Malnutrition, in conditions such as kwashiorkor and pyloric stenosis, results from inadequate intake of nutrients despite a good appetite, and manifests as weight loss associated with protective metabolic responses such as decreased basic metabolic rate and preservation of lean body mass at the expense of fat mass. Cachexia differs from malnutrition in several key ways. First, despite the fact that the cachexic person is "starving," he or she is anorexic. Second, in normal starvation the metabolic rate decreases as a protective mechanism. This protective reduction in metabolic rate is not observed in cachexia. Resting energy expenditure is high in patients with cachexia from renal failure (9,10). Third, in simple starvation fats are preferentially lost and there is preservation of lean body mass. In cachexia, lean tissues are wasted and fat stores are relatively underutilized (11). Finally, the abnormalities in malnutrition can usually be overcome simply by supplying more food or altering the composition of the diet. To date this approach has not proven to be successful in cachexic patients. Stimulation of nutritional intake with megestrol acetate fails to restore the loss of lean body mass in cancer patients, whereas weight gain achieved is the result of an accumulation of adipose tissue and water (12). There are fundamental metabolic abnormalities in cachexic patients that prevent them from utilizing dietary nutrients effectively. One important point about cancer cachexia is that the presence and severity of cachexia has no correlation to the size of the tumor. The tumor does not represent a "metabolic sink" for ingested nutrients. If this were the case, increasing nutrient intake would result in more rapid tumor growth, an outcome that is not observed clinically (11). Furthermore, parabiosis experiments in animals demonstrated that cachexia is observed in the nontumor-bearing partner, indicating that circulating factors are largely responsible for this phenomenon (11).
Was this article helpful?