Sufficient sleep in childhood is fundamental to proper development as well as preventing behavioral or emotional complications later in adulthood (Gregory & Sadeh, 2012; Bruni, 2010). Sleep is controlled by a 24-hour cycle of hormonal regulation termed the circadian rhythm, which is controlled by different environmental inputs such as light (Reppert & Weaver, 2002). Previous research has also demonstrated that light exposure at night can delay the night phase production of specific hormones that promote sleep (Zeitzer, Dijk, Kronauer, Brown, & Czeisler, 2004; Chang, Aeschbach, Duffy, & Czeisler, 2015), which in turn delays sleep onset. Such studies involving the effects that light may have on sleep have focused on adult subjects, however, and it is important to explore this idea in childhood to promote proper development. The first aim of this study was to examine the effects of light exposure in the hour before bedtime on different measures of sleep in middle childhood. The second aim was to determine the genetic and environmental contributions to light exposure and sleep. A diverse sample of 490 twin children was assessed at 8 years of age. Twins followed a week long protocol in which they wore actigraph watches that collected data on both light and sleep. Zero-order correlations with subsequent multilevel regression analyses showed that any light exposure in the hour before bedtime was significantly positively associated with sleep onset latency. Twin intraclass correlations indicated no heritability for light exposure, but did indicate some heritability ranging from 7-66% for the sleep indicators. Overall, these findings regarding the impacts of sleep in childhood build upon an area of research that has only been explored in adulthood. These impacts of light on sleep in childhood suggest that possible interventions ought to be explored for implementation to minimize the long-term effects of altered sleeping patterns in childhood.

This study examined whether social support available to parents moderated the heritability of parent-reported social approach at 12 months (N = 286 twin pairs, 52.00% female) and social competence at 30 months (N = 259 twin pairs, 53.30% female). Genetic and environmental covariance across age is also reported. Social support consistently moderated genetic influences on children’s social approach and competence, such that heritability was highest when parents reported low social support. Shared environment was not moderated by social support and explained continuity across age. Findings provide further evidence that genetic and environmental influences on development vary across context. When parents are supported, environmental influences on children’s social competence are larger, perhaps because support helps parents provide a broadly promotive environment.

The purpose of the current study was to use structural equation modeling-based quantitative genetic models to characterize latent genetic and environmental influences on proneness to three discrete negative emotions in middle childhood, according to mother-report, father-report and in-home observation. One primary aim was to test the extent to which covariance among the three emotions could be accounted for by a single, common genetically- and environmentally-influenced negative emotionality factor. A second aim was to examine the extent to which different reporters appeared to be tapping into the same genetically- and environmentally-influenced aspects of each emotion. According to mother- and father-report, moderate to high genetic influences were evident for all emotions, with mother- and father-report of fear and father-report of anger showing the highest heritability. Significant common environmental influences were also found for mother-report of anger and sadness in both univariate and multivariate models. For observed emotion, anger was moderately heritable with no evidence for common environmental variance, but sadness, object fear and social fear all showed modest to moderate common environmental influences and no significant genetic variance. In addition, cholesky decompositions examining genetic and environmental influences across reporter suggested that despite considerable overlap between mother-report and father-report, there was also reporter-specific variance on anger, sadness, and fear. Specifically, there were significant common environmental influences on mother-report of anger- and sadness that were not shared with father-report, and genetic influences on father-report of sadness and fear that were not shared with mother-report. In-home observations were not highly correlated enough with parent-report to support multivariate analysis for any emotion. Finally, according to both mother- and father-report, a single set of genetic and environmental influences was sufficient to account for covariance among all three negative emotions. However, fear was primarily explained by genetic influences not shared with other emotions, and anger also showed considerable emotion-specific genetic variance. In both cases, findings support the value of a more emotion-specific approach to temperament, and highlight the need to consider distinctions as well as commonalities across emotions, reporters and situations.