A review of endocrine changes in anorexia nervosa

RK Støving, J Hangaard, M Hansen-Nord… - Journal of psychiatric …, 1999 - Elsevier
RK Støving, J Hangaard, M Hansen-Nord, C Hagen
Journal of psychiatric research, 1999Elsevier
Anorexia nervosa is a syndrome of unknown etiology. It is associated with multiple
endocrine abnormalities. Hypothalamic monoamines (especially serotonin), neuropeptides
(especially neuropeptide Y and cholecystokinin) and leptin are involved in the regulation of
human appetite, and in several ways they are changed in anorexia nervosa. However, it
remains to be clarified whether the altered appetite regulation is secondary or etiologic.
Increased secretion of corticotropin-releasing hormone and proopiomelanocortin seems to …
Anorexia nervosa is a syndrome of unknown etiology. It is associated with multiple endocrine abnormalities. Hypothalamic monoamines (especially serotonin), neuropeptides (especially neuropeptide Y and cholecystokinin) and leptin are involved in the regulation of human appetite, and in several ways they are changed in anorexia nervosa. However, it remains to be clarified whether the altered appetite regulation is secondary or etiologic. Increased secretion of corticotropin-releasing hormone and proopiomelanocortin seems to be secondary to starvation, however, there is evidence that it may maintain and intensify anorexia, excessive physical activity and amenorrhea. Hypothalamic amenorrhea, which is a diagnostic criterion in anorexia nervosa, is not solely related to the low body weight and exercise. Growth hormone resistance with low production of insulin-like growth factor I and high growth hormone secretion reflect the nutritional deprivation. The nutritional therapy of patients with anorexia nervosa might be improved by administering an anabolic agent such as growth hormone or insulin-like growth factor I. So far none of the endocrine abnormalities have proved to be primary, however, there is increasing evidence that some of these might participate in a vicious circle.
Elsevier
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