Abstract
Daytime napping is a common, heritable behavior, but its genetic basis and causal relationship with cardiometabolic health remain unclear. Here, we perform a genome-wide association study of self-reported daytime napping in the UK Biobank (n = 452,633) and identify 123 loci of which 61 replicate in the 23andMe research cohort (n = 541,333). Findings include missense variants in established drug targets for sleep disorders (HCRTR1, HCRTR2), genes with roles in arousal (TRPC6, PNOC), and genes suggesting an obesity-hypersomnolence pathway (PNOC, PATJ). Association signals are concordant with accelerometer-measured daytime inactivity duration and 33 loci colocalize with loci for other sleep phenotypes. Cluster analysis identifies three distinct clusters of nap-promoting mechanisms with heterogeneous associations with cardiometabolic outcomes. Mendelian randomization shows potential causal links between more frequent daytime napping and higher blood pressure and waist circumference.
14 Authors
- Hassan S. Dashti
- Iyas Daghlas
- Jacqueline M. Lane
- Yunru Huang
- Miriam S. Udler
- Heming Wang
- Hanna M. Ollila
- Samuel E. Jones
- Jaegil Kim
- Andrew R. Wood
- Michael N. Weedon
- Stella Aslibekyan
- Marta Garaulet
- Richa Saxena
1 Application
Application ID | Title |
6818 | Sleep and chronotype and their causal links with cardiometabolic and chronic inflammatory diseases |