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ABSTRACT
Objective/Background
Stress is a strong predictor for poor sleep quality. However, little is known about the mechanism of this association or the respective contribution of genetic and environmental factors. This study aims to investigate general distress as a mediator and cognitive/emotional control as a moderator in the stress–sleep relationship and estimate the influence of gene and environment in this mechanism using a national representative sample.
Participants
1,255 middle-aged and elderly Americans and a subset of 296 twins.
Methods
The Pittsburgh Sleep Quality Index, the Perceived Stress Scale, the Mood and Anxiety Symptom Questionnaire and the Self-Control Scale assessed sleep quality, perceived stress, general distress, and emotional/cognitive control. Structural equation modeling was used to test the mediating and moderating effect. ACE models on MZ and DZ twins were used to separate the contribution of genetic and environmental factors. Finally, a co-twin design was nested in the SEM to control for the genetic and familial confounds in the stress–sleep relationship.
Results
General distress mediated the relationship between stress and sleep while emotional/cognitive control buffered the impact of stress on general distress. 7.69% of the variance in sleep quality was explained by genetic and familial factors and 8.26% was explained by individual-specific factors. Emotional/cognitive control only moderated the individual-specific association between stress and sleep.
Conclusions
Gene/family factors and individual factors explained an equivalent proportion of the stress–sleep relationship. The genetic and familial association between stress and sleep is more robust, whereas the individual-specific association can be buffered by regulation strategies.
Author contributions
Yueqin Hu contributed to the conception of the work, data analysis, result interpretation, drafting the manuscript and critical revision. Marieke Visser contributed to literature review, data analysis, drafting the manuscript and critical revision. Sierra Kaiser contributed to data analysis and critical revision. All authors approved the final version to be published.
Disclosure statement
No potential conflict of interest was reported by the authors.