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The interaction between polygenic risk and environmental influences

A direct test of the 3P model of insomnia in adolescents

Bibliographic Data

ID21344908
AuthorsJuan J Madrid-Valero (0000-0002-3450-1159, Department of Health Psychology, Faculty of Health Sciences University of Alicante Alicante Spain, corresponding author), Nicola L Barclay (0000-0002-6500-9909, Centre for Statistics in Medicine, Nuffield Department of Orthopaedics, Rheumatology, and Musculoskeletal Sciences University of Oxford Oxford UK), Alice M Gregory (0000-0003-2222-7823, Department of Psychology Goldsmiths, University of London London UK, corresponding author)
Year2024
Volume65
Issue3
Pages308-315
Publication date2024-03-01
Open AccessYes
TypeARTICLE
VenueJournal of Child Psychology and Psychiatry (JOURNAL)
Journal identifiersISSN: 0021-9630 • E-ISSN: 1469-7610
PublisherWiley (PUBLISHER • GB)
DOI10.1111/jcpp.13895
PMID37792459
OpenAlexW4387326767
LanguageEN
References cited46

BACKGROUND: Stress is a universal phenomenon and one of the most common precipitants of insomnia. However, not everyone develops insomnia after experiencing a stressful life event. This study aims to test aspects of Spielman's '3P model of insomnia' (during adolescence) by exploring the extent to which: (a) insomnia symptoms are predicted by polygenic scores (PGS); (b) life events predict insomnia symptoms; (c) the interaction between PGS and life events contribute to the prediction of insomnia symptoms; (d) gene-environment interaction effects remain after controlling for sex. METHODS: The sample comprised 4,629 twins aged 16 from the Twin Early Development Study who reported on their insomnia symptoms and life events. PGS for insomnia were calculated. In order to test the main hypothesis of this study (a significant interaction between PGS and negative life events), we fitted a series of mixed effect regressions. RESULTS: The best fit was provided by the model including sex, PGS for insomnia, negative life events, and their interactions (AIC = 26,158.7). Our results show that the association between insomnia symptoms and negative life events is stronger for those with a higher genetic risk for insomnia. CONCLUSIONS: This work sheds light on the complex relationship between genetic and environmental factors implicated for insomnia. This study has tested for the first time the interaction between genetic predisposition (PGS) for insomnia and environmental stressors (negative life events) in adolescents. This work represents a direct test of components of Spielman's 3P model for insomnia which is supported by our results

Biology · Heritability · Insomnia · Primary Insomnia · Psychiatry · Sleep disorder · Stressor · Structural equation modeling · Twin study · Clinical Psychology · Cognitive Abilities and Testing · Genetic Associations and Epidemiology · Genetics · Medicine · Psychology · Sleep and related disorders

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