This study reports on the description of children’s distinct trajectories of intrusive grief, baseline predictors of grief trajectories, and the association of grief trajectories with mental health, substantive abuse and disordered grief six and fifteen years following baseline assessment. The study uses data on 244 parentally-bereaved children ages 8–16 at baseline. Four distinct trajectories were identified using Growth Mixture Modeling over four waves of assessment across 6 years. The trajectories were labeled high chronic grief, moderate chronic grief, grief recovery (starts high but decreases over 6 years of assessment) and grief resilience (chronic low grief). Baseline factors associated with chronic high or moderate chronic levels of grief included depression, traumatic cause of death (homicide or suicide), active inhibition of emotional expression, active coping, child age and gender. At the six-year assessment, trajectories were associated with internalizing mental health problems, higher level of traumatic grief, and aversive views of the self. At the fifteen-year assessment, trajectories were associated with intrusive grief. The results are interpreted in terms of consistency with prior evidence of children’s long-term grief, theoretical processes that may account for chronic grief and implications for the development of preventive and treatment interventions.

There is strong evidence for a general psychopathology dimension which captures covariance among all forms of psychopathology, yet its nature and underlying association with personality remain unclear. This study examined the co-development of general psychopathology and four high-risk personality traits: anxiety sensitivity, negative thinking, sensation seeking, and impulsivity. Data from two large Australian school-based randomised controlled trials of substance use prevention programs were analysed (N = 2,083, mean age at baseline = 13.49 years). Adolescents completed self-report measures of psychopathology symptoms and personality at baseline, one-, two-, and three-years post-baseline. Latent curve models with structured residuals, were used to examine the co-development of general psychopathology (extracted from a higher-order model) and personality traits from 13 to 16 years of age, controlling for age, sex, and cohort. Higher than usual levels of anxiety sensitivity and impulsivity were associated with higher than usual levels of general psychopathology at subsequent time points, and higher than usual levels of general psychopathology were associated with higher than usual levels of negative thinking at later time points. Sensation seeking was unrelated to general psychopathology. These findings enhance our understanding of the meaning and validity of general psychopathology, highlighting potential personality-based prevention and intervention targets.

Personality pathology is hypothesized to be an important factor in shaping identity, yet longitudinal evidence linking dimensional measures of identity and personality pathology remains scarce. To address this knowledge gap and shed light on the reciprocal dynamics proposed by the alternative model of personality disorder, we conducted a comprehensive seven-year study involving 372 emerging adults from a community sample (MageT1 = 21.98 years, SDT1 = 1.13; 57% females). Pathological personality traits were assessed using the short form of the Personality Inventory for DSM-5 (PID-5 SF) while identity was assessed with the Dimensions of Identity Development Scale (DIDS). Cross-lagged analyses in Mplus revealed that personality pathology consistently predicts subsequent different levels of identity seven years later, whereas only one significant pathway from identity to personality pathology was found. Notably, negative affectivity and detachment emerge as the most influential pathological personality trait, whereas no significant effects were found for disinhibition and psychoticism. In summary, our study uncovered compelling longitudinal associations that underscore the pivotal role of pathological personality traits in the development of identity. Implications and suggestions for future research are discussed.

Neglect remains understudied compared to other forms of maltreatment. While studies have shown that neglect has negative effects on mental health in adolescence, yet unresolved is whether these impacts result from critical period or cumulative effects. In the present article, we use a novel approach to compare these two hypotheses from the impact of two types of neglect, failure to provide (FTP) and lack of supervision (LOS), on adolescent depression and internalizing symptoms. Data derive from the LONGSCAN consortium, a diverse, multi-site, prospective study of children from approximately age 2–16. Despite our hypothesis that the critical period of early childhood would have the greatest impact on adolescent internalizing mental health, exposure to neglect during the critical period of adolescence (ages 12–16) was the best-fitting model for the effects of FTP neglect on depression, and the effects of LOS neglect on both depression and internalizing symptoms. The cumulative model (exposure across all time periods) best explained the effects of FTP neglect on internalizing symptoms. Results were robust to the addition of control variables, including other forms of maltreatment. These findings demonstrate that responding to neglect into adolescence must be considered as urgent for child welfare systems.

Children’s neural responses to emotions may play a role in the intergenerational transmission of anxiety. In a prospective longitudinal study of a community sample of N = 464 mother–child dyads, we examined relations among maternal anxiety symptoms when children were infants and age 5 years, child neural responses to emotional faces (angry, fearful, happy) at age 3 years, and child internalizing symptoms at age 5 years. Path analyses tested whether amplitudes of event-related potential (ERP) components selected a priori (N290, Nc, P400) (a) mediated associations between maternal anxiety symptoms in infancy and child internalizing symptoms at 5 years and/or (b) moderated associations between maternal anxiety symptoms at 5 years and child internalizing symptoms at 5 years. Mediating effects were not observed for any of the ERP measures. Nc and P400 amplitudes to angry faces and Nc amplitude to happy faces moderated the effect of maternal anxiety at 5 years on child internalizing symptoms at 5 years. Effects were not related to maternal depressive symptoms. Differential sex effects were not observed. The findings suggest that larger neural responses to emotional faces may represent a biological risk factor that amplifies vulnerability to the development of internalizing symptomatology in young children exposed to maternal anxiety.

Early adversity increases risk for child mental health difficulties. Stressors in the home environment (e.g., parental mental illness, household socioeconomic challenges) may be particularly impactful. Attending out-of-home childcare may buffer or magnify negative effects of such exposures. Using a longitudinal observational design, we leveraged data from the NIH Environmental influences on Child Health Outcomes Program to test whether number of hours in childcare, defined as 1) any type of nonparental care and 2) center-based care specifically, was associated with child mental health, including via buffering or magnifying associations between early exposure to psychosocial and socioeconomic risks (age 0–3 years) and later internalizing and externalizing symptoms (age 3–5.5 years), in a diverse sample of N = 2,024 parent–child dyads. In linear regression models, childcare participation was not associated with mental health outcomes, nor did we observe an impact of childcare attendance on associations between risk exposures and symptoms. Psychosocial and socioeconomic risks had interactive effects on internalizing and externalizing symptoms. Overall, the findings did not indicate that childcare attendance positively or negatively influenced child mental health and suggested that psychosocial and socioeconomic adversity may need to be considered as separate exposures to understand child mental health risk in early life.

Callous-unemotional (CU) traits represent a risk factor for persistent, severe levels of externalizing problems. Irritability may predict the development of CU traits for some individuals, who are thought to acquire them in reaction to negative environmental experiences. Models on the development of CU traits have emphasized the socializing role of harsh parenting to the neglect of negative peer experiences. The present study 1) tested primary and alternative models of physical and relational peer victimization as socialization agents in relations between irritability and CU traits; and 2) considered hypothalamic-pituitary-adrenal-axis functioning as a moderator of these associations. Gender moderation was also considered. Aims were tested from middle childhood to adolescence using data from the NICHD Study of Early Child Care and Youth Development, which includes a large national sample (N = 1,077) and multiple methods and informants for the constructs of interest. Positive associations between irritability, peer victimization, and CU traits were supported, with indirect effects on CU traits supported specifically from peer victimization through increases in irritability. Associations between relational victimization, irritability, and CU traits may be particularly salient for females, whose experiences have been neglected to date. However, effects were small, and replication efforts are needed.

Although childhood maltreatment is associated with externalizing symptoms, not all individuals with these experiences develop externalizing behaviors and some exhibit positive adjustment. To address this multifinality, we used latent growth curve modeling to identify trajectories of (a) externalizing symptoms and (b) subjective wellbeing from late adolescence through young adulthood, determine whether types of childhood maltreatment and domains of executive functioning (EF) are associated with initial levels and growth (slopes) of externalizing symptoms or subjective wellbeing, and investigate whether EF moderates these relations. Participants were youth recruited at ages 10–12 (N = 775; 69% male, 31% female; 76% White, 21% Black/African American, 3% multiracial). We examined EF at ages 10–12, childhood maltreatment reported retrospectively at age 25, and externalizing symptoms and subjective wellbeing at multiple points between ages 16 and 28. Experience of childhood maltreatment and certain EF domains were associated with externalizing symptoms and subjective wellbeing at age 16. EF domains were associated with rate of change in externalizing problems, though not in expected directions. EF variables moderated the relation between maltreatment and initial levels of both outcomes and change in externalizing symptoms. Findings have implications for intervention efforts to mitigate externalizing problems and bolster positive adjustment.

Despite the added value of multisystem (relative to traditional single-system) approaches for characterizing biological processes linked to risk for psychopathology (e.g., neuroendocrine stress responsivity; Buss et al., 2019; Quas et al., 2014), no study to date has evaluated whether multisystem processes may serve as viable biological targets of intervention. Utilizing a multiple-levels-of-analysis approach (Cicchetti & Dawson, 2002), this person-centered study examined whether stress-adapted patterns of hypothalamus–pituitary–adrenal (HPA) axis and sympathetic-adrenomedullary (SAM) system co-activation were amenable to change following the Building a Strong Identity and Coping Skills intervention (BaSICS; Wadsworth et al., 2022). Preadolescents exposed to concentrated poverty (n = 112, Mage = 11.78 years, 57.1% female, 54% assigned to intervention; 40% Hispanic, 63% Black, 20% White) completed questionnaires and the Trier Social Stress Test at both pre- and posttest. Multitrajectory modeling of cortisol and alpha-amylase levels identified four pretest and posttest HPA-SAM co-activation profiles. At pretest, youth exhibiting Asymmetric Nos. 1 & 2 HPA-SAM co-activation reported greater maladjustment relative to youth with Symmetric Nos. 1 & 2 co-activation. Youth exhibiting Asymmetric No. 1 co-activation at pretest were more likely to exhibit Symmetric No. 1 co-activation following BaSICS relative to control. Findings highlight the potential of BaSICS to restore neuroendocrine stress response function in impoverished youth, pointing to HPA–SAM co-activation as a potential biological target of preventive intervention in this population.

Depression is transmitted within families, but the mechanisms involved in such transmission are not clearly defined. A potential marker of familial risk is the neural response to errors, which may play a role in depression symptoms and is known to be partially heritable. Here, 97 mother-daughter dyads completed a Flanker task while electroencephalography markers of error monitoring were recorded: the error-related negativity (ERN) and response-locked delta and theta power. We assessed whether these measures of neural response to errors 1) were associated with history of recurrent major depressive disorder (MDD) and current depression symptoms among mothers, 2) were correlated among mother-daughter dyads, and 3) were associated with maternal history of recurrent MDD and maternal symptoms of depression among daughters. A history of recurrent MDD was associated with blunted delta and increased theta among mothers. Across mothers, delta and theta were negatively and positively associated, respectively, with current depression symptoms. Mothers’ and daughters’ ERN were positively correlated. Finally, current maternal depression symptoms were negatively associated with delta power in daughters. These results suggest that neural responses to errors may be implicated in the intergenerational transmission of depression. These results also support the relevance of delta oscillations to understanding pathways to depression.

Building on the sensitization hypothesis, the present work aimed to examine how parent-adolescent conflict might be associated with heightened emotional reactivity to peer conflicts, which in turn shape the development of adolescent internalizing psychopathology. Participants were 108 Taiwanese adolescents between the ages of 18 and 19 (Mage = 18.53, SDage = 0.39; 64% female) who completed baseline assessments, 14-day daily surveys, and 6-month follow-up assessments. Emotional reactivity was measured by calculating the daily association between peer conflict and positive and negative emotions. Results indicated that greater baseline parent-adolescent conflict was associated with higher negative emotional reactivity to peer conflicts, which then predicted increased depressive symptoms and anxiety symptoms 6 months later. Moreover, greater positive emotional reactivity to peer conflicts (i.e., more declines in positive emotions in response to peer conflicts) predicted increased depressive symptoms. Thus, the findings of the current study support and extend the sensitization hypothesis and suggest that parent-adolescent conflict may contribute to family-of-origin sensitization in non-familial, interpersonal contexts. The results have key implications for understanding adolescent developmental psychopathology associated with family conflicts and emotional reactivity.

The increased risk for psychopathology associated with interpersonal violence exposure (IPV, e.g., physical abuse, sexual assault) is partially mediated by neurobiological alterations in threat-related processes. Evidence supports parsing neural circuitry related to transient and sustained threat, as they appear to be separable processes with distinct neurobiological underpinnings. Although childhood is a sensitive period for neurodevelopment, most prior work has been conducted in adult samples. Further, it is unknown how IPV exposure may impact transient-sustained threat neural interactions. The current study tested the moderating role of IPV exposure on sustained vmPFC-transient amygdala co-activation during an fMRI task during which threat and neutral cues were predictably or unpredictably presented. Analyses were conducted in a sample of 212 community-recruited youth (M/SDage = 11.77/2.44 years old; 51.9% male; 56.1% White/Caucasian). IPV-exposed youth evidenced a positive sustained vmPFC-transient amygdala co-activation, while youth with no IPV exposure did not show this association. Consistent with theoretical models, effects were specific to unpredictable, negative trials and to exposure to IPV (i.e., unrelated to non-IPV traumatic experiences). Although preliminary, these findings provide novel insight into how childhood IPV exposure may alter neural circuity involved in specific facets of threat processing.

Preschool anxiety is highly prevalent and well known to predict risk for future psychopathology. The present study explores whether a diagnosis of an anxiety disorder in preschool interacts with (a) social skills and (b) cognitive ability to longitudinally predict psychopathology, two well-known protective factors, among a sample of 207 children measured at preschool (Mage = 4.34 years) and early childhood (Mage = 6.61 years). To assess social skills and cognitive ability, we utilized the Social Skills Rating Scale and the Differential Abilities Scale, respectively. To assess psychopathology, we utilized the parent report of the Preschool Age Psychiatric Assessment. Hierarchical linear regression models revealed significant interactions between both social skills and cognitive ability with preschool anxiety. We observed that social skills protected against emergent psychopathology for both children with and without anxiety, although this association was stronger for children with preschool anxiety. Contrastingly, cognitive ability served as a protective factor against future psychopathology primarily among children without preschool anxiety. Results from this study identify targets for future intervention and inform our understanding of how preschool anxiety, a common disorder among young children, shapes future psychopathology risk in childhood.

The field of developmental psychopathology has grown broadly. Here, I draw upon lessons learned from Dante Cicchetti to highlight areas that show promise for continued disciplinary advancement. These include attention to equifinality and multifinality in the conceptualization of initial study designs, and more emphasis on specificity in accounting for developmental change. A shift from reliance on external events and towards greater diversity of research approaches will allow researchers to devote attention to the variety of ways that individuals come to understand and then respond to their own life experiences. The field of developmental psychopathology holds tremendous promise for advancing basic science about human development that can be applied to create interventions that improve the well-being of individuals and address significant societal issues.

The importance of interactions between child temperament and parenting has been accepted ever since Thomas and Chess (1977) proposed their “goodness-of-fit” construct, but over the last three decades, pertinent research has grown exponentially. Researchers examining child characteristics that can moderate the effects of socialization have tested increasingly complex, nuanced, and sophisticated models, largely inspired by the highly influential frameworks of child plasticity or differential susceptibility (Belsky & Pluess, 2009). Yet, multiple questions remain unsettled. We addressed four such questions as applied to predicting children’s observed disregard for rules at age 4.5 in a study of 200 community families from the US Midwest. (a) We examined children’s observed negative emotionality at 16 months, most commonly seen as a plasticity “trait,” but separating anger and fear proneness, which may differently moderate effects of socialization. (b) We examined two separate aspects of observed parental socialization at age 3, mutually responsive orientation and power assertion. (c) We distinguished analytically diathesis-stress from differential susceptibility. (d) We examined all effects in mother– and father–child relationships. We supported both diathesis-stress and differential susceptibility, depending on the facet of negative emotionality, the aspect of socialization considered, and parental gender, highlighting the nuanced nature of the processes involved.

Emotion regulation, as a typical “top-down” emotional self-regulation, has been shown to play an important role in children’s oppositional defiant disorder (ODD) development. However, the association between other self-regulation subcomponents and the ODD symptom network remains unclear. Meanwhile, while there are gender differences in both self-regulation and ODD, few studies have examined whether their relation is moderated by gender. Five hundred and four children (age 6–11 years; 207 girls) were recruited from schools with parents and classroom teachers completing questionnaires and were followed up for assessment six months later. Using moderation network analysis, we analyzed the relation between self-regulation and ODD symptoms, and the moderating role of gender. Self-regulation including emotion regulation, self-control, and emotion lability/negativity had broad bidirectional relations with ODD symptoms. In particular, the bidirectional relations between emotion regulation and ODD3 (Defies) and between emotion lability/negativity and ODD4 (Annoys) were significantly weaker in girls than in boys. Considering the important role of different self-regulation subcomponents in the ODD symptom network, ODD is better conceptualized as a self-regulation disorder. Each ODD symptom is associated with different degrees of impaired “bottom-up” and “top-down” self-regulation, and several of the associations vary by gender.

This study explores patterns of self-regulation and emotional well-being among Syrian refugee children in Lebanon, employing a person-centered approach, responding to theoretical challenges articulated by Dante Cicchetti and other psychologists. Using latent profile analysis with data from 2,132 children, we identified seven distinct profiles across cognitive regulation, emotional-behavioral regulation, interpersonal regulation, and emotional well-being. These profiles showed significant heterogeneity in patterns of self-regulation across domains and emotional well-being among Syrian children. Some profiles consistently exhibited either positive (“Well-regulated and Adjusted”) or negative (“Moody and Frustrated”) functioning across all domains, while others revealed domain-specific challenges, e.g., particularly sensitive to interpersonal conflict. This heterogeneity in the organization of self-regulatory skill and emotional well-being challenges the traditional homogeneous view of child development in conflict settings. The study also underscores the profiles’ differential associations with demographic characteristics and experiences, with school-related experiences being particularly salient. We discuss the implications of these findings for future research in developmental psychopathology on self-regulation and emotional well-being in conflict-affected contexts. In addition, we advocate for tailored interventions to meet the diverse needs of children affected by conflict.

Limited data exists on the role of attachment in influencing the development and wellbeing of refugee children. Herein we describe patterning and correlates of attachment in an Australian sample of adolescent Tamil refugees. Sixty-eight adolescents, aged 10–18, were assessed for trauma exposure, mental health problems and pattern of attachment. Attachment representations were assessed by discourse analysis of structured attachment interviews. Mothers of the adolescents were assessed for post-migration family stressors, depression, and post-traumatic stress disorder (PTSD) using self-report measures. Inhbitory A and A+ patterns of attachment predominated. Attachment insecurity was associated with child trauma exposure (β = .417), post-migration family stressors (β = .297) and maternal PTSD (β = .409). Path modeling demonstrated that attachment insecurity mediated associations of child trauma exposure, family stressors and maternal PTSD with child mental health problems, the model yielding adequate fit (Comparative Fit Index [CFI] = .957; standardized root mean square residual [SRMR] = .066; R2 .449). Our cross-sectional findings suggest that compromised attachment security is one potential mechanism by which the adverse effects of refugee family trauma and adversity are transmitted to children. Resettlement policy and psychosocial services should aim to preserve and/or reestablish attachment security in child-caregiver relationships through policy that reduces family stressors and interventions that bolster parental mental health and caregiver sensitivity.

School connectedness may offset mental health risks associated with childhood adversity. The present study examined the potential protective effects of school connectedness against childhood adversity when predicting adolescent mental health outcomes in 9,964 individuals (51% female, 81% white) from the Millennium Cohort Study. Structural equation models were fitted to examine the longitudinal relationships between childhood adversity, school connectedness, and adolescent mental health. Childhood adversity was a risk factor, predicting greater internalizing and externalizing problems and lower levels of positive mental health. School connectedness was a promotive factor as it predicted fewer mental health problems and greater positive mental health. Furthermore, school connectedness at age 11 was protective against childhood adversity when predicting internalizing and externalizing problems at age 14. That is, students with a history of adversity who felt more connected to school were less likely to exhibit internalizing and externalizing symptoms than those who felt less connected to school. Only school connectedness at age 11 was protective against childhood adversity, indicating that feeling connected to school at younger ages may disrupt processes linking childhood adversity to adolescent mental health. Schools should foster students’ feelings of connectedness to protect vulnerable individuals and benefit all pupils’ mental health.

Prenatal glucocorticoid exposure has been negatively associated with infant neurocognitive outcomes. However, questions about developmental timing effects across gestation remain. Participants were 253 mother-child dyads who participated in a prospective cohort study recruited in the first trimester of pregnancy. Diurnal cortisol was measured in maternal saliva samples collected across a single day within each trimester of pregnancy. Children (49.8% female) completed the Bayley Mental Development Scales, Third Edition at 6, 12, and 24 months and completed three observational executive function tasks at 24 months. Structural equation models adjusting for sociodemographic covariates were used to test study hypotheses. There was significant evidence for timing sensitivity. First-trimester diurnal cortisol (area under the curve) was negatively associated with cognitive and language development at 12 months and poorer inhibition at 24 months. Second-trimester cortisol exposure was negatively associated with language scores at 24 months. Third-trimester cortisol positively predicted performance in shifting between task rules (set shifting) at 24 months. Associations were not reliably moderated by child sex. Findings suggest that neurocognitive development is sensitive to prenatal glucocorticoid exposure as early as the first trimester and underscore the importance of assessing developmental timing in research on prenatal exposures for child health outcomes.