ABSTRACT
Neurochemical research on a relationship between 5-hydroxytryptamine [5-HT; serotonin] and feeding shows that brain 5-HT metabolism is increased following the ingestion of a particularly carbohydrate rich diet. Increased metabolism may generate a neurochemical signal for the termination of the meal which is evidenced by pharmacological research on experimental animals and clinical reports. Receptor research shows that appetite suppressant effects of 5-HT are manifested by the stimulation of 5-HT-2B/5-HT-2C receptors located postsynaptically. Drugs with selectivity selectively towards 5-HT-1A receptors decreased the availability of 5-TH at these sites and elicited hyperphagia in experimental animals. It has been observed in clinical studies that availability of tryptophan [the precursor of 5-HT] to the brain is increased in anorexia associated with various diseases. However, psychological loss of appetite, as observed in anorexia nervosa, cannot be explained by the above hypothesis because evidence for enhanced 5-HT metabolism is lacing. On the other hand, underweight patients with clinical symptoms of anorexia nervosa exhibited low basal levels of 5-HIAA, a major metabolite of 5-HT, in the cerebrospinal fluid. Food restriction and self imposed dieting precipitate anorexia nervosa. Although brain 5-HT metabolism is increased following starvation, restricted feeding decreases it and the 5-HT synthesis rate, particularly in the hypothalamus. It is, therefore, possible that decreased presynaptic activity may provoke a compensatory up-regulation of postsynaptic receptors to precipitate anorexia nervosa. A greater sensitivity of these hypophagic serotonergic mechanisms in the female may put women at a greater risk to the disease