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  Vol. 58 No. 9, September 2001 TABLE OF CONTENTS
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Association of Serotonin and Cortisol Indices With Childhood Abuse in Bulimia Nervosa

Howard Steiger, PhD; Lise Gauvin, PhD; Mimi Israël, MD; Naomi Koerner, BA; N. M. K. Ng Ying Kin, PhD; Joel Paris, MD; Simon N. Young, PhD

Arch Gen Psychiatry. 2001;58:837-843.

Background  Bulimia nervosa (BN) is reported to co-occur with childhood abuse and alterations in central serotonin (5-hydroxytryptamine [5-HT]) and cortisol mechanisms. However, findings also link childhood abuse to anomalous 5-HT and cortisol function, and this motivated us to explore relationships between childhood abuse and neurobiological variations in BN.

Methods  Thirty-five bulimic and 25 nonbulimic women were assessed for childhood physical and sexual abuse, eating symptoms, and comorbid psychopathological tendencies. These women provided blood samples for measurement of platelet hydrogen-3–paroxetine binding and serial prolactin and cortisol responses following oral administration of the partial 5-HT agonist meta-chlorophenylpiperazine (m-CPP).

Results  Bulimic women showed markedly lower mean ± SD density (Bmax) of paroxetine-binding sites (631.12 ± 341.58) than did normal eaters (1213.00 ± 628.74) (t54 = -4.47; P = .001). Paroxetine binding did not vary with childhood abuse. In contrast, measures of peak change on prolactin levels after m-CPP administration ({Delta}-peak prolactin) indicated blunted response in abused bulimic women (7.26 ± 7.06), nonabused bulimic women (5.62 ± 3.95), and abused women who were normal eaters (5.73 ± 5.19) compared with nonabused women who were normal eaters (13.57 ± 9.94) (F3,51 = 3.04, P = .04). Furthermore, individuals reporting childhood abuse showed decreased plasma cortisol levels relative to nonabused women who were normal eaters.

Conclusion  Findings imply that BN and childhood abuse are both generally associated with reduced 5-HT tone but that childhood abuse may be somewhat more specifically linked to reduced cortisol levels (ie, hypothalamic-pituitary-adrenal axis) activity.


From the Eating Disorders Program, Douglas Hospital, Verdun (Drs Steiger and Israël and Ms Koerner); Department of Psychiatry, McGill University, Montreal (Drs Steiger, Israël, Ng Ying Kin, Paris, and Young); Research Centre, Douglas Hospital, Verdun (Drs Israël, Ng Ying Kin, Paris, and Young); and Department of Social and Preventive Medicine and Groupe de Recherche Interdisciplinaire en Santé (GRIS), University of Montreal, Montreal (Dr Gauvin), Quebec.

Corresponding author and reprints: Howard Steiger, PhD, Eating Disorders Program, Douglas Hospital, 6875 LaSalle Blvd, Verdun, Quebec, Canada H4H 1R3.







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