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Sleep traits causally affect epigenetic age acceleration: a Mendelian randomization study.

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Investigating sleep disorders and epigenetic aging, this study found insomnia may accelerate aging via the GrimAge clock. Early sleep disorder interventions could potentially impact aging and related diseases.

Keywords:
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Area of Science:

  • Genetics
  • Chronobiology
  • Epigenetics

Background:

  • Sleep disorders (SDs) are prevalent in older adults.
  • Epigenetic clocks, measuring DNA methylation (DNAm), accurately predict biological aging and are linked to age-related diseases.

Purpose of the Study:

  • To explore the causal links between sleep traits and epigenetic clock measures.
  • Utilizing Mendelian randomization (MR) to investigate these relationships.

Main Methods:

  • Genome-wide association study (GWAS) data for epigenetic clocks (HannumAge, IEAA, PhenoAge, GrimAge) and sleep traits were sourced from large biobanks (UKB, 23andMe, Finngen).
  • Multiple MR methods (IVW, MR-Egger, WM, etc.) were applied to assess causality.
  • Rigorous quality control analyses were conducted.

Main Results:

  • Self-reported insomnia showed a potential causal link to accelerated aging as measured by the GrimAge clock.
  • GrimAge acceleration exhibited a slight inverse association with self-reported insomnia.
  • Epigenetic clocks, particularly PhenoAge and GrimAge, demonstrated weak influences on sleep traits.

Conclusions:

  • Findings suggest a potential bidirectional relationship between insomnia and epigenetic aging.
  • Early intervention for sleep disorders may offer a strategy to mitigate aging and associated diseases.
  • Further research is needed to uncover the underlying biological mechanisms.