Mary M. Boggiano

Putative contributors to the secular increase in obesity: exploring the roads less traveled

Objective:To investigate plausible contributors to the obesity epidemic beyond the two most commonly suggested factors, reduced physical activity and food marketing practices.Design:A narrative review of data and published materials that provide evidence of the role of additional putative factors in contributing to the increasing prevalence of obesity.Data:Information was drawn from ecological and epidemiological studies of humans, animal studies and studies addressing physiological mechanisms, when available.Results:For at least 10 putative additional explanations for the increased prevalence of obesity over the recent decades, we found supportive (although not conclusive) evidence that in many cases is as compelling as the evidence for more commonly discussed putative explanations.Conclusion:Undue attention has been devoted to reduced physical activity and food marketing practices as postulated causes for increases in the prevalence of obesity, leading to neglect of other plausible mechanisms and well-intentioned, but potentially ill-founded proposals for reducing obesity rates.

Ten Putative Contributors to the Obesity Epidemic

The obesity epidemic is a global issue and shows no signs of abating, while the cause of this epidemic remains unclear. Marketing practices of energy-dense foods and institutionally-driven declines in physical activity are the alleged perpetrators for the epidemic, despite a lack of solid evidence to demonstrate their causal role. While both may contribute to obesity, we call attention to their unquestioned dominance in program funding and public efforts to reduce obesity, and propose several alternative putative contributors that would benefit from equal consideration and attention. Evidence for microorganisms, epigenetics, increasing maternal age, greater fecundity among people with higher adiposity, assortative mating, sleep debt, endocrine disruptors, pharmaceutical iatrogenesis, reduction in variability of ambient temperatures, and intrauterine and intergenerational effects as contributing factors to the obesity epidemic are reviewed herein. While the evidence is strong for some contributors such as pharmaceutical-induced weight gain, it is still emerging for other reviewed factors. Considering the role of such putative etiological factors of obesity may lead to comprehensive, cause specific, and effective strategies for prevention and treatment of this global epidemic.

Feeding and reward: Perspectives from three rat models of binge eating

Research has focused on understanding how overeating can affect brain reward mechanisms and subsequent behaviors, both preclinically and in clinical research settings. This work is partly driven by the need to uncover the etiology and possible treatments for the ongoing obesity epidemic. However, overeating, or non-homeostatic feeding behavior, can occur independent of obesity. Isolating the variable of overeating from the consequence of increased body weight is of great utility, as it is well known that increased body weight or obesity can impart its own deleterious effects on physiology, neural processes, and behavior. In this review, we present data from three selected animal models of normal-weight non-homeostatic feeding behavior that have been significantly influenced by Bart Hoebels 40+-yr career studying motivation, feeding, reinforcement, and the neural mechanisms that participate in the regulation of these processes. First, a model of sugar bingeing is described (Avena/Hoebel), in which animals with repeated, intermittent access to a sugar solution develop behaviors and brain changes that are similar to the effects of some drugs of abuse, serving as the first animal model of food addiction. Second, another model is described (Boggiano) in which a history of dieting and stress can perpetuate further binge eating of palatable and non-palatable food. In addition, a model (Boggiano) is described that allows animals to be classified as having a binge-prone vs. binge-resistant behavioral profile. Lastly, a limited access model is described (Corwin) in which non-food deprived rats with sporadic limited access to a high-fat food develop binge-type behaviors. These models are considered within the context of their effects on brain reward systems, including dopamine, the opioids, cholinergic systems, serotonin, and GABA. Collectively, the data derived from the use of these models clearly show that behavioral and neuronal consequences of bingeing on a palatable food, even when at a normal body weight, are different from those that result from simply consuming the palatable food in a non-binge manner. These findings may be important in understanding how overeating can influence behavior and brain chemistry.

PYY3-36 as an anti-obesity drug target.

The neuropeptide Y (NPY)/peptide YY (PYY) system has been implicated in the physiology of obesity for several decades. More recently, Batterham et al. 2002 ignited enormous interest in PYY3‐36, an endogenous Y2‐receptor agonist, as a promising anti‐obesity compound. Despite this interest, there have been remarkably few subsequent reports reproducing or extending the initial findings, while at the same time studies finding no anti‐obesity effects have surfaced. Out of 41 different rodent studies conducted (in 16 independent labs worldwide), 33 (83%) were unable to reproduce the reported effects and obtained no change or sometimes increased food intake, despite use of the same experimental conditions (i.e. adaptation protocols, routes of drug administration and doses, rodent strains, diets, drug vendors, light cycles, room temperatures). Among studies by authors in the original study, procedural caveats are reported under which positive effects may be obtained. Currently, data speak against a sustained decrease in food intake, body fat, or body weight gain following PYY3‐36 administration and make the previously suggested role of the hypothalamic melanocortin system unlikely as is the existence of PYY deficiency in human obesity. We review the studies that are in the public domain which support or challenge PYY3‐36 as a potential anti‐obesity target.

High intake of palatable food predicts binge-eating independent of susceptibility to obesity: an animal model of lean vs obese binge-eating and obesity with and without binge-eating

Objective:To determine the stability of individual differences in non-nutritive ‘junk’ palatable food (PF) intake in rats; assess the relationship of these differences to binge-eating characteristics and susceptibility to obesity; and evaluate the practicality of using these differences to model binge-eating and obesity.Design:Binge-eating prone (BEP) and resistant (BER) groups were identified. Differential responses to stress, hunger, macronutrient-varied PFs, a diet-induced obesity (DIO) regimen and daily vs intermittent access to a PF+chow diet, were assessed.Subjects:One hundred and twenty female Sprague–Dawley rats.Measurements:Reliability of intake patterns within rats; food intake and body weight after various challenges over acute (1, 2, 4 h), 24-h and 2-week periods.Results:Although BEP and BER rats did not differ in amount of chow consumed, BEPs consumed >50% more intermittent PF than BERs (P<0.001) and consistently so (α=0.86). BEPs suppressed chow but not PF intake when stressed, and ate as much when sated as when hungry. Conversely, BERs were more affected by stress and ate less PF, not chow, when stressed and were normally hyperphagic to energy deficit. BEP overeating generalized to other PFs varying in sucrose, fat and nutrition content. Half the rats in each group proved to be obesity prone after a no-choice high fat diet (DIO diet) but a continuous diet of PF+chow normalized the BEPs high drive for PF.Conclusion:Greater intermittent intake of PF predicts binge-eating independent of susceptibility to weight gain. Daily fat consumption in a nutritious source (DIO-diet; analogous to a fatty meal) promoted overeating and weight gain but limiting fat to daily non-nutritive food (PF+chow; analogous to a snack with a low fat meal), did not. The data offer an animal model of lean and obese binge-eating, and obesity with and without binge-eating that can be used to identify the unique physiology of these groups and henceforth suggest more specifically targeted treatments for binge-eating and obesity.

The Pavlovian power of palatable food: lessons for weight-loss adherence from a new rodent model of cue-induced overeating

Objective:Relapsing to overeating is a stubborn problem in obesity treatment. We tested the hypothesis that context cues surrounding palatable food (PF) intake have the power to disrupt caloric regulation even of less PF. Context cues are non-food cues that are in the environment where PF is habitually eaten.Design:Rats were conditioned to associate intake of Oreo cookies as the PF to cages with distinct context cues that differed from cues in cages where they were only given chow. PF naturally stimulated greater caloric intake. The rats were then tested in the PF cage with only chow available to determine whether the PF-paired cues, alone, could elicit overeating of plain chow.Subjects:Non-food-deprived female Sprague–Dawley rats.Measurements:Intake of plain chow under PF-paired cues vs chow-paired cues was compared. This was also measured in tests that included a morsel of PF as a priming stimulus. We also controlled for any effect of binge-prone vs binge-resistant status to predict cued-overeating.Results:Rats consumed significantly more chow when exposed to context cues paired earlier with PF than with chow (P<0.01). This effect occurred using various cues (for example, different types of bedding or wallpaper). The effect was strengthened by priming with a morsel of PF (P<0.001) and was unaffected by baseline differences in propensity to binge on PF.Conclusion:Context-cues associated with PF intake can drive overeating even of a less PF and abolish the ability of rats to compensate for the calories of a PF primer. Just as drug-associated context cues can reinstate drug-addiction relapse, PF-paired cues may trigger overeating relapses linked to weight regain and obesity. This model should help identify the reflex-like biology that sabotages attempts to adhere to healthy reduced calorie regimens and call greater attention to the cue-factor in the treatment of binge eating and obesity.

Motives for eating tasty foods associated with binge-eating. Results from a student and a weight-loss seeking population ☆

The aim of this study was to use the Palatable Eating Motives Scale (PEMS) to determine if and what motives for eating tasty foods (e.g., junk food, fast food, and desserts) are associated with binge-eating in two diverse populations. BMI and scores on the PEMS, Yale Food Addiction Scale (YFAS), and Binge-eating Scale (BES) were obtained from 247 undergraduates at the University of Alabama at Birmingham (UAB) and 249 weight-loss seeking patients at the UAB EatRight program. Regression analyses revealed that eating tasty foods to forget worries and problems and help alleviate negative feelings (i.e., the 4-item Coping motive) was associated with binge-eating independently of any variance in BES scores due to sex, age, ethnicity, BMI, other PEMS motives, and YFAS scores in both students (R² = .57) and patients (R² = .55). Coping also was associated with higher BMI in students (p < 0.01), and in patients despite their truncated BMI range (p < 0.05). Among students, the motives Conformity and Reward Enhancement were also independently associated with binge-eating. For this younger sample with a greater range of BES scores, eating for these motives, but not for Social ones, may indicate early maladaptive eating habits that could later develop into disorders characterized by binge-eating if predisposing factors are present. Thus, identifying ones tasty food motive or motives can potentially be used to thwart the development of BED and obesity, especially if the motive is Coping. Identifying ones PEMS motives should also help personalize conventional treatments for binge-eating and obesity toward improved outcomes.

Binge Eating in Rats Produced by Combining Dieting with Stress

This unit describes a rodent model of binge eating based on cyclic restriction, refeeding, footshock, and intermittent access to palatable food. These conditions mimic dieting, stress, and “junk” food indulgence, respectively, all common etiological and maintenance factors in human binge eating. Four groups of rats are used: one subjected to cyclic food restriction, another to acute footshock stress, another to both of these (R + S), and a control. Neither cyclic restriction nor stress alone produces binge eating, but the R + S rats, despite satiety, double their intake of palatable food in a discrete period of time (i.e., binge) when stressed. This protocol recapitulates critical properties of human binge eating, namely preference for palatable food, dieting‐ and stress‐induced vulnerability to binging, and eating for reward versus metabolic need. This protocol permits study of the psychobiological underpinnings of binge eating and possibly also of addiction, impulsivity, and depression, which are co‐morbid with binge eating.

Testosterone and social evaluative stress: The moderating role of basal cortisol

Research has suggested that stressful situations lead to a decrease in testosterone, whereas concern with ones social status increases testosterone. However, results from studies examining testosterone reactivity in stressful situations that involve evaluation by others (hence status concerns) are inconsistent. Furthermore, there is a lack of research examining individual differences in testosterone responses in such situations. In this study 85 male participants underwent the Trier Social Stress Test (TSST, which includes performing speech and arithmetic tasks in front of two critical evaluators) and practiced solving puzzles. Testosterone and cortisol levels were assessed from saliva. Across participants, testosterone increased from baseline to peak levels following the stressor tasks. Importantly, the increase in testosterone was larger for participants with lower basal cortisol. Hence, lower basal cortisol (which is known to be associated with low social fearfulness) may help one to mobilize a larger testosterone response in situations that involve social-evaluative stress. Given the hypothesized adaptive role of a larger testosterone response in social competition situations, the results suggest that there may be long-term benefits in learning to lower ones social fearfulness in situations involving potential for negative evaluation by others.

Body composition and endocrine status of long-term stress-induced binge-eating rats

Clinical binge eating runs a protracted course. The etiology of binge eating remains perplexing in part because, in humans, it is difficult to isolate and assess the independent and aggregate impact of various contributing variables. Using rats, we found that footshock stress and a history of caloric restriction (S+R), combine synergistically to induce binge eating. Stress and dieting are also strong antecedents and relapse factors in human eating disorders. Here we report further behavioral and physiological parallels to human binge eating. Like the protracted course of human binge eating, young female Sprague-Dawley rats continued to binge eat after 23 restriction/stress cycles (7 months) and this despite experiencing no significant weight loss during the restriction phases. Stress alone reduced adiposity by 35% (p<0.001) but S+R rats had no significant fat loss. An endocrine profile of normal plasma leptin and insulin levels but marked elevation of plasma corticosterone levels was found only in the binge-eating (S+R) rats (p<0.01), also paralleling endocrine profiles reported in clinical binge-eating studies. These behavioral and physiological similarities between this animal model and clinical binge eating increase its utility in understanding binge eating. Importantly, our findings also highlight the stubborn nature of binge eating: once a critical experience with dieting and stress is experienced, little if any further weight loss or food restriction is necessary to sustain it.