ArticlesCatabolism of aging: is it an inflammatory process?Roubenoff, RonennAuthor Information Department of Molecular Medicine, Millennium Pharmaceuticals Inc., Cambridge and Department of Medicine and Nutrition, Tufts University, Boston, Massachusetts, USA Curr Opin Clin Nutr Metab Care 6:295–299. © 2003 Lippincott Williams & Wilkins. Correspondence to Ronenn Roubenoff, MD, MHS, Millennium Pharmaceuticals, 75 Sidney Street, Cambridge, MA 02139, USA Tel: +1 617 4441537; fax: +1 617 551 7963; e-mail: [email protected] Current Opinion in Clinical Nutrition and Metabolic Care 2003, 6:295–299 Current Opinion in Clinical Nutrition and Metabolic Care: May 2003 - Volume 6 - Issue 3 - p 295-299 doi: 10.1097/01.mco.0000068965.34812.62 Buy Metrics Abstract Aging causes loss of many of the anabolic signals to muscle that are present in young adulthood. Recent research suggests that there is also an increase in catabolic signals with age. Purpose of review Research in the field of sarcopenia is evolving rapidly, and the process is now recognized as an important cause of frailty and morbidity in the elderly. This review focuses on recent developments in the field, especially regarding the role of catabolic stimuli in causing sarcopenia. Recent findings There is now an impressive body of literature implicating increased interleukin-6 levels in successfully aging adults. New data indicate that high interleukin-6 levels carry a poor prognosis, although it is not clear if the cytokine has primarily a causal or counter-regulatory function. Interleukin-6 and other cytokines could function through direct catabolic effects, or by causing reduced dietary energy intake (the anorexia of aging), or by inducing insulin resistance or lowering growth hormoneinsulin-like growth factor-I concentrations. Furthermore, apoptosis has now been linked to sarcopenia, suggesting that an inflammatory signal could trigger loss of muscle cells in the elderly even in the absence of overt inflammatory disease. © 2003 Lippincott Williams & Wilkins, Inc.