Debilitating cancer cachexia is multifactorial, but many of the etiologies and most of the resulting effects are similar to those seen in malnourished patients without cancer. From the work in human beings and experimental animals, nutritional support of the tumor-bearing host can replenish lean body mass, visceral protein components, and immunocompetence. This induction of anabolism, however, depends on time, content, the method of administration of hyperalimentation solutions; the initial and continuing catabolic response of the patient, as well as the degree of initial malnutrition; the energy expenditure of the patient required during oncologic therapy; and the expertise of the physician administering nutritional support. Increased tumor stimulation resulting from intravenous hyperalimentation (IVH) has never been observed in humans; the stimulatory effects of IVH on animal tumor systems have been identified only in previously depleted animals, and then growth rates have not been out of proportion to that of the host or to that of otherwise healthy animals. Animal data suggest that tumor growth characteristics can be affected by nutritional state and the exact substrates administered, ie, amino acids, carbohydrates, or fat. Further evidence suggests that the apparent enhanced tumor growth can be used to increase responsiveness to cell cycle-specific chemotherapeutic agents during nutritional repletion. Current evidence supports the use of intravenous hyperalimentation in malnourished cancer patients who have effective oncologic therapeutic options; such patients should not be denied these options simply on the basis of severe nutritional cachexia.
Adenocarcinoma Animals