BACKGROUND
Insomnia symptoms are associated with vulnerability to age-related morbidity and mortality. Cross-sectional data suggest 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.
METHODS
We examined the association of epigenetic age and immune cell aging with sleep in the Women’s Health Initiative (WHI) study (N=2,078; Age M(SD)=64.5(7.1) 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 or less; long-sleep >8hrs), epigenetic age, naïve T cell (CD8+CD45RA+CCR7+), and late differentiated T cells (CD8+CD28−CD45RA−).
RESULTS
Insomnia symptoms were related to advanced epigenetic age, B(SE)=1.02(.37), P=0.005, after adjustments for covariates. Insomnia symptoms were also associated with more late differentiated T cells (B(SE)=.59(.21), P=.006), but not with naïve T cells. Self-reported short and long sleep duration were unrelated to epigenetic age. Short sleep, but not long sleep, was associated with fewer naïve T cells (P<.005) and neither were related to late differentiated T cells.
CONCLUSIONS
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 naïve T cells. In this large population based study of women in the United States, insomnia symptoms are implicated in accelerated aging.