A twin and molecular genetics study of sleep paralysis and associated factors
Dan Denis, C. French, R. Rowe, H. Zavos, P. Nolan, M. Parsons, A. Gregory
Journal of Sleep Research February 9, 2015 DOI: 10.1111/jsr.12282 (opens in new tab) via Semantic Scholar
Summary
AI-generated from the abstractSleep paralysis is moderately heritable (53%) in a UK sample of 862 twins and siblings aged 22–32 years. Poor sleep quality, anxiety symptoms, and exposure to threatening events were each independently associated with sleep paralysis. Variants in the PER2 gene showed some association, but this did not survive correction for multiple testing. The authors conclude that factors disrupting sleep cycles appear linked to sleep paralysis and that future research should explore circadian-rhythm and sleep-homeostasis polymorphisms.
Study at a glance
| Characteristics | Observational cohort (twin/sibling study) Peer reviewed |
|---|---|
| Sample size | 862 |
| Population | Twins and siblings aged 22–32 years from England and Wales (34% male) |
| Keywords | Psychology Medicine Biology |
| Key finding | Sleep paralysis is moderately heritable (53%), and self-reported sleep quality, anxiety symptoms, and threatening events are each independently associated with it. |
Abstract
Sleep paralysis is a relatively common but under‐researched phenomenon. In this paper we examine prevalence in a UK sample and associations with candidate risk factors. This is the first study to investigate the heritability of sleep paralysis in a twin sample and to explore genetic associations between sleep paralysis and a number of circadian expressed single nucleotide polymorphisms. Analyses are based on data from the Genesis1219 twin/sibling study, a community sample of twins/siblings from England and Wales. In total, data from 862 participants aged 22–32 years (34% male) were used in the study. This sample consisted of monozygotic and dizygotic twins and siblings. It was found that self‐reports of general sleep quality, anxiety symptoms and exposure to threatening events were all associated independently with sleep paralysis. There was moderate genetic influence on sleep paralysis (53%). Polymorphisms in the PER2 gene were associated with sleep paralysis in additive and dominant models of inheritance—although significance was not reached once a Bonferroni correction was applied. It is concluded that factors associated with disrupted sleep cycles appear to be associated with sleep paralysis. In this sample of young adults, sleep paralysis was moderately heritable. Future work should examine specific polymorphisms associated with differences in circadian rhythms and sleep homeostasis further in association with sleep paralysis.