Disorganized attachment is associated with a host of negative developmental outcomes, leading to a growing interest in preventative interventions targeting the attachment relationship in infancy. The objective of this meta-analysis was to assess the effectiveness of interventions that aimed to prevent or reduce rates of disorganization among children at risk. We performed a literature search using PsycINFO, MEDLINE, and ProQuest databases for studies published between January 1989 and August 2016. All 16 studies (N = 1,360) included a control condition and reported postintervention rates of organized and disorganized attachments assessed by the Strange Situation Procedure. Results showed that, overall, interventions were effective in increasing rates of organized attachment compared to control conditions (d = 0.35, 95% CI [0.10–0.61]). Moderator analyses demonstrated that interventions were more effective (a) in more recently published studies than in older studies, (b) for maltreated samples than nonmaltreated samples, and (c) as children increased in age. These results have important implications for future development, tailoring, and implementation of attachment-based intervention programs.

Although behavioral and experimental studies have shown links between victimization and antisocial behavior, the neural correlates explaining this link are relatively unknown. In the current study, we recruited adolescent girls from a longitudinal study that tracked youths’ reports of peer victimization experiences annually from the second through eighth grades. Based on these reports, 46 adolescents were recruited: 25 chronically victimized and 21 nonvictimized. During a functional magnetic resonance imaging scan, participants completed a risk-taking task. Chronic peer victimization was associated with greater risk-taking behavior during the task and higher levels of self-reported antisocial behavior in everyday life. At the neural level, chronically victimized girls showed greater activation in regions involved in affective sensitivity, social cognition, and cognitive control, which significantly mediated victimization group differences in self-reported antisocial behavior.

Maternal depression negatively impacts children's development, yet few studies have focused on fathering and the family process in cases of maternal depression. A community cohort of married/cohabitating women was recruited on the second postbirth day (N = 1,983) and maternal depression repeatedly assessed across the first year and again at 6 years to form two cohorts: mothers chronically depressed from birth to 6 (N = 46) and nondepressed controls (N = 103). At 6 years, mother–child, father–child, and family interactions were observed. In families of depressed mothers, both mother and father exhibited lower sensitivity and higher intrusiveness, and children displayed lower social engagement during interactions with mother and father. Fathering moderated the effects of maternal depression on the family process. When fathers showed low sensitivity, high intrusiveness, and provided little opportunities for child social engagement, the family process was less cohesive, implying a decrease in the family's harmonious, warm, and collaborative style. However, in cases of high father sensitivity, low intrusiveness, and increased child engagement, the family process was unaffected by maternal depression. Findings describe both comparability and compensatory mechanisms in the effects of fathering on family life when maternal care is deficient, highlight the buffering role of fathers, and underscore the importance of father-focused interventions when mothers are depressed.

The developmental course of daily functioning prior to first psychosis-onset remains poorly understood. This study explored age-related periods of change in social and role functioning. The longitudinal study included youth (aged 12–23, mean follow-up years = 1.19) at clinical high risk (CHR) for psychosis (converters [CHR-C], n = 83; nonconverters [CHR-NC], n = 275) and a healthy control group (n = 164). Mixed-model analyses were performed to determine age-related differences in social and role functioning. We limited our analyses to functioning before psychosis conversion; thus, data of CHR-C participants gathered after psychosis onset were excluded. In controls, social and role functioning improved over time. From at least age 12, functioning in CHR was poorer than in controls, and this lag persisted over time. Between ages 15 and 18, social functioning in CHR-C stagnated and diverged from that of CHR-NC, who continued to improve (p = .001). Subsequently, CHR-C lagged behind in improvement between ages 21 and 23, further distinguishing them from CHR-NC (p < .001). A similar period of stagnation was apparent for role functioning, but to a lesser extent (p = .007). The results remained consistent when we accounted for the time to conversion. Our findings suggest that CHR-C start lagging behind CHR-NC in social and role functioning in adolescence, followed by a period of further stagnation in adulthood.

Although borderline personality disorder (BPD) traits decline from adolescence to adulthood, comorbid psychopathology such as symptoms of major depressive disorder (MDD), alcohol use disorder (AUD), and drug use disorders (DUDs) likely disrupt this normative decline. Using a longitudinal sample of female twins (N = 1,763), we examined if levels of BPD traits were correlated with changes in MDD, AUD, and DUD symptoms from ages 14 to 24. A parallel process biometric latent growth model examined the contributions of genetic and environmental factors to the relationships between developmental components of these phenotypes. Higher BPD trait levels predicted a greater rate of increase in AUD and DUD symptoms, and higher AUD and DUD symptoms predicted a slower rate of decline of BPD traits from ages 14 to 24. Common genetic influences accounted for the associations between BPD traits and each disorder, as well as the interrelationships of AUD and DUD symptoms. Both genetic and nonshared environmental influences accounted for the correlated levels between BPD traits and MDD symptoms, but solely environmental influences accounted for the correlated changes between the two over time. Results indicate that higher levels of BPD traits may contribute to an earlier onset and faster escalation of AUD and DUD symptoms, and substance use problems slow the normative decline in BPD traits. Overall, our data suggests that primarily genetic influences contribute to the comorbidity between BPD features and substance use disorder symptoms. We discuss our data in the context of two major theories of developmental psychopathology and comorbidity.

The role of environmental adversity in the development of high callous–unemotional (CU) traits in children is controversial. Evidence speaks to the traits being largely independent of adversity; however, recent data shows that those with high CU traits and high adversity and/or high anxiety might differ in important ways from those with no such history. We tested this using emotion recognition (ER) skills. We tested whether maltreatment history and anxiety levels moderated the relationship between level of CU traits and ER skills in N = 364 children with behavioral problems who were 3 to 16 years old. As hypothesised, in the full sample, the relationship between CU traits and ER differed according to maltreatment history, such that CU traits were associated with poorer recognition for those with zero or negligible history of maltreatment. This moderation of the CU-ER relationship by maltreatment was inconsistent across subgroups, however, and for the cohort utilizing youth self-report of maltreatment, high CU traits were associated with poor ER in those with lower anxiety levels. Maltreatment history and/or anxiety levels can identify different emotional impairments associated with high CU traits, and the impairments might be characteristic of “primary” high CU traits defined as occurring independently of maltreatment and/or high anxiety.

Early maturation, indexed by pubertal development (PD), has been associated with earlier initiation and greater frequency of adolescent substance use, but this relationship may be biased by confounding factors and effects that change across development. Using a population-based Finnish twin sample (N = 3,632 individuals), we conducted twin modeling and multilevel structural equation modeling of the relationship between PD and substance use at ages 12–22. Shared environmental factors contributed to early PD and heavier substance use for females. Biological father absence was associated with early PD for boys but not girls, and did not account for the relationship between PD and substance use. The association between early PD and heavier substance use was partially due to between-family confounds, although early PD appeared to qualitatively alter long-term trajectories for some substances (nicotine), but not others (alcohol). Mediation by peer and parental factors did not explain this relationship within families. However, higher peer substance use and lower parental monitoring were themselves associated with heavier substance use, strengthening the existing evidence for these factors as targets for prevention/intervention efforts. Early maturation was not supported as a robust determinant of alcohol use trajectories in adolescence and young adulthood, but may require longer term follow-up. Subtle effects of early PD on nicotine and illicit drug use trajectories throughout adolescence and adulthood merit further investigation.

In a randomized controlled trial, the Observational Randomized Controlled Trial of Childhood Differential Susceptibility (ORCHIDS study), we tested whether observed parental affect and observed and reported parenting behavior are mechanisms of change underlying the effects of the behavioral parent training program the Incredible Years (IY). Furthermore, we tested whether some children are more susceptible to these change mechanisms because of their temperamental negative affectivity and/or serotonin transporter linked polymorphic region (5-HTTLPR) genotype. Participants were 387 Dutch children between 4 and 8 years of age (M age = 6.31, SD = 1.33; 55.3% boys) and their parents. Results showed that although IY was successful in improving parenting behavior and increasing parental positive affect, these effects did not explain the significant decreases in child externalizing problems. We therefore found no evidence for changes in parenting behavior or parental affect being the putative mechanisms of IY effectiveness. Furthermore, intervention effects on child externalizing behavior were not moderated by child negative affectivity or 5-HTTLPR genotype. However, child 5-HTTLPR genotype did moderate intervention effects on negative parenting behavior. This suggests that in research on behavioral parent training programs, “what works for which parents” might also be an important question.

While the trajectory of self-esteem from adolescence to adulthood varies from person to person, little research has examined how differences in early developmental processes might affect these pathways. This study examined how early motor skill development interacted with preterm birth status to predict self-esteem from adolescence through the early 30s. We addressed this using the oldest known, prospectively followed cohort of extremely low birth weight (<1000 g) survivors (N = 179) and normal birth weight controls (N = 145) in the world, born between 1977 and 1982. Motor skills were measured using a performance-based assessment at age 8 and a retrospective self-report, and self-esteem was reported during three follow-up periods (age 12–16, age 22–26, and age 29–36). We found that birth weight status moderated the association between early motor skills and self-esteem. Stable over three decades, the self-esteem of normal birth weight participants was sensitive to early motor skills such that those with poorer motor functioning manifested lower self-esteem, while those with better motor skills manifested higher self-esteem. Conversely, differences in motor skill development did not affect the self-esteem from adolescence to adulthood in individuals born at extremely low birth weight. Early motor skill development may exert differential effects on self-esteem, depending on whether one is born at term or prematurely.

The error-related negativity (ERN) is a negative deflection in the event-related potential occurring when individuals make mistakes, and is increased in children with internalizing psychopathology. We recently found that harsh parenting predicts a larger ERN in children, and recent work has suggested that variation in the brain-derived neurotrophic factor (BDNF) gene may moderate the impact of early life adversity. Parents and children completed measures of parenting when children were 3 years old (N = 201); 3 years later, the ERN was measured and diagnostic interviews as well as dimensional symptom measures were completed. We found that harsh parenting predicted an increased ERN only among children with a methionine allele of the BDNF genotype, and evidence of moderated mediation: the ERN mediated the relationship between parenting and internalizing diagnoses and dimensional symptoms only if children had a methionine allele. We tested this model with externalizing disorders, and found that harsh parenting predicted externalizing outcomes, but the ERN did not mediate this association. These findings suggest that harsh parenting predicts both externalizing and internalizing outcomes in children; however, this occurs through different pathways that uniquely implicate error-related brain activity in the development of internalizing disorders.

Liability to substance use disorder (SUD) is largely nonspecific to particular drugs and is related to behavior dysregulation, including reduced cognitive control. Recent data suggest that cognitive mechanisms may be influenced by exposure to neurotropic infections, such as human herpesviruses. In this study, serological evidence of exposure to human herpesvirus Herpes simplex virus Type 1 (HSV-1), cytomegalovirus (CMV), and Epstein–Barr virus (EBV) as well as Toxoplasma gondii was determined in childhood (age ~11 years) in 395 sons and 174 daughters of fathers with or without SUD. Its relationships with a cognitive characteristic (IQ) in childhood and with risk for SUD in adulthood were examined using correlation, regression, survival, and path analyses. Exposure to HSV-1, EBV, and T. gondii in males and females, and CMV in males, was associated with lower IQ. Independent of that relationship, EBV in females and possibly in males, and CMV and possibly HSV-1 in females were associated with elevated risk for SUD. Therefore, childhood neurotropic infections may influence cognitive development and risk for behavior disorders such as SUD. The results may point to new avenues for alleviating cognitive impairment and SUD risk.

Growing evidence from developmental psychology and social neuroscience emphasizes the importance of third-party harm aversion for constructing morality. A sensitivity to interpersonal harm emerges very early in ontogeny, as reflected in both the capacity for implicit social evaluation and an aversion for antisocial agents. Yet it does not necessarily entail avoidance toward inflicting pain to others. Later, an understanding that harmful actions cause suffering emerges, followed by an integration of rules that can depend on social contexts and cultures. These developmental findings build on a burgeoning literature, which suggests that the fundamental nature of moral and social cognition, including their motivational and hedonic value, lies in general computational processes such as attention, approach–avoidance, social valuation, and decision making rather than in fully distinct, dedicated neural regions for morality. Bridging the gap between cognition and behaviors and the requisite affective, motivational, and cognitive mechanisms, a developmental neuroscience approach enriches our understanding of the emergence of morality.

Recent research suggests that psychosocial resources and life stressors are mediating pathways explaining socioeconomic variation in young adults' health risks. However, less research has examined both these pathways simultaneously and their genetic moderation. A nationally representative sample of 11,030 respondents with prospective data collected over 13 years from the National Study of Adolescent to Adult Health was examined. First, the association between early cumulative socioeconomic adversity and young adults' (ages 25–34) cardiometabolic disease risk, as measured by 10 biomarkers, through psychosocial resources (educational attainment) and life stressors (accelerated transition to adulthood) was examined. Second, moderation of these pathways by the serotonin transporter linked polymorphic region gene (5-HTTLPR) was examined. There was evidence for the association between early socioeconomic adversity and young adults' cardiometabolic disease risk directly and indirectly through educational attainment and accelerated transitions. These direct and mediating pathways were amplified by the 5-HTTLPR polymorphism. These findings elucidate how early adversity can have an enduring influence on young adults' cardiometabolic disease risk directly and indirectly through psychosocial resources and life stressors and their genetic moderation. This information suggests that effective intervention and prevention programs should focus on early adversity, youth educational attainment, and their transition to young adulthood.

Behavioral inhibition (BI) is a temperament identified in early childhood that is associated with risk for anxiety disorders, yet only about half of behaviorally inhibited children manifest anxiety later in life. We compared brain function and behavior during extinction recall in a sample of nonanxious young adults characterized in childhood with BI (n = 22) or with no BI (n = 28). Three weeks after undergoing fear conditioning and extinction, participants completed a functional magnetic resonance imaging extinction recall task assessing memory and threat differentiation for conditioned stimuli. While self-report and psychophysiological measures of differential conditioning and extinction were similar across groups, BI-related differences in brain function emerged during extinction recall. Childhood BI was associated with greater activation in subgenual anterior cingulate cortex in response to cues signaling safety. This pattern of results may reflect neural correlates that promote resilience against anxiety in a temperamentally at-risk population.

Callous–unemotional (CU) traits characterize a subgroup of youths with conduct problems who exhibit low empathy, fearlessness, and elevated externalizing behaviors. The current study examines the role of aberrant amygdala activity and functional connectivity during a socioemotional judgment task in youths with CU traits, and links these deficits to externalizing behaviors. Functional magnetic resonance imaging was used to compare neural responses in 18 healthy youths and 30 youths with conduct problems and varying levels of CU traits as they evaluated the acceptability of causing another person to experience each of several emotions, including fear. Neuroimaging analyses examined blood oxygenation level dependent responses and task-dependent functional connectivity. High-CU youths exhibited left amygdala hypoactivation relative to healthy controls and low-CU youths primarily during evaluations of causing others fear. CU traits moderated the relationship between externalizing behavior and both amygdala activity and patterns of functional connectivity. The present data suggest that CU youths' aberrant amygdala activity and connectivity affect how they make judgments about the acceptability of causing others emotional distress, and that these aberrations represent risk factors for externalizing behaviors like rule breaking and aggression. These findings suggest that reducing externalizing behaviors in high-CU youths may require interventions that influence affective sensitivity.

Genetic variation in the oxytocin receptor gene (OXTR) is associated with several psychiatric conditions characterized by deficits in executive functioning (EF). A specific OXTR variant, rs2254298, has previously been associated with brain functioning in regions implicated in EF. Moreover, birth weight variation across the entire range is associated with individual differences in cortical structure and function that underlie EF. This is the first study to examine the main and interactive effect between rs2254298 and birth weight on EF in children. The sample consisted of 310 children from an ongoing longitudinal study. EF was measured at age 4.5 using observational tasks indexing working memory, cognitive flexibility, and inhibitory control. A family-based design that controlled for population admixture, stratification, and nongenomic confounds was employed. A significant genetic association between rs2254298 and EF was observed, with more copies of the major allele (G) associated with higher EF. There was also a significant interaction between rs2254298 and birth weight, such that more copies of the major allele in combination with higher birth weight predicted better EF. Findings suggest that OXTR may be associated with discrete neurocognitive abilities in childhood, and these effects may be modulated by intrauterine conditions related to fetal growth and development.

The current study used data from two longitudinal samples to test whether self-regulation, depressive symptoms, and aggression/antisociality were mediators in the relation between a polygenic score indexing serotonin (5-HT) functioning and alcohol use in adolescence. The results from an independent genome-wide association study of 5-hydroxyindoleacetic acid in the cerebrospinal fluid were used to create 5-HT polygenic risk scores. Adolescents and/or parents reported on adolescents’ self-regulation (Time 1), depressive symptoms (Time 2), aggression/antisociality (Time 2), and alcohol use (Time 3). The results showed that 5-HT polygenic risk did not predict self-regulation. However, adolescents with higher levels of 5-HT polygenic risk showed greater depression and aggression/antisociality. Adolescents’ aggression/antisociality mediated the relation between 5-HT polygenic risk and later alcohol use. Deficits in self-regulation also predicted depression and aggression/antisociality, and indirectly predicted alcohol use through aggression/antisociality. Pathways to alcohol use were especially salient for males from families with low parental education in one of the two samples. The results provide insights into the longitudinal mechanisms underlying the relation between 5-HT functioning and alcohol use (i.e., earlier aggression/antisociality). There was no evidence that genetically based variation in 5-HT functioning predisposed individuals to deficits in self-regulation. Genetically based variation in 5-HT functioning and self-regulation might be separate, transdiagnostic risk factors for several types of psychopathology.

High conflict and low warmth in families may contribute to immune cells developing a tendency to respond to threats with exaggerated inflammation that is insensitive to inhibitory signaling. We tested associations between family environments and expression of genes bearing response elements for transcription factors that regulate inflammation: nuclear factor kappa B (NF-κB) and glucocorticoid receptor. The overall sample (47 families) completed interviews, questionnaires, and 8-week daily diary assessments of conflict and warmth, which were used to create composite family conflict and warmth scores. The diaries assessed upper respiratory infection (URI) symptoms, and URI episodes were clinically verified. Leukocyte RNA was extracted from whole blood samples provided by a subsample of 42 children (8–13 years of age) and 73 parents. In children, higher conflict and lower warmth were related to greater expression of genes bearing response elements for the proinflammatory transcription factor NF-κB, and more severe URI symptoms. In parents, higher conflict and lower warmth were also related to greater NF-κB–associated gene expression. Monocytes and dendritic cells were implicated as primary cellular sources of differential gene expression in the sample. Consistent with existing conceptual frameworks, stressful family environments were related to a proinflammatory phenotype at the level of the circulating leukocyte transcriptome.

Extant research consistently links youth externalizing problems and later maladaptive outcomes, and these behaviors are particularly detrimental given their relative stability across development. Although an array of risk and protective factors for externalizing problems have been identified, few studies have examined factors reflecting the multiple social–ecological levels that influence child development and used them to predict longitudinal trajectories of externalizing problems. The current study examined externalizing behavior trajectories in a sample of 1,094 at-risk youth (539 boys, 555 girls) from the Longitudinal Studies in Child Abuse and Neglect multisite longitudinal study of child maltreatment. Normed Child Behavior Checklist externalizing scores were used to estimate group trajectories via growth-based trajectory modeling at ages 10, 12, 14, and 16 using the SAS PROC TRAJ procedure. Model fit was assessed using the Bayes information criterion and the Akaike information criterion statistics. Analyses revealed optimal fit for five distinct behavioral trajectories: low stable, mid-increasing, mid-decreasing, medium high, and high stable. Multinomial logistic regressions revealed that a combination of risk and protective factors at individual, family, school, and neighborhood levels contribute to distinct trajectories of externalizing problems over time. Predictors of low and decreasing trajectories can inform interventions aimed at addressing externalizing problems among high-risk adolescents.

The current project seeks to integrate literatures on personality risk for antisocial behavior (ASB) by examining how callous–unemotional traits relate to (a) the development of disinhibited traits and (b) the association between disinhibited traits and ASB. In Study 1, using a nationally representative sample of youth (N > 7,000), we examined whether conduct problems and lack of guilt assessed during ages 4–10 years predicted levels of and changes in disinhibited traits over the course of adolescence, and moderated associations between these traits and ASB. High levels of childhood conduct problems were associated with higher levels of impulsivity, sensation seeking, and ASB in early adolescence, whereas lack of guilt was associated with lower levels of sensation seeking. Neither conduct problems nor lack of guilt significantly predicted changes in impulsivity or sensation seeking, and associations among changes in sensation seeking, impulsivity, and ASB were also consistent across levels of conduct problems and lack of guilt. In Study 2, using a cross-sectional sample of adolescents (N = 970), we tested whether callous–unemotional traits moderated associations between disinhibited traits and ASB. Consistent with the results of Study 1, associations between disinhibited personality and ASB were consistent across a continuous range of callous–unemotional traits.