Family dysfunction plays an important role in cyberbullying and cybervictimization. However, little research has investigated the longitudinal relations and the mediating mechanisms between them during adolescence. This study examined the longitudinal relations between family dysfunction and cyberbullying and cybervictimization, along with whether depressive symptoms function as mediators between them at the within-person level. A total of 3,743 Chinese adolescents (46.2% females; Mage = 9.92 years; SD = 0.51) participated a five-wave longitudinal study with a 6-month time interval. The results of random intercept cross-lagged panel model found that: (1) family dysfunction directly predicted depressive symptoms and vice versa at the within-person level; (2) depressive symptoms directly predicted cyberbullying and cybervictimization at the within-person level, but not vice versa; (3) family dysfunction indirectly predicted cyberbullying and cybervictimization via depressive symptoms at the within-person level; (4) at the between-person level, there were significant associations among family dysfunction, depressive symptoms, cyberbullying and cybervictimization. The results are discussed on the basis of the mechanisms that lead to cyberbullying and cybervictimization.

Although atypical theta and alpha activity may be biomarkers of attention-deficit/hyperactivity disorder (ADHD) outcomes such as atypical affective processing and attention, the exact nature of the relations of these characteristics is unknown. We examined in age- and sex-matched adolescents (N = 132; Mage = 14.944, years, SD = .802) with and without ADHD, whether resting state (RS) theta and alpha power or theta and alpha event-related synchronization (ERS) during affect regulation (1) differ between adolescents with and without ADHD; (2) are differentially associated with event-related potential (ERP) and parent- and self-report measures of affective processing and inattention, given ADHD status and sex, and (3) are differentially lateralized, given ADHD status and sex. Adolescents with ADHD exhibited lower RS frontal-midline alpha power than adolescents without ADHD. In adolescents with ADHD, right parietal theta ERS was positively associated with the ERP measure of elaborate affective/motivational processing and right parietal RS alpha power was negatively associated with self-reported positive affectivity. In adolescents without ADHD, associations were nonsignificant. There was no disassociation of theta and alpha activity with affective processing and inattention. Consistent with clinical impressions, the between-group difference in frontal-midline theta ERS was more marked in boys than girls.

Maternal antenatal anxiety is an emerging risk factor for child emotional development. Both sex and epigenetic mechanisms, such as DNA methylation, may contribute to the embedding of maternal distress into emotional outcomes. Here, we investigated sex-dependent patterns in the association between antenatal maternal trait anxiety, methylation of the brain-derived neurotrophic factor gene (BDNF DNAm), and infant negative emotionality (NE). Mother–infant dyads (N = 276) were recruited at delivery. Maternal trait anxiety, as a marker of antenatal chronic stress exposure, was assessed soon after delivery using the Stait-Trait Anxiety Inventory (STAI-Y). Infants’ BDNF DNAm at birth was assessed in 11 CpG sites in buccal cells whereas infants’ NE was assessed at 3 (N = 225) and 6 months (N = 189) using the Infant Behavior Questionnaire-Revised (IBQ-R). Hierarchical linear analyses showed that higher maternal antenatal anxiety was associated with greater 6-month-olds’ NE. Furthermore, maternal antenatal anxiety predicted greater infants’ BDNF DNAm in five CpG sites in males but not in females. Higher methylation at these sites was associated with greater 3-to-6-month NE increase, independently of infants’ sex. Maternal antenatal anxiety emerged as a risk factor for infant’s NE. BDNF DNAm might mediate this effect in males. These results may inform the development of strategies to promote mothers and infants’ emotional well-being.

Neuroscience research underscores the critical impact of adverse experiences on brain development. Yet, there is limited understanding of the specific pathways linking adverse experiences to accelerated or delayed brain development and their ultimate contributions to psychopathology. Here, we present new longitudinal data demonstrating that neurocognitive functioning during adolescence, as affected by adverse experiences, predicts psychopathology during young adulthood. The sample included 167 participants (52% male) assessed in adolescence and young adulthood. Adverse experiences were measured by early maltreatment experiences and low family socioeconomic status. Cognitive control was assessed by neural activation and behavioral performance during the Multi-Source Interference Task. Psychopathology was measured by self-reported internalizing and externalizing symptomatology. Results indicated that higher maltreatment predicted heightened frontoparietal activation during cognitive control, indicating delayed neurodevelopment, which, in turn predicted higher internalizing and externalizing symptomatology. Furthermore, higher maltreatment predicted a steeper decline in frontoparietal activation across adolescence, indicating neural plasticity in cognitive control-related brain development, which was associated with lower internalizing symptomatology. Our results elucidate the crucial role of neurocognitive development in the processes linking adverse experiences and psychopathology. Implications of the findings and directions for future research on the effects of adverse experiences on brain development are discussed.

Studies found support for a link between pubertal timing and self-regulation in low-resource environments. This link could potentially explain a link between pubertal timing and early risk behavior. This study builds on this body of research by examining the mediated effect of pubertal timing on sexual activity through self-regulation in 728 adolescents and their families in a group with poor resources and a group with adequate resources. Income-to-Needs (ITN) was measured at age 7.5 to establish two groups (low-ITN and Medium/High-ITN). Pubertal timing was measured at age 10.5, self-regulation was assessed at age 14 and operationalized with effortful control, and sexual activity was assessed at age 16. Structural equation modeling was employed to test the hypothesized model in both groups. The link between pubertal timing and sexual activity mediated by effortful control was only significant in the low-ITN group. Specifically, more advanced pubertal maturity was associated with lower levels of adolescents’ effortful control, which in turn was associated with more sexual activity at age 16. Findings were partially replicated with a drug use index replacing sexual activity. This study shows a different operating link from pubertal timing to effortful control and subsequent risk behavior in resource-poor environments. Implications are discussed.

Sipping, an early form of alcohol initiation, is associated with aspects of psychopathology and personality that reflect long-term risk for harmful alcohol use. In the Adolescent Brain and Cognitive Development cohort (N = 11,872), sipping by age 9–10 was concurrently associated with impulsivity, other aspects of externalizing, and prodromal schizophrenia symptoms. Still, these associations were cross-sectional in nature, leaving open the possibility that these features of psychopathology and personality might not reflect long-term risk for alcohol consumption and related harm across development. Here, we attempted to replicate baseline concurrent associations across three waves of data to extend concurrent associations to prospective ones. Most cross-sectional associations replicated across waves, such that impulsivity, other aspects of externalizing, reward sensitivity (e.g., surgency, sensation seeking), and prodromal schizophrenia symptoms were associated with increased odds of having sipped alcohol by the age of 12. Nevertheless, not all concurrent associations replicated prospectively; impulsigenic features did not reflect long-term risk for sipping. Thus, some psychopathology features appeared to reflect stable risk factors, whereas others appeared to reflect state-dependent risk factors. All told, sipping might not reflect long-term risk for harmful alcohol use, and the nature of sipping may change across development.

There is a wealth of literature characterizing social difficulties in autism spectrum disorder (ASD). However, little work has replicated longitudinal findings from typical development that adolescent social competence predicts positive adult outcomes in ASD. The current study examined social competence trajectories from 2 to 26 and the utility of three social competence measures collected in adolescence in predicting work, residential status, friendship, and romantic outcomes in a longitudinal cohort (n = 253) of ASD. Using group-based trajectory modeling, we identified two patterns of social competence development: a low trajectory characterized by slow linear gains throughout childhood and plateauing in adulthood, and a high trajectory characterized by steeper linear gains in childhood followed by decline in adulthood. Regression models indicated one social competence measure, Vineland Social-AE scores, significantly predicted employment, residential status, and friendships in adulthood. One other social competence measure, SSQ total scores, also significantly predicted friendship in adulthood. Only nonverbal IQ at 9 predicted the likelihood of having ever had a romantic relationship. These findings highlight the role of social competence in both atypical and typical development and suggest the social impairments associated with ASD do not necessarily impact all realms of social functioning equally.

A central goal in the field of developmental psychopathology is to evaluate the complex, dynamic transactions occurring among biological, psychological, and broader social-cultural contexts that predict adaptive and maladaptive outcomes across ontogeny. Here, I briefly review research on the effects of a history of childhood maltreatment on parental, child, and dyadic functioning, along with more recent studies on the intergenerational transmission of trauma. Because the experience and sequelae of child maltreatment and the intergenerational transmission of trauma are embedded in complex biopsychosocial contexts, this research is best conceptualized in a developmental psychopathology framework. Moreover, there is a pressing need for investigators in this area of study to adopt dynamic, multi-level perspectives as well as using developmentally guided, sophisticated research methods. Other directions for research in this field are suggested, including the implementation of collaborative interdisciplinary team science approaches, as well as community-based participatory research, to increase representation, inclusion, and equity of community stakeholders. A greater focus on cultural and global perspectives is also recommended.

Literature examining emotional regulation in infants with autism spectrum disorder (ASD) has focused on parent report. We examined behavioral and physiological responses during an emotion-evoking task designed to elicit emotional states in infants. Infants at an increased likelihood for ASD (IL; have an older sibling with ASD; 96 not classified; 29 classified with ASD at age two) and low likelihood (LL; no family history of ASD; n = 61) completed the task at 6, 12, and 18 months. The main findings were (1) the IL-ASD group displayed higher levels of negative affect during toy removal and negative tasks compared to the IL non-ASD and LL groups, respectively, (2) the IL-ASD group spent more time looking at the baseline task compared to the other two groups, and (3) the IL-ASD group showed a greater increase in heart rate from baseline during the toy removal and negative tasks compared to the LL group. These results suggest that IL children who are classified as ASD at 24 months show differences in affect, gaze, and heart rate during an emotion-evoking task, with potential implications for understanding mechanisms related to emerging ASD.

Early-life adversity accelerates the maturation of affect-related circuitry, which might be a short-term adaptation with long-term tradeoffs. Sexual trauma is associated with a particularly strong impact on pubertal development and mental health outcomes. Our objective was to test the relations between trauma type, affective network maturity, and mental health outcomes in young women with trauma history. Trauma-exposed women aged 18–29 completed a clinical interview (n = 35) and an fMRI scan (n = 28). We used a public data set to train a machine learning algorithm to predict age from resting-state affective network connectivity and calculated network maturity as the difference between predicted and true age. We also performed principal component analysis on mental health outcomes and retained two components: clinical and state psychological outcomes. Compared to nonsexual trauma (n = 17), sexual trauma (n = 11) was associated with greater affective network maturity. In addition, for sexual trauma only, greater affective network maturity was associated with better clinical but not state psychological outcomes. These results suggest that sexual trauma during development might uniquely alter the maturational trajectory of affect-related circuitry, with distinct mental health consequences in emerging adulthood. Whereas delayed affective network maturation is associated with adverse clinical outcomes, accelerated affective network maturation might confer resilience in survivors.

Children differ in their environmental sensitivity (ES), which can be measured observationally or by self-report questionnaire. A parent-report scale represents an important tool for investigating ES in younger children but has to be psychometrically robust and valid. In the current multistudy, we validated the parent-report version of the Highly Sensitive Child (HSC-PR) scale in Italian children, evaluating its factorial structure (Study 1, N = 1,857, 6.2 years, age range: 2.6–14 years) through a multigroup Confirmatory Factory Analysis in preschoolers (n = 1,066, 4.2 years) and school-age children (n = 791, 8.8 years). We then investigated the HSC-PR relationship with established temperament traits (Study 2, N = 327, 4.3 years), before exploring whether the scale moderates the effects of parenting stress on children’s emotion regulation (Study 3, N = 112, 6.5 years). We found support for a bi-factor structure in both groups, though in preschoolers minor adaptations were suggested for one item. Importantly, the HSC-PR did not fully overlap with common temperament traits and moderated the effects of parenting stress on children emotion regulation. To conclude, the HSC-PR performs well and appears to capture ES in children.

Maternal depressive symptoms (MDS) in the postnatal period may impact children’s later development through poorer quality parent-child interactions. The current study tested a specific pathway from MDS (child age 9 months) to child receptive vocabulary (4 ½ years) through both self-reported and observed parent-child verbal interactions (at both 2 and 4 ½ years). Participants (n = 4,432) were part of a large, diverse, contemporary pre-birth national cohort study: Growing Up in New Zealand. Results indicated a direct association between greater MDS at 9 months and poorer receptive vocabulary at age 4 ½ years. There was support for an indirect pathway through self-reported parent-child verbal interactions at 2 years and through observed parent-child verbal interactions at 4 ½ years. A moderated mediation effect was also found: the indirect effect of MDS on child vocabulary through observed verbal interaction was supported for families living in areas of greater socioeconomic deprivation. Overall, findings support the potential role of parent-child verbal interactions as a mechanism for the influence of MDS on later child language development. This pathway may be particularly important for families experiencing socioeconomic adversity, suggesting that effective and appropriate supportive parenting interventions be preferentially targeted to reduce inequities in child language outcomes.

Intimate partner violence (IPV) represents a significant public health concern. Adverse childhood experiences (ACEs) represent one risk factor for IPV, however, the results of existing research on the association between ACEs and IPV demonstrate mixed findings. The present research sought to meta-analytically examine the association between ACEs and (a) IPV perpetration and (b) IPV victimization. Moderator analyses were conducted to determine factors that may impact the association between ACEs and IPV involvement. Electronic searches were conducted in MEDLINE, Embase, and PsycINFO in August of 2021. One-hundred and twenty-three records were screened for inclusion. All studies included a measure of ACEs and IPV victimization or perpetration. Among the 27 studies and 41 samples included in the meta-analysis, 65,330 participants were included. The results of the meta-analyses demonstrated that ACEs were positively associated with IPV perpetration and victimization. Significant methodological and measurement moderators further inform our understanding of ACEs and IPV involvement. The present meta-analyses demonstrates that trauma-informed approaches to IPV screening, prevention, and intervention may be useful, given that individuals who are involved with IPV may be more likely to possess a history of ACEs exposure.

Contemporary biological and contextually based theoretical frameworks have conceptualized how stress exposure may influence adaptation in youth. However, nearly all of this scholarship neglects the role of specific contextual features and/or biological processes that are involved in ethnic-racial minority youth’s responses and adaptation to sociocultural stressors. Drawing on the theoretical principles of the developmental psychopathology framework and contemporary models of stress and adaptation, this article proposes a new multisystem model that explains how multiple levels and systems within and outside of individual youth influence their sociocultural adaptation. We provide empirical evidence to support components of this multisystem model. We propose that research based on our new theoretical framework will capture the sociocultural experiences of ethnic-racial minority youth by centering processes that are relevant to their lived experiences, coping, and adjustment. In doing so, this model will inform psychosocial interventions focused on promoting healthy adaptation among ethnic and racial diverse youth. Finally, we offer recommendations to guide future research on stress and adaptation among ethnic and racial diverse youth, in particular, and developmental psychopathology more broadly.

This study examined children’s exposure to family adversity, hostile reactivity to parental conflict, and negative family representations as mediators of the prospective relation between their temperamental exuberance and externalizing symptoms. Participants included 243 preschool children (Mage = 4.60 years; 56% girls) and parents (48% Black; 16% Latinx) in a multi-method and multi-informant study with three annual measurement occasions. Structural equation model results specifically supported children’s hostile reactivity to parental conflict and negative family representations as mediators. Exuberance predicted residualized increases in children’s hostile reactivity and negative family representations over a 1-year period. In turn, children’s hostile reactivity and negative family representations predicted their greater externalizing symptoms 1 year later after controlling for prior externalizing symptoms. Results are discussed in the context of their relation and refinement of temperamental models of developmental psychopathology.

Greater unpredictability in childhood from the level of the caregiver-child dyad to broader family, home, or environmental instability is consistently associated with disruptions in cognitive, socioemotional, behavioral, and biological development in humans. These findings are bolstered by experimental research in non-human animal models suggesting that early life unpredictability is an important environmental signal to the developing organism that shapes neurodevelopment and behavior. Research on childhood unpredictability has surged in the past several years, guided in part by theoretical grounding from the developmental psychopathology framework (shaped largely by Dr. Dante Cicchetti’s innovative work). The current review focuses on future directions for unpredictability research, including probing intergenerational effects, the role of predictability in resilience, cultural and contextual considerations, and novel developmental outcomes that should be tested in relation to childhood unpredictability. We urge the integration of multidisciplinary perspectives and collaborations into future research on unpredictability. We also provide ideas for translating this research to real-world practice and policy and encourage high-quality research testing whether incorporating predictability into interventions and policy improves developmental outcomes, which would support further dissemination of these findings.

Parenting can protect against the development of, or increase risk for, child psychopathology; however, it is unclear if parenting is related to psychopathology symptoms in a specific domain, or to broad liability for psychopathology. Parenting differs between and within families, and both overall family-level parenting and the child-specific parenting a child receives may be important in estimating transdiagnostic associations with psychopathology. Data come from a cross-sectional epidemiological sample (N = 10,605 children ages 4–17, 6434 households). Parents rated child internalizing and externalizing symptoms and their parenting toward each child. General and specific (internalizing, externalizing) psychopathology factors, derived with bifactor modeling, were regressed on parenting using multilevel modeling. Less warmth and more aversive/inconsistent parenting in the family, and toward an individual child relative to family average, were associated with higher general psychopathology and specific externalizing problems. Unexpectedly, more warmth in the family, and toward an individual child relative to family average, was associated with higher specific internalizing problems in 4–11 (not 12–17) year-olds. Less warmth and more aversive/inconsistent parenting are broad correlates of child psychopathology. Aversive/inconsistent parenting, is also related to specific externalizing problems. Parents may behave more warmly when their younger children have specific internalizing problems, net of overall psychopathology.

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.