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Journal of Aging Research
Volume 2011 (2011), Article ID 721390, 6 pages
Research Article

Shorter Leukocyte Telomere Length in Midlife Women with Poor Sleep Quality

1Robert Wood Johnson Foundation Health and Society Scholars Program, Center for Health and Community, University of California San Francisco, 3333 California Street, Suite 465, San Francisco, CA 94118, USA
2Department of Psychiatry, University of California, San Francisco, CA 94143, USA
3Department of Biochemistry, University of California, San Francisco, CA 94143, USA
4Department of Psychology, Rutgers University, New Brunswick, NJ 08901, USA
5Department of Nutrition, Rutgers University, New Brunswick, NJ 08901, USA

Received 22 July 2011; Accepted 19 August 2011

Academic Editor: J. Woo

Copyright © 2011 Aric A. Prather et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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 ( 𝑟 = 0 . 1 4 , 𝑃 = 0 . 0 3 ), independent of age, BMI, race, and income ( 𝑏 = 5 5 . 4 8 , S E = 2 7 . 4 3 , 𝑃 = 0 . 0 4 ). 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.