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Copyright © February 1st, 2014 by Alan Aragon Home: www.alanaragon.com/researchreview Correspondence:

Copyright © February 1st, 2014 by Alan Aragon Home: www.alanaragon.com/researchreview Correspondence: aarrsupport@gmail.com

Correspondence: aarrsupport@gmail.com 2 Hormones and addiction. By David A. Wiss, MS, RDN, CPT
Correspondence: aarrsupport@gmail.com 2 Hormones and addiction. By David A. Wiss, MS, RDN, CPT
2 Hormones and addiction. By David A. Wiss, MS, RDN, CPT 11 Structural balance theory:
2
Hormones and addiction.
By David A. Wiss, MS, RDN, CPT
11
Structural balance theory: does your butt care
about your biceps?
By Menno Henselmans

15 Overfeeding polyunsaturated and saturated fat causes distinct effects on liver and visceral fat accumulation in humans. Rosqvist F, Iggman D, Kullberg J, Jonathan Cedernaes J, Johansson HE, Larsson A, Johansson L, Ahlström H, Arner P, Dahlman I, Risérus U. Diabetes. 2014 Feb 18. [Epub ahead of print] [PubMed]

16 Can we say what diet is best for health? Katz DL, Meller S. Annu Rev Public Health. 2014 Mar 18;35:83-103. [PubMed]

Annu Rev Public Health. 2014 Mar 18;35:83-103. [ PubMed ] 17 Effects of supplementing n-3 fatty

17 Effects of supplementing n-3 fatty acid enriched eggs and walnuts on cardiovascular disease risk markers in healthy free-living lacto-ovo- vegetarians: a randomized, crossover, free-living intervention study.

Burns-Whitmore B, Haddad E, Sabaté J, Rajaram S. Nutr J 2014, 13:29 [Epub ahead of print] [PubMed]

S. Nutr J 2014, 13:29 [Epub ahead of print] [ PubMed ] 18 Resistance training in

18 Resistance training in overweight women on a ketogenic diet conserved lean body mass while reducing body fat. Jabekk PT, Moe IA, Meen HD, Tomten SE, Høstmark AT. Nutr Metab (Lond). 2010 Mar 2;7:17. [PubMed]

AT. Nutr Metab (Lond). 2010 Mar 2;7:17. [ PubMed ] 20 In defense of the bros.
20 In defense of the bros. By Bryan Krahn, CSCS 22 Should you stop counting
20
In defense of the bros.
By Bryan Krahn, CSCS
22
Should you stop counting calories and macros?
By Armi Legge

24 Does “reverse dieting” build metabolic capacity?

By Alan Aragon

dieting” build metabolic capacity? By Alan Aragon 26 Interview with Tom Venuto. By Alan Aragon Ala

26 Interview with Tom Venuto.

By Alan Aragon

By Alan Aragon 26 Interview with Tom Venuto. By Alan Aragon Ala n Aragon’s Research Review
By Alan Aragon 26 Interview with Tom Venuto. By Alan Aragon Ala n Aragon’s Research Review
Hormones and Addiction. David A. Wiss, MS, RDN, CPT Introduction It has been known for

Hormones and Addiction.

David A. Wiss, MS, RDN, CPT

Introduction

It has been known for some time that individuals with substance

use disorders (SUDs) have significant vitamin and mineral deficiencies. 1-6 In the past decade, investigators have begun to explore alterations in both neuro-circuitry and nutrition-related hormones (i.e. leptin, ghrelin, insulin) in the SUD population to better understand eating behavior during drug use, recovery, and long-term abstinence. The connection between nutrition behavior and addiction recovery have important implications that are not frequently addressed in clinical practice. According to Virmani et al, 7 drug abuse appears to be a risk factor for metabolic syndrome, which is a cluster of risk factors for cardiovascular disease. Given that weight gain following abstinence from drugs is a source of major personal suffering, there is a pressing need for a more detailed understanding of the effects of drug addiction on dietary intake. 8

It is well known that drug addicts share many of the same brain

imaging 9 and behavioral 10 characteristics as compulsive overeaters. However, since the "reward" or hedonic value associated with food in humans is tied to memory, emotions, and individual characteristics, food perception is difficult to assess at

a group level. 11 Meanwhile, evidence supporting the concept of

food addiction is becoming widely accepted. The purpose of this review is to examine both drugs of abuse and contemporary palatable food to determine if there is a link addiction between

hormones acting on reward-related dopamine pathways that stimulate or inhibit feeding. The majority of neuro-hormonal research is conducted in animal models, so unless specified as human research, it can be assumed that physiological observations of the brain are extrapolated from rodents.

The mesolimbic dopamine system is considered a primitive part of the brain that consists of the ventral tegmental area (VTA) which contains dopamine neurons that project to cortico-limbic structures such as the nucleus accumbens (pleasure center), medial prefrontal cortex (cognition), hippocampus (memory), and amygdala (emotional reactivity). The VTA receives direct and indirect input from the hypothalamus, which governs several endocrine processes through communication with various glands. The VTA is involved in somatic processes including body temperature, sleep, and appetite, and influences neurological mechanisms that underlie mood and motivational states. Direct evidence that leptin and ghrelin modulates the hypothalamic pathway has begun to emerge, implying reward- related information that drives feeding behavior at the level of the VTA.

Coll et al 12 have suggested the presence of an integrated system in which adipocyte-derived signals (i.e. leptin) provide long- term information to the brain about the state of nutrient stores, whereas a variety of signals (many not addressed in this article) triggered by eating have important roles in influencing meal

initiation and termination. Adam and Epel 13 have highlighted the role of chronic stress and elevated cortisol (a glucocorticoid controlled by the hypothalamus) in the dysregulation of this finely balanced system. This may cause impaired sensitization of satiety signals leading to increased food intake and subsequent visceral fat accumulation. Corticotrophin-releasing factor is released during stress, which stimulates the reward system. 14 Stress has been linked to drug relapse and is a significant cause of failure in dieters, and can actually become a conditioned incentive for food, possibly explaining the phenomenon of "comfort food." 15 Wiss found that individuals with a history of substance abuse reported more difficulty controlling overeating when depressed. 16

Food addiction

Highly palatable food can stimulate endogenous opioid release 17 and trigger dopamine activity in the brain. 18 Palatable food is processed food that typically contains added sugars, salt, and fat. Recent evidence depicts dopamine circuits as a major site of convergence where metabolic/hormonal and visceral sensory cues interact to regulate eating behavior by way of a "gut-brain dopamine axis." 19 Food addiction has been associated with binge eating disorder as well as obesity. 20 According to Heber and Carpenter, 21 obesity-associated inflammation modulated by leptin in the brain may promote addictive behaviors leading to a self-perpetuating cycle of addiction to food, as well as drugs/alcohol and process addictions such as gambling.

Other researchers have challenged the notion that drug addiction and food addiction are near-identical processes, since there are unique evolutionary contexts across species with different environmental pressures, resulting in significant differences between rodents and humans. 22 Such differences can include food availability, visual appeal, economics and incentives, social routines for eating, alternative reinforcement, and the impact of advertising. 23 Other differences in the prefrontal cortex (which weighs pros and cons) are not sufficiently integrated into the current animal models of food intake. The full behavioral consequences of metabolic hormones acting on dopamine neurons will require further investigation. Meanwhile, several authors have identified leptin as the indirect link between overeating and addiction, suggesting that many leptin-deficient individuals meet criteria for food addiction. 14

Leptin

Leptin is produced and secreted by adipose tissue to increase metabolic rate. In human populations plasma leptin is positively associated with fat mass. 24 Leptin is described as anorexigenic because it is responsible for initiating the starvation response (decreases food intake). Evidence suggests that leptin-mediated modulation of central dopamine circuits provides a neural pathway by which changes in leptin levels lead to adaptive behavioral responses in feeding. 25 De Araujo et al showed that the reward value of sucrose was increased by fasting, yet decreased by leptin via a reduction in dopamine signaling. 26 In other words, a hungry individual with lower leptin levels will assign a higher reward value of food compared to an individual who is satiated (dopamine release and firing is inhibited in the nucleus accumbens when satiated). Interestingly, high

in the nucleus accumbens when satiated). Interestingly, high Ala n Aragon’s Research Review – February/March 2014
in the nucleus accumbens when satiated). Interestingly, high Ala n Aragon’s Research Review – February/March 2014

circulating levels of leptin have no pronounced effect on metabolism and feeding, whereas low levels may trigger a physiological condition where the body perceives a hungry state and simultaneously enhances motivation for obtaining food. 27

The failure of elevated leptin levels to control or reverse obesity suggests the possibility of a leptin-resistant state. High-fat diets can induce leptin resistance and is emerging as a cause and consequence of weight gain. 28 Leptin resistance is considered analogous to the concept of insulin resistance, both of which can correlate to obesity. According to Coll et al, 12 leptin resistance occurs when circulating leptin fails to reach its target receptors in the brain, when leptin receptors have decreased expression, when there is attenuation of the intracellular leptin signaling cascade, or when enzymatic dysfunction exists. Additionally, altered leptin signaling due to genetic mutations have been implicated in obesity. 29 Meanwhile, the concept of leptin resistance remains controversial.

As evidence that leptin regulates the activity of the mesolimbic

dopamine system by its actions on VTA dopamine neurons continues to grow, recent data indicates that leptin not only regulates the homeostatic center of the hypothalamus but also the hedonic system by affecting subjective desires for food. 30 Food deprivation decreases circulating leptin levels, which has been used to study the impact of leptin on brain reward centers. While still not fully understood, it is known that leptin has action extending to the brain reward circuits thereby contributing to preference for highly palatable foods. Recent research suggests

that the leptin-dopamine interaction appears to be bi-directional,

as dopamine has been shown to negatively influence leptin

action in the lateral hypothalamus. 31 Data collected by Davis et al indicate that leptin signaling within the lateral hypothalamus regulates energy homeostasis and metabolism, whereas midbrain leptin modulates effort-based responding for food via mesolimbic dopamine. 32 Hormone-influenced neuroplasticity infers behavioral changes that include an elevated preference for high-fat and high-sugar diets commonly associated with the phenomenon of food addiction. 33

Human research using functional magnetic resonance imaging (fMRI) measured responses to visual food stimuli in obese

subjects compared to controls. 34 As expected, obese participants had significantly higher plasma leptin concentrations, possibly experiencing a state of leptin resistance. Meanwhile, Kalra states that hypothalamic leptin insufficiency rather than "leptin resistance" leads to decreased energy expenditure, increased energy intake, and consequential obesity. 35 Grosshans et al found

a significant positive correlation between plasma leptin

concentration and brain activation in the ventral striatum (area which includes the nucleus accumbens) during the presentation

of visual food cues, 34 strongly suggesting that the homeostatic

feedback mechanism between leptin and mesolimbic reward

function is impaired in obese subjects.

Ghrelin

Ghrelin has opposing effects with leptin, stimulating appetite by activating orexigenic neurons in the hypothalamus. Additionally, ghrelin receptors have also been identified in the VTA,

hippocampus, and amygdala. 36 Both ghrelin and leptin play a central role in the neuroendocrine regulation of food intake and energy homeostasis. 30 Ghrelin is stomach-derived and will decrease after eating thus contributing to satiety. Leptin counters the effects of ghrelin thereby decreasing relentless hyperphagia. The sight of food significantly elevates ghrelin levels in non- obese healthy volunteers. 37 In obese human subjects, ghrelin levels are lowered, whereas post-meal ghrelin levels remain higher than in lean individuals. 38 Direct injection of ghrelin in the VTA and nucleus accumbens increases feeding behavior. 39 Recent findings suggest that the VTA but not the nucleus accumbens is the direct target site for ghrelin's action on sweet food motivation. 40 Ghrelin also enhances intake of artificially sweetened food (saccharin), implying a role in feeding behavior regardless of caloric content. 41

Dickson et al suggest that the ghrelin system alters the set point of the dopaminergic neurons in the VTA, thereby enhancing the ability of rewarding substances to activate the midbrain dopamine system. 42 Anticipatory physiological responses to scheduled meals can be learned through ghrelin's interaction with central nervous system (CNS) reward pathways that stimulate motivation to eat 28 via increased release and activity of VTA dopamine. 23 While regular or palatable food by itself activates the mu opioid receptor pathway in the VTA, systemic ghrelin switches the dominant opioid receptor pathway from mu to kappa only for highly rewarding food. 43 These findings suggest a pivotal role of ghrelin in regulation of food incentives and hedonics. Meanwhile, other investigators have concluded that ghrelin primarily exerts motivational effects on feeding, rather than hedonic or opioid-related effects. 44

The central ghrelin signaling system interfaces neurobiological circuits involved in reward from both food and chemical drugs including alcohol. Increased ghrelin signaling could contribute to the overconsumption and preference for high-calorie food 45 and alcohol, a high-calorie beverage. 46 Whether or not ghrelin plays a significant role in losing control over drug-taking behavior is yet to be determined. Humans subjected acutely to psychosocial stress displayed increased plasma ghrelin, particularly "emotional eaters" where ghrelin did not decline acutely following food consumption. 47 Since stress has been linked to drug relapse and is a significant cause of failure in dieters, it is possible that stress-related increases in ghrelin are a risk factor for substance-seeking behavior. Some authors have suggested that ghrelin antagonists have therapeutic potential for the treatment of obesity by suppressing overconsumption of sweet food. 48 Similarly, ghrelin agonists might increase the motivation to eat, which could be helpful in cases where the drive to eat is insufficient. 44 Kawahara et al recommends further study on the role of ghrelin in regulating the mesolimbic dopamine system in response to drugs of abuse and alcohol. 43

Insulin

While widely studied in connection with the regulation of blood glucose, the CNS effects of insulin remain to be elucidated. Much like leptin, insulin is an adiposity signal, is anorexigenic, and attenuates food reward. Leptin gene therapy represses insulin secretion and can potentially ameliorate diabetes. 35 In

and can potentially ameliorate diabetes. 3 5 In Ala n Aragon’s Research Review – February/March 2014
and can potentially ameliorate diabetes. 3 5 In Ala n Aragon’s Research Review – February/March 2014

metabolic circumstances in which plasma insulin or leptin levels are low (starvation and reduced adiposity), signaling would be decreased and drive for food intake increased. Insulin and dopamine work together to orchestrate both the motivation to engage in consumptive behavior and to calibrate the associated reward, particularly related to hedonic feeding. 49 More specifically, insulin depresses dopamine concentration in the VTA, which may suppress salience of food once satiety is reached.

Similar to ghrelin, there are insulin receptors in the hypothalamus, VTA, hippocampus, and amygdala. 36 In humans, insulin secretion is decreased by ghrelin, and vice versa. 50,51 There is also evidence that the insulin receptor signaling pathway interferes with leptin signaling, indicating that hyperinsulinemia contributes to the pathogenesis of leptin resistance. 52 Chronic hyperinsulinemia promotes obesity by interfering with leptin extinguishing of dopamine clearance in the nucleus accumbens, which is a hallmark of addiction. 53 Insulin resistance may directly or indirectly impact neural pathways driving desires to consume highly caloric foods and ultimately influence further adiposity. 54 These authors also reported that during exposure to stress, desire to eat is exacerbated in obese humans but not lean individuals. In obese individuals, evidence of insulin resistance can lead to alterations in food craving even in a relaxed state.

Daws et al reviewed the potential impact of impaired insulin signaling in obesity and stimulant abuse suggesting that insulin- influenced dopamine transmission can affect the ability of drugs to exert their neurochemical and behavioral effects. 55 According to these authors, insulin receptors are present in brain and are found on midbrain dopamine neurons, and the interplay between insulin signaling and drug-induced increases in extracellular dopamine may contribute to the high comorbidity of eating disorders and drug abuse. Improvements in brain dopamine function by normalizing or bypassing disruptions in insulin signaling might be effective in treating addictions.

Alcohol

Leptin

The course of alcoholism is associated with suppressed secretion of ghrelin and leptin, both of which influence the hypothalamic- pituitary-adrenal system. 56 Increasing leptin concentrations have been correlated with the course of alcohol withdrawal in human females. 57 While alcohol attenuates the secretion of leptin in the short run (6-8 hours) in non-alcoholic, non-obese human subjects, 58 chronic alcoholism has been linked to elevated leptin. 24 This may indicate that fat tissue of alcoholic patients is sensitized to release more leptin than controls, however levels do normalize after six months of abstinence. 24 Lenz et al reported that lower levels of leptin were correlated with lower levels of alcohol craving in males, 59 while the opposite is true for women. 57 There is epidemiological support for a link between familial alcoholism and risk for obesity in women, and possibly for men. 60 Some authors have suggested that alcoholic men outnumber women four to one, highlighting neurological and hormonal differences that may account for these observed

difference. 61 Further investigations into the relationship between leptin and alcohol craving accounting for differences in gender as well as the nutritional status of subjects are clearly warranted.

Ghrelin

The rewarding properties of alcohol require ghrelin. 62 Alcohol- dependent patients have increased ghrelin levels when intoxicated and during early abstinence, increasing during the first week of alcohol withdrawal. 57 It is likely that elevated ghrelin can account for measurable changes in hunger and appetite during alcohol withdrawal. The common practice of healthy individuals drinking an alcoholic beverage before a meal suggests that alcohol stimulates appetite. Jerlhag et al suggest that by increasing the incentive value of rewards such as alcohol, hyperghrelinemia may play a pathophysiological role in the disease process that leads to addiction. 62 The authors conclude that modulation of ghrelin signaling constitutes a potential target for treatment of alcohol-related disorders. Other human research led by Leggio and colleagues have confirmed the findings that ghrelin plays a key role in alcohol-seeking behavior, 46 highlighting the key role of dopamine in the neurobiology of alcohol craving. The authors conclude that antagonizing ghrelin via homeostatic stabilization might lead to new and innovative ways to provide effective treatment for alcohol use disorders.

Insulin

Abstinent alcoholic human subjects have exhibited significantly blunted responses in blood glucose when exposed to intravenous 2-Deoxy-D-glucose. 63 Subjects exhibited trends towards both blunted responses in glucagon and insulin. Authors speculate that that nervous system damage attributable to the effects of alcohol exposure is responsible for the insufficient hormonal response, particularly neurons in the hypothalamus, as well as the adrenal medulla. It has been established that alcohol- dependent subjects during the first month of abstinence report maximal pleasure response to the sweetness significantly more frequently than control subjects, 64 consistent with the concept of "reward deficiency syndrome.” 65 The percentage of alcohol- dependent subjects preferring the maximum concentration of sucrose decreased over time. Those alcohol-dependent subjects who reported abstinence at six months were significantly less likely to prefer the maximum sweetness than were the subjects who did not maintain abstinence. Krahn et al propose that sweet preferences should be tested as a predictor of future abstinence. 64 Positive associations between the consumption of any type of alcoholic beverage and anthropometric markers of adiposity have been reported. 66

Taken together, the apparent link between alcohol abuse and sugar abuse and the subsequent blunted hormonal responses highlight the negative impact of substance use on the endocrine system, providing support for the need for dietary intervention in supporting long-term abstinence and recovery. Manipulation of the insulin signaling system should not rely solely on pharmacological intervention but rather should focus on normalizing the altered dopamine-glucose link via interventions in nutrition behavior, which has proven to be challenging in the light of the science on food addiction.

challenging in the light of the science on food addiction. Ala n Aragon’s Research Review –
challenging in the light of the science on food addiction. Ala n Aragon’s Research Review –

Stimulants

Methamphetamine

Crystal methamphetamine (meth) use may be associated with the onset of disordered eating or used as an efficient weight loss mechanism for those with established eating disorders. 67 Food restriction has been shown to enhance the central rewarding effect of amphetamine. 68 Research by Jerlhag et al demonstrates that the ghrelin signaling system is required for indirect measures of the rewarding properties of amphetamine, as well as cocaine. 69 The authors highlight the fact that food restriction leading to elevated ghrelin facilitates the acquisition of drug- seeking behavior in rats, attributable to the dopaminergic regions of the nucleus accumbens and VTA. Hyperghrelinemia observable in SUD patients raises important questions regarding the physiological role of ghrelin influencing not only food intake and appetite, but also a broader role in reward induced by addictive drugs such as alcohol, amphetamine, and cocaine. 69 The potential for a gradual normalization of ghrelin levels through medical nutrition therapy appears indicated for patients with methamphetamine use disorders.

Cocaine

Research using positron emission tomography (PET) brain imaging has suggested that deficits in dopamine signaling are similar for cocaine-addicted and obese rats. 11 The authors

suggest that dopamine binding ability in the D2R/D3R sites can

be used to predict future body weight and cocaine preference. A

small sample of human cocaine addicts in an inpatient setting reported preference for the highest concentration of sweet solutions, which is in agreement with sweet-preference expressed by alcoholics. 64,72 Clearly sugar reinforces depleted reward pathways in the brain resulting from cocaine abuse. Meanwhile, research conducted on rats has shown that antagonism of ghrelin receptor function has reduced the development of cocaine sensitization, strongly supporting the view that ghrelin receptors are partially responsible for modulating reinforcement/reward function. 70

A sample of female crack cocaine users presented with lower

levels of plasma leptin during early abstinence in comparison with healthy controls, consistently increasing during detoxification. 71 The authors speculate that leptin levels may increase in abstinence only as a consequence of improved diet or weight gain. Consistent with the link between leptin and inflammation reported by Heber and Carpenter 21 and Levandowski et al 71 highlights the fact that disruption of energy homeostasis could interfere with clinical responses to cocaine treatment, since cocaine addicts demonstrate increased immune response inflammation both at the baseline and in response to stress and cue imagery conditions. 73

According to recent research conducted by Ersche et al, 8 cocaine-dependent men (not abstinent) reported increased food intake, specifically foods high in fat and carbohydrate. There was an expected trend towards lower levels of circulating leptin in the cocaine group, directly interfering with metabolic processes (impaired energy balance). In other words, the higher fat intake was associated with less fat storage, suggesting an

inhibition of leptin production that facilitates overeating. The overeating in cocaine-dependent individuals often pre-dates recovery, with the effect masked by lack of weight gain. Taken together, investigators found that cocaine abuse results in an imbalance between fat intake and storage, leading to excessive weight gain during recovery. 8 For many individuals, it is likely that dysfunctional eating pre-dates the initiation of drug use as well. According to Wiss and Waterhous, 74 patients with SUDs often develop disordered and dysfunctional eating patterns during abstinence, and eating disorder patients can similarly progress into substance abuse. Traditionally addiction has been addressed first, however delaying eating disorder treatment can hinder recovery, therefore it is important to alert treatment providers who treat patients with dual diagnoses how to assess and address both disorders simultaneously.

Ecstasy

Ecstasy is a popular club drug classified as an empathogen or entactogen often mixed with stimulants. In humans, abuse of this drug reduces eating, although there is research to suggest that women who use ecstasy are not necessarily taking it as deliberate means of weight control. 75 In rats, ecstasy was shown to cause significant decreases in serum leptin and increases in serum ghrelin, both of which recovered to baseline after 24 hours. 76 Long-term effects of altered hormonal levels related to ecstasy and stimulant abuse require further evaluation, with more emphasis on behavioral parameters such as food intake.

Opiates

Acute food deprivation (24 hours) reinstated heroin-seeking in rats, and this effect was attenuated by leptin infusions. 77 Similar to other substances of abuse, decreased activity in the mesolimbic dopaminergic reward system (VTA and nucleus accumbens) following leptin administration is likely to account for this effect. Not surprisingly, Nolan and Scagnelli found that methadone-treated human patients had a higher consumption of sweets, a higher eagerness to consume sweet foods, and a willingness to consume larger quantities desired by controls. 78 In another sample of human patients on methadone maintenance, basal serum leptin concentrations were significantly decreased compared to controls. 79 These findings were independent of BMI, body fat, and insulin sensitivity.

Recent research has also shown that chronic food restriction (14 days of mild restriction) led to robust heroin-seeking behavior in rats. 80 The authors acknowledge the "stress aspect" of food restriction on reward-seeking behavior, meanwhile recognizing that the state of hunger by itself was not sufficient to induce augmentation of heroin-seeking. D'Cunha et al concluded that ghrelin is likely more responsible than leptin for mediating the effect of food restriction on heroin-seeking following prolonged abstinence. 80 These findings are in agreement with Maric et al who provided evidence that activation of ghrelin receptors is sufficient to induce increases in drug-taking and drug-seeking behaviors. 81 Meanwhile, these authors point out that ghrelin is not required for this mechanism since treatment with a ghrelin receptor antagonist had no effect on drug-taking or food deprivation-induced reinstatement of extinguished heroin- seeking.

reinstatement of extinguished heroin- seeking. Ala n Aragon’s Research Review – February/March 2014
reinstatement of extinguished heroin- seeking. Ala n Aragon’s Research Review – February/March 2014

Nutrition and addiction treatment

Disordered Eating

Drug abuse is a risk factor for eating disorders 82 and has been shown to have both genetic and environmental influences. 83 Even a remote history of SUD can negatively impact weight loss in adults 84 and adolescents. 85 Sobriety time has been positively associated with increased sugar use. 86 Substance abuse linked to low distress tolerance can lead to excessive consumption of food. 87 Fischer et al found that problems of alcohol use were associated with binge eating and purging, and that a tendency to act rashly when distressed was associated with both behaviors. 88 In one study, nearly 40% of women in SUD treatment met criteria for an eating disorder most commonly binge eating disorder followed by bulimia nervosa. 89 Men in SUD treatment reported bingeing and the use of food to satisfy drug cravings during the first six months, with weight concerns and distress about efforts to lose weight during months 7-36. 90

Interventions and Outcomes

Positive associations between nutrition interventions and substance abuse outcomes have been reported, where nutrition education was the differentiating factor. 91 An educational intervention on the nutrition behavior of alcohol-dependent patients led to 80% of participants reporting continual abstinence after six months. 92 A six-week environmental/educational intervention to improve dietary intake and reduce excessive weight gain among men in residential treatment reported greater reductions in total energy, percentage of energy from sweets, daily servings of fats, oils, and sweets, and BMI over the intervention period. 90 The findings provide evidence that such interventions can be successful despite challenges met in residential substance abuse facilities. A series of nutrition workshops in a substance abuse program (SAP) in the US prison system led to significant improvements in nutrition and general health, with a trend towards improvements in social ties. 93 A review article on the drug-addicted prison population in the UK builds a convincing argument for the inclusion of more nutritious options in prisons, concluding that such changes are overall likely to make sound economic sense in terms of prisoner health, mood, behavior, and recidivism rates. 94

Upcoming Trends

Betty Ford is a world-renowned treatment center in California that has recently merged with Hazelden in Minnesota. Betty Ford utilizes a treatment model that includes measures to prevent post-detoxification overeating. Patients are provided with access to dietitians and exercise is emphasized, helping patients to plan for expected changes in eating and the reinforcing effects of food. At Breathe Life Healing Center in Los Angeles, a registered dietitian nutritionist is an integrated member of the treatment team, approving all food and beverages that enter the campus, planning nutritionally balanced meals and snacks, teaching educational courses, and working with patients individually to mediate dysfunctional eating behavior and disrupt addictive tendencies. Exercise is also a mandatory component of treatment. It is possible that data supporting the effectiveness of improved nutrition and exercise behavior during the course of treatment will eventually be reported.

Discussion

The most substantial health burden arising from addiction lies not in the direct effects of intoxication but in the secondary effects on physical health. 8 There is strong evidence to support that food and drugs are competing for overlapping reward mechanisms. When the immediate crisis of substance abuse has been resolved, there is a likely compensatory increase drive for food intake to achieve weight recovery and a likely overshoot, leading to increased adiposity. 13 Ravenous food consumption may be due to "rebound appetite" in the wake of the hypothalamic suppression from drug use. Making healthful food choices after abstinence has been achieved may be very challenging. Sobriety is associated with new emotions, anxiety, and uncertainty. It is easy to seek a predictable and comforting response from food. This may lead to overeating, relapse, compromised quality of life, and the development of chronic disease. Caffeine and nicotine abuse should also be addressed since they are highly addictive substances that can perpetuate substance-seeking behavior. Additionally, the impact of stress and adequate sleep should not be ignored, as they too can have profound effects on the endocrine and reward systems.

The modern epidemic of obesity may be in part related to reward and hedonic mechanisms, and that failure of regulatory systems might be related to dysregulation of reward systems. Normalizing the disrupted leptin signaling cascade in the obese brain may be sufficient to decrease motivation for food reward, and interventions targeting the central leptin system and/or other hypothalamic hormones regulated by leptin should be considered for the treatment of drug addicts with comorbid eating disorders. Kalra has proposed trials involving gene therapy aimed at reinstating leptin circuitry in drug addicts. 35 More realistically, weight gain during substance abuse recovery should be monitored and controlled (gradual rather than drastic) in order to counter the associated adaptations in nutrition-related hormones. In order to accomplish this, exposure to highly palatable foods with addictive potential should be minimized.

Educational efforts alone have not reduced use of drugs of dependence. Successful efforts have required both individuals and societal intervention including taxation, regulation, and/or interdiction. Similar efforts targeting the food industry may be required to combat the rising epidemics of food addiction, obesity, and binge eating disorder. Given that individuals with a history of SUD are at higher risk for developing food-intake- related dysfunction, there is a substantial need for nutrition interventions in addiction recovery, and registered dietitian nutritionists should become vital members of the treatment team. Currently, there is no requirement for nutrition education and counseling in substance abuse treatment. Anecdotal reports suggest that most treatment centers allow unlimited or excessive amounts of highly palatable foods to patients. While food restriction can lead to relapse, over-indulgence can perpetuate the cycle of addictive behavior and contribute significantly to healthcare burden. The best intervention appears to lie somewhere in between these extremes, which will require additional clinical expertise in treatment settings. The need for firm commitment to intervention protocols as well as ongoing supervision and consultation is warranted for successful program implementation in residential drug-treatment facilities. 90

in residential drug-treatment facilities. 9 0 Ala n Aragon’s Research Review – February/March 2014
in residential drug-treatment facilities. 9 0 Ala n Aragon’s Research Review – February/March 2014

It is important to acknowledge other relevant hormones, cytokines, and neuropeptides not mentioned in this article, which can include but are not limited to: neuropeptide Y, peptide YY, agouti-related peptide, cholecystokinin, galanin, melanocortin, adiponectin, thyroid hormones (i.e. thyroxine), reproductive hormones (i.e. prolactin), posterior pituitary hormones (i.e. oxytocin).

Conclusions and Further Implications for Nutritionists

Restoration of nutritional status in SUD recovery should look beyond correction of vitamin/mineral status and body weight, but should also account for recovery of dysfunctional neural circuitry and altered hormones. Before a successful nutrition intervention can occur, it is of paramount importance to heal gut function to promote optimal nutrient absorption throughout the gastrointestinal tract. Next, preventing over-exposure to highly palatable foods is critical in repairing addictive processes in the brain. Finally, restoration of hormone levels should occur through gradual yet progressive changes in eating behavior, although there is limited data to support this approach given the presence of confounding variables over extended periods of time. From my own experience in clinical practice, utilizing several small feedings throughout the day is an effective approach towards preventing spikes and subsequent drops in insulin. Given that insulin can block leptin, this technique may be effective in gradually normalizing leptin levels, although to my knowledge there is no data in the SUD population to support this claim. Similarly, stable insulin levels achieved through regular and consistent feeding patterns may prevent ghrelin from increasing to abnormal levels. The mantra I encourage with my SUD patients is "never hungry, never full" and the evidence reviewed herein provides strong support for this approach. Gradual increases in fiber intake throughout the recovery process can improve gut function, minimize undesirable insulin spikes, and promote satiety. For detailed recommendations regarding nutrition therapy during SUD recovery for specific substances of abuse, refer to Wiss and Waterhous. 74

The current trend towards over-medicating SUD patients while failing to address and improve nutrition behavior should be aggressively challenged. Consider this is a call to order for data collection linking drug addiction to reward-related hormones, specifically demonstrating the importance of medical nutrition therapy in SUD recovery over short periods (1-6 months) and longer periods (6-36 months). Without this data, it will be difficult to substantiate the need for nutrition interventions in addiction recovery at the policy level. Nutrition interventions during recovery may prevent or minimize the onset of chronic illness, improving resource allocation. Public health measures should be considered critical.

Public health measures should be considered critical. David A. Wiss, MS, RDN, CPT, is the founder

David A. Wiss, MS, RDN, CPT, is the founder of Nutrition In Recovery, which specializes in the nutritional management of: Food Addiction, Substance Abuse, Eating Disorders, Weight Management, Sports Nutrition, and General Wellness. Mr. Wiss has shared his expertise with a myriad of eating disorder and addiction facilities throughout the greater Los Angeles area. He is on the executive committee of the

Behavioral Health Nutrition Dietetic Practice Group, and is the Research and Grants Committee Chair for the Los Angeles District of the California Dietetic Association. David is a co-founder of Dietitians for Professional Integrity (www.integritydietitians.org). Learn more about his private practice at:

www.NutritionInRecovery.com Facebook.com/NutritionInRecovery Twitter: @DavidAWiss Email: DavidAWiss@NutritionInRecovery.com

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Structural balance theory: does your butt care about your biceps? by Menno Henselmans

Everything that sucks is good for you. That’s what our intuition tells us. Give someone a piece of food that tastes disgusting and tell them it’s really good for them. They’ll take your word for it. Give someone a piece of this cheesecake and afterwards tell them it’s healthy and they’ll go ‘Yeah, right’. Even worse, if you tell them beforehand, they’ll enjoy the cheesecake less. 1 We readily believe that stretching is good for us because it hurts and it’s boring, even though stretching often doesn’t help at all. Bodybuilders take this masochistic ‘no pain no gain’ outlook on life to extremes. Unseasoned chicken with sauceless rice and plain broccoli, anyone? One particular fitness concept that has completely escaped scientific scrutiny because of its inherent plausibility is structural balance theory. To show that nothing escapes the truth, I will hereby shine the light of science on this theory.

Structural balance theory 101

I was going to call this ‘structural balance theory for dummies’, but this didn’t seem applicable, because structural balance theory doesn’t seem to have any advanced version. In fact, it has no operational definition at all.* Structural balance theory was popularized by Charles Poliquin in the 90s and it has since spread like a hooker’s legs in the fitness community. The theory in its currently most common form is that your body tries to maintain a certain balance between muscular strength in every part of the body or in every movement pattern (as I said, the definition varies depending on who you ask). If any body part or movement pattern becomes overdeveloped, the nervous system shuts it down to prevent further imbalance. For example, a weak rotator cuff is often said to limit bench press strength. Specifically, Poliquin proposed the following strength ratios for perfect structural balance in the upper body.

[Footnote]*: According to Popper’s falsifiability criterion, this alone would make it pseudoscience.

criterion, this alone would make it pseudoscience. Before analyzing this theory, I should say that although

Before analyzing this theory, I should say that although I have previously also reviewed Poliquin’s BioSignature Modulation, I am only interested ideas, not their creators. As president Roosevelt said with equal arrogance and eloquence, “Great minds discuss ideas; average minds discuss events; small minds discuss people.” The fact that Poliquin is the man behind both theories is simply an unfortunate coincidence of his ability to come up with plausible theories without supporting them with evidence. What’s the point of discussing theories that do not at least seem to make sense? You don’t see me criticize CrossFit’s use in bodybuilding, for example. That is like taking candy from

a child. (CrossFit, like circuit training, was designed as a bit-of-

everything

bodybuilding or

powerlifting program.)

social

workout,

not an optimal

Back

to

the

interesting

stuff:

does

your

body

care

about

structural

balance?

I’ll

look

at

structural

balance

from

7

perspectives.

1. Antagonist inhibition for strength

Structural balance theory says that if the biceps gets stronger and the triceps doesn’t, biceps activity will be restrained by the nervous system. Like one of the horses pulling a carriage being reined back by the driver because it was trying to run faster than the other horses. Sounds plausible, right?

Plausible but deceptive. A more valid analogy would be a carriage being pulled by 2 horses in opposite directions. Horse Triceps wants to move to the dumbbell rack to do overhead extensions, but horse Biceps wants to move to the mirror to look at his guns. This situation is regulated by antagonist co- activation. Antagonist co-activation is the activity of muscles with the opposite function of the prime movers (the agonists). For example, during a biceps curl the triceps is an antagonist. Antagonist co-activation is required to stabilize movement. The triceps basically corrects for overenthusiastic actions of the biceps. Now here’s where the research gets interesting. When the prime movers become stronger, it is not their activity that is restrained by the nervous system but that of the antagonists. 2 So during a curl, the stronger your biceps gets, the weaker your triceps contracts. The motor cortex, the part of your brain that controls movement, learns to maximally contract the biceps during a curl with minimal interference from the triceps.

This makes evolutionary sense. It is an efficient adaptation. A limitation on prime mover activity would be highly unadaptive. Since nature only cares about function and adaptivity, we see extreme structural imbalance between antagonists in nature in various animals. A good example is the jaws of a crocodile. Some crocodiles have a bite force of 3,700 pounds per square inch (psi). 18 That’s the equivalent of 16,460 newtons, roughly the force needed to lift 3691 pounds (1677 kg). You may be able to clench your teeth into a piece of unseasoned chicken with 150 to 200 psi (890 newtons). Yet you can easily hold a croc’s jaws shut because the muscles that open instead of close the jaw are extremely weak. In humans, we see this in a less extreme form in the weakness of the tibialis anterior on your shins compared to the strength of the calves. Opposite function, opposite strength level.

of the calves. Opposite function, opposite strength level. Ala n Aragon’s Research Review – February/March 2014
of the calves. Opposite function, opposite strength level. Ala n Aragon’s Research Review – February/March 2014

2. European weightlifting secrets

The original idea of using strength ratios for various exercises came from European weightlifters. They used ratios between the Olympic lifts and accessory movements like the squat to assess how to improve the Olympic lifts. If a lifter didn’t progress in the Clean & Jerk and her front squat was comparatively weak, getting stronger in the front squat became a priority.

This may seem like structural balance training, but it’s not. The accessory exercises chosen were highly specific to the corresponding Olympic lift. Front squats build the Clean & Jerk, because the catching position of the C&J is essentially a front squat.

In this case, it’s a matter of using different exercises to cause morphological and neural adaptations in the same muscle groups (muscle growth and power). It has nothing to do with structural balance with other parts of the body. Front squats are a better exercise choice to gain muscle and strength, but the Olympic lifts themselves are required for the nervous system to master the Snatch and the Clean & Jerk. Front squats build the foundation and the Olympic lifts convert this potential into exercise specific power.

In fact, Olympic weightlifters are an excellent example of athletes who are not structurally balanced. Many of them do nothing but squats and Olympic lifts. That means almost all of their training is in the frontal plane: the bar only goes up or down vertically. Imagine that, decades of Olympic weightlifters held back because they didn’t know their performance in the Scott barbell curl wasn’t structurally balanced.

3. “A muscle is just a dumb piece of meat.”

That’s what my friend and colleague Børge Fagerli says in our seminars together to explain that muscle growth is mostly a local process. The stimulus for muscle growth tension, muscle damage or metabolic stress occurs in the muscle and the subsequent adaptation follows in the same place. Almost everything we know about the mechanisms of muscle growth happens within the muscle. The following is a rough overview of how muscle grows. 3-5

1. When you put tension on a muscle, its muscle fibers deform and trigger chemical activity (mechanotransduction).

2. The muscle fibers release growth factors like insulin- like growth factor 1 (IGF-1) and myokines like IL-6 to signal the need for repair (myogenic signaling).

3. The mTOR master enzyme integrates all the signals for muscle growth, such as amino acid availability and the presence of growth factors, and then translates this information for your genes (translation initiation).

4. Your genes are located within muscle cell nuclei that function as command centers in their region of a muscle fiber. They contain the blueprint to create new proteins.

5. Nearby satellite cells are activated and fuse to the muscle fibers to enlarge them (myonuclear addition) and aid in the creation of more new muscle proteins.

As such, there is no plausible physiological mechanism by which one body part could limit growth in another (which is what structural balance theory claims).

4. Does training your legs make your upper body bigger?

Strength training newbies are often told to exercise their legs. When they protest that they don’t really care about leg muscle growth, they’re told that training their legs will make their upper body larger too. The arguments are:

A) Heavy compound leg work like squats increases the production of anabolic hormones. The increases in circulating testosterone, growth hormone and IGF-1 then amplify the training effect in other body parts.

B) The body grows best in proportion. Your body won’t build a Schwarzeneggerian torso on chicken legs. AKA structural balance theory.

The research in support of argument A, the effect of hormones, is methodologically weak and inconsistent. 3,6-8 In the only 2 studies in which training the lower body increased the effect of training the upper body (or the other way around), the participants performed squats immediately before training their biceps. 9,10 The authors concluded that this timing is ideal, since the biceps is trained exactly when anabolic hormone concentrations are at their peak. So, if there’s any validity at all to the idea that training your legs makes your upper body bigger (or the other way around), the mechanism is hormonal and it has nothing to do with structural balance theory.

In other words, your body does not care about structural balance between the upper and lower body. You only need to look around you to see that upper and lower body growth are only proportionate in people who train their whole body equally.

Look at how top-heavy some ring gymnasts are.

Look at the freakily large quads of sprint cyclists.

Look at the amazing physiques of wheelchair bodybuilders and the performance of wheelchair athletes.

Also, compare chicken leg syndrome to Brazilian booty syndrome (nature, how I love thee).

5. The cross-training effect

If you only train your right biceps, your left biceps will become stronger too. Not only that, your triceps gets stronger too, even on the untrained side. 13 This is called the cross-training effect. Is this finally proof of structural balance theory? How can cross- training occur if muscle is just dumb meat?

Cross-training has nothing to do with muscular adaptations. Researchers have used every measurement technique known to mananthropometric measurements, imaging techniques, analysis of the muscle cross-sectional area, etc.to see if the untrained limb gets bigger. It doesn’t. 11,12

The mastermind behind the cross-training effect is your nervous system, mainly your brain (specifically the motor cortex). Many parts of your body are operated by some of the same parts of

parts of your body are operated by some of the same parts of Ala n Aragon’s
parts of your body are operated by some of the same parts of Ala n Aragon’s

your nervous system. So when the nervous system learns how to recruit your muscles on one side of your body, some of these neural adaptations can also be used by the other side. That’s why some researchers now call it the cross-education effect. 11,12

This is a form of structural balance, but it is in fact the complete opposite of structural balance theory. Structural balance theory says that when your right biceps gets too strong relative to your triceps or your other arm, it is shut down. What the cross- education effect and antagonist co-activation both show is that this doesn’t happen. Instead, the triceps, even the other arm, adapts along with the biceps. Basically, your body automatically maintains structural balance, although putting it this way is misleading. A better way to put it is that your body cares about strength symmetry both within a limb (e.g. triceps/biceps) and across limbs (e.g. right arm/left arm).

6. Sports injuries

Why does your body care about strength symmetry but not structural balance? Because strength asymmetry puts you at risk for injury, at least outside of the gym in uncontrolled settings like sports. 14-17 The body doesn’t care about aesthetics, but 160,000+ years of human evolution sure taught it to care about injuries. 21 Balance in the actual structures of your body, like proportionate muscle development, is irrelevant as long as everything is functional. If you never use your legs, having chicken legs is not dysfunctional. Yet if you use your legs and one leg is stronger than the other, the stronger leg is at risk for overuse injuries and the weaker leg is not adapted to cope with the forces generated by both legs.

Thus, the relevance of strength symmetry depends on the type of exercise you do. Arm wrestlers specializing in only 1 arm are a good example of how extreme strength asymmetry can still be functional. Physique athletes should care about symmetry and proportion in body parts, but strength asymmetry is rarely a cause for concern. Strength athletes mostly use a barbell or other type of symmetric implement like rings, kegs or bars. As long as these movements remain symmetric, correcting strength asymmetry is rarely needed. Other athletes involved in sports that do not automatically lead to symmetric strength development have to pay attention to thisespecially in uncontrolled and high impact sports.

7. Removing body parts

If you’re not convinced of the body’s disregard for structural balance, let’s look at an extreme example. We’ve looked at how the body responds to muscle growth of muscles with opposing functions, muscles on the other limb and muscles on the upper vs. lower half of the body. But what happens when there is extreme structural imbalance between muscles with the same function (synergists)? This scenario rarely occurs in humans because these muscles will be activated together, and will therefore grow together. Fortunately (?), we can do much more extreme experiments on animals.

Researchers have looked at what happens when you surgically remove body parts (ablation) or cut them off from the nervous system (denervation) in various animals. 19,20 When you remove a

muscle with the same function or even a division (head) of the same muscle, what is left becomes stronger. Compensatory hypertrophy occurs in the remaining muscle. This again makes no sense from a structural balance perspective, which would require that the remaining body part becomes weaker to retain structural balance. But it makes perfect sense from an evolutionary perspective. The body adapts without concern for anything but function. Lost half of your calves? Better learn to walk on the other half.

Conclusion

Structural balance theory is good broscience: plausible at a glance, but ill-defined and completely lacking in scientific study. Closer inspection reveals that it has no plausible neural or physiological mechanism, it makes no evolutionary sense, it cannot explain the wide display of structural imbalance in nature and sports, and it does not correspond with any empirical .except an anecdote from Charles Poliquin.

It is the power of a well-told story. From childhood onwards, we like to believe stories. They make things real for us. Like a poison to our judgment, they make us forget context and forego reason. Let science be the antidote to anecdote, and reject structural balance theory.

antidote to anecdote, and reject structural balance theory. More of Menno’ s articles are accessible at

More of Menno’s articles are accessible at his website, bayesianbodybuilding.com. Menno’s ideas on everything related to fat loss and muscle

hypertrophy can be seen in his course on optimal program

upcoming

seminar in Miami with Børge Fagerli, who I interviewed in

of

AARR.

the

and

his

2012

August

issue

References

1. Raghunathan R, Walker Naylor R, Hoyer WD. The Unhealthy = Tasty Intuition and Its Effects on Taste Inferences, Enjoyment, and Choice of Food Products. Journal of Marketing: October 2006, Vol. 70, No. 4, pp. 170-184. [AMA]

2. . Dal Maso F, Longcamp M, Amarantini D. Training-related

decrease in antagonist muscles activation is associated with increased motor cortex activation: evidence of central mechanisms for control of antagonist muscles. Exp Brain Res.

2012 Aug;220(3-4):287-95. [PubMed]

3. Mitchell CJ, Churchward-Venne TA, Bellamy L, Parise G, Baker SK, Phillips SM. Muscular and systemic correlates of resistance training-induced muscle hypertrophy. PLoS One.

2013 Oct 9;8(10):e78636. [PubMed]

4. Schoenfeld BJ. The mechanisms of muscle hypertrophy and their application to resistance training. J Strength Cond Res.

2010 Oct;24(10):2857-72. [PubMed]

5. West DW, Burd NA, Staples AW, Phillips SM. Human exercise-mediated skeletal muscle hypertrophy is an intrinsic process. Int J Biochem Cell Biol. 2010 Sep;42(9):1371-5.

Int J Biochem Cell Biol. 2010 Sep;42(9):1371-5. [ PubMed ] Ala n Aragon’s Research Review –
Int J Biochem Cell Biol. 2010 Sep;42(9):1371-5. [ PubMed ] Ala n Aragon’s Research Review –

6.

Phillips SM. Strength and hypertrophy with resistance training:

chasing a hormonal ghost. Eur J Appl Physiol. 2012 May;112(5):1981-3; author reply 1985-7. [PubMed]

7. West DW, Burd NA, Tang JE, Moore DR, Staples AW, Holwerda AM, Baker SK, Phillips SM. Elevations in ostensibly anabolic hormones with resistance exercise enhance neither training-induced muscle hypertrophy nor strength of the elbow flexors. J Appl Physiol (1985). 2010 Jan;108(1):60-7. [PubMed]

8. West DW, Kujbida GW, Moore DR, Atherton P, Burd NA, Padzik JP, De Lisio M, Tang JE, Parise G, Rennie MJ, Baker SK, Phillips SM. Resistance exercise-induced increases in putative anabolic hormones do not enhance muscle protein synthesis or intracellular signalling in young men. J Physiol.

2009 Nov 1;587(Pt 21):5239-47. [PubMed]

9. Hansen S, Kvorning T, Kjaer M, Sjøgaard G. The effect of short-term strength training on human skeletal muscle: the importance of physiologically elevated hormone levels. Scand J Med Sci Sports. 2001 Dec;11(6):347-54. [PubMed]

10. Rønnestad BR, Nygaard H, Raastad T. Physiological elevation of endogenous hormones results in superior strength training adaptation. Eur J Appl Physiol. 2011 Sep;111(9):2249-59. [PubMed]

11. Farthing JP, Borowsky R, Chilibeck PD, Binsted G, Sarty GE. Neuro-physiological adaptations associated with cross- education of strength. Brain Topogr. 2007 Winter;20(2):77-88. Epub 2007 Oct 12. [PubMed]

12. Carroll TJ, Herbert RD, Munn J, Lee M, Gandevia SC. Contralateral effects of unilateral strength training: evidence and possible mechanisms. J Appl Physiol (1985). 2006 Nov;101(5):1514-22. [PubMed]

13. Sariyildiz M, Karacan I, Rezvani A, Ergin O, Cidem M. Cross- education of muscle strength: cross-training effects are not confined to untrained contralateral homologous muscle. Scand J Med Sci Sports. 2011 Dec;21(6):e359-64. [PubMed]

14. Knapik JJ, Bauman CL, Jones BH, Harris JM, Vaughan L. Preseason strength and flexibility imbalances associated with

athletic injuries in female collegiate athletes. Am J Sports Med.

1991 Jan-Feb;19(1):76-81. [PubMed]

15. Nadler SF, Malanga GA, DePrince M, Stitik TP, Feinberg JH. The relationship between lower extremity injury, low back pain, and hip muscle strength in male and female collegiate athletes. Clin J Sport Med. 2000 Apr;10(2):89-97. [PubMed]

16. Devan MR, Pescatello LS, Faghri P, Anderson J. A Prospective Study of Overuse Knee Injuries Among Female Athletes With

Muscle Imbalances and Structural Abnormalities. J Athl Train.

2004 Sep;39(3):263-267. [PubMed]

17. Burnham RS, May L, Nelson E, Steadward R, Reid DC. Shoulder pain in wheelchair athletes. The role of muscle imbalance. Am J Sports Med. 1993 Mar-Apr;21(2):238-42. [PubMed]

18. Erickson GM, Gignac PM, Steppan SJ, Lappin AK, Vliet KA, Brueggen JD, Inouye BD, Kledzik D, Webb GJ. Insights into the ecology and evolutionary success of crocodilians revealed through bite-force and tooth-pressure experimentation. PLoS One. 2012;7(3):e31781. [PubMed]

19. Snow MH. Satellite cell response in rat soleus muscle undergoing hypertrophy due to surgical ablation of synergists. Anat Rec. 1990 Aug;227(4):437-46. [PubMed]

20. Walsh JV Jr, Burke RE, Rymer WZ, Tsairis P. Effect of

compensatory hypertrophy studied in individual motor units in medial gastrocnemius muscle of the cat. J Neurophysiol. 1978 Mar;41(2):496-508. [PubMed]

21. Wells JC, Stock JT. The biology of the colonizing ape. Am J Phys Anthropol. 2007;Suppl 45:191-222. [PubMed]

Am J Phys Anthropol. 2007;Suppl 45:191-222. [ PubMed ] Ala n Aragon’s Research Review – February/March
Am J Phys Anthropol. 2007;Suppl 45:191-222. [ PubMed ] Ala n Aragon’s Research Review – February/March
Overfeeding polyunsaturated and saturated fat causes distinct effects on liver and visceral fat accumulation in

Overfeeding polyunsaturated and saturated fat causes distinct effects on liver and visceral fat accumulation in humans.

Rosqvist F, Iggman D, Kullberg J, Jonathan Cedernaes J, Johansson HE, Larsson A, Johansson L, Ahlström H, Arner P, Dahlman I, Risérus U. Diabetes. 2014 Feb 18. [Epub ahead of print] [PubMed]

BACKGROUND: Excess ectopic fat storage is linked to type 2 diabetes. The importance of dietary fat composition for ectopic fat storage in humans is unknown. PURPOSE: We investigated liver fat accumulation and body composition during overfeeding saturated (SFA) or polyunsaturated (PUFA) fat. DESIGN:

LIPOGAIN was a double-blind, parallel-group, randomized trial. Thirty-nine young and normal-weight individuals were overfed muffins high in SFA (palm oil) or n-6 PUFA (sunflower oil) for 7 weeks. Liver fat, visceral (VAT), subcutaneous abdominal (SAT), and total adipose tissue (TAT), pancreatic fat, and lean tissue was assessed by MRI. Transcriptomics were performed in SAT. RESULTS: Both groups gained similar weight. SFA however markedly increased liver fat compared with PUFA and caused 2-fold larger increase in VAT than PUFA. Conversely, PUFA caused a nearly 3-fold larger increase in lean tissue than SFA. Increase in liver fat directly correlated with changes in plasma SFA and inversely with PUFA. Genes involved in regulating energy dissipation, insulin resistance, body composition and fat cell differentiation in SAT were differentially regulated between diets, and associated with increased PUFA in SAT. CONCLUSION: In conclusion, overeating SFA promotes hepatic and visceral fat storage whereas excess energy from PUFA may instead promote lean tissue in healthy humans. SPONSORSHIP: The sponsors had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; or preparation, review, or approval of the manuscript.

Study strengths

The question of dietary fatty acids on health is huge and largely unsolved. This study is innovative since it’s the first to compare the overfeeding effects of the major source of omega-6 PUFA in the diet (linoleic acid) with the major source of SFA (palmitic acid). The study was meticulously blinded. Quality control was bolstered by subjects receiving dietary counseling from a Registered Dietitian (RD) every two weeks, and maintaining a daily food diary. Erythrocyte membrane fatty acid composition objectively assessed compliance to the treatment protocols.

Study limitations

The authors acknowledged several limitations. First off, the results might be limited to the subject profile (healthy, young relatively lean lacto-ovo vegetarians with low baseline levels of hepatic and visceral fat). The authors conceded that their results still need confirmation in older populations and individuals with type 2 diabetes or non-alcoholic fatty liver disease (NAFLD). The short study duration (7 weeks) leaves open questions about the long-term. Fixed spectrum models examined by the MRI methods used do not cover the full range of lipids.

Comment/application

do not cover the full range of lipids. Comment/application As depicted above, the main findings were

As depicted above, the main findings were unanimously more favorable changes in the PUFA overfeeding compared to SFA. Despite similar gains in total bodyweight (1.6 kg, accomplished by consuming an additional 750 kcal/day from fat-fortified muffins). The ratio of lean:fat tissue gained in the PUFA group was 1:1, whereas it was 1:4 in SFA, indicating an overall better lean-partitioning effect of surplus energy from PUFA. Furthermore, liver fat and visceral fat deposition was significantly greater in SFA. It’s notable that physical activity did not change or differ between groups through throughout the trial, which strengthens the validity of the other outcomes.

It was a diligent decision to use palmitic acid in the SFA condition since it’s the most common SFA in the food supply, including plant foods. However, the effects seen in this study cannot necessarily be generalized to all SFAs. Palm oil was used in the SFA overfeeding arm. Palm oil’s track record in the literature on markers of cardiovascular health has generally been neutral to positive. 1-7 However, the present study clearly shows superior results of omega-6 PUFA-rich sunflower oil in the context of overfeeding. The authors speculate that this could be due in part to the greater ease of oxidation, thus potentially lowering the production of non-esterified fatty acids, which in turn would lower triacylglycerol synthesis in the liver. Despite the interesting results seen in the present study, I would caution against generalizing this comparison to all SFA vs PUFA sources. There could be other constituents within foods that can differently influence outcomes. More comparisons are needed.

differently influence outcomes. More comparisons are needed. Ala n Aragon’s Research Review – February/March 2014
differently influence outcomes. More comparisons are needed. Ala n Aragon’s Research Review – February/March 2014

Can we say what diet is best for health?

Katz

18;35:83-103. [PubMed]

DL,

Meller

S.

Annu

Rev

Public

Health.

2014

Mar

ABSTRACT: Diet is established among the most important influences on health in modern societies. Injudicious diet figures among the leading causes of premature death and chronic disease. Optimal eating is associated with increased life expectancy, dramatic reduction in lifetime risk of all chronic disease, and amelioration of gene expression. In this context, claims abound for the competitive merits of various diets relative to one another. Whereas such claims, particularly when attached to commercial interests, emphasize distinctions, the fundamentals of virtually all eating patterns associated with meaningful evidence of health benefit overlap substantially. There have been no rigorous, long-term studies comparing contenders for best diet laurels using methodology that precludes bias and confounding, and for many reasons such studies are unlikely. In the absence of such direct comparisons, claims for the established superiority of any one specific diet over others are exaggerated. The weight of evidence strongly supports a theme of healthful eating while allowing for variations on that theme. A diet of minimally processed foods close to nature, predominantly plants, is decisively associated with health promotion and disease prevention and is consistent with the salient components of seemingly distinct dietary approaches. Efforts to improve public health through diet are forestalled not for want of knowledge about the optimal feeding of Homo sapiens but for distractions associated with exaggerated claims, and our failure to convert what we reliably know into what we routinely do. Knowledge in this case is not,

as of yet, power; would that it were so. SPONSORSHIP: None listed.

My commentary

Since this is a review paper, it’s not conducive to my normal

assessment of methodological strengths & weaknesses. What I’ll

do is offer my commentary. The cool thing is that the full text of

this article is available here, so you have the freedom to dig into

it on your own. Before I comment on the sections that jumped

out at me, let me first mention the general structure of the paper.

A summary of several major diet types is given: low-carb, low-

fat, low-glycemic, Mediterranean, mixed/balanced such as DASH & DPP, Paleolithic, vegan, & other (table here). After these summaries, an attempt is made to elucidate commonalities among the diets that lead to better health.

In their assessment, the authors take an impressively rigorous

look at each of the dietary regimes. The thorough-ness of the paper makes it quite refreshing. When discussing low-carb diet, they mentioned the interesting angle of an “Eco-Atkins” approach (reviewed in the August 2010 AARR), which essentially is a vegetarian version of the Atkins diet. 8 Interestinglyat least in my viewthis foreshadowed a potential bias in the authors’ perspective. Funny enough, the bias

I initially detected dropped down like a hammer in their final analysis (I’ll get to that).

Keep in mind that I’m seeing a very subtle and delicate bias, but

a bias nonetheless. The authors step outside of the

health/nutrition realm per se, and delve into the realm of ethico-

economics by stating that, An emphasis on meat is an inefficient basis for feeding a global population now in excess of seven billion. Ethical concerns have been raised about meat- eating in general and in particular with regard to the treatment of animals associated with feeding multitudes, along with concerns about the environmental costs of heavily animal-based diets.” While this statement is still defensible, it certainly borders on irrelevance given the specific topic of human health effects of the various diets.

In contrast to the authors reaching outside of the nutritional ‘box’ to challenge low-carb, the diets they virtually exempt the “mixed, balanced” diets (DASH & DPP) from any significant criticism aside from an odd couple of oddly placed references to the potential link between dairy intake and cancer 9,10 when discussing the DASH diet. Once again, this set off my bias sensors. The DASH diet is rife with all of the trappings of 1980’s saturated fat phobia (maximum of 6% of calories) and cholesterol phobia (150 mg max). Challenging this, a recent systematic review and meta-analysis by Chowdhury et al that examined 32 observational studies (n=512,420) and 27 randomized controlled trials ( n=105,085) found no clear support for the traditional recommendation to increase poly-unsaturated

fat intake and decrease saturated fat intake. 11 In another recent meta-analysis, Ramsden et al had similar findings, that no lowering of cardiovascular risk factors was evident from

substituting unsaturated fats

The DASH diet is rooted in the attempt to lower blood pressure, and in addition to its other restrictions, it aims to cap sodium at 2300 mg/day, with a footnote that 1500 mg was found to be even better at lowering blood pressure in those with pre-existent hypertension. Of course, this may be perfectly appropriatefor hypertensives. However, there are adjacent clinical consequences to consider. Graudal et al recently analyzed 167 intervention studies and found that alongside decreased blood pressure, sodium restriction also caused a 2.5% increase in cholesterol, and a 7% increase in triglyceride. 13

Moving toward the final analysis, the authors of the present paper summed up the compatible elements of each of the diets reviewed as: Limited refined starches, added sugars, processed foods; limited intake of certain fats; emphasis on whole plant foods, with or without lean meats, fish, poultry, seafood.” This is where I feel they should have halted the progression of their conclusions and recommendations. However, they continue onward and end up paying tribute to journalist Michael Pollan’s famous saying by relaying, nearly verbatim, his recommendation to eat food, not too much, mostly plants. 14

There’s a certain degree of eloquence in that conclusion, but it’s an oversimplification. At best, it’s too vague (at what point in processing is food not food?). At worst, it’s misleading and dismissive of the delicate contingencies of individual dietary needs driven by preference, tolerance, and various physiological demands. Given the broad gamut of diet types (from plant to animal-dominant) that have shown similar clinical effectiveness for various parameters, the “mostly plants” clause remains speculative. It’s not definitively supported by the current evidence, especially when the rule is applied to percentage of total energy. So, can we say what diet is best for health? On an individual basis, yes we can. On a universal basis, we cannot.

in place of saturated fats. 12

basis, we cannot. in place of saturated fats. 1 2 Ala n Aragon’s Research Review –
basis, we cannot. in place of saturated fats. 1 2 Ala n Aragon’s Research Review –
Effects of supplementing n-3 fatty acid enriched eggs and walnuts on cardiovascular disease risk markers

Effects of supplementing n-3 fatty acid enriched eggs and walnuts on cardiovascular disease risk markers in healthy free-living lacto-ovo-vegetarians: a randomized, crossover, free-living intervention study.

Burns-Whitmore B, Haddad E, Sabaté J, Rajaram S. Nutr J 2014, 13:29 [Epub ahead of print] [PubMed]

BACKGROUND: Plant and marine n-3 fatty acids (FA) may favorably modify select markers of cardiovascular disease risk. Whether supplementing the habitual diet of lacto-ovo- vegetarians (LOV) with walnuts (containing alpha-linolenic acid, ALA) and n-3 FA enriched eggs (containing primarily docosahexaenoic acid, DHA and ALA) would have equivalent effects on CVD risk factors is explored in this study. METHODS: In this study, 20 healthy free-living LOVs following their habitual diet were randomly assigned in a crossover design to receive one of three supplements: n-3 FA enriched egg (6/week), walnuts (28.4 g, 6/week) or a standard egg, 6/week (control) for 8 weeks each with 4-wk

washout between treatments. Erythrocyte membrane fatty acids, serum lipids and inflammatory markers were measured at the end of each treatment. RESULTS: Dietary compliance was observed by an expected increase in erythrocyte membrane ALA following the walnut treatment and in DHA following the n-3 FA enriched egg treatment. Walnut treatment lowered serum triacylglycerol, total cholesterol and Apo B (p < 0.05) compared to the standard egg but not the n-3 FA enriched egg treatment. However, walnut treatment significantly reduced total: HDL cholesterol ratio compared to both egg treatments. There were no differences between treatments for any of the inflammatory markers. CONCLUSION: For LOV, a direct source of DHA such as n-3 FA enriched eggs seems necessary to increase membrane levels of DHA. However for producing an overall favorable blood lipid profile, daily consumption of a handful of walnuts rich in ALA may be a preferred option for lacto-ovo vegetarian. SPONSORSHIP: This work was supported by the American Egg Board

Fellowship; Agriculture Research Institute (Grant) from California State Polytechnic University, Pomona; California Walnut Commission (in-kind donation of walnuts); Chino Valley Ranchers (in-kind donation of eggs).

Study strengths

This study is the first to ever compare the blood lipid-altering effects of walnuts with that of n-3 fatty acid-enriched eggs and regular eggs. This investigation is highly relevant to lacto-ovo vegetarians, who comprise a large segment of the vegetarian population, and who could benefit from fortification and supplement tactics to optimize their diets further. A crossover design helped alleviate the compromised statistical power of the relatively small subject number (n=20). Participants received diet counseling and their intervention foods from a Registered Dietitian (RD) every two weeks during the treatment periods, which bolstered compliance with the experimental protocols.

Study limitations

This was a free-living study, which is beneficial for testing “real- world” conditions, but the trade-off is that it also allows for a higher degree of inter-individual dietary variation, and thus less control. Nevertheless, it was reported (according to recall data) that energy, carbohydrate, fiber, total fat, saturated fat, and monounsaturated fat were not significantly different between the three treatments, which lessens this concern. However, a potential confounder was the higher protein intake in the supplemental egg conditions. Specific data regarding habitual physical activity levels were missing, and would have provided

some useful insight. A final limitation is that the results might be limited to the subject profile (healthy, normolipidemic). The

must be used in

authors further acknowledge that,

interpretation of the results for people with chronic diseases, people that consume other animal products and people that may

caution

exhibit sensitivity to dietary cholesterol.”

Comment/application

sensitivity to dietary cholesterol.” Comment/application As seen above, one of the main findings of this study

As seen above, one of the main findings of this study was that the walnut treatment showed a significant decrease in total cholesterol, triglyceride, and apo B compared to the standard eggs but not the n-3 FA-enriched eggs. However, the total-C:

HDL-C ratio was lower in the walnut treatment compared to both the egg treatments. In this sense, it can be said that walnuts have more favorable effects on blood lipids than both the standard and the n-3 eggs. Notably, that the n-3 eggs caused lower cholesterol levels than the standard eggs but not to a statistically significant degree. The other main finding was that n-3 eggs were more effective at increasing membrane levels of DHA, which has implications for cardiovascular disease prevention. 15 The ALA content of walnuts was insufficient at causing a similar effect via endogenous conversion to DHA. The practical application suggested by these outcomesat least for lacto-ovo vegetariansis to cover the bases by consuming both walnuts as well as a direct DHA source like n-3-enriched eggs.

as well as a direct DHA source like n-3-enriched eggs. Ala n Aragon’s Research Review –
as well as a direct DHA source like n-3-enriched eggs. Ala n Aragon’s Research Review –
Resistance training in overweight women on a ketogenic diet conserved lean body mass while reducing

Resistance training in overweight women on a ketogenic diet conserved lean body mass while reducing body fat.

Jabekk PT, Moe IA, Meen HD, Tomten SE, Høstmark AT. Nutr Metab (Lond). 2010 Mar 2;7:17. [PubMed]

BACKGROUND: The aim of the present study was to compare the effects of 10 weeks resistance training in combination with either a regular diet (Ex) or a low carbohydrate, ketogenic diet (Lc+Ex) in overweight women on body weight and body composition. METHODS: 18 untrained women between 20 and 40 years with BMI >/= 25 kg*m-2 were randomly assigned into the Ex or Lc+Ex group. Both groups performed 60-100 min of varied resistance exercise twice weekly. Dietary estimates were based on two 4-day weighed records. Body composition was estimated using Dual Energy X-ray Absorptiometry. Fasting blood samples were analyzed for total-, HDL- and LDL-cholesterol, triacylglycerols, and glucose. RESULTS: 16 subjects were included in the analyses. Percentage of energy (En%) from carbohydrates, fat and protein was 6, 66, and 22 respectively in the (Lc+Ex) group and 41, 34, 17 in the Ex group. Mean weight change (pre-post) was -5.6 +/- 2.6 kg in Lc+Ex; (p < 0.001) and 0.8 +/- 1.5 kg in Ex; (p = 0.175). The Lc+Ex group lost 5.6 +/- 2.9 kg of fat mass (p = 0.001) with no significant change in lean body mass (LBM), while the Ex group gained 1.6 +/- 1.8 kg of LBM (p = 0.045) with no significant change in fat mass (p = 0.059). Fasting blood lipids and blood glucose were not significantly affected by the interventions. CONCLUSION:

Resistance exercise in combination with a ketogenic diet may reduce body fat without significantly changing LBM, while resistance exercise on a regular diet may increase LBM in without significantly affecting fat mass. Fasting blood lipids do not seem to be negatively influenced by the combination of resistance exercise and a low carbohydrate diet. SPONSORSHIP: Ketolyse AS, Norway.

Study strengths

This study is innovative since it’s the first and still the only one to compare the chronic effect of a ketogenic diet with a conventional diet in subjects undergoing progressive resistance training. Every exercise session was supervised by research personnel. Body composition was assessed via dual X-ray absorptiometry (DXA). Urine reagent strips were used to objectively assessed the adherence of the ketogenic diet group. 4-day weighed food records were taken at the 4th and 7th week of the intervention in order to analyze dietary intake.

Study limitations

The authors gave a detailed description of the ketogenic group’s diet programming (specific carbohydrate restriction with ad libitum intake of protein and fat-rich foods, dietary guide book, use of reagent strips to detect ketosis). Surprisingly, they completely omitted any of the programming details of the regular/control diet or whether or not the subjects were issued any interventional instructions at all. Several limitations are acknowledged by the authors: small study sample (16 subjects completed), insulin sensitivity not measured, neither was albumin bound fatty acids, plasma lipoprotein distribution or fatty acid distribution. They further acknowledged that only fasting values were assessed and that they did not measure sex or

thyroid hormones, catecholamines, glucagon, or corticosteroids all of which could have played roles in the metabolic effects of the diets. A final acknowledged limitation was that menstrual cycle was not coordinated with blood collection. I would add that the use of untrained subjects leaves question about how trained subjects might respond in a similar comparison.

Comment/application

might respond in a similar comparison. Comment/application \ Above is the breakdown of the diets in

\Above is the breakdown of the diets in all of their disparate glory, and as we go over the results, it will help to refer to how these differences played in. The ketogenic group lost a significant amount of total bodyweight (5.6 kg), while the control group slightly gained (0.8 kg). The weight lost in the ketogenic group was almost exclusively body fat, while no significant change in fat mass was seen in the control group. Interestingly, the control group gained a significant amount of lean body mass (1.8 kg), while the ketogenic group had no significant lean mass change.

The greater drop in total bodyweight in the ketogenic group can at least partially be attributed to the discrepancy in total caloric intake (217 kcals more in the control condition). However, this was not a statistically significant difference. Nevertheless, it would explain about 2 kg of the 5.6 kg fat mass lost in the ketogenic group. Regarding the greater fat loss in the ketogenic group, the authors speculate that greater satiety, increased lipolysis (via decreased insulin and increased catecholamines and glucagon), decreased carbohydrate-mediated de novo lipogenesis, and decreased glucose-driven triacylglycerol formation in the fat cell.

Interestingly (and perhaps due to bias), they don’t include the lower energy intake in their speculation of the ketogenic diet’s greater fat loss, but they point to the higher energy intake of the control group in their speculation about the latter’s increase in lean mass (which was not seen in the ketogenic group). A second speculation they made about this lack of increased LBM was that the state of ketosis could have driven a higher use of amino acids for glucose production. This is far-fetched compared to the simpler explanation that glycogen is a component of lean mass, and a higher carbohydrate intake results in greater glycogen storage.

Interestingly, the authors did not discuss the fat loss advantage of the ketogenic group’s higher protein intake. A recent meta- analysis by Clifton et al noted that a three-fold greater effect on fat mass was found in studies where a difference between the diets of only 5% energy from protein was maintained. 16 This happens to be the exact protein intake difference between the diets in the present study.

intake difference between the diets in the present study. Ala n Aragon’s Research Review – February/March
intake difference between the diets in the present study. Ala n Aragon’s Research Review – February/March
1. Chong YH, Ng TK. Effects of palm oil on cardiovascular risk. Med J Malaysia.

1. Chong YH, Ng TK. Effects of palm oil on cardiovascular risk. Med J Malaysia. 1991 Mar;46(1):41-50. [PubMed]

2. Elson CE. Tropical oils: nutritional and scientific issues. Crit Rev Food Sci Nutr. 1992;31(1-2):79-102. [PubMed]

3. Ebong PE, Owu DU, Isong EU. Influence of palm oil (Elaesis guineensis) on health. Plant Foods Hum Nutr. 1999;53(3):209-22. [PubMed]

4. Edem DO. Palm oil: biochemical, physiological, nutritional, hematological, and toxicological aspects: a review. Plant Foods Hum Nutr. 2002 Fall;57(3-4):319-41. [PubMed]

Sambanthamurthi R, Tan YA. Palm fruit

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for palm oil with a cautionary note on interesterification. J Am Coll Nutr. 2010 Jun;29(3 Suppl):253S-284S. [PubMed]

7. Oyewole OE, Amosu AM. Public health nutrition concerns on consumption of red palm-oil (RPO): the scientific facts from literature. Afr J Med Med Sci. 2010 Dec;39(4):255-62; discussion 263-5. [PubMed]

8. Jenkins DJ, Wong JM, Kendall CW, Esfahani A, Ng VW, Leong TC, Faulkner DA, Vidgen E, Greaves KA, Paul G, Singer W. The effect of a plant-based low-carbohydrate ("Eco-Atkins") diet on body weight and blood lipid concentrations in hyperlipidemic subjects. Arch Intern Med.

2009 Jun 8;169(11):1046-54. [PubMed]

9. Lampe JW. Dairy products and cancer. J Am Coll Nutr.

2011 Oct;30(5 Suppl 1):464S-70S. [PubMed]

10. Song Y, Chavarro JE, Cao Y, Qiu W, Mucci L, Sesso HD, Stampfer MJ, Giovannucci E, Pollak M, Liu S, Ma J.Whole milk intake is associated with prostate cancer-specific mortality among U.S. male physicians. J Nutr. 2013

Feb;143(2):189-96. [PubMed]

11. Chowdhury R, et al. Association of Dietary, Circulating, and Supplement Fatty Acids With Coronary Risk: A Systematic Review and Meta-analysis. Ann Intern Med.

2014 Mar;160(6):398-406. [AIM]

12. Ramsden CE1, Zamora D, Leelarthaepin B, Majchrzak- Hong SF, Faurot KR, Suchindran CM, Ringel A, Davis JM, Hibbeln JR. Use of dietary linoleic acid for secondary prevention of coronary heart disease and death: evaluation of recovered data from the Sydney Diet Heart Study and updated meta-analysis. BMJ. 2013 Feb 4;346:e8707. [PubMed]

13. Graudal NA, Hubeck-Graudal T, Jürgens G. Effects of low- sodium diet vs. high-sodium diet on blood pressure, renin, aldosterone, catecholamines, cholesterol, and triglyceride (Cochrane Review). Am J Hypertens. 2012 Jan;25(1):1-15. [PubMed]

14. Pollan M. 2007. Unhappy meals. New York Times Mag., Jan. 28. [NYT]

15. Holub BJ. Docosahexaenoic acid (DHA) and cardiovascular disease risk factors. Prostaglandins Leukot Essent Fatty Acids. 2009 Aug-Sep;81(2-3):199-204. [PubMed]

16. Clifton PM, Condo D, Keogh JB. Long term weight maintenance after advice to consume low carbohydrate, higher protein diets - A systematic review and meta analysis. Nutr Metab Cardiovasc Dis. Nutr Metab Cardiovasc Dis. 2014 Mar;24(3):224-35 [PubMed]

Metab Cardiovasc Dis. 2014 Mar;24(3):224-35 [ PubMed ] Ala n Aragon’s Research Review – February/March 2014
Metab Cardiovasc Dis. 2014 Mar;24(3):224-35 [ PubMed ] Ala n Aragon’s Research Review – February/March 2014
In defense of the bros. Bryan Krahn, CSCS They say the first step towards recovery

In defense of the bros. Bryan Krahn, CSCS

They say the first step towards recovery is admitting you have a problem. So here goes: I’m Bryan and I’m a bro.

In my defense, I can’t help my bro-styling ways. My muscle building teeth were cut in the late ‘80’s and 90’s, the salad days of bro bodybuilding. This era was also pre-internet, when a muscle-head’s only resources were ghostwritten Weider magazines and the occasional re-run of ESPN’s American Muscle.

That left a huge void for muscle building information so we looked to our only legitimate source for guidance and inspiration -- other bodybuilders.

Now there’s nothing wrong with a little observational evidence. In fact, were a law suddenly passed that young bodybuilders couldn’t read about training and nutrition online anymore and could only copy what the top natural pros are doing -- no questions asked -- hypertrophy rates across the country would double, and internet memes like Do You Even Lift would cease to exist.

Problem is, throw steroids into the mix and suddenly things get dicey. It’s because almost everything works -- if you take enough gear. The most cockamamie training schemes will produce pumps and big PR’s, while asinine “tilapia and MCT oil” type-diets will shred fat with negligible lean mass lost.

It’s not surprising (and a little depressing) that some bros go their whole lives believing that training and diet play second fiddle to the type and quantity of gear they take.

It’s also not surprising that the most ridiculous bro-isms happen to be contest prep related. Take a bodybuilder on a long, hard prep, when each pound of weight lost is accompanied by a 10% increase in anxiety, and now throw in an extra-healthy dose of anabolics -- forget the braintrust at Weider University, this is the true source of much bro science.

Everyone’s heard that higher reps with lighter weights when dieting “etches in the cuts and brings out striations.” Yes, it’s those 30-rep sets of cable flyes that’s bringing out Mongo’s coveted pectoral-deltoid separation, not the Draconian diet he’s been following for 16-weeks, the hours of cardio, or the pharmaceutical cocktail from his “life extension doc.”

Sometimes though, the pre-contest broscience goes beyond amusing and into dangerous. How many bodybuilders have missed pre-judging in favor of the hospital because some gym scientist had them cut water too soon, or were told to channel their inner wrestler and wear garbage bags in the sauna to lose that “last bit of water they’re holding.”

I remember a guru telling me (with a straight face) that his prized competitor’s peak weak would include two hours of

cardio and only a half-cup of water -- a day. His argument:

“He’s a redhead, and gingers hold water more.” I’m not sure if his client won his show. I’m more surprised he even survived.

Of course, those are extreme examples, but evidence-based guys all say the real problem with broscience is that when it trickles down into the mainstream it holds the maturation of the entire industry back.

For example, spiking insulin with a big dose of high glycemic carbs post workout became “a thing” in gym culture to “halt catabolism in its tracks and kickstart anabolism.” Forget that the practice is really only necessary for high intensity athletes performing multiple exercise bouts in a day (or that many bodybuilders doing it are also injecting insulin), now Mrs. Jones thinks she needs a massive sugar bomb after her Zumba class so she can “recover.”

Then there’s clean eating, a nice bro-ism in theory for making better food choices that’s been twisted and perverted by misinformed zealots and unleashed upon the mainstream diet industry.

Yes, cut enough sugary or fatty foods from your menu and you’ll lose weight. If labeling the ones you cut out “dirty” helps keep you on track, fine. However, we now have an entire generation of bros swearing off dairy, wheat, and all forms of “white death” (sugar) because it’s “dirty” or “toxic.” As a result, destructive behaviors like binge eating and orthorexia are reportedly on the rise in seemingly “healthy” fitness populations.

I realize you’ve heard all this before. I could’ve easily saved 1000 words and wrote, “So yeah, broscience is bad, m’kay?”

Here’s the thing. I kinda like broscience.

Okay, let me re-phrase, cause saying I like broscience is basically saying I accept pseudo science or bad science. Even when broscience has proven to be true -- like weight trainers needing more protein -- you can’t turn a blind eye to the many

times it’s been flat-out wrong. As they say, even a broken clock

is correct twice a day.

I just have a soft spot for broscientists. Not the marketing

hucksters cherry picking data to convince me I can eat all the carbs I want after 9 pm (EDT) and not gain fat. The real bros -- the guys in the gym experimenting, inventing techniques, and tweaking exercises. Those bros are my peeps.

Broscientists like that are who got me excited about lifting weights. I remember the day I befriended my first real-life bodybuilder and convinced (begged) him to let me train with him. I didn’t receive a sterile lecture about loading parameters and the importance of activation drills -- we did wide grip pull- ups for a wide back, 21’s to make the biceps more vascular, and heavy dumbbell pullovers to expand the rib cage while developing a serratus “three fingers deep.”

It might’ve been “wrong” or “gym science” but it also spoke to

my teenage mind and motivated me. And years later, long after

teenage mind and motivated me. And years later, long after Ala n Aragon’s Research Review –
teenage mind and motivated me. And years later, long after Ala n Aragon’s Research Review –

I’ve abandoned many of my bro-isms, I still see the things I did -

- even the incorrect things -- as essential to my development.

After all, I started as an ADHD-afflicted teenager and yet here I am, still training, in my fourth decade of life. Had those first

workouts been less experiential and more sterile and educational,

I doubt I would’ve continued past age 20.

To that end, even as the industry matures (thanks in part to the people involved in this Research Review) and evidence-based practices supplant outdated or erroneous ones, I still hold onto a few bro-isms. I even champion a few of my own that I’ve come up with.

I’m convinced that weak bodyparts are usually the bodyparts you have trouble getting a pump in, while strong bodyparts typically need just a set or two.

I’m convinced that calves grow best when you train them daily and when you throw the kitchen sink at them -- at least until that stops working.

I’m convinced that if you’re not experiencing any hunger or loss of energy on a diet after the first few weeks then you need to cut your calories. (Or at least cut back on your stimulants. Meh, do what you want.)

Those are some of my bro-isms. If any evidence for them exists,

I haven’t seen it, but until the likes of Schoenfeld or Aragon

decide to torpedo them, I’ll consider them bro-true. Which should be the metric for all good broscience -- it’s what you believe based on experience and intuition and good old observation. If one day science validates your beliefs, great! But if what you believe turns out to be wrong, then it’s incumbent on you to revise your theories. Trust me, it doesn’t make you less of

a bro.

So train hard, keep records, and make adjustments to your approach till you find what works for your body, all the while keeping a close eye on the objective science.

And go easy on the bros! Cause even the most buttoned-up, lab coat wearing, evidence-based guy will tell you that bodybuilding is a beautiful amalgam of art and science. The bros are the artistic side of our muscle-building pursuit, and without them, what we do would be a lot less colorful.

and without them, what we do would be a lot less colorful. Bryan Krahn, BA, CSCS,

Bryan Krahn, BA, CSCS, is a fitness consultant, writer, editor, and online coach. He's been published like, a lot, under his own name and has ghost written for many prominent figures in the fitness scene. He blogs about training, eating, and New York City at bryankrahn.com. And yes, he even lifts.

York City at bryankrahn.com . And yes, he even lifts. Ala n Aragon’s Research Review –
York City at bryankrahn.com . And yes, he even lifts. Ala n Aragon’s Research Review –

Should you stop counting calories and macros?

By Armi Legge

Should you stop counting calories and macros? By Armi Legge Introduction You know that calories count

Introduction

You know that calories count if you want to lose fat. (If not, go to the AARR index and search for “calorie.” Read for an hour and come back).You also know that your macronutrient intake is extremely important if you want to build muscle, lose fat, or be healthy.

The logical conclusion, therefore, is to start counting calories. If calories in versus calories out is true, then you should strictly control your calorie intake, right? That can work well, but not for everyone or forever.

Here are 4 reasons even obsessive bodybuilders and athletes should consider not counting calories or macros, at least for a while.

1) It can drive you to overeat.

As odd as this might sound, this is a common problem. It’s basic economics. When something is in short supply, you value it more. If you have a very specific limit on how many calories you can eat, that number becomes increasingly more important throughout the day. Often, this gets to the point you can’t stop thinking about your diet.

On one hand, that’s a good thing. Calories should be a little “scarcer” while you’re dieting. On the other hand, this can drive you a little nuts.

There is some indirect evidence this is true, too. People who are intrinsically motivated to lose weight, who focus more on

behaviors like preparing healthy meals than hitting specific numbers, are generally able to lose more weight and keep it off longer than people who are motivated by external rewards or punishments. 1

If you’ve ever counted calories and gone over, it’s easy to feel like you’ve failed, which is a kind of self punishment. While I’m stretching a bit, most evidence indicates that more rigid control techniques, like counting calories, aren’t as effective in the long- run. They also tend to increase your risk of binge eating and other eating disorders. 1

From an anecdotal standpoint, many of the people I’ve worked with have had similar experiences. They don’t necessarily feel like failures if they go over their calories, but they’re so sick of being constrained by their calorie and macronutrient targets that overeating is almost like a “screw you,” to their diet. Obviously this isn’t true for everyone, but it can happen.

2) It can be painfully inconvenient.

Say you’re at a friend’s house, a restaurant, or a camping trip. Suddenly you don’t have a nice kitchen anymore to weigh your food, or a handy app or spreadsheet to count calories and macros.

Or, maybe you’re out with friends, and they decide to go to a restaurant. You already have a meal planned, but you also don’t want to be the “Oh, I have to get up early, have fun without me,” person. That sucks.

Maybe you went out with your friends and sat awkwardly while everyone else ordered food. Or, you get 50 calories worth of tomato soup, so you can go home and eat broccoli and chicken breasts to hit your macros.

Yes, you can always eyeball your portions and estimate your macros while eating out. However, if you’re kind of obsessive, like me, it’s hard to make yourself do that in the real world. It also makes eating more complicated, which brings us back to problem number 1.

This becomes even more of an issue while traveling.

3. It’s extremely difficult while traveling.

If you like traveling, like me, counting calories and macros can be hard. It’s almost as bad as dealing with TSA employees.

You’ll probably encounter new foods which you can’t identify, or even pronounce. Try estimating the macros of Gai Pad Med Ma Muang, a Thai chicken dish with cashews, honey, peppers, and other vegetables. Good luck.

Another problem is that you have less time while traveling, and your normal routine is shattered, which makes it even harder to stick to your meal plan and thus calories and macros.

You can generally find simpler foods while traveling if you know where to look, but that’s not always possible or fun.

know where to look, but that’s not always possible or fun. Ala n Aragon’s Research Review
know where to look, but that’s not always possible or fun. Ala n Aragon’s Research Review

If you use an app like MyFitnessPal to count calories and it runs out of battery (damn iPhone), then you’re really screwed.

If you’re traveling for more than about two weeks, you’ll probably need a different system for dieting.

If you’re traveling less than two weeks, you can generally make calorie counting work, not that you’d want to.

4. It can be stressful and distracting.

There’s a concept in economics called “externality,” where one action has unintended consequences in another area.

While calorie counting might seem to only take a few minutes per day, you’ll often spend a significant amount of time thinking about food and what you’ll eat to hit your macros.

There have been times when I’m out with friends, got a little hungry, and immediately started thinking about how I was going to hit my calories and macros if we got food. These thoughts can creep into almost every other aspect of your life such as work, time with family, etc.

Instead of being able to enjoy your food, you can’t stop thinking about how many grams of carbs, protein, and fat you still need to eat, or if you’ve eaten too much.

It’s exhausting.

At this point, you may think that you don’t need to ever count calories or macros. Or you think I’m an idiot, so let me explain. Calorie Counting Also Works, so be Flexible

Counting calories and macros works extremely well for some people. I have friends who’ve been doing it with no problem for years. Some of them weigh their food every day, too.

They’re happy with their system, and it’s helped them stay extremely lean.

In other cases, you might have to count calories. If you’re getting extremely lean for a bodybuilding competition or a photo shoot, it might be worth the inconvenience and stress to count calories for a few weeks or months.

However, there are others who get sick of counting calories and macros, and run into all of the problems listed above. When that happens, if they don’t have a system in place to stay on track, they often gain weight or feel so out of control they’re a nervous wreck.

If the only way you know to control your diet and stay lean is through counting calories and macros, and that stops working for you, you’re screwed.

Your new goal is to become comfortable with multiple kinds of dieting. As long as you’re in a calorie deficit, you’ll lose fat.

There are all kinds of methods you can use to accomplish that, which don’t involve counting calories or macros.

If you’re sick of meticulously tracking your food, look at this as a wakeup call. Try something new.

Here’s your challenge.

If you’ve been counting calories and macros, go one week without it. Yes, if you’re a OCD like me, this will be a little scary. All the more reason to do it.

Assuming you don’t enter a speed eating contest, it’s hard to gain much of any fat in one week. The benefits on the other hand, can be huge.

If you find that you enjoy your new style of eating, try it for another week. Keep doing it as long as you can while improving or maintaining your physique and performance.

If you feel anxious on the first day, don’t wuss out. Give the system at least a week.

After going at least a week without tracking, and you’d still rather count calories and macros, go for it. Just make sure the benefits are worth the added effort and inconvenience, and don’t give up on a more relaxed approach completely.

There’s also nothing wrong with using a hybrid approach -- counting calories and macros some days, and “freestyling” it on others. That’s what I do while cutting.

Ultimately, you’ll get lean and stay that way using the system that’s easiest for you to maintain. Or you can just go Paleo. 2

easiest for you to mai ntain. Or you can just go Paleo. 2 Armi Legge is

Armi Legge is the editor of Evidence Magazine, a monthly publication that helps you automate your diet and training, so you can have the body you want and move on with your life. Learn more about it here.

References

1. Pelletier L, Dion S, Slovinec-D'Angelo M, Reid R. Why Do You Regulate What You Eat? Relationships Between Forms of Regulation, Eating Behaviors, Sustained Dietary Behavior Change, and Psychological Adjustment. Motivation and Emotion. 2004;28(3):245277.

2. LOL

Motivation and Emotion. 2004;28(3):245 – 277. 2. LOL  Ala n Aragon’s Research Review – February/March
Motivation and Emotion. 2004;28(3):245 – 277. 2. LOL  Ala n Aragon’s Research Review – February/March
Does “reverse dieting” build metabolic capacity? By Alan Aragon Background I have received numerous incarnations

Does “reverse dieting” build metabolic capacity?

By Alan Aragon

Background

I have received numerous incarnations of the question titling this section. It relates to the transition period into caloric maintenance or surplus after prolonged dieting for several weeks or months. To the best of my knowledge, the term “reverse dieting” has its origins in competitive bodybuilding, where the post-contest period is commonly treacherous ground when it comes to the ravenous gorging of foods that were avoided during prep. One of two unfavorable outcomes can occur.

The lesser of the evils is that the competitor ends up filling glycogen stores and looking fuller and tighter the next day, wishing this was the look that made it to the stage the day before. The competitor then returns to the scheduled maintenance or off-season intake, and hums right along, accepting the eventual reality of not being contest-lean, but also enjoying the lack of severe restriction in terms of food type and/or amount.

The more brutal scenario is when this post-contest feeding frenzy continues for the next few days (or weeks), resulting in rapid fat gains that boomerang the competitor to pre-competition level body fat levels and beyond. The adverse psychological impact is a discussion that’s beyond the scope of this article, but for now, suffice it to say that it ain’t a good thing.

In my observations, the latter scenario is far more common after prep periods, especially preps that are very severe in their caloric deficit and/or the limits placed on the range of foods “allowed” to be consumed. Diets based on a narrow set of supposedly “clean” foods often fail to benefit prep beyond more flexible approaches emphasizing macronutrient targets. An under- recognized downside is that they can also create a devastating aftermath by accumulated feelings of deprivation, triggering a vicious backlash against the pre-contest diet.

Enter “reverse dieting”

The broad definition of reverse dieting is a gradual, incremental re-introduction of calories (mostly from carbohydrate) into the diet for a prolonged period after the dieting phase. There is no universal or “official” set of reverse dieting rules, but the general incarnation in coaching circles is to increase carbohydrate (and to a lesser degree, fat and protein) on a weekly basis, to the order of roughly 5-10 g carbs/week (I’ve also heard of figures like 10- 20 g thrown around) until maintenance levels are hit, at which point a decision is made to either hold steady or continue into a ‘bulking’ or surplus phase.

Given a scenario where someone’s daily maintenance carb target is 300 g, using the lower incremental range of 5-10 g/week, if a contest diet ended someone off at, say, 150 g/day, then it could take 15-30 weeks (almost 4-8 months) to arrive at maintenance- level carb intake. Using the higher range of a 10-20 g weekly

carb increment, it would take nearly 1-2 months to hit maintenance carb levels. Ironically, the reverse dieting period has been described as being as difficult or even more so than the dieting period in terms of the willpower and self-control required to not binge everything back. It’s also ironic that instead of phasing into a more psychologically relaxed off-season phase, reverse dieting can have a tendency to perpetuate the obsessiveness inherent in the pre-contest phase. Therefore, for some competitors, there really is no actual break from dietary micromanagement, regardless of season.

Observations, claims, & perspectives

One of the most obvious and concrete benefits of reverse dieting

is that it draws a hard line protecting against the post-contest

binge, which in severe cases can put back most or all of the competitor’s body fat in a matter of a few days. Along with that comes the physical discomfort of bloating and edema, not to mention the psychological stress of the rapid disappearance of the hard-fought aesthetics. However, beyond this, the benefits of reverse dieting are more subtle. In some cases, the claimed benefits tread well into speculative/hypothetical ground, despite being asserted as factual.

One of the popular claims is that reverse dieting builds metabolic capacity. In other words, it increases the amount you

can eat (emphasis on carbs) as a matter of maintenance intake. In light of the starvation-level carb & total kcal intakes common among pre-contest diets, this increased maintenance carb intake

is seen as a godsend. It allows competitors to begin their contest

prep at a higher carb intake, and end off at a higher intake as well. This avoidance of starvation-level intake has also been claimed to prevent so-called metabolic damage, characterized by stalled weight loss despite continued efforts to reduce caloric intake or increase exercise output. So, before I answer the question about building metabolic capacity, let’s take a closer look at the opposite phenomenon.

It’s important that the metabolic damage concept be viewed in an objective/critical light, since it has a tendency to lend itself to fairy tales. Metabolic damage is actually a dramatized version of what researchers know as adaptive thermogenesis (AT), defined as the margin of decrease in resting energy expenditure (REE) that cannot be accounted for by losses in lean/metabolically active tissue. The highest margin of AT was seen recently in Johanssen et al reported 29.4% drop in resting metabolic rate after massive weight loss in obese subjects in a nationally televised competition. 1 Significant AT was apparent since this metabolic rate drop was 504 kcal greater than what the loss of lean mass would have predicted; it amounted to an AT of 18.8%. Keep in mind that this is after a mean weight loss of 57.6 kg (126.7 lb) in 6 months. It’s not likely that physique competitors will significantly exceed that degree of metabolic slowing. In a more typical example, Liebel et al showed that in obese subjects,

a 10% or greater weight loss resulted in a 15% greater REE reduction than predicted by body composition change. 2

It should also be noted that none of the subjects in Liebel et al’s

or Johanssen et al’s research were on an optimally designed progressive resistance training program with optimized macronutrient targets, so it's entirely possible for AT in well- designed programs to be significantly less than what has been

programs to be significantly less than what has been Ala n Aragon’s Research Review – February/March
programs to be significantly less than what has been Ala n Aragon’s Research Review – February/March

reported in the literature. Another thing I’d like to point out about metabolic damage-related claims is the unreliability of self-reported intake and output. For example, Lichtman et al found that obese subjects with a reported history of ‘diet resistance’ under-reported food intake by an average of 47%, and over-reported physical activity by 51%. 3 Furthermore, under-reporting intake might be greater among women than men (especially in overweight women). 4 At this point I would encourage the reader to refer back to the April/May 2013 issue

of AARR for further insight by Lyle McDonald on perception

versus realities of metabolic damage.

Raising metabolic capacity

Aside from preventing post-contest binging, the reported benefits of reverse dieting center around higher caloric

(especially carb) intakes for maintenance. There are also reports

of maintaining impressive levels of leanness during the reverse

dieting period, despite the incremental intake hikes. There are at least five factors explaining these intriguing phenomena.

One would be that the gradual increases in carbohydrate

facilitate increases in resistance training performance, which can translate to an increased training energy expenditure. In support

of

this, Paoli et al recently saw an unprecedented 22.6% increase

in

REE in a 22-hour post-exercise period as a result of a protocol

involving a rest-pause-type of technique where heavy loads were

taken to failure. 5 This results would be reflective of trainees who are able to train progressively while maintaining a high intensity

of effort.

A second possibility is an increase in non-exercise activity

thermogenesis (NEAT) occurring alongside the graduated increases in energy intake. A memorable example supporting this possibility is research by Levine et al, who fed non-obese adults 1000 kcal above their maintenance needs for 8 weeks. 6 On average, 432 kcal was stored, and 531 kcal was burned. Nearly two-thirds of the latter (336 kcal) was attributable to NEAT. Now here’s the interesting finding that warrants special attention within the context of this discussion: the metabolic responses to the caloric surplus was highly variable, ranging from a 89 kcal decrease to a 692 kcal increase. It’s the latter occurrence that would explain the maintenance of leanness during reverse dieting, but it’s the former that should also caution against assuming it will work spectacularly for everyone.

A third explanation for increased metabolic capacity is the

increased REE associated with gains in fat-free mass, which are

inevitable alongside progressive training combined with increasing energy intake.

A fourth factor is the return of the metabolic rate-regulating

hormonal milieu towards normal. Most notably in this aspect is thyroid activity, which is suppressed under prolonged hypocaloric conditions, especially those involving carbohydrate restriction. Classic research by Pasquali et al showed that

carbohydrate intake can be a thyroid-regulating factor independent of total caloric intake. 7

A fifth and very likely explanation is simply a combination of

the previous factors, where the collective result appears to be the

metabolic miracle of staying lean while increasing calories-in,

and ending up at a higher maintenance caloric requirement at the end of a reverse dieting cycle.

Conclusions

So, to answer the question, does reverse dieting increase

metabolic capacity? Yes it canbut not by magic, not as effectively for some as for others, and not necessarily by virtue

of its gradual nature. While a regimented, gradual transition to

maintenance or surplus can prevent binging, dragging out this process by making it too gradual is not necessarily optimal from a recovery and progression standpoint.

A recent comprehensive case study by Rossow et al examined

the 6-month prep and 6-month recovery period of a professional drug-free bodybuilder. 8 During the prep phase, markers of metabolic stress were substantially elevated. Increases in cortisol and ghrelin were seen with consurrent decreases were seen in leptin, testosterone, red blood cell count, hematocrit, thyroid (T3 & T4), and resting energy expenditure. It’s reasonable to postulate that that reverse dieting variants that are too gradual result in keeping the trainee at a subpar recovery rate. The sooner a trainee can fully alleviate this physiologically ‘insulted’ state, the betterof course without sabotaging it all by binging.

Since there’s a lack of objective research to lean on in this area, I’ll offer my opinion. I personally would not recommend taking more than a 2-week period to transition from deficit to maintenance, and I would not recommend taking more than 4 weeks to go from deficit to surplus. The objective would be to transition as quickly as possible, and not let shifts in scale weight or body fat regain mess with your head. So, if you can transition even more quickly than the aforementioned timeframesgreat. That means more time in recovery, and a faster track toward growth. Physique competitors need to come

to grips with the reality that the vast majority cannot stay within

spitting distance of contest-leanness without compromising muscle gains in the off-season.

References

1. Johannsen DL, Knuth ND, Huizenga R, Rood JC, Ravussin E, Hall KD. Metabolic slowing with massive weight loss despite preservation of fat-free mass. J Clin Endocrinol Metab. 2012 Jul;97(7):2489-96. [PubMed]

2. Leibel RL, Rosenbaum M, Hirsch J. Changes in energy expenditure resulting from altered body weight. N Engl J Med. 1995 Mar 9;332(10):621-8. [PubMed]

3. Lichtman SW1, Pisarska K, Berman ER, Pestone M, Dowling H, Offenbacher E, Weisel H, Heshka S, Matthews DE, Heymsfield SB. Discrepancy between self-reported and actual caloric intake and exercise in obese subjects. N Engl J Med. 1992 Dec 31;327(27):1893-8. [PubMed]

4. Garriguet D. Under-reporting of energy intake in the Canadian Community Health Survey. Health Rep. 2008 Dec;19(4):37-45. [PubMed]

5. Paoli A, Moro T, Marcolin G, Neri M, Bianco A, Palma A, Grimaldi K. High-Intensity Interval Resistance Training (HIRT) influences resting energy expenditure and respiratory ratio in non-dieting individuals. J Transl Med. 2012 Nov 24;10:237. [PubMed]

6. Levine JA, et al. Role of nonexercise activity thermogenesis in resistance to fat gain in humans. Science. 1999 Jan 8;283(5399):212-4. [Pubmed]

7. Pasquali R, Parenti M, Mattioli L, Capelli M, Cavazzini G, Baraldi G, Sorrenti G, De Benedettis G, Biso P, Melchionda N. Effect of dietary carbohydrates during hypocaloric treatment of obesity on peripheral thyroid hormone metabolism. J Endocrinol Invest. 1982 Jan-Feb;5(1):47- 52. [Pubmed]

8. Rossow LM1, Fukuda DH, Fahs CA, Loenneke JP, Stout JR. Natural bodybuilding competition preparation and recovery: a 12-month case study. Int J Sports Physiol Perform. 2013 Sep;8(5):582-92. [Pubmed]

Sports Physiol Perform. 2013 Sep;8(5):582-92. [ Pubmed ] Ala n Aragon’s Research Review – February/March 2014
Sports Physiol Perform. 2013 Sep;8(5):582-92. [ Pubmed ] Ala n Aragon’s Research Review – February/March 2014
Interview with Tom Venuto. Tom is one of the true legends of the industry, and

Interview with Tom Venuto.

Tom is one of the true legends of the industry, and has earned a reputation as one of the rare few guys who you can’t say anything bad about. I’ve known Tom personally since 2008 when he began his subscription to AARR. It’s a special honor to have him here for a one-on-one interview about a topic he probably has more knowledge about than anyone else:

transformations.

Tom The Icon! First off I want to thank you for agreeing to do this interview, I realize that you are a busy international man of mystery & intrigue, and donating your insight & expertise here is much appreciated. The first thing I'd like to ask is how the transformation 'games' originated in your audience, and what has it developed into today, in terms of scope, size, & magnitude. You mentioned playing somewhat of a Bill Phillips role (for those who can recall the earlier days of EAS & Body for Life), and I think that's a really noble and challenging position to have a foot in.

Thanks for the flattering, if not embellished intro Alan, and it’s a privilege to contribute to AARR again. Through the 1990’s and into the 2000’s I was deep into natural bodybuilding competition and busy establishing myself in the fitness business. That was indeed the Phillips / EAS / Muscle Media era. Everyone in the industry noticed the conspicuous success of the Body For Life challenge back then, and that definitely planted the seeds as inspiration for our future Burn the Fat Challenge. Originally, however, our first body transformation contest was born by accident.

In November of 2008 I wrote a motivational call to action type of article that urged my readers to get in better shape over the thanksgiving and Christmas holidays rather than let themselves go, and to start right away, not procrastinate until the new year. That article produced a huge response but then everyone went on their merry way. Then in January, having almost forgotten about the challenge I laid down 7 weeks earlier, I was again deluged with messages like this one: “Hey Tom, I accepted your holiday fitness challenge and I just wanted to say thank you for the motivation. This was the first time ever I actually lost fat over the holidays… I even ate cookies and pie without guilt this year – I was just careful to keep it in moderation and fit it into my calorie budget like you told me to. Thanks again.” Some people even sent me their progress pictures.

That’s when I knew we were on to something. So the following year, we formalized it, created a competition structure and announced our first Burn the Fat Holiday challenge. We offered great prizes, including a trip for two to Maui for the male and female winners. Each contestant took progress photos, set goals, tracked their weight and body composition, recorded progress in a journal every week and wrote an essay at the end. Doing it in an online forum with thousands of members turned out to be fantastic for accountability and community support.

Critics said we were crazy to run a transformation contest at that time of year, but it was a hit. More than 1000 people entered. It

was 49 days (7 weeks) simply because that was the length of time from thanksgiving week into the new year. In the summer, we launched a second event because so many people said they needed the motivation again. We made it 98 days assuming that

twice the

(surprisingly that was not always the case). More than 2000 people entered that event. We’ve been sponsoring the challenges with steady participation ever since and have started new performance-based fitness challenges as well.

time would allow twice the transformation

Performance-based fitness challenges as well? That's a great idea. Do you run these alongside the regular body comp transformations? I'd love to hear some memorable examples of both a) the physical transformations, and b) the performance transformations. What makes these particular cases stand out to you?

Today we run performance-based challenges alongside the before and after photo / body comp transformation contests to appeal to people with different motivations. We discovered from earlier events that some people won’t post “half-naked” pictures online no matter how big the incentives are. We also found that even though we judged our contests based on personal improvement and not the absolute best physique, some people got demotivated if they felt like they never had a chance to win. Photos-optional fitness performance challenges got those people involved.

We’ve done the usual thing you see on a lot of “gamified” sites, like push ups, pull ups, plank time, deadlifts and other workout challenges, but the real success for us was the “fitness habits challenge.” We made a list of what actions and behavior changes would create lasting success if they became habits. We kept score and awarded points every day for things like writing goals, posting nutrition in a journal, tracking the training sessions and reporting results every week for accountability.

Then we started events like our Mt Everest Challenge which requires 2903 floors to the “summit” and our 1 million step challenge, which involves taking just over 10,000 steps in 98 days, as tracked with a pedometer. We used a leaderboard and have a group at Fitbit as well. The combination of an attainable goal, prizes, accountability and friendly competition made this a huge success and we got thousands of people off the couch. We had three people do over 3 million steps and none were endurance athletes. One of them, Marc Chabot, age 55, dropped 52 pounds in 98 days. These contests made me a big fan of gadgets or apps that make you accountable for your activity, training and nutrition.

For the before and after transformations, we have hundreds of case studies from every age group and background. Two types stand out the most. First, the success stories from “real people” who have either overcome serious adversities like injury or just ordinary life challenges like being busy that most people use as excuses. Cynthia Cardenas for example, won one of our 49-day events while being a stay at home mom of 5 kids all under the age of 8, including homeschooling 2 of them. Because dropout rates are so high for all kinds of diets as well as fitness contests, the second group that really stands out is the long-term “maintainers,” not just the “big losers” at the end of each contest. Brian Nordberg is like the poster man for this. He dropped 122 lbs, kept it off more than 4 years and since gained

122 lbs, kept it off more than 4 years and since gained Ala n Aragon’s Research
122 lbs, kept it off more than 4 years and since gained Ala n Aragon’s Research

over 20 pounds of muscle. He’s now a participant in the National Weight Control Registry. You can see both of them at Burn the Fat Blog or on the back cover of my book.

Fascinating & impressive cases, Tom. Are there key qualities (work ethic, approach, habits, etc) you find as common threads among folks who are able to successfully transform? Or, are there really no consistently common threads at all among the long-term success stories (I'm not discounting that possibility).

I’ve seen people with big differences in dietary approaches – food choices (vegetarian or carnivore), meal schedules (three meals or six meals), macronutrients (high-carb, low-carb and everywhere in between) and so on all become equally successful, as long as they adhered to the big picture principles, such as maintain a calorie deficit for fat loss, get optimal protein levels and so on. But there are definitely common threads among all the success stories.

First, absolutely, work ethic is high on the list. I’ve never heard a transformation contest finalist or winner say, “That was easy.” More often, I’ve heard the polar opposite: “I worked harder than I ever have in my life for this event.”

Second is using mental training strategies: visualization or mental rehearsal, self-image modification, goal setting, relaxation or meditation, affirmations or motivational scripting, self-talk, working on belief systems, and so on. Some type of conscious work on mindset is always there.

Third is doing nutrition by the numbers. Not everyone tracks calories and macronutrients, especially long-term, so I wouldn’t say this is mandatory, but it correlates highly with success. In our contests, I’d estimate at least 90% of the top finishers and winners logged nutrition with spreadsheets, software or apps.

Fourth is accountability through tracking and self-monitoring. It’s like the classic business management and sports coaching maxims: “what gets measured gets improved” and “if you don’t measure it, you can’t manage it.” In the best transformations we see people consistently tracking actions and performance, including training and nutrition journals. They also track outcomes such as weight, body composition, measurements and progress photos. Collecting progress data weekly also provides a feedback loop system to help with course corrections.

Fifth is a social support system, which in our case, is built into the challenge because we host our contest in an online forum with thousands of members. We usually also see a strong personal support system from friends or family, but in the cases where someone doesn’t get the kind of support they need from their immediate social circle, they always say their online support system made all the difference

diet, high physical activity, supportive environment, good coping mechanisms (for handling stress, etc), self monitoring progress, journaling food and training, less sedentary leisure time, consistent eating patterns and more home cooking/less eating at restaurants.

If someone is following these guidelines, you’d think they’d be a sure thing for making it into the long-term maintainer group. But it’s not always that easy to predict who sticks with it and who relapses. Knowing about these strategies and doing them are two different things. Long-term weight control is a huge challenge for a lot of people and it’s always complicated with a lot of distractions, obstacles or bumps in the road. The phrase I hear a lot is, “Life got in the way.” The real question is what makes people follow through with these maintenance behaviors without getting derailed.

I believe one reason is that maintainers expect problems and accept adversity as part of the process and have mental and physical strategies to get through it and forge onward. In a word, they’re resilient. The maintainers get knocked down and get back up quickly, over and over again. The relapsers get knocked down and stay down. The difference is in the way each person thinks about and explains adversity. I could go on and on about this, but to keep this brief, I’d highly recommend looking up Martin Seligman’s work in positive psychology on learned helplessness and explanatory style if you want to learn more. I think he nailed it.

Another difference between the maintainers and the relapsers is in whether the motivation is purely extrinsic and temporary or it’s also intrinsic and long-term. Purely external rewards like a trip to Hawaii can be incredible short-term motivators. I’ve heard people say they worked harder, specifically hoping to win that vacation, than they’ve ever worked for anything in their lives and they did it – they won. Unfortunately, I’ve seen some of those overall winners regain the fat they lost afterwards, because when the contest and vacation were over, they had nothing else to keep them going. Short-term win, long-term fail.

On the other hand, we’ve seen people enter our contest, and agree that a trip to Hawaii would be amazing, but they said their biggest motivator was getting healthy for their family. After a recent checkup, their doctor said, “You’re not going to live long enough to see your kids (or grandkids) grow up if you don’t change your ways.” That was the turning point. Staying healthy for family isn’t a short-term goal with an end date – it’s an intrinsic and long-term motivation a value – and that’s what keeps them going.

Final question: Any interesting motivational lessons you've learned from these long-term success cases? Can you speak about the unpredictability of which people (even contest winners) relapse and which make their transformations last?

winners) relapse and which make their transformations last? Tom Venuto is a natural bodybuilder and the

Tom Venuto is a natural bodybuilder and the author of Burn the Fat, Feed the Muscle. Tom received his degree in exercise science and has been involved in the fitness industry since 1989, including 15 years as a personal trainer before he became a full-time writer, publisher and online coach. You can visit Tom at www.BurnTheFatBlog.com

Most of our contest winners who’ve also kept the fat off long- term are succeeding by using the same best practices you’d see in the research on long-term maintainers, like what comes out of the National Weight Control Registry studies; calorie controlled

or learn more about the new

2014

hardcover edition of

his

book

at

Here is an interesting VICE episode (20:38) documenting a strongman training facility in Iceland. If

Here is an interesting VICE episode (20:38) documenting a strongman training facility in Iceland.

documenting a strongman training facility in Iceland. If you have any questions, comments, suggestions, bones of

If you have any questions, comments, suggestions, bones of contention, cheers, jeers, guest articles you’d like to submit, or any feedback at all, send it over to aarrsupport@gmail.com.

feedback at all, send it over to aarrsupport@gmail.com . Ala n Aragon’s Research Review – February/March
feedback at all, send it over to aarrsupport@gmail.com . Ala n Aragon’s Research Review – February/March