This study provides initial evidence for an association between sleep quality and leukocyte telomere length, a marker of immune cell aging, among a sample of healthy midlife women. Specifically, we found that women reporting poorer subjective sleep quality had shorter LTL, independent of age, body mass index, race, and income, thus, providing preliminary evidence that LTL may reflect a potential biological mechanism linking sleep and age-related disease.
In the full sample (N
= 245), levels of perceived stress accounted for variance in the relationship between sleep quality and telomere length. However, when analyses were limited to those participants whose sleep quality in the past week was typical of their sleep over the past three months (N
= 201), sleep quality was a significant predictor of LTL, independent of perceived stress, indicating that the chronicity of sleep problems may be an important qualifier in this association. This is consistent with a prior investigation of caregiving stress and LTL, which found that duration of caregiving and not merely being a caregiver was associated with telomere attrition [11
The biological mechanisms underlying the association between sleep quality and telomere attribution remain to be elucidated. Indeed, disrupted sleep quality has been associated with cortisol secretion [33
], enhanced autonomic activation [34
], and elevated proinflammatory cytokine production [35
], which may contribute to variation in LTL. Recent work suggests that LTL, in addition to being a promising biomarker of cellular aging, may also be an important contributor to disease pathogenesis [36
]; rodent models lacking telomerase have implicated telomere attrition as a mechanism leading to mitochondrial damage, increased oxidative stress, and structural and functional damage to cardiac tissue [36
]. Relatedly, it is possible that chronically disturbed sleep is related to diminished telomerase activity; however, no study has yet examined whether telomerase activity varies by quality or duration of sleep.
There are a number of limitations of the current study. The cross-sectional nature of the study precludes any causal inferences regarding sleep quality and LTL. In addition, we relied on self-reported sleep measures, and more than 67% of the participants described their sleep as “fairly good” or “very good.” Future studies would benefit from using more ecologically valid measures of sleep, including in-home polysomnography and actigraphy, as well as sampling within a population with greater variation in quality of sleep; the latter could be accomplished by including a more comprehensive measure of subjective sleep quality. Importantly, participants in the current study were predominantly Caucasian, well educated, in a high-income bracket, and included only women. Thus, the present findings are potentially restricted to this sample of women, and the possibility exists that other components of sleep, such as duration and latency, would be associated with LTL in a more diverse sample of participants. Furthermore, while perceived stress was assessed, other related psychological constructs and measures of stressful life events often related to sleep quality were not tested here. This is important given converging evidence that suggests that childhood trauma is a strong predictor of short LTL in later life [37
]. Additional studies are needed to determine the extent to which psychological factors account for the observed association between sleep quality and LTL. Finally, we did not assess for the presence of clinical sleep disorders, such as obstructive sleep apnea (OSA), in this study. This is an important issue given that adults with OSA have been shown to exhibit shorter LTL compared to those without OSA [39
]. Notably, the presence of OSA in children is associated with longer LTL [40
]. While the influence of OSA on LTL requires further clarity, the association of sleep quality and LTL in the present study was independent of BMI, a common correlate of OSA.
The alarming increase in the prevalence of age-related diseases suggests that greater attention be placed on identifying biomarkers of cellular aging and modifiable behaviors that may slow the rates of illness. The present study provides the first evidence that poorer subjective sleep quality is associated with shorter LTL, and additional research using prospective samples and objective measures of sleep is warranted. Sleep is a modifiable health behavior, and while the clinical significance of LTL remains to be elucidated, this study provides promising results that sleep quality may be an important factor explaining variation in cellular aging and later health.