The Effects of Genetic Background for Diurnal Preference on Sleep Development in Early Childhood

Nat Sci Sleep. 2021 Feb 16:13:219-228. doi: 10.2147/NSS.S287163. eCollection 2021.

Abstract

Purpose: No previous research has examined the impact of the genetic background of diurnal preference on children´s sleep. Here, we examined the effects of genetic risk score for the liability of diurnal preference on sleep development in early childhood in two population-based cohorts from Finland.

Participants and methods: The primary sample (CHILD-SLEEP, CS) comprised 1420 infants (695 girls), and the replication sample (FinnBrain, FB; 962 girls) 2063 infants. Parent-reported sleep duration, sleep-onset latency and bedtime were assessed at three, eight, 18 and 24 months in CS, and at six, 12 and 24 months in FB. Actigraphy-based sleep latency and efficiency were measured in CS in 365 infants at eight months (168 girls), and in 197 infants at 24 months (82 girls). Mean standard scores for each sleep domain were calculated in both samples. Polygenic risk scores (PRS) were used to quantitate the genetic risk for eveningness (PRSBestFit) and morningness (PRS10kBest).

Results: PRSBestFit associated with longer sleep-onset latency and later bedtime, and PRS10kBest related to shorter sleep-onset latency in CS. The link between genetic risk for diurnal preference and sleep-onset latency was replicated in FB, and meta-analysis resulted in associations (P<0.0005) with both PRS-values (PRSBestFit: Z=3.55; and PRS10kBest: Z=-3.68). Finally, PRSBestFit was related to actigraphy-based lower sleep efficiency and longer sleep latency at eight months.

Conclusion: Genetic liability to diurnal preference for eveningness relates to longer sleep-onset during the first two years of life, and to objectively measured lowered sleep efficiency. These findings enhance our understanding on the biological factors affecting sleep development, and contribute to clarify the physiological sleep architecture in early childhood.

Keywords: chronotype; cohorts; early childhood; genetic risk; sleep.

Grants and funding

This work was supported by The Academy of Finland (#134880 and #253346 to TP; #308588 to EJP, #308589 to LK; # 134950 and #253270 to HK; #277557 to OSH; #315035 to IMM; and #326631 to AK), the Signe and Ane Gyllenberg foundation, the Yrjö Jahnsson Foundation, the Foundation for Pediatric Research, the Finnish Cultural Foundation, the Competitive Research Financing of the Expert Responsibility area of Tampere University Hospital, the Arvo ja Lea Ylppö Foundation, Finnish State Grants for Clinical Research (ERVA), and The Medical Society of Tampere.