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.