Abstract
Anorexia nervosa is a psychosomatic disorder in which the interplay between psychological and biological factors is particularly apparent. The illness appears to develop from a variety of psychosocial and sociocultural stressors, but when the syndrome is fully developed the symptoms are stereotyped. It is possible that, at this point, a characteristic neurobiological syndrome exists, such as occurs in endogenous depression. Evidence to support this hypothesis has developed in recent years. A variety of abnormalities of neuroendocrine function indicate hypothalamic dysfunction in the acute, underweight stages of anorexia nervosa (Vigersky and Loriaux 1977). Various neuroendocrine abnormalities documented in anorexia nervosa include abnormal regulation of growth hormone, gonadotropins, thyrotropin-stimulating hormone, cortisol, defects in urinary concentration or dilution, and failure to regulate core body temperature. Investigators in endocrinology have speculated that these endocrine abnormalities might be secondary to changes in brain neurotransmitter function or metabolism. The dexamethasone suppression test, a biological marker of endogenous depression, is abnormal in many patients with anorexia nervosa (Gerner and Gwirtsman 1981). A large amount of data in animals implicates monoamines, particularly catecholamines and serotonin, in the normal hypothalamic regulation of appetite. A catecholamine hypothesis of the etiology of anorexia nervosa and bulimia has been proposed by Leibowitz (Leibowitz, to be published).
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Ebert, M.H., Kaye, W.K., Gold, P.W. (1984). Neurotransmitter Metabolism in Anorexia Nervosa. In: Pirke, K.M., Ploog, D. (eds) The Psychobiology of Anorexia Nervosa. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-69594-0_7
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DOI: https://doi.org/10.1007/978-3-642-69594-0_7
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