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.

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.

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.

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.

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.

Cognitive abilities are heritable and influenced by socioeconomic status (SES). It is critical to understand the association between SES and cognition beyond genetic propensity to inform potential benefits of SES-based interventions and to determine if such associations vary across (i) cognitive domains, (ii) facets of SES, and/or (iii) genetic propensity for different aspects of cognition. We examined the contributions of neighborhood socioeconomic advantage, family income, and polygenic scores (PGS) for domains of cognition (i.e., general cognitive ability, executive function, learning and memory, fluid reasoning) in a sample of children (ages 9–10; n = 5549) most genetically similar to reference populations from Europe. With some variability across cognitive outcomes, family income and PGS were independently significantly associated with cognitive performance. Within-sibling analyses revealed that cognitive PGS associations were predominantly driven by between-family effects suggestive of non-direct genetic mechanisms. These findings provide evidence that SES and genetic propensity to cognition have unique associations with cognitive performance in middle childhood. These results underscore the importance of environmental factors and genetic influences in the development of cognitive abilities and caution against overinterpreting associations with PGS of cognitive and educational outcomes as predominantly direct genetic effects.

Suicide rates are rising among U.S. youth, yet our understanding of developmental mechanisms associated with increased suicide risk is limited. One high-risk pathway involves an interaction between heritable trait impulsivity and emotion dysregulation (ED). Together, these confer increased vulnerability to nonsuicidal self-injury (NSSI), suicide ideation (SI), and suicide attempts (SAs). Previous work, however, has been limited to homogeneous samples. We extend the Impulsivity × ED hypothesis to a more diverse sample of adolescents (N = 344, ages 12–15 at Baseline, 107 males and 237 females) who were treated for major depression and assessed four times over two years. In multilevel models, the impulsivity × ED interaction was associated with higher levels and worse trajectories of NSSI, SI, and SAs. As expected, stressful life events were also associated with poorer trajectories for all outcomes, and NSSI was associated with future and concurrent SI and SAs. These findings extend one developmental pathway of risk for self-harming and suicidal behaviors to more diverse adolescents, with potential implications for prevention.

Autism spectrum disorder prevalence more than quadrupled in the United States between 2000 and 2020. Ice storm-related prenatal maternal stress (PNMS) predicts autistic-like trait severity in children exposed early in gestation. The objective was to determine the extent to which PNMS influences the severity and trajectory of autistic-like traits in prenatally flood-exposed children at ages 4–7 years and to test moderation by sex and gestational timing. Soon after the June 2008 floods in Iowa, USA, 268 women pregnant during the disaster were assessed for objective hardship, subjective distress, and cognitive appraisal of the experience. When their children were 4, 5½, and 7 years old, mothers completed the Social Communication Questionnaire (SCQ) to assess their children’s autistic-like traits; 137 mothers completed the SCQ for at least one age. The final longitudinal multilevel model showed that the greater the maternal subjective distress, the more severe the child’s autistic-like traits, controlling for objective hardship. The effect of PNMS on rate of change was not significant, and there were no significant main effects or interactions involving sex or timing. Prenatal maternal subjective distress, but not objective hardship or cognitive appraisal, predicted more severe autistic-like traits at age 4, and this effect remained stable through age 7.

Similar to adults with posttraumatic stress disorder, children with early life adversity show bias in memory for negative emotional stimuli. However, it is not well understood how childhood adversity impacts mechanisms underlying emotional memory. N = 56 children (8–14 years, 48% female) reported on adverse experiences including potentially traumatic events and underwent fMRI while attending to emotionally pleasant, neutral, or negative images. Post-scan, participants completed a cued recall test to assess memory for these images. Emotional difference-in-memory (DM) scores were computed by subtracting negative or positive from neutral recall performance. All children showed enhancing effects of emotion on recall, with no effect of trauma load. However, children with less trauma showed a larger emotional DM for both positive and negative stimuli when amygdala or anterior hippocampal activity was higher. In contrast, highly trauma-exposed children demonstrated a lower emotional DM with greater amygdala or hippocampal activity. This suggested that alternative neural mechanisms might support emotional enhancement of encoding in children with greater trauma load. Whole-brain analyses revealed that right fusiform activity during encoding positively correlated with both trauma load and successful later recall of positive images. Therefore, highly trauma-exposed children may use alternative, potentially adaptive neural pathways via the ventral visual stream to encode positive emotional events.

Childhood maltreatment is linked with later depressive symptoms, but not every maltreated child will experience symptoms later in life. Therefore, we investigate whether genetic predisposition for depression (i.e., polygenic score for depression, PGSDEP) modifies the association between maltreatment and depressive symptoms, while accounting for different types of maltreatment and whether it was evaluated through prospective and retrospective reports. The sample included 541–617 participants from the Quebec Longitudinal Study of Child Development with information on maltreatment, including threat, deprivation, assessed prospectively (5 months–17 years) and retrospectively (reported at 23 years), PGSDEP and self-reported depressive symptoms (20–23 years). Using hierarchical linear regressions, we found that retrospective, but not prospective indicators of maltreatment (threat/deprivation/cumulative) were associated with later depressive symptoms, above and beyond the PGSDEP. Our findings also show the presence of gene–environment interactions, whereby the association between maltreatment (retrospective cumulative maltreatment/threat, prospective deprivation) and depression was strengthened among youth with higher PGSDEP scores. Consistent with the Diathesis-Stress hypothesis, our findings suggest that a genetic predisposition for depression may exacerbate the putative impact of maltreatment on later depressive symptoms, especially when maltreatment is retrospective. Understanding the gene–environment interplay emerging in the context of maltreatment has the potential to guide prevention efforts.

Child maltreatment impacts approximately one in seven children in the United States, leading to adverse outcomes throughout life. Adolescence is a time period critical for the development of executive function, but there is little research examining how abuse and neglect may differently affect the developmental trajectories of executive function throughout adolescence and into young adulthood. In the current study, 167 adolescents participated at six time points from ages 14 to 20. At each time point, adolescents completed behavioral tasks measuring the three dimensions of executive function (working memory, inhibitory control, and cognitive flexibility). Neglect and abuse in early life (ages 1–13) were reported at ages 18–19. Unconditional growth curve models revealed age-related improvement in all three executive function dimensions. Conditional growth curve models tested the prospective effects of recalled neglect and abuse on the developmental trajectories of executive function. The results revealed that neglect was associated with developmental changes in working memory abilities, such that greater levels of neglect during ages 1–13 were associated with slower increases in working memory abilities across ages 14–20. These findings highlight the adverse consequences of early neglect experiences shown by delayed working memory development during adolescence into young adulthood.

Parenting behaviors play an important role in the transmission of depressive symptoms from mothers to children. Although reduced positive affect is a central feature of depression, models of intergenerational transmission have neglected maternal socialization of positive affect as a mediating mechanism. This study investigated whether maternal responses to infant positive affect mediate the link between mothers’ and toddlers’ depressive symptoms. A community sample of 128 mothers (58% White) and their infants (Mage = 6.65 months, SD = 0.53 at first visit) participated in 3 assessments over a 1-year period. Assessments included self-reports of postpartum depressive symptoms, observational measures of maternal responses to infant positive affect and maternal sensitivity, and mother report of toddlers’ depressive problems. Mediation analyses revealed that mothers with elevated postpartum depressive symptoms displayed fewer supportive responses to their infants’ positive affect. In turn, infants who received fewer supportive responses had more depressive problems in toddlerhood. The indirect effect of postpartum depressive symptoms on toddlers’ depressive problems via maternal supportive responses remained significant after controlling for maternal sensitivity. Findings suggest that maternal responses to infant positive affect play a unique role in the intergenerational transmission of depressive symptoms. The theoretical and practical implications of these findings are discussed.

We investigated cross-sectional and longitudinal associations between neonate microbial exposure and emerging behavioral temperament measures at the ages of 1, 2, and 3 years. Infants and mothers (n = 335) were extracted from the Kuopio Birth Cohort Study. Temperament was assessed using the Infant Behavioral and Early Childhood Behavioral Questionnaires. Microbial samples were collected from oral cavity at birth and the bacterial profiles were assessed using 16S rRNA gene sequencing. Microbial diversity was characterized using alpha and beta diversity metrics. Analyses were performed for the most abundant genera. The sample was analyzed as a whole, as well as divided into subgroups representing no antibiotic use during birth (n = 198) and those with antibiotic use during birth (n = 137). No significant associations were observed between microbial profiles and behavioral measures after Bonferroni corrections. Nevertheless, our pre-correction results indicated an association between increased behavioral temperament surgency in the first year and beta diversity (high abundance of Bacteroides, Faecalibacterium and Blautia, low abundance of Lactobacillus) in the antibiotic use group. Additionally, pre-corrections, a high relative abundance of Staphylococcus was associated with increased surgency through years 1, 2, and 3 in the no antibiotics group, prompting consideration into a possible link between antibiotic use and emerging behavioral temperament.