Data are presented concerning the early predictors of adaptational success and failure among 72 children attending their 1st years of elementary school in a violent Washington, D.C., neighborhood. Adaptational failures were defined as those children who were doing poorly or failing in school and rated by their parents as suffering clinically significant levels of behavior problems. Adaptational successes were defined as children whose performance as students was rated in the average to excellent range and whose parent-rated levels of behavior problems were within the normal range. Despite the fact that these children were being raised in violent neighborhoods, had been exposed to relatively high levels of violence in the community, and were experiencing associated distress symptoms, community violence exposure levels were not predictive of adaptational failure or success. Instead, adaptational status was systematically related to characteristics of the children's homes. More specifically, the children's chances of adaptational failure rose dramatically as a function of living in unstable and/or unsafe homes. Moreover, it was not the mere accumulation of environmental adversities that gave rise to adaptational failure in these children. Rather, it was only when such adversities contaminated or eroded the stability and/or safety levels of the children's homes that the odds of their adaptational failure increased. We argue that this erosion of the quality of the child's microsystem (i.e., family) by adversities and pressures in the exosystem (i.e., community) is not an inevitable process. Although not yet well understood, it is a process over which families have and must exercise control. The implications of these data for improving children's chances of physical, psychological, and academic survival in violent neighborhoods are considered.

An overview is provided of recent twin, molecular genetic, and magnetic resonance imaging studies that are helping to inform a model of developmental vulnerability to adult psychopathy. Although the current evidence base suggests that children with high levels of callous–unemotional traits are genetically and neurocognitively vulnerable to developing psychopathic and antisocial behaviors, existing research also clearly indicates that environmental influences play an important role. One potential implication is that interventions for children with antisocial behavior and callous–unemotional traits may need to be tailored to take into account their distinct pattern of neurocognitive vulnerability, as revealed by developmental neuroimaging studies. Specifically, interventions that pursue punishment-oriented or explicit empathy induction strategies may be less effective with this group of antisocial children. By contrast, preliminary evidence suggests that enhancing positive parenting and parental involvement, as well as applying consistent rewards may represent more promising intervention approaches.

This study focused on empathic and prosocial orientations in preschool children who vary in externalizing problems. Children were categorized as low, moderate, or high risk for developing disruptive behavior disorders, depending on severity of current behavior problems. Hypothetical and real encounters with others in distress were used to examine children's affect, behavior, autonomic activity, and social cognitions. When children witnessed someone in distress, empathic concern and prosocial behaviors were present at similar levels for all risk groups. However, moderate and high-risk children were less able than low-risk children to remain positively engaged with distress victims. Girls showed more prosocial behavior than boys, and boys showed more anger than girls. During sadness mood inductions to assess autonomic activity, risk groups did not differ on heart rate or vagal tone. Girls showed higher skin conductance than boys, with high-risk girls showing the highest levels. Higher heart rate (and heart rate deceleration) predicted empathic concern and prosocial behavior, whereas lower heart rate was associated with aggression and avoidance, irrespective of risk. Although biological correlates of emotions and behaviors that reflect caring versus indifference to others' distress are identified, they do not support an early direct link to externalizing psychopathologies.

We studied the developmental trends of temperament and character in a longitudinal population-based sample of Finnish men and women aged 20–45 years using the Temperament and Character Inventory model of personality. Personality was assessed in 1997, 2001, and 2007 (n = 2,104, 2,095, and 2,056, respectively). Mean-level changes demonstrated qualitatively distinct developmental patterns for character (self-directedness, cooperativeness, and self-transcendence) and temperament (novelty seeking, harm avoidance, reward dependence, and persistence). Character developed toward greater maturity, although self-transcendence decreased with age. However, self-transcendence was the strongest predictor of overall personality change. Cohort effects indicated lower level of self-transcendence and higher level of self-directedness and cooperativeness in younger birth cohorts. Regarding temperament, novelty seeking decreased and persistence increased slightly with age. Both high novelty seeking and high persistence predicted overall personality change. These findings suggest that temperament and character traits follow different kinds of developmental trajectories.

This review discusses neurobiological studies of oppositional defiant disorder and conduct disorder within the conceptual framework of three interrelated mental domains: punishment processing, reward processing, and cognitive control. First, impaired fear conditioning, reduced cortisol reactivity to stress, amygdala hyporeactivity to negative stimuli, and altered serotonin and noradrenaline neurotransmission suggest low punishment sensitivity, which may compromise the ability of children and adolescents to make associations between inappropriate behaviors and forthcoming punishments. Second, sympathetic nervous system hyporeactivity to incentives, low basal heart rate associated with sensation seeking, orbitofrontal cortex hyporeactiviy to reward, and altered dopamine functioning suggest a hyposensitivity to reward. The associated unpleasant emotional state may make children and adolescents prone to sensation-seeking behavior such as rule breaking, delinquency, and substance abuse. Third, impairments in executive functions, especially when motivational factors are involved, as well as structural deficits and impaired functioning of the paralimbic system encompassing the orbitofrontal and cingulate cortex, suggest impaired cognitive control over emotional behavior. In the discussion we argue that more insight into the neurobiology of oppositional defiance disorder and conduct disorder may be obtained by studying these disorders separately and by paying attention to the heterogeneity of symptoms within each disorder.

The ability to effectively regulate emotions and a secure attachment style are critical for maintaining mental health across the life span. The experience of childhood maltreatment interferes with normal development of emotional regulation and dramatically increases risk for a wide range of psychiatric disorders in adulthood. The central nervous system oxytocin systems are critically involved in mediating social attachment and buffering psychophysiological responses to stress. We therefore investigated the impact of childhood maltreatment and an oxytocin receptor (OXTR) single nucleotide polymorphism (rs53576) and their interaction on emotional dysregulation and attachment style in adulthood in a sample of low-income, African American men and women recruited from primary care clinics of an urban, public hospital. Consistent with prior research, we found that the severity of childhood maltreatment was associated with increased levels of emotional dysregulation in adulthood. Childhood maltreatment was also positively associated with ratings of disorganized/unresolved adult attachment style and negatively associated with ratings of secure adult attachment style. There was no direct association between rs53576 and emotional dysregulation or ratings of adult attachment style. However, there were significant interactions between rs53576 and childhood maltreatment in predicting level of adult emotional dysregulation and attachment style. Specifically, G/G genotype carriers were at risk for increased emotional dysregulation when exposed to three or more categories of childhood abuse. In addition, G/G genotype carriers exhibited enhanced disorganized adult attachment style when exposed to severe childhood abuse compared to A/A and A/G carriers. Our findings suggest that A allele carriers of OXTR rs53576 are resilient against the effects of severe childhood adversity, by protection against emotional dysregulation and disorganized attachment.

Using data from two long-term longitudinal projects, we investigated reciprocal relations between maternal reports of physical discipline and teacher and self-ratings of child externalizing behavior, accounting for continuity in both discipline and externalizing over time. In Study 1, which followed a community sample of 562 boys and girls from age 6 to 9, high levels of physical discipline in a given year predicted high levels of externalizing behavior in the next year, and externalizing behavior in a given year predicted high levels of physical discipline in the next year. In Study 2, which followed an independent sample of 290 lower income, higher risk boys from age 10 to 15, mother-reported physical discipline in a given year predicted child ratings of antisocial behavior in the next year, but child antisocial behavior in a given year did not predict parents' use of physical discipline in the next year. In neither sample was there evidence that associations between physical discipline and child externalizing changed as the child aged, and findings were not moderated by gender, race, socioeconomic status, or the severity of the physical discipline. Implications for the reciprocal nature of the socialization process and the risks associated with physical discipline are discussed.

Child maltreatment and polymorphisms of the serotonin transporter (5-HTT) and monoamine oxidase A (MAOA) genes were examined in relation to depressive symptomatology. Adolescents (M age = 16.7 years) from low socioeconomic backgrounds with a history of child maltreatment (n = 207) or no such history (n = 132) were interviewed and provided buccal cells for genetic analysis. Gene × environment interactions were observed. Heightened depressive symptoms were found only among extensively maltreated youth with low MAOA activity. Among comparably maltreated youth with high MAOA activity, self-coping strategies related to lower symptoms. Sexual abuse and the 5-HTT short/short genotype predicted higher depression, anxiety, and somatic symptoms. This Gene × Environment interaction was further moderated by MAOA activity level. The results highlight the protective functions of genetic polymorphisms and coping strategies in high risk youth and offer direction for understanding resilience and its promotion from a multiple levels of analysis perspective.

The hypothalamic–pituitary–adrenal (HPA) axis is a primary mechanism in the allostatic process through which early life stress (ELS) contributes to disease. Studies of the influence of ELS on children's HPA axis functioning have yielded inconsistent findings. To address this issue, the present study considers multiple types of ELS (maternal depression, paternal depression, and family expressed anger), mental health symptoms, and two components of HPA functioning (traitlike and epoch-specific activity) in a long-term prospective community study of 357 children. ELS was assessed during the infancy and preschool periods; mental health symptoms and cortisol were assessed at child ages 9, 11, 13, and 15 years. A three-level hierarchical linear model addressed questions regarding the influences of ELS on HPA functioning and its covariation with mental health symptoms. ELS influenced traitlike cortisol level and slope, with both hyper- and hypoarousal evident depending on type of ELS. Further, type(s) of ELS influenced covariation of epoch-specific HPA functioning and mental health symptoms, with a tighter coupling of HPA alterations with symptom severity among children exposed previously to ELS. Results highlight the importance of examining multiple types of ELS and dynamic HPA functioning in order to capture the allostatic process unfolding across the transition into adolescence.

This study of 71 low-income mothers and infants examined whether the disorganized/disoriented (D) infant attachment classification is best viewed as a single category or whether at least two subgroups exist, corresponding to the forced-secure and forced-insecure alternate classifications. Correlates of the D classification as a whole, and of the two subtypes of disorganized behavior, were examined in five domains, including 6-month stability, maternal childhood history of loss, severity of maternal psychosocial risk, maternal behavior toward the infant at home, and infant mental development. Results indicated that the two subtypes of disorganized infant attachment behavior differed in age of emergence, maternal childhood history, severity of associated family risk factors, and the extent of the mother's lack of involvement with the infant at home. Across both D subtypes, disorganization of attachment strategies was associated with less optimal maternal behavior at home and with decreased mental development scores at 18 months. Results are discussed in relation to Main and Hesse's (1990) theory of the role of fear-inducing parental behavior in the genesis of disorganized infant attachment behavior and in relation to Aber, Allen, Carlson, and Cicchetti's (1989) concept of secure readiness to learn.

Williams syndrome is a rare genetic disorder in which, it is claimed, language abilities are relatively strong despite mild to moderate mental retardation. Such claims have, in turn, been interpreted as evidence either for modular preservation of language or for atypical constraints on cognitive development. However, this review demonstrates that there is, in fact, little evidence that syntax, morphology, phonology, or pragmatics are any better than predicted by nonverbal ability, although performance on receptive vocabulary tests is relatively good. Similarly, claims of an imbalance between good phonology and impaired or atypical lexical semantics are without strong support. There is, nevertheless, consistent evidence for specific deficits in spatial language that mirror difficulties in nonverbal spatial cognition, as well as some tentative evidence that early language acquisition proceeds atypically. Implications for modular and neuroconstructivist accounts of language development are discussed.The preparation of this paper was supported by the Williams Syndrome Foundation (United Kingdom) and the Medical Research Council. I thank Courtenay Norbury and Kate Nation for comments on the manuscript and Chris Jarrold, Jill Boucher, and Teresa McCormack for many useful discussions.

This study examined the effects of stressful environments on physiological and affective functioning among 131 maltreated school-aged children attending a summer day camp. Sixty-six nonmaltreated children also attending the camp served as a comparison group. Salivary Cortisol measures were obtained daily at 10:00 a.m. and at 4:00 p.m. Depression was measured using the Child Depression Inventory. Children with scores of 19 or higher were classified as depressed. Internalizing and externalizing behavior problems were determined from the Teacher Report Form of the Child Behavior Checklist. Children with t scores of 70 or higher were classified as having clinical levels of these problems. Maltreated children had slightly elevated afternoon Cortisol concentrations, but their morning concentrations did not differ significantly from those of nonmaltreated children. Neither clinical levels of depression, internalizing, or externalizing problems were predictive of the elevated afternoon values. Depression among maltreated children was, however, associated with altered activity of the hypothalamic-pituitary-adrenocortical (HPA) axis. Depressed maltreated children had lower morning Cortisol concentrations compared to nondepressed maltreated children and were more likely to show a rise rather than the expected decrease in Cortisol from morning to afternoon. These data replicated earlier findings. There was no evidence that depressed, nonmaltreated children exhibited this change in diurnal Cortisol activity.

The present study attempted to determine the direction and etiology of the robust relationship between childhood externalizing (EXT) symptoms and parent–child conflict using a genetically informative longitudinal model and data from the ongoing Minnesota Twin Family Study. Participants consisted of 1,506 same-sex twins assessed at ages 11 and 14, and their parents. The relationship between EXT and parent–child conflict from ages 11 to 14 was examined within a biometrical cross-lagged design. The results revealed three primary findings: first, the stability of conflict and externalizing over time is largely, although not solely, a result of genetic factors. Second, there appears to be a bidirectional relationship between conflict and EXT over time, such that both conflict and EXT at 11 independently predict the other 3 years later. Finally, the results are consistent with the notion that parent–child conflict partially results from parental responses to their child's heritable externalizing behavior, while simultaneously contributing to child externalizing via environmental mechanisms. These results suggest a “downward spiral” of interplay between parent–child conflict and EXT, and offer confirmation of a (partially) environmentally mediated effect of parenting on child behavior.This research was funded in part by USPHS grants (DA05147, DA13240, AA09367, AA00175, MH 65137), a National Institutes of Mental Health training grant (MH17069 to S.A.B.), and a Doctoral Dissertation Fellowship (S.A.B.). We also thank Hennepin County Medical Center in Minneapolis for the research time that enabled the primary author to conduct this study.

This paper examines the relationship between self-esteem in adolescence and later mental health, substance use, and life and relationship outcomes in adulthood. The investigation analyzed data from a birth cohort of approximately 1,000 New Zealand young adults studied to the age of 25. Lower levels of self-esteem at age 15 were associated with greater risks of mental health problems, substance dependence, and lower levels of life and relationship satisfaction at ages 18, 21, and 25. Adjustment for potentially confounding factors reduced the strength of these associations to either moderate or statistically nonsignificant levels. It was concluded that the effects of self-esteem during adolescence on later developmental outcomes were weak, and largely explained by the psychosocial context within which self-esteem develops.

The family is one of the primary contexts of child development. Marital and parent–child conflict (family conflict) are common and predict a wide range of negative behavioral and emotional outcomes in children. Thus, an important task for developmental researchers is to identify the processes through which family conflict contributes to children's psychological maladjustment, as well as vulnerability and protective factors in the context of family conflict. In the current paper, we aim to advance a conceptual model that focuses on indices of children's autonomic nervous system (ANS) functioning that increase vulnerability or provide protection against psychological maladjustment in the context of family conflict. In doing so, we provide a selective review that reflects the state of the science linking family conflict, children's ANS activity, and child psychological adjustment, and offer directions and guidance for future research. Our hope is to accelerate research at the intersection of family conflict and ANS functioning to advance understanding of risk and resilience among children.

The secure working model classification of adult attachment, as derived from Main and Goldwyn's (in press) Adult Attachment Interview scoring system, was considered in terms of earned-security and continuous-security. Earned-security was a classification given to adults who described difficult, early relationships with parents, but who also had current secure working models as indicated by high coherency scores; continuous-security referred to a classification in which individuals described secure early attachment relationship with parents and current secure working models. Working models of attachment were classified as earned-secure, continuous-secure, or insecure in a sample of 40 parents of preschool children. Comparisons among the classifications were conducted on a measure of depressive symptoms and two sets of ratings of observed parenting styles. Adults with earned-secure classifications had comparable depressive symptomatology to insecures, with 30% of the insecures, 40% of the earned-secures, and only 10% of the continuous-secures having scores exceeding the clinical cut-off. The rate of depressive symptomatology in the earned-secure group suggests that reconstructions of past difficulties may remain emotional liabilities despite a current secure working model. With regard to parenting styles with their preschoolers, the behavior of earned-secure parents was comparable to that of the continuous-secures. This refinement in conceptualizing secure working models suggests ways for understanding variation in pathways to competent parenting as well as a possible perspective on how adults' adverse early experiences may continue to place them and their children at risk.

This article examines what it means to have a self. My focus is on the essential components of self-experience, the kind of psychological architecture required to construct a self, rather than on the configurations or qualities of individual “selves.” I adopt a developmental perspective and indicate how early childhood autism may afford unique insights into the role of perceptual-affective and interpersonal experience in determining the normal child's developing awareness of self.

We hypothesized that hyperactivity defines the first stage and that antisocial problems define a second stage in a progression that leads eventually to early-onset delinquency. As expected, a structural equation model (SEM) showed that a latent construct for hyperactivity was significantly related to a latent construct for antisocial problems. We hypothesized that this path reflected a shared mechanism, disrupted parental discipline. A second SEM showed that the relation between hyperactivity and antisocial behavior really reflected a shared disruption in parental discipline. A third SEM showed that having antisocial parents was uniquely correlated with antisocial children but not with hyperactivity. A fourth SEM showed that early-onset delinquency was predicted by a latent construct for antisocial child; but when this was partialed out, the contribution for hyperactivity was nonsignificant.

Recent studies have focused on the behavioral and neurobiological sequella of exposure to early adverse events. We hypothesize that early adverse experiences result in an increased sensitivity to the effects of stress later in life and render an individual vulnerable to stress-related psychiatric disorders. This vulnerability may be mediated by persistent changes in corticotropin-releasing-factor (CRF)-containing neurons, the hypothalamic–pituitary–adrenal axis, and the sympathetic nervous system. We therefore present an overview of the CRF system and its role as a mediator in the development of the stress response, major depression, and posttraumatic stress disorder. The literature pertaining to behavioral and neurobiological alterations associated with exposure to early adverse life events in rodents, nonhuman primates, and humans is reviewed. We focus on animal models that precipitate depressive and anxiety symptoms while producing neuroendocrine alterations that mimic those seen in adults with those disorders. The literature integrating neurobiological and behavioral consequences of early life stress is also reviewed, focusing primarily on infants born to mothers with depression and on infants who were abused or neglected.

This article presents an overview of work conducted at the Institute of Psychiatry over the past 30 years on childhood depression. The work began with the basic question of definition and measurement. Epidemiological studies showed that depressive symptoms were quite common in children and were a good, if nonspecific, indicator of psychological disturbance. Further work in both epidemiological and clinical samples provided some evidence for the validity of a depressive syndrome. However, this work also showed that these depressive syndromes represented a heterogeneous group of phenomena. The validity of major depressive disorder in children was therefore tested further in longitudinal and family-genetic studies. These studies supported the validity of the concept but confirmed that there was heterogeneity in respect to both developmental stage at the time of onset and comorbidity with conduct disorder. We concluded that there are probably several different kinds of depressive syndromes in children. Some are strongly linked with depressive disorders in adulthood, but others are probably better conceptualized as part of another psychopathological problem altogether.