Preventing Muscle Poverty

Sarcopenia, a continual, age-related muscle-wasting process, initiates its degenerative impact on health by the third decade of life. Approximately two-thirds of male and one-third of female sexagenarians present overt symptoms of sarcopenia. By 2025, those over 60 years of age will represent nearly 19% of the U.S. population. Among the elderly alone, this condition will directly cost healthcare more than $20 billion.

A combination of neurological factors, nutritional components, some hormones, metabolic dynamics, immunological factors, and the absence of physical activity contribute to the muscle atrophy and loss of muscle strength typically evident through physical weakness, decreased mobility, and, ultimately, disability and loss of independence (Doherty, T.J., 2003).

Aging presents numerous health challenges, many of which involve inflammatory processes. Sarcopenia, including sarcopenic obesity, may represent a chronic low-grade inflammation, which is indicated by the elevation of several nonspecific biomarkers such as interleukin-6 and C-reactive protein. These markers of acute inflammation observed in sarcopenia reflect the loss of muscle mass, loss of muscle and grip strength, impaired gait, and a decline in functional abilities such as walking.

The sedentary nature of obesity contributes to the inflammatory burden. The chronic expression of adipokines, including hormones and inflammatory cytokines, from a substantial volume of adipose tissue contributes to insulin resistance. This tissue, now considered a new endocrine organ, actively participates in the secretion and accretion of pro-inflammatory substances, which exacerbate muscle erosion, decrease muscle strength, and, ultimately, reduce muscle mass such that a person’s physical mobility is further compromised (Jensen, G.L., 2008). This functional decline of voluntary muscle leads to increased fat deposition in this tissue and decreased insulin sensitivity.

The Longitudinal Aging Study Amsterdam examined the possible role of vitamin D and parathyroid hormone (PTH) as determinants of sarcopenia (Visser, M. et al., 2003). Previous investigations among the elderly indicated vitamin D deficiency is evident in 30–90% of the population, depending on the cut-off criteria, such as low serum calcium, phosphate, and vitamin D levels, and elevated alkaline phosphatase activity (Lips, P., 2001). Based on seasonal serum vitamin D values alone, at least 30 studies among more than 3,000 subjects in Europe and Asia indicated that vitamin D deficiency ranged from 6–90%. Vitamin D deficiency was typically associated with muscle weakness and decreased muscle mass. This association is consistent with our understanding that vitamin D functions to preserve the function of type II muscle fibers through the interaction with vitamin D receptors (VDR) in muscle tissue (Montero-Odasso, M. and Duque, G., 2005). Importantly, the array of VDR receptor polymorphisms further complicate the aging presentation since there are several VDR genotypes associated with other non-muscle functions, including cognition, depression, and balance capability.

Several studies among the elderly have also indicated increased PTH levels as part of the clinical picture of low vitamin D, renal insufficiency, and low intake of dietary calcium (Freaney, R. et al., 1993). These kinds of studies indicate vitamin D metabolites and PTH can affect skeletal muscle metabolism, modulate calcium flux in muscle tissue, and influence the production of inflammatory mediators in muscle. Considering the high prevalence of vitamin D deficiency and decreased VDR expression with aging, normalizing and maintaining muscle function and muscle tone during the golden years remains an area of intense research.

Regular consumption of eiscosapentaenoic acid (EPA), an omega-3 polyunsaturated fatty acid naturally found in fatty, cold-water fish, may reduce inflammation associated with cardiovascular disease. Another potential benefit of EPA consumption, as demonstrated in mice, is the reduction of skeletal muscle inflammation associated with increased levels of the pro-inflammatory cytokine TNF-α (Magee, P. et al., 2008). While it is clear that the inflammatory process and muscle atrophy are complex processes, the role of dietary components and their influence on modulating inflammatory markers and skeletal muscle restoration or regeneration among older people remains uncertain (Tidball, J.G., 2005).