Morales-Muñoz Isabel, Kantojärvi Katri, Uhre Veli-Matti, Saarenpää-Heikkilä Outi, Kylliäinen Anneli, Pölkki Pirjo, Himanen Sari-Leena, Karlsson Linnea, Karlsson Hasse, Paavonen E Juulia, Paunio Tiina
Department of Public Health Solutions, Finnish Institute for Health and Welfare, Helsinki, Finland.
Institute for Mental Health, School of Psychology, University of Birmingham, Birmingham, UK.
Nat Sci Sleep. 2021 Feb 16;13:219-228. doi: 10.2147/NSS.S287163. eCollection 2021.
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.
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).
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.
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.
以往尚无研究探讨昼夜偏好的遗传背景对儿童睡眠的影响。在此,我们在芬兰的两个基于人群的队列中,研究了昼夜偏好易感性的遗传风险评分对幼儿睡眠发育的影响。
主要样本(儿童睡眠研究,CS)包括1420名婴儿(695名女孩),复制样本(芬兰脑研究,FB;962名女孩)包括2063名婴儿。在CS中,分别在3个月、8个月、18个月和24个月时评估家长报告的睡眠时间、入睡潜伏期和就寝时间;在FB中,分别在6个月、12个月和24个月时进行评估。在CS中,对365名8个月大的婴儿(168名女孩)和197名24个月大的婴儿(82名女孩)进行基于活动记录仪的入睡潜伏期和睡眠效率测量。在两个样本中均计算每个睡眠领域的平均标准分数。使用多基因风险评分(PRS)来量化晚睡倾向(PRSBestFit)和早睡倾向(PRS10kBest)的遗传风险。
在CS中,PRSBestFit与较长的入睡潜伏期和较晚的就寝时间相关,而PRS10kBest与较短的入睡潜伏期相关。昼夜偏好的遗传风险与入睡潜伏期之间的联系在FB中得到了重复,荟萃分析得出两个PRS值均存在关联(P<0.0005)(PRSBestFit:Z=3.55;PRS10kBest:Z=-3.68)。最后,PRSBestFit与8个月时基于活动记录仪测量的较低睡眠效率和较长入睡潜伏期相关。
晚睡倾向的遗传易感性与生命最初两年较长的入睡时间以及客观测量的较低睡眠效率有关。这些发现增进了我们对影响睡眠发育的生物学因素的理解,并有助于阐明幼儿期的生理睡眠结构。