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Alan Aragons Research Review February & March 2013 [Back to Contents] Page 1

Copyright September 1st, 2013 by Alan Aragon

Home:www.alanaragon.com/researchreview

Correspondence:[email protected]

2 Clearing up common misunderstandings thatplague the calorie debate, part 3: eat less, movemore.

By Alan Aragon

5 Strength and body composition changes inrecreationally strength-trained individuals:comparison of one versus three sets resistance-training programmes. [Critiqued byBrad Schoenfeld,PhD(c), CSCS, CSPS, FNSCA].

Baker JS, Davies B, Cooper SM, Wong DP, Buchan DS,Kilgore L. BioMed Research International, vol. 2013,Article ID 615901, 6 pages, 2013. doi:10.1155/2013/615901[Hindawi]

7 Belief beyond the evidence: using the proposedeffect of breakfast on obesity to show 2 practicesthat distort scientific evidence.

Brown AW, Bohan Brown MM, Allison DB. Am J ClinNutr. 2013 Sep 4. [Epub ahead of print] [PubMed]

9 Whey protein supplementation during resistancetraining augments lean body mass.

Volek JS, Volk BM, Gmez AL, Kunces LJ, Kupchak BR,Freidenreich DJ, Aristizabal JC, Saenz C, Dunn-Lewis C,Ballard KD, Quann EE, Kawiecki DL, Flanagan SD,Comstock BA, Fragala MS, Earp JE, Fernandez ML, BrunoRS, Ptolemy AS, Kellogg MD, Maresh CM, Kraemer WJ. JAm Coll Nutr. 2013 Apr;32(2):122-35. [PubMed]

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

Christensen AS, Viggers L, Hasselstrm K, Gregersen SNutr J. 2013 Mar 5;12:29. doi: 10.1186/1475-2891-12-29[PubMed]

12 Are Americas nutrition professionals in the pocketof Big Food? [my commentary on the article byJoseph Mercola]

By Alan Aragon

14 Interview with Karen Pendergrass, founder ofPaleo Movement Magazine.

By Alan Aragon
http://www.alanaragon.com/researchreviewmailto:[email protected]:[email protected]://www.lookgreatnaked.com/about_brad.phphttp://www.lookgreatnaked.com/about_brad.phphttp://www.lookgreatnaked.com/about_brad.phphttp://www.hindawi.com/journals/bmri/2013/615901/cta/http://www.hindawi.com/journals/bmri/2013/615901/cta/http://www.hindawi.com/journals/bmri/2013/615901/cta/http://www.ncbi.nlm.nih.gov/pubmed/24004890http://www.ncbi.nlm.nih.gov/pubmed/24004890http://www.ncbi.nlm.nih.gov/pubmed/24004890http://www.ncbi.nlm.nih.gov/pubmed/24015719http://www.ncbi.nlm.nih.gov/pubmed/24015719http://www.ncbi.nlm.nih.gov/pubmed/24015719http://www.ncbi.nlm.nih.gov/pubmed/23497350http://www.ncbi.nlm.nih.gov/pubmed/23497350http://www.ncbi.nlm.nih.gov/pubmed/23497350http://alanaragon.com/researchreviewhttp://www.ncbi.nlm.nih.gov/pubmed/23497350http://www.ncbi.nlm.nih.gov/pubmed/24015719http://www.ncbi.nlm.nih.gov/pubmed/24004890http://www.hindawi.com/journals/bmri/2013/615901/cta/http://www.lookgreatnaked.com/about_brad.phpmailto:[email protected]://www.alanaragon.com/researchreview

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Clearing up common misunderstandings that plaguethe calorie debate, part 3: eat less, move more.

By Alan Aragon

____________________________________________________

Welcome to the Wild West

Epidemic is no longer a strong enough word to describe theobesity problem. The United States has been called theepicenter of an obesity pandemic.1Obesity is a global problem,we know that. Whats kind of embarrassing for Westerners like

myself is that the Western lifestyle is the unofficial poster-modelof obesogenicity. The Westernization of any given populationusually implies a set-up for obesity-related disease. Since theWestern lifestyle is characterized by physical inactivity andovereating,2,3doing the opposite (eating less and moving more)is a seemingly obvious solution. Its well-established that weightloss over the long-term is achieved via sustaining an energydeficit, and indeed eating less and/or moving more is the onlyway to do this regardless of whatever clever food choices orenergy expenditure tactics are employed. One or both roads must

lead to one place: an energy deficit.

Conversely, weight gain over time can only be reached through asustained caloric surplus by whatever overt or discreet meansthis is achieved. There are a multitude of hypotheses behindwhat caused the rise of obesity that began about four decadesago. However, the most plausible explanation is somewhatanticlimactic. Swinburn et al investigated the major drivers ofthe US obesity epidemic and found that increased energy intakeby ~500kcal/day for adults and ~350 kcal/day for children ismore than sufficient to explain the US epidemic of obesity.4Iwould also add that there is evidence indicating a reduction inenergy-out as well.5,6 These factors combined quite elegantly

account for the expansion of the nations waistline. We eat moreand move less.

However, is telling the public to simply eat less and move morean effective way to solve the obesity problem? Unfortunatelynot, even though its essentially true. Ill discuss why this adviceon its own doesnt always work, and Ill then propose some

alternative advice.

Problems with eating less

The implication behind eating less is consuming less totalcalories. Alright, clear enough, but does it matter where thecalorie cuts are made? Yes it does, and it cant be assumed thatthe public knows the finer details of this. There is a bounty ofresearch showing the advantage of consuming sufficient protein(approximately 1.2-2.3 g/kg; one recent review suggested arange of 1.8-2.7 g/kg) while dieting in order to minimize lossesof lean mass.7,8 Protein also leads the macronutrients in itsthermic and satiating effect.9 It therefore does not make goodsense to target protein when cutting back intake. Theproportional decrease of fat versus carbohydrate is a flexiblematter subject to individual preference, tolerance, and goals. Insupport of this, Soenen et al recently demonstrated that weight

loss and weight-maintenance advantages depend on the high-protein, rather than the low-carb aspect of the diet.10

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

practical limit to eating less. At some point, eating less can leadto eating nothing. Thats not sustainable, nor is it fun. So, thequestion now becomes whether or not certain circumstances canbenefit from aggressive deficits, and the answer is yes. Anaggressive caloric deficit is an effective intervention tactic for asevere state of obesity. There is a substantive and consisten

body of evidence indicating that in the initial stage of dieting, agreater weight loss is associated with greater short- and long-term success in weight loss maintenance.11,12However, keep inmind that the quick-initial weight loss model does notnecessarily apply to everyone. In lean/athletic subjects, slow-and-steady weight loss is more protective of lean mass.13

Perhaps the most confounding and insidious problem witheating less is the double-whammy of reduced resting energyexpenditure combined with increased hunger. Adaptivethermogenesis (a decrease in resting energy expenditure beyondwhat can be attributed to losses in lean mass) was discussed at-length in the July 2013 issue. Now its time to address hunger

issues. While eating less can reliably induce weight loss, it canalso reliably induce hunger. An increased drive to eat can lead tothe sabotage of weight loss efforts, so the dieter is stuck in atough position. At this point I have to interject with the conceptthat this is supposed to happen. It might appear to be a problemfor the dieter, but as far as the body is concerned, the sabotagingof dieting efforts is a victory against death.

Its useful to get familiar with the known mechanisms that drive

the homeostasis of bodyweight, since they give a clearer pictureof why the advice to simply eat less, move more often fails

Boguszewski et al eloquently summarize the complexity of thesituation as follows:14

The human body is endowed with a complex physiologicasystem that maintains relatively constant body weight and fa

stores despite the wide variations in daily energy intake and

energy expenditure. With weight loss, compensatory

physiological adaptations result in increased hunger and

decreased energy expenditure, while opposite responses are

triggered when body weight increases. This regulatory system is

formed by multiple interactions between the gastrointestina

tract (GIT), adipose tissue, and the central nervous system

(CNS) and is influenced by behavioural, sensorial, autonomic

nutritional, and endocrine mechanisms.

That was such a beautiful encapsulation of whats involved, that

its a shame I didnt write it myself. Back on topic, its important

to note that the body launches a more pronounced defensiveresponse against weight loss than it does against weight gainThis makes sense, since we as a species evolved to surviveprolonged periods of famine. As evidenced by the currenobesity pandemic, humans have not gracefully adapted to thehistorically recent perpetual abundance of food combined withthe elimination of the obligatory link between physical activityand survival (i.e., chasing our food down versus driving to thestore to buy it).

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The harmony of physiological factors regulating the bodys

defense against weight loss is downright symphonic. The centralnervous system (CNS) communicates with the adipose tissue,gastrointestinal tract, and pancreas in what can rightly be seen asa conspiracy to keep bodyweight from changing. Ill touchbriefly upon insulin and leptin to illuminate an important sectionof this symphony, and also to illustrate the complexity ofbodyweight homeostasis, given that this interplay is only one ofmany weight-regulatory systems in the body.

Leptin is a peptide hormone primarily secreted by the adiposetissue. Our understanding of leptins role in bodyweightregulation is still very incomplete, but we do know that it aids inappetite control (at least in part) by stimulating anorexigenicneurons and inhibiting orexigenic ones. In addition to increasingenergy expenditure, leptin serves to reduce food intake, whichcollectively is a set-up for weight loss. But of course, the body issmarter than that. Leptin levels rise and fall in tandem with theamount of body fat one carries. So, the lower your bodyfatlevels, the less capacity leptin has to work its magic. Lowerleptin levels result in a higher activation of neuropeptide Y(NPY), the brains most abundant neurotransmitter, which also

happens to be the primary hunger signal in response to caloric

restriction.15

Insulin, a peptide hormone produced by the pancreas, is similarto leptin in the sense that its an adipose signal. Like leptin,

serum insulin levels mirror body fat levels. And also like leptin,insulin elevations are anorexigenic. Thus, they both haveregulatory effects on food intake. The twist in the saga is howinsulin and leptin have opposite effects on adipose tissue. Leptinstimulates lipolysis (the breakdown lipids and mobilization offatty acids), while insulin inhibits lipolysis and stimulateslipogenesis. Kiefer and Habener have thus proposed anadipoinsular axis which they summarize as follows (along

with a diligent disclaimer of ex vivo and animal data):

There is now growing evidence that leptin also acts tosuppress insulin production from pancreatic -cells. Because

insulin is adipogenic and increases the expression of leptin,

there is a bidirectional feedback loop between adipose tissue

and pancreatic islets, termed the adipoinsular axis. The majority

of evidence in support of an adipoinsular axis has come from

studies in rodents or cell lines, but there is also evidence to

suggest that a similar pathway exists in humans.

In essence, insulin and leptin share similar/overlappingbiological effects, but the unintuitive reality is that they alsohave opposing actions that keep each other in check. Toreiterate, insulin and leptin are adiposity signals, but they are a

mere drop in the bucket within the larger body of knownhomeostatic regulators. The influence of gastrointestinalpeptides and endocannabinoids on appetite and bodyweightregulation could fill chapters on their own.

The practical take-away from this information is that you cantsimply focus on any single factor in isolation, since its

inevitably integrated into a regulatory system with a multitude ofchecks and balances. Another point to reiterate is that the energybalance imposedeither a surplus or deficitis the single mostpowerful dictator of the fate and function of these

neuroendocrine factors. So, weight loss certainly can occur byeating less. But this says very little about the bodys plan to

counteract this by decreasing energy expenditure and increasinghunger.

Problems with moving more

This part of the discussion is far less esoteric and abstract, so goahead and exhale. Moving more implies voluntarily increasingenergy expenditure. Clear enough, but does it matter how this

increase is executed? Yes it does. And just as in the case ofeating less, it cant be assumed that the public knows the deta ilsthat can make or break long-term success. The advice to movemore can evoke a wide range of different aims. Some might hearthe advice and start shopping around for a Crossfit gymmembership. Others might look at their work schedule andagonize over whether theres enough time for a walk beforerushing to the office.

The main problem I see with the move more objective is that it

automatically leads people to think in terms of increased trainingtime. This can be a deal-breaker for the majority of workingpeople in the industrialized world who feel that they have notime to spare. This is especially the case for those who fee

maxed-out in terms of their time investment in exercise. Thelatter individuals need to review their options of increasing theirtraining intensity, especially if eating less is out of the question.

Speaking of training intensity, the objective to move harder is

just as legitimate as the objective to move more. Imposing mypersonal preference would be to change the mantra to movemore weight. Progressive resistance training has only recentlyreceived recognition for its positive effects on cardiometabolichealth,17-19whereas it traditionally has been viewed as a meansto improve musculoskeletal strength.

There are obvious limits to resistance training in terms of loadprogression, and these limits will vary widely with the

individual. I just want to dispel the nearly automatic tendency toadd minutes to the evening treadmill session or miles to themorning jog. At the same time, I dont want to portray some sorof false dichotomy where you have to do either one or the otheror that one mode is inherently superior to the other. The natureof the exercise increase, whether its based on intensity

frequency, or duration, must once again be dictated by youguessed it individual preference, tolerance, and goal. Movingmore essentially becomes a matter of progressing properly.

Moving more carries an additional implication that the energyexpenditure increase must consist of formal exercise. Theproblem is that not everyone equates exercise with excitement or

pleasure. In fact, many view exercise as a form of torture. Nonexercise activity (including recreational activity) is perfectlylegitimate and effective for fulfilling the move moreobjective.20For exercise-phobic individuals, we can strategicallymodify move more into sit less and then progress fromthere.

A final problem with the move more mantra is the reluctance

to engage in exercise due to the belief that it simply doesnwork. The purported ineffectiveness of exercise as a weight losstool regularly makes it rounds through various popular media

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Some gurus go as far as promoting the idea that exercise onlyincreases the tendency to gain weight. This is simply incorrect.A relatively recent meta-analysis by Wu et al found that diet plusexercise caused significantly greater weight loss than dietalone..21 This weight loss was significantly greater in trialslasting a year or more, suggesting that exercise has long-termbenefits to weight loss.

Conclusions & potential solutions

Fundamentally speaking, eating less and moving more is a validapproach for weight loss and obesity prevention. However, thedevil is in the details. Specific strategies must be implemented inorder to increase the chances of long-term success. In the case ofeating less, the brunt of the caloric reduction should be fromcarbohydrate and/or fat (depending on personal preference) inorder to reap the lean mass-preserving and satiating effect ofprotein.

This is not to say that more-is-better when it comes to protein.The point of diminishing returns where protein intake impingesupon a dieters carbohydrate and/or fat allotment can be avoided

by setting an upper limit of protein intake at approximately agram per pound of bodyweight. Another strategy to hedge

against the bodys multitude of defenses against weight loss is topurposely reserve more rapid weight loss for the initial phase ofa program (roughly within the first 3-6 months), or for the initial10-20% drop in bodyweight depending on the severity of theobesity at the start of the program. The remainder of the weightloss programming should accommodate a slower pace.

Advice to move more can be interpreted in many ways, withvarying degrees of productivity (and counterproductivity). Aswith diet composition, exercise programming and progressionshould be tailored to individual preference, tolerance, and goals.Moving more has practical limits that must be respected, as doeseating less. The recommendation to eat less and move more is

not sufficient on its own to cover the many nuances andcontingencies associated with long-term weight loss success orimprovements in body composition. But then again, Eat less,move more! is far catchier than, Maintain an energy deficitwith appropriate macronutrient targets and personally preferred

foods while training with properly individualized programming

and progression.

References

1. Katz DL. Pandemic obesity and the contagion of nutritionalnonsense. Public Health Rev. 2003;31(1):33-44. [PubMed]

2. Nedeltcheva AV, Kessler L, Imperial J, Penev PD. Exposure torecurrent sleep restriction in the setting of high caloric intake

and physical inactivity results in increased insulin resistanceand reduced glucose tolerance. J Clin Endocrinol Metab. 2009Sep;94(9):3242-50. [PubMed]

3. Nedeltcheva AV, Kilkus JM, Imperial J, Kasza K, SchoellerDA, Penev PD. Sleep curtailment is accompanied by increasedintake of calories from snacks. Am J Clin Nutr. 2009Jan;89(1):126-33. [PubMed

4. Swinburn B, Sacks G, Ravussin E. Increased food energysupply is more than sufficient to explain the US epidemic ofobesity. Am J Clin Nutr. 2009 Dec;90(6):1453-6. [PubMed]

5. Economic Research Service, USDA. Food Availability (Per

Capita) Data System: Summary Findings. Last Updated MonAug 20, 2012. http://www.ers.usda.gov/data-products/foodavailability-(per-capita)-data-system/summary-findings.aspx

6. King DE, Mainous AG 3rd, Carnemolla M, Everett CJAdherence to healthy lifestyle habits in US adults, 1988-2006Am J Med. 2009 Jun;122(6):528-34. [PubMed]

7. Churchward-Venne TA, Murphy CH, Longland TM, PhillipsSM. Role of protein and amino acids in promoting lean massaccretion with resistance exercise and attenuating lean massloss during energy deficit in humans. Amino Acids. 2013Aug;45(2):231-40. [PubMed]

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

9. Halton TL, Hu FB. The effects of high protein diets onthermogenesis, satiety and weight loss: a critical review. J AmColl Nutr. 2004 Oct;23(5):373-85. [PubMed]

10. Soenen S, Bonomi AG, Lemmens SG, Scholte J, Thijssen MAvan Berkum F, Westerterp-Plantenga MS. Relatively high

protein or 'low-carb' energy-restricted diets for body weighloss and body weight maintenance? Physiol Behav. 2012 Oct10;107(3):374-80. [PubMed]

11. Anderson JW, Konz EC, Frederich RC, Wood CL. Long-termweight-loss maintenance: a meta-analysis of US studies. Am JClin Nutr. 2001 Nov;74(5):579-84. [PubMed]

12. Nackers LM, Ross KM, Perri MG. The association betweenrate of initial weight loss and long-term success in obesitytreatment: does slow and steady win the race? Int J Behav Med2010 Sep;17(3):161-7. [PubMed]

13. Garthe I, Raastad T, Refsnes PE, Koivisto A, Sundgot-BorgenJ. Effect of two different weight-loss rates on body compositionand strength and power-related performance in elite athletesInt J Sport Nutr Exerc Metab. 2011 Apr;21(2):97-104[PubMed]

14. Boguszewski CL, Paz-Filho G, Velloso LA. Neuroendocrinebody weight regulation: integration between fat tissuegastrointestinal tract, and the brain. Endokrynol Pol. 2010 Mar-Apr;61(2):194-206. [PubMed]

15. Minor RK, Chang JW, de Cabo R. Hungry for life: How thearcuate nucleus and neuropeptide Y may play a critical role in

mediating the benefits of calorie restriction. Mol CelEndocrinol. 2009 Feb 5;299(1):79-88. [PubMed]

16. Kieffer TJ, Habener JF. The adipoinsular axis: effects of leptinon pancreatic beta-cells. Am J Physiol Endocrinol Metab. 2000Jan;278(1):E1-E14. [PubMed]

17. Sundell J. Resistance Training Is an Effective Tool againstMetabolic and Frailty Syndromes. Adv Prev Med2011;2011:984683. [PubMed]

18. Warner SO, Linden MA, Liu Y, Harvey BR, Thyfault JPWhaley-Connell AT, Chockalingam A, Hinton PS, DellspergerKC, Thomas TR. The effects of resistance training onmetabolic health with weight regain. J Clin Hypertens(Greenwich). 2010 Jan;12(1):64-72. [PubMed]

19. Conceio MS, Bonganha V, Vechin FC, de Barros Berton RP

Lixandro ME, Nogueira FR, de Souza GV, Chacon-MikahiMP, Libardi CA. Sixteen weeks of resistance training candecrease the risk of metabolic syndrome in healthy

postmenopausal women. Clin Interv Aging. 2013;8:1221-8[PubMed]

20. Levine JA. Nonexercise activity thermogenesis--liberating thelife-force. J Intern Med. 2007 Sep;262(3):273-87. [PubMed]

21. Wu T, Gao X, Chen M, van Dam RM. Long-term effectivenessof diet-plus-exercise interventions vs. diet-only interventionsfor weight loss: a meta-analysis. Obes Rev. 2009May;10(3):313-23. [PubMed]
http://www.ncbi.nlm.nih.gov/pubmed/14656042http://www.ncbi.nlm.nih.gov/pubmed/14656042http://www.ncbi.nlm.nih.gov/pubmed/14656042http://www.ncbi.nlm.nih.gov/pubmed/19567526http://www.ncbi.nlm.nih.gov/pubmed/19567526http://www.ncbi.nlm.nih.gov/pubmed/19567526http://www.ncbi.nlm.nih.gov/pubmed/19567526http://www.ncbi.nlm.nih.gov/pubmed/19567526http://www.ncbi.nlm.nih.gov/pubmed/19567526http://www.ncbi.nlm.nih.gov/pubmed/19828708http://www.ncbi.nlm.nih.gov/pubmed/19828708http://www.ncbi.nlm.nih.gov/pubmed/19828708http://www.ers.usda.gov/data-products/food-availability-(per-capita)-data-system/summary-findings.aspxhttp://www.ers.usda.gov/data-products/food-availability-(per-capita)-data-system/summary-findings.aspxhttp://www.ncbi.nlm.nih.gov/pubmed/19486715http://www.ncbi.nlm.nih.gov/pubmed/19486715http://www.ncbi.nlm.nih.gov/pubmed/19486715http://www.ncbi.nlm.nih.gov/pubmed/23645387http://www.ncbi.nlm.nih.gov/pubmed/23645387http://www.ncbi.nlm.nih.gov/pubmed/23645387http://www.ncbi.nlm.nih.gov/pubmed/22150425http://www.ncbi.nlm.nih.gov/pubmed/22150425http://www.ncbi.nlm.nih.gov/pubmed/22150425http://www.ncbi.nlm.nih.gov/pubmed/15466943http://www.ncbi.nlm.nih.gov/pubmed/15466943http://www.ncbi.nlm.nih.gov/pubmed/15466943http://www.ncbi.nlm.nih.gov/pubmed/22935440http://www.ncbi.nlm.nih.gov/pubmed/22935440http://www.ncbi.nlm.nih.gov/pubmed/22935440http://www.ncbi.nlm.nih.gov/pubmed/11684524http://www.ncbi.nlm.nih.gov/pubmed/11684524http://www.ncbi.nlm.nih.gov/pubmed/11684524http://www.ncbi.nlm.nih.gov/pubmed/20443094http://www.ncbi.nlm.nih.gov/pubmed/20443094http://www.ncbi.nlm.nih.gov/pubmed/20443094http://www.ncbi.nlm.nih.gov/pubmed/21558571http://www.ncbi.nlm.nih.gov/pubmed/21558571http://www.ncbi.nlm.nih.gov/pubmed/21558571http://www.ncbi.nlm.nih.gov/pubmed/20464707http://www.ncbi.nlm.nih.gov/pubmed/20464707http://www.ncbi.nlm.nih.gov/pubmed/20464707http://www.ncbi.nlm.nih.gov/pubmed/19041366http://www.ncbi.nlm.nih.gov/pubmed/19041366http://www.ncbi.nlm.nih.gov/pubmed/19041366http://www.ncbi.nlm.nih.gov/pubmed/10644531http://www.ncbi.nlm.nih.gov/pubmed/10644531http://www.ncbi.nlm.nih.gov/pubmed/10644531http://www.ncbi.nlm.nih.gov/pubmed/21991450http://www.ncbi.nlm.nih.gov/pubmed/21991450http://www.ncbi.nlm.nih.gov/pubmed/21991450http://www.ncbi.nlm.nih.gov/pubmed/20047634http://www.ncbi.nlm.nih.gov/pubmed/20047634http://www.ncbi.nlm.nih.gov/pubmed/20047634http://www.ncbi.nlm.nih.gov/pubmed/24072967http://www.ncbi.nlm.nih.gov/pubmed/24072967http://www.ncbi.nlm.nih.gov/pubmed/24072967http://www.ncbi.nlm.nih.gov/pubmed/17697152http://www.ncbi.nlm.nih.gov/pubmed/17697152http://www.ncbi.nlm.nih.gov/pubmed/17697152http://www.ncbi.nlm.nih.gov/pubmed/19175510http://www.ncbi.nlm.nih.gov/pubmed/19175510http://www.ncbi.nlm.nih.gov/pubmed/19175510http://www.ncbi.nlm.nih.gov/pubmed/19175510http://www.ncbi.nlm.nih.gov/pubmed/17697152http://www.ncbi.nlm.nih.gov/pubmed/24072967http://www.ncbi.nlm.nih.gov/pubmed/20047634http://www.ncbi.nlm.nih.gov/pubmed/21991450http://www.ncbi.nlm.nih.gov/pubmed/10644531http://www.ncbi.nlm.nih.gov/pubmed/19041366http://www.ncbi.nlm.nih.gov/pubmed/20464707http://www.ncbi.nlm.nih.gov/pubmed/21558571http://www.ncbi.nlm.nih.gov/pubmed/20443094http://www.ncbi.nlm.nih.gov/pubmed/11684524http://www.ncbi.nlm.nih.gov/pubmed/22935440http://www.ncbi.nlm.nih.gov/pubmed/15466943http://www.ncbi.nlm.nih.gov/pubmed/22150425http://www.ncbi.nlm.nih.gov/pubmed/23645387http://www.ncbi.nlm.nih.gov/pubmed/19486715http://www.ers.usda.gov/data-products/food-availability-(per-capita)-data-system/summary-findings.aspxhttp://www.ers.usda.gov/data-products/food-availability-(per-capita)-data-system/summary-findings.aspxhttp://www.ncbi.nlm.nih.gov/pubmed/19828708http://www.ncbi.nlm.nih.gov/pubmed/19567526http://www.ncbi.nlm.nih.gov/pubmed/19567526http://www.ncbi.nlm.nih.gov/pubmed/14656042

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Strength and body composition changes inrecreationally strength-trained individuals:comparison of one versus three sets resistance-training programmes. [Critiqued by Brad Schoenfeld,PhD(c), CSCS, CSPS, FNSCA].

__________________________________________________________________________

Baker JS, Davies B, Cooper SM, Wong DP, Buchan DS, Kilgore

L. BioMed Research International, vol. 2013, Article ID 615901,6 pages, 2013. doi:10.1155/2013/615901 [Hindawi]

PURPOSE: The purpose of this study was to determine theeffects of increasing the volume of weight-training from one tothree sets upon body composition and muscular strength.METHODS:Sixteen male weight-trainers volunteered to act assubjects and were randomly assigned to one of two traininggroups. Supervised weight-training targeting the upper body wasconducted three times per week for eight weeks using one set(n=8) or three sets (n=10) of six repetitions to fatigue. Subjectswere measured before and after the training intervention for (1)strength performance ( and kg) and (2) adiposity (sum of sevenskinfold thicknesses in mm). RESULTS:Both training groups

improved significantly (20.7%) in terms of muscular strength (P< 0.05 ) with no differences being observed between the one set(21.98% increase) and three set group (20.71% increase) afterthe training interventions (P > 0.05). Significant decreases werealso observed for skinfold measures in the one set group (P carb>soy was also seenGains in maximal bench press and squat strength weresignificant in all groups, with no between-group differencesInterestingly, while the whey group topped the field to anonsignificant degree in bench press gains, it had the lowestincrease in squatting strength (44%) compared to the carb (62%)and soy group (65%). But again, these differences were not

significant.

The authors attribute the superior lean mass gains in the wheygroup to its greater elevations in fasting and post-exerciseleucine concentrations. It has been proposed that a thresholddose of leucine required to maximize muscle protein synthesis isapproximately 2-3 g, or 0.05 g/kg.10The leucine content of thewhey protein isolate is about 10.9%, whereas in soy proteinisolate its 8% (chart here).11 So, in the 22g doses used in thepresent study, whey crosses over that leucine threshold while

soy does not reach it. In recent work by Joy et al, no significantdifferences were seen in the body composition and performanceimprovements resulting from a 48 g dose of whey versus riceprotein, presumably because both doses met the leucine

threshold.12

While its plausible that the superior lean mass gains in the whey

group could have been due to the higher leucine content ofwhey, Churchward-Venne et al13 recently found that low dosesof whey fortified with EAA or leucine to match the content of athreshold dose of whey (25 g) elicited a lower anabolic

response than the full dose of whey protein. This means thathere could be other factors intrinsic to whey protein(independent of its leucine content) that promote lean mass gain.
http://www.ncbi.nlm.nih.gov/pubmed/24015719http://www.ncbi.nlm.nih.gov/pubmed/24015719http://www.ncbi.nlm.nih.gov/pubmed/24015719http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3488566/table/T3/http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3488566/table/T3/http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3488566/table/T3/http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3488566/table/T3/http://www.ncbi.nlm.nih.gov/pubmed/24015719

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

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

BACKGROUND:Medical nutrition therapy is recognized as animportant treatment option in type 2 diabetes. Most guidelinesrecommend eating a diet with a high intake of fiber-rich food

including fruit. This is based on the many positive effects of fruiton human health. However some health professionals haveconcerns that fruit intake has a negative impact on glycemiccontrol and therefore recommend restricting the fruit intake. Wefound no studies addressing this important clinical question. Theobjective was to investigate whether an advice to reduce theintake of fruit to patients with type 2 diabetes affects HbA1c,bodyweight, waist circumference and fruit intake. METHODS:This was an open randomized controlled trial with two parallelgroups. The primary outcome was a change in HbA1c during 12weeks of intervention. Participants were randomized to one oftwo interventions; medical nutrition therapy + advice toconsume at least two pieces of fruit a day (high-fruit) or medicalnutrition therapy + advice to consume no more than two pieces

of fruit a day (low-fruit). All participants had two consultationswith a registered dietitian. Fruit intake was self-reported using 3-day fruit records and dietary recalls. All assessments were madeby the "intention to treat" principle. RESULTS: The studypopulation consisted of 63 men and women with newlydiagnosed type 2 diabetes. All patients completed the trial. Thehigh-fruit group increased fruit intake with 125 grams (CI 95%;78 to 172) and the low-fruit group reduced intake with 51 grams(CI 95%; -18 to -83). HbA1c decreased in both groups with nodifference between the groups (diff.: 0.19%, CI 95%; -0.23 to0.62). Both groups reduced body weight and waistcircumference, however there was no difference between thegroups. CONCLUSIONS: A recommendation to reduce fruitintake as part of standard medical nutrition therapy in

overweight patients with newly diagnosed type 2 diabetesresulted in eating less fruit. It had however no effect on HbA1c,weight loss or waist circumference. We recommend that theintake of fruit should not be restricted in patients with type 2diabetes. SPONSORSHIP:None listed.

Study strengths

This study is conceptually strong; it examines practical/realisticnon-pharmacological steps that might aid in the management oftype 2 diabetes (T2D), a global problem that continues to rise.This is the first controlled trial to compare the effect ofrestricting fruit intake to 2 per day with consuming at least 2 perday on glycemic control in adults with T2D. Both groups hadtwo consultations (one consultation in the beginning and one atthe end of the study period) with an experienced registereddietitian. Compliance to the interventions was good. One subjectwho failed to comply was excluded, but this did not affect theoutcomes. Subjects were instructed to eat fresh, whole fruit onlyand to exclude fruit juice, canned and dried fruit from their diet,or keep it as low as possible. This was a good move since itminimized the confounding effects of the consumption ofrefined, fruit-based products that could skew the aim of thestudy.

Study limitations

According to the authors, the study was prematurely terminated

due to limited time and research funding. First of all, that sucks

Secondly, the authors did not specify how much of the 12-week

intervention had to be cut short (or whether it indeed lasted 12

weeks but was originally intended to be longer). This is a rather

important reporting omission. Another limitation was the

reliance on a 3-day food record at only 2 points in the

intervention (before and after). Increasing the frequency of the

submission of diet reports or having the subjects keep a daily

record would have increased the accuracy of the intake

journaling. Another limitation was the lack of tracking and

analyzing the diet overall. At minimum, it would have been

useful to see how the high-fruit and low-fruit treatments

impacted macronutrient intake.

A final limitation (from a public health reporting perspective)

was the misleading definition of a fruit serving, which was the

amount of fruit that contains 10 g carbohydrate (e.g., 100 grams

apple, 50 grams banana or 125 grams orange). The problem I see

with this is that a typical whole fruit contains about double this

amount of carbohydrate. For example, a medium-sized banana

(118 g) contains 27 g carbohydrate. A medium-sized apple (182

g) contains 25 g carbohydrate. So, without reading the full text

one could easily assume that the amount of fruit assigned in the

study was at least double the actual amount consumed.

Comment/application

The main finding of this study was a lack of significantdifference in glucose control improvements between the highfruit and low-fruit interventions; both decreased HbA1cTherefore, the common recommendation for newly diagnosedT2D patients to limit fruit servings to 2 per day was nosupported by these findings. In addition, both groups showedsignificant decreases in bodyweight and waist circumferencewith no between-group differences. Interestingly, a tendencytowards reduced body weight and waist circumference was seenin the high-fruit group. However, given the relatively loosecontrol of the variables, these favorable trends in the higher-fruitgroup should be viewed with caution. Still, it should be notedthat the favorable results of the higher fruit consumption havebeen supported by recent observational research by Muraki et awho found that greater whole-fruit consumption is significantlyassociated with lower risk of T2D, while greater fruit juiceconsumption was associated with a higher risk.14 Interventionaresearch has also shown a consistency of positive effects of fruitintake.15-17Thus far it looks that whole fruit consumption to theorder of 2 servings (or possibly more) is not an inherent threat toglucose control or bodyweight/composition in those with T2Deven in the context of not meticulously tracking total carb intake
http://www.ncbi.nlm.nih.gov/pubmed/23497350http://www.ncbi.nlm.nih.gov/pubmed/23497350http://www.ncbi.nlm.nih.gov/pubmed/23497350http://www.ncbi.nlm.nih.gov/pubmed/23497350

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9. Schlundt DG, Hill JO, Sbrocco T, Pope-Cordle J, Sharp T. Therole of breakfast in the treatment of obesity: a randomizedclinical trial. Am J Clin Nutr. 1992 Mar;55(3):645-51.[PubMed]

10.Norton LE. Optimal protein intake to maximize muscleprotein synthesis: Examinations of optimal meal protein

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11. Norton LE, Wilson GJ, Layman DK, Moulton CJ, Garlick PJ.Leucine content of dietary proteins is a determinant of

postprandial skeletal muscle protein synthesis in adult rats.Nutr Metab (Lond). 2012 Jul 20;9(1):67. [PubMed]

12. Joy JM, Lowery RP, Wilson JM, Purpura M, De Souza EO,Wilson SM, Kalman DS, Dudeck JE, Jger R. The effects of8 weeks of whey or rice protein supplementation on bodycomposition and exercise performance. Nutr J. 2013 Jun20;12(1):86. [Epub ahead of print] [PubMed]

13. Churchward-Venne TA, Burd NA, Mitchell CJ, West DW,Philp A, Marcotte GR, Baker SK, Baar K, Phillips SM.

Supplementation of a suboptimal protein dose with leucine oressential amino acids: effects on myofibrillar protein synthesisat rest and following resistance exercise in men. J Physiol.

2012 Jun 1;590(Pt 11):2751-65. [PubMed]14. Muraki I, Imamura F, Manson JE, Hu FB, Willett WC, van

Dam RM, Sun Q. Fruit consumption and risk of type 2diabetes: results from three prospective longitudinal cohort

studies. BMJ. 2013 Aug 28;347:f5001. [PubMed]

15. Madero M, Arriaga JC, Jalal D, Rivard C, McFann K, Prez-Mndez O, Vzquez A, Ruiz A, Lanaspa MA, Jimenez CRJohnson RJ, Lozada LG. The effect of two energy-restricteddiets, a low-fructose diet versus a moderate natural fructosediet, on weight loss and metabolic syndrome parameters: arandomized controlled trial. Metabolism. 2011

Nov;60(11):1551-9. [PubMed]16. de Oliveira MC, Sichieri R, Venturim Mozzer R. A low-

energy-dense diet adding fruit reduces weight and energy

intake in women. Appetite. 2008 Sep;51(2):291-5. [PubMed]

17. Rodrguez MC, Parra MD, Marques-Lopes I, De Morentin BEGonzlez A, Martnez JA. Effects of two energy-restricted dietscontaining different fruit amounts on body weight loss andmacronutrient oxidation. Plant Foods Hum Nutr. 2005

Dec;60(4):219-24. [PubMed]
http://www.ncbi.nlm.nih.gov/pubmed/20300012http://www.ncbi.nlm.nih.gov/pubmed/20300012http://www.ncbi.nlm.nih.gov/pubmed/20300012http://www.ncbi.nlm.nih.gov/pubmed/19661829http://www.ncbi.nlm.nih.gov/pubmed/19661829http://www.ncbi.nlm.nih.gov/pubmed/19661829http://www.ncbi.nlm.nih.gov/pubmed/21925535http://www.ncbi.nlm.nih.gov/pubmed/21925535http://www.ncbi.nlm.nih.gov/pubmed/21925535http://www.ncbi.nlm.nih.gov/pubmed/21955734http://www.ncbi.nlm.nih.gov/pubmed/21955734http://www.ncbi.nlm.nih.gov/pubmed/21955734http://www.ncbi.nlm.nih.gov/pubmed/15883552http://www.ncbi.nlm.nih.gov/pubmed/15883552http://www.ncbi.nlm.nih.gov/pubmed/15883552http://www.ncbi.nlm.nih.gov/pubmed/20112153http://www.ncbi.nlm.nih.gov/pubmed/20112153http://www.ncbi.nlm.nih.gov/pubmed/20112153http://www.sciencedirect.com/science/article/pii/S0889157596900216http://www.sciencedirect.com/science/article/pii/S0889157596900216http://www.sciencedirect.com/science/article/pii/S0889157596900216http://www.ncbi.nlm.nih.gov/pubmed/14513075http://www.ncbi.nlm.nih.gov/pubmed/14513075http://www.ncbi.nlm.nih.gov/pubmed/14513075http://www.ncbi.nlm.nih.gov/pubmed/1550038http://www.ncbi.nlm.nih.gov/pubmed/1550038http://www.ncbi.nlm.nih.gov/pubmed/1550038http://agro-food-industry.teknoscienze.com/pdf/norton_AF2_09.PDFhttp://agro-food-industry.teknoscienze.com/pdf/norton_AF2_09.PDFhttp://agro-food-industry.teknoscienze.com/pdf/norton_AF2_09.PDFhttp://www.ncbi.nlm.nih.gov/pubmed/22818257/http://www.ncbi.nlm.nih.gov/pubmed/22818257/http://www.ncbi.nlm.nih.gov/pubmed/22818257/http://www.ncbi.nlm.nih.gov/pubmed/23782948http://www.ncbi.nlm.nih.gov/pubmed/23782948http://www.ncbi.nlm.nih.gov/pubmed/23782948http://www.ncbi.nlm.nih.gov/pubmed/22451437http://www.ncbi.nlm.nih.gov/pubmed/22451437http://www.ncbi.nlm.nih.gov/pubmed/22451437http://www.ncbi.nlm.nih.gov/pubmed/23990623http://www.ncbi.nlm.nih.gov/pubmed/23990623http://www.ncbi.nlm.nih.gov/pubmed/23990623http://www.ncbi.nlm.nih.gov/pubmed/21621801http://www.ncbi.nlm.nih.gov/pubmed/21621801http://www.ncbi.nlm.nih.gov/pubmed/21621801http://www.ncbi.nlm.nih.gov/pubmed/18439712http://www.ncbi.nlm.nih.gov/pubmed/18439712http://www.ncbi.nlm.nih.gov/pubmed/18439712http://www.ncbi.nlm.nih.gov/pubmed/16395633http://www.ncbi.nlm.nih.gov/pubmed/16395633http://www.ncbi.nlm.nih.gov/pubmed/16395633http://www.ncbi.nlm.nih.gov/pubmed/16395633http://www.ncbi.nlm.nih.gov/pubmed/18439712http://www.ncbi.nlm.nih.gov/pubmed/21621801http://www.ncbi.nlm.nih.gov/pubmed/23990623http://www.ncbi.nlm.nih.gov/pubmed/22451437http://www.ncbi.nlm.nih.gov/pubmed/23782948http://www.ncbi.nlm.nih.gov/pubmed/22818257/http://agro-food-industry.teknoscienze.com/pdf/norton_AF2_09.PDFhttp://www.ncbi.nlm.nih.gov/pubmed/1550038http://www.ncbi.nlm.nih.gov/pubmed/14513075http://www.sciencedirect.com/science/article/pii/S0889157596900216http://www.ncbi.nlm.nih.gov/pubmed/20112153http://www.ncbi.nlm.nih.gov/pubmed/15883552http://www.ncbi.nlm.nih.gov/pubmed/21955734http://www.ncbi.nlm.nih.gov/pubmed/21925535http://www.ncbi.nlm.nih.gov/pubmed/19661829http://www.ncbi.nlm.nih.gov/pubmed/20300012

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Are Americas nutrition professionals in the pocket of

Big Food? [my commentary on the article by JosephMercola]

By Alan Aragon________________________________________________

Intro & background

I have to admit that when someone linked me to this article, myBS defenses immediately went up since its author, JosephMercola, is a physician who is notorious in the science-basedhealth & fitness community for being quacky. He has a longhistory of warnings and battles with the FDA over false andillegal product claims.1 Nevertheless, I gave the article a look,and some very provocative points were raised, and this includedMercolas video interview with public health lawyer MicheleSimon. Simon has become somewhat of an iconic whistle-blower questioning the alliances of the Academy of Nutritionand Dietetics (AND), formerly called the American DieteticAssociation. Her 50-page critical analysis of ANDs corporateties with the food industry can be downloadedhere.

Since I got my undergraduate degree in nutrition & dieteticswith an AND-compliant curriculum taught mainly by registereddietitians (RDs), I find this conflict very interesting. Lets take a

look at some of the gripes against the AND, and how legitimatethey may (or may not) be.

The excerpt above captures the heart of the problem, while alsocapturing the sensationalistic nature of Mercolas delivery. Its a

biased slant to imply that sponsorships are bought solely bymajor junk food purveyors. They are other sponsors whose

products would not accurately be described as junk food. Heresa compilation of the largest vendors at the ANDs annua

meeting (officially called the Food & Nutrition Conference &ExpoFNCE):2

While the above revenue might make some folks jaws drop, its

important to note that AND sponsorship revenue was $1.85million, which is only 5% the total revenue.2 What plays the

largest role in keeping AND afloat are membership dues, whichin 2011 amounted to $11.16 million. Clearly, sponsorship moneyis not the backbone of the ANDs financial health, as somedisgruntled folks mistakenly believe.

Nevertheless, there is still the problem of how the corporatesponsors influence the continuing education of RDs, who areconsidered to be the most legitimate professionals in terms of

expertise in food and nutrition. The list of accredited continuingeducation providers for RDs include Pepsico Nutrition, NestleHealthcare Nutrition, Coca-Cola Company Beverage Institutefor Health and Wellness, Kraft Foods Global, and ConAgraFoods Science Institute. Thats an incomplete list, but its clear

how these companies involvement with producing continuing

education materials for RDs harbors an uncomfortably highpotential for conflict between science and commerce.

Its interesting to note that RDs (at least the ones who could bereached, more on that in a bit) are for the most part approving ofthe majority of the ANDs corporate sponsors. Here are the

results of a 2009 poll:2

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

Mills, Nestl, Kraft, and all of the major junk food purveyors

buy sponsorships to be at the Academy of Nutrition andDietetics annual trade organization meetings. They typically

end up having the largest booths on the expo floor. Besides

showcasing their food products, theyre also allowed to

sponsor or hold educational sessions at the meeting.
http://www.mercola.com/forms/background.htmhttp://www.mercola.com/forms/background.htmhttp://www.youtube.com/watch?v=qkuNejVGhTQhttp://www.youtube.com/watch?v=qkuNejVGhTQhttp://www.eatdrinkpolitics.com/about/http://www.eatdrinkpolitics.com/about/http://www.eatdrinkpolitics.com/about/http://www.eatdrinkpolitics.com/wp-content/uploads/AND_Corporate_Sponsorship_Report.pdfhttp://www.eatdrinkpolitics.com/wp-content/uploads/AND_Corporate_Sponsorship_Report.pdfhttp://www.eatdrinkpolitics.com/wp-content/uploads/AND_Corporate_Sponsorship_Report.pdfhttp://www.eatdrinkpolitics.com/wp-content/uploads/AND_Corporate_Sponsorship_Report.pdfhttp://www.eatdrinkpolitics.com/about/http://www.eatdrinkpolitics.com/about/http://www.youtube.com/watch?v=qkuNejVGhTQhttp://www.mercola.com/forms/background.htmhttp://www.mercola.com/forms/background.htm

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According to Reitshamer et al,3 only 13% of the dietitianssurveyed disapproved of all corporate sponsorship, and 68% saidthat it depends who the sponsor is. 83% say they should have asay in who is allowed to become a sponsor of the AND.Interestingly, 47% of members are unaccepting of increasedmembership fees in order to reduce sponsorship. More insiderdetails about this survey was reported here, where nutritiongraduate student Colby Vorland discusses his emailcommunication with the authors.4 Suffice it to say thatReitshamer et al did not have the budget to pay for access to theentire AND membership, so they were only able to access 10%of the membership through a second-hand process dictated bystate and district affiliates. As such, the poll could potentially beskewed in favor of member approval of the sponsors.

Rage against the machine

Having grown up in the dietetics curriculum, it was an unsaid

rule that you shouldnt mess with the parent organization unless

youre ready for a slap on the hand. So, it was surprising to findout about Dietitians for Professional Integrity (DPI), whoseinception appears to be largely inspired by Michele Simons

expos. Its a fast-growing group, reported have roughly 4000

members. DPI describes itself as such:Dietitians for Professional Integrity is composed of Registered

Dietitians, Dietetic Technicians, dietetics students, and other

concerned individuals who do not support the Academy of

Nutrition and Dietetics' current sponsorship model. We believe

these sponsorships pose a serious conflict of interest for a

nutrition organization and harm our credential and reputation.

DPI founderAndy Bellatiset up a formalonline petitioncallingfor the ANDs administrative executives to sever the ties with

companies that concentrate on the sale of refined/processedjunk food. Bellati asserts that the petition is the result ofcountless grievances from RDs to the AND, which has beenlargely unresponsive to their concerns. The following excerptfrom the petition captures the frustration:

When junk food giants are allowed to sponsor our conferences

and provide continuing "education" to Registered Dietitians,

our credential -- which we worked hard for and value -- loses

credibility in the eyes of the public. These alliances run so deep

that dietitians can attend webinars where these companies

tell them that soda is unfairly vilified, and that sugary cereals

are a healthful way for children to start their day to earn

continuing education credits for re-certification.

While the sugary cereals comment is debatable, one thing thatreally bugs me and makes me empathize with the DPI is theirlong-standing attempt to convince the administrators of the

FNCE to include a structured point-counterpoint session aboutthe ANDs corporate ties with Big Food. This would have been

an excellent step forward in exposing the benefits and detrimentsof this model. The DPI requested that the panel discussion be atleast partially composed of RDs. In a stroke of bad decision-making, the AND chose not to assemble a point-counterpointsession, but rather to have journalist Michael Specter andpsychology professor Paul Rozin give their viewpoints (sessiondescription here). Neither of those individuals is a registereddietitian, and no point-counterpoint discussion will take place. I

see this as a multi-faceted insult to the dietetics professionalswho provide vital support and sustenance to the AND.

Potential solutions

The following are Simons recommended steps (verbatimtoward resolving the AND/Big Food alliance problem:2

1) Greater Transparency: AND should make more detailsavailable to the public (or at least to members) regardingcorporate sponsorshipfar beyond what it currentlyprovides in its annual reports.

2) Request Input from Membership: Trade group policiesshould reflect the desires of its members. Many RDsobject to corporate sponsorship but dont know how to

make their voices heard.

3) Meaningful Sponsorship Guidelines: AND shouldimplement much stronger and more meaningfusponsorship guidelines, possibly looking to the Hungerand Environmental Nutrition Dietetic Practice Groups

stricter guidelines as a model.

4) Reject Corporate-Sponsored Education: AND shouldreject outright corporate-sponsored continuing education

as well as corporate-sponsored education sessions at itsannual meeting. AND should also consider placing moredistance between its credentialing arm and the mainorganization.

5) Increased Leadership on Nutrition Policy: In recent yearsANDs leadership has taken important steps to improveits policy agenda and create a positive presence inWashington. However, while the staff in the D.C. office islobbying on behalf of ANDs membership, education

sessions are being taught to RDs by Coke and Hersheys

This disconnect will continue to undermine ANDs

credibility on critical policy issues until the conflicts areresolved.

I agree with all of these suggestions. In my view, #4 is the mostimportant, since its the root of the problem. If the mea ns forcommercial objectives to influence educational materials areeliminated or minimized, then less bias will make its way intothe knowledge base of RDs. Suggestion #2 is crucially importantas well, since lending a deaf administrative ear to the memberswill only continue to brew civil unrest, and degrade the unity ofthe organization from the inside-out. I would add a 6th step toSimons list, and that would be to offer (or even mandate) extra

non-industry-funded courses on scientific/critical thinking andresearch methodology so that no RD is unarmed in the face ofdubious claimsby the food industry or other.

References

1. Barrett S. FDA Orders Dr. Joseph Mercola to Stop Illegal ClaimsQuackwatch. May 7, 2013. [Quackwatch]

2. Simon M. And now a word from our sponsors: Are Americas nutritionprofessionals in the pocket of Big Food? Jan 2013. [Eat Drink Politics AND Corporate Sponsorship - Full PDF]

3. Reitshamer E, Schrier MS, Herbold N, Metallinos-Katsaras E. Membersattitudes toward corporate sponsorship of the Academy of Nutrition andDietetics. Journal of Hunger & Environmental Nutrition. Sep 2013;8(3DOI: 10.1080/19320248.2013.817169 [JHEN]

4. Vorland C. Member attitudes toward corporate sponsorship of AND[Nutsci.org]
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Interview with Karen Pendergrass, founder of PaleoMovement Magazine.

By Alan Aragon

____________________________________________________

The following is an interview with Karen Pendergrass, which I

conducted shortly after she publicly interviewed me (here). Im

pleased to have her relay her knowledge about a controversial

topic that has been the object of my criticism for some time now.

Karens full bio plus links are listed at the end of the

interview...enjoy!

__________________________________________________

1. First of all, Id like to thank you for accepting this

interview, Im certain that the AARR audience will

appreciate your insight. What if any are your main

criticisms of the Paleo diet itself (whichever variant you want

to address), as well as the Paleo community at-large?

Thanks for asking me to do an interview, and I hope it givesyour readers something to chew on. Now, as far as generalcriticisms of the Paleo Diet itself,or as far as the concept of itgoes, I have none to report. Heres why:

1) Evolution via natural selection is the central dogma ofBiology.

2) The Paleo Diet serves as a logical framework based onevolutionary theory.

3) The Paleo Diet as an evolutionary template gives us thebasis for testable health predictions.

4) The Evolutionary Theory is a good framework forhypothesis generation.

Now, Its really not as far-fetched as one may think to apply the

evolutionary theory to diet. Heres a perfect example:

Evolutionarily and biologically speaking, I know that my cat isan obligate carnivore, and evolved to be that way over eons. Yet,I fed her Royal Canin Urinary SO for years because thats wha

the veterinarian prescribed her for chronic urinary tracinfections. Initially, I trusted the judgement of my vet, but mycat never improved. I postulated that my obligate carnivore of acat was biologically maladapted to her prescribed diet ofchicken, corn, rice, and soymeal, and I hypothesized that my catwould improve if I switched her to a raw cat food diet consistingof muscle and organ meat. Unwittingly, my cat Flip became ascience experiment. Luckily, it worked for her, and she hasnt

had a UTI since the transition, 4 years ago.

See, not outlandish. Read on.

The concept of the evolutionary diet, or Paleo Diet itself isapplied with a similar basis, often for similar reasons, but tohumans. The theory is that the Paleo Diet is the one which

humans are physiologically best suited for, since humans (homosapiens and homo sapiens sapiens) evolved following thisdietary pattern. So, people across the world are testing thistheory with an n=1 experimental design. Its a large-scaledscience experiment, and of course, results vary. Some find after30 days of eliminating grains, legumes, and dairy that theycannot reintroduce them well, while some find that they do jusfine. I think its good to know your personal limitations. In tha

capacity, the Paleo Diet is probably the best baseline to test yourdietary limitations from.

This is where I am probably going to get crucified by my owncommunity. We use evolution as a reason to adopt the PaleoDiet, but then we often forget what evolution is really about, theincredible ability for adaptation. Within my own community, Ioften hear No one is adapted to grains and legumes and dairy.

Trust me, I sincerely wish that were true, but it likely isnt.

While researching insecticide applications on monocrops, Ilearned that with every new insecticide class, cases of resistancesurfaced within 2 to 20 yearsthis type of prolonged exposure

artificially selects for resistance. We saw the same thing happenwith Methicillin-Resistant Staph. Aureus (MRSA). This, as I seeit, is part of the natural selection and evolution process.

I could be wrong, but this is how it makes sense to me for nowIf your ancestors were initially maladapted to their dietswhichis likely since early agrarian societies werent as healthy relative

to hunter-gatherer societies according to surveys of dental cariesand bone densities by physical anthropologistsagriculturalistswould have had selective pressures to adapt. If it takes 2 to 20years for insects to adapt, it seems likely that over the course of
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10,000 years of selective pressures from a Neolithic,agricultural-diet, would render some population of adaptedhumans.

By that accord, it also makes sense that the longer your ancestorshad adopted a Neolithic Diet, the greater your chances of beingwell-adapted are. Perhaps this is why studiesof aboriginalpopulations indicate that they experience an abnormally greaterrate of diseases of civilization when they adopt Neolithic

diets*. It may also explain why some specific ethnicities

experience abnormally greater rates of Neolithic diseases andautoimmune conditions, as well. Perhaps not enough time haspassed to exert enough selective pressure to manifest intoadaptation. Its not a perfect explanation, because there are

confounding groups like the Inuit, but it does merit furtherinspection.

Overall, the concept of the Paleo Diet can be viewed as simplyanother application of evolutionary theory to generate ahypothesis and test it. I have no qualms with that, and I dont

think anyone should in the name of science.

2. What do you feel are the most significant benefits (to

human health, the environment, or other) of going Paleothat are unique to the diet?

Talk about a loaded question there, Alan. Thats like asking me

to condense my 400+ page book into a few short paragraphs, andtheres no way I could really do justice to any of my arguments

in such a short interview, but Ill try.

In short, while some humans may have adapted to the post-agricultural-revolution diet, the planet has not. After 4 years ofreading, researching, and toiling over the concept of agriculturalsustainability, I have concluded that the Paleo Diet, and Paleo-esque diets hold the key to turning the clock back onenvironmental destruction that has occurred over the past 15,000

years, and I firmly believe it is the only diet that can besustainable in the long-term. Unfortunately, because the PaleoDiet is meat-based, many sustainability experts have erroneouslydeclared that the Paleo Diet is the worst, and that meat-free dietsthat obtain protein from plant sources are the best.

One way agricultural sustainability is often discussed belies theAnimal production is destroying the planet with greenhouse

gasses and pollutants so we should stop eating meat notion.

Then theres the idea that We should eat on a lower trophic

level because it must enable us to feed more people. Using bothof these rationales, it would appear, without further inspection,that grains and legumes are certainly superior protein sources for

the environment and food security. After all, we are often toldthat the only way to feed the planet is by increasing grainagricultural yields to meet the food demands of the projected 9billion global population of 2050.

While it is unequivocally true that 95% of the animal productionin this country is destroying this planet, we are throwing theproverbial baby out with the bathwater here by lumping allanimal production methods together. Not all animal productionmethods are created equally. Some are far more beneficial than

anyone dares give credit to (lest you be called a flesh-eatingmurderer), and because we fail to recognize that well-managedlivestock actually nets a negative carbon footprint and have theunique capacity to restore previously degraded lands and reverseprocesses of the burgeoning desertification crisis,* we havecommitted the logical fallacy of composition and are missingopportunities to save the planet via (generalization alert:) falsepretenses of moral superiority and misinformation.

Whats really missing in the environmental sustainability sect is

the bigger picture, the critical analysis, the Malcolm Gladwell-ian viewpoint of agricultural sustainability with an ecologicalens, if you will. While environmentalists, conservationists, andsustainability enthusiasts examine current issues and make futureforecasts, history is largely (and inexplicably) ignored.

In the study of agricultural sustainability and eco-restoration, Ihave used the Paleolithic Era as a baseline to compare all otheragricultural systems to. This is because 15,000 years ago whilehumans were hunter-gatherers, the vast majority of ecosystemswere functioning properly in the illustrious closed-loop nutrientcycle, food distribution was equitable, plants were efficientlyrunning the carbon cycle, animals aptly did their job of

maintaining the health of their prospective ecosystems, and thehealth of the soil was excellent. Gleaning information from thePaleolithic Era is a great place to learn about sustainability fromnot because it tells us what mightwork, but what hasworked.

The question is, what significant environmental changes couldhave caused these properly functioning systems to go awry on aglobal scale?

Its a common theory that the advent of agriculture was the

cause of these systems to falter, I agree, and there is plenty ofevidence to support that. The areas where humans first adoptedagriculture is highly correlated with distinct periods ounprecedented soil infertility, deforestation, desertification, and

other types of land degradation.** The truth is, the AgriculturalRevolution is really just one large science experiment that hasfailed miserably, but we continue with its proliferation anywayYou may have thought, perhaps, that through time and vasttechnological advances that we were able to mitigate theseconcerns, but we have not. In fact, technological advances haveonly served to make conditions like soil erosion and soiinfertility worse. Agricultural advances like monocultures, or

the agricultural practice of producing a single plant species overa relatively large area for a prolonged period of time, have beenimplicated in the process of:

1) Desertification2) Deforestation

3) Land Degradation4) Depleted Water Tables5) Climate Change

6) Habitat Loss and Extinction

Monocultures are the bane of our existence. This includesmonocultures of grains, monocultures of legumes, andmonocultures of animals, otherwise known as ConcentratedAnimal Feeding Operations (CAFOs). I can assure you, there areno monocultures that exist in nature because monocultures do
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not respect the basic tenets of ecology. Unfortunately, foodsfrom monocultures make up the bulk of our diets today, and yetsomehow, the inherent dangers of monocultures are alsoinexplicably ignored when we propose solutions to feeding theplanet. This baffles me.

To feed the world and heal the environment, it will requirebolstering food systems that focus on bioregionalism andfacilitating wildlife. It will require a system that fostersbiodiversity and reduces global reliance on monocultures. Its

going to require an overhaul of current food systems and anumber of paradigm shifts, including a new way to assessagricultural sustainability.

Sustainability is a hot topic these days, and everyone fromfarmers to square-rimmed hipsters drinking PBR endeavor todiscuss it. Unfortunately, there isnt really a universal definitionfor the word sustainable, so people generally throw facts

around without critically assessing a dietary plan or agriculturalsystem by its survivability. This is disconcerting because if the

goal is to reverse these ecological damages incurred over the last15,000 years and prepare for the next 100, we need to definesustainability so that we can objectively assess possible

solutions. We need guidelines. We need criteria. We need targetsto hit.

I propose that we universally accept and define agriculturalsustainability on a scale reflecting a systems capacity tocontinue to function productively in the event of any particular

economic, political, environmental, or food system disruption.Examples of these types of disruptions and their impact on foodsystems should be assessed by environmentalists,conservationists, ecologists, and biologists for theirsurvivability, and even culpability in the disruption itself.

The three top environmental offenders are the monocultures ofgrains, the monocultures of legumes, and the monocultures of

animals; this Industrial Agriculture system exists because wecontinuously buy into it as a society. The Standard AmericanDiet, Vegan Diet, Vegetarian Diet, and Paleo Diet, all have theirown unique set environmental pitfalls. Each still relies tooheavily on unsustainable forms of agriculture that are culpable inenvironmental destruction. Either we are purchasingmonoculture grains and legumes directly in the form of cereals,breads, and pastas, or we are purchasing them indirectly in theform of grain and soy-fed animals who live in confinement. Icannot tell which is worse.

What I can tell, is that the current system isnt working. Stephen

Hawking thinks were screwedand need to find a way off this

planet, and although I may be delusional... I think the Paleo Dietoffers us a fighting chance.

We have yet to find a dietary discipline that has proven itselfsustainable, except for the hunter-gatherer, Paleo Diet. Wehave yet to find a dietary discipline that has proven itselfecological sound, except for the hunter-gatherer, Paleo Diet.Again, the Agricultural Revolution is really just a failed scienceexperiment. Like Wendell Berry said, We didnt know what we

were doing because we didnt know what we were undoing.

We still dont know what we have undone, and continue to undo

Back to the original question, what significant environmentabenefit is unique to the Paleo Diet?

As the Paleo Movement has progressed, our focus has shiftedfrom simply what to eat, to where to get our food from. It is

now commonly known amongst Paleo adherents that findinglocal farms who produce pastured animals raised on species-appropriate diets is the best way to improve food quality, but

also alleviate other environmental and health concerns. Animalsthat are raised in this manner that perform their ecologicafunctions foster, not hamper, the most important thing thaenvironmental sustainability hinges upon: biodiversity. Its also

an excellent way to decentralize our food system, another vitalstep towards agricultural sustainability.

If we can promote the proliferation of decentralized farming byfinancially supporting these types of animal husbandry practicesinstead of purchasing foods from CAFOs, we can change thedirection of the market and change the direction ofenvironmental destruction. We can go from focusing on effortsto maintain the health of the soils, to repair the health of thesoils. We can reverse the processes of climate changedesertification, land degradation, and losses of biodiversity. Ifthe goal is to decentralize, eschew monocultures, promoteecological function, and improve biodiversity we canaccomplish much of this by gradually adhering to a moreorthodox type of Paleo Diet.

Is there another diet that could be adhered to without relying onmonocultures? Absolutely, I think all diets can be done withourelying on monocultures, but I suspect that it would belogistically nightmarish. But the real question is, which dietarydiscipline is most capable of reinstating biodiversity, feeding theplanet, reversing land degradation, decentralizing, and weaningoff the tit of Industrial Agriculture?

Honestly, I cant say with absolute certainty that I have the exact

answer, I can only say with absolute certainty that what we aredoing now is going to push us over the biodiversity cliff intooblivion, and we really should go back to the drawing board tocome up with better solutions. We have already entered the6thmass extinction,and our current extinction rate estimated to be1,000 to 10,000 times greater than the historical, backgroundrate.

In conclusion, I suspect that the Paleo Diet has the uniquepotential to be environmentally far superior than any otherdietary discipline. Im hedging my bets on what worked in the

past, since technological advances in the agrarian sect don

seem to adequately replace or respect the vast complexities ofnatural systems. And I dont suspect they ever will.

*Savory Institute Carbon Restoring Climate Through Capture

and Storage of Soil Carbon Through Holistic Planned Grazing

White Paper April 2013

**Andrew Kimbrell (Ed.) Fatal Harvest: The Tragedy of

Industrial Agriculture. Washington DC: Island Press Chapter

Farming in Natures Image, page 68
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3. The most current prevalence estimates of celiac disease

fall below one percent of the general population, while a

recent study estimated non-celiac gluten intolerance at about

half a percent of the population. Since there are several types

of gluten-free grains available commercially, how is it

justified to recommend a complete avoidance of all grain

types? Id like to hear your stance on this, since its one of

the logical impasses Ive found consistent with all variants of

the Paleo doctrine.

The American Autoimmune Related Diseases Associationestimates that there are around50 million people in the UnitedStates with an autoimmune condition, and suggests that itsprevalence may be increasing. To put that another way, that is 1in 6 individuals.

It seems to me that most people are under the impression thatgluten avoidance only makes sense for individuals with CeliacsDisease. Actually, I think it makes sense for all people who haveautoimmune conditions because of therole that it appears to playin theetiology of autoimmune disease.

Gluten is made up of two types of proteins, gliadins andglutenins. During the digestion process, gluten is broken down

into strings of amino acids, called peptides. Because gluten isnot degraded by heat or by digestion, it remains an intact,undigested 33-mer long polypeptide, and if it enters intosystemic circulation, an autoimmune response may occur if thepeptide sequence mimics the three-dimensional structure of anindividuals tissues. In this event, the immune system confuses

non-self proteins with self-proteins, a case of mistaken identityknown asmolecular mimicry. It is widely accepted that this iswhat happens in individuals with Celiacs Disease.

The immune system has a number of recognition or

identification mechanisms which allow the body to distinguishbetween its own proteins, and foreign proteins. This

identification system allows for foreign bodies to be discovered,identified, and subsequently destroyed. This makes perfect senseevolutionarily speaking, so that the body will initiate an immuneresponse to intrusions by viruses, bacteria, etc. When anantigen,or foreign invader is presented, immunoglobulins make

antibodies to combat them. There are IgA, IgG, IgM, IgE, andIgD subclasses of antibodies, and certain antibodies have beenlinked to the pathogenesis of autoimmune conditions, namelyanti-gliadin antibodies, which have been widely accepted as ahallmark for Celiacs Disease.

Research has shown elevated levels of anti-gliadin antibodies inseveral autoimmune conditions, not just Celiacs Disease. Thisis including, but not limited to:

Autoimmune Diabetes Multiple Sclerosis Rheumatoid Arthritis Psoriatic Arthritis Autism (not an autoimmune condition, but still interesting) Rett Syndrome Lupus Crohns Disease Ulcerative Colitis

Graves Disease Antiphospholipid Syndrome Pemphigus vulgaris

I had never heard ofPemphigus Vulgarisbefore.

Perhaps we (as in the 1 in 6 of us with autoimmune conditions)should consider avoiding gluten altogether. But should we avoidall grains like the plague? After all, most of the grains on themarket aregluten-free...

A study entitled Mucosal recovery and mortality in adults with

Celiac Disease after treatment with a gluten-free diet concludesthat Mucosal recovery was absent in a substantial portion ofadults with [Celiac Disease] after treatment with a [gluten-free-diet]. Immunoreacitvity was still presented.

While research is still inconclusive, its also hypothesized that

impaired intestinal barrier function is required in thedevelopment of autoimmunity. Because gliadin and otherprolamins are associated with the development of intestinadamage and zonulin release, they may be implicated in theprocess of autoimmune disease, aside from causing molecularmimicry in susceptible individuals.

Just because a grain is gluten-free doesnt mean it doesnt causeimmunoreactivity, and is safe for people with autoimmuneconditions. For instance:

The prolaminzeinin corn was found to illicit immunoreactivityin individuals with Celiacs Disease. I cant pull official figuresfrom the USDA after the federal funding lapse (their website isshut down) to illustrate how much corn is in our food, but I cantell you from experience that most gluten-free products use cornas the starch source.

Rice has the prolaminorzenin ,which is now causing rice to bereevaluated as a hypoallergenic food, since it is recognized as a

common and severe cause of food protein-induced enterocolitissyndrome. This is interesting, since enterocolitis is commonlyinduced by an autoimmunetargeting of glial cells.Though, I stilthink white rice may be relatively benign, but I may be wrongMillet and Sorghum arePanicoid grainswith zein-likeprolaminswhich are notably also resistant to digestion, and it is suggestedthat theyact likezeins, which are also implicated in the processof molecular mimicry.

Grain Prolamin % Total Protein

Wheat Gliadin 69

Rye Secalinin 50

Oats Avenin 16

Barley Hordein 52Millet Panicin 40

Corn Zein 55

Rice Orzenin 5

Sorghum Kafirin 52

Fun fact: approximately 56% of the protein consumed globallycomes from wheat, rye, oats, barley, millet, corn, rice, andsorghum*.
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This begs the question, does research justify gliadin abstinencefor individuals with autoimmune conditions? Are water-insoluble prolamins safe for people with compromised gutfunction? Clearly, more succinct information is needed.

But for the 1 in 6 who have a diagnosed, undiagnosed, ormisdiagnosed autoimmune condition, it appears logical that theycould benefit by removing all grains which have been noted toillicit immunoreactivity, which goes beyond the traditionalgluten-free approach, whether the research blatantly suggests

it or not. Though there are other factors that could causemolecular mimicry (likerotovirus,and certain types ofbacteria)it should be no wonder that so many people with previousautoimmune conditions report such drastic improvementsadhering to a more than just gluten-free, but a grain-free, PaleoDiet.

Now you may hav