Self-inflicted injury (SII) in adolescence is a serious public health concern that portends prospective vulnerability to internalizing and externalizing psychopathology, borderline personality development, suicide attempts, and suicide. To date, however, our understanding of neurobiological vulnerabilities to SII is limited. Behaviorally, affect dysregulation is common among those who self-injure. This suggests ineffective cortical modulation of emotion, as observed among adults with borderline personality disorder. In borderline samples, structural and functional abnormalities are observed in several frontal regions that subserve emotion regulation (e.g., anterior cingulate, insula, dorsolateral prefrontal cortex). However, no volumetric analyses of cortical brain regions have been conducted among self-injuring adolescents. We used voxel-based morphometry to compare cortical gray matter volumes between self-injuring adolescent girls, ages 13–19 years (n = 20), and controls (n = 20). Whole-brain analyses revealed reduced gray matter volumes among self-injurers in the insular cortex bilaterally, and in the right inferior frontal gyrus, an adjacent neural structure also implicated in emotion and self-regulation. Insular and inferior frontal gyrus gray matter volumes correlated inversely with self-reported emotion dysregulation, over-and-above effects of psychopathology. Findings are consistent with an emotion dysregulation construal of SII, and indicate structural abnormalities in some but not all cortical brain regions implicated in borderline personality disorder among adults.

Drawing on five waves of longitudinal data from 392 families (52% female; mean age of wave 1 [Mage_W1] = 12.89, standard deviation [SD] = .48; Mage_W5 = 21.95, SD = .77; 199 European American and 193 Mexican American families; 217 intact and 175 stepfather families), this study documented transactional relations of mothers’ and fathers’ depressive symptoms with youth's symptomatology from early adolescence to young adulthood. Trait and time-varying cross-lagged models revealed that both mothers’ and fathers’ between- and within-person differences in depressive symptoms were associated with youth's internalizing and externalizing symptoms. Whereas each parent's depressive symptoms uniquely contributed to youth's internalizing symptoms, however, only mothers’ depressive symptoms influenced youth's externalizing symptoms. Although reciprocal effects of youth's internalizing symptoms on parents’ depressive symptoms were not significant, youth's externalizing symptoms predicted changes in mothers’ depressive symptoms over time. Moderation analyses revealed distinct transactional patterns by family ethnicity and child gender, but not by family structure. This study revealed dynamic transactions among family members’ symptomatology that point to opportune times and targets for intervention efforts aimed at mitigating the negative impact of parents’ depressive symptoms on youth's adjustment.

The impact of maltreatment spreads across many developmental domains and extends across the entire life span. Identifying unidirectional or bidirectional drivers of developmental cascades of the effects of maltreatment experiences is critical to efficiently employing interventions to promote resilient development in maltreated children. This 1-year longitudinal study utilized a multiple-levels approach, investigating “bottom-up” and “top-down” cascades using structural equation modeling between cortisol regulation, externalizing behavior, and peer aggression. Neither a bottom-up model driven by cortisol regulation nor a top-down model driven by peer aggression fit the data well. Instead, lower rates of externalizing behavior at Year 1 most strongly predicted improvements at all levels of analysis (reduced cortisol, externalizing behavior, and peer aggression) at Year 2. These results provide initial indication of a mechanism through which interventions for maltreated children may be most effective and result in the most substantial positive changes across developmental domains.

Childhood maltreatment robustly predicts adolescent externalizing behaviors (EB; e.g., violence, delinquency, substance use) and may crystalize patterns of EB by influencing sensitivity to the social environment (e.g., parenting, friendships). In a nationally representative sample of 9,421 adolescents, we modeled latent growth curves of EB from age 13 to 32 years. Next, we explored whether maltreated youth differed from nonmaltreated youth in their sensitivity to parental closeness, friendship involvement, and polymorphisms from dopamine genes linked to EB (dopamine receptors D2 and D4, dopamine transporter). Overall, maltreated youth had significantly higher levels of EB across adolescence and adulthood; however, maltreated and nonmaltreated youth showed similar patterns of EB change over time: violent behavior decreased in adolescence before stabilizing in adulthood, whereas nonviolent delinquency and substance use increased in adolescence before decreasing in the transition to adulthood. Maltreatment reduced sensitivity to parental closeness and friendship involvement, although patterns varied based on type of EB outcome. Finally, none of the environmental effects on EB were significantly moderated by the dopamine polygenic risk score after accounting for multiple testing. These findings underline the enduring effects of early maltreatment and implicate that maltreatment may contribute to long-term risk for EB by influencing children's sensitivity to social relationship factors in adolescence.

We tested the hypothesis that high activity levels in infancy would predict self-regulatory problems and later symptoms of attention deficit and hyperactivity disorder (ADHD) in a longitudinal study of British families (N = 321). Infants’ activity levels were assessed at 6 months, using 3 informants’ reports from the Infant Behavior Questionnaire (IBQ) and ActiGraphs during baseline, attention, and restraint tasks. At a mean of 33 months, the children were assessed on self-regulatory tasks; at a mean of 36 months, 3 informants reported symptoms of ADHD. At a mean of 7.0 years, the children were assessed on executive function tasks; 3 informants reported on the child's symptoms of ADHD; and diagnoses of disorder were obtained using the Preschool Age Psychiatric Assessment. Informants’ reports of high activity levels at 6 months predicted ADHD symptoms in early childhood and diagnoses of ADHD with clinical impairment at age 7. The IBQ activity scale was also associated with the children's later performance on self-regulation tasks in early and middle childhood. Activity level in infancy reflects normal variation and is not a sign of psychopathology; however, these findings suggest that further study of the correlates of high activity level in infancy may help identify those children most at risk for disorder.

A low resting heart rate across development from infancy to young adulthood relates to greater aggression/hostility. Adult aggression and a high heart rate relate to health risk. Do some aggressive individuals retain low heart rate and less health risk across development while others show high heart rate and more risk? A longitudinal sample of 203 men assessed as teens (age 16.1) and adults (mean age 32.0) permitted us to assess (a) stability of heart rate levels and reactivity, (b) stability of aggression/hostility, and (c) whether change or stability related to health risk. Adults were assessed with Buss–Perry measures of aggression/hostility; teens with the Zuckerman aggression/hostility measure. Mean resting heart rate, heart rate reactivity to speech preparation, and aggression/hostility were moderately stable across development. Within age periods, mean heart rate level, but not reactivity, was negatively related to hostility/aggression. Maintaining low heart rate into adulthood was related to better health among aggressive individuals relative to those with increasing heart rate into adulthood. Analyses controlled for weight gain, socioeconomic status, race, health habits, and medication. Low heart rate as a characteristic of hostile/aggressive individuals may continue to relate to better health indices in adulthood, despite possible reversal of this relationship with aging.

Children with prenatal tobacco exposure (PTE) exhibit early self-regulatory impairments, reflecting a life-course persistent propensity toward behavioral disinhibition. Previously, we demonstrated the protective role of parental responsiveness for reducing the risk of exposure-related disruptive behavior in adolescence. Here, we expanded this line of inquiry, examining whether responsiveness moderates the relation of PTE to a broader set of behavioral disinhibition features in early childhood and testing alternative diathesis-stress versus differential susceptibility explanatory models. PTE was assessed prospectively using interviews and bioassays in the Midwestern Infant Development Study (MIDS). Mother-child dyads (N = 276) were re-assessed at approximately 5 years of age in a preschool follow-up. We quantified maternal responsiveness and child behavioral disinhibition using a combination of directly observed activities in the lab and developmentally sensitive questionnaires. Results supported a diathesis-stress pattern. Children with PTE and less responsive mothers showed increased disruptive behavior and lower effortful control compared with children without PTE. In contrast, exposed children with more responsive mothers had self-regulatory profiles similar to their non-exposed peers. We did not observe sex differences. Findings provide greater specification of the protective role of maternal responsiveness for self-regulation in children with PTE and help clarify mechanisms that may underscore trajectories of exposure-related behavioral disinhibition.

We examined genetic and environmental contributions to the development of symptoms of attention-deficit/hyperactivity disorder (ADHD) in preschool children. ADHD symptoms in siblings at 1.5, 3, and 5 years of age were investigated in a population-based sample from the prospective Norwegian Mother and Child Cohort Study. The longitudinal contributions of additive genetic, shared, twin-specific, and unique environmental influences were estimated using biometric structural equation models. Heritability of ADHD symptoms ranged from 54% to 70%. There was evidence of partially new genetic influences at successive ages, with genetic correlations ranging from .58 to .89. Contributions from shared environmental factors and twin-specific factors were minor. The importance of unique environmental effects appeared to increase across ages, and was mostly specific to a given age. There was no evidence suggesting that this pattern differs across males and females. Symptoms of ADHD are highly heritability in young children from as early as 1.5 years of age. Longitudinal stability of ADHD symptoms is mainly attributable to genetic influences, but there is also some evidence for age-specific genetic influences. These findings contribute to our understanding of development of ADHD early in life, and can guide future molecular genetics studies.

The current study examined trajectories of maternal and paternal depression in the year following the birth of an infant sibling, and relations with family risk factors and firstborn children's internalizing and externalizing behavior problems. Latent class growth analysis was conducted on 231 families in a longitudinal investigation (prebirth and 1, 4, 8, and 12 months postbirth) and revealed four classes of families: both mother and father low in depressive symptoms (40.7%); mother high–father low (25.1%); father high–mother low (24.7%), and both mother and father high (9.5%). Families with both mothers and fathers high on depressive symptoms were higher on marital negativity, parenting stress, and children's internalizing and externalizing problems, and lower on marital positivity and parental efficacy than other classes. Children, parents, and marital relationships were more problematic in families with fathers higher on depressive symptoms than in families in which mothers were higher, indicating the significant role of paternal support for firstborn children undergoing the transition to siblinghood. Maternal and paternal depression covaried with an accumulation of family risks over time, no doubt increasing the likelihood of children's problematic adjustment after the birth of their infant sibling.

Emerging literature suggests fathers may contribute uniquely to child development and emotional health through play. In the present study, a multiple mediational model was analyzed using data from 476 families that participated in the NICHD Study of Early Child Care and Youth Development. After accounting for infant–mother attachment, infant temperament, and family income and stability, a significant indirect effect from father–child play quality to adolescent internalizing symptoms was found through father-reported child emotional dysregulation, B = –.05, 95% confidence interval; CI [–.14, –.01]. Specifically, in first grade, dyads where fathers were rated highly on sensitivity and stimulation during play, and children demonstrated high felt security and affective mutuality during play, had children with fewer father-reported emotional dysregulation problems in third grade, B = –.23, 95% CI [–.39, –.06]. Children with fewer emotional dysregulation problems had lower self-reported internalizing symptoms at age 15, B = .23, 95% CI [.01, .45]. Mothers’ ratings of children's emotional dysregulation were not a significant mediator. Results are discussed regarding the importance of father–child play for children's adjustment as well as the usefulness of inclusion of fathers in child developmental research.

Research suggests that genetic variants linked to hypothalamic-pituitary-adrenal (HPA)-axis functioning moderate the association between environmental stressors and depression, but examining gene–environment interactions with single polymorphisms limits power. The current study used a multilocus genetic profile score (MGPS) approach to measuring HPA-axis–related genetic variation and examined interactions with acute stress, chronic stress, and childhood adversity (assessed using contextual threat interview methods) with depressive symptoms as outcomes in an adolescent sample (ages 14–17, N = 241; White subsample n = 192). Additive MGPSs were calculated using 10 single nucleotide polymorphisms within HPA-axis genes (CRHR1, NR3C2, NR3C1, FKBP5). Higher MGPS directly correlated with adolescent depressive symptoms. Moreover, MGPS predicted stronger associations between acute and chronic stress and adolescent depressive symptoms and also moderated the effect of interpersonal, but not noninterpersonal, childhood adversity. Gene–environment interactions individually accounted for 5%–8% of depressive symptom variation. All results were retained following multiple test correction and stratification by race. Results suggest that using MGPSs provides substantial power to examine gene–environmental interactions linked to affective outcomes among adolescents.

Growing research has documented distinct developmental sequelae in insecure and secure parent–child relationships, supporting a model of early attachment as moderating future developmental processes rather than, or in addition to, a source of direct effects. We explored maladaptive developmental implications of infants’ anger proneness in 102 community families. Anger was assessed in infancy through observations in the Car Seat episode and parents’ ratings. Children's security with parents was assessed in the Strange Situation paradigm at 15 months. At preschool age, child negativity (defiance and negative affect) was observed in interactions with the parent, and at early school age, oppositionality was rated by parents and teachers. Security was unrelated to infant anger; however, it moderated associations between infant anger and future maladaptive outcomes, such that highly angry infants embarked on a negative trajectory in insecure, but not in secure, parent–child dyads. For insecure, but not secure, mother–child dyads, infants’ mother-rated anger predicted negativity at preschool age. For insecure, but not secure, father–child dyads, infants’ anger in the Car Seat predicted father- and teacher-rated oppositional behavior at early school age. Results highlight the developmentally complex nature of the impact of attachment, depending on the relationship with mother versus father, type of measure, and timing of effects.

The aim of this study is to examine the role of repeated exposure to rocket attacks in the links between personality vulnerability (dependency and self-criticism) and internalizing/externalizing psychopathology. A main-effect vulnerability model (personality leads to psychopathology) was compared with a main-effect scarring model (psychopathology leads to personality vulnerability). Also, a stress-diathesis pattern (personality vulnerability is activated under stress) was compared to a dual-vulnerability pattern (either personality vulnerability or stress, but not both, lead to psychopathology). Israeli adolescents (N = 362) repeatedly exposed to rocket attacks were assessed annually over 3 years. In 2008 and 2010, personality and psychopathology were assessed. Cumulative exposure was measured as the sums of exposure across the three assessment waves. Theoretical models were tested via Autoregressive Cross-Lagged Structural Equation Modeling analyses. Baseline dependency and self-criticism were associated with an increase in anxiety, whereas baseline depression was associated with an increase in dependency. Under low, not high, levels of rocket exposure, self-criticism and depression were longitudinally associated. Violence commission was associated with an increase in dependency under high, not low, cumulative exposure. Results are consistent with both scarring and vulnerability models, and with both stress-diathesis and dual-vulnerability patterns of adolescent risk and resilience.

Using a family systems perspective, we examined the trajectories of father-child and mother-child closeness and conflict across Grades 1, 3, 4, 5, and 6, and their associations with child depressive symptoms across middle childhood among 685 families in the Eunice Kennedy Shriver National Institute of Child Health and Human Development Study of Early Child Care and Youth Development (SECCYD). Father-child and mother-child relationship conflict increased, whereas relationship closeness decreased from Grades 1 to 6. Girls with more slowly increasing father-child conflict, and more slowly decreasing father-child closeness, were at lower risk for depressive symptoms. Boys with more slowly increasing mother-child conflict were at lower risk for depressive symptoms. These findings highlight the important roles of both father-child and mother-child relationships in children's emotional adjustment during middle childhood.

The 5-HTTLPR polymorphism of the serotonin transporter has been shown to play a role in autism spectrum disorders (ASD). Moreover, disaster-related prenatal maternal stress (PNMS) has also been shown to be associated with ASD. However, no study to date has examined whether these two factors, either individually or in combination, are predictive of ASD traits in the same sample. We hypothesized that children, particularly boys, with the LL genotype exposed to high levels of disaster-related PNMS would exhibit higher levels of ASD traits compared to boys with the LS or SS genotypes and girls regardless of genotype. Genotype and ASD levels obtained using the Australian normed Autism Spectrum Rating Scales – Short Form were available for 105 30-month-old children exposed to varying levels of PNMS following the 2011 Queensland Flood. For boys, higher ASD traits were associated with the 5-HTTLPR LL genotype in combination with either a negative maternal appraisal of the flood, or high levels of maternal composite subjective stress, PSTD-like or peritraumatic dissociation symptoms. For girls, maternal peritraumatic dissociation levels in combination with the 5-HTTLPR LS or SS genotype were associated with higher ASD traits. The present findings are the first to demonstrate that children’s genotype moderates effects of disaster-related PNMS on ASD traits, with different pattern according to child sex.

Potential long-term associations between repetitive negative thinking and mother-infant interactions have received little attention. The current longitudinal study including N = 62 mother-infant dyads investigated both maternal and infant behavior in face-to-face interactions as a function of pre- and postnatal maternal repetitive negative thinking when infants were aged around 4 months. We hypothesised that mothers with a strong tendency to engage in repetitive negative thinking would react less contingently to their infants’ behavior compared to mothers with a weak tendency to engage in repetitive negative thinking. Furthermore, we hypothesised that infants of mothers high in repetitive negative thinking would differ from infants of mothers low in repetitive negative thinking in their reactions in the still-face task. Contrary to expectations, there was no difference in maternal contingency between mothers high versus low in repetitive negative thinking. However, infant behavior in the still-face task differed as a function of maternal repetitive negative thinking status. Specifically, infants of mothers high in repetitive negative thinking spent more time with object/environment engagement than infants of mothers who were low in repetitive negative thinking, and they also protested less frequently. These findings are discussed in terms of their relevance for the intergenerational transmission of mental disorders.

Young sexual minority men (YSMM) experience more victimization and are at higher risk for mental health and substance use problems compared with heterosexual youth. We attempt to understand change over time in the experience of these constructs among YSMM. Data were taken from a diverse community-based sample of YSMM (N = 450, baseline mean age 18.93) surveyed every 6 months for 2.5 years. Multilevel modeling was used to model within-person change in victimization, internalizing symptoms, externalizing symptoms, alcohol frequency, marijuana use, and illicit drug use. We tested the indirect effect of concurrent and time-lagged victimization on the association between age and mental health and substance use. Victimization, internalizing symptoms, and externalizing symptoms decreased over time. Concurrent victimization was associated with higher internalizing symptoms, externalizing symptoms, alcohol use, marijuana use, and illicit drug use. Analysis of indirect effects suggested that the association between victimization and mental health and substance use outcomes decreased as participants transitioned from adolescence into adulthood. This study found that the reduction in victimization that YSMM experience as they grow older is associated with a reduction in negative mental health and substance use outcomes. Prevention efforts to limit victimization exposure may reduce health disparities for YSMM.

Childhood adversity can negatively impact development across various domains, including physical and mental health. Adverse childhood experiences have been linked to aggression and substance use; however, developmental pathways to explain these associations are not well characterized. Understanding early precursors to later problem behavior and substance use can inform preventive interventions. The aim of the current study was to examine neurobiological pathways through which childhood adversity may lead to early adolescent problem behavior and substance use in late adolescence by testing two prospective models. Our first model found that early adolescent externalizing behavior mediates the association between childhood adversity and alcohol, cigarette, and marijuana use in late adolescence. Our second model found that activation in the anterior cingulate cortex (ACC) during an inhibitory control task mediates the association between childhood adversity and early adolescent externalizing behavior, with lower ACC activation associated with higher levels of adversity and more externalizing behavior. Together these findings indicate that the path to substance use in late adolescence from childhood adversity may operate through lower functioning in the ACC related to inhibitory control and externalizing behavior. Early life stressors should be considered an integral component in the etiology and prevention of early and problematic substance use.

Previous research has shown that problematic parent–child, peer, and romantic partner relationships are associated with an increased likelihood for major depressive disorder (MDD). Less research has evaluated the developmental unfolding of how these interpersonal relationship features are both an antecedent versus a consequence of MDD symptoms from adolescence through young adulthood. These gaps were evaluated using a large community sample (N = 1,127; 54% female, 96% white) via a developmental cascade model. Results showed support for significant antecedent effects, as greater parent–child relationship problems at ages 11 and 17 predicted rank-order increases in MDD symptoms at ages 14 and 20. Supporting a developmental cascade of problematic social relationships, greater parent–child relationship problems at ages 11 and 14 also predicted greater subsequent rank-order increases in antisocial peer affiliation at ages 14 and 17. Greater affiliation to antisocial peers at age 20 predicted greater rank-order increases in romantic relationship problems at age 24, which in turn predicted greater MDD symptoms at age 29. Cross-effects were generally small (βs ≤ .16), illustrating other factors may be relevant to the development or consequences of MDD. Nonetheless, findings support the importance of efforts to strengthen social support networks to offset risk as well as potentially treat depression.

Bullying has been understudied among preschool children, especially those from Chinese American families. Previous research has also neglected the dimensional effects of psychological control on child bullying development. This study examined two psychological control dimensions, love withdrawal and guilt induction, and their effects on children's bullying aggressive behavior using a longitudinal design. Participants were first-generation Chinese American mothers (N = 133; mean age [Mage] = 37.82) and their preschool children (Mage = 4.48). Chinese immigrant mothers reported their psychologically controlling parenting and teachers rated children's bullying aggressive behaviors in the school setting. Confirmatory factor analyses were conducted to establish the psychometric properties and cross-wave measurement equivalence of the study constructs. Cross-lagged structural equation modeling analysis indicated that maternal love withdrawal prospectively predicted more bullying aggressive behavior, whereas guilt induction predicted less bullying aggressive behavior in children 6 months later. These results held after controlling for the initial level of children's problem behaviors and demographic variables (child age, gender, and maternal education). For child effects, child bullying aggressive behavior predicted more maternal guilt induction over time but not love withdrawal. Our findings highlight the importance of construct specificity and cultural context in understanding associations between parenting and child development.