Genome-wide association analyses of sleep disturbance traits identify new loci and highlight shared genetics with neuropsychiatric and metabolic traits
Jacqueline M. Lane,
Simon G Anderson,
David A. Bechtold,
Max A Little,
AnneMarie I Luik,
Frank AJL Scheer,
Shaun M. Purcell,
Simon D Kyle,
Deborah A. Lawlor,
David W. Ray,
Martin K Rutter,
Posted 24 Oct 2016
bioRxiv DOI: 10.1101/082792 (published DOI: 10.1038/ng.3749)
Posted 24 Oct 2016
Chronic sleep disturbances, associated with cardio-metabolic diseases, psychiatric disorders and all-cause mortality1,2, affect 25-30% of adults worldwide3. While environmental factors contribute importantly to self-reported habitual sleep duration and disruption, these traits are heritable4-9, 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 (rG=0.29, p=1.90x10-13) and between increased excessive daytime sleepiness and increased adiposity traits (BMI rG=0.20, p=3.12x10-09; waist circumference rG=0.20, p=2.12x10-07). Note: Martin K Rutter and Richa Saxena contributed equally and are joint senior authors on this manuscript.
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