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COMPILATION NUTRITION

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ARTICLES WRITTEN BY ALAN ARAGON, LYLE


MCDONALD AND WILL BRINK

COMPILATED BY @fitnessoriol

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A Primer on Nutrition Part 1
In many articles on the site, I go into a rather great deal of detail on various aspects of human nutrition and
the various nutrients that comprise it. However, I find that it’s often exceedingly useful to go back to basics
and discuss the fundamentals (this applies to all topics, not just nutrition). Where appropriate, I’ll point
readers to other articles on the site (or my books) which discuss a given topic in more detail than I want to
cover here.
To keep the piece manageable, I’m going to divide it into two parts with Part 2 being run on Thursday. Today
I want to look at the issue of essential vs. non-essential nutrients as well as protein and carbohydrates. On
Thursday, I’ll tackle the issue of dietary fats along with everything else (fiber, alcohol, vitamins and minerals).

Essential vs. Non-essential Nutrients

The body has a requirement for somewhere around 60 nutrients on a daily basis for normal
functioning. Please note: as nutritional science has progressed, it’s now become apparent that many, many
more nutrients may contribute to optimal health, although they are not necessarily required for survival. Put
differently, you can live without consuming them but you might be healthier or perform better if you did eat
them.
I should also mention that this list of 60 nutrients includes things such as air and water that, while they aren’t
considered as nutrients per se, are usually not an issue. Put differently, if you’re having issues obtaining
adequate amounts of air or water, you have bigger problems to deal with.
Of more relevance to today’s article, nutritional science often groups nutrients into the categories of essential
and nonessential (recently the terms indispensable and dispensable have come into vogue) which is what
I’d like to discuss next. For quick summary, there are roughly 8 essential amino acids, 2 essential fatty acids,
a host of vitamins and minerals and a few others substances that are required on a daily basis. You might
note that carbohydrates were not listed as an essential nutrient, a topic I’ll come back to below.
So what is an essential nutrient as opposed to a non-essential nutrient? I’m actually going to answer that
by explaining what a non-essential nutrient is first. Contrary to what it sounds like, the term non-essential
(or dispensable) doesn’t mean that the nutrient isn’t essential for life; rather, it’s not essential that the nutrient
be obtained from the diet itself.
Translating that into English, there are some nutrients (such as glucose, certain fatty acids and just over half
of the amino acids) that can be made in the body from other sources. For example, many amino acids can
be made in the body via metabolism from other amino acids; as well, glucose can be made in the body from
a number of different substances. So while these nutrients are essential for life and survival, it is not
essential that they be obtained from the diet.
At the same time, there are nutrients that cannot be made by the body (the vitamins and minerals are
examples, so are the essential fatty acids and roughly the other half of the amino acids) and are hence
considered essential nutrients. That is, it is essential that they be obtained from the diet (generally on a daily
basis).
In short, to be considered essential, a nutrient must meet two primary criteria:
1. That nutrient is required for survival
2. That nutrient cannot be made in sufficient quantities (or at all) by the body
So if a nutrient isn’t required to keep you alive, it’s not essential (even if consuming it improves health or
what have you). If it’s required for life but the body can make sufficient amounts of it, it’s still not essential

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to get it from the diet; hence it is not an essential nutrient. Only when a given nutrient is both required for
survival and can’t be made in the body in sufficient amounts is it an essential nutrient in terms of what I’m
talking about here.
Although I want to keep this piece focused on the basics, I should probably mention one odd exception which
is Vitamin D (currently getting a lot of press, and for good reason, in various places). Vitamins and minerals,
generally, can’t be made in the body and must come from the diet. But while Vitamin D can be obtained
from the diet (many foods are fortified with it), and is an essential nutrient, it is actually made by the body in
response to sunlight hitting the skin.
I want to make it clear that the above is a bit of a simplification and the topic of essential and non-essential
nutrients can be made considerably more complicated. For example, some nutrients can be considered
conditionally essential. That is, under normal conditions, the body may make plenty of a given nutrient
(meaning that it is not required that the nutrient come from the diet) but under other conditions the body
needs more than it can make. Under those conditions (usually involving things like disease and severe
trauma), a nutrient that is normally non-essential becomes essential (must be obtained from the diet). Hence
conditionally essential.
.

Protein
The word protein come from a Greek word meaning “the first” which is meant to signify its primary role in
human nutrition. While you can survive rather extended periods without carbohydrate or fats in the diet, a
long-term lack of protein intake leads to a loss of body tissue (muscle and organ protein), function and
eventually death.
Whole dietary proteins are made up of smaller units called amino acids of which ~20 occur in the diet (there
are many more that occur in the body). Of those 20 or so amino acids, roughly eight are considered essential
meaning that they must come from the diet on a daily basis. Under certain conditions, such as stress and
trauma, some amino acids also become conditionally essential; glutamine is perhaps the most commonly
cited example with much higher amounts that can be made in the body being required under those kinds of
conditions. There are other examples but few would be relevant outside of some very very specific situations
(usually involving severe malnutrition or disease).
A primary distinction between protein and carbohydrate/fat is that only protein contains dietary nitrogen
(which is technically an essential nutrient). Since humans can’t ‘fix’ nitrogen from the air like plants, we have
to obtain it from the diet. And that nitrogen is found in the individual amino acids that make up whole food
proteins. Also, while there can be some interconversion of protein (more accurately, amino acids) to carbs
or fat (this last one is very rare), neither carbs nor fat can be made into amino acids.
Proteins/amino acids have a number of crucial roles in the human body but most of them are structural
(meaning the protein is used to build things). Many hormones are made of protein (some examples are IGF-
1 and Growth Hormone), your organs, muscles, skin and hair all contain protein; protein has numerous other
roles in the body as well. Protein can also be used to produce energy in the body, usually by conversion to
other nutrients (almost always glucose). For example, during long-term aerobic exercise, the breakdown of
amino acids (specifically leucine) can provide 5-10% of the total energy generated.
Something to note is that, in contrast to carbohydrate (which is stored in both muscle and liver) and fat (which
is stored on your butt and stomach), there is no real storage form of protein unless you count the relatively
small amount floating around in the bloodstream and the protein that makes up your muscles and

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organs. But this isn’t a true storage form like for carbohydrates and fats since, in general, breaking down
body protein is a bad thing (as I mentioned above).
In the diet, protein is found to some degree in almost all foods with the exception of pure fats like vegetable
oils and such and some totally refined carbohydrates such as candy (e.g. jelly beans). Fruits and vegetables
contain fairly small amounts of protein (perhaps a gram or two per serving) while beans and nuts can contain
significant amounts of protein. But most people in modern society get their protein from animal based
products: meat (red meat, chicken, fish), milk, cheeses, etc.
In terms of caloric content, protein has traditionally been assigned a value of 4 kilocalories/gram (~16.8 kj/g)
but this is currently a topic of some debate. Because of how it is digested and assimilated in the body, at
least one researcher is suggesting strongly that protein be given a lower caloric value (roughly 3.2 kcal/g or
13 kj/g) than the traditional value.
I covered a great deal of detail regarding different dietary proteins on the site in What’s Are Good Sources
of Protein; of course The Protein Book also discusses this topic in detail.

Carbohydrate

The term carbohydrate refers to a number of different organic compounds ranging from simple sugars (e.g.
glucose and fructose) to disaccharides (e.g. sucrose, lactose) all the way up to starches (long chains of
individual carbohydrate molecules bound together). Because of it’s chemical structure, you will often see
carbohydrate abbreviated as CHO (for carbon, hydrogen, oxygen).
In the body, carbohydrate’s role is primarily energetic, that is it provides energy (through breakdown) in
various tissues of the body. Most tissues in the body can use glucose for fuel and, quite in fact, most will
use glucose if it is available (they will switch to using fats or ketones if glucose is not available in sufficient
amounts). A few tissues of the body can only use glucose for fuel.
And while the above might suggest that dietary carbohydrates are essential, this isn’t the case. Recall from
the discussion above that, to be considered essential a nutrient must not only be required by the body but
cannot be made in sufficient quantities. And, as I’ve also discussed elsewhere, the body is able to produce
some carbohydrate from the breakdown of other nutrients, specifically about half of the amino acids, glycerol
(the backbone of both dietary and body fat) and lactate.
In general this process (called gluconeogenesis which simply means the production of new glucose) is able
to cover the body’s basic daily needs. As well, with low-carbohydrate diets, there is a whole body shift in
fuel use from carbs to fats and ketones which reduces carbohydrate requirements. This is discussed to
some degree in nearly all of my books but the greatest detail can be found in The Ketogenic Diet.
I would finish by noting that high-intensity exercise tends to increase carbohydrate requirements beyond
what the body can make putting carbohydrates into the conditionally essential category I discussed above
(e.g. the body needs more than it can produce itself). For those individuals who wish to perform high-
intensity activity such as intensive weight training or even high intensity metabolic work, some amount of
carbohydrates generally becomes required in the diet. The issue of daily carbohdyrate requirements is
discussed in much more detail in How Many Carbohydrates Do You Need?
Carbohydrates can be stored within the body in the liver or muscle as glycogen (a long chain of glucose
molecules bonded to each other) and is found in small amounts (~5-10 grams total) as free glucose in the
bloodstream. Liver glycogen exists primarily to help maintain blood glucose levels while glycogen within
skeletal muscle can only be used by the muscle that it’s stored in; it can’t be released back into the
bloodstream.

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Dietarily, traditionally carbohydrates have been divided somewhat simply into two major categories (this is
especially true in athletic subcultures but is often used generally) which are fibrous and starchy. Please note
that this is mainly a division of convenience but it tends to be useful practically so I’ll stick with it.
Fibrous carbohydrates generally refers to vegetables which, with a few exceptions, tend to contain very small
amounts of digestible carbohydrate while containing a lot of fiber. Pretty much any vegetable you care to
name (with the handful of exceptions mentioned next) will fall into this category of carbohydrates and it’s
often stated that you can eat these types of carbohyrates ‘without limit’ due to their generally low caloric
content. I’ll come back to this shortly.
Starchy carbohydrates are, more or less, everything else: breads, pasta, rice, and grains, basically any
carbohydrate that contains a good bit of digestible carbohydrate. I should note that there are a few starchy
vegetables such as carrots, peas, corn and potatoes: vegetables which contain larger amount of digestible
carbohydrate and which need to be counted as starches in terms of real-world meal planning. Fruits, while
not technically a starch, are usually grouped with starches since they contain quite a bit of digestible
carbohydrate (the majority of which are simple sugars).
Explaining the caloric value of carbohydrates can be somewhat confusing. Starchy carbohydrates are
generally assigned an average value of 4 calories per gram (16 kj/g) although this can vary slightly from food
to food. Fiber is where it gets more confusing; as I recently discussed in Fiber – It’s Nature’s Broom, some
types of fiber can be broken down to other things in the intestine and, recently, fiber has been given a caloric
value of 1.5-2 kcal/g (~6.3-8.4 kj/g). While this isn’t a large amount given most people’s average fiber intake,
for people who are eating enormous amounts of vegetables (which don’t just contain fiber, mind you), the
calories can start to add up.
And with those topics covered, I’ll stop here for today. On Thursday, I’ll take another quick look at dietary
fats along with the ‘everything else’ category of human nutrition: alcohol, vitamins, minerals and fiber (again).

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A Primer on Nutrition Part 2
On Monday, in A Primer on Nutrition Part 1, I discussed essential vs. inessential (aka indispensable vs.
dispensable) nutrients along with the basics of both protein and carbohydrates. Today I want to finish taking
a look at the basics of nutrition by looking at fat/cholesterol and then wrapping up ‘everything else’ including
alcohol, vitamins/minerals and fiber (somewhat separate from vegetables).

.Fat and Cholesterol

Although I recently examined Fat and Cholesterol in some detail in A Primer on Dietary Fats Part 1 and A
Primer on Dietary Fats Part 2 back in May, I want to take a briefer, more streamlined look at them in today’s
article. Readers wanting more details can click the above links.
Even though they are chemically and nutritionally distinct substances, dietary fat and cholesterol are so
linked in the minds of most people that I’m going to discuss them together. As well, along with the never-
ending debate over carbohydrates in the diet, the issue of dietary fats is one of almost constant debate in
both nutritional sciences and among nutritional experts. I’m not going to get into those debates in any real
detail here (since it’s about the basics) but interested readers can read Carbohydrate and Fat Controversies
Part 1 and Carbohydrate and Fat Controversies Part 2 if they want more details.
First let met get cholesterol out of the way since I don’t actually have a tremendous amount to say about it.
Cholesterol plays a number of roles in the body not the least of which is involvement in the structure of cell
membranes in the body. As well, cholesterol provides the ‘base’ for the steroid hormones, testosterone,
estrogen, progesterone and others are synthesized out of cholesterol in the body.
Of course, when most people hear the word ‘cholesterol’, they immediately think heart disease and, certainly,
one aspect of cholesterol metabolism in the body is that it can cause atherosclerotic plaques (essentially the
cholesterol builds up in arteries, potentially blocking blood flow).
Please note: I am vastly simplifying a much more complicated topic.
And this tends to be the source of much confusion, especially among the lay public, about diet; they confuse
dietary cholesterol intake with blood cholesterol (aka blood lipid) levels. I’d note, and again this is more
complicated than I want to cover here, that blood cholesterol levels are only one of several contributors to
the issue of heart disease. Others contribute.
But there tends to be an idea that dietary cholesterol intake is a primary determinant of blood cholesterol
levels when, simply, this isn’t generally the case. Certainly a percentage of people seem to be sensitive to
dietary cholesterol intake (in terms of how their blood cholesterol responds) but, in the majority, dietary
cholesterol intake per se has very little impact on blood lipid levels.
As well, your body generally makes more cholesterol (in the liver) than you eat in a day; that’s unless dietary
cholesterol intake is exceedingly high. Additionally, the live modifies how much cholesterol it produces
depending on daily intake. If dietary cholesterol intake goes up, the liver makes less; if dietary cholesterol
intake goes down, the liver makes more. The body is smart that way.
Rather, the types and amounts of dietary fat being consumed play a far larger role in blood lipid
levels. Frankly, I don’t have much more to say about dietary cholesterol, it’s simply not that big of a deal
unless you are in that small percentage of folks who are sensitive to it. Rather, I want to talk a bit more
about dietary fats.
Of course, a primary role of dietary fats in the body is to be used for energy and it was assumed for many
years that this was the only real role of fat, to provide energy storage. This was especially true of stored

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body fat which was thought for decades to provide only a passive storage depot of energy; rather it turns out
that fat cells do much more in the body, producing hormones and such that affect myriad processes
elsewhere in the body (a topic I’ve discussed at length on the site and in my books)..
Fats are also found in the cell membranes of various tissues (and the type of fat stored there can affect
various cellular processes). As well, fats can be used to make eicosanoids, chemical messengers made
from specific fatty acids that affect numerous biological processes. Specific dietary fats can also affect gene
expression in certain cells, impacting on things like fat storage and oxidation and many others.
From an energetic standpoint, fats are typically assigned a caloric value of 9 kilocalories/gram (~38 kj/g);
there are slight differences between specific fatty acids however. As well, there is some evidence that
different fats have a slightly different propensity to be stored vs. burned after consumption although the
differences between the fatty acids are relatively small. I’d mention for completeness that dietary cholesterol
has no energetic value to the body.
The biggest controversies regarding dietary fat usually revolve around the health effects of its consumption.
It’s not unfair to say that, for many years now, dietary fat has been the whipping boy of the nutritional world
(though carbohydrates are taking that role in recent years): fat makes you fat, fat causes heart disease and
cancer, fat is probably responsible for terrorism in the US and the decline in the family unit. You name it and
the problem has probably been blamed on dietary fat by certain groups. At the other extreme are folks who
argue that dietary fats have no health negatives, that they can be consumed effectively without limit or
concern.
As with so many extremist stances, the truth is a little different and tends to lie somewhere in the middle.
In the past ten years or so, the issue of fat quality (i.e. type of fat) has become just as important as that of
fat quantity (i.e. amount of fat). Simply put: all fats are not the same in terms of their effects on health. As
well, whether a specific fat is good, bad or neutral in terms of health depends to a great degree on the
context in which it’s eaten; this is a concept that neither extremist group can seem to wrap their heads
around.
Whether the person is active or inactive, fat or lean, the rest of their diet, gaining or losing weight, and a host
of others all contribute to the effect a given fat will have on the body. I’m not going to go into further details
here, I’d suggest you read Carbohydrate and Fat Controversies Part 1 and Carbohydrate and Fat
Controversies Part 2 for more details.
In any case, dietary fats are generally divided into four distinct categories, I’m going to look at each in brief
next.

Trans-Fats
Trans-fatty acids are a man-made fat made by bubbling hydrogen through vegetable oil to make it semisolid
with a longer shelf-life; I’d note that there are naturally occurring trans-fatty acids found in foods as
well. Margarine is probably the example most readers are familiar with although trans-fatty acids (also called
partially hydrogenated vegetable oils) are commonly found in most processed foods (there is currently a big
push for trans-fat free foods to be produced commercially).
Of the four types of fats, trans-fatty acids have the least amount of debate around them; their intake at even
low levels tends to have exceedingly detrimental impacts on things like blood lipid levels and diabetes
risk. Due to the high reliance on processed foods in the modern diet, trans-fatty acid intake is thought to be
at least one part of the problems being seen in the modern world (note: there are certainly other contributors).

Saturated Fats

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Saturated fats are found almost exclusively in animal products (two exceptions are coconut and palm kernel
oil) and are solid at room temperature. Traditionally, the impact of saturated fats on blood lipid levels and
heart disease risk has been thought to be universally negative but it turns out to be much more complicated
than this. While some saturated fats do reliably raise blood cholesterol levels (primarily due to an impact on
liver metabolism), others are completely neutral. Anybody interested in this topic may wish to read the
journal article Saturated Fats: What Dietary Intake.
As well, as I mentioned above there is far more to heart disease risk than just blood cholesterol levels. And,
as also noted above, the overall impact of any fat (including saturated fats) on health risk depends on the
context of their intake. In one context (e.g. low fruit/vegetable/anti-oxidant intake, high stress, inactivity, high
body fat, excessive total energy intake), a high saturated fat intake may be exceedigly harmful. In a different
context (e.g. high fruit/vegetable intake, low stress, high activity, low body fat, appropriate energy intake),
they may have no effect. I hope that any of the pro-saturated fat folks reading this article will read this
paragraph a couple of times before they leave me comments about how I’m anti-saturated fats.
I’d finish by noting that saturated fats are not an essential nutrient. They aren’t required for life and, even if
they were, the body can produce them from other sources.

Monounsaturated Fats
Monounsaturates are present in almost all foods which contain fat and are liquid at room temperature (quite
in fact, the majority of fat in most ‘high-fat’ foods is monounsaturated). Olive oil is arguably the most well-
known of the monounsaturated fats and has received a great deal of attention as a relatively healthy fat.
Monounsaturates have a neutral, if not beneficial, effect on health and it’s thought that the high olive oil
consumption among Mediterraneans is partly responsible for their robust health (there are ceertainly other
factors involved here).
Like saturated fats, monounsaturated fats are not an essential nutrients, they may confer health benefits but
they are not required for survival.

Polyunsaturated Fats
Polyunsaturated fats are found primarily in vegetable oils and are liquid at room temperature. They are
generally claimed to have a positive effect on human health although, as always, things are a little more
complicated than that. Polyunsaturated fats come in two major “flavors”, referred to generally as omega-
three and omega-6 fatty acids.
The omega-3 fatty acids include a number of different fatty acids including the ‘parent’ fatty acid alpha-
linoleic acid (ALA) found in things such as flax oil along with the fish oils (EPA and DHA). I would be surprised
if anybody reading this hadn’t heard of the fish oils or their benefits. In sum, fish oils do just about everything,
they decrease inflammation, help with depression (especially while dieting), decrease enzymes involved in
fat storage and increase the levels of enzymes involved in fat burning. I’d finish by noting that the conversion
of ALA to EPA is fairly low and the further conversion of EPA to DHA is basically insignificant. For this
reason, taking preformed fish oils is generally required to impact body levels of EPA/DHA to any great
degree.
Similarly, the omega-6 fatty acids include a host of different fatty acids including linolenic acid (LA), found in
many vegeteable oils, along with things such as arichnidonic acid (AA) which are made from metabolism or
LA within the body.
I’d note that both the w-3 and w-6 fatty acids are part of a more general class of fats called essential fatty
acids, that is they are essential nutrients; that is, as explained in A Primer on Nutrition Part 1, they are

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required for life and cannot be made within the body. In the modern diet, it’s generally pretty easy to get w-
6 fatty acids through the diet, unless folks consume fatty fish, w-3 are much harder to come by (hence the
general need for some type of supplementation).
Now, there is some controversy over w-3 and w-6 intake with excessive w-6 intake being thought to cause
some health problems (such as inflammation). In the modern diet, the intake of w-6 fatty acids to w-3 is
about 20-25:1 or so and it’s been thought that a ratio closer to 1:1 or 4:1 would be healthier with the excessive
w-6 intake causes problems. Some groups have even blamed current health problems less on saturated fat
intake and more on a high w-6 intake due to the use of vegetable oils in the modern diet.
However, as I discussed in more detail in A Primer on Dietary Fats Part 2, current research calls this into
question with mortality rate generally decreasing with increasing w-6 intake and some research suggesting
no real impact on inflammation of ‘excessive’ w-6 intake. I’m not going to go into any real detail here, please
read that article for more information.

Dietary Fats: Summing Up

I expect the issue of dietary fats to remain an area of controversy for some time to come. New functions of
dietary fats are still being found and the impact of dietary fats on overall health (not simply limited to heart
disease) will continue to be examined. As I noted above, I feel that the impact of a given type of dietary fat
on health is entirely context dependent, an issue that the individuals involved in both sides of the debate
seem to have missed. Since I’ve discussed this in detail in other articles linked in this piece along with
touching on it briefly above, I won’t discuss it further.

Everything else: Fiber, Alcohol, Vitamins and Minerals

I recently looked in some detail at fiber in Fiber – It’s Nature’s Broom and only want to touch on it in brief
here. While not an essential nutrient (e.g. you won’t die if you don’t eat it), fiber does play a number of
important roles in human health in nutrition. If nothing else, high-fiber intakes tend to keep people full and,
generally, high-fiber diets are associated with greater weight loss or at least less weight gain. There are
other effects as well, see the above article for the details.
Fiber can be subdivided into a variety of different categories but, practically speaking, the main ones of
importance are soluble and insoluble fiber. Soluble fibers mix in water and take up a lot of space in the
stomach, it also holds food in the stomach longer: this tends to increase feelings of fullness. In contrast
insoluble fibers don’t mix with water but help with bowel regularity and keep the colon healthy.
Both types of fiber appear to be important to human health and both are found in varying degrees in foods
such as fruits and vegetables (grains have varying amounts of fiber depending on how processed they are).
Alcohol isn’t really a nutrient in that it provides nothing of actual nutritional value except for calories. Even
there, alcohol intake doesn’t seem to scale with predicted weight gain although nobody is quite sure why
this is the case. Some studies suggest that some alcohol calories go ‘missing’ but nobody can figure out
where they are. Alcohol also tends to impact on metabolism in a way that can promote fat gain. Certainly
alcohol can have a place in any diet (with a large body of research suggesting that moderate alcohol intake
has health benefits depending on the specifics) but excessive amounts can cause varying problems.
Finally there are vitamins and minerals which serve innumerable roles in the body and which include a host
of essential nutrients (again, can’t be made in the body, required for life). Minerals such as calcium are
structural (e.g. bone) along with being involved in cellular signalling. Iron is involved, of course, in the

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formation of red blood cells, important for overall health and performance. Zinc is involved in immune system
function and a host of other processes (including appetite regulation). Vitamins act as nutritional co-factors
and are necessary for the body to function optimally.

Vitamins and minerals are found to some degree in all foods with amounts and types depending on the
specific food. Fruits and vegetables tend to be nutritional powerhouses in this regards but some vitamins
and minerals are optimally consumed in foods of animal origin (for example, the iron in red meat is absorbed
roughly ten times better than the iron in vegetable source foods and B12 can only be found ‘naturally’ in
animal source foods).
In that context, I’d note that a class of nutrients called phytochemicals are only found in plant foods and there
is currently a great deal of interest in the health benefits of these compounds. They aren’t essential by any
stretch but may confer health benefits. Various anti-oxidant nutrients are also found in varying amounts in
these foods and, while anti-oxidant supplementation has generally shown little to no real health benefits,
diets high in food-based anti-oxidants have been found to confer many health benefits.

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A Primer on Dietary Fats – Part 1
For the past 30 years or so, ever since people started talking about cholesterol and heart disease, there has
been a combination of concern and confusion over the topic of dietary fats in the diet. In this article, I want
to take a look at some of the topics involved to see if I can help to clear up some of the confusion.
Today I want to look at some general issues, including the major categories of dietary fats, the difference
between cholesterol and triglycerides, and then look briefly at the impact of dietary cholesterol on blood
cholesterol levels. On Friday, in Part 2, I’ll look in some detail at the different types of dietary triglycerides
and address some of the current controversy over their effects on health.

Triglycerides, Cholesterol and Everything Else

While people tend to throw around the term dietary fat somewhat loosely, the fact is that not all of the fat
that we consume on a daily basis is the same. And here I’m not talking about saturated vs. unsaturated
fats. Quite in fact, dietary fats (more generally known as lipids) come in distinct chemical types.
Now, the primary two that folks eat on a day to day basis are triglycerides (TGs) and dietary cholesterol with
dietary triglyceride contributing the bulk (over 90% of the total) of the dietary fat that we consume on a day
to day basis.
However, there is also a small amount of lipid that come from sources such as various phospholipids and
other fat based compounds; since they tend to make up a very small percentage of the total daily fat intake,
I’m not going to spend any time discussing them.
Rather, I want to focus primarily on dietary triglyceride and cholesterol.
For completeness, I should note that there are also dietary diglycerides (two fatty acids bound to a glycerol
molecule) which may have some slight fat loss benefits. In the Ultimate Diet 2.0, I mentioned Enova Oil
(which is apparently no longer being produced), a diglyceride oil that can increase fat loss slightly over the
length of a diet. Dietary diglycerides may also be a bit more filling in the short-term (compared to dietary
triglycerides) due to how they are processed in the body; this may also give them some benefit for dieting.
For true completeness, there has also been some recent interest in the use of free fatty acids in terms of
appetite control, although I’ve yet to see a commercial product that contained them. In any case, the primary
source of dietary fat in the diet will be dietary triglycerides with cholesterol playing a secondary role.

Triglycerides and Cholesterol: What’s the Difference?

For several decades now, many people have been confused about dietary triglyceride versus dietary
cholesterol, with many seeming to think that they are identical or at least related.
The confusion most likely stems from the extreme focus on blood cholesterol and heart disease risk that
really started in the late 1970’s and 1980’s. Since many of the foods that people were becoming concerned
with (e.g. ‘high-fat’ meat or eggs) tend to contain a lot of dietary cholesterol as well, people seemed to link
the two substances in their minds.
And while it’s true that high-fat animal foods are generally also high in cholesterol, this isn’t always the case;
some low-fat foods (such as certain types of shellfish) can actually be high in cholesterol despite being low
in total fat content. However, in general, high-fat animal foods tend to be high in cholesterol as well and I
suspect this is where much of the confusion about the two stems from.
But structurally and chemically, dietary fats and cholesterol couldn’t be more different.

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Cholesterol is what is termed a steroid molecule. It has a complex ring like structure and one of it’s main
functions in the body is as a precursor molecule for other compounds with a similar structure (such as
testosterone, cortisol, estrogen, progesterone and others).
In contrast, the dietary fats that make up the majority of our daily intake are more accurately called
triglycerides (or tri-acyl-glycerols if you want to be fancy). They have a chemical structure where three fatty
acid chains (‘tri’ = three) are bound to a molecule of glycerol (which is where the ‘glyceride’ part of the name
comes from)..

Of Dietary Cholesterol and Blood Cholesterol

As I mentioned above, I think that part of the confusion over dietary fat and cholesterol came out of the focus
on blood cholesterol levels and heart disease that really got rolling in the 70’s and continued well into the
80’s. And when that was combined with the fact that many of the ‘off-limit’ high-fat foods (such as eggs)
were also high in dietary cholesterol, it’s actually easy to see where the confusion comes from.
Now I’m actually not going to get into the big debate/argument/controversy over the role of blood cholesterol
in heart disease. Sufficed to say that I think both groups of extremists, both those that think blood cholesterol
is the primary concern as well as those who think it is no concern at all are misguided; I find this is true of
most extremist stances. At best, I think blood cholesterol levels are one of several factors that contribute to
the development or not of heart disease; but there are certainly others. I’ll leave the topic at that.
In any case, what is often forgotten is that the body actually makes more cholesterol (in the liver) than most
people would eat in a day. As well, the body tend to adapt to changing dietary cholesterol intakes. When
you eat less dietary cholesterol, the body will make more; when you eat more, the body makes less.
And this is why a lot of the concern over dietary cholesterol per se is a bit misplaced; for most people the
intake of dietary cholesterol has little to no impact on blood cholesterol on the first place. It’s worth
mentioning that a certain percentage of people seem to be responders to dietary cholesterol intake in terms
of how their blood cholesterol is affected.
Rather, it is the intake of specific types of triglycerides that seems to have a far larger role on blood
cholesterol levels; exercise also plays a role and there are strong genetic factors which determine blood
cholesterol levels as well.
But since that discussion of different types of dietary triglycerides is going to be fairly long, I’m going to save
it for Part 2 which I’ll post on Friday.
Read A Primer on Dietary Fats – Part 2.

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A Primer on Dietary Fats – Part 2
In A Primer on Dietary Fats – Part 1, I looked at some basic concepts related to dietary fat/lipids including
the different primary types of lipid (triglycerides, cholesterol and the ‘other stuff’) as well as the difference
between triglyceride and cholesterol. Finally, I looked at the issue of dietary cholesterol and blood
cholesterol briefly.
Today I want to finish up by looking at more detail at the issue of dietary triglycerides. As I mentioned in
Part 1, dietary triglycerides (TGs) make up the bulk of the fat that we consume in a day, providing over 90%
of our total fat intake. Therefore, understanding what the different ‘types’ of TG are along with how they
affect the body is important.

Types of Dietary Triglyceride

As I mentioned in A Primer on Dietary Fats – Part 1, a fat/TG molecule consists of three fatty acid chains
bound to a backbone molecule of glycerol. And while people tend to talk about different types of fats (e.g.
saturated fat or unsaturated fat), it’s actually the specific fatty acids that differ in terms of their chemical
structure. For simplicity, I’ll simply refer to the different types of ‘fats’ and leave it at that.
Things such as chain length, degree of saturation and chemical conformation all go into distinguishing one
fat from another but I’ll try to avoid boring people with that level of detail. Fats are pretty much universally
subdivided into four primary categories which are
1. Trans-Fat
2. Monounsaturated Fat
3. Saturated Fat
4. Polyunsaturated fat
And there’s no reason for me to go against that grain. Below, I want to look briefly at each type of fat, where
it’s found in the diet, what types of effects it has on the body, and address any of the lingering controversies
that currently exist.

Trans Fat

Since there is little to no debate or controversy over the role of trans-fatty acids (often abbreviated TFAs) in
human health, I figured I’d tackle it first. In recent years, it’s fairly safe to say that trans-fatty acids (aka
partially hydrogenated vegetable oils) have gotten the most press in terms of their negative health
effects. And there is much truth to this.
Trans-fatty acids are a semi-solid fat which are made by bubbling hydrogen through vegetable oil (hence
the name partially hydrogenated vegetable oil). This is done to make vegetable oils (which can often be
unstable and go rancid) more shelf-stable; that’s important when foods sit on the shelf for a long
time. Margarine is a classic example that most will be familiar with, a semi-solid made by bubbling hydrogen
through vegetable oil.
And while there are naturally occurring trans-fatty acids that occur in small amounts in foods, quantitatively
most of the trans-fats that people will consume will come from the intake of processed foods.
The problem is that the process of partial hydrogenation changes the chemical structure of the vegetable oil
from what is called a cis-configuration (the form that most dietary fatty acid are found in) to a trans-
form. Hence the name trans-fatty acid. Without going into a lot of unnecessary details, simply accept that

13
the body is meant to use cis-fatty acids, not trans-fatty acids; it’s got to do with the chemical shape of the
fatty acid.
For that reason, intake of a large amount of trans-fatty acids causes a number of problems in the body.
Quoting from a a recent review on the metabolic effects of trans-fatty acids:
TFA [trans-fatty acid] consumption causes metabolic dysfunction: it adversely affects circulating lipid levels,
triggers systemic inflammation, induces endothelial dysfunction, and, according to some studies, increases
visceral adiposity, body weight, and insulin resistance…Consistent with these adverse physiological effects,
consumption of even small amounts of TFAs (2% of total energy intake) is consistently associated with a
markedly increased incidence of coronary heart disease.
Now, I’m rarely a fan of nutritional absolutes but this is one place where I’m willing to make one: trans-fatty
acids really have no place in human nutrition and this is a place where there is little disagreement in the
field. They provide absolutely no benefits that I’m aware of and their impact on human health would appear
to be wholly negative.

Monounsaturated Fat

If there is another fat over which there is really no argument or controversy in the field it’s monounsaturated
fat. At worst, monounsaturated fats are fairly neutral from a health perspective (especially in terms of the
effects on blood cholesterol levels) and there is also evidence that intake of monounsaturated fats may have
health benefits.
Quite in fact, it’s thought that part of the benefit of various Mediterranean diets is related to the large intake
of olive oil (arguably the primary dietary monounsaturated fat) in the diet. It’s certainly worth mentioning that
other aspects of their diet such as a large vegetable/anti-oxidant intake is assuredly contributing to the good
health observed; that is, it’s not just the olive oil.
In any case, outside of being a source of calories (excessive calories causing fat gain, of course), there’s no
real indication that mono-unsaturated fats have any real negatives in terms of human health.
The primary mono-unsaturated fat is oleic acid which is found in very high amounts in olive oil (hence the
name). It’s worth noting that oleic acid actually tend to be the primary fatty acid found in most ‘high-fat’ foods
(you can check this for yourself at the USDA database) including the ones that most think of as containing
large amounts of saturated fat. A couple of examples appear in the table below.

Food Serving Size Total Fat Saturated Fat Monounsaturated fat

Ground Beef 100 grams 10 grams 4 grams 4 grams

Whole Egg 1 Large 5 grams 1.5 grams 2 grams

Because of it’s prevalence in the food supply, olive oil will often make up a fairly large proportion of someones
total dietary fat content without much effort. However, when people are looking to ‘add fat’ to their diet (for
whatever reason), it would be hard for them to go wrong in using a source of mono-unsaturated fat or Olive
oil. It can be added to salads and I know of some brave souls who throw it directly into protein drinks when
they need to raise calories.

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I’d mention that, for people (like me) who don’t like the taste of olive oil, there is a high oleic safflower oil
available for people who want to add more oleic acid to their diet.

Saturated Fat

For a couple of decades now, saturated fat has been the veritable whipping boy of the nutritional world
(forced out of the number one position by trans-fatty acids only recently). Blamed for everything in the world
including heart disease and probably terrorism, saturated fats have received the brunt of negative press
when it comes to the issue of dietary fats.
However, in recent years, there has been a counterargument regarding saturated fat intake that they are of
no health risk at all, that the real problem is with excessive polyunsaturated fatty acids/vegetable oils
(discussed next), etc.
This has led to a lot of confusion for people.
Now, anybody who has regularly read this site knows that I tend to shy away from nutritional extremism, I
usually find that whenever there are competing extremist positions, the truth generally lies somewhere in the
middle.
This is certainly the case for saturated fat in my opinion. Now, for anybody who reads nutritional research,
there is little to no argument that saturated fat can cause a variety of problems. Whether you’re looking at
blood lipid levels, inflammation, etc. there’s really little debate in the field and there are a zillion and one
studies that support that excessive saturated fat intake can cause a variety of health problems.
However, as always it gets more complicated.
A a huge part of the problem is that the term saturated fats actually refers to a category that includes a
number of different fatty acids. Lauric acid, palmitic acid, stearic acid and many others are all included under
the general heading of saturated fat.
And at least part of the problem is that they don’t all act the same way in the body. Some specific saturated
fatty acids have distinctly negative effects on the body, others do not. For anybody truly interested in the
science of this topic, I’d recommend the paper Saturated Fats: What Dietary Intake which examines the
issue in some detail.
As well, as I have discussed in other articles on this site such as Carbohydrate and Fat Controversies Part
1 and Carbohydrate and Fat Controversies Part 2, I think there is a huge issue of context in terms of the
effect of saturated fat (or any nutrient for that matter) on overall health.
For someone who is lean, active, eating plenty of fruits and vegetables, who is in caloric balance there
appears to be no real danger (in a health context) to an increased intake of saturated fats. One study I recall
in cyclists found that, as long as they were in caloric balance, an increase intake of saturated fats had no
impact on blood cholesterol one way or the other.
It’s worth mentioning in this context that some research suggests that saturated fat is required for optimal
hormone levels (e.g. testosterone) so trying to reduce saturated fat excessively may be a mistake for athletes
in the first place.
But not all individuals are lean, active athletes who are eating lots of fruits and vegetables who are in caloric
balance. For someone who is overweight (which is an inflammatory state in and of itself), inactive (which
has a host of negative health effects), is under a lot of stress, not eating sufficient fruits and vegetables, etc.
, saturated fats may have a very different impact on the body.
There is often also an impact of weight loss or weight gain in terms of how saturated fats affect blood lipid
levels; in general when weight is lost, blood cholesterol levels improve almost irrespective of the type of fat

15
consumed. But when weight is being gained or even maintained, often blood cholesterol levels worsen with
a high saturated fat intake.
I should mention that the changes that typically occur in blood cholesterol levels with changing saturated fat
intake tend to occur in both the ‘good’ and ‘bad’ cholesterol fractions. That is, when saturated fat is reduced,
both good and bad cholesterol typically goes down and vice versa. Therefore the overall impact on health
risk is a bit more complex than many think.
In any case, I think that saying that saturated fats are good, bad or neutral is too simplistic. Context, as
always, is important and I find that many of the extremists in each group tend to forget that. What is
drastically unhealthy in one context may be neutral or at least irrelevant in another. Which still won’t stop
some very silly comments from appearing on this article as people accuse me of being ‘anti-saturated fat’.
In any case, finishing up, saturated fats are found more or less exclusively in animal source products and
are typically solid at room temperature. A couple of odd exceptions are coconut and palm kernel oil (both
of which contain a lot of saturated fat but primarily in the form of medium chain triglycerides, discussed
below). As well, milk fat contains a decent amount of saturated fat.
From a body fat perspective, it’s at least worth mentioning that saturated fats tend to be stored a bit more
easily than polyunsaturated fats (more accurately, when polyunsaturated fats are consumed, the body tends
to burn them off a bit more readily) but the effect is not massive.

Polyunsaturated Fat

And finally we come to polyunsaturated fats. Almost always liquid at room temperature (unless found in
foods), the key polyunsaturated fats are the omega-3 and omega-6 fatty acids (which you’ll often see referred
to as w-3/w-6 or n-3/n-6). This naming simply refers to the structure of the individual fatty acid and it’s not
worth going into any more details than that.
The two primary polyunsaturated fats are alpha-linolenic acid (ALA, not to be confused with the supplement
alpha-lipoic acid) which is an w-3 fatty acid and linoleic acid (LA) which is an w-6 fatty acid. Among other
things, ALA and LA have the distinction of being the two essential fatty acids (EFAs), that is it is essential
that they be obtained from the diet for optimal health. This is in contrast to all of the other types of fat
discussed, none of which is actually essential for life or health.
Strictly speaking, you could live forever if you never consumed another gram of saturated, monounsaturated
or trans fat. But a long enough deficiency of either ALA or LA would eventually cause a host of health
problems and eventually death. It’s worth mentioning that it takes the absolutely most artificial of diets
(usually completely fat free diets served in a hospital setting) to generate a true ALA or LA deficiency; even
the worst diet will tend to cover bare minimum requirements of both. In fact, it took years of research to even
determine that there were essential fatty acids because causing a true deficiency was so difficult.
When saturated fats started to become ‘the enemy’ in the 70’s and 80’s, there was a big push for an
increased intake of vegetable oils in the diet. That is, if people were going to eat a lot of fat, it was thought
that eating more vegetable oils would be better than saturated fats.
As always, things are not quite so simple and, as I noted above, some groups think that the increased intake
of vegetable oils is actually the cause of many health problems blamed on saturated fats.
Ok, now everybody is really confused, let me see if I can unconfuse things.
Both ALA and LA turn out to have a massive number of effects in the body ranging from modulating gene
expression, producing or inhibiting inflammation and a host of others; they are also involved in the production
of eicosanoids, short-lived chemical signalling molecules that do a zillion different things in the body. It’s

16
worth mentioning that many of these effects are mediated by compounds formed by the metabolism of ALA
and LA within the body.
That is, ALA and LA are sort of ‘parent compounds’ for other things in the body. For example, LA is converted
to gamma-linoleic acid which may have anti-inflammatory effects (and many women swear helps with
PMS). LA is also converted to arachidonic acid (AA) which is an inflammatory compound that may be
involved in muscle growth. ALA undergoes extensive metabolism and can be converted to EPA and DHA
(the fish oils, I’ll spare you the full names) which I’ll come back to below.
Of more importance, although both are essential fatty acids, ALA and LA often have different and frequently
opposing effects; in general, the effects of the w-3 fatty acids tend to be ‘good’ and the effects of w-6 are
‘bad’ although, as always it’s far more complex than that.
This is important because there has been concern regarding the modern diet that the ratio of w-6:w-3 fatty
acids is causing a variety of health problems.
For example, it’s thought that our evolutionary diet had a ratio of w-6:w-3 intake of between 1:1 and 4:1; the
modern diet contains somewhere around 20-25:1. This skewed ratio is due both to the abundance of w-6
in the food supply as well as the exceeding lack of w-3 fatty acids in the modern diet. Because of this, finding
ways to boost the w-3 content of foods (such as high w-3 eggs) is a huge area of research.
And it’s been argued that this skewed ratio is contributing to a myriad of health problems, not the least of
which is inflammation and increased heart disease risk (with an increased intake of w-6 being blamed for
the problem). Current research calls this into question, however.
Quoting from a recent review titled “Too much linoleic acid promotes inflammation, doesn’t it?” by Kevin
Fritsche
Existing evidence in humans, though limited, fails to show a link between higher dietary LA intake, or higher
plasma LA, and greater inflammation in vivo. In fact, some of the data suggest the opposite may be true [my
note: he’s saying that increased LA intake may be ant-inflammatory].
Quoting from another paper titled “The role of dietary n-6 fatty acids in the prevention of cardiovascular
disease.” by Walter Willett:
Because n-6 fatty acids are the precursors of proinflammatory eicosanoids, higher intakes have been
suggested to be detrimental, and the ratio of n-6 to n-3 fatty acids has been suggested by some to be
particularly important. However, this hypothesis is based on minimal evidence, and in humans higher intakes
of n-6 fatty acids have not been associated with elevated levels of inflammatory markers…In the United
States, for example, intake of n-6 fatty acids doubled and coronary heart disease (CHD) mortality fell by 50%
over a period of several decades. In a series of relatively small, older randomized trials, in which intakes of
polyunsaturated fat were increased (even up to 20% of calories), rates of CHD were generally reduced.
Basically, a lot of the concern over high w-6:w-3 ratios may be misplaced but I’m not going to get into the
debate beyond that.
For the most part, I don’t think worrying about w-6 intake is much of an issue. On even the most moderate
fat diet, w-6 intake will be generally be more than sufficient and trying to consume more is rarely
necessary. Whether or not intakes need to be explicitly reduced and what impact that will actually have is
something to let the nutrition researchers argue about for the time being.
Rather I want to focus on the w-3 fatty acids about which there is far less debate; at this point about a zillion
studies (+-a million) have shown benefits of increased w-3 intake on a myriad of health
parameters. Decreased inflammation, improved blood lipid levels (including decreased triglyceride levels),
decreased risk of heart disease, decreased depression and even fat loss have all been found from w-3
supplementation.

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Now, recall from above that both w-3 and w-6 fatty acids undergo significant processing in the body with
ALA being converted downstream to EPA and DHA, at least potentially. It’s EPA and DHA that I want to talk
about now.
Readers are probably more familiar with EPA and DHA as fish oils since that is how they are typically referred
to. As you might expect, both compounds are found in large amounts in fatty fish (free range animals often
have a larger proportion of w-3 fatty acids as well).
Quite in fact, the original interest in fish oils came from the observation that cultures (such as the Alaskan
Inuit) had low rates of heart disease despite a ‘high-fat’ intake. It turned out that the large intake of fish oils
were a huge part of that.
And while ALA is still technically considered the ‘essential fatty acid’, it’s looking more and more like it’s
actually the EPA and DHA that are doing the majority of the ‘good’ things in the body (and that they may do
different things in the body meaning that they are both important). Whether ALA actually does anything
indepdently of its conversion to EPA/DHA is currently being debated.
And here’s why this is a problem: outside of vegetarians/vegans, the conversion of ALA to EPA/DHA is
extremely small in adults. When ALA is supplemented (for example, from flax oil), the actual conversion to
EPA is only about 4-5%. And the conversion of EPA to DHA is negligible; that is, supplementing the parent
compound doesn’t raise body stores of DHA at all (in fact, supplementing with EPA doesn’t raise DHA either).
This topic is discussed in some detail in the research review Extremely Limited Synthesis of Long Chain
Polyunsaturates in Adults: Implications for Their Dietary Essentiality and Use as Supplements.
But the point holds, simply ensuring sufficient intake of ALA (e.g. from flax or another vegetable oil) does not
ensure that there will be a significant increase in EPA or DHA which appear to be the key fats in terms of
improving health; in fact it’s almost certain that it won’t raise EPA/DHA sufficiently to be of benefit. In my
opinion, the only way to ensure adequate EPA/DHA intake is by ensuring a daily intake from preformed
sources.
For people who consume fatty fish (or perhaps free range meat) on a regular basis, that is generally an
adequate source. For everyone else, supplementing with either pills or liquids will generally be necessary
to ensure a sufficient daily intake.
And, as I stated in the research review I linked to above, while w-3 fortified foods are becoming available, I
find that they are not cost effective; rather than buying high w-3 eggs, it’s far cheaper to buy normal eggs
and take an w-3 supplement.
I’m not going to get into dosing issues here since that’s really beyond what I wanted to talk about in this
article; I’ll address that at a later date. An absolute bare minimum would be a combined intake of EPA/DHA
of 500mg per day. A standard 1 gram fish oil capsule typically contains 180 mg EPA and 120 mg DHA (300
mg of total fish oil) so that would be only 2 pills per day. There is evidence that more may be beneficial for a
variety of goals but, again, I’ll save that discussion for a later article.

Summing Up

So what started out as a primer on dietary fats got a little bit longer than I had intended. Hopefully now you
understand the difference between dietary cholesterol and triglycerides along with understanding what the
different types of dietary triglycerides are and what roles they might or might not have in the body. I’ve also
tried to address some of the current confusion and controversy that currently exists over the different types
of fats.

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I also realize that I didn’t address much in the way of practical recommendations. Frankly, assuming folks
are consuming a moderate fat diet (perhaps 20-25% of their total calories), outside of ensuring that they get
sufficient amounts of EPA/DHA on a daily basis and mostly avoid trans fat intake, I’m not sure it’s worth
being that concerned with.
Most ‘high-fat’ foods contain a mix of saturated and monounsaturated fats and ensuring sufficient w-6 intake
is rarely an issue unless dietary fat intake is kept extremely low for long periods or the diet is very artificially
set up.
It’s usually w-3 fatty acids that are lacking in most diets and ensuring their intake will do most of the good in
my opinion. As noted up above, if an athlete needed to consciously add more fat calories (for example an
endurance athlete who can’t meet their caloric needs), a separate source of monounsaturated fats would be
the first choice.
I also realize that didn’t talk extensively about Enova Oil or speciality oils like Medium Chain Triglycerides
(MCT’s). That will have to wait for a later article.

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A Primer on Dietary Carbohydrates – Part 1
Having previously done a fairly detailed Primer on Dietary Fats, I wanted to do something similar on the topic
of carbohydrates (in the future I’ll do one for protein as well). In this article, I’m not going to look at many of
the debates surrounding the issues of carbohydrate intake (in terms of body weight, body fat, or health), you
can read Carbohydrate and Fat Conteroversies Part 1 and Carbohdyrate and Fat Controversies Part 2 for
somewhat of an examination of that. Rather, I just want to focus on some basic definitions and concepts
since there tends to be a lot of general confusion over the topic of carbohydrates.
.

What is a Carbohydrate?

The term carbohydrate is sort of an overall classification referring to a number of different organic
compounds, which I’m going to detail below. You may often see the abbreviation CHO (for Carbon,
Hydrogen and Oxygen) to refer to carbohydrate. Although fiber is a carbohydrate, I’m not going to discuss
fiber in detail in this article; rather I’d refer you to Fiber – It’s Natures Broom for a detailed look.
As I have discussed in many articles on the site, the primary role of carbohydrate in the body is energetic,
that is it is broken down in cells to provide energy through a variety of pathways. At the same time, strictly
speaking, carbohydrate is not an essential dietary component; that is, you can survive without eating it at all
(an explanation of essential vs. inessential nutrients can be found in A Primer on Nutrition Part 1). How
many carbohydrates should be consumed in the human diet is a topic of endless debate and controversy,
I’d refer readers to How Many Carbohydrates Do You Need? for a detailed look at the topic.
Now, another term that is sometimes used to describe carbohydrates is saccharides and, with that trivial
note made, there are three primary classes of carbohydrates which I’m going to first list and then describe
in more detail below in terms of what they are, what they do in the body and where they are found in the
food supply.
1. Monosaccharides
2. Oligosaccharides
3. Polysaccharides
To keep the article length under control, I’m only going ot discuss the monosaccharides today. I’ll discuss
oligosaccharides and polysaccharides (along with an article summary on Tuesday of next week).
.

Monosaccharides

The term monosaccharide refers to a single ‘sugar’ molecule (‘mono’ = single; saccharide = ‘sugar’) and are
often referred to as simple sugars. The monosaccharides are glucose (blood sugar), fructose (fruit sugar)
and galactose (milk sugar). I should mention that there are other monosaccharides but the above three are
the ones primarily found in the diet.
One that does come up on fitness forums (due to its use in many sports products) is dextrose which is simply
d-glucose. The ‘d’ refers to the chemical structure (normal glucose would be more accurately described l-
glucose and you can technically have both d- and l-fructose) and I’ll leave it to the organic chemistry nerds
to worry about it beyond that. Simply recognize that both dextrose and glucose are a form of glucose
(effectively they are molecular mirror images).
Now, free glucose is found in some foods (fruit has some and many types of candy will contain glucose)
although it’s primarily associated with blood sugar (when diabetics are measuring their ‘blood sugar levels’

20
they are measuring blood glucose levels specifically). This is because glucose is the type of sugar found
almost exclusively in the bloodstream of humans. Quite in fact, almost all other dietary carbohydrates will
either be converted to or simply appear in the bloodstream as free glucose.
This is certainly true of dietary fructose, found primarily in fruits (hence the name) which must first be
converted to glucose (in the liver) prior to release. That is, contrary to some claims being made, free fructose
is almost never found in the bloodstream in large quantities unless it was put there through infusion. Rather,
dietary fructose will either be stored in the liver as glycogen (see below) before being converted to glucose
and released into the bloodstream, or simply converted to glucose and released after consumption. Again,
free fructose is rarely found in the bloodstream in appreciable quantities even when it’s consumed in the
diet.
I should probably mention that fructose got a lot of press one point as either a superior sweetener or a sugar
that was ideal for diabetics. In terms of the latter, due to it’s slow digestion and general lack of effect on
blood sugar or insulin response, dietary fructose was thought to be superior to sucrose. However, it’s turning
out to be much more complicated than that. Excess dietary fructose (and please note my use of the word
‘excess’) can cause problems in terms of raising blood triglycerides and having other negative effects.
So, while the fear and scare-mongering of the anti-fructose brigade (who are often looking at insanely non-
physiological amounts of fructose; amounts that simply aren’t achievable in a normal human diet) tends to
be a lot of nonsense, there’s little doubt that too much fructose can be a bad thing. I’d note, and this is
discussed in some detail in the article (and especially comments section) of Straight Talk about High-
Fructose Corn-Syrup: What it is and What it Aint that the fructose mainly becomes and issue when it’s being
mainlined as part of sugary sodas.
It would take an absurd amount of say, fruit, to provide enough fructose to the diet to cause problems. The
liver can generally handle approximately 50 grams of fructose or so before you start to see conversion to
triglycerides or other negatives (when you divide the studies up into those that find problems versus those
that don’t, 50 g/day is about where the cutoff occurs). While that intake level might be easily achievable by
someone consuming a lot of sugary soda, given taht an average piece of fruit is roughly 7% fructose (e.g. 7
grams fructose per 100 grams of fruit), well..that’s a lot of fruit (~7 average pieces per day). But, in my
opinion, anyone consuming gallons of sugary soda per day has bigger issues in their diet than the
HFCS/fructose intake. But I digress.
Finally is galactose, or milk sugar, found, as you might imagine in milk and dairy products. I don’t have much
to say about this one here but will come back to it below. I’d only note that galactose tends to be metabolized
similarly to fructose in the body; that is it’s dealt with in the liver. Since galactose tends to make up a fairly
small amount of the overall diet (unless massive amounts of dairy are being consumed), I don’t usually
consider this worth worrying about.
As a final note, there are a host of other types of monosaccharides that can either occur in small amounts
in the diet or be made. Ribose is one simple sugar, for example, that was one promoted to improve
performance. Some of the sugar alcohols (e.g. xylitol) also fall into the category of monosaccharide but
since they are modified carbohydates (simple sugars with an alcohol molecule tacked on), I’m not going to
discuss them here.
Simply while there are far more monosaccharides that can be found in the diet (or at least obtained), glucose
and fructose are going to be the major players (and glucose more than fructose); galactose intake will depend
entirely on dairy intake or the lack thereof.
And that’s where I’m going to wrap it up for today. On Tuesday of next week, I’ll discuss oligo- and poly-
saccharides and sum up the topic overall.
Read a Primer on Dietary Carbohydrates – Part 2

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A Primer on Dietary Carbohydrates – Part 2
In a Primer on Dietary Carbohydrates – Part 1, I took a brief look at what carbohydrates are and listed the
three primary categories of dietary carbohydrates which are monosaccharides, oligosaccharides and
polysaccharides. As well, I looked in some detail at the monosaccharides (simple sugars) which are glucose
(dextrose), fructose and galactose. Today, I want to examine the other two major categories of dietary
carbohydrates: oligosaccharides and polysaccharides.

Oligosaccharides

The term oligosaccharide is used to refer to any carbohydrate chain between 2-10 molecules long (‘oligo’ =
‘several’ or as I like to call it ‘a buncha'; ‘saccharide’ = sugar). Chemically, that is, an oligosaccharide, is a
buncha monosaccharides that are chemically bonded together but there are only 2-10 of them in the chain
(this will make more sense when I discuss polysaccharides).
And while some of the longer chains may be found in small amounts in the diet or in specialty food products
(e.g. some maltodextrins which are a combination of maltose and dextrose may be about this length) by and
large the primary oligosaccharides are the disaccharides, two sugar molecules bound together. I’ve listed
the primary dietary disaccharides in the table below including what two sugars they are made up of along
with where they are generally found in the diet.
.

Name Combination of Where Found

Sucrose Glucose + Fructose Too many places to list

Lactose Glucose + Galactose Dairy products

Maltose Glucose + Glucose Malt Beverages (Beer!)

.
While I’m hesitant to mention high-fructose corn-syrup (HFCS) in this article, I’m going to bring it up since it
is also a combination of glucose and fructose (like sucrose), as discussed in the article Straight Talk about
High-Fructose Corn-Syrup: What it is and What it Aint. I’d only ask that you take any comments about HFCS
to that article instead of this one since most of what needs to be said is there and needn’t be repeated
here. Simply recognize that, nutritionally, HFCS and sucrose are essentially identical in that both are made
up of roughly 1/2 glucose an 1/2 fructose; that’s all I’m going to say about it.
Sucrose is arguably what most think of when they think of ‘sugar’. Table sugar is pure sucrose and sucrose
has traditionally been used as a sweetener for, well, forever in various forms (including cane sugar, refined
sucrose and many many others). As a sweetener, sucrose is used in various candies, as a sweetener in
some sodas and is also found occurring in many foods whether naturally occurring (even fruit contains some
sucrose) or man-made.
Lactose, as mentioned is a mixture of 1/2 glucose and 1/2 galactose and is found in dairy products. Many
people are probably familiar with lactose due to issues of lactose intolerance. Lactose intolerance occurs
due to an inability to digest lactose in the stomach due to either the complete lack (or more usually an
inadequate amount) of the enzyme lactase in the stomach. Lactose intolerance typically develops shortly
after weaning (if it happens at all) and is more common in ethnic groups who did not evolve consuming milk
past that point. As a very gross generalization, the darker someones skin, the more likely there is for lactose
intolerance to be present.

23
The symptoms of lactose intolerance generally include gas, diarrhea and stomach upset; this is due to the
undigested lactose hitting the colon where it ferments. Individuals with lactose intolerance (not to be
confused with a true milk allergy, see A Quick Look at Food Intolerances and Allergies) must either avoid
dairy products, consume special lactose removed products (e.g. Lactaid milk) or consume lactase
supplements with dairy products. Lactose intolerance and how to deal with it (for example, some with more
minor lactose intolerance can consume dairy with meals) is discussed in more detail in The Protein Book.
Maltose, as noted above, is used primarily to brew beer and make malt drinks, it is also produced during the
digestion of the polysaccharides (discussed next). As well, maltodextrins are often found/used in specialty
food products. But for the most part sucrose and lactose are the primary oligo/di -saccharides found in the
‘normal’ diet. Even if we include HFCS as a disaccharide, it’s generally made for commercial products and
doesn’t occur naturally in the diet (to my knowledge).
.

Polysaccharides

And finally are the polysaccharides, a term that refers to chains of sugar molecules which can range from
several hundred to many thousands long (‘poly’ = ‘many’). In terms of the human diet, polysaccharides
almost universally refers to starch which is simply a long, long (long) chain of glucose molecules strung
together. Even there there are slight distinctions with recent research finding differences between what are
termed amylose and amylopectin, both of which are found in dietary starches. The difference has to do
with the molecular structure: amylose is simply a straight chain of glucose molecules while amylopectin has
a branching structure.
Both types of carbohydrates are found in dietary starches although amylose is usually more prevalent. Both
high amylopectin and high amylose starches are available (e.g. waxy corn is 98% amylopectin) for specific
food purposes. Foods such as grains (refined or otherwise), potatoes, etc. are all food examples of starches
that are eaten in various proportions in the human diet.
Polysaccharides actually start digestion in the mouth due to an enzyme called alpha-amylase. You can test
this by putting a piece of bread or something in your mouth and chewing without swallowing; after some time
you’ll get a very sweet taste in your mouth due to the breakdown of starch to free glucose. The old
‘carbohydrate blocker supplements’ (usually derived from white kidney bean) were actually alpha-amylase
blockers, they prevented digestion of carbohydrates in the mouth. Unfortunately, they didn’t do anything for
the next step in digestion which occurs mainly in the stomach. There, the long chains of starch molecules
are broken down into smaller and smaller chains (producing some maltose for example) until the free glucose
is available for absorption.
Although this isn’t related to the diet specifically, in the body (specifically muscle and liver) long chains of
starch are called glycogen. Again, these are simply long chains of glucose that are bonded together (in the
liver, fructose is converted to glucose before being stored as liver glycogen) for breakdown at some later
date. Some recent work even suggests that there may be small stores of glycogen in the brain or fat cells
but the majority will be found in muscle and liver cells. On average, the liver may hold about 50 grams of
carbohydrates and the skeletal muscle of an average sized person about 300-400 grams. These values can
be doubled with carbohydrate loading.
A question that I have seen enough times to think it worth addressing is why meat doesn’t provide
carbohydrate to the diet due to the presence of glycogen in muscle (animal meat is just muscle). And the
major part of the answer is that, after death, the glycogen will be broken down as part of the process of the
animal going into rigor. If you ate it fresh off the kill, depending on whether or not the animal stored glycogen

24
or not (not all animals do), there might very well be glycogen still present. But I’m talking fresh off the kill,
like Ted Nugent you just shot it in the head with an arrow and you dig in with a knife right then fresh off the
kill. If you don’t do that, the glycogen will be gone.
I should also mention another type of starch which is ‘resistant starch’, this is actually a type of starch that is
resistant to digestion, hence the name. That is, it passes through the stomach and intestines without
digestion (and may have certain health or weight loss benefits because of it). Resistant starch is found
naturally in small amounts in some foods but most of the focus seems to be on developing commercial foods
higher in resistant starch.
Finally, fiber would technically be discussed here as a polysaccharide but, as I mentioned in Primer on
Dietary Carbohydrates – Part 1, I already detailed fiber in Fiber – It’s Nature’s Broom and would refer readers
there for more detail so I won’t spend much more time on it here. Just realize that the various fibers are long
chains of, generally indigestible, carbohydrate molecules (I say ‘generally’ as some fibers are metabolized
in the colon to short-chain fatty acids as discussed in the linked article).

Summary

And that’s that, a primer on dietary carbohydrates. Carbohydrates refers to a general class of compounds
containing Carbon, Hydrogen and Oxygen (hence CHO) including monosaccharides (simple sugars),
oligosaccharides (chains of 2-10 molecules) and polysaccharides (long chains of molecules including
fiber). I’ve summarized the primary types of dietary carbohydrates in the chart below.
.

Common Name What it Is Where It’s Found

MonoSaccharide

Glucose Blood sugar Bloodstream, various foods

Fructose Fruit sugar Fruit

Galactose Milk sugar Dairy

Dextrose D-glucose Specialty nutrition products

Oligosaccharides

Sucrose Table sugar Glucose + Fructose Just about everywhere

Lactose Milk sugar Glucose + Galactose Dairy

Maltose N/A Glucose + Glucose Malt Beverages/Beer

HFCS (sort-of) Glucose + Fructose Commercial foods such as soda

Polysaccharides

Starch Starch Amylose/Amylopectin Starches (ha ha)

Resistant Starch Resistant Starch Resistant Starch Small amounts in foods, specialty products

Fibers Fiber Cellulose, etc. Vegetables, Grains, Fruits

Glycogen Glycogen Long chains of glucose Skeletal muscle, liver

25
Nutrient Metabolism Overview
This article actually represents the entirety of Chapter 4 of the Revised Rapid Fat Loss Handbook.
In this chapter, I want to give readers a very brief and simplified overview of human metabolism and nutrient
use. Which, for those who know a lot about the topic will realize, is an understatement of vast proportion.
The complexities of human metabolism can and do fill up hundreds of pages in physiology books and this
chapter should be taken with that in mind.

The Basics: Energy and Building Blocks

Very simplistically speaking, we can divide the uses of the nutrients (discussed last chapter) into three
categories, of which I only really want to talk about two. One category, which I won’t discuss much has to do
with the vitamins and minerals which both act, essentially, as nuts and bolts in the body. They fulfill any
number of different roles; depending on which one you’re talking about. While critical to human health, they
simply aren’t that important to the topic of this book. If you’re interested, go get yourself a book on vitamins
and minerals and go to town. All I’m going to say is that you should make an effort to ensure your vitamin
and mineral intake. A basic one-per-day multivitamin should probably be good “nutritional insurance” for
everyone, the obsessed can look at versions containing mega-doses or what have you of the different
nutrients.
The second category is for use as building blocks. Most parts of the human body are in a constant state of
breakdown and buildup and nutrients must come in to the body to provide building blocks for those
processes. One I imagine all readers are familiar with is that of calcium (a mineral) being the building block
for bones. Additionally, skeletal muscle, organs and many hormones have amino acids (coming from protein)
as their building blocks. As well, both fats and cholesterol play a role as a building block for cell membranes
and a few other substances in the body.
The third category, and the one I’ll spend the most time on in this chapter, is as an energy (fuel) source.
Even as you sit reading this and growing bored, your body is using energy at some rate. So your brain, your
heart and other organs, skeletal muscle, liver and even your fat cells are using energy, although the rates at
which each uses energy varies from high (e.g. brain, liver) to extremely low (e.g. fat cells). Surprisingly and
quite contrary to common belief, at rest skeletal muscle doesn’t burn that many calories. The idea that adding
muscle mass will turn you into a calorie burning inferno is simply incorrect.

Where Does the Energy Come From?


So where does that energy come from? At the lowest level of cellular function, the only form of energy that
your cells can use directly is something called adenosine triphosphate (ATP). I doubt that factoid is very
helpful to readers except perhaps as the answer to a Trivial Pursuit or game show question. If you happen
to sit around having polite conversation about ATP, please send me an email: I want to hang out with you.
Of more use to us, the body generates ATP from the burning (oxidation or combustion to use a more sciency
term) of either glucose from carbohydrate or fatty acids from fats. Under specific circumstances protein can
be used to produce ATP, either directly or via the conversion to either glucose or fat (usually protein is
converted to glucose to be used for fuel). I’ll come back to this below.
With a few exceptions that I’ll talk about in a second, every tissue in your body can use either carbohydrate
or fat for fuel. What determines which they use? For the most part, it’s the availability of carbohydrates: when
carbs are available (because you’re eating plenty of them), those tissues will use carbohydrates, in the form

26
of glucose, for fuel. When carbs are not available (because you’re restricting them), the body will switch to
using fat for fuel. That fat can either come from your diet or from the fat stored on your butt or stomach. This
has another implication that is often forgotten in weight/fat reduction programs: when you eat more
carbohydrates, your body uses less fat for energy; when you eat less carbohydrates, your body uses more
fat for energy.
So what about those exceptions? A few tissues in your body such as the brain/central nervous system and
one or two others can’t use fatty acids for fuel; they can only use glucose. The brain is the main one I want
to talk about here. It’s usually (and incorrectly) stated that the brain can only use glucose for fuel, and this is
true if you only consider glucose, amino acids, and fat as potential fuel sources. But this leaves out a fourth,
extremely important, fuel source: ketones (also known as ketone bodies). Ketones are made from the
breakdown of fat in the liver and function as a fat-derived fuel for the brain during periods of
starvation/carbohydrate restriction.
I’ll talk about starvation in more detail in a second but I want to mention that, after a few weeks in ketosis (a
state where ketones build up in the bloodstream such that fuels such as the brain start using them for
energy), the brain can derive 75% of its total energy from ketone metabolism. The other 25% comes from
glucose.

So Aren’t Carbohydrates Essential?

At this point you may be slightly confused about the role of carbohydrates in the diet. In the last chapter, I
stated that carbohydrates weren’t an essential nutrient and above I mentioned that a few tissues can only
use glucose and that even the brain gets about 25% of its total fuel requirements from glucose after
adaptation to ketosis. So if those tissues still require glucose for energy, you may be wondering how
carbohydrates aren’t essential in the diet. Remember from the last chapter what the two requirements of an
essential nutrient are
 That nutrient is required for the proper function of the body.
 The body can’t make that nutrient in sufficient quantities.
The second criterion is the reason that dietary carbohydrate is not an essential nutrient: the body is able to
make as much glucose as the brain and the few other tissues need on a day-to-day basis. I should mention
that the body is not able to provide sufficient carbohydrate to fuel high intensity exercise such as sprinting
or weight training and carbs might be considered essential for individuals who want to do that type of
exercise.
So how is the glucose made? The answer is a biochemical process with the unwieldy name of
gluconeogenesis, which simply means the making of new glucose. This process primarily occurs in the liver.
When necessary, the body can make glucose out of a number of other substances including glycerol (which
comes from fat metabolism), lactate and pyruvate (which comes from carbohydrate metabolism), and certain
amino acids (from protein).
Which brings me back around to the topic of protein as a fuel source for the body. Readers may have read
that “carbohydrates spare protein” and this is part of the basis for that claim: when carbohydrates are being
eaten in sufficient quantities, the body has no need to break down protein for fuel. By extension, when
carbohydrates are being restricted for whatever reason, some proportion of protein will be used to make
glucose, leaving less to be used for building blocks. This has an important implication for dieting, namely
that protein requirements go up when you’re restricting either calories or carbohydrates.

27
What About Starvation?

Now seems like as good of a time to talk about starvation, the consumption of zero food. I should mention
that therapeutic starvation (as it was called) was tried during the middle of the 20th century for weight loss,
frequently causing rather rapid losses of weight. But it had an unfortunate problem, which I’m going to
address below. For now, let’s look at starvation and what happens.
So let’s say you stop eating anything and look at what happens (a much more detailed examination of this
and many other topics can be found in my first book The Ketogenic Diet). Over the first few hours of
starvation, blood glucose and insulin levels both drop. This signals the body to break down glycogen (stored
carbohydrate) in the liver to release it into the bloodstream. As well, the body starts mobilizing fat from fat
cells to use for fuel. After 12-18 hours or so (faster if you exercise), liver glycogen is emptied. At this point
blood glucose will drop to low-normal levels and stay there. Blood fatty acids will have increased significantly
by this point.
After a day or so, most cells in the body, with a few exceptions, are using fatty acids for fuel. Obese
individuals may derive over 90% of their total fuel requirements from fat while leaner individuals may only
derive about 75% of the total from fat. So far so good, right, the body is mobilizing and utilizing an absolute
ton of fatty acids for fuel: 90% of your total energy expenditure if you’re fat and 75% if you’re lean (I’ll talk
about what fat and lean is in another chapter).
There must be a drawback and here it is: the few tissues that require glucose are getting it via
gluconeogenesis in the liver. As above, gluconeogenesis occurs from glycerol, lactate, pyruvate and amino
acids. Now, if the person isn’t eating any protein, where are those amino acids going to have to come from?
That’s right, from the protein that is already in the body. But recall from last chapter that there really isn’t a
store of protein in the body, unless you count muscles and organs. Which means that, during total starvation,
the body has to break down protein tissues to provide amino acids to make glucose. The body starts eating
its own lean body mass to make glucose to fuel certain tissues. This is bad.
Now, as fatty acids start to accumulate and be burned in the liver, ketones will start to be produced. Initially,
for reasons totally unimportant to this book, muscles will use the majority of ketones that are produced. As I
mentioned above, after a few weeks, the brain will adapt so that it is using ketones and deriving most of its
fuel from them; the small remainder comes from the glucose being produced via gluconeogenesis.
Now, the adaptation to ketosis occurs for a profoundly important reason. Once again, much of the glucose
produced in the body is from amino acids which are coming from the protein in muscle (and to a lesser
degree, organs). If such a breakdown continued in the long term, so much muscle would be lost that the
individual who was starving would be unable to move. Quite in fact, the loss of too much lean body mass
(muscle and organs) causes death. The shift to using ketones decreases the need to break down body
protein to make glucose.
As I mentioned above, therapeutic starvation was often used in the cases where rapid weight loss was
needed. And while it did generate rather high levels of weight and fat loss, it had as a problem the loss of
excessive body protein. So researchers decided to find a way to try and generate similar levels of weight/fat
loss while sparing LBM. And that’s the topic of the next chapter.

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Calories, Nutrients or Food?
In this article, I want to look at a somewhat fundamental aspect of general nutrition; that is the distinction
between calorie intake, nutrient intake, and food intake. This is relevant for the simple fact that the average
person doesn’t think in terms of calorie intake, and they probably don’t think in terms of nutrient intake.
Rather, they think in terms of eating food; thus it’s important to examine the distinction between those three
‘categories’ of intake.

Calories

Ignoring the fringe that claims that the calorie counting theory is invalid or doesn’t work, most diet books deal
predominantly with calories (everywhere but the US, joules are used). They’ll discuss caloric intake (from
food) or caloric expenditure (from activity) or compare the two. In discussing what is happening to the body
(weight gain or loss), they’ll compare the energy balance equation which compares calories in to calories
out.
So what, you ask, is a calorie? A calorie is a measure of heat. One calorie is the amount of heat needed to
raise the temperature of 1 gram of water by 1 degree Celsius. Fascinating stuff, this nutritional science.
You’ll also frequently see kilocalorie (kcal) used. Technically one kcal is equal to 1000 calories (kilo = 1000).
In the US, most people use calories and kilocalories interchangeably, although it’s incorrect to do so. You’ll
sometimes see ‘cal’ with a lower-case ‘c’ used to mean a calorie and ‘Cal’ with an upper-case ‘C’ to mean
kilocalorie but that’s just too much to pay attention to.
Without boring you with some true minutiae, this simply has to do with keeping the numbers reasonable and
easier to deal with.In the real world, people mean kilocalories when they say calories even if pedantic
nutritional types get their panties all twisted over it. I use calories to mean kilocalories just because it’s easier
and, let’s face it, everybody knows what I mean.
As noted above, in all countries but the United States, the energy value of foods are measured in joules
which is just another measure of energy. If you really need to convert for some reason, 1 calorie is equal to
4.2 joules (or 1000 cal = 4,200 joules). I always hate having to convert when I read research studies. Let’s
see, they gave them 5000 joules per day, divide by 4.2, carry the one, umm, where’s that damn calculator.
Ok, it’s 1200 calories per day. The nice researchers list energy intake in both joules and calories, because
they realize that most people in the US are too dumb to understand metric.
To give you an idea of some representative numbers, your average non-huge male at about 170 pounds
has a daily maintenance energy need of about 2700 calories or so (11,340 joules or 11.3 megajoules), a
female of 135 lbs about 2000 calories (8,400 joules or 8.4 megajoules). That number is subject to change
and scales with weight (larger individuals having higher daily energy needs; smaller individuals lower). This
is discussed in more detail in Metabolic Rate: Overview.
I’d note that you can Quick Estimate Maintenance Calories with the following values: 14-16 calories/lb
current bodyweight for men and for 13-15 cal/lb for women. Keep in mind that these are only estimates.
So you know, the calorie values (with joule conversions for non-American readers) for the macronutrients
are:
 Protein: 4 calories per gram (16.8 joules/gram)
 Carbohydrate: 4 calories per gram (16.8 joules/gram)
 Fat: 9 calories per gram (37.8 joules/gram)
 Alcohol: 7 calories per gram (29.4 joules/gram)

29
Note: these are average values and can vary very slightly (i.e. protein ranges from about 3.8 to 4.2 cal/gram
depending on the specific type of protein). Worrying about slight difference in energy content between
different sources of protein or carbs is taking anal-compulsion to a whole new level. I shant mention it again.
That’s right…shant.
When researchers determine the calorie values of foods (i.e. what you see when you read the food labels),
they do it by burning the foods in something called a bomb calorimeter and measuring how much heat is
given off. A potential problem is that the human body is not a bomb calorimeter and that simple fact affects
the energy balance equation. That is to say, just because a gram of protein burned in a bomb calorimeter
has 4 calories doesn’t mean your body derives 4 calories from it energy wise.
I suppose I should mention fiber which is (or at least should be) consumed in gram amounts each day and
is therefore considered a macronutrient (fiber is usually considered a subset of carbohydrates). Fiber has a
number of important benefits but providing a lot of energy to the body isn’t one of them for the most part.
It’s generally stated that humans don’t derive any calories from fiber, since we lack the enzymes necessary
to break it down like cows. This isn’t strictly speaking true, our lower intestine may break down fiber to short
chain fatty acids which are used for energy by the micro-organisms living in our gut.
Although there is ongoing debate in this area, a caloric value of 1.5-2 cal/gram for fiber is the currently
accepted value. Even then, since a fiber intake for most people these days probably doesn’t top 25
grams/day, that’s only about 35-50 calories total per day. A massive 100 grams of fiber/day (you’d have to
eat a tree) would 150-200 calories which would be significant.
For all practical purposes, unless your fiber intake is ungodly high, we can ignore the caloric content of fiber.
You can also ignore the fiber grams for carbohydrate count if you’re keeping track of those for some reason
(such as a ketogenic diet).

Macronutrients

Of course, we don’t eat calories which is why people often get confused when that’s all that’s being talked
about. Rather, we consume the various macronutrients (protein, carbs, fat and alcohol) which provide
calories to the body during their metabolism. As the chart above shows, the different nutrients provide the
body with different caloric values; a gram of protein and a gram of fat will provide 4 and 9 calories/gram
respectively.
Even then, just looking at the calories values are misleading because the different nutrients provide energy
(calories) to the body with varying efficiency. In processing (and depending on how the processing occurs),
the body may derive slightly different amounts of energy from different nutrients. Consuming 400 calories
from carbohydrates may not have the same overall effect on metabolism as consuming 400 calories from
fat or protein, even though the caloric value of all three is identical.
The main place this shows up is in something called the thermic effect of food (TEF), which refers to the
amount of calories that are used by the body in processing. For example, in storage as glycogen,
carbohydrates burn off 3-6% of the total energy ingested. Fat, in contrast, may only use 3% of its total energy
content in storage.
Protein uses the most energy in processing, anywhere from 15-25% of its total energy value depending on
the source. This can add up when very large scale substitutions of carbohydrate or fat with protein is made
and this is at least part of why higher protein diets tend to outperform lower protein diets.

30
Even alcohol can lead to a ‘loss’ of energy by causing changes in liver function that serve to burn off excess
calories; this seems to be more of a pathological adaptation than something people should seek out.
I want to mention here, and I’ll come back to this later, that the effect of whole body metabolism due to the
above effects are generally fairly small, especially compared to all of the other variables that affect energy
balance such as activity levels. For example, shuffling around carbs and fat might affect metabolic rate by a
total of 3%. So for every 100 calories of fat you replaced with carbs, you’d burn 3 more calories per day.
Contrast that, for example, to the daily variance in food intake which may approach 23% (i.e. under
uncontrolled conditions, someone’s caloric intake might vary by 23% from day to day). Protein has the largest
potential to affect metabolic rate but there is generally a limit to how much protein can be consumed to this
effect tends to be somewhat limited as well. Unless you’re looking at very large-scale replacement of carbs
or fat with protein, the overall effect simply isn’t that large.
The distinction between calories and nutrients also becomes important when we start to consider the specific
mechanisms which cause the body to lose or gain fat and muscle (I’m not talking about insulin by the way).
Simply looking at caloric intake vs. expenditure may be misleading under certain circumstances. Looking at
the actual nutrient balance (nutrient intake vs. nutrient burning) is more important in determining what’s really
going on in the body. This will make more sense soon.

Food

Now, of course, we don’t eat individual nutrients, at least not under most real-world conditions. That is, you
don’t typically sit down and pick from a tub of protein, a container of fat and a container of carbohydrate; not
unless you’re an obsessed athlete or bodybuilder. Rather, you probably derive your nutrients (and hence
your calories) from food.
This is perhaps one of the most important distinctions that needs to be made because the source of a given
nutrient (or calories) can affect things such as fullness and hunger, energy levels, overall health and body
composition. Consuming 100 grams of digestible carbohydrates from a sweet potato and 100 grams of
digestible carbohydrates from a candy bar may provide identical amounts of carbohydrate (100 grams) and
calories (400 calories) to the body; but that doesn’t mean that they will have identical effects on bodily
function.
Hormone levels, fullness and health can all be impacted by the source of nutrients/calories. Different sources
of nutrients and calories may contain other substances (vitamins and minerals, phytonutrients, fiber) that
may be of relevance. Individual taste preferences also come into play here: humans eat for reasons that
may be wholly unrelated to the macronutrient composition of the food. We eat because things taste good or
for social or cultural reasons; only obsessed athletes pick foods based on their macronutrient profile or
caloric content.

The Point
All food contains nutrients in some proportion or another, and those nutrients provide energy in the form of
calories to the body. From a very simplistic sense, this means that all that matters from a bodily energy
standpoint is the caloric content: 3000 calories are always 3000 calories regardless of where they come
from. And to a first approximation, and assuming a few other factors are taken into account, looking at
calories does give us a good indication of what’s going on.

31
Unfortunately, this simplistic approach isn’t always sufficient for our needs and we have to get into more
detail. The amounts of nutrients ingested affects whole body fuel metabolism, hormone levels and a whole
host of other factors that may be relevant to body composition, health or overall function.
So even though carbs and protein both contain 4 calories/gram, that doesn’t automatically make them
identical in terms of their actual physiological effect on the body. From a strictly physiological standpoint,
looking at macronutrient intake tends to be sufficient, we can determine what’s going on in the body based
on the amounts and proportions of the different nutrients being consumed.
But this is only correct when we consider strict physiology and the simple fact is that humans are more than
just a collection of physiological processes. This is especially true when you start looking at real world eating
behavior.
Even then, since we generally don’t eat individual nutrients, it become relevant to consider the food source
of those nutrients in the discussion. Foods not only contain different amounts of the various macronutrients
but may contain other compounds that are relevant to the overall discussion.
Understand me here? Issues such as hunger control, long-term adherence, individual variance, athletic
performance, and a few others all go into the determination of what food might or might not be a better
choice under a given set of circumstances.
Additionally, whether you’re looking at intake under controlled or uncontrolled conditions tends to vastly
affect what conclusions are drawn; some foods are easier to overeat and their consumption under
uncontrolled conditions may lead to increase caloric intake and fat gain. I discuss this topic in more detail in
Is a Calorie a Calorie.

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Carbohydrate and Fat Controversies: Part 1
Although there are still many Protein Controversies (usually regarding kidney health, bone health, etc.),
nowhere in the dietary world is there quite as much controversy as over carbohydrate versus fat intakes.
In this article, I want to look at carbohydrate and fat intake in terms of the various arguments and debates
that tend to surround them.
The main controversy here revolves around what amounts of carbohydrates and/or fat are ideal, healthy,
recommended, etc. and that’s what I’ll focus on. I’m not going to deal with body composition explicitly in this
article, I’ll save that for another day.

Two (or Three) Dietary Camps

Generally, folks fall into one of two camps regarding whether they think carbohydrates or fats are good or
bad. For a couple of decades now, the mainstream of dietary advice has been more or less stuck in the
mindset of ‘fat is evil and ‘carbohydrate is good’.
Various attempts to promote so-called ‘high-fat’ or ‘low-carb’ diets have usually been shot down as fads
although there is increasing research evidence that, at least for some individuals (usually those with insulin
resistance) higher fat intakes and lowered carbohydrates may be both beneficial and preferred.
However, for the most part, I’d say that mainstream dietitians are still on the carbs = good, fat = bad
bandwagon with higher fat/lower carbohydrate diets being relegated to the diet ‘fringe’.
Both groups can bring impressive (or at least impressive looking) data to the table but, as usual, extreme
stances are invariably incorrect and the truth lies somewhere in the middle; this particularly debate is no
different.
The third group (and the one I put myself in) recognizes that whether or not carbohydrates or fats are ‘good’
or ‘bad’ depends on the context. The source of the carb or fat, the rest of the diet, the goal of the individual,
genetics, activity, etc. all factor into this issue. So while it may be convenient to give simplistic
recommendations of the ‘X is bad, Y is good’ variety, simple in this case tends to be incorrect.
Perhaps the most succinct way of describing what I’m going to detail is that there are no good or bad foods
only good or bad diets. That is, within the context of one type of diet or individual situation, a specific food
may be excellent; under other conditions it may be a poor choice.

What does the Body Require?


So that some of my comments will make sense, I need to cover a smidgen of nutrient physiology, mainly
having to do with the issue of carbohydrate ‘requirements’ (a topic I cover in detail in How Many
Carbohydrates Do You Need).
As I think I’ve managed to work into every book I’ve ever written, there is no strict physiological requirement
for carbohydrates (this factoid is often used by the low-carb diet groups as part of the rationale for their
dietary approach).
Most tissues in the body can readily use fatty acids for fuel just as easily as glucose. There are a few tissues
such as the renal medulla, red blood cells and one or two other that can only use glucose. However, those
cells essentially make their own glucose by recycling lactate (produced from glucose metabolism) back into
glucose.
The brain is in its own weird category. Under most conditions, it relies exclusively on glucose. And while it
can’t use fatty acids directly, it can use a fatty acid derived fuel in the form of ketone bodies. After roughly

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three weeks of adaptation to using ketones, the brain may only need 25 grams/day of glucose or so, which
can be made by the body (in the liver and kidney) from sources such as lactate, pyruvate, amino acids and
glycerol.
Even the American Dietetic Association bible, the RDA Handbook, states that there is no requirement for
dietary carbohydrates. Any decent nutrition or physiology book will state the same. Despite this basic
biological fact, many researchers and diet authorities still insist that the majority (50-60% or more) of the
human diet should come from carbohydrates.
I’ve seen papers where researchers point out that the body requires no carbohydrates which then go on to
say that a proper diet should contain at least 50% carbohydrates. It doesn’t make much sense.
At the same time, outside of a small essential fatty acid requirement (a few grams per day from the fish oils,
EPA/DHA), fats aren’t truly required by the body either. All of the tissues I mentioned above will use glucose
if you provide it (the heart is an exception, almost exclusively relying on fatty acids for fuel) and the body can
make fatty acids out of other sources if need be (this pathway isn’t utilized massively in humans, although a
few conditions will make it relevant).
So, outside of the small essential fatty acid requirement, one could make an argument for there being no
physiological requirement for fats either.
What does the body then require on a day to day basis if there is no real requirement for either carbohydrates
or fats? Well, outside of the basics like water and air, roughly eight amino acids are essential to get from the
diet, there’s the small essential fatty acids requirements and of course vitamins and minerals. Everything
else, strictly speaking is optional.
I would note that, to avoid starving to death, sufficient calories will be required. Since it’s generally unrealistic
to consume your entire daily caloric requirement from protein, that means that carbs, fats, or a combination
of the two, will generally be needed to supply sufficient energy to the body.
But, as noted above, most tissues in the body show a great deal of flexibility, using carbs when they are
available and fats when carbs aren’t available. Note also that the body has its own store of fuel, primarily in
the form of body fat that is mobilized when sufficient amounts of other nutrients aren’t available

So Why Do Most Argue that Carbs are Good and Fats are Bad?

Despite the fact that there is no physiological requirement for carbohydrates in the human diet, the most
common dietary recommendation in modern times is generally to reduce fat intake and increase
carbohydrate intake. I’m going to address the issue starting from that standpoint.
A good question might be why is this stance taken. While I can’t read the minds of these folks (and I hate to
contribute to grain lobby USDA conspiracy theories), I think the reasons is actually fairly simple: we have to
eat something.
There’s usually a limit to how much protein can be reasonably consumed (and most authorities seem to be
against ‘high’ protein intakes as well) so that means that the rest of the diet (in terms of energy) must come
from either carbohydrate or fat.
In the 70’s, the stigma against dietary fat started to develop and it all pretty much went from there. Fat was
implicated as the cause of heart disease, stroke, obesity, you name it and excessive fat intake was blamed.
Since people have to eat something and because of the general stigma against a high fat intake (some of
which is warranted, some of which isn’t), policy makers recommend a high-carbohydrate intake by default.
The bigger question is whether or not this is a scientifically defensible position.
I’ll address this issue in more detail in Carbohydrate and Fat Controversies: Part 2

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Carbohydrate and Fat Controversies: Part 2
In Carbohydrate and Fat Controversies: Part 1, I begun an examination of the argument over carbohydrate
and fat intakes in the human diet, explaining that, contrary to popular argument, most extremist stances in
this debate are incorrect. In Part 2, I want to continue addressing the issue by looking at both sides of the
debate.

Examining Both Sides of the Debate

As noted, the usual argument goes that high-fat diets cause high-cholesterol, heart disease, cancer, obesity
and the rest, as evidenced by the high incidence of those disease in modern diets (which are typically high
in fat). But that’s a questionable conclusion to draw.
Modern diets are also high in carbohydrates (and mainly the highly refined, high GI, low-fiber stuff that the
body often doesn’t handle well), low in fruits and vegetables, and generally contain the wrong types of fats
(an excess of saturated and trans fats with insufficient amounts of healthy fats). Such an intake is typically
coupled with inactivity, the folks eating them tend to be overweight/obese, smoking and alcohol play a role,
etc. That is, there are a number of inter-related factors at work here.
Pinning the blame entirely on fat intake or expecting only a reduction in fat to fix the problem is disingenuous:
there are a lot of variables at work here. Some research suggests that the entirety of the problem rests with
excessive saturated fat intake with the other variables (activity, fruits and vegetables, etc.) playing a relatively
minor role. It’s awfully hard to tease out all of the relationships when there are this many variables at play.
Similar comments can be made in terms of obesity. Fat is more calorically dense than carbohydrates and
studies comparing high-fat (40%) to low-fat (25%) meals find that people tend to eat more in the higher fat
conditions; this is usually referred to as passive over-consumption and leads to excess calorie intake. These
studies have problems, mind you, but that’s beyond the scope of this article. The point does stand, though,
that dietary fat is tasty (giving food mouth feel) and folks do tend to eat more of foods that taste good.
But while it’s common to blame obesity on high-fat diets, not all researchers agree. Some cultures have fairly
high fat intakes but have no problems with obesity and researchers are starting to realize that fat isn’t the
ONLY problem. Increasing intakes of refined carbohydrates (contributing large numbers of calories to the
diet), decreasing activity, increasing portion sizes and other factors all contribute. You can’t dismiss an
excessive fat intake as part of the obesity problem; it’s simply not the sole factor. I don’t want to get into a
massive discussion of the carb versus fat debate in terms of caloric intake, preferring to focus on the health
issues here.
The fact is that not all studies link a high fat intake to an increased risk of disease. For example, recent
analyses of our ancestral diet (what we ate during 99.9% of our evolution) suggests a much higher fat intake
and much lower daily carbohydrate intake. Exact numbers vary depending on what assumptions you use
but carb intakes of 20-40% (most of which came from low GI, high fiber fruits and vegetables; grains were
almost non-existent), fat intakes of 28-60% (which had a significantly different quality than our current diet),
and protein intakes of 19-35% of total calories are the current best estimates.
Studies of extant hunter-gatherer societies show little incidence of any of the diseases of modern society
and it’s thought that our evolutionary diet was NOT atherogenic (promoting heart disease) despite the high
fat intake.
The reasons for this are many-fold, of course and that’s the key to keep in mind when you consider fat
intakes and potential health problems. In our ancestral diet, fiber intakes were monstrous, averaging 100-

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150 grams per day. As well, despite the high fat intake, the source of that fat was far, far different than our
modern intake. Much higher intakes of polyunsaturated and mono-unsaturated fats and far lower intakes of
saturated fat were fairly typical. Activity levels were also much higher and folks generally stayed pretty lean.
Alcohol intake was low or non-existent, as was smoking. Although our ancestors dealt with various stresses,
they didn’t deal with the kinds of chronic stress that occurs in modern societies.
Related to this, studies of the Mediterranean diet have found few problems in terms of heart disease and all
the rest despite a relatively high fat intake (40% of total calories). Although the reasons are, as always, multi-
factorial some of the contributing factors are that the fat intake is primarily from mono-unsaturated sources
(e.g. olive oil).
As well, a tremendous amount of fresh vegetables are typically consumed (with far less reliance on refined
carbohydrates). Other factors such as activity, bodyweight, moderate alcohol intake and lowered stress
levels probably play a role. Studies of the Alaskan Inuit show similar results, despite an extremely high-fat
intake, heart disease is almost unheard of. This has typically been attributed to the high intake of fish oils
but there may be genetic adaptations as well.
Of course, some studies on low-carbohydrates diets (which are typically high in fat) will show a big
improvement in blood lipid levels; this is especially true for individuals with insulin resistance. I’d note that
this effect primarily occurs when weight is lost; in studies of very low-carbohydrate diets where weight is
gained, blood lipid levels often get much much worse.
Thus, whether or not you’re gaining or losing weight probably impacts on whether or not dietary fat is a
health risk. I’d note that studies in cyclists find that high intakes of saturated fat don’t pose a health problem
as long as the athletes are in calorie balance. As I mentioned above, activity (which will affect whether
ingested dietary fat is stored or burned off) plays a big role here.
Studies in diabetics are finding that higher mono-unsaturated fat intakes (and lowered carbohydrate) intakes
may be healthier than the converse. This, of course, only holds if calories are strictly monitored and controlled
to avoid weight gain. When weight is gained, from nearly any dietary approach, blood sugar control in
diabetics worsens.
Of course, there’s a flip side to the anti-fat dogma and reducing fat to extreme levels can cause its own set
of problems. First and foremost, most people find extremely low-fat diets to be tasteless and this tends to
limit adherence in the long-term (as I mentioned above, high-fat diets tend to be very tasty and people
frequently eat too much).
And while caloric intake typically goes down in the short-term, folks frequently end up increasing caloric
intake because they are hungry all the time. Dietary fat slows gastric emptying (keeping food in the gut
longer) although some work suggests that this effect is lost with chronically high-fat diets. Extremely low-fat
diets tend to leave people hungrier for this reason.
There is also evidence that the fat-soluble vitamin absorption may be impaired when fat intake is taken too
low. And while total cholesterol typically decreases when fat intake is lowered, the decrease occurs in both
the good (HDL) and bad (LDL) sub-fractions so overall health risk may not be improved. From a body
recomposition or performance standpoint, some studies show a lowering of testosterone with very low fat
diets.
There is another set of issues that crops up as well. Again, it relates to the simple fact that people have to
eat something. In reducing fat intake, most people increase carbohydrate intake. Most researchers would
say that this is just fine as long as the increase comes in the form of unrefined, high fiber, complex
carbohydrates. I would say that most researchers need to get out of the lab and look at the real world for a
while.

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The simple fact is that the majority of people who reduce fat do NOT increase carbohydrate intake from
unrefined, high-fiber, complex sources. This is especially apparent in the US (I can’t speak for other
countries) where companies rapidly jumped on the ‘fat is bad’ bandwagon and brought tons of ‘low-fat’ high-
carbohydrate sources that were highly refined to market.
Such foods may have as many, if not more, calories than the same higher-fat items. Even when they don’t,
humans play a cute psychological game, tending to eat more of a given food when they are told it’s low or
no-fat.
Recent studies are finding that, when carbs are increased from those sources, other problems show up. In
addition to the changes in blood cholesterol I mentioned above (both the good and bad subfraction
decrease), the increase in refined carbohydrate intake causes an increase in blood triglyceride levels and
small LDL particles; both of which are independent risk factors for heart disease and all the rest. The
chronically high insulin levels which commonly occur with such a diet cause other problems including insulin
resistance and all of the issues that accompany it.
I should probably note, and this could certainly be an entirely separate article, that the new scapegoat for
obesity and all of the health problems in the world is excessive carbohydrate intake, with a lot of the focus
on insulin release. I don’t have space here to address that side of the argument, a future topic for another
day.
Sufficed to say that while there is certainly an element of truth to this (in that excessive intakes of any nutrient,
and that includes refined carbohydrates, is bad), it’s still true that simplistically arguing that ‘fat is good and
carbs are bad’ is just as moronic as arguing that ‘carbs are good and fat is bad’. Again, it depends on the
context.

Summing Up

Now, I want to make it very clear that I’m not trying to make this either a pro-fat or anti-carbohydrate article
or trying to make a low-carbohydrate diet the default choice for anybody. My point is simply that the idea that
‘fat is bad’ and ‘carbs are good’ (or the opposite) is too simplistic to be meaningful.
Not all fat is bad and not all carbs are good. The source, the composition of the rest of the diet, the total
amounts you’re eating of each, your activity level and other variables all factor in. Whether you’re talking
about health risk or obesity, you can’t simply pin the blame on one factor or the other.
So, under conditions of high caloric intake, with a high intake of refined carbohydrates (meaning chronically
high insulin levels), poor quality fat choices (too much saturated fat and/or too little unsaturated fats), little
activity, minimal fruit and vegetable intake, etc. a high-fat intake is probably very detrimental from a health
standpoint. Sadly, this describes a fairly typical diet in the modern world (especially the US).
In contrast, with reduced or even controlled caloric intake (such that bodyweight goes down or is maintained)
and most of the fat coming from unsaturated sources (note: excessive polyunsaturated fats has its own set
of problems), a high fruit and vegetable intake, reasonable activity levels, keeping body fat levels down, etc.
higher fat intakes may be no problem at all. In some situations, an increased fat intake (again, from healthy
sources within the context of activity and a high fruit and vegetable intake) may be beneficial compared to
the alternatives (e.g. increasing carbohydrate intake).

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How Many Carbohydrates Do You Need?
A perennial question, argument and debate in the field of nutrition has to do with how many carbohydrates
people should be eating. While the nutritional mainstream is still more or less advocating a large amount of
daily carbohydrate (with fat being blamed for the health problems of the modern world), groups often
considered at the ‘fringe’ of nutrition are adamant that carbohydrates are the source of all evil when it comes
to health, obesity, etc. They advocate lowering carbohydrates and replacing them with dietary protein, fat or
both.
This is a topic that I discussed in some detail in Carbohydrates and Fat Controversies Part 1 and
Carbohydrate and Fat Controversies Part 2 and I’d recommend readers take a look at those for a slightly
different look at the issue than what is discussed here.
Arguments over recommended carbohydrate intake have a long history and it doesn’t appear to be close to
ending any time soon. Typical mainstream recommendations have carbohydrates contributing 50% or more
of total calories while many low-carbohydrate advocates suggest far fewer (ranging from the 40% of the
Zone diet to close to zero for ketogenic diets).
This article looks at the topic in detail. And while I originally wrote it quite a while back (some of you have
probably seen it before), it was nice going over it with fine toothed comb for an update. While the majority of
it stands up well over time, I was able to make some slight changes to the values, along with removing some
original stuff that wasn’t really relevant. Enjoy.

Introduction

It’s safe to say that most carbohydrate recommendations that you will see are put in terms of percentages,
you should be eating 45% of your calories as carbs, or 65% or whatever number is being used.
As I discussed in Diet Percentages: Part 2, I don’t like this method. Rather, putting nutrient recommendations
in terms of grams per kilogram or per pound is generally more valid (with one exception I discuss below).
The percentages are simply meaningless without knowing how many carbohydrates are being provided in
terms of gram amounts.
In that context, a typical ketogenic/low-carbohydrate diet might contain 0.5 g/lb (~1 gram/kilogram) of
carbohydrate. An average moderate carb diet (such as The Zone or Duchaine’s Isocaloric Diet) might contain
1 g/lb (~2 g/kg) of carbohydrate or slightly more. A typical high-carbohydrate diet would, of course contain
more than that (perhaps 2-3 g/lb or more). Typical recommendations for endurance athletes are in the 3-4
g/lb (6-8 g/kg) range and carb-loading may require 5-8 g/lb (10-16 g/kg) of carbohydrate.
Still, whether you’re looking at carb recommendations in terms of percentages of g/lb (g/kg), there is still a
huge discrepancy between different experts. Some recommend lots of carbs, some recommend medium
amounts, some recommend almost none.
Who’s right? Well, I am. Because rather than giving some single carbohydrate recommendation (that can’t
possibly take into account all possible situations), I look at the individual and their needs to decide how many
carbohydrates should be consumed daily.
Which is what I’m going to look at in detail in this article. The punchline, of course is that I’ll end up concluding
that how many carbohydrates someone needs (or should consume) daily depends on the same factors that
affect other nutrient recommendations: goals, preferences, types and amounts of activity, and our old friend,
genetic variation. By the end of the discussion, I’ll have set both minimum and maximum intake values
depending on different conditions that might crop up. Let’s start with minimum amounts.

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Are Carbohydrates Essential?

Despite oft-heard claims to the contrary, there is no actual physiological requirement for dietary
carbohydrate. Even the RDA handbook acknowledges this, right before recommending that a prudent diet
should contain a lot of carbohydrates.
To understand why carbs aren’t essential, I need to discuss the concept of an essential nutrient briefly. And,
in brief, an essential nutrient is defined as:
1. Any nutrient that is required for survival.
2. Can’t be made by the body.
Quoting from my own Rapid Fat Loss Handbook:
The second criterion is the reason that dietary carbohydrate is not an essential nutrient: the body is able to
make as much glucose as the brain and the few other tissues need on a day-to-day basis from other sources.
I should mention that the body is not able to provide sufficient carbohydrate to fuel high intensity exercise
such as sprinting or weight training and carbs might be considered essential for individuals who want to do
that type of exercise. I’ll come back to exercise later in this article.
But from the standpoint of survival, the minimum amount of carbohydrates that are required in a diet is zero
grams per day. The body can make what little it needs from other sources. What, you ask, are those other
sources? Read on.

Where Does the Glucose that the Body Makes Come from?

When carbohydrates are restricted completely, the body still has a small requirement for glucose (although
this decreases over time) and the body has to find something to make glucose out of. That something is
lactate and pyruvate (produced from glucose metabolism), glycerol (from fat metabolism) and some amino
acids. It’s the amino acid use that can be problematic since they have to come from somewhere.
Now, if no food is being consumed (e.g. total starvation), that somewhere is generally muscle tissue (the
body will also break down liver proteins); the body will readily break down body protein to scavenge the
amino acids it needs to produce glucose. In doing so, the muscle released alanine and glutamine (produced
in the muscle from the breakdown of leucine and the branch chained amino acids, so you know) which can
be converted to glucose in the liver. This process goes by the unwieldy name of gluconeogenesis which just
means the production of new glucose.
Protein losses during total starvation are extremely high to start, gradually decreasing as the brain switches
over to using ketones for fuel (this reduces the body’s glucose requirements which means less protein has
to be broken down to make glucose). Even so, during complete starvation there is always some loss of body
protein. Over long periods of time, this goes from harmful (because function is compromised from muscle
loss) to downright fatal. Especially as folks get extremely lean and body protein breakdown increases.
In this context, an under-appreciated fact of liver and protein metabolism (but discussed in detail in The
Protein Book) is that over half of all ingested amino acids are broken down in the liver in the first place. A
good portion of those can be used to make glucose and this is especially true when carbohydrates are
restricted.
Switching from starvation to dieting, this is fundamentally a big part of why protein requirements go up when
folks are dieting, more of the ingested protein is being used in the liver to make glucose, meaning that more

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total protein has to be ingested to make sure there is sufficient amounts to support things like protein
synthesis in skeletal muscle.
I don’t want to discuss this in detail here (since this article is about carbohydrates) but the topic is covered
to some degree in nearly all of my books. My original Ketogenic Diet had a thorough examination of protein
sparing on a diet and, of course The Protein Book discusses how protein requirements change during dieting
in detail.
I’d also note that, as long as protein intake is sufficiently high (e.g. the diet is covering the increased
breakdown of protein in the liver and elsewhere), the amount of carbohydrates which are truly required is
still zero; this is the basis of my Rapid Fat Loss Handbook approach: eliminate all non-essential nutrients
(including carbohydrates) and provide only those that are essential (in this case large amounts of high-quality
protein and essential fatty acids) to generate the largest deficit and maximum fat loss per day.
But, let’s assume that you don’t just want to eat massive amounts of protein, how many carbohydrates are
needed to limit (or prevent) protein loss on a diet?

How Many Carbs Do I Need to Spare Protein Loss?

Early research into the topic of starvation and low-carbohydrate dieting found that as few as 15 grams of
carbohydrates per day can limit nitrogen loss in the body. And raising carbohydrate intake to 50 grams per
day severely limits the need for the body to use amino acids for gluoconeogenesis (which is why I suggested
setting daily carbs on the low-carb days of The Ultimate Diet 2.0 at 50 grams).
This occurs via at least two mechanisms:
1. The increased carb intake maintains blood glucose and insulin at a higher level (inhibiting cortisol
release).
2. The carbohydrate provides glucose for the brain, limiting the need to break down body protein.
Basically, in the context of dieting, dieters can either jack up dietary protein to cover the increased
carbohydrate requirements of dieting or simply eat slightly more carbohydrates to provide them directly. Both
have the same end-result. 15-50 grams per day limits the body’s need to break down protein and will allow
protein requirements to be set lower than a diet providing essentially zero carbohydrates per day.

But What About Ketosis?

Since I’m going to use the term in just a second, I need to define what it means. When fatty acid burning is
ramped up to high levels (as when carbohydrates are restricted), the body starts producing ketone bodies
in the liver. As noted above, many tissues in the body can use ketones for fuel, basically they are an
alternative energy source to glucose when it’s not available. When ketones build up in the bloodstream
beyond a certain point, a condition called ketosis is said to develop. In contrast to the diabetic ketoacidosis
(which occurs in poorly treated Type I diabetics), dietary ketosis is not dangerous and is an adaptation by
the body to total starvation.
Many diets such as The Atkins Diet and other very low-carbohydrate diets are based around establishing
ketosis for various reasons which are beyond the scope of this article. I only bring this up as most ketogenic
diets set a carbohydrate intake level of roughly 30 grams per day (allowing some vegetables but little else)
although I’ve never found support for that specific value.

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I bring this up in the context of this article as many people start such diets with the specific goal of developing
ketosis (again, for a variety of reasons). Since many books give the 30 g/day value for a ketogenic diet, folks
get a little anxious about carb intakes that are higher than that.
However, strictly speaking, any diet with less than 100 g/day of carbohydrate will cause ketosis to develop
to some degree (more ketones will be generated as carbs are lowered). I’d note that many ketogenic dieters
use Ketostix to track ketosis, small sticks that measure urinary ketone levels. These are misleading for a
number of reasons, not the least of which is that while ketosis (as defined by blood concentrations of ketones)
may develop, urinary ketones don’t always show up, especially as carbs are raised to nearer the 100 g/day
high end.
In any case, an intake of 15-50 grams per day of carbohydrate will still allow ketosis to develop and those
ketogenic dieters attempting to ‘eat as few carbs as possible’ might want to consider that in the context of
not only providing much needed food variety (at 50 g/day, even a small amount of fruit can often be fit in)
but also in the context of the protein sparing issues I discussed above.
Getting to the point, although the physiological requirement for dietary carbohydrates is zero, we might set
a practical minimum (in terms of preventing excessive body protein loss) at 50 grams per day. I’d note again
that, within the context of The Rapid Fat Loss Handbook approach, carbs are limited to essentially trace
amounts; however protein (which makes up the majority of the diet) is set high enough to limit muscle loss.
However, not everyone functions well in ketosis. They get brain fuzzed, lethargic and just generally feel
awful. Even with weeks of being on a ketogenic diet, they never seem to adapt completely. That’s not a good
recipe for long-term adherence to a diet or healthy functioning or training.
Tangentially, I’d note that this seems to be related to inherent levels of insulin sensitivity. Individuals with
good insulin sensitivity, who typically run well on carbohydrates, tend to not do well on low-carbohydrate
diets. In contrast, individuals with insulin resistance often do far better reducing carbohydrates and that often
means going to ketogenic levels. Finally, some people seem to have the metabolic flexibility to do well with
either diet. I address this issue in more detail in article Insulin Sensitivity and Fat Loss.
So what if people want to avoid ketosis? In general, assuming zero or very low levels of activity, an intake
of 100-120 grams of carbohydrates per day will prevent the development of ketosis, just providing the brain
with enough carbohydrates to function ‘normally’. So, for folks who want (or need) to just avoid ketosis, 100-
120 grams per day will act as a practical limit. Again, this won’t quite work as a recommendation for people
involved in high-intensity activity since not all of the incoming carbs will be available for the brain.
So, summing up mid-article, the absolute requirement for carbohydrates is zero grams per day. However,
depending on protein intake, a practical minimum for carbs lies between 50 grams/day (if someone functions
well in ketosis) to 100-120 grams per day (if they don’t function well in ketosis). Let me mention very
specifically that I’m not suggesting those numbers are a recommended level, I’m simply using them to
represent a practical minimum value.
As a final note, before addressing the issue of exercise, I want to note that the above values above don’t
change significantly with body size (e.g. it’s one of the few places that an absolute number of carbs, rather
than an amount set relative to bodyweight is appropriate). Most of the above discussion deals with the
carbohydrate requirements of the brain which, for the most part, doesn’t change massively with body size.
A 120 pound female and a 200 pound male have roughly similar carbohydrate requirements for their brains
because brain size simply doesn’t differ that much between them.

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The Impact of Exercise

So far I haven’t considered the impact of activity on all of this as this can affect daily carbohydrate
requirements. I’d comment that all exercise is not the same and different types of activities will affect
carbohydrate requirements very differently. The type, amount and intensity of activity will impact on
carbohydrate requirements.
Typical low intensity aerobic/cardiovascular work doesn’t generally use a lot of carbohydrate. So if someone
were only performing that type of activity (i.e. walking 3-5 times per week), there wouldn’t be any real need
to increase carbohydrate intake over the above minimum. They might want to increase carbohydrates to
higher levels than that (for various reasons) but, strictly speaking, they probably don’t need to.
The carbohydrate requirements for weight training actually aren’t that great. I did some rough calculations
in The Ketogenic Diet and concluded that, for every 2 work sets (assuming a set length of 30-45 seconds)
or so, you’ll need 5 grams of carbohydrates to replenish the glycogen used.
So if you did a workout containing 24 work sets, you’d only need about 60 extra grams (24 sets * 5 grams/2
sets = 60 grams) of carbohydrate to replace the glycogen used. So if you were starting at the bare minimum
of 50 grams per day and were doing roughly 24 sets/workout, you’d need to consume an additional 60 grams
(total 110 grams/day) to cover it. If you didn’t function well in ketosis and were starting at the 100-120 g/day,
you’d increase to 160-180 g/day. I’d note that, for the average male lifter, this works out to about 1 g/lb or
~2 g/kg lean body mass carbohydrate per day
In this context, bodybuilding nutrition (much of which has been determined empirically over the years) has
long recommended carbohydrate intakes ranging from 1 g/lb on fat loss diets to 3 g/lb for mass gains so
we’re definitely in that range at this point. General recommendations for strength athletes by the nutrition
mainstream are in the range of 5-7 g/kg or 2.2-3 g/lb so these values are all pretty consistent.
Higher intensity cardiovascular exercise is a little bit harder to pinpoint in terms of carbohydrate requirements
and can vary pretty significantly depending on the intensities and volumes. A sprinter running 60m repeats
isn’t using a lot of glycogen, a trained endurance athlete working near their lactate threshold for extended
periods can deplete glycogen fairly completely in 1-2 hours. Even at lower intensities, the 2-6 hour sessions
done by endurance athletes can completely deplete both muscle and liver glycogen stores on a daily basis.
Full skeletal muscle glycogen depletion for these athletes might represent 300-400 grams of total
carbohydrate or more. For an average sized endurance athlete this might represent 3 g per pound or ~6
g/kg on a more or less daily basis. Under less extreme circumstances, carbohydrate requirements won’t be
as high. And while current recommendations for endurance athletes are in the 7-10 g/kg (3-4.5 g/lb) range,
studies show that most athletes consume closer to 5 g/kg (2.2 g/lb).
However, only the most highly trained athletes are going to be able to do that on a daily basis. Even with
exercise, the average recreational trainee won’t have carb requirements near that level. Essentially, if
competition athletes are getting sufficient carbohydrate intake at a level of ~5 g/kg (roughly 2 g/lb), I see little
reason for the average individual to consume more or for people to recommend that they consume more.
I should note that the above sections assume that maintenance of muscle glycogen is the goal. Under some
situations (generally fat loss), glycogen depletion, or maintenance of glycogen at a lowered level is the goal.
This means that an athlete or dieter may deliberately under consume carbohydrates such that, over some
time period, glycogen concentrations decline. In such a situation, where someone deliberately wanted to
maintain muscle glycogen at lower levels, the above values would be too high since they are aimed at full
glycogen repletion after heavy exercise.

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Of course, there are also situations where dieters or athletes want to increase muscle glycogen levels far
above normal; this will require higher carbohydrate intakes than the values above.

Is There a Maximal Level of Carbohydrate Intake?

Logically, a practical upper limit for carbohydrates intake would be a situation where they made up 100% of
someone’s total energy intake. An average individual has a daily caloric intake in the realm of 14-16 cal/lb.
Since carbs have 4 calories/gram, this would represent a maximum intake of roughly 4 grams/lb (8.8 g/kg).
Of course, athletes involved in heavy training (who are burning far more calories than 14-16 cal/lb) have
higher caloric (and hence carbohydrate requirements). But for the typical person at maintenance, a realistic
upper limit would be ~4 g/lb and this would leave no room for either dietary protein or fat (without going over
maintenance calories).
Of course, there are also situations where a dieter or athlete wants to super-compensate their muscle
glycogen levels; that is load the skeletal muscle far above the levels which are normally maintained. This is
often done by endurance athletes looking to improve performance and various cyclical diets (such as my
Ultimate Diet 2.0) use glycogen compensation for anabolic (muscle building) purposes.
Generally speaking, to generate maximal levels of glycogen requires first depleting the skeletal muscle with
the combination of heavy training and a low-carbohydrate diet. Given those conditions, carbohydrate intakes
in the realm of 16 g/kg (a little over 7 grams/pound) of lean body mass can be tolerated over a 24 hour
period. This probably represents a practical maximum for carbohydrate intake but it would only be achievable
under this very specific situation.

Summing Up

So let’s sum up, looking at both practical minimum and maximum carbohydrate intakes under different
circumstances. For illustrative purposes, after each of the g/lb recommendations, I’ll give an absolute number
of carbohydrate, assuming an athlete with 160 pounds of lean body mass.

Carbohydrate Grams for an athlete


Circumstance
Requirement1 with 160 lbs. LBM

Physiological Requirement 0 g/day 0 g/day

PracticalMinimum to Avoid Muscle


50 g/day 50 g/day
Breakdown2

Practical Minimum for Individuals Who


100-120 g/day 100-120 g/day
Function Poorly In Ketosis3

Additional Amount to Sustain Low Minimal approaching


Minimal approaching zero
Intensity Exercise zero

Additional Amount Needed to Sustain 5 g carbs. per 2 work 5 g carbs. per 2 work
Weight Training sets4 sets4

Average Recommendations in
1-3 g/lb. 160-480 g/day
Bodybuilding Nutrition

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Average Recommendations by
2-3 g/lb 320-480 g/day
Mainstream Nutritionists

Average Intake for Endurance Athletes 2 g/lb 320 g/day

Recommended Intake for Endurance


3-4.5 g/lb 480-720 g/day
Athletes

Practical Maximum for Non-Carb Loading


4 g/lb 640 g/day
Individuals

Maximal Intakes for Carb-Loading ~7 g/lb 1120 g/day

1. All values are in g/lb. To convert to g/kg, multiply by 2.2.


2. Note: If protein intake is sufficient, this amount of carbohydrate is not required.
3. All values above this line assume no exercise and do not change significantly with body
weight.
4. Assumes a set length of 30-45 seconds.
Clearly the above represents a pretty drastic range of carbohydrate requirements, depending on the
specifics. For a typical male with 160 pounds of lean body mass, daily carbohydrate intake could range from
the physiological requirement of zero grams per day to a near maximum of 1120 g/day during a carb-load.
Which makes it no wonder that people are confused.
Simply, the question “How Many Carbohydrates Do You Need?” has no singular answer. The goals of the
person, the amount and type of activity, their individual needs (e.g. insulin sensitive vs. resistant, whether or
not they function well in ketosis or not), their individual goals all determine how many carbs are ideal in the
diet.

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Body Composition Recommendations
In previous articles in this ‘series’,I’ve addressed the question What Does Body Composition Mean?, showed
you how to do Body Composition Calculations, and taken a look at Body Composition Numbers. Over two
articles, Measuring Body Composition Part 1 and Measuring Body Composition Part 2, I looked at different
methods that, even if they don’t measure body composition exactly, will at least allow tracking of progress
of some sort. In the last article, I discussed some of the Problems with Measuring Body Composition.
Finally, in this article, I want to give some concrete recommendations on how to put this information to use,
with some specific recommendations about measuring and tracking body composition. First off I want to
discuss one last potential problem with body composition measurements; then I’ll make some specific
recommendations about which methods to use, when to measure body composition and how best to make
use of the information I’ve presented.

Lean Body Mass/Fat Mass Problems

As I’ve at least mentioned in earlier articles in this series, all lean body mass and all fat mass aren’t identical
and this provides another place where body composition measurements can be a problem. For example,
there are at least three primary types of body fat (in The Stubborn Fat Solution I describe five different types
but that’s more detail than we need here) which are
1. Visceral fat (deep, around the gut)
2. Subcutaneous fat (under the skin, the stuff we can see)
3. Essential fat
And depending on which method of measuring body composition you’re using, loss of one vs. the other is
difficult to track (e.g. calipers only measure subcutaneous fat). Now, the essential fat issue isn’t a big one
since you won’t generally be losing that and, if you are, you’re probably starving to death and about to die.
But an inability to measure losses of visceral fat by some methods causes problems because measurements
that don’t measure it will show visceral fat loss as a loss of lean body mass (which leads people to think that
they are losing muscle mass). Calipers are a prime example, since you can’t pinch visceral fat with them, a
loss of visceral fat on a diet will show up as LBM loss by those calculations.
As I discussed in What Does Body Composition Mean?, lean body mass (LBM) actually constitutes a lot of
different things including muscle mass, glycogen, water, minerals, organs and a few others. For this reason,
some researchers have started to differentiate between essential LBM (muscle and organ mass) and
inessential LBM (connective tissue).
In general, inessential LBM tends to be lost first and essential LBM later. However, depending on the setup
of the diet (primarily protein intake and whether or not the person is exercising), there can be essential LBM
loss early in a fat loss diet. Just looking at LBM loss can’t differentiate between the two.
Now, the LBM issue can be avoided to some degree if someone is performing resistance training (which
everyone should be while dieting). What’s happening to strength in the weight room tends to act as a rough
metric for what’s happening to muscle mass; if someone is more or less maintaining their strength levels,
odds are that muscle mass isn’t being lost. If strength is dropping like a rock, muscle is probably being lost.
It’s worth nothing that rank beginners can’t even use that method because beginners can gain strength
(through neurological adaptations) even if they are losing muscle mass.
Which isn’t to say that I think body composition monitoring is useless; if that were the case I wouldn’t have
written 6 articles about it. I’m just trying to make the point that it’s not perfect.

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Mass Gaining

Although I’ve focused primarily on fat loss in this series (simply because, statistically more people are trying
to lose fat), the same comments and issues apply equally when someone is trying to gain mass or
strength. Athletes and bodybuilders want to know the composition of the weight that they are gaining, how
much muscle mass they are gaining versus how much fat.
And the same issues that I’ve discussed crop up. Many methods of measuring body composition can’t
measure changes in glycogen and water (and certain diets and supplements will use this to their advantage,
causing the body to hold more glycogen and water to make the lifter think that they are gaining radical
amounts of lean body mass).

So What do I Recommend?

Ok, enough of that, let’s look at what I actually recommend folks use to track changes in body composition,
starting from the least to the most complex. Normally, I suggest a combination of methods rather than just
one since that tends to help avoid problems inherent to any single method. These recommendations apply
to both fat loss and muscle gain plans.
The simplest method, of course is the mirror which I imagine nearly everyone has. You can get naked if you
want to (put them on the Internet and you might make some good money) or wear a bathing suit. As I noted
in Measuring Body Composition Part 1, if you can be honest with yourself, the mirror may tell you all you
need to know. Unfortunately, it’s difficult for most to be honest. As well, things like lighting, water retention
can impact visual appearance and few folks can be truly objective with what they are seeing.
The other problem with the mirror that i noted was that small daily or weekly changes can be tough to see
and people may get depressed when it doesn’t appear that anything seems to be happening. Enter
pictures. Taken 4-6 weeks apart, these will often provide much more visual indication of what’s going on
since the contrast will tend to be greater. It’s the same phenomenon by which you don’t think anything is
physically happening but then you run into someone you haven’t seen for a couple of months and they go
“My god, you look totally different.” Again, make sure to wear the same outfit, put the camera the same
distance away, use the same lighting, etc. to make the pictures as comparable as possible.
Next up would be the standard bathroom scale. I think I covered this one pretty thoroughly already. For
individuals carrying a lot of fat, the scale can actually work pretty well by itself since weight loss will pretty
much be identical to fat loss. As individuals get leaner (perhaps 15% for males and about 22% for females),
this is no longer the case and weight changes by themselves can be misleading. Females have the
additional issue that changes in water balance can screw everything up. I’ll come back to this when I talk
about when and how often to measure.
I should mention that tracking weight changes along with performance in the weight room can often be most
of all that’s needed during a fat loss diet. If weight is dropping but strength in the weight room is staying
consistent (and the person isn’t a beginner), that indicates that what is being lost is not muscle mass; by
extension it should be fat.
The next addition would be the tape measure, which can at least give you some indication of where the
weight (hopefully fat) is coming off. For fat loss purposes, it’s often useful enough to measure one or two
indicator areas. For men, changes typically occur around the midsection: when the waist is going down, fat
is being lost, if it’s going up, fat is being gained. Women might use thigh.

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Of course, if someone is trying to gain muscle mass, measuring the target muscle groups would be logical;
along with changes in strength in the weight room, this can tell you what’s going on (e.g. is the target muscle
group growing or not).
A related method to the tape measure is to use clothing as a gauge. You might have a standard pair of pants
or dress or whatever that you try on every so often. If it’s fitting more loosely, you’re losing weight and/or
fat. If it’s tighter, well…..
Related to this, it’s worth noting that studies of successful weight losers have been found to monitor their
weight more regularly (and a piece of clothing that you wear regularly is a quick way to do this); contrast that
to people who wear nothing but elastic band clothing and one day ‘wake up fat’ without ever noticing what’s
happening.
It’s worth commenting again, that that tape measure can be misleading as well. A drop in tape measure
measurement might suggest muscle loss but actually be due to glycogen and water depletion. A loss of 1/2″
or more on the arms isn’t uncommon with complete glycogen depletion (as occurs in my Ultimate Diet 2.0
plan). Bodybuilders tend to hate carbohydrate depletion for this reason: they feel flat and small and can’t
get a pump in the gym.
As I mentioned other methods such as the Body Mass Index can be used to track changes and, for untrained
individuals, can actually be used to get a rough estimate of body composition (I use this method in both The
Rapid Fat Loss Handbook and A Guide to Flexible Dieting). Waist/hip ratio can tell you a little bit about
what’s going on too.
I should note again that there are reasonably accurate equations that use the tape measure to estimate
actual body fat percentage and they can be used in that fashion in addition to just tracking changes in
girth. The links to the equations can be found in Measuring Body Composition Part 2. For individuals without
access to one of the other true body composition methods, this is a workable compromise.
Although the Tanita scales are very popular, my concerns with most people’s inability to adequately
standardize hydration status leads me to not recommend them widely. I suppose if you always measure at
the same time of the week and day, they can be at least workable. And they do avoid a lot of the issues
with proper caliper technique.
Which brings me to calipers which I still tend to recommend the most widely. Once folks get decent at
measuring themselves, they can track changes fairly reasonably. Even if the actual equations aren’t used,
like the tape measure, certain key sites can be tracked to measure changes in body fat. Males will typically
use abdominal or the iliac crest (the love handle) and females can measure the thigh. Often that one
measurement alone tells you everything you need to know even if you can’t actually estimate true body fat
percentage from it.
The higher tech methods such as underwater weighing, DEXA or the BodPod might be used if you can get
access to them relatively cheaply (or free); I’m told that BodPod readings can be had fairly cheaply if you
can actually find a place that has a one. DEXA is also useful for females to keep tabs on bone density to
save them problems down the road (when they get older).
As I mentioned in a previous article, something that may be worth doing it calibrating one of the lower tech
methods with the higher-tech method. So get a caliper reading done along with underwater weighing or
DEXA or what have you to see how closely they match up. Then just use the cheaper methods going
forwards.

My Ideal

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If I had to pick a single combination of methods for most applications, it would probably be the scale, a tape
measure, and calipers. And probably throw in the mirror and pictures for good measure. The mirror/picture
will give you an idea of what’s happening visually and between changes in weight, selected tape measure
measurements and caliper readings, you should be able to keep pretty good track of what’s changing (or
not) physically with either a diet or muscle mass gain program.
As I mentioned above, for the exceedingly low-tech out there, simply looking at scale weight and strength
levels in the gym will tell most of what’s going on. If fat loss is the goal, you want a drop in weight with little
to no change in strength in the weight room. If that’s happening, most of what you’re losing is fat (or at least
it’s not muscle mass). For muscle gain it’s a bit more difficult but as long as you keep weight gain per week
reasonable (0.5-1 lb per week or so), if you’re getting stronger in a medium repetition range, odds are most
of what you’re gaining should be muscle mass.
Again, I know a lot of folks like BIA scales and, as long as you control hydration state, they can work ok. I’m
personally still biased to calipers since, once you learn to use them, I think they work better. And they are
cheaper if nothing else.

When to Measure

As I discussed in Problems with Measuring Body Composition, although all methods of measuring body
composition can have issues with true accuracy, arguably we are more concerned with consistency. That
is, we want to be able to compare measurements over time to one another to see what the changes are.
And one aspect of consistency is actually taking the measurements under the same conditions. Now, there
are a couple of weird exceptions where you would deliberately take measurements under different conditions
(e.g. to determine if a carb-load worked or not) but, under most circumstances, taking any measurements
under identical conditions is important to be able to know what’s going on.
So, depending on preference, you might take 10 minutes every Monday morning to take a quick set of
measurements. So first thing, after going to the bathroom (but before eating), hop on the scale, throw a tape
measure around a couple of key sites (again, usually waist for men and thigh for women) and do a couple
of quick caliper measurements. Write it down and then get on with your day. This will give you
measurements that you can compare week to week to see what’s happening. Of course, if you’re doing
pictures, you may need to pick a different time of day so that you have time to do it without rushing. My point
is simply that you need to keep everything consistent.
What won’t work is measuring at drastically different times since this won’t make the measurement
comparable. Doing a set of measurements on a Friday afternoon after you’ve eaten several meals and been
running around all day to first thing Monday morning after you wake up won’t give values that are meaningful.
And while people do this all the time, you can’t compare measurements taken immediately after a workout
to those taken before it (we’ve all seen people get on the scale before and after training, to see how much
weight they ‘lost’ I imagine). Sweat and water redistribution to the skin will throw everything off. So pick
one time to measure and keep it consistent.
Oh yeah, if you’re using tape measure measurements to check changes in muscle size, a question that often
comes up is whether or not to take the measurement flexed or unflexed. At the end of the day it doesn’t
matter, make your choice and keep it consistent. That’s all that matters, the consistency so that you can
compare measurements.
Regarding calipers, if you’re not going to do your own measurements (and some of the spots are impossible
to get at unless you’re a contortionist), it’s best to have the same person do them every time since individual

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technique can vary a bit. This is a problem as most commercial gyms have a lot of employee turnover and
the same person who took you measurements initially may not even be working there now. In that case,
consider teaching your significant other to do it. Or your kids; make them useful for something other than
pooping and leaving their toys on the floor.
Finally, there’s women who, as always, have the most interesting issues. Changes over the menstrual cycle,
especially with water balance, can make tracking real changes in body composition a real pain in the ass. As
well, there is just huge variation in this; some women gain little water and others will swing 10 pounds in a
week. This will not only throw off the scale (and of course BIA) but also tape measure and calipers.
For women, it may be best to stay away from weekly measurements and just measure once a month and
compare those values. Or, if weekly measurements are made, only compare the same weeks of the
month. So compare week 1 to week 1 (of hte next month )and week 2 to week 2. If you try to compare
week 1 (when you’re not holding water) to week 2 (when you are), you are likely to go crazy becuase of the
changes.

How often to Measure

Let’s face it, most people measure themselves too often.. As I mentioned, we’ve all seen people get on the
scale before and after a workout, presumably to see how much weight they lost during the workout. I’ve
seen guys trying to get big do the same, I guess they want to see how much muscle they built (ha ha). At
home, dieters will get on the scale before and after they poop just to watch the numbers drop. I’ve done it
and you have too.
Clearly this isn’t effective as changes can’t happen that quickly and, in general, I see little reason to measure
more than weekly. And sometimes, or in specific situations, even that can be misleading. Between shifts in
water weight (that happen to everyone), women’s menstrual cycles, etc. weekly measurements may indicate
that nothing is actually happening when it is.
One solution to this is to take a rolling average of changes and plot them on a spreadsheet. As long as they
are showing a trend downwards over time, that’s most of what matters. If you don’t know how to do this, get
one of your nerd friends to set it up for you in Xcel.
Add to this an odd phenomenon that is often referred to as the “whoosh” (a topic I discussed seriously in
The Stubborn Fat Solution). What sometime happens, and this is assuredly related to issues related to
water balance, is that someone will be dieting for a few weeks with no changes. Suddenly, almost overnight,
there is the “whoosh”; they wake up several pounds lighter and visibly leaner. Suddenly the diet that wasn’t
working” for 3 weeks just generated a massive change. My point being that this can make weekly tracking
annoying and misleading from time to time.
At the same time, it’s also possible to track things far too infrequently. As I mentioned above, studies of
successful dieters show that regular tracking of weight and body composition is one way that they avoid
weight regain; basically by keeping tabs on what’s happening, they know when they are starting to slip off
the wagon and can tighten up their diet or exercise program. This is probably a good strategy for folks who
have to really fight to keep from falling back into old dietary and non-exercise habits.
What doesn’t work is avoiding the scale or mirror or tape measure for months on end and then ‘waking’ up
with the same 42 inch waist you started with. Measuring at least semi-regularly during weight maintenance,
perhaps every 2-4 weeks, is a good way to keep yourself honest. If the numbers start to go the wrong
direction, it’s time to get a little more diligent about your diet and training.

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In general, body composition doesn’t change that drastically week to week although there are
exceptions. On extreme diets, such as The Rapid Fat Loss Handbook, often there are visible and
measurable changes week to week. But on more moderate diets, usually changes week to week are not
much more than background noise to the measurements.
And in that situation measuring too often can lead people to think that things aren’t working and make them
start doing goofy things (like drastically increasing activity, cutting calories severely, or abandoning the diet
outright). Measuring every 2-4 weeks is probably better and it is worth commenting that if you haven’t seen
any visible or measurable changes in 4 weeks, your diet and training probably should be modified becuase
it’s not working very well.
One odd exception that I’ve seen is that beginners (and usually females more than men) often won’t see
any changes in the first 4 weeks of their new fat loss program. This can be frustrating and cause a lot of drop
outs. So they’ll be plugging along with the exercise and diet program and nothing is changing. But then
they invariably get the “whoosh” about week 4 or perhaps a little bit later; it always happened by week 8 in
any case. Almost overnight, they drop 4-5 pounds and look visibly different. Patience is a virtue here and I
highly recommend that folks just starting out show a little patience when they start trying to lose fat (or gain
muscle).
Another exception to the above is folks who are very lean and this usually means contest bodybuilders or
athletes. When body fat levels are already very low it’s not uncommon to see changes occurring much faster
and tracking every 1-2 weeks may be necessary to keep tabs on what’s going on (there is often a time
constraint here so it’s critical to keep tabs on the changes). Measuring weekly with calipers, etc. may be
necessary to make sure they are coming in on time.
Of course, those athletes aren’t immune to the “whoosh” either and often 2 weeks of apparently no changes
will be met with a massive change almost overnight. This seems to be very individuals, folks who are prone
to water retention see “stalls” and “whooshes” and those who don’t usually don’t.
If you’re wondering why the huge discrepancy between the very lean and folks carrying a lot of fat in terms
of changes, I think it’s actually pretty simple math. When someone is carrying 30-60 pounds of fat, a 1
pound loss per week isn’t very much (3% or less of the total) and that’s less than what the best body
composition method can actually pick up. In contrast, when someone is very lean and down to the last few
pounds of fat, even a small fat loss may represent a massive percentage of what’s left; it’s not unheard of
for bodybuilders to change visually day to day at the end of their diets.

Summing it all Up

Whew, so that’s that. Pretty much everything I have to offer about measuring body composition. I’ve
explained What Does Body Composition Mean?, showed you how to do Body Composition Calculations,
and taken a look at Body Composition Numbers.
In Measuring Body Composition Part 1 and Measuring Body Composition Part 2, I looked at different
methods that, even if they don’t measure body composition exactly, will at least allow tracking of progress
of some sort. Finally. I discussed some of the Problems with Measuring Body Composition.
In this article, I’ve given my specific recommendations (and ideal combination of methods) that I think will let
people best track changes in body composition to see if their diet and exercise program is working. No
single method is perfect by itself but using a combination can give a pretty good indication of what’s actually
going on.

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I strongly belive that folks who are dieting (or trying to gain muscle mass) should be tracking some aspect
of body composition changes. What method is used may ultimately be less important than some method is
used.
As a strength coach buddy of mine likes to say “If you’re not assessing, you’re guessing” and that applies
here. If you’re not tracking some aspect of what’s changing about your body, you can’t know if what you’re
doing is effective.
With that said, keep in mind that none of the methods currently available are perfect. Use them intelligently
but don’t live and die by them.

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Different Glycemic Indexes of Breakfast Cereals Are Not Due to
Glucose Entry into Blood but to Glucose Removal by Tissue.
Schenk S et. al. Different glycemic indexes of breakfast cereals are not due to glucose entry into
blood but to glucose removal by tissue. Am J Clin Nutr. (2003) 78(4):742-8.

BACKGROUND: The glycemic index (GI) of a food is thought to directly reflect the rate of digestion and
entry of glucose into the systemic circulation. The blood glucose concentration, however, represents a
balance of both the entry and the removal of glucose into and from the blood, respectively. Such direct
quantification of the postprandial glucose curve with respect to interpreting the GI is lacking in the literature.
OBJECTIVE: We compared the plasma glucose kinetics of low- and high-GI breakfast cereals. DESIGN: On
2 occasions, plasma insulin concentrations and plasma glucose kinetics (by constant-rate infusion of [6,6-
(2)H(2)]glucose) were measured in 6 healthy males for 180 min after they fasted overnight and then
consumed an amount of corn flakes (CF) or bran cereal (BC) containing 50 g available carbohydrate.
RESULTS: The GI of CF was more than twice that of BC (131.5 +/- 33.0 compared with 54.5 +/- 7.2; P <
0.05), despite no significant differences in the rate of appearance of glucose into the plasma during the 180-
min period. Postprandial hyperinsulinemia occurred earlier with BC than with CF, resulting in a 76% higher
plasma insulin concentration at 20 min (20.4 +/- 4.5 compared with 11.6 +/- 2.1 micro U/mL; P < 0.05). This
was associated with a 31% higher rate of disappearance of glucose with BC than with CF during the 30-60-
min period (28.7 +/- 3.1 compared with 21.9 +/- 3.1 micro mol. kg(-)(1). min(-)(1); P < 0.05). CONCLUSION:
The lower GI of BC than of CF was not due to a lower rate of appearance of glucose but instead to an earlier
postprandial hyperinsulinemia and an earlier increase in the rate of disappearance of glucose, which
attenuated the increase in the plasma glucose concentration.

My comments: This is another older paper that I wanted to talk about since it ties in somewhat with the
feedback on milk below. In way of introduction, I should probably define glycemic index (GI) for readers
who aren’t familiar with it.
The GI is used to rate carbohydrates by examining the blood glucose response to 50 grams of digestible
carbohydrates. After fasting, subjects are first given some reference food; this used to be glucose but
researchers now use white bread. The blood glucose response to white bread is defined as 100. Then, the
test food is given and the blood glucose response is measured and compared to that of the test food. A
food that shows 60% of the blood glucose response to white bread is given a GI of 60.
It has commonly been assumed that GI and insulin response are related and bodybuilders and athletes
commonly use GI to determine which foods are or are not acceptable to eat (especially on a fat loss
diet). Low GI foods are usually assumed to digest slowly and it is the slow rate of glucose into the
bloodstream which causes the low GI.
A massive number of foods have been tested for GI although there is still much debate as to the validity of
GI in meal planning. GI can vary significantly by food and how it is prepared, as well as between
individuals. Also, GI is measured for 50 gram quantities of foods (that’s 50 grams of digestible
carbohydrates). But this can be misleading; for example, carrots are very high on the GI scale but few
people would eat 50 grams of digestible carbohydrates worth of carrots in a sitting. To counter this, some
researchers have proposed a measure called the glycemic load (GL) which is the total amount of digestible
carbohydrate multiplied by the GI. This at least recognizes that, in the real world, carbohydrate intake

53
varies. GL can be lowered by either picking lower GI foods or by eating less total carbohydrate, or some
combination of the two.
Additionally, GI tends to be affected by other nutrients (protein, fat and fiber) although not always in the way
you’d think (and not all research finds a significant impact of protein and fat). For example, protein tends to
lower the GI of carbohydrates but insulin levels often increase when you add protein to carbs.
For reference, the most complete site on the web for information about GI is Rick Mendosa’s Site.
Which brings us to the above study. As mentioned above, bodybuilders and athletes usually assume that a
low GI means a low insulin response but the study above draws that conclusion into question. Rather it
found that the low GI food showed a lower blood glucose response because it generated a higher early
insulin response (clearing blood glucose out of the bloodstream) at the 30 minute mark (by 60 minutes, both
foods showed similar insulin levels). Quoting directly from the paper "Bran cereal has a low GI because a
more rapid insulin-mediated increase in tissue glucose uptake attenuates the increase in blood glucose
concentration, despite a similar rate of glucose entry into the blood."
That is to say, both foods released glucose into the bloodstream at similar rates, but the bran cereal showed
faster uptake due to a higher initial insulin spike, which lowered the overall GI response.
The researchers also noted that the bran cereal contained more protein than the corn flakes and this is
probably what caused the higher insulin response (and lower blood glucose) which ties into my comments
above.
Somehow, I don’t think bodybuilders would argue that combining low GI carbs with protein is bad for fat loss,
yet here we have an (as of yet unreplicated paper) showing that the initial insulin response is higher;
essentially, the higher initial insulin response caused the lower GI in this case. Yet most bodybuilders also
believe that high insulin is detrimental to fat loss. Here we have a study that I think questions that idea. At
the very least, the small initial insulin spike certainly wouldn’t appear to be hurting things, it’s likely that
sustained insulin levels would be more problematic by limiting the ability to mobilize fat for fuel.
Then again, at least one study found that spiking insulin (high GI condition) resulted in a larger rebound in
blood fatty acid levels (after blood glucose crashed) compared to keeping insulin low but stable (low GI
condition) so maybe there’s more to this picture than we yet realize.

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Carbs & Fat: Friends After All?
Here’s a true story… On a fitness message board, a member cautioned another against having
peanut butter with his oatmeal. “Why not?” asked the confused youth. The pseudo-educated
guy answered, “This is bad, never, especially while cutting, do you mix carbs and fats. PWO
should be pro/carb.” I had to go into that thread and straighten things out. Yes, I’ll admit that I
get kick out of breaking up a good bro-down. This incident was in 2004, and the last time I
checked, we’re dangerously close to half a decade past that. Believe it or not, people still parrot
this guideline.

Context-switching & oversimplification

In the same absolutist vein that The Zone Diet warns against consuming carbs without fat along
with it, some of you may be aware of the opposite recommendation to avoid combining fats and
carbs. It’s been suggested that when insulin levels are high, dietary fat in circulation has a better
chance of making into the storage depots. This is misleading because it’s assumes a singular
transient event will develop into the multi-factorial condition of over-fatness. Furthermore, it
mistakenly ordains insulin as the almighty agent of fat gain (or inhibition of fat loss). Let’s clear
up this mess, shall we?

How did this start?

Despite small fluctuations, the Standard American Diet (SAD) has traditionally been higher in
carbohydrate (52%) and fat (33%), with protein (15%) taking up the least dietary space [1].
Since the prevalence of obesity has risen to belt-popping proportions in the US over the last
three decades, it’s easy to claim that the high-carb/high-fat combination will keep you nice and
plump. However, fitness buffs are typically on a high-protein/anti-carb kick, so the separation of
carbs and fat in this population would have minimal impact either way. Still, the no-carbs-with-
fat dictum has been adopted by many individuals in search of the edge; the magic secret.

A little horse sense

One of the biggest logical flaws of the “don’t mix carbs with fat” philosophy is that it’s extremely
rare for individuals consuming more than one or two meals per day to be in a truly fasted state
aside from waking in the morning. For most of us, there’s a constant meal absorption overlap
that keeps insulin, glucose, amino acids, and lipids in the blood above fasting levels. Since we
spend most of our waking hours in the ‘fed state’, it’s flat-out silly to think we can avoid this
overlap by simply separating our carb and fat intake by a few hours. So, is this mixture of
substrates in circulation a bad thing for fat loss in the first place? Buckle up, here comes the
cold, hard data.

Separation anxiety

One thing that really bugs me is when someone makes an adamant claim about how the body
works, but has no objective evidence to back it up. Such is the case with claiming that mixing
fats and carbs is the ticket to fat gain (or fat retention). To my knowledge, there’s only a single
study directly comparing the separation of carbs and fats versus their combination [2]. Both
groups lost a significant amount of bodyweight. Although not to a degree of statistical
significance, the combination group had greater weight and fat loss. The researchers concluded
that despite popular belief, the separation of macronutrients (carbs and fat in particular) had no
metabolic benefit over consuming them together.

More proof that having fat with carbs won’t hinder fat loss

A relatively recent trial examined the effects of 3 diets consisting of roughly 1400 kcals each for
8 weeks, followed by 4 weeks of maintenance [3]. The diets had the following macronutrient
proportions: a) very low fat (70% carb, 10% fat, 20% protein), b) high unsaturated fat (50%
carb, 30% fat, 20% protein), and c) very low carb (4% carb, 61% fat, 35% protein). Since none

55
of the groups were told to separate their fat and carb intake, the high unsaturated fat group
should have lost the least amount of fat because of all that dreadful mixing, right? On the
contrary, no significant differences were seen in total weight loss, or loss of bodyfat percent.
And here’s the kicker: this lack of difference in bodyfat reduction was seen despite the distinctly
different effects each diet had on fasting insulin levels.

Another recent trial compared two 1500 calorie diets, a non-ketogenic diet and a ketogenic one
[4]. Insulin sensitivity was equally improved between the groups. No inhibition of fat loss was
seen in the non-ketogenic diet despite the fact that it was moderate in both fat (30%) and carbs
(40%). In fact, the non-keto group lost more bodyweight and bodyfat than the keto group,
although neither of these effects was statistically significant. It appears that any threat of
fat/carb combining slowing fat loss is imagination-based.

Nails in the coffin, anyone?

The current body of research focuses on obese, deconditioned, or untrained subjects. And still,
the moderate-carb/fat-combining fails to show a fat loss disadvantage over carb-restricted or
carb-separated conditions. Putting athletic subjects through the same conditions would show
even LESS of a difference. Since fit folks have far better glucose and insulin metabolisms than
the unconditioned obese, nit-picky combination or separation would be a nonfactor for fat loss.

The bottom line is that as long as you’re aware of your macronutrient targets for the day, go
ahead and sludge that peanut butter into your oatmeal if your little heart desires it. Leave the
neurotic eating behaviors for those with a lot of faith in fairy tales.

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Diet Percentages: Part 1
Commonly, when you see diet plans laid out, the intake of the various macronutrients (protein, carbohydrate,
fat) is presented in terms of percentages of total caloric intake. So you might see a diet which was 60%
carbohydrates, 30% protein and 10% fat or some other set of percentages. Or you’ll see recommendations
that ‘…athletes only need 15% of their calories from protein.’ or ‘don’t eat more than 30% of your total calories
from fat’, that sort of thing.
In this article, I want to teach readers what these percentages mean and how to use them (if you so desire)
either analyze a given diet, set up a diet, or figure out what a food label means.
A quick recap on calories
In a previous chapter I gave you the caloric content of the various macronutrients. To save you needless
paging, I’ll review them here.
 Protein: 4 calories/gram
 Carbohydrate: 4 calories/gram
 Fat: 9 calories/gram
 Alcohol: 7 calories per gra

Calculating percentages

With the above values in hand, and using some basic math, we can do several different operations in terms
of diet and food analysis. Let’s look at each one in turn. I’ll give examples but don’t read too much into the
numbers. They are only examples.

Operation 1: Setting up diets based on percentages


Probably the most common use of methods is to do actual diet set up, to determine how many grams of
each nutrient someone will be consuming. Let’s say we have a 170 pound male with a maintenance calorie
level of roughly 2700 calories per day and let’s say we wanted to put him on a diet that was 60%
carbohydrate, 20% protein and 20% fat (again, don’t read too much into these values, I’m using them for
example only). We want to find out how many grams of each nutrient he will be consuming per day.
Step 1: Calculate total calories of each macronutrient
The first thing we’d do is multiply his total caloric intake (2700 cal/day) by the percentages of each
macronutrient as this will tell us how many calories will be coming from each nutrient. To convert
percentages, just divide by 100 so 20% becomes 0.20, 60% becomes 0.60, etc.
The calculations appear below
 Carbohydrate: 2700 * 0.60 = 1620 calories from carbohydrate
 Protein: 2700 * 0.20 = 540 calories from protein
 Fat: 2700 * 0.20 = 540 calories from fat
 Note: It should be obvious that the percentages need to total 100% (or 1.0).
Step 2: Determine total grams from each macronutrient
Now we simply divide the total calories from each macronutrient by the caloric content of each macronutrient.
This tells us how many grams of each food our guy will be eating each day.
 Carbohydrate: 1620 calories / 4 cal/gram =405 grams carbohydrate
 Protein: 540 cal / 4 cal/gram = 135 grams protein
 Fat = 540 calories / 9 cal/gram = 60 grams fat per day

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So this particular diet, with 2700 calories and 60% carbs, 20% protein and 20% fat yields a diet of 405 grams
of carbohydate, 135 grams of protein and 60 grams of fat per day. For the remainder of the diet setup, you’d
divide that up across some number of meals including pre- and post-workout, all that jazz.

Operation 2:
Working Backwards Part 1: Determining Diet Composition
You can just as easily work the math backwards, to determine what percentage of each nutrient a given diet
is. Let’s say someone was eating 150 grams of protein, 200 grams of carbohydrate, and 50 grams of fat and
we want to find out how many total calories they are eating and what the percentages of the diet are.
Step 1: Determine caloric intake
First you simply mutiply the total grams of each nutrient by the caloric content of that nutrient. That tells you
how many calories they are eating each day
 Protein: 150 grams * 4 cal/gram = 600 calories from protein
 Carbs: 200 grams * 4 cal/gram = 800 calories from carbs
 Fat: 50 grams * 9 cal/gram = 450 calories from fat
 From those values, you can calculate total daily caloric intake by simply adding up the numbers.
 Total calories = 600 + 800 + 450 = 1850 calories per day.
Step 2: Determine percentage from each nutrient
Now simply divide the calories from each nutrient by the total number of calories being consumed to
determine the percentage each nutrient is providing. Multiply the decimal amount by 100 to get the
percentage
 Protein: 600 calories/1850 calories = 0.32 * 100 = 32%
 Carbs: 800/1850 = 0.43 * 100 = 43%
 Fat: 450/1850 = 0.24 * 100 = 24%.
So our example person is consuming 1850 calories per day with 32% from protein, 43% from carbs and 24%
from fat.

Operation 3:
Working Backwards Part 2: Determining Food or Meal Composition
You can use the identical math above to determine the composition of a given food (based on the food label)
or a given meal.
So say you wanted to determine the macronutrient percentages on a food or a meal that contained 10 grams
of protein, 20 grams of carbohydrates, and 9 grams of fat.
Step 1: Determine calories from each nutrient
First you’d simply multiply the total grams of each nutrient by the caloric content of that nutrient.
 Protein: 10 grams * 4 cal/gram = 40 calories
 Carbohydrate: 20 grams * 4 cal/gram = 80 calories
 Fat: 9 grams * 9 cal/gram = 81 cal
Although most food labels list the total caloric content, even if they don’t, you can easy figure it out by adding
up the totals above. This food/meal would contain 201 calories (40 cal + 80 cal + 81 cal)
Step 2: Determine percentages from each nutrient
Now you simply divide the total calories from each nutrient by the total calories in the food.
 Protein: 40 calories/201 calories = 0.2 * 100 = 20% calories from protein
 Carbohydrate: 80 calories/201 calories = 0.4 * 100 = 40% calories from carbohydrate

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 Fat: 81 calories/201 calories = 0.4 * 100 = 40% calories from fat
So this food or meal would contain 201 calories, with 20% protein, 40% carbs and 40% fat. Whether those
percentages mean anything is the topic of the next chapter

A note on food labels


Many people become perplexed when they do the math above on food labels and find that the caloric content
listed isn’t the same as what they calculate. So you might see a food that was listed as containing 212
calories with 10 grams protein, 20 grams of carbs and 9 grams of fat (which, as above, only yields 201
calories). There are a couple of reasons that this happens.
The first is that determining the caloric content of a given food isn’t doesn’t give perfect values, there is
always a little bit of slop. As well, the 4, 9 and 4 cal/g values are rounded values in the first place. Finally,
food labels almost always round off the values for protein, carbs and fat grams (for example, a food
containing less than 0.5 g of fat can list it as 0 grams of fat). If the food listed above actually contained 10.5
grams of protein (44 calories), 20.5 grams of carbs (84 calories) and 9.5 grams of fat (85 calories), that
would make up for the difference in values.
Ultimately, these types of tiny differences are no big deal. Even under the best circumstances, caloric
estimates are only estimates and there’s always going to be a little bit of slop either direction. We’re not
doing clinical nutrition here and, as long as it’s not excessive, small discrepancies in calore values are
nothing worth worrying about.
In Diet Percentages: Part 2, I’ll explain why I think using percentages to set up diets is a mistake.

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Diet Percentages: Part 2
Now that you know how to do the calculations from Diet Percentages: Part 1, in this article I want to talk
about some of the problems inherent in setting up diets based on percentages.

Reviewing basic physiology

On a day to day basis, your body has certain nutrient requirements, a topic which is discussed in detail
elsewhere in this book. As described in those chapters, those nutrient requirements are generally related to
how much you weigh (or how much lean body mass you have). There are a few exceptions, places where
the requirements for a given nutrient are absolute which I’ll mention when necessary.
For example, at any given moment, nearly all of the tissues in your body are utilizing some amount of protein
for various processes. Your liver, your kidneys, your muscles, your fat cells, your gut are all using protein for
protein synthesis and energy needs. Meaning that the more of those tissues you have, the more protein you
need; the less of those tissues you have the less protein that you need.
The same goes for carbohydrate and fat. Your body is using energy at some rate (set by your metabolic rate
which is fundamentally related to your body mass but also determined by factors such as hormones, the
temperature and other factors) and that means providing energy at some level related to bodyweight. Since
carbohydrate and fat are your body’s primary energy yielding nutrients, that means that they are required in
some amount related to bodyweight. In addition, fat is being used for other structural processes and is going
to be required in some amounts relative to bodyweight as well. And although those values may change
(based on activity and other factors such as genetics, age, etc.), they are still going to change relative to
your bodyweight. Some numerical examples:
The RDA for protein is set at 0.8 g protein/kg body weight (0.36 g/lb) while dieters may need as much as 1.5
g/kg (0.68 g/lb) to avoid excessive protein loss. Endurance athletes need protein at roughly 1.2-1.4 g
protein/kg (0.54-0.63 g/lb) and weight trainers may need 1.6-1.8 g protein/kg (0.72-0.81 g/lb). Most
bodybuilders use 1 g/lb as a rough estimate and this isn’t too far off from the value of 0.8 g/lb.
So someone who weighs 200 lbs and is sedentary needs about 72 grams of protein per day; if they were
dieting, they’d need at least 136 g/day; if they are an endurance athlete, they need between 108-126 grams
of protein per day; if they are weight training, they may need 144-164 grams of protein per day. Note, at this
point, that I’ve said nothing about percentages.
And while there’s no true requirement for carbohydrates, studies show that maintaining daily endurance
performance may take 5 g carbohydrates/kg (2.2 g/lb); glycogen supercompensation requires amounts on
the order of 10 g carbohydrates/kg (4.5 g/lb).
For the most part, fat intakes in relation to bodyweight haven’t really been determined, and most research
still simplistically talks in terms of percentages. A minimal intake of 3-6 grams of linolenic acid, and 1-2 grams
of linoleic acid has been suggested to avoid deficiency syndromes. As discussed elsewhere, whether this
represents an optimal amount in terms of health or body recomposition is debatable. Even then, it seems
impossible that some fixed amount of either linoleic acid or alpha-linolenic acid would apply to everyone
regardless of bodyweight.
But this is all sort of tangential to my point which is that nutrient requirements are related to your bodyweight
or lean body mass.

Why is this a problem?


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So why is this a problem? When someone puts protein, carb, or fat requirements in terms of percentages
only for a diet setup, it doesn’t necessarily have any relevance to what that person actually needs. For
example, it’s not uncommon to see diets for bodybuilders set up with 25-30% protein. Others take a more
conservative 15% and use that across the board for athletes or general intake. But what do those
percentages actually mean? Obviously nothing unless you also know how many calories that person is
eating.
Let’s use our 200 lb example individual above and look at his protein intake. Let’s split the middle value for
weight training and say he actually needs 150 g/day of protein and put him at two different caloric extremes:
1000 cal/day (a starvation diet) vs. 10,000 calories/day (Parillo style). Let’s set protein at 30% which most
would say is sufficient (or excessive depending on who you’re talking to).
1000 cal/day at 30% yields 300 calories from protein, or 75 grams of protein. He’d need 60% protein on
1000 cal/day to get 150 grams of protein per dya. 10,000 cal/day at 30% yields 3000 calories from protein,
or 750 grams of protein. Although both diets are 30% protein, the first is half of what our guy actually needs
(75 g/day vs. 150 g/day); the second diet has 5 times as much protein as he actually needs. Yes, these are
extreme examples and deliberately chosen that way. But they point out that the percentage itself has no
relevance whatsoever to what our guy’s actual requirements are.
Now, the typical counter-response to what I wrote above is that the percentage values are assumed to be
based on some fairly average caloric intake. That is, if we were to put our 200 lb guy (150 g/protein required
per day) on a more ‘average’ 2400 cal/day (12 cal/lb) and 30% protein, he will come out with a protein intake
of 2400 * 0.3 = 800 cal from protein yielding 200 grams/day or 1 gram per pound. Yes, a little higher than
the 150 g/day but not excessively so. And that’s fine, percentage based diets are going to be roughly valid
within a certain caloric range. The problem is that isn’t always how they are applied and that’s certainly not
how the percentages are typically interpreted.

More problems: interpretation and usage

It’s quite common to see statements of “Such and such is a high-fat diet and hence bad.” or “High-protein
diets are bad”, things of that nature. Most commonly, those statements are based on the percentages of a
given nutrient in a diet. For example, diets containing 30% or less total calories from fat are generally
considered ‘low-fat’ while, by definition, higher fat intakes are considered high-fat. But this can be terribly
misleading as well as misused. Here’s an example.
Let’s say we have a person who’s currently eating 2000 calories of which 150 grams (600 calories) are
protein, 176 grams (707 calories) are carbs, and 77 grams (693 calories) of fat. Using the math from the last
chapter, this yields a diet that is 30% protein, 35% carbohydrate, and 35% fat. Most would refer to this as a
high-fat diet and deem it bad because it contains 35% fat calories. They would probably also call it ‘low-
carbohydrate’ and ‘high-protein’ based on the percentages.
Ok, so let’s say we add 200 grams (800 calories) of carbohydrates (let’s use table sugar just because) to
the diet without changing anything else. Total calories now go to 2800 and the percentage of calories from
fat drops 35% to 25% (protein drops from 30% to 21%, carbs increase from 35% to 53%), even though the
total fat intake in grams hasn’t changed. By typical naming conventions a ‘high-fat’ diet has now magically
become a ‘low-fat’ diet and nobody will have a problem with the protein or carbohydrate intake, based on
the percentages. Of course, total fat intake in grams didn’t change. Neither has protein intake in grams. All
we did was skew the percentages by adding 200 grams of table sugar to the diet. And I don’t think anybody

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would argue that adding 200 grams of table sugar to this diet is particularly healthy. Yet many clueless folks
would automatically assume or claim that the second diet (25% fat) is healthier than the first (35% fat)
because it’s a ‘low-fat’ diet even though both diets contain the same number of grams of fat.
On a related note, many food companies will use this strategy as well. By simply adding table sugar to a
food, to increase the caloric content, they can drive the percentage of calories from fat downwards below
30% and call it a low-fat food. You can make vegetable oil (100% fat calories at 14 grams fat/140 calories)
a low-fat food if you add enough table sugar to it. Does that make it healthy because it’s now ‘low-fat’?
Obviously not. Or perhaps not so obviously because some folks fixate so hard on the percentages that they
miss the forest for the trees.
Using the same starting diet from above, say we decide to take all of the carbohydrates out of the same diet.
Now it contains 150 grams of protein (600 calories), zero grams of carbs, and 77 grams of fat (693 calories)
and 1293 total calories. Now it contains 46% protein and 54% fat. Most would call this a high-protein, high-
fat diet and go into an apoplectic fit even though it contains the exact same number of grams of protein and
fat as the previous diet. By simply changing the total carb and caloric content, we can skew the percentages.
But we haven’t changed a damn thing in terms of absolute protein or fat intake.
Or an even more extreme example, let’s say we decide to move this guy to nothing but protein (as in my
Rapid Fat Loss Handbook). Now he’s eating nothing but 150 grams of protein per day. That’s a 100% protein
diet, which most would call ‘high-protein’. First they’d freak out, then they’d tell you that his kidneys are going
to fall out of his ass. Except that it contains no more and no less protein than the previously two described
diets; once again, by manipulating the total caloric content of the diets we’ve changed the percentages even
if we really haven’t changed the gram intake.
On that note, this is a common criticism of ‘low-carbohydrate’ and/or ‘ketogenic diets’. Most will call them
high-protein and/or high-fat because the percentage of total calories from protein and fat is very high. But
this can be misleading because ketogenic diets are also commonly low in total calories. Studies typically
show that total protein and fat intake change very little when people move to ketogenic diets. Rather, total
calorie and carbohydrate content come down, and the percentage from fat and protein go up. Nitwit diet
critics will look at the high fat percentage and condemn the diet, without looking at the actual gram intake.
Another example: one of the popularly referenced studies by lower-carbohydrate diet advocates refers to a
group of athletes given only 40% of total calories from carbohydrates, who are able to maintain performance.
This is frequently used (by low-carbohydrate diet proponents) to argue that a diet of 40% carbs is sufficient
and/or that ‘high-carb’ diets are unnecessary. Here’s the problem: because of the extremely high total caloric
intake in these athletes, 40% of total calories still yielded in excess of 400 grams of carbohydrates per day
(a far cry from the 150-200 grams/day you might get on a typical lowered-carb diet). So even though it was
‘low-carbohydrate’ by percentage standards, it was still high-carbohydrate relative to their bodyweight needs.
Even at only 40% total calories, they still got close to the 5 g/kg value listed above needed to sustain
glycogen stores. Once again, the percentage had absolutely no relevance to the actual gram intake.
And, finally, here’s a rather humorous example from my college days. At some point or another, during a
nutrition class, a professor of mine had made the rather common statement that “As long as you don’t eat
foods with more than 30% total fat calories, you will be fine” something to that effect. It seemed like a logical
extension of trying to get total fat intake below 30%: make sure no individual food contains more than 30%
fat calories and you should be safe. At some later date, I took him a cookie recipe of mine that contained
approximately 20 calories/cookie and 1 gram of fat (the cookies were mostly air, with a little sugar and some
chocolate chips). My professor bristled, because these cookies contained nearly 50% of calories from fat (9
calories out of a total 20). Well, yeah, but they still only contained 1 gram of fat/cookie. ONE GRAM. A cookie
that was 200 calories and 30% fat (70 calories) would contain 8 grams of fat even though it’s below the

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magical 30% cutoff point. Yet he would have considered the second a better food choice based on just the
percentage even though it had 10 times as many calories and 8 grams of fat vs. 1. Go figure.

Making my point

Looking simply at the percentages of a given nutrient contained within a diet or food can lead people down
entirely incorrect paths. Whether it’s in setting up a diet, on intrepreting a given diet, looking at the
percentages alone is a mistake. A 15% protein diet might contain too much protein if calories are absurdly
high, and far too little protein if the calories are very low. And a diet which contains ‘only’ 40% carbohydrate
may contain more than enough actual carbohydrates by grams as long as the total caloric intake is high
enough. A diet which was considered ‘high-fat’ by percentage can be made ‘low-fat’ by simply adding
carbohydrates/calories/sugar to the diet but that’s not necessarily improving anything.
As I pointed out early in this chapter and elsewhere, daily nutrient requirements are (generally) based on
bodyweight, not the percentage of that nutrient in a diet. If someone requires, say, 1 gram of protein per
pound of bodyweight, they need 1 gram per pound whether it represents 10%, 50% or 100% of their total
calories. If someone needs 5 g/kg of carbs to maintain performance, that’s what they need whether it’s 40%
of their total calories or 60% of their total calories. If they need X grams of fat (X not really having been
established at this point except for minimal essential fatty acid requirements), they need X grams no matter
the percentage. Are we clear now on the different between percentages and total grams? I certainly hope
so.

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Energy Density
Today I want to cover another fundamental aspect of nutrition that is somewhat easy to confuse. That
concept is referred to as energy density. Energy density integrates, in a fashion, the concepts of calories,
nutrients and food intake (a topic discussed in detail in the article Calories, Nutrients or Food?).
First I want to define energy density before looking at some examples that will hopefully make the concept
a bit more clear. Finally, I’ll look at applications of the energy density concept in terms of dieting, weight
gain, etc.

What is Energy Density?

Conceptually, energy density refers to how many calories are found in a given weight or volume or food. Ok,
what does that mean. Let’s say that you have 1 gram of each of the three macronutrients which are protein,
carbohydrates and fat. We know that these are given calorie values of 4 cal/g for protein and carbs and 9
cal/g for fat. Clearly, in this simple example, fat has over twice the energy density of either carbs or fat (9
cal in one gram vs. 4 cal in one gram).
This basic fact is generally interpreted one of two ways depending on whether a given author is pro- or anti-
fat (and of course what the context is). Pro-fat authors will contend (usually in the context of exercise
performance) that since fat contains twice the calories of carbohydrates, it provides more energy to the body
on a gram per gram basis (again, the context is usually exercise performance). While there is an element
of truth to this it leaves out some important information that I’m not going to get into in this article.
In contrast, anti-fat authors (usually coming at it from an obesity or weight gain standpoint) tend to blame
high caloric intakes (and hence obesity) on a high fat intake because of it’s high energy density. That is,
frequently diets higher in fat are also higher in calories because of the increased energy density.

But Wait…

Unfortunately, just looking at things as simply as above is misleading for the reasons I outlined in Calories,
Nutrients or Food?. First and foremost, people don’t generally eat pure nutrients, they eat food. And, as
discussed in that article, most foods are a combination of nutrients (e.g. milk contains protein, carbs and fat,
meat contains protein and usually fat, most carb sources contain some protein). Even in those cases where
folks (read: OCD athletes) may choose pure nutrients, most humans eat mixed meals containing multiple
foods and that affects the overall energy density of the meal.
Of perhaps more relevance is that most foods also contain other non-nutrient compounds such as air, water,
ash, fiber, etc. Put differently, 100 grams of say chicken won’t contain 100 grams of protein; rather, the
amount of protein will be diluted by the presence of not only other nutrients but the other compounds that
are present.
If this is difficult to understand, an easy example might be soup which is mostly water. So say you make a
soup containing potatoes, vegetables, ground beef, some vegetable oil, spices and what have you. Each of
the foods you put in will contain some amounts of carbohydrates, proteins and fat and each will fall
somewhere in terms of their energy density. However, a cup of that soup will likely have a fairly low energy
density because most of the volume is water.
Another example would be to compare two cups of pasta to one cup of pasta with one cup of steamed
vegetables. Both meals are 2 cups (in terms of the total volume) but the second meal would contain far less

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calories due to the vegetables; and since the total volume of both meals is the same, the energy density
(calories per unit weight/volume) would also be lower. In this specific case, the low energy density food
dilutes the higher energy density food and brings the overall energy density of the meal/dish down.
Alternately, let’s take a typical 100 grams baked potato which contains about 46 grams of digestible
carbohydrate; hopefully readers can sort of imagine about how big that would be (this is just a standard size
baked potato). Now contrast that to 100 grams of pure table sugar which will contain very nearly 100 grams
of carbohydrate; I bet you can imagine just how little sugar that would be.
In both cases we’re looking at 100 grams of total food but the caloric content of each is drastically different
(about 200 calories vs. 400) as is the energy density. The potato will have an energy density of 200
calories/100 grams food compared to the 400 calories/100 grams food in the table sugar.
Of course, 100 grams of pure fat would contain nearly 900 calories and still have the highest energy density
of all.
Here’s an example that will help to illustrate just how large a role water content plays in all of this. Two cups
of grapes will contain about 100 calories while 2 cups of raisins (dried grapes) might contain nearly 800
calories. This is because the raisins have had most of the water and air content removed during the drying
process. Same volume, same food, but drastically different energy densities.
One thing I would note is that, although fat is often blamed for the high-energy density of the diet, this isn’t
always true. Food companies have come up with amazingly creative ways to make low-fat high-carb foods
be exceedingly energy dense by removing water, air and fiber.
Most dietetics types seem to assume that a high-carb diet will be non-energy dense but they are assuming
that people are eating naturally occurring carbohydrates such as potatoes; in the real world this is rarely the
case. When you start moving into heavily processed carbohydrates, the energy densities can get up there
pretty quickly.
As a general rule, foods high in water and fiber tend to be pretty low on the energy density scale and food
that lack either tend to be much higher. Pure oils tend to have the highest energy densities (which is why I
strongly recommend measuring them out, even if you don’t measure anything else in most of my books) and
vegetables tend to have the lowest, everything else is somewhere in the middle.

Why Does This Matter?

Ok, enough explanation, why is this important. Energy density starts to become important when you are
looking at food intake in the real world, both in terms of dieting and gaining weight (for athletes). A lot of this
has to do with fullness and satiety, a topic I discussed somewhat in 9 Ways to Deal with Hunger on a Diet.
Some research suggests that humans eat a fixed weight of food each day (other research says this is not
the case and I’ll let the scientists argue it out for the time being); thus people who eat higher energy density
foods invariably end up eating more total calories. Basically, if you are going to eat 2 pounds of food per day
(I’m pulling this number out of thin air), you will end up consuming more calories if you eat high energy
density foods vs. low energy density foods.
Even if this isn’t entirely the case, high energy density foods tend to make it easier to overconsume calories
compared to low energy-density equivalents. This is especially true when you’re looking at uncontrolled
diets (e.g. where people are not tracking calories), a topic I keep harping on but one that people keep
confusing with other issues of the diet.

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Simply put, foods with a low energy density will contain a relatively small number of calories in a large bulk
or volume of food. As noted above, vegetables, fruits and other unrefined carbohydrates typically have a
low energy density although even that’s not always the case as mentioned above
Foods with a high energy density will contain a large number of calories in a relatively small amount of food.
This generally includes high-fat foods but can also include highly refined carbohydrates. I mentioned this
above but I want to look at that issue in a little more detail.
It looks at first glance that high fat foods will always be more energy dense than similar amounts of
carbohydrates or protein and that fact has been used as part of the campaign to lower dietary fat to help
with the obesity problem. But is this always the case, are high-fat foods always higher energy density than
high-carbohydrate foods?
Let’s take our baked potato example, containing about 46 grams of carbohydrate in a 100 gram potato. So
it contains about 200 calories/100 grams. Let’s say we add 10 grams of fat in the form of butter (making anti-
fat crusaders cringe) to the potato which adds 90 calories. Our potato/butter combination contains 290
calories in 110 grams of food.
Now let’s contrast this 110 grams of candy and let’s say it contains ~100 grams of sugar, or 400 calories.
So the baked potato/butter combination contains 290 calories/110 grams of food while the candy contains
400 calories/100 grams of food. Despite being ‘high-fat’, the potato-butter combination has a lower energy
density than the zero-fat high-sugar food its being compared to.
Semi-tangentially, while the anti-fat crusaders tend to blame high-fat diets for every malady known to man,
there are real-world examples, such as the classic Mediterranean diet (which often contains up to 40% fat
as total calories), where a high-fat diet doesn’t cause problems. Much of this is that the overall diet is still
fairly low energy density because there are a tremendous amount of vegetables being eaten.
Despite having a high fat content, the Mediterranean diet has an overall low energy density because of the
other foods that are present in such abundance. This is in contrast to most Western diets that tend to not
only be high in fat but low in foods such as fruits and vegetables that would dilute the energy density of the
fat.
As I mentioned above, one of the reasons that fat is so often blamed for its role in causing obesity is its high
energy density. This is obviously true if you’re talking about pure fat (which few people eat) and it’s generally
true that high fat foods have a high energy density. This difference is especially prevalent if they are
compared to low-fat unrefined carbohydrate foods likes fruits, vegetables and unrefined grains. You know,
the foods that nobody really eats but that anti-fat crusaders think people are eating.
As I alluded to above, a low-fat diet isn’t automatically a low energy-density diet. Many highly refined high-
carbohydrate foods have a high energy density because the water, air, fiber, etc. has been removed. More
and more, food companies have brought low-fat/high-carbohydrate but also high energy density foods to
market.
Even diet staples such as pasta can have a surprisingly large number of calories in a fairly small volume.
Such foods may be low (or even no) fat but still have a very high energy density. This not only makes them
easy to overconsume but also means that they can contribute a rather large number of calories to the diet
without providing much bulk.
To really drive this into the ground, a high-fat diet isn’t automatically a high energy density diet any more
than a low-fat diet is automatically a low-energy density diet. The types and amounts of other foods in the
diet play a major role and, in my experience, what dietetics types think people are eating in the real world
isn’t what people are actually eating in the real world.

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Which isn’t to say that an excessive fat intake isn’t contributing to the energy density (or caloric content) of
the modern diet; of course it is. Dietary fat simply isn’t the only factor contributing to the problem of caloric
overconsumption.

So Which is Better?

You may be thinking after the above discussion that choosing a low energy-density diet is always superior. If
you’re talking about weight loss or even general health, there is probably much truth to that. For people who
won’t or aren’t going to count calories, choosing low energy density foods will tend to reduce caloric intake
without doing anything else. For people on a diet, foods with a lower energy density tend to be more filling,
helping to keep hunger at bay.
But there are exceptions to this. Often times, people want or need to gain weight (especially athletes). In
that situation, when very high caloric intakes may be required, low energy density foods can actually make
it impossible to get in sufficient calories. Admittedly, this probably isn’t a situation that applies to the majority
but it does come up. Trying to get 6000 calories per day eating nothing but low energy density foods can
be a near impossibility and consuming higher energy density foods may be necessary to get the job done.
A related issue are the high-carbohydrate refeeeds that I recommend in my books (such as A Guide to
Flexible Dieting and The Rapid Fat Loss Handbook). When the goal is to deliberately overconsume a lot of
carbohydrates, people invariably get into trouble trying to do low-energy density, high-fiber foods. Not only
can’t they get sufficient calories in to make the refeed worthwhile, but the high-fiber tends to make them
explode (if you get my meaning). Similarly, in the post-workout period, higher energy density foods may be
preferred due to a faster rate of digestion and the hormonal response.
And, of course, for people who are actively tracking calories, some of the above becomes much less
relevant. As I discuss in Is A Calorie A Calorie?, much of this type of stuff only really matters when people
aren’t tracking calories (because of the impact of different food choices on spontaneous food intake). For
people who do track daily calories, clearly some higher energy density foods can be worked in (if desired)
because total calories will still be controlled.

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Dissecting the Energy Needs of the Body – Research Review

Title and Abstract

McClave SA, Snider HL. Dissecting the energy needs of the body. Curr Opin Clin Nutr Metab Care. (2001)
4(2):143-7.
The majority of the resting energy expenditure can be explained by the energy needs of a few highly
metabolic organs, making up a small percentage of the body by weight. The relationship of the specific size,
individual metabolism, and proportional contribution to the actual body weight and total energy expenditure
for each of these organs is a dynamic process throughout growth and development, the onset of disease,
and changes in nutritional status. Defining the energy needs of the individual tissues and organ systems
immeasurably enhances our understanding of the body’s response to these clinical processes, which
otherwise could not easily be evaluated by focusing solely on total energy expenditure, fat-free mass,
nitrogen imbalance, or actual body weight. Recently reported studies have served mainly to reinforce
concepts described previously, and clarify some areas of controversy.
.

Background

Last month, I answered a Q&A on Reducing Body Fat Percentage by Gaining Muscle and in that article I
mentioned that the actual caloric burn of skeletal muscle is actually quite low compared to what is often
claimed. In the comments section someone mentioned a recent seminar where the value of 50 cal/lb for
muscle was thrown out and asked for clarification on my claim.
Unlike previous research reviews, today’s paper isn’t an actual study but rather a review paper so my
discussion will be a little bit different in terms of what I want to look at. The paper itself is actually fairly
technical and I don’t want to focus so much on the technical aspects as on the concepts and implications
that the paper deals with as they pertain to issues of body composition.
More specifically I want to look at some of the common claims that are often thrown around in the world of
body composition such as “Adding muscle mass significantly raises metabolic rate.” and “Fat cells burn no
calories, they are metabolically inert.” While this paper was examining the issue from a different perspective,
it actually provides good data on both questions.
Specifically today’s paper examines in some detail how different tissues of the body (e.g. muscle vs. fat vs.
organs) contribute to the body’s resting energy expenditure. As well, factor such as disease,
growth/development and under-nutrition are examined in terms of how they impact on different tissues in
the body and their energy expenditure.
As I discuss in detail in Metabolic Rate Overview, there are four primary components to total daily energy
expenditure: Resting Energy Expenditure (REE), Thermic Effect of Activity (TEA), Thermic Effect of Food
(TEF) and Non-Exercise Activity Thermogenesis/Spontaneous Physical Activity (NEAT/SPA).
Of those four, resting energy expenditure plays the major role in total daily energy expenditure, generally
comprising 65-70% of the total. So looking at the differential impact of each tissue on REE tends to
give pretty decent picture of what’s going on.
.

The Paper

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The paper begins with an introduction to the overall concepts, pointing out estimating REE in individuals of
different body sizes has been classically difficult. While body weight per se is a decent indicator, REE actually
tends to scale better with body surface area. However, this gives no indication of which tissues (and in what
proportion) are contributing to overall REE.
Readers may have seen the statement that ‘The largest predictor of REE is lean body mass” and there is
certainly some truth to that. However, lean body mass (aka fat free mass) only predicts 53-88% of the
variability in energy expenditure. There are a number of reasons for this not the least of which being that
lean body mass/fat free mass is not a single homogeneous tissue.
Rather, as discussed in What Does Body Composition Mean, lean body mass represents organs, skeletal
muscle, bone, skin and basically everything in the body that isn’t fat mass. And as you’ll see shortly, each
of those tissues burns very different numbers of calories on a day to day basis. Which means that variability
in the amounts and proportions of those tissues will impact on overall resting energy expenditure.
Next the paper discusses the different methodologies used to estimate the resting energy expenditure of
different tissues. I don’t want to get into huge detail on this. Suffice to say that newer technology has allowed
for more and more accurate methods of estimating the caloric expenditure of different tissues in the body.
While they are still not error-free (nothing in science ever is), some of the newer methods of measurement
may explain why some of the oft-held beliefs about caloric expenditure and values that are often thrown out
are turning out to be wrong. Of course that also means that future developments may render current values
incorrect.
.

The Normal Human

The next topic addressed in the paper is an examination of the different tissues and how they contribute to
resting energy expenditure in a fairly ‘average’ human being. I’ve reproduced Table 1 from the paper below,
honestly this was the main reason I wanted to examine this paper, to get this chart up on the site.
.

Organ or Metabolic Rate Metabolic Rate % Overall Weight in Weight in %Body


Tissue (kcal/kg/day) (kcal/lb/day) REE Kg Lb Weight

Adipose 4.5 2.0 4 15 33 21.4%

Muscle 13 5.9 22 28.2 61.6 40

Other 12 5.4 16 23.2 51 33.1

Liver 200 90.9 21 1.8 3.96 2.6

Brain 240 109 22 1.4 3.08 2.0

Heart 400 181 9 0.3 0.66 0.5

Kidneys 400 181 8 0.3 0.66 0.5

Other refers to bone, skin, intestines and glands.


Note: the lungs have not been measured for methodological reasons but have been estimated at
200 kcal/kg similar to the liver.
.
As you can see above, and quite contrary to what is commonly stated, skeletal
muscle actually has a fairly low resting energy expenditure, roughly 6 calories per

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pound. This is contrast to very old values of 100 calories/pound or even more
recent claims that a pound of muscle will raise metabolic rate by 40-50 calories
per pound.
Additionally, an in contrast to what is commonly claimed, fat cells do burn
calories. Admittedly the value is not massive (roughly 2 calories per pound) but
the idea that fat cells are completely inert is also incorrect. We now know that fat
cells produce a variety of hormones, etc. (e.g. leptin, adiponectin) and that
expends calories. Again, not much per unit mass of fat, but for someone carrying
a lot of fat mass, this does add up.
Perhaps of more relevance, and getting back to the paper per se, the primary
contributor to resting energy expenditure comes from the organs with the liver,
heart, kidneys and brains contributing roughly 70-80% of total resting energy
expenditure. This is despite the fact that they only make up approximately 7% of
total body weight. That is, despite their relatively small weight, they are simply
massively metabolically active on a day to day basis.
In contrast, while skeletal muscle may contribute roughly 40% of total weight (a
little bit less in women), it only contributes 28% of total resting energy
expenditure. Essentially, the relatively small caloric burn of a single pound of
muscle mass is made up for by the sheer quantity of it. Which doesn’t change
the fact that adding muscle mass still won’t have a massive impact on resting
energy expenditure.
To put that into mathematical perspective, gaining 20 pounds of muscle would be
expected to increase resting energy expenditure by approximately 120 calories
per day. Certainly that does have an impact overall (equivalent to perhaps 10
minutes per day of moderate intensity cardio) but also keep in mind the time
frames involved to gain that much muscle mass. Expecting that adding a bit of
muscle to have massive impacts on metabolic rate in the short-term is simply
unrealistic; a few pounds gained simply won’t have any major impact.
Rather, I would expect that any real impact of building muscle mass on The
Energy Balance Equation is going to come through the training done to
stimulate/maintain muscle mass increases along with the caloric cost of building
the muscle in the first place. But once it’s there, the caloric expenditure at rest
of skeletal muscle is simply very low.
.

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Factors Affecting Energy Expenditure

Having examined the average contribution of different tissues to the body, the researchers then look at a
host of other topics, only a few of which I’m going to really look at in any detail.
Growth and development is covered first, examining how the ratios of energy expenditure to body weight
changes over the lifespan. Since most reading this are full grown adults, the changes that occur from
childhood to maturity don’t seem that relevant.
One issue of some importance is covered next and that’s the effect of differences in body size between
individuals. In general, if you look at two people of different body sizes, larger folks tend to have lower
resting energy expenditures relative to their body mass. This is most likely related to differences in the
proportion of organ weight (recall from above that the organs contribute the most to overall resting energy
expenditure) to total body weight.
Meaning this: on average, organ weight won’t vary much between individuals. So if one person is larger
than another, that difference in size is likely to occur through changes in either muscle mass or fat tissue,
neither of which makes massive contributions to resting energy expenditure (and differences in body
composition won’t have nearly the impact that most think given the relatively small difference in caloric
expenditure between muscle mass and fat mass).
Practically, this means that equations that estimate resting energy expenditure based solely on body weight
will tend to overestimate larger individuals to some degree. Of course, as I recently discussed in Adjusting
the Diet, since all estimates of energy expenditure and/or caloric intake have to be adjusted based on real-
world changes anyhow, I’m not sure how important this is practically.
I should probably address a question that I imagine will come up in the comments, given the enormous
variability in energy expenditure per pound of tissue, where does the quick estimate of 10-11 calories/pound
(22-24 cal/kg) come from? And the answer is that it’s basically a weighted average of the above values. That
is, if you took the values for caloric expenditure/unit weight times their contribution to overall weight and
worked it out, you’d get a value that was pretty close to the quick estimate value. Again, this will tend to vary
based on actual body size due to differences in the relative contribution of each tissue to the body’s total
weight.
Next the researchers looked at the impact of both undernutrition and refeeding on energy expenditure at
rest. During underfeeding, they point out that skeletal muscle and fat are generally the major tissue lost
while organs are spared. This tends to have the impact of raising the relative proportion of energy
expenditure to body weight (because the low energy expenditure tissues are being lost). Of course, with
extended dieting, there is also an adaptive component of metabolic rate reduction as all tissues in the body
tend to slow their overall energy expenditure.
In contrast, during refeeding, there is often a hypermetabolic state that occurs, possibly due to increases in
protein synthesis, core temperature and the thermic effect of food. As well, there are a number of hormonal
effects that occur when calories are raised, a topic I discuss in more detail in The Full Diet Break, all of which
may have potentially beneficial impacts on overall energy expenditure and metabolic rate.
Finally the researchers examine the impact of disease and injury on energy expenditure but I don’t find that
terribly relevant to this article.
.

Summing Up

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The main point that I wanted to make with today’s research review was to clear up some of the oft-held (and
unfortunately incorrect) ideas regarding the impact of things like skeletal muscle mass and fat mass on
resting energy expenditure. Based on current data, the idea that skeletal muscle burns massive numbers
of calories would appear to be 100% incorrect.
Rather, skeletal muscle actually burns fairly few calories on a per pound basis; it primarily has a major impact
on resting energy expenditure because there is a good bit of it. But adding even moderate amounts of
muscle are unlikely to massively impact on energy expenditure. As noted above, I expect the major effect
to be from the effort of stimulating muscle mass gains along with the energy needed to synthesize that
muscle tissue. But once it’s there it doesn’t burn many calories.
Rather, the majority of resting energy expenditure is generated by the organs which, despite their small size,
burn a massive number of calories per unit weight. Someone on the support forum jokingly asked “So how
do I hypertrophy my liver?”
Finally, fat cells, while not having much of a calorie burn do burn calories. In fact, they are only about 1/3rds
of the burn of skeletal muscle (2 cal/lb vs. 6 cal/lb respectively). While low, someone carrying a lot of fat will
have this add up and it will contribute to overall resting energy expenditure.

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Dieting Psychology Versus Dieting Physiology
Over the next series of articles, I want to look at both physiological and psychological reasons that diets can
fail.
But before doing that I need to make something very clear: the distinction I’m making between psychology
and physiology is simply for convenience, it’s not one that really truly exists.
That is to say, psychology impacts on physiology and physiology impacts on psychology and the days of
pretending the body and mind are separate non-interacting entities are long, long gone. Again, I’ll make the
separation primarily for reasons of convenience, it will save me some needless complexity in the upcoming
discussion. Just keep in mind that it’s an artificial and non-existent separation in reality.
Modern science, for example the field of psychoneuroimmunology, recognizes that the brain and body are
in a constant state of interaction and involvement with one another. This is sort of the basis for the idea that
you can think yourself sick, or for the idea that people with a more positive attitude are more likely to survive
certain diseases (such as cancer). Your thought processes can impact on such workings of your body as
immune function.
Put more simply, how you think affects how your body works and how your body works can affect how you
think or feel.
Incidentally, for anybody who is interested in this topic, I would highly, highly, highly recommend almost any
of the books by science writer Robert Sapolsky, especially his book Why Zebras Don’t Get Ulcers where this
topic is discussed in some detail (primarily wrt: cortisol and stress). This is literally one of my top-5 books
ever and I cannot recommend it too highly.
Anyhow, while you’re sitting there reading this, I want you to start thinking about something that really makes
you angry. Taxes, gas prices, my inability to blog consistently, take your pick. Really get a good anger going.
Now stop for a second and pay attention to your body: odds are that your heart rate is up, if we measured
blood pressure it would be increased too, you might be breathing a little bit harder, you get the idea. The
mere act of thinking about something that upset you had a strong physiological effect throughout your body.
Here’s another example in the reverse direction: everybody knows how they get really lethargic and lazy
when they are sick with something like the flu or a bad cold or what have you. It’s as if when you are sick
your body is deliberately trying to get you to lay around all day and rest. This turns out to basically be the
case.
When you are sick, your body releases short-lived chemicals called cytokines, some of which are
inflammatory. Inflammatory cytokines, in addition to making you feel like warmed over crap when you have
the flu or something, they also directly impact on the brain and your motivation to move around.
I’d note that a similar mechanism has been suggested as a primary cause of overtraining; called the cytokine
hypothesis of overtraining I think it ties together a lot of conflicting and contradictory data on the topic. It
explains changes in performance along with behavior and ties together the previous held (but wrong idea)
of local versus central overtraining. It turns out that they are the same thing and local effects (tissue damage)
is causing central effects (behavior and motivation changes).
Essentially constant/chronic/excessive inflammation locally (in the muscles you’re training) causes an
increase in inflammatory cytokines and this is responsible for the lack of motivation to train and lethargy that
often sets in. Essentially, your body (your muscles) are trying to ‘tell’ your brain to give it a rest and take
some down-time. Of course, humans, being the stubborn folks that we are, often choose to ignore or over-
ride these signals.
This has a lot of relevance to the issue of dieting failure which is what I’ll be talking about next.

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Excluding the Middle
This is going to be one of those seemingly pointless posts that doesn’t say a whole lot (and I’ll try to keep it
short); it’s mainly just a background type of thing that I want to put up once so that I can just link to it in the
future since I’ll be referring to it repeatedly. I figure most of my readers will still be hungover from July 4th
celebration anyhow and won’t really be paying attention or able to focus on anything more detailed.
What I want to discuss is a concept that I call ‘excluding the middle’ but which is more formally referred to
as a logical fallacy called ‘the false dilemma‘, the ‘either/or fallacy’ or a whole host of other things. It’s
something I see a lot in both Internetz articles and Internetz arguments.
In brief, people have a tendency to play this cute little game where a given situation can either be exactly
one thing (their preference) or exactly one other thing where that other thing is some ludicrous stupid-ass
extreme example that they use to attempt to prove their preference simply by how extreme (and dumb) it
is. But compared to something stupid, anything is better by comparison.
As an example, I am apparently quoted as having said that “…compared to the Standard American Diet, a
diet of bug spray and skittles would be healthier.” One extreme compared to another and the second is
only better because of the awfulness of the first. Except that I was joking…mostly. In most arguments, the
folks falling prey to this trap are not.
Now, whether or not this is just some aspect of human nature where we want things to be one thing or
another, or because people are bad at making logical arguments or what I have no idea. Nor do I really
care. It’s called a logical fallacy for a reason and I’m going to give you four explicit examples to try to get
my point across.
But simply, life is not binary and most things comes in varying degrees of extreme and shades of gray. As
my favorite author once put it “The universe can count beyond two.” He was using this statement in a
different context (to point out that most things fall into a yes/no/maybe type of situation and there are rarely
simply yes/no answers) but it applies here too. Hopefully this little piece will help you count beyond two.
.

The HIT Example

For those who live under a rock, HIT refers to High Intensity Training (not to the confusingly similarly named
HIIT or High-Intensity Interval Training). Developed by Arthur Jones (as much to market Nautilus equipment
or anything else) but truly popularized by Mike Mentzer (who called it Heavy Duty training), HIT has more or
less become synonymous with doing 1 set to failure of a given exercise (interestingly, Jone’s original HIT
was not like this at all and was actually a fairly moderate volume of training). Yes, there’s more to it. No, I’m
not going into details here because it doesn’t matter.
But in arguments with HIT’ers, if you suggest doing more than one set, you typically see a great example of
what I’m talking about. Specifically, you will often see the statement to the effect of “If you’re going to do
more than 1 set, why not do 10, or 20, or 80?” HIT’ers see the world in two simple binary situations: either
you stop at one set or you do as many sets as possible.
That is, they don’t seem to have considered that one could do say, 4-8 sets of an exercise. That the options
are just 1 and ‘all’. And since 1 set is better than ‘all’ sets, clearly it’s the correct choice.
They are excluding the middle: It’s not as if you can’t do a moderate number of sets (say 4-8 or whatever
number might be optimal) and the only options are 1 or ‘all of them’.
.

The Clean Eater Example

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The idea of eating ‘clean’ is one that runs rampant in the physique sports. Simply stated, ‘eating clean’
means eating only unprocessed foods in the diet. Well, except when it’s inconvenient, it’s always amusing
watching rabid clean freaks rationalize foods that don’t fit their definition (Crystal Light comes to mind) while
eliminating foods (such as dairy) which clearly do fit their definition. And when you get into arguments with
clean freaks and suggest that it’s not required to eat clean 100% of the time, you will often get a response
to the effect of “I guess I could go binge on junk food and McDonald’s and pizza at every meal, sure.”
I’d note that clean freaks often include a ‘cheat day’ where they go out of their way to eat the most junk
humanly possible, often to the point of making themselves sick. As well, many fall into the trap whereby if
even a gram of an ‘unclean’ food passes their lips, they have ruined their diet and must go binge on
everything they can get their hands on. They need to read A Guide to Flexible Dieting.
In the clean freak’s mind, there are two binary options: you either eat clean 100% or you’re eating nothing
but junk food at every meal every day. The idea that you might ‘eat clean’ (whatever those words mean to
you) 80-90% of the time and include selective ‘unclean foods’ (whatever that means to you) the other 10-
20% of the time is simply an inconceivable one to many.
They are excluding the middle: it’s clean 100% of the time (except when it’s not) or junk food 100% of the
time, you can’t do anything in the middle. Even though you clearly can. And most do, and more probably
should.

The Paleo Diet Example

Arguing with rabid paleo folks is about the same as arguing with the clean eating crowd. I can recall specific
arguments where the suggestion that grains (which represent unholy evil to the paleo crew) can be part of
an overall diet was met with the counter-argument of “I’d never eat a diet that is 80% carbs.” Or something
to that effect.
That is, the paleo eater seems to see the world as one of two things: you are either a strict paleo eater
consuming nothing but meats, veggies, fruits and other paleo-approved ™ foods (and I’d note here that the
paleo folks are about as flexible with their definitions as the clean eaters, routinely rationalizing foods that
they want to eat while ignoring others based on whim) or you’re living on nothing but refined grains.
It’s one or the other, if you’re not 100% paleo, you’re 100% at the other extreme. Apparently that whole
concept of an athletic diet where you eat lots of protein, fruits, vegetables AND some amount of grains is
simply inconceivable. Despite the fact that athletes and bodybuilders have done that for decades.
They are excluding the middle: your diet is either 100% paleo (except for the exceptions they justify) or
you’re eating 80% refined grains. There is no possible middle ground that they can conceptualize.
.

The HIIT/LSD Example

Now I am talking about High-Intensity Interval Training along with the whole silly either-or argument that is
going on in the world of conditioning and cardiovascular training (something I’ve written about at length in
the Steady State vs. Interval Training series). Basically, and this is mostly a marketing thing/a backlash to
the over-emphasize on low-intensity cardio of previous years, folks have flip flopped and it’s all intervals all
the time.
Coaches will argue to the effect of “I would never have an athlete do low intensity work, marathon runners
have a poor power output” or something roughly to the effect. You’ll see similar stupidity aimed at folks

75
aiming to lose fat where the statement is something akin to “Hours of low intensity work burn off muscle.” As
if the only way to do aerobic work is by doing hours and hours of it every day.
Apparently 45-60 minutes of low intensity work can’t be done even if dieters and contest bodybuilders have
done exactly that for about 30 years. Nor can a mix of low intensity work (i.e. 2-3 sessions per week or
more) plus some interval work (1-2 session). Or some other mixture depending on your goals and
needs. You know, like just about every endurance athlete in the world.
They are excluding the middle: It’s either nothing but interval sessions at every workout OR you’re training
for the Tour De France and doing 30 hours per week of aerobic work, you can’t do anything in the middle.
.

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Fundamental Principles Versus Minor Details
In that I am a bit obsessive compulsive about my field of interest, I have a driving desire to read anything
and everything related to it. I also happen to particular enjoy older books as you generally find that what
you think is a brand spanking new idea in the world of training or diet was being done 30 years ago by
someone smarter than you.
A little while back, in trying to fix my own ignorance about swimming, I read what is often considered a classic
in the field of training literature which is the book “The Science of Swimming” by James ‘Doc’
Counsilman. Written in 1968, the book represented one of the first attempts to apply much in the way of
science to the technique of swimming. Suffice to say that swimming is very strange and, so far as I can tell
even in 2010, nobody is exactly sure how swimming ‘works’. That is, in terms of what’s going on
mechanically in the water.
But this is not an article about swimming, rather there is a particular quote in the book that really resonated
with me (especially after some of the silliness I had been seeing on the support forum) and that prompted
this article. In discussing technique considerations and stroke mechanics, Counsilman writes:
Do not subordinate fundamental principles to minor details.
It’s quotes like these, ones that are so to the point and clear that really stand out for me. It’s also the sign
of a truly knowledgeable person: people who know their field can express complicated ideas in simple
language. People who use complex language to confuse you don’t really know what they are talking
about. But that’s a different topic for a different day.
In this specific case, Counsilman was talking about worrying about details of stroke mechanics (or trying to
fix or alter them) without paying attention to the fundamentals of proper stroke mechanics. Because the
fundamental principles outweigh the minor details by miles. But it applies equally well to the issues of diet
and training.
As I’ve written about in a previous article How Detail Oriented Do You Need to Be, with the advent of the
Internet (along with other forms of constantly running media) people are absolutely overwhelmed with
information, much of it dealing with what can only be termed completely irrelevant details. That is, stuff that
just isn’t likely to make an iota of difference to anything in the real world. I think the reason for this trend is
that writing about the basics and the fundamentals all the time isn’t sexy or interesting. It certainly doesn’t
sell magazines.
.

Let’s Get the Big Exception Out of the Way

Certainly, there is a time and a place where details can matter. As discussed in How Detail Oriented Do
You Need to Be usually it’s people who are at the very extreme high level of performance or leanness looking
for that next level up. Yeah, fine, if I’m trying to diet a male down to 5% body fat without muscle loss, the
details may start to matter (though amusingly some can do it without ever moving past the most basic of
approaches). An elite athlete looking for that last bit of performance is in that position where all of the
esoteric stuff, the insane details, start to matter.
But those tend to represent such a tiny percentage of the training or dieting population as to be almost
irrelevant. They may be the more interesting subgroup (because coaches like getting up their own butts
with this stuff too) but they aren’t the largest percentage of the training or dieting population.
And while everyone on the Internet thinks that they are advanced, the simple fact is that most are not; most
would be served by simplifying more than complexifying. As well, the individuals in the situations above

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have spent years working on the fundamentals to the point that they are so well entrenched that they needn’t
be worried about. At that point the details can matter.
.

So Let’s Talk about Everybody Else

As I mentioned, by the definition of the word ‘most’, most people training or altering their diet are not in the
above situations, looking for that last bit of a percentage point gain where details may start to matter. Which
unfortunately, doesn’t stop them from all too often focusing on the minor details to such a degree that one
of two damaging things happens which are:
1. They never actually get started on their plan.
2. They manage to completely forget about the fundamental principles.
Both are clearly a problem and I want to talk about both in some detail.
.

Just Do Something

One of the primary end results of the unnecessary focus on details is that people often spend weeks (or
months) looking for the perfect program, the perfect diet. And invariably they are focusing on the minor,
minor, minor details that separate different successful programs. So one program has such and such a set
and rep scheme, another slightly different. One training program might be more frequency based, another
more intensity based (as discussed in A Quick Look at Some Popular Hypertrophy Programs).
I see people do it all the time: asking for a compare and contrast of one training program vs. another. Is one
‘better’ than the other? What about this third one? What about this one? What about that one?
The same holds for diet. One uses carb-cycling of some form or fashion on a daily basis, another uses big-
carb refeeds less frequently (most of my plans), a third does something else entirely. And every approach
seems to work stunningly (at least for some people) or not at all (in others). But that gets into the issue of
context more than anything else; what is right (or potentially ideal) for one person or one situation is not right
for another. Context matters.
Of more relevance, what often happens is that people get so overwhelmed at focusing on the details that
they never act. They spend weeks looking for the perfect diet or training program (which doesn’t really exist
in the first place, at best all programs have pros and cons and are, at most, best under a given set of
circumstances) and lose time when they should simply be doing something.
Because, at the end of the day, assuming the training or diet isn’t completely and utterly moronic (and make
no mistake, there are plenty of those out there) actually doing something is always better than talking about
it for weeks on end.
Yet it’s that latter pattern I see altogether too many falling into: people spend days and weeks and longer
asking about this plan versus the other plan, this program versus the other. Time that would be more
productively spent actually starting any one of the myriad programs that they’ve asked about.
And this is especially true at the beginner stage (less so at the intermediate stage although the same
principles still hold). When you’re starting out in training or diet, the ‘nice’ thing is that everything works. One
set, three sets, it all works; for the most part any non-idiotic diet will be effective to some degree for
generating weight or fat loss.
Hell, some of the idiotic stuff usually works at this level simply because it’s better than what the person was
doing beforehand. It’s not that the new approach is better so much as what was left behind was awful. But
at this point, the details just don’t matter. What matters is actually doing something. You usually won’t find

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out if something is right for you ahead of time unless you just hunker down and try it. So stop worrying and
start hunkering.
Once again, as folks get more advanced, the details can start to matter. Basically, you often have to worry
more and more about less and less as you try to get to higher levels of performance or leanness or
muscularity. But by the time someone truly reaches that stage, they usually know enough about how their
body responds, on top of having years of fundamentals under their belt, that they either know what to do
next or how to proceed. As mentioned above, while everyone wants to think that they are advanced, the
reality is that they are not.
.

Forgetting Fundamental Principles

Make no mistake, I often get rather focused on details, and many articles on this site reflect that. Of course,
I try my best to balance those out with articles looking fundamental concepts; that is, the basics that are
important and should underlie all intelligently set up approaches. That’s why I write the primers on various
topics and try to look at fundamental principles instead of just getting up my own butt with complicated details
(that fascinate me but are often not globally very relevant).
It’s worth noting that most of my own complicated approaches to things are aimed at the advanced people
in the first place. The Ultimate Diet 2.0 is an advance diet for advanced dieters; it’s aimed at people for
whom the details matter. Even there, while the overall structure of the diet is a bit complicated, any given
day actually isn’t.
The information in The Stubborn Fat Solution is equally detail oriented. But again, it’s aimed at folks looking
at the last little bits of fat, the stuff that doesn’t come off easily without an attention to such details. For
everyone else, such details are not needed: that training and dieting gets done is more important than how
it gets done exactly.
But the fundamental principles must always be adhered to, even in the advanced/complicated programs. It’s
simply that the details are less relevant for the non-advanced. So, for example, as I looked at in The
Fundamentals of Fat Loss Diets Part 1 and The Fundamentals of Fat Loss Diets Part 2, there are a set of
fundamental principles of fat loss diets that I consider crucial to success, first and foremost among them the
creation of a suitable caloric deficit.
And, frankly, any approach that meets those principles in one form or fashion will be a ‘good’ program. So
while I have my approach and Alan Aragon has his and someone like Borge Fagerli (Blade) has another,
and Martin Berkhan has his intermittent fasting approach; if you looked at all those plans in terms of the
fundamental principles, you’d see that they all met them. They may differ slightly in details and approach
but the fundamentals are always present.
A similar article could be written (and I will eventually write it) regarding training principles for growth or
strength gains. There are fundamental principles (revolving around intensity, frequency, volume, etc.) that
all intelligent programs must meet. How they are met is less relevant than that they are met in some form
or fashion. And while people will argue endlessly about the (apparent) differences in application; when you
get down to the fundamentals most programs are not as different as you think. Not the good ones anyhow.
The problem comes in when people start focusing on details (that may or may not be relevant) to the
exception of those fundamental principles. So people want some magic combination of foods or whatever
to get around the necessity to create a caloric deficit; they hope that they can avoid the fundamental principle
of fat loss (an imbalance between energy intake and output) with some minor detail. That’s when the
problems start.

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I can’t count the number of times someone has come on the support forum with a question about “Why am
I stalling/why am I not losing weight?” and they can’t even answer the basic questions of “How many calories
are you eating per day? How much protein? How many total carbs? How much total dietary fat?” They
can tell you just about everything about their diet except the relevant stuff: how much.
So they are worrying about the glycemic index of one food versus another and one protein source versus
another and whether 12.7% of one nutrient is better or worse than 17.2% of the same nutrient and one
supplement versus another and….. And they haven’t even figured out how much they are currently eating
per day, or their total macronutrient intake or anything else that actually matters. On and on it goes and I’m
sure readers can see this for themselves across the Internet.
.

Making My Point

Make no mistake, worrying about minor details can have value in certain circumstances and don’t
misconstrue what I’m saying here. For some it’s a true physiological need; those advanced people who
need to worry about the details because they are at a level that matters. But, as I noted above, those folks
have already spent so much time on the fundamentals that they are in a position where it may matter.
For others, there is often a psychological need to worry about details. There is a type of dieter I once saw
Dan Duchaine describe as ‘wanting all the plumbing’ who tends to follow diet and training programs better
when they have an insane amount of details to worry about. They may not need them in the sense of a true
physiological need but they want them and will only be happy if they have them present.
And, to a degree, a lot of what is written in the athletic and bodybuilding literature (those subcultures being
towards the obsessive end of things) is geared towards that; giving people a lot of details that are often
irrelevant to worry about and obsess about. Certainly psychological needs are important and have to be
taken into account but those details must be placed on top of a basic of fundamentals. Many of those folks
often learn over time that the details aren’t really that relevant anyhow. But starting out they often need/want
those details to be happy or to follow their program.
Because what you usually find is this: once you get the fundamental principles in order, most of the minor
details don’t matter very much. At the very least, they don’t add nearly to the results that most people hope
for. And until you get the fundamental principles in place, the minor details don’t matter at all. That’s on top
of the situation where obsessing about those details prevent someone from ever actually acting in the first
place.
As Doc said so clearly and succinctly: Do not subordinate fundamental principles to minor details.

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How Detail Oriented Do You Need to Be?
If the internet has accomplished one thing, it’s making people extremely obsessive compulsive about the
most minute details of their training program and diet. Arguments and flame wars erupt over the absolutely
least consequential of things. How many minutes should pass between sets, how long after workout before
you drink your liquid beef aminos with waxy maize starch, stuff like that.
Of course, I’m as guilty as everyone else, I worry about such things and my books often contribute to the
problem by providing fairly detail-oriented approaches to diet and training. However, I’m often writing for a
fairly small population of folks (trying to reach the extreme low-end of leanness) for whom such details may
matter.
Now, in my experience, a lot of people are attracted to complex approaches whether they need them or not,
it’s just part of their psychological profile. At the same time, an equal number are plenty happy with nothing
but basic simple guidelines.
Ultimately, all of this is just an introduction to the topic this article is about which is “How detail oriented do
you need to be?” in terms of your training or diet. Of course, the short-answer is that “It depends.” Now let’s
look at the long answer.

The Long Answer

How detail oriented you need or have to be depends on a lot of factors. One of these is where you’re starting
out. Someone going from 30% bodyfat to 25% bodyfat or just trying to lose a few pounds won’t have to pay
nearly the attention to the details as the individual trying to get from 10% bodyfat to 5% bodyfat with no
muscle loss.
Wanna lose weight? It’s simple: Eat less, exercise more, repeat. Get a few basic details correct and that’s
really about everything you need to know in the initial stages or if you aren’t trying to get super lean.
Everything else, quite seriously, is just details. For the record, same thing for muscle gain but in reverse,
more or less. If you don’t care how much fat you gain, just eat a lot, train hard, sit on your butt as much as
possible and be done with it.
Since that latter group, the folks who are worried about the last few percentage points, probably describes
only a tiny percentage anyhow, you’re probably wondering why I brought it up. To drastically oversimplify, I
have found two types of individuals, psychlogically speaking, when it comes to diet and exercise advice.

Group 1: Keep it Simple Stupid

The first group isn’t really that detail oriented, they just want some basic easy-to-follow advice that will help
them get moving towards their goal. They usually like to make the smallest, least intrusive changes to their
diet and exercise programs when they start and they tend to go through a lot of anxiety if they have too much
to deal with in terms of details.
If making small changes will get you to where you want to be, more power to you. I’ll absolutely be the first
to tell you to make the smallest changes you have/need to, as long as they are producing the results you
want. If you don’t need the hassle of all of the details, don’t stress yourself out about them. Basically, keep
it simple as long as it’s working. In actuality, I see a lot of people drastically over-complicating things long
before it’s needed. Which brings us to group 2.

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Group 2: All the Plumbing

Then there’s the second group: they want all the details and then some. Some refer to this as nutrition (or
training) with “all the plumbing”. Based on the kinds of email questions I regularly get, I’m used to getting the
“all the plumbing” types of questions. As I noted above, people are obsessed with just about any possible
bit of diet or training minutiae you could conceive of even if it’s not necessary. They time their workouts to
the minute, their sets to the second, and measure their post-workout drinks to the gram. They worry about
details so minute as to have literally no relevance to real-world results.
We can really divide Group 2 into two separate groups. The first are folks who are simply more ready to
make changes to their diet and exercise program when they have everything laid out to the last detail. They
tend to be drawn towards very complicated dietary approaches that have a lot of details to keep up with
(cyclical ketogenic diets being a prime example) because it fulfills a psychological aspect of the diet. I know,
I used to be one of these types of people. Still am to some degree. I want to make it clear up front that
meeting psychological goals is as important as meeting the physiological ones.
The second group consists of an even smaller percentage of folks: they want all the plumbing because they
truly need it. They are the natural bodybuilder who loses too much muscle dieting down and hopes there’s
a magic solution (better yet, a magic pill). Or a sprinter who needs to drop 10 lbs. of accumulated fat, without
losing performance, in 8 weeks, for a competition (that was an actual email I got one time, and I told the guy
he was basically out of luck without using drugs). They are meticulous about all the details because they
have to be, not because they necessarily want to be. I’d surmise that this sub-group would rather not have
to pay so much attention to the details if they didn’t have to.
There is much to be said for group 2 individuals, at least with regards to short-term success. Folks in this
group tend to get overall faster and better results because of their attention to detail. But it seems that overall
long-term success can be up in the air.
Basically, when they are on their diets, they are ON THEIR DIETS (!!!) and the results come as a
consequence. But when they fall off the wagon, they fall off hard. So they tend to alternate between two
extremes: one of anal-compulsion and one of total indifference. These extremes correspond to being in
shape and not being in shape respectively.

Finding balance

It would be relatively safe to say that a balance of the two different groups is probably ideal for most
applications (excepting the subgroup of group 2 who have to track the details or risk failure). Somewhere
between complete devotion/compulsion and total slackness will work for the majority of folks. We’ll talk more
about finding balance way later on in this book.
It’s pretty safe to say that bodybuilders and athletes (especially bodybuilders) are almost always in the
second group, whether they are very good or not. To say that they are obsessive compulsive is putting it far
too mildly. Psychotically obsessed is more like it. Even folks who don’t have a prayer of ever reaching a
decent level of competitive bodybuilding will worry about every detail under the sun. The psychology just
seems to accompany the activity in this case. Meaning that folks who tend to get drawn to bodybuilding in
the first place tend to be detail obsessed, control freaks. I don’t mean that as a negative, necesssarily, just
a statement of fact.

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As a side-note: some psychologists have commented that most top athletes are slightly obsessive
compulsive in the true sense of the term, others have even tried to turn it into a psychological syndrome as
a bad thing. Whatever. I’d argue that most people at the top of any field are a bit compulsive; if they weren’t,
they wouldn’t reach the top level because there’d always be someone willing to work a little bit harder who
would surpass them.
Of course, obsessive dedication is part of the price to be paid for high performance and maximal results.
That’s also a big part of the reason group 2 folks get the results they get. Sure you can’t deny genetics, good
coaching, drugs, etc. but the fact that they are so attentive to ALL the details ALL the time makes a big
difference in the level of performance that these individuals ultimately achieve. At the elite level, genetics,
equipment and everything else tend to be fairly equal across the board and it comes down to who worked
the hardest and smartest. There are, of course, exceptions.
Then again, a lot of very dedicated people don’t get the results they want (or think they should) usually
because they are getting bad advice. So don’t equate obsession with automatic success. A crappy diet or
training program is a crappy diet or training program no matter how dedicated you are. A lot of people will
stick to really crappy diet or training programs far longer than any reasonable person should, usually because
a ‘guru’ told them it was the right way to do things. This leads to the my most important rule of training and
diet. Call it Lyle’s Rule #1 :

If something isn’t working, change it.

My general rule of thumb is that if some dietary or training change hasn’t generated some type of progress
within 4 weeks, it’s time to try something else. Sure, there are exceptions and I’ll note them as we go but
something that hasn’t done anything in a month isn’t going to magically start working. Seriously, no matter
who the guru is or how smart you think they are, if the advice isn’t producing results in a reasonable time
frame, it’s time to move on. You have little to lose (you’re making zero progress to begin with, and you can’t
do any worse than that) and everything to gain.
Oh yeah, that goes for any advice I might give you in this book too: if it’s not working for you in a reasonable
time frame, try something else. I’m as fallible as the next guy and have given some pretty crappy pieces of
advice in my life. Like I said before, I’m all about honesty here.
While I’m on the topic, I suppose I should mention the Corrolary to Rule #1 which is

If it’s not broken, don’t mess with it.

Yes, I know, this isn’t a new idea but it is absolutely true. It’s quite common to have someone doing
everything just fine, losing fat without losing any muscle or gaining muscle at a good rate, to make a change
simply for the sake of making a change.
This is depressingly true with pre-contest bodybuilders and newbie athletes; they’ll freak out 2 weeks
beforehand and start doing goofy stuff. They’ll change their diet, experiment with some untested strategy
and it always does more harm than good. If something is working, don’t mess with it.
You also see it out of simple impatience: body recomposition takes time and humans are not good at waiting.
We want it NOW, and that attitude tends to make folks change things to try and generate results faster.
Seriously, if what you’re doing is generating the results you want, leave it the hell alone. Change simply for
the sake of change is just as bad as not changing something when it’s not working. When we get there, I’ll

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give you guidelines for what I consider good progress in terms of fat loss or muscle gain. If you’re meeting
those numbers already, then what you’re doing is fine. Don’t mess with it.

Making a Choice Between Groups

Now. there’s also no reason that you have to be in one group or the other. It’s not uncommon for individuals
to begin in group 1 (making small, manageable changes to their diets and exercise programs), begin to see
some nice progress, and become more detail oriented as the time passes or such detail become necessary
to reach the next level. There’s actually a lot to be said for making the changes gradually, because they are
more likely to become part of your daily patterns, instead of some extreme approach that you won’t stick to
in the long term.
Which do I think is better? As I said in the introduction “It depends”. If you came to me as an athlete with 5
weeks to accomplish some nearly impossible goal, I’d say you better pay attention to the details. If you’re a
newbie starting out on a weight loss or exercise journey, I’d be more inclined to argue for keeping it simple
initially and getting more detail-focussed as needed.

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Comparing the Diets: Part 1
If you read diet literature, it seems as if there are nearly an infinite number of dietary approaches out there.
However, once you start looking at it in terms of generalities, you find that this isn’t really the case. The
number of distinct dietary approaches is actually quite minimal.
I’m going to ignore the really weird stuff that’s out there, by the way. Food combining, metabolic typing, I
consider all of that to be voodoo nutrition. If such approaches work for you, fantastic, but I doubt they are
working for the reasons you think they are working.
In general, folks have generally divided themselves into three different ‘camps’ when it comes to diet. All of
the groups tend to proclaim loudly that their approach is best and all are quite able to bring research to the
table to support their diet in some degree.
Testimonies always abound about how a specific diet just did amazing things and you can find them for any
diet out there. A bigger cynic might conclude that all diets work (as long as they meet a few basic
requirements) and to, a great degree, there is some truth to this. As long as a diet gets you to eat less, you
should lose at least some weight.
At the same time, you can always find folks who did poorly on a given approach. It’s easy (and a copout) to
blame the dieter and there are situations where a given diet may simply be inappropriate (or less than ideal)
for a given situation. A dieter may fail on a diet for the simple reason that it doesn’t meet their needs, a topic
I discuss in How Dieters Fail Diets.
But that doesn’t change the rather loud proclamations of the various dietary camps that they have the ONE
TRUE DIET ™. It’s not far from claims of having the ONE TRUE RELIGION ™ in a lot of ways.
What few of these groups are willing to admit or acknowledge, and what I’ve tried to make a recurring theme
in this book is that different diets are more or less appropriate depending on the situation. Each of the
different diets may be the ‘correct’ approach, simply at different times and under different sets of
circumstances.
Rather than promoting a specific diet as being optimal under all situations, I take the stance that the choice
of diet (for example high vs. low-carbohydrate) is context specific: different diets are more or less appropriate
under a given set of conditions. Sure, I’d sell more copies of my books if I told you I had the ONE TRUE
DIET (TM) but that’d be bullshit because I don’t think it’s true.
Frankly, I feel that this is a big part of why you can always find someone reporting near magical results with
a given diet: whether by design or by accident, they stumbled on the diet that happened to meet their specific
needs. At the same time, it’s easy to find people who weren’t so lucky: who by design or accident picked the
absolutely wrong diet for their situation. Results, as would be expected, are poor.
As I mentioned above, you might note in this regards, that diet gurus almost never report their failures (or
they blame failure on the dieter), focusing only on those individuals who got stunning results. To say that
this is intellectually dishonest would be an understatement.
I’m going to present, discuss and describe three distinct dietary approaches in this and the next two articles:
high carb/low-fat, moderate carb/moderate fat and low-carb/high fat. If you read Dan Duchaine’s Bodyopus,
they should seem quite familiar as he described a standard high-carb/low-fat diet, the Isocaloric diet and
finally his take on the ketogenic diet, Bodyopus.
However, the way Dan’s book was written, it almost seemed as if dieters were supposed to move
sequentially through each diet: starting with the standard high-carb approach, then to Isocaloric, finally to
Bodyopus. Figuring that most people were ‘used’ to seeing the standard approach first, he described it first;
it was pandering to the psychological hangups of dieters as much as anything else.

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I am going to take a different approach in this article series. Rather than have folks pick a diet at random,
find out that it’s not appropriate for them (losing valuable dieting time) and then try the next diet, I prefer to
take a broader approach.
First I want to discuss each of the three diets in terms of their pros and cons and under what situations and
conditions they might be ideal or less so. Odds are you’ll find a description of your specific situation (or
something close to it) in that discussion. That should point you towards which approach might be ideal for
you and you can look at the detail chapters to get the specifics of the how to optimize the diet. Of course, I
can’t predict every possible situation, in some cases you might have to take a stab at one of the dietary
approaches and then make modifications.
I’ll say it again, for the slow of reading: none of the three diets described in this book is the ‘best’ across the
board. Not high-carb, not moderate carb, not low-carb (so please quit calling me the keto guru). Put
differently, I am absolutely NOT an advocate of a given dietary approach except inasmuch as it meets the
needs of the individual. I’ll rant about this one last time in the next chapter.

One More time: Protein Intake

Before continuing, I want to harp on the issue of protein intake one more time, an issue I discuss in more
detail in Is A Calorie A Calorie? In this article series, I’m mainly going to focus on manipulations in
carbohydrate and fat intake; I assume protein intake to be set adequately and identically in each of the three
diets I’m going to discuss. Basically, this isn’t a discussion of how low-carb diets are ‘better’ but only because
they happen to get people eating more protein. Understand, protein intake is taken to be sufficient and
identical regardless of the rest of the diet.
That assumption means a protein intake of 1-1.5 g/lb (roughly 1.8-3.0 g/kg or thereabouts). Again, that
means that, in this discussion, I’ll be focusing primarily on variations on carbohydrate and fat content since,
as I’ve mentioned before, that’s generally what’s being shuffled around.

Defining Terms

Even though I threw around the terms high, moderate and low above in terms of carbohydrate and fat content
above, I’m not happy with them. As I discussed Diet Percentages, such terms tend to be generally
meaningless. A diet containing nothing but 50 grams of protein per day might be ‘high-protein’ because it’s
a 100% protein diet but it’s ‘low-protein’ compared to what the body actually might require. As well, as much
as I don’t like percentage based diets, I need some way to differentiate the various diet camps from one
another. I’m not saying mine are necessarily correct, simply that that’s what I’ll be using. But so we’re clear
I’m going to use the following terminology:
Low-fat: anything below 30% of total calories (this is the standard definition) Note: to athletes and obsessive
dieters, low-fat usually means 10% or ‘as low as I can get it’
Moderate-fat: 30-40% of total calories Note: some researchers use 25-35% as moderate fat
High-fat: anything above 40% of total calories
Low-carbohydrate: less than 20% of total calories
Note: a true ketogenic diet contains, by definition, less than 100 g carbs/day. But while all ketogenic diets
are low-carbohydrate, not all low-carbohydate diets are ketogenic
Moderate-carbohydrate: 20-45% of total calories

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High-carbohydrate: 45% of total calories or higher
Since protein intake will always be set at about the same level (between 1.0-1.5 g/lb which is generally
between 25 and 40% of total calories), I’m not going to bother defining terms for it. You can call it low-protein
or high-protein or Susan for all I care; I consider it the proper protein intake and that’s all that matters.
So, using those numbers, a traditional athletic ‘low-fat’ diet would contain approximately 60% carbohydrates,
30% protein and 10% fat. Moderate fat diets such as The Zone, Dan’s Isocaloric diet and others contain
anywhere 30-33% protein, 33-40% carbs, and 30-33% fat on average. A typical low-carbohydrate/high-fat
diet would contain 30% protein, 20% carbs or less and 50% fat or more.
I want to make the point once more that such percentages don’t necesarily have any relevance to actual
human needs, which are better expressed in terms of g/lb or g/kg. I’m simply using them for convenience
here. Again, read Diet Percentages if you’re unclear on why I’m saying this.
To be continued in Comparing the Diets: Part 2.

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Comparing the Diets: Part 2
In Comparing the Diets: Part 1, I made some introductory comments about the different primary approaches
to dieting which are high-carbohydrate/low-fat, moderate carb/moderate fat, and low-carbohydrate/high-fat.
I also defined my terms as to what I mean by high, moderate and low. In the next parts of this article series,
I want to examine each of the three major dietary camps, along with their pros and cons so that I can provide
recommendations on which diet might be the most appropriate for a given situation or individual.
A quick note on the percentage nutrient notation: as much as possible I tried to adhere to a format where
the percentages represent percentages from protein/carbohydrates/fat in that order. So a notation of
30/60/10 means a diet where 30% of the calories are protein, 60% are carbs and 10% are fat.

High-Carb/Low-Fat

While trends are beginning to show shifts, the high-carb/low-fat diet is arguably the de facto standard
recommendation for both health, weight loss and athletic performance. At the same time, it’s becoming more
common to criticize this diet on various grounds, blaming it for increasing obesity and health problems among
the general public. You can read more about Carbohydrate and Fat Controversies elsewhere on the site.
Research is finding that, among certain populations, such a diet can do more harm than good. For examples,
individuals with insulin resistance tend to get better health benefits from lowered carbohydrates.
Among more fringe diet groups, a diet based around high-carbs and low-fat has become an almost
unspeakable evil. Claims that you can’t lose fat on high carbs or can’t get ripped, or whatever, are becoming
more and more common.
Now, if you still think of me as the keto-guy you’re probably expecting me to shit all over this diet interpretation
or take the fringe stance on it. With some qualifications, I’ll say up front that you’re wrong. The reality is that
there are plenty of folks out there who have made high-carb/low-fat diets work and work well.
In fact, over the years it’s probably safe to say that most contest bodybuilders have gotten into shape on
such a diet. Folks in the National Weight Control Registry (NWCR, which tracks successful dieters and their
habits) reports most using some version of a high-carbohydrate diet (although more recent surveys have
identified smaller groups succeeding in the long-term with low-carb diets).
It’d be absurd to dismiss it out of hand even if that’s what most people do.
At the same time, it’s probably safe to say that a lot of folks don’t do particularly well on such a diet, although
it depends on a lot of interacting variables. The question is what differentiates the groups: why does such a
diet work for some but not others? It’s easy and convenient to say that the drug use among top bodybuilders
makes such a diet workable but this is too pat of an answer. Nor does it explain the NWCR folks. In my
opinion, the answer is more complex.
Now, upfront I will say that I think a 30/60/10 diet is a little unbalanced to begin with. My main problem is
that the dietary fat is too low. As I discussed in Comparing the Diets: Part 1 the technical definition of a low-
fat diet is anything less than 30% and the actual government recommended high-carb/low-fat diet is actually
closer to 15% protein, 45-50% carbs and 30% fat or thereabouts.
As you might imagine, I find this lacking in protein for body recomposition or optimal athletic performance
even if it’s probably ok for the average person (even there recent research supports a benefit of higher
protein intakes, approaching 25% for fat loss diets even in the non-athletic). Frankly, my ideal high-carb/low-

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fat diet would be in the realm of 25-40% protein, 50% carbs and 20-25% fat although, as I’ve discussed
before, the percentages themselves are fairly meaningless.
The first problem that typically crops up is that people take a diet that should be ‘ok’ (either 30/60/10 or
15/45-50/30) and screw it up completely. The problem is primarily one of interpretation. It’s not uncommon
to see dieters, especially women, turn a 30/60/10 diet into a 10/80/10 diet and they do it by overemphasizing
high GI refined junk (the government and researchers thinks that folks are getting their carbs from unrefined
grains but this is generally incorrect).
Endurance athletes, who tend to overemphasize carbohydrates frequently do the same thing: many, in my
experience, are protein deficient (and studies are suggesting that very low fat intakes can hamper endurance
performance). That takes a diet that was right on the edge of being imbalanced to begin with and screws it
up even further.
I can track a majority of high-carb diet failures directly to such a mistake in interpretation. And, if you take
someone from 10/80/10 to anything else and the results will look like magic. It’s not so much that the new
approach is magical as the original approach was screwed up. Just about anything is better than something
stupid.
Ignoring this major problem, let’s assume someone actually sets up a 30/60/10 diet more or less ‘correctly’
in terms of amounts. There can still be problems. The first is one of taste. A 10% fat diet is literally a non-fat
diet and the small amounts of naturally occurring fats in non-fat foods tend to readily fill up the small fat
allotment. Many people find such diets to be tasteless and bland which compromises adherence and
research shows that moderate fat diets (discussed in Part 3 of this series) show better adherence than very
low-fat diets.
Bodybuilders will just suck it up, of course; they are used to dieting with food that tastes like shit and a
common statement is that ‘When I diet, I just make sure I don’t eat anything that tastes good.’ Typical macho
crap. But the rest of humanity is unlikely to stick to a diet that they don’t find palatable.
With such an extremely low fat intake, there can also be problems with essential fatty acid intake which can
be difficult to meet with so little of a fat intake. Even Dan Duchaine’s high-carb/low-fat diet required 8%
essential fats for a total of nearly 18% total fat content (this changed a 30/60/10 diet to 30/52/18 which is
damn close to my ideal anyhow).
There is a certain minimal fat requirement, if for no other reason than to ensure adequate absorption of fat-
soluble vitamins. Extremely low-fat diets can cause their own set of health problems and this is clearly a
place where lower isn’t better.
Another problem that crops up has to do with the types of carbohydrates being eaten. Researchers and
other well-meaning types seem to assume that this is going to be the source of carbohydrates among the
general public but this is generally not the case. Most of the athletes and bodybuilders who follow such a
diet emphasize low GI, unrefined, high-fiber foods; in my experience, most of your typical dieters do not. It’s
one thing to eat 60% of your total calories from carbohydrates when all the foods you’re eating have a GI
that is extremely low.
As soon as you start making breads, pastas and other high GI foods a larger source of your total
carbohydrates you run into a few problems. First is that the speed of digestion is fairly fast, a problem made
worse by the low fat intake and generally low fiber intake of high GI food sources (and most peope don’t eat
enough vegetables or fruit which would provide some much needed fiber). Along with that, the glycemic load
(which is the Glycemic Index * the number of carbs eaten)) goes up fast meaning blood glucose can be all
over the map. For folks with even moderate insulin resistance (see below) this causes all kinds of problems.
Along with that, most of the higher GI carbs can be surprisingly high in calories. So while 2 oz of uncooked
pasta may only contain 40 some odd grams of carbohydrates and 200 calories, an average large bowl of

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past may easily contain two or three times that. This can easily amount to hundreds of calories. Bodybuilders
and athletes are typically obsessive compulsive to begin with, and measure all their food intake; your
average dieter is not. So where an athlete will know exactly how many calories they are getting from the
pasta or rice, the average person will end up eating too many calories.
That’s ignoring all of the highly refined, high-carbohydrate low-fat foods that food companies brought to
market (Snackwell’s anyone?). As above, researchers seem to think that most people are increasing their
carbohydrate intake from moderately refined sources but that’s simply not the case in my experience.
As soon as people heard that fat was bad and carbs were good, and food companies rushed high GI non-
fat carb foods to market, folks went crazy. Studies even found that, subconsciously, folks figured they could
eat more when it was low-fat. Any benefit from lowering the fat content was more than compensated for.
Basically, very high carbohydrate intakes tend to work best when the source of those carbs are low on the
GI. If you’re willing to eat almost nothing but low GI carbohydrates in the first place, a high-carb diet will
probably work. If not…
Related to this issue is meal frequency. Bodybuilders and athletes eating high-carb diets spread out the
carbohydrates over 6 or more meals meaning their total carbohydrate intake per meal isn’t actually that
large. That, along with the low GI and high fiber intake minimizes problems with blood glucose swings and
the resulting problems. Your average dieter, eating 3 large meals per day, with high GI carbohydrates and
too little fiber will generally run into problems with such a high-carbohydrate intake.
Another related issue has to do with activity. Athletes who are burning a tremendous number of carbohydrate
calories per day can tolerate/handle many more carbohydrates without problems than someone who is
engaging in little to no activity (your average person). This is discussed in detail in How Many Carbohydrates
Do You Need?
A bodybuilder or endurance athlete doing 2 hour workouts on a nearly daily basis may be able to tolerate
(and may in fact need) such high carbohydrate intakes; someone walking briskly 30 minutes per day three
times per week does not.
Related to the activity issue is that of insulin sensitivity. Insulin sensitivity refers to how well (or how poorly)
tissues respond to insulin. With high insulin sensitivity, small amounts of insulin generate a large response.
With poor insulin sensitivity (insulin resistance), the body has to produce more insulin to get tissues to
respond. Recent research has shown a clear link between Insulin Sensitivity and Fat Loss in terms of what
diet is optimal.
Individuals who are highly insulin sensitivity handle high carbohdyrate intakes to a better degree than folks
with poor insulin sensitivity. I should mention, in this regards, that even folks with substandard insulin
sensitivity can sometimes handle high-carbohydrate intakes when insulin sensitivity has been temporarily
elevated (such as with glycogen depletion). This is relevant because certain dietary approaches (such as
cyclical diets like my Ultimate Diet 2.0) use this ‘trick': they elevate insulin sensitivity temporarily and then
load in lots of carbohydrates before insulin sensitivity goes back to substandard levels.
So what determines insulin sensitivity? Well, there are a lot of factors. First, there’s a genetic component,
activity affects it drastically (improving it), so does diet. Diets high in refined, high GI carbs tend to impair
insulin sensitivity, so do diets high in saturated fats. Fish oils and unsaturated fats generally improve insulin
sensitivity. A crucial determinant of insulin sensitivity is body fat percentage.
Obese individuals frequently become insulin resistant, which causes problems with carbohydrate intakes
are excessive (moreso when they are high on the glycemic index). One of the main problems has to do with
hunger and appetite. Under conditions of relative insulin resistance, a high carbohydrate intake (especially
with very low fat intakes) tends to spike blood glucose levels, which spikes insulin, which crashes blood
glucose.

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This tends to cause rebound hunger, making calorie control nearly impossible. It also makes people feel
crappy with alternating periods of high and low energy. Studies are finding that high-carbohydrate/low-fat
diets, especially when the carbs are high on the GI, cause detrimental effects on various health parameters
in insulin resistant individuals.
Additonally, some people seem to be carbohydrate ‘addicts’. While it’s debatable whether or not this is a
true addiciton, many people find that eating carbohydrates makes them want to eat more carbohydrates.
Whether this effect is hormonal or just a taste effect is debatable but it is real.
For such individuals, a high-carb/low-fat diet can cause problems in terms of calorie control. It’s all good and
well to tell such people to suck it up, or that dieting is supposed to be a test of willpower, but any diet that
makes people feel lethargic and hungry all the time (from crashing blood glucose or simply the ‘taste’ of
carbs) is not likely to be followed for very long.
As a final issue, empirically, high-carbohydrate diets can cause problems with stubborn fat mobilzation. The
mechanisms are discussed in a later chapter but folks with a lot of lower body fat can have problems getting
extremely lean on high-carb diets unless they reduce the GI to very low levels. That means pretty much
veggies and the few low GI starches. Women seem to crave carbohydrates more than men and sticking to
such a diet can be a losing proposition.
Continued in Comparing the Diets Part 3.

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Comparing the Diets: Part 3
Having examined the traditional high-carbohydrate/low-fat in Comparing the Diets: Part 2, I now want to look
at the second major diet ‘type'; moderate-carb/moderate-fat.
A quick note on the percentage nutrient notation: as much as possible I tried to adhere to a format where
the percentages represent percentages from protein/carbohydrates/fat in that order. So a notation of
30/60/10 means a diet where 30% of the calories are protein, 60% are carbs and 10% are fat.

Moderate-Carb/Moderate-Fat

The next major dietary camp refers to any diet consisting of relatively moderate carbohydrate and dietary fat
intakes. This includes diets such as Barry Sear’s “The Zone”, Dan Duchaine’s “Isocaloric diet”, 30/40/30
nutrition and others. Such diets generally recommend a macronutrient split based on fairly equal amounts
of protein, carbs and fat. Various scientific rationales, usually involving hormonal control are typically given.
The Zone, for example, recommends a 30/40/30 split while Dan’s Isocaloric diet is 33/33/33. Some
bodyuilding gurus recommend 40% protein with 30% carbs and fats, for what it’s worth. In the research
realm, cutting edge diabetic diets are in the realm of 15% protein (too low for athletes but protein can
stimulate insulin release in diabetics), 40-45% carbs and up to 40% fat from mono-unsaturated sources. All
of those approaches to fall within the description of moderate carbohydrate and moderate fat I gave last
chapter.
Although I find a lot of the scientific rationales given for such diets to be pseudoscience at best, I do think
that this type of moderate approach is probably close to ideal for most individuals. As I mentioned above,
my ideal high-carb/low-fat diet is already close to 25-30% protein, 45-55% carbohydrate and 20-30% fat or
so and moving from that to an Isocaloric or Zone diet is a rather minimal change to begin with.
But rather than focus on issues of eicosanoid balance or what have you, I simply think of such diets in terms
of the fact that they tend to control blood glucose and hunger better because of the lowered carbs and higher
fat content. It’s a fairly simple trick, the increased dietary fat (and usually fiber) slows gastric emptying; the
decreased carb intake decreases the overall glycemic load.
Such diets also allow more food freedom and taste better than their near zero fat counterparts; this adds up
to increased adherence. Frankly, if the various diet book authors had simply said “Hey, here’s a diet that
better controls blood glucose and insulin and blunts hunger by slowing gastric emptying and it doesn’t taste
like cardboard so you’ll stick with it better.” instead of making up physiology, I don’t think there’d be as much
criticism of such diets.
So what people might find such an approach to be ideal? As I described above, for that small percentage of
individuals who are genetically very insulin sensitive, or who are burning a tremendous number of calories
(from carbs) with daily or near daily workouts, the high-carb/low-fat diet described in Comparing the Diets:
Part 2 intakes are probably more appropriate. At the very least, they can be tolerated. Since that describes
a rather small percentage of people in the first place, I find the moderate- carb/moderate-fat approach more
appropriate under most conditions.
For people burning less calories (or carbs) during the day, there’s simply no real need for the high
carbohydrate intakes of the high-carb/low-fat diet. Folks doing more realistic levels of activity (perhaps an
hour of weight training 3-4X/week and moderate cardio), carb requirements simply aren’t that high. Again,
read How Many Carbohydrates Do You Need? for more details.

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From a caloric control issue, by lowering carbohydrates, and raising dietary fat, digestion is slowed and blood
glucose levels tend to even out (note: the major effect is from reducing carbohydrates, fat is simply a caloric
ballast). This generally means more stable energy levels and less pronounced hunger. This also allows
foods higher on the GI to be chosen if desired with less of a problem.
Basically, while it’s generally better to choose lower GI foods from a health standpoint but GI becomes far
less crtical when total carbohydrate intake is decreased. Remember that the glycmic load is the GI times the
grams of digestible carbs: reduce digestible carb intake and GI becomes less important. Breads, pasta, rice
and the rest can be consumed in controlled amounts on such a diet with far fewer problems. I’d note again
that these foods may not provide much actual food volume when calories are restricted.
Another potential benefit is that, by reducing carbohydrate intake, muscle glycogen is generally maintained
at slightly lower level. As I’ve discussed in books such as the Ultimate Diet 2.0, lowering muscle glycogen
enhances whole-body fat burning. At the same time, the moderate carb intakes should be sufficient to sustain
performance in all but the most extensive types of training.
Moderate-carb/moderate-fat diets also tend to limit problems with insulin resistance related blood sugar
crashes as a consequence of both reduced carbohydrate intake and increased dietary fat. However, some
extremely insulin resistant individuals still run into problems with even moderate carbohydrate intakes. For
such people, a more drastic decrease in carbohydrates may be necessary.
As well, those individuals who find that eating carbohydrates makes them want to eat more carbohydrate
can also run into problems even with moderate carbohydrate intake. As I discuss in The Stubborn Fat
Solution, lowering carbs tends to enhance stubborn body fat mobilization; however larger reductions than
those which occur in the moderate-carb/moderate fat diet may be necessary for extremely lean dieters.
I should mention, that moderate carb/moderate fat diets tend to be more of a planning hassle than the other
diets, especially at first. While I don’t believe that you have to be exact in the percentages (as long as you
get in the ballpark, you’ll be fine), it can still be a pain in the butt to figure out meal plans.
From a simplicity standpoint, it’s pretty easy to reduce fat and it’s pretty easy to reduce carbs; getting
moderate amounts of each can be a hassle. As well, with practice and time, it becomes relatively trivial to
eyeball meals to get in the right ratio.
And that’s that for the moderate-fat/moderate-carb approach.
I’ll discuss low-carbohydrate/high-fat diets in Comparing the Diets: Part 4.

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Comparing the Diets: Part 4
Having examined the moderate-carb/moderate fat diet in Comparing the Diets: Part 3, I now want to turn my
attention to one of the more contentious dietary approaches out there: low-carbohydrate/high-fat diets. I’ll
also provide an end-of-article chart showing how the different dietary approaches may be more or less useful
in a given situation.
A quick note on the percentage nutrient notation: as much as possible I tried to adhere to a format where
the percentages represent percentages from protein/carbohydrates/fat in that order. So a notation of
30/60/10 means a diet where 30% of the calories are protein, 60% are carbs and 10% are fat.

Low-Carbohydrate/High-Fat

And finally we come to the low-carbohydrate or ketogenic diet, the diet with perhaps the greatest amount of
controversy and argument surrounding it. Now, at the risk of beating a dead horse, and since I find many of
my critics to be a little slow on the uptake, I’m going to go off on one last rant about this topic.
Rant mode on:
If you think of me as the keto-guru, you’re probably expecting me to advocate the ketogenic/low-carb diet
over all the others. People seem to think since my first book The Ketogenic Diet was about nothing but, I
must be the diet’s strongest promoter. It makes me wonder if these morons actually read the book since I
made it clear there that I didn’t feel that ketogenic diets were necessarliy ideal. I repeated this multiple times
within that book. People didn’t get it.
I’ve actually found two different criticisms of my attitude towards ketogenic diets, depending on whether the
critic is pro- or anti-ketogenic diets.
First is the group that feels that, since I didn’t write negatively about keto-diets, I must be their biggest
advocate. Since they dislike ketogenic diets on some level, they feel that I should as well. Anyone who writes
honestly and fairly about them is, by definition, in favor of them. This is moronic by the way.
The second groups seems to feel that since I didn’t say that ketogenic diets are magic, I must not believe in
them. Since they think the diet is magic, they think I should too.
Both groups, as usual, are guilty of projecting their own personal biases onto me. Both groups are apparently
unable to count beyond two, since they see the world in a rather simplistic ‘for/against’ way.
To make things clear to both groups, I’m going to sum up my attitude towards ketogenic diets one more time.
I’ll be using simple words as much as possible.
My opinion on ketogenic diets is this: ketogenic diets are one of many (ok, three) dietary approaches
available. They have advantages and disadvantages (like all diets). They are appropriate under some
circumstances, relatively neutral under others, and entirely inappropriate under still other circumstances.
They are not magic but they work tremendously well for some people and absolutely horribly for other. There
are still questions regarding their long-term effects.
Of course, you could make the same statement about any dietary approach as I’ve discussed throughout
this series. They all have pros and cons, advantages and disadvantages. But since keto diets are among
the most contentious, and since my name is essentially equated with the ketogenic diet, I’m having to make
my stance that much more clear.
The point I’m trying to make, and one that I will continue to make (probably for the rest of my life since
morons will always think of me as the keto-guru), is that, it’s a matter of context, always. Whether a given
diet, or training program, or supplement or drug is ‘the best’ always depends on context.

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And if you continue to think that I only advocate or believe in ketogenic diets after reading that, I strongly
suggest you go get your head checked for signs of trauma because you would seem to have a rather large
comprehension problem.
Rant mode off
Now, I want to point out again, while a ketogenic diet is a low-carbohydrate diets, not all low-carbohydrate
diets are ketogenic diets. As detailed in the article How Many Carbohydrates Do You Need, an intake of
carbs below 100 g/day is required to induce ketosis to any measurable degree (most ketogenic authors set
an initial daily limit of 30 grams/day but I’ve never found a rationale for this recommendation). Not all low-
carb diets reduce carbohydrates below the 100 g/day level so not all will induce ketosis. However, for the
sake of typing and reading simplicity, I’m going to refer to all diets in this section as ketogenic (again, by
definition containing 100 grams carbohdyrate or less per day).
For the purposes of this section, and as mentioned in Comparing the Diets Part 1 I’m going to set carbs at
20% or less of total intake for a low-carbohydrate diet. Protein will be set at 30% (and possibly higher) and
the remainder of the diet will be fat (in this example, 50%). As carbs go lower, fat intake goes higher, of
course, up to the limit of 0% carbs and 70% fat. I should also mention that some authors prefer to do low-
carbohydrate diets as nearly all protein affairs, with little to no dietary fat. My own Rapid Fat Loss Handbook
takes this very approach but it also sets out to generate a massive daily deficit.
I should probably mention that ketogenic diets actually come in a few varieties. First are the standard or
strict ketogenic diets (SKD) where carbohydrates are kept reduced for extended (or unlimited) periods. Most
of the mainstream low-carb/keto diets fall into this category.
Second are the modified ketogenic diets which come in two flavors. The first is diets which reduce
carbohydrates throughout the day but allow small amounts of carbs before, during, and/or after training. We
named those targeted ketogenic diets (TKD) in my book The Ketogenic Diet and I’ll stick with that name.
Finally are the cyclical ketogenic diets (CKD) such as Bodyopus, The Anabolic Diet, and Rob Faigan’s NHE
diet which alternates periods of ketogenic dieting with phases of high-carb intakes. Since all of these diets
revolve around a ketogenic/low-carbohydrate phase, I’ll discuss them together.
Let’s look at the SKDs first and when and where they might be appropriate. Frankly, I could probably just tell
you that, if you don’t meet the requirements for either of the previous two diets, some type of ketogenic diet
is going to be appropriate for you; it’s a choice by exclusion. To be safe, I’ll include a little more commentary
than that.
Obviously, folks who aren’t doing much (or any) activity, ketogenic diets tend to be appropriate. Now, it’s
easy to simply say ‘You should exercise and eat more carbs’ but this isn’t always possible. In cases of
extreme obesity, or injury, or just plain laziness, exercise (especially intense exercise) may be out of the
question. Since carbohydrate requirements are going to be extremely low (approaching the minimums
discussed in How Many Carbohydrates Do You Need?), a ketogenic diet can be appropriate under those
conditions.
Even individuals doing nothing but low-intensity activity (think walking and such), carbohydrate requirements
are rarely very high. Low-carbohydrate diets are also appropriate under those conditions. There is some
evidence that a low-carb diet might be useful for ultraendurance athletes (who typically perform for hours on
end at fairly low intensities) but the data is mixed and the issue contentious; at some point I’ll write a full
article (or book) about that topic alone. I’ll talk about higher intensity exercise performance in a second.
I’ve also found that folks with extreme insulin resistance do better in terms of energy levels and
hunger/appetite control when they reduce carbohydrates, as I discuss in Insulin Sensitivity and Fat Loss, fat
loss may be greater as well. They go from constant energy swings to more stable energy. Research typically
report rather significant improvements in many health parameters such as blood cholesterol and triglyceride

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levels although this depends on total caloric intake and fat source as well. But for those individuals with
severe insulin resistance and the resultant hyperinsulinemia (high-insulin levels), a near complete reduction
of carbs may be necessary to bring glucose and insulin levels under control.
Along those lines, some people simply feel better on low-carbohydrate (especially ketogenic diets). They
feel mentally more aware and function better, especially after a few weeks of adaptation. At the same time,
some folks never seem to adapt to such diets, always feeling brain fuzzed, lethargic and all the rest. Many
folks couldn’t care either way. Is this genetics, a micronutrient imbalance, individual variance? I have no
idea, but I’ve seen it enough times to know it happens.
My general experience, in terms of giving you some guidelines to go on is this: if you feel fine, meaning that
you function well with no major energy swings on a carb-based diet, odds are you’ll feel horrible on a
ketogenic diet. You probably have good insulin sensitivity, high levels of activity, are fairly lean and are
genetically well suited to run on carbohydrates. Don’t mess with it.
If you’re one of those individuals who always feels lagged out and un-energetic on high-carbohydrate diets
(or get major energy crashes after a high-carb meal), you’ll probably tend to feel wonderful on a low-
carbohydrate diet. You may be inactive, carrying too much fat, or simply be genetically insulin resistant,
meaning your body isn’t set up to handle lots of carbohydrates.
This is where individual variance starts to play a role. I suspect that the differences in response have to do
with many of the factors described in the previous sections: activity, insulin sensitivity and the rest. At the
same time, research is finding that some people seem to be better adapted to using fat for fuel while others
do not (meaning their bodies prefer carbohydrates).
Genetics most certainly plays a role. Unfortunately, at present there’s no easy way to know who will do best
with higher fat and who won’t. Use the guidelines above: if you feel good on high-carbs, you’ll probably feel
terrible on low-carbs and vice versa. Some people seem to have the metabolic flexibilty to handle either
approach at which point it’s more an issue of preference and the other related issues.
While I feel that a moderate carbohydrate/moderate fat diet will probably be sufficient for all but the most
extreme cases, there are always those individuals for whom a nearly complete reduction in carbohydrate
intake may be necessary.
And, as above, for those folks for whom even moderate amounts of carbs make them hungry for more
carbohydrates (this tends to be far more true for starches than anything else), a complete removal of them
may be necessary at least for the time being. I’ve found that, after time on a ketogenic diet, most people lose
their taste for the high GI starches as their taste buds adapt. Frequently they can go back to a more moderate
carb/moderate fat approach without getting into problems.
This is actually an important point, even for athletic individuals. Even with the most stalwart dietary discipline,
athletes can have problems reducing calories on a diet because of the presence of what we might call ‘diet-
breaker’ foods. That is, even in small amounts, certain foods make people cheat and overeat. While dietary
fat can be problematic here, starches and sugars are typically what’s craved on a diet.
Now, as anyone who read my rather torturous Bodyopus diaries so long ago knows, I am (well, used to be)
one of those individuals. Even the smallest taste of starch made me want to eat more. Keeping bread or
what have you in the house meant a diet that was destined to fail. Over time, I’ve found balance, I can (and
usually do) use a moderate-carb/moderate-fat diet without running into too many problems.
As well, even athletic individuals can suffer from some degree of insulin resistance (at a genetic level) and
may not handle carbohydrates well. In Bodyopus, Dan wrote that he felt most bodybuilding failures were do
to poor insulin sensitivity. While I think it would be more clear to say that it’s due to poor nutrient sensitivity
and uptake, the general idea is still sound. This is discussed in more detail in the articles on Calorie
Partitioning.

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For those individuals, even who are highly athletic, a complete removal of the diet breaker foods (or foods
that interact negatively with genetically poor insulin sensitivity) may be a necessary evil. As above, while I
think moderate carb/moderate fat diets will probably do most of the work this isn’t always the case. Some
people will have to remove those foods entirely from their diet to be able to stick with it.
As well as I’ve mentioned throughout this article series, stubborn fat (ab/low-back fat for men and hip-thigh
fat for women) comes off better when carbs are restricted. The Stubborn Fat Solution details the along with
how to utilize low-carbohydrate intakes and specific training protocols to target stubborn fat.
So now we have a contradiction, even highly active individuals (meaning high carbohydrate requirements)
may find a situation where carbohydrates need to be restricted to very low levels. The question then becomes
of how to sustain exercise performance on such restricted carbohydrate intakes.
Most critics of ketogenic diets would simply say ‘Eat more carbs’ but, as above, this may not be an option
(also, as above, these people are idiots who can’t see past a single dietary approach). So we have to
compromise. Modified ketogenic diets are that compromise: they let folks use ketogenic diets while trying to
maintain performance with the inclusion of carbs at specific times.
To date, two primary solutions have been developed, both of which I mentioned above. The first, and perhaps
the simplest is the Targeted Ketogenic Diet (TKD). The TKD allows varying amounts (usually 25-50 grams)
of high GI carbohydrates before, during or after training with carbohydrates being severely restricted the rest
of the day. This accomplishes a few things. First, it allows dieters to eat some of the diet breaker foods, but
under controlled circumstances. This helps deal with some of the psychological issues involved with dieting.
Second, it goes a long way towards sustaining exercise performance by providing carbs around training.
Third, since insulin resistance isn’t much of a problem right around training, the high GI stuff that everybody
likes to eat can be eaten fairly ‘safely’ (from a blood glucose/insulin release point of view).
Even extremely insulin resistant/pre-diabetic individuals can usually eat carbs right after an intense workout
without problems, as exercise elevates insulin sensitivity to high levels temporarily (there is also insulin
indepdendent glucose uptake during exercise so the body can utilize glucose without having to increase
insulin levels).
The second solution, and the one I suspect most readers are aware of is the cyclical ketogenic diet (CKD).
A CKD refers to any diet which alternates periods of low-carbohydrate (or ketogenic eating) with periods of
high-carbohydrate eating. Diets such as DiPasquale’s Anabolic Diet and Metabolic Diet, Dan’s Bodyopus,
and Faigan’s NHE are all examples of CKD’s. My own Ultimate Diet 2.0, of course, represents the pinnacle
of cyclical diets of this sort.
CKD’s are another compromise diet approach: they switch between a ketogenic/low-carbohydrate phase
(for anywhere from 5 or more days) and a high-carb phase (lasting from 12 to 48 hours or more) to restore
muscle glycogen and hopefully generate an anabolic response. They are for those athletic individuals who,
for one reason or another, needs to restrict carbohydrates severely, but sustain exercise performance.
Active individuals with severe (diagnosed) insulin resistance or even the beginning of Type II diabetes tend
to fare poorly on CKDs; the extended carb-load period causes all of the problems that they are trying to
avoid in the first place. The TKD is more appropriate for them.
On that note, I should mention a seemingly contradictory situation, that of endurance athletes. Interest in fat
loading and fat adapting endurance athletes has been a long-term project for exercise physiologists and
some research suggests that some endurance athletes can benefit from following a low-carbohydrate/high-
fat diet for some period of time (5-21 days) and improve performance (more recent research suggests that
it kills sprint performance even within the context of a long-duration event).
This is especially true for ultra-endurance athletes who may perform for many hours at submaximal
intensities, relying predominantly on fat for energy. A recent series of studies found that fat adapting cyclists

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for 5 days followed by a 1 day carb-load (similar to a CKD) improved performance in some athletes. The fat
adaptation increased fat utilization at lower intensities but the carb-load made sure that sufficient glycogen
was available for high intensity efforts. Again, this is a topic deserving it’s own full article or book so I won’t
get into many details here.

Summing Up Low-Carb Diets

So summing up the section on low-carbohydrate diets. As above, we have two basic flavors of low-carb diet.
The first is simply a diet in which carbohydrates are restricted for extended periods of time. Such diets are
appropriate (and may be desired) for individuals who aren’t doing much, if any, exercise (or are only doing
low-intensity activity), who may have severe problems with insulin resistance, who have such an extreme
carbohydrate ‘addiction’ that a full removal of starches may be required to control hunger.
The second flavor, the modified low-carbohydrate diets come in two separate groups. They are for those
individuals who need (for some reason) to lower carbohydrates to low levels but still need to sustain exercise
performance. First are the targeted type diets which have dieters restrict carbohydrates except around
exercise (this is actually a very common approach to diet setup in bodybuilding literature). Second are the
cyclical diets that alternate some period of low-carbohydrate dieting with periods of high-carbohydrate intake
to refill muscle glycogen (and sometimes, it’s argued, to stimulate a growth response).

Finally, the Chart You’ve Been Waiting For

Ok, now you’ve hopefully got a better idea of which diet approach may be the most ideal for you. To make
it a little more clear, I’m going to try to summarize all of the above information into a chart so you can see
how the different variables interact.

Activity Insulin Carb Carb Stubborn


Diet
Level Sensitivity Choices Addict Fat

High-carb/low-
High High Low GI No NO
fat

Mod carb/mod-
Medium Low-moderate Medium GI Maybe Yes/Maybe
fat

Standard Keto Low Low N/A Yes Yes

Targeted Keto High Low N/A Yes Yes

Cyclical Keto High Low N/A Yes Yes

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Comparison of the Atkins, Zone, Ornish and LEARN Diets for
Change in Weight and Related Risk Factors Among Overweight
Premenopausal Women – Research Review

Title and Abstract

Gardner CD et. al. Comparison of the Atkins, Zone, Ornish, and LEARN diets for change in weight and
related risk factors among overweight premenopausal women: the A TO Z Weight Loss Study: a randomized
trial. JAMA. (2007) 297(9):969-77.
CONTEXT: Popular diets, particularly those low in carbohydrates, have challenged current
recommendations advising a low-fat, high-carbohydrate diet for weight loss. Potential benefits and risks have
not been tested adequately. OBJECTIVE: To compare 4 weight-loss diets representing a spectrum of low
to high carbohydrate intake for effects on weight loss and related metabolic variables. DESIGN, SETTING,
AND PARTICIPANTS: Twelve-month randomized trial conducted in the United States from February 2003
to October 2005 among 311 free-living, overweight/obese (body mass index, 27-40) nondiabetic,
premenopausal women. INTERVENTION: Participants were randomly assigned to follow the Atkins (n = 77),
Zone (n = 79), LEARN (n = 79), or Ornish (n = 76) diets and received weekly instruction for 2 months, then
an additional 10-month follow-up. MAIN OUTCOME MEASURES: Weight loss at 12 months was the primary
outcome. Secondary outcomes included lipid profile (low-density lipoprotein, high-density lipoprotein, and
non-high-density lipoprotein cholesterol, and triglyceride levels), percentage of body fat, waist-hip ratio,
fasting insulin and glucose levels, and blood pressure. Outcomes were assessed at months 0, 2, 6, and 12.
The Tukey studentized range test was used to adjust for multiple testing. RESULTS: Weight loss was greater
for women in the Atkins diet group compared with the other diet groups at 12 months, and mean 12-month
weight loss was significantly different between the Atkins and Zone diets (P<.05).
Mean 12-month weight loss was as follows: Atkins, -4.7 kg (95% confidence interval [CI], -6.3 to -3.1 kg),
Zone, -1.6 kg (95% CI, -2.8 to -0.4 kg), LEARN, -2.6 kg (-3.8 to -1.3 kg), and Ornish, -2.2 kg (-3.6 to -0.8 kg).
Weight loss was not statistically different among the Zone, LEARN, and Ornish groups. At 12 months,
secondary outcomes for the Atkins group were comparable with or more favorable than the other diet
groups. CONCLUSIONS: In this study, premenopausal overweight and obese women assigned to follow
the Atkins diet, which had the lowest carbohydrate intake, lost more weight and experienced more favorable
overall metabolic effects at 12 months than women assigned to follow the Zone, Ornish, or LEARN diets.
While questions remain about long-term effects and mechanisms, a low-carbohydrate, high-protein, high-fat
diet may be considered a feasible alternative recommendation for weight loss.

Background

When this paper came out a couple of years ago, there was a ton of press about this study with further
claims of low-carb metabolic advantages (several fitness related blogs have already stated that the Atkins
diet generated significantly greater weight losses) based on it; of course as you’ll see the claims that were
made based on the results aren’t quite as astounding as made them out to be.
I want to point out up front that I am hardly against low-carb diets even though my comments about them
often leads people to think that especially when people start talking about ‘metabolic advantages’ of such

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diets. For goodness sake, my first book The Ketogenic Diet was dedicated to nothing but low-carbohydrate
diets and many of my diet books incorporate some type of carbohydrate restriction.
However, while I like low-carb diets and think that they are appropriate under some (but assuredly not all)
situations, I don’t believe that the research supports much of a metabolic advantage (in terms of being able
to lose more weight/fat at the same or higher caloric intakes). If such diets have an advantage in terms of
dieting, it tends to have more to do with adherence and food intake due to appetite suppression. Which is
still a benefit, mind you. But is different than what is often being claimed.
I would entreat people to reread the above paragraph two or three more times before they start entering
comments about how I’m anti-lowcarb diets.

The Study

Which brings us to this week’s study. The researchers set out to compare 4 diets of drastically different
carbohydrate intake. The first was Atkins which is a very low-carbohydrate diet. The second was the Zone
which is a moderate carb diet (40% carbs, 30% protein, 30% fat). The third is something called the LEARN
diet which is your basic food Pyramidy type of diet with 55-60% carbs and saturated fat below 10% of total
calories. Finally was Dean Ornish’s extremely high-carbohydrate, very low-fat (10% or less) diet. These diets
were chosen to represent the spectrum of diets from very low carbohydrate to very high carbohydrate.
The subjects were premenopausal women between the ages of 25-50 with a body mass index between 27
and 40 who had been weight stable for the previous 2 months. Folks were excluded for various reasons.
311 subjects entered the study and were randomly assigned to one of the four groups with about 70 subjects
per group.
All subjects were given a copy of the respective book and a dietitian explained the details of the diet to each.
For the first 8 weeks of the study, all subjects attended a 1 hour class per week. For the remaining 10 months
of the study, they were on their own.
Subjects did receive email and phone contact from the staff between the 2 and 6 month mark and the 6 and
12 month mark and small financial incentives were given for completing the data collection at the 2, 6 and
12 month time point.
Diet was assessed by a 3 day food recall (I’ll come back to this below) and energy expenditure was estimated
by a 7 day activity recall. Subjects were measured for height, weight, body fat was done by DEXA. A number
of blood measures including total cholesterol and blood triglycerides were measured. So was fasting insulin
and blood glucose along with blood pressure.

The Results

Ok, before getting into the details, I want to look at the overall results since that’s most of what people
focused on. After 12 months on the diet, the respective weight losses were
 Atkins: 4.7 kg (10.3 lbs)
 Zone: 1.6 kg (3.5 lbs)
 LEARN: 2.6 kg (5.7 lbs)
 Ornish: 2.2 kg (4.8 lbs)
So yes, the Atkins group did get better results, 2.5 kg or more weight loss than the other diets over the span
of a year. And, according to the self-reported food intakes (an issue that I’ll discuss momentarily), they did
it eating the same number of calories as the other groups with both groups reporting a reduction in food

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intake over the length of the study. AHA, more weight loss on the same calories, there’s your metabolic
advantage….
Ok, first and foremost, let’s be realistic: regardless of the fact that Atkins got double the weight loss, those
results suck. Ten pounds weight loss in one year amounts to a 3/4 lb weight loss per month in the Atkins
group and half or less than that in the other groups. By contrast, low-calorie diets that are highly controlled
can generate a 7kg/15 lb weight loss over 4 weeks. My own Rapid Fat Loss Handbook can do that in 2
weeks in some people.
Yes, fine, the study points out that even small weight losses can improve health but what dieter would be
happy with that? Not many. More like 10 lbs weight loss in 2 months. I didn’t pick that value out of a hat.
The paper shows changes in body weight at each of the 2, 6 and 12 month time spans. And Table 3 in the
paper, which I show below shows how each diet affected weight. It tells the entire tale so far as I’m
concerned.

There are a few key observations to make from this. The first is this: at the 2 month mark, the Atkins group
was already 4kg down in body weight while the other groups had lost about 2.5 kg or so. Recall from above
that the total difference in weight loss between Atkins and the other groups was only about 2kg. So most of
the difference between the diets occurred in the first 2 months.
Now, it’s well-established that ketogenic diets can cause significant water loss in the first couple of weeks,
water loss can range from 1-15 lbs over that time frame. I’m a little guy but I can drop 7 lbs in 3 days of
carbohydrate restriction or about 2.5 kg. So the 2 kg ‘advantage’ of the Atkins diet not only could be due to
water loss but in all likelihood is due to water loss. Other studies, lasting from 4 days to 2 weeks show the
same 2kg difference in weight loss. All of which occurs early on and likely represents water drops due to
carbohydrate restriction.
Another interesting point is that over the next 10 months, the Zone, LEARN and Ornish group didn’t lose an
additional pound and even showed a slight trend towards regain. Read that and let it sink in for a few
minutes. Over a 12 month diet, after a small weight loss in the first 2 months, there was no additional weight
loss for the next 10 months.
Rather, the entirety of their weight loss occurred during the first 8 weeks when they went to weekly meetings
and they didn’t lose an ounce for the remaining 10 months. In contrast, the Atkins group had lost about 2
kg more at the 6 month mark and regained over a kilogram at the 12 month mark, leading to the final results
reported above.
As mentioned, the groups all self-reported eating roughly the same number of calories and reducing their
caloric intake over the length of the study. But let’s think about that rationally for a second: are we to honestly
believe that the three groups which didn’t lose an additional pound over 10 months truly ate less over that
time period? Was every single person in this study one of the metabolic miracles that exist in droves on the
Internet, that can eat less let magically maintain weight?
Or is it more likely, as with tons of studies done previously, that they were under-reporting their food intake
and actually eating more (possibly quite a bit more as studies of carb based diets show a systematic under-
reporting of anywhere from 30-50%) than they thought or said they were?
Now, call me a cynic but I think you know where my opinion on this lays. As I discuss in the research review
Ketogenic Low-Carbohydrate Diets have no Metabolic Advantage over Nonketogenic Low-Carbohydrate
Diets, when calories are strictly controlled (and protein intake is identical), there is simply no metabolic
advantage or greater fat loss to be had. Another study, which I will eventually review for the site was unable
to find any measurable difference in metabolic rate for ketogenic vs. carb-based diets. As well, caloric
misreporting on carb-based diets is known to be prevalent and the only logical answer to the claims of this

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study (e.g. the Atkins dieters lost more weight despite ‘eating the same amount’) is that the self-reported
food intakes are invalid (as they usually are).
So even was slightly greater for the Atkins diet, it’s not because of any inherent metabolic advantage. It’s
because, under uncontrolled conditions, people on ketogenic diets typically eat less. In this study, they only
ate a little bit less because they only lost about 2 lbs over the 10 months of the uncontrolled study period.
It’s worth noting that the researchers point out that the weight loss trajectories, meaning the trends over time,
indicate that the Atkins dieters were regaining weight. So over a longer time period for the study, the
differences in weight loss would have been even smaller between the Atkins group and the others.
I should mention that based on the self-reported food intakes, a lot of the criticism of this study has to do
with overall compliance to the actual diets. For example, Ornish has complained that the dieters were eating
30% fat when he prescribes only 10% fat; hence it wasn’t his diet. And the Atkins dieters were eating almost
35% carbs at the end of the study. So it wasn’t really an Atkins diet.
There is some truth to this and does raise some questions about the inherent validity of the study. However,
it also raises the point that, in free living subjects, people usually suck at adhering or properly following
diets. So even with those flaws, this study probably represents how people actually diet in the real world.
I should mention that some of the health measures (blood lipids, etc) did show a slight advantage to one or
the other diets but the differences were small and hardly significant. You could generate more changes with
just about any reasonable diet that actually too a decent amount of weight/fat off of someone than with the
pitiful results this study found.

Summing Up

First, what I’m not saying. As usual, folks will find a way to read this as “Lyle dislikes low-carbohydrate diets”
which is incorrect. Like all dietary approaches they have their pros and cons and are appropriate in some
conditions and not in others.
For many people, they make controlling calories easier, for people with insulin resistance they often improve
health parameters to a greater degree than carb-based diets. Those are advantages to be sure but they
aren’t the ones that most are fixated on (e.g. the idea that you’ll somehow lose tons of weight and fat while
ignoring caloric intake).
Clearly, despite some of the current claims, simply reducing carbs doesn’t magically ‘cure’ obesity if calories
don’t come down. And studies like this demonstrate that. Even if the Atkins diet was slightly superior to the
other diets, the simply fact is that the overall weight loss was minor in all groups (this is a common finding
among many studies where caloric restriction isn’t put into place).
Ten pounds total weight loss (or even true fat loss) in a year of dieting is crap results, plain and simple;
whether or not it was slightly better than the other approahces wouldn’t seem to be that massively
significant. Especially when you consider that 8 of those 10 pounds occurred in the first 2 months, meaning
that there was only 2 lbs more net weight loss over the next ten months of the study (the equivalent of 0.2
lbs weight loss per month).

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All Diets Work: Qualification
In An Introduction to the Psychology and Physiology of Dieting, I made a statement that I imagine many will
take some issue with; that statement was, in effect, that all diets work. At least to some degree.
I want to qualify that a little bit.
Fundamentally, any diet that is restricted in calories will cause weight loss. Of course, dieters, ideally,
shouldn’t only be concerned with the scale. The composition of what is lost is important too and, generally
speaking, dieters want to lose fat not muscle (or just shift water around).
I want to point out that for the extremely overweight, lean body mass (LBM) loss isn’t considered as huge of
an issue among dieting researchers. When becoming obese, roughly 25% of the total weight gained is lean
body mass. Some of this is actual muscle tissue (check out the calves and thighs on fat people) but some
of it is just connective tissue to support the extra fat mass.
Some researchers are now delineating between essential lean body mass (skeletal muscle, organs) and
inessential lean body mass (connective tissue). Losing the second may be required for an individual to get
even close to an ‘ideal’ body weight, whatever that is.
However, when you’re talking about relatively lean individuals, where there isn’t a lot of inessential LBM to
lose, the focus does tend to shift on avoiding any LBM loss. I’d note here that glycogen, water and minerals
show up as LBM loss.
Depending on the measurement method used, even visceral fat loss can show up as LBM loss. Lean folks
often panic when various body composition measurements show that they are losing LBM but they are just
dehydrated, glycogen depleted, etc.
And there’s little doubt that here, all diets are not equivalent in terms of how well they spare LBM.
So my statement that ‘all diets work’ isn’t entirely true once you start concerning yourself with the composition
of the weight that is lost.
Without going into massive detail (which is sort of a tangent from what I want this series of articles to be
about), the primary determinants of LBM loss on a diet tend to be protein intake (which must be sufficient)
and proper resistance training (which sends a ‘signal’ to maintain muscle). Other issues such as essential
fatty acid intake, etc. are also relevant but protein and training are the big ones.
But assuming that a diet sets protein at sufficient levels, provides essential fatty acids and includes the
proper kind of training, frankly, they all diets work assuming that the person actually follows the diet.
There is, however, one other major requirement for that statement to be true and that’s the existence of a
caloric deficit (e.g. caloric intake must be less than caloric expenditure).
But, you say, so many diet books comment that caloric restriction doesn’t work or that calories don’t count
or some other silly shit like that. That’s the topic for the next post to stay tuned.

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What Are Good Sources of Protein? – Introduction
In recent years, thanks to emerging research, diet books and popular articles, the general public is starting
to become aware of something that many athletes (especially bodybuilders) have been saying for a while:
higher protein diets are better for weight/fat loss and improved health. In addition, athletes have long been
on the search for nutrients or foods that can improve their performance or their adaptation to the training
they put themselves through.
Between those two groups, a question that often comes up is “What are good sources of protein?”
Many websites offer simple answers to that question, generally revolving around whatever protein they
happen to sell; the answer, as always, is far more complicated than that. A large number of variables go into
the declaration of what a good source of protein is and, as always, what is good in one context may not be
good in another.
That is to say, the decision over what a good source of protein happens to be is entirely context dependent.
So, in my usual way, I’m going to dissect the question and look at all of the factors that go into determining
what constitutes a good source of protein. In this first part of this article series, I’m simply going to introduce
and define some terms, I’ll look at each in detail in forthcoming parts of this series (over the next few days).
Before continuing, I’d mention that this topic was of sufficient interest to me that I wrote an entire book on
the topic, The Protein Book. Much of what I’ll be presenting will be excerpted from that project.
I’d also note before continuing that there is still a lot of very outdated information about the ‘dangers’ of high-
protein diets. I address them in detail in the article Protein Controversies, on this site. And with that out of
the way, let me start answering the question “What are good sources of protein?”
The topics I’m going to discuss in each of the following articles, relating to what makes a protein source good
(or bad, or middling) are the following:

Digestibility: Before a protein can be used by the body, it has to be digested and absorbed into the
bloodstream for use by the body. Proteins vary in their digestibility and, logically, a protein that is poorly
digested will be a poor source simply because less of what’s being eaten is being made available to the
body. A topic related to digestibility is the speed of digestion and there has been interest since about the
late 90’s in how a given protein’s digestion speed affects how it is used by the body.

Protein Quality: In one sense, the topic of protein quality could be used as an overall look at many of the
other topics I’m going to discuss. In general, protein quality is a measure of how well or poorly a given
protein is used by the body. I’d note that how you define the word ‘use’ here depends also on context. Are
we talking about a protein’s ability to sustain life, build muscle, improve performance, improve health? Some
measures of protein quality take into account digestion while others do not (which is why I’ll discuss digestion
separately), the amino acid profile of the protein tends to be one of the biggest determinants of quality.

Amino Acid Profile: Again, tying in with the issue of protein quality, there is the issue of the amino acid
profile of a given protein. For background, amino acids are simply the building blocks of protein, and there
are 18-22 distinct amino acids depending on who you talk to (not all sources recognize all of the amino
acids). Each one is found in differing proportions in different food protein sources and, under certain
circumstances, that profile will affect how it is used in the body or how it functions.

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Presence or Absence of Other Nutrients: While often ignored, the presence or absence of other nutrients
in a given protein source also impacts on how good of a protein it may be. For example, some protein
sources contain high levels of iron, B12 and zinc while others do not; the presence of absence of the omega-
3 fatty acids (fish oils) may also be relevant. Calcium is also a consideration.
Other Factors: There are a number of other potential factors surrounding protein that might determine which
is a good or bad source under a given context. For example, proteins may show different effects on appetite,
or blood sugar control, or what have you. There is also the issue of cost and availability along with the
amount of protein in a given amount of whole food proteins. I’ll cover those as a catch-all final category in
this series before summing up and looking at a variety of whole food proteins and how they rank on each
category.
So those are the major topics I’m going to cover in this series of articles. While it will take a bit of time to
cover all of the information I want to cover, by the end of the series you’ll know the answer to the question
“What are good sources of protein?“

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What Are Good Sources of Protein? – Speed of Digestion Part 1
In the last article, What are good sources of protein – Digestibility, I examined some basics of protein
digestibility and presented data on the gross digestibility of varying proteins. Summing up, animal source
proteins such as meat, milk and eggs show extremely high (90%+) digestion while vegetable source proteins
show much lower values.
However, the efficiency of digestion alone is not the only factor which goes into answering the question What
are good sources of protein?
Recently (and by that I mean the late 90’s or so), an interest in the speed of digestion and how that impacts
on various aspects of human physiology has occurred. It’s turning out that proteins can digest at fairly
different rates and this turns out to affect various physiological processes; the main two are protein synthesis
and protein breakdown. As with the last article, I’m going to talk about these terms in brief before moving
onto the main thrust of today’s article.
Because I have a lot of information to cover, I’m going to break the topic down into two parts. In Part 1
today, I need to cover a bit more background physiology and talk about the original study that kicked off the
entire interest in speed of digestion. In Part 2 (tomorrow), I’ll finish up with some other recent
developments. As always, all of this information can be found in a more detailed and expanded fashion in
The Protein Book.

Protein Turnover: The Combination of Protein Synthesis and


Protein Breakdown

Early ideas about the body held that the different tissues such as fat cells and skeletal muscle (see What
Does Body Composition Mean for a little more detail) were essentially static and unchanging. This turns out
to be incorrect. At any given time in the body, pretty much all of the cells in your body are undergoing a
constant process of breakdown (where larger structures are broken down into smaller) and synthesis (where
smaller structures are combined to make larger).
So as you sit here reading this, your fat cells are both breaking down and re-synthesizing the triglyceride
(fat) stored in them. Bone is undergoing the same constant processes as well. Of course, the same holds
for protein tissues.
Right this moment, your liver is breaking down and remaking various proteins, and your skeletal muscle is
in a constant source of breakdown and re-synthesis. While this is actually energetically very costly, and
seems wasteful, it turns out to give the human body an incredible adaptability and ability to deal with stress.
The combination of breakdown and re-synthesis is referred to, generally, as turnover. In the context of
protein based tissues, this is referred to as protein turnover.
I should note that different tissues in the body break down at drastically different rates. So while liver proteins
may break down and be completely re-synthesized in a number of hours, skeletal muscle is turning over
more slowly. Tissues such as organs, tendons and ligaments turn over much more slowly. As you’ll see,
this actually has some implications for what I’m going to talk about in just a moment.
What happens overall to a given tissue (e.g. whether it grows, shrinks or stays the same) depends on the
relative rate of synthesis and breakdown. Simply:
 If synthesis is greater than breakdown, there will be an increase in the amount of that tissue.
 If breakdown is greater than synthesis, there will be a decrease in the amount of that tissue.
 If breakdown equals synthesis, there will be no change in the amount of that tissue.

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This also means that, fundamentally, we have two different ways to have an impact on the amount of a given
tissue. Let’s say for example that someone wants to increase the amount of muscle that they have. They
can either try to increase protein synthesis, decrease protein breakdown, or cause both to occur.
This is an important distinction because various things (such as nutrients, training, drugs) can differentially
affect each process. As you’ll see in just a second, speed of digestion is one of those things and the rate of
digestion of a given protein can affect protein synthesis vs. breakdown differently.

The Now Infamous Boirie Study

Back in 1997, a research group in France published the first paper on the topic of slow and fast
proteins. Titled, “Slow and fast dietary proteins differently modulate postprandial protein accretion.”, this is
the paper that kicked off the entire field of fast and slow proteins.
In that paper, subjects were fed either casein or whey, the two proteins found in milk (see Milk: The New
Sports Drink? A Review – Research Review for more information), and blood amino acid level along with
whole body protein synthesis and breakdown were measured. I’d note that both proteins were given after a
morning fast with no other nutrients (carbohydrates or fat) provided. This is important because the results
of this study don’t necessarily hold when other nutrients are being consumed, or someone is consuming a
given protein later in the day (when other meals are still digesting).
The researchers found the following: whey spiked blood amino acid levels faster than casein, but blood
amino acid levels dropped more quickly as well. Casein, in contrast, took much longer to digest, actually
providing amino acids for around 8 hours to the body (you might consider that data point the next time you
hear that you have to eat every three hours or your muscles will fall off, a topic I cover in Meal Frequency
and Energy Balance).
I actually want to clarify that a bit since there has been a lot of confusion over what the study actually
found. Both casein and whey hit the bloodstream at about the same time (about an hour in), that is, whey
didn’t actually get into the system faster. However, whey spiked blood amino acid levels higher at that one
hour point. Figure 1 (taken from The Protein Book) shows this.

Note that both proteins enter the bloodstream at about the same time, around the one hour mark. Whey
simply spikes blood amino acids faster (before falling back to baseline levels around hour 4). Casein, in
contrast raises amino acid levels to a much lower level but they are sustained for hours (in the graphic, at
the 7 hour mark, blood amino acid levels were still above where they started).
So it’s not that whey gets into the system faster, it just spikes blood amino acid levels higher at the same
time point (about an hour after consumption).
Now, the next bit of this study was an examination of the effects of these proteins on protein synthesis and
breakdown. Basically, it was found that whey raised protein synthesis with no effect on protein breakdown
while casein decreased protein breakdown without affecting protein synthesis.
Hence, whey become known as an ‘anabolic’ protein (anabolic just means making bigger things out of
smaller things) and casein was an ‘anti-catabolic’ protein (catabolic means making smaller things out of
bigger things, and anti-catabolic means that casein prevents that).
I’d also note that more of the whey was burned for energy (oxidized) compared to the casein.
This, of course, got taken wildly out of context to sell protein powders. However, note above I said that the
research was looking at whole-body protein synthesis and breakdown. It wasn’t examining skeletal muscle

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per se. It’s just as logical to conclude that the whey stimulated liver protein synthesis as skeletal muscle but,
of course, supplement companies don’t ever talk about that.
And with that I’m going to wrap up Part 1. In Part 2 (tune in tomorrow), I’ll talk about more recent research
and some implications of speed of digestion for answering the question What are good sources of protein?
Go to What Are Good Sources of Protein – Speed of Digestion Part 2

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What Are Good Sources of Protein? – Speed of Digestion Part 2
Yesterday, in What are Good Sources of Protein? – Digestion Speed Part 1, I looked briefly at the issue of
protein turnover and synthesis and then looked even more briefly at the now infamous Boirie study that
kicked off the interest in fast and slow proteins.
Summing up, that study found that whey and casein (the two proteins found in milk) digested at different
speeds, with whey being a ‘fast’ protein that spiked amino acid levels before dropping (after 3-4 hours), and
casein being a ‘slow’ protein that raised amino acid levels more gradually but remaining stable for an
extended period (7-8 hours).
Of more relevance, the researchers also found that the whey protein stimulated whole-body protein synthesis
without much effect on protein breakdown while casein decreased protein breakdown with little effect on
protein synthesis; I’d note that there was also an increase in the oxidation (burning for energy) of the whey
protein. Thus whey became known as an ‘anabolic’ protein and casein an ‘anti-catabolic’ protein.

More Commentary About the Boirie Study

One other note that I didn’t mention yesterday. The researchers also looked at how each protein impacted
on net leucine balance, that is how much leucine was actually stored in the body (this is used as an indicator
of what’s going on with other amino acid levels).
Despite the fact that the whey actually stimulated more protein synthesis, the casein had the larger impact
on leucine balance; at the end of the feeding period, the body had stored more leucine with the
casein. Phrased a bit differently, it looked as if decreasing protein breakdown was more important than
increasing protein synthesis in terms of whole body leucine (and therefore, protein balance).
This study essentially created an entirely new industry in the world of sports nutrition. Interestingly (or
amusingly depending on your perspective), the study was interpreted variously depending on whether the
company in question was selling whey or casein. Companies selling whey focused on the increase in protein
synthesis; those selling casein either pointed to the increased oxidation of whey or the fact that casein had
a greater impact on net leucine balance.
Various practical suggestion came out of this as well at least in the world of sports nutrition, whey protein
was suggested for first thing in the morning to get aminos into the bloodstream as quickly as possible. I’d
note again that this isn’t exactly the case and I realize that this is a little bit confusing. As shown in Figure
of in What Are Good Sources of Protein? – Speed of Digestion Part 1 both casein and whey start to appear
in the bloodstream at about the same time point; however, whey certainly raises blood amino acid levels
more quickly at that point. In contrast, casein was suggested for bedtime to provide aminos throughout the
fasting period to stave off muscle breakdown.
Almost without exception, whey was suggested as the best protein for after training to get aminos into the
bloodstream more quickly. As noted yesterday, not only is this not true but there is emerging data (discussed
in detail in The Protein Book) that fast proteins after training are not the optimal choice for promoting lean
body mass gains, slow proteins or a combination of slow and fast proteins appear to be more effective. I’d
refer readers back to my article on Milk: The New Sports Drink? A Review where milk outperformed soy (a
fast protein) for promoting lean body mass gains.
Others suggested that the combination of whey and casein should be superior to either in isolation; the whey
provides a quick hit of aminos to boost protein synthesis while the casein provided a longer source of aminos

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to blunt protein breakdown. In many ways, this third group would turn out to be closer to correct than either
the whey-only or casein-only groups. But I’m getting ahead of myself.

But Wait, There’s More

As I also noted yesterday, one limitation of the study in question was that the protein was given without any
other nutrients (carbs or fats) and were given to folks who had fasted overnight; of course it didn’t involve
any type of training (which can change the dynamics of how protein is used in the body).
Frankly, the extrapolations being made about whey or casein from the study in question were poor for this
(and other reasons).
Of course, later research ended up addressing some of these issues. A followup study titled “Influence of
the protein digestion rate on protein turnover in young and elderly subjects.” looked at the impact of whey
and casein when it was combined with carbohydrates and fats. And the differences between the two
basically disappeared under these conditions.
While whey still got aminos into the bloodstream a touch more quickly, the casein meal still had the edge in
terms of net leucine retention. It’s important to note that, in both of the original studies, the amount of protein
given in the whey and casein group weren’t identical; the casein group got a bit more protein and that alone
might have explained the greater gain in protein.
A third study provided identical amounts of casein and whey in mixed meals to either young or elderly folks;
in that study the whey group came out a bit ahead in the young but way ahead in the older subjects (older
here means 72 years old). This suggested that, even in the context of mixed meals, whey had a slight edge.
I’d note here that emerging research shows that older individuals respond very different to protein than
younger; their muscles appear to become insensitive to protein to some degree and various interventions
(such as protein pulse feeding or fast proteins) which spike blood amino acids appear to be vastly
superior. In younger individuals, this doesn’t appear to be as significantly the case.
In any case, the data on the topic was clearly pretty mixed and, in the context of a mixed meal (which is how
most people eat), while whey might have a slight edge over casein it was small at best.
I’d note that none of the above applies to nutrition around training, which is a topic that I’ll have to cover in a
separate article. Training changes the dynamics of a many things including how protein is used by the body
so the data discussed so far doesn’t really apply to that specific situation.

The Impact of Previous Meals on Digestion Speed

Finally, before moving on, a final topic that I’ve mentioned above, which is the fact that most of the studies
done feed the protein to folks after an overnight fast. While this makes the studies less complicated, it
doesn’t indicate what happens when a meal is being consumed while another is still digesting.
Unfortunately, this area is poorly studied, I’m not aware of any work that has examined if the fast/slow protein
concept has any relevance to a meal being eaten later in the day. I’d only note again that whole food meals
take much longer to digest than is often claimed, a moderate sized meal may still be digesting 5-6 hours
later. Even if a ‘fast’ protein is consumed, there’s no guarantee it will still act ‘fast’ if there’s still food sitting
in the gut. Again, I’m unaware of any research on this topic.

What About Other Proteins?

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So far all I’ve focused on is whey and casein as these are the proteins that have been predominantly
studied. Unfortunately, there is far less data on the speed of digestion of other proteins. Soy has been
examined and appears to be a fast protein; note from my article Milk: The New Sports Drink? A Review that
milk was found to be superior to soy protein for gains in lean body mass with training. This is thought to be
due to the rapid digestion and amino acid profile of soy.
Beyond that not a tremendous amount of data exists. One researcher collected what is available and I’ve
reproduced his data (originally printed in The Protein Book) in the table below

Protein Absorption Rate (g/hour)

Raw Egg Protein * 1.4

Cooked Egg Protein * 2.9

Pea Protein 3.5

Milk Protein 3.5

Soy Protein Isolate 3.9

Casein Isolate 6.1

Whey Isolate 8-10

Tenderloin Pork Steak * 10.0

* Measurements marked with an asterisk should be considered as the roughest estimates as the
studies used indirect measurements of protein digestion.
Clearly there is a large variety for protein digestion rates although, as noted, some of the above values
should be taken as very rough estimates.
I’d note again that this has some implication for the idea that you must eat protein every three hours. With
the exception of whey, where 40 grams of protein would take roughly 4 hours for complete absorption), all
proteins listed would still be digesting for far longer than the magic 3 hour period.
Once again, this is getting a bit too long so I’m going to save the final bit of this discussion for Part 3, which
I’ll post on Monday. In that article I’ll look at the current fascination in the sports nutrition industry with protein
hydrolysates along with a few minor topics.

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What Are Good Sources of Protein? – Speed of Digestion Part 3
Ok, somehow this mini-topic got a little bit out of control (I have a lot to say) so I want to wrap up the
discussion on speed of digestion and move into the other topics that go into answering the question What
are good sources of protein?

Whole Foods vs. Protein Powders

I finished up What are Good Sources of Protein? Speed of Digestion Part 2 with a short chart showing the
estimated digestion speeds of various proteins, including some whole foods. As someone brought up in the
comments, it’s unfortunate that there isn’t more data for whole foods because of the fact that, outside of
athletes, most people are eating whole food protein sources, not protein powders, to obtain the majority of
their daily protein.
And, in that chart, with the exception of an estimated value for tenderloin that seems impossibly high, most
whole food proteins were on the slow end of the digestion scale. This actually makes perfect sense. Whole
food proteins are generally contained within a matrix of connective tissue and such (e.g. think of the chewing
that you have to put into eating meats such as beef, tuna, or chicken) and that alone will slow the process
of digestion down. Basically, even without direct data, I’d expect most whole food proteins to be slowly
digesting proteins.
Research using whole food meals find that amino acids are still be released into the bloodstream up to 5
hours after eating them; this certainly supports the idea that whole food proteins take a long time to
digest. Other researchers have suggested that a given meal will maintain the body in an anabolic state for
5-6 hours so clearly whole food proteins aren’t digesting particularly quickly.
Basically, the majority of proteins that people who aren’t obsessed athletes will be eating are going to be
slowly digesting proteins.
The primary exception that I’ve examined, of course, is whey protein which digests quickly; soy isolate is
also a fast protein (another that I’ll mention briefly in a second is pea protein hydrolysate). Now, whey has
some nice characteristics in terms of its amino acid profile (discussed in a later segment of this article), it
may improve immune system function, and have other functional health benefits. Outside of athletes, life
extension folks and the obsessed health types, I’m not sure that whey protein powder is going to make up a
major source of protein for the majority of people.
However, this brings me in a very roundabout way to a related topic having to do with protein powders and
the different forms that they come in.

Types of Protein Powder: Concentrates, Isolates and Hydrolysates

On this note, before moving on, I want to make a couple of quick comments about protein powders since,
as usual, there is a lot of confusion, hype and outright lies being made about them. Quoting directly from
The Protein Book:
Protein powders come in three primary forms which are isolates, concentrates and hydrolysates. Protein
concentrates typically contain roughly 80% protein with 5-6% carbohydrate and fat while isolates may
contain up to 90% protein. Hydrolysates are simply isolates or concentrates which have been pre-digested
(digestion of protein is called hydrolysis) by subjecting them to specific enzymes. Practically speaking, you
will typically pay the least for a protein concentrate, more for an isolate and the most for a protein

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hydrolysate. Because of the presence of free form amino acids in protein hydrolysates, they often have a
more bitter taste than either concentrates or isolates.
In the last couple of years, there has been a real push by supplement companies for expensive (and often
bitter tasting) hydrolysates based on the claim that they digest much more quickly than either isolates or
concentrates and thus super-speed amino acids to just worked muscles.
Ignoring the question of whether faster is actually better (see below), there is the question of whether
hydrolysates actually do digest significantly faster than protein isolates. Limited research is available and
while one study showed that pea protein hydrolysate digested more quickly than other concentrates, this
data can’t be applied to any protein except pea protein.
One study compared the digestion speed of whey and casein to their respective hydrolysates and the simple
fact is that there was no significant difference in digestion speed. Quoting from the results:
The rate of gastric emptying for all solutions was found to fit an exponential pattern (r=0.92–1).Solutions
were emptied at similar rates, with half-times of (mean ± S.E.M.) 21.4±1.3, 19.3±2.2, 18.0±2.5 and 19.4±2.8
min,for the whey hydrolysate, casein hydrolysate, casein and whey protein,respectively.
Basically, there was no real difference (maybe a couple of minutes faster for the hydrolysates) between
whey isolate and its hydrolysate and casein and its hydrolysate.
Translation: there is no advantage to whey or casein hydrolysates in terms of digestion speed. None. Well,
unless you think paying three times the price and accepting an often bitter taste is an advantage.
Which brings me in a roundabout way to the final topic of this series within the series:

Is Faster Digestion Better?

Although this question would pretty much never come up with regards to general health and nutrition, it is
one that is relevant to sports nutrition (and as noted in part 2, older individuals may obtain beneifts from fast
proteins). Is it better for protein to be quickly digesting or slowly digesting?
Of course the answer is context dependent and depends on what the goal is. For the majority of applications,
I hope that readers get the basic idea that I think slower digesting proteins, or a mix of slow and fast are
generally superior to fast proteins by themselves.
This is especially true for non-athletic applications where I think most should simply stick with whole food
proteins most of the time anyhow; in the context of a mixed meal, that will mean that the proteins being
consumed will digest slowly.
As I noted in What are Good Sources of Protein? Speed of Digestion Part 2, there is emerging data that
older folks may benefit from spikes of amino acids in terms of offsetting age-related muscle protein
breakdown. So that is clearly one exception to my general belief that slower or slow/fast mixes are best
under most conditions.
Now, a recent trend in sports nutrition is to consume nutrients (carbs, protein) around the entire training bout,
this often means before, during and after training. I actually spend about 35 pages discussing this issue in
The Protein Book examining the most recent research and giving specific recommendations for both
strength/power and endurance athletes in terms of when, how much and what to consume around training
for different types of workouts. I’m not going to repeat that here, clearly.
As discussed thoroughly in that chapter, there is emerging data that a slow or mixed fast/slow protein
following training is superior to a fast protein alone (I realize that this goes against what all of the supplement
companies are saying but, as usual, they are taking research out of context to sell product).

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Readers might simply refer back to my article on Milk: The New Sports Drink – A Review as research clearly
showed that milk (a combination of whey and casein, that is a combined slow/fast protein) was superior to
soy protein (a fast protein) for supporting muscle mass gains. Post-training, slow or a combination of fast
and slow is simply superior to a rapidly digesting protein.
But that’s after training and folks are currently consuming protein before and during workouts these
days. Under those situations, clearly a slowly digesting protein is inappropriate if for no other reason than
having protein sitting in the gut digesting while you try to train is a good way to throw up.
For pre- and during-workout protein intake, I recommend a quickly digesting protein such as whey or a good
soy isolate. That is one condition where, clearly, a fast digestion speed will be superior. Under most others,
I feel that a slower digesting protein or at the very least a combination of slow and fast will give the best
results.
There are other possible exceptions to the above, which I’ll come back to later in this series. As a primary
example, some research suggests that hormonal impact of a fast protien like whey may blunt hunger better
than slowly digesting proteins such as casein.
However, empirically, I can’t say I’ve seen this be the case: most report that casein (a slow protein) or milk
protein isolate (a protein powder containing both whey and casein) keeps people fuller on a diet by sitting in
the stomach longer. Again, I’ll come back to this in more detail when I talk about dieting.
And that’s that for speed of digestion. On Wednesday, I’ll look quickly at protein quality before moving onto
the rest of the topics I outlined in the Introduction to this series.
Go to What Are Good Sources of Protein – Protein Quality

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What Are Good Sources of Protein? – Micronutrient Content
As I move towards wrapping up this series this week, I need to discuss a couple of other topics of relevance
to the question of what are good sources of protein. A good bit of what’s been discussed in other sections
was a bit on the theoretical/sciency end of things and I’m going to keep the next couple of topics a lot more
applied.
Today I want to look at an issue that I don’t think is addressed as much as it could be when folks are looking
at protein source; that topic is the presence (or absence) of other nutrients. Outside of a few select groups
(that often get a majority of their protein from isolated sources such as protein powders or amino acids),
most people get their daily protein from whole food sources and whole foods contain other nutrients. Some
of those nutrients may be beneficial, some of them may be detrimental; all need to be considered when
looking at protein sources and deciding which are good, bad, or neutral.
The major ‘extra’ nutrients I want to look at in this article are zinc, iron, B12, calcium. In the next part of this
article series, I’ll take a look at the issue of dietary fat content, both in terms of good and bad fats. This is
simply to keep the length a bit more manageable.

Zinc

Zinc is an essential mineral involved in an amazing number of processes in the body including immune
system function, appetite (a lot of early research showed that zinc deficiency did weird things to appetite,
zinc has been shown to regulate leptin levels as well) and hormone levels (zinc deficiency can reduce
testosterone levels). Since the body doesn’t store zinc, its intake is required on a daily basis.
Zinc is found to varying degrees in most protein foods with oysters containing the most zinc of any food (this
probably explains the idea that oysters are an aphrodisiac, given the role of zinc intake on testosterone
levels) Red meat, liver and crab meat contain the highest levels after that, chicken is a fairly close
second. Eggs and milk are not fantastic sources of zinc although cheese has reasonable amounts.
Grains and cereals, along with beans (often a prime source of protein in vegetarian diets) are relatively poor
sources of zinc. As well, compounds in these foods tend to impair zinc absorption in the gut.
Vegetarian diets are often zinc deficient and females (especially female athletes) who have a habit of
removing sources of protein such as red meat and chicken also often come up zinc deficient. I’m a huge
believer in lean red meat for most people, especially athletes and ensuring adequate zinc intake is one of
those reasons.

Iron

Iron is another essential mineral, also involved in a staggering number of processes. Arguably the most
well-known role of iron in the body has to do with keeping red blood cells healthy and working. A lesser
known effect of iron has to do with thyroid conversion in the body; very low levels of iron can cause problems
with thyroid production in the liver. Restoring iron levels to normal reliably improves thyroid conversion, can
increase metabolic rate and improves thermoregulation.
In the diet there are two types of iron which are called heme-iron and non-heme iron. Heme iron is absorbed
roughly 10 times more effectively than non-heme. Like zinc, the best sources of iron (especially heme iron)
are meats, especially red meat, liver and organ meats. Chicken is also a good source of iron; interesting

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research has found that both red meat and chicken contain a factor that improves non-heme iron absorption
by the body.
While many non-meat sources contain reasonable amounts of iron (and many food are iron fortified in the
modern world), the iron is typically of the non-heme variety; as well the presence of other compounds in
those foods often impairs the iron absorption. I’d note that vitamin C increases iron absorption and
consuming some with iron containing foods is one way to improve iron absorption; cooking with a cast-iron
skillet also increases the iron content of foods.
Females, due to the loss of menstrual blood each month are at a higher risk for iron deficiency than men (in
this vein it’s interesting to note that women are more likely to have thyroid problems, I have to wonder if
these two issues aren’t related) and females (especially athletes) along with vegetarians are likely to be iron
deficient. This is especially true for female athletes who have a habit of removing red meat out of their
diet. That, along with possibly increased requirements from training, along with slight blood losses each
month add up to iron deficiency.
I’d note that too much iron can be as bad as too little, iron acts as a pro-oxidant in the body; men should be
very careful about going out of their way to take extra iron and many multivitamins for men have no iron in
them for this reason. While women lose some iron each month, excessive iron intake can build up stores in
men and cause many problems.
Basically, as with zinc, meat protein, especially red meat is the winner here. This is yet another reason that
I think lean red meat (which has also been shown to lower blood pressure and improve blood lipid levels)
should be part of any healthy diet. Female athletes especially should probably be consuming lean red meat
multiple times per week; supplementation may also be necessary.

B12

Vitamin B12 is, as its name suggests, one of the B vitamins. It plays critical roles in the body not the least
of which is brain function. While B12 requirements are staggeringly tiny, and the body can actually build up
a fairly long store of B12 (in the liver), deficiencies are not unheard of.
B12 is ONLY found in animal source products and vegetarians are often at risk for deficiency for this
reason. Females who remove animal source proteins from their diet are, as with zinc and iron, at risk for
deficiency.
I’d note that there is an oddity with B12 in that a specific factor is required in the stomach for B12 absorption;
some people lack this. Even with plenty of B12 in the diet, they don’t absorb it and can end up with
deficient. This can cause something called megoblastic anemia (this is a bit of weirdness to do with red
blood cells) along with mental fuzziness. People who lack the absorption factor can’t simply supplement
normal B12, they have to get a specific form called Methylcobalamin and this will have to be taken forever
to avoid deficiency.
For everyone else, simply ensuring sufficient protein intake from animal source proteins will provide plenty
of B12.

Calcium

Finally, I want to talk about calcium. Known primarily for its effects on bone health, calcium is turning out to
play a number of other major roles. Early research found an effect on blood pressure of high dairy intakes
and more recently some work has found an impact of calcium (and dairy foods seem to work better in this

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regards) on fat loss; the mechanism is still unclear although calcium may be affecting fat absorption from
the gut, fat oxidation in the body, or some other aspect.
As well, the exact reason that dairy calcium seems to work better is an issue of some question; it may be
due to greater absorption of dairy calcium compared to non-dairy calcium or it may have something to do
with another factor inherent to dairy products.
The most well-known source of calcium in the human diet is, of course, dairy products. While there is calcium
in many vegetable source proteins (vegetarians often claim that broccoli has more calcium than milk), the
presence of other compounds in vegetables impairs absorption of the calcium that is present. Meats, grains
and nuts are a poor source of dietary calcium.
I’d note, tangentially, that while there has been a long-standing belief that high-protein intakes are bad for
bone health but this isn’t supported by current research. As detailed in Protein Controversies, a high protein
intake is only a problem when calcium intake is insufficient; a high protein intake along with plenty of calcium
actually improves bone health.
As discussed The Protein Book, I am a big believer that low-fat dairy products should be part of any healthy
diet. Not only do dairy foods provide an excellent combination of slow and fast proteins, they provide the
most available source of dietary calcium and seem to improve body composition and calorie partitioning.
As well, as I discuss in Contest Dieting Part 1, I also think that the weird bodybuilder ideas about dairy on a
contest prep are not only invalid but actually do more to harm fat loss than anything else.
Of course, not everyone can consume dairy, either due to a true allergy (which is rare) or a lactose
intolerance (which is more common). Of course, lactose free dairy products do exist (for example, Lactaid
Milk) and there are pills of varying sorts which help with lactose digestion (either by providing the necessary
enzyme or helping the gut to start producing more naturally). Failing that, calcium supplements would be
indicated for someone who can’t consume dairy (for whatever reason).

Summing Up

There are a number of important micro-nutrients that can go into the decision of What are good sources of
protein. Zinc, Iron and B12 are all critical nutrients which are found in the largest and most well-absorbed
amounts in animal sources foods. Lean red meat (to avoid excessive fat intake), chicken, seafish can all be
good sources of those foods; vegetarians and others who try to limit their intake of those foods (for either
good or bad reasons) can be at risk for deficiency.
Dietary calcium plays an enormous number of roles in the body; while the most well-known is bone health,
current research indicates that sufficient calcium (and dairy calcium appears to be superior to non-dairy
calcium) can lower blood pressure and decrease body fat levels through a variety of mechanisms. I strongly
believe that no- or low-fat dairy products should be part of any healthy or athletic diet for those and other
reasons. Individuals with lactose intolerance have a number of potential solutions but if dairy simply can’t
be consumed, supplements are at least adequate.
In the next part of this sub-series, I’ll look at the issue of dietary fat and its presence or absence in various
dietary protein sources. This will include a quick look at both the contentious issue of saturated fat as well
as the importance of the omega-3 fish oils.
Go to What Are Good Sources of Protein – Dietary Fat Content

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What Are Good Sources of Protein? – Amino Acid Profile Part 1
Continuing from Wednesday’s article on What are good sources of protein? – Protein Quality, I want to talk
a little bit about the amino acid profile of proteins and how that impacts on the answer to the question What
are good sources of protein.
I’m going to actually divide this into two parts to keep it from getting too long. In Part 1, I’ll discuss some
basic concepts and look at how the amino acid profile of various proteins relates to supporting basic bodily
function. In Part 2, which I’ll run on Monday, I’ll discuss the possibility that athletes have specific amino acid
requirements above and beyond what’s necessary to support basic function.

What are Amino Acids?

Now, as I’ve mentioned but not gone into any great detail in this series, amino acids are simply the building
blocks of protein. Depending on which reference source you use, there are 18-22 different amino acids that
occur in the human food supply. Whole food proteins are simply long chains of these amino acids bonded
together. Typically whole food proteins are extremely long chains of amino acids, as I discussed in What
are good sources of protein? – Digestibility, these long chains are cut into smaller and smaller chunks during
digestion until only single amino acids and chains of 2-3 amino acids are actually absorbed.
I’d note that individual amino acids are often sold for either health or sports performance purposes. Readers
may be familiar with the amino acid L-tryptophan which is often sold as a sleep aid. L-Tryptophan converts
to serotonin in the brain which is involved in sleep. Take L-tryptophan on an empty stomach and you get
drowsy because of increased brain serotonin levels.
In the athletic realm, all kinds of products are available. The branched-chain amino acids (BCAA) L-leucine,
L-isoleucine and L-valine have been pushed for years to athletes; recently there has been a big push for
isolated leucine for a number of reasons that I’ll touch on in Part 2.
Another example is L-carnitine, an amino acid involved in fat metabolism that has been sold as a fat loss aid
for years (it doesn’t work by the way). I, myself, have recommended the amino acid L-tyrosine (which
converts in the brain to adrenaline and noradrenaline) as part of a stimulant cocktail to improve performance.
You may be wondering what the ‘L-‘ means above; it refers to the chemical structure of the amino acid (to
be technical, it’s an organic chemistry notation that stands for levorotary). There are also ‘D-‘ amino acids
(the ‘D’ stands for dextrorotary). The human body only uses the ‘L-‘ form of amino acids; the ‘D-‘ form can
actually be toxic.

Essential vs. Non-essential Amino Acids

I should note that the amino acids are usually subdivided into essential amino acids and inessential or non-
essential amino acids. It’s important to note that both are absolutely essential for life, the term
inessential/non-essential simply means that those amino acids don’t need to be obtain from the diet; the
body can make them. The essential amino acids can only come from the diet; hence they are ‘essential’.y
I should also note things aren’t actually quite this simple, some amino acids which are inessential under
normal conditions can become essential under others; glutamine is perhaps the most well known
example. Under normal conditions, glutamine is inessential, the body can make what it needs. However,
under conditions of massive stress (such as blunt force trauma, burn injuries or sepsis), the body can’t make
as much glutamine as it needs; glutamine becomes conditionally essential under those conditions.

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And while there are a few other odd exceptions to the essential/inessential distinction, they tend to be rare
and not very relevant under most conditions, so I won’t talk about them.

Why do Amino Acids matter?

Now, as mentioned in What are good sources of protein? – Digestibility, after being broken down in the gut
and intestine, proteins then appear in the bloodstream as amino acids. These are then used in the body for
various processes such as the synthesis of new proteins.
Your heart, liver and many other organs are made of protein, skeletal muscle contains about 20% protein
(most of it is actually water), your hair and skin is made of protein, there are numerous enzymes and liver
proteins made in your body every day; all are synthesized from incoming amino acids from the diet.
Recall from What are good sources of protein – Speed of Digestion Part 1, that the tissues in the human
body are in a constant state of turnover, which is the combination of breakdown and re-synthesis. So skeletal
muscle is being broken down and remade, so is hair, skin, etc. Of course, since no process in the body
processed with 100% efficiency, some of the broken down amino acids are lost.
That is, fundamentally, the basis for human protein requirements; the amino acids lost in the process of
breakdown and re-synthesis have to be replaced from the diet. Otherwise, there will be a gradual loss of
protein tissues in the body (as occurs in complete starvation). Lose enough body protein (about 40%) and
you die.
Now, since the body is actually using specific amino acids for these various processes, it’s actually a little
more accurate to say that the body has specific ‘amino acid requirements’ rather than ‘protein requirements’
per se. I’d note that there is also a general ‘nitrogen requirement’ (that can only be met with dietary protein)
but I don’t want to get into that level of detail.
As a final note, I want to mention that the tissues in the human body that use proteins all use them in varying
proportions and amounts. That is, the amino acid profile of say, your liver, or a specific enzyme may not be
the same as skeletal muscle, hair or bone. Basically, the tissue you’re focusing on will determine what the
ideal amino acid profile ‘might be’. I’ll come back to this.

Back to Protein Quality

Now, as I mentioned in What are good sources of protein – Protein Quality, one of the determinations of
protein quality has to do with how well or poorly a given protein fulfills the amino acid requirements of the
body and the above discussion basically explains why. Every day your body loses some amino acids which
have to be replaced. One determinant of a protein’s quality is how well it matches the body’s need for those
specific amino acids.
Now, I should mention again that most of the work on protein quality deals with the issue of general health,
especially in those people who are not getting sufficient protein, protein from high quality sources, and who
aren’t eating much in the first place. That is, the research is aimed at folks in third world countries.
The goal is to find ways of improving overall health and bodily function in people who are starving to
death. And the focus is basically on keeping them healthy overall, that is meeting the amino acid
requirements of the whole body in terms of keeping the basic stuff functioning well (or at least
passably). Issues such as optimizing athletic performance or increasing muscle mass are not the focus.
Not only does this mean it has questionable relevance to those of us lucky enough to live in a modern world
where protein and food is generally very available, it also means that it isn’t aimed at athletes or individuals

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involved in training (which tends to be the group I focus on). It’s conceivable (and, of course, supplement
companies pander to this idea) that athletes or individuals in hard training might have specific requirements
for amino acids.
That is to say, it’s conceivable that someone involved in a strength/power sport (powerlifting, bodybuilding,
etc.) might require a different amino acid profile to support the growth of skeletal muscle; an endurance
athlete might conceivably need a specific amino acid profile to support the synthesis of mitochondria (the
powerhouse of the cell) or enzymes involved in energy production. This topic is drastically under studied.
But, simply (and of course this is discussed in great detail in The Protein Book), amino acid requirements
can be sub-divided into the amino acid requirements needed to support basic health and bodily function
(what most research deals with) and the amino acid requirements (if any) to optimize athletic performance.

Meeting Basic Bodily Requirements

Now, for reasons I’m not going to get to, the amino acid requirements for 2-5 year old children are actually
used to examine whether or not a specific protein is sufficient. That is, any dietary protein which has an
amino acid profile that meets or exceeds the requirements for 2-5 year old children is considered sufficient
to support the basic needs of adults.
I’d note that, in keeping with the section on essential/inessential amino acid discussion above, the real focus
is on whether or not a given protein can meet the essential amino acid requirements of the body. Assuming
sufficient protein is being consumed in the first place, the inessential amino acid profile isn’t that relevant.
And as I show in Table 2 on Page 56 of The Protein Book (which I’m not going to reproduce here), basically
all high quality proteins, and this even includes soy protein, can meet the basic amino acid needs of an adult
human being. Human milk, cows milk, eggs, beef, whey and soy all contain amino acids far in excess of the
requirements for 2-5 year old children; by extension this means that they can readily meet the requirements
for adults.
This is in keeping with the discussion of the PDCAAS from What are good sources of protein – Protein
Quality showing that proteins such as soy (which were typically thought of as low quality) are more than
sufficient to meet adult human essential amino acid requirements. Assuming adeequate dietary protein is
being eaten in the first place (and this is basically never an issue in the modern world), all proteins easily
meet human protein requirements.
Which doesn’t make them all identical or equivalent mind you; there may be reasons (such as the presence
or absence of other nutrients such as iron, zinc, or calcium, or the fatty acid profile) to choose one protein
over another. But from the standpoint of amino acid profile, there isn’t much of a functional difference
between proteins (I’d note, rather tangentially, that recent work has suggested that fish protein per se seems
to have benefits on insulin sensitivity, possibily due to the high taurine content).
Which, as noted above, doesn’t really address the issue of athletes and possible differences in
requirements. But that will have to wait for Part 2.

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What Are Good Sources of Protein? – Amino Acid Profile Part 2
In What are good sources of protein? – Amino Acid Profile Part 1, I examined the issue of amino acid profile,
primarily as it relates to general health and wellness. My basic conclusion, based on the research is that
basically any high quality protein source (and this is eminently true in the modern world where people get
plenty of protein from mixed sources along with lots of total calories) more than adequately meet the amino
acid requirements of adult humans.
Today, I want to continue that by looking at some issues specific to athletes and those involved in heavy
exercise training. It’s fairly well established that athletes need more protein than sedentary individuals
although there is still great argument over just how much is needed.
Two specific amino acids that tend to get focused on by athletes are the branched chain amino acids
(BCAAs) and glutamine, I’ll give a quick primer on those before discussing any of the other specific issues.
There are a number of different ways by which by which exercise training might increase protein/amino acids
requirements. This includes the use of amino acids for energy directly during exercise, other pathways of
interest (see below), and finally the actual adaptation to training. I also want to touch briefly on the issue of
dieting.
To keep this from getting too long, I’m only going to discuss energy use and the other pathways today. Since
it will be the longest part, on Thursday or Friday, I’ll look at the issue of the actual adaptations to training and
how that might impact on specific amino acid requirements; I’ll also look at the issue of glutamine and BCAA
supplementation in that regards. I’ll discuss dieting then as well.
Again, I can’t really do these topics full justice in this article, it took me 225 pages to cover it all in The Protein
Book and anybody who wants the full discussion (and all of my study references) should pick up that book.

BCAA: A Primer

The branched chain amino acids (BCAA) refer to three individual amino acids, leucine, isoleucine and
valine. They are so named because of their branching structure. It’s been known for years that they are
treated differently in the body than the other aminos; while other aminos can all be degraded in the liver,
BCAA metabolism is fairly specific to skeletal muscle. In a very real sense, BCAA are muscle food. I should
note that while BCAA are primarily used in the muscle, they can also be burned there directly for energy.
The BCAA can not be made within the body and must be obtained by the diet. In that context, I’d note that
all high quality proteins actually contain quite a bit of BCAA. Proteins such as meat typically contain about
15% BCAA by weight (e.g. 100 grams of protein will provide about 15 grams of BCAA) while dairy proteins
such as whey and casein contain more. Some forms of whey contain as much as 25% BCAA by weight
(e.g. 100 grams of whey protein will provide 25 grams of BCAA), casein comes in at about 20%.
Quoting from The Protein Book about this:
A typical diet containing high quality protein will provide 15-20 grams of BCAAs for every
100 grams of protein ingested (25); diets containing a significant amount of whey protein
will contain slightly more than this. A 100 kg athlete consuming 3.0 g/kg protein, or 300
grams of protein per day, would be expected to be consuming 45-60 grams of BCAAs per
day; again, this value would be slightly higher if a large amount of whey protein was being
consumed.
This is an important point because the grand majority of studies which have shown benefits from BCAA
supplementation have done so without first providing adequate protein in the first place. And as is always

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the case with such things; nutrients do very different things when they are shoring up a deficiency or
inadequacy than when they are not.

Glutamine: A Primer

Glutamine is a non-essential amino acid (e.g. under normal conditions it can be made in sufficient amounts)
although under conditions of very high stress (trauma, burn injury), the body may need more. Crafty
supplement manufacturers have tried to liken heavy training to that level of stress which is, frankly, absurd.
Glutamine plays a number of roles in the body, early research showed that it could stimulate protein
synthesis when added to cell culture. Glutamine is also involved in immune system function, I’ll talk about
this further on. Glutamine is also involved in acid-base balance, some have suggested its consumption on
a high-protein diet to help buffer acid production. I suggested glutamine for GH release (GH has some fat
mobilizing properties) in The Ultimate Diet 2.0.
As it turns out, the body actually synthesizes a lot of glutamine per day, anywhere from 20-60 grams per
day. As it also turns out, a lot of this glutamine is being synthesized from other amino acids, including the
BCAA.
As noted above, BCAA can be burned in skeletal muscle directly (and this increases when glycogen has
been depleted) and this tends to produce ammonia which the body buffers by converting to glutamine to be
sent to the liver. Basically, glutamine is used by the body to transport amino from muscle to other places
where it can be disposed of; glutamine is also used heavily by the gut, immune system and kidneys.

Exercise and Amino Acid Requirements: Energy Use During


exercise

One source of increased protein requirements during exercise has to do with the direct use of amino acids
for energy during exercise. Generally speaking this is fairly specific to endurance training where ~5-10% of
the total energy requirements of exercise can be from the burning of amino acids. Specifically, the branched
chain amino acids, and especially leucine, can be used directly for energy by exercising muscle.
This does suggest that increased BCAA intake during endurance exercise might be beneficial and, to this
point, studies have found that the consumption of small amounts (10-12 grams per hour) of rapidly digesting
protein with carbohydrate can decrease muscle damage, may improve recovery between bouts and may
improve performance. But, for reasons beyond the scope of this article, I strongly feel that a quickly digesting
whole protein such as whey is superior to isolated BCAA in this case.
Because of the vast differences in energetics between weight training and endurance training, there typically
isn’t a lot of burning of amino acids during resistance training. It’s conceivable that extremely high-volume
training, which depletes muscle glycogen could increase BCAA burning but this is unlikely with anything but
the most insane training volumes.
Outside of possible effects on immune system function, there’s really not much role for glutamine in terms
of energy production during exercise. Consuming adequate carbohydrate (~30-60 grams per hour) with
small amounts of protein (e.g. 10-12 grams of whey protein which will provide 3-4 grams of BCAA) will do
more to protect immune system function than glutamine could ever do.

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Exercise and Amino Acid Requirements: Other Pathways of
Interest

Although they haven’t been studied much, there are other potential pathways that use amino acids that
contribute to increased protein requirements by athletes. Quoting again from The Protein Book:
In addition to all of the body’s uses of protein described above, there are a number of
processes of extra importance to athletes. This includes the repair and replacement of
damaged proteins, remodeling of the proteins within muscle, bone, tendon and ligaments,
maintenance of optimal functioning of all of the metabolic pathways that use amino acids
(presumably these pathways are up regulated in athletes due to training), supporting lean
body mass gains, supporting immune system function, and possibly others (4).
Each of these pathways, might conceivably all require a different amino acid pattern for optimal
functioning. However, this area is woefully understudied so I can’t comment much.
I do want to discuss the immune system issue a little bit; clearly an athlete who is sick isn’t training well and
if they aren’t training they certainly aren’t getting better. Protecting immune system function in athletes (and
the problems tend to occur with volume more than intensity) is a key aspect of sports nutrition.
The amino acid glutamine is a key amino in terms of immune system function and there was some interest
at one point in using glutamine to prevent immune system function; some studies supported that idea, others
did not. As it turned out, BCAA turned out to work better; recall from above that BCAA can be converted to
glutamine and BCAA turn out to ‘protect’ glutamine status in the body.
Ensuring sufficient BCAA intake may help protect the immune system during periods of high-volume training
and at least one study in endurance athletes found that BCAA supplementation even in the context of
adequate daily protein did help; given that many endurance athletes don’t consume sufficient protein in the
first place, BCAA might play a role. I’d note that simply raising protein intake to adequate levels would be
better than trying to shore up an inadequacy with supplements.
As I mentioned above, I’d note that simply ensuring sufficient carbohydrate during training usually does more
to keep immune system functioning well than anything else. The combination of carbs and small amounts
of high quality protein (e.g. whey) should be sufficient under most conditions but endurance athletes doing
very high volume might consider additional BCAA.
Resistance training, in general, tends not to have the negative effects on immune system function that high-
volume endurance training does. I suppose athletes who were doing very high volume resistance training
on a near daily basis might have issues but I’d see that as a problem with their training program more than
their nutrition. And given that athletes involved in resistance training typically consume a lot more protein
than the average endurance athlete, BCAA intake will go up automatically without the need for
supplementation.

Summing Up

Quickly summing up this article, I looked briefly at BCAA and glutamine in general in terms of their
metabolism before looking at two pathways of interest to athletes that might impact on specific amino acid
requirements.
The first was energy use during exercise; generally relegated to endurance athletes only, there is evidence
that the BCAA can be burned directly for energy during exercise, conceivably raising requirements. Studies

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have shown that the consumption of small amounts of protein during endurance exercis can limit muscle
damage and may improve both recovery and performance. I feel that whole proteins such as whey will
generally be superior to isolated supplements.
Resistance training, in general, doesn’t burn protein for energy unless the workouts are very voluminous and
very long. While amino acid or protein intake during resistance trianing can still be valuable (for reasons I’ll
discuss in Part 3) it has less to do with energy provision and more to do with overall adaptation and growth.
There are other pathways such as connective tissue and immune system function that are likely to be
upregulated by heavy training; unfortunately these are poorly studied. Immune system is an area of great
interest; while early studies suggested a role for glutamine in protecting the immune system during periods
of high-volume training, not all studies were positive and BCAA probably play a bigger role by protecting
glutamine status in the body.
At the end of the day, consuming adequate carbs during training (with or without small amounts of protein)
does more to protect immune function but athletes involved in very heavy high-volume training might
consider extra BCAA to keep from getting sick.
In Part 3, I’ll take a detailed look at the adaptations that occur with training along with how they might impact
on amino acid requirements; again focusing on the BCAA and glutamine. I’ll also touch on dieting since that
is a topic of much importance and relevance to many people.
I know this series is getting long and some folks want me to wrap it up and get to the point but I have a lot
to say and a lot of information to cover. I will finally answer the original question What are good sources
of protein? at the end of this series and give specific recommendations. So please be patient.

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What Are Good Sources of Protein? – Amino Acid Profile Part 3
In What Are Good Sources of Protein? – Amino Acid Profile Part 2, I looked a little bit at both the branched-
chain amino acids (BCAAs) and glutamine before examining two distinct pathways by which exercise not
only increases overall protein requirements but might impact on the specific amino acid profile needed by
the body to support heavy training.
In the final part of this sub-series within the series, I want to look at the final way that training can potentially
impact on specific amino acid requirements. I’ll also touch on dieting at the very end.

Exercise and Amino Acid Requirements: Skeletal Muscle


Adaptation

Although there are certainly other adaptations occurring to training (e.g. neural, cardiovascular), one of the
primary places where adaptation to regular training occurs in skeletal muscle. Both endurance training and
heavy resistance training stimulate specific adaptations in skeletal muscle that work to improve performance
in the long run.
Something to keep in mind is that resistance training and endurance training stimulate very different
adaptations. Resistance training generally causes an increase in the actual contractile tissue in skeletal
muscle; in contrast, endurance training stimulates increases in mitochondria along with the enzymes
responsible for energy production.
In premise this means that strength/power athletes (who typically engage in heavy resistance training) and
endurance athletes might require different amounts of specific amino acids to support the
specific adaptations in those tissues. Without going into a lot of detail, it simply doesn’t work that way.
Quoting again from The Protein Book:
The liver acts essentially as a gate to ensure that the AAs which are required by the body are released into
the bloodstream while any that aren’t needed are simply disposed of via oxidation. Even if a protein with the
absolutely identical AA profile to skeletal muscle was consumed, this in no way guarantees that AAs in that
proportion will appear in the bloodstream in the first
place.
As an example of this, you might recall from What Are good sources of protein – Speed of Digestion Part 1
that whey consumed by itself simulates amino acid burning; essentially any time the body sees an excess
of aminos compared to what’s needed, it will simply burn off the excess aminos.
Now, one possible exception to this are the branched chain amino acids (BCAA) which I’d remind you are
leucine, isoleucine, and valine. Unlike other amino acids which can all be degraded in the liver, the BCAA
are used primarily in skeletal muscle.
In a very real fashion, the BCAA are muscle food and there has been huge interest in BCAA, especially
among the weight lifting subculture, and for seemingly good reason.
It’s been known for years that the BCAA themselves can specifically turn on protein synthesis in skeletal
muscle and, more recently, it’s been found that this effect is specific to the amino acid leucine (which works
through a molecular receptor called mTOR).
Put simply: leucine turns on protein synthesis and this has led to the suggestion that lots of BCAA around
training, or extra leucine, can be useful to stimulate protein synthesis.
And there certainly seem to be studies to support that. However, they all suffer from the same major flaw in
my opinion: they are looking at BCAA supplementation in the context of insufficient protein intake. Or they

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are looking at older folks who, as I mentioned in a previous part of this series, respond to protein differently
than younger folks.
As an example, one study that is being cited currently compared either a small amount of protein (~13 grams
per hour) with carbs to a small amount of protein with an absurd amount of leucine (the same 13 grams of
protein with an additional 6 grams of leucine) taken post-workout. Not only did the leucine only have a tiny
effect, what’s not mentioned about this study is that the drinks were given for 6 hours after training which is
hardly relevant to a single post-workout drink. As well, 13 grams of protein is far below what’s optimal post-
workout; had sufficient protein been given in the first place, I doubt the extra leucine would have done
anything.
As another example, one of the classic studies cited to support BCAA around training was an Italian study
that compared the impact of BCAA to NOTHING on strength improvements. Of course the BCAA was
superior because consuming something around training is going to be better than consuming nothing around
training. But what if they had compared it to whey protein during training? Or whey plus carbohydrates (my
recommendation). Would the BCAA still have been superior? I doubt it.

There is the additional fact that even if you stimulate protein synthesis with BCAA or leucine specifically, it
won’t matter if there aren’t sufficient amounts of the other aminos present. You can turn on protein synthesis
all you want with BCAA or leucine, without the other building blocks for skeletal muscle, it won’t make any
difference. There is also the simple fact that the primary stimulus for increased muscle in the body is training,
not protein. Most Americans eat tons of protein and get lots of BCAA, they aren’t growing muscle because
they aren’t training and giving the body a stimulus to store the extra protein.
You can turn on all the protein synthesis that you want with dietary modifications, as it turns out the body
simply breaks down more protein later in the day to compensate. Unless someone is training, muscle mass
simply doesn’t increase due to these kinds of dietary manipulations.
Finally is the issue I talked about in What are good sources of protein? – Amino Acid Quality Part 2: all high
quality proteins contain lots of the BCAA in the first place, ranging from 15-25% depending on the source
(most sources are around 15%, casein comes in around 20% and whey can range from 23-25% BCAA). Of
that BCAA, a fairly large chunk is leucine.
A bodybuilder consuming say 250 grams of protein (e.g. 1.5 grams per pound at around 170 pounds) will be
getting, somewhere between 40-50 grams of BCAA depending on the sources. Someone consuming a lot
of whey or casein will get a bit more, someone living on nothing but meat will get slightly less. But someone
eating that much protein is already getting a lot of leucine in their diet, at each meal; throwing in another
gram or two is not going to do much.
The same holds for BCAA as a whole; I just see it as unlikely that, unless someone adds a truly absurd
amount, it’s going to matter in the context of the already large amount of BCAA coming in. And, as noted
above, unfortunately the studies don’t really answer that question; they all look at BCAA supplementation
under conditions of what I consider inadequate protein in the first place.
I would note that around training nutrition may be a slightly different situation, as I discussed in Milk: The
New Sports Drink – A Review, milk protein was superior to soy for promoting lean body mass gains although
this probably had as much to do with speed of digestion (milk protein was slower than soy) as amino acid
profile per se.
There was also some indication that the soy protein, because of its amino acid profile, was preferentially
used by the gut and this may have played a role. Again, around workout nutrition appears to be a place
where things are a little bit different than the rest of the day, simply because of the acute increase in both

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protein synthesis and breakdown. Around workout nutrition is discussed in extreme detail (35 pages worth
of detailed information) in The Protein Book.
But assuming an athlete is coming sufficient amounts of high-quality protein from mixed sources, and eating
enough calories, there is simply no reason to believe that any protein source will significantly impact on
adaptation to training or preferentially support adaptations in either contractile tissue or mitochondrial
function.

Dieting

A final topic I want to discuss before I wrap up this series next week is the issue of dieting. Throughout the
discussion about protein quality and amino acid requirements, one of the assumptions I’ve been making
(along with high-quality proteins from mixed sources) is that sufficient calories are being consumed; clearly
this isn’t the case when dieting.
It’s been known for at least three decades that total protein requirements go up during dieting; while
bodybuilders were perhaps the first to realize this, research is finally catching up with their empirical
knowledge.
Recent studies have found that ‘high-protein’ diets (and this is usually defined in terms of the percentage of
protein in the diet) are superior for dieting for a number of reasons: research has found that high protein
diets keep people fuller (making it easier to keep calories controlled), help to prevent some of the metabolic
slowdown that otherwise occurs, spares lean body mass and helps to stabilize blood glucose.
While dieting, the body tends to use more amino acids to produce energy, both the branched chain amino
acids and alanine are used in the liver to produce glucose and this is probably where much of the increased
requirement for those aminos comes from. In that alanine in skeletal muscle is produced by the metabolism
of glutamine, this might suggest an increased glutamine requirement during dieting.
But other than simply eating more protein, is any one protein optimal in terms of its amino acid profile? The
answer is yes. One researcher has examined dairy proteins, and specifically leucine content, while dieting
and has found that they tend to improve blood glucose maintenance and spare lean body mass while
dieting. As I’ve mentioned throughout this series, I’m a big fan of dairy proteins (whey, casein, milk, yogurt)
and this is one reason. You can read more of the reasons in Contest Dieting Part 1.
There is also some interesting evidence that fish protein (specifically cod as I recall) may improve insulin
and possibly leptin sensitivity; it was suggested that this might be due to the specific amino acid content,
especially taurine. This might explain why, empirically bodybuilders found that diets based around a LOT of
white fish worked well.
Unfortunately, that’s about the limit of the research into specific amino acid requirements in terms of whole
proteins. So what about supplements?
One study in wrestlers examined massive dose BCAA (~52 grams per day) and showed a slight increase in
visceral fat mass and a sparing of lean body mass. However, it didn’t give adequate protein in the first place,
the wrestlers were only given about 1.2 g/kg (a little less than 0.6 grams of protein per pound) which is less
than half of what’s needed on a diet to spare lean body mass loss.
I’m only aware of one study that has examined glutamine directly for its effects on a diet; no effect was seen
even at massive doses (35 grams per day). And while I’ve suggested small doses of glutamine to boost GH
(GH has mild lipolytic properties as discussed in the Stubborn Fat Solution), no study has tested directly if
this actually increases fat loss.

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Summing Up

Both resistance training and endurance training increase overall protein requirements and the specific
adaptations (e.g. contractile tissue in strength athletes, mitochondria in edurance athletes) seen with
different types of training suggests that there might be optimal amino acid profiles to support the specific
adaptations; little research has examined this.
As well, there are distinct physiological reasons, having to do with how the body as a whole and the liver
specifically regulates blood amino acid levels, that makes this idea fairly untenable. The amino acid profile
that shows up in the bloodstream tends to have very little relation to the amino acid of the proteins being
eaten and the body will simply ensure that the aminos which are needed reach the target tissues and the
ones that are not are disposed of.
Assuming sufficient high-quality proteins are being consumed in the first place, there should be more than
enough of all of the amino acids present without any specific amino acid profile being required.
A possible exception to this are the branched chain amino acids (BCAAs) which generally escape liver
metabolism and are used preferentially by skeletal muscle. While some studies have suggested role for
BCAA in a variety of processes important to athlete (e.g. leucine specifically stimultes protein synthesis),
every study that has suggested a benefit of BCAA or isolated leucine has done so within the context of
inadequate dietary protein in the first place. Given a lifter consuming 3.0 g/kg (~1.4 g/lb) of protein, the high
BCAA content of all high-quality dietary proteins make additional BCAA or leucine moot in my opinion.
One possible exception is around training where, at least in one study, milk protein was superior to soy
protein in terms of promoting lean body mass; this had as much to do with the speed of digestion as the
amino acid profile per se.
There is also evidence that, while dieting, high intakes of leucine and the BCAA may spare lean body mass
and help to maintain blood glucose. Given the other benefits of dairy proteins as a whole (e.g. some aspect
of dairy products increases fat loss), I’d suggest lifters focus on those whole proteins rather than isolated
amino acids supplements per se.
In the next part of this series, I’ll start to wrap things up by looking at how the presence or absence of other
nutrients (such as zinc, iron, the omega-3 fatty acids) impact on the answer to the question What are good
sources of protein?

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What Are Good Sources of Protein? – Digestibility
In the introduction to this series of articles, I briefly described a number of different aspects of dietary protein
that go into answering the question what is a good source of protein. I’d mention again that ‘good’ in this
sense can only be defined in a context-specific way. The protein that might be a good source under one set
of conditions may not be a good source under another. That will make more sense as I go through the
series.
Today I want to talk about the issue of protein digestibility; to keep the length down I’ll save speed of digestion
for Part 3 of the series. Once again I’ll note that much of what will appear in this and subsequent articles in
this series is being excerpted or paraphrased from The Protein Book, my complete look at the issue of dietary
protein.
One final note: While The Protein Book is fully referenced, with over 500 research studies cited, I will not be
citing references on this series of articles unless absolutely absolutely necessary.

A Primer on Protein Digestion

While the breakdown of protein begins in the mouth through the mechanical act of chewing, almost no actual
digestion occurs there. Rather, chewed protein hits the stomach where digestion and breakdown occurs via
hydrochloric acid and the enzyme pepsinogen.
The majority of protein digestion occurs in the small intestine where protein is broken down into smaller and
smaller amino acid (AA, the building blocks of protein) chains via a variety of protein digesting enzymes. You
can think of proteins as being a long chain of the AAs, the enzymes basically act like scissors, cutting the
chains into smaller and smaller bits.
Prior to absorption into the bloodstream, whole proteins have been broken down to provide single AAs along
with two and three AA chains (called di- and tri-peptides); further breakdown occurs in the intestinal cells
themselves, finally releasing individual amino acids into the bloodstream.
Generally speaking, AA chains larger than three in length will not be absorbed to any appreciable degree. I’d
note that occasionally very small amounts of longer amino acid chains can slip through and this is especially
the case in situations like leaky gut syndrome where the normal functioning of the gut has been
compromised.
This is actually a very bad thing as the body tends to launch immune/allergic responses to the presence of
undigested protein in the bloodstream; which is a big part of why the gut is set up to not allow larger protein
chains into the bloodstream under normal circumstances.
Related to this is a recurrent idea, usually in sports nutrition, of supplements containing protein based
hormones such as Growth Hormone (GH), Insulin-Like Growth Factor 1 (IGF-1) or others being orally
consumed. This can’t work due to the way human digestion of protein works, such peptide hormones will
simply be digested in the gut and lose their biological availability.
Let me put this a different way: major pharmaceutical companies have been trying to make an oral insulin
(another protein based hormone) for diabetic treatment and have basically given up on it; it took weirdly
functioning drugs and there were huge problems with implementation. If the big drug companies haven’t
figured out how to do it, neither has the protein powder company claiming it in their ads.

So What is Digestibility?

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Now, the above makes it sound like all ingested protein gets into the bloodstream after digestion but this is
far from the case. No process in the human body works at 100% efficiency and this is one of them. For
various reasons, a proportion of all ingested nutrients will escape digestion, continuing through the intestine
to eventually end up in your poop. Fat is typically absorbed with up to 97% efficiency and carbs can vary
quite a bit depending on what you’re talking about. But what about protein?
Researchers define protein digestibility as the amount of protein absorbed into the body relative to the
amount that was consumed. A quick note: researchers are actually measuring nitrogen absorption and
excretion, rather than protein or amino acids per se, but I don’t want to get into the technical details of that
here.
So, for example, they might feed someone 50 grams of protein and then see how much comes out the other
end. Let’s say that 5 grams of protein show up in the poop. That means that 45 grams of the 50 grams
ingested were actually absorbed and that protein would have a digestibility of 90% (45 grams absorbed/50
grams ingested = 0.90 * 100 = 90%).
If 50 grams of protein were fed and 25 grams showed up in the poop, that protein would have a digestibility
of only 50% (25 grams absorbed/50 grams ingested = 0.50 * 100 = 50%). Get it?
I want to note that a lot of very silly claims are often made about protein digestibility. Companies selling
protein powders argue that the digestibility of their product is impossibly high, vegetarians usually ignore the
research on this topic to claim that vegetarian proteins have higher digestibility than animal source proteins,
on and on it goes. The research on this is extremely clear and I’ve reproduced the chart from The Protein
Book on the digestibility of common foods below.

Food Source Protein Digestibility (%)

Egg 97

Milk and Cheese 97

Mixed US Diet 96

Peanut Butter 95

Meat and Fish 94

Whole Wheat 86

Oatmeal 86

Soybeans 78

Rice 76

Source: National Research Council. Recommended Dietary Allowances, 10th ed. National
Academy Press, 1989.

Looking at the chart above, two major things stand out. The first is that, contrary to the occasional vegetarian
claim, vegetable source proteins have a significantly lower digestibility than animal source proteins.
This actually has relevance for an issue beyond the scope of this article: protein requirements. Because
they provide less available protein from consumption, a larger amount of vegetable proteins have to be
consumed to meet human (or athletic) requirements.
The second is that commonly available animal-source food source proteins have extremely high
digestibilities, 94-97%. This means that for every 100 grams of protein consumed, 94-97 grams are being
digested and assimilated by the gut.

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Given that this likely represents the very high end of digestibility for humans (no process in humans is ever
100%). The odds of a given commercial product being significantly above this is unlikely. As well, even if it
were the overall real-world impact would be small.
That is, let’s say a given over-priced commercial protein powder achieved a true 99% digestibility. For every
100 grams consumed, you absorb 99 grams of protein. That’s only 2-5 more grams than a much cheaper
whole-food protein. And given that you’ll likely be paying 2-3 times as much for the ‘magic protein powder’,
this seems a pretty silly path to pursue.
Which isn’t to say that the protein powder might not have other advantages in a certain circumstance. For
example, perhaps the protein powder digests more quickly than the food; this might be valuable under certain
circumstances (or negative in others). Which is as good a bridge as I can give to the topic I’m going to
discuss in Part 3 of this series: Digestion Speed.

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Ketogenic Diets: High-fat or High-Protein – Q&A
Question: I’m familiar with the “true” ketogenic diet of 90% fat which historically is a medical diet used to
assist in controlling seizure prone individuals, but it has the added advantage of being a fantastic way to
shed weight while keeping the brain fed. In your RAPID FAT LOSS diet, you say it’s basically a ketogenic
diet but without the dietary fat – why? If I were to choose between the 2 ketogenic diets, why choose 90-
95% PROTEIN over 90-95% FAT????

Answer: The issue, as always, comes down to a matter of context. The original epilepsy ketogenic diet was
developed, as you note to control seizures. And for whatever reason, at least one aspect of that was
developing very, very deep degrees of ketosis. For this reason, a very high dietary fat content and lowish
protein intake is necessary. This is for reasons discussed in Ketosis and the Ketogenic Ratio – Q&A. Protein
has about a half anti-ketogenic effect and too much dietary protein can inhibit ketosis. Which makes the
epilepsy diet not work. So in that context, the diet had to be set up with very high fat and low protein.
And while such a diet may make people lose WEIGHT quickly, simply losing WEIGHT is not necessarily the
goal. Rather, the goal is (or should be) to lose FAT while maintaining MUSCLE mass. I discussed this
difference in some detail in the Rapid Fat Loss Handbook itself (as well as in every other of my books) or
you can read the article What Does Body Composition Mean?
That is, people who want to change body composition aren’t just interested in weight loss per se, they want
to maximize fat loss while (generally speaking) minimizing the loss of lean body mass. And the simple fact
is that a 90% fat ketogenic diet, due to the low protein content won’t do that. Rather, dietary protein has to
be set at a certain level to avoid lean body mass losses.
And since the explicit goal of the Rapid Fat Loss Handbook diet is to maximize fat loss (again while
minimizing lean body mass loss) that also means cutting calories to the bone. That means reducing dietary
fat to minimal levels (only essential fatty acids). And, mind you, such a diet would be wholly inappropriate
(it wouldn’t work) for epilepsy treatment.
And that’s your answer. If the goal were epilepsy treatment, the high-fat ketogenic diet would be the
appropriate choice (I’d point anyone interested in this topic to The Ketogenic Diet: A Treatment for Epilepsy,
3rd Edition (Paperback) by Freeman, Freeman and Kelly). But assuming the goal is maximal fat loss with
no muscle loss (e.g. the goal of most who read my site), a higher protein intake is required and the very
high-fat version of the ketogenic diet would be wholly inappropriate.
And, in the context of Rapid Fat Loss Handbook, given the explicit goals of that diet, that means keeping fat
intake very low (limited only to essential fatty acids and the tagalongs that are unavoidable with whole
foods). Of course, more moderate ketogenic diets with sufficient dietary protein and higher dietary fat
intakes can also be set up as described in my first book The Ketogenic Diet. The rate of fat loss will simply
be slower on such a diet due to the higher caloric intake. But that may be a reasonable compromise for
reasons discussed in Setting the Deficit – Small, Moderate, or Large.
Hope that clears it up and thanks for the question.

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Effects of Soy Protein and Soybean Isoflavones on Thyroid
Function in Healthy Adults and Hypothyroid Patients – Research
Review

Title and Abstract

Messina M, Redmond G. Effects of soy protein and soybean isoflavones on thyroid function in healthy adults
and hypothyroid patients: a review of the relevant literature. Thyroid. (2006) 16:249-58.
Soy foods are a traditional staple of Asian diets but because of their purported health benefits they have
become popular in recent years among non-Asians, especially postmenopausal women. There are many
bioactive soybean components that may contribute to the hypothesized health benefits of soy but most
attention has focused on the isoflavones, which have both hormonal and nonhormonal properties. However,
despite the possible benefits concerns have been expressed that soy may be contraindicated for some
subsets of the population. One concern is that soy may adversely affect thyroid function and interfere with
the absorption of synthetic thyroid hormone. Thus, the purpose of this review is to evaluate the relevant
literature and provide the clinician guidance for advising their patients about the effects of soy on thyroid
function. In total, 14 trials (thyroid function was not the primary health outcome in any trial) were identified in
which the effects of soy foods or isoflavones on at least one measure of thyroid function was assessed in
presumably healthy subjects; eight involved women only, four involved men, and two both men and women.
With only one exception, either no effects or only very modest changes were noted in these trials. Thus,
collectively the findings provide little evidence that in euthyroid, iodine-replete individuals, soy foods, or
isoflavones adversely affect thyroid function. In contrast, some evidence suggests that soy foods, by
inhibiting absorption, may increase the dose of thyroid hormone required by hypothyroid patients. However,
hypothyroid adults need not avoid soy foods. In addition, there remains a theoretical concern based on in
vitro and animal data that in individuals with compromised thyroid function and/or whose iodine intake is
marginal soy foods may increase risk of developing clinical hypothyroidism. Therefore, it is important for soy
food consumers to make sure their intake of iodine is adequate.

Introduction

Soy protein is one of those topics that seems to be a perennial topic of debate and argument with staunch
pro- and anti-soy people out there making all kinds of seemingly good arguments for either the benefits or
dangers of soy protein. As is usually the case with extremist positions, I find that the reality lies somewhere
in the middle.
Now, I think that part of the problem, as I explained in a seminar a few weeks ago, is how people, at least
those in the United States (I can’t speak to the rest of the world) tend to approach things. Folks are prone
to extremes in the first place and nowhere is this more prevalent than in the health field.
Whenever some nutrient is discovered to be ‘healthy’, invariably people figure that more must be better and
start mega-dosing it. This invariably leads to some sort of backlash as people learn (often the hard way)
that more is, in fact, not better. Then they invariably go on a crusade against that nutrient not realizing that
their own extreme behavior (rather than the nutrient itself) was the actual cause of the problem.
One of my favorite examples is that of oat bran back in the 80’s. Discovered to improve blood lipid levels,
people starting eating mountains of the stuff, 50+ grams per day. People were putting down horse-doses of

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the stuff because, you know, more is better. Until it was found that such massive fiber intakes, especially
from isolated sources, had the potential to cause vitamin and mineral deficiencies by binding them up before
they could be absorbed.
Which brings me in a roundabout way to the issue of today’s research review on soy protein and thyroid
function. As per usual, there are camps on both sides of the debate for soy protein having either a beneficial
or negative effect on thyroid hormones. And also as per usual, the truth of the matter, in terms of how soy
protein affects thyroid hormones lies somewhere in the middle and depends on other factors. Today’s review
looks at them.

Background

To give readers a brief background on the topic, the thyroid gland releases two primary hormones T4 and
T3 (thyroxine and trio-iodothyronine respectively) in a ratio of roughly 80:20 in response to the signal sent
by TSH (thyroid stimulating hormone). That is to say, most of the thyroid released from the thyroid gland
itself is the relatively inactive T4. Most T3 is actually made in other tissues (especially the liver but also in
many other cells) from the metabolism of T4 via an enzyme called 5′-deiodinase.
Now, I imagine most readers think of T3 in terms of its effects on body weight or body fat and it’s certainly
true that T3, along with the catecholamines (adrenaline/noradrenaline or epinephrine/norepinephrine
depending on which side of the pond you’re on) are two of the primary regulators of human metabolic rate. Of
course, thyroid controls about a billion other things in the body too and, as one example, low T3 status can
cause depression.
I should mention that iodine intake plays a crucial role in thyroid metabolism with inadequate intake of iodine
causing thyroid problems. There are many other micronutrients that are involved in this conversion process
as well; these include selenium and iron (iron deficiency can impair thyroid conversion, yet another reason
to eat red meat while dieting).
Now soy proteins are known to contain hormonal mimics called phytoestrogens. This include genistien,
daidzein and others. A great deal of controversy exists over the impact of these types of compounds in the
human diet; while phytoestrogens may have some beneficial effects (especially in post-menopausal women
for whom low estrogen can predispose towards heart disease and bone loss) other research shows negative
impacts. A lot of whether positive or negative impacts are seen depends on what’s being looked at and, of
course, the dose studied.
The effect of phytoestrogens in men is far less studied and understood. While many are concerned that the
phytoestrogens present in soy may negatively impact on testosterone levels the reality is that the studies
done to date, using moderate doses of soy/phytoestrogens, have found little to no impact (higher doses are
often seen to cause issues).
There is likely to be a sex and population specific response to these compounds and whether or not soy has
an impact on anything at all depends heavily on the amount being consumed. Small amounts of soy protein
tend to have minimal or no effects on most things studied (such as testosterone levels) while large daily
amounts are often seen to have an effect.
There’s an old saw in medicine that the dose makes the poison and this is certainly one of those situations.
And, as I noted in the introduction, I think part of the backlash against soy has more to do with the human
nature of people thinking more is better than with the nutrient itself. As I mention below, the actual soy intake
among Asian cultures doesn’t appear to be that high in the first place (and anyone who is worried about the

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impact on testosterone levels might consider that Asians, as a whole, don’t seem to be having many
problems with fertility or making babies).
Again, I’m not going to focus on all of the potential effects of soy (e.g. on hormones such as testosterone)
here; I only want to look at the impact, or potential impact of soy protein on thyroid hormone metabolism.

The Paper

So with that background out of the way, on to today’s research review, a review paper on the impact of soy
protein on thyroid hormone status and metabolism. As I noted above, there are two primary thyroid
hormones, T4 and T3 and it appears that soy may have an impact on both.
Early work, in animals, had supported the idea that soy proteins could actually increase thyroid (mainly T4)
output and this is likely where a lot of the pro-soy claims come from in terms of thyroid status (e.g. some will
claim that soy will help fat loss by raising thyroid hormones).
However, as the paper points out, studies suggests a very different effect in humans with soy protein having
little to no direct impact on thyroid hormone output. This is yet another place where extrapolating from animal
research just doesn’t pan out. Of course, there is also animal research suggesting a negative impact of soy
protein, primarily the phytoestrogens, on animal thyroid status, something the pro-soy folks seem to ignore
when they claim that soy will increase thyroid output.
Beyond that, at least in individuals with normal thyroid function, soy protein appears to have little to no impact
on overall thyroid status. The review examined 14 different studies (as noted above, 8 in women, 4 in men
and 2 in both) and, with one exception, found little to no impact of soy intake on any measure of thyroid
hormone status. I’ll spare you all of the details, only the punchline is of any real importance. Again, that’s
in individuals with otherwise normal thyroid function.
However, in individuals with pre-existing low-thyroid (hypothyroid) symptoms, soy proteins can cause
problems. Research has shown that soy protein intake may increase the dose of thyroid medication needed
(the soy appears to impair uptake of thyroid medication) and individuals who are on thyroid hormones may
need to avoid soy protein immediately around the intake of their medication.
Another review (Doerge DR. Goitrogenic and estrogenic activity of soy isoflavones. Environ Health Perspect.
(2002) 110 Suppl 3:349-53.2002) has shown, using mainly animal work, that the phytoestrogens in soy can
impair the enzyme (thyroid peroxidase) responsible for proper thyroid hormone production. That same
review found that while soy protein itself could not induce a hypothyroid state, a high phytoestrogen intake
coupled with a low iodine intake could.
I bring up this last point because one of the main providers of iodine in the modern diet is iodized salt and
even there, diet surveys have shown a downward trend in overall iodine intake (due to a reliance on
processed food and less iodinization of salt). It’s worth noting that seaweed (another stable in Asian culture)
is another good source of iodine. Even if Asian cuisine did contain a tremendous amount of soy, it would
seem that the intake of seaweed, by providing iodine, would help to prevent problems from occurring.
Basically, I could see how a high intake of soy products (which are being used to fortify many foods such as
cereals and protein bars, in addition to the use of soy protein powders) coupled with a misguided attempt to
reduce salt intakes excessively (as is often seen in many ‘health-conscious’ individuals) could potentially
cause proteins with overall thyroid metabolism.
But, and this goes to my comments earlier in the article, this is only an issue with people insistent on taking
aspects of their diet to extremes. People who are really consuming a massive amount of soy protein on a
daily basis (that intake level not being seen in the Asian cultures in the first place) who also are trying to

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minimize sodium intake could be putting themselves at potential risk. And this is moreso the case if there is
a pre-existing problem.

Summing Up

So we have several different issues at stake here in terms of how soy protein might impact on thyroid
hormone status.
Clearly individuals with no pre-existing thyroid problems don’t need to worry much about soy. And, no, I’m
not saying that folks should therefore eat as much of it as possible. Just that they needn’t go out of their
way to avoid any and all source of soy in their diet.
But what about people who do have a pre-existing thyroid problem?
First and foremost, anybody who is on thyroid medication should avoid consuming soy immediately before
or after taking their medication as soy protein appears to impair absorption of thyroid medication. Individuals
insistent (for whatever reason) on consuming soy near to the intake of their thyroid medication will need to
increase their dose to compensate. This, of course, should be dealt with through your medical
provider/health professional.
As well, individuals with pre-existing thyroid problems (and it’s worth mentioning that females, which tend to
be the primary target for soy foods, are more likely to have thyroid problems than men) may need to limit
their soy intake on a day to day basis. This is especially the case for individuals intent on reducing their
sodium intake.
So…recommendations.
Trying to avoid every last bit of soy intake (for example, a typical soy protein fortified cereal may contain a
few grams at most of soy) seems misguided to me, most studies examining a variety of endpoints find that
it’s only when soy protein intake is excessive that any sorts of problems start. Even in the case of hypothyroid
individuals, soy only appears to be a problem when iodine intake is insufficient in the first place.
Clearly, living on nothing but soy foods and soy fortified products is misguided as well. As I mentioned
above, the soy intake among most Asian cultures isn’t actually that massive in the first place and I suspect
that much of the backlash against soy is primarily to do with people taking a little of a good thing, assuming
a lot was better, and causing themselves problems because of it.
To me a happy medium seems the best; assuming no pre-existing thyroid problems, soy products are
probably safe in moderation. What’s moderation? In The Protein Book, I suggested a daily maximum of
perhaps 20-25 grams of soy protein on a daily basis. Based on the average phytoestrogen content of most
soy proteins (generally 2-3 mg phytoestrogen per gram of soy protein), that will keep most people below the
threshold where any sorts of issues start to crop up.
I should mention that many foods are currently being fortified with soy protein (check the labels) and people
may already be consuming soy protein in some amounts without knowing it. Adding more (e.g. through a
soy protein powder) may very well take people above the level I suggested above.
Frankly, unless someone is a fairly strict vegetarian or vegan, there are enough other high quality protein
sources (such as meat, dairy products, whey, etc.) that I don’t see the need to consume massive amounts
of soy in the first place. But neither do I think it’s a horrible protein that no-one should ever eat because it
will make their testosterone drop and give men boobs.
Soy, like all proteins has a variety of pros and cons and, in moderation, can make up part of a healthy or
sports oriented diet. Thinking that it is evil and must be eliminated is as silly as thinking it’s the best protein
ever and people should consume tons of it.

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137
The effect of protein timing on muscle
strength and hypertrophy: a meta-analysis

This is an Open Access article distributed under the terms of the Creative Commons Attribution
License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use,
distribution, and reproduction in any medium, provided the original work is properly cited. The
Creative Commons Public Domain Dedication waiver
(http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this

article, unless otherwise stated. Abstract

Protein timing is a popular dietary strategy designed to optimize the adaptive response to
exercise. The strategy involves consuming protein in and around a training session in an effort to
facilitate muscular repair and remodeling, and thereby enhance post-exercise strength- and
hypertrophy-related adaptations. Despite the apparent biological plausibility of the strategy,
however, the effectiveness of protein timing in chronic training studies has been decidedly mixed.
The purpose of this paper therefore was to conduct a multi-level meta-regression of randomized
controlled trials to determine whether protein timing is a viable strategy for enhancing post-
exercise muscular adaptations. The strength analysis comprised 478 subjects and 96 ESs, nested
within 41 treatment or control groups and 20 studies. The hypertrophy analysis comprised 525
subjects and 132 ESs, nested with 47 treatment or control groups and 23 studies. A simple pooled
analysis of protein timing without controlling for covariates showed a small to moderate effect on
muscle hypertrophy with no significant effect found on muscle strength. In the full meta-
regression model controlling for all covariates, however, no significant differences were found
between treatment and control for strength or hypertrophy. The reduced model was not
significantly different from the full model for either strength or hypertrophy. With respect to
hypertrophy, total protein intake was the strongest predictor of ES magnitude. These results
refute the commonly held belief that the timing of protein intake in and around a training session
is critical to muscular adaptations and indicate that consuming adequate protein in combination
with resistance exercise is the key factor for maximizing muscle protein accretion.

Background

Protein timing is a popular dietary strategy designed to optimize the adaptive response to exercise
[1]. The strategy involves consuming protein in and around a training session in an effort to
facilitate muscular repair and remodeling, and thereby enhance post-exercise strength- and
hypertrophy-related adaptations [2]. It is generally accepted that protein should be consumed just
before and/or immediately following a training session to take maximum advantage of a limited
anabolic window [3]. Proponents of the strategy claim that, when properly executed, precise
intake of protein in the peri-workout period can augment increases in fat-free mass [4]. Some
researchers have even put forth the notion that the timing of food intake may have a greater
positive effect on body composition than absolute daily nutrient consumption [5].

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A number of studies support the superiority of protein timing for stimulating increases in acute
protein synthesis pursuant to resistance training when compared to placebo [6-9]. Protein is
deemed to be the critical nutrient required for optimizing post-exercise protein synthesis. The
essential amino acids, in particular, are believed primarily responsible for enhancing this response,
with little to no contribution seen from provision of non-essential amino acids [10,11]. Borsheim et
al. [10] found that a 6 g dose of essential amino acids (EAAs) consumed immediately post-
exercise produced an approximate twofold increase in net protein balance compared to a
comparable dose containing an approximately equal mixture of essential and non-essential amino
acids, indicating a dose–response relationship up to 6 g EAAs. However, increasing EAA intake
beyond this amount has not been shown to significantly heighten post-exercise protein synthesis
[2]. There is limited evidence that carbohydrate has an additive effect on enhancing post-exercise
muscle protein synthesis when combined with amino acid ingestion [12], with a majority of studies
failing to demonstrate any such benefit [13-15].

Despite the apparent biological plausibility of the strategy, the effectiveness of protein timing in
chronic training studies has been decidedly mixed. While some studies have shown that
consumption of protein in the peri-workout period promotes increases in muscle strength and/or
hypertrophy [16-19], others have not [20-22]. In a review of literature, Aragon and Schoenfeld
[23] concluded that there is a lack of evidence to support a narrow “anabolic window of
opportunity” whereby protein need to be consumed in immediate proximity to the exercise bout to
maximize muscular adaptations. However, these conclusions were at least in part a reflection of
methodological issues in the current research. One issue in particular is that studies to date have
employed small sample sizes. Thus, it is possible that null findings may be attributable to these
studies being underpowered, resulting in a type II error. In addition, various confounders including
the amount of EAA supplementation, matching of protein intake, training status, and variations in
age and gender between studies make it difficult to draw definitive conclusions on the topic. Thus,
by increasing statistical power and controlling for confounding variables, a meta-analysis may help
to provide clarity as to whether protein timing confers potential benefits in post-exercise skeletal
muscle adaptations.

A recent meta-analysis by Cermak et al. [24] found that protein supplementation, when combined
with regimented resistance training, enhances gains in strength and muscle mass in both young
and elderly adults. However, this analysis did not specifically investigate protein timing per se.
Rather, inclusion criteria encompassed all resistance training studies in which at least one group
consumed a protein supplement or modified higher protein diet. The purpose of this paper
therefore is to conduct a meta-analysis to determine whether timing protein near the resistance
training bout is a viable strategy for enhancing muscular adaptations.

Methodology

Inclusion criteria

Only randomized controlled trials or randomized crossover trials involving protein timing were
considered for inclusion. Protein timing was defined here as a study where at least one treatment
group consumed a minimum of 6 g essential amino acids (EAAs) ≤ 1 hour pre- and/or post-

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resistance exercise and at least one control group did not consume protein < 2 hours pre- and/or
post-resistance exercise. Resistance training protocols had to span at least 6 weeks and directly
measure dynamic muscle strength and/or hypertrophy as a primary outcome variable. There were
no restrictions for age, gender, training status, or matching of protein intake, but these variables
were controlled via subgroup analysis using meta-regression.

Search strategy

To carry out this review, English-language literature searches of the PubMed and Google Scholar
databases were conducted for all time periods up to March 2013. Combinations of the following
keywords were used as search terms: “nutrient timing”; “protein supplementation”; “nutritional
supplementation”; “protein supplement”; “nutritional supplement”; “resistance exercise”;
“resistance training”; “strength training”. Consistent with methods outlined by Greenhalgh and
Peacock [25], the reference lists of articles retrieved in the search were then screened for any
additional articles that had relevance to the topic. Abstracts from conferences, reviews, and
unpublished dissertations/theses were excluded from analysis. A total of 34 studies were identified
as potentially relevant to this review. To reduce the potential for selection bias, each of these
studies were independently perused by two of the investigators (BJS and AAA), and a mutual
decision was made as to whether or not they met basic inclusion criteria. Study quality was then
assessed with the PEDro scale, which has been shown to be a valid measure of the methodologic
quality of RCTs [26] and possesses acceptable inter-rater reliability [27]. Only those studies
scoring ≥5 on the PEDro scale--a value considered to be of moderate to high quality [27]-were
accepted for analysis. Any inter-reviewer disagreements were settled by consensus and/or
consultation with the third investigator. Initial pre-screening revealed 29 potential studies that
investigated nutrient timing with respect to muscular adaptations. Of these studies, 3 did not meet
criteria for sufficient supplemental protein intake [28-30] and in another the timing of
consumption was outside the defined post-workout range [31]. Thus, a total of 25 studies
ultimately were deemed suitable for inclusion. Two of the studies were subsequently excluded
because they did not contain sufficient data for calculating an effect size and attempts to obtain
this information from the authors were unsuccessful [19,32], leaving a total 23 studies suitable for
analysis. The average PEDro score of these studies was 8.7, indicating an overall high level of
methodological quality. Table 1 summarizes the studies meeting inclusion criteria.

Table 1. Summary of studies meeting inclusion criteria

Coding of studies

Studies were read and individually coded by two of the investigators (BJS and AAA) for the
following variables: Descriptive information of subjects by group including gender, body mass,
training status (trained subjects were defined as those with at least one year resistance training
experience), age, and stratified subject age (classified as either young [18–49 years] or elderly
[50+ years]; whether or not total daily protein intake between groups was matched; whether the
study was an RCT or crossover design; the number of subjects in each group; blinding (classified
as single, double, or unblinded); duration of the study; type of hypertrophy measurement (MRI,
CT, ultrasound, biopsy, etc.) and region/muscle of body measured, if applicable; lean body mass

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measurement (i.e. DXA, hydrostatic weighing, etc.), if applicable, and; strength exercise (s)
employed for testing, if applicable. Coding was cross-checked between coders, and any
discrepancies were resolved by mutual consensus. To assess potential coder drift, 5 studies were
randomly selected for recoding as described by Cooper et al. [50]. Per case agreement was
determined by dividing the number of variables coded the same by the total number of variables.
Acceptance required a mean agreement of 0.90.

Calculation of effect size

For each 1-RM strength or hypertrophy outcome, an effect size (ES) was calculated as the pretest-
posttest change, divided by the pretest standard deviation (SD) [51]. The sampling variance for
each ES was estimated according to Morris and DeShon [51]. Calculation of the sampling variance
required an estimate of the population ES, and the pretest-posttest correlation for each individual
ES. The population ES was estimated by calculating the mean ES across all studies and treatment
groups [51]. The pretest-posttest correlation was calculated using the following formula [51]:

Statistical analyses

Meta-analyses were performed using hierarchical linear mixed models, modeling the variation
between studies as a random effect, the variation between treatment and control groups as a
random effect nested within studies, and group-level predictors as fixed effects [53]. The within-
group variances were assumed known. Observations were weighted by the inverse of the sampling
variance [51]. An intercept-only model was created, estimating the weighted mean ES across all
studies and treatment groups. Second, a basic model was created which only included the class of
the group (treatment or control) as a predictor. A full model was then created with the following
predictors: the class of the group (treatment or control), whether or not the groups were protein
matched, training status (experienced or novice), blinding (double, single, or none), gender (male,
female, or mixed), age (young or old), body mass in kg, and the duration of the study in weeks.
The full model was then reduced by removing one predictor at a time, starting with the most
insignificant predictor [54]. The final model represented the reduced model with the lowest
Akaike’s Information Corrected Criterion (AICC) [55] and that was not significantly different
(P > 0.05) from the full model when compared using a likelihood ratio test (LRT). Model
parameters were estimated by the method of restricted maximum likelihood (REML) [56]; an
exception was during the model reduction process, in which parameters were estimated by the
method of maximum likelihood (ML), as LRTs cannot be used to compare nested models with
REML estimates. Denominator df for statistical tests and CIs were calculated according to Berkey
et al. [57]. The treatment/control classification variable was not removed during the model
reduction process.

Separate analyses were performed for strength and hypertrophy. ESs for both changes in cross-
sectional area (CSA) and FFM were pooled in the hypertrophy analysis. However, because
resistance exercise is associated with the accretion of non-muscle tissue, separate sub-analyses
on CSA and FFM were performed. Because the effect of protein timing might interact with whether
the treatment and control groups were matched for total protein intake, an additional model was
created that included an interaction term between the treatment/control classification variable and

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the protein match variable. Also, because the effect of protein timing might vary by training
experience, a model was created that included an interaction term between the treatment/control
classification variable and the training status variable. Adjustment for post hoc multiple
comparisons was performed using a simulation-based procedure [58]. All analyses were
performed using SAS Enterprise Guide Version 4.2 (Cary, NC). Effects were considered significant
at P ≤ 0.05. Data are reported as means (±SEs) and 95% CIs.

Results

Study characteristics

The strength analysis comprised 478 subjects and 96 ESs, nested within 41 treatment or control
groups and 20 studies. The weighted mean strength ES across all studies and groups was
1.39 ± 0.24 (CI: 0.88, 1.90). The hypertrophy analysis comprised 525 subjects and 132 ESs,
nested with 47 treatment or control groups and 23 studies. The weighted mean hypertrophy ES
across all studies and groups was 0.47 ± 0.08 (CI: 0.31, 0.63).

Basic model

There was no significant difference between the treatment and control for strength
(difference = 0.38 ± 0.36; CI: -0.34, 1.10; P = 0.30). The mean strength ES difference between
treatment and control for each individual study, along with the overall weighted mean difference
across all studies, is shown in Figure 1. For hypertrophy, the mean ES was significantly greater in
the treatment compared to the control (difference = 0.24 ± 0.10; CI: 0.04, 0.44; P = 0.02). The
mean hypertrophy ES difference between treatment and control for each individual study, along
with the overall weighted mean difference across all studies, is shown in Figure 2.

Full model

In the full meta-regression model controlling for all covariates, there was no significant difference
between the treatment and control for strength (difference = 0.28 ± 0.40; CI: -0.52, 1.07;
P = 0.49) or hypertrophy (difference =0.16 ± 0.11; CI: -0.07, 0.38; P = 0.18).

Reduced model: strength

After the model reduction procedure, only training status and blinding remained as significant
covariates. The reduced model was not significantly different from the full model (P = 0.73). In the
reduced model, there was no significant difference between the treatment and control
(difference = 0.39 ± 0.36; CI: -0.34, 1.11; P = 0.29). The mean ES for control was 0.93 ± 0.31 (CI:
0.32, 1.54). The mean ES for treatment was 1.31 ± 0.30 (CI: 0.71, 1.92).

Reduced model: hypertrophy

After the model reduction procedure, total protein intake, study duration, and blinding remained
as significant covariates. The reduced model was not significantly different from the full model

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(P = 0.87). In the reduced model, there was no significant difference between the treatment and
control (difference = 0.14 ± 0.11; CI: -0.07, 0.35; P = 0.20). The mean ES for control was
0.36 ± 0.09 (CI: 0.18, 0.53). The mean ES for treatment was 0.49 ± 0.08 (CI: 0.33, 0.66). Total
protein intake (in g/kg) was the strongest predictor of ES magnitude (estimate = 0.41 ± 0.14; CI:
0.14, 0.69; P = 0.004).

To confirm that total protein intake was mediator variable in the relationship between protein
timing and hypertrophy, a model with only total protein intake as a covariate was created. The
difference between treatment and control was not significant (difference = 0.14 ± 0.11; CI: -0.07,
0.35,; P = 0.19). Total protein intake was a significant predictor of ES magnitude
(estimate = 0.39 ± 0.15; CI: 0.08, 0.69; P = 0.01). Figure 3 shows the total protein intake-
adjusted ES’s for each study, as well as the overall effect from the meta-regression with only
total protein intake as a covariate.

Interactions

For strength, the interaction between treatment and training status was nearly significant
(P = 0.051), but post hoc comparisons between treatment and control within each training status
classification were not significant (adjusted P = 0.47 for difference within non-experienced groups,
and adjusted P = 0.99 for difference within experienced groups). There was no significant
interaction between treatment and whether groups were protein matched (P = 0.43). For
hypertrophy, there was no significant interaction between treatment and training status (P = 0.63)
or treatment and protein matching (P = 0.59).

Hypertrophy sub-analyses

Separating the hypertrophy analysis into CSA or FFM did not materially alter the outcomes. For
FFM, there was no significant difference between treatment and control (difference = 0.08 ± 0.07;
CI: -0.07, 0.24; P = 0.27). Total protein intake remained a strong predictor of ES magnitude
(estimate = 0.39 ± 0.07; CI: 0.25, 0.53; P < 0.001). For CSA, there was no significant difference
between treatment and control (difference = 0.14 ± 0.16; CI: -0.17, 0.46; P = 0.37). Total protein
intake was again a predictor of ES magnitude (estimate = 0.55 ± 0.24; CI: 0.08, 1.20; P = 0.02).

Discussion

This is the first meta-analysis to directly investigate the effects of protein timing on strength and
hypertrophic adaptations following long-term resistance training protocols. The study produced
several novel findings. A simple pooled analysis of protein timing without controlling for covariates
showed a significant effect on muscle hypertrophy (ES = 0.24 ± 0.10) with no significant effect
found on muscle strength. It is generally accepted that an effect size of 0.2 is small, 0.5 is
moderate, and 0.8 and above is a large, indicating that the effect of protein timing on gains in
lean body mass were small to moderate. However, an expanded regression analysis found that
any positive effects associated with protein timing on muscle protein accretion disappeared after
controlling for covariates. Moreover, sub-analysis showed that discrepancies in total protein intake
explained the majority of hypertrophic differences noted in timing studies. When taken together,

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these results would seem to refute the commonly held belief that the timing of protein intake in
the immediate pre- and post-workout period is critical to muscular adaptations [3-5].

Perceived hypertrophic benefits seen in timing studies appear to be the result of an increased
consumption of protein as opposed to temporal factors. In our reduced model, the amount of
protein consumed was highly and significantly associated with hypertrophic gains. In fact, the
reduced model revealed that total protein intake was by far the most important predictor of
hypertrophy ES, with a ~0.2 increase in ES noted for every 0.5 g/kg increase in protein ingestion.
While there is undoubtedly an upper threshold to this correlation, these findings underscore the
importance of consuming higher amounts of protein when the goal is to maximize exercise-
induced increases in muscle mass. Conversely, total protein intake did not have an impact on
strength outcomes and ultimately was factored out during the model reduction process.

The Recommended Dietary Allowance (RDA) for protein is 0.8 g/kg/day. However, these values
are based on the needs of sedentary individuals and are intended to represent a level of intake
necessary to replace losses and hence avert deficiency; they do not reflect the requirements of
hard training individuals seeking to increase lean mass. Studies do in fact show that those
participating in intensive resistance training programs need significantly more protein to remain in
a non-negative nitrogen balance. Position stands from multiple scientific bodies estimate these
requirements to be approximately double that of the RDA [59,60]. Higher levels of protein
consumption appear to be particularly important during the early stages of intense resistance
training. Lemon et al. [61] displayed that novice bodybuilders required a protein intake of 1.6-
1.7 g/kg/day to remain in a non-negative nitrogen balance. The increased protein requirements in
novice subjects have been attributed to changes in muscle protein synthetic rate and the need to
sustain greater lean mass rather than increased fuel utilization [62]. There is some evidence that
protein requirements actually decrease slightly to approximately 1.4 g/kg/day in well-trained
individuals because of a greater efficiency in dietary nitrogen utilization [63], although this
hypothesis needs further study.

The average protein intake for controls in the unmatched studies was 1.33 g/kg/day while average
intake for treatment was 1.66 g/kg/day. Since a preponderance of these studies involved
untrained subjects, it seems probable that a majority of any gains in muscle mass would have
been due to higher protein consumption by the treatment group. These findings are consistent
with those of Cermak et al. [24], who found that protein supplementation alone produced
beneficial adaptations when combined with resistance training. The study by Cermak et al. [24]
did not evaluate any effects regarding timing of intake, however, so our results directly lend
support to the theory that meeting target protein requirements is paramount with respect to
exercise-induced muscle protein accretion; immediate intake of dietary protein pre and/or post-
workout would at best appear to be a minor consideration. The findings also support previous
recommendations that a protein consumption of at least 1.6 g/kg/day is necessary to maximize
muscle protein accretion in individuals involved in resistance training programs [61].

For the matched studies, protein intake averaged 1.91 g/kg/day versus 1.81 g/kg/day for
treatment and controls, respectively. This level of intake for both groups meets or exceeds
suggested guidelines, allowing for a fair evaluation of temporal effects. Only 3 studies that

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employed matched protein intake met inclusion criteria for this analysis, however. Interestingly, 2
of the 3 showed no benefits from timing. Moreover, another matched study actually found
significantly greater increases in strength and lean body mass from a time-divided protein dose
(i.e. morning and evening) compared with the same dose provided around the resistance training
session [19]. However, this study had to be excluded from our analysis because it lacked
adequate data to calculate an ES. The sum results of the matched-protein studies suggest that
timing is superfluous provided adequate protein is ingested, although the small number of studies
limits the ability to draw firm conclusions on the matter.

This meta-analysis had a number of strengths. For one, the quality of studies evaluated was high,
with an average PEDro score of 8.7. Also, the sample was relatively large (23 trials encompassing
478 subjects for strength outcomes and 525 subjects for hypertrophy outcomes), affording good
statistical power. In addition, strict inclusion/exclusion criteria were employed to reduce the
potential for bias. Combined, these factors provide good confidence in the ability draw relevant
inferences from findings. Another strength was the rigid adherence to proper coding practices.
Coding was carried out by two of the investigators (BJS and AAA) and then cross-checked between
coders. Coder drift was then assessed by random selection of studies to further ensure consistency
of data. Finally and importantly, the study benefited from the use of meta-regression. This
afforded the ability to examine the impact of moderator variables on effect size and explain
heterogenecity between studies [64]. Although initial findings indicated an advantage conferred by
protein timing, meta-regression revealed that results were confounded by discrepancies in
consumption. This ultimately led to the determination that total protein intake rather than
temporal factors explained any perceived benefits.

There are several limitations to this analysis that should be taken into consideration when drawing
evidence-based conclusions. First, timing of the meals in the control groups varied significantly
from study to study. Some provided protein as soon as 2 hours post workout while others delayed
consumption for many hours. A recent review by Aragon and Schoenfeld [23] postulated that the
anabolic window of opportunity may be as long as 4–6 hours around a training session, depending
on the size and composition of the meal. Because the timing of intake in controls were all treated
similarly in this meta-analysis, it is difficult to determine whether a clear anabolic window exists
for protein consumption beyond which muscular adaptations suffer.

Second, the majority of studies evaluated subjects who were inexperienced with resistance
exercise. It is well-established that highly trained individuals respond differently to the demands of
resistance training compared with those who lack training experience [65]. In part, this is
attributed to a “ceiling effect” whereby gains in muscle mass become progressively more difficult
as a trainee gets closer to his genetic hypertrophic potential. There also is emerging evidence
showing that regimented resistance exercise attenuates anabolic intracellular signaling in rodents
[66] and humans [67], conceivably diminishing the hypertrophic response. Our sub-analysis failed
to show an interaction effect between resistance training status and protein timing for either
strength or hypertrophy. However, statistical power was low because only 4 studies using trained
subjects met inclusion criteria. Future research should therefore focus on determining the effects
of protein timing on muscular adaptations in those with at least 1 year or more of regular,
consistent resistance training experience.

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Third, in an effort to keep our sample size sufficiently large, we pooled CSA and FFM data to
determine hypertrophy ES. FFM is frequently used as a proxy for hypertrophy, as it is generally
assumed that the vast majority of the gains in fat free mass from resistance training are
myocellular in nature. Nevertheless, resistance exercise also is associated with the accretion of
non-muscle tissue as well (i.e. bone, connective tissue, etc.). To account for any potential
discrepancies in this regard, we performed sub-analyses on CSA and FFM alone and the results
essentially did not change. For FFM, the difference between treatment and control was not
significant (P = 0.27), with a ES difference of -0.08. Protein intake again was highly significant,
with an ES impact of ~0.2 per every 1 g/kg/day. For CSA, the difference between treatment and
control was not significant (P = 0.37), with a ES difference of -0.14. Protein intake was again
significant (P = 0.02) with an ES impact of ~0.33 per every 0.5 g/kg.

Finally and importantly, there was a paucity of timing studies that attempted to match protein
intake. As previously discussed, our results show that total protein intake is strongly and positively
associated with post-exercise gains in muscle hypertrophy. Future studies should seek to control
for this variable so that the true effects of timing, if any, can be accurately assessed.

Practical applications

In conclusion, current evidence does not appear to support the claim that immediate (≤ 1 hour)
consumption of protein pre- and/or post-workout significantly enhances strength- or hypertrophic-
related adaptations to resistance exercise. The results of this meta-analysis indicate that if a peri-
workout anabolic window of opportunity does in fact exist, the window for protein consumption
would appear to be greater than one-hour before and after a resistance training session. Any
positive effects noted in timing studies were found to be due to an increased protein intake rather
than the temporal aspects of consumption, but a lack of matched studies makes it difficult to draw
firm conclusions in this regard. The fact that protein consumption in non-supplemented subjects
was below generally recommended intake for those involved in resistance training lends credence
to this finding. Since causality cannot be directly drawn from our analysis, however, we must
acknowledge the possibility that protein timing was in fact responsible for producing a positive
effect and that the associated increase in protein intake is merely coincidental. Future research
should seek to control for protein intake so that the true value regarding nutrient timing can be
properly evaluated. Particular focus should be placed on carrying out these studies with well-
trained subjects to better determine whether resistance training experience plays a role in the
response.

Competing interests

The authors declare that they have no competing interests.

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Casein Hydrolysate and Anabolic Hormones and Growth –
Research Review
I want to try something a little bit different for today’s research review. Rather than looking at a single study
in the kind of obsessive detail that only I and three readers really care about, I want to look at multiple studies
but in lesser detail. Not only will this hopefully make the article a bit more relevant and readable, it will let
me address more than a single topic at once.
With the sheer volume of research appearing on a weekly basis, this will at least help me to look at data in
a more timely fashion. I’d mention that, for anyone who wants an even better look at a lot of studies, you’d
be well served to consider Alan Aragon’s monthly Research Review which I reviewed in the confusingly titled
Alan Aragon Research Review – Product Review.
In any case, today I want to look at two recent studies which are:
1. Deglaire et al. Hydrolyzed dietary casein as compared with the intact protein reduces postprandial
peripheral, but not whole-body, uptake of nitrogen in humans. Am J Clin Nutr. (2009) 90(4):1011-22.
2. West et. al. Elevations in ostensibly anabolic hormones with resistance exercise enhance neither
training-induced muscle hypertrophy nor strength of the elbow flexors. J Appl Physiol. 2009 Nov 12.
For each study I’ll give a brief background to the topic, look at what was done and then jump straight to the
conclusions with some final summing up. As noted above, some of the detail will be left out but I figure that
anyone who is that interested in the details of methodology and such will simply get ahold of the full paper
and read it themselves.
.

Deglaire et al. Hydrolyzed dietary casein as compared with the


intact protein reduces postprandial peripheral, but not whole-body,
uptake of nitrogen in humans. Am J Clin Nutr. (2009) 90(4):1011-22.

BACKGROUND: Compared with slow proteins, fast proteins are more completely extracted in the splanchnic
bed but contribute less to peripheral protein accretion; however, the independent influence of absorption
kinetics and the amino acid (AA) pattern of dietary protein on AA anabolism in individual tissues remains
unknown. OBJECTIVE: We aimed to compare the postprandial regional utilization of proteins with similar
AA profiles but different absorption kinetics by coupling clinical experiments with compartmental modeling.
DESIGN: Experimental data pertaining to the intestine, blood, and urine for dietary nitrogen kinetics after a
15N-labeled intact (IC) or hydrolyzed (HC) casein meal were obtained in parallel groups of healthy adults (n
= 21) and were analyzed by using a 13-compartment model to predict the cascade of dietary nitrogen
absorption and regional metabolism. RESULTS: IC and HC elicited a similar whole-body postprandial
retention of dietary nitrogen, but HC was associated with a faster rate of absorption than was IC, resulting
in earlier and stronger hyperaminoacidemia and hyperinsulinemia. An enhancement of both catabolic (26%)
and anabolic (37%) utilization of dietary nitrogen occurred in the splanchnic bed at the expense of its further
peripheral availability, which reached 18% and 11% of ingested nitrogen 8 h after the IC and HC meals,
respectively. CONCLUSIONS: The form of delivery of dietary AAs constituted an independent factor of
modulation of their postprandial regional metabolism, with a fast supply favoring the splanchnic dietary
nitrogen uptake over its peripheral anabolic use. These results question a possible effect of ingestion of
protein hydrolysates on tissue nitrogen metabolism and accretion.

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My Comments: Ever since the pioneering work in the 90’s on fast and slow proteins, there has been
continued interest in the digestion speed of proteins and how that impacts on metabolism, performance and,
of course, muscle growth. In recent years, there have been many claims made for the superiority of faster
proteins to slower in terms of ‘speeding amino acids to muscle’ in terms of promoting growth.
As well, as many may note, a recent commercial product (T-nations Anaconda), who’s anabolic claims were
analyzed in perhaps the most commented article on the site in Alan’s Aragon’s guest article Supplement
Marketing on Steroids, has recently been released to the market.
For background, hydrolysates are simply whole proteins that have been pre-digested (through the addition
of enzymes during production) to some degree. The theory being that, due to this pre-digestion, the
hydrolysate will be digested in the stomach faster, getting aminos into the bloodstream faster and,
presumably, having a better effect on skeletal muscle than slower proteins.
But is it true? Guess.
The above study examined this issue by feeding 21 subjects 2 test meals containing ~26.5 grams of either
intact casein or it’s hydrolysate; the protein had been marked with radioactive nitrogen so that it’s fate after
ingestion could be tracked over the next 8 hours. The test meals also contained 96 grams of carbohydrate
and 23 grams of fat; this is worth noting as adding other nutrients to fast proteins often makes them behave
more like slow proteins. I’ll spare you the methodology, sufficed to say that tracking protein after it enters
the body is brutally complicated and involves a lot of modelling and various measurements of blood amino
acid levels and such.
Here’s what the study found. Over the time course studied (8 hours after ingestion), the hydrolyzed casein
product showed greater losses from digestion (that is, less was absorbed). As well, a greater amount of
the hydrolysate was oxidized for energy through deamination (a process by which the amino group is
stripped off the carbon backbone). Finally, a larger amount of the casein hydrolysate was used by the
splanchnic bed (gut and intestines) with significantly less of the total protein reaching the bloodstream or
peripheral tissues (muscles).
To quote the researchers:
Despite similar overall net postprandial protein utilization, our results indicate important differences in
metabolic partitioning and kinetics between protein sources characterized by a preferential utilization of
dietary nitrogen by for splanchnic protein syntheses after HC [hydrolyzed casein] ingestion at the expense
of the incorporation into peripheral tissues.
Translating that into English: hydrolyzed casein is digested more poorly, gets burned for energy to a greater
degree and gets used more by the gut than intact casein; the end result of this is that hydrolyzed casein
provides LESS amino acids to skeletal muscle after ingestion than intact casein protein.
So not only is the claim that hydrolysates are better at providing aminos faster to skeletal muscle wrong, the
reality is actually exactly reversed: intact casein is better for providing aminos to the muscle. I’d note that
other studies have found this as well: in one, intact protein provided MORE branched-chain amino acids into
the bloodstream than a hydrolyzed form.
I’d add to this that, as I discussed in The Protein Book, other data supports the idea that slower proteins may
actually be superior to faster proteins for muscle growth; in one set of studies, for example, milk protein (a
mix of slow and fast proteins) resulted in greater hypertophy than soy (a fast protein) over 8 weeks of training
and supplementation. As well hydrolyzed proteins tend to taste like bleach; it’s no coincidence that
Anaconda has to come with a separate flavoring intensifier: hydrolysates are gag-inducing. They can’t be
consumed straight.
Summing up: Hydrolysates are not only not superior to intact protein in terms of providing amino acids to
skeletal muscle, they are distinctly inferior. Their fast digestion speed leads to greater digestive losses,

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more oxidation via deamination and provides less amino acids to skeletal muscle. That’s on top of tasting
like vomit. Or at least making you want to.
.

West et. al. Elevations in ostensibly anabolic hormones with


resistance exercise enhance neither training-induced muscle
hypertrophy nor strength of the elbow flexors. J Appl Physiol. 2009
Nov 12.

The aim of our study was to determine whether resistance exercise-induced elevations in endogenous
hormones enhance muscle strength and hypertrophy with training. Twelve healthy young men (21.8 +/- 1.2
y, BMI = 23.1 +/- 0.6 kg(.)m(-2)) independently trained their elbow flexors for 15 weeks on separate days
and under different hormonal milieu. In one training condition, participants performed isolated arm curl
exercise designed to maintain basal hormone concentrations (low hormone, LH); in the other training
condition, participants performed identical arm exercise to the LH condition followed immediately by a high
volume of leg resistance exercise to elicit a large increase in endogenous hormones (High Hormone, HH).
There was no elevation in serum growth hormone (GH), insulin-like growth factor (IGF-1) or testosterone
after the LH protocol, but significant (P < 0.001) elevations in these hormones immediately and 15 and 30
min after the HH protocol. The hormone responses elicited by each respective exercise protocol late in the
training period were similar to the response elicited early in the training period indicating that a divergent
post-exercise hormone response was maintained over the training period. Muscle cross-sectional area
increased by 12% in LH and 10% in HH (P < 0.001) with no difference between conditions (condition x
training interaction, P = 0.25). Similarly, type I (P < 0.01) and type II (P < 0.001) muscle fiber CSA increased
with training with no effect of hormone elevation in the HH condition. Strength increased in both arms but
the increase was not different between the LH and HH conditions. We conclude that exposure of loaded
muscle to acute exercise-induced elevations in endogenous anabolic hormones enhances neither muscle
hypertrophy nor strength with resistance training in young men. Key words: testosterone, growth hormone,
IGF-1, anabolism.
My Comments: For several decades now, there has been intense focus on the acute hormonal response
to training. This started back in the 80’s where researchers, interested in growth did a rather cursory
examination of elite powerlifters and bodybuilders, made some assumptions about muscle size, made some
even bigger assumptions about how they trained, and then proceeded to reach some staggeringly poor
conclusions.
Basically, what they observed was that bodybuilders were bigger than powerlifters, which is debatable in the
first place. They also observed that powerlifters typically used low reps and long rest periods and
bodybuilders (remember: this was the Arnold era) trained with high reps and short rest periods. Thus they
concluded that high reps and short rest stimulated muscle growth and went looking for reasons why this was
the case. I’d note that this is not really how you’re supposed to do science: you don’t reach your conclusion
and go find reasons why it’s right. You test hypotheses and draw your conclusions from that. But I digress.
And the main focus for a while was potential differences in hormonal response to training, primarily focusing
on testosterone and growth hormone (GH). The basic study design that was followed was to compare the
acute hormonal response to either 3 sets of 5 repetitions with a long rest interval (3 minutes) to sets of 10
with a 1 minute rest interval. Repeatedly, studies showed that the first type of training boosted testosterone

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and the second GH. Entire training schemes have grown out of this but there was a problem: nobody ever
bothered to see if these acute (usually less than 10-15 minute) bumps in hormones actually did anything.
Nevermind that this makes little sense anyhow for a variety of reasons. Not the least of which is that women
have higher GH levels than men and get a bigger GH response to training, yet they don’t grow better. If
anything, with the known impact of testosterone on muscle growth, if there was to be any benefit to this,
you’d expect the lower rep/heavy work to be superior. Yet the researchers were arguing that it wasn’t. There
was a logic missing in the argument (not the least of which being the assumption that powerlifters had smaller
muscles than bodybuilders) that seemed to get skipped over.
In addition to the science, there is a long held belief, echoed in various places (including the comments
section of another contentious article I wrote titled Squats vs. Leg Press for Big Legs) that certain
movements, notably squats and deadlifts, will have full-body growth stimulating properties, generally
mediated through the hormonal response.
It’s not uncommon to see people recommending things like “If you want big arms, squat/train legs.” for
example. Essentially, heavy leg work is touted as being the key to overall growth. Nevermind that the same
people who make this argument will often complain about “All those guys in the gym with huge upper bodies
and no legs” without realizing that the two ideas contradict one another (that is, if leg training is required for
growth, how can guys get huge upper bodies without training legs). But I digress again.
In any case, this study examined the issue directly with a somewhat confusing study design: twelve healthy
young men trained their biceps on different days of the week under different training conditions. In what
they called the low-hormone condition, the biceps were trained all by themselves; no other exercise was
done. In the other called the high-hormone condition, the biceps were trained and then a large-volume of
leg training was done to elevate the supposedly anabolic hormones.
Does that make sense, all subjects trained both arms, but on different days and under different
conditions. And the training was far enough apart that the hormonal response from the leg training wouldn’t
have impacted the low-hormone training session. This training was followed for 15 weeks and subjects
consumed protein both before and after the training (so there was nutritional support).
Hormone levels were measured and while there was no significant change in hormones in the low-hormone
situation, in the high-hormone situation, there were increases in lactate, growth hormone, free and total
testosterone and IGF-1 with the peak occurring approximately 15 minutes after the leg work.
And, if the hormonal response to heavy leg training actually has any impact, what you’d expect to see is that
one arm, the one trained along with the leg training, would grow better.
Did it happen? Guess.
Both maximal strength and muscle cross sectional area increased identically in both arms to the tune of a
20% vs. 19% increase in strength for low- vs. high-hormones and an increase in skeletal muscle cross
sectional area of 12% vs. 10% in low- vs. high-hormones. These differences were not statistically significant.
Quoting the researchers:
Despite vast differences in hormone availability in the immediate post- exercise period, we found no
differences in the increases in strength or hypertrophy in muscle exercised under low or high hormone
conditions after 15 weeks of resistance training. These findings are in agreement with our hypothesis and
previous work showing that exercise-induced hormone elevations do not stimulate myofibrillar protein
synthesis (36) and are not necessary for hypertrophy (37). Thus, our data ((36) and present observations),
when viewed collectively, lead us to conclude that local mechanisms are of far greater relevance in regulating
muscle protein accretion occurring with resistance training, and that acute changes in hormones, such as
GH, IGF-1, and testosterone, do not predict or in any way reflect a capacity for hypertrophy.

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I don’t think it gets any clearer than that and I’d note that another recent study titled “Resistance exercise-
induced increases in putative anabolic hormones do not enhance muscle protein synthesis or intracellular
signalling in young men.” by the same group found the exact same thing.
Summing Up: Leg training has no magic impact on overall growth, most of which is determined locally
(through mechanisms of tension and fatigue mediated by changes in local muscular metabolism). If you
want big arms, train arms. If you want big legs, train legs.
And if folks are wondering why empirically ‘folks who train legs hard’ seem to get big compared to those who
don’t, I’d offer the following explanation: folks willing to toil on heavy leg work work hard. Folks too lazy to
train legs hard often don’t. And it’s the overall intensity of the training that is causing the difference, not the
presence or absence of squats per se. Which is why guys who only hammer pecs and guns get big pecs
and guns even if they couldn’t find the squat rack in the gym: the small acute hormonal responses to training
are simply irrelevant to overall growth.

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Excess Protein and Fat Storage – Q&A

Question: I have done a lot of study in diets and nutrition but to this day I have not been able to get any
concrete evidence on what happens with excess protein in the body and I’m hoping you can help.
To make things simple, lets take a theoretical diet consisting of 5000 calories of pure protein for a 60kg,
175cm female.
Many people claim that excess protein will get wasted while others say that all excess calories eventually
end up being stored as fat.
I have done my own research on the breakdown of protein into amino acids and I understood it as: some of
the amino acids are wasted while others will go through the cycle of conversion and will still be used by the
body for energy.

Answer: Ok, first things first. The example given above is absurdly non-physiological. The satiating power
of protein would make such a high protein consumption impossible. That is, 5000 calories of pure protein is
1250 grams of pure protein. Can’t be done. Beyond that, while the biochemical pathways for the conversion
of protein to fat do exist in humans, the likelihood of it ever happening in any but the most absurdly non-
physiological circumstances are effectively nil.
Let me put this in perspective. Despite a lot of claims to the contrary, the actual conversion of carbohydrate
to fat in humans under normal dietary conditions is small approaching insignificant (a topic I discussed at
least briefly in Nutrient Intake, Nutrient Storage and Nutrient Oxidation).
Make no mistake, the conversion of carbs to fat (a process called de-novo lipogenesis or DNL) can happen
but the requirements for it to happen significantly are fairly rare in humans under most conditions (to discuss
this in detail would require a full article, interested readers can search Medline for work by Hellerstein or
Acheson on the topic).
At least one of those is when daily carbohydrate intake is just massive, fulfilling over 100% of the daily
maintenance energy requirements. And only then when muscle glycogen is full. For an average sized male
you’re looking at 700-900 grams of carbohydrate daily for multiple days running.
Which means that the odds of protein being converted to fat in any quantitatively meaningful fashion is simply
not going to happen. Certain amino acids are processed to a great degree in the liver (as I discuss in The
Protein Book) and this can produce glucose, ketones and a few other things. But triglycerides (the storage
form of ‘fat’) isn’t one of them.
I imagine that if protein were going to be converted to fat, it would first have to be converted to glucose and
only if the amount produced were then in excess of daily maintenance requirements would there be
conversion to fat. But as noted above, this simply isn’t going to happen under any even reasonably normal
circumstances. No human could eat enough protein on a daily basis for it to occur.
What will happen, as discussed in Nutrient Intake, Nutrient Storage and Nutrient Oxidation. is that amino
acid oxidation (burning for energy) will go up somewhat although, as discussed in that article, it’s a slow
process and isn’t complete.
So, as noted above, while the pathway exists for protein to be stored as fat, and folks will continue to claim
that ‘excess protein just turns to fat’, it’s really just not going to happen under any sort of real-world
situation. Certainly we can dream up odd theoretical situations where it might but those won’t apply to 99.9%
of real-world situations.

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Red Meat and Health – have we been blaming the wrong thing?

Frequent consumption of red and processed meat has been shown in population studies
to be positively correlated with cardiovascular disease [1-3], cancer and type 2 diabetes.
Recent meta-analyses also indicate that it increases total mortality [4]. Hence, a high
meat intake (regardless of its fat quantity and quality) is generally perceived to be
unhealthy and something that should be avoided. However, although there are many
studies documenting these associations, results are not always consistent and there are
several methodological issues which weakens the strength of their findings (more on
that in a bit). In the same way as the putative health risks of red meat consumption is
investigated, its documented health benefits (which I will cover below) are equally as
important and must be given a fair chance in the establishment of public health
messages in relation to red meat consumption. In this article I will therefore cover both
the risks and benefits associated with red meat consumption, and after having taken all
the scientific data into consideration, argue that meat has been unfairly blamed…

This is a long article (7 pages excluding references) so here’s a printer-friendly


download version for you who prefer to read away from the computer and/or want to
share it with others.

The “bad” side of meat – supposed harm to health

Cardiovascular disease (heart attack, stroke and coronary heart disease)

In a study that found a significant positive association between servings of red meat and
the risk of coronary heart disease (adjusted for age), this effect became non-significant
(meaning it could have occurred by chance) after controlling for age, body weight,
smoking, alcohol, physical activity, energy intake and family history of coronary heart
disease in the multivariate analysis [1]. Another study reported found that red meat was
associated with an increased risk of mortality from coronary heart disease, but their
classification of red meat included processed meats [5]. Similar inconsistencies have
been observed in [1, 6], because there is no universal agreement of which meats should
be classed as processed or not [7, 8]. A recent meta-analysis from Harvard Medical
School concluded that unprocessed red meat intake is not associated with coronary heart
disease (relative risk per 100-g serving per day), while processed meat intake is

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associated with 42% higher risk of coronary heart disease (relative risk per 50-g serving
per day) [9]. This study also found that consumption of unprocessed or processed meat
were not associated with stroke [9].

Much evidence is based on studies that have investigated dietary patterns rather than
meat consumption in relation to risk of cardiovascular disease [2, 10-13]. However,
when looking at dietary pattern analyses and comparisons we have to remember that
these types of studies make it impossible to isolate the effects of red meat alone, which
is what the whole red meat – health diatribe is all about.

A typical Western dietary pattern has been identified that is high in red meat and meat
products, low in fruit and vegetables and coupled with a sedentary lifestyle, smoking
and high alcohol intake [14]. This type of diet has been associated with a 22% greater
risk of mortality from cardiovascular disease than a prudent dietary pattern that is high
in fruit and vegetables, legumes, poultry and whole grains [15]. Bearing in mind the
very well documented health promoting effects of fruit and vegetables [16], this doesn’t
come as a surprise.

Including red meat as part of the typical Western dietary pattern erroneously implies
that red meat cannot be part of a healthy dietary pattern characterized by a high intake
of for example fruit and vegetables, oily fish and legumes. This has been proven in
several less frequently cited studies, which demonstrated that when red meat is
included is such a healthy dietary pattern, it is not related with cardiovascular disease
mortality [17, 18].

Cancer

Based on epidemiological studies it is assumed that meat, especially red meat, enhances
risk for cancer, particularly of the colon, breast and prostate [19]. One of the 10
universal guidelines for healthy nutrition in a report of the World Cancer Research Fund
released at the end of 2007 is to “limit intake of red meat and avoid processed meat”, as
a result of the “convincing evidence” for an association with an increased risk of
colorectal cancer development [20]. However, as it turns out, the allegedly “convincing
evidence” is not at all that convincing [21]. For those unfamiliar with scientific
parlance, saying that something has “convincing evidence” is a very bold statement.

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According to the scientific norms, that kind of statement requires that all different types
of studies behind the evidence point in the same direction. This, coupled with the fact
that the World Cancer Research Fund presented its “convincing evidence” in only one
page of text f the 517-page report, has made several leading cancer researchers raise
their eye-brows [21, 22].

The flaws with World Cancer Research Fund report are obvious when we look at
statistics for meat intake and colon cancer incidence. According to this report, if we
decrease our meat intake, then our risk of colorectal cancer will decrease too… In the
UK during the period 1963 to 1998 the intake of red meat decreased by 25% [23]. Far
from falling substantially, the incidence of colorectal cancer increased substantially!
[23] Similarly, in Norway the intake of red meat has remained steady or has even
decreased at a time when their risk of colorectal cancer increased by 50% [23]. The lack
of linkage between meat intake and colorectal cancer risk can be illustrated further by
comparing the countries in the European Union. Meat consumption in the UK is less
than that in any of the other EU and Mediterranean countries [24] and yet the colorectal
cancer risk is much higher [23]. Spain has a very much higher intake of red meat but
still the third lowest colorectal cancer risk [23].

One main flaw (there are several!) with the epidemiological studies that have
investigated the relation between meat intake and cancer, is that they haven’t separated
the effects of processed and unprocessed meat, and not taking consideration to cooking
methods [25]. The most supported mechanism behind the putative carcinogenic effect of
meat is the formation of mutagenic compounds, HCAs (heterocyclic aromatic amines)
and PAHs (polycyclic aromatic hydrocarbons), when meat is cooked at high
temperatures to a well-done state [26, 27]. However, very few studies have assessed the
method of cooking when measuring meat consumption. Therefore, in the largest studies,
the effects of red meat per se have not been isolated from the effects of processing or
cooking temperatures. Of the few studies which have considered these factors, some
found an increased risk of colon cancer with high intakes of well or very well done red
meat compared to low intakes [28], whilst others found no increase in risk [29, 30]. The
diverging findings can be explained by the fact that approximately 80% of colon cancer
cases are thought to be caused by modifiable diet and lifestyle factors [31] and red meat
(whether processed or not) is only one factor among a myriad of other strongly

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influential factors, including intake of fruit and vegetables, physical activity level,
obesity and smoking.

A notable study is further supporting this [32]; here 265 000 Japanese persons were
followed for 25 y. A detaileddiet history was taken at recruitment and regularly updated.
Vegetable intake was stratified into four intake groups (daily, often, sometimes, and
never) and then analyzed in relation to meat consumption and cancer risk in each group.
As expected, the daily vegetable intake group had very much lower cancer rates than the
never vegetable eating group, with the other two groups intermediate. Interestingly, in
the group who ate green-yellow vegetables daily, there was an inverse relation between
meat intake and colorectal cancer, meaning that a higher meat intake in the context a
vegetable rich dietary pattern actually is associated with a lower colorectal cancer
incidence! In the group who never ate vegetables there was, as expected, a positive
relation between meat intake and cancer of the colon and rectum (the higher the meat
intake, the higher the cancer incidence). Thus is seems as if meat is a risk factor, then it
is only manifest among those who do not eat sufficient amounts of the protective
factors. This is supported by a recent study demonstrating that a high consumption of
fruit and vegetables is associated with a reduced risk of colon cancer [33].

Type-2 diabetes

Intake of red meat has also been associated with type-2 diabetes [34]. A meta-analysis
that pooled the results from 12 population studies, found that when comparing high vs.
low intake, the risk for type-2 diabetes was increased by 21% for unprocessed red meat
and 41 % for processed red meat [34]. However, the absolute amount eaten varied
greatly, and because the included studies didn’t properly control for influencing
variables like body weight and physical activity, the researchers themselves admitted
that it is possible that these confounding factors could have explained the observed
association, and not necessarily the meat intake [34]. This is underscored by another
study which found that the effect of unprocessed meat intake on type-2 diabetes is
modified by body weight [35], which in turn is a function of physical activity and
caloric intake.

In contrast, a more recent and more detailed meta-analysis, which pooled the results
from 20 population studies, concluded that red meat intake is not associated with type-2

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diabetes [9]. In agreement with the previous meta-analysis, an association between
processed meat intake and type-2 diabetes was found, even though the increase in risk
was lower, 19% per 50 g serving/day [9].

All-cause mortality

In March 2012, a media attention grabbing study was published that investigated the
association between red meat intake and mortality. This large study prospectively
followed 37 698 men from the Health Professionals Follow-up Study (1986-2008) and
83 644 women from the Nurses’ Health Study (1980-2008) who were free of
cardiovascular disease (CVD) and cancer at baseline. Diet was assessed by validated
food frequency questionnaires and updated every 4 years. The results showed that, after
having adjusted for major lifestyle and dietary risk factors, adding 1 serving (3 oz) of
unprocessed red meat or processed red meat per day to one’s regular diet was
associated with a 13% and 20% greater chance of dying from all causes, respectively.

It was also estimated that substitutions of 1 serving per day of other foods (including
fish, poultry, nuts, legumes, low-fat dairy, and whole grains) for 1 serving per day of
red meat were associated with a 7% to 19% lower mortality risk. It was further
estimated that 9.3% of deaths in men and 7.6% in women in this study could have been
prevented at the end of follow-up if all the individuals consumed fewer than 0.5
servings per day (approximately 42 g/d) of red meat. The conclusion of this study stated
that red meat consumption is associated with an increased risk of total, CVD, and
cancer mortality, and that substitution of other healthy protein sources for red meat is
associated with a lower mortality risk [4].

My first question about this study was how it assessed lifestyle related risk factors.
What jumped at me right off the bat when I was reading through the research
publication was that the researchers, while using validated food frequency
questionnaires, did not use validated lifestyle and physical activity assessment
questionnaires. As I said in the meat – fat loss article, questionnaires are infamous for
being inaccurate and bias prone. So if a questionnaire is used, it better be validated
(which mean that what it is supposed to measure reasonably correlates to the results
obtained with a more exact labor intensive measurement tool)! This fact, coupled with

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the finding that associations between diet and mortality are confounded by fitness [36],
greatly weakens the conclusions drawn in this study.

To put the red meat – mortality data in context, and to illustrate the importance of
fitness, I want to cite a study that investigated the association of cardiovascular fitness
(measured by total duration during a maximal treadmill exercise test, and not a
nonsense questionnaire!) and mortality [37]. Compared with the least fit men and
women, the most fit men and women had 43% and 53% lower risk for all-cause
mortality, and 47% and 70% lower risk of cardiovascular disease mortality, respectively
[38]!!! Put this next to the meat – mortality data stating a 13-20% increase in mortality
risk by eating red meat, and you get the point; red meat only plays a tiny, if any, role in
the overall life style – mortality relation. It’s pretty obvious that the problem is not the
red meat, but our lazy asses!!!

The importance of distinguishing between unprocessed and processed red meat

The most robust and reliable evidence to date of how unprocessed and processed red
meat consumption may influence risk of cardio-metabolic diseases comes from the
Harvard Medical School meta-analysis. The findings of different relationships of
unprocessed versus processed red meat (bacon, hot dogs, salami etc.) consumption with
coronary heart disease and type-2 diabetes (no effect of unprocessed red meat but
increased risk with processed red meat, as outlined above) underscore the need to better
characterize which particular components of meats that may increase cardio-metabolic
risk [9]. The Harvard researchers also criticized the World Cancer Research Fund –
American Institute for Cancer Research statement that both red and processed meat
consumption increases colorectal cancer (see above), because they didn’t distinguish
between processed and unprocessed red meat [9].

At least in the United States, where most of the studies have been performed, processed
meats contain, on average, similar saturated fat and lower cholesterol and heme iron
compared with red meats, suggesting that differences in these constituents may not
account for different associations with disease risk [9]. This is a very important fact
because both saturated fat, cholesterol and heme iron have been condemned for being
the “meat evils”. From this data, we can draw the following conclusions:

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1) Unprocessed red meat per see is NOT harmful.

2) Processed red meat can increase the risk for heart disease and type-2 diabetes, but
this is not due to its content of saturated fat, cholesterol or heme iron.

Thus, it is other constituents in processed red meat that are contributing to the observed
health risk association.

Processed meats contain preservatives and additives that can increase the risk of
cardiovascular disease, type-2 diabetes or cancer. These may include nitrites, nitrates,
and heterocyclic amines formed during cooking. Nitrosamines formed during cooking
may be toxic to pancreatic cells [39]. In addition, advanced glycation end products
formed in meat and high fat products through heating and processing have been
associated with insulin resistance in mice, and with diabetes complications in humans
[40].

In particular, nitrates and their byproducts (eg, peroxynitrite) promote atherosclerosis


and vascular dysfunction, reduce insulin secretion, and impair glucose tolerance, and
streptozotocin, a nitrosamine-related compound, is a known diabetogenic compound. In
observational studies in children, nitrites and nitrous compounds are associated with
type 1 diabetes mellitus [41, 42], and nitrite concentrations in adults have been used as a
biomarker of endothelial dysfunction [43] and impaired insulin resistance [44].
However, the types of foods that are commonly replaced when individuals consume
unprocessed versus processed meats could also account for their different associations
with risk [9]. Ask yourself if you are more likely to eat veggies with a piece of steak, or
with a hot dog, bacon and egg combo, or a salami meal…?

The meat and potato war…

I want to bring up another point showing that red meat has been unfairly attacked.
While meat is blamed for generating risky heterocyclic amines during high temperature
cooking (for example over open flames), nobody talk about the high levels of
acrylamide that are formed during the frying, roasting, or baking of carbohydrate rich
foods, especially potatoes and cereal products [45, 46]. And acrylamide possesses a
range of hazardous effects and is known to induce carcinogenicity, genotoxicity,
neurotoxicity and reproductive toxicity [45].
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Let’s take a look at the average daily intakes for heterocyclic amines (from red meat)
and acrylamide (from potatoes and cereals):

Average daily intakes for heterocyclic amines is in the range 2.5 – 26 ng/kg body
weight/day [47-49].

Average daily intakes for acrylamide is in the range 370-490 ng/kg body weight/day
[50, 51]

This clearly shows that acrylamide intakes are 20 to 150 times higher than that of
heterocyclic amines! Makes me wonder if the potato and celery industry has some
lobbying going behind the public health recommendations that urge us to lower our red
meat intake…

Red meat and fat intake

Many people avoid red meat because of its total fat, saturated fat and cholesterol
content. In an upcoming article I critically examine and explain the flaws in the diet-
heart hypothesis (ie, the presumed link between saturated fat intake and cardiovascular
disease) that has led to the long-standing public health recommendations for limiting
saturated fat intake as a means to prevent cardiovascular disease. If you are more
concerned about the purported fat intake – obesity relation, check out my other article
on meat and fat loss. As illustrated by the popularity of low-carb, high-fat diets (also a
topic for another article) your fat intake will not automatically make you fat. For those
of you who still have dietary fat phobia, here are the hard facts.

The fat content and fatty acid profile in red meat is often misunderstood. The first thing
to note is that most of the fat can easily be trimmed off before cooking. There is
confusion among consumers about the impact of lean meat and meat fat on human
health, because it is commonly, but incorrectly thought that lean meat tissue has the
same saturated fat content as the visible fat of meat. Once visible fat is trimmed, lean
red meat often contains less than 5-10% lipid [52]. And in high quality lean red meats,
like the ones you can find at Eat To Grow, there is very little fat marbling within the
meat. Lean meat is relatively higher in polyunsaturated fat and lower in saturated fat
compared with the visible fat of meat [52]. The saturated fat content of lean red meat is
less than 2-3g/100g (3.5 oz) lean red meat (for example in Eat To Grow‘s flank steak
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and beef tenderloin) compared with more than 37g/100g (3.5 oz) of visible fat from red
meat. Eat To Grow‘s meat cuts are also very low in cholesterol.

The main fat in lean meat tissue is in phospholipid form, which makes up the major
portion of the cell membrane structure, and these are rich in polyunsaturated fats [53].
The other main fat in lean meat is the “regular” fat (more precisely known as
triglyceride or triacylglycerol) which is predominantly saturated and monounsaturated
fat [53]. The phospholipid fat in lean red meat is relatively constant and independent of
the total fat content, whilst the content of “regular” fat increases as the total fat level
increases [54]. Therefore, as the total fat content of lean red meat increases there is an
increase in saturated and monounsaturated fat content. In other words, the fatty acid
composition of meat depends on the total lipid content of the meat [53-56].

In lean beef, over half and up to 70% of fatty acids are monounsaturated or
polyunsaturated, which are the types recommended by health professional and
government agencies such as the American Heart Association and the Dietary
Guidelines for Americans [57, 58]. Also, one-third of the saturated fat in red meat is
stearic acid, which, unlike other long-chain saturated fatty acids, is neutral in its effects
on blood cholesterol levels in humans [59, 60].

Lean beef contains around 10 g total fat (you can find even leaner cuts at Eat To Grow),
no more than 4.5 g of saturated fat, and less than 95 mg cholesterol per 3-ounce serving
[61]. This fat profile readily fits into a heart-healthy diet. Based on the American Heart
Association’s dietary fat recommendations, the total, saturated fat and cholesterol intake
goals are 30%, 10%, and 300 mg, respectively [57]. For an average person consuming a
2,000 calorie diet, the numbers will be 67 g total fat and 22 g saturated fat/day. As noted
above, a 3-ounce serving of lean beef contains levels of total and saturated fat well
below these limits, and cholesterol levels below the recommendation of <300 mg/day.
You could fit in 3-4 lean meat servings per day and still be within those targets. And
there is overwhelming evidence showing that lean red meat is as effective as chicken in
blood cholesterol lowering diets, and therefore has a well deserved place in diets for
cholesterol and lipid control [52, 62-65].

The good side of meat – health promoting nutrients

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The inordinate focus on red meat as the evil has distracted attention from its unique
nutritional characteristics, which contribute to a healthy diet.

Meat is not only composed of fat and protein; it also contains essential nutrients which
appear exclusively in meat (vitamin A, vitamin B12) and micronutrients for which meat
is the major source because of either high concentrations or better bioavailability
(folate, iron, selenium, zinc) [19, 66-69]. In particular, vitamin A, folate and selenium
are reported to be cancer-preventive [19, 66].

Red meat being the major source of vitamin B12 is especially notable because vitamin
B12, together with folate and vitamin B6 (also found in ample amounts in red meat), is
required by the methylation cycle, which keeps the level of homocysteine under control.
Homocysteine is not only a risk factor for cardiovascular disease [70-72], but also for
cognitive decline and dementia [73-76] and vascular injury [77]. Thus, getting all these
three vitamins in a highly bioavaliable form in one single food is a pretty good deal. An
interesting effect of homocysteine is that it inhibits NO (nitric oxide) production in
blood vessels and contributes to vascular dysfunction [78-80]. NO is an essential
vasodilatory molecule and many supplements are marketed as being NO-boosters (I will
save a discussion about those supps for another article). The take home here is that by
eating red meat you will ensure to cover you vitamin requirements for preventing
homocysteine levels to rise, and thereby avoid the homocysteine-induced NO synthesis
inhibition.

Also, the iron in meat is in an especially highly bioavaliable form called heme iron,
which is much more bioavailable than non-haem iron found in plant sources [67, 69, 81-
83]. Red meat in particular is recognized as a significant source of hem iron compared
to poultry and fish [84]. Iron is vital for many cellular processes in the body and, as a
component of hemoglobin, is essential to maintaining adequate transport of oxygen in
the blood. Therefore, even mild suboptimal status before the onset of anemia can
negatively impact health [85]. Iron-deficiency anemia is a major nutritional deficiency,
being particularly prevalent among children and young women [85]. Therefore, cutting
out or lowering meat intakes could have a seriously negative impact on iron status and
increase the risk for anemia.

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Meat is a also a good source of vitamin D [69]. In particular, the vitamin D metabolite
25-hydroxycholecalciferol [25(OH)D3] is found in significant quantities in meat and
liver and is assumed to have a high biological activity, resulting in better and faster
absorption from the diet compared with its parent compound [86]. Furthermore, it has
been suggested that components of meat protein may enhance the utilization of vitamin
D in humans, particularly where exposure to sunshine is limited [87].

In addition, meat is a good source of choline, taurine, carnosine, coenzyme Q10,


creatine and glutathione [88, 89]. Glutathione levels in red meat are estimated to be 12-
26mg/100g in beef [90] and most meats contain approximately twice the level of
glutathione of poultry and up to ten times the content found in fish [88].

Conclusion

Red meat, when part of healthy diet combined with regular exercise, does not pose any
harm. Actually, in this context, red meat, thanks to it providing high quality protein
together with valuable nutrients, is actually a very sound strategy for both health
promotion, sports performance and muscle growth. The scientific reports on the
detrimental health effects of red meat have to be interpreted with their methodological
flaws in mind, and evaluated against the background diet. The meat-potato war clearly
illustrates this. Also, there is compelling evidence showing that the supply of beneficial
protective dietary factors, and people’s lifestyles, are probably more important that our
red meat intake per see.

While high-heat food preparation causes formation of cancer-promoting substances,


meat also contains cancer-protecting nutrients (vitamin A, folate and selenium). The
latter can be optimized by a diet rich in fruit and vegetables, which contain a myriad of
bioactive cancer-protective substances. Also, the amount of cooking dependent cancer-
promoting substances can be reduced by avoiding open flame grilling and well done
meats.

So the answer the question in the title “have we been blaming the wrong thing?” =
YES!

Looking at all the scientific evidence, it is safe to say that the most appropriate
conclusion to be drawn is that it is laziness, manifested as lack of regular physical
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activity, and lack of veggies that are the culprits behind the associations, and not the red
meat!

Meat is a popular food especially among bodybuilders and strength athletes. Taking into
consideration the intense training regimens these individuals partake in, if you are one
of them, or if you train regularly just for health promotion, you have nothing to fear. To
the contrary, thanks to the high quality protein red meat supplies, eating it together with
your veggies is a smart strategy to build muscle, increase performance, and improve
your health.

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Is there a limit to how much protein the body can use
in a single meal?

Introduction

A longstanding belief in fitness circles is that the body can only use a certain amount of protein
per meal, and the excess is either oxidized or excreted. The ballpark range thrown around is 20-
30 grams, with 30 grams being perhaps the most common figure.

This guideline has led many trainees to go through the pains of consuming multiple doses of
protein throughout the day, banking that it will maximize muscle anabolism or muscle retention.

Well, true or not, this concept fits in nicely with another longstanding fitness “rule” that you have
to eat at least six times per day in order to keep the body’s metabolism revving high. Since the
meal frequency and metabolism dogma has been thoroughly debunked [1-5], it’s time to dig into
the topic of whether there’s a limit to effective protein dosing, and if so, what that limit might be.

Looking at simple logic first

Let’s imagine an experiment involving two relatively lean 200 lb individuals. For the purposes of
this illustration, I’ll assign a daily amount of protein known to adequately support the needs of
the athletic population. We’ll give Person A 150 g protein spread over five meals at 30 g each.
We’ll give Person B the same amount of protein, but in a single meal. Let’s say that this meal
consists of a 16 oz steak, chased with a shake containing two scoops of protein powder.

If we really believed that only 30 g protein can be handled by the body in a single meal, then
Person B would eventually run into protein deficiency symptoms because he supposedly is only
absorbing a total of 30 g out of the 150 g we’re giving him. At 30 g/day, he’s only getting 0.33
g/kg of bodyweight, which isn’t even half of the already-low RDA of 0.8 g/kg. If the body worked
this way, the human species would have quickly become extinct. The human body is more
efficient and effective than we give it credit for.

The body will take all the sweet time it needs to effectively digest and absorb just about
whatever dose you give it. Person A will have shorter digestion periods per meal in order to
effectively absorb and utilize the small meals. Person B will have a longer digestion period in
order to effectively absorb and utilize the large meal. While the truth in this logic seems self-
evident, the important question is whether or not it’s supported by scientific research. Let’s look
at the evidence, starting with immediate-effect (acute) studies, then move on to the longer-term
trials.

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Research examining speed of absorption

A thorough literature review by Bilsborough and Mann compiled data from studies by various
investigators who measured the absorption rates of various protein sources [6]. Oddly, an
amino acid mixture designed to mimic the composition of pork tenderloin made the top spot, at
10 g/hour, while whey took a close second at 8-10 g/hour. Other proteins fell in their respective
spots below the top two, with little rhyme or reason behind the outcomes. As a matter of trivia,
raw egg protein was the most slowly absorbed of them all at 1.3 g/hour.

It’s important to note that these data have some serious limitations. A major one is the variance
of the methods used to determine the absorption rates (i.e., intravenous infusion, oral ingestion,
ileal ingestion). Most of the methods are just too crude or far-fetched for serious consideration.
Another limitation is that these figures could be skewed depending upon their concentration in
solution, which can affect their rate of gastric evacuation. Another factor to consider is the timing
of ingestion relative to exercise and how that might differentially affect absorption rates. Finally,
short-term data leaves a lot open to question.

Short-term research supporting the magic limit

I’ve heard many folks parrot that the maximal anabolic effect of a single protein dose is limited
to 20 grams, citing recent work by Moore and colleagues [7]. In this study’s 4-hour post-exercise
test period, 40 g protein did not elicit a greater anabolic response than 20 g. I’d interpret these
outcomes with caution. Fundamentally speaking, protein utilization can differ according to
muscle mass. The requirements of a 140-lb person will differ markedly from someone who’s a
lean 200. Additionally, a relatively low amount of total volume was used (12 sets total). Typical
training bouts usually involve more than one muscle group and are commonly at least double
that volume, which can potentially increase the demand for nutrient uptake. Finally, the
conclusion of the authors is questionable. They state explicitly,

“…we speculate that no more than 5-6 times daily could one ingest this amount (~20 g) of
protein and expect muscle protein synthesis to be maximally stimulated.”

So, they’re implying that 100-120 grams of protein per day is maximal for promoting muscle
growth. Wait a minute, what? Based on both the bulk of the research evidence and numerous
field observations, this is simply false [8,9].

In another recent study, Symons and colleagues compared the 5-hour response of a moderate
serving of lean beef containing 30 g protein with a large serving containing 90 g protein [10].
The smaller serving increased protein synthesis by approximately 50%, and the larger serving
caused no further increase in protein synthesis, despite being triple the dose. The researchers
concluded that the ingestion of more than 30 g protein in a single meal does not further
enhance muscle protein synthesis. While their conclusion indeed supports the outcomes of their

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short-term study, it’s pretty easy to predict the outcomes in muscle size and strength if we
compared a total daily protein dose of 90 g with 30 g over a longer trial period, let alone one
involving a structured exercise protocol. This brings me to the crucial point that acute outcomes
merely provide grounds for hypothesis. It’s not completely meaningless, but it’s far from
conclusive without examining the long-term effects.

Longer-term research challenging the magic limit

If we were to believe the premise that a 20-30 g dose of protein yields a maximal anabolic
effect, then it follows that any excess beyond this dose would be wasted. On the contrary, the
body is smarter than that. In a 14-day trial, Arnal and colleagues found no difference in fat-free
mass or nitrogen retention between consuming 79% of the day’s protein needs (roughly 54 g) in
one meal, versus the same amount spread across four meals [11].

Notably, this study was done on young female adults whose fat-free mass averaged 40.8 kg
(89.8 lb). Considering that most non-sedentary males have considerably more lean mass than
the female subjects used in the aforementioned trial, it’s plausible that much more than 54 g
protein in a single meal can be efficiently processed for anabolic and/or anti-catabolic purposes.
If we extrapolated the protein dose used in this study (79% of 1.67g/kg) to the average adult
male, it would be roughly 85-95 g or even more, depending on just how close someone is to the
end of the upper limits of muscular size.

When Arnal and colleagues applied the same protocol to the elderly population, the single-dose
treatment actually caused better muscle protein retention than the multiple-dose treatment
[12]. This raises the possibility that as we age, larger protein feedings might be necessary to
achieve the same effect on protein retention as lesser amounts in our youth.

IF research nailing the coffin shut?

Perhaps the strongest case against the idea of a dosing limit beyond which anabolism or
muscle retention can occur is the recent intermittent fasting (IF) research, particularly the trials
with a control group on a conventional diet. For example, Soeters and colleagues compared two
weeks of IF involving 20-hour fasting cycles with a conventional diet [13]. Despite the IF
group’s consumption of an average of 101 g protein in a 4-hour window, there was no difference
in preservation of lean mass and muscle protein between groups.

In another example, Stote and colleagues actually reported an improvement in body


composition (including an increase in lean mass) after 8 weeks in the IF group consuming one
meal per day, where roughly 86 g protein was ingested in a 4-hour window [14]. Interestingly,
the conventional group consuming three meals spread throughout the day showed no
significant body composition improvements.

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Keep in mind that bioelectrical impedance (BIA) was used to determine body composition, so
these outcomes should be viewed with caution. I’ve been highly critical of this study in the past,
and I still am. Nevertheless, it cannot be completely written off and must be factored into the
body of evidence against the idea of a magic protein dose limit.

Conclusion & application

Based on the available evidence, it’s false to assume that the body can only use a certain
amount of protein per meal. Studies examining short-term effects have provided hints towards
what might be an optimal protein dose for maximizing anabolism, but trials drawn out over
longer periods haven’t supported this idea. So, is there a limit to how much protein per meal can
be effectively used? Yes there is, but this limit is likely similar to the amount that’s maximally
effective in an entire day. What’s the most protein that the body can effectively use in an entire
day? The short answer is, a lot more than 20-30 g. The long answer is, it depends on several
factors. In most cases it’s not too far from a gram per pound in drug-free trainees, given that
adequate total calories are provided [8,9].

In terms of application, I’ve consistently observed the effectiveness of having approximately a


quarter of your target bodyweight in both the pre- and post-exercise meal. Note: target
bodyweight is a surrogate index of lean mass, and I use that to avoid making skewed
calculations in cases where individuals are markedly over- or underweight. This dose surpasses
the amounts seen to cause a maximal anabolic response but doesn’t impinge upon the rest of
the day’s protein allotment, which can be distributed as desired. On days off from training,
combine or split up your total protein allotment according to your personal preference and
digestive tolerance. I realize that freedom and flexibility are uncommon terms in physique
culture, but maybe it’s time for a paradigm shift.

In sum, view all information – especially gym folklore and short-term research – with caution.
Don’t buy into the myth that protein won’t get used efficiently unless it’s dosed sparingly
throughout the day. Hopefully, future research will definitively answer how different dosing
schemes with various protein types affect relevant endpoints such as size and strength. In the
mean time, feel free to eat the whole steak and drink the whole shake, and if you want to get the

best bang for your buck, go for a quality protein blend such as Nitrean!

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Exercise and Weight/Fat Loss: Part 1
I think it was last year some time that Time magazine ran an article to the effect of “Exercise will make you
fit but it won’t make you thin.” I remember someone asking me about this (it might have been my mom) and
I wasn’t really sure what the issue was; I had written back in my first book The Ketogenic Diet about some
of the realities of exercise and fat loss. Most of my other books have at least dealt with the issue to some
degree.
I suppose the issue isn’t really one of the realities of exercise and fat/weight loss but rather how the message
was misinterpreted. Many have held up exercise as some sort of panacea for all things, health, fitness and
of course what everyone is really interested in: losing weight/fat and I suspect the message got a bit garbled
as it so often does: people figured that they could do a bit of easy exercise and the pounds would just melt
right off.
The realities, unfortunately, are often quite a bit different and in this series of articles (which I’ll hopefully
keep to a mere two parts), I want to look at the possible ways that exercise might impact on one’s overall
body recomposition goals. You’ll notice that I used the word ways plural in that sentence; while most focus
on the direct role of exercise on fat loss (via direct calorie and/or fat burning) it turns out that there are more
ways than just that for exercise to impact on things.
For the most part, I’m going to sort of cluster all exercise in one big grouping for the sake of simplicity. Clearly
resistance training and aerobic training aren’t the same and have differential effects; when needed I’ll make
distinctions between them. It’s important to realize that most research on exercise and fat loss have used
obese individuals (researchers by and large not being interested in lean folks trying to get leaner) and that
has potentially other impacts on a lot of this. Again, as needed, I’ll make note of this.
Today, since it will take the most verbiage, I’m only going to look at the primary way that exercise can (or
can not) impact on body recomposition goals and that is in terms of its impact on total weight loss; that is
the quantity of weight lost. I’ll note ahead of time that I am going to confusingly jump back and forth between
fat and weight although they are not the same thing. This will make more sense in Part 2 when I attempt to
cover all of the other ways that exercise may potentially impact on things.

Quantity of Weight Loss

Most commonly, exercise is held up as a way of either directly causing weight/fat loss or for increasing the
amount of weight/fat lost when added to a diet with the focus primarily on the direct effects of exercise on
calorie/fat burning either during the exercise bout or afterwards. As noted above since it will take the longest,
that’s the only issue I’m going to look at today. Basically, I’m going to give a reality check on the impact of
realistic amounts of exercise in terms of its impact on body weight/body fat. It’s not a reality many are happy
with.
In previous articles as well as in my books, most recently in the Training the Obese Beginner series, I’ve
made the comment that, generally speaking, the only people who can burn a tremendous number of calories
during exercise are trained athletes; and they aren’t the ones that usually need it. That statement appears
to have confused some people but the point I was trying to make is that the number of calories that can be
burned with realistic amounts of exercise in beginners is usually fairly low.
In my first book The Ketogenic Diet, I cited some paper or another indicating that most untrained folks can
burn perhaps 5-10 cal/minute in exercise if you’re talking about sustainable intensities; this might hit 15
cal/minute but that would be for high intensity interval-type training.

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However, the duration of that activity tends to be exceedingly limited and the total average calorie burn for
the activity will be lower due to the rest intervals. As well, this isn’t an intensity of training that can be done
frequently. Even achieving 10 cal/minute would be fairly challenging for an relatively untrained/low-trained
individual.
Of course, as training status goes up, folks can burn proportionally more calories. A moderately trained
individual might be able to burn 10 cal/minute fairly easily and hit 15 cal/minute for extended periods if they
are willing to work a bit. 20 cal/minute might be achievable for short periods but, again, the total burned
during activity would be balanced out by the low intensity nature of the rest intervals.
As I discussed in Steady State vs. Intervals and EPOC: Practical Application, when I have compared interval
sessions of varying types to steady state training with a Powermeter, the total caloric expenditure is usually
about identical because of how the rest intervals affect the average intensity. The steady state sessions are
far easier to complete and can be done more frequently as well.
A very highly trained athlete might be able to burn 15 cal/minute as a matter of course, 20 cal/minute if they
are willing to work and hit even higher values for high intensity training. Certainly these athletes sometimes
need to drop fat (usually to improve power to weight ratio) and they have the advantage of being able to
burn a tremendous number of calories with even low intensity activity. Simply tacking on an ‘easy’ 30-45
minutes to their normal training can burn a pretty large number of calories making fat loss relatively easy
without much change in diet. But that last group is not who we are realistically talking about here.
I’d note that the above values are for cardiovascular activities. People always ask about calorie burn during
weight training and it’s harder to pin down values. It also depends staggeringly on the type of activities done
(e.g. whole body vs. isolation exercises), rest intervals, rep ranges, etc. Clearly repetition clean and jerk
will burn a lot more calories than barbell curls.
On average, studies have found a calorie burn of 7-9 cal/minute seems to be about right (again with huge
variability) but that only holds for the actual work time and a lot of time in the weight room is usually spent
resting. When we have tracked calorie burn for various types of weight training (ranging from Olympic lifting
to isolation machine work) with tools such as the Bodybugg/GoWearFit or Polar heart rate monitors, a calorie
burn of 300-400 cal/hour is about the average.
So with the above values in hand, let’s look at realistically what we might expect in terms of weight loss using
the values for a typical untrained/low fitness level individual assuming a calorie burn of 5-10 cal/minute and
various durations and frequencies. I’m going to compare 30 vs. 60 minutes and 3 vs. 6 days/week to
estimate total caloric expenditure.
And here’s where the confusing bit comes in, to put in this in real world terms I’m going to move from weight
loss to fat loss with the assumed value of a 3500 calorie deficit to lose one pound of fat; of course this
assumes that 100% fat is being lost which is not always a safe assumption. I’d note that total weight lost
will be higher if a larger proportion of muscle is lost, an issue I discussed in The Energy Balance Equation.
I want to note up front that there is a HUGE assumption built into the following calculations: that nothing else
is changing. Not diet, not activity at other times during the day (some studies find that people compensate
for exercise based energy expenditure by moving less later in the day), nothing. The only change we’re
making here is by adding exercise to an otherwise static situation. For reasons far beyond the scope of
what I want to talk about right now, this is not a good assumption. It simply makes the math easier.

Calorie Estimated Fat Estimated Fat


Duration Burn/Workout 3X/Week 6X/Week
Burn Loss Loss

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30
5 cal/min 150 calories 450 calories 0.128 pounds 900 calories 0.25 pounds
minutes

60 1800
5 cal/min 300 calories 900 calories 0.25 pounds 0.51 pounds
minutes calories

30 1800
10 cal/min 300 calories 900 calories 0.25 pounds 0.51 pounds
minutes calories

60 1800 3600
10 cal/min 600 calories 0.51 pounds 1.1 pounds
minutes calories calories

.
Frankly, the results are pretty dismal; you don’t even get to a one pound fat loss per week until you reach 6
days/week of an hour of fairly challenging exercise every day. Certainly the folks who think that brisk walking
for 30 minutes a few times per week is going to have a major impact on much of anything without a complete
overhaul in diet are incorrect; the impact is simply negligible.
It’s also worth mentioning that the above caloric expenditure is actually somewhat of an overestimation since
it includes the calories that would be burned by simply sitting around doing nothing. That is, if you did nothing
during that hour, you’d burn perhaps 60-100 calories/hour or so depending on that activity. The above
values include that resting expenditure so the actual impact on energy expenditure above and beyond
normal are going to be slightly lower.
But it’s fairly easy based on the above values (which again represent a massive number of assumptions in
the first place) to see how many people have concluded that exercise is worthless for fat loss. And certainly
a majority of studies (including most of the big meta-analyses) have reached that conclusion: compared to
dieting alone, exercise tends to add very little to the quantity of weight lost. Even added to a diet, exercise
tends to impact on the total weight loss marginally at most; the diet is doing most of the work in terms of the
actual quantity of weight lost (here I’m switching back to talking just about weight).
And this is simple mathematics, removing 1000 calories/day from the diet can be achieved with relatively
more or less ease (depending on how bad the diet is to start with); the average beginner simply can’t burn
that many calories with any realistic amount of exercise. At a low intensity and a calorie burn of 5 cal/min,
that would require 200 minutes of activity per day, over 3 hours. At a challenging 10 cal/min, you’re looking
at 100 minutes, an hour and forty minutes. This is simply beyond what most people can, are willing, or have
time to do.
This is also why I mentioned the huge assumption that diet is unchanging in the above estimations; another
conclusion often reached is that exercise is worthless as the amount of calories that can be burned can be
offset by even a small increase in food intake. An average bagel may contain 250 calories (or more if they
are the big ones), you can overcome the deficit generated by the lower amounts of activity with a small
increase in food intake.
I’d mention that the only impact of exercise on weight/fat loss tends to be due to the deficit created; studies
where the calories from activity are replaced by increasing food intake show no changes in anything. That
is to say, if you compensate for the activity by eating more (an issue I’ll talk about later), nothing really
happens.
In this vein, most of the exercise and diet studies have used fairly low-moderate amounts of activity (in line
with the above chart) and few have progressed anything over the course of the study, volume or intensity;
most show neglible effects on much of anything (even the much vaunted interval studies only show maybe
a 1-2 lbs fat loss over 12 weeks compared to steady state training).

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The latter is a problem to me since no good fitness program would be so static without some progression in
frequency, duration, intensity or all three as folks got fitter and were able to handle more or harder
training. As I mentioned in the Training the Obese Beginner series, one consequence of regular fitness
training is an improvement in fitness, allowing folks to train at higher levels (both driving fitness higher as
well as burning more calories).
So while realistic amounts of exercise may not be able to play a major role initially in weight loss, over time
it not only adds up (albeit in depressingly small amounts) but can end up contributing further down the road
as fitness improves. That’s in addition to some other indirect ways that exercise may help that I’ll talk about
shortly. Finally, there turns out to be a huge area where exercise has been shown to play a role that I’ll talk
about when I wrap up the series.
I’d note before moving on that some studies using fairly large amounts of activity (one that comes to mind
had subjects cycle 2 hours/day 6 days/week) have shown a greater impact on weight and fat losses. But
these amounts of activities are usually considered to be fairly unrealistic for most people. I’m simply making
the point that for people who can do a lot of activity (one person on my forum actually got into the habit of
doing 8 hours of low intensity cycling during the day believe it or not) there can be an impact.
But the simple fact is that, for the average untrained individual, realistic amounts of activity are unlikely to
have massive direct impacts on either body weight or body fat; the caloric expenditure simply isn’t significant
enough to impact on anything. As well, changes in diet have the potential to make a much greater
contribution to the creation of a caloric deficit; removing 500 or even 1000 calories per day from the diet can
usually be achieved much more readily than adding the same amount of activity. At least in certain
populations.
But as noted in the introduction, there are several other ways that exercise can positively impact on weight/fat
loss goals. Those will be the topic of Part 2 on Friday.
Read Exercise and Weight/Fat Loss: Part 2

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Exercise and Weight/Fat Loss: Part 2
On Tuesday in Exercise and Weight/Fat Loss: Part 1, I took a somewhat thorough look at some of the
realities of exercise and weight/fat loss in terms of the direct impact on caloric expenditure. And the fairly
depressing conclusion is that moderate/realistic amounts of exercise (for the typical person) are unlikely to
have enormous effects in terms of body weight/body fat per se, or in increasing the total amount of weight/fat
loss when added to a diet.
Certainly larger amounts of exercise can approach significance (and as folks become fitter, they can burn
more calories with activity) but the idea that a little bit of exercise is going to have a massive impact on
anything is fairly misguided. However, there are more ways that exercise might positively impact on
weight/fat loss (especially when combined with changes in diet) and that’s what I want to look at today. I’d
mention that readers should check out PJ Striet’s comments in Exercise and Weight/Fat Loss: Part 1 for
some other potential benefits of exercise outside of weight and fat loss per se.

Quality of Weight Lost

In Exercise and Weight/Fat Loss: Part 1 I sort of confusingly jumped back and forth between weight and fat
loss (mainly using fat loss as a way of estimating how much exercise might actually impact on things); for
the most part the big meta-analyses and a lot of studies have focused more on total weight lost in response
to exercise with most of them finding, at best, a small impact.
However, anyone who hasn’t had their head under a rock for the past couple of decades, or who has read
anything on this website, knows that there is more to the overall equation than just weight loss. As I discuss
in some detail in What Does Body Composition Mean? the body is made of a number of different components
including muscle mass, organs, water, connective tissues, minerals, fat, etc.
Just looking at changes in body weight can be misleading; it’s more important to look at what’s happening
to body composition; that is, under most circumstances, folks want to lose fat while minimizing or eliminating
the loss of lean body mass (especially muscle mass).
Does exercise help with that? That is, does the addition of exercise to a diet change the proportion of what’s
lost; that is does it change the quality of weight lost (ideally shifting the loss towards more fat and less muscle
mass). And when you look at the studies the answer is a big old it depends. A lot of which has to do with
the specifics of the diet (especially the amount of protein provided) and the type of exercise done.
For the most part, exercise is found to have a protein sparing effect of some sort; that is less muscle and
more fat is lost in response to the same caloric deficit. It’s not universal with not all studies finding an impact
(depending on the, type, frequency, duration and intensity of activity) but certainly the trend is for that.
And here is a place where there does seem to be a difference in what type of activity being done with studies
(and practical experience) finding that resistance training (especially coupled with adequate protein intake)
being superior to aerobic activity (or a low protein intake) for limiting lean body mass loss and, thus increasing
fat loss in response to a diet. And while more mixed, there is some suggestion that this helps to limit the
normal drop in metabolic rate that tends to occur with weight loss.
Put differently, as I phrased it in The Rapid Fat Loss Handbook, if there’s a single type of exercise to do
while dieting, it’s proper resistance training. Coupled with an adequate protein intake, that alone tends to
limit (or eliminate) lean body mass losses such that the weight which is lost (in response to the caloric deficit)
comes predominantly from fat mass.

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So this is a place where even if exercise doesn’t increase the quantity of total weight loss per se (i.e. how
much the scale actually changes), it can impact on the quality of weight lost; with proper exercise causing
more fat and less muscle loss than would otherwise occur. Here again, proper resistance exercise,
especially coupled with adequate protein, seems to be superior to aerobic activity or diets with insufficient
protein. You can read more about proper resistance training in Weight Training for Fat Loss Part 1 and
Weight Training for Fat Loss Part 2.
.

Accountability/Adherence

Perhaps one of the most potentially beneficial places that exercise can play a role during weight loss is with
adherence. I’ve mentioned this in articles before but, for many people, the simple fact of doing some sort of
exercise on a given day makes it more likely for them to stick to their diet. The underlying logic seems to be
along the lines of “I worked out today, why would I blow my diet?”
In a lot of ways, this may actually be one of the single most important aspects of successful weight loss
attempts, long-term adherence to the plan. I’ve ‘joked’ about this before, saying that the best diet is the one
that you can stick to and there is much truth to this joke; at the end of the day after you work through all of
the potential benefits of one diet versus another or what have you, the best one for a given individual is the
one that they can stick to in the long-term. If regular daily activity of some sort helps an individual adhere to
their dietary plan, that benefit alone may be more important than any actual metabolic effects of the exercise
bout itself.
Basically, for some people there seems to be a psychological coupling of exercise with good dietary habits
on a day to day basis and clearly that can be of benefit. Of course, there is a potential negative that needs
to be considered: when/if people stop exercising often their dietary habits fall off just as quickly.
In fact, one odd study years ago looked at this issue comparing diet, exercise and diet+exercise for both
short- and long-term results. It found that the diet+exercise group ran into problems such that, when subjects
stopped exercising, their diet habits fell apart too.
There is another potential place that this can backfire which I’m going to look at next.
.

Exercise and Hunger/Appetite

The impact of exercise on hunger and/or appetite is, to put it mildly, complicated. This is because human
hunger/appetite (I’m not going to bother making the distinction between the two here) is exceedingly complex
being an interplay of biology, psychology and environment. These are often separated out for convenience
but they all interact.
Looking solely at biology, overall exercise seems to have a beneficial overall impact on acute hunger,
showing a decrease at least in the short-term (other work has shown that the overall hunger/appetite
regulation system works more effectively when regular activity is performed).
This seems to be related to increased levels of various gut hormones involved in signalling fullness, as well
exercise can increase leptin transport into the brain (other studies suggest that long-term aerobic activity
may improve leptin sensitivity which is good given that obesity is generally associated with leptin resistance
in the brain). There may still be as of yet undiscovered mechanisms for exercise to impact on
hunger/appetite.
Other work suggests that even if exercise can increase hunger, any increase in food intake tends to be less
than the energy burnt during the activity itself; that is exercise still has an overall benefit. It’s worth

174
mentioning that even here there tends to be a large degree of individuality, some people compensate for the
energy expenditure of activity better than others and this may be part of what contributes to individual
differences in results.
One thing I noticed years ago (and forgot to mention in the Training the Obese Beginner series) is that
beginners often seem to get a slight increase in hunger following activity, at least in the first few weeks of
training. I suspect this is due to their general over-reliance on glucose for fuel (falling blood glucose being
one of many stimuli for hunger). At about the week 4 mark, as their bodies started to get the first adaptation
to training and started to use more fat for fuel; this effect generally went away.
It’s worth noting that emerging research suggests that there may be gender differences in this effect (along
with many others) with women, as usual, getting the short end of the stick when it comes to exercise and
hunger regulation. And this is consistent with earlier studies showing that, under uncontrolled eating
conditions, women are less likely to lose weight in response to exercise than men.
Of course, the above tends to interact massively with the psychology of the individual and whether or not
they are consciously controlling their food intake. That second issue is a major confound in a lot of studies
that people tend to forget about when they compared different studies.
However, this isn’t always the case and one trap that many exercisers often fall into is assuming that their
exercise bout has burned far more calories than it has (you’ll hear folks figuring they must have burned at
least 1000 calories in an hour of moderate activity when the reality is probably closer to 400-500) and figuring
that they’ve ‘earned’ that big post-exercise junk-food meal.
As I mentioned in Exercise and Weight/Fat Loss: Part 1 it’s usually quite trivial to overcome all but the most
massive exercise related energy expenditures. You can put down 1000+ calories in a big post-workout meal
with ease, more than compensating for the energy burn of the activity.
But as much as anything I feel that this comes down to an issue of misinformation and education; people
need to be realistic about the number of calories they are burning during activity. It’s simply almost never
as high as they think and realizing this is a first step to avoiding habits that will tend to not only offset but
actually reverse any beneficial impact of activity.
.

Weight Loss Maintenance

As a final topic, I want to look at an issue that is perhaps more important in the big scheme of things than
actual weight loss per se. The rather simple fact that needs to be recognized is that weight/fat loss per se
isn’t really the hard part; people consistently do and can lose fat/weight all the time.
The issue is with keeping it off. That is to say, although people successfully lose weight/fat all the time, they
usually end up gaining it back. Frankly, I am of the opinion that strategies to lose fat/weight are no longer
the important issue, rather research and practice needs to find out what makes people so poor at long-term
adherence to dietary changes (or behavioral changes of all types) and find solutions to that. Is it biological,
psychological, is the distinction even meaningful? And how do we fix it?
But beyond that issue, this is one place where exercise has routinely shown to have a benefit with regards
to overall body weight/body fat reduction programs. That is, while most studies have not found a massive
impact of exercise on weight/fat loss per se, the impact on weight loss maintenance seems to be much much
larger.
Both epidemiological and intervention studies have found that maintenance of regular activity following
weight loss is associated with better long-term weight maintenance (I’d note that keeping protein intake high

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also has benefits) but with one major caveat: it takes quite a bit of activity (I’d note that this seems to assume
that the diet is relatively uncontrolled after the active weight loss period).
Various lines of research suggest that a weekly exercise energy expenditure of 2500-2800 calories per week
is required to maintain the lowered body weight. If we assume an average of 5-10 cal/min for low to moderate
intensity activity, this works out to between 280-500 minutes of exercise per week or somewhere between
40-70 minutes of activity (depending on intensity and frequency) per day.
Again, the above seems to assume that the diet is relatively more uncontrolled following the actual weight-
loss intervention which isn’t automatically a good assumption. But it does put into perspective what may be
required in terms of daily activity to maintain weight loss.
.

Summing Up

So that’s a (for me anyhow) fairly brief look at the potential impact of exercise on weight/fat loss. As I
discussed in some detail in Exercise and Weight/Fat Loss: Part 1, the unfortunate reality is that all but the
most extensive exercise programs are unlikely to have much of an overall impact on the absolute quantity
of weight lost, especially in the absence of dietary changes.
The average beginner/overweight individual simply can’t burn enough calories in realistic amounts of
exercise to have much of an impact. Reducing caloric intake through various means (discussed in detail in
other articles on the site) will almost always have a larger impact on overall energy balance.
However, that doesn’t make exercise useless and there are other ways that activity can positively (and
negatively) impact on the overall goal of weight/fat loss. The first of those is in shifting the quality of weight
lost; even if exercise doesn’t affect the total magnitude of scale change, proper activity (with resistance
training coupled with sufficient protein intake being superior to aerobic work/low protein) can decrease the
loss of lean body mass and increase the total loss of fat.
There are also potential benefits to adherence/accountability with some people essentially coupling daily
activity with adhering to their diet. Anything that makes someone stick to their diet in the long-term can only
be beneficial. As noted, this can sometimes backfire, where the person then loses all good dietary habits if
their exercise program is interrupted for whatever reason.
In terms of hunger and appetite, exercise seems to have an overall beneficial impact but interactions with
the individual psychology of the dieter can affect this greatly; some people will rationalize the consumption
of food based on a misunderstanding of their actual calorie burn. This can completely overcome any benefit
of the exercise in terms of energy expenditure.
Finally, exercise appears to have the greatest potential benefit in terms of long-term weight loss
maintenance; here studies have shown that regular exercise improves long-term weight loss
maintenance. However, it takes quite a bit with upwards of an hour or more of daily activity required to
completely offset post-diet weight gains.

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Fat Loss for Athletes: Part 1
Losing body fat is often an issue for athletes and there are various and sundry (yes, sundry) reasons that
they either want or need to do this. Clearly for the physique sports (bodybuilding, fitness, figure), it’s an issue
of appearance. For performance sports (everything else), losing fat or weight can often improve
performance. Either the athlete can get into a lower weight class (if their sport has such) or they can improve
their strength or power to weight ratio, improving performance.
I’d note, and this would be a topic for an entirely separate article, that leaner is not always better. Most sports
end up having an ideal level of leanness where higher and lower levels aren’t consistent with optimal
performance. Many athletes will over train or lose muscle mass and performance in the quest to get as lean
as possible and this often does more harm than good.
Unfortunately, athletes often approach the goal of fat loss in an absolutely awful way. It’s altogether too often
assumed that they should simply do what the bodybuilders do since bodybuilders are, at least for one day
per year, the leanest folks of them all.
The problem with this mentality is that, fundamentally, the physique sports aren’t performance oriented
(fitness competitions are sort of an exception since the fitness round does require quite a bit of performance
oriented training). But bodybuilders and figure girls aren’t usually interested in performance per se, it’s all
about looking good on stage. What happens in the gym or in training is only a means to an end in this
regards. So some of the dietary and training approaches that bodybuilders would follow might not be
appropriate for a performance-oriented athlete.
At the same time, there are clearly some good ideas that have come out of the physique sports; to say that
individuals in those activities are competitive dieters isn’t far off and they have figured out a lot of good things
(much of which modern research has subsequently validated). You simply can’t apply them wholly
uncritically to every sport. I’d also note that some performance sports (women’s gymnastics and figure
skating jump to mind) also have an aesthetic aspect to them; little girls are being judged on appearance and
body in addition to how well they can fling themselves through the air.
In this article, I want to talk about how athletes of different sorts can go about best losing body fat without
sacrificing (too-much) performance. The parentheses may seem odd but it’s not always possible to
completely avoid performance (strength, power, etc.) loss while dieting down. As long as the reduction in fat
or total weight is greater than the performance loss, the strength/power to weight ratio still usually goes up.
To avoid talking about every sport known to god and man, I’m going to subdivide sports into one of three
rough categories (I’d note that I used the same three in my protein book and usually apply this scheme in
some fashion in all of my fat loss books) which are

Pure strength/power: Think Powerlifting, Olympic lifting, throwing events, etc. These are athletes who do
the bulk of their training as strength/power training of some sort and their sports don’t require endurance or
metabolic conditioning outside of work capacity considerations to handle their massive training loads. The
competition itself usually involves very little endurance component (unless you consider sitting on your ass
for 3 hours between squat and bench while you eat sandwiches to require endurance).

Pure endurance sports: This includes cycling, running, swimming, cross country skiing and anything of
that sort. Any sport where the majority of training is pretty much pure endurance style training (lower intensity,
long durations) goes in this category. And yes, trust me I realize that many of these athletes also do stuff in
the weight room and higher intensity interval work is done. I’m talking about the majority of training that they

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do. In competition, the events can actually vary pretty significantly in terms of duration and intensity. An hour
criterium race for a cyclist is a very different event than a 5 hour stage race; same for a 5k vs. marathon in
running. Regardless, the majority of training done in these sports is of the long-duration endurance type.

Mixed sports: And then there’s mostly everything else, sports that end up having to cover all of the bases
with both a good bit of strength/power work (in the weight room or on the track sprinting) and metabolic
conditioning (which can take on a variety of forms, I’ll talk about this a bit below). Football, basketball, hockey,
mixed martial arts, boxing, wrestling, etc. all belong here. These are athletes that need high levels of
strength/power (varying with the sport) and high levels of metabolic conditioning (which also varies with
sport). Competitions usually require these athletes to express strength/power over and over and over again.
Of course, I’m sure there are going to be sports (Curling? Archery? Extreme Frisbee?) that don’t fit neatly
into any of the above categories. Since I doubt they have the same requirements (outside of technical stuff)
of the main three categories, I’m not too worried about them.
Simplistically, when I look at fat loss, I take 5 components into consideration in their rough order of
importance. I’ll look at each below.
1. Total calories and the rate of fat loss
2. Protein intake
3. Fat intake
4. Carbohydrate intake
5. Training and how it can or should be changed when fat loss is the goal.
Yeah, I know. Cutting edge shit there. I’m only spelling it out so that I can look at each within the context of
each of the types of sports I discussed above. I’d note that frankly components 1-4 (and especially 1) are
the more important aspects when fat loss is the goal. All of the training in the world won’t overcome a diet
that sucks. Ok, maybe ALL of the training in the world but you pedantic assholes know what I mean.
Continued in Fat Loss for Athletes: Part 2.

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Fat Loss for Athletes: Part 2
In Fat Loss for Athletes: Part 1, I addressed some basic concepts regarding fat loss for athletes including a
look at the different ‘categories’ of athletes that I delineate and a hierarchy of factors that can or should be

modified when an athlete is trying to lose fat. In Part 2, I want to look at the first 4 of those factors.

1. Total Calories and the Rate of Fat Loss

As mentioned above, this is the single most important aspect of fat loss as far as I’m concerned. It’s usually
pretty trivial to out-eat the calories burned from training and if you don’t control calories you’re not going to
lose fat no matter what you do. And all of the weird macronutrient manipulations still don’t make a shit’s
worth of difference if calories aren’t controlled so you can stop worrying about food combining, or not eating
carbs after 6pm or whatever. With no exception all of those strategies only work to hide caloric restriction in
the guise of something else. It’s still calories at the end of the day.
So the next question comes in terms of where to set calories. A typically generic recommendation used by
bodybuilders is 10-12 cal/lb starting weight depending on metabolism (higher value for higher, lower value
for lower) and this isn’t bad for someone doing fairly moderate amounts of training (e.g. an hour or so daily).
But for athletes with very high caloric requirements this will be too low.
Many endurance athletes can have energy requirements up near 20 cal/lb, occasionally higher. Athletes
who have to do a lot of metabolic work will have elevated requirements as well. Strength/power athletes can
vary massively; Ol’ers have been reported to have fairly high caloric requirements but when you train 4-6
hours/day, even with low reps, this isn’t shocking.
Arguably a better way to adjust calories is to first determine maintenance calories (the number that will
maintain your current weight) and then reduce it by 10-20% as a starting point (I’d note that fatter athletes
can usually sustain a larger deficit than leaner). This should then be adjusted based on real world changes
in fat loss and performance changes.
A reasonable goal for fat loss might be 1-1.5 lbs fat loss/week with no major reduction in performance. If an
athlete is losing less than that, a further reduction in calories (or increase in activity, discussed below) may
be needed. If an athlete is losing more than 2 pounds per week or performance is crashing, calories would
be adjusted upwards by 10%. Eventually that sweet spot will be found. Note that as folks get lighter and
caloric requirements go down, calories will eventually have to be adjusted down even further to keep fat loss
going.
Finally I’d note that lighter athletes (women, lighter males in weight class sports) may have to be happy with
half of that fat loss, 0.5-0.75 pounds per week. Yeah, I know, that’s only 2 pounds per month. Tough titty,
don’t get fat next time.

2. Protein Intake

After calories have been set, the single next most important aspect of a fat loss diet is protein intake as
consuming sufficient protein is perhaps the single key to limiting (or eliminating) muscle and performance
loss. It’s also where a lot of athletes not of the strength/power type fuck up.
Endurance athletes tend to overemphasize carbs as it is, they often get sufficient protein only by dint of
eating so much food; when calories are restricted protein goes down and problems start. Females often
seem to fear fat and protein altogether, living on starch. Performance craters.

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Getting large amounts of dietary protein is one place that bodybuilders and other strength athletes have long
been ahead of the curve, especially while dieting. As modern research has found that higher protein intakes
have numerous fat loss benefits (including but not limited to sparing muscle loss, maintaining blood glucose
at stable levels, blunting hunger, limiting drops in metabolic rate), bodybuilders can just give a hearty “We
told you so” to the labcoats who said they were full of shit for so many years.
Of more interest, and seemingly ignored by most mainstream dietitians, protein requirements go UP when
calories go down, yet most diets seem to reduce protein. Research proved that fact 30 years ago, why the
RD’s haven’t caught on is anybody’s guess.
As outlined in detail (and with full references) in The Protein Book, I recommend that pure strength/power
athlete consume at least 1.4-1.5 g/lb protein. In some cases (usually athletes seeking extreme leanness) 2
g/lb may be required. I see no reason for more than this. Since, as you’ll see, strength/power athletes don’t
generally have the high carbohydrate requirements of other athletes (although this depends on the specifics
of the sport), they can ‘get away’ with more protein and less carbohydrates without hurting their training.
Endurance athletes, who could normally get by with perhaps 0.7-0.9 g/lb under maintenance conditions,
should increase their protein intake to at least 1.2-1.4 g/lb while dieting. Given the often absurd caloric
requirements for endurance athletes, this more than allows for sufficient intakes of other macronutrients to
support training and recovery.
Mixed sport athletes have to ‘cover’ the requirements for both their strength/power and metabolic training
and should use the high end of recommendations at 1.5 g/lb. Again, this can potentially go higher if extreme
levels of leanness need to be reached. The problem, as I’ll discuss below, is that these athletes often need
more carbohydrate in their diet and consuming too much protein tends to limit carb intake. This can hurt
performance. So it becomes a greater balancing act. These athletes need to eat enough protein to spare
muscle loss, while still allowing sufficient carbohydrate to maintain training.

3. Fat Intake

You might be surprised that I put fat intake before carbohydrate intake but outside of setting up ketogenic
(very-low-carbohydrate) diets, this is how I do things. The reason is this: very low fat diets tend to do negative
things to hormones, on top of making the diet bland and tasteless. More often than not very low-fat diets
leave the dieter exceptionally hungry which makes it harder to control calories. So before folk worry about
carbohydrate, they need to take care of dietary fat.
Now, while I don’t generally like diets set up by percentages, fat intake is where I do exactly that. 20-25%
total calories from fat is usually about right for most situations. Sometimes it may be a bit higher, it’d be a
rare situation indeed where I’d take it much lower. I’ve sometimes used a rough intake of 0.45 g/lb and that’s
a good starting point but issues of total caloric intake become a problem here and that can’t always be
adhered to.
Of the total fat intake, the only requirement are fish oils. A minimum of 6X1 grams standard capsules (180
mg EPA/120 mg DHA) should be taken daily. This can be increased to 10 capsules per day for athletes who
are either larger, simply want to, or have the calories to do it.
Beyond that, I don’t get overly hung up on fat intake. Research shows that both MCT’s and di-glycerides (in
the form of Enova oil) can slightly increase fat loss during a diet but the impact is not massive, maybe a few
tenths of a pound a week if that. Both fats do seem to help control appetite which might be one reason to
include them in a diet.

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4. Carbohydrates

So all that’s left is carbohydrate and this is generally where my diets will vary the most. As discussed in How
Many Carbohydrates Do You Need, the simplest comment I can make is that carbohydrate requirements
can vary….a lot.
It’s also one place where following the lead of bodybuilders can get athletes into trouble. Recall from above
that, for the most part, bodybuilding is not a performance sport, it’s an aesthetic one. Maintaining
performance in the gym is purely secondary to coming in ripped. So carbohydrates are often removed
completely from the diet to achieve this. Depending on the type of sport you’re talking about, this can either
be workable or about the single worst thing that an athlete can do.
A pure strength/power athlete who’s dieting and doing repeat triples in the weight room or what have you
may not need many (or any) carbs in their diet. As mentioned, bodybuilders often cut carbs down or nearly
out to get to the pinnacle of leanness. Those athletes can often get away with a carb intake of perhaps 1
g/lb or even lower. Carb cycling approaches tend to be popular, common and successful, carbs can be
higher on training days and cut down on non-training days to facilitate a larger caloric deficit and greater fat
loss.
Endurance athletes typically have the highest carbohydrate requirements although even that depends on
the type of training they’re doing. An hour spin on the bike doesn’t require that many carbs, a 6 hour ride
may deplete glycogen almost completely. Carb intake here can vary massively. Maintenance carb
recommendations for these athletes often approach 10-12 g/kg (4.5-5.5 g/lb or so) but this has to be cut
back while dieting to some degree. If volume is high enough, an intake of 2-3 g/lb might work, a lot of it will
depend on where calories are set.
Mixed sports athletes are generally going to have carb requirements somewhere in the middle. It’ll probably
end up being higher than 1 g/lb on heavy training days but unlikely to reach the higher levels of endurance
athletes. So you might see 1.5-2 g/lb as a rough average.
At the end of the day, much of the above discussion is moot. Once you’ve set calories, set protein and set
fat, carbs will simply be what’s left. So that makes more sense, let me set up a sample diet for a 200 lb
strength/power athlete with 15% bodyfat (170 lbs lean body mass) and with an estimated maintenance
calorie intake of 16 cal/lb on training days. So his maintenance requirement is 3200 calories/day.
1. Set calories: 20% deficit. 3200 * 0.20 = 640 calories. 3200 – 640 = 2560 cal/day
2. Set protein: 1.5 g/lb lean body mass = 255 grams protein * 4 cal/g = 1020 cal/day
3. Set fat: 25% of total calories. 2560 * 0.25 = 640 calories / 9 cal/g = 71 grams
4. Set carbs: 2560 calories – 1020 calories from protein – 640 calories from fat = 900 calories / 4 cal/g =
225 grams. Just slightly over 1 g/lb.
Now, if his calories had to be lowered for some reason, he’d make the reduction from carbohydrate. So if he
needed to take another 200 calories per day out of his diet, he’d reduce his carbs by 50 grams more to 175
grams. Hopefully you get the idea.
Those calories would be roughly spread across however many meals the athlete will be eating during the
diet. Of course, there’s no reason that they have to be spread completely evenly, many people like to put
more of their carbs earlier in the day or around training and slightly more fat and less carbs in the evening.
It’s all fine.
On the timing issue, I strongly feel that at least some proportion of every athlete’s daily carbs and protein
should come around heavy training sessions. A lot of athletes try to cut out those calories but I think it’s a

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mistake. It is usually done out of some misguided idea about GH release or fat loss; female athletes do it
because they think they are ‘saving’ calories but all they are doing is hurting themselves in the long run.
Total fat loss will be mostly determined by the caloric deficit, insufficient calories around heavy training only
hurts performance and recovery which is never a good thing on a diet. Carb cuts should therefore come
mainly from meals not around training. Fat intake at those meals can be slightly increased as well.
Which isn’t to say that the same amount of pre/during/post workout nutrients would be consumed on a diet
as when mass gains or performance improvements are the goal. Just that something should still be
consumed around most workouts (low-intensity metabolic stuff being the major exception). If you eat too
many calories around training, you don’t end up with enough at the other meals to stay full.
Continued in Fat Loss for Athletes: Part 3.

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Fat Loss for Athletes: Part 3
Having talked generally about fat loss and defined some terms in Fat Loss for Athletes: Part 1, along with
examining issues of diet in Fat Loss for Athletes: Part 2, I want to finish out this article series by examining
how training can or should be modified. Finally, I want to make a few comments about when in their training
year athletes should attempt to lose fat.

5. Training and Fat Loss

The final issue I want to discuss regarding fat loss for athletes is how training can or should be modified
while dieting. Again, this is a place where a lot of people make mistakes and where (especially given the
role of anabolics in bodybuilding preparation since about the 80’s) following bodybuilders can be problematic.
I’ll come back to this below.
Once again, I’m going to address the three different general categories of athletes that I described in Fat
Loss for Athletes: Part 1. Additionally, I’m going to look at training in terms of both weight room work (of any
sort) and metabolic work (this includes both standard aerobic training along with intervals).
Weight training can, of course, be subdivided into several different categories. From very heavy, low-
repetition strength or power work (5’s or less) to more bodybuilding oriented hypertrophy work (generally 6-
15 reps) to higher rep, metabolic-style depletion work (15-20 reps or more, usually with short rest periods),
weight training covers a lot of ground.
Is one best for fat loss? Of course not, they each have their pros and cons. One approach that is all too
commonplace in the weight room (and this is an idea that came out of bodybuilding in the 80’s) is that heavy
weights should be replaced by higher reps for cuts. While this certainly works when anabolics are present
to protect muscle mass, it’s absolutely the worst thing that a natural athlete can do to maintain muscle mass.
Tension builds muscle, removing heavy tension overload causes muscle and strength to go away; not what
most athletes want when they diet. Simply, if an athlete can only do one type of weight training while dieting,
it should be a lowered volume (see comments below) of heavy work to maintain muscle. The caloric deficit
and any metabolic work can take care of fat loss.
However, that doesn’t mean that higher rep/metabolic style weight training of various sorts (think barbell
complexes, KB circuits, sled dragging might even fit here, and stuff like that) can’t have a use as well.
Between the hormonal response, glycogen depletion (which increases whole body fat usage), and a
somewhat larger calorie burn, these types of training can certainly enhance fat loss. But they should only be
done in conjunction with a maintenance volume of heavy work. I’ll come back to this below.
In terms of other types of metabolic training (e.g. steady state cardio and intervals), the world seems to have
subdivided itself into two distinct camps of late. As the idea that interval training is not only the best way to
lose fat but (seemingly) the only way, the idea that low intensity steady state cardio can have any use for fat
loss has more or less disappeared. Some are even claiming (wrongly I’d add) that steady state cardio can
make dieters fatter. Apparently the four decades of bodybuilders who got contest lean doing nothing but low-
intensity steady state didn’t realize that all of that cardio was detrimental. You can read more about this in
the extended series of articles on Steady State vs. Interval Training here on the site.
Frankly, addressing this topic in detail is beyond the scope of this article. Within the context of the room I
have here, I will only say that both intervals and steady state cardio can have their role depending on the
specifics. The simple fact is that athletes can’t do high intensity training daily and most athletes will be training

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daily for fat loss. If every workout is high intensity, especially when calories are reduced, only bad things can
happen.

A Quick Comment on Volume and Frequency of Training for Fat


Loss

Another idea that appears to have come out of 80’s era (read: steroid fueled) bodybuilding dieting is that
volume and frequency of training should go UP while dieting. This is, of course, completely ass-backwards.
Recovery is always hampered when calories are restricted, trying to increase the frequency of high-intensity
training (e.g. weight training or intervals) is a recipe for disaster. If anything, the frequency (and especially
the volume) of high-intensity work should be reduced somewhat when calories are restricted to avoid over
training in the long-run.

Strength/Power Athletes
The grand majority of training done by strength/power athletes is, of course, strength power training. Yes,
some type of general prep/work capacity work is often done (sled dragging for powerlifters, extensive tempo
running for sprinters, etc) but anybody who doesn’t have their head up their ass knows that long-duration
endurance training is about the worst choice for these types of athletes because it stimulates adaptations in
the muscle that are not conducive to maximal performance.
Put a bit differently, you show me a powerlifter or shotputter that runs and I’ll show you a guy who is not
performing optimally. Show me one of those athletes who decides to start running for fat loss and I’ll show
you one who just destroyed his performance.
Training for these athletes, therefore, must revolve around the same types of training that they are doing for
their sport. As noted above, at least some volume of heavy training should be done while dieting to maintain
current strength and muscle mass levels. However, research clearly shows that the volume and frequency
of training can be cut back rather significantly.
Reductions in both of up to 2/3rds (so total sets and/or days of training can be reduced) are fine but ONLY
if the intensity (weight on the bar) is maintained. So an athlete who was doing 6 sets of 3 in the back squat
could conceivably cut back to 2 sets of 3 as long as he keeps the weight on the bar the same. If the intensity
is cut back, strength and muscle mass will suffer. Again, some volume of heavy work must be kept in.
To that, other types of work to facilitate fat loss can be added. Barbell complexes or KB circuits could be
used in the weight room to increase caloric expenditure, etc. (the complexes would replace the volume of
heavy work that had been reduced) for example. Other types of GPP, sled dragging (with lighter weights
and shorter rest intervals) and such would be another way of increasing caloric expenditure to hasten fat
loss as well.
As mentioned above, strength/power athletes wouldn’t generally want to add a bunch of steady state
endurance training as this will tend to harm leg strength. About the only exception to this is steady state
‘cardio’ that is so low intensity that it won’t cut into strength. I’m talking about things like brisk walking here,
just very low intensity activity to burn a few calories. Big guys can burn a few hundred calories with nothing
but that level of work which will add up over time without cutting into leg strength or recovery.
Interval training is a possibility here although I’d strongly suggest that a non-impact exercise method be
used. Three hundred pound athletes plus sprinting equal joint injuries. As well, interval workouts of this type
should be counted as a high-intensity leg workout. Trying to add a day or two of heavy lower body intervals

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to a weekly training schedule that already includes a significant amount of lower body weight room work is
another recipe for disaster. Something has to give.
As noted above, weight training frequency can realistically be cut much further back than most think, one
heavy leg workout per week will maintain leg strength for quite some time (athletes shouldn’t generally have
to diet that long in the first place), allowing other lower body work to be done. Frankly, metabolic weight work
of the barbell complex/KB/etc. kind may be a better fit for pure strength/power athletes.

Endurance Athletes
In modern endurance sports training, there is not a massive amount of weight training done for the most part
(although this can depend on the sport). However, for those endurance athletes who are lifting, the same
suggestions as above apply. At least some volume of heavy work should be maintained but the volume and
frequency should be reduced. This could conceivably be replaced by complexes, etc. but, in general, this
probably isn’t hugely necessary as I’ll explain below.
As expected, the majority of training of pure endurance athletes is of the endurance type. And this actually
gives them a fairly big advantage for fat loss. A trained endurance athlete can usually burn a significant
number of calories without working very hard. Simply adding an extra 30 minutes of easy training per day
can burn a significant number of calories without heavily cutting into recovery; this also allows the reduction
in food intake to be less (e.g. burn 300 extra calories with low intensity activity and reduce food intake by a
couple hundred to get about a pound of fat loss per week). Used properly, these types of easy aerobic
workouts can have an active recovery effect as well.
As far as interval training goes, most endurance athletes do intervals at some time during the season. How
much can be added to that when calories are restricted is pretty debatable. I’d expect most endurance
athletes to be focusing on fat loss during a general preparation phase (when interval training is usually pretty
low) and adding a bunch of high intensity training when the goal is lots of low-intensity volume is backwards.
As noted above, simply adding a bit of volume daily with a slight reduction in calories should do most of the
work for a typical endurance athlete.

Mixed Sports
And finally we come again to the mixed sports, the athletes whose training invariably has to cover all of the
bases in terms of both a fairly large amount of strength/power work along with a good bit of metabolic work.
In the same way that strength/power athletes can and should reduce their heavy training, mixed sports
athletes looking for fat loss should do the same. Total volume and/or frequency of heavy work can be
reduced significantly. This can be replaced by some metabolic type stuff of the barbell complex, KB, GPP
variety.
Metabolic work for these athletes can vary massively but, depending on where they are in their season,
some type of interval training or slightly increased volume of low-intensity work could reasonably be done to
increase caloric expenditure. Like endurance athletes above, the likelihood of adding yet more interval
training to an already heavy training load are pretty slim. Rather, adding slightly to the volume of work already
being done may be the best approach.

When to Lose Fat


Although I didn’t list this topic in the original list in Part 1 of this series, a final issue of importance for athletes
is when to lose body fat during the year. Bodybuilders and physique athletes have it somewhat simpler in
this regards since they aren’t so performance oriented. And most don’t use any type of periodization in the

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first place. The simply focus on gaining muscle until a contest is chosen and then move into dieting at that
time.
Athletes usually have an annual plan of some sort and may have specific competitions that they need to be
prepared for. This means that fat loss and dieting periods can’t be chosen at random as it could potentially
hurt their ability train or peak effectively.
In general, I think that losing fat should be the focus of any type of general physical preparation (GPP) phase.
Yes, I know that they have gone the way of the dodo in modern sports training but most athletes still do
some period of training when the volume is relatively higher and the intensity lower. Since maximum
performance isn’t the goal, a small reduction in calories with a slight shift in training to facilitate fat loss is
possible during this time.

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Set points, Settling points, and Bodyweight Regulation Part 1
Having explained why the separation of psychology and physiology is a false separation in Dieting
Psychology vs. Dieting Physiology, I want to discuss quickly some of the physiology behind diet failures.
This is a topic that I discuss in detail in nearly all of my recent books and I’m not going to spend endless time
on it here (trying to eventually get back to the psychological factors behind diet failures).
A long standing debate in the world of obesity research revolves around the idea that bodyweight (or perhaps
body fat) is regulated. What does that mean exactly?
Think about your thermostat (yes, this is the example I always use): you set it to keep the house at 80
degrees and it continually senses the temperature (via a thermometer). If the temperature goes above 80
degrees, the air conditioning comes on; if it drops below 80, the heat comes on. This is a regulated system.
Your cruise control in the car works the same way: you set the speed you want to maintain and it either gives
more or less gas to the engine in an attempt to maintain that level.
For some 50 odd years, it’s been thought that bodyweight/body fat are regulated similarly; that is the body
is attempting to maintain some set level (called the set point) and is adjusting things like appetite, behavior,
movement, etc. to do so.
A great deal of animal research supports this model: starve a rat and its metabolic rate slows, it moves
around less (conserving energy), it’s appetite goes up such that when you give it free access to food again
it will eat until it reaches its starting weight at which point things go back to normal. The same occurs when
you fatten it up, metabolic rate goes up, activity goes up, appetite/hunger go down and it rapidly returns to
its starting weight when you stop force feeding it. The rat is, somehow, trying to maintain weight at a set
level.
Quick note: and this ties into that research review I did on homeostatic vs. hedonic pathways a few weeks
back: exposed to certain types of diets (in rat lingo, this is called a cafeteria diet and consists of calorically
dense tasty foods), most rats will readily maintain a weight that is above their set point (when exposed to a
more typical rat diet). That is, the tastiness of the food can overcome any homeostatic attempts to prevent
weight gain. This is important and something I’ll come back to later in this series.
Some research has found a similar effect in humans although the studies tend to be very mixed on this (I’ll
address why in a later blog post): when you diet down a human being, often you see metabolic rate
decreasing far more than you’d expect based on the loss of body weight alone. That is, based on the weight
loss, say you expected metabolic rate to drop by 200 calories; but when you measure it it really drops by
300. That extra 100 calories is more than predicted and suggests that the body is ‘adapting’ to the weight
loss in an attempt to not only slow further fat loss but also to get bodyweight/body fat back up when food
becomes available again.
There are other adaptations, folks often decrease their activity levels (conserving energy), fat burning goes
down and fat storage goes up, appetite often goes up so that people eat more when food is made available.
In common parlance, this is often referred to as the ‘starvation response’ and, yes, there is something to it.
Unfortunately, it’s basically the price that has to be paid for losing body fat to any significant level. People
talk constantly about avoiding the starvation response and things of that nature but the only way to avoid it
completely is to never lose fat.
In any case, perhaps the classic study in this regards is the Minnesota semi-starvation study, a 6 month
study undertaken during the mid 20th century where a number of lean male war objectors were placed on
50% of their maintenance calories for the entire time while forced to engage in quite a bit of daily activity (5-
6 miles walking per day).

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In that study, after reaching the lower limits of human body fat levels (about 5%) and showing a host of
adaptations (including an obsession with food), the men showed uncontrolled hunger when food was made
available and rapidly ate themselves back up beyond their initial body fat level.
This has been termed post-starvation hyperphagia (a technical word that means overeating). Of course, it’s
crucial to realize just how lean these men got; the response to less severe diets or fat loss is exactly that:
less severe. A lot of this also depends on the nature of the intervention (e.g. type of diet) and the population
studied. Initial body fat percentage plays a huge role here for reasons you’ll learn about in future blog posts.
Unlike in rats however, in humans, overfeeding doesn’t have nearly as reliable an impact in terms of
increasing metabolic rate and it looks increasingly like any bodyweight regulation system present in
humans is assymetrical: that is it protects against weight loss far more so than it protects against weight
gain.
Put a bit differently and most realize this on some level: for most it’s far harder to lose weight than it is to
gain it.
The reasons for this are a bit obscure but it’s thought that since humans never had any real evolutionary
pressure to not get fat (e.g. we had no real predators and, during evolution, few could have gotten or stayed
fat for extended periods), the body never had to develop defenses against weight gain. In contrast, starving
to death was a very real reality in our evolutionary past and the body developed a number of ways of
‘defending’ against weight loss.
Moved into modern times (where food is readily available and activity levels continue to drop), this is a bad
bad thing.
For completeness, I should note that there are exceptions, some people appear to show a pronounced
response to overfeeding which is now being called NEAT (non-exercise activity thermogenesis) or SPA
(spontaneous physical activity); some folks ramp these up to high levels when subjected to increased caloric
intakes, burning off the excess calories instead of storing them as fat.
These are the people for whom gaining weight is often difficult: invariably when they try to increase food
intake, not only do they sub-conciously start moving around more (burning off the excess calories), their
hunger shuts off. You probably had one of these guys in your high school, the one who was always fidgeting
and bouncing his leg and all of that; it turns out that the caloric expenditure from that type of activity adds up
significantly over a day.
Hunger also seems to shut off more rapidly in these folks as well. They are often the folks who also claim “I
eat a ton and can’t gain weight” but when you look at their food intake, they either aren’t eating much at all
or they eat a single big meal and get so full that they don’t eat much else for the rest of the day (or next day).
Unfortunately, NEAT seems to be quite genetic and researchers still haven’t really figured out the exact
causes or if this can be applied to help in any practical way. It probably has to do with not only the various
hormones involved in all of this (which I’ll discuss in a later blog post) but how the brain responds to them.
In any case, all of the above supports the basic idea of a set point in humans: human metabolic rate, etc.
clearly adapts (and does so more than weight loss alone would predict) to caloric restriction and weight/fat
loss.
Unfortunately, it doesn’t appear to adapt nearly as well to overfeeding and weight gain.
Even more unfortunately, this isn’t the end of the story and determining exactly what sets the setpoint or
whether or not it can change in the long-term is an area of continuing debate. Most of what I’ve seen suggests
that, if setpoint can change, it only goes up. I’ve seen nothing to suggest that it ever comes back down, even
over years of maintaining a lowered body weight.
Additionally, not everyone agrees with the idea of a biological setpoint anyhow, some researchers feel that
a settling point is a better description of what’s going on.

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Set Points, Settling Points and Bodyweight Regulation Part 2
In Set Points, Settling Points and Bodyweight Regulation Part 1, I took a little bit of a look at the issue of
bodyweight regulation and the concept of the set point, examining various bits of research supporting the
existence of such a thing. At the end of that piece, I also mentioned that not all researchers believe in the
concept of a set point, feeling instead that a settling point is a more accurate representation of what’s
actually going on.
Recall from Part 1 that the set point idea basically says that the body will attempt to defend some body
weight (or body fat) level (or perhaps range) by adjusting things such as metabolic rate, activity, hunger, etc.
in response to changes in weight or fat.
I’d mention, and I’ll come back to this in a future blog post that it’s most likely body fat levels that are being
regulated, more than absolute body weight per se.
This almost suggests that any attempt to alter body weight or body fat levels is futile because of the body’s
defenses (and some have interpreted the concept in exactly that fashion). This is especially true when it
comes to weight/fat loss as the human body appears to defend against weight/fat loss much moreso than
against weight/fat gain.
In contrast, the essential idea of a settling point is that bodyweight/body fat levels will ‘settle’ at a given point
based on the environment. The availability (or lack thereof) of food (and how tasty it is), the amount of activity
done, all work to adjust where the body will settle.
So if you take the average human being and put them in America, with tasty inexpensive food readily
available and very little activity required on a daily basis, their body weight will ‘settle’ at a certain point that
may be somewhat high.
Now change their diet, or enforce a large amount of exercise, presumably their body weight will settle at
some lower point (regardless of set point). At least assuming that the intervention to diet/activity is
maintained.
Now take that same person and put them in a third world country where massive amounts of food aren’t
available and high amounts of activity have to be done daily to obtain it; bodyweight will presumably settle
at the lowest level.
This would tend to occur absolutely regardless of any biological set point.
And, as usual, there is data to support both concepts. And, given recent understanding that a variety of
systems regulate body weight (including homeostatic and hedonic), it seems pretty obvious to me that both
set point and settling point concepts are working to regulate body weight/fat levels.
Nobody can deny that the body fights back (to relatively greater or lesser degrees) when weight/fat levels
change, especially when weight/fat is lost.
At the same time it’d be asinine to think that humans are little more than automatons driven by a homeostatic
drive to eat with no control over what goes into their mouth.
As well, clearly the environment plays a huge role in eating behavior. Increasing portion sizes, exposure to
food advertising and a host of other factors all impact on eating behavior regardless of homeostatic systems.
An excellent synthesis of these ideas came in a 2002 paper titled “Putting behavior back into feeding
behavior: a tribute to George Collier.”
Quoting from the abstract:
“The combination of these data with George’s insightful idea, has merged into a modification of the popular
Set-Point Theory of the regulation of body weight. The alternative “Settling Zone” Theory suggests that
whereas biology may determine a range of body weights (adiposity) that are maintained fairly constant for

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long periods of time, within this “zone”, the behaviors responsible for controlling energy intake and energy
expenditure are influenced primarily by environmental and cognitive stimuli.”
Essentially, while the set point may be working to keep people within some range of body fat levels, even
within that range individual behaviors and environment will affect where within that range folks will end up.
This model manages to tie pure biology in with pure psychology which, as I noted earlier, is a false separation
in the first place.
And, I’d note again, it’s becoming abundantly clear that, regardless of set points or settling points or whatever
you want to call it, the prevailing environment and individual behaviors can overcome either.
For most people given the current environment (which researchers are now terming obesigenic, meaning
that it generates obesity), this means maintaining a much higher bodyweight/body fat level than you’d expect
based on the set point concept (note again that any homeostatic system defending against weight gain
appears to be pretty weak).
I’d note also, and this is a contentious issue, that some evidence suggests that the set point can go up
(apparently permanently) with the maintenance of chronic obesity. Other things such as pregnancy, puberty
and a couple of others may be able to permanently move the set point up as well.
However, there are clearly subgroups of dieters and athletes who, through various behavioral means
(generally involving dietary choice and activity) can clearly maintain bodyweight and bodyfat levels that are
presumably below (or at least at) their biological setpoint.
Of course, contest dieters (bodybuilders, figure competitors) often work like to hell to diet down far below
their set point. Fighting against hunger, metabolic slowdown, etc. these individuals clearly can and do reach
the extreme lower limits of human body fat levels (roughly 3-5% for men and 7-9% for women). Few maintain
that in the long-term of course and most suffer from the post-starvation hyperphagia I mentioned in Friday’s
post.
Horror stories of competitors gaining weight rapidly and massively following a strict 12-16 week diet are
plentiful, many people will finish their contest preparation and go on month-long food binges (with no training)
afterwards. Some of this is clearly physiological, some of it is psychological and, again, there are overlaps
in the system.
I’ll continue with some of the physiology behind this system next time and (finally, really, I promise) move
into psychological stuff after that.

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9 Ways to Deal with Hunger on a Diet
Diets fail for a lot of reasons but one of the primary ones is simply hunger. I discussed this sort of tangentially
in the research review Why Do Obese People not Lose More Weight When Treated with Low-Calorie Diets
and one of the comments on that article is what prompted me to write this article.

What is Hunger?

To say that human hunger is complicated is a vast understatement. To cover it in detail would require a
series of articles or perhaps an entire book. Research continues to uncover numerous interacting and
overlapping hormones (such as leptin, ghrelin, peptide YY, GLP-1 and others) that monitor how much and
what someone is eating (along with their body weight) and those all send a signal to the brain that drives a
number of processes, not the least of which is hunger.
Now, it would be truly simple if that’s all there was to it but humans also eat/get hungry for non-physiological
reasons. We get hungry out of boredom, because we are at a party and it’s expected that we eat, because
we just saw a commercial for some food we like and many others.
Simplistically, we might differentiate these different drivers of hunger into physiological and psychological
factors although, as I discussed in the article Dieting Psychology vs. Dieting Physiology, the distinction
between the two is not only false but increasingly fuzzy. Physiological drives can manifest themselves as
‘psychological’ hunger and psychological factors can affect physiology.
However, even though the distinction is a false one, it is often useful practically to make that division and I”ll
be doing so through the rest of that article.
Sufficed to say that human hunger is exceedingly complicated and finding out ways to deal with hunger while
dieting is a huge first step in making diets more effective. And with that said, in no particular order of
importance, here are 9 Ways to Deal with Hunger on a Diet.

1. Eat More Lean Protein

While dietitians continue to squabble over whether carbohydrates or fats are more filling in the short-term,
the data is actually abundantly clear: protein beats them both out. Increasing amounts of research has
shown that both acutely and in the long-term, higher protein intakes help blunt hunger. It also helps that, as
long as you’re dealing with sources of lean protein (low-fat fish, skinless chicken, even low-fat red meat), it
can be tough to get a lot of calories from protein in the first place.
I’d also note that there are many other reasons to consume sufficient amounts of lean protein on a weight
loss diet including blood glucose stability and sparing of muscle mass loss. It’s also worth mentioning that
a lot of the benefits that are often attributed to ‘low-carbohydrate’ diets have more to do with the increased
protein intake; the benefits occur because they are ‘high-protein’.

2. Eat Fruit

For odd reasons fruit has gotten a bad rap for dieting, at least in the athletic and bodybuilding subculture but
little could be further from the truth. One aspect of hunger has to do with the status of liver glycogen, when

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liver glycogen is emptied, a signal is sent to the brain that can stimulate hunger; the corollary is that
replenishing liver glycogen tends to make people feel fuller.
The fructose component of fruit works to refill liver glycogen and folks who include a moderate amount of
fruit in their weight loss diets often report feeling much less hungry. That’s in addition to the other benefits
of fruit (fiber, nutrients). Oh yeah, eat whole fruit, stay away from fruit juice.

3. Eat More Fiber

No list of this sort would be complete without the mention of fiber. Fiber can help with hunger in at least two
ways. The first is that the physical ‘stretching’ of the stomach is one of many signals about how much food
has been eaten; when the stomach is physically stretched the brain thinks you’re full. High-fiber/high-volume
foods (e.g. foods that have a lot of volume for few calories) accomplish that most effectively.
Additionally, fiber slows gastric emptying, the rate at which food leave the stomach. By keeping foods in the
stomach longer, a high-fiber intake keeps folks full longer. Basically, mom was right, eat your vegetables.

4. Eat (At-Least) Moderate Amounts of Dietary Fat

Ignoring the debate I mentioned above about carbs versus fat and hunger, the simple fact is that exceedingly
low-fat diets tend to leave a lot of people hungry in both the short- and long-term. Tying in with my comments
about fiber in Number 3, dietary fat also slows gastric emptying (hence the aphorism that high-fat meals
really stick to the ribs). While dietary fat does little to blunt hunger in the short-term, moderate intakes tend
to keep people fuller longer between meals since the meal sits in the stomach longer.
As well, exceedingly low-fat diets often taste like cardboard, tying into some of the comments I made initially
about psychological effects of dieting; people won’t follow a diet that doesn’t taste good for very long. Dietary
fat gives food a certain mouth-feel and very low-fat diets remove that, leaving people dissatisfied. The diet
usually ends shortly after that.
Research has shown that moderate fat diets improve adherence to dieting and, with rare exceptions, I don’t
suggest taking dietary fat much lower than 20-25% of total calories on a fat loss diet. In some cases (such
as very low-carbohydrate diets), it may be higher than this.

5. Exercise

I’m hesitant to mention exercise in this article simply because the response to it can vary drastically in terms
of hunger control on a diet. Doing the topic justice would take a complete article in and of itself but here I’m
going to give a quick overview.
Basically, through myriad overlapping mechanisms, exercise has the potential to increase hunger, decrease
hunger or have no effect. Some of the effects are purely physiological. On the one hand, exercise increases
leptin transport into the brain which should help some of the other hunger signals work better. On the other
hand, some people can get a blood glucose crash with exercise (this is especially true in the early stages of
a program) and this can stimulate hunger. Most research suggests that exercise has, if anything, a net
benefit in terms of hunger control but it’s even more complicated than that.
Whether or not exercise helps with hunger control ends up interacting with psychological factors that I’m not
going to detail here. Some research suggests that people ‘couple’ exercise with their diet. The underlying

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psychlogy seems to be along the lines of “I exercised today, why would I ruin that by blowing my diet.” That’s
good.
However, another category of people often use exercise as an excuse to eat more. The underlying
psychology seems to be “I must have burned at least 1000 calories in exercise, I earned that cheeseburger
and milkshake.” Of course, since people basically always over-estimate how many calories they burned
with exercise, they end up doing more harm than good.
The short-version of this point is this: for some people, regular exercise (and it may not be anything more
than a brisk walk) has a profound benefit on keeping them on their diet. And for others it tends to backfire.

6. Consider Intermittent Fasting (IF’ing)

IF’ing is a current dietary trend that, while exact definitions vary, basically refers to a pattern where someone
fasts for some portion of the day (perhaps 16-20 hours) and eats most of their food during a short ‘eating
period’. Various interpretations are out there but there is emerging research showing a variety of health
benefits from this style of eating.
In the context of this article, IF’ing can be particularly valuable for smaller dieters who simply don’t get to eat
a lot of food each day. A small female trying to subsist on 1000-1200 calories per day and trying to eat 3-4
times per day is only getting a few small, relatively unsatisfying meals per day.
However, if that same dieter fasts most of the day (many find that hunger goes away after an initial spike in
the morning), she can eat 1-2 significantly larger (and more satisfying) meals later in the day.
If you’re interested in IF’ing, I’d direct you to Martin Berkhan’s Leangains.com for the absolute best source
of IF information on the net. Martin is currently working on a book on IF’ing and I, for one, can’t wait to see
it.

7. Use Appetite Suppressants

The history of diet drugs is a mixed bag but, for the most part, diet drugs have fallen into one of two major
categories: metabolic enhancers and appetite suppressants. Sometimes the drugs do both. Now, used
without changes in diet and activity, these drugs tend to only have small and transient effects.
But the simple fact is that they can help a diet. The old Dexatrim (containing pseudoephedrine HCL) was
actually very nice in that it blunted hunger without over-stimulating the person but it’s not available any
more. I’m personally a big fan of the ephedrine/caffeine stack.
Despite scare-mongering to the contrary, EC used properly (e.g. don’t take 3X the recommended dose) is
actually quite safe and has both potent appetite suppressant effects along with boosting metabolic rate
slightly. Hell, I thought EC was important enough that I gave it an entire chapter in The Rapid Fat Loss
Handbook.
Which isn’t to say that I think every dieter should be using/abusing appetite suppressants from day 1. At
least try the non-drug strategies first; but when the hunger is clawing at you making you want to quit your
diet, consider using one.

8. Be more Flexible Towards Your Dieting

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This is another topic that really deserves a book to fully discuss. I’d say that I need to write that book but
the fact is that I already did, the topics I’m going to briefly look at here are discussed in detail in A Guide to
Flexible Dieting.
Let me address this topic with a question “What would you do if I told you you could never have something
again?” Assume it’s something you like or want, how would you react? Odds are you’d want it that much
more, right. It’s human nature, we want what we’re told we can’t have.
Guess what, that’s dieting. Or at least how many dieters approach dieting. Many diets are predicated on
some food being bad, off-limits or what have you; dieters go into the diet thinking “I can’t ever eat XXX again
in my life” which just makes them want XXX that much more. This is one of the psychological aspects of
hunger I mentioned in the introduction.
And, of course, the followup to this is that when dieters do eventually eat XXX (and they will), then they just
feel guilty and miserable, figure the diet is blown and eat the entire bag or box of XXX and abandon the diet
altogether.
It’s truly a damaging approach to dieting and research has clearly shown that the type of rigid dieter I’m
describing above (who expects absolute perfection from their diet or it’s a failure) do worse than more flexible
dieters.
The reality is that, within the context of a long-term diet, even small deviations don’t really do much harm
(unless the person goes berserk and makes it harmful). That is, say you’re on a diet and you eat a couple
hundred calories of cookies because you really wanted them. If you’ve dieted the past 6 days, that’s no big
deal. However, if you decide that you are a worthless piece of crap with no willpower and eat another 1000
calories of cookies; well you made it into a problem. Understand?
I always recommend that dieters use strategies like free meals (non-diet meals, preferably eaten out of the
house), refeeds (extended periods of deliberate high-carbohydrate over-consumption) and full diet breaks
(periods of 10-14 days where the diet is abandoned for maintenance) when they diet. It keeps people from
falling into the rigid dieting trap that, invariably, backfires. Again, all of the details can be found in A Guide
to Flexible Dieting.

9. Suck it Up or Stay Fat

I want to make it clear that I’m not being facetious with the title of this one; and I’m only being slightly
obnoxious. Even if you do everything I talked about above, apply every strategy perfectly, the reality is that
you will probably still have some hunger on a diet.
Well…too bad. The simple fact is that losing weight requires eating less than you’re burning and this will, at
some point, generate hunger. Now, there are exceptions, extremely overweight individuals often find that
they have no appetite in the initial stages of dieting but the reality is that eventually hunger will rear it’s ugly
head.
At which point every dieter is faced with a fundamental choice which, put simply is this “What’s more
important to me, losing weight, or eating this food?” I’d note that this is also a reason I’m so adamant about
the flexible dieting strategies, at least one way of dealing with food cravings is to include them in the diet in
a controlled fashion. That way the dieter is controlling the diet, instead of the other way around.
But even with that, hunger is a reality of dieting no matter what else you do. Now, you can try to reframe it
(Tom Venuto in his new book suggested telling yourself that “Hunger is fatness leaving the body.”) or you
can simply accept it (yes, I know, very Zen) and move on.

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But none of that makes the hunger away, it’s just you trying to trick yourself out of feeling bad about it. When
that point is reached, there are only two options that I’m going to put very bluntly.
You can suck it up or stay fat.
After you’ve gotten your protein and fruit and fiber and fat and appetite supressants and exercise and flexible
dieting strategies down pat, when hunger rears its ugly head, those are the only two options left.

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Rapid Fat Loss Without Weight Training – Q&A
Question: I’m beginning a rehab program for a diastasis recti. I’m male, 58. I’m in fairly decent cardio shape
(resting heartrate of 52 and can do 30 second intervals at 85-95% MHR; I try to do 15-20 minutes of variable
paced warmup followed by the intervals and cooldown.)
However, I’m significantly overweight (6′ 220; ~35% body fat by a cheap scale) which is obviously a
contributor to the diastasis. You can see why the idea of rapid fat loss is attractive. The thing is, for the first
6 weeks on the diastasis program, strength
training is out of the picture. I’m doing my cardio on a VersaClimber, which at least works my legs fairly well.
Would the rapid fat loss protocol work OK under these conditions? It sounds as though to try it I would need
to put in more time on the climber and skip the intervals for the duration.

Answer: The short answer is that, at your current body fat percentage, yes, the Rapid Fat Loss Handbook
program can be done without weight training. This is an issue that I discuss in the book as well as in the
article Initial Body Fat and Body Composition Changes but, simply, the higher your initial body fat
percentage, the less muscle you are likely to lose under any circumstances (and by extension the leaner
you are the more muscle you tend to lose, although this depends on a host of variables). The primary
function of resistance training on any diet is to maintain muscle mass (as discussed in Weight Training for
Fat Loss Part 1 and Weight Training for Fat Loss Part 2) but when the risk of muscle mass loss is reduced,
the importance of weight training is lessened.
An additional factor, also discussed in the book is that there is often an increase in lean body mass (and this
represents both muscle mass and connective tissue) when people gain body fat. From the standpoint of
obtaining a ‘normal’ body weight (whatever ‘normal’ means here) losing that ‘extra’ LBM is thought to be
beneficial or necessary by some obesity experts.
Finally, at least in relative beginners, even cardiovascular exercise (and the Versaclimber is one of the rare
machines that has both an upper and lower body component) has some effect on sparing muscle mass
loss. So the inclusion of that (although with volumes cut back to match the recommendations in the book)
should be sufficient until you abdominal issue has healed and you can begin resistance training.
Hope that helps and good luck!

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Protein Intake While Dieting – Q&A
Question: You refer to “adequate protein intake” as important, but what do you consider adequate? In my
case — calorie restriction of ~750-1000 kcals below BMR coupled with regular strength training? Is there a
percentage of intake you consider ideal, and is it higher while dieting versus maintenance (to prevent muscle
loss during times of restriction)?

Answer: The above question actually came through in the comments section of Exercise and Weight/Fat
Loss: Part 2 and I thought it was important enough to address explicitly since it’s a place where I still see
many mainstream diets and dieters making mistakes. It’s worth noting that bodybuilders and other strength
athletes have been promoting higher protein intakes while dieting for decades and this is yet another place
where modern science has ended up validating those beliefs many years after the fact.
The question of adequate protein under different conditions is one that has a long history of debate, the
issue of maintenance requirements as well as protein intakes for athletes is still highly debated with science
on both sides of the story (for details you can refer to The Protein Book).
With regards dieting specifically, this was a topic of much study in the 60’s and 70’s as researchers started
looking past the simple issue of weight loss and into that of changes in body composition; the goal moved
from weight loss per se to that of generating fat loss while minimizing lean body mass and muscle mass
loss.
After much toing and froing and research had been done it was eventually found that a protein intake of
about 1.5 g/kg of lean body mass (LBM; note that researchers actually used Ideal Body Weight but this is a
rough proxy for LBM) was necessary to spare LBM losses in a non-training obese individual consuming low
calories.
This is about double the DRI for protein (at 0.8 g/kg) at maintenance calories. So for an overweight individual
at say 200 pounds and 30% body fat (this would give them an LBM of 140 lbs or 63 kg), that would be a
protein intake of 95 grams of protein per day. Please note that this value is simply a minimum and dieters
may still find that higher protein intakes are beneficial from a hunger blunting effect or what have you (see
below).
In that context, I’d mention that at least one of the studies I referred to in Exercise and Weight/Fat Loss: Part
2 that found no benefit of resistance training gave something like 40 grams of protein to the subjects; far
less than necessary or adequate. So it’s no surprise that no protein sparing effect of exercise was seen; the
diet was inadequate in the first place.
It’s worth noting that more recent research supports further benefits of increased protein intakes while
dieting, beyond simple lean body mass maintenance. Protein is the most filling nutrient (meaning that higher
protein intakes tend to control hunger better) and studies have found that higher protein intakes can help to
stabilize blood sugar levels while dieting which has benefits from both an energy level and appetite
standpoint. Protein high in the amino acid leucine (with the dairy proteins whey and casein being the two
proteins highest in leucine) seem to have extra benefit in this regard.
Now, as individuals get leaner, protein requirement tend to go up further for reasons discussed in other
articles on this site. As well, regular training tends to further increase protein requirements. So lean athletes
trying to lose fat while sparing lean body mass loss need even higher protein intakes than this. And we’ve
known for decades now that caloric intake per se tends to impact on protein requirements; as caloric intake
goes down, protein requirements go up. And vice versa.
While less data on this group is available, bodybuilders and athletes have long used a protein intake of 2.2
g/kg (1 g/lb) lean body mass as a generalized intake level and as folks get very lean, intakes of 3.3 g/kg (1.5

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g/lb) of lean body mass may be required to stave off muscle loss while dieting. In some very extreme cases,
such as the near protein only diet approach of my own Rapid Fat Loss Handbook even higher protein intakes
may be required for very lean individuals.
So basically we have an intake continuum ranging from about 1.5 g/kg (0.68 g/lb) as a minimum for the
obese non-training individual up to a high of around 3.3 g/kg (1.5 g/lb) of protein per pound of lean body
mass for very lean heavily training athletes or bodybuilders with middle ground values being found in
between those two extremes. You’ll note that I didn’t put any of those values in terms of percentages for
reasons discussed in Diet Percentages: Part 1 and Diet Percentages: Part 2.
So that’s what I mean by ‘adequate protein on a diet’ when I use that phrase. It’s context dependent with
the primary variables being body fat percentage (as this goes up, protein requirements go down), caloric
intake (as caloric intake goes down, protein requirements go up and vice versa), and activity (with regular
activity generally increasing protein requirements).

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The Fundamentals of Fat Loss Diets Part 1
I did an online interview of some sort a while back and one of the questions I was asked was this “What are
the basic components of fat loss diet that you would recommend? That is, if you had to give the most general
fat loss diet approach, what would it be?” Another way of phrasing the question might be thus: What’s the
simplest fat loss diet you can draw up, with the fewest details for people to get obsessive over?
This is actually a very good question and, while I can generally answer it in about 4 sentences, I’m going to
do my best to stretch it out into a full length article by overexplaining everything and giving at least some of
my rationale for the different recommendations. In many places, I’ll be linking out to other articles on the site
that go into individual topics in more detail.
Since this is going to get long, I’m actually going to divide the article into two parts. Today I’m going to focus
on what is probably the most contentious area of diet set up, on Tuesday next week, I’ll cover the other
factors that I use to set up a basic fat loss diet.

Complexity vs. the Fundamentals

It’s quite common, and this is true in all aspects of, well, everything, for people to want to get into really
involved interpretations before they have the fundamentals down. I see it in training and I see it in diet; of
course the industry tends to pander to that by providing unbelivably complicated training and diet programs
that, for most people, simply aren’t necessary.
People always want advanced training programs long before they have the basics down; and they tend to
be drawn to overly complicated diet plans when they don’t even have the basics down. I have probably
contributed to this to some degree as I do tend to write complicated dieting approaches from time to time
(e.g. The Ultimate Diet 2.0).
Of course, there are times, usually for very lean folks dealing with all of the myriad issues involved in getting
very lean that necessitate such complex approaches. The UD2, for example, is an advanced diet for
advanced dieters; it’s assumed in that book that the folks reading it have spent a couple of years getting the
fundamentals in place. That’s why I didn’t spend any time discussing those fundamentals in that book; if
you don’t already have the basics of eating and nutrition down, you aren’t ready for it. Unfortunately, that
doesn’t stop people from trying from time to time.
But at the end of the day, and again this is true in training and in diet, the fundamentals are the most
important. Until you have those in place, none of the advanced stuff makes a difference. And, generally
speaking, you find that once you have the fundamentals in place, the advanced stuff doesn’t add that
much. Again, in specific situations, worrying about the details matters (e.g. very lean natural bodybuilders
trying to get super lean); for most people it doesn’t.
I’d note, semi-tangentially, that there tend to be individual personality differences in how people approach
these kinds of topics. Some people are, shall we say, a bit obsessive compulsive (I’m one of them) about
things like nutrition and training. They are the ones who, as Dan Duchaine once phrased it, want nutrition
with ‘all the plumbing’. They want diets to be set out in terms of how many seconds to wait between sets,
protein and amino acid recommendations must be set to the milligram, etc. Amusingly, these folks want all
of the details whether they are necessary or not in the first place (usually they are not).
At the other extreme are people who get overwhelmed by that type of information, they want easy
generalities and lots of detail puts them off. Many people are somewhere in between the two, they want

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enough details to get the job done well but not so much that they get paralyzed by it. But I’m getting off
topic.

The Fundamentals of Fat Loss

Ok, before I talk details, let me spell out how I would set up the most basic fat loss diet on the planet. These
criteria are in order of importance, by the way and are:
1. Create an appropriate caloric deficit/set caloric intake appropriately
2. Set protein intake
3. Set dietary fat intake
4. Everything else depends
Anyone who has read any of my books may recognize this to some degree since I tend to focus on the first
3 and leave 4 up to the specifics of the situation. Now, I’m actually going to spend a bit of time on #1 and
for that reason will discuss #2-4 next Tuesday so that this doesn’t get too long to read.

Create an Appropriate Caloric Deficit/Set Calories

Ok, this is probably the one that will cause the most controversy which is why I’m going to spend the most
time on it. A constant and never-ending cry, and one that has recently come back to life due to some popular
but misguided books, is that calories don’t count, or thermodynamics doesn’t apply to humans or other
nonsense. In that vein, a current meme (look it up) is that the energy balance equation is incorrect for
various reasons; I addressed this in some detail a little while back in the article The Energy Balance Equation.
In case you can’t take the time to go read it in full, I’ll only say that the people saying that calories in vs.
calories out don’t understand the energy balance equation; in fact I saw some hysterical examples of this in
a recent thread on a fitness forum, people tossing out examples that they thought disproved the energy
balance equation but which only showed that they really had no idea what they were talking about. Again,
the problem isn’t with the equation, the problem is with people who don’t understand what it
represents. Read the article for more.
But the simple fact is this, the ONLY way to force the body to call on stored energy (e.g. body fat) is to create
an imbalance between energy intake (from food) and energy expenditure (this side of the equation comprises
a number of factors discussed in detail in Metabolic Rate Overview). That’s why this is the primary criterion
in how I set up fat loss diets. I don’t give a damn what else you do, if you haven’t created an imbalance
between intake and expenditure (and you’ll see that there are different ways of achieving this goal), nothing
else will matter.

Creating the Deficit: Different Paths to the Same Goal

Now, there are many different ways to create this imbalance and I think that also lends itself to
confusion. Each of the below can work to some degree and makes it look like it’s not just calories in vs.
calories out. But it still is.
For example, a traditional way is to simply reduce total food intake, that is reduce the quantity of food such
that less calories are being eaten. Certainly this works because, by definition, eating less means you’re
taking in less calories than when you were eating more.

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Another is to change the quality of food but this tends to introduce a subtle confound that most people seem
to forget (and that I discuss in detail in Is a Calorie a Calorie): some foods are relatively harder to overeat
than others. Or, put differently, some food are easier to overeat than others.
If changing the quality of food eaten causes people to eat less, and that causes weight/fat to be lost, it’s
easy to confuse the quality of the food with the total caloric expenditure. But it’s not the quality of the food
per se that is causing the weight/fat loss or gain; it’s the change in total caloric intake due to the change in
food quality.
I would mention that changing the macronutrient content of the diet can have a small impact in this
regards. For the most part, switching out carbs and fat doesn’t do much despite what many claim. The
difference in the thermic effect of food for carbs vs. fat is about 3% so for every 100 calories you switch out
one for the other, you might see a 3 calorie difference in energy expenditure.
I’d note that carbs have a the advantage here with a thermic effect of 6% compared to 3% for fat. But the
effect tends to be so small as to be irrelevant unless you are looking at whole scale changes to diet. Again,
if you replace 100 calories of fat with carbs, you burn 3 more calories per day. If you replace 1000 calories
of fat with carbs, you burn 30 calories more per day; you’ll lose an extra pound of fat every 116 days. Whoop
de doo.
And while I know someone is going to bring up the issue of gluconeogenesis on ketogenic diets in the
comments, I’ll only point out that the impact of this is small and disappears after about 2-3 weeks (when the
body shifts to using ketones for fuel). As well, any increase in expenditure from this pathway is balanced
against a loss of the thermic effect of carbs.
As well, direct research (by Brehm) shows that there is no difference in resting metabolic rate for ketogenic
vs. carb-based diets; the thermic effect of food was higher in the high-carb condition. If there were a true
metabolic advantage in terms of energy expenditure for ketogenic diets, someone would have been able to
measure it by now. They haven’t and they aren’t going to and all of the theorizing about it doesn’t change
the fact that direct research hasn’t supported the concept.
Now, protein has the biggest impact in terms of the thermic effect of food, switching out carbs or fat with
protein tends to increase the energy out side of the equation but you have to make pretty large scale changes
for it to be particularly significant. I’d note that protein also tends to be the most filling of all the nutrients
and studies show that increasing dietary protein intake tends to cause people to eat less calories. Which is
another huge confound; if increasing protein makes folks spontaneously eat less, it looks like it was adding
the protein per se that did the magic. But it wasn’t, it was the effect of increasing protein on total energy
intake that caused the fat loss. Like I said, a subtle confound that people tend to miss a lot.
Another way of course is to use activity to increase energy expenditure. That increases the energy out side
of the energy balance equation. I’ll do a full article on the role of activity in weight/fat loss (and it’s more
complicated than I’m making it sound here since I don’t have space to cover it in full) but this is one valid
way to do it. Activity not only increases energy expenditure but also impacts on the quality of weight loss
(e.g. fat vs. muscle) and can impact on appetite (both positively or negatively depending on the
specifics). Again, I don’t have space to cover it here but will in a future article.
The problem for most is that the amount of calories that can be expended by most people in exercise is not
large. An irony that I”ve mentioned before is that the only people who can usually burn a ton of calories in
activity are trained athletes; and they usually don’t need to lose fat. But the reality is that an hour of activity
for most people will not burn a staggering number of calories. Usually caloric restriction per se or a
combination of cutting calories and increasing activity is going to be more realistic.
And before you start typing out comments about how all of the above is flawed and thermodynamics doesn’t
hold for humans or all of that other nonsense, consider the following realities:

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1. The number of people who have lost fat by making excuses about thermodynamics and other nonsense:
zero.
2. The number of people who have lost fat by creating a deficit in one of the ways I’ve mentioned: all of
them.
End of discussion.
Of course, someone will point to someone who did lose fat without ‘counting calories’ but invariably they did
something dietarily that I described above: made a wholesale change to the types of food that they were
eating that caused them to spontaneously eat less food. Which still makes me right; they created an
imbalance between intake and expenditure, they just did it in a way that looked ‘different’ than simply
counting calories. But it still had the same end result. They still created a caloric deficit, it was simply
‘hidden’ by what looked like something else.
And make no mistake, I would love it to be different, I would love to be able to tell you how to magically lose
fat without some change in your eating or activity or creating an imbalance in the energy balance equation;
I want magic to be real too. And when I figure that magic out, I’ll be a billionaire. And until that happens,
the reality is that to lose fat you must create some imbalance between intake and expenditure. It may not
be what you want to hear but it is the truth.

Setting Calories

Ok, with that introduction out of the way, how do you set calories for a basic fat loss diet? A value that has
been used for absolutely years is 10-12 cal/lb, and I explain where that value comes from to some degree
in How to Estimate Maintenance Calories. Essentially it’s a 20% reduction from a rough maintenance
estimate of ‘About 15 cal/lb or so’.
I’d note that this is your basic moderate deficit diet, as I discuss in Setting the Deficit – Small, Moderate or
Large there can be various pros and cons to using smaller or larger deficits. But, once again, here I’m
focusing on simplicity and the basics and trying to avoid any source of complication.
In general, 10-12 cal/lb tends to be a decent starting point for fat loss diets. Please note that this is only a
starting point and will always have to be adjusted based on real-world changes. Some people with high
activity levels may need higher calories than that, and folks with lower daily activity levels may need less.
In the modern world, with daily activity levels going down (especially if you work in a sedentary job), lower
caloric intakes are altogether too often required. I have known many people who had to go to 8 cal/lb with
an hour per day of low to moderate intensity cardio to lose fat effectively. I was one of them back when my
daily activity entailed sitting in front of the computer all day and doing an hour or so of weight training a few
times per week. Now that I train about 18 hours per week, I can diet with higher calories if needed.
I’d note that, for various reasons discussed in Lean Mass or Total Weight to Set Calorie Levels, I tend to use
total weight to set starting caloric intake levels. As noted in the paragraph above, you always have to make
adjustments based on real-world changes in body composition and it’s simply faster and easier to use total
weight; it avoids issues with trying to get a good estimate of body fat percentage and saves people the
trouble of all that pesky math. In my books I often use a more complicated approach but this article is about
simplicity so use total weight.
And that ends Part 1 of the article. In Part 2, which I’ll post next Tuesday, I’ll address points 2-4 from the
section above: protein requirements, fat intake, and the ‘it depends’ part of the diet. See you then.
Read A Primer on Fat Loss Diets Part 2.

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The Fundamentals of Fat Loss Diets Part 2
On Friday, in The Fundamentals of Fat Loss Diets Part 1, I started to answer the following question: “What’s
the simplest fat loss diet you can draw up, with the fewest details for people to get obsessive over?”
In that article, I listed the following 4 topics that make up the ‘base’ of a fat loss diet, again in order of
importance:
1. Create an appropriate caloric deficit/set caloric intake appropriately
2. Set protein intake
3. Set dietary fat intake
4. Everything else depends
In Part 1, I looked at the issue of calorie balance and setting calories appropriately. As I stated there, despite
claims to the contrary on various places on the Internet, without the creation of a caloric deficit (either through
manipulation of energy intake OR energy expenditure), no fat loss can occur.
In Part 1, I also provided a rough starting point for caloric intake of 10-12 calories per pound of total body
weight. As noted in that article, this is only a starting point and, depending on the specific, relatively higher
or lower caloric intakes may be more appropriate.
While much of this variability is due to differences in daily activity level and/or individual physiology, there
are also various pros and cons to using larger or smaller deficits, a topic I discuss in Setting the Deficit –
Small, Moderate or Large.
Today I want to look at the other three components listed above, protein intake, dietary fat intake and then
the everything else depends catetgory which is where the individual variability comes in.

Set Protein Intake

After total calories, the single most important aspect of a fat loss diet, as any readers of my books know, is
total protein intake. There are a number of reasons for this not the least of which is this: one major concern
during fat loss is the loss of lean body mass (which includes but is not limited to skeletal muscle as discussed
in What Does Body Composition Mean).
Now, in the early days of nutritional science, researchers did a lot of work trying to determine things like
whether or not carbohydrates or dietary fats were more protein sparing (e.g. did their intake prevent the loss
of protein) but eventually someone had the bright idea to just test eating more dietary protein. In what should
not have been a surprise, the most protein sparing nutrient turned out to be…dietary protein. That is,
providing sufficient dietary protein on a diet was truly the key to limiting (or preventing) the loss of body
protein during fat loss.
There are, mind you, many other reasons to eat more dietary protein on a fat loss diet. Another huge benefit
is that, of all three macronutrient (protein, carbohydrates, dietary fats), protein is the most filling. That is, it
tends to blunt appetite/hunger (the distinction is not important here) the most. This was actually such an
important role for dietary protein that I made it #1 on the list of 9 Ways to Deal with Hunger on a Diet.
Additionally, research (primarily by a researcher named Layman) has shown that, in contrast to
carbohydrate, increasing dietary protein tends to keep blood glucose more stable while dieting. This is
important as falling blood sugar can trigger hunger and specifically carbohydrate cravings.
So, as mentioned above, providing sufficient amounts of dietary protein on a diet is key, that’s why it’s the
second most important factor I look at in terms of setting up a basic fat loss diet. But how much do you ask?

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Now, researchers have an annoying tendency of putting protein and other dietary requirements in terms of
percentages but, as I discuss in Diet Percentages there are many problems with this. That’s why, in all of
my books, you will find protein requirements set relative to body, weight in terms of grams/pound or
grams/kilogram.
I’d note that, in general, it’s better to use lean body mass to set protein intake, rather than total body
weight. I’d also note that, for lean individuals (e.g. a male at 10-12% body fat), the difference is relatively
negligible. However, for individuals carrying a lot of body fat, the difference in total and lean body mass
makes it important to take the difference into account. This is discussed in more detail in The Protein Book.
That actually depends. A variety of factors go into protein requirements while dieting, the two major ones
being initial body fat percentage and activity level. In general, fatter individuals tend to lose less lean body
mass than leaner individuals and this means that they don’t need as much dietary protein to spare lean body
mass. This is discussed in more detail in Initial Body Fat and Body Composition Changes
Which doesn’t mean that they may still not benefit from higher protein intakes (in terms of appetite or blood
glucose control) but, strictly speaking, it may not be required from the standpoint of sparing lean body mass
loss. As folks get leaner, protein requirements go up and I find that many nutritionists do not take this factor
into account; they give the same protein intake requirements for lean as for overweight individuals.
An additional factor is activity as this is known to affect protein requirements as well. Contrary to what most
think, some early research actually suggests that regular activity reduces protein requirements (by improving
the body’s utilization of what is being consumed) but I’d say the majority suggests that regular activity
increases protein requirements and I tend to err on the side of too much rather than too little in this
regards. I’d also note, and this is a topic for another day, that aerobic activity and weight training have
somewhat different effects on both protein requirements (and lean body mass sparing during a diet).
So how much? Bodybuilders have long used a protein recommendation of 1 g/lb body weight (2.2 g/kg)
while dieting and this certainly a decent starting point. As noted above, I tend to err on the side of too much
than too little and for lean athletes dieting, a protein intake of 1.5 g/lb (3.3 g/kg) may be a better starting
place.
Again, there is some individual variability in this; some people seem to get by with less protein than
others. But for lean individuals a protein intake of 1-1.5 g/lb (2.2-3.3 g/kg) is usually about right. I’d note that
in extreme situations, such as my Rapid Fat Loss Handbook diet, even higher intakes may be required. But,
once again, this article is about the most generic diet I can set up.
For very overweight individuals, less protein than this is probably required on a strict physiological
basis. Assuming no activity, as little as 0.7 g/lb (~1.5 g/kg) may be sufficient. If weight training or other
activity is added this can go up. Frankly, the old bodybuilder value of 1 g/lb (2.2 g/kg) of lean weight may
be perfectly sufficient.
Again, individuals carrying a lot of body fat should use lean mass to determine protein intake values not total
weight. This means having some way of estimating body fat percentage and the amount of lean mass can
be calculated using the equations in Body Composition Calculations.

Set Dietary Fat Intake

After calories and protein are set, the next issue I look at in terms of fat loss diet is the dietary fat
intake. Again, there are multiple reasons for this. At the very least, there is a small but important daily
requirement for the essential fatty acids. This topic is discussed in A Primer on Dietary Fats and all of my
books but I’ll recap briefly here.

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In short, there are two essential fatty acids, that is fats that must be consumed on a daily basis for optimal
health and function. Those two fatty acids, in this case are the w-3 and w-6 fatty acids (strictly speaking,
those terms refer to a class of different fatty acids but that’s more complexity than I want to get into). The
parent fatty acids are alpha-linolenic acid and linoleic acid respectively and these are metabolized
extensively to other fatty acids.
In the case of alpha-linolenic acid (w-3), the main metabolites we are concerned with are EPA and DHA
which are more commonly known as the fish oils. They do a staggering number of things in the body and,
honestly, if I saw a list of claimed benefits and had not read the research, I’d think someone were selling me
a bill of goods.
But they do have all of those benefits and more: they decrease inflammation, may enhance fat loss, inhibit
fat storage, and may impact positively on appetite. The w-3 fatty acids are also the ones in the shortest
supply in the modern diet unless folks eat a lot of high-fat fish on a consistent basis. I’d note that simply
consuming things like flax oil and such (sources of ALA) are not ideal; the conversion to EPA/DHA is tiny
and, in general, I recommend explicit supplementation of the fish oils while dieting.
In the case of linoleic acid (w-6) there are a number of products including arachidonic acid and others. In
general, obtaining w-6 fatty acids are not a problem, they are plentiful in the diet. And while they don’t
appear to have the massive health negatives that are often claimed for them (see A Primer on Dietary Fats
Part 2 for a bit more about this), they aren’t usually a problem to obtain in the modern diet. If someone is
eating just about any dietary fat, they will fulfill the requirements for the w-6’s.
However the requirement for the above fatty acids is quite small, a few grams per day at most. Even the
maximum fish oil intake I recommend is only 6-10 standard 1 gram capsules and most folks will get sufficient
w-6 from the fat intake in the other foods they are eating. That’s not much fat.
But that’s also not the only reason to consume dietary fat on a standard generic fat loss diet and I actually
tend to start with a higher amount than this. Why? There are really two primary reasons and both speak to
dietary adherence. This is actually far more important than I think many people realize: any diet, no matter
how wonderful, isn’t any good if people can’t stick with it.
As people found out the hard way in the 80’s, extremely low-fat diets tend to be bland, boring and leave
people feeling really hungry all the time. Research has even supported this, moderate fat diets tend to
generate better dietary adherence in the long-term than very low-fat diets. Allowing moderate dietary fat
intakes means more potential variety in dietary intake (when you’re limited to near zero fat foods, the list of
what you can eat can become very small) and dietary fat provides mouth feel, a sensory issue that makes
food taste better. Simply: people don’t stick with diets that taste like shit for long.
An additional factor, and one I’ve mentioned in several of my books is that moderate amounts of dietary fat
tend to blunt hunger in the long-term (e.g. between meals). Now, this is actually more complicated than I’m
making it sound but I’m not getting into the details here. Basically, while dietary fat doesn’t blunt hunger in
the short-term (e.g. in the course of a single meal), it tends to keep people fuller between meals. This
occurs for a few reasons.
The first is that dietary fat tends to slow how quickly meals empty from the stomach (this is called gastric
emptying). Very low-fat meals tend to digest quickly, people often get hungrier sooner which makes diet
adherence a problem. I’m sure all readers are familiar with the concept of a meal that ‘sticks to their ribs’
and this is the genesis of this aphorism: meals with even moderate dietary fat sit in the gut longer, keeping
the person fuller.
Additionally, research has shown that moderate fat (as opposed to low- or high-fat meals) keep blood
glucose more stable, presumably much of this is mediated by a slowing of gastric emptying. Moderate in
this case is about 10-14 grams total fat per meal.

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So, in my ‘most generic diet’, I tend to set dietary fat levels at a nice moderate level; enough to get the
benefits above without crowding out the rest of the calories. Now, despite my comments about percentages
above, most dietary fat research has only used percentages and I tend to default to that here, suggesting
20-25% dietary fat as as starting place for the generic fat loss diet.
On 10-12 cal/lb this works out to a range of 0.22-0.33 g/lb (0.48-0.72 g/kg). For a 200 lb. (90kg) dieter, this
would equate to 44-66 grams of fat per day. Which, across 4-6 meals per day is right about 10-14 grams of
fat per meal. Isn’t math fun?
But this amount will allow not only easy intake of the essential fatty acids but allow for some other foods and
dietary fat to be included in the meal to make the diet more palatable; it also fits the research with blood
glucose stability and hunger blunting between meals.
Now, as with other aspects of the diet, there may be times when less or more dietary fat is appropriate, at
the risk of repeating myself again and again, the above is simply for the most generic fat loss diet there is.

A Quick Summary

Ok, let me recap the first three components of the diet. I’m going to assume a 200 lb (90 kg) dieter with 15%
body fat (so he has 30 pounds body fat and 170 pounds lean body mass). His super generic basic fat loss
diet would be the following
1. Calories: 200 lb * 12 cal/lb = 2400 calories/day
2. Protein: 170 lbs * 1.5 g/lb = 255 grams/day (1020 calories/day)
3. Fat: 200 lbs * 0.33 g/lb = 66 grams/day (594 calories/day)
You might note that his total protein and fat don’t add up to the daily total. Rather, he’s only fulfilled 1600
calories per day with those. That leaves 800 calories which would be generically assigned to
carbohydrate. That’s 200 grams or 1 g/lb total weight, another common value often used for basic diet set
up.
And that might be a great generic fat loss diet for this person but that brings us finally to:

Everything Else Depends

Essentially in setting up the generic diet, I set calories, set protein and set fat. Those are the three aspects
of the diet that I consider most important. You can think of them as the ‘essential’ aspects of the fat loss
diet. Everything else, as you can imagine depends.
In the quick summary above, I went ahead and calculated out what a typical dieters overall diet would be
assuming that the remaining calories of the day went into carbohydrates. But this isn’t an automatic
assumption. That’s where it gets complicated. Issues such as activity level, insulin sensitivity and the
specifics of the diet all go into how I would determine what, if any modifications would be made to the generic
template.
I addressed these in some detail in the 4-part article series Comparing the Diets. And while I can’t look at
those all in detail in this article (and I tried to put my general ‘scheme’ for how I work this stuff out in A Guide
to Flexible Dieting) I do want to look at a couple of examples where the ‘it depends’ bit might get modified
for their individual needs.
Clearly daily activity is one of those factors and impacts on many issues I’ve discussed not the least of which
is caloric intakes. As I mentioned in The Fundamentals of Fat Loss Diets Part 1, while 10-12 cal/lb tends to
be a good starting point for caloric levels, it can vary. Individuals with very high daily activities (usually

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athletes in training) will tend to find that those values are too low. By the same token, individuals with very
low daily activities (e.g. you ride a desk) may have to go lower than that to effectively lose fat. I’ve seen
sedentary folks need to go as low as 8 cal/lb (and that’s with an hour of exercise per day) to effectively lose
fat.
Activity also impacts on carbohydrate requirements. As discussed in How Many Carbohyrates Do You Need,
activity levels can drastically affect carbohydrate (and of course calorie) requirements. Individuals involved
in large amounts of activity will not only find that they need more than the generic 12 cal/lb for dieting but
might find that the above 1 g/lb carb intake is insufficient for training and recovery. In contrast, someone
with limited or no activity during the day might find that reducing carbohydrate (and replacing those carbs
with dietary fat) might be a more appropriate choice. That would be in addition to possibly needing to reduce
caloric intake in total.
In a related vein, insulin sensitivity seems to impact on whether or not individuals do better or worse with
higher carbohydrate or higher fat diets, as I discuss in Insulin Sensitivity and Fat Loss. Now, in general, with
increasing body fat, insulin sensitivity tends to decrease (note that this is absolutely NOT universal;
overweight individuals can be insulin sensitive and lean folks can be insulin resistant). As well, individuals
carrying more weight often can not or simply don’t engage in regular activity. The combination of those two
factors interact to mean that lower carbohydrates and higher dietary fat intakes are often more appropriate.
There are others, of course. Individual variance, food preferences, etc. all go into modifications of the generic
diet template. I don’t have space to address them all here but hopefully have given people a starting
point. The generic diet template is exactly that, it’s a summary of what I consider the three most important
factors to any fat loss diet: caloric intake, protein intake, dietary fat intake. Those three tend to be relatively
unchanging in my diet plans (although there are exceptions, The Rapid Fat Loss Handbook is very low in fat
but it’s also meant to be short-term). Everything else depends on the those factors that they depend on.
And that’s a Primer on Fat Loss Diets.

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The Effect of Two Energy-Restricted Diets, a Low-Fructose Diet vs.
a Moderate Natural Fructose Diet – Research Review

Madero M et. al. The effect of two energy-restricted diets, a low-


fructose diet versus a moderate natural fructose diet, on weight
loss and metabolic syndrome parameters: a randomized controlled
trial. Metabolism. 2011 May 27. [Epub ahead of print]

One of the proposed causes of obesity and metabolic syndrome is the excessive intake of products
containing added sugars, in particular, fructose. Although the ability of excessive intake of fructose to induce
metabolic syndrome is mounting, to date, no study has addressed whether a diet specifically lowering
fructose but not total carbohydrates can reduce features of metabolic syndrome. A total of 131 patients were
randomized to compare the short-term effects of 2 energy-restricted diets-a low-fructose diet vs a moderate
natural fructose diet-on weight loss and metabolic syndrome parameters. Patients were randomized to
receive 1500, 1800, or 2000 cal diets according to sex, age, and height. Because natural fructose might be
differently absorbed compared with fructose from added sugars, we randomized obese subjects to either a
low-fructose diet (<20 g/d) or a moderate-fructose diet with natural fruit supplements (50-70 g/d) and
compared the effects of both diets on the primary outcome of weight loss in a 6-week follow-up period. Blood
pressure, lipid profile, serum glucose, insulin resistance, uric acid, soluble intercellular adhesion molecule-
1, and quality of life scores were included as secondary outcomes. One hundred two (78%) of the 131
participants were women, mean age was 38.8 ± 8.8 years, and the mean body mass index was 32.4 ± 4.5
kg/m(2). Each intervention diet was associated with significant weight loss compared with baseline. Weight
loss was higher in the moderate natural fructose group (4.19 ± 0.30 kg) than the low-fructose group (2.83 ±
0.29 kg) (P = .0016). Compared with baseline, each intervention diet was associated with significant
improvement in secondary outcomes. Reduction of energy and added fructose intake may represent an
important therapeutic target to reduce the frequency of obesity and diabetes. For weight loss achievement,
an energy-restricted moderate natural fructose diet was superior to a low-fructose diet.

Background

Every since John Parillo said that fruit makes you fat over 30 years ago, fruit has
held an odd place in the world of dieting. It’s quite common to see contest dieters
talking about ‘dropping out fruit’ and removing fruit from the diet is not an
uncommon recommendation when someone stalls on their diet.
More recently, the rabid furor and hype over refined fructose (and especially High-
fructose corn syrup or HFCS) has only added to this. If reports I’m seeing are
right, the consumption of fructose and/or HFCS will make you fat, drive up blood
pressure and make your muscles fall off. HFCS is responsible for the problems
with the economy (when Obama isn’t being blamed), the war in Iraq and just

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general human meanness and unhappiness. Ok, I may be exaggerating slightly
but it’s only slightly.
I addressed the issue of HFCS in Straight Talk About High-Fructose Corn Syrup: What it is and

What it Ain’t. – Research Review, an article that drew quite the share of comments (inane and otherwise)
and I’d point readers towards that article for a more detailed look at what I’m going tot talk about next.
Make no mistake, studies have clearly shown that excessive fructose intake (and this is usually due to an
excessive HFCS intake and that is typically due to the consumption of non-diet soda) cause problems. But
often the studies are, well, let’s just call them silly. They almost always revolve around the chronic intake of
simply non-physiological intakes of whatever is being studied (sometimes pure fructose, sometimes HFCS).
In one that people like to cite at me, rats (rarely a good model for humans) were fed a 60% fructose diet for
6 straight months and this induced leptin resistance. I was actually going to do a research review on it
(mainly to point out everything wrong with it) but couldn’t be bothered. The short version is that a 60%
fructose diet isn’t even possible in humans. Humans don’t do well with large amounts of pure fructose intake
as it causes stomach upset.
And if you’re going to argue that most fructose in the diet comes from HFCS (which is about half fructose),
that means that the equivalent 60% fructose diet in a human would consist of 120% of the diet being from
HFCS. Except that that is impossible.
I’d mention, humorously, that the rats didn’t actually gain weight during the 6 months of fructose overfeeding;
rather, it was during the high-fat part of the study that the weight gain occurred. But the anti-HFCS crusaders
(who are often pro-fat) missed that point since they seem to only read abstracts on this stuff. Not that it
applies in either case because it’s freaking rats and the diet was completely impossible for a human to
achieve in the first place.
In another study, humans were given 200 grams of pure fructose to see what happened. I don’t recall the
details but the results were negative. First and foremost, that’s 800 calories of pure fructose which is just a
ton. Second, again going by the fact that HFCS is only about 1/2 fructose (the other half is glucose) that
would be the equivalent of someone eating 400 grams of HFCS. 1600 calories per day just from HFCS.
That’s about 16 standard sized non-diet sodas per day (or one super duper mega insane Big Gulp). Now,
I’m not saying that’s healthy, I’m not disagreeing that that is a problem. But have you ever seen someone
drinking that much soda who didn’t have the rest of their diet look like absolute shit? Usually the ones
refilling the 128oz cup with coke are eating a ton of other junk food. My point being that the HFCS may not
be the only thing causing issues here. Yet folks are fixated on HFCS as the source of all evil.
Which isn’t to say that smaller amounts of fructose don’t or can’t cause issues. I wrote an article over 10
years ago looking at this issue and it was clear that beyond a certain level (about 50 grams of pure fructose
per day) there was the potential for issues. At the time, the big endpoint had to do with blood
triglycerides. Fructose is metabolized almost exclusively in the liver (quite in fact almost zero incoming
fructose will ever reach the bloodstream in humans) and this is a rate limited process. Above a certain point,
fructose starts being converted to fat in the liver.
It’s worth mentioning that some studies have also found that, because it doesn’t raise insulin, fructose
consumption doesn’t blunt fat oxidation after you eat it. So while eating a ton of fructose at once (which is
abnormal) can cause fat production in the liver, the body burns more fat. Almost as if it all sort of cancels
out.
But the above invariably was looking at either absurd levels of pure fructose or HFCS. What about fruit? To
a degree, fruit has become sort of guilty by association. One of the sugars in fruit is fructose and the hysteria

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over HFCS (again coming primarily from non-diet soda and refined foods) and the fructose content has
caused people to lose their minds.
Basically, people have written off anything containing HFCS or fructose IN ANY AMOUNT. If either are on
the label, that food is ‘evil’. Evil I tell you. Even consider eating it and your muscles will fall off and you’ll
explode with fat. You’ll start beating your pets and probably become a serial killer and end up with your
story on Law and Order: SVU. Fructose is serious stuff if Internet message boards are to be believed.
But it’s key to realize that fruit doesn’t even contain that much fructose in the first place, about 7% by
weight. So a 100 gram piece of fruit (a medium sized apple or banana for reference) might contain about 7
grams of fructose in addition to the other calories. Even if you use a 50 grams per day cutoff, that’s 7 medium
pieces of fruit. Not impossible but that’s a lot of fruit.
A second issue is that fruit, as opposed to pure fructose or HFCS, contains other stuff, micronutrients, anti-
oxidants, flavonols and everything else that might, just might, impact on how it’s metabolized in the
body. You can’t automatically throw out the fruit with the dishwater (yes, I’m mixing my metaphors) because
studies of purified fructose/HFCS using insane amounts have found problems.
Finally is an issue that the dynamics of how nutrients are handled while dieting (that is, in a hypocaloric
state) are often vastly different than when someone is weight stable or gaining weight. So yeah, it’s pretty
clear that large amounts of fructose/HFCS are a big issue for the average person who is inactive, gaining
weight and for whom the entirety of their diet is pretty much crap. But that doesn’t mean that fruit as part of
an overall hypocaloric weight/fat loss diet is automatically the same problem. And that, finally brings us to
today’s paper.
.

The Paper

The researchers set out to address two questions. The first was whether a calorie
restricted diet that specifically restricts fructose would improve markers of the
metabolic syndrome. They also hypothesized that a diet high in natural fructose
(From fruit) would be superior to one where fruits were limited.
Towards this end, 131 patients were recruited of which 107 finished the study, all
were obese (average body fat 40%) and nearly 80% of the subjects were
women. After determining basal caloric requirements, subjects were placed on
meal plans of 1500, 1800 or 2000 calories. The diet itself consisted of 55% carbs,
15% protein and 30% fat and the main difference between the two groups was
the fructose content. One group was limited to less than 10 grams of fructose
per day, the other was allowed 50-70 grams of fructose per day coming almost
exclusively from fruits.
Food was not provided for the subjects (arguably the biggest limitation of the
study); rather they were given meal plans and had to record their food intake at
least once weekly (food reports can be notoriously inaccurate and I’ll come back

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to this). Adherence to the diet was defined as at least 80% attendance for
scheduled clinic visits.
A variety of things were measured including weight and waist measurement along
with body fat percentage. A Tanita BIA scale was used and I’d note (as I discuss
in Measuring Body Composition: Part 1 and Measuring Body Composition: Part
2) BIA is not a perfect method as it can be drastically impacted by changes in
hydration state. A vast number of metabolic variables including blood glucose,
blood pressure, insulin, creatinine, uric acid cholesterol, triglycerides and others
were also measured. A measure of quality of life was also made in both groups.
The study lasted 6 weeks and these were the results.
In terms of changes in the measured health parameters there were no significant
differences between groups in terms of anything. The fructose group showed a
slightly better drop in blood glucose (no surprise there) and the low-fructose group
showed a slightly better drop in blood pressure; neither of these reached
statistical significance.
I’d comment here that this isn’t uncommon: in a dieting situation, most things
change/improve as a function of the weight/fat loss and diet composition tends
not to matter. This is a point lost on many who look at dieting situations (such as
a recent study where a high fat intake caused no problems when weight was
being lost) and extrapolate it to situations where someone is weight stable or
gaining weight. Basically, weight/fat loss tends to trump just about everything
else but that doesn’t meant that the same results will be seen if the person is
gaining weight.
But what about the weight/fat loss? The two groups’ weight losses were 4.19+-
0.30 kg and 2.83 +-0.29kg after six weeks. And perhaps to the surprise of many,
the high-fructose group was the one that lost the greater amount of weight. Body
Fat percentage also dropped 2.09+-6.32% in the low-fructose group compared to
2.89+-6.33% in the high-fructose group but this wasn’t statistically significant. The
BMI drop was also higher in the high-fructose group but the change in waist to
hip ratio was not.
I’d note that there was massive overlap in total weight loss and I’ve reproduced
the actual results below.

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Like I said, a huge amount of overlap even if the weight drop was larger in the
high-fructose group. There was an improvement in quality of life in both groups
with no difference between them.
.
My Comments

Ok, so what does this paper say? I think the first point I’d make is that this current
idea that carbs make you fat or prevent weight/fat loss is clearly incorrect. I wish
someone would send this paper to Gary Taubes to help him try to remove his
head from his ass. Both groups lost a significant amount of weight and fat and
did it eating 55% carbohydrate.
And clearly, at least in the population tested (obese subjects, mostly women),
fructose in the form of fruit caused no problems. At worst, the high-fructose diet
was no worse than the low-fructose diet (in terms of all health parameters
measured).
And, at least looking at weight loss, it may have been slightly superior. The
researchers had no real explanation for the differential given that the caloric
intakes were supposed to be identical. They suggest that perhaps the higher
intake of anti-oxidants, etc. from the fruit might have played a role. They also
point out that the low-fructose diet had a higher glycemic load (since natural fruits
had to be replaced by higher glycemic index carbs, I doubt this given the Glycaemic
Index Effects on Fuel Partitioning in Humans – Research Review.

Rather, I suspect that the difference in weight loss is just a weird artifact of the
study especially given that there was no significant difference in changes in body
fat percentage or waist/hip ratio. While higher insulin doesn’t really impact on
fuel utilization, it does impact on water retention, causing the kidney to resorb
water. Lowering insulin (as would occur in the fructose group) might have caused
greater water loss.
There is also the issue of the diet not being perfectly controlled since only meal
plans were given. Fructose tends to blunt hunger in many people (this occurs
through a vagally mediated mechanism in the liver which sends a fullness signal);
perhaps the high-fructose group ate a bit less. Again, this isn’t really supported
by the lack of body fat or waist/hip ratio changes.

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Regardless, clearly the idea that the data on massive intakes of either fructose
or HFCS doesn’t seem to apply to fructose coming from fruit. At least not in the
population tested. As I mentioned above, the fruit group did at least as well on
all measured markers and was slightly superior in terms of weight loss. The idea
that fruit needs to be eliminated because it contains fructose would seem to be
flawed, at least in this group.
Of course, readers of this site are wondering if this applies to leaner individuals
and this study can’t answer that question. I’d note that for every anecdotal report
of someone removing fruit and getting lean, there are just as many (and many
coaches) who keep fruit in the diet and their guys get plenty lean. One is Borge
Fagerli (aka Blade) who has found, in many clients, that the re-addition of fruit to
the diet helps people get lean. But that’s not research, just his observation.

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Why Big Caloric Deficits and Lots of Activity Can Hurt Fat Loss
This week, several people have brought a recent case-study to my attention and asked me for comment. In
it, a 51 year old female began marathon training along with a (self-reported) low calorie diet and either
appears to have gained weight or not lost weight (she also showed a very depressed metabolic rate, nearly
30% below predicted).
By raising her calories gradually, her body fat (as measured by BIA) came down and her metabolic rate
increased. Now, without more details, it’s hard to really comment on this and the link to the case study is
the total amount of information available.
But we’ve got an older (either post-menopausal or peri-menopausal) woman, undisclosed anti-depressant
medication, self-reported food intake and a method of body fat measurement that is, at best, problematic
(read Methods of Body Composition Measurement Part 2 for more details). Odd things happen metabolically
around menopause, some medications can cause issues, food reporting is notoriously inaccurate and BIA
isn’t ideal to track changes. Then again, the measured metabolic rate change is pretty interesting; something
was going on.
That said, I’ve mentioned in previous articles that one oddity that I’ve seen (and personally experienced)
over the years is one where the combination of very large caloric deficits and very large amounts of activity
(especially higher-intensity activity) can cause problems for people either stalling or slowing fat loss.
Like my previous article on The LTDFLE, or Long-term Delayed Fat Loss Effect, this is one of those oddities
that seems to crop up more often than you’d expect. It’s also one where there’s not a ton of research but I
will happily provide a good bit of speculation on what I think may be going on.
I’d also note that the combination of big caloric deficits and large amounts of activity clearly isn’t detrimental
to everyone. Some folks can get away with it but, for many, it tends to backfire more than anything else.

First, Some Background

Back in my early 20’s, I remember a very specific client I had. She was a little bit, well, to be honest nuts. She
was older, I think she had gone through menopause but I wouldn’t swear to that. In any case, she started
working with me, determined to lose weight and immediately jumped into something like 2 hours of cardio
per day and cut calories massively. She claimed 600 calories per day and I won’t even try to describe her
diet; it was insane (breakfast was supposedly one-half an egg and to this day I’m not entirely sure how you
eat half an egg).
Now, I didn’t know much at that point but I had this general idea that too much activity and too few calories
was a bad thing. For weeks on end I entreated her to either cut her activity or raise her calories. She
adamantly refused; how could that possibly work? I tried to point out that what she was doing wasn’t working
either and she could hardly do worse by trying something different but that line of logic went nowhere.
In any event, at one point she went on a cruise or a vacation or something. And what do you think she
did? Exercised less and ate more like everybody does on vacation. And she came back something like 5
pounds lighter (some of which may very well have been The LTDFLE mind you). “See, see.” I told her, “You
ate more and exercised less and good things happened.”
And she immediately went back to a massive caloric deficit and over-exercising. But that’s how it goes
sometimes.
Later in my 20’s, mind you, I’d do the same thing during the now infamous Bodyopus experience (probably
the singular experience that taught me what NOT to do during a fat loss diet). Frustrated by stalled fat loss

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(I had dieted far too long at that point in the first place), I worked even harder, cutting calories further and
adding more activity. That coupled with some genuinely awful ‘carb-loads’ took fat loss to a standstill.
In addition to those case studies, this is a phenomenon that I’ve seen elsewhere including the support forum,
I imagine readers run into it constantly: people (frequently but not always women) who try to combine
excessive caloric deficits with massive amounts of activity (often with a lot of that activity being high-intensity
activity) and nothing is happening. And if you can get them to reduce activity (or just cut back the intensity
to reasonable level) or increase calories, things invariably start to work better.
.

What’s Going On: Let’s Talk About Cortisol

Cortisol is one of those hormones that I imagine everyone reading this has heard about and about which a
lot of misinformation exists. Simply cortisol is a stress hormone, released by the body in response to nearly
all kinds of stress. In the fitness/bodybuilding world, cortisol has gotten an almost exclusively negative
reputation (cortisol is ‘bad’ in the way that testosterone and thyroid are ‘good’) although this is simplistically
incorrect.
Rather, whether cortisol does good things or bad things in the body depends on how it’s released. Simply
(and I’d simply, ha ha, refer folks to Robert Sapolsky’s amazing book Why Zebras Don’t Get Ulcers for a
detailed look at this; I also talk about cortisol in The Stubborn Fat Solution), acute pulses of cortisol tend to
do good things and be adaptive and chronic elevations in cortisol tend to be bad and be maladaptive.
For example, the morning cortisol pulse helps to promote fat mobilization. In contrast, a chronic elevation
of cortisol (especially in the face of high insulin levels) tend to promote visceral fat accumulation. As a non-
fitness related topic, acute pulses of cortisol tend to be good for memory (why we often remember stressful
situations in such detail) while chronic elevations (as often seen in depression) make memory go down the
toilet. And there are endless other examples of where acute cortisol pulses are good and chronic elevations
are bad; again see Sapolsky’s book for details.
In any case, dieting in general is a stress. And of course training is a stress. And the more extreme you do
of each, the more of a stress occurs. And I suspect that a lot of what is going on when folks try to combine
excessive caloric deficits with massive amounts of activity is that cortisol just goes through the roof (there’s
another issue I’ll come back to at the end that relates to this). Simply, you get these massive chronic
elevations in cortisol levels.
Tangentially, this is also one reason I suspect that various types of cyclical dieting help with some of this
issue. For at least brief periods, when calories are raised to maintenance or above, you break the
diet/training induced elevations in cortisol. This of course assumes that the person isn’t mentally stressed
to the nines by raising calories like that but I’m getting ahead of myself.
.

So Why is This Bad?

As noted above, chronic elevations in cortisol can cause a lot of bad things to happen. One of them is simply
water retention and I’ve mentioned in previous articles that water retention can mask fat loss, sometimes for
extremely extended periods. I talked about this in some detail in The LTDFLE and suspect that some of the
‘fat loss’ is actually just water loss when calories are raised and cortisol mediated water retention
dissipates. Reducing total training (volume, frequency, intensity or some combination) does the same thing.
But that’s probably not all of what’s going on. Another effect of chronically elevated cortisol levels is leptin
resistance in the brain. I’m not going to talk about leptin endlessly here again, you can read the Bodyweight

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Regulation Series for more information. When the normal leptin signal to the brain is blocked, a lot of things
can go wrong metabolically and I suspect that this is part of the problem.
In this vein, although not necessarily related to cortisol per se, at least one study found that the addition of
6 hours per week of aerobic activity to a very low calorie diet (in this case a protein sparing modified fast)
caused a larger decrement in metabolic rate than the diet alone. The body appears to monitor caloric
availability (simplistically caloric intake minus output) and if it gets too low, bad things can happen.
This is why I so strongly suggested AGAINST the inclusion of much cardio in The Rapid Fat Loss Handbook;
it causes more harm than good. Invariably, the biggest source of failure on that plan is when people ignore
my advice and try to do a bunch of cardio. And fat loss stops.
In any case, there are several different plausible mechanisms by which the combination of excessive caloric
deficits an large amounts of activity can cause problems. Whether it’s simply cortisol related water retention,
a drop in metabolic rate due to leptin resistance or something else, something is going on. From a more
practical standpoint, for a lot of people, the combination simply doesn’t work. Mind you, some seem to get
away with it but not all.
.

An Additional Variable

There is another variable that I have noticed over the years in looking at this issue. As odd as it sounds, it
has to do with personality. In discussing this, for example, I’ve often noted that the people who seem to
have the biggest issues with the whole lots of cardio/big caloric deficit tend to be a little bit ‘tightly wound’ (to
put it politely). A bit less politely they are stress cases.
You can almost ‘hear’ the stress in their typing. Every post has lots of exclamation points and there is this
undercurrent of “I MUST LOSE FAT NOW!!!!!!” in their posts. When fat loss stalls for a day, they freak out
and want to cut calories or go add another hour of cardio. You can almost ‘see’ the tension in them as they
sit hammering at the keyboard looking for solutions.
And this is an issue because these types of folks already over-secrete cortisol. As a true oddity, there is the
issue of amenorrhea (loss of menstrual cycle). Typically it’s been thought to be related to body fat levels or
caloric intake and this is a general cause. But there is often a type of amenorrhea seen in women without
any of the normal predisposing factors. In this case, it’s all due to mental stress.
Basically, there is a subset of folks who are already high-level stress cases. They tend to be drawn to harder
is better in the first place, tend to be resistant to change (like my client from my early 20’s) and their already
high level of cortisol production is simply amplified by the combination of too much activity and too few
calories. And suggestions to raise calories and/or reduce activity are invariably met by resistance (again,
like my client from ages ago). What they really need is to just chill the hell out.
But invariably the approach that they are intuitively drawn to is the wrong one for them: moderate deficits
and moderate activity always work better in those folks. It’s getting them to do it that’s the hard part.
Tangentially, I suspect that the classic hardgainer is of a typical type but that’s another topic for another day.
.

Summing Up

So that’s that, a look at one of the oddities of fat loss, the situation where the combination of excessive
caloric deficits and excessive amounts of activity seem to hurt rather than help fat loss, along with some
gross speculation (and just enough research to make it sound like I know what I’m talking about) on what
may be going on.

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In a practical sense, of course, most of the background isn’t that relevant. The simple facts for the majority
of folks is this: you can either cut calories hard OR do large amounts of activity. But you can’t do both. Well
you can do both, you just probably shouldn’t under most circumstances.

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Why Do Obese People not Lose More Weight When Treated with
Low-Calorie Diets?

Title

Heymsfield SB et. al. Why do obese patients not lose more weight when treated with low-calorie diets? A
mechanistic perspective. Am J Clin Nutr. 2007 Feb;85(2):346-54.

Abstract

Maximal weight loss observed in low-calorie diet (LCD) studies tends to be small, and the mechanisms
leading to this low treatment efficacy have not been clarified. Less-than-expected weight loss with LCDs can
arise from an increase in fractional energy absorption (FEA), adaptations in energy expenditure, or
incomplete patient diet adherence. We systematically reviewed studies of FEA and total energy expenditure
(TEE) in obese patients undergoing weight loss with LCDs and in patients with reduced obesity (RO),
respectively. This information was used to support an energy balance model that was then applied to
examine patient adherence to prescribed LCD treatment programs. In the limited available literature, FEA
was unchanged from baseline in short-term (<12 wk) treatment studies with LCDs; no long-term (>/=26 wk)
studies were found. Review of doubly labeled water and respiratory chamber studies identified 10 reports of
TEE in RO patients (n = 150) with long-term weight loss. These patients, who were weight stable, had a TEE
almost identical to measured or predicted values in never-obese subjects (weighted mean difference: 1.3%;
range: -1.7-8.5%). Modeling of energy balance, as supported by reviewed FEA and TEE studies, suggests
that obese subjects participating in LCD programs have a weight loss less than half of that predicted. The
small maximal weight loss observed with LCD treatments thus is likely not due to gastrointestinal adaptations
but may be attributed, by deduction, to difficulties with patient adherence or, to a lesser degree, to metabolic
adaptations induced by negative energy balance that are not captured by the current models.

My Comments

Over decades of their use, the simple fact is that low calorie diets (LCDs) mostly fail. And I’m not simply
talking about the fact that most people will regain any weight lost. The simple fact is that even the total weight
loss seen with such diets is often fairly small. A total loss of 5-10kg (roughly 10-20 lbs) over a year’s span is
a typical result. And while that might be great for someone who who is lean, for someone at 250-300 lbs, it’s
not terribly significant.
Tangentially I’d note that from a health standpoint, even small weight losses of 5-10% of body weight can
improve various health and metabolic markers. Even if most people probably won’t be satisfied with that
rate of loss. One of the questions is why the results are so poor, especially given that, based on the caloric
deficit created, a much greater loss should occur.
Setting out to examine the (surprisingly) limited amount of data on this topic, this paper first examined
representative weight loss studies of LCD’s. Although the study sample was far from comprehensive, they
typically showed a weight loss of anywhere from 25-50% of what was predicted based on the deficit created.

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I should note that this included both high and low-carb diet studies so this shouldn’t be taken as a ‘the calorie
theory of weight loss is wrong’ kind of argument.
The study, thankfully mentions that there are three different ways of setting up a deficit, something I’ve
discussed variously. The first is by making an absolute reduction in food intake (i.e. 500 calories/day). The
second (my preferred method) is to reduce food intake by some percentage (for example 20%) below
baseline. The third, and worst in my opinion, is to use an absolute level such as ‘Women get 1200
calories/day and men get 1700 calories/day’. I discuss this topic in some detail in my first book The
Ketogenic Diet.
The paper then set out to examine three major possibilities (based on a host of assumptions that they discuss
in some detail but that I’m going to skip over) for the failure of actual weight loss to reach what is predicted.

Possibility 1: An Increase in Food Absorption

The first possibility considered is that there is an adaptation towards increased absorption of food in the gut
with dieting. However, research fails to support this contention. Absorption rates of ~95% or so are seen for
most ingested nutrients and this is true in both the pre- and post-obese (dieted down individuals). The study
also points out that even a 5% increase in food absorption would only amount to about 100 calories per day
extra which still wouldn’t be able to explain the observed results. So possibility 1 is unlikely to be the cause
of the observed results.

Possibility 2: A Reduced Metabolic Rate

The second possibility considered was that a reduction in total energy expenditure is the cause. That is,
some studies have shown that individuals who are actively dieting have a lower than predicted metabolic
rate (as well, calories burned during activity goes down as you lose body mass) than individuals at the same
weight who aren’t/haven’t had to diet.
However, and I’ll come back to this below, the study chose to examine studies looking at post-obese
individuals at weight maintenance in their analysis. And such studies invariably show a fairly small difference
(maybe 1-5% tops, I should note that these are studies in obese individuals, much greater drops have been
seen in leaner individuals) between predicted energy expenditure and actual energy expenditure in the post-
obese.
However, I think this is misleading because it’s the drop during active dieting that would be contributing to
the difference in actual versus predicted weight loss. In their defense, the researchers did address this in
the discussion but why they chose this particular data set for their analysis I’m not sure.
The authors do thankfully note that the work they examined on total energy expenditure in the weight stable
state isn’t exactly the same as what happens during active dieting. Numerous (but not all) studies show a
drop in energy expenditure (both in terms of basal metabolic rate as well as overall activity, people tend to
move less when they diet) during active dieting.
Additionally, there is work showing a fairly large variability in this (a topic I’ve discussed at length before). In
one study I recall, subject’s metabolic rates dropped anywhere from 50-200 calories/day by week 2. Clearly
the subjects with the larger metabolic rate drop are going to get less weight loss over time because their net
deficit is smaller.
Put differently say you put two people on a 500 calorie per day deficit and one person shows a drop in
metabolic rate of 50 calories/day while another shows a drop of 200 calories/day. The first is still maintaining

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a 450 cal/day deficit, the seconds deficit has been cut to 300 calories. Over a month’s time that will add up
to 1.5 pounds difference in fat loss between the two despite being on ‘the same diet’.
At the same time, the researchers point out that “..changes occur in EE (energy expenditure) that could
reduce the prescribed energy deficit, but these decrements in EE appear to be tied to the energy deficit, the
rate of weight loss, or both, and thus they would slow weight loss but not result in a premature plateau
because, by definition, that plateau occurs at the point of energy balance.”
Which is a convoluted way of saying that, even if you’re ona 50% daily deficit, and energy expenditure drops
by 25%, that’s still insufficient to STOP weight loss. Because you still have a 25% deficit. The drop will simply
slow things down. That is, the decrease in metabolic rate with dieting can only ever slow the rate of fat loss,
it can’t ever stop it completely.

Possibility 3: Adherence

Thus, by default, they basically conclude that the failure of LCD’s comes down to problems with adherence.
That is, people lose less weight on the diets because they are not really following them. This would also
explain the tendency to start regaining weight at some point, people start reverting to old eating habits.
Related to this, in the discussion, they discuss a paper which used self-reporting of dietary compliance
(relative to Zone, Atkins and carb-based diets) in terms of results. The first observation in that study is that
the subjects who started with low levels dietary compliance ended up with even worse levels. Put bluntly,
the people who started the diet half-assed, ended up doing the diet all-assed.
Additionally, the subjects reporting the greatest dietary compliance lost 20kg (45 lbs) whereas the low
compliance folks lost negligible weight. It’s a conclusion that is unbelievably obvious but really bears making
explicit: people who actually follow/stick to a diet lose weight and those who don’t don’t.

Discussion

So overall, it appears that the major determinant of overall diet success is simply one of adherence. Changes
in food absorption can’t explain the difference between predicted and actual weight loss and, with the
caveats mentioned above, it doesn’t appear that metabolic rate can either (although individual variance in
metabolic rate change might explain differences between individuals on the same diet).
The researchers did acknowledge the limitations of their study, the limited amount of data, the short-time
frames over which most studies are done (a year or less) and the fact that they didn’t examine
exercise/physical activity in terms of how it impacts or changes during dieting.
This is important for a number of reasons not the least of which is that some people will start to decrease
their daily activity (subconsciously) on a diet, reducing their daily activity energy expenditure. While this
wouldn’t show up as an actual measurable drop in resting metabolic rate, it would still serve to reduce the
net deficit.
The paper concludes:
A critical need therefore exists for elucidating the basis of poor patient adherence to prescribed energy
deficits. This research effort could lead to even greater clinical benefits for the many obese patients with
weight related comorbidities.
Basically, the question is no longer one of what type of diet to put someone on, it’s a question of how to
actually get people to stick to a diet in the long-term. I couldn’t agree more and expressed that very opinion
in A Guide to Flexible Dieting.

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After decades of research, we know about pretty much all there is to now about dieting and fat loss in my
opinion at this point. We know how, from a biological standpoint, to get people to lose weight and/or fat.
I think the bigger question is figuring out why people are so bad at changing habits in the long term or the
short-term for that matter. Until that question is answered, it seems that only the small percentage of people
willing to change their habits and, most importantly, keep them changed FOREVER are going to succeed.

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Why Do People Change Body Composition?
In previous articles, I’ve addressed the issue of What Does Body Composition Mean?, shown folks how to
do Body Composition Calculations, examined Body Composition Numbers and looked at methods of
Measuring Body Composition.
However, something I haven’t looked at may be a much more fundamental question which is this: why do
people want to change their body composition? That is, what reasons (good or bad) might people have for
wanting to change their body composition in the first place. That’s the topic of this piece.
While the overall goal of body recomposition typically means losing fat and/or gaining muscle there are some
situations where gaining fat or losing muscle may also be desired. I’ll look at each topic below.

Why Do People Want to Lose Fat?

At any given time, some ludicrous percentage of the population is trying to lose weight and/or fat. I’d note
that if you’re unclear on the distinction, you should really read What Does Body Composition Mean? before
you go any further. As I noted above, the motivations or reasons for this goal can vary significantly
depending on the population you’re looking at.
It’s probably safe to say that bodybuilders and other physique athletes are the ones who are at least the
most visible in terms of their extreme levels of fat loss; they are often the most successful as well. While
their goals are often also vanity driven, the simple fact is that reducing body fat to an appropriate level is
required for competition purposes. In the case of bodybuilding, this can often reducing body fat to what are
unhealthy levels.
A male may reach 3-4% body fat on competition day, females have been measured in the single digits as
well although few will maintain those levels for very long. This does some nasty things to hormones and
women can do real damage to their health if they try to maintain that level for extended periods. As noted,
most don’t but some try.
Figure and fitness has become more relaxed in recent years with higher body fat levels and ‘softer’ looks
being the goal. But fat loss is usually a primary goal for these types of individuals (it’s not a stretch to say
that they are professional dieters).
Even bodybuilders with no interest in stepping on stage typically wants to keep their body fat levels low
enough to have some definition (to be ‘buff’) in the common parlance; this is often accompanied with a desire
to gain muscle mass. These folks don’t typically like to hear that body fat often has to increase to some
degree to make optimal gains in muscle mass.
Female physique types, who are usually less interested in massive muscles in the first place (there are
exceptions, females who want to be massive and/or beastly strong) and tend to be more concerned about
just looking good.
Performance athletes frequently want to drop fat (or sometimes just weight) to either improve performance
or simply make it into a specific weight class. Clearly, in some cases, losing fat and/or weight helps
performance by increasing the strength/power to weight ratio. Endurance athletes tend to benefit from being
lighter because the less mass they have to move against gravity, the faster they go. There are occasional
exceptions (heavyweight rowers come to mind).
However, taken to extremes, dropping too much weight or fat can cause performance to plummet. Whether
this is due to the reduced weight/fat per se or simply the effort (excessive + dietary restriction) required to
make it happen is difficult to determine and probably both contribute.

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For sports performance, there is usually an optimal level of bodyfat but optimal isn’t the same as
minimal. Many athletes get confused about the distinction.
Many weight class athletes will dehydrate (sometimes severely) to make a lower weight class and there are
some horror stories associated with this if it’s done incorrectly. There have been some deaths associated
with this practice and severe dehydration is no joking matter. If nothing else, dehydration past about the 2%
of total weight level tends to hurt performance. Which won’t stop athletes in these sports from doing it if
necessary.
Mild dehydration generally only requires a couple of days of low-carb, protein only diets and caffeine and is
usually reasonably well-tolerated. More extreme levels of dehydration can require prescription diuretics and
near death experiences; what a lot of people don’t hear about is the IV fluids used to rehydrate these athletes
after they get off the scale.
Returning to physique athletes, bodybuilders often dehydrate themselves to improve appearance, to look
more ‘cut'; by reducing the water underneath the skin, muscle definition is improved. Stories of problems
with heavy-duty diuretics, ranging from cramping to passing out and death, are out there.
Of course, not everyone wants to lose fat for athletic, performance or bodybuilding reasons. While many
will pay at least lip service to the idea of losing weight or fat for health reasons, let’s face up to the facts: the
grand majority of people who pursue fat loss do it for vanity driven reasons. Put bluntly: they want to look
better naked. Which isn’t necessarily a bad goal, mind you, but let’s at least be honest about it.
Related to this, some people tie in their sense of self-confidence with their physique; when they’re lean
they’re confident, when they’re not, they’re not. Others are doing it to meet some societally driven idea of
‘perfection’ or ‘beauty’. I’ll leave argument over that to the sociologists.
It’s worth mentioning that while this used to apply primarily to women, there are an increasing number of
men showing issues with eating disorders and other unhealthy eating and training habits (including a
massive increase in elective plastic surgery for men). At one point it was thought that eating disorders only
occurred in men but this is clearly not the case. Both anorexia and bulimia are potentially fatal.
Of course, some individuals want, have to or need to lose fat/weight for health reasons. High blood
cholesterol, high blood pressure, Syndrome X (aka Type II diabetes), arthritis, etc. are all often positively
impacted by even moderate amounts of weight loss. Research suggests that as little as a 10% weight loss
(e.g. 20 lbs for a 200 lb person, 30 lbs for a 300 lb person) can drastically improve health parameters.

Why Do People Want to Gain Fat?

It’s interesting to note that in many non-modern cultures, fatness is not the social negative that it tends to be
in the Western world. Women are frequently moved into fattening tents prior to marriage, and one culture
even has a ritual fattening period that signals a boy’s growth into a man. I’d note that there’s no real trick to
this: they accomplish this fattening by making the victims eat a lot and sit on their butts all day.
It’s probably fair to say that in most Western cultures, it’d be a little unusual for someone to specifically want
to gain fat; there are always exceptions. Here are a few.
For some athletes (especially female) increasing bodyfat may actually be healthier for them in the long-
term. Studies show that women’s hormones (and men’s for the record) can be severely disrupted under
certain conditions (usually the combination of a low body fat and excessive caloric restriction) and this can
cause bone loss and other problems at a very early age. Studies of female gymnasts have found bone
densities similar to that seen in severe osteoporosis in old women. This is not a good thing.

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For other athletes, such as a football lineman or a sumo wrestler, the quality of weight gained may not be as
critical as just being a walking human wall. Carrying extra fat may actually be beneficial since it can provide
some protection against the other large men who are going to be running into you at high speeds with
violence on their mind.
Of course, gaining fat for the sake of gaining fat is almost always a poor idea health-wise (and there has
been an alarming increase in death at a young age among athletes in sports where the body weight
requirements keep going up and up and up), unless someone was unhealthily lean in the first place.
But sports performance and optimal health aren’t always compatible. If being 350-400 lbs (with 40% body
fat) is required to be a pro football lineman and make the big bucks, so be it. I’d note that taking the fat off
after they retire is often a real problem for these types of athletes. They tend to be so used to eating
everything in sight that the idea of not doing so is a very rough change to make.
Finally, sometimes non-athletic individuals need to gain weight or fat as well. Although relatively more rare,
some individuals are unhealthily underweight or underfat. I’m not talking about the anorexic eating disorder
types (who need to be medically supervised during their weight gain) but folks who simply can’t seem to gain
enough weight to be healthy, energetic and vigorous. This tends to be a small percentage of the population
but anybody who reads this site regularly knows that I’m all about completeness.

Why Do People Want to Gain Muscle?

The same individuals who typically want to reduce fat for either cosmetic or performance reasons frequently
want to gain muscle mass for the very same reasons. Bodybuilders may need (or simply want) to gain muscle
mass to improve their size and overall shape. This may be overall size increases or just increases in specific
muscle groups for reasons of symmetry and balance.
Performance athletes may find that performance increases with more muscle and strength although how
much of each depends strongly on the type of sport. Many athletes (e.g. sprinters) have to balance out the
requirement for strength and power with carrying too much body weight. It is often a fine balance. Other
sports aren’t quite as demanding for that balance and if more muscle mass leads to more strength and
power, performance often goes up.
For some athletes (especially endurance), too much muscle mass is a hindrance and will slow them down
beyond a certain point. Heavyweight rowers tend to be an odd exception since their weight is supported by
the boat. As with body fat, optimal levels of muscle mass, enough for efficient performance, but not so much
that it slows the athlete down is the goal for these athletes.
There are also athletes who can’t gain too much muscle because of aesthetic requirements of their sport
(i.e. gymnastics and figure skating).
Even the general public is often interested in some amount of muscle mass gain in this day and age. Like
fat loss, most of this tends to be driven by cosmetic reasons. Males want to ‘be buff’ and females are finding
that even small amounts of muscle mass drastically improve their appearance.
Of course, there can also be health benefits to gaining muscle mass. Massive amounts of research is
focusing on the muscle loss that can occur with aging and finding ways to improve muscle mass (usually
through training and nutritional intervention) in an increasingly aging population is key is important for both
health and functional reasons (e.g. being able to carry your own groceries or get up out a chair without help).
Of course, in extreme situations such as wasting (cancer, AIDS, etc.) maintaining muscle mass is of equal
health importance. As it turns out, the loss of too much muscle mass will cause death and finding ways to
slow or stop the loss of muscle that occurs is of huge importance.

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Why Do People Want to Lose Muscle?

Possibly even more rare are the situations where someone wants to lose muscle. Frequently these are ex-
athletes who have no desire to maintain their muscle mass once their competitive days are over.
More commonly are athletes for whom losing muscle mass may actually improve performance. Generally
these tend to be endurance athletes who, for some reason, gained excessive amounts of muscle mass
(either deliberately or through involvement in another sport) often in non-functional muscles.
A big upper body is typically a hindrance for an athlete such as a road cyclist since it’s just dead weight to
be hauled around the course. Losing it may improve performance.
In this vein, there is a story that is often told about Lance Armstrong who, after losing a large amount of
weight (including some upper body muscle mass) due to his bout with cancer, was a much better cyclist
because of it. In this case, losing non-functional muscle could only improve his power to weight ratio.
Finally, as I noted in Weight Training for Fat Loss Part 1, extremely obese individuals often gain some lean
body mass (some of which is muscle) in the process of becoming obese. Most obesity experts expect, and
don’t necessarily mind, that that ‘extra’ lean body mass is lost when weight is lost. In fact, up to 25% of the
total weight lost may come from lean body mass without anybody getting too concerned in that situation.

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10 Tips to Deal with Holiday Weight Gain
This was originally written and run back in 2008 (and I believe every year since then) and as we enter the
holiday season again (with Halloween candy finally leaving the aisles, thank goodness), it’s just as relevant
now as it was then. So without further adeiu, I give you the annual running of 10 Tips to Deal with Holiday
Weight Gain. Enjoy!
For the body obsessed or even normal dieters, the holiday period from around October through to January
can be a true minefield. Between the specific holidays of Halloween (mercifully passed), Thanksgiving and
Christmas, along with endless goody baskets and parties, folks can run into problems maintaining the habits
they strive to follow the rest of the year.
A lot of strategies exist to deal with this time, especially among the body obsessed, although I’d consider
few of them particularly healthy from a mental or psychological standpoint. One is to become a social pariah.
Can’t control your food at parties? Simply skip all of them. While this might avoid food issues, it’s also a way
to make your friends and co-workers think you’re an anti-social asshole. Which is fine, I guess, if you are
an anti-social asshole. But it won’t do much for your inter-work relationships.
Another common one is to take the needed meal or food (e.g. turkey, broccoli, plain sweet potato) with you
in a Tupperware bowl. I’ve heard of folks doing this at Thanksgiving dinner, usually so that they can sit and
look down upon their family members with an air of superiority. “Oh, I can’t believe you’d eat that, that’s why
you’re fat.” Newsflash folks, not only are we talking about a borderline eating disorder at this point (see also:
orthorexia/Chris Shugart), that kind of insanity just makes your family uncomfortable. So don’t do it. Better
to stay home than be an asshole.
Of course, at the other extreme are the dis-inhibited eaters who just go completely crazy and eat everything
in sight, gaining a considerable amount of weight and fat in the three months of holidays. It can happen and
I’m not saying that it can’t. Of course, if you’re a bodybuilder or powerlifter, you can just say “I’m bulking” as
you shovel down the third piece of cake but I’ll assume that you actually want to keep a lid on weight/fat
gains during this time period. Balance please.
As always, being a middle of the road kind of guy that I am, I’m going to suggest some strategies that, while
not quite as disturbed as taking broccoli with you to Thanksgiving, also doesn’t put you in the trap of gorging
on fudge. In no real particular order of importance, here are 10 Tips to Deal with Holiday Weight Gain
from getting out of hand over the holidays.

1. Make Better Bad Choices

I forget who I stole this idea from offhand but it’s nothing new. The simple fact, and I’ll come back to this in
point 10, is that many people fall into the trap of “If I’m going to eat junk, I might as well jam as much of the
worst stuff I can down my food hole.” That’s silly.
Instead, try to make better bad choices. Limit portions (you know that you don’t really NEED three pieces of
cake to be satisfied). Pick the lower calorie or lower fat/high-carb stuff at the dessert table. People training
hard can handle an influx of carbs acutely better than fat so pick that stuff. Maybe have a little bit of two or
three different desserts, just get a taste and move on. You get the idea.

2. Take a Lowered Fat/Calorie Dessert or Dish to the Party

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Whether a work party or holiday dinner, it’s not uncommon for people to bring their own thing to add to the
food table. So make something that you’ve de-fatted or lowered in calories, there are zillions of recipes out
there. And, please, I’m not talking about black bean ‘cake’ that you think tastes like the real thing.
Find a happy medium between the high-sugar/high-fat stuff and clean eating. Most American desserts have
about twice the sugar and butter that they usually need and, who knows, you might even convert someone
into realizing that they can eat sweets without it having to be 1000 calories per piece.

3. Train with a Bit Higher Volume Prior to the Event

One of the best ways to increase the ‘sink’ for incoming calories is to deplete muscle glycogen. When you
do that by using a higher volume (more sets, higher reps) of training, not only do you increase fat oxidation,
you give incoming carbs somewhere to go for storage instead of being used for energy.
You can simply bump up your volume a bit in the days before a specific event where you know there will be
junk. Even a heavy training session on the day of the party can be beneficial here. And, bonus, you’ll be
pumped at the party. Great for pulling that hot co-worker so you can both be really uncomfortable the next
day at the water cooler.
Train in a nice hypertrophy zone (get about 40 reps per muscle group) and you’ll increase protein synthesis
so that incoming calories will support growth. Training also tends to acutely blunt hunger so if you train right
before the party, you’ll be less likely to overeat. Well, unless you’re a typically dis-inhibited eater who falls
into the trap of “I trained, I deserve 10 pieces of fudge.”

4. Start with Lots of Lean Protein and Vegetables Before Hitting


the Dessert Table

This one is for the body obsessed and dieters alike. Lean protein has the highest short-term satiating power
(this means it keeps you full) and the high-bulk of vegetables helps to fill your stomach which also sends a
fullness signal. I’ve yet to be at a holiday party that didn’t have a vegetable plate (limit the high-fat dip) or
plate of cold cuts. Load up on that to get some fullness going before you hit the desserts. You won’t be as
hungry and, assuming you don’t like eating yourself sick, this alone will do damage control.

5. Have a High-Protein Snack with some Vegetables or Fruit


about 30′ Beforehand

If you’re in a situation where Number 4 won’t work or won’t be available, have a small snack before the party
or dinner. Some lean protein, veggies and fruit about 30 minutes will give you a feeling of fullness and help
to limit overconsumption of ‘junk’ at the party.

6. Consider Intermittent Fasting on the Day of the Event

Intermittent Fasting (IF’ing) is a recent dietary approach that involves not eating for 14-18 hours per day and
then either having an ‘eat period’ of roughly 4-6 hour or even a single meal. There’s some interesting
research on it and I’ll discuss it at a later date on the site. But it’s one good way to deal with holiday parties.

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Know that you’ve got a 7pm dinner party where there will be lots of yummy food? Try IF’ing (or only have
small meals of lean protein and veggies) most of the day. Unless you go completely berserk, you’ll be unlikely
to exceed your entirely daily caloric requirement in the one meal. If you can train beforehand, even better.

7. Consider a Short Mini-Diet in the Days Before the Event

Let’s say you have an event or two coming up on the weekend and you know that there will be lots of food
and you may have control issues. Well, consider doing a short, possibly hardcore diet in the days before.
My Rapid Fat Loss Handbook would be perfect, 4 days of it can actually reduce body fat by 1-4 pounds
(depending on your size) and you can schedule the free meal and/or refeed for your events. Call it pro-active
damage control.

8. Ok, I Was Actually Kidding in the Introduction About the


Tupperware

Let’s face it, you know that nothing tastes as good as lean feels, you know how good discipline feels, you
know that you’re better than all of those weak willed candy and dessert eaters; you read Chris Shugart’s
insane ramblings and actually take his bullshit seriously. You know the truth. You know you’re better than
them and 50 years from now when you’re old and decrepit, you’ll know that it was worth it, sticking to your
diet 365 days a year and never actually enjoying a moment of life.
So you go ahead and take your Tupperware with chicken breast, broccoli and sweet potato and eat it while
everyone else around you actually gets some joy out of life and you feel miserable, alone, deprived and
isolated. Know deep down that you’re not only physically superior but also morally superior.
No, really, I’m seriously kidding about this, don’t do it. If you do, I hope someone pins you to the ground and
force feeds you fudge until you throw up. Just because you’re an asshole.

9. Stay Off the Damn Scale

No matter what happens, folks often see the scale spike up after a big party; this is especially true after
Thanksgiving. The typical carb-depleted trainee is especially prone to this; the high-carb intake of your typical
holiday event along with extra sodium both can jack up scale weight a bit. But you know deep down it’s not
really fat. The simple fact is that, unless you go nuts, you can’t eat enough in a single meal to put on
appreciable fat. It’s only water and it’ll come right back off in a few days.
But stay off the scale anyhow.

10. Don’t Be Your Own Worst Enemy

This goes back to what I alluded to in point 1, a lot of people fall into a dreadful trap over the holidays, figuring
that if they’ve eaten a little bit of junk food, clearly they’ve blown it and might as well retire to the corner with
the entire tray of fudge and eat themselves sick.
I’m going to quote from the foreword of my own A Guide to Flexible Dieting here:

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Then the problem hits. Maybe it’s something small, a slight deviation or dalliance. There’s a bag
of cookies and you have one or you’re at the mini mart and just can’t resist a little something that’s not on
your diet. Or maybe it’s something a little bit bigger, a party or special event comes up and you know you
won’t be able to stick with your diet. Or, at the very extreme, maybe a vacation comes up, a few days out of
town or even something longer, a week or two. What do you do?

Now, if you’re in the majority, here’s what happens: You eat the cookie and figure that you’ve blown your
diet and might as well eat the entire bag. Clearly you were weak willed and pathetic for having that cookie,
the guilt sets in and you might as well just start eating and eating and eating.

Or since the special event is going to blow your diet, you might as well eat as much as you can and give up,
right? The diet is obviously blown by that single event so might as well chuck it all in the garbage.

Sound familiar? Yeah I thought it might. The above is amazingly prevalent and exceedingly destructive.
Extremely rigid dieters fall into a trap where they let events such as the holidays become a problem because
of their own psychology. They figure that one piece of dessert has ruined all of their hard efforts so they
might as well eat ALL the dessert. Which is, of course, nonsense. Say that piece of dessert has a few
hundred calories, or say 500 calories. In the context of a weekly plan that is calorie controlled with training,
that’s nothing.
Unless the person lets it become something. They figure 500 calories is the end of the world and eat an
additional 5000 calories. Instead of just taking it in stride and realizing that it’s not big deal, they make it a
big deal with their own reaction.
Simply, don’t do that. Realize that there is only so much damage you can do in the short-term. Apply the
other strategies in this article and realize, at the end of the day, what you did for one meal that week simply
doesn’t matter if the rest of the week was fine. Not unless you make it.
And that’s that, 10 strategies I hope will help you to enjoy the holidays. Eat a piece of cake for me.

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A time-efficient reduction of fat mass in 4 days with exercise and
caloric restriction – Research Review

Calbet, JA et. al. A time-efficient reduction of fat mass in 4 days


with exercise and caloric restriction. Scand J Med Sci Sports. 2014
Mar 6. doi: 10.1111/sms.12194. [Epub ahead of print]

To determine whether a fast reduction in fat mass can be achieved in 4 days by combining caloric restriction
(CR: 3.2 kcal/kg body weight per day) with exercise (8-h walking + 45-min arm cranking per day) to induce
an energy deficit of ∼5000 kcal/day, 15 overweight men underwent five experimental phases: pretest,
exercise + CR for 4 days (WCR), control diet + reduced exercise for 3 days (DIET), and follow-up 4 weeks
(POST1) and 1 year later (POST2). During WCR, the diet consisted solely of whey protein (n = 8) or sucrose
(n = 7) (0.8 g/kg body weight per day). After WCR, DIET, POST1, and POST2, fat mass was reduced by a
mean of 2.1, 2.8, 3.8, and 1.9 kg (P < 0.05), with two thirds of this loss from the trunk; and lean mass by 2.8,
1.0, 0.5, and 0.4 kg, respectively. After WCR, serum glucose, insulin, homeostatic model assessment, total
and low-density lipoprotein cholesterol and triglycerides were reduced, and free fatty acid and cortisol
increased. Serum leptin was reduced by 64%, 50%, and 33% following WCR, DIET, and POST1,
respectively (P < 0.05). The effects were similar in both groups. In conclusion, a clinically relevant reduction
in fat mass can be achieved in overweight men in just 4 days by combining prolonged exercise with CR.
.

Background

I’ve discussed the impact (or rather, the often non-impact) of exercise on weight/fat loss a number of times
on the site under most circumstances. The reality being (as most studies show) that the types of realistically
achievable amounts of exercise by the average obese individual is simply too low to massively impact on
energy balance or total weight/fat loss. Certainly there is some effect (that is enhanced when it is combined
with caloric restriction) but it’s rarely massive with most research showing that the primary role of exercise
being improved weight maintenance.
However, there is the occasional paper that comes along that imposes a fairly large amount of activity and
generates a fairly large amount of fat loss. One that comes to mind (that I cannot find at the moment) had
subjects bicycle for 2 hours/day 6 days/week and saw a significant fat loss over the length of the
study. Every so often, someone will come along on a forum and ask if doing some absurd amount of activity
will generate massive fat loss (one person I recall from a forum decided to do something like 6-8 hours of
low intensity cycling, while seated at his desk, and keeping calories stable and just lost fat at a staggering
rate).
Which leads right into the paper I want to look at today.

The Paper

As the title of the paper suggests, the researchers wanted to see whether or not a significant amount of fat
mass could be lost in a mere 4 days; building on previous research they actually looked at the combination
of a very large amount of activity along with extremely severe caloric restriction.

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They also decided to look at whether diet composition (pure protein vs. carbohydrate) would exert any
differential effects based on the idea that dietary protein is better at sparing lean mass lost. Finally they did
follow ups on the subjects at both short- and long-term (4 weeks and 1 year post intervention). A host of
health measures and hormonal measurements (insulin sensitivity and leptin for example) were also
done. Body composition was measured both with DEXA and Bioimpedance (to get a measure of changes
in body water).
So specifics: the subjects were aged 18-55 and had been weight stable for at least three months; all had
body fat percentages between 20 and 40% (the average was 31%+- 5% or so) and the study ended up with
7 subjects in the sucrose group and 8 in the protein group (it was a small study). The study was divided into
five distinct phases. Phase 1 was one week of normal activity. Phase 2 was the actual 4-day intervention
which was followed by Phase 3 which was 3-days of a normal diet and limited activity which was meant to
stabilize hydration status. Phase 4 was four weeks where subjects could eat and exercise by their own
choice and Phase 5 was a one year follow-up.
Ok, so the intervention; as I mentioned above there were two components. The first was the exercise
component (remember again that this was a 4-day intervention). For exercise, each day the subjects
followed an overnight fast with 45 minutes of one-arm cranking exercise (at 15% maximal intensity) followed
by 8 hours of walking at 4.5 km/h (2.8 mph) for a total of 35 km (21 miles) of walking per day. None of that
is a typo; it was 8 hours and 45 minutes of exercise a day all at very low intensities. I can’t find in the paper
where they indicate why they decided on this protocol (especially the initial 45 minutes of arm cranking).
The diet was equally extreme, subjects were given 3.2 kcal/kg (1.4 kcal/lb) which was roughly a 90% deficit
from their maintenance energy intake. So a 100kg (220 pound) subject would have been consuming 308
calories. Again, not a typo and the total daily deficit was calculated to be around 5500 calories/day. Protein
was set at the DRI (formerly the RDA) of 0.8 g/kg (0.36 g/lb).
The subjects either received nothing but whey protein (so about 75 grams of protein per day for our 100kg
example subject) or pure sucrose (table sugar) along with some minerals and fluid; they were allowed a
rehydrating drink (which looked more or less like Gatorade) during the day. Repeating from the above, this
was followed for only 4 days before the subjects were moved back to maintenance calories and rehydrated
to stabilize their body weight.
As you might expect, the results were as extreme as the protocol. I’ve indicated the total losses from
baseline below.

Fat Loss LBM Loss (*)

Phase 2 (4 days) -2.1 kg (-4.6 lbs) -2.8 kg (-6.2 lbs)

Phase 3 (3 more days) -2.8 kg (-6.1 lbs) -1.0 kg (-2.2 lbs)

Phase 4(4-week Follow up) -3.8 kg (-8.4 lbs) -0.5 kg (-1.1 lbs)

Phase 5 (1-Year Followup) -1.9 kg (-4.2 lbs) -0.4 kg (-0.88 lbs)

*This loss of lean mass only amounted to 15% of the total loss or so, actually below the
theoretically “expected” 25% loss of LBM that is thought to be normal and par for the course.
If you’re wondering why I didn’t make a distinction between the protein group and the sucrose group in terms
of losses, it’s because there was no difference. Both groups lost the same amount of fat mass and lean
mass and the protein showed no lean mass sparing effect. I’d also note that most of the loss was in the
form of trunk fat (and probably some visceral fat loss) which is known to have greater negative impacts on
health than fat carried in other places.

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I’d noted in passing that the intervention showed equally extreme impacts on measures of insulin sensitivity
along with a lowering of glucose and insulin, plasma triglycerides and cholesterol. Note that most of these
had returned to baseline by the four week followup.

Conclusions

As the researchers conclude “The present investigation reveals that whole-body fat mass can be reduced
by ~3kg with a 4-day intervention combining a reduction of energy intake (to barely 10% of the habitual level)
and 9h of low-intensity exercise per day.” They add that “…despite no specific request for lifestyle changes,
subjects lost an additional kilogram of fat during the 4 weeks after the intervention.”
One question worth addressing is why the protein group wasn’t superior to the sucrose only group which is
in contrast to previous studies on the topic. The researches suggest that the extremity of the caloric deficit
along with the very low-calories was probably part of this. They add that “It remains to be determined
whether better preservation of LM could be achieved with a higher intake or other types of proteins.” I’d
comment that this doesn’t really remain to be determined.
As I discuss in detail in The Protein Book (and in fact based an entire dietary approach around in The Rapid
Fat Loss Handbook) it’s been known for quite some time that higher protein intakes (starting at 1.5 g/kg or
at least double what this study provided) is required to limit lean body mass losses when calories are
restricted. As well, given the very low protein intake in this study, a slower digesting protein such as casein
or milk protein would probably have proved superior.
As the researchers themselves point out “…in the absence of dietary carbohydrate and the presence of
significant catabolic stress most of this protein may have undergone oxidation or ketogenesis to maintain
hepatic gluconeogenesis.” (translation to non-nerd: the protein was burned off or converted to ketones to
produce glucose in the liver).
They add “Our results also indicate that when the energy deficit is very high, ingestion of the recommended
dietary requirements for protein (0.8 g/kg or 0.36 g/lb) does not prevent loss of body protein any more
effectively than the same amount of energy provided in the form of sucrose.” Honestly this is the most
perplexing part of the study to me: it’s 2014 and beyond well established that this amount of protein is
insufficient on a diet.
I’m not sure I have much to add beyond that and I also don’t mean to present this paper as a protocol to be
followed. Even the authors comment “The present proof-of-concept study does not propose an alternative
treatment for obesity. Although most of the subjects tolerated the intervention relatively well, all complained
of muscle and joint pain, individuals who are less strongly motivated would probably not tolerate this type of
intervention.” They also aren’t sure what caused the continued loss of a small amount of fat at the 1-year
mark.
Basically I just thought it was an interesting little paper in that it showed what is at least biologically plausible
or feasible in the short-term. I’ve seen the occasional person apply something along those lines (usually
the massive amounts of daily low-intensity activity without the extreme caloric deficit) and see some fairly
stunning results. It’s still not very applicable to the majority although with the increase of some of the new
walking/standing desks it might be.

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How Dieters Fail Diets
Note: The following is the entirety of Chapter 5 from A Guide to Flexible Dieting.
In this chapter, I want to discuss some two of the primary ways that dieters tend to sabotage their own efforts
on a diet, that is the way that dieters fail diets. These two ways are being too absolute and expecting
perfection and by thinking only in the short-term.
And before you complain about how bad it is form wise to write a short introductory paragraph instead of just
going straight into the text, I’ll defend my style choice by explaining that I don’t like starting a chapter with a
bold-faced sub-category. So there.

Too Absolute/Expecting Perfection


Perhaps the single biggest reason I have found for dieters failing in their diet effects is that many dieters try
to be far too absolute in their approach to the diet something I alluded to in the foreword. When these people
are on their diet they are ON THE DIET(!!!). Which is altogether fine as long as they stay on the diet. The
problem is that any slip, no matter how small, is taken as complete and utter failure. The diet is abandoned
and the post-diet food binge begins. As I’ve said repatedly, this tends to puts the fat (and frequently a little
extra) back on faster than before.
We have all either known (or been) the following person: one cookie eaten in a moment of weakness or
distraction, the guilt sets in, and the rest of the bag is GONE (perhaps inhaled is the proper word). Anything
worth doing is worth overdoing, right? Psychologists refer to such individuals as rigid dieters, they see the
world in a rather extreme right or wrong approach, either they are on their diet, and 100% perfection is
expected, or they are off their diet, shovelling crap in as fast as it will go. I’m quite sure this type of attitude
is not limited to dieting, probably any behavior you care to name finds people at one extreme or the other.
As a side note, you can oftentimes see the same attitude with people starting an exercise program. The first
few weeks go great, workouts are going well, then a single workout is missed. The person figures that any
benefits are lost because of missing that one workout and they never go back to the gym.
Now, I could probably go on for pages about this one topic but I’ll spare you the verbiage. My main point out
that there are times (most of them) when obsessive dedication or the expectation of perfection becomes a
very real source of failure. Sure, if it drives you towards better and better results, such an attitude will work.
But only until you finally slip. Note that I said ‘until you slip’ not ‘if you slip’. In most cases, it’s a matter of
when, not if you’re going to break your diet. There are exceptions, some of which I’ll mention below, but for
the majority of dieters, I would say that expecting perfection is pretty much expecting failure.
If you take the attitude that anything less than absolute perfection is a failure, you’re pretty much doomed
from the start. Now, there are some exceptions, places where results have to obtained in a very short time
frame and you can’t really accept mistakes. Athletes who have a short time to get to a certain level of bodyfat
or muscle mass, for whom victory or defeat may hinge on their ability to suffer for long enough are one. I
mentioned some others in my last booklet, individuals who have to accomplish some drastic goal in a very
short period of time; even there I included some deliberate breaks for both psychological and physiological
reasons. But in the grand majority of cases, this type of obsessive, no-exceptions attitude tends to cause
more problems that it solves.
Keeping with this idea, psychologists frequently talk about something called the 80/20 principle which says
that ‘If you’re doing what you’re supposed to do 80% of the time, the othe 20% doesn’t matter’. While there
are certainly exceptions (try avoiding crack or heroin for 80% of the time), it certainly applies to dieting and
exercise under the grand majority of conditions.

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If the changes you’ve made to your diet and exercise program stay solid for 80% of the time, the other 20%
is no big deal. Not unless you make it one. And that’s really the issue, that 20% problem only becomes one
if the dieter decides (either consciously or unconciously) to make it a problem. Once again, the exception is
for those folks under strict time frames, who don’t have the option to screw up. For everyone else, seeking
perfection means seeking failure.

Focusing Only on the Short-Term

The second primary way that dieters fail diets is focusing only on the short-term and this applies in a couple
of different ways. The first is a reality issue. Ignoring diets promising quick easy weight loss (my Rapid Fat
Loss Handbook caused rapid weight loss, a great deal of which was water, but it sure isn’t an easy diet),
about the best you can usually do with true fat loss is somewhere between 1.5-3 lbs/week (heavier
individuals can lose more).
Sure you can drop a lot more total weight if you factor in water weight and other contributors but true fat loss
typically peaks at about that rate (some lighter women may have trouble even losing one pound of fat per
week)
For the sake of example, let’s say 2 lbs/week can be reasonably expected for a fatter individual. For someone
with a large amount of fat to lose, 50 or 100 pounds, this may mean one-half to a full year of dieting. Possibly
more since it’s rare to see perfectly linear fat loss without stalls or plateaus.
Consider the reality of that, you may have to alter eating and exercise habits for nearly a year just to reach
your goal. Do you really expect to be hungry and deprived for that entire period? I thought not. If you have a
lot of weight/fat to lose, you need to start thinking in thte long-term, you will need to make changes to diet or
activity (or both) and maintain them in the long-term.
As a second issue: a lot of dieters seem to think that once they have lost the weight with one diet or another,
they can revert to their old habits and keep the weight off. So they change their eating habits drastically,
drop the weight and then go right back to the way of eating that made them fat. And, to their apparent
surprise, they get fat again. “You can never go back again.” as the old saying goes. If you go back to the
diet and exercise habits that made you fat in the first place, you’ll just get fat again.
This actually makes a profound argument for making small, livable changes to your eating and activity habits
and avoiding the type of extreme approach that I described in my last booklet. The simple reason being that
small changes seem to be easier to maintain in the long-term, even if they don’t generate results as rapidly.
And that’s actually sort of the trade-off, the types of small changes that tends to be sustainable in the long-
term tend to cause weight/fat loss that is so painfully slow (or minimal) as to be almost irrelevant; and the
types of extreme approaches that generate rapid results tend to be nearly impossible to stick to in the long-
term. In my last booklet, my compromise was to use the Rapid Weight Loss approach as a short-term
approach and then use it to move into a maintenance approach. But I digress.
At the end of the day, here’s the painful reality that all dieters must come to terms with: the only way to both
lose fat AND maintain that loss in the long-term is to maintain at least some of the diet and exercise habits
you changed in the long-term. Forever, basically even though that’s a little too depressing to consider. Maybe
we should just think long-term instead. Hopefully we’ll get genetic engineering soon enough to make it a not-
forever kind of deal.
Dieters (or anyone seeking to change a long-standing behavior) must stop thinking of diets as a short-term
behavior change, you’ll have to maintain at least some of those changes in the long-term. Now, I’ll point out
here that the strategies used for weight/fat loss and maintenance aren’t necessarily going to be the same

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(nor should they be). As I talked about in the Rapid Fat Loss Handbook, there are situations where an
extreme diet can be used initially and used to move into a proper maintenance phase. A lot of diet
researchers and diet book authors miss this point, thinking that the diet that you followed to lose the
weight/fat must or should be the same as the one you use to maintain that loss.
I do think it’s helpful is the diet that caused the fat loss can be used to move into a maintenance approach
(again, something I discussed in some detail in the last booklet and will make mention of in this one) but
they needn’t be the same. If eliminating all of the carbohdyrates from your diet makes it easier to lose fat in
the long run, and you are able to move back to a maintenance diet that contains some carbohydrates, I don’t
see what the problem is. Once again, the diet you use to lose the fat doesn’t necessarily have to be thes
same diet as you use to maintain that fat loss. If nothing else, you get to eat more when you move back to
maintenance, the types of foods you allow yourself may change as well.
Summing up this section, it’s not that diets per se fail, it’s that diets that are only followed short-term fail. The
body is really good at storing incoming calories as fat after a diet and if you return to old eating habits, you
can just watch the pounds come flying back on.
To hopefully cement this point in your mind, studies of successful dieters (those who have lost weight and
kept it off for some period of time, usually 2-5 years) have shown several very consistent behaviour patterns
of which this is one: they maintain the dietary and exercise changes they have made in the long-term. If
you’re not going to maintain at least some of your changed dietary and exercise habits in the long-term, you
might as well not bother (with one major exception discussed below).

One Exception to the Comments Aabove

There is, however, one major exception to the above that I should probably mention (and that I discuss in
greater detail in my Rapid Fat Loss Handbook). There are individuals who, for whatever reason, only have
to be in shape for a very short period of time, a day or three at the most, who don’t necessarily care if the
results are maintained long-term or not.
Usually it’s a bodybuilder preparing for a contest, or even a model who has a particularly important photo
shoot. Or a woman who needs to drop 20 lbs for her wedding or a male who needs to impress people at his
high school reunion. Even athletes who have to make a weight class sometimes have to do scary stuff to
get where they need to be, usally involving fluid restriction and frequently severe dehydration. But the
consequences of not making weight (whatever they may be) are greater than the extreme approaches that
tend to be used.
In situations like that, whether it’s healthy or not, extremely restrictive and/or even slightly dangerous
approaches are frequently used. We may not like them, we may not condone them but sometimes the ends
justifies the means because a few pounds may mean the difference in getting a big paycheck/winning the
contest/looking good in your wedding gown or not.
In these situations, long-term maintenance isn’t necessarily the goal. No sane bodybuilder expects to
maintain contest shape year-round, and no weight class athlete expects to maintain a severe state of
dehydration year round. They get in shape for their event, and relax to some degree for the rest of the time.
So the above sections really are aimed at the person looking to lose fat and keep it off long-term.
In that case, where maintenance is just as important as the loss itself, absolute attitudes and focusing only
on the short-term hurt far more than they help, and should be avoided as much as possible. In addition to
the strategies I’m going to discuss in this booklet, this means taking a very different attitude towards dieting.

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First you have to let go of your absolutist attitudes, which can be hard. Second, you need to start taking the
long-view to both your weight loss and dietary and exercise habits. I’ll come back to this in later chapters.

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Around Workout Nutrition While Dieting – Q&A
Question: Should I continue with around workout nutrition while dieting?

Answer: Since summer time is approach and everyone (more or less) is dieting to look good at the pool,
this is a question that comes up fairly often. I’ll be honest that I spent years going around and around with
this one in my head before finally coming to some conclusions about it. These are those conclusions.
The usual rationale for avoiding around workout nutrition while dieting goes something like this: if you
consume nutrients (especially carbohydrate) during or after training, you will either impair fat
mobilization/burning by increasing insulin levels or impair the hormonal response (growth hormone gets
brought up a lot) and slow fat loss. Some suggest only consuming protein around training for this reason
although they all seem to forget that protein (and especially the Branched Chain Amino Acids) raise insulin.
A related idea is of doing training first thing in the morning fasted to take maximum advantage of the increase
in blood fatty acids which occur during the overnight fast. And certainly, for certain types of activity
(especially low intensity aerobic activity), there is certain some truth to this. Of course, those types of
activities don’t generally require much in the way of around workout nutrition in the first place.
Certainly this strategy has been used for decades by contest prepping bodybuilders or other athletes who
need to lean out. As I discuss in detail in The Stubborn Fat Solution, for individuals looking to shed the last
bit of stubborn fat, there is probably some rationale to this strategy due to the profound impact of insulin on
fat mobilization. Of course, for people who can’t work out first thing in the morning or fasted, there are also
ways to get around that (discussed in the book) and still deal with stubborn fat.
But what about higher intensity activities such as weight training or more intense types of metabolic work,
should around workout nutrition still be maintained (to at least some degree) while dieting?
The short-answer, in my opinion, is yes. Here’s the longer answer.
First let’s look at metabolic work, cardio and interval type work. For the most part, concerns about impairing
fat oxidation during higher intensity activity with the consumption of during workout nutrition don’t seem to
be warranted in the first place.
As Alan Aragon reviews in his book Girth Control, research clearly shows that the consumption of carbs
during moderate and higher intensity aerobic activity doesn’t negatively impact fat oxidation in the first
place. Basically, it’s only low intensity aerobic activity where this is an issue and, as noted above, that type
of training doesn’t require much in the way of nutritional support in the first place.
I’d even go further and argue that proper during workout nutrition during higher intensity activities can help
with fat loss simply because it tends to improve intensity and performance, allowing people to work harder
and/or longer which burns more calories which is far more important in the big scheme of fat loss.
Trying to perform higher intensity training when blood sugar is down often goes badly (there is a lot of
individual variability in this). From a fat loss standpoint, I consider being able to train effectively far more
important than any small benefits from a hormonal or other perspective.
Of course, I’d make the same argument for weight training (with the exception of activities done specifically
to deplete muscle glycogen); the ability to maintain training intensity in the weight room (which is the key to
maintaining muscle mass) is far more important in the big scheme of things than any small hormonal effect
or what have you. As well, weight training doesn’t generally use fat for fuel to any great degree in the first
place. Worrying about ‘impairing fat burning’ during weight training sessions is missing the point.
It’s also worth noting that much of the concern over post-workout nutrition under these conditions may be
equally misplaced. It’s usually feared that consuming carbs after a workout will impair any post-workout fat
burn (I’d note that any effect from this is very small in the first place).

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However, research shows that following high-intensity (aerobic) activity, the body continues to use fat for
fuel even when carbs are consumed immediately after workout; under those conditions the carbs go to refill
glycogen stores but the body continues to use fat for energy production.
And given that proper post-workout nutrition is one of the key aspects to improving overall recovery (always
at a premium when folks are dieting), I think that the benefits of maintaining at least some around workout
nutrition outweigh any slight negatives in the case.
Finally, there is also the often forgotten fact that most of the ‘fat burning’ that happens during a diet doesn’t
occur during training (especially weight training) in the first place. Rather, it’s what happens the other 23
hours of the day that will have the biggest impact on overall fat loss. And that’s mostly related to diet.
Don’t get me wrong, exercise clearly contributes to fat loss through a variety of mechanisms but, again, it’s
less the hour you spent training and what happens in the other 23 hours of the day that will maximally affect
fat loss.
Basically, at least if you’re talking about moderate to high-intensity types of training, I think the benefits of
around workout nutrition far outweigh any of the negatives. During workout nutrition can help to maintain
training intensity and proper post-workout nutrition improves recovery. I think those benefits far outweigh
any small or nonexistent negatives that might occur.
Basically, rather than cut carbs/protein from around hard training sessions, I’d rather see those cuts
(especially carbohdyrates) coming from other meals of the day. Some dieters will actually take this to the
extreme of only consuming carbohydrates around training and eating no starchy carbs the rest of the day.
This is essentially the Targeted Ketogenic Diet (TKD) that I discussed in my first book The Ketogenic Diet
and it can provide any benefits of a full-blown low-carbohydrate diet while still allowing trainees to maintain
training intensity and recovery from high-intensity worouts.
However, that may not be desired or required for all dieters. Some people do poorly on low-carbohdyrate
diets and will need to consume some carbs at other meals of the day in addition to any around training
nutrition. This means that, in most cases, the amount of around workout nutrition consumed may have to
be scaled back somewhat.
Someone consuming a lot of calories around training may leave themselves with almost nothing to eat the
rest of the day on a diet and scaling the values back may be necessary. I can’t give recommendations
beyond that since a lot will depend on how much is being consumed around training in the first place.
A trainee consuming a very large amount of carbs and protein post-workout (e.g. 100 grams carbs/40 grams
protein) might cut that in half while dieting; someone consuming a small amount in the first place (e.g. 20-
30 grams of each) might not cut back anything at all.
Of course, I also think that training volume (especially in the weight room) should be reduced while dieting
in the first place which means less requirement for around workout nutrition in the first place. But talking
about weight training on a diet is another topic for another day.
But I don’t think that around workout nutrition should be eliminated while dieting completely, especially for
moderate to high-intensity training sessions. The benefits from being able to maintain training intensity and
recovery far outweigh any small benefits from the hormonal response or what have you (especially given
that most fat loss happens outside of the gym anyhow).

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Does Your Mind Stop You From Losing Weight?

It’s interesting to note; the single most important factor to not just getting the weight
off, but keeping it off, is between our ears. That is, how people approach the issue,
psychologically speaking, is an essential component of success. And yet, 8 zillion
weight loss books and programs out there, and at best, this aspect of weight loss gets lip
service only.

Many diet programs out there don’t address the psychological aspect of why people fail
to be successful with long-term weight loss. However, quite a few studies exist that
have looked at just that. In many respects, the psychological aspect is the most
important for long-term weight loss, and probably the most underappreciated
component.

Studies that compare the psychological characteristics of people who have successfully
kept the weight off to people who have regained the weight, see clear differences
between these two groups. For example, one study that looked at 28 obese women who
had lost weight but regained the weight that they had lost, compared to 28 formerly
obese women who had lost weight and maintained their weight for at least one year and
20 women with a stable weight in the healthy range, found the women who regained the
weight:

• Had a tendency to evaluate self-worth in terms of weight and shape

• Had a lack of vigilance with regard to weight control

• Had a dichotomous (black-and-white) thinking style

• Had the tendency to use eating to regulate mood.

The researchers concluded:

“The results suggest that psychological factors may provide some explanation as to
why many people with obesity regain weight following successful weight loss.”

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This particular study was done on women, so it reflects some of the specific
psychological issues women have – but make no mistake here – men also have their
own psychological issues that can sabotage their long term weight loss efforts. (6)

Additional studies on men and women find psychological characteristics such as


“having unrealistic weight goals, poor coping or problem-solving skills and low self-
efficacy” often predict failure with long term weight loss. (7) On the other hand,
psychological traits common to people who experienced successful long term weight
loss include “…an internal motivation to lose weight, social support, better coping
strategies and ability to handle life stress, self-efficacy, autonomy, assuming
responsibility in life, and overall more psychological strength and stability.” (8)

The main point of this section is to illustrate that psychology plays a major role in
determining if people are successful with long-term weight loss. If it’s not addressed as
part of the overall plan, it can be the factor that makes or breaks your success. This,
however, is not an area most nutrition programs can adequately tackle and should not be
expected to. However, the better programs do generally attempt to help with motivation,
goal setting, and support. Lack of support is one important issue I identified early,
having personally trained so many people, and getting feedback from my articles, etc.
That’s why my Fat Loss Revealed Program comes with a private forum where people
can get support, advice, and get answers to their questions.

If you see yourself in the above lists from the groups that failed to maintain their weight
long term, then know you will need to address those issues via counseling, support
groups, etc. Don’t expect any weight loss program to cover this topic adequately but do
look for programs that attempt to offer support, goal setting, and resources that will
keep you on track.

Note: the above is a modified section from a report I did called “The Big Picture of
Permanent Weight Loss.” More info on the topic of successful long term weight loss,
the citations from the studies mentioned above, etc can be found in that report if
interested.

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Adjusting the Diet
In various places on the site, I have made the comment that such things as caloric intake and activity will
have to be adjusted based on real-world fat loss. For example, in the Q&A on How to Estimate Maintenance
Caloric Intake, I pointed out that one of the reasons that I use the quick estimates for such things as
maintenance calories and setting initial caloric intakes is that they always have to be adjusted anyhow.
Today I want to talk about how I do that adjustment, note that if you’ve read either The Rapid Fat Loss
Handbook or A Guide to Flexible Dieting, this is the same information in the last chapter where I talk about
setting up moderate deficit diets and how to adjust them. I’d only note that the same basic information can
be used when either small or larger deficit are used as discussed in Setting the Deficit-Small, Medium or
Large.

.A Quick Note about Water Balance

Before I get into the meat of the article, there is one topic I want to bring up first. Many people have an
expectation of fat loss being this nice weekly linear thing that occurs in a predictable fashion. And certainly,
for some people this can be the case. However, for an equally large number of people (and I’d probably
tend to argue that these folks are in the majority), fat loss does not occur in a predictable linear fashion.
Rather, there are often stops and starts or, as it’s often referred to on the Internets, stalls and whooshes. I
discussed this topic in some seriousness in The Stubborn Fat Solution and excerpted that bit in the article
Of Whooshes and Squishy Fat. The main culprit here is almost always water retention which can mask fat
true fat loss and make it look as if a diet that is otherwise set up perfectly (and working just fine) actually
isn’t.
People vary in how predisposed they are to this occurring. Some folks seem to retain water like crazy,
especially if they try to combine hard deficits with excessive and or too intensive of activity. Women of
course have an additional factor of shifts in water balance throughout the menstrual cycle. Even that is
massively variable, some women gain little to no water weight throughout the month, others can hold an
extra 5-10 pounds (2.5-5kg or so) easily.
Coupled with a generally slower rate of fat loss in the first place, women can go nuts trying to figure out if
their diet is working or not. Put differently, let’s say a woman is on a moderate deficit diet and should be
losing right around 1 pound of fat per week. If she is holding an extra 5-10 pounds of water, it could take 5-
10 weeks before she actually sees that her diet is working.
Of course, if the water retention is related to menstrual cycle stuff, what she should see if times of the month
when her weight/fat is down (below where she started) and other times when it’s not. Plotting weight or
some attempt to measure body composition on a monthly basis to see what the overall trend is is probably
going to be more beneficial than looking at it on a week to week basis.
My point in bringing this up is actually not just to depress people. Rather, I’m pointing out that what I’m going
to discuss in this article in terms of adjusting the diet can be done too often. For folks who have issues with
water retention (who may see big drops every couple of weeks rather than smaller drops weekly), trying to
gauge true weekly fat loss and adjust the diet is usually a losing proposition.
Rather, those folks may have to only look at what’s happening every 2 weeks to decide when and if to adjust
their diet. Women with major menstrual cycle swings may even have to chart their monthly trends to see
what’s happening and only make adjustments every 4 weeks.

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Yes, I know this is a pain but at this point there’s really no solution for it. All of the methods that we have to
measure body composition are too inaccurate to get around this and the point I want everybody to really
take home is that expecting predictable weekly fat loss may not be realistic depending on individual
propensity to hold water or not.
.

Back to the Point

Accepting the above, that water balance can throw off expectations on a week to week (or even month to
month) basis in terms of fat loss, the first necessary data point is what the predicted or expected fat loss
actually is. I gave some examples of this in Setting the Deficit-Small, Medium or Large and clearly the
expected fat loss will depend on two things: the size of the dieter and the size of the deficit. Bigger dieters
and/or bigger deficits mean faster expected fat loss and vice versa.
For the purpose of this article, I’m going to use a relatively ‘average sized’ dieter and a moderate deficit with
a weekly expectation of approximately 1-1.5 pounds per week of true fat loss. This would be a reasonable
degree of fat loss for a relatively ‘average sized’ male using a moderate deficit (20-25% below maintenance);
again the numbers would be different for smaller/larger dieters and/or smaller/larger deficits.
Based on that, the chart below is how I’d adjust calories (either by reducing food intake or increasing activity,
again a topic I’ll address another day in terms of which may be better or worse) based on measured weekly
(or bi-weekly) fat loss.
.

Average Weekly Fat Loss Is There Performance Loss Adjustment

Less than 1 lb/week Reduce Calories by 10%

1-1.5 lbs/week No Change

2+ lbs/week No

Yes Increase Calories by 10%

.
Frankly, there’s nothing that exciting in the chart and it should be fairly self-explanatory. If your predicted fat
loss is 1-1.5 lbs/week (and you’re not messing up your calories somehow, through mis-measurement or
what have you) and you’re not achieving that, you need to reduce calories further (or increase activity to
burn the extra).
Clearly, if you’re hitting your goal numbers right on the spot, don’t change anything.
Of course, there are times when the actual weekly weight loss ends up being larger than expected. Some
of this can be water or what have you but not always. And that leads me to an explanation of the middle
column.
As I discussed in Weight Training for Fat Loss, one of the primary metrics that should be used while dieting
(for non-athletes) is the maintenance of poundages in the gym. Now, it’s not always possible to maintain
100% of strength (and this tends to be a bigger issue as folks get to lower and lower body fat levels) but if
major dropoffs are being seen and training is correct, that usually indicates that muscle is being lost. In that
situation, the deficit must be reduced, either food intake should be increased or some of the extra activity
(usually excessive cardio) should be reduced.
Of course, the same would go for athletes who are trying to reduce body fat levels, if some useful metric of
their performance (e.g. run time, cycling power output, whatever) is worsening, then the deficit is too
aggressive and calories should be increased (with any ‘junk’ or extra activity being reduced if necessary).

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I’d note that, strictly speaking, I could have included the performance loss column for any of the weekly fat
losses. Some people even doing everything ‘right’ simply can’t achieve optimal fat loss results without
performance loss. They will need to use less agressive deficits (again either reducing food intake or
increasing activity) to avoid major performance falloffs.
.

Summing Up

And that’s how I adjust diets. Honestly, there’s nothing too majorly complicated to it and there are basically
three steps.
First off you need to have some idea of what the expected or possible fat loss for a given deficit is. I’d note
that people always want fat loss to be faster than it is no matter what they do. If they are losing 1 pound per
week, they want 2 pounds per week. If they are losing 2 pounds per week, they want 4 pounds per week. If
they are losing 5 pounds per week, they will want 10 pounds per week. This is just human nature but it’s
not always realistic.
Certainly there are ways to do this (usually involving monster daily deficits as discussed in Setting the Deficit-
Small, Medium or Large) but even there there is going to be some expected degree of fat loss based on the
deficit that is created. You need to know what is realistic based on the deficit that is being created.
Second there needs to be some awareness of the issues related to whooshes, stalls and water
balance. This basically relates to how frequently you are going to decide whether your current activity level
and deficit need to be examined and/or adjusted in the first place. Folks vary in how much of an effect this
has.
Women, on average, have bigger issues but some men also deal with it. If you know that you take 2 weeks
before you see a drop, clearly using a single week of measurement to make a decision is a mistake. If you’re
a woman with major monthly swings, you may have to only examine true fat loss on a 4 week cycle, using
what happens weekly (or daily as is sometimes the case) will not only drive you nuts but be inaccurate.
And then you simply compare the expected fat loss to the actual fat loss. If what happened is less than
what’s predicted (and you’re not mis-measuring food or something), then you need to increase the deficit
slightly. If you’re right in the sweet spot, losing what you’d predict, don’t change anything. And if you’re
losing more than predicted, you may need to increase calories (or decrease activity).
I usually use small adjustements here, 10% is usually fine for increases or decreases. Then stay there for
whatever time period is appropriate for you individually and adjust again. Eventually you’ll nail it down to
exactly where you need to be.
Since I imagine someone will ask about this in the comments, I’d note that, as people lose weight/fat, and
maintenance requirements fall (both as a function of body mass loss along with the adaptive adjustments),
often caloric intake has to be reduced further (or activity increased) to maintain the same degree of weight/fat
loss. This is something I’ll address in more detail in a later article.
Finally, another consideration is performance loss. If you’re a general weight trainer or physique athlete,
poundages in the gym are the usual metric. If they are cratering you are probably losing muscle; regardless
of the weekly fat loss, you need to reduce the size of the deficit. You need to either increase calories or
reduce volume (usually cardio). For performance athletes, there should be some performance metric that
you’re tracking to judge if your diet is doing more harm than good. If that metric is going down, you need to
reduce the size of the deficit.

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Introduction to Dieting
I am credited with having made the following statement on an internet newsgroup “Diet books tell you that
you don’t have to reduce calories to lose weight, and then trick you into doing it anyway.” In this article, I
want to look at some basic concepts related to dieting, the myriad weight-loss diets that exist, etc.

Mainstream dieting

Arguably the simplest diet of all is a rather basic ‘just eat less’ approach to weight loss (or ‘just eat more’
approach to weight gain). By making a conscious effort to eat less food over the course of the day, folks
reduce calories and lose weight. There’s no magic, it’s simply food proportioning. Such an approach to
dieting isn’t fundamentally flawed and, when it works, it works fine.
At the next level of ‘complexity’ are what we might term good food/bad food types of diets. Most people seem
to carry around the idea that some foods are good for them while others are bad (in terms of bodyweight or
health or what have you) and diets in this category feed into that psychology. Generally, a good food/bad
food dichotomy is emphasized over the actual quantity of food being consumed (many such diets will loudly
exclaim that calories don’t matter, only the source of those calories).
Even the standard low-fat prescription is based around the idea that fat is ‘bad’, being the cause of obesity,
and that by eating less of it, you’ll lose weight and be healthier. It’s been estimated, for example that for
every 1% reduction in fat intake, a person will lose 1.6 g/day. So a 10% fat reduction would result in a 16
g/day loss, about 2.5 kg (~5 lbs) over a 2 month span. Yippee. Of course, going into that estimation is the
huge assumption that the dieter won’t compensate by eating more of the non-proscribed foods.
A more frequently occuring idea revolves around carbohydrates. Diets such as SugarBusters and others
paint refined sugar as the enemy, while more extreme diets such as The Atkins Diet, Protein Power and
the South Beach Diet paint all carbohydrates (vegetables excluded) as the enemy. Since carbohydrates
typically make up a rather large (50% or more) of total daily energy intake, restricting or removing them has
the potential to cause rather large scale caloric reduction.
Typically such diets fixate on one individual aspect of humans physiology in terms of weight gain and use
that to defend the argument of why a given food is ‘bad’. Anti-fat books will focus on the fact that dietary fat
is stored as fat far more easily than other nutrients while anti-carb books usually focus on insulin levels.
What few of these books admit is that the ‘bad’ foods in question typically contain a lot of calories and are
foods that people like to eat a lot of. Meaning that it’s easy to consume too many calories when you eat
those foods. By decreasing intake of such foods, dieters generally end up eating less calories and losing
weight. There’s no magic, it’s simply disguised caloric restriction.
Other diet books take the slightly opposite approach, advocating that you eat certain foods (usually
vegetables or high-bulk, high-fiber starches) in large amounts. I remember a study done years ago where
subjects were required to eat 2 lbs of potatoes per day and they could eat anything else as long as they ate
the potatoes. Of course, since the potatotes filled them up, they didn’t eat much else so they ended up eating
fewer calories and losing weight. Such diets require that you eat these foods first in a meal and then you
can eat ‘anything you want’.
Fiber is frequently touted as a miracle weight loss food and diets forcing you to eat metric assloads of high-
fiber, high-bulk (and hence filling) vegetables work a similar way: by forcing you to fill up on low-calorie foods,
you eat less of the higher calorie foods and lose weight. One recent diet book tricks people into eating less
(all this after telling them for pages that calorie counting doesn’t work) by switching out starches with fiber;

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automatically reducing their calories. Another best-selling diet book (no names) goes on for pages about
how calories don’t count, and then puts everyone on a low-calorie diet with a complicated ‘block’ based
system.
Then there are ‘simple’ diets that aren’t so simple. They typically revolve around complicated sets of rules
(such as food combining) while still telling the dieter to ‘eat all they want’. Again this is just a trick, when you
look at the rules you find that they actually are quite limiting. For example, diets that only let you eat fat with
protein (a common food combining approach) means that you can only eat fat (with all of its calories) at
roughly half of your meals. Compared to a diet where you can eat fat at all of your meals, this will generally
cause you to eat less. As well, since most people don’t have a taste for pure fat per se, but rather the
combination of sugar and fat (donuts anyone?), preventing people from combining carbs and fats makes
them unable to eat stuff they’d otherwise over-consume.
Two different diets requires that you fast (or eat small amounts of lean protein and veggies) most of the day
with one big ‘reward’ meal at the end of the day. But even that reward meal has a bunch of rules: start with
veggies, then lean proteins, then starches (one diet limits the ‘reward’ meal to an hour as well). Over the
course of 24 hours, you can’t help but eat less with such a diet: you’re eating only tiny amounts (or nothing
at all) and you’re ‘eat all you want meal’ has a set of rules that prevents you from eating that much.
Now, many of these diets will occasionally make admissions that calorie counting may be necessary (usually
when the diet stops working) but most focus predominantly on one food or another, based on the (sometimes
valid) assumption that eating less of that food will make people eat less without thinking too much about it.
You might think that I have a problem with such simplistic dietary prescriptions but you’d be wrong. As I
discuss in How Detail Oriented Do You Need to Be many people respond best to diets that make simple,
rather non-intrusive demands on their food intake. If switching out one food for another, or cutting
back/down/out on a certain food makes them eat less without thinking about it all the better. Obviously, up
to a point, such diets work.
I’ve used this approach commonly with my personal training clients (non-athletic/bodybuilder types). I would
look at their diet from a qualitative standpoint and make simple, non-obnoxious suggestions. One client, for
example, was drinking three or four regular sodas per day. I suggested he switch to diet soda, automatically
cutting many hundreds of calories out of his diet; he lost weight without doing anything else, having to count
his food, or feeling deprived.
Other approaches, such as switching from full fat to lower fat milk, or reducing refined starch intakes can
frequently work just as well. Now that protein has been shown to be the most filling of the nutrients,
spontaneously causing people to eat less, I’m expecting a slew of new diet books based around that concept.
Now, I want to make it clear that I do have a big problem with diet books that tell people that calories don’t
count becuase that’s obviously and quite simply not the case. Calories always count. It’s simply that, under
certain dietary circumstances, people eat less (or more) calories and that affects weight gain. Simply put, if
a given food makes you overeat (this goes for ‘healthy’ foods too), it’ll make you gain weight. If you eat less
of that food, odds are you’ll lose weight. Tricky diet book authors hide what is, ultimately, simple caloric
restriction in complicated rules and regulations. Eat this, don’t eat that, eat this with that but not with the
other, don’t eat after 6pm, that kind of thing.
Admittedly, diets that trick people into eating less without making them aware of it can be actually very
beneficial, which is why I’m not against them entirely. Psychologically, knowing that you have to eat less
food tends to cause anxiety, hunger and problems with adherence. That is, frequently simply being aware
that you’re eating less will make you hungry as a consequence. This is truly a case where ignorance is bliss.
As long as such a simple diet ensured adequate protein intake and essential fatty acids, I’d have no real
problem with it. Many simple diets do not.

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Unfortunately, such approaches don’t always work, or they only work temporarily. There are many reasons
for failures at this level (the topic of why diets fail is discussed in greater detail in an upcoming chapter). The
usual culprits in my experience have to do with the craftiness of the human body and the human mind. Over
time, the body will almost always compensate to reductions in caloric intake, whether the compensation is
conscious or not.
In one classic study, for example, subjects were given a high-fat yogurt and either told it was low-fat or
normal fat. The folks who thought it was low-fat ate more of it. This was, of course, during the time when
people had heard the message that ‘fat was bad’ and nothing else mattered. Which is why the slew of ‘non-
fat’ foods that came to market didn’t do what was expected: people simply compensated by eating more of
them. The same appears to hold for all of the no-calorie sweeteners.
Psychologically, people figure that since they are eating no-calorie foods, they can eat more of the higher
calorie stuff and they end up compensating. Folks on simple ‘eat less of X’ diets frequently end up eating
more of the other foods allowed on the diet. Studies where fat is reduced with no attention paid to caloric
intake generally find an initial weight loss followed by a gain when people invariably start eating more total
calories from other sources. You’d expect the same on other diets and recent studies of low-carbohydrate
dieting are finding similar results: initial weight loss followed by either a plateau or weight gain as people
start eating more.
This is especially true when a given diet book entreats dieters to ‘eat all they wish’ as long as they avoid the
forbidden foods. Even if the book only means ‘eat until you’re full and stop’, crafty humans will find a way to
turn ‘eat as much as you wish’ into ‘eat as much as I can'; they’ll still end up eating too many calories and
weight loss will stop. Alternately, they may not realize that, as weight is lost and caloric requirements go
down, food intake has to decrease as well. The diet that was once calorically restricted is now a maintenance
calorie diet.
There’s a potentially bigger problem that I see quite a bit. When these books have programmed such diet
failures with a ‘calories don’t count’ message, it becomes impossible to make folks realize that the source of
the stall is a simple calorie issue. They’ll find every reason under the sun why the weight isn’t coming off,
anything to avoid facing up to the fact that they are going to have to start counting calories. They are not
different.
There are other problems with such diets (and dieting in general) that I don’t have space to cover here. But,
in summary, I’m all in favor of such simple diet changes as long as they are working. For many people they
work, at least for some time period. And, as long as they are working, I have no real problem with them. But
when such approaches stop working, it’s time to move into real dieting.

Real Dieting

As appealing as simple diets are, there are times when they simply won’t suffice. It may be a situation where
a simple diet has stopped producing results. Alternately, many people prefer (on a psychological level) more
complex and/or controlled diets. Finally, there is that small percentage that has to acheive maximal results
in a certain time period, for whom simple diets simply won’t do. Again, this is discussed in more detail in the
article How Detail Oriented Do You Need to Be.
So what do I mean by ‘real dieting’? Real dieting consists of counting calories, weighing and measuring
foods, and paying attention to macronutrient intakes. It’s more of a hassle (causing more anxiety) than simple
dieting but, if you’re in one of the situations described above, you don’t have a choice. Actually, you do have
a choice which is to stop getting results: stay fat or quit gaining muscle. I’ll assume that that’s no-choice
meaning that you will have to move to real dieting.

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I’ll be the first to admit that real dieting isn’t nearly as much fun as the simpler version. However, it does offer
some benefits. One of these is control; by knowing how much and what you’re eating, you can develop some
expectations as to what types of weight changes to expect. This allows for better manipulation of the different
dieting variables. By comparing what you’d expect to what you’re actually getting, you can make the
appropriate changes.
A second benefit of real dieting is that it makes you aware of your actual food intake. As I’ve mentioned other
articles on the site, most people have a tremendous tendency to mis-estimate their true caloric intake.
Dieters typically underestimate and folks trying to gain weight do the opposite.
By actually measuring it (meaning measuring food portions and using a food counter book), you develop
food awareness. Over time, that type of awareness becomes more or less automatic, you can get a generally
good idea of how many calories a given meal might have or how much you’re eating in a day’s span. Until
you’ve spent some time directly measuring your food, odds are you’re going to mis-estimate.
A third, and perhaps the most important benefit has to do with troubleshooting. Now, there are a lot of factors
can cause diets to fail, I’ll discuss some of them in detail in an upcoming chapter. At the very least, by
tracking your actual intake, you can avoid some of the simpler fuckups.
For example, with a simple diet, there’s usually no guarantee that you’re eating sufficient amounts of protein,
or getting your essential fatty acids every day. By tracking and being aware of your actual intakes of such
things you can avoid those problems. Tracking things won’t solve all of the problems related to dieting, but
you can avoid the really egregious ones
A very real problem with simple diets has to do with caloric intake. Sometimes, the reason a dieter isn’t
losing weight is because they are simply eating too much. In more rare cases, eating too little (especially for
extremely prolonged periods of time) can be the problem. But unless you know what you’re currently eating
with some reasonable amount of accuracy, you can’t know if that amount should be adjusted upwards or
downwards.
I guess the primary benefit of real dieting real dieting over more simple approaches can be summed up in
the word ‘control’. You can control your nutrient intakes to ensure that no major problems occur, and you
have control over what to do when other problems show up. By knowing your intake, you can make
predictions as to what types of results should be occurring. If they don’t, you’ll be in a better place to make
an informed decision over what to change.

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Not Losing Fat at 20% Deficit, What Should I do? – Q&A
Question: If someone is looking to reduce body fat and is not showing progress at 20% below their calorie
maintenance level, what would be the next logical step to induce fat loss? This person engages in regular
aerobic and resistance training.

Answer: The first question I would ask this person is if they had just started their diet and exercise program. I
have often see this sort of weird ‘delay’ in fat loss when people first start a new diet/exercise program. And
this tends to be far more so the case for women than for men (men always have it easier).
Trainees would be doing everything ‘right’ and absolutely nothing measurable would happen for the first four
weeks. And then sometime after week 4, there will be this big change in body composition, seemingly
overnight. On the Internet, this is often called the ‘whoosh’ (which usually comes after a ‘stall’).
Which, of course raises the question of what is causing this to occur. Some of it may have to do with gene
expression in terms of mobilizing and burning fat off the body, these pathways seem to take some time to
get up to full speed when people are just starting out. Some of it may simply be the error in terms of making
caliper measurements and our ability to measure small changes with current technology. I suspect a lot of
it has to do with water balance. When in doubt, I just chalk it up to voodoo magic and acknowledge that it
happens even if we don’t exactly know why.
I honestly suspect that weirdness in water balance plays a huge role in this; and there is a lot of individual
variance in how much people are prone to retain water (simply, some are more prone than others). I
discussed the ‘whoosh’ phenomenon in The Stubborn Fat Solution and honestly think that water retention
and such tend to ‘mask’ true fat loss in a lot of cases, at least over the short term. Then seemingly overnight,
it looks like someone has lost several pounds of fat; people wake up leaner and lighter. At some point in the
future, I’ll write a full article about the topic.
And while the above applies to both men and women fairly equally, women have an additional issue which
is the changes in water balance throughout the month due to the menstrual cycle. As I discussed in Body
Composition Recommendations, some women can shift fairly significant amounts of water over the duration
of their monthly cycle. That will tend to overwhelm all but the most extreme rates of fat loss.
Trying to measure fat or weight loss in women on a week to week basis is often a futile endeavor and females
may have to measure only once per month (ideally at the same point in the cycle) to get any sort of consistent
or comparative measures. Women should generally pick a specific point in their cycle and make all
measurements then to track changes month to month.
Another option is to measure weekly but only compare the same week of the cycle each month. So week 1
of the cycle would be compared to week 1 of the cycle a month down the road, week 2 is compared to week
2, you get the idea. What doesn’t work is comparing week 1 to week 3 because the body may be holding a
ton of water during one of the weeks and not during the other making comparison impossible.
Tangentially, an idea that seems to come in and out of fashion in bodybuilding circles is that of a water
load. Bodybuilders who think that they are holding water may bump up water intake fairly significantly for a
few days before cutting it back to normal levels. This can often help the body to normalize water balance
and may help get past the water retention issue.
I’ve often also seen refeeds (high-carbohydrate overfeeding as discussed in A Guide to Flexible Dieting)
trigger whooshes. A bit more accurately, people get fed up with dieting for a month with no visible results,
say ‘screw this’ and go pig out. And frequently wake up several pounds lighter and looking leaner. I just try
to structure and control it a a bit better with structured refeeds.

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Something else to consider has to do with the issue of the estimation equations for maintenance intake. As
I discussed in How to Estimate Maintenance Caloric Intake, I use a rough estimate for maintenance of 14-
16 cal/lb (31-35 cal/kg). A standard moderate deficit is usually a 20% reduction which puts most people in
the range of 10-12 cal/lb (22-26.5 cal/kg).
However, those values are only estimates which have to be adjusted based on real world fat loss (I’ll discuss
how I make adjustments in a later article). In modern times, with decreasing amounts of daily activity, I’m
finding that many people, unless they engage in quite a bit of exercise during the day, find that even 10 cal/lb
doesn’t generate significant fat loss. Because their true maintenance is lower than the estimate.
I have known people who have to go to 8 cal/lb (often with an hour of activity daily) to lose fat at any
reasonable rate. So if you’re basing the 20% reduction on one of the estimation equations, that may be
getting you into trouble. If your true maintenance isn’t actually 15 cal/lb, using a 20% reduction from that
starting point won’t yield appreciable fat loss because true maintenance is lower than the equation is
predicting.
A related issue is that, contrary to what some seem to believe, maintenance caloric expenditure is not static,
it can vary somewhat with changing diet and activity (both up and down). During dieting, many people tend
to move around a bit less during the day, due to fatigue and lethargy, and this reduces the pre-diet
maintenance level, offsetting some of the supposed deficit.
An additional factor has to do with systematic mismeasurement of food. And here I’m not talking about
people just grossly mis-estimating their food intake; rather, I’m talking about folks who are measuring the
amounts of food they’re eating but making mistakes in their measurement (a point made in some detail in
Leigh Peele’s Fat Loss Troubleshoot). If you’re using cup or teaspoon (or whatever your metric equivalent)
measures to track your food, it’s very possible to end up eating more than you think because you’re still mis-
measuring things.
A good example is peanut butter, if you load a tablespoon (supposedly 16 grams and about 100 calories
according to the label) fully and then actually weight it on a digital scale, it will invariably be more than 16
grams. And since we all know that you actually overfill the spoon and and lick the sides, well….it’s easy to
get a lot more calories than you’re actually writing down. And over the course of multiple meals per day, this
adds up.
Depressingly, even vegetables, which are often thought of as ‘free foods’ on a diet, can be a problem in this
regards. Due to hunger, some dieters start eating enormous amounts of vegetables (e.g. a head of
cauliflower) and when you actually go look up the amount of digestible calories this provides, it does start to
add up.
For smaller dieters who don’t have a huge deficit in the first place, it’s possible to eliminate the deficit almost
entirely because of this type of thing. Correlating your cup/spoon measures on an actual digital scale may
be necessary to make sure you’re not doing this. Yes, this is a pain in the ass and yes this starts pushing
people towards insane levels of obsessive compulsive neuroticism. But in some cases it’s absolutely
necessary to ensure that what you think you’re eating is actually what you are eating.
However, assuming that none of the above is the actual problem, what would I recommend someone in this
situation do? It’s easy, if a 20% deficit is not generating reasonable enough fat loss, I’d suggest increasing
the deficit by an additional 10% (this can be done by reducing calories or increasing activity a bit) for a month
to see what happens. If that’s still not working, maybe go another 10% for a month. And if nothing has
happened by then, I’d suggest getting some blood work done because something would appear to be
profoundly wrong.

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Is Rapid Fat Loss Right For You?
As we enter the new year, coming out of nearly three straight months of too much food and too little training,
it’s nearly guaranteed that people will be stepping up their weight loss efforts. Now, there are and always
have been a million and one (only a slight exaggeration) diet books out there, including mine. Fast diets,
long-term diets, you name it and someone has written a book about it.
In this context, a question worth examining is whether or not it’s better to go into a gradual, slow approach
to weight loss, making small changes to habits or to just jump in feet first and go for rapid weight
loss. Psychologically, many people are inherently drawn to faster programs because they get the weight off
sooner. It’s just human nature, people always want more faster now. But is faster better or worse than a
slower approach to weight loss?
It’s taken almost as a matter of faith in the fitness world that slower rates of weight loss are superior to faster
rates, that diets generating faster weight loss always cause faster rates of regain and poorer long-term
results. As I’ll mention below, there is certainly some data to support that.
It’s also often suggested that dieters set more moderate weight loss goals (e.g. lose ten pounds vs. 40
pounds) compared to larger ones; this is based on the idea that smaller goals are more realistic and more
likely to succeed.
But just because something is a long-standing dogma doesn’t make it true. And if it were as simple as
slower is always better, I wouldn’t be bothering to write this article.

Fast vs. Slow Initial Weight Loss

It might come as a shock to many readers, who have only ever seen the standard dogma, that a fair amount
of data actually shows that a faster/greater initial weight loss is often associated with better long-term
maintenance. Yup, that’s right, better weight maintenance. Not worse.
In a 2000 review titled “Lessons from obesity management: greater initial weigh loss improves long-term
maintenance.” (1) along with a more recent review (2), it’s actually pointed out that a good deal of research
has found that more rapid initial weight loss actually shows better long-term weight maintenance.
Quoting from reference 1 (pg. 17):
However, against this notion speaks numerous post hoc analyses of weight loss intervention studies showing
that a greater initial weight loss, usually achieved in the first 2-4 weeks of treatment, is associated with a
better long-term outcome, i.e. a sustained weight loss 1-5 years later.
As one example, Astrup (3) showed that the group of dieters who had lost the most weight at week 36 (17.7
kg vs. 9.8kg) had maintained more weight loss 2-5 years later (they were still down 7.1 kg vs. a 2.8 kg weight
GAIN). Other research supports that conclusion as well; that is, in many studies, a faster rate and greater
amount of weight loss is predictive of better long-term weight maintenance rather than worse.

What’s Going On?

Now, analyzing studies after the fact can be a problem, it’s easy to confuse correlation with causation. For
example, it’s well established that some people lose weight more easily than others due to differences in
biology, hormones such as thyroid, leptin and others, etc. Perhaps the folks who lose weight the most readily
early on are the ones who are biologically more likely to keep it off in the long-term.

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For this reason it’s crucial that controlled studies, where the rate of weight loss is manipulated be performed.
Not a lot of work has been done in this area but what work has been done is certainly supportive of the idea.
In one study, subjects were placed on either a very low calorie diet or a conventional diet so that they would
lose the same amount of weight over different times frames (8 vs. 17 weeks). Both groups lost 13.6 kg but,
of course, the rate of weight loss was double in the very low energy group. Weight loss maintenance was
higher by 2.4 kg at one year and 3 kg at two years although this wasn’t statistically significant (4).
Even if the long-term results weren’t any better, to quote again from the review (1): “At least this study does
not support that a rapid weight loss influences long-term outcome adversely.”
Now, a problem with many dieting studies is that the often use multi-factorial approaches to weight loss and
this can make it difficult to isolate out what’s doing what. For example, some studies will examine diet with
behavioral therapy or exercise, or diet with or without diet drugs, or some combination of all of
those. Figuring out what’s driving what can be difficult. Maybe it was the diet, maybe it was the drugs,
maybe it was the behavioral intervention, maybe it was the combination of everything tested.
And this in part explains some of the research showing a worse effect from very low calorie rapid weight loss
approaches; many of them contain exactly zero nutritional re-education as they are based around protein
powder and pre-mixed type diets. They may generate stunningly fast weight loss but they don’t do anything
to help with long-term maintenance. No change in food habits, nothing.
As I clearly state in The Rapid Fat Loss Handbook:
I will be the first to admit that just measuring out powders makes it extremely easy to
control food intake….The problem in my mind is that, while this approach to dieting generates amazing
weight/fat loss in the short term, it does nothing to teach or retrain overall eating habits in the longer term.
Basically, to have any chance of succeeding in the long-term, any diet approach (whether slow or fast) must
contain an element of nutritional education. Along with generating quick weight loss, the diet should work
to help the person learn good long-term eating habits.
It’s also beneficial if aspects such as increased physical activity are included. As I’ve discussed in many of
my books, and once again going against the dogma on the topic: at realistic levels, exercise actually has at
most a small impact on total weight loss (although proper exercise spares lean mass loss and increases fat
loss as a result). However, it’s absolutely critical for long-term weight maintenance. Any diet or training
program that doesn’t set the person up with tools for long-term maintennace is a bad one, simple as that.
Of course, this is exactly how I set up The Rapid Fat Loss Handbook and why I did it the way that I did. The
program is a rapid weight/fat loss plan but I explicitly built it around whole foods rather than
supplements. That way, even while it’s generating rapid weight and fat loss, it’s also giving the dieter a
better baseline diet (built around plenty of lean protein, vegetables, and essential fatty acids).
As well, exercise (primarily weight training with only small amounts of cardio required or recommended) is
recommended during the diet, with an increase in aerobic type activity when the dieter either moves into
maintenance or a moderate type of dieting approach; again this is consistent with the research on the
topic. The book spends quite some time on moving to maintenance as well, with both a non-counting and
counting approach to the mainteance period.
On that last note, many have found that The Rapid Fat Loss Handbook plan is a great way to kickstart a
more moderate diet. I think much of this is psychological, it can be depressing watching the scale drop by
a pound a week; a rapid initial fat loss is psychologically gratifying for many people and often sets the dieter
up to move into a more moderate approach (which the book details how to set up).
Quoting from another paper on the topic (5):
[Very low calorie diet] with active follow-up treatment seems to be one of the better treatment modalities
related to long-term weight-maintenance success.

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In this context, follow-up treatment included behavior therapy, nutritional education and exercise. An
extreme diet followed for 2-4 weeks before moving into maintenance may represent a nearly ideal
compromise in this regards.
The benefits of a rapid initial weight loss are present along with the potential benefits of longer-term more
moderate approaches to dieting (many of which are discussed my book A Guide to Flexible Dieting).

Is Faster Always Better?

As much as the research may support them, in the real-world rapid weight loss plans are absolutely not
appropriate for everyone. The main exception are folks who have shown a pattern of on-again/off-again or
binge type eating; they invariably tend to have poor success with extreme diets. While they may do
stunningly on the diet but they won’t move to maintenance well (or at all) and will end up flip-flopping between
two extremes.
For those individuals, a plan like The Rapid Fat Loss Handbook is probably the worst choice and I don’t
recommend even attempting it; even if the diet succeeeds in the short-term, it is as likely to fail in the long-
term as anything else. For those extremist individuals who have trouble moving out of a diet without losing
control, the ideas in A Guide to Flexible Dieting are probably more beneficial.
But for many individuals, given the information discussed above, it’s becoming clear from the research that
rapid weight loss plans, as long as they include certain factors such as nutritional re-education, exercise,
etc. may be superior to more moderate approaches.

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Bodyweight Regulation: Leptin Part 1
As I noted Set Points, Settling Points and Bodyweight Regulation Part 2, although I’ve been using
bodyweight/body fat during this discussion, it’s probably more likely that it is body fat levels per se that are
being regulated. Today you’ll see why and from here on out I’ll only talk about bodyfat regulation.
With early research (I’m talking the 1950’s) having established the existence of some type of setpoint (again,
primarily in animal models), early researchers had to sort of guess what might be going on in terms of
regulating body fat levels.
Essentially they postulated that the brain of the animal must be responding in some form or fashion to a
hormone that scaled with body fat levels. They could only postulate what it was and it would take another
40 years before a major candidate would make itself known.
In 1994, the gene for a hormone that would eventually be called leptin (from the Greek “leptos” for thin) was
discovered in the OB (OB stands for obesity) mouse. The OB mouse had been studied for decades and was
spontaneously overweight with a low resting metabolic rate, low levels of activity, etc. It ate a lot, put on fat
easily, etc. Here’s what it looks like compared to a normal lean mouse.

Superficially, the OB mouse appeared to be similar to obese humans (except furrier).


It turns out that the OB/OB mouse doesn’t produce leptin at all, it has a gene defect and makes zero leptin.
Inject it with synthetic leptin and it loses weight rapidly.
After the discovery of leptin, the news was abuzz with thoughts that the cure for obesity was finally here.
Companies spent a lot of money getting the rights to leptin, thinking it would fix the global obesity problem
and they’d make zillions of dollars.
So researchers went about measuring blood levels of leptin in humans of varying weight expecting obese
humans to produce no leptin.
To their dismay, it turned out that obese individuals invariably had very high levels of leptin and it was
suggested that, in a similar vein to insulin resistance (where the body no longer responds appropriately to
the hormone insulin), the body or brain had become leptin resistant. There was plenty of leptin floating
around but it wasn’t sending the right signal to the brain to turn off appetite and reduce body fat.
I’d note in this regards that two other rat strains, the DB (for diabetic) and DIO (dietary induced obesity) rat
show varying degrees of leptin resistance (the existence of resistance to the supposed regulating hormone
was also postulated back in the 50’s). In the case of the DB rat, it’s complete and genetic; in the DIO rat it
develops with increasing obesity.
A variety of things induce leptin resistance including high blood triglyceride levels and even leptin itself;
when elevated chronically, leptin induces resistance to itself.
I’d note that it is currently being debated if leptin resistance is truly the cause for what’s going on and other
models, such as the leptin insufficiency theory are being discussed as well; in this concept, a lack of leptin
in the brain (but not in the body) is the problem. In either case, the signal from leptin isn’t being sent properly.
I’ll talk about what that signal is in the next post.
And while a handful of individuals have been found who produce no leptin (and who respond to injectable
leptin with massive weight loss and a normalization of metabolic rate), studies which injected leptin levels in
the obese showed disappointing or no weight loss.
Which doesn’t make leptin useless, mind you; it was simply being used incorrectly because researchers
didn’t quite understand what it was actually doing or supposed to be doing. Many people still don’t.

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Before wrapping this up, I want to note that leptin isn’t the only candidate hormone for body weight regulation;
as it turns out insulin is also a key player here (insulin also scales with bodyfat). Direct injection of insulin
into the brains of animals reliably reduces food intake and bodyweight.
There is also evidence, which I’ll discuss later, that there is a gender difference in how the brain responds
to either leptin or insulin. Given that leptin scales mostly with subcutaneous fat (generally higher in women)
and insulin scales mostly with visceral fat (generally higher in men), this will turn out to make some logical
sense.
Of course, there are other factors here as well. Hormones such as cholecystokinin, peptide YY, ghrelin as
well as blood glucose, blood fatty acids, amino acids, and others being discovered damn near daily are all
sending an integrated signal to the brain about what’s going on in the body.
As well, varying hormones work on relatively longer or shorter time frames. For example, insulin can change
in a matter of minutes, leptin may take hours, ghrelin operates on a meal to meal basis, etc. This makes for
a very complicated system. But I’m getting ahead of myself.
Oh yeah, it goes without saying that most of this information is discussed to one degree or another in almost
all of my books. There are links to individual ones on the side rail or you can go to the store.

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Bodyweight Regulation: Leptin Part 2
In the Bodyweight Regulation: Leptin Part 1, I talked primarily about leptin (and a bit about insulin,and a very
little bit about the other hormones) and its discovery and how it may be the (or at least one of the) long-
sought after hormones involved in regulating bodyweight. Today I want to take a quick look at what leptin is
and how it’s regulated. Next time I’ll look at what leptin is doing (or not doing as the case may be).
Leptin is a protein hormone released primarily from fat cells although skeletal muscle, the gut and possibly
the brain releases it too. But, in terms of overall quantity, fat cells are the primary place where leptin is
synthesized and released.
Note: those of you still laboring under the false idea that fat cells are simply inert storage cells need to get
out of the 1970’s and get up to date. Fat cells are turning out to be an endocrine organ in their own right,
releasing a host of hormones and chemicals that have effects all over the body; leptin is but one of them.
Quite in fact, leptin scales scarily well with body fat percentage, as I noted on Wednesday, primarily with
subcutaneous body fat percentage. The higher the level of body fat, the higher the leptin level and vice
versa. Males below 10% body fat may have no detectable leptin in their bloodstream.
I’d note that, probably for hormonal reasons, women generally have 2-3 times as much leptin as men at any
given level of bodyfat. There is also some evidence for gender differences in how leptin responds in women
versus men to things like diet and exercise; more importantly, women’s brains may respond to leptin
differently than men.
Tangentially, I suspect that this may be part of what’s involved in terms of why women generally have a
harder time losing fat (a topic I discussed in some detail in my Bromocriptine booklet and that I’m delving
even more heavily into right now).
However, leptin doesn’t only scale with body fat percentage, it is also related heavily to food intake,
specifically carbohydrate metabolism in the fat cell.
In response to both over- and under-feeding, leptin changes quite rapidly.
When someone starts a diet, leptin may drop by 30-50% within about a week, obviously they haven’t lost
that much of their body fat. After that rapid initial drop, drops in leptin are much slower scaling with body fat
loss.
By the same token, with even short-term overfeeding, leptin can come up far more quickly than body fat is
gained. This latter fact is part of the basic premise behind refeeding and cyclical dieting; short-term very high
carbohydrate/caloric intakes can raise leptin without causing significant fat gain.
I’d note that, in the short-term, only carbohydrate intake affects leptin leptin levels; fat overfeeding has no
effect. In addition, changes in fat mass per se don’t regulate leptin in the short-term (less than 48 hours).
Rather, it’s the effect of glucose metabolism within the fat cell that is affecting leptin synthesis and release.
This is why my diets always base refeeds around periods of high-carbohydrate intakes, acutely this is the
only way to affect leptin levels in the short-term.
In essence, leptin is telling your body two different things:
1. How much fat you’re carrying.
2. How much you’re eating.
From the standpoint of bodyweight regulation and physiology, these are important things for the body to
know about.
I want to note again that, as I mentioned in the last post, insulin is also a player in bodyweight regulation,
scaling primarily with visceral fat and there is evidence that men’s and women’s brains are relatively more
or less sensitive to the two hormones.

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Women’s brains appear to respond more to changes in leptin while men’s respond more to insulin. As you’d
expect, these effects are probably mediated by differences in hormone levels and it appears that estrogen
improves the sensitivity of the brain to leptin. While not tested in humans, estrogen injected into male rats
increases the response to leptin.
As I discussed in a previous research review, there is also evidence that estrogen exerts a leptin like signal
in the brain as well.
I’d mention that, from a practical standpoint (regarding refeeds), this doesn’t particularly matter in that both
leptin and insulin will primarily be increased via high-carbohydrate refeeds.
In any case, leptin (and insulin and, of course, the other hormones I mentioned last time) are sending a
signal to the brain about body fat levels and food intake, making them likely candidates for bodyweight
regulation. So how are they working exactly?
That’s what I’ll talk about next time (still focusing on leptin but starting to address some of the other hormones
as well).

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Bodyweight Regulation: Leptin Part 3
Ok, so now that you know what leptin is and a little bit about what regulates leptin levels, I want to look at
what leptin ‘does’ in the body. The short answer is a whole lot of things.
Here’s the long answer:
Like most hormones in the body, leptin has effects nearly everywhere in the body. In skeletal muscle, it’s
involved in promoting fat oxidation, it impacts on fat cell metabolism directly, liver metabolism, is involved in
immune system function (which may be why dieters get sick when they get very lean) and more recent
research is implicating effects on brain function, neurogenesis, breathing and a whole host of other stuff.
Of some interest, leptin levels are crucially involved in both puberty and fertility, it’s been known for decades
that a certain level of body fat was required for puberty to hit and achieving critical levels of leptin appears
to play a role in allowing puberty to begin.
The handful of folks who don’t produce leptin never hit puberty, for example and it’s thought that some of
the reason children may be hitting puberty sooner is because increasing childhood obesity is causing them
to hit that critical level sooner.
In a similar vein, leptin is a key factor in regulating fertility, essentially it ‘tells’ the body and brain that it’s
well fed enough to spend calories on things like reproduction and making babies. This at least partly explains
why dieters are very low levels of body fat lose both sex drive and the ability to function.
Loss of menstrual cycle is a well known effect of dieting and intensive training and while it was always
thought to be related to body fat levels per se, it appears that energy availability (which, remember, leptin
tells the body about) is a bigger factor. Essentially, when the body ‘senses’ that energy availability is
insufficient, it shuts down what are essentially ‘extra activities’ such as reproduction.
In this vein, the most recent ideas about what leptin ‘does’ in the body are that it acts as an adipometer, a
measurement of energy stores that tells the brain whether there are sufficient calories available to spend
them on things like making bone, maintaining immune function, etc. Essentially the same concept I’m
describing here.
My point being that leptin does a lot of stuff in the body, but that’s not mainly what I want to talk about here.
Rather, in keeping with the theme of this blog series, I want to talk about leptin’s potential roles in
bodyweight/bodyfat regulation.
When it was originally discovered, leptin was originally conceived as an ‘anti-obesity’ hormone, it was
thought that leptin should act to prevent weight gain. This led one researcher to quip (and I’m paraphrasing
here) that “If leptin is meant to act as an anti-obesity hormone, it has to go down in history as the most
ineffective hormone in the human body” or something roughly to that effect.
As I mentioned in previous blog posts, obese individuals invariably have high levels of leptin, raising levels
in those folks does little to generate weight loss and because of that failure, everyone sort of moved on in
terms of using leptin as a treatment for weight loss.
The problem is that early ideas about leptin were conceptually incorrect; rather than acting as an ‘anti-
obesity’ hormone per se, leptin appears to act as more of an ‘anti-starvation’ hormone. That is, leptin doesn’t
act to prevent weight gain, it acts to keep you from starving to death.
This reconceptualization would go a long way towards explaining the apparent assymmetry in the
bodyweight regulation system I discussed previously: the body doesn’t defend against weight gain very well,
it defends tenaciously against weight loss.
Various research found that the drop in leptin was a key aspect triggering (or at least mediating) the effects
of starvation (dieting is just starvation on a smaller scale) in humans. In that vein, several studies had

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individuals diet before replacing leptin to pre-diet levels. This raised metabolic rate, normalized thyroid and
increased fat loss. For example.
Basically while trying to raise leptin in overweight individuals is pretty much a bust, preventing leptin from
dropping on a diet (or raising it back to normal levels after weight has been lost) is where the real action is.
In this vein, recent work has found that females suffering from amenorrhea (a loss of menstrual cycle)
respond to replacement levels of leptin with improvements in reproductive function, bone health, thyroid and
overall hormonal axes, etc. Without weight gain.
So now you know basically what leptin ‘does’ in the body at least conceptually: it signals the brain about
energy stores (both body fat levels and energy intake) and appears to act primarily as an anti-starvation
hormone. Next time I’ll look at mechanistically some of what it does (e.g. impact on appetite, etc) and then
about how to go about dealing with this on a diet.

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Bodyweight Regulation: Leptin Part 4
Don’t worry, slowly, I’m getting to the point.
So when you are in an energy deficit and/or losing body fat, leptin levels drop.
Although I haven’t talked much about the role of exercise here I’d only note that whether or not the deficit
comes from caloric restriction or exercise per se doesn’t appear to have much of an effect on how much
leptin drops.
Basically, the body appears to be sensing ‘energy availability’ (defined as energy intake minus expenditure)
and adjusting things based on that. I’d, of course, note that exercise still plays plenty of other crucial roles
(including psychological, which I am getting back to slowly but surely) in terms of dieting and fat loss.
In any case, what happens now?
Well, a bunch of stuff. Leptin interacts with various part of the brain but the hypothalamus (where the setpoint
is primarily thought to be regulated) appears to be the key aspect. In conjunction with the other hormones I
haven’t talked much about yet, when leptin drops a bunch of other neurochemicals change. These all have
complicated names like Neuropeptide Y (NPY), Agouti Related Peptide (AgRP), Pro-opiomelanocortin
(POMC) and Cocaine Activated Receptor Transcript (CART). The names are not that important practically.
When these hormones change, they cause other changes further downstream that affect all aspects of
metabolism.
There are other regulators as well, in my little Bromocriptine booklet, I pointed out that brain dopamine levels
go down when leptin goes down and this appears to play a role in the overall metabolic adaptation to dieting.
The whole idea in that booklet was to use a dopamine agonist to ‘trick’ the brain into thinking it was fed, it
worked for about half of the people who tried it; I’m still trying to determine what the cause of the variance
was.
Lowered dopamine has a secondary effect that low leptin makes animals (mice and rats at least) more likely
to addict to drugs when you starve them (there are other mechanisms at work here, of course): they need
something to drive the dopamine/reward system. There is also evidence that obese individuals have
impaired dopamine signalling in the brain.
In any case, POMC/AGRP/NPY/CART have further downstream effects and regulate things like metabolic
rate (which drops when you diet), appetite/hunger (which go up when you diet), activity levels (you tend to
get lethargic, burning less calories in daily activity), hormone levels (including thyroid via TRH/TSH and
reproductive hormones via LH/FSH), etc. Testosterone and thyroid generally go down as does nervous
system output, cortisol goes up. You get the idea.
Please note again that the extent of these changes depends to a great degree on the extent of the diet and
the body fat level of the individual: someone dropping from 35% to 30% body fat might see only small
changes (or almost none at all) in these parameters, someone who is getting leaner at the 15% range is
seeing bigger problems and someone at 5% body fat (e.g. a natural male bodybuilder) is undergoing massive
adaptation.
This is a big part of why dieting gets so much harder as people get leaner, muscle loss accelerates,
hormones are crashing, etc. My Ultimate Diet 2.0 goes into much more detail on this topic.
Basically, the body undergoes an overall adapatation that attempts to slow fat/weight loss (via reductions in
metabolic rate and activity) and seek out food, these adaptations become stronger the leaner the individual
gets (you’ll see that this has implications for how to fix it). I’d note that there is more to the overall adaptation
to dieting than just the central effects in the brain; for example, impaired conversion of T4 to T3 in the liver
is a well known effect of dieting.

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Of course, various hormones have other peripheral effects in terms of energy balance and fat loss; for
example leptin directly stimulates fat oxidation in skeletal muscle and a known adaptation to fat loss is a
decrease in fat oxidation.
There is also that post-starvation hyperphagia I talked about in an earlier post, whereby signals from fat cells
drive hunger to extreme levels when food is made available. Which, I’d note is pretty much always in modern
society.
Note again (this ties in with my comments above) that the original observation of post-starvation hyperphagia
was made in males who were kept on 50% maintenance calories for 6 months, ultimately reaching a body
fat percentage of ~5% (that is, the lower limits of human body fat levels). Someone going from 35% to 30%
isn’t going to experience nearly that effect and there’s going to be a continuum of responses from fatter to
leaner that’s going to occur.
Finally (ok, probably not finally), leptin also impacts on how well or how poorly other appetite hormones in
the body send their signals to the brain (that’s in addition to those other hormones sending a signal to the
hypothalamus). For example, cholecystokinin (CCK) is a hormone released from the gut primarily in
response to protein or fat intake; it’s involved in making you feel full after a meal. As is turns out, in rats at
least, CCK doesn’t work as well when leptin is low.
Hardcore dieters (e.g. contest bodybuilders and figure/fitness competitors) are well aware of this: when they
start getting very lean, even if they do everything ‘right’ at a given meal (i.e. lots of lean protein, moderate
fat, fiber, moderate amounts of low GI carbs), they simply don’t stay full very long. Because all of the short-
term fullness signals just aren’t working as well.
That’s because leptin is essentially setting the overall ‘tone’ of the brain in terms of how it responds to other
signals. The various hormones that determine when you get hungry or full aren’t working as well when leptin
is lowered from dieting and fat loss. Leptin certainly isn’t the only hormone involved in all of this; but it’s
definitely one of the most important ones.
Finally, next time, what to do about all of this (short of not dieting and just staying fat and happy).

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Bodyweight Regulation: Leptin Part 5
Summarizing what I’ve discussed so far:
1. Human bodyweight appears to be biologically regulated, that is it makes some attempt (that can be
overcome by environment, of course) to maintain body fat within some range or level.
2. The system regulating body fat is assymetrical, for most people it defends against fat loss much more
strongly than against weight gain.
3. For proper regulation, the body needs a way of ‘knowing’ two things: how much fat you’re carrying and
how much you’re eating; a variety of hormones play a role here.
4. At least in terms of indicating the amount of body fat is present, the hormones leptin and insulin appear
to play a major role. Leptin scales with subcutaneous body fat levels (higher in women), insulin scales with
visceral fat levels (usually higher in men); there is some indication of a gender difference in response to the
different hormones.
Leptin and insulin also both change with changing food intake; leptin levels can drop significantly within a
few days of dieting even with no change in body fat levels. Insulin changes meal to meal.
5. When people reduce calories and lose fat, leptin levels drop, and this appears to be a major part of the
overall adaptations to dieting in terms of metabolic rate, hunger, etc.
While leptin certainly isn’t the only hormone involved it appears to be one of the major ones not only having
direct effects but also impacting how well or how poorly other hormones (such as CCK) work in the brain.
6. While studies have found that raising leptin in overweight individuals typically does little (for reasons
related to either leptin resistance or insufficiency in the brain), preventing leptin from dropping during a diet
(or raising it) appears to reverse many of adaptations that occur.
Point 6 raises a question that someone actually brought up in the comments: why can’t I find leptin for
sale?
And the answer is that it has never (and I suspect will never) been made available outside of research. When
I originally wrote my Bromocriptine booklet, an effective dose of leptin came in around $1000 PER DAY. The
last time I looked (about a month ago), it’s down to about $500 per day. That’s assuming a chemical company
would sell it to you.
That’s not a typo mind you, leptin makes growth hormone look cheap.
For various reasons, it simply hasn’t been developed for human use outside of research applications. Why?
I can’t say for sure. I suspect it’s because drug companies primarily want weight loss drugs that cause weight
loss and leptin doesn’t do that.
They don’t seem to want drugs that simply make dieting work better. I’d note that the average dieter isn’t
looking for that type of compound either. Drugs that generate weight loss without the person having to
change their behavior patterns are the real goal.
There is also the issue of leptin being a peptide hormone, meaning it would have to be injected. Injectable
drugs are a bitch practically and there’s been a huge push to develop diabetic solutions not involving
injectable insulin for that reason; the odds of the typical person injecting leptin twice daily while dieting are
slim.
Bodybuilders would, of course, but that small percentage of people trying to get to 5% body fat are not the
target market of the drug companies.
End result: nobody is developing leptin for commercial use so far as I can tell and I doubt this will change.
But for dieters and especially the very lean, injectable leptin would be a godsend fixing a majority of the
problems that occur with dieting. Unfortunately, it’s a pipe dream at this point.
Where does that leave us?

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Bodyweight Regulation: Leptin Part 6
In Bodyweight Regulation: Leptin Part 5, I explained that, while injectable leptin would be a true boon for
dieters, it appears unlikely that it will ever reach commercial or clinical use.
This leaves us with other approaches (e.g. nutritional, supplements, training) to attempt to manipulate either
leptin levels or signaling.
There are basically three places where dieters might impact leptin levels and/or activity in terms of fighting
off the adaptations to dieting.
1. Production at the fat cell
2. Signaling in the brain
3. Transport into the brain
Leptin production in the fat cell
I talked a little bit about #1 in a previous post, when I talked about refeeds. At this point, and this topic is
discussed to some degree in nearly every book I’ve written at this point, interjecting high carbohydrate, high
calorie refeeds of varying lengths (anywhere from 5 hours to 3 days) is (currently) the best way to raise leptin
while dieting.
One of the interesting (and often missed points) is that, as dieters get leaner (and leptin drops more and
more), refeeds need to become larger and/or more frequent. That is, rather than necessarily dieting harder
as they get leaner, some people are actually doing better by ‘breaking their diet’ (with specific high-carb
refeeds) more frequently.
I’d note again that leptin production is related primarily to carbohydrate intake in the short-term, high-fat
refeeds aren’t the best way to raise leptin levels. I’d also note that single ‘cheat’ meals won’t impact on leptin
levels significantly as leptin doesn’t really change on a meal to meal basis.
Tangent: I’d note that, in this regards, some of the work being done with intermittent fasting and every other
day refeeds has relevance here as some data suggests that leptin may be maintained better with that
approach to dieting. But until I get Martin Berkhan in here from LeanGains for an interview and dig into it
more, I’m not going to talk much about IF’ing as a dietary strategy other than to say: there’s some compelling
shit going on here.
An additional strategy, talked about in some detail in my Guide to Flexible Dieting is the idea of full diet
breaks, periods of 10-14 days in-between periods of active dieting where calories are brought back to
maintenance (and carb intakes brought back to at least moderate levels).
Not only does this provide a psychological break from the grind of continuous dieting, it helps to ‘reset’ some
of the metabolic adaptations that occur with dieting. Leptin levels will come up, thyroid conversion in the liver
is improved, etc. Assuming dieters have no strict time constraints, I strongly feel that inserting full diet breaks
every so often (how often depends on body fat levels) is important for long-term success. Again, for both
physiological and psychological reasons.
There are at least two other regulators of leptin levels here, both zinc and Vitamin E intake appears to
regulate leptin production and I have suggested supplementation of both in the past to try to help raise leptin.
How much (if any) impact this actually has I can’t say.
Leptin action in the brain
Although it seems a bit out of order, I want to jump next to leptin activity in the brain. This is part of the area
that gets generally referred to as ‘leptin sensitivity’ in the literature and is, unfortunately, poorly studied and
even more poorly characterized.
What causes it, what (if anything) can be done about it is a huge question mark although finding ways to
improve leptin sensitivity would probably also have huge benefits. Similar to improving insulin sensitivity,

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increasing leptin sensitivity would mean that the same level of hormone sends a larger signal. A supplement
or drug that increased leptin sensitivity would be expected to do some very nice things.
I would mention that there is indirect evidence that regular exercise improves leptin sensitivity. I say indirect
because measuring leptin sensitivity in humans is very difficult. Improved leptin sensitivity is being inferred
from the fact that endurance athletes often have leptin levels below what you’d expect given their body fat
level; this suggests increased sensitivity. Again, it’s hard to measure in humans.
It does appear that increasing levels of leptin induce resistance to itself (I’ll spare you the mechanism) so it’s
conceivable that reducing leptin levels (e.g. with a diet) could transiently reduce leptin resistance/improve
leptin sensitivity. How much of an effect or how long this would take is currently unknown.
If this were the case, would provide more support for cyclical dieting approaches such as my Ultimate Diet
2.0. During dieting periods, leptin levels would go down (but sensitivity would go up); during periods of
deliberate overfeeding, improved leptin sensitivity (until such time as it went down again) could possibly be
taken advantage of.
A similar logic could be applied to weight gain, eventually chronic overfeeding/weight gain might potentially
induce leptin resistance; inserting periods of dieting to deliberately lower leptin might offset this.
While I’m on the topic, I should mention that leptin resistance can occur at other tissues such as skeletal
muscle (I haven’t talked much about leptin’s actions there).In animals at least, both exercise and fish oils
increase skeletal muscle leptin sensitivity.
Leptin transport into the brain
The final topic I want to talk about is that of leptin transport into the brain, something else I haven’t really
talked about in this series. But it’s thought that leptin transport issues at the blood brain barrier may be part
of the overall ‘leptin resistance syndrome’ and impaired leptin transport into the brain may be part of the
problem. It’s thought that leptin transport into the brain can become saturated, that is, once leptin gets above
a certain level in the bloodstream, no more can be transported into the brain.
But leptin transport into the brain is also actively regulated by the blood brain barrier, by a variety of things,
let’s look at a few:
High blood triglycerides tend to reduce leptin transport and it’s interesting to note that, despite being high in
fat, low-carbohydrate diets often reduce blood TG levels; is enhanced leptin transport part of the often
observed appetite blunting effect that is often seen (along with other potential mechanisms of course)?
In a similar vein, high-carbohydrate diets, especially combined with low levels of activity often raise blood
triglyceride levels, probably hindering leptin transport into the brain.
Both insulin and epinephrine increase leptin transport into the brain. Tying in with my comments above, this
might be another reason that high-carbohydrate refeeds ‘work’ after a period of dieting; between (potentially)
increased leptin sensitivity in the brain and insulin increasing leptin transport, there is a brief period where
leptin signalling should be increased.
The supplements ephedrine and synephrine would be expected to increase leptin transport, ephedrine by
raising epinephrine levels and synephrine by directly binding to beta-receptors.
And, of course exercise raises levels of epinephrine and, at least transiently should increase leptin transport
into the brain. In that vein, quite a bit of research suggests that the body better regulates food intake when
exercise is performed, increased leptin transport (and signalling) might be part of the mechanism.
And while I can’t find the paper now, I seem to recall a rat study suggesting that long-term (4 months if my
memory isn’t failing me) fish oil supplementation could increase leptin transport into the brain. But it would
likely take a very very long time to occur in humans.

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And, at least for the time being that’s pretty much all I have to say about leptin. Next time, I’ll take a quick
look at some of the other hormones involved in this system before (finally) moving onto some psychological
issues that play a role in dieting.

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We Are What We Absorb II: Proteins, amino acids, and
peptides

This is a topic so large it could take stacks of text books (and it does!) and many
semesters in college and years of research afterward, so an exhaustive review is both
beyond the scope of this article and my brain!

There’s a few key areas however I plan to address in this article people will find helpful
to making smart decisions the over hyped ads for protein, amino acids, and peptides
don’t cover. For the most part, I recommend whole protein sources, such as whey, eggs,
lean meats, fish etc. in terms of dietary protein* intakes, but some individual amino
acids can be of benefit in specific applications. Those applications may be sports
performance related, general health, or medical, but I’m getting ahead of myself.

Back In The Day…

Back in the day when I was taking my first nutrition courses and reading what research
existed - right after the Pleistocene era – the mantra of nutrition was that digested
proteins were broken down into individual amino acids during digestion and absorbed,
and that was that. As with virtually all overly simplified models generated from the
early research examining human nutrition and physiology, it was wrong. To this day
however, there are still those who believe it, but I digress. However, most know that
ingested proteins are broken down primarily into small peptides and individual amino
acids. The fact is, to this day, human digestion, absorption, and utilization of nutrients
we ingest is still being elucidated with more discoveries being made than most people
realize or appreciate. It’s amazing to me however the number of people – some
educated enough in the sciences to know better – who think digestion, absorption, and
utilization of the food we eat can be summarized as “it get’s dumped into the acid in
your stomach, then absorbed via voodoo, the end.” Human digestion, absorption, and
utilization of the nutrients we ingest, is an incredibly complex process, that as
previously mentioned, still being elucidated. If you want to get a glimpse of how
complex, the Encyclopedia Britannica site has a nice write up on that, and remember:
digestion, absorption, and utilization of protein is but one very small aspect of it.

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As mentioned previously, there are benefits and potentially unique effects to using
individual amino acids, but studies indicate peptides are better absorbed and or utilized
than individual amino acids. What that suggests is, even if the goal is to derive benefits
from a singe amino acid (e.g., Leucine, Glutamine, etc.), it’s likely best to get it in
peptide form. For example, instead of taking L-leucine alone as the free amino acid, to
increase intakes of L-leucine, ingesting a leucine rich peptide is likely to be the superior
approach. The science and understanding of the value of peptides in human nutrition, be
it for health, performance, increased muscle mass, etc., is an evolving area of research
yielding useful findings, and still in it’s early stages in fact. Because this is such a wide-
open and extensive topic, I’m going to stay focused on a few key issues, such as the
value of using individual amino acids or “free” amino acids vs. peptides even if the goal
is to increase levels of a specific amino acid.

Free Amino Acid vs. Peptide Absorption and


Utilization

Studies find that diets fed to animals with identical amino acid composition, but fed as
either free amino acids or as whey derived peptides, finds peptides have a greater
nutritive value than free amino acids and greater tendency toward production of lean
body mass. Additional human studies find the same effect, although not all studies
concur in humans. The protein efficiency ration (P.E.R) is superior with peptides over
whole proteins or free amino acids (FAA), and as alluded to above, digestion of whole
proteins in humans produces mostly peptides for absorption and possible utilization vs.
FAA.** Why are peptides more easily absorbed over FAA? Some amino acids have
relatively low solubility for starters. As pointed out in part one of this series, solubility
is essential and often rate limiting to digestion, absorption, and perhaps utilization of
various nutrients we ingest:

“It’s well established that compounds with poor solubility are poorly absorbed and
have poor bioavailability. Compounds must be solubilized by the body before they can

266
be absorbed. It’s accurate to say that solubilization, absorption, and metabolism are
three key steps that modulate oral bioavailability of an ingested compound. In many
cases, there’s a direct relationship to the solubility of the compounds or nutrient and
it’s bioavailability.”

Other possible reasons why FAA are not as readily absorbed and utilized compared to
peptides may be an interference with amino acid transporters, and the tendency of FAA
to be oxidized by the liver, the different availability to gut flora of peptides vs. FAA,
and differences in osmolarity between peptides and FAA which can impact gastric
emptying and nutrient utilization. However, the reiterate, although the data is strongly
supportive of the conclusions I’m making in this section, it’s far from conclusive and
research is ongoing.

What of hydrolysates?

“Pre digested” proteins or hydrolysates yield peptides of varying lengths and appear to
have some unique effects and advantages to whole “native” proteins or FAA alone.
However, a major limitation of the differences between native proteins and
their hydrolysates is that all hydrolysis does not yield the same hydrolysate end-
product. That is to say, the degree of hydrolysis varies considerably between products
yielding relatively large protein fragments down to di and tri peptides and combinations
there of.

Unfortunately, the degree of hydrolysis is rarely reported in studies much less on


product labels, leaving both those reading studies and buying products essentially in the
dark. “On paper” hydrolysates should be of value, but the complete lack of
standardization in both the research and end product sold to consumers makes them
difficult to recommend at this time. Of course, if one is attempting to increase their
intake of specific amino acid, hydrolysates are not the right choice for that goal
regardless as they will supply the amino acid profile of the hydrolyzed protein vs. a
specific amino acid.

Specific Peptide Products.

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Science focused companies have developed promising peptide technology. For
example, Glanbia Nutritionals has developed a unique method of developing peptides
that are rich in a given amino acid. Because L-Leucine is getting so much attention in
the literature and sports nutrition community, *** I’ll focus on their Leucine peptide.
The technology is called PepForm® and is already being added to various formulas on
the market and can be identified by looking for the PepForm® logo on product
labeling. The product yields a soluble and highly bioavailable peptide rich in a specific
amino acid (in this case Leucine) and preliminary results with the PepForm® Leucine
peptide product have been very encouraging; testing both PER values in animals as well
as absorption characteristics in human volunteers.****

Typical of the supplement industry, some companies who have identified the obvious
benefits of peptides rich in Leucine – or other amino acids – simply responded by
invented marketing terms and using buzz words like “micro enhanced delivery techno
functional peptide delivery system” to lead consumers to assume there’s legit peptide
technology in their products when they don’t… Such is the reality of the supplement
industry, so per usual, consumers need to read labels and do a little digging on their own
to see what’s got legit peptide tech behind it and what’s marketing mumbo jumbo.

Conclusion

The reader should understand I have attempted to distill down an extensive amount of
technical information while doing my level best to be accurate in the “take home”
recommendations and conclusions. Whole protein sources should make up the majority
of dietary protein intake, hydrolysates show great promise but don’t appear ready for
“prime time” and if one is attempting to increase their intake of a specific amino acid,
peptide form appears the superior choice, even if the goal is to increase the intake of a
specific amino acid. Some additional info on new technologies I’m looking at for
improved absorption and bioavailability can be found HERE if interested in some
visuals.

Additional Comments:

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* = Why? Because whole protein sources deliver many nutrients beyond just protein or
amino acids and should make up the majority of protein intake in any well rounded
nutrition plan.

** = How is the PER figured? The PER is based on the weight gain of a test subject
divided by its intake of a particular protein during the test period done with growing
animals. The PER is one commonly used method for evaluating the quality of protein
sources, but there are other methods, such a biological value (BV), net protein
utilization (NPU) and the more recent PDCAAS. None are perfect, all have their
potential drawbacks, nor reflect a 1:1 relationship to their score and how much muscle a
person may gain from them, etc. As a rule, protein sources with higher scores
PER/BV/NPU scored tend to be the more “complete” proteins, and or better choices for
active people looking to gain or retain muscle, but that’s beyond the scope of this article
and a topic of for a future article.

*** = The amino acid Leucine is getting a great deal of attention recently and rightly so.
Leucine appears the most important amino acid of the in BCAA’s and is an essential
nutritional anabolic driver. Leucine, acts as an essential signaling molecule in the
mTOR cascade and a critical amino acid for increasing skeletal muscle protein synthesis
as well suppressing muscle protein degradation. That’s what we call in science a “win
win”!

**** = As tested in animals vs. an equal amount of free form L-leucine, PepForm® was
found to have lead to increased lean body mass when compared to matched free form L-
Leucine in the diet of rats. In a group of human volunteers, PepForm lead to serum
leucine levels known to trigger protein synthesis in humans, but these results have not
been published in the peer reviewed literature to date.

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A 45-Minute Vigorous Exercise Bout Increases Metabolic Rate for
14 Hours – Research Review

Knab AM et. al. A 45-Minute Vigorous Exercise Bout Increases


Metabolic Rate for 14 Hours. Med Sci Sports Exerc. 2011 Feb 8.
[Epub ahead of print]
INTRODUCTION: The magnitude and duration of the elevation in resting energy expenditure following
vigorous exercise have not been measured in a metabolic chamber. This study investigated the effects of
inserting a 45-min vigorous cycling bout into the daily schedule versus a controlled resting day on 24-h
energy expenditure in a metabolic chamber.
METHODS: Ten male subjects (ages 22 to 33 yrs) completed two separate 24-h chamber visits (one rest
and one exercise day) and energy balance was maintained for each visit condition. On the exercise day,
subjects completed 45-min of cycling at 57% Wattsmax (mean±SD, 72.8±5.8% VO2max) starting at 11:00
am. Activities of daily living were tightly controlled to ensure uniformity on both rest and exercise days. The
area under the energy expenditure curve for exercise and rest days was calculated using the trapezoid rule
in the EXPAND procedure in the Statistical Analysis Systems (SAS) and then contrasted.
RESULTS: The 45-min exercise bout resulted in a net energy expenditure of 519±60.9 kcal (P<0.001). For
14-h post-exercise, energy expenditure was increased 190±71.4 kcal compared to the rest day (P±0.001).
CONCLUSION: In young male subjects, vigorous exercise for 45-min resulted in a significant elevation in
post-exercise energy expenditure that persisted for 14-h. The 190 kcals expended post-exercise above
resting levels, represented an additional 37% to the net energy expended during the 45-min cycling bout.
The magnitude and duration of increased energy expenditure following a 45-min bout of vigorous exercise
may have implications for weight loss and management.

Background

In recent years there has been a focus on the calorie burn that occurs after
training, referred to in science terms as EPOC (Excess Post-exercise Oxygen
Consumption). A variety of different types of training (usually revolving around
brief duration, high-intensity methods such as interval training or circuits) have
been proposed with the major effect of such activity being in the EPOC that is
created.
Now, EPOC used to be thought to be related to something called the ‘oxygen
debt’, essentially the difference in how much oxygen the body needed to sustain
activity and how much was available. We now know that it’s related to a host of
other processes but these aren’t really that relevant practically. What is relevant
from a fat/weight loss point of view is how large the EPOC is and whether or not
it contributes meaningfully to the overall caloric expenditure of an individual.

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In a previous research review with the imposing title of Effects of Exercise Intensity and

Duration on the Excess Post-Exercise Oxygen Consumption I examined a monster review on the topic. In
brief, looking at the data in aggregate, the study concluded that intensity was more important than duration
in terms of the EPOC created.
And while the relative EPOC was higher for high-intensity activities (that is the percentage increase), the
absolute level of EPOC was still pretty irrelevant (maybe 30-50 calories). The researchers concluded that
the primary impact of exercise was still through the calories burned during the activity itself: the absolute
EPOC was fairly irrelevant to the total whether an individual did long-duration low-intensity activity or short-
duration high-intensity activity. Their conclusion based on review of the data was:
The manipulation of energy balance for these individuals should not be concerned with generating large
EPOCs but focused on both the energy expended during the actual exercise and the design of programmes
that enhance compliance.
The compliance issue is actually quite relevant given that the intensities used in the interval studies are
generally exceedingly high and unlikely to be performed consistently by most people, especially beginning
and/or overweight exercises (for more on this topic, please read Training the Obese Beginner series). An
added issue that I have talked about variously on the site is that many people looking for fat loss train daily;
trying to perform high-intensity activity too frequently is a recipe for disaster. Read the previous review for
the details, or the series on Steady State vs. Interval Training that it was a part of if you’re particularly bored.
However, several people have asked me about a recent study that seems to contradict the above
conclusions, as it found that the EPOC following what was terms ‘vigorous’ activity was significant and it’s
that paper I want to look at today.
.

The Study

The study recruited 10 male subjects, aged 23-33 years who were capable of
bicycling for 45 minutes continuously. Body composition was measured via DEXA
and the subjects all underwent VO2 max testing using a fairly standard
protocol. The subjects performed two ‘exercise’ sessions. In the first they sat
quietly in a metabolic chamber (which was measuring the actual energy
expenditure); in the second they performed actual exercise.
Basically, the ‘sitting quietly’ was the control condition, the researchers had to
see how many calories the subjects burned at rest and in the following hours so
that they could determine the difference in caloric expenditure and EPOC
following the actual workout.
The exercise bout consisted of 45 minutes of cycling at 57% maximum wattage
(so if a subjects Vo2 max wattage occurred at 300watts, they cycled at 171 watts),
this put them at roughly 70% of their VO2 max; the duration was chosen to
represent a midpoint for some rather standard recommendations for

271
activity. There was actually a short (4 minute) warm-up before the main set along
with a short cool-down but I’m not going to bother detailing it.
Food intake was controlled (this can be a huge confound to a lot of these studies
as eating raises metabolic rate and a lot of early exercise and metabolic rate
studies confused the increase from eating with an increase from the exercise
session); it is important to note that food intake was increased on the exercise
day to maintain energy balance That is, the subjects were not in a caloric deficit
during the period following the training session. The subjects stayed in the
metabolic chamber following the exercise session and this is how the caloric
expenditure following the exercise bout was determined.
For the exercise bout itself, the session burned a total of 519 +- 60 calories so
about 11 calories per minute for the 45 minute exercise session. This is
consistent with it being a vigorous intensity. And over the next 14 hours (including
3 hours of sleep), the subjects burned an additional 144+-50 calories with the
majority of this occuring in the first 9 hours after training.
This EPOC represented a whopping 37% of the actual exercise bout energy
expenditure, far higher than what was reported (usually 15% or less) in the
LaForgia review I linked to above. And the total impact of the exercise bout was
an energy expenditure of ~750 calories above and beyond the resting
condition. The researchers conclude
“The 24-h net energy expenditure difference between exercise and rest days was 750 kcal, a meaningful
quantity over time if two or three such exercise bouts are inserted into the weekly schedule and energy
intake is controlled.”
Fair enough. And obviously a workout burning 750 cal/session (including the workout and EPOC) is
meaningful.

My Comments

I think the first issue worth addressing is why this particular study found such a
difference compared to previous studies, such as the ones reviewed in the
LaForgia review I linked above. Certainly there could be methodological
differences; for example this study used a metabolic chamber to get an accurate
measure of caloric expenditure, other studies using a different method (such as
Douglas bags, think big balloon looking things that folks breathe in for later
analysis) might be getting different measurements.

272
Another has to do with the fact that the subjects were deliberately kept in energy
balance, and fed an additional 660 calories to offset the energy expenditure of
the exercise bout. The researchers state:
The increased energy intake balanced against energy expenditure (energy flux) has been shown in several
studies to contribute to the elevated 24-h energy expenditure on exercise days or in trained individuals.
Of course this is a problem with applying this study to a dieting/fat loss situation where, by definition, you
can’t be in energy balance (since you have to create a deficit by not replacing the exercise induced energy
expenditure with more food). This study needs to be re-done under conditions where energy intake isn’t
increased to see if the same big increase in EPOC is seen under dieting conditions (as that would have
actual application to fat loss).

The final reason that contributed is likely this: the workout tested in this study
was HARD. As I noted above, subjects pedalled at a workrate equal to 57% of
their max wattage output. This corresponded to 70% of VO2 max which
corresponds to roughly 85% of maximum heart rate. Quite in fact, the heart rate
measured during the activity was 163 +-16 beats per minute. This would be
equivalent to the Sweet Spot training that I discussed the Methods of Endurance
Training series. I’ll come back to this.
Without going into the details of what determines the EPOC, the researchers
state fairly simply that:
The magnitude of post-exercise energy expenditure is greatest when the body experiences significant
physiologic stress during prolonged and high intensity exercise.
Basically, through whatever specific mechanisms (and a host have been implicated), the ‘afterburn’ effect is
maximized when you massively disrupt homeostasis in the body. And this tends to occur most significantly
for workouts that are a combination of high-intensity AND high-volume (i.e. long-duration).
Earlier studies tended to either look at EPOC following longer duration lower-intensity work or short-duration
high-intensity work (such as interval training). And the simple fact is that neither tend to cause the greatest
homeostatic changes to the body: the longer duration stuff is too easy and the high-intensity stuff is too
short. In contrast, this workout had the subjects working pretty damn near their maximal steady state level
(for most this falls around 170-180 beats per minute). Anybody who has done this type of training can attest
to the fact that it’s work.
Conceptually this is no different than what I discussed in the Reps Per Set for Optimal Growth where an
intensity of 80-85% of maximum tends to put you in the range where you get both a high stimulus intensity
coupled with a high-volume. Higher intensities limit volume (both per set and per workout) and lower
intensities don’t tend to have the stress associated with it even if you do more total volume. Somewhere in
the middle you get that maximal response where you combine high-intensity AND a high-volume.
In that vein, having done all three types of workout (long-durations at piss easy intensities, interval work of
varying durations, long sessions at sweet spot), by far and away the sweet spot training is the hardest. Long
duration/low intensity stuff is mainly just dull. It’s not hard, just boring (and your butt gets sore on the
bike). The high-intensity stuff certainly hurts but the work bouts are too short for you to really suffer; the
workout is over before it gets too awful.

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In contrast, working for extended periods near your maximal output level is just uncomfortable as hell and
the duration makes it pretty gruelling as the minutes tick slowly by. This is even more true on a bike where
the stress tends to be localized to the legs (running at this pace is a bit easier since the stress is ‘spread out’
a bit more.
That’s what this study did. Most folks can go about an hour at their maximum steady state; this study was
45 minutes at maybe 90% of that intensity. It’s a tough workout, most can’t do it that frequently and this
would be more true if they are dieting and/or including weight training as well. So while these study results
are certainly interesting, and it’s clear that EPOC can be significant at least under the conditions tested
(essentially energy balance and a hard/long workout), I find it questionable how relevant this is to real-world
dieting situations where calories are lowered and/or weight training is being done.

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Acid Diet (High-Meat Protein) Effects on Calcium Metabolism and
Bone Health – Research Review

Cao JJ, Nielsen FH. Acid diet (high-meat protein) effects on


calcium metabolism and bone health. Curr Opin Clin Nutr Metab
Care. 2010 Aug 16. [Epub ahead of print]
PURPOSE OF REVIEW: Update recent advancements regarding the effect of high-animal protein intakes
on calcium utilization and bone health.
RECENT FINDINGS: Increased potential renal acid load resulting from a high protein (intake above the
current Recommended Dietary Allowance of 0.8 g protein/kg body weight) intake has been closely
associated with increased urinary calcium excretion. However, recent findings do not support the assumption
that bone is lost to provide the extra calcium found in urine. Neither whole body calcium balance nor bone
status indicators, negatively affected by the increased acid load. Contrary to the supposed detrimental effect
of protein, the majority of epidemiological studies have shown that long-term high-protein intake increases
bone mineral density and reduces bone fracture incidence. The beneficial effects of protein such as
increasing intestinal calcium absorption and circulating IGF-I whereas lowering serum parathyroid hormone
sufficiently offset any negative effects of the acid load of protein on bone health.
SUMMARY: On the basis of recent findings, consuming protein (including that from meat) higher than current
Recommended Dietary Allowance for protein is beneficial to calcium utilization and bone health, especially
in the elderly. A high-protein diet with adequate calcium and fruits and vegetables is important for bone
health and osteoporosis prevention.

Background

For decades now, it’s often been thought, felt or claimed that a high dietary protein intake had a detrimental
effect on calcium metabolism and bone health; certainly many groups promoting low-protein dietary
approaches tend to echo/parrot this idea.
This idea came around in the mid-20th century but was based on some, shall we say, questionable
research. In it, totally purified proteins were given (that is, no other nutrients were present) and a loss of
calcium in the body (in the urine) was documented. It was simply assumed that this had a negative impact
on bone health.
Despite later research showing that it was much more complicated than this (i.e. that proteins containing
other nutrients had different effects and that other parts of the diet played a major role in the overall effect),
this idea is simply repeated as if it were still unquestionably true. I dealt with this issue to some degree in
The Protein Book, in a chapter called Protein Controversies, which is reproduced here on the main site.
As well, there has long been a secondary data set (seemingly ignored by anti-protein folks) showing that
higher protein diets actually IMPROVE bone healing following things such as breaks or fractures. Clearly
the idea that ‘protein is bad for bone’ is a bit more complicated than just a soundbite. The review paper I
want to look at today examines the topic in some detail.
.

The Paper

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The paper begins by pointing out that bone is over 50% protein to begin with and that there has long been
concern that the modern Western diet is detrimental to bone health due to the production of acids within the
body. This is something I imagine readers have at least seen mentioned in recent years (I get the occasional
question about it) with some going so far as to claim that the body’s pH is THE KEY to all health (some even
claim that a drop in cellular pH is the cause of cancer).
While it’s not quite that cut and dry, clearly the modern Western diet tends to promote the production of
metabolic acids and at least some degree of metabolic acidosis. This is due to a number of factors including
a high protein intake (proteins are acid promoting), insufficient fruit and vegetable intake (both of which are
net base producing for the most part), along with other factors such as sodium and potassium balance
(excessive sodium intake relative to potassium can increase the acid load of the body). You can find long
lists of foods online in terms of their net acid or base producing potential.
And certainly, as discussed briefly in Protein Controversies, acidosis can cause problems in the body. It’s
relevant to today’s paper in that the body appears to buffer this acid load by releasing calcium, presumably
from bone. In that current research is suggesting that the RDA for protein is actually too low for some
populations (notably older individuals) and with the current interest in high-protein diets for weight/fat loss
and maintenance, it’s important to know whether or not these dietary approaches are having negative
impacts on bone health.
The paper looks in some detail at the issue of acid/base balance and calcium metabolism. As noted above,
the generation of metabolic acids causes a number of effects in the body, all of which could potentially impact
negatively on calcium metabolism and bone health. As well, studies clearly show both that:
1. The generation of metabolic acids causes increased calcium loss in the urine
2. Counteracting acidosis with base-forming minerals (e.g. potassium bicarbonate) decreases calcium
excretion
While the above is clear, the direct impact of dietary protein on bone health is a bit less clear with the results
of more direct epidemiological data showing mixed results in terms of the actual impact on bone health. As
well, citing a review by Fenton, the paper points out that:
…neither calcium balance nor the bone resorption marker, N-telopeptides, was affected by diet-induced
changes in net renal acid excretion despite a significant linear relationship between an increase in renal net
acid excretion and urinary calcium.
That is, while it’s clear that increased dietary acid load causes increased urinary calcium excretion, it’s less
clear if this has any real direct impact on the body’s net calcium balance or overall bone health.
Moving on to more direct effects, the paper looks at the very old data (using primarily purified proteins)
showing that for every increase in dietary protein by 1 gram, there was a 1 mg increase in urinary calcium
loss (raising the question of why not simply scale calcium intake to protein intake to offset this); this led to
the assumption that bone health was being compromised.
However, in direct contrast to this, the majority of epidemiological studies find that a higher protein intake is
associated with increased bone mineral density with only a few finding a negative impact. As well, while
weight loss per se tends to cause a decline in bone health, some research has found that high-protein weight
loss diets reduce the loss of bone mineral content; that is, high-protein intakes on a diet are beneficial.
The primary acid formation from protein comes from the sulfur containing amino acids (cysteine and
methionine) and these are found in higher amounts in animal vs. vegetable proteins; it’s often been assumed
that a higher vegetable protein intake would therefore have less of an impact on bone health.
However, this also turns out to be incorrect; the paper points out that studies of high-meat protein intakes
either show no overall effect on net calcium balance and a higher animal protein intake is actually associated

276
with increased bone mineral density; as well studies show a negative association between vegetable protein
and bone mineral density.
It’s worth noting that strength/power athletes, who have traditionally consumed a high-protein diet are
typically found to have higher bone densities compared to sedentary individuals. As the paper points out:
Changes in bone mass, muscle mass and strength track together; thus maintenance or an increase in
muscle mass and function maintains or enhances bone strength and mineral density.
And while the increase in urinary calcium excretion with increasing protein cannot be simply ignored, current
data suggest that this isn’t actually due to a loss of bone mass. Rather, increased protein intake leads to
increased calcium absorption from the gut; the loss in the urine is simply due to more calcium being
absorbed. The increased loss is simply due to more being absorbed from the diet; interestingly, this effect
is more pronounced when calcium intake is low to begin with.
In terms of mechanism, higher protein intakes raise levels of the hormone IGF-1, which stimulates bone
formation; this probably explains the benefits of a high-protein intake on bone healing. As well, high protein
intakes have been shown to decrease levels of parathyroid hormone (PTH), a hormone that is involved in
the loss of bone mass. Low protein intakes are associated with increased PTH and lowered bone mineral
density.
Finally, as I mentioned in the introduction, you can’t simply look at protein intake outside of the rest of the
diet and there are clear interactions with other nutrients. I mentioned above that protein intake interacts with
calcium intake, increased absorption. As well, a high protein intake has been shown to increase bone health
in older individuals when calcium and Vitamin D are supplemented. Finally, ensuring a sufficient intake of
fruits and vegetables (which neutralize the acid load of protein) should help to ensure the impact of dietary
protein on bone health is positive rather than negative.
Summing up, the researchers conclude thus:
Although a high meat or protein intake increases renal acid load and urinary calcium excretion, recent
findings do not support the claim that bone is the source of the extra calcium lost in the urine. In addition,
evidence is lacking that shows high-protein intakes, including that from animal sources, affect whole body
calcium balance or contribute to osteoporosis development and fracture risk.
.

Summing Up

I don’t have a whole lot to add to the above conclusion. Clearly the negative impact of dietary protein on
bone health would appear to be overstated to some degree. Under certain circumstances (low
calcium/Vitamin D intake, insufficient intake of fruits and vegetables), it’s certainly possible that a high-protein
intake could have negative impacts. But again this comes down to an issue of context. And in the context
of sufficient net acid neutralizing foods (fruits, vegetables, sufficient potassium intake) along with sufficient
calcium/Vitamin D intake, the impact of protein on bone health would appear to be positive overall.

277
Antioxidant and Vitamin D Supplements for Athletes: Sense or
Nonsense? – Research Review

Powers S et. al. Antioxidant and Vitamin D supplements for


athletes: Sense or nonsense? J Sports Sci. 2011 Aug 11. [Epub
ahead of print]
The idea that dietary supplements can improve athletic performance is popular among athletes. The use of
antioxidant supplements is widespread among endurance athletes because of evidence that free radicals
contribute to muscle fatigue during prolonged exercise. Furthermore, interest in vitamin D supplementation
is increasing in response to studies indicating that vitamin D deficiency exists in athletic populations. This
review explores the rationale for supplementation with both antioxidants and vitamin D and discusses the
evidence to support and deny the benefits of these dietary supplements. The issue of whether athletes
should use antioxidant supplements remains highly controversial. Nonetheless, at present there is limited
scientific evidence to recommend antioxidant supplements to athletes or other physically active individuals.
Therefore, athletes should consult with their health care professional and/or nutritionist when considering
antioxidant supplementation. The issue of whether athletes should supplement with vitamin D is also
controversial. While arguments for and against vitamin D supplementation exist, additional research is
required to determine whether vitamin D supplementation is beneficial to athletes. Nevertheless, based upon
the growing evidence that many athletic populations are vitamin D deficient or insufficient, it is recommended
that athletes monitor their serum vitamin D concentration and consult with their health care professional
and/or nutritionist to determine if they would derive health benefits from vitamin D supplementation.

Background

Supplements for athletic performance have been a part of the landscape for decades and athletes are always
looking for an edge in terms of either promoting adaptations to training, recovery, or outright
performance. And while many in the field tend to think of me as anti-supplement, this really sort of misses
my issue with supplements. Because I’m not anti-supplement; rather I’m simply anti-bs.
I’m also anti-anything that takes focus away from the factors that actually do matter, namely things like
training, diet, lifestyle, etc. And the sad fact is that all too many athletes try to use supplements in place of
proper training, attention to their diet, etc. It goes to something I discussed ad nauseum in the thankfully
finished Why the US Sucks at Olympic Lifting series, quick fixes are more appealing than things that take
work. And popping a pill is easier than working your nuts off in the gym or watching your diet.
And the reality is that most claims made for most supplements are about 99% bs and 1% “Well, maybe”. Of
course, that never stops athletes, who fall prey to the logic of “IF this is the next big thing, I don’t want to
miss out on it.” Of course, supplement industries pander to that very thought process; that’s how they make
shocking amounts of money off of desperate athletes.
I’ve been in this field for over 2 decades and in that time I’ve seen thousands of products come and go,
always with the same hype and exciting ad copy claiming that they are the solution for the woes of athletes,
only to disappear months later to be replaced by the newest crop of crap. Because over that 20 years, I can
count the number of products that even came close to living up on maybe two hands. That gives
supplements about a 99.9% failure rate; in my mind it’s absurd to hold any opinion about anything new

278
except to assume it’s crap until proven otherwise. But I’m sort of getting off track here and really only want
to focus on two specific supplements since they relate to today’s paper.
Because for about three decades, one ‘class’ of supplements that has been popular (and very often
recommended) is that of anti-oxidants. In short, these are compounds that help to scavenge or ‘deal with’
what are called reactive oxygen species (ROS) in the body. These are produced under various conditions
(including exercise) and one early theory of aging and bodily damage was that the production of ROS was
part of the overall breaking down of the body. With the logical solution being to simply take these nutrients
in doses ranging from reasonable to ‘Oh my god, you want me to take how much?’ levels. I can fondly
remember Colgan and his laundry list of high-dose anti-oxidants in Optimum Sports Nutrition (an excellent
book so long as you ignore every word about supplements) for example.
More recently, there has been great interest in Vitamin D status, both from a general health standpoint
(Vitamin D deficiency is literally being considered a current vitamin deficiency epidemic and there is actually
a staggering amount of data that this is the case) and from an athletic standpoint (and data going back to
the 1920’s actually suggested this very early on). Vitamin D does about a million and one things in the body
but one thing it is strongly related to is muscular function and performance; I even mentioned explicitly in the
Why the US Sucks at Olympic Lifting that one advantage that Kenyan runners may have is the ability to train
outdoors year round (the same holds for Jamaican sprinters) and this may maintain better Vitamin D status
compared to athletes who live in harsher environments.
Which is all just a lead up to today’s paper, a relatively short review on both anti-oxidant and Vitamin D (and
calcium) supplementation for athletes, looking at the role that they play in the body and arguments both for
and against the use of either by athletes.

The Paper

The paper starts by looking at the role of antioxidants in the body. As I mentioned above, ROS are produced
in the body under a variety of conditions including exercise and there is at least some evidence that ROS
may cause fatigue during exercise when they are produced in large quantities; this is along with potentially
causing overall bodily damage through oxidative stress (also caused by things like pollution and smoking for
example) and muscle damage.
And this provided the idea that providing supplemental anti-oxidants (which include but are not limited to
compounds such as Vitamin A, Vitamin C, Vitamin E, beta-carotone and a host of others; the list of potential
anti-oxidant compound seems to grow daily). However, with the exception of N-Acetyl Cysteine, which
appears to reduce fatigue during some types of submaximal exercise (and it’s thought that this occurs by
reducing ROS fatigue in breathing muscles, believe it or not), most studies supplementing anti-oxidants have
not found any impact on performance.
Even the studies on anti-oxidant supplementation on muscle damage and oxidative damage are pretty
mixed, probably reflecting differences in the type, amount and intensity of exercise along with the specific
anti-oxidants and doses that were supplemented. Basically, outside of NAC and submaximal endurance
performance, the data is far from conclusive.
Moving to arguments for anti-oxidant supplementation, the paper examines three potential reasons that
athletes might consider anti-oxidant supplementation. First is the known increase in ROS production during
activity, coupled with the general principle that the compounds are pretty much non-toxic even at relatively
high levels. This is sort of a ‘It probably won’t hurt and might help’ kind of argument. Kind of weak.

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A second argument has to do with the role of excessive ROS on muscle fatigue but, as I noted above, with
the exception of NAC, most supplementation studies have shown no performance benefit of anti-oxidants
so this argument pretty much fails. The final argument that they address is the idea that many athletes have
poor or insufficient diets (note that most anti-oxidants in the diet come from fruits and vegetables) and that
an athlete who’s diet is poor may need supplementation. Which is equally weak for a number of reasons I
won’t go into just yet.
In terms of arguments against anti-oxidants, the paper examines a number of arguments against
supplementation. First they point out that while exercise certainly does increase ROS production it’s very
transient (and this does distinguish it from the pollution or smoking examples which may be generating more
chronic levels). As well, the body already has an in-built system to deal with ROS production; quite in fact it
increases it’s activity with training.
That is, by exposing the body to ROS in moderate amounts, it adapts by being better able to handle further
ROS production (some have even theorized that high-dose antioxidant supplementation might be harmful
down the road by limiting the body’s upregulation of it’s inbuilt system).
In a related vein, there is considerable evidence and this has been accumulating for a while that the
production of ROS is part of the overall adaptation to training (and the data here is more geared towards
endurance athletes than strength/power athletes). That is, the production of ROS, like inflammation and a
whole host of other things that occur with training appear to be part of the overall training stimulus; blocking
this with high-dose supplementation could conceivably limit the adaptations to training.
Finally is the simple fact that studies are routinely showing that individual anti-0xidant supplementation (as
opposed to diets high in natural anti-oxidants; that is diets including lots of fruits and vegetables) either have
no real benefit to health or may actually be harmful and increase mortality in the long-term. The authors
conclude that outside of ensuring a mixed, energy sufficient diet (which should provide adequate ‘natural’
anti-oxidants) that there is no reason for athletes to supplement with individual high-dose anti-oxidants. I’ll
come back to this when I wrap-up below.
Moving on the authors next address Vitamin D along with calcium (since it’s a bit tough to separate the
two). Vitamin D is a bit odd among the vitamins for a number of reasons, not the least of which that it can
actually be produced by the body specifically in response to sun exposure. The authors overview the
metabolism of Vitamin D but I won’t repeat that here, go Wikipedia it if you must know.
Vitamin D is critical in the body for a number of reasons, not the least of which is bone health; in this vein,
adequate Vitamin D status is required for optimal calcium absorption in the body. As well, Vitamin D
regulates genes all over the body, controls inflammation and immune system function; a great deal of
research has focused on low Vitamin D status and colon cancer. Of more relevance to athletes is that
Vitamin D status is tied to muscular function and Vitamin D is involved in the expression of a number of
genes involved in muscular function and performance; all issues relevant to athletes.
There’s actual a considerable history of evidence on the issue of Vitamin D and performance although it’s
only recently that researchers have realized that Vitamin D might be playing a role. Let me explain: back in
the early part of the 20th century, it was observed that athletes often made less progress during the winter
months in terms of strength or performance and that exposure to ultraviolet light improved trainability and
strength gains. We now clearly know that UVB exposure would have had one effect of increasing Vitamin
D synthesis in the body and as discussed in Athletic Performance and Vitamin D, this may have been the
mechanism at work.
Of more relevance, recent research is finding that almost everyone is Vitamin D deficient, all over the world.
This is due to a number of factors including things like overuse of sunscreen, working indoors, poor diet,
etc. Both calcium and Vitamin D come from the diet (and many foods are fortified with both) but, as I

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mentioned, Vitamin D is an oddity among the vitamins in that it can be produced by the body, specifically in
response to direct sun exposure.
Moving to Vitamin D status, the authors point out that determination of optimal level of Vitamin D in the body
is still a bit of a controversial area. It’s generally considered that Vitamin D levels below 50 nmol/L (or 20
ng/mL) is a sign of deficiency while levels below 80 nmol/L (32 ng/mL) is insufficient. What level is optimal
is harder to determine but a concentration of 100-250 nmol/l (or 40-100 ng/ML) is thought to be ideal.
It’s worth mentioning that while there is less work on the Vitamin D status of athletes, what work exists
suggests that many athletes show Vitamin D insufficiency or outright deficiency levels; depending on the
study and the definition used this may be as high as 90% of the athletes tested. This is especially true for
athletes involved in indoor sports, or who train in areas with a harsh winter that limits sun exposure (while
Vitamin D levels go up during summer training, they are only maintained for perhaps a month or so without
supplementation or sun exposure. Interestingly, even athletes in sunny areas, such as Qatar may be at risk
for deficiency, probably due to athletes preferring to train after sundown since it’s about a billion degrees
during the day. It’s only athletes who live in temperate year round sunny climates that are likely to not be at
risk for Vitamin D deficiency.
And from that standpoint alone, supplementation is probably warranted for athletes who train indoors or who
live in cold weather areas where sun exposure for a great part of the year simply isn’t available (note that
the use of a tanning bed would be another option so long as the duration are moderate).
Mind you, the direct data on Vitamin D and athletic performance isn’t major except for what I talked about
above, a handful of studies have examined it and there does appear to be a positive correlation between
Vitamin D status and things like strength and muscle force, along with decreased risk of stress fracture
(important for athletes in high-impact activities). Mind you, claims such as “The higher the Vitamin D status
the better your performance” are absolutely not supported by current research; it’s likely that it’s more an
issue of correcting a highly likely deficiency or insufficiency.
In terms of arguments against supplementation, the main one is the overall lack of data indicating a
performance boost; mind you that keeping an athlete healthy in general terms (and Vitamin D contributes to
immune system function and bone health) is just as critical here. An injured or sick athlete isn’t training nor
performing and the realities of Vitamin D deficiency should be addressed regardless of whether or not it
improves performance.
The other argument against has to do with toxicity, as a fat soluble vitamin, it is possible to take too much
Vitamin D. It does take pretty stupid levels but athletes often fall into a ‘more is better’ trap. But this is more
to do with ensuring that athletes don’t do stupid things and take 5X the recommended dose than the
supplement itself. I’d note that roughly 30 minutes of direct sun exposure pretty much maxes out Vitamin D
synthesis (at roughly 10,000 IU’s) in the body and this might be taken as a rough realistic maximum daily
intake level. Others have set more conservative maximum intake levels of 4000 IU’s/day; at the current time
it’s not really known what level of supplementation is toxic or problematic.
Finally the authors note that there is individual difference in the absorption and utilization of Vitamin D and
this could conceivably impact on how a given athlete responds to supplementation (a great deal of research
suggested a problem with Vitamin D levels in obesity but that’s a different research review). The authors
recommend that, while there is little evidence that Vitamin D supplementation will improve performance
(outside of correcting a deficiency), athletes should monitor their Vitamin D levels and supplement as
needed. Again I’ll give my recommendations below.
.

My Comments

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For the most part what I wrote above doesn’t really differ to any signicant degree from what I wrote in the
articles Supplements Part 1 and Supplements Part 2. In terms of anti-oxidant supplementation, I’m really
not a fan under most circumstances. Not only do they not appear to have much if any benefit, especially
taken in isolated form in high-doses, they may actually be detrimental to training adaptations. Using them
during a primary training phase could slow adaptations. In contrast, athletes in heavy competition might
consider supplementation; some studies do show decreased muscle soreness and damage and taking them
during a heavy competition schedule might be worthwhile simply to keep the athlete in one piece. That’s in
addition to NAC having a potential ergogenic benefit before certain types of endurance performance.
In terms of Vitamin D, outside of those athletes who can train consistently in the sun, I think supplementation
is probably mandatory. Few athletes live in climates where outdoor sun exposure is available year round
and the simple fact is that even if optimal levels occur during summer training, they only maintain about a
month or so after the stimulus of regular sun exposure is removed.
Athletes who’s sports keep them indoors, or who live in areas with actual winter (where training is done
indoors by choice or there is simply limited sun exposure) will find Vitamin D levels falling rapidly, potentially
compromising immune system function, bone health and even trainability. Supplementation (or going to the
tanning bed a few times per week for reasonable amounts of time, perhaps 30 minutes 2-3X/week) will serve
to maintain optimal Vitamin D status during those time periods.
And while it would be ideal for athletes to get regular blood work to determine levels along with their response
to supplementation it’s not cheap work to do and has to be done at least twice. For athletes that can get it
done, I’d mention that it takes, on average, 100 IU of Vitamin D to raise levels by 1 ng/mL. So an athlete
with a Vitamin D level of 30 ng/mL who wants to get to 50 ng/mL would need 2000 IU’s per day.
As I noted above, 30 minutes of direct sun exposure generates 10,000 IU’s of Vitamin D and that appears
to be the maximum the body will synthesize. A daily intake of half that should be more than safe and is in
keeping with other maximum daily recommendations of 4000 IU/day. And outside of extreme deficiencies,
that level should cover most folks (that is if we assume levels drop to an insufficient 20-30 ng/mL during the
winter, 5000 IU/day would be expected to raise that to 70-80 ng/mL right in the middle of the optimal range).
I’d note in closing that, as a fat soluble vitamin, Vitamin D should be taken with a fat containing meal for
optimal absorption, Vitamin D is also a supplement that can be taken only weekly (i.e. 35,000 IU’s all at once
or what they’d get from 5000 IU’s per day for a week) for athletes who are bad about taking pills.

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Are Blood Flow and Lipolysis in Subcutaneous Adipose Tissue
Influenced by Contractions in Adjacent Muscle in Humans –
Research Review

Title and Abstract

Stallknecht B et. al. Are blood flow and lipolysis in subcutaneous adipose tissue influenced by contractions
in adjacent muscles in humans? Am J Physiol Endocrinol Metab. 2007 Feb;292(2):E394-9.
Aerobic exercise increases whole-body adipose tissue lipolysis, but is lipolysis higher in subcutaneous
adipose tissue (SCAT) adjacent to contracting muscles than in SCAT adjacent to resting muscles? Ten
healthy, overnight-fasted males performed one-legged knee extension exercise at 25% of maximal workload
(Wmax) for 30 minutes followed by exercise at 55% Wmax for 120 minutes with the other leg and finally
exercised at 85% Wmax for 30 minutes with the first leg. Subjects rested for 30 minutes between exercise
periods. Femoral SCAT blood flow was estimated from washout of (133)Xe and lipolysis was calculated from
femoral SCAT interstitial and arterial glycerol concentrations and blood flow. In general, blood flow as well
as lipolysis was higher in femoral SCAT adjacent to contracting than adjacent to resting muscle (time 15-30
min: blood flow: 25% Wmax: 6.6 +/- 1.0 vs. 3.9 +/- 0.8 ml 100 g(-1) min(-1), P < 0.05; 55% Wmax: 7.3 +/-
0.6 vs. 5.0 +/- 0.6, P < 0.05; 85% Wmax: 6.6 +/- 1.3 vs. 5.9 +/- 0.7, P > 0.05; lipolysis: 25% Wmax: 102 +/-
19 vs. 55 +/- 14 nmol 100 g(-1) min(-1), P = 0.06; 55% Wmax: 86 +/- 11 vs. 50 +/- 20, P > 0.05; 85% Wmax:
88 +/- 31 vs. -9 +/- 25, P < 0.05). In conclusion, blood flow and lipolysis are generally higher in SCAT adjacent
to contracting than adjacent to resting muscle irrespective of exercise intensity. Thus, specific exercises can
induce “spot lipolysis” in adipose tissue. Key words: exercise, spot lipolysis, microdialysis.

Background

The idea of spot reduction is one that has floated around the fitness body recomposition world for
decades. Men want the ever desirable six-pack and can be seen doing abs until the cows come home,
women try to slim hips and thighs with endless reps on the inner/outer thigh machine.
Hour long ‘abs’ or ‘buns/thighs’ classes filled with nearly an hour of high rep movements for the specific area
can be found in most commercial gyms. Even in the bodybuilding world, where people really should know
better, some still argue that spot reduction can occur and that working a given muscle group will help reduce
fat in that specific area. I addressed this topic somewhat in The Stubborn Fat Solution since some of what
I discuss in that book could readily be confused with spot reduction (it’s not).
For the most part, the idea of spot reduction has been resoundly denied by folks in the field (with the
occasional heretic or book seller suggesting it is still possible). Various lines of research are usually cited
including those showing no difference in skinfolds in the arms of tennis players (who typically use one arm
more than the other).
An example I’ve often used is that “If spot reduction worked, people who ate a lot should have skinny faces.”
A bit silly but I think it gets the point across. If working a specific muscle group reduced fat only in that area,
that’s how it should work. But it doesn’t. Or certainly doesn’t seem to. But, for the most part, the idea hasn’t
been directly tested to my knowledge.

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In that context, I should note for the sake of background that there are three primary steps involved in fat
loss that might potentially be influenced although today’s study only focuses on two. Those steps are
1. Lipolysis (the actual fat breakdown)
2. Blood flow (critical for transport of the broken down fat to other tissues for ‘burning’)
3. Oxidation (the actual ‘burning’ of fat in tissues such as the liver or skeletal muscle)
Is it possible that performing local activity can impact on some aspect of the above in a way that might make
spot reduction or performing endless reps of local exercises worthwhile in terms of fat loss? That’s what
today’s study set out to examine: do contractions in a specific muscle impact on either lipolysis or blood flow
(oxidation was not measured) in the adjacent fat cells.
And although it was published several years ago, it still seems to be making the rounds (being cited as
‘evidence’ for spot reduction); as well, the idea of spot reduction is one that refuses to die. So it’s worth
seeing what the real or potentially real effects actually are.
.

The Study

Using a couple of different methods (that I’m not going to detail) to measure actual blood flow and lipolysis ,
the study had subjects perform lower body exercise (they called it one leg leg extension but this probably
means one legged cycling) at various intensities while resting the other leg. That way, blood flow/lipolysis
could be measured for the exercise versus the unexercised leg.
This allowed them to compare lipolysis and blood flow in response to local exercise to the non-exercised
control leg. This is actually critically important as any type of whole body exercise would tend to have
systemic effects; that is impacting on fuel metabolism all over the body. By limiting exercise to a single leg,
the researchers were able to measure the response only in the fat cells close to the muscles being worked
and compare that to the unworked msuscle to see what differences occurred.
Exercise was performed at 25%, 55% and 85% of maximum power output with a 30 minute break and the
subjects switched legs from one intensity to the next. This also acted as a control so that the previous bout
of exercise wasn’t impacting on the next bout, since the previously exercised leg got the longer break. As
mentioned above, blood flow and lipolysis was compared between the exercised leg and the rested leg to
see what difference the exercise had.
.

Results

And, as indicated in the abstract above, both lipolysis and blood flow were increased for the exercised vs.
non-exercised leg although this only occurred at the two lower intensities of exercise. At the highest
intensity of exercise, no change was seen.
Before getting to specific numbers, a question worth addressing is why this would have happened. The
researchers proposed two possible reasons for their observation.
First, local changes in hormones (or a synergy between changes in hormones and blood flow) are most
likely responsible but there is a larger question of why this would occur in the first place, a point that the
researchers specifically made. By why I mean why the system would work that way in terms of improving
physiological functioning.
The reason for asking this question is this: fat mobilized from a specific area of body fat (say the thigh) can’t
actually be used for fuel by the muscle underneath it (e.g. the quadriceps). The blood flow of skeletal muscle

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and fat cells are separate and any fat mobilized from an adjacent area will go into local circulation; again, it
can’t be used directly by that muscle.
So there’s no really logical physiological reason that working a given muscle would would cause fatty acids
to be mobilized; that muscle can’t use them. Of course, physiology doesn’t have to be logical to work a
certain way and worrying about the reasons why instead of the observation of what happened can make you
lose the forest for the trees.
Related to this, the researchers point out clearly that there is no indication that these results will actually
result in spot reduction as fat stores in the affected areas could simply be replenished after the exercise
bout. They didn’t measure fat storage after the exercise bout stopped and process that occurs quite often
is fatty acid re-esterification, basically mobilized fat that isn’t burned off elsewhere in the body simply gets
stored back in the fat cell. In some exceedingly strange cases, fat mobilized in one area of the body can be
restored in fat cells somewhere else.
The researchers also suggest that localized increase in temperature, which can also impact on blood flow
may have also been involved in the measured response. I discuss this aspect of fat cell mobilization in The
Stubborn Fat Solution as local temperature is known to impact on blood flow in the area. Cold tends to
cause vasoconstriction and heat vasodilation so there might actually be some logic to those rubber belts and
such that warm the area before exercise.
In any case, for whatever reasons, through whatever mechanism, working a given muscle for 30 minutes at
low to moderate intensities did increase fat cell lipolysis in blood flow.
Aha! Spot reduction is possible, right? Hang on.
Although clearly local exercise did impact on fat cell lipolysis and blood flow, you might note something I left
out of the above discussion: the acutal quantitative impact of this. That is, how much extra fat was actually
mobilized for fuel, potentially to be burned off.
Addressing that very thing, based on the measured changes in blood flow and lipolysis, the researchers
estimate that, in 30 minutes of local exercise, an additional .6-2.1 milligrams (one milligram is one thousandth
of a gram) per 100 grams of adipose tissue adjacent to contracting muscle was mobilized.
Let me put that in context. First let’s assume that you’re carying a whopping 5 kg (11.1 pounds) of fat in a
specific area.
If local exercise can mobilize 0.6-2.1 milligrams of fat per 100 grams of fat mass, that works out to:
0.6-2.1 mg/100 grams * 1000 grams/kg * 5 kg = 30-105 milligrams of fat.
Or 0.03-0.1 gram of extra fat mobilized in 30 minutes of activity.
Now, a single pound of fat (0.454 kg) contains about 400 grams of fat so our hypothetical 11.1 pounds of fat
contains 4,440 grams of fat. And 30 minutes of local activity mobilized at most 0.1 gram of fat. Whoo
hoo. You’ll be ripped in about 1000 years.
.

Summing Up

And, so far as I’m concerned, that should be the death knell for the idea of spot reduction. Yes, there
appears to be an effect whereby working a given muscle impacts on local fat cell metabolism but the effect
is completely and utterly irrelevant in quantatitive terms. The amount of fat mobilized due to increased
hormones or blood flow is simply insignificant to anything in the real world.
There is also the fact that, compared to something like full body cardio types of activities, local single muscle
group activities burn tiny amounts of calories. Doing cardio for 30 minutes at even a reasonable caloric burn

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of 5 cal/minute (very easy) burns 150 calories. If you get say 90% fat utilization for fuel, you’ve burned 15
grams of fat. Compared to the 0.1 gram you might mobilize doing crunches or leg lifts.
As well, the whole body activity will impact on fuel utilization and hormones in ways that much more
massively impact on lipolysis and blood flow. Simply, spending an hour doing localized exercise pales in
comparison to the fat loss effects of even moderate cardio. Wasting time with ab or buns/thighs classes is
simply a waste of time in terms of any sort of local fat reduction.

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AMPK: Master Metabolic Regulator
This is a very technical article that I wrote a while back for a now defunct online magazine. If you’re extremely
interested in some of the underlying molecular level reasons ‘why’ certain things happen in the body, this is
an article for you. If not, I’d suggest pulling something else out of the archive. There isn’t a ton of application
to be had out of this article; as stated it’s more of a ‘why things happen'; at best, it will help explain some of
the issues that go along with both dieting/fat loss and gaining muscle, along with a lot of the underlying
physiology of my Ultimate Diet 2.0. I guess that’s something anyhow.
The molecule I want to talk about is called AMP-activated protein kinase or AMPk for short, a compound that
is turning out to be one of the major metabolic regulators in the liver, skeletal muscle, fatty acids, and the
brain. This is especially true if you’re talking about the regulation of glucose uptake and utilization, fatty acid
intake and oxidation, and appetite. Ok, maybe I have your attention again.

What is AMPk and How is it Regulated (1)

I’m not going to bore you with a detail of the structure of AMPk. Sufficed to say that it’s a heterotrimeric
compound (translation to nonscientist: contains 3 different parts which are different from each other) which
are all regulated differently. Sparing you unnecessary details, AMPk is turned on when the cellular energy
state of the cell drops. Basically, anything that causes the cell to use energy (ATP is broken down to produce
energy and ADP, and the ATP/ADP ratio is a key activator of AMPk) will activate AMPk. As well, specifically
in muscle, levels of glycogen may also regulate AMPk: it appears that high levels of glycogen inactivate
AMPk and lowered levels of glycogen activate it.
Ok, let’s get more specific. A number of cellular stresses can activate AMPk. This includes metabolic poisons
(DNP anybody?), glucose deprivation, ischemia (decreased blood flow), hypoxia (insufficient oxygen),
oxidative stress and hyperosmotic stress. With the possible exception of DNP use, none of these are going
to occur in healthy athletes. A chemical activator of AMPk called AICAR (NOT to be confused with acetyl-l
carnitine or ALCAR) is being used in research as a chronic activator of AMPk. I thought I had heard rumors
that someone was going to try to bring it to market as a fat loss product. As I’m going to explain below, for
athletes/bodybuilders, use of such a compound would be a tremendously bad idea.
So what else? Well, I already mentioned that glycogen depletion may play a role (this is probably part of why
glycogen depletion increases whole body fat utilization). Probably the most relevant activator of AMPk is
exercise and muscular contraction, both of which shift both the ATP/ADP ratio as well as the
creatine/phosphocreatine ratio. I should mention that exercise also activates AMPk in liver and fat cells and
this appears to result from exercise induced release of certain molecules such as interleukin-6 (released
from muscle cells during intense activity, especially when glycogen is depleted). Also, systemic changes in
fuel availability during exercise is involved in the activation of AMPk in tissues like liver and fat cells.
AMPk is also controlled by a variety of hormones. Leptin and adiponectin, released primarily from fat cells
in response to nutrient surplus, both activate AMPk in peripheral tissues. Leptin also appears to decrease
AMPk levels in the brain (I’ll come back to this paradox below) while ghrelin (released from the stomach in
response to eating less) increases levels of AMPk in the brain.

What Does AMPk Do?

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Although it’s likely that AMPk is involved in cellular control in most cells of the body, I’m going to focus
primarily on liver, skeletal muscle fat cells, and the brain (specifically the hypothalamus, which is the area
primarily involved in appetite/hunger and bodyweight regulation) with AMPk playing a role in carb, fat and
protein metabolism in peripheral tissues and bodyweight regulation in the brain.
With regards to carbs, AMPk activation inhibits glycogen storage and increases glucose uptake, it appears
to be very involved in improving insulin sensitivity for this reason. Insulin sensitizing drugs such as metformin
and the thiazolidinediones (TZD’s) appear to work at least partially through AMPk activation. Note that the
TZD’s tend to increase bodyfat and metformin hasn’t been found to cause a drastic decrease in fat mass by
itself either (2) although it seems to improve the results of low-carbohydrate diets in insulin resistant/obese
individuals .
So what about fat metabolism? In the liver, AMPk activation decreases fatty acid and cholesterol synthesis.
In muscle cells, AMPk activation increases fatty acid oxidation (i.e. you burn more fat). It also appears that
AMPk activation is one of the keys to how endurance training causes adaptations such as increased
mitochondrial protein synthesis (3). In fat cells, AMPk activation decreases both fatty acid synthesis and
lipolysis (by inhibiting hormone sensitive lipase).
Ok, so far so good, right? With the exception of the inhibition of lipolysis, it sounds like AMPk activation is a
good thing, increased glucose uptake, increased fatty acid oxidation in skeletal muscle cells. So why not just
jack up AMPk levels all the time and get ripped?
The first reason I alluded to in the UD2.0, a low cellular energy state inhibits protein synthesis. And it looks
like AMPk activation is part of the mechanism. In a rat model, AMPk activation has been shown to suppress
protein synthesis by down regulating another molecular target called the mammalian target of rapomyacin,
or mTOR (4) which is heavily involved in protein synthesis.
Although this hasn’t been shown in humans to my knowledge, the general picture is that AMPk activation
turns off energetically costly processes (such as protein synthesis) and turns on energy producing processes
(such as glucose and fat oxidation). So an AMPk inhibition of skeletal muscle protein synthesis would be
consistent in humans. I’ll note that years ago, Dan Duchaine commented how insulin sensitizers (of which
metformin was one of the ones in use) caused muscle loss and I have to wonder if this isn’t part of the
mechanism.
The second reason has to do with the effects of AMPk activation in the brain where AMPk activation has a
rather negative effect, which is to increase appetite. Recall from above that I mentioned that both leptin and
ghrelin affect AMPk levels in the brain. Well, it’s time to talk about that. As mentioned, ghrelin, which tends
to increase appetite and food intake increases AMPk levels in the brain while leptin, which tends to decrease
appetite and food intake (sort-of) decreases AMPk. As well, nutrient availability affects brain AMPk (probably
through leptin and ghrelin). Eat more and brain AMPk goes down, eat less and brain AMPk goes up (5).
Increased activity of hypothalamic AMPk via AICAR also increases food intake (6). I’ll come back to the
ramifications of all of this below.
I want to mention that the mechanism whereby leptin increases AMPk levels in muscle but decreases them
in brain is currently unknown (7). That is, leptin has opposite effects on AMPk in muscle/fat/liver cells versus
the brain.

Putting it All Together

So now a few things may start to come together in terms of dieting or mass gains or what have you. When
you eat less (diet), a lot of things occur. One of those is going to be a decreased cellular energy charge (an

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effect which may be increased by glycogen depletion and, of course, exercise). Fat oxidation goes up, insulin
sensitivity goes up, good things happen in terms of fat loss. But the drawback is that, due to changes in
hormone levels and AMPk signaling you get hungry. As well, protein synthesis is inhibited (this is a huge
part of why it’s so hard to gain muscle while losing fat at the same time).
AMPk and its function also explains one of the older models of hypertrophy whereby protein synthesis was
acutely depressed during exercise. Activation of AMPk during exercise directly inhibits mTOR and protein
synthesis. The recovery of cellular energy post-workout allows protein synthesis to increase and growth to
occur. Note also the huge push on the provision of amino acids, specifically leucine, post-workout as leucine
directly activates mTOR, turning on protein synthesis.
A question that comes to mind (which I have no answer to): can leucine’s activation of mTOR override the
AMPk suppression of mTOR either during exercise or while dieting? High dose BCAA may decrease muscle
loss on a diet, could this be a potential mechanism?
In reverse, consider what happens when you’re eating above maintenance. AMPk will be inhibited (except
during exercise) meaning no inhibition of protein synthesis. Also, assuming decent brain leptin sensitivity,
appetite and food intake will be kept under control. However, this comes at the expense of decreased fat
oxidation (part of why folks tend to gain fat as they gain muscle).
Basically, AMPk (and, make no mistake, there are multiple other pathways involved) help to explain why it’s
so hard to have it all: fat loss with muscle gain. As described in the UD2.0, the mechanisms needed to
maximize fat loss are more or less directly antagonistic to those mechanisms involved in muscle gain and
vice versa. Which is why the UD2.0 was broken up into discrete fat loss and muscle gain phases which were
alternated every few days.

A Few Words About Application


As mentioned in the introduction, this article didn’t really present a whole lot useful, I’m wondering why I’m
wasting your time with it. Clearly, the most potent tool we have to activate AMPk and increase fat oxidation
and the rest is exercise. Dieting in general probably activates AMPk as well although I can’t recall seeing it
directly studied.
The effects of both can be increased by depleting glycogen (ala the UD2) but this comes with the price of
inhibited protein synthesis. Which is why I’m so adamant about all diets having a refeed/anabolic phase at
some point. You need to turn off diet induced catabolism although I should note that AMPk activation is only
one of many mechanisms (including insulin, cortisol, etc, etc.)
Under non-dieting circumstances, although AMPk will be activated during training, impairing protein
synthesis, providing nutrients afterwards (i.e. carbs + proteins) is known to reverse the catabolic processes
and turn on anabolic processes. Making me wonder if pre- or during-workout nutrition can actually prevent
the activation of AMPk in the first place (by limiting the drop in cellular energy charge). To my knowledge, it
hasn’t been studied but it would make some logical sense.

A Final Question about AMPk and Fat Loss


From the standpoint of treating obesity and insulin resistance, AMPk appears to be an attractive target.
However, the contradiction described above has to be dealt with. Ideally you’d want to activate AMPk in
peripheral tissues such as muscle and fat cells while decreasing AMPk in the brain (to reduce or control food
intake).
Clearly leptin injections are one way of doing that but leptin injections are unlikely to work in obese
individuals, due to leptin resistance, in the first place. Of course, lean athletes and bodybuilders aren’t obese

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and probably have decent leptin sensitivity. This is probably one of the reasons refeeds ‘work’, by raising
leptin, we are activating AMPk in skeletal muscle (explaining why people often lean out after a refeed) and
inhibiting it in the brain. Is there any other way? Well, maybe.
One study (again, in rats) found that alpha-lipoic acid ingestion decreased AMPk in the brain while increasing
it in skeletal muscle in rats (8). I should note that the doses used were high and a very informal poll on my
forum doesn’t seem to indicate that ALA was having any such effect in terms of fat loss or appetite. If
anything, people noted an increase in appetite, most likely mediated by a decrease in blood glucose via
insulin sensitization. Would consuming ALA while eating sufficient carbs allow us to achieve the same effects
without increasing hunger? I don’t know. There is also the dose issue.
But it does point out that increasing AMPk in muscle while decreasing it in the brain is possible and future
drugs or nutrient compounds may allow us to get the best of both worlds. Unfortunately, there is still the
issue of muscle loss due to the inhibition of protein synthesis that would occur with chronic muscular
activation of AMPk. At this point, I have no idea how to sidestep that. Would sufficient amounts of protein,
BCAA or even just leucine be sufficient to activate mTOR against the inhibition occurring due to AMPk? Or
would another drug or nutrient be required to prevent muscle loss against chronic AMPk activation. At this
point, it’s all speculation; hopefully more research will help to answer these questions.

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Bodyweight Regulation Wrap-Up: Other Hormones
Ok, although this is one of those topics that truly could have endless posts made about it, most of what I
wanted to cover regarding bodyweight regulation and such was covered in the posts on leptin.
However, as I mentioned in that series, leptin turns out to be far from the only hormone involved in this.
I already talked a little about insulin in that series but there are still more hormones of some importance.
With more likely to be discovered as time goes on. Oxyntomodulin, GLP-1, PP and others are being
discussed in recent reviews and further research will go towards determining what in the hell is actually
going on.
Tangentially, this is one of the big problems in trying to find a true ‘solution’ to the issue of weight loss and
obesity: the human body has a number of overlapping, integrated and redundant pathways that all send
signals to the brain. Fix one and something else eventually steps in to fill the role and cause problems.
From a pharmacological standpoint, this likely means that multiple drug therapy will be required; I also
suspect that research and testing will help to identify whether any given individual has a specific pathway
that is more of a contribution, perhaps allowing drug or nutritional therapy to be more individually tailored.
However, this is likely to be years off from practical application.
Anyhow, I want to finish up by talking about a few of these other hormones focusing on three main ones:
Cholecystokinin, ghrelin and Peptide YY as these three currently have the most research on them.

Cholecystokinin
Cholecystokinin, or CCK, was one of the first fullness hormones found, originally discovered back in the late
1960’s. Released from the intestines in response to nutrient intake, it goes to the brain, binds to its specific
receptor and helps to signal fullness on a meal to meal basis. CCK doesn’t appear to play much of a role in
the long-term regulation of bodyweight, its simply a fullness signal in response to meals.
Nutritionally, protein, fat and fiber play a primary role in stimulating CCK with carbohydrate having a much
smaller effect; this may explain part of the appetite blunting effect of many low-carbohydrate diets (which
are generally high in protein, fat and fiber).
As I mentioned in a previous post, CCK doesn’t work very well when leptin is low explaining why lean dieters
can do everything ‘right’ nutritionally and still be a hungry an hour later.

Ghrelin
Released primarily from the stomach, ghrelin goes to the brain where, predictable, there is a specific
receptor. Among other functions, ghrelin raises levels of growth hormone. But that’s far from all.
Ghrelin also stimulates hunger (the only hormone so far found to do so) and appears to be a key hormone
in initiating the hunger that goes along with meals; ghrelin drops prior to hunger and injection of ghrelin
stimulates hunger specifically.
Even more interestingly, there is research suggesting that ghrelin levels become entrained to normal meal
times.
So if you normally eat at 3pm (or whatever), you’ll likely find yourself becoming hungry at 3pm; this appears
to occur from changes in ghrelin. I suspect this explains why people often have problems changing meal
frequency, at least until ghrelin re-entrains itself to the new frequency.
That is, moving from a higher to lower frequency of meals is often accompanied by hunger at the previously
‘normal’ meal times. Moving from lower to higher is often accompanied by a lack of hunger until the body

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adjusts to the new frequency. I haven’t seen any work examining how long this takes but empirically it seems
like it’s a couple of weeks or so.
Increased ghrelin also negatively impacts on pretty much all aspects of metabolism, slowing metabolism and
increasing fat storage, at least it does this in rats with daily infusion.
In this vein, I’ve heard rumors that ghrelin is being promoted as a bulking aid for athletes and bodybuilders,
both for the appetite increasing effects and the GH release. Given the negative aspects of ghrelin on
metabolism, this is truly an awful idea unless the goal is to just get really fat.
In contrast, a ghrelin antagonist might be a very nice thing indeed for dieting. There appears to be work on
orally available ghrelin antagonists going on.
As it turns out, ghrelin changes in the opposite direction of leptin; while leptin falls on a diet, ghrelin goes up.
It almost goes without saying that leptin levels have a hand in controlling ghrelin; leptin appears to restrain
both grhelin release from the gut and its stimulation of hunger.
So dieting, as usual is a double whammy in this regards: leptin goes down as ghrelin is going up with the
reduction in leptin being partly responsible for the increase in ghrelin.
Ghrelin appears to play a role in both short- and long-term hunger and long-term bodyweight regulation. As
mentioned above, ghrelin goes up prior to a meal; it also comes back down after eating.
However, ghrelin levels also increase overall with a loss of weight/bodyfat, decreasing when weight is
gained. Individuals with a high BMI have lower ghrelin (and the idea of ghrelin resistance has been thrown
around) and anorexics have higher ghrelin (which decreases with refeeding).
Nutritionally, carbohydrates appear to play a primary role in regulating ghrelin levels with dietary fat having
less of an impact, the effect of protein is currently unclear. In one study, a high carbohydrate/low-fat diet
generated weight loss without the normal increase in ghrelin levels.
And although only tested in anorexics, at least one study showed that the consumption of non-caloric fiber
reduced ghrelin levels. Consuming small amounts of guar gum or psyllium fiber between meals might help
to keep ghrelin down during a diet.
Perhaps ironically, it appears that low-sodium intakes increase ghrelin levels (although there is a racial
effect). As I discussed in this article, I wonder if the low-sodium intakes taht contest bodybuilders and figure
competitors often obsess about isn’t making things worse rather than better.
In one study increases in ghrelin with weight loss were related primarily to fat free mass loss but not body
fat loss per se. As good reason as any to ensure that the diet is set up to prevent lean body mass loss.
Of some interest, one of the ways that bariatric surgery appears to be so successful is that, despite the
massive weight loss generated, there is often no increase in ghrelin levels as would be seen with diet induced
weight loss.
This may explain why weight is so rapidly lost, seemingly without hunger, with that surgery. I’d note that
research also suggests that other hormone (such as Peptide YY, discussed next, and Glucagon like peptide
1, are more relevant to the hunger suppressing effect of the surgery).

Peptide YY
Finally is peptide YY (PYY), another important hormone released primarily from the small intestine. Like
CCK, PYY decreases hunger and appetite although it may do so for longer periods. Infusion of PYY blunts
hunger in humans for up to 24 hours.
More physiologically, PYY increases with 15 minutes of eating and may stay elevated for up to 5 hours. Of
some relevance to the issue of overweight, obese individuals have been found to have lower basal PYY
levels and less of an increase with meals.

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Of course, since this is all interconnected, administration of PYY has been shown to reduce fasting PYY
levels as well as preventing the normal increase in ghrelin before meals.
Nutritionally, PYY appears to be related primarily to the energy content of the meal although work suggests
that dietary fat has the biggest impact on PYY. The appetite supressing effect of protein appears to be
related to increased PYY levels as well. Fiber increases PYY as well.
Of some interest, one study comparing a lowcarb/highfat to highcarb/low fat diet found that the lowcarb/high
fat diet had a greater sustained effect on PYY levels in obese individuals.

Where does this all leave us?


As I mentioned above, there’s a lot of interacting and overalapping things going on when it comes to
appetite/hunger and bodyweight/bodyfat regulation. Even looking at the above hormones it’s clearly
complicated without worrying about leptin, insulin, blood glucose and everything else.
For example, one study finds that high carbs and low fat is better for supressing ghrelin while another finds
that lowcarb and high fat has a bigger impact on peptide YY (which may be low in the obese to begin with).
Which diet is better?
Looking at individual macronutrients carbs have the largest impact in supressing ghrelin while protein, fat
and fiber appear to have the biggest impact on CCK and peptide YY.
Is one hormone relatively more important than the other or is a moderate approach to dieting, where each
meal contains all four macronutrients (plenty of lean protein, moderate fat, dietary fiber and moderate
amounts of carbohydrates) going to be superior by targetting all of the gut hormones (in addition to providing
the greatest dietary flexibility and variety)?
Is keeping ghrelin from going up relatively more important than increasing CCK and PYY or does it simply
depend on the individual? If raising PYY with plenty of protein, fat and fiber not only helps with short-term
fullness but also blunts ghrelin increases (as infusion studies suggest) does that avoid the whole issue since
you accomplish both (increased PYY and lowered ghrelin) with the same intervention?
Does all of this lend more credence to the use of low-carbohydrate diets for the treatment of obesity? There’s
an additional interaction of diet with insulin sensitivity as well; something I haven’t talked about in this series
but discuss in Insulin Sensitivity and Fat Loss.
As I noted above, my gut (ha ha, get it?) says that different individuals are going to be relatively more or less
responsive to the different hormones.
If ghrelin is a bigger issue than the other hormones (and insulin sensitivity is good), then a high carb/low-fat
diet may very well be the superior choice for a given individual. If PYY is dominant (and insulin sensitivity is
poor), a low-carb/higher fat diet may be the best choice.
I’m not saying that I have the answers, I’m not sure anybody does at this point. As noted, I suspect that we
will get to the point that basic testing of gut hormone levels, insulin sensitivity, etc. will get us to the point that
diet optimization can occur. I’m not sure when that’s going to happen, though.

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Adding Muscle While Losing Fat – Q&A
Question: Is it possible to stay at the same weight and replace fat weight with LBM, by making decent
strength gains over time? (i.e by not actually leaning out and then mass packing etc). Can the body use the
extra calories that are needed for new muscle gain from existing fat stores on the body? I’m assuming this
is the case for beginners, but how about intermediates/advanced trainees? If so, roughly what sort of time
frame would be needed to say drop 10lbs fat and replace with the same amount in muscle? Thanks.

Answer: I’m willing to argue that if there is a single question (or related set of questions) that comes up
perennially in the field of training and nutrition, it’s something akin to the above. The idea of ‘gaining muscle
while losing fat’ in general or, better yet ‘replacing every pound of fat lost with muscle’ is sort of the holy grail
of training and nutrition and a great deal of approaches that are supposed to generate that very thing have
been thrown out over the years.
In essence, this is the basis of bodyrecomposition, you train and eat in such a way as to end up with more
muscle and less fat than you had before. People on forums either want to know how to accomplish the
above or make statements such as “I want to gain muscle without gaining weight.” implying that they are
replacing every pound of lost fat with the exact same pound of muscle. Others will hide it in the math of the
situation, wanting to move from one weight/body fat percentage to another without recognizing what that
implies for the numerical changes that they are seeking.
Now, when I was younger and only thought I knew what I was talking about, I would often say that the above
was impossible to accomplish. In hindsight, impossible was a bit too strong of a term; clearly it’s not
impossible as it does happen. But it can sure be difficult depending on the situation.
There are a handful of situations where the combination of muscle gain and fat loss occur relatively
readily. The first of those is in overfat beginners. I want to really stress the term overfat in the above
sentence. This phenomenon doesn’t happen in lean beginners for reasons I’m going to explain in a second.
A second situation where this phenomenon occurs readily is folks returning from a layoff. Folks who are
previously lean and muscular but who get out of shape (whether deliberately or not) often find that they get
back into shape much faster than they did initially: they seem to magically replace fat with muscle. In fact,
with the advent of before/after transformation pictures for supplements, this has become a growth industry:
people who are already in great shape will deliberately get out of great shape so that they can quickly reattain
their previous shape in a short period. Apparently there is huge money in selling such before/after pictures
to help move supplements.
But that’s not really what the question was asking which had more to do with this idea: can the body use
calories stored in fat cells to support muscle growth, essentially shunting calories from fat to muscle and
achieving the holy grail: fat loss with concomitant muscle gain.
And, as a generality, this tends to be difficult for reasons that I discussed in some detail in the Ultimate Diet
2.0 and Calorie Partitioning Part 1 and Calorie Partitioning Part 2.
And this brings me back to my comment about overfat beginners as I think this explains some of the
physiology involved. Please note that I’ve never really seen this topic studied directly and much of what I’m
going to write is based on either observation or other known aspects of physiology that I feel tie into the
issue.
So consider an individual who is carrying quite a bit of fat and not very much muscle. Your typical overfat
beginner trainee. Let’s look a bit at what’s going on physiologically for this person.
One consequence of the excess body fat is a systemic insulin resistance and this is especially true for fat
cells. Basically, when fat cells start to get full, they become more resistant to further caloric storage. That

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is to say: insulin resistance actually develops as an adaptation to obesity and this is one reason that obesity
is often associated with things like hyperglycemia, hypertriglyercidemia and hypercholesterolemia; the fat
cells get so full that they stop accepting more calories. So instead of being stored, glucose, triglycerides
and cholesterol sit in the bloodstream. In that vein, and quite contrary to popular belief, insulin resistance
actually predicts weight loss and insulin sensitivity weight gain but that’s another topic for another day.
So we have a situation in overfat folks where fat cells are sort of trying to ‘push calories away’ from the fat
cells. That’s point #1.
The second thing to consider is the untrained state and the fact that when people start training, they always
make gains in both strength and muscle mass faster. That is, beginners have the potential to gain muscle
at a much faster rate (and more easily in terms of the stimulus needed) than someone trained. As well, keep
in mind that regular training (both resistance training and cardio) improve muscular insulin sensitivity and
nutrient uptake in that one specific tissue (training is probably the most powerful tool in our arsenal to improve
nutrient uptake in that specific a fashion). That’s point #2.
So consider the combination: we have a situation with overfat beginners where fat cells are very insulin
resistant and essentially trying to push calories away. Now we throw training on that, not only sending a
muscle building stimulus via training but increasing nutrient uptake into skeletal muscle through effects on
skeletal muscle nutrient uptake/insulin sensitivity.
And what happens under those circumstances is exactly what you’d expect: the body appears to take
calories out of fat cells and use them to build muscle. And this is effectively what is happening due to the
combination of the above two factors. But the combination of the two is required. A lean beginner won’t see
the above because they don’t have the fat to lose/fat energy to shunt to the muscle. And as they get more
advanced, the rate of muscle gain slows way down. Again, it’s the combination of overfat and beginner
status that comes together here to let some magic occur.
And even there you’re not going to see the body replacing one pound of fat with one pound of muscle for
very long. The rates of the different processes are simply too different. What you might see is an initial shift
where muscle ‘replaces’ fat due to the calorie shunting effect but invariably it slows down and either muscle
gain or (more frequently) fat loss becomes dominant.
Now, having looked at the specific situation of an overfat beginner, let’s look at what happens as one of two
things (or both happen): the person becomes leaner and/or achieves a higher training status.
A known adaptation to fat loss is an improvement in insulin sensitivity especially in fat cells. This is part of
why fat loss becomes more difficult as folks get leaner as well as why the risk of weight/fat gain is higher at
the end of the diet (you’re MORE insulin sensitive). This means that the fat cells not only have less stored
fat to give up but it becomes more difficult to get it out of there.
I discussed some of the reasons for this in detail in The Stubborn Fat Solution along with protocols to get
around it. But the point is made: as folks get leaner, getting fat out of fat cells becomes more difficult. Some
of the hormonal mechanisms involved are also discussed in Calorie Partitioning Part 1 and Calorie
Partitioning Part 2.
Furthermore, as folks become better trained, it becomes more difficult to gain muscle under any
condition. The training stimulus is higher and the impact of training is lessened.
So the situation that was in place for the overfat beginner has reversed itself in someone who is leaner
and/or better trained. Fat cells are no longer insulin resistant and ‘pushing fat calories’ away; quite in fact
they are ready to take up excess calories at any time. And since training has a lesser impact on muscle
growth, the odds of getting the calorie shunting effect becomes lower and lower approaching nil. Again,
that’s on top of all of the hormonal stuff discussed in the above articles (e.g. fat loss and muscle gain requires
different hormonal situations).

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Which is why a lot of the approaches advocated for ‘gaining muscle while losing fat’ aren’t very effective. In
fact, I’d tend to argue that most people’s attempts to achieve the above results in them simply spinning their
wheels, making no progress towards either goal. Because invariably they set up a situation where neither
training nor diet is optimized for either fat loss or muscle gain. Calories are too high for fat loss and too low
to support muscle gains and outside of that one overfat beginner situation, the physiology simply isn’t going
to readily allow what they want to happen to happen.
But more specific approaches can be effective in achieving this goal. The Ultimate Diet 2.0 has often
generated muscle gains while people dieted to single digit body fat levels (I’d note that the gain in muscle
never reaches equality with the fat loss) but it also alternates specific dieting and gaining phases during the
week.
Many of the intermittent fasting (IF’ing) approaches do this more acutely and I’d suggest anybody interested
go to Martin Berkhan’s Lean Gains site for more information about IF. There are others, things like every
other day refeeds (EOD refeeds) which are discussed in some detail in my The Bodyrecomposition Support
Forums. But all of those approaches are alternating dieting phases (lowered calories, a net ‘catabolic’ state)
with gaining phases (increased calories, a net ‘anabolic’ state).
But none of those approaches generate a muscle gain to equal the fat loss, at best they generate a small
muscle gain in the face of a much larger fat loss (e.g. someone might lose a lot of fat while gaining a pound
or two of muscle or what have you). But for the non-beginner/non-returning from a layoff trainee that’s about
the best you’re going to get. Potential rates of muscle gain are never going to approach the potential rate
of fat loss once folks are past the beginner stage. Even in the beginner stage, it’s generally always easier
to lose fat much faster than you can gain muscle.
So the idea of replacing every pound of lost fat with exactly one pound of muscle will be essentially
impossible for the intermediate/advanced trainee. There’s simply not enough fat/the fat cells dont want to
‘give up their calories’ and the ability to stimulate rapid muscle gains isn’t there any more.
A followup question might be what about fatter but more advanced trainees. Certainly in that situation, fat
cell insulin sensitivity/etc. can approach what is occurring with the overfat beginner but there is still the issue
of rate of muscle gain being drastically slowed. It’s probably possible briefly at the start of the diet to get
some caloric shunting but it’s never going to approach a 1:1 gain in muscle with fat loss; the potential rate
of fat loss (1-2 lbs/week) to rates of muscle gain (0.5 lbs/week if you’re lucky) simply doesn’t exist.
As a final comment, I can say without hesitation that someone will post in the comments that they managed
to achieve the above results in some form or fashion. And while there are always going to be exceptions to
any generality, that doesn’t tend to disprove the generality. And generally speaking, the above is what
happens in the real world.

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Carbohydrate Intake and Depression – Q&A
Question: I’m a 45 year old female. I currently weigh 221lbs. I’ve lost 30lbs in the last three months. My
protein intake is roughly 120 to 130 grams per day. I’m limiting my carb intake to 180 to 200 grams a day. I
suffer from life long depression and I find that when I limit by carb intake I slowly slide into a depressed state
after two or three months (it’s happening to me now). My sleep is disturbed, I develop anxiety I’m bitchy as
hell and I’m dragging ass. Is there a correlation between carb intake and production of neurotransmitters?
If so, how can I eliminate the effect lower levels of carbs is having on me? Any information is greatly
appreciated.

Answer: Dieting in general tends to lower serotonin in the brain and this can cause depression in susceptible
people. Interestingly, this effect seems to be more likely to occur in women than men (women being more
susceptible to depression in general). In my experience, low carbohydrate/higher proteins diets tend to be
even worse in this regards for reasons I’ll explain now.
First and foremost, nutrient intake per se affects the production of neurotransmitters with the effects being
both direct and indirect.
In a very direct way, specific amino acids are the precursors for specific neurotransmitters in the
brain. Tryptophan is a precursor for serotonin in the brain and the amino acid tyrosine (as well as
phenylalanine which converts into tyrosine in the body) is the precursor for dopamine (and subsequently
adrenaline/noradrenaline).
As an extreme example of this, researchers will sometimes use something called acute tryptophan depletion
(accomplished by providing an amino acid solution containing all of the amino acids except tryptophan) to
drastically lower brain levels of serotonin. This is used to test various things but, among other things, it tends
to cause acute depression in those who are susceptible. However, this is a pretty extreme type of
intervention, decreasing blood tryptophan levels massively (by about 80%); in dieting, tryptophan levels only
drop by about 10%.
As usual, it gets more complicated. The different amino acids have different transporters in the body and
some amino acids use the same transporter; this means that different amino acid can compete for transport.
Specifically relevant to this topic is the fact that both the branched chain amino acids (BCAAS), tyrosine and
phenylalanine and tryptophan all use a transporter called the Large Neutral Amino Acid (LNAA)
transporter. Again, this means that they compete for transport, meaning that levels of the different amino
acids can affect the transport of the other. Which means that the relative amounts of the different amino
acids will impact on how much is getting into a specific tissue in the body; in this case the brain.
If there is a large amount of tryptophan relative to the other LNAA, there will be greater serotonin production
in the brain; if there is less tryptophan relative to the other LNAA, there will be less tryptophan transport into
the brain and impaired serotonin production.
This brings us to one potential problem with higher protein intakes per se: most dietary proteins contain a lot
more LNAA than they do tryptophan. One exception is a derivative of whey called alpha-lactalbumin which
has the highest tryptophan content of any dietary protein; recent studies have found that consumption of this
protein can increase the ratio of tryptophan to the LNAA in the bloodstream, increasing brain serotonin
synthesis. For comparison, while most dietary proteins may ony contain about 2 grams of tryptophan per
100 grams, alpha-lactalbumin contains nearly 5 grams of tryptophan per 100 grams.
As well, there is an interaction with the carbohydrate intake of the diet. Diets very high in carbohydrates and
low in protein are known to raise plasma tryptophan and serotonin levels (which is probably why such diets
make some people sleepy and dopey). It’s worth mentioning that unless dietary protein is taken to

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exceedingly low levels (below 5% of total calories), the real-world impact of high-carbohydrates and low-
protein isn’t that massive in terms of its effect on serotonin levels in the brain.
However this may explain why some people who are prone to depression tend to crave low-protein/high-
carbohydrate foods at certain times (stress, seasonal affective disorder), they are trying to self-medicate
themselves and improve serotonin levels.
In any case, let me explain why carbohydrates can impact on all of this since this will help clear up why
lowering carbohydrates can cause problems.
The reason is this, the uptake of some of the LNAA (especially the branched chain amino acids) are insulin
sensitive; for example, when insulin levels go up, blood levels of the BCAA go down. This shifts the
tryptophan:LNAA ratio towards tryptophan such that more gets transported into the brain, potentially
increasing serotonin production.
The corollary to that is that when carbohydrates are reduced (and high quality dietary protein is increased),
there is the potential for serotonin levels to be reduced. Between the increased intake of LNAA from most
high-quality proteins, decreased clearance of them due to reduced insulin levels and the overall effect of
dieting in general on plasma tryptophan levels, this all adds up to problems for people at risk for depression.
Which is a long way of answering your question with a resounding yes.
Both dieting in general and low carbohydrate/higher protein diets in specific can cause issues with
depression in susceptible people. I do find it a bit surprising that what I consider fairly moderate intakes of
both protein and carbohydrates are causing you to experience this but some of it may depend on the depths
of depression you experienced (e.g. your genetic susceptibility).
It may also explain why it takes a good 2-3 months for your symptoms to show up, a very low carbohydrate
(e.g. 100 grams per day or less) and/or higher protein diet would probably cause things to go south that
much faster.
Ok, so that’s what’s going on, what are the solutions? I wouldn’t tend to generally recommend lowering
dietary protein and increasing carbohydrates (higher protein diets having a number of benefits in terms of
weight and fat loss) but, depending on the specifics of your situation (e.g. training, etc.) that might be one
option.
Assuming it isn’t, here are some things to consider:
1. Add the protein I mentioned above, alpha-lactalbumin to your daily protein intake. High in tryptophan, it
will help support serotonin synthesis. Consuming some near bedtime might help with sleep, taking it at other
times throughout the day may help with overall mood. In this context, I’d note that having a relatively higher
carb/lower protein meal at dinner time may help with some of the sleep issues.
2. Consider supplementing with 5-hydroxytryptophan. 5-HTP is another precursor to serotonin in the brain
that many have used to deal with depression and sleep problems. Doses seem to vary significantly but 50-
100 mg taken up to three times daily may be worth considering to keep serotonin levels from falling while
dieting.
3. Given that your symptoms only show up after 2-3 months of dieting, I’d strongly suggest taking a full diet
break (discussed in detail in A Guide to Flexible Dieting) between periods of active dieting. Basically,
perhaps every 2 months, take 2 weeks to raise calories and carbohydrates to restore brain serotonin levels
back to normal. Then you can enter another phase of active dieting, stopping before the depression really
sets in to take another full diet break. I think you get the idea.
I hope that helps and good luck.

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Dietary Guidelines on Fat Intake – were there ever any
evidence to support the low-fat recommendation?

In an effort to slash heart disease, the Dietary Guidelines for Americans [1] have since
1977 been urging people to:

1. Reduce total fat consumption to 30% of total caloric intake.

2. Reduce saturated fat consumption to 10% of total energy intake.

Government issued dietary guidelines are highly authoritative and regarded by a


majority as being backed by solid research. However, as it turns out, this is not the
case…

Dietary recommendations regarding intake of total and saturated fat are highly
controversial, and the debate is heating up. A recent systematic review and meta-
analysis of six studies that were available 1977, when the first version of the Dietary
Guidelines for Americans was published, shows: [2]

- Dietary interventions that reduce total and/or saturated fat intakes result in no
differences in all-cause mortality, and non-significant differences (meaning could be
due to chance) in coronary heart disease mortality.

- While lower total fat and saturated fat intakes led to significant reductions in mean
total cholesterol levels, this did not result in significant differences in coronary heart
disease or all-cause mortality.

————–
NOTE:

As I described in a previous article, total cholesterol levels tells nothing; it is a far too
crude measure. One has to look at each cholesterol and lipoprotein fraction, and their
respective particle distributions, in order to get an idea about the cardiovascular risk
profile. I covered this in more detail in a previous article “Blood Cholesterol Testing –
don’t let the routine standard lipid panel fool you!”

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In the context of this discussion, it is notable that replacing carbs with fat beneficially
reduces atherogenic lipoprotein (i.e. cholesterol carrying) particles.[3]

————–

Thus, the available randomized controlled trials (RCT; the gold standard type of study
in scientific nutrition research [4, 5]) clearly did NOT support the introduction of these
dietary fat recommendations in order to reduce heart disease and mortality.

Astonishingly, five of the six RCTs did not even examine either a total fat consumption
of 30%, or a saturated fat consumption of 10%, of energy intake.[2] The trials
investigated administration of vegetable oil, the replacement of saturated fats with
vegetable oil, and an approximate 20% fat diet. Only one single RCT examined the
consequence of a 10% saturated fat diet… and here comes the kicker… reported a
HIGHER incidence of all-cause mortality and coronary heart disease deaths in the low
saturated fat group.[6]

The conclusion from this analysis is:

“Dietary advice [on fat intakes] not merely needs review; it should not have been
introduced.”

Comments

Since the 1980s we have been indoctrinated by supposedly authoritative guidelines to


believe that dietary fat, and especially saturated fat, is “bad”. Even the most uneducated
citizens know how “bad” it is it to eat fat, right!?

This undue focus on total fat and saturated fat as a dietary villain for heart disease has
greatly distracted attention away from the risks posed by other foods and nutrients, such
as carbohydrates [7-12], processed foods [13-16], and fruits/vegetables.[17-20] In
addition, we have to remember that it is not just about eating too much of something
harmful; too little of something health promoting may be as deleterious for our health
and wellbeing. This brings up the issue of reductionism vs. holism [21], i.e. the
importance to look at the whole dietary picture. This is especially important when it
comes to saturated fat intakes, as the carbohydrate content of the overall diet will

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tremendously impact how the body metabolizes ingested fats.[22, 23] In addition, if you
reduce intake of one thing, what you replace it with may be even more important.[8, 24]

Perhaps the most disturbing issue is that guidelines originating from authorities are
supposed to be evidence based; meaning, based on the totality of evidence.[25] Thus,
even if the government issued dietary goals back in 1977 were wrong, one would expect
that the accumulating body of scientific evidence over the past few decades, showing
that dietary fat is not a villain [26-32], would have impelled the authorities to modify
their recommendations….not so!

We can only hope that the 2015 edition of the Dietary Guidelines for Americans – after
38 years – will embrace the fact that science (including nutrition science) is an evolving
discipline and finally update their old-school low-fat mantra … the world is not flat
anymore!

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Dieting Psychology Versus Dieting Physiology
Over the next series of articles, I want to look at both physiological and psychological reasons that diets can
fail.
But before doing that I need to make something very clear: the distinction I’m making between psychology
and physiology is simply for convenience, it’s not one that really truly exists.
That is to say, psychology impacts on physiology and physiology impacts on psychology and the days of
pretending the body and mind are separate non-interacting entities are long, long gone. Again, I’ll make the
separation primarily for reasons of convenience, it will save me some needless complexity in the upcoming
discussion. Just keep in mind that it’s an artificial and non-existent separation in reality.
Modern science, for example the field of psychoneuroimmunology, recognizes that the brain and body are
in a constant state of interaction and involvement with one another. This is sort of the basis for the idea that
you can think yourself sick, or for the idea that people with a more positive attitude are more likely to survive
certain diseases (such as cancer). Your thought processes can impact on such workings of your body as
immune function.
Put more simply, how you think affects how your body works and how your body works can affect how you
think or feel.
Incidentally, for anybody who is interested in this topic, I would highly, highly, highly recommend almost any
of the books by science writer Robert Sapolsky, especially his book Why Zebras Don’t Get Ulcers where this
topic is discussed in some detail (primarily wrt: cortisol and stress). This is literally one of my top-5 books
ever and I cannot recommend it too highly.
Anyhow, while you’re sitting there reading this, I want you to start thinking about something that really makes
you angry. Taxes, gas prices, my inability to blog consistently, take your pick. Really get a good anger going.
Now stop for a second and pay attention to your body: odds are that your heart rate is up, if we measured
blood pressure it would be increased too, you might be breathing a little bit harder, you get the idea. The
mere act of thinking about something that upset you had a strong physiological effect throughout your body.
Here’s another example in the reverse direction: everybody knows how they get really lethargic and lazy
when they are sick with something like the flu or a bad cold or what have you. It’s as if when you are sick
your body is deliberately trying to get you to lay around all day and rest. This turns out to basically be the
case.
When you are sick, your body releases short-lived chemicals called cytokines, some of which are
inflammatory. Inflammatory cytokines, in addition to making you feel like warmed over crap when you have
the flu or something, they also directly impact on the brain and your motivation to move around.
I’d note that a similar mechanism has been suggested as a primary cause of overtraining; called the cytokine
hypothesis of overtraining I think it ties together a lot of conflicting and contradictory data on the topic. It
explains changes in performance along with behavior and ties together the previous held (but wrong idea)
of local versus central overtraining. It turns out that they are the same thing and local effects (tissue damage)
is causing central effects (behavior and motivation changes).
Essentially constant/chronic/excessive inflammation locally (in the muscles you’re training) causes an
increase in inflammatory cytokines and this is responsible for the lack of motivation to train and lethargy that
often sets in. Essentially, your body (your muscles) are trying to ‘tell’ your brain to give it a rest and take
some down-time. Of course, humans, being the stubborn folks that we are, often choose to ignore or over-
ride these signals.
This has a lot of relevance to the issue of dieting failure which is what I’ll be talking about next.

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Ketogenic Low-Carbohydrate Diets have no Metabolic Advantage
over Nonketogenic Low-Carbohydrate Diets – Research Review

Title and Abstract

Johnston CS et. al. Ketogenic low-carbohydrate diets have no metabolic advantage over nonketogenic low-
carbohydrate diets. American Journal of Clinical Nutrition. (2006) 83: 1055-1061
Background:Low-carbohydrate diets may promote greater weight loss than does the conventional low-fat,
high-carbohydrate diet. Objective:We compared weight loss and biomarker change in adults adhering to a
ketogenic low-carbohydrate (KLC) diet or a nonketogenic low-carbohydrate (NLC) diet. Design:Twenty
adults [body mass index (in kg/m2): 34.4 ± 1.0] were randomly assigned to the KLC (60% of energy as fat,
beginning with 5% of energy as carbohydrate) or NLC (30% of energy as fat; 40% of energy as carbohydrate)
diet. During the 6-wk trial, participants were sedentary, and 24-h intakes were strictly
controlled. Results:Mean (±SE) weight losses (6.3 ± 0.6 and 7.2 ± 0.8 kg in KLC and NLC dieters,
respectively; P = 0.324) and fat losses (3.4 and 5.5 kg in KLC and NLC dieters, respectively; P = 0.111) did
not differ significantly by group after 6 wk. Blood ß-hydroxybutyrate in the KLC dieters was 3.6 times that in
the NLC dieters at week 2 (P = 0.018), and LDL cholesterol was directly correlated with blood ß-
hydroxybutyrate (r = 0.297, P = 0.025). Overall, insulin sensitivity and resting energy expenditure increased
and serum -glutamyltransferase concentrations decreased in both diet groups during the 6-wk trial (P <
0.05). However, inflammatory risk (arachidonic acid:eicosapentaenoic acid ratios in plasma phospholipids)
and perceptions of vigor were more adversely affected by the KLC than by the NLC diet. Conclusions:KLC
and NLC diets were equally effective in reducing body weight and insulin resistance, but the KLC diet was
associated with several adverse metabolic and emotional effects. The use of ketogenic diets for weight loss
is not warranted.

Introduction

Pretty much without fail, every decade seems to see the resurgence of the idea that extremely low-
carbohydrate diets have a ‘metabolic advantage’ over carb-based diets; that is the claim is made that the
very low-carbohydrate diet will generate more weight or fat loss at the same (or sometimes even a higher
calorie level).
Now, before I continue let me say that I have nothing against low-carbohydrate diets. My first book The
Ketogenic Diet was about nothing but and many of my dietary approaches often have low- or at least lowered
carbohydrate phases to them as they tend to generate certain biological effects that I’m seeking.
As well, research clearly shows that, for some people, lowering carbohydrates can have profound health
benefits and in some cases a near removal of dietary carbohydrates (except for things like fruits and
vegetables) may be profoundly beneficial.
However, the weight and fat loss claims are a bit trickier. There is certainly an element of truth to the idea
that low-carb diets generate more total weight loss but this issue is confounded by the issue of water
loss. Between a drop in insulin (insulin causes the kidney to resorb water) and a dehydrating effect of
ketones themselves, very-low carbohydrate diets can cause significant water loss.
As I discussed at length in The Ketogenic Diet, water loss can range from 1-15 pounds depending on size
(even small individual may lose a rapid 3-4 pounds, of primarily water, in the first days of carbohydrate

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restriction). This tends to make comparisons of weight loss pretty meaningless. This is even more true
when you consider that the difference in total weight loss between low- and high-carb diets is usually only a
few pounds anyhow.
However, other recent studies have used more accurate methods of measuring body composition and
several do seem to find a greater fat loss for the low-carbohydrate diet compared to the higher carbohydrate
diet. Often with the low-carbohydrate diets reporting that they are eating the same (or occasionally) more
calories. Aha, a metabolic advantage.
Well…maybe.
I have two primary issues with most of the studies that have been done, one of which I referred to
above. That is the issue of caloric self-reporting. The grand majority of studies done to date have allowed
people to self-report their food intake and this introduces a staggering number of issues. Because, simply,
people really suck at it. Relying on them to tell you how much they are actually eating means not having
any real idea as to what’s going on.
The other, potentially bigger issue, revolves around protein intake. In general, and this is especially true if
you are comparing a typical very-low carbohydrate diet to a high-carbohydrate diet, the lower carbohydrate
diet will contain significantly more protein.
This is simply a function of what foods can be eaten on the diet. Logically, when most of your diet revolves
around meat, you will tend to eat more protein than when it doesn’t. But this tends to make comparing the
diets problematic for reasons I discussed in the article Is a Calorie a Calorie.
Now, at this point there is little to no debate that higher protein diets have a number of inherent benefits to
lower protein diets. Benefits to dieters include increased satiety, better maintenance of metabolic rate while
dieting, better blood glucose maintenance, less lean body mass loss and others I’m sure I’m forgetting.
But now we’re not talking about ‘low-carbohydrate diets’ per se, we’re talking about ‘high-protein diets'; that
is the comparison is no longer about the carbohydrate content of the diet but about the protein content. In
fact, some researchers argue that the ‘benefit’ of supposed low-carbohydrate diets comes from the increased
protein intake, rather than the carbohydrate content per se.

In any case, that’s a brief look at the two main issues I have with a lot of the low-carbohydrate vs. other diet
research that is out there. Between self-reported food intake (which tends to be all over the map) along with
variable protein intake (with the low-carbohydrate diet group usually eating more protein), it’s hard to draw
any solid conclusion about what’s actually going on.

The Study

Enter the study I want to look at today; while it’s a couple of years old it does a good job of addressing both
of the issues I brought up above (in fact, their introduction and mine cover basically the same exact issues).
Researchers recruited 20 overweight subjects (which they admitted was a small sample size), both men and
women and placed them on either a ketogenic low-carbohydrate diet (essentially an Atkins type of diet) or a
moderate-carbohydrate non-ketogenic diet (like the Zone and it’s worth noting that Barry Sears is one of the
authors on the paper) for 6 weeks. Exercise was not performed.
The researchers examined a number of different variables including fat loss, insulin sensitivity, blood lipid
levels, inflammation and energy levels. Resting metabolic rate was also measured.

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One nice thing about this study is that the researchers went out of their way to make sure that both diets
were equal in both calories and protein (almost anyhow, the very low carb diet was a touch higher in
protein). The composition of both diets appears in the table below:

Ketogenic Diet Non-Ketogenic Diet

Calories 1500 1500

Protein (Grams) 125 117

Carbohydrate (Grams) 33 157

Fat (Grams) 100 50

The ketogenic diet was also slightly higher in saturated fat than the non-ketogenic diet (21% vs. 9% of the
total calories).
Now, you might be wondering how the researchers ensured that the diets were actually met; another strength
of the study was that all food was provided to the study subjects. Lunches were actually prepared and
served to the subjects at the testing facility Monday through Friday; all other meals were prepared for the
subjects to take home with them for consumption. This is likely the reason that the sample size was so
small, it gets expensive to provide all food to subjects in studies like this.

The Results

In terms of weight and fat loss, at the end of 6 weeks both groups had lost roughly the same amount of
weight (6.3kg for the ketogenic diet, and 7.2 kg for the non-ketogenic diet; this was not statistically
significant). As well, the loss of body fat was the same (3.4 kg in the ketogenic diet and 5.5 kg in the non-
ketogenic diet; again this was not statistically different even if the non-ketogenic diet seems to have lost ~4
pounds more fat). There was no significant change in fat free mass for either diet.
It’s worth noting that body composition measurements were made with a Tanita BIA device; as I discussed
in Measuring Body Composition Part 2, BIA has its share of problems and can be thrown off by hydration
status, which is affected by the carbohydrate content of the diet. It would have been nice had the study used
a more accurate method; one not so impacted by hydration state.
Hunger ratings improved for both diets with no difference between diets. An oft-heard claim is that ketogenic
diets cause hunger blunting due to the presence of ketones or what have you; but this study does not support
that. Given that protein is the most filling nutrient, the effect seems to be mediated by the increased protein
content, not decreasing carbohydrates per se.
Somewhat oddly, the researchers found that weight adjusted resting energy expenditure went up but as it
did so equally in both groups, this was more likely related to the protein content of the diets (remember,
identical) than the carbohydrate intake per se.
Looking at blood lipids, the results were actually quite mixed. Low-density lipoprotein (LDL) went up in 5 of
the ketogenic dieters and down in the other 4; LDL went up in 2 of the non-ketogenic dieters and down in
the remaining 8. HDL levels fell in both groups.
The researchers also found that one marker of inflammation was significantly higher in the ketogenic diet
compared to the non-ketogenic diet; no explanation for this was given. Some studies link saturated fat to
inflammation and the slightly higher saturated fat intake in the ketogenic diet might have been part of this.
Insulin sensitivity was improved in both groups with no differences between the diets.

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In terms of energy levels, there were no differences except that the non-ketogenic dieters scored higher on
a rating of vigor-activity than the ketogenic dieters. I’d note that, in my experience, the response to full blown
ketogenic diets is highly variable: some people feel awful and others feel completely energized.
This tends to show an interaction with insulin sensitivity as I discuss in Insulin Sensitivity and Fat Loss with
individuals with poorer insulin sensitivity often feeling fantastic on low-carb diets and vice versa. As well,
ensuring adequate mineral intake (sodium, potassium, magnesium, calcium) tends to be key to limiting
fatigue on very-low carbohydrate diets.
Summing up, the researchers conclude:
In the current study, the KLC [ketogenic low-carb] diet did not offer any significant metabolic advantage over
the NLC [non-ketogenic low-carb] diet. Both diets were effective at reducing total body mass and insulin
resistance, but, because blood ketones were directly related to LDL-cholesterol concentrations and because
inflammatory risk was elevated with adherence to the KLC diet, severe restrictions in dietary carbohydrate
are not warranted.
Well….maybe.

My Comments

This study certainly has a couple of strengths, controlled calorie levels (with food provision) and equal protein
intake between groups being the two main ones. Weaknesses are the small sample size and the use of
Tanita body fat measurement to track body composition. Changes in water balance can affect that method
significantly and diets that manipulate carbohydrate content tend to impact significantly on water levels in
the body.
With that said, this study adds to the data set suggesting that, if calories and protein intake are identical,
there is little to no metabolic advantage (in terms of fat or weight loss) to full blown ketogenic diets. They
work at least as well, mind you, but not better.
Now, as I discuss in the series of articles on Comparing the Diets, there still may be circumstances where
very-low carbohydrate/ketogenic diets may still be preferred, even given the researchers comments above.
For many individuals, the biggest ‘metabolic advantage’ of very-low carbohdyrate diets may be one of
food/calorie control. Many people seem to show what might be popularly called ‘carbohydrate addiction’ (a
term that is massively debated among obesity researchers) where eating even small amounts of carbs
makes them want to eat more. In that case, a full blown removal of carbohydrates from the diet may be the
only realistic way to limit caloric intake.
Related to this, for many, spending time on a very-low carbohydrate diet seems to change taste preferences:
carbohydrates can often be reintroduced after some period without the loss of food control that occurred
prior to the diet.
I mentioned in the introduction that severely insulin resistant individual seem to get health benefits from
extreme carbohydrate restriction. For leaner dieters, as I discuss in both The Ultimate Diet 2.0 and The
Stubborn Fat Solution, extreme carbohydrate restriction tends to help with stubborn lower body fat
mobilization.
But clearly in other situations, moderate carbohydrates diets (still containing sufficient protein mind you) may
be superior. For people who can control their food intake, many simply feel better with more moderate
carbohydrate intakes, their training (especially high intensity training such as weights) doesn’t suffer as
much, and they don’t feel quite as lethargic. Again, these issues are discussed in detail in the Comparing
the Diets series.

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I guess my point is that there is too much variance between individuals and their needs to claim that any
single diet is inherently superior for all people and all situations. As this study suggests, given identical
calories and protein intake, there doesn’t seem to be any inherent metabolic advantage in terms of total fat
loss to a full blown ketogenic diet, at least not when compared to a moderate carbohydrate diet with an
identical amount of protein.
As I’ve noted above, there may be other ‘advantages’ unrelated to fat loss that are still important. Basically,
the choice of diet may come down to other issues than fat loss per se. A diet that makes someone feel
terrible isn’t one that they are likely to stick to for very long; a diet that does is one that may be the ‘superior’
one for that person.
Finally, finally, if you want to hear more about my thoughts on this whole issue, Jimmy Moore of the Livin La
Vida Lowcarb blog has just put up an audio interview we did a couple of months ago. We talk about
everything related to low-carb diets you could imagine.

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Is Fat the Preferred Fuel Source in the Body – Q&A
Question: I’ve seen it claimed (by members of the paleo diet movement) that fat is the preferred fuel source
of the body and, for that reason, dietary fat should make up a large part of the diet (i.e. 40-70% of total
calories). Is this true?

Answer: Ok, before addressing this question in terms of the physiology involved, I want to get a little bit
pedantic (or at least semantic) and look at what it means for something to be ‘preferred’. According to the
dictionary definition preferred means “more desirable than another” but what does that really mean?
Let’s say that you’re thirsting for a caffeinated beverage so I offer you two drinks, coffee and tea. Since you
like coffee more, you choose to drink coffee. In this case, coffee is preferred. Let’s contrast that to a situation
where I offer you tea or nothing. You choose tea because it’s the only option available. In that second
situation, tea wouldn’t really be your preferred choice (a true pedant would argue that you still preferred it to
nothing but bear with me), it’s a choice by exclusion: you’re thirsty and with only one option you drink what
you’re given. Don’t worry I’m getting to the point.
So let’s turn to human physiology and talk about what fuel the body ‘prefers’ to use, with the above definition
in mind. Now, for the most part, all tissues in the body can generate energy (ATP for the biochemically
minded) from either glucose or fatty acids. There are a few exceptions, mind you; the brain uses almost
exclusively glucose but shifts to mostly ketones under certain conditions. What the brain can’t use is fatty
acids directly for energy. There are a couple of other weird ones, a handful of tissues in the body that only
use glucose: the retina is one, part of the kidney, there’s a third I’m forgetting. There’s one other exception
to this that I’ll come back to at the end.
But ignoring those exceptions most tissues can use either fatty acids or glucose for fuel (there is a separate
issue of metabolic flexibility, the body’s ability to shift back and forth but that’s getting into a different
topic). And although both are stored in the body to be sure, this has to do with dietary intake, carbohydrates
versus fat intake.
So what happens when you provide the body with both carbs and fats in the diet? Which fuel source is
preferred? Well the answer is clear: carbs. That is, when you give the body both carbs and fats (or more
generally when carbs are available), the body will use the carbs for fuel and store the fat. Carbs are clearly,
by the definition I bored you with above, the preferred choice. Reiterating: if the body is given a choice of
carbs or fats, it will prefer carbs for fuel. No question and no debates.
Now, if you remove all of your dietary carbohydrates, as in a low-carbohydrate/ketogenic diet, the body does
make a huge shift towards relying almost exclusively on fatty acids (and ketones) for fuel. But this is akin to
my second example above, when I only offered you tea; it’s only a choice by exclusion where the body
switches to using predominantly fats for fuel because that’s all that is available. But that’s not the definition
of preferred; it’s only a choice relative to nothing.
So, you ask, where did this idea that fat is the preferred source of fuel by the body come from? Mind you,
it’s not new and the paleo diet people aren’t the first to make this claim. Well remember the other exception
I mentioned above to the general idea that most tissues in the body can and (and in fact) will use glucose or
fat depending on what’s available?
That exception is heart (cardiac) tissue. For fairly logical reasons (i.e. the heart can’t ever be in a situation
where energy isn’t available) cardiac muscle tissue prefers fatty acids to glucose for fuel. But it’s the lone
exception in the body and certainly (and fairly obviously) is not representative of the rest of the body.
So while it’s clear that the body can and will shift fuel source choice depending on what’s available, the idea
that ‘fat is the preferred fuel source in humans’ is incorrect.

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Ketosis, Carbohydrates and the Brain – Q&A
Question: I’ve been doing the CKD effectively. However, I have a major exam on Friday. Is there any effect
on limited carbs on cognitive processes? Does limiting carbs ( 20g / day) have a negative effect or could it
retard my performance on a major exam, i.e. MCATs, Series7, etc? Is there any study or suggestion you
could give based on your research?

Answer: First a quick definition for anyone who isn’t familiar with the abbreviation: as discussed in the
Comparing the Diets Series , a CKD refers to a cyclical ketogenic diet. This is simply a diet that alternates
between periods of very low-carbohydrate eating (typically 4-6 days) and very high-carbohydrate eating (1-
3 days). Dan Duchaine’s Bodyopus, Mauro DiPasquale’s Anabolic Diet and my own Ultimate Diet 2.0 are
all examples of CKD’s. My first book The Ketogenic Diet discusses CKD’s generally in mind-numbing detail.
Now back to the question: does ketosis negatively impact on cognitive function? And the answer is one
huge it depends. Certainly early studies found that, in the short-term (first 1-3 weeks), low-carbohydrate
diets tend to cause some problems. For this reason short-term studies (usually a week long) tend to report
decrements in a lot of things including cognitive performance.
Empirically, as well, many report fatigue, lethargy and a sort of mental ‘fog’ until they adapt to the diet (the
brain adjusts to using ketones for fuel over those first 3 weeks). I’d note that supplementing with sodium,
potassium and magnesium seems to go a long way towards limiting or eliminating that feeling of fatigue.
So, for most I certainly wouldn’t recommend starting a very low-carbohydrate/ketogenic diet right before
some major test or cognitive challenge. Odds are it’s going to cause problems.
But what about someone who has adapted to being in ketosis. There there tends to be huge variance. Some
people are sort of neutral to it but I know of many who report far better brain functioning when they are in
ketosis. I couldn’t tell you the mechanism, this is just one of those self-reported things. But it tends to be
highly variable (and I can’t think of any studies that have examined cognitive performance after long-term
adaptation to low-carbohydrate diets).
CKD’s add another complication, outside of some exercise research on Cyclical Ketogenic Diets and
Endurance Performance that looked only at performance, I’m unaware of any work on CKD’s and cognitive
performance. I bring this up as some people do report changes switching back and forth between very low
and very high carbohydrate intakes.
Quite in fact, many who find that they feel ‘great’ in ketosis feel a bit dopey or sleepy when they switch back
to high carb intakes. This is probably related to either blood glucose swings or a big increase in brain
serotonin (which tends to cause lethargy and fatigue) but it does occur.
Similarly, some seem to go through at least a brief re-adaptation (in terms of fatigue, etc.) going back from
high carbs to low-carbs. Again, this is pretty variable, many people can switch back and forth from one
extreme to the other and don’t seem to notice anything. I have no idea why, just reports I’ve seen.
So back to the question, should you switch out of ketosis for your test? It’s a hard question to answer and
you’d have to think back to your previous switches from low- to high-carbs during the CKD. If you find that
you’re fully adapted to ketosis and function fine mentally, and that you get dopey going back to high-carbs,
I’d probably suggest you stay on low-carbs through the test.
If you’re one of those people who don’t seem to have ever fully adapted to being in ketosis (they do exist),
you might want to move back to at least moderate carbs a day or two before your test. Unfortunately, there’s
just too much variability for me to give you any advice beyond that.

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Ketosis and The Ketogenic Ratio – Q&A
Question: Do you still believe in the ketogenic ratio for getting into ketosis? I am having trouble showing
ketones. Any tips? Sorry to bother you again but can drinking 2 gal of water per day dilute your urine so you
don’t show ketones?

Answer: Ok, let me take these on one at a time.


In my first book The Ketogenic Diet, I talked about something called the ketogenic ratio (KR) which is an
equation/concept used in the planning of ketogenic diets for epilepsy patients. The equation basically gives
you the potential ketone producing potential of a given meal depending on the relative ketogenic or anti-
ketogenic effect of the different macronutrients.
So the KR of a given combination of nutrients can be estimated with the following equation:

Protein turns out to be partially ketogenic (46%) and partially anti-ketogenic (58%), reflecting the fact that
some amino acids can be made into ketones, while other are made into glucose). Carbohydrate is 100%
anti-ketogenic and fat is mostly (90%) ketogenic (the 10% anti-ketogenic is due to the fact that the glycerol
portion of triglycerides, explained in A Primer on Dietary Fats, can be converted to glucose in the liver).
Quoting from that section of The Ketogenic Diet:
This equation represents the relative tendency for a given macronutrient to either promote or prevent a
ketogenic state (1). Recalling from the previous chapter that insulin and glucagon are the ultimate
determinants of the shift to a ketotic state, this equation essentially represents the tendency for a given
nutrient to raise insulin (anti-ketogenic) or glucagon (pro-ketogenic).
For the treatment of epilepsy, the ratio of K to AK must be at least 1.5 for a meal to be considered ketogenic
(1). Typically, this results in a diet containing 4 grams of fat for each gram of protein and carbohydrate, called
a 4:1 diet. More details on the development of ketogenic diets for epilepsy can be found in the references,
as they are beyond the scope of this book.
However, invariably when people tried to apply the KR to low-carbohydrate fat loss diets, one of two things
happened. If the person set calories appropriately and used the KR, the protein intake ended up being far
too low (because dietary fat had to be so damn high). Alternately, if they set protein appropriately and tried
to scale dietary fat to the proper ratio, the caloric intake ended up being too high.
The former was a poor choice from the standpoint of protein sparing; the second limited (or eliminated fat
loss).
So basically I threw out the ketogenic ratio. As noted above, it’s crucial for the development of epilepsy
treatment diets (anyone wanting more information on this topic should purchase the excellent The Ketogenic
Diet: A Treatment for Epilepsy by Freeman, Freeman and Kelly.
But for dieters and folks seeking body recomposition, it made setting up appropriate diets impossible.
Additionally, there isn’t convincing evidence in my opinion that ketosis is crucial for the benefits of the diet.
Yes, ketones are protein sparing but only when dietary protein intake is inadequate in the first place. When
protein is set appropriately (e.g. 1-1.5 g/lb lean body mass as discussed in The Protein Book), the
development of ketosis isn’t that critical to spare protein. Simply, protein is the most protein sparing nutrient
and other things (e.g. ketones vs. carbohydrates) only matter if protein is inadequate in the first place.
Even the hunger blunting effects of ketosis is up to debate and much of the recent literature on the topic
suggests that it is actually the increased dietary protein intake that is causing the decreased hunger, rather
than the presence of ketones per se.

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Which is a long way of saying that I don’t think that the ketogenic ratio, or even the development of ketosis
is important to the overall success (or failure for that matter) of low-carbohydrate diets. In the Ultimate Diet
2.0, I addressed this rather explicitly in a section titled “What About Ketosis?”

For the most part, I simply see ketosis as a “side-effect” of fat loss (burning to be more accurate), more than
something to be explicitly sought out. That is, when you accelerate fat oxidation with the methods above,
you tend to enter ketosis. Ketosis in and of itself isn’t any big deal. For that reason, I won’t talk about
monitoring ketone levels with Ketostix or anything like that. Frankly, using a low-carbohydrate/ketogenic diet
for the fat loss phase of the UD2 has more to do with lowering insulin, raising catecholamines, and ramping
up fat oxidation; ketosis is simply a tangential effect.
Which brings me to your second set of questions. For background, low-carb dieters have often used a
product called Ketostix which change color to indicate the concentration of ketones in the urine. Yes, you
pee on them and they change color to indicate the presence or absence of ketones in the urine.
There are a number of problems with Ketostix not the least of which is that urinary ketone concentration is
at best a very indirect indicator of what’s going on in the body. True ketosis is defined in terms of blood
concentrations (terms ketonemia), not urine (terms ketonuria). But since you can’t easily measure ketones
in the blood (no, you can’t put blood on the Ketostix, I tried it years ago and it doesn’t work), the next best
thing is urinary ketones.
Now, obviously, if you have ketones in your urine, you certainly have them in your bloodstream. However,
the absence of ketones in the urine doesn’t mean that you’re not still in ketosis (as defined by blood
concentrations). You might be in ketosis as measured by blood levels but simply not be excreting any in the
urine. Or not excreting enough to change the Ketostix.
Basically, there are a variety of things that influence whether or not there are enough ketones present to be
excreted in the urine in sufficient quantities to make the Ketostix change colors. For example, you might not
be making ketones in sufficient quantities (this happens in lean people, especially if they are very active),
lots of water can dilute your urine and the ketone concentration, some other variables can impact on whether
or not you show ketones on the Ketostix.
As you might imagine, at the end of the day, I don’t think focusing on ketosis per se (or the lack thereof) or
the Ketostix is very valuable. You can develop deep ketosis by gorging on dietary fat (especially Medium
Chain Triglycerides) but your calories will be so high that you won’t be losing much, if any fat, that way. And
you can lose fat without ever showing a single ketone in the urine. Basically, there’s just no real correlation
between ketosis, what the Ketostix are showing and fat loss.
Basically, I have seen too many dieters focusing on the Ketostix instead of what’s important: relative amounts
of fat and lean body mass lost. Focus on the latter, if you’re losing fat and maintaining lean body mass, your
diet (low-carbohydrate or otherwise) is working, whether you are in ketosis or not.

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Metabolic Rate Overview
In the article You Are Not Different, I made reference to the concept of energy balance and it’s time to expand
on that concept. In the most simplistic form, we can define energy balance as Energy balance = energy in –
energy out.
Energy in is food, since this is the only place that human can absorb energy (calories and joules are both
measures of energy). That side of the equation is relatively simple, just add up your total caloric intake.
Actually it’s not because the different macronutrients are handled a little bit differently from one another so
it’s not simply calories, but that’s another topic for another section. Energy out is the topic of the next several
chapters but ultimately represents how many calories you expend in a day.
Long-term changes in energy balance are what ultimately determine what happens to the body. A long-term
excess of energy balance (energy in exceeds energy out) will lead to a gain of body mass; a long-term deficit
in energy balance (energy out exceeds energy in) leads to a decrease in body mass. Whether that changed
body mass is made up of fat, muscle, or some combination depends on a few factors.
It’s the energy out side of the equation, usually referred to as metabolic rate, that I want to talk about now.
Over the next several chapters, I want to address the various components of metabolic rate, as well as how
they are affected by such things as obesity, gender, exercise, diet, etc. This will ultimately lead into a
discussion of setting calorie levels for different goals. I’ll be throwing around three letter acronyms (TLAs)
like mad in these chapters so be forewarned.
Most sources differentiate four different components of total energy expenditure (TEE): basal or resting
metabolic rate, the thermic effect of activity, the thermic effect of food, and an adaptive component. Lets look
at each.

Basal or Resting Metabolic Rate (BMR or RMR)

Although many sources tend to use these terms interchangeably, they are not really the same thing. Both
roughly represent the number of calories needed to sustain the body’s most basic functions, which I’ll discuss
in a second. The real difference comes in how they are measured. Basal metabolic rate (BMR) technically
refers to the absolute minimum amount of energy needed by your body to sustain itself. A true measurement
of BMR requires that you be sleeping which is impractical (you’ll sometimes see it referred to as sleeping
metabolic rate or SMR in research).
Instead, most studies and labs measure resting metabolic rate (RMR) instead. RMR is measured in the
morning before eating, while resting quietly and generally gives values that are 5-15% greater than true BMR
(even being awake means you burn slightly more calories). But it is far more practical to measure RMR in
most cases and it’ll be what I refer to from now on.
As stated above, RMR refers to the energy needed to sustain the body’s most basic functions. As you sit
reading and growing more bored by the minute, literally thousands of cellular reactions are proceeding within
your body. Your brain is using glucose for fuel, your eye muscles are using energy as you scan the page,
your heart is beating, your muscles are somewhat tense as you sit in the chair. Protein in your muscles is
being broken down and resynthesized, as are fatty acids in your fat cells (these are called futile cycles since
they don’t really accomplish anything but they do require energy). Your cells are constantly cycling sodium
into the cell and potassium out (called the Na/K+ pump) using up energy in the process. On and on it goes
and all of it uses energy.

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So you know, adenosine triphosphate (ATP) is the ‘currency’ of energy used by the body at its most
fundamental level; it is the only substance that can be used directly for energy production. Other substances
(i.e. carbohydrate, fat, protein and alcohol) are used to produce ATP.
RMR is determined primarily by the amount of lean body mass you have. Although it varies somewhat from
study to study, the amount of LBM appears to predict roughly 65% of the variance in RMR is attributed to
differences in lean body mass. That is to say, more lean body mass will mean a higher RMR and vice versa.
Given all other things equal (and they never are), someone with more lean body mass will have a higher
RMR. To be honest, total body weight gives a damn good estimate of RMR even if you don’t factor in lean
body mass but LBM is probably a better predictor.
I want to be clear that here I’m using lean body mass generally to include muscle. organs, brain, etc. Quite
in fact, your muscles don’t actually use that much total energy on a daily basis. Despite making up nearly
40% of your total body mass, muscles only contribute about 25% of your total RMR. In contrast, your organs
account for nearly 60% of your total RMR because they are so much more active.
Contrary to popular belief, fat does use a small amount of calories and also contributes to RMR. It’s not huge
mind you, maybe 3 calories per pound but it adds up. Someone carrying 50-100 lbs of fat is burning 150-
300 calories per day to sustain that fat.
Gender also affect RMR. Bad news for the ladies, on average men have a higher BMR than females. Some
of this is simply a consequence of having more LBM. That is, at any given body weight, a male will typically
have less fat and more LBM. But even if you factor out those differences (and all of the rest), women still
typically run about a 3% lower BMR than men. The cause is probably hormonal, differences in the levels
(and sensitivity) to hormones such as leptin, thyroid, insulin, the catecholamines. Even estrogen and
progesterone affect BMR slightly. However, it gets even more complicated than that: during a woman’s
menstrual cycle, BMR can vary quite a bit.
Age also affects RMR, as folks get older, RMR decreases slightly. Some of this decrease is simply an effect
of losing lean body mass but some of it probably represents a general slowing down of bodily functions.
If you include other variables such as fat mass, gender, and age, you can predict about 85% of the variance
in RMR. That is, knowing LBM, fat mass, gender and age, you can predict RMR with about 85% accuracy.
That still leaves 15% unaccounted for; that 15% is basically the genetic lottery. But let’s put that 15% in
perspective.
Say you have two people with an estimated RMR of 2000 cal/day (ignore for now how we’ve estimated it)
based on the above factors. That value could actually vary by 15% (300 cal/day) or so. That’s 300 cal total
variance or 150 cal/day either way. So you might see actual RMR values as high as 2150 cal/day or as low
as 1850 cal/day. This gets into the genetics stuff I talked about very early on in this book and relates to both
weight gain and loss.
Someone with a low relative metabolic rate (which typically accompanies some other defects such as
decreased fat oxidation and problems regulating hunger and appetite) is going to be predisposed to obesity
if they are given a typical American diet. As well, given the same type of fat loss diet, they aren’t going to
lose as quickly. Either they will have to cut calories more, do more activity (i.e. exercise), or simply accept a
slower rate of weight/fat loss.
Once again, look at our two folks from above, with a predicted metabolic rate of 2000 cal but a variance of
300 cal/day either way. If we put both folks on a 1500 cal/day diet, we would expect vastly different results.
The person with a metabolic rate of 2150 cal/day is creating an 650 cal/day deficit, just over a pound a week
fat loss. The person with a metabolic rate of 1850 cal/day is only generating a 350 cal/day deficit, barely 0.5
lbs/week weight/fat loss. To achieve the same rate of loss, the second person would either have to cut

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calories by 500 (to a piddly 1000 cal/day), increase activity significantly (an hour plus of aerobics or so), or
some combination of the two.
Research is currently underway to determine what the specific defects are which lead some people to have
a lower than normal metabolic rate. While the specific factors haven’t been worked out, it likely represents
differences in levels of various hormones (insulin, thyroid, leptin, the catecholamines) as well as overall
sensitivity to those hormones. Other genetic variations, for example in UCP (see below) may also play a
role.
As we’ll see in the next chapter, the decrease in RMR with dieting is partially due to dropping levels of insulin,
thyroid, catecholamines and especially leptin. Increases in RMR with overfeeding occur for the reverse
reasons.
There is some debate over whether exercise affects changes RMR. Some studies have documented a
higher RMR (for body weight) in aerobically trained athletes compared to sedentary folks, but others have
not. Any effect is likely to be small.
Weight training, by increasing muscle mass, should have a small effect on BMR as well although not all
studies have shown this to be the case. Unfortunately, the most recent research points out just how small
the effect is: at rest, a pound of muscle burns about 6 calories. The old values of 40-100 cal/lb were simply
vast overestimations and unless you can add an absolute ton of muscle mass, you’re unlikely to increase
resting metabolic rate significantly (not that adding muscle doesn’t have other benefits).
Overall, RMR makes up anywhere from 50-70% of your total daily energy expenditure. If you’re wondering
about the spread, it has to do with the variable nature of activity. For someone expending a massive amount
of calories per day in exercise (think an endurance athlete spending 4+ hours training), RMR will make up
relatively (as a percentage) less of the total. For someone who is relatively sedentary, BMR will make up a
larger percentage. The absolute amount of calories burned won’t change, mind you, simply the percentage
coming from RMR.
I’ll give you some more detailed equations in the next chapter but, on average, RMR can be estimated simply
by multiplying body weight by 10-11 calories/pound (22-24 cal/kg). So someone weighing 150 lbs has a
RMR estimate of 1500-1650 calories/day.

Thermic Effect of Food (TEF)

The thermic effect of food (TEF, also known as specific dynamic action or SDA or Dietary Induced
Thermogenesis or DIT) refers to the slight bump in metabolic rate that occurs after eating, due to processing
and utilization of the ingested nutrients. For example, protein has to be broken down and processed in the
liver which requires energy. As well, the simple act of eating protein stimulates protein synthesis in various
tissues (organs, liver, muscle) as well. All of which takes energy. Carbohydrates get broken down to glucose,
which goes through the liver, some processing, etc. Fat undergoes the least processing. There are
exceptions such as medium chain triglycerides (MCTs) which undergo quite a bit of processing in the liver,
causing a slight bump in metabolic rate (via TEF) in the process.
As it turns out, different nutrients have different individual TEF’s. Protein turns out to have the highest, to the
tune of 20-30%. Meaning that of the total protein calories you eat, 20-30% is lost in processing. Carbohydrate
stored as glycogen requires about 5-6% of the total calories. Carbohydrate converted to fat (which generally
doesn’t happen in very significant amounts) uses up ~23% of the total calories as TEF. Most fats have a tiny
TEF, maybe 2-3% (because they can be stored as fat in fat cells with minimal processing).

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Since it’s usually impractical to sit and figure out the individual TEFs for each nutrient, the normal estimate
used is 10% of total caloric intake. So if you consume 3000 calories per day of a relatively ‘normal’ mixed
diet, you can assume that your TEF is about 300 calories per day or so. You also generally find that, with
the exception of extreme diets (such as all protein), shuffling macronutrients has a pretty minimal overall
impact on metabolic rate via TEF.
For example, consider the difference in TEF for carbs versus fat: 5-6% vs. 3%. That means that, for every
100 calories of each you ate, you’d burn 5-6 or 3 calories. So if you replaced 100 calories of fat with 100
calories of carbohydrates, you’d burn a whopping 2-3 extra calories via TEF. If you replaced 1000 calories
of fat with 1000 calories of carbohydrates, you’d burn 20-30 more calories. If you were able, by some means,
to replace 2000 calories of fat with carbohydrates, you would burn 40-60 more calories via TEF. One study
found that metabolism was about 4% higher (100 calories per day or so) for the higher carb versus the higher
protein diet. That still only amounts to an extra pound lost per month or so. Nothing to write home about to
be sure.
About the only time that TEF can become considerable is when you replace carbohydrates or fat with protein.
For every 100 calories of carbs/fat replaced with protein, you’d expect to burn about 25 calories more (30
cal for protein vs. 3-6 for carbs/fat). So a doubling of protein from 60 to120 grams/day might increase TEF
by 80 calories/day. Triple it to 180 grams/day and TEF could increase by 150 calories. The 20-30% TEF of
protein can become even more significant at extreme intakes. However, for the most part, such extreme
intakes aren’t practical or used outside of the bodybuilding subculture. In all but the most extreme diets,
protein stays fairly static and carbs and fats are shuffled around; the effect is typically minimal in terms of
TEF.
Finally, I should mention that some research has found that insulin resistant individuals may have an
impaired TEF response to eating, with a rough 50% reduction occurring. This could conceivably become
significant. For example, on a 3000 cal/day diet, the estimated TEF would be 300 calories. Cut that in half
and you only get a 150 cal/day increase in energy expenditure via TEF. Over a month’s time that would
amount to 4,500 calories or about 1.5 lbs difference. I’d assume that correcting the insulin resistance by
losing fat, lowering insulin and various other interventions would correct this defect and allow TEF to work
normally.

Thermic Effect of Activity (TEA)

The thermic effect of activity (TEA) refers to all activity above and beyond basal levels. If you get off the
couch and walk around, that goes into TEA. Do chores around the house, TEA. Go to the gym and work out,
TEA. Because of extreme differences in daily activity levels, TEA is the most variable of all the components
of total energy expenditure ranging from 10-100% over basal levels. Relatively sedentary individuals may
burn a mere 10-30% over BMR during the day. Extremely active individuals (think athletes engaged in
several hours of training per day) can burn 50-100% over BMR through activity. This make figuring out TEA
a real hassle, simply because of the variance involved. There are some rough estimates but that’s all they
really are, I’ll address this in a little bit.
The calorie burn from TEA technically comes from two separate factors: calories burned during the activity
and calories burned afterwards. Caloric expenditure during activity can be pretty variable. Someone trotting
along on the treadmill may only be burning 5-10 calories/minute. An elite athlete may be capable of burning
20 cal/min or more for extended periods of time. Weight training can burn roughly 7-9 cal/min although this

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depends on the exercises done, number of reps and rest periods. Depending on the duration and intensity
of a given workout, the caloric expenditure can range from irrelevant to extreme.
First and foremost, there is typically an increase in caloric expenditure (referred to as excess post-exercise
oxygen consumption or EPOC) but this tends to be variable as hell. Despite commonly held belief, there is
a fairly inconsequential increase in caloric expenditure following aerobic exercise. You may have read that
aerobics raises RMR for 24 hours but this happens to be completely false (the studies suggesting this were
flawed for a variety of technical reasons).
Rather, the amount of bump in RMR (i.e. calories burned after the aerobic session) from aerobics depends
on both the duration and intensity of the workout. A typical aerobic workout, done at low intensity for short
durations (what one friend of mine calls Weak Assed Morning Cardio since most people do it in the morning)
may burn an additional 5-10 calories total after the workout. Yippee.
At higher intensities, or taken to exhaustion, the RMR bump from aerobics can approach 100-150 calories
total. But this typically requires intensities and/or exercise durations that the average person simply won’t or
can’t do. Only a well-trained athlete would be able to accomplish the types of workloads needed to elevate
BMR significantly with aerobics, and they don’t generally need to lose fat in the first place.
A specialized type of aerobic activity, referred to as interval training (sprint training basically) appears to
elevate RMR to a much greater degree than typical aerobic workouts but exact numbers are difficult to
obtain.
Weight training is a different story entirely. Studies have shown that properly done weight training can raise
RMR by quite a bit for anywhere from 24-36 hours. One recent study, using a mere 12 sets measured a total
caloric burn of 700 calories over baseline in the two days after the workout. This can add up quickly.
I should mention, briefly, one of the great contradictions of exercise: the individuals who really need to burn
the most calories with activity (typically overweight and out of shape) usually aren’t capable of it; and the
folks who can burn tons of calories (highly trained lean athletes) don’t need it. Of course, given time,
untrained individuals can drastically increase their capacity to burn calories during exercise, as their fitness
improves (and they lose weight) so this shouldn’t be taken as a reason not to exercise. I’m simply trying to
point out some of the realiities.

A Quick Note
I should note that RMR and TEF are relatively static for the most part, except during the most extreme diets
(where TEF and RMR will both crash). A 10 lb muscle weight gain may only raise BMR by 60 calories or so.
Ignoring the adaptive component of metabolic rate (see next section), a 10 lb weight loss would only reduce
metabolic rate by about 100 calories per day.
It’d take eating 1000 extra calories to burn an additional 100 calories via TEF (and you’d still end up with
900 calories extra that would get stored). Those same 100 calories could be burned with 10-20 minutes of
moderate to high intensity exercise. I’ll talk about this some more in a few chapters. Excepting massive
weight loss or gains, which can affect RMR significantly, perhaps the single place you can most affect caloric
expenditure is with activity.

Adaptive Component

The adaptive component of total energy expenditure is sort of a catch-all category for anything that doesn’t
neatly fit into the other categories. Even then, the adaptive component (sometimes called thermogenesis

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which simply means the production of heat) can be divided up into an obligatory component and a facultative
component. We needn’t get that detailed.
Generally the adaptive component refers to changes in energy expenditure due to environmental changes.
It fundamentally represents a change in metabolic efficiency, meaning you are burning more or less calories
at the same bodyweight than you’d expect.
For example, in cold weather, there is an increase in calorie burn via shivering. Fever or injury can raise
metabolic rate by 10% or more due to the increased cellular turnover and hormonal response that occurs.
Weight training that causes muscle damage increases the rate of protein turnover, which is a big part of the
calorie burn that occurs after the workout.
During dieting, in addition to the drop in BMR due to loss of weight, there can be an adaptive decrease in
metabolic rate due to hormonal changes (meaning you burn less calories than you’d expect based on the
change bodyweight so even though you’ve lost only 10 lbs, BMR may have dropped by far more than 100
calories/day). As it turns out, some people have adaptive drops that are larger than others and this
contributes to some of the variance in weight/fat loss between people.
I’ve already mentioned brown adipose tissue (BAT) in previous chapters. While BAT is responsible for the
adaptive component of metabolic rate in animals and newborns, as I already told you, adult humans don’t
have much BAT
However, because of their research into BAT, scientists discovered a new class of proteins called uncoupling
proteins (UCPs). To avoid an unnecessarily technical discussion, simply realize that UCPs tend to lead to a
wasteage of energy in the mitochondria of cells to generate heat. The first UCP, UCP1 (aka thermogenenin)
was found in BAT which I already told you we don’t have much of; we can ignore it. However, two additional
UCPs (UCP2 and UCP3) have also been found in human muscle and fat cells.
Originally it was hoped that UCP2 and 3 would play a role in humans similar to UCP1 in animals but it doesn’t
appear to be the case. Rather, it looks like UCP 2 and 3 are mainly involved in fuel use, especially fatty acid
oxidation (burning). When fatty acid levels increase, for example during fasting, UCP levels in skeletal
muscle go up to help burn them off. This isn’t to say that drugs (or supplements) that affected UCP might
not benefically influence energy expenditure, only that UCPs weren’t the holy grail of fat loss that they were
originally hoped to be.
A final, and interesting part of the adaptive component of metabolic rate is something researchers have
given the cutesy wootsey name of Non-exercise Adaptive Thermogenesis or NEAT (this lets them make all
kinds of cute paper titles along the lines of ‘Decreased weight gain, a NEAT explanation’ because scientists
are amazingly unfunny).
NEAT more or less refers to fidgeting, moving around, basically weird spontaneous movement that burns
off calories without really accomplishing much. If you remember back to high school, there was always that
one skinny guy who was always fidgeting his hands, bouncing his leg, that kind of thing. He was burning
calories at a much greater rate than you might expect. Even chewing gum all day can burn up a lot of
calories.
It turns out that NEAT can account for 200-900 calories/day of caloric expenditure and there is a massive
variance between people in how much change they get. This is especially true during overfeeding; some
people ramp up NEAT to super high levels and stay lean, others don’t and get fat easily.
To put that in perspective, 900 calories per day is equivalent to about an hour and a half of hard exercise.
That’s a ton of calories burned through nothing but fidgeting. Unfortunately, it also looks like NEAT is
genetically determined; either you upregulate NEAT during overfeeding or you don’t. One more thing, in this
particular study, women consistently had the smallest NEAT response.

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In addition, it looks like the capacity to increase NEAT is tied to the adaptive downregulation of metabolism
during dieting. One study found that the same people who were best able to increase metabolism during
overfeeding had the smallest drop in metabolic rate during dieting and vice versa; the folks who’s metabolism
went up the least during overfeeding had the biggest drop in metabolic rate during dieting.
Researchers referred to this as ‘spendthrift’ (store excess calories poorly, lose weight easily) and ‘thrifty’
(store excess calories easily, lose weight poorly) phenotypes. We might call them the genetically blessed
and the genetically fucked. The latter individuals not only have the hardest time losing fat because their
metabolisms crash the hardest and fastest, they will tend to store fat the most readily.

Summing Up

The changes in overall body mass (increase or decrease) ultimately comes down to long-term energy
balance which is represented by energy in (via food) and energy out (via metabolic rate). Total energy
expenditure is determined by four components.
The first is basal metabolic rate (BMR) which represents the number of calories needed to sustain the basic
functions of your body.
The second is the thermic effect of food (TEF) which represents the calories expended in processing the
food that you eat.
The third is the thermic effect of activity (TEA) which refers to any and all calories burned above and beyond
BMR. Chores, just sitting up in a chair, and exercise all contribute to TEA.
Finally, there is an adaptive component of metabolic rate which is a catch-all category for a variety of different
metabolic processes. This includes changes due to environmental factors such as cold, sickness (fever),
changes because of increased or decreased food intake, or the cutely named NEAT which is just fidgeting
and basic moving around.

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Permanent Metabolic Damage – Q&A
Question: Lately I’ve seen a lot of hype regarding metabolic damage that can occur when dieting to very
low body fat levels, where individuals permanently “damage” their metabolisms to the point where they are
getting fat on 800-900 calories a day. It’s said to occur when losing weight too fast or trying to do too much
cardio on top of a very low caloric intake.
This sounds like bro-hype but I’m wondering: Is there any truth to this phenomenon?

Answer: This seemed a good followup Q&A after last Friday’s Lean Body Mass Maintenance and Metabolic
Rate Slowdown – Q&A since it’s semi-related and I seem to have total writer’s block regarding anything
approximating a feature article right now.
There are several issues at stake here and I’m going to address them in reverse order. Certainly I have
seen some weirdness occur (and there is at least one study to support this) where excessive cardio in the
face of a large caloric deficit can cause problems, not the least of which is stalled fat/weight loss. In that
study, the combination of a very large deficit plus about 6 hours of cardio seemed to decrease metabolic
rate more than the diet alone. This is something I intend to cover in more detail at a later date.
This, along with personal observations, was what led me to strongly suggest against doing a lot of cardio on
The Rapid Fat Loss Handbook program; in fact I’d say that a majority of failures on that program can be
tracked to people trying to do too much cardio and it doing more harm than good. Invariably, the folks who
minimize activity (beyond the basic weight workouts) and let the deficit of the diet do the work do better in
terms of fat loss. So certainly there is an element of truth to that.
However, we need to look at magnitudes here and do a bit of reality checking. Several in fact.
The first is to look at the food intake. 700-900 calories is not a lot of food and, typically, at the end of a
contest diet, hunger is simply off the map. I find it doubtful that someone is truly consuming that little food
on a day to day basis at the end of a contest diet.
Note that I did not say impossible (anorexics certainly seem to do this); I’m simply doubtful that someone is
consuming that little food in the face of extreme hunger on a day to day basis. They may be reporting that
that is their true food intake but I’d be doubtful that it was truly that low on an everyday basis.
Now, as discussed in the Q&A I linked above (as well as in other articles on the site and in my books), there
is no doubt that the body undergoes a variety of rather annoying adaptations to reduced calories and fat
loss. Reduced metabolic rate, reduced spontaneous activity, etc. all occur and this works to slow fat
loss. But what we’re really dealing with here is a magnitude issue.
First and foremost, if someone is claiming to get fat on only 900 calories per day, that implies that their actual
total daily energy expenditure is actually LESS than that. That is, as I discuss in some detail in The Energy
Balance Equation, we know that to actively gain fat requires a caloric surplus (relative to expenditure).
To gain fat at say 900 calories, and to do so at any fast rate would imply that daily energy expenditure was
significantly less than that. For example, assume that someone eating only 900 calories per day were
gaining fat at a rate of 1 pound per week. That would imply a 500 cal/day surplus or a total daily energy
expenditure of 400 calories per day.
For an average sized male who started out with a maintenance energy expenditure of 2700 calories per day
that would be an 85% reduction. For an smaller female who started with perhaps a 1700 calorie/day
maintenance, that would be a 75% reduction from where they started. And simply, that level of reduction is
far and beyond everything that’s ever been measured in the history of research on this topic.
Now, some might argue that the stressors of competition dieting haven’t been examined and they’d probably
be right; to my knowledge, no-one has examined the metabolic rate of a bodybuilder following an extreme

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contest diet. Quite in fact, most studies don’t examine lean individuals at all but there is one study that is
possibly relevant which is the seminal Minnesota Semi-Starvation Study.
I’ve talked about this study before and it represents one of the most massively well-controlled studies on the
topic ever done (or that will ever be done). In it, war objectors were placed on approximately a 50% reduction
from maintenance calories (which only put them around 1500 calories/day or thereabouts in the first place)
and were held there for 6 straight months. Activity (walking) was enforced and most men reached the lower
limits of body fat percentage by the end of it. I’d note that only men were studied so it’s possible that women,
who are prone to showing more resistance to fat loss, could show a differential response.
And the total reduction in daily energy expenditure only amounted to 40% (of which the majority of that was
due to the weight loss). Weight and fat loss had basically stopped at the end of the study which makes
sense; the original 50% deficit had been reduced to at most 10% due to the 40% reduction in metabolic rate.
The bottom line is that no study I’ve ever seen has suggested that total daily energy expenditure could be
reduced to the levels that are implied by ‘gaining fat rapidly at 700-900 calories/day’.
So what’s going on? Certainly some bad hormonal things go on when you combine heavy activity with heavy
deficits for extended periods to low body fat levels (I’d note that various types of cylical dieting such as my
own Ultimate Diet 2.0 and Martin Berkhan’s Intermittent Fasting approach seem to side-step at least some
of this). Thyroid levels drops, nervous system output drops, testosterone levels crater, cortisol goes through
the roof.
And I would suspect/suggest that it is this last effect that is being observed and taken as evidence of
‘metabolic damage’. In a water depleted, glycogen depleted bodybuilder coming out of a contest diet, water
balance is going to go absolutely crazy and cortisol is one mediator of this. Water retention secondary to
glycogen storage will also contribute.
So you have a situation where a post-contest bodybuilder may be seeing just massive swings in water weight
(which can appear like rapid fat gain) following the contest; especially when you consider the normal runaway
hunger that tends to occur at that point.
Between glycogen storage and simple cortisol mediated water retention, I can’t see any other reason to
explain the observation. Even one day of overeating carbs can cause massive water retention (for example,
shifts in water weight of 7-10 pounds over a day or two are not uncommon on cyclical diets) and I suspect
that’s what is being observed.
Which is all a long way of saying the following: certainly there is evidence of metabolic derangement when
you diet people down to low levels of body fat, this can probably be made worse if you undergo the normal
severe overtraining cycle that most dieters go through at that point. But I don’t see any physiological way
that true rapid FAT gain can occur at such low calorie levels. I’d suspect that water retention (and a bit of
neurosis equating water weight gain with true fat gain) is the primary culprit here.

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Permanent Metabolic Damage Followup – Q&A
About 10 days ago I posted a Q&A titled Permanent Metabolic Damage dealing with the claim that, following
extreme contest diets, bodybuilders and other physique competitors have ‘damaged’ their metabolic rate so
irrevocably that they are able to gain significant amounts of fat consuming only 700-900 calories per day. I’ll
let you read that piece to see my answer. But in the comments sections were several questions that seemed
worth addressing although they weren’t all exactly related to the specific topic I was addressing.

Question: I suppose a follow-up question to this answer is just how rare it would be to cross a true “point of
no return” where you may have fouled up your internal physiology to where it may never be able to rebound.
Or is it usually a case of time and reversing some of the actions that cause it in the first place? i.e. the longer
and more extreme the descent, the longer it will take to recover, but recovery is entirely possible
Would clinically severe eating disorders probably be the only instances where someone could allow things
to devolve to such a degree that any sort of irreparable damage may have been done to some part of the
body and its normal functioning?

Answer: First let me say that I am not and do not claim to be any sort of expert on the topic of eating
disorders. It’s simply not been a major area of interest of mine. I think it’s worth considering that what is
going on in something like anorexia or bulimia is quite different than what is going on with the topic I was
primarily addressing in the original Q&A, to wit contest diets in bodybuilders/physique athletes.
For example, if nothing else we can see massive differences in the nutritional intake of a dieting
bodybuilder/physique competitor (typically based around high protein intakes and ‘healthy’ foods) as
opposed to the near complete absence of food in the anorexic or the alternation of binging and purging in
the bulimic.
With that said, what little literature I have looked at in terms of recovery from eating disorders doesn’t lead
me to believe that there is any sort of permanent damage. So long as a ‘normal’ weight is regained (here
we’re typically looking at the anorexic), things come more or less back to normal. Even in the seminal
Minnesota study, metabolic rate eventually rebounded to normal; of course the subjects had regained all of
the fat they had lost as well for that to occur.
But again, this is really outside of my major sphere of interest; if anyone reading this has expertise that can
contribute to this question, I think we’d all love to see it.

Question: Layne Norton once said that from the day one begins to eat normally again, it can take anywhere
from 3-4 months to completely restore BMR to 100% from post-dieting levels. Although he didn’t cite it, do
you know of any studies roughly reflecting this extended time frame? I’m only referring to restoration of
normal hormone output and, thus, adaptive thermogenesis, since if the weight loss were maintained, BMR
would still be relatively lower than it was pre-diet simply by virtue of a lower final body weight.
Answer: No direct research on this comes to mind immediately although it may exist. I think the problem is
that, usually in looking at post-diet ‘recovery’ there is almost always a regain in body fat which tends to color
the issue. For example, in the Minnesota study that I mentioned in the question above, following the 6
months of semi-starvation, the men were allowed to eat as much as they wanted. And they went nuts, eating
massive numbers of calories and regaining fat. Which normalized metabolic rate eventually but doesn’t
really apply to what you seem to be describing.

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Frankly, I’m not 100% sure that hormones will ever return to completely normal (see next question) assuming
that the lowered body weight/body fat level is maintained. They can be improved by raising calories to
maintenance for sure. This is part of the rationale behind The Full Diet Break although that’s really meant
to break up periods of explicit dieting (I also suggest it at the end a diet to start normalizing things). Which
is a long way of saying “I don’t know” If Layne has a reference for that, I’d love to see it.

Question: So there is evidence of metabolic derangement, but do you think it is permanent even when
returning to normal caloric intake?

Answer: The studies of the post-obese (see next question) suggest that, even at weight maintenance (i.e.
when calories have been returned to normal), there is still a small overall reduction in basal metabolic rate
(on the order of perhaps 5%) compared to someone who is ‘naturally’ of that weight. Meaning that if you
compare someone who is 180 pounds without dieting to someone who has dieted down to 180 pounds, the
second person will show a slightly reduced metabolic rate compared to the predicted values. But the effect
is slight when calories are brought back to maintenance.
As I discussed in the original Q&A, it looks like the main impact in terms of reducing daily energy expenditure
is on spontaneous activity levels; this probably explains why exercise seems to have so much bigger of an
impact on weight maintenance than weight loss (as I discussed in Exercise and Weight/Fat Loss Part 2).
I am unaware of any research examining if this is maintained in the long-term (i.e. will the post-obese
continue to show decreases in spontaneous activity). However, the long-term studies of the post-obese
(ranging from 2-5 years if my memory serves correctly) suggest that the effect on basal metabolic rate never
goes away. So yes, it’s effectively permanent; it’s simply small.

Question: I’m also wondering about the permanence of any such metabolic adaptations. It seems likely to
me that metabolism would return to normal at some point. If so, how long would it take? It seems like I read
something about this in a discussion of the Minnesota study, but I’d have to go searching to see if I’m
remembering correctly.

Answer: As noted in the question above, what data I’ve seen looking at the post-obese in the long-term
suggest that there is a slight reduction in basal metabolic rate that doesn’t appear to ever go away. At least
not in any practical time frame. Based on what we know about the issue of setpoint (discussed in Set Points,
Settling Points and Bodyweight Regulation Part 1) I wouldn’t expect this to ever truly go away. I imagine
someone will ask the logical followup to this in the comments which is “So what about people who get and
stay lean in the long-term, how do they do it?” Maybe addressing that will get me past my writer’s block to
write an actual article about it.

Question: I am a clinical nutritionist at clinic where we see a lot of people with “screwed up metabolisms”.
In a different vein, there are the people who got fat from overeating and eating the wrong types of foods and
became insulin resistant. Now they have to eat low calorie diets otherwise they gain weight.
One of my clients weighs 360 lbs and her BMR according to the the InBody is 2700 calories. The girl eats
maybe 1200 calories a day and maintains that weight. Reversing insulin resistance by eating the proper
foods and incorporating resistance training obviously helps. I am wondering if there is an approach to
increasing calories systematically when working to reverse insulin resistance without gaining weight?

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Answer: This is really a bit outside of what the original Q&A was discussing but I’ll address it anyhow;
certainly there can be metabolic derangements that occur in obesity (what’s cause and what’s effect is often
hard to determine). However, it’s highly unlikely that your client is truly maintaining her weight on 1200
calories per day if her measured BMR is that high (meaning that her total daily energy expenditure is even
higher); insulin resistance or not, that’s simply a physiological impossibility.
The more likely (and exceedingly common) issue is that she’s simply consuming more food than she’s aware
of or self-reporting. Because even in studies of insulin resistance, when calories are reduced (and and
accurately monitored), weight/fat loss occurs. So either she’s a physiological anomaly or she’s not really
eating 1200 calories per day. And my experience (along with a large body of research) suggests that it’s
the latter issue that’s the cause of the problem.
Thanks for the questions folks!

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Another Look at Metabolic Damage
Originally I was going to do a full writeup of the recent study making the rounds suggesting that both low-
and high-repetition training generate the same muscle growth but I’m going to save that until next week; this
topic makes more logical sense given last week’s video on BMI and weighing frequency. It was also
stimulated by a private message I got on FB regarding the topic.
That topic, of course is the idea of metabolic damage, something I have written about on the site
previously. But rather than write something new, I just got permission from Alan Aragon to reproduce an
interview I originally did for his (highly recommended) research review. It’s only $10 a month and chock full
(that’s right, CHOCK!) of the most current research on diet and training along with interviews with top current
coaches and feature articles on all topics big and small. Go subscribe, subscribe now.
Ok, so what exactly are we talking about here? As originally claimed, metabolic damage referred to a
phenomenon wherby dieters (typically females) who had been on low calories and performing a large
amount of cardio (i.e. typical physique sport contest prep)
1. Stopped losing fat despite maintained low calories/high activity
2. Started regaining fat despite those same maintained low calories/high activity
Hence their metabolism was damaged. I’m mainly bringing this up as the original concept has been
somewhat, err let’s be nice and say, “modified” from the original (now being called metabolic adaptation, a
concept I’ve been personally writing about for over a decade in pretty much all of my books).
And with that out of the way I reprint my original interview with Alan Aragon (did I mention that you should
subscribe to his research review). Everything in bold is Alan, the other dense walls of texts are me.

My big question for you is related to the whole “metabolic damage” concept. Coaches and
competitors involved in bodybuilding & physique contest prep – predominantly women – often
report cases of consuming very low calories (i.e., in the 700-1000 kcal range), combines with high
volumes of cardio (i.e., 2+ hours per day), and all this without any weight loss. What are your initial
thoughts on this, as far as validity and/or mechanisms behind it.
First and foremost, I have myself written about how the odd combination of very low calories and excessive
cardio can, in some people, cause problems. Some of it is metabolic which I’ll come back to. But most of it
is simply due to one thing: water retention. It’s a little known fact that cortisol has cross-reactivity with the
aldosterone receptor (aldosterone is the primary hormone for retaining water). But while cortisol only has
about 1/100th the affinity for the receptor, there can be about 10,000 times as much. We know that cortisol
causes water retention (Cushing’s patients who are often on high-dose cortisone have this problem).
1. Now, dieting raises cortisol.
2. Cardio raises cortisol.
3. Mental stress raises cortisol.
So combine your typical headcase female dieter (who is already mentally stressing themselves out), add a
massive caloric restriction, add tons of cardio. And cortisol goes through the roof. And this is worse in some
personality types. You can always tell them on Internet forums, they type in all caps with lots of !!! (Subject
line: NEED TO LOSE WEIGHT NOW!!!). You can sense the stress in their life in how they write. And what
these people do other than mentally stressing themselves out is further physically stress themselves out.
And when weight loss stops, they stress harder, cut calories harder, do more cardio. And make it worse.
I mean, hell, a woman can easily shift 10 pounds of water weight across her menstrual cycle. That’s not
uncommon in this kind of stress condition. Now add to that the fact that a typical female dieter if she’s lucky,
might be getting 1 pound of true fat loss per week. If her stress (due to mental, diet and physical factors) is

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causing her to retain 10 pounds of water it will appear that her diet is not working for 10 full weeks. During
which time she will lose her absolute shit.
What always works in these types of dieters is chilling the fuck out (weed would help too). Raising calories,
lowering cardio, a good lay. There’s no metabolic magic, cortisol finally drops when you get them stop being
crazy for a couple of days and they experience the magical whoosh (or the LTDFLE, check my site for
details). Boom, weight drops by 5+ pounds overnight.
All water. Well mostly. But clearly they didn’t have a 5 pound deficit in one day. They just finally dropped the
water they’d been holding.
So that’s part 1. Any questions before I move on to part 2?

Clear so far, please continue…


So, for the most part I think that’s a lot of what’s going on the fat loss is just being masked by severe water
retention. I say this simply because getting folks to rest a couple of days, raise calories (especially from
carbs, the increase in insulin lowers cortisol levels) and “refeed” invariably causes that big weight
drop/whoosh effect. It has to be water.
However, that isn’t to say that there aren’t metabolic effects that can occur due to that combination of
variables (low calories and high activity).
I’m going to assume (and hope) that your readers are familiar with leptin. If not, basically it signals to the
brain (and elsewhere) about energy stores in the body (and how much you’re eating) and when it drops it
induces much of what is often incorrectly called the “starvation response” or “metabolic damage”. I say
incorrectly because this simply represents a normal ADAPTATION to dieting that occurs because the body,
fundamentally, doesn’t give a damn that you need to look good on stage. It wants to keep you from starving
to death.
So falling leptin causes a host of things to occur: metabolic rate slows, hunger increases, you get lethargic,
thyroid goes down, testosterone drops, and a whole bunch of other shit goes wrong.
Pretty much everything bad that happens with dieting is controlled, to at least some degree by leptin levels
especially at the level of the brain. On that note, studies that have given leptin replacement following dieting
show a reversal of these effects; but don’t get your hopes up leptin is an injectable drug and still many
hundreds of dollars per day. But drug using bodybuilders have basically been sort of fixing all of the
peripheral problems with drugs: anabolics to counter falling testosterone, thyroid meds for thyroid, cortisol
blockers, appetite suppressants, stimulants to keep energy levels up. Raising leptin would be more elegant
(as it would fix the problem centrally in the brain) but difficult. Refeeds and full diet breaks (discussed on
my site and in my books) help a lot. Injectable leptin would be skippy but way too expensive. The leptin-
mimicking supplements are all bullshit.
I bring this up because cortisol, among its other fun features, induces leptin resistance in the brain. Like
insulin resistance in skeletal muscle (where the cells don’t respond to insulin properly), leptin resistance
means that what leptin is around doesn’t send a sufficient signal to the brain. So in those folks who are
already psychotically stressed and cutting calories and doing too much cardio, the massive increase in
cortisol will have that effect centrally in the brain.
But, wait…there’s more…

WHOOT!!! Keep going.


Ok, so finishing up, which is not to say that there is not a metabolic adaptation/adjustment to dieting and fat
loss; that’s really never been up to debate. Once again, we have this leptin system that basically evolved to

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keep us from starving to death. In that regards, a lot of people think of leptin as an anti-obesity hormone but
this is incorrect. Leptin does very little to keep us from getting fat (which had no evolutionary disadvantages
until recently); leptin exists to keep us from starving to death. And fundamentally, dieting is just controlled
starving to death. But the same things occur.
Now the determinants of total metabolic rate are multi-fold, typically divided up into the following four
categories:
1. BMR: Basal metabolic rate (also called RMR or resting metabolic rate): this is just the basal processes
to run your body.
2. TEF: Thermic effect of food, the extra calories you burn from eating. Quick-estimated at 10% or so it
actually depends on the nutrient eaten.
3. TEE: Thermic effect of exercise. The calories burned through exercise.
4. SPA/NEAT: Spontaneous physical activity/Non-Exercise Activity Thermogenesis: This is a newer
category and separate from thermic effect of exercise, it’s the calories you burn moving around,
fidgeting, changing postures. It happens to be massively individual.
But all 4 respond to changing food intake and body weight. So as soon as you start dieting, TEF automatically
goes down a bit since you are eating less food. Less food means less TEF (note that this has NOTHING to
do with meal frequency). BMR goes down as you lose weight because a smaller body burns fewer calories.
So do the calories burned during exercise; at any given absolute intensity, a smaller person burns less
calories.
Again, SPA/NEAT is a big question mark since it varies so much. But you generally tend to be more lethargic
during the day when you diet, so you end up moving around less, burning fewer calories in total. And while
it’s great to think that you can consciously impact this, NEAT is subconscious. At best you can offset it with
more exercise (part of why competitors usually raise cardio volume or intensity during a cut).
Even with that said, research has typically divided the drop in metabolic rate into two different components.
One part is simply due to the reduction in bodyweight. As I said above, a smaller body burns fewer calories
and there’s really not much that can be done about this (wearing a weighted vest might have a small impact
on at least TEE). Get lighter and you burn fewer calories.
There’s nothing you can do about this short of NOT LOSING WEIGHT. Which goes against the point of a
cut. And yes, I’m using weight and fat interchangeably here: for anybody but a drug-using competitor, fat
loss is going to mean weight loss. Don’t get picky.
But there is also evidence for what is called an adaptive component of metabolic rate reduction. Let me
explain. Let’s say that someone loses twenty pounds and based on all of the math you’d expect a drop in
metabolic rate of 10%. But when you measure it you actually see a reduction in 15%.
That is, the drop in metabolic rate is greater than what you’d predict based on the drop in bodyweight. That
extra 5% is the adaptive component of metabolic rate reduction. And it’s hormonally driven, the drop in leptin,
the drop in thyroid levels (conversion of T4 to T3 is impaired on a diet), there is a drop in sympathetic nervous
system activity (part of why the ephedrine/caffeine stack helps, it offsets this drop), you get the idea.
The thing is that not every study has found this. Some do some don’t. A lot of it depends on starting body
fat, the length of the diet, genetic individuality and all that stuff. But in dieting bodybuilders or fitness people,
it is going to have an impact. But the preponderance of studies say that it does exist; I’d certainly expect it
to occur in lean hard dieting physique athletes who is who we are concerned with (typically when it doesn’t
show up is in studies of extremely overfat individuals whose hormones don’t really get mucked up until they
have lost a lot of weight).
A-ha, you say, now we have an explanation for the so-called metabolic damage (and note that I’ve seen this
term used to refer to a couple of different things: one is that weight/fat loss stops despite a huge deficit; a

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more extreme claim is that competitors start to regain fat even in the face of low calories/high activity). But
wait, there’s more. And yes I’m almost done.
Ready for the big payoff?

I would have to be a crazy person to stop you here. Let it rip, Brofessor McDonald.
Actually I only have a BB (Bachelor of Bro-osity). I didn’t feel like doing advanced academic work to get my
MB (Master of Bro-osity) or BrD (Doctor of Bro-osity). Note: I told you this was email and Alan and I were
being a little bit silly.
Anyhow, I’ve looked at water retention (which I think is a big part of this) and some of what goes into
metabolic rate adaptation. And yes it does occur. No one is doubting that. But that raises the important
question. Is the drop in metabolic rate that occurs during dieting sufficient to stop weight loss in its tracks
despite a claimed low caloric intake and high-activity level?
Actually, before I get to that, let me expand on the above sentence. You might note my use of the word
“claimed” in regards to low-caloric intake. Because there’s an issue here that often gets overlooked. One of
the known adaptations to dieting and getting lean is a massive increase in hunger. And even with the
strongest willed competitor/dieter, often it becomes overwhelming. Geared bodybuilders often use appetite
suppressants, the EC stack has been used perennially but the reality is that getting very lean means being
hungry.
And that means binges. You can go to endless forums where competitors, men and women alike report
losing their minds and going on a binge of varying types. Some go carb-crazy, some of the “clean-eaters”
will have that one taste of something forbidden and go on a Blizzard binge that makes them sick. But most
don’t really like to talk about it.
That is, these binges, as often as not go un-reported. So the dieter who is claiming 1200 calories with tons
of cardio tends to often conveniently “forget” about the day they spent eating every piece of garbage they
could stuff down their gullet. And in light female competitors, if the binges get crazy enough it can readily
offset the deficit being created during the week.
But irrespective of that, let’s address what seems like a fairly simple question: Can the drop in metabolic
rate, due to the drop in bodyweight and the adaptive component EVER be sufficient to completely eliminate
true fat loss?
And the answer, at least based on the last 80 years of studies into the topic (in humans, NOT animal models)
says no. Perhaps the classic study in this regard was the oft-quoted (and oft- misunderstood) Minnesota
Semi-Starvation Study. In it, a dozen or so war objectors got to avoid going to war and arguably got into
something worse. That is, researchers wanted to study long- term starvation as might occur during war or
famine or being held in a prisoner camp.
Specifically the men were put on 50% of their maintenance calories, subject to forced daily activity (walking,
NO weight training) and basically had their lives controlled and managed for 6 months. And in various sub-
analyses, it was found that, by the end of the study the total drop in metabolic rate was nearly 40%. That is,
of the original 50% deficit in calories, 80% of it had been offset. Of that 40%, a full 25% was simply due to
the reduced bodyweight. Again, lighter bodies burn less calories and there’s no getting around it. But that
also means that the adaptive component of metabolic rate reduction was only 15%. Which is about the
largest drop ever measured (most studies measure less).
But here’s the punchline, the men had also reached the limits of human leanness. They were in the realm
of 4-5% body fat by this point in the study. Even though their fat loss had basically stopped (and at some
points in the study WEIGHT loss stopped due to severe water retention) it didn’t occur until they reached
ultimate leanness (NB: the claims of bodybuilders to be 2-3% bodyfat is a measurement error). And even

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they were still losing tiny amounts of weight/fat. It just wouldn’t have amounted to much since most of the
deficit had been offset by the metabolic rate reduction.
Now some will (and may rightly) point out that the study was only in men and women’s bodies may be
different. And they are correct; I’ve written about this myself (my odd little book on Bromocriptine talks about
it in some detail). Certainly women’s bodies do some strange things in this regard, they are more
evolutionarily, err, evolved, to hold onto calories and fat stores than men (and there’s some profoundly goofy
shit that can occur where they shift upper body fat stores to their legs, discussed in my book The Stubborn
Fat Solution). So I suppose it’s conceivable that there might be a woman or three for whom this could occur.
Maybe. Not that that woman has ever shown up in a well-controlled study in 50 years. But I suppose she
might exist. She probably rides my invisible unicorn.
Because in no study that i have ever seen or ever been aware of has the drop in metabolic rate (whether
due to the drop in weight or adaptive component) EVER exceeded the actual deficit whether in men or
women. Fine, yes, it may offset things, it may slow fat loss (i.e. if you set up a 30% caloric deficit and
metabolic rate drops by 20%, your deficit is only 10% so fat loss is a lot slower than expected or predicted)
but it has never been sufficient to either stop fat loss completely (or, even to address the even stupider claim
being made about this, to cause actual fat gain).
But even when the drop in metabolic rate is massive, sufficient to drastically slow fat loss, even when it
occurs it’s only when that person’s body has more or less reached the limits of leanness in the first place.
So for ‘hundreds of women who are self-reporting this in emails’ to a certain coach to exist, well; just let me
call that what it is: bullshit.
I think what’s really going on is you have a bunch of neurotic crazed female dieters, who are misreporting
their food intake (especially the crazy food binges we KNOW happen in this population) and who are holding
onto massive amounts of water due to the combination of low calories, high-cardio and being batshit stressed
mentally about the whole process. And who magically start losing fat again when their poorly controlled 1200
calories becomes a well-controlled 1250 calories, well….you’ll have to call me incredulous about the whole
thing.
Because the science doesn’t support it in any way shape or form. No study in humans in 50 years has ever
shown the claimed phenomenon. I mean not ever. Not a single study showing truly stopped fat loss in the
face of a controlled deficit much less fat regain. And with plenty of other mechanisms (like water retention)
to explain the “apparent” lack of fat loss that make more logical sense (Occam’s razor for the win).
And that’s my take on the issue. Now it’s time for a nap.

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Coffee, Diabetes and Weight Control – Research Review

Title and Abstract

Greenberg JA et. al. Coffee, diabetes, and weight control. Am J Clin Nutr. (2006) 84(4):682-93.
Several prospective epidemiologic studies over the past 4 y concluded that ingestion of caffeinated and
decaffeinated coffee can reduce the risk of diabetes. This finding is at odds with the results of trials in humans
showing that glucose tolerance is reduced shortly after ingestion of caffeine or caffeinated coffee and
suggesting that coffee consumption could increase the risk of diabetes. This review discusses epidemiologic
and laboratory studies of the effects of coffee and its constituents, with a focus on diabetes risk. Weight loss
may be an explanatory factor, because one prospective epidemiologic study found that consumption of
coffee was followed by lower diabetes risk but only in participants who had lost weight. A second such study
found that both caffeine and coffee intakes were modestly and inversely associated with weight gain. It is
possible that caffeine and other constituents of coffee, such as chlorogenic acid and quinides, are involved
in causing weight loss. Caffeine and caffeinated coffee have been shown to acutely increase blood pressure
and thereby to pose a health threat to persons with cardiovascular disease risk. One short-term study found
that ground decaffeinated coffee did not increase blood pressure. Decaffeinated coffee, therefore, may be
the type of coffee that can safely help persons decrease diabetes risk. However, the ability of decaffeinated
coffee to achieve these effects is based on a limited number of studies, and the underlying biological
mechanisms have yet to be elucidated.

My Comments

Caffeine is another one of those compounds about which there is endless argument and debate. Some feel
that it is evil, too much causes all manners of problems, and should be eliminated completely. Others like
me feel that the only problem with caffeine is when there isn’t enough of it.
Specific to this research review, it’s often been claimed that caffeine raises insulin, causes insulin resistance
and deteriorates blood glucose control. Thus individuals suffering from the Metabolic Syndrome/Insulin
Resistance/Pre-Type II diabetes (all being the same name for essentially the same thing) should avoid it.
But what does the research actually say in this regards?
First and foremost, there is actual some truth to the idea that caffeine can cause problems with blood glucose
control and insulin levels, at least if you’re looking at high doses of caffeine right before a meal tested under
acute (single meal) conditions.
Typically doses of 5 mg/kg are given which is 500 mg of caffeine for a 100kg (220 lb) person. Under those
conditions, at least in short-term studies, problems are often seen. This is an enormous amount of caffeine.
Putting this in a real world perspective, a typical soda or cup of coffee might contain 60-100 mg of caffeine,
or approximately 1/5th to 1/8th the amount used in most studies. Of course, we all know people who’s idea
of caffeine intake means drinking the entire pot and, in that situation, the above might actually apply. But
the person drinking a soda with a meal or a cup of coffee won’t even be close.
At the same time, epidemiological studies (which are not the strongest data set in my opinion) suggest that
regular caffeine/coffee intake may actually be beneficial in terms of limiting the incidence of diabetes and
may play a role in weight loss.
So clearly it’s a bit more complicated than it looks (or is claimed) and this paper set out to uncomplicate
things.

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The first data set the review looked at was epidemiological data. Now, I’m no fan of epidemiology in general,
there can be a lot of confounding factors when you’re trying to determine what causes what. At best, that
kind of data gives a starting point and some possible correlational data to do direct work; at worst it’s useless.
That said, looking at 20 studies on the topic, the researchers found that 17 of the 20 showed a beneficial
effect of habitual coffee/caffeine intake on diabetes and glucose metabolism, 3 found no effect and none
showed a negative effect.
Getting a bit more detailed, four of the studies suggested that non-caffeine components of coffee were
involved (that is, pure caffeine and coffee per se may have different effects, a topic I’ll come back to below)
and four studies found an effect of decaf coffee (suggesting that non-caffeine components are playing a role
here). One study suggested that the impact of coffee was due to an effect on body weight (weight loss)
which was the next topic of the paper and what I’ll discuss next.
Looking first at rat data, the paper examines data showing that caffeine can reduce bodyweight, fat pad
weight and even fat cell number. However, humans aren’t rats and human data on this topic is mixed at best.
One human study found no impact of caffeine on weight loss but as mentioned above it may be that coffee
and other non-caffeine components explains the epidemiological data.
Next up, the paper looked at the impact of caffeine on thermogenesis (calorie burning) and lipolysis (fat
mobilization). It comments that a habitual caffeine of 600 mg/day (~6 strong cups of coffee) could lead to an
extra caloric expenditure of 100 cal/day (equivalent to walking about 1 mile for a 150 lb person). This effect
also occurs with ground and instant coffee, but not decaf so the effect is probably mediated via the caffeine
itself. Do note that the body can develop tolerance to these effects so any effect might not be very long
lasting.
Related to this, caffeine has also been shown to increase lipolysis (fat mobilization) and fat oxidation and
both caffeine and coffee have this effect; decaf does not so it’s clearly an effect of the caffeine per se.
Interestingly, both the impact on lipolysis and fat oxidation is more pronounced in non-obese than obese
individuals; leaner individuals, probably due to a greater sensitivity to lipolytic stimuli, get a larger effect.
In any case, I want to expand on that a bit, even if caffeine is having a negative impact on insulin sensitivity
or insulin levels, the simple fact is that it increases fat mobilization. Combined with a caloric deficit or
exercise, this means that those fatty acids can be burned off the body. The idea that caffeine is somehow
bad on a diet because of an impact on insulin sensitivity is missing the forest for the trees; caffeine increases
fat mobilization and burning and that’s what matters in the long run for losing body fat.
The paper also mentions that caffeine may increase energy expenditure. Doses of 3-30 mg/kg in rats
increase spontaneous activity and this type of activity (called NEAT or non-exercise activity thermogenesis
in humans) can amount to a fairly considerable energy expenditure. Basically, caffeine may help with weight
loss by making you move around more. Again, decaf does not have this effect.
Additionally, a very well known effect of caffeine is improved exercise performance. Caffeine pre workout
decreases fatigue, causes more fat to be used (sparing glycogen) and has a host of other effects. By allowing
exercisers to work harder, caloric expenditure can be increased. Which can only facilitate fat loss.
The next topic discussed has to do with the direct impact of caffeine/coffee on insulin and blood glucose
tolerance with a majority of short-term studies showing a negative impact of coffee/caffeine on glucose
tolerance when given right before a carbohydrate containing meal.
Note that caffeine was not found to raise insulin or blood glucose when not given with a carbohydrate meal;
the fear of caffeine on low-carb diets (it’s often claimed that caffeine will raise insulin and should be avoided
on such diets) appears to be unfounded. However, this data is at odds with the epidemiological data
suggesting that chronic caffeine/coffee intake decreases diabetes risk.

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Data comparing the effects of decaf to caffeinated coffee suggests a possible explanation; decaf coffee
tends to lower blood glucose, suggesting the presence of non-caffeine compounds in coffee that may
beneficially impact on blood glucose levels.
Note also that animal research suggests a tolerance to any impact of caffeine on blood glucose levels
although this has not been studied in humans. However, humans are known to develop a tolerance to the
stimulant, thermogenic and other effects of caffeine, it may be that chronic intake of caffeine has a very
different effect on blood glucose levels that studies looking at single dose intakes.
Mechanistically, caffeine probably impacts on blood glucose tolerance by raising blood fatty acids and
catecholamine levels, both of which impair skeletal muscle insulin sensitivity. That is, the way that caffeine
might have an impact on insulin resistance (and thus indirectly insulin levels when carbohydrates are
consumed) is by its effects on lipolysis.
Additionally, the potential impact of coffee/caffeine on fullness was noted but this has not been well
researched in humans, some studies indicate higher satiety in folks using coffee/caffeine habitually.
Next the paper delved into other potential health effects. Acutely, caffeine/coffee can raise blood pressure a
bit but the body develops partial tolerance rapidly. High caffeine intakes have been found, in animal studies,
to cause problems with pregnancy; as well, it may potentiate the negative effects of alcohol and tobacco in
this regards. Intakes of >3 cups/day of coffee can decrease fetal birth weight.
Additionally, caffeine withdrawal can cause headaches, irritability, anxiety, depression, drowsiness and
fatigue. Folks wanting to reduce their caffeine/coffee intake (for whatever reason) should do so gradually to
avoid problems.
High doses of caffeine can also contribute to the risk of kidney stones in elderly individuals and could cause
problems with osteoporosis; this is mainly seen with daily calcium intake is low to begin with.
Early research suggested a link between coffee and an elevation of blood lipids but this turns out to only
hold for boiled coffee, not brewed.
Finally, the paper discussed the issue of non-caffeine compounds in coffee that might have additional effects
on the body. One (I’ll spare you the name) has been shown to decrease glucose uptake from the intestine,
this might offset negative potential effects of caffeine on blood glucose levels (caffeine alone accelerates
glucose uptake from the gut).
Another compound (called a quinide) was shown to enhance glucose uptake and insulin sensitivity in rats,
and both the high antioxidant content of coffee along with the magnesium intake may improve insulin
sensitivity in the long-term; this might explain the discrepancy in the short-term and epidemiological data.
More research into the non-caffeine components of coffee still needs to be done.

Application

So what’s the take home in this? Caffeine/coffee intake appears to have different effects when looked at in
the short and long term; looking only at acute dosing studies (esp with extremely high doses of caffeine)
aren’t that relevant to how people actually consume caffeine (over the long term).
In the short-term, caffeine can impact positively on a number of factors (such as delaying fatigue during
exercise, increasing lipolysis, and increasing fat oxidation and caloric expenditure) but negatively on others
(decreased glucose tolerance/increased insulin response, slight increase in blood pressure).
However, longer term studies suggest that habitual caffeine/coffee intake is, overall, beneficial: it decreases
the risk of diabetes and may contribute to preventing weight gain Tangentially, of course, any benefit of

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coffee/caffeine itself is going to be more than outweighed if you fill it up with sugar, cream and other high
calorie goodies.
My take on the topic: used in reasonable amounts, caffeine pretty much does nothing but help fat loss. The
impact on insulin sensitivity is overstated (in my opinion) only applying to acute studies with massive
doses. The known impact of caffeine on lipolysis and improving exercise performance is so well-established
as to be beyond debate.
So use caffeine, just don’t go nuts with it.

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Fiber – It’s Natures Broom
Years ago I remember lamenting (and writing somewhere) that I was fairly sick of reading research papers
on how eating more fiber was good for people, how it was time for nutritional science to move into relatively
more interesting things than a topic that had literally been beaten to death.
Thankfully, soon thereafter leptin was discovered and nutritional researchers could start looking at things
more interesting than why eating high-fiber vegetables were good for you (a nutritional tidbit that I file under
the ‘Grandma was right’ category).
Even so, there is still some confusion regarding fiber out in the world of nutrition regarding fiber. And boring
or not, it’s a topic worth clearing up. So today I want to take a fairly comprehensive look at dietary fiber,
what it is, what it does in the body, how it impacts on things like body composition (and health to a lesser
degree) and finish by looking at some (admittedly vague recommendations).
.

What is Fiber?

Generally speaking, fiber is included within the category of dietary carbohydrates (many athletes or
bodybuilders divide carbohydrates into starchy and fibrous for example). But fiber is distinct enough to be
considered separately from other types of digestible carbohydrates. Perhaps surprisingly, defining what is
and isn’t a fiber is actually a more complicated issue than most would think.
Chemistry, botanical and physiology types all sort of want to use different definitions and spend altogether
too much time arguing about what is and what isn’t a fiber. Since I’m less interested in chemical or botanical
issue than physiological ones, I won’t bore people with the details of those of those definitions and
arguments. Rather, I’m interested in the physiological effects and, hence, the physiological definitions.
Even there there are two primary definitions which are used:
1. Soluble vs. insoluble (aka viscous vs. non-viscous)
2. Fermentable vs. infermentable
I suspect that most are at least passingly familiar with the first definition above. If not, here’s what it
means. Soluble fibers go into solution in liquid. A good example is guar gum, if you put a spoonful in water
and mix it, it will turn into this gel-like mass; that’s because it’s soluble in fluid. Insoluble fibers, in contrast
don’t do this, you can mix them until the cows come home but they won’t ever go into solution.
I suspect that readers are relatively less familiar with the fermentable vs. infermentable definitions. I’ll come
back to this below when I talk about the caloric value of fiber but, simply, some fibers can be fermented
(specifically by bacteria in the intestine) into other things (e.g. short-chain fatty acids, CO2 or methane) while
others are infermentable (they cannot be converted into those other things).
.

What Does Fiber Do?

Fiber has a number of different effects in the body which are relevant to both health and body
composition. It’s worth noting that, strictly speaking, fiber is not an essential nutrient. That is, you won’t die
if you don’t eat it regularly (or at all) and there are cultures such as the Alaskan Inuit and the African Masai
that subsist on a diet that is essentially devoid of fiber. However, that doesn’t mean that a sufficient intake
of dietary fiber isn’t good for you or can’t provide either health or body composition benefits.

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Below, I’ve listed a bunch of the major effects of dietary fibers (and note that some of these occur in the
upper GI tract, others in the lower but I’m not getting into that much detail) in terms of their physiological
effects.
1. Promoting fullness/satiety
2. Slowing gastric emptying
3. Decreasing nutrient absorption
4. Improved glycemic control, secondary to delayed gastric emptying and impaired nutrient absorption
5. Decreasing blood cholesterol
6. Decreasing mineral absorption
7. Effects on insulin sensitivity via fermentation to short-chain fatty acids
8. A number of effects relevant to colon cancer
9. Helps with poopin’
I want to touch on each below although I’m going to focus more on some than others.

Satiety
One of the myriad signals for fullness during or after a meal has to do with the physical stretching of the
stomach. And high-bulk foods are far more likely to do this than low-bulk foods. In this context, meals or
foods high in fiber generally contain a lot of bulk in few calories (a topic I discussed in more detail in Energy
Density).
Thus they tend to make people feel fuller both in the short- and long-term. In this context, I recall a rather
‘brilliant’ study a few years back which found that people who ate salad first in a meal ate less total calories;
the high-bulk, high-fiber items filled them up so that they ate less of the more calorie dense foods. Another
one for the ‘Grandma knew best’ file.
In a slightly different context, it’s worth noting that individuals who have trouble meeting their energy
requirements (e.g. athletes or ‘hardgainers’) may find it better to save salads for the end of the meal
specifically so that they don’t get full too soon before eating the higher calorie part of the meal.

Slowing Gastric Emptying


As I mentioned above, soluble fibers tend to form a gel-like substance in liquids and one consequence of a
high soluble fiber intake is that gastric emptying (the rate at which foods empty the stomach) is slowed when
they are eaten. Basically, they cause the chyme (the partially digested nutrients in the gut) to form this big
gel which empties the stomach more slowly. This, along with the physical stretching of the stomach tends
to keep people fuller in the longer term because the food stays in the gut longer.

Impaired Nutrient Absorption


Another effect, again primarily seen with soluble fibers, is an impairment of nutrient absorption, and this
holds for carbohydrates, fats and dietary protein. Essentially, due to the gel-like mass that is formed,
digestive enzymes can’t get access to the other nutrients so that more is carried out of the body. This means
that high-fiber diets will result in less total caloric absorption, basically the left-hand side of the equation
discussed in The Energy Balance Equation will be lower when a large amount of soluble fiber is consumed.
I’d note that the effect isn’t massive, fiber may reduce total fat absorption by about 3%, protein by 5%. I
can’t find a good value for carbohydrates at the moment. Put more concretely, an increase in dietary fiber
from 18 to 36 grams per day might reduce total caloric absorption by 100 calories per day.

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Now, depending on how you want to look at this, it can be seen as either a good or bad thing. For individuals
trying to lose weight, higher fiber diets will not only have positive effects on fullness and the rest but will
result in less total calories being absorbed from the diet. Again, the high-fiber nature will reduce the Energy
In side of the equation (which only counts calories which are actually absorbed).
On the other hand, for athletes or bodybuilders, the impact of a high-fiber intake could be seen as
detrimental, especially given that soluble fibers impact on protein absorption. While it would be nice if fiber
only impacted on carb or fat absorption, that simply isn’t the case. As well, for athletes with very high energy
demands, losing digestible energy due to a high fiber intake might not be the best thing. Again, I’d note that
the total impact isn’t massive but it is worth considering.

Improved Glycemic Control


One of the most well-known and talked about effects of a high-fiber intake is improvement in blood glucose
control. Between the slowing of gastric emptying and impairment of carbohydrate digestion, high soluble
fiber intakes tend to improve blood sugar control; rather then seeing larger spikes (due to rapid digestion)
which can be followed by crashes, blood sugar levels are balanced out. In that crashing blood glucose can
be another stimulus for hunger, this can have an additional impact on hunger control between meals
(especially important when dieting).

Decreasing Blood Cholesterol


I’m actually not going to talk about the impact of fiber intake on blood cholesterol levels in great
detail. Sufficed to say that high-fiber intakes tend to improve blood lipid levels and do this through a variety
of different and inter-related mechanisms. If you want more detail than that, pick up a nutrition textbook.

Impairment of Mineral Absorption


In addition to global impacts on carbohydrate, protein and fat absorption, dietary fibers can also negatively
affect mineral absorption especially calcium, magnesium, sodium and potassium. I’d note that, in general,
this isn’t really an issue for concern unless the intake of those nutrients is insufficient in the first place.
As well, when fiber intake is increased from foods (as opposed to dietary supplements), there is generally
an increase in mineral intake in the first place which should help to offset any issues. For example, the fiber
intakes of our evolutionary diet is thought to be massive (some have estimated it at 100-150 grams per day)
but nutrient deficiencies aren’t seen; this is most likely due to the fact that the fiber is coming from nutrient
dense fruits and vegetables.
However, when people start adding horse-doses of fiber supplements to their diet, problems can start. Older
readers may remember the bran craze in the 80’s, when bran was found to lower cholesterol, people starting
eating it in massive amounts. But they were often doing it from purified sources rather than whole
foods. While this may have improved cholesterol levels, it ended up causing issues with mineral imbalances
because the massive fiber intake was not accompanied by an increase in nutrient intake.

Effect on Insulin Sensitivity via Fermentation to Fatty Acids


As I mentioned above, another categorization of fiber is that of fermentable vs. non-fermentable, referring to
whether a given fiber can be fermented (via the bacteria in the gut) to other things. The other things that
most are familiar with are hydrogen, carbon dioxide and methane; these are what cause the gassiness that
can occur with high-fiber intakes. Specifically, methane is what give farts their wonderful smell.

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But fiber can also be fermented to short-chain fatty acids such as acetate, propionate and butyrate that are
re-absorbed into the body and which have a variety of physiological effects. One of those is to provide
calories, a topic I’ll come back to shortly. But the other is to impact on fuel metabolism.
The short-chain fatty acids provided by fiber fermentation impact on both fat cell metabolism and insulin
sensitivity. And while these short-chain fatty acids positively impact on insulin sensitivity, they appear to do
it by blunting the release of fatty acids from the fat cell. Yes, that says what you think it says: high-fiber
intakes may be limiting fatty acid release from fat cells. I’ll come back to this below.

A Number of Effects Relevant to Colon Cancer


Again, not a topic I’m going to get into much detail on. Sufficed to say, high-fiber intakes have a number of
physiological effects that reduce the risk of colon cancer. Get a textbook for more.

Helps with Poopin’


And, of course, possibly the most well known effect a high-fiber intake is regularity and comfort in
pooping. That’s actually what the title of this piece refers to, I have often commented that fiber is nature’s
broom. It helps sweep stuff through the intestines and out the other end. It does this through a number of
mechanisms.
First and foremost, fiber speeds the transit time of food from one end of the intestines to the other. So rather
than sitting in the intestines, it moves towards the exit more quickly. As well, fiber contributes to fecal bulk,
essentially the size of the poo that is produced. This increase in bulk also pulls more water into the fecal
mass which makes the poop softer and easier to pass. Both of these latter effects further contribute to the
decreased transit time and all of this contributes to better regularity.
And, at the end of the day, who can argue with a good poop?
.

Fiber and Energy Balance

Relevant to issues of body composition, fiber can contribute in a number of ways to The Energy Balance
Equation. As noted above, fiber impacts on caloric absorption (decreasing it, generally) along with fullness
(which may cause people to spontaneously eat less) along with blood glucose control and several other
mechanisms. In general, the effect is to reduce either total food intake or caloric absorption, facilitating
weight loss.
I’d mention again that the effect of fiber on fat cell metabolism via the conversion to short-chain fatty acids
is perplexing, one way of looking at this is that high-fiber intakes might hurt with fat loss. This might become
more relevant when people get very lean and fatty acid mobilization is becoming more difficult (for reasons
discussed in The Stubborn Fat Solution). At the same time, real-world results call the real-world significance
of this into question. High-fiber intakes have been part of hardcore diets for decades and folks seem to be
doing alright.
Depending on the goal (e.g. weight loss vs. weight gain), this can be seen as good or bad depending on the
context. For individuals trying to lose weight, most of the effects of a high-fiber diet could be seen as
generally positive. Being fuller with more stable blood sugar and absorbing fewer calories would seem a
good thing.
As noted above, for individuals trying to increase their energy intake and/or gain weight, a high-fiber intake
could potentially be a negative. Between making the individual fuller at a given meal and/or keeping them

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fuller longer during the day, along with impairment of caloric absorption, high-fiber intakes might have a
negative impact overall for some people.
.

Newsflash: Fiber Provides Calories to Humans

But there is another effect of fiber on energy balance that often goes unappreciated. Backing up, it’s often
stated that fiber provides no calories to the body since humans lack the enzymes necessary to digest it. This
has often been taken even further to claim that high-fiber vegetables are ‘negative calorie foods’, that is they
take more calories to digest than they provide (assumed to be zero).
Here’s the thing: it’s not true. Not entirely anyhow.
Above I discussed the issue of fermentation of some types of fiber to short-chain fatty acids which are then
reabsorbed by the body. Well, those fatty acids provide calories to the body. While there is still some debate
in the area, researchers have assigned a caloric value to fiber of 1.5-2 cal/gram (depending on the specific
type).
Admittedly this is an average and will depend on the specifics of the diet and the type of fiber but, simply,
the idea that fiber provides no calories to the body is not true. While the caloric value of fiber is still lower
than starchy carbohydrates (4 cal/g), it is not zero.
.

How Much and What Kind of Fiber?

So how much fiber do we need? As noted above, strictly speaking fiber is not an essential nutrient; you
might be healthier with it but if you never ate another gram you would not die. You might want to die when
you tried to poop but you wouldn’t actually die without it.
But due to the non-essentiality of fiber for human survival, it’s hard to make specific recommendations for
daily fiber intake.
The American Dietetic Association recommends an intake of 10-13 grams of fiber per 1000 calories
consumed. This is roughly 20-30 grams per day for an average day’s diet of 2000-3000 calories per day. It’s
worth noting that the average fiber intake in the modern diet is about 10-11 grams/day which is far below
this. Most people would probably benefit from eating more fiber but they’d also generally benefit from eating
more fruits and vegetables generally.
As I mentioned, our evolutionary diet is thought to have contained absolutely massive amounts of fiber on
average, intakes of 100-150 grams/day has been thrown around in some scientific papers. I would note
again that this would have come from the intake of massive amounts of fruits and vegetables, providing
numerous other nutrients (especially minerals and vitamins) that wouldn’t be found if you tried to get that
much fiber from supplements.
In that context, it’s worth mentioning that high-fiber foods, typically fruits and vegetables, contain tons of
other nutrients important to health or what have you so looking only at the fiber content can be a bit
misleading. Getting adequate amounts of high-fiber fruits and vegetables on a daily basis has benefits far
beyond just the fiber content; getting some at each meal would seem to be a good thing.
And yes, I am waffling on this. There is very little hard and fast data on optimal fiber intakes for any goal. Too
little is bad, too much is probably bad. Somewhere between those two extremes is about right. People
eating the modern diet get too little fiber and should increase it. I’ve seen some meal plans that, frankly,
included absurd amounts of fiber (folks with eating disorders often do this type of thing to stave off the
gnawing hunger). Find balance, people.

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Depending on meal frequency, somewhere between 5-10 grams of fiber per meal would seem a decent
place to start. That should provide anywhere from 30-60 grams of fiber per day, covering average
recommendations without being excessive.
I would note that if you fiber intake is currently low, do NOT try to increase it drastically in a short period of
time. The body needs time to adapt to big increases in any nutrient intake and people who jump their fiber
intakes massively often pay a hard price in terms of gas and such.
Finally, on the topic of types of fibers, I don’t get overly concerned with it. The soluble/insoluble fibers can
be further subdivided into a whole host of other categories but I consider this nutritional minutiae of little real
relevance. If you strive to consume a variety of fruits and high-fiber vegetables on a day to day basis, you’ll
get a mix of fibers and cover your bases.
In specific situations, fiber supplements may play a role (for example, soluble fibers such as guar gum can
be put into yogurt/protein powder mixtures to thicken it up and/or help with fullness on a diet). And many
will use psyllium husks as a form of insoluble fiber if they are having issues with constipation or what have
you. But, for the most part, I’d rather see people increase their intakes of high-fiber whole foods rather than
use purified supplements.

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Endurance Training and Obesity: Effect on Substrate Metabolism
and Insulin Sensitivity.

Title and Abstract

Venables MC AND AE Jeukendrup. Endurance training and obesity: effect on substrate metabolism and
insulin sensitivity. Med Sci Sports Exerc. 2008 Mar;40(3):495-502.
PURPOSE:: Obesity and type 2 diabetes mellitus are disease states associated with hallmark features such
as insulin resistance and an impaired ability to oxidize lipids. It has recently been reported that an optimal
exercise intensity for fat oxidation (FATmax) exists; we hypothesize that continuous exercise training at this
specific intensity can lead to greater improvements in fat oxidation and insulin sensitivity than a eucaloric
interval training program. METHODS:: In a counterbalanced, crossover design, eight sedentary, obese, but
otherwise healthy male participants performed two 4-wk blocks of endurance training, either at a
predetermined intensity eliciting maximal fat oxidation (TPCON) or at 5-min intervals of +/- 20% FATmax
(TPINT). During the week preceding the exercise training and 48 h after the final exercise bout, an OGTT,
V O2max test, steady-state exercise, and measurements of body composition were undertaken. Diet was
controlled the day before all trials (50% carbohydrate, 35% fat, and 15% protein; ~2900 kcal.d). Variables
were compared using two-way repeated-measures analyses of variance. RESULTS:: It was shown that fat
oxidation rates were increased by 44% after TPCON (0.24 +/- 0.01 vs 0.35 +/- 0.03 g.min, P < 0.05) but not
after TPINT, and the whole-body insulin sensitivity index was increased by 27% after TPCON (P < 0.05).
These changes occurred despite no change in body weight, body mass index (BMI), waist to hip ratio (WHR),
percent body fat (%BF), or V O2max. CONCLUSIONS:: A continuous exercise training protocol that can
elicit high rates of fat oxidation increases the contribution of fat to substrate oxidation during exercise and
can significantly increase insulin sensitivity compared with a eucaloric interval protocol.

My Comments:

After putting up Steady State vs. Interval Training: An Introduction, I thought this would be an interesting
study to examine (before really delving into the topic) since most of what tends to be written is along the
lines of intervals are always superior to steady state cardio.
Now, let me make a couple of things clear.
First, I am in no-way anti-interval training, although I expect those with poor reading comprehension may
‘hear’ what I’m saying that way. Rather I’m against the uncritically applied idea that somehow intervals are
ALWAYS superior or that steady state is somehow either useless (or, as some claim, detrimental).
Second, this study was not looking at fat loss per se, so some might want to dismiss it out of hand in terms
of its relevance to the debate. Maybe, maybe not. Improving health (and insulin sensitivity is one marker of
health) is just as important as getting lean, and that is what this paper looked at.
As a bit of introduction, it’s recently come to light that one major cause of insulin resistance in obesity has to
do with the accumulation of fat within skeletal muscle. Referred to as intramuscular triglyceride (IMTG), fat
stored within skeletal muscle appears to play a big role in how well (or poorly) the muscle can utilize glucose
and respond to insulin. I’d note that it’s a touch more complicated than that for reasons I don’t want to get
into.

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Oddly, studies of endurance athletes usually find not only increased IMTG but improved insulin sensitivity,
throwing something of a wrench into the whole idea. Various ideas have been thrown around to try to explain
this but, among other things, it appears that there is a defect in the mitochondria in skeletal muscle of obese
people that appears to contribute to the IMTG-related insulin resistance; whether this defect causes or is
caused by obesity is currently being debated. Of more relevance is the question of whether or not it can be
‘fixed’ with proper training (e.g. to improve mitochondrial functioning).
The point being that the difference between fat people with large amounts of IMTG and trained endurance
athletes with high levels of IMTG is probably related to the improved mitochondrial functioning in the
endurance guys.
Now, it’s well established that regular exercise improves insulin sensitivity although previous studies have
been split as to whether the effect is a function of intensity or volume. Some work says that only high intensity
works, other suggests that low-intensity works, I’ve seen some work that it depends on the number of calories
burned, one study suggests that it’s the duration of training.
But given the major role of IMTG in insulin resistance, the current paper set out to see if endurance training
at an intensity that caused maximal fat oxidation (e.g. ‘burned’ the most fat during activity) would improve
insulin sensitivity more than an interval program that was set up to burn an identical number of calories.
Eight obese males with no major health issues were recruited and followed the same training program. After
a three day break-in including an exercise test to determine the exercise intensity where they burned the
most fat (called FatMax) and a test of insulin sensitivity they all did the continuous program
for 4 weeks, followed by another set of tests, followed by a 6 week washout period. Then another 3 days of
testing, 4 weeks of the interval training program and then another 3 days of testing. A variety of measures
were taken including an oral glucose tolerance test, body composition, etc. The diet was set to avoid weight
loss on either exercise program. This is important because weight loss by itself tends to improve insulin
sensitivity so often the effects of the exercise program are mediated by weight loss.
The continuous exercise program consisted of 5 days/week at the intensity shown to elicit FatMax, starting
at 30 minutes and increasing by 10′ per week to a maximum of 60′ by week 4. It turned out that this occurred
at an intensity of roughly 45% VO2 max which corresponds to about 60% of maximum heart rate.
The interval program consisted of alternating periods of 5 minutes either 20% above or 20% below the
intensity of FatMax, again starting at 30 total minute and increasing by 10 minutes to an hour by week 4.
Five days per week. So 5 minutes were done at 65% VO2 max or 75% max heart rate or so alternated with
5 minutes at 25% Vo2 max (very low % max heart rate).
Body composition changed in neither group and the average energy expenditure for the workouts were the
same.
Of some interest, only the continuous group showed an increase in fat oxidation during exercise, the interval
group did not. This meant, to quote the researchers “…the reduction in RER during exercise meant that
there was significant increase in the fat oxidation rate during exercise. Rates of fat oxidation increased by
44% after [continuous training] but no change was observed after [interval training].”
Tangentially and with a tone of snarkiness, I’d point out that this pretty much flies in the face of most of the
‘Aerobic exercise is bad because you adapt to it’ arguments. Yeah, they adapted….by burning more fat for
fuel with no reduction in caloric expenditure. How awful.
Of more relevance to this paper, since fat oxidation during exercise may or may not relevant to fat loss
anyhow, only the continuous group showed increases in insulin sensitivity and this was correlated with the
increases in fat oxidation. Given that one adaptation to chronic endurance training is to use more IMTG, and
given that only the continuous group increased fat oxidation, this makes sense.

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Getting into the discussion, the researchers address some of the observations, especially as it pertains to
earlier work. Most of this I addressed above having to do with different study results and intensity, volume
and such.
One issue I do want to address is the intensity and duration of the interval group’s training since I suspect
this is where most of the pro-interval crowd will find a ‘flaw’ in the study. It’s true that 5 minutes of interval
work at roughly 75% of max heart rate is not a tremendously high intensity.
The researchers specifically mention one interval study (by Talanian) which used an interval workout of 10X4
minutes at 90% VO2 max (this is pretty close to maximum heart rate) and found an increase in insulin
sensitivity, possibly due to the higher total energy expenditure. The researchers only noted that “..the
intensity used by Talanian et .al. would far exceed the tolerance of the obese sedentary male.” True that, no
sedentary individual would handle such a workload.
And, yes, I realize that many of the popular fat loss interval programs use much shorter bouts which are
more likely to be done. Of course a short interval program of 5X30 seconds hard/30 seconds easy wouldn’t
come close to burning as many calories as the study of Talanian (or this one) either.

Summing Up

This study compared improvements in fat oxidation and insulin sensitivity for obese males either performing
30-60 minutes of steady state cardio (at an intensity set to elicit maximal fat oxidation) or an equal calorically
burning interval session. Steady state exercise was superior in all parameters. Let’s see if the folks claiming
to use ‘science’ to support interval training cite this one.
In the next part of the Interval vs. Steady State series, I get a little bit silly in Pole Vaulting for a Hot Body.

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Different Glycemic Indexes of Breakfast Cereals Are Not Due to
Glucose Entry into Blood but to Glucose Removal by Tissue.
Schenk S et. al. Different glycemic indexes of breakfast cereals are not due to glucose entry into
blood but to glucose removal by tissue. Am J Clin Nutr. (2003) 78(4):742-8.
BACKGROUND: The glycemic index (GI) of a food is thought to directly reflect the rate of digestion and
entry of glucose into the systemic circulation. The blood glucose concentration, however, represents a
balance of both the entry and the removal of glucose into and from the blood, respectively. Such direct
quantification of the postprandial glucose curve with respect to interpreting the GI is lacking in the literature.
OBJECTIVE: We compared the plasma glucose kinetics of low- and high-GI breakfast cereals. DESIGN: On
2 occasions, plasma insulin concentrations and plasma glucose kinetics (by constant-rate infusion of [6,6-
(2)H(2)]glucose) were measured in 6 healthy males for 180 min after they fasted overnight and then
consumed an amount of corn flakes (CF) or bran cereal (BC) containing 50 g available carbohydrate.
RESULTS: The GI of CF was more than twice that of BC (131.5 +/- 33.0 compared with 54.5 +/- 7.2; P <
0.05), despite no significant differences in the rate of appearance of glucose into the plasma during the 180-
min period. Postprandial hyperinsulinemia occurred earlier with BC than with CF, resulting in a 76% higher
plasma insulin concentration at 20 min (20.4 +/- 4.5 compared with 11.6 +/- 2.1 micro U/mL; P < 0.05). This
was associated with a 31% higher rate of disappearance of glucose with BC than with CF during the 30-60-
min period (28.7 +/- 3.1 compared with 21.9 +/- 3.1 micro mol. kg(-)(1). min(-)(1); P < 0.05). CONCLUSION:
The lower GI of BC than of CF was not due to a lower rate of appearance of glucose but instead to an earlier
postprandial hyperinsulinemia and an earlier increase in the rate of disappearance of glucose, which
attenuated the increase in the plasma glucose concentration.

My comments: This is another older paper that I wanted to talk about since it ties in somewhat with the
feedback on milk below. In way of introduction, I should probably define glycemic index (GI) for readers
who aren’t familiar with it.
The GI is used to rate carbohydrates by examining the blood glucose response to 50 grams of digestible
carbohydrates. After fasting, subjects are first given some reference food; this used to be glucose but
researchers now use white bread. The blood glucose response to white bread is defined as 100. Then, the
test food is given and the blood glucose response is measured and compared to that of the test food. A
food that shows 60% of the blood glucose response to white bread is given a GI of 60.
It has commonly been assumed that GI and insulin response are related and bodybuilders and athletes
commonly use GI to determine which foods are or are not acceptable to eat (especially on a fat loss
diet). Low GI foods are usually assumed to digest slowly and it is the slow rate of glucose into the
bloodstream which causes the low GI.
A massive number of foods have been tested for GI although there is still much debate as to the validity of
GI in meal planning. GI can vary significantly by food and how it is prepared, as well as between
individuals. Also, GI is measured for 50 gram quantities of foods (that’s 50 grams of digestible
carbohydrates). But this can be misleading; for example, carrots are very high on the GI scale but few
people would eat 50 grams of digestible carbohydrates worth of carrots in a sitting. To counter this, some
researchers have proposed a measure called the glycemic load (GL) which is the total amount of digestible
carbohydrate multiplied by the GI. This at least recognizes that, in the real world, carbohydrate intake
varies. GL can be lowered by either picking lower GI foods or by eating less total carbohydrate, or some
combination of the two.

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Additionally, GI tends to be affected by other nutrients (protein, fat and fiber) although not always in the way
you’d think (and not all research finds a significant impact of protein and fat). For example, protein tends to
lower the GI of carbohydrates but insulin levels often increase when you add protein to carbs.
For reference, the most complete site on the web for information about GI is Rick Mendosa’s Site.
Which brings us to the above study. As mentioned above, bodybuilders and athletes usually assume that a
low GI means a low insulin response but the study above draws that conclusion into question. Rather it
found that the low GI food showed a lower blood glucose response because it generated a higher early
insulin response (clearing blood glucose out of the bloodstream) at the 30 minute mark (by 60 minutes, both
foods showed similar insulin levels). Quoting directly from the paper "Bran cereal has a low GI because a
more rapid insulin-mediated increase in tissue glucose uptake attenuates the increase in blood glucose
concentration, despite a similar rate of glucose entry into the blood."
That is to say, both foods released glucose into the bloodstream at similar rates, but the bran cereal showed
faster uptake due to a higher initial insulin spike, which lowered the overall GI response.
The researchers also noted that the bran cereal contained more protein than the corn flakes and this is
probably what caused the higher insulin response (and lower blood glucose) which ties into my comments
above.
Somehow, I don’t think bodybuilders would argue that combining low GI carbs with protein is bad for fat loss,
yet here we have an (as of yet unreplicated paper) showing that the initial insulin response is higher;
essentially, the higher initial insulin response caused the lower GI in this case. Yet most bodybuilders also
believe that high insulin is detrimental to fat loss. Here we have a study that I think questions that idea. At
the very least, the small initial insulin spike certainly wouldn’t appear to be hurting things, it’s likely that
sustained insulin levels would be more problematic by limiting the ability to mobilize fat for fuel.
Then again, at least one study found that spiking insulin (high GI condition) resulted in a larger rebound in
blood fatty acid levels (after blood glucose crashed) compared to keeping insulin low but stable (low GI
condition) so maybe there’s more to this picture than we yet realize.

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Dissecting the Energy Needs of the Body – Research Review

Title and Abstract

McClave SA, Snider HL. Dissecting the energy needs of the body. Curr Opin Clin Nutr Metab Care. (2001)
4(2):143-7.
The majority of the resting energy expenditure can be explained by the energy needs of a few highly
metabolic organs, making up a small percentage of the body by weight. The relationship of the specific size,
individual metabolism, and proportional contribution to the actual body weight and total energy expenditure
for each of these organs is a dynamic process throughout growth and development, the onset of disease,
and changes in nutritional status. Defining the energy needs of the individual tissues and organ systems
immeasurably enhances our understanding of the body’s response to these clinical processes, which
otherwise could not easily be evaluated by focusing solely on total energy expenditure, fat-free mass,
nitrogen imbalance, or actual body weight. Recently reported studies have served mainly to reinforce
concepts described previously, and clarify some areas of controversy.
.

Background

Last month, I answered a Q&A on Reducing Body Fat Percentage by Gaining Muscle and in that article I
mentioned that the actual caloric burn of skeletal muscle is actually quite low compared to what is often
claimed. In the comments section someone mentioned a recent seminar where the value of 50 cal/lb for
muscle was thrown out and asked for clarification on my claim.
Unlike previous research reviews, today’s paper isn’t an actual study but rather a review paper so my
discussion will be a little bit different in terms of what I want to look at. The paper itself is actually fairly
technical and I don’t want to focus so much on the technical aspects as on the concepts and implications
that the paper deals with as they pertain to issues of body composition.
More specifically I want to look at some of the common claims that are often thrown around in the world of
body composition such as “Adding muscle mass significantly raises metabolic rate.” and “Fat cells burn no
calories, they are metabolically inert.” While this paper was examining the issue from a different perspective,
it actually provides good data on both questions.
Specifically today’s paper examines in some detail how different tissues of the body (e.g. muscle vs. fat vs.
organs) contribute to the body’s resting energy expenditure. As well, factor such as disease,
growth/development and under-nutrition are examined in terms of how they impact on different tissues in
the body and their energy expenditure.
As I discuss in detail in Metabolic Rate Overview, there are four primary components to total daily energy
expenditure: Resting Energy Expenditure (REE), Thermic Effect of Activity (TEA), Thermic Effect of Food
(TEF) and Non-Exercise Activity Thermogenesis/Spontaneous Physical Activity (NEAT/SPA).
Of those four, resting energy expenditure plays the major role in total daily energy expenditure, generally
comprising 65-70% of the total. So looking at the differential impact of each tissue on REE tends to
give pretty decent picture of what’s going on.
.

The Paper

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The paper begins with an introduction to the overall concepts, pointing out estimating REE in individuals of
different body sizes has been classically difficult. While body weight per se is a decent indicator, REE actually
tends to scale better with body surface area. However, this gives no indication of which tissues (and in what
proportion) are contributing to overall REE.
Readers may have seen the statement that ‘The largest predictor of REE is lean body mass” and there is
certainly some truth to that. However, lean body mass (aka fat free mass) only predicts 53-88% of the
variability in energy expenditure. There are a number of reasons for this not the least of which being that
lean body mass/fat free mass is not a single homogeneous tissue.
Rather, as discussed in What Does Body Composition Mean, lean body mass represents organs, skeletal
muscle, bone, skin and basically everything in the body that isn’t fat mass. And as you’ll see shortly, each
of those tissues burns very different numbers of calories on a day to day basis. Which means that variability
in the amounts and proportions of those tissues will impact on overall resting energy expenditure.
Next the paper discusses the different methodologies used to estimate the resting energy expenditure of
different tissues. I don’t want to get into huge detail on this. Suffice to say that newer technology has allowed
for more and more accurate methods of estimating the caloric expenditure of different tissues in the body.
While they are still not error-free (nothing in science ever is), some of the newer methods of measurement
may explain why some of the oft-held beliefs about caloric expenditure and values that are often thrown out
are turning out to be wrong. Of course that also means that future developments may render current values
incorrect.
.

The Normal Human

The next topic addressed in the paper is an examination of the different tissues and how they contribute to
resting energy expenditure in a fairly ‘average’ human being. I’ve reproduced Table 1 from the paper below,
honestly this was the main reason I wanted to examine this paper, to get this chart up on the site.
.

Organ or Metabolic Rate Metabolic Rate % Overall Weight in Weight in %Body


Tissue (kcal/kg/day) (kcal/lb/day) REE Kg Lb Weight

Adipose 4.5 2.0 4 15 33 21.4%

Muscle 13 5.9 22 28.2 61.6 40

Other 12 5.4 16 23.2 51 33.1

Liver 200 90.9 21 1.8 3.96 2.6

Brain 240 109 22 1.4 3.08 2.0

Heart 400 181 9 0.3 0.66 0.5

Kidneys 400 181 8 0.3 0.66 0.5

Other refers to bone, skin, intestines and glands.


Note: the lungs have not been measured for methodological reasons but have been estimated at
200 kcal/kg similar to the liver.
.
As you can see above, and quite contrary to what is commonly stated, skeletal
muscle actually has a fairly low resting energy expenditure, roughly 6 calories per

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pound. This is contrast to very old values of 100 calories/pound or even more
recent claims that a pound of muscle will raise metabolic rate by 40-50 calories
per pound.
Additionally, an in contrast to what is commonly claimed, fat cells do burn
calories. Admittedly the value is not massive (roughly 2 calories per pound) but
the idea that fat cells are completely inert is also incorrect. We now know that fat
cells produce a variety of hormones, etc. (e.g. leptin, adiponectin) and that
expends calories. Again, not much per unit mass of fat, but for someone carrying
a lot of fat mass, this does add up.
Perhaps of more relevance, and getting back to the paper per se, the primary
contributor to resting energy expenditure comes from the organs with the liver,
heart, kidneys and brains contributing roughly 70-80% of total resting energy
expenditure. This is despite the fact that they only make up approximately 7% of
total body weight. That is, despite their relatively small weight, they are simply
massively metabolically active on a day to day basis.
In contrast, while skeletal muscle may contribute roughly 40% of total weight (a
little bit less in women), it only contributes 28% of total resting energy
expenditure. Essentially, the relatively small caloric burn of a single pound of
muscle mass is made up for by the sheer quantity of it. Which doesn’t change
the fact that adding muscle mass still won’t have a massive impact on resting
energy expenditure.
To put that into mathematical perspective, gaining 20 pounds of muscle would be
expected to increase resting energy expenditure by approximately 120 calories
per day. Certainly that does have an impact overall (equivalent to perhaps 10
minutes per day of moderate intensity cardio) but also keep in mind the time
frames involved to gain that much muscle mass. Expecting that adding a bit of
muscle to have massive impacts on metabolic rate in the short-term is simply
unrealistic; a few pounds gained simply won’t have any major impact.
Rather, I would expect that any real impact of building muscle mass on The
Energy Balance Equation is going to come through the training done to
stimulate/maintain muscle mass increases along with the caloric cost of building
the muscle in the first place. But once it’s there, the caloric expenditure at rest
of skeletal muscle is simply very low.
.

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Factors Affecting Energy Expenditure

Having examined the average contribution of different tissues to the body, the researchers then look at a
host of other topics, only a few of which I’m going to really look at in any detail.
Growth and development is covered first, examining how the ratios of energy expenditure to body weight
changes over the lifespan. Since most reading this are full grown adults, the changes that occur from
childhood to maturity don’t seem that relevant.
One issue of some importance is covered next and that’s the effect of differences in body size between
individuals. In general, if you look at two people of different body sizes, larger folks tend to have lower
resting energy expenditures relative to their body mass. This is most likely related to differences in the
proportion of organ weight (recall from above that the organs contribute the most to overall resting energy
expenditure) to total body weight.
Meaning this: on average, organ weight won’t vary much between individuals. So if one person is larger
than another, that difference in size is likely to occur through changes in either muscle mass or fat tissue,
neither of which makes massive contributions to resting energy expenditure (and differences in body
composition won’t have nearly the impact that most think given the relatively small difference in caloric
expenditure between muscle mass and fat mass).
Practically, this means that equations that estimate resting energy expenditure based solely on body weight
will tend to overestimate larger individuals to some degree. Of course, as I recently discussed in Adjusting
the Diet, since all estimates of energy expenditure and/or caloric intake have to be adjusted based on real-
world changes anyhow, I’m not sure how important this is practically.
I should probably address a question that I imagine will come up in the comments, given the enormous
variability in energy expenditure per pound of tissue, where does the quick estimate of 10-11 calories/pound
(22-24 cal/kg) come from? And the answer is that it’s basically a weighted average of the above values. That
is, if you took the values for caloric expenditure/unit weight times their contribution to overall weight and
worked it out, you’d get a value that was pretty close to the quick estimate value. Again, this will tend to vary
based on actual body size due to differences in the relative contribution of each tissue to the body’s total
weight.
Next the researchers looked at the impact of both undernutrition and refeeding on energy expenditure at
rest. During underfeeding, they point out that skeletal muscle and fat are generally the major tissue lost
while organs are spared. This tends to have the impact of raising the relative proportion of energy
expenditure to body weight (because the low energy expenditure tissues are being lost). Of course, with
extended dieting, there is also an adaptive component of metabolic rate reduction as all tissues in the body
tend to slow their overall energy expenditure.
In contrast, during refeeding, there is often a hypermetabolic state that occurs, possibly due to increases in
protein synthesis, core temperature and the thermic effect of food. As well, there are a number of hormonal
effects that occur when calories are raised, a topic I discuss in more detail in The Full Diet Break, all of which
may have potentially beneficial impacts on overall energy expenditure and metabolic rate.
Finally the researchers examine the impact of disease and injury on energy expenditure but I don’t find that
terribly relevant to this article.
.

Summing Up

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The main point that I wanted to make with today’s research review was to clear up some of the oft-held (and
unfortunately incorrect) ideas regarding the impact of things like skeletal muscle mass and fat mass on
resting energy expenditure. Based on current data, the idea that skeletal muscle burns massive numbers
of calories would appear to be 100% incorrect.
Rather, skeletal muscle actually burns fairly few calories on a per pound basis; it primarily has a major impact
on resting energy expenditure because there is a good bit of it. But adding even moderate amounts of
muscle are unlikely to massively impact on energy expenditure. As noted above, I expect the major effect
to be from the effort of stimulating muscle mass gains along with the energy needed to synthesize that
muscle tissue. But once it’s there it doesn’t burn many calories.
Rather, the majority of resting energy expenditure is generated by the organs which, despite their small size,
burn a massive number of calories per unit weight. Someone on the support forum jokingly asked “So how
do I hypertrophy my liver?”
Finally, fat cells, while not having much of a calorie burn do burn calories. In fact, they are only about 1/3rds
of the burn of skeletal muscle (2 cal/lb vs. 6 cal/lb respectively). While low, someone carrying a lot of fat will
have this add up and it will contribute to overall resting energy expenditure.

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Extremely Limited Synthesis of Long Chain Polyunsaturates in
Adults: Implications for their Dietary Essentiality and use as
Supplements
Plourde M, Cunnane SC. Extremely limited synthesis of long chain polyunsaturates in adults:
implications for their dietary essentiality and use as supplements. Appl Physiol Nutr Metab. 2007
Aug;32(4):619-34.
There is considerable interest in the potential impact of several polyunsaturated fatty acids (PUFAs) in
mitigating the significant morbidity and mortality caused by degenerative diseases of the cardiovascular
system and brain. Despite this interest, confusion surrounds the extent of conversion in humans of the parent
PUFA, linoleic acid or alpha-linolenic acid (ALA), to their respective long-chain PUFA products. As a result,
there is uncertainty about the potential benefits of ALA versus eicosapentaenoic acid (EPA) or
docosahexaenoic acid (DHA). Some of the confusion arises because although mammals have the necessary
enzymes to make the long-chain PUFA from the parent PUFA, in vivo studies in humans show that
asymptotically equal to 5% of ALA is converted to EPA and <0.5% of ALA is converted to DHA. Because
the capacity of this pathway is very low in healthy, nonvegetarian humans, even large amounts of dietary
ALA have a negligible effect on plasma DHA, an effect paralleled in the omega6 PUFA by a negligible effect
of dietary linoleic acid on plasma arachidonic acid. Despite this inefficient conversion, there are potential
roles in human health for ALA and EPA that could be independent of their metabolism to DHA through the
desaturation – chain elongation pathway.

My comments: By way of introduction, early nutrition research was very concerned with determining what
were the essential nutrients for human health and survival. By definition, an essential nutrient is one that is
 Required by the body for survival
 Can’t be made by the body
It’s a bit more complicated than that and there are some nutrients which are defined as conditionally essential
(glutamine is one) but this covers the basics.
Vitamins and minerals are essential, about half of the amino acids are essential and, as early research fought
to determine, it turns out that some fatty acids are essential. These are called, generally, the EFAs and, as
we now know there are two of them.
Due to methodological issues that I won’t detail, determining what fatty acids were actually essential was
actually a fairly difficult problem in the early part of the 20th century. In early research, it was thought that
there were three EFAs, alpha-linoleic acid (ALA, not to be confused with alpha-lipoic acid, an insulin
sensitizer), linolenic acid (LA), and arachidonic acid (AA). When it was found that rats could make AA out of
LA, it was dropped, leaving two EFAs. I’d note that, at one point, it was thought that LA was the only EFA
but, as we now know, both ALA and LA are essential fatty acids.
These two fatty acids are also often referred to by their chemical names (which have to do with their
structure) which are omega-3 (n-3,w-3) for ALA and omega-6 (n-6, w-6) for LA.
Now, both LA and ALA are metabolized in the body (this includes a variety of processes including oxidation
in the liver) to other compounds, I’ll spare everyone the biochemical details.
LA is metabolized to gamma-linoleic acid and then eventually to arachidonic acid. As mentioned above, this
is why AA was removed from the list of EFAs, since the body can synthesize it from LA, it’s not essential.

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ALA is metabolized to EPA (you don’t want to know the full name) which is further metabolized to DHA (same
comment). EPA and DHA are more commonly referred to as the fish oils since they are found in high
amounts in fatty fish.
Now, for the most part, I’m not going to talk much about the LA->AA pathway. The reason is that excess
LA/AA is actually detrimental to the body. AA has inflammatory characteristics and excess LA (esp. in relation
to ALA) is thought to be a harmful to the body. I’d note that studies show that the current ratio of LA:ALA is
around 25:1. It’s thought that a ratio of 4:1 or lower would be better.
Bottom line, most of us get way too much LA in the first place, unless you eat essentially a zero fat diet you
get most of what you need, there’s no real need to make lots of AA from a health or survival standpoint.
Of more concern is the EPA/DHA issue which is what I want to discuss in more detail. Both are critical for
things like optimal health, fat burning, etc. It looks like DHA may be even more important. Babies accumulate
DHA in their brains and babies who either don’t receive sufficient DHA (from the diet) or have a rare genetic
syndrome can end up with brain damage. DHA is present in large amounts in cellular membranes. Basically,
sufficient DHA intake is critical.
Which brings us to the real topic of this week’s paper: Can the body convert ALA to EPA/DHA in sufficient
amounts? Because, if it can, then using a source of ALA such as flaxseed oil is sufficient. If it can’t, then
intake of preformed EPA/DHA via fish oils is going to be required.
Now it’s clear that the human body possesses the enzymatic machinery to convert ALA to EPA/DHA. But
there is an issue of whether the conversion process can occur in sufficient amounts.

Fish Oil: Just The Facts • By Alan Aragon • 7-05-07

The Dawn of Fat Phobia

If you have a few years under your belt, then you can still remember what I call
the “Fat-Free 80’s.” Think back to a time when dietary fat was the enemy. Ah,
yes... A time when fat-free products lined the outer shelves of the supermarket.
A time when it was not a bad thing to get a box of Entemann’s cinnamon rolls,
as long as they were the FAT-FREE cinnamon rolls. Health Valley made some
positively disgusting fat-free cookies, along with a host of other fat-free products
that tasted like sugary cardboard. And we can’t forget the 75% sugar weight
gainer products, those were priceless. 1,000, 2000, 4,000 calories per serving,
and all you had to do was mix about a cup of powder into your favourite drink.
No worries though, these gainers were virtually fat-free! What we were led to
believe was that fat-free products equated to fat-free physiques. Unfortunately,
that was far from the truth.

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During the 1980’s, a disturbing climb in national obesity rates occurred, and
steadily kept its course. Large behavioral trend studies such as the National
Health and Nutrition Examination Study (NHANES II & III), the Behavioral Risk
Factor Surveillance System (BRFSS), and the Calorie Control Council Report
(CCCR) collectively showed a 31% increase in overweight prevalence from
1976-1991. The punch line? This increase in weight was accompanied by an
11% decrease in percentage of calories from fat (from 41.0% to 36.6%). The
most recent report by the BRFSS shows a further decrease in fat intake to 33%,
accompanied by an increase in obesity from 11.6% to 22.1%. This is a 90.5%
increase in US obesity from 1990-2002[1]. It’s obvious that dietary fat is not the
evil culprit in the expansion of the population’s waistline.

A Brief Evolution of Our Knowledge of Fats

As indicated by the fat-free product boom a couple of decades back, there


indeed was the widespread belief that ALL fats were a substance to be
minimized, or avoided altogether. But with the forward march of research, we
came to understand that different fats had different effects on health. Since it’s
human nature to think in black and white terms, the great divide initially fell
between saturated (SFA) and mono- or polyunsaturated fatty acids (MUFA &
PUFA). SFA were thought to be the root of all evil, conjuring images of arterial
plaque and eventual heart failure, while unsaturated fat was regarded as a
universally angelic substance. This turned out to be a gross oversimplification of
reality.

The intricacies and widely varying sources and subtypes of SFA is another
article altogether, but suffice it to say that it’s not that simple to pigeonhole them
as unhealthy. SFA are not created equal. They have markedly variable
physiological effects from the detrimental all the way to the beneficial. Given
this, it depends on which ones you want throw onto the theoretical chopping
block. Stearic acid, an SFA abundant in meat & milk fat, has been consistently
observed to actually reduce blood platelet aggregation [2]. This is a good thing.
In contrast, trans fats (found in high concentrations in commercially baked

352
goods as well as processed & fried foods) have been observed to negatively
impact blood lipids by not only lowering HDL, but increasing LDL as well [3].

Ironically, experimental research exists on healthy humans showing the least fat
was oxidized on the MUFA fat dietary treatment, and the most fat oxidized on a
trans fat diet [4]. This result echoes what’s been seen in rats as well. It appears
that the tighter the control of the study, the less “superior” unsaturated fats turn
out to be for any presumed effect on body composition compared to SFA.
Throw in the fact that a reducing SFA intake and increasing the degree of
unsaturation of fatty acids in the diet reduces testosterone levels [5], and then
you have yet another wrinkle in the mix to concern yourself with.

Then you have medium-chain triacylglycerols (MCT), which are SFAs that
exhibit physiological behavior that’s closer to carbohydrate than fat. MCT has
been hyped to death by those who sell it. But the point is that they are a type of
SFA that may potentially have minor benefits on body composition. I personally
wouldn’t spend a dime on them, but they nevertheless illustrate the fact that
SFAs are a complex and highly varied group of compounds in terms of
physiological effect. As always, the effects of each type of fat undoubtedly vary
with the population in question, as well as individual response.

Finally, with the black and white fallacy of saturated versus unsaturated fats out
of the way, we can now shift the focus on fish oils, which happen to be a rich
source of a particular class of fatty acids under intense study, the omega 3’s.

Enter The Omega-3 Fatty Acids

Omega-3 fatty acids are essential for normal growth and development, but are
noted specifically for their powerful influence over multiple physiological
processes. Alpha-linolenic acid (ALA), one of the two essential fatty acids (EFA)
that the body cannot biosynthesize and must get from the diet, is an omega-
3. EFA are precursors to a class of biologically significant compounds called
eicosanoids, which include prostaglandins, leukotrienes, and thromboxanes.
Eicosapentanoic acid (EPA) and docosahexanoic acid (DHA) can be derived

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from fish oil, and to a lesser degree, flaxseed oil. Consumption of EPA and DHA
has an appreciable number of positive health effects, including decreases in
blood platelet aggregation, lowered blood pressure, enhancement of smooth
muscle function, decreased inflammation, alleviation of dyslipidema, and
treatment of mood disorders [6-9]. There’s even emerging evidence pointing to
the benefits of omega-3 fatty acids on bone health [10].

Archaeological research postulates that humans were biologically designed to


thrive on a diet whose ratio of omega-6 to omega-3 fatty acids was
approximately 1:1, and unlikely greater than 4:1. Today, consumption of n-6 to
n-3 fatty acids is estimated at roughly 25:1 [11]. This is due in part to a
predominance of omega-6 oils available commercially in our food supply (corn
oil, sunflower oil, safflower oil, refined packaged grain products & pastries) and
a relative minority of omega-3 sources (fatty marine fish such as salmon,
mackerel, herring, and flaxseed oil, walnuts, & small amounts in canola oil).
Industrial production of omega-6-rich animal feeds has also resulted in animal
tissues (livestock, eggs, and cultured fish) rich in omega-6 and poor in omega-3
fatty acids. This disproportionately high intake of omega 6’s biases our
physiology towards thrombosis, hyperlipidemia, and vasoconstriction. The
reverse of those effects occurs simply by increasing the proportion of omega-
3’s.

Fish Oil as a Fat Loss Supplement?

So far, the resume of fish oil’s health effects is very extensive. But can it add fat
loss to the list as well? The buzz in the supplement industry would certainly
want consumers to believe so. But as always, the answer can only begin to
reveal itself in the research. Human studies examining the effect of fish oil
supplementation on body composition are scarce, but that makes it easy to pick
them apart.

A decade ago, Couet and colleagues investigated the effect of replacing 6g of


visible dietary fat with 6g of fish oil in healthy adults over a 3-week period, done
12 weeks after a 3-week control diet period [12]. Bodyfat mass and respiratory

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quotient decreased in the fish oil phase. It’s important to note that the flaws in
this study’s design are grave enough to almost completely invalidate it.
Extremely small sample size (6 subjects total), short trial period (3 weeks), and
a complete absence of randomization or treatment balance (opening the distinct
possibility for seasonal variation, among other errors) are the main fatal knocks
that render this data nearly useless.

In contrast, 2 more recent studies conducted within the past 3 years looking at
weight-loss diets supplemented with omega-3’s have not observed any
significant effects on body composition beyond what was caused by dietary
restriction alone [13,14]. But it’s never that simple, since things may differ
according to the population and protocol. In contrast to the previous two trials,
Kunesova’s team examined the effects of omega-3 supplementation on
severely obese female inpatients undergoing a 3-week very low calorie (525
kcal) in-patient weight reduction treatment [15]. Calories were controlled to
accommodate the supplemental omega-3, which was 2.8g/day. Result? The
omega-3 supplemented group lost 1.5 kg bodyweight, and 2.2 cm more off the
waist than the control group.

How about more relevant populations? As of this writing, there are only three
trials in existence examining the effect of omega-3 supplementation combined
with a structured aerobic exercise program on body composition. Let’s dig in. In
1989, Warner and colleagues looked at the effect of walking or jogging 3
days/week for 45–50 minutes at 75-80% maximal heart rate in hyperlipidemic
subjects randomly assigned to 1 of 4 groups: fish oil + exercise, fish oil alone,
corn oil, or control [16]. Body fat was reduced only in the fish oil + exercise
group. These data are severely limited by the absence of an exercise-only
control group, leaving a huge question mark open regarding the relative
contribution of exercise to the bottom line result. A year later, Brilla and
Landerholm conducted a well-designed study on healthy, previously sedentary
men [17]. This trial did contain an exercise-only control group, and no effect of
fish oil on body fat was observed.

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In the most recent fish oil + exercise study to date, Hill’s team examined the
effect of fish oil supplementation (6g) on overweight
hypertensive/hyperlipidemic subjects (24 men and 41 women) over a 12 week
period [18]. Exercise was 3 days/week walking at 75% predicted maximal heart
rate for 45 minutes. Body composition was assessed by dual energy X-ray
absorptiometry (DEXA). Predictably, fish oil supplementation improved blood
lipids and arterial vasodilation. As for body composition, fish oil by itself didn’t
cause any bodyfat reduction from baseline levels, whereas the sunflower oil
control gained bodyfat , but to an insignificant degree. However, fish oil +
exercise caused a 1.1% greater bodyfat reduction compared to the sunflower oil
+ exercise control (1.2% reduction versus a 0.1% reduction in the sunflower oil
group). But here's the kicker... The daily intake of the exercising fish oil group averaged
143.4 kcals less than the exercising control group. Factoring in the reduced calories of the fish
oil group, we’re now looking at a difference of 0.32 kg (0.7 lb) -- less than a pound more weight
loss in the fish oil group in 12 weeks.

The Dark Side of Over-doing Fish Oil Supplementation

Yes, Luke, there is always a dark side. In the world of unchecked marketing
hype, fish oil has definitely gotten the “more is better” stamp. The problem is,
EPA and DHA have a well-documented ability to suppress the body’s immune
response. Although not as consistent as the immune effects, data also exist on
the ability of EPA and DHA to increase bleeding time and oxidation. Let’s take a
look at a couple of the published peer-reviewed research that no one in the
fitness industry talks about.

Thies and colleagues examined the 12-week effect of various fatty acid
supplement mixes on healthy subjects [19]. Various blends of placebo oil and
oils rich in ALA, GLA, AA, DHA, or EPA (720mg) + DHA (280mg) were
compared. Total fat intake from the 9-capsule dose was 4 g/d. The EPA/DHA
treatment was the only one that had a negative effect on immunity, significantly
decreasing natural killer cell activity by 48%. This effect was reversed after 4
weeks of ceasing intake of the supplement.

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Rees and colleagues investigated the effects of various amounts of EPA on
immune markers in young and older men [20]. In a 12-week study, EPA was
incorporated into plasma and mononuclear cell phospholipids. Supplemental
EPA in amounts of 1.35, 2.7, and 4.05g/day caused a dose-dependent
decrease in neutrophil respiratory burst, indicating the suppression of a cellular
defense against immunity threats. This effect was seen in the older, but not the
younger men. Based on these and the previous data, if you’re not a spring
chicken, and immunity is an issue, you might not want to go hog-wild on the fish
oil dosing.

Suggested Use & Take-Home Tips

The cardio-protective benefits of increasing the dietary proportion of omega-3


fatty acids is seen consistently in trials involving various populations and
protocols. Fish oil is one of the few supplements that actually has a substantial
body of scientific evidence backing it up. However, it’s easy to think in terms of
pills instead of food. Those who love fish (and have the time or resources to
prepare or order it) can simply increase or maintain their intake of fatty fish such
as salmon, mackerel, lake trout, herring, albacore tuna, and sardines.

The American Heart Association (AHA) recommends at least two servings of


fish per week for the general population. Think of a palm-sized piece as a
serving. For those with high triacylglycerol levels, a supplemental 2-4g of
combined EPA/DHA is their suggested therapeutic dose. However, note that
caution is advised against supplementing more than 3g combined
EPA/DHA outside of a physician’s care, since some individuals may risk
excessive bleeding [21]. 3 g combined EPA/DHA typically is contained within 10
one-gram capsules. I recommend maxing out your whole food options first
before going the supplemental route. There’s always more complete and
synergistic nutrition contained within whole foods. Having 3-6 oz fatty fish a
minimum of 4 times a week would exempt most healthy folks from needing fish
oil supplementation. For those who can’t or won’t eat fish, there’s always fish oil
capsules, which thankfully are inexpensive, and more convenient than getting
your omega-3’s through fish.

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The amount of EPA/DHA per capsule may vary with the brand. Capsules can
contain anywhere from 250-500mg. Most healthy folks don’t need more than 3-
6 one-gram capsules per day to meet or exceed the amounts that show
benefits. There are no definitive conclusions about optimal proportion of
EPA:DHA, so to error on the side of safety, I recommend finding roughly an
even mix. It’s common and perfectly acceptable for products to contain slightly
more EPA than DHA. If at all possible, make sure your supplement is verified by
the USP (United States Pharmacopoeia) for the peace of mind that you’re
getting what the label is claiming. I would also error on the side of safety and
keep them refrigerated. As a side note, there’s a widespread belief that ALA
from flaxseed is worthless for increasing EPA/DHA since the conversion is
inefficient. However, Harper’s team recently saw 3g ALA/day (from 5.2g
flaxseed oil) raise plasma EPA levels by 60% at the end of a 12-week trial [22].

Looking at the body of evidence as a whole, fish oil (or increased fish
consumption) has great potential for improving cardiovascular health. But for
reducing body fat, the effects are minor to nonexistent. Let’s not forget that fish
oil isn’t some magical negative-calorie food. It still contains 9 calories per gram,
and no matter how much of those calories are used in its processing within the
body, it’s still a net gain in calories after consumption. To sum everything up,
fish oil has health benefits, as well as potential risks. It’s certainly not a matter of
more-is-better. It might have minor fat loss effects in the obese and overweight
population, but their fat loss effect in general is far from conclusively
established. Get a variety of fats in your diet, and get them from whole foods
whenever possible. Fish oil is merely one of many agents that can contribute to
optimal health within the context of well-balanced nutrition. Keep it in
perspective, and keep your eye on the facts.
Without going into the ridiculous detail of this week’s paper, the short-answer is basically “No, it can’t.” Now,
there are some methodological issues with the studies having to do with the amount (giving large amounts
of ALA can cause an underestimation of true conversion) given and some other stuff but the bulk of the data
points to the simple conclusion that the human body is simply terrible at converting ALA to EPA/DHA. In fact,
studies using flax oil supplementation show no change in DHA levels. None. It will raise EPA a bit but the
conversion to DHA is essentially zero.
There are two odd exceptions to the above that I want to mention. The first is in vegans. Due to zero intake
of animal foods, they have zero intake of DHA. But while they show lower levels of DHA, they don’t show

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deficiency symptoms. While more research needs to be done, presumably pathways of
conversion/production of DHA are up-regulated under this situation.
The other is in extreme w-3 deficiency, where plasma DHA levels typically rise after ALA supplementation.
This is just a classic feedback loop, and occurs for other nutrients as well (for example, absorption of certain
minerals will increase the more deficient someone is).
But beyond that, the overall impact of ALA supplementation plasma levels of EPA is small, for DHA
essentially nil. And given the critical importance of both EPA/DHA on human health, fat loss and
performance, the bottom line is that this makes ALA (via flaxseed oil or what have you) an insufficient
replacement for preformed fish oils.
As a couple of final comments, I’d also note that supplementation of EPA doesn’t raise DHA levels either.
Since all commercial fish oils I’ve ever seen contain both EPA/DHA, this is a fairly non-issue. But it is yet
another reason why ALA by itself is insufficient. Not only is the conversion of ALA to EPA small, the
conversion of EPA to DHA is simply nil, hence ALA won’t impact on the body’s DHA levels.
Having established that ALA intake is ineffective at increasing EPA/DHA levels, a final and related question
to address is whether ALA has any effects above and beyond what EPA/DHA are doing. This week’s paper
mentions one possibility which is a mild impact of ALA supplementation on cardiovascular disease. It also
notes that EPA/DHA supplementation has a greater effect. Other researchers (not all agree) feel that the
true EFAs are EPA/DHA, and that ALA is simply a parent compound that is not essential in its own right.
Currently I tend to agree with this stance.

Summing up: the body requires EPA/DHA for optimal function. This includes fat loss, prevention of a lot of
diseases, controlling inflammation, etc. While the body has the machinery to convert alpha-linolenic acid
(ALA, found in high quantities in flaxseed oil), the amount of that conversion is small for conversion to EPA
and negligible for DHA. Hence I don’t feel that ALA/flax oil is an appropriate EFA source. You need to be
taking preformed EPA/DHA (in either capsule or liquid form). This was one of the changes I made to the
second edition of the Rapid Fat Loss Handbook (the first edition allowed for flax to substitute for fish oil).

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Fish Oil Intake for Inflammation
Q: I read in quite a lot of places that fish oil capsules or cod liver oil are a great supplement for
controlling inflammation and improving nutrient partitioning, but no one gives any information about
dosing. I have no idea how much of this stuff to ingest. Have you formed any guidelines as a result
of your research?

A: A fairly standard dose of fish oil in the studies is the equivalent of 6X1 gram capsules. The average
capsule has 180 mg epa and 120 dha so 6 capsules will provide 1020 mg epa and 720mg dha for a total of
1.8 grams of total fish oil. I would consider this basically the minimum daily amount that would be beneficial
on any level.
Some work has identified that the body will hit a limit (in terms of plasma saturation) on DHA at 1.2 grams
per day which is the equivalent of 10X1 gram fish oil capsules. That would also provide 1.8 grams EPA for
a total of 3 grams per day of fish oil. Under most conditions, I think this is more than enough.
A friend who uses fish oiils to control her arthritis will often go as high as 15X1 gram capsules although I
haven’t seen that supported in the literature. I’d note that higher doses are not better here (although some
are currently recommending absurd amounts). Excessive fish oil can impair the body’s ability to mount a
proper immune response, as well as impairing insulin release.
Carlson’s fish oil contains roughly the equivalent of 4X1 gram fish oil capsules per tsp., I don’t know the
values on cod liver oil offhand.
My current generic recommendation is the middle level, 10X1 gram capsules per day for 3 grams total fish
oil. This should provide maximal benefits (in terms of partitioning and health) with minimum negatives.
Individuals trying to control a specific excessive inflammatory condition may wish to experiment with higher
doses (15X1 grams capsules or 3-4 tsp Carlson’s fish oil per day).

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Hormonal Responses to a Fast-Food Meal Compared with
Nutritionally Comparable Meals of Different Composition –
Research Review

Title and Abstract

Bray GA et. al. Hormonal Responses to a Fast-Food Meal Compared with Nutritionally Comparable Meals
of Different Composition. Ann Nutr Metab. 2007 May 29;51(2):163-171 [Epub ahead of print]
Background: Fast food is consumed in large quantities each day. Whether there are differences in the acute
metabolic response to these meals as compared to ‘healthy’ meals with similar composition is unknown.
Design: Three-way crossover. Methods: Six overweight men were given a standard breakfast at 8:00 a.m.
on each of 3 occasions, followed by 1 of 3 lunches at noon. The 3 lunches included: (1) a fast-food meal
consisting of a burger, French fries and root beer sweetened with high fructose corn syrup; (2) an organic
beef meal prepared with organic foods and a root beer containing sucrose, and (3) a turkey meal consisting
of a turkey sandwich and granola made with organic foods and an organic orange juice. Glucose, insulin,
free fatty acids, ghrelin, leptin, triglycerides, LDL-cholesterol and HDL-cholesterol were measured at 30-min
intervals over 6 h. Salivary cortisol was measured after lunch. Results: Total fat, protein and energy content
were similar in the 3 meals, but the fatty acid content differed. The fast-food meal had more myristic (C14:0),
palmitic (C16:0), stearic (C18:0) and trans fatty acids (C18:1) than the other 2 meals. The pattern of nutrient
and hormonal response was similar for a given subject to each of the 3 meals. The only statistically significant
acute difference observed was a decrease in the AUC of LDL cholesterol after the organic beef meal relative
to that for the other two meals. Other metabolic responses were not different. Conclusion: LDL-cholesterol
decreased more with the organic beef meal which had lesser amounts of saturated and trans fatty acids
than in the fast-food beef meal.

My Comments

For a couple of decades, there has been an ongoing argument regarding the issue of ‘is a calorie a calorie’
in terms of changes on body composition and other parameters. I discuss this topic in Is a Calorie a
Calorie?
Fundamentally, my belief is that, given identical macro-nutrient intakes (in terms of protein, carbs, and fats)
that there is going to be little difference in terms of bodily response to a given meal. There may be small
differences mind you (and of course research supports that) but, overall, they are not large. And certainly
not of the magnitude that many make it sound like.
It’s worth nothing that there are a couple of built-in assumptions to my argument, all of which are detailed in
the article I linked to above but I want to briefly reiterate them here.
A tediously typical argument of the ‘a calorie isn’t a calorie’ types is usually something along the lines of
“Clearly eating 3000 calories of jelly beans isn’t the same as eating 3000 calories of chicken breast and
vegetables.” Well…no shit.
But at that point, the argument is about more than food quality, it’s also about the macro-nutrient
content. And of course the diet containing zero protein will be bad. But, again that has zip to do with it
being clean and everything to do with there being no protein.

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My basic assumptions in this argument are that both protein and essential fatty acid requirements are being
met. Beyond that, I find most of the obsession over food quality to be pretty pointless. Again, this is
discussed in more detail in the article linked above so I won’t get into it here.
Now it’s worth noting that a great deal of the difference seen between ‘eating clean’ and ‘eating unclean’ has
to do with caloric intakes. I’ve pointed out repeatedly that, and this is especially true when people are not
counting their calories, certain eating patterns tend to make people eat more than others. It’s easier to
overeat donuts than broccoli.
Clearly, someone eating a 2000 calorie fast food meal will obviously get a different response than someone
eating a 500 or even 1000 calorie clean meal. But as with the argument above, at this point there is more
than one variable changing; it’s not just about clean vs. unclean, you’re comparing meals of drastically
different caloric value.
A far more logical comparison would be to look at ‘unclean’ vs ‘clean’ meals containing the same caloric
value and the same macro-nutrient content; by controlling those two variables, the only thing being examined
will be the quality of the food (rather than the total quantity or the macro-nutrient profile).
Especially when you’re talking about bodybuilders and athletes who are typically controlling their caloric
content. Under those conditions, I argue that there will be no significant difference between the two; given
identical macros and calories, there is simply no real-world difference in a clean vs. unclean meal in terms
of its effects on body composition (health and other effects such as hunger control are separate, albeit
important, issues).
However, even there the clean freaks will make the counter-argument: they contend that even if the macros
and calories are identical, the unclean meal will still be worse. This is usually based on an assumed
difference in hormonal response (usually insulin).
So who’s right?
Unfortunately, very little research has actually examined this topic in any sort of controlled way (there are at
least two studies showing that high sucrose diets generate identical weight and fat losses as lower sucrose
diets). At least until this paper came along
The study’s explicit goal was to see if the metabolic response to a fast-food meal would differ to a ‘healthy’
meal of similar macro-nutrient and caloric value.
Towards this end six overweight men and two women were recruited to take part in the study although the
data in the women was excluded due to the low number and possible gender effects.
Each subject consumed each of the three test meals on different days with one week in between trials. A
standard breakfast was provided at 8am and the test meal was given at exactly 12pm and blood samples
were taken every 30 minutes for the first 4 hours and every 60 minutes for the next two hours. Blood glucose,
blood lipids, insulin, leptin, ghrelin and free fatty acids were measured.
The test meals consisted of the following:.
 Fast food meal: A Big Mac, french fries and root beer sweetened with high fructose corn syrup
purchased at the restaurant itself.
 Organic beef meal: this meal used certified organic rangefed ground beef; cheddar cheese; hamburger
bun made with unbleached all purpose naturally white flour, non-iodized salt, non-fat powdered milk,
natural yeast, canola oil, and granulated sugar; sauce made from canola mayonnaise and organic
ketchup; organic lettuce, onion and dill pickles; French fries made from organic potatoes and fried in
pure pressed canola oil; and root beer made with cane sugar.
 Organic turkey meal: this consisted of a turkey sandwich made from sliced, roasted free-range turkey
breast with no antibiotics or artificial growth stimulants; cheddar cheese; 60% whole wheat bread made
with whole wheat and unbleached all-purpose naturally white flours, non-iodized salt, non-fat powdered

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milk, yeast, vital wheat gluten, canola oil, and granulated sugar; pure pressed canola oil and canola
mayonnaise, stone ground mustard; organic lettuce; accompanied by a granola made with Blue Diamond
whole natural almonds, Nature’s path organic multigrain oatbrain flakes, wholesome sweeteners
evaporated cane juice, Spectrum Naturals pure pressed canola oil, clover honey, Sonoma organically
grown raisins and dried apples. The beverage was an organic orange juice.
So the study was comparing a commercial fast food meal to two carefully designed organic meals (one beef,
one turkey) from the above list of ingredients.
The composition of each meal was as follows:

Meal Calories Protein Carbs Fat

Fast Food 1044 28.2 151 53

Organic Beef 1154 28 163 60.2

Organic Turkey 1260 34 170 49

It’s important to note that while the meals were similar, they were not identical in composition; it would have
been better if the meals had been completely identical.
The biggest difference between meals had to do with the fatty acid composition: the fast food meal contained
twice as much saturated and nearly 8 times as much trans-fatty acids with half of the oleic acid compared
to the organic beef meal (which is no surprise). Interestingly, the fast food meal actually contained more
linoleic acid than the organic beef meal. The turkey meal had less saturated fat but similar amounts of linoleic
and linolenic acid to the fast food meal, with the lowest amount of trans fats.
So what happened?
In terms of the blood glucose and insulin response, no difference was seen between any of the meals and
this is true whether the data was presented in terms of percentage or absolute change from baseline. The
same held true for the ratio of insulin/glucose, no change was seen between any of the meals. Please read
those sentences again: the blood glucose and insulin response were identical for all three meals despite one
being a fast food ‘unclean’ meal and the other two being organic ‘clean’ meals.
Fatty acid levels showed slight differences, dropping rapidly and then returning to baseline by 5 hours in the
beef meals but 6 hours in the turkey meal. Blood triglyceride levels reached a slightly higher peak in the
organic beef and turkey meals compared to the fast food meal but this wasn’t significant.
Changes in leptin were not significant between groups; ghrelin was suppressed equally after all three meals
but rose above baseline 5 hours after the fast-food lunch but returned only to baseline in the other two meals.
The only significant difference found in the study was that LDL cholesterol decreased more after both of the
organic meals compared to the fast food meal, HDL and total cholesterol showed no change after any of the
meals. This was thought to be due to differences in the fatty acid content of the meals (saturated fat typically
having a greater negative impact on blood lipid levels than other types of fat).
However, beyond that, there were no differences seen in the response of blood glucose, insulin, blood fatty
acids or anything else measured.
Now, the study does have a few limitations that I want to mention explicitly.
1. The study only looked at a single meal. It’s entirely possible that a diet based completely around fast
food would show different effects.
2. The sample size was small: 6 overweight men and two women. It’s possible that differences would have
shown up with more subjects. A related question is whether lean individuals would respond

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differently. Perhaps but I doubt it. As I discussed in The Influence of the Subjects’ Training State on
the Glycemic Index, GI and insulin response are even less relevant in trained individuals.
However, with that said (along with the fact that the meals weren’t exactly identical), the basic fact is this:
the metabolic response between the three meals was essentially identical. There were no differences in
either insulin or blood glucose, the fatty acid profile makes perfect sense given the composition of the meals
and blood lipids showed basically no change.

Application

This study basically backs up what I’ve been saying for years: a single fast food meal, within the context of
a calorie controlled diet, is not death on a plate. It won’t destroy your diet and it won’t make you immediately
turn into a big fat pile of blubber. And, frankly, this can be predicted on basic physiology (in terms of nutrient
digestion) alone. It’s just nice to see it verified in a controlled setting.
It’s not uncommon for the physique obsessed to literally become social pariahs, afraid to eat out because
eating out is somehow defined as ‘unclean’ (never mind that a grilled chicken breast eaten out is
fundamentally no different than a grilled chicken breast cooked at home) and fast food is, of course, the
death of any diet. This is in addition to the fact that apparently eating fast food makes you morally inferior
as well. Well, that’s what bodybuilders and other orthorexics will tell you anyhow.
Except that it’s clearly not. Given caloric control, the body’s response to a given set of nutrients, with the
exception of blood lipids would appear to be more determined by the total caloric and macro content of that
meal more than the source of the food.
In terms of the hormonal response, clean vs. unclean just doesn’t matter, it’s all about calories and macros.
Which is what I’ve been saying all along.

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Glycaemic Index Effects on Fuel Partitioning in Humans –
Research Review

Title and Abstract


Diaz EO et. al. Glycaemic index effects on fuel partitioning in humans. Obes Rev.
(2006) 7:219-26.
The purpose of this review was to examine the role of glycaemic index in fuel partitioning and body
composition with emphasis on fat oxidation/storage in humans. This relationship is based on the hypothesis
postulating that a higher serum glucose and insulin response induced by high-glycaemic carbohydrates
promotes lower fat oxidation and higher fat storage in comparison with low-glycaemic carbohydrates. Thus,
high-glycaemic index meals could contribute to the maintenance of excess weight in obese individuals and/or
predispose obesity-prone subjects to weight gain. Several studies comparing the effects of meals with
contrasting glycaemic carbohydrates for hours, days or weeks have failed to demonstrate any differential
effect on fuel partitioning when either substrate oxidation or body composition measurements were
performed. Apparently, the glycaemic index-induced serum insulin differences are not sufficient in magnitude
and/or duration to modify fuel oxidation.

Background

The glycemic index (GI) of foods is yet another place where endless argument and debate exists in the world
of nutrition, especially as it applies to body composition.
In the early days of nutrition, as many may recall, carbohydrates were rather simplistically divided into simple
and complex sources with the even simpler belief that ‘simple = bad’ and ‘complex = good’. While this was
applied to general health and such, one of the major applications and concerns over carbohydrate intake
had to do with diabetic meal planning.
When it became clear that simple vs. complex was insufficient, researchers went looking for more accurate
methods of measuring the differences between carbohydrates. Sometime in the 80’s, the GI was born.
Conceptually, the GI refers to the blood glucose response to a given carbohydrate food. A little more
technically, the GI of a food relates to the area under the curve (AUC for nerdy types) of blood glucose
versus time after the ingestion of a fixed amount of a test food.
Researchers would first test a fixed amount (currently 50 grams digestible carbohydrate) of some standard
food, they originally used pure glucose but switched to white bread years later. The blood glucose response
to that standard food was defined as having a GI value of 100. I want to make it clear that this value has no
inherent meaning, it was simply a defined value.
Then other foods were tested, again 50 grams of digestible carbohydrate (perhaps baked potato or cereal)
were given by itself after an overnight fast and the blood glucose response was measured. The GI of that
food was then defined relative to the 100 value of the test standard. So a GI of 80 meant that the test food
had 80% of the blood glucose response of the test food; a GI of 120 means that it had 120% the blood
glucose response of the test food. Again, keep in mind that these values don’t really ‘mean’ anything, they
are just relative value.

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In any case, from the standpoint of diabetic meal planning, the GI seemed important as it would let diabetics
decide which foods would have the best effect on blood glucose levels without causing problems. Of course,
for a variety of reasons, the GI concept was also adopted by athletes and the physique obsessed.
I’d note that there is much more to the GI than I have space to go into here, I’ll be writing a full article on it
soon enough. Sufficed to say that GI becomes much more complicated when you start mixing foods
together, or the person isn’t fasted (e.g. you’ve eaten a meal). Even the aerobic training status of a person
modifies the GI as I detail in the research review The Influence of the Subject’s Training State on the
Glycemic Index.
In any event, the big argument over the GI of foods at least with regards to body composition usually involves
the insulin response and potential impact on things like fat mass and fuel utilization. It was usually inferred
that a higher GI value (remember, larger and/or longer blood glucose response) meant a bigger insulin
response and for the physique obsesses, insulin equals badness.
I’d note that things aren’t this simple and at least one study suggests that foods with a lower GI may have a
lower GI because of a LARGER initial insulin response as detailed in Different Glycemic Indexes of Breakfast
Cereals Are Not Due to Glucose Entry into Blood but to Glucose Removal by Tissue.

The Paper
But I’m getting off topic. What today’s paper looks at is the idea of whether differences in the insulin response
(from foods differing in GI) actually have meaningful differences in terms of their effect on insulin, fuel
utilization or body composition.
Because that’s the real issue: there’s no debate that foods differing in GI generate different blood glucose
responses, there is indication that this impacts on the insulin response. But the bottom line question is
whether those differences in hormonal response actually meaningfully affect anything.
In looking at the topic, the researchers examined a variety of different data sets including more acute studies
along with those looking at actual changes in body composition.
The short-, mid- and long-term studies typically examined things like blood glucose, insulin, blood fatty acid
levels, carb and fat oxidation and/or energy expenditure over periods ranging from 6-24 hours (or longer)
after the ingestion of foods or meals differing in GI. I’m not going to detail each and every one but, with one
or two exceptions, the majority simply found no significant difference in things like fatty acid suppression or
fuel oxidation despite significant differences in blood glucose and insulin response. Even longer term
intervention studies of 30 days to 10 weeks found no significant impact on weight or body composition for
diets designed with different GI levels.
So in terms of data directly examining the topic, the researchers comment that:
High fasting serum insulin concentration or high first-phase serum insulin response to intravenous glucose
has been proposed as a risk factor for weight gain.This may have led Ludwig to state that ‘functional
hyperinsulinemia associated with high-GI diets ma promote weight gain by preferentially directing nutrients
away from oxidation in muscle and towards storage in fat’. Evidence for this hypothesis is still lacking since
no effects of GI on fuel partitioning have been demonstrated to date.
Of course, there are studies suggesting that lower GI diets generate more weight loss than higher GI but
there are often subtle confounds including the fact that typically GI is not the only difference between
diets. Often, with changes in the GI come differences in fiber intake, energy density of the diet, at least one
study I can think of changed protein intake between groups. So concluding that the GI per se is having an
impact is incorrect.

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It’s worth mentioning that low GI foods are often claimed to better control appetite than higher GI foods. And
about half of the studies examining this do find this effect, with the other half finding no real effect. As I
discuss in Is a Calorie a Calorie, this is another confound, if eating lower GI foods causes someone to eat
less total food, they will tend to lose weight but it’s not due to the GI of the foods per se. As well, if high GI
foods make people eat more, they will tend to gain fat, as a function of eating more.
But this is far different than claiming that high GI foods will make someone gain fat (and/or lose muscle) at
an identical caloric intake, an argument that does not seem to be supported by the above studies looking at
fuel utilization directly.
I should note that there is at least some indication of an interaction between high and low GI diets and insulin
sensitivity, as I discuss in Insulin Sensitivity and Fat Loss, at least one study has shown that people with
insulin resistance lose more weight with lower GI diets while those with higher insulin sensitivity actually do
better with higher GI diets.
Wrapping up the paper, the researchers examine the impact of insulin on fuel utilization in general terms
mentioning that both the magnitude and duration of insulin response has the potential to affect fuel and fat
utilization. Without detailing all of the information, they conclude
Taking into account all of the above arguments, we speculate that under postprandial conditions, GI-induced
serum insulin differences are not sufficient in magnitude and/or duration to modify fat oxidation.
Given that even tiny increases in insulin pretty much shut off fat oxidation, this actually isn’t surprising. As I
discussed in The Stubborn Fat Solution, even fasting levels of insulin inhibit fat cell lipolysis by 50% from
maximal rates and almost any increase in insulin is sufficient to shut off lipolysis completely.
As this research review points out, it simply doesn’t appear that some vs. more insulin has any major impact
on this. I’d note, mind you, that fat cell metabolism can also be impacted by eating even if insulin doesn’t
increase; oral ingestion of pure dietary fat also shuts down lipolysis but that’s beyond the scope of this article.

Summing Up

Ok, what does this all mean and what am I saying? First let me clarify what I am not saying. I don’t want
folks to read this as a suggestion to go scarf down as much high GI, refined stuff as they can put down their
gullets. That would be asinine although I’m sure someone will manage to read this article as advocating
exactly that.
Even if there is no significant impact on acute fuel utilization, fat oxidation or storage in the short-term for
higher GI vs. lower GI foods, that doesn’t suggest that eating nothing but high GI foods is the way to
automatically go.
As I noted above, for many people lower GI foods tend to control hunger better and, in general, lower GI
foods are typically less refined, contain more fiber and nutrients, etc. Even if there are no significant
differences in how they impact on fuel utilization, health should always be a consideration. There are other
issues such as the glycemic load (a topic I’ll discuss in some detail later) and overall health as well.
But from the standpoint of fuel utilization, fat oxidation and the rest, there appears to be no meaningful
differences in the impact of higher vs. lower GI foods in humans (the study also examined animal data where
things, as usual, are different but simply don’t apply to non-rats).
I find that many people become nearly clinically insane over the issue of GI, it becomes a level of absolute
dietary extremism that is simply not necessary. For these folks, anything without a super low GI is a devil
food and will cause one’s muscles to instantly fall off and be replaced by body fat.

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And as with so many other topics, that’s just not the case. Small differences in GI, especially within the
context of mixed meals and lean individuals who are training regularly appear to have no significant impact
on overall fuel utilization, fat oxidation, or anything else.

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Lean Mass or Total Weight to Set Calorie Levels – Q&A
Question: Should I use lean body mass or total weight to set my caloric intake?
Or should I use goal weight?

Answer: First off let me address the second question, using goal weight. With few exceptions I don’t
recommend using goal weight to set anything for the simple reason that most people tend to pick a goal
weight that is exceedingly unrealistic and this tends to make them set calories very strangely. That is, unless
someone sets a goal weight that is perhaps 10-20% below their current weight, using goal weight will tend
to do odd things. So I don’t recommend it.
As to the first question, as usual it depends and there are pros and cons to each method. Let’s look at them
and then I’ll explain why I tend to use total weight regardless.
Part of the complication is that total daily energy expenditure has several components to it; classically these
included resting energy expenditure (REE), the thermic effect of food (TEF), and the thermic effect of activity
(TEA).
Recently, interest in non-exercise activity thermogenesis (NEAT) and spontaneous physical activity (SPA)
has also been generated based on the observation that people differ greatly in their ability to burn off excess
calories through NEAT/SPA. This topic is discussed in more detail in Metabolic Rate Overview.
And while a good deal of work shows that resting energy expenditure is related primarily to lean body
mass. It’s worth noting that lean body mass includes a lot more than muscle mass, something that is often
forgotten. I’m not aware of any work linking the thermic effect of food to lean body mass specifically. The
calories burned during activity tends to be related to total body weight (since you’re moving the entirety of
you weight) and, depending on how active someone is, this can actually make up a fairly large portion of
total energy expenditure. So while part of daily energy expenditure is certainly related to lean body mass,
not all of it is.
As an additional complication, there is the issue of getting an accurate measurement of lean body mass in
the first place, a topic that I discussed recently in Problems with Measuring Body Composition. Admittedly
this is a minor issue as many body composition methods can get you within 3-5% of true body composition
and any variance in lean body mass based on that inaccuracy will be fairly small.
As a final issue, there is the simple fact that no matter how you estimate your starting calorie levels, it’s never
more than an estimate (this is something that is altogether too often forgotten) and it will always have to be
adjusted based on real world changes in body weight and body fat.
For this reason, I tend to simply use current total body weight and go from there. It’s faster and easier, and
unless you’re dealing with extremes (e.g. of age, body composition, activity) tends to get most people within
shooting distance anyhow.
So, as I discussed in How to Estimate Maintenance Caloric Intake, for someone engaging in about an hour
of moderate intensity activity per day, I will tend to assume a maintenance caloric intake of between 14-16
calories per pound current body weight. Is this a perfect value correct for everyone? No. Is it pretty close
most of the time? Yes.
I’d note that, in recent years, due to drastically decreasing daily activity (outside of the gym), this value is
often turning out to be a bit too high and many people are ending up towards the lower end (or lower than
14 cal/lb) as often as not. Sitting in front of the computer all day burns squat for calories, even being on
one’s feet burns significantly more.
So an individual weighing 170 pounds would have an estimated maintenance caloric intake between
 170 pounds X 14 calories per pound = 2380 calories

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 170 pounds X 16 calories per pound = 2720 calories
Just to simplify the math, let’s split the middle and assume a maintenance level of about 2500 calories for
this person.
Depending on the goals, I’d make adjustments to caloric intake based on that starting point. A fairly standard
moderate deficit fat loss diet might be a 20-25% reduction from maintenance. Or 500-625 calories per day
for an intake of 1875-2000 calories per day.
Which, as it turns out is about 11-12 calories per pound total weight. And, as I discussed in How to Estimate
Maintenance Caloric Intake, a very common moderate deficit calorie level is ~10-12 calories per pound
anyhow. So we could have saved a lot of time by just using that value in the first place.
More extreme diets would use larger deficits, of course. For example, the low-calorie phase of my Ultimate
Diet 2.0 uses a full 50% reduction from maintenance which would bring our subject to 1250 calories per
day. But that’s a different kind of diet since there are only 4 low-calorie days before raising them again.
Of course for muscle gain, you’d go the opposite direction, perhaps increasing calories by that same 20-
25% (depending on a host of factor). So you might end up at 3000-3125 calories per day or 17.5-18 calories
per pound. I typically use 16-18 cal/lb as a starting point for muscle gain and, as you can see, even using a
slightly more complicated method yields an identical value. So I tend to just use the fast one (with total
weight) and then make adjustments from there.
Again, let me reiterate that these are all only rough estimates; they should only be treated as such rather
than as holy writ. While I don’t have the space to go into the approach I use to adjust calories (both are
discussed in the final chapters of both The Rapid Fat Loss Handbook and A Guide to Flexible Dieting), the
key is that those values must be adjusted based on real world changes in body weight and/or body fat levels.
And since this is true whether or not you use lean body mass or total weight, I tend to just use faster estimates
using total weight and then adjust from there. Outside of extreme situations, this typically works well enough
and since you have to adjust things anyhow, I don’t see much of a benefit to using the more complicated
approaches.
I hope that answers the question.

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Homeostatic and Non-Homeostatic Pathways Involved in the
Control of Food Intake and Energy Balance.
Berthoud H. Homeostatic and non-homeostatic pathways involved in the control of food intake and
energy balance. Obesity (Silver Spring). 2006 Aug;14 Suppl 5:197S-200S.
A neural network sensitive to leptin and other energy status signals stretching from the hypothalamus to the
caudal medulla has been identified as the homeostatic control system for the regulation of food intake and
energy balance. While this system is remarkably powerful in defending the lower limits of adiposity, it is weak
in curbing appetite in a world of plenty. Another extensive neural system that processes appetitive and
rewarding aspects of food intake is mainly interacting with the external world. This non-homeostatic system
is constantly attacked by sophisticated signals from the environment, ultimately resulting in increased energy
intake in many genetically predisposed individuals. Recent findings suggest a role for accumbens-
hypothalamic pathways in the interaction between non-homeostatic and homeostatic factors that control
food intake. Identification of the neural pathways that mediate this dominance of cortico-limbic processes
over the homeostatic regulatory circuits in the hypothalamus and brainstem will be important for the
development of behavioral strategies and pharmacological therapies in the fight against obesity.

My comments: this isn’t the kind of uber-technical paper I usually like to deal with in the research review
because I don’t figure most readers care so much about the detailed neurobiological stuff; they want
application. But this will tie in heavily with a future article series examining the physiological and
psychological issues that relate to dieting and fat loss and gives some important background to them.
The basic gist of this paper is that the body has two different systems that ‘regulate’ food intake (and by
extension, body weight). Those are homeostatic and non-homeostatic systems.
Some definitions are in order:
Regulation simply refers to the idea that a certain system, via feeding back onto itself, will maintain itself
within a fairly narrow range. The best example of a regulated system I can give you is that of your thermostat
or maybe cruise control. Your thermostat takes input (temperature), runs that through the processor (what
you want the temperature to be) and sets up an output (turns on the heat or the air conditioning). So,
depending on where you set the thermostat, the temperature in your house stays fairly stable. That’s a
regulated system. The idea that bodyweight is regulated has been around for 50 years and the subject of
much debate. I’ll write about that at some later date, at this point simply accept that some level of regulation
is going on.
The homeostatic system has to do with the idea that the body tries to maintain some specific ‘set point’ in
terms of bodyweight or body fat. Basically this system takes incoming signal (from hormones like leptin,
insulin, blood glucose, ghrelin, peptide YY and a host of other stuff) and makes adjustments in appetite,
hormones, metabolic rate and activity to compensate.
The non-homeostatic system has less to do with internal signaling and more to do with how the body interacts
with the external world. So when you are bombarded by food advertising, super size options (lots of food at
a low price), appetizers (Awesome Blossom anyone?), and all you can eat buffets, these interact with the
non-homeostatic system.
This paper basically lays out a quick review of the different systems before getting into the (complicated)
neurobiology of how they work.
The homeostatic generally works better for defending against weight loss than weight gain. There are a
bunch of complicated reasons for this, perhaps the simplest of which is that starving to death is very bad,

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while being fat was never really a bad thing in our evolutionary past. So the body developed a system to
fight like hell agains weight loss but work fairly ineffectively against weight gain. Simply, for most people it’s
far far easier to gain weight than it is to lose it. I’ll be getting into the details of this system as I continue to
talk about leptin in coming issues but the above is the basic gist of it.
The non-homeostatic system has less to do with internal biology and everything to do with external
environment. It also ties in with what is described as the hedonic system of eating: simply put, we eat
because it is pleasurable. Essentially, the non-homeostatic system deals with issues related to food intake
that are not governed by the homeostatic/internal system. The paper goes into the details, I don’t think they
are that relevant for most readers, it has to do with how certain parts of the brain (the nucleus accumbens)
“provide an interface between motivation and behavioral action.”
And this is where things get kind of interesting. One of the most eye-opening papers I may have read in
recent years was by a research named Juan De Castro who looks at real-world eating habits (as opposed
to what you might see in a lab or controlled setting). Basically he made the huge point that humans eat for
reasons often totally unrelated to hunger. That is, it’s a convenient and easy trap to fall into to think of humans
like rats: a gut and a nervous system with appetite being rigidly controlled by the set point. But it’s not that
simple. Even rats can be fattened far past their set point with what is called a cafeteria diet (think cookie
dough). Give them access to enough high calorie tasty food and they will over-ride any internal set point or
homeostatic mechanism.
And the same holds for humans which a point De Castro made and which the non-homeostatic system
appears to be involved with. The non-homeostatic system explains why so many humans appear to so easily
override any internal homeostatic system that is operating. An abundance of food cues (tv advertising) and
the easy availability of highly palatable calorie dense foods (would you like to Supersize that for only 39
cents?) and even the social environment all tend to promote food intakes far outside of any homeostatic
system involved.
De Castro’s work has demonstrated this routinely. For example, the amount of food consumed goes up
almost linearly with the number of people at an event. Now you know why you eat so much at holiday
gatherings. People typically eat more on the weekends than during the weekdays. How much food is
presented to you (all you can eat buffet anybody) also affects food intake: the more food on the plate, the
more you tend to eat. So does greater food variability: the more variety at a given meal, the more people
tend to eat. Think about the next time you are gorging on 18 different kinds of food at Thanksgiving dinner.
To quote one of his papers “Changes in intake can be detected with different levels of the number of people
present, food accessibility, eating locations, food color, ambient temperatures and lighting, and temperature
of foods, smell of food, time of consumption, and ambient sounds.” None of which has to do with any
internally set system one bit.
But goes a long way towards explaining why restaurants (who are in the business of getting you to eat more)
do what they do, and why most people in a modern environment have so many problems avoiding weight
gain unless they impose a tremendous amount of self-discipline. It may also explain why bodybuilders and
athletes, who are typically the most successful at dieting are succeeding: many of their behaviors explicitly
avoid much of what De Castro’s work has demonstrated. By eating a low variety of food,s rarely if ever going
out (many become social pariahs and refuse to go out with friends for fear of screwing up their near
pathological eating patterns), avoiding most places where supersizing or buffet style eating would be a
problem, etc they avoid many of the problems. Suggesting that type of approach (become a food obsessed
hermit) to the non-obsessed is generally a recipe for disaster but recognizing that there are aspects of eating
behavior that are not simply internally determined may be of some use. At the very least, recognizing those
types of situations which tend to promote overconsumption is not a bad thing.

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A point that I really want to drive home before wrapping this up is this:
I don’t want it to sound like these are completely separate pathways controlling food intake, which would be
easy to do.
Rather, the systems are overlapping and integrated and separating them is more a function of convenience
(and a reflection that they do represent slightly different things).
Here’s a quick example: the reward system in the brain is primarily dependent on dopamine. So the body
releases dopamine in the brain in response to rewarding things (a bit more accurately, it turns out that it’s
the expectation of rewarding things that releases dopamine) and this is what makes them rewarding.
Readers may have heard about the famous study were rats had a level wired up to fire the reward pathway
in their little rat brains; they would sit there hammering away at the lever over and over, ignoring food, water,
etc. That’s how powerful the dopamine/reward pathway can be.
Dopamine is also highly involved in addiction and addicting stimuli (such as drugs) tend to drive dopamine
levels.
Now, one of the key hormones involved in the homeostatic system is leptin which I’ve been rambling about
variously for damn near 10 years. Leptin does a lot of things in the body but, among them, arguably its
primary role is as a signal to the brain about two things: how much fat you’re carrying and how much you’re
eating on a day to day basis.
As it turns out, leptin appears to drive dopamine levels in the brain. When leptin drops, so do dopamine
levels (this is discussed in more detail in my little book that most don’t even know about, on the drug
Bromocriptine).
As it turns out, when you starve rats, they are more likely to become addicted to various substances, because
of the drop in dopamine.
My point simply being that changes in the homeostatic system (for example, in response to fat loss or food
restriction) are overlapping with the non-homeostatic (or hedonic) system. Everybody has noticed that food
seems to ‘taste better’ when you’re hungry and these changes are probably why.

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Low Body Fat in Women, Stubborn Low Back Fat, and Skinny Fat
Training
I haven’t done a Q&A in a while and the mailbag is getting a bit full. So in lieu of boring everyone with
another 20-part series on some minutial detail of training, here’s a bunch of questions.

Question: Hello. Do you know any females who are successfully and consistently living at at lower body fat
10-12% using a keto/ low carb diet? Thank you!

Answer: First and foremost, 12% is about the lower limit of essential fat in women. While you will sometimes
have women estimated lower than that, this is an artifact of the equations. A woman at 10% body fat is
dead. Even at 12%, almost all women will show massive hormonal issues, a lack of health and vigor. This
shouldn’t even be a goal for women, it’s unrealistic and physically damaging in the long-run.
About the lowest body fat I’d suggest any woman even attempt to maintain long-term is 15-16% bodyfat. She
will have a cut upper body, 6-pack abs and legs should be fairly lean (depending on her body fat distribution
patterns) but, assuming she’s not doing anything completely idiotic with her diet and training, she should be
ok. Some women won’t even be able to maintain that low level without a loss of menstrual cycle, energy
and mental problems and will have to skew higher.
And honestly this has nothing to do with dietary choice. Keto or carb-based, a woman is not going to easily,
or more importantly, healthily maintain that low level of body fat year round. Nor should that be a goal.

Question: Hello. I have been bodybuilding for 5 years, I estimate that I am around 12-13% body fat. My
main problem in the lower abs and lower back fat that doesn’t seem do go whatever I do. Which book would
be beneficial for my case?

Answer: For men with normal “male” (yes, I’m using the whitecisgendered heteronormative term for this,
suck on it) body fat patterning, abs and low back are always the last place to go. A man will have ripped
delts and pecs, shredded legs and still be sloppy around the waist. It’s just part of being a man (for a woman
with normal “female” body fat patterns, hips and thighs are the stubborn area).
Stubborn fat is stubborn for a variety of reasons including adrenoreceptor density, poor blood flow; stubborn
fat even stores different types of triglcyerides than non-stubborn fat. All of this makes it harder to get rid of.
But it’s by no means impossible.
The first necessary thing is patience, most men will need to get to 10% body fat or lower for ab and low back
fat to really go away. Yeah, yeah, patience, how long is that going to take So far as a book, The Stubborn
Fat Solution would of course be the suggestion I’d make. It not only will explain to you every reason WHY
stubborn fat is stubborn (in often excruciating detail) but will give you diet, supplement and workout protocols
to mobilize it as effectively as possible.
Good luck!

Question: Hi Lyle, I recently got a DEXA scan to measure my body composition and the results were not
good. at 5’11, I weighed in at 166 lbs but discovered my body fat was very high – 25.5%. This meant I only
had a mere 123 lbs of LBM. This was even after lifting for a few months, gaining about 10lbs (not sure of the

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composition of this), so building muscle and losing fat at the same time is probably out of the question as
I’m not a total beginner.
Now I’m not sure whether to lose fat or try gain muscle; I would have to go as low as 137 – 140 lbs to get in
the 10-12% BF range, which seems very low for someone of my height. Conversely I’m not sure about trying
to gain muscle at such a high body fat % – I’d likely end up pushing 30% by the time I get any significant
amount of muscle gain, and also because I’d likely have issues with insulin sensitivity at such a high starting
bf%. I’m not sure how I should approach this as I’m probably not advanced enough for a recomp diet like
your UD2.0. any advice on what me or people in a similar situation should do? Thanks, CR

Answer: This an exceedingly common question and, for those who haven’t read all 350 articles on my site
(shame on you!), the numbers he’s using in the above have to do with my general suggestion to stay between
10-15% body fat or thereabouts for gaining muscle. Certainly recomposition is a great goal and sometimes
achievable but most approaches tend to make people spin their wheels. And as a beginner trainee, an
approach like the Ultimate Diet 2.0 is inappropriate.
Now, a first comment: for reasons I’m unclear on, DEXA scans seem to systematically result in higher body
fat percentages than other methods such as calipers (which is where my numbers come from). A number
of recent pros have gotten DEXA scans when they were obviously in contest shape.
While calipers or visual estimates might have put them at 4-5% body fat (about the lower limit for men),
DEXA put them at like 9-10%. So there is something going on that makes the methods incomparable but
I’m not sure what (anybody reading this who knows, PLEASE leave a comment). The numbers I use will
always be lower than the numbers DEXA spits out. But even if we adjust the above value of 23% downwards
by 5% or so, the person asking the question is still slightly outside of my ideal range (he’s near the high end
cutoff but would need to diet first in my approach).
On that note, please understand that the 10-15% value is not an absolute. I constantly have people go “Well
I use 12-17% and that works fine” Yes, fantastic. Thank you for being even more pedantic than me. Body
fat estimation is ONLY an estimate and there s a 1-2% error bar anywhere you go (so my 10-15% is really
8-12% to 13-17% in the first place).
My primary point in using the 10-15% (this is for men by the way, women use 17-22% or so since they have
more essential fat) is to keep people from bulking when they are too fat (and end up having calorie
partitioning issues and/or having to diet for a year to get lean again) or trying to get so lean (single digits)
that they have other issues. 10-15% is good rough RANGE. It’s not an absolute number. I’m mainly just
trying to keep people from scuttling themselves by giving them a range that will work for most and keep them
from doing something dumb.
Beyond that, what is CR to do? Since he doesn’t have a lot of lean body mass, he’s obviously hesitant to
diet (as the old saying goes, you can’t define bone) down specifically although it really isn’t a problem in my
book. But I understand a male trainee not wanting to be an even smaller version of himself or to be 140
pounds at his height.
Bulking in the strictest sense, is out of the question since at his current bodyfat, he’ll run into all of the issues
I mentioned above and discuss in detail in the linked article: he may have calorie partitioning problems and
he’ll end up at such a high body fat when all is said and done that getting lean again will take forever. What
to do?
Honestly, despite his assertion that he’s been lifting a few months, he is still a beginner. And will be for 3-6
more months. And his body fat is still high enough that he can probably gain strength and muscle slowly as
he leans out. This is one of those situations where gaining muscle while you lose fat is relatively easier: the
combination of being an overfat beginner allows a physiology for this to happen.

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So this is a place where I’d suggest a slight deficit (10-20% from maintenance), moderate low intensity cardio
and a well set up beginner training program. Bodyfat should come off slowly, strength will go up and muscle
mass should go up gradually as well. When he has a year of training, he can re-assess where he is and will
be ready for more specific dieting or gaining cycles. But I don’t think he needs them now.

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Growth Hormone (GH) Release and Fat Loss – Q&A
On Tuesday of last week I ran a research review on Casein Hydrolysate and Anabolic Hormones and Growth
looking at two papers, one of which was a paper showing that the acute hormonal response (in terms of
testosterone and growth hormone) to weight training had zero impact on growth. In the comments section,
at least three different people asked a semi-related question that I’ve reproduced below and which I want to
address in some detail today.

Question: A common recommendation bandied about by trainers is to place any LISS cardio after “lactate
training” or whatever they choose to call higher intensity work, and they say that if fat loss is the aim, this will
milk every last bit of effectiveness out of the low intensity work (versus keeping it a separate session entirely).
And they usually say that increased lactate leads to increased GH, leads to increased lipolysis, so that when
the low intensity work comes after the much higher intensity work, you oxidize more of the fat they claim
gets mobilized. So does this pairing of LISS cardio after high(er)-intensity work still make it at least
somewhat more effective (from a fat-loss standpoint) than when performed separately? And if so, is it more
due to other things you mentioned (glycogen depletion, effect of the catecholamines, etc.), so that the
intended effect is the same, it was just the purported reason for the effect that most of these trainers had
wrong (namely implicating a GH-induced increase in lipolysis as the reason)?

Answer: There’s no doubt that growth hormone (GH) is involved in lipolysis although, compared to
hormones such as insulin and the catecholamines (epinephrine/norepinephrine aka
adrenaline/noradrenaline) it plays a distinctly secondary role. There are other hormones of course,
testosterone, estrogen, progesterone, Interleukin-6 and a new player called atrial-natriurietic peptide (ANP)
all play a role as well. Here I’m only going to talk about GH.
First let me define a single term which is lipolysis. This refers to the breakdown of stored fat (technically:
triglycerides) in fat cells for release into the bloodstream. While there are more steps involved in losing fat
(and the specific pathways are all discussed in some detail in The Stubborn Fat Solution), clearly if you can’t
get the fat out of the cell in the first place, little else matters. Lipolysis simply refers to that process, whereby
fatty acids stored within fat cells are broken down to be released into the bloodstream, hopefully to be burned
elsewhere in the body (generally skeletal muscle or liver).
For example, while studies of injectable GH have generally crapped out in terms of muscle growth (there is
an increase in lean body mass but it’s primarily water and connective tissue, not actual muscle mass), it has
shown impact on fat loss. As well, the nighttime GH pulse has been shown to be important for lipolysis the
next day. Finally, during periods of fasting or even low-carbohydrate diets, studies clearly show that blocking
the normal GH response not only limits lipolysis, but this ends up increasing muscle loss (because the body
doesn’t have fatty acids to burn).
So far so good right?
Add to that a host of studies done primarily during in the 80’s by William Kraemer and his group showing
that certain training protocols (notably higher reps and short rest periods; 3X10 with 1′ rest was typically
used) elevate GH and you can see where folks got the idea that training in this fashion would be good for
fat loss.
I think the first place I saw this idea floated was Charles Poliquin’s original German Body Composition
Training. Claimed to be based on German research into the hormonal response to training, it was based

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arund multiple sets of high reps with short-rest, the premise of which being to raise GH (and lactate
production during training seemed to be involved somehow) to increase fat loss.
More specifically to today’s question, many trainers will use that type of training (using various permutations
of Metabolic Training, discussed in some detail in Weight Training for Fat Loss Part 1 and Weight Training
for Fat Loss part 2) to be followed up by low-intensity cardio. The idea being that the GH response will
promote lipolysis and the low-intensity cardio will then ‘burn off the fatty acids’.
And here’s we run into the problem with the idea: the time course. Because while GH is certainly involved
in lipolysis, it’s effects are pretty slow to occur. Cutting ot the chase, after a big GH pulse, you don’t really
see a big increase in lipolysis or blood fatty acids until about the 2 hour mark. Which means that a protocol
based around the idea of elevating GH during the intense portion so that cardio done a few minutes after
will burn off the fatty acids mobilized by the GH pulse is fundamentally incorrect from a physiological point
of view.
But that doesn’t mean it doesn’t work. Quite in fact, the premise is still fairly sound, this is just a place where
I’m being picky about the mechanism. As discussed in Weight Training for Fat Loss Part 1 this type of
training still has metabolic effects that can be conducive to fat loss (even acutely), they simply aren’t related
to the GH pulse in any form or fashion.
Rather, increases in epinephrine/norepinhrine will have a much stronger acute effect on fat mobilization, and
the glycogen depletion due to this type of training tends to enhance fat oxidation in skeletal muscle. Quite
in fact, the two advanced protocols in my Stubborn Fat Solution are at least superficially similar to this type
of training, high-intensity work followed by low-intensity work. But GH isn’t the mechanism behind it.
So bascially, what the person asking the question wrote in the second-half of his question. The combination
of high-intensity followed by low-intensity work can still be effective for fat loss, it’s simply not for the
mechanism stated. The impact of GH on fat loss is simply too slow to be involved. Rather, other
mechanisms related to hormonal response, glycogen depletion, etc. are what are involved and
responsible. GH simply isn’t relevant to the process in that short of a term.

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Insulin Sensitivity and Fat Loss
Over the years, bodybuilding nutrition has divided itself into three fairly distinct categories (I’m going to leave
out the ones I consider voodoo nonsense) which are high-carb/low-fat, moderate carb/moderate fat, and
low-carbohydrate. Low carb-diets can be further subdivided into high or low fat as well as cyclical or non-
cyclical. I discuss each in more detail in Comparing the Diets.
In theory, you can make arguments for or against any of these approaches in terms of superiority. In the real
world, it’s not quite that simple. You can always find folks (and this is true whether they are bodybuilders or
just general dieters) who either succeeded staggeringly well or failed miserably on one or another
approaches.
Before going on, I want to mention that protein recommendations tend not to vary that significantly between
diets and most of the arguments tend to revolve around the varying proportions of carbohydrate and fats in
the diet and that’s what I’ll be focusing on here. Simply, I don’t consider low-protein fat loss diets in the
equation at all for the simple fact that they don’t work for anybody but the extremely obese. Any dieting
bodybuilder or athlete needs 1-1.5 g/lb lean body mass of protein on a diet. Possibly more under certain
circumstances.
My general experience has been that individuals who respond very well to high-carbohydrate/lower fat diets
tend to do very poorly on low-carb/higher-fat diets. They feel terrible (low energy and a mental fog that never
goes away), don’t seem to lean out very effectively and it just doesn’t work.
This cuts both ways: folks who don’t respond well to higher carbs do better by lowering carbs and
increasing dietary fat. Sometimes that means a moderate carb/moderate fat diet, sometimes it means a full
blown ketogenic diet. I should also note that some people seem to do just as well on one diet as another.
Some of this may simply be related to adherence although this tends to be less of an issue in bodybuilders
(who take obsessiveness to a new level). Carb-based diets make some people hungry even if they follow all
the ‘rules’; so they eat more and don’t lose fat effectively. For many of those people, reducing carb intake
allows better calorie control in the long-term. People who hate moderation tend to like cyclical ketogenic
diets, they can handle no-carbs during the week and massive carb-ups on the weekend; moderate carbs
drive them crazy.
But how does all of the above help the neophyte dieter looking to diet down. Put differently, how can
someone know ahead of the fact what diet might be optimal for them? Current research is starting to explore
a link between diet and genetics and suggesting biological differences in how people respond to diet; that
might explain some of the real-world results I described above.
With regards to fat intake, studies have identified what researches call low and high-fat phenotypes
(phenotype is just a technical word for the interaction between your genetics and your environment) (1).
Some people appear to be better able to increase fat burning in response to higher fat intakes; they stay
lean in the face of such an intake. Others, however, do no such thing. Other aspects of metabolism and
appetite were associated with being either a high- or low-fat phenotype.
Unfortunately, no practical way of determining which one you might be ever came around. It was also never
exclusively determined if the effect was due to inherent biology or simply adaptation to a habitual diet. But
the point still stands, biologically, some people seem better able to increase fat oxidation in response to
higher fat intakes than others. I think this goes part of the way to explaining the response (good or bad) to
high-fat ketogenic diets. People who upregulate fat oxidation well tend to thrive on them; people who don’t
just get bloated and don’t lose fat well.
More recently, an interaction between diet effectiveness and both insulin sensitivity and insulin secretion
after a meal has been proposed (2). Noting that all of the research to date has been on obese individuals

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(not dieting bodybuilders), I still think it explains some of what is going on. As well as allowing us to predict
ahead of time which diet someone might do best on.

A Very Brief Primer on Insulin Secretion and Sensitivity

To understand the research I want to talk about next, I need to briefly discuss two different but somewhat
related aspects of insulin metabolism: insulin sensitivity/resistance and insulin secretion.
As I imagine all of the readers of this know, insulin is a storage hormone released in response to eating with
carbohydrates having the largest impact on insulin secretion, protein having the second greatest and fat
having little to no impact on insulin secretion. Insulin sensitivity refers to how well or poorly the body responds
to the hormone insulin. Individuals who are insulin resistant tend to have higher baseline insulin levels
because the body is releasing more in response to try and overcome the resistance.
And while a great majority of insulin resistance is determined by lifestyle (training and diet play a huge role,
as does body fatness), so do genetics. At the same bodyfat level, insulin sensitivity can vary nearly 10 fold
for genetic reasons. So it’s possible that even lean athletes and bodybuilders could have some degree of
genetic insulin resistant (I’ll talk about how to determine this at the end of the article). As it turns out,
individuals also differ in how much or how little insulin they release following a standardized meal; some
people release more insulin than others in response to a meal. While this can be related to baseline insulin
sensitivity, it doesn’t have to be.
It turns out that both issue relate to fat/weight gain or loss (2). In contrast to what is generally believed, good
overall insulin sensitivity tends to correlate with weight/fat gain and insulin resistance is thought to be an
adaptation to prevent further fat/weight gain. However, some research suggests that a tendency to release
too much insulin in response to feeding may predispose people towards weight/fat gain. One huge confound
in all of this, mind you, is that high insulin secretion tends to make people eat more. Studies of diabetics find
that decreasing insulin secretion with drugs tends to cause a spontaneously lower food intake (2).

The Impact of Insulin Sensitivity or Insulin Secretion on Response


to Different Diets

While the research is in its infancy, there have been studies examining the weight loss response relative to
either insulin sensitivity or insulin secretion. For the most part, no major difference in terms of weight loss
has been found in subjects with different insulin sensitivities (2). However, at least one study found that the
specific diet given interacted with baseline insulin sensitivity to determine the magnitude of weight loss (3).
In that study, obese women with either high or low insulin sensitivity were placed on either a high carb (60%
carb, 20% fat) or low carb (40% carb, 40% fat) diets.
So there were four groups: high carb/insulin sensitive, high carb/insulin resistant, low carb/insulin sensitive,
low carb/insulin resistant. The results were intriguing: insulin sensitive women on the high carb diet lost
nearly double the weight as insulin sensitive women on the low-carb diet. Similarly, insulin resistant women
lost twice the weight on the low-carb diet as on the high carb diet. Unfortunately, it’s not clear what caused
the divergent results. The researchers mentioned a gene called FOXC2 which is involved in energy
expenditure and found that it was upregulated in the individuals who responded best to diet; further research
into this topic is needed (3).

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Even less data relates to insulin secretion status and diet although a recent study suggests that it may (4).
In that study, subjects were given either a high glycemic load (60% carbs, 20% protein, 20% fat) or a low
GL diet (40% carbs, 30% protein, 30% fat diet) and weight loss was examined relative to baseline insulin
secretion. In that study, subjects with high insulin secretion lost more weight on the low glycemic load diet
while subjects in the low insulin secretion group lost slightly more on the high glycemic load diet.

Getting to the Point

Overall, I think the limited data available on both high and low fat phenotypes as well as how individuals with
differing baseline insulin sensitivity/secretion respond to diets supports the observations occurring in the real
world in terms of both subjective feelings on a given diet as well as the weight/fat loss response. So how
can we put this to use?
Unfortunately, there’s no easy way to see if you’re a high or low fat phenotype so I’ll focus on insulin
sensitivity. There are a lot of complicated and impractical ways to determine insulin sensitivity and insulin
secretion. All involve blood work and looking at either baseline insulin or blood glucose or how insulin
changes in response to a meal.
However, in practice, there are signs as to whether you have good insulin sensitivity or not and possibly
whether you over-secrete insulin. Here’s two very simple questions to ask yourself regarding your response
to diet.
1. On high-carbohydrate intakes, do you find yourself getting pumped and full or sloppy and bloated? If
the former, you have good insulin sensitivity; if the latter, you don’t.
2. When you eat a large carbohydrate meal, do you find that you have steady and stable energy levels or
do you get an energy crash/sleep and get hungry about an hour later? If the former, you probably have
normal/low levels of insulin secretion; if the latter, you probably tend to over-secrete insulin which is
causing blood glucose to crash which is making you sleepy and hungry.
I consider it most likely that superior bodybuilders couple excellent insulin sensitivity with low insulin
secretion in response to a meal. This would tend to explain why bodybuilders have often gravitated towards
high carb/low-fat diets and been successful on them.
At the same time, mediocre bodybuilders frequently get less than stellar results from that same diet.
Lowering carbs and increasing dietary fat seems to be more effective in that case some of the low-carb
bulking strategies out there probably work better for those individuals. The same goes for fat loss. Cyclical
low-carb diets such as my Ultimate Diet 2.0 or the more generic cyclical ktogenic diet (CKD) described in
my first book The Ketogenic Diet allow such individuals to briefly enjoy the benefits of heightened muscular
insulin sensitivity.

Putting it Into Practice

If you have good insulin sensitivity and low insulin secretion, odds are you will do well with a traditional
bodybuilding type of diet which means high protein, highish carbs and low fat. Let’s say you’re consuming 1
g/lb of protein at 12 cal/lb. That’s 33% protein. If you go to 1.5 g/lb, that’s 50% protein. That leaves you with
50-67% of your calories to allocate between fat and carbohydrate. 15-20% dietary fat is about the lower limit
as it becomes impossible to get sufficient essential fatty acids below that intake level. So, at 1 g/lb, your diet
will be roughly 33% protein, 47-52% carbs (call it 45-50%) and 15-20% fat. If protein goes to 50% of the
total, carbs should come down to 35% of the total with 15% fat.

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If you’re not insulin sensitive and/or have high insulin secretion, a diet lower in carbs and higher in fat (don’t
forget that protein can raise insulin as well) is a better choice. Assuming, again, 40% protein, a good starting
place might be 40% protein, 20-30% carbs and 20-30% fat. A further shift to a near ketogenic (or cyclical
ketogenic) diet may be necessary, 40% protein, 10-20% carbs and the remainder fat may be the most
effective. If protein is set higher, up to 50% protein, carbs would be set at 10-20% with the remainder (20-
30%) coming from dietary fat.

Summing Up

Hopefully the above has given you some insight into choosing what might be an optimal fat loss diet without
having to go through so much tedious trial and error. However, please don’t treat the above as more than a
starting point. Adjustments to diet in terms of calories or nutrient intake should always be based on real world
fat loss. You should be tracking your fat loss every 2 weeks (4 at the most); if you’re not losing at a reasonable
rate (1-1.5 lbs fat loss/week), you need to adjust something.
Bio: Lyle McDonald received his BS in physiology from UCLA in 1993 and has been obsessed with all
aspects of human performance (training, nutrition, supplements) since then. He has written extensively about
fat loss, especially low carbohydrate dieting. He is currently working on a book covering all aspects of protein
nutrition for athletes as well as an approach to getting rid of stubborn bodyfat. His website is
http://www.bodyrecomposition and his books can be ordered there by clicking on the store link.

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Lean Body Mass Maintenance and Metabolic Rate Slowdown –
Q&A
Question: I am a little confused when it comes to metabolic slowdown. The reason for my confusion is that
as far as I can figure, if my LBM remains approximately the same throughout the diet, then my energy
expenditure should also remain basically the same. Granted, maintaining LBM is difficult but for arguments
sake let’s assume that LBM is maintained within a +/- 5% range. So for an individual with 150lbs of LBM that
amounts to 7.5lbs. My assertion(correct or not) is that metabolic slowdown cannot occur beyond what that
7.5lbs of LBM used in the first place?
Is this a faulty assumption? I’ve read on many a website that the body goes into “starvation mode”, however
that argument doesn’t sit well with me. Either the body requires X amount of energy to function, or it doesn’t.
I think “starvation mode” might simply be reduced activity in general, so for a relatively insane individual
(read:athlete) who is willing to push hard on a restrictive diet, metabolic slowdown shouldn’t be an issue?

Answer: I suspect that some of this comes down to an issue of semantics (you sort of get to part of what
I’m going to talk about in your second paragraph) but some of it doesn’t. The short answer to your question
is that your assumption isn’t entirely correct; even with 100% maintenance of lean body mass (LBM) there
can still be some metabolic slowdown. Now here’s the longer answer.
First and foremost, we need to define some terms and what’s meant by metabolic rate since I suspect that’s
part of where some of the confusion is coming from. On a daily basis, an individual’s total daily energy
expenditure is given by three components, which I’ve discussed in detail in Metabolic Rate Overview. They
are
1. Resting/Basal Metabolic Rate (RMR/BMR; what I suspect you’re referring to above)
2. Thermic Effect of Food (TEF)
3. Thermic Effect of Activity (TEA)
Where TEA has now been divided into two distinct components: the thermic effect of exercise and non-
exercise activity thermogenesis (NEAT). The distinction being that the first is calories burned during formal
exercise and the second, NEAT, is the calories burned during activities such as daily moving around,
fidgeting, moving from sitting to standing, etc. I discussed the potentially major impact of NEAT in a recent
research review on Role of Nonexercise Activity Thermogenesis in Resistance to Fat Gain in Humans.
Now, each of the above is determined by various factors including body composition, diet, etc. And all of
them are affected by dieting and the loss of body mass. Studies have repeatedly shown that individuals who
have been dieted down to a given weight will have a lower than predicted metabolic rate compared to
someone who didn’t diet to that weight. That is, someone who ‘naturally’ weighs 200 pounds will have a
higher total energy expenditure than someone who dieted down to 200 pounds.
So what’s causing this reduction in total energy expenditure. A majority of the ‘metabolic slowdown’ that
occurs is due simply to the loss of body mass. Because larger bodies burn more calories (both at rest and
during activities) and smaller bodies burn less.
But that’s not the only cause of metabolic slowdown here. There is also an adaptive component of metabolic
rate slowdown that is mediated by changes in hormones: leptin, insulin, thyroid, catecholamines. As these
change (decrease) on a diet, you find that tissues burn fewer calories per unit mass. I’d mention that not all
studies find this, about half do and half don’t. That is, your assumption that a given body composition always
burns the identical number of calories on a day to day basis isn’t entirely correct.

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Of course, an important question is how much of a change this amounts to. During active weight loss, the
impact is relatively greater (because hormones tend to be more greatly affected); at weight maintenance
(once a person has stabilized), the impact isn’t huge. In some studies of the post-obese (folks who have
been dieted down and maintained at that weight) show a relatively modest 5% or so reduction in RMR. The
effect exists but is not massive; it’s also highly variable, with people showing relatively more or less of an
effect.
There is also evidence that individuals move around less when they lose/are losing weight. As James
Krieger recently wrote on his Weightology.net website, it looks like changes in activity (especially NEAT) are
the far larger contribution to the reduction in overall energy expenditure on a day to day basis; the number
of calories burned in that activity also appear to be reduced due to improved muscular efficiency.
In that study, decreases in RMR were about 150 calories per day but reductions in activity expenditure were
up in the 300 calorie plus range with the total effect being over 400 calories. This is likely why daily activity
has such a profound impact on weight maintenance as I discussed in Exercise and Weight/Fat Loss Part 2:
since the body is ‘automatically’ decreasing activity energy expenditure, you have to make up for it.
So basically you’re both correct and incorrect. The greatest impact on total daily energy expenditure
certainly appears to be due to decreased spontaneous activity during the day. However, there is also an
added component of a reduction in resting energy expenditure due to changes in RMR, even with complete
maintenance of lean body mass. Some of this is due to simply being smaller, some of it is an adaptive
reduction in metabolic rate due to shifting hormone levels (which, again, not all studies find).
And semi-tangentially, a long while back I had written an article as a background primer to something I had
intended to write about alcohol. Well, now I don’t have to since Martin Berkhan over at Leangains.com has
written it. In his article The Truth about Alcohol, Fat Loss and Muscle Gain he pretty much covers everything
you could ever want to know about the topic.

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How to get most out of your Creatine – what form,
dose and supplementation strategy?

Creatine is one of the few dietary supplements that have a very solid scientific support
for its efficacy in increasing strength, explosive performance and muscle mass. So the
question in not whether it is effective, but rather how to supplement it to reap maximal
effectiveness?

There are several theories on how to take creatine; some say your should load and then
lower the dose, while others say you can get good results by a low dosage regimen
without loading. Yet others say you should cycle the creatine and take breaks from it in
between cycles. And then we have the issue of dosages and how to ingest it. In addition
there is a lot of confusion about the myriad for creatine forms that claim to be superior
over the golden standard creatine monohydrate. Are the new fancy creatine-super-duper
formulations really worth their price? Let’s review it all here and see what the research
is saying.

Creatine forms

When creatine first came out on the market it was creatine monohydrate. This is also the
form of creatine that has been used in all the scientific studies that showed its
performance enhancing and muscle growth stimulating effects. Because creatine rapidly
became so popular, manufacturers came up with different creatine variants and started
to make specific claims that their creatine formula is superior. Not so! Don’t let yourself
get fooled and ripped off! Stick to the golden standard creatine monohydrate.

For more info on different creatine forms and formulation, check out

Will Brink’s article “The Creatine Grave Yard”

Creatine supplementation protocols

There are basically three creatine supplementation protocols. Here’s an overview of


them with recommended effective dosages:
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Loading followed by Maintenance protocol

Loading phase: Supplement with 0.3 g creatine/kg body weight/day (0.14


g/lb/body weight/day) for 5-6 days to maximize muscle creatine stores.

Maintenance phase: Supplement with 0.03 g creatine/kg body weight/day (0.014


g/lb/body weight/day) thereafter to maintain elevated muscle creatine stores.

Low-Dose protocol

Supplement with 3-5 g creatine per day for at least 8 weeks to increase muscle creatine
stores.

Cycling protocol

Load/maintain for 12-16 weeks, and then take a break for 3-6 weeks. After the break,
start another cycle with the loading phase followed by a maintenance phase followed by
a break for a desired numbers of cycles.
Most studies that have shown performance enhancing effects used the creatine loading
protocol. The purpose the creatine loading is to maximize creatine storage in the
muscles. The magnitude of the increase in muscle creatine content is important because
studies have reported that performance improvements are dependent on the increase in
muscle creatine (1, 2). In a typical creatine loading phase, a dose of 20-30 g creatine (5-
6 g taken four times per day) is taken during 5-6 days (3, 4).

To find out your optimal loading dose, multiply your body weight in pound (lb) with
0.14 (or multiply your body weight in kg with 0.3). Thus, for a male weighing 220 lb
(100 kg) and a female weighing 140 lb (63 kg), the appropriate loading dose is 30-31 g
(220×0.14 or 100×0.3) and 20 g (140×0.14 or 63×0.3), respectively.

Thereafter,a maintenance dose is taken with the purpose to maintain the elevated muscle
creatine stores. A maintenance dose corresponding to 0.03 g/kg/body weight/day (0.014
g/lb/body weight) is enough to maintain elevated muscle creatine levels (4).

To find out your optimal maintenance dose, multiply your body weight in pound (lb)
with 0.014 (or multiply your body weight in kg with 0.03). Thus, for a male weighing
220 lb (100 kg) and a female weighing 140 lb (63 kg), the appropriate maintenance dose
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is 3 g (220 x 0.014 or 100 x 0.03) and 2 g (140 x 0.014 or 63 x 0.03), respectively.
Some people might prefer a slightly higher maintenance dose of 5 g per day. Cessation
of creatine maintenance doses after loading causes muscle creatine stores to return to
baseline within 4-6 weeks (4-8).

An alternative supplementation protocol is to ingest 3-5 g creatine per day (with no


loading phase) for at least 28-30 days (4, 9). Studies have shown that this method can
increase muscle creatine levels as effectively as the creatine loading (4). However, this
low-dose creatine supplementation will result in a more gradual and slower increase in
muscle creatine levels compared to the more rapid loading protocol, and it will therefore
take longer before any performance enhancement will be noticeable. Thus, the constant
low-dose creatine supplementation protocol is only beneficial for people who cannot do
the loading phase because of for example a busy working schedule. Also, while loading
dosages of 20-30 g creatine per day are well tolerated in the majority of individuals,
some can experience gastrointestinal upset (for example diarrhea) when large daily
dosages of creatine are consumed(10-12). For those people, the constant low-dose
creatine supplementation protocol is the way to go. Some discomfort can occur if
creatine is incompletely dissolved before ingestion (12). Thus, make sure to dissolve the
creatine powder properly, especially if you are taking larger doses.

Listen to Will Brink’s take on loading versus not loading.

Finally, we have the cycling protocol of creatine supplementation (13-15). One


argument behind creatine cycling is that it will keep the body’s ability to synthesize
creatine, intact. However, while the body’s endogenous synthesis of creatine (which
amounts to about 1 g per day (16, 17)) is decreased during creatine supplementation (8),
cessation of creatine supplementation merely causes the creatine levels in the body to
return to baseline (4, 5). If creatine supplementation were to permanently decrease the
body’s capability to synthesize creatine, the creatine levels in the body would have
dropped below baseline (pre-supplementation) levels, which would have caused an
increased fatigue and loss of strength. This does not happen (5, 6, 8, 14, 18, 19). Thus,
cycling of creatine supplementation has no scientific foundation and is completely
unnecessary. It confers no advantage over loading + chronic maintenance. Continuous
creatine supplementation without cycling actually might confer multiple health benefits
(which I will cover in a separate article).

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For more check out Will Brink’s great video on creatine cycling.

The Importance of dissolving your creatine before ingestion

This is the most common mistake people who take creatine do; they put it in
their protein shakes and scoop it down. However, this isn’t a very smart thing to do
because creatine has to be dissolved in order for the body to absorb all of it. This will
also prevent stomach upsets. And to dissolve creatine, it has to be put into warm (not
boiling!) water and stirred. If you cannot get really warm water from the tap (or if you
are drinking bottled water), heat up the glass in the micro and then dissolve the creatine
in it. I personally dissolve my creatine like this before going to the gym (I add in beta-
alanine as well) and drink it when I get back home from the gym. By then it has cooled
down to room temperature. I mix in 2 packets of stevia for flavor, as I don’t like to
drink plain lukewarm water. Of course, you can mix in some protein powder if you
want (just don’t put it in the fridge, see below).

Will has done a great video on the importance of dissolving creatine.

Usually, 5 g creatine should dissolve in about 2/3 glass of water. if you take more
creatine, you have to add more water.

Note that you cannot put the glass with your dissolved creatine in the fridge, as it will
cause the creatine to precipitate, which ruins the whole point of dissolving it in the first
place. The reason for this is that, stated in scientifically terms, the solubility of a solute
(creatine) is a function of the temperature of the solvent (water). Thus, dissolve your
creatine AND drink it dissolved.

Bottom Line

When supplementing with creatine I therefore recommend the classic loading / chronic
maintenance supplementation protocol. To get maximal effects ingest your creatine with
high GI carbs and protein (13, 20). Also, take the majority of your creatine during the
loading phase after your workouts, and during the chronic maintenance phase take the
whole 3-5 g dose in the meal right after your workouts. The reason for this is that co-
ingestion of creatine, protein and carbohydrates increases muscular retention of dietary
creatine (13, 20). And when creatine is ingested after workouts the uptake of creatine

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into muscles is further increased, and results in even greater muscle thickness (3, 21-
23). And remember to dissolve your creatine before you ingest it, which will prevent
stomach upset and help your body absorb more of it

Insulin Levels and Fat Loss – Q&A


Question: I know I’ve bothered about this on the forum but I still haven’t received a clear response from
anyone. From my understanding of insulin from not only your writings but the web in general when food is
consumed insulin is secreted.
Insulin is responsible for pushing nutrients to their respective targets and if necessary creating fat. It also
inhibits fat loss.
So given a negative caloric balance while trying to achieve fat loss with adequate protein fish oils and say
100 grams of carbs, how does the body bypass insulin’s effect on fat loss inhibition?
Does the insulin just deplete itself and fat oxidation resumes?
What about differences in GI and its effect on insulin.
Does equal carb intake of say white rice vs .brown rice elicit the same insulin response but at different
portions varying over time?
If both white rice and brown rice are equal in calories and nutrients and let’s say right before bed I consume
it, but still consuming at negative caloric balance. Would I still burn the fat equally to brown rice?
Possibly a bit lengthy but I would appreciate a response if you could. An insulin column would be fantastic

on your new site and would eliminate a lot of repetitive questions! nice job on the site and thanks for all
you do.

Answer: This is going to be a long answer because, frankly, there is a lot of misinformation and
misunderstanding about insulin and, as usual, I got a lot to say.
This is because, in a lot of ways, insulin is a schizophrenic hormone. Depending on what folks read (e.g.
bodybuilding literature), they will be told that insulin is great, it’s the most anabolic hormone in the body, it’s
key to getting big. And if you read other stuff (a lot of mainstream dieting literature), you’ll hear that insulin
is the devil, it makes you fat and ruins your health. Who’s right? Well, everybody…sort of.
As the question above states, it’s best to think of insulin as a generalized storage hormone rather than being
good or bad; and what it does, as always, depends on the context. I should mention that insulin not only
affects peripheral tissues such as the liver, muscle and fat cell; it also has central effects in the brain. I
discuss this in Bodyweight Regulation: Part 1 and that series of articles.
When elevated (and I’d note here that while carbohydrate has the primary effect on raising insulin, protein
also raises insulin; as well, the combination of protein and carbohydrate raises insulin more than either
alone), insulin pushes nutrients into cells. So insulin stimulates glycogen storage in the liver, it also enhances
glycogen storage in skeletal muscle. And while insulin isn’t that critically involved in protein synthesis per
se, it does decrease protein breakdown; as discussed in The Protein Book, this is important for maximal
increases in muscle mass. So far so good.
But insulin also is involved in fat storage which is where it gets its ‘bad’ characterization. Insulin activates
an enzyme called lipoprotein lipase which is involved in breaking fatty acids off of chylomicrons for
storage. However, this isn’t the only important step in fat storage.

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Contrary to popular belief (espoused by people still reading literature from the 1970’s), insulin is neither the
only nor single most important hormone involved in fat storage. Rather, a little compound called acylation
stimulation protein (ASP) has been described as “the most potent stimulator of fat storage in the fat cell”. And
ASP levels can go up without an increase in insulin (although insulin plays a role).
As another effect of insulin on body-fat levels, and this is discussed in some detail in The Stubborn Fat
Solution, insulin drastically inhibits lipolysis (fat mobilization) from fat cells. Even fasting insulin levels inhibit
lipolysis by up to 50%, even small increases essentially turn off lipolysis completely. Some could easily
interpret this as meaning that ‘eating carbs stops fat loss’. Or it might lead them to conclude that a
carbohydrate based diet would make fat loss impossible.
Tangentially I’d note, and one weird little study supports this, that spiking insulin (and letting it crash back
down) might be superior for fat loss than the standard strategy of trying to keep insulin low but stable all day
long. The reason is that even tiny amounts of insulin block lipolysis, if you keep insulin low but stable all
day, you are effectively impairing lipolysis. But the study in question showed that blood fatty acid levels
came back up much faster when insulin was spiked (which crashed blood glucose back down, lowering
insulin). The drawback, mind you, is that rapidly falling blood glucose tends to make people hungry and
calorie control would be nearly impossible with this strategy. And, as you’ll see below, in a hypocaloric
situation, it probably doesn’t matter a bit.
Anyhow, despite the sometimes seen mentality that you must ‘cut carbs to get lean’, four decades of practical
experience (and endless clinical research) show that that is simply not the case: bodybuilders (well, some
bodybuilders) have gotten plenty lean on carb-based diets (of course, others have failed miserably) so it’s
obviously not as simple as many would make it. That’s because whether a high-carb, moderate-carb, or
low-carb diet is most appropriate for someone depends on the circumstances; a topic I discuss in Comparing
the Diets.
Which brings me the long way around to the first question above. What is happening in terms of fat loss on
a diet that is hypocaloric (below maintenance levels, that is the person is burning more calories than they
are consuming) but contains sufficient protein and essential fatty acids but with say 100 grams of
carbohydrate? Don’t the carbs prevent fat loss by raising insulin? What’s going on?
To understand what’s going on, I need to explain two terms which are the post-prandial and post-absorptive
phases.
Post-prandial phase: this is just a technical term for ‘after you’ve eaten a meal’. In this situation, nutrients
are being absorbed and digested from the gut and released into the bloodstream, a whole host of hormones
are being released (depending on the macronutrient content of the meal) and the body will generally be in
an anabolic state (meaning that more nutrients are being stored than are being released from storage).
Post-absorptive stage: This is what happens between post-prandial phases. Eventually what you’ve eaten
has all been digested, absorbed and either burned for energy or stored in various tissues. When this
happens, hormone levels change an the body starts shifting to an overall catabolic state (I’m using this term
generally here to indicate that the body is releasing more nutrients from storage than are being stored).
So throughout the day, the body is shifting between the post-prandial phase and the post-absorptive phase
as you eat, that food gets digested and absorbed, and the body starts to draw on stored nutrients (hopefully
stored fat in fat cells).
And when you lower caloric intake, over a 24 hour period, the body will end up spending relatively more time
in the post-absorptive (remember: body burning stored nutrients) than post-prandial (remember: body storing
ingested nutrients) phase. This is simply a consequence of having less nutrients coming in relative to what’s
being burned.

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On a diet, meals are smaller (or activity is higher, or both) so any given meal will only maintain an anabolic
state for so long (and that time period will be shorter than if the person were eating more) before the body
shifts back to burning stored nutrients. So even in the face of dietary carbohydrate intake, the body still will
tap into stored fat; hence fat loss.
I’d note that theoretically this might mean that eating less frequently would improve fat loss, since the body
would spend more time between meals in the post-absorptive stage. Of course, this is probably offset by
each meal being larger and therefore taking longer to digest and I tend to doubt it matters in the long-
run. Some interesting research into intermittent fasting suggests that there is more to it than that but that’s
another topic for another day.
And this brings me to the second part of the above question, the glycemic index (GI) and insulin. Which
requires another long explanation. The GI was developed back in the 80’s to help with diabetic meal
planning. Basically it involves feeding folks a fixed amount of a reference carbohydrate (studies have
typically used either 50 grams or 100 grams of digestible carbs and while glucose was the original test food,
they now use white bread) with blood glucose being measured over a several hour period. The glucose
response to the reference food is defined as having a GI of 100.
Then, whatever food was being tested (again either 50 or 100 grams of digestible carbs were given) and
blood glucose was measured, researchers compared the blood glucose response of the test food to the
reference food. If the blood glucose response was say, 80% of the reference food, the test food was given
a GI of 80. If the blood glucose response was 120% of the test food, that’s a GI of 120. You get the idea.
And lower GI values basically meant that the test food was generating a smaller blood glucose response
than the reference food.
GI is far from perfect, there is massive individual variability, many foods will show a different GI depending
how you cook them and, as soon as you start mixing foods or adding things like protein, fiber and fat,
GI changes (almost always going down). So GI in and of itself ends up not saying very much in the big
scheme of things. An additional confound is training. As I discuss in the research review The Influence of
the Subjects’ Training State on the Glycemic Index, people who are better aerobically trained show a lower
GI response than those who are less well trained.
Now, it was always pretty much assumed that the GI was indicative of the insulin response and that lower
GI foods caused a lower insulin response than higher GI foods; this is part of where dieters originally got
fixated on the issue. However, it looks like it’s not quite that simple. While there was some brief interest in
an Insulin Index (II) which measured the insulin response to foods in the same way GI does, research seems
to have stopped as soon as it started.
As well as I discuss this in detail in the research review article Different Glycemic Indexes of Breakfast
Cereals Are Not Due to Glucose Entry into Blood but to Glucose Removal by Tissue there is some evidence
that low GI foods are low GI because they generate a fast initial insulin response.
That is, it’s important to realize that the blood glucose response of a food is determined by both its rate of
digestion and entry into the bloodstream as well as the rate of glucose storage in tissues such as
muscle. And it looks like low GI foods are not necessarily digesting more slowly but that a fast initial insulin
response is clearing more blood glucose. To quote from the summary of that research article:
“Bran cereal has a low GI because a more rapid insulin-mediated increase in tissue glucose uptake
attenuates the increase in blood glucose concentration, despite a similar rate of glucose entry into the blood.”
In this regards, I’d note that adding protein to carbs has been known to lower the GI for a couple of
decades. However, it’s also been established that adding protein to carbs increases the insulin
response. Which is consistent with the conclusions of the paper above, by increasing insulin, protein lowers
blood glucose levels giving a lower effective GI. Just not for the reason that most people think. And I

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daresay that most of the ‘insulin is evil’ people are going to argue that eating more protein hurts fat loss, yes
protein increases the insulin response to carbs. While increasing the insulin response. Go figure.
Which is a long way of saying that I don’t think the GI and insulin response matter much (although see my
final comments below). If there is much effect of GI on fat loss, it’s more likely to be mediated through food
intake and fullness as lower GI foods generally make people feel fuller and often cause decreased food
intake. As I discuss in detail in Is a Calorie a Calorie, this is the typical confound in these types of studies:
certain food types often make people spontaneously eat less, causing fat and weight loss and people
confuse the food itself with the reduction in food intake that it causes.
It’s also worth noting that a 2006 review paper titled Glycaemix Index Effects on Fuel Partitioning in Humans
examined this issue and concluded that:
“Apparently, the glycaemic index-induced serum insulin differences are not sufficient in magnitude and/or
duration to modify fuel oxidation.”
Basically, at least outside of the absolute extremes (where it’s possible that some of this stuff might matter),
it just doesn’t really seem to matter much outside of any influence on food intake (e.g. if a certain food keeps
you fuller and you eat less, it’s good for fat loss; if it doesn’t, it’s not). Basically:
The GI doesn’t truly indicate the insulin response in the first place, if it does it appears that low-GI foods may
be generating a faster initial insulin response in the first place, and none of this seems to meaningfully impact
on fuel utilization anyhow. Certainly any tiny differences in GI between brown and white rice are going to be
utterly irrelevant for 99% of cases.
Now, to wrap this up, I’d note that most studies done on this topic are drawing conclusions from average
responses and emerging evidence suggests that it’s a bit more complicated than this. In the article Insulin
Sensitivity and Fat Loss, I detail some recent work suggesting that the insulin sensitivity of a given individual
interacts with diet; the punchline of that article is that individuals who are insulin resistant (and/or show a
pronounced early insulin response to food intake) seem to get superior results from a lower GI/lower-
carbohydrate diet. In contrast, individuals with high insulin sensitivity show superior results on a carb-based
diet. Which is something I’ve observed for the last 15 years since writing my first book The Ketogenic Diet.
Ok, I know that was long but, as noted initially, there’s a lot of confusion over insulin and I have a lot to say
on the topic. Hopefully I answered your question.

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Impact of the Menstrual Cycle on Determinants of Energy Intake –
Reseach Review

Title and Abstract

L Davidsen et. al. Impact of the menstrual cycle on determinants of energy balance: a putative role in weight
loss attempts. International Journal of Obesity (2007) 31, 887-890
Abstract: Women’s weight and body composition is significantly influenced by the female sex-steroid
hormones. Levels of these hormones fluctuate in a defined manner throughout the menstrual cycle and
interact to modulate energy homeostasis. This paper reviews the scientific literature on the relationship
between hormonal changes across the menstrual cycle and components of energy balance, with the aim of
clarifying whether this influences weight loss in women. In the luteal phase of the menstrual cycle it appears
that women’s energy intake and energy expenditure are increased and they experience more frequent
cravings for foods, particularly those high in carbohydrate and fat, than during the follicular phase. This
suggests that the potential of the underlying physiology related to each phase of the menstrual cycle may
be worth considering as an element in strategies to optimize weight loss. Studies are needed to assess the
weight loss outcome of tailoring dietary recommendations and the degree of energy restriction to each
menstrual phase throughout a weight management program, taking these preliminary findings into account.

Background

Compared to men, women get the short end of the stick in almost everything related to body composition.
Their bodies fight back harder, they lose both weight and fat slower (even given an identical intervention),
they gain muscle more slowly, etc. Then again, they do get that whole multiple orgasm thing so there is at
least some good that comes along with the bad.
In any case, there are a lot of potential reasons for things to be this way and it’s been theorized that the
importance of women in keeping humanity alive (by raising children) during famines is a huge part of the
gender discrepancy. For example, women are more likely to be in the super-obese category and far more
likely to survive famines than men. While even men’s bodies fight back, the simple fact is that women’s
pretty much always fight back more.
Of course, the biggest potential impact on all of this is hormones which differ drastically between men and
women. It’s been known for a while that women’s fuel utilization changes during their menstrual cycle, as
does appetite and potentially energy expenditure.
In this vein, it’s been suggested that dieting (and training) might or should be modified during the menstrual
cycle to match up physiologically with what is going on in a woman’s body; I’ll come back to this a bit below.
That’s what today’s research review is about, a look at how things such as energy intake, appetite, energy
expenditure and body weight change throughout a woman’s cycle, as well the impact of birth control is briefly
examined along with some issues related to PMS and food cravings.

The Paper

The first section of the paper is simply a review of the hormonal changes which occur during a normal
menstrual cycle. Although there is variability, the typical woman’s full cycle is 28 days (this is an average)

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which is typically divided up into 4 distinct phases. With menstruation taken as day 1, we can define early
follicular phase (day 1-4), late follicular (days 5-11), periovulation (day 12-15), and luteal phase (days 16-
28).
A number of hormones change during the cycle but the two that I’m going to focus on are estrogen and
progesterone. During the early follicular phase, both estrogen and progesterone are relatively low. Estrogen
(estradiol in the graphic below) shows a peak in the late follicular phase followed by a drop. Progesterone
starts a slow increase through ovulation and both estrogen/progesterone peak in the middle of the luteal
phase before returning to baseline.
The paper notes that body temperature typically goes up after ovulation (for example, some women try to
use changes in body temperature to predict fertility), remains high during the luteal phase before returning
to baseline at or after the start of menstruation.
This pattern of hormonal change between estrogen (estradiol) and progesterone is shown in the graphic
below. Estradiol is the blue line, progesterone the black line. You needn’t worry about the green and red
lines (LH and FSH respectively) within the context of today’s research review.

The paper then examined research on energy (food) intake during different parts of the menstrual cycle. In
animals, energy intake is reduced at ovulation (when estrogen peaks) and increases after ovulation when
progesterone is peaking; this has long been interpreted as indicating that progesterone drove food intake.
Research in humans has generally borne out that pattern, higher energy intakes during the luteal phase and
lower intakes during the follicular phase; the increase in food intake has generally been reported to be
between 90-500 calories day.
It’s interesting to note that some research suggests that it is falling estrogen rather than increasing
progesterone that drives hunger. As I discussed in the research review on Crosstalk Between Estrogen and
Leptin Signalling in the Hypothalamus, estrogen appears to either improve leptin signalling in the brain or
send a leptin-like signal to the brain directly; falling estrogen would reduce overall signalling which would
tend to facilitate hunger.
Of course, there is also some reason to think that it’s a combination effect of estrogen and progesterone that
is having the overall effect. Given everything that’s changing at once, it is often difficult to determine exactly
which hormone (or how they are interacting) is having a specific effect.
Tangentially, the paper mentions that estrogens might play an important role for weight and fat loss loss
through inhibition of food intake. I’d also mention that a good bit of data suggests that estrogen is actually
lipolytic, helping to mobilize fatty acids during aerobic activities. In fact, if you inject men with estrogen, they
will mobilize fatty acids more effectively as well.
It’s actually even more complicated than this and estrogen can be seen to be having both positive and
negative effects on fat loss (and regional fat loss). I discuss this in more detail in The Stubborn Fat Solution;
sufficed to say that idea that ‘estrogen is bad’ in terms of fat loss is a simplistically incorrect one.
I bring this up for a couple of reasons. It’s interesting to note that with increasing fat loss, estrogen levels
typically drop, this is probably part of what drives hunger in women as they get leaner (I’d note that falling
estrogen certainly doesn’t seem to make lower body fat mobilization any easier for female dieters which I
think throws a major wrench in the idea that estrogen is responsible for women’s hip/thigh fat).
As well, there is an idea that comes up among some female dieters of wanting to ‘banish estrogen’ for a
variety of reasons (whether fat loss or otherwise). Given that estrogen may be doing many beneficial things
in terms of fat loss, this idea is probably going to do more harm than good. I’d also mention that low estrogen
causes major problems with bone density, trying to get rid of it will cause major problems down the road.

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Finally, the paper notes that some of the drive for appetite may be mediated by changes in blood glucose
homeostasis. Empirically, some women seem to be more prone to hypoglycemia during certain phases of
the menstrual cycle and falling blood sugar can stimulate hunger. Ensuring that blood glucose levels stay
stable might be extremely beneficial during those periods. For example, consuming moderate amounts of
fruit during that part of the cycle (to ensure that there is always some liver glycogen to be released to maintain
blood glucose) would be a useful strategy.
The next part of the paper examines changes in macronutrient intake, food cravings and PMS. Studies, as
usual, are inconsistent showing variously increases in carb, fat and protein intake during the luteal phase.
Some of this may simply be related to being hungrier in general with no clear increase in desire for a specific
nutrient.
Some research has indicated that the increase in carbohydrate intake is due to a specific craving although,
with chocolate (a combination of carbs, fat and other micronutrients) being the most craved item, other
possibilities exist. Cravings for a sugar/fat combo or something else entirely may be functioning here.
Alternately, the issue could simply be one of a magnesium deficiency; some research indicates that
magnesium supplements help with PMS related cravings and chocolate tends to be high in magnesium;
women may simply be self-medicating an important micronutrient. In this vein, many females report that
their cravings are ameliorated if not eliminated when they are supplementing magnesium (e.g. 400 mg of
magnesium citrate at bedtime, which can also help with sleep).
Next, the paper looks at the impact of menstrual cycle on energy expenditure (this brings us back to the
increased body temperature I noted above). The major increase in energy expenditure occurs also during
the luteal phase (when hunger is increased) with increases of 2.5-11.5% having been reported.
It’s important to note that this only amounts to a daily increase in energy expenditure of 90-280 calories per
day. That would be contrasted to the potential increase in food intake of 90-500 calories. That is, while
energy expenditure is up during the luteal phase, so is appetite; increases in energy intake can easily
overwhelm the small increase in energy output if food intake isn’t controlled.
The increase in metabolic rate is thought to be primarily related to the increasing progesterone levels. So
while increasing progesterone may not be driving the increased appetite, it may be stimulating metabolic
rate slightly during the luteal phase.
Next, the study examined the impact of birth control pills on body weight, first pointing out that there a number
of different types of birth control containing synthetic estrogen, progesterone or possibly both. I mention this
because, given the differences in each of the hormones (and their interactions), it becomes fairly inaccurate
to talk about the ‘effects of birth control’ on any of this; different types are likely to have different effects and
this can vary depending on the woman as well.
Studies have examined the impact of birth control on energy intake and several find an increase in both total
energy intake and fat intake; others have found no effect. With limited research it’s hard to tell if this is an
issue of different types of birth control or possibly individual variance. Empirically women seem to respond
extremely differently to birth control. Some go crazy, some get suicidal, some gain weight, some don’t, etc.
etc.
Of course, the same can be said for female responses to the menstrual cycle in general; some have crippling
PMS and out of control hunger, others are hit at most mildly or notice almost nothing at all. Differences in
hormone levels, sensitivity, etc. all contribute to the mystery that is woman.
As far as energy expenditure, while one study showed a small increase in basal metabolic rate of 5% with
birth control intake, others have found no effect. Again, type of pill and individual variance is probably at play
here (e.g. you might expect progesterone dominant pills to have the biggest impact on metabolic rate).

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Looking at body weight, most studies have apparently reported no substantial change in body weight with
birth control pills although many show a trend towards increased body weight. One exception is Depo-
Provera injections which are associated with weight gain.
Finally the paper looks at potential implications for dieting and weight loss. The paper argues that considering
which phase of the menstrual cycle the female in when starting a diet may be important. They argue that
starting the diet premenstrually when hunger and food cravings are most intense may be a bad idea, just
from an adherence standpoint.
Instead, starting a diet following menstruation or in the late follicular phase when food cravings and hunger
are less may make compliance easier. They also suggest that increasing total energy intake 5-8 days before
menstruation (when hunger/energy expenditure are at their highest) may prevent a suboptimal caloric intake
(which can make folks lethargic) and help with long term adherence to a diet. While I doubt most females
would be willing to break their diet 5-8 days out of every month, at least raising calories slightly to avoid loss
of control due to out of control hunger might be a worthwhile consideration.
Of course, it’s also easy to look at that from the other direction; in theory at least, keeping calories controlled
during periods when energy expenditure is up (for hormonal reasons) might generate superior fat loss. Of
course, that also means keeping calories controlled when hunger is at its worst. Life, she is full of
compromises.
The paper also argues that as chocolate is seemingly irreplaceable due to cravings, small amounts of dark
chocolate should be allowed to improve dietary adherence. Interestingly, I first read that idea in an older
book called Why Women Need Chocolate which was an interesting look at the idea of biologically driven
food cravings.
I’d note again that many females note that these types of cravings are almost eliminated if they supplement
with magnesium so I’m not sure that the idea that chocolate is irreplaceable is exactly true. Of course, dark
cocoa has a lot of health benefits anyhow and there are certainly worth things for a female to consume.
However, given that I wrote a book called A Guide to Flexible Dieting arguing that allowing food flexibility
can improve adherence, I think there is a lot of logic in their argument in a general sense. At the end of the
day, better to allow a small controlled amount of chocolate than feel deprived and end up eating the entire
bag. An extra 100 calories is always better than an extra 1000 calories in the long-term.
The same goes for the increased hunger that occurs when estrogen levels drop in the late follicular phase;
if allowing a few hundred extra calories acutely avoids a massive loss of control, that would seem beneficial
in the long-term.

Summing Up

So that’s a look at some of the things that can occur (good and bad) in terms of food intake, energy
expenditure during the menstrual cycle. It should be obvious that massive changes in hormones, including
the interactions between estrogen and progesterone drive a great deal of processes that can impact on a
woman’s food intake, energy expenditure and, of course, body weight.
I’d note again that the above processes tend to be exceedingly variable between women and while
generalizations can be made from studies, women may need to track things like body temperature, weight
and appetite through a couple of months to get an idea of how their bodies respond. Body temperature can
be tracked as can things such as training capacity (some women find it very difficult to train effectively during
certain periods of their cycle), appetite, etc.

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In periods when hunger is off the map and/or blood glucose seems to keep crashing, increasing food intake
slightly (and including moderate fruit) may be beneficial. For those women able to keep food intake under
control during the part of the cycle when body temperature is up, increased fat loss may be possible.
Supplementing with various nutrients such as magnesium and fish oils seems to help with PMS symptoms
and may help with food cravings during particularly difficult periods. Alternately, that may be a good time to
include free meals or refeeds as discussed in A Guide to Flexible Dieting; rather than trying to fight the
body’s tendencies (and losing control completely), finding ways to work with them may be better in terms of
long-term results. Allowing controlled amounts of craved foods tends to help avoid problems with guilt and
eating the whole box. Just keep it controlled.
I’d note, in concluding, that other more involved strategies have been suggested from time to time. Things
like synchronizing the intake of carbs or fats with different parts of the cycle (e.g. eating relatively more carbs
when carb metabolism is dominant and less when fat metabolism is dominant) have been suggested. I’m
not sure, practically, how well they’ve panned out but if anybody has any experience with the idea, I’d love
to hear about it in the comments section.

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How We Get Fat
Ok, this is going to be a bit ranty but, trust me, I write better when I’m upset. If the Internet has proven
anything to me over the years it’s this: basic literacy is sorely lacking. Because the comments in response
to the article I wrote on Tuesday, Excess Protein and Fat Storage – Q&A indicate that not only can people
not understand rather basic concepts, they insist on reading things into what I am saying that I have never
said. I could rant about making uncritical inferences but I’ll spare everyone that.
In that piece I answered a very specific question with a very specific answer. I made no implications of
anything beyond the exact answer I gave to that specific question. And somehow people managed to read
all kinds of asinine stuff into it, things that I never said or even began to imply. It’d amaze me if I hadn’t seen
people do this consistently over the past 15 years.
The basic confusion in that article was that folks interpreted my saying that carbs and protein can’t be
converted to fat as ‘Lyle says you can’t get fat overeating carbs and protein’. Which I absolutely didn’t
say. But people inferred, incorrectly. Basically, what I said and what they heard were not the same thing.
I’d note before continuing that if folks had taken 30 seconds to click on and read the article I linked Nutrient
Intake, Oxidation and Storage, they would have realized the mistake they were making as I specifically said
that overeating carbs can still make you fat, just not through direct conversion (rather through indirect
mechanisms). But in addition to a lack of basic literacy, laziness seems to be endemic on the net as
well. And for not taking a couple of minutes to read the piece that I specifically linked to, a bunch of people
got confused and then aggro.
I’d also note that if folks reading the protein piece had taken time to read the, I dunno, 200+ other articles
on the site, they’d realize that I am making no such claim that you can eat all the carbs you want (or that
lowcarb diets are superior, or whatever nonsensical conclusions they reached). Or that one specific dietary
approach (e.g. lowcarbs) is automatically superior to another.
But rather than do that, they took a single article, addressing a single specific question, and ran with it. That’s
not a good thing to do, you can’t take a single answer to a single specific question out of context and take
that to represent what I believe. Well you can but it’s stupid to do so. That’s what a lot of people did.
But since they couldn’t do any of that, couldn’t take the time to even read the single linked article much less
the rest of what’s on the site, rather than writing about something more interesting today, I’m going to clear
it up once and for all. And I still expect someone to read this completely wrong and go around the Internet
mis-representing what I’m saying. I’m used to it at this point.
.

How We Get Fat Part 1: Energy Intake Exceeds Energy Output

At a fundamental level, fat storage occurs when caloric intake exceeds caloric output, a topic I discussed in
some detail in The Energy Balance Equation. Now, I know that a lot of people claim that basic
thermodynamics don’t hold for humans. Simply, they are wrong. Invariably, the studies used to support this
position are based on a faulty data set: to whit, they are drawing poor conclusions about what people SAY
that they are eating.
For example, one popular book bases one of its many incorrect theses on a 1980 report suggesting that the
obese ate the same number of calories as the lean. Ergo, obesity was caused by something else. The
problem is this, the data set is wrong. A fact we’ve known for nearly 30 years but that the author was
somehow unable to become aware of in his ‘5 years of dedicated research’.

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Study after study after study over the past 30 years shows that the obese systematically under-report their
food intake (by up to 30-50%) and over-report their activity (by about the same). So when they say they are
only eating 1800 calories per day, they may be eating 2400-3600 calories per day. And their activity isn’t
nearly what they think.
And when you put those same folks in controlled metabolic ward conditions and control their food intake
and/or activity output…voila, the energy balance equation holds. It’s only when you believe the (incorrect)
self-reported data that it doesn’t.
And make no mistake I am NOT saying that the obese are lying about their intake, not consciously
anyhow. Most people simply suck at knowing how much they are actually eating. Leave them to self-report
it and they almost always screw it up. If you’re mistaken enough to believe the self-reported values, you
reach even more screwed up conclusions about things.
In that vein, I have found that the chronically underweight “I can’t gain weight no matter what I do” are
invariably vastly over-estimating what they are eating. That is, they are eating far less than they think. Other
studies show that ‘health conscious people’ tend to under-report their true ‘junk food’ and dietary fat intake;
to appear more healthy they conveniently forget or leave out that trip to the burger joint.
Put differently, this isn’t something that only occurs in the obese (so spare me accusations of ‘hating the
obese’ or some nonsense). Am I clear or are people going to misinterpret me some more in the comments
and claim I said that fat people lie about their food intake? Because I’m not saying anything of the sort. Make
no mistake, I’m sure some do lie about it; most are just clueless about how much they are actually eating.
Now let me make it clear that there is obviously a lot more going on here, hormones and all manners of other
stuff impact on the energy balance equation. For example, chronically elevated cortisol does a lot of nasty
things in terms of reducing metabolic rate (reducing the energy out side of the equation) as well as negatively
impacting on calorie partitioning (where calories go when you eat them as discussed in Calorie Partitioning
Part 1 and Part 2). But for the most part, a lot of that is outside of our control. It’s relevant but you can’t do
much with most of it. So I’ll focus on calories.
.

How We Get Fat Part 2: Nutrient Intake, Oxidation and Storage Part
Deux

The primary storage of fat in the body is in fat cells, duh. Most of that is found in what is called subcutaneous
fat, which is found under the skin. There is also fat stored around the gut area called visceral fat (this
surrounds the organs). Fat can also be stored in ‘bad’ places like the liver and pancreas under certain
conditions; this is called ectopic fat storage.
I’m going to focus here on subcutaneous fat. There, whether or not fat is stored or removed comes down to
a concept called fat balance, which I discuss in some detail in The Ultimate Diet 2.0. You can think of fat
balance as the fat specific equivalent of energy balance. That is
Net Change in Fat Stores = Fat Stored – Fat Burned
I’d note that the same nutrient balance holds for protein, carbohydrates and alcohol (which I’m not going to
talk about today). That is, the net effect on bodily stores, whether protein or carbohydrate stores in the body
increases, decreases or stays the same comes down to the balance of protein/carb stored vs. protein or
carbs/burned.
So at a fundamental level, fat gain occurs when fat storage exceeds fat burning (technically oxidation). And
fat loss occurs when fat oxidation exceeds fat storage. I’d note that both processes take place in some
amounts throughout the day, controlled by a host of processes I’m not going to talk about. Just recognize

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that what happens over time in terms of your fat stores comes down to the relationship between those two
processes: fat storage – fat oxidation.
So what determines fat oxidation and fat storage rates?
.

How We Get Fat Part 3: Back to Nutrient Intake, Oxidation and


Storage

Now, here’s where people got confused by Excess Protein Intake and Fat Storage – Q&A, and where they
would have been unconfused by clicking the linked article on Nutrient Intake, Oxidation and Storage. In fact,
I’d suggest you go read it right now, it’s not that long and since I’m not going to retype all of it here (that’s
why I wrote it the first time), it’d be a good idea. I’ll wait.
However, since I know most of you will have just ignored my suggestion to actually read that piece, I’m going
to summarize a few points from it (as well as from the Q&A):
1. Carbs are rarely converted to fat and stored as such
2. When you eat more carbs you burn more carbs and less fat; eat less carbs and you burn less carbs
and more fat
3. Protein is basically never going to be converted to fat and stored as such
4. When you eat more protein, you burn more protein (and by extension, less carbs and less fat); eat less
protein and you burn less protein (and by extension, more carbs and more fat)
5. Ingested dietary fat is primarily stored, eating more of it doesn’t impact on fat oxidation to a significant
degree
Let’s work through this backwards. When you eat dietary fat, it’s primary fate is storage as its intake has
very little impact on fat oxidation (and don’t ask me a bunch of questions about “But people say you have to
eat fat to burn fat?” in the comments. That idea is fundamentally wrong but would take an entire article to
address). It also doesn’t impact greatly on the oxidation of the protein or carbohydrates.
Carbohydrates are rarely converted to fat (a process called de novo lipogenesis) under normal dietary
conditions. There are exceptions when this occurs. One is with massive chronic overfeeding of carbs. I’m
talking 700-900 grams of carbs per day for multiple days. Under those conditions, carbs max out glycogen
stores, are in excess of total daily energy requirements and you see the conversion of carbohydrate to fat
for storage. But this is not a normal dietary situation for most people.
A few very stupid studies have shown that glucose INFUSION at levels of 1.5 total daily energy expenditure
can cause DNL to occur but this is equally non-physiological. There is also some evidence that DNL may
be increased in individuals with hyperinsulinemia (often secondary to obesity). There’s one final exception
that I’ll use to finish this piece.
But when you eat more carbs, you burn more carbs and burn less fat. And that’s why even if carbs aren’t
directly converted to fat and stored as such, excess carbs can STILL MAKE YOU FAT. Basically, by
inhibiting fat oxidation, excess carbs cause you to store all the fat you’re eating without burning any of it
off. Did you get that? Let me repeat it again.
Carbs don’t make you fat via direct conversion and storage to fat; but excess carbs can still make you fat by
blunting out the normal daily fat oxidation so that all of the fat you’re eating is stored. Which is why a 500
cal surplus of fat and a 500 cal surplus of carbs can both make you fat; they just do it for different reasons
through different mechanisms. The 500 calories of excess fat is simply stored; the excess 500 calories of
carbs ensure that all the fat you’re eating is stored because carb oxidation goes up and fat oxidation goes
down. Got it? If not, re-read this paragraph until it sinks in.

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Oh yeah, the same holds for protein. Protein isn’t going to be converted to and stored as fat. But eat excess
protein and the body will burn more protein for energy (and less carbs and fat). Which means that the other
nutrients have to get stored. Which means that excess protein can still make you fat, just not by direct
conversion. Rather, it does it by ensuring that the fat you’re eating gets stored.
Of course protein also has the highest thermic effect, more of the incoming calories are burned off. So
excess protein tends to have the least odds of making you fat under any conditions; but excess protein can
make you fat. Just not by direct conversion to fat; rather it’s indirectly by decreasing the oxidation of other
nutrients.
Ok, is the above clear enough? Because I can’t really explain it any simpler but will try one last time using
bullet points and an example. Let’s assume someone is eating at exactly maintenance calories. Neither
gaining nor losing fat. Here’s what happens with excess calories. Assume that all three conditions represent
identical increases in caloric intake, just from each of the different macros. Here’s what happens
mechanistically and why all three still make you fat:
1. Excess dietary fat is directly stored as fat
2. Excess dietary carbs increases carb oxidation, impairing fat oxidation; more of your daily fat intake is
stored as fat
3. Excess dietary protein increases protein oxidation, impairing fat oxidation; more of your daily fat intake
is stored as fat
Got it? All three situations make you fat, just through different mechanisms. Fat is directly stored and carbs
and protein cause you to store the fat you’re eating by decreasing fat oxidation.
And I’d note again, since someone will invariably misread this that that doesn’t mean that a low-carb and/or
low-protein diet is therefore superior for fat loss. I’m not saying that and don’t think that I am. Because in
such a situation, while you may be burning more fat, you’re also eating more dietary fat. So net fat balance
can be unchanged despite the dicking around with macronutrient content. It still comes down to the deficit.
.

The Obvious Question: Why Not Just Eat Zero Dietary Fat?

And now I’ll answer the question that I know every person who has read (and hopefully understood) the
above is asking: so if carbs and protein are rarely converted to and stored as fat, and make you fat by
decreasing fat oxidation and causing all ingested dietary fat to get stored as fat, can’t I eat as much as I want
of protein and carbs so long as my dietary fat intake is zero?
And the asnswer is still no. Remember how I teased you above with one other exception, when carbs are
converted to fat for storage? That exception is when dietary fat is below about 10% of total daily
calories. Under that condition, the body ramps up de novo lipogenesis. So you still get fat.
Because the body is usually smarter than we are. Under conditions where dietary fat intake is ‘adequate’
(meaning 10% of total calories or more), the primary fate of that fat is storage and protein and carbs are
used for other things. And when dietary fat is too low, the body will start converting ingested carbs (and
probably protein, though it would still be rare) to fat for storage.
Oh yeah, the other question you’re going to ask in the comments “What about alcohol?” That’s going to
require a full article so be patient. I know that’s another thing lacking on the Internet but so be it.
And I really hope that clears things up. If it doesn’t, read this piece and the linked articles until it is.

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Meal Frequency and Energy Balance

Introduction

I read a tremendous number of research papers each week in order to keep up with the rapidly changing
field of nutrition, physiology, and all topics related to body recomposition. From time to time, I like to review
research papers that I think are interesting to my readers; while these are usually new papers, sometimes,
I also go back to older papers that happen to be relevant or important. This week’s paper is one of those
older papers that addresses one of the longer-standing myths in the field of weight loss, that of meal
frequency.

Title
Bellisle F et. al. Meal frequency and energy balance. Br J Nutr. (1997) 77 (Suppl
1):S57-70.

Abstract

Several epidemiological studies have observed an inverse relationship between people’s habitual frequency
of eating and body weight, leading to the suggestion that a ‘nibbling’ meal pattern may help in the avoidance
of obesity. A review of all pertinent studies shows that, although many fail to find any significant relationship,
the relationship is consistently inverse in those that do observe a relationship.
However, this finding is highly vulnerable to the probable confounding effects of post hoc changes in dietary
patterns as a consequence of weight gain and to dietary under-reporting which undoubtedly invalidates some
of the studies
We conclude that the epidemiological evidence is at best very weak, and almost certainly represents an
artefact. A detailed review of the possible mechanistic explanations for a metabolic advantage of nibbling
meal patterns failed to reveal significant benefits in respect of energy expenditure.
Although some short-term studies suggest that the thermic effect of feeding is higher when an isoenergetic
test load is divided into multiple small meals, other studies refute this, and most are neutral. More importantly,
studies using whole-body calorimetry and doubly-labelled water to assess total 24 h energy expenditure find
no difference between nibbling and gorging. Finally, with the exception of a single study, there is no evidence
that weight loss on hypoenergetic regimens is altered by meal frequency. We conclude that any effects of
meal pattern on the regulation of body weight are likely to be mediated through effects on the food intake
side of the energy balance equation.

My comments

Perhaps one of the longest standing dogmas in the weight loss and bodybuilding world is the absolute
necessity of eating frequently for various reasons. Specific to weight loss, how many times have you heard
something along the lines of “Eating 6 times per day stokes the metabolic fire.” or “You must eat 6 times per
day to lose fat effectively.” or “Skipping even one meal per day will slow your metabolic rate and you’ll hoard
fat.” Probably a lot

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Well, guess what. The idea is primarily based on awful observational studies and direct research (where
meal frequency is varied within the context of an identical number of calories under controlled conditions)
says that it’s all basically nonsense. The basic premise came, essentially out of a misunderstanding of the
thermic effect of food (TEF) also called dietary induced thermogenesis (DIT) which are the calories burned
in processing of the food you eat.
While TEF differs for the different nutrients, on average it constitutes about 10% of a typical mixed diet (this
varies between nutrients and slight differences may be seen with extreme variations in macronutrient intake).
So every time you eat, your metabolic rate goes up a little bit due to TEF
Aha! Eat more frequently and metabolic rate goes up more, right? Because you’re stimulating TEF more
often. Well, no. Here’s why:
Say we have two people, both eating the same 3000 calories per day from identical macronutrients. One
eats 6 meals of 500 calories/meal while the other eats 3 meals of 1000 calories/meal and we’ll assume a
TEF of 10%. So the first will have a TEF of 50 calories (10% of 500) 6 times/day. The second will have a
TEF of 100 calories (10% of 1000 calories) 3 times/day. Well, 6X50 = 300 calories/day and 3X100 = 300
calories/day. There’s no difference.
Of course, if you increase food intake from, say, 1500 calories to 2000 calories, you will burn more with TEF;
but this has nothing to do with meal frequency per se, it has to do with eating more food. I only bring this
up because I’ve seen people (try to) argue the positive effect of TEF by dredging up studies where folks ate
more total calories. Of course TEF goes up, but not because they are eating more frequently; rather it’s
because they are eating more food in total.
I want to address that last bit a little bit more since the fact that TEF goes up with increasing food intake is
often used to argue that “metabolism chases intake” and to make arguments for eating more to get lean.
Here’s the problem with this ‘logic’. Assuming an average 10% TEF, increasing food intake from 1500
calories to 2000 calories per day will increase caloric expenditure by 50 calories. But you had to eat 500
more calories to get it. So even if you burn 50 calories more, you’re still consuming 450 more calories than
you would have otherwise. Basically, the logic is akin to saying “I saved $100 by spending $1000 because
what I bought was 10% off”. Right, but you’re still out $900 that you wouldn’t have spent and you’d have
saved $1000 if you hadn’t bought it in the first place. The same logic applies here.
Which brings me, the long way around, to the above review paper which examined not only earlier
observational work but also direct studies of varying meal frequency on either weight loss (during such
studies) or metabolic rate. And, with the exception of a poorly done study on boxers (which I’ll discuss a bit
below), they found no effect of varying meal frequency on any of the examined parameters. No increase in
metabolic rate, no increase in weight loss, no nothing. What’s going on?
They concluded that earlier studies finding an effect of meal frequency on weight gain (or loss) had more to
do with changes in appetite or food intake, not from a direct impact on metabolic rate. For example, early
observational studies found that people who skipped breakfast were heavier and this still resonates today
with the idea that skipping breakfast makes you fatter. However, the review points out that this may be
confusing cause and effect: people often start skipping meals to lose weight.
I’d note, tangentially and I’ll come back to this below, that there is no data in humans that skipping a single
meal or even a day’s worth of meals does anything to metabolic rate. Human metabolism simply doesn’t
operate that quickly and various research into both fasting and intermittent fasting show, if anything, a slight
(~5% or so) increase in metabolic rate during the initial period of fasting. The idea that skipping breakfast or
a single meal slows metabolic rate or induces a starvation response is simply nonsensical.
Basically, there are a lot of confounding issues when you start looking at observational work on diet and
body weight. As I discussed in detail in Is A Calorie A Calorie, you often find that certain eating patterns

403
impact on caloric intake. And it’s those changes in caloric intake (rather than the eating patterns themselves)
that are causing changes in weight
For example, some early studies actually found that eating more frequently caused weight gain, mainly
because the foods being added were snacks and were in addition to normal food intake. In that situation, a
higher meal frequency led to greater food intake and weight gain. But it wasn’t the meal frequency per se
that caused the weight gain, it was the fact that folks were eating more.
Other studies have shown that splitting one’s daily calories into multiple smaller meals helps to control
hunger: people tend to eat less when they split their meals and eat more frequently. But, again, this isn’t an
issue of meal frequency per se, it’s because food intake is decreased. When folks eat less, they lose weight
and IF a higher meal frequency facilitates that, it will cause weight loss. But, at the risk of being repetitive,
it’s not because of effects on metabolic rate or any such thing; it’s because folks ate less and eating less
causes weight loss.
I’d note that the above observation isn’t universal and some people report that the simple act of eating makes
them hungrier. Many people are finding that an intermittent fasting protocol, where they don’t eat anything
for most of the day followed by one or two big meals works far far better for food control than the standard
of eating many small meals per day. Again, this isn’t a universal and I’m currently examining differences
between people to determine who will respond best to a given pattern.
I’d also note that there is a fair amount of literature that eating more frequently has benefits in terms of blood
glucose control, blood lipid levels and other health markers. I’d add to that the recent work on caloric
restriction and intermittent fasting (a topic I’ll look at in a later article) is finding massive benefits (especially
for the brain) from less frequent meals. So even this topic isn’t as simple as ‘more frequent meals is healthier’.
However, this is all tangential to the claims being made for metabolic rate. Whether you eat 3 meals per day
or 6, if your daily caloric intake is identical, you will expend the same number of calories per day from TEF.
While work in rats and mice, for whom everything happens faster, has found that a single meal can lower
metabolic rate, this is irrelevant to humans. Skipping a meal will not affect human metabolic rate at all.
Quite in fact, it takes at least 3-4 days of fairly strict dieting to impact on metabolic rate (and some work on
fasting shows that metabolic rate goes UP acutely during the first 72 hours of fasting); a single meal means
nothing. You will not go into ‘starvation mode’ because you went more than 3 hours without a meal. Nor will
your muscles fall off as an average sized food meal takes 5-6 hours to fully digest, as I discuss in The Protein
Book.
Now, all of the above is only looking at the quantity of weight loss, not the quality. For athletes and dieters,
of course, sparing lean body mass and losing fat is a bigger goal than how much weight is actually lost.
Which brings me to the boxer study that everybody loves to cite and nobody seems to have read (except
me as I spent years tracking down the full text of the paper).
In this study, boxers were given either 2 or 6 meals per day with identical protein and calories and examined
for lean body mass lost; the 2 meal per day group lost more lean body mass (note: both groups lost lean
body mass, the 2 meal per day group simply lost more). Aha, higher meal frequency spares lean body mass.
Well, not exactly.
In that study, boxers were put on low calories and then an inadequate amount of liquid protein was given to
both groups and the meals were divided up into 2 or 6 meals. But the study design was pretty crappy and I
want to look at a few reasons why I think that.
First and foremost, a 2 vs. 6 meal per day comparison isn’t realistic. As discussed in The Protein Book, a
typical whole food meal will only maintain an anabolic state for 5-6 hours, with only 2 meals per day, that’s
simply too long between meals and three vs. six meals would have been far more realistic (I would note that
the IF’ing folks are doing just fine not eating for 18 hours per day).

404
Additionally is the use of a liquid protein that confounds things even more. Liquids digest that much more
quickly than solid foods so the study was basically set up to fail for the low meal frequency group. They were
given an inadequate amount of rapidly digesting liquid protein too infrequently to spare muscle loss. But
what if they had been given sufficient amounts of solid protein (e.g. 1.5 g/lb lean body mass) at those same
intervals? The results would have been completely different.
As discussed in The Protein Book in some detail, meal frequency only really matters when protein intake is
inadequate in the first place. Under those conditions, a higher meal frequency spares lean body mass. But
when protein intake is adequate in the first place (and again that usually means 1.5 g/lb lean body mass for
lean dieters), meal frequency makes no difference. And that’s why the boxer study is meaningless so far as
I’m concerned. An inadequate amount of liquid protein given twice per day is nothing like how folks should
be dieting in the first place.
In any case, let me sum up the results of this review: Meal frequency per se has essentially no impact on
the magnitude of weight or fat loss except for its effects on food intake. If a high meal frequency makes
people eat more, they will gain weight. Because they are eating more. And if a high meal frequency makes
people eat less, they will lose weight. Because they are eating less. But it’s got nothing to do with stoking
the metabolic fire or affecting metabolic rate on a day to day basis. As the researchers state above:
We conclude that any effects of meal pattern on the regulation of body weight are likely to be mediated
through effects on the food intake side of the energy balance equation.
And that’s that.

Practical Application

The take home of this paper should be fairly clear and I’m going to focus primarily on dieting and weight/fat
loss here. I’m also going to assume that your protein intake is adequate in the first place; if you’re not getting
sufficient protein during your diet, you have bigger problems than meal frequency can solve.
Before summing up, one last thing, from a practical standpoint, I sometimes wonder if the people who are
adamant about 6 meals/day have ever worked with a small female athlete or bodybuilder. A 120 lb female
may have a daily food intake of 1200 calories/day or less on a diet.
Dividing that into 6 meals gives her 200 calorie ‘meals’. More like a snack. 4 meals of 300 calories or even
3 meals of 400 calories is a much more livable approach than a few bites of food every 3 hours.
By the same token, a very large male with very high caloric requirements (for dieting or mass gaining for
example) may find that fewer larger meals are difficult to get down or cause gut discomfort, eating more
frequently may be the only way to get sufficient daily calories.
But again, these are all completely tangential to any (non-existent) impacts of meal frequency on metabolic
rate or what have you.
So here’s the take home:
 If eating more frequently makes it easier to control/reduce calories, it will help you to lose weight/fat.
 If eating more frequently makes it harder to control/reduce calories, or makes you eat more, you will gain
weight.
 If eating less frequently makes it harder for you to control/reduce calories (because you get hungry and
binge), it will hurt your efforts to lose weight/fat.
 If eating less frequently makes it easier for you to control/reduce calories (for any number of reasons),
then that will help your efforts to lose weight/fat

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I personally consider 3-4 meals/day a workable minimum for most, 3 meals plus a couple of snacks works
just fine too. High meal frequencies may have benefits under certain conditions but are in no way mandatory.
And, in case you missed it the first time through: eating more frequently does NOT, I repeat DOES NOT,
‘stoke the metabolic fire’.

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Meal Frequency and Mass Gains
The issue of meal frequency for muscle mass gains would seem to be pretty well decided,
right? Bodybuilders have been pushing for 6 (or more) meals per day spread out every 2.5-3 hours for
decades and this is taken as an almost de-facto requirement for success in terms of optimal mass gains.
Then again, the people who have used Intermittent Fasting (for examples, check out Martin Berkhan’s
LeanGains.com) appear to be making exceedingly good progress in terms of muscle gain despite not eating
for 14-16 hours during the day suggesting that perhaps the above dogma regarding meal frequency isn’t
quite as well established as folks might think.
Now, I’ve discussed meal frequency previously, in terms of its effects on weight, body fat and body
composition in the research review on Meal Frequency and Energy Balance and won’t rehash those points
here. Rather, what I want to discuss here is the potential impact of meal frequency on mass gains for
athletes trying to increase muscle mass.
And since I covered the topic in exceeding detail in The Protein Book, I’m simply going to excerpt that section
of that chapter. I’d note that I cover a tremendous number of other topics related to meal frequency in that
chapter including many practical issues along with the impact of meal frequency on muscle mass
maintenance during fat loss.
I’d also note that apparently Layne Norton (a professional natural bodybuilder and all around smart guy who
is doing scientific research on the issue of protein and muscle gain) has been experimenting with the ideas
I’m going to discuss below (he calls it protein bolusing) but I have no idea how or if it actually panned out.
Finally I’d note that I’m not going to include the reference list for this excerpt. It’s in the book.

Optimal meal frequency: A theoretical approach

In Chapter 3, I discussed how eating impacted on both protein synthesis and breakdown following a meal.
To briefly recap, an increase in blood AAs primarily stimulates protein synthesis with a much lesser impact
on protein breakdown; in contrast, increasing insulin levels appears to primarily decrease protein breakdown
with only a small impact on protein synthesis. With that information as background, I now want to examine
the topic of meal frequency from a slightly more theoretical standpoint by examining two separate questions:
1. Is it possible to eat too frequently?
2. How long will a typical meal maintain the body in an anabolic state?
By determining a potential maximum and minimum amount of time that should pass between meals, an
optimal meal frequency can be developed. As well, I want to examine the idea that different meal frequencies
might be optimal under different conditions (i.e. maintenance versus mass gains versus dieting).

Is it possible to eat too frequently?

It’s not uncommon to read about bodybuilders or other athletes taking the eat-more-frequently dictum to
extreme levels, eating every one to two hours. The idea behind this is the idea that optimal results should
occur by maintaining a near continuous influx of nutrients into the body. I imagine if they could find a way to
do it, some enterprising athletes would set up a continuous intravenous drip with carbohydrates, amino acids
and essential fatty acids.

407
This may not be a good idea in the first place. Some research, primarily using amino acid infusion, suggests
that skeletal muscle can become insensitive to further stimulation of protein synthesis. In one study, amino
acids were infused for several hours to 70% over normal levels (17). Protein synthesis increased after
roughly 30 minutes and was maintained for the next two hours at which point protein synthesis decreased
back to baseline.
Importantly, this decrease occurred despite the maintenance of high levels of blood amino acids.
Additionally, there was an increase in urea production (a waste product of protein metabolism), indicating
that the excess AAs were simply being catabolized in the liver to be excreted in the urine; that is, those AAs
were wasted and never utilized by the muscle.
The researchers took this as a suggestion that there might be a maximum amount of protein synthesis that
can occur at any one given time before a “muscle full” situation is reached (18). Perhaps more interestingly,
based on the amounts of AAs infused, the researchers estimated that only 3.5 grams of AAs would be
required to result in this “muscle full” situation (18). I want to make it very clear that this doesn’t mean that
3.5 grams of orally ingested AAs would cause the same effect. Rather, this represented the delivery of 3.5
grams of AAs to the muscle itself.
However, the total amount of dietary protein to achieve this amount wouldn’t be huge. Most dietary proteins
are roughly 40-50% EAAs, and due to processing in the liver, slightly less than half of the ingested AAs
actually make it into the bloodstream. To provide 3.5 g EAAs to skeletal muscle would require roughly 15-
20 grams of whole protein over a two hour time span.
Interestingly, other more direct research supports this value. In a study I described in an earlier chapter,
subjects received doses of EAAs ranging from zero to 20 g EAAs and protein synthesis was studied (19). In
young subjects, muscle protein synthesis was maximized with an intake of 10 g EAAs and there was no
further increase with 20 g EAAs. This represents roughly 20-25 grams of whole protein.
Consumed every three waking hours (roughly six meals per day), this would allow for a maximum protein
intake of 120 grams per day before skeletal muscle protein synthesis is maxed out. For a 100kg (220 pound)
athlete, this is only 1.2 g/kg, lower than even the most conservative estimates discussed in Chapter 4. As
discussed previously, this research is a difficult to reconcile with other, much higher recommendations or
empirical results.
However, recall from Chapter 4 that dietary protein has more functions for athletes than simply the
stimulation of protein synthesis. Although the amount described above might very well maximize skeletal
muscle protein synthesis, optimizing the function of other important pathways of AA metabolism would very
likely raise requirements even further (20). As well, while excess amino acids may simple be oxidized off,
there is evidence that increased AA oxidation is involved in the overall “anabolic drive” of the body.
Finishing up this discussion, in their most recent study, the same group examined the effect on protein
synthesis of a variety of doses of infused AAs (21). Infusing AAs at four different ranges, the group saw a
similar pattern to their earlier work, an initial increase in protein synthesis followed by a return to baseline
despite maintenance of high AA levels. Additionally, while the lower infusion rates caused a significant
increase in protein synthesis, further increases at the higher concentration levels showed smaller additional
benefits. Essentially, providing low to moderate amounts of AAs gave the greatest result.
Finally, and perhaps most interestingly, the paper demonstrated conclusively that it was extracellular AA
concentrations (rather than the concentration of AAs inside the muscle cell) that were involved in stimulating
protein synthesis. The researchers suggested the existence of some type of amino acid “sensor” in the
muscle cell membrane that sensed AA levels. The study also suggested that it was the changes in
extracellular AA concentration, rather than the absolute amounts that were driving the changes in protein

408
synthesis. That is, it was the change from lower to higher that had the effect more than the absolute amount
of AAs present.
Along with the indication of a “resistance” to further stimulation of protein synthesis, it appears that raising
AA concentrations (after a meal) followed by a decrease in concentrations yield the best results. Basically,
spacing meals apart and allowing blood AA levels to drop, rather than maintaining AA concentrations at
continuously stable levels, appears to have the greatest impact on protein synthesis. Unfortunately, this still
gives no indication of how far apart those meals need to be spaced to allow a “resensitization” of the muscle
to a subsequent increase in AA concentrations.
Additionally, since it was based on an amino acid infusion, it’s unclear how this would relate exactly to the
consumption of meals. Between digestion and the hormonal response that occurs with eating, it may very
well be that eating protein would yield a different result than what the above research found using AA
infusion.
In this vein, it’s interesting to look back at the original casein versus whey research that I discussed in
Chapter 2. In that study, whey protein showed an initial spike in protein synthesis followed by an increase in
amino acid oxidation in the liver, a pattern not dissimilar to the work examined above (22). It seems plausible
that once whey had maximally stimulated protein synthesis, the remaining AAs were simply metabolized in
the liver.
In contrast, when very small amounts of whey (a few grams at a time) were sipped over a six hour span to
mimic the effects of casein, there was no increase in amino acid oxidation (23); however the impact on
protein synthesis was also smaller. It may very well be that flooding the body with large amounts of AAs
simply overloads the muscle’s ability to utilize amino acids, causing the excess to be burned off. This would
also be consistent with the fact that the slower protein, casein, actually generated a higher overall gain in
leucine in the body compared to whey; by never overloading the body’s protein synthetic machinery, overall
better results were obtained.
Related to the above research, another group compared the body’s use of leucine with subjects either given
small hourly meals or three separate meals (24). They found that protein oxidation was decreased (by 16%)
in the group given three meals. Essentially, providing amino acids too frequently appears to decrease the
body’s utilization of those aminos. Rather, having discrete meals where blood amino acid levels first increase
(stimulating protein synthesis without overloading the body’s ability to utilize AA’s) and then decrease for
some time (so that muscle can become “sensitive” to the effect of aminos again) would seem to be ideal.
At this point it would appear that eating too frequently (less than every three hours) has no real benefit, and
could possibly be detrimental due to the muscle becoming insensitive to the impact of amino acids. It’s
interesting to note the preliminary report above which found increased LBM gains with three versus six meals
per day. Perhaps by spacing the meals further apart, greater stimulation of protein synthesis occurred when
protein was eaten.
For the remainder of this chapter, I’ll take three hours to represent the minimum amount of time that should
pass between meals. Eating more frequently is unlikely to be beneficial and may very well have a negative
effect.

How long does a meal maintain the body in an anabolic state?

Having looked at the possibility that eating too frequently might actually be detrimental (or at least not
particularly beneficial) given how long a typical meal takes to digest, I want to look at how long a given meal
might possibly maintain an anabolic state.

409
Mentioned above, considering the relatively slow rate of protein and other nutrient digestion, it appears that
even a moderate sized meal maintains an anabolic state for at least five to six hours (8). Individual whole
food meals are still releasing nutrients into the bloodstream at the 5-hour mark (7). Very slowly digesting
proteins such as casein may still be releasing AAs into the bloodstream seven to eight hours after ingestion
(22). Considering this research, we might set a conservative limit of five hours as the absolute longest time
that should pass between eating some source of dietary protein during waking hours.

Summary: Theoretical examination of meal frequency

It appears that eating too frequently could potentially be detrimental to the goal of gaining muscle mass in
that muscle tissue becomes insensitive to further stimulation by amino acids, increasing protein oxidation in
the liver. Eating more frequently than every three hours would seem to not only be unnecessary (based on
the rate of digestion of whole proteins) but could possibly be detrimental.
Given a moderately sized whole food meal, the body will generally remain in an anabolic state for at least
five to six hours (and possibly longer depending on the foods chosen). Conservatively, we might use five
hours as the upper limit cutoff for time between meals.
This yields a duration between meals of anywhere from three to five hours. This should keep the body in an
overall anabolic state without causing problems related to too frequent or too infrequent consumption of
meals.
Full time athletes with time to eat very frequently are probably best served with the higher meal frequency
simply to ensure adequate caloric intake. Again, smaller individuals with lower total energy intakes may want
to use slightly larger meals eaten slightly less frequently for practical reasons. Similarly, individuals who work
jobs and are unable to fit in a meal every three hours needn’t worry obsessively about becoming catabolic.
A solid food meal containing a high quality protein, carbohydrates, fat and some fiber eaten every five hours
will maintain an anabolic state readily.

Protein distribution throughout the day

Related to the topic of meal frequency is the question of whether the day’s protein should be spread evenly
throughout the day, or if some other pattern of intake might be superior.
As discussed above, one early study examined whether providing 25% of protein at breakfast and lunch and
50% at dinner had any impact on nitrogen balance compared to spreading the protein evenly across the
day’s three meals; no difference was found (9).
More recent work has examined a dietary strategy called “protein pulse” feeding. With that approach, 80%
of the day’s protein was given at lunch with only 10% at the other two meals; this was compared to a “spread”
pattern where the day’s protein intake was distributed evenly across four meals. In elderly women, the
“pulse” pattern led to a greater protein gain compared to the “spread” pattern (25). However, in younger
women, the “spread” pattern was superior and led to a greater nitrogen balance (26).
There is a substantial and increasing amount of data that putting some amount of the day’s protein around
training is beneficial, a topic that is discussed in detail in the next chapter. Outside of ensuring adequate
protein before, during and after training, there is no real indication that distributing the day’s protein in any
pattern other than a basic spread pattern is beneficial (again, except possibly for older individuals).
So, for example, take an athlete who will be consuming 200 grams of protein per day with 40 grams of that
placed around training. That leaves 160 grams of protein to be evenly distributed across the day’s other

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meals. With a four meal per day frequency, that yields 40 grams of protein per meal; at six meals per day,
the athlete would consume roughly 27 grams of protein at each meal.

Is there an optimal intake pattern for different goals?

In the chapter on protein requirements, I mentioned Tipton and Wolfe’s contention that any discussion of
protein requirements has to be context dependent: that is, the goals of the athlete determine what is optimal
in terms of protein intake. While they were talking primarily about total daily protein intake, this idea can be
extended to other aspects of nutrition including protein intake throughout the day and how it might interact
with specific training goals.
Logically, gaining muscle mass versus maintaining muscle mass at maintenance calories versus trying to
maintain muscle mass under conditions of caloric restriction (dieting) are different situations, potentially
requiring different optimal intakes of protein, AAs, meal frequency or protein intake pattern. The possibility
exists that different patterns of protein intake (in terms of both timing and type of protein) might exist for
different goals (27).
For practical purposes, I’m going to consider the following discussion in terms of two different goals: muscle
mass maintenance (either at maintenance calories or while dieting) and muscle mass gain. I want to note
that most of this discussion will be somewhat hypothetical since little direct research exists to date.
The background for this discussion can be derived from a topic I’ve discussed previously in the book in terms
of how different patterns of protein digestion (i.e. fast versus slow) can influence whole body metabolism
differently.
Recapping briefly, large spikes in amino acid concentration appear to stimulate protein synthesis (recall also
the infusion data I discussed above) with little to no impact on protein breakdown. In contrast, maintaining
constant low levels of AAs appears to reduce protein breakdown with less of an impact on protein synthesis.
Consuming very large amounts of protein at once (as in the protein “pulse” studies discussed above) has an
effect similar to a fast protein such as whey, spiking blood amino acids and promoting protein synthesis as
well as oxidation (28).
In contrast, spreading protein out in smaller amounts throughout the day has an effect closer to that of
casein, inhibiting protein breakdown with a smaller impact on protein synthesis (28).
I’d mention again that, in the original whey versus casein study, reducing protein breakdown via casein had
a larger impact on net leucine balance compared to whey. Recall also that adding whey to other food, which
had the effect of slowing down digestion, had a similar effect.
Given that data, it may very well be that simply maintaining relatively constant low levels of amino acids (with
a spike around training, discussed next chapter) is optimal for all goals. This would be conceptually similar
to the strategy of keeping insulin low but stable during the day with a spike around training. This is essentially
the strategy that bodybuilders have empirically settled on under all situations: they eat small amounts of
protein, carbohydrates and fat throughout the day with a relatively larger intake of nutrients around training.
With regards to muscle mass maintenance and dieting, there is little to discuss: based on the direct research
available as well as the general difficulty in stimulating protein synthesis when calories are reduced, a
slow/spread pattern of protein intake is clearly optimal. Maintaining continuous low levels of amino acids
throughout the day (in addition to increasing total protein intake) to limit the body’s need to mobilize stored
body protein from muscle and other tissues should be the goal. A combination of slow proteins combined
with evenly spaced meals to keep blood AA levels stable throughout the day would seem to be optimal.

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But is this also the optimal pattern for gaining muscle mass? On the one hand there is the suggestive study
above where a group receiving three meals per day gained more LBM than a group receiving six per day;
as well there is the research suggesting that maintaining constant levels of AAs might cause skeletal muscle
to become “insensitive” to further stimulation; increasing extracellular levels of AAs and then allowing them
to fall again appears to be superior. Both of these data points suggest that keeping blood AA levels stable
throughout the day might not be optimal from the standpoint of muscle mass gains.
Another recent study throws a wrench in the typically held bodybuilder idea that simply maintaining
continuous levels of amino acids with frequent meal feeding is optimal (29). In that study, two groups were
compared. The first received three whole food meals while the second received the same three meals with
an essential amino acid (EAA) supplement in-between. I should note that the study suffered from one huge
design flaw: the groups got different amounts of total protein. It should have also tested a group that got 6
whole food meals and the same amount of protein as the EAA supplemented group.
Recognizing that limitation, the study made at least three major observations. The first was that the EAA
supplement generated a greater protein synthetic response than the whole meals. The second was that the
EAA supplement generated an anabolic response even when given in-between meals. That is to say, the
previously consumed meal, which was still digesting when the supplement was given, didn’t blunt the effect
of the EAA supplement. Finally, the EAA supplement didn’t blunt the anabolic response to the meal. Of
course, the study didn’t examine what impact this would actually have in the long-term on muscle mass
gains but is interesting nonetheless.
This study suggests that a potential pattern at least worth experimenting with for athletes seeking maximal
muscle mass gains would be to alternate between slower digesting meals with faster acting sources
(perhaps a whey protein drink or an EAA supplement) throughout the day (25).
It also plausible that a combination of slow and fast protein sources at a given meal could give the best of
both worlds: a spike in AAs to stimulate protein synthesis followed by a slower increase to inhibit protein
breakdown. Preliminary data that I discussed back in Chapter 2 supports that idea as well although it was
being primarily applied to protein intake following resistance training. It’s interesting to note that old school
bodybuilders often consumed copious amounts of milk to gain lean body mass as milk protein is a mixture
of whey and casein.

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Milk as an Effective Post-Exercise Rehydration Drink

Title
Shirreffs SM et al. Milk as an effective post-exercise rehydration drink. Br J Nutr (2007): Pg 1-8

Abstract

The effectiveness of low-fat milk, alone and with an additional 20 mmol/l NaCl, at restoring fluid balance after
exercise-induced hypohydration was compared to a sports drink and water. After losing 1·8 (SD 0·1) % of
their body mass during intermittent exercise in a warm environment, eleven subjects consumed a drink
volume equivalent to 150 % of their sweat loss. Urine samples were collected before and for 5 h after
exercise to assess fluid balance. Urine excretion over the recovery period did not change during the milk
trials whereas there was a marked increase in output between 1 and 2 h after drinking water and the sports
drink. Cumulative urine output was less after the milk drinks were consumed (611 (SD 207) and 550 (SD
141) ml for milk and milk with added sodium, respectively, compared to 1184 (SD 321) and 1205 (SD 142)
ml for the water and sports drink; P,0·001). Subjects remained in net positive fluid balance or euhydrated
throughout the recovery period after drinking the milk drinks but returned to net negative fluid balance 1 h
after drinking the other drinks. The results of the present study suggest that milk can be an effective post-
exercise rehydration drink and can be considered for use after exercise by everyone except those individuals
who have lactose intolerance.

My comments

In addition to glycogen replenishment and the promotion of recovery and adaptation to training, the issue of
re-hydration after exercise (endurance training more so than resistance training) is also of importance and
finding ways to optimally rehydrate the body following dehydration is a critical aspect of sports nutrition.
During endurance exercise, fluid loss usually exceeds fluid intake and athletes end up slightly dehydrated
at the end of the bout and even small amounts of dehydration can negatively impact on exercise performance
(i.e. at the next training session). While re-hydration when training once per day usually isn’t too big of an
issue, many athletes train more frequently than this and finding ways to optimally rehydrate (again, in
addition to issues of recovery, etc.) is important.
Previous work had found that the addition of both sodium and potassium to fluids was a key in re-hydration,
thus the popularity of drinks such as Gatorade and Powerade both of which also provide carbohydrate for
glycogen replenishment.
With the exception of one study which examined the role of a whole food meal on re-hydration, most studies
have used various experimental solutions, so this week’s study set out to examine a more commonly found
beverage (low fat milk) in terms of its effects on rehydration following exercise.
The study recruited eleven healthy male volunteers who were physically active but described as not being
accustomed to exercise in a warm environment.
Following a familiarization trial, subjects performed an exercise trial in a warm/humid room consisting of 10
minute bouts at 2 w/kg workload. Body weight was measured in-between bouts with the exercise stopped
when the subjects had lost 1.7% of their starting body weight.

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One of four drinks was provided starting at 20 minutes after exercise. The drinks were 2% milk, 2% milk
with added sodium, water, or Powerade. The total drink volume given was equal to 150% of the total weight
lost in four equal amounts (every 15 minutes for an hour); subjects were monitored for an additional 4
hours. No food or drink was allowed and urine production was measured every hour by having the subjects
pee. Subjective measurements of hunger and thirst were made every hour as well (in addition to before and
immediately after the exercise bout).
All subjects lost roughly 1.8 kg of weight during the exercise bout and the total amount of fluid given over
the hour of recovery drinking was 1.8 l (slightly under half a gallon).
In terms of urine production (a measurement of the amount of ingested fluid retained by the both), both milk
trials showed significantly less urine output compared to either water or Powerade with no real difference
between the milk and milk plus sodium drinks.
Similar results were seen looking at net fluid balance, due to decreased urine output, the milk groups
reattained fluid balance after 4 hours while the water/Powerade groups were still slightly dehydrated.
Finally, subjective rating of thirst went up after the exercise bout but decreased with re-hydration, with no
difference between drinks. Feelings of hunger also increased throughout recovery although both milk groups
and the Powerade reduced hunger more than water. Subjects also reported that the Powerade was sweeter
and slightly more palatable compared to the milk drinks which were reported as being saltier and more
bitter. No other differences were seen.
The researchers concluded that milk (with or without extra sodium) was superior to either water or Powerade
at rehydration although the slight differences seen at the end of the study are unlikely to significantly impact
on exercise performance in temperate climates.
They suggest that at least part of this is due to the quantities of both sodium and potassium in milk; as
mentioned both electrolytes are important in helping the body retain the fluid consumed following
exercise. They also note that the digestion rate of milk is going to be slower than either water or Powerade
due to the presence of protein and fat in addition to the carbohydrate; this might have affected the body’s
utilization of the milk for re-hydration compared to the other drinks. In keeping with this, subjects in the milk
group reported greater fullness, probably due to the length of time it took for the milk to be fully absorbed.
So this study adds to previous data showing that milk can be useful for recovery (in terms of protein
synthesis) following either resistance training or endurance training, as I’ve discussed in previous
newsletters.
At the same time, the amount of fluid consumed (nearly a half gallon of milk) is significant and some people
might not find milk terribly appealing following an exhaustive exercise bout. It would be interesting to see if
a protein/carbohydrate drink containing either dextrose/maltodextrin and whey or milk protein isolate (with
similar amounts of electrolytes to what is found in milk) promoted the same level of re-hydration following
exercise. I suspect that it would and this might provide an easier way to promote both training adaptations
and re-hydration following exercise. This would probably be easier than trying to drink 16-32 oz of milk
following exercise.
An additional issue, of course, is that of lactose intolerance but the availability of lactose reduced or removed
milk (cf. Lactaid/DairyEase) should make this less of an issue.

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Mixed Brain Fuel – Q&A
Question: On a ketogenic diet, how rapidly does the brain flip between glucose and ketones for fuel? Can
it use both fuel sources simultaneously?

Answer: The above question sort of encompasses a few different potential things and I’m not 100% sure
which you’re asking so I’ll just cover them all. First realize that one fuel that the brain cannot use is fatty
acids, at least not directly. This has led to the oft-stated belief that the brain can only use glucose. But this
is incorrect as the brain has an alternative fat derived fuel which are ketones (or ketone bodies, the two
major of which are beta-hydroxybutyrate and acetyl-acetate).
Ketones are produced primarily in the liver (from the breakdown of fatty acids) and exist predominantly as
an alternative fuel source for the brain (they can also be used by skeletal muscle) during periods of low-
carbohydrate availability. This probably was originally important during periods of complete starvation; now
very low-carbohydrate diets (defined here as any diet containing less than 100 grams per day of
carbohydrates) effectively ‘exploit’ this mechanism.
Now, on a carbohydrate based diet, the brain runs essentially on 100% glucose since ketones are generally
not produced in significant amounts under those conditions (there are a couple of odd exceptions, one is
following very long duration endurance exercise where a post-exercise ketosis can occur due to changes in
fuel metabolism). So what happens when you remove most or all carbohydrates from the diet? Does the
brain magically switch to using ketones? For the most part, no. Studies done way back when show that
there is an adaptation phase that may last about 3 weeks while the brain ramps up its ability to use ketones
for fuel.
Even there, after that roughly 3 week period, the brain still only derives about 75% of its total fuel
requirements (about 400 calories per day or thereabouts) from ketones; the other 25% come from glucose
(which the body can produce through a variety of pathways that I won’t detail here; all of this is explained in
excruciating detail in my first book The Ketogenic Diet). Mind you, this is only relevant on a very low-
carbohydrate diet. Even if the brain could still use ketones on a carb-based diet they wouldn’t be produced
in large enough amounts for it to be relevant.
So I think that answers at least part of your question: when first starting a low-carbohydrate diet, it takes the
brain about 3 weeks to adapt to using ketones for fuel; even then it only gets about 75% of its total fuel from
them. This scans pretty well with what many experience on the diet, they don’t feel fantastic for the first 2-3
weeks of the diet (while they are adapting). Some of that, mind you, is related more to mineral intake than
anything else (early studies found that sufficient intake of sodium, potassium and magnesium eliminated all
of the fatigue and lethargy that occurred on very low carbohydrate diets).
But there is a related question that often comes up which has to do with switching back and forth between
fuels (this is especially relevant for some cyclical ketogenic diets such as what’s described in The Ketogenic
Diet or in my Ultimate Diet 2.0). Here I am unaware of any research on the topic and most of what I have to
say is just based on empirical evidence, what people have reported over the 15+ years they’ve been giving
me feedback.
Certainly early in the diet there is often a period where the alternation of high and low carbs often causes
some people distress, they get the same headaches and issues going from high-carbs back to low-carbs for
a couple of weeks. Probably just a function of ‘interrupting’ the adaptation to ketone metabolism in the brain
and there might be some rationale to doing 2-3 straight weeks of a ketogenic diet prior to inserting refeeds
or carb-loads.

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At the same time, after more extended periods on the diet (perhaps 6-8 weeks), switching back and forth
from a carb-based to a ketone-based brain metabolism seems to cause most people no problems. They can
sort of drop in and out of ketosis (even throughout the day under certain conditions) and not really notice
anything one way or the other. Interestingly, even after extended periods off of a low-carbohydrate diet,
most people don’t report the same early adaptation phase that they went through the first time on the diet;
they go back onto a ketogenic diet and don’t notice anything.
This suggests to me that there is some type of long-term and/or almost permanent change in the brain in
terms of its ability to use ketones for fuel with long-term exposure to them. Again, I have exactly zero
research to back this up; it’s just an observation. But even there you’d still expect to see the same basic
75/25 split, just with an easier switching back to ketone metabolism after that initial adaptation phase.
Hope that answers your question.

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Milk: The New Sports Drink? A Review

Title
Roy BD. Milk: the new sports drink? A Review. J Int Soc Sports Nutr. 2008 Oct 2;5:15

ABSTRACT

There has been growing interest in the potential use of bovine milk as an exercise beverage, especially
during recovery from resistance training and endurance sports. Based on the limited research, milk appears
to be an effective post-resistance exercise beverage that results in favourable acute alterations in protein
metabolism. Milk consumption acutely increases muscle protein synthesis, leading to an improved net
muscle protein balance. Furthermore, when post-exercise milk consumption is combined with resistance
training (12 weeks minimum), greater increases in muscle hypertrophy and lean mass have been observed.
Although research with milk is limited, there is some evidence to suggest that milk may be an effective post-
exercise beverage for endurance activities. Low-fat milk has been shown to be as effective, if not more
effective, than commercially available sports drinks as a rehydration beverage. Milk represents a more
nutrient dense beverage choice for individuals who partake in strength and endurance activities, compared
to traditional sports drinks. Bovine low-fat fluid milk is a safe and effective post exercise beverage for most
individuals, except for those who are lactose intolerant. Further research is warranted to better delineate the
possible applications and efficacy of bovine milk in the field of sports nutrition.

My Comments

Milk, like all aspects of nutrition is often surrounded by controversy. From the nutjob tinfoil on the head anti-
milk zealots to bodybuilders who say that milk makes you smooth, milk is often thought of as a terrible food
for adult humans to eat.
Yet, objectively milk is an excellent source of high quality protein (a mix of casein and whey), carbohydrates
(lactose, which admittedly some people have problems digesting) along with providing fluids, highly bio-
available calcium, and electrolytes. Old time lifters often built large amounts of muscle mass with a program
of squats and a gallon of milk per day; the idea is still around in various incarnations. In contrast to the anti-
milk zealots, milk has been shown to have a number of potential health benefits beyond any sporting
applications that may exist.
I’m not going to address the controversy regarding milk here, sufficed to say I’m on the side of milk (and
dairy foods in general) being excellent for athletes and folks trying to improve body recomposition. The
combination of both fast whey and slow casein is excellent for a lot of sporting and athletic applications, dairy
calcium improves body composition, etc. And while dairy does contain quite a bit of sodium (which is what I
suspect causes the issues with ‘smoothness’ for contest bodybuilders), this is only an issue on the day of
the contest. Dropping milk out 16 weeks out can only hurt fat loss, not help it.
You can read more about that in Contest Dieting Part 1. As well I discuss dairy proteins (both supplemental
and whole food) in detail in The Protein book.

Which brings me in a roundabout way to today’s article which examines recent research examining the
potential of milk as a sports drink.

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The paper first examines much of what I talked about above, the overall macronutrient profile of milk. In that
the recent area of research for sports nutrition revolves around carbohydrate, protein/amino acid intake,
along with fluids and electrolytes, milk ends up covering all of those nutritional bases.
As noted above, milk contains a combination of both casein (a slow digesting protein) and whey (fast acting),
along with a large proportion of the branched chain amino acids (BCAA). It also contains carbohydrates
(lactose, see my note at the end of this piece), along with minerals, both sodium and potassium. Of course,
milk automatically contains fluid and hydration/fluid balance is also important for optimal performance and
recovery.
Moving on the paper first examines research on milk and resistance training adaptations. A number of
studies have been performed from acute (single drink) studies to longer work looking at lean body mass
gain. In one acute study, both fat free and whole milk were shown to improve protein synthesis following
training; the whole milk worked better although the researchers weren’t sure why.
Of more interest, milk was shown to be superior to a soy based drink (both drinks contained identical protein,
carbs and calories) in terms of lean body mass gains over 3-8 weeks. In addition, not only did the milk group
gain more lean body mass, they lost a bit of fat. Of some interest, it was thought that the superiority of the
milk was due to its slower digestion compared to the soy (a fast protein). As I detail in The Protein Book, in
contrast to recurring beliefs that whey is superior post-workout, research shows that a slow or combination
slow and fast protein following training appears to be superior in terms of lean body mass gains.
Quoting from the paper’s conclusion:
“Consumption of low-fat milk appears to create an anabolic environment following resistance training and
over the long term with training, it appears that greater gains in lean mass and muscle hypertrophy can be
obtained. Furthermore, milk may also lead to greater losses of body fat when it is consumed following
resistance training.”
Now, moving onto endurance training, it’s first important to note that endurance athletes have a couple of
issues to deal with (in terms of both performance and recovery) that strength trainers don’t necessarily have
to deal with. This includes hydration and performance during training/competition as well as glycogen re-
synthesis and re-hydration following training. While those certainly can be an issue following very voluminous
strength training, they tend to be a bigger issue for endurance type training.
Now, about a zillion studies (give or take a couple hundred thousand) have looked at the impact of carb
intake on endurance performance. The research is mixed and whether or not carbs help depends on the
duration and intensity of training. Of more relevance here, some research has examined whether adding
small amounts of protein during endurance competition can help performance. Some of it finds a benefit,
some of it doesn’t; there is still some controversy over this issue.
In this vein, some work has examine the impact of milk during endurance training. While some potential
benefits (such as increased blood amino acid levels) were seen, no performance benefits were seen and
the subjects reported a fuller stomach due to the milk; this was likely due to the milk more slowly emptying
from the stomach. This isn’t a good thing and what research has found a benefit of protein during endurance
training invariably used faster proteins (whey or casein hydrolysate). I would not recommend milk during
training.
However, as a post-workout drink, milk appears to be a good choice for endurance athletes. Some work has
found that the combination of protein and carbs leads to better glycogen re-synthesis, however no research
has directly examined milk in this context. One study compared chocolate milk to a commercial carbohydrate
drink and found that the chocolate milk was at least as good at promoting performance as the carb drink.

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With regards to hydration, a previous research review I did examined Milk as an Effective Post-Exercise
Rehydration Drink, finding that milk was superior to water or commercial carbohydrate drinks for re-hydration
following endurance exercise, presumably due to the sodium and potassium content.
Quoting again from the paper itself, the researchers conclude that
“The limited literature that does exist suggests that milk is as effective as commercially available sports
drinks at facilitating recovery for additional performance…Furthermore, milk is also a very effective beverage
at promoting fluid recovery following dehydrating exercise in the heat.”
The bottom link is that milk can be an effective post-workout drink for both resistance trainers and endurance
athletes.

Practical Application

Clearly the research to date suggests that milk may be a superior post-workout drink following resistance
training (at least compared to a fast protein like soy) and may have benefits for endurance athletes as well
in terms of promoting glycogen synthesis, recovery and re-hydration following training.
Anyone who has read The Protein Book (or my other books for that matter) knows that I’m big on milk and
milk proteins, they have massive advantages in terms of their protein content, dairy calcium, and other
effects. Milk is readily available, tasty and relatively inexpensive.
However, there are a couple of caveats. For large athletes who need a large amount of carbohydrates or
protein following training, milk may not be an ideal way of getting it. A typical 8-oz serving of milk contains
roughly 12 grams of carbohydrates and 8 grams of protein. A large resistance training athlete might need 4-
5X that many nutrients following training and drinking that much milk may not be feasible.
A compromise solution might be to use milk as a base and add extra nutrients (such as maltodextrin or
dextrose powder for carbs and protein powder for protein) to achieve a higher nutrient density than milk itself
can provide. So 16 oz. (2 cups) of milk with extra carbs/protein would get the benefits of milk along with
sufficient nutrients for larger athletes to recovery. Similar comments would apply to endurance athletes who
often need very large amounts of carbs following exhaustive training; drinking 4+ cups of milk following
training may not be feasible.
As a final comment, if there is one major problem with milk for many people, it’s the presence of lactose
(milk-sugar). Lactose, like all digestible carbohydrates requires a specific enzyme to be broken down called
lactase. However, some people lose the ability to produce lactase/digest lactose; this can occur either
completely or relatively (in the latter case, folks can handle small amounts of dairy).
Lactose intolerance, which should not be confused with a true milk allergy, can cause stomach upset, gas,
and diarrhea in predisposed people; it’s racially based and some ethnicities are more or less likely to have
problems. For those with lactose intolerance, but who wish to use milk following training there are several
options.
The first is to find a source of lactose free milk. Brands such as Lactaid add lactase to milk to digest the
lactose into glucose and galactose; this typically results in sweeter milk but without the offending lactase.
Lactase pills are also available which can be taken with milk to help with digestion. Finally, there are products
which claim to increase lactase levels in the gut and some people find that milk consumed with other food is
tolerable; additionally, regular yogurt consumption can improve the ability to digest lactose.

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Nuts and Bodyweight – Q&A
Question: I have a follow-up to the article you posted on Monday regarding 10 Tips to Deal with Holiday
Weight Gain. A lot of parties I attend during the holidays have various sorts of nuts as snacks and my
question is how they impact on body weight. I have read that they are healthy but they also seem to contain
a lot of calories, what’s the deal with them? Thank you.

Answer: Nuts are sort of strange nutritionally. On the one hand they are generally very nutritious, they
provide a decent amount of quality protein and, although sometimes high in fat, the fats they contain are
generally of the healthy kind, nuts are generally high in fiber as well. Nuts are also a good source of
magnesium, Vitamin E and research indicates that they may contain important phyto-chemical compounds
beneficial to human health; diets containing nuts have also been shown to improve blood lipid profiles.
On the other hand, they can be extremely nutritionally dense (that is, providing a lot of calories in a very low
volume). This gives them the potential to negatively affect body weight.
However, a fairly large body of research indicates that nuts don’t seem to impact body weight negatively, at
all. That is, various research studies have provided some amount of nuts in addition to the normal diet to
see what happens to body weight. In general, the addition of nuts has had limited or no impact on body
weight. Phrased differently, despite the addition of calories from nuts, weight doesn’t change/isn’t affected.
What’s going on?
Research has identified three possible mechanisms to account for the observed results.

Satiety: Nuts appear to increase fullness and calories from nuts seem to be compensated later in the day.
That is, it’s suggested that the calories from nut intake results in a spontaneous decrease in food intake later
in the day such that total energy balance is unchanged.
One type of study, called a preload study has examined this, providing a fixed number of calories from nuts
and then seeing what happens to spontaneous food intake at a buffet type meal later on. Invariably, nut
intake (one study tested almonds, chestnuts, and peanuts) causes people to eat less at the buffet meal
However, despite the impact of nuts on fullness, this still isn’t sufficient to account for the lack of an impact
on body weight from nut consumption and other mechanisms must be at work.

Increased Energy Expenditure: Some work has identified an increase in energy expenditure due to nut
intake; some research has found an increase in resting energy expenditure with chronic nut intake as well.
This could be due to the protein content (protein has the largest effect on TEF for example), the fatty acid
profile, or both.

Increased Fecal Energy Loss: With nut consumption, there is increased energy loss in your poop, that is,
some proportion (one study found a 7% increase) of ingested calories are excreted without absorption. This
is likely due to the fiber content of the nuts or some other compound that limits digestive/absorption capacity
for nuts.
The three factors above have been shown to account for 95% of the total energy value of the nuts so there
is still a small amount unaccounted for. In any case, nuts, despite their high energy content, simply don’t
seem to have the negative impact on body weight that one might expect. Which, mind you, doesn’t mean
that you can eat them with no attention to portions or intake of other food, recall that a big part of the above

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effect is due to caloric compensation. If you’re adding a ton of calories from nuts and don’t end up reducing
your intake from other sources, the potential for fat/weight gain certainly is there.
Which is basically a long way of saying to eat them, just not without paying some attention to overall intake.
Reference:
Mattes, RD. The Energetics of Nut Consumption. Asia Pac J Clin Nutr (2008) 17 (S1): 337-339.

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Nutrient Intake, Nutrient Storage and Nutrient Oxidation
This is going to be a bit of technical/unapplied article, I’m going to try to keep it short and to the point and
mainly it serves as a background for some topics I want to talk about in the near future (especially alcohol)
so just be forewarned as you start on this. When people talk about diet, it’s common to divide the various
nutrients that humans consume into two gross categories which are:
1. Macronutrients: nutrients consumed in large amounts (‘macro’ = large)
2. Micronutrients: nutrients consumed in small mounts (‘micro’ = small)
So macronutrient refers to protein, carbohydrates, fats and alcohol, those nutrients that, when they are
consumed are generally consumed in gram or larger amounts. The micronutrients refers to vitamins and
minerals which are usually consumed in very small amounts (e.g. the DRI for Vitamin C is 60mg where 1mg
is 1/1000th of a gram). I’m not going to talk about micronutrients in this article and will only focus on the
macronutrients, specifically protein, carbohydrate, fat and alcohol.
I’m also going to assume that you’re getting your nutrients through food and it’s going in through your mouth.
Certainly nutrients can be given via infusion but this is usually done in a hospital setting (sometimes athletes
will rehydrate and carb-load with IV fluids and glucose, mind you) and I’ll assume you’re not doing that.
.

Digestive Efficiency and Your Poop

Clearly anything you eat has to go through the process of chewing, swallowing and into the stomach for
digestion. There a bunch of stuff happens where the nutrients are broken down to one degree or
another. And either they get absorbed (moving into special cells to be released into the bloodstream, or
lymphatic system in the case of dietary fats) or not. If you’re particularly interested in the digestion processes
of the different macronutrients, I’d refer you to the specific articles:
A Primer on Dietary Fats Part 1 for fat digestion.
A Primer on Dietary Carbohydrates Part 1 for carb digestion.
What are Good Sources of Protein-Digestibility for protein digestion.
Nutrients that aren’t absorbed in the stomach move further down the intestine where in some cases (for
example, certain fibers), they are digested by special bacteria and re-enter the bloodstream as short-chain
fatty acids. This is discussed in Fiber – It’s Nature’s Broom.
Nutrients that pass that stage eventually come out the other end in your poo and we needn’t talk about that
much more. I’ll only note in this regards that digestive efficiency in humans is generally very high. Fats are
absorbed with about 97% efficiency (e.g. if you eat 100 grams fat, you’ll absorb 97 grams of them), animal
source proteins are about 90-95%, vegetable source proteins can be in the 80% range and carbohydrates
vary drastically depending on their form, fiber content, etc. But for the most part, with the exception of high-
fiber foods, you’re not losing a lot of calories in your poop.
I would note, having said more about poop than necessary at this point, that there appears to be slight
differences (based on the gut bacteria present) in how efficiently individuals absorb calories from the diet
but this only amounts to perhaps a 100 cal/day difference between the highest and lowest people. OF
course, in cases of specific disease where there is nutrient malabsorption, all these comments go out the
window but I won’t talk about that here. I’ll assume you have a normally functioning gut, etc.
.

Fates of Ingested Nutrients: Oxidation or Storage

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So what happens after nutrients get through the stomach and intestines and into the body? Broadly
speaking, there are two primary fates for nutrients at this point which are oxidation or storage. A third that I
should at least mention is that, under certain conditions, nutrients will sort of ‘sit’ in the bloodstream either
causing problems there or eventually being excreted in the urine. Outside of various pathophysiologies (e.g.
runaway diabetes where glucose is lost in the urine in large amounts), the urine excretion route is generally
minimal approaching insignificant and I won’t focus on it further here.
Oxidation simply refers to the direct burning of fuels for energy. This can occur in the liver, skeletal muscle
and a few others places and all 4 macronutrients can strictly speaking undergo oxidation after ingestion. So
fatty acids from dietary fat ingestion can be used to produce energy, carbohydrate can be burned off, a little
appreciated fact is that under normal circumstances as much as half of all dietary protein ingested gets
metabolized in the liver via a process called deamination with some of it simply being burned off for energy.
Storage should be fairly clear and the nutrients (with the exception of alcohol) can be ‘stored’ in the body for
later use. Carbohydrates can be stored as liver or muscle glycogen, under rare circumstances they are
converted to and stored as fat. Dietary fat is stored either in fat cells or can be stored within muscle as intra-
muscular triglyceride (IMTG). Under certain pathological conditions, fat gets stored in places it’s not
supposed to go, a situation called ectopic fat storage. In a very real sense there’s no true store of dietary
protein although amino acids from protein digestion are used to make various proteins and hormones in the
body. Skeletal muscle is, in essence, a ‘store’ of protein in the body. There is no store of alcohol in the body.
Which is the segue into the only real point I have to make in this piece: as it turns out, the size of a nutrient’s
store in the body is inversely related to the body’s propensity to oxidize it after ingestion. This is especially
true in terms of the size of the store relative to the amount consumed on a daily basis.
Put a little more clearly, the better the body’s ability to store a given nutrient, the less it tends to alter/increase
oxidize that nutrient after ingestion. And vice versa, the smaller the store in the body of a given nutrient
relative to intake levels, the more likely the body is to oxidize that nutrient after ingestion. I’ve shown the
implications of this in the table below and will make comments about specific nutrients below that.
.

Nutrient Size of store relative to daily intake Oxidation increase due to intake

Fat Very high Low

Carbohydrate Roughly equal High

Protein Moderate Moderate

Alcohol None Perfect

Fat

Body fat stores are effectively unlimited as individuals reaching 1000 lbs (and 70-80% body fat) have
demonstrated. Even a relatively lean male at 180 lbs and 12% body fat is carrying 21 pounds of fat. Each
pound contains maybe 400 grams of actual stored fat and that means about 8500 grams of fat stored in the
body. Contrast this to a relatively high daily intake of perhaps 100-150 grams per day and you can see that
the body’s store of fat is much much higher than what you eat on a day. And most people aren’t 12% body
fat.
But for the most part, ingested dietary fat has little impact on fat burning in the body; that is, when you eat
dietary fat, your body doesn’t increase fat oxidation. One exception is if an absolutely massive amount of
fat (like 80 g) is consumed all at once but even then the effect is fairly mild. Some specific fats, notably

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medium chain triglycerides, are somewhat of an exception to this; they are oxidized in the liver
directly. Rather, the primary controller of dietary fat oxidation in the body is how many carbohydrates you’re
eating, which I’ll explain momentarily.

Carbohydrate
For carbohydrate, the body’s stores are relatively close to the daily intake. A normal non-carb loaded person
may store 300-400 grams of muscle glycogen, another 50 or so of liver glyogen and 10 or so in the
bloodstream as free glucose. So let’s say 350-450 grams of carbohydrate as a rough average. On a
relatively normal diet of 2700 calories, if a person eats the ‘recommended’ 60% carbs, that’s 400 grams. So
about the amount that’s stored in the body already.
For this reason, the body is extremely good at modulating carbohydrate oxidation to carbohydrate
intake. Eat more carbs and you burn more carbs (you also store more glycogen); eat less carbs and you
burn less carbs (and glycogen levels drop). This occurs for a variety of reasons including changing insulin
levels (fructose, for example, since it doesn’t raise insulin, doesn’t increase carbohydrate oxidation) and
simple substrate availability. And, as it turns out, fat oxidation is basically inversely related to carbohydrate
oxidation.
So when you eat more carbs, you burn more carbs and burn less fat; eat less carbs and you burn less carbs
and burn more fat. And don’t jump to the immediate conclusion that lowcarb diets are therefore superior for
fat loss because lowcarb diets are also higher in fat intake (generally speaking). You’re burning more fat,
but you’re also eating more. But that’s a topic that I’ve not only addressed previously on the site but may
look at in more detail in a future article with this piece as background.

Protein
The body’s total protein stores (and note again that this isn’t a true store in the sense of body fat and
glycogen) is maybe 10-15kg or so when you add it all up. Which is pretty high compared to an average daily
intake. The DRI for protein is only about 50-60 grams per day for the average person and even folks eating
200-300 grams per day are still eating far less protein than stored. Which is why protein oxidation rates can
change with intake.
As I mentioned above, an under-appreciated fact is that about half of all ingested dietary protein is
metabolized in the liver (details on this can be found in The Protein Book). Some of it is oxidized for energy
while others are converted into other things (including glucose and ketones) for use elsewhere. But, protein
oxidation rates do change in response to intake. So, when protein intake goes up, oxidation will increase;
when protein intake goes down, oxidation rates decrease. This change isn’t immediate (as it more or less
is for carbohydrates) and takes 3-9 days to occur but mis-understanding of this process has led to some
goofy ideas such as protein cycling.
But it also explains one other issue of importance to protein which has to do with speed of digestion. Early
studies, including the oft-cited study on whey and casein by Boirie find that fast proteins are burned off for
energy to a greater degree than slower digesting proteins. Since the body doesn’t have anywhere to store
the rapidly incoming amino acids, it simply burns off more for energy. This, along with differences in handling
(e.g. the fact that fast proteins are absorbed by the gut as discussed in Casein Hydrolysate and Anabolic
Hormones and Growth – Research Review) are a big part of why slower digesting proteins invariably lead
to better overall protein retention in the body; not only does more make it into the bloodstream but less is
burned for fuel.

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Alcohol
And, finally, as noted above, there is absolutely no store of alcohol in the body. None
whatsoever. Effectively, alcohol is seen as a sort of metabolic ‘toxin’ or ‘poison’ to the body. And this means
that alcohol oxidation is 100% perfect, that is, the body will effectively do everything in its power to get rid of
the alcohol increasing alcohol oxidation to maximum (which means decreasing the oxidation of other
nutrients consumed with that alcohol) so that the alcohol can be gotten rid of.
I’m going to ask readers not to read anything into the above paragraph, don’t infer or try to draw conclusions
about how alcohol might or mightn’t fit into the diet in terms of anything. As it turns out, alcohol is an oddity
among nutrients with seemingly contradictory effects on things. I’m going to address that in detail in a
forthcoming article and, for now, just take the above as some much needed background information.
.

Summing Up

And that’s that. After consumption and digestion, nutrients have a couple of primary fates in the body which
are oxidation (burning) and storage (for use later). And, as it turns out, the propensity for the body to store
or oxidize a given nutrient is related to the body’s built-in store relative to intake. In the case of dietary fat,
where stored fat is much higher than daily intake, the body tends to store incoming fat and burn very little. Fat
intake per se has very little impact on fat oxidation rates.
Rather, the rate of fat oxidation is related to carbohydrate intake as the body is able to precisely alter
carbohdyrate oxidation to changing intake. Eat more carbs and burn more carbs (and less fat); eat less
carbs and burn less carbs (and more fat). Protein is somewhere in the middle, oxidation can increase or
decrease relative to intake but the effect takes time (3-9 days). Finally is alcohol, with no storehouse in the
body, alcohol oxidation will take 100% precedence over everything else when it is consumed. I’ll discuss
the implications of this in an article on alcohol (and it’s rather schizoid effects on body weight and body
composition in a later article).

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Muscle Growth and Post-Workout Nutrition
In recent years, there has been huge interest in the topic of around workout nutrition for promoting optimal
gains in strength and muscle size (prior to that, most interest had to to with recovery from exhaustive
endurance exercise). And, as is so often the case, as research has developed, many ideas, some good and
some bad, have developed out of that.
Early research into post-workout nutrition focused almost exclusively on endurance athletes and, really, the
only issue of importance was refilling muscle glycogen and re-hydrating the athlete. For this reason the
focus was on carbohydrates and fluids with little else considered. At some point, I recall it being the mid-
90’s some early work suggested that adding protein to post-workout carbohydrates was beneficial in terms
of glycogen re-synthesis and a new dietary trend started to form.
Now, it turns out to be a bit more complicated than that whether additional protein actually increases
glycogen synthesis depends on a host of factors, primarily how much carbohydrate is provided. Simply, if
sufficient carbohydrate is given following training, adding protein has no further benefit in terms of promoting
glycogen re-synthesis.
In situations where insufficient carbs are consumed (by choice or otherwise), extra protein helps. Which
isn’t to say that additional protein following training isn’t valuable for endurance athletes even if carbohydrate
are sufficient but that’s not really the topic of today’s article.
While individuals involved in the strength sports and bodybuilding were quick to jump onto the post-workout
carb/protein bandwagon, the research wasn’t really aimed at them. As well, there has always been a bit of
a disconnect in using work on endurance athletes (who may be doing hours of exhaustive work) and trying
to apply it to individuals in the weight room.
Differences in volume of training, fuel use and goals make using data on one group inappropriate for
application to the others. It’s still common to see well-meaning nutritionists use the same guidelines for both
strength/power athletes (including bodybuilders) and endurance athletes but that is simply silly.
In any case, work examining the impact of various combinations of post-workout nutrients in terms of
promoting strength or hypertrophy would come later and, at this point, a huge amount of work has been
done. I’m not going to get into every detail (the issue is discussed in absurd detail, 35 pages worth, in The
Protein Book) of post-workout nutrition and will focus the article simply on the issue of protein, carbohydrates
and the combination of the two in terms of how they impact on post-workout recovery and muscle growth.
To understand what I’m going to say and why I think some current recommendations (especially the one
saying that you only need protein post-workout) are not consistent with the research, I need to get into a few
details regarding how training impacts on muscle growth and how nutrients impact on this. Don’t worry about
the dense text, there’s a pretty graphic below to help explain it all. A pretty, pretty graphic.
.

How Does Muscle Grow?

Endlessly on the site, I’ve talked about how the primary stimulus for growth is progressive tension overload
(with fatigue being a secondary factor) but, believe it or not, that’s not what I’m going to talk about
here. Rather, I want to get a bit deeper into the processes of muscle growth. I’m not going to get full-blown
molecular on you, just a bit more detail than I usually go into.
Now, the ultimate goal of getting bigger muscles is, well, getting bigger muscles. But what does that actually
mean? Skeletal muscle is composed of a variety of different elements including protein (about 100-120
grams of actual protein per pound of muscle and yes I’m mixing grams and pounds), water (making up the

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majority), connective tissues, glycogen, minerals and a few other things. I’m going to focus on the actual
protein component of it since that’s the bit that actually generates force, etc.
Protein in your muscle is no different than the protein found in dietary protein, it’s a long-chain of amino acids
that have been attached to one another in the structure that makes up skeletal muscle (the various fibers
and such). But how does this process work?
Simply, there are two competing processes that go into what ultimately happens to muscle mass which are
protein synthesis and protein breakdown. Protein synthesis is simply the act of attaching amino acids into
one another and making them into muscle. This is an energetically costly process and occurs through the
actions of ribosomes (little cellular messengers that you learned about in 7th grade biology) acting under the
instructions of mRNA (something else you forgot about from high school). So training turns on genes which
get translated into mRNA which tell the ribosomes what to build and how to do it. That’s protein synthesis
and you can think of it as ‘good’ when it comes to muscle growth.
The competing process is protein breakdown which is the opposite. Various specialty enzymes work against
you, cleaving off amino acids from the already built skeletal muscle. This happens under the influence of
hormones and other factors. Most tend to think of protein breakdown as ‘bad’ in the sense of muscle growth
but it’s a touch more complicated than that. The ability to break down and rebuild tissues in the body (a
process which is ongoing constantly, even when you’re ‘at rest’), provides the human body with a lot of
adaptations flexibility. That is, it allows the body to adapt to changing demands and remodel itself based on
the signal it gets from whatever is going on in your life. In that sense, protein breakdown is not ‘bad’.
Now, what happens to your muscle mass ultimately depends on the balance between these two competing
processes. I’ve tried to illustrate this below with three possible scenarios.
1. Protein synthesis > Protein breakdown = Muscle mass increases
2. Protein synthesis = Protein breakdown = No change in muscle mass
3. Protein synthesis < Protein breakdown = Muscle mass decreases
Assuming your goal is bigger muscles, clearly 1 is the goal. But this also means that there are two primary
ways that we can potentially impact on muscle growth. We can either increase protein synthesis, decrease
protein breakdown or do both at the same time. And doing both at the same time would be expected to have
the biggest impact.
There’s one more factoid you need to know which is this: heavy resistance training increases the rates of
both protein synthesis AND breakdown. That is, training doesn’t just turn on one or another, it turns on
both. This is probably a mechanism to help with the previously mentioned remodeling process. But both
happen following training.
And with that background, now let’s look at how nutrients interact with all of this.
.

Protein, Carbohydrates or Both, Oh My!

While athletes are rarely that interested in technical details and only want the practical applications, to
understand everything I want to talk about I need to look at a bit more detail, specifically how protein and
carbohydrates interact with the processes of protein synthesis and breakdown discussed above. And it
basically works out like this:
1. Protein (amino acids) stimulate protein synthesis but have no impact on protein breakdown.
2. Insulin (secondary to carb consumption) inhibits protein breakdown with no impact on protein synthesis.
It’s actually a touch more complex than this. Protein can impact on protein breakdown under certain
conditions and insulin can impact directly on protein synthesis (and there happens to be a big difference in

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terms of what happens at rest vs. after training). But for the most part, following training, the above will hold
true.
Which leads us towards an ideal of post-workout nutrition. First and foremost I should point out that if you
train and don’t eat anything afterwards (and this assumes you haven’t eaten a few hours before), the body
will actually remain in a net catabolic state. That is, protein breakdown will be greater than protein
synthesis. That’s bad. But only really applies if you’re training first thing in the morning after a fast (how
many studies are done) and haven’t eaten anything.
But let’s assume that you eat something following training. Should it be protein, carbs, both, or some other
combination? First let’s look at the single feeding studies. That is, let’s say that you could only choose one
or the other following training, which should you choose. The answer there is clearly protein alone which
will be vastly superior to carbohydrate alone. Because while consuming carbohydrates will decrease protein
breakdown, only protein will increase protein synthesis (and provide the building blocks for building new
muscle).
And this is also where a rather silly idea has come from in the post-workout recommendations. Folks will
often state that “You only need protein post-workout because carbs don’t effect protein synthesis.” This is
true but ignores the impact of decreasing protein breakdown on net protein gain.
Certainly increasing protein synthesis appears to be relatively more important than decreasing protein
breakdown but the simple fact is that you get the biggest overall effect if you target both at the same
time. Which means a combination of protein and carbohydrates.
I should probably mention dietary fat and the simple fact is that fat intake post-workout is woefully
understudied. One study found no difference in anything with a meal containing fat vs one not-containing
fat (so you folks insanely obsessed with not slowing gastric emptying by consuming dietary fat can stop
worrying) but beyond that there’s little research. One study did find that full fat milk promoted protein
synthesis better than skim milk following training but nobody is sure why. It wasn’t because more calories
were consumed because the researchers also tested enough skim milk to match the calories of the whole
milk; whole milk was still superior.
In any case, that’s the overall conclusion that I draw from looking at the body of literature: while protein alone
is superior to carbohydrates alone, the combination of the two will have the greatest impact on promoting
muscle growth (as well as having other beneficial effects on muscle glycogen, etc). How much of each? Well
that depends on a host of other factors that will have to wait for a later article (or see The Protein Book).
I’ve shown this schematically in the graphic below, showing how both training and nutrients impact on the
processes discussed above.

Arrows are neat!


So that’s that: protein is better than carbohydrate following training but protein plus carbohydrates is optimal.
Good luck with your muscles.

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Muscle Gain Mistakes
Although it may seem strange to talk about how to gain weight as we approach the holidays (where people
typically gain weight without trying very hard), the simple fact is that, for athletes and bodybuilders, the winter
(when it’s cold outside and you’re covered up) has always been one of the primary times that trainees focus
on muscle gain.
You can worry about being lean and having a six pack when it’s warm and you don’t look stupid being mostly
nude. The winter is a good time to pack on some muscle mass and justify all that Halloween candy (“I’m
bulking, bro”).
But in the same way that many diets fail for a lot of reasons, there are equally common reasons that trainees
fail to make the muscular gains that they desire. I want to look at several of them, addressing potential
solutions along the way

Not eating enough

Outside of poor training (which can be either too much or too little), not eating enough is the number one
mistake I see most trainees making who can’t gain muscle. This is true even of individuals who swear up,
down and sideways that they eat a ton but no matter what they can’t gain weight. It’s been said that
‘hardgainers’ tend to be overtrainers and undereaters and there is much truth to that.
Almost invariably, when you track these big eaters, they really aren’t eating that much. Research has
routinely shown that overweight individuals tend to under-estimate food intake (e.g. they think they are eating
much less than they actually are) but in my experience ‘hardgainers’ are doing the opposite: vastly
overestimating how much they are actually eating in a given day, or over the span of a week.
Similarly, although such trainees may get in a lot of food acutely, invariably they often compensate for those
high-caloric intakes by lowering calories on the following day (or even in the same day). So while they might
remember that one big-assed lunch meal, they won’t remember how they ate almost nothing later in the day
because they got full.
Some people simply lack the appetite to eat sufficient amounts to gain muscle (or any weight at all). While
they may be able to force feed calories for a little bit, their appetite regulatory mechanisms kick in and they
unconsciously reduce calories. Their bodies also tend to upregulate metabolic rate better than others, so
they burn off more calories (a phenomenon called non-exercise activity thermogenesis or NEAT).
But the simple fact is this: if such ‘big-eaters’ were actually eating as much as they think they are, they would
be at least gaining some body fat, even if they were gaining zero muscle. If a trainee swears he’s eating a
ton, but he’s not even gaining body fat, I know he’s still not eating enough (or even as much as he thinks he
is).
Since I’m talking about body fat, I might as well address another very common cause of poor muscle gain
and that’s trainees who fear putting on even an ounce of body fat. They’ll deliberately keep their calories low
all the time and then wonder why they aren’t magically synthesizing muscle mass out of thin air. At this point,
I’m not even including the folks who want to lose fat and gain muscle at the same time.
The simple physiological fact is that, to gain muscle, you have to provide not only the proper training stimulus,
but also the building blocks for the new tissue. This means not only sufficient protein (see below) but also
sufficient calories and energy. While it’s wonderful to hope that the energy to build new muscle will be pulled
out of fat cells, the reality is that this rarely happens (there are some odd exceptions such as folks beginning
a program, and those returning from a layoff).

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And while there are extremes (such as my Ultimate Diet 2.0 or some of the intermittent fasting schemes)
that allow people to put on muscle while remaining lean, they always invariably alternate periods of low and
high calories. With the high calorie part of the diet (e.g. the weekend on the UD2) providing sufficient protein
and energy to drive muscle mass gains.
Now, although this is a slightly different topic, I entreat trainees not to take the ‘Eat enough to gain’ to the
opposite extreme. While GFH (look it up) can work for many people, eating so much food that a trainee gains
a disproportionate amount of fat is just as much of a mistake as not eating enough in the first place.
Unless you’re a sumo wrestler or football lineman, eventually the fat has to come off; the more you put on
while gaining muscle mass, the longer you have to diet. Which is not only a psychological chore but often
results in performance or muscle mass losses (especially if you diet badly).
What I’m getting at is some optimum level, an intake sufficient to provide sufficient calories and protein for
muscle growth without becoming a total fat-ass. Which isn’t very helpful without some starting points which
I’ll present now.
Muscle magazine claims notwithstanding, a natural trainee is usually doing damn well to gain 0.5 pounds of
muscle per week (and a female might gain half of that). Yes, you’ll occasionally see a faster rate of gain but
much more than that (especially for sustained periods) tends to be rare.
And while that may not sound like much, realize that a 0.5 lb per week muscle gain over the course of a year
comes out to 26 pounds of lean body mass. And most won’t get that past their first year of training.
However, to get that rate of muscle mass gain will usually require some amount of fat gain, depending on
how much over maintenance you’re eating, this might be an additional half pound of fat per week. So a
reasonable weekly or monthly weight gain rate might be 1 pound per week or 4 pounds per month of which
about half should be muscle and the other half fat.
Short dieting cycles can be inserted to take off the fat of course, a number of people on my forum have been
using the Rapid Fat Loss Handbook to strip off fat between short bulking cycles so that they can get back
to normal training.
I’d note that this shouldn’t take a huge number of calories over maintenance. Assuming a trainee is not
burning off excessive calories through either a ton of cardio (or NEAT), you’re not looking at much more than
500 calories over maintenance to support about the maximum rate of muscle gain for a natural lifter. I’d
suggest putting a majority of that on training days (and around training) with a lesser surplus on non-training
days. That should help keep fat gains down somewhat.
Of course, this will have to be adjusted based on real world changes in body composition. If you’re not
gaining any weight, you need to up calories. If you’re gaining a disproportionate amount of fat, you need to
cut things back.

Problems with Protein Intake

While less common than simply not eating enough, I have found many individuals to have problems with
inadequate protein intake when it comes to the desire to build muscle. Although they don’t usually want or
need to gain a lot of muscle, endurance athletes tend to be the worst in terms of not getting enough protein,
since they frequently overemphasize carbohydrates to such a ridiculous degree. But even among weight
trainers, occasionally you find someone who simply won’t eat sufficient protein to support gains in muscle
mass. Considering the rather high protein intake of even the average American, anywhere from 2-3 times
the RDA, this is a little odd.

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What usually happens is that these individuals have fallen into the trap of the endurance athlete and
overemphasized carbohydrates to the point of neglecting protein (and usually fat as well); this was a much
bigger problem in the 80’s and 90’s when sports nutritionists overemphasized carbs but isn’t heard of now
(now, the opposite extreme, carbs are the devil, is more often seen).
Sometimes, in their quest to eliminate dietary fat from their diet, trainees quit eating meat, this seems to
occur a lot among female trainees. Vegetarians can have greater problems but even eggs, fish and chicken
can fulfill protein requirements easily. And while there is the occasional claim of someone building a lot of
muscle with a true vegan diet, I’d say that most who claim veganism turned to that AFTER building up their
muscle mass with a more traditional diet.
Occasionally you find someone who just doesn’t like protein very much. Women, moreso than men, tend to
underconsume protein and overconsume carbohydrates. As low as the RDA for women is (44 grams/day),
I’ve still run into women who aren’t even getting that much protein a day in their diet. You get the idea.
The point being that some people just don’t get enough protein. As with sufficient calories, adequate protein
is critical for gains in muscle mass. The common number that is thrown out is 1 g/lb body mass and this is a
good starting place. As I detail in The Protein Book, raising protein to 1.5 g/lb (another common value) may
have small, cumulative benefits that current research can’t turn up. It usually can’t hurt unless it prevents
sufficient intake of the other nutrients.
I would note that, for natural lifters, I don’t see much point to intakes over 1.5 g/lb. An exception is hardcore
diets but I’m talking about muscle gain here. As caloric intake goes up, protein requirements go down and
suggestions to eat 2 g/lb for naturals seems more of a ploy to sell protein powder than anything physiological.
As a final comment on protein intake, it’s very common to find wannabe bodybuilders taking protein intake
to the other extreme, and making it the entirety of their daily diet. This ultimately sort of ties into the first
problem I talked about: inadequate calorie intake. For the kinds of caloric intakes that many people need to
gain muscle/weight at any decent rate, it’s nearly impossible to consume enough protein to do it. It’s also
inefficient as hell, both metabolically and financially but those are separate issues.
For example, a 170 lb male may have a maintenance caloric requirement of around 2500 calories/day. To
gain weight, he may need three thousand or more calories per day. Three thousand plus calories or more
from protein alone is nearly impossible to achieve.
This is on top of the fact that protein calories aren’t used as efficiently for energy as calories from
carbohydrates or fats (this can be great for weight control but is a real detriment for weight/muscle gain).
That’s on top of the fact that protein plus carbohydrates is far more anabolic than protein or carbohydrates
by themselves. Studies have shown that, once protein requirements are met, more muscle is gained by
adding dietary energy (from carbs or fat) than from just plugging in more protein.
Is sufficient protein crucial for muscle mass gains? Yes.
Is it all a lifter should be eating? Absolutely not.
I suppose, for completeness, I should discuss the issue of protein quality, an issue that trainees (and
especially bodybuilders) get themselves endlessly wound up about. In short (and, this is discussed in
massive detail in The Protein Book), at an intake of 1.5 g/lb. from varied high quality sources, it just doesn’t
matter. Quality matters hugely when you have someone eating a small amount of some single shitty protein.
This describes conditions in third world countries, this doesn’t describe conditions for an American athlete
eating plenty of protein from meat, fish, dairy, whey, casein, etc.
Which isn’t to say that different proteins don’t have varying pros and cons or aren’t more or less appropriate
around training or what have you. I’m simply saying that, given sufficient protein and energy from high quality
sources, protein quality isn’t nearly the issue that people (read: supplement companies) make it out to be. It
certainly won’t be a deal breaker for muscle gains.

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Training Issues: Cardio

Of course, diet isn’t the only place trainees run into problems, there are also issues related to training. To
get it out of the way, let me talk about cardio training and mass gains, an area where opinions vary widely.
Some say to do no cardio, some suggest it daily; the current fad of ‘intervals are the best for everything’ has
people doing intervals multiple times per week while trying to gain muscle. What’s going on?
Frankly, for all but the most extreme hardgainer types (the guys who burn off a ton of calories when they try
to gain weight), I think the inclusion of some cardio can be beneficial. It can help with appetite (by increasing
it), keep conditioning up a bit, tends to improve recovery and may help alleviate some fat gain. Perhaps most
importantly, it keeps the fat burning metabolic pathways running so that, when dieting is resumed, fat loss
seems to occur faster.
However, too much will certainly hurt things. Reams of data suggest interference effects of excessive cardio
on strength (and muscle mass gains); I won’t even bore you with the molecular mechanisms here (you can
read AMPk: Master Metabolic Regulator for the details). But it’s only when it’s done excessively or at too
high of an intensity (cough, cough, intervals) that it’s a problem.
I know that everything on the internet is true but this fad of keeping in lots of intervals when you’re trying to
get stronger and bigger is frankly pretty stupid so far as I’m concerned. 20-30 minutes of boring old standard
low to medium intensity cardio done 2-4 times per week is plenty and, surprise surprise, your legs might
actually grow because you aren’t overtraining them with two weight sessions and two interval sessions per
week.

Training issues: Weights

Of course, where the real problems usually start in terms of training is the weight room. To say that the
training being performed by most individuals in most weight rooms sucks is an understatement. The problem
is that much of the advice being followed is coming out of the professional bodybuilding ranks at least as it
is disseminated through the bodybuilding magazines.
Yes, the internet has helped out with this and there’s a lot more realistic information out there but a lot of
people are still trying to follow programs based on the training of elite drugged out bodybuilders. And,
contrary to popular belief, 99% of internet trainees are not elite, or advanced. A lot of them aren’t even
intermediates. But they are trying to follow programs aimed at those folks.
In my experience, the typical approach of blasting a muscle group once per week for an insane number of
sets and exercises simply doesn’t work for the majority. Yes, fine, there are some who do fine on it. They
usually have good genetics and hormones. But the number who failed completely with that type of training
is legion. You can’t use the minority who succeed on it and ignore the majority who didn’t.
There’s a lot of reasons that type of training isn’t ideal for most people, this isn’t the place to discuss it. Fine,
you get real sore, and you’re real tired coming out of the gym. But who cares if you aren’t making progress?
Being sore and exhausted wasn’t the goal of this the last time I looked.
I should note that many fall at the opposite extreme of training, hitting a bodypart for one set once per week
or what have you. They’ll go to complete muscular failure, hit the hard isometric hold and be blown out and
shaking when they leave the gym. Again, since being tired isn’t the main goal, who cares. This can be just
as big of a mistake for another set of reasons that I’m not going to discuss here.

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The bottom line is that, in my opinion, in my experience, and in the realm of a lot of good research, something
in between those two extremes appears to be best. A weekly training frequency of 3-4 times per week is
usually quite doable although, for many (older trainees especially), four days may be pushing it unless the
workouts are kept very short. And yes, some people get away training six days per week but they are usually
in and out of the gym very quickly.
This will allow each bodypart to be hit roughly twice per week or, at the least, once every 5 days (about the
lowest frequency I recommend for naturals). Upper/lower splits are popular but there are other ways to
approach it as well.
A moderate number of sets, perhaps 4-8 per bodypart (more for larger, less for smaller) is usually about
right as well. Research suggests that 40-60 contractions per bodypart per workout seems to give the optimal
response. 4 sets of 10 would be at the low end of that, 8 sets of 8 (perhaps 2 exercises for 4 sets of 8 reps
each) would be at the high end. A typical workout might last 60-90 minutes depending on how it’s split up.
One final comment on training before I wrap this up: an insidious (and stupid) idea that is out there (especially
in the realm of bodybuilding) is that trainees should focus on irrelevant things: the feel, the squeeze, the
pump. This is crap and guys who do this, unless they are on drugs, simply don’t grow. Muscle grows as a
function of progressive tension overload, if you’re not adding weight to the bar over time, you’re not growing.
This doesn’t mean that you have to add weight at every workout, but if you’re not gradually going heavier
over time, you won’t be growing either.

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Mind Over Milkshakes: Mindsets, Not Just Nutrients, Determine
Ghrelin Response – Research Review

Mind over milkshakes: Mindsets, not just nutrients, determine


ghrelin response. Crum AJ et. al. Health Psychol. 2011 May 16.
[Epub ahead of print]

Objective: To test whether physiological satiation as measured by the gut peptide ghrelin may vary
depending on the mindset in which one approaches consumption of food. Methods: On 2 separate
occasions, participants (n = 46) consumed a 380-calorie milkshake under the pretense that it was either a
620-calorie “indulgent” shake or a 140-calorie “sensible” shake. Ghrelin was measured via intravenous blood
samples at 3 time points: baseline (20 min), anticipatory (60 min), and postconsumption (90 min). During the
first interval (between 20 and 60 min) participants were asked to view and rate the (misleading) label of the
shake. During the second interval (between 60 and 90 min) participants were asked to drink and rate the
milkshake. Results: The mindset of indulgence produced a dramatically steeper decline in ghrelin after
consuming the shake, whereas the mindset of sensibility produced a relatively flat ghrelin response.
Participants’ satiety was consistent with what they believed they were consuming rather than the actual
nutritional value of what they consumed. Conclusions: The effect of food consumption on ghrelin may be
psychologically mediated, and mindset meaningfully affects physiological responses to food. (PsycINFO
Database Record (c) 2011 APA, all rights reserved).
.

Background

Ok, in addition to having possibly the coolest title of any paper I’ve reviewed on
the site, this is also one of the weirdest papers I’ve looked at. But I’ve seen it
getting a lot of press and, of course, have to put in my own two cents, if for no
other reason than I suspect many people will take the findings far out of
context. First, some necessary background; this will probably take more space
than discussing the actual paper itself.

In recent years, the number of factors in the body controlling hunger has
multiplied by leaps and bounds. Leptin was discovered in 1994 or so and since
then numerous other compounds have been identified that play some role in
hunger, appetite, body weight regulation or even body composition. One of those
is ghrelin, which I also talked about in more detail in the Bodyweight Regulation
Series.
In brief, ghrelin is a compound released from the gut in response to a whole host
of physiological factors. Among other things, ghrelin binds to a receptor in the
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brain and stimulates growth hormone release (useless trivia for the day: ghrelin
was a compound where the brain receptor was discovered before the hormone
itself was discovered; it was actually the presence of the receptor that drove
researchers to go look for what was supposed to bind to it).
More relevant to today’s article, increases in ghrelin stimulate hunger (and alter
fuel utilization and calorie partitioning, at least in animal models) and acute
injections of ghrelin reliably increase hunger. As well, ghrelin antagonists reliably
blunt hunger. Please note that ghrelin is one of those hormones where, in a
sense, high levels are ‘bad’ and low levels are ‘good’, at least from the standpoint
of things like hunger and appetite. As is to be expected, as leptin levels fall on a
diet, ghrelin typically goes up.
One of the oddities of ghrelin was that levels appeared to change in anticipation
of meal time. That is, through some mechanism (that so far as I could tell was
never determined), ghrelin levels would go up just prior to normal meal times. So
if you habitually ate lunch at 12pm, ghrelin would go up right before then, lowering
blood sugar and making you hungry. Scientists call this entrainment and ghrelin
levels would entrain to normal meal times through some mechanism or another.
Tangentially, this probably explains why changing meal frequency is at least
initially difficult: ghrelin levels are changing in accord with your normal meal times
and get out of synch with the new one. So if you’re trying to increase meal
frequency, you initially find that you’re simply not hungry when you’re supposed
to eat.
And if you’re trying to decrease meal frequency, for a few days at least, you’re
ravenous at the times you used to normally eat, at least initially. However, over
a few days time, ghrelin entrains to the new meal frequency and you stop being
hungry when you used to eat, only getting hungry when you’re habitually eating.
Most of the early studies on ghrelin looked at how food intake, calorie intake and
macronutrient intake and such were impacting on ghrelin levels. Carbs seemed
to have a greater impact than fat, protein was unclear (at least the last time I
looked at the research); mind you ghrelin is not the only hormone of relevance. I
look at a bunch of the others in Bodyweight Regulation Wrap-Up: Other Hormones.
The total caloric value of the meal seemed to play a determining role; more calories dropped ghrelin more
than fewer calories. I seem to recall one odd study where sham feeding (I think they gave them noncaloric
fiber or something) reduced ghrelin which is the first indication that something weird was going on: how could
thinking you were eating something lower ghrelin? Ok, that’s the first half of the background on this paper.

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The bottom line is that the above is all good and well and interesting and relevant. And would be the final
word in all of this if humans were nothing more than a gut and a nervous system. That is, if we just responded
in a lovely deterministic way to changes in hormones, this would all be a lot simpler. Sadly, that’s not the
case.
Big brained humans have this thing called self-awareness, sometimes we even use it for our own
benefits. We can think, reason, etc. and this impacts on many things including hunger, appetite, food
choices, etc. So while most animals will pretty much eat when hungry and not when full, it’s not nearly so
clear cut in the case of humans.
Humans will eat out of boredom, depression, because they are at a party. Most eat more on the weekends
and there is a reliable relationship between the number of people at a meal and how much people eat: more
people and folks eat more food. My point is that you can’t just look at the physiology of what’s going on and
ignore the psychology or other aspects.
A simple example is that of anorexia, or even dieting in a more general sense: in the case of full blown
anorexia there is a situation where despite presumably massive drive to eat, the individual consciously
chooses not to do so (I’d note here a brand new study, that I am still trying to get ahold of where researchers
are suggesting a metabolic ‘brokenness’ contributing to anorexia and driving the psychology; I suspect it’s a
complex loop where one is driving the other).
Even dieters, in the face of hunger, make conscious choices whether or not to ‘obey’ the signals being sent
by hormones. Basically, humans do not represent some deterministic system where you just look at the
hormones and go ‘This is what’s going to happen’. And if that didn’t complicate things enough, it’s clear that
people differ in their psychological approach to things like eating.
Researchers often talk about things like restrained and unrestrained eaters, rigid versus flexible dieters (a
topic I looked at in my own A Guide to Flexible Dieting), disinhibited eaters and others and there are clearly
different psychologies when it comes to how people approach eating, food restriction, overeating.
And it won’t be surprising to find that all of the above psychological (along with physiological) stuff differs to
at least some degree for lean versus obese individuals. We already know that there can be an insensitivity
to leptin in the brains of the obese (whether this is a cause or effect of obesity is still up to debate) and there
is evidence of differing sensitivity to other hormones such as ghrelin, GLP-1, PPY and the rest of the mix.
Basically, human hunger and appetite and real-world food intake is very complicated and something the
strangest things impact on food intake in a way that you might not necessarily predict ahead of time (i.e. who
would have thought that having more people present at a meal would lead to higher food intakes). One of
those is related to belief or how people can often rationalize certain food choices because of the situation or
what else they are eating.
Here’s a classic example that will finally segue into today’s paper: back during the low-fat craze someone
did a study more or less along the following lines. Folks were given a food (I think it was frozen yogurt) and
then ‘told’ that it was either low-fat or full/high-fat yogurt. Note that the yogurt was identical in both cases,
they were simply told that they were being given different types. Subjects who thought they were eating the
low-fat yogurt ate more. Presumably they rationalized that since it had less calories/fat, they could eat more
of it and this, among many other factors, has been held up as one reason that the whole low-fat movement
failed.
You might also look at this as the Oreo/skim milk or double cheeseburger/diet coke effect whereby people
rationalize eating something crappy because they are ‘balancing’ it out with something healthy or
whatever. This is often given as a reason that things like diet sodas fail to impact on bodyweight; some
people simply justify eating more of the other stuff because they aren’t getting calories from the diet
soda. Yes, there’s more to it than that but this introduction is already way too long.

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My point is this: human appetite and hunger is clearly an interaction between physiology and psychology,
not that you can ever really separate the two (as I discussed in Dieting Psychology vs. Physiology before I
lost the plot of what I was trying to talk about). Because physiology impacts on psychological function. And,
as today’s study shows, psychological function impacts on the physiology of eating behavior. Ok, on to the
paper.
.

The Paper

46 participants, between the ages of 18-35, within a normal to overweight BMI


were recruited to take part in two separate sessions for the study. Of those 46
people, 65% of the subjects were women, 56% were white, 12% African
American, 11% Asian American, 10% Hispanic/Latino and 11% other. Subjects
were told that the Yale nutritional center was working on two different milkshake
with differing nutrient contents that they would sample and that the goal of the
study was to evaluate whether or not the shakes tasted different and to examine
the body’s reaction to the different shakes.
Basically, they were lied to; the milkshakes were identical in composition, but
were presented with two different labels, which I’ve shown below.

So the indulgent shake was presented as a high fat, high calorie shake and the sensible shake was touted
as being low fat and low calorie. Again, the shakes were actually identical in terms of their nutrient and
caloric content, all that differed was the labelling. Each day lasted 2.5 hours divided into two time
intervals. In the first interval, after 20 minute rest period, blood was drawn at 60 and 90 minutes and the
subjects were asked to rate the label of the shake in terms of hunger ratings.
In the second interval, subjects drank the shake within 10 minutes and were asked again to rate hunger
along with taste (including smell and taste along with enjoyment and healthiness). If you’re wondering how
hunger is rated, it’s done subjectively through something called a Visual Analog Scale (VAS), a little graphic
doodad that ranks things from 0-100; it’s subjective as hell but used commonly.
Measurements of ghrelin were made from the blood draws and subjects also filled out a questionnaire to
determine their degree of dietary restraint and this was used to see if there was any effect of dietary restraint
on the other variables measured.
So what about the results. Not shockingly, subjects rated the sensible shake as 7 times healthier than the
indulgent shake and the degree of restraint had no impact on this. Basically, they firmly believed that the
sensible shake was healthier. No differences were seen in the ratings of tastiness between shake
conditions.
Ok, let’s look at ghrelin first since this seems to be where most of the Internet punditry is focusing. The
indulgent group showed a much higher rise in ghrelin prior to consumption of the shake followed by an
equally significant drop after consumption. In contrast, the sensible shake situation found a fairly flat ghrelin
change: there was a small increase with little change downwards. I’ve shown the actual changes in ghrelin
in the graph below and you can see the clear difference in ghrelin response pattern for the two conditions.
..

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Looking solely at this physiological response, the researchers state:
When drinking the shake in an indulgent mindset, participants’ levels of ghrelin reflected a moderate level of
physiological craving followed by a significant level of physiological satiety…when drinking the shake in a
sensible mindset, suggesting that, despite consuming the same nutrient contents, they were not
physiologically satisfied.
So good intersting stuff, mindset affects physiology and the folks who thought they were indulging had a
significantly different ghrelin response, suggesting of differences in both craving and satiety, than those who
thought they were eating the sensible shake. Clearly how you approach your diet meals or whatever can
impact your physiology and all you have to do is adjust your mindset to sail along in your diet. Right?
But, now, you’re wondering, what’s the catch in all of this because we all know I wouldn’t be discussing this
paper if there wasn’t something more going on? Be patient, I know this is long but bear with me.
.

My Comments

Today’s paper is certainly interesting, if nothing else it indicates that an


individual’s mindset going into eating something can affect at least one marker of
physiology, in this case ghrelin. Specifically, the ghrelin response to the shake
intake was based on the person’s expectancies of the shake rather than it’s actual
caloric content. And that’s what the researchers talked about in the abstract: how
mindset affected this one singular physiological response.
That’s most of what I’ve seen people focusing on in their commentary about this
study on the Internets (one title was “It’s All About the Hormones”). It’s also why
I spent so much time in the introduction trying to point out that humans aren’t just
physiological automatons responding to changing hormones in this
fashion. Because it’s not just about the hormones in humans. There’s way more
going on.
Before moving on the researchers point out something that most seem intent on
ignoring: this was a single meal study. As the researchers state:
Although the effects of such psychologically mediated differences in subsequent
consumption or long-term alterations in weight were not measured in this
particular study, future research on the impact of this phenomenon on metabolic
maintenance is warranted.
I don’t disagree and in the real-world the above matters since what is seen acutely often doesn’t translate at
all to the long-term; you often see compensation at the next meal or the next day or whatever and it all
balances out in the wash. Simply, few conclusions can be drawn from this one study in terms of food intake
across a day, a week, a month.

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Don’t misread me: I’m not saying it won’t or couldn’t have an impact. It might or it might not. But it might
also all balance out given that there are other systems regulating things as well. There is also the fact that,
as I discussed in Homeostatic and Non-Homeostatic Pathways Involved in the Control of Food Intake and
Energy Balance the physiological systems present in humans can clearly and easily be overwhelmed by
non-physiological factors (such as how many people you are eating with).

Looking at their results, the researchers get into a whole speculative discussion
about how some of the mindset of dieter’s about their food might be contributing
negatively to overall results. For example, based on data that increased ghrelin
tends to drive hunger and lower metabolic rate (at least in animal models), they
speculate that:
The relatively flat ghrelin profiles in response to consuming the shake in a
sensible mindset may be placing participants in a psychologically challenging
state marked by increased appetite and decreased metabolism.
Two problems with this. One they didn’t measure metabolic rate and speculating
from what is mostly animal data is a mistake. But that’s not the bigger issue here,
it’s time to focus on their claim of increased appetite (or perhaps less blunting of
hunger).
Did you notice something missing in my discussion of the study above? Like how
I mentioned that they measured hunger using a Visual Analog Scale early on but
then didn’t say anything more about it? It’s because I was saving it for now. In a
single throwaway sentence hidden at the end of the results section that nobody who has just read the
abstract will actually see, the researchers state what I think is the truly important finding that everyone seems
to be ignoring:
For the measure of hunger, these analyses produces no significant main or interaction effects as a function
of shake, time or restrained eating.
Translated into English that means this: despite the changes in ghrelin as a physiological marker of craving
and satiety there was no difference in hunger between the indulgent and sensible condition and dietary
restraint had no impact on this. So the differential ghrelin response, while interesting, didn’t amount to
anything in the real-world in terms of actual hunger ratings differences between the two mindsets. Please
read that sentence again until it sinks in.
Hell, the researchers didn’t even bother to provide the VAS hunger data for the different conditions anywhere
in the paper. They just went through this whole involved discussion on ghrelin and everything else and then,
as an afterthought mentioned “Oh yeah, there was no difference in actual hunger.” And they didn’t mention
it in the abstract.

So while the physiological response they measured is nifty as hell and certainly
worthy of more research, the simple fact is that it didn’t amount to any real world
difference in actual hunger. Which is important because people are already
taking this paper completely out of context, going from the hormonal response

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(which was different based on mindset) and extrapolating that to differences in
hunger (which was not different based on mindset).
A question might be why there was no difference in hunger and the best the
researchers could do was to say:
This study did not find any significant differences with respect to subjective
hunger regardless of mindset after participants consumed the milkshake. This
result may have been a function of the measuring timing (hunger levels were
assessed 10 min prior to ghrelin changes as opposed to simultaneously or
subsequently), or the manner in which hunger was measured (visual analog
scale).
Basically they are crapping on their own measurement methodology to try to
dismiss their non-result. Don’t get me wrong, maybe they would have seen a
difference in hunger had they measured things differently. At least they used the
word ‘may’ above.
I’d note that the VAS is used extensively to measure hunger and has been for
years now; so far as I know, it’s pretty accurate and able to discriminate different
levels of hunger. So saying ‘The measurement method we choose might have
sucked’ is kind of weak given that VAS is a commonly used measure. And, of
course there are other potential reasons that their nifty physiological response
didn’t generate a real world change in hunger.
Maybe those small changes in ghrelin were irrelevant to overall hunger drive (the
graph looks pretty impressive but the absolute difference in ghrelin wasn’t
huge). Maybe that kind of small change just isn’t enough to have an
impact. Maybe you need to factor in the myriad other hormones such as leptin,
GLP-1, PPY and the rest when you look at this; there are too many overlapping
systems here to just focus on a small difference in ghrelin response and then
extrapolate to the entire system. Or maybe it was something else going on. We
don’t really know until more research is done and speculating is kind of pointless
at the end of the day.
What we do know is this: psychological mindset impacted on the response of a
singular hormone that is important in terms of hunger drive and satiety. But
despite a measured physiological change in that hormone that differed between
groups, there was no difference in real world hunger based on psychological

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mindset. The hormonal response simply didn’t amount to anything in the real
world.
And that last paragraph above is really my main point, and yes I took a long time
to get to it. Everywhere I’m seeing folks prattle about ‘thinking themselves thin’
hoping that thinking that what they are eating is more indulgent than it is while
dieting will lower ghrelin and make them be less hungry. But that’s absolutely not
what the paper found as there was no difference in actual hunger ratings based
on mindset.
As well, I think you could just as easily parse this paper to suggest that the
indulgent group would be more likely to overconsume calories due to the early
increase in ghrelin. That is, if increasing ghrelin drives hunger, who’s to say that
folks won’t eat more of a food if they put themself in an indulgent mindset?
Especially if they aren’t in the artificial situation where regardless of hormonal response, they are being given
a fixed calorie shake to drink.
Mind you, the study didn’t find this either since, beating the dead horse, hunger ratings didn’t differ at any
time point for either group. But it would be just as accurate an interpretation of the physiological response
as assuming that the drop in ghrelin will decrease hunger (which it didn’t).

So here we have a fascinating paper, clearly things are more complex than we
even thought up until this point, and this study shows that psychological mindset
can impact on at least one measure of the physiology of hunger regulation (the
mechanism wasn’t even guessed at). Hopefully more work on this will determine
not only if there is an impact but what the mechanism of it all is.
But at the end of the day, it didn’t amount to any actual change in real world
hunger which is what matters. More research is needed but drawing unwarranted
conclusions from this paper is a mistake even if that’s what the Internet is doing
right now. So the physiological response while interesting as all hell simply had
no real-world impact on actual hunger. That’s the bottom line.

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What You Need To Know About Caffeine

Someone once said “there’s no sunshine without coffee.” I tend to agree. However,
there’s a great deal more to understand regarding the benefits of caffeine – the central
nervous system stimulant most people associate with coffee – and its effects on mental
acuity, performance, etc. In this article I’m going to cover what people really need to
know about this topic, and suggest a way to get the most bang for your money when it
comes to this highly popular beverage and supplement.

The Basics….

Caffeine – a compound in the methylxanthine family – has its effects through various
mechanisms on the central nervous system, and to be honest, I doubt those mechanisms
are of great interest to most readers, so I won’t bother with an extensive discussion on it
here. Suffice to say, caffeine positively impacts memory, performance, endurance,
coordination and increases arousal, vigilance, while reducing fatigue, to name a few
effects. Anyone who has used straight caffeine knows the stuff works, which is why the
military, for example, adds it to gum as well as other things like bars and such. We all
know the “energy drink/shot” category is all the rage these days even outside the gym
setting. Although caffeine is not for everyone to be sure, it’s amazingly non-toxic. OK,
so users of caffeine either know all this, or have at least experienced it, and don’t need
much convincing it’s effective stuff for its intended uses. Let’s move into the more
interesting info of this article, shall we?

Coffee Vs. Caffeine

Here’s where things get interesting, at least to science nerds like me. Most people think
of coffee and caffeine as essentially interchangeable terms with the same effects.
However, caffeine and coffee have very different effects and when we discuss the
various positive effects of caffeine on performance or mental acuity, we are in fact
talking about straight caffeine vs. coffee. That reality often comes as a surprise to many,
but it’s true. Caffeine and coffee have different effects and it’s straight caffeine that has
the pronounced effects on performance, mental acuity, and others briefly outlined
above.

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Studies have been carried out that used coffee matched for caffeine content vs. pure
caffeine, and find it’s the straight caffeine that has the major impact on what we all
generally associate with caffeine. Probably the most extensive study that compares
coffee to caffeine was entitled Metabolic and exercise endurance effects of coffee and
caffeine ingestion (1). This study found in a nutshell:

“…This study was designed to compare the metabolic and exercise endurance
responses to the ingestion of the same amounts of caffeine as a coffee beverage and as
pure caffeine with water. The caffeine was consumed in the same volume of coffee or
water in the same period of time. It resulted in very similar plasma concentrations of
plasma methylxanthines [meaning the caffeine appeared to be absorbed equally from
the different sources], but only when it was consumed independent of coffee was there
an enhancement of endurance. In addition, in this trial the initial impact on circulating
epinephrine [adrenaline] concentration was greatest. Thus it appears that some
component(s) in coffee interferes with the normal ergogenic response of caffeine.”

So for the non-science readers, what does the above mean? Essentially, coffee matched
for caffeine content to caffeine capsules failed to have the same effects on adrenaline
response (feeling “jacked up”) and endurance as straight caffeine. “Why is that, Will?!”
is the obvious thought you have! No, I’m not a mind reader, just the obvious question.
Coffee is a complex biological substance with literally hundreds of compounds that are
dissolved along with caffeine during the brewing process, all of which ends up in your
coffee mug. Some of these compounds have effects completely separate from caffeine,
and more important to this article, effects that appear to counteract the effects of
caffeine. Besides the more obvious stuff found in coffee (e.g., lipids, carbohydrates, and
proteins) you find compounds of potential metabolic importance, such as nicotinic acid,
opiate-receptor antagonists, and cholinomimetics (agents that exert an effect “opposite”
to adrenaline). Interestingly one group of researchers isolated a cholinomimetic
compound from both regular and decaffeinated coffees that, when injected into rats,
resulted in decreases in heart rate and blood pressure. Thus, a compound that has direct
counter regulatory effects to that of caffeine (and adrenaline).

Additional support for that is the fact these researchers also added pure caffeine to decaf
coffee matched for dose to straight caffeine, and the effects were still inferior to caffeine
alone on performance as well as other effects one usually associates to coffee vs.

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caffeine. According to the researchers from the above paper, “One possibility to account
for this difference is that one or more of the multitude of compounds in coffee
beverages antagonize the actions of caffeine, resulting in a reduced response.”
We know what the caffeine antagonist is in tea (from Camellia sinensis—the leaves that
make white, green, oolong, and black teas). It is called L-theanine and you can buy it as
a stand alone dietary supplement, and it’s also in some “relaxing” drinks and
supplements. L-theanine combined with caffeine reduces both the blood pressure
elevation and the alertness boosting effects of caffeine alone (2).

Caffeine Content of Coffee

As the previous section outlines, if you want to enjoy your cup of coffee because it
tastes good, and gives you a coffee buzz – that’s likely due to a variety of naturally
occurring compounds in the coffee in addition to the caffeine – go for it. I won’t be
giving up my mug of strong morning coffee either. However, if you are looking
specifically to get the known effects of caffeine on performance, increased alertness,
etc., use straight caffeine.
Even if you are attempting to drink coffee for its caffeine content, that’s a hit or miss
strategy. Researchers visited a variety of specialty coffee store for 6 consecutive days
and tested a wide range of coffees and found the caffeine content varied considerably
(3). According to these researchers:

“There was a wide range in caffeine content present in caffeinated coffees ranging from
58 to 259 mg/dose. The mean (SD) caffeine content of the brewed specialty coffees was
188 (36) mg for a 16-oz cup. Another notable find is the wide range of caffeine
concentrations (259-564 mg/dose) in the same coffee beverage obtained from the same
outlet on six consecutive days.”

So the same cup of coffee purchased from the same vendor (Starbucks) over six
consecutive days ranged from 259 to 564 mg of caffeine!!! That’s like power gulping
3.2 to just over 7 small cans of Red Bull®—over 15-30 minutes (see below). If you
want to try and experiment to confirm what the earlier mentioned study found regarding
the different effects coffee has from straight caffeine, try 600mg of pure caffeine some
time. Your head may explode, but you will never doubt again what an equal amount of
caffeine feels like that can be found in a really strong cup of coffee.

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So What About the Energy Drinks?

The “energy drink” category is all the rage these days, and cans of Red Bull and others
of the ilk fly off the shelves. This has proven to be a very profitable market segment for
sellers of these products. There’s nothing inherently problematic with them, but to get
your 80mg of caffeine (the dose listed for Red Bull for example) you have to ingest
additional stuff you may not want, be it sugar, various synthetic sweeteners, etc. and
you are paying an exorbitant amount per serving compared to what you get from
them. Bang for the buck, these products are generally a poor deal in my view.

The same researchers who measured the caffeine content in coffees did a separate study
and examined the caffeine content of a variety of sodas and energy drinks. Sodas such
as Coke Classic had similar caffeine content to those energy drinks at the lower end of
their caffeine content, such as KMX, which had 33.3mg of caffeine to Coke Classic’s
29.5mg but the caffeine content could vary. Interestingly, they found just 67mg of
caffeine in a small can of Red Bull, a drop from the 80mg that is claimed to be inside
(4) They summarize their findings:

“The caffeine content of 10 energy drinks, 19 carbonated sodas, and 7 other beverages
was determined. In addition, the variability of the caffeine content of Coca-Cola
fountain soda was evaluated…The caffeine concentration of the caffeinated energy
drinks ranged from none detected to 141.1 mg/serving. The caffeine content of the
carbonated sodas ranged from none detected to 48.2 mg/serving, and the content of the
other beverages ranged from < 2.7 to 105.7 mg/serving.”

Take home is, I don’t have any beef per se with the energy drink/shot category of
products, but I also don’t see them as a value for the money spent considering what you
get, and I don’t like the taste of most of them (which admittedly is a subjective
experience) and for me, they don’t make sense to spend money on.

Cost effective Caffeine

OK, so coffee is great stuff, but does not deliver the true caffeine experience, and
energy drinks are, in my view, an overly expensive and unneeded method of getting

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caffeine. What next? A product called Fein came on my radar a few months back while
at a show. I asked for some samples, tried it, and liked it It’s simplicity at its best: an
inexpensive, essentially tasteless, easy to use way of getting pure caffeine when I want
it—and it has zero calories and no artificial ingredients. It comes in a tiny packet of
powder which can be used when and where I need it. At less then .50 cents per serving
for a 75mg dose of caffeine that I can put into whatever I want, it’s a winner in my
view.

Personally, I like to make my own energy drink before I go to the gym by mixing a
packet of Fein and a packet of Crystal Light added to my water bottle, and I’m good to
go. One can simply add Fein to water and have caffeine water. Hell, add it to oatmeal or
a protein shake in the morning if you want.

As caffeine, usually via coffee and or energy drinks, is used by virtually all segments of
society, I would say there are few who would not find this product both cost effective
and effective for added energy, alertness, improved endurance, and other known
benefits of caffeine.

Effective doses of caffeine varies widely with people, so some experimentation is


needed. One study showed that a dose of pure caffeine as low as 12.5mg—in regular
caffeine users—improved mental function. Generally speaking, for those who have been
exposed to caffeine before – which is most human beings on the planet – 75 to 100mg is
a good starting dose in my experience. Those particularly sensitive to stimulants, might
try 25-50mg to start.

Obviously caffeine is a stimulant and, as with all stimulants, has its possible drawbacks,
like insomnia if you take it too late in the day. Although caffeine has been shown to be
exceedingly non-toxic, general warnings apply (like check with your doc before you
take it if you have high blood pressure, are taking psychiatric drugs, or are pregnant), so
make sure caffeine is right for you before proceeding.

Conclusion

That’s my report on my favorite type of product: effective, cheap, and well researched.
Caffeine – particularly in the form of Fein – fits that bill for me. If you all give it a try,

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let me know your feedback to see if it jibes with my own experiences. People interested
in Fein can get more info at their web site: www.GetFein.com

See you in the gym!

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The Effects of Arachidonic Acid (ARA) On Strength &
Muscle Mass

NOTE: The brand of ARA used in the study covered in this article – the brand
with longest track record and most extensive feedback by users – is X Factor by
Molecular Nutrition. For companies looking to carry ARA, the manufacturer of
ARA is Cargill and the contact (wholesale inquiries only)
is sales@arachidonic.com

I recently did a video on ARA which discusses this study that found ARA had positive
effects on strength and muscle mass, but was not able to give details because it had yet
to be published as an abstract or full paper. The study results are now public and I cover
them below. Two previous articles on ARA ( Part I), by Monica M cover why ARA is
a generally misunderstood fatty acid and not a a negative to health, (part II ) covered the
safety of ARA as a supplement. Finally, Part III, cuts through the hype and bro-science
to give details on ARA and it’s use as a supplement for increasing strength and muscle
mass! My understanding is a full paper is in process that will also examine the specific
mechanisms of ARA and its impact on strength, muscle mass, and performance.

This study looked at the effects of 1.5g per day of ARA for 8 weeks on muscle
hypertrophy, body composition, strength, and power, compared to a placebo matched
control. For those who don’t enjoy reading abstracts and studies, here’s the cliffs notes
followed by the full details:

• The group receiving 1.5g of ARA had in increase in lean body mass (LBM) of approx
3%, corresponding to 3.5 lb (1.6 kg) compared to no changes in the placebo group

• Muscle thickness increased in the group receiving ARA (+9.5%) vs. the placebo
group (+4.7%).

• There was an improvement in anaerobic power (via Wingate test which measures 30
second maximal output), which increased in the group getting ARA (+10.7%) vs. the
placebo group (+3.8%).

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• The group receiving ARA increased their bench press and leg press strength to a
greater degree than the placebo group.

Full Study Details:

Effects of Arachidonic Acid Supplementation on Skeletal Muscle Mass,


Strength, and Power

Jacob Ormes1, Matthew H. Sharp, Jordan M. et al.

Department of Health Sciences and Human Performance, The University of Tampa,


Department of Health and Exercise Science, Auburn University

Introduction

Arachidonic acid (ARA) is a long-chain omega-6 polyunsaturated fatty


acid that can be integrated into membrane phospholipids and it is the primary
substrate for COX-2-mediated biosynthesis of prostaglandins [1].
Previous research found that ARA could enhance power and tended to
increase strength and hypertrophy [2]. However, a lack of power likely
prevented these values from reaching significance. Therefore, the purpose
of this study was to investigate the effects of 8 weeks of arachidonic
acid supplementation in individuals participating in a periodized resistance
training program on skeletal muscle hypertrophy, body composition,
strength, and power relative to a placebo matched control.

Materials & Methods

Thirty recreationally-trained males aged 20.4 ± 2.1 years with a respective


average leg press and bench press of 231.5 ± 55.6 kg and 103.9 ± 26.8 kg
and a minimum of 1 year of resistance training experience were recruited
for the study. All subjects participated in an 8-week, 3-day per week,
resistance-training program that was split-focused on multi-joint movements
such as leg press, bench press, and bent-over rows. Ultrasonography
measured muscle thickness of the quadriceps, dual-energy X-ray
absorptiometry (DEXA) determined lean body mass, power, and strength

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of the bench press and leg press were determined at weeks 0, and 8 of
the study.

Results

There were time, and group-by-time interactions for LBM (p<0.05) in


which LBM increased from pre (Placebo 57.7± 4.8kg; ARA 57.6 ± 5.0kg,)
to post (Placebo 57.8 ± 5.6kg; ARA 59.3 ± 5.0 kg,) only in ARA group, but
not the placebo. Delta change of LBM was significantly greater in the ARA
group (1.62 ± 0.01kg) than the placebo (0.09 ± 0.7) (p<0.05). The Delta
change for muscle thickness was greater in the ARA group (.47 ± .08 cm)
than the placebo (.25 ± .04 cm) (p<0.05). There was a time, and group by
time interaction for wingate power, in which power increased to a greater
extent in ARA (723.01± 104.53 W to 800.66 ± 112.60 W) than the placebo
(738.75 ± 129.76 to 766.51 ± 136.52 W). Delta change for total strength
was greater in the ARA group (109.92 ± 33.25) than the placebo (75.78
± 12.41).

Conclusions

These results suggest that ARA supplementation can positively augment


adaptations in strength and skeletal muscle hypertrophy in resistance-
trained men. Athletes and everyday individuals looking to maximize
their body composition, strength, and power could use ARA as an ergogenic
aid.

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The Dieter’s Paradox – Research Review

Chernev A. The Dieter’s Paradox. Journal of Consumer


Psychology. (2001) 21: 178-183.

Abstract

Despite the vast public policy efforts to promote the consumption of healthy foods and the public’s growing
concern with weight management, the proportion of overweight individuals continues to increase. An
important factor contributing to this obesity trend is the misguided belief about the relationship between a
meal’s healthiness and its impact on weight gain, whereby people erroneously believe that eating healthy
foods in addition to unhealthy ones can decrease a meal’s calorie count. This research documents this
misperception, showing that it is stronger among individuals most concerned with managing their weight—
a striking result given that these individuals are more motivated to monitor their calorie intake. This finding
has important public policy implications, suggesting that in addition to encouraging the adoption of a healthier
lifestyle among overweight individuals, promoting the consumption of healthy foods might end up facilitating
calorie overconsumption, leading to weight gain rather than weight loss.
.

Background

In introducing today’s paper, I am reminded of an old joke/quip to the effect that “All that separates man from
the animals is our ability to rationalize.” I’d add “And accessorize” but that’s neither here nor there. But the
reality is that humans are able to do a wide variety of mental gymnastics in how they approach
life. Effectively, we appear to be slave to what psychologists call cognitive biases, ways in which we think
about the present, past, future or ourselves that often lead us to make some fascinatingly bad choices. This
is a topic that many recent books has discussed in a variety of contexts.
And while I don’t know if I can say that it occurs to a greater degree in terms of eating and health behaviors,
there is no doubt that people often engage in some exceedingly interesting mental gymnastics when it comes
to those topics. Some of this is conscious but much of it can be chalked up to either unconscious behaviors,
misunderstandings (or a lack of information/education) or mishearing/misinterpreting the message. And
these types of things, as much as anything else, often derail many people’s attempts to eat healthy, lose
weight or simply avoid weight gain.
In the realm of exercise for example, many people grossly overestimate the actual caloric expenditure from
activity, as I discussed in Normal Weight Men and Women Overestimate Energy Expenditure – Research
Review, and this leads them to either expect far more of an impact on weight loss than is realistic or to eat
more calories than they actually need based on the assumption that they burned it off during activity.
In the arena of eating, this issue can show up in a myriad ways. A classic example of a
misunderstanding/garbling of the message occurred back in the 80’s during the low-fat eating craze. While
it’s hard to say where the blame lies, the general public sort of got the message that so long as they kept fat
intake low, nothing else really mattered. Caloric intake and portions went out the window.
Food companies capitalized on this by rushing plenty of energy dense, high-calorie (but low-fat) foods to
market and it all went wrong. Studies routinely found that people ate more food when it was labelled ‘low-

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fat’ compared to one that was labelled as being higher in fat. Either consciously or unconsciously, they gave
themselves permission to eat more of it. And often ended up consuming more calories than they would have
otherwise.
Another example deals with artificial sweeteners where you often see a pattern where artificial sweetener
(or diet soda) intake is associated with weight gain (or a lack of weight loss). And while there is some
speculation that artificial sweeteners do some odd things in the brain in terms of driving appetite, it’s probably
more related to people rationalizing that they can eat more of something else because they are getting less
calories by choosing diet soda or using artificial sweeteners. That is, they figure that since they are ‘saving
so many calories’ by making one choice, they end up compensating (or more than compensating) by
choosing something unhealthy. Call this the skim milk and chocolate cake or Diet Coke and cheeseburger
approach to eating.
I’d note before continuing that this much of the above rationalizing tends to be more for people who are only
paying somewhat ‘superficial’ attention to ‘eating well’ (or some other fairly abstract goal). That is, the type
of thing I’m going to talk about doesn’t generally occur among folks who are diet obsessed and track macros
or calories or what have you. Rather it’s for folks who, while they may say that they are concerned with their
diet or body weight or body fat, are focusing on the wrong things (a topic I addressed in more detail in
Fundamental Principles vs. Minor Details).
Finally type of behavior seems to occur more prevalently in people who tend to divide foods into ‘good’ and
‘bad’ categories (a category that many popular diets and dietary approaches tend to promote). ‘Good’ foods
become equated with healthy and, altogether too often, can be eaten without consequence (i.e. weight
gain). Researchers call this the ‘health halo’ by which supposed ‘healthy foods’ have a halo of invincibility
around them In the same vein ‘bad’ foods are equated with being unhealthy and this categories are not only
absolute but cause us to do some of those strange mental gymnastics when it comes to how we approach
our food intake.
You can find examples of this all over the place where people assume that ‘healthy/good’ foods can be eaten
in uncontrolled amounts whereas the tiniest amount of ‘unhealthy/bad foods’ mean that the diet has failed,
the dieter is immoral and weak, and health will simply be destroyed (this is seen at the greatest extreme in
a psychological condition called orthorexia whereby people see food as a moral choice judging not only
themselves but others by the foods that they choose to eat). You can see some good examples of this in
the comments section of Straight Talk About High-Fructose Corn Syrup: What it is and What it Ain’t. –
Research Review.
Which basically segues into today’s paper which examines a behavior pattern that is often seen whereby
folks tend to get fixated (or perhaps ‘blinded’ is a better word) by the concept of ‘healthy’ foods and end up
missing the forest for the trees when it comes to their food and caloric intake. There is also evidence that
people who are (or at least state that they are) more ‘weight conscious’ are even more prone to make these
kinds of mis-estimations which was a secondary aim of the study.
.

The Paper

The study recruited 934 people, of whom the majority (74.2%) were female aged anywhere from under 20
to over 50. Subjects were then shown 4 meals which either consisted of ‘unhealthy’ foods or those same
unhealthy foods coupled with a healthy option. The four meals, with the healthy addition shown in
parentheses, were a hamburger (three celery sticks), bacon and cheese waffle sandwich (small organic
apple), chili with beef (small salad without dressing) and meatball pepperoni cheesesteak (celery/carrot side

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dish). So, for example, subjects were either shown a bacon and cheese waffle sandwich (which sounds
amazing in so many ways) either by itself or side by side with a small organic apple.
Half the subjects were shown the unhealthy choice alone and the other half were shown the combination of
the unhealthy choice with it’s healthy add-on and they were asked to estimate the caloric value of the
meals. I’d mention that this design is problematic because it’s not comparing how a given individual might
rank each of the two meals; rather it’s comparing the average estimate of the caloric value of the different
meals between people. All subjects were also asked to rate how concerned they were with managing their
weight on a scale of 1-5 (with 5 being extremely concerned).
The study generated a total of 2750 total observations of the different meals and, on average, subjects
estimated that the unhealthy meal alone contained 691 calories. Now, logically it’s obvious that a food
consisting of an unhealthy item PLUS a healthy item would have to have more calories than the unhealthy
item alone. Clearly two foods can’t have less calories than either food alone.
Yet, on average, subjects estimated the unhealthy plus healthy choice as having only 648 calories. I’d
mention that as a third part of the study, a separate group was asked if they believed that the healthy foods
contained negative calories and this was not the case. So it doesn’t appear to have been the case where
subjects figured that the healthy addition was literally ‘reducing’ the caloric value of the food by containing
negative calories. Rather, the ‘health halo’ effect caused people to systematically underestimate the caloric
value of the combination of an unhealthy and healthy food.
But it gets even odder. When the estimates were ranked by how folks reported their concern with managing
their weight, the values changed even more. The most ‘weight conscious’ subjects estimated the unhealthy
meal as containing 711 calories while the combination of the unhealthy and healthy choice was only 615
calories. In contrast, the non-weight conscious individuals estimates were only 684 for the unhealthy choice
versus 658 for the combination and there was a direct relationship between how weight conscious the
subjects were and their mis-estimate of the different meals.
.

My Comments

I really don’t have a ton to add to the above, the paper goes into lot of discussion that I’ll spare you here
since it’s a lot of detailed examination of the possible underlying mechanisms behind these types of odd
cognitive biases. One point that was made was that while one might expect more motivated/involved people
to have less problems with these types of conceptual biases, this research found the opposite. To whit:
The negative calorie bias is more pronounced for more involved/motivated individuals. Thus when evaluating
vice/virtue combinations, greater motivation does not necessarily result in greater accuracy but instead can
lead to more biased judgments.
I would add that I think really has more to do with what I mentioned in the background above, the issue isn’t
with dietary motivation per se but rather with how people often conceptualize the process. By focusing on
things like good/bad foods, clean vs. unclean eating, meal frequency exclusively or organic vs. non, people
lose sight of the issue of portions and calories which are what really matter when it comes down to it. They
rely on estimates which are oh so often off. And which appear to be colored heavily by the cognitive biases
that many humans are so prone towards.
Make no mistake, certain types of eating patterns often automatically get people to reduce their intake, often
by the outright removal of a so-called ‘bad’ food. What is defined as good or bad depends on the diet in
question and certainly these types of good/bad approaches to dieting can work in at least the short-term
(and sometimes longer than that). The problem is when people start focusing on the goodness/badness of

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the foods they are eating to the exclusion of everything else. That’s when it often goes wrong; this is not
helped by many dietary approaches telling folks that calories/portions don’t count and that focusing only on
the aforementioned ‘good/healthy’ foods is all that matters.
In this vein, the paper’s author notes that:
In particular, the negative calorie illusion has been shown to be less pronounced when individuals pay
attention to the quantity of the combined items, instead of focusing solely on the healthy/unhealthy aspects
of the items.
In a related vein, the author points out that:
Another public issue raised by this research concerns the viability of promoting the very notion of
stereotyping foods into vices and virtues. Despite it’s intuitive appeal as a decision heuristic to simplify
choice, vice/virtue categorizations focuses consumers’ attention only on one aspect of the meal [my note:
whether the food is a ‘vice’ or a ‘virtue’] and ignores other important aspects such as its overall quantity.
And I really think that that’s the big take home message of this rather odd paper: people often get so fixated
and focused on the wrong things that they end up hamstringing their own attempts to reach their
goals. Because while it’s all well and good to focus on healthy/unhealthy, good/bad, clean/unclean or
whatever, at the end of the day quantities always count. When people lose sight of that and focus on the
wrong aspects exclusively, they often end up hurting their own progress. This paper just points out one way
that this happens.
I’ll finish by pointing interested readers to a book by the paper’s author titled The Dieter’s Paradox: Why
Dieting Makes Us Fat that addresses not only this research but a great deal of other research looking at
similar issues. How humans tend to categorize foods into good and bad and how it can lead them to make
a lot of really weird assumptions about what they are actually eating. It was a pretty fascinating read and
shows how many different ways we can end up screwing our own progress by relying on our (often incorrect)
intuition, primarily by focusing on the wrong factors that are relevant to what we are eating.

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The Science Of Bomb Proof Coffee

In Part I of Bomb Proof Coffee, I cover what’s in it and why, as well as how to make
it, doses, sources, etc in video form HERE. If you’re new to Bomb Proof Coffee you’ll
want to watch those videos for all the info you need to get started. This article will add
some of the supporting science on the ingredients in Bomb Proof Coffee.

The obvious first ingredient to cover is the coffee. Coffee just continues to show itself
to a have a wide variety of health benefits for both the brain and body. Not surprisingly,
not all coffee is created and the levels of beneficial compounds depends on the type of
processing and other factors. As the coffee itself is not the main focus of Bomb Proof
Coffee per se, the Life Extension has a good article HERE covering the topic and offers
a coffee with especially high levels of beneficial compounds found in coffee that might
make a good choice for the coffee used in Bomb Proof Coffee.

Cocoa

Cocoa (the main ingredients in chocolate), is rich in various polyphenols (including


flavonoids/flavanols) and other bio active compounds such as amines,
alkaloids, tyramine, magnesium, procyanidins, phenylethylamine, and N-
acylethanolamines. Cocoa has been shown to reduce blood pressure, improve insulin
resistance and improved endothelial function. A meta analysis found that the highest
levels of chocolate consumption were associated with a 37% reduction in cardiovascular
disease, and a 29% reduction in stroke compared with the lowest level of intake, an
that’s despite the sugar and fat content of chocolate; reduced insulin resistance and
reduced serum insulin levels were associated with the chocolate consumption. There are
various studies that also suggest direct cognitive benefit of cocoa ingestion as well as
neruo protection. The flavanol epicatechin is believed to be the main source of benefit,
but there’s a wide range of compounds in cocoa and it’s highly likely there’s synergism
between epicatechin and other flavanols as well as other compounds found in cocoa,
many of which are still being elucidated. As mentioned via the vids on Bomb Proof
Coffee, not all cocoa is created equal and the highest levels of beneficial compounds is
found in cocoa that has not been “Dutch Processed” which is exposed to alkalization.
The vast majority of cocoa sold commercially has been Dutch Processed/exposed to

455
alkalization. The exact dose for optimal effects is unclear at this time and research is
ongoing, but the dose recommended in Bomb Proof Coffee – if you’re using high
quality cocoa that has not been exposed to alkalization – should have you covered well.
See videos for more information on that. Cocoa, similar to coffee, is a highly
complex ingredient, which may have synergism when ingested together.

L- Tyrosine

L-Tyrosine (Tyrosine) is an amino acid and essential precursor or “building block” for
the neurotransmitters responsible for maintaining metabolic rate and mental acuity
under stress. L-Tyrosine is the direct precursor to stimulatory neurotransmitters such as
epinephrine (i.e. adrenaline) and norepinephrine as well as certain thyroid hormones and
dopamine. Tyrosine is found in protein-rich foods and can also be synthesized in the
body from the amino acid phenylalanine. Under stressful conditions, however, food
sources and phenylalanine-to-tyrosine conversion may be inadequate to maintain the
essential neurotransmitters needed for optimal performance and mental focus. Several
studies done by the US Army found animals given supplemental L-Tyrosine were more
resistant to cold temperatures than those not getting the amino acid. Studies with
humans given supplemental L-Tyrosine have found improved cognitive function when
subjected to cold temperatures. One recent study found that 2000 mg (2 grams) L-
Tyrosine reduced the effects of stress and fatigue on cognitive tasks performance for 21
cadets subjected to a demanding military combat training course. Other studies have
confirmed that tyrosine is a stress-fighting nutrient. Elite soldiers often go for days
without sleep, which seriously compromises their mental acuity and performance.
Several studies have found L-Tyrosine may be able to counteract some of the negative
effects of prolonged sleeplessness on cognitive tasks and performance. As a further test
of Tyrosine’s efficacy, 36 Navy SEALs ingested L-Tyrosine during Winter Warfare
training. Either tyrosine or a placebo was consumed by the men, who were then exposed
to temperatures as low as -10° F. The study found L-Tyrosine prevented the decline in
mental acuity common to extreme cold conditions in the group of SEALS receiving the
supplement. Many athletes have found the use of L-Tyrosine to be helpful as a pre-
workout stimulant, as well as students, businessmen, etc., in need of improved mental
acuity. Prolonged stress and physical exertion can deplete the body of L-Tyrosine and
reduce the levels of neurotransmitters needed for peak performance under pressure.

456
Some studies also show L-Tyrosine may reduce levels of the catabolic (muscle-wasting)
hormone cortisol. Additional studies done by the Naval Aerospace Medical Research
Laboratory, Massachusetts Institute of Technology (MIT), the US Army, and other
locations suggest L-Tyrosine may be useful in counteracting stress-related performance
decrement and mood deterioration by increasing depleted levels of catecholamines
(especially norepinephrine) in the brain. Tyrosine is a key “anti stress” nutrient. Some
find L-Tyrosine a mood elevator. Dose and timing are essential to maximizing the
effects of L- Tyrosine.

Creatine

As mentioned in the vids, creatine has an extensive list of potential health benefits, and
my most recent article on that topic is covered HERE via the Life Extension
Foundation. Specific to cognitive and neuro protection, creatine has been found to
improve brain metabolism and energetics, reduces mental fatigue, improve memory and
cognition and following extended sleep deprivation, creatine
supplementation improved performance of complex “executive” tasks involving
decision-making skills. Creatine is also highly neuro protective and helps protect the
brain from a wide range of insults. That’s just the tip of the proverbial ice berg on the
benefits of creatine, which should be taken as the monohydrate form. For those who
want in-depth information on the various health benefits of creatine should read the
article linked above, and my free report they can grab HERE and or, check out the many
free articles and vids on the BrinkZone. As I state in the vids, anyone who is surprised
to see creatine in a mental focus, cognitive, health formula does not know creatine! The
addition of creatine to a neuro-cognitive, mental energy/focus and health formula is the
proverbial “no brainer.” No pun intended!

Coconut oil

People need to realize first off, coconut oil is a fad of late being pushed hard for a wide
variety of proposed health benefits, some poorly supported by the science, some vastly
over exaggerated, which I cover in a vid on coconut oil HERE if interested. That’s not
to say coconut oil is without potential value, but its main use in Bomb Proof Coffee is
not as “magic fat” but as a useful and pleasant tasting way to mix the cocoa and small
amount of skim milk into an emulsion, which improves taste and possible absorption of

457
the cocoa compounds. Yes, a small amount of medium chain triglycerides (MCTs) will
come from the addition of the coconut oil, and there’s some potential cognitive benefits
from MCTs, and I’ll tweak recs as future studies suggest. For now, consider the addition
coconut oil to Bomb Proof Coffee as functional and good tasting vs. as an active part of
the recipe as the other ingredients are listed above. However, if one wants to add more
coconut oil to this recipe than I call for (see vids ) there’s no harm done to the effects of
the other ingredients.

NOTE: Some studies suggest that milk can block the absorption of the important health
promoting flavonoids found in cocoa negating the benefits (Nature, 424:1013, August
28, 2003). It’s unlikely the very small amount of skim milk recommended for Bomb
Proof Coffee will negatively impact absorption. However, the skim milk is for taste and
assisting the foaming (emulsion) created while preparing Bomb Proof Coffee and is not
essential to the effects. One can leave it out if worried about the small amount of skim
milk negating the benefits of the cocoa, but I wouldn’t worry about it. Conversely, it’s
recommend you keep added dairy to a minimum so large amounts of typical additions
to coffee (e.g., half & half, cream, etc) are not recommended.

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The LTDFLE
Over the many years I’ve been involved in the fat loss game, I’ve seen some weird stuff happen. When I
was in my 20’s and only thought I knew what I was talking about (as opposed to now when I’m simply usually
sure I do), I had observed one of the things I’m going to talk about today but didn’t have any real clue why it
happened. With clients or whatever, the only answer I could give was “Because it does.” or “Magic!”.
Now, I have a bit more clue what’s going on, or at least what I think is going on so I’m going to share one of
these with you (I’ll address others in future articles). Today I want to talk about something that I like to call
the LTDFLE, an acronym that I genuinely hope you will use at every possible chance on forums to confuse
people, and which will make sense shortly.
.

The LTDFLE

Anyone who has had the headache-inducing misfortune of reading (or trying to read) Supertraining by Mel
Siff and Yuri Verkoshansky may have a clue where I’m going with this section heading. In that book, one
topic that is discussed rather endlessly is the long-term delayed training effect (LTDTE), a phenomenon
whereby strength/performance gains often show up considerably (e.g. 2-4 weeks) after the heavy training
has been done. This can actually be explained fairly simply through a two-model fitness/fatigue theory of
adaptation but I’m getting way off track.
LTDFLE stands for Long-Term Delayed Fat Loss Effect (I’d note that I have also seen a LTDGE which is a
Long-Term Delayed Growth Effect but that’s another topic for another article). Basically, this is the
phenomenon whereby fat loss continues to occur even after the diet has been ended and/or calories have
been raised back towards/to maintenance or even above. In the same way that fitness sometimes continues
to increase after the period of heavy loading, it’s almost as if there is some type of fat loss inertia whereby
the diet continues working even after the person ends it.
Now, I talked about a similar phenomenon in the article Of Whooshes and Squishy Fat, a situation where,
usually after the diet is broken (for a meal or a day), folks often wake up lighter and leaner. But that’s more
of an acute thing that I think can clearly be related to water retention/the release of such that happens when
people break their diets (deliberately or otherwise).
The LTDFLE is a bit different and can last from 4-7 days (on average). During that time, and note that this
only happens after fairly prolonged dieting, as calories are brought up, people continue to get visibly and
measurably leaner. Skinfolds continue to drop, other measurements will continue to change in the direction
of a decreased body fat.
I’ve observed the LTDFLE in myself, in trainees/clients and it’s something that a lot of bodybuilders
(depending on how nuts they go) experience in the first few days after a show. After all that work, after all
that effort, they end up looking their best 2-3 days after the post-contest binge has started.
In fact, there’s actually even a weird study from back in the late-90’s that saw this although the researchers
had no clue what was actually going on (because nutrition researchers don’t read enough basic
science/endocrinology). In it, folks were dieted hard for 4 weeks and then progressively refed (raising
calories over the 5th week towards maintenance). Body weight kept going down in Week 5 despite the
gradually increasing calories (as I recall, they didn’t measure body composition).
.

What’s Going On?

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Now, it seems fairly obvious that at least some of the LTDFLE is due to water retention and water balances,
just like the acute whooshes discussed in Of Whooshes and Squishy Fat. Although there is a great deal of
variance, people often retain water (both under the skin and possibly within fat cells) when they are dieting
hard and restricting calories and much of this is related to increases in the hormone cortisol (please note
that water retention is profoundly more complicated than this). Raising calories/carbohydrates and/or
reducing training tends to shut down cortisol release. Suddenly the body stops freaking out and water is
dropped. But I wouldn’t expect water loss to explain a full week of visual changes. A day, maybe two,
sure. But not the 4-7 days that the LTDFLE typically runs.
An additional factor that is certainly involved, and especially with folks on low-carbohydrate diets who are
doing a lot of training, is replenishing muscle glycogen. As carbs are raised, the body starts sucking up
carbs (this has an additional effect of pulling water into muscle which probably also accounts for water shifts),
they fill out and start to look better. This is assuredly a big part of why bodybuilders often look better 2 days
after their show; instead of looking stringy and flat on stage, they get full and pumped. If water is being
dropped from the body at the same time, all the better from a visible standpoint. Please note that muscle
glycogen is only increased if the caloric increase comes from carbohdyrates; pigging out on high-fat fare

won’t get it done. The Influence of the Subject’s Training State on the
Glycemic Index.
Mettler S et. al. The influence of the subjects’ training state on the glycemic index. Eur J. Clin Nutr
(2007 ) Jan;61(1):19-24.

Objective:To determine the glycemic index (GI) dependence on the training state of healthy adult
males.Subjects and design:Young, adult males of normal body mass index and normal glucose tolerance
were tested twice with a 50 g reference glucose solution and twice with a breakfast cereal containing 50 g
of available carbohydrates in a randomized order. Ten subjects were sedentary (SE), 12 were moderately
trained (MT) and 12 were endurance trained (ET). Blood glucose, insulin and glucagon were
measured.Results:The GI differed significantly between SE and ET subjects (P=0.02, mean difference: 23
GI units, 95% CI=3-42 GI units). The GI of the MT subjects was intermediary, but did not differ significantly
from the SE or ET subjects. The insulin index did not differ significantly between the groups
(P=0.65).Conclusion:The GI of the commercially available breakfast cereal depended on the training state
of the healthy males. The training state is the first reported factor influencing the GI that is subject specific
rather than food specific.European Journal of Clinical Nutrition advance online publication, 12 July 2006

My comments: For readers who aren’t familiar with the concept, the glycemic index (GI) is a measure of
how a given food affects blood glucose levels. It was introduced over 25 years ago as a more accurate
measure of foods (as opposed to earlier schemes that simply used simple versus complex carbs) for
diabetics and has been researched extensively since that time.
To determine GI, first a standard food is given. This used to be 50 or 100 grams of pure glucose but now
50 grams of white bread is used as the standard. Blood glucose is tracked over time and the area under the
curve for blood glucose is given a value of 100. Other foods are then tested (again, 50 grams of digestible
carbs are given) and the ratio of area under the curve to the test food gives the GI. So a food that has 75%
of the area under the curve is given a GI of 75, a food which has 20% of the area under the curve is given a
GI of 20. A food that gave 120% of the area under the curve has a GI of 120; you get the idea.

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While I’m at it, I want to mention a related/similar concept called the insulin index (II) which is functionally
identical to the GI but looking at insulin response. Although research into the II seems to have stopped
almost immediately after it started, it will come up in this week’s review.
Over the years, an absolutely tremendous number of foods have been tested and GI lists can be found in a
variety of places (one of THE most thorough sources for GI information is Rick Mendosa’s amazing GI
site). GI becomes interesting because the results aren’t always what you expect.
Some ‘simple’ carbs have a much lower GI than other ‘complex’ carbs. For example, sucrose (table sugar)
has a medium high GI (about 70) while some GI measurements for potatos are much higher. Full fat ice
cream has a low GI (due to the fat content) and fructose (fruit sugar) has an extremely low GI (about 20)
because of how it is metabolized by the liver.
However, the use of the GI is still debated in terms of its utility. Factors such as how the food is prepared,
the presence of other nutrients (fiber, fat, protein), and the effects of previous meals all impact on GI. For
non-diabetics, it’s especially questionable how relevant the GI actually is. Bodybuilders and athletes often
use GI as a proxy for insulin response under the assumption that low GI means low insulin which is good.
Up until this point, essentially all of the research into GI has suggested that the impact of a given food is
independent of the individual, having only to do with the food itself.
However, this week’s research review brings that into question. Following up on an earlier paper (by the
same group) which found a difference in GI between sedentary and endurance trained individuals, it sought
to measure the GI in three different groups of individuals: sedentary folks, moderately trained individuals
(defined as aerobic exercise 2-3X/week on average) and trained (aerobic exercise 4X/week on average with
some being competitive endurance athletes). Only males were studied so its unknown if these results apply
to females.
A standard GI test was done with 50 grams of glucose and then a meal of (seriously) Kellog’s Special K with
partial skim milk providing 50 grams of carbohydrate, 14 grams of protein, 4.6 grams of fat and 1.7 grams of
fiber was given and blood glucose and insulin response was measured. GI and II were calculated for all
groups.
And, as with the previous study, the endurance trained group showed a significantly lower glycemic response
for both the glucose and cereal meal as well as an average GI response that was 23 points (with a range of
3-42 units) less for the cereal meal (GI was about 80 for sedentary, 65 for moderately trained and 57 for
endurance trained). This was nearly identical to the previous study which found a 25 point difference. The
moderately trained group was square in the middle.
Although the absolute insulin response was different across groups (highest in sedentary, medium in
moderately trained, lowest in endurance trained), the insulin index was not different between the groups. Nor
was the absolute insulin response different between the glucose and cereal trial, the same amount of insulin
was released despite the difference in GI.
Unfortunately, the researchers couldn’t pin down a mechanism for this response although it’s clearly related
somehow to training status, probably insulin sensitivity (how well skeletal muscle responds to the hormone
insulin). Given the differences in absolute insulin response (although the insulin index was no different), this
would seem the logical conclusions.
So what does this paper tell us? First and foremost, in endurance trained individuals, choosing foods based
on glycemic index may be that much less relevant; regular endurance training will decrease the effective GI
significantly. Additionally, endurance training reduces the absolute amount of insulin released in response
to a given carb load. Given the effect of regular training on insulin sensitivity, this makes a certain level of
sense.

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An unanswered question by this paper is whether regular resistance training will have the same effect. While
weight training can certainly improve insulin sensitivity, there is also evidence that extremely heavy lifting
(which causes significant muscle damage) can negatively impact on insulin sensitivity. So the question is
still unanswered.
Perhaps more interestingly is how little endurance training is needed to have at least some impact on both
glycemic and insulin responses. Even two to three days/week had an impact although a greater frequency
had a larger impact. Strength/power athletes (including bodybuilders) might want to include a moderate
amount of aerobic work (2-3X/week at low intensity) solely for that purpose, to improve glycemic and insulin
responses to carb intake.

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Of course, the increase in glycogen/water mediated lean body mass will have a small effect on actual body
fat percentage but, as discussed in Reducing Bodyfat by Gaining Muscle – Q&A, the effect is not large. It
doesn’t hurt, of course, but it certainly doesn’t explain all of it.
But even with that, it does seem that actual fat is still being lost, skinfolds get measurably smaller and people
look leaner (and depending on what’s done next, often the skinfolds stay down suggesting that it’s more
than just a transient water shift magic trick). So beyond the above explanations, what’s really going on. I
suspect that at least some of it is related to leptin kinetics. If you’re not familiar with leptin and what it does,
I’d suggest you take the time to read the 6-part series on Bodyweight Regulation: Leptin. I’ll wait.
As I’ve discussed in my various books and in the article The Full Diet Break, leptin starts to increase fairly
quickly when calories and carbohydrates are raised, even 5 hours of over-eating carbs can raise leptin. With
even a few days of eating more calories/carbs, leptin will go up. And while many of the effects of leptin aren’t
immediate (which is part of why I recommend 10-14 days for a full diet break), some of them might be.
Leptin is part of what regulates cortisol levels for example (leptin inhibits cortisol release) so at the very least,
increasing leptin would help to reduce water retention. But some work has also shown a direct effect of leptin
on fat cells in terms of lipolysis; leptin also promotes fat oxidation in skeletal muscle and elsewhere, perhaps
the increase in leptin is directly stimulating actual fat loss. Of course, that explanation is predicated on leptin
going up/having a greater impact on things than the excess of calories coming in has on fat gain.
Related to that are thyroid hormone kinetics. On a diet, conversion of the relatively inactive T4 to the more
active T3 goes down in the liver and this rebounds fairly quickly when calories (and especially carbohydrates)
are raised. Tangentially, this is why I recommend a minimum of 100-150 grams of carbohydrates per day
during a The Full Diet Break; that’s what is required to normalize T3 production in the liver. As well, leptin is
involved in the control of thyroid stimulating hormone (TSH) so increasing leptin may also be driving thyroid
output.
Now, T3 has both short-term and long-term effects on metabolism with most of the long-term effects being
related to changes in gene expression; those take time to maximally occur (at least 14 days). But T3 can
also be degraded to T2 which has immediate metabolic effects on energy expenditure and it seems possible
that increases in T3 and subsequent breakdown to T2 might be raising metabolic rate enough to not only
offset the increased calories but also to generate extra fat loss. That might explain part of the LTDFLE as
well.
I mentioned gene expression above, this is just a nerd term referring to changes in which genes are turned
‘on’ or ‘off’ (simplistically speaking) in various cells. And gene expression changes in response to dieting,
caloric intake, activity, etc. While some changes happen pretty quickly others take longer; it’s not an
instantaneous process. Many have observed that often a diet takes a solid week or so to start ‘working’ and
this may be related to slower changes in gene expression when someone moves from an above
maintenance caloric intake to a below maintenance caloric intake.
And the same may be working in reverse, the body is still effectively in a ‘fat burning mode’ for some period
of time after calories are raised. Along with any direct effects of leptin and/or thyroid on lipolysis/fat
oxidation/metabolic rate and the shifts in water balance, the situation is still simply this: people often keep
getting leaner in the first week off their diet (again, this assumes that they don’t go totally nuts with food
intake).
I’d note in this regards that my own Ultimate Diet 2.0 actually takes advantage of this to get a short-term
sidestep of the energy balance equation: for about 24 hours following the 4 hard days of dieting/glycogen
depletion, even in the face of massive carbohydrate intake, the body preferentially stores the incoming carbs
as glycogen while using fatty acids for fuel (part of why fat intake has to be kept low during the carb-

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load). Folks may be at literally double maintenance caloric intake and still be losing fat. Magic? No, just
good science. Ok, maybe a little magic.
.

Summing Up

And that’s the oddity that is the LTDFLE: that magic period where, despite raising calories, you keep leaning
out and losing fat. It’s only about 7 days at the longest and can be shorter if people go really nuts with their
food intake. This is especially true if a lot of high-fat foods are consumed for extended periods. Empirically,
making the LTDFLE work the best seems to involve raising carbohydrate intake moreso than dietary fat. In
that vein, in the short-term 2-3 days), leptin levels are only responsive to increasing dietary carbohydrate
intake, not fat.
So that’s the LTDFLE, an oddity of fat loss that tends to occur after fairly prolonged dieting when calories
are raised. It’s not universal and doesn’t always happen but when it does, enjoy it. Before I finish, let me
make one thing very clear which is that the LTDFLE only occurs after fairly prolonged actual dieting (which
can still contain free meals and refeeds as discussed in A Guide to Flexible Dieting). Don’t think that you’re
going to get the magic effect of the LTDFLE by half-assing it for a couple of weeks and then raising calories
and voila.
In a future article, I’ll look at another specific oddity of fat loss, the situation where combining a large caloric
deficit with too much activity can actually hurt rather than help weight/fat loss. But that’s for another day.

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What’s Causing My Muscles to Cramp – Q&A
Question: I have been following a very low-carbohydrate diet and taking the ephedrine/caffeine stack for
the past 4 months. Recently I have been having problems with cramping in the gym, I find that if I get too
close to failure on a set, I get very bad cramps. I’m drinking plenty of water and taking a multivitamin and I
can’t figure out what’s wrong. Please help.

Answer: Cramping is unfortunately a very complicated topic and while many simple solutions are often
thrown out, they don’t always seem to work. Usually the culprit is issues with hydration per se or electrolyte
levels; electrolytes are things like potassium, calcium, sodium and magnesium they are involved in
transmission of the electrical signals in the body. Hence their name.
I’d note that hydration and electrolyte levels are intertwined as the amount of water in the body affects the
relative concentrations of the electrolytes in the body. So if there is more water present, the relative
concentration of each of the electrolytes will be lower because the water will dilute them. By the same token,
if you are dehydrated, the relative concentrations of the electrolytes goes up.
Most ideas about cramping tend to focus on a single electrolyte, potassium was blamed for quite some time
which is the basic origin of the ‘eat a banana to stop cramping’ idea. Bananas are an excellent source of
dietary potassium.
The problem is that cramping is way more complicated than this and can be related to all of the different
electrolytes, not simply the absolute amounts of each but the interactions between them. Fixing the problem
often entails trying different things to figure out what’s causing the problems for a given individual.
Now, a potential issue specific to very low-carbohydrate diets (less than 100 grams of carbohydrate per day)
and cramping per se is that these diets cause water loss. As well, the water losses can vary massively from
a low of perhaps 1-2 pounds up to 10-15 pounds in larger individuals. As well, very low-carb diets cause
electrolyte losses and this can cause cramping and fatigue.
As I detailed in my first book The Ketogenic Diet, very low-carb dieters need to supplement their daily
electrolyte intake with the following at a bare minimum:
 3-5 grams extra sodium hydrochloride
 1 gram potassium
 300 mg magnesium
Not only should this help with cramping issues, this has also been shown to fix some of the fatigue issues
that often beset people when they start ketogenic diets. Of course, an adequate calcium intake is important
under all conditions for bone health. How much you need depends solely on how much dairy foods you’re
eating so whether or not you need to supplement extra will depend on that variable.
While you generally have to supplement magnesium separately, you can cover at least some of the
potassium and sodium requirements with something like LiteSalt. This is a table salt that contains 1/2 sodium
chloride (standard table salt) and 1/2 potassium chloride. It tastes just like normal salt but gives a better
balance of sodium and potassium. I’d note that pure potassium salt tends to be a bit bitter which is why I
don’t recommend it; most won’t use it regularly.
So the above would be a good first step. I’d note that empirically high doses of the amino acid l-taurine
seems to help with cramps in some people. If your hydration is good and you’re getting the above
electrolytes but are still having problems with cramping, you should consider adding l-taurine to the mix.
I should also mention that stimulants in general and the Ephedrine/caffeine stack (as well as the drug
clenbuterol) can cause cramps. This is even more true on low-carbohydrate diets. The reason is that they
both cause calcium to flow into the muscles, essentially putting them in a low-level state of contraction. When

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you put heavy training on top of this, cramping often occurs. This is likely just an interaction between the
low-carbohydrate diet causing dehydration and electrolyte loss, the EC/Clen causing calcium to go into the
muscle and then throwing training on top of it. It’s not very much fun.
I’d note that even for individuals who aren’t on very low-carbohydrate diets, cramping can still occur
especially if they do a lot of training in the heat; as well some of the extremist attitudes towards diet such as
‘Never eat sodium’ among bodybuilders and other trainees can cause problems. Again, this can be related
to both hydration and electrolyte imbalance. Unfortunately, it’s nearly impossible to give more than vague
guidelines on this.
Recent research has found that water and salt loss during training can vary about 10-fold between people.
This makes giving a specific single guideline (e.g. drink 1 gallon water) impossible even if people try to do it
to keep things simple.
At least in terms of training, the old guideline was that you should weigh yourself before and after workout
and for every 1 kg (2.2 lbs) of weight lost, you needed 1 liter (32 oz, 4 cups) of fluid to replace it. This turns
out to be wrong, you actually need 1.5 liters (48 oz, 6 cups) of fluid to replace every 1kg of weight lost.
Please note that you don’t have to pound this right after training, but you need to consume that much extra
over the course of the day to cover losses. Athletes who do a lot of training in the heat who don’t replace
fluid losses can get into trouble pretty quickly.
As well, note that plain water is actually the worst rehydration drink out there. As I discussed in Milk as an
Effective Post-Exercise Reydration Drink, fluids containing sodium and potassium are retained far better
than those that don’t. Milk also provides good carbohydrates and high-quality protein so it does double duty
after training if you can stomach it.
I’d note that, again, weight loss during a given bout of training can vary many fold. One athlete might lose
1-2 kg (2-4.5 lbs) and another might lose 8kg (17 lbs). Like I said, it’s impossible to give a specific value of
how much fluid to consume because of this. Weighing before and after for a few workouts will tell you what
your personal hydration requirements are.
I’d also mention that sodium losses during activity are just as variable and calculations show that one athlete
might only lose a gram or two of sodium during training while another can lose upwards of 20 grams. I am
currently unaware of any non-laboratory way to determine sodium losses during training.
But I also don’t believe in heavily restricting sodium for athletes; training in the heat requires that electrolytes
be replaced and liberal use of something like the LiteSalt I mentioned above is a good idea for a number of
reasons.
So anyhow, that’s sort of a basic look at cramping. It’s a place where I wish I could give more firm guidelines
but they simply don’t exist. There is just too much variability and what works for one may not work for
another. In general, it tends to be related to hydration and electrolyte intake and this tends to be more of an
issue on very low-carbohydrate diets. But it can become an issue on carb-based diets as well.
So make sure you’re getting sufficient fluids, don’t skimp on salt (and get a sodium/potassium salt) and
consider supplementation if you’re still having issues. Some people seem more prone to have issues with
stimulants as well so if they are causing cramping, you may need to drop them completely.

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Of Whooshes and Squishy Fat
A few weeks back I answered a question about Not Losing Fat at a 20% Deficit, What Should I Do? and
among other things, one comment I made had to do with a water retention that often occurs during fat loss
which can mask fat loss and make it appear as if the diet is not working. I also mentioned specifically that I
had written (with a straight-face no less) about whooshes in The Stubborn Fat Solution, along with a related
phenomenon which I call squishy fat.
In any case, to expand on that issue, I’m going to excerpt the chapter section from The Stubborn Fat Solution
dealing with both phenomena. With that introduction, I give you (again, with a straight face)…

Of Whooshes and Squishy Fat

Before you freak out and think you’ve entered some weird Internet forum where people talk about stalls and
whooshes, please bear with me; there’s actually some physiological rationale to what I’m going to discuss.
Many people have noted that fat loss is often discontinuous, that is it often happens in stops and starts. So
you’ll be dieting and dieting and doing everything correctly with nothing to show for it. Then, boom, almost
overnight, you drop 4 pounds and look leaner.
What’s going on? Back during my college days, one of my professors threw out the idea that after fat cells
had been emptied of stored triglyceride, they would temporarily refill with water (glycerol attracts water, which
might be part of the mechanism). So there would be no immediate change in size, body weight or
appearance. Then, after some time frame, the water would get dropped, the fat cells would shrink. A weird
way of looking at it might be that the fat loss suddenly becomes ‘apparent’. That is, the fat was emptied and
burned off days or weeks ago but until the water is dropped, nothing appears to have happened.
For nearly 20 years I looked for research to support this, I was never sure if it was based on something from
the 50’s or he just pulled it out of thin air as an explanation. Recently, one paper did suggest that visceral
fat can fill up with water after massive weight loss but that’s about it.
Somewhat circumstantially, people using Bioimpedance body fat scales (which use hydration to estimate
body fat levels) have noted that body fat appears to go up right before a big drop. This implicates water
balance as the issue here.
As well, women, who have more problems with water retention, seem to have bigger issues with stalls and
whooshes than men. Further, some individuals who have done dry carb-loads (high carbohydrate refeeds
without drinking a lot of water) have seen them occur; presumably the body pulls water into the muscles and
out of other tissues (fat cells). In lean individuals, appearance is often drastically improved with this
approach, it doesn’t do much for those carrying a lot of fat.
I’d note that dry carb-loads suck because you’re so damn thirsty. Interestingly, even normal refeeds often
work in this regards, perhaps the hormonal effect ‘tells’ the body to chill out and release some water. So not
only do refeeds seem to improve stubborn fat mobilization the next day (as discussed above), they may help
the body drop some water so that you can see what is happening.
Finally, many have reported whooshes following an evening which included alcohol. A mild diuretic, this
would also tend to implicate water balance issues in the whoosh phenomenon.
I’d also note that this isn’t universal, lean dieters often see visual improvements on a day to day basis; a lot
seems to depend on whether or not they tend to retain water in general. Folks who do have problems with
water retention tend to have stalls and whooshes, those who don’t show nice consistent visual changes.

467
On a related topic, I wanted to discuss something else that often happens when people are getting very lean
and dealing with stubborn body fat: the fat gets squishy, feeling almost like there are small marbles under
the skin. Yes, very scientific, I know. That’s the best I can do.
As folks get very lean, down to the last pounds of fat, the skin and fat cells that are left will often change
appearance and texture. It will look dimply (as the fat cells which are supporting the skin shrink and the skin
isn’t supported) and feel squishy to the touch. This is bad in that it looks really weird, but it’s good because
it means that the fat is going away. I have nothing truly profound to say about this topic, just realizes that it
happens and usually indicates good things are happening.

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Flexible vs. Rigid Dieting
With the holidays looming, and all of the food and candy that that entails, I wanted to write a quick article
post about a topic that I consider very important. In fact, it’s so important to the goal of long-term body
composition changes that I wrote an entire book (A Guide to Flexible Dieting) about it.
Over the years, I’ve seen a particular pattern that is pretty endemic among the body obsessed: that is what
dietary behavior researchers would call rigid dieting patterns (restrained dieting might be a little more
accurate here but I don’t want to get into the distinction that deeply).
Rigid dieters are the folks who are, to some degree or another, always controlling their overall food intake.
They never relax, they never allow themselves to ‘cheat’ (a term I dislike for various reasons). And, sort of
like the type of athlete I talked about in Goal vs. Process Oriented Athletes: Part 1 before, they often see
better short-term results.
The problem is that, if something happens and they go off their diet for whatever reason, they end up going
completely off their diet. Contest bodybuilders have some of the worst problems with this, 12-16 weeks of
total deprivation leads into a 4-6 week food orgy where weight and fat are both regained rapidly, no training
is done, etc. The cycle repeats annually.
In research, extremely rigid dieters are often heavier (mainly because of the cheats and binges they undergo
when they break their diets) and often have poorer long-term success than what are called flexible dieters.
Flexible dieters allow for, well, flexibility in their lives. They realize that a little bit of something that isn’t ‘on
their diet’ is no big deal in the big scheme of things, they often weigh less, etc. In my experience, while the
short-term results may not be as great, the long-term results are usually better.
This type of self-destructive rigid dieting behavior manifests in other ways as well. How many times have
you (or someone you know) started a diet and things were going just fine. But then you had a little bit of
something not on your diet, a cookie or whatever. The guilt sets in, clearly you blew your diet, might as well
eat the whole bag, right?
But step back and think about it rationally.
Say you’ve been dieting well for 6 straight days and then, one day, you have a cookie or two. What is that,
100 calories, maybe 150. Can that 150 calories truly derail the previous 6 days? Hell, think about it more, if
you were to adjust your daily caloric intake so that you took out 150 calories elsewhere to account for the
cookies, have you done any harm at all? Of course not.
But if you decide that your diet is clearly blown and you then eat the entire bag, to the tune of 1000 calories.
Well now you HAVE done yourself a ton of damage. But not through the eating of the first two cookies.
Rather, through the psychological damage that can occur when you think in absolute terms. Either you are
on your diet perfectly (100% adherence), or you’re not.
I’d note that some gurus actually seem to approach dieting, especially physique contest dieting, by promoting
rigid behaviors. A very short list of acceptable foods is given and anything eaten that isn’t on the list means
failure. At least that’s how it’s programmed into the dieter.
Of course, many diets (mine included) also allow a ‘cheat’ day or mea. of some sort or another. Now, used
properly, these can be extremely useful. I’ve prepped bodybuilders to contest shape with diets that included
1-3 days of controlled overfeeding per week.
I’d note that I don’t like looking at them as ‘cheat’ days as, invariably, this psychologically programs the dieter
to go out of their way to eat the worst crap they can lay their hands on. The stories I’ve seen, dieters
deliberately force feeding themselves junk to the point of sickness during their ‘cheat’ days.

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In contrast, I prefer to refer to ‘free’ meals (normal meals that are a little less rigid than whatever diet you’re
on) or ‘refeeds’ (high carb/high calorie days). I also program in full diet breaks, periods of 10-14 days when
you go off your diet and eat at maintenance. This is all described in The Guide to Flexible Dieting.
But the way that many use them becomes an abuse. The goal of a free meal is a psychological break from
your diet, refeeds exist to exert a specific physiological response (raising leptin and others), so do full diet
breaks. The goal is to make your diet work better, not eliminate all of the progress of the previous week by
eating three cheesecakes until you want to vomit.
So let my tie this in with holiday eating. At some point over the next six to eight weeks, you know you’ll find
yourself at a holiday party with tons of junk food, sweets and such. If you consider yourself ‘hardcore’, you
might even be obnoxious enough to take your Tupperware container of chicken breast, rice and broccoli
with you. And you’ll feel miserable watching everybody else eat the stuff you know you really want during it.
God forbid you have a piece of candy, odds are that will lead into an orgy of food consumption.
So instead, how about going to that same party with a different mentality. Plan to allow yourself a bit of ‘junk’
and realize that, in the big scheme of things, it doesn’t make an ounce of difference. You’re not going to put
on three pounds of fat because you had a couple of piece of chocolate, your muscles aren’t going to fall off
because you only got 25 grams of protein from ham instead of your ideal mix of whey, casein and gemma
protein.
However, you might find that you enjoyed the holidays a whole lot more without feeling deprived OR falling
into the trap of eating like a maniac out of guilt.

Testosterone and Fat Loss – The Evidence

It is well documented that obesity may cause hypogonadism, and that hypogonadism
may cause obesity [1-4] This has generated debate about what condition comes first;
obesity or hypogonadism? And what should be the first point of intervention?

In this article I will summarize data from several reviews on the associations of
hypogonadism and obesity [1-4], and make the case that these conditions create a self-
perpetuating vicious circle. Once a vicious circle has been established, it doesn’t matter
where one intervenes; one can either treat the obese condition or treat hypogonadism
first. The critical issue is to break the vicious circle as soon as possible before
irreversible health damage arises.

Nevertheless, as I will explain here, treating hypogonadism first with testosterone


replacement therapy may prove to be a more effective strategy because it to a large
extent “automatically” takes care of the excess body fat and metabolic derangements. In
addition, treating hypogonadism first also confers psychological benefits that will help
obese men become and stay more physically active.

Key Points [1-4]


470
• Traditional obesity treatments with diet and exercise programs are notorious for failing
in long-term maintenance of weight loss due to lack of adherence. Anti-obesity drugs
have limited efficacy and may not be without adverse effects.

• In the prospective Massachusetts Male Aging Study (MMAS), non-obese men who
became obese had a decline of testosterone levels comparable to that of 10 years of
aging.

• Testosterone deficiency and obesity each contribute independently to a self-


perpetuating vicious cycle.

• Long-term testosterone therapy in men with hypogonadism improves body


composition, metabolic syndrome components and quality of life, and thereby can help
break the vicious cycle.

• Treatment of hypogonadism with long-term testosterone therapy, with or without


lifestyle modifications, effectively treats obesity by correcting testosterone deficiency;
one physiological root cause of obesity.

• In contrast to the U-shaped curve for weight loss seen with traditional obesity
treatments, which are characterized by weight loss and weight regain, treatment with
testosterone therapy results in a continuous reduction in obesity parameters (waist
circumference, weight and BMI) for >5 years, or until metabolic abnormalities return to
healthy ranges.

• The significant effectiveness of testosterone therapy in combating obesity in


hypogonadal men remains largely unknown to doctors. Educational efforts are therefore
critical to bring research findings into clinical practice in order to improve patient care
and health outcomes.

WHAT IS KNOWN

Obesity, classified by the American Medical Association in 2013 as a disease, is an


epidemic that is rapidly spreading globally. Obesity is the most common preventable
disease and the most common modifiable risk factor for several chronic diseases [5, 6];
it is notable that obesity is an independent risk factor for cardiovascular disease [7, 8]

471
and type 2 diabetes [9, 10], as well as an independent cause of increased morbidity and
mortality.[5] With the contemporary pervasive unhealthy food habits and sedentary
lifestyles, it is anticipated that the prevalence of obesity and its health consequences will
continue to rise.[11] Over the last decade, an escalation in diabetes incidence has
paralleled the rapid increase in obesity prevalence, constituting a global health
crisis.[12] The concurrent occurrence of obesity and diabetes in the same individual,
known as “diabesity” is also rising in prevalence at a fast pace.[13, 14]

A comprehensive program of lifestyle modification can produce a 7% to 10% reduction


of body weight and clinically meaningful improvements in several cardiovascular risk
factors, including the prevention of type 2 diabetes.[15] However, long-term
maintenance of lifestyle induced weight loss is notoriously difficult and fails for the
large majority.[16] In turn, anti-obesity drugs have limited efficacy and adverse side
effects that limit their use.[5, 17]

Thus, few effective treatment options for lasting weight loss are available to obese
individuals. This is a serious issue, as obesity is an escalating epidemic posing a
tremendous burden on both the individual and public level. According to a recently
published report “Overcoming obesity: An initial economic analysis” from the
McKinsey Global Institute (MGI),” obesity is one of the top three preventable social
burdens (along with smoking and violence/war/terrorism) generated by human beings”
imposing an estimated annual global direct economic burden amounting to 2 trillion
USD.[18]

Therefore, new interventions are urgently needed to combat this alarming preventable
threat to society. A new line of reasoning has suggested that it is time to test hormonal
theories about why people get fat.[19] Testosterone is a promising candidate.

WHAT NEW STUDIES SHOW

Multiple lines of evidence, from experimental to observational studies, and randomized


controlled trials of both testosterone therapy and testosterone deprivation, show the
critical role of testosterone in regulation of body fat metabolism and body
composition.[1-4]

472
Obesity as a cause of hypogonadism – Evidence that obesity leads to low
testosterone

Multiple observational studies in community-dwelling men suggest that obesity leads to


decreased testosterone. Cross-sectional analyses show that obese men have lower
testosterone levels than age-matched non-obese men.[20, 21] In the prospective
Massachusetts Male Aging Study (MMAS), non-obese men who became obese had a
decline of testosterone levels comparable to that of 10 years of aging.[22] Another
prospective study confirmed that weight gain results in a proportional decrease in
testosterone levels at follow-up.[23] Obesity, metabolic syndrome, diabetes and
dyslipidaemia have been identified as risk factors of incident hypogonadism.[24]

Support that obesity is a cause of hypogonadism comes from studies of weight loss
(induced by either low-calorie dieting or bariatric surgery) which show increases in
testosterone levels proportional to the amount of weight lost.[25]

Hypogonadism as a cause of obesity – Evidence that low testosterone leads to


obesity

There is also ample evidence, both from experimental and human studies, to suggest the
reverse. Lower baseline testosterone levels independently predict an increase in intra-
abdominal fat after 7.5 years of follow-up.[26] Experimental induction of
hypogonadism in healthy men aged 20-50 years, significantly increases body fat mass
within 16 weeks, indicating that severe testosterone deficiency rapidly causes body fat
gain.[27] Moreover, men with prostate cancer receiving androgen deprivation therapy
show marked increases in total body fat mass and abdominal visceral fat within 6
months.[28]

Further proof of the causal role of testosterone in the pathogenesis of obesity comes
from a growing number of studies showing that testosterone therapy significantly
reduces several markers of obesity, (including weight, waist circumference and
BMI)[29-33], total body fat mass [34-39] and intra-abdominal fat mass.[39-42]

While testosterone is most known for its effect on libido and sexual function, it plays a
key role in fat, carbohydrate and protein metabolism as well.[39, 43-47] The exact
mechanisms by which testosterone acts on pathways to control metabolism are not fully
473
clear. Nevertheless, data from animal, cell and clinical studies show that testosterone at
the molecular level controls the expression of important regulatory proteins involved in
energy and substrate metabolism.[43] The cumulative effects of testosterone on these
biochemical pathways would account for the overall benefits seen with testosterone
therapy on fat loss and body composition.

Low testosterone and obesity: a self-perpetuating vicious cycle

When taking into consideration both sides of the testosterone – obesity link, it becomes
clear that a bidirectional relationship exists between testosterone and obesity, initiating
and reinforcing a self-perpetuating cycle (figure 1).

Figure 1: Bidirectional relationship between low testosterone and obesity, initiating and
reinforcing a self-perpetuating cycle. Click to see full image.

On the one hand, increasing body fat suppresses the HPT (hypothalamic-pituitary-
gonadal) axis by multiple mechanisms; via increased insulin resistance, metabolic
syndrome and diabetes [48, 49], and elevation in estradiol and cortisol levels.[50, 51]
Because of its mechanistic and clinical evidence, it has been suggested that obesity-
induced hypogonadism should be regarded as a distinct clinical entity and subtype of
(hypogonadotrophic) hypogonadism.[52]

On the other hand, low testosterone promotes accumulation of total and visceral fat
mass, thereby inducing and/or exacerbating the gonadotropin inhibition, which will
further reduce testosterone levels.[48, 50, 51] Testosterone may exert a bi-phasic effect
on metabolism; an acute improvement in insulin sensitivity that occurs rapidly within a
few days to few weeks of treatment, before loss of fat mass becomes evident; and a
long-term effect achieved when a significant reduction of total and visceral body fat
occurs.[2]

A recent placebo-controlled study investigated the effects of testosterone therapy on


obesity, HbA1c, hypertension and dyslipidemia in hypogonadal diabetic patients.[53] It
was found that testosterone therapy did break the metabolic vicious circle by raising
testosterone levels, and it was concluded that re-instituting physiological levels of
testosterone has an important role in reducing the prevalence of diabetic
complications.[53]
474
Psychological effects – Adherence to lifestyle changes

Testosterone therapy as an obesity treatment confers additional benefits in that it


consistently improves mood and feelings of energy, and reduces fatigue [54-58]; this in
turn may bolster motivation to adhere to diet and exercise regimens designed to combat
obesity.[2] This has been demonstrated in studies that added testosterone or placebo to
diet and exercise recommendations or structured programs.[59, 60]

In one study the placebo group showed initial reduction in waist circumference after 18
weeks, but it returned toward baseline as soon as 12 weeks later, indicating the transient
effect of the physician’s advice to improve life style.[59] In another study, adding
testosterone therapy to a 1 year-long supervised diet and exercise program resulted in
greater improvements in testosterone levels, waist circumference, glycosylated
hemoglobin HbA1c), fasting plasma glucose, high-density lipoprotein cholesterol
(HDL), triglyceride levels, compared to the placebo group that was on the same diet and
exercise program. [60] The larger reduction in waist circumference by adding
testosterone to a diet + exercise program, compared to the same diet + exercise program
alone, is especially notable (figure 2).[60]

Figure 2: Waist circumference in 32 men with newly diagnosed type 2 diabetes in the
DIMALITE (Diabetes Management by Lifestyle and Testosterone) study. Click to see
full image.

It has been suggested that hypogonadism is “the common denominator between the
development of insulin resistance in the long term and the immediate experience of
fatigue”.[61] Androgens, by improving mitochondrial function, control the sense of
energy and vitality, and the “pick-up-and-go” mentality, as well as possibly influences
the pathogenesis of insulin resistance, type 2 diabetes and cardiovascular disease.[61]
Therefore, testosterone therapy, by addressing a root cause of obesity, can help obese
men adhere to exercise programs and thereby not only break the vicious circle, but also
initiate a health promoting circle.

CONCLUSION and COMMENTS

Restoring testosterone levels in hypogonadal obese men will relatively quickly break
the self-perpetuating vicious circle, and transform it into a “health promoting circle.”
475
And restoring testosterone levels in hypogonadal men who are not yet obese may help
prevent excess body fat accumulation and thereby serve as a primary prevention
strategy. I will outline the promising results of using testosterone replacement therapy
as a primary prevention strategy in an upcoming article.

It is of utmost interest that in contrast to the U-shaped curve for weight loss seen with
traditional obesity treatments, which are characterized by weight loss and weight regain,
treatment with testosterone therapy results in a continuous reduction in obesity
parameters (waist circumference, weight and BMI) for >5 years, or until metabolic
abnormalities return to healthy ranges.[29-33]

Testosterone therapy has been proposed to be a new potential obesity treatment


modality in hypogonadal men with excessive body fat mass and metabolic
derangements.[2] It should be underscored that the contribution of testosterone therapy
to combating obesity remains largely unknown to medical professionals.[2] It is
therefore important to highlight the promising research on the anti-obesity effects of
testosterone therapy and help implement its research findings into clinical practice, for
the benefit of a growing population of suffering hypogonadal men.

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Role of Nonexercise Activity Thermogenesis in Resistance to Fat
Gain in Humans – Research Review

Levine JA et. al. Role of nonexercise activity thermogenesis in


resistance to fat gain in humans. Science. (1999) Jan
8;283(5399):212-4.

Humans show considerable interindividual variation in susceptibility to weight gain in response to overeating.
The physiological basis of this variation was investigated by measuring changes in energy storage and
expenditure in 16 nonobese volunteers who were fed 1000 kilocalories per day in excess of weight-
maintenance requirements for 8 weeks. Two-thirds of the increases in total daily energy expenditure was
due to increased nonexercise activity thermogenesis (NEAT), which is associated with fidgeting,
maintenance of posture, and other physical activities of daily life. Changes in NEAT accounted for the 10-
fold differences in fat storage that occurred and directly predicted resistance to fat gain with overfeeding
(correlation coefficient = 0.77, probability < 0.001). These results suggest that as humans overeat, activation
of NEAT dissipates excess energy to preserve leanness and that failure to activate NEAT may result in ready
fat gain.

Background

There has long been a question of why some people seem to be able to ‘eat anything they want’ and remain
thin while others can do no such thing; in fact this is often used as an argument that The Energy Balance
Equation is wrong.
More in fact, the paper I’m going to talk about today was once trotted out by several individuals as ‘proof’
that The Energy Balance Equation was incorrect. Unfortunately all their discussion really ended up proving
was that, as I suggest in The Energy Balance Equation, the issue was not the equation, but that they had
no clue what they were talking about. But I’m getting ahead of myself.
Certainly we all have seen, known (or in lucky situations been) that person who seems to ‘eat anything they
want’ without gaining appreciable weight. This is in contrast to those people who seem to be able to simply
look at food and get fat. What’s going on?
At least part of what’s going on, and this is outside of the paper I’m going to discuss today, is that these folks
in question often don’t eat as much as you think they are. Certainly you may see them gorging on food
acutely (at a single meal, perhaps out with friends) but what you often don’t see is what they are doing the
rest of the day, or the day before, or the day after.
So while you may see the single enormous meal, what you don’t see is the smaller or non-existent meals
that they are eating at other times of the day. Or the compensations that occur a day or two later to drastically
reduce their food intake and keep them in energy balance in the long-term. So while you may assume that
they eat like that all day every day, you don’t know that for sure.
But as it turns out, that’s not all that’s going on. As I discussed in The Energy Balance Equation one mistake
people often make is assuming that the output side of the equation is static; that the energy output of a given

477
individual is invariant over time. Thus if you plug in X calories and the person doesn’t gain exactly Y weight,
the equation must be invalid. This is wrong for a bunch of reasons discussed in that article not the least of
which being that the out side of the equation changes in response to cahnges in food intake, activity and
obesity.
For example, in response to both increases and decreases in food intake (as well as body weight), we know
that basal or resting metabolic rate (BMR/RMR) can go up and down. Similarly, the thermic effect of food
(TEF) is related to the amount (and type) of food being eaten and will adjust upwards or downwards as well.
Activity of varying sort can be affected by energy intake as well as body weight (e.g. larger bodies burn more
calories in movement). Clearly the idea that the out side of The Energy Balance Equation is unchanging is
wrong. Yet people keep pretending that it is when they simply look at calories in or out and what they think
should happen to body weight without accounting for those changes.
But as it turns out, changes in the above three factors don’t seem sufficient to explain some of what is seen
when people are overfed with studies finding a huge individual variance in how much fat is gained with
identical amounts of overfeeding and that brings me in a very roundabout way to today’s paper; while over
10 years old, this was a seminal study that goes a long way towards explaining the odd observation that
some people are seemingly able to ‘eat’ whatever they want and not get fat. The researchers wanted to try
to determine mechanistically what might be causing that to occur.
.

The Paper

It’s been known for quite some time that people show a rather large amount of variability in terms of actual
fat/weight gain in response to overfeeding and the researchers wanted to try to figure out some of the
mechanistic reasons why this might be the case.
Towards this goal, the study recruited 16 people (12 males and 4 female) who underwent body composition
measurement (via DEXA) and total energy expenditure (measured by doubly labeled water) who were then
overfed by 1000 calories per day for 8 straight weeks.
I’d note that both basal metabolic rate and TEF were measured via indirect calorimetry, mainly to see if
changes there could explain anything about the measured results. As a control, subjects were required to
maintain their exercise type activity at very low levels; this was done to prevent folks from trying to
compensate for the increased caloric intake by simply exercising more. While slightly artificial in terms of
how people often work in the real world, this was simply a way of controlling the study to see what else might
be going on.
Over the course of the study, an average of 432 cal/day was stored and 531 was dissipated through
increased energy expenditure: this accounted for 97% of the total (note: this means that the energy equation
was essentially balanced in that all calories were accounted for, either being stored or burned; none
magically went anywhere else). However, looking at the averages obscure what was really happening.
Moving to individual results, fat gain varied from a low of 0.36 kg (0.79 lbs) to 4.23 kg (9.3 lbs) a 10 fold
variance despite the same 1000 calorie/day increase in energy intake. Changes in BMR and TEF were
unable to explain this difference. BMR went up only 5% accounting for 8% of the extra energy while TEF
went up 14%, simply in response to the increased food intake; none of those changes showed any correlation
with changes in fat mass. As I noted above, exercise type activity was clamped at low levels so changes
there can’t explain the difference either.
And that brings us to NEAT, an acronym referring to Non-Exercise Activity Thermogenesis. As the
researchers define it:

478
NEAT is the thermogenesis that accompanies physical activities other than volitional exercise, such as the
activities of daily living, fidgeting, spontaneous muscle contraction, and maintaining posture when not
recumbent.
Basically, think of NEAT as the calorie burn associated with all activities that aren’t formal exercise. And
that’s where the researchers saw the massive difference between subjects; while the average increase in
NEAT across all subjects was 336 cal/day, the individual changes in NEAT varied from -98 (that is it actually
went down in at least one person) to +692 cal/day.
That is, in at least one subject, approximately 700 calories of the 1000 extra was burned off via NEAT. That’s
in addition to the increase in BMR and TEF which would have burned off even more of the total calories. The
researchers calculated that the increase in NEAT in the greatest responder would be the equivalent of
strolling for 15 minutes per hour during waking hours.
In this vein, in the review of the Bodybugg/GoWearFit I mentioned that even small increases in activity over
the course of the day can end up having a massive impact on overall energy balance because of how it can
really add up. The subjects with the increase in NEAT effectively had that happen without trying.
Of more importance, changes in NEAT directly predicted fat gain (or the lack thereof): people who showed
the greatest increase in NEAT showed the smallest fat gain and vice versa. I’d note in finishing out the
paper that the four worst responders in terms of NEAT were the 4 female subjects; this really isn’t news
inasmuch as we’ve also known for decades that women get the short end of the stick in terms of both weight
gain and loss.
I’d also mention that this paper did nothing to determine the mechanisms behind NEAT (later studies have
tried, and done poorly, at determining what is the actual cause of the increase in NEAT) only mentioning that
NEAT seems to be a familial trait (suggesting a genetic basis). Other later studies have shown that NEAT
is essentially subconscious, people either do it or don’t.
.

My comments:

There’s really not a huge amount to say about this paper; it’s a point of interest without a lot of practical
application. I only bring it up to make the point that many people’s assumptions about what does or does
not disprove The Energy Balance Equation tend to stem with their misunderstanding of things; especially
their failure to realize that the out side of the equation is not static. And this goes especially for the NEAT
component of energy expenditure, with individual increases in NEAT varying massively from one person to
another.
Of more relevance, not only is the out side of the equation not static, there appears to be quite a bit of
variability involved. While some people get effectively no (or a negative) increase in NEAT with overfeeding,
which makes their gaining of fat quite easy, others have essentially won the genetic lottery: in response to
overfeeding, they subconsciously ramp up small calorie burning activities that add up over the course of the
day to burn off the excess.
To beat that dead horse, the equation isn’t wrong, the out side of the equation in terms of NEAT simply
differs massively between people especially in terms of the NEAT response. The people who can apparently
‘eat like gluttons’ and not gain weight appear to have a physiological mechanism by which they burn off the
excess, essentially protecting them from fat gain.
In that vein, I’d mention at least one other study that compared the response to overfeeding and dieting in
terms of metabolic rate adjustment. It found that those individuals who showed the greatest increase in

479
metabolic rate to overfeeding showed the least drop in response to dieting; by contrast those people who
showed the least increase to overfeeding showed the biggest drop with dieting.
That study posited the existence of spendthrift (big increase with overfeeding/small decrease with dieting)
and thrifty (small increase with overfeeding/big decrease with dieting) physiologies. Clearly the first has as
huge benefit in terms of both avoiding weight gain as well as losing it if necessary; the second group will
have a much larger problem.
As I mentioned above, follow up work to this seminal paper has done little to determine the mechanisms
behind it (which might lead to some way of increasing NEAT in those not disposed to it). It appear to be
genetic and more or less subconscious. Of course, that doesn’t stop people from consciously trying to do
things to increase their activity levels and energy expenditure outside of formal exercise. All of the old
behavioral strategies such as taking the stairs instead of the elevator, parking further away, etc. all end up
adding up over time.

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Static Stretching and Refined Grain Intake by Paleo Man –
Research Review

Taylor KL et. al. Negative effect of static stretching restored when


combined with a sport specific warm-up component. J Sci Med
Sport. (2009) 12(6):657-61.

There is substantial evidence that static stretching may inhibit performance in strength and power activities.
However, most of this research has involved stretching routines dissimilar to those practiced by athletes.
The purpose of this study was to evaluate whether the decline in performance normally associated with static
stretching pervades when the static stretching is conducted prior to a sport specific warm-up. Thirteen netball
players completed two experimental warm-up conditions. Day 1 warm-up involved a submaximal run
followed by 15 min of static stretching and a netball specific skill warm-up. Day 2 followed the same design;
however, the static stretching was replaced with a 15 min dynamic warm-up routine to allow for a direct
comparison between the static stretching and dynamic warm-up effects. Participants performed a
countermovement vertical jump and 20m sprint after the first warm-up intervention (static or dynamic) and
also after the netball specific skill warm-up. The static stretching condition resulted in significantly worse
performance than the dynamic warm-up in vertical jump height (-4.2%, 0.40 ES) and 20m sprint time (1.4%,
0.34 ES) (p<0.05). However, no significant differences in either performance variable were evident when the
skill-based warm-up was preceded by static stretching or a dynamic warm-up routine. This suggests that the
practice of a subsequent high-intensity skill based warm-up restored the differences between the two warm-
up interventions. Hence, if static stretching is to be included in the warm-up period, it is recommended that
a period of high-intensity sport-specific skills based activity is included prior to the on-court/field performance.

My Comments: As I discussed recently in The Importance of Context, people these days seem to love them
some absolutes and there tends to be no shortage of them to go around, especially when it comes to
training. Always do this, never do that, you get the idea. The situational context is irrelevant, there are
simply black and white absolutes that apply across the board.
And a recent never is that you should never ever static stretch before high-intensity training of any sort with
endless coaches and gurus repeating that idea. And certainly this seems to be based on quite a body of
research. A number of studies have shown that extensive static stretching done immediately prior to various
types of exercise performance such as vertical jumping, sprinting and weightlifting impair strength and/or
power output.
Now, as I mentioned in Warming Up for the Weight Room Part 1, even if static stretching does decrease
strength and power outputs, there may still be times to do it before training. Usually this is in the case of a
severe muscular tightness that impairs either technique or safety. In that context, proper technique and not
hurting the person is far outweighed by any decrease in performance.
However, I made another point in that article which was this: many of the studies don’t really reflect how
athletes typically go about their training. That is, anyone who has trained as an athlete or actually coached
athletes in the real world knows that it’s fairly rare (especially among strength/power type athletes,
endurance guys are often years behind the curve) to go straight from static stretching immediately into high-
performance work. At the very least some type of drills are generally done between the two, usually more
than that (e.g. multiple progressive intensity sports specific warm-ups) is done.

481
There is also an issue of the extent of stretching: many of the negative performance studies have used levels
of static stretching that far exceed what most athletes would ever do in practice (again, something anyone
who’s actually worked with athletes would know). That is, it would be rare to hold a stretch for 2-4 minutes
in the real world, static stretching of perhaps 30 seconds per muscle group would be far more realistic. Yet
it is generally that type of extremely prolonged static stretching that has been tested and found to impair
performance (some studies have shown shorter stretching periods to have a similar negative impact).
Which brings us to today’s study which set to test the above in a more real-world type of situation.
The study examined 13 netball players from the Australian Institute of Sport. Both groups first performed a
sub-maximal run as a general warm-up. Then one group performed static stretching (9 stretches held for
30 second each) and the other performed a dynamic warm-up consisting of 16 rather common dynamic
movements. Both the static and dynamic warm-ups lasted 15 minutes. After a short-rest, both groups were
tested on 20m sprint and vertical jump. Then both groups performed a netball specific skill warm-up
consisting of various short sprints, shuffling, accelerations, direction changes and jumping. Then the
performance tests were performed a second time to see if anything had changed.
And the results? Well, in keeping with previous work, the static stretching routine did in fact hurt performance
on the 20 m sprint and vertical jumping compared to the dynamic warm-up. However, after performing the
specific skills warm-ups described above, results were no different on the second set of performance
tests. That is, any loss of performance due to static stretching was eliminated simply by performing a variety
of sport specific skills prior to the maximal effort testing.
Basically, by testing the athletes in a situation that more accurately reflects how athletes actually train, they
found that much of the concern over static stretching is unfounded. As they state in the discussion:
The results suggest that if an inhibitory effect was present after static stretching, that the SKILL component
of the warm-up routine was able to dissipate the negative effect. This supports the suggestion by Young
and Behm that practice attempts of the required tests may offset potential negative effects of static
stretching.
The also note that their results are in contrast to another study examining both a dynamic performance
warm-up and a static-stretching warm-up but in that study, the static stretching was done after the
performance warm-up and immediately prior to the testing. Basically, order of warm-up matters which I also
discussed in Warming Up for the Weight Room Part 1. And so long as it’s followed by some sort of dynamic,
skill specific, progressive warm-up (e.g. progressively heavier warm-up sets in the weight room, increasingly
faster pickups in sprinting, etc), static stretching appears to not be quite the absolute no-no that many have
made it out to be.
Quoting from the researchers conclusions:
The most important findings from this study were that a dynamic warm-up routine is superior to static
stretching when preparing for powerful performance; however, these differences can be eliminated if
followed by a moderate to high intensity sport specific skill warm-up.
Summing Up: Basically, static stretching is only a problem if it’s done too extensively (e.g. stretches held
for very extended periods) and is not followed by appropriate sport-specific warm-ups between the end of
static stretching and maximal performance (testing or training). Which isn’t how real athletes generally train
anyhow. Which is something any performance coach who has actually worked with athletes should know
anyhow.

Mercader J. Mozambican grass seed consumption during the


middle stone age. Science. (2009) 326(5960):1680-3.

482
The role of starchy plants in early hominin diets and when the culinary processing of starches began have
been difficult to track archaeologically. Seed collecting is conventionally perceived to have been an irrelevant
activity among the Pleistocene foragers of southern Africa, on the grounds of both technological difficulty in
the processing of grains and the belief that roots, fruits, and nuts, not cereals, were the basis for subsistence
for the past 100,000 years and further back in time. A large assemblage of starch granules has been
retrieved from the surfaces of Middle Stone Age stone tools from Mozambique, showing that early Homo
sapiens relied on grass seeds starting at least 105,000 years ago, including those of sorghum grasses.
My Comments: In recent years, there has been quite an explosion in interest in the supposed diet of our
paleolithic ancestors, essentially in an attempt to explain part of why humans are having so much trouble
with the modern diet. So far as I can tell the first paper was written in the Mid-80’s or so but even more
recently it’s become quite the fad/cult/area of interest for a lot of people.
Now, while an entire article could be written about this, it’s important to note that nobody knows for sure
what we ate during our evolution. Even researchers in the field (Cordain and Eaton are two of the major
ones) have arrived at rather drastically different conclusions about what our diets contained based on their
assumptions because it’s all basically a lot of guesswork. We end up with estimations based on a bunch of
assumptions and not much more.
Much of it comes from an analysis of a book called the Ethnographic Atlas, a work done years ago by non-
scientists who wrote down (sort-of) what extant non-modernized people were eating. From that, various
researchers, making various assumptions about the relative proportions of animal and vegetable foods in
the diet have thrown out some ideas about what our evolutionary diet contained. Those researchers have
often reached utterly differing ideas based on which built-in assumptions they started with. Other
suggestions about our ancestral diet have been made by examining the current intake of extant hunter-
gatherer tribes with the implicit assumption that their food intake is representative of our intake during our
evolution.
I’d note that it’s unlikely that there was any singular evolutionary diet in the first place. Humans have shown
the ability to adjust to all but the most extreme environments and show an amazing ability to adapt to
drastically differing diets as well. Human ancestors evolving in say Alaska would have had far different foods
available than someone living in the arid plains in Africa. Even examining the extant hunter-gatherer tribes
demonstrates this in spades: the diet of an Alaskan Inuit is radically different from say an African Bushman
simply due to the difference in environment and what is available to them. So there is no single ancestral
diet in terms of the quantities, proportions or types of food that would have been eaten in the first place.
At best we can probably say with some degree of certainty that our ancestors didn’t have many of the foods
available to us today. That is, Cap’n Crunch, Ben and Jerry’s Ice Cream and Bud Light weren’t part of our
evolutionary diet because they didn’t exist (much to the loss of our ancestors). Beyond that, we can’t say
with much certainty what they did eat; it’s mostly guessing because folks weren’t alive to say for sure. And
while it may be safe to assume that extant hunter-gatherer tribes are representative, it’s still an assumption.
Now, while there are many different interpretations to the ‘paleo-diet’ craze, at least one thing that most
seem to agree on was that refined grains were absolutely not part of the evolutionary diet. Bloggers,
apparently unclear on the concept of irony, go on constantly about how ‘Paleo man didn’t have grains, so
you shouldn’t eat them.’ Apparently that same logic doesn’t apply to the computers they use to blog with,
the Internet that they blog on, their Blackberries that they use to Twitter about their blog updates, modern
cars that they use to get to work or the houses they live in. Paleo man didn’t have those either but I don’t
see these folks giving those up. Guess they only want to give up the easy stuff when it’s convenient. But I
digress.

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That is, it’s generally assumed that refined grains (being currently blamed for much of modern health
problems) weren’t a major part of our diet until the agricultural revolution, about 10,000 years ago. It’s also
assumed that that span of time is insufficient for man to have evolved to deal with them. I’ll only address
this second assumption by pointing readers to a new book called The 10,000 Year Explosion: How
Civilization Accelerated Human Evolution wherein the authors make a rather good argument that, contrary
to common belief, not only did human evolution continue once humans became civilized, that it accelerated.
Rather, in looking at today’s second paper, I want to address that first assumption: that our evolutionary diet
was devoid of any type of refined cereal grain. I imagine that, if you’ve read this far, you can guess what I’m
going to say about it and what the second study concluded.
The researchers were examining cave artifacts in a cave site in Mozambique which have been dated to
somewhere between 42000 and 105,000 years ago. They mention that excavation in 2007 retrieved 555
artifacts. Of those, 70 stone tools were analyzed and were chosen to represent the broadest range of
potential plant uses. This includes scrapers, grinders, points, flakes and miscellaneous tools. These were
analyzed and while 20% contained no starch residue, the other 80% were found to contain starch granules
with the number on each tool ranging from 1 to 650. It’s worth noting that the quantity of granules found on
the scrapers was massively larger than what is found naturally in the cave, that is, they were brought into
the cave.
The majority of starch granules (89%) were identified as sorghum, a grass showing a large complex of
cultivated, wild and weedy types. The researchers note that the starch granules found on the tools analyzed
are structurally identical to modern sorghum plants. As the researchers state:
The Mozambican data show that Middle Stone Age groups routinely brought starchy plants to their cave
sites and that starch granules go attached to and preserved on stone tools. I cannot prove that starch from
all stone tools represents direct tool function…These early grinders are simply modified cobbles and core
tools, with a suspected use that conforms to the technological action of “diffuse resting percussion” and
“pounding”, which allows the grinding of plant materials.
Put differently, while more research will certainly be needed to verify or refute this claim, data that is a bit
more direct than “Assumptions based on a book some guys wrote years and years ago” suggest that as far
back as 100,000 years ago, humans had found a way to refine and consume at least some grains for their
diet. Or as the researchers state more directly in the abstract above:
A large assembly of starch granules has been retrieved from the surfaces of Middle Stone Age tools from
Mozambique, showing that early Homo Sapiens relied on grass seeds starting at least 105,000 years ago,
including those of sorghum grasses.
And even if you don’t buy the argument of the book I referenced above, that 10,000 years is more than
sufficient to allow adaptation to changes in diet, it would be hard to argue that 105,000 years isn’t time
enough to adapt to some degree.

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Straight Talk About High-Fructose Corn Syrup: What it is and What
it Ain’t. – Research Review

Title
White JS. Straight talk about high-fructose corn syrup: what it is and what it ain’t. Am J Clin Nutr. 2008
Dec;88(6):1716S-1721S.Click here to read Links

Abstract

High-fructose corn syrup (HFCS) is a fructose-glucose liquid sweetener alternative to sucrose (common
table sugar) first introduced to the food and beverage industry in the 1970s. It is not meaningfully different
in composition or metabolism from other fructose-glucose sweeteners like sucrose, honey, and fruit juice
concentrates. HFCS was widely embraced by food formulators, and its use grew between the mid-1970s
and mid-1990s, principally as a replacement for sucrose. This was primarily because of its sweetness
comparable with that of sucrose, improved stability and functionality, and ease of use. Although HFCS use
today is nearly equivalent to sucrose use in the United States, we live in a decidedly sucrose-sweetened
world: >90% of the nutritive sweetener used worldwide is sucrose. Here I review the history, composition,
availability, and characteristics of HFCS in a factual manner to clarify common misunderstandings that have
been a source of confusion to health professionals and the general public alike. In particular, I evaluate the
strength of the popular hypothesis that HFCS is uniquely responsible for obesity. Although examples of pure
fructose causing metabolic upset at high concentrations abound, especially when fed as the sole
carbohydrate source, there is no evidence that the common fructose-glucose sweeteners do the same. Thus,
studies using extreme carbohydrate diets may be useful for probing biochemical pathways, but they have
no relevance to the human diet or to current consumption. I conclude that the HFCS-obesity hypothesis is
supported neither in the United States nor worldwide.

My Comments

I think it’s just human nature, people seem to have a need to find a single enemy that is the cause of all
woes under the sun. The one that causes obesity, diabetes, and all manners of health
problems. Nutritionally, I’ve watched the enemy change over the years. In the 80’s it was dietary fat, which
was blamed for all the problems of humanity. During the 90’s, things started to shift and carbohydrates
became the enemy. About the same time, trans-fatty acids became the one thing that people MUST NOT
EAT or they would seemingly drop dead nearly instantly.
And now, as we enter 2009, if there is a single nutrient that is blamed for everything that is wrong in the
world, it is high-fructose corn syrup (HFCS). Much of this started with a 2004 paper by Bray where he
correlated changes in HFCS intake with changes in obesity, suggesting that it was the increase in HFCS
intake that was driving obesity. This was taken, as usual, far out of context into the popular realm of
magazines, newspapers and tv soundbites.
Nowhere is this more prevalent than in the athletic/bodybuilding and fat loss arena where people are simply
losing their ever-loving minds over anything with HFCS. Any food that dare list high-fructose corn syrup on
its label (even if the total quantity is obviously miniscule) is immediately deemed to be evil, a destroyer of

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not only one’s physique but a corrupter of children, a direct line to Satan himself. Ok, maybe I’m
exaggerating but not by much.
This paper addresses this idea, by looking at the hypothesis that somehow HFCS is uniquely obesity or
health-problem causing beyond simply being a source of calories. The author states that several
assumptions must be found to be true to accept this idea as fact. They are:
 HFCS and sucrose are significantly different
 HFCS must be uniquely obesity-promoting
 HFCS must be predictive of US obesity
 HFCS must be predictive of global obesity
 Eliminating HFCS from the food supply must significantly reduce obesity
I won’t detail in full every one of his arguments; the punch line of course is that none of these actually turn
out to be true. Yes, HFCS and foods containing them often contribute a large number of calories to the diet
and clearly that alone causes problems; but there is nothing special about HFCS to warrant the fear about
it that many seem to have developed.

What is HFCS and Is it Really Different than Sucrose?

Historically, HFCS was developed back in the 50’s as an alternative to cane sugar for food preparations. The
reasons why HFCS is superior for foods than cane sugar isn’t really that relevant; sufficed to say that HFCS
is more stable and has replaced your basic cane sugar/sucrose in a lot of foods.
Now, a lot of the silliness, especially in the fitness world about HFCS probably comes out of two things. The
first is a generally anti-fructose, anti-fruit idea that started about 30 years ago with John Parillo. Fruit is
considered forbidden on a diet; nevermind that it helps a LOT of people with hunger (liver glycogen status
is one of many signals to the brain) and seems to do something good for thyroid status for many people.
The second is a general confusion about what HFCS actually is, the problem is with the name, the ‘high-
fructose’ part of it suggests to people that HFCS is much higher in fructose content that it actually
is. However this is not the case as the chart below shows. The percentage of either fructose or glucose is
shown for each of the types of sugars (HFCS-42, HFCS-55, Corn Syrup, Pure Fructose, Pure Sucrose,
Invert Sugar, Honey).

HFCS- HFCS- Corn Invert


Fructose Sucrose Honey
42 55 Syrup Sugar

Fructose
42 55 0 100 50 45 49
Content

Glucose
53 42 100 0 50 45 43
Content

As the chart clearly shows, HFCS-42 is only 42% fructose, lower than sucrose, invert sugar or honey (which
is often considered a ‘healthy’ sugar, at least in the hippie subculture). HFCS-55 is 55% fructose which is
only slightly more fructose than the other sugars. It’s worth noting that there are products such as HFCS-
80 and 90 which contain 80 and 90% fructose but they aren’t used widely commercially.

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The point being that despite it’s name, HFCS is actually no higher in fructose than many other sugars such
as sucrose (table sugar), invert sugar or honey. The ‘high-fructose moniker’ is simply a poor choice of names
but HFCS will not provide any greater amount of fructose to the diet than those other sugars.
Additionally, despite Bray’s assertion that increases in HFCS corrleates with increases in obesity, the paper
points out that he looked at the relationship in isolation. During the time that HFCS intake was going up,
daily food intake was also increasing, by about 500 calories per day from 1980 to the year 2000.
Additionally, intake data shows that total sugar intake did not increase over that time frame, and as HFCS
intake was going up, sucrose intake was going down; leading to no change in overall sugar intake. Rather,
what people were eating more of was grains and dietary fat. There is simply no basis to conclude that
increasing HFCS intake has any correlation with rising rates of obesity.
Additionally, while it is often claimed that HFCS is sweeter than sucrose (with that being argued that HFCS
will increase intake of itself), this is also untrue. While pure crystalline fructose IS sweeter than sucrose,
HFCS is identical in sweetness. Increasing use of HFCS in the US food supply did not increase the relative
sweetness of those foods.
Of course, the caloric value for HFCS and sucrose is identical at 4 calories/gram. In that sucrose appears
to have been swapped out for HFCS in a more or less 1:1 ratio, there is no reason to believe that HFCS
intake is increasing caloric intake outside of simply being a source of calories.
Finally, the paper looks at the issue of absorption and metabolism of sucrose vs. HFCS. While fructose is
metabolized differently than glucose (in terms of the transporters used and how it is handled in the liver),
keep in mind that HFCS is only about half-fructose, just like sucrose. Fructose malabsorption is a problem,
mind you, but only when large amounts of fructose by-itself is consumed, this does not apply to HFCS.
Quoting from the paper:
Sucrose, HFCS, invert sugar, honey an many fruits and juices deliver the same sugars in the same ratios to
the same tissues within the same time frame to the same metabolic pathways. Thus…it makes essentially
no metabolic difference which one is used.
So, again, while HFCS is certainly a source of calories (and many HFCS containing foods are easily
overconsumed), there is nothing special about HFCS that makes it uniquely problematic. Fruit juice or a
sucrose containing soda would function identically in the body.

Is HFCS Uniquely Obesity Promoting?

Much of the concern over HFCS has to do with the fructose content as stated above; and a lot of very silly
studies have come out recently showing that massive intakes of fructose by itself are problematic in terms
of health or obesity.
One that is making the rounds now showed that feeding rats a 60% fructose diet for 6 months caused leptin
resistance. But let’s be realistic. For someone on a 3000 calorie/day diet that would be the equivalent of
450 grams of pure fructose per day. Every day. For six straight months. This simply has no relevance to
any real human diet.
As the paper states:
A pure fructose diet is surely a poor model for HFCS, because HFCS has equivalent amounts of
glucose. Because no one would eat a pure fructose diet, such experimentation must be recognized as highly
artificial and highly prejudicial and not at all appropriate to HFCS.

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Rather, diets examining sucrose intake make a much more appropriate model for HFCS. Not much has
been done comparing HFCS to sucrose but what has been shows no metabolic difference between the two;
exactly what would be expected due the fact that they have nearly identical composition.

Does HFCS predict either US or Global Obesity?

In a word, no. While Bray’s original analysis suggested a correlation between increasing HFCS intake and
US obesity, that relationship no longer holds. Despite reduced HFCS intake in the last few years, obesity
continues to increase. Simply, HFCS cannot explain the continuous rise in US obesity.
Moving to the global arena, there is simply no relationship between HFCS intake and obesity rates with the
two countries showing the highest rates of obesity showing the lowest intake of HFCS.

Will Eliminating HFCS from the Food Supply Affect Obesity?

You can probably guess the answer which is no. Given that HFCS and sucrose are nearly identical in
composition, given that HFCS has replaced sucrose intake in the human diet over the past 30 years, given
that they are handled metabolically identically, given that they have the identical caloric value, replacing
HFCS with sucrose will simply have no effect on anything. Except perhaps to raise prices since sucrose is
higher than HFCS.

Conclusion

The paper concludes, as you might imagine, by reiterating the points I’ve made above. HFCS is in no way
unique amount sugars, with a composition identical to sucrose as well as the supposedly ‘healthy’
honey. Increased caloric intake since the 1970’s is the driver for increased obesity, with no relationship with
HFCS intake per se.
In that all fructose-glucose solutions (whether HFCS, sucrose or honey) are metabolized in exactly the same
fashion in the body, there is simply no reason to think that HFCS per se is particularly obesity promoting
outside of being a caloric source.

Application

Now, since I know some people will mis-interpret this piece, I want to be clear: the paper is not saying that
people can or should be consuming HFCS in massive amounts. Many HFCS containing foods contain
massive numbers of calories.
This is especially true of sweetened sodas and it’s interesting to note that a good bit of data suggests that
such drinks can be consumed in massive amounts without signalling the body about their caloric content;
but this has more ot do with their fluid nature than their composition.
What I’m getting at with this research review is that the near insane over-reaction and concern to any food
containing any amount of HFCS among certain groups. Folks on forums are throwing out the baby with the
bathwater under the gross misunderstanding that HFCS per se is a unique evil which it clearly isn’t. Within
the context of a calorically controlled diet, there is no reson to believe it will have any differential impact
beyond every other sugar that has ever been used.

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