Abstract
Cachexia in cancer patients is a major cause of morbidity and mortality. The syndrome of cachexia seems to be a facet of the inflammatory response to injury. This proinflammatory state is driven by an interdependent web of mediators such as cytokines, neurotransmitters, prostaglandins, neuroendocrine hormones, and tumor-derived catabolic factors. The resulting metabolic response to cancer prevents the effective use of calories provided and therefore blocks anabolism. The most promising interventions in cancer cachexia seem to depend on modulation of the inflammatory state (including nonsteroidal anti-inflammatory drugs and fish oil–based preparations). Suppression of the inflammatory milieu seems to allow nutrition to have an anabolic effect, resulting in gains in lean tissue with the potential to improve patient survival and quality of life.
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