This study provides insights into the roles played by perceived stress and social support in the relationship between cumulative risk exposure (CRE) and adolescent emotional distress. Preregistered longitudinal moderated mediation analyses were used to test hypotheses relating to the association between CRE and later emotional distress; the mediating role of perceived stress in the relationship between CRE and later emotional distress; and, the moderating effects of peer and adult-level family support on the relationship between CRE and later perceived stress, among N = 19,159 adolescents over three annual waves (at ages 11/12, 12/13, 13/14). Analyses revealed that CRE significantly predicted later adolescent emotional distress. This relationship was partially mediated by perceived stress. Both peer and adult-level family support significantly moderated the impact of CRE on later perceived stress (i.e., adolescents reporting higher levels of support perceived significantly lower levels of stress resulting from CRE compared to those reporting lower levels of support). These findings provide critical empirical evidence of the roles played by perceived stress and social support in the relationship between CRE and adolescent emotional distress, with consequent implications for intervention.

Based on a multiwave, two-year prospective design, this study is the first to examine the extent to which multilocus hypothalamic–pituitary–adrenal axis (HPA axis)-related genetic variants, childhood maltreatment, and recent stress jointly predicted prospective changes in adolescent depressive symptoms. A theory-driven multilocus genetic profile score (MGPS) was calculated to combine the effects of six common polymorphisms within HPA-axis related genes (CRHR1, NR3C1, NR3C2, FKBP5, COMT, and HTR1A) in a sample of Chinese Han adolescents (N = 827; 50.2% boys; Mage = 16.45 ± 1.36 years). The results showed that the three-way interaction of HPA-axis related MGPS, childhood maltreatment and recent interpersonal, but not noninterpersonal, stress significantly predicted prospective changes in adolescent depressive symptoms. For adolescents with high but not low HPA-axis related MGPS, exposure to severe childhood maltreatment predisposed individuals more vulnerable to recent interpersonal stress, exhibiting greater prospective changes in adolescent depressive symptoms. The findings provide preliminary evidence for the cumulative risk mechanism regarding gene-by-environment-by-environment (G × E1 × E2) interactions that underlie the longitudinal development of adolescent depressive symptoms and show effects specific to interpersonal stress.

Psychopathology is intergenerationally transmitted through both genetic and environmental mechanisms via heterotypic (cross-domain), homotypic (domain-specific), and general (e.g., “p-factor”) pathways. The current study leveraged an adopted-at-birth design, the Early Growth and Development Study (57% male; 55.6% White, 19.3% Multiracial, 13% Black/African American, 10.9% Hispanic/Latine) to explore the relative influence of these pathways via associations between adoptive caregiver psychopathology (indexing potential environmental transmission) and birth parent psychopathology (indexing genetic transmission) with adolescent internalizing and externalizing symptoms. We included composite measures of adoptive and birth parent internalizing, externalizing, and substance use domains, and a general “p-factor.” Age 11 adolescent internalizing and externalizing symptom scores were the average of adoptive parent reports on the Child Behavior Checklist (n = 407). Examining domains independently without addressing comorbidity can lead to incorrect interpretations of transmission mode. Therefore, we also examined symptom severity (like the “p-factor”) and an orthogonal symptom directionality score to more cleanly disentangle transmission modes. The pattern of correlations was consistent with mostly general transmission in families with youth showing comorbid internalizing and externalizing symptoms, rather than homotypic transmission. Findings more strongly supported potential environmental or evocative mechanisms of intergenerational transmission than genetic transmission mechanisms (though see limitations). Parent-specific effects are discussed.

Adolescents often experience heightened socioemotional sensitivity warranting their use of regulatory strategies. Yet, little is known about how key socializing agents help regulate teens’ negative emotions in daily life and implications for long-term adjustment. We examined adolescent girls’ interpersonal emotion regulation (IER) with parents and peers in response to negative social interactions, defined as parent and peer involvement in the teen’s enactment of emotion regulation strategies. We also tested associations between rates of daily parental and peer IER and depressive symptoms, concurrently and one year later. Adolescent girls (N = 112; Mage = 12.39) at temperamental risk for depressive disorders completed a 16-day ecological momentary assessment protocol measuring reactivity to negative social interactions, parental and peer IER, and current negative affect. Results indicated that adolescents used more adaptive strategies with peers and more maladaptive strategies with parents in daily life. Both parental and peer IER down-regulated negative affect, reflected by girls’ decreased likelihood of experiencing continued negative affect. Higher proportions of parental adaptive IER predicted reduced depressive symptoms one year later. Findings suggest that both parents and peers effectively help adolescent girls down-regulate everyday negative emotions; however, parents may offer more enduring benefits for long-term adjustment.

Sensory differences and anxiety disorders are highly prevalent in autistic individuals with and without ADHD. Studies have shown that sensory differences and anxiety are associated and that intolerance of uncertainty (IU) plays an important role in this relationship. However, it is unclear as to how different levels of the sensory processing pathway (i.e., perceptual, affective, or behavioral) contribute. Here, we used psychophysics to assess how alterations in tactile perception contribute to questionnaire measures of sensory reactivity, IU, and anxiety. Thirty-eight autistic children (aged 8-12 years; 27 with co-occurring ADHD) were included. Consistent with previous findings, mediation analyses showed that child-reported IU fully mediated an association between parent-reported sensory reactivity and parent-reported anxiety and that anxiety partially mediated an association between sensory reactivity and IU. Of the vibrotactile thresholds, only simultaneous frequency discrimination (SFD) thresholds correlated with sensory reactivity. Interestingly, we found that sensory reactivity fully mediated an association between SFD threshold and anxiety, and between SFD threshold and IU. Taken together, those findings suggest a mechanistic pathway whereby tactile perceptual alterations contribute to sensory reactivity at the affective level, leading in turn to increased IU and anxiety. This stepwise association can inform potential interventions for IU and anxiety in autism.

Maternal insensitivity to children’s emotional distress (e.g., expressions of sadness or fearfulness) is one mechanism through which maternal alcohol dependence may increase children’s risk for psychopathology. Although emotion dysregulation is consistently associated with psychopathology, it remains unclear how or why alcohol dependence’s effects on caregiving responses to children’s distress may impact children’s emotion regulation over time, particularly in ways that may engender risks for psychopathology. This study examined longitudinal associations between lifetime maternal alcohol dependence symptoms, mothers’ insensitivity to children’s emotional distress cues, and children’s emotional reactivity among 201 mother-child dyads (Mchild age = 2.14 years; 56% Black; 11% Latino). Structural equation modeling analyses revealed a significant mediational pathway such that maternal alcohol dependence predicted increases in mothers’ insensitivity to children’s emotional distress across a one-year period (β = .16, p = .013), which subsequently predicted decreases in children’s emotional reactivity one year later (β = −.29, p = .009). Results suggest that mothers with alcohol dependence symptoms may struggle to sensitively respond to children’s emotional distress, which may prompt children to suppress or hide their emotions as an adaptive, protective strategy. The potential developmental benefits and consequences of early, protective expressive suppression strategies are discussed via developmental psychopathology frameworks.

Prenatal glucocorticoid exposure has been negatively associated with infant neurocognitive outcomes. However, questions about developmental timing effects across gestation remain. Participants were 253 mother-child dyads who participated in a prospective cohort study recruited in the first trimester of pregnancy. Diurnal cortisol was measured in maternal saliva samples collected across a single day within each trimester of pregnancy. Children (49.8% female) completed the Bayley Mental Development Scales, Third Edition at 6, 12, and 24 months and completed three observational executive function tasks at 24 months. Structural equation models adjusting for sociodemographic covariates were used to test study hypotheses. There was significant evidence for timing sensitivity. First-trimester diurnal cortisol (area under the curve) was negatively associated with cognitive and language development at 12 months and poorer inhibition at 24 months. Second-trimester cortisol exposure was negatively associated with language scores at 24 months. Third-trimester cortisol positively predicted performance in shifting between task rules (set shifting) at 24 months. Associations were not reliably moderated by child sex. Findings suggest that neurocognitive development is sensitive to prenatal glucocorticoid exposure as early as the first trimester and underscore the importance of assessing developmental timing in research on prenatal exposures for child health outcomes.

This study replicated and extended Narayan and colleagues’ (2018) original benevolent childhood experiences (BCEs) study. We examined associations between adverse and positive childhood experiences and mental health problems in a second sample of low-income, ethnically diverse pregnant individuals (replication). We also examined effects of childhood experiences on perinatal mental health problems while accounting for contemporaneous support and stress (extension). Participants were 175 pregnant individuals (M = 28.07 years, SD = 5.68, range = 18–40; 38.9% White, 25.7% Latina, 16.6% Black, 12.0% biracial/multiracial, 6.8% other) who completed standardized instruments on BCEs, childhood maltreatment and exposure to family dysfunction, sociodemographic stress, and perinatal depression and post-traumatic stress disorder (PTSD) symptoms. They completed the Five-Minute Speech Sample at pregnancy and postpartum to assess social support from the other biological parent. Higher family dysfunction predicted higher prenatal depression symptoms, while higher BCEs and prenatal social support predicted lower prenatal PTSD symptoms. Prenatal depression and prenatal PTSD symptoms were the most robust predictors of postnatal depression and PTSD symptoms, respectively, although higher postnatal social support also predicted lower postnatal PTSD symptoms. Findings replicated many patterns found in the original BCEs study and indicated that contemporaneous experiences are also associated with perinatal mental health problems.

The moral self-concept (MSC) describes how children view themselves as moral agents. Research suggests that the MSC may relate to moral behavior, yet little is known about how MSC relates to moral behavior in preschoolers. One hundred six low-income children (Mage = 52.78 months, SD = 6.61 months) and their teachers participated in this study. In the fall, children completed a MSC puppet task measure. In the fall and spring, teachers reported via children’s survey prosocial behavior and aggressive behavior. We used a person-centered approach to identify profiles of MSC, which revealed two profiles of behavior: comforting prosocials and helpful aggressors. Comforting prosocials showed a moderate preference for comforting, a slight preference for helping, and a slight preference for avoiding aggression. Helpful aggressors had a moderate aversion to comforting, a strong preference for helping, and a slight preference for aggressive behavior. Subsequent analysis of covariance analysis revealed that MSC profiles did not differ in concurrent behavior but did differ in behavior 6 months later. The comforting prosocial group participated in more aggression than the helpful aggressors. Additionally, analysis of covariance analysis of change in aggression scores over time showed that comforting prosocials aggression increased, while helpful aggressors aggression decreased. Both groups over time decreased in prosocial behavior, but to different degrees. Overall, findings reveal that the MSC in preschoolers may relate to future not concurrent moral behavior.

Parental depression is a risk factor for children’s cognitive and psychological development. Literature has found reciprocal relations between parental depression and child psychopathology and effects of parental depression on children’s cognition. The present study is the first to examine reciprocity among parental depression and child cognition, and pathways to child psychopathology. Structural equation models were conducted using data from the Early Head Start Research and Evaluation Project, a nationally representative sample of 3,001 economically marginalized families. Measures were collected in four waves from 14 months to 10–11 years. Reciprocal associations emerged between maternal and paternal depression at from 14 months to 5 years. Reciprocal parental depression was associated with greater psychopathology at age 10–11. Maternal depression predicted poorer child cognition, which indirectly predicted increased depression in mothers of children aged 3–5 through paternal depression, and in fathers at age 3, through earlier paternal depression. This study was unable to parse within- and between-person effects. Additionally, data for paternal depression was limited to ages 2 and 3. Findings emphasize the transactional nature of child cognition and child and parent psychopathology, supporting family focused intervention and prevention efforts that target parent psychopathology and child cognition.

Researchers often aim to assess whether repeated measures of an exposure are associated with repeated measures of an outcome. A question of particular interest is how associations between exposures and outcomes may differ over time. In other words, researchers may seek the best form of a temporal model. While several models are possible, researchers often consider a few key models. For example, researchers may hypothesize that an exposure measured during a sensitive period may be associated with repeated measures of the outcome over time. Alternatively, they may hypothesize that the exposure measured immediately before the current time period may be most strongly associated with the outcome at the current time. Finally, they may hypothesize that all prior exposures are important. Many analytic methods cannot compare and evaluate these alternative temporal models, perhaps because they make the restrictive assumption that the associations between exposures and outcomes remains constant over time. Instead, we provide a tutorial describing four temporal models that allow the associations between repeated measures of exposures and outcomes to vary, and showing how to test which temporal model is best supported by the data. By finding the best temporal model, developmental psychopathology researchers can find optimal windows for intervention.

Studies show that war leads to an increase in harsh parenting and a decrease in parental warmth, which in turn has a devastating impact on children’s development. However, there is insufficient research on the factors that affect parenting in post-conflict regions. In addition, most previous studies on the role of parenting in the context of war rely on self-reports, which are subject to a number of limitations. To complement existing research, the present cross-sectional study used behavioral observations of 101 mothers and their 6–12 year old children to assess parenting in post-conflict northern Uganda. The aim of the current study was to explore associations between observed maternal warmth and coercion and self-reported socioeconomic status (e.g., mother’s educational level) as well as maternal (e.g., posttraumatic stress disorder), child (e.g., externalizing problems), and social contextual factors (e.g., family violence). Results show a link between observed parenting, child characteristics, and family violence. Higher levels of children’s externalizing problems were associated with more severe maternal coercion. In addition, a negative association was found between family violence and maternal warmth. Findings are discussed in terms of their implications for prevention and intervention programs and the use of behavioral observations in post-conflict environments.

Although resilient youth provide an important model of successful adaptation to adversity, we know relatively little about the origins of their positive outcomes, particularly the role of biological mechanisms. The current study employed a series of methylome-wide association studies to identify methylomic biomarkers of resilience in a unique sample of 276 twins within 141 families residing in disadvantaged neighborhoods. Results revealed methylome-wide significant differentially methylated probes (DMPs) for social and academic resilience and suggestive DMPs for psychological resilience and resilience across domains. Pathway analyses informed our understanding of the biological underpinnings of significant differentially methylated probes. Monozygotic twin difference analyses were then employed to narrow in on DMPs that were specifically environmental in origin. Our findings suggest that alterations in the DNA methylome may be implicated in youth resilience to neighborhood adversity and that some of the suggestive DMPs may be environmentally engendered. Importantly, our ability to replicate our findings in a well-powered sample was hindered by the scarcity of twin samples with youth exposed to moderate to substantial levels of adversity. Thus, although preliminary, the present study is the first to identify DNA methylation biomarkers of academic and social resilience.

To determine the validity of parent reports (PRs) of ADHD in preschoolers, we assessed hyperactivity/impulsivity (HI) and inattention (IN) in 1114 twins with PRs at 1.5, 2.5, 4, 5, 14, 15, and 17 years, and teacher-reports at 6, 7, 9, 10, and 12. We examined if preschool PRs (1) predict high HI/IN trajectories, and (2) capture genetic contributions to HI/IN into adolescence. Group-based trajectory analyses identified three 6–17 years trajectories for both HI and IN, including small groups with high HI (N = 88, 10.4%, 77% boys) and IN (N = 158, 17.3%, 75% boys). Controlling for sex, each unit of HI PRs starting at 1.5 years and at 4 years for IN, increased more than 2-fold the risk of belonging to the high trajectory, with incremental contributions (Odds Ratios = 2.5–4.5) at subsequent ages. Quantitative genetic analyses showed that genetic contributions underlying preschool PRs accounted for up to a quarter and a third of the heritability of later HI and IN, respectively. Genes underlying 1.5-year HI and 4-year IN contributed to 6 of 8 later HI and IN time-points and largely explained the corresponding phenotypic correlations. Results provide phenotypic and genetic evidence that preschool parent reports of HI and IN are valid means to predict developmental risk of ADHD.

The finding that victims’ psychological problems tend to be exacerbated in lower-victimization classrooms has been referred to as the “healthy context paradox.” The current study has put the healthy context paradox to a strict test by examining whether classroom-level victimization moderates bidirectional within- and between-person associations between victimization and psychological adjustment. Across one school year, 3,470 Finnish 4th to 9th graders (Mage = 13.16, 46.1% boys) reported their victimization, depressive symptoms, anxiety, and self-esteem. Three types of multilevel models (cross-lagged panel, latent change score, and random-intercept cross-lagged panel) were estimated for each indicator of psychological adjustment. Findings indicated that the healthy context paradox emerges because classroom-level victimization moderates the prospective effect of victimization on psychological problems, rather than the effect of psychological problems on victimization. In classrooms with lower victimization, victims not only experience worse psychological maladjustment over time compared to others (between-person changes), but also higher maladjustment than before (absolute within-person changes).

Alexithymia (difficulties identifying and describing feelings) predicts increased risks for psychopathology, especially during the transition from childhood to adolescence. However, little is known of the early contributors to alexithymia. The language hypothesis of alexithymia suggests that language deficits play a primary role in predisposing language-impaired groups to developing alexithymia; yet longitudinal data tracking prospective relationship between language function and alexithymia are scarce. Leveraging data from the Surrey Communication and Language in Education cohort (N = 229, mean age at time point 1 = 5.32 years, SD = 0.29, 51.1% female), we investigated the prospective link between childhood language development and alexithymic traits in adolescence. Results indicated that boys with low language function at ages 4–5 years, and those who later met the diagnostic criteria for language disorders at ages 5–6 years, reported elevated alexithymic traits when they reached adolescence. Parent-reported child syntax abilities at ages 5–6 years revealed a dimensional relationship with alexithymic traits, and this was consistent with behavioral assessments on related structural language abilities. Empirically derived language groups and latent language trajectories did not predict alexithymic traits in adolescence. While findings support the language hypothesis of alexithymia, greater specificity of the alexithymia construct in developmental populations is needed to guide clinical interventions.

Parents’ responses to their children’s negative emotions are a central aspect of emotion socialization that have well-established associations with the development of psychopathology. Yet research is lacking on potential bidirectional associations between parental responses and youth symptoms that may unfold over time. Further, additional research is needed on sociocultural factors that may be related to the trajectories of these constructs. In this study, we examined associations between trajectories of parental responses to negative emotions and adolescent internalizing symptoms and the potential role of youth sex and racial identity. Adolescents and caregivers (N = 256) completed six assessments that spanned adolescent ages 13–18 years. Multivariate growth models revealed that adolescents with higher internalizing symptoms at baseline experienced increasingly non-supportive parental responses over time (punitive and distress responses). By contrast, parental responses did not predict initial levels of or changes in internalizing symptoms. Parents of Black youth reported higher minimization and emotion-focused responses and lower distress responses compared to parents of White youth. We found minimal evidence for sex differences in parental responses. Internalizing symptoms in early adolescence had enduring effects on parental responses to distress, suggesting that adolescents may play an active role in shaping their emotion socialization developmental context.

The previously observed heterogeneity in developmental and intergenerational trajectories of childhood trauma may root from interindividual differences in the way trauma-exposed individuals have resolved these experiences. The current study explored whether distinctive patterns of impaired mentalization in relation to trauma could be identified in a sample of 825 pregnant women who experienced childhood maltreatment and whether these heterogeneous patterns were marked by significant differences in internalized and externalized problems during pregnancy, intimate partner violence, personality dysfunctions, and antenatal attachment. A latent profile analysis applied to the seven subscales of the Failure to Mentalize Trauma Questionnaire unraveled interindividual variability in mentalizing impairments among pregnant women exposed to childhood maltreatment by identifying five distinctive types of psychological responses to trauma, each being associated in cross-sectional analyses with a specific set of symptoms and dysfunctions. Overall, the study highlights the need for tailored interventions based on the individuals’ specific impairments in mentalizing trauma and calls for future developmental research exploring the longitudinal correlates of the five documented profiles of trauma processing.

Childhood maltreatment is associated with wide-ranging psychopathology at all stages of life. In the current study, we investigated whether posttraumatic stress disorder (PTSD) severity mediated the association between childhood maltreatment and internalizing and externalizing disorders among 262 South African trauma-exposed adolescents (aged 12–18 years). Childhood maltreatment and PTSD symptom severity were assessed using the Childhood Trauma Questionnaire and the Child PTSD Checklist, respectively. Psychiatric disorders were assessed utilizing the Kiddie-Schedule for Affective Disorders and Schizophrenia-Present and Lifetime version and were grouped into internalizing or externalizing disorders. Hierarchal logistic regression was used to assess the association of childhood maltreatment subtype with internalizing and externalizing disorders, controlling for age and gender, with PTSD symptom severity added to the final model. We found that sexual abuse was significantly associated with internalizing disorders, although this effect was no longer significant when PTSD was added to the model demonstrating that PTSD mediated the association between sexual abuse and internalizing disorders. Physical abuse, but not PTSD, was associated with externalizing disorders. Physical abuse, emotional neglect, and PTSD were associated with comorbid internalizing and externalizing disorders. These findings have implications for intervention and prevention strategies targeted at trauma-exposed adolescents with a history of childhood maltreatment.

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