11 - Nov - 2012

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Alan Aragons Research Review November 2012 [Back to Contents] Page 1

Copyright November 1st, 2012 by Alan Aragon Home: www.alanaragon.com/researchreview Correspondence: [email protected]

2 Complex problems, simple solutions.

By Matt Perryman

5 Timing of food intake predicts weight loss

effectiveness. Garaulet M, Gmez-Abelln P, Alburquerque-Bjar JJ, Lee YC, Ordovs JM, Scheer FA. Int J Obes (Lond). 2013 Jan 29. doi: 10.1038/ijo.2012.229. [Epub ahead of print]

ed[PubM ] 6 Carbohydrate co-ingestion with protein does not

further augment post-prandial muscle protein accretion in older men.

Hamer HM, Wall BT, Kiskini A, de Lange A, Groen BB, Bakker JA, Gijsen AP, Verdijk LB, van Loon LJ. Nutr Metab (Lond). 2013 Jan 25;10(1):15. [Epub ahead of print] PubMed[ ]

7 Concurrent training in elite male runners: The influence of strength versus muscular endurance training on performance outcomes.

Sedano S, Marn PJ, Cuadrado G, Redondo JC. J Strength ond Res. 2013 Jan 2. [Epub ahead of print] [C PubMed]

8 No effect of 1 or 7 days green tea extract ingestion

on fat oxidation during exercise. Randell RK, Hodgson AB, Lotito SB, Jacobs DM, Boon N,

Mela DJ, Jeukendrup AE. Med Sci Sports Exerc. 2012 Dec 14 [PubMed]

9 Effects of increased meal frequency on fat

oxidation and perceived hunger. Ohkawara K, Cornier M, Kohrt WM, Melanson EL. Effects

of increased meal frequency on fat oxidation and perceived hunger. Obesity 2012. Epub ahead of print. DOI: 10.1002/oby.20032 [Obesity]

11 Sports science professor Tim Noakes goes full

low-carb, part 3. By Alan Aragon

14 Nicotine and fat loss.

By Kurtis Frank and Sol Orwell

18 Chronic nutrient timing studies.

By Alan Aragon & Brad Schoenfeld


C omplex problems, simple solutions. By Matt Perryman _________________________________________________ Introduction Let's ask a simple question. When your car breaks down, you take it to your local mechanic. He knows his way around cars like I know my way around the liquor store. You know he'll track down the problem, fix it, and do it so well you won't think twice about it when you pick your car up. Are you going to ask him about his graduate degree in automotive engineering? My readers, including you AARR regulars, will be aware of my love for science. I believe that, on balance, scientific research is the ultimate arbiter of facts about the natural world, including our bodies. Over the last few years, however, my interests have zoomed out to the larger picture. The details of knowledge, and what that "on balance" implies, rate high on my list. What is a fact? How do we determine a fact about a living organism? How do we take those facts and make them relevant to our training and nutrition? Keeping those questions in mind, are we, as trainers and coaches and athletes, meant to be engineers, well versed in theory and engrossed in the deep layers of design, or more like the mechanic who may not have the first clue about how to design a car, but is so familiar with how it works that he can tell you what's wrong by hearing the engine idle? I'd like to have a look at these two distinct, but related, questions: what kind of knowledge do we need, and on a deeper level, what kind of knowledge can we ultimately have about living organisms in the first place? A New Biology

A society that permits biology to become an engineering discipline, that allows that science to slip into the role of changing the living world without trying to understand it, is a danger to itself. Modern society knows that it desperately needs to learn how to live in harmony with the biosphere. Today more than ever we are in need of a science of biology that helps us to do this, shows the way. An engineering biology might still show us how to get there; it just doesnt know where "there" is.

Carl Woese recently passed away at the age of 84, and it is to my regret that I only became aware of his work after his death. Woese had a long and interesting career, including the discovery of the "third kingdom" of life, the microbial archaea that may be the oldest form of life on Earth. Woese's work on the evolutionary origins of life via molecular phylogeny set him apart from the orthodoxy of the time,

although he would eventually be vindicated. He was nothing if not a big thinker, and as the quote above, taken from his 2004 paper "A New Biology for a New Century", suggests, he set his sights on the biggest target of all: the way we think about biology as a discipline.1 Woese argued that biology needed a guiding vision, and one distinct from those that drive it in previous centuries. He identifies a problem near and dear to my interests: how we can analyze wholes in terms of parts (and vice-versa)? Western science has long treated life as explainable in terms of the most fundamental parts atoms and forces a view which leaves the living world explained away as a "sea of tiny atomic particles". Woese rejects this picture, calling it the "colorless, reductionist world of 19th century classical physics", and instead advocates a richer perspective. "The time has come," he writes, "to replace the purely reductionist 'eyes-down' molecular perspective with a new and genuinely holistic, 'eyes-up,' view of the living world, one whose primary focus is on evolution, emergence, and biologys innate complexity." Readers of my blog will find familiar sentiments there; I find myself captivated by this suggestion and in large agreement with it. The conceptual viewpoint is no mere philosophical curiosity. Woese believed that the reductionist picture creates many problems, not the least of which being "that the biologists sense of what is important and what is fundamental was retooled to conform to the classical physicists perception thereof." From there, we see the inevitable spillover into the very concept of organism, of what it means to explain, of what biology itself really is and how it relates to other sciences. Before you know it, this understanding has crept into academia and society itself, to such an extent that it "is impossible to discuss modern biology without the cacophony of materialistic reductionism throughout." For Woese, this biology of materialism and molecules is an incomplete biology, and we have been looking at the essence of biology with the wrong lens. Indeed, true complexity, the vast 'nonlinear' world that physics now recognizes to exist, is beyond the purview of classical physics.

Lets stop looking at the organism purely as a molecular machine. The machine metaphor certainly provides insights, but these come at the price of overlooking much of what biology is. Machines are not made of parts that continually turn over, renew. The organism is. Machines are stable and accurate because they are designed and built to be so. The stability of an organism lies in resilience, the homeostatic capacity to reestablish itself.

Instead of the tired machine imagery, he suggests the metaphor of an eddy or whirlpool in a stream of water -- one which can withstand a child poking a stick into it. "Organisms are resilient patterns in a turbulent flow," he offers. For biology to survive as a discipline and move forward, it must move away from the


focus on parts and pieces. Doing so means "an emphasis on holistic, 'nonlinear,' emergent biology with understanding evolution and the nature of biological form as the primary, defining goals of a new biology." I'd reiterate that this is no crank at work, but one of the brightest minds to work in modern biology. I am inclined to agree with his points; I believe that when speaking of biological organisms, we are dealing not just with different scales but with a different type of being from familiar "dead" objects. And this, of course, has implications for not only biology as a science but what we (believe we) know about our bodies. A New Perspective

The reductionism and mechanicism Woese and many others so deeply abhor may be regarded as the Big Perspective ("vision") that has guided much of western science hitherto...All scientific endeavors are 'finite' because of..our perspectives. But this is no reason for despair; we can always try to change our perspectives.

The idea of an objective, God-like point of view, detached from the observer, is appealing and it has formed the basis of Western science since the beginning (the blame is typically placed at Descartes's feet, but the roots go back to Plato). However, it's also impossible to justify without taking for granted Descartes's "mind stuff" as distinct from the physical realm of matter and energy. The consequence is that there can be no "view from nowhere"; we are limited to an essentially human way of viewing the world. The idea called perspectivism has its roots in Nietzsche's writings. Modern philosophers of science have modernized the idea in the form of "scientific perspectivism", acknowledging the lack of a privileged, objective point of view while preserving the useful features of science. For a quick overview, we can look at a paper by Werner Callebaut.2 Callebaut argues that we may better understand "so-called universal laws of nature" as "defining highly generalized models that characterize a scientific perspective." Newton's laws characterize one point of view, Einstein's another, evolutionary biology still another. This has a profound implication, namely that our scientific theories only apply to specific and limited aspects of the world, and never with any total precision. We're left with a notion of "science" that leaves theory and observation closely entangled, far more than the "objective" story leads us to believe. Ronald Giere, who has argued for such a perspectivist model of science, adds:

Consensus among scientists on a particular scientific perspective arises out of both social interactions among members of a scientific community and interactions with the world, typically mediated by complex instrumentation. But just as scientists do in this way succeed in creating more detailed or more general, or

otherwise more desirable, perspectives on the world, so those of us who study science as a human activity can do the same. It is the best any of us can do.

(Emphasis added). This is not to deny that there is a real, objective "something" independent of us, but rather to suggest that our knowledge of that "something" must depend on a perspective rather than a God's eye view. What we know, then, is highly dependent on the specific domain or area under investigation. Move outside of that and you must adopt a new perspective. Take, for example, the currently popular belief that you can understand how muscles grow or fat is mobilized or how metabolism responds to exercise or diet entirely by analyzing studies that focus on the networks of biomolecules in single cells. Drawing on Pubmed stories about what happens in a living cell say, the sequence of molecular events that we understand to trigger protein synthesis in response to weight-training creates a necessarily incomplete picture; it is a wonderful and rich story about what goes on there, and it is also entirely dependent on the tools, methods, and theories which investigate life on that scale. Move out of that domain, say to an eating-and-exercising athlete, and you're left no better off. What happens in cells might hint at why some methods work, but we cannot simply theorize from specifics about cells to specifics about the how of real life. What Now? I left quite a bit out of these papers for brevity's sake as well as avoiding tiresome technical language, though I'd suggest reading them in full if you have any interest in these topics.3 It's important to note the position here; I am not talking about these papers as factual truths, but rather ideas to consider. I hope it's apparent that the situation may not be as simple a story as "science establishes objective facts without fail" (which usually translates to ripping selected papers out of a brief Pubmed search to "prove" something or other). That is one possible view, but in light of the discussion above (and make no mistake, this is a real and on-going debate), I am not convinced things work that way. We see that biology might not be what we think and worse yet, neither is science. What we observe depends, to some extent, on the theories and concepts by which we filter and give meaning to observations themselves. And we're stuck using that toolkit to study objects which may not be playing by the rules we're using to study them. In biology, what appears simple can be unimaginably complex and what appears complex beyond comprehension might be describable with a few simple rules. Based on all this, you might wonder if there's a way forward if we wish to be "evidence based" in our nutrition and exercise. Aren't we simply paralyzed by the raw complexity, by the uncertainty of it all? If we can't know facts and truths, how are we meant to proceed? I'm going to argue that we're in the exact opposite position: the lack of knowledge and fundamental


uncertainty are to our benefit. First of all, having only few truly "right" answers means it's also very hard to screw up. There is no optimum that you must strive to seek; the very idea of "optimum", as you would expect from an assembly line in a factory, is a phantom. Good enough is not just "good enough" it's all there is. It's a matter of scale; we may be ignorant (and ignorant of our ignorance) about biology in strict analytical terms, but at the top, where we live and play and eat, the complexity smooths out to simple guidelines. This has led me to a position that I might as well call pragmatism. By this I simply mean that there are no rules, no strict workouts or dietary plans, no need to obsess about hypothetical perfection. You don't have to appeal to experts with special, secret knowledge or worry about all the things you may love to worry about. Good enough is all there is. Instead of being driven by factoids from published research, you work by heuristics (guidelines, or rules-of-thumb), and you tinker. "Tinkering" is a word I've picked up from Nassim Taleb, who argues along similar lines: some phenomena are just not like machines that can be picked apart and analyzed in fine detail. The best we can do is watch and experiment.4 You can pick up heuristics by watching people train, by seeing what has worked and only then see if perhaps there is any biological explanation to lend support (or not). I would suggest being a skeptic with regard to any hard "rules" about training or nutrition, no matter where they come from. The tacit knowledge of the practitioner, the technician, is what we should see knowledge driven by observation, not by the abstract theory of formal science.5 For me, that is the lesson. Do something, do it with an open mind, and base your knowledge, as a practitioner, on outcomes rather than abstractions. Evidence comes from many places, and science itself is not as certain a bedrock as it can seem and that's okay. We are mechanics, not engineers. _

_________________________________________________

EDITORSS NOTE: More of Matts brotacular writings can be found at Myosynthesis.com. __________________________________________________ References 1. Woese, Carl R. A New Biology for a New Century.

Microbiology and Molecular Biology Reviews 68, no. 2 (2004): 173186. [PubMed]

2. Callebaut, Werner. Scientific Perspectivism: A Philosopher of Sciences Response to the Challenge of Big Data Biology. Studies in History and Philosophy of Science Part C: Studies in History and Philosophy of Biological and Biomedical Sciences 43, no. 1 (2012): 69-80. [PubMed]

3. If you're interested in a more detailed account of perspectivism, have a look at: Giere, Ronald N. Scientific Perspectivism. Chicago: University of Chicago Press, 2006.

4. See Taleb, Nassim. Antifragile: Things That Gain From Disorder. New York: Random House, 2012. Taleb's discussion of how we "fragilize" complex systems, including our own bodies, in our efforts to control and smooth out volatility including our compulsion to "do something" is applicable to our efforts in training and nutrition.

5. For more on this topic, see: Polanyi, Michael. Personal Knowledge: Towards a Post-Critical Philosophy. Chicago: University of Chicago Press, 1974.


Timing of food intake predicts weight loss

eness. effectiv Garaulet M, Gmez-Abelln P, Alburquerque-Bjar JJ, Lee YC, Ordovs JM, Scheer FA. Int J Obes (Lond). 2013 Jan 29. doi: 10.1038/ijo.2012.229. [Epub ahead of print] [PubMed] BACKGROUND: There is emerging literature demonstrating a relationship between the timing of feeding and weight regulation in animals. However, whether the timing of food intake influences the success of a weight-loss diet in humans is unknown. OBJECTIVE: To evaluate the role of food timing in weight-loss effectiveness in a sample of 420 individuals who followed a 20-week weight-loss treatment. METHODS: Participants (49.5% female subjects; age (means.d.): 4211 years; BMI: 31.45.4kgm(-2)) were grouped in early eaters and late eaters, according to the timing of the main meal (lunch in this Mediterranean population). 51% of the subjects were early eaters and 49% were late eaters (lunch time before and after 1500 hours, respectively), energy intake and expenditure, appetite hormones, CLOCK genotype, sleep duration and chronotype were studied. RESULTS: Late lunch eaters lost less weight and displayed a slower weight-loss rate during the 20 weeks of treatment than early eaters (P=0.002). Surprisingly, energy intake, dietary composition, estimated energy expenditure, appetite hormones and sleep duration was similar between both groups. Nevertheless, late eaters were more evening types, had less energetic breakfasts and skipped breakfast more frequently that early eaters (all; P0.05). CONCLUSION: Eating late may influence the success of weight-loss therapy. Novel therapeutic strategies should incorporate not only the caloric intake and macronutrient distribution-as is classically done-but also the timing of food. SPONSORSHIP: This study was supported by grants from Tomas Pascual and Pilar Gomez-Cuetara Foundations, Spanish Government of Science and Innovation, Seneca Foundation, NHLBI, NIDDKD, and USDA. S

tudy strengths A novel aspect of this study is the reporting of not just bodyweight, but also energy expenditure, physical activity (in METs), appetite hormones, and CLOCK genes, whose single nucleotide polymorphisms (SNPs) have been associated with weight loss or obesity depending on within-day timing of food intake. Sample size was relatively large (420 subjects), and trial duration was long (~20 weeks). Subjects met with a nutritional professional every 2 weeks, who counseled them on the range of dietary and behavioral program aspects. Energy and macronutrient records were software-analyzed. Study limitations The authors acknowledged a couple of limitations. First, the Harris-Benedict equation was used to predict energy requirements, and they conceded that this ...is not very accurate to assess energy expenditure, especially during weight loss. they also admitted that the groups could have had differences in resting energy expenditure that went undetected. A solution for this confounder would be the doubly labeled water technique, which is a more accurate/objective measure of energy

expenditure.1,2 Dietary intake was self-reported, and this introduces considerable error potential, as opposed to a more controlled model where food (at least the main meals) are provided by the lab. Its noteworthy, however, that the aforementioned measures of control are rare due to their astronomical expense in long trials with large subject numbers. Body composition was not measured, and the subjects results cannot necessarily be generalized to athletic populations. Comment/application A quick perusal could lead many to assume that the over-arching message is that eating later means getting fatter. However, its important to note that only the timing of lunch (early as opposed to late) was associated with a significantly greater loss of bodyweight. The timing of breakfast or dinner was not found to have any impact on bodyweight change. This finding deserves emphasis since it runs contrary to the automatic assumption that people will make namely, that dinner must be consumed early in order to effectively lose weight. However, taking a look at the chart above, the mean weight loss between the differing breakfast and dinner timing was practically identical. Upon closer examination of what qualified as a statistically significant difference in weight loss between the late and early lunch eaters amounted to a difference of 2.2 kg in 5 months hardly anything to get overly excited about, considering the potential confounders discussed. The authors found that late eaters happened to skip breakfast more frequently than early eaters, which they felt could be a contributing factor to their lesser weight loss. Curiously, they posited that the late lunch may prolong a semi-fasted state and induce glucose metabolism impairments. However, these speculations have questionable grounds due to the majority of controlled interventions that do not support them.3-7 The present findings, although interesting, dont exactly rock the boat of evidence. Replication with tighter control would be required. Ill conclude by quoting recent work by Sofer et al, who found opposite & potentially more relevant

utcomes despite concentrating energy intake later in the day:8 o ...our studies have demonstrated that manipulation of dietary carbohydrate distribution led to changes in the daily curves of leptin, ghrelin and adiponectin that coincided with improved hunger/satiety status, persistence in the weight loss process, anthropometric outcomes, insulin sensitivity, metabolic syndrome parameters and inflammatory status.

Carbohydrate co-ingestion with protein does not further augment post-prandial muscle protein ccretion in older men. a

Hamer HM, Wall BT, Kiskini A, de Lange A, Groen BB, Bakker JA, Gijsen AP, Verdijk LB, van Loon LJ. Nutr Metab (Lond). 2013 Jan 25;10(1):15. [Epub ahead of print] [PubMed] BACKGROUND: A blunted muscle protein synthetic response to protein ingestion may contribute to the age related loss of muscle tissue. We hypothesized that the greater endogenous insulin release following co-ingestion of carbohydrate facilitates post-prandial muscle protein accretion after ingesting a meal-like bolus of protein in older males. METHODS: Twenty-four healthy older men (75+/-1 y) were randomly assigned to ingest 20 g intrinsically L-[1-13C] phenylalanine-labeled casein protein with (PRO-CHO) or without (PRO) 40 g carbohydrate. Ingestion of specifically produced intrinsically L-[1-13C] phenylalanine labeled protein allowed us to assess post-prandial incorporation of dietary protein derived amino acids into muscle protein. Blood samples were collected at regular intervals, with muscle biopsies being obtained prior to and 2 and 6 h after protein ingestion. RESULTS: Plasma glucose and insulin concentrations showed a greater increase in PRO-CHO compared with PRO (P


Concurrent training in elite male runners: The influence of strength versus muscular endurance raining on performance outcomes. t

Sedano S, Marn PJ, Cuadrado G, Redondo JC. J Strength Cond es. 2013 Jan 2. [Epub ahead of print] [R PubMed]

BACKGROUND: Much recent attention has been given to the compatibility of combined aerobic and anaerobic training modalities. However few of these studies have reported data related to well-trained runners, which is a potential limitation. PURPOSE: Therefore, due to the limited evidence available for this population, the main aim was to determine which mode of concurrent strength-endurance training might be the most effective at improving running performance in highly-trained runners. METHODS: Eighteen well-trained male runners (age 23.7 1.2 yr) with a maximal oxygen consumption (VO2max) higher than 65 mLkgmin were randomly assigned into one of the three groups: Endurance-only Group (EG; n=6), who continued their usual training, which included general strength training with Thera-band latex-free exercise bands and endurance training; Strength Group (SG; n=6) who performed combined resistance and plyometric exercises and endurance training; Endurance-Strength Group (ESG; n=6) who performed endurance-strength training with loads of 40% and endurance training.. The study comprised 12 weeks of training in which runners trained 8 times a week (6 endurance sessions and 2 strength sessions) and 5 weeks of detraining. The subjects were tested on three different occasions (counter movement jump height, hopping test average height, one-repetition-maximum, running economy, VO2max, maximal heart rate (HRmax), peak velocity, rating of perceived exertion and 3-km time trial were measured). RESULTS: Findings revealed significant time x group interaction effects for all almost tests (p


No effect of 1 or 7 days green tea extract ingestion on fat oxidation during exercise. Randell RK, Hodgson AB, Lotito SB, Jacobs DM, Boon N, Mela DJ, Jeukendrup AE. Med Sci Sports Exerc. 2012 Dec 14 [PubMed] PURPOSE: The aim of this study was to investigate the effects of 1 day and 7 days ingestion of a green tea extract (GTE) on whole body fat oxidation during moderate-intensity exercise. METHODS: Thirty one males completed two exercise trials (60 min cycle 50% Wmax). Following the baseline trial (Day 0) subjects were randomly assigned to one of three conditions involving a week supplementation of; 1) 7 days placebo (PLA); 2) 6 days of PLA followed by 1 day of GTE (GTE1); 3) 7 days of GTE ingestion (GTE7). The morning after the supplementation week, subjects consumed an additional supplement and completed a second exercise trial (Day 8). VO2 and VCO2 measurements were taken during exercise to calculate whole body fat oxidation rates. Blood samples, for analysis of plasma fatty acids (FAs), glycerol and epigallocatechin gallate (EGCG), were collected at rest and during exercise. RESULTS: On Day 8 the plasma kinetics and maximal plasma concentrations of EGCG were similar in the GTE1 and GTE7 group (206 28 and 216 25 ngmL-1 respectively). One day of GTE ingestion did not affect markers of lipolysis during the exercise bout. Seven days of GTE ingestion significantly increased plasma glycerol during exercise (P=0.045) and plasma FAs during exercise (P=0.020) as well as at rest (P= 0.046). However, fat oxidation did not change in any of the groups. CONCLUSIONS: There was no effect of 1 day GTE ingestion on markers of lipolysis or fat oxidation during exercise. Seven days of GTE ingestion increased lipolysis, indicated by increased plasma FA and glycerol concentrations, but did not result in significant changes in fat oxidation. SPONSORSHIP: This work was supported by a research grant from Unilever Plc. S.L, D.J and D.M are employees of Unilever. R.R, A.H and A.J have no professional relationship with the company involved in this study and have no conflict of interests. N.B was a previous employee of Unilever however had no conflict of interest at the time of results interpretation. S

tudy strengths

This study is the first to measure the effect of green tea extract (GTE) on fat oxidation rates in humans, while also taking into account plasma catechin levels. Its also the first to directly compare the effects of 1 & 7 days of GTE ingestion on fat oxidation during 60 minutes of moderate-intensity exercise. The lab provided subjects all of their meals the day before the trial. To bolster compliance, daily text messages were sent to the

subjects to take their supplements, supplement logs were kept daily as well. Subjects were also required to return all empty cans when they visited the lab. Inclusion criteria involved choosing subjects who consumed a maximum of 400 mg caffeine per day in order to exclude those who might be desensitized to caffeines effects. Study limitations The outcomes might be limited to the short trial duration (7 days). Sample size was small (10-11 subjects per treatment arm). Moderately trained subjects were chosen, so the results might not be generalizable to other populations. As acknowledged by the authors, highly trained endurance athletes have less chance of showing significant effects on fat oxidation since they have high pre-existent whole-body fat oxidation rates as a result of muscular adaptations to their training protocols. A final limitation is that the results might not be relevant outside of the exercise testing protocol used, which was 60 minutes of cycling at 55% VO2max. These findings are not necessarily applicable to different training modes or to significantly higher or lower intensities. Comment/application

The main findings of this study were twofold. There was no significant difference in circulating EGCG after the 7-day and 1-day dosing of GTE/caffeine. Perhaps the most important finding, depicted above, was the lack of significant difference in fat oxidation between all three conditions, and this lack of effect on fat oxidation was seen despite an increase in lipolysis (fat mobilization, indicated by an increase in plasma fatty acid levels at rest and during exercise after 7 days of GTE/caffeine supplementation). The authors speculate that the 7 day trial period might not have been long enough to form functional compounds (i.e., proteins and enzymes) involved with upregulation of fatty acid oxidation. The bigger picture of GTEs effectiveness should be taken into consideration. Human research on the chronic effects of GTE as a weight loss supplement has shown a consistency of positive effects on fat oxidation. However, the effects tend to be small.18 To quote the conclusion of a recent systematic review of green tea catechins (GTC) by Phung et al:19 The administration of GTCs with caffeine is associated with statistically significant reductions in BMI, body weight, and [waist circumference]; however, the clinical significance of these reductions is modest at best. Current data do not suggest that GTCs alone positively alter anthropometric measurements.


Effects of increased meal frequency on fat oxidation nd perceived hunger. a

Ohkawara K, Cornier M, Kohrt WM, Melanson EL. Effects of increased meal frequency on fat oxidation and perceived hunger. Obesity 2012. Epub ahead of print. DOI: 10.1002/oby.20032 [Obesity] BACKGROUND: Consuming smaller, more frequent meals is often advocated as a means of controlling body weight, but studies demonstrating a mechanistic effect of this practice on factors associated with body weight regulation are lacking. METHODS: The purpose of this study was to compare the effect of consuming 3 (3M) vs. 6 meals (6M) per day on 24-h fat oxidation and subjective ratings of hunger. Lean (BMI0.05) in 24 h EE (8.7 0.3 vs. 8.6 0.3 mj.d-1), 24 h RQ (0.85 0.01 vs. 0.85 0.01) or 24 h fat oxidation (82 6 vs. 80 7 g.day-1) between 3M and6M, respectively. There was no difference in fullness24 h AUC, but hunger AUC (41850 2255 vs. 36612 2556 mm.24 h, P=0.03) and desire to eat AUC (47061 1791 vs. 41170 2574 mm.24 h, P=0.03) were greater during 6M than 3M. CONCLUSION: We conclude that increasing meal frequency from3 to 6 per day has no significant effect on 24 h fat oxidation, but may increase hunger and the desire to eat. SPONSORSHIP: Funding was provided by Research Fellowships of the Japan Society for the Promotion of Science for Young Scientists. Research support was provided by the University of Colorado Clinical and Translational Science Award and Nutrition and Obesity Research Center. Study strengths This study is innovative since surprisingly enough its the first to ever compare a traditional meal pattern (3 meals) versus smaller, more frequent meals (6 meals) on 24-hour fat oxidation and perceived hunger. A 3-day outpatient energy & macronutrient stabilization period followed each tightly controlled whole room calorimeter-based test day. All meals were provided to the subjects during both the lead-in and of course during calorimeter day. The calorimeter protocol included 2 bouts of bench-stepping exercise (72 steps per minute for 20 minutes) in order to mimic free-living activity. Subjects physical activity was monitored and tracked throughout the calorimeter period via accelerometer. The inherently compromised statistical power by the small number of subjects was alleviated by a crossover design. S

tudy limitations

Several limitations were diligently acknowledged by the authors (it bears repeating that this is refreshing to see since not all studies admit potential faults). First off, acute effects were examined, so long-term effects of this particular design are open to speculation. Secondly. the subjects were relatively lean, so the

relevance of these results to overweight or obese individuals can be questioned. Third, the women studied were not all in the same menstrual phase. Fourth, appetite-related hormones were not directly measured. a final limitation relayed by the authors is worth quoting, since they truly seemed to be reaching on this one (I find this amusing since most authors do whatever possible to avoid listing limitations): Finally, we performed our studies under isocaloric conditions to specifically study the effects of meal frequency, but given the higher ratings of hunger and lower fullness during 6M, we would expect intake to be increased during 6M under ad libitum conditions, an effect which needs to be studied directly. C

omment/application

The main findings were twofold. First off, fat oxidation and energy were not significantly different between the 3 and 6 meal-per-day treatments. Secondly and perhaps most notably perceiver hunger and desire to eat were greater in the 6 meal than the 3 meal condition. The latter results are in line with recent work by Leidy et al, who compared varying protein levels consumed within 3 or 6 meals and found that the higher meal frequency led to lower fullness ratings.20 Leidy et al found that PYY, a gut peptide associated with appetite reduction, was 9%

wer in the higher meal frequency condition. lo The present study adds to a very small body of research examining the question of meal frequencys effect on 24-hour fat oxidation. Only two other studies have specifically compared different meal frequencies on 24-hour fat oxidation, and the results were inconsistent with each other. Verboeket-van de Venne and Westerterp found no difference between 2 versus 7 meals per day,21 while Smeets & Westerterp-Plantenga found that 3 meals resulted in greater fat oxidation than 2 meals.22 The authors of the present study noted that the results of Smeets & Westerterp-Plantenga may have been attributable to the slightly (though non-significantly) lower energy balance in the 3-meal condition. In contrast, the present study achieved nearly zero-balance, which was nearly identical between conditions. a

As always, its important to consider the evidence of meal frequency on macro-effects. A comprehensive review of the research in this area was done in my critique of the ISSN position stand on meal frequency, and the majority of the evidence does not support the idea that higher frequency equals better weight loss or improvements in body composition.7 After I wrote the latter review in April 2011, more recent meal frequency research has since been published. A 6-month study by Bachman and Raynor found no significant differences in body mass index or energy intake between a 3 meal per day group and a grazing group that ate at least 100 cal every 2-3 hours.23 In contrast to Leidy et al,20 the grazing group reported a ignificant reduction in hunger by the end of the trial. s

The authors of the present study concluded that, although popular advice dictates that a grazing pattern is superior to lesser meal frequency for the goal of weight control, grazing was not seen to impart any advantages toward this end. In fact, the higher hunger and lower fullness ratings of the grazing condition render it a potentially inferior approach for dieters. In my observations, one size does not fit all, and meal frequency is best optimized according to individual preference.


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3. Sensi S, Capani F. Chronobiological aspects of weight loss in obesity: effects of different meal timing regimens. Chronobiol Int. 1987;4(2):251-61. [PubMed]

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

5. Keim NL, Van Loan MD, Horn WF, Barbieri TF, Mayclin PL. Weight loss is greater with consumption of large morning meals and fat-free mass is preserved with large evening meals in women on a controlled weight reduction regimen. J Nutr. 1997 Jan;127(1):75-82. [PubMed]

6. Sofer S, Eliraz A, Kaplan S, Voet H, Fink G, Kima T, Madar Z. Greater weight loss and hormonal changes after 6 months diet with carbohydrates eaten mostly at dinner. Obesity (Silver Spring). 2011 Oct;19(10):2006-14. [PubMed]

7. Aragon AA. A critique of the ISSN position stand on meal frequency. April 4, 2011. [Leangains].

8. Sofer S, Eliraz A, Kaplan S, Voet H, Fink G, Kima T, Madar Z. Changes in daily leptin, ghrelin and adiponectin profiles following a diet with carbohydrates eaten at dinner in obese subjects. Nutr Metab Cardiovasc Dis. 2012 Aug 14. [Epub ahead of print] [PubMed]

9. US Census Bureau, US Dept of Commerce. 2010 Census shows 65 and older population growing faster than total US population. Nove 30, 2011. [USCB]

10. Staples AW, Burd NA, West DW, Currie KD, Atherton PJ, Moore DR, Rennie MJ, Macdonald MJ, Baker SK, Phillips SM. Carbohydrate does not augment exercise-induced protein accretion versus protein alone. Med Sci Sports Exerc. 2011 Jul;43(7):1154-61. [PubMed]

11. Moore DR, Robinson MJ, Fry JL, Tang JE, Glover EI, Wilkinson SB, Prior T, Tarnopolsky MA, Phillips SM. Ingested protein dose response of muscle and albumin protein synthesis after resistance exercise in young men. Am J Clin Nutr. 2009 Jan;89(1):161-8. [PubMed]

12. Yang Y, Breen L, Burd NA, Hector AJ, Churchward-Venne TA, Josse AR, Tarnopolsky MA, Phillips SM. Resistance exercise enhances myofibrillar protein synthesis with graded intakes of whey protein in older men. Br J Nutr. 2012:1-9. [PubMed]

13. Pennings B, Groen B, de Lange A, Gijsen AP, Zorenc AH, Senden JM, van Loon LJ. Amino acid absorption and subsequent muscle protein accretion following graded intakes of whey protein in elderly men. Am J Physiol Endocrinol Metab. 2012 Apr 15;302(8):E992-9. [PubMed]

14. Paavolainen L, Hkkinen K, Hmlinen I, Nummela A, Rusko H. Explosive-strength training improves 5-km running time by improving running economy and muscle power. J Appl Physiol. 1999 May;86(5):1527-33. [PubMed]

15. Aagaard P, Andersen JL, Bennekou M, Larsson B, Olesen JL, Crameri R, Magnusson SP, Kjaer M. Effects of resistance training on endurance capacity and muscle fiber composition in young top-level cyclists. Scand J Med Sci Sports. 2011 Dec;21(6):e298-307. [PubMed]

16. Mikkola J, Vesterinen V, Taipale R, Capostagno B, Hkkinen K, Nummela A. Effect of resistance training regimens on treadmill running and neuromuscular performance in recreational endurance runners. J Sports Sci. 2011 Oct;29(13):1359-71. [PubMed]

17. Aagaard P, Andersen JL. Effects of strength training on endurance capacity in top-level endurance athletes. Scand J Med Sci Sports. 2010 Oct;20 Suppl 2:39-47. [PubMed]

18. Hursel R, Viechtbauer W, Dulloo AG, Tremblay A, Tappy L, Rumpler W, Westerterp-Plantenga MS. The effects of catechin rich teas and caffeine on energy expenditure and fat oxidation: a meta-analysis. Obes Rev. 2011 Jul;12(7):e573-81. [PubMed]

19. Phung OJ, Baker WL, Matthews LJ, Lanosa M, Thorne A, Coleman CI. Effect of green tea catechins with or without caffeine on anthropometric measures: a systematic review and meta-analysis. Am J Clin Nutr. 2010 Jan;91(1):73-81. [PubMed]

20. Leidy HJ, Armstrong CL, Tang M, Mattes RD, Campbell WW. The influence of higher protein intake and greater eating frequency on appetite control in overweight and obese men. Obesity (Silver Spring). 2010 Sep;18(9):1725-32. [PubMed]

21. Verboeket-van de Venne WP, Westerterp KR. Influence of the feeding frequency on nutrient utilization in man: consequences for energy metabolism. Eur J Clin Nutr. 1991 Mar;45(3):161-9. [PubMed]

22. Smeets AJ, Westerterp-Plantenga MS. Acute effects on metabolism and appetite profile of one meal difference in the lower range of meal frequency. Br J Nutr. 2008 Jun;99(6):1316-21. Epub 2007 Dec 6. [PubMed]

23. Bachman JL, Raynor HA. Effects of manipulating eating frequency during a behavioral weight loss intervention: a pilot randomized controlled trial. Obesity (Silver Spring). 2012 May;20(5):985-92. [PubMed]


Sports science professor Tim Noakes goes full low-carb, part 3. By Alan Aragon Onward into the sunset Welcome to the final installment of my critique of Tim Noakes carbophobic manifesto for the masses.1 As with the previous, Ill interject my commentary between key sections of Noakes article. Lets begin where we left off, with Noakes warning that carbs can be the kiss of death, even for competitive endurance athletes. Noakes appears to be reaching for anything he can grasp. So, there are chunkier competitors who finish slower in marathons? Stop the presses, how can this be true ? Of course, its easy to guess the hypothesis hell present (carbohydrate addiction and carbohydrate resistance, stuff thats been discussed in the last issue). However, the thing that bugs me in most in the above section is his passive acceptance of body mass index (BMI = weight in kg divided by height in meters squared), particularly within the context of athletic populations. I laughed out loud at him calling it an excellent proxy for whether one is eating the right amount of energy each day. Really? Wow...

he NHLBIs BMI guidelines are as follows:2 T Underweight:


Noakes is essentially recommending that children and babies go on the Atkins diet (remember banting is a colloquialism for the Harvey/Banting diet, which was a forerunner of the Atkins diet). His claim that many baby formulas are full of sugar and carbohydrate and cannot provide the proper nutrients for optimum development is questionable on a couple of counts. First of all, infant formula composition, unlike most food products, is actually regulated. The nutrient content of infant formula sold in the United States is regulated by the FDA, and these regulations are based on standards set by the American Academy of Pediatrics (AAP), which is not some rinky-dink operation that flies by the seat of its pants. The AAP is a professional/scientific organization that is heavily involved in research, continuing medical education, and the improvement of clinical practice guidelines. Keep in mind that Im not saying that major health organizations are exempt from critical analysis. However, I would say that Noakes suggestion that infant diets should consist mostly of fat and protein is silly, given that mature human breast milk, by volume, has been reported to consist of 3-5% fat, 0.8-0.9% protein, 6.9-7.2% carbohydrate (mainly as lactose).7 Further challenging Noakes protein/fat-centric recommendations for infants, Koletzko et al reported that protein intake is 5580% higher in formula-fed babies than in breastfed infants, which has raised concerns of what the long-term impact might be. Their research warrants a direct quote (my underlined emphasis added):8

We randomly assigned healthy infants who were born at term to receive for the first year infant formula and follow-on formula with higher or lower protein contents, respectively. The follow-up data obtained at age 2 y indicate that feeding formula with reduced protein content normalizes early growth relative to a breastfed reference group and the new World Health Organization growth standard, which may furnish a significant long-term protection against later obesity.

Similarly children who are obese already at a young age willmost likely have CR and carbohydrate addiction and wouldbenefitenormouslybybanting.Thereisalsogrowinginterestthat, at the other end of the age spectrum, the elderly brain(like mine) requires a high fat intake to protect it from thedetrimentaleffectsofaging.

concentrations. Ifanyof these threevalues iselevated, it isasureindicationthatoneisheadingforadultonsetdiabetesandthequickeroneadoptsapreventive,lowcarbohydratediet,thebetter.

What Noakes nebulously labels as carbohydrate resistance is better referred to as impaired glucose tolerance (IGT), which presents itself when challenged with an oral glucose load. Impaired fasting glucose (IFG) may or may not accompany IGT, but both conditions are associated with pre-diabetes. IGT is characterized by having a certain degree of insulin resistance, so these descriptors can be interchanged. The most objective test for glucose tolerance (which can interchangeably be considered a test for insulin sensitivity) is the hyperinsulinemic-euglycemic clamp technique, which requires a steady intravenous infusion of insulin. Circulating glucose level is then clamped at a normal fasting concentration, and blood samples are then taken to monitor serum glucose so that a steady fasting level can be maintained. The degree of insulin sensitivity is directly proportional to the glucose uptake by target tissues. In other words, the less glucose that's taken up by tissues during the procedure (and the more insulin required to get the job done), the more insulin resistant/less insulin-sensitive someone is. A detailed review of these concepts and diagnostic criteria can be found in peer-reviewed full text here.9

Sonowtomydietarychoices.RecallthatIamprofoundlyCRsothatImustrestrictcarbohydratesasmuchaspossibletodelaytheonsetofdiabetesforaslongaspossible,hopefullyforeversothatIwillsuccumbfromsomeother,lessdestructive(but)terminalillness.SoIrestricttheintakeofthefoodslistedbelow.Ihavefounditeasiestsimplytoremoveallfrommydiet.ThosewithlesserdegreesofCR(andcarbohydrateaddiction)willnotneedtobeasrestrictiveasamI.

Noakes then goes on to list the foods that he completely avoids, which include sugar, soft drinks, bread, rice, potatoes, porridge, breakfast cereals, high-energy fruits like bananas, all confectionary (cakes & sweets), desserts, products containing artificial sweeteners such as diet sodas, and vegetable oils with a high omega-6 content. I find this list amusing for many reasons, but Im still waiting for Noakes to provide some sort of quantitative allowance for carbohydrates, which he does in the following passage:

The finalpoint ishowdoesonedetermine ifone isCRornot.Firstisthefamilyhistory.Ifthereisaclosefamilymemberwithadultonsetdiabetes,thenoneismorelikelytobeCR.Secondisonesweighthistory.Thosewhowereheavy(obese)aschildrenare very likely to be CR.Alternatively a history of progressiveweight gain through adult life or with pregnancy or at themenopause, and an inability to forestall weight gain wheneatingahighcarbohydratedietisalsoverysuggestive.Frequentfailedattempts to loseweightwhen following themoreusualcalorierestrictedbutstillhighcarbohydratediet, isalsohighlyuggestive.sFinally when the CR is advanced it can be diagnosed withcertainty with a fasting blood sample that shows elevatedfastingglucose,insulinandglycosylatedhaemoglobin

HowevertherealpointisthatifoneisasCRasamI,onehastomake choicesof (i)howmuch carbohydrateonewants toeateachday.Ilimitmyselftobetween5075gramsadayasthatisthe amount that allows me to regulate my body weighteffortlessly without hunger and (ii) which carbohydratesourceswillprovidethatscantyamountofcarbohydrate.Ihavechosen to get mymiserly grams of carbohydrate from highlynutritiousvegetablesanddairyproduce,not fromwholegraincereals.Othersmightbeadvisedtomakeadifferentchoice.

So, there it is. Since Noakes is restricting his carb intake to 50-75 grams a day, his diet defaults to the exclusion of the aforementioned foods. The foods he allows himself are eggs, fish, organic/grass-fed meat, dairy (I was surprised at this), non-

starchy vegetables, nuts (except for peanuts and cashews, wihch he considers to be high in carbohyrates), and fruits (only those with a lower carbohydrate concentration. He allows himself tea and coffee, but unsweetened of course. One thing Noakes is careful about doing is not specifically pushing his personal carbohydrate intake on the reader, although its purported benefit for everyone across the board is heavily implied. My opinion? Great, hes restricting carbs and self-righteously loving it. Good for him, I hope this is his personal long-term solution to controlling overall caloric intake which is really the heart of the matter, not carbohydrate per se. An overconsumption of total calories leading to progressively excessive body fat was likely the largest contributor to Noakes diagnosis of pre-diabetic status, which was probably hastened by his likely neglect for resistance/strength training, which we now know is potentially the most powerful mode of exercise for improving glucose tolerance.


Apparently, Noakes has an open-minded approach to supplementation, which can be a double-edged sword. The case for omega-3 supplementation has been challenged in the peer-reviewed literature repeatedly within the past year. A widely publicized systematic review/meta-analysis by Rizos et al concluded that omega-3 PUFA supplementation was not associated with a lower risk of all-cause mortality, cardiac death, sudden death, myocardial infarction, or stroke.10 Another recent systematic review/meta-analysis by Kotwal et al is worth quoting since it nicely sums up the general trend of the findings:11

Recommendations for the use of fish oil supplements are included in a number of guidelines, but the neutral outcomes of recent large trials have served to weaken rather than strengthen the evidence base. Although it remains possible that fish oil supplements will produce health benefits through the prevention of vascular complications, the size of these gains are probably smaller than previously believed, and both physician and patient expectations may need to be reset.

Noakes then recommends that the reader seek counseling from a registered dietitian (RD), but also acknowledges that not all RDs will cozy up to the approach of carbohydrate restriction. As a solution to this, Noakes proposes that consumers should approach RDs and tell them specifically that they want to bant, and this in turn might eventually increase the number of RDs who are willing to engage in it. To me, this sounds like a futile effort since the majority of RDs will not do a cursory Google search for the specifics of the Harvey/Banting diet. Rather, a large segment are more prone to seek information from the Evidence Analysis Library (EAL) of the Academy of Nutrition & Dietetics (formerly the American Dietetics Association). The EAL is a resource designed to assist RDs in clinical judgement.

Much of the ANDs literature (including the EAL) contains content which in large part is highly critical and cautionary of low-carb dieting. A prime example is the ANDs most recent position paper on weight loss, which states the following:12

The EAL also notes that safety has not been evaluated for long-term, extreme restrictions of carbohydrates 35% of energy from carbohydrates) and specifically recommends that practitioners use caution in suggesting a low-carbohydrate diet for even short-term use in patients with osteoporosis, kidney disease, or in patients with increased ow-density lipoprotein cholesterol. l

The AND has carried on a long-standing tradition of harboring an anti-low-carb undercurrent. I disagree with the tenacity of their caution toward the clinical viability of carbohydrate restriction, since this has been demonstrated as an effective tactic in a growing body of literature spanning beyond the past decade.13 At the same time, its unscientific to ignore the full range of evidence showing the effectiveness of a very wide range of macronutrient set-ups across a wide range of populations. This is where individual programming comes in, rather than assuming that a single dietary approach is the end-all.

Ialsocurrentlysupplementmyeatingwithomega3 fattyacidcapsules(1.62g/day).Thevalueofomega3supplementationseemstobeuniversallyaccepted.Iamalsoexperimentingwithsupplementationofarangeofvitaminsbutthisisstillaworkinprogress as ismy choiceof thebest vegetables and salads tolimit the CR and two other medical tendencies that genetictestinghasrevealed.

R

eferences 1. Noakes T. Tim Noakes on Carbohydrates. June 18, 2012. [Health 24] 2. National Heart, Lung, and Blood Institute. Clinical Guidelines on the

identification, evaluation, and treatment of overweight and obesity in adults: the evidence report. September, 1998. [NHLBI]

3. Romero-Corral A, Montori VM, Somers VK, Korinek J, Thomas RJ, Allison TG, Mookadam F, Lopez-Jimenez F. Association of bodyweight with total mortality and with cardiovascular events in coronary artery disease: a systematic review of cohort studies. Lancet. 2006 Aug 19;368(9536):666-78. [PubMed]

4. Flegal KM, Graubard BI, Williamson DF, Gail MH. Cause-specific excess deaths associated with underweight, overweight, and obesity. JAMA. 2007 Nov 7;298(17):2028-37. [PubMed]

5. Kyle UG, Schutz Y, Dupertuis YM, Pichard C. Body composition interpretation. Contributions of the fat-free mass index and the body fat mass index. Nutrition. 2003 Jul-Aug;19(7-8):597-604. [PubMed]

6. Abernathy RP, Black DR. Healthy body weights: an alternative perspective. Am J Clin Nutr. 1996 Mar;63(3 Suppl):448S-451S. [PubMed]

7. Jenness R. The composition of human milk. Semin Perinatol. 1979 Jul;3(3):225-39. [PubMed]

8. Koletzko B, von Kries R, Closa R, Escribano J, Scaglioni S, Giovannini M, Beyer J, Demmelmair H, Anton B, Gruszfeld D, Dobrzanska A, Sengier A, Langhendries JP, Rolland Cachera MF, Grote V. Can infant feeding choices modulate later obesity risk? Am J Clin Nutr. 2009 May;89(5):1502S-1508S. [PubMed]

9. American Diabetes Association. Diagnosis and classification of diabetes mellitus. Diabetes Care. 2005 Jan;28 Suppl 1:S37-42. [PubMed]

10. Rizos EC, Ntzani EE, Bika E, Kostapanos MS, Elisaf MS. Association between omega-3 fatty acid supplementation and risk of major cardiovascular disease events: a systematic review and meta-analysis. JAMA. 2012 Sep 12;308(10):1024-33. [PubMed]

11. Kotwal S, Jun M, Sullivan D, Perkovic V, Neal B. Omega 3 Fatty acids and cardiovascular outcomes: systematic review and meta-analysis. Circ Cardiovasc Qual Outcomes. 2012 Nov;5(6):808-18. [PubMed]

12. Seagle HM, Strain GW, Makris A, Reeves RS; American Dietetic Association. Position of the American Dietetic Association: weight management. J Am Diet Assoc. 2009 Feb;109(2):330-46. [PubMed]

13. Hession M, Rolland C, Kulkarni U, Wise A, Broom J. Systematic review of randomized controlled trials of low-carbohydrate vs. low-fat/low-calorie diets in the management of obesity and its comorbidities. Obes Rev. 2009 Jan;10(1):36-50. [PubMed]


N icotine and fat loss. By Kurtis Frank and Sol Orwell N

icotine as a fat burner?

Recently, nicotine (primary stimulatory compound found in cigarettes, also used as a means in isolation to reduce cravings for cigarettes) has become more commonly used for fat burning purposes. The link between weight loss and nicotine initially comes from epidemiological research, where a consistent correlation between less weight and nicotine usage exists (mostly attributed to less food intake secondary to both social factors and appetite suppression), but a recent surge of popularity has occurred with athletes and lay persons looking to ose weight. l

A good deal of the popularity can be traced back to an article titled, Can Nicotine Safely Burn Fat and Build Muscle? The Surprising Facts1 by the author John Kiefer, best known for developing a popular dietary method called Carb Back-Loading. Independent of whether or not nicotine can be used as a fat burner and muscle building agent, the article itself does not constitute sufficient evidence to recommend nicotine, and its use of references warrants critique. Adrenaline Diabetes Adrenaline Diabetes was the term used by the author to define a state where the body becomes resistant to the effects of catecholamines and catecholamine mimetics which is supposedly similar in phenotype to true type II diabetes, specifically insulin resistance. This phrase was used in regards to the supposed decreased efficacy of classical fat burners such as ephedrine or clenbuterol, as these compounds target and interact with the same receptors as adrenaline. As any new phrase or

henomena, it needs to be proven to actually exist. p He supports the existence of this phenomenon (that the body can become insensitive to catecholamines such as adrenaline) with four citations: the last three of which are review articles which can be found by merely doing a Pubmed search for Beta-adrenergic (the receptor in question) and desensitization and the first is an acute experiment.2 This study was in vitro (outside of the body), and saturated a cell to acutely induce beta-adrenergic insensitivity in order to assess how the cell responds to it. This study does not support the claim of adrenaline diabetes, which would be characterized by chronic insensitivity in a living model rather than an acute study. All receptors can be desensitized pretty effectively if we override them acutely in itro. v

Oddly, the actual desensitization response to anything that acts on this receptor class is not too straight forward and it seems longer lasting ligands (things that circulate in the blood for

longer periods of time) have more potential for desensitization while shorter agonists, like catecholamines themselves should be (fight or flight response should be short in nature) either inert or potentiated. This is normally seen in studies on asthmatics as long-term bronchodilators (typically acting on the same receptors) tend to induce some degree of insensitivity while ephedrine, a short acting one, seems to be potentiated in vivo.3 This is because when the agonist is removed of culture, the receptor gets resensitized within hours if not minutes.4 Quick to be insensitive, quick to be sensitive; this makes the claim of drenaline diabetes very inaccurate if not operationalized further.

IreadanarticlecalledCanNicotineSafelyBurnFatandBuildMusclebyKiefer,andIwaswonderingifnicotineisaseffectiveforfatlossasitsportrayedtobeinthatarticle.Thanksinadvance.

a Much of the article supporting Nicotine as the next best fat burner was built on this notion that catecholamine mimetics are subpar since you can become resistant to them. This is an unsubstantiated claim, as it was not supported in the article and no currently accepted disease state is characterized by a chronic state of adrenaline insensitivity at the receptor level. B

ut wait, there's more? Not really.

To follow up the supposed hit to catecholamine/catecholamine mimetic's efficacy, Nicotine was supported as a great option due to being a muscle builder (via mTOR activation) and a fat burner (via AMPK activation). Both are proteins in the cytoplasm of a cell, and are central points of metabolism sort of like crossroads or junction points; they seem to regulate many mechanisms in the body. mTOR is characterized as the cell protecting and growth mediator (alongside some other ones) and AMPK acts as a nutrient sensor protein, activated during energy deficits to increase glucose and fat uptake into cells and their ubsequent catabolism into ATP. s

The claim of nicotine activating mTOR was drawn from an article noting that nicotine was the main ingredient in cigarette secondhand smoke that may cause insulin resistance, and that this was tied into mTOR activation which was shown in vitro.5 For those unaware, although mTOR itself is activated by the insulin receptor it sends a signal back to the first post-receptor substrate, IRS-1, to desensitize the receptor. This is a homeostatic mechanism in the cell and a nice example of regulation, and how mTOR activation can cause insulin esistance. r

The fact that, by this same mechanism, nicotine induces insulin resistance was not mentioned. The closest mention was citation 15, where it was said that carbs alongside nicotine increases fat storage in a cell relative to carbohydrate along; this is theoretically plausible assuming the mTOR link, it is just unfortunate that the citation is wholly irrelevant and does not actually say anything about pairing carbohydrates with nicotine nor an increase in fatty acid accumulation.6 The aforementioned mTOR study was also cited for nicotine can induce insulin resistance in the morning, with no actual evidence of the morning being relevant (beyond a reference to the authors diet plan, which uses a circadian rhythm and insulin sensitivity

anipulation). m That being said, mTOR in that one study was induced in vitro so there does appear to be a degree of activation there. Whether or not this is even relevant practically is not known, it is currently the only study that exists on the topic and at best is preliminary


e vidence.

The second claim of AMPK activation causing nutrient uptake was also an in vitro study, where an increase in nitric oxide caused an increase in peroxynitrate (a free radical) which then induced AMPK. The study was conducted in immortalized fat cells, which is again a preliminary study (a nicely conducted one t that) which needs replication. a

The problem here is that mTOR and AMPK have a yin-yang relationship in all cell lines, when one gets activated it suppresses the other.7 Reliance on in vitro studies to support claims made it seem like you can have your cake and eat it too, but unless a novel pathway suddenly appears in the future that can prevent crosstalk it seems likely that both of the above are active. Either one of them will overcome the other, or they will

egate. n No evidence exists to support a localized mTOR in skeletal muscle and AMPK in adipose either (this is a currently unknown but theoretically plausible nutrient partitioning effect) so touting these two mechanisms of action for nicotine is, at best, an unfortunate result of relying too much on in vitro evidence and not accounting for cellular crosstalk (when one protein or receptor interacts with another). At worst, its a hasty misuse of science, resulting in largely irrelevant supporting data. On the topic of nicotine as a fat burner There is a lot of research on nicotine that can be found currently, which dwindles in amount when you control for nicotine per se (excluding cigarettes) and when you look at studies that induce weight loss rather than those that prevent weight regain after smoking cessation the latter of which are fairly common. We have one (cited by the aforementioned article) that shows an acute increase in metabolic rate following usage of up to 2 mg nicotine gum paired with caffeine in otherwise healthy men,8 and one in otherwise healthy smokers only reporting a thermogenic response in men,9 and we have one study that noted in non-smoking using a 15mg patch that 1.6 kg was lost over 91 days, although after 6 months the difference was no longer apparent.10 The former two studies support the notion that a fat burning effect may exist (which appears to be mediated via an acetylcholine-induced release of catecholamines as per the first study, so I guess it is a good thing that 'adrenaline diabetes' doesn't exist) and the latter supports the notion of appetite uppression causing a reduction in weight even when blinded. s

Animal studies suggest that the mechanisms of weight loss are mediated via acetylcholine receptors (as blocking these receptors block the weight loss), although this implicates both increased atecholamines as well as appetite suppression. c

That is basically it. For the purposes that many people are using it for (anti-smoking aids ingested with exercise and diet for the purpose of body fat loss) it is a very underresearched topic. M

isinterpretation of science

At several points in this article, references were cited in support of the claims. 26 in total, all conveniently hidden behind a Like this on social media form of pseudo-paywall (where the benefit is in exposure rather than finances). All citations and their

espective claims are analyzed as follows: r Citations 1-4 were collectively in support of adrenaline

diabetes, with three being reviews on desensitization of the beta-adrenergic receptors11 on adverse effects of these agonists12 and one on the receptor category (GPRC) in general13 with the last one being the acute study mentioned previously.14 None of these citations mention nor support the notion of chronic catecholamine insensitivity nor the oncept of adrenaline diabetes. c

Citation 5 was used in support of Nicotine, like other

stimulants, raises lipoprotein lipase in muscle tissue but lowers it in fat cells; Translation: your muscles can absorb and burn triglycerides easily, but your fat cells cant store it. In short, nicotine makes it harder to get fat., the article in question15 assessed cardiac muscle tissue rather than skeletal

uscle tissue, which are markedly different metabolically. m Citation 6 was used to mention how nicotine can locally act

via a different receptor class as do catecholamine mimetics; this one appears to be a correct citation to an intervention.16 Citation 7 is the mTOR study17 which itself is a good

preliminary study. The following claims were derived from this article; What makes nicotine so effective for cutting and general fat loss is the fact that its also an effective stimulator of the mTOR pathway, When youre cutting, youre in a state of calorie deprivation, which automatically decreases TOR. Nicotine, however, turns it back on, and Nicotine is a prime regulator of TOR. A single in vitro tudy does not constitute such a claim. s

Related, Citation 26 is also the exact same study, and was

used to support ingesting nicotine earlier in the day can cause transient insulin resistance despite the time of day not being relevant in this study. The former part was used to

ention Carb-Back Loading, the author's diet program. m Citation 8 is a link to AMPK activation in fat cells via

oxidant stress.18 This is a pretty good study mechanistically, but the claims it was in support of were First, free-radical accumulation during training can ignite muscle growth, but its a hermetic response. Elevating it for a while is good, but elevating it for too long is bad which aside from the religious typo of 'hormetic', this study was conducted in fat cells which are not muscle cells and the claim AMPK activation also prevents fat cellsonce againfrom storing fat is an absolute, which is false. AMPK is activated by literally hundreds of phytonutrients to varying degrees, and Nicotine barely activates AMPK relative to the reference drugs of Curcumin, Metformin, or Berberine all of which do

ot abolish fat gain. n Citation 9 claims that Nicotine stimulates one of these

myostatin-bashing pathways (in reference to novel pathways to downregulate Myostatin) and can be found here.19 The study compared a high myostatin active bull genotype against a low active and noted a correlation between the expression of the nicotinic acetylcholine recepetor (what nicotine acts upon) and noted an inverse correlation with myostatin enhanced genotype and nicotinic receptor expression. There was not even an in vitro study


conducted to assess how nicotine influences myostatin; this study being even more preliminary than the previous in vitro studies. Citations 10 and 11 were used to support nicotine enhancing

working memory. They are correct translations of what the tudies claim (one review20, one rat intervention21). s

Citation 12 was used to support the statement that working

memory is your ability to reason correctly, succinctly, and efficiently rather than the currently accepted definition of (give or take a few words) the system that actively holds multiple pieces of transitory information in the mind. The study noted correlations with working memory and other aspects of cognition, and hypothesized that working memory could consist of more.22 The article uses it, either intentionally or accidentally, to try and make the aforementioned citations 10 and 11 more vast in their implications, to then say nicotine can make you smarter. I won't debate as to whether nicotine can or cannot make you smarter, but the above citation was used to misinterpret the forementioned two. a

Three citations support the claim Nicotine, because of its

unique receptor stimulation on fat cells, causes them to dump fat like a drunk sorority girl puking her guts out after a party. We have already discussed citation 6 (making a reappearance), which simply discusses which receptors nicotine acts on. Citation 13 is the aforementioned citation 5 (duplicated), which assessed cardiac muscle tissue, not skeletal tissue. Citation 14 is a review on brain energy homeostasis,23 discussing how nicotine interacts with appetite. This literally has nothing to do with dumping fat either technically (lipolysis) or for long term fat-burning effects; it supports somebody eating less. To defend the notion that nicotine is not suited to a high

carbohydrate diet and that fat cells exposed to nicotine and insulin simultaneously can actually increase the rate of fat storage in fat cells, the following Citation 15 was made note of.24 Insulin and Dexamethasone were incubated in cells, and then nicotine was added; there was no nicotine-only cell, only an insulin+dex control cell (which actually increases LPL, adding nicotine increased it further). There is absolutely no way this study can at all support the claims made. Citation 16 was used to support The fat-dumping potential

of nicotine also increases with physical activity. The study never measured serum free fatty acids, NEFAs, nor triglycerides; only metabolic rate (which appeared to be slightly but synergistically increased).25 This is a poor way o phrase the benefits seen in the study. t

Uncoupling protein 1 (UCP1) is a protein in mitochondria

that regulates uncoupling, a release of potential energy as heat in response to a variety of stimuli; activation of UCP1 might cause weight loss as it wastes energy for heat. Anyways, this was a topic mentioned in the article (Citation 17) as caloric restriction was said to reduce UCP1 activity; the study noted a decrease at 48 hours of starvation, yet a spike at 56 hours that was unexplained.26 This is hardly conclusive of the claim.

Citation 18 and 19 do not support the claim of Nicotine re-

stimulates UCP1...so you keep burning fat even if you drop calories. as neither induced caloric restriction previous to the experiment.27,28 Citations 20-22 were used to support the appetite-

suppressive effect of nicotine, and these citations appear to e legitimate.29-31 b

Citation 23 was mentioned as mTOR may also augment

tumor cell growth (context dependent) and the author made note that Curcumin could negate this effect. It is again an in vitro study,32 but Curcumin does appear to antagonize the proliferative effects of nicotine in this cell line (via inhibitin

TOR activation and the subsequent genomic signalling). m Citation 24 was mentioned in support of how nicotine clears

slower in the evening (despite taking 24 hours to clear the body, which will always cross over into one evening at least). The study merely made not of several issues that ould alter the pharmacokinetics of nicotine patches.33 c

Citation 25 was used in the middle of a paragraph talking

about nicotine dosing, and is a study noting synergism between nicotine and caffeine.34 It seems out of place here (possibly being used to recommend 1mg given what the study and article says), but reappears in the section saying to stack with caffeine where it makes more sense. There does appear to be some slight synergy with caffeine and nicotine in a dose-dependent manner, as assessed by this study using doses up to a 2mg/200mg nicotine/caffeine combination on acute thermogenic response. No clue where the claim about for fat loss and mobilization during training came in, since there was no training in this study.

Overall, this article offers a number of interesting speculations, but its also a good example of how citations do not necessarily mean that the topic on hand is scientific. References in blog posts are just links, and these links can be poorly directed and misinterpreted. Summation In sum, Nicotine is a promising anti-obesity drug, and the anti-inflammatory effects of it can theoretically confer more benefit to obese persons than classical stimulants. The aforementioned claim needs to be studied though, as studies on nicotine and inducing weight loss are surprisingly scarce. There is no evidence to currently support nicotine as a muscle building agent beyond a single in vitro study of questionable practical significance, and the fat burning effects of nicotine do not appear to be greater than that of classical stimulants such as ephedrine or caffeine. The concept of adrenaline diabetes most likely does not exist, and especially not the same degree as chronic insulin resistance, and as such nicotine is unlikely to exert more weight loss to athletes than classical stimulants (mentioned

efore). b Nicotine is another possible option to add to a supplement regimen or to throw into your minds database; it does not currently revolutionize anything pertaining to fat loss or muscle-building.


Kurtis Frank and Sol Orwell are the co-founders of Examine.com, a compendium of available scientific research on supplementation and nutrition. In my opinion, its the most diligent resource of its kind. The sites nicotine page is currently in progress and can be seen here. __________________________________________________ R

eferences 1. Kiefer J. Can Nicotine Safely Burn Fat and Build Muscle? The

Surprising Facts. Accessed November 21, 2012. [Dangerously Hardcore]

2. Bawa-Khalfe T, Altememi GF, Mandyam CD, Schwarz LA, Eikenburg DC, Standifer KM. The presence of beta2-adrenoceptors sensitizes alpha2A-adrenoceptors to desensitization after chronic epinephrine treatment. BMC Pharmacol. 2007 Dec 20;7:16. [PubMed]

3. Astrup A, Lundsgaard C, Madsen J, Christensen NJ. Enhanced thermogenic responsiveness during chronic ephedrine treatment in man. Am J Clin Nutr. 1985 Jul;42(1):83-94. [PubMed]

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5. Bergman BC, Perreault L, Hunerdosse D, Kerege A, Playdon M, Samek AM, Eckel RH. Novel and reversible mechanisms of smoking-induced insulin resistance in humans. Diabetes. 2012 Dec;61(12):3156-66. [PubMed]

6. Chajek-Shaul T, Scherer G, Barash V, Shiloni E, Caine Y, Stein O, Stein Y. Metabolic effects of nicotine on human adipose tissue in organ culture. Clin Investig. 1994 Jan;72(2):94-9. [PubMed]

7. Xu J, Ji J, Yan XH. Cross-talk between AMPK and mTOR in regulating energy balance. Crit Rev Food Sci Nutr. 2012;52(5):373-81. [PubMed]

8. Jessen AB, Toubro S, Astrup A. Effect of chewing gum containing nicotine and caffeine on energy expenditure and substrate utilization in men. Am J Clin Nutr. 2003 Jun;77(6):1442-7. [PubMed]

9. Perkins KA, Sexton JE, DiMarco A. Acute thermogenic effects of nicotine and alcohol in healthy male and female smokers. Physiol Behav. 1996 Jul;60(1):305-9. [PubMed]

10. Newhouse P, Kellar K, Aisen P, White H, Wesnes K, Coderre E, Pfaff A, Wilkins H, Howard D, Levin ED. Neurology. 2012 Jan 10;78(2):91-101. [PubMed]

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12. Sears MR. Adverse effects of beta-agonists. J Allergy Clin Immunol. 2002 Dec;110(6 Suppl):S322-8. [PubMed]

13. Premont RT.Once and future signaling: G protein-coupled receptor kinase control of neuronal sensitivity. Neuromolecular Med. 2005;7(1-2):129-47. [PubMed]

14. Bawa-Khalfe T, Altememi GF, Mandyam CD, Schwarz LA, Eikenburg DC, Standifer KM. The presence of beta2-adrenoceptors sensitizes alpha2A-adrenoceptors to desensitization after chronic epinephrine treatment. BMC Pharmacol. 2007 Dec 20;7:16. [PubMed]

15. Sztalryd C, Hamilton J, Horwitz BA, Johnson P, Kraemer FB. terations of lipolysis and lipoprotein lipase in chronically nicotine-treated rats. Am J Physiol. 1996 Feb;270(2 Pt 1):E215-23.

16. Andersson K, Arner P. Systemic nicotine stimulates human adipose tissue lipolysis through local cholinergic and catecholaminergic receptors. Int J Obes Relat Metab Disord. 2001 Aug;25(8):1225-32. [PubMed]

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smoking-induced insulin resistance in humans. Diabetes. 2012 Dec;61(12):3156-66. [PubMed]

18. An Z, Wang H, Song P, Zhang M, Geng X, Zou MH. Nicotine-induced activation of AMP-activated protein kinase inhibits fatty acid synthase in 3T3L1 adipocytes: a role for oxidant stress. J Biol Chem. 2007 Sep 14;282(37):26793-801. [PubMed]

19. Sadkowski T, Jank M, Zwierzchowski L, Siadkowska E, Oprzadek J, Motyl T. Gene expression profiling in skeletal muscle of Holstein-Friesian bulls with single-nucleotide polymorphism in the myostatin gene 5'-flanking region. J Appl Genet. 2008;49(3):237-50. [PubMed]

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25. Perkins KA, Sexton JE, Epstein LH, DiMarco A, Fonte C, Stiller RL, Scierka A, Jacob RG. Acute thermogenic effects of nicotine combined with caffeine during light physical activity in male and female smokers. Am J Clin Nutr. 1994 Sep;60(3):312-9. [PubMed]

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uscle Strength & Hypertrophy in Chronic Nutrient Timing Studies Compiled by Brad Schoenfeld & Alan Aragon M What follows is an update of the collection of chronic nutrient timing studies first presented in the September 2012 issue of AARR. Two studies are added, and the chart is not a pasted image file like the previous (its now intrinsically part of this document), so it should be more clearly visible. _____________________________________________________________________________________________________ KEY: yellow = significant benefits from timing nutrients near training; no background color = no significant benefits from timing nutrients near training; blue = total protein (including supplementation) was matched between experimental & placebo/control conditions. Note that the baseline/habitual protein amounts listed are the average of the groups compared.

Study

Subjects

Supplementation

Total Protein intake habitual or baseline vs with supp

Protein Matched with Control?

Measure- ment Method

Training Protocol

Strength Results

Body composition Results

Esmarck et al, 2001

13 untrained elderly males

10 g milk/soy protein combo consumed either immediately or 2 hours after exercise

1.05 g/kg (supplement increased this to 1.18 g/kg)

Yes

MRI and muscle biopsy

Progressive resistance training consisting of multiple sets of lat pulldown, leg press and knee extension performed 3 days/wk for 12 wks

Immediate intake increased both dynamic and isokinetic Strength, whereas delayed intake only improved dynamic strength.

Significant increase in muscle CSA with immediate vs. delayed supplementation

Bird et al, 2006

32 untrained young men

6% CHO solution, 6 g EAA mixture, combined CHO + EAA supplement or placebo consumed during exercise

Not specified, but a range was listed:15% of 9.8-13.7 MJ; 87.8-122.7g.

No DXA Progressive resistance training consisting of 3 sets of 8-10 repetitions for all the major muscles performed 2 days/wk for 12 wks

Immediate pre-post supplementation caused greater increases in 1RM in 2 out of 3 exercises

CHO + EAA caused the greatest gains in fat-free mass and muscle fiber CSA relative to placebo

Cribb and Hayes, 2006

23 young recreational male body- builders

1 g/kg of a supplement containing 40 g whey isolate, 43 g glucose, and 7 g creatine monohydrate consumed either immediately before and after exercise, or early morning & late evening


Yes DXA and muscle biopsy

Progressive resistance training consisting of exercises for the major muscle groups performed 3 days/wk for 10 wks

Immediate pre-post supplementation caused greater increases in 1RM in 2 out of 3 exercises

Significant increases in lean body mass and muscle CSA of type II fibers in immediate vs. delayed supplementation

Willoughby et al, 2007

19 untrained young males

20 g whey-dominant protein or 20 g dextrose consumed 1 hour before and after exercise


No Hydro- static weighing, muscle biopsy, surface measurements

Progressive resistance training consisting of 3 sets of 6-8 repetitions for all the major muscles performed 4 days/wk for 10 wks

Protein supplementation caused greater increases in relative strength (maximal strength corrected for bodyweight) in bench press & leg press

Significant increase in total body mass, fat-free mass, and thigh mass with protein vs. carb supplementation

Verdijk et al, 2009

28 untrained elderly males

10 g casein hydrolysate or placebo consumed immediately before and after exercise


No DXA, CT, and muscle biopsy

Progressive resistance training consisting of multiple sets of leg press and knee extension performed 3 days/wk for 12 wks

1RM leg press & leg extension strength increased, with no significant difference between groups

No significant differences in muscle CSA increase between groups

Hoffman et al, 2009

33 well-trained young males

Supplement containing 42 g protein (milk/collagen blend) and 2 g carbohydrate consumed either immediately before and after exercise, or early morning & late evening


Yes DXA Progressive resistance training consisting of 3-4 sets of 6-10 repetitions of multiple exercises for the entire body peformed 4 days/wk for 10 wks.

1RM & 5 RM bench press & squat strength increased, with no significant difference between groups

No significant differences in total body mass or lean body mass between groups.

Burk et al, 2009

13 untrained young males

Two casein-dominant protein dose

11 - Nov - 2012

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