The clinical phenotype of bulimia nervosa patients is more complex. The bingeing and purging behaviors of these patients are suggestive of problems with impulse control and satiety regulation. A series of systematic studies with structured interviews (4–6) showed that about one-fourth to one-third of bulimia nervosa patients met the threshold criteria for a cluster B (impulsive) personality disorder. For example, the study by Braun et al. (6) showed that 26% of bulimia nervosa patients had a cluster B personality disorder diagnosis and 19% had a diagnosis of borderline personality disorder. These findings seem to confirm the phenotype of bulimia nervosa as an impulsive disorder. Neuroendocrine studies added further confirmation. Low levels of CSF 5-hydroxyindoleacetic acid (5-HIAA) with impulsive, suicidal, and aggressive behavior have been demonstrated by Asberg et al. (7) and Brown et al. (8). Animal studies have shown that impaired serotonergic function leads to overeating and obesity (9). Several studies have indicated deficient serotonergic function in bulimic patients. Jimerson et al. (10) showed that patients with more severe binge eating have lower CSF 5-HIAA levels than do control subjects. Brewerton et al. (11) demonstrated that bulimic patients have a blunted prolactin response to m-chlorophenylpiperazine (m-CPP), and McBride et al. (12) showed that these patients have a reduced prolactin response to the serotonin agonist fenfluramine. Unfortunately, the clinical phenotype in bulimia nervosa is more complex.