ArticleAging2025
Evaluating the nonlinear effects of sleep duration on biological aging across phenotypic, genomic, and epigenomic data.
Article in Aging, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed.
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
Short and long sleep durations have been inconsistently linked to aging and health outcomes, potentially due to underexplored nonlinear associations. Using phenotypic and genomic data from the UK Biobank (n=442,664), we applied multivariable linear regression, restricted cubic splines, and Mendelian randomization (MR) to analyze nonlinear relationships between self-reported sleep duration and biomarkers of accelerated aging: PhenoAge acceleration (PhenoAgeAccel), BioAge acceleration (BioAgeAccel), and leukocyte telomere length (LTL). Functional annotation analyses were performed to assess potential shared biological pathways using epigenomic profiles. Observational analyses supported U-shaped phenotypic associations between sleep duration and PhenoAgeAccel/BioAgeAccel, with optimal sleep around 7 h/d. For LTL, linear models suggested a U-shape, while spline models indicated an inverted reverse J-pattern. MR analyses corroborated the deleterious impacts of insufficient, but not excessive, sleep, by revealing a threshold nonlinear relationship between increasing genetically-predicted sleep duration up to 7 h/d and lower PhenoAgeAccel/BioAgeAccel, and a linear relationship with longer LTL. Cell-type enrichment analyses connected short sleep to BioAgeAccel/LTL through pathways related to muscle maintenance and immune function. These findings suggest that extending sleep may mitigate accelerated aging, though further research is needed to clarify the underlying biological mechanisms and whether excessive sleep also contributes causally to biological aging.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.