The regulation of gonaddropin secretion was studied in anorexia nervosa, in voluntarily starving healthy subjects, and in the starved rat. In all cases, a hype thalamic disturbance is observed, msuMng in an impaired ability to secrete gonadotropin-rdeasing hormone (GnRH) from the d i a n eminence. This effect is weightdependent in man and animals. The central neurofransmifters noradrenaline, dopamine, dymphin, and prostaglandin โฌ2 are involved in the regulation of GnRH release. A decreased advity of the cat&amineq$c system and an increased activity of the endorphinergic system may be responsiMe for the impaired GnRH rekase.
From the earliest' descriptions of anorexia nervosa it was clear that besides disturbed eating behavior and weight loss there is an endocrine dysfunction, since all the female patients had amenorrhea. Recent years have seen many endocrine studies in anorexia nervosa, so that by now, the endocrine abnormalities in anorexia nervosa are well documented. There remains, however, a basic question that has not yet been answered: Are the endocrine symptoms only a consequence of starvation or are they caused by some unknown hypothalamic dysfunction that may also be responsible for the eating disorder?
In an earlier study we looked into the 24-hour sleep-wake patterns of gonadotropin secretion (Pirke et al., 1979). We obtained blood samples at half-hour intervals in which luteinizing hormone (LH) was measured. During the night, sleep was monitored polygraphically. The study was done one week after admission to the hospital and was repeated each time the patient had re-gained10% of his ideal weight (IBW). Fig. shows a typical set of LH patterns.