Although a robust literature has linked stable, high levels of fear across childhood to increased risk for anxiety problems, less is known about alternative pathways to anxiety. We tested two putatively normative developmental pathways of early fearfulness for their distinct associations with behavioral (anxiety-related behaviors and symptoms) and biological (diurnal cortisol) markers of anxiety risk in middle childhood in a community-based sample (n = 107). Steeper increases in fear from 6 to 36 months predicted more parent-reported anxiety symptoms at age 8 years. In addition, children who exhibited steep increases in fear during infancy were overrepresented among children with diagnoses of separation anxiety disorder at age 8 years. Finally, we showed that steeper increases in fearfulness in infancy predicted flatter slopes of diurnal cortisol at age 8 years for girls. Thus, differences in stranger fear across infancy may indicate varying degrees of risk for anxious behaviors in later childhood.

This study expanded the Benevolent Childhood Experiences scale (termed the “BCEs-Original” scale) with 10 new multisystem items and identified a subset of items (termed the “BCEs-Revised” scale) that are systematically less commonly reported across samples. Total BCEs-Revised scores were tested against total BCEs-Original scores and three dimensions of childhood adversity (maltreatment, threat, and deprivation) as predictors of young adulthood mental health problems (depression, anxiety, and PTSD symptoms). Hypotheses expected stronger inverse associations of BCEs-Revised scores than BCEs-Original scores with all mental health problems. Participants were 1,746 U.S. young adults (M = 26.6 years, SD = 4.7, range = 19–35 years; 55.3% female, 42.4% male, 2.3% gender non-conforming; 67.0% White, 10.3% Asian, 8.6% Black, 8.4% Latine, 5.7% other) who completed a 20-item BCEs scale and well-validated instruments on childhood adversities and mental health problems. Compared to BCEs-Original scores, BCEs-Revised scores were significantly more strongly inversely associated with all mental health outcomes. Compared to childhood threat and deprivation, maltreatment was significantly more strongly associated with PTSD symptoms. After controlling for current depression symptoms, BCEs-Revised scores interacted with maltreatment to predict PTSD symptoms. Maltreatment and BCEs-Revised scores also influenced PTSD symptoms in person-oriented analyses. The BCEs-Revised scale has strong psychometric properties and unique strengths in research and practice. Implications for multisystem resilience are discussed.

Although familial adversity is associated with poorer outcomes in childhood and adulthood, little research has looked at the influence of stability or transition between distinct familial adversity subgroups or the impact in adolescence. Using data from the 9-month, 3-, 5-, and 14-year time waves of the Millennium Cohort Study (n > 18,000), we used latent class analysis to identify distinct classes of early familial adversity (marital instability/conflict, “suboptimal” parenting, economic disadvantage, and parental mental health problems) and the impact of these adversity classes on adolescent (a) mental health (including self-harm), (b) risk taking, (c) criminality, and (d) victimization. Four profiles were identified largely differing on economic hardship, family composition, and parental conflict. Across the first three time points, 72% of the sample remained stable, with the remainder transitioning between classes. Adolescents in the higher risk groups (particularly categorized by economic hardship or high parental conflict) had poorer outcomes in adolescence. Transitioning to a higher adversity group at any time in the first 5 years was associated with poorer outcomes but was particularly pronounced when the transition occurred when the child was under 3 years. These findings demonstrate the broad consequences of early familial adversity and the need for targeted early support for at-risk families.

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.

This study tested whether the association between interparental conflict and adolescent externalizing symptoms was moderated by a polygenic composite indexing low dopamine activity (i.e., 7-repeat allele of DRD4; Val alleles of COMT; 10-repeat variants of DAT1) in a sample of seventh-grade adolescents (Mean age = 13.0 years) and their parents. Using a longitudinal, autoregressive design, observational assessments of interparental conflict at Wave 1 predicted increases in a multi-informant measurement of youth externalizing symptoms 2 years later at Wave 3 only for children who were high on the hypodopaminergic composite. Moderation was expressed in a “for better” or “for worse” form hypothesized by differential susceptibility theory. Thus, children high on the dopaminergic composite experienced more externalizing problems than their peers when faced with more destructive conflicts but also fewer externalizing problems when exposed to more constructive interparental conflicts. Mediated moderation findings indicated that adolescent reports of their emotional insecurity in the interparental relationship partially explained the greater genetic susceptibility experienced by these children. More specifically, the dopamine composite moderated the association between Wave 1 interparental conflict and emotional insecurity 1 year later at Wave 2 in the same “for better” or “for worse” pattern as externalizing symptoms. Adolescent insecurity at Wave 2, in turn, predicted their greater externalizing symptoms 1 year later at Wave 3. Post hoc analyses further revealed that the 7-repeat allele of the dopamine receptor D4 (DRD4) gene was the primary source of plasticity in the polygenic composite. Results are discussed as to how they advance process-oriented Gene x Environment models of emotion regulation.

We appreciate both the opportunity to co-edit this Special Section of Development and Psychopathology and the thoughtful commentaries provided by Marjorie Beeghly, Marc Bornstein, Robert Emde, and David Oppenheim. Their commentaries review historical perspectives, provide new insights, and suggest future horizons for the study of emotional availability (EA) within a developmental psychopathology framework. Along with the collection of empirical studies in this Special Section, they begin to chart a course for further growth and integration of EA into the field of developmental psychopathology. Taking stock of the research on EA, we realize that there is now a sufficient corpus to suggest that research focusing on this construct, as operationalized by the EA Scales (Biringen, Robinson, & Emde, 1998) is entering a more mature phase of inquiry. In the last 14 years, research on EA, including several special journal issues on the topic (see Biringen & Easterbrooks, 2008; Easterbrooks & Biringen, 2000, 2005, 2009), has explored the methodological concerns, reliability, and validity of the EA Scales and application across different samples and ages. This “critical mass” of knowledge (more than 100 peer-reviewed publications) supports the current focus on asking incisive questions for the field of developmental psychopathology (Cicchetti & Toth, 1995, 2009).

The bully/victim relationship was studied in a sample of elementary school children (N = 1,289 in first, third, and fifth grades). Three questions were tested. Does bullying involve a power differential between bully and victim? Are bully/victim dyads participants in a relationship, whether mutual liking or disliking? Does the gender composition of the bully/victim dyad moderate power differential and relational context patterns? Hierarchical linear modeling was used to analyze predictors of the reputational strength of bully/victim ties. The findings revealed that the bully/victim dyads most frequently nominated by peers were characterized by asymmetries in social status, where bullies were increasingly more popular than their victims, and by asymmetries in aggression, where bullies were increasingly less aggressive than their victims. Bullies and victims were likely to select one another as among the children that they least like. Most effects with respect to aggression, popularity, and relationships were moderated by the gender composition of the bully/victim dyad. Implications for a developmental psychopathology perspective on peer bullying and victimization are highlighted.

The authors tested whether emerging borderline personality disorder (BPD) symptoms mediated the association between childhood physical abuse (CPA) and aggression among incarcerated girls. Participants were 121 incarcerated adolescent girls (13–19 years old). Three forms of aggression (relational, overt, and violent offending behavior) and exposure to CPA by a parental figure were assessed using self-report inventories, whereas BPD symptoms were evaluated using a structured interview. Mediation models, including tests of indirect effects, were conducted in which each form of aggression was predicted from CPA with BPD symptoms entered as a mediator. A divergent pattern emerged in which BPD symptoms mediated the relationship between CPA and violent offending, but not less severe forms of overt aggression. Relational aggression, although correlated with CPA, was not associated with BPD symptoms. Implications for the conceptualization and treatment of girls' aggression within the context of interpersonal functioning are discussed.

Adverse effects of early exposure to parental mood disturbance on child adjustment have been documented for both mothers and fathers, but are rarely examined in tandem. Other under-researched questions include effects of changes over time in parental well-being, similarities and contrasts between effects of parental mood disturbance on children's internalizing versus externalizing problems, and potential mediating effects of couple relationship quality. The current study involved 438 couples who reported symptoms of depression and anxiety at each of four time points (i.e., last trimester of pregnancy and 4, 14, and 24 months postbirth). Mothers and fathers also rated their couple relationship quality and their child's socioemotional adjustment at 14 months, as well as internalizing and externalizing problems at 24 months. Latent growth models indicated direct effects of (a) maternal prenatal well-being on externalizing problems at 24 months, and (b) paternal prenatal well-being on socioemotional problems at 14 months. Internalizing symptoms at 24 months showed only indirect associations with parental well-being, with couple relationship quality playing a mediating role. Our findings highlight the importance of prenatal exposure to parental mood disturbance and demonstrate that, even in a low-risk sample, poor couple relationship quality explains the intergenerational stability of internalizing problems.

Parents serve important functions in regulating children's responses to stress and challenge. However, the parental characteristics that modulate the effectiveness of parents as stress buffers remain to be fully characterized. To address this gap, this study examined parental characteristics and behaviors that may explain variation in parents’ ability to buffer cortisol responses to acute stress of 180 children (ages 9–11 years old, M = 9.9 years, SD = .58). Children were randomly assigned to either participate in a public speaking task, the Trier Social Stress Test – modified for children (TSST-M) or a control condition. Children in the TSST-M condition were randomly assigned to prepare for the public speaking task either with their parent (N = 59) or alone (N = 60), whereas 61 children were assigned to the control condition (no TSST-M). We found that parental education moderated the effect of condition on children's responses to acute stress. Children whose parents had lower levels of education exhibited reduced cortisol responses in the parent condition compared to the alone condition, showing a buffered pattern of reactivity. In contrast, children of parents with high levels of education displayed higher cortisol reactivity in the parent condition compared to the alone and control conditions. Parental education was also positively associated with higher levels of state anxiety within the parent condition. These results suggest that highly educated parents may emphasize performance over comfort, amplifying their children's state anxiety and cortisol responses to a public performance.

Research findings in psychoneuroimmunology document reliable, bidirectional linkages among psychological processes, the nervous system, and the immune system. However, available data are based almost entirely on animal and adult human studies; the application to children and adolescents is uncertain. We capitalized on the experimental leverage provided by a routine vaccination to examine the link between mood symptoms and the immune response to a vaccine challenge in early adolescence. One hundred twenty-six 11-year-olds for whom vaccine response data were available were assessed at prevaccination and 4 weeks, 3 months, and 6 months following vaccination; self-report ratings of depression and anxiety as well as measures of psychosocial and somatic risk were assessed prior to vaccine response. Analyses indicated that children's internalizing mood symptoms were associated with elevated and persistently higher antibody responses, with evidence extending to two of the four serogroups. The associations remained after controlling for multiple possible confounders (social class, body mass index, sleep, psychosocial risk, and pubertal status). The observed enhanced vaccine response associated with depressive and anxious symptoms in early adolescence may reflect an important developmental difference in immune system–brain interplay between adults and children, and it underscores the need for further developmental studies of psychoneuroimmunology.

Social anxiety is one of the most commonly reported mental health problems among adolescents, and it has been suggested that parenting style influences an adolescent's level of anxiety. A context-dependent effect of oxytocin on human social behavior has been proposed; however, research on the oxytocin gene (OXT) has mostly been reported without considering contextual factors. This study investigated the interactions between parenting style and polymorphic variations in the OXT gene in association with social anxiety symptoms in a community sample of adolescents (n = 1,359). Two single nucleotide polymorphisms linked to OXT, rs4813625 and rs2770378, were genotyped. Social anxiety and perceived parenting style were assessed by behavioral questionnaires. In interaction models adjusted for sex, significant interaction effects with parenting style were observed for both variants in relation to social anxiety. The nature of the interactions was in line with the differential susceptibility framework for rs4813625, whereas for rs2770378 the results indicated a diathesis–stress type of interaction. The findings may be interpreted from the perspective of the social salience hypothesis of oxytocin, with rs4813625 affecting social anxiety levels along a perceived unsafe–safe social context dimension.

Attachment and Biobehavioral Catch-up (ABC) demonstrates efficacy in improving parent and child outcomes, with preliminary evidence for effectiveness in community settings. The objective of this study was to assess the effectiveness of a community-based ABC implementation in improving parent outcomes as well as to examine potential mediators and moderators of intervention effectiveness. Two hundred parents and their 5- to 21-month-old infants recruited from an urban community were randomly assigned to receive ABC or be placed on a waitlist. The majority of participants had a minority racial or ethnic background. Before intervention, parents completed questionnaires about sociodemographic risk and adverse childhood experiences. At both baseline and follow-up, parents reported depression symptoms and were video-recorded interacting with their infant, which was coded for sensitivity. The ABC intervention predicted significant increases in parental sensitivity and, among parents who completed the intervention, significant decreases in depression symptoms. Changes in parental depression symptoms did not significantly mediate the intervention effects on sensitivity. Risk variables did not moderate the intervention effects. The results indicate that ABC shows promise for improving parent outcomes in community settings, supporting dissemination.

Many young adolescents are embedded in neighborhoods, schools, and homes where alcohol and drugs are frequently used. However, little is known about (a) how witnessing others' substance use affects adolescents in their daily lives and (b) which adolescents will be most affected. The current study used ecological momentary assessment with 151 young adolescents (ages 11–15) to examine the daily association between witnessing substance use and antisocial behavior across 38 consecutive days. Results from multilevel logistic regression models indicated that adolescents were more likely to engage in antisocial behavior on days when they witnessed others using substances, an association that held when substance use was witnessed inside the home as well as outside the home (e.g., at school or in their neighborhoods). A significant Gene × Environment interaction suggested that the same-day association between witnessing substance use and antisocial behavior was significantly stronger among adolescents with, versus without, the dopamine receptor D4 seven repeat (DRD4-7R) allele. The implications of the findings for theory and research related to adolescent antisocial behavior are discussed.

Fathers are a crucial source of support for children following the birth of an infant sibling. This study examined whether fathers were more vulnerable to the effects of interparental conflict than mothers, and whether there was a subsequent spillover cascade from interparental conflict to children's externalizing behavior problems. We followed 241 families after the birth of a second child. Mothers and fathers reported on interparental conflict and parental efficacy at 1 and 4 months postpartum and punitive discipline and firstborn children's externalizing behavior problems across a longitudinal investigation (prenatal and 4, 8, and 12 months postpartum). For both mothers and fathers, interparental conflict prenatally predicted decreased parental efficacy following the birth. Fathers’ lower parental efficacy was significantly associated with increased punitive discipline toward the older sibling at 4 months, whereas mothers’ lower parental efficacy was not. Coercive family processes were present between mothers’ and fathers’ punitive discipline and older siblings’ externalizing behavior problems. Results were inconsistent with the father vulnerability hypothesis in that both mothers and fathers were vulnerable to interparental conflict, which in turn spilled over to create coercive family processes that exacerbated children's externalizing behavior problems in the year following the birth of a second child.

The cultural differences hypothesis is the assertion that there are large differences between Whites and racial/ethnic minorities in the United States, while there are small differences between- (e.g., African Americans and Latinos) and within- (e.g., Latinos: Mexican Americans and Cuban Americans) minority groups. Conversely, the cultural similarities hypothesis argues that there are small differences between Whites and minorities, and these differences are equal or smaller in magnitude than differences between and within minorities. In this study, we conducted a second-order meta-analysis focused on psychopathology, to (a) test these hypotheses by estimating the absolute average difference between Whites and minorities, as well as between and within minorities, on levels of psychopathology, and (b) determine if general and meta-analytic method moderators account for these differences. A systematic search in PsycINFO, Web of Science, and ProQuest Dissertations identified 16 meta-analyses (13% unpublished) on 493 primary studies (N = 3,036,749). Differences between Whites and minorities (d+ = 0.23, 95% confidence interval [0.18, 0.28]), and between minorities (d+ = 0.30, 95% confidence interval [0.12, 0.48]) were small in magnitude. White–minority differences remained small across moderators. These findings support the cultural similarities hypothesis. We discuss their implications and future research directions.

While child self-regulation is shaped by the environment (e.g., the parents’ caregiving behaviors), children also play an active role in influencing the care they receive, indicating that children's individual differences should be integrated in models relating early care to children's development. We assessed 409 children's observed temperamental behavioral inhibition (BI), effortful control (EC), and the primary caregiver's parenting at child ages 3 and 5. Parents reported on child behavior problems at child ages 3, 5, and 8. Mediation analyses were conducted to examine relations between child temperament and parenting in predicting child problems. BI at age 3 was positively associated with structured parenting at age 5, which was negatively related to child internalizing and attention-academic problems at age 8. In contrast, parenting at child age 3 did not predict child BI or EC at age 5, nor did age 3 EC predict parenting at age 5. Findings indicate that child behavior may shape the development of caregiving and, in turn, long-term child adjustment, suggesting that studies of caregiving and child outcomes should consider the role of child temperament toward developing more informative models of child–environment interplay.

Attention-deficit hyperactivity disorder (ADHD) is a common, chronic, and impairing disorder, yet presentations of ADHD and clinical course are highly heterogeneous. Despite substantial research efforts, both (a) the secondary co-occurrence of ADHD and complicating additional clinical problems and (b) the developmental pathways leading toward or away from recovery through adolescence remain poorly understood. Resolving these requires accounting for transactional influences of a large number of features across development. Here, we applied a longitudinal cross-lagged panel network model to a multimodal, multilevel dataset in a well-characterized sample of 488 children (nADHD = 296) to test Research Domain Criteria initiative-inspired hypotheses about transdiagnostic risk. Network features included Diagnostic and Statistical Manual of Mental Disorders symptoms, trait-based ratings of emotional functioning (temperament), and performance-based measures of cognition. Results confirmed that ADHD symptom domains, temperamental irritability, and working memory are independent transdiagnostic risk factors for psychopathology based on their direct associations with other features across time. ADHD symptoms and working memory each had direct, independent associations with depression. Results also demonstrated tightly linked co-development of ADHD symptoms and temperamental irritability, consistent with the possibility that this type of anger dysregulation is a core feature that is co-expressed as part of the ADHD phenotype for some children.

Symptoms of anxiety and depression are prevalent among adolescents and associated with impairment in multiple domains of functioning. Moreover, anxiety and depression frequently co-occur, with estimated comorbidity rates as high as 75%. Whereas previous research has shown that anxiety symptoms predict increased depressive symptoms over time, the relation between depressive symptoms and later anxiety symptoms has been inconsistent. The present study examined dynamic relations between anxiety and depressive symptoms across adolescence and explored whether these longitudinal relations were moderated by maternal history of anxiety, family relationship quality, or children's attributional style. Participants included 240 children (M age = 11.86 years; 53.9% female) and their mothers, who were assessed annually for 6 years. Children reported on their depressive symptoms and mothers reported on their child's anxiety symptoms. Dynamic latent change score models indicated that anxiety symptoms predicted subsequent elevations in depressive symptoms over time. Depressive symptoms predicted subsequent elevations in anxiety symptoms among children who had mothers with a history of anxiety, reported low family relationship quality, or had high levels of negative attributions. Thus, whereas anxiety symptoms were a robust predictor of later depressive symptoms during adolescence, contextual and individual factors may be important to consider when examining relations between depressive symptoms and subsequent change in anxiety symptoms.

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.