Genome-wide association study identifies genetic loci for self-reported habitual sleep duration supported by accelerometer-derived estimates.

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Abstract

Sleep is an essential state of decreased activity and alertness but molecular factors regulating sleep duration remain unknown. Through genome-wide association analysis in 446,118 adults of European ancestry from the UK Biobank, we identify 78 loci for self-reported habitual sleep duration (p < 5 × 10-8; 43 loci at p < 6 × 10-9). Replication is observed for PAX8, VRK2, and FBXL12/UBL5/PIN1 loci in the CHARGE study (n = 47,180; p < 6.3 × 10-4), and 55 signals show sign-concordant effects. The 78 loci further associate with accelerometer-derived sleep duration, daytime inactivity, sleep efficiency and number of sleep bouts in secondary analysis (n = 85,499). Loci are enriched for pathways including striatum and subpallium development, mechanosensory response, dopamine binding, synaptic neurotransmission and plasticity, among others. Genetic correlation indicates shared links with anthropometric, cognitive, metabolic, and psychiatric traits and two-sample Mendelian randomization highlights a bidirectional causal link with schizophrenia. This work provides insights into the genetic basis for inter-individual variation in sleep duration implicating multiple biological pathways.

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Most cited references 36

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Self-reported and measured sleep duration: how similar are they?

Diane S. Lauderdale, Kristen Knutson, Lijing L. Yan … (2008)

Recent epidemiologic studies have found that self-reported duration of sleep is associated with obesity, diabetes, hypertension, and mortality. The extent to which self reports of sleep duration are similar to objective measures and whether individual characteristics influence the degree of similarity are not known. Eligible participants at the Chicago site of the Coronary Artery Risk Development in Young Adults Study were invited to participate in a 2003-2005 ancillary sleep study; 82% (n = 669) agreed. Sleep measurements collected in 2 waves included 3 days each of wrist actigraphy, a sleep log, and questions about usual sleep duration. We estimate the average difference and correlation between subjectively and objectively measured sleep by using errors-in-variables regression models. Average measured sleep was 6 hours, whereas the average from subjective reports was 6.8 hours. Subjective reports increased on average by 34 minutes for each additional hour of measured sleep. Overall, the correlation between reported and measured sleep duration was 0.47. Our model suggests that persons sleeping 5 hours over-reported their sleep duration by 1.2 hours, and those sleeping 7 hours over-reported by 0.4 hours. The correlations and average differences between self-reports and measured sleep varied by health, sociodemographic, and sleep characteristics. In a population-based sample of middle-aged adults, subjective reports of habitual sleep are moderately correlated with actigraph-measured sleep, but are biased by systematic over-reporting. The true associations between sleep duration and health may differ from previously reported associations between self-reported sleep and health.

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Ontogenetic development of the human sleep-dream cycle.

H Roffwarg, W Dement, Rubén Muzio (1966)

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A prospective study of self-reported sleep duration and incident diabetes in women.

N T Ayas, D. P. White, W K Al-Delaimy … (2003)

Short-term sleep restriction results in impaired glucose tolerance. To test whether habitually short sleep duration increases the risk of developing diabetes, we studied a cohort of 70,026 women enrolled in the Nurses Health Study, without diabetes at baseline, and who responded to a question about daily sleep duration in 1986. Subjects were followed until 1996 for the diagnosis of diabetes (1,969 cases). Long and short sleep durations were associated with an increased risk of diabetes diagnosis. The relative risks (RRs) for short (slept or =9 h per day) sleepers were 1.57 (95% CI 1.28-1.92) and 1.47 (1.19-1.80), respectively. After adjustment for BMI and a variety of confounders, the RR was not significantly increased for short sleepers (1.18 [0.96-1.44]) but remained modestly increased for long sleepers (1.29 [1.05-1.59]). We then performed a similar analysis using only symptomatic cases (n = 1,187). Adjusted RRs for symptomatic diabetes were modestly elevated in both short (1.34 [1.04-1.72]) and long (1.35 [1.04-1.75]) sleepers. Our data suggest that the association between a reduced self-reported sleep duration and diabetes diagnosis could be due to confounding by BMI, or sleep restriction may mediate its effects on diabetes through weight gain. Sleep restriction may be an independent risk factor for developing symptomatic diabetes.

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Author and article information

Journal

Journal ID (iso-abbrev): Nat Commun

Title: Nature communications

Publisher: Springer Science and Business Media LLC

ISSN (Electronic): 2041-1723

ISSN (Print): 2041-1723

Publication date (Electronic): Mar 07 2019

Volume: 10

Issue: 1

Affiliations

[1 ] Center for Genomic Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, 02114, MA, USA.

[2 ] Broad Institute, Cambridge, 02142, MA, USA.

[3 ] Genetics of Complex Traits, University of Exeter Medical School, Exeter, EX2 5DW, UK.

[4 ] Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, 02114, MA, USA.

[5 ] Netherlands eScience Center, Amsterdam, 1098 XG, The Netherlands.

[6 ] Division of Sleep and Circadian Disorders, Department of Medicine, Brigham and Women's Hospital, Boston, 02115, MA, USA.

[7 ] Division of Sleep Medicine, Harvard Medical School, Boston, 02115, MA, USA.

[8 ] Northeastern University College of Science, 176 Mugar Life Sciences, 360 Huntington Avenue, Boston, MA, 02015, USA.

[9 ] Division of Cardiovascular Sciences, School of Medical Sciences, Faculty of Biology, Medicine and Health, The University of Manchester, Manchester, M13 9PL, UK.

[10 ] Division of Endocrinology, Diabetes & Gastroenterology, School of Medical Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Manchester, M13 9PL, UK.

[11 ] MRC Integrative Epidemiology Unit at the University of Bristol, Bristol, BS8 2BN, UK.

[12 ] Population Health Sciences, Bristol Medical School, University of Bristol, Bristol, BS8 2BN, UK.

[13 ] Department of Physiology, University of Murcia, Murcia, 30100, Spain.

[14 ] IMIB-Arrixaca, Murcia, 30120, Spain.

[15 ] Sleep and Circadian Neuroscience Institute, Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, OX3 7LF, UK.

[16 ] Department of Mathematics, Aston University, Birmingham, B4 7ET, UK.

[17 ] Media Lab, Massachusetts Institute of Technology, Cambridge, 02139, MA, USA.

[18 ] Medical Chronobiology Program, Division of Sleep and Circadian Disorders, Departments of Medicine and Neurology, Brigham and Women's Hospital, Boston, 02115, MA, USA.

[19 ] Clinic for Psychiatry and Psychotherapy, Medical Centre - University of Freiburg, Faculty of Medicine, University of Freiburg, Freiburg, 79106, Germany.

[20 ] VA Boston Healthcare System, Boston, 02132, MA, USA.

[21 ] Deprtment of Social and Behavioral Science, Harvard TH Chan School of Public Health, Boston, 02115, MA, USA.

[22 ] Department of Epidemiology, Erasmus Medical Center, Rotterdam, 3015, The Netherlands.

[23 ] Department of Psychiatry, Brigham & Women's Hospital, Harvard Medical School, 02115, Boston, MA, USA.

[24 ] Departments of Medicine, Brigham and Women's Hospital and Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, 02115, MA, USA.

[25 ] Manchester Diabetes Centre, Manchester University NHS Foundation Trust, Manchester Academic Health Science Centre, Manchester, M13 9PL, UK.

[26 ] Center for Genomic Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, 02114, MA, USA. rsaxena@partners.org.

[27 ] Broad Institute, Cambridge, 02142, MA, USA. rsaxena@partners.org.

[28 ] Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, 02114, MA, USA. rsaxena@partners.org.

Article

Publisher Item ID: 10.1038/s41467-019-08917-4

DOI: 10.1038/s41467-019-08917-4

PMC ID: 6405943

PubMed ID: 30846698

SO-VID: e091d57a-5cc0-45af-b878-b1c0ca1b9eb3

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Genome-wide association study identifies genetic loci for self-reported habitual sleep duration supported by accelerometer-derived estimates.

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Most cited references 36

Self-reported and measured sleep duration: how similar are they?

Ontogenetic development of the human sleep-dream cycle.

A prospective study of self-reported sleep duration and incident diabetes in women.

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Cited by 198

Most referenced authors 7,946