Genome-wide association analysis of self-reported daytime sleepiness identifies 42 loci that suggest biological subtypes

Heming Wang, Jacqueline M. Lane, Samuel E. Jones, Hassan S. Dashti, Hanna M. Ollila, Andrew R. Wood, Vincent T. van Hees, Ben Brumpton, Bendik S. Winsvold, Katri Kantojärvi, Teemu Palviainen, Brian E. Cade, Tamar Sofer, Yanwei Song, Krunal Patel, Simon G. Anderson, David A. Bechtold, Jack Bowden, Richard Emsley, Simon D. Kyle, Max A. Little, Andrew S. Loudon, Frank A. J. L. Scheer, Shaun M. Purcell, Rebecca C. Richmond, Kai Spiegelhalder, Jessica Tyrrell, Xiaofeng Zhu, Christer Hublin, Jaakko A. Kaprio, Kati Kristiansson, Sonja Sulkava, Tiina Paunio, Kristian Hveem, Jonas B. Nielsen, Cristen J. Willer, John-Anker Zwart, Linn B. Strand, Timothy M. Frayling, David Ray, Deborah A. Lawlor, Martin K. Rutter, Michael N. Weedon, Susan Redline and Richa Saxena ()
Additional contact information
Heming Wang: Brigham and Women’s Hospital and Harvard Medical School
Jacqueline M. Lane: Broad Institute
Samuel E. Jones: University of Exeter Medical School
Hassan S. Dashti: Broad Institute
Hanna M. Ollila: Broad Institute
Andrew R. Wood: University of Exeter Medical School
Vincent T. van Hees: Netherlands eScience Center
Ben Brumpton: Norwegian University of Science and Technology
Bendik S. Winsvold: Norwegian University of Science and Technology
Katri Kantojärvi: National Institute for Health and Welfare
Teemu Palviainen: HiLIFE, University of Helsinki
Brian E. Cade: Brigham and Women’s Hospital and Harvard Medical School
Tamar Sofer: Brigham and Women’s Hospital and Harvard Medical School
Yanwei Song: Massachusetts General Hospital
Krunal Patel: Massachusetts General Hospital
Simon G. Anderson: The University of Manchester
David A. Bechtold: University of Manchester
Jack Bowden: MRC Integrative Epidemiology Unit at the University of Bristol
Richard Emsley: University of Manchester
Simon D. Kyle: University of Oxford
Max A. Little: Aston University
Andrew S. Loudon: University of Manchester
Frank A. J. L. Scheer: Brigham and Women’s Hospital and Harvard Medical School
Shaun M. Purcell: Brigham and Women’s Hospital and Harvard Medical School
Rebecca C. Richmond: MRC Integrative Epidemiology Unit at the University of Bristol
Kai Spiegelhalder: University of Freiburg
Jessica Tyrrell: University of Exeter Medical School
Xiaofeng Zhu: Case Western Reserve University
Christer Hublin: HiLIFE, University of Helsinki
Jaakko A. Kaprio: HiLIFE, University of Helsinki
Kati Kristiansson: National Institute for Health and Welfare
Sonja Sulkava: National Institute for Health and Welfare
Tiina Paunio: National Institute for Health and Welfare
Kristian Hveem: Norwegian University of Science and Technology
Jonas B. Nielsen: University of Michigan
Cristen J. Willer: University of Michigan
John-Anker Zwart: Oslo University Hospital and University of Oslo
Linn B. Strand: Norwegian University of Science and Technology
Timothy M. Frayling: University of Exeter Medical School
David Ray: John Radcliffe Hospital
Deborah A. Lawlor: MRC Integrative Epidemiology Unit at the University of Bristol
Martin K. Rutter: University of Manchester
Michael N. Weedon: University of Exeter Medical School
Susan Redline: Brigham and Women’s Hospital and Harvard Medical School
Richa Saxena: Brigham and Women’s Hospital and Harvard Medical School

Nature Communications, 2019, vol. 10, issue 1, 1-12

Abstract: Abstract Excessive daytime sleepiness (EDS) affects 10–20% of the population and is associated with substantial functional deficits. Here, we identify 42 loci for self-reported daytime sleepiness in GWAS of 452,071 individuals from the UK Biobank, with enrichment for genes expressed in brain tissues and in neuronal transmission pathways. We confirm the aggregate effect of a genetic risk score of 42 SNPs on daytime sleepiness in independent Scandinavian cohorts and on other sleep disorders (restless legs syndrome, insomnia) and sleep traits (duration, chronotype, accelerometer-derived sleep efficiency and daytime naps or inactivity). However, individual daytime sleepiness signals vary in their associations with objective short vs long sleep, and with markers of sleep continuity. The 42 sleepiness variants primarily cluster into two predominant composite biological subtypes - sleep propensity and sleep fragmentation. Shared genetic links are also seen with obesity, coronary heart disease, psychiatric diseases, cognitive traits and reproductive ageing.

Date: 2019
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DOI: 10.1038/s41467-019-11456-7

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