Runze Jana, Euser Saskia, Oosterman Mirjam, Dolan Conor V, Koopman-Verhoeff M Elisabeth, Bakermans-Kranenburg Marian J
Clinical Child and Family Studies, VU University Amsterdam, the Netherlands.
Leiden Consortium on Individual Development, Leiden University, the Netherlands.
Compr Psychoneuroendocrinol. 2021 Oct 14;8:100094. doi: 10.1016/j.cpnec.2021.100094. eCollection 2021 Nov.
To date, behavioral genetic studies investigated either sleep or cortisol levels in middle childhood, but not both simultaneously. Therefore, a pertinent question is the degree to which genetic factors and environmental factor contribute to the correlation between sleep and cortisol levels. To address this question, we employed the classical twin design. We measured sleep in 6-9-year-old twins (N = 436 twin pairs, "Together Unique" study) over four consecutive nights using actigraphy, and we measured morning cortisol on two consecutive days. Sleep duration, sleep efficiency, and wake episodes were used as indicators of sleep. Morning cortisol level was used as cortisol indicator. A structural equation model was fitted to estimate the contribution of additive genetic effects (A), shared (common) environmental effects, (C) and unique environmental effects (E) to phenotypic variances and covariances. Age, cohort, and sex were included as covariates. The heritability of sleep duration, sleep efficiency, and wake episodes were 52%, 45%, and 55%, respectively. Common environmental factors played no significant role. High genetic correlations between sleep duration and sleep efficiency and high genetic correlations between sleep efficiency and wake episodes were found. Shared environmental (29%) and unique environmental factors (53%) explained the variance in morning cortisol levels. Because the sleep and cortisol measures were found to be uncorrelated, we did not consider genetic and environmental contributions to the association between the sleep and cortisol measures. Our findings indicate that sleep duration, sleep efficiency, and wake episodes in children are mostly impacted by genetic factors and by unique environmental factors (including measurement error).
迄今为止,行为遗传学研究要么调查童年中期的睡眠情况,要么调查皮质醇水平,但未同时对两者进行研究。因此,一个相关问题是遗传因素和环境因素在多大程度上导致了睡眠与皮质醇水平之间的相关性。为了解决这个问题,我们采用了经典的双生子设计。我们使用活动记录仪连续四个晚上测量了6至9岁双胞胎(N = 436对双胞胎,“Together Unique”研究)的睡眠情况,并连续两天测量了早晨的皮质醇水平。睡眠时间、睡眠效率和觉醒次数被用作睡眠指标。早晨皮质醇水平被用作皮质醇指标。我们拟合了一个结构方程模型,以估计加性遗传效应(A)、共享(共同)环境效应(C)和独特环境效应(E)对表型方差和协方差的贡献。年龄、队列和性别被作为协变量纳入。睡眠时间、睡眠效率和觉醒次数的遗传率分别为52%、45%和55%。共同环境因素没有起到显著作用。我们发现睡眠时间和睡眠效率之间以及睡眠效率和觉醒次数之间存在高度遗传相关性。共享环境因素(29%)和独特环境因素(53%)解释了早晨皮质醇水平的方差。由于发现睡眠和皮质醇测量值不相关,我们没有考虑遗传和环境因素对睡眠与皮质醇测量值之间关联的贡献。我们的研究结果表明,儿童的睡眠时间、睡眠效率和觉醒次数主要受遗传因素和独特环境因素(包括测量误差)的影响。