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|Title:||Genome-wide association analyses of sleep disturbance traits identify new loci and highlight shared genetics with neuropsychiatric and metabolic traits|
|Citation:||Nature Genetics, 2017; 49(2):274-281|
|Publisher:||NATURE PUBLISHING GROUP|
|Jacqueline M Lane, Jingjing Liang, Irma Vlasac, Simon G Anderson, David A Bechtold, Jack Bowden, Richard Emsley, Shubhroz Gill, Max A Little, Annemarie I Luik, Andrew Loudon, Frank A J L Scheer, Shaun M Purcell, Simon D Kyle, Deborah A Lawlor, Xiaofeng Zhu, Susan Redline, David W Ray, Martin K Rutter, Richa Saxena|
|Abstract:||Chronic sleep disturbances, associated with cardiometabolic diseases, psychiatric disorders and all-cause mortality¹’², affect 25–30% of adults worldwide³. Although environmental factors contribute substantially to self-reported habitual sleep duration and disruption, these traits are heritable⁴¯⁹ and identification of the genes involved should improve understanding of sleep, mechanisms linking sleep to disease and development of new therapies. We report single- and multiple-trait genome-wide association analyses of self-reported sleep duration, insomnia symptoms and excessive daytime sleepiness in the UK Biobank (n = 112,586). We discover loci associated with insomnia symptoms (near MEIS1, TMEM132E, CYCL1 and TGFBI in females and WDR27 in males), excessive daytime sleepiness (near AR–OPHN1) and a composite sleep trait (near PATJ (INADL) and HCRTR2) and replicate a locus associated with sleep duration (at PAX8). We also observe genetic correlation between longer sleep duration and schizophrenia risk (rg = 0.29, P = 1.90 × 10−¹³) and between increased levels of excessive daytime sleepiness and increased measures for adiposity traits (body mass index (BMI): rg = 0.20, P = 3.12 × 10⁻⁹; waist circumference: rg = 0.20, P = 2.12 × 10⁻⁷).|
|Keywords:||Behavioural genetics; genome-wide association studies|
|Rights:||© 2017 Nature America, Inc., part of Springer Nature. All rights reserved.|
|Appears in Collections:||Medicine publications|
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