8 - Oct - 2013

12 Vemma a fairy tale of hope, a reality of nope.
By Alan Aragon
14 Interview with Eric Helms about his latest peerreviewed publication on protein needs of lean,
trained athletes in an energy deficit.
By Alan Aragon
Copyright October 1st, 2013 by Alan Aragon
Home: www.alanaragon.com/researchreview
Correspondence: aarrsupport@gmail.com
The neurophysiology of human appetite.

By Andrew Abbate
Interval training in the fed or fasted state improves

body composition and muscle oxidative capacity
in overweight women.
Gillen JB, Percival1 ME, Ludzki1 A, Tarnopolsky MA,
Gibala MJ. Obesity. 2013 Nov;21(11): 2249-55. [Wiley
Online]
Metabolic effects of milk protein intake strongly

depend on pre-existing metabolic and exercise
status.
Melnik BC, Schmitz G, John SM, Carrera-Bastos P,
Lindeberg S, CordainL. Nutr Metab (Lond). 2013
Oct;10(1)60: doi:10.1186/1743-7075-10-60 [N&M]
Undenatured type II collagen (UC-II(R)) for joint

support: a randomized, double-blind, placebocontrolled study in healthy volunteers.
Lugo JP, Saiyed ZM, Lau FC, Molina JP, Pakdaman MN,
Shamie AN, Udani JK. J Int Soc Sports Nutr. 2013 Oct
24;10(1):48. [JISSN]
10 Resistance training reduces fasted- and fed-state

leucine turnover and increases dietary nitrogen
retention in previously untrained young men.
Moore DR, Del Bel NC, Nizi KI, Hartman JW, Tang JE,
Armstrong D, Phillips SM. J Nutr. 2007 Apr;137(4):985-91.
[PubMed]
Alan Aragons Research Review October 2013
[Back to Contents]
Page 1
The neurophysiology of human appetite.

By Andrew Abbate
____________________________________________________
We have reached an age where weight control has been turned
upside down from an instinctual, highly regulated system, to a
process requiring considerable cognitive effort. - Peters et al.,
2002
Embracing the prevailing intersection between anthropology and
physiology that the Paleo Diet/Movement debate continually
inspires, Id like to start from the beginning of human
consciousness to introduce this topic. However, since thats a
textbook-length undertaking, well substitute breadth for depth
and focus on the key component that facilitates human hunger
urges, dopamine. When we come out on the other side well
hopefully have at least partially demystified the conscious
barrier between instinct and will, the dueling cerebral forces that
dictate our diet decisions. On an unconscious physiological
level, driving food intake upstream (before) dopamine
fluctuations, we are dealing with the command center of brain
activity, where the primary signals originate: The hypothalamus
(via regulatory neuropeptides such as leptin, cholecystokinin,
ghrelin, orexin, insulin, neuropeptide Y, and through the sensing
of nutrients, such as glucose, amino acids and fatty acids) is
recognized as the main brain region regulating food intake as it
relates to caloric and nutrition requirements, as Volkow (a
remarkable lady whose research is consistently compelling) and
colleagues summarize concisely.1 Note: bolded above are the
two neuropeptides are delve into later on.
Again, my questions here are big, and only half-answered in the
lab because animals dont express cognitive control comparable
to that observed in humans. However, the unconscious
physiological similarities mentioned above are still operative, so
this raises questions relevant to our dopaminergic examination:
at what point does eating more become not worth it? How is that
impetus to eat consciously manipulatable? And at what point
does this internal monologue become obsessive, pathological,
disorderly? Now, as much as Id like to explore eating disorders,
I am not a mental health professional, so well leave that topic
on the shelf. However, as a fitness enthusiast and scientist I can
certainly divulge the fundamental neurological inputs to the
hunger equation, behavioral and biochemical, specifically with
respect to dopamine, so well compress the scope: How does
dopamine control the human appetite, how can conscious control
affect hunger, and how do other hormones cooperate with
dopaminergic appetite modulation?
see in lower species is analogous to whats underneath all those

folded lobes (also known as convolutions) of the neocortex,
down to the bare essentials for life-maintenance in many species
for which there is no substantial cortex. A monkey brain image
is an adequate visual aid to inform an understanding of why
some monkey behaviors are easily anthropomorphized, theres a
little neocortex in there.
Image source: http://www.nibb.ac.jp/brish/Gallery/cortexE.html Unrelated:

The mouse brain kind of looks like a mouse, which is funny.
Within the neocortex is a still massive subsection called the

prefrontal cortex (PFC), and this is the part that we consult
before reaching for a bite of chocolate cake, and then another,
and then maybe just one more. For a relatively long period in
scientific history we had evidence that the PFC was primarily
responsible for causing impulsive decisions, not preventing
them. But in 1992 Duvauchelle and colleagues, expanding on
some of their previous work, solidified a young hypothesis that
the PFC plays some role in modulating dopamine release in the
reward center of the brain.2 Then in 2008 Del Arco and Mora
expanded on this further by demonstrating that the PFC
modulates reward-seeking behavior charged by dopamine and
environment can play a significant role on how these two brain
regions, PFC and reward center, interact.3 That is, translated to
human practicality, our environment affects our reward-seeking
behavior, and that necessarily includes hunger.
The cerebral evolution that guided the course of our primitive

human family tree, the expansion of our brains neocortex, is
really that change that made us us. The neocortex is the place
where our conscious thoughts originate and go on to propagate
actions its the processing center that hosts all the
extraordinary phenomena of conscious human cognition. If you
look at human brains relative to other species what youll really
It wasnt until early 2010 that human brain imaging revealed a

dynamic interconnectivity between the PFC and other parts of
the brain, showing that, yes, the PFC is responsible for charging
those immediate reward desires, those consecutive bites of cake;
but we now know that it also innervates temperance, that, I
want more but its not really worth it internal monologue.
Diekhof and Gruber dub this paradigm the desire-reason
dilemma.4 And knowing this, that the same part of the brain that
encourages reward-seeking also suppresses it, will be important
in understanding how this all relates to appetite. When instinct
and will collide, the PFC becomes a battleground, and sudden
food-seeking urges are not always the end result when satiety
and dopamine collide.
[Back to Contents]
The prefrontal cortex (PFC), behavior and food
Page 2
Dopamine and appetite

A basic understanding of dopamine is necessary to take all of
this in its proper context, and chances are you all already know
that in normal people, elevated brain dopamine enhances mood,
reinforces incentive (i.e. its a motivating hormone: doing
something you enjoy causes its release, and dopamine itself
motivates you to keep going), and it facilitates just about every
facet of human behavior from involuntary muscle control to
belief in the supernatural.5 However, when examining
dopamines behavioral effects with respect to appetite, there is a
crucial distinction that many scientists have failed to consider
until recently, affect versus motivation, or liking versus
wanting.6
In a laboratory setting, liking and wanting are best separated by
examining palatability, or how the brain responds to different
tastes, because sensory taste input is entirely dissociated from
desire to eat.7 It is therefore possible to measure wanting
independently, isolating the instances when desire is causative.
Wanting food, hunger, is an active pursuit of a known reward, or
as Finlayson et al. reports, Wanting implies a direction, not just
a force. Therefore, obtaining a measure of wanting [a specific
food] can be dissociated from a non-specific drive to eat.8 This
foundation is important if we want to decouple dopamine and
desire from inter-individual preferences, and it helps us elucidate
specific neurochemical impulses linking dopamine and hunger.
The other side predicts, expectedly, that if dopamine sensitivity

function is compromised, perhaps if dopamine receptors are
fewer in a persons reward center, that person is more
susceptible to compulsive eating and obesity.1,10,11 Now, back
the neurocircuit discrepancy When we talk about a mismatch
in the expected reward vis-a-vis the actual reward, we are only
focussing on the conscious part of the reward center activity
when reason trumps desire, and this is where the PFC comes
back into play. The expected reward response can only win out
if we are reflecting on a memory; in this case memory of the
reward is received by a different brain region called the
amygdala. The PFC then relays impulses to the reward center in
response to cues initiated by presenting an image, a reminder,
any kind of cue of a desirable object, including food and
addictive drugs.12,13 If the conscious inhibitory response is strong
enough, we resist. What Volkow and her colleagues are saying
when they reference the expected reward overpowering our
conscious control is that the cue (desire) overpowers control
(reason), and this is because of a compromised response to
dopamine in the reward center.1,14,15 If its still unclear, take a
look at this image, keeping in mind some of the keywords
mentioned above and acknowledging that the (-) sign connecting
the PFC and the reward center is what happens when reason
takes control and we decide not to eat:
Although I alluded to its role a few paragraphs ago, we still

havent fully addressed the mechanism dopamine exercises in
human appetite, the big question: does dopamine increase
hunger or suppress it? The answer lies in the complex,
inextricable overlap between two distinct neurocircuits: the
hypothalamic, unconscious system (as mentioned in the first
paragraph) and the reward system (as also mentioned in the first
paragraph the one largely inhibited by that reason-desire
dilemma processed in the PFC).1,4 What happens when these
circuits malfunction or miscommunicate is presumably what
happens when we compulsively overeat, the dopamine procured
from eating is not enough, so we crave more. When it happens
chronically, a pathological mechanism comes into play, and
thats one reason we can now define obesity as a disease state.
Examining obesity through a pathological lens, this overlap
suggests conditional, repeatedly compromised dopamine
responses in the reward center. Volkow and others elaborate on
this paradigm, describing it as the point at which the expected
reward (processed by memory circuits) over-activates the reward
and motivation circuits while inhibiting the cognitive control
circuit.9 To better understand how the cognitive control circuit
in the PFC is overpowered, lets restructure that model by first
going back to a well-defined role for dopamine, then look at an
image that clears things up a bit better: If dopaminergic function
is normal, dopamine response to food consumption decreases
appetite. That foundation is very well established and,
considering neurosciences nuanced nature, its quite convenient
that we can accept it; however, keep in mind that we are hinging
this assumption not on dopamine levels themselves, but rather
dopamine sensitivity, which involves receptor function and
interaction with hormones.
Larger/complete diagram here:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3124340/figure/F1/
Palatability, that taste preference we established in the first

paragraph, also comes back into the picture when we examine
cued responses processed initially in the amygdala, should we be
afforded the luxury of only remembering and craving the foods
we enjoy.9,16 Stress eating is also a common response in
dopamine-compromised people, likely because what were
craving in these compulsory instances is more-so dopamine than
nutrition.9 Apparently, dopamine sensitivity plays the critical
role in modulating appetite, which opens the door to
interdisciplinary research perspectives that connect dopamine
insensitivity, the other ways it manifests itself, and obesity risk,
but for the analysis at hand we should acknowledge that
behavioral conditioning is not always effective, and will-power
may not be enough for people predisposed to dopamine
insensitivity to resist hedonic urges. However, for many of us,
[Back to Contents]
Page 3
behavioral conditioning can be the antidote to memory input

from craving cues, preventing that overpowering effect its
observable in practice and statistically verifiable in science, but
heres a very important detail that I touched upon in the first
paragraph: palatability is not a necessary factor in addictive
eating patterns, because even nonpalatable foods can come to
be desired and potentially over-consumed.23
To recap and simplify, food consumption elevates dopamine,
and if the response to that increase in dopamine is not adequate,
appetite can go on uninhibited.9 The type of food, palatability of
food, and macronutrient content of food cannot be isolated
because in pathological over-consumption, palatability is not
necessary, and different cravings for different macronutrient
compositions depends on too many independent variables e.g.
gender, age, hunger state, time of day, and phase of the
menstrual cycle.23,24
You can create animals that do not produce dopamine, said
Volkow. They die of starvation. They dont eat. Its as dramatic
26
as that.
So, knowing (a) a normal dopamine response to food

consumption will innervate normal satiety and (b) modulating
dopamine systems can affect hunger, we can move on to two of
the upstream players in appetite control, which expectedly work
through dopamine, and now that the arduous information is laid
out, the picture becomes clearer (at least for ghrelin).
Ghrelin, the hunger hormone produced in the stomach, is
released in response to low energy status.25 In 2012, Kern and
colleagues examined the interaction between ghrelin and
dopamine agonism in mice with chemically induced anorexia
in short, they discovered that ghrelin increases appetite when its
receptor couples with a specific type of dopamine receptor,
inactivating it.17 Followup research in 2013 further elucidated
ghrelins dopaminergic role in appetite by reporting that direct
stimulation of dopamine receptors decreases ghrelins appetite
stimulating effects, and removing the ghrelin receptor attenuates
proper dopamine-induced satiety.18 These insights unite Volkow
et al.s research and Avena et al.s research, which take
somewhat opposing stances on how dopamine modulates
appetite.9,11,19 All research considered, the key observation we
can extract from ghrelins interaction with dopamine receptors is
that dopamine levels themselves do not necessarily reflect
normal dopamine sensitivity, as stressed earlier.
Dopamine itself motivates reward-seeking, sometimes in the

form of food. Its dopamine sensitivity that were examining
when trying to figure out when things go awry, and leptin keeps
that dopamine sensitivity sustained in the reward center while
simultaneously increasing conscious inhibition of food intake by
increasing conscious control in the PFC.21 Leptin also increases
dopamine synthesis in the reward center, possibly to reinforce
normal dopamine sensitivity and therein normal appetite
regulation.21 All-in-all, we can say that leptin closes the
perceived gap between between predicted reward and actual
reward, which is a roundabout way of saying, again, that leptin
reinforces normal dopamine signaling, and compromised leptin
sensitivity can reinforce compulsive eating behavior, an
unfortunate positive feedback loop.1,22
An open-ended question: Are Oreos really more addictive
than cocaine?
At first glance this hypothesis, recently propagated through
mainstream media, seems outrageous, and it is a duplicitous
situation in which science antagonizes logic. Food and drugs, as
we can surmise from understanding how dopamine motivates
reward, are inextricably related in addiction research, and this
paradigm presents a treacherous pattern, comparing exogenous,
pharmacological responses with endogenous, homeostatic
responses clearly there is much more to the story. Gently
intertwining logic and science, lets first return to the brain
comparison image presented in the introduction to this article,
mouse brain versus human brain. The PFC can inhibit our
reward-seeking urges with food and drugs. Mice cant do this.
Mice do not have conscious control over their decisions. So
when we examine compulsive behavior in the reward center,
which mice and humans both have, and take conscious control
completely out of the equation, we lose explanatory power
comparing the two models. For a human model, lets turn back
to Dr. Volkow in a lecture summary published in April of 2012:
Many experts dismiss food as an addictive substance because
it doesnt lead to most people behaving like addicts
compulsively seeking food despite negative consequences. So,
the reasoning goes, food cant be as addictive as a drug like
crack cocaine. What that fails to recognize, however, is that
crack cocaine itself isnt as addictive as is commonly believed.
If you look at people who take drugs, the majority are not
addicted, Volkow said. Indeed, even for drugs like crack and
26
heroin, fewer than 20% of users become addicted.
Next, lets take leptin, which would presumably have an

opposite effect on dopaminergic appetite stimulus, since we
know that leptin suppresses appetite in healthy adults.1 Notably,
leptin is far more dynamic and difficult to disambiguate than
ghrelin for self-explanatory reasons; its just a more dynamic
hormone. For example, we know that leptin decreases reward
response to food intake and cue-induced appetite induction by
decreasing dopaminergic firing rate in the reward center.20
Thats a mouthful, so lets back up. Thinking about food makes
us crave food, and leptin makes that craving less intense. This
may seem contradictory, since weve seemingly established that
decreased dopamine signaling would lead to increased appetite,
but to clear up the contradiction we need to rehash dopamines
quintessential role in motivating reward-seeking behavior.
This is where I want to leave you to formulate your own

hypotheses about food and addiction. Its a complex, polarized
topic in neuroscience and a relevant, emotionally charged topic
in cultural discussions about obesity. From here, I think logic
[Back to Contents]
In contrast, if you look at the proportion of people who are

currently obese some 34% of adults over 20 its a
significantly larger group. Add in those who are overweight, and
fully two-thirds of Americans clearly have significant difficulties
controlling their food intake. So, measured by the proportion of
those who behave in health-risking ways with each substance,
food could actually be considered several times more
27
addictive than crack.
Page 4
Volkow ND, Wang GJ, Baler RD. Reward, dopamine and

the control of food intake: implications for obesity. Trends
Cogn Sci. 2011 Jan;15(1):37-46. [PubMed]
2. Duvauchelle CL, Levitin M, MacConell LA, Lee LK,
Ettenberg A. Opposite effects of prefrontal cortex and
nucleus accumbens infusions of flupenthixol on stimulantinduced locomotion and brain stimulation reward. Brain
Res. 1992 Mar 27;576(1):104-10. [PubMed]
3. Del Arco A, Mora F. Prefrontal cortex-nucleus accumbens
interaction: in vivo modulation by dopamine and glutamate
in the prefrontal cortex. Pharmacol Biochem Behav. 2008
Aug;90(2):226-35. [PubMed]
4. Diekhof EK, Gruber O. When desire collides with reason:
functional interactions between anteroventral prefrontal
cortex and nucleus accumbens underlie the human ability to
resist impulsive desires. J Neurosci. 2010 Jan
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5. Beninger RJ. The role of dopamine in locomotor activity
and learning. Brain Res. 1983 Oct;287(2):173-96. [PubMed]
6. Finlayson G, King N, Blundell JE. Liking vs. wanting food:
importance for human appetite control and weight
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[PubMed]
7. Berridge KC. Measuring hedonic impact in animals and
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8. Finlayson G, King N, Blundell JE. Is it possible to
dissociate 'liking' and 'wanting' for foods in humans? A
novel experimental procedure. Physiol Behav. 2007 Jan
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10. Volkow ND, Wang GJ, Maynard L, Jayne M, Fowler JS,
Zhu W, Logan J, Gatley SJ, Ding YS, Wong C, Pappas N.
Brain dopamine is associated with eating behaviors in
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11. Avena NM, Rada P, Hoebel BG. Evidence for sugar
addiction: behavioral and neurochemical effects of
intermittent, excessive sugar intake. Neurosci Biobehav
Rev. 2008;32(1):20-39. [PubMed]
12. Roesch MR, Olson CR. Impact of expected reward on

neuronal activity in prefrontal cortex, frontal and
supplementary eye fields and premotor cortex. J
Neurophysiol. 2003 Sep;90(3):1766-89. [PubMed]
13. Wilson SJ, Sayette MA, Fiez JA. Prefrontal responses to
drug cues: a neurocognitive analysis. Nat Neurosci. 2004
Mar;7(3):211-4. [PubMed]
14. Petrovich GD, Ross CA, Holland PC, Gallagher M. edial
prefrontal cortex is necessary for an appetitive contextual
conditioned stimulus to promote eating in sated rats. J
Neurosci. 2007 Jun 13;27(24):6436-41. [PubMed]
15. Volkow ND, Fowler JS, Wang GJ, Goldstein RZ. Role of
dopamine, the frontal cortex and memory circuits in drug
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16. Mark GP, Smith SE, Rada PV, Hoebel BG. An appetitively
conditioned taste elicits a preferential increase in
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17. Kern A, Albarran-Zeckler R, Walsh HE, Smith RG. Apoghrelin receptor forms heteromers with DRD2 in
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18. Romero-Pic A, Novelle MG, Folgueira C, Lpez M,
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receptors attenuates the orexigenic action of ghrelin.
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peripheral regulation of appetite. J Neuroendocrinol. 2009
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20. Scarpace PJ, Zhang Y. Leptin resistance: a prediposing
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21. Fulton S, Pissios P, Manchon RP, Stiles L, Frank L, Pothos
EN, Maratos-Flier E, Flier JS. Leptin regulation of the
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22. Farooqi IS, Bullmore E, Keogh J, Gillard J, O'Rahilly S,
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23. White MA, Whisenhunt BL, Williamson DA, Greenway
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25. Maier C, Schaller G, Buranyi B, Nowotny P, Geyer G,
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26. National Survey on Drug Use and Health. Substance Use
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Humans. April 05, 2012 [TIME Health & Family]
[Back to Contents]
and science can find common ground given what we know about
dopamine and appetite, informing a behavioral approach best
centered on habitual moderation, avoiding overeating itself
rather than avoiding certain foods. A generalization rarely best
suits practical application, but in this case I think its the best we
can do: instead of saying, some foods are addictive, we might
be better off saying, some behaviors are addictive, where
overconsumption is a conditioned, but breakable habit in
otherwise healthy people.
________________________________________________________________________________________________________
Andy Abbate graduated pre-medical from Boston College in 2013 with

a BA in Economics, extensive undergraduate coursework in
biochemistry and graduate-level coursework in analytical and organic
chemistry. He is currently pursuing an MS in Biomedical Science at
Drexel University and hopes to continue graduate-level study in
biological neuroscience.
________________________________________________________________________________________________________
References
1.
Page 5
Interval training in the fed or fasted state improves

body composition and muscle oxidative capacity in
overweight women.
Gillen JB, Percival1 ME, Ludzki1 A, Tarnopolsky MA, Gibala
MJ. Obesity. 2013 Nov;21(11): 2249-55. [Wiley Online]
OBJECTIVE: To investigate the effects of low-volume highintensity interval training (HIT) performed in thefasted (FAST)
versus fed (FED) state on body composition, muscle oxidative
capacity, and glycemiccontrol in overweight/obese women.
METHODS: Sixteen women (27 8 years, BMI: 29 6 kg/m2,
VO2peak: 28 3 ml/kg/min) were assigned to either FAST or
FED (n = 8 each) and performed 18 sessions of HIT (10 60-s
cycling efforts at 90% maximal heart rate, 60-s recovery) over
6 weeks. RESULTS: There was no significant difference
between FAST and FED for any measured variable. Body mass
was unchanged following training; however, dual energy X-ray
absorptiometry revealed lower percent fat in abdominal and leg
regions as well as the whole body level (main effects for time, P
0.05). Fat-free mass increased in leg and gynoid regions (P
0.05). Resting muscle biopsies revealed a training-induced
increase in mitochondrial capacity as evidenced by increased
maximal activities of citrate synthase and -hydroxyacyl-CoA
dehydrogenase (P 0.05). There was no change in insulin
sensitivity, although change in insulin area under the curve was
correlated with change in abdominal percent fat (r = 0.54, P
0.05). CONCLUSIONS: Short-term low-volume HIT is a timeefficient strategy to improve body composition and muscle
oxidative capacity in overweight/obese women, but fed- versus
fasted-state training does not alter this response.
SPONSORSHIP: Natural Science and Engineering Research
Council (NSERC) operating grant and McMaster University
internally sponsored research grant to MJG.
Study strengths
This study is conceptually strong since it investigates a question
thats been hotly debated for what seems to be over a decade
now. The interesting twist is the use of high-intensity interval
training (HIIT) instead of low-intensity steady-state (LISS),
which is a welcome variation on the theme since HIIT better
economizes training duration. This is the first study to ever
examine the effect of fed versus fasted HIIT on glucose control,
muscle metabolic capacity measured via citrate synthase (CS)
and -hydroxyacyl-CoA (-HAD) activity, and body composition.
Training sessions were supervised. Pre-training breakfasts were
standardized & duplicated on testing day. Maintenance of
normal diet habits was confirmed with 3-day diet records at the 3
& 6-week points via nutritional software. Body composition was
assessed via DXA.
since the subjects used were untrained/obese. Another limitation

was the absence of resistance training. Cardio-only programs are
not optimal, but this limitation is somewhat of a necessarily evil
given the nature of this investigation, which is focused on
comparing feeding effects on a single training mode. It also
would have been useful if the authors reported the macronutrient
intakes of the subjects in each group, since after all, they went
through the trouble of software-analyzing diet records, and this
information would have been useful. A final limitation is that the
results might be limited to the training protocol used, which was
three sessions per week consisting of 10 cycles of 60 seconds at
90% of maximal heart rate alternated with 60 seconds of
recovery at 50 W.
Comment/application
The main finding was a lack of significant difference between

conditions in any of the parameters assessed, regardless of
differences in nutritional intake around training sessions. As
seen above, this included a lack of significant difference in body
composition change (in addition to a lack of differences in
glucose control & mitochondrial capacity). Interestingly, this
was the first study to ever observe a gain in fat-free mass as a
result of low-volume HIIT in women.
The authors acknowledged two limitations the absence of a

control group doing conventional endurance-type training, and
the inability to assess sex-based differences (the sample was all
women). I would add to this that the results are not necessarily
applicable to lean/athletic subjects looking to push the limits
Something that might be easy to overlook (but that the authors

diligently acknowledged), was the trend toward a greater lean
mass increase in the fed group (P = 0.07, as shown above).
Although this greater increase in lean mass did not reach
statistical significance, it conjures the question of whether a
significant difference would become apparent in a trial lasting
longer than 6 weeks. It would also be interesting to see how
changes in lean mass would be influenced by a concurrent
progressive resistance training program. With perhaps a single
exception,1 the research that actually assess body composition
shows that HIIT is effective for reducing fat mass.2 However, the
present study additionally indicates the lean mass-increasing
potential of HIIT especially in the fed state (though not seen
here to a statistically significant degree). Its important to note
that the recomp effect (decrease in fat mass and increase in
lean mass) seen in the present study is not too surprising since
the subjects were overweight/obese and untrained.
[Back to Contents]
Study limitations
Page 6
Metabolic effects of milk protein intake strongly

depend on pre-existing metabolic and exercise status.
Melnik BC, Schmitz G, John SM, Carrera-Bastos P, Lindeberg
S, CordainL. Nutr Metab (Lond). 2013 Oct;10(1)60:
doi:10.1186/1743-7075-10-60 [N&M]
ABSTRACT: Milk protein intake has recently been suggested
to improve metabolic health. This Perspective provides evidence
that metabolic effects of milk protein intake have to be regarded
in the context of the individuals pre-existing metabolic and
exercise status. Milk proteins provide abundant branched-chain
amino acids (BCAAs) and glutamine. Plasma BCAAs and
glutamine are increased in obesity and insulin resistance, but
decrease after gastric bypass surgery resulting in weight loss and
improved insulin sensitivity. Milk protein consumption results in
postprandial hyperinsulinemia in obese subjects, increases body
weight of overweight adolescents and may thus deteriorate preexisting metabolic disturbances of obese, insulin resistant
individuals. SPONSORSHIP: None listed.
Commentary
Since this paper is a narrative review instead of a controlled
experiment, its simply not conducive for critique based on
methodological strengths and limitations. Instead, Ill do some
general commentary, focusing on the assertions of the paper that
are not adequately supported by scientific evidence. Before I get
into that, heres some background on the present review. Melnik
et al wrote this paper in response to a recent paper by McGregor
and Poppitt, who reviewed a substantive body of literature on
milk protein showing a diversity of favorable effects on
metabolic health and body composition.3 Melnik et al felt it was
warranted to challenge these views and throw in some
cautionary notes that were purportedly overlooked. What
follows are boxed excerpts alternated with my commentary.
Palaeolithic, physically active hunter-gatherers consumed
structural proteins like fish and meat. In contrast, modern
Neolithic humans have mutated into physically inactive
individuals, who particularly consume signalling proteins from
milk providing abundant fast dietary proteins leading to high
plasma BCAA and glutamine levels [15]. Palaeolithic dairy-free
diets exhibit lower insulin levels with improved insulin
sensitivity protecting against the development of diseases of
civilization [16-19].
and Dhaliwal compared the 12-week effects of either whey,

casein, or glucose supplementation in overweight and obese
subjects and found whey to actually improve fasting lipids and
insulin levels.4 Finally, the papers they reference in support of
the claim that Palaeolithic dairy-free diets exhibit lower insulin
levels with improved insulin sensitivity were all speculative
pieces rooted in nothing more than hypothesis. It would be
impossible to support such a claim with objective, controlled
data yet the authors boldly point the finger at dairy
consumption as a key factor in the diseases of civilization. This
is quite a bodacious leap of logic.
In obese subjects, oral administration of leucine induces
exaggerated and prolonged postprandial hyperinsulinemia
without significant changes of blood glucose levels [34-36]. In
children, daily intake of 53 g milk protein, but not of 53 g meat
induced hyperinsulinemia and insulin resistance under fasting
conditions [10].
The
concern
surrounding
prolonged
postprandial
hyperinsulinemia without significant changes in in blood glucose
levels is immaterial considering that this was the result of
ingesting isolated leucine (or in one of the studies, leucine plus
glucose). Ironically, one of the studies Melnik et al cited simply
did not support their disdain for BCAA. To quote Hoppe et al,5
In the milk-group, fasting s-insulin concentrations doubled,
which caused the insulin resistance to increase similarly. In the
meat-group, there was no increase in insulin and insulin
resistance. As the BCAAs increased similarly in both groups,
stimulation of insulin secretion through BCAAs is not
supported.
Note that the latter results were seen in a 7-day study on 8 yearold children, so they should be viewed in a highly preliminary
light.
In overweight adolescents daily intake of 35 g whey protein or
casein significantly increased fasting plasma insulin levels [37].
Thus, there is substantial evidence that increased milk protein
consumption in obese individuals persistently over-stimulates
insulin secretion, which in the long term may promote early
onset of -cell apoptosis. [...] Supplementation of milk protein
(either 35 g whey protein, skim milk protein, or casein) to
overweight adolescents further increased body weight [37].
The above excerpt appears in the introductory paragraph of the

paper, and it encompasses several dubious presumptions. First of
all, its painting a guilt-by-association picture. Clearly, its
fallacious to assume a causal relationship between the presence
of dairy in the diet and the so-called diseases of civilization. In
addition, they make a false distinction between structural
proteins and signaling proteins since the examples they use both
contain each type. Fish and meat are both rich sources of
BCAAs, which the authors rail against throughout their paper.
They call milk an abundant provider of fast dietary proteins.
However, its relatively elementary knowledge that 80% of milk
protein is the slowly digested/absorbed casein, with the faster
protein (whey) rounding out the minority. Nevertheless, recent
research directly refutes the fear of fast milk proteins being
agents of glucose control impairment/insulin resistance. Ellis
Reference #37 in Melnik et als paper is cited twice in attempt to

support the claim that milk protein consumption is a special
agent of increased fasting insulin levels and weight gain. What
they fail to mention is that this was a 12-week study involving
the addition of 1 liter (32 oz or 4 cups) of milk-based beverage
to the normal/habitual diet of overweight adolescent subjects.6
One of the treatments was a liter of skim milk, which contains
roughly 350 kcal. The other 2 treatments (whey & casein-based
beverages) had similar kcal content. This put the subjects in the
experimental groups under a sustained hypercaloric balance, so
weight gain should be an obvious outcome compared to the
control condition which was water.
[Back to Contents]
Melnik et al close their paper by blaming milk protein for

prostate cancer via mTORC1 activation.7 They also cite
Page 7
epidemiological data to support a link to prostate cancer and

high intakes of dairy.8,9 In support of this concern, Tseng et al
proposed that dairy consumption can potentially raise prostate
cancer risk through a calcium-mediated pathway.10 Newmark
and Heaney have countered that the phosphate content may be a
more likely source of prostate cancer risk from high dietary
intake of dairy products.11 However, keep in mind that these
data are observational, and thus speculative in nature.
In stark contrast to the hypotheses of Melnik et al, a role for milk
proteins in cancer prevention (yes, bold) has been proposed by
Parodi as follows:12
Various experiments showed that tumour prevention by
dietary whey protein was accompanied by increased
glutathione levels in serum and tissues as well as enhanced
splenic lymphocyte proliferation, phagocytosis and natural
killer, T helper and cytotoxic T cell activity. Whey protein
components, beta-lactoglobulin, alpha-lactalbumin and serum
albumin were studied infrequently, but results suggest they
have anticancer potential.
In addition to the latter research, Huncharek et al pooled the data

from 45 observational studies using a meta-analytic method, and
found that observational studies do not support an association
between dairy product use and an increased risk of prostate
cancer.13
As the trusty clich goes, correlation does not automatically
equal causation. There is evidence of an inverse association
between dairy intake and certain cancers. In a recent review of
the evidence, Lampe states the following:14
illustrate how observational data must be viewed as merely

hypothesis-generating, rather than conclusive or confirmative.
Naturally, I was curious about the Dairy Councils stance on the
prostate cancer issue, so I dug up what they had to say:18
Results of epidemiological studies of dairy foods or dairy food
nutrients such as calcium and prostate cancer are inconsistent,
with studies showing either a positive (35-39) or no (40-44)
association. [...] Also, an increased risk for prostate cancer is
associated with calcium intakes (>1,500 mg/day) exceeding
current dietary recommendations (45,47-49).
On the note of foods and cancer risk, a very amusing satirical

piece was recently run in the American Journal of Clinical
Nutrition. Schoenfeld and Ioannidis conducted a systematic
review of 50 common ingredients in cookbooks and found that
80% of them were associated with cancer risk or benefit in the
epidemiological literature.19 The authors take-home message is
that epidemiology is a messy soup of variables that must be
viewed skeptically. This quote captures the essence of their
satire and undercurrent of truth:
Given that we examined the effects most specific to individual
ingredients, we did not examine more complex analyses
involving nutritional pathways, biochemical nutritional
measurements, and metabolites or combinations of
ingredients. However, we hypothesize that similar patterns of
research conduct and reporting also apply to these other
aspects of nutritional epidemiology.
For most cancers, associations between cancer risk and intake

of milk and dairy products have been examined only in a small
number of cohort studies, and data are inconsistent or lacking.
Meta-analyses of cohort data available to date support an
inverse association between milk intake and risk of colorectal
and bladder cancer and a positive association between diets
high in calcium and risk of prostate cancer.
By the same logic Melnik et al employ to blame milk protein for

prostate cancer, it can also be said that milk protein will also
save you from colorectal and bladder cancer. But obviously, this
claim cannot be made based on observational data. Nevertheless,
the possibility of a high dairy intake being a causal factor in the
pathogenesis of prostate cancer cannot be completely dismissed.
At the same time, it cannot be presumed true, due to the lack of
controlled data supporting this hypothesis.
Melnik et als claim that milk protein is the specific culprit
behind prostate cancer must therefore be viewed with caution, as
should the very nature of epidemiological outcomes. An
example of what I consider to be a highly questionable
association thats been replicated in the literature is red meat
consumption raising the risk for type 2 diabetes (T2D).15,16 There
could be a slew of unaccounted variables at play that
erroneously indict red meat. Similar implausibility is evident in a
recent prospective cohort study by de Koning et al, who found
that red meat intake within a low-carbohydrate diet was
associated with increased risk for T2D.17 Another of my favorite
face-palm outcomes is the daily consumption of eggs increasing
the risk for T2D.18 These biologically implausible outcomes
[Back to Contents]
Page 8
Undenatured type II collagen (UC-II(R)) for joint

support: a randomized, double-blind, placebocontrolled study in healthy volunteers.
Lugo JP, Saiyed ZM, Lau FC, Molina JP, Pakdaman MN,
Shamie AN, Udani JK. J Int Soc Sports Nutr. 2013 Oct
24;10(1):48. [JISSN]
BACKGROUND: UC-II contains a patented form of
undenatured type II collagen derived from chicken sternum.
Previous preclinical and clinical studies support the safety and
efficacy of UC-II in modulating joint discomfort in osteoarthritis
and rheumatoid arthritis. The purpose of this study was to assess
the efficacy and tolerability of UC-II in moderating joint
function and joint pain due to strenuous exercise in healthy
subjects. METHODS: This randomized, double-blind, placebocontrolled study was conducted in healthy subjects who had no
prior history of arthritic disease or joint pain at rest but
experienced joint discomfort with physical activity. Fifty-five
subjects, who reported knee pain after participating in a
standardized stepmill performance test, were randomized to the
placebo (n = 28) or the UC-II (40 mg daily, n = 27) cohort for
120 days. Joint function was assessed by measuring knee flexion
and knee extension as well as time to experiencing and
recovering from joint pain following strenuous stepmill exertion.
RESULTS: After 120 days of supplementation, subjects in the
UC-II group exhibited a statistically significant improvement in
average knee extension compared to placebo (81.0 +/- 1.3o vs
74.0 +/- 2.2o; p = 0.011) and to baseline (81.0 +/- 1.3o vs 73.2
+/- 1.9o; p = 0.002). The UC-II cohort also demonstrated a
statistically significant change in average knee extension at day
90 (78.8 +/- 1.9o vs 73.2 +/- 1.9o; p = 0.045) versus baseline. No
significant change in knee extension was observed in the placebo
group at any time. It was also noted that the UC-II group
exercised longer before experiencing any initial joint discomfort
at day 120 (2.8 +/- 0.5 min, p = 0.019), compared to baseline
(1.4 +/- 0.2 min). By contrast, no significant changes were seen
in the placebo group. No product related adverse events were
observed during the study. At study conclusion, five individuals
in the UC-II cohort reported no pain during or after the stepmill
protocol (p = 0.031, within visit) as compared to one subject in
the placebo group. CONCLUSIONS: Daily supplementation
with 40 mg of UC-II was well tolerated and led to improved
knee joint extension in healthy subjects. UC-II also
demonstrated the potential to lengthen the period of pain free
strenuous exertion and alleviate the joint pain that occasionally
arises from such activities. SPONSORSHIP: InterHealth
Nutraceuticals, Inc., Benicia, California.
prevalence of both diseases. If consistently demonstrated as

effective, its fair to speculate that UC-IIs availability &
affordability would be reasonable since its not some exotic or
scarce material (its derived from chicken sternum).
Study limitations
The authors diligently acknowledge two limitations. First, the
time to onset of initial pain was limited to a 10-minute interval,
which casts some doubt about the clinical importance of such a
short assessment period. Secondly, its possible that the subjects
might have early signs of arthritis that do not meet formal
diagnostic criteria (thereby reducing the validity of the claim that
UC-II is effective for those with no prior history of arthritic
disease). This possibility also points to the potential limitation of
not directly assessing inflammatory biomarkers, which could
provide a more objective set of data on the effects of UC-II.
Comment/application
The main findings were that UC-II significantly improved knee

range of motion (extension), as well as increased time of
exercising before experiencing joint discomfort, as depicted
above. The authors thus concluded:
UC-II is a unique ingredient that supports healthy joints.
Previous studies have focused on the efficacy of this ingredient
in OA subjects. By including healthy subjects in this study, and
using non-disease endpoints as a measure of efficacy, it is
believed that the benefits that derive from UC-II usage now
extends to include healthy individuals.
This study presents novel findings since its the first to examine
the effect of undenatured type 2 collagen (UC-II) in subjects
who experienced knee pain after strenuous physical exertion but
had no prior history of arthritic disease. Subjects, clinical staff,
and data analysis/management staff remained blinded as to who
received treatment or placebo. I would also add that nonpharmacological (natural) therapies for managing pain related
to osteoarthritis and rheumatoid arthritis are important, given the
Regarding safety, three studies aside from the present one are
cited indicating the absence of adverse effects in humans and
animals in trials lasting up to 90 days.20-22 Particularly
impressive is a 24-week multicenter intervention by Wei et al
who found that sternally derived type 2 chicken collagen (likely
very similar to that used in the present study) significantly
improved symptoms of rheumatoid arthritis at a daily dose of 0.1
mg (the present study used 40 mg).23 Although it was not as
potent as the comparator (the drug methotrexate), it had a lower
incidence of adverse effects. The evidence overall suggests that
UC-II is a promising non-drug therapy option for those suffering
from rheumatoid arthritis or osteoarthritis and possibly for
those with joint pain that does not fit standard diagnostics.
[Back to Contents]
Study strengths
Page 9
Resistance training reduces fasted- and fed-state

leucine turnover and increases dietary nitrogen
retention in previously untrained young men.
Moore DR, Del Bel NC, Nizi KI, Hartman JW, Tang JE,
Armstrong D, Phillips SM. J Nutr. 2007 Apr;137(4):985-91.
[PubMed]
PURPOSE: We aimed to determine the impact of intense resistance
training, designed to increase lean body mass (LBM), on both fasted
and fed whole body protein kinetics in untrained young men.
METHODS: Twelve healthy males (22 +/- 2 y of age; BMI, 24.3
+/- 2.4 kg/m(2)) participated in a 12-wk (5-d/wk) resistance training
program. Before and after training, a primed constant infusion of [1(13)C]leucine was used to measure whole body leucine turnover,
protein breakdown, and nonoxidative leucine disposal in the fasted
and fed states. Participants were studied during 5-d controlled diet
periods that provided a moderate protein intake [1.4 g/(kg body
wt/d)]. We estimated protein turnover and nitrogen balance.
RESULTS: Training increased LBM (61.6 +/- 6.9 vs. 64.8 +/- 6.7
kg, P < 0.05). After training, whole body leucine turnover was
reduced (P < 0.01) in both fasted (167 +/- 18 vs. 152 +/- 17) and fed
(197 +/- 23 vs. 178 +/- 21) states [all values micromol/(kg LBM .
h)]. Training-induced decreases (P < 0.01) in protein breakdown
occurred in the fasted (165 +/- 18 vs. 144 +/- 17) and fed (111 +/23 vs. 93 +/- 20) states. Following training, nonoxidative leucine
disposal was similarly reduced (P < 0.01) in the fasted (144 +/- 18
vs. 126 +/- 18) and fed (151 +/- 20 vs. 133 +/- 19) states. Nitrogen
balance was more positive after training (13.7 +/- 8.1 vs. 33.4 +/12.5 g/(kg LBM/d), P < 0.01) indicating an increased retention of
dietary nitrogen. CONCLUSIONS: The increase in nitrogen
balance after training demonstrates a more efficient utilization of
dietary nitrogen, suggesting that protein requirements for novice
weightlifters are not elevated. SPONSORSHIP: Supported by a
grant from the Natural Sciences and Engineering Research Council
(NSERC) of Canada (S.M.P.).
Study strengths
This study is innovative since it was the first to examine the
effect of resistance training on whole-body protein metabolism
(via leucine kinetics) in the fasted and fed state. By default, it
investigated whether protein intake at 1.4 g/kg is necessary or
beneficial under resistance training conditions, but the
interesting aspect was seeing whether the physiological demand
for this level of intake increases or decreases over time. DXA
was used to assess body composition. The progressive resistance
training sessions were supervised by research personnel. Threeday diet records were software-analyzed at the start, midpoint,
and end of the study. Dietary control overall was tight.
subjects. A final limitation would be the lack of a comparison

group consuming protein at a higher-end dose that might
optimize the rate of muscular gains (~1.8 g/kg). It would have
been interesting to see whether this dose could have exceeded
the LBM gains seen with 1.4 g/kg, despite hypercaloric
conditions.
Comment/application
The main findings were three-fold. First the expected set of

outcomes: progressive resistance training caused a significant
increase in LBM, muscle fiber hypertrophy, and maximal
strength. Secondly, resistance training caused a reduction in both
postabsorptive (fasting) and postprandial (fed) protein turnover
after resistance training in young men and are the result of
decreases in whole-body protein breakdown and protein
synthesis, as indicated by leucine kinetics. Finally, as shown in
the table above, nitrogen balance was more positive after
training compared with before training.
The present study supports and extends the findings of a
previous study from the same lab. Hartman et al observed
similar outcomes (increase in strength, LBM, and net protein
balance, and nitrogen balance).24 The training-induced reduction
in protein turnover and higher net protein balance combined with
increased nitrogen balance led them to a similar conclusion as
the authors of the present study that dietary protein
requirements decrease as a result of resistance training.
The authors acknowledge that measuring leucine turnover

cannot assess tissue-specific changes (i.e., skeletal muscle
protein flux); it can only estimate changes at the whole-body
level. However, they also measured changes in LBM and muscle
fiber cross-sectional area, so this minimized the assessment gaps
that mere leucine kinetics might leave. I would add to this that
nitrogen balance (another whole-body index of protein turnover)
has limited accuracy in representing actual muscle protein status;
it typically over-estimates it. Furthermore, the results seen in this
study could be limited to hypercaloric conditions in untrained
Its notable that not all previous work agrees with the present
study. Others have observed increased leucine turnover as a
result of resistance training, particularly in older subjects. 25 Its
tempting to conclude that, based on the present studys results,
resistance training decreases protein requirements. However, its
important to consider that lean, trained athletes in hypocaloric
conditions have benefited from substantially higher intakes than
1.4 g/kg.26 Furthermore, its likely that rigorous, periodized
training programs (especially ones that include over-reaching
phases) can to impose higher protein demands. Combining highvolume, periodized, progressive training with hypocaloric
conditions is not likely to yield the increase in nitrogen retention
and reduction in leucine turnover seen in the present study.
[Back to Contents]
Study limitations
Page 10
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Kassapa C, Trichopoulos D, Ardanaz E, Larraaga N, Tormo
MJ, Gonzlez CA, Quirs JR, Snchez MJ, Bingham S, Khaw
KT, Manjer J, Berglund G, Stattin P, Hallmans G, Slimani N,
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Song Y, Chavarro JE, Cao Y, Qiu W, Mucci L, Sesso HD,
Stampfer MJ, Giovannucci E, Pollak M, Liu S, Ma J. Whole
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Tseng M, Breslow RA, Graubard BI, Ziegler RG. Dairy,
calcium, and vitamin D intakes and prostate cancer risk in the
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[Back to Contents]
Page 11
Vemma a fairy tale of hope, a reality of nope.

By Alan Aragon
________________________________________________
Intro & background

Vemma (an acronym for vitamins, essential minerals,
mangosteen, aloe + green tea) is a privately held direct sales
company that uses multilevel marketing (MLM also called
network marketing) to generate revenue. Vemma was founded in
2004 by Benson K. Boreyko, who has a long history of running
large MLM businesses prior to launching Vemma, whose 2012
revenue totaled $117 million. According to Vemma, their US
revenue saw a 46% increase over last year, followed by Canada
with 34%, and Europe with a 22% increase (full press release
here). Its safe to say that Vemma is no small business.
directly above takes up almost all of the space on Vemmas

home page. The picture of the guy next to his slick, black BMW
is 22 year-old Alex Morton, featured in a press release as one of
Vemmas success stories. Here is a video clip of his sales pitch,
where he proudly claims hes earning $3500 per week (at 6:38
into the vid). Anyone whos sat through an MLM presentation
knows that they play on the audiences fear of working a few
decades for an ungrateful corporation and retiring broke, like the
majority. Either join the MLM, or accept a miserable life
doomed to financial hardship. Thats the absurdly false dilemma
put forth by the recruiter. At these sales meetings, the value of a
college education is dismissed or downplayed, and the
conventional road of climbing the corporate ladder is
discouraged and mocked. New recruits are told that within 3-5
years after joining, they can create enough residual income to
become financially free. This is the age-old promise of MLMs
in general, its not just a pitch exclusive to Vemma.
Although the idea of achieving financial independence in a few
short years of part-time effort sounds attractive to many, the
reality of the matter is much less exciting. Have a look at
Vemmas own 2012 income dislosure report:
Like many modern MLMs, Vemmas product line is focused on

nutritional products marketed to promote health and wellness.
Tied in with this is the promise of financial success through
recruitment into their sales force. Heres an example of
Vemmas advertising copy:
The foundation of Vemma's success lies firmly in the results
achieved from our clinically studied, single-formula product
line. At the company's core is our mission to help others by
enhancing their well-being, and offering an income stream to
people who introduce others to a product line they believe in.
Targeting the youth
While Vemma is hyped as a cash machine ready to dish out

riches to all who join in, the hard numbers tell a different story.
Notice how 85.73% of the sales force makes between $667.78
and $3260.73 per year. Thats a measly $55.64 to $271.72 per
month. According to the US Census Bureau (spreadsheet here),
the average (mean) annual household income in the US is
$69,677. Less than one percent of Vemma reps earn this.
The products
Vemma reported an 85% increase in sales recruits in the US in

2012. Its reasonable to speculate that a growing proportion of
these recruits are high school and college-aged. The screen shot
There are four Vemma product lines thus far: 1) Vemma, a

vitamin & mineral-fortified mangosteen-based drink that also
contains aloe; 2) Verve, a series of mangosteen-based energy
drinks containing anywhere from 5 to 70 kcal and 40 to 160 mg
caffeine; 3) Bod-e, a series of products sold as transformation
packs that include a vitamin & mineral-fortified protein shake,
mangosteen & caffeine-based burn, fiber-based cleanse,
mangosteen based rest which supposedly enhances the bodys
nightly restorative processes, and thirst, a mangosteen-based,
vitamin/mineral-fortified beverage aimed at hydrating and
providing electrolytes minus the high sugar content of typical
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Page 12
electrolyte replacement drinks; 4) Next is a vitamin & mineralfortified, mangosteen-based beverage aimed at children 2-12
years of age. All four Vemma product lines have similar
ingredients with slight variations, but all contain mangosteen and
vitamin/mineral fortification. This product template is common
in MLM because its a proven hit. The underlying formula is to
tout the benefits of some exotic fruit juice, and include it in a
line of products that cover the range of health/fitness goals and
insecurities of the general public. The recurrent thoughts I had
while reading through these product labels were, Wow, that
caffeine could add up, and Wow, what a superfluous degree of
vitamin and mineral fortification.
Scientific support?
Like any smart MLM, Vemma boldly claims that its products
have a solid foundation in research. They lean heavily on the
academic credentials of their product formulator and Chief
Scientific Officer, Ybing Wang. MD, PhD. But the question is,
how strong is the research evidence behind their products? You
would think that theres a mountain of research supporting
Vemma by the way the sales reps glorify this aspect of it.
However, there are only 2 published studies examining the
Vemma product specifically. One examined immune response,
and the other examined bioavailability. Lets take a closer look.
Tang et al investigated the 30-day effect of Vemmas flagship
product (the vitamin/mineral-fortified mangosteen-based juice)
on immune function and subjective self-appraisal of well-being.1
The investigators found that Vemma enhanced both innate and
acquired immune responses while lowering C-reactive protein (a
biomarker of inflammation). Subjective self-appraisals of overall
health status in the Vemma treatment were also signicantly
improved compared to the control condition.
While these results are mildly interesting, they still lack any real
value. Why? Because the placebo control was merely fructose
and water. A much more practical design would have compared
Vemma with some widely commercially available fruit juice or
fruit juice blend taken with (or without) an equivalent
supplemental amount of vitamins and minerals. As it stands,
Vemma cant claim to impart exclusive health benefits. For
example, concord grape juice which is inexpensive and widely
available has been shown to benefit immunity and increase
antioxidant levels.2 And keep in mind, you can purchase concord
grape juice without having to endure a pushy sales speech.
The other Vemma study tested bioavailability and antioxidant
effects of a single dose.3 Antioxidant capacity increased, and the
bioavailability of -mangostin as well as B2 and B5 were
observed. But once again, this was compared with a fructose
solution, and the same lack of practical relevance applies. Aside
from these two Vemma studies, a more extensive body of
research has been published on mangosteen itself. This raises the
question of whether mangosteens health effects are worth the
investment. Thus far, the answer appears to be nope. Heres
an excerpt from the conclusion of a recent scientific literature
review by Gutierrez-Orozco and Failla:4
Controlled intervention trials of the efficacy of xanthones in
human volunteers, as well as characterization of the
absorption, metabolism and elimination of these compounds,
remain quite limited. Also, the potential toxicity of chronic

ingestion of formulations containing mangosteen pericarp and
its extracts has received minimal attention. Despite the
numerous health claims on advertising sites for producers and
retailers of products and beverages containing mangosteen,
there is insufficient scientific evidence at this time to support
the use of mangosteen containing supplements as enhancers of
health and useful adjuvants for treatment of various
pathophysiological illnesses.
Cause for concern

What Vemma does particularly well is capitalize on the caffeinedriven energy drink craze that has swept the younger
generation like wildfire. According to a recent ISSN position
stand, energy drinks are the most popular dietary supplement in
the US adolescent and young adult population aside from
multivitamins.5 Seifert et al recently reviewed the adverse
consequences and extent of energy drink consumption among
children, adolescents, and young adults.6 Their cautionary notes
are worth quoting:
Energy drinks have no therapeutic benefit, and many
ingredients are understudied and not regulated. The known
and unknown pharmacology of agents included in such
drinks, combined with reports of toxicity, raises concern for
potentially serious adverse effects in association with energy
drink use.
Concluding thoughts
The MLM business model inevitably makes you view everyone
you meet as means to increase revenue. Seeing people as
walking dollar signs is not the healthiest mindstate to dwell in.
Ive tried MLM for a short stint back in high school (more than
20 years ago), and Im hearing the identical sales script from the
new generation of MLMs such as Vemma. When you combine
the desperate hustle of network marketing with relatively
ineffective products that carry the risk of adverse effects, you
have a good recipe for saying, no thanks.
References
1.
2.
3.
4.
5.
6.
Tang YP, Li PG, Kondo M, Ji HP, Kou Y, Ou B. blind, placebocontrolled trial. J Med Food. 2009 Aug;12(4):755-63. [PubMed]
Rowe CA, Nantz MP, Nieves C Jr, West RL, Percival SS. Regular
consumption of concord grape juice benefits human immunity. J
Med Food. 2011 Jan-Feb;14(1-2):69-78. [PubMed]
Kondo M, Zhang L, Ji H, Kou Y, Ou B. Bioavailability and
antioxidant effects of a xanthone-rich Mangosteen (Garcinia
mangostana) product in humans. J Agric Food Chem. 2009 Oct
14;57(19):8788-92. [PubMed]
Gutierrez-Orozco F, Failla ML. Biological activities and
bioavailability of mangosteen xanthones: a critical review of the
current evidence. Nutrients. 2013 Aug 13;5(8):3163-83. [PubMed]
Campbell B, Wilborn C, La Bounty P, Taylor L, Nelson MT,
Greenwood M, Ziegenfuss TN, Lopez HL, Hoffman JR, Stout JR,
Schmitz S, Collins R, Kalman DS, Antonio J, Kreider RB.
International Society of Sports Nutrition position stand: energy
drinks. J Int Soc Sports Nutr. 2013 Jan 3;10(1):1. [PubMed]
Seifert SM, Schaechter JL, Hershorin ER, Lipshultz SE. Health
effects of energy drinks on children, adolescents, and young adults.
Pediatrics. 2011 Mar;127(3):511-28. [PubMed]
[Back to Contents]
Page 13
Interview with Eric Helms about his latest peerreviewed publication on protein needs of lean, trained
athletes in an energy deficit.
By Alan Aragon
____________________________________________________
_
A systematic review of dietary protein during caloric
restriction in Resistance Trained Lean Athletes: A Case for
Higher Intakes.
Helms ER, Zinn C, Rowlands DS, Brown SR. Int J Sport Nutr
Exerc Metab. 2013 Oct 2. [Epub ahead of print] [PubMed]
BACKGROUND: Caloric restriction occurs when athletes
attempt to reduce body fat or make weight. There is evidence
that protein needs increase when athletes restrict calories or
have low body fat. PURPOSE: The aims of this review were to
evaluate the effects of dietary protein on body composition in
energy-restricted resistance-trained athletes and to provide
protein recommendations for these athletes. METHODS:
Database searches were performed from earliest record to July
2013 using the terms protein, and intake, or diet, and weight,
or train, or restrict, or energy, or strength, and athlete. Studies
(N = 6) needed to use adult ( 18 yrs), energy-restricted,
resistance-trained (> 6 months) humans of lower body fat
(males 23% and females 35%) performing resistance
training. Protein intake, fat free mass (FFM) and body fat had
to be reported. RESULTS: Body fat percentage decreased (0.5%
to 6.6%) in all study groups (N = 13) and FFM decreased (0.3 to
2.7kg) in nine of 13. Four groups gained or did not lose FFM.
They had the highest body fat, smallest magnitudes of energy
restriction or underwent novel resistance training stimuli. Two
groups lost non-significant amounts of FFM. The same
conditions that existed in the groups that did not lose FFM
existed in the first group. These conditions were not present in
the second group, but this group consumed the highest
protein intake in this review (2.5-2.6g/kg). CONCLUSION:
Protein needs for energy-restricted resistance-trained athletes
are likely 2.3-3.1g/kg of FFM scaled upwards with severity of
caloric restriction and leanness. SPONSORSHIP: No funding
was provided for this research.
Thanks so much for agreeing to do this interview in the midst
of sledging through your doctoral work. My first question is,
what gave you the idea or the impetus to ask the research
question (protein needs of lean/trained subjects in dieting
conditions)?
Alan, happy to as I'm between projects. This review was the

second chapter of my masters thesis which I recently submitted
and my PhD doesn't officially start until January. Plus, the true
purpose of my research-based education is adding to the body of
knowledge in my field. This includes not just publication, but
dissemination and engaging the people interested in my work.
Your readers are exactly the folks I'm trying to serve and help,
so I see this interview as part of my academic and life goals!
As to where the research impetus came from, that stems from
my personal goals and goals of 3DMuscleJourney. Among these
goals, and my focus as a part of the team, is using science to
approach bodybuilding in an evidence-based fashion. To do so
we need researchers to ask questions relevant to the sport;

specifically questions where confusion and contention lie. I
decided to stop wishing more researchers would look at
bodybuilding related topics, get over my insecurities, and do it
myself (not to say I'm the only bodybuilding researcher out
there, but there aren't many of us).
One contentious question at the top of my list was related to the
debate over protein intake. There are smart people on both sides
of the fence who have very different opinions on
protein recommendations. Bodybuilders typically recommend
higher protein intakes than most scientists and nutritionists.
I believe that central to this difference of opinion is context.
Bodybuilders see the biggest physique changes during contest
prep, and this is also when nutrition is most important. The
experience of seeing your physique at it's peak during a period of
intense nutritional focus, almost always with a high protein
approach, influences the perspective by which bodybuilders see
nutrition (I know it has for me). Additionally, one of the biggest
gaps in the literature is protein intake in athletic populations
during hypocaloric periods. In essence, the primary experience
that influences bodybuilders to have a "high protein bias" is
woefully understudied. Bodybuilders primarily have anecdote to
argue their case, and their opponents have research that is at best
only semi-applicable to counter it.
So, in order to help out this impasse I decided to tackle this
understudied area with my thesis. In fact the title of my thesis is
"Exploring protein and macronutrient intakes in lean
bodybuilders during caloric restriction". To start any thesis you
have to become intimately familiar with the research that does
exist. The experience of sifting through all this research for a
few years culminated in this publication.
I remember how your recently published paper in IJSNEM
started out (way back!), as I had the privilege of you getting
my feedback & critique. I'm curious to know how you took
on the direction of conducting a systematic review, since its
original form - if I recall correctly - could have been
considered more of a narrative review. I like how the paper
is more sterile & concise now, but I also miss a lot of the
background detail that was in the original work. It's always
amazing how papers often evolve into completely different
animals once they hit publication. So, here's my question what would you say are the greatest strengths of your paper?
And on the other hand, if you didn't have any word limits or
obligation to focus so tightly, what aspects of
the paper would you go into more depth about?
My first masters wasn't research-based, but I learned to be an
informed consumer and reviewer of research. That said, I had
never attempted a review of this scope. Thus, I started with an
organic, broad, comprehensive, and in hindsight, unorganized
approach. I dedicated hours every day, starting with the reviews,
working my way back through their reference lists, reading the
game-changing papers through the last four decades, reading the
underlying theoretical papers on metabolism and methodologies
related to protein, and then I went back and read it all again with
a renewed perspective and understanding.
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Page 14
At this point, I started doing more focused Boolean searches. I

ended up exhausting probably 99% of the research on protein
needs under hypocaloric conditions, and probably 2/3rds to
3/4ths of the published work on protein intake in athletes. I
wrote and edited as I reviewed, letting subtopics define
themselves. I plugged these sections into a semi-coherent first
draft, although looking back it was a review of everything
remotely related to the question rather than a clear paper that
could be applied in practice.
The first people to see it were folks like yourself: practitioners
with their proverbial ear to the ground of research. This was to
make sure I didn't miss important things in the field and that I
hadn't considered. The next step was getting it to my supervisors
who knew the peer review process and knew what academic
writing had to be. This process brought the word count down
from over ten thousand to just under seven. It also shifted away
from citing every piece of work ever published, to focusing on a
clear logic-chain leading to a conclusion.
When the dust settled it was a focused paper that I was proud of
and I submitted it to IJSNEM. At the time it was in fact still in
narrative review form. The transition into a systematic review
came after submission and I'll go into that further in answer to
your question about the peer review process.
As far as the paper's greatest strengths, I would say besides the
fact that it covers a very understudied topic in a systematic
fashion, the determination of protein intake by fat free mass
rather than total body mass is it's greatest strength. Believe it or
not, this also came out of the peer review process, so I'll save
further discussion on this topic for your question about peer
review as well.
Finally, as to your question about word limits and a tight focus,
I'm glad I had to tighten it. It made the paper more honest. For
example, before submission I had a section dedicated to studies
suggesting there might be benefits of high (over 2g/kg) protein
intakes for strength athletes even during non-hypocaloric
periods. The purpose was to illustrate that the "jury is still out"
on high protein intakes in general. However, it was the most
biased section and not relevant to the main point. I searched
specifically for papers showing the benefits of high protein
intakes, and while the fact that I found them is noteworthy,
presenting them in isolation is inherently an incomplete and
biased view of the literature and I'm glad I removed it.
I was also happy to trim down the section on methodologies of
determining protein requirements. I went into too much depth,
covered obscure methodologies, and got away from the main
point: we need to be looking directly at changes in body
composition and performance, not surrogate measures of protein
balance.
question on their own. Either they were on what I would call

"semi-resistance-trained" populations like recreational exercisers
or non strength athletes who do some resistance training, or
when they were on dedicated resistance-trained populations
something else was missing. For example, the length of the
interventions was incredibly short (1 to 2 weeks) or a high
protein intake was compared to a very low protein intake with
nothing in the middle.
The one study that was on highly trained natural bodybuilders
during contest prep that was 11 weeks long, and had a high
protein group compared to a moderately high protein group was
almost perfect. Except for one crucial thing, it was a study of
hypocaloric vs hypercaloric conditions not protein. Meaning
while the high protein experimental group was hypocaloric, the
moderately high protein control group was not! So while a great
study that did observe and record protein intake and body
composition changes in a relevant population, it didn't answer
the question. In fact no study alone has been able to answer the
question "what is the optimal protein intake in dieting strength
athletes?". So, the review looked at all the studies that met
certain criteria collectively to see what shook out. Essentially
looking at each study as an individual data point, each one filling
in the gaps where other studies were lacking.
In piecing the paper together, what were your most
significant "light bulb" moments? Were there any points
that you thought, "Ah-hah! I learned something new, and so
will the readers of this review."
The biggest one for me was when I looked at the study by Elia et
al., (1999). Seeing that lean individuals during starvation utilized
two to three times the amount of protein for energy that obese
individuals during starvation utilized really made some things
click for me. This study illustrates quite clearly that a caloric
deficit does different things in someone with higher body fat
than in someone with lower body fat. It illustrates that having a
low body fat level and being hypocaloric each independently
increase how much protein is used for energy. This was not
necessarily a new concept, but the clear delineation and also the
magnitude of the difference in physiology were both "light bulb"
moments you could say.
We both know that, unfortunately, not everyone will access
the full-text, let alone read it. People will inevitably make
flash-judgments and assumptions based solely on the
abstract. What are the main "zingers" or "knowledge
bombs" or crucial points of the paper that you feel are far
from captured in the abstract?
I could never "have my cake and eat it too". All the studies I
found were imperfect in their ability to answer the research
First off I don't actually like the abstract in it's current form! It is
going to change and be more clear when it moves from "in
press" to final publication. However, even with the clarity
changes I won't be able to explain one crucial point related to
nutritional order of importance. Before we can start playing
around with optimizing macronutrient ratios, caloric intake has
to be appropriately set. I learned through my research that the
size of the caloric deficit is more important in terms of muscle
loss/muscle maintenance than the macronutrient breakdown.
[Back to Contents]
As you sifted through the literature, what were the most

common limitation(s) you found with the studies on protein
requirements for the population in question?
Page 15
A high protein intake is only beneficial up to the point where it

doesn't force down other macronutrients to detrimental levels.
When dieting you're working with a limited caloric intake, and if
calories are set too low to start, a high protein intake can be
detrimental. To illustrate the importance of proper caloric intake,
let me state that I would rather have someone below my
protein recommendations at a 20% calorie deficit (80% of
maintenance) than I would have someone within them but at a
40% calorie deficit (60% habitual). The former will probably be
more protective of muscle. Now that said, a 20% caloric deficit
with a protein intake within my recommended range would most
likely be the best choice, but I wanted to make that point just to
illustrate the importance of energy balance over macronutrient
breakdown.
But why is calorie intake so important? Well, for a few reasons.
Metabolically, the less abundant fat and carbohydrate are, the
more we will convert protein to energy and thus the greater
likelihood of catabolizing muscle. But, probably of
equal importance is remembering that a resistance training
stimulus is going to be more important than protein intake for
maintaining muscle. That means enough fat and carbohydrate
needs to stay in the diet to maintain productive training. So
really what the abstract doesn't express is that if you crash diet,
no amount of protein is going to save you from the negative
consequences. In fact, a high protein intake could be worse than
a moderate protein intake in this situation if it forces carbs and
fat so low that your lifting suffers. (BTW it so common for
people put to put the proverbial "cart before the horse" when it
comes to their diets that I made a 6 part youtube series on how to
get your priorities straight nutritionally:
http://www.youtube.com/watch?v=GAvW6xBZjSk
What were the most challenging aspects of putting the paper
together - in terms of either the process or the content itself?
Some might be surprised by this, but I'm not a detail guy, I'm a
big picture thinker. This is a double-edged sword in research; on
one hand I tend to avoid big mistakes that some very analytical,
detail-oriented researchers make like focusing on one specific
metabolic pathway, or an in vitro physiological response and
extrapolating a conclusion that is incorrect when applied in the
real world. But, on the other hand I get ripped to pieces when it
comes time to edit my work. Consistent use of acronyms, proper
citation formatting, obscure grammar rules, proper scientific
nomenclature, and journal manuscript guidelines are all absolute
headaches for me. These aspects of scientific writing frustrate
me to no end, and let's just say I rely on the strengths of my
colleagues. My primary supervisor for my thesis was Dr. Caryn
Zinn. She has a great mind for detail and she was an invaluable
part of the editing and quality control process for not just this
paper but my entire thesis.
authors of papers not included in the main analysis. Some never

returned my emails, another couldn't release the data because of
institutional policy, and in one case when I received the data not
all of it had been properly processed and analysed.
In the end, I had to employ the help of my colleague and friend
Scott Brown (the fourth author) to do statistical back
calculations with the data we were able to get to impute the
missing data points. That is how we were able to create the
forest plot and tables in the review. This was a review of just six
studies, imagine the work that goes into a review that looks at 60
studies!
What are the most rewarding aspects of having completed &
published it? It's still barely in press, so I'd imagine these
positive things (invitations to speak, acknowledgment from
peers & students, etc.) are just trickling in.
Like you said, it's been in press only a few weeks at the time that
I am writing this, but there are still some definitive rewarding
outcomes. Publishing this paper in and of itself was hugely
rewarding. As I'm sure you recently experienced after writing
your fantastic review of nutrient timing with Brad Schoenfeld,
the simple act of writing and publishing your first manuscript is
incredibly satisfying. Looking back at nearly two years of
thinking, writing and revising to come to this point puts a big
smile on my face and makes it all worth it. Besides that, I would
say this interview is something I'm hugely proud of as it is an
honor to be in the AARR.
Thanks, Eric! Its definitely an honor to have you contribute,
for both myself and the AARR readership. Can you tell me
how the peer review process went for this paper? I'm going
to take a wild guess that you didn't have too much battling to
do with the reviewers.
The peer review process was incredibly important and beneficial
for this paper. Some talk of the horrors of peer review and how it
can go wrong, often rightfully so, but in this case the process
was grueling but incredibly positive. I had two reviewers and an
editor who all acknowledged the importance of this review.
There was consensus that it needed to be published as it
reviewed an understudied area, challenged existing beliefs, and
was important for practice, education, and research. So, while
the reviewers had plenty of critique, it was with the intention of
getting it ready for publication.
Another challenging aspect of a review is getting the data you

need! To properly do a review you often need not only the full
text of a study, but often parts of the data that wasn't included in
its published form. To get the fat free mass and body fat
percentage data delineated by gender from each study, I had to
contact the authors of the six papers I reviewed and some
One reviewer felt quite strongly that protein intake needed to be

dictated based on fat free mass rather than total body mass. The
reviewer used my own logic to convince me that this was the
way to go. In the review I pointed out that protein needs are
likely proportionate to fat free mass and that the vast majority of
protein research during hypocaloric periods has been done on
obese and overweight populations. Thus, existing protein
guidelines based on total body mass are inherently skewed. So
the reviewer challenged me to break the trend, and reanalyze the
data based on fat free mass. So, I went back and analyzed the
protein intake in each study as grams per kilogram of fat free
mass. This allowed me to make a more definitive, evidencebased recommendation rather than just piggy-backing on Phillips
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Page 16
and Van Loon's (2011) recommendation of 1.8-2.7g/kg of total

body mass for athletes during hypocaloric periods as I had
initially.
The second reviewer wanted this review to become a systematic
review. The reviewer felt that the information was too cluttered,
and that the logic-train would be better supported in this format.
It was incredibly difficult to retroactively transform a narrative
review into a systematic. Luckily, when it came down to it, I did
do "a systematic review" of the literature initially (even if it was
circuitous and unorganized); so this transformation was actually
possible.
However, to make the full transformation I had to develop a
qualitative rating scale to judge each study, and myself and a
coauthor had to independently rate each study and then reach a
consensus when we disagreed. We had to impute and back
calculate statistics to make the forest plot as I mentioned earlier.
I had to retrace the steps of my database search to provide the
exact search string that provided the included studies and
provide a flow chart of how we located, included and excluded
each study, and finally I had to change the format of the paper.
My original sub topics that I started with had to become
introduction, methods, results, and conclusions sections. When
the dust cleared after two rounds of revisions, I had a finished
product that was substantially better than when it was initially
submitted. But boy did it transform.
How would you suggest the readers 'run with' the
information presented in your review? In other words, do
you consider it more of a contemplative piece given data
that's not definitive, or more of an actionable piece for
putting the conclusions to practice?
The research has limitations (as all research does) and therefore
the review is not perfect nor completely definitive (and few
reviews are). I sincerely hope that subsequent reviews and
studies down the line bridge gaps, fill in holes and bring more
clarity and context to the research question. However, in the end
I think this is an actionable review that provides sound,
evidence-based guidelines for coaches, nutritionists and athletes
to put into practice.
Could you give us a glimpse into your own primary research
on protein needs of athletic subjects in a deficit, and what
sort of illuminating results you observed?
I have to be careful going into too much detail in this area
because I have submitted this research for publication and it is
currently in review. If I make the full results public the journal
won't be interested in publishing my work. That said, let me
share what I can.
I studied lean, resistance trained males during substantial caloric
restriction and observed changes over two 2-week periods in
maximal strength, body composition, athlete specific stress and
mood state. However, I did what no other study has yet done, I
matched carbohydrate intake and calorie intake, and had one
group follow a moderately high protein intake while the other
followed a high protein intake. Essentially, I probed the lower

and upper thresholds of the range I recommended in my review.
I found that more fat free mass was retained in the higher protein
group, but the amount was trivial in magnitude. Had the trial
been longer this may have reached a more practically
meaningful level, but I can only speculate. Strength overall
showed a neutral mean effect in response to the intervention, but
there was a substantial amount of individual variation and some
folks seemed to particularly have issues with the higher protein
diet which I think was due to it skirting the lower limits
of acceptable fat intakes for some participants (there are
mechanisms by which this could degrade resistance training).
More intriguing was the clear outcome that the higher protein
group maintained lower levels of athlete specific stress, fatigue,
and mood disturbance and had less diet dissatisfaction compared
to the moderately high protein group. We know from studies on
overtraining that psychological stress is typically the first sign
that appears before things start to go downhill physiologically.
So, this is a pretty important finding, it also has implications
about adherence during longer diets. That said, really we need
more research on longer term caloric restriction, but that is really
hard to do.
Last question any other projects or irons in the fire you
want to mention?
Quite a few actually. Besides the study I just mentioned that is in
review, I have written and submitted two other reviews for
publication. Both are reviews designed to provide evidence
based recommendations for natural bodybuilding contest
preparation; one for nutrition, one for training. You may have
heard of one of my co authors, I believe his name is Adam
Aragorn or something like that? No but in all seriousness, I am
really stoked about the manuscripts we've written together along
with Peter Fitschen and Professor John Cronin. I think these two
reviews synthesize research on the topic of bodybuilding like no
other papers have in history.
____________________________________________________
A trainer since 2002, Eric Helms co-owns 3D Muscle Journey LLC, a
consulting business for drug-free physique and strength athletes.
He researches nutrition and exercise and has published with the
National Strength and Conditioning Association and International
Journal of Sports Nutrition and Exercise Metabolism. An athlete
himself, he holds professional status with the Professional Natural
Bodybuilding Association and competes internationally in raw
powerlifting. He holds two masters degrees in exercise science and
sports nutrition, respectively, certifications in strength and
conditioning, nutrition, and personal training, and he is pursuing his
PhD in strength and conditioning at AUT University in New Zealand.
http://www.3dmusclejourney.com/
http://www.youtube.com/team3dmj
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Page 17
Researchers are not renowned for their writing eloquence.

Illustrating this, I might have found the longest sentence ever
printed in the peer-reviewed scientific literature, thanks to
Knudsen and Poulsen:*
The authors consider on this basis that the 90-day, rodent
feeding study with one high dose level and a dietary design
based upon compositional data on the GM food and toxicity data
on the gene product is sensitive and specific enough to verify the
presence/absence of the biological/nutritional/toxicological
effects of the novel gene insert and further by the use of spiking
able to separate potentially unintended effects of the novel gene
product from other unintended effects at the level of intake
defined in the test and within the remit of the test.
*Knudsen I, Poulsen M. Comparative safety testing of genetically
modified foods in a 90-day rat feeding study design allowing the
distinction between primary and secondary effects of the new genetic
event. Regul Toxicol Pharmacol. 2007 Oct;49(1):53-62. [PubMed]
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.
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12 Vemma a fairy tale of hope, a reality of nope.

The neurophysiology of human appetite.

Interval training in the fed or fasted state improves

Metabolic effects of milk protein intake strongly

Undenatured type II collagen (UC-II(R)) for joint

10 Resistance training reduces fasted- and fed-state

Alan Aragons Research Review October 2013

The neurophysiology of human appetite.

see in lower species is analogous to whats underneath all those

Image source: http://www.nibb.ac.jp/brish/Gallery/cortexE.html Unrelated:

Within the neocortex is a still massive subsection called the

The cerebral evolution that guided the course of our primitive

It wasnt until early 2010 that human brain imaging revealed a

Alan Aragons Research Review October 2013

The prefrontal cortex (PFC), behavior and food

Dopamine and appetite

The other side predicts, expectedly, that if dopamine sensitivity

Although I alluded to its role a few paragraphs ago, we still

Larger/complete diagram here:

Palatability, that taste preference we established in the first

behavioral conditioning can be the antidote to memory input

So, knowing (a) a normal dopamine response to food

Dopamine itself motivates reward-seeking, sometimes in the

Next, lets take leptin, which would presumably have an

This is where I want to leave you to formulate your own

Alan Aragons Research Review October 2013

In contrast, if you look at the proportion of people who are

Volkow ND, Wang GJ, Baler RD. Reward, dopamine and

12. Roesch MR, Olson CR. Impact of expected reward on

Alan Aragons Research Review October 2013

Andy Abbate graduated pre-medical from Boston College in 2013 with

Interval training in the fed or fasted state improves

since the subjects used were untrained/obese. Another limitation

The main finding was a lack of significant difference between

The authors acknowledged two limitations the absence of a

Something that might be easy to overlook (but that the authors

Alan Aragons Research Review October 2013

Metabolic effects of milk protein intake strongly

and Dhaliwal compared the 12-week effects of either whey,

The above excerpt appears in the introductory paragraph of the

Reference #37 in Melnik et als paper is cited twice in attempt to

Alan Aragons Research Review October 2013

Melnik et al close their paper by blaming milk protein for

epidemiological data to support a link to prostate cancer and

In addition to the latter research, Huncharek et al pooled the data

illustrate how observational data must be viewed as merely

On the note of foods and cancer risk, a very amusing satirical

For most cancers, associations between cancer risk and intake

By the same logic Melnik et al employ to blame milk protein for

Undenatured type II collagen (UC-II(R)) for joint

prevalence of both diseases. If consistently demonstrated as

The main findings were that UC-II significantly improved knee

Alan Aragons Research Review October 2013

Resistance training reduces fasted- and fed-state

subjects. A final limitation would be the lack of a comparison

The main findings were three-fold. First the expected set of

The authors acknowledge that measuring leucine turnover

Alan Aragons Research Review October 2013

Macpherson RE, Hazell TJ, Olver TD, Paterson DH, Lemon

Alan Aragons Research Review October 2013

Vemma a fairy tale of hope, a reality of nope.

Intro & background

directly above takes up almost all of the space on Vemmas

Like many modern MLMs, Vemmas product line is focused on