Genetic determinants of daytime napping and effects on cardiometabolic health

Daytime napping is a common, heritable behavior, but its genetic basis and causal relationship with cardiometabolic health remains unclear. Here, we performed a genome-wide association study of self-reported daytime napping in the UK Biobank ( n =452,633) and identified 123 loci of which 60 replicated in 23andMe research participants ( n =541,333). Findings included missense variants in established drug targets ( HCRTR1, HCRTR2 ), genes with roles in arousal ( TRPC6, PNOC ), and genes suggesting an obesity-hypersomnolence pathway ( PNOC, PATJ ). Signals were concordant with accelerometer-measured daytime inactivity duration and 33 signals colocalized with signals for other sleep phenotypes. Cluster analysis identified 3 clusters suggesting distinct nap-promoting mechanisms with heterogeneous associations with cardiometabolic outcomes. Mendelian randomization showed potential causal links between more frequent daytime napping and higher systolic blood pressure, diastolic blood pressure, and waist circumference.