Summary
This genome-wide association study of over 452,000 UK Biobank participants identified 42 genetic loci influencing self-reported daytime sleepiness, with enrichment in brain-expressed genes and neuronal transmission pathways. The study demonstrates that daytime sleepiness variants cluster into two predominant biological subtypes — sleep propensity and sleep fragmentation — and share genetic links with obesity, cardiovascular disease, psychiatric conditions, and cognitive traits. These findings suggest distinct biological mechanisms underlying excessive daytime sleepiness and implicate shared genetic architecture with multiple chronic health conditions.
UK applicability
The findings are directly applicable to UK populations, as the primary analysis used the UK Biobank cohort of 452,071 participants. The identified genetic variants and their associations with sleepiness, obesity, coronary heart disease, and psychiatric conditions may inform UK clinical and public health strategies for identifying high-risk individuals and understanding the biological heterogeneity of sleep disorders.
Key measures
Self-reported daytime sleepiness, genetic risk score (42 SNPs), sleep duration, sleep chronotype, accelerometer-derived sleep efficiency, daytime naps/inactivity, restless legs syndrome, insomnia, obesity, coronary heart disease, psychiatric disease, cognitive traits, reproductive ageing
Outcomes reported
The study identified 42 genetic loci associated with self-reported daytime sleepiness through genome-wide association analysis in 452,071 UK Biobank participants. The findings were validated in independent Scandinavian cohorts and examined for associations with objective sleep measures, other sleep disorders, and cardiometabolic and psychiatric traits.
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