Parental Nurturance Moderates the Etiology of Youth Resilience.

Parenting behaviors are among the most robust predictors of youth resilience to adversity. Critically, however, very few studies examining these effects have been genetically-informed, and none have considered parenting as an etiologic moderator of resilience. What's more, despite the multidimensionality of resilience, extant etiologic literature has largely focused on a single domain. The current study sought to fill these respective gaps in the literature by examining whether and how parental nurturance shapes the etiology of academic, social, and psychological resilience, respectively. We employed a unique sample of twins (N = 426 pairs; ages 6-11) exposed to moderate-to-severe levels of environmental adversity (i.e., family poverty, neighborhood poverty, community violence) from the Twin Study of Behavioral and Emotional Development in Children. As expected, parental nurturance was positively correlated with all forms of resilience. Extended univariate genotype-by-environment interaction models revealed that parental nurturance significantly moderated genetic influences on all three domains of resilience (academic resilience A1= -0.53, psychological resilience A1= -1.22, social resilience A1= -0.63; all p < .05), such that as parental nurturance increased, genetic influences on youth resilience decreased. Put another way, children experiencing high levels of parental nurturance were more resilient to disadvantage, regardless of their genetic predisposition towards resilience. In the absence of nurturing parenting, however, genetic influences played an outsized role in the origins of resilience. Such findings indicate that parental nurturance may serve as a malleable protective factor that increases youth resilience regardless of genetic influences.

Elucidating the role of negative parenting in the genetic v. environmental influences on adult psychopathic traits.

BACKGROUND: Psychopathic traits involve interpersonal manipulation, callous affect, erratic lifestyle, and antisocial behavior. Though adult psychopathic traits emerge from both genetic and environmental risk, no studies have examined etiologic associations between adult psychopathic traits and experiences of parenting in childhood, or the extent to which parenting practices may impact the heritability of adult psychopathic traits using a genetically-informed design. METHODS: In total, 1842 adult twins from the community reported their current psychopathic traits and experiences of negative parenting during childhood. We fit bivariate genetic models to the data, decomposing the variance within, and the covariance between, psychopathic traits and perceived negative parenting into their genetic and environmental components. We then fit a genotype × environment interaction model to evaluate whether negative parenting moderated the etiology of psychopathic traits. RESULTS: Psychopathic traits were moderately heritable with substantial non-shared environmental influences. There were significant associations between perceived negative parenting and three of four psychopathy facets (interpersonal manipulation, erratic lifestyle, antisocial tendencies, but not callous affect). These associations were attributable to a common non-shared environmental pathway and not to overlapping genetic effects. Additionally, we found that primarily shared environmental influences were stronger on psychopathic traits for individuals with a history of greater negative parenting. CONCLUSIONS: Utilizing a genetically-informed design, we found that both genetic and non-shared environmental factors contribute to the emergence of psychopathic traits. Moreover, perceptions of negative parenting emerged as a clear environmental influence on the development of interpersonal, lifestyle, and antisocial features of psychopathy.

Genetic versus environmental influences on callous-unemotional traits in preadolescence: The role of parenting and parental psychopathology.

Children with callous-unemotional (CU) traits are at risk for severe conduct problems. While CU traits are moderately heritable, parenting also predicts risk. However, few studies have investigated whether parenting factors (e.g., acceptance, conflict, parental psychopathology) moderate the etiology of CU traits, while accounting for gene-environment correlations. To address this knowledge gap, we used data from 772 twin pairs from the Adolescent Brain and Cognitive Development Study to test bivariate models that explored overlapping etiological influences on CU traits and child reports of their parenting environment. We also used gene-by-environment interaction models to test whether parenting moderated genetic versus environmental influences. There were no overlapping etiological influences on CU traits and parental acceptance, but modest genetic and non-shared environmental overlap between CU traits and family conflict. Parental acceptance and psychopathology moderated non-shared environmental influences, with stronger non-shared environmental influences on CU traits among children who experienced lower parental acceptance and greater parental psychopathology. Family conflict only moderated environmental influences when models did not covary for conduct problems. Parental acceptance and parental psychopathology may be specific environmental protective and risk factors for CU traits, whereas family conflict may represent a general environmental risk factor for both CU traits and conduct problems.

Neighborhood features moderate genetic and environmental influences on children's social information processing.

Neighborhood is a key context where children learn to process social information; however, the field has largely overlooked the ways children's individual characteristics might be moderated by neighborhood effects. We examined 1,030 six- to 11-year-olds (48.7% female; 82% White) twin pairs oversampled for neighborhood disadvantage from the Twin Study of Behavioral and Emotional Development in Children. We evaluated neighbor reports (N = 1,880) of neighborhood structural and social characteristics as moderators of genetic and environmental influences on children's social processing. Although there was no evidence of moderation for children's hostile attributions, there was robust evidence that the social and structural characteristics of the neighborhood moderated the genetic and environmental origins of children's positive expectations of aggressive behavior. Specifically, we found that genetic influences on aggressive expectations increased in the presence of neighborhood deprivation and decreased in the presence of protective social processes and availability of resources. Such findings suggest that protective neighborhood social processes may buffer against the development of aggressive expectations during middle childhood by suppressing the expression of genetic influences on those outcomes. In doing so, they suggest that neighborhood social processes may be able to promote youth resilience to neighborhood deprivation "under the skin." (PsycInfo Database Record (c) 2024 APA, all rights reserved).

Associations of depression and anxiety symptoms in childhood and adolescence with epigenetic aging.

BACKGROUND: Childhood anxiety and depression symptoms are potential risk factors for accelerated biological aging. In child and adolescent twins, we tested whether these symptoms were associated with DNA methylation (DNAm) aging, a measure of biological aging. METHODS: 276 twins (135 pairs, 6 singletons) had DNAm assayed from saliva in middle childhood (mean = 7.8 years). Residuals of five different DNAm age estimates regressed on chronological age were used to indicate accelerated aging. Anxiety and depression symptoms were assessed in middle childhood and early adolescence using the Child Behavior Checklist. Mixed effect regression was used to examine potential relationships between anxiety or depression symptoms, and accelerated DNAm age. MZ twin difference analysis was then utilized to determine if associations were environmentally-driven or due to genetic or shared-environment confounding. RESULTS: Anxiety and depression symptoms were not associated with accelerated DNAm aging in middle childhood. In early adolescence, only the Wu clock was significant and indicated that each one symptom increase in anxiety symptoms had an associated age acceleration of 0.03 years (~0.4 months; p = 0.019). MZ twin difference analysis revealed non-significant within-pair effects, suggesting genetic and shared environmental influences. LIMITATIONS: Sample is predominantly male and white. Generalizability to other populations may be limited. CONCLUSION: Accelerated DNAm aging of the Wu clock in middle childhood is associated with anxiety, but not depression, symptoms in early adolescence. Further, this association may be the result of shared genetic and environmental influences. Accelerated DNAm aging may serve as an early risk factor or predictor of later anxiety symptoms.

Identifying Patterns of Youth Resilience to Neighborhood Disadvantage.

The present report describes the motivation for the Michigan Twin Neurogenetic Study (MTwiNS), which seeks to illuminate underlying biological mechanisms through which familial and community factors support resilience (i.e., adaptive competence in the face of adversity) in youth exposed to neighborhood disadvantage. To accomplish these goals, we must first understand how resilience manifests in this cohort. The current study uncovers evidence of three domains of youth resilience: psychiatric health, social engagement, and scholastic success. Although all three domains were relatively stable across a one-to-two year period, variability in this stability was observed. Additionally, although resilience in one domain was quite common, resilience across all 3 domains was less common. Finally, we show substantial variability in resilience within and across families, with substantial co-twin discordances that can be leveraged in future analyses that examine promotive contexts that are environmental in origin.

The Etiology of Resilience to Disadvantage.

BACKGROUND: Although early-life exposure to chronic disadvantage is associated with deleterious outcomes, 40-60% of exposed youth continue to thrive. To date, little is known about the etiology of these resilient outcomes. METHODS: The current study examined child twin families living in disadvantaged contexts (N=417 pairs) to elucidate the etiology of resilience. We evaluated maternal reports of the Child Behavior Checklist to examine three domains of resilience and general resilience. RESULTS: Genetic, shared, and nonshared environmental influences significantly contributed to social resilience (22%, 61%, 17%, respectively) and psychiatric resilience (40%, 28%, 32%, respectively), but academic resilience was influenced only by genetic and nonshared environmental influences (65% and 35%, respectively). These three domains loaded significantly onto a latent resilience factor, with factor loadings ranging from .60 to .34. A common pathway model revealed that the variance common to all three forms of resilience was predominantly explained by genetic and non-shared environmental influences (50% and 35%, respectively). CONCLUSIONS: These results support recent conceptualizations of resilience as a multifaceted construct influenced by both genetic and environmental influences, only some of which overlap across the various domains of resilience.