@article {Dashti274977, author = {Hassan S Dashti and Samuel E Jones and Andrew R Wood and Jacqueline M Lane and Vincent T. van Hees and Heming Wang and Jessica A Rhodes and Yanwei Song and Krunal Patel and Simon G Anderson and Robin Beaumont and David A Bechtold and Jack Bowden and Brian E Cade and Marta Garaulet and Simon D Kyle and Max A Little and Andrew S Loudon and Annemarie I Luik and Frank AJL Scheer and Kai Spiegelhalder and Jessica Tyrrell and Daniel J Gottlieb and Henning Tiemeier and David W Ray and Shaun M Purcell and Timothy M Frayling and Susan Redline and Deborah A Lawlor and Martin K Rutter and Michael N Weedon and Richa Saxena}, title = {GWAS in 446,118 European adults identifies 78 genetic loci for self-reported habitual sleep duration supported by accelerometer-derived estimates}, elocation-id = {274977}, year = {2018}, doi = {10.1101/274977}, publisher = {Cold Spring Harbor Laboratory}, abstract = {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.}, URL = {https://www.biorxiv.org/content/early/2018/04/19/274977}, eprint = {https://www.biorxiv.org/content/early/2018/04/19/274977.full.pdf}, journal = {bioRxiv} }