Abstract
Anorexia nervosa is a disorder that has been known to physicians for centuries; yet an understanding of its pathophysiology and successful treatment has been elusive. Studies of the hypothalamic-pituitary axis have demonstrated that pituitary responsiveness to hypothalamic releasing factors and hypothalamic responsiveness to feedback stimuli are normal except that gonadotropin release does not result from clomiphene citrate administration. The latter, with other evidence (abnormal thermoregulatory responses, partial diabetes insipidus and insulin insensitivity1), implicates hypothalamic dysfunction as an integral part of the disease. It is not clear whether this dysfunction is secondary to the malnutrition that results from the disease, . . .
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