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.