NatureMay 13, 2026

Sleep patterns linked to biological aging in middle and older age

Longevity & Aging Weekly Brief ↗PubMed ↗DOI ↗OA ↗

Updated May 14, 2026

Abstract

A U-shaped relationship exists between sleep duration and biological age gaps across nine brain and body systems, with 6.4 to 7.8 hours of sleep associated with the lowest biological age gaps.

Short (<6 hours) and long (>8 hours) sleep durations are linked to a higher risk of systemic diseases and increased all-cause mortality compared to normal sleep duration (6-8 hours).
Evidence from genetic correlations and survival predictions indicates associations between sleep duration and conditions such as depression and diabetes.
Long sleep duration's relationship with late-life depression may be mediated by biological ageing clocks, while short sleep duration shows a direct connection.
Mendelian randomization suggests that while disease may influence sleep, it does not provide strong evidence for a causal relationship.

Simplified

Optimal sleep has a vital role in promoting healthy ageing and enhancing longevity. Here we propose Sleep Chart to assess the relationship between self-reported sleep duration and 23 biological ageing clocks derived from in vivo imaging, plasma proteomicsand metabolomics. First, a systemic, U-shaped pattern emerges between sleep duration and biological age gaps across nine brain and body systems and three omics technologies. The sample-specific lowest biological age gaps are achieved between 6.4 and 7.8 h of sleep duration, varying by organ and sex in the UK Biobank (aged 37-84 years). Furthermore, short (<6 h) and long (>8 h) sleep duration, compared with a normal sleep duration (6-8 h), are associated with increased risk of systemic diseases beyond the brain and all-cause mortality, with evidence from genetic correlations and time-to-incident survival predictions, such as depression and diabetes. Finally, the pathways by which long and short sleep duration are associated with late-life depression differ: ageing clocks may partially mediate the pathway for long sleep duration, while short sleep duration shows a more direct link. Although Mendelian randomization does not provide strong evidence that disease causally affects sleep, it cannot completely exclude such reverse causality. Our findings suggest a cross-organ, multi-omics U-shaped relationship between sleep duration and biological ageing clocks, highlighting the potential of sleep optimization to promote healthy ageing, lower disease risk and extend longevity. 1 2 3

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Competing interests: The authors declare no competing interests.

PubMed

Sleep patterns linked to biological aging in middle and older age

Abstract

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