During
tumor growth,
anorexia and reduced food intake markedly contribute to the development of
malnutrition, thus worsening overall patients' survival. A better understanding of the pathophysiology of eating behavior may lead to new and more effective
therapies, aiming at counteracting the detrimental effects of
anorexia and reduced food intake on nutritional status and survival in
cancer patients. Brain
tryptophan and
serotonin concentrations seem to play a pivotal role in the regulation of eating behavior. Increased brain
serotonin activity is indeed associated with a reduction of food intake. It has been recently hypothesized that increased availability of
tryptophan to the brain and the consequent increased
serotonin activity may represent the pathogenic mechanism for
cancer-associated
anorexia. According to this hypothesis, the modulation of brain
serotonin activity may result in an improvement of
anorexia. Reducing brain
tryptophan availability represents a possible mechanism to restore brain
serotonin activity to normal. There is evidence that the
oral administration of
neutral amino acids competing with
tryptophan for brain entry results in a significant improvement of
cancer anorexia. The same treatment may also be effective in improving secondary
anorexia, which is associated with other
chronic illnesses, including renal and
liver failure,
sepsis, and so forth, sharing a similar pathogenic mechanism.