Disruptive behavior increases the risk of developing more severe behavior problems later in life, including antisocial and criminal behavior. Parents behavior, and possibly their genetic makeup as well, plays a key role in shaping their children’s disruptive behavior. We examined gene-environment (parenting) correlations as underlying mechanisms for disruptive child behavior in a cross-sectional study. Polygenic scores for disruptive and externalizing behavior (PGS-DB and PGS-EXT) and parent-reported harsh and warm-supportive parenting were measured in 288 Dutch parent-child pairs (Child Mage = 6.26, SD = 1.31, 48% girls) with above-average parent-reported disruptive behavior. Harsh and warm-supportive parenting and children’s PGS-DB were associated with disruptive child behavior (β = .23, .10 and .15, respectively), but no evidence emerged for gene-environment correlations or genetic nurture. However, harsh parenting was found to partially mediate the link between parental PGS-EXT and disruptive child behavior (β = .04). These findings suggest that the choice of polygenic scores may influence the ability to detect genetic nurture as a relevant mechanism underlying disruptive child behavior.

Physical and sexual abuse have far-reaching mental and behavioral health consequences, extending across the lifespan and, in some cases, across generations. However, empirical work in this area is limited by cross-sectional study designs, short follow-up durations, and data analytic techniques that fail to capture the nuanced developmental processes through which caregivers and children impact one another. The present study investigated the cross-lagged and bidirectional pathways between maternal childhood victimization, depression, harsh parenting, and their children’s externalizing symptoms over a 10-year period. Participants were 818 mother-child dyads prospectively identified as at-risk for family violence when children were four years old. Traditional cross-lagged panel modeling (CLPM) and random-intercept cross-lagged panel modeling (RI-CLPM) documented that maternal depression, harsh parenting, and child externalizing problems — all predicted by mothers’ early abuse experiences — exacerbated one another across time. Discrepancies between the CLPM and RI-CLPM highlighted the advantages, disadvantages, and methodological implications of each approach. Findings highlight maternal psychopathology and parenting as key mechanisms in the intergenerational impact of abuse, emphasizing the importance of trauma-informed, parent-mediated interventions for breaking long-term cycles of family dysfunction. The present findings support separating out between-person, trait-like components when interpreting cross-lagged associations, as these may confound within-person effects.

Past studies that examined externalizing and internalizing symptoms in separate samples have found different trajectories associated with harsh parenting. The present study uses a complex set of longitudinal modeling to investigate the developmental trajectories of internalizing and externalizing symptoms associated with harsh parenting. We also explore the moderation of socioeconomic status and ethnicity by testing differences between income and racial groups. Using bivariate and multigroup latent change score modeling, we analyzed 12,909 participants from the Millennium Cohort Study. Results of the bivariate latent change score model showed that harsh parenting had a bidirectional association with externalizing symptoms but only a unidirectional association with internalizing symptoms. A further analysis using multi-group modeling showed that the association between harsh parenting and externalizing and internalizing symptoms differed across ethnic backgrounds but much less on socioeconomic status. Specifically, initial levels of harsh parenting predicted an increase in externalizing symptoms among White participants but not in non-White participants, and these ethnic differences cut across socioeconomic status classifications in a test of the interaction of ethnicity and socioeconomic status. Taken together, our findings suggest that the prevailing cultural norms surrounding harsh parenting may affect the degree to which it negatively impacts children’s mental health.

The present study examined several distinct indicators of regulation (i.e., task-based executive function, surveyed child effortful control, and surveyed household chaos) as moderators of longitudinal bidirectional links between developmental changes in harsh parenting (HP) and child externalizing behaviors (EXT) from age 9 to 14 years. The sample included 311 children (50.4% female; 111 White or European American; 97 Hispanic or Latino; 103 Black or African American). We conducted cross-lagged panel analyses and utilized multiple reporters (mother, father, and child). Regarding bidirectionality between HP and EXT, findings were mixed depending on informant, but overall more child effects than parent effects or bidirectional effects emerged. Child and household regulation moderated certain effects, providing initial evidence of the potential role of regulations in bidirectional links between HP and EXT. The present study adds impetus to considering child self-regulation and household chaos as critical features influencing the bidirectional link between parenting and child functioning.

Deficits in executive functioning both run in families and serve as a transdiagnostic risk factor for psychopathology. The present study employed twin modeling to examine parenting as an environmental pathway underlying the intergenerational transmission of executive functioning in an at-risk community sample of children and adolescents (N = 354 pairs, 167 monozygotic). Using structural equation modeling of multi-informant reports of parenting and a multi-method measure of child executive functioning, we found that better parent executive functioning related to less harsh, warmer parenting, which in turn related to better child executive functioning. Second, we assessed the etiology of executive functioning via the nuclear twin family model, finding large non-shared environmental effects (E = .69) and low-to-moderate heritability (A = .22). We did not find evidence of shared environmental effects or passive genotype–environment correlation. Third, a bivariate twin model revealed significant shared environmental overlap between both warm and harsh parenting and child executive functioning (which may indicate either passive genotype–environment correlation or environmental mediation), and non-shared environmental overlap between only harsh parenting and child executive functioning (indicating an effect of harsh parenting separable from genetic confounds). In summary, genetics contribute to the intergenerational transmission of executive functioning, with environmental mechanisms, including harsh parenting, also making unique contributions.

Childhood adversity is thought to undermine youth socioemotional development via altered neural function within regions that support emotion processing. These effects are hypothesized to be developmentally specific, with adversity in early childhood sculpting subcortical structures (e.g., amygdala) and adversity during adolescence impacting later-developing structures (e.g., prefrontal cortex; PFC). However, little work has tested these theories directly in humans. Using prospectively collected longitudinal data from the Fragile Families and Child Wellbeing Study (FFCWS) (N = 4,144) and neuroimaging data from a subsample of families recruited in adolescence (N = 162), the current study investigated the trajectory of harsh parenting across childhood (i.e., ages 3 to 9) and how initial levels versus changes in harsh parenting across childhood were associated with corticolimbic activation and connectivity during socioemotional processing. Harsh parenting in early childhood (indexed by the intercept term from a linear growth curve model) was associated with less amygdala, but not PFC, reactivity to angry facial expressions. In contrast, change in harsh parenting across childhood (indexed by the slope term) was associated with less PFC, but not amygdala, activation to angry faces. Increases in, but not initial levels of, harsh parenting were also associated with stronger positive amygdala–PFC connectivity during angry face processing.

Parental alcohol dependence is a significant risk factor for harsh caregiving behaviors; however, it is unknown whether and how harsh caregiving changes over time and across parenting contexts for alcohol-dependent mothers. Furthermore, to our knowledge, no studies have examined whether and how distinct dimensions of child characteristics, such as negative emotionality modulate harsh caregiving among alcohol-dependent mothers. Guided by parenting process models, the present study examined how two distinct domains of children's negative emotionality—fear and frustration—moderate the association between maternal alcohol dependence and maternal harshness across discipline and free-play contexts. A high-risk sample of 201 mothers and their two-year-old children were studied over a one-year period. Results from latent difference score analyses indicated that harsh parenting among alcohol-dependent mothers increased over time in the more stressful discipline context, but not in the parent–child play context. This effect was maintained even after controlling for other parenting risk factors, including other forms of maternal psychopathology. Furthermore, this increase in harsh parenting was specific to alcohol-dependent mothers whose children were displaying high levels of anger and frustration. Findings provide support for specificity in conceptualizations of child negative emotionality and parenting contexts as potential determinants of maladaptive caregiving among alcohol-dependent mothers.