RT Journal Article SR Electronic T1 GWAS in 446,118 European adults identifies 78 genetic loci for self-reported habitual sleep duration supported by accelerometer-derived estimates JF bioRxiv FD Cold Spring Harbor Laboratory SP 274977 DO 10.1101/274977 A1 Hassan S Dashti A1 Samuel E Jones A1 Andrew R Wood A1 Jacqueline M Lane A1 Vincent T. van Hees A1 Heming Wang A1 Jessica A Rhodes A1 Yanwei Song A1 Krunal Patel A1 Simon G Anderson A1 Robin Beaumont A1 David A Bechtold A1 Jack Bowden A1 Brian E Cade A1 Marta Garaulet A1 Simon D Kyle A1 Max A Little A1 Andrew S Loudon A1 Annemarie I Luik A1 Frank AJL Scheer A1 Kai Spiegelhalder A1 Jessica Tyrrell A1 Daniel J Gottlieb A1 Henning Tiemeier A1 David W Ray A1 Shaun M Purcell A1 Timothy M Frayling A1 Susan Redline A1 Deborah A Lawlor A1 Martin K Rutter A1 Michael N Weedon A1 Richa Saxena YR 2018 UL http://biorxiv.org/content/early/2018/04/19/274977.abstract AB 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 mortality1,2. 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 (n=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.