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Article
January 1989

Central and Peripheral ACTH and Cortisol Levels in Anorexia Nervosa and Bulimia

Author Affiliations

From the Department of Psychiatry, UCLA School of Medicine, Los Angeles (Dr Gwirtsman); Western Psychiatric Institute, Pittsburgh (Dr Kaye); National Institute of Alcohol and Alcohol Abuse (Dr George), and Biological Psychiatry Branch (Dr Gold), National Institute of Mental Health, Bethesda, Md; the Department of Psychiatry, Beth Israel Hospital, Boston (Dr Jimerson); and the Department of Psychiatry, Vanderbilt School of Medicine, Nashville, Tenn (Dr Ebert).

Arch Gen Psychiatry. 1989;46(1):61-69. doi:10.1001/archpsyc.1989.01810010063009
Abstract

• To explore the relationship of central and peripheral adrenocorticotropic hormone (ACTH, or corticotropin) levels to hypothalamo-pituitary-adrenal axis dysfunction in patients with eating disorders, levels of cerebrospinal fluid (CSF) and plasma ACTH, cortisol, and 24-hour urinary free cortisol were measured in 16 patients with anorexia nervosa (60% ±1.1% of ideal body weight), 14 patients with bulimia (93.2% ±4.6% of ideal body weight), and 11 healthy age-matched women volunteers. The CSF, plasma, and urinary free cortisol levels were elevated in underweight anorexic patients and showed declines following weight recovery. Cortisol-binding globulin levels were similar in anorexics and controls. In contrast, underweight anorexics showed low CSF ACTH levels that returned to normal following weight recovery, and their plasma ACTH levels were normal. On hospital admission, bulimic patients demonstrated normal ACTH and cortisol levels. After their abstinence from binge-purge episodes, the CSF ACTH levels decreased significantly. Positive relationships were found among CSF, plasma, and urinary cortisol levels, and inverse relationships were seen between cortisol measures and CSF ACTH levels in patients with eating disorders. Secretion of ACTH into the CSF may respond to feedback by cortisol or, alternatively, may be suppressed by the hypersecretion of corticotropin-releasing hormone, leading to the depletion of the pro-opiomelanocortin molecule.

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