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P017 Differences in genetic risk for insomnia, hypersomnia and chronotype in bipolar disorder subtypes
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  1. Katie JS Lewis1,2,
  2. Alexander Richards1,
  3. Robert Karlsson3,
  4. Ganna Leonenko1,
  5. Samuel E Jones4,
  6. Hannah Jones5,6,7,
  7. Katherine Gordon-Smith8,
  8. Liz Forty1,
  9. Valentina Escott-Price1,
  10. Michael J Owen1,2,
  11. Michael N Weedon4,
  12. Lisa Jones8,
  13. Nick Craddock1,2,
  14. Ian Jones1,2,
  15. Mikael Landén3,9,
  16. Michael C O’Donovan1,2 and
  17. Arianna Di Florio1,2
  1. 1Medical Research Council Centre for Neuropsychiatric Genetics and Genomics, Institute of Psychological Medicine and Clinical Neurosciences, School of Medicine, Cardiff University, Cardiff, UK
  2. 2National Centre for Mental Health, Cardiff University, Cardiff, UK
  3. 3Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden
  4. 4Genetics of Complex Traits, University of Exeter Medical School, Exeter, UK
  5. 5Centre for Academic Mental Health, Population Health Sciences, Bristol Medical School, University of Bristol, Bristol, UK
  6. 6Medical Research Council (MRC) Integrative Epidemiology Unit (IEU), University of Bristol, Bristol, UK
  7. 7NIHR Biomedical Research Centre at University Hospitals Bristol NHS Foundation Trust and the University of Bristol, Bristol, UK
  8. 8Department of Psychological Medicine, University of Worcester, Worcester, UK
  9. 9Institute of Neuroscience and Physiology, Sahlgenska Academy at the Gothenburg University, Gothenburg, Gothenburg, Sweden

Abstract

Introduction Insomnia, hypersomnia and evening chronotype are common in bipolar disorder (BD) but research examining the role of genetics is mixed. Stratifying by bipolar subtypes could elucidate this relationship and inform sleep and BD research. Aim: to determine whether genetic liability to insomnia, hypersomnia and chronotype differ between bipolar subtypes (type 1, BD-I or type 2, BD-II).

Method Case-control study of 4672 participants with BD (67% female, 3404 BD-I, 1268 BD-II) enrolled in the Bipolar Disorder Research Network and 5714 controls (49% female) recruited from the 1958 British Birth Cohort and UK Blood Service. All participants were of European ancestry. BD subtypes were determined by semi-structured psychiatric interview and case notes. Genetic liability to sleep traits was assessed using genetic risk scores (GRS), which were derived using alleles from genome-wide association studies of insomnia, sleep duration, daytime sleepiness and chronotype. Analyses used multinomial regression to determine whether GRS for insomnia, hypersomnia (daytime sleepiness or sleep duration) and chronotype were associated with BD-I or BD-II when compared to controls.

Results Insomnia GRS were associated with increased risk of BD-II (RR=1.14, 95% CI=1.07–1.21, P=8.26 × 10–5) but not BD-I (RR=0.98, 95% CI=0.94–1.03, P=0.409) relative to controls. Sleep duration GRS were associated with increased relative risk of BD-I (RR=1.10, 95% CI=1.06–1.15, P=1.13 × 10–5), but not BD-II (RR=0.99, 95% CI=0.93–1.06, P=0.818). Daytime sleepiness and chronotype GRS did not distinguish bipolar subtypes.

Discussion Bipolar subtypes differ in genetic liability to insomnia and sleep duration, providing further evidence that bipolar subtypes should be considered separately in research on sleep in BD. The distinct findings for sleep duration and daytime sleepiness support existing literature suggesting that these are distinct subtypes of hypersomnia.

http://dx.doi.org/10.1136/bmjresp-2019-bssconf.17

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