Mental health problems often begin in early childhood. However, the associations of various individual and contextual risk factors with mental health in the preschool period are incompletely understood, particularly in low- to middle-income countries (LMICs) where multiple risk factors co-exist. To address this gap, we prospectively followed 981 children in a South African birth cohort, the Drakenstein Child Health Study, assessing pre-and postnatal exposures and risk factors. The predictive value of these factors for child mental health (assessed by the Child Behavior Checklist) was modeled using structural equation modeling. We identified two key pathways to greater externalizing behavior: (1) prenatal exposure to substances (alcohol and smoking) directly predicted increased externalizing behavior (β = 0.24, p < 0.001); this relationship was partially mediated by an aspect of infant temperament (negative emotionality; β = 0.05, p = 0.016); (2) lower socioeconomic status and associated maternal prenatal depression predicted more coercive parenting, which in turn predicted increased externalizing behavior (β = 0.18, p = 0.001). Findings in this high-risk LMIC cohort cohere with research from higher income contexts, and indicate the need to introduce integrated screening and intervention strategies for maternal prenatal substance use and depression, and promoting positive parenting across the preschool period.

Incremental prediction of aggression from callous–unemotional (CU) traits is well established, but cross-cultural replication and studies of young children are needed. Little is understood about the contribution of CU traits in children who are already aggressive. We addressed these issues in prospective studies in the United Kingdom and Colombia. In a UK epidemiological cohort, CU traits and aggression were assessed at age 3.5 years, and aggression at 5.0 years by mothers (N = 687) and partners (N = 397). In a Colombian general population sample, CU traits were assessed at age 3.5 years and aggression at 3.5 and 5.0 years by mother report (N = 220). Analyses consistently showed prediction of age-5.0 aggression by age-3.5 CU traits controlling for age-3.5 aggression. Associations between age-3.5 CU traits and age-5.0 aggression were moderated by aggression at 3.5 years, with UK interaction terms, same informant, β = .07 p = .014 cross-informant, β = .14 p = .002, and in Colombia, β = .09 p = .128. The interactions arose from stronger associations between CU traits and later aggression in those already aggressive. Our findings with preschoolers replicated across culturally diverse settings imply a major role for CU traits in the maintenance and amplification of already established aggression, and cast doubt on their contribution to its origins.

This article reviews ways in which quantitative genetic approaches to developmental psychopathology can elucidate normal development. A few examples from genetics are discussed to highlight how investigations of abnormal functioning can inform the study of normal functioning. Two topics that provide bridges between the normal and abnormal are presented in greater detail. Most important is a new quantitative genetic technique that assesses empirically genetic and environmental links between the normal and abnormal. A second topic involves quantitative genetic approaches to environmental analyses, as highlighted by the examination of nonshared environmental factors. Such examinations of the environment are essential in studies of psychopathology, and their application to abnormal development can elucidate processes of normal development. We believe that forging links between the normal and abnormal is the core task of developmental psychopathology and that quantitative genetics is not only compatible with this goal, but essential to it.

In this study, we sought to combine two lines of research to better understand risk for the intergenerational transmission of depression. The first focuses on the role of maternal criticism as a potential mechanism of risk for depression in youth while the second builds from interpersonal and stress generation models regarding the potential impact of youth depression on future escalations in maternal criticism. Specifically, we examined the role of maternal criticism within a transactional mediation model using data from a multi-wave study. Participants were 251 mother–offspring pairs consisting of mothers with (n = 129) and without (n = 122) a history of major depressive disorder (MDD) during their child’s lifetime who completed assessments every 6 months for 2 years. We found support for the hypothesized transactional mediational model in which maternal expressed emotion-criticism (EE-Crit) mediated the link between maternal history of MDD and residual change in youth’s depressive symptoms over the previous 6 months and, reciprocally, youth depressive symptoms mediated the relation between maternal MDD history and residual change in EE-Crit 6 months later. These results indicate that maternal criticism and offspring depressive symptoms may contribute to a vicious cycle of depression risk, which should be considered for interventions targeted toward youth at risk of developing MDD.

Previous research has established that parental marital discord is associated with higher levels of offspring externalizing behaviors, but it is unclear how parental relationship functioning is associated with the genetic and environmental variance on a factor of externalizing problems. Thus, the current study assessed how parental marital discord moderates genetic and environmental variance on offspring externalizing problems at two different ages: childhood and late adolescence. That is, the magnitude of genetic and environmental influences on offspring externalizing at ages 11 and 17 was examined as a function of parental marital discord. Consistent with a diathesis–stress model of psychopathology, it was hypothesized that with increasing marital discord, genetic influences on externalizing would be more pronounced. Rather, results indicated that for the 11-year-old sample, nonshared environmental influences were greater when parental marital discord was low, and comparatively, shared environmental influences contributed more to the variance in externalizing problems when parental marital discord was high. No moderation was found for the 17-year-old cohort. In contrast to studies that do not find an effect of the shared environment, these results provide evidence that the common rearing environment has an impact on externalizing problems in preadolescent children.

Refugee children are often exposed to substantial trauma, placing them at increased risk for mental illness. However, this risk can be mitigated by a capacity for resilience, conferred from multiple ecological systems (e.g., family, community), including at an individual biological level. We examined the ability of hair cortisol concentrations and polygenic scores for mental health to predict risk and resilience in a sample of Syrian refugee children (n = 1359). Children were categorized as either at-risk or resilient depending on clinical thresholds for posttraumatic stress disorder, depression, and externalizing behavior problems. Logistic regression was used to examine main and interacting effects while controlling for covariates. Elevated hair cortisol concentrations were significantly associated with reduced resilience (odds ratio (OR)=0.58, 95%CI [0.40, 0.83]) while controlling for levels of war exposure. Polygenic scores for depression, self-harm, and neuroticism were not found to have any significant main effects. However, a significant interaction emerged between hair cortisol and polygenic scores for depression (OR=0.04, 95%CI [0.003 0.47]), suggesting that children predisposed to depression were more at risk for mental health problems when hair cortisol concentrations were high. Our results suggest that biomarkers (separately and in combination) might support early identification of refugee children at risk for mental health problems.

In spring 2020, U.S. schools universally transitioned to online learning due to the COVID-19 pandemic’s onset, thus creating a natural experiment for examining adolescents’ risk and resilience during an ongoing school crisis response. This longitudinal study used a daily-diary approach to investigate the role of social support in the link between remote learning and psychological well-being across 64 days among a national sample of adolescents (n = 744; 42% Black, 36% White, 22% Other ethnicity/race; 41% boys; 72% eligible for free/reduced-priced lunch; Mage=14.60, SDage=1.71, age-range = 12–17 years). On days when youth attended remote learning, they reported lower daily positive affect, more daily stress, and higher parent social support. There were no significant differences in the effect of remote learning on affect or stress by race or economic status. On days when youth experienced more parent support, they reported lower daily stress and negative affect and higher daily positive affect. On days when youth experienced more peer support, they reported higher daily positive affect. Overall, the study highlights the impact of pandemic-onset remote learning on adolescents’ psychological well-being and emphasizes the need for future research on school crisis contingency planning to address these challenges.

The current study evaluated risk factors in adolescence on problem drinking and emotional distress in late adolescence and emerging adulthood, and meeting criteria for diagnosed disorders in adulthood. The study included 501 parents and their adolescent who participated from middle adolescence to adulthood. Risk factors in middle adolescence (age 18) included parent alcohol use, adolescent alcohol use, and parent and adolescent emotional distress. In late adolescence (age 18), binge drinking and emotional distress were assessed, and in emerging adulthood (age 25), alcohol problems and emotional distress were examined. Meeting criteria for substance use, behavioral, affective, or anxiety disorders were examined between the ages of 26 and 31. Results showed parent alcohol use predicted substance use disorder through late adolescent binge drinking and emerging adulthood alcohol problems. Behavioral disorders were indirectly predicted by adolescent and emerging adult emotional distress. Affective disorders were indirectly predicted by parent emotional distress through adolescent emotional distress. Finally, anxiety disorders were predicted by parent alcohol use via adolescent drinking; parent emotional distress via adolescent emotional distress, and through adolescent alcohol use and emotional distress. Results provided support for the intergenerational transmission of problem drinking and emotional distress on meeting criteria for diagnosed psychiatric disorders in adulthood.

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.

This longitudinal study aimed to validate the biosocial theory of borderline personality disorder (BPD) by examining the transactional relationship between individual vulnerabilities and parental invalidation, and their links to BPD symptoms. We recruited a sample of 332 adolescents (mean age = 14.18 years; 58.3% female) residing in Singapore and administered self-report measures across three time-points (six months apart). Results from our path analytic model indicated that parental invalidation, impulsivity, and emotional vulnerability exhibited unique predictive associations with emotion dysregulation six months later. There was also a reciprocal prospective relationship between emotion regulation difficulties and BPD symptoms. Using random-intercepts cross-lagged panel models, we found partial evidence for a within-individual reciprocal relationship between parental invalidation and emotional vulnerability, and a unidirectional relationship of within-individual changes in impulsivity positively predicting changes in parental invalidation six months later. Overall, the study provided partial empirical support for the biosocial model in a Singaporean context.

Greater childhood adversity predicts a higher likelihood of later self-injurious thoughts and behaviors (SITB). There is little research focused on whether the timing of childhood adversity predicts SITB. The current research examined whether the timing of childhood adversity predicted parent- and youth-reported SITB at age 12 and 16 years in the Longitudinal Studies of Child Abuse and Neglect (LONGSCAN) cohort (n = 970). We found that greater adversity at age 11–12 years consistently predicted SITB at age 12 years, while greater adversity at age 13–14 years consistently predicted SITB at age 16 years. These findings suggest there may be sensitive periods during which adversity may be more likely to lead to adolescent SITB, which can inform prevention and treatment.

Twin studies demonstrate significant environmental influences and a lack of genetic effects on disordered eating before puberty in girls. However, genetic factors could act indirectly through passive gene–environment correlations (rGE; correlations between parents’ genes and an environment shaped by those genes) that inflate environmental (but not genetic) estimates. The only study to explore passive rGE did not find significant effects, but the full range of parental phenotypes (e.g., internalizing symptoms) that could impact daughters’ disordered eating was not examined. We addressed this gap by exploring whether parents’ internalizing symptoms (e.g., anxiety, depressive symptoms) contribute to daughters’ eating pathology through passive rGE. Participants were female twin pairs (aged 8–14 years; M = 10.44) in pre-early puberty and their biological parents (n = 279 families) from the Michigan State University Twin Registry. Nuclear twin family models explored passive rGE for parents’ internalizing traits/symptoms and twins’ overall eating disorder symptoms. No evidence for passive rGE was found. Instead, environmental factors that create similarities between co-twins (but not with their parents) and unique environmental factors were important. In pre-early puberty, genetic factors do not influence daughters’ disordered eating, even indirectly through passive rGE. Future research should explore sibling-specific and unique environmental factors during this critical developmental period.

Little effort has been made to integrate developmental cascades with maternal/paternal parenting in a single investigation. The present study seeks to test cascading effects among academic and internalizing/externalizing symptoms and their associations with maternal/paternal parenting across three time points from 8 to 10 years. Data for this investigation came from a nationally representative prospective cohort study of children born in April through July of 2008 in South Korea who were followed up annually. The sample included 1,598 families (48.5% girls). Parents rated their parenting and teachers rated children’s internalizing/externalizing problems and academic performance. Structural equation modeling showed that externalizing problems were negatively related to academic performance. Academic performance was negatively related to internalizing problems and positively related to maternal/paternal authoritative parenting, which in turn led to children’s higher academic performance. Bidirectional relations were found between academic performance and externalizing problems and between paternal authoritative parenting and children’s internalizing problems. Findings suggested cascading effects and their associations with parenting were not attributable to child gender, intelligence, or socioeconomic differences. These findings lend support to adjustment erosion and academic incompetence models and underscore the need for greater attention to the role that fathering may play in children’s development and mothering.

How we are influenced by our environment is a fundamental question in developmental science. Theories and empirical research have claimed that some individuals are susceptible to environmental influences and others are much less susceptible. The present study addressed four questions: (1) Is environmental susceptibility a continuous or categorical construct? (2) Is environmental susceptibility unidimensional (i.e., domain general) or multidimensional (i.e., domain specific)? (3) Are there genetic contributions to individual differences in environmental susceptibility? (4) What are the temperamental characteristics of different environmental susceptibility patterns? We used child- and mother-report data from a sample of 11-year-old twins (N = 1,507) and applied a novel data-driven approach to assess an environmental susceptibility space, based on simultaneous associations between multiple environmental exposures (18 measures relating to parenting, parent, peer, and twin relationships) and developmental outcomes (10 measures relating to empathy, prosocial behavior, aggression, and self-esteem). The results suggest that the environmental susceptibility space we assessed is better conceptualized as continuous and multidimensional. Different children showed susceptibility to different contexts and variation in domain-general versus domain-specific patterns. A comparison of distances between monozygotic and dizygotic twins within the space demonstrated genetic contributions. Finally, susceptibility patterns could not be differentiated based on a specific temperament trait, but rather related to temperament profiles.

Recent initiatives have focused on integrating transdiagnostic biobehavioral processes or dispositions with dimensional models of psychopathology. Toward this goal, biobehavioral traits of affiliative capacity (AFF) and inhibitory control (INH) hold particular promise as they demonstrate transdiagnostic stability and predictive validity across developmental stages and differing measurement modalities. The current study employed data from different modes of measurement in a sample of 1830 children aged 5–10 years to test for associations of AFF and INH, individually and interactively, with broad dimensions of psychopathology. Low AFF, assessed via parent-report, evidenced predictive relations with distress- and externalizing-related problems. INH as assessed by cognitive-task performance did not relate itself to either psychopathology dimension, but it moderated the effects observed for low AFF, such that high INH protected against distress symptoms in low-AFF participants, whereas low INH amplified distress and externalizing symptoms in low-AFF participants. Results are discussed in the context of the interface of general trait transdiagnostic risk factors with quantitatively derived dimensional models of psychopathology.

During early life-sensitive periods (i.e., fetal, infancy), the developing stress response system adaptively calibrates to match environmental conditions, whether harsh or supportive. Recent evidence suggests that puberty is another window when the stress system is open to recalibration if environmental conditions have shifted significantly. Whether additional periods of recalibration exist in adulthood remains to be established. The present paper draws parallels between childhood (re)calibration periods and the perinatal period to hypothesize that this phase may be an additional window of stress recalibration in adult life. Specifically, the perinatal period (defined here to include pregnancy, lactation, and early parenthood) is also a developmental switch point characterized by heightened neural plasticity and marked changes in stress system function. After discussing these similarities, lines of empirical evidence needed to substantiate the perinatal stress recalibration hypothesis are proposed, and existing research support is reviewed. Complexities and challenges related to delineating the boundaries of perinatal stress recalibration and empirically testing this hypothesis are discussed, as well as possibilities for future multidisciplinary research. In the theme of this special issue, perinatal stress recalibration may be a mechanism of multilevel, multisystem risk, and resilience, both intra-individually and intergenerationally, with implications for optimizing interventions.

Children of alcoholics (COAs) are at risk for elevated internalizing and externalizing symptoms. Yet, little is known about the familial and behavioral adjustments of COAs following parental separation. Using an ecological–transactional framework, we examined how multiple risk factors contributed to the formation of different alcoholic family structures and how living in heterogeneous family structures affected COAs’ behavioral problems. The Michigan Longitudinal Study, a multiwave study on initially intact alcoholic and control families with preschool-age children (n = 503), was used to evaluate outcomes of offspring, when families either remained intact or were separated when the child was aged 12–14. Alcoholic families who later transitioned into stepfamilies were characterized with higher paternal antisociality, marital aggression, and serious family crises than alcoholic families that remained intact. COAs in stepfamilies (but not in single-parent families) exhibited higher levels of internalizing and externalizing symptoms in preadolescence compared with those in alcoholic intact families, in part because of elevated behavioral risk at age 3. Structural equation modeling indicated that the aggregated risk of stepfamily residence directly related to COAs’ internalizing and indirectly related to COAs’ externalizing problems, partially mediated by family stressors. Findings suggest targeting COAs in separated families for early intervention.

Mapuche represents the largest indigenous group in Chile amounting to nearly 10% of the total population. In a longitudinal cohort of 12,398 children, we analyzed the role of ethnicity in physical and psychosocial development of Mapuche and nonindigenous Chilean toddlers (age 2.5 years), taking into account sociodemographic and caregiver characteristics. As indicated by our univariate analysis, the Mapuche developmental niche was characterized by lower income, lower maternal education, poorer quality of the home environment, longer breastfeeding, and higher parental stress. Physical development showed higher body mass index. Mapuche children showed less externalizing problems. We then analyzed the incremental contribution of ethnicity in a series of hierarchical regressions with the second wave of developmental measurements (age 4.5 years) as outcome variables, showing a significant but modest incremental contribution of ethnicity to the prediction of children's development between 2.5 and 4.5 years of age. Controlling for environmental variables, Mapuche showed less externalizing and internalizing, behavior problems. Socioeconomic status, quality of the home environment, and parenting stress were stronger predictors of socioemotional development than ethnicity per se.