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

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.

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 Hoebel’s 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 phenotype. 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.

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 þ 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 450% more intermittent PF than BERs (Po0.001) and consistently so (a ¼ 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 þ 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 þ 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.

Objective-Binge-eating involves an abnormal motivation for highly palatable food in that these foods are repeatedly consumed despite their binge-triggering effects and life-affecting consequences associated with binge-eating. We determined if rats identified as binge-eating prone (BEP) similarly display abnormal motivation for palatable food.Method-Food-sated BEP and binge-eating resistant (BER) rats were given voluntary access to palatable food paired with increasing intensity of footshock. Later, they were exposed to a period of cyclic caloric restriction-refeeding.Results-BEPs consumed significantly more and tolerated higher levels of footshock for palatable food than BERs. Cyclic restriction-refeeding increased BERs' tolerance of shock for palatable food.Discussion-Previously observed parallels of the rat BEP model to human binge-eating can now be extended to include an abnormal motivation for palatable food. This model should prove useful in identifying specific genes that interact with the nutritional environment to mediate bingeeating and may point to novel physiological targets to treat compulsive overeating. KeywordsBED; obesity; rats; motivation; footshock; compulsive overeating; compulsivity; emotional eating; caloric restriction; dieting; bulimia Binge-eating is characterized by the compulsion to seek out and consume large quantities of food in a discrete time period (1). While the macronutrient composition of binges is often similar to normal meals (2), it is highly palatable food that is greatly craved and preferred during binges. These are foods that are typically high in sucrose and fat and, because they are calorie-dense, are commonly "forbidden" between binges (3-7). The motivation to repeatedly seek out and consume palatable food can be construed as abnormal given the many consequences that result from ingesting these foods. For example, palatable foods are known to trigger binges (7,8), and they contribute to weight gain and ensuing preoccupation with weight gain (7)(8). Binges lead to worsening body image, low self-esteem, mood disturbances, increased perceived life stress, and adverse medical consequences (9-13). Repeatedly returning to intake of palatable foods with full knowledge that a binge, along with worsening of binge-eating symptoms and consequences, is likely to follow cannot be regarded as adaptive.Animal models are valuable in that they aid in identifying the physiological underpinnings of complex human behaviors, of which binge-eating is certainly an example. The validity of an animal model of binge-eating is in part contingent on the number of clinical features it reproduces. One feature not previously investigated in these models is the compulsive nature of eating palatable food despite aversive consequences. Consuming significantly more palatable food can imply an increased motivation for that food. However, tolerating punishment for it is stronger evidence of abnormal motivation for palatable foods. Therefore, the main goal of this study was to ascertain whether bing...