Internationally adopted postinstitutionalized (PI) children are at risk for lower levels of emotion understanding. This study examined how postadoption parenting influences emotion understanding and whether lower levels of emotion understanding are associated with behavior problems. Emotion understanding and parent mental state language were assessed in 3-year-old internationally adopted PI children (N = 25), and comparison groups of children internationally adopted from foster care (N = 25) and nonadopted (NA) children (N = 36). At 5.5-year follow-up, PI children had lower levels of emotion understanding than NA children, a group difference not explained by language. In the total sample, parent mental state language at age 3 years predicted 5.5-year emotion understanding after controlling for child language ability. The association of parent mental state language and 5.5-year emotion understanding was moderated by adoption status, such that parent mental state language predicted 5.5-year emotion understanding for the internationally adopted children, but not for the NA children. While postadoption experience does not erase negative effects of early deprivation on emotion understanding, results suggest that parents can promote emotion understanding development through mental state talk. At 5.5 years, PI children had more internalizing and externalizing problems than NA children, and these behavioral problems related to lower levels of emotion understanding.

Studies in rodents, nonhuman primates, and humans suggest that epigenetic processes mediate between early life experiences and adult phenotype. However, the normal evolution of epigenetic programs during child development, the effect of sex, and the impact of early life adversity on these trajectories are not well understood. This study mapped the genome-wide DNA methylation changes in CD3+ T lymphocytes from rhesus monkeys from postnatal day 14 through 2 years of age in both males and females and determined the impact of maternal deprivation on the DNA methylation profile. We show here that DNA methylation profiles evolve from birth to adolescence and are sex dependent. DNA methylation changes accompany imposed weaning, attenuating the difference between males and females. Maternal separation at birth alters the normal evolution of DNA methylation profiles and targets genes that are also affected by a later stage maternal separation, that is, weaning. Our results suggest that early life events dynamically interfere with the normal developmental evolution of the DNA methylation profile and that these changes are highly effected by sex.

This prospective longitudinal study examines the long-term influence of intimate partner violence (IPV) exposure in utero. We hypothesized that (a) prenatal IPV increases risk for internalizing and externalizing problems as well as for a profile of dysregulated cortisol reactivity, and (b) patterns of cortisol hyper- and hyporeactivity are differentially associated with internalizing and externalizing problems. The participants were 119 10-year-old children. Their mothers reported their IPV experiences and distress during pregnancy. Child and maternal reports of internalizing and externalizing problems as well as lifetime IPV exposure were obtained. Salivary cortisol was assessed at baseline, 20 min, and 40 min after challenge. The results partially supported our hypotheses: Exposure to IPV during pregnancy predicted child-reported internalizing and externalizing problems, mother ratings of child externalizing problems, and a profile of high cortisol secretion before and after stress challenge. The results were significant above and beyond the influence of maternal distress during pregnancy and IPV that occurred during the child's life. In addition, a profile of high cortisol secretion was associated with maternal reports of child internalizing behaviors. Findings support the growing consensus that prenatal stress can lead to lasting disruptions in adaptation and highlight the need for more longitudinal examinations of prenatal IPV exposure.

Transactional cascades among child internalizing and externalizing symptoms, and fathers’ and mothers’ posttraumatic stress disorder (PTSD) symptoms were examined in a sample of families with a male parent who had been deployed to recent military conflicts in the Middle East. The role of parents’ positive engagement and coercive interaction with their child, and family members’ emotion regulation were tested as processes linking cascades of parent and child symptoms. A subsample of 183 families with deployed fathers and nondeployed mothers and their 4- to 13-year-old children who participated in a randomized control trial intervention (After Deployment: Adaptive Parenting Tools) were assessed at baseline prior to intervention, and at 12 and 24 months after baseline, using parent reports of their own and their child's symptoms. Parents’ observed behavior during interaction with their children was coded using a multimethod approach at each assessment point. Reciprocal cascades among fathers’ and mothers’ PTSD symptoms, and child internalizing and externalizing symptoms, were observed. Fathers’ and mothers’ positive engagement during parent–child interaction linked their PTSD symptoms and their child's internalizing symptoms. Fathers’ and mothers’ coercive behavior toward their child linked their PTSD symptoms and their child's externalizing symptoms. Each family member's capacity for emotion regulation was associated with his or her adjustment problems at baseline. Implications for intervention, and for research using longitudinal models and a family-systems perspective of co-occurrence and cascades of symptoms across family members are described.

Deviance proneness models propose a multilevel interplay in which transactions among genetic, individual, and family risk factors place children at increased risk for substance use. We examined bidirectional transactions between impulsivity and family conflict from middle childhood to adolescence and their contributions to substance use in adolescence and emerging adulthood (n = 380). Moreover, we examined children's, mothers’, and fathers’ polygenic risk scores for behavioral undercontrol, and mothers’ and fathers’ interparental conflict and substance disorder diagnoses as predictors of these transactions. The results support a developmental cascade model in which children's polygenic risk scores predicted greater impulsivity in middle childhood. Impulsivity in middle childhood predicted greater family conflict in late childhood, which in turn predicted greater impulsivity in late adolescence. Adolescent impulsivity subsequently predicted greater substance use in emerging adulthood. Results are discussed with respect to evocative genotype–environment correlations within developmental cascades and applications to prevention efforts.

We propose a novel developmentally informed framework to push research beyond a focus on comorbidity between discrete diagnostic categories and to move toward research based on the well-validated dimensional and hierarchical structure of psychopathology. For example, a large body of research speaks to the validity and utility of the internalizing and externalizing spectra as organizing constructs for research on common forms of psychopathology. The internalizing and externalizing spectra act as powerful explanatory variables that channel the psychopathological effects of genetic and environmental risk factors, predict adaptive functioning, and account for the likelihood of disorder-level manifestations of psychopathology. As such, our proposed theoretical framework uses the internalizing and externalizing spectra as central constructs to guide future psychopathology research across the life span. The framework is particularly flexible, because any of the facets or factors from the dimensional and hierarchical structure of psychopathology can form the focus of research. We describe the utility and strengths of this framework for developmental psychopathology in particular and explore avenues for future research.

Accumulating evidence suggests that the experience of early life adversity is a risk factor for a range of poor outcomes across development, including poor physical health in adulthood. The biological embedding model of early adversity (Miller, Chen, & Parker, 2011) suggests that early adversity might become embedded within immune cells known as monocytes/macrophages, programming them to be overly aggressive to environmental stimuli and insensitive to inhibitory signals, creating a “proinflammatory phenotype” that increases vulnerability to chronic diseases across the life span. We tested this hypothesis in the present study. Adolescent girls (n = 147) had blood drawn every 6 months across a 2.5-year period. To assess inflammatory responses to challenge, their monocytes were stimulated in vitro with a bacterial product, and production of the cytokine interleukin-6 was quantified. Hydrocortisone was added to cultures to assess the cells’ sensitivity to glucocorticoids’ anti-inflammatory signal. Using cluster analyses, we found that early life adversity was associated with greater odds of displaying a proinflammatory phenotype characterized by relatively larger interleukin-6 responses and relatively less sensitivity to glucocorticoids. In contrast, ongoing social stress was not associated with increasing odds of being categorized in the proinflammatory cluster. These findings suggest that early life adversity increases the probability of developing a proinflammatory phenotype, which, if sustained, could forecast risk for health problems later in life.

This report uses 6-year outcomes of the Oregon Divorce Study to examine the processes by which parenting practices affect deviant peer association during two developmental stages: early to middle childhood and late childhood to early adolescence. The participants were 238 newly divorced mothers and their 5- to 8-year-old sons who were randomly assigned to Parent Management Training—Oregon Model (PMTO®) or to a no-treatment control group. Parenting practices, child delinquent behavior, and deviant peer association were repeatedly assessed from baseline to 6 years after baseline using multiple methods and informants. PMTO had a beneficial effect on parenting practices relative to the control group. Two stage models linking changes in parenting generated by PMTO to children's growth in deviant peer association were supported. During the early to middle childhood stage, the relationship of improved parenting practices on deviant peer association was moderated by family socioeconomic status (SES); effective parenting was particularly important in mitigating deviant peer association for lower SES families whose children experience higher densities of deviant peers in schools and neighborhoods. During late childhood and early adolescence, the relationship of improved parenting to youths' growth in deviant peer association was mediated by reductions in the growth of delinquency during childhood; higher levels of early delinquency are likely to promote deviant peer association through processes of selective affiliation and reciprocal deviancy training. The results are discussed in terms of multilevel developmental progressions of diminished parenting, child involvement in deviancy producing processes in peer groups, and increased variety and severity of antisocial behavior, all exacerbated by ecological risks associated with low family SES.

Children entering out-of-home (OoH) care have often experienced multiple forms of maltreatment and are at risk of psychiatric disorder and poor long-term outcome. Recent evidence shows high rates of disinhibited attachment disorder (DAD) among maltreated adolescents in UK OoH care (Kay & Green, 2013). This study aimed to further understand the mechanisms of outcome in this group through investigation of social cognitive functioning. Patterns of theory of mind (ToM) and social information processing were assessed alongside DAD behavior and psychopathology in 63 adolescents in UK OoH care (mean age = 176 months, SD = 22; 48% male; 89% White British) and 69 low-risk comparison adolescents (mean age = 171 months, SD = 17; 46% male; 87% White British). Compared to low risk, OoH adolescents showed a hostile attribution bias and ToM deficit, but this was confounded by language ability. ToM was associated with reduced hostile attribution and responding biases and increased social competence, which was further associated with lower levels of externalizing psychopathology. There was no association between social cognition and core features of DAD. Social cognitive deficits and biases may play a role in the high rates of externalizing psychopathology and relationship functioning difficulties in maltreated samples. Future research should assess alternative cognitive mechanisms for DAD.

Information-processing biases may contribute to the intergenerational transmission of depression. There is growing evidence that children of depressed mothers exhibit attentional biases for sad faces. However, findings are mixed as to whether this bias reflects preferential attention toward, versus attentional avoidance of, sad faces, suggesting the presence of unmeasured moderators. To address these mixed findings, we focused on the potential moderating role of genes associated with hypothalamic–pituitary–adrenal axis reactivity. Participants included children (8–14 years old) of mothers with (n = 81) and without (n = 81) a history of depression. Eye movements were recorded while children passively viewed arrays of angry, happy, sad, and neutral faces. DNA was obtained from buccal cells. Children of depressed mothers exhibited more sustained attention to sad faces than did children of nondepressed mothers. However, it is important that this relation was moderated by children's genotype. Specifically, children of depressed mothers who carried reactive genotypes across the corticotropin-releasing hormone type 1 receptor (CHRH1) TAT haplotype and FK506 binding protein 5 (FKBP5) rs1360780 (but not the solute carrier family C6 member 4 [SLC6A4] of the serotonin transporter linked polymorphic region [5-HTTLPR]) exhibited less sustained attention to sad faces and more sustained attention to happy faces. These findings highlight the role played by specific genetic influences and suggest that previous mixed findings may have been due to genetic heterogeneity across the samples.

This study tested a transactional hypothesis predicting early adult sexual coercion from family maltreatment, early adolescent gang affiliation, and socialization of adolescent friendships that support coercive relationship norms. The longitudinal study of a community sample of 998 11-year-olds was intensively assessed in early and middle adolescence and followed to 23–24 years of age. At age 16–17 youth were videotaped with a friend, and their interactions were coded for coercive relationship talk. Structural equation modeling revealed that maltreatment predicted gang affiliation during early adolescence. Both maltreatment and gang affiliation strongly predicted adolescent sexual promiscuity and coercive relationship norms with friends at age 16–17 years. Adolescent sexual promiscuity, however, did not predict sexual coercion in early adulthood. In contrast, higher levels of observed coercive relationship talk with a friend predicted sexual coercion in early adulthood for both males and females. These findings suggest that peers have a socialization function in the development of norms prognostic of sexual coercion, and the need to consider peers in the promotion of healthy relationships.

Affective family processes are associated with the development of depression during adolescence. However, empirical description of these processes is generally based on examining affect at the individual or dyadic level. The purpose of this study was to examine triadic patterns of affect during parent–adolescent interactions in families with or without a depressed adolescent. We used state space grid analysis to characterize the state of all three actors simultaneously. Compared to healthy controls, triads with depressed adolescents displayed a wider range of affect, demonstrated less predictability of triadic affective sequences, spent more time in and returned more quickly to discrepant affective states, and spent less time in and returned more slowly to matched affective states, particularly while engaged in a problem-solving interaction. Furthermore, we identified seven unique triadic states in which triads with depressed adolescents spent significantly more time than triads with healthy controls. The present study enhances understanding of family affective processes related to depression by taking a more systemic approach and revealing triadic patterns that go beyond individual and dyadic analyses.

The last decade has been marked by an increased interest in relating epigenetic mechanisms to complex human behaviors, although this interest has not been balanced, accentuating various types of affective and primarily ignoring cognitive functioning. Recent animal model data support the view that epigenetic processes play a role in learning and memory consolidation and help transmit acquired memories even across generations. In this review, we provide an overview of various types of epigenetic mechanisms in the brain (DNA methylation, histone modification, and noncoding RNA action) and discuss their impact proximally on gene transcription, protein synthesis, and synaptic plasticity and distally on learning, memory, and other cognitive functions. Of particular importance are observations that neuronal activation regulates the dynamics of the epigenome's functioning under precise timing, with subsequent alterations in the gene expression profile. In turn, epigenetic regulation impacts neuronal action, closing the circle and substantiating the signaling pathways that underlie, at least partially, learning, memory, and other cognitive processes.

It is well known that comorbidity is the rule, not the exception, for categorically defined psychiatric disorders, and this is also the case for internalizing disorders of depression and anxiety. This theoretical review paper addresses the ubiquity of comorbidity among internalizing disorders. Our central thesis is that progress in understanding this co-occurrence can be made by employing latent dimensional structural models that organize psychopathology as well as vulnerabilities and risk mechanisms and by connecting the multiple levels of risk and psychopathology outcomes together. Different vulnerabilities and risk mechanisms are hypothesized to predict different levels of the structural model of psychopathology. We review the present state of knowledge based on concurrent and developmental sequential comorbidity patterns among common discrete psychiatric disorders in youth, and then we advocate for the use of more recent bifactor dimensional models of psychopathology (e.g., p factor; Caspi et al., 2014) that can help to explain the co-occurrence among internalizing symptoms. In support of this relatively novel conceptual perspective, we review six exemplar vulnerabilities and risk mechanisms, including executive function, information processing biases, cognitive vulnerabilities, positive and negative affectivity aspects of temperament, and autonomic dysregulation, along with the developmental occurrence of stressors in different domains, to show how these vulnerabilities can predict the general latent psychopathology factor, a unique latent internalizing dimension, as well as specific symptom syndrome manifestations.

This study examined trajectories of aggression and rule breaking during the transition from childhood to adolescence (ages 9–15), and determined whether these trajectories were predicted by lower order personality facets, overreactive parenting, and their interaction. At three time points separated by 2-year intervals, mothers and fathers reported on their children's aggression and rule breaking (N = 290, M age = 8.8 years at Time 1). At Time 1, parents reported on their children's personality traits and their own overreactivity. Growth mixture modeling identified three aggression trajectories (low decreasing, high decreasing, and high increasing) and two rule-breaking trajectories (low and high). Lower optimism and compliance and higher energy predicted trajectories for both aggression and rule breaking, whereas higher expressiveness and irritability and lower orderliness and perseverance were unique risk factors for increasing aggression into adolescence. Lower concentration was a unique risk factor for increasing rule breaking. Parental overreactivity predicted higher trajectories of aggression but not rule breaking. Only two Trait × Overreactivity interactions were found. Our results indicate that personality facets could differentiate children at risk for different developmental trajectories of aggression and rule breaking.

Stress has been shown to have a causal effect on risk for depression. We investigated the role of cognitive ability as a moderator of the effect of stressful life events on depressive symptoms and whether this varied by gender. Data were analyzed in two adolescent data sets: one representative community sample aged 11–12 years (n = 460) and one at increased familial risk of depression aged 9–17 years (n = 335). In both data sets, a three-way interaction was found whereby for girls, but not boys, higher cognitive ability buffered the association between stress and greater depressive symptoms. The interaction was replicated when the outcome was a diagnosis of major depressive disorder. This buffering effect in girls was not attributable to coping efficacy. However, a small proportion of the variance was accounted for by sensitivity to environmental stressors. Results suggest that this moderating effect of cognitive ability in girls is largely attributable to greater available resources for cognitive operations that offer protection against stress-induced reductions in cognitive processing and cognitive control which in turn reduces the likelihood of depressive symptomatology.

In the present investigation, differential methylation analyses of the whole genome were conducted among a sample of 548 school-aged low-income children (47.8% female, 67.7% Black, M age = 9.40 years), 54.4% of whom had a history of child maltreatment. In the context of a summer research camp, DNA samples via saliva were obtained. Using GenomeStudio, Methylation Module, and the Illumina Custom Model, differential methylation analyses revealed a pattern of greater methylation at low methylation sites (n = 197 sites) and medium methylation sites (n = 730 sites) and less methylation at high methylation sites (n = 907 sites) among maltreated children. The mean difference in methylation between the maltreated and nonmaltreated children was 6.2%. The relative risk of maltreatment with known disease biomarkers was also investigated using GenoGo MetaCore Software. A large number of network objects previously associated with mental health, cancer, cardiovascular systems, and immune functioning were identified evidencing differential methylation among maltreated and nonmaltreated children. Site-specific analyses were also conducted for aldehyde dehydrogenase 2 (ALDH2), ankyrin repeat and kinase domain containing 1 (ANKK1), and nuclear receptor subfamily 3, group C, member 1 (NR3C1) genes, and the results highlight the importance of considering gender and the developmental timing of maltreatment. For ALDH2, the results indicated that maltreated girls evidenced significantly lower methylation compared to nonmaltreated girls, and maltreated boys evidenced significantly higher methylation compared to nonmaltreated boys. Moreover, early onset–not recently maltreated boys evidenced significantly higher methylation at ALDH2 compared to nonmaltreated boys. Similarly, children with early onset–nonrecent maltreatment evidenced significantly higher methylation compared to nonmaltreated children at ANKK1. The site-specific results were not altered by controlling for genotypic variation of respective genes. The findings demonstrate increased risk for adverse physical and mental health outcomes associated with differences in methylation in maltreated children and indicate differences among maltreated children related to developmental timing of maltreatment and gender in genes involved in mental health functioning.

This study examines the interplay between individual and social–developmental factors in the development of positive functioning, substance use problems, and mental health problems. This interplay is nested within positive and negative developmental cascades that span childhood, adolescence, the transition to adulthood, and adulthood. Data are drawn from the Seattle Social Development Project, a gender-balanced, ethnically diverse community sample of 808 participants interviewed 12 times from ages 10 to 33. Path modeling showed short- and long-term cascading effects of positive social environments, family history of depression, and substance-using social environments throughout development. Positive family social environments set a template for future partner social environment interaction and had positive influences on proximal individual functioning, both in the next developmental period and long term. Family history of depression adversely affected mental health functioning throughout adulthood. Family substance use began a cascade of substance-specific social environments across development, which was the pathway through which increasing severity of substance use problems flowed. The model also indicated that adolescent, but not adult, individual functioning influenced selection into positive social environments, and significant cross-domain effects were found in which substance-using social environments affected subsequent mental health.

This study investigated the influences of neighborhood factors (residential stability and neighborhood disadvantage) and variants of the serotonin transporter linked polymorphic region (5-HTTLPR) genotype on the development of substance use among African American children aged 10–24 years. To accomplish this, a harmonized data set of five longitudinal studies was created via pooling overlapping age cohorts to establish a database with 2,689 children and 12,474 data points to span ages 10–24 years. A description of steps used in the development of the harmonized data set is provided, including how issues such as the measurement equivalence of constructs were addressed. A sequence of multilevel models was specified to evaluate Gene × Environment effects on growth of substance use across time. Findings indicated that residential instability was associated with higher levels and a steeper gradient of growth in substance use across time. The inclusion of the 5-HTTLPR genotype provided greater precision to the relationships in that higher residential instability, in conjunction with the risk variant of 5-HTTLPR (i.e., the short allele), was associated with the highest level and steepest gradient of growth in substance use across ages 10–24 years. The findings demonstrated how the creation of a harmonized data set increased statistical power to test Gene × Environment interactions for an under studied sample.

Using a sample of 228 females with and without childhood attention-deficit/hyperactivity disorder followed prospectively across 16 years, we measured childhood neurocognitive vulnerability via executive dysfunction using teacher-reported cognitive and learning problems. We then ascertained relations between dimensionally measured internalizing and externalizing psychopathology during adulthood and showed that childhood neurocognitive vulnerability reliably predicted such associated psychopathology. We identified six serial mediation pathways from childhood neurocognitive vulnerability to adult psychopathology through three early- and late-adolescent domains: individual (self-control and delay of gratification), peer (rejection/conflict and acceptance/friendship), and school (academic performance and school failure). The serial indirect effects occurred for the pathways from childhood neurocognitive vulnerability through early-adolescent academic performance, to late-adolescent school failure, to adult associated psychopathology, and from neurocognitive vulnerability through adolescent self-control and then the ability to delay gratification, to adult psychopathology. Furthermore, these indirect effects, plus two others, were moderated by parental distress during childhood and early adolescence, such that under conditions of high distress, the serial indirect effects were weaker than when parental distress was low. We discuss the potential importance of behavioral self-regulation and educational success for later psychological functioning, especially among girls, as well as implications for ontogenic process models of psychopathology.