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Biological and clinical insights from genetics of insomnia symptoms

Research output: Contribution to journalArticle

  • Jacqueline M. Lane
  • Samuel E Jones
  • Hassan S Dashti
  • Jack Bowden
  • Deborah A. Lawlor
  • Martin K Rutter
  • Michael N Weedon
  • Richa Saxena
Original languageEnglish
Pages (from-to)387–393
Number of pages7
JournalNature Genetics
Volume51
Issue number3
Early online date25 Feb 2019
DOIs
DateAccepted/In press - 25 Jan 2019
DateE-pub ahead of print - 25 Feb 2019
DatePublished (current) - Mar 2019

Abstract

Insomnia is a common disorder linked with adverse long-term medical and psychiatric outcomes. The underlying pathophysiological processes and causal relationships of insomnia with disease are poorly understood. Here we identified 57 loci for self-reported insomnia symptoms in the UK Biobank (n = 453,379) and confirmed their effects on self-reported insomnia symptoms in the HUNT Study (n = 14,923 cases and 47,610 controls), physician-diagnosed insomnia in the Partners Biobank (n = 2,217 cases and 14,240 controls), and accelerometer-derived measures of sleep efficiency and sleep duration in the UK Biobank (n = 83,726). Our results suggest enrichment of genes involved in ubiquitin-mediated proteolysis and of genes expressed in multiple brain regions, skeletal muscle, and adrenal glands. Evidence of shared genetic factors was found between frequent insomnia symptoms and restless legs syndrome, aging, and cardiometabolic, behavioral, psychiatric, and reproductive traits. Evidence was found for a possible causal link between insomnia symptoms and coronary artery disease, depressive symptoms, and subjective well-being.

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    Rights statement: This is the accepted author manuscript (AAM). The final published version (version of record) is available online via Springer Nature at https://doi.org/10.1038/s41588-019-0361-7 . Please refer to any applicable terms of use of the publisher.

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