Inanition is the opposite of obesity and is characterized by extreme weight loss. It can be caused by inadequate availability of food or by pathophysiologic conditions that greatly decrease the desire for food, including psy-chogenic disturbances, hypothalamic abnormalities, and factors released from peripheral tissues. In many instances, especially in those with serious diseases such as cancer, the reduced desire for food may be associated with increased energy expenditure, causing serious weight loss.
Anorexia can be defined as a reduction in food intake caused primarily by diminished appetite, as opposed to the literal definition of "not eating." This definition emphasizes the important role of central neural mechanisms in the pathophysiology of anorexia in diseases such as cancer, when other common problems, such as pain and nausea, may also cause a person to consume less food. Anorexia nervosa is an abnormal psychic state in which a person loses all desire for food and even becomes nauseated by food; as a result, severe inanition occurs.
Cachexia is a metabolic disorder of increased energy expenditure leading to weight loss greater than that caused by reduced food intake alone. Anorexia and cachexia often occur together in many types of cancer or in the "wasting syndrome" observed in patients with acquired immunodeficiency syndrome (AIDS) and chronic inflammatory disorders. Almost all types of cancer cause both anorexia and cachexia, and more than half of cancer patients develop anorexia-cachexia syndrome during the course of their disease.
Central neural and peripheral factors are believed to contribute to cancer-induced anorexia and cachexia.
Several inflammatory cytokines, including tumor necrosis factor-a, interleukin-6, interleukin-1 b, and a proteolysis-inducing factor, have been shown to cause anorexia and cachexia. Most of these inflammatory cytokines appear to mediate anorexia by activation of the melanocortin system in the hypothalamus. The precise mechanisms by which cytokines or tumor products interact with the melanocortin pathway to decrease food intake are still unclear, but blockade of the hypo-thalamic melanocortin receptors appears to almost completely prevent their anorexic and cachectic effects in experimental animals. Additional research, however, is needed to better understand the pathophysiologic mechanisms of anorexia and cachexia in cancer patients and to develop therapeutic agents to improve their nutritional status and survival.
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