Editors' ChoiceAging

Catch some T’s

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Science Translational Medicine  30 Mar 2016:
Vol. 8, Issue 332, pp. 332ec53
DOI: 10.1126/scitranslmed.aaf6469

Sleep disturbances in older adults are common and frequently multifactorial. The incidence of insomnia, for instance, increases with age, and the symptoms of insomnia are associated with increased risk of disease and death. Multiple mechanisms have been proposed to account for this increased risk, including basic biological processes that promote aging such as telomere shortening. In a recent study, Carroll et al. assessed markers of biological aging in individuals with clinical insomnia compared with healthy controls.

The authors recruited 126 participants age 50 to 88 years who were either healthy controls without insomnia or had insomnia determined by reported difficulty with initiating or maintaining sleep or having chronic non-restorative sleep. All participants had telomere length measured in peripheral blood mononuclear cells by real-time quantitative polymerase chain reaction. The key finding of the study is that participants with insomnia aged ≥70 years had significantly shorter telomere lengths compared with age-matched healthy controls. A difference in telomere length was not seen in adults 60 to 69 years old without and with insomnia. These findings suggest that disrupted sleep accelerates normal cellular aging.

Major limitations of the study include the cross-sectional design and the lack of objective sleep measures. Participants were diagnosed with insomnia based on clinical criteria of self-reported sleep quality. Future studies using objective sleep tests such as actigraphy or polysomnography will help to define specific sleep parameters associated with shortened telomere length. Sleep disorders other than insomnia, such as periodic leg movements during sleep and sleep-disordered breathing, also increase with age and were not directly assessed in this study. Controlling for these other sleep factors in prospective studies with longitudinal assessments of both sleep and telomere length will help to establish whether a direct causal relationship exists between insomnia and short telomeres. The study also assumes that telomere length in peripheral blood mononuclear cells is representative of general cellular senescence, although this may be a reasonable assumption, as peripheral blood cell telomere length is considered a marker for immune cell aging and is positively correlated with telomere length in other body tissues. Despite these limitations, the findings of this study open up a new avenue of research into a potential sleep-mediated mechanism that increases the risk of age-related diseases.

J. E. Carroll et al., Insomnia and telomere length in older adults. Sleep 39, 559–564 (2016). [Abstract]

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