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Anorexia in Cancer Patients¹

Medical Oncology Section, Department of Medicine and Cancer Center, Northwestern University School of Medicine, Chicago, Illinois 60611

The pathophysiology of anorexia in cancer patients is poorly understood and has been difficult to study because of multiple variables that influence the clinical picture. This essay reviews current understanding of food intake control in normals and attempts to relate this to observations in cancer patients. Hypothalamic centers can either stimulate or suppress feeding behavior, but there is no evidence of alteration of these centers in cancer patients. Sensory input from the mouth may influence feeding behavior. Recent studies have delineated changes in taste sensation in cancer patients that can be correlated with patient symptoms, extent of tumor involvement, and caloric intake. Sensors within the gastrointestinal tract influence the quantity of food eaten; there may be alterations in the function of these sensors in cancer patients, but no direct study of this is available. Thermostatic sensors also influence food intake; it is possible that the heat generated by tumor metabolism may tend to reduce food intake, but this also requires further study. Glucosensitive receptors exist in the brain and the liver, and it is possible that the increased metabolic activity in the liver that occurs in cancer may stimulate hepatic receptors to lead to suppression of appetite, but this requires further study. Liposensitive and amino acid-sensitive receptors also influence normal food intake regulation, and alterations in metabolism in the cancer patient such as amino acid imbalances may be anorexigenic. Since eating behavior is controlled by several apparently redundant cues or control mechanisms, there probably is a hierarchy among these cues, and aberration of a cue high on the hierarchical scale may predominate over others. Future research should further delineate the hierarchical ranking of food intake cues and controls in normals and in patients with cancer.

¹ 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 from the National Cancer Institute.