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. 2025 Mar;100(2):135-164.
doi: 10.1177/00914150241231192. Epub 2024 Feb 12.

Sleep Duration Polygenic Risk and Phenotype: Associations with Biomarkers of Accelerated Aging in the Baltimore Longitudinal Study of Aging

David W Sosnowski  1 , Emily J Smail  1 , Brion S Maher  1 , Ann Zenobia Moore  2 , Pei-Lun Kuo  2 , Mark N Wu  3 , Dominique V Low  4 , Katie L Stone  5   6 , Eleanor M Simonsick  2 , Luigi Ferrucci  2 , Adam P Spira  1   7   8
Affiliations

Sleep Duration Polygenic Risk and Phenotype: Associations with Biomarkers of Accelerated Aging in the Baltimore Longitudinal Study of Aging

David W Sosnowski et al. Int J Aging Hum Dev. 2025 Mar.

Abstract

We sought to explore whether genetic risk for, and self-reported, short sleep are associated with biological aging and whether age and sex moderate these associations. Participants were a subset of individuals from the Baltimore Longitudinal Study of Aging who had complete data on self-reported sleep (n = 567) or genotype (n = 367). Outcomes included: Intrinsic Horvath age, Hannum age, PhenoAge, GrimAge, and DNAm-based estimates of plasminogen activator inhibitor-1 (PAI-1) and granulocyte count. Results demonstrated that polygenic risk for short sleep was positively associated with granulocyte count; compared to those reporting <6 hr sleep, those reporting >7 hr demonstrated faster PhenoAge and GrimAge acceleration and higher estimated PAI-1. Polygenic risk for short sleep and self-reported sleep duration interacted with age and sex in their associations with some of the outcomes. Findings highlight that polygenic risk for short sleep and self-reported long sleep is associated with variation in the epigenetic landscape and subsequently aging.

Keywords: age acceleration; aging; biomarkers; epigenetics; polygenic risk; sleep duration.

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