Sosnowski David W, Smail Emily J, Maher Brion S, Moore Ann Zenobia, Kuo Pei-Lun, Wu Mark N, Low Dominique V, Stone Katie L, Simonsick Eleanor M, Ferrucci Luigi, Spira Adam P
Department of Mental Health, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD, USA.
Longitudinal Studies Section, Translational Gerontology Branch, Intramural Research Program, National Institute on Aging, Baltimore, MD, USA.
Int J Aging Hum Dev. 2025 Mar;100(2):135-164. doi: 10.1177/00914150241231192. Epub 2024 Feb 12.
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 ( = 567) or genotype ( = 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.
我们试图探究睡眠不足的遗传风险以及自我报告的短睡眠是否与生物衰老相关，以及年龄和性别是否会调节这些关联。研究参与者是巴尔的摩纵向衰老研究中的一部分个体，他们拥有关于自我报告睡眠（n = 567）或基因型（n = 367）的完整数据。研究结果包括：内在霍瓦斯年龄、汉努姆年龄、表型年龄、格里姆年龄，以及基于DNA甲基化的纤溶酶原激活物抑制剂-1（PAI-1）和粒细胞计数估计值。结果表明，短睡眠的多基因风险与粒细胞计数呈正相关；与报告睡眠<6小时的人相比，报告睡眠>7小时的人表现出更快的表型年龄和格里姆年龄加速以及更高的PAI-1估计值。短睡眠的多基因风险和自我报告的睡眠时间在与某些结果的关联中与年龄和性别存在相互作用。研究结果强调，短睡眠的多基因风险和自我报告的长睡眠与表观遗传景观的变化以及随后的衰老相关。
