Adrenocorticotropin-Stimulated Adrenal Androgen Secretion in Anorexia Nervosa: Impaired Secretion at Low Weight with Normalization after Long-Term Weight Recovery

Abstract

Adrenal androgen secretion is decreased in patients with anorexia nervosa. To assess the reversibility of the decreased secretion with recovery of body weight, we measured ACTH-stimulated adrenal androgen levels at different stages of recovery. Basal plasma GH and somatomedin-C levels also were measured, because both have been proposed as potential stimuli for adrenal androgen secretion. When studied at low body weight [58 +/- 3% (+/- SEM) ideal BW], women with anorexia nervosa had decreased ACTH-stimulated levels of dehydroepiandrosterone (DHA), DHA sulfate (DHAS), and androstenedione and decreased DHA to cortisol, DHAS to cortisol, and androstenedione to cortisol ratios compared to normal women. Women who had recently completed a refeeding program (within 2-4 weeks, 81 +/- 2% ideal BW) had an increased somatomedin-C level compared to low weight patients, but similar ACTH-stimulated adrenal androgen levels. Long term weight-recovered women (86 +/- 4% ideal BW, recovery for more than 6 months, with resumption of menses), however, had significant increases in ACTH-stimulated DHA and DHAS levels and DHA to cortisol and DHAS to cortisol ratios, and their hormone levels and ratios were not different from those in normal women. GH levels fell during weight recovery, although the values in the three patient groups did not differ significantly. We conclude that the recovery of adrenal androgen secretion while GH levels were falling provides evidence against a direct effect of GH as a stimulus for adrenal androgen secretion. The recovery of somatomedin-C before the recovery of adrenal androgens, however, and the positive correlation between plasma somatomedin-C and the integrated level of plasma DHAS (r = 0.50; P less than 0.02) are consistent with the hypothesis that somatomedin-C is a stimulus for adrenal androgen secretion.

Clinical and Biochemical Determinants of Bone Metabolism and Bone Mass in Adolescent Female Patients with Anorexia Nervosa

“…This contrasts with other studies in which patients presented high GH secretion (25), high IGFBP-1, and low IGFBP-3 accompanying low IGF-I (26), although in the study of Argente et al (27), IGF-I, IGFBP-3, and GHBP low levels did not correlate with the GH secretory status, which could be independently increased or decreased. Other studies have also shown high cortisol secretion (28 -30) and low DHEA-S response to ACTH stimulation (31), and in accordance with the clinical characteristics previously mentioned, our patients presented normal urinary cortisol excretion and normal serum DHEA-S.…”

Androgens in Women with Anorexia Nervosa and Normal-Weight Women with Hypothalamic Amenorrhea

“…Interventional studies would be necessary to investigate this possible mechanism further. Previous reports in small numbers of women have shown variably low (11)(12)(13)(14)(15)(16)(17)(18), normal (6 -10), or elevated (15,23) androgens or DHEAS levels in women with anorexia nervosa. Some of these studies compared androgen or preandrogen levels with published normal ranges, instead of with those of recruited healthy control groups.…”

Brain tissue volume segmentation in patients with anorexia nervosa before and after weight normalization

“…Several studies have shown that IGF-1 levels are reduced in patients with protein caloric malnutrition (Grant, Hambley, Becker, & Pimstone, 1973;Hintz, Suskind, Amatayakul, Thanangkul, & Olson, 1978;Smith et al, 1981;Soliman et al, 1986). Others have found that IGF-1 levels are reduced in patients with anorexia nervosa (Counts, Gwirtsman, Carlsson, Lesem, & Cutler, 1992;Golden et al, 1994;Grinspoon, Baum, et al, 1996;Grinspoon, Gulick, et al, 1996;Hall, Lundin, & Pó voa, 1988;Hill, Hill, McClain, Humphries, & McClain, 1993;Hochberg et al, 1992;Rappaport, Prevot, & Czernichow, 1980;Tanaka, Maesaka, & Suwa, 1985;Winterer et al, 1985). As in anorexic patients, CT and MRI studies of patients with protein caloric malnutrition have demonstrated reduced brain tissue volumes, which are reversible following nutritional normalization (Gunston, Burkimsher, Malan, & Sive, 1992;Househam, 1991;Househam & De Villiers, 1987).…”