A Mendelian randomization study investigating the role of sleep traits and their joint effects on the incidence of atrial fibrillation.
Summary
Using one-sample and factorial Mendelian randomization in UK Biobank (with partial replication in HUNT2), genetic liability to insomnia symptoms and short sleep duration each increased AF risk. Combined sleep traits conferred the highest risk but without statistical interaction, indicating additive effects and reinforcing sleep health as a modifiable AF prevention target.
Key Findings
- Genetic predisposition to insomnia symptoms increased AF risk (HR 1.14; 95% CI 1.07–1.21) in UK Biobank.
- Genetic predisposition to short sleep (≤6 h vs 7–8 h) increased AF risk (HR 1.14; 95% CI 1.04–1.26) in UK Biobank.
- Factorial MR showed additive (non-interacting) increases when sleep traits co-occurred; findings were not consistently replicated in HUNT2.
Clinical Implications
Screen and manage insomnia symptoms and short sleep in patients at risk for AF; prioritizing behavioral and, when appropriate, pharmacologic sleep interventions may reduce incident AF.
Why It Matters
The study strengthens causal inference for sleep traits in AF using MR and explores joint effects, guiding both clinical counseling and public health interventions on sleep hygiene.
Limitations
- Replication in HUNT2 was inconsistent, limiting generalizability.
- Sleep traits were self-reported and may suffer from measurement error.
Future Directions
Interventional trials targeting insomnia and short sleep to evaluate AF prevention, with harmonized sleep phenotyping and wearable device validation.
Study Information
- Study Type
- Cohort
- Research Domain
- Prevention
- Evidence Level
- II - Prospective cohort analyses combined with Mendelian randomization for causal inference.
- Study Design
- OTHER