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.

The present study examined the intergenerational transmission of internalizing and externalizing symptom severity, which indexes comorbidity, and symptom directionality, which indicates differentiation toward externalizing versus internalizing problems. Data are from 854 male and female, same-sex adult twin pairs born between 1926 and 1971 (32–60 years old, M = 44.9 years, SD = 4.9 years) from the Twin and Offspring Study in Sweden and their adolescent offspring (11–22 years old, M = 15.7 years, SD = 2.4 years, 52% female). Children-of-twins models revealed additive (9%) and dominant (45%) genetic and nonshared environmental (47%) influences on twins’ symptom severity, and additive genetic (39%) and nonshared environmental (61%) influences on twins’ symptom directionality. Both comorbid problems and preponderance of symptoms of a particular – internalizing versus externalizing – spectrum were correlated across parent and child generations, although associations were modest especially for directionality (i.e., transmission of specific symptom type). By interpreting findings alongside a recent study of adolescent twins, we demonstrate that the intergenerational transmission of symptom severity and symptom directionality are both unlikely to be attributable to genetic transmission, are both likely to be influenced by direct phenotypic transmission and/or nonpassive rGE, and the intergenerational transmission of symptom severity is also likely to be influenced by passive rGE.

This research examines maternal smoking during pregnancy and risk for poorer executive function in siblings discordant for exposure. Data (N = 173 families) were drawn from the Missouri Mothers and Their Children study, a sample, identified using birth records (years 1998–2005), in which mothers changed smoking behavior between two pregnancies (Child 1 [older sibling]: Mage = 12.99; Child 2 [younger sibling]: Mage = 10.19). A sibling comparison approach was used, providing a robust test for the association between maternal smoking during pregnancy and different aspects of executive function in early-mid adolescence. Results suggested within-family (i.e., potentially causal) associations between maternal smoking during pregnancy and one working memory task (visual working memory) and one response inhibition task (color-word interference), with increased exposure associated with decreased performance. Maternal smoking during pregnancy was not associated with stop-signal reaction time, cognitive flexibility/set-shifting, or auditory working memory. Initial within-family associations between maternal smoking during pregnancy and visual working memory as well as color-word interference were fully attenuated in a model including child and familial covariates. These findings indicate that exposure to maternal smoking during pregnancy may be associated with poorer performance on some, but not all skills assessed; however, familial transmission of risk for low executive function appears more important.

Father absence has a small but robust association with earlier age at menarche (AAM), likely reflecting both genetic confounding and an environmental influence on life history strategy development. Studies that have attempted to disambiguate genetic versus environmental contributions to this association have shown conflicting findings, though genomic-based studies have begun to establish the role of gene–environment interplay in the father absence/AAM literature. The purpose of this study was to replicate and extend prior genomic work using the Avon Longitudinal Study of Parents and Children (ALSPAC), a prospective longitudinal cohort study (N = 2,685), by (a) testing if an AAM polygenic score (PGS) could account for the father absence/AAM association, (b) replicating G×E research on lin-28 homolog B (LIN28B) variation and father absence, and (c) testing the G×E hypothesis using the PGS. Results showed that the PGS could not explain the father absence/AAM association and there was no interaction between father absence and the PGS. Findings using LIN28B largely replicated prior work that showed LIN28B variants predicted later AAM in father-present girls, but this AAM-delaying effect was absent or reversed in father-absent girls. Findings are discussed in terms genetic confounding, the unique biological role of LIN28B, and using PGSs for G×E tests.

The generalist genes specialist environment model, when applied to developmental psychopathology, predicts that genetic influences should explain variance that is shared across internalizing and externalizing problems, whereas environmental influences should explain variance that distinguishes the two overarching problem types. The present study is a direct test of this hypothesis, leveraging a sample of 708 twins and siblings (aged 10–18 years, 93% White) from the United States. Measures of severity of symptoms, regardless of type, and of directionality of symptoms – whether the adolescent tended to exhibit more externalizing or internalizing problems – were subjected to genetic (A), shared environmental (C), and nonshared environmental (E) (ACE) variance decompositions. As expected, severity of problems was under substantial genetic influence, but there were also significant shared and nonshared environmental influences. Contrary to the generalist genes specialist environment model, directionality of problem type was also under considerable genetic influence, with modest nonshared environmental influence. Findings corroborate existing evidence from other designs highlighting the role of familial influences (including generalist genes) in comorbidity of adolescent internalizing and externalizing problems, but suggest that the specialist environments hypothesis may not be the key factor in distinguishing problem type.

Several aspects of mother–child relationships are associated with children's internalizing problems. We examined longitudinal associations between mother–child conflict and children's internalizing problems in middle childhood. Specifically, we examined whether conflict and children's internalizing problems predict each other longitudinally in a sample of children from 3rd through 6th grade (N = 1,364) and their mothers using a cross-lagged panel model with random intercepts. In line with expectations, we found stable between-family differences in both mother–child conflict and children's internalizing problems. Contrary to expectations, we did not find that mother–child conflict and children's internalizing problems showed significant cross-lagged associations. However, mother–child conflict and children's internalizing problems had correlated errors at each wave, indicating that these two constructs covary with each other concurrently at multiple times across development, independent of stable between-family associations (i.e., as one increases, so does the other, and vice versa). The results of this study point to the importance of using statistical approaches that can disentangle between-family differences from within-family processes. In future studies, shorter time scales (e.g., weeks or months) may better capture dynamic associations between parent–child conflict and internalizing problems.

We observed gendered coping strategies and conflict resolution outcomes used by adolescents and parents during a conflict discussion task to evaluate associations with current and later adolescent psychopathology. We studied 137 middle- to upper-middle-class, predominantly Caucasian families of adolescents (aged 11–16 years, 65 males) who represented a range of psychological functioning, including normative, subclinical, and clinical levels of problems. Adolescent coping strategies played key roles both in the extent to which parent–adolescent dyads resolved conflict and in the trajectory of psychopathology symptom severity over a 2-year period. Gender-prototypic adaptive coping strategies were observed in parents but not youth, (i.e., more problem solving by fathers than mothers and more regulated emotion-focused coping by mothers than fathers). Youth–mother dyads more often achieved full resolution of conflict than youth–father dyads. There were generally not bidirectional effects among youth and parents’ coping across the discussion except boys’ initial use of angry/hostile coping predicted fathers’ angry/hostile coping. The child was more influential than the parent on conflict resolution. This extended to exacerbation/alleviation of psychopathology over 2 years: higher conflict resolution mediated the association of adolescents’ use of problem-focused coping with decreases in symptom severity over time. Lower conflict resolution mediated the association of adolescents’ use of angry/hostile emotion coping with increases in symptom severity over time. Implications of findings are considered within a broadened context of the nature of coping and conflict resolution in youth–parent interactions, as well as on how these processes impact youth well-being and dysfunction over time.

The Missouri Mothers and Their Children Study (MO-MATCH) was specifically designed to critically investigate prenatal environmental influences on child attention problems and associated learning and cognitive deficits. The project began as a pilot study in 2004 and was formally launched in 2008. Participants in the study were initially identified via the Department of Vital Statistics birth record (BR) database. Interview and lab-based data were obtained from: (1) mothers of Missouri-born children (born 1998–2005), who smoked during one pregnancy but not during another pregnancy; (2) biological fathers when available; and (3) the children (i.e., full sibling pairs discordant for exposure to maternal smoking during pregnancy (SDP). This within-mother, between-pregnancy contrast provides the best possible methodological control for many stable maternal and familial confounding factors (e.g., heritable and socio-demographic characteristics of the mother that predict increased probability of SDP). It also controls for differences between mothers who do and do not smoke during pregnancy, and their partners, that might otherwise artifactually create, or alternatively mask, associations between SDP and child outcomes. Such a design will therefore provide opportunities to determine less biased effect sizes while also allowing us to investigate (on a preliminary basis) the possible contribution of paternal or other second-hand smoke exposure during the pre, peri, and postnatal periods to offspring outcome. This protocol has developed a cohort that can be followed longitudinally through periods typically associated with increased externalizing symptoms and substance used initiation.

We examined how genotype–environment correlation processes differ as a function of adolescent age. We tested whether adolescent age moderates genetic and environmental influences on positivity and negativity in mother–adolescent and father–adolescent relationships using parallel samples of twin parents from the Twin and Offspring Study in Sweden and twin/sibling adolescents from the Nonshared Environment in Adolescent Development Study. We inferred differences in the role of passive and nonpassive genotype–environment correlation based on biometric moderation findings. The findings indicated that nonpassive gene–environment correlation played a stronger role for positivity in mother– and father–adolescent relationships in families with older adolescents than in families with younger adolescents, and that passive gene–environment correlation played a stronger role for positivity in the mother–adolescent relationship in families with younger adolescents than in families with older adolescents. Implications of these findings for the timing and targeting of interventions on family relationships are discussed.

This study examined genetic and environmental influences on associations among marital conflict about the child, parental monitoring, sibling relationship negativity, and peer delinquency during adolescence and initiation of illegal drug use by young adulthood. The sample comprised data collected longitudinally from same-sex sibling pairs and parents when the siblings were 10–18 years old (M = 14.5 and 12.9 years for Child 1 and Child 2, respectively) and 20–35 years old (M = 26.8 and 25.5 years for Child 1 and Child 2, respectively). Findings indicate four factors that explain the initiation of illegal drug use: two shaped by genetic influences and two shaped by environments shared by siblings. The two genetically shaped factors probably have distinct mechanisms: one a child-initiated coercive process in the family and the other parent and peer processes shaped by the child's disclosure. The environmentally influenced factors seem distinctively shaped by poor parental monitoring of both sibs and the effects of siblings on each other's deviancy.