Despite identified concurrent socioeconomic disparities in children's sleep, little research has examined pathways explaining such associations. This study examined the quality of the home environment as a direct predictor of sleep and potential mediator of associations between early life socioeconomic status and objective and subjective indicators of sleep in middle childhood. A socioeconomically and ethnically diverse sample of 381 twin children (50% female; 46.6% lower middle class or living at or below the poverty line; 26% Hispanic/Latino) were assessed at 12 months for SES and eight years using gold-standard home environment interviews and actigraphy-measured sleep. Multilevel mediation path models indicated that lower early SES and lower quality concurrent home environments were associated with shorter sleep durations, longer sleep latencies, and greater sleep timing variability. The home environment significantly mediated associations with sleep duration and sleep timing variability. The findings illustrate an important target in the prevention of poor childhood and adolescent sleep.
Twin factor mixture modeling was used to identify temperament profiles, while simultaneously estimating a latent factor model for each profile with a sample of 787 twin pairs (Mage =7.4 years; SD = .84; 49% female; 88.3% Caucasian), using mother- and father-reported temperament. A 4-profile, 1-factor model fit the data well. Profiles included ‘Regulated, Typical Reactive’, ‘Well-regulated, Positive Reactive’, ‘Regulated, Surgent’, and ‘Dysregulated, Negative Reactive.’ All profiles were heritable, with heritability lower and shared environment also contributing to membership in the ‘Regulated, Typical Reactive’ and ‘Dysregulated, Negative Reactive’ profiles.
This study examined the extent to which subordinate dimensions of negative emotionality were genetically and environmentally distinct in a sample of 1316 twins (51% female, 85.8% Caucasian, primarily middle class, mean age = 7.87 years, SD = .93), recruited from Wisconsin hospital birth records between 1989 and 2004. Cholesky, independent pathway, and common pathway models were fitted for mother-report, father-report, and in-home observation of temperament. Although findings support the use of negative emotionality, there were heritable aspects of anger and fear not explained by a common genetic factor, and shared environmental influences common to anger and sadness but not fear. Observed fear was independent from observed anger and sadness. Distinctions support specificity in measurement when considering implications for child development.
Development involves synergistic interplay among genotypes and the physical and cultural environments, and integrating genetics into experimental designs that manipulate the environment can improve understanding of developmental psychopathology and intervention efficacy. Consistent with Differential Susceptibility Theory, individuals can vary in their sensitivity to environmental conditions including intervention for reasons including their genotype. As a consequence, understanding genetic influences on intervention response is critical. Empirically, we tested an interaction between a genetic index representing sensitivity to the environment and the Family Check-Up intervention. Participants were drawn from the Early Steps Multisite randomized prevention trial that included a low income and racial/ethnically diverse sample of children and their families followed longitudinally (n=515). As hypothesized, polygenic sensitivity to the environment moderated the effects of the intervention on 10-year-old children’s symptoms of internalizing psychopathology, such that children who were genetically sensitive and were randomly assigned to the intervention had fewer symptoms of child psychopathology than genetically sensitive children assigned to the control condition. A significant difference in internalizing symptoms assessed with a clinical interview emerged between the intervention and control groups for those 0.493 standard deviations above the mean on polygenic sensitivity, or 25% of the sample. Similar to personalized medicine, it is time to understand individual and socio-cultural differences in treatment response and individualize psychosocial interventions to reduce the burden of child psychopathology and maximize wellbeing for children growing up in a wide range of physical environments and cultures.
Previous approaches for creating polygenic risk scores (PRSs) do not explicitly consider the biological or developmental relevance of the genetic variants selected for inclusion. We applied gene set enrichment analysis to meta-GWAS data to create developmentally targeted, functionally informed PRSs. Using two developmentally matched meta-GWAS discovery samples, separate PRSs were formed, then examined in time-varying effect models of aggression in a second, longitudinal sample of children (
n
=
515, 49% female) in early childhood (2–5 years old), and middle childhood (7.5–10.5 years old). Functional PRSs were associated with aggression in both the early and middle childhood models.
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