Abstract
Study objectives:
To investigate whether sleep traits are associated with the risk of biological aging using a case-control design with Mendelian randomization (MR) analyses.
Methods:
We studied 336,559 participants in the UK Biobank cohort, including 157,227 cases of accelerated biological aging and 179,332 controls. PhenoAge, derived from clinical traits, estimated biological ages, and the discrepancies from chronological age were defined as age accelerations (PhenoAgeAccel). Sleep behaviors were assessed with a standardized questionnaire. Propensity Score Matching (PSM) matched control participants to age-accelerated participants, and a conditional multivariable logistic regression model estimated odds ratio (OR) and 95% confidence intervals (95% CI). Causal relationships between sleep traits and PhenoAgeAccel were explored using linear and nonlinear Mendelian randomization (MR) methods.
Results:
A U-shaped association was found between sleep duration and PhenoAgeAccel risk. Short sleepers had a 7% higher risk (OR = 1.07; 95% CI: 1.03-1.11), while long sleepers had an 18% higher risk (OR = 1.18; 95% CI: 1.15-1.22), compared to normal sleepers (6-8 hours/day). Evening chronotype was linked to higher PhenoAgeAccel risk than morning chronotype (OR = 1.14; 95% CI: 1.10-1.18), while no significant associations were found for insomnia or snoring. Morning chronotype had a protective effect on PhenoAgeAccel risk (OR = 0.87, 95% CI: 0.79-0.95) per linear MR analysis. Genetically predicted sleep duration showed a U-shaped relationship with PhenoAgeAccel, suggesting a non-linear association (P non-linear < 0.001).
Conclusions:
The study suggests that improving sleep can slow biological aging, highlighting the importance of optimizing sleep as an intervention to mitigate aging's adverse effects.
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