Department of Health Psychology, Faculty of Health Sciences, University of Alicante, 03690, Alicante, Spain.
Department of Human Anatomy and Psychobiology, University of Murcia, Campus de Espinardo, 30100, Murcia, Spain.
Behav Genet. 2022 Sep;52(4-5):236-245. doi: 10.1007/s10519-022-10111-0. Epub 2022 Aug 25.
The genetic and environmental underpinnings of sleep quality have been widely investigated. However, less is known about the etiology of the different sleep quality components and their associations. Subjective sleep quality has been studied most commonly using the Pittsburgh Sleep Quality Index (PSQI). Therefore, this work aimed to study the structure of sleep quality dimensions in a population-based twin sample by examining the etiology of the associations among the PSQI components themselves and between them. The sample comprised 2129 participants from the Murcia Twin Registry. In order to study the phenotypic, genetic and environmental structure of the PSQI we used three alternative multivariate twin models including all seven sub-scales of the PSQI (subjective sleep quality, latency, duration, efficiency, disturbances, use of sleeping medication and daytime dysfunction): a multivariate model (with seven separate correlated factors), a common pathway model and an independent pathway model. The multivariate correlated factors model showed the best fit to the data. All twin models indicated significant genetic overlap among most of the PSQI components, except daytime dysfunction and use of sleep medication. Bivariate heritability explained between 25 and 50% of the covariance for most associations between dimensions. Furthermore, the common pathway model showed that around one third of the variance (0.32; CI 95% 0.18.0.43) of a latent factor common to all questionnaire dimensions is explained by genetic factors. Genetic influences on a latent factor common to all questionnaire dimensions produced the same heritability estimates as the PSQI global score. However, sleep quality dimensions showed considerable specificity regarding its genetic-environmental structure.
睡眠质量的遗传和环境基础已被广泛研究。然而，对于不同睡眠质量成分的病因及其关联知之甚少。主观睡眠质量通常使用匹兹堡睡眠质量指数 (PSQI) 进行研究。因此，这项工作旨在通过检查 PSQI 成分本身以及它们之间的关联的病因，研究基于人群的双胞胎样本中睡眠质量维度的结构。该样本包括来自 Murcia 双胞胎登记处的 2129 名参与者。为了研究 PSQI 的表型、遗传和环境结构，我们使用了三种替代的多变量双胞胎模型，包括 PSQI 的所有七个子量表（主观睡眠质量、潜伏期、持续时间、效率、干扰、使用睡眠药物和日间功能障碍）：多变量模型（有七个独立相关因素）、共同途径模型和独立途径模型。多变量相关因素模型最适合数据。所有双胞胎模型都表明，除了日间功能障碍和使用睡眠药物外，大多数 PSQI 成分之间存在显著的遗传重叠。双变量遗传率解释了大多数维度之间关联的协方差的 25%至 50%。此外，共同途径模型表明，所有问卷维度共有的潜在因素的方差的三分之一左右（0.32；95%CI 0.18.0.43）由遗传因素解释。遗传因素对所有问卷维度共有的潜在因素的影响产生了与 PSQI 总评分相同的遗传率估计值。然而，睡眠质量维度在其遗传-环境结构方面表现出相当大的特异性。
