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Biol Psychiatry. 2017 Jan 15;81(2):136-144. doi: 10.1016/j.biopsych.2016.07.008. Epub 2016 Jul 26.

Epigenetic Aging and Immune Senescence in Women With Insomnia Symptoms: Findings From the Women's Health Initiative Study.

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Cousins Center for Psychoneuroimmunology, Semel Institute for Neuroscience and Human Behavior, Los Angeles. Electronic address:
Cousins Center for Psychoneuroimmunology, Semel Institute for Neuroscience and Human Behavior, Los Angeles.
Department of Human Genetics, Los Angeles.
Department of Geriatrics, David Geffen School of Medicine, Los Angeles.
HudsonAlpha Institute for Biotechnology, Huntsville, Alabama.
Department of Medicine, Stanford University, Palo Alto, California.
Department of Human Genetics, Los Angeles; Department of Biostatistics, Fielding School of Public Health, University of California, Los Angeles, Los Angeles.



Insomnia symptoms are associated with vulnerability to age-related morbidity and mortality. Cross-sectional data suggest that accelerated biological aging may be a mechanism through which sleep influences risk. A novel method for determining age acceleration using epigenetic methylation to DNA has demonstrated predictive utility as an epigenetic clock and prognostic of age-related morbidity and mortality.


We examined the association of epigenetic age and immune cell aging with sleep in the Women's Health Initiative study (N = 2078; mean 64.5 ± 7.1 years of age) with assessment of insomnia symptoms (restlessness, difficulty falling asleep, waking at night, trouble getting back to sleep, and early awakenings), sleep duration (short sleep 5 hours or less; long sleep greater than 8 hours), epigenetic age, naive T cell (CD8+CD45RA+CCR7+), and late differentiated T cells (CD8+CD28-CD45RA-).


Insomnia symptoms were related to advanced epigenetic age (β ± SE = 1.02 ± 0.37, p = .005) after adjustments for covariates. Insomnia symptoms were also associated with more late differentiated T cells (β ± SE = 0.59 ± 0.21, p = .006), but not with naive T cells. Self-reported short and long sleep duration were unrelated to epigenetic age. Short sleep, but not long sleep, was associated with fewer naive T cells (p < .005) and neither was related to late differentiated T cells.


Symptoms of insomnia were associated with increased epigenetic age of blood tissue and were associated with higher counts of late differentiated CD8+ T cells. Short sleep was unrelated to epigenetic age and late differentiated cell counts, but was related to a decline in naive T cells. In this large population-based study of women in the United States, insomnia symptoms are implicated in accelerated aging.


Aging; Epigenetic; Immunosenescence; Insomnia; Methylation; Sleep

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