6 - July - 2014

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Alan Aragon’s Research Review – July 2014 [Back to Contents ] Page 1 Copyright © July 1st, 2014 by Alan Aragon Home: www.alanaragon.com/researchreview Correspondence: [email protected] 2 The Walking Dead: GM food hysteria and the naturalistic fallacy. By Mike Israetel, PhD 5 Poor posture is not likely causing you pain. By Steinar Ekren 7 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 ] 8 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 ] 9 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. Acheson KJ, Schutz Y, Bessard T, Anantharaman K, Flatt JP, Jéquier 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? By Alan Aragon

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Alan Aragon

Transcript of 6 - July - 2014

  • Alan Aragons Research Review July 2014 [Back to Contents] Page 1

    Copyright July 1st, 2014 by Alan Aragon

    Home: www.alanaragon.com/researchreview

    Correspondence: [email protected]

    2 The Walking Dead: GM food hysteria and the

    naturalistic fallacy.

    By Mike Israetel, PhD

    5 Poor posture is not likely causing you pain.

    By Steinar Ekren

    7 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]

    8 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]

    9 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.

    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? By Alan Aragon

  • Alan Aragons Research Review July 2014 [Back to Contents] Page 2

    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 anti-GM 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.

    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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    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.

    3) Baseless via philosophy

    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

    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.

    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 [Back to Contents] Page 4

    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.

    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. American Association for the Advancement of Science (AAAS), Board of Directors (2012). Legally Mandating GM Food Labels Could Mislead and Falsely Alarm Consumers. [AAAS]

    2. A decade of EU-funded GMO research (2001-2010) (PDF). Directorate-General for Research and Innovation. Biotechnologies, Agriculture, Food. European Union. 2010.

    3. Ronald, Pamela (2011). "Plant Genetics, Sustainable Agriculture and Global Food Security". Genetics 188 (1): 1120. [PubMed]

    4. American Medical Association (2012). Report 2 of the Council on Science and Public Health: Labeling of Bioengineered Foods.

    5. 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]

    6. 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]

    7. 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]

  • Alan Aragons Research Review July 2014 [Back to Contents] Page 5

    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 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.

    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. 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 [Back to Contents] Page 6

    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: [email protected] 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):363-71 [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. Leg-length 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 [Back to Contents] Page 7

    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 follow-up 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. 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

    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.

    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 (

  • Alan Aragons Research Review July 2014 [Back to Contents] Page 8

    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]

    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. Pre- and 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. 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 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

    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. Comment/application

    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.

    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 9

    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% one-repetition 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

  • Alan Aragons Research Review July 2014 [Back to Contents] Page 10

    significant difference in nitrogen balance at P0 & P6 was seen in the untrained group.

    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): A 4-hour peri-workout period (the timespan between the pre-and post-exercise meal) is relatively common. However, while a 6-hour 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

    has limited relevance to the populations most likely to aim for optimizing muscle hypertrophy through timing tactics.

    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.

    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 post-exercise 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 post-exercise 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.

  • Alan Aragons Research Review July 2014 [Back to Contents] Page 11

    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:

    Study limitations

    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-

    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/low-carb 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.

    On a relate note, previous research by Acheson et al21 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 [Back to Contents] Page 12

    1. Frigolet ME, Ramos Barragn VE, Tamez Gonzlez M.

    Low-carbohydrate diets: a matter of love or hate. Ann Nutr Metab. 2011 Oct;58(4):320-34. [PubMed]

    2. Westman EC, Feinman RD, Mavropoulos JC, Vernon MC, Volek JS, Wortman JA, Yancy WS, Phinney SD. Low-carbohydrate nutrition and metabolism. Am J Clin Nutr. 2007 Aug;86(2):276-84. [PubMed]

    3. Hu T, Mills KT, Yao L, Demanelis K, Eloustaz M, Yancy WS Jr, Kelly TN, He J, Bazzano LA. Effects of low-carbohydrate diets versus low-fat diets on metabolic risk factors: a meta-analysis of randomized controlled clinical trials. Am J Epidemiol. 2012 Oct 1;176 Suppl 7:S44-54. [PubMed]

    4. Gardner CD, Kiazand A, Alhassan S, Kim S, Stafford RS, Balise RR, Kraemer HC, King AC. Comparison of the Atkins, Zone, Ornish, and LEARN diets for change in weight and related risk factors among overweight premenopausal women: the A TO Z Weight Loss Study: a randomized trial. JAMA. 2007 Mar 7;297(9):969-77. [PubMed]

    5. Tay J, Brinkworth GD, Noakes M, Keogh J, Clifton PM. Metabolic effects of weight loss on a very-low-carbohydrate diet compared with an isocaloric high-carbohydrate diet in abdominally obese subjects. J Am Coll Cardiol. 2008 Jan 1;51(1):59-67. [PubMed]

    6. Robinson MJ, Burd NA, Breen L, Rerecich T, Yang Y, Hector AJ, Baker SK, Phillips SM. Dose-dependent responses of myofibrillar protein synthesis with beef ingestion are enhanced with resistance exercise in middle-aged men. Appl Physiol Nutr Metab. 2013 Feb;38(2):120-5. [PubMed]

    7. Symons TB, Sheffield-Moore M, Mamerow MM, Wolfe RR, Paddon-Jones D. The anabolic response to resistance exercise and a protein-rich meal is not diminished by age. J Nutr Health Aging. 2011 May;15(5):376-81. [PubMed]

    8. Pateyjohns IR, Brinkworth GD, Buckley JD, Noakes M, Clifton PM.. Comparison of three bioelectrical impedance methods with DXA in overweight and obese men. Obesity (Silver Spring). 2006 Nov;14(11):2064-70. [PubMed]

    9. Bosse JD, Dixon BM. Dietary protein to maximize resistance training: a review and examination of protein spread and change theories. J Int Soc Sports Nutr. 2012 Sep 8;9(1):42. [PubMed]

    10. Kopple JD. Uses and limitations of the balance technique. JPEN J Parenter Enteral Nutr. 1987 Sep-Oct;11(5 Suppl):79S-85S. [PubMed]

    11. Aragon AA, Schoenfeld BJ. Nutrient timing revisited: is there a post-exercise anabolic window? J Int Soc Sports Nutr. 2013 Jan 29;10(1):5. [PubMed]

    12. Schoenfeld BJ, Aragon AA, Krieger JW. The effect of protein timing on muscle strength and hypertrophy: a meta-analysis. J Int Soc Sports Nutr. 2013 Dec 3;10(1):53. [PubMed]

    13. Mitchell CJ, Churchward-Venne TA, Parise G, Bellamy L, Baker SK, Smith K, Atherton PJ, Phillips SM. cute post-exercise myofibrillar protein synthesis is not correlated with resistance training-induced muscle hypertrophy in young men. PLoS One. 2014 Feb 24;9(2):e89431. [PubMed]

    14. Mayhew DL, Kim JS, Cross JM, Ferrando AA, Bamman MM (2009) Translational signaling responses preceding resistance training-mediated myofiber hypertrophy in young and old humans. J Appl Physiol 107: 16551662 [PubMed]

    15. Glynn EL, Fry CS, Drummond MJ, Dreyer HC, Dhanani S, Volpi E, Rasmussen BB. Muscle protein breakdown has a minor role in the protein anabolic response to essential amino acid and carbohydrate intake following resistance exercise. Am J Physiol Regul Integr Comp Physiol. 2010 Aug;299(2):R533-40. [PubMed]

    16. Lowery L, Daugherty A, Miller B, Dye S, Liming L. The effect of habitually large protein intake on renal function of strength athletes: an update. J In Soc Sports Nutr. 2011 Nov, 8(Suppl 1):P33 [JISSN]

    17. Chen JD, Wang JF, Li KJ, Zhao YW, Wang SW, Jiao Y, Hou XY. Nutritional problems and measures in elite and amateur athletes. Am J Clin Nutr. 1989 May;49(5 Suppl):1084-9. [PubMed]

    18. Kim H, Lee S, Choue R.. Metabolic responses to high protein diet in Korean elite bodybuilders with high-intensity resistance exercise. J Int Soc Sports Nutr. 2011 Jul 4;8(1):10. [Pubmed]

    19. Cribb PJ, Hayes A. Effects of supplement timing and resistance exercise on skeletal muscle hypertrophy. Med Sci Sports Exerc. 2006 Nov;38(11):1918-25. [PubMed]

    20. Hoffman JR, Ratamess NA, Tranchina CP, Rashti SL, Kang J, Faigenbaum AD. Effect of protein-supplement timing on strength, power, and body-composition changes in resistance-trained men. Int J Sport Nutr Exerc Metab. 2009 Apr;19(2):172-85. [PubMed]

    21. Acheson KJ, Flatt JP, Jquier E. Glycogen synthesis versus lipogenesis after a 500 gram carbohydrate meal in man. Metabolism. 1982 Dec;31(12):1234-40. [PubMed]

  • Alan Aragons Research Review July 2014 [Back to Contents] Page 13

    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 Setting goals isnt bad, but thats only the first step. Unfortunately, thats where most people stop, and its part of they fail. The following five-step process is, in my view, more effective. 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. Unless you have a specific event planned like a race, photo-shoot, or bodybuilding competition, dont worry about setting a deadline. That generally encourages you to rush, and its unnecessary. 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. 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 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.

    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? What would their diet look like? How often are they training? 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. 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.

    Do you know roughly how much youre eating? Are you really being as consistent with your training as you could be? Are you sticking to your sleep schedule every night? There will always be more habits you can work on in the future, so focus on the most important one today. Pick one. Need more sleep? 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. Use one of these apps to block websites like Facebook after a certain time.

  • Alan Aragons Research Review July 2014 [Back to Contents] Page 14

    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. If you want to go to bed earlier, get in bed five minutes earlier than last night. In the beginning, actually doing your habit is more important than how well, or how much, you do. If you keep this up, youll see results. Heres an example. In the winter of 2012, I was living in the Blue Ridge Mountains of Virginia. Despite the temperature being less than 20 degrees

    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. 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. Now I dont even think about it. 5 Steps to Fail-Proofing Your Weight Loss Goals

    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 [Back to Contents] Page 15

    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. 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.

    2. Maltz M. Psycho-Cybernetics: a New Technique for Using Your Subconscious Power. Wilshire Book Company; 1969. Available at: http://www.amazon.com/Psycho-Cybernetics-Technique-Using-Subconscious-Power/dp/B000BHN4K0

    3. 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]

    4. Johnson F, Pratt M, Wardle J. Dietary restraint and self-regulation in eating behavior. International Journal of Obesity (2005). 2012;36(5):665674. [PubMed]

    5. Collins RL, Lapp WM. The temptation and restraint inventory for measuring drinking restraint. Br J Addict. 1992;87(4):625633. [PubMed]

    6. 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]

  • Alan Aragons Research Review July 2014 [Back to Contents] Page 16

    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 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

    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 pre-existent 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.

    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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    of the studies included in the analysis? For the recent meta-analysis 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.

    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.

    The evidence hierarchy in practice

    The Scottish Intercollegiate Guidelines Network (SIGN) has developed a system for grading recommendations in evidence-based 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

    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

    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

    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

  • Alan Aragons Research Review July 2014 [Back to Contents] Page 18

    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. 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. References

    1. National Heart, Lung, and Blood Institute. Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults Updated April 2011. [NHLBI]

    2. Slavin JL, Lloyd B. Health benefits of fruits and vegetables. Adv Nutr. 2012 Jul 1;3(4):506-16. [PubMed]

    3. 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]

    4. 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

    stand: creatine supplementation and exercise. J Int Soc Sports Nutr. 2007 Aug 30;4:6. [PubMed]

    5. 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]

    6. Harbour R, Miller J. A new system for grading recommendations in evidence based guidelines. BMJ. 2001 Aug 11;323(7308):334-6. [PubMed]

    7. Schoenfeld BJ, Aragon AA, Krieger JW. The effect of protein timing on muscle strength and hypertrophy: a meta-analysis. J Int Soc Sports Nutr. 2013 Dec 3;10(1):53. [PubMed]

    8. Blobaum P. Physiotherapy Evidence Database (PEDro). J Med Libr Assoc. Oct 2006; 94(4): 477478. [PMC]

    9. 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]

    10. Aragon AA. Hierarchy of Evidence Strength (original schematic). AARR. July, 2014.

    11. 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]

    12. Phillips SM, Van Loon LJ. Dietary protein for athletes: from requirements to optimum adaptation. J Sports Sci. 2011;29 Suppl 1:S29-38. [PubMed]

    13. 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]

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    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 [email protected].

    Table of ContentsEditor's Cut: The Walking Dead: GM food hysteria and the naturalistic fallacy.Alternate Perspective: Poor posture is not likely causing you pain.Nutrition & Exercise:Low carbohydrate versus isoenergetic balanced diets for reducing weight and cardiovascular risk: a systematic review and meta-analysis.Protein supplementation with low fat meat after resistance training: effects on body composition and strength.

    Supplementation: Effect of timing of protein and carbohydrate intake after resistance exercise on nitrogen balance in trained and untrained young men.Less Recent Gem: Glycogen storage capacity and de novo lipogenesis during masive carbohydrate overfeeding in man.Study Comment ReferencesIn the Lay Press: How to set weight loss goals that work [part 2]. Good Question: Is being evidence-based an abused concept in the fitness industry?