Event Abstract

The genetic liability for insomnia is associated with lower amount of slow wave sleep in young and healthy individuals

  • 1 GIGA-Cyclotron Research Center In Vivo Imaging, University of Liege, Belgium
  • 2 Walloon Excellence in Life Sciences and Biotechnology (WELBIO), Belgium
  • 3 Université de Liège, Belgium
  • 4 Other
  • 5 Department of Neurology, University Hospital Liège, Belgium
  • 6 Surrey Sleep Research Centre, University of Surrey, United Kingdom
  • 7 GIGA-In silico Medicine, University of Liège, Belgium
  • 8 Netherlands Institute for Neuroscience (KNAW), Netherlands

Introduction. Identifying risk factors for insomnia in individuals that are likely to develop insomnia is needed to develop prevention strategies. Novel genetic tools using results of large case-control genome wide association studies (GWAS) allow to predict the liability for complex diseases based on full-genome common genetic variations. Here, we applied such tools to assess the link between the genetic liability of developing insomnia and sleep phenotypes in young and healthy adults not reporting any sleep complaint. Methods. Electroencephalography was recording during 8h baseline sleep in 360 healthy young male volunteers with normal sleep (aged 22.09 y ± 2.71). Sleep architecture, the percentage and latency of each sleep stage, and the total number, hourly rate and mean duration of awakenings were extracted from automatic sleep scoring (Aseega, Physip). Blood samples were collected in all participants to assess common Single Nucleotide Polymorphisms (SNPs) over the entire genome. Individual liability for insomnia was computed based on whole genome SNPs using the summary-statistics of a case-control GWAS seeking for genetic determinants of insomnia (Hammerschlag et al. Nat Genet 2017;49:1584–1592, https://ctg.cncr.nl/software/summary_statistics). Results. Generalized linear mixed model reveal significant associations of one's genetic risk score for insomnia with the percentage of sleep stage 2 (r = 0.13, p <0.05) and the percentage of sleep stage 3 (r = -0.12, p < 0.05). These results suggest that higher liability for insomnia is associated with lower percentage of slow wave sleep while it is associated with higher percentage of lighter sleep. The results remain significant after adjusting for age. Conclusion. These results show that individual genetic liability for insomnia is linked to sleep lower amount of what is considered most important to dissipate sleep need (i.e. slow wave sleep) in young and healthy individuals. These findings could help identifying novel prevention targets for insomnia.


FNRS, ULiège, ARC, FEDER, Welbio, FMRE, Clerdent Foundation

Keywords: insomnia, Sleep, EEG, Genetics, aging

Conference: Belgian Brain Congress 2018 — Belgian Brain Council, LIEGE, Belgium, 19 Oct - 19 Oct, 2018.

Presentation Type: e-posters


Citation: Ghaemmaghami P, Muto V, Jaspar M, Meyer C, Elansary M, VanEgroo M, Berthomier C, Lambot E, Brandewinder M, Luxen A, Degueldre C, Salmon E, Archer SN, Phillips C, Dijk D, Posthuma D, Van Someren E, Collette F, Georges M, Maquet P and Vandewalle G (2019). The genetic liability for insomnia is associated with lower amount of slow wave sleep in young and healthy individuals. Front. Neurosci. Conference Abstract: Belgian Brain Congress 2018 — Belgian Brain Council. doi: 10.3389/conf.fnins.2018.95.00069

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Received: 23 Aug 2018; Published Online: 17 Jan 2019.

* Correspondence: Dr. Pouya Ghaemmaghami, GIGA-Cyclotron Research Center In Vivo Imaging, University of Liege, Liège, Liège, 4000, Belgium, ghaemmaghami.pouya@gmail.com

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