Clonidine stimulation in anorexia nervosa: Growth hormone, cortisol, and beta-endorphin responses

Abstract

Clinical and biochemical findings link anorexia nervosa (AN) and primary affective disorders (PAD). Clonidine, an α 2-adrenoceptor agonist, has been shown to blunt growth hormone (GH) response and greatly lower plasma cortisol in PAD patients. We examined the GH, cortisol, and β-endorphin (β-EP) responses to an acute clonidine challenge (150 μg i.v. as a bolus) before and after 30 days of treatment with desmethylimipramine in 14 women with AN. Both before and after treatment, the AN patients showed normal plasma GH and cortisol responses, but an increased plasma β-EP response. The increased β-EP response in AN was independent of weight and depressive symptomatology. Our data indicate that α 2-adrenoceptors involved in the control of GH and adrenocorticotropic hormone are not altered in AN. The increased β-EP response may indicate elevated opioid activity in the hypothalamo-pituitary system of AN patients.