Development and Psychopathology has been a premier resource for understanding stressful childhood experiences and the intergenerational continuity of psychopathology. Building on that tradition, we examined the unique and joint influences of maternal stress on children’s effortful control (age 7) and externalizing behavior (age 11) as transmitted via genetics, the prenatal environment, and the postnatal environment. The sample included N = 561 adopted children and their biological and adoptive parents. Path models identified a direct effect of biological mother life stress on children’s effortful control (β = −.08) and an indirect effect of her life stress on child externalizing behavior via effortful control (β = .52), but no main or indirect effects of biological parent psychopathology, prenatal stress, or adoptive mother adverse childhood experiences (ACES). Adoptive mother ACES amplified the association between biological mother life stress and child effortful control (β = −.08), externalizing behavior (β = 1.41), and the indirect effect via effortful control, strengthening associations when adoptive mothers reported average or high ACES during their own childhoods. Results suggest that novel study designs are needed to enhance the understanding of how life stress gets “under the skin” to affect psychopathology in the offspring of adults who have experienced stress.

Parent-Child interaction therapy (PCIT) has been shown to improve positive, responsive parenting and lower risk for child maltreatment (CM), including among families who are already involved in the child welfare system. However, higher risk families show higher rates of treatment attrition, limiting effectiveness. In N = 120 child welfare families randomized to PCIT, we tested behavioral and physiological markers of parent self-regulation and socio-cognitive processes assessed at pre-intervention as predictors of retention in PCIT. Results of multinomial logistic regressions indicate that parents who declined treatment displayed more negative parenting, greater perceptions of child responsibility and control in adult–child transactions, respiratory sinus arrhythmia (RSA) increases to a positive dyadic interaction task, and RSA withdrawal to a challenging, dyadic toy clean-up task. Increased odds of dropout during PCIT's child-directed interaction phase were associated with greater parent attentional bias to angry facial cues on an emotional go/no-go task. Hostile attributions about one's child predicted risk for dropout during the parent-directed interaction phase, and readiness for change scores predicted higher odds of treatment completion. Implications for intervening with child welfare-involved families are discussed along with study limitations.

Dishion and Patterson's work on the unique role of fathers in the coercive family process showed that fathers' coercion explained twice the variance of mothers' in predicting children's antisocial behavior and how treatment and prevention of coercion and promotion of prosocial parenting can mitigate children's problem behaviors. Using these ideas, we employed a sample of 426 divorced or separated fathers randomly assigned to Fathering Through Change (FTC), an interactive online behavioral parent training program or to a waitlist control. Participating fathers had been separated or divorced within the past 24 months with children ages 4 to 12 years. We tested an intent to treat (ITT) mediation hypothesis positing that intervention-induced changes in child problem behaviors would be mediated by changes in fathers' coercive parenting. We also tested complier average causal effects (CACE) models to estimate intervention effects, accounting for compliers and noncompliers in the treatment group and would-be compliers in the controls. Mediation was supported. ITT analyses showed the FTC obtained a small direct effect on father-reported pre–post changes in child adjustment problems (d = .20), a medium effect on pre–post changes in fathers' coercive parenting (d = .61), and a moderate indirect effect to changes in child adjustment (d = .30). Larger effects were observed in CACE analyses.

We examined time-ordered associations between children's compliance behavior and maternal respiratory sinus arrhythmia (RSA) in a sample of 127 child-maltreating (physical abuse, physical neglect, emotional abuse) and 94 non-maltreating mothers and their preschool-aged children. Child prosocial and aversive compliance behaviors and maternal RSA were continuously collected during a joint challenge task. Child behavior and mother RSA were longitudinally nested within-person and subjected to multilevel modeling (MLM), with between-person child maltreatment subtype and level of inconsistent parenting modeled as moderators. Both child maltreatment type and inconsistent parenting moderated the effects of child compliance on maternal RSA. Increases in children's prosocial compliance behaviors led to decreasing RSA in physically abusive mothers 30s later (i.e., increasing arousal), but predicted increases in non-maltreating mothers’ RSA (i.e., increasing calm). Inconsistent parenting (vacillating between autonomy-support and strict control) also moderated the effects of children's compliance behavior on maternal physiology, weakening the effects of child prosocial compliance on subsequent maternal RSA. These findings highlight variations in mothers’ physiological sensitivity to their children's prosocial behavior that may play a role in the development of coercive cycles, and underscore the need to consider individual differences in parents’ physiological sensitivity to their children to effectively tailor interventions across the spectrum of risk.

Neurobehavioral disinhibition (ND) is a complex condition reflecting a wide range of problems involving difficulties with emotion regulation and behavior control. Respiratory sinus arrhythmia (RSA) is a physiological correlate of emotion regulation that has been studied in a variety of at-risk populations; however, there are no studies of RSA in children with ND. Data were drawn from a prospective longitudinal study of prenatal substance exposure that included 1,073 participants. Baseline RSA and RSA reactivity to an attention-demanding task were assessed at 3, 4, 5, and 6 years. ND was assessed at ages 8/9, 11, and 13/14 years via behavioral dysregulation and executive dysfunction composite measures. Greater exposure to early adversity was related to less RSA reactivity at 3 years, increases in RSA reactivity from ages 3 to 6 years, and increased behavioral dysregulation from ages 8/9 to 13/14. RSA reactivity was examined as a moderator of the association between early adversity and changes in ND. A significant Early Adversity × RSA Reactivity quadratic interaction revealed that children with decelerations in RSA reactivity exhibited increases in behavioral dysregulation, regardless of their exposure to early adversity. However, greater exposure to early adversity was related to greater increases in behavioral dysregulation, but only if children exhibited accelerations in RSA reactivity from ages 3 to 6 years. The results contribute to our understanding of how interactions across multiple levels of analysis contribute to the development of ND.

The negative effects of prenatal substance exposure on neurobiological and psychological development and of early adversity are clear, but little is known about their combined effects. In this study, multilevel analyses of the effects of prenatal substance exposure and early adversity on the emergence of neurobehavioral disinhibition in adolescence were conducted. Neurobehavioral disinhibition has previously been observed to occur frequently in multiproblem youth from high-risk backgrounds. In the present study, neurobehavioral disinhibition was assessed via behavioral dysregulation and poor executive function composite measures. Data were drawn from a prospective longitudinal investigation of prenatal substance exposure that included 1,073 participants followed from birth through adolescence. The results from latent growth modeling analyses showed mean stability but significant individual differences in behavioral dysregulation and mean decline with individual differences in executive function difficulties. Prior behavioral dysregulation predicted increased executive function difficulties. Prenatal drug use predicted the emergence and growth in neurobehavioral disinhibition across adolescence (directly for behavioral dysregulation and indirectly for executive function difficulties via early adversity and behavioral dysregulation). Prenatal drug use and early adversity exhibited unique effects on growth in behavioral dysregulation; early adversity uniquely predicted executive function difficulties. These results are discussed in terms of implications for theory development, social policy, and prevention science.

Four different sources for cascade effects were examined using 9-year process and outcome data from a randomized controlled trial of a preventive intervention using the Parent Management Training—Oregon Model (PMTO™). The social interaction learning model of child antisocial behavior serves as one basis for predicting change. A second source addresses the issue of comorbid relationships among clinical diagnoses. The third source, collateral changes, describes events in which changes in one family member correlate with changes in another. The fourth component is based on the long-term effects of reducing coercion and increasing positive interpersonal processes within the family. New findings from the 9-year follow-up show that mothers experienced benefits as measured by standard of living (i.e., income, occupation, education, and financial stress) and frequency of police arrests. It is assumed that PMTO reduces the level of coercion, which sets the stage for a massive increase in positive social interaction. In effect, PMTO alters the family environment and thereby opens doors to healthy new social environments.

This paper presents experimental tests of the Oregon delinquency model applied within a randomized design of an at-risk sample of single mothers and their elementary school-aged sons. In the theoretical model, ineffective parenting practices and deviant peer association serve as the primary mechanisms for growth in adolescent delinquent behavior and early arrests. Multiple-method assessments of 238 mothers and sons include delinquency as measured by teacher reports and official arrest records, parenting skills measured by observations of parent–child interactions, and deviant peer association as reported by focal boys. Analyses of the 9-year follow-up data indicate that the Oregon model of parent management training significantly reduced teacher-reported delinquency and police arrests for focal boys. As hypothesized, the experiments demonstrated that improving parenting practices and reducing contacts with deviant peers served as mediating mechanisms for reducing rates of adolescent delinquency. As predicted, there was also a significant delay in the timing of police arrests for youth in the experimental as compared to the control group.

We hypothesized that hyperactivity defines the first stage and that antisocial problems define a second stage in a progression that leads eventually to early-onset delinquency. As expected, a structural equation model (SEM) showed that a latent construct for hyperactivity was significantly related to a latent construct for antisocial problems. We hypothesized that this path reflected a shared mechanism, disrupted parental discipline. A second SEM showed that the relation between hyperactivity and antisocial behavior really reflected a shared disruption in parental discipline. A third SEM showed that having antisocial parents was uniquely correlated with antisocial children but not with hyperactivity. A fourth SEM showed that early-onset delinquency was predicted by a latent construct for antisocial child; but when this was partialed out, the contribution for hyperactivity was nonsignificant.