Clinical evidence suggests that initial attempts to regulate weight gain quickly become habit-like in individuals with eating disorders. These behaviors are controlled excessively in patients with Anorexia Nervosa (AN) and are controlled more intermittently, with periods of lost control, in patients with Bulimia Nervosa (BN). We suspect that abnormalities in frontostriatal systems that subserve self-regulatory control and habit learning may contribute to the development and perpetuation of AN and BN. We summarize previous findings and present a pathophysiological model that provides a framework for understanding the shared and non-shared clinical phenotypes of AN and BN. Whereas dysregulated control systems produce heightened self-regulatory control, permitting individuals with AN to sustain excessive dietary restriction, dysregulated control systems likely result in impaired self-regulatory control in patients with BN, releasing feelings of hunger and urges to binge, thereby resulting in overeating. Interactions with cultural ideals of thinness and impaired habit learning systems may then allow the dieting behaviors of individuals with restricting-type AN to spiral into the habitual and restrictive eating behaviors that typify the disorder. Although these cultural factors likely contribute to the compensatory purging behaviors in BN, interactions with normal habit learning systems may explain the higher recovery rate of BN relative to AN, in which habit learning may be impaired. We describe neuroimaging methods that we are using to test these hypotheses and emphasize the potential utility of studying AN and BN early in the course of illness, to disentangle their causes from epiphenomena or compensatory responses. We believe that this innovative approach to studying eating disorders will lend explanation to the perplexing fact that although many young people diet and overeat at some point in time, only some go on to develop eating disorders.