This was a prospective longitudinal multisite study of the effects of prenatal cocaine and/or opiate exposure on temperament in 4-month-olds of the Maternal Lifestyle Study (N = 958: 366 cocaine exposed, 37 opiate exposed, 33 exposed to both drugs, 522 matched comparison). The study evaluated positivity and negativity during The Behavior Assessment of Infant Temperament (Garcia Coll et al., 1988). Parents rated temperament (Infant Behavior Questionnaire; Rothbart, 1981). Cocaine-exposed infants showed less positivity overall, mainly during activity and threshold items, more negativity during sociability items, and less negativity during irritability and threshold items. Latent profile analysis indicated individual temperament patterns were best described by three groups: low/moderate overall reactivity, high social negative reactivity, and high nonsocial negative reactivity. Infants with heavy cocaine exposure were more likely in high social negative reactivity profile, were less negative during threshold items, and required longer soothing intervention. Cocaine- and opiate-exposed infants scored lower on Infant Behavior Questionnaire smiling and laughter and duration of orienting scales. Opiate-exposed infants were rated as less respondent to soothing. By including a multitask measure of temperament we were able to show context-specific behavioral dysregulation in prenatally cocaine-exposed infants. The findings indicate flatter temperament may be specific to nonsocial contexts, whereas social interactions may be more distressing for cocaine-exposed infants.

A heightened synchrony between the mother's and infant's facial affect predicts adverse infant development. We know that maternal psychopathology is related to mother–infant facial affect synchrony, but it is unclear how maternal psychopathology is transmitted to mother–infant synchrony. One pathway might be maternal emotion dysregulation. We examined (a) whether maternal emotion dysregulation is positively related to facial affect synchrony and (b) whether maternal emotion dysregulation mediates the effect of maternal psychopathology on mother–infant facial affect synchrony. We observed 68 mothers with mood disorders and their 4- to 9-month-old infants in the Still-Face paradigm during two play interactions. The mother's and infant's facial affect were rated from high negative to high positive, and the degree of synchrony between the mother's and infant's facial affect was computed with a time-series analysis. Emotion dysregulation was measured with the Difficulties in Emotion Regulation Scale, and psychopathology was assessed with the Symptom Checklist–90–Revised. Higher maternal emotion dysregulation was significantly associated with higher facial affect synchrony; emotion dysregulation fully mediated the effect of maternal psychopathology on facial affect synchrony. Our findings demonstrate that maternal emotion dysregulation rather than maternal psychopathology per se places mothers and infants at risk for heightened facial affect synchrony.

Environmental risk predicts disrupted basal cortisol levels in preschool children. However, little is known about the stability or variability of diurnal cortisol morning levels or slope patterns over time in young children. This study used latent profile analysis to identify patterns of the hypothalamic–pituitary–adrenal axis activity during the preschool period. Using a community sample (N = 306), this study measured income, cumulative risk, and children's diurnal cortisol (morning level and slope) four times across 2.5 years, starting when children were 36 months old. Latent profile analysis profiles indicated that there were predominantly stable patterns of diurnal cortisol level and slope over time and that these patterns were predicted by income and cumulative risk. In addition, there were curvilinear relations of income and cumulative risk to profiles of low morning cortisol level and flattened diurnal slope across time, suggesting that both lower and higher levels of income and cumulative risk were associated with a stress-sensitive physiological system. Overall, this study provides initial evidence for the role of environmental risk in predicting lower, flattened basal cortisol patterns that remain stable over time.

Guided by emotional security theory, this study examined the temperamental precursors of distinctive profiles of children's responses to interparental conflict. Participants included 243 children (M = 4.6 years) and their parents across two annual measurement occasions. Temperamental constructs of frustration proneness, approach, positive affect, activity level, and effortful control were assessed through multiple methods, informants, and contexts. Behavioral observations of children's responses to interparental conflict at each wave yielded four profiles: secure (i.e., efficiently address direct threat), mobilizing (i.e., vigilance to potential threat and social opportunities), dominant (i.e., directly defeat threat), and demobilizing (i.e., reduce salience as a target of hostility). Results supported hypotheses on the distinct constellations of temperament in predicting subsequent change in the four security profiles.

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.

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 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.

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.

The present investigation extends research on Gene × Environment interactions and youth risk behavior by linking multilevel contextual factors, such as community disadvantage and protective parenting practices, to both parental and youth dopamine D4 receptor (DRD4) genotypes. We expected community disadvantage to influence youth risk behavior via a series of indirect effects involving protective parenting and youth's planful future orientation when both parents’ and youth's DRD4 status was considered. Genetic moderation processes also were tested to determine whether they conformed to a diathesis–stress or a differential susceptibility model. Hypotheses were investigated with data from 361 rural African American youth and their parents assessed 3 times when youth were ages 16 to 19. Community disadvantage interacted with parental DRD4 status to predict low levels of protective parenting. Protective parenting, in turn, interacted with youth DRD4 status to forecast increases in youth's planful future orientations, a proximal influence on changes in risk behavior. The Parental DRD4 × Community Disadvantage interaction, but not youth DRD4 × Protective Parenting, conformed to a differential susceptibility model. Indirect effect analyses revealed a significant indirect path linking community disadvantage to youth risk behavior through a series of multilevel Gene × Environment interaction processes.

Studies support a link between adolescent romantic involvement and depression. Adolescent romantic relationships may increase depression risk by introducing chronic stress, and genetic vulnerability to stress reactivity/emotion dysregulation may moderate these associations. We tested genetic moderation of longitudinal associations between adolescent romantic involvement and later depressive symptoms by a polymorphism in the serotonin transporter linked polymorphic region gene (5-HTTLPR) and examined contributory roles of chronic stress and family discord. Three hundred eighty-one youth participated at ages 15 and 20. The results indicated that 5-HTTLPR moderated the association between age 15 romantic involvement and age 20 depressive symptoms, with strongest effects for short homozygotes. Conditional process analysis revealed that chronic stress functioned as a moderated mediator of this association, fully accounting for the romantic involvement–depression link among short/short genotypes. Also, romantic involvement predicted later depressive symptoms most strongly among short-allele carriers with high family discord. The results have important implications for understanding the romantic involvement–depression link and the behavioral and emotional correlates of the 5-HTTLPR genotype.

Anxiety sensitivity (AS), the belief that anxious arousal is harmful, is a malleable risk factor that has been implicated in anxiety and depression symptoms in adolescents. Although there is some evidence that adolescents possess distinct developmental trajectories, few studies have explored this topic. This study examined the developmental trajectory of AS in 248 adolescents (M age = 11.0 years, SD = 0.82; 56% male) across 6 years, beginning when children were age 11. This study also examined the influence of AS trajectories on anxiety and depression at age 16. Finally, this study examined the utility of AS classes in identifying anxiety and depression growth. Three AS classes were found, described by normative-stable, high-stable, and high-unstable trajectories. Adolescents in the high-stable and the high-unstable AS classes had higher levels of anxiety and depression at age 16 than did adolescents in the normative-stable AS class. In addition, the anxiety and depression trajectories fit by AS class mirrored the AS class trajectories. These findings suggest three AS trajectories can be identified in adolescents. These trajectories are discussed in relation to a developmental perspective of AS.

Late adolescence and emerging adulthood (specifically ages 15–24) represent a period of heightened sexual risk taking resulting in the greatest annual rates of sexually transmitted infections and unplanned pregnancies in the US population. Ongoing efforts to prevent such negative consequences are likely to benefit from a deepening of our understanding of biological mechanisms through which sexual risk taking emerges and biases decision making during this critical window. Here we present a neuroscience framework from which a mechanistic examination of sexual risk taking can be advanced. Specifically, we adapt the neurodevelopmental triadic model, which outlines how motivated behavior is governed by three systems: approach, avoidance, and regulation, to sexual decision making and subsequent risk behavior. We further propose a testable hypothesis of the triadic model, wherein relatively decreased threat-related amygdala reactivity and increased reward-related ventral striatum reactivity leads to sexual risk taking, which is particularly exaggerated during adolescence and young adulthood when there is an overexpression of dopaminergic neurons coupled with immature top-down prefrontal cortex regulation. We conclude by discussing how future research based on our adapted triadic model can inform ongoing efforts to improve intervention and prevention efforts.

Longitudinal research on mental health development beyond adolescence among nonclinical populations is lacking. This study reports on psychiatric disorder trajectories from late adolescence to young adulthood in relation to childhood and adolescent risk factors. Participants were recruited for a prospective longitudinal study tracing a community sample of 5-year-old children with communication disorders and a matched control cohort to age 31. Psychiatric disorders were measured at ages 19, 25, and 31. Known predictors of psychopathology and two school-related factors specifically associated with language disorder (LD) were measured by self-reports and semistructured interviews. The LD cohort was uniquely characterized by a significantly decreasing disorder trajectory in early adulthood. Special education was associated with differential disorder trajectories between LD and control cohorts, whereas maltreatment history, specific learning disorder, family structure, and maternal psychological distress were associated with consistent trajectories between cohorts. From late adolescence to young adulthood, childhood LD was characterized by a developmentally limited course of psychiatric disorder; maltreatment was consistently characterized by an elevated risk of psychiatric disorder regardless of LD history, whereas special education was associated with significantly decreasing risk of psychiatric disorder only in the presence of LD.

We aimed to analyze the impact of several parenting factors on the relationship between psychopathy and antisocial behavior. Nine hundred youths and their mothers reported on parent–youth interactions, and youth self-report measures of psychopathy, delinquency and violent behavior were taken. Multiple regression was used to test for the significance of interactions between parenting and psychopathy scores. In terms of delinquency, linear interactions between psychopathy and the level of conflict with parents and parents' knowledge of their youths' whereabouts/youths' willingness to disclose information were found based on the data reported by the youths. Data reported by mothers indicated a linear interaction between psychopathy and parents' knowledge/youth disclosure, and a quadratic interaction of conflict with parents. For violence, we used logistic regression models to analyze moderation. No interaction effects between psychopahy scores and parenting factors were found. Youths' reports of high conflict with parents and parents' knowledge/youth disclosure showed to have an impact on violence regardless of the level of psychopathic traits. Implications for the prevention and treatment are discussed.

To investigate familial influences on the full range of variability in attention and activity across adolescence, we collected maternal ratings of 339 twin pairs at ages 12, 14, and 16, and estimated the transmitted and new familial influences on attention and activity as measured by the Strengths and Weaknesses of Attention-Deficit/Hyperactivity Disorder Symptoms and Normal Behavior Scale. Familial influences were substantial for both traits across adolescence: genetic influences accounted for 54%–73% (attention) and 31%–73% (activity) of the total variance, and shared environmental influences accounted for 0%–22% of the attention variance and 13%–57% of the activity variance. The longitudinal stability of individual differences in attention and activity was largely accounted for by familial influences transmitted from previous ages. Innovations over adolescence were also partially attributable to familial influences. Studying the full range of variability in attention and activity may facilitate our understanding of attention-deficit/hyperactivity disorder's etiology and intervention.

Adolescent internalizing and externalizing psychopathology is strongly associated with adult psychiatric morbidity, including psychotic disorders. This study examined whether internalizing or externalizing trajectories (continuity/discontinuity of symptoms) from middle childhood were associated with adolescent psychotic-like experiences (PLEs). Prospective data were collected from a community sample of 553 children (mean age = 10.4 years; 50% male) and their primary caregivers. Participants completed questionnaire reports of internalizing and externalizing psychopathology and PLEs at baseline, and again approximately 2 years later. Logistic regression was used to examine the association of adolescent PLEs with four trajectories of internalizing and externalizing psychopathology (persistent, incident, remitting, and none), controlling for a range of potential confounders and sampling bias. Significant associations were identified between adolescent PLEs and the incident internalizing (adjusted odds ratio [adj. OR] = 2.96; 95% confidence interval [CI] = 1.60–5.49) and externalizing psychopathology (adj. OR = 2.14; 95% CI = 1.11–4.14) trajectories, as well as the persistent internalizing (adj. OR = 1.90; 95% CI = 1.13–3.18) and externalizing (adj. OR = 1.81, 95% CI = 1.02–3.19) trajectories. Children with remitting psychopathology trajectories were no more likely to present later PLEs than those who never experienced psychopathology. While for many individuals symptoms and illness remit during development without intervention, this study provides important insights regarding potential targets and timing for delivery of early intervention and prevention programs.

Much research has examined Moffitt's developmental taxonomy, focusing almost exclusively on the distinction between life-course persistent and adolescence-limited offenders. Of interest, a handful of studies have identified a group of individuals whose early childhood years were marked by extensive antisocial behavior but who seemed to recover and desist (at least from severe offending) in adolescence and early adulthood. We use data from the Cambridge Study in Delinquent Development to examine the adult adjustment outcomes of different groups of offenders, including a recoveries group, in late middle adulthood, offering the most comprehensive investigation of this particular group to date. Findings indicate that abstainers comprise the largest group of males followed by adolescence-limited offenders, recoveries, and life-course persistent offenders. Furthermore, the results reveal that a host of adult adjustment problems measured at ages 32 and 48 in a number of life-course domains are differentially distributed across these four offender groups. In addition, the recoveries and life-course persistent offenders often show the greatest number of adult adjustment problems relative to the adolescence-limited offenders and abstainers.

Childhood maltreatment can disturb brain development and subsequently lead to adverse socioemotional and mental health problems across the life span. The long-term association between childhood maltreatment and resting–wake brain activity during adulthood is unknown and was examined in the current study. Forty-one medically stable and medication-free military veterans (M = 29.31 ± 6.01 years, 78% male) completed a battery of clinical assessments and had [18F]-fluorodeoxyglucose positron emission tomography neuroimaging scans during quiet wakefulness. After statistically adjusting for later-life trauma and mental health problems, childhood maltreatment was negatively associated with brain activity within a priori defined regions that included the left orbital frontal cortex and left hippocampus. Childhood maltreatment was significantly associated with increased and decreased brain activity within six additional whole-brain clusters that included the frontal, parietal–temporal, cerebellar, limbic, and midbrain regions. Childhood maltreatment is associated with altered neural activity in adulthood within regions that are involved in executive functioning and cognitive control, socioemotional processes, autonomic functions, and sleep/wake regulation. This study provides support for taking a life span developmental approach to understanding the effects of early-life maltreatment on later-life neurobiology, socioemotional functioning, and mental health.

Individuals with autism spectrum disorder (ASD) experience higher rates of psychopathology than their typically developing peers or peers with other intellectual or developmental disabilities. Little is known about the developmental course of psychiatric symptoms such as internalizing and externalizing behaviors in this population. Individual characteristics and aspects of the family environment may explain variability in outcomes for adults with ASD. The present study extends our current understanding of psychopathology among individuals with ASD by examining group-based trajectories of internalizing and externalizing symptoms in adulthood. Overall, the results showed that symptoms became less severe over time. Distinct patterns of change in psychopathology were observed and associated with differential profiles of psychotropic medication use, comorbid mental health diagnoses, and residential placement. The likelihood of following each developmental trajectory was estimated based on characteristics of the adults with ASD (gender, adaptive behavior, and autistic symptoms) and maternal expressed emotion (criticism and warmth). Maternal criticism and warmth were identified as key risk and protective factors, respectively, with important implications for future research and intervention for individuals with ASD.

Drawing from developmental psychology and psychopathology, we propose a new, developmentally informed approach to parenting interventions that focuses on elucidating changes in the unfolding developmental process between the parent and child. We present data from 186 low-income mothers of toddlers, randomly assigned to a child-oriented play group or a play-as-usual group. We examined the maladaptive cascade from child difficulty to mother adversarial, negative parenting to child maladjustment, well documented in the literature. The measures incorporated multiple observations and reports. As expected, the sequence from child difficulty (pretest) to mother adversarial, negative parenting (Posttest 1, after 3-month intervention) to child maladjustment (Posttest 2, 6 months later) was present in the play-as-usual group, but absent, or defused, in the child-oriented play group. The findings are consistent with a view of intervention presumably enhancing the mother–child relationship, which in turn served to moderate future mother–child dynamics, altering its otherwise anticipated negative trajectory. A closer examination of the cascade revealed that, at Posttest 1, mothers in the play-as-usual group engaged in more adversarial, negative parenting (controlling for pretest) than did mothers in the child-oriented play group when their children were of high difficulty. The intervention appears to exert its primary influence on the cascade by weakening the link between child difficulty and maternal adversarial, negative parenting.