This paper offers a new model for bulimia nervosa (BN) that explains both the initial impulsive nature of binge eating and purging as well as the compulsive quality of the fully developed disorder. The model is based on a review of advances in research on BN and advances in relevant basic psychological science. It integrates transdiagnostic personality risk, eating disorder specific risk, reinforcement theory, cognitive neuroscience, and theory drawn from the drug addiction literature. We identify both a state-based and a trait-based risk pathway, and we then propose possible state-by-trait interaction risk processes. The state-based pathway emphasizes depletion of self-control. The trait-based pathway emphasizes transactions between the trait of negative urgency (the tendency to act rashly when distressed) and high-risk psychosocial learning. We then describe a process by which initially impulsive BN behaviors become compulsive over time, and we consider the clinical implications of our model.

The presence of binge eating behavior in early middle school predicts future diagnoses and health difficulties. The authors showed that this early binge eating behavior can, itself, be predicted by risk factors assessed in elementary school. We tested the acquired preparedness model of risk, which involves transactions among personality, psychosocial learning, and binge eating. In a sample of 1,906 children assessed in the spring of fifth grade (the last year of elementary school), the fall of sixth grade, and the spring of sixth grade, we found that fifth grade negative urgency (the personality tendency to act rashly when distressed) predicted subsequent increases in the expectancy that eating helps alleviate negative affect, which in turn predicted subsequent increases in binge eating behavior. This transactional risk process appeared to continue to occur at later time points. Negative urgency in the fall of sixth grade was predicted by fifth grade pubertal onset, binge eating behavior, and expectancies. It, in turn, predicted increases in high-risk eating expectancies by the spring of sixth grade, and thus heightened risk.

Eating disorders and obesity have become predominant in human society. Their association to modern lifestyle, encompassing calorie-rich diets, psychological stress, and comorbidity with major diseases are well documented. Unfortunately the biological basis remains elusive and the pharmacological treatment inadequate, in part due to the limited availability of valid animal models. Human research on binge eating disorder (BED) proves a strong link between stress exposure and bingeing: state-levels of stress and negative affect are linked to binge eating in individuals with BED both in laboratory settings and the natural environment. Similarly, classical animal models of BED reveal an association between acute exposure to stressors and binging but they are often associated with unchanged or decreased body weight, thus reflecting a negative energy balance, which is uncommon in humans where most commonly BED is associated with excessive or unstable body weight gain. Recent mouse models of subordination stress induce spontaneous binging and hyperphagia, altogether more closely mimicking the behavioral and metabolic features of human BED. Therefore the translational relevance of subordination stress models could facilitate the identification of the neurobiological basis of BED and obesity-associated disease and inform on the development of innovative therapies.

Purpose To examine longitudinal risk factors and short-term risk correlates for the development of extreme forms of restrictive eating among adolescent dieters. Methods Data from Project EAT, a population-based study of 2,516 students aged 12-18, were collected in 1998-1999 (Time 1) and 5 years later (Time 2). Within this sample, 243 adolescents who reported dieting but not engaging in disordered forms of restrictive eating (e.g., fasting, skipping meals) at Time 1 were followed to determine the self-reported psychological, familial, and social variables predicting initiation of disordered restrictive eating at Time 2. To investigate short-term risk correlates of initiating disordered restrictive eating, the same risk factors were also compared cross-sectionally at Time 2 between the dieters who had and had not initiated disordered restrictive eating. Poisson regression models with robust standard errors were fit for each predictor adjusted for covariates. Results Depressive symptoms and low self-esteem were significantly associated with the initiation of disordered restrictive eating in both longitudinal and cross-sectional analyses. Poor family communication/caring and maternal dieting significantly predicted long-term risk for escalating restrictive eating severity; whereas, individual body image issues (i.e., weight concerns, body dissatisfaction) and social concerns (i.e., weight-related teasing, peer dieting) were significant short-term correlates of initiating disordered restrictive eating. Conclusions Depressive symptoms and low self-esteem may be especially important targets for risk identification and prevention for disordered restrictive eating. Intervening upon family influences may decrease long-term risk, while intervening upon body image and responses to social influences may decrease short-term risk for disordered restrictive eating.

Objective The very early engagement in bulimic behaviors, such as binge eating, may be influenced by factors that dispose individuals to impulsive action as well as by factors that dispose individuals to depressive symptomatology. Using a longitudinal design, we conducted the first test of the simultaneous operation of both risk factors as children transition from elementary to middle school. Method In a sample of 1,906 children, we assessed risk for impulsive action (negative urgency, which is the tendency to act rashly when distressed, and eating expectancies, which are learned anticipations that eating will alleviate negative mood) and risk for depression (negative affect and depressive symptomatology) and binge eating behavior at three time points using a longitudinal design: the end of fifth grade (last year of elementary school: T0), the beginning of sixth grade (first year of middle school: T1), and the end of sixth grade (T2). Results Both the impulsive action and depression pathways predicted very early engagement in binge eating: each accounted for variance beyond the other. Mediation tests found that T1 eating expectancies mediated the predictive influence of T0 negative urgency on T2 binge eating (z = 2.45, p < .01) and that T1 depressive symptoms mediated the influence of T0 negative affect on T2 binge eating (z = 2.04, p < .05). Discussion In children, elevated levels of both negative urgency and negative affect predict early binge eating. This finding has important clinical implications because there are different interventions for the two different risk processes.