It has been hypothesized that corticotropin-releasing hormone (CRH) is an integral mediator in the pathophysiology of anorexia nervosa. This hypothesis is based on a) studies on patients with eating disorders which found elevated CRH levels in the cerebrospinal fluid and an abnormal response of the hypothalamopituitary (HYPAC) axis to intravenous CRH, and b) the discovery that the central administration of CRH to rats causes an acute anorectic state. Human and animal data supporting this hypothesis are reviewed, and important problems with the data base and the interpretation of these data are discussed. Appropriate directions for future research are highlighted.
|Original language||English (US)|
|Number of pages||11|
|State||Published - Dec 1 1989|