While the detrimental effect of interparental conflict on adolescent depression is well-established, the underlying mechanisms linking the two continue to be inadequately understood. This study investigated the mediating role of family functioning and the moderating role of cultural beliefs about adversity in the association between interparental conflict and adolescent depression. The samples included 651 Chinese adolescents (mean age at Time 1 = 13.27 years; 56.5% girls) from a two-wave longitudinal study with data spanning 1 year. The findings from path modeling analyses provided evidence for the mediating role of family functioning; these findings indicated that interparental conflict can damage family functioning, which in turn exacerbates the risk of adolescent depression. The moderating role of cultural beliefs about adversity was also demonstrated by interactions between interparental conflict and cultural beliefs about adversity, as well as, family functioning and cultural beliefs about adversity. The results indicated a buffering role of cultural beliefs about adversity on the deleterious effect of interparental conflict on adolescent depression. They also suggested that lower levels of family functioning was associated with increased depression among adolescents were lower in cultural beliefs about adversity.

Identifying the mechanisms linking early experiences, genetic risk factors, and their interaction with later health consequences is central to the development of preventive interventions and identifying potential boundary conditions for their efficacy. In the current investigation of 412 African American adolescents followed across a 20-year period, we examined change in body mass index (BMI) across adolescence as one possible mechanism linking childhood adversity and adult health. We found associations of childhood adversity with objective indicators of young adult health, including a cardiometabolic risk index, a methylomic aging index, and a count of chronic health conditions. Childhood adversities were associated with objective indicators indirectly through their association with gains in BMI across adolescence and early adulthood. We also found evidence of an association of genetic risk with weight gain across adolescence and young adult health, as well as genetic moderation of childhood adversity's effect on gains in BMI, resulting in moderated mediation. These patterns indicated that genetic risk moderated the indirect pathways from childhood adversity to young adult health outcomes and childhood adversity moderated the indirect pathways from genetic risk to young adult health outcomes through effects on weight gain during adolescence and early adulthood.

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.

Exposure to childhood adversity is a powerful risk factor for psychopathology. Despite extensive efforts, we have not yet identified effective or scalable interventions that prevent the emergence of mental health problems in children who have experienced adversity. In this modified Delphi study, we identified intervention strategies for effectively targeting both the neurodevelopmental mechanisms linking childhood adversity and psychopathology – including heightened emotional reactivity, difficulties with emotion regulation, blunted reward processing, and social information processing biases, as well as a range of psychopathology symptoms. We iteratively synthesized information from experts in the field and relevant meta-analyses through three surveys, first with experts in intervention development, prevention, and childhood adversity (n = 32), and then within our study team (n = 8). The results produced increasing stability and good consensus on intervention strategy recommendations for specific neurodevelopmental mechanisms and symptom presentations and on strength of evidence ratings of intervention strategies targeting youth and parents. More broadly, our findings highlight how intervention decision making can be informed by meta-analyses, enhanced by aggregate group feedback, saturated before consensus, and persistently subjective or even contradictory. Ultimately, the results converged on several promising intervention strategies for prevention programming with adversity-exposed youth, which will be tested in an upcoming clinical trial.

The current investigation utilized a developmental psychopathology approach to test the hypothesis that multigenic (i.e., dopaminergic and serotonergic genes) and multienvironmental factors interactively contribute to developmental pathways of antisocial behavior (ASB). A sample of 8,834 Caucasian individuals from the National Longitudinal Study of Adolescent to Adult Health (Add Health) were used to (a) examine the developmental pathways of ASB from age 13 to 32 using growth mixture modeling, (b) compute weighted multigenic risk scores (Add Health MRS) for ASB from six well-characterized polymorphisms in dopamine and serotonin genes, and (c) test the interaction between the Add Health MRS and a measures of support (incorporating indicators of both positive and negative support from parents and schools). Four pathways of adolescent to adult ASB emerged from the growth mixture models: low, adolescence-peaked, high decline, and persistent. Add Health MRS predicted the persistent ASB pathway, but not other ASB pathways. Males with high Add Health MRS, but not low MRS, had significantly greater odds of being in the adolescence-peaked pathway relative to the low pathway at low levels of school connectedness. Nonfamilial environmental influences during adolescence may have a cumulative impact on the development of ASB, particularly among males with greater underlying genetic risks.

This study reports findings from the administration of a social problem-solving training (SPST) intervention to juvenile detainees in the Connecticut Youth Detainee Program. SPST is a cognitive behavioral intervention that teaches children and youth how to more effectively cope with interpersonal stress and conflict. In the current study, we tested whether SPST could decrease depressive symptoms in a sample of detained adolescent offenders. The study used a randomized-control design with detention staff administering the intervention. The results showed that SPST, as a main effect, was not more effective in reducing depressive symptoms than treatment as usual. However, the effectiveness of SPST was moderated by fluid intelligence. Juvenile detainees with high intelligence scores were most likely to benefit from SPST compared to treatment as usual. It was surprising that, for those with lower intelligence scores, SPST increased depressive symptoms relative to treatment as usual. These results help fill a critical need for intervention effectiveness data on juvenile detainees and indicate that SPST may not be useful for reducing outcomes such as depression.

Studies using the Emotional Availability Scales have burgeoned in the past decade. The collection of papers included in this Special Section represents the latest innovations in research with this paradigm. Consistent with a developmental psychopathology perspective, these papers evaluate emotional availability in a variety of typical, at-risk, international, and intergenerational samples of children and caregivers, with many utilizing longitudinal designs or employing measures from multiple levels of analysis. One study begins to translate findings from this body of research into a promising intervention program. Although further growth and refinement in research with this paradigm is needed, the results to date begin to place the construct of emotional availability into a complex, dynamic biopsychosocial context, and promise to inspire a new generation of studies. In this commentary, some of the key contributions and challenges of this collection of studies are highlighted using a developmental psychopathology framework.

The present investigation extends research on Gene × Environment interactions and youth risk behavior by linking multilevel contextual factors, such as community disadvantage and protective parenting practices, to both parental and youth dopamine D4 receptor (DRD4) genotypes. We expected community disadvantage to influence youth risk behavior via a series of indirect effects involving protective parenting and youth's planful future orientation when both parents’ and youth's DRD4 status was considered. Genetic moderation processes also were tested to determine whether they conformed to a diathesis–stress or a differential susceptibility model. Hypotheses were investigated with data from 361 rural African American youth and their parents assessed 3 times when youth were ages 16 to 19. Community disadvantage interacted with parental DRD4 status to predict low levels of protective parenting. Protective parenting, in turn, interacted with youth DRD4 status to forecast increases in youth's planful future orientations, a proximal influence on changes in risk behavior. The Parental DRD4 × Community Disadvantage interaction, but not youth DRD4 × Protective Parenting, conformed to a differential susceptibility model. Indirect effect analyses revealed a significant indirect path linking community disadvantage to youth risk behavior through a series of multilevel Gene × Environment interaction processes.

This study explores the coherence between different raters of adolescent psychopathology and examines the coherence of these ratings with earlier and later events associated with the development of psychopathology. In particular, teachers', mothers', and adolescents' ratings of the 13-year-old adolescents are examined. Additionally, the earlier factors of attachment status, environmental stress, and the friendship network are related to the different ratings. Both earlier factors and rater judgments are used to examine subsequent use of psychotherapy. The results show little coherence between raters on the presence of psychopathology in 13-year-olds and little coherence between earlier events and subsequent raters' judgments of psychopathology. However, earlier stress events and teachers' ratings of 13-year-olds' psychopathology are related to subsequent therapy use.

Perceived threat in youth’s environments can elevate risk for mental health, social, and neurocognitive difficulties throughout the lifespan. However, few studies examine variability in youth’s perceptions of threat across multiple contexts or evaluate outcomes across multiple domains, ultimately limiting our understanding of specific risks associated with perceived threats in different contexts. This study examined associations between perceived threat in youth’s neighborhood, school, and family contexts at ages 9–10 and mental health, social, and neurocognitive outcomes at ages 11–12 within a large US cohort (N = 5525) enrolled in the Adolescent Brain Cognitive DevelopmentSM Study (ABCD Study®). Latent profile analysis revealed four distinct profiles: Low Threat in all contexts, Elevated Family Threat, Elevated Neighborhood Threat, and Elevated Threat in all contexts. Mixed-effect models and post hoc pairwise comparisons showed that youth in Elevated Threat profile had poorer mental health and social outcomes 2 years later. Youth in the Elevated Family Threat profile uniquely showed increased disruptive behavior symptoms, whereas youth in the Elevated Neighborhood Threat profile predominantly displayed increased sleep problems and worse neurocognitive outcomes 2 years later. Together, findings highlight the importance of considering perceptions of threat across multiple contexts to achieve a more nuanced developmental picture.

Over the last four decades the transactional model has emerged as a central fixture of modern developmental science. Despite this, we are aware of no principled approach for determining (a) whether it is actually necessary to invoke transactional mechanisms to explain observed patterns of stability in a given domain of adaptive functioning and (b) the extent to which transactional processes, once identified in aggregate, are accounted for by measured domains with which an aspect of adaptive functioning is theoretically in transaction. Leveraging the fact that transactional mechanisms produce excess stability in an outcome domain above and beyond autoregressive processes, along with the basic logic of mediational analysis, we introduce two novel indexes for studying transactional processes strategically. We apply these metrics to data from the NICHD Study of Early Child Care and Youth Development cohort on mother- and teacher-reported externalizing problems and social competence along with teacher-reported and objective assessments of academic skills acquired in Grades 1, 3, and 5. During this developmental period we find that (a) transactional contributions to stability are strongest for teacher-reported outcomes, next strongest for mother-reported outcomes, and relatively weak for objective assessments of academic skills and (b) observed maternal sensitivity (but not child-reported friendship quality) accounts for a modest proportion of the total transactional effects operative in most of the domains of adaptive functioning we studied. Discussion focuses on extending the logic of our approach to additional waves of measurement.

Although there is growing recognition that disadvantaged contexts attenuate genetic influences on youth misbehavior, it is not yet clear how this dampening occurs. The current study made use of a “geographic contagion” model to isolate specific contexts contributing to this effect, with a focus on nonaggressive rule-breaking behaviors (RB) in the families’ neighbors. Our sample included 847 families residing in or near modestly-to-severely disadvantaged neighborhoods who participated in the Michigan State University Twin Registry. Neighborhood sampling techniques were used to recruit neighbors residing within 5km of a given family (the mean number of neighbors assessed per family was 13.09; range, 1–47). Analyses revealed clear evidence of genotype–environment interactions by neighbor RB, such that sibling-level shared environmental influences on child RB increased with increasing neighbor self-reports of their own RB, whereas genetic influences decreased. Moreover, this moderation appeared to be driven by geographic proximity to neighbors. Sensitivity analyses further indicated that this effect was specifically accounted for by higher levels of neighbor joblessness, rather than elements of neighbor RB that would contribute to neighborhood blight or crime. Such findings provocatively suggest that future genotype–environment interactions studies should integrate the dynamic networks of social contagion theory.

The functioning of the hypothalamic–pituitary–adrenal (HPA) axis is implicated in the etiology and maintenance of depressive and posttraumatic stress disorder (PTSD) symptoms. However, different maltreatment experiences as well as the increased sensitivity of the HPA axis during puberty may alter associations between the HPA axis and mental health. To address these gaps, the current study examined the potential bidirectional associations between cortisol reactivity to a stressor, PTSD symptoms, and depressive symptoms among early adolescents across two time points, 1 year apart (n = 454; Mage = 10.98 at Time 1 and Mage = 12.11 at Time 2). Multiple-group path models tested the pathways between cortiol reactivity and mental health prior to and during puberty, for different types of maltreatment . Overall, the results showed that associations between cortisol output and symptoms of PTSD and depression were driven by those in the midst of puberty. Specifically, higher cortisol output at Time 1 was linked with higher levels of subsequent PTSD and depressive symptoms for neglected youth who had reached puberty. However, depressive symptoms predicted subsequent lower cortisol output for the physical abuse and emotional abuse groups. These findings demonstrate longitudinal links between cortisol, depressive symptoms, and PTSD symptoms among youth with different types of maltreatment histories and highlight the need to consider the reorganization of the stress system during puberty in order to advance our understanding of the HPA axis and mental health.

Researchers have begun to examine the psychological toll of the ongoing global COVID-19 pandemic. Data are now emerging indicating that there may be long-term adverse effects of the pandemic on new mothers and on children born during this period. In a longitudinal study of maternal mental health and child emotional development during the pandemic, we conducted online assessments of a cohort of women at two time points: when they were pregnant at the beginning of the surge of the pandemic in the United States (baseline, N = 725), and approximately 1 year postpartum (follow-up, N = 296), examining prenatal and postnatal maternal mental health, prenatal pandemic-related stress, and infant temperament. Pandemic-related stress at baseline was associated with concurrent depressive symptoms and infant negative affect at follow-up. Baseline maternal depressive symptoms were associated with follow-up depressive symptoms, which in turn were also associated with infant negative affect. Pandemic-related stress during pregnancy may have enduring effects on infant temperament. These findings have important implications for our understanding of the emotional development of children who were in utero during the COVID-19 pandemic.

We studied the conservation scores of 21 schizophrenic and schizotypal children (aged 6;7–12;5 years) and 21 yoked normal mental age matches and their relationship to the Kiddie Formal Thought Disorder Scale measures. Like the normal children, the schizophrenic/schizotypal subjects were able to recognize the invariance of two dimensional space, number, and substance, but not of weight. Unlike the normal children, the schizophrenic/schizotypal children were poor conservers of continuous and discontinuous matter, and this was related to their illogical thinking scores. Age and IQ accounted for the conservation competence of the normal children. The conservation skills of the patients, however, were associated with the severity of their formal thought disorder scores, not with their age or IQ. The developmental approach employed in this study enabled further clarification of the cognitive parameters of formal thought disorder in middle childhood. We discuss the developmental, clinical, and possible information processing implications of these findings.

I argue that Mundy and Sigman (1989) are right to question Leslie's (1987) explanation of the autistic syndrome, but that they do so for the wrong reasons. They assert that there is a lag between the emergence of joint-attention and pretence. However, evidence for the lag is equivocal because it depends on the behavioral criteria for each skill. Moreover, even if there were a lag, it could be argued that the relatively early appearance of joint-attention simply shows that a decoupling device is available before its recruitment for pretence. More problematic, with regard to Leslie's theory, is the finding that autistic children can engage in certain forms of pretence. This result suggests that autistic children suffer not from a general incapacity to conjure up imaginary entities or properties, but from a more specific impairment in the ability to imagine mental states that they are not currently experiencing.

Overgeneral autobiographical memory, the tendency to report general memories when asked to report specific event recollections, has been implicated in the development and maintenance of psychopathology. The dominant model of overgeneral memory, the CaR-FA-X model (Williams et al., 2007), proposes that three cognitive processes (increased rumination and avoidance, and reduced executive control) either independently, or in interaction, interfere with successful memory retrieval. Although psychopathology increases significantly during adolescence, no research has tested this model in its entirety, including interaction effects, longitudinally in community youth. We tested the model with 323 adolescents (152 females, 171 males) across four annual assessment points. Increased avoidance predicted higher proportions of overgeneral memories from Time 3 to Time 4, but this association was stronger for youth with elevated depressive symptoms across the four waves, and limited to memories generated in response to negative cue words. This finding may indicate that youth with stable higher levels of depression remember in an overgeneral way to avoid re-elicitation of negative event-related emotions. In youth with lower depression levels across time, the CaR-FA-X mechanisms did not predict overgeneral memory.

In this three-generation longitudinal study of familial depression, we investigated the continuity of parenting styles, and major depressive disorder (MDD), temperament, and social support during childrearing as potential mechanisms. Each generation independently completed the Parental Bonding Instrument (PBI), measuring individuals’ experiences of care and overprotection received from parents during childhood. MDD was assessed prospectively, up to 38 years, using the semi-structured Schedule for Affective Disorders and Schizophrenia (SADS). Social support and temperament were assessed using the Social Adjustment Scale – Self-Report (SAS-SR) and Dimensions of Temperament Scales – Revised, respectively. We first assessed transmission of parenting styles in the generation 1 to generation 2 cycle (G1→G2), including 133 G1 and their 229 G2 children (367 pairs), and found continuity of both care and overprotection. G1 MDD accounted for the association between G1→G2 experiences of care, and G1 social support and temperament moderated the transmission of overprotection. The findings were largely similar when examining these psychosocial mechanisms in 111 G2 and their spouses (G2+S) and their 136 children (G3) (a total of 223 pairs). Finally, in a subsample of families with three successive generations (G1→G2→G3), G2 experiences of overprotection accounted for the association between G1→G3 experiences of overprotection. The results of this study highlight the roles of MDD, temperament, and social support in the intergenerational continuity of parenting, which should be considered in interventions to “break the cycle” of poor parenting practices across generations.

Evidence suggests that early trauma may have a negative effect on cognitive functioning in individuals with psychosis, yet the relationship between childhood trauma and cognition among those at clinical high risk (CHR) for psychosis remains unexplored. Our sample consisted of 626 CHR children and 279 healthy controls who were recruited as part of the North American Prodrome Longitudinal Study 2. Childhood trauma up to the age of 16 (psychological, physical, and sexual abuse, emotional neglect, and bullying) was assessed by using the Childhood Trauma and Abuse Scale. Multiple domains of cognition were measured at baseline and at the time of psychosis conversion, using standardized assessments. In the CHR group, there was a trend for better performance in individuals who reported a history of multiple types of childhood trauma compared with those with no/one type of trauma (Cohen d = 0.16). A history of multiple trauma types was not associated with greater cognitive change in CHR converters over time. Our findings tentatively suggest there may be different mechanisms that lead to CHR states. Individuals who are at clinical high risk who have experienced multiple types of childhood trauma may have more typically developing premorbid cognitive functioning than those who reported minimal trauma do. Further research is needed to unravel the complexity of factors underlying the development of at-risk states.

The way that people internalize adverse experiences plays an important role in the development of psychopathology. The Pathogenic Belief Scale (PBS) is intended to operationalize a transtheoretical understanding of repetitive patterns of emotion-laden beliefs that develop in childhood and continue to influence people's current experience. Using a cross-sectional survey design, we recruited a large heterogeneous sample of 246 clinic outpatients and 732 adults in the community. Besides the PBS, measures of adverse parenting experiences and common psychopathology were administered. An exploratory factor analysis of the total sample of 978 participants was conducted followed by a convergent validity analysis for the 246 clinic outpatients. The three-factor solution included “cannot rely on others,” “undeserving,” and “interpersonal guilt,” and it showed good psychometric properties, including convergent validity with the measures of adverse parenting experiences and psychopathology. The 34-item PBS offers a promising self-report measure that could help delineate and understand the pathogenic beliefs that heterogeneous samples of patients may hold. Pathogenic beliefs may be relevant to the psychotherapy process, regardless of model or theoretical context.