ean 10 Almonds vs complex carbohydrates in a weight

reduction program.
Wien MA, et al. Int J Obes Relat Metab Disord. 2003
Nov;27(11):1365-72. [Medline]

12 Soy claims & controversies: what does science

have to say?
By Alan Aragon

Copyright © February 1st, 2010 by Alan Aragon

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

2 Supplemental BCAA: limitations & applications.

By Alan Aragon

5 Lack of suppression of circulating free fatty acids

and hypercholesterolemia during weight loss on a
high-fat, low-carbohydrate diet.
Hernandez TL, et al. Am J Clin Nutr. 2010 Jan 27. [Epub
ahead of print] [Medline]
6 Twelve weeks of moderate aerobic exercise
without dietary intervention or weight loss does
not affect 24-h energy expenditure in lean and
obese adolescents.
van der Heijden GJ, Sauer PJ, Sunehag AL. Am J Clin Nutr.
2010 Mar;91(3):589-96. Epub 2010 Jan 27. [Medline]

7 The effects of a pre-workout supplement

containing caffeine, creatine, and amino acids
during three weeks of high-intensity exercise on
aerobic and anaerobic performance.
Smith AE, et al. J Int Soc Sports Nutr. 2010 Feb 15;7(1):10.
[Epub ahead of print] [JISSN]
8 Effect of n-3 fatty acids and antioxidants on
oxidative stress after exercise.
McAnulty SR, et al. Med Sci Sports Exerc. 2010 Feb 13.
[Epub ahead of print] [Medline]

9 Postexercise fat oxidation: effect of exercise

duration, intensity, and modality.
Warren A, et al. Int J Sport Nutr Exerc Metab. 2009
Dec;19(6):607-23. [Medline]

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


Supplemental BCAA: limitations & applications.
By Alan Aragon
Introduction
For several years now, branched chain amino acids (BCAA:
leucine, isoleucine, and valine) have been among the biggest-
selling supplements in the fitness and sports nutrition market. I
refuse to seek out a reference for that statement, because it’s so
blatantly obvious. The rationale appears compelling; BCAAs
account for 35–40% of the dietary essential amino acids in body
protein and 14–18% of the total amino acids in muscle proteins.1
Leucine is thought to play a critical role in modulating protein
synthesis in skeletal muscle via multiple signaling pathways
including the phosphorylation of ribosomal protein S6 Kinase,
eukaryotic initiation factor (eIF)4E binding protein-1, and
eIF4G.2 A key regulator of these mechanisms is the protein
kinase called the mammalian target of rapamycin (mTOR),
which is intimately linked to leucine availability.
While there is plenty of science behind the role of BCAA in
muscle protein synthesis and the prevention of muscle protein
breakdown, the benefit of supplementing the diet with BCAA on
top of a pre-existing sufficiency is controversial. The following
discussion will focus on the limitations and potential
applications of BCAA supplementation for the purpose of
muscle growth and preservation in the face of training and
various phases of dieting.
BCAA content of foods
One of the most overlooked aspects when discussing the utility
of BCAA supplementation is the pre-existent content of BCAA
within the diet. Here’s just a handful of common examples:
ƒ At approximately 25% BCAA (5 g per 20 g scoop), whey is
exemplary in this regard.
ƒ Most lean animal flesh is roughly 17-18% BCAA (5 g per 6
oz portion).
ƒ In the plant food realm, tofu and soy protein isolate are quite
comparable at roughly 15-18% BCAA.
ƒ Cottage cheese is roughly 10-13% BCAA (2-3 g per cup).
ƒ Depending on fat level, other cheeses are roughly 7%
BCAA (2 g per oz).
ƒ Beans and peas are roughly 4-5% BCAA (2-3 g per cup,
cooked measure).
ƒ Nuts are about 2% BCAA by calories (4 g per cup).
Figuring that the typical OCD fitness nut’s protein intake
averages at about 15% BCAA, an example intake of 200 g
protein would amount to 30g BCAA for the day.
Leucine dose & the maximal anabolic effect of a meal
Donald Layman and his protégé Layne Norton are two of the
field’s foremost experts on the effect of leucine and protein
synthesis. According to Layne’s presentation at the 5th Annual
ISSN Conference, 3-4 g leucine per meal is the amount that’s
likely to maximally stimulate muscle protein synthesis.3 This
Alan Aragon’s Research Review – February 2010
corresponds to a leucine dosage range of 0.045-0.06 g/kg. This
hypothesis is based on acute research by Paddon-Jones et al4 and
Tipton et al.5 A 3-4 g leucine dose is achievable by consuming
one of the following examples:
ƒ 6-8 oz of most land & sea animal flesh.
ƒ 1.5-2 scoops of whey (assuming roughly a 20 g scoop).
ƒ 2-2.5 scoops soy protein.
ƒ 1.5 cups of cottage cheese.
ƒ 3 oz parmesan cheese.
ƒ 6-8 g supplemental BCAA (most brands have leucine,
isoleucine, and valine in a 2:1:1 proportion).
ƒ Of course, you can also buy supplemental leucine and dose
3-4 g straight-up, sort of like fairy dust. However, this might
not be optimal. A recent literature review by Balage and
Dardevet concluded the following:6
“There is some evidence that long-term leucine availability
is sufficient to improve muscle mass or performance during
exercise training. However, it needs to be associated with
other amino acids to be efficient (for example, through
leucine-rich proteins).”
Is free-form BCAA better for anabolism than BCAA within
food?
Some would argue that free-form BCAA are more beneficial
because they aren’t protein-bound within the matrix of food and
can be more quickly absorbed. Some folks believe that BCAA
within food (or bound to intact proteins as in the case of whey
concentrate and whey isolate) don’t cause a rapid enough rise
and fall in amino acid levels, which supposedly compromises the
anabolic response.
The above idea is based on the so-called protein stat hypothesis,
which suggests that there’s a membrane-bound sensor (likely to
be extracellular) which detects and is influenced by relative
changes in amino acid concentrations rather than absolute
changes.7 The protein stat hypothesis attempts to explain the
refractory response seen in muscle protein synthesis when amino
acid (AA) levels are kept constantly elevated. That is, protein
synthesis begins to decline despite elevated AA levels.
Speculation points to drops in insulin (after initial elevation)
being at least partially responsible for the refractory response to
sustained AA levels, since the time course of plasma insulin
somewhat reflects the decline in muscle protein synthesis.8,9
Avoiding the refractory response vs. clinging to optimism
Assuming that the protein stat hypothesis holds truth, a potential
solution is to ingest BCAA for rapid increases & subsequent
rapid drops in extracellular amino acid levels in attempt to
circumvent the refractory response seen with sustained amino
acid elevations. A popular recommendation is to dose roughly 5-
10 g BCAA between meals. The research cited to support this
tactic is infusion data by Bohe et al8 and a highly lopsided study
by Paddon-Jones et al.10 By the end of the test period of the latter
study, the experimental group consumed 45g EAA and 90g
CHO above and beyond the control group, which (predictably)
resulted in greater protein synthesis. Another design flaw was
that the control group's protein intake totalled 64g for the day,
while the supplemented group averaged 109g. Essentially, this
[Back to Contents] Page 2
was a comparison of insufficient protein intake versus barely
adequate intake.
The point I’m trying to get across is that between-meal BCAA
dosing is based largely on optimistic assumptions involving the
protein stat hypothesis. This tactic stakes its claims on the basis
of short-term data (some of it being infusion data), not on any
long-term research examining effects on body composition or
training performance. These data don’t exist...yet.
Waiting for the goods to hit the Pubs
To my knowledge, an unpublished study by Stoppani et al is the
only one that has examined the chronic effects of BCAA dosing
on top of a pre-existent high protein intake on subjects
undergoing a structured training program. I’ve been anticipating
its full-text arrival in the Journal of the International Society of
Sports Nutrition, but it’s currently only published as a poster
presentation.11 In the meantime, the outcomes of this trial are
intriguing enough to warrant some commentary.
3 during-training protocols were compared: 1) 28 g carbs from
Gatorade, 2) 28 g whey, and 3) 4 scoops of Xtend, containing 14
g BCAA. There are a few aspects about the results of this trial
that seem far-fetched:
ƒ Despite the subjects being strength-trained (not novices), the
whey group gained 2 kg LBM, and the BCAA group gained
4 kg in 8 weeks. This is an exceptionally high rate of gain
for drug-free subjects, trainees who aren’t on a post-dieting
rebound, and subjects who aren’t in the initial phase of
creatine loading.
ƒ To top it off, the BCAA group lost more fat than the whey
group (2% vs 1%, respectively), and gained more benching
and squatting strength than the whey group as well.
ƒ The above results occurred despite an abundant daily
protein intake of 2.2-2.4 g/kg.
ƒ The marked advantage of the BCAA treatment in all
parameters boils down to a mere 7 g more BCAA than the
whey group.
ƒ The based on a lack of research evidence, the vitamin B-6,
citrulline malate, and glutamine in Xtend are not likely to be
significant ergogenic contributors to the superior results of
the BCAA group.
More details excluded from the abstract can be seen in this
forum post. The skeptic in me is tempted to chalk up some of the
results to not just funding source (Scivation), but also the
longstanding friendship between Jim Stoppani and the Scivation
staff. The fact is, there’s no way to quantify the degree of
commercial bias inherent in this trial – or any other for that
matter. So, once again, it will boil down to how optimistic you
choose to be towards a single study if/when it gets published.
Challenging the benefit of BCAA while dieting
Traditionally, the use of supplemental BCAA, even among
conservative enthusiasts and competitors, is during prolonged
hypocaloric states where the main goal is weight or fat loss.
However, as you’ll soon see, supplementing with BCAA might
prove to make dieting even tougher to endure. For some time
now, I’ve been a proponent of using intact protein sources such
Alan Aragon’s Research Review – February 2010
as whey or flesh for this purpose instead of BCAA. Stick with
me on this explanation. During times of aggressive dieting, a
potential case can be made for the caloric economy of using
essential amino acids to replace a portion of intact proteins,
which contain non-essential amino acids (NEAAs don’t
contribute to protein synthesis). However, this calorie savings
is minor. Take whey protein for example. It’s about 25% BCAA.
If someone used a good 20g of BCAA surrounding the workout,
it would take about 80 g of whey to match that BCAA dose. So,
with the whey dose, you’re getting an extra 240 kcals beyond
what you’d get with just BCAA. If we assume 4 training bouts
per week, this amounts to a 960 kcals per week more than using
just BCAA, which totals out to 3840 kcals per month. In a 3-
month dieting phase, we’re looking at a “disadvantage” of just a
little over 3 lbs. Here’s a simple solution: start your dieting prep
2 weeks early, and stick with the whey. This will impart a
number of advantages:
ƒ You’ll save money.
ƒ You’ll get just as much BCAAs, plus the rest of the EAAs.
ƒ You’ll get several other beneficial compounds within whey
that are missing from isolated BCAA, including lactoferrin,
immunoglobins, lactoperoxidase, and glycomacropeptide.12
ƒ Whey and/or flesh (& other intact protein sources) are likely
to cause greater satiety than just taking BCAA.
This leads me to my next point: you might just exacerbate
hunger by supplementing with BCAA while dieting. Any claims
of greater fullness while dosing BCAA are likely due to the
accompanying water intake, not the BCAA.
BCAA for appetite stimulation?
In clinical circles, a relatively well-known use of BCAA is to
treat liver disease.13 However, a more esoteric use of BCAA is
as an antianorexic-anticachexic agent. In other words, BCAA
has been successfully used in humans as a therapeutic modality
to treat conditions where a lack of appetite can lead to physical
wasting.14 The benefit of BCAA for this purpose instead of
appetite drugs is a lack of adverse side effects. The main
mechanism through which BCAA is thought to work its
appetite-stimulating magic is by competing with tryptophan for
entry into the brain, thus reducing the production of serotonin, a
satiating neurotransmitter.
The unanswered question is whether BCAA’s appetite-
stimulating effect in diseased subjects can be extrapolated to the
healthy population pursuing the goal of eating more for muscular
growth. It’s also tempting to deduce that the potential orexigenic
effect of BCAA supplementation would contraindicate its use
during dieting – a time when the last thing you want to do is
increase the drive to eat. In contrast to the hunger-spiking
potential of BCAA is the satiating effect of whey seen
repeatedly in research.15-17 This is another reason whey wins for
dieting purposes – you still get the BCAA, but you also get
greater appetite control. For those seeking a theoretically sound
tactic to increase the drive to eat, BCAA seems to be a safe bet.
Conclusions & applications
BCAA is abundant in protein-rich diets common to athletes and
fitness enthusiasts. On this basis alone, it’s difficult to justify
[Back to Contents] Page 3
supplementing such diets with additional BCAA. Dosing free- 12. Marshall K. Therapeutic applications of whey protein.
form BCAA between meals to circumvent the refractory Altern Med Rev. 2004 Jun;9(2):136-56. [Medline]
phenomenon is not much more than optimistic hypothesizing. 13. Charlton M. Branched-chain amino acid enriched
It’s based on acute data in the absence of long-term research supplements as therapy for liver disease. J Nutr. 2006
examining concrete endpoints like gains in size and strength, or Jan;136(1 Suppl):295S-8S. [Medline]
preservation of lean mass under chronic hypocaloric conditions. 14. Laviano A, et al. Branched-chain amino acids: the best
Replacing intact proteins with BCAA only minimally compromise to achieve anabolism? Curr Opin Clin Nutr
economizes caloric consumption during dieting. Furthermore, it Metab Care. 2005 Jul;8(4):408-14. [Medline]
misses the beneficial biofractions of intact proteins like whey, 15. Burton-Freeman BM. Glycomacropeptide (GMP) is not
and has the potential to stimulate appetite. While this has limited critical to whey-induced satiety, but may have a unique role
applications for weight gain (or preventing weight loss), in energy intake regulation through cholecystokinin (CCK).
supplementing with BCAA is typically done during dieting Physiol Behav. 2008 Jan 28;93(1-2):379-87. [Medline]
phases where appetite stimulation is desired least. Ironic, isn’t it? 16. Veldhorst MA, et al. Dose-dependent satiating effect of
whey relative to casein or soy. Physiol Behav. 2009 Mar
References 23;96(4-5):675-82. [Medline]
17. Akhavan T, et al. Effect of premeal consumption of whey
1. Shimomura Y, et al. Nutraceutical effects of branched-chain
protein and its hydrolysate on food intake and postmeal
amino acids on skeletal muscle. J Nutr. 2006
glycemia and insulin responses in young adults. Am J Clin
Feb;136(2):529S-532S. [Medline]
Nutr. 2010 Feb 17. [Epub ahead of print] [Medline]
2. Kimball SR, Jefferson LS. Signaling pathways and
molecular mechanisms through which branched-chain
amino acids mediate translational control of protein
synthesis. J Nutr. 2006 Jan;136(1 Suppl):227S-31S.
[Medline]
3. Norton L. Optimal Protein Intake & Meal Frequency to
Support Maximal Protein Synthesis & Muscle Mass. June
2008. [ISSN]
4. Paddon-Jones D, et al. Amino acid ingestion improves
muscle protein synthesis in the young and elderly. Am J
Physiol Endocrinol Metab. 2004 Mar;286(3):E321-8.
[Medline]
5. Tipton KD, et al. Postexercise net protein synthesis in
human muscle from orally administered amino acids. Am J
Physiol. 1999 Apr;276(4 Pt 1):E628-34. [Medline]
6. 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]
7. Norton L. Optimal protein intake to maximize muscle
protein synthesis: Examinations of optimal meal protein
intake and frequency for maximizing muscle mass in
athletes. Agro Food Ind. High-Tech. 2009
Mar/Apr;20(2):54-57. [AFI]
8. Bohe J, et al. Latency and duration of stimulation of human
muscle protein synthesis during continuous infusion of
amino acids. Physiol. 2001 Apr 15;532(Pt 2):575-9.
[Medline]
9. Norton, L.E., et al. Translational controls of skeletal muscle
protein synthesis are delayed and prolonged associated with
ingestion of a complete meal. 2007 Experimental Biology
meeting abstracts, p. 221. Abstract #694.6. [Exp Biol]
10. Paddon-Jones D, et al. Exogenous amino acids stimulate
human muscle anabolism without interfering with the
response to mixed meal ingestion. Am J Physiol Endocrinol
Metab. 2005 Apr;288(4):E761-7 [Medline]
11. Stoppani J, et al. Consuming a supplement containing
branched-chain amino acids during a resistance-training
program increases lean mass, muscle strength and fat loss.
Proceedings of the Sixth International Society of Sports
Nutrition (ISSN) Conference and Expo. June 2009. [JISSN]

Alan Aragon’s Research Review – February 2010 [Back to Contents] Page 4


Lack of suppression of circulating free fatty acids and
hypercholesterolemia during weight loss on a high-fat,
low-carbohydrate diet.
Hernandez TL, et al. Am J Clin Nutr. 2010 Jan 27. [Epub ahead
of print] [Medline]
BACKGROUND: Little is known about the comparative effect
of weight-loss diets on metabolic profiles during dieting.
OBJECTIVE: The purpose of this study was to compare the
effect of a low-carbohydrate (</=20 g/d) with a high-
carbohydrate (55% of total energy intake) diet on fasting and
hourly metabolic variables during active weight loss. DESIGN:
Healthy, obese adults (n = 32; 22 women, 10 men) were
randomly assigned to receive either a carbohydrate-restricted
diet [High Fat: mean +/- SD body mass index (BMI; in kg/m(2)):
35.8 +/- 2.9] or a calorie-restricted, low-fat diet (High Carb:
BMI: 36.7 +/- 4.6) for 6 wk. A 24-h in-patient feeding study was
performed at baseline and after 6 wk. Glucose, insulin, free fatty
acids (FFAs), and triglycerides were measured hourly during
meals, at regimented times. Remnant lipoprotein cholesterol was
measured every 4 h. RESULTS: Patients lost a similar amount
of weight in both groups (P = 0.57). There was an absence of
any diet treatment effect between groups on fasting triglycerides
or on remnant lipoprotein cholesterol, which was the main
outcome. Fasting insulin decreased (P = 0.03), and both fasting
(P = 0.040) and 24-h FFA (P < 0.0001) increased within the
High Fat group. Twenty-four-hour insulin decreased (P < 0.05
for both groups). Fasting LDL cholesterol decreased in the High
Carb group only (P = 0.003). In both groups, the differences in
fasting and 24-h FFA at 6 wk were significantly correlated with
the change in LDL cholesterol (fasting FFA: r = 0.41, P = 0.02;
24-h FFA: r = 0.52, P = 0.002). CONCLUSION: Weight loss
was similar between diets, but only the high-fat diet increased
LDL-cholesterol concentrations. This effect was related to the
lack of suppression of both fasting and 24-h FFA.
SPONSORSHIP: Clinical Translational Research Institute at
the University of Colorado at Denver.
Study strengths
All subjects attended weekly group sessions. Here’s something I
haven’t seen: each session was audiotaped and forwarded to
Foster (the lead investigator) and his staff, who reviewed the
sessions to ensure that the curriculum was being followed
accurately by the treatment providers. In addition to the weekly
sessions, compliance to the diets was monitored by measuring
urine ketones at later time points in the parent study.
Study limitations
At 16 subjects per treatment arm, this sample size was larger
than what’s typically seen in diet-related research. Nevertheless,
the authors themselves criticize their sample as being small.
They continue the self-critique by acknowledging that the use of
only healthy obese subjects is limiting since the adverse effects
seen could possibly have been amplified in a more relevant
population – individuals with known cardiovascular disease
(CVD). Dietary records were not taken, which negated the
possibility of any software-based dietary analysis. It would have
Alan Aragon’s Research Review – February 2010
been useful to examine the proportion of fatty acid types
consumed (i.e., poly- mono-, and saturated fatty acids), as well
as the types of carbohydrate and predominant sources of protein.
The degree of control was not even between the diets compared.
The high-carb group’s macronutrient composition (modeled
after the USDA Pyramid) was projected to be ~30% fat, 15%
protein, and 55% carbohydrate. On the other hand, the only
concrete guideline for the low-carb diet was to keep
carbohydrates at approximately 20 grams per day. There were no
specifics set for the remaining protein and fat intake, except to
eat until full. This type of loose programming opens up the
possibility of excessive variability of protein and fat intake
among subjects in the low-carb group. This doesn’t blow the
whole point of the study, but it’s a rather severe design flaw.
Comment/application
There was no significant difference in weight loss between the
groups. I found this surprising, since low-carb treatments tend to
yield more weight loss, especially during the first 6 months.
Thus far, only 1 of 5 long-term trials1 shows a significant weight
loss difference at or past the 12-month mark.2-5 The present
study – within the longer parent study – was only 6 weeks, so I
would have expected to see at least the initial effect of less water
weight due to less glycogen storage in the low-carb group. Not
to mention, the superior satiating effect of a higher protein intake
tends to result in less total caloric consumption. It would also
have been fair to anticipate greater weight loss in the low-carb
group if it involved more protein, and thus a greater thermic
effect. Of course, the potential thermic advantage in the low-carb
group may have been offset by high fat intakes. This can only be
speculated over in the absence of formal dietary analysis.
The present trial raised some concern about the adverse health
potential of the low-carb treatment. While fasting LDL levels
decreased in the high-carb group, they showed a non-significant
increase in the low-carb group. However, it’s notable that the
patterning of LDL was not directly measured. That is, only total
levels of the different lipoproteins were measured, but not the
subtypes. A method capable of determining this is the vertical
auto profile (VAP) method.6 Of relevance here, the VAP test can
distinguish the non-atherogenic larger LDL particle (pattern A)
from the small, dense LDL particle (pattern B) that poses the
risk. Without the use more sophisticated means such as VAP,
lipoprotein assessment is rather nebulous and crude. Another
concern was the low-carb group’s increased fasting and 24-hour
free fatty-acid (FFA) levels. The high-fat diet’s failure to
suppress FFA poses the threat of an overproduction VLDL
triglycerides, which are associated with increased atherogenicity.
Recent research by Bradley et al has also supported the idea that
low-carb, high-fat dieting might pose some cardiovascular risk.7
They found that systemic arterial stiffness increased in the low-
carb group (60% fat, 20% carbohydrate), but not in the low-fat
group (20% fat, 60% carbohydrate), and saw no significant
difference in weight loss or body composition change between
groups over the 8-week trial. Notably, all food intake was lab-
provided instead of self-selected/self-reported. Despite the
adverse effects seen in the present trial’s low-carb treatment,
insufficient control was imposed to draw any firm conclusions.
Still, the “low-carb/high-fat is always healthier” camp shouldn’t
ignore studies like this one.
[Back to Contents] Page 5
Twelve weeks of moderate aerobic exercise without
dietary intervention or weight loss does not affect 24-h
energy expenditure in lean and obese adolescents.
van der Heijden GJ, Sauer PJ, Sunehag AL. Am J Clin Nutr.
2010 Mar;91(3):589-96. Epub 2010 Jan 27. [Medline]
BACKGROUND: Exercise might have a persistent effect on
energy expenditure and fat oxidation, resulting in increased fat
loss. However, even without weight loss, exercise results in
positive metabolic effects. The effect of an aerobic exercise
program on 24-h total energy expenditure (TEE) and its
components-basal (BEE), sleep (SEE), and awake sedentary
(SEDEE) energy expenditure and substrate oxidation-has not
been studied in lean and obese adolescents. OBJECTIVE: The
objective was to test the hypothesis that 24-h energy expenditure
and fat oxidation increase in lean and obese adolescents after 12
wk of moderate aerobic exercise without dietary intervention
and weight loss. DESIGN: Twenty-eight postpubertal Hispanic
adolescents (13 lean [mean +/- SE: age, 15.3 +/- 0.3 y; body
mass index (BMI; in kg/m(2)), 20.2 +/- 0.7; body fat, 18.7 +/-
1.6%] and 15 obese [age, 15.6 +/- 0.3 y; BMI, 33.1 +/- 0.9; body
fat, 38.1 +/- 1.4%]) completed a 12-wk aerobic exercise program
(4 x 30 min/wk at > or =70% of VO(2 peak)) without weight
loss. Energy expenditure and substrate oxidation were quantified
by 24-h room calorimetry at baseline and postexercise.
RESULTS: This aerobic exercise program did not affect 24-h
TEE, BEE, SEE, or SEDEE in lean or obese participants. In
obese adolescents, respiratory quotient (RQ) and substrate
oxidation also did not change. In lean adolescents, 24-h RQ and
RQ during SEE decreased (both P < 0.01) and fat oxidation
increased (P < 0.01). CONCLUSION: 12-wk aerobic exercise
program did not increase TEE, BEE, SEE, or SEDEE in either
lean or obese sedentary adolescents. Furthermore, 24-h fat
oxidation did not change in the obese adolescents, whereas it
increased in the lean adolescents. SPONSORSHIP: NICHD
RO1 HD044609, Baylor General Clinical Research Center grant
MO1-RR-00188-34, and USDA CRIS 6250-51000-046.
Study strengths
This study addresses the important question of how to alleviate
the youth obesity problem that’s particularly prevalent among
minority populations.8 This is perhaps the first trial to ever
examine the chronic effect of exercise on 24-hour total energy
expenditure (TEE), as well as its subcomponents: basal energy
expenditure (BEE), sleep energy expenditure (SEE), and awake
sedentary energy expenditure (SEDEE). Whole-room
calorimetry was used. To control for variability in dietary intake
on baseline versus postexercise measurements, subjects
received, before both studies, an identical diet whose caloric
content was individually determined. The food was delivered to
the subjects by the metabolic research kitchen. To isolate the
effect of exercise, participants were told not to maintain their
habitual diet, but follow the controlled diet provided the week
before both study occasions.
Study limitations
To get the obvious out of the way, the outcomes of this trial may
be limited to the population studied (adolescents). The outcomes
may be limited to the exercise protocol used (70% VO2max for
Alan Aragon’s Research Review – February 2010
30 minutes, 4 times per week). A more ideal program would
have involved resistance training, as opposed to merely
endurance-type aerobic training. Although part of the aim of the
study was to examine the effect of exercise without dietary
intervention, diet records generally provide valuable information
for analysis and interpretation of results.
Conclusion/application
Unsurprisingly, the lean subjects experienced decreased
carbohydrate oxidation and increased fat oxidation as a result of
the exercise program, while the obese subjects showed no
change in substrate oxidation. Despite that, the present trial’s
lack of effect on 24-hour energy expenditure in either subset
might lead to hasty conclusions of the uselessness of exercise.
However, this would be a mistake. The same protocol in
previous research on similar subjects showed an improvement in
hepatic and peripheral insulin sensitivity,9 as well as decreased
visceral and hepatic fat content.10 Due to these results, the
authors of the present trial offer the following conclusion:
“These findings indicate that aerobic exercise may have its
major effects on the cellular level in muscle (41) and liver (42),
not reflected by changes in whole-body energy expenditure and
substrate oxidation. […] We speculate that an exercise program
with a greater effect on lean body mass and/or a combined
exercise and weight-loss intervention would be required to
achieve a significant increase in energy expenditure and fat
oxidation.”
The body of research examining the effect of exercise on energy
expenditure is equivocal. For example, Kirk et al found that a
minimal amount of resistance training (11-minute workout, 3
days per week, consisting of 9 exercises, one set each to 3-6
repetition max) significantly increased sleeping and resting
metabolic rate.11 However, the latter outcomes were not seen in
obese prepubertal girls who underwent a 5-month strength
training program.12 In contrast, a 16-month trial by Potteiger et
al involving a combination 3-5 weekly aerobic training sessions
showed an increase in resting metabolic rate.13
Apparently, increases in 24-hour energy expenditure are not
necessary for improvements in both insulin sensitivity or
reduction of visceral and hepatic fat, as seen in the studies I
referenced earlier. Nevertheless, a desirable scenario would
include these improvements in addition to an increase in resting
metabolism, since the latter would be more optimal – at least in
individuals whose goal is weight (or net fat) loss. It’s tempting
to assume this can be done simply by increasing training
intensity. However, in obese subjects, exercise intensity might
not make any major difference in fat oxidation, given equal
energy expended during exercise. For example, Saris and
Schrawen found no difference in 24-hour substrate oxidation
between obese subjects doing a 30-minute high-intensity interval
protocol or a 60-minute linear low-intensity protocol.14
Ultimately, it might not be realistic in the obese population to
strive for improvement in fat loss and insulin sensitivity in
addition to an increase in 24-hr energy expenditure. In light of
previous work, this trial shows that beneficial health effects of
exercise can occur independently of its thermic effects – or in
this case, lack thereof.
[Back to Contents] Page 6

The effects of a pre-workout supplement containing
caffeine, creatine, and amino acids during three weeks
of high-intensity exercise on aerobic and anaerobic
performance.
Smith AE, et al. J Int Soc Sports Nutr. 2010 Feb 15;7(1):10.
[Epub ahead of print] [JISSN]
BACKGROUND: A randomized, single-blinded, placebo-
controlled, parallel design study was used to examine the effects
of a pre-workout supplement combined with three weeks of
high-intensity interval training (HIIT) on aerobic and anaerobic
running performance, training volume, and body composition.
METHODS: Twenty-four moderately-trained recreational
athletes (mean +/- SD age = 21.1 +/- 1.9 yrs; stature = 172.2 +/-
8.7 cm; body mass = 66.2 +/- 11.8 kg, VO2max = 3.21 +/- 0.85 l
* min-1, percent body fat = 19.0 +/- 7.1%) were assigned to
either the active supplement (GT, n=13) or placebo (PL, n=11)
group. The active supplement (Game Time(R), Corr-Jensen
Laboratories Inc., Aurora, CO) was 18g of powder, 40 kcals, and
consisted of a proprietary blend including whey protein,
cordyceps sinensis, creatine, citrulline, ginseng, and caffeine.
The PL was also 18g of powder, 40 kcals, and consisted of only
maltodextrin, natural and artificial flavors and colors. Thirty
minutes prior to all testing and training sessions, participants
consumed their respective supplements mixed with 8-10 oz of
water. Both groups participated in a three-week HIIT program
three days per week, and testing was conducted before and after
the training. Cardiovascular fitness (VO2max) was assessed
using open circuit spirometry (Parvo-Medics TrueOne(R) 2400
Metabolic Measurement System, Sandy, UT) during graded
exercise tests on a treadmill (Woodway, Pro Series,
Waukesha,WI). Also, four high-speed runs to exhaustion were
conducted at 110, 105, 100, and 90% of the treadmill velocity
recorded during VO2max, and the distances achieved were
plotted over the times-to-exhaustion. Linear regression was used
to determine the slopes (critical velocity, CV) and y-intercepts
(anaerobic running capacity, ARC) of these relationships to
assess aerobic and anaerobic performances, respectively.
Training volumes were tracked by summing the distances
achieved during each training session for each subject. Percent
body fat (%BF) and lean body mass (LBM) were assessed with
air-displacement plethysmography (BOD POD, Life
Measurement, Inc., Concord, CA). RESULTS: Both GT and PL
groups demonstrated a significant (p=0.028) increase in
VO2max from pre- to post-training resulting in a 10.3% and
2.9% improvement, respectively. CV increased (p=0.036) for the
GT group by 2.9%, while the PL group did not change (p=0.256;
1.7% increase). ARC increased for the PL group by 22.9% and
for the GT group by 10.6%. Training volume was 11.6% higher
for the GT versus PL group (p=0.041). %BF decreased from
19.3% to 16.1% for the GT group and decreased from 18.0% to
16.8% in the PL group (p=0.178). LBM increased from 54.2 kg
to 55.4 kg (p=0.035) for the GT group and decreased from 52.9
kg to 52.4 kg in the PL group (p=0.694). CONCLUSIONS:
These results demonstrated improvements in VO2max, CV, and
LBM when GT is combined with HIIT. Three weeks of HIIT
alone also augmented anaerobic running performance, VO2max
Alan Aragon’s Research Review – February 2010
and body composition. SPONSORSHIP: Corr-Jensen
Laboratories Inc., Aurora, CO, USA
Study strengths
Overall, this design was pretty straightforward without much
room for flaws beyond the typical and obvious. The placebo
treatment was calorie-matched with the experimental treatment
(40 kcal). The exercise testing protocol is applicable to various
team sports that involve repeated bouts of high-intensity efforts.
This is perhaps the first study to ever examine the chronic effects
of a pre-exercise supplement on high-intensity interval running.
Study limitations
Although the subjects were instructed to maintain their usual
dietary habits, no diet records or analysis was done. This
removes an important element of control, especially since body
composition was one of the endpoints to be assessed. The short
study duration leaves open questions about the effectiveness of
the supplement over a period of months or longer.
Comment/application
Granted that industry-sponsored trials almost always yield
positive results their own product is tested, several aspects about
this supplement (Game Time) made its effectiveness beyond
placebo surprising. First of all, the creatine dose (1.5 g/day) was
less than what would normally be effective, even for a
maintenance dose. The absence of a loading phase combined
with the short 3-week duration further casts doubt on just how
much the creatine contributed to the ergogenic effect. Secondly,
the caffeine dose (100 mg/day) was significantly below the
typically effective range of 3-9mg/kg seen in the literature. That
takes care of the 2 compounds in the supplement with the most
solid base of research rationale for their use.
Cordyceps sinensis, another ingredient thrown into this
product’s proprietary blend of ingredients, has failed to enhance
exercise performance on its own15 or within an herbal formula.16
Therefore, it’s tough to imagine why the authors would
speculate that it could have worked synergistically with the other
ingredients in the supplement. The same doubt can rightly be
placed on the combined 0.75 g dose of citrulline and rhodiola –
both of which lack a solid research basis for use as ergogenic
aids. Rhodiola has an inconsistent track record in humans,17 and
citrulline has actually been seen to reduce endurance capacity
compared to placebo.18 Arginine AKG has been shown in one
study to increase peak power when taken with creatine,19 but the
unspecified dose in the present supplement leaves questions
about its sufficiency. Such is the nature of proprietary blends;
it’s an economical loophole for listing an “impressive” battery of
ingredients. Furthermore, Arginine has been touted as a
precursor for nitric oxide production, which can potentially
result in better nutrient delivery via increased blood flow.
However, arginine supplementation has repeatedly failed to
enhance exercise-related parameters.20-24 What we have left in
the mix is 1 g BCAA and 9 g whey.
Game Time costs 60 bucks for a 20 servings, which will get you
a total of 30 g creatine, 2000 mg caffeine, 180 g whey, and 20g
BCAA. Here’s the punchline: you can buy these ingredients
separately in these amounts for a total of 10 bucks or less.
[Back to Contents] Page 7
Effect of n-3 fatty acids and antioxidants on oxidative
stress after exercise.
McAnulty SR, et al. Med Sci Sports Exerc. 2010 Feb 13. [Epub
ahead of print] [Medline]
PURPOSE: n-3 fatty acids are known to exert multiple
beneficial effects including anti-inflammatory actions which
may diminish oxidative stress. Supplementation with antioxidant
vitamins has been proposed to counteract oxidative stress and
improve antioxidant status. Therefore, this project investigated
the effects of daily supplementation in 48 trained cyclists over 6
wks and during 3-d of continuous exercise on F2-isoprostanes
(oxidative stress), plasma n-3 fatty acids, and antioxidant status
(Oxygen Radical Antioxidant Capacity (ORAC) and Ferric
Reducing Antioxidant Potential (FRAP)). DESIGN: Cyclists
were randomized into n-3 fatty acids (N3) (N=11) (2,000 mg
eicosapentaenoic acid (EPA) and 400 mg docosahexaenoic acid
(DHA)), a vitamin-mineral complex (VM) (N=12) emphasizing
vitamins C (2000 mg), E (800 IU), A (3000 IU) and selenium
(200 ug), a vitamin-mineral and n-3 fatty acid combination
(VN3) (N=13), or placebo (P) (N=12). Blood was collected at
baseline and pre- and post-exercise. A 4x 3 repeated measures
ANOVA was performed to test main effects. RESULTS: After
exercise, F2-isoprostanes were higher in N3 (Treatment effect
P=0.014). EPA and DHA plasma values were higher after
supplementation (Interaction effect P=0.001 and P=0.006,
respectively) in both n-3 supplemented groups. ORAC declined
similarly among all groups after exercise. FRAP exhibited
significant interaction (P=0.045) and significantly increased after
exercise in VN3 and VM (P<0.01). CONCLUSION: This study
indicates supplementation with n-3 fatty acids alone significantly
increases F2-isoprostanes after exhaustive exercise. Lastly,
antioxidant supplementation augments plasma antioxidant status
and modestly attenuates but does not prevent the significant n-3
fatty acid associated increase in F2-isoprostanes post exercise.
SPONSORSHIP: Cooper Aerobics Center, Dallas, Texas.
Study Strengths
Points for pioneering: this is the first study to ever directly
examine the effect of omega-3 (denoted in the literature as n-3)
fatty acid supplementation on oxidation indicators after
exhaustive exercise. Trained cyclists were used. Subjects had an
orientation session with a dietitian at the outset of the program in
attempt to standardize their intake. To insure compliance with
the protocol, subjects received weekly calls and daily emails
reminding them to return the empty supplement boxes. Among
the other indexes assessed, F2-isoprostane levels were measured.
This is considered to be the gold standard for determining levels
of oxidative stress.
Study limitations
Although it wasn’t the aim of this study, measures of cycling
performance (as opposed to just markers of oxidative stress)
would have made the outcomes more meaningful and concrete.
Another limitation of this design was the absence of postexercise
nutrition, which in prolonged endurance sports is usually an
immediate and significant part of the protocol. We could take
this a step further and consider that rides lasting 3 hours usually
have some sort of intra-exercise nutrient intake, whether it’s a
Alan Aragon’s Research Review – February 2010
dilute carbohydrate solution such as Gatorade or a carb-protein
combination like Accelerade, or similar home-brewed sports
drink. It’s likely that nutrients ingested during and postexercise
would influence measures of oxidative stress, but such a
treatment arm was missing from this design. For example,
Brown et al, who observed an unexpected reduction in
antioxidant capacity in subjects who consumed a whey protein
bar, but no such effect in subjects consuming the soy protein bar
or in the training-only group.25
Comment/application
The authors of the present trial seemed particularly concerned
with the large increase (53% above pre-exercise levels) in F2-
isoprostanes, which are products lipid peroxidation. The
implications of this can be profound since F2-isoprostanes are
elevated in a number of acute and chronic disease states.26 To be
fair, however, this resulted from a daily dose of 2000 mg EPA
plus 400 mg DHA. This is a far larger dose than what most
sensible people are prone to taking, especially EPA. Most fish
oil products are available in 1-1.2g gel caps, containing
anywhere from roughly 180-410 mg EPA and 120-274 mg
DHA. With that said, there indeed are individuals out there who
heartily apply the more-is-better principle to supplementation.
With all the good press fish oil has gotten over the last decade or
so, it’s a perfect candidate for overconsumption by overzealous
health/fitness enthusiasts.
Interestingly, n-3 supplementation has been shown in other
studies to decrease F2-isoprostanes. Mori et al found 2 separate
treatments, either daily fish meals or fish oil supplementation,
lowered urinary F2-isoprostane levels by 20-27%, indicating a
reduction in oxidative stress.27 Similarly, a 3-month study by
Nalsen et al found that 2.4 g combined EPA & DHA
significantly reduced F2-isoprostane levels. But, as noted by the
authors of the present study, the subjects in the aforementioned
trials were not undergoing regular, exhaustive endurance
exercise.28 To quote their speculations: “Since the concentration
of F2-isoprostanes was so drastically increased postexercise
versus other treatments, we hypothesize that consumption of
high amounts of n-3fa (14) does not increase peroxidation until
a state of high oxidative stress is initiated.”
In the present study, large doses of antioxidant micronutrients
(2000 mg of vitamin C, 800 IU of vitamin E, 3000 IU of vitamin
A, and 200 mcg selenium) coingested with the n-3 fatty acids
reduced the 53% rise in F2-isoprostanes to a 32.8% rise. While
this might seem like a good thing at first glance, there’s a
notable body of research indicating that antioxidant
supplementation is questionably beneficial, and even potentially
adverse:29 “Although there is some evidence to show that both
antioxidants can reduce indices of oxidative stress, there is little
evidence to support a role for vitamin C and/or vitamin E in
protecting against muscle damage. Indeed, antioxidant
supplementation may actually interfere with the cellular
signalling functions of ROS, thereby adversely affecting muscle
performance.” The moral of the story is that more is not always
better when it comes to n-3 supplementation. In addition, things
can get more complicated when we need to turn to a supplement
to do damage control of another supplement (while doing
potential damage of its own).
[Back to Contents] Page 8

Postexercise fat oxidation: effect of exercise duration,
intensity, and modality.
Warren A, et al. Int J Sport Nutr Exerc Metab. 2009
Dec;19(6):607-23. [Medline]
PURPOSE: Postexercise fat oxidation may be important for
exercise prescription aimed at optimizing fat loss. The authors
examined the effects of exercise intensity, duration, and
modality on postexercise oxygen consumption (VO2) and
substrate selection/ respiratory-exchange ratio (RER) in healthy
individuals. DESIGN: Three experiments (n = 7 for each)
compared (a) short- (SD) vs. long-duration (LD) ergometer
cycling exercise (30 min vs. 90 min) matched for intensity, (b)
low- (LI) vs. high-intensity (HI) cycling (50% vs. 85% of
VO2(max)) matched for energy expenditure, and (c) continuous
(CON) vs. interval (INT) cycling matched for energy
expenditure and mean intensity. All experiments were
administered by crossover design. RESULTS: Altering exercise
duration did not affect postexercise VO2 or RER kinetics (p >
.05). However, RER was lower and fat oxidation was higher
during the postexercise period in LD vs. SD (p < .05). HI vs. LI
resulted in a significant increase in total postexercise energy
expenditure and fat oxidation (p < .01). Altering exercise
modality (CON vs. INT) did not affect postexercise VO2, RER,
or fat oxidation (p > .05). CONCLUSIONS: These results
demonstrate that postexercise energy expenditure and fat
oxidation can be augmented by increasing exercise intensity, but
these benefits cannot be exploited by undertaking interval
exercise (1:2-min work:recovery ratio) when total energy
expenditure, duration, and mean intensity remain unchanged. In
spite of the apparent benefit of these strategies, the amount of fat
oxidized after exercise may be inconsequential compared with
that oxidized during the exercise bout. SPONSORSHIP: None
listed.
Study strengths
In a rather elegant design, 3 treatments were done to satisfy
questions regarding duration, intensity, and modality on
postexercise fat oxidation. A crossover was implemented, so
each subject got a chance to undergo each treatment. This tactic
minimizes intersubject variability, and serves to alleviate the
limited statistical power inherent in small sample sizes.
Endogenous substrate availability during testing was controlled
by subjects refraining from all forms of recreational exercise 24
hours prior, recording their diet and activity 48 hours prior, and
duplicating that for each trial. Diet composition was assessed via
software. To further control substrate use, subjects consumed a
standardized meal the night before, no later than 10 hours before
testing. The experimental trials were done at the same time in
the day in order to minimize variations of circadian effects on
metabolism.
Study limitations
The outcomes of this trial may be limited to women, given the
all-female sample used. Additionally, these outcomes may not
necessarily be smoothly extrapolable to other types of exercise
Alan Aragon’s Research Review – February 2010
aside from cycling. Perhaps the most glaring limitation of this
study was the short postexercise assessment period (90 minutes).
It would have been far more telling to extend this period to 24
hours, and of course, it would have been ideal to stretch the trial
out over several weeks.
Comment/application
The results of each experiment is summarized in the following
table, and I’ll provide more specifics to follow:
ƒ EXPERIMENT A: While exercise intensity was matched
(50% of VO2max), increasing exercise duration from 30
minutes to 90 minutes increased total energy expenditure and
fat oxidation during and after the exercise bout.
ƒ EXPERIMENT B: When energy expenditure during exercise
was matched, increasing exercise intensity from 50% to 85%
of VO2max reduced total fat oxidation during exercise but
increased energy expenditure and fat oxidation during the 90
min after exercise.
ƒ EXPERIMENT C: This greater fat-oxidative effect of
increasing exercise intensity could not be exploited by
undertaking an interval-type protocol (90 minutes consisting
of intervals of 60 seconds at 85% of VO2max interspersed
with 120 seconds at 30% of VO2max), compared to a
continuous treatment matched for total energy expenditure
and duration (90 minutes at 50% of VO2max).
The authors of the present trial acknowledge the outcome of
Experiment C conflicts with other research showing the greater
fat-oxidative effect of high-intensity interval work compared to
continuous work matched for energy expenditure. They also
assert that it’s difficult to resolve this discrepancy due to the
variable nature of interval exercise protocols in the literature.
For example, Trapp et al observed higher rates of adipose tissue
lipolysis as a result of an interval protocol involving 8-12
seconds of supramaximal work interspersed with 12-36 seconds
of recovery.30 This points to the possibility that either the
intensity peaks in the present study weren’t high enough to elicit
residual effects, or the lows were too low (or too long – or both).
What’s clear is that the present study’s outcomes can’t be
blanketly assumed of all interval protocols, due to a wide range
of possible variations of intensity and duration of the intervals.
Finally, an important point the authors make is the practical
insignificance of the actual amount of residual oxidation:
“However, the additional energy expended after high intensity
exercise is trivial when energy expenditure that occurs during
the exercise bout is considered.”
[Back to Contents] Page 9
Almonds vs complex carbohydrates in a weight
reduction program.
Wien MA, et al. Int J Obes Relat Metab Disord. 2003
Nov;27(11):1365-72. [Medline]
PURPOSE: To evaluate the effect of an almond-enriched (high
monounsaturated fat, MUFA) or complex carbohydrate-enriched
(high carbohydrate) formula-based low-calorie diet (LCD) on
anthropometric, body composition and metabolic parameters in a
weight reduction program. DESIGN: A randomized, prospective
24-week trial in a free-living population evaluating two distinct
macronutrient interventions on obesity and metabolic syndrome-
related parameters during weight reduction. SUBJECTS: In
total, 65 overweight and obese adults (age: 27-79 y, body mass
index (BMI): 27-55 kg/m(2)). DESIGN: A formula-based LCD
enriched with 84 g/day of almonds (almond-LCD; 39% total fat,
25% MUFA and 32% carbohydrate as percent of dietary energy)
or self-selected complex carbohydrates (CHO-LCD; 18% total
fat, 5% MUFA and 53% carbohydrate as percent of dietary
energy) featuring equivalent calories and protein. MAIN
OUTCOME MEASUREMENTS: Various anthropometric, body
composition and metabolic parameters at baseline, during and
after 24 weeks of dietary intervention. RESULTS: LCD
supplementation with almonds, in contrast to complex
carbohydrates, was associated with greater reductions in
weight/BMI (-18 vs -11%), waist circumference (WC) (-14 vs -
9%), fat mass (FM) (-30 vs -20%), total body water (-8 vs -1%)
and systolic blood pressure (-11 vs 0%), P=0.0001-0.05. A 62%
greater reduction in weight/BMI, 50% greater reduction in WC
and 56% greater reduction in FM were observed in the almond-
LCD as compared to the CHO-LCD intervention. Ketone levels
increased only in the almond-LCD group (+260 vs 0%, P<0.02).
High-density lipoprotein cholesterol (HDL-C) increased in the
CHO-LCD group and decreased in the almond-LCD group (+15
vs -6%, P=0.05). Glucose, insulin, diastolic blood pressure, total
cholesterol, triglycerides, low-density lipoprotein cholesterol
(LDL-C) and LDL-C to HDL-C ratio decreased significantly to a
similar extent in both dietary interventions. Homeostasis model
analysis of insulin resistance (HOMA-IR) decreased in both
study groups over time (almond-LCD: -66% and CHO-LCD: -
35%, P<0.0001). Among subjects with type 2 diabetes, diabetes
medication reductions were sustained or further reduced in a
greater proportion of almond-LCD as compared to CHO-LCD
subjects (96 vs 50%, respectively). CONCLUSIONS: Our
findings suggest that an almond-enriched LCD improves a
preponderance of the abnormalities associated with the
metabolic syndrome. Both dietary interventions were effective in
decreasing body weight beyond the weight loss observed during
long-term pharmacological interventions; however, the almond-
LCD group experienced a sustained and greater weight reduction
for the duration of the 24-week intervention. Almond
supplementation of a formula-based LCD is a novel alternative
to self-selected complex carbohydrates and has a potential role
in reducing the public health implications of obesity.
SPONSORSHIP: This research was supported in part by a
General Clinical Research Center Grant NIH (M01RR00043)
awarded to the City of Hope National Medical Center, a satellite
center of the University of Southern California, and, the Almond
Board of California.
Alan Aragon’s Research Review – February 2010
Study strengths
With 52 subjects completing this 24-month trial, we’re looking
at an unusually large sample size and lengthy trial duration. Both
groups were equally matched on total calories, protein,
cholesterol and saturated fat. Subjects in the almond group were
provided weekly prepackaged allotments of whole unblanched
unsalted almonds. The amount of almonds was chosen
methodically (84g, or 3 oz), based on published data showing
positive alterations in blood lipids using this amount of almonds
under isocaloric conditions. Subjects completed daily food and
exercise records and met with a dietitian weekly.
Study limitations
In contrast to the almond group receiving its experimental agent
prepackaged from the lab, the carb group was relegated to a self-
selected combination of complex carb-based foods from which
they were instructed to compile the caloric equivalent of 84 g
almonds. They were also instructed to consume 2 tbsp safflower
oil per day in order to meet their essential fatty acid needs. This
creates more complexity (i.e., another step to either accidentally
miss or double-up on) in addition to the self-selection of starch
foods. Bioelectrical impedance (BIA) was used so assess body
composition, instead of a more reliable method such as DXA.
Comment/application
The almond group significantly outperformed the carb group on
several important anthropomorphic and metabolic parameters
including a 62% greater reduction in weight/BMI, 50% greater
reduction in waist circumference, 56% greater reduction in fat
mass (no difference in lean mass change), more total bodyweight
loss, a 31% greater magnitude of improvement in insulin
sensitivity. In addition, more patients in the CHO-LCD group
(62%) than in the almond-LCD group (50%) were able to reduce
their antihypertensive medications. The authors of the present
study were surprised that the almond group lost more weight
than the carb group, especially since the diets were isocaloric,
and physical activity (although self-reported) did not differ
significantly between groups. Their speculations for why this
occurred are centered around increased satiety and the inhibition
of absorption of fat calories within nuts by their fiber
component. In support of this, there’s noteworthy evidence
indicating the utility of nut consumption in controlling body
weight. A recent review by Mattes and Dreher elucidates the
following points:31
ƒ Mechanistic studies indicate high satiating capability and low
metabolizable energy (poor bioavailability leading to
inefficient energy absorption) properties of nuts.
ƒ Compensatory dietary responses account for 55-75% of the
energy provided by nuts (this is a heck of a lot).
ƒ Routine nut consumption is associated with elevated resting
energy expenditure and thermogenic effect of feeding,
resulting in further dissipation of the energy they provide.
ƒ Comparisons of regimens including or excluding nuts show
better compliance & greater weight loss when nuts are
permitted.
In sum, the present study indicates that nuts are good for your
health, and can serve as a discreet weapon in the war on the
waistline. I’d also reiterate that starches might be easier to
overeat, especially when they’re not prepackaged by the lab.
[Back to Contents] Page 10

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Redox Signal. 2008 Aug;10(8):1405-34. [Medline]
27. Mori TA, et al. Effect of omega 3 fatty acids on oxidative
stress in humans: GC-MS measurement of urinary F2-
isoprostane excretion. Redox Rep. 2000;5(1):45-6.
[Medline]
28. Nalsen C, et al. Dietary (n-3) fatty acids reduce plasma F2-
isoprostanes but not prostaglandin F2alpha in healthy
humans. J Nutr. 2006 May;136(5):1222-8. [Medline]
29. McGinley C, et al. Does antioxidant vitamin
supplementation protect against muscle damage? Sports
Med. 2009;39(12):1011-32. [Medline]
30. Trapp EG, et al. Metabolic response of trained and untrained
women during high-intensity intermittent cycle exercise.
Am J Physiol Regul Integr Comp Physiol. 2007
Dec;293(6):R2370-5. [Medline]
31. Mattes RD, Dreher ML. Nuts and healthy body weight
maintenance mechanisms. Asia Pac J Clin Nutr.
2010;19(1):137-41. [Medline]
[Back to Contents] Page 11

Soy claims & controversies: what does science have
to say?
By Alan Aragon
Introduction
The soy bean, also called soya bean, is a legume native to East
Asia. It was introduced to the United States in the mid 1700’s
but has been consumed throughout Asia long before recorded
history. In more recent times, Soy has gained a dual-reputation
of being a “health” food as well as some sort of evil thing to
avoid. In this article I’ll look at a selection of common claims
behind soy, and attempt to clear up the confusion with current
research-based evidence. I’ll also sneak in a comment on the
potential commercial bias therein.
Does soy have feminizing effects in men?
Soy contains isoflavones, which have potentially estrogenic
effects. This has raised the concern that men consuming soy
might experience adverse hormonal changes. A recent meta-
analysis by researchers of Johns Hopkins University found that
neither soy foods nor isoflavone supplements significantly alter
testosterone levels in men [1]. Of interest to the athletic
population, 12 weeks of supplementation with soy protein did
not decrease testosterone levels or hinder lean body mass gains
in men engaged in a resistance training program [2]. Therefore,
the evidence does not support the idea that soy is likely to cause
feminizing effects in men.
Does soy protect against breast cancer in women?
Breast cancer rates among women in Asian countries are
substantially lower than those among women in Western
countries. This has lead to a lot of investigation of dietary factors
that might be involved. Since soy is a staple food throughout
Asia, it’s under ongoing study as a possible protective food.
Three separate meta-analyses came to the similar conclusion that
that soy intake may be associated with a decreased risk of breast
cancer [3-5]. Although this area of study has been focused on
postmenopausal women, there’s fairly strong research evidence
that soy is protective against breast cancer in premenopausal
women as well [6].
Does soy protect against prostate cancer?
Prostate cancer is the leading type of cancer in men, occurring
mostly in the older population. The most recent meta-analyses
involving various study designs show that consumption of soy
foods is associated with a reduction in prostate cancer risk in
men [7,8].
Does soy adversely affect thyroid function?
A comprehensive literature review done by researchers at Loma
Linda University concluded that there is not enough evidence
that in iodine-replete individuals with normally functioning
thyroids, soy foods, or isoflavones adversely affect
thyroid function [9]. However, in hypothyroid patients, some
evidence suggests that soy foods taken in excess may increase
Alan Aragon’s Research Review – February 2010
the dose of thyroid hormone medication required by hypothyroid
patients. The review also states that hypothyroid adults need not
avoid soy foods completely. Still, there’s a theoretical concern
that in individuals with compromised thyroid function, soy foods
may increase the risk of developing hypothyroidism. Therefore,
it’s important for soy consumers who have known thyroid issues
to make sure that they moderate their intake of soy. It’s also
been suggested that to make sure that iodine is adequate, but
iodine deficiency is rare in industrialized countries due to
enrichments in the food supply.
Does soy protect against osteoporosis?
The majority of the research done on soy’s effect on bone has
been on menopausal women. As indicated by 2 recent meta-
analyses [10,11], the bulk of the evidence shows that the intake
of soy increases bone mineral density and stimulate bone
formation.
Does soy protect against cardiovascular disease?
This area of study is not as clear-cut as the rest, since most of it
is based on epidemiological studies. This type of research is
uncontrolled, and thus it’s limited by many possible unaccounted
variables. Nevertheless, soy intake has been positively correlated
with the prevention of cardiovascular disease [12]. Part of this
mechanism may be attributed to soy isoflavones’ ability to lower
LDL and total cholesterol [13].
Do soy-based infant formulas have endocrine effects?
A fairly recent study done at the Kaplan Medical Center in
Jerusalem found that breast tissue (denoted as “breast buds”)
was more prevalent in the second year of life in soy formula-fed
infants compared to breast-fed infants and those fed dairy-based
formula [14]. Nursing and consuming dairy-based formulas
showed a decline in the prevalence of breast buds in the
second year of life, whereas infants fed a soy-based formula did
not. The American Academy of Pediatrics (AAP) discourages
the use of soy-based formula unless the infant has galactosemia
and hereditary lactase deficiency, which is a rare occurrence [15].
They strongly assert that, “Soy protein-based formulas are
not designed for or recommended for preterm infants.”
Political considerations
Commercially-vested sponsors of soy research include (but are
not limited to) the Soy Nutrition Institute, Solae Company, Fuji
Foundation for Protein Research, and even the US Government.
Speaking of the latter, under the administration of the USDA’s
Agricultural Marketing Service, the Soybean Promotion and
Research Program has the following goals and objectives [16]:
“The  program’s  goal  is  to  strengthen  the  position  of  soybeans  in 
the  marketplace  and  to  maintain  and  expand  domestic  and 
foreign markets and uses for soybeans and soybean products. It is 
funded by a mandatory assessment of 0.5 of 1 percent of the net 
market price of soybeans. All producers marketing soybeans must 
pay  the  assessment.  Assessments  under  the  national program 
average $40‐50 million ($56.7 in fiscal year 2008) annually and are 
used  to  fund  promotional  and  informational  campaigns  and  to 
conduct  research with  the  objective  of  expanding  and  improving 
the use of soybeans and soybean products.”
[Back to Contents] Page 12
Tying it together
The alarmist venom directed towards the soy industry by fringe
anti-establishment groups is, for the most part, overhyped. Other
than the potential concerns in those with pre-existent
hypothyroidism, known allergies to soy and soy-based products
(more common in children than adults), and soy-based formula
use in preterm infants, consumption of soy is relatively harmless,
and in many cases beneficial to health. In adults, endocrinologic
risk is minimal due to the greatly reduced proportional
contribution of isoflavones in a normal balanced diet. Concerns
of soy having a testosterone-lowering effect on men have not
been solidly supported in the scientific literature.
Soy has been a staple part of some of the healthiest regions in
the world, including Asia-Pacific populations like the
Okinawans. It’s not surprising that research has for the most part
supported its numerous health claims, including protection
against osteoporosis (in menopausal women), prostate cancer,
and breast cancer. Nevertheless, it’s important to be careful of
perceiving soy as a “superfood” based on positive press it’s been
receiving in the scientific literature. It’s also important to realize
that the soy industry has a staggering amount of financial
capability to make sure this positive press continues.
analysis of randomized controlled trials. Eur J Clin Nutr.
2008 Feb;62(2):155-61. Epub 2007 Mar 28. [Medline]
11. Ma DF, et al. Soy isoflavone intake increases bone mineral
density in the spine of menopausal women: meta-analysis of
randomized controlled trials. Clin Nutr. 2008 Feb;27(1):57-
64. Epub 2007 Dec 11. [Medline]
12. Rimbach G, et al. Dietary isoflavones in the prevention of
cardiovascular disease--a molecular perspective. Food
Chem Toxicol. 2008 Apr;46(4):1308-19. [Medline]
13. Taku K, et al. Effects of extracted soy isoflavones alone on
blood total and LDL cholesterol: Meta-analysis of
randomized controlled trials. Ther Clin Risk Manag. 2008
Oct;4(5):1097-103. [Medline]
14. Zung A, et al. Breast development in the first 2 years of life:
an association with soy-based infant formulas. J Pediatr
Gastroenterol Nutr. 2008 Feb;46(2):191-5. [Medline]
15. Bhatia J, et al. Use of soy protein-based formulas in infant
feeding. Pediatrics. 2008 May;121(5):1062-8. [Medline]
16. USDA Agricultural Marketing Service. Soybean Promotion
and Research Program Background Information. Last
Modified Date: 05/12/2009. [USDA-AMS]

References
1. Hamilton-Reeves JM, et al. Clinical studies show no effects
of soy protein or isoflavones on reproductive hormones in
men: results of a meta-analysis. Fertil Steril. 2009 Jun 11.
[Epub ahead of print] [Medline]
2. Kalman D, et al. Effect of protein source and resistance
training on body composition and sex hormones. J Int Soc
Sports Nutr. 2007 Jul 23;4:4. [Medline]
3. Qin LQ, et al. Soyfood intake in the prevention of breast
cancer risk in women: a meta-analysis of observational
epidemiological studies. J Nutr Sci Vitaminol (Tokyo).
2006 Dec;52(6):428-36. [Medline]
4. Trock BJ, et al. Meta-analysis of soy intake and breast
cancer risk. J Natl Cancer Inst. 2006 Apr 5;98(7):459-71.
[Medline]
5. Badger TM, et al. Soy protein isolate and protection against
cancer. J Am Coll Nutr. 2005 Apr;24(2):146S-149S.
[Medline]
6. Lee SA, et al. Adolescent and adult soy food intake and
breast cancer risk: results from the Shanghai Women's
Health Study. Am J Clin Nutr. 2009 Jun;89(6):1920-6. Epub
2009 Apr 29. [Medline]
7. Yan L, Spitznagel EL. Soy consumption and prostate cancer
risk in men: a revisit of a meta-analysis. Am J Clin Nutr.
2009 Apr;89(4):1155-63. Epub 2009 Feb 11. [Medline]
Steve Troutman interviewed Matt Perryman in a 3-part series
8. Hwang YW, et al. Soy food consumption and risk of
that’s well worth the read: Part 1, Part 2, Part 3.
prostate cancer: a meta-analysis of observational studies.
Nutr Cancer. 2009;61(5):598-606. [Medline]
9. Messina M, Redmond G. Effects of soy protein and soybean
isoflavones on thyroid function in healthy adults and
hypothyroid patients: a review of the relevant literature.
If you have any questions, comments, suggestions, bones
Thyroid. 2006 Mar;16(3):249-58. [Medline] of contention, cheers, jeers, guest articles you’d like to
10. Ma DF, et al. Soy isoflavone intake inhibits bone resorption submit, or any feedback at all, send it over to
and stimulates bone formation in menopausal women: meta- aarrsupport@gmail.com.

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