Background. Accumulating evidence supports leukocyte telomere length (LTL) as a biological marker of cellular aging. Poor sleep is a risk factor for age-related disease; however, the extent to which sleep accounts for variation in LTL is unknown. Methods. The present study examined associations of self-reported sleep duration, onset latency, and subjective quality with LTL in a community-dwelling sample of 245 healthy women in midlife (aged 49–66 years). Results. While sleep duration and onset latency were unrelated to LTL, women reporting poorer sleep quality displayed shorter LTL ( , ), independent of age, BMI, race, and income ( , , ). When analyses were restricted to participants for whom sleep patterns were chronic, poorer sleep quality predicted shorter LTL independent of covariates and perceived psychological stress. Conclusions. This study provides the first evidence that poor sleep quality explains significant variation in LTL, a marker of cellular aging. 1. Introduction The elderly (65 year or older) population is growing at a remarkable rate, expected to exceed 72 million in the United States by 2030 [1]. This growth is likely to lead to increasing prevalence in age-related disease, including cardiovascular disease, diabetes, and various forms of cancer. The burden of this population on the health care system will be formidable, thus, highlighting the importance of identifying markers of cellular aging implicated in the onset and progression of disease. Emerging evidence supports telomere length as a correlate and potential mechanism underling rates of diseases. Telomeres are DNA-protein complexes that cap chromosomal ends, conferring chromosomal stability [2, 3]. Shorter leukocyte telomere length is a putative risk factor for several chronic conditions, including hypertension [4], atherosclerosis [5], type 2 diabetes mellitus [6, 7], and predicts risk for cardiovascular and all-cause mortality [8–10]. There are several psychological and behavioral factors associated with telomere length, including psychological distress [11], personality characteristics [12], poor diet [13], cigarette smoking [14, 15], and leading a sedentary lifestyle [16, 17]. Interestingly, sleep, a modifiable health behavior that often worsens with age [18] and is repeatedly predictive of rates of chronic disease [19–21], has yet to be evaluated. Prior laboratory and epidemiologic evidence supports associations between disrupted sleep and several plausible biological pathways to disease, including alterations in cellular immune function [22]; however, this work has not
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