Journal of Clinical Endocrinology & Metabolism, Vol 65, 1278-1281, Copyright © 1987 by Endocrine Society

ARTICLES

Growth hormone (GH) response to GH-releasing hormone in depression

KP Lesch, G Laux, H Pfuller, A Erb and H Beckmann
Department of Psychiatry, University of Wurzburg, West Germany.

To explore the GHRH-GH-somatomedin axis integrity in major depressive disorder, 11 drug-free patients and normal subjects matched for age, sex, ovarian status, and body weight received 1 microgram/kg synthetic human GHRH-44 amide as an iv bolus dose. Compared to the normal subjects, the depressed patients had reduced mean basal serum GH levels [2.2 +/- 0.5 (+/- SE) vs. 1.1 +/- 0.2 ng/mL (micrograms/L); P less than 0.05] and a significant attenuation of the net GH response to GHRH [1346 +/- 499 vs. 217 +/- 46 ng.min/mL (micrograms.min/L); P less than 0.01]. The blunted GH responses occurred in the face of significantly increased plasma somatomedin C (Sm-C) levels [1.1 +/- 0.2 vs. 0.6 +/- 0.1 U/mL; P less than 0.05]. The magnitude of GH responses to GHRH did not differ between men and women and was not significantly correlated with age, body weight, baseline serum GH levels, or plasma Sm-C levels in either individual groups or both groups combined. The increased plasma Sm-C levels in the depressed patients could have resulted from diurnal hypersecretion of GH, and the diminished GH responses to GHRH may reflect normal Sm-C-mediated feedback at the level of the pituitary. The presumed GH hypersecretion may be due to decreased hypothalamic somatostatin release and/or hyperactivity of GHRH- containing neurons. Thus, the pathological process resulting in abnormal GH secretory patterns associated with depression may occur primarily at a suprapituitary site.