Distinct roles of chronotype, daytime napping, and sleep duration in biological and functional aging: a univariable and multivariable Mendelian randomization study

Mar 13, 2026Clinical epigenetics

Different impacts of sleep timing, daytime naps, and sleep length on biological and functional aging

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Abstract

Napping is adversely associated with telomere length and cognitive performance.

Napping correlates negatively with telomere length, suggesting a potential link to cellular aging.
Facial aging shows a positive association with napping, indicating that it may contribute to visible signs of aging.
, an epigenetic measure of biological age, is positively influenced by napping.
Longer sleep duration is linked to lower frailty, suggesting that it may have protective effects on physical health.
Chronotype is associated with facial aging and cognition, with later chronotypes potentially leading to worse outcomes.

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BACKGROUND: Sleep traits have been linked to aging, but observational designs cannot separate correlated sleep behaviors or establish causality. We used (MR) to estimate both total and direct effects of chronotype, daytime napping, and sleep duration on multidimensional aging outcomes.

METHODS: Two-sample MR used large GWAS instruments for the three sleep traits against leukocyte telomere length, facial ageing, epigenetic clocks (IEAA, HannumAge, PhenoAge, ), frailty index, and cognitive performance. Inverse-variance weighted (IVW) was primary, with MR-Egger, weighted median, and MR-PRESSO as sensitivity analyses. Univariable MR (UVMR) estimated total effects; multivariable MR (MVMR) estimated direct effects accounting for intercorrelations.

RESULTS: In UVMR, napping was adversely associated with telomere length (β = - 0.11, 95% CI - 0.18 to - 0.05, PFDR = 0.002), facial ageing (β = 0.05, 0.01-0.09, PFDR = 0.036), GrimAge (β = 0.96, 0.09-1.83, PFDR = 0.048), frailty (β = 0.32, 0.20-0.45, PFDR < 0.001), and cognition (β = - 0.16, - 0.29 to - 0.03, PFDR = 0.036); HannumAge was nominal (β = 0.53, - 0.29-1.35, PFDR = 0.275). Chronotype related to HannumAge (β = 0.46, 0.15-0.78, PFDR = 0.032) with borderline links to IEAA (β = 0.36, 0.07-0.66, PFDR = 0.060) and poorer cognition (β = - 0.04, - 0.08 to - 0.01, PFDR = 0.060). Sleep duration was inversely associated with frailty (β = -0 .17, - 0.26 to - 0.08, PFDR = 0.001). In MVMR, napping retained associations with GrimAge (β = 1.08, 0.02-2.15, P = 0.046) and frailty (β = 0.29, 0.15-0.43, P < 0.001), while links to telomere length and cognition attenuated. Chronotype became protective for facial ageing (β = -0 .03, - 0.05 to - 0.01, P = 0.011) and cognition (β = 0.09, 0.01-0.17, P = 0.036) and showed no independent association with epigenetic clocks. The inverse association between sleep duration and frailty strengthened (β = - 0.36, - 0.49 to - 0.22, P < 0.001).

CONCLUSIONS: Sleep traits show distinct, partly independent causal links with aging: excessive napping adversely influences GrimAge and frailty; longer sleep duration independently protects against frailty; and chronotype benefits facial ageing and cognition after accounting for other sleep behaviors.

Key numbers

-0.11

Decrease in Telomere Length

Association with daytime napping in UVMR analysis.

0.32

Increase in Frailty Index

Association with daytime napping in UVMR analysis.

-0.03

Decrease in Facial Aging

Association with chronotype in MVMR analysis.

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Distinct roles of chronotype, daytime napping, and sleep duration in biological and functional aging: a univariable and multivariable Mendelian randomization study

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