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<jats:p>Chronic sleep disturbances, associated with cardio-metabolic diseases, psychiatric disorders and all-cause mortality<jats:sup>1,2</jats:sup>, affect 25–30% of adults worldwide<jats:sup>3</jats:sup>. While environmental factors contribute importantly to self-reported habitual sleep duration and disruption, these traits are heritable<jats:sup>4–9</jats:sup>, 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 <jats:italic>MEIS1, TMEM132E, CYCL1, TGFBI</jats:italic> in females and <jats:italic>WDR27</jats:italic> in males), excessive daytime sleepiness (near <jats:italic>AR/OPHN1</jats:italic>) and a composite sleep trait (near <jats:italic>INADL</jats:italic> and <jats:italic>HCRTR2</jats:italic>), as well as replication of a locus for sleep duration (at <jats:italic>PAX-8</jats:italic>). Genetic correlation was observed between longer sleep duration and schizophrenia (r<jats:sub>G</jats:sub>=0.29, <jats:italic>p</jats:italic>=1.90x10<jats:sup>−13</jats:sup>) and between increased excessive daytime sleepiness and increased adiposity traits (BMI r<jats:sub>G</jats:sub>=0.20, <jats:italic>p=</jats:italic>3.12x10<jats:sup>−09</jats:sup>; waist circumference r<jats:sub>G</jats:sub>=0.20, <jats:italic>p=</jats:italic>2.12x10<jats:sup>−07</jats:sup>).</jats:p>

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Journal article


Cold Spring Harbor Laboratory

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