GWAS in 446,118 European adults identifies 78 genetic loci for self-reported habitual sleep duration supported by accelerometer-derived estimates
Dashti HS., Jones SE., Wood AR., Lane JM., van Hees VT., Wang H., Rhodes JA., Song Y., Patel K., Anderson SG., Beaumont R., Bechtold DA., Bowden J., Cade BE., Garaulet M., Kyle SD., Little MA., Loudon AS., Luik AI., Scheer FAJL., Spiegelhalder K., Tyrrell J., Gottlieb DJ., Tiemeier H., Ray DW., Purcell SM., Frayling TM., Redline S., Lawlor DA., Rutter MK., Weedon MN., Saxena R.
<jats:title>Abstract</jats:title><jats:p>Sleep is an essential homeostatically-regulated state of decreased activity and alertness conserved across animal species, and both short and long sleep duration associate with chronic disease and all-cause mortality<jats:sup>1,2</jats:sup>. Defining genetic contributions to sleep duration could point to regulatory mechanisms and clarify causal disease relationships. Through genome-wide association analyses in 446,118 participants of European ancestry from the UK Biobank, we discover 78 loci for self-reported sleep duration that further impact accelerometer-derived measures of sleep duration, daytime inactivity duration, sleep efficiency and number of sleep bouts in a subgroup (<jats:italic>n</jats:italic>=85,499) with up to 7-day accelerometry. Associations are enriched for genes expressed in several brain regions, and for pathways including striatum and subpallium development, mechanosensory response, dopamine binding, synaptic neurotransmission, catecholamine production, synaptic plasticity, and unsaturated fatty acid metabolism. Genetic correlation analysis indicates shared biological links between sleep duration and psychiatric, cognitive, anthropometric and metabolic traits and Mendelian randomization highlights a causal link of longer sleep with schizophrenia.</jats:p>