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Acheson KJ, Schutz Y, Bessard T, Anantharaman K, Flatt

JP, Jquier E. Am J Clin Nutr. 1988 Aug;48(2):240-7.


[PubMed]

13 How to set weight loss goals that work [part 2].


By Armi Legge

16 Is being evidence-based an abused concept in


the fitness industry?
Copyright July 1st, 2014 by Alan Aragon
Home: www.alanaragon.com/researchreview
Correspondence: aarrsupport@gmail.com

By Alan Aragon

The Walking Dead: GM food hysteria and the


naturalistic fallacy.
By Mike Israetel, PhD

Poor posture is not likely causing you pain.


By Steinar Ekren

Low carbohydrate versus isoenergetic balanced


diets for reducing weight and cardiovascular risk:
a systematic review and meta-analysis.
Naude CE, Schoonees A, Senekal M, Young T, Garner P4,
Volmink J. PLoS One. 2014 Jul 9;9(7):e100652. [PubMed]

Protein supplementation with low fat meat after


resistance training: effects on body composition
and strength.
Negro M, Vandoni M, Ottobrini S, Codrons E, Correale L,
Buonocore D, Marzatico F. Nutrients. 2014 Aug
4;6(8):3040-9. [PubMed]

Effect of timing of protein and carbohydrate intake


after resistance exercise on nitrogen balance in
trained and untrained young men.
Mori H. Physiol Anthropol. 2014 Aug 6;33(1):24. [Epub
ahead of print] [PubMed]

11 Glycogen storage capacity and de novo


lipogenesis
during
masive
carbohydrate
overfeeding in man.
Alan Aragons Research Review July 2014

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Page 1

The Walking Dead: GM food hysteria and the


naturalistic fallacy.
By Mike Israetel, PhD
____________________________________________________
Intro: Zombie Nation
Im not gonna lie, zombie movies scare the crap out of me. I
watched Dawn of the Dead (the newer one) and didnt sleep for
a week. I have yet to see World War Z, and probably never will
because Im too big of a wuss. The thought of the undead
coming back to life after being repeatedly killed and the thought
of a hopeless battle against them are just a bit too much for the
faint of heart, I guess.
Luckily, zombies are an entirely fictional entitynothing like
them exists in real life. Well, almost, as the trend with anti-GM
food (food manufactured with the use of genetically modified
organisms) seems to be quite zombie-like. In much the same
way that zombies simply stand up and continue advancing after
being presumed dead, the anti-GM food movement continues to
be revitalized year after year, claiming the lack of safety and
healthiness of GM foods despite a daunting amount of evidence
against their cause. How does a movement like this keep coming
back even after the strongest scientific offensives seem
victorious? Lets take a look, starting with the basics first; is the
evidence really that strong against the anti-GM food position,
and is the evidence against GM foods really that weak?
Before getting into the evidence, a couple of caveats are in order:
a) The anti-GM food movement I am arguing against is NOT
the group of people that demand thorough and rational food
testing and confirmation of safety for ALL new and exotic food
products, including GM foods. I am wholly in support of such
testing, and believe that it should be quite stringent. However,
when you have people claiming that GM foods are not proven
safe in the long term (on principle of being GM) while many
studies of such foods are 20 years and older, were not dealing
with a rational demand for sane food testing any longer. It is this
latter group which Im seeking to debunk.
b) GM foods and agribusiness are NOT the same thing. Im not
arguing for or against Monsanto or any other large agricultural
corporation. Im arguing about GM foods on principle.
Companies of various kinds (including those that produce
wholly non-GM products) have various kinds of ethical and
procedural records, and should be judged accordingly. Lumping
them in with the GM foods issue is not intellectually honest.
Because Monsanto is NOT an argument.
Well then, lets get into the fun How do the claims of the antiGM food movement stack up against the evidence? Well take a
look at three different views here (though they are not the only
views that can be taken):
1) The examination of anti-GM food claims via the scientific
(peer review) process.
2) The examination of claims of conspiracy against the truth
in regards to GM safety.
Alan Aragons Research Review July 2014

3) The examination of the claims that GM foods are somehow


at their core more potentially dangerous than natural
foods.
The merits of GM hysteria:
1) Baseless via peer review
This section wont be very long at all. Why not? Because the
empirical case against the safety and health of GM foods is
practically non-existent. As a matter of fact, literature review
upon literature review shows that GM foods are some of the
safest engineered food products manufactured to-date.1-7
Not only do all of the major reviews suggest overwhelming
evidence for the health and safety of GM foods, these reviews
are conducted by numerous independent scientific bodies, many
of which originate from various countries and world regions.
Were not talking about a single approval paper by the U.S.
FDAwere talking about the FDA equivalents of dozens of
countries (even the whole European Union) confirming the lack
of evidence for the safety concerns proposed for GM foods. To
make matters even more one-sided, some of the studies
conducted are on the verge of being 30 years long, still showing
no long-term damage of any kind from GM food consumption.
If you read the FAQs of some of the more savvy anti-GM
organizations, they sound quite a bit more reserved in their
critiques of GM food research, using terms like may potentially
be dangerous to replace more aggressive language used in past
years and decades. This is a very good sign, as it reflects that at
least the less radical segments of the anti-GM food movement
have resigned to argue in ways other than via the peer review
process. And that brings us to our next point...
2) Baseless via conspiracy
If you cant win the argument against GM foods in the arena of
academic peer review and strictly controlled studies, then the
tactic of burning the whole arena down may present itself as
desirable. The anti-GM food conspiracy movement does just
that, with an unsettling amount of success in reaching out to the
lay public.
For a long time, the anti-GM food movement has consistently
tried to paint the entire peer review process as corrupt. The most
common allegation is that the same people who oversee large
regulatory bodies that conduct the studies are former lobbyists
for big agribusiness companies, and that even the smaller
research projects are often mostly funded by agribusiness. This
is of course thought to imply that the majority (if not nearly all)
of the peer-reviewed research on the matter is not to be taken
seriously, and is largely a veil for the wrongdoings of
corporations who can pay off anyone they please.
Interestingly, many of the above allegations are in fact true to
some extent. YES, agribusiness does fund a lot of the research
on GM food safety. YES, some regulatory bodies have panel
members that are quite cozy with industry executives. These are
certainly areas of potential concern to watch. However, there are
two incredibly giant hurdles of fundamentality that have not yet
been jumped over by anti-GM food activists in regard to the
issue of conspiracy:
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Page 2

a) The first and likely biggest problem for the pro-conspiracy


view is that there is a uniformity of research conclusions,
irrespective of investigation agency funding or paneling. That is,
labs and panels that are NOT funded or associated with
agribusiness or other pro-GM interests find largely the same
thing that more suspiciously funded labs and agencies do: that
GM foods are so far safe and healthy for human consumption. It
would indeed be a very curious finding if pro-GM labs found
GM foods to be very safe and neutral or even anti-GM labs
found them to have consistently serious dangers. Sort of like Iran
denying nuclear testing while every single other national nuclear
agency disagrees. But this is not even remotely the case with
GM foods, which is a big problem for the conspiracy view.
b) The second-biggest problem for the conspiracy view is that,
well...theres no evidence for the conspiracy! When the Soviet
Union and the West were waging a cold war against each other
for more than 40 years, there was plenty of conspiracy from both
sides in influencing the governments of neutral nations. And,
much as would be expected, the evidence for such conspiracy is
quite impressive. Records of central intelligence agencies
spying, threatening, poisoning, manipulating, infiltrating, and
well, you name itall the fun things required to sway people in
a certain political direction. Thats a lot of work, and leaves
quite the trail even if incredible efforts to retain secrecy are
taken. On the other hand, solid evidence of a pro-GM conspiracy
is almost entirely lacking. Aside from a couple of questionable
incidents here and there, the real evidence for a pro-GM
conspiracy is just not there. And before you say well thats the
why its a conspiracy!! we must be careful. If the evidence is
not there, HOW do people know that bribery and data
falsification is occurring? Are they making it up simply because
they believe it likely?
We mustnt forget that even a small conspiracy is incredibly
difficult to pull off. In a free society, getting several people to do
what they dont want is VERY difficult, while getting the
members of many national agricultural governing bodies to
perform a massive top-down cover up is almost impossible. The
NSA cant keep their own employees from talking, but somehow
Monsanto literally owns the entire scientific communitythe
medals, honors, awards and adorations for heroism of the
scientists to come out against the conspiracy is somehow not
incentive enough in this case. Scientists in Soviet Russia
managed to defect and spill secrets (the punishment for which
was death, if not worse), but for some reason Monsanto or some
secret cabal of agribusinesses has managed to keep over 100
independent scientific bodies in line without even a KGB to help
them out. Now, is this possible? YES. Whats the evidence for
it? Terrible. And until the evidence for conspiracy starts to look
like the Iran vs. The World nuclear arms debate, Im going to
leave the conspiracy for the guys in tinfoil hats.

the philosophical perspective? Doesnt the artificial process of


genetic modification of organisms by itself imply a higher risk to
consumers of such foods? Arent natural foods safer by default?
It turns out that this is indeed not the case.
Firstly, there is NO REASON to think that more natural (in
this case understood to mean incrementally less modified by
humans) foods are somehow healthier or safer than less
natural foods. Nature may be our mother, but shes a cruel step
parent at best if that analogy holds. The plants and animals we
eat for our survival are just themselves trying to survive, and
care not an iota about human health and safety. They are
designed to survive themselves, and not to somehow serve and
protect humankind. That leaf or berry can as easily be poisonous
as it can be nutritious.
Humans have been co-evolving with certain food sources for
quite a while, so the argument can be made that our physiology
is used to the consumption of those food sources (cows, lettuce,
etc) and thus harm is less likely. Thats a fine argument to
make (though much of the reason those products are as
nutritious as they are stems from artificial selection which is
itself genetic modification), but such an argument must then be
taken to its rational implications; for example that Caucasians
should be VERY WEARY of consuming acai berries, since none
of our ancestors ever evolved in proximity with them. Ive not
yet heard a single anti-GM food proponent make that argument.
Secondly, there seems to be no fundamental difference in the
END RESULT of food that has been artificially selected (bred)
vs. food that has been genetically spliced in the laboratory.
Whatever the method of gene transplant between organisms, the
final result is in a biological way no different between
modalities. Whether completely natural vs. artificially selected
vs. laboratory spliced, the ONLY result of a GM modification of
foods is the appearance of several new genes in the new food.
These genes code for specific proteins, which then have their
own effects on human physiology, or interact with other food
proteins to express their effects. Its the same result no matter
the route. As a matter of fact, when eating a completely natural
exotic fruit, youre exposing your body to potentially hundreds
of new proteins! If eating artificially selected (farm bred) fruits,
youre exposing yourself to perhaps dozens of new proteins.
However, if youre consuming GM foods, then many times only
ONE new protein or at most several proteins are present. These
proteins have been extensively tested for their effects in both
isolation and integration with the whole food. Given all that, for
some reason the GM foods are the scary onesand I just dont
get it.

So, the evidence for the purported risks of GM foods is lacking,


and the possibility that a conspiracy to alter the state of the
scientific community is the cause of this lack isalso
lackingboth in a big way. If the evidence is just not strong that
GM foods cause a special need for concern, what about taking

Thirdly, when we are comparing two foods for their health and
safety, which one would you rather eat: an exotic new amazon
fruit, as yet only consumed by indigenous peoples, or a food
item which has been meticulously designed by the best food
scientists and tested into absurdity for its nearly universal health
and safety for multiple species of animals, including humans?
Why would we be less suspicious of something cobbled together
by natural processes without a speck of care for the survival of
humans than a food product that was carefully modified and
tested? Oftentimes, the philosophical argument of the anti-GM
food movement rests on well, do you REALLY want to eat a

Alan Aragons Research Review July 2014

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3) Baseless via philosophy

Page 3

food designed in a lab? Well, yesactually I would and I dont


see whats so baffling about that.
Why wouldnt we prefer something so thoughtfully engineered?
When you get sick, you dont go out and eat random grasses but
rather get a prescription for lab-designed medicine. Is food any
different? Careful of your answer If the first thoughts that pop
into your head when you read lab designed food are Bruce
Banner, the X-men, and other such genetic labs gone wrong
tales, perhaps a step back must be taken and a deeper, almost
universal human tendency needs examination. That tendency is
the proclivity of humans to prefer natural over artificial on
principle, otherwise known as the naturalistic fallacy. This
tendency runs VERY deeply in many people, and seems to be
the main culprit behind the brunt of the anti-GM food
movement.
An old and tired foe: the primary factor for GM hysteria
Different zombie tales propose different explanations for why
zombies get back up after their apparent death. A curse, a virus,
or an alien organism seem to be Hollywoods top choices. For
the anti-GM food movement, the elixir of endless life seems
likely to be the naturalistic fallacy itself.
The naturalistic fallacy (or argument from nature, if we want to
get really technical) is the idea that IF something is natural,
THEN it must be good. In the realm of GM foods, the logic is
that IF a food is more natural, THEN it must be better than a GM
alternative. This fallacy also expresses itself in the prominent
disgust many people have towards even the idea of laboratory
engineering of food.
If you look at the anti-GM food movement without the bias of
the naturalistic fallacy, the pro-GM argument begins to look so
one-sided as to resemble the debate on the historical actuality of
the moon landing. Just going on evidence would lead us to the
conclusion that while demanding ever-continued testing is
desirable, GM foods are in no way prima facie to be considered
more dangerous or less healthy than more natural foods. When
all of the wrapping paper comes off, it is precisely the
naturalistic fallacy that keeps the majority of the anti-GM food
movement afloat.
The problem with the naturalistic fallacy is that, wellits a
fallacy! Its simply not true, and blinds the adherents from
seeing a clearer picture of the world. The more we can get away
from entertaining this fallacy (which means we must be more
vigilant in exposing it when it arises), the more rational and
proactive our discourse on many issues will become, the least
important of which is certainly not GM foods.
Conclusion: the path towards clearer thought
Technological progress is amazing and awesome in just about
every way. Over the centuries, technology has allowed us to live
fuller, longer, less painful, and more fulfilling lives. Future
developments in medical, agricultural, materials, and computer
technology promise almost unimaginable benefits, quite similar
to how unimagined our current technological benefits were to
past generations.
Alan Aragons Research Review July 2014

However, like all progress, the technological kind comes with its
share of potential risks, pitfalls, and dangers. There are
legitimate dangers in adopting nanomaterials, artificial
intelligence, and GM foods. These potential dangers and pitfalls
must be carefully studied and great efforts must be made to
avoid them. However, if the naturalistic fallacy continues to
keep us occupied with imagined problems, we risk missing the
real ones. Lets let the zombies finally rest in peaceso that we
can focus on THE IMPENDING WAR AGAINST THE
MACHINES!!! FEAR YOUR TOASTER! NO ONE IS
SAFE!!!!
;)
Thanks for reading.
___________________________________________________
Mike Israetel is an assistant professor of
exercise science at the University of Central
Missouri. Born in Moscow, Russia, Mike earned
his PhD in Sport Physiology at East Tennessee
State University, where he also served as a
strength coach and sport scientist to Division I
Athletes as well as the head sport nutrition
consultant to the US Olympic Training Site in
Johnson City, TN. Michael's educational
background complements his experiences
as a competitive powerlifter and bodybuilder.
While focusing primarily on his full-time job of teaching and research in the
academic world, Mike is the head science consultant to Renaissance
Periodization and works with some athletes directly to help them with their
strength and body composition goals. http://renaissanceperiodization.com/

____________________________________________________
References
1.

2.
3.
4.
5.

6.
7.

American Association for the Advancement of Science


(AAAS), Board of Directors (2012). Legally Mandating
GM Food Labels Could Mislead and Falsely Alarm
Consumers. [AAAS]
A decade of EU-funded GMO research (2001-2010) (PDF).
Directorate-General for Research and Innovation.
Biotechnologies, Agriculture, Food. European Union. 2010.
Ronald, Pamela (2011). "Plant Genetics, Sustainable
Agriculture and Global Food Security". Genetics 188 (1):
1120. [PubMed]
American Medical Association (2012). Report 2 of the
Council on Science and Public Health: Labeling of
Bioengineered Foods.
United States Institute of Medicine and National Research
Council (2004). Safety of Genetically Engineered Foods:
Approaches to Assessing Unintended Health Effects.
National Academies Press. Free full-text. National
Academies Press. pp R9-10. [NAP]
Key S, Ma JK, Drake PM (June 2008). "Genetically
modified plants and human health". Journal of the Royal
Society of Medicine 101 (6): 2908. [PubMed]
Nicolia A, et al (March 2014). An overview of the last 10
years of genetically engineered crop safety research.
Critical Reviews of Biotechnology 34(1):77-88. [PubMed]

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Page 4

Poor posture is not likely causing you pain.


By Steinar Ekren
________________________________________________
Legions of personal trainers and physical therapists are doing
posture screenings nowadays to see if their clients deviate from
the perfect posture only observed with the Kings Guard. This is
usually done under the presumption that bad posture will lead to
pain.
Are you sure about that? Even skilled, formally trained
practitioners who screen people can be inaccurate in visually
assessing their clients postures. For example, Fedorak et al
found poor inter-rater reliability of visual assessment of cervical
& lumbar lordosis among a diverse sample of clinicians
(orthopedic surgeons, physical therapists, chiropractors,
physiatrists, and rheumatologists).1 Maybe an improper
posture does not matter at all? Its possible that youre wasting
a lot of money and time since a considerable body of evidence
casts doubt upon the idea that bad posture leads to pain. 2-5

Ask a person with poor posture if they can go into a perfect


posture. In most cases they can. This is because your posture is
controlled by your brain and nervous system and is an adaption
to the conditions you live under. If youre sitting at your work
desk with a kyphotic posture every day youre most likely going
to develop a bad posture. Does it make sense to you that
natural adaptions to the environment will automatically lead to
pain? No way!
What about people that do feel pain and do have a bad posture?
In many cases, it seems its the other way around; your pain is
causing the bad posture.6 Some people want a good posture for
aesthetics and thats okay of course. Doing exercises for proper
posture for 10 minutes a day when youre sitting 8 hours a day
in the same old bad posture is probably not gonna do the trick.
If a person wishes to improve posture its probably better to
constantly keep that posture until its a subconscious act.
Keep in mind that static posture is not the same as dynamic
posture. That means just because you look like a hunchback, it
doesnt mean you cant do a perfect squat or deadlift. The idea
that poor posture will automatically lead to pain is about as
absurd as saying that an asymmetric pelvis making your left leg
2mm longer than the other is going to lead to pain. Research has
not shown a consistent association of leg-length inequality with
pain at the greater trochanter7 or low back.8 Furthermore, tight
hamstring or psoas muscles failed to correlate with current back
pain or incidence of back pain.9
Interestingly, having a strong core might not reliably prevent
back pain down the road. Illustrating this, Helewa et al found no
significant differences in low back pain as a result of abdominal
strength exercise combined with back education versus back
education alone.10 However, the investigators advised caution
toward these results since they could have been confouded by
noncompliance to the exercise program. If you wish to do some
form of prehab, the best ways seem to be exercise/movement.
This recommendation also holds true with the management of
chronic low back pain, as reported in a systematic review by
Liddle et al.11 In addition, be sure to maintain proper technique,
a reasonable degree of training variation, and good
health/nutritional status.

Upper- and Lower Crossed Syndrome have been defined as two


conditions where you dont have perfect posture, but short and
tight muscles and long and inhibited muscles. I think thats a
weird description considering muscles cant get longer or shorter
since they are anchored in bone or soft tissue via tendons. The
conditions are more an attempt at placing people into categories
than an actual diagnosis. If you have been told you have one of
these, you can relax. Theres virtually no chance it will lead to
pain just because you have slightly more anterior tilt in your
pelvis than the person doing the posture screening.

In conclusion: posture screenings should not be done as a matter


of standard assessment for clients unless they specifically ask
for it. In that case, describe to them how the research supporting
the relationship between posture and pain is questionable, at
best. Making the hasty leap of telling clients that theres
something wrong with them can actually lead to pain through a
psychogenic phenomenon known as the nocebo effect. This is
essentially the opposite of a placebo effect. A nocebo effect is
when an inert or harmless condition leads to harm via the
subjects false expectations. A recent meta-analysis by Petersen
et al found that the overall moderate to large magnitude of
nocebo effects were similar to those of placebo effects.12 Thus,
practitioners need to be aware of, and minimize nocebo effects
when dealing with patients or clients.
________________________________________________

Alan Aragons Research Review July 2014

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Page 5

Steinar Ekren is personal trainer,


Rehab Trainer, writer, and
lecturer at various fitness-related
courses. His passions are
educating others and himself in
all aspects of the fitness field. He
specializes in pain science and
helping people manage and
eliminate their pain trough
evidence-based methods. Steinar
can be reached via the following:
Email: steinarekrenpt@gmail.com
Facebook: https://www.facebook.com/steinar.a.ekren
Website (under construction as yet): www.steinarekren.com

____________________________________________________
References
1.

Fedorak C, Ashworth N, Marshall J, Paull H. Reliability of the


visual assessment of cervical and lumbar lordosis: how good
are we? Spine (Phila Pa 1976). 2003 Aug 15;28(16):1857-9.
[PubMed]
2. Widhe T. Spine: posture, mobility and pain. A longitudinal
study from childhood to adolescence. Eur Spine J. 2001
Apr;10(2):118-23. [PubMed]
3. Lewis JS, Green A, Wright C. Subacromial impingement
syndrome: the role of posture and muscle imbalance. Shoulder
Elbow Surg. 2005 Jul-Aug;14(4):385-92. [PubMed]
4. Roffey DM, Wai EK, Bishop P, Kwon BK, Dagenais S. Causal
assessment of awkward occupational postures and low back
pain: results of a systematic review. Spine J. 2010
Jan;10(1):89-99. [PubMed]
5. Edmondston SJ, Chan HY, Ngai GC, Warren ML, Williams
JM, Glennon S, Netto K. Postural neck pain: an investigation
of habitual sitting posture, perception of 'good' posture and
cervicothoracic kinaesthesia. Man Ther. 2007 Nov;12(4):36371 [PubMed]
6. Hirata RP, Ervilha UF, Arendt-Nielsen L, Graven-Nielsen T.
Experimental muscle pain challenges the postural stability
during quiet stance and unexpected posture perturbation. J
Pain. 2011 Aug;12(8):911-9. [PubMed]
7. Segal NA, Harvey W, Felson DT, Yang M, Torner JC, Curtis
JR, Nevitt MC; Multicenter Osteoarthritis Study Group. Leglength inequality is not associated with greater trochanteric
pain syndrome. Arthritis Res Ther. 2008;10(3):R62. [PubMed]
8. Soukka A, Alaranta H, Tallroth K, Helivaara M. Leg-length
inequality in people of working age. The association between
mild inequality and low-back pain is questionable. Spine (Phila
Pa 1976). 1991 Apr;16(4):429-31. [PubMed]
9. Hellsing AL. Tightness of hamstring- and psoas major muscles.
A prospective study of back pain in young men during their
military service. Ups J Med Sci. 1988;93(3):267-76. [PubMed]
10. Helewa A, Goldsmith CH, Lee P, Smythe HA, Forwell L. Does
strengthening the abdominal muscles prevent low back pain--a
randomized
controlled
trial.
J
Rheumatol.
1999
Aug;26(8):1808-15. [PubMed]
11. Liddle SD, Gracey JH, Baxter GD. Advice for the management
of low back pain: a systematic review of randomised controlled
trials. Man Ther. 2007 Nov;12(4):310-27. [PubMed]
12. Petersen GL, Finnerup NB, Colloca L, Amanzio M, Price DD,
Jensen TS, Vase L. The magnitude of nocebo effects in pain: A
meta-analysis. Pain. 2014 Aug;155(8):1426-1434. [PubMed]
Alan Aragons Research Review July 2014

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Page 6

Low carbohydrate versus isoenergetic balanced diets


for reducing weight and cardiovascular risk: a
systematic review and meta-analysis.
Naude CE, Schoonees A, Senekal M, Young T, Garner P4,
Volmink J. PLoS One. 2014 Jul 9;9(7):e100652. [PubMed]
BACKGROUND: Some popular weight loss diets restricting
carbohydrates (CHO) claim to be more effective, and have additional
health benefits in preventing cardiovascular disease compared to
balanced weight loss diets. METHODS: We compared the effects of
low CHO and isoenergetic balanced weight loss diets in overweight and
obese adults assessed in randomised controlled trials (minimum followup of 12 weeks), and summarised the effects on weight, as well as
cardiovascular and diabetes risk. Dietary criteria were derived from
existing macronutrient recommendations. We searched Medline,
EMBASE and CENTRAL (19 March 2014). Analysis was stratified by
outcomes at 3-6 months and 1-2 years, and participants with diabetes
were analysed separately. We evaluated dietary adherence and used
GRADE to assess the quality of evidence. We calculated mean
differences (MD) and performed random-effects meta-analysis.
Nineteen trials were included (n=3209); 3 had adequate allocation
concealment. FINDINGS: In non-diabetic participants, our analysis
showed little or no difference in mean weight loss in the two groups at
3-6 months (MD 0.74 kg, 95%CI -1.49 to 0.01 kg; I2=53%; n=1745,
14 trials; moderate quality evidence) and 1-2 years (MD 0.48 kg,
95%CI -1.44 kg to 0.49 kg; I2=12%; n=1025; 7 trials, moderate quality
evidence). Furthermore, little or no difference was detected at 3-6
months and 1-2 years for blood pressure, LDL, HDL and total
cholesterol, triglycerides and fasting blood glucose (>914 participants).
In diabetic participants, findings showed a similar pattern.
CONCLUSIONS: Trials show weight loss in the short-term
irrespective of whether the diet is low CHO or balanced. There is
probably little or no difference in weight loss and changes in
cardiovascular risk factors up to two years of follow-up when
overweight and obese adults, with or without type 2 diabetes, are
randomised to low CHO diets and isoenergetic balanced weight loss
diets. SPONSORSHIP: This review was funded by the Effective
Health Care Research Consortium and the South African Medical
Research Council.

However, at the 12 years, the low-carb diet group showed


better adherence in 3 trials while the balanced diet group showed
better adherence in 5 trials. This led the authors to propose that
diminished compliance is ...more likely in extreme dietary
changes such as drastic restrictions of entire food groups.
A major limitation unaddressed by the authors is that the cutoff
point for classifying a diet as low-carb was too liberal to
satisfy most definitions adopted by the proponents of low-carb
diets. Meeting the low-carb criteria were diets with less than
45% of energy as carbohydrate. This is at odds with the common
proportional definition of a true low-carb diet, where the high
end of intake would be 30% of total energy.1 Its even a further
cry from very-low carb (VLCD), whose upper cutoff point is
20%, and even more disparate from the very-low-carb/ketogenic
diet (VLCKD), which proportionally is about 4-10% of total
energy (<20-50 g/day).2 As such, the primary complaint of lowcarb advocates who read the present study is that the type of diet
they favor was not actually examined. Carbohydrate intake in
the vast majority of low-carb studies in this analysis were well
above VLCD & VLCKD levels (see Table 6), averaging in the
mid-30%s.
Comment/application
The main finding of the present meta-analysis was a lack of
significant difference in weight loss and cardiovascular disease
risk reduction in isoenergetic comparisons of low-carb (<45%
CHO) and balanced diets (45-65% CHO). To reiterate, the
results were confounded by poor adherence, which got worse
with time. Nevertheless, no significant differences in weight loss
were seen at either 3-6 months or 1-2 years. These findings are
similar to those of a recent meta-analysis by Hu et al,3 who
found no significant differences in reductions in body weight
and waist circumference from low-carb ( 45% CHO) versus
low-fat (30% fat) diets in controlled interventions lasting 6
months or more. Importantly, the carbohydrate proportion in the
low-carb diets averaged 23%, which is within the realm of what
most low-carb advocates would consider to be legitimately lowcarb.

As acknowledged by the authors, adherence to both types of


diets was poor, and got worse in the long-term follow-ups. The
lack of adherence to the low-carb diets was objectively indicated
by a very low incidence of urinary ketosis after 6 months. At 3-6
months, 5 trials showed better adherence to the low-carb diets,
while four trials showed better adherence to the balanced diet.

Theres a lot of dogma and selective perception on both sides,


but its particularly strong among low-carb proponents, who tend
to see carbohydrate restriction or minimization as the allencompassing answer to alleviating obesity and cardiovascular
disease risk. The A to Z trial by Gardner et al4 is popularly
cited by low-carbers since it found the Atkins Diet to outperform
the rest of the diets for weight loss at 12 months, and either
matched or beat the other diets (Zone, Ornish, and LEARN) for
improving blood lipid profile and glucose control. However, its
noteworthy that the weight loss differences were not statistically
significant by the trials end. Subsequently, Tay et al5 sought to
tighten up the lack of control of total caloric intake that may
have confounded the A to Z trial. Perhaps not so surprisingly,
under isocaloric conditions, no significant difference in weight
loss were seen between a very-low-carb (4% CHO) and a highcarb (46% CHO) diet over a 6-month period in abdominally
obese subjects. Notably, this lack of weight loss advantage was
seen despite a higher protein intake in the low-carb group.
Effects on blood pressure, CRP, and insulin were similar, but the
low-carb dieters experienced a greater increase in HDL, greater
decrease triglyceride levels, and a highly variable LDL response.
The latter concerned the authors to a degree of stating that the
high-carb diet had more favorable blood lipid effects.

Alan Aragons Research Review July 2014

[Back to Contents]

Study strengths
The authors explicitly listed what they felt were the strengths of
this meta-analysis (especially compared to previous reviews):
Explicit cut-off ranges for macronutrients for treatment and
control diets; the complete macronutrient profile of
intervention diets had to be available.
Only included isoenergetic diet comparisons.
Only included interventions with a diet component alone,
or combined interventions that were similar to prevent
confounding by co-interventions.
Only included randomised controlled trials.
Only included studies with 12 wks or more follow-up; and
outcomes were grouped by defined lengths of follow-up.
Study limitations

Page 7

Protein supplementation with low fat meat after


resistance training: effects on body composition and
strength.
Negro M, Vandoni M, Ottobrini S, Codrons E, Correale L,
Buonocore D, Marzatico F. Nutrients. 2014 Aug 4;6(8):3040-9.
[PubMed]

anabolism (roughly 1.8 g/kg or more). An important but


unaddressed limitation of the study is that total daily protein was
not matched between the treatment and control group. The beef
added 20 g protein above and beyond the control group, which
makes it impossible to know whether the greater total amount or
the timing of the treatment imparted the advantage.

BACKGROUND: Beef is a nutrient-rich, high-quality protein


containing all the essential amino acids in proportions similar to
those found in human skeletal muscle. METHODS: In order to
investigate the efficacy of a beef supplementation strategy on
strength and body composition, we recruited 26 young healthy
adults to participate in a resistance-training program of eight
weeks, based on the use of isotonic machines and free weights at
75% of one repetition maximum. Subjects were randomly
divided into two groups, food group and control group, of 12 and
14 subjects respectively. Food group were supplemented after
resistance training with a 135 g serving of lean beef (tinned
meat), providing 20 g of protein and 1.7 g of fat. No
supplementation was provided to control group. Fat mass, fat
free mass, lean mass, assessed by bioelectrical impedance
analyzer, and muscle strength, assessed by one repetition
maximum test, were evaluated in all subjects both at the
beginning (week 0) and at the end (week 8) of the study. Preand post-training differences were evaluated with paired t-tests
while group differences for each outcome parameter was
evaluated with independent t-tests. RESULTS: At the end of
the study the food group showed a significantly decrease in fat
mass (week 0: 15.0 6.7 kg; week 8: 13.1 7.6 kg; : -1.9 2.9
kg; p < 0.05) and a significantly increase in fat free mass (week
0: 52.8 kg 9.4; week 8: 55.1 kg 10.9; : 2.3 2.5 kg; p <
0.01). No significant differences in lean mass were found in
either food group or control group. No significant differences in
one repetition maximum tests were found between food group
and control group. CONCLUSION: Tinned meat can be
considered a nutrition strategy in addition to other proteins or
amino acid supplements, but as with any other supplementation
strategy, a proper nutrition plan must be coupled.
SPONSORSHIP: None listed.

Comment/application

Study strengths
This study is innovative since its the first to examine the
chronic effect of post-exercise beef on muscle strength &
hypertrophy in subjects undergoing resistance training, whereas
previous research on beef ingestion near training only examined
acute effects on muscle protein synthesis.6,7 All training sessions
were closely monitored to insure that the subjects carried out the
prescribed protocol.
Study limitations

The main findings of the present study were a significant


increase in fat-free mass (FFM) and a significant decrease in fat
mass (FM) in the beef group. Maximal strength increased
significantly in both groups, with no significant between-group
differences.
While the common interpretation of the results is that beef
supplementation had a positive effect on muscle mass, the
authors make an explicit distinction between FFM (all fat-free
bodily tissue) and LM (the muscle component specifically). Fact
of the matter is that there was no statistically significant increase
in LM in either group, through in absolute numbers, the beef
group had a slight increase while the control group had a slight
decrease. In addressing this lack of significant LM increase, the
authors speculate that it may have been due to a low total daily
protein intake, or it could have been due to the slow-digesting
nature of beef, whose essential amino acid availability did not
spike up quickly enough to take advantage of the heightened
sensitivity in the post-exercise period. The authors thus proposed
that in the case of beef, pre-exercise consumption might be the
ticket to special effects. In reference to research by Symons et
al,7 the authors posit the following:
...consuming a slowly digested protein-rich mixed meal 60 min
prior to exercise, may be the physiological equivalent of
ingesting a rapidly digested protein source (e.g., whey protein)
3060 min post-exercise.

The authors acknowledged that the sample size (26 subjects


completed the study) and duration (8 weeks) are potential
limitations. I would add that bioelectrical impedance analysis
(BIA) used to assess body composition has been found to be
useful for assessing groups, but individual assessment lacks
reliability.8 Although software analysis of subjects habitual diet
was done at the outset of the trial, there was no indication that
journaling or analysis was done at subsequent points in order to
assess for consistency. Another limitation was that total daily
protein intake was reported to be approximately 1.0 g/kg, with
the beef treatment bumping this up to about 1.3 g/kg both of
which are below levels known to maximize rates of muscle

Whats clear in the above speculation is that the authors are


stuck on the idea that the post-exercise anabolic window was
missed, thus the LM gains didnt occur. I would offer another
possibility, which is that difference in total protein intake or
spread between groups could possibly have been insufficient
to significantly influence muscle size and strength. To illustrate
my point, Boss and Dixon found that a superior effect of the
higher protein treatment had an average spread of 66.1%
g/kg/day.9 In contrast, the present study had a spread of roughly
28%. And once again, dietary control in this design was minimal
to begin with, so its difficult to place a high degree of
confidence in the outcomes. Add to this the error potential of
BIA, and questions are left lingering.

Alan Aragons Research Review July 2014

[Back to Contents]

Page 8

Effect of timing of protein and carbohydrate intake


after resistance exercise on nitrogen balance in
trained and untrained young men.
Mori H. Physiol Anthropol. 2014 Aug 6;33(1):24. [Epub ahead
of print] [PubMed]
BACKGROUND: Resistance exercise alters the post-exercise
response of anabolic and catabolic hormones. A previous study
indicated that the turnover of muscle protein in trained
individuals is reduced due to alterations in endocrine factors
caused by resistance training, and that muscle protein
accumulation varies between trained and untrained individuals
due to differences in the timing of protein and carbohydrate
intake. We investigated the effect of the timing of protein and
carbohydrate intake after resistance exercise on nitrogen balance
in trained and untrained young men. METHODS: Subjects were
10 trained healthy men (mean age, 23 +/- 4 years; height, 173.8
+/- 3.1 cm; weight, 72.3 +/- 4.3 kg) and 10 untrained healthy
men (mean age, 23 +/- 1 years; height, 171.8 +/- 5.0 cm; weight,
64.5 +/- 5.0 kg). All subjects performed four sets of 8 to 10
repetitions of a resistance exercise (comprising bench press,
shoulder press, triceps pushdown, leg extension, leg press, leg
curl, lat pulldown, rowing, and biceps curl) at 80% onerepetition maximum. After each resistance exercise session,
subjects were randomly divided into two groups with respect to
intake of protein (0.3 g/kg body weight) and carbohydrate (0.8
g/kg body weight) immediately after (P0) or 6 h (P6) after the
session. All subjects were on an experimental diet that met their
individual total energy requirement. We assessed whole-body
protein metabolism by measuring nitrogen balance at P0 and P6
on the last 3 days of exercise training. RESULTS: The nitrogen
balance was significantly lower in the trained men than in the
untrained men at both P0 (P <0.05) and P6 (P <0.01). The
nitrogen balance in trained men was significantly higher at P0
than at P6 (P <0.01), whereas that in the untrained men was not
significantly
different
between
the
two
periods.
CONCLUSION: The timing of protein and carbohydrate intake
after resistance exercise influences nitrogen balance differently
in trained and untrained young men. SPONSORSHIP: None
listed.
Study strengths
This study is novel since it compared protein/carb timing effects
in trained versus untrained subjects. This is an important concept
since trained subjects traditionally exhibit greater resistance to
treatment effects due to their closer proximity to their genetic
potential. Therefore, when significant effects are seen in trained
subjects, it increases the possibility that the treatment has
meaningful effects. Dietary intake was well-controlled during
the experimental periods.

measured after a period of weeks). Nitrogen balance assessment


tends to overestimate intake and underestimate output of
nitrogen, which can lead to falsely positive balances.10
Its important to note that short-term responses to immediate
pre- and/or post-exercise protein feedings, which indeed have
shown positive effects on muscle protein synthesis (MPS), do
not reliably predict long-term muscular adaptations.11 This is
exemplified by the recent meta-analysis on protein timing I did
with Brad Schoenfeld and James Krieger, where no significant
differences in strength or hypertrophy were found between the
consumption of protein (containing at least 6 g EAA) within an
hour of either side of the resistance training bout, versus at least
2 hours away from the training bout.12
Interestingly, 3 out of the 5 protein-matched studies initially
considered for our meta-analysis did not find a significant effect
of timing protein closer to the bout (note that the vast majority of
supposed timing studies do not match total daily protein
between groups). Out of the 23 studies that made it into the
analysis, only 3 studies matched protein between groups, and
thus were true timing studies. 2 of the 3 protein-matched studies
did not find a significant effect of timing protein closer to the
bout. Furthermore, a sub-analysis of the protein-matched studies
did not show a significant effect of timing. Regression analysis
of the 23 studies revealed that a greater total daily protein intake
(mean of 1.66 g/kg in the treatment groups versus 1.33 g/kg in
the controls) rather than timing within the anabolic window
was the primary factor influencing hypertrophy. However, only
2 studies that matched protein involved trained subjects, so there
clearly is a need for more research in this population.
In a more recent example of short-term response failing to
reflect long-term adaptations, Mitchell et al found that muscle
protein synthesis (MPS) rates after the first session of resistance
training and substantial protein-carb ingestion had no
relationship with MRI-measured muscle volume or DXAmeasured lean body mass.13 Similarly, previous work by
Mayhew et al found no significant relationship between mixed
muscle FSR (fractional synthetic rate) and hypertrophy.14 A
limitation worth noting is that the aforementioned studies did not
measure muscle protein breakdown (MPB), which is the other
side of protein turnover that determines net protein balance.
However, Mitchel et al stated that MPS is the main locus of
control and is far more responsive to nutritional and contractile
stimuli in regulating changes in muscle size than MPB.13 This
assertion is partly based on research by Glynn et al,15 who found
that post-exercise MPB did not differ between the ingestion of
20 g EAA plus 30 versus 90 g carbohydrate. MPB accounted for
less than 30% of the improvement in net protein balance, leading
them to conclude that MPB plays only a minor role in the postexercise net anabolic response.
Comment/application

First and foremost, this study examined short-term effects on


whole-body protein status via nitrogen balance. It did not
measure muscle-specific protein balance, nor did it measure
muscle hypertrophy or strength effects (which can only be

This study found that trained subjects had a significantly lower


nitrogen balance (suggesting better protein retention) than
untrained subjects in both the immediate post-exercise
supplementation condition (P0) and in the 6-hour delayed
condition (P6). Perhaps most importantly, nitrogen balance in
the trained group was significantly higher at P0 than at P6. No

Alan Aragons Research Review July 2014

[Back to Contents]

Study limitations

Page 9

significant difference in nitrogen balance at P0 & P6 was seen in


the untrained group.

has limited relevance to the populations most likely to aim for


optimizing muscle hypertrophy through timing tactics.

Upon initial perusal of this study (in the provisional version


thats not fully formatted), I hastily assumed that a 6-hour lag
was compared with immediate nutrient consumption. However,
a closer look at the study timeline shows that in both conditions,
lunch was consumed 2 hours after the training bout. So, from
breakfast to the following meal, a 4-hour period (7 am to 11am)
was compared with a 6-hour period (7 am to 1 pm):

On a quick sidenote, some who have read the study closely


noticed that energy intake was higher in the trained subjects
(3170 kcal) than the untrained subjects (2750 kcal). This 420
kcal difference might appear to be an unfair advantage for the
trained subjects, but this is accounted for by their significantly
higher mean bodyweight than the untrained subjects (72.3 kg vs
64.4 kg). When prescribing energy intake, bodyweight is one of
the fundamental determinants. The higher the bodyweight, the
higher the maintenance intake requirement.

A 4-hour peri-workout period (the timespan between the pre-and


post-exercise meal) is relatively common. However, while a 6hour peri-workout period is not necessarily a unicorn scenario,
in my observations, its quite rare, especially with trainees
whose primary goal is to gain size and/or strength. These
individuals rarely experience 6-hour lapses between meals due
to the volume of food they must consume in order to gain weight
(increased meal frequency prevents the necessity to force down
huge meals).
Notably, protein content in the lunch meals were 32.1 g in the
trained group and 29.1 g in the untrained group. This is
sufficient to elicit a robust MPS response. Based on the results,
its tempting to conclude that trained subjects have a narrower
window of opportunity for post-exercise nutrient dosing to
maximize the anabolic response. However, a subtle but
potentially important detail was that although both trained and
untrained subjects consumed protein at 1.5 g/kg, untrained
subjects had a higher percentage of fat mass and lower
percentage of lean mass. So, in terms of protein intake per unit
of lean mass, more was consumed by the untrained subjects (1.8
g/kg LBM vs 1.7 g/kg LBM). This difference could have at least
partially explained the better nitrogen retention in the untrained
subjects.
Along these lines, an important principle to bear in mind is that
the higher the daily total protein intake, the less of an impact that
specific timing of its constituent doses has on muscular
adaptations to training. Athletes whose primary aims are size
and strength typically consume substantially more protein than
the 1.5 g/kg prescribed in the present study. For example,
Lowery et al found that protein-seeking strength trainers
reported an intake of 2.5 g/kg.16 Chen et al reported that elite
athletes in a variety of sports all consumed more than 2 g/kg, and
among them, weightlifters and swimmers consumeed more than
3 g/kg.17 In another example, Kim et al studied the dietary habits
and nutritional status of elite Korean bodybuilders, who reported
an intake of 4.3 g/kg.18 Therefore, a protein intake of 1.5 g/kg
Alan Aragons Research Review July 2014

Once again, Id emphasize that despite the intriguing outcomes


seen in this study, its still short-term data. The body of chronic
studies at-large casts doubt upon the efficacy of timing nutrients
near training for increasing strength and/or hypertrophy.
Regarding chronic studies using trained subjects, perhaps the
strongest support for timing nutrients near the training bout is a
2006 study by Cribb & Hayes,19 who found that found that
timing a supplement consisting of 40 g protein, 43 g
carbohydrate, and 7 g creatine immediately pre- and postexercise resulted in greater size and strength gains than
positioning the supplement doses away from the training bout.
Now, heres something plenty of people either miss or purposely
ignore. A chronic study involving resistance-trained subjects
done after Cribb & Hayes study did not replicate its findings.
Hoffman et al20 found no significant changes in body
composition or between-group differences in strength gain when
comparing immediate pre- and post-exercise supplementation
(containing 42 g protein) with the supplement placed away from
each side of the training bout. This lack of effect was attributed
to a sufficient total daily protein consumption combined with an
advanced lifting status.
Ultimately, what we have is a body of inconclusive evidence
regarding the effectiveness of timing nutrients (most
importantly, protein) as close to the training bout as possible.
My colleagues and I will continue to chip away at this grey area
with further research. In the meantime, Ill end off with the
practical recommendations outlined by myself and Brad
Schoenfeld, which establish strong safeguards against missing
the window, but also allow flexibility:11
Due to the transient anabolic impact of a protein-rich meal
and its potential synergy with the trained state, pre- and postexercise meals should not be separated by more than
approximately 34 hours, given a typical resistance training
bout lasting 4590 minutes. If protein is delivered within
particularly large mixed-meals (which are inherently more
anticatabolic), a case can be made for lengthening the interval
to 56 hours. This strategy covers the hypothetical timing
benefits while allowing significant flexibility in the length of the
feeding windows before and after training.

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Page 10

Glycogen storage capacity and de novo lipogenesis


during masive carbohydrate overfeeding in man.
Acheson KJ, Schutz Y, Bessard T, Anantharaman K, Flatt JP,
Jquier E. Am J Clin Nutr. 1988 Aug;48(2):240-7. [PubMed]
OBJECTIVE: The metabolic balance method was performed on
three men to investigate the fate of large excesses of carbohydrate.
METHODS: Glycogen stores, which were first depleted by diet (3
days, 8.35 +/- 0.27 MJ [1994 +/- 65 kcal] decreasing to 5.70 +/1.03 MJ [1361 +/- 247 kcal], 15% protein, 75% fat, 10% carb) and
exercise, were repleted during 7 day carbohydrate overfeeding (11%
protein, 3% fat, 86% carb) providing 15.25 +/- 1.10 MJ (3642 +/263 kcal) on the first day, increasing progressively to 20.64 +/- 1.30
MJ (4930 +/- 311 kcal) on the last day of overfeeding. Glycogen
depletion
was
again
accomplished
with
2
days
of carbohydrate restriction (2.52 MJ/day [602 kcal/day], 85%
protein, and 15% fat). RESULTS & CONCLUSIONS: Glycogen
storage capacity in man is approximately 15 g/kg body weight and
can accommodate a gain of approximately 500 g before net lipid
synthesis contributes to increasing body fat mass. When the
glycogen stores are saturated, massive intakes of carbohydrate are
disposed of by high carbohydrate-oxidation rates and substantial de
novo lipid synthesis (150 g lipid/day using approximately 475 g
CHO/day)
without
postabsorptive
hyperglycemia.
SPONSORSHIP: Nestl Co, Switzerland.

Study strengths
This was the first study to ever systematically assess the upper
limit of glycogen storage after glycogen depletion and massive
carbohydrate overfeeding in humans. It produced a number of
interesting results that have been valuable to our understanding
of various conditions that affect the accumulation of fat mass.
Diets were prepared by trained dietitians. A respiration chamber
was used to assess energy expenditure. All variables were tightly
controlled. The study protocol is outlined as follows:

circuit indirect calorimetry, including ventilated hood system which are standard and commonly used) rather than design
shortcomings. The results may also be limited to the
composition of the diets. The excess carbohydrate was largely
composed of sugared fruit juices of known uniform
composition and energy content. It would have been interesting
and useful to see an actual sample menu of such an extreme
degree of carbohydrate overfeeding (which gradually increased
from 836 g to 1073 g on days 4 to 10 thats a lot of carbs).
Comment/application

The above diagram elegantly depicts the results. Total


bodyweight decreased by 0.8 kg during the 3-day high-fat/lowcarb phase (69-79 g P, 45-59 g C, 142-171 g F) plus exercise
designed to deplete glycogen. Total bodyweight increased by 4.6
kg by the end of the 7-day high-carb/low-fat phase (114-142 g P,
836-1073 g C, 12-20 g F). 2 days into this phase, mean 24-hour
non-protein respiratory quotient exceeded 1.00, indicating the
start of de novo lipogenesis (DNL), which is the conversion of
dietary carbohydrate into fat. Notably, it was not until glycogen
stores had increased by about 500 g that carbohydrate oxidation
and glycogen storage became insufficient to dispose of all the
dietary carbs, thereby initiating DNL.
During the last 3 days of the high-carb/low-fat phase, DNL
produced an average of 142 g fat per day. The fat produced
specifically via DNL was estimated at 580 g. Overall fat gain by
the end of this phase was 1.1 kg. After 4 days into this phase,
glycogen stores were saturated and had increased by
approximately 770 g. The values of the subjects with the top-3
highest amounts of stored glycogen were 1146, 654, and 629 g,
leading to the conclusion that maximal glycogen storage
capacity in humans is approximately 15 g/kg of bodyweight, and
that DNL can become significant in the case of massive
carbohydrate overfeeding. In this case, DNL was initiated on the
2nd day. Carb intake on day 1 was 836 g, and day 2 was 900 g.

The nature of this study was exploratory, so the limitations were


mainly confined to the error potential inherent within the
instruments (pedometry, portable heart rate monitors, open-

On a relate note, previous research by Acheson et al 21 found that


a single 500 g carbohydrate meal (consisting of bread, jam, and
fruit juice) consumed by healthy young men led to a 346 g gain
in glycogen storage while 133 g carb, 17 g fat, and 29 g protein
were oxidized during the 10 hour post-meal assessment period.
The important finding was that no net fat synthesis occurred
(although fat oxidation was suppressed). Its notable that the
subjects were not glycogen-depleted upon consuming the test
meal, so its likely that they had at least 200 g glycogen stored,
yet DNL still did not occur from the 500 g carb-bomb.

Alan Aragons Research Review July 2014

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Study limitations

Page 11

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Page 12

How to set weight loss goals that work [part 2].


By Armi Legge
____________________________________________________
Set a goal, achieve it.
Some hot, sweaty woman was doing push-ups on the screen
above the squat rack.
The voiceover kept playing the same clichd inspirational
sayings like pain is weakness leaving the body, and if you
dont know where youre going, youll never get there.
Sweaty hot girl started doing sit-ups.
If youre interested in fitness, youre expected to have goals. If
youre a trainer, your clients expect you to lay out a roadmap to
their goal and hold them accountable.
Goals are overrated, especially when it comes to weight loss. As
you learned in the last edition of AARR, goal setting can
sometimes encourage people to think in the short-term, along
with several other problems.1

On average, it took people 66 days to master a new habit. But


there were huge differences in how long it took people to adopt
their chosen habits.
It only took people 20 days to start drinking a glass of water
after breakfast. In other cases, like doing 50 sit-ups after
drinking coffee in the morning, people still hadnt adopted the
habit after the entire 84 days of the study. If they had maintained
the same rate of progress, it would have taken them 254 days to
make the habit automatic.
Dont worry about reminding yourself of your goal on a frequent
basis. In fact, I encourage you to put it in the back of your mind.
That allows you to focus on more important things, which youll
learn about in a moment.
2. Imagine the kind of person who would achieve and
maintain this goal.
Think about the kind of person you want to become. This is
where you get to indulge in your fantasies about being jacked,
lean, strong, or whatever you want.
Then think about the kind of habits that person would use to get
there. What would mister six-pack" do every day?

Setting goals isnt bad, but thats only the first step.
Unfortunately, thats where most people stop, and its part of
they fail.

What would their diet look like?

The following five-step process is, in my view, more effective.

If you want to be 8% body fat, that kind of person is going to be


eating most of their calories from whole foods, training
consistently, and getting enough sleep.

How often are they training?

1. Set a goal.
Write down roughly how much you want to weigh.
If you want to figure out your target weight and how much fat
youd need to lose to reach a certain body fat percentage, read
the August 2011 issue of AARR.

You cant achieve your goals overnight, but you can start
practicing the habits that will help you achieve your goals
immediately. The latter is more important.
3. Pick the most important habit that will help you achieve
this goal.

Unless you have a specific event planned like a race, photoshoot, or bodybuilding competition, dont worry about setting a
deadline. That generally encourages you to rush, and its
unnecessary.

Do you know roughly how much youre eating?

Your goal is just a starting place, and your main job is to master
the habits that will help you accomplish that goal. The problem
is that it takes everyone different amounts of time to adopt a new
habit.

Are you sticking to your sleep schedule every night?

The rule about a habit taking 21 days to form is completely


wrong. That idea was based on one doctors experience working
with limb amputees. He found that, on average, it took them 21
days to adjust to the loss of their limb.2

Need more sleep?

Are you really being as consistent with your training as you


could be?

There will always be more habits you can work on in the future,
so focus on the most important one today. Pick one.

Set an alert on your calendar to go to bed on time every night.


Create a routine before bed, like reading for 30 minutes,
listening to music, or writing in a journal.

In one study, participants were asked to pick a behavior theyd


like to turn into a habit.3 Most of these were health related, like
eat a piece of fruit with lunch.

Use one of these apps to block websites like Facebook after a


certain time.

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Feel like you dont have time for workouts?


Wake up five minutes earlier every day this week, and watch
five minutes less of television in the evenings. If you do that
every day, thats 25 minutes per week, or about two hours extra
per month.
No time to prepare meals?
Block off time on your calendar and treat it like a business
meeting. Give up something less important, like surfing
Facebook or feeding your children. (Just kidding, Facebook is
far too important).
Only focus on one habit at a time. Its fine to put some energy
toward another habit, but you need to put most of your effort
into one.
The big three that most people need to work on are their diet,
exercise, and sleep. In my case, I had the first two covered, but I
wasnt getting enough consistent sleep. So thats what I focused
on.
4. Break your habit into the smallest possible step.
Make it so easy you cant say no. Leo Babauta
We all overestimate our ability to stick to habits.
We tell ourselves that well be active every day, despite the fact
were barely making time to train three times per week right
now.
We tell ourselves well prepare all of our own meals, despite
eating out several times a day for months.
We tell ourselves well get up at 5:00 am every morning, despite
the fact were used to sleeping till 9:00 am right now.
The key to making lasting behavior change is to start small. My
general rule is that I should be almost embarrassed to tell a
friend about my progress.
If you want to start cooking at home, make one dish per day. It
could be as simple as making coffee.
If you want to start lifting weights, do one set.

for several weeks straight, I rode my bike and ran over 25 hours
per week, all outside.
I told myself, before every workout, that I only had to go for ten
minutes. If I wanted to stop after that, I could. I only missed two
workouts all winter, and thats because there was over a foot of
snow on the ground.
I started using that rule when I was four years old. After 10 years
of consistent training, I was still using the 10-minute rule to get
through 5-hour long workouts.
5. Create a routine.
The best way to get rid of an old habit is to replace it with a new
one. In fact, just trying to suppress an old habit without finding a
replacement often causes people to relapse.4,5
The best way to develop a new habit is to fuse it to something
you already do every day.6
For example, lets say you spend your lunch break reading
Cracked.com articles. First, you decide to replace that habit with
walking around your building during that time.
You decide to start walking immediately after you finish eating
you fuse it to your lunch.
Lets say you want to stop eating as much junk food after dinner.
You decide to replace that time with reading. You keep a book
in the middle of the dinner table, and as soon as youre finished,
you pick it up, go into another room, and start reading.
Heres an example from my life.
From 2010 to late 2013, I did 90% of my work standing. I didnt
even have a chair in my room.
When I started working on my first book, I stopped using a
standing desk. I was too stressed about reaching my deadline to
care.
About a month ago, I tried to start using a standing desk again,
but it was much harder than I remembered. In order to develop
the habit again, I fused it to my daily writing.

In the beginning, actually doing your habit is more important


than how well, or how much, you do.

Every morning, I write for 2-3 hours. I started standing for the
first five minutes of my writing. I never kept a timer, and I
naturally started standing longer and longer every day. After
several weeks I was back to writing for 2-3 hours while
standing.

If you keep this up, youll see results.

Now I dont even think about it.

Heres an example.

5 Steps to Fail-Proofing Your Weight Loss Goals

In the winter of 2012, I was living in the Blue Ridge Mountains


of Virginia. Despite the temperature being less than 20 degrees

Weight loss is never fun or easy, but you can make it a lot less
painful if you set the right kind of goals.

Alan Aragons Research Review July 2014

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If you want to go to bed earlier, get in bed five minutes earlier


than last night.

Page 14

S.M.A.R.T. goals are better than none, but theyre far from
optimal. They encourage you to focus on the outcome, rather
than your daily behaviors. Its the latter that matters.
But developing a new habit isnt easy, and it takes time. This
system will help your new habits stick.
1. Set a goal without a deadline, and write it down.
2. Imagine the kind of person who would be able to
accomplish that goal. What behaviors are they doing
every day?
3. Pick the top three most important habits that will help you
achieve this goal.
4. Break your habit into the smallest possible step.
5. Create a routine.
You are the sum of your daily habits, so focus on those instead
of listening to the hot girl on your gym television.
__________________________________________________
My name is Armi Legge, and Im the editor of
EvidenceMag.com, a website that helps
obsessive people, like you, simplify their
health and fitness. If youd like to see some of
my best articles, click here.

___________________________________________________
References
1.

2.

3.
4.
5.
6.

Lisa D OMESADGMHB. Goals Gone Wild: The


Systematic Side Effects of Over-Prescribing Goal Setting.
Hardvard Business School. 2009. Available at:
http://ssrn.com/abstract=1332071.
Maltz M. Psycho-Cybernetics: a New Technique for Using
Your Subconscious Power. Wilshire Book Company; 1969.
Available at: http://www.amazon.com/Psycho-CyberneticsTechnique-Using-Subconscious-Power/dp/B000BHN4K0
Lally P, van Jaarsveld CHM, Potts HWW, Wardle J. How
are habits formed: Modelling habit formation in the real
world. Eur J Soc Psychol. 2010;40(6):9981009. [EJSP]
Johnson F, Pratt M, Wardle J. Dietary restraint and selfregulation in eating behavior. International Journal of
Obesity (2005). 2012;36(5):665674. [PubMed]
Collins RL, Lapp WM. The temptation and restraint
inventory for measuring drinking restraint. Br J Addict.
1992;87(4):625633. [PubMed]
Gollwitzer PM, Sheeran P. Implementation Intentions and
Goal Achievement: A Metaanalysis of Effects and
Processes. In: Zanna MP, ed. Advances in Experimental
Social Psychology. Volume 38. Advances in Experimental
Social Psychology. Academic Press; 2006:69119
T2.[KOPS]

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Is being evidence-based an abused concept in the


fitness industry?
By Alan Aragon
____________________________________________________
The short answer
I was recently asked this question by someone who was
frustrated by the new generation of fitness professionals jumping
on what he felt was the science bandwagon. My short answer
to his question was a question of my own: Is this a bad thing?
I personally have not seen enough desire to be evidence-based
for any widespread abuse to occur among fitness trainers,
strength coaches, dietitians/nutritionists, and the like. As
someone who feels partially responsible for inspiring the new
generation of science-bandwagoneers, I actually wish more
fitness professionals cared about being evidence-based. Instead,
what Im seeing is a more pervasive pursuit of commercial profit
in a fast-growing, highly competitive fieldat the expense of
being evidence-based. With that out of the way, I will concede
that that among those with noble intentions is a certain degree of
misuse due to a misunderstanding of the concept. I discussed the
concept of evidence-based fitness way back in the August 2009
issue of AARR, so its time for my current thoughts on the topic.
Evidence 101
There are a number of incarnations of the grades of evidence, but
they are all fundamentally similar. A practical, straight-forward
model by National Heart, Lung, and Blood Institute (NHLBI)
lists the evidence categories as follows, with Category A being
the strongest (larger image here):1

ignoring observational evidence and placing all bets on


experimental evidence (specifically, randomized controlled trials
or RCTs). While RCTs are indeed considered the gold standard
of research due to their capability of demonstrating causation,
this doesnt mean all other types of research should be ignored.
Epidemiology (which includes cross-sectional, case-control, and
cohort studies) falls under the umbrella of observational
research, which is only capable of drawing correlations or
associations. The saying that correlation does not necessarily
equal causation is often provoked by bold claims based on
observational research, which is best for generating hyptheses
rather than arriving at firm conclusions, due to a lack of control
of a multitude of potentially confounding variables. Put another
way, observational research is good for generating questions
whose answers can be more rigorously investigated via
experimental research.
However, to reiterate, observational research should not be
automatically ignored because of its limitations. In the study of
chronic disease, epidemiological research is an important part of
the evidence spectrum. Its often not logistically, financially, or
ethically feasible to carry out RCTs long enough to exploit
disease endpoints. For example, theres only a small body of
controlled human interventions examining the effect of different
levels fruit and vegetable consumption on biomarkers of health
status.2 However, disease prevention via fruit & vegetable
consumption is biologically plausibleparticularly when we
piece together the epidemiological evidence with the
interventional & mechanistic research on the compounds in
fruits & vegetables.3 More RCTs on the effect of various fruits &
vegetables on relevant biomarkers that would satisfy everyone
would be great to see, but extremely difficult to execute.
On the note of RCTs, their strength lies in their degree of
control. However, their external validity (the extent to which
their results can be generalized) is often limited to a narrow
scope of utility. In other words, an RCT can have a high degree
of internal validity (very well-controlled, with error and bias
meticulously minimized), but how much relevance does it have
to you or the situation youre concerned with? Oftentimes RCTs
are presented as evidence with little or no regard to the
population studied or the protocol employed. Here a short list of
the questions that must be asked when evaluating the study:
Was it primary or secondary research? If it was primary,
what type of study was it? Was it observational, or
experimental? How diligent was the suppression of
potential confounding variables? What were the main
limitations of the study?
If it was secondary research, how thorough was the review
of the topic? Cherry-picking the research to support preexistent bias is unfortunately a constant threat to the
objectivity of secondary research papers. The latter is
sometimes due to the author having some sort of brand to
defend. In any case, conveniently ignoring evidence in
order to defend personal dogma is highly unscientific.

An important idea to reinforce is that evidence exists on a


continuum of strength. Its not a binary or black-and-white
matter. Lately, Ive observed a trend among fitness folks toward
Alan Aragons Research Review July 2014

If it was a meta-analysis, what were the inclusion criteria?


Were studies of particular importance or impact excluded,
and why? Was attention paid to the methodological quality
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Page 16

of the studies included in the analysis? For the recent metaanalysis on protein timing I did with Brad Schoenfeld and
James Krieger,7 study quality was assessed according to
the PEDro Rating Scale,8 which is an elegant yes/no rubric
composed of 11 criteria. A minimum score of 5 (out of a
maximum of 11) was required for studies to be considered
for inclusion in the analysis, and the average PEDro score
of the 23 studies we analyzed was 8.7, indicating high
overall quality.9
Who or what was studied, animals or humans? If humans
were studied, is their health or training status applicable to
your concern? Does the nutrition and/or training protocol
imposed on the subjects reflect the question youre
investigating? Refer to the March 2010, July 2012, and
January 2013 issues of AARR for further discussion on the
relevance limitations of animal research.
Was the study short- or long-term? As discussed in this
issue on page 9, short-term responses are often unreliable
for predicting long-term adaptations.
If the results reached statistical significance, were they
large enough to have practical significance? Sometimes
statistically significant differences are practically
meaningless. There are plenty of examples of this in diet
comparisons with significant differences in weight loss
that amount to 1-2 kg or less by the end of trials lasting
several weeks or months (were talking about changes that
can occur within a typical week or even a day).
Conversely, its possible for effects to not reach statistical
significance, but be large enough to have practical
significance or clinical importance over time. For statistics
tutorials, refer to the March 2011, May 2011, and January
2014 issues of AARR. Also, here is a good basic read on
interpreting health-related statistics.

The hierarchy of study types presented above is based on


guidelines set by the Agency for Healthcare Research and
Quality (AHRQ), formerly known as the Agency for Health
Care Policy and Research, which is one of 12 agencies within
the United States Department of Health and Human Services
(HHS). Ive taken the liberty to adapt this concept to what I call
the Hierarchy of Evidence Strength:10

Was the dosing or programming adequate or relevant?


RCTs can have a high degree of internal validity but barely
reflect with occurs in the real world (or the specific niche
youre concerned with).
Any replication? Independent replication of positive results
strengthens the validity of research findings. Ample,
replicated support versus one-hit-wonder status (with
repeated failure) is exemplified by comparing the track
record of creatine monohydrate4 versus ZMA5 for
improving muscular strength. A convergence of evidence
from hundreds of studies is what creatine has under its belt.
Now, just because a compound has limited research
support (or one-hit-wonder status) does not mean it should
be completely dismissed; it just has to be viewed in a more
cautious, tentative light.

There are many incarnations of this type of hierarchy, but my


goal was to simplify it and make it as relevant as possible to
health & fitness-related professions. Notice at the bottom of the
hierarchy, we have anecdote, tradition, and authority. Its
important to keep in mind that although these forms of evidence
are prone to the most bias, they are part of the evidence
hierarchy, nonetheless. Thus, they should not be automatically
dismissed or ignored.
A note about anecdotal evidence

The Scottish Intercollegiate Guidelines Network (SIGN) has


developed a system for grading recommendations in evidencebased guidelines. The following schematic is an overview of
their grading process, and notice its hierarchy of study types, and
the similarity to the NHLBI evidence categories (larger image
here).6

Anecdotal evidence is an interesting animal. It ranges from


valuable to useless, depending on the source of the anecdote. On
one end, anecdotes or personal testimonies about dieting or
training techniques from highly educated, highly accomplished
people (without any ulterior motives) hold much more
credibility than techniques touted by the uneducated,
unaccomplished folks especially those with hidden agendas.
So, its false to assume that all anecdotal data are worthless.
There is plenty of uncharted ground in the literature, so

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The evidence hierarchy in practice

Page 17

automatically dismissing anecdotes and unpublished information


is foolish. There indeed have been cases where the age-old
habits & lore of folks in the trenches were validated by research.
Take protein, for example. Prior to the past decade or so, many
authoritative figures in scientific circles scoffed at, and warned
against the uselessness of consuming protein at levels beyond
the RDA of 0.8 g/kg. We now have substantial scientific support
for the benefits of consuming protein at about 2-3 times the
RDA for certain athletic populations.11-13
Although anecdotal evidence shouldnt be automatically tossed
out, remember that its inescapably confounded by cognitive
biases, perhaps the most common being confirmation bias. Keep
an open mind, but remain skeptical in the absence of objective
evidence. Individual response should be the ultimate guide for
programming adjustments, but using the research as a starting
platform is the best way to minimize the extent of trial and error
in discovering whats optimal.

5.

6.
7.

8.
9.

Do you even lift?


A common question raised in online debates goes something
like, How come all the guys who are quick to post research
dont even look like they lift? Granted that this is a false
generalization, the apparent tendency of highly knowledgeable
folks to have unremarkable physiques has a plausible
explanation (other than laziness). Gifted trainees for whom great
results happen with minimal or haphazard effort have less
motivation to dig in, read, & learn all they possibly can in order
to put a dent in their mediocre genetics. On the other hand, some
folks were dealt a truly bum hand, and have to bleed for every
sliver of progress. This prompts a more rigorous investigation
and acquisition of knowledge toward battling their limitations.
Keep in mind that there are legions of guys with subpar
knowledge and subpar physiques, so a converse generalization
can be made. As well, there are guys with high levels of
scientific knowledge and impressive physiques, so making the
generalization that lots of book smarts is exclusive to those
with unimpressive physiques is yet another fallacy. In my
observations, the majority of folks with the best of both worlds
(spectacular knowledge and spectacular physiques) dont like to
argue muchunfortunately.

10.
11.

12.
13.

stand: creatine supplementation and exercise. J Int Soc


Sports Nutr. 2007 Aug 30;4:6. [PubMed]
Wilborn CD1, Kerksick CM, Campbell BI, Taylor LW,
Marcello BM, Rasmussen CJ, Greenwood MC, Almada A,
Kreider RB. Effects of Zinc Magnesium Aspartate (ZMA)
Supplementation on Training Adaptations and Markers of
Anabolism and Catabolism. J Int Soc Sports Nutr. 2004 Dec
31;1(2):12-20. [PubMed]
Harbour R, Miller J. A new system for grading
recommendations in evidence based guidelines. BMJ. 2001
Aug 11;323(7308):334-6. [PubMed]
Schoenfeld BJ, Aragon AA, Krieger JW. The effect of
protein timing on muscle strength and hypertrophy: a metaanalysis. J Int Soc Sports Nutr. 2013 Dec 3;10(1):53.
[PubMed]
Blobaum P. Physiotherapy Evidence Database (PEDro). J
Med Libr Assoc. Oct 2006; 94(4): 477478. [PMC]
Moseley AM, Herbert RD, Sherrington C, Maher CG.
Evidence for physiotherapy practice: a survey of the
physiotherapy evidence database (PEDro) Aust J
Physiother. 2002;10(1):4349. [PubMed]
Aragon AA. Hierarchy of Evidence Strength (original
schematic). AARR. July, 2014.
Helms ER, Zinn C, Rowlands DS, Brown SR. A systematic
review of dietary protein during caloric restriction in
resistance trained lean athletes: a case for higher intakes. Int
J Sport Nutr Exerc Metab. 2014 Apr;24(2):127-38.
[PubMed]
Phillips SM, Van Loon LJ. Dietary protein for athletes:
from requirements to optimum adaptation. J Sports Sci.
2011;29 Suppl 1:S29-38. [PubMed]
Campbell B, Kreider RB, Ziegenfuss T, La Bounty P,
Roberts M, Burke D, Landis J, Lopez H, Antonio J.
International Society of Sports Nutrition position stand:
protein and exercise. J Int Soc Sports Nutr. 2007 Sep 26;4:8.
[PubMed]

References
1.

2.
3.

4.

National Heart, Lung, and Blood Institute. Clinical


Guidelines on the Identification, Evaluation, and Treatment
of Overweight and Obesity in Adults Updated April 2011.
[NHLBI]
Slavin JL, Lloyd B. Health benefits of fruits and vegetables.
Adv Nutr. 2012 Jul 1;3(4):506-16. [PubMed]
Boeing H1, Bechthold A, Bub A, Ellinger S, Haller D,
Kroke A, Leschik-Bonnet E, Mller MJ, Oberritter H,
Schulze M, Stehle P, Watzl B. Critical review: vegetables
and fruit in the prevention of chronic diseases. Eur J Nutr.
2012 Sep;51(6):637-63. [PubMed]
Buford TW1, Kreider RB, Stout JR, Greenwood M,
Campbell B, Spano M, Ziegenfuss T, Lopez H, Landis J,
Antonio J. International Society of Sports Nutrition position

Alan Aragons Research Review July 2014

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Page 18

Here is a nice, quick read by Jamie Hale on the mythology


behind the all-natural label and its surrounding concepts:
http://www.maxcondition.com/page.php?169

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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Page 19

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