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June 1997

Decreased Serotonin Function in Bulimia Nervosa

Author Affiliations

From the Department of Psychiatry, Beth Israel Deaconess Medical Center and Harvard Medical School (Drs Jimerson, Wolfe, Metzger, and Levine), and the Department of Biostatistics, Harvard School of Public Health (Dr Finkelstein), Boston, Mass; and the Nathan Kline Institute for Psychiatric Research, Orangeburg, and the New York State Psychiatric Institute, College of Physicians & Surgeons, Columbia University, New York (Mr Cooper). Dr Levine is now with the Department of Psychiatry, St Mary's Hospital, Waterbury, and Yale University School of Medicine, New Haven, Conn.

Arch Gen Psychiatry. 1997;54(6):529-534. doi:10.1001/archpsyc.1997.01830180043005

Background:  Evidence that serotonin-active antidepressant medications decrease binge eating in patients with bulimia nervosa has fueled interest in the hypothesis that abnormal serotonergic neurotransmitter function contributes to symptoms of the disorder. To evaluate this hypothesis, we employed pharmacological challenge testing to compare serotonin function in patients with bulimia nervosa and healthy controls.

Methods:  Neuroendocrine response patterns were compared for 15 nonhospitalized, medication-free, normal-weight women with bulimia nervosa and 14 age-matched healthy female controls. Behavioral assessment included ratings of eating disorder symptoms, depression, and anxiety. Serotonergic response patterns were assessed by measuring the increase in serum prolactin concentration during 5 hours following single- dose, oral administration of 60 mg of d, l-fenfluramine hydrochloride (Pondimin).

Results:  For patients with bulimia nervosa, the fenfluramine-stimulated increase in serum prolactin concentration was significantly less than for controls. Within the patient group, the frequency of binge eating episodes during the 4 weeks prior to the study exhibited a significant inverse correlation with serotoninstimulated prolactin secretion.

Conclusion:  Our study provides new evidence that impaired central nervous system serotonergic responsiveness may contribute to the onset or maintenance of abnormal eating patterns in patients with bulimia nervosa.

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