Associations between low birth weight and prenatal anxiety and later psychopathology may arise from programming effects likely to be adaptive under some, but not other, environmental exposures and modified by sex differences. If physiological reactivity, which also confers vulnerability or resilience in an environment-dependent manner, is associated with birth weight and prenatal anxiety, it will be a candidate to mediate the links with psychopathology. From a general population sample of 1,233 first-time mothers recruited at 20 weeks gestation, a sample of 316 stratified by adversity was assessed at 32 weeks and when their infants were aged 29 weeks (N = 271). Prenatal anxiety was assessed by self-report, birth weight from medical records, and vagal reactivity from respiratory sinus arrhythmia during four nonstressful and one stressful (still-face) procedure. Lower birth weight for gestational age predicted higher vagal reactivity only in girls (interaction term, p = .016), and prenatal maternal anxiety predicted lower vagal reactivity only in boys (interaction term, p = .014). These findings are consistent with sex differences in fetal programming, whereby prenatal risks are associated with increased stress reactivity in females but decreased reactivity in males, with distinctive advantages and penalties for each sex.

Children born prematurely at very low birth weight (<1500 g) are at increased risk for impairments affecting social functioning, including autism spectrum disorders (e.g., Johnson et al., 2010). In the current study, we used the Happé–Frith animated triangles task (Abell, Happé, & Frith, 2000) to study social attribution skills in this population. In this task, typical viewers attribute intentionality and mental states to shapes, based on characteristics of their movements. Participants included 34 preterm children and 36 full-term controls, aged 8–11 years. Groups were comparable in terms of age at test, gender, handedness, and socioeconomic status; they also performed similarly on tests of selective attention/processing speed and verbal intelligence. Relative to full-term peers, preterm children's descriptions of the animations were less appropriate overall; they also overattributed intentionality/mental states to randomly moving shapes and underattributed intentionality/mental states to shapes that seemed to be interacting socially. Impairments in the ability to infer the putative mental states of triangles from movement cues alone were most evident in children displaying more “autistic-like” traits, and this may reflect atypical development of and/or functioning in, or atypical connections between, parts of the social brain.

Neurobehavioral disinhibition (ND) is a complex condition reflecting a wide range of problems involving difficulties with emotion regulation and behavior control. Respiratory sinus arrhythmia (RSA) is a physiological correlate of emotion regulation that has been studied in a variety of at-risk populations; however, there are no studies of RSA in children with ND. Data were drawn from a prospective longitudinal study of prenatal substance exposure that included 1,073 participants. Baseline RSA and RSA reactivity to an attention-demanding task were assessed at 3, 4, 5, and 6 years. ND was assessed at ages 8/9, 11, and 13/14 years via behavioral dysregulation and executive dysfunction composite measures. Greater exposure to early adversity was related to less RSA reactivity at 3 years, increases in RSA reactivity from ages 3 to 6 years, and increased behavioral dysregulation from ages 8/9 to 13/14. RSA reactivity was examined as a moderator of the association between early adversity and changes in ND. A significant Early Adversity × RSA Reactivity quadratic interaction revealed that children with decelerations in RSA reactivity exhibited increases in behavioral dysregulation, regardless of their exposure to early adversity. However, greater exposure to early adversity was related to greater increases in behavioral dysregulation, but only if children exhibited accelerations in RSA reactivity from ages 3 to 6 years. The results contribute to our understanding of how interactions across multiple levels of analysis contribute to the development of ND.

The emergence and persistence of conduct problems (CPs) during early childhood is a robust predictor of behavior problems in school and of future maladaptation. In this study we examined the reciprocal influences between observed coercive interactions between children and caregivers, oppositional and aggressive behavior, and growth in parent report of early childhood (ages 2–5) and school-age CPs (ages 7.5 and 8.5). Participants were drawn from the Early Steps multisite randomized prevention trial that includes an ethnically diverse sample of male and female children and their families (N = 731). A parallel-process growth model combining latent trajectory and cross-lagged approaches revealed the amplifying effect of observed coercive caregiver–child interactions on children's noncompliance, whereas child oppositional and aggressive behaviors did not consistently predict increased coercion. The slope and initial levels of child oppositional and aggressive behaviors and the stability of caregiver–child coercion were predictive of teacher-reported oppositional behavior at school age. Families assigned to the Family Check-Up condition had significantly steeper declines in child oppositional and aggressive behavior and moderate reductions in oppositional behavior in school and in coercion at age 3. Results were not moderated by child gender, race/ethnicity, or assignment to the intervention condition. The implications of these findings are discussed with respect to understanding the early development of CPs and to designing optimal strategies for reducing problem behavior in early childhood with families most in need.

Autism spectrum disorders (ASDs) are characterized by social impairments, including inappropriate responses to affective stimuli and nonverbal cues, which may extend to poor face-emotion recognition. However, the results of empirical studies of face-emotion recognition in individuals with ASD have yielded inconsistent findings that occlude understanding the role of face-emotion recognition deficits in the development of ASD. The goal of this meta-analysis was to address three as-yet unanswered questions. Are ASDs associated with consistent face-emotion recognition deficits? Do deficits generalize across multiple emotional expressions or are they limited to specific emotions? Do age or cognitive intelligence affect the magnitude of identified deficits? The results indicate that ASDs are associated with face-emotion recognition deficits across multiple expressions and that the magnitude of these deficits increases with age and cannot be accounted for by intelligence. These findings suggest that, whereas neurodevelopmental processes and social experience produce improvements in general face-emotion recognition abilities over time during typical development, children with ASD may experience disruptions in these processes, which suggested distributed functional impairment in the neural architecture that subserves face-emotion processing, an effect with downstream developmental consequences.

Children with histories of disorganized attachment exhibit diverse problems, possibly because disorganization takes at least two distinctive forms as children age: controlling–punitive and controlling–caregiving. This variation in the developmental legacy of disorganization has been attributed primarily to variations in children's rearing experiences. Here an alternative explanation of these divergent sequelae of disorganization is evaluated: one focused on genotype. Structural equation modeling was applied to data on 704 Norwegian children to test whether the catechol-O-methyltransferase Val158Met genotype moderates the effect of disorganized attachment, which was measured dimensionally at 4 years of age using the Manchester Child Attachment Story Task, on changes in aggressive behavior and social competence from ages 4 to 6. Children who scored high on disorganization and were homozygous for the valine allele displayed significantly greater increases in aggression and decreases in self-oriented social skills (e.g., self-regulation and assertiveness) over time than did their disorganized counterparts carrying the methionine allele, whereas disorganized children carrying the methionine allele increased their other-oriented social skill (e.g., cooperation and responsibility) scores more than did valine-homozygous children. These results are consistent with the controlling–punitive and controlling–caregiving behaviors observed in disorganized children, suggesting that the children's genotype contributed to variations in the social development of disorganized children.

Despite widespread recognition that the physiological systems underlying stress reactivity are well coordinated at a neurobiological level, surprisingly little empirical attention has been given to delineating precisely how the systems actually interact with one another when confronted with stress. We examined cross-system response proclivities in anticipation of and following standardized laboratory challenges in 664 4- to 14-year-olds from four independent studies. In each study, measures of stress reactivity within both the locus coeruleus-norepinephrine system (i.e., the sympathetic and parasympathetic branches of the autonomic nervous system) and the corticotrophin releasing hormone system (i.e., the hypothalamic–pituitary–adrenal axis) were collected. Latent profile analyses revealed six distinctive patterns that recurred across the samples: moderate reactivity (average cross-system activation; 52%–80% of children across samples), parasympathetic-specific reactivity (2%–36%), anticipatory arousal (4%–9%), multisystem reactivity (7%–14%), hypothalamic–pituitary–adrenal axis specific reactivity (6%–7%), and underarousal (0%–2%). Groups meaningfully differed in socioeconomic status, family adversity, and age. Results highlight the sample-level reliability of children's neuroendocrine responses to stress and suggest important cross-system regularities that are linked to development and prior experiences and may have implications for subsequent physical and mental morbidity.

The present study incorporates a person-based approach to identify spillover and compartmentalization patterns of interpartner conflict and maternal parenting practices in an ethnically diverse sample of 192 2-year-old children and their mothers who had experienced higher levels of socioeconomic risk. In addition, we tested whether sociocontextual variables were differentially predictive of theses profiles and examined how interpartner-parenting profiles were associated with children's physiological and psychological adjustment over time. As expected, latent class analyses extracted three primary profiles of functioning: adequate functioning, spillover, and compartmentalizing families. Furthermore, interpartner-parenting profiles were differentially associated with both sociocontextual predictors and children's adjustment trajectories. The findings highlight the developmental utility of incorporating person-based approaches to models of interpartner conflict and maternal parenting practices.

Building on research on cumulative risk and psychopathology, this study examines how cumulative risk exposure is associated with altered diurnal cortisol rhythms in an ethnically diverse, low-income sample of youth. In addition, consistent with a diathesis-stress perspective, this study explores whether the effect of environmental risk is moderated by allelic variation in the serotonin transporter linked polymorphic region (5-HTTLPR) gene. Results show that youth with greater cumulative risk exposure had flatter diurnal cortisol slopes, regardless of 5-HTTLPR genotype. However, the association of cumulative risk with average cortisol output (area under the curve [AUC]) was moderated by the 5-HTTLPR genotype. Among youth homozygous for the long allele, greater cumulative risk exposure was associated with lower cortisol AUC, driven by significant reductions in cortisol levels at waking. In contrast, there was a trend-level association between greater cumulative risk and higher cortisol AUC among youth carrying the short allele, driven by a trend-level increase in bedtime cortisol levels. Findings are discussed with regard to the relevance of dysregulated diurnal cortisol rhythms for the development of psychopathology and the implications of genetically mediated differences in psychophysiological adaptations to stress.

Physically maltreated children are at risk for developing externalizing behavioral problems characterized by reactive aggression. The current experiment tested the relationships between individual differences in a neural index of social information processing, histories of child maltreatment, child negative affect, and aggressive behavior. Fifty boys (17 maltreated) performed an emotion recognition task while the P3b component of the event-related potential was recorded to index attention allocation to angry faces. Children then participated in a peer-directed aggression task. Negative affect was measured by recording facial electromyography, and aggression was indexed by the feedback that children provided to a putative peer. Physically maltreated children exhibited greater negative affect and more aggressive behavior, compared to nonmaltreated children, and this relationship was mediated by children's allocation of attention to angry faces. These data suggest that physical maltreatment leads to inappropriate regulation of both negative affect and aggression, which likely place maltreated children at increased risk for the development and maintenance of externalizing behavior disorders.

The link between the experience of peer victimization (PV) and future psychological maladjustment has been consistently documented; however, little is known about intermediary cognitive processes that underlie this relation or how these processes vary across childhood. The present study examined the prospective relations between physical and relational PV and the development of negative and positive automatic thoughts and self-cognitions. Self-reports of cognitions and peer nomination measures of victimization were obtained from 1,242 children and young adolescents (Grades 3 through 6) in a two-wave longitudinal study. The results revealed that PV predicted significant increases in negative views of the self, world, and future and decreases in self-perceived competence for girls under 11 years of age, with the effect being stronger for younger girls. PV was not significantly associated with changes in positive or negative self-cognitions for older girls or for boys of any age. These findings support the hypothesis that PV may be linked to future psychopathology through its influence on self-cognitions, but only for girls.

Many African American adolescents experience racial discrimination, with adverse consequences; however, stability and change in these experiences over time have not been examined. We examined longitudinal patterns of perceived racial discrimination assessed in Grades 7–10 and how these discrimination trajectories related to patterns of change in depressive and anxious symptoms and aggressive behaviors assessed over the same 4-year period. Growth mixture modeling performed on a community epidemiologically defined sample of urban African American adolescents (n = 504) revealed three trajectories of discrimination: increasing, decreasing, and stable low. As predicted, African American boys were more frequent targets for racial discrimination as they aged, and they were more likely to be in the increasing group. The results of parallel process growth mixture modeling revealed that youth in the increasing racial discrimination group were four times more likely to be in an increasing depression trajectory than were youth in the low stable discrimination trajectory. Though youth in the increasing racial discrimination group were nearly twice as likely to be in the high aggression trajectory, results were not statistically significant. These results indicate an association between variation in the growth of perceived racial discrimination and youth behavior and psychological well-being over the adolescent years.

Childhood adversities have been proposed to modify later stress sensitivity and risk of depressive disorder in several ways: by stress sensitization, stress amplification, and stress inoculation. Combining these models, we hypothesized that childhood adversities would increase risk of early, but not later, onsets of depression (Hypothesis 1). In those without an early onset, childhood adversities were hypothesized to predict a relatively low risk of depression in high-stress conditions (Hypothesis 2a) and a relatively high risk of depression in low-stress conditions (Hypothesis 2b), compared to no childhood adversities. These hypotheses were tested in 1,584 participants of the Tracking Adolescents' Individual Lives Survey, a prospective cohort study of adolescents. Childhood adversities were assessed retrospectively at ages 11 and 13.5, using self-reports and parent reports. Lifetime DSM-IV major depressive episodes were assessed at age 19, by means of the Composite International Diagnostic Interview. Stressful life events during adolescence were established using interview-based contextual ratings of personal and network events. The results provided support for all hypotheses, regardless of the informant and timeframe used to assess childhood adversities and regardless of the nature (personal vs. network, dependent vs. independent) of recent stressful events. These findings suggest that age at first onset of depression may be an effective marker to distinguish between various types of reaction patterns.

This study examined separate developmental trajectories of anxious and depressive symptoms from childhood to adolescence (9–15 years) in a community-based sample (N = 290). At three measurement points, mothers and fathers reported on their children's anxious and depressive symptoms, and at Time 1 they reported on lower order child personality facets and on their parenting. By means of growth mixture modeling, three developmental trajectories were identified for anxious symptoms: steady low (82%), moderate increasing–decreasing (5.9%), and high declining groups (12.1%). For depressive symptoms, two developmental trajectories were found: steady low (94.1%) and moderate increasing groups (5.9%). Higher shyness, irritability, and altruism predicted membership in more problematic anxious and depressive groups. The personality facets energy, optimism, compliance, and anxiety were unique predictors for class membership for anxious symptoms, and the effects of shyness, irritability, and compliance were moderated by overreactive parenting. Shyness and irritability increased the probability of following the moderate increasing–decreasing anxiety trajectory, but only in the context of high or average levels of overreactive parenting. Compliance increased the probability of following the moderate increasing–decreasing and high decreasing trajectories in the context of high overreactive parenting. Our results indicate that childhood personality facets differentiate trajectories of anxious and depressive symptoms in theoretically compelling ways.

Although adolescence is characterized by hormonal changes and increased disinhibited behaviors, explanations for these developmental changes that include personality and environmental factors have not been fully elucidated. We examined the interactions between psychosocial stress and the traits of negative emotionality and constraint on impulsive and risk-taking behaviors as well as salivary cortisol reactivity in 88 adolescents. In terms of behavioral outcomes, analyses revealed that negative emotionality and constraint were protective of impulsivity and risk taking, respectively, for adolescents in the no-stress condition; personality did not relate to either behavior in the stress condition. Low-constraint adolescents in the stress condition engaged in less risk taking than low-constraint adolescents in the no-stress condition, whereas there was no effect of stress group for high-constraint adolescents. In terms of cortisol reactivity, analyses revealed that low-constraint adolescents in the stress condition exhibited greater cortisol reactivity compared to high-constraint adolescents, which suggests that low-constraint adolescents mobilize greater resources (e.g., increased cognitive control, heightened attention to threat) in stressful situations relative to nonstressful ones. These results demonstrate that two facets of disinhibition and cortisol reactivity are differentially affected by psychosocial stress and personality (and their interactions) in adolescents.

Social disorganization theory posits that individuals who live in disadvantaged neighborhoods are more likely to engage in antisocial behavior than are those who live in advantaged neighborhoods and that neighborhood disadvantage asserts this effect through its disruptive impact on social ties. Past research on this framework has been limited in two respects. First, most studies have concentrated on adolescent males. In contrast, the present study focused on a sample of adult African American females. Second, past research has largely ignored individual-level factors that might explain why people who grow up in disadvantaged neighborhoods often do not engage in antisocial behavior. We investigated the extent to which genetic variation contributes to heterogeneity of response to neighborhood conditions. We found that the impact of neighborhood disadvantage on antisocial behavior was mediated by neighborhood social ties. Further, the analysis indicated that the effects of neighborhood disadvantage and social ties on antisocial behavior were moderated by genetic polymorphisms. Examination of these moderating effects provided support for the differential susceptibility model of Gene × Environment. The effect of Gene × Neighborhood Disadvantage on antisocial behavior was mediated by the effect of Gene × Neighborhood Social Ties, providing support for an expanded view of social disorganization theory.

Maternal depression is an established risk factor for child conduct problems, but relatively few studies have tested whether children's behavioral problems exacerbate mothers' depression or whether other child behavioral characteristics (e.g., self-regulation) may mediate bidirectional effects between maternal depression and child disruptive behavior. This longitudinal study examined the parallel growth of maternal depressive symptoms and child oppositional behavior from ages 2 to 5; the magnitude and timing of their bidirectional effects; and whether child inhibitory control, a temperament-based self-regulatory mechanism, mediated effects between maternal depression and child oppositionality. A randomized control trial of 731 at-risk families assessed children annually from ages 2 to 5. Transactional models demonstrated positive and bidirectional associations between mothers' depressive symptoms and children's oppositional behavior from ages 2 to 3, with a less consistent pattern of reciprocal relations up to age 5. Mediation of indirect mother–child effects and child evocative effects depended on the rater of children's inhibitory control. Findings are discussed in regard to how child evocative effects and self-regulatory mechanisms may clarify the transmission of psychopathology within families.

The present study compared two theories of the association between romantic involvement and adjustment: a social timetable theory and a developmental task theory. We examined seven waves of longitudinal data on a community based sample of 200 participants (Wave 1 mean age = 15 years, 10 months). In each wave, multiple measures of substance use, externalizing symptoms, and internalizing symptoms were gathered, typically from multiple reporters. Multilevel modeling revealed that greater levels of romantic involvement in adolescence were associated with higher levels of substance use and externalizing symptoms but became associated with lower levels in adulthood. Having a romantic partner was associated with greater levels of substance use, externalizing symptoms, and internalizing symptoms in adolescence but was associated with lower levels in young adulthood. The findings were not consistent with a social timetable theory, which predicts that nonnormative involvement is associated with poor adjustment. Instead, the findings are consistent with a developmental task theory, which predicts that precocious romantic involvement undermines development and adaptation, but when romantic involvement becomes a salient developmental task in adulthood, it is associated with positive adjustment. Discussion focuses on the processes that may underlie the changing nature of the association between romantic involvement and adjustment.

This study examined whether a family-based preventive intervention for inner-city children entering the first grade could alter the developmental course of attention-deficit/hyperactivity disorder (ADHD) symptoms. Participants were 424 families randomly selected and randomly assigned to a control condition (n = 192) or Schools and Families Educating Children (SAFE) Children (n = 232). SAFE Children combined family-focused prevention with academic tutoring to address multiple developmental–ecological needs. A booster intervention provided in the 4th grade to randomly assigned children in the initial intervention (n =101) evaluated the potential of increasing preventive effects. Follow-up occurred over 5 years with parents and teachers reporting on attention problems. Growth mixture models identified multiple developmental trajectories of ADHD symptoms. The initial phase of intervention placed children on more positive developmental trajectories for impulsivity and hyperactivity, demonstrating the potential for ADHD prevention in at-risk youth, but the SAFE Children booster had no additional effect on trajectory or change in ADHD indicators.