Changes in brain serotonin and tryptophan concentrations probably represent one of the most important mechanisms in the regulation of eating behavior both in experimental animals and in humans. Anorexia, which accompanies numerous diseases, e.g., cancer, liver cirrhosis, and uremia, may recognize an increased brain availability of tryptophan as a common pathogenic mechanism. This will lead to a rise in brain serotonin synthesis, which, in turn, is responsible for a reduction in food intake. According to this hypothesis, the anorexia observed in various diseases could be improved either by a decrease in the cerebral synthesis of serotonin or by a reduction in the entry of tryptophan into the brain.