RT Journal Article
SR Electronic
T1 Genome-wide association analyses of sleep disturbance traits identify new loci and highlight shared genetics with neuropsychiatric and metabolic traits
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 082792
DO 10.1101/082792
A1 Jacqueline M. Lane
A1 Jingjing Liang
A1 Irma Vlasac
A1 Simon G. Anderson
A1 David A. Bechtold
A1 Jack Bowden
A1 Richard Emsley
A1 Shubhroz Gill
A1 Max A. Little
A1 AnneMarie I. Luik
A1 Andrew Loudon
A1 Frank A.J.L. Scheer
A1 Shaun M. Purcell
A1 Simon D. Kyle
A1 Deborah A. Lawlor
A1 Xiaofeng Zhu
A1 Susan Redline
A1 David W. Ray
A1 Martin K. Rutter
A1 Richa Saxena
YR 2016
UL http://biorxiv.org/content/early/2016/10/24/082792.abstract
AB 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).