3 - April - 2014

12 Protein: is it really as bad as they say it is?
By Dylan Klein
17 Dr. Brad Schoenfeld gives the inside scoop on his

new study comparing hypertrophy-type and
strength-type training.
Interviewed by Alan Aragon
Copyright April 1st, 2014 by Alan Aragon
Home: www.alanaragon.com/researchreview
Correspondence: aarrsupport@gmail.com
20 Response to: Cardiovascular disease mortality

and cancer incidence in vegetarians: a metaanalysis and systematic review.
By Robert Hoenselaar
The compelling case against 'food addiction.'

By Evelyn Kocur
Processed foods: contributions to nutrition.

Weaver CM, Dwyer J, Fulgoni VL 3rd, King JC, Leveille
GA, Macdonald RS, Ordovas J, Schnakenberg D. Am J Clin
Nutr. 2014 Apr 23. [Epub ahead of print] [PubMed]
The effects of 12 weeks of beta-hydroxy-betamethylbutyrate free acid supplementation on

muscle mass, strength, and power in resistancetrained individuals: a randomized, double-blind,
placebo-controlled study.
Wilson JM, Lowery RP, Joy JM, Andersen JC, Wilson SM,
Stout JR, Duncan N, Fuller JC, Baier SM, Naimo MA,
Rathmacher J. Eur J Appl Physiol. 2014 Mar 6. [Epub ahead
of print] [PubMed]
Vitamin D and multiple health outcomes: umbrella

review of systematic reviews and meta-analyses of
observational studies and randomised trials.
Theodoratou E, Tzoulaki I, Zgaga L, Ioannidis JP. BMJ.
2014 Apr 1;348:g2035. [PubMed] [Full Text]
10 Variability in muscle size and strength gain after

unilateral resistance training.
Hubal MJ, Gordish-Dressman H, Thompson PD, Price TB,
Hoffman EP, Angelopoulos TJ, Gordon PM, Moyna NM,
Pescatello LS, Visich PS, Zoeller RF, Seip RL, Clarkson
PM. Med Sci Sports Exerc. 2005 Jun;37(6):964-72.
[PubMed]
Alan Aragons Research Review April 2014
[Back to Contents]
Page 1
The compelling case against 'food addiction.'

By Evelyn Kocur
_________________________________________________________________
The concept of food addiction has been elevated from obscure

conjecture to almost universally accepted scientific fact within
the past two decades. That this has happened so relatively
quickly is understandable given the predicament Western nations
are in, with obesity rates rising year after year, seemingly
unabated. Simply put, food addiction seems a rather plausible
explanation for the overconsumption fueling this obesity
epidemic. But does it stand up to scientific testing? I submit that
the answer is a resounding No! What follows should convince
you as well.
eating more, and drinking more in the form of sodas and coffee
concoctions. Estimates vary, but it is not controversial that our
average caloric intake has risen substantially since the 1970s,
and this alone is sufficient to explain the obesity epidemic.4
While nutritional researchers sought to identify culprit foods
from an energy standpoint, others sought to identify the reasons
that prompted this uptick in intake. Food addiction came of age.
The most convincing evidence of food that has emerged has to
be the deluge of juxtaposed brain activity scans showing some
known addictive drug alongside sugar. Who isnt convinced by
the brain scans in Figure 1?5 Similar pictures are seen
everywhere these days , offered up as scientific proof that
sugar is addictive. It doesnt hurt that sugar is also a white
powder that it lends itself well to creating images with white
lines, mirrors and drug paraphernalia. In 2013, the biggest
nutrition headline was: Rats find Oreos as addictive as cocaine. 6
The nature of addiction: physiology or psychology?

Whenever the topic of addiction comes up, the debate ensues
over whether it is physiological or psychological in nature. The
proponents of the food addiction concept have made this part
easy, however, as they have chosen the model put forth in the
American Psychiatric Associations DSM-IV,1 and that model is
predicated on physical dependence. This is important because,
researchers often point to symptoms they can evoke while failing
to establish the primary physical dependence. In the scientific
literature, it was TG Randolph who first drew analogies between
alcohol addiction and food addiction.2 He focused on
physiological measures of addiction size of dose and frequency
of dosing in his attempts to draw parallels. But these two
measures have posed the same conundrum for alcohol and food.
If alcohol is addictive and fairly widely used, why doesnt
everyone who drinks become an addict? The reality is that it is
highly likely that everyone who ingests a certain amount of
alcohol frequently enough will develop a physical dependence.
Psychological factors factor more in the how and why someone
might come to ingest those amounts in the first place, but once
physical dependence sets in are largely irrelevant to the question
of why the person still partakes despite negative consequences.
An addiction model for food that is predicated on these same
diagnostics must meet the criterion for physical dependence or it
fails. When the first chapter of Overeaters Anonymous was
founded in the 1960s, it was modeled after Gamblers
Anonymous, which was in turn modeled after the 12 Step
program of Alcoholics Anonymous. Researchers, like the rest of
us, are no doubt influenced by the existence of OA and its focus
on treating compulsive eating (addiction) considered to be the
cause of overweight and obesity.3 Obesity was still relatively
rare in those times, so these ideas didnt really catch on then as
they have now. Now that a sizeable minority, or perhaps even a
majority, seems to have been effected, and externally driven
addiction seems to be a more acceptable explanation.
Figure 1. Your Brain on Sugar
But its not just sugar, its seemingly all foods, or at least any
food even the flimsiest case can be made against. Never mind
that the same regions of the brain light up during sex, exercise,
making silly faces at babies and petting puppies. In the 1980s
and 1990s it was fatty foods and McDonalds was a favorite
target. More recently, its sugary foods and carbohydrates in
general, and McDonalds is still a favorite target. Documentaries
and videos, be they mainstream,7,8 lamestream,9 or somewhere in
between,10 and countless media reports have sought to convince
us that certain foods are indeed addictive and the cause of our
battle with the bulge.
The common sense case against food addiction
By the 1990s, the obesity epidemic that had begun a decade or

so before, was gaining steam and researchers clamored to
identify a cause. Alongside a veritable explosion of fast food
restaurants and packaged convenience foods, Americans were
Whenever a concept is advanced with such fervor as to be

presumed fact, the part of my brain responsible for skepticism
would light the heck out of one of those scans! Step back and
think about this. Pick the food agent you are most convinced is
addictive sugar generally fits that bill for most and draw
analogies to alcohol. See if it all even makes sense. A true
alcoholic is physically addicted to ethanol. Take it away and
he/she will get the DTs.11 You wouldnt serve a teetotaler light
beer because it contains just a little alcohol. You wouldnt put
Metamucil in a martini to render the ethanol benign. Yet the
mountain of literature implicating sugar sucrose and/or HFCS
as an addictive agent fails the simple fruit test. One of the
foremost crusaders against sugar, Dr. Robert Lustig, had this to
say in a recent interview:12
[Back to Contents]
Brain images seal the deal
Page 2
People always say to me, "What about fruit? It has sugar.

But I have nothing against fruit, because it comes with its
inherent fiber, and fiber mitigates the negative effects.
If sucrose were addictive like ethanol, then it wouldnt matter
how much fiber it came packed with. Numerous similar
analogies could be drawn relating other aspects of food and
alcohol, none of which rescue the case for food addiction.
Wait a minute. This is Alan Aragons Research Review.
Wheres the science?
Honestly I could have ended the article with my last section, but
the scientists have brought out the big guns to convince you food
addiction is real and the diet gurus have seized on it to sell you
their detoxes and clean eating plans. So now Im going to turn
those guns right back at them and present my case for why it is
not. Yes, their own research often, and accidentally, refutes
their claims. The vast majority of addiction research is carried
out in our close friend and evolutionary relative, the rat. (That
is a tongue in cheek reference to recent assertions by two
researchers cited in this article claiming rats are very good
models for human behavior!) Humans present far too many
ethical issues for considerable research in this field, rats do not.
Now while I dont share the researchers full enthusiasm for
broad similarities between rats and humans, I rather celebrate the
differences and what those differences can help elucidate. Rats
eat throughout the 24 hour cycle, though more during their
active periods. They dont eat at regular intervals or consume
meals in a human sense. When fed chow they get balanced and
complete nutrition with every bite. They dont eat out of
emotional distress, diet to fit into that little black dress, or give a
rats behind what the other rats think of their waistline. In other
words, as imperfect as they are to mimic the totality of human
behavior, they can be helpful in isolating the part we are
interested in: What physiological effects do foods have on the
brain, and do those effects alter energy intake and body weight?
If youre going to try propose food addiction as a concept, youll
need to model it after established addictions. So off to the DSM
went the researchers for the list of substance dependence criteria.
The first three are (i) tolerance, (ii) withdrawal, and (iii)
overconsumption. This is important, because merely
overconsuming something does not an addiction make.
Researchers have been invariably successful in getting rats
addicted to alcohol. If you put it in their water supply, they
become addicted with ad libitum access. It takes a while, but it
will happen. Pretty soon researchers discovered that they could
shorten that time by employing an intermittent access
protocol.13,14 Such protocols promote binges resulting in larger
doses of alcohol at one time. If they can get rats hooked on
alcohol (and other drugs) in this fashion, then they should be
able to replicate this with food. Just force them to consume the
addictive food. Right?
Your standard rat feeding protocol is to allow ad libitum access
to a species appropriate chow, usually 10-15% fat, 15-20%
protein, and the balance consisting of grains for carbohydrate in
the 60-70% of energy range. This is used as the control in most
every rat nutritional study out there. So they fed rats sugar (in
their drinking water or in their chow), and they fed them fats,
and they fed them combinations thereof, with and without the
flavors of human foods added. They even fed them the actual
junky human snack foods! Care to guess what happened? Here

is a summary.
Ad libitum chows: Rats fed chows enriched in refined
carbohydrate (35% sucrose/30% cornstarch) or a sweet-fat
chow (45% fat/17% sucrose) in ad libitum fashion
consumed the same or even fewer calories vs. controls, but
gained more weight due to food efficiency.15 It is difficult
to find high fat diets that do not contain sucrose, but in a
study where sucrose was controlled between a low and high
fat diet, the rats fed the high fat diet consumed more and
became obese.16
Ad Libitum junk food diets: Rats fed standard chow but
offered a rotating selection of human snack foods, ranging
from jelly beans to pepperoni to cheese doodles, reduced
their consumption of chow considerably yet consumed
almost one-third more in total calories than their chow-fed
counterparts. Needless to say, they became very obese.15 In
another study, rats fed a modified chow (powdered chow
and sweetened condensed milk) along with several human
snack foods also consumed significantly more calories and
became obese.17
There is no mention in any of these various studies of rats
engaging in binge-like behaviors associated with addiction.
Next, here are a couple of studies where chronic ad libitum diets
have been switched after prolonged periods:
Study One:18 Rats were fed either a cafeteria diet (like ref.
17) or a standard chow ad libitum for 16 weeks. Half of
each diet group was then switched to the other diet for 9
days. This one is worth including the graphs in Figure 2.
The long term intake for Caf rats was roughly double that of
Chow rats. Rats switched from Caf to Chow dropped intake
below that of the long term intake of the Chow rats. Rats
that had been accustomed to bland Chow? They appear to
have gone a bit wild, roughly tripling their intake and
exceeding habitual Caf intake by around 50% of what the
Caf rats consumed long term!
Figure 2. Effect of switching diet on weight and intake.
[Back to Contents]
Page 3
Study Two:19 These rats were given the same diet as the
low fat (refined carbohydrate, REF) diet in reference 15
or standard chow (CON) ad libitum for 6 months. The REF
rats gained roughly 20% more body weight CONs. At 6
months the rats were subjected to a lever pressing test to
ascertain motivation. After training to press a lever to
dispense sugar water, the number of lever presses required
for dispensing was progressively increased. The REF rats
demonstrated less motivation by taking longer between
attempts. This was repeated with plain water to the same
result. Nine days after the diet switch, the motivation test
was again conducted. The REF rats remained less motivated
despite consuming the CON diet, and vice versa with the
CON rats suffering no impaired motivation from the REF
diet.
To me, Study Two is one of those accidental gems where the
researchers set out to prove some other beliefs, and never even
realized their results undercut another premise they appear to
hold dear. The REF diet is described as a human junk food diet
(when at such low fat levels it simply is not!) and junk foods are
described as addictive and obesogenic in the discussion of the
paper. Study One employed a more obesogenic human junk
food diet, yet there was no mention of addictive-like
withdrawal behavior. It is conceivable that this was simply
overlooked or not noted in that study, but in Study Two, the test
for motivation involved sugar, a purported addictive agent, as
reward for completing the task. If long term exposure to a
35% sucrose diet caused addiction, one would expect the rats to
be more highly motivated to obtain still more sugar, not less.
Further, when they were withdrawn for a period, one might
expect them to chew through the apparatus to get at the sugar, or
at least try! Instead, they showed less enthusiasm than the
presumably non-addicted rats, could care less if the reward was
water or sugar-water, and demonstrated the same lack of
motivation for the sugar water even after having been deprived
of their fix. This is very compelling evidence against sugar
addiction per se, straight from a study that would otherwise seem
to favor the food addiction paradigm.
So... What exactly does one have to do to evoke addiction-like
behaviors in rats? Intermittent restriction of sugar, fat, or
combinations thereof. These are summarized nicely in a review
article by Avena et.al. entitled Sugar and fat bingeing have
notable differences in addictive-like behavior 20
Intermittent Sugar Water: By alternating access to sugar
water to 12 hours on/off and delaying sugar access several
hours into the circadian feeding cycle, rats increase sugar
intake. They also binge the most in the first hour of access
and engage in larger meals during the access period than
ad libitum fed rats. The rats compensate for the caloric
intake by decreasing chow intake (available ad libitum).
Thus total 24 hour intake remained the same as ad libitum
access rats and they remain normal weight.
Intermittent Fat Access: Rats will binge on shortening
made available for only two hours a day. Interestingly,
restricting access to only 3 times per week leads to a greater
effect. Again, however, the rats compensate with reduced
chow intake and remain normal weight.
Sweet-fat intermittent restriction:21 Rats were provided

only 2 hours of access per day to a sweet-fat chow with ad
libitum access to a standard (bland low fat) chow. After
three weeks, some rats were consuming almost 60% of their
total daily calories within those 2 hours. Although they
reduced chow intake during the other 22 hours, this was not
sufficient to offset binge intake completely, thus total intake
was greater, and these rats gained weight.
I find it amazing that Avena has co-authored a mass media diet
book entitled Why Diets Fail: Because Youre Addicted to
Sugar, given her unique involvement in developing the methods
to elicit bingeing in rats.
Summary of the research
Taken together, these rat studies paint a picture that is rather
more simple that you might think, especially if youve ever
found yourself stuck in the PubMed rat maze on this topic.
1.
2.
3.
4.
5.
6.
Sugar supplied in water or substituted for other

carbohydrate in a standard rodent chow does not induce
overconsumption, but may lead to weight gain due to
food efficiency.
Fat replacing carbohydrate in substantial proportion in a
standard
rodent
chow
does
not
induce
overconsumption, but predictably leads to weight gain
due to food efficiency.
Sugar and fat together generally lead to modest weight
gain due to food efficiency and/or mild increases in
intake due to increased palatability.
Sugar + fat + flavor = high palatability. This leads to
considerable overeating and weight gain due to excess
consumption (food efficiency may be a factor as well).
General feeding behavior remains normal, however.
Intermittent access to sugar or fat can result in binge
behavior, but rats compensate for the calories consumed
during binges. Thus, total intake remains the same and
the rats remain a normal weight.
Intermittent access to a more palatable sugar-fat chow,
with free access to regular chow, leads to severe
binging in such a way that rats cannot completely
compensate for the caloric excesses by limiting intake
of regular chow. This leads to weight gain.
Similar observations to these have been made by various

researchers using various protocols. Although often
accompanied by impressive neurobiological and neurochemical
changes, as well as brain scans lit up like the sky on the Fourth
of July, the behaviors simply do not support a substance
dependence addiction model like that developed for alcohol and
cocaine, or even caffeine.
In the real world humans become addicted to such substances
with a predictable pattern, though on differing timescales and/or
prevented limited exposure. The person engages in optional
intake of a non-life sustaining, mind altering compound. With
repeated exposure a tolerance develops thus requiring more of
the agent over time to produce the same effect. As intake
increases to compensate for the tolerance, a physical dependence
[Back to Contents]
Page 4
develops as the body/brain becomes accustomed to this new

normal. If the substance is then removed, withdrawal symptoms
ensue, sometimes quite severe, and even life-threatening,
producing strong cravings for the substance. Since withdrawal
symptoms are alleviated with consumption of the substance, this
drives the cycle of addiction. The evidence is simply not there to
support this mechanism for foods or their particular components
to result in physical dependence.
9.
10.
11.
12.
13.
The take-away message

Im often asked what negative results such as those Ive laid out,
provide people with in terms of actionable information. In this
current environment of pseudoscience and guru-speak gushing
from every corner of the media, I believe that there is benefit to
just presenting it at all. Consider it a deprogramming of sorts.
There is a lesson to be learned from these rats in terms of what
actually causes the addiction-like behaviors. It is restriction
that triggers the physiological addiction cycle, such as it
exists, with food. At least that is the conclusion that the research,
conducted by the proponents of the alternative concept, leads us
to.
____________________________________________________
Evelyn Kocur holds a B.S. in Biology from
Rensselaer Polytechnic Institute and an
M.S. in Materials Science (Metallurgy)
from The University of Connecticut
where
she
studied
corrosion
phenomenon. She is a former research
scientist in the pharmaceutical and
electronic materials industries and
currently teaches college math and
science. Following her personal
interests in nutritional science, Evelyn
began blogging as CarbSane at The Carb-Sane Asylum in 2010 focusing
on nutrition and diabetes research. Her first book, Restriction
Addiction: Why the "cure" for food addiction may just be the cause,
and
how
to
break
the
cycle,
is
available
at:
http://carbsanity.blogspot.com/p/restriction-addiction.html
____________________________________________________
References
1.
2.
3.
4.
5.
6.
7.
8.
14.
15.
16.
17.
18.
19.
20.
21.
Fat Head Movie

The Skinny on Obesity
http://en.wikipedia.org/wiki/Delirium_tremens
Feb. 2014 NYT Interview called Learning to Cut the Sugar
with
Dr.
Lustig,
by
Anahad
OConnor.
http://well.blogs.nytimes.com/2014/02/19/learning-to-cutthe-sugar
Hopf, FW et.al. Motivation for alcohol becomes resistant to
quinine adulteration after 3-4 months of intermittent alcohol
self-administration. Alcohol Clin Exp Res. Sep 1, 2010;
34(9): 15651573. [PubMed]
Loi, B et.al. Increase in alcohol intake, reduced flexibility
of alcohol drinking, and evidence of signs of alcohol
intoxication in Sardinian alcohol-preferring rats exposed to
intermittent access to 20% alcohol. Alcohol Clin Exp Res.
2010 Dec; 34(12):2147-54. [PubMed]
Sampey, BP et.al. Cafeteria Diet Is a Robust Model of
Human Metabolic Syndrome With Liver and Adipose
Inflammation: Comparison to High-Fat Diet. Obesity.
2011 June;19(6): 11091117. [PubMed]
Woods, SC et.al. A Controlled High-Fat Diet Induces an
Obese Syndrome in Rats. J. Nutr. 2003 April; 133(4):
1081-1087. [PubMed]
Hansen, MJ et.al. Adaptive responses in hypothalamic
neuropeptide Y in the face of prolonged high-fat feeding in
the rat. J. Neurochem. 2003 Dec; 88(4): 909-916.
[PubMed]
South, T et.al. Neurological and stress related effects of
shifting obese rats from a palatable diet to chow and lean
rats from chow to a palatable diet. Physiol Behav. 2012 Feb
28;105(4):1052-7. [PubMed]
Blaisdell, A et.al. Food quality and motivation: A refined
low-fat diet induces obesity and impairs performance on a
progressive ratio schedule of instrumental lever pressing in
rats. Physiol Behav. 2014 Apr 10;128:220-5. [PubMed]
Avena, NM et.al. Sugar and Fat Bingeing Have Notable
Differences in Addictive-like Behavior. J Nutr. 2009
Mar;139(3): 623628. [PubMed]
Berner, LA et.al. Bingeing, Self-restriction, and Increased
Body Weight in Rats With Limited Access to a Sweet-fat
Diet. Obesity. 2008 Sept; 16(9): 19982002. [PubMed]
DSM-IV Alcohol Abuse and Dependence. Office of the

Surgeon General (US); National Institute on Alcohol Abuse
and Alcoholism (US); Substance Abuse and Mental Health
Services Administration (US). Rockville (MD): Office of
the Surgeon General (US); 2007.
http://www.ncbi.nlm.nih.gov/books/NBK44358/
Randolph, TG. The descriptive features of food addiction;
addictive eating and drinking. Q J Stud Alcohol. 1956 Jun;
17(2):198-224. [PubMed]
Overeaters Anonymous
Swinburn, B et.al. Increased food energy supply is more
than sufcient to explain the US epidemic of obesity. Am J
Clin Nutr. 2009 Dec;90(6):1453-6. [PubMed] [Full PDF]
What Happens to Your Brain on Sugar, Explained by
Science
Rats find Oreos as addictive as cocaine
Supersize Me
The Men Who Made Us Fat
[Back to Contents]
Page 5
Processed foods: contributions to nutrition.

Weaver CM, Dwyer J, Fulgoni VL 3rd, King JC, Leveille GA,
Macdonald RS, Ordovas J, Schnakenberg D. Am J Clin Nutr.
2014 Apr 23. [Epub ahead of print] [PubMed]
My commentary
As a scientific statement by the American Society for Nutrition
(ASN), this paper is not conducive to the typical critique of
strengths and limitations inherent in experimental studies. Its
essentially an updated review of the state of the science. The
reason it jumped out at me when choosing literature to review is
because the term processed foods carries strongly negative
connotations, and much of this vilification is simply not
warranted. Its true that food processing in certain cases has
indeed created problems, particularly in cases of
overconsumption of highly refined food products displacing
whole & less-refined foods. However, processing has also
contributed significantly to the improvement of human health.
The latter is widely overlooked, especially with the constant
barrage of sensationalistic media messages that are universally
against food processing. The chart below (Table 5 in the text)
summarizes the wide array of consumer benefits of current and
developing food processing technologies. Notice that a recurring
benefit is the enhancement of well-being and quality of life.
One aspect that rings loudly with me personally is the ability of

food processing technology to optimize nutrition for populations
such as infants, pregnant mothers, and the elderly. Also, through
the isolation of various compounds, food processing technology
has played a tremendous role in not just the enhancement of
athletic performance through supplementation, but for
populations at risk for essential nutrient deficiencies. A recent
review by van Boekel et al list the most important benefits of
food processing as follows:1
Food safety (pathogens): The main benefit of food
processing is inactivation of food-borne pathogens, as is
normally required by Food Safety Legislation.
Food safety (other aspects): inactivation of natural toxins
and enzymes, prolongation of shelf-life.
Nutritional value: improved digestibility, bioavailability of
nutrients.
Sensory quality: taste, texture and flavor. Functional health
benefits: e.g. probiotics, prebiotics,
Maillard reaction products (MRPs), flavonoids, other food
constituents and their reaction products.
Convenience: availability of ready-to-eat and semiprepared
foods, e.g. microwavable frozen meals.
Cost: economy of scale
Diversity: independence from the seasonal availability of
foods, and introduction of global food supply chain.
Quality of life: improved because less time required for food
supply and preparation.
[Back to Contents]
Page 6
Study limitations
The effects of 12 weeks of beta-hydroxy-betamethylbutyrate free acid supplementation on muscle
mass, strength, and power in resistance-trained
individuals: a randomized, double-blind, placebocontrolled study.
Wilson JM, Lowery RP, Joy JM, Andersen JC, Wilson SM,
Stout JR, Duncan N, Fuller JC, Baier SM, Naimo MA,
Rathmacher J. Eur J Appl Physiol. 2014 Mar 6. [Epub ahead of
print] [PubMed]
INTRODUCTION: Studies utilizing beta-hydroxy-betamethylbutyrate (HMB) supplementation in trained populations
are limited. No long-term studies utilizing HMB free acid
(HMB-FA) have been conducted. Therefore, we investigated the
effects of 12 weeks of HMB-FA supplementation on skeletal
muscle hypertrophy, body composition, strength, and power in
trained individuals. We also determined the effects of HMB-FA
on muscle damage and performance during an overreaching
cycle. DESIGN: A three-phase double-blind, placebo- and dietcontrolled randomized intervention study was conducted. Phase
1 was an 8-week-periodized resistance-training program; Phase
2 was a 2-week overreaching cycle; and Phase 3 was a 2-week
taper. Muscle mass, strength, and power were examined at
weeks 0, 4, 8, and 12 to assess the chronic effects of HMB-FA;
and assessment of these, as well as cortisol, testosterone, and
creatine kinase (CK) was performed at weeks 9 and 10 of the
overreaching cycle. RESULTS: HMB-FA resulted in increased
total strength (bench press, squat, and deadlift combined) over
the 12-week training (77.1 18.4 vs. 25.3 22.0 kg, p < 0.001);
a greater increase in vertical jump power (991 168 vs.
630 167 W, p < 0.001); and increased lean body mass gain
(7.4 4.2 vs. 2.1 6.1 kg, p < 0.001) in HMB-FA- and placebosupplemented groups, respectively. During the overreaching
cycle, HMB-FA attenuated increases in CK (-6 91 vs.
277 229 IU/l, p < 0.001) and cortisol (-0.2 2.9 vs.
4.5 1.7 g/dl, p < 0.003) in the HMB-FA- and placebosupplemented groups, respectively. CONCLUSION: These
results suggest that HMB-FA enhances hypertrophy, strength,
and power following chronic resistance training, and prevents
decrements in performance following the overreaching.
SPONSORSHIP: this research was funded in part through a
grant from Metabolic technologies Inc. JMW, rPl, JMJ, JcA, and
SMcW declare no competing interests. Jr, JF, and SB are
employed by Metabolic technologies, Inc.
Study strengths
The authors did not specifically acknowledge any limitations of

their study. This is odd, since its pretty much standard practice
to do so, even if the limitations are disclaimed in the same breath
(which is common as well). A limitation that is not noted in the
text but is noted by the lead author in this video (starting from 17
inutes in) is the following:
These [subjects] were very unique individuals. What we did
was put them through the most brutal protocol you can
imagine possible. I cant even describe how brutal this
protocol is. And so what we did was for an entire semester, we
filtered through individuals we felt that were mentally and
physically able to withstand this brutal bout of training. [...] All
these guys were genetically outstanding, you could tell they
had full muscle bellies, they were essentially jacked. You could
tell that they were extreme responders to training. Now, in
most studies you just recruit anybody, and you could have
non-responders, moderate responders, high-responders. We
filtered so we had purely high-responders to training.
This highly selective recruitment process places severe

limitations on the extrapolability of the outcomes to other
subjects who arent necessarily genetically gifted for size and
strength gains. Its possible that the results seen in this study are
only achievable in a very narrow segment of the trained
population with extraordinarily high mental fortitude and
physiological responsiveness to extremely rigorous training. One
population of relevance could be the military (especially elite
forces on prolonged missions), who are subjected to extreme
conditions and constant over-reaching.
The next limitation I want to point out involves the reporting of
the data. As seen in the data tables (full study here), the standard
deviations are identical at all time points between the control and
intervention group in every variable at multiple testing sessions.
Ive personally never seen anything like it, and Ive seen plenty
of data tables in the sports nutrition literature. When questioned
about this on the ISSNs Facebook page, lead author Jacob
Wilson responded that, ...we used a covariant analysis and
reported the adjusted means as was requested by the reviewers.
This is very very common in the scientific papers. I asked
James Krieger (the stats wiz behind the recent protein timing
meta-analysis I did with him & Brad Schoenfeld) for his
feedback, and heres what he said:
It looks like they are reporting the pooled standard
deviation, which is unusual to report but does not indicate
their statistical analysis is flawed. I dont see anything wrong
with the stats that they ran. There are ways to get variance
data at each time point (rather than a pooled variance) using
SAS (which is what they used) even if you report adjusted
means. Im surprised the reviewers let them just go with the
pooled SD, which is not very meaningful when examining the
outcomes.
This study is innovative since its the first to ever examine the
chronic effects of the free acid form of HMB (HMB-FA) in
trained subjects on a monitored, periodized resistance training
program. Blinding was meticulous on both sides of the
experiment. The design was also unique since its the first to
include an over-reaching period (in addition to the other novel
conditions). The authors provided the details of the training
program in a supplemental document (downloadable here, full
study PDF here). Diet was standardized and designed by a
registered dietitian who counseled the subjects throughout the
study. Compliance with supplementation was over 98%.
A final limitation Id like to point out is the omission of

testosterone data from the manuscript. This is unfortunate since
the dramatic results of the subjects raised questions about
anabolic steroid use. The manuscript states that there were no
[Back to Contents]
Page 7
significant changes in free or total testosterone, but no data are

listed in support. Luckily, in a heated Facebook debate where
this data was demanded, Wilson graciously provided it:
The HMB group had a remarkable LBM gain of 7.4 kg (16.28

lb) while dropping 3.5 kg (7.7 lb) body fat. In contrast, the
placebo group gained 2.1 kg (4.62 lb) LBM while losing 1.7 kg
(3.74 lb) body fat. These are both favorable scenarios, but
clearly the HMB groups results especially the LBM gain is
nothing short of astounding. What makes it particularly
impressive was that these subjects were resistance-trained; they
were not novices primed for huge leaps in muscle size and
strength.
The LBM gains seen in the present study have been met with
severe skepticism since theyre superior to what has been
observed by Bhasin et al,2 whose subjects were on a
supraphysiological dose of testosterone (600 mg/week).
However, its important to note that dramatic results from HMB
are not completely anomalous. What Wilson et al saw is
essentially a replication of Kraemer et als 2009 study,3 which
also reported spectacular changes in body composition,
including similar gains in LBM to those seen in the present
study. However, their subjects were not trained, so dramatic
results are less surprising (as opposed to the present study, where
the trained subjects were closer to their potential for muscle
mass). Furthermore, Kraemer et al used calcium HMB, whereas
the free acid form was used in the present study.
The main findings were that HMB-FA increased strength by

more than threefold that of placebo (vertical jump increased
markedly as well), both groups gained LBM (although
insignificantly in the placebo group), and both lost fat (although
insignificantly in the placebo group). Below are the numbers:
The present study has been referred to as an example of one that

defies the rule that only overweight novices can experience a
significant degree of simpultaneous fat loss and muscle gain
(A.K.A. recomposition or recomp). However, despite the
subjects being trained, Im not surprised that recomp occurred in
both groups. Both the HMB and placebo groups began the trial
at approximately 21% body fat, which is not particularly lean.
On a final note, HMB has an equivocal track record of
effectiveness, as shown in a recent review by Zanchi et al (their
table of studies shows considerable hit & miss).4 Wilson et al
would probably argue that theres a scarcity of studies
examining the effect of HMB within the context of sufficiently
rigorous, periodized training program of sufficient length.
[Back to Contents]
As seen above, all subjects total testosterone levels were all

within normal range throughout the trial.
Comment/application
Page 8
Vitamin D and multiple health outcomes: umbrella

review of systematic reviews and meta-analyses of
observational studies and randomised trials.
Theodoratou E, Tzoulaki I, Zgaga L, Ioannidis JP. BMJ. 2014
Apr 1;348:g2035. [PubMed] [Full Text]
OBJECTIVE: To evaluate the breadth, validity, and presence of
biases of the associations of vitamin D with diverse outcomes.
DESIGN: Umbrella review of the evidence across systematic
reviews and meta-analyses of observational studies of plasma 25hydroxyvitamin D or 1,25-dihydroxyvitamin D concentrations and
randomised controlled trials of vitamin D supplementation. DATA
SOURCES: Medline, Embase, and screening of citations and
references. ELIGIBILITY CRITERIA: Three types of studies
were eligible for the umbrella review: systematic reviews and metaanalyses that examined observational associations between
circulating vitamin D concentrations and any clinical outcome; and
meta-analyses of randomised controlled trials assessing
supplementation with vitamin D or active compounds (both
established and newer compounds of vitamin D). RESULTS: 107
systematic literature reviews and 74 meta-analyses of observational
studies of plasma vitamin D concentrations and 87 meta-analyses of
randomised controlled trials of vitamin D supplementation were
identified. The relation between vitamin D and 137 outcomes has
been explored, covering a wide range of skeletal, malignant,
cardiovascular, autoimmune, infectious, metabolic, and other
diseases. Ten outcomes were examined by both meta-analyses of
observational studies and meta-analyses of randomised controlled
trials, but the direction of the effect and level of statistical
significance was concordant only for birth weight (maternal vitamin
D status or supplementation). On the basis of the available evidence,
an association between vitamin D concentrations and birth weight,
dental caries in children, maternal vitamin D concentrations at term,
and parathyroid hormone concentrations in patients with chronic
kidney disease requiring dialysis is probable, but further studies and
better designed trials are needed to draw firmer conclusions. In
contrast to previous reports, evidence does not support the argument
that vitamin D only supplementation increases bone mineral density
or reduces the risk of fractures or falls in older people.
CONCLUSIONS: Despite a few hundred systematic reviews and
meta-analyses, highly convincing evidence of a clear role of vitamin
D does not exist for any outcome, but associations with a selection
of outcomes are probable. SPONSORSHIP: The authors did not
receive funding.
Study strengths
This is the largest analysis of vitamin Ds clinical outcomes ever
done: 107 systematic literature reviews, 74 meta-analyses of
observational studies, and 87 meta-analyses of randomized
controlled trials (RCTs). Its rare to see analyses of this breadth
since, frankly, its a hell of a lot of work. This analysis provides
a relatively comprehensive summary of the existing literature. It
also attempted to account for the extent of bias and
heterogeneity in the observational vitamin D literature.
Study limitations
As acknowledged by the authors, the analysis was unable to
assess the relationship between vitamin D supplementation dose
and effect size in RCTs. Furthermore, the effect of different
choices of comparison groups or of varying vitamin D
distributions and median differences of the observational studies
could not be assessed either. Importantly and as a general
principle of pooled study data the quality of the analysis is

dependent on the quality of the studies comprising it. Quoting
the authors, ...some health related outcomes were poorly
covered, and we have flagged this gap.
Comment/application
The salient finding of this umbrella analysis was a lack of
support for the effectiveness of vitamin D supplementation on its
own to do what its most commonly touted for increasing bone
mineral density & reducing risk of fractures. The essence of the
general findings are well-captured in this excerpt of the
discussion:
Vitamin D might not be as essential as previously thought in
maintaining bone mineral density. [...] The lack of convincing
associations and the relative dearth of probable associations
(table 6) suggest that evidence for benefits that may be reaped
from population-wide vitamin D supplementation is weak.
Probable associations, where highly significant effects appear in
randomised trials, hold the most promise for clinical
translation, but they pertain to specific populations (children,
pregnant women, patients with chronic kidney disease), and
even in these cases the evidence is not sufficient to make
universal recommendations about daily intake.
Seeing that this conclusion is at odds with a sizable body of

literature suggesting of the benefits of vitamin D
supplementation,5-10 I contacted Dr. Michael F. Holick, who is
perhaps the most prolific and renowned vitamin D researcher in
the world. Heres his emailed response to me regarding the
umbrella review by Theodoratou et al:
There continues to be a lot of misinformation written by
people who have little or no experience in the field of vitamin D
but somehow believe that they can write about it. Please see
the enclosed letter I recently wrote regarding another metaanalysis that was flawed.
Holick attached a letter of dissent (full text here),11 which

includes the following primary counterpoints:
The medical model of evidence was used to assess the
evidence of the health benefits of vitamin D, which is not
necessarily appropriate for natural compounds.
The more appropriate way to establish causality is through
application of Hill's criteria for causality in a biological
system.
Most RCTs were poorly designed and had poor compliance,
thus compromising the detection of a beneficial effect.
By claiming that, the hypothesis that variations in
25(OH)D concentrations would essentially be a result, and
not a cause, of ill health and inflammation, the authors
would also have to pre-suppose inverse correlations between
solar UVB doses and cancer incidence and mortality rates
noted in ecological studies were due to confounding factors.
Their hypothesis connecting ill health and inflammation as
the cause for reduction in blood concentrations of 25(OH)D
is flawed and lacking supporting literature, which the
authors misrepresented in attempt to substantiate this claim.
[Back to Contents]
Page 9
Comment/application
Variability in muscle size and strength gain after
unilateral resistance training.
Hubal MJ, Gordish-Dressman H, Thompson PD, Price TB,
Hoffman EP, Angelopoulos TJ, Gordon PM, Moyna NM,
Pescatello LS, Visich PS, Zoeller RF, Seip RL, Clarkson PM.
Med Sci Sports Exerc. 2005 Jun;37(6):964-72. [PubMed]
PURPOSE: This study assessed variability in muscle size and
strength changes in a large cohort of men and women after a
unilateral resistance training program in the elbow flexors. A
secondary purpose was to assess sex differences in size and strength
changes after training. METHODS: Five hundred eighty-five
subjects (342 women, 243 men) were tested at one of eight study
centers. Isometric (MVC) and dynamic strength (one-repetition
maximum (1RM)) of the elbow flexor muscles of each arm and
magnetic resonance imaging (MRI) of the biceps brachii (to
determine cross-sectional area (CSA)) were assessed before and
after 12 wk of progressive dynamic resistance training of the
nondominant arm. RESULTS: Size changes ranged from -2 to
+59% (-0.4 to +13.6 cm), 1RM strength gains ranged from 0 to
+250% (0 to +10.2 kg), and MVC changes ranged from -32 to
+149% (-15.9 to +52.6 kg). Coefficients of variation were 0.48 and
0.51 for changes in CSA (P = 0.44), 1.07 and 0.89 for changes in
MVC (P < 0.01), and 0.55 and 0.59 for changes in CSA (P < 0.01)
in men and women, respectively. Men experienced 2.5% greater
gains for CSA (P < 0.01) compared with women. Despite greater
absolute gains in men, relative increases in strength measures were
greater in women versus men (P < 0.05). CONCLUSION: Men and
women exhibit wide ranges of response to resistance training, with
some subjects showing little to no gain, and others showing
profound changes, increasing size by over 10 cm and doubling their
strength. Men had only a slight advantage in relative size gains
compared with women, whereas women outpaced men considerably
in relative gains in strength. SPONSORSHIP: National Institutes of
Health Grant no. 5R01NS040606-03.
As depicted above, out of the 585 subjects, 232 showed a 1525% increase in CSA, 10 particularly high responders
experienced over a 40% increase in CSA, while on the opposite
end of the spectrum, 36 subjects showed less than a 5% increase
in CSA. The range of size changes was notable due to an actual
decrease in CSA on the low end of the range (-2 to +59%).
Formal examination of individual dietary intake would likely
have explained any drop in CSA, but the range of responses is
strikingly broad nevertheless. Men had 2.5% greater gains in
CSA than women. Next up are the strength effects.
Study strengths
The large number of subjects (585 total) heightened statistical
power and allowed a comparison of gender differences. Crosssectional area (CSA) of the upper arm musculature was
measured via magnetic resonance imaging (MRI), as opposed to
merely circumference, which cannot distinguish between lean
and fat tissue. Training was periodized, with reps beginning at
12 RM and progressing to 6 RM. All of the assessment and
training techniques/protocols were videotaped and shared by all
the sites in order to standardize the methods as much as possible.
Study limitations
Subjects over 40 years-old were excluded from the study,
leaving open questions about the applicability of these outcomes
to older populations. Dietary control was minimal, aside from
the instruction to maintain usual habits. It would have been
helpful to analyze the macronutrient composition of subjects
habitual intake, since variations especially in protein intake
can significantly impact gains in muscle size and strength during
resistance training programs.12,13 Its possible that the results
could be limited to the untrained population, as well as the
training protocol used on the targeted muscles (3 exercises for
the biceps, 2 exercises for the triceps, 3 sets per exercise).
Sessions per week were not specified which is unfortunate
since that leaves us with a very vague idea of total volume.
Out of the 585 subjects, 232 subjects 232 showed a 40-60%

increase in 1 RM, 36 high responders showed over 100%, and 12
unfortunate subjects had less than a 5% increase in 1 RM. Men
had greater variability in isometric strength gains, while
womens gains varied more greatly in dynamic strength. Women
experienced greater gains in strength, while men had slightly
greater gains in size. It would be interesting to see this
experiment done on trained subjects. Testosterone levels were
not associated with CSA variability. The authors attribute this to
the subjects 40-year age cutoff, citing a review by Matsumoto14
suggesting that functionally significant age-related decreases in
testosterone levels do not occur until roughly age 60 and up.
[Back to Contents]
Page 10
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
van Boekel M1, Fogliano V, Pellegrini N, Stanton C, Scholz

G, Lalljie S, Somoza V, Knorr D, Jasti PR, Eisenbrand G. A
review on the beneficial aspects of food processing. Mol
Nutr Food Res. 2010 Sep;54(9):1215-47. [PubMed]
Bhasin S, Storer TW, Berman N, Callegari C, Clevenger B,
Phillips J, Bunnell TJ, Tricker R, Shirazi A, Casaburi R.
The effects of supraphysiologic doses of testosterone on
muscle size and strength in normal men. N Engl J Med.
1996 Jul 4;335(1):1-7. [PubMed]
Kraemer WJ1, Hatfield DL, Volek JS, Fragala MS, Vingren
JL, Anderson JM, Spiering BA, Thomas GA, Ho JY, Quann
EE, Izquierdo M, Hkkinen K, Maresh CM. Effects of
amino acids supplement on physiological adaptations to
resistance training. Med Sci Sports Exerc. 2009
May;41(5):1111-21. [PubMed]
Zanchi NE1, Gerlinger-Romero F, Guimares-Ferreira L, de
Siqueira Filho MA, Felitti V, Lira FS, Seelaender M,
Lancha AH Jr. HMB supplementation: clinical and athletic
performance-related
effects
and
mechanisms
of
action.Amino Acids. 2011 Apr;40(4):1015-25. [PubMed]
Grber U, Spitz J, Reichrath J, Kisters K, Holick MF.
Vitamin D: Update 2013: From rickets prophylaxis to
general preventive healthcare. Dermatoendocrinol. 2013 Jun
1;5(3):331-347. [PubMed]
Wacker M, Holick MF. Vitamin D - effects on skeletal and
extraskeletal health and the need for supplementation.
Nutrients. 2013 Jan 10;5(1):111-48. [PubMed]
Wacker M, Holick MF. Sunlight and Vitamin D: A global
perspective for health. Dermatoendocrinol. 2013 Jan
1;5(1):51-108. [PubMed]
Holick MF. Vitamin D: evolutionary, physiological and
health perspectives. Curr Drug Targets. 2011 Jan;12(1):418. [PubMed]
Cranney A1, Weiler HA, O'Donnell S, Puil L. Summary of
evidence-based review on vitamin D efficacy and safety in
relation to bone health. Am J Clin Nutr. 2008
Aug;88(2):513S-519S. [PubMed]
Holick MF. Vitamin D: importance in the prevention of
cancers, type 1 diabetes, heart disease, and osteoporosis.
Am J Clin Nutr. 2004 Mar;79(3):362-71. [PubMed]
Holick MF, Grant WB. Correspondence: Vitamin D status
and ill health. The Lancet Diabetes & Endocrinology,
Volume 2, Issue 4, Pages 273 - 274, April 2014 [Lancet]
Schoenfeld BJ, Aragon AA, Krieger JW. The effect of
protein timing on muscle strength and hypertrophy: a metaanalysis. J Int Soc Sports Nutr. 2013 Dec 3;10(1):53.
[PubMed]
Cermak NM, Res PT, de Groot LC, Saris WH, van Loon LJ.
Protein supplementation augments the adaptive response of
skeletal muscle to resistance-type exercise training: a metaanalysis. Am J Clin Nutr. 2012 Dec;96(6):1454-64.
[PubMed]
Matsumoto AM. Andropause: clinical implications of the
decline in serum testosterone levels with aging in men. J
Gerontol A Biol Sci Med Sci. 2002 Feb;57(2):M76-99.
[PubMed]
[Back to Contents]
Page 11
Protein: is it really as bad as they say it is?

By Dylan Klein
____________________________________________________
Introduction & background

Early last March a provocative study published by Levine et al 1
in the prestigious Cell Metabolism has really shaken up the
nutritional science world ever since one of the authors of the
study suggested that eating a diet higher in protein is potentially
more harmful than smoking cigarettes. Talk about rustling some
jimmies!
Now, before we go any farther, lets keep one thing in mind: this
was not a randomized controlled trial wherein participants were
randomly assigned to either high or low protein groups and
followed for a period of time at which point various health
outcomes could be tallied and assessed. No, instead this study
was part epidemiological and part rodent research, each of which
has their own serious limitations when extrapolating to health
policy and human physiology. That being said, Levine et al
reported that in people aged 50-years and over, moderate and
high protein intakes were associated with increased type 2
diabetes mortality, but not cardiovascular disease (CVD),
cancer, or all-cause mortality. However, when the study
population was split into persons aged 50-65 and those 66 and
over, high and moderate protein intakes were associated with
increased mortality from cancer and all-causes in the 50-65 age
group, but not the latter. In addition, when animal protein was
accounted for, the harmful associations between protein intake
and mortality risks disappeared, suggesting that animal proteins,
and not plant-based proteins, are potentially harmful at higher
intakes during middle-age. With respect to those over 65, it
appears that higher protein intake had a protective effect and was
not associated with increased disease mortality risk, save type 2
diabetes. But wait, theres more!
In subsequent analysis the investigators looked at insulin-like
growth factor-1 (IGF-1) and its association with protein intake
and mortality risks. In recent years insulin and IGF-1 have been
suggested to contribute to the pathogenesis of cancer, due to
their similar intracellular signaling pathways and downstream
effects on various targets that favor cell survival rather than
death.2 Therefore, cells which should probably die are instead
salvaged and are at an increased likelihood of becoming
cancerous through various metabolic reprogramming
mechanisms. This has prompted a recent interest in examining
the potential therapeutic effects of low-carbohydrate and/or
ketogenic diets in treating cancer due to their ability to
drastically reduce serum levels of glucose and insulin3 two

factors that are predictive of future cancer risk and cancerrelated mortality.4-6 The current study, however, chose to focus
only on protein and IGF-1. So, what did the researchers find?
They found that IGF-1 levels were positively associated with
protein intakes and that for every 10ng/mL increase in IGF-1 for
those ages 50-65, mortality risk of cancer increased by about
9%. No association was observed in those over 65. But thats not
all!
Next, the investigators used a mouse model to confirm that their
associations were more than just associations. In doing so, a
relatively standard mouse strain (C57BL/6) was split into two
groups that were given isocaloric diets, either high or low in
calories from protein. Next, these mice were artificially given
cancer via a subcutaneous injection of murine melanoma cells.
The researchers then tracked tumor growth/progression in the
high and low protein groups. At the end of study period, it was
shown that the tumors from the mice on the high protein diet
grew much faster and were much larger than the tumors from the
mice consuming the low protein diet. Moreover, mice in the low
protein group had significantly lower serum IGF-1 and
significantly higher levels of IGF-binding protein-1 (IGFBP-1; a
binding protein that doesnt allow IGF-1 to bind to its receptor
and exert its effects). In addition, using a second geneticallymodified mouse model (GHRKO) that lacked both the growth
hormone receptor and IGF-1, tumor progression was strongly
inhibited compared to control mice that did have both the
receptor and the normal levels of the hormone. In aggregate,
these rodent models suggest that IGF-1 and its downstream
signaling pathways are likely contributing to tumor progression
and the increase in cancer mortality. Moreover, by reducing
protein intake one can potentially limit the growth of cancerous
tumors.
While there was even more going on in the recent study (you
never get off easy with a Cell paper) Im not going to bore you
to tears with the rest of the article. The bottom line is, to quote
the concluding remarks of the authors:
Overall, our human and animal studies indicate that a low
protein diet during middle age is likely to be beneficial for the
prevention of cancer, overall mortality, and possibly diabetes
through a process that may involve, at least in part, regulation
of circulating IGF-1.
My take on the matter
First off, and I know Im preaching to the choir, correlation does
not equal causation. While epidemiological data may show
interesting associations as well as lay the groundwork for future
research, it does not show cause and effect. Second, speaking of
cause and effect, there are absolutely no well-controlled,
randomized trials looking at protein intake and either cancer
mortality, type 2 diabetes mortality, or overall mortality in any
aged population, regardless of health status. Lastly, rodent
research needs to be taken with a grain of salt. While rodents do
serve a vital role in medical and nutrition research, the data
should not be blindly extrapolated to humans and formulated
[Back to Contents]
Page 12
into health policy until a substantial body of evidence has

accrued. This, however, is not the case. Therefore, if we are to
evaluate this study based on the aforementioned criteria, I see
nothing to convincingly sway my mind that protein is in any way
shape or form harmful to health and I havent even gotten to
the substantial methodological weaknesses contained within the
paper itself; which is exactly what we will get to next!
I'm not upset that you lied to me, I'm upset that from now
on I can't believe you.
women were below physiologically plausible in every single one

of the nine NHANES studies. Men, however, did manage to
provide mean energy intakes that were plausible in three of the
nine studies unfortunately Levine et al used recall data from
one of the six that didnt. Furthermore, at no point during those
39 years did more than 43% of overweight and obese women
and 49% of overweight and obese men report realistic energy
intakes. The mean amount of caloric underreporting for women
was about -365kcals while men underreported by about 281kcals.
Perhaps the greatest short-coming of the recent paper (and

believe me, there is plenty), is the investigators reliance on
NHANES food recall data. To help illustrate the absolute futility
of the NHANES survey, a press release last October regarding a
recent study looking at the validity of NHANES food intake data
reads, 40 years of federal nutrition research fatally flawed.
And while it might seem like a bit of an over exaggeration, I
think I can convince you that it most certainly is not.
This, however, should come to no surprise. Studies comparing

24-hour dietary recalls to doubly-labeled water have shown time
and time again that respondents, especially overweight and
obese subjects, underreport their energy intakes. 8 Moreover,
studies using metabolic biomarkers have also shown that
compared to urinary nitrogen measurements, respondents also
misreport their protein intakes (i.e. over- or under-report);9-11
which brings me back to the Cell Metabolism study.
First off, for those unaware, NHANES stands for National

Health and Nutrition Examination Survey and, to quote the CDC
directly:
By using NHANES dietary recall data, the researchers were

assuming that a single, 24-hour dietary recall which has been
shown to be highly inaccurate with regards to both energy and
protein intakes was 1) accurate, and 2) representative of the
respondents diets for the next 18 years! Thats right, mortality
data was accessed for subjects at 18 years post interview with
not a single follow-up measurement of dietary intake in between.
I dont know about you, but I dont possess that kind of faith
nor would I try to suggest that protein is more harmful that
smoking cigarettes when the only data Im using to compare diet
and mortality is completely laughable. Therefore, in my eyes,
this study does a horrible job at trying to pin mortality risk on a
single macronutrient which by itself is just outright ridiculous.
[It is] designed to assess the health and nutritional status of

adults and children in the United States [] The NHANES
interview includes demographic, socioeconomic, dietary, and
health-related questions. The examination component consists of
medical, dental, and physiological measurements, as well as
laboratory tests administered by highly trained medical
personnel. Findings from this survey [are] [] used in
epidemiological studies and health sciences research, which
help develop sound public health policy, direct and design
health programs and services, and expand the health knowledge
for the Nation.
The key thing to know here is that all dietary information is
recorded as part of a one-time, 24-hour dietary recall. During
this process participants try to accurately recall their previous
days dietary intake under the supervision of a trained dietitian.
From this survey total calories, protein, carbohydrate, and fat are
calculated, as well as a whole host of other dietary estimations.
Thus, the entire validity of the NHANES survey rests upon the
respondents ability to accurately and truthfully recall their
previous days nutrition. Yeah, you can see where this is
headed
"There are three kinds of lies: lies, damned lies, and

statistics."
Moving on to Levine et als analysis of the mortality data, I will
simply quote the remarks from a scathing unpublished (read:
rejected) letter-to-the-editor, written by an all-star team of
protein researchers, namely Donald Layman, Arne Astrup, Peter
Clifton, Heather Leidy, Douglas Paddon-Jones, and Stuart
Phillips. Their critique reads:
In an effort to see just how valid NHANES diet recall data really
is, Archer et al7 analyzed the 39-year history of the multiple
NHANES surveys (from 1971 through 2010) and compared
those intakes to what they estimated to be realistic total daily
energy expenditures for men and women based on the Schofield
predictive equations plus an additional activity factor of 1.35.
Anything reported below this value was deemed not
physiologically credible. So, what did Archer and company
find?
[Levine et al.] used Hazard Ratio (HR) analysis and concluded

that the [high protein] group had a 73-fold increased risk of
dying from diabetes. The HR and confidence interval (CI) were
reported as 73.52 (4.47 1,209.70). To our knowledge, that is
the highest HR ever reported for any dietary component and
certainly for one within dietary guidelines of the [Institutes of
Medicine]. The CI with a 400-fold range and an upper value of
1,209.70 with 6-significant figures of accuracy is not credible.
Hazard Ratio analysis is a standard method for clinical studies
with equal treatment groups and survival as a primary outcome,
but have important a priori criteria for their use: 1) equal size
groups, 2) no evidence of selection or group bias, and 3) linear
outcomes over time. The present study fails to meet all three
criteria.
What they found was that during the almost four decades-long
history of the NHANES, the mean reported energy intakes for
Indeed, with respect to a priori 1, there were 436 persons in the

low protein group, 4,800 persons in the moderate protein group,
[Back to Contents]
The reason why NHANES is fatally flawed
Page 13
and 1,145 persons in the high protein group when comparing

protein intakes to mortality risk. Not quite equal size groups by
any stretch of the imagination. Thus, coupled with laughable
dietary recall data we have highly biased and inappropriate
statistical analysis leading to misleading results about diet and
mortality. It appears that Mark Twain was right after all.
A brief break from reality
Now that weve established that NHANES is basically useless
when it comes to drawing any meaningful relationships between
diet and disease mortality, along with the authors untenable
statistical analysis that would make anyone wonder how this
paper got published in the first place, lets for a moment suspend
reality and take at face value the findings of Levine et al If we
are to take such a huge leap of faith, then the next obvious
question to ask is, what does the rest of the literature say on the
subject? That is to say, what are the associations between
protein and overall, cancer, and type 2 diabetes mortality? Well,
folks, youre in luck, because thats exactly where Im going
next!
Protein and all-cause mortality
First, lets start with protein and all-cause mortality. In a recent
2013 systematic review and meta-analysis of the available
observational research looking at low-carbohydrate as well as
low-carbohydrate, high-protein diets (LCHP),12 it was shown
that both types of diets are associated with an increased risk of
overall death. While you may be spitting out your bullet-coffee
right now, keep in mind that this isnt to condemn protein, per
se. Due to the nature of a LCHP diet, or any diet wherein you
manipulate macronutrient content, you cant simply say that its
the increase in protein thats leading to increased mortality and
neglect the fact that you also reduced carbohydrate intake as
well. Moreover, this was a meta-analysis of observational
studies only; there is absolutely no well-controlled randomized
data to support the contention that higher protein intakes lead to
increased mortality. Thus, as it stands now, there is no
convincing data to suggest lowering your protein intake to
increase your chances of living a longer and healthier life. In
fact, a good case can be made for many different populations to
consume more protein than what is suggested by the RDA13 a
topic that Ive covered previously on my site.
Levine et al also caution the intake of animal-based proteins in
favor of plant-based proteins due to the fact that they observed
no apparent mortality risk when animal protein was controlled
for. While some research may suggest that vegetarian and/or
vegan diets may confer additional health benefits, such as a
longer lifespan, the fact of the matter is that vegans and
vegetarians also take part in a whole host of other healthful
things, such as not smoking, not drinking, actually eating fruits
and vegetables, and most importantly, exercising.14-16 The fact
that they eat less animal products has nothing to do with their
supposed increased longevity and better health. Indeed, when
health-conscious meat-eating individuals are compared to
vegans and vegetarians, there is absolutely no difference in
overall mortality rates.17 Therefore, its not the meat that is
detrimental to health; rather, its the lifestyle that meat-eaters
tend to follow (in general) that imposes negative health
outcomes. As a matter of fact, some research suggests that

vegetarians are actually less healthy in terms of cancer, allergies,
and mental health disorders, as well as experiencing a poorer
overall quality of life compared to individuals who do eat
animal-based protein.18 Thus, when other healthful
characteristics are controlled for, there is absolutely no benefit to
eating plant-based proteins in terms of overall mortality or
general health.
Protein and cancer mortality
Not surprisingly, the literature here is considerably lacking wellcontrolled randomized research. Nevertheless, in a recent 2013
systematic review19 the authors examined five different cohorts
from five different observational studies and concluded that the
research looking at protein and cancer mortality is, so far,
inconclusive. Similar conclusions were made about protein
intakes and risk of developing various types of cancers. So
again, there is absolutely no convincing evidence to suggest
lowering ones intake of protein in order to reduce the risk of
dying from disease.
Regarding Levine et als rodent model that showed a highprotein diet increases tumor size and growth, it should be noted
that there is contradictory rodent evidence to suggest that
increasing protein intake along with decreasing carbohydrate
intake can actually significantly inhibit tumor size and growth,
contrary to what was shown in the current study. Indeed, in 2007
a group of Canadian researchers20 showed that, in mice injected
with human prostate cancer cells, a diet higher in protein (45%
of total calories) and lower in carbohydrate (10% of total
calories) led to significantly lower tumor volume and tumor
volume-to-bodyweight ratios after 9-weeks compared to a diet
high in carbohydrate (40% of total calories) and lower in protein
(10% of total calories). Moreover, the high-protein diet also had
significantly lower levels of plasma insulin/IGF-1, as well as
protein levels of phosphorylated Akt (an indicator of
insulin/IGF-1 signaling) in tumor cell lysates. This is
diametrically opposite of what Levine et al propose.
More recently, in 2011 Ho et al21 showed that tumor progression
is significantly inhibited by a high-protein (58% of total calories)
low-carbohydrate (15% of total calories) diet compared to a
more Westernized diet with ~23% of calories from protein.
Based on these studies it would seem that high intakes of protein
do not necessarily promote tumor progression but can actually
be part of a diet that slows tumor growth granted that
carbohydrate intake is also reduced. It should be noted, however,
that these studies did differ in methodology, in both the strains
of mice used, as well as the types of cancerous cells that were
injected; therefore, it is hard to accurately compare study
outcomes. Nonetheless, the assertion that high protein intakes
increase cancer mortality risk or promote tumor progression is
far from settled science.
Protein and type 2 diabetes
Lastly, lets take a look at the literature surrounding protein
intake and type 2 diabetes. In clinical trials, increasing the
protein to carbohydrate ratio during a weight loss diet has been
shown to improve glucose regulation in both obese22 and type 2
diabetic subjects,23-26 sometimes even better than traditional
[Back to Contents]
Page 14
weight loss diets that impose similar weight reductions.27,28

Moreover, it has even been shown that higher protein diets
improve glucose homeostasis in type 2 diabetics without weight
loss.29,30 When a structured exercise program is thrown into the
mix something considerably lacking in the conversation about
health and disease overall higher protein lower carbohydrate
diets can be equally, if not more, effective at improving blood
glucose levels after 12 weeks.31 Finally, in a 2012 meta-analysis
it was shown that LCHP diets were no worse than lower protein
higher carbohydrate diets at reducing HbA1c, fasting blood
glucose, and fasting plasma insulin levels,32 while a 2013 metaanalysis showed that there was a significant decrease in HbA1c
in persons who consumed higher protein diets.33 Thus, it appears
that, compared to lower protein intakes, higher protein diets can
be just as effective, if not more so, at controlling and/or
improving type 2 diabetes.
Dylan earned his BSc in nutritional sciences

and dietetics from Rutgers University where
he is currently pursuing his PhD in
nutritional biochemistry and physiology.
Dylan writes regularly on his blog/website,
Calories in Context, where he covers a wide
range of nutrition and performance-related
topics. Dylan has experience as a sport
nutritionist for the Rutgers Football and
Ranger Army Challenge teams and also
works with the lay public, both in-person
and via e-mail correspondence, where he
specializes in fat loss, muscle gain, and body re-composition. For more
information, you can visit his site at nutridylan.com or e-mail him at
decline104@gmail.com.
________________________________________________________________________________________________________
________________________________________________________________________________________________________
References
1. Levine ME, Suarez JA, Brandhorst S, Balasubramanian P,
Cheng CW, Madia F, Fontana L, Mirisola MG, GuevaraAguirre J, Wan J, et al: Low protein intake is associated with a
major reduction in IGF-1, cancer, and overall mortality in the
65 and younger but not older population. Cell Metab 2014,
19:407-417. [PubMed]
2. Klement RJ, Kammerer U: Is there a role for carbohydrate
restriction in the treatment and prevention of cancer? Nutr
Metab (Lond) 2011, 8:75. [PubMed]
3. Klement RJ, Champ CE: Calories, carbohydrates, and cancer
therapy with radiation: exploiting the five R's through dietary
manipulation. Cancer Metastasis Rev 2014. [PubMed]
4. Goodwin PJ, Ennis M, Pritchard KI, Trudeau ME, Koo J,
Madarnas Y, Hartwick W, Hoffman B, Hood N: Fasting insulin
and outcome in early-stage breast cancer: results of a
prospective cohort study. J Clin Oncol 2002, 20:42-51.
[PubMed]
5. Stattin P, Bjor O, Ferrari P, Lukanova A, Lenner P, Lindahl B,
Hallmans G, Kaaks R: Prospective study of hyperglycemia and
cancer risk. Diabetes Care 2007, 30:561-567. [PubMed]
6. Weiser MA, Cabanillas ME, Konopleva M, Thomas DA,
Pierce SA, Escalante CP, Kantarjian HM, O'Brien SM:
Relation between the duration of remission and hyperglycemia
during induction chemotherapy for acute lymphocytic leukemia
with a hyperfractionated cyclophosphamide, vincristine,
doxorubicin, and dexamethasone/methotrexate-cytarabine
regimen. Cancer 2004, 100:1179-1185. [PubMed]
7. Archer E, Hand GA, Blair SN: Validity of U.S. nutritional
surveillance:National Health and Nutrition Examination Survey
caloric energy intake data, 1971-2010. PLoS One 2013,
8:e76632. [PLoS ONE]
8. Hill RJ, Davies PS: The validity of self-reported energy intake
as determined using the doubly labelled water technique. Br J
Nutr 2001, 85:415-430. [PubMed]
9. Lissner L, Troiano RP, Midthune D, Heitmann BL, Kipnis V,
Subar AF, Potischman N: OPEN about obesity: recovery
biomarkers, dietary reporting errors and BMI. Int J Obes
(Lond) 2007, 31:956-961. [PubMed]
10. Heerstrass DW, Ocke MC, Bueno-de-Mesquita HB, Peeters
PH, Seidell JC: Underreporting of energy, protein and
potassium intake in relation to body mass index. Int J
Epidemiol 1998, 27:186-193. [PubMed]
11. Subar AF, Kipnis V, Troiano RP, Midthune D, Schoeller DA,
Bingham S, Sharbaugh CO, Trabulsi J, Runswick S, BallardBarbash R, et al: Using intake biomarkers to evaluate the extent
of dietary misreporting in a large sample of adults: the OPEN
study. Am J Epidemiol 2003, 158:1-13. [PubMed]
[Back to Contents]
As far as contradictory evidence that suggests that lowcarbohydrate and/or high total/animal protein diets might
increase the risk of type 2 diabetes, all such studies are
observational in methodology and do not indicate cause and
effect.34-38 We do know, however, that diets higher in
total/animal protein tend to be associated with lower fruit and
vegetable intake and higher intakes of processed foods and
sugars (i.e. all the makings of a crappy diet). Indeed, in a recent
meta-analysis looking that the link between dietary patterns and
type 2 diabetes risk,39 it was shown that diets that conformed
more to what would be considered a healthy diet (i.e. less
processed grains and more fruits and vegetables) was associated
with reduced risk of type 2 diabetes while diets that were
considered unhealthy (i.e. higher in processed grains/meats
and refined sugars) were associated with increased risk of type 2
diabetes. What this goes to show is that having a well-balanced
diet is probably more important than limiting or increasing a
single macronutrient without regard to the rest of your daily
intake. In the end, a crappy diet is a crappy diet. I dont care how
much protein you are or arent eating.
Wrapping up
In the end, it doesnt look like the recent Cell Metabolism study
is anything to lose sleep over. Horrible study methodology
paired with biased statistics and a body of shabby inconclusive
and/or contradictory observational research suggests that
reducing your protein intake should be the last thing on your list
of dietary amendments (no comment about Alans PAP!).
And with that I will leave you with the concluding remarks from
the aforementioned unpublished letter-to-the-editor, written by
Layman et al:
Our overall assessment of [the Cell Metabolism] paper is that
the conclusions and analyses are biased and flawed. While there
is growing consensus that a moderate protein intake between 1.0
and 1.5 g/kg/d may confer health benefits beyond those afforded
by the current RDA for protein, we also recognize there are gaps
in the current knowledge base and encourage discussion of
important contradictory evidence/data. Future research must be
well designed, rigorously reviewed, and credibility
communicated. Unfortunately, the article by Levine et al.
presents conclusions not supported by their own analyses or the
greater literature.
Page 15
12. Noto H, Goto A, Tsujimoto T, Noda M: Low-carbohydrate

diets and all-cause mortality: a systematic review and metaanalysis of observational studies. PLoS One 2013, 8:e55030.
[PubMed]
13. Bauer J, Biolo G, Cederholm T, Cesari M, Cruz-Jentoft AJ,
Morley JE, Phillips S, Sieber C, Stehle P, Teta D, et al:
Evidence-based recommendations for optimal dietary protein
intake in older people: a position paper from the PROT-AGE
Study Group. J Am Med Dir Assoc 2013, 14:542-559.
[PubMed]
14. Baines S, Powers J, Brown WJ: How does the health and wellbeing of young Australian vegetarian and semi-vegetarian
women compare with non-vegetarians? Public Health Nutr
2007, 10:436-442. [PubMed]
15. Pollard J, Greenwood D, Kirk S, Cade J: Lifestyle factors
affecting fruit and vegetable consumption in the UK Women's
Cohort Study. Appetite 2001, 37:71-79. [PubMed]
16. Gacek M: [Selected lifestyle and health condition indices of
adults with varied models of eating]. Rocz Panstw Zakl Hig
2010, 61:65-69. [PubMed]
17. Chang-Claude J, Hermann S, Eilber U, Steindorf K: Lifestyle
determinants and mortality in German vegetarians and healthconscious persons: results of a 21-year follow-up. Cancer
Epidemiol Biomarkers Prev 2005, 14:963-968. [PubMed]
18. Burkert NT, Muckenhuber J, Grossschadl F, Rasky E, Freidl
W: Nutrition and health - the association between eating
behavior and various health parameters: a matched sample
study. PLoS One 2014, 9:e88278. [PLoS ONE]
19. Pedersen AN, Kondrup J, Borsheim E: Health effects of protein
intake in healthy adults: a systematic literature review. Food
Nutr Res 2013, 57. [PubMed]
20. Venkateswaran V, Haddad AQ, Fleshner NE, Fan R, Sugar LM,
Nam R, Klotz LH, Pollak M: Association of diet-induced
hyperinsulinemia with accelerated growth of prostate cancer
(LNCaP) xenografts. J Natl Cancer Inst 2007, 99:1793-1800.
21. Ho VW, Leung K, Hsu A, Luk B, Lai J, Shen SY, Minchinton
AI, Waterhouse D, Bally MB, Lin W, et al: A low
carbohydrate, high protein diet slows tumor growth and
prevents cancer initiation. Cancer Res 2011, 71:4484-4493.
[PubMed]
22. Farnsworth E, Luscombe ND, Noakes M, Wittert G, Argyiou
E, Clifton PM: Effect of a high-protein, energy-restricted diet
on body composition, glycemic control, and lipid
concentrations in overweight and obese hyperinsulinemic men
and women. Am J Clin Nutr 2003, 78:31-39. [PubMed]
23. Parker B, Noakes M, Luscombe N, Clifton P: Effect of a highprotein, high-monounsaturated fat weight loss diet on glycemic
control and lipid levels in type 2 diabetes. Diabetes Care 2002,
25:425-430. [PubMed]
24. Gannon MC, Nuttall JA, Damberg G, Gupta V, Nuttall FQ:
Effect of protein ingestion on the glucose appearance rate in
people with type 2 diabetes. J Clin Endocrinol Metab 2001,
86:1040-1047. [PubMed]
25. Gannon MC, Nuttall FQ, Saeed A, Jordan K, Hoover H: An
increase in dietary protein improves the blood glucose response
in persons with type 2 diabetes. Am J Clin Nutr 2003, 78:734741. [PubMed]
26. Boden G, Sargrad K, Homko C, Mozzoli M, Stein TP: Effect
of a low-carbohydrate diet on appetite, blood glucose levels,
and insulin resistance in obese patients with type 2 diabetes.
Ann Intern Med 2005, 142:403-411. [PubMed]
27. Layman DK, Shiue H, Sather C, Erickson DJ, Baum J:
Increased dietary protein modifies glucose and insulin
28.
29.
30.
31.
32.
33.
34.
35.
36.
37.
38.
39.
homeostasis in adult women during weight loss. J Nutr 2003,

133:405-410. [PubMed]
Luscombe ND, Clifton PM, Noakes M, Farnsworth E, Wittert
G: Effect of a high-protein, energy-restricted diet on weight
loss and energy expenditure after weight stabilization in
hyperinsulinemic subjects. Int J Obes Relat Metab Disord
2003, 27:582-590. [PubMed]
Nuttall FQ, Gannon MC, Saeed A, Jordan K, Hoover H: The
metabolic response of subjects with type 2 diabetes to a highprotein, weight-maintenance diet. J Clin Endocrinol Metab
2003, 88:3577-3583. [PubMed]
Gannon MC, Nuttall FQ: Control of blood glucose in type 2
diabetes without weight loss by modification of diet
composition. Nutr Metab (Lond) 2006, 3:16. [PubMed]
Bowden RG, Lanning BA, Doyle EI, Slonaker B, Johnston
HM, Scanes G: Systemic glucose level changes with a
carbohydrate-restricted and higher protein diet combined with
exercise. J Am Coll Health 2007, 56:147-152. [PubMed]
Santesso N, Akl EA, Bianchi M, Mente A, Mustafa R, HeelsAnsdell D, Schunemann HJ: Effects of higher- versus lowerprotein diets on health outcomes: a systematic review and
meta-analysis. Eur J Clin Nutr 2012, 66:780-788. [PubMed]
Ajala O, English P, Pinkney J: Systematic review and metaanalysis of different dietary approaches to the management of
type 2 diabetes. Am J Clin Nutr 2013, 97:505-516. [PubMed]
de Koning L, Fung TT, Liao X, Chiuve SE, Rimm EB, Willett
WC, Spiegelman D, Hu FB: Low-carbohydrate diet scores and
risk of type 2 diabetes in men. Am J Clin Nutr 2011, 93:844850. [PubMed]
Halton TL, Liu S, Manson JE, Hu FB: Low-carbohydrate-diet
score and risk of type 2 diabetes in women. Am J Clin Nutr
2008, 87:339-346. [PubMed]
Pan A, Sun Q, Bernstein AM, Manson JE, Willett WC, Hu FB:
Changes in red meat consumption and subsequent risk of type 2
diabetes mellitus: three cohorts of US men and women. JAMA
Intern Med 2013, 173:1328-1335. [PubMed]
Schulze MB, Schulz M, Heidemann C, Schienkiewitz A,
Hoffmann K, Boeing H: Carbohydrate intake and incidence of
type 2 diabetes in the European Prospective Investigation into
Cancer and Nutrition (EPIC)-Potsdam Study. Br J Nutr 2008,
99:1107-1116. [PubMed]
Sluijs I, Beulens JW, van der AD, Spijkerman AM, Grobbee
DE, van der Schouw YT: Dietary intake of total, animal, and
vegetable protein and risk of type 2 diabetes in the European
Prospective Investigation into Cancer and Nutrition (EPIC)-NL
study. Diabetes Care 2010, 33:43-48. [PubMed]
Alhazmi A, Stojanovski E, McEvoy M, Garg ML: The
association between dietary patterns and type 2 diabetes: a
systematic review and meta-analysis of cohort studies. J Hum
Nutr Diet 2013. [Wiley Online]
[Back to Contents]
Page 16
What follows is an interview with my colleague and personal

friend, Dr. Brad Schoenfeld about his recent publication* thats
been generating lots of discussion. My questions are in bold.
Enjoy the discussion, and big thanks to Brad for the insight &
expertise!
between groups. On the other hand, hypertrophy was virtually

identical between groups, which was mildly surprising but
certainly not a shock. There is no question that mechanical
tension is the overriding factor in promoting muscle growth. My
thought going into the study was that the increased effects of
metabolic stress from the bodybuilding style training might
provide be additive to the response, but the results of the study
suggest that they may in fact be redundant. Thus, the study
provides important information as to a mechanistic hypothesis
for hypertrophy, whereby increased mechanical tension from
greater loads will offset any growth-related beneficial impact of
metabolic stress. The hypothesis requires further study since we
did not directly investigate mechanistic influences.
*Schoenfeld BJ, Ratamess NA, Peterson MD, Contreras B, Tiryaki-Sonmez G,

Alvar BA. Effects of different volume-equated resistance training loading
strategies on muscular adaptations in well-trained men. J Strength Cond Res.
2014 Apr 7. [Epub ahead of print] [PubMed]
What have been the most common criticisms youve received

about the study, and how have you responded to these
criticisms?
Dr. Brad Schoenfeld gives the inside scoop on his new

study comparing hypertrophy-type and strength-type
training.
Interviewed by Alan Aragon
____________________________________________________
____________________________________________________
First off, congrats on the publication of the paper, which
breaks ground since its the first to compare a volumeequated strength-type versus a hypertrophy-type program
on trained subjects. What was the spark that inspired this
investigation? Id like some insight on the inception of the
idea and initial motivation to carry this out.
The genesis of this study actually dates back well over a decade.
As a former competitive bodybuilder, the subject of maximizing
hypertrophy has always been a big interest. It was perplexing to
me that the vast majority of studies on hypertrophy 1) used
untrained subjects and, 2) were carried out using routines that
werent very practical to how lifters actually train. So when I
decided to pursue an academic career, I set my focus on carrying
out a study that addressed these issues and thus had real practical
implications for hard-training lifters. I actually proposed a
variation of the study I eventually conducted during my masters
degree work at the University of Texas but ultimately decided to
do a project rather than a thesis (which incidentally was
published as a review paper called The mechanisms of muscle
hypertrophy and their application to resistance training in the
JSCR) and save the study for my PhD dissertation. It turned out
to be a big plus in that I hit the ground running once I began my
doctoral work; all my scholarly efforts were directed to making
the study happen. On that note, I need to give a big shout out to
my dissertation committee here: Dr. Brent Alvar, Dr. Nick
Ratamess, and Dr. Mark Peterson. We had numerous strategy
sessions about every aspect of the study and they all were a huge
help in fine-tuning the methodology so it had maximum impact.
There have been a number of criticisms levied at the study, most

of which can be attributed to a lack of appreciation of the
complexities of the research process. Ive heard everything from
complaints that the sample size was too low to that the training
period was too short to the fact that I didnt use actual
bodybuilders and powerlifters. If I lived in Fantasy Land Id
have loved to be able to recruit 50 natural elite-level
bodybuilders and powerlifters and assess their gains over a 6
month training protocol. In real life this simply isnt feasible.
Most people have no clue as to how difficult it is to pull off a
study like this. Simply getting the initial 20 subjects that met
inclusion criteria was a huge chore and then having the resources
to carry out the training was equally difficult (the study required
60 hours of fully supervised training each week, necessitating 6
research assistants and lots of gym space!). So before criticizing,
its important to have a comprehension of what it takes to
conduct research. We did an a priori power analysis and the
number of subjects was sufficient to detect differences at a
moderate effect size. The time frame of 8 weeks has been shown
to be quite sufficient to see changes in muscular adaptations, and
in fact we saw fairly robust increases in both strength and
hypertrophy. And the average resistance training experience of
the subjects was 4+ years, which provides a good gauge of most
guys lifting.
My research hypothesis was that the powerlifting routine would

produce slightly greater strength gains and that the bodybuilding
routine would produce slightly greater hypertrophy. The study
supported my hypothesis as to strength; the powerlifting group
did in fact show significantly greater increases in max bench
press strength and a trend for greater increases in squat strength
A fair criticism that has been levied is why I didnt simply

manipulate the reps/sets and control for other variables (i.e.
session-to-session exercises, rest intervals, etc). I struggled with
this decision and had an extensive discussion about it with my
dissertation committee. Ultimately I felt that the study would
have greatest utility if it reflected the usual and customary
training practices of each respective athlete (i.e. powerlifter vs.
bodybuilder). Its important to understand that the greater the
control employed, the less generalizable results are in practice.
For example, Ive been questioned as to why it was necessary
for the bodybuilders use a split routine and the powerlifters a
total body routine. Well, a central concept amongst bodybuilders
is that increasing metabolic stress is an important factor in
maximizing a hypertrophic response. Performing multiple
exercises for the same muscle group in a workout has been
shown to enhance metabolic stress. So has reducing rest
[Back to Contents]
After designing the study and getting it started, what results

did you anticipate? How were the actual outcomes different
from what you hypothesized from the outset?
Page 17
intervals. On the other hand, powerlifters generally train

different muscle groups each session with longer rest intervals to
reduce fatigue and thus increase their ability to move heavy
weight. If I would have standardized these components between
groups, then it would have compromised the generalizability of
one or the other. So this study was merely the first piece in a
larger puzzle. I have a number of additional studies in the
pipeline that will now build on this work by seeking to exert
further control and hopefully tease out the influence of specific
variables on the hypertrophic response to resistance training.
In the studys discussion section, this excerpt stands out to
me:
HT protocol took approximately ~17 minutes to perform,
while the ST protocol required a time commitment of more
than 1 hour. Given the similar hypertrophic gains in the biceps
brachii between groups, HT was a much more time-efficient
strategy for eliciting these increases. Moreover, personal
communication with subjects both during and after the study
revealed that those in the ST group generally felt highly
fatigued both physically and mentally from the workouts while
those in the HT group tended to report being willing and able
to extend the duration of training sessions. It therefore stands
to reason that the HT group could have endured additional
volume in their routines while those in the ST group.
Is it reasonable then to conclude that this study provides
further evidence that given equal training volume due to
its greater efficiency of effect and greater tolerability, a
moderate intensity allowing 10 RM sets (with a range of 8-12
reps) with shorter (~90 sec) interset rest is a more favorable
option than a higher intensity of 3 RM sets with longer (~3
min) rest intervals for the specific goal of hypertrophy?
Bingo! The efficiency aspect is huge here. Because of the time
commitment required in powerlifting group, we had to limit the
number of exercises performed to 3 per workout (an upper body
pushing movement, an upper body pulling movement, and a
lower body movement). Maximizing whole body hypertrophy
would need to include a substantial number of additional
exercises to target various other areas of the body (i.e. calves,
middle and rear delts, hamstrings, etc). Adding these into the
powerlifting group would have required well over 2 hours of
training per session, which in itself isnt feasible for a lot of
people. Whats more, training at high volumes with very heavy
loads as was the case in the powerlifting group simply isnt
sustainable over the long-haul. Exit interviews with the subjects
revealed that every one of them felt fatigued and had sore joints
at the end of the 8 week period. The constant grinding and
taxation of their resources was overburdening. The bodybuilding
group on the other hand all expressed an ability and desire to
perform greater volumes. Taken together and given the clear
dose-response relationship between training volume and muscle
growth, Id say that primary hypertrophy-related benefit of
bodybuilding training is that it allows for the performance of
high volumes in a manner that doesnt overtax recovery
capacity. This essentially validates the hypertrophy range for
the goal of maximizing increases in size, although perhaps not
for the reasons often given.
What have been the most common misinterpretations of

your study that youve seen expressed in the media online
or other?
Far too many fitness enthusiasts are little more than arm-chair
researchers who simply draw conclusions based on the abstract
of a study. This is highly misguided. With respect to my study,
many have concluded from the abstract that it doesnt matter
whether you perform powerlifting or bodybuilding training to
maximize growth. As discussed above, this takes the results out
of context. Its imperative to read the entire study to appreciate
the specifics of what we did, what we found, and how the
findings correspond to practical applications for program design.
A large portion of the discussion section is dedicated to the
studys implications as well as its limitations. As the readers of
your newsletter can hopefully see from what Ive covered here,
the topic is a lot more nuanced than what you can derive from
the abstract.
In retrospect, what aspects of the studys design or execution
would you have done differently knowing what challenges
(or mishaps/shortcomings) were in store?
This is a great question and one that Ive actually given a great
deal of thought. I always try to assess what Ive done, learn from
my experiences, and then use the knowledge to improve future
endeavors. A major benefit I had in this instance was a very
experienced and knowledgeable team of researchers who I
consulted with regularly, which made for what I think was a
very tight research design. Thus, upon reflection, the only thing I
would have changed would be to require that all subjects
squatted on a regular basis. The subjects in the study were all
experienced lifters, but several of them performed only machinebased lower body exercises (i.e. leg presses, leg extensions, etc).
Given that squatting involves a steep learning curve even in
those with good initial leg strength, it ended up causing a fairly
large variance in the 1RM squat results. The upshot was a
negative impact on statistical power, impairing our ability to
detect significance in this outcome measure (as stated, the study
showed a trend for greater max squat strength in the powerlifting
group, but this was obscured by the large standard deviations).
Accordingly, Im currently carrying out a study that is
investigating 10 rep vs. 30 rep sets in well-trained lifters and the
inclusion criteria required that all subjects performed the squat
on a weekly basis.
Could you please indulge in the hypothetical for a minute
and speculate about how a combination protocol (i.e., one
combining hypertrophy and strength rep ranges) would do
in comparison to the pre-existing protocols you examined for
the goal of maximal strength? Same question for
hypertrophy? Thanks!
I would say there is strong evidence that combining loading
ranges has a synergistic impact on both strength and
hypertrophy. From a strength standpoint, the moderate rep
training would conceivably allow for greater hypertrophic
increases (via higher volumes). Studies show a clear positive
relationship between muscle CSA and the ability to produce
[Back to Contents]
Page 18
force. Thus, increases in hypertrophy by moderate rep training

would therefore translate into greater gains in maximal strength.
It also could be argued that the moderate rep training would
alleviate potential joint-related issues associated with continually
training with very heavy loads. Most strength athletes include
assistance exercises in their training, and this has a sound
theoretical basis which is supported by the results of my study.
With respect to hypertrophy, I would expand on the previous
recommendations and offer that maximal muscle growth is
achieved by training throughout the full spectrum of rep ranges.
Low reps facilitate greater strength increases (as demonstrated in
this study), which can translate into heavier loads used in the
moderate rep ranges; and high reps (>20 per set) facilitate
improvements in buffering capacity that can help to stave off
fatigue during moderate rep training. Thus, a program that
focuses on the hypertrophy range but incorporates heavy and
light loading zones would seemingly be the ideal approach.
Another interesting point to consider is that there might be
differences in fiber-type adaptations with each loading zone. We
did not conduct a biopsy analysis so I cant say for sure, but
there is evidence that bodybuilders have greater type I
hypertrophy compared to powerlifters and this may be a function
of training methodology. Also, recent work from my lab shows
that very high reps (>30 per set) might specifically target type I
fibers to a greater degree than heavy or moderate reps. Given
that maximal muscle size is predicated on maximizing
hypertrophy in all fiber types, it is logical that the full-spectrum
of rep ranges should be targeted to achieve this goal.
One final and important point to note is that any and all
recommendations must be customized to the individual. It is
often lost that research studies show only the means of the
groups tested, and dont reflect the fact that large interindividual differences are usually seen within groups. That
certainly was the case here. There are responders and nonresponders to training along a wide continuum, and these
differences have been largely attributed to ones ability to
express various genes. This doesnt mean some people wont
respond to resistance training, just that it will require substantial
alterations in program design to maximize their genetic
potential.
____________________________________________________
Brad Schoenfeld, PhD, CSCS, CSPS, FNSCA, is a
lecturer in the exercise science department for
Lehman College and is the head of their
human performance laboratory. His primary
research interests focus on elucidating the
mechanisms of muscle hypertrophy and their
application to resistance training. He has
published over 40 peer-reviewed journal
articles and currently serves on the Board of
Directors for the NSCA. He is author of the
book, "The M.A.X. Muscle Plan" which is
available at all major bookstores and on
Amazon.com. He maintains an active blog on his website:
http://www.lookgreatnaked.com/
[Back to Contents]
Page 19
Response to: Cardiovascular disease mortality and

cancer incidence in vegetarians: a meta-analysis and
systematic review.
By Robert Hoenselaar
________________________________________________
Dear editor,
In a recently published systematic review, Huang et al describe
results from cohort studies linking vegetarianism to all-cause
mortality and disease incidence.1 However, their interpretation
of the data raises several concerns. Seven studies were included
in the analysis. Data as described by the authors was compared
to the data as described in the articles referred to. The results can
be seen in Table 1.
The first study included was published by Ogata et al in 1984.2
According to Huang et al, this was a cohort study with a followup period of 23 years (1955-1978). Even though they state that
the cohort was compared to a general Japanese male population
for mortality rates. Since the Food Frequency Questionnaire
(FFQ) was completed in 1981 - after the follow-up period - this
is not a prospective study for dietary variables by definition.
According to Huang et al, 4,352 Zen priests were included, of
which 1,396 died. But Ogata et al state that only 1,887 male
FFQs were included in the analysis. And it is not clear how
many of these participants died. Moreover, Huang et al state that
adjustments were made for several variables, including alcohol
intake and exercise. Ogata et al did not adjust for these
covariates. Instead, they pointed to several possible weaknesses
of the study. In the discussion part, the authors state that one
must go through a strict training process in order to become a
Zen priest. Anyone who is not healthy physically or mentally
would not be able to bear such training. The cohort therefore,
seems to be slightly healthier than the general population. Also,
Zen priests are less likely to smoke, and they live in less polluted
areas.
The second study was published by Berkel and the Waard in
1983.3 According to Huang et al, this was a cohort study also,
with a follow-up time of 10 years (1968-1977). However,
mortality rates for the Seventh-Day Adventist (SDA) population
were compared to mortality rates for the general Dutch
population in 1972. Huang et al conclude that the relative risk
(RR) for all-cause mortality = 0.45 (0.41-0.49). But no data was
provided about dietary intakes/vegetarianism in any way. Huang
et al seem to have simply assumed that all SDAs were
vegetarians and that all subjects among the Dutch population
were meat eaters. In addition, Huang et al state that the RR was
adjusted for the BMI, alcohol intake, education and exercise.
Berkel and the Waard do not mention any adjustments for
covariates. In the discussion part of the article they even state
that characteristics of the SDA life-style include abstinence from
the use of tobacco and alcoholic beverages. And that there is a
strong recommendation for a (lacto-ovo) vegetarian diet. They
do not state that all SDAs were vegetarians. These authors

conclude that abstinence from cigarette smoking is likely to be
the main factor explaining the low mortality from ischaemic
heart disease in SDAs.
The third study was published by Beeson et al in 1989 regarding
the Adventist Health Study.4 According to Huang et al, the
follow-up period lasted from 1976 to 1988 and 14,044 deaths
were found among the cohort of 28,952 subjects. Beeson et al
continuously state that the follow-up period lasted from 1975 to
1982 for all-cause mortality. They also state that 6,151 subjects
died over the follow-up period in the total population of 59,081
subjects. Among the incidence population of 34,198 subjects a
total of only 2,716 subjects died. Huang et al show that 8,003
vegetarians were compared to 20,949 nonvegetarians. Beeson et
al do not link vegetarianism or dietary intakes to any
mortality/disease end point in any way. Huang et al possibly
extracted their data about this cohort from a review article by
Key et al. (Key 1998; Key 1999).5,6 These authors provided the
same death rate ratio (DRR) as Huang et al (DRR = 0.80; 95%
CI = 0.74-0.87). Key et al show that only 3,564 deaths were
found in this cohort and that adjustments were made for age, sex
and smoking in addition to the adjustments Huang et al defined
for the cohort.
The fourth study was published by Chang-Claude et al in 2005.7
Though these authors state that 535 study participants had died
within the follow-up period, their data shows that there were
only 456 deaths in the prospective analysis of mortality from all
causes. Possibly, Huang et al mistakenly used the 535 deaths
included in the comparison of death rates between the entire
cohort and the general German population.
The fifth study was published by Key et al in 1996.8 ChangClaude et al state that effects in this cohort were adjusted for
age, sex, smoking, alcohol intake, BMI and education. But
effects were not adjusted for the latter 3 possible confounders.
Key et al even stated that a limitation of the questionnaire was
that it was short and did not include several important food
groups (for example alcoholic drinks). According to Huang et al,
1,343 deaths were found among vegetarians and exactly 2 times
as much deaths (2,686) were found among nonvegetarians. Key
et al show that only 1,343 subjects died in the entire cohort.
Moreover, in 2003 Key et al again published data about the same
cohort [9]. This time with a longer period of follow-up. 2,346
deaths were found after 19 years of follow-up. And the DRR
was 1.03 (0.95-1.13) for vegetarians vs nonvegetarians.
The sixth study was published by Thorogood et al in 1994. 10
Huang et al state that 1.938 deaths were found, and define a RR
of 1.01 (0.89-1.14) for vegetarians vs non-vegetarians. But
Thorogood et al showed that only 404 subjects died within the
cohort. And that non-meat eaters had a lower mortality risk than
meat eaters: DRR = 0.80 (0.65-0.99). Again, data was available
about the same cohort after a longer follow-up period. In 2003,
Key et al also published data about this cohort. The RR found
after this follow-up period is 1.01 (0.89-1.14), suggesting that
Huang et al actually refer to this article for their data. But this
article also shows that less subjects died, namely 1,131.
[Back to Contents]
Page 20
The last study was published by Key et al in 2009.11 Huang et al

described the RR correctly. But stated that 2,965 deaths were
found among 64,234 participants. Key et al show that 64,234
participants and 2,965 deaths were used to calculate standardized
mortality ratios in table 1 of their article. While table 3 of their
article shows that 47,254 participants and 1,513 deaths were
used to calculate the RR provided by Huang et al.
Most of the studies included in the analysis by Huang et al

provided standardized mortality ratios (SMRs) comparing death
rates between cohorts and the entire population for the country
of interest. Table 2 shows that SMRs for the cohorts were
consistently much lower than SMRs for the general population.
But it is also shown that, within these cohorts, both vegetarians
and non-vegetarians had similar SMRs. In several of the articles
[Back to Contents]
Page 21
included, the authors concluded that these lower mortality ratios

were found because the study populations had a healthy lifestyle,
with low proportions of smokers and obesity7-9,11 and therefore
are not comparable to the general population.7,12 Thorogood et
al10 stated that "Volunteers in cohort studies are known to have
lower rates of cancer and other serious diseases at recruitment to
studies and therefore to have a low initial mortality, which will
contribute to the low overall mortality." This is called the
"healthy volunteer effect."4,9,11 For the Adventist Health Study,
Beeson et al defined this effect as follows: "Table 8
demonstrates that, as expected, there is substantial healthy
volunteer response bias, firstly to the census questionnaire and
then again to the lifestyle questionnaire. Age-standardized
mortality rates increase over the duration of the study, perhaps
stabilizing by 1980. Notice also the step down in rates among
respondents to the lifestyle questionnaire, with a gradual
increase through the end of the study."
Most RRs/DRRs were > 1 meaning that prospective data does

not confirm the theory that vegetarians may have lower mortality
rates than nonvegetarians. Key et al mention that because of the
healthy volunteer effect, people who are already ill and therefore
likely to die within a few years are much less likely to join this
type of study than are people who are healthy. 9,11 For the "Health
Food Shoppers Study" and the "Oxford Vegetarian Study"
authors attempted to investigate the extent to which the healthy
volunteer effect (resulting in lower than expected mortality
during the first few years of a cohort study) might have
influenced the results.10,12 DRRs were recalculated excluding
deaths occurring during the first 5 years of a subject joining the
study. DRRs slightly increased from 1.03 and 1.01 to 1.05 and
1.09 for the Health Food Shoppers Study and The Oxford
Vegetarian Study, respectively.
Table 2 also describes prospective data for comparisons within

the cohorts. Prospective data was available for 4 cohorts only.
The way Huang et al present their data, suggests that prospective

analyses were undertaken: cohort studies were included in the
analysis, and table 1 of their article shows the follow-up period
for all studies included. For two of the studies in their analysis
[Back to Contents]
Page 22
no prospective data was available. Cohorts including Zen priests

or Dutch SDAs - which were assumed to be vegetarians - were
compared to the general population - which was assumed to
consist of meat eaters only - for mortality ratios. Also, data from
the Adventist Mortality Study was not included in their metaanalysis. Though this data was available from 2 of the references
used by the authors.5,6 The DRR for this cohort was 0.83 (95%
CI = 0.76-0.92) for vegetarians vs nonvegetarians. Looking at
the references used, it is often not clear how Huang et al
interpreted the data included in their analysis: numbers of
participant, deaths, follow-up periods and covariates used for
adjustments did not always match the original data. The authors
include both prospective and ecological (SMRs) data to calculate
an effect size which would describe the effect of a vegetarian
lifestyle on mortality end points. Their tables clearly show that
most effect sizes favoring the vegetarian lifestyle are driven by
the ecological data from Ogata et al and from Berkel and de
Waard. If analyses are restricted to prospective data, metaanalyses will probably show that vegetarians do not have lower
mortality rates for total circulatory diseases, cancer and all-cause
mortality compared to nonvegetarians. Over a decade ago, Key
et al found no evidence that vegetarians have lower mortality
rates than nonvegetarians. A DRR of 0.95 (0.82-1.11) was found
after meta-analysis of 5 prospective studies.5,6 Since then, only
one more prospective study was published, examining
vegetarians. A DRR of 1.05 (0.93-1.19) was found for
vegetarianism in the EPIC-Oxford Study.11 Excluding the first 5
years of follow-up from the analysis might even further attenuate
any evidence for an association, but little data is available about
this effect. In conclusion: Both vegetarians and nonvegetarians
in cohort studies have lower mortality rates compared with the
general population. Prospective data shows little evidence that
vegetarians may live longer than nonvegetarians.
____________________________________________________
Robert Hoenselaar is a dietitian and
research journalist, living in the
Netherlands. He published 4 articles about
the relation between saturated fat and
cardiovascular diseases in the scientific
literature. Showing that results and
conclusions about this association, as
described by leading advisory committees,
do not reflect the available scientific
literature. Currently, he runs a website with daily news about diet,
supplements, sports and health: http://www.foodanddisease.com/
3.
Berkel J, de Waard F. Mortality pattern and life expectancy

of Seventh-Day Adventists in the Netherlands. Int J
Epidemiol. 1983 Dec;12(4):455-9. [PubMed]
4. Beeson WL, Mills PK, Phillips RL, Andress M, Fraser GE.
Chronic disease among Seventh-day Adventists, a low-risk
group. Rationale, methodology, and description of the
population. Cancer. 1989 Aug 1;64(3):570-81. [PubMed]
5. Key TJ, Fraser GE, Thorogood M, Appleby PN, Beral V,
Reeves G et al. Mortality in vegetarians and nonvegetarians: a collaborative analysis of 8300 deaths among
76,000 men and women in five prospective studies. Public
Health Nutr. 1998 Mar;1(1):33-41. [PubMed]
6. Key TJ, Fraser GE, Thorogood M, Appleby PN, Beral V,
Reeves G et al. Mortality in vegetarians and nonvegetarians:
detailed findings from a collaborative analysis of 5
prospective studies. Am J Clin Nutr. 1999 Sep;70(3
Suppl):516S-524S. [PubMed]
7. Chang-Claude J, Hermann S, Elibur U, Steindorf K,
Lifestyle determinants and mortality in German vegetarians
and health-conscious persons: results of a 21-year followup. Cancer Epidemiol Biomarkers Prev. 2005
Apr;14(4):963-8. [PubMed]
8. Key TJ, Thorogood M, Appleby PN, Burr ML. Dietary
habits and mortality in 11,000 vegetarians and health
conscious people: results of a 17 year follow up. BMJ. 1996
Sep 28;313(7060):775-9. [PubMed]
9. Key TJ, Appleby PN, Davey GK, Allen NE, Spencer EA,
Travis RC. Mortality in British vegetarians: review and
preliminary results from EPIC-Oxford. Am J Clin Nutr.
2003 Sep;78(3 Suppl):533S-538S. [PubMed]
10. Thorogood M, Mann J, Appleby P, McPherson K. Risk of
death from cancer and ischaemic heart disease in meat and
non-meat eaters. BMJ. 1994 Jun 25;308(6945):1667-70.
[PubMed]
11. Key TJ, Appleby PN, Spencer EA, Travis RC, Roddam
AW, Allen NE. Mortality in British vegetarians: results
from the European Prospective Investigation into Cancer
and Nutrition (EPIC-Oxford). Am J Clin Nutr. 2009
May;89(5):1613S-1619S. [PubMed]
12. Appleby PN, Key TJ, Thorogood M, Burr ML, Mann J.
Mortality in British vegetarians. Public Health Nutr. 2002
Feb;5(1):29-36. [PubMed]
Editors note: I asked Robert to contribute to AARR immediately

after discovering his impressive work (http://canceranddiet.nl/),
and lucky for us, he obliged.
References
1.
2.
Huang T, Yang B, Zheng J, Li G, Wahlqvist ML, Li D.

Cardiovascular disease mortality and cancer incidence in
vegetarians: a meta-analysis and systematic review. Ann
Nutr Metab. 2012;60(4):233-40. [PubMed]
Ogata M, Ikeda M, Kuratsune M. Mortality among Japanese
Zen priests. J Epidemiol Community Health. 1984
Jun;38(2):161-6. [PubMed]
[Back to Contents]
Page 23
This full-length documentary (52:58) on the honey badger is

absolutely fascinating.
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 24

3 - April - 2014

Uploaded by

Document Information

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

3 - April - 2014

Uploaded by

Copyright:

Available Formats

12 Protein: is it really as bad as they say it is?

17 Dr. Brad Schoenfeld gives the inside scoop on his

20 Response to: Cardiovascular disease mortality

The compelling case against 'food addiction.'

Processed foods: contributions to nutrition.

The effects of 12 weeks of beta-hydroxy-betamethylbutyrate free acid supplementation on

Vitamin D and multiple health outcomes: umbrella

10 Variability in muscle size and strength gain after

The compelling case against 'food addiction.'

The concept of food addiction has been elevated from obscure

The nature of addiction: physiology or psychology?

Figure 1. Your Brain on Sugar

By the 1990s, the obesity epidemic that had begun a decade or

Whenever a concept is advanced with such fervor as to be

Alan Aragons Research Review April 2014

Brain images seal the deal

People always say to me, "What about fruit? It has sugar.

junky human snack foods! Care to guess what happened? Here

Figure 2. Effect of switching diet on weight and intake.

Sweet-fat intermittent restriction:21 Rats were provided

Sugar supplied in water or substituted for other

Similar observations to these have been made by various

develops as the body/brain becomes accustomed to this new

The take-away message

Fat Head Movie

DSM-IV Alcohol Abuse and Dependence. Office of the

Alan Aragons Research Review April 2014

Processed foods: contributions to nutrition.

Alan Aragons Research Review April 2014

One aspect that rings loudly with me personally is the ability of

The authors did not specifically acknowledge any limitations of

This highly selective recruitment process places severe

A final limitation Id like to point out is the omission of

Alan Aragons Research Review April 2014

significant changes in free or total testosterone, but no data are

The HMB group had a remarkable LBM gain of 7.4 kg (16.28

The main findings were that HMB-FA increased strength by

The present study has been referred to as an example of one that

Alan Aragons Research Review April 2014

As seen above, all subjects total testosterone levels were all

Vitamin D and multiple health outcomes: umbrella

principle of pooled study data the quality of the analysis is

Seeing that this conclusion is at odds with a sizable body of

Holick attached a letter of dissent (full text here),11 which

Out of the 585 subjects, 232 subjects 232 showed a 40-60%

Alan Aragons Research Review April 2014

van Boekel M1, Fogliano V, Pellegrini N, Stanton C, Scholz

Alan Aragons Research Review April 2014

Protein: is it really as bad as they say it is?

Introduction & background

drastically reduce serum levels of glucose and insulin3 two

into health policy until a substantial body of evidence has

women were below physiologically plausible in every single one

Perhaps the greatest short-coming of the recent paper (and

This, however, should come to no surprise. Studies comparing

First off, for those unaware, NHANES stands for National

By using NHANES dietary recall data, the researchers were

[It is] designed to assess the health and nutritional status of

"There are three kinds of lies: lies, damned lies, and

[Levine et al.] used Hazard Ratio (HR) analysis and concluded

Indeed, with respect to a priori 1, there were 436 persons in the

Alan Aragons Research Review April 2014

The reason why NHANES is fatally flawed

and 1,145 persons in the high protein group when comparing