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A LTHOUGH biologic age may be impossible to define completely, it will be better understood by uncovering biomarkers of aging. In the future, these biomarkers might guide preventive or therapeutic interventions before clinical onset of age-related disease. Leukocyte telomere length (LTL) might be such a biomarker because it ostensibly records the accruing burden of inflammation and oxidative stress, processes thought to contribute to aging and disease pathogenesis (1-3). LTL undergoes progressive shortening with age, and in the general population, it is comparatively short in individuals with atherosclerosis or those at risk for this aging-related disease (4). The evidence for LTL as an overall biomarker of aging remains unclear, though, due to variation in the strength of detected associations, differences in results based on measurement method and selected outcome, lack of data coupling longitudinal measurements of LTL and aging phenotypes, and theoretical considerations of whether a single marker can accurately and strongly record aging across the life span (5-7).
Sanders et al. (Tue,) studied this question.
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