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LETTER TO THE EDITOR |
Division of Geriatric Medicine Saint Louis University Health Sciences Center and Geriatric Research, Education and Clinical Center Veterans Administration Medical Center St. Louis, Missouri
To the Editor:
Iannuzzi-Sucich and colleagues (1) draw on the findings of an elegant study to further substantiate the valid threat of sarcopenia to aging humans. Refreshingly, they depart from the populist strategy of simply emphasizing the logical consequence of functional disability and attempt to define useful predictors of sarcopenia. Notably, the authors identify body mass index as a strong predictor of skeletal muscle mass in both men and women. However, within the context of their discussion, nutritional considerations, though mentioned, are addressed tangentially almost as mere conjecture. Roubenoff, in an earlier issue of the Journal, aptly describes sarcopenia as "both a process and outcome" (2). Clearly, with emerging evidence, delineating the pathophysiological processes underlying sarcopenia is more mystifying and less relevant to practicing clinicians than appreciating the logical outcome of frailty. Undoubtedly, establishing a definitive cure for sarcopenia must be preceded by accurate determination of the underlying pathophysiology. However, from the practicing geriatricians' standpoint, the availability of reliable predictors of sarcopenia is invaluable in developing effective intervention strategies.
Multiple convincing links exist between suboptimal nutrition and sarcopenia. Plausible theories implicate a complex interplay between age-related anorexia, appetite dysregulation, cytokine proliferation, and altered endocrinological profiles. Attempts have been made to link neuropeptide Y, cholecystokinin, nitric oxide, and opioids to sarcopenia by way of appetite suppression (3,4). Hyperleptinemia in older men is associated with low testosterone levels, thereby raising the specter of leptin as a likely culprit in older adults with sarcopenia (5). Cytokines have also been linked with sarcopenia through their anorectic effect. Other multistep pathophysiological theories invoke vitamin B12 and folate deficiencies in the genesis of sarcopenia by way of increased homocysteine levels, atherosclerosis, and consequent peripheral vascular disease (4). Thus, logical scientific deduction would lead one to conclude that nutritional considerations play a major role in sarcopenia and consequent functional disability (68).
This study by Iannuzzi-Sucich and colleagues identifying predictors of sarcopenia, namely hypogonadism in men and low body mass index in both genders, is critical to the evolution of appropriate intervention protocols (1). Unfortunately, the significance of their findings to the clinical readership is undercut by their seemingly casual and rather cursory mention of good nutrition, exercise, and testosterone replacement therapy as treatment-preventive options. In view of the masculinizing effects, testosterone replacement is likely to remain a gender-based therapy, leaving nutritional management and physical exercise as the only other practical options.
In approaching sarcopenia, geriatric health professionals may well benefit from adoption of the politically controversial "preemptive strike" approach. Rather than postpone the development of intervention protocols until precise etiological characterization of sarcopenia, identification of reliable predictive indices should prompt institution of appropriate countermeasures. To this end, nutritional therapy should be heralded as a pivotal domain in the management of sarcopenia.
Far too often in medicine, practical and obvious treatment strategies are unjustly deferred until the vast armamentarium of scientific tools unearth the precise pathophysiology of the disease process in question. The paradox in geriatrics is that most preventive measures are intuitive, simple, cost effective, and readily accessible. From the practical standpoint, preventive strategies for sarcopenia are immediately obvious. As we await the unveiling of the pathogenesis, it may do us well to remember that "... Science is the knowledge of consequences, and dependence of one fact upon another" (9). Accordingly, preempting the consequences of sarcopenia by simply controlling the negative impact of risk factors may effectively retard the decline, and indeed death, of the frail older adult (10,11).
Acknowledgments
Address correspondence to Margaret-Mary G. Wilson, MD, Division of Geriatric Medicine, Saint Louis University School of Medicine, 1402 S. Grand Blvd., M238, St. Louis, MO 63104. E-mail: wilsonmg{at}slu.edu
REFERENCES
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