Fight Aging!

An important goal in the research community is to build a robust measure of biological age, the burden of age-related damage and dysfunction contributing to disease and mortality, that can be used to rapidly assess the quality of any potential intervention to slow or reverse aging. One of the reasons why the longevity field moves slowly is that, in the absence of a robust measure of biological age, it takes a long time to assess any given therapy by running life span studies in mice, and repeating such studies in humans is infeasible. So there is relatively little drive to compare, contrast, and optimize approaches shown to slow or reverse aging in laboratory species. One might hope that a robust measure of biological age would speed up the research community's efforts to build a basis for greater human longevity.

There are obviously a great many existing biomarkers of aging, some of which are very straightforward to measure. Grip strength is a popular one, and today's open access paper advocates for imaging of the degree of fat infiltration into muscle tissue. The issue is that these measures are not known to be robust. Either their relationship with outcomes in aging varies greatly from individual to individual, or they cannot be trusted to accurately reflect effects on outcomes produced by interventions. Any measure of aging can be calibrated against any specific form of treatment for aging, to determine whether or not it is helpful in that case, but then one is back to needing long-running, expensive studies to make progress. It doesn't help the bigger picture because it doesn't accelerate the field.

Myosteatosis: an emerging biomarker of aging

Adipose tissue infiltration into skeletal muscle (i.e., myosteatosis) has emerged as an independent contributor to metabolic disorders and declines in skeletal muscle function with age. It remains unclear whether myosteatosis is a marker of aging or simply a consequence of disease or disuse. This review summarizes evidence from population-based epidemiologic studies that utilized non-invasive imaging to measure myosteatosis and to evaluate age-related changes among community-dwelling middle aged and older adults.

Myosteatosis consistently increased with age, independent of weight change, and the burden of myosteatosis was greater among women, and non-White racial and Hispanic ethnic groups after accounting for physical activity levels, chronic disease burden, and overall body size. Myosteatosis accumulation is not uniform throughout the body and is differentially associated with clinically meaningful age-related outcomes, including changes to gait, balance, muscle strength, and physical function. Hormonal, cellular, genetic, and lifestyle differences comprise the biological pathways that may lead to age-related increases in myosteatosis.

Future work in diverse populations using standardized imaging methodologies could include longitudinal measures of biological markers to better understand the biological precursors that accompany the phenotypic change. In conclusion, while myosteatosis does not accumulate uniformly with age across sex, race, or anatomical location, evidence from several well-characterized epidemiologic studies supports myosteatosis as a potential marker of aging, independent of weight change, body size, activity level, or chronic disease burden.