ean

12 Bytes of baloney.
By Alan Aragon
 
 

14 Quick responses from the authors.

Copyright © July 1st, 2010 by Alan Aragon

Home: www.alanaragon.com/researchreview
Correspondence: aarrsupport@gmail.com

2 Logic Does Not Apply Part 2: Breakfast (critique of

the article).
By Alan Aragon

6 High-intensity exercise and carbohydrate-reduced

energy-restricted diet in obese individuals.
Sartor F, et al. Eur J Appl Physiol. 2010 Jul 14. [Epub ahead
of print] [Medline]

7 Weight and metabolic outcomes after 2 years on a

low-carbohydrate versus low-fat diet: a
randomized trial.
Foster GD,, et al. Ann Intern Med. 2010 Aug 3;153(3):147-
57. [Medline]

8 The effects of adding leucine to pre and

postexercise carbohydrate beverages on acute
muscle recovery from resistance training.
Stock MS, et al. J Strength Cond Res. 2010 Jul 14. [Epub
ahead of print] [Medline]

9 Ergogenic effects of betaine supplementation on

strength and power performance.
Lee EC, et al. J Int Soc Sports Nutr. 2010 Jul 19;7(1):27.
[Epub ahead of print] [Medline]

10 Eating behavior and obesity at Chinese buffets.

Wansink B, Payne CR. Obesity (Silver Spring). 2008
Aug;16(8):1957-60. [Medline]

Alan Aragon’s Research Review – July 2010 [Back to Contents] Page 1

 Here’s a brief synopsis of hormonal‐happenings around 7 AM for 
the  average  person.  Cortisol  levels  elevate  naturally  through  the 
Logic Does Not Apply Part 2: Breakfast (critique of the 1‐9
night   and  peak
2,9‐14
.  Uh  oh,  cortisol  is  catabolic  and  without 
article). food, the body’s going to start eating all that hard‐earned muscle, 
By Alan Aragon right?  Wrong.  Catabolic  only  describes  the  process  of  something 
____________________________________________________ being  broken  down  for  energy.  Cortisol,  when  acting  without 
elevated insulin levels and in a natural manner — so without being 
constantly  elevated  like  during  chronic  stress  —  triggers  the 
Breakfast sucks: a reasonable conclusion?
breakdown  of  triglycerides  into  free‐fatty  acids  (FFAs)  for 
1,2,14‐28
EliteFTS recently published a spirited, well-written, heavily- metabolization  and  triggers  lipolysis .  Cortisol,  in  the 
referenced anti-breakfast article by John Kiefer that’s been morning, accelerates fat burning. 
causing quite a commotion.1 After numerous emails asking for
my feedback, I’ve decided to buckle down and do it AARR This segment actually deserves a “So, what?” response, but I’ll
style, instead of a less technical, more blog-friendly critique. So, oblige it to clear some things up about the idea that elevated
without further ado, let’s dig in. My comments will follow cortisol in the morning accelerates fat burning. In support of this
Kiefer’s boxed quotes. claim, Kiefer’s very first reference is a study on insulin-
 
The Logic  dependent diabetics.2 The limited relevance is obvious.
 
All  metabolic  arguments  aside,  scientists  have  witnessed  that  However, the next reference gives us a little more to talk about.
healthy, smart people eat breakfast; therefore, breakfast must be  Samra et al concluded that the morning rise in plasma cortisol
key. (Of course, from here, there are endless theories on why it’s  plays an important role in the regulation of lipolysis in adipose
so important: the body’s been starving all night and needs food to  tissue in normal healthy adults.3 Sounds exciting, but should we
function;  if  you  eat  a  lot  of  food  in  the  morning  it  sparks  interpret this to mean that skipping breakfast per se causes
metabolism and you burn off all the food and some fat; since the  quicker body fat reduction than skipping any other meal? This is
brain  needs  carbs  to  function,  supplying  the  body  with  a  low‐fat  essentially what Kiefer is claiming, but this study simply did not
breakfast gets the mind working at peak performance; etc.)  investigate the effect of differing meal placement. Instead, it
compared drug-mediated suppression of cortisol (via
Other than that being the longest parenthesized disclaimer I’ve metyrapone) versus the absence of cortisol suppression. A third
ever read, I can agree with his sentiment. As far as dietary treatment involved the infusion of hydrocortisone sodium
dogma goes, breakfast is more than a meal; it’s almost a culture succinate in addition to an infusion of metyrapone.
with its own built-in peer pressure. Furthermore, it’s definitely
Furthermore, this trial measured lipolysis, a term which tends to
an important subject of grain industry-funded research.
get interchanged with fat oxidation (also called fatty acid
  oxidation), when they are related yet distinctly different
The Reality  phenomena. Lipolysis is the breakdown of triacylglycerol into
 
The only reasonable conclusion the facts support is that breakfast  free fatty acids (this can be viewed as ‘mobilization’ step) while
sucks.  fat oxidation is the breakdown of fatty acids into energy (this can
  be viewed as the final ‘burning’ step). Although it’s easy to
It’s no secret that I’m not a fan of breakfast. When working with a 
make the assumption, the rate of lipolysis is not a limiting factor
new client in a  physique or strength sport or the average person 
trying to lose a few pounds, more often than not, the first thing I 
to fat oxidation, as I’ll touch upon shortly.
say  is,  “stop  eating  breakfast.”  Brian  Carroll  loves  the  excuse  to  Given all this, using the latter research as a basis for the claim
skip  breakfast  as  do  a  large  number  of people I  work  with.  Like  I  that breakfast sucks for fat loss is a Grand Canyon-sized leap.
once thought, they believe that breakfast is critical to mental and  The subsequent fifteen references in the article were either
physical performance and they force themselves to eat it whether  equally or less relevant to the claim in terms of the samples and
they want to or not. 
protocols (i.e., rodent studies, patients with Cushing’s syndrome,
acute or short-term effects). Note: a longer list of references does
Okay, so a red flag comes up pretty early in the article. Breakfast not necessarily equal better evidence for the case.
sucks? He’s not a “fan” of breakfast, and more often than not,
issues the order to stop eating it? Hmmm... I wouldn’t say I’m a Kiefer goes on to discuss ghrelin’s appetite-stimulatory and
fan of any meal in particular (I adore them equally), so I guess I growth hormone-releasing properties, and how this peaks
can partially agree. He then drops the name of powerlifter Brian roughly 2 hours after waking without breakfast. Despite the
Carroll, which I would do too, if he was my client. so-what factor, there’s nothing very concerning until he states
the following, where I sensed him telegraphing his next zinger.
Again, I’m in agreement with him that meals (breakfast or other)
shouldn’t be forced down when you’re not hungry for them, Every  day  the  body  starts  as  a  fat‐burning  furnace.  Even  during 
unless your goals are on the fringes away from the general exercise,  without  eating  breakfast,  the  body  burns  far  higher 
fitness population. Competitive eaters would vouch for this, as levels  of  fat  than  normal52,53  and  causes  up  regulation  of  the 
would certain competitive athletes with a limited timeframe to enzymes  necessary  to  burn  fat,  allowing  fat  to  be  metabolized 
54
increase their scale weight. The problem with his tone is that you faster . 
can already see where he’s headed in terms of bias.
Alan Aragon’s Research Review – July 2010 [Back to Contents] Page 2
Firstly, I don’t disagree that in many cases, the body burns more Before jumping to the conclusion that Martin et al demonstrated
fat during fasted training. However, what ultimately matters that breakfast sucks, we have to seriously consider the
most is net fat balance beyond the short term. limitations of their study. Let’s first begin by examining the
macronutritional stats of the two breakfasts:
Furthermore, there are examples in the literature showing the
contrary, particularly in trained subjects. Horowitz et al ƒ Low-energy breakfast: 109.8 kcal, 1gP, 17gC, 4.2gF
examined the effect of high-glycemic carbohydrate ingestion ƒ High-energy breakfast: 706.5 kcal, 14.9gP, 118.3gC, 19.3gF
during either low intensity exercise (25% VO2 max) or high-
moderate intensity (68% VO2 max). Subjects did a 2-hr cycling Do those stats seem a bit odd? If so, then have a look at the
bout, consuming either a carb solution or a noncaloric placebo at actual food composition of each breakfast, and you’ll notice that
30-minute intervals. In the low-intensity group, fat oxidation did these meals are hardly reflective of what the typical
not dip below that of the fasted group until 80-90 minutes into health/fitness-oriented individual would consume:
the bout. In the high-moderate intensity group, there was no
difference in fat oxidation between the fasted and fed groups at
any point in the trial. Interestingly, (remember I mentioned I’d
touch on this), in both of the fed groups, the rate of lipolysis was
20-25% greater than fat oxidation during the final hour of the
bout. To quote their conclusion directly:4
“In summary, carbohydrate ingestion and the resultant insulin
response during exercise suppressed lipolysis. However, the
lipolytic rate remained in excess of fat oxidation after
carbohydrate ingestion during both low- and moderate-intensity
exercise, indicating that this suppression in lipolysis was not
responsible for reducing fat oxidation.”
In a similar example, Febbraio et al examined the effects of pre
&/or during-training carbohydrate ingestion compared to fasted
conditions in endurance-trained subjects who exercised for 2 hrs
at 63% VO2 max.5 No difference was seen in total fat oxidation Notice in the above chart that the primary macronutritional
between the fasted and fed subjects, despite the elevated insulin difference between the two breakfasts was roughly 83g carbs,
levels in the fed groups, who consumed a relatively high amount 79g of which came from refined sources (bread & jam). Perhaps
of carbohydrate (up to 2g/kg 30 minutes before testing, plus the most crucial detail to consider is that dietary intake aside
2g/kg during testing). Notably, time trial performance was better from breakfast was not tightly controlled, and this critically
in the carb-fed groups. jeopardizes the validity of the authors’ conclusions. The high-
  energy breakfast treatment also had more total energy intake
Now  contrast  with  what  happens  as  soon  as  you  eat  breakfast,  overall, and since protein and fat intakes of both conditions were
one  that  contains  around  30  grams  or  more  of  carbs.  As  is  well  the same, the extra daily intake (the authors calculated 1483 kJ,
known,  insulin  levels  raise  with  the  rise  in  blood  sugar,  kick‐
or 354.2 kcal) in the bigger breakfast condition were from
starting  a  downward  spiral:  the  early‐morning  release  of  insulin 
55 carbohydrate - mainly in the form of bread & jam. So, there you
reduces fat burning for the entire rest of the day ; while cortisol 
have it. It’s simply not logical to conclude that the larger
levels remain high, the insulin release causes new empty fat cells 
to  be  created
56‐64
;  and  the  insulin  lowers  levels  of  ghrelin  and 
breakfast per se was the culprit causing the unfavorable
growth hormone
29‐31, 51
.  outcomes when the treatments were not equal in macronutrition
or total calories.
So, is it possible for early-morning insulin elevation from In the following section, Kiefer finally discusses more concrete
breakfast per se to reduce fat burning for the rest of the day? The research he feels validates his negative view toward breakfast.
reference cited to support this claim is a 2-week study by Martin
et al,6 who compared the effects of a low-energy & a high- So what happened when researchers studied two groups, one that 
ate most of their calories in the beginning of the day, to simulate 
energy breakfast, and a series of less favorable outcomes was
the  no‐eating‐after‐seven  routine,  and  the  other  that  skipped 
seen in the high-energy breakfast condition. Fasting
breakfast and ate most of their meals in the latter half of the day? 
triacylglycerol levels were higher and HDL-cholesterol levels
Damn  if  I  shouldn’t  be  embarrassed:  the  group  that  ate  most  of 
were lower as a result of the high-energy breakfast. Indeed, as their calories early in the day, including a big breakfast, lost more 
Kiefer mentioned, the high-energy breakfast induced a strong weight than the other group . 
65
inhibition of fat oxidation throughout the day. These results led  
the authors to conclude the following: Hold on: there’s more to this story. The researchers also looked at 
body composition before and after. The morning group lost more 
“Although long-term adaptation to a high-energy breakfast weight  but  lost  a  lot  more  muscle  and  a  lot  less  fat.  The  night 
cannot be excluded, the high-energy breakfast in this study did group  lost  almost  exclusively  fat  and  preserved  muscle65‐69.  Who 
not appear to be favourable to health. Our results do not support knew, maybe there is something to this science stuff after all? 
the current advice to consume more energy at breakfast.”

Alan Aragon’s Research Review – July 2010 [Back to Contents] Page 3

In the above segment, he cites a study by Keim et al,7 who found
that larger intake earlier in the day resulted in more weight loss
but less lean mass preservation than the same intake shifted
more towards the later part of the day. However, Kiefer
exaggerates by saying that the morning group lost “a lot more
muscle and a lot less fat.” This is a very misleading
oversimplification of the actual outcomes. Here’s the chart from
the study:
Solid triangles represent the mean of 6 subjects who received large
evening meals (PM pattern) in period 1, and large morning meals
(AM pattern) in period 2. Open circles represent the mean of
4 subjects who received AM pattern in period 1 and PM pattern in
period 2.
When viewing the above chart above, keep in mind that the
study had 3 phases. The initial phase was a stabilization period
to establish weight maintenance. Each subsequent experimental
period lasted 6 weeks. In Period 1, the subjects were split into 2
groups, one of which consumed 70% of daily caloric intake over
two meals in the AM, while the other group did the same, except
in the PM. Period 2 simply consisted of the same protocol in
Period 1, but with the subjects in each group crossing over to the
other treatment (the AM group switched over to the PM
protocol, and vice-versa).
When examining the data in its entirety, Kiefer’s statement is not
only exaggerated, but incomplete. Ultimately, it’s just plain
false. While there indeed was a significantly greater loss of fat
mass in the PM pattern in Period 1, fat mass loss was not
significantly different between groups in Period 2. Averaging
both periods, bodyfat in the PM pattern decreased from 36.3%
to 33.8 (2.5%). Bodyfat in the AM pattern decreased from
35.3% to 33.5% (1.8%). This makes the absolute difference in
Alan Aragon’s Research Review – July 2010
bodyfat reduction between the AM & PM patterns less than 1%
more in the PM pattern. This is not only minor in terms of real-
world significance over a 6 week period, but it also didn’t reach
statistical significance in this study. Have a look at the chart
below that sums up the overall changes in body composition:
Loss of lean mass by the end of 6 weeks was 1.03 kg greater in
the AM pattern. While this was a statistically significant
decrease, the authors themselves state that since the components
of the fat free mass weren’t measured, it’s still open to
speculation about whether or not this was merely water loss. I’ll
quote their discussion of the study’s limitations directly:
“In consideration of the inconsistent meal pattern effects on
body fat mass, the nature of this observation should be explored
further to determine if the greater loss of fat mass associated
with large PM meals was a true, but transient meal pattern
response or an artifact of our cross-over design.”
Clearly, there’s a big difference between Keifer’s dramatic
interpretation of this study’s outcomes and what actually
occurred. Furthermore, although this study was well done, it still
carries the limitation of being a single study in dire need of
replication using a larger number of subjects. Additional
criticism can be made about the relevance and applicability of
the disproportionately carb-heavy test diet, which consisted of
88 g protein, 293 g CHO, and 49 g fat.
No  matter  what  I  say  about  fat  loss,  someone  will  say  that 
skipping breakfast turns people into mental sloths. Does it really? 
You  think  so?  [...]  Do  experiments  prove  that  breakfast  improves
cognitive abilities? Yes, if the person is malnourished70‐73 
Here’s one of the few segments of the article where I don’t
completely butt heads with Kiefer. Recently, Hoyland et al
examined the convoluted, messy body of breakfast research.8
For the first time ever, systematic review methodology was used
to evaluate the effects of breakfast on cognitive performance in
well-nourished children and nutritionally at-risk children. After
wringing out the data of 45 studies published between 1950 and
2008, they concluded that the evidence overall shows positive
effects of breakfast on cognitive performance compared to
omitting breakfast. However, they also found that these effects
were more easily demonstrated in “nutritionally vulnerable”
children. They also mentioned that the majority of the studies
had some degree of industry sponsorship, which inevitably puts
research at risk for positive outcome bias.
A point reiterated throughout the review was that the overall
quality of the studies was poor. Methodological problems
plagued several aspects of the research, including a lack of
isocaloric matching, questionable developmental stage
appropriateness of the cognitive performance testing, lack of
control for inter-individuality of glucoregulation, failure to
describe statistical procedures, and a lack of appropriate methods
to track biomarkers during cognitive activity.
[Back to Contents] Page 4
  
Someone  in  a  forum  also  referenced  an  article  stating  that  2. Dineen S, et al. Effects of the normal nocturnal rise in
skipping  breakfast  primes  the  body  to  get  fat  and  slows  fat  cortisol on carbohydrate and fat metabolism in IDDM. Am J
burning, which is the opposite of the truth, but the article goes on  Physiol. 1995 Apr;268(4 Pt 1):E595-603. [Medline]
to  say  that  all  of  this  can  be  avoided  by  adding  some  branched‐ 3. Van Proeyen, et al. Effects of training in the fasted state in
chain  amino  acids  in  lieu  of  breakfast  and  suggests  leucine,  conjunction with fat-rich diet on muscle metabolism. Med
isoleucine  and  valine.  This  is  probably  a  bad  idea,  as  the  amino  Sci Sports Exerc. 2010 May;42(5):42. [MSSE]
acid  leucine  stimulates  insulin  release  without  the  presence  of  4. Horowitz JF, et al. Substrate metabolism when subjects are
85‐86
glucose   and  may  cause  the  same  reactions  as  a  carby  fed carbohydrate during exercise. Am J Physiol. 1999
breakfast.  May;276(5 Pt 1):E828-35. [Medline]
5. Febbraio MA, et al. Effects of carbohydrate ingestion before
The above quote is more evidence of Kiefer becoming highly and during exercise on glucose kinetics and exercise
indiscriminate with the application of his preset philosophical performance. J Appl Physiol. 2000 Dec;89(6):2220-6.
framework. Saying that the ingestion of branched chain amino [Medline]
acids (BCAA) at breakfast time is likely a bad idea due to an 6. Martin A, et al. Is advice for breakfast consumption
insulin-mediated mechanism is just plain unsupportable with justified? Results from a short-term dietary and metabolic
anything more than wild assumptions mixed with a heavy dose experiment in young healthy men. Br J Nutr. 2000
of imagination. Sep;84(3):337-44. [Medline]
 
As  far  as  strength  is  concerned,  there  is  little  effect  as  long  as  7. Keim NL, et al. Weight loss is greater with consumption of
glycogen  stores  remain  adequate
87‐88
,  hence  the  application  of  large morning meals and fat-free mass is preserved with
Carb Back‐Loading™ to strength, power and physique athletes.  large evening meals in women on a controlled weight
reduction regimen. J Nutr. 1997 Jan;127(1):75-82.
To end things off, Kiefer throws in the above comment implying [Medline]
the uselessness of pre-workout carbohydrate ingestion for a 8. Hoyland A, et al. A systematic review of the effect of
range of athletic pursuits. The problem is, he cites a couple of breakfast on the cognitive performance of children and
out-dated reviews discussing research that doesn’t necessarily adolescents. Nutr Res Rev. 2009 Dec;22(2):220-43.
support his case. For example, one of the studies discussed is a [Medline]
classic by Lambert et al,9 who found that ingesting a 9. Lambert CP, et al. Effects of carbohydrate feeding on
carbohydrate dose of 1g/kg immediately before resistance multiple bout resistance exercise. J Strength Cond Res.
training, and then an additional dose (0.17g/kg) after the 5th, 1991;5(4):192-7. [JSCR]
10th and 15th sets resulted in 18.8% more sets and 15.5% more 10. Kiefer J. Carb Back-loading. June, 2010. [EliteFTS]
repetitions than the noncaloric placebo control treatment. These
outcomes were just shy of statistical significance, but the actual
effects are too large to dismiss.
While I admire innovative ideas, seeing that Kiefer trademarked   
a dietary method (Carb Back-Loading™)  immediately
heightened my BS sensors. I did a little digging and found a
recent article of his where he recommends limiting non-fiber
carbohydrate intake to 30 grams between waking until mid-to-
late afternoon (when the workout occurs). He then describes his
personal postexercise nutrition protocol as follows (I bolded the
part that might make you spit your drink onto your keyboard): 10
 
After  training,  the  only  meal  I  keep  low‐fat  is  my  post‐workout 
shake, which is zero fat. It contains 50 grams of protein, 100 grams 
of  a  glucose‐based  carb  powder  with  no  other  caloric  nutrients. 
Otherwise, the latter half of the day is filled with high‐carb meals, 
but  not  necessarily  low‐fat.  The  sharp  spike  in  metabolism  that 
accompanies the rush of carbs helps burn the dietary fat through 
the hours of sleep. 

To the above quote, I actually have no comment – mainly due to

speechlessness. I’ll wrap this up by thanking John Kiefer for
writing a genuinely thought-provoking article. Based on the
research, as well as my observations in the field, I wouldn’t say
that breakfast sucks...I’d say it depends.

References
1. Kiefer J. Logic Does Not Apply Part 2: Breakfast. July,
2010. [EliteFTS] [Corrected Reference List]
Alan Aragon’s Research Review – July 2010 [Back to Contents] Page 5

High-intensity exercise and carbohydrate-reduced
energy-restricted diet in obese individuals.
Sartor F, et al. Eur J Appl Physiol. 2010 Jul 14. [Epub ahead of
print] [Medline]
PURPOSE: Continuous high glycemic load and inactivity
challenge glucose homeostasis and fat oxidation. Hyperglycemia
and high intramuscular glucose levels mediate insulin resistance,
a precursor state of type 2 diabetes. The aim was to investigate
whether a carbohydrate (CHO)-reduced diet combined with
high-intensity interval training (HIIT) enhances the beneficial
effects of the diet alone on insulin sensitivity and fat oxidation in
obese individuals. METHODS: Nineteen obese subjects
underwent 14 days of CHO-reduced and energy-restricted diet.
Ten of them combined the diet with HIIT (4 min bouts at 90%
VO(2peak) up to 10 times, 3 times a week). RESULTS: Oral
glucose insulin sensitivity (OGIS) increased significantly in both
groups; [diet-exercise (DE) group: pre 377 +/- 70, post 396 +/-
68 mL min(-1) m(-2); diet (D) group: pre 365 +/- 91, post 404
+/- 87 mL min(-1) m(-2); P < 0.001]. Fasting respiratory
exchange ratio (RER) decreased significantly in both groups
(DE group: pre 0.91 +/- 0.06, post 0.88 +/- 0.06; D group: pre
0.92 +/- 0.07, post 0.86 +/- 0.07; P = 0.002). VO(2peak)
increased significantly in the DE group (pre 27 +/- 5, post 32 +/-
6 mL kg(-1) min(-1); P < 0.001), but not in the D group (pre 26
+/- 9, post 26 +/- 8 mL kg(-1) min(-1)). Lean mass and resistin
were preserved only in the DE group (P < 0.05).
CONCLUSION: Fourteen days of CHO-reduced diet improved
OGIS and fat oxidation (RER) in obese subjects. The energy-
balanced HIIT did not further enhance these parameters, but
increased aerobic capacity (VO(2peak)) and preserved lean mass
and resistin. SPONSORSHIP: N.W. Wales NHS Grant.
Study strengths
This study is unique in that it’s the first to compare the effect of
high-intensity interval training (HIIT) on carbohydrate-
restricted, hypocaloric conditions with the effect of dieting
alone. Body composition was assessed via dual X-ray
absorptiometry (DXA). A high degree of dietary control was
imposed due to the lab-provided diet. Furthermore, subjects
were required to report any deviations to the assigned diet. In the
case of noncompliance, the following days’ intake was adjusted
to maintain the assigned diet values. Both heart rate and rating of
perceived exertion were used in order to ensure that the targeted
exercise intensity was hit. An activity correction factor was used
to account for individual variations in physical activity, and the
caloric intake of the diet + exercise group (DE) was increased
via the activity correction factor to compensate for the extra
energy burned during training.
Study limitations
On the whole, this study was well-controlled, so its primary
limitation is conceptual. In this day and age, a “cardio-only”
training program is not optimal, nor is it realistic in some cases.
In an ideal word, this trial would have examined a protocol
involving resistance training and/or cardio training. It’s
somewhat predictable that exercise imposed upon hypocaloric
Alan Aragon’s Research Review – July 2010
conditions would further the desired adaptations. So, simply
comparing weight training with HIIT under these conditions
would have been a more interesting investigation. Another
obvious limitation was the short 14-day trial duration. The
authors themselves concede that the small sample size had the
potential to mask differences between groups.
Comment/application
As the chart above indicates, the diet-only (D) group lost a
significant amount of weight. However, pan down and notice
that that the DE group gained a significant amount of lean body
mass, while the D group lost lean mass. These outcomes weren’t
too surprising. They concurred with past research showing the
lean mass-preserving superiority of higher-intensity work or
HIIT compared to lower-intensity/steady state aerobic work.1,2
Another predictable outcome was the cardiovascular fitness
increase in DE. A notable detail here was the increase in lean
mass despite a relatively low habitual daily protein intake at
baseline (91.7g in DE, 90.4g in D) and an even lower protein
intake during the carb-restricted intervention (70.9 g in DE,
62.7 g in D). It’s reasonable to speculate that the HIIT was a
novel and strong enough stimulus to elicit “newbie gains” in
lean mass despite the sup-optimal protein intake.
Interestingly, there were no significant differences in the
increased insulin sensitivity in both groups. The authors noted
that the lack of additional insulin-sensitizing effect of exercise
was likely due to an offsetting effect by the compensatory
energy intake in the DE group required to keep the deficit
matched with the D group. In support of this, they cite an acute
study by Black et al, who found no significant effect of moderate
aerobic exercise on insulin sensitivity when energy balance was
preserved (via postexercise carbohydrate intake).3 Refer to last
month’s issue to see the broader context of the latter study.
Predictably, leptin decreased in both groups. A less-publicized
adipokine called resistin was unaltered in the DE group, but to
the surprise of the authors, increased in the D group. This is
potentially concerning since resistin elevations have been
associated with decreased insulin sensitivity, but this finding is
still equivocal. The authors speculate that the increase in resistin
was somehow counteracted by the HIIT.
An important detail to keep in mind was that although
carbohydrate intake was reduced, it wasn’t necessarily low-carb
in the typical sense (163g in DE, 147g in D). This can partially
explain the zero dropout rate, and the general lack of difference
seen in insulin sensitivity improvement.
[Back to Contents] Page 6
Weight and metabolic outcomes after 2 years on a
low-carbohydrate versus low-fat diet: a randomized
trial.
Foster GD,, et al. Ann Intern Med. 2010 Aug 3;153(3):147-57.
[Medline]
BACKGROUND: Previous studies comparing low-
carbohydrate and low-fat diets have not included a
comprehensive behavioral treatment, resulting in suboptimal
weight loss. Objective: To evaluate the effects of 2-year
treatment with a low-carbohydrate or low-fat diet, each of which
was combined with a comprehensive lifestyle modification
program. DESIGN: Randomized parallel-group trial.
(ClinicalTrials.gov registration number: NCT00143936) Setting:
3 academic medical centers. Patients: 307 participants with a
mean age of 45.5 years (SD, 9.7 years) and mean body mass
index of 36.1 kg/m(2) (SD, 3.5 kg/m(2)). Intervention: A low-
carbohydrate diet, which consisted of limited carbohydrate
intake (20 g/d for 3 months) in the form of low-glycemic index
vegetables with unrestricted consumption of fat and protein.
After 3 months, participants in the low-carbohydrate diet group
increased their carbohydrate intake (5 g/d per wk) until a stable
and desired weight was achieved. A low-fat diet consisted of
limited energy intake (1200 to 1800 kcal/d; </=30% calories
from fat). Both diets were combined with comprehensive
behavioral treatment. Measurements: Weight at 2 years was the
primary outcome. Secondary measures included weight at 3, 6,
and 12 months and serum lipid concentrations, blood pressure,
urinary ketones, symptoms, bone mineral density, and body
composition throughout the study. RESULTS: Weight loss was
approximately 11 kg (11%) at 1 year and 7 kg (7%) at 2 years.
There were no differences in weight, body composition, or bone
mineral density between the groups at any time point. During the
first 6 months, the low-carbohydrate diet group had greater
reductions in diastolic blood pressure, triglyceride levels, and
very-low-density lipoprotein cholesterol levels, lesser reductions
in low-density lipoprotein cholesterol levels, and more adverse
symptoms than did the low-fat diet group. The low-carbohydrate
diet group had greater increases in high-density lipoprotein
cholesterol levels at all time points, approximating a 23%
increase at 2 years. Limitation: Intensive behavioral treatment
was provided, patients with dyslipidemia and diabetes were
excluded, and attrition at 2 years was high. CONCLUSION:
Successful weight loss can be achieved with either a low-fat or
low-carbohydrate diet when coupled with behavioral treatment.
A low-carbohydrate diet is associated with favorable changes in
cardiovascular disease risk factors at 2 years. SPONSORSHIP:
National Institutes of Health.
Study strengths
A couple of obvious strengths were the long duration (2 years),
and large sample (307 participants from 3 separate sites). Both
male and female subjects were used, and as far as diet trials go,
this was the first to assess adverse symptoms, bone status, and
comprehensive behavioral therapy.
Study limitations
Although the effective behavioral treatment can be seen as a
design strength (it provides useful data for follow-up
Alan Aragon’s Research Review – July 2010
investigations), it also presents a variable that makes it difficult
to extrapolate the results to the general population – much of
which may not have access to such therapy. As noted by the
authors, since the low-carb treatment was based on the Atkins
model (which increases carbohydrate intake over time), the
effects of sustained, severe carbohydrate restriction (20g/day)
could not be assessed. They also noted that their findings are
potentially limited to individuals without diabetes or
hypercholesterolemia. Attrition (drop-out) was high. By the 2-
year mark, 32% of the low-fat group and 42% of the low-carb
dropped out, or were intermittently absent from participating in
the study. Finally, while several measures were taken to ensure
dietary compliance, the food was not provided by the lab.
Comment/application
Depicted above is perhaps the most important finding. No
significant difference in weight loss between groups was seen at
any point in the study (although a trend toward greater weight
loss in the low-carb group was seen at 3 months). Notably,
DXA-assessed body composition did not differ between groups
at any point in the study either. These outcomes reinforce the
premise that total energy is what matters for weight loss, rather
than the proportion of fat versus carbohydrate energy in the diet.
The assessment also included bone density, which was not
different between groups. This outcome challenges the popular
assumption that low-carb diets are harmful to skeletal health.
Predictably, HDL increased to a greater degree in the low-carb
group. Although LDL was increased in the low-carb group and
decreased in the low-fat group at months 3 and 6, but not
significantly different at the 2-year mark. The authors diligently
noted that interpreting changes in LDL is only possible by
examining the subparticles.4 Increases in LDL resulting from
isocaloric replacement of carbohydrate with fat has been shown
to raise the larger LDL particle, which is neutral – while the
smaller particle is associated with atherogenesis.5 Ultimately, the
authors felt that these changes in LDL were not clinically
important, since there was no significant difference in LDL
levels between the groups in the long term.
An interesting assessment was the reporting of adverse
symptoms: bad breath, hair loss, constipation, and dry mouth. Of
all of these, only constipation persisted after the 6 months in the
low-carb group (slightly double that of the low-fat group at the
2-year mark). These outcomes challenge the idea that the
unsavory aspects of severe carbohydrate restriction must be
endured permanently. In sum, this study provides some of the
strongest evidence to-date that diets should be individualized
according to personal preference, rather than dogmatically
glorifying fat over carbohydrate intake, or vice-versa.
[Back to Contents] Page 7

The effects of adding leucine to pre and postexercise
carbohydrate beverages on acute muscle recovery
from resistance training.
Stock MS, et al. J Strength Cond Res. 2010 Jul 14. [Epub ahead
of print] [Medline]
[Medline
PURPOSE: The present study examined the effects of adding
leucine to pre and postexercise carbohydrate beverages on
selected markers of muscle damage, delayed-onset muscle
soreness (DOMS), and squat performance for up to 72 hours
after lower-body resistance training. DESIGN: Seventeen
resistance trained men (mean +/- SD age 22.9 +/- 2.9 years) and
3 resistance trained women (mean +/- SD age 21.6 +/- 2.6 years)
performed 6 sets of squats to fatigue using 75% of the 1
repetition maximum. Each subject consumed a carbohydrate
beverage 30 minutes before and immediately after exercise with
or without the addition of 22.5 mg.kg (45 mg.kg total) of leucine
in a randomized, double-blind fashion. RESULTS: Serum
creatine kinase (CK), lactate dehydrogenase (LDH), and DOMS
were analyzed immediately before (TIME1), 24 (TIME2), 48
(TIME3), and 72 (TIME4) hours after exercise. The subjects
repeated the squat protocol at TIME4 to test recovery. No
differences were observed between groups for squat
performance, defined as the total number of repetitions
performed during 6 sets of squats, for both TIME1 and TIME4.
The addition of leucine did not significantly decrease CK and
LDH activity or DOMS. CONCLUSIONS: These results
suggested that adding leucine to carbohydrate beverages did not
affect acute muscle recovery and squat performance during both
initial testing and during a subsequent exercise bout 72 hours
later in resistance trained subjects. SPONSORSHIP: Financial
support for this study was awarded through a UNLV Graduate
and Professional Student Association Grant.
Study strengths
Given the hype surrounding leucine supplementation (and
BCAA supplementation in general), this is a timely topic for
research to address. This is the first study to isolate the effects of
adding leucine to a carbohydrate solution on recovery from
lower-body resistance exercise. This is also the first study to
monitor dietary intake for up to 72 hours postexercise. Dietary
intake was analyzed via software, and was tracked throughout
the study via food logs that were submitted to the research staff
at each visit to the lab.
Study limitations
The most obvious limitation here is the acute (short-term) nature
of the trial. Also, the sample was small, and a between-subjects
design was used – that is, each subject underwent only one of the
treatments. The authors could have reduced some of the
confounding variability of response by using a within-subject
design (also called a repeated measures design, or crossover),
where each subject gets a chance to undergo both treatments.
Indeed, they acknowledge that there was a large amount of
variability in creatine kinase (CK, a marker of muscle protein
breakdown), and thus, the results should be viewed and
interpreted with caution.
Alan Aragon’s Research Review – July 2010
Comment/application
As the above chart depicts, the salient finding was a lack of
significant difference in CK levels between the leucine-carb and
the carb-only group. Furthermore, lactate dehydrogenase (LDH
– another marker of muscle damage) and delayed-onset muscle
soreness (DOMS) were not different between groups either.
Notably, this was despite the combination of amino acids and
carbohydrate, which have been seen to have not only an additive
effect on antiproteolysis and fiber hypertrophy, but a synergistic
benefit, as Bird et al demonstrated with a 6 g dose of EAA
combined with a 6% carbohydrate solution.6
I was pleased to see that the authors’ speculations over this lack
of effect concurred with my original hunch, which was that the
diets likely had sufficient protein (and thus sufficient BCAA) to
offset any additional effect of supplemental leucine. As indicated
by the nutritional breakdown above, the average protein intake
was 1.62 g/kg in the leucine-carb group and 1.65 g/kg in the
carb-only group. According to the preponderance of the
literature on the athletic population, this amount is sufficient for
causing and/or maintaining positive muscular adaptations.7-9
Balage and Dardevet offer the following explanation behind
leucine supplementation’s inconsistent track record for
improving muscle mass and performance:10
“…when free leucine is added in a diet, it is rapidly absorbed
and its plasma concentration increases before that of the other
amino acids coming from the digestion of the proteins present in
the diet. Then, muscle protein synthesis machinery may be
activated by this leucine increase (via mTOR activation) but
cannot translate into protein synthesis because of the lack of
simultaneous availability of the other amino acids (as substrates
for protein synthesis).
To provide a contrasting example to the outcomes of the present
study, the authors cite research by Coombes and McNaughton
who found a daily dose of 12 g BCAA decreased CK and LDH
resulting from 120 minutes of ergometer work at 70%
VO2max.11 However, this isn’t necessarily the best study for
comparison given the drastically different training protocol. In
sum, isolated leucine supplementation is yet to yield compelling
results for resistance trainees with ample dietary leucine via their
typical protein intake. However, I’m sure the ads will continue.
[Back to Contents] Page 8
Ergogenic effects of betaine supplementation on
strength and power performance.
Lee EC, et al. J Int Soc Sports Nutr. 2010 Jul 19;7(1):27. [Epub
ahead of print] [Medline]
PURPOSE: We investigated the ergogenic effects of betaine
(B) supplementation on strength and power
performance. DESIGN: Twelve men (mean SD age, 21 3 yr;
mass, 79.1 10.7 kg) with a minimum of 3 months resistance
training completed two 14-day experimental trials separated by a
14-day washout period, in a balanced, randomized, double-blind,
repeated measures, crossover design. Prior to and following 14
days of twice daily B or placebo (P) supplementation, subjects
completed two consecutive days (D1 and D2) of a standardized
high intensity strength/power resistance exercise challenge
(REC). Performance included bench, squat, and jump tests.
RESULTS: Following 14-days of B supplementation, D1 and
D2 bench throw power (1779 90 and 1788 +/- 34 W,
respectively) and isometric bench press force (2922 297 and
2503 +/- 28 N, respectively) were increased (p < 0.05) during
REC compared to pre-supplementation values (1534 +/- 30 and
1498 +/- 29 W, respectively; 2345 +/- 64 and 2423 +/-84 N,
respectively) and corresponding P values (1374 +/- 128 and
1523 +/- 39 W; 2175 +/- 92 and 2128 +/- 56 N, respectively).
Compared to pre-supplementation, vertical jump power and
isometric squat force increased (p < 0.05) on D1 and D2
following B supplementation. However, there were no
differences in jump squat power or the number of bench press or
squat repetitions. CONCLUSION: B supplementation increased
power, force and maintenance of these measures in selected
performance measures, and these were more apparent in the
smaller upper-body muscle groups. SPONSORSHIP: Dansico,
Inc. Ardsley, NY.
Study strengths
There is a relatively scant body of research examining the
ergogenic potential of betaine. So, at least conceptually, this
study can still be considered novel. A within-treatment
experimental design was used (another name for a crossover
design) in order to alleviate the confounding variability within
the small sample. Betaine supplementation occurred at
standardized times for each subject. The time of testing was
standardized for each subject as well. The exercise testing
protocol involved both upper and lower body exercises, making
the results more broadly applicable. The protocol included both
isometric as well as isotonic testing. Urine specific gravity was
measured to control hydration status.
Study limitations
An obvious limitation is the short trial duration (14 days).
Healthy, recreationally active men were used, but there was no
definition provided (a minimum experience of 3 months of
resistance training). Thus it’s open to speculation whether or not
the outcomes would apply to more highly trained populations
who would most likely be seeking out the competitive edge via
supplementation. Aside from the submission of 3-day diet
records, there wasn’t any strict control or formal dietary analysis
done. Tight dietary monitoring is critical for strengthening the
validity of the outcomes in supplement research.
Alan Aragon’s Research Review – July 2010
Comment/application
As the above graphic depicts,12 betaine and its related
metabolites are interesting and important biological compounds
regardless of their relative effectiveness (or ineffectiveness) as
an ergogenic aid. It occurs naturally in microorganisms, plants,
animals, and many foods. Sugar beets, wheat, spinach, and
shellfish are a few examples of foods that contain measurable
amounts of betaine. Within the body, betaine is produced by the
oxidation of choline. Betaine acts as a methyl donor involved
with the conversion of homocysteine to methionine. Methionine
is converted to S-adenosylmethionine (SAMe), the primary
methyl donor for numerous biochemical reactions in the liver
and various other tissues.
Given the multifunctional properties of SAMe, it indeed has
been investigated as a dietary supplement. Those of you who
work in or shop at supplement retailers undoubtedly seen SAMe
on the shelves. Recent reviews have indicated SAMe as an
effective therapeutic agent against the risk for Alzheimer’s
disease,13 treating alcoholic liver disease,14 and depression.15
SAMe has also been pretty heavily touted as an anti-arthritic
agent, and is commonly included in joint support supplements.
However, a recent systematic review by Rutjies et al found that
the routine use of SAMe to treat osteoarthritis of the knee and
hip is not advisable due to a lack of clinically relevant effects
within a scant body of poorly designed studies.16
Like the present one, prior studies haven’t been spectacular, but
did show some promise. In an acute effect trial by Armstrong et
al,17 5 g betaine in a both water and carb-electrolyte solution
caused a positive trend toward longer sprint time at 85%
V02max compared to the control treatments. In a 15-day study
by Hoffman et al,18 1.25 g betaine taken twice per had no
significant effect on total repetitions performed to exhaustion at
75% 1RM, or in the number of repetitions performed at 90% of
both peak and mean power in the bench press. However, betaine
caused a greater number of repetitions performed in the squat on
days 7-8, and a similar trend was seen on days 14-15. No
differences between groups were seen in vertical jump and
bench press throw power, or in the Wingate test. Hoffman et al
thus concluded that betaine “appeared to” improve the endurance
and quality of reps in the squat – which is a nice way of saying it
helped a tiny bit.
The present trial’s positive outcomes add to the very preliminary
body of research examining betaine’s effectiveness for
performance enhancement. However, longer trial durations in
future research with better dietary control are necessary to
consider betaine useful for this purpose.
[Back to Contents] Page 9

Eating behavior and obesity at Chinese buffets.
Wansink B, Payne CR. Obesity (Silver Spring). 2008
Aug;16(8):1957-60. [Medline]
PURPOSE: The aim of this study was to investigate
whether the eating behaviors of people at all-you-can-eat
Chinese buffets differs depending upon their body mass.
The resulting findings could confirm or disconfirm
previous laboratory research that has been criticized for
being artificial. DESIGN: Trained observers recorded
the height, weight, sex, age, and behavior of 213 patrons
at Chinese all-you-can-eat restaurants. Various seating,
serving, and eating behaviors were then compared across
BMI levels. RESULTS: Patrons with higher levels of
BMI were more likely to be associated with using larger
plates vs. smaller plates (OR 1.16, P < 0.01) and facing
the buffet vs. side or back (OR 1.10, P < 0.001). Patrons
with higher levels of BMI were less likely to be
associated with using chopsticks vs. forks (OR 0.90,P <
0.05), browsing the buffet before eating vs. serving
themselves immediately (OR 0.92, P < 0.001), and
having a napkin on their lap vs. not having a napkin on
their lap (OR 0.92, P < 0.01). Patrons with lower BMIs left more
food on their plates (10.6% vs. 6.0%, P < 0.05) and chewed
more per bite of food (14.8 vs. 11.9, P < 0.001).
CONCLUSIONS: These observational findings of real-world
behavior provide support for laboratory studies that have
otherwise been dismissed as artificial SPONSORSHIP: None
listed.
Study strengths
Well, how can a study about Chinese buffets not be interesting?
Since this was an observational study rather than an
interventional study, it’s not necessarily conducive to my typical
strengths/weaknesses critique. However, this study did have its
sizable share of technical merits. First of all, it was a rather
large-scale study. From unobtrusive locations in the restaurants,
22 trained observers monitored and coded the behavior of 213
patrons at 11 all-you-can eat Chinese buffets across the United
States. The observers underwent 2 training sessions involving
weight, height, and age estimation. Photos of various people and
their weights were provided as further visual benchmarks to use
when estimating weight.
Furthermore, a visual body shape chart of 32 body typologies
(16 for men; 16 for women) was used to enhance and to assess
the accuracy of their estimates. To further reinforce the accuracy
of height estimation, observers were actually trained to use the
known height of buffet glasses as benchmarks from which to
estimate the height if the patrons as they served themselves.
Study limitations
As an observational study, this type of research is incapable of
demonstrating cause-and-effect. It’s limited to suggesting
correlations/associations between variables. Causal relationships
can only be determined by randomized controlled trials (RCTs),
which attempt to isolate the independent & dependent variables
while as many extraneous/confounding variables as possible are
Alan Aragon’s Research Review – July 2010
controlled. Still, the covert, systematic coding of behaviors of
those in a free-living environment can provide useful data, and
new ideas for further research in both the observational and
experimental sectors. A final limitation is that not all the
outcomes here may apply to cuisine outside of Chinese food.
Comment/application
The chart above outlines the relationship between the patrons’
eating behaviors and the range of body mass index (BMI)
brackets. The authors echo my thoughts that this study can only
draw associations between variables rather than elicit causal
relationships. However, they make the point that, “…these
findings are notably consistent with important principles of food
intake that have been isolated only in highly controlled—but
sometimes artificial—laboratory situations.”
Behavior associations that have been consistent with controlled
experiments are either related to food convenience (i.e., serving
one’s self without browsing first or using a fork instead of
chopsticks), consumption norms (using larger plates), and rather
esoteric principles such as salience (facing the food instead of
side- or back-positioning). However, other findings are less
consistent with the outcomes of controlled experiments, such as
leftovers and the number of chews per bite of food. A
confounding aspect of the latter is that bite size decreases as the
meal’s consumption progresses. Since the authors used 10 bites
as a surrogate measure for an entire meal, this could potentially
have lead to the overestimation of the average chews per bite.
Nevertheless, BMI was inversely correlated with number of
chews per bite.
For those unfamiliar with Dr. Brian Wansink, the principal
investigator of the present study, he has become a sort of
celebrity among academic folks and the lay public alike. The
following quote is from study’s conclusion: “The silver lining to
all of these findings, in tandem with laboratory findings, is that
they reinforce that small changes in one’s environment may
lessen one’s tendency to overeat.”
Wansink’s practical recommendations from this study boil down
to making food less convenient to access (i.e., keeping serving
bowls off the table), using smaller plates, and by altering the
presentation & thus salience of food (i.e., using a fruit bowl
instead of a cookie jar).
[Back to Contents] Page 10
1. Tremblay A, et al. Impact of exercise intensity on body
fatness and skeletal muscle metabolism. Metabolism. 1994
Jul;43(7):814-8. [Medline]
2. Grediagin A, et al. Exercise intensity does not effect body
composition change in untrained, moderately overfat
women. J Am Diet Assoc. 1995 Jun;95(6):661-5. [Medline]
3. Black SE, et al. Improved insulin action following short-
term exercise training: role of energy and carbohydrate
balance. J Appl Physiol. 2005 Dec;99(6):2285-93.
[Medline]
4. Berneis KK, Krauss RM. Metabolic origins and clinical
significance of LDL heterogeneity. J Lipid Res. 2002
Sep;43(9):1363-79. [Medline]
5. Krauss RM, et al. Separate effects of reduced carbohydrate
intake and weight loss on atherogenic dyslipidemia. Am J
Clin Nutr. 2006 May;83(5):1025-31; quiz 1205. [Medline]
6. Bird SP, et al. Independent and combined effects of liquid
carbohydrate/essential amino acid ingestion on hormonal
and muscular adaptations following resistance training in
untrained men. Eur J Appl Physiol. 2006 May;97(2):225-38.
Epub 2006 Mar 24. [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. 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]
9. Tipton KD, Wolfe RR. Protein and amino acids for athletes.
J Sports Sci. 2004 Jan;22(1):65-79. [Medline]
10. Balage M, Dardevet D. Long-term effects of leucine
supplementation on body composition. Curr Opin Clin Nutr
Metab Care. 2010 Jan 25. [Epub ahead of print] [Medline]
11. Coombes JS, McNaughton LR. Effects of branched-chain
amino acid supplementation on serum creatine kinase and
lactate dehydrogenase after prolonged exercise. J Sports
Med Phys Fitness. 2000 Sep;40(3):240-6. [Medline]
12. [No authors listed] Betaine. Monograph. Altern Med Rev.
2003 May;8(2):193-6. [Medline]
13. Shea TB, Chan A. S-adenosyl methionine: a natural
therapeutic agent effective against multiple hallmarks and
risk factors associated with Alzheimer's disease. J
Alzheimers Dis. 2008 Feb;13(1):67-70. [Medline]
14. Purohit V, et al. Role of S-adenosylmethionine, folate, and
betaine in the treatment of alcoholic liver disease: summary
of a symposium. Am J Clin Nutr. 2007 Jul;86(1):14-24.
[Medline]
15. Williams AL, et al. S-adenosylmethionine (SAMe) as
treatment for depression: a systematic review. Clin Invest
Med. 2005 Jun;28(3):132-9. [Medline]
16. Rutjes AW, et al. S-Adenosylmethionine for osteoarthritis
of the knee or hip. Cochrane Database Syst Rev. 2009 Oct
7;(4):CD007321. [Medline]
17. Armstrong LE, et al. Influence of betaine consumption on
strenuous running and sprinting in a hot environment. J
Strength Cond Res. 2008 May;22(3):851-60. [Medline]
18. Hoffman JR, et al. Effect of betaine supplementation on
power performance and fatigue. J Int Soc Sports Nutr. 2009
Feb 27;6:7. [Medline]

Alan Aragon’s Research Review – July 2010 [Back to Contents] Page 11


Bytes of baloney.
By Alan Aragon
A butterfly’s wings
The butterfly effect is a concept in chaos theory where small
initial differences can cause large differences in the behavior of a
system. The common example here is the potential of the flap of
a butterfly’s wings in one part of the world affecting the weather
in another part of the world through a dynamic, exponential
chain of events. I tend to see this same idea applying to online
information. Its accuracy is critical because of how rapidly or
“virally” it can spread. While the internet has become a
spectacular boon for legitimate educators, it has also evolved
into a highly potent campaign platform for bull crap.
By the end of this short lesson…
A perfect example of the flap of a butterfly’s wings is the video
depicted above (link here). The company producing it gives the
impression of being a formal educational outfit which for many
layfolk raises the video’s credibility. In fairness, I haven’t
evaluated the rest of their videos, but based on the one we’re
examining, I’d be weary of their body of work. To quote the
above video’s introduction, “By the end of this short lesson,
you’ll be able to explain the answers to the following questions
to your friends.” So, right off the bat, they’re encouraging the
word-of-mouth spreading of this purported wisdom. Here are the
questions that they claim to answer:
1. Why are acid reflux medications one of the fastest
growing groups of medication in the US?
2. Why is it that Americans have the highest consumption of
calcium in the world, yet poor bone health?
3. How could a diet soda with zero calories make you gain
weight?
They move on to discuss the idea the foods differ in their place
along the acid-alkaline continuum, and duly mention that the
Alan Aragon’s Research Review – July 2010
body has multiple mechanisms in place that preserve the pH
balance of the blood, otherwise death would quickly ensue. They
go on to mention that problems occur when the body is forced to
work “overtime” by the consuming too much of the following
acid-forming foods: coffee, alcoholic beverages, soft drinks,
processed foods, fried foods, high-fructose corn syrup, sugar,
artificial sweeteners, and animal proteins.
When laying down the general rules of how to spot acidic foods,
they reiterate various animal products. In the process, they also
mention tea. They also mention high stress levels as being an
acid-forming agent. For the alkaline foods, they mention various
vegetables and fruits. They correctly mention that as a general
rule, the more processed the food, the more acid-forming it will
be. They also correctly mention that just because a food is acid-
forming, that doesn’t mean it’s unhealthy. Blueberries and
walnuts are used as examples of this.
So far, there isn’t anything glaringly inaccurate about the
categorization of foods as generating more acid or alkaline end-
products. In fact, their disclaimer that certain acid-forming foods
can be good for you was a diligent move. But, from this point,
things start to go from equivocal to downright wacky.
Addressing question 1
Examples of “typical American meals” consisting of processed
foods are given (hamburgers, hot dogs, fries, potato chips, soda,
beer, etc). They claim that these meals are detrimental because
of their acid-forming nature, which causes the body to fight to
preserve balance by drawing upon and leeching out its alkaline-
forming minerals like calcium, magnesium, iodine, potassium,
and sodium. This is where they tie in the answer to question 1,
claiming that since acid reflux medications block acid
production, their widespread use is due to acid-forming
foods. Is it really this simple? The short answer is, no.
The pathogenesis of gastroesophageal reflux disease (GERD) is
multi-factorial, rather than simple and singular, as the video
suggests. In other words, acid reflux cannot be easily solved
with a simple list of foods to eat and foods to avoid. The factors
involved with the development of GERD are both anatomical
and functional. The primary mechanism of the reflux is called
transient lower esophageal sphincter relaxation (TLESR), and is
thought to account for the majority of reflux occurrences.
An increased number of TLESR episodes may lead to GERD,
but the underlying causes of these functional disorders are not
completely understood nor accounted for. According to research
done on twins,1,2 GERD may also have a strong genetic
component, since hereditability accounted for 31%-43% of the
likelihood of developing the disease.
In terms of gathering the research as a whole and making heads
or tails of it, Festi and colleagues conducted a comprehensive
examination of the literature on this topic spanning from 1999 to
2008,3 and their findings simply do not support our neat little
Youtube video. I’ll quote the authors directly:
“In conclusion, no definitive data exist regarding the role of diet
and, in particular, of specific foods or drinks, in GERD clinical
manifestations.”
[Back to Contents] Page 12
Instead of specific foods or drinks being special agents of reflux weight gain. Once again, we have to demand sufficient scientific
disease, a far stronger association exists with excess backing for this claim.
bodyweight.3-5 Weight loss has been repeatedly seen to reduce
I personally could not find any research showing a causal
GERD symptoms and manifestations, regardless of whether the
relationship between artificially sweetened soft drinks and
weight loss occurred by diet or surgery. In their paper, Festi et al
weight gain, let alone research indicating a thyroid-mediated
are very clear in their assertion that there is no definitive data
mechanism for this phenomenon. Among the research that does
pointing to specific dietary choices that alleviate or prevent
exist, the majority of studies lasting beyond the acute phase have
reflux disease. As the research stands, religiously fixating on
demonstrated the superior effectiveness of artificially sweetened
acid/alkaline food charts is highly questionable for the treatment
beverages to sugar-sweetened ones for weight loss.11-14
or prevention of GERD.
Therefore, the claim that diet soft drinks cause weight gain is
nothing but a false alarm.
Addressing question 2
The video closes by recommending more rest and relaxation to
The 2nd question was, why is it that Americans have the highest
decrease stress, and actively choosing foods that are highly
consumption of calcium in the world, yet poor bone health? To
alkaline, and use their product called the Food Target that ranks
begin with, this question contains false assumptions. First off, it
foods on an acid-alkaline basis. They further suggesting
implies that correlation automatically equals causation, which is
monitoring your own pH via litmus strips for the saliva and urine
false. There are a multitude of factors leading to brittle bones
(as if there’s not enough ways for people to compulsively obsess
(not the least of which is insufficient weight-bearing activity and
over themselves).
an actual lack of bone-building nutrition, including calcium
intake). Pointing the finger at acid-forming foods (the video
Let the flapping commence
indicts dairy) is false.6,7 Secondly, the US is not the highest the
highest per-capita consumer of calcium in the world nor is it the Hopefully this critique will initiate its own butterfly effect; one
largest per-capita consumer of dairy (more info here & here). that might counteract the progression of nonsense propagated
online.
Back to the question, the makers of the video answer this
question by saying that an acid-forming diet forces the body to
use its mineral stores to neutralize blood pH, causing the
References
leeching of calcium from bone. Keep in mind that this is right
after using dairy as an example. They go on to blame acidic 1. Cameron AJ, et al. Gastroesophageal reflux disease in
beverages (soda, coffee, energy drinks, alcohol). monozygotic and dizygotic twins. Gastroenterology. 2002
Jan;122(1):55-9. [Medline]
The important question is, how solid is the research evidence
2. Mohammed I, et al. Genetic influences in gastro-
behind these claims? The short answer is, no again. The idea that
oesophageal reflux disease: a twin study. Gut. 2003
acid-forming diets are the culprit in osteoporosis has been
Aug;52(8):1085-9. [Medline]
refuted by no less than 3 separate meta-analyses by Fenton et al,
3. Festi D, et al. Body weight, lifestyle, dietary habits and
and I’ll quote the concluding segments of each one:8-10
gastroesophageal reflux disease. World J Gastroenterol.
ƒ “Dietary advice that dairy products, meats, and grains are 2009 Apr 14;15(14):1690-701. [Medline]
detrimental to bone health due to “acidic” phosphate 4. Hampel H, et al. Meta-analysis: obesity and the risk for
content needs reassessment. There is no evidence that gastroesophageal reflux disease and its complications. Ann
higher phosphate intakes are detrimental to bone health.” 8 Intern Med. 2005 Aug 2;143(3):199-211. [Medline]
5. El-Serag HB, et al. Obesity is an independent risk factor for
ƒ “There is no evidence from superior quality balance studies
GERD symptoms and erosive esophagitis. Am J
that increasing the diet acid load promotes skeletal bone
Gastroenterol. 2005 Jun;100(6):1243-50. [Medline]
mineral loss or osteoporosis. Changes of urine calcium do
6. Heaney RP. Calcium, dairy products and osteoporosis. J Am
not accurately represent calcium balance. Promotion of the
Coll Nutr. 2000 Apr;19(2 Suppl):83S-99S. [Medline]
“alkaline diet” to prevent calcium loss is not justified.” 9
7. Heaney RP. Protein and calcium: antagonists or synergists?
ƒ “Evidence suggests a linear association between changes in Am J Clin Nutr. 2002 Apr;75(4):609-10. [Medline]
calcium excretion in response to experimental changes in 8. Fenton TR, et al. Phosphate decreases urine calcium and
net acid excretion. However, this finding is not evidence that increases calcium balance: a meta-analysis of the
the source of the excreted calcium is bone or that this osteoporosis acid-ash diet hypothesis. Nutr J. 2009 Sep
calciuria contributes to the development of osteoporosis.” 10 15;8:41. [Medline]
9. Fenton TR, et al. Meta-analysis of the effect of the acid-ash
Addressing question 3 hypothesis of osteoporosis on calcium balance. J Bone
Miner Res. 2009 Nov;24(11):1835-40. [Medline]
The final question deals with the video’s attention-grabbing
10. Fenton TR, et al. Meta-analysis of the quantity of calcium
headline of how a diet soda with zero calories can “cause”
excretion associated with the net acid excretion of the
weight gain. According to them, the phosphoric acid contained
modern diet under the acid-ash diet hypothesis. Am J Clin
within diet sodas can cause the body to leech out iodine, which
Nutr. 2008 Oct;88(4):1159-66. [Medline]
regulates thyroid function. An improperly functioning thyroid
can result in the slowing of metabolism, which in turn results in

Alan Aragon’s Research Review – July 2010 [Back to Contents] Page 13

11. Bellisle F, Drewnowski A. Intense sweeteners, energy
intake and the control of body weight. Eur J Clin Nutr.
2007;61:691–700. [Medline]
12. Porikos KP, Booth G, Van Itallie TB. Effect of covert
nutritive dilution on the spontaneous food intake of obese
individuals: a pilot study. Am J Clin Nutr. 1977;30:1638–
44. [Medline]
13. Tordoff MG, Alleva AM. Effect of drinking soda sweetened
with aspartame or high-fructose corn syrup on food intake
and body weight. Am J Clin Nutr. 1990;51:963–9.
[Medline]
14. Raben A, et al. Sucrose compared with artificial sweeteners:
different effects on ad libitum food intake and body weight
after 10 wk of supplementation in overweight subjects. Am
J Clin Nutr. 2002;76:721–9. [Medline]

 
 

Responses from the authors about the study below.1

The following is a response I got from Dr. Steven Sayers,

regarding the N:
The “N” you see is the designation of Newtons (which is the
standard way in journals you express force). It would be so
much easier if we could just use lbs! To convert lbs to N, just
multiply the number of lbs by 4.44822162

The following is a response I got from Bryan Mann to the

following AARR subscriber comment, “Looking at the fulltext,
it's still not clear to me how the fourth set determinted the
"initial weight" for next week's session.”
Everything is based on an estimated 6rm for the APRE6
routine. So if week one, my third set is 225 lbs and I do 13
reps, I use the adjustment chart and see to add 15 lbs on for
my 4th set, which would be 240 lbs. I again do 13 reps, I look
at the adjustment chart and see to add on another 15 lbs. This
adjustment makes this estimated 6RM 255lbs which is what
the first 3 sets are based off of. So in week 2 you would do
10 at about 130 lbs, 6 at about 195 lbs, and 255 lbs for
maximal repetitions.

1. Mann JB, et al. The effect of autoregulatory progressive resistance

exercise vs. linear periodization on strength improvement in college
athletes. J Strength Cond Res. 2010 Jun 10. [Epub ahead of print]
[Medline]

In this video, rapper/actor LL Cool J is a guest on The View, and

gets put on the spot with an impromptu workout.

If you have any questions, comments, suggestions, bones of

contention, cheers, jeers, guest articles you’d like to submit, or
any feedback at all, send it over to aarrsupport@gmail.com.

Alan Aragon’s Research Review – July 2010 [Back to Contents] Page 14