An accelerated longitudinal research design was used to examine heterogeneity in the developmental co-occurrence of peer relational victimization and aggression and of peer overt victimization and aggression from age 4.5 to 10.5 years. Data were gathered from four cohorts of children in kindergarten to Grade 3 (N = 503) on six occasions across 2 years. Psychopathology, peer, and social–cognitive factors were examined as predictors of the joint trajectories. Sequential process latent growth mixture models identified four distinct subgroups for the relational trajectories (co-occurring increasing aggression, co-occurring increasing victimization, high chronic victimization, typical low risk) and four distinct subgroups for the overt trajectories (co-occurring decelerating aggression, high chronic victimization, moderate chronic victimization, typical low risk). Membership in the co-occurring trajectories was associated with psychopathology and membership in the chronic victimization trajectories was related to internalizing and social–cognitive problems but also peer likeability.

Heavy episodic drinking (HED) is a major public health concern, and youth who engage in HED are at increased risk for alcohol-related problems that continue into adulthood. Importantly, there is heterogeneity in the onset and course of adolescent HED, as youth exhibit different trajectories of initiation and progression into heavy drinking. Much of what is known about the etiology of adolescent HED and alcohol-related problems that persist into adulthood comes from studies of predominantly White, middle-class youth. Because alcohol use and related problems vary by race/ethnicity and socioeconomic status, it is unclear whether previous findings are relevant for understanding developmental antecedents and distal consequences of adolescent HED for minoritized individuals. In the current study, we utilize a developmental psychopathology perspective to fill this gap in the literature. Using a racially and economically diverse cohort followed from adolescence well into adulthood, we apply group-based trajectory modeling (GBTM) to identify patterns of involvement in HED from age 14 to 17 years. We then investigate developmental antecedents of GBTM class membership, and alcohol-related distal outcomes in adulthood (∼ age 31 years) associated with GBTM class membership. Results highlight the importance of adolescent alcohol use in predicting future alcohol use in adulthood.

Utilizing a large (N = 739), ancestrally homogenous sample, the current study aimed to better understand biological risk processes involved in the development of depressive symptoms in maltreated, African American children age 8-12 years. Maltreatment was independently coded from Child Protective Services records and maternal report. Self-reported depressive symptoms were attained in the context of a week-long, summer research camp. DNA was acquired from buccal cell or saliva samples and genotyped for nine polymorphisms in four hypothalamic-pituitary-adrenal (HPA)-axis-related genes: FKBP5, NR3C1, NR3C2, and CRHR1. Salivary cortisol samples were collected each morning (9 a.m.) and late afternoon (4 p.m.) throughout the week to assess HPA functioning. Results revealed that experiences of maltreatment beginning prior to age 5 were most predictive of depressive symptoms, whereas maltreatment onset after age 5 was most predictive of HPA axis dysregulation (blunted daytime cortisol patterns). Multigenic risk did not relate to HPA functioning, nor did it moderate the relationship between maltreatment and HPA activity. There was no mediation of the relationship between maltreatment and depressive symptoms by HPA dysfunction. Results are interpreted through a developmental psychopathology lens, emphasizing the principle of equifinality while carefully appraising racial differences. Implications for future research, particularly the need for longitudinal studies, and important methodological considerations are discussed.

Childhood maltreatment and mental health problems are common among young people placed out-of-home. However, evidence on the impact of maltreatment on the course of mental health problems in at-risk populations is sparse. The aim of this longitudinal study is twofold: (a) describe the course of mental health problems and the shift in symptom patterns among adolescents in youth residential care into young adulthood and (b) assess how childhood maltreatment is related to the course of mental health problems. One hundred and sixty-six adolescents in Swiss youth residential care were followed up into young adulthood (36.1% women; MAge-Baseline = 16.1 years; MAge-Follow-Up = 26.4 years). Latent transition analysis was employed to analyze transitions of symptom patterns and their association with maltreatment exposure. We found three latent classes of mental health problems: a “multiproblem”-class (51.8% baseline; 33.7% follow-up), a “low symptom”-class (39.2% baseline; 60.2% follow-up), and an “externalizing”-class (9.0% baseline; 6.0% follow-up). Individuals in the “multiproblem”-class were likely to transition towards less-complex symptom patterns. Higher severity of self-reported childhood maltreatment was associated with more complex and persistent mental health problems. Our study underlines the need for collaboration between residential and psychiatric care systems within and after care placements, with a specialized focus on trauma-informed interventions and care.

Although common, little is known about the potential impacts of sibling victimization, and how best to ameliorate these. We explored longitudinal associations between sibling victimization and mental health and wellbeing outcomes, and promotive and risk factors that predicted better or worse outcomes following victimization. Data were from >12,000 participants in the Millennium Cohort Study, a longitudinal UK birth cohort, who reported on sibling victimization at age 11 and/or 14 years. We identified potential risk and promotive factors at family, peer, school, and neighborhood levels from age 14 data. Mental health and wellbeing outcomes (internalizing and externalizing problems, mental wellbeing, self-harm) were collected at age 17. Results suggested that over and above pre-existing individual and family level vulnerabilities, experiencing sibling victimization was associated with significantly worse mental health and wellbeing. Having no close friends was a risk factor for worse-than-expected outcomes following victimization. Higher levels of school motivation and engagement was a promotive factor for better-than-expected outcomes. This indicates that aspects of the school environment may offer both risk and promotive factors for children experiencing sibling victimization at home. We argue that effective sibling victimization interventions should be extended to include a focus on factors at the school level.

The current study explored dynamics of secure state attachment expectations in everyday life in middle childhood, specifically state attachment carry-over and reactivity to experiences of caregiver support in the context of stress. In two independent samples (one community sample, N = 123; one adoption sample, N = 69), children (8–12 years) daily reported on their state attachment for respectively 14 and 7 consecutive days. Additionally, they reported daily on their experiences of distress and subsequent experiences of caregiver support. Results in both samples indicated that secure state attachment on a day-to-day basis is characterized by a significant positive carry-over effect, suggesting that state attachment fluctuations are (partially) self-predictive. In Study 1, experiencing no support following distress significantly related to intraindividual decreases in secure state attachment; in Study 2, experiencing effective support during distress related to intra-individual increases in secure state attachment. Taken together, the current studies provide novel and important insights into how state attachment temporally evolves on a day-to-day basis in middle childhood.

Research has supported a link between insecure attachment and disordered eating in adolescents; however, how this influence is exerted remains unclear. This study explored whether depressive symptoms constitute a pathway through which insecure attachment to parents predicts subsequent development of disordered eating in the transition from childhood to adolescence. The study also examines whether there are differential effects regarding the attachment figure, child's gender, or reciprocity between variables. A community-based sample of Spanish youth (n = 904; 49.4% girls) was followed biennially from age 10 to 16 years. Attachment, depressive symptoms, and disordered eating were measured using the Inventory of Parental and Peer Attachment, Children's Depression Inventory, and Children's Eating Attitudes Test, respectively. Prospective data were analyzed using a dynamic panel model, which accounts for unmeasured time-invariant factors. Whereas insecure attachment to the father did not predict later depression or disordered eating, higher insecure attachment to the mother at ages 10 and 12 years predicted more disordered eating at ages 14 and 16 years via increased depressive symptoms at ages 12 and 14 years. No child's gender-specific or reverse mediational effects were found. This study suggests that an increase in depressive symptoms might be one mechanism by which insecure attachment exerts its influence on the development of eating disorders symptomatology in adolescence. Intervention efforts aimed at strengthening particularly the mother–child attachment relationship may reduce the vulnerability to develop depressive symptoms and disordered eating.

Stress associated with caring for a mentally ill spouse can adversely affect the health status of caregivers and their children. Adding to the stress of caregiving is the stigma often placed against spouses and children of people with mental illness. Contrary to mental illness, many physical disorders such as cancer may be less stigmatized (expect pulmonary cancer). In this study, we measured externalized and internalized stigma, as well as psychological (depressive symptoms and stressful life events) and physiological (basal salivary cortisol levels) markers of stress in 115 spouses and 154 children of parents suffering from major depressive disorder, cancer, or no illness (control group). The results show that spouses and children from families with parental depression present significantly more externalized stigma than spouses and children from families with parental cancer or no illness, although we find no group differences on internalized stigma. The analysis did not show a significant group difference either for spouses or their children on depressive symptomatology, although spouses from the parental depression group reported greater work/family stress. Finally, we found that although for both spouses children the awakening cortisol response was greater on weekdays than on weekend days, salivary cortisol levels did not differ between groups. Bayes factor calculated on the null result for cortisol levels was greater than 100, providing strong evidence for the null hypothesis H0. Altogether, these results suggest an impact of stigma toward mental health disorder on psychological markers of stress but no impact of stigma on physiological markers of stress. We suggest that these results may be due to the characteristics of the families who participated in the present study.

Understanding how youth perceive household economic hardship and how it relates to their behavior is vital given associations between hardship and behavioral development. Yet, most studies ignore youth’s own perceptions of economic hardship, instead relying solely on caregiver reports. Moreover, the literature has tended to treat economic hardship as a stable force over time, rather than a volatile one that varies month-to-month. This study addressed extant limitations by collecting monthly measures of economic hardship, specifically caregiver- and youth-reported material deprivation and youth-reported financial stress, and youth internalizing and externalizing problems from 104 youth–caregiver dyads (youth: 14–16 years, 55% female, 37% Black, 43% White) over nine months. We examined month-to-month variability of these constructs and how youth-reports of material deprivation and financial stress predicted their behavior problems, controlling for caregiver-reports of material deprivation. We found that hardship measures varied month-to-month (ICCs = 0.69–0.73), and youth-reported material deprivation positively predicted internalizing when examining both within- and between-individual variability (β = .19–.47). Youth-reported financial stress positively predicted within-individual variation in externalizing (β = .18), while youth reports of material deprivation predicted externalizing when looking between families (β = .41). Caregiver-reported material deprivation was unrelated to youth behavior when accounting for youth perceptions of economic hardship.

Comorbidity of internalizing and externalizing problems and its risk and protective factors have not been well incorporated into developmental research, especially among racial minority youth from high-poverty neighborhoods. The present study identified a latent comorbid factor as well as specific factors underlying internalizing and externalizing problems among 592 African American adolescents living in economically disadvantaged neighborhoods (291 male; M age = 15.9 years, SD = 1.43 years). Stressful life events and racial discrimination were associated with higher comorbid problems, whereas stressful life events and exposure to violence were associated with higher specific externalizing problems. Collective efficacy was associated with both lower specific externalizing problems and lower comorbid problems. Moreover, high collective efficacy buffered the risk effects of stressful life events and racial discrimination on comorbid problems. Our results demonstrated the advantages of latent variable modeling to understanding comorbidity by articulating impacts of risk factors on comorbid and specific components underlying internalizing and externalizing problems. They also highlighted the protective effect of collective efficacy in mitigating risks for these problems. Broadly, these findings call for more studies on comorbidities in developmental psychopathology among youth from diverse sociocultural backgrounds.

Conduct disorder (CD), characterized by youth antisocial behavior, is associated with a variety of neurocognitive impairments. However, questions remain regarding the neural underpinnings of these impairments. To investigate novel neural mechanisms that may support these neurocognitive abnormalities, the present study applied a graph analysis to resting-state functional magnetic resonance imaging (fMRI) data collected from a national sample of 4,781 youth, ages 9–10, who participated in the baseline session of the Adolescent Brain Cognitive DevelopmentSM Study (ABCD Study®). Analyses were then conducted to examine the relationships among levels of CD symptomatology, metrics of global topology, node-level metrics for subcortical structures, and performance on neurocognitive assessments. Youth higher on CD displayed higher global clustering (β = .039, 95% CIcorrected [.0027 .0771]), but lower Degreesubcortical (β = −.052, 95% CIcorrected [−.0916 −.0152]). Youth higher on CD had worse performance on a general neurocognitive assessment (β = −.104, 95% CI [−.1328 −.0763]) and an emotion recognition memory assessment (β = −.061, 95% CI [−.0919 −.0290]). Finally, global clustering mediated the relationship between CD and general neurocognitive functioning (indirect β = −.002, 95% CI [−.0044 −.0002]), and Degreesubcortical mediated the relationship between CD and emotion recognition memory performance (indirect β = −.002, 95% CI [−.0046 −.0005]). CD appears associated with neuro-topological abnormalities and these abnormalities may represent neural mechanisms supporting CD-related neurocognitive disruptions.

Childhood adversity has been associated with hypothalamic–pituitary–adrenal axis dysregulation, which is associated with mental and physical health consequences. However, associations between childhood adversity and cortisol regulation in the current literature vary in magnitude and direction. This multilevel meta-analysis examines the association between childhood adversity and diurnal cortisol measures, as well as potential moderators of these effects (adversity timing and type, study or sample characteristics). A search was conducted in online databases PsycINFO and PubMed for papers written in English. After screening for exclusion criteria (papers examining animals, pregnant women, people receiving hormonal treatment, people with endocrine disorders, cortisol before age 2 months, or cortisol after an intervention), 303 papers were identified for inclusion. In total, 441 effect sizes were extracted from 156 manuscripts representing 104 studies. A significant overall effect was found between childhood adversity and bedtime cortisol, r = 0.047, 95% CI [0.005, 0.089], t = 2.231, p = 0.028. All other overall and moderation effects were not significant. The lack of overall effects may reflect the importance of the timing and nature of childhood adversity to adversity’s impact on cortisol regulation. Thus, we offer concrete recommendations for testing theoretical models linking early adversity and stress physiology.

To test the transmission of mental health difficulties from mother to child, we examined mediation through emotion reminiscing conversations and child language. Maternal depression symptoms were measured at 9 months post-partum, and child mental health outcomes were measured at age 8 years. Emotion reminiscing conversations between 1,234 mother-child pairs (624 boys, 610 girls) were recorded as part of a large, diverse, longitudinal cohort Growing Up in New Zealand. The 1,234 reminiscing conversations were transcribed and coded for maternal elaboration and emotion resolution quality (mother and child). The coded reminiscing variables did not mediate the pathway from maternal depression to child mental health outcomes; however, each maternal reminiscing variable together with child language skill serially mediated the relationship from maternal depression symptoms to child-reported anxiety and depression symptoms, and parent-reported child externalizing symptoms. Language as a skill and it’s use as a tool for making shared meaning from past events are highlighted as possible mechanisms for the intergenerational transmission of mental health difficulties. These findings point to potential opportunities for early interventions, including prevention of and support for postnatal depression, family intervention in reminiscing training, and supporting child language development.

The body of scientific knowledge accumulated by the scholarly disciplines such as Developmental Psychopathology can achieve meaningful public impact if wielded and used in policy decision-making. Scientific study of how policymakers use research evidence underscores the need for researchers’ policy engagement; however, barriers in the academy create conditions in which there is a need for infrastructure that increases the feasibility of researchers’ partnership with policymakers. This need led to the development of the Research-to-Policy Collaboration model, a systematic approach for developing “boundary spanning” infrastructure, which has been experimentally tested and shown to improve policymakers’ use of research evidence and bolster researchers’ policy skills and engagement. This paper presents original research regarding the optimization of the RPC model, which sought to better serve and engage scholars across the globe. Trial findings shed light on ways to improve conditions that make good use of researchers’ time for policy engagement via a virtual platform and enhanced e-communications. Future directions, implications, and practical guidelines for how scientists can engage in the political process and improve the impact of a collective discipline are also discussed.

Indices of cumulative risk (CR) have long been used in developmental research to encode the number of risk factors a child or adolescent experiences that may impede optimal developmental outcomes. Initial contributions concentrated on indices of cumulative environmental risk; more recently, indices of cumulative genetic risk have been employed. In this article, regression analytic methods are proposed for interrogating strongly the validity of risk indices by testing optimality of compositing weights, enabling more informative modeling of effects of CR indices. Reanalyses of data from two studies are reported. One study involved 10 environmental risk factors predicting Verbal IQ in 215 four-year-old children. The second study included an index of genetic CR in a G×E interaction investigation of 281 target participants assessed at age 15 years and then again at age 31 years for observed hostility during videotaped interactions with close family relations. Principles to guide evaluation of results of statistical modeling are presented, and implications of results for research and theory are discussed. The ultimate goals of this paper are to develop stronger tests of conjectures involving CR indices and to promote methods for improving replicability of results across studies.

Alcohol use and dependence are strongly affected by variation in aldehyde dehydrogenase (ALDH2) and, to a lesser extent, alcohol dehydrogenase (ADH1B) genes. We use this genetic variation with an adoption design to test the causal role of alcohol use on other drug use, as well as the moderating role of adoptive parent, sibling, and peer alcohol use. Longitudinal models were run on 412 genotyped adopted individuals of East Asian ancestry with multiple assessments between ages 14 and 40. We found robust associations between alcohol frequency, quantity, and maximum drinks and ALDH2, but not ADH1B, status. The magnitude of the ALDH2 protective effect increased with age, particularly for maximum drinks, though estimates were smaller than previously reported in ancestrally similar individuals in East/North-East Asian countries. These results suggest that sociocultural factors in Minnesota may reduce the protective effects of ALDH2. We found that peer alcohol use, but not parent or sibling use, predicted adopted offspring’s use, and that these environmental influences did not vary by ALDH2 status. Finally, we did not find strong evidence of associations between ALDH2 status and tobacco, marijuana, or illegal drug use, contrary to expectation if alcohol serves as a gateway to use of other drugs.

Peer victimization and depressive symptoms are highly relevant risks during adolescence. Understanding the dynamic patterns of interactions between peer victimization and depressive symptoms as well as gender differences in these variables can improve intervention strategies for adolescents navigating this critical transition period. In the present study, a large sample of Chinese adolescents reported peer victimization and depressive symptoms in four survey waves at six-month intervals. A total of 2534 adolescents (51.9% boys, M = 12.98 ± 0.60 years) were included in the latent change score (LCS) analysis. The results supported the reciprocal effects model obtained in the full sample. Changes in peer victimization were influenced by prior changes in depressive symptoms over time, and changes in depressive symptoms were influenced by prior levels of peer victimization. There were also gender differences, with boys exhibiting depressive symptom-driven effects on peer victimization, while girls exhibiting peer victimization-induced depressive symptoms. The dynamic relationships between peer victimization and depressive symptoms that promote and constrain each other in adolescents are elucidated in this study. Differentiating effects on boys and girls is crucial for enhancing the effectiveness of practical interventions.

Following a network analysis approach, the present study aims to explore the pattern of mutual relationships between failure in reflective functioning (RF) – defined as hypomentalization – problematic social networking sites use (PSNSU), attachment anxiety and avoidance, and childhood maltreatment among emerging adults, with a focus on gender differences. The study sample comprises N = 1,614 emerging adults (Mage = 23.84; SD = 3.21; 50% identified themselves as women) who completed online self-assessment measures. Results showed significantly greater PSNSU, hypomentalization, childhood emotional abuse, and both attachment avoidance and anxiety among women. Indeed, within the network analysis, performed separately for men and women, network-specific associative patterns were observed; yet also similarities have emerged. Within the women’s network, differently from males, attachment avoidance connects, through attachment anxiety, to emotional abuse, mood modification related to PSNSU, and hypomentalization. Nonetheless, hypomentalization was central in both networks, functioning as a hub between attachment anxiety, the PSNSU cluster, and the childhood maltreatment cluster. These results shed light on the use of social network sites as a potential maladaptive emotion regulation strategy, particularly among women. In this regard, the role of RF should be considered as a key treatment target to reduce PSNSU and support the use of adaptive emotion regulation strategies.

Mid-adolescence is a critical time for the development of stress-related disorders and it is associated with significant social vulnerability. However, little is known about normative neural processes accompanying psychosocial stress at this time. Previous research found that emotion regulation strategies critically influence the relationship between stress and the development of psychiatric symptoms during adolescence. Using functional magnetic resonance imaging (fMRI), we examined neural responses to acute stress and analyzed whether the tendency to use adaptive or maladaptive emotion regulation strategies is related to neural and autonomic stress responses. Results show large linear activation increases from low to medium to high stress levels mainly in medial prefrontal, insulae and temporal areas. Caudate and subgenual anterior cingulate cortex, neural areas related to reward and affective valuations, showed linearly decreasing activation. In line with our hypothesis, the current adolescent neural stress profile resembled social rejection and was characterized by pronounced activation in insula, angular and temporal cortices. Moreover, results point to an intriguing role of the anterior temporal gyrus. Stress-related activity in the anterior temporal gyrus was positively related to maladaptive regulation strategies and stress-induced autonomic activity. Maladaptive coping might increase the social threat and reappraisal load of a stressor, relating to higher stress sensitivity of anterior temporal cortices.