Although neurocognitive impairments in theory of mind and in executive functions have both been hypothesized to play a causal role in autism, there has been little research investigating the explanatory power of these impairments with regard to autistic symptomatology. The present study examined the degree to which individual differences in theory of mind and executive functions could explain variations in the severity of autism symptoms. Participants included 31 verbal, school-aged children with autism who were administered a battery of tests assessing the understanding of mental states (knowledge and false belief) and executive control skills (working memory, combined working memory and inhibitory control, and planning) and who were behaviorally evaluated for autism severity in the three core symptom domains. Whereas theory of mind and executive control abilities explained the significant variance beyond that accounted for by language level in communication symptoms, neither explained the significant variance in reciprocal social interaction or repetitive behaviors symptoms. These findings are discussed in terms of a proposed distinction between higher level, cognitive–linguistic aspects of theory of mind and related executive control skills, and more fundamental social–perceptual processes involved in the apprehension of mental state information conveyed through eyes, faces, and voices, which may be more closely linked to autistic deficits in social reciprocity.This research was supported by grants from the National Institute on Child Health and Human Development (RO3 HD37898) to Robert Joseph and from the National Institute on Deafness and Other Communication Disorders (PO1 DC03610) to Helen Tager–Flusberg. In addition, this study was conducted as part of the NICHD/NIDCD Collaborative Programs of Excellence in Autism. We thank the following individuals for their assistance in collecting and preparing the data reported in this article: Susan Bacalman, Laura Becker, June Chu, Susan Folstein, Anne Gavin, Margaret Kjelgaard, Lauren McGrath, Echo Meyer, and Shelly Steele. We are especially grateful to the children and families who generously participated in this study.

This study tested a developmental cascade model of peer rejection, social information processing (SIP), and aggression using data from 585 children assessed at 12 time points from kindergarten through Grade 3. Peer rejection had direct effects on subsequent SIP problems and aggression. SIP had direct effects on subsequent peer rejection and aggression. Aggression had direct effects on subsequent peer rejection. Each construct also had indirect effects on each of the other constructs. These findings advance the literature beyond a simple mediation approach by demonstrating how each construct effects changes in the others in a snowballing cycle over time. The progressions of SIP problems and aggression cascaded through lower liking, and both better SIP skills and lower aggression facilitated the progress of social preference. Findings are discussed in terms of the dynamic, developmental relations among social environments, cognitions, and behavioral adjustment.

The hypothesis was tested that weak theory of mind (ToM) and/or emotion recognition (ER) abilities are specific to subjects with autism. Differences in ToM and ER performance were examined between autistic (n = 20), pervasive developmental disorder—not otherwise specified (PDD-NOS) (n = 20), psychiatric control (n = 20), and normal children (n = 20). The clinical groups were matched person-to-person on age and verbal IQ. We used tasks for the matching and the context recognition of emotional expressions, and a set of first- and second-order ToM tasks. Autistic and PDD-NOS children could not be significantly differentiated from each other, nor could they be differentiated from the psychiatric controls with a diagnosis of ADHD (n = 9). The psychiatric controls with conduct disorder or dysthymia performed about as well as normal children. The variance in second-order ToM performance contributed most to differences between diagnostic groups.

The MacArthur Story Stem Battery was used to examine maternal and self-representations in neglected, physically abused, sexually abused, and nonmaltreated comparison preschool children. The narratives of maltreated children contained more negative maternal representations and more negative self-representations than did the narratives of nonmaltreated children. Maltreated children also were more controlling with and less responsive to the examiner. In examining the differential impact of maltreatment subtype differences on maternal and self-representations, physically abused children evidenced the most negative maternal representations; they also had more negative self-representations than nonmaltreated children. Sexually abused children manifested more positive self-representations than neglected children. Despite these differences in the nature of maternal and self-representations, physically and sexually abused children both were more controlling and less responsive to the examiner. The investigation adds to the corpus of knowledge regarding disturbances in the self-system functioning of maltreated children and provides support for relations between representational models of self and other and the self-organizing function that these models exert on children's lives.

We examined the relations between emotionality, emotion processing, and aggression in 182 first- and second-grade children. Consistent with Tomkins' and Izard's theoretical predictions, emotionality correlated with emotion processing. In particular, the happiness component of emotionality correlated with emotion attribution accuracy and empathy, the anger component correlated with anger attribution bias and empathy, and the fear component correlated with fear attribution bias. Multiple emotion processing deficits—including emotion attribution accuracy, anger attribution bias, and self-report of empathy—placed children at risk for heightened levels of teacher-reported aggression. Mediational analyses revealed that an emotion processing risk index fit a model of significant partial mediation between happiness and aggression but not between anger and aggression. The results suggest the multifaceted manner in which children's emotion experiences may influence the development of aggressive tendencies.The authors thank the teachers, staff, parents, and students of the Smyrna, DE, school district for their enthusiastic participation in this project and the dedicated work of Fran Haskins and our many research assistants at the University of Delaware.

This paper presents experimental tests of the Oregon delinquency model applied within a randomized design of an at-risk sample of single mothers and their elementary school-aged sons. In the theoretical model, ineffective parenting practices and deviant peer association serve as the primary mechanisms for growth in adolescent delinquent behavior and early arrests. Multiple-method assessments of 238 mothers and sons include delinquency as measured by teacher reports and official arrest records, parenting skills measured by observations of parent–child interactions, and deviant peer association as reported by focal boys. Analyses of the 9-year follow-up data indicate that the Oregon model of parent management training significantly reduced teacher-reported delinquency and police arrests for focal boys. As hypothesized, the experiments demonstrated that improving parenting practices and reducing contacts with deviant peers served as mediating mechanisms for reducing rates of adolescent delinquency. As predicted, there was also a significant delay in the timing of police arrests for youth in the experimental as compared to the control group.

By adolescence, appraisal of one's past life experience becomes critical to the stage-salient issue of identity formation. This study examined adolescents' perceptions of their maltreatment experiences. It scrutinized the combined and unique contribution of five maltreatment types (i.e., physical abuse, sexual abuse, psychological abuse, neglect, and exposure to family violence) to variance in adolescent adjustment. It was predicted that these maltreatment types would account for significant variance in adjustment when controlling for the context variables of age, sex, socioeconomic status, IQ, and stressful life events. Adolescents (N = 160, aged 11–17) were randomly selected from the open caseload of a child protection agency. Participants completed global severity ratings regarding their experiences of the five types of maltreatment, as well as a battery of measures assessing self- and caretaker-reported externalizing and internalizing symptomatology. The youths' maltreatment ratings significantly predicted self-reported adjustment, even when controlling for all context variables. Psychological maltreatment was the most predictively potent maltreatment type, and enhanced the predictive utility of other maltreatment types. Significant sex differences in the sequelae of perceived maltreatment were evident. Also, interactions between youths' ratings and those obtained from CPS files were detected. The findings were consistent with recent research in child maltreatment, and contribute to our understanding of developmental psychopathology among adolescents.

We report a graded relationship between neighborhood socioeconomic status (SES) and children's antisocial behavior that (a) can be observed at school entry, (b) widens across childhood, (c) remains after controlling for family-level SES and risk, and (d) is completely mediated by maternal warmth and parental monitoring (defined throughout as supportive parenting). The children were participants in the Environmental Risk Longitudinal Twin Study (N = 2,232), which prospectively tracked the development of children and their neighborhoods across childhood. Direct and independent effects of neighborhood-level SES on children's antisocial behavior were observed as early as age 5, and the gap between children living in deprived versus more affluent neighborhoods widened as children approached adolescence. By age 12, the effect of neighborhood SES on children's antisocial behavior was as large as the effect observed for our most robust predictor of antisocial behavior: sex (Cohen d = 0.51 when comparing children growing up in deprived vs. more affluent neighborhoods in comparison to Cohen d = 0.53 when comparing antisocial behavior among boys vs. girls). However, these relatively large differences in children's levels and rate of change in antisocial behavior across deprived versus more affluent neighborhoods were completely mediated by supportive parenting practices. The implications of our findings for studying and reducing socioeconomic disparities in antisocial behavior among children are discussed.

Many young people who are mistreated by an adult, victimized by bullies, criminally assaulted, or who witness domestic violence react to this violence exposure by developing behavioral, emotional, or learning problems. What is less well known is that adverse experiences like violence exposure can lead to hidden physical alterations inside a child's body, alterations that may have adverse effects on life-long health. We discuss why this is important for the field of developmental psychopathology and for society, and we recommend that stress-biology research and intervention science join forces to tackle the problem. We examine the evidence base in relation to stress-sensitive measures for the body (inflammatory reactions, telomere erosion, epigenetic methylation, and gene expression) and brain (mental disorders, neuroimaging, and neuropsychological testing). We also review promising interventions for families, couples, and children that have been designed to reduce the effects of childhood violence exposure. We invite intervention scientists and stress-biology researchers to collaborate in adding stress-biology measures to randomized clinical trials of interventions intended to reduce effects of violence exposure and other traumas on young people.

This research investigated the developmental stages (pubertal status) and contexts (early or late timing relative to peers, and a context of stressful versus supportive peer relationships) in which the sex difference in depression unfolds. A sample of 158 youth (ages 9.6–14.8) and their caregivers provided information at two waves, 1 year apart, on puberty, peer stress, and depression. Pubertal status and timing (actual and perceived) interacted with sex to predict depression. Sex differences in depression were evident at particular levels of pubertal status and timing, both actual and perceived. Depression was associated with more mature pubertal status and early timing (both actual and perceived) in girls, but with less mature pubertal status and late timing (actual and perceived) in boys. These patterns held concurrently, and often over time, particularly in a context of stressful peer relationships (peer stress moderated sex-differentiated associations between puberty and depression). Of note, there were no significant sex differences in depression at any particular age. Thus, this research highlights important distinctions among the contributions of age, pubertal status, pubertal timing, and perceived timing to the sex difference in adolescent depression. More broadly, these findings contribute to our growing understanding of the interactions among physical, social, and psychological processes involved in the sex difference in adolescent depression.

Borderline personality disorder (BPD) is a highly prevalent, chronic, and debilitating psychiatric problem characterized by a pattern of chaotic and self-defeating interpersonal relationships, emotional lability, poor impulse control, angry outbursts, frequent suicidality, and self-mutilation. Recently, psychopathology researchers and theorists have begun to understand fundamental aspects of BPD such as unstable, intense interpersonal relationships, feelings of emptiness, bursts of rage, chronic fears of abandonment and intolerance for aloneness, and lack of a stable sense of self as stemming from impairments in the underlying attachment organization. These investigators have noted that the impulsivity, affective lability, and self-damaging actions that are the hallmark of borderline personality occur in an interpersonal context and are often precipitated by real or imagined events in relationships. This article reviews attachment theory and research as a means of providing a developmental psychopathology perspective on BPD. Following a brief review of Bowlby's theory of attachment, and an overview of the evidence with respect to the major claims of attachment theory, I discuss individual differences, the evidence that these differences are rooted in patterns of interaction with caregivers, and how these patterns have important implications for evolving adaptations and development. Following this discussion, I present recent work linking attachment theory and BPD, focusing on the implications for understanding the etiology and treatment of BPD. In conclusion, I address some of the salient issues that point to the direction for future research efforts.

A person-oriented approach was adopted to examine joint developmental trajectories of physical and indirect aggression. Participants were 1183 children aged 2 years at the initial assessment and followed over 6 years. Most children followed either low or declining trajectories of physical aggression (PA), but 14.6% followed high stable trajectories. Approximately two-thirds of participants followed low indirect aggression (IA) trajectories (67.9%), and one-third (32.1%) followed high rising trajectories. The results combining both PA and IA group memberships indicate that most children (62.1%) exhibit desisting levels of PA and low levels of IA. A significant proportion followed a trajectory of moderately desisting PA and rising IA (14.2%), and 13.5% followed high level trajectories of both forms of aggression. Virtually no children were high on one type and low on the other. Multinomial regressions analyses were used to predict joint trajectory group membership from selected child and family variables measured at 2 years. Young motherhood and low income predicted membership in the high PA-high IA trajectory, but only hostile parenting remained significant after family processes variables were entered in the model. Being a boy, young motherhood, and hostile parenting were generally associated with higher levels of PA. Girls were more likely than boys to follow a trajectory of desisting PA and rising IA. The results suggest that some children, mostly girls, reduce their use of PA and tend to increase their use of IA, and that highly physically aggressive children also tend to be highly indirectly aggressive. Early family risk characteristics and hostile parenting interfere with the socialization of aggression.This research was supported by research grants from Quebec's FQRSC and CIQSS, Canada's CIHR and SSHRC, the Canadian Institute for Advanced Research, the Molson foundation, St-Justine Hospital's Research Center, and the University of Montréal. We thank Danielle Forest (University of Montréal) for her work on data analysis and Franck Larouche (Statistics Canada) for his sustained commitment to assist us in managing the data.

Accumulating research suggests that psychopathy can be disaggregated into low-anxious primary and high-anxious secondary variants, and this research may be important for understanding antisocial youths with callous–unemotional traits. Using model-based cluster analysis, the present study disaggregated 165 serious male adolescent offenders (M age = 16) with high scores on the Youth Psychopathic Traits Inventory into primary and secondary variants based on the presence of anxiety. The results indicated that the secondary, high-anxious variant was more likely to show a history of abuse and scored higher on measures of emotional and attentional problems. On a picture version of the dot-probe task, the low-anxious primary variant was not engaged by emotionally distressing pictures, whereas the high-anxious secondary variant was more attentive to such stimuli (Cohen d = 0.71). Although the two groups differed as hypothesized from one another, neither differed significantly in their emotional processing from a nonpsychopathic control group of offending youth (n = 208). These results are consistent with the possibility that the two variants of psychopathy, both of which were high on callous–unemotional traits, may have different etiological pathways, with the primary being more related to a deficit in the processing of distress cues in others and the secondary being more related to histories of abuse and emotional problems.

This research examined three possible models to explain how childhood social adversity and recent stress interact to predict depression in youth: stress sensitization, stress amplification, and stress inoculation. Drawing from a stress-sensitization theory of depression, we hypothesized that exposure to childhood adversity, in the form of disruptions in critical interpersonal relationships, would lower youths' threshold for depressive reactions to recent interpersonal stress. We expected that this pattern of stress sensitization would be most salient for girls negotiating the pubertal transition. These hypotheses were examined in two studies: a longitudinal, questionnaire-based investigation of 399 youth (M = 11.66 years) and a concurrent, interview-based investigation of 147 youth (M = 12.39 years). Findings supported the role of stress-sensitization processes in pubertal girls and prepubertal boys, and stress-amplification processes in prepubertal girls. Childhood social adversity specifically predicted sensitization to recent interpersonal, but not noninterpersonal, stress. These findings build on prior theory and research by suggesting that early adversity exerts context-specific effects that vary across gender and development. Future research will need to identify the specific mechanisms underlying this stress-sensitization process.We express our appreciation to the students, teachers, and principals of the participating schools for their facilitation of this study. We also thank Constance Hammen, Kate Harkness, and Eva Pomerantz for their helpful comments; Melissa Caldwell, Alyssa Clark, Colleen Conley, Alison Dupre, Heidi Gazelle, and Kathryn Kurlakowsky for their assistance in data collection and management; and Shannon Daley for consultation on statistical analyses. This research was supported by a University of Illinois Research Board Beckman Award, a William T. Grant Foundation Faculty Scholars Award, and National Institute of Mental Health Grant MH59711 awarded to Karen D. Rudolph.

Mundy and Sigman (1989) present a challenge to the metarepresentational theory of autism. Their argument holds if it is assumed that the capacity for metarepresentation only emerges at 12–24 months old in normal development, as manifested in pretend play. However, I present reasons for postulating that the capacity for metarepresentation may be present from as early as 7–9 months of age, manifested in joint-attention behaviors. If this account has any validity, then the metarepresentational theory of autism is unaffected by Mundy and Sigman's challenge. In addition, I highlight some problems in Mundy and Sigman's alternative model of autism. These criticisms aside, their article is without doubt important and opens up critical questions both for models of the origins of autism and of a theory of mind in normal development.

Childhood adversity is associated with increased risk for psychopathology. Neurodevelopmental pathways underlying this risk remain poorly understood. A recent conceptual model posits that childhood adversity can be deconstructed into at least two underlying dimensions, deprivation and threat, that are associated with distinct neurocognitive consequences. This model argues that deprivation (i.e., a lack of cognitive stimulation and learning opportunities) is associated with poor executive function (EF), whereas threat is not. We examine this hypothesis in two studies measuring EF at multiple levels: performance on EF tasks, neural recruitment during EF, and problems with EF in daily life. In Study 1, deprivation (low parental education and child neglect) was associated with greater parent-reported problems with EF in adolescents (N = 169; 13–17 years) after adjustment for levels of threat (community violence and abuse), which were unrelated to EF. In Study 2, low parental education was associated with poor working memory (WM) performance and inefficient neural recruitment in the parietal and prefrontal cortex during high WM load among adolescents (N = 51, 13–20 years) after adjusting for abuse, which was unrelated to WM task performance and neural recruitment during WM. These findings constitute strong preliminary evidence for a novel model of the neurodevelopmental consequences of childhood adversity.

Evidence indicates that maternal prenatal distress predicts problematic health and behavioral outcomes in children as well as infant/child cortisol levels and negative emotionality as reviewed here. Evidence that these physiological and behavioral characteristics themselves moderate environmental effects on development in a “for better and for worse” manner consistent with Belsky's differential susceptibility hypothesis and Boyce and Ellis' notions of biological sensitivity to context raises the prospect that susceptibility to rearing is a function of nurture (i.e., fetal environment), consistent with Boyce and Ellis' proposal that plasticity can be shaped by developmental experience. This hypothesis is supported by new findings from the National Institute of Child Health and Human Development Study of Early Child Care and Youth Development showing that low birth weight, a marker for an adverse prenatal environment, predicts infant difficult temperament, which is a susceptibility factor that we previously showed as moderating, in a for better and for worse manner, the effects of parenting and child care quality on socioemotional functioning. Moreover, recent Gene × Environment interaction research raises the prospect that some fetuses may be more susceptible to such “prenatal programming of postnatal plasticity” as a result of their genetic makeup. If this proves true, it will be consistent with the conclusion that early developmental plasticity is a function of both nature and nurture and may be evolutionarily adaptive, a further possibility considered in the discussion.

The concurrent and predictive influence of deviant peers on boys' disruptive and delinquent behavior was examined in a community sample of fourth- and seventh-grade boys, who were followed-up over six data waves. Analyses were conducted separately for three different types of behavior problems: authority conflict, covert, and overt disruptive behavior. Consistent with the existing literature, concurrent relations between peers' and boys' disruptive behavior were expected to be significant. A more informative test, however, was whether exposure to deviant peers resulted in boys' subsequent initiation of disruptive behavior. Although peer influences were expected in the predictive analyses, the relations were hypothesized to differ by type of behavior. The potential moderating effects of hyperactivity and poor parenting practices were also examined to test the hypothesis that boys who are already at risk for behavior problems will be more susceptible to deviant peer influence. Results supported the significant concurrent and predictive relation between exposure to deviant peers and boys' engagement in disruptive and delinquent behavior. There were no significant moderating effects of attention-deficit hyperactivity disorder (ADHD) or parenting practices on peer influence.

Children with autism are developmentally delayed in following the direction of another person's gaze in social situations. A number of studies have measured reflexive orienting to eye gaze cues using Posner-style laboratory tasks in children with autism. Some studies observe normal patterns of cueing, suggesting that children with autism are alert to the significance of the eyes, whereas other studies reveal an atypical pattern of cueing. We review this contradictive evidence to consider the extent to which sensitivity to gaze is normal, and ask whether apparently normal performance may be a consequence of atypical (nonsocial) mechanisms. Our review concludes by highlighting the importance of adopting a developmental perspective if we are to understand the reasons why people with autism process eye gaze information atypically.

There is clear evidence that the mother's stress, anxiety, or depression during pregnancy can alter the development of her fetus and her child, with an increased risk for later psychopathology. We are starting to understand some of the underlying mechanisms including the role of the placenta, gene–environment interactions, epigenetics, and specific systems including the hypothalamic–pituitary–adrenal axis and cytokines. In this review we also consider how these effects may be different, and potentially exacerbated, in different parts of the world. There can be many reasons for elevated prenatal stress, as in communities at war. There may be raised pregnancy-specific anxiety with high levels of maternal and infant death. There can be raised interpersonal violence (in Afghanistan 90.2% of women thought that “wife beating” was justified compared with 2.0% in Argentina). There may be interactions with nutritional deficiencies or with extremes of temperature. Prenatal stress alters the microbiome, and this can differ in different countries. Genetic differences in different ethnic groups may make some more vulnerable or more resilient to the effects of prenatal stress on child neurodevelopment. Most research on these questions has been in predominantly Caucasian samples from high-income countries. It is now time to understand more about prenatal stress and psychopathology, and the role of both social and biological differences, in the rest of the world.