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Nutrition Modulation of Cachexia/Proteolysis

Rafat Siddiqui, PhD^*,, Darshak Pandya, DO^*,, Kevin Harvey, BS^* and Gary P. Zaloga, MD^*,

^* Methodist Research Institute of Clarian Health Partners, Indianapolis, Indiana; and the Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana

Correspondence: Gary P. Zaloga, MD, Medical Director, Methodist Research Institute, 1812 N Capitol Ave, Wile Hall, Room 120, Indianapolis, IN 46202. Electronic mail may be sent to gzaloga{at}clarian.org.

Cachexia represents progressive wasting of muscle and adipose tissue and is associated with increased morbidity and mortality. Although anorexia usually accompanies cachexia, cachexia rarely responds to increased food intake alone. Our knowledge of the underlying mechanisms responsible for cachexia remains incomplete. However, most states of cachexia are associated with underlying inflammatory processes and/or cancer. These processes activate protein degradation and lipolytic pathways, resulting in tissue loss. In this article, we briefly review the pathophysiology of cachexia and discuss the role of specific nutrient supplements for the treatment of cachexia. The branched chain amino acid leucine, the leucine metabolite β-hydroxy-β-methylbutyrate, arginine, glutamine, -3 long chain fatty acids, conjugated linoleic acid, and polyphenols have demonstrated some efficacy in animal and/or human studies. Optimal treatment for cachexia is likely aimed at maximizing muscle and adipose synthesis while minimizing degradation.

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