Aktuelle Ernährungsmedizin 2007; 32 - F2_4
DOI: 10.1055/s-2007-983370

Cortisol as a mediator of central fat accumulation in anorectic patients during weight gain

V Haas 1, 2, 3, M Kohn 2, MJ Müller 3, S Clarke 4, S Madden 5, H Lochs 1, K Gaskin 6
  • 1Med. Klinik m. Schw. Gastroenterologie, Hepatologie und Endokrinologie, Universitätsklinikum Charité, Berlin, Germany
  • 2The Departments of Adolescent Medicine
  • 5Psychological Medicine, and
  • 6The James Fairfax Institute of Paediatric Nutrition, The Children's Hospital at Westmead, Sydney, Australia
  • 3Institut für Humanernährung und Lebensmittelkunde der Christian-Albrechts-Universität zu Kiel, Germany
  • 4The Centre of Research into Adolescent's Health, Westmead Hospital, Sydney, Australia

Introduction: Preferential accretion of body fat (BF) after a period of starvation also termed has already been described in humans in the classic Minnesota starvation study in 1950 (1). In convalescent patients with Anorexia Nervosa (AN), weight gain resulted in an accumulation of trunk fat (2), yet the role of steroid hormones on fat redistribution during weight gain in AN has not been investigated.

Subjects and Methods: BMI, total and regional fat, waist circumference and plasma levels of cortisol (cort), estradiol (E2), testosterone (T), leptin and adiponcetin (ApN) were assessed in 81 adolescent AN (15.0±1.6y) before ('T0'), and in 15 of these also after 7 months of therapeutically induced weight gain ('T1'). Data was compared to a healthy and normal weight sex- and age-matched control group (C, n=29).

Results: At T0, BMI (16.3±1.6 vs. 20.0±2,2kg/m2) total BF (6.6±3.1 vs. 14.6±5.2kg) and waist (59.6±4.3 vs. 65.6±6.0cm) were significantly reduced in AN when compared to C. In AN, cort was significantly higher (374±109 vs. 173±59 nmol/L), E2 significantly lower (86±36 vs. 119±43pmol/L), and T was unchanged (1.8±0.9 vs. 1.9±0.7 nmol/L). After weight gain (+5.4±3.0kg), there was evidence of central fat accumulation in AN: trunk fat increased from 39 to 43% of total fat (p=0.003), whereas extremity fat decreased, albeit not significantly, from 54 to 52%. At T1, cort remained elevated in AN (317±107 nmol/L), but E2 and T were within the normal range (129±133pmol/L and 1.8±0.7 nmol/L, respectively). Increases in trunk fat showed a positive association with baseline cort and with the failure to decrease cort with weight gain, as well as with changes in T (p<0.05). Increases in waist were positively associated with baseline cort (p<0.05), and negatively but weakly with baseline E2 (p=0.08).

Conclusions: Nutritional recovery at the presence of hypercortisolemia might lead to central fat accumulation in AN patients. The metabolic consequences of this change in fat distribution pattern remain unclear.

References: (1) Keys A, et al.: The Biology of Human Starvation. Minneapolis: University of Minnesota Press, 1950:303–64. (2) Mayer L et al.: Body fat redistribution after weight gain in women with anorexia nervosa. Am J Clin Nutr 2005;81:1286–91.