The growth of cancer leads to profound alterations of host organs and functions. The overall result is cachexia, a syndrome characterized primarily by weakness, anorexia, and the depletion and redistribution of host components. Cachexia is the consequence of anatomical alterations, decreased food intake or absorption, and altered metabolism.

Anatomical alterations are always present in a cancer patient. It has been repeatedly observed, however, that the degree of cachexia bears no simple correlation to tumor burden, tumor cell type, or anatomical site of involvement.

The consequences of impaired food intake or food absorption are a major contributor to the overall morbidity of the cancer patient. Depletion of protein and/or fat stores, hypovitaminoses, and decrease in the concentration of trace elements, variously combined, lead to states nearly identical to kwashiorkor or marasmus. Clear guidelines for recognition of these states have been set recently for cancer patients. Awareness of these syndromes is of enormous clinical importance since they are potentially reversible by the modern techniques of hyperalimentation.

It is also important to recognize metabolic effects produced by tumors and independent of either anatomical alterations or insufficient delivery of nutrients. Such effects, exemplified by the endocrine syndromes produced by nonendocrine tumors, are of substantial conceptual importance inasmuch as they imply secretion by the tumor of toxic substances that act at sites distant from the sites of anatomic involvement. The study of such defects might well pave the way to understanding of the mechanisms of cancer aggression.

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Presented at the Conference on Nutrition and Cancer Therapy, November 29 to December 1, 1976, Key Biscayne, Fla. Supported in part by Contract NO1-CP-65779-56 from the National Cancer Institute, NIH, Department of Health, Education, and Welfare.

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