Binge-Eating Disorder: Prevalence, Predictors, and Management in the Primary Care Setting

Genetic risk factors appear to play a strong role in the development of BED. Risk for BED tends to aggregate in families independently of the risk for obesity, although the presence of BED in a first-degree relative does increase risk for obesity [97]. Heritability estimates for BED range from 45% to 57% [98,99], which is greater than the heritability estimate for subthreshold binge eating (ie, overeating with a sense of loss of control, 41%) [100]. In addition, symptom-level analyses support moderate genetic contributions for each BED symptom [98], supporting the integrity of the diagnostic criteria. Finally, shared environment appears to play a very small role in the familial transmission of BED, and the contribution of unique environmental factors in development of BED appears to be substantial [97,101].

With regard to the neurobiological underpinnings of BED, it appears that BED may be associated with hypersensitivity to reward, a phenomenon that is strongly associated with the striatum and dopaminergic mechanisms [102,103]. In support of this hypothesis, Davis et al [102] reported that BED was differentially related to genotypes that reflect a greater density of D2 receptors and higher D2 binding potential as compared to obese controls. Additionally, greater increases in striatal DA and unique activation patterns in the right ventral striatum have been demonstrated in individuals with BED as compared to obese non-BED controls in response to food-related stimuli [103,104]. Other findings have implicated the orbitofrontal cortex (OFC) in BED, which is another brain region responsible for reward processing, particularly as it relates to the hedonic value of food stimuli [103]. Increased volume of grey matter has been documented in individuals with BED and bulimia as compared to normal weight controls, and stronger medial OFC activation while viewing pictures of food was observed in individuals with BED as compared to individuals with bulimia, overweight controls, and normal controls [105].

Difficulties with affect regulation have also been implicated in the development of BED. Two theories that implicate a primary and specific role for affect regulation in BED are cited most frequently in the extant literature: the affect regulation theory and the escape theory. The affect regulation theory [106] posits that BE is a conditioned response to negative affect which is correspondingly negatively reinforced by reductions in negative affect, which could occur during or after BE. Escape theory [107] posits that aversive self-awareness causes negative affect, which in turn triggers BE. BE is then negatively reinforced by reductions in negative affect during a binge via an escape from self-awareness that is accomplished through cognitive narrowing to the immediate stimulus environment. In contrast to the affect regulation theory, escape theory predicts that negative affect will increase after BE when self-awareness is restored. Results regarding changes in affect during BE episodes are conflicting as to whether BE is associated with decreases, no change [108–110], or even increases in negative affect. In particular, a meta-analytic review of 36 studies that examined affect via ecological momentary sampling found moderate increases in negative affect following binge episodes [111]. To some degree, results of this meta-analysis may not generalize to BED, per se, given that it included other binge eating groups, such as those with bulimia nervosa. However, in general, studies suggest that negative affect is an antecedent for BE and increased negative affect may be a consequence of BE, at least among women. More information is needed regarding aversive self-awareness before and after BE, cognitive narrowing, and changes in affect during BE. As such, the current state of the literature provides only partial support for affect regulation models of BED in women. Furthermore, it remains unknown if these results will generalize to men.