Reagan S. Breitenstein

Young children who are capable of regulating their behaviors and emotions are better able to meet the demands of the classroom environment (Blair, 2002; McCormick et al., 2015; O’Connor et al., 201...

Transitioning from high school to college can be challenging and put young adults at risk for problematic mental health, particularly for those with bullying victimization histories. Bullying detrimentally impacts psychological well-being and mental health, both concurrently and in the future. Social support positively influences college students’ emotional, social, and academic performance. However, few studies have examined the extent to which different types of bullying, as well as different sources of social support, may interact to predict mental health symptoms. Further, few studies examine associations between bullying victimization and mental health symptoms across the transition from high school to college. We examined three sources of social support (and their composite) measured during college as moderators between high school bullying victimization (traditional, cyberbullying) and college mental health (anxiety, depressive symptoms) in a sample of young adults from the Southeast United States (n = 329). Thus, we hypothesized that social support may protect college students from the harmful effects of bullying on mental health. Multivariate linear regressions revealed that higher levels of both traditional and cyberbullying during high school predicted worse mental health during college, and higher levels of social support in college predicted better concurrent mental health. However, social support did not moderate links between either type of bullying victimization in high school and mental health in college. Our findings provide evidence for institutions and educators regarding the importance of fostering social support (e.g., developing new friendships, maintaining existing support systems with close family or friends) for young adults as they transition to college.

Children’s poor sleep is a risk factor for lower cognitive functioning and internalizing and externalizing problems. It is unclear whether genetic and environmental influences vary based on sleep assessment and no studies to date have examined genetic and environmental contributions to links between multiple objective and subjective sleep indicators. Further, nearly all heritability studies rely on subjective parent- or self-report measures of sleep duration and problems. Given these gaps in the literature, we (1) modeled genetic and environmental influences on multiple objective and subjective sleep indicators and (2) estimated genetic and environmental covariances between objective and subjective sleep indicators in middle childhood. Participants were 608 twin children (MZ = 178, same-sex DZ = 234, opposite-sex DZ = 190) assessed at 8 years of age (SD = 0.63 years). Objective nighttime sleep duration, efficiency, sleep onset latency (SOL), midpoint time, and midpoint variability were collected from actigraph watches worn for 7 nights (M_nights = 6.83, SD = 0.62). Children’s nighttime sleep duration and daytime sleepiness were assessed via parent report. Findings suggested high additive genetic influence on objective sleep quantity and quality, whereas objective SOL, sleep midpoint time, midpoint variability, parent-reported sleep duration, and daytime sleepiness were largely influenced by the shared environment. Common genetic factors explained associations between objective sleep quantity and quality, but genetics did not account for links with parent-reported sleep duration, midpoint time, or midpoint variability. Thus, objective and parent-reported assessments of children’s sleep have unique genetic etiologies and should not be used interchangeably in the sleep literature.

Adverse experiences in childhood are associated with altered hypothalamic–pituitary–adrenal (HPA) axis function and negative health outcomes throughout life. It is now commonly accepted that abuse and neglect can alter epigenetic regulation of HPA genes. Accumulated evidence suggests harsh parenting practices such as spanking are also strong predictors of negative health outcomes. We predicted harsh parenting at 2.5 years old would predict HPA gene DNA methylation similarly to abuse and neglect, and cortisol output at 8.5 years old. Saliva samples were collected three times a day across 3 days to estimate cortisol diurnal slopes. Methylation was quantified using the Illumina Infinium MethylationEPIC array BeadChip (850 K) with DNA collected from buccal cells. We used principal components analysis to compute a summary statistic for CpG sites across candidate genes. The first and second components were used as outcome variables in mixed linear regression analyses with harsh parenting as a predictor variable. We found harsh parenting significantly predicted methylation of several HPA axis genes, including novel gene associations with AVPRB1, CRHR1, CRHR2, and MC2R (FDR corrected p < 0.05). Further, we found NR3C1 methylation predicted a steeper diurnal cortisol slope. Our results extend the current literature by demonstrating harsh parenting may influence DNA methylation similarly to more extreme early life experiences such as abuse and neglect. Further, we show NR3C1 methylation is associated with diurnal HPA function. Elucidating the molecular consequences of harsh parenting on health can inform best parenting practices and provide potential treatment targets for common complex disorders.

Rumination is an involuntary cognitive process theorized to prolong arousal and inhibit proper emotion regulation. Most available research has examined individual differences in cognitive dispositions to ruminate about stress as a risk marker for psychopathology and other health problems. This intensive longitudinal study extended previous research by examining day-to-day associations of rumination about stress with objectively-measured actigraph-based sleep and diurnal salivary cortisol activity. Sixty-one healthy participants (M_age = 20.91) completed up to five ecological momentary assessments (EMA) each day and wore actigraph wristwatches for eight days (N = 488). On three of these days, participants provided five saliva samples assayed for cortisol (N = 910). On average, greater daily stress levels were associated with shorter sleep duration and higher waking cortisol levels. In day-to-day analyses, greater daily stress levels, when combined with ruminating about daily stress more than usual, was associated with higher waking cortisol levels the following morning. Ruminating more than usual about daily stress, in the context of low-stress days, was also associated with flatter diurnal cortisol slopes the next day. These findings highlight the potential influences of daily stress, and rumination about stress, on sleep and diurnal cortisol activity – two important markers of health and well-being.

Individual differences in cognitive function are due to a combination of heritable and non-heritable factors. A large body of evidence from clinical, cognitive, and pharmacological neuroscience implicates dopaminergic gene variants as modulators of cognitive functions. Neuroepigenetic studies demonstrate environmental factors also influence complex phenotypes by affecting gene expression regulation. To evaluate the mechanism of environmental influence on cognitive abilities, we examined if epigenetic regulation of dopaminergic genes plays a role in cognition. Using a DNA methylation profiling microarray, we used a monozygotic (MZ) twin difference design to evaluate if co-twin differences in methylation of CpG sites near six dopaminergic genes predicted differences in response inhibition and memory performance. Studying MZ twins allows us to assess if environmentally driven differences in methylation affect differences in phenotype while controlling for the influence of genotype and shared family environment. Response inhibition was assessed with the flanker task and short-term and working memory were assessed with digit span recall. We found MZ co-twin differences in DRD4 gene methylation predicted differences in short-term memory. MZ differences in COMT, DBH, DAT1, DRD1, and DRD2 gene methylation predicted differences in response inhibition. Taken together, findings suggest methylation status of dopaminergic genes may influence cognitive functions in a dissociable manner. Our results highlight the importance of the epigenome and environment, over and above the influence of genotype, in supporting complex cognitive functions.

Children's sleep has both environmental and genetic influences, with stressful family environmental factors like household chaos and marital conflict associated with sleep duration and quality (El‐Sheikh, Buckhalt, Mize, & Acebo, 2006; Fiese, Winter, Sliwinski, & Anbar, 2007). However, it is less clear whether sibling conflict is related to sleep duration and children's sleep problems (e.g., nighttime wakings, parasomnias). In addition, few studies have tested whether associations between sleep and stressful family environmental factors are accounted for by an underlying set of genes or shared and unique environmental factors. Participants were 582 twins with sleep assessed longitudinally at 12, 30 months, and 5 years of age. Sibling conflict was assessed at 5 years. Greater sibling conflict was associated with shorter sleep duration and greater number of total sleep problems, over and above the influence of general household stress and other covariates. The heritability of sleep duration increased with age. Shared environmental factors accounted for the covariance between sibling conflict and sleep duration and total sleep problems. Findings hold promise for interventions, including educating parents about fostering positive sibling relationships and healthy sleep habits.