Binge eating is a recalcitrant symptom of bulimia nervosa, binge-eating disorder (BED), and the binge/purge subtype of anorexia nervosa. Binge eating is rooted in gene-environment interactions, but the biology of these interactions is largely unknown. This chapter describes a simple and reliable animal model of binge eating that is based on such an interaction: a significant inherent difference in eating patterns when palatable food (PF) is encountered in the environment. Roughly one-third of rats exhibit a binge-like pattern of intake of PF despite normal intake when only chow is available. The PF intake of these binge-eating prone (BEP) rats is significantly and consistently greater than that of binge-eating-resistant (BER) rats. Also described are subsequent experimental manipulations that reveal additional parallels between BEP rats and human binge-eating behavior, including preference for and abnormal intake of PF when stressed, binge eating in the absence of hunger and despite evidence of satiety, motivation to obtain and eat PF despite punishing consequences, and age of onset shortly after puberty. The model also dissociates binge eating from obesity proneness such that four subgroups can be obtained that resemble bulimia nervosa (binge eating with compensatory restriction to prevent obesity), BED (binge eating with propensity for obesity), frank obesity (obesity proneness without binge eating), and healthy controls (non-binge-eating, obese-resistant rats). These behavioral profiles render the BEP/BER model a useful tool to uncover some of the genetic and epigenetic substrates distinguishing BEDs. It can also be used to develop and test more targeted treatments against these life-threatening conditions. © 2013 Springer Science+Business Media, LLC.