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Chronic sleep disturbances, associated with cardio-metabolic diseases, psychiatric disorders and all-cause mortality 1,2 , affect 25–30% of adults worldwide 3 . While environmental factors contribute importantly to self-reported habitual sleep duration and disruption, these traits are heritable 4–9 , and gene identification should improve our understanding of sleep function, mechanisms linking sleep to disease, and development of novel therapies. We report single and multi-trait genome-wide association analyses (GWAS) of self-reported sleep duration, insomnia symptoms including difficulty initiating and/or maintaining sleep, and excessive daytime sleepiness in the UK Biobank (n=112,586), with discovery of loci for insomnia symptoms (near MEIS1, TMEM132E, CYCL1, TGFBI in females and WDR27 in males), excessive daytime sleepiness (near AR/OPHN1 ) and a composite sleep trait (near INADL and HCRTR2 ), as well as replication of a locus for sleep duration (at PAX-8 ). Genetic correlation was observed between longer sleep duration and schizophrenia (r G =0.29, p =1.90x10 −13 ) and between increased excessive daytime sleepiness and increased adiposity traits (BMI r G =0.20, p= 3.12x10 −09 ; waist circumference r G =0.20, p= 2.12x10 −07 ).

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