Are some children genetically predisposed to poor sleep? A polygenic risk study in the general population

Abstract

BackgroundTwin studies show moderate heritability of sleep traits: 40% for insomnia symptoms and 46% for sleep duration. Genome‐wide association studies (GWAS) have identified genetic variants involved in insomnia and sleep duration in adults, but it is unknown whether these variants affect sleep during early development. We assessed whether polygenic risk scores for insomnia (PRS‐I) and sleep duration (PRS‐SD) affect sleep throughout early childhood to adolescence.MethodsWe included 2,458 children of European ancestry (51% girls). Insomnia‐related items of the Child Behavior Checklist were reported by mothers at child's age 1.5, 3, and 6 years. At 10–15 years, the Sleep Disturbance Scale for Children and actigraphy were assessed in a subsample (N = 975). Standardized PRS‐I and PRS‐SD (higher scores indicate genetic susceptibility for insomnia and longer sleep duration, respectively) were computed at multiple p‐value thresholds based on largest GWAS to date.ResultsChildren with higher PRS‐I had more insomnia‐related sleep problems between 1.5 and 15 years (BPRS‐I < 0.001 = .09, 95% CI: 0.05; 0.14). PRS‐SD was not associated with mother‐reported sleep problems. A higher PRS‐SD was in turn associated with longer actigraphically estimated sleep duration (BPRS‐SD < 5e08 = .05, 95% CI: 0.001; 0.09) and more wake after sleep onset (BPRS‐SD < 0.005 = .25, 95% CI: 0.04; 0.47) at 10–15 years, but these associations did not survive multiple testing correction.ConclusionsChildren who are genetically predisposed to insomnia have more insomnia‐like sleep problems, whereas those who are genetically predisposed to longer sleep have longer sleep duration, but are also more awake during the night in adolescence. This indicates that polygenic risk for sleep traits, based on GWAS in adults, affects sleep already in children.