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Preliminary Studies

Elizabeth A. Young, MD; Stanley J. Watson, MD, PhD; Joan Kotun, MD; Roger F. Haskett, MD; Leon Grunhaus, MD; Virginia Murphy-Weinberg, RN; Wylie Vale, PhD; Jean Rivier, PhD; Huda Akil, PhD

Arch Gen Psychiatry. 1990;47(5):449-457.

Abstract
• Studies in depression using a maximal stimulatory dose of corticotropin releasing factor have concluded that elevated resting cortisol levels in depressed patients exert a negative feedback effect on the corticotroph, resulting in a decreased corticotropin response. In this preliminary report, we examine the effects of a submaximal dose of corticotropin releasing factor on the release of another corticotroph secretory product, β-lipotropin—β-endorphin. We observed a decreased β-lipotropin—β-endorphin response in depressed subjects, but a normal adrenal cortisol response. Although the total β-lirotropin—β-endorphin response was decreased, the initial secretory response did not differ between patients and normal controls. Rather, the patients appeared to turn off secretion faster. This rapid shutoff was seen in all patients regardless of resting cortisol levels, suggesting that resting cortisol levels alone do not explain the decreased response seen in depressed patients.

Author Affiliations
From the Mental Health Research Institute, Department of Psychiatry, University of Michigan, Ann Arbor (Drs Young, Watson, Kotun, Haskett, Grunhaus, and Akil and Ms Murphy-Weinberg); and the Clayton Foundation, Laboratories for Peptide Biology, the Salk Institute, La Jolla, Calif (Drs Vale and Rivier).

Footnotes
Accepted for publication August 16, 1989.

Read in part before the 41st Annual Society of Biological Psychiatry Meeting, Washington, DC, May 9, 1986.

Reprint requests to Mental Health Research Institute, University of Michigan, 205 Washtenaw Pl, Ann Arbor, MI 48109-0720 (Dr Young).

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