Home: Correspondence:: Ala N Aragon's Research Review - February & March 2013)

10 Effect of fruit restriction on glycemic control in
patients with type 2 diabetes--a randomized trial.

Christensen AS, Viggers L, Hasselstrm K, Gregersen S.
Nutr J. 2013 Mar 5;12:29. doi: 10.1186/1475-2891-12-29.
[PubMed]
12 Are Americas nutrition professionals in the pocket

of Big Food? [my commentary on the article by
Joseph Mercola]
Copyright September 1st, 2013 by Alan Aragon
Home: www.alanaragon.com/researchreview
Correspondence: aarrsupport@gmail.com
By Alan Aragon
14 Interview with Karen Pendergrass, founder of

Paleo Movement Magazine.
By Alan Aragon
2
Clearing up common misunderstandings that

plague the calorie debate, part 3: eat less, move
more.
By Alan Aragon
Strength and body composition changes in

recreationally
strength-trained
individuals:
comparison of one versus three sets resistancetraining programmes. [Critiqued by Brad Schoenfeld,
PhD(c), CSCS, CSPS, FNSCA].
Baker JS, Davies B, Cooper SM, Wong DP, Buchan DS,
Kilgore L. BioMed Research International, vol. 2013,
Article ID 615901, 6 pages, 2013. doi:10.1155/2013/615901
[Hindawi]
Belief beyond the evidence: using the proposed

effect of breakfast on obesity to show 2 practices
that distort scientific evidence.
Brown AW, Bohan Brown MM, Allison DB. Am J Clin
Nutr. 2013 Sep 4. [Epub ahead of print] [PubMed]
Whey protein supplementation during resistance

training augments lean body mass.
Volek JS, Volk BM, Gmez AL, Kunces LJ, Kupchak BR,
Freidenreich DJ, Aristizabal JC, Saenz C, Dunn-Lewis C,
Ballard KD, Quann EE, Kawiecki DL, Flanagan SD,
Comstock BA, Fragala MS, Earp JE, Fernandez ML, Bruno
RS, Ptolemy AS, Kellogg MD, Maresh CM, Kraemer WJ. J
Am Coll Nutr. 2013 Apr;32(2):122-35. [PubMed]
Alan Aragons Research Review February & March 2013
[Back to Contents]
Page 1
loss and weight-maintenance advantages depend on the highprotein, rather than the low-carb aspect of the diet.10
Clearing up common misunderstandings that plague
the calorie debate, part 3: eat less, move more.
By Alan Aragon
____________________________________________________
Welcome to the Wild West
Epidemic is no longer a strong enough word to describe the
obesity problem. The United States has been called the
epicenter of an obesity pandemic.1 Obesity is a global problem,
we know that. Whats kind of embarrassing for Westerners like
myself is that the Western lifestyle is the unofficial poster-model
of obesogenicity. The Westernization of any given population
usually implies a set-up for obesity-related disease. Since the
Western lifestyle is characterized by physical inactivity and
overeating,2,3 doing the opposite (eating less and moving more)
is a seemingly obvious solution. Its well-established that weight
loss over the long-term is achieved via sustaining an energy
deficit, and indeed eating less and/or moving more is the only
way to do this regardless of whatever clever food choices or
energy expenditure tactics are employed. One or both roads must
lead to one place: an energy deficit.
Conversely, weight gain over time can only be reached through a
sustained caloric surplus by whatever overt or discreet means
this is achieved. There are a multitude of hypotheses behind
what caused the rise of obesity that began about four decades
ago. However, the most plausible explanation is somewhat
anticlimactic. Swinburn et al investigated the major drivers of
the US obesity epidemic and found that increased energy intake
by ~500kcal/day for adults and ~350 kcal/day for children is
more than sufficient to explain the US epidemic of obesity. 4 I
would also add that there is evidence indicating a reduction in
energy-out as well.5,6 These factors combined quite elegantly
account for the expansion of the nations waistline. We eat more
and move less.
However, is telling the public to simply eat less and move more
an effective way to solve the obesity problem? Unfortunately
not, even though its essentially true. Ill discuss why this advice
on its own doesnt always work, and Ill then propose some
alternative advice.
Problems with eating less
Another problem with the advice to eat less is that theres a

practical limit to eating less. At some point, eating less can lead
to eating nothing. Thats not sustainable, nor is it fun. So, the
question now becomes whether or not certain circumstances can
benefit from aggressive deficits, and the answer is yes. An
aggressive caloric deficit is an effective intervention tactic for a
severe state of obesity. There is a substantive and consistent
body of evidence indicating that in the initial stage of dieting, a
greater weight loss is associated with greater short- and longterm success in weight loss maintenance.11,12 However, keep in
mind that the quick-initial weight loss model does not
necessarily apply to everyone. In lean/athletic subjects, slowand-steady weight loss is more protective of lean mass.13
Perhaps the most confounding and insidious problem with
eating less is the double-whammy of reduced resting energy
expenditure combined with increased hunger. Adaptive
thermogenesis (a decrease in resting energy expenditure beyond
what can be attributed to losses in lean mass) was discussed atlength in the July 2013 issue. Now its time to address hunger
issues. While eating less can reliably induce weight loss, it can
also reliably induce hunger. An increased drive to eat can lead to
the sabotage of weight loss efforts, so the dieter is stuck in a
tough position. At this point I have to interject with the concept
that this is supposed to happen. It might appear to be a problem
for the dieter, but as far as the body is concerned, the sabotaging
of dieting efforts is a victory against death.
Its useful to get familiar with the known mechanisms that drive
the homeostasis of bodyweight, since they give a clearer picture
of why the advice to simply eat less, move more often fails.
Boguszewski et al eloquently summarize the complexity of the
situation as follows:14
The human body is endowed with a complex physiological
system that maintains relatively constant body weight and fat
stores despite the wide variations in daily energy intake and
energy expenditure. With weight loss, compensatory
physiological adaptations result in increased hunger and
decreased energy expenditure, while opposite responses are
triggered when body weight increases. This regulatory system is
formed by multiple interactions between the gastrointestinal
tract (GIT), adipose tissue, and the central nervous system
(CNS) and is influenced by behavioural, sensorial, autonomic,
nutritional, and endocrine mechanisms.
The implication behind eating less is consuming less total

calories. Alright, clear enough, but does it matter where the
calorie cuts are made? Yes it does, and it cant be assumed that
the public knows the finer details of this. There is a bounty of
research showing the advantage of consuming sufficient protein
(approximately 1.2-2.3 g/kg; one recent review suggested a
range of 1.8-2.7 g/kg) while dieting in order to minimize losses
of lean mass.7,8 Protein also leads the macronutrients in its
thermic and satiating effect.9 It therefore does not make good
sense to target protein when cutting back intake. The
proportional decrease of fat versus carbohydrate is a flexible
matter subject to individual preference, tolerance, and goals. In
support of this, Soenen et al recently demonstrated that weight
That was such a beautiful encapsulation of whats involved, that

its a shame I didnt write it myself. Back on topic, its important
to note that the body launches a more pronounced defensive
response against weight loss than it does against weight gain.
This makes sense, since we as a species evolved to survive
prolonged periods of famine. As evidenced by the current
obesity pandemic, humans have not gracefully adapted to the
historically recent perpetual abundance of food combined with
the elimination of the obligatory link between physical activity
and survival (i.e., chasing our food down versus driving to the
store to buy it).
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Page 2
The harmony of physiological factors regulating the bodys

defense against weight loss is downright symphonic. The central
nervous system (CNS) communicates with the adipose tissue,
gastrointestinal tract, and pancreas in what can rightly be seen as
a conspiracy to keep bodyweight from changing. Ill touch
briefly upon insulin and leptin to illuminate an important section
of this symphony, and also to illustrate the complexity of
bodyweight homeostasis, given that this interplay is only one of
many weight-regulatory systems in the body.
Leptin is a peptide hormone primarily secreted by the adipose
tissue. Our understanding of leptins role in bodyweight
regulation is still very incomplete, but we do know that it aids in
appetite control (at least in part) by stimulating anorexigenic
neurons and inhibiting orexigenic ones. In addition to increasing
energy expenditure, leptin serves to reduce food intake, which
collectively is a set-up for weight loss. But of course, the body is
smarter than that. Leptin levels rise and fall in tandem with the
amount of body fat one carries. So, the lower your bodyfat
levels, the less capacity leptin has to work its magic. Lower
leptin levels result in a higher activation of neuropeptide Y
(NPY), the brains most abundant neurotransmitter, which also
happens to be the primary hunger signal in response to caloric
restriction.15
Insulin, a peptide hormone produced by the pancreas, is similar
to leptin in the sense that its an adipose signal. Like leptin,
serum insulin levels mirror body fat levels. And also like leptin,
insulin elevations are anorexigenic. Thus, they both have
regulatory effects on food intake. The twist in the saga is how
insulin and leptin have opposite effects on adipose tissue. Leptin
stimulates lipolysis (the breakdown lipids and mobilization of
fatty acids), while insulin inhibits lipolysis and stimulates
lipogenesis. Kiefer and Habener have thus proposed an
adipoinsular axis which they summarize as follows (along
with a diligent disclaimer of ex vivo and animal data):
There is now growing evidence that leptin also acts to
suppress insulin production from pancreatic -cells. Because
insulin is adipogenic and increases the expression of leptin,
there is a bidirectional feedback loop between adipose tissue
and pancreatic islets, termed the adipoinsular axis. The majority
of evidence in support of an adipoinsular axis has come from
studies in rodents or cell lines, but there is also evidence to
suggest that a similar pathway exists in humans.
In essence, insulin and leptin share similar/overlapping

biological effects, but the unintuitive reality is that they also
have opposing actions that keep each other in check. To
reiterate, insulin and leptin are adiposity signals, but they are a
mere drop in the bucket within the larger body of known
homeostatic regulators. The influence of gastrointestinal
peptides and endocannabinoids on appetite and bodyweight
regulation could fill chapters on their own.
The practical take-away from this information is that you cant
simply focus on any single factor in isolation, since its
inevitably integrated into a regulatory system with a multitude of
checks and balances. Another point to reiterate is that the energy
balance imposed either a surplus or deficit is the single most
powerful dictator of the fate and function of these
neuroendocrine factors. So, weight loss certainly can occur by

eating less. But this says very little about the bodys plan to
counteract this by decreasing energy expenditure and increasing
hunger.
Problems with moving more
This part of the discussion is far less esoteric and abstract, so go
ahead and exhale. Moving more implies voluntarily increasing
energy expenditure. Clear enough, but does it matter how this
increase is executed? Yes it does. And just as in the case of
eating less, it cant be assumed that the public knows the details
that can make or break long-term success. The advice to move
more can evoke a wide range of different aims. Some might hear
the advice and start shopping around for a Crossfit gym
membership. Others might look at their work schedule and
agonize over whether theres enough time for a walk before
rushing to the office.
The main problem I see with the move more objective is that it
automatically leads people to think in terms of increased training
time. This can be a deal-breaker for the majority of working
people in the industrialized world who feel that they have no
time to spare. This is especially the case for those who feel
maxed-out in terms of their time investment in exercise. The
latter individuals need to review their options of increasing their
training intensity, especially if eating less is out of the question.
Speaking of training intensity, the objective to move harder is
just as legitimate as the objective to move more. Imposing my
personal preference would be to change the mantra to move
more weight. Progressive resistance training has only recently
received recognition for its positive effects on cardiometabolic
health,17-19 whereas it traditionally has been viewed as a means
to improve musculoskeletal strength.
There are obvious limits to resistance training in terms of load
progression, and these limits will vary widely with the
individual. I just want to dispel the nearly automatic tendency to
add minutes to the evening treadmill session or miles to the
morning jog. At the same time, I dont want to portray some sort
of false dichotomy where you have to do either one or the other,
or that one mode is inherently superior to the other. The nature
of the exercise increase, whether its based on intensity,
frequency, or duration, must once again be dictated by you
guessed it individual preference, tolerance, and goal. Moving
more essentially becomes a matter of progressing properly.
Moving more carries an additional implication that the energy
expenditure increase must consist of formal exercise. The
problem is that not everyone equates exercise with excitement or
pleasure. In fact, many view exercise as a form of torture. Nonexercise activity (including recreational activity) is perfectly
legitimate and effective for fulfilling the move more
objective.20 For exercise-phobic individuals, we can strategically
modify move more into sit less and then progress from
there.
A final problem with the move more mantra is the reluctance
to engage in exercise due to the belief that it simply doesnt
work. The purported ineffectiveness of exercise as a weight loss
tool regularly makes it rounds through various popular media.
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Page 3
Some gurus go as far as promoting the idea that exercise only

increases the tendency to gain weight. This is simply incorrect.
A relatively recent meta-analysis by Wu et al found that diet plus
exercise caused significantly greater weight loss than diet
alone..21 This weight loss was significantly greater in trials
lasting a year or more, suggesting that exercise has long-term
benefits to weight loss.
6.
7.
Conclusions & potential solutions

Fundamentally speaking, eating less and moving more is a valid
approach for weight loss and obesity prevention. However, the
devil is in the details. Specific strategies must be implemented in
order to increase the chances of long-term success. In the case of
eating less, the brunt of the caloric reduction should be from
carbohydrate and/or fat (depending on personal preference) in
order to reap the lean mass-preserving and satiating effect of
protein.
This is not to say that more-is-better when it comes to protein.
The point of diminishing returns where protein intake impinges
upon a dieters carbohydrate and/or fat allotment can be avoided
by setting an upper limit of protein intake at approximately a
gram per pound of bodyweight. Another strategy to hedge
against the bodys multitude of defenses against weight loss is to
purposely reserve more rapid weight loss for the initial phase of
a program (roughly within the first 3-6 months), or for the initial
10-20% drop in bodyweight depending on the severity of the
obesity at the start of the program. The remainder of the weight
loss programming should accommodate a slower pace.
Advice to move more can be interpreted in many ways, with
varying degrees of productivity (and counterproductivity). As
with diet composition, exercise programming and progression
should be tailored to individual preference, tolerance, and goals.
Moving more has practical limits that must be respected, as does
eating less. The recommendation to eat less and move more is
not sufficient on its own to cover the many nuances and
contingencies associated with long-term weight loss success or
improvements in body composition. But then again, Eat less,
move more! is far catchier than, Maintain an energy deficit
with appropriate macronutrient targets and personally preferred
foods while training with properly individualized programming
and progression.
References
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Katz DL. Pandemic obesity and the contagion of nutritional

nonsense. Public Health Rev. 2003;31(1):33-44. [PubMed]
Nedeltcheva AV, Kessler L, Imperial J, Penev PD. Exposure to
recurrent sleep restriction in the setting of high caloric intake
and physical inactivity results in increased insulin resistance
and reduced glucose tolerance. J Clin Endocrinol Metab. 2009
Sep;94(9):3242-50. [PubMed]
Nedeltcheva AV, Kilkus JM, Imperial J, Kasza K, Schoeller
DA, Penev PD. Sleep curtailment is accompanied by increased
intake of calories from snacks. Am J Clin Nutr. 2009
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Swinburn B, Sacks G, Ravussin E. Increased food energy
supply is more than sufficient to explain the US epidemic of
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King DE, Mainous AG 3rd, Carnemolla M, Everett CJ.
Adherence to healthy lifestyle habits in US adults, 1988-2006.
Am J Med. 2009 Jun;122(6):528-34. [PubMed]
Churchward-Venne TA, Murphy CH, Longland TM, Phillips
SM. Role of protein and amino acids in promoting lean mass
accretion with resistance exercise and attenuating lean mass
loss during energy deficit in humans. Amino Acids. 2013
Aug;45(2):231-40. [PubMed]
Phillips SM, Van Loon LJ. Dietary protein for athletes: from
requirements to optimum adaptation. J Sports Sci. 2011;29
Suppl 1:S29-38. [PubMed]
Halton TL, Hu FB. The effects of high protein diets on
thermogenesis, satiety and weight loss: a critical review. J Am
Coll Nutr. 2004 Oct;23(5):373-85. [PubMed]
Soenen S, Bonomi AG, Lemmens SG, Scholte J, Thijssen MA,
van Berkum F, Westerterp-Plantenga MS. Relatively highprotein or 'low-carb' energy-restricted diets for body weight
loss and body weight maintenance? Physiol Behav. 2012 Oct
10;107(3):374-80. [PubMed]
Anderson JW, Konz EC, Frederich RC, Wood CL. Long-term
weight-loss maintenance: a meta-analysis of US studies. Am J
Clin Nutr. 2001 Nov;74(5):579-84. [PubMed]
Nackers LM, Ross KM, Perri MG. The association between
rate of initial weight loss and long-term success in obesity
treatment: does slow and steady win the race? Int J Behav Med.
2010 Sep;17(3):161-7. [PubMed]
Garthe I, Raastad T, Refsnes PE, Koivisto A, Sundgot-Borgen
J. Effect of two different weight-loss rates on body composition
and strength and power-related performance in elite athletes.
Int J Sport Nutr Exerc Metab. 2011 Apr;21(2):97-104.
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Boguszewski CL, Paz-Filho G, Velloso LA. Neuroendocrine
body weight regulation: integration between fat tissue,
gastrointestinal tract, and the brain. Endokrynol Pol. 2010 MarApr;61(2):194-206. [PubMed]
Minor RK, Chang JW, de Cabo R. Hungry for life: How the
arcuate nucleus and neuropeptide Y may play a critical role in
mediating the benefits of calorie restriction. Mol Cell
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Kieffer TJ, Habener JF. The adipoinsular axis: effects of leptin
on pancreatic beta-cells. Am J Physiol Endocrinol Metab. 2000
Jan;278(1):E1-E14. [PubMed]
Sundell J. Resistance Training Is an Effective Tool against
Metabolic and Frailty Syndromes. Adv Prev Med.
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Whaley-Connell AT, Chockalingam A, Hinton PS, Dellsperger
KC, Thomas TR. The effects of resistance training on
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(Greenwich). 2010 Jan;12(1):64-72. [PubMed]
Conceio MS, Bonganha V, Vechin FC, de Barros Berton RP,
Lixandro ME, Nogueira FR, de Souza GV, Chacon-Mikahil
MP, Libardi CA. Sixteen weeks of resistance training can
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Levine JA. Nonexercise activity thermogenesis--liberating the
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Wu T, Gao X, Chen M, van Dam RM. Long-term effectiveness
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May;10(3):313-23. [PubMed]
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Page 4
Strength and body composition changes in

recreationally
strength-trained
individuals:
comparison of one versus three sets resistancetraining programmes. [Critiqued by Brad Schoenfeld,
PhD(c), CSCS, CSPS, FNSCA].
__________________________________________________________________________
Baker JS, Davies B, Cooper SM, Wong DP, Buchan DS, Kilgore
L. BioMed Research International, vol. 2013, Article ID 615901,
6 pages, 2013. doi:10.1155/2013/615901 [Hindawi]
PURPOSE: The purpose of this study was to determine the
effects of increasing the volume of weight-training from one to
three sets upon body composition and muscular strength.
METHODS: Sixteen male weight-trainers volunteered to act as
subjects and were randomly assigned to one of two training
groups. Supervised weight-training targeting the upper body was
conducted three times per week for eight weeks using one set
(n=8) or three sets (n=10) of six repetitions to fatigue. Subjects
were measured before and after the training intervention for (1)
strength performance ( and kg) and (2) adiposity (sum of seven
skinfold thicknesses in mm). RESULTS: Both training groups
improved significantly (20.7%) in terms of muscular strength (P
< 0.05 ) with no differences being observed between the one set
(21.98% increase) and three set group (20.71% increase) after
the training interventions (P > 0.05). Significant decreases were
also observed for skinfold measures in the one set group (P <
0.05). CONCLUSIONS: One set of high intensity resistance
training was as effective as three sets for increasing the strength
of muscle groups in the upper body. The one set protocol also
produced significantly greater decreases in adiposity.
SPONSORSHIP: None listed.
__________________________________________________________________________
One of the biggest controversies in the field of exercise science

is whether multi-set programs are superior to those employing
only a single set. To date, numerous studies have investigated
the topic and the compelling body of research indicates that
higher training volumes are associated with greater muscular
adaptations. Using a sophisticated statistical technique called
meta-regression where the results of all relevant studies are
pooled for analysis, Krieger determined that multi-set protocols
produce a 46% greater increase in strength and a ~40% greater
increase in hypertrophy compared to single-set training.1,2 These
findings held true for both novice and experienced lifters. What's
most striking is the large magnitude of differences between
protocols, which would be considered practically meaningful by
any standard. Despite what seems to be an open-and-shut case in
favor of multiple sets, however, the subject continues to be a
heated source of debate amongst some fitness professionals.
The purpose of the study in question was to evaluate the effects
of 1- versus 3-set resistance training routines on indices of
strength and body composition. The researchers recruited 16
young, recreationally trained subjects to participate in the study.
The author's stated definition of "recreationally trained" was
having at least 1 year of resistance training experience. This
definition is rather ambiguous and the study did not report
average number of years trained. In the discussion section, the
authors acknowledge that, "Subjects here would be categorized

as high performing new trainees or lower performing novices at
entry and high performance novices at exit." The implication
here is that average training experience was probably around a
year at most.
Participants were randomly assigned to either a 1-set or a 3-set
group. The routine consisted of 6 reps of 9 different free-weight
exercises for the upper body with 2-3 minutes rest between sets.
Exercises included the bench press, inclined bench press,
dumbbell flyes, biceps curl with barbell, biceps curl with
dumbbells, hammer curl with dumbbells, seated shoulder press
behind neck, lateral raises, and upright row. Training was carried
out 3 times a week for 8 weeks. All sets were performed to
volitional failure. Pre- and post-study testing measures included
1RM testing in the bench press, biceps curl, and shoulder press.
Body composition was assessed by 7-site skinfold testing.
Results of the study showed that both groups significantly
increased their 1RM values on all of the exercises tested, with no
strength differences found between groups. Sum of skinfolds
decreased significantly in the 1-set group with no significant
changes noted in the 3-set group (indicating that the 1-set group
lost more body fat). On the surface, these findings seem to
provide evidence that single set training is as effective as multiset training in promoting favorable adaptations in muscle
strength and even better at improving body composition. Based
on the methodology employed in the study, however, its
limitations substantially hinder our ability to draw conclusions
as to the topic at hand.
The most glaring issue with the study is that the exercise
protocol was highly uncharacteristic of how most people train.
The single-set group performed 3 sets per muscle each session
for a total of 9 sets per muscle per week; this is more indicative
of typical multi-set regimens as opposed to what is normally
considered a true single-set routine. Thus, the real point of
discussion raised by the study is not about training with single
versus multiple sets; rather, it is whether performing 9 sets per
muscle group per week is superior to 27 sets. The results of this
study would seem to indicate that there is not a significant
difference for strength increases when performing more than 9
sets per muscle group per week. It was suggested by the authors
that the higher volume of training by the multi-set group might
have resulted in an overtrained state, which could conceivably
have hampered gains. This warrants further study as no markers
of overtraining were measured in this study.
A potential confounding issue here is the fact that the
researchers did not control for the possibility that subjects
performed other resistance exercise during the course of the
protocol (at least this was not stated in the study). If subjects did
indeed perform additional sets of exercises for the target muscle
groups, which cannot be determined based on the write up, it
would certainly confound results. Moreover, the performance of
exercises targeting the back musculature (which were curiously
excluded from the protocol) would have had an impact on the
biceps and chest as well.
Another possible confounder is the fact that intraclass
correlation coefficients (ICC) were not mentioned for the
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Page 5
exercises used in 1RM testing. In short, an ICC is a measure of

the ability of the evaluator to replicate a given measure. By
failing to state the ICC from their lab, one is left to wonder
whether the researchers had the requisite skills to carry out
strength testing in a manner that would provide valid results.
An additional point to consider in the present study is its small
sample size; only 16 subjects were recruited for inclusion. Small
sample sizes are common in longitudinal training studies given
their time-intensive nature, which raises the potential of a type II
error, i.e. an inability to detect a significant difference due to a
lack of statistical power. Considering the null findings, we
cannot rule out that this was an issue here.
Finally, the study design employed by the researchers precludes
our ability to draw any firm inferences with respect to body
composition. The finding that subjects in the 1-set group -- who
performed ~66% less exercise than the 3-set group -- would
achieve a greater reduction in body fat makes little sense. There
are a couple of potential explanations to account for this highly
illogical finding. For one, skinfold testing was used as the
measurement instrument. This technique is known to be highly
dependent on the skill of the practitioner and thus prone to
technical error. For another, the researchers allude to the fact that
dietary monitoring was poor. It is well-established that caloric
balance is the key to weight loss, as dictated by the First Law of
Thermodynamics. Thus, it can only be concluded that any body
fat reductions were either the result of inaccurate measurements
or perhaps that the 1-set group achieved a greater caloric deficit
over the course of the study.
In conclusion, the body of research shows multiple sets to be
superior to single sets for increasing muscular strength. Given
the methodological limitations noted herein, the present study
does little to refute such opinion. The study does, however, add
to the literature with respect to determining the threshold of
volume necessary to optimize muscular strength. The findings
suggest that performing more than about 9 sets does not have
additional utility for increasing strength-related gains in those
with a year or so of lifting experience. This is a topic that
requires further research, particularly attention to employing
better control over confounding variables and using larger
sample sizes. It also should be noted that the study only looked
at training the muscles of the upper body; results therefore
cannot necessarily be generalized to lower body training. Again,
this requires further study.
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Page 6
Belief beyond the evidence: using the proposed effect

of breakfast on obesity to show 2 practices that distort
scientific evidence.
Brown AW, Bohan Brown MM, Allison DB. Am J Clin Nutr.
2013 Sep 4. [Epub ahead of print] [PubMed]
BACKGROUND: Various intentional and unintentional factors
influence beliefs beyond what scientific evidence justifies. Two
such factors are research lacking probative value (RLPV) and
biased research reporting (BRR). OBJECTIVE: We
investigated the prevalence of RLPV and BRR in research about
the proposition that skipping breakfast causes weight gain,
which is called the proposed effect of breakfast on obesity
(PEBO) in this article. DESIGN: Studies related to the PEBO
were synthesized by using a cumulative meta-analysis. Abstracts
from these studies were also rated for the improper use of causal
language and biased interpretations. In separate analyses, articles
that cited an observational study about the PEBO were rated for
the inappropriate use of causal language, and articles that cited a
randomized controlled trial (RCT) about the PEBO were rated
for misleadingly citing the RCT. RESULTS: The current body
of scientific knowledge indicates that the PEBO is only
presumed true. The observational literature on the PEBO has
gratuitously established the association, but not the causal
relation, between skipping breakfast and obesity (final
cumulative meta-analysis P value <10-42), which is evidence of
RLPV. Four examples of BRR are evident in the PEBO
literature as follows: 1) biased interpretation of one's own
results, 2) improper use of causal language in describing one's
own results, 3) misleadingly citing others' results, and 4)
improper use of causal language in citing others' work.
CONCLUSIONS: The belief in the PEBO exceeds the strength
of scientific evidence. The scientific record is distorted by RLPV
and BRR. RLPV is a suboptimal use of collective scientific
resources. SPONSORSHIP: Supported by the National Institute
of Diabetes and Digestive and Kidney Diseases (NIDDK
P30DK056336 and NIDDK T32DK62710).
Study strengths
This study is conceptually strong since it tackles a delicate and
important topic involving long-held beliefs about breakfast, and
challenges the validity of reporting in the literature thereof. In
order to establish the existence of the widely held proposed
effect of breakfast on obesity (PEBO the idea that breakfast
consumption prevents obesity and the opposite promotes it) a
wide range of literature, including lay media, scientific, and
governmental sources were searched through. In order to assess
research lacking probative value (RLPV characterized by
questions that have already been sufficiently answered, or
designed in such a way that cannot advance the scientific
knowledge of the question), a cumulative meta-analysis was
done, which involved one published meta-analysis3 and 3
systematic reviews.4-6
Study limitations
of results and inappropriate use of causal language is an

interesting element identified by the present study.
Comment/application
The main findings were 4-fold. First of all, PEBO (the idea that
breakfast consumption prevents obesity and the opposite
promotes it) was found to be widely stated as true by a range of
sources, including popular television media (Dr. Oz), the
Surgeon General, Mayo Clinic, Academy of Nutrition &
Dietetics, and Johns Hopkins Bloomberg School of Public
Health. Secondly, the research evidence (both controlled and
observational) is equivocal; it does not clearly confirm or refute
the PEBO. Thirdly, RLPV (research lacking probative value)
was indicated by the detection of gratuitous replication of
associations between breakfast and obesity. Lastly, BRR
(biased research reporting) was found. To quote the manuscript:
26-50% of the studies were ascribed greater inferential
strength than the study designs warranted. [...] These results
show that a sizeable number of citations of Schlundt et al (10)
were misleading (62% of the PEBO-relevant citations), and they
were almost exclusively biased in favor of breakfast.
In addition to misleadingly citing other investigators results,

there was the improper use of causal language. For example, a
misleading positive statement was made by Booth et al7 who
said, Daily consumption of breakfast is important in weight
control... The authors failed to provide qualification for this
claim. An example of a misleading negative statement was by
Berkey et al8 who said, However, a randomized clinical trial of
obese women found that those who stopped eating breakfast lost
the most weight... The authors did not properly qualify this
claim, since there were two groups in the study in question
(Schlundt et al9), habitual breakfast skippers and habitual
breakfast eaters. It would be more accurately reported that
subjects who had to make the most substantial changes in eating
(i.e., habitual breakfast skippers assigned to eat breakfast and
habitual breakfast eaters assigned to skip breakfast) achieved
better results.
The authors of the present study speculate that a vicious cycle
initiated by frequent assertions (i.e., breakfast is the most
important meal of the day) causing a halo effect, wherein other
positive aspects are attributed to breakfast, such as a proposed
ability to prevent obesity. Subsequent to these pervasive
assertions is the exposure to research with unneeded replication,
which is confounded by misleading statements of causality. This
leads to the potential for confirmation bias, which can
insidiously manifest as not only the selective seeking of
agreeable data, but the avoidance or denial of disagreeable data.
This excerpt from the conclusion is worth quoting:
Although we hope that the results presented in the current
article will help individuals identify biased reporting in their
own work (ourselves included), it is the peer review process
that may be best improved by raising awareness of bias.
The main limitation was not necessarily design-related, but

rather that the bulk of the breakfast-related research was
observational as opposed to interventional, and thus unable to
demonstrate causation. Ironically, the misleading interpretation
Ultimately, there is insufficient evidence supporting the PEBO,

despite its prevalent promotion in various media. The following
very nicely done schematic (bravo, Brown et al) illustrates the roles
of BRR and RLPV in perpetuating presumptions about PEBO.
[Back to Contents]
Page 7
Diagram Key:
A. Exposure to such phrases as breakfast is the most
important meal of the day may predispose individuals to
believe positive things about breakfast because of the halo
effect, or cognitive bias created by these phrases.
B. The RLPV related to the PEBO may enhance this
predisposition to believe the PEBO through the mere
exposure effect (the development of a preference based
merely on familiarity) particularly when the research is
presented in a biased manner, such as in the presence of
BRR.
C. Individuals tend to seek out information confirming their
point of view and reject or avoid seeking information to the
contrary (confirmation bias) to prevent or reduce cognitive
dissonance (the discomfort of holding two or more
conflicting beliefs). This can result in retaining a biased
sample of information.
D. This is a hypothetical graph of the comparison of strength
of conviction compared with the strength of existing
evidence supporting the PEBO.
E. Collectively, these cognitive biases may predispose
researchers to bias their research reporting, which would in
turn feed the cycle of false presumptions about the effect of
breakfast on obesity.
[Back to Contents]
Page 8
staff. Body composition was assessed with dual X-ray

absorptiometry (DXA).
Whey protein supplementation during
training augments lean body mass.
resistance
Volek JS, Volk BM, Gmez AL, Kunces LJ, Kupchak BR,
Freidenreich DJ, Aristizabal JC, Saenz C, Dunn-Lewis C,
Ballard KD, Quann EE, Kawiecki DL, Flanagan SD, Comstock
BA, Fragala MS, Earp JE, Fernandez ML, Bruno RS, Ptolemy
AS, Kellogg MD, Maresh CM, Kraemer WJ. J Am Coll Nutr.
2013 Apr;32(2):122-35. [PubMed]
BACKGROUND: Compared to soy, whey protein is higher in
leucine, absorbed quicker and results in a more pronounced increase
in muscle protein synthesis. OBJECTIVE: To determine whether
supplementation with whey promotes greater increases in muscle
mass compared to soy or carbohydrate, we randomized nonresistance-trained men and women into groups who consumed daily
isocaloric supplements containing carbohydrate (carb; n = 22), whey
protein (whey; n = 19), or soy protein (soy; n = 22). METHODS:
All subjects completed a supervised, whole-body periodized
resistance training program consisting of 96 workouts (9 months).
Body composition was determined at baseline and after 3, 6, and 9
months. Plasma amino acid responses to resistance exercise
followed by supplement ingestion were determined at baseline and 9
months. RESULTS: Daily protein intake (including the
supplement) for carb, whey, and soy was 1.1, 1.4, and 1.4 gkg body
mass(-1), respectively. Lean body mass gains were significantly (p
< 0.05) greater in whey (3.3 1.5 kg) than carb (2.3 1.7 kg) and
soy (1.8 1.6 kg). Fat mass decreased slightly but there were no
differences between groups. Fasting concentrations of leucine were
significantly elevated (20%) and postexercise plasma leucine
increased more than 2-fold in whey. Fasting leucine concentrations
were positively correlated with lean body mass responses.
CONCLUSIONS: Despite consuming similar calories and protein
during resistance training, daily supplementation with whey was
more effective than soy protein or isocaloric carbohydrate control
treatment conditions in promoting gains in lean body mass. These
results highlight the importance of protein quality as an important
determinant of lean body mass responses to resistance training.
SPONSORSHIP: This study was funded by a grant from the Dairy
Research Institute, Rosemont, Illinois.
Study strengths
This is the first study to compare whey versus soy protein over a
period longer than 6 months (this one was 9 months). 5-day diet
records were assessed during one-on-one sessions with
registered dietitians. Subjects were weighed weekly, and those
showing a trend for weight gain or loss were flagged and
counseled by the nutrition team in order to adjust intake to
regain maintenance. Dietary intake data were analyzed via
software. Protein intake including supplementation was targeted
to be ~1.4 g/kg. This was adequate to support muscular
adaptations to training, but not so high as to mask differences in
protein types. Supplementation compliance was enforced via
ingestion in the presence of research personnel, as well as
monthly unannounced urine testing for the detection of paraaminobenzoic acid (PABA), which the supplement was spiked
with. Based on PABA testing, compliance was 82%. The
resistance training program was progressive, nonlinear, and
periodized. Exercise sessions were supervised by the training
Study limitations
This study was very well-controlled and executed, so its
limitations and methodological shortcomings are minimal. The
only way to tighten things up would be to remove the food &
beverage responsibility from the subjects, but complete intake
provision for a fairly large sample size over a 9 month period is
just not feasible. Another limitation is that the results of this
study might only apply to untrained (or not highly trained)
subjects. The subjects eligibility depended upon not
participating in a systematic, high-intensity resistance program
within 1 year prior to enrollment. The micronutritional
composition of the supplements was not matched, but this is
understandable due to the different food sources of each.
However, whats odd (and admittedly a reach as far as potential
confounding effect) was the disparate amounts of sodium in the
whey and soy supplements, which were 154 mg & 402 mg,
respectively.
Comment/application
The main finding was that whey protein supplementation was
superior to soy and carbohydrate supplementation for increasing
lean mass. Although carbohydrate supplementation led to greater
lean mass gain than soy, the difference did not reach statistical
significance. All groups dropped similar, nonsignificant amounts
of body fat without any significant between-group differences,
but the performance hierarchy of whey>carb>soy was also seen.
Gains in maximal bench press and squat strength were
significant in all groups, with no between-group differences.
Interestingly, while the whey group topped the field to a
nonsignificant degree in bench press gains, it had the lowest
increase in squatting strength (44%) compared to the carb (62%)
and soy group (65%). But again, these differences were not
significant.
The authors attribute the superior lean mass gains in the whey
group to its greater elevations in fasting and post-exercise
leucine concentrations. It has been proposed that a threshold
dose of leucine required to maximize muscle protein synthesis is
approximately 2-3 g, or 0.05 g/kg.10 The leucine content of the
whey protein isolate is about 10.9%, whereas in soy protein
isolate its 8% (chart here).11 So, in the 22g doses used in the
present study, whey crosses over that leucine threshold while
soy does not reach it. In recent work by Joy et al, no significant
differences were seen in the body composition and performance
improvements resulting from a 48 g dose of whey versus rice
protein, presumably because both doses met the leucine
threshold.12
While its plausible that the superior lean mass gains in the whey
group could have been due to the higher leucine content of
whey, Churchward-Venne et al13 recently found that low doses
of whey fortified with EAA or leucine to match the content of a
threshold dose of whey (25 g) elicited a lower anabolic
response than the full dose of whey protein. This means that
there could be other factors intrinsic to whey protein
(independent of its leucine content) that promote lean mass gain.
[Back to Contents]
Page 9
Study limitations
Effect of fruit restriction on glycemic control in
patients with type 2 diabetes--a randomized trial.
Christensen AS, Viggers L, Hasselstrm K, Gregersen S. Nutr J.
2013 Mar 5;12:29. doi: 10.1186/1475-2891-12-29. [PubMed]
BACKGROUND: Medical nutrition therapy is recognized as an
important treatment option in type 2 diabetes. Most guidelines
recommend eating a diet with a high intake of fiber-rich food
including fruit. This is based on the many positive effects of fruit
on human health. However some health professionals have
concerns that fruit intake has a negative impact on glycemic
control and therefore recommend restricting the fruit intake. We
found no studies addressing this important clinical question. The
objective was to investigate whether an advice to reduce the
intake of fruit to patients with type 2 diabetes affects HbA1c,
bodyweight, waist circumference and fruit intake. METHODS:
This was an open randomized controlled trial with two parallel
groups. The primary outcome was a change in HbA1c during 12
weeks of intervention. Participants were randomized to one of
two interventions; medical nutrition therapy + advice to
consume at least two pieces of fruit a day (high-fruit) or medical
nutrition therapy + advice to consume no more than two pieces
of fruit a day (low-fruit). All participants had two consultations
with a registered dietitian. Fruit intake was self-reported using 3day fruit records and dietary recalls. All assessments were made
by the "intention to treat" principle. RESULTS: The study
population consisted of 63 men and women with newly
diagnosed type 2 diabetes. All patients completed the trial. The
high-fruit group increased fruit intake with 125 grams (CI 95%;
78 to 172) and the low-fruit group reduced intake with 51 grams
(CI 95%; -18 to -83). HbA1c decreased in both groups with no
difference between the groups (diff.: 0.19%, CI 95%; -0.23 to
0.62). Both groups reduced body weight and waist
circumference, however there was no difference between the
groups. CONCLUSIONS: A recommendation to reduce fruit
intake as part of standard medical nutrition therapy in
overweight patients with newly diagnosed type 2 diabetes
resulted in eating less fruit. It had however no effect on HbA1c,
weight loss or waist circumference. We recommend that the
intake of fruit should not be restricted in patients with type 2
diabetes. SPONSORSHIP: None listed.
According to the authors, the study was prematurely terminated

due to limited time and research funding. First of all, that sucks.
Secondly, the authors did not specify how much of the 12-week
intervention had to be cut short (or whether it indeed lasted 12
weeks but was originally intended to be longer). This is a rather
important reporting omission. Another limitation was the
reliance on a 3-day food record at only 2 points in the
intervention (before and after). Increasing the frequency of the
submission of diet reports or having the subjects keep a daily
record would have increased the accuracy of the intake
journaling. Another limitation was the lack of tracking and
analyzing the diet overall. At minimum, it would have been
useful to see how the high-fruit and low-fruit treatments
impacted macronutrient intake.
A final limitation (from a public health reporting perspective)
was the misleading definition of a fruit serving, which was the
amount of fruit that contains 10 g carbohydrate (e.g., 100 grams
apple, 50 grams banana or 125 grams orange). The problem I see
with this is that a typical whole fruit contains about double this
amount of carbohydrate. For example, a medium-sized banana
(118 g) contains 27 g carbohydrate. A medium-sized apple (182
g) contains 25 g carbohydrate. So, without reading the full text,
one could easily assume that the amount of fruit assigned in the
study was at least double the actual amount consumed.
Comment/application
This study is conceptually strong; it examines practical/realistic

non-pharmacological steps that might aid in the management of
type 2 diabetes (T2D), a global problem that continues to rise.
This is the first controlled trial to compare the effect of
restricting fruit intake to 2 per day with consuming at least 2 per
day on glycemic control in adults with T2D. Both groups had
two consultations (one consultation in the beginning and one at
the end of the study period) with an experienced registered
dietitian. Compliance to the interventions was good. One subject
who failed to comply was excluded, but this did not affect the
outcomes. Subjects were instructed to eat fresh, whole fruit only
and to exclude fruit juice, canned and dried fruit from their diet,
or keep it as low as possible. This was a good move since it
minimized the confounding effects of the consumption of
refined, fruit-based products that could skew the aim of the
study.
The main finding of this study was a lack of significant

difference in glucose control improvements between the highfruit and low-fruit interventions; both decreased HbA1c.
Therefore, the common recommendation for newly diagnosed
T2D patients to limit fruit servings to 2 per day was not
supported by these findings. In addition, both groups showed
significant decreases in bodyweight and waist circumference,
with no between-group differences. Interestingly, a tendency
towards reduced body weight and waist circumference was seen
in the high-fruit group. However, given the relatively loose
control of the variables, these favorable trends in the higher-fruit
group should be viewed with caution. Still, it should be noted
that the favorable results of the higher fruit consumption have
been supported by recent observational research by Muraki et al
who found that greater whole-fruit consumption is significantly
associated with lower risk of T2D, while greater fruit juice
consumption was associated with a higher risk.14 Interventional
research has also shown a consistency of positive effects of fruit
intake.15-17 Thus far it looks that whole fruit consumption to the
order of 2 servings (or possibly more) is not an inherent threat to
glucose control or bodyweight/composition in those with T2D,
even in the context of not meticulously tracking total carb intake.
[Back to Contents]
Study strengths
Page 10
\
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2.
3.
4.
5.
6.
7.
8.
9.
Krieger JW. Single vs. multiple sets of resistance exercise for

muscle hypertrophy: A meta-analysis. J Strength Cond Res.
2010 Apr;24(4):1150-9. [PubMed]
Krieger JW. Single versus multiple sets of resistance exercise:
a meta-regression. J Strength Cond Res. 2009 Sep;23(6):1890901. [PubMed]
Horikawa C, Kodama S, Yachi Y, Heianza Y, Hirasawa R, Ibe
Y, Saito K, Shimano H, Yamada N, Sone H. Skipping
breakfast and prevalence of overweight and obesity in Asian
and Pacific regions: a meta-analysis. Prev Med. 2011 Oct;53(45):260-7. [PubMed]
Mesas AE, Muoz-Pareja M, Lpez-Garca E, RodrguezArtalejo F. Selected eating behaviours and excess body weight:
a systematic review. Obes Rev. 2012 Feb;13(2):106-35.
[PubMed]
Rampersaud GC, Pereira MA, Girard BL, Adams J, Metzl JD.
Breakfast habits, nutritional status, body weight, and academic
performance in children and adolescents. J Am Diet Assoc.
2005 May;105(5):743-60; quiz 761-2. [PubMed]
Szajewska H, Ruszczynski M. Systematic review
demonstrating that breakfast consumption influences body
weight outcomes in children and adolescents in Europe. Crit
Rev Food Sci Nutr. 2010 Feb;50(2):113-9. [PubMed]
Booth CK, Reilly C, Farmakalidis E. Mineral composition of
Australian ready-to-eat breakfast cereals. J Food Compost Anal
1996;9:13547. [Science Direct]
Berkey CS, Rockett HR, Gillman MW, Field AE, Colditz GA.
Longitudinal study of skipping breakfast and weight change in
adolescents. Int J Obes Relat Metab Disord. 2003
Oct;27(10):1258-66. [PubMed]
Schlundt DG, Hill JO, Sbrocco T, Pope-Cordle J, Sharp T. The
role of breakfast in the treatment of obesity: a randomized
clinical trial. Am J Clin Nutr. 1992 Mar;55(3):645-51.
[PubMed]
15. Madero M, Arriaga JC, Jalal D, Rivard C, McFann K, PrezMndez O, Vzquez A, Ruiz A, Lanaspa MA, Jimenez CR,
Johnson RJ, Lozada LG. The effect of two energy-restricted
diets, a low-fructose diet versus a moderate natural fructose
diet, on weight loss and metabolic syndrome parameters: a
randomized
controlled
trial.
Metabolism.
2011
Nov;60(11):1551-9. [PubMed]
16. de Oliveira MC, Sichieri R, Venturim Mozzer R. A lowenergy-dense diet adding fruit reduces weight and energy
intake in women. Appetite. 2008 Sep;51(2):291-5. [PubMed]
17. Rodrguez MC, Parra MD, Marques-Lopes I, De Morentin BE,
Gonzlez A, Martnez JA. Effects of two energy-restricted diets
containing different fruit amounts on body weight loss and
macronutrient oxidation. Plant Foods Hum Nutr. 2005
Dec;60(4):219-24. [PubMed]
10. Norton LE. 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]
11. Norton LE, Wilson GJ, Layman DK, Moulton CJ, Garlick PJ.
Leucine content of dietary proteins is a determinant of
postprandial skeletal muscle protein synthesis in adult rats.
Nutr Metab (Lond). 2012 Jul 20;9(1):67. [PubMed]
12. Joy JM, Lowery RP, Wilson JM, Purpura M, De Souza EO,
Wilson SM, Kalman DS, Dudeck JE, Jger R. The effects of
8 weeks of whey or rice protein supplementation on body
composition and exercise performance. Nutr J. 2013 Jun
20;12(1):86. [Epub ahead of print] [PubMed]
13. Churchward-Venne TA, Burd NA, Mitchell CJ, West DW,
Philp A, Marcotte GR, Baker SK, Baar K, Phillips SM.
Supplementation of a suboptimal protein dose with leucine or
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14. Muraki I, Imamura F, Manson JE, Hu FB, Willett WC, van
Dam RM, Sun Q. Fruit consumption and risk of type 2
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studies. BMJ. 2013 Aug 28;347:f5001. [PubMed]
[Back to Contents]
Page 11
Are Americas nutrition professionals in the pocket of

Big Food? [my commentary on the article by Joseph
Mercola]
products would not accurately be described as junk food. Heres

a compilation of the largest vendors at the ANDs annual
meeting (officially called the Food & Nutrition Conference &
Expo FNCE):2
By Alan Aragon
________________________________________________
Intro & background

I have to admit that when someone linked me to this article, my
BS defenses immediately went up since its author, Joseph
Mercola, is a physician who is notorious in the science-based
health & fitness community for being quacky. He has a long
history of warnings and battles with the FDA over false and
illegal product claims.1 Nevertheless, I gave the article a look,
and some very provocative points were raised, and this included
Mercolas video interview with public health lawyer Michele
Simon. Simon has become somewhat of an iconic whistleblower questioning the alliances of the Academy of Nutrition
and Dietetics (AND), formerly called the American Dietetic
Association. Her 50-page critical analysis of ANDs corporate
ties with the food industry can be downloaded here.
Since I got my undergraduate degree in nutrition & dietetics
with an AND-compliant curriculum taught mainly by registered
dietitians (RDs), I find this conflict very interesting. Lets take a
look at some of the gripes against the AND, and how legitimate
they may (or may not) be.
While the above revenue might make some folks jaws drop, its
important to note that AND sponsorship revenue was $1.85
million, which is only 5% the total revenue.2 What plays the
largest role in keeping AND afloat are membership dues, which
in 2011 amounted to $11.16 million. Clearly, sponsorship money
is not the backbone of the ANDs financial health, as some
disgruntled folks mistakenly believe.
Nevertheless, there is still the problem of how the corporate
sponsors influence the continuing education of RDs, who are
considered to be the most legitimate professionals in terms of
expertise in food and nutrition. The list of accredited continuing
education providers for RDs include Pepsico Nutrition, Nestle
Healthcare Nutrition, Coca-Cola Company Beverage Institute
for Health and Wellness, Kraft Foods Global, and ConAgra
Foods Science Institute. Thats an incomplete list, but its clear
how these companies involvement with producing continuing
education materials for RDs harbors an uncomfortably high
potential for conflict between science and commerce.
Its interesting to note that RDs (at least the ones who could be
reached, more on that in a bit) are for the most part approving of
the majority of the ANDs corporate sponsors. Here are the
results of a 2009 poll:2
As Michele discovered, food companies like Coca-Cola, General

Mills, Nestl, Kraft, and all of the major junk food purveyors
buy sponsorships to be at the Academy of Nutrition and
Dietetics annual trade organization meetings. They typically
end up having the largest booths on the expo floor. Besides
showcasing their food products, theyre also allowed to
sponsor or hold educational sessions at the meeting.
The excerpt above captures the heart of the problem, while also
capturing the sensationalistic nature of Mercolas delivery. Its a
biased slant to imply that sponsorships are bought solely by
major junk food purveyors. They are other sponsors whose
[Back to Contents]
Page 12
According to Reitshamer et al,3 only 13% of the dietitians

surveyed disapproved of all corporate sponsorship, and 68% said
that it depends who the sponsor is. 83% say they should have a
say in who is allowed to become a sponsor of the AND.
Interestingly, 47% of members are unaccepting of increased
membership fees in order to reduce sponsorship. More insider
details about this survey was reported here, where nutrition
graduate student Colby Vorland discusses his email
communication with the authors.4 Suffice it to say that
Reitshamer et al did not have the budget to pay for access to the
entire AND membership, so they were only able to access 10%
of the membership through a second-hand process dictated by
state and district affiliates. As such, the poll could potentially be
skewed in favor of member approval of the sponsors.
see this as a multi-faceted insult to the dietetics professionals

who provide vital support and sustenance to the AND.
Potential solutions
The following are Simons recommended steps (verbatim)
toward resolving the AND/Big Food alliance problem:2
1) Greater Transparency: AND should make more details
available to the public (or at least to members) regarding
corporate sponsorshipfar beyond what it currently
provides in its annual reports.
2) Request Input from Membership: Trade group policies
should reflect the desires of its members. Many RDs
object to corporate sponsorship but dont know how to
make their voices heard.
3) Meaningful Sponsorship Guidelines: AND should
implement much stronger and more meaningful
sponsorship guidelines, possibly looking to the Hunger
and Environmental Nutrition Dietetic Practice Groups
stricter guidelines as a model.
4) Reject Corporate-Sponsored Education: AND should
reject outright corporate-sponsored continuing education,
as well as corporate-sponsored education sessions at its
annual meeting. AND should also consider placing more
distance between its credentialing arm and the main
organization.
5) Increased Leadership on Nutrition Policy: In recent years,
ANDs leadership has taken important steps to improve
its policy agenda and create a positive presence in
Washington. However, while the staff in the D.C. office is
lobbying on behalf of ANDs membership, education
sessions are being taught to RDs by Coke and Hersheys.
This disconnect will continue to undermine ANDs
credibility on critical policy issues until the conflicts are
resolved.
Rage against the machine

Having grown up in the dietetics curriculum, it was an unsaid
rule that you shouldnt mess with the parent organization unless
youre ready for a slap on the hand. So, it was surprising to find
out about Dietitians for Professional Integrity (DPI), whose
inception appears to be largely inspired by Michele Simons
expos. Its a fast-growing group, reported have roughly 4000
members. DPI describes itself as such:
Dietitians for Professional Integrity is composed of Registered
Dietitians, Dietetic Technicians, dietetics students, and other
concerned individuals who do not support the Academy of
Nutrition and Dietetics' current sponsorship model. We believe
these sponsorships pose a serious conflict of interest for a
nutrition organization and harm our credential and reputation.
DPI founder Andy Bellati set up a formal online petition calling

for the ANDs administrative executives to sever the ties with
companies that concentrate on the sale of refined/processed
junk food. Bellati asserts that the petition is the result of
countless grievances from RDs to the AND, which has been
largely unresponsive to their concerns. The following excerpt
from the petition captures the frustration:
When junk food giants are allowed to sponsor our conferences
and provide continuing "education" to Registered Dietitians,
our credential -- which we worked hard for and value -- loses
credibility in the eyes of the public. These alliances run so deep
that dietitians can attend webinars where these companies
tell them that soda is unfairly vilified, and that sugary cereals
are a healthful way for children to start their day to earn
continuing education credits for re-certification.
While the sugary cereals comment is debatable, one thing that

really bugs me and makes me empathize with the DPI is their
long-standing attempt to convince the administrators of the
FNCE to include a structured point-counterpoint session about
the ANDs corporate ties with Big Food. This would have been
an excellent step forward in exposing the benefits and detriments
of this model. The DPI requested that the panel discussion be at
least partially composed of RDs. In a stroke of bad decisionmaking, the AND chose not to assemble a point-counterpoint
session, but rather to have journalist Michael Specter and
psychology professor Paul Rozin give their viewpoints (session
description here). Neither of those individuals is a registered
dietitian, and no point-counterpoint discussion will take place. I
I agree with all of these suggestions. In my view, #4 is the most

important, since its the root of the problem. If the means for
commercial objectives to influence educational materials are
eliminated or minimized, then less bias will make its way into
the knowledge base of RDs. Suggestion #2 is crucially important
as well, since lending a deaf administrative ear to the members
will only continue to brew civil unrest, and degrade the unity of
the organization from the inside-out. I would add a 6th step to
Simons list, and that would be to offer (or even mandate) extra
non-industry-funded courses on scientific/critical thinking and
research methodology so that no RD is unarmed in the face of
dubious claims by the food industry or other.
References
1.
2.
3.
4.
Barrett S. FDA Orders Dr. Joseph Mercola to Stop Illegal Claims.

Quackwatch. May 7, 2013. [Quackwatch]
Simon M. And now a word from our sponsors: Are Americas nutrition
professionals in the pocket of Big Food? Jan 2013. [Eat Drink Politics
AND Corporate Sponsorship - Full PDF]
Reitshamer E, Schrier MS, Herbold N, Metallinos-Katsaras E. Members
attitudes toward corporate sponsorship of the Academy of Nutrition and
Dietetics. Journal of Hunger & Environmental Nutrition. Sep 2013;8(3)
DOI: 10.1080/19320248.2013.817169 [JHEN]
Vorland C. Member attitudes toward corporate sponsorship of AND.
[Nutsci.org]
[Back to Contents]
Page 13
Interview with Karen Pendergrass, founder of Paleo

Movement Magazine.
By Alan Aragon
____________________________________________________
1) Evolution via natural selection is the central dogma of

Biology.
2) The Paleo Diet serves as a logical framework based on
evolutionary theory.
3) The Paleo Diet as an evolutionary template gives us the
basis for testable health predictions.
4) The Evolutionary Theory is a good framework for
hypothesis generation.
Now, Its really not as far-fetched as one may think to apply the
evolutionary theory to diet. Heres a perfect example:
Evolutionarily and biologically speaking, I know that my cat is
an obligate carnivore, and evolved to be that way over eons. Yet,
I fed her Royal Canin Urinary SO for years because thats what
the veterinarian prescribed her for chronic urinary tract
infections. Initially, I trusted the judgement of my vet, but my
cat never improved. I postulated that my obligate carnivore of a
cat was biologically maladapted to her prescribed diet of
chicken, corn, rice, and soymeal, and I hypothesized that my cat
would improve if I switched her to a raw cat food diet consisting
of muscle and organ meat. Unwittingly, my cat Flip became a
science experiment. Luckily, it worked for her, and she hasnt
had a UTI since the transition, 4 years ago.
See, not outlandish. Read on.
The concept of the evolutionary diet, or Paleo Diet itself is
applied with a similar basis, often for similar reasons, but to
humans. The theory is that the Paleo Diet is the one which
humans are physiologically best suited for, since humans (homo
sapiens and homo sapiens sapiens) evolved following this
dietary pattern. So, people across the world are testing this
theory with an n=1 experimental design. Its a large-scaled
science experiment, and of course, results vary. Some find after
30 days of eliminating grains, legumes, and dairy that they
cannot reintroduce them well, while some find that they do just
fine. I think its good to know your personal limitations. In that
capacity, the Paleo Diet is probably the best baseline to test your
dietary limitations from.
The following is an interview with Karen Pendergrass, which I

conducted shortly after she publicly interviewed me (here). Im
pleased to have her relay her knowledge about a controversial
topic that has been the object of my criticism for some time now.
Karens full bio plus links are listed at the end of the
interview...enjoy!
__________________________________________________
1. First of all, Id like to thank you for accepting this
interview, Im certain that the AARR audience will
appreciate your insight. What if any are your main
criticisms of the Paleo diet itself (whichever variant you want
to address), as well as the Paleo community at-large?
This is where I am probably going to get crucified by my own

community. We use evolution as a reason to adopt the Paleo
Diet, but then we often forget what evolution is really about, the
incredible ability for adaptation. Within my own community, I
often hear No one is adapted to grains and legumes and dairy.
Trust me, I sincerely wish that were true, but it likely isnt.
While researching insecticide applications on monocrops, I
learned that with every new insecticide class, cases of resistance
surfaced within 2 to 20 years this type of prolonged exposure
artificially selects for resistance. We saw the same thing happen
with Methicillin-Resistant Staph. Aureus (MRSA). This, as I see
it, is part of the natural selection and evolution process.
Thanks for asking me to do an interview, and I hope it gives

your readers something to chew on. Now, as far as general
criticisms of the Paleo Diet itself, or as far as the concept of it
goes, I have none to report. Heres why:
I could be wrong, but this is how it makes sense to me for now:

If your ancestors were initially maladapted to their dietswhich
is likely since early agrarian societies werent as healthy relative
to hunter-gatherer societies according to surveys of dental caries
and bone densities by physical anthropologists agriculturalists
would have had selective pressures to adapt. If it takes 2 to 20
years for insects to adapt, it seems likely that over the course of
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Page 14
10,000 years of selective pressures from a Neolithic,

agricultural-diet, would render some population of adapted
humans.
By that accord, it also makes sense that the longer your ancestors
had adopted a Neolithic Diet, the greater your chances of being
well-adapted are. Perhaps this is why studies of aboriginal
populations indicate that they experience an abnormally greater
rate of diseases of civilization when they adopt Neolithic
diets*. It may also explain why some specific ethnicities
experience abnormally greater rates of Neolithic diseases and
autoimmune conditions, as well. Perhaps not enough time has
passed to exert enough selective pressure to manifest into
adaptation. Its not a perfect explanation, because there are
confounding groups like the Inuit, but it does merit further
inspection.
Overall, the concept of the Paleo Diet can be viewed as simply
another application of evolutionary theory to generate a
hypothesis and test it. I have no qualms with that, and I dont
think anyone should in the name of science.
2. What do you feel are the most significant benefits (to
human health, the environment, or other) of going Paleo
that are unique to the diet?
Talk about a loaded question there, Alan. Thats like asking me
to condense my 400+ page book into a few short paragraphs, and
theres no way I could really do justice to any of my arguments
in such a short interview, but Ill try.
In short, while some humans may have adapted to the postagricultural-revolution diet, the planet has not. After 4 years of
reading, researching, and toiling over the concept of agricultural
sustainability, I have concluded that the Paleo Diet, and Paleoesque diets hold the key to turning the clock back on
environmental destruction that has occurred over the past 15,000
years, and I firmly believe it is the only diet that can be
sustainable in the long-term. Unfortunately, because the Paleo
Diet is meat-based, many sustainability experts have erroneously
declared that the Paleo Diet is the worst, and that meat-free diets
that obtain protein from plant sources are the best.
One way agricultural sustainability is often discussed belies the
Animal production is destroying the planet with greenhouse
gasses and pollutants so we should stop eating meat notion.
Then theres the idea that We should eat on a lower trophic
level because it must enable us to feed more people. Using both
of these rationales, it would appear, without further inspection,
that grains and legumes are certainly superior protein sources for
the environment and food security. After all, we are often told
that the only way to feed the planet is by increasing grain
agricultural yields to meet the food demands of the projected 9
billion global population of 2050.
anyone dares give credit to (lest you be called a flesh-eating

murderer), and because we fail to recognize that well-managed
livestock actually nets a negative carbon footprint and have the
unique capacity to restore previously degraded lands and reverse
processes of the burgeoning desertification crisis,* we have
committed the logical fallacy of composition and are missing
opportunities to save the planet via (generalization alert:) false
pretenses of moral superiority and misinformation.
Whats really missing in the environmental sustainability sect is
the bigger picture, the critical analysis, the Malcolm Gladwellian viewpoint of agricultural sustainability with an ecological
lens, if you will. While environmentalists, conservationists, and
sustainability enthusiasts examine current issues and make future
forecasts, history is largely (and inexplicably) ignored.
In the study of agricultural sustainability and eco-restoration, I
have used the Paleolithic Era as a baseline to compare all other
agricultural systems to. This is because 15,000 years ago while
humans were hunter-gatherers, the vast majority of ecosystems
were functioning properly in the illustrious closed-loop nutrient
cycle, food distribution was equitable, plants were efficiently
running the carbon cycle, animals aptly did their job of
maintaining the health of their prospective ecosystems, and the
health of the soil was excellent. Gleaning information from the
Paleolithic Era is a great place to learn about sustainability from,
not because it tells us what might work, but what has worked.
The question is, what significant environmental changes could
have caused these properly functioning systems to go awry on a
global scale?
Its a common theory that the advent of agriculture was the
cause of these systems to falter, I agree, and there is plenty of
evidence to support that. The areas where humans first adopted
agriculture is highly correlated with distinct periods of
unprecedented soil infertility, deforestation, desertification, and
other types of land degradation.** The truth is, the Agricultural
Revolution is really just one large science experiment that has
failed miserably, but we continue with its proliferation anyway.
You may have thought, perhaps, that through time and vast
technological advances that we were able to mitigate these
concerns, but we have not. In fact, technological advances have
only served to make conditions like soil erosion and soil
infertility worse. Agricultural advances like monocultures, or
the agricultural practice of producing a single plant species over
a relatively large area for a prolonged period of time, have been
implicated in the process of:
1)
2)
3)
4)
5)
6)
Desertification
Deforestation
Land Degradation
Depleted Water Tables
Climate Change
Habitat Loss and Extinction
While it is unequivocally true that 95% of the animal production

in this country is destroying this planet, we are throwing the
proverbial baby out with the bathwater here by lumping all
animal production methods together. Not all animal production
methods are created equally. Some are far more beneficial than
Monocultures are the bane of our existence. This includes

monocultures of grains, monocultures of legumes, and
monocultures of animals, otherwise known as Concentrated
Animal Feeding Operations (CAFOs). I can assure you, there are
no monocultures that exist in nature because monocultures do
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Page 15
not respect the basic tenets of ecology. Unfortunately, foods

from monocultures make up the bulk of our diets today, and yet
somehow, the inherent dangers of monocultures are also
inexplicably ignored when we propose solutions to feeding the
planet. This baffles me.
To feed the world and heal the environment, it will require
bolstering food systems that focus on bioregionalism and
facilitating wildlife. It will require a system that fosters
biodiversity and reduces global reliance on monocultures. Its
going to require an overhaul of current food systems and a
number of paradigm shifts, including a new way to assess
agricultural sustainability.
Sustainability is a hot topic these days, and everyone from
farmers to square-rimmed hipsters drinking PBR endeavor to
discuss it. Unfortunately, there isnt really a universal definition
for the word sustainable, so people generally throw facts
around without critically assessing a dietary plan or agricultural
system by its survivability. This is disconcerting because if the
goal is to reverse these ecological damages incurred over the last
15,000 years and prepare for the next 100, we need to define
sustainability so that we can objectively assess possible
solutions. We need guidelines. We need criteria. We need targets
to hit.
I propose that we universally accept and define agricultural
sustainability on a scale reflecting a systems capacity to
continue to function productively in the event of any particular
economic, political, environmental, or food system disruption.
Examples of these types of disruptions and their impact on food
systems
should
be
assessed
by
environmentalists,
conservationists, ecologists, and biologists for their
survivability, and even culpability in the disruption itself.
The three top environmental offenders are the monocultures of
grains, the monocultures of legumes, and the monocultures of
animals; this Industrial Agriculture system exists because we
continuously buy into it as a society. The Standard American
Diet, Vegan Diet, Vegetarian Diet, and Paleo Diet, all have their
own unique set environmental pitfalls. Each still relies too
heavily on unsustainable forms of agriculture that are culpable in
environmental destruction. Either we are purchasing
monoculture grains and legumes directly in the form of cereals,
breads, and pastas, or we are purchasing them indirectly in the
form of grain and soy-fed animals who live in confinement. I
cannot tell which is worse.
were doing because we didnt know what we were undoing.

We still dont know what we have undone, and continue to undo.
Back to the original question, what significant environmental
benefit is unique to the Paleo Diet?
As the Paleo Movement has progressed, our focus has shifted
from simply what to eat, to where to get our food from. It is
now commonly known amongst Paleo adherents that finding
local farms who produce pastured animals raised on speciesappropriate diets is the best way to improve food quality, but
also alleviate other environmental and health concerns. Animals
that are raised in this manner that perform their ecological
functions foster, not hamper, the most important thing that
environmental sustainability hinges upon: biodiversity. Its also
an excellent way to decentralize our food system, another vital
step towards agricultural sustainability.
If we can promote the proliferation of decentralized farming by
financially supporting these types of animal husbandry practices
instead of purchasing foods from CAFOs, we can change the
direction of the market and change the direction of
environmental destruction. We can go from focusing on efforts
to maintain the health of the soils, to repair the health of the
soils. We can reverse the processes of climate change,
desertification, land degradation, and losses of biodiversity. If
the goal is to decentralize, eschew monocultures, promote
ecological function, and improve biodiversity we can
accomplish much of this by gradually adhering to a more
orthodox type of Paleo Diet.
Is there another diet that could be adhered to without relying on
monocultures? Absolutely, I think all diets can be done without
relying on monocultures, but I suspect that it would be
logistically nightmarish. But the real question is, which dietary
discipline is most capable of reinstating biodiversity, feeding the
planet, reversing land degradation, decentralizing, and weaning
off the tit of Industrial Agriculture?
Honestly, I cant say with absolute certainty that I have the exact
answer, I can only say with absolute certainty that what we are
doing now is going to push us over the biodiversity cliff into
oblivion, and we really should go back to the drawing board to
come up with better solutions. We have already entered the 6th
mass extinction, and our current extinction rate estimated to be
1,000 to 10,000 times greater than the historical, background
rate.
What I can tell, is that the current system isnt working. Stephen
Hawking thinks were screwed and need to find a way off this
planet, and although I may be delusional... I think the Paleo Diet
offers us a fighting chance.
In conclusion, I suspect that the Paleo Diet has the unique

potential to be environmentally far superior than any other
dietary discipline. Im hedging my bets on what worked in the
past, since technological advances in the agrarian sect dont
seem to adequately replace or respect the vast complexities of
natural systems. And I dont suspect they ever will.
We have yet to find a dietary discipline that has proven itself

sustainable, except for the hunter-gatherer, Paleo Diet. We
have yet to find a dietary discipline that has proven itself
ecological sound, except for the hunter-gatherer, Paleo Diet.
Again, the Agricultural Revolution is really just a failed science
experiment. Like Wendell Berry said, We didnt know what we
*Savory Institute Carbon Restoring Climate Through Capture

and Storage of Soil Carbon Through Holistic Planned Grazing
White Paper April 2013
**Andrew Kimbrell (Ed.) Fatal Harvest: The Tragedy of
Industrial Agriculture. Washington DC: Island Press Chapter:
Farming in Natures Image, page 68
[Back to Contents]
Page 16
Graves Disease
Antiphospholipid Syndrome
Pemphigus vulgaris
3. The most current prevalence estimates of celiac disease

fall below one percent of the general population, while a
recent study estimated non-celiac gluten intolerance at about
half a percent of the population. Since there are several types
of gluten-free grains available commercially, how is it
justified to recommend a complete avoidance of all grain
types? Id like to hear your stance on this, since its one of
the logical impasses Ive found consistent with all variants of
the Paleo doctrine.
I had never heard of Pemphigus Vulgaris before.
The American Autoimmune Related Diseases Association

estimates that there are around 50 million people in the United
States with an autoimmune condition, and suggests that its
prevalence may be increasing. To put that another way, that is 1
in 6 individuals.
A study entitled Mucosal recovery and mortality in adults with

Celiac Disease after treatment with a gluten-free diet concludes
that Mucosal recovery was absent in a substantial portion of
adults with [Celiac Disease] after treatment with a [gluten-freediet]. Immunoreacitvity was still presented.
It seems to me that most people are under the impression that

gluten avoidance only makes sense for individuals with Celiacs
Disease. Actually, I think it makes sense for all people who have
autoimmune conditions because of the role that it appears to play
in the etiology of autoimmune disease.
While research is still inconclusive, its also hypothesized that

impaired intestinal barrier function is required in the
development of autoimmunity. Because gliadin and other
prolamins are associated with the development of intestinal
damage and zonulin release, they may be implicated in the
process of autoimmune disease, aside from causing molecular
mimicry in susceptible individuals.
Gluten is made up of two types of proteins, gliadins and

glutenins. During the digestion process, gluten is broken down
into strings of amino acids, called peptides. Because gluten is
not degraded by heat or by digestion, it remains an intact,
undigested 33-mer long polypeptide, and if it enters into
systemic circulation, an autoimmune response may occur if the
peptide sequence mimics the three-dimensional structure of an
individuals tissues. In this event, the immune system confuses
non-self proteins with self-proteins, a case of mistaken identity
known as molecular mimicry. It is widely accepted that this is
what happens in individuals with Celiacs Disease.
The immune system has a number of recognition or
identification mechanisms which allow the body to distinguish
between its own proteins, and foreign proteins. This
identification system allows for foreign bodies to be discovered,
identified, and subsequently destroyed. This makes perfect sense
evolutionarily speaking, so that the body will initiate an immune
response to intrusions by viruses, bacteria, etc. When an antigen,
or foreign invader is presented, immunoglobulins make
antibodies to combat them. There are IgA, IgG, IgM, IgE, and
IgD subclasses of antibodies, and certain antibodies have been
linked to the pathogenesis of autoimmune conditions, namely
anti-gliadin antibodies, which have been widely accepted as a
hallmark for Celiacs Disease.
Research has shown elevated levels of anti-gliadin antibodies in
several autoimmune conditions, not just Celiacs Disease. This
is including, but not limited to:
Autoimmune Diabetes
Multiple Sclerosis
Rheumatoid Arthritis
Psoriatic Arthritis
Autism (not an autoimmune condition, but still interesting)
Rett Syndrome
Lupus
Crohns Disease
Ulcerative Colitis
Perhaps we (as in the 1 in 6 of us with autoimmune conditions)

should consider avoiding gluten altogether. But should we avoid
all grains like the plague? After all, most of the grains on the
market are gluten-free...
Just because a grain is gluten-free doesnt mean it doesnt cause

immunoreactivity, and is safe for people with autoimmune
conditions. For instance:
The prolamin zein in corn was found to illicit immunoreactivity
in individuals with Celiacs Disease. I cant pull official figures
from the USDA after the federal funding lapse (their website is
shut down) to illustrate how much corn is in our food, but I can
tell you from experience that most gluten-free products use corn
as the starch source.
Rice has the prolamin orzenin ,which is now causing rice to be
reevaluated as a hypoallergenic food, since it is recognized as a
common and severe cause of food protein-induced enterocolitis
syndrome. This is interesting, since enterocolitis is commonly
induced by an autoimmune targeting of glial cells. Though, I still
think white rice may be relatively benign, but I may be wrong.
Millet and Sorghum are Panicoid grains with zein-likeprolamins,
which are notably also resistant to digestion, and it is suggested
that they act like zeins, which are also implicated in the process
of molecular mimicry.
Grain
Wheat
Rye
Oats
Barley
Millet
Corn
Rice
Sorghum
Prolamin
Gliadin
Secalinin
Avenin
Hordein
Panicin
Zein
Orzenin
Kafirin
% Total Protein
69
50
16
52
40
55
5
52
Fun fact: approximately 56% of the protein consumed globally

comes from wheat, rye, oats, barley, millet, corn, rice, and
sorghum*.
[Back to Contents]
Page 17
This begs the question, does research justify gliadin abstinence

for individuals with autoimmune conditions? Are waterinsoluble prolamins safe for people with compromised gut
function? Clearly, more succinct information is needed.
But for the 1 in 6 who have a diagnosed, undiagnosed, or
misdiagnosed autoimmune condition, it appears logical that they
could benefit by removing all grains which have been noted to
illicit immunoreactivity, which goes beyond the traditional
gluten-free approach, whether the research blatantly suggests
it or not. Though there are other factors that could cause
molecular mimicry (like rotovirus, and certain types of bacteria)
it should be no wonder that so many people with previous
autoimmune conditions report such drastic improvements
adhering to a more than just gluten-free, but a grain-free, Paleo
Diet.
Now you may have read all of that and thought to yourself that
youre Scott-free because you dont have an autoimmune
condition. Unfortunately, research still indicates that non-Celiac
individuals still experience mucosal changes and damage to
enterocytes (gut cells) in the intestines of people who have a
high gluten-containing diets. So, if enterocytes are damaged, gut
permeability is increased, prolamins like gliadin get into
systemic circulation, and youre just lucky enough to be 1 in 6
with a genetic predisposition for an autoimmune disease... Ill let
you postulate what could potentially happen next.
And since family history of autoimmune disorders, and certain
ethnicities can increase your chances of getting an autoimmune
disease significantly, one could easily justify going grain-free
even if youre healthy, just as a preventative measure.
*Stoskopf NC: Cereal Grain Crops. Reston, Reston Publishing
Company, 1985
4) I have often challenged people to provide controlled
research evidence showing the adverse effect of whole grain
and legume consumption in humans (as opposed to ex vivo
or animal data). People invariably fail to meet this request,
given those specific methodological parameters. I do not
claim to be aware of every bit of research in existence, so I
would love to see data that Im unaware of. Could you
provide any evidence that fits these conditions? To reiterate,
it has to be controlled intervention rather than
observational, and it has to be in living, healthy humans.
these questions are unfalsifiable at the moment, unless a study is,

or has been, conducted.
Maybe we need to find someone to fund this specific type of
research. NuSI?
5) Assuming you were able to find the indicting evidence in
the previous question, how can you reconcile the
recommendation for everyone to avoid grains and legumes in
light of the evidence indicating their beneficial health effects
(which outweigh the evidence of their adverse effects in an
admittedly mixed and complex body of literature)?
I can reconcile the recommendation to avoid grains and legumes
for a proscribed time period easily as a means to test individual
susceptibilities. Why not? The studies are out there that grains
and legumes have been implicated in exacerbating conditions
like leaky gut, autoimmune conditions, neurological conditions,
etc., but of course these studies are performed on individuals
who are already unhealthy. If you have any health condition,
even headaches, Id suggest it giving Paleo a go.
And you are unequivocally, absolutely, 100% right that the
literature is mixed, and youre right that the studies that favor
grain and legume consumption far outweigh the literature that
favor grain and legume cessation. A few things could account
for this:
1) Funding mechanisms that favor publishing several studies
with specific outcomes (Please read Bending Science: How
Special interest Corrupt Public Health Research)
2) Inadequate controls (directly confounding the evidence)
Hopefully this is not misconstrued as me saying that is no
evidence to support possible dietary benefits of grains and
legumes, I have seen pretty tight studies that have indicated
possible therapeutic properties. I am, however, just saying that I
ask a lot more questions when there is conflicting evidence, and
for the sake of circumventing a political discussion, Ill leave
you with this cartoon.
I scoured for studies to address this exact question with the

parameters that youve set, and I came up short.
So this is similar to the If a tree falls in the woods, does it make
a sound? question. If there are no in vivo, random controlled
trials on healthy humans to show what happens on every
physiological level when grains or legumes are consumed, do
adverse affects really happen?
Critics cannot say that grains and legumes dont cause healthy
individuals to experience any physiological damages, just as I
cant say that they do, given the parameters that youve set for
this question. So at this juncture, all hypothesis surrounding
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Page 18
6) How do you feel about the ban on potatoes issued by the

Paleo Godfather, Loren Cordain?
that is something that you are avoiding. You should likely avoid
asparagus and spinach root too if that is a real concern.
Paleo Godfather? If Im not mistaken, I think that title belongs to

Robb Wolf.
If you have a pathological metabolic issue that requires

abstaining from high-glycemic index, carbohydrate-rich foods,
perhaps you might want to skip it. Other than that, Id say they
are fine. And Paleo. But hey, Im no anthropologist.
For the record, I dont think anyone in this community agrees
with anyone 100%. Because the fundamental basis of the Paleo
diet itself is hypothetical, the entire community partakes in the
process of hashing out the Paleo-ness of a specific food.
Now, Lorens reasoning for issuing that ban as you call it was
for 3 reasons:
1) Potatoes have high glycemic indexes.

2) Most potatoes are consumed in highly processed forms.
3) Potatoes have saponins, or glycoalkaloids.
Because a food has a high glycemic index, or because it is often
prepared in such a way that is processed does not make a potato
inherently unhealthy. What is, perhaps, of concern is the saponin
or glycoalkaloid content, so lets delve into that.
Saponins are thought to bind and poke holes in enterocytes (gut
cells), and have been shown to increase gut permeability and
sensitization to dietary antigens (like food stuffs recognizable by
the immune system). So they may want to be avoided by people
who have autoimmune conditions or intestinal permeability
already.
In a Paleo Diet update, Loren says that:
Potato saponins can be lethally toxic in the bloodstream in
sufficient concentrations because these glycoalkaloids inhibit a
key enzyme (acetyl cholinesterase) required for the synthesis of
acetylcholine, a neurotransmitter required for nerve impulse
conduction....the highest concentrations of these toxic
glycoalkaloids appear in potato foods containing the skins.
Perhaps the answer is to remove the skins. Here is a graph by

Stephen Guyenet about the saponin content of various potatoes if
7) Whats your stance on the other Paleo no-no: dairy?

I do not think dairy is not inherently bad, and I dont believe for
a second that our Paleolithic ancestors wouldnt have had
access to it, since that had been one of the first the underlying
reasons behind its avoidance that I had heard back in 2009. If I
was a hunter-gatherer and I had just killed a nursing cow, theres
no way Id have passed up an opportunity to drink its milk.
Ive also heard the argument that we are the only animals that
would drink the milk of another animal, and therefore we
shouldnt do it. Well, I dont know any other animals that have
moral dilemmas about killing animals, either. Even still, thats
a poor reason not to do something. Wed have to have a better
reason than that.
But as far as my stance goes? My official stance is that I dont
have an official stance. I thought I did, but Im in the process of
reevaluating my stance on milk since a paper I received threw
me for a loop. I am still rock solid on never suggesting dairy
products from a CAFO, unless you were starving. Dont ever
expect me to waiver on that.
But before, Id have suggested dairy products from a grass-fed
operation with the caveat that you didnt have an autoimmune
condition or compromised gut lining or gut flora. I think most
paleo proponents would agree that this is sage advice.
The study that I received basically iterated that grass-fed dairy
may be beneficial for individuals with autoimmune conditions,
even though every study I had previously seen indicated that
dairy was detrimental for individuals with an autoimmune
condition. Because of this conflicting evidence, I no longer have
an official stance.
These were the thought processes of mine in light of this study:
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Page 19
1) I wonder if weve committed the same logical fallacy with

milk and autoimmune disease that was committed when we
lumped all forms of animal husbandry in with CAFOs. If
the sources of milk that was used in these studies that
determined that it was detrimental to individuals with
autoimmune conditions was not considered in the outcome,
then controls werent properly controlled. Our information
is skewed.
2) I asked myself, is milk inherently unhealthy? What is the
purpose of a mothers milk? To grow a healthy baby and
populate the gut flora, of course. Aha!
3) Is it possible then, that the milk from a corn and soy-fed
cow with chronic mastitis and gut
dysbiosis could exacerbate a
human autoimmune condition
with accompanying gut dysbiosis?
And by that same token, is it
possible that the milk from a
healthy cow could serve to
regulate human gut dysbiosis and
therefore,
alleviate
some
symptoms
of
autoimmune
conditions?
about the overkill theory of extinction. Vegetarianism didnt

wipe out 100 genera (not species, genera) of large animals
(weighing over 100 lbs) in the past 50,000 years*, and evidence
suggests that our species required much larger quantities of
animal foods to instigate larger brain development.**
Some researchers have suggested that the some of the earliest
humans 200,000 years ago consumed grains. Though this may
seem like a perfect opportunity to suggest that the Paleo Diet is
based on false pretenses, it appears that some of the research
that seems to have elucidated a cereal-based diet for our earlier
ancestors may not have been accurate. According to current
research, the stable isotopic data does not indicate grass
consumption by early hominin species in Africa.
Sorry I didnt have anything more solid

to report since Ive now got more
questions than answers. Again, more
information is needed.
8. What do you feel are the most
significant misunderstandings or
knowledge gaps that are harbored by the non-Paleo side of
the fence? In other words, what are the main things you feel
that Paleo critics are overlooking?
I have heard critics suggest that the Paleo Diet as we currently
practice it is based on false pretenses, since early humans were
largely vegetarian pointing to Homo erectus as a case-in-point
example. Though Homo erectus was human, our modern human
species, the Homo sapiens sapiens, and their Homo sapiens
predecessors were definitely not vegetarian.
To further illustrate the folly of using Homo erectus, or any
other hominid species other than our homo sapiens as an
example for comparison, we should know that we are also
99.5% genetically identical to chimpanzees. Just because two
species are genetically similar does not mean that they thrive on
the same diets or function in exactly the same environments.
Comparing us to Homo Erectus is like comparing us to a
chimpanzee.
If you are trying to determine a more accurate Paleo Diet,
clearly it would be better to compare homo sapiens sapiens to...
homo sapiens.
The other, and single-most disconcerting thing I have seen on

the other side of the fence is the assumption that what Paleo
adherents are experiencing is simply a placebo effect. This is
poor scientific thinking, and a cop-out for when you don't have a
theory that is substantial enough to explain the phenomenon, if
you will, of Paleo successes. Initially, I couldnt wrap my head
around how anyone could be well-adapted to eating grains, but it
was clear that some people were. So instead of throwing my
hands in the air and exclaiming that everyone is hiding their
symptoms, I had to look for other theories which could explain
my experiences, and the experiences of others as well.
Its why I like evolution. Its still a theory, sure but it helps
put so many of the pieces of the puzzle together.
*Twilight of the Mammoths: Ice Age Extinctions and the
Rewilding of America Paul S. Martin University of California
Press Page 1
**The Evolution of Hominin Diets: Integrating Approaches to
the Study of Palaeolithic Subsistence. Jean-Jacques Hublin pp
24-25
And if you really think that our human (Homo sapiens sapiens)
ancestors we were largely vegetarian, I highly suggest you take a
gander at Paul S. Martins Twilight of the Mammoths and learn
9. Tell us more about your Paleo-related projects you have in

the works. What goals and objectives do you aim to
accomplish with them? What do you see as the main
challenges or obstacles in ahead?
[Back to Contents]
Page 20
My main projects:
1) Eat Paleo Save the World: Sustainability from an
Omnivores Perspective is my book that is coming soon,
which is essentially the long-version of the answer to #2.
2) The Paleo Movement Magazine, which is the media
outlet arm of...
3) The Paleo Foundation, the umbrella nonprofit that
houses two food certification labels (Paleo Approved
and Paleo Friendly), organizes Paleo Movement events,
and has programs like sending food to troops overseas,
and grant programs for farmers who are interested in
accepting the Paleo Approved challenge, and
documenting and drafting procedural outlines for raising
animals using techniques suggested in Eat Paleo, Save
the World, just to see if they can come up better animal
farming solutions that are economically viable and more
sustainable than current farming methods.
My aim with all of my three projects is simple. I want to
effectuate change in the food system, and I think the Paleo
Movement will be instrumental in making that change.
Everything I have done thus far has been in the vein of spreading
awareness, fostering unity, and growing the movement. Thats
the answer youll find on paper.
The other aim of those projects is that they fuel my biggest
passion, which is helping people get better. My heart drops when
I hear of people who have experienced anything remotely similar
to what I have and need help. For me, these endeavors arent just
business, they are personal. I want people to know that when
they are told theres no cure that it doesnt mean theres no
hope.
About Karen Pendergrass:

Karen is the Founder of the the Paleo Foundation, a non-profit
organization whose mission is to strengthen, unify, and further
the Paleo Movement; President of the Paleo Movement
Magazine, and author of Eat Paleo, Save the World, a
publication serving to legitimize the Paleo Movement in the
fields of agricultural sustainability, biodiversity conservation,
and restorative ecology.
After a near-death experience with a slew of health conditions
including Celiacs Disease, Liver Disease, Fibromyalgia,
Neurological Disorders, and PCOS in 2009, Pendergrass
became particularly interested in nutrition, autoimmune
conditions, and species-appropriate diets for humans and
market animals alike which later spawned a deeper interest in
sustainable agriculture. She currently resides in Marina del Rey,
California.
Links:
Paleo Movement Magazine: http://paleomovement.com
Eat Paleo Save the World:
https://www.facebook.com/EatPaleoSaveTheWorld
The Paleo Foundation:
https://www.facebook.com/paleo.approved?ref=hl
Linkedin: http://www.linkedin.com/profile/view?id=77031109
Twitter: https://twitter.com/PaleoApproved
Im expecting some monumental obstacles in the next few years,

but Ill hold on anyway.
For one, getting a nonprofit
organization up and running smoothly is no simple feat, and Ill
need a lot of people who share my vision of the future, and
recognize a need for change on my side. Ive been planning this
for three years and Im just now making moves on it. For two,
trying to convince people to care about the environment is going
to be an exercise in futility and I will be left banging my head
against a wall. Then there are the toes that I expect Ill be
stepping on and the fallout from that... that will be fun. Not.
But if those are the greatest obstacles I encounter, Ill consider
myself lucky.
10. Whats your favorite dessert? Do you ever violate Paleo
Law?
If I violate Paleo Law, will the Paleo Police issue me a citation?
I think my favorite dessert of all-time is either peanut butter
cheesecake or peanut butter fudge. And when I knowingly
violate Paleo Law I can assure you that there is peanut butter
involved. And probably dairy too, if that counts.
And yes, when I eat peanut butter, I am a hypocrite! A sick one
at that!
____________________________________________________
[Back to Contents]
Page 21
Sometimes its easy to slip into the oversimplistic, black-orwhite judgement of the significance of outcomes based on the
arbitrary p-value of <0.05. Hat-tip to Eric Helms for
recommending the following slideshow by Alan Batterham and
Will Hopkins (Powerpoint or PDF format).
If you have any questions, comments, suggestions, bones of

contention, cheers, jeers, guest articles youd like to submit, or
any feedback at all, send it over to aarrsupport@gmail.com.
[Back to Contents]
Page 22

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10 Effect of fruit restriction on glycemic control in

patients with type 2 diabetes--a randomized trial.

12 Are Americas nutrition professionals in the pocket

14 Interview with Karen Pendergrass, founder of

Clearing up common misunderstandings that

Strength and body composition changes in

Belief beyond the evidence: using the proposed

Whey protein supplementation during resistance

Alan Aragons Research Review February & March 2013

Another problem with the advice to eat less is that theres a

The implication behind eating less is consuming less total

That was such a beautiful encapsulation of whats involved, that

Alan Aragons Research Review February & March 2013

The harmony of physiological factors regulating the bodys

In essence, insulin and leptin share similar/overlapping

neuroendocrine factors. So, weight loss certainly can occur by

Some gurus go as far as promoting the idea that exercise only

Conclusions & potential solutions

Katz DL. Pandemic obesity and the contagion of nutritional

Alan Aragons Research Review February & March 2013

Capita) Data System: Summary Findings. Last Updated Mon.

Strength and body composition changes in

One of the biggest controversies in the field of exercise science

authors acknowledge that, "Subjects here would be categorized

exercises used in 1RM testing. In short, an ICC is a measure of

Alan Aragons Research Review February & March 2013

Belief beyond the evidence: using the proposed effect

of results and inappropriate use of causal language is an

In addition to misleadingly citing other investigators results,

The main limitation was not necessarily design-related, but

Ultimately, there is insufficient evidence supporting the PEBO,

Alan Aragons Research Review February & March 2013

Alan Aragons Research Review February & March 2013

staff. Body composition was assessed with dual X-ray

According to the authors, the study was prematurely terminated

This study is conceptually strong; it examines practical/realistic

The main finding of this study was a lack of significant

Alan Aragons Research Review February & March 2013

Krieger JW. Single vs. multiple sets of resistance exercise for

10. Norton LE. Optimal protein intake to maximize muscle

Alan Aragons Research Review February & March 2013

Are Americas nutrition professionals in the pocket of

products would not accurately be described as junk food. Heres

Intro & background

As Michele discovered, food companies like Coca-Cola, General

According to Reitshamer et al,3 only 13% of the dietitians

see this as a multi-faceted insult to the dietetics professionals

Rage against the machine

DPI founder Andy Bellati set up a formal online petition calling

While the sugary cereals comment is debatable, one thing that

I agree with all of these suggestions. In my view, #4 is the most

Barrett S. FDA Orders Dr. Joseph Mercola to Stop Illegal Claims.

Interview with Karen Pendergrass, founder of Paleo

1) Evolution via natural selection is the central dogma of

The following is an interview with Karen Pendergrass, which I

This is where I am probably going to get crucified by my own

Thanks for asking me to do an interview, and I hope it gives

I could be wrong, but this is how it makes sense to me for now:

Alan Aragons Research Review February & March 2013

10,000 years of selective pressures from a Neolithic,

anyone dares give credit to (lest you be called a flesh-eating

While it is unequivocally true that 95% of the animal production

Monocultures are the bane of our existence. This includes