ean

12 The effects of supraphysiologic doses of

testosterone on muscle size and strength in
normal men.
Bhasin S, et al. N Engl J Med. 1996 Jul 4;335(1):1-7.
[Medline]

14 It’s time to rant about the sport of bodybuilding.

By Alan Aragon

Copyright © October 1st, 2011 by Alan Aragon

Home: www.alanaragon.com/researchreview
Correspondence: aarrsupport@gmail.com 16 Can BCAA metabolism in rodents be extrapolated
to humans?
By Alan Aragon

2 The modern anti-grain crusade: should any of its

claims be taken seriously?
By Alan Aragon

8 The effects of low and high glycemic index foods

on exercise performance and beta-endorphin
responses.
Jamurtas AZ, et al. J Int Soc Sports Nutr. 2011 Oct
20;8(1):15. [Epub ahead of print] [Medline]

9 Eating frequency is higher in weight loss

maintainers and normal-weight individuals than in
overweight individuals.
Bachman JL, et al. J Am Diet Assoc. 2011
Nov;111(11):1730-4. [Medline]

10 Effects of 28 days of resistance exercise while

consuming commercially available pre- and post-
workout supplements, NO-Shotgun and NO-
Synthesize on body composition, muscle strength
and mass, markers of protein synthesis, and
clinical safety markers in males.
Spillane M, et al. Nutr Metab (Lond). 2011 Nov 3;8(1):78.
[Epub ahead of print] [Medline]

11 Ingestion of 10 grams of whey protein prior to a

single bout of resistance exercise does not
augment Akt/mTOR pathway signaling compared
to carbohydrate.
Cooke MB, et al. J Int Soc Sports Nutr. 2011 Nov 8;8(1):18.
[Epub ahead of print] [Medline]

Alan Aragon’s Research Review – October 2011 [Back to Contents] Page 1


The modern anti-grain crusade: should any of its
claims be taken seriously?
By Alan Aragon
_______________________________________________
Introduction & background
There’s plenty of passionate anti-grain press in both the lay and
academic media. A noisy legion of researchers, journalists, and
trainers have made grain-bashing a big part of their career. For
some, it’s their sole identity. It resembles a crusade because
these folks rail against grains as if they’ve been deceived &
oppressed, and are now on a mission to expose the conspiracy
behind those evil grass seeds. Their intentions are sincere, but
how strong is the evidence supporting their contentions? I’ve
already addressed the Paleolithic argument against grains in the
December 2009 Editor’s Cut, so in this article, I won’t belabor
any speculations about what Fred Flintstone did or did not eat. In
the following discussion, I’ll examine the scientific support for
the most common gripes against cereal grains.
“Grains are unhealthy, and should be avoided.”
This is the perfect claim to kick things off because it’s a vague,
over-assumptive statement that ignores context. First off, there
are several types of grains consumed across the globe, including
rice, buckwheat, sorghum, oats, millet, barley, rye, quinoa,
amaranth, wheat, triticale, corn, and teff. Which grains are being
addressed as harmful to health? Specific types are rarely
elucidated. Instead, grains in general get the “bad” stamp, and
this is nothing more than an ignorant dismissal of the research
associating1-4 & directly demonstrating5-10 positive health effects
of several of the aforementioned species. If anyone wants to
complain that much of the research on grains is industry-funded,
then they would also have to concede that the same is true for
the low-carb diet research. Secondly, the statement implies that a
single food in and of itself can be “unhealthy.” This is false,
unless the ridiculous assumption is made that it’s the only food
in the diet. I would also add that strict avoidance of any food can
be unhealthy from a psychological standpoint.11,12
“Grains are to blame for the high prevalence of obesity.”
I’ll make the educated guess that most of you reading this don’t
need an explanation about why this is false. But just in case
anyone is unaware, a chronic energy surplus that isn’t used for
building lean tissue will result in the accumulation of fat mass.
Blaming grains as the cause of fat gain is blatantly illogical
because it carries the implication that nothing else in the diet
contributes to the caloric surplus. Not to mention, it completely
ignores the energy-out side of the equation, which involves a
decrease in physical activity due to things such as labor-saving
technology, television, the internet, sedentary entertainment, and
increased time sitting at the work desk. The energy balance
equation is simple in principle, but it has several important
aspects that are often overlooked. These details have been
thoroughly covered by Lyle McDonald.13,14
Alan Aragon’s Research Review – October 2011
Giacco et al recently reviewed the available scientific literature
on grain consumption and found a couple of interesting things.15
First off, they found that epidemiological studies unanimously
show that a higher whole grain consumption is associated with a
lower BMI. However, they also found that controlled
interventions have largely failed to show the weight loss
superiority of whole grain versus refined grain intake.
Perhaps the most compelling case against the claim that grains
are inherently fattening is that long-term (1 year or longer)
controlled studies comparing diets of widely varying
carbohydrate content have failed to show significant differences
in weight loss.16-21 Importantly, this lack of significant weight
loss difference was consistently seen despite the use of sedentary
subjects consuming sub-optimally constructed diets, in terms of
both macronutrition and food selection. Optimizing & actually
matching protein intake, improving food selection (though
moderating or minimizing highly refined foods), and adding a
structured training program would further diminish the chance of
weight loss differences.
If the “grains are fattening” claim was true, then vegetarians
(well-known for their staple consumption of grains) would be at
a higher risk for excessive weight gain. Although correlation
does not necessarily equal causation, no peer-reviewed research
in existence associates vegetarianism with a higher incidence of
being overweight or obese. In fact, the opposite is consistently
observed.22-26
“Grains contain phytates and oxalates, which are antinutrients
that reduce the bioavailability of essential minerals.”
Let’s first establish that phytates and oxalates are not exclusively
contained in grains. They exist in a wide range of plant foods,
including green/leafy vegetables.27 Ironically, green veggies are
often consumed ad nauseam by the same folks who avoid grains
because of antinutritional concerns. But the illogic doesn’t stop
there. Since antinutrients are part of a plant’s defense
mechanism against predatory threats, some folks view these
antinutrients as completely inedible. Selectively claiming that
certain plants should not be eaten because they were designed to
resist consumption is the same as claiming that no one should eat
animals with scales, shells, claws, or the ability to bite.
On a more serious note, scenarios indeed exist where mineral
bioavailability can be compromised. Once again, vegetarianism
makes a good illustration, since the elimination of meat and
increased consumption of phytates from grains and legumes can
reduce the absorption of iron and zinc.28 Still, this concern does
not have definitive scientific support, particularly in the case of
industrialized populations with diverse and abundant food
supplies. To quote a review by Hunt,29
“...adverse health effects from lower iron and zinc
absorption have not been demonstrated with varied
vegetarian diets in developed countries, and moderately
lower iron stores have even been hypothesized to reduce the
risk of chronic diseases”
Keep in mind that these reductions in nutrient bioavailability are
of questionable significance in vegetarian diets. In the case of
varied, omnivorous diets, these concerns would be even more
minimal & trivial.
[Back to Contents] Page 2
Another potential concern is wheat consumption reducing the
absorption of calcium. Weaver et al investigated this question
through a series of randomized crossover studies and found that
with the exception of wheat bran cereal, whole wheat flour
products did not reduce calcium absorption when coingested
with milk.30 In related research, Andersson et al found that wheat
bran in amounts typically consumed did not significantly effect
mineral absorption.31 Although increasing the amount of bran
increased fecal output, no significant effect on calcium, zinc, and
iron balance was seen. In yet another example, Sandström et al
found that a large intake of oat bran (142g incorporated into
bread consumed at 3 meals) did not affect zinc absorption of an
otherwise low-fiber animal protein-based diet.32
“Grains are to blame for widespread vitamin D deficiency.”
Vitamin D deficiency is a legitimate concern. It’s widespread, to
the point of peer-reviewed headlines calling it a pandemic.33
Unsurprisingly, alarmists are quick to shake the guilty finger at
grain consumption. However, this isn’t an objective view of the
situation. In terms of direct evidence, there’s only one human
study suggesting that an increased grain consumption can
compromise 25(OH)D (vitamin D3) status. Way back in 1983,
Batchelor & Compston found that the plasma elimination half-
life of vitamin D3 (time it takes for the blood plasma level to
decrease by 50%) was shorter in subjects on a high-fiber diet.34
This means that systemic elimination of vitamin D3 was faster in
the high-fiber group. Since the high-fiber treatment involved the
addition of 60g of wheat bran (adding 20g fiber to the diet),
grains once again got the guilty stamp.
However, it’s rarely mentioned that despite this, plasma vitamin
D3 levels in both groups were still within the normal range, and
the mean value was not significantly different between the
normal & high-fiber groups. Furthermore, there was no
significant correlation between the plasma vitamin D3 levels and
plasma half-life for any of the subjects in either group. So, while
this study is often cited as damning evidence against grains, it’s
actually just preliminary food for thought.
An important point to be made is that grains – or any single
dietary factor in isolation – cannot cause vitamin D deficiency.
Vitamin D deficiency is a multifactorial process, and for cereal
fiber (or any type of fiber) to be a contributor, other factors must
be in play in order for it to even be an issue. Speaking of which,
the most commonly cited factors in the global vitamin D3
deficiency problem are decreased penetration of UVB radiation
(from less direct sunlight, the use of sunscreen, population
residence shifts to higher latitudes, etc), age-related decreases in
7-dehydrocholesterol (the precursor of vitamin D3 in the skin),
and obesity.33,35
Interestingly, secular trends in obesity are similar to that of
vitamin D deficiency. This has led to the wonky speculation that
vitamin D deficiency is the cause of obesity.36 However, it’s far
more likely to be the opposite way around. Illustrating this,
Wortsman et al compared vitamin D3 production via ultraviolet
radiation and pharmacological oral dose in obese and non-obese
subjects.37 The results were striking. The increase in blood
vitamin D3 levels was 57% less in the obese than the non-obese
subjects. This was unexpected because not only does the
Alan Aragon’s Research Review – October 2011
increased skin surface area of obese subjects provide a greater
opportunity for cutaneous absorption (which should thus lead to
greater production of D3), but there was no difference in 7-
dehydrocholesterol (the precursor of vitamin D3 in the skin)
between the groups. These outcomes clearly indicate that the
greater amount of fat in obese individuals acts as a barrier (or
entrapment depot) against vitamin D3 release into circulation.
“Grains cause inflammation, the root of all disease.”
First off, inflammation is not the root of all disease. I addressed
this claim in detail in the August 2010 Editor’s Cut, but to
briefly sum it up, there are several origins of disease, and
inflammation is just one of them. Furthermore, chronic, low-
grade inflammation is often a symptom of disease rather than a
causal agent. However, this doesn’t click well with the over-
simplistic path of reasoning that grains cause inflammation,
inflammation is the root of all disease, and therefore grains are
the primary agents of disease.
Now let’s examine the more important question: is it even
accurate to say that grains cause inflammation? Observational
research suggests that whole grains and refined grains have
divergent effects. Whole grains consistently show an inverse
correlation with inflammation, while refined grains are
positively correlated with inflammation.38-41
There’s a limited number of controlled interventions on this
topic, but they’re important because they can demonstrate cause
& effect. Katcher et al found that 3 daily servings of whole grain
foods was more effective than refined grains for reducing
inflammation (indexed by C-reactive protein - CRP) and
abdominal fat.42 Importantly, both treatments reduced
cardiovascular disease (CVD) risk factors. A counter-argument
to these results might be that weight loss that was the primary
agent in CVD risk improvement, rather than grains per se.
Nevertheless, grain consumption – whether whole or refined –
did not prevent these improvements from occurring under
dieting conditions.
In a 6-week crossover study that did not involve weight loss,
Andersson et al found that moderately overweight subjects who
added either whole or refined grain products to their habitual
diets experienced no significant change in glucose control, lipids
blood pressure, antioxidative activity, biomarkers of
inflammation, or fibrinolytic activity. Though this study is
limited by its short duration and small number of subjects, it still
showed that the adding 3-4 small servings of wheat-based
products to a pre-existent set of dietary habits had neutral
effects, regardless of whether they’re whole or refined.
One of the better-designed intervention studies on this topic thus
far is a recent one by Tighe et al,45 which had a larger sample
than Katcher et al, longer duration & larger sample than
Andersson et al, and overall better dietary control. Tighe et al
compared the effects of a control diet (refined foods), a wheat
treatment (3 servings), and a wheat + oats treatment (1 serving
of wheat, 2 servings of oats). None of the treatments affected
markers of inflammation, but improvements in blood pressure
and pulse pressure were seen in both whole grain groups. Unlike
[Back to Contents] Page 3
that of Andersson et al’s study, this protocol was not designed to
induce weight loss.
In another recent (longer & larger) trial by Brownlee et al, an
increased consumption of various types of whole grains had no
significant effect on any of the risk factors assessed, including
inflammation.46 Once again, this protocol was not hypocaloric.
Therefore, based on the outcomes of the limited controlled
research thus far, any ‘special’ health effects from whole grain
consumption might be limited to dieting conditions.
In study on its way to press as of this writing, Guevara-Cruz et al
compared the effect of a food supplement containing 7g
dehydrated nopal, 4g chia seeds, 20g oats, 32 g soy protein, 1g
flavoring, and 0.02g Splenda with a placebo containing 30 g
calcium caseinate, 30g maltodextrin, 1g flavoring, and 0.02g
Splenda.47 Subjects with the metabolic syndrome were put on
moderately hypocaloric diets, and the supplements were
consumed twice per day. Both groups lost weight, but only the
experimental treatment decreased triacylglycerol levels, CRP
(indicating decreased inflammation), and improved glucose
tolerance. Since the supplement was a mix of ingredients, it’s
impossible to know the relative contribution of each to the
beneficial effects seen. However, it’s clear that the oat content,
which comprised a significant proportion of the supplement, did
not suppress its anti-inflammatory action.
Collectively, none of these trials indicate an inflammatory effect
of grain consumption.
“Gluten intolerance is widespread, and mainstream science is
in denial of it.”
Celiac disease (CD) is a gluten-dependent autoimmune disorder
of the small intestine. It’s still poorly understood and difficult to
diagnose. There are 8-10 different assays available to diagnose
and monitor CD. There’s ongoing controversy over which of
these tests are best for screening versus confirming the presence
of the disease, as well as which isotypes of the various
antibodies should be used in the panels. Given this, it’s not
surprising that estimates of CD prevalence range widely, from
0.3-1.2%.48 The diagnostic difficulty of CD only adds to the
uncertainty of the prevalence of gluten intolerance (also called
non-celiac gluten sensitivity, NCGS or GS). GS is characterized
by CD-like symptoms such as abdominal pain, discomfort, or
bloating as a result of wheat ingestion despite the absence of any
indication of CD on standard immunological tests.
In the recent past, GS was dismissed by the scientific community
as a quack diagnosis. It probably didn’t help that going gluten-
free has been a popular trend among hypochondriacs and neo-
hippies. However, GS is beginning to gain serious scientific
consideration. In a recent review, Bizzaro et al present clinical,
laboratory, and experimental evidence that GS and CD are
distinctly separate entities.48 The authors admit that GS also
lacks definitive diagnostic criteria, so here is their practical
recommendation for identifying it:
“Until now, in the absence of one or more specific markers,
once CD has been excluded, the best available test for
diagnosing GS is the “gold standard” of food sensitivity
testing, e.g., gluten elimination diet for 2-3 months. If, with
Alan Aragon’s Research Review – October 2011
the gluten-free diet, remission of symptoms is obtained, a
definitive demonstration of GS can be counted if the
symptoms reappear upon open challenge (gluten
reintroduction).”
Grains that contain gluten are wheat (including spelt, durum,
semolina, bulgur, kamut, faro), barley, rye, and triticale. Oats are
an inherently gluten-free grain, but still can be contaminated by
shared processing means with other gluten-containing grains.49
The Whole Grains Council lists the following companies
catering to those seeking uncontaminated oats: Bob’s Red Mill,
Cream Hill Estates, GF Harvest, Avena Foods, Legacy Valley,
and Gifts of Nature.
“Grains contain lectins, which do all kinds of damage.”
Lectins are carbohydrate-binding proteins that are ubiquitous in
the plant kingdom. Most plants contain one or more type of
lectin. The concern with lectins is that some types may have
evolved as a toxic defense against threats to survival of the plant
species. Their effect on humans ranges from harmless to
dangerous. Lectins have a surprisingly wide range of uses. An
interesting factoid is that a particular subunit of a lectin called
risin, found in the castor bean plant, is being tested for cancer
treatment due to its ability to enter cells through endocytosis and
completely block protein synthesis.50
Grains, legumes, and even vegetables in the family solanaceae
(also called nightshades) such as potatoes and tomatoes have
received some pretty mean scrutiny due to the lectins they
contain. This includes allegations of these lectins causing
increased gut permeability by binding surface glycans of the
epithelial cells, disrupting the intestinal barrier and impairing
immunological function. A recent review by Carrera-Bastos et al
discusses research showing that a lectin in wheat called wheat
germ agglutinin (WGA) can bind insulin and leptin receptors,
which in turn can cause insulin and leptin resistance.51 This has
the potential to precipitate or exacerbate symptoms of the
metabolic syndrome.
While this all sounds very menacing, the data supporting these
concerns is far from definitive. Frankly, it’s not very compelling.
It’s largely speculative since it’s based primarily on animal
models and in vitro data. To their credit, the authors of this anti-
Neolithic article swallow their pride and admit the following
despite its lack of support for their cause: 51
“Unfortunately, the effects of lectins and saponins on
intestinal permeability, endotoxemia, and inflammation have
been poorly studied in humans to allow us to draw significant
conclusions.”
Controlled trials showing (potentially) adverse effects
There are 2 trials worth reviewing, and I’m giving them their
own section because they are exceptions to the rule. First up is a
relative oldie (done in 1989), but a standout nonetheless.52 The
DART (Diet And Reinfarction Trial) by Burr et al found that
subjects advised to eat fatty fish had a 29% reduction in 2 year
all-cause mortality compared with those did not receive this
advice. And now for the kicker - subjects advised to increase
fiber intake had a slightly higher mortality than their
[Back to Contents] Page 4
counterparts, though not to a statistically significant degree.
Ness et al did a 10-year follow-up study of DART and found
that the increases in fish and fiber intake had significantly
diminished but were still in present.53 It was concluded that fat
and fiber advice had no clear effect on coronary or all-cause
mortality. To quote the authors:
“The fact that the initial increased risk of coronary death
and deaths from all causes in men who were given advice to
eat more cereal fibre was not maintained suggests that
increased fibre intake is not harmful.”
Next up is a study by Jenkins et al, who found that adding cereal
fiber (wheat bran, 19 g/day) did not affect glycemic control or
standard risk factors for coronary heart disease.54 The kicker
here was that the increased fiber treatment slightly raised levels
of oxidized LDL, which is considered to be atherogenic. In a
commentary of this trial, Jacobs & Steffen point out a staggering
flaw: 44 of the 67 people who began the study dropped out,
increasing the possibility of skewed outcomes resulting from
incomplete/unaccounted data.55 However, Jacobs concedes that
wheat fiber appears to have limited effectiveness compared to
brans that are high in soluble fiber like oat bran. Incidentally,
oats have the strongest support from controlled trials for their
beneficial effect on heart disease risk factors.8
Summary points
ƒ Saying that all grains are unhealthy and should be avoided
is just as biased as saying that all grains are superfoods that
should be consumed in massive amounts by all. Both
extremes are overzealous and unobjective.
ƒ Claiming that grains cause obesity is false on many counts.
Obesity is a multifactorial condition that is ultimately
attributable to the accumulation of an unused energy
surplus over time (which is governed by behavioral,
hormonal, & genetic factors); it’s not attributable to any
particular type of food.
ƒ Grains contain antinutrients such as phytates and oxalates,
but so do most commonly consumed plant foods. Fiber-
mediated reductions in nutrient bioavailability are of
questionable functional significance, especially in the case
of varied, omnivorous diets in developed countries with
abundant food supplies.
ƒ The idea that grains are the cause of the vitamin D
deficiency pandemic is an oversimplification based on
insufficient evidence. The high prevalence of vitamin D
deficiency is based on a combination of factors. An
important one is excess bodyfat’s ability to impair vitamin
D3 bioavailability.
ƒ Observational & interventional research has consistently
shown that grains have no significant impact on
inflammation. The idea that inflammation is the root of all
disease is an oversimplification, but oh is it catchy.
ƒ Estimates of celiac disease (CD) prevalence range from
0.3-1.2%. Gluten sensitivity (GS) shares similar symptoms
with CD, but does not register as CD in clinical tests, and
is often (mistakenly) assumed to not exist. An emerging
body of evidence indicates that GS is a indeed a separate
condition from CD.
Alan Aragon’s Research Review – October 2011
ƒ Lectins have widely variable impacts on health. The lectins
in grains (wheat in particular) & legumes have been
alleged to cause a host of diseases resulting from increased
gut permeability. These concerns have an interesting
hypothetical framework, but lack support from controlled
human trials.
ƒ Wheat appears to be the most problematic and least
protective of the grains, so it should be the first choice for
moderation, minimization, or in some cases where it’s
warranted – elimination.
Conclusions
In response to the title of this article, I would say that all of the
claims should be taken seriously enough to investigate the
evidence behind them. The problem is, all of those claims
(except for the emerging legitimacy of non-celiac gluten
intolerance and the equivocal performance of wheat) have not
earned solid scientific support. But let’s for a moment give the
litigators the benefit of the doubt, and assume there’s a certain
amount of risk from consuming grains (& the other usual
suspects). Did it ever occur to them that despite the potential
negatives, the positives are strong enough to provide a net
benefit to physical & psychological health for those who lead
active, balanced lives? The current evidence says yes.
An important point to consider is that well-constructed diets
draw their carbohydrate allotment from a variety of sources, and
their total energy content is rarely dominated by grains in the
first place. The anti-grain camp’s black & white assumptions
often function as arguments against the nonexistent. Another big
message that needs to sink in is that grains are not the health
treasures that the agricultural industry paints them out to be. By
the same token, they are not the poison-dipped darts that
evidence-ignoring alarmists insist they are. Grains are, for the
most part, neutral. Their goodness or badness depends on whose
mouth they land in, and how aware that person is.
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minerals from vegetarian diets. Am J Clin Nutr. 2003
Sep;78(3 Suppl):633S-639S. [Medline]
30. Weaver CM, et al. Human calcium absorption from whole-
wheat products. J Nutr. 1991 Nov;121(11):1769-75.
[Medline]
31. Andersson H, et al. The effects of breads containing similar
amounts of phytate but different amounts of wheat bran on
calcium, zinc and iron balance in man. Br J Nutr. 1983
Nov;50(3):503-10. [Medline]
32. Sandström B, et al. A high oat-bran intake does not impair
zinc absorption in humans when added to a low-fiber animal
protein-based diet. J Nutr. 2000 Mar;130(3):594-9.
[Medline]
33. Holick MF. The vitamin D deficiency pandemic and
consequences for nonskeletal health: mechanisms of action.
Mol Aspects Med. 2008 Dec;29(6):361-8. Epub 2008 Sep 2
[Medline]
34. Batchelor AJ, Compston JE. Reduced plasma half-life of
radio-labelled 25-hydroxyvitamin D3 in subjects receiving a
high fiber diet. Br J Nutr. 1983 Mar;49(2):213-6. [Medline]
35. Holick MF, Chen TC. Vitamin D deficiency: a worldwide
problem with health consequences. Am J Clin Nutr. 2008
Apr;87(4):1080S-6S. [Medline]
36. Foss YJ. Vitamin D deficiency is the cause of common
obesity. Med Hypotheses. 2009 Mar;72(3):314-21. Epub
2008 Dec 2. [Medline]
37. Wortsman J, et al. Decreased bioavailability of vitamin D in
obesity. Am J Clin Nutr. 2000 Sep;72(3):690-3. [Medline]
38. Anderson AL, et al. Dietary patterns, insulin sensitivity and
inflammation in older adults. Eur J Clin Nutr. 2011 Sep 14.
doi: 10.1038/ejcn.2011.162. [Epub ahead of print]
[Medline]
39. Qi L, et al. Whole-grain, bran, and cereal fiber intakes and
markers of systemic inflammation in diabetic women.
Diabetes Care. 2006 Feb;29(2):207-11. [Medline]
[Back to Contents] Page 6
40. Masters RC, et al. Whole and refined grain intakes are 55. Jacobs DR Jr, Steffen LM. Wheat bran, whole grain, and
related to inflammatory protein concentrations in human food synergy. Diabetes Care. 2002 Sep;25(9):1652-3.
plasma. J Nutr. 2010 Mar;140(3):587-94. [Medline] [Medline]
41. Lutsey PL, et al. Whole grain intake and its cross-sectional
association with obesity, insulin resistance, inflammation,
diabetes and subclinical CVD: The MESA Study. Br J Nutr.
2007 Aug;98(2):397-405. Epub 2007 Mar 29. [Medline]
42. Jensen MK, et al. Whole grains, bran, and germ in relation
to homocysteine and markers of glycemic control, lipids,
and inflammation 1. Am J Clin Nutr. 2006 Feb;83(2):275-
83. [Medline]
43. Katcher HI, et al. The effects of a whole grain-enriched
hypocaloric diet on cardiovascular disease risk factors in
men and women with metabolic syndrome. Am J Clin Nutr.
2008 Jan;87(1):79-90. [Medline]
44. Andersson A, et al. Whole-grain foods do not affect insulin
sensitivity or markers of lipid peroxidation and
inflammation in healthy, moderately overweight subjects. J
Nutr. 2007 Jun;137(6):1401-7. [Medline]
45. Tighe P, et al. Effect of increased consumption of whole-
grain foods on blood pressure and other cardiovascular risk
markers in healthy middle-aged persons: a randomized
controlled trial. Am J Clin Nutr. 2010 Aug 4. [Epub ahead
of print] [Medline]
46. Brownlee IA, et al. Markers of cardiovascular risk are not
changed by increased whole-grain intake: the WHOLEheart
study, a randomised, controlled dietary intervention. Br J
Nutr. 2010 Jul;104(1):125-34. Epub 2010 Mar 23.
[Medline]
47. Guevara-Cruz M, et al. A dietary pattern including nopal,
chia seed, soy protein, and oat reduces serum triglycerides
and glucose intolerance in patients with metabolic
syndrome. J Nutr. 2011 Nov 16. [Epub ahead of print]
[Medline]
48. Bizzaro N, et al. Cutting-Edge Issues in Celiac Disease and
in Gluten Intolerance. Clin Rev Allergy Immunol. 2010 Dec
23. [Epub ahead of print] [Medline]
49. Thompson T. Gluten contamination of commercial oat
products in the United States. N Engl J Med. 2004 Nov
4;351(19):2021-2. [Medline] [NEJM – go here to view the
comparison chart].
50. Ajit Varki, et al. Chapter 30, Plant Lectins. Essentials of
Glycobiology, 2nd Edition. Cold Spring Harbor (NY): Cold
Spring Harbor Laboratory Press; 2009. [NCBI]
51. Carrera-Bastos P, et al. The western diet and lifestyle and
diseases of civilization. Research Reports in Clinical
Cardiology. 2001;2:15-35. [Dovepress]
52. Burr ML, et al. Effects of changes in fat, fish, and fibre
intakes on death and myocardial reinfarction: diet and
reinfarction trial (DART). Lancet. 1989 Sep
30;2(8666):757-61. [Medline]
53. Ness AR, et al. The long-term effect of dietary advice in
men with coronary disease: follow-up of the Diet and
Reinfarction trial (DART). Eur J Clin Nutr. 2002
Jun;56(6):512-8. [Medline]
54. Jenkins DJ, et al. Effect of wheat bran on glycemic control
and risk factors for cardiovascular disease in type 2
diabetes. Diabetes Care. 2002 Sep;25(9):1522-8. [Medline]

Alan Aragon’s Research Review – October 2011 [Back to Contents] Page 7


The effects of low and high glycemic index foods on
exercise performance and beta-endorphin responses.
Jamurtas AZ, et al. J Int Soc Sports Nutr. 2011 Oct 20;8(1):15.
[Epub ahead of print] [Medline]
PURPOSE: The aim of this study was to examine the effects of
the consumption of foods of various glycemic index values on
performance, beta-endorphin levels and substrate (fat and
carbohydrate) utilization during prolonged exercise. DESIGN:
Eight untrained healthy males underwent, in a randomized
counterbalanced design, three experimental conditions under
which they received carbohydrates (1.5 gr . kg-1 of body weight)
of low glycemic index (LGI), high glycemic index (HGI) or
placebo. Food was administered 30 min prior to exercise.
Subjects cycled for 60 min at an intensity corresponding to 65%
of VO2max, which was increased to 90% of VO2max, then they
cycled until exhaustion and the time to exhaustion was recorded.
Blood was collected prior to food consumption, 15 min prior to
exercise, 0, 20, 40, and 60 min into exercise as well as at
exhaustion. Blood was analyzed for beta-endorphin, glucose,
insulin, and lactate. RESULTS: The mean time to exhaustion
did not differ between the three conditions. There was a
significant interaction in glucose and insulin response (P < 0.05)
with HGI exhibiting higher values before exercise. beta-
endorphin increased significantly (P < 0.05) at the end of
exercise without, however, a significant interaction between the
three conditions. Rate of perceived exertion, heart rate,
ventilation, lactate, respiratory quotient and substrate oxidation
rate did not differ between the three conditions.
CONCLUSION: The present study indicates that ingestion of
foods of different glycemic index 30 min prior to one hour
cycling exercise does not result in significant changes in exercise
performance, beta-endorphin levels as well as carbohydrate and
fat oxidation during exercise. SPONSORSHIP: None listed.
Study strengths
This investigation is novel since it’s perhaps the first to examine
the effects of varying glycemic index (GI) on beta-endorphins
along with substrate utilization during endurance exercise. The
relevance of beta-endorphin levels is that they may be a part of
the poorly understood mechanism behind the suppression of
glucose decline during prolonged exercise resulting from low-GI
carbohydrate ingestion prior to the bout. A crossover design was
implemented so that all subjects underwent each experimental
treatment. This helped alleviate the statistical limitation of a
small sample size (8 subjects). Carbohydrate intake in the days
prior to testing was standardized (6-8g/kg) in order to minimize
intersubject variations in glycogen levels. Dietary intake was
tracked & analyzed with software.
Study limitations
Aside from the small number of subjects, they were also
untrained, which potentially limits the applicability of the results
to this population. Another limitation was the use of a time-to-
exhaustion (TTE) protocol, rather than a time trial with a fixed
amount of work to be completed in the fastest time possible. The
latter protocol is more reflective of actual race conditions. The
authors acknowledge that the abrupt intensity increase (to 90%
Alan Aragon’s Research Review – October 2011
VO2max to exhaustion after an hour at 65% VO2max) might not
accurately show performance and metabolic responses in trained
competitors. Also, the results might be limited to the test foods,
which were dried apricots for the low-GI treatment, and white
bread with strawberry jam for the high-GI treatment. A final
limitation is that the absence of protein and fat in these test
meals do not reflect typical pre-event nutrition. As illustrated in
recent research by Dodd et al which showed that differential
glycemic effects of otherwise isolated carbohydrate sources
greatly diminish within the context of a typical mixed meal.1
Comment/application
The main practical finding, depicted above, is the lack of
significant difference in endurance capacity between the high &
low-GI treatments. I chose to relay this particular graph showing
the individual results, because look at the outlying performance
of subject #6. It looks like someone should seriously consider
taking up endurance competition! This lack of performance
difference adds to the mixed outcomes seen in previous trials
comparing the effect of high & low-GI pre-exercise meals. To
quote a recent review by Donaldson et al:2
“Athletes are commonly instructed to consume low-GI (LGI)
carbohydrate (CHO) before exercise, but this recommendation
appears to be based on the results of only a few studies, whereas
others have found that the GI of CHO ingested before exercise
has no impact on performance.”
Donaldson et al concluded that until further well-designed
studies can provide sufficient weight of evidence in favor of
specific GI-based recommendations for endurance athletes, a
focus on total amount of carbohydrate is warranted. A scarcely
studied area is the effect of GI on high-intensity, intermittent
exercise - which is more characteristic of team sports rather than
individual endurance sports. Investigating this question, Little et
al recently compared the effect of low-GI (lentil) and high-GI
(potato & egg white) pre-exercise meal.3 Despite a lower rating
of perceived exertion (RPE) in the low-GI treatment, no
significant differences were seen in the distance covered during
a 90-min high-intensity intermittent running test. Notably, the
test meals resembled mixed meals consumed in the real world.
Back to the present study, an interesting finding was a lack of
difference in respiratory quotient (RQ – indicating the relative
oxidation of carbohydrate & fat) despite significantly greater
insulin elevations in the high-GI treatment. Furthermore, beta-
endorphin responses did not differ between treatments. I’ll make
the bold prediction that in future studies, GI will continue to be a
factor that fails to consistently influence training performance.
[Back to Contents] Page 8
Eating frequency is higher in weight loss maintainers
and normal-weight individuals than in overweight
individuals.
Bachman JL, et al. J Am Diet Assoc. 2011 Nov;111(11):1730-4.
[Medline]
BACKGROUND/PURPOSE: Eating frequency has been
negatively related to body mass index (BMI). The relationship
between eating frequency and weight loss maintenance is
unknown. This secondary analysis examined eating frequency
(self-reported meals and snacks consumed per day) in weight
loss maintainers (WLM) who had reduced from
overweight/obese to normal weight, normal weight (NW)
individuals, and
overweight (OW)
individuals. METHODS:
Data collected July 2006
to March 2007 in
Providence, RI, included
three 24-hour dietary
recalls (2 weekdays, 1
weekend day) analyzed
using Nutrient Data
System for Research
software from 257 adults
(WLM n=96, 83.3%
women aged 50.0±11.8
years with BMI 22.1±1.7;
NW n=80, 95.0% women
aged 46.1±11.5 years with
BMI 21.1±1.4; OW n=81, 53.1% women aged 51.4±9.0 years
with BMI 34.2±4.1) with plausible intakes. Participant-defined
meals and snacks were ≥50 kcal and separated by more than 1
hour. RESULTS: Self-reported physical activity was highest in
WLM followed by NW, and then OW (3,097±2,572 kcal/week,
2,062±1,286 kcal/week, and 785±901 kcal/week, respectively;
P<0.001). Number of daily snacks consumed was highest in
NW, followed by WLM, and then OW (2.3±1.1 snacks/day,
1.9±1.1 snacks/day, and 1.5±1.3 snacks/day, respectively;
P<0.001). No significant group differences were observed in
mean number of meals consumed (2.7±0.4 meals/day).
CONCLUSIONS: Eating frequency, particularly in regard to a
pattern of three meals and two snacks per day, may be important
in weight loss maintenance. SPONSORSHIP: This research
was supported by grants nos. R01DK066787 and R01DK074721
from the National Institutes of Health.
Study strengths
The topic of eating frequency is still under-investigated despite
its widespread level of interest in clinical & fitness circles, so
any research in this vein is a welcome surprise. A strong design
aspect was the inclusion of not just overweight & normal-weight
subjects, but also weight loss maintainers. This study was the
first yet to compare those groups in the context of eating
frequency. As is common with observational studies, this one
examined a larger number of subjects than typically seen in
controlled interventions. A nice touch was the examination of
the relationships between eating frequency variables, energy
intake, and BMI – even if the data is mainly inferential in nature.
Alan Aragon’s Research Review – October 2011
Study limitations
The most profound limitation of the present study is that its
cross-sectional design is observational rather than interventional.
This renders it impossible to demonstrate a causal relationship
between eating frequency and bodyweight; it can only draw
associations, which ultimately are subject to confirmation by
controlled interventions. Dietary intake & physical activity were
self-reported, which them subject to considerable inaccuracy.
Data was collected retrospectively from two separate studies,
which increases the potential for unaccounted differences
between the groups.
Comment/application
As seen above, the primary finding was that although no
difference was seen in the number of main meals, normal-weight
subjects consumed the highest number of daily snacks, weight
loss maintainers came in second, while overweight subjects
consumed the lowest number of daily snacks. Unsurprisingly,
overweight subjects had the highest energy intake and the lowest
physical activity (785 kcal/week). Interestingly – and not too
surprisingly either – weight loss maintainers had the highest
physical activity level (3097 kcal/week).
One thing the authors diligently point out is that the difference in
snacking between overweight subjects and the other 2 groups
was relatively small - about 0.5 to 0.8 snacks/per day. The
potential to blow this study’s title way out of proportion is
enormous, considering that we’re talking about a difference of
less than one snack per day that was associated with the
differences seen. Proponents of the typical 6-a-day meal pattern
common in fitness/wellness circles are almost certain to cite this
study as back-up for their stance. However, the authors
themselves said this “…does not suggest a so-called grazing
(eating every 2 to 3 hours) style of eating frequency in those with
lower BMI. For WLM and NW, the eating pattern was
consuming approximately three meals plus two snacks per day.”
On the note of observational research, the present study looked
at a relatively narrow slice of the general population. A recent
systematic review by Mesas et al examined 153 studies (73 of
which were published 2008 or later) and find no consistent
relationship between excess weight and a host of factors
including skipping breakfast, eating frequency, snacking, and
consumption of large food portions.4
[Back to Contents] Page 9

Effects of 28 days of resistance exercise while
consuming commercially available pre- and post-
workout supplements, NO-Shotgun and NO-
Synthesize on body composition, muscle strength and
mass, markers of protein synthesis, and clinical safety
markers in males.
Spillane M, et al. Nutr Metab (Lond). 2011 Nov 3;8(1):78.
[Epub ahead of print] [Medline]
OBJECTIVE: The effects of 28 days of heavy resistance
training while ingesting the pre- and post-workout supplements,
NO-Shotgun(R) and NO-Synthesize(R) were determined on
body composition, muscle strength and mass, markers of protein
synthesis, and clinical safety markers. METHODS: Nineteen
non-resistance-trained males participated in a resistance training
program 4 times/week for 28 days while either ingesting 27
g/day of carbohydrate (CARB) or NO-Shotgun(R) 30 min pre-
exercise and 27 g/day of carbohydrate or NO- Synthesize(R) 30
min post-exercise (NOSS). Data were analyzed with separate 2 x
2 ANOVA (p < 0.05). Results: RESULTS: Total body mass
was increased in both groups (p = 0.001), but not different
between groups. Fat mass was unchanged with CARB, but
NOSS decreased fat mass (p = 0.026). Both groups increased
fat-free mass (p = 0.001); however, the increases were greater
with NOSS (p = 0.023). NOSS underwent greater increases in
upper-body (p = 0.023) and lower-body (p = 0.035) strength than
CARB. Myofibrillar protein significantly increased in both
groups (p = 0.041), with NOSS being greater than CARB (p =
0.049). All of the MHC isoforms were significantly increased in
both groups; however, NOSS was greater than CARB for MHC
1 (p = 0.013) and MHC 2A (p = 0.046). All of the myogenic
regulatory factors were significantly increased in both groups;
however, NOSS was greater than CARB for Myo-D (p = 0.038)
and MRF-4 (p = 0.001). For the whole blood and serum clinical
chemistry markers, all variables remained within normal clinical
ranges. CONCLUSIONS: Heavy resistance training for 28
days, with NO-Shotgun(R) and NO-Synthesize(R) ingested
before and after exercise, respectively, significantly improved
body composition and increased muscle mass and performance
without abnormally impacting any of the clinical chemistry
markers. SPONSORSHIP: This study was supported by an
independent research grant from VPX (Davie, FL) awarded to
Baylor University.
Study strengths
Free weight bench press and angled leg press was used for
strength testing. While the use of lab-based instruments such as
isokinetic dynamometers, etc can measure force output to a finer
degree, they may not always accurately reflect the performance
of gym-based, or free weight movements. Dietary intake was
analyzed with software. Body composition was assessed with
dual X-ray absorptiometry (DXA).
Study limitations
The authors do not specify the actual ingredient breakdown of
either of the products, so I’ll link them here (NO-Shotgun, NO-
Synthesize). Since the supplements are “proprietary blends,”
exact doses of each ingredient within the mixture are not
specified. This is a tactic supplement companies use to cut costs
while still maximizing the number of ingredients on the label,
Alan Aragon’s Research Review – October 2011
which gives customers a greater impression that the product is
loaded with goodies. As the authors acknowledge, “attempting
to isolate which specific ingredient has the greatest impact on
our outcome measures is not feasible.” While the subjects were
recreationally active, they were still described as “non-resistance
trained,” so effects might be less apparent in the well-trained
population. Another limitation is the relatively short (28-day)
trial duration. Perhaps the most important limitation was a
failure to match macronutrition between the groups. More on
this in a second.
Comment/application
The NO-Shotgun/NO-Synthesize (NOSS) treatment significantly
outperformed the carbohydrate comparator for every strength
and body composition parameter except total bodyweight &
body water (which were not significantly different from baseline
in either group). Collectively, NOSS’s main ingredients are
casein, whey, BCAA, creatine, citrulline malate, arginine, beta-
alanine, histidine, lysine, phenylalanine, threonine, histidine,
methionine, and tyrosine. Aside from the protein, creatine and
beta-alanine have the strongest evidence bases. Of note, in
addition to creatine monohydrate (CM), the products contain
novel forms of creatine (including taurinate, gluconate, & ethyl
ester). Again, this mainly serves to wow the consumer into
thinking something special is being consumed. However, a
recent review by Jäger et al concluded the following:5 “…there
is little to no evidence supporting marketing claims that these
newer forms of creatine are more stable, digested faster, and
more effective in increasing muscle creatine levels and/or
associated with fewer side effects than CM.”
An easily overlooked design shortcoming is that each serving of
the pre & post-exercise supplement contained 20 g protein. By
the end of the trial, dietary protein intake of the groups did not
differ significantly (1.31g/kg in the carb group, 1.25g/kg in the
NOSS group). However, as I confirmed with one of the research
assistants at Baylor University, the table above reported dietary
intake, and did not include supplemental intake. This is a crucial
detail, since the addition of 40 g protein taken 4 times per week
(training days) & 20 g 3 times per week (off days) increases the
average daily protein intake by 31.42 g, which hikes the protein
intake of the NOSS group to 1.63 g/kg. Unlike that of the carb
group, the NOSS group’s protein intake lands squarely in the
middle of what’s considered optimal for strength and size
gains.6,7 A more fair & honest assessment of the product’s
“special effects” would be to compare it with a simple (& far
cheaper) whey/creatine combo, in which case I would bet
against a meaningful difference.
[Back to Contents] Page 10
Ingestion of 10 grams of whey protein prior to a single
bout of resistance exercise does not augment
Akt/mTOR pathway signaling compared to
carbohydrate.
Cooke MB, et al. J Int Soc Sports Nutr. 2011 Nov 8;8(1):18.
[Epub ahead of print] [Medline]
BACKGROUND: This study examined the effects of a whey
protein supplement in conjunction with an acute bout of lower
body resistance exercise, in recreationally-active males, on
serum insulin and insulin like growth factor 1 (IGF-1) and
Akt/mTOR signaling markers indicative of muscle protein
synthesis: insulin receptor substrate 1 (IRS-1), AKT, mammalian
target of rapamycin (mTOR), p70S6 kinase (p70S6K) and 4E-
binding protein 1 (4E-BP1). METHODS: In a randomized,
double-blind, cross-over design, 10 males ingested 1 week apart,
either 10 g of whey protein (5.25 g EAAs) or carbohydrate
(maltodextrose), 30 min prior to a lower-body resistance
exercise bout. The resistance exercise bout consisted of 4 sets of
8-10 reps at 80% of the one repetition maximum (RM) on the
angled leg press and knee extension exercises. Blood and muscle
samples were obtained prior to, and 30 min following
supplement ingestion and 15 min and 120 min post-exercise.
Serum and muscle data were analyzed using two-way ANOVA.
RESULTS: No significant differences were observed for IGF-1
(p > 0.05). A significant main effect for Test was observed for
serum insulin (p<0.01) at 30 min post-ingestion and 15 and 120
min post-exercise, with no Supplement x Test interaction (p >
0.05). For the Akt/MTOR signaling intermediates, no significant
Supplement x Test interactions were observed (p > 0.05).
However, significant main effects for Test were observed for
phosphorylated concentrations of IRS, mTOR, and p70S6K, as
all were elevated at 15 min post-exercise (p < 0.05).
Additionally, a significant main effect for Test was noted for 4E-
BP1 (p < 0.05), as it was decreased at 15 min post-exercise.
CONCLUSIONS: Ingestion of 10 g of whey protein prior to an
acute bout of lower body resistance exercise had no significant
preferential effect compared to carbohydrate on systemic and
cellular signaling markers indicative of muscle protein synthesis
in untrained individuals. SPONSORSHIP: This work was
supported by Glanbia Nutritionals, Twin Falls, ID, USA and the
Exercise and Biochemical Nutrition Laboratory at Baylor
University.
Study strengths
Anabolic effects of protein intake surrounding training is still an
under-studied area with conflicting outcomes, so additional
research in this area is welcomed. A crossover design helped
alleviate the compromised statistical power of the small number
of subjects. To control dietary variables, 2-day food & fluid
intake prior to testing was recorded and analyzed with software.
Study limitations
The authors responsibly acknowledged a host of limitations (this
isn’t always done, nor is it required). Protein synthesis was not
directly assessed; only indirect molecular markers were
measured. Also, no treatment-free control was used as a means
to directly compare with carbohydrate & whey. Another
limitation was the lack of other doses compared with 10 g.
Establishing a dose-response curve with the addition of a 20, 30,
and 40-g dose would be ideal, but not apparently this is not
Alan Aragon’s Research Review – October 2011
feasible, since I haven’t seen it done in protein studies. In a rare
moment of diligence, the authors admit that the study’s focus on
effects in the acute postexercise period excludes the certainty of
effects at later points (6, 24, or 48 hours) which might be more
reliable indicators of MPS. I would add to this that even 48-hour
effects still leave training performance or body composition
effects over weeks and months open to speculation. Non-
acute/longer-term trials are only a handful, but they are the ones
that hold the most weight of consideration. Thus far, the non-
acute evidence is insufficient for recommending specific protein
dosing & timing regimes relative to training, as long as total
daily needs are met (see the December 2010 issue for review).
Also, the results may be limited to the volume of the training
bout (8 sets total, 8-10 reps at 80% of 1RM). A final limitation is
that the subjects used had not been engaged in regular resistance
training for at least 1 year prior to the study, so the outcomes
might not be applicable for more experienced trainees.
Comment/application
The main finding of the present study was a lack of postexercise
difference in IGF-1, insulin, and Akt/mTOR signaling between
the protein and carbohydrate treatments – collectively suggesting
a lack of differential effect on muscle protein synthesis. In the
above chart, I circled the insulin values because they’re
substantially higher than seen in previous research. Tang et al
reported an insulin peak at just under 30 µIU/ml at the 30-minute
mark, and this was from 10 g whey plus 21 g fructose.8
However, this was ingested postexercise, whereas the present
study’s treatment was taken 30 minutes pre-exercise. Staples et
al saw insulin peak at roughly 19 µIU/ml with 25 g whey,9
which is more than double the present study’s dose, eliciting less
than half the insulin peak. But again, this was ingested
postexercise. The relevance here is that both treatments in the
present study caused insulin elevations within the range known
to maximally inhibit muscle protein breakdown (15-30 µIU/ml).9
The insulin peaks occurred at the start of the training bout, and
insulin was still significantly elevated 15 minutes postexercise.
An important note is that the lack of Akt/mTOR signaling does
not necessarily equate to an absence of muscle protein synthesis.
For example, Tang et al’s postexercise dosing of 10 g whey + 21
g fructose stimulated muscle protein synthesis to a greater
degree than the carb-only treatment (10g maltodextrin + 21 g
fructose), and this occurred despite a lack of mTOR activation.8
[Back to Contents] Page 11
 the typical range in hormone replacement therapy is roughly
100-300 mg/week. The authors admitted that their chosen dose
The effects of supraphysiologic doses of testosterone (600 mg/week) was the highest yet administered in any study of
on muscle size and strength in normal men. athletic performance. The point is, while the dose used in this
Bhasin S, et al. N Engl J Med. 1996 Jul 4;335(1):1-7. [Medline] study is indeed supraphysiological, it’s only a snippet of the
range used by competitive & recreational athletes (who often
BACKGROUND: Athletes often take androgenic steroids in an stack multiple anabolic/androgenic drugs). Another potential
attempt to increase their strength. The efficacy of these limitation is the novice-oriented training protocol, which was a
substances for this purpose is unsubstantiated, however. full-body routine based on compound movements, with a set
METHODS: We randomly assigned 43 normal men to one of number of repetitions (6 per set), regardless of the prescribed
four groups: placebo with no exercise; testosterone with no load intensity, which varied between 70, 80, & 90% of 1 RM for
exercise; placebo plus exercise; and testosterone plus exercise.
each of the thrice-weekly workouts. A final limitation is that the
The men received injections of 600 mg of testosterone enanthate
length of the study still leaves open questions regarding the
or placebo weekly for 10 weeks. The men in the exercise groups
long-term safety (& other effects) of this dose of testosterone.
performed standardized weight-lifting exercises three times
weekly. Before and after the treatment period, fat-free mass was Comment/application
determined by underwater weighing, muscle size was measured
by magnetic resonance imaging, and the strength of the arms and
legs was assessed by bench-press and squatting exercises,
respectively. RESULTS: Among the men in the no-exercise
groups, those given testosterone had greater increases than those
given placebo in muscle size in their arms (mean [+/-SE] change
in triceps area, 424 +/- 104 vs. -81 +/- 109 square millimeters; P
< 0.05) and legs (change in quadriceps area, 607 +/- 123 vs. -131
+/- 111 square millimeters; P < 0.05) and greater increases in
strength in the bench-press (9 +/- 4 vs. -1 +/- 1 kg, P < 0.05) and
squatting exercises (16 +/- 4 vs. 3 +/- 1 kg, P < 0.05). The men
assigned to testosterone and exercise had greater increases in fat-
free mass (6.1 +/- 0.6 kg) and muscle size (triceps area, 501 +/-
104 square millimeters; quadriceps area, 1174 +/- 91 square
millimeters) than those assigned to either no-exercise group, and
greater increases in muscle strength (bench-press strength, 22 +/-
2 kg; squatting-exercise capacity, 38 +/- 4 kg) than either no-
exercise group. Neither mood nor behavior was altered in any
group. CONCLUSIONS: Supraphysiologic doses of
testosterone, especially when combined with strength training,
increase fat-free mass and muscle size and strength in normal
men. SPONSORSHIP: Supported by grants from the National
Institutes of Health, General Clinical Research Center, Clinical
Research Infrastructure Initiative, and the Research Centers for
Minority Institutions.
Study strengths The main findings were that supraphysiologic doses of
testosterone increase muscular mass and strength. The results of
The use of anabolic-androgenic steroids (AAS) became publicly this study silenced the then-common doubters of the striking
prominent as early as the 1960s, with their use by German
effectiveness of AAS. A notable outcome was the 6.1 kg (13.42
athletes (mostly female) in the Olympic Games.11 The present
lb) fat-free mass gain in the AAS + exercise group (4 kg more
study is a big deal because it was the first one to properly control
than placebo + exercise), in just 10 weeks. This is substantial,
experimental variables and examine the effects of AAS in
especially when compared to the initial fat-free mass gain from
healthy humans. Protein and energy intake were standardized at
creatine supplementation, which is roughly 2 kg greater than
1.5 g/kg and 36 kcal/kg. Body composition was determined via
placebo in 12 weeks.12 Given this, it’s not a stretch to say that
hydrostatic weighing, and muscle size was determined by
magnetic resonance imaging (MRI). A standout strength of this testosterone is twice as effective as creatine for putting on lean
design was a comprehensive set of treatment arms, including a mass – at least within the timeframe mentioned.
non-training group that was administered testosterone. Particularly illustrative of the testosterone’s potency (highlighted
in the chart above) is that fat-free mass, triceps area, and
Study limitations quadriceps area were greater in the non-training AAS group than
While I’ve seen cases where significantly higher testosterone the training + placebo group. In addition, the significant strength
doses were used (over 1000 mg/week), 600 mg/week is toward gains occurring in the non-training AAS group indicate
the middle-high end of what’s commonly used by strength increased muscular functionality as opposed to purely a bloating
athletes and bodybuilders who aren’t part of extreme/more-is- effect. Another notable outcome was the lack of differences in
better camp. One athlete I personally know stays jacked as hell mood & blood lipids, with the exception of a slight drop in HDL
on a prescribed replacement dose of 250 mg/week. Anecdotally, in the exercising placebo group.
Alan Aragon’s Research Review – October 2011 [Back to Contents] Page 12
1. Dodd H, et al. Calculating meal glycemic index by using
measured and published food values compared with directly
measured meal glycemic index. Am J Clin Nutr. 2011 Aug
10. [Epub ahead of print] [Medline]
2. Donaldson CM, et al. Glycemic index and endurance
performance. Int J Sport Nutr Exerc Metab. 2010
Apr;20(2):154-65. [Medline]
3. Little JP, et al. Effect of low- and high-glycemic-index
meals on metabolism and performance during high-
intensity, intermittent exercise. Int J Sport Nutr Exerc
Metab. 2010 Dec;20(6):447-56. [Medline]
4. Mesas AE, et al. Selected eating behaviours and excess
body weight: a systematic review. Obes Rev. 2011 Sep 28.
doi: 10.1111/j.1467-789X.2011.00936.x. [Epub ahead of
print] [Medline]
5. Jäger R, Analysis of the efficacy, safety, and regulatory
status of novel forms of creatine. Amino Acids. 2011
May;40(5):1369-83. Epub 2011 Mar 22. [Medline]
6. Campbell B, et al. International Society of Sports Nutrition
position stand: protein and exercise. J Int Soc Sports Nutr.
2007 Sep 26;4:8. [Medline]
7. Wilson J, Wilson GJ. Contemporary issues in protein
requirements and consumption for resistance trained
athletes. J Int Soc Sports Nutr. 2006 Jun 5;3:7-27.
[Medline]
8. Tang JE, et al. Minimal whey protein with carbohydrate
stimulates muscle protein synthesis following resistance
exercise in trained young men. Appl Physiol Nutr Metab.
2007 Dec;32(6):1132-1138. [Medline]
9. Greenhaff PL, et al. Disassociation between the effects of
amino acids and insulin on signaling, ubiquitin ligases, and
protein turnover in human muscle. Am J Physiol Endocrinol
Metab. 2008 Sep;295(3):E595-604. [Medline]
10. Staples AW, et al. Carbohydrate does not augment exercise-
induced protein accretion versus protein alone. Med Sci
Sports Exerc. 2010 Dec 1. [Epub ahead of print]. [Medline]
11. Basaria S. Androgen abuse in athletes: detection and
consequences. J Clin Endocrinol Metab. 2010
Apr;95(4):1533-43. Epub 2010 Feb 5. [Medline]
12. Persky AM, Brazeau GA. Clinical pharmacology of the
dietary supplement creatine monohydrate. Pharmacol Rev.
2001 Jun;53(2):161-76. [Medline]

Alan Aragon’s Research Review – October 2011 [Back to Contents] Page 13


It’s time to rant about the sport of bodybuilding.
By Alan Aragon
________________________________________________________________
Why am I writing this?
I’m writing this because I’ve been a big fan of bodybuilding
since childhood. I was one of those kids who drooled over the
super hero physiques in comic books and on magazine covers.
Bodybuilding is an artform that can be finely customized to fit
the standards of the individual. In my personal view, the primary
competition is yourself, and the goal is make improvements &
maintain those improvements. However, recent conversations
with competitors along with an incident at the last Mr. Olympia
made me realize that I don’t like where the sport is headed (more
on that later).
Keep in mind, I’m fully aware that since its inception in the
1950’s, competitive bodybuilding has progressively distanced
itself from mainstream acceptance due to an increasing level of
“freakiness” of the physiques. Some people don’t consider
bodybuilding a “real” sport; they liken it to a beauty pageant or a
twisted foray into narcissism and unnecessary self-sacrifice.
While the definition of “sport” is more of a philosophical debate
than anything, I think we can all agree that bodybuilding,
defined simply as the process of gaining muscle and losing fat,
can improve physical and psychological health, as long as
extreme measures are avoided.
Conflict with moderation
Still, there will always be those who fail to see the point in
pursuing any endeavour unless it’s taken to extremes. After all,
where’s the fun in moderation? And since when have sports
been about restraining or compromising the results? How can
anyone become a world champion at any sport unless they are
willing to pull out all the stops to get there? Well, using any
means necessary to win is exactly what I feel is the problem
with bodybuilding, at least at the higher levels of formal
competition.
It’s well-known that anabolic-androgenic steroids (AAS) and a
host of other accompanying drugs are a standard part of
bodybuilding competition outside of “natural” organizations.
And even among the latter, there’s a wide range of looseness and
stringency in testing and policies against drug use. As a fan of
bodybuilding, I’ve come to look past this and become
desensitized to it. With extremely rare exceptions, there’s
Alan Aragon’s Research Review – October 2011
absolutely no way to be on a level playing field with national
and professional-level competitors without AAS. Nearly 100%
of the athletes are using.
Although I’ve never done AAS (& don’t plan to – heck, I’m not
even on creatine), I still admire the spectacular results of the
non-natty competitors. The appreciation of such physiques is
similar in principle to the appreciation of modified race cars that
are not street-legal. I’m fully aware that it’s the idea of drug
abuse is perhaps the strongest factor that alienates bodybuilding
from the mainstream. AAS use is common in a wide range of
mainstream professional sports, including major league baseball
and American football.1,2 However, since performance
enhancement is a more discrete result than huge/shredded
muscles, drug use in mainstream sports is much easier for the
masses to digest (or deny).
Well-oiled machines
For quite some time, I’ve known that some competitors inject
site enhancement oil (SEO) directly into lagging muscles in
order to bring their size up to par with the rest of the physique.
There are a number of different SEOs used for this purpose, but
the most well-known is synthol, consisting mostly of medium-
chain triglyceride, with a minor proportion of lidocaine and
alcohol. Synthol administration is rarely discussed openly.
Protocols vary, but in general, it involves repeated injections (in
some cases the injections are daily), and the process is invariably
described as extremely painful. Over time, the muscle fascia can
stretch and potentiate more tissue growth, which can give the
swelling a relative degree of permanence.
Unsurprisingly, synthol use has its risks, including the obvious
such as muscle deformation & microbial infection, and the more
insidious such as pulmonary embolism/occlusion, myocardial
infarction, and cereberal stroke.3 The most famous abuser of
SEO is Gregg Valentino, who gained international notoriety
from his appearances in the TV documentary The Man Whose
Arms Exploded and the movie documentary Bigger, Stronger,
Faster. Valentino’s edgy sense of humor and childlike
candidness has earned him a surprising level of celebrity. His
regular column and other media work for Muscular
Development magazine keeps him in the public eye (and
presumably out of trouble).
Valentino’s battle with an upper arm infection from using un-
sterile needles is legendary. Its documentation on film is a major
part of what connected him to his audience. Not all of us have
pulled Valentino-esque stunts, but we can all relate to injuring
ourselves through careless error. Similarly, the following video
shows a patient being treated for a severe infection in his upper
arm. Do not watch this unless you are impervious to nastiness.
This ranks among the utmost disgusting things I’ve ever seen, so
please heed my warning. Here’s the clip.
A lesser known site-specific enhancer is formebolone, called
esiclene in lay circles. Formebolone is a steroid that’s been used
to treat patients with nephrosis & renal insufficiency4 and
children with non-pituitary growth retardation.5 In a similar
fashion to synthol, bodybuilders inject the drug directly into
muscles where it causes localized inflammation. But unlike the
more permanent effects of synthol, formebolone’s inflammation
[Back to Contents] Page 14
only lasts 4-5 days. Its transient effects render it a short-term
precontest tactic to bring up weak bodyparts, rather than a part
of the regular routine.
Eye-opening feedback
I recently engaged in a discussion at Bodybuilding.com about
the prevalence of SEO use among the pros. While it’s still
speculative, the consensus was that the SEO use is rampant in
the pro ranks. I’ll quote one of the members because he earned
his pro card by winning the 2007 NABBA Mr. Universe, and has
better inside knowledge than the average person:
“I respect your opinion and no I do not have any physical
evidence, so take what I'm saying with a grain of salt. Yes,
most pros do use synthol, in fact it's usually a basic protocol
in most people’s prep. Even in amateurs it’s widespread. I'm
not going to say that I agree with it or disagree, but it's
something you have to do to give you that edge, and
everyone, myself included, will be willing to use these to gain
that extra edge. Any lagging bodyparts or certain areas of
the muscle that are difficult to bring up can easily be
manipulated by oil. Just takes some knowledge on where to
hit the muscle and how much oil to use. It hurts like a bitch,
the most painful injections you'll ever do in your life.”
The above passage & the feedback of others combined with the
recently dethroned Mr. Olympia Jay Cutler’s lumpy left bicep
(pictured here) finally got it through my thick skull that I may
have been naive in my perception of pro bodybuilding. I’m still
trying to wrap my head around the possibility that SEO use is
standard practice for most pros. After digging around online and
finding this decade-old forum post, I truly felt like I’ve been
living under a rock. The post is linked to a perfectly named
website, howtodoinjections.com, which provides vivid pictorial
instructions on SEO administration.
original definition, that it’s no longer bodybuilding. The
bodybuilding community as a whole frowns upon the use of
implants. I’m not talking female breast implants, but those
designed to bring up stubborn muscles like calves. One of the
most famous cases of implants (or other site-specific
enhancement) was when Lou “The Incredible Hulk” Ferrigno
made a comeback to the Mr. Olympia stage in 1992 with fairly
obvious lower-leg augmentation. Should synthol, esiclene, and
other such means of muscle modification be viewed in the same
light as implants? In my opinion, all of those tactics defeat the
original purpose of bodybuilding.
References
1. Lippi G, et al. Biochemistry and physiology of anabolic
androgenic steroids doping. Mini Rev Med Chem. 2011
May;11(5):362-73. [Medline]
2. Ambrose PJ. Drug use in sports: a veritable arena for
pharmacists. J Am Pharm Assoc (2003). 2004 Jul-
Aug;44(4):501-14; quiz 514-6. [Medline]
3. Pupka A, et al. The usage of synthol in the body building.
Polim Med. 2009;39(1):63-5. [Medline]
4. Esposito R, et al. Anabolic agents in kidney disease: the
effect of formebolone on protein synthesis in patients with
renal insufficiency or nephrosis. Curr Med Res Opin.
1975;3(1):43-5. [Medline]
5. Cuatrecasas Membrado JM, Bosch Banyeres JM. Study of
non-hypophysiary growth retardation treated with
formebolone. An Esp Pediatr. 1985 Jan;22(1):27-32.
[Medline]

According to one of the forum members, a popular SEO retailer

is Synthetek.com, which also provides a detailed instructions
page. I was blown away upon seeing this for the first time. And
it wasn’t that I didn’t know that SEO use existed – it was the
shameless, matter-of-fact nature of it that left me flabbergasted.

Where do you draw the line?

Answering this question is a matter of personal philosophical
ideals. At some point, bodybuilding can stray so far from its

Alan Aragon’s Research Review – October 2011 [Back to Contents] Page 15

 Selected outcomes relevant to the question

Can BCAA metabolism in rodents be extrapolated to

humans?
By Alan Aragon
 
             I read the Editor’s Cut in the March 2010 issue of AARR 
            (Newsflash:  rats  are  not  humans).  If  I  understood  it 
correctly, the article was mainly in response to studies showing 
adverse  effects  of  high  fructose  doses  fed  to  rodents.  You 
made  it  clear  that  carbohydrate  metabolism  in  rats  is  far 
different  from  humans,  especially  regarding  de  novo 
lipogenesis.  But  I’m  wondering  whether  the  same  applies  to 
protein metabolism. I’ve heard people say that rats are a good 
model  for  protein  metabolism,  implying  that  we  can  trust 
rodent  studies  on  BCAA  and  such.  I  would  very  much 
appreciate some clarification on this. Thanks Alan!  

You’re in luck. I found a study that’s directly relevant to

this question. Here’s the abstract: As seen in the chart above, humans and rats have vastly different
________________________________________________________________ distributions of branched chain amino acid aminotransferase
(BCAT). These differences in the muscle and liver are of
A molecular model of human branched-chain amino acid particular importance, and I’ll explain why. BCAT is an enzyme
metabolism that catalyzes the first step of the breakdown of BCAA into their
Suryawan A, et al. Am J Clin Nutr. 1998 Jul;68(1):72-81.. respective alpha-keto acids (BCKA), as seen in the diagram
[Medline] below.1 The oxidation of BCAA in humans occurs primarily in
skeletal muscle, while the catabolism of the other essential
To establish an accurate molecular model of human branched- amino acids occurs in the liver.1 In the chart above, notice how
chain amino acid (BCAA) metabolism, the distribution, activity, the relative proportion of BCAT activity in the liver and muscle
and expression of the first 2 enzymes in the catabolic pathway-- of humans and rats is highly disparate. Rats have very high
branched-chain-amino-acid aminotransferase (BCAT) and BCAT activity in muscle, but very little in the liver. Humans
branched-chain alpha-keto acid dehydrogenase (BCKD) have nearly a 13-fold lower concentration of muscle BCAT than
complex--were determined in human tissues. The same enzyme rats, but about triple their liver BCAT activity. This might sound
activities were measured in rat and African green monkey like jibberish at this point, but stick with me.
tissues. Overall, the activities of BCAT and BCKD were higher
in rat than in human and monkey tissues; nevertheless, the ratio
of the 2 activities was similar in most tissues in the 3 species.
Total oxidative capacity was concentrated in skeletal muscle and
liver (> 70%) with muscle having a higher proportion of the total
in humans and monkeys. In humans, brain (10-20%) and kidney
(8-13%) may contribute significantly to whole-body BCAA
metabolism. Furthermore, in primates the high ratio of
transaminase to oxidative capacity in the entire gastrointestinal
tract serves to prevent loss of essential BCAA carbon and raises
the possibility that the gastrointestinal tract contributes to the
plasma branched-chain alpha-keto acid pool. Quantitative
polymerase chain reaction was used to examine expression of
human branched-chain alpha-keto acid dehydrogenase kinase
(BCKDK), the key enzyme that regulates the activity state of the
human BCKD complex and human BCAT isoenzymes. To
design the primers for the polymerase chain reaction, human
BCKDK was cloned. BCKDK message was found in all human
tissues tested, with the highest amount in human muscle. As in
rats, there was ubiquitous expression of mitochondrial BCAT,
whereas mRNA for the cytosolic enzyme was at or below the
limit of detection outside the brain. Finally, the role of BCAA in
body nitrogen metabolism is discussed.

Alan Aragon’s Research Review – October 2011 [Back to Contents] Page 16

The second step in BCAA catabolism is the irreversible
oxidative decarboxylation of BCKA to form coenzyme A (CoA)
compounds, as seen in the diagram on the previous page. This is
the rate-limiting step of BCAA catabolism and is tightly
regulated.2 This process is catalyzed by the branched-chain
alpha-keto acid dehydrogenase (BCKD) complex.

As seen above, BCKD capacity in rat muscle & liver is

markedly different from that in humans. Rats have a far greater
BCAA oxidative capacity than humans. Collectively, these
differences suggest the possibility that BCAA metabolism in rats
can’t reliably be extrapolated to humans due to its greater
efficiency. To quote the authors, “...there may be more limited
transfer of metabolites between skeletal muscle and liver in
primates than in rats.”
Extensive research has been done on BCAA metabolism in rats.
Some of it has raised hopes for therapeutic and ergogenic
applications in humans supplemented with BCAA. A recent
example is work by Wilson et al (Layne Norton was part of this
team), who found that rats administered Leucine and/or a
glucose-sucrose mix at 135 minutes post-meal maintained peak
muscle protein synthesis (MPS) through the 180-minute mark,
whereas MPS in the non-supplemented group peaked at 90
minutes dropped down to baseline levels at 180 minutes.3 These
findings lend support to the idea that dosing BCAA between
meals can extend the meals’ anabolic effect. However, the
chronic effect of BCAA supplementation on top of an abundance
of BCAA bound to an ample intake of dietary protein in humans
remains unaddressed.
Ultimately, based on fundamental differences in BCAA and
carbohydrate metabolism, it’s not justified to get too excited (or
too disappointed) with rodent results until they’re sufficiently
replicated in relevantly designed human trials.

References
1. Shimomura Y, et al/ Nutraceutical effects of branched-chain Here are some rather spectacular time-lapse photo sequences
amino acids on skeletal muscle. J Nutr. 2006 Feb;136(2):529S- taken by the crew of expeditions 28 & 29 onboard NASA’s
532S. [Medline] International Space Station from August to October, 2011. It’s 5
2. Harris RA, et al. Studies on the regulation of the mitochondrial minutes long, watch it in full screen & HD for the full effect.
alpha-ketoacid dehydrogenase complexes and their kinases.
Adv Enzyme Regul. 1997;37:271-93. [Medline]
3. Wilson GJ, et al. Leucine or carbohydrate supplementation
reduces AMPK and eEF2 phosphorylation and extends If you have any questions, comments, suggestions, bones of
postprandial muscle protein synthesis in rats. Am J Physiol contention, cheers, jeers, guest articles you’d like to submit, or
Endocrinol Metab. 2011 Sep 13. [Epub ahead of print] any feedback at all, send it over to aarrsupport@gmail.com.
[Medline]

Alan Aragon’s Research Review – October 2011 [Back to Contents] Page 17