Psychopathology is intergenerationally transmitted through both genetic and environmental mechanisms via heterotypic (cross-domain), homotypic (domain-specific), and general (e.g., “p-factor”) pathways. The current study leveraged an adopted-at-birth design, the Early Growth and Development Study (57% male; 55.6% White, 19.3% Multiracial, 13% Black/African American, 10.9% Hispanic/Latine) to explore the relative influence of these pathways via associations between adoptive caregiver psychopathology (indexing potential environmental transmission) and birth parent psychopathology (indexing genetic transmission) with adolescent internalizing and externalizing symptoms. We included composite measures of adoptive and birth parent internalizing, externalizing, and substance use domains, and a general “p-factor.” Age 11 adolescent internalizing and externalizing symptom scores were the average of adoptive parent reports on the Child Behavior Checklist (n = 407). Examining domains independently without addressing comorbidity can lead to incorrect interpretations of transmission mode. Therefore, we also examined symptom severity (like the “p-factor”) and an orthogonal symptom directionality score to more cleanly disentangle transmission modes. The pattern of correlations was consistent with mostly general transmission in families with youth showing comorbid internalizing and externalizing symptoms, rather than homotypic transmission. Findings more strongly supported potential environmental or evocative mechanisms of intergenerational transmission than genetic transmission mechanisms (though see limitations). Parent-specific effects are discussed.

Introduced in the context of developmental psychopathology by Cicchetti and Rogosh in the Journal, the current paper incorporates the principles of equifinality and multifinality to support the use of tiered models to prevent the development of emerging child psychopathology and promote school readiness in early childhood. We use the principles of equifinality and multifinality to describe the limitations of applying one intervention model to address all children presenting with different types of risk for early problem behavior. We then describe the potential benefits of applying a tiered model for having impacts at the population level and two initial applications of this approach during early childhood. The first of these tiered models, Smart Beginnings, integrates the use of two evidenced-based preventive interventions, Video Interaction Project, a universal parenting program, and Family Check-Up, a selective parenting program. Building on the strengths of Smart Beginnings, the second trial, The Pittsburgh Study includes Video Interaction Project and Family Check-Up, and other more and less-intensive programs to address the spectrum of challenges facing parents of young children. Findings from these two projects are discussed with their implications for developing tiered models to support children’s early development and mental health.

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.

Studies found support for a link between pubertal timing and self-regulation in low-resource environments. This link could potentially explain a link between pubertal timing and early risk behavior. This study builds on this body of research by examining the mediated effect of pubertal timing on sexual activity through self-regulation in 728 adolescents and their families in a group with poor resources and a group with adequate resources. Income-to-Needs (ITN) was measured at age 7.5 to establish two groups (low-ITN and Medium/High-ITN). Pubertal timing was measured at age 10.5, self-regulation was assessed at age 14 and operationalized with effortful control, and sexual activity was assessed at age 16. Structural equation modeling was employed to test the hypothesized model in both groups. The link between pubertal timing and sexual activity mediated by effortful control was only significant in the low-ITN group. Specifically, more advanced pubertal maturity was associated with lower levels of adolescents’ effortful control, which in turn was associated with more sexual activity at age 16. Findings were partially replicated with a drug use index replacing sexual activity. This study shows a different operating link from pubertal timing to effortful control and subsequent risk behavior in resource-poor environments. Implications are discussed.

Externalizing behavior in early adolescence is associated with alcohol use in adolescence and early adulthood and these behaviors often emerge as part of a developmental sequence. This pattern can be the result of heterotypic continuity, in which different behaviors emerge over time based on an underlying shared etiology. In particular, there is largely a shared genetic etiology underlying externalizing and substance use behaviors. We examined whether polygenic risk for alcohol use disorder predicted (1) externalizing behavior in early adolescence and alcohol use in adolescence in the Early Steps Multisite sample and (2) externalizing behavior in adolescence and alcohol use in early adulthood in the Project Alliance 1 (PAL1) sample. We examined associations separately for African Americans and European Americans. When examining European Americans in the Early Steps sample, greater polygenic risk was associated with externalizing behavior in early adolescence. In European Americans in PAL1, we found greater polygenic risk was associated with alcohol use in early adulthood. Effects were largely absent in African Americans in both samples. Results imply that genetic predisposition for alcohol use disorder may increase risk for externalizing and alcohol use as these behaviors emerge developmentally.

Some children are more affected by specific family environments than others, as a function of differences in their genetic make-up. However, longitudinal studies of genetic moderation of parenting effects during early childhood have not been conducted. We examined developmental profiles of child behavior problems between 18 months and age 8 in a longitudinal parent–offspring sample of 361 adopted children. In toddlerhood (18 months), observed structured parenting indexed parental guidance in service of task goals. Biological parent psychopathology served as an index of genetic influences on children’s behavior problems. Four profiles of child behavior problems were identified: low stable (11%), average stable (50%), higher stable (29%), and high increasing (11%). A multinominal logistic regression analysis indicated a genetically moderated effect of structured parenting, such that for children whose biological mother had higher psychopathology, the odds of the child being in the low stable group increased as structured parenting increased. Conversely, for children whose biological mother had lower psychopathology, the odds of being in the low stable group was reduced when structured parenting increased. Results suggest that increasing structured parenting is an effective strategy for children at higher genetic risk for psychopathology, but may be detrimental for those at lower genetic risk.

Aggressive behavior in middle childhood can contribute to peer rejection, subsequently increasing risk for substance use in adolescence. However, the quality of peer relationships a child experiences can be associated with his or her genetic predisposition, a genotype–environment correlation (rGE). In addition, recent evidence indicates that psychosocial preventive interventions can buffer genetic predispositions for negative behavior. The current study examined associations between polygenic risk for aggression, aggressive behavior, and peer rejection from 8.5 to 10.5 years, and the subsequent influence of peer rejection on marijuana use in adolescence (n = 515; 256 control, 259 intervention). Associations were examined separately in control and intervention groups for children of families who participated in a randomized controlled trial of the family-based preventive intervention, the Family Check-Up . Using time-varying effect modeling (TVEM), polygenic risk for aggression was associated with peer rejection from approximately age 8.50 to 9.50 in the control group but no associations were present in the intervention group. Subsequent analyses showed peer rejection mediated the association between polygenic risk for aggression and adolescent marijuana use in the control group. The role of rGEs in middle childhood peer processes and implications for preventive intervention programs for adolescent substance use are discussed.

Differential susceptibility theory (DST) posits that individuals differ in their developmental plasticity: some children are highly responsive to both environmental adversity and support, while others are less affected. According to this theory, “plasticity” genes that confer risk for psychopathology in adverse environments may promote superior functioning in supportive environments. We tested DST using a broad measure of child genetic liability (based on birth parent psychopathology), adoptive home environmental variables (e.g., marital warmth, parenting stress, and internalizing symptoms), and measures of child externalizing problems (n = 337) and social competence (n = 330) in 54-month-old adopted children from the Early Growth and Development Study. This adoption design is useful for examining DST because children are placed at birth or shortly thereafter with nongenetically related adoptive parents, naturally disentangling heritable and postnatal environmental effects. We conducted a series of multivariable regression analyses that included Gene × Environment interaction terms and found little evidence of DST; rather, interactions varied depending on the environmental factor of interest, in both significance and shape. Our mixed findings suggest further investigation of DST is warranted before tailoring screening and intervention recommendations to children based on their genetic liability or “sensitivity.”

This study examined the long-term effects of a randomized controlled trial of the Family Check-Up (FCU) intervention initiated at age 2 on inhibitory control in middle childhood and adolescent internalizing and externalizing problems. We hypothesized that the FCU would promote higher inhibitory control in middle childhood relative to the control group, which in turn would be associated with lower internalizing and externalizing symptomology at age 14. Participants were 731 families, with half (n = 367) of the families assigned to the FCU intervention. Using an intent-to-treat design, results indicate that the FCU intervention was indirectly associated with both lower internalizing and externalizing symptoms at age 14 via its effect on increased inhibitory control in middle childhood (i.e., ages 8.5–10.5). Findings highlight the potential for interventions initiated in toddlerhood to have long-term impacts on self-regulation processes, which can further reduce the risk for behavioral and emotional difficulties in adolescence.

The Early Growth and Development Study (EGDS) is a prospective adoption study of birth parents, adoptive parents and adopted children (n = 561 adoptees). The original sample has been expanded to include siblings of the EGDS adoptees who were reared by the birth mother and assessed beginning at age 7 years (n = 217 biological children), and additional siblings in both the birth and adoptive family homes, recruited when the adoptees were 8–15 years old (n = 823). The overall study aims are to examine how family, peer and contextual processes affect child and adolescent adjustment, and to examine their interplay (mediation, moderation) with genetic influences. Adoptive and birth parents were originally recruited through adoption agencies located throughout the USA following the birth of a child. Assessments are ongoing and occurred in 9 month’s intervals until the adoptees turned 3 years of age, and in 1 to 2 year intervals thereafter through age 15. Data collection includes the following primary constructs: child temperament, behavior problems, mental health, peer relations, executive functioning, school performance and health; birth and adoptive parent personality characteristics, mental health, health, context, substance use, parenting and marital relations; and the prenatal environment. Findings highlight the power of the adoption design to detect environmental influences on child development and provide evidence of complex interactions and correlations between genetic, prenatal environmental and postnatal environmental influences on a range of child outcomes. The study sample, procedures and an overview of findings are summarized and ongoing assessment activities are described.

To advance research from Dishion and others on associations between parenting and peer problems across childhood, we used a sample of 177 sibling pairs reared apart since birth (because of adoption of one of the siblings) to examine associations between parental hostility and children's peer problems when children were ages 7 and 9.5 years (n = 329 children). We extended conventional cross-lagged parent–peer models by incorporating child inhibitory control as an additional predictor and examining genetic contributions via birth mother psychopathology. Path models indicated a cross-lagged association from parental hostility to later peer problems. When child inhibitory control was included, birth mother internalizing symptoms were associated with poorer child inhibitory control, which was associated with more parental hostility and peer problems. The cross-lagged paths from parental hostility to peer problems were no longer significant in the full model. Multigroup analyses revealed that the path from birth mother internalizing symptoms to child inhibitory control was significantly higher for birth parent–reared children, indicating the possible contribution of passive gene–environment correlation to this association. Exploratory analyses suggested that each child's unique rearing context contributed to his or her inhibitory control and peer behavior. Implications for the development of evidence-based interventions are discussed.

Building on prior work using Tom Dishion's Family Check-Up, the current article examined intervention effects on dysregulated irritability in early childhood. Dysregulated irritability, defined as reactive and intense response to frustration, and prolonged angry mood, is an ideal marker of neurodevelopmental vulnerability to later psychopathology because it is a transdiagnostic indicator of decrements in self-regulation that are measurable in the first years of life that have lifelong implications for health and disease. This study is perhaps the first randomized trial to examine the direct effects of an evidence- and family-based intervention, the Family Check-Up (FCU), on irritability in early childhood and the effects of reductions in irritability on later risk of child internalizing and externalizing symptomatology. Data from the geographically and sociodemographically diverse multisite Early Steps randomized prevention trial were used. Path modeling revealed intervention effects on irritability at age 4, which predicted lower externalizing and internalizing symptoms at age 10.5. Results indicate that family-based programs initiated in early childhood can reduce early childhood irritability and later risk for psychopathology. This holds promise for earlier identification and prevention approaches that target transdiagnostic pathways. Implications for future basic and prevention research are discussed.

Several research teams have previously traced patterns of emerging conduct problems (CP) from early or middle childhood. The current study expands on this previous literature by using a genetically-informed, experimental, and long-term longitudinal design to examine trajectories of early-emerging conduct problems and early childhood discriminators of such patterns from the toddler period to adolescence. The sample represents a cohort of 731 toddlers and diverse families recruited based on socioeconomic, child, and family risk, varying in urbanicity and assessed on nine occasions between ages 2 and 14. In addition to examining child, family, and community level discriminators of patterns of emerging conduct problems, we were able to account for genetic susceptibility using polygenic scores and the study's experimental design to determine whether random assignment to the Family Check-Up (FCU) discriminated trajectory groups. In addition, in accord with differential susceptibility theory, we tested whether the effects of the FCU were stronger for those children with higher genetic susceptibility. Results augmented previous findings documenting the influence of child (inhibitory control [IC], gender) and family (harsh parenting, parental depression, and educational attainment) risk. In addition, children in the FCU were overrepresented in the persistent low versus persistent high CP group, but such direct effects were qualified by an interaction between the intervention and genetic susceptibility that was consistent with differential susceptibility. Implications are discussed for early identification and specifically, prevention efforts addressing early child and family risk.

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 racially/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 SD above the mean on polygenic sensitivity, or 25% of the sample. Similar to personalized medicine, it is time to understand individual and sociocultural differences in treatment response and individualize psychosocial interventions to reduce the burden of child psychopathology and maximize well-being for children growing up in a wide range of physical environments and cultures.

Maternal trauma is a complex risk factor that has been linked to adverse child outcomes, yet the mechanisms underlying this association are not well understood. This study, which included adoptive and biological families, examined the heritable and environmental mechanisms by which maternal trauma and associated depressive symptoms are linked to child internalizing and externalizing behaviors. Path analyses were used to analyze data from 541 adoptive mother–adopted child (AM–AC) dyads and 126 biological mother–biological child (BM–BC) dyads; the two family types were linked through the same biological mother. Rearing mother's trauma was associated with child internalizing and externalizing behaviors in AM–AC and BM–BC dyads, and this association was mediated by rearing mothers’ depressive symptoms, with the exception of biological child externalizing behavior, for which biological mother trauma had a direct influence only. Significant associations between maternal trauma and child behavior in dyads that share only environment (i.e., AM–AC dyads) suggest an environmental mechanism of influence for maternal trauma. Significant associations were also observed between maternal depressive symptoms and child internalizing and externalizing behavior in dyads that were only genetically related, with no shared environment (i.e., BM–AC dyads), suggesting a heritable pathway of influence via maternal depressive symptoms.

The current study utilized a longitudinal design to explore the effect of early child impulsivity and rejecting parenting on the development of problematic behaviors in adolescence and early adulthood. Using a low-income sample of 310 mothers and their sons, we examined the direct and interactive effects of child impulsivity and rejecting parenting at age 2 on aggression and substance use at ages 12, 15, and 22, as well as risky sexual behavior at ages 15 and 22. Results revealed that rejecting parenting at age 2 predicted greater aggression at age 12 and risky sexual behavior at ages 15 and 22. Early impulsivity had few direct effects on later outcomes, with the exception of greater substance use at age 22. Instead, impulsivity emerged as a significant moderator in the link between rejecting parenting and aggression at all three ages and substance use at age 15. Specifically, early rejecting parenting predicted greater aggression and substance use only for children high in impulsivity. Findings highlight the potential for early child and parenting risk factors to have long-term implications for adjustment, with the combination of high impulsivity and rejecting parenting being particularly deleterious for problems of aggression throughout adolescence and into early adulthood.

There is now ample evidence that the quality of early attachment experiences shapes expectations for supportive and responsive care and ultimately serves to scaffold adaptation to the salient tasks of development. Nonetheless, few studies have identified neural mechanisms that might give rise to these associations. Using a moderately large sample of low-income male participants recruited during infancy (N = 171), we studied the predictive significance of attachment insecurity and disorganization at age 18 months (as measured in the Strange Situation Procedure) for patterns of neural activation to reward and loss at age 20 years (assessed during a reward-based task as part of a functional magnetic resonance imaging scan). Results indicated that individuals with a history of insecure attachment showed hyperactivity in (a) reward- and emotion-related (e.g., basal ganglia and amygdala) structures and (b) emotion regulation and self-referential processing (cortical midline structures) in response to positive and negative outcomes (and anticipation of those outcomes). Further, the neural activation of individuals with a history of disorganized attachment suggested that they had greater emotional reactivity in anticipation of reward and employed greater cognitive control when negative outcomes were encountered. Overall, results suggest that the quality of early attachments has lasting impacts on brain function and reward processing.