tients (e.g., eicosapentaenoic acid and ibuprofen) are more effective than parenteral nutrition in stabilizing weight loss (Tisdale, 1998).

Parenteral nutrition may be used to improve patients’ nutritional status and enable them to receive complete doses of chemotherapy or radiation therapy. However, in prospective randomized clinical trials, parenteral nutrition has not had a significant effect either on a patient’s survival or on symptoms and toxicities (Body, 1999).

New treatments for cachexia include thalidomide, dronabinol (THC, tetrahydrocannabinol) and cannabis, and melatonin. THC stimulates appetite and increases body weight in patients with HIV and cancer. However, it is unclear whether THC or cannabis is more effective. Gorter (1999) argues that cannabis may be better tolerated than THC alone because cannabis stimulates the appetite like pure THC but includes other cannabinoids that decrease the psychotropic side effects of THC. Neuropeptide agonists and antagonists currently used to treat obesity may also have an effect on cancer anorexia-cachexia, especially when combined with other agents that affect the breakdown of muscle and protein (Inui, 1999). Clinical trials are needed to test the effectiveness of all the treatments discussed above.

Patients with cachexia often have greater concentrations of proinflammatory cytokines (i.e., tumor necrosis factor alpha, interleukin-1, interleukin-6 [IL-6], serotonin, interferon gamma) (Mantovani et al., 1998; Yeh and Schuster, 1999). When the concentrations of these cytokines are reduced, patients often gain weight. According to Tisdale (Tisdale, 1998), IL-6 is the only cytokine that is correlated with the development of cancer cachexia. Although it seems safe to say that cytokines are involved in cancer cachexia, the specific roles of these cytokines in the production of cachexia are still unclear.

Animal models of anorexia and cachexia have been developed. Emery (1999) placed a transplantable Leydig cell tumor in Fischer rats. Rats with this tumor showed a 20–40 percent decrease in food intake and an increase in energy expenditure compared with controls. Potential explanations for these effects include postprandial metabolism of carbohydrate caused by a greater rate of hepatic glycogen synthesis via the indirect pathway and maintenance of this increased rate of hepatic glycogen synthesis for a longer time after a meal. Another animal model of cachexia involves ciliary neurotrophic factor (a type of IL-6), which decreased muscle mass in experimental animals but did not have a direct effect on muscle in vitro (Tisdale, 1998).

A better understanding of the link between cancer cachexia and cytokines should lead to the development and testing of new pharmacologic agents. For example, megestrol acetate downregulates the synthesis and release of cytokines and increases appetite, body weight, and quality of life in patients with cachexia, and medroxyprogesterone acetate reduces the in



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