We examined whether adolescents’ loneliness and social withdrawal mediated the association between maternal depressive symptoms and adolescent suicidality. Secondary analyses on the Québec Longitudinal Study of Child Development data were conducted (n = 1,623). Each mother completed the Centre for Epidemiologic Studies Depression Scale (at child ages 5 months, 1.5, 3.5, 5, and 7 years). Adolescent's social withdrawal (adolescent, father, and teacher reported at 10, 12, and 13 years) and loneliness (adolescent reported at 10, 12, and 13 years), were assessed using items from the Social Behavior Questionnaire and the Loneliness and Social Satisfaction Questionnaire, respectively. Adolescents completed self-reports to assess suicidal thoughts and attempts at 13, 15, 17, and 20 years. Children of mothers with higher levels of maternal depressive symptoms had an increased risk for suicidality (OR = 1.15, 95% CI: 1.03–1.28). Loneliness explained 16% of the total effect of maternal depressive symptoms on adolescent suicidality (indirect effect OR = 1.02, 95% CI: 1.00–1.04). There was no indirect effect of maternal depressive symptoms on adolescent suicidal outcomes via social withdrawal (indirect effect OR = 1.00, 95% CI: 0.99–1.02). Interventions that target loneliness may be beneficial for decreasing the risk for suicidality among adolescents of mothers with depressive symptoms.

COVID-19 changed the landscape of employment and financial security in the USA, contributing to multi-systemic disruptions in family life. Using dyadic, daily-diary parent–adolescent data from a nationwide American sample (18,415 daily assessments; 29 days: 4/8/2020–4/21/2020 and 5/18/2020–6/1/2020; N = 635 parent–adolescent dyads), this intensive longitudinal study investigated how COVID-19-related job loss and working-from-home (WFH) arrangements influenced parents’ and children’s daily affect indirectly through family functioning (i.e., parent–adolescent conflict, inter-adult conflict, and parental warmth) and whether these links varied by family socioeconomic status (SES). Parental employment status was linked to these family relational dynamics, which were then connected to parents’ and adolescents’ daily affect. Although SES did not moderate these links, low-income families were more likely to experience job loss, parent–adolescent conflict, and inter-adult conflict and less likely to WFH than higher-income families. As inter-relations within the family are a malleable point for intervention, clinicians working with families recovering from the fiscal impact of the COVID-19 pandemic are encouraged to use approaches that strengthen family relationships, especially between adolescents and their parents. Unemployment subsidies are discussed as a means to support families struggling with job loss, and organizations are urged to consider the benefits of WFH on employee health and work-life balance.

Childhood anxiety disorders (CAD) are a common childhood mental disorder and understanding early developmental pathways is key to prevention and early intervention. What is not understood is whether early life stress predictors of CAD might be both mediated by infant cortisol reactivity and moderated by infant attachment status. To address this question, this exploratory study draws on 190 women recruited in early pregnancy and followed together with their children until 4 years of age. Early life stress is operationalized as maternal depression measured using the Structured Clinical Interview for the DSM, Childhood Trauma Questionnaire, Parenting Stress Index, and antenatal maternal hair cortisol concentrations. Infant cortisol reactivity was measured at 12 months together with the Strange Situation Procedure and CAD assessed at 4 years of age using the Preschool Age Psychiatric Assessment. There was no direct association between attachment classification and CAD. Furthermore, infant cortisol reactivity neither mediated nor attachment moderated the association of early life stress predictors and CAD. However, only for infants with organized attachment classifications, higher maternal antenatal depression, and hair cortisol were associated with a higher risk of CAD.

We examined the associations of middle childhood and adolescence nighttime sleep duration with adolescence internalizing and externalizing behavior problems per the Youth Self-Report (YSR) and the Child Behavior Checklist (CBCL) questionnaires, in a cohort of 889 Colombian schoolchildren. We estimated adjusted differences with 95% confidence intervals (CI) in mean behavior problem t-scores in standardized units between recommended sleep duration categories and as a continuous exposure using multiple linear regression and restricted cubic spline models, respectively. Compared with sleep duration within recommendations, middle childhood sleep above recommendations was related to 4.6 (95% CI: 1.6, 7.6; p = .004) and 5.4 (95% CI: 1.2, 9.7; p = .01) adjusted units higher YSR and CBCL externalizing problem scores, respectively. In continuous exposure analyses, this association seemed restricted to children aged ≥11 years. Longer sleep, both in categories and as a continuous exposure, was also associated with increased CBCL internalizing problems. Results did not differ by sex or weekend/weekday sleep. Sleeping under recommendations in middle childhood was not significantly related to behavior problems; nevertheless, shorter sleep in adolescence, in both categorical and continuous scales, was significantly related to behavior problems. In conclusion, behavior problems in adolescence are associated with longer sleep in middle childhood and shorter sleep in adolescence.

Autism spectrum disorder (ASD) is a common neurodevelopmental disorder characterized by deficits in social communication and presence of restricted, repetitive behaviors, and interests. However, individuals with ASD vary significantly in their challenges and abilities in these and other developmental domains. Gene discovery in ASD has accelerated in the past decade, and genetic subtyping has yielded preliminary evidence of utility in parsing phenotypic heterogeneity through genomic subtypes. Recent advances in transcriptomics have provided additional dimensions with which to refine genetic subtyping efforts. In the current study, we investigate phenotypic differences among transcriptional subtypes defined by neurobiological spatiotemporal co-expression patterns. Of the four transcriptional subtypes examined, participants with mutations to genes typically expressed highly in all brain regions prenatally, and those with differential postnatal cerebellar expression relative to other brain regions, showed lower cognitive and adaptive skills, higher severity of social communication deficits, and later acquisition of speech and motor milestones, compared to those with mutations to genes highly expressed during the postnatal period across brain regions. These findings suggest higher-order characterization of genetic subtypes based on neurobiological expression patterns may be a promising approach to parsing phenotypic heterogeneity among those with ASD and related neurodevelopmental disorders.

Research on marital quality and child well-being is currently limited by its common use of geographically constrained, homogenous, and often cross-sectional (or at least temporally limited) samples. We build upon previous work showing multiple trajectories of marital quality and data from the National Longitudinal Survey of Youth-1979 (NLSY79) regarding mothers and their children (inclusive of ages 5–14). We examine how indicators of child well-being are linked to parental trajectories of marital quality (happiness, communication, and conflict). Results showed children whose parents had consistently poor marital quality over the life course exhibited more internalizing and externalizing problems, poorer health, lower quality home environments, and lower math and vocabulary scores than children of parents in consistently higher-quality marriages. Group differences remained stable over time for child health, home environment, and vocabulary scores. Group differences for internalizing problems declined over time, whereas group differences increased for externalizing problems and math scores. Initial advantages for females across nearly all indicators of child well-being tended to shrink over time, with boys often moving slightly ahead by mid adolescence. We discuss the implications of these findings in regard to children's development and well-being and suggest treating marriage as a monolithic construct betrays important variation within marriage itself.

Both preterm birth and early institutional deprivation are associated with neurodevelopmental impairment—with both shared and distinctive features. To explore shared underlying mechanisms, this study directly compared the effects of these putative risk factors on temperament profiles in six-year-olds: Children born very preterm (<32 weeks gestation) or at very low birthweight (<1500 g) from the Bavarian Longitudinal Study (n = 299); and children who experienced >6 months of deprivation in Romanian institutions from the English and Romanian Adoptees Study (n = 101). The former were compared with 311 healthy term born controls and the latter with 52 nondeprived adoptees. At 6 years, temperament was assessed via parent reports across 5 dimensions: effortful control, activity, shyness, emotionality, and sociability. Very preterm/very low birthweight and postinstitutionalized children showed similarly aberrant profiles in terms of lower effortful control, preterm = −0.50, 95% CI [−0.67, −0.33]; postinstitutionalized = −0.48, 95% CI [−0.82, −0.14], compared with their respective controls. Additionally, postinstitutionalized children showed higher activity, whereas very preterm/very low birthweight children showed lower shyness. Preterm birth and early institutionalization are similarly associated with poorer effortful control, which might contribute to long-term vulnerability. More research is needed to examine temperamental processes as common mediators of negative long-term outcomes following early adversity.

To understand the complex relationships between autism spectrum disorder (ASD) and other frequently comorbid conditions, a growing number of studies have investigated the emergence of ASD during infancy. This research has suggested that symptoms of ASD and highly related comorbid conditions emerge from complex interactions between neurodevelopmental vulnerabilities and early environments, indicating that developing treatments to prevent ASD is highly challenging. However, it also suggests that attenuating the negative effects of ASD on future development once identified is possible. The present paper builds on this by conceptualizing developmental delays in nonsocial skills as the potential product of altered caregiver–infant interactions following the emergence of ASD during infancy. And, following emerging findings from caregiver–infant dyadic head-mounted eye-tracking (D-ET) research, it also suggests that a multiple pathway model of joint attention can provide mechanistic insights into how ASD alters the ability of caregiver and infant to create a context for infant learning. The potential for this view to inform early intervention is further discussed and illustrated through D-ET data collected prior to and following a brief, parent-mediated intervention for infant ASD. While promising, further research informing how a multiple pathway model of joint attention can inform ASD early intervention is needed.

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

Deficits in executive functioning both run in families and serve as a transdiagnostic risk factor for psychopathology. The present study employed twin modeling to examine parenting as an environmental pathway underlying the intergenerational transmission of executive functioning in an at-risk community sample of children and adolescents (N = 354 pairs, 167 monozygotic). Using structural equation modeling of multi-informant reports of parenting and a multi-method measure of child executive functioning, we found that better parent executive functioning related to less harsh, warmer parenting, which in turn related to better child executive functioning. Second, we assessed the etiology of executive functioning via the nuclear twin family model, finding large non-shared environmental effects (E = .69) and low-to-moderate heritability (A = .22). We did not find evidence of shared environmental effects or passive genotype–environment correlation. Third, a bivariate twin model revealed significant shared environmental overlap between both warm and harsh parenting and child executive functioning (which may indicate either passive genotype–environment correlation or environmental mediation), and non-shared environmental overlap between only harsh parenting and child executive functioning (indicating an effect of harsh parenting separable from genetic confounds). In summary, genetics contribute to the intergenerational transmission of executive functioning, with environmental mechanisms, including harsh parenting, also making unique contributions.

This reflection on the history and future of developmental resilience science (DRS) highlights its co-emergence with developmental psychopathology (DP), as well as the roles of this journal and its founding editor, Dante Cicchetti, in the evolution of these intertwined domains of scholarship. A remarkable constellation of scholars at the University of Minnesota shaped the course of both conceptual frameworks and their dissemination. I describe fundamental assumptions common to DP and DRS frameworks that reflect their common roots and the pervasive influence of systems theory on developmental science. I describe four waves of DRS and key principles of DRS at the present time. In conclusion, I consider the possibility that a fifth wave of DRS is emerging with a focus on understanding patterns of multisystem, multilevel processes of resilience and their implications for interventions in the context of interacting, interdependent, and complex adaptive systems. I close this commentary with questions for future research and a hopeful outlook on the future of human resilience.

Greater maternal depressive symptoms are consistently associated with higher levels of behavioral difficulties in children, emerging in early childhood and with long-lasting consequences for children’s development. Interventions promoting early relational health have been shown to have benefits for children’s behavior; however, these impacts are not always realized in the context of maternal depression. This study examined whether tiered programs could address this limitation by focusing on both parenting, through universal primary prevention, and psychosocial stressors and parent mental health, through tailored secondary prevention. Analysis of a randomized controlled trial (RCT) of the Smart Beginnings (SB) intervention was conducted to determine whether SB attenuated the association between maternal depression and early childhood internalizing and externalizing behaviors. Maternal depression significantly predicted both internalizing and externalizing behaviors in linear regression models. Further, there was a significant interaction between maternal depression and treatment group, such that among mothers with higher depressive symptoms, the SB treatment attenuated the magnitude of the association between depression and child behavior. Findings suggest that while parenting support is important for all families, it may be particularly critical for those with higher levels of depression and underscores the need to consider multidimensional family processes in both research and clinical practice.

Bullying victimization is common in adolescence and has been associated with a broad variety of psychopathology and alcohol use. The present study assessed time-varying associations between bullying victimization and alcohol use through internalizing and externalizing symptoms and whether this indirect association throughout time is moderated by personality. This 5-year longitudinal study (3,800 grade 7 adolescents) used Bayesian multilevel moderated mediation models: independent variable was bullying victimization; moderators were four personality dimensions (anxiety sensitivity, hopelessness, impulsivity, and sensation seeking); internalizing symptoms (anxiety, depressive symptoms) and externalizing symptoms (conduct, hyperactivity problems) were the mediators; and alcohol use, the outcome. Results indicated significant between, within, and lagged effects on alcohol use through internalizing and externalizing symptoms. There were significant between and within effects on alcohol use through internalizing symptoms for adolescents with high anxiety sensitivity and hopelessness, and significant between, within, and lagged effects on alcohol use through externalizing symptoms for adolescents with high impulsivity and sensation seeking. These findings implicate two risk pathways that account for how bullying victimization enhances alcohol use risk and emphasize the importance of personality profiles that can shape the immediate and long-term consequences of victimization.

Teenage childbearing (age 15–19 years) represents a significant public health issue that can generate considerable deleterious, multigenerational consequences for teen-childbearing mothers and their offspring. However, few studies have examined the potential mediating mechanisms that may explain if and how teen childbearing is associated with the development of offspring psychopathology. The current study used a developmental model to test the mediating role of chronic child maltreatment in the relationship between teen childbearing and offspring internalizing symptoms in childhood and emerging adulthood. The study participants were 384 individuals from socioeconomically disadvantaged, ethnically diverse backgrounds, assessed across two longitudinal waves of data (i.e., ages 10–12 and 18–20). The sample included maltreated and nonmaltreated children, all of whom were comparable in terms of family income. Structural equation modeling was conducted to test direct and indirect pathways from teen childbearing to offspring psychopathology. A multigenerational developmental cascade was found such that individuals born to mothers who began their childbearing in adolescence were more likely to experience chronic maltreatment during childhood, which in turn predicted greater internalizing symptoms throughout childhood and emerging adulthood. Using a developmental psychopathology framework, the results are discussed with regard to implications for prevention and early intervention.

Effects of stresses associated with extremely preterm birth may be biologically “recorded” in the genomes of individuals born preterm via changes in DNA methylation (DNAm) patterns. Genome-wide DNAm profiles were examined in buccal epithelial cells from 45 adults born at extremely low birth weight (ELBW; ≤1000 g) in the oldest known cohort of prospectively followed ELBW survivors (Mage = 32.35 years, 17 male), and 47 normal birth weight (NBW; ≥2500 g) control adults (Mage = 32.43 years, 20 male). Sex differences in DNAm profiles were found in both birth weight groups, but they were greatly enhanced in the ELBW group (77,895 loci) versus the NBW group (3,424 loci), suggesting synergistic effects of extreme prenatal adversity and sex on adult DNAm profiles. In men, DNAm profiles differed by birth weight group at 1,354 loci on 694 unique genes. Only two loci on two genes distinguished between ELBW and NBW women. Gene ontology (GO) and network analyses indicated that loci differentiating between ELBW and NBW men were abundant in genes within biological pathways related to neuronal development, synaptic transportation, metabolic regulation, and cellular regulation. Findings suggest increased sensitivity of males to long-term epigenetic effects of extremely preterm birth. Group differences are discussed in relation to particular gene functions.

Previous cross-sectional work has consistently found associations between neuroticism and impulsivity and nonsuicidal self-injury (NSSI). However, there are few longitudinal studies of personality risk factors for NSSI. In this study, we examined associations between individual differences in temperament at age 3 and NSSI from ages 9 to 15. At age 3, 559 preschool-aged children (54% male; Mage = 42.2 months [SD = 3.10]) completed laboratory assessments of temperament. Parents also completed questionnaires about their child’s temperament. Children completed a diagnostic interview assessing NSSI engagement at ages 9, 12, and 15. By the age 15 assessment, 12.4% of adolescents reported engaging in NSSI. In univariate models, we found that higher levels of observed sadness and maternal-reported sadness and anger were associated with increased risk for NSSI. In multivariate models, female sex and maternal-reported anger were significantly associated with greater likelihood of NSSI. Laboratory observed sadness and impulsivity were associated with a higher likelihood of NSSI. This work extends the literature on personality risk factors associated with NSSI by finding longitudinal associations between early childhood negative affect and later NSSI engagement during adolescence.

The recent introduction of the induced pluripotent stem cell technology has made possible the derivation of neuronal cells from somatic cells obtained from human individuals. This in turn has opened new areas of investigation that can potentially bridge the gap between neuroscience and psychopathology. For the first time we can study the cell biology and genetics of neurons derived from any individual. Furthermore, by recapitulating in vitro the developmental steps whereby stem cells give rise to neuronal cells, we can now hope to understand factors that control typical and atypical development. We can begin to explore how human genes and their variants are transcribed into messenger RNAs within developing neurons and how these gene transcripts control the biology of developing cells. Thus, human-induced pluripotent stem cells have the potential to uncover not only what aspects of development are uniquely human but also variations in the series of events necessary for normal human brain development that predispose to psychopathology.

Autism spectrum disorder (ASD) is heterogeneous and likely entails distinct phenotypes with varying etiologies. Identifying these subgroups may contribute to hypotheses about differential treatment responses. The present study aimed to discern subgroups among children with ASD and anxiety in context of the five-factor model of personality (FFM) and evaluate treatment response differences to two cognitive-behavioral therapy treatments. The present study is a secondary data analysis of children with ASD and anxiety (N=202; ages 7–13; 20.8% female) in a cognitive behavioral therapy (CBT) randomized controlled trial (Wood et al., 2020). Subgroups were identified via latent profile analysis of parent-reported FFM data. Treatment groups included standard-of-practice CBT (CC), designed for children with anxiety, and adapted CBT (BIACA), designed for children with ASD and comorbid anxiety. Five subgroups with distinct profiles were extracted. Analysis of covariance revealed CBT response was contingent on subgroup membership. Two subgroups responded better to BIACA on the primary outcome measure and a third responded better to BIACA on a peer-social adaptation measure, while a fourth subgroup responded better to CC on a school-related adaptation measure. These findings suggest that the FFM may be useful in empirically identifying subgroups of children with ASD, which could inform intervention selection decisions for children with ASD and anxiety.

Traditional categorical approaches to classifying personality disorders are limited in important ways, leading to a shift in the field to dimensional approaches to conceptualizing personality pathology. Different areas of psychology – personality, developmental, and psychopathology – can be leveraged to understand personality pathology by examining its structure, development, and underlying mechanisms. However, an integrative model that encompasses these distinct lines of inquiry has not yet been proposed. In order to address this gap, we review the latest evidence for dimensional classification of personality disorders based on structural models of maladaptive personality traits, provide an overview of developmental theories of pathological personality, and summarize the Research Domain Criteria (RDoC) initiative, which seeks to understand underlying mechanisms of psychopathology. We conclude by proposing an integrative model of personality pathology development that aims to elucidate the developmental pathways of personality pathology and its underlying mechanisms.

Developmental psychopathology started as an intersection of fields and is now a field itself. As we contemplate the future of this field, we consider the ways in which a newer, interdisciplinary field – human developmental neuroscience – can inform, and be informed by, developmental psychopathology. To do so, we outline principles of developmental psychopathology and how they are and/or can be implemented in developmental neuroscience. In turn, we highlight how the collaboration between these fields can lead to richer models and more impactful translation. In doing so, we describe the ways in which models from developmental psychopathology can enrich developmental neuroscience and future directions for developmental psychopathology.