Brain serotonin activity contributes to satiety. Theoretically, binging behavior is consistent with reduced serotonin function, whereas anorexia nervosa is consistent with increased serotonin activity. Brain serotonin abnormalities could also contribute to psychopathologic behaviors such as dysphoric mood, disturbance of impulse control, and obsessionality, as well as neuroendocrine disturbances. In fact, disturbances of serotonin have been found in acutely ill anorexia nervosa patients. Tryptophan, an essential amino acid found in the diet, is the precursor of serotonin. Thus serotonin disturbances could be secondary to dietary abnormalities. However, disturbances of serotonin activity appear to persist after long-term weight recovery from anorexia nervosa. While speculative, it is possible that increased serotonin activity could contribute to the pathogenesis of restricted eating and obsessional behaviors in this illness. Physiologic and pharmacologic evidence suggest that patients with normal weight bulimia have reduced serotonin activity when acutely ill. Such disturbances, even if secondary to dietary abnormalities, may still contribute to dysphoric mood and binging behavior.