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Genetic determinants of daytime napping and effects on cardiometabolic health

By Hassan S Dashti, Iyas Daghlas, Jacqueline Lane, Yunru Huang, Miriam Udler, Heming Wang, Hanna Ollila, Samuel Edward Jones, Jaegil Kim, Andrew R. Wood, 23andMe Research Team, Sian Ellard, Stella Aslibekyan, Marta Garaulet, Richa Saxena

Posted 16 Jun 2020
medRxiv DOI: 10.1101/2020.06.12.20129858

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.

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