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Altered response to meta‐chlorophenylpiperazine in anorexia nervosa: Support for a persistent alteration of serotonin activity after short‐term weight restoration
Author(s) -
Frank Guido K.,
Kaye Walter H.,
Weltzin Theodore E.,
Perel James,
Moss Howard,
McConaha Claire,
Pollice Christine
Publication year - 2001
Publication title -
international journal of eating disorders
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.785
H-Index - 138
eISSN - 1098-108X
pISSN - 0276-3478
DOI - 10.1002/eat.1054
Subject(s) - serotonin , medicine , anorexia nervosa , endocrinology , psychology , appetite , mood , placebo , prolactin , weight loss , eating disorders , hormone , psychiatry , receptor , obesity , alternative medicine , pathology
Objective Patients with anorexia nervosa (AN) have disturbances of appetite and behaviors, such as dysphoria, inhibition, and obsessions, that could be related to altered serotonin activity. To investigate such relationships, we administered meta‐chlorophenylpiperazine (m‐CPP), a relatively serotonin‐specific drug. Methods To avoid the confounding effects of malnutrition or weight loss, we studied 12 patients with restricting‐type AN between 5 and 17 days after a return to a normal weight and while on a stable dietary intake. We compared them to 12 healthy control women (CW). m‐CPP was administered double blind and placebo controlled. Results Although weight restored, AN women had lower body weight and increased ratings for depression and obsessionality compared with CW. After m‐CPP, AN women had an elevation in mood and a reduction in body image distortion when compared with placebo. After m‐CPP, groups had similar cortisol, adrenocorticotropin (ACTH), and growth hormone responses whereas AN women had an uncertain reduction in prolactin response. Discussion These data support other studies that suggest that altered serotonin activity persists after weight restoration in AN patients. The finding that m‐CPP temporarily improved mood and reduced body image distortions supports the hypothesis that altered serotonin activity may contribute to the pathophysiology of AN. © 2001 by John Wiley & Sons, Inc. Int J Eat Disord 30: 57–68, 2001.