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.

This paper examined whether childhood maltreatment increases the risk of living in neighborhoods with less desirable characteristics (i.e., more disorder and disadvantage, less social cohesion, social control and advantage, and fewer resources) in middle adulthood and whether these neighborhood characteristics influence subsequent illicit drug use. Using a prospective cohort design study, court documented cases of childhood abuse and neglect and matched controls (n = 833) were first interviewed as young adults (mean age = 29 years) from 1989 to 1995 and again in middle adulthood from 2000 to 2002 (mean age = 40 years) and 2003 to 2005 (mean age = 41 years). In middle adulthood, individuals with histories of childhood abuse and neglect were more likely to live in neighborhoods with more disorder and disadvantage and less social cohesion and advantage compared to controls and to engage in illicit drug use during the past year. Path analyses showed an indirect effect on illicit drug use via neighborhood disorder among maltreated children, even after accounting for drug abuse symptoms in young adulthood, although this was sex specific and race specific, affecting women and Whites. Overall, child abuse and neglect places children on a negative trajectory that dynamically influences negative outcomes at multiple levels into middle adulthood.

Children born to older fathers are at higher risk to develop severe psychopathology (e.g., schizophrenia and bipolar disorder), possibly because of increased de novo mutations during spermatogenesis with older paternal age. Because severe psychopathology is correlated with antisocial behavior, we examined possible associations between advancing paternal age and offspring violent offending. Interlinked Swedish national registers provided information on fathers' age at childbirth and violent criminal convictions in all offspring born from 1958 to 1979 (N = 2,359,921). We used ever committing a violent crime and number of violent crimes as indices of violent offending. The data included information on multiple levels; we compared differentially exposed siblings in within-family analyses to rigorously test causal influences. In the entire population, advancing paternal age predicted offspring violent crime according to both indices. Congruent with a causal effect, this association remained for rates of violent crime in within-family analyses. However, in within-family analyses, we found no association with ever committing a violent crime, suggesting that factors shared by siblings (genes and environment) confounded this association. Life-course persistent criminality has been proposed to have a partly biological etiology; our results agree with a stronger biological effect (i.e., de novo mutations) on persistent violent offending.

Previous research documented a robust link between difficulties in self-regulation and development of externalizing problems (i.e., aggression and delinquency). In this study, we examined the longitudinal additive and interactive genetic and environmental covariation underlying this well-established link using a twin design. The sample included 131 pairs of monozygotic twins and 173 pairs of same-sex dizygotic twins who participated in three waves of annual assessment. Mothers and fathers provided reports of externalizing problems. Teacher report and observer rating were used to assess twin's attention regulation. The etiology underlying the link between externalizing problems and attention regulation shifted from a common genetic mechanism to a common environmental mechanism in the transition across middle childhood. Household chaos moderated the genetic variance of and covariance between externalizing problems and attention regulation. The genetic influence on individual differences in both externalizing problems and attention regulation was stronger in more chaotic households. However, higher levels of household chaos attenuated the genetic link between externalizing problems and attention regulation.

Prenatal androgen exposure has been associated with aggressive behavior in adults. It is less clear whether this association holds for childhood externalizing behavior. This study tests the hypothesis that increased prenatal androgen exposure is associated with aggressive behavior and attention problems in childhood. The ratio of the length of the second finger digit relative to the fourth digit, which is a marker for prenatal testosterone exposure, was assessed in 239 male and female fifth grade schoolchildren from Jintan, China, together with parent and teacher ratings of aggression and attention problems. Increased aggression and attention problems were both significantly associated with a lower ratio of the length of the second finger digit relative to the fourth digit ratios in boys but not girls. The effects remained significant after controlling for early adversity. These findings are the first to establish a relationship between an indirect indicator of fetal androgen exposure and any child psychopathology in Chinese children, and the observed effect size in boys was stronger than in male adults in Western studies. The results provide limited cross-cultural support for the importance of prenatal androgen exposure in contributing to the development of externalizing behavior problems in children, and they suggest that such effects may be specific to boys who may be relatively more vulnerable to early prenatal influences.

Early parent–child attachment has been extensively explored as a contributor to children's future adaptive or antisocial outcomes, but the specific developmental mechanisms remain to be fully understood. We examined long-term indirect developmental sequelae of early security in two longitudinal community samples followed from infancy to early school age: the Family Study (102 mothers, fathers, and infants) and the Parent–Child Study (112 mothers and infants). Constructs at multiple levels (child characteristics, parent–child security, parental discipline, and child antisocial outcomes) were assessed using a range of methods (extensive behavioral observations in a variety of settings, informants' ratings). Both studies supported the proposed model of infant attachment as a potent catalyst that moderates future developmental socialization trajectories, despite having few long-term main effects. In insecure dyads, a pattern of coercion emerged between children who were anger prone as toddlers and their parents, resulting in parents' increased power-assertive discipline. Power assertion in turn predicted children's rule-breaking conduct and a compromised capacity to delay in laboratory paradigms, as well as oppositional, disruptive, callous, and aggressive behavior rated by parents and teachers at early school age. This causal chain was absent in secure dyads, where child anger proneness was unrelated to power assertion, and power assertion was unrelated to antisocial outcomes. Early insecurity appeared to act as a catalyst for the parent–child dyad embarking on a mutually adversarial path toward antisocial outcomes, whereas security defused such a maladaptive dynamic. The possible mechanisms of those effects were proposed.

Two studies examined the nature and processes underlying the joint role of interparental aggression and maternal antisocial personality as predictors of children's disruptive behavior problems. Participants for both studies included a high-risk sample of 201 mothers and their 2-year-old children in a longitudinal, multimethod design. Addressing the form of the interplay between interparental aggression and maternal antisocial personality as risk factors for concurrent and prospective levels of child disruptive problems, the Study 1 findings indicated that maternal antisocial personality was a predictor of the initial levels of preschooler's disruptive problems independent of the effects of interparental violence, comorbid forms of maternal psychopathology, and socioeconomic factors. In attesting to the salience of interparental aggression in the lives of young children, latent difference score analyses further revealed that interparental aggression mediated the link between maternal antisocial personality and subsequent changes in child disruptive problems over a 1-year period. To identify the family mechanisms that account for the two forms of intergenerational transmission of disruptive problems identified in Study 1, Study 2 explored the role of children's difficult temperament, emotional reactivity to interparental conflict, adrenocortical reactivity in a challenging parent–child task, and experiences with maternal parenting as mediating processes. Analyses identified child emotional reactivity to conflict and maternal unresponsiveness as mediators in pathways between interparental aggression and preschooler's disruptive problems. The findings further supported the role of blunted adrenocortical reactivity as an allostatic mediator of the associations between parental unresponsiveness and child disruptive problems.

Extremes in fearful temperament have long been associated with later psychopathology and risk pathways. Whereas fearful children are inhibited and anxious and avoid novel events, fearless individuals are disinhibited and more likely to engage in aggressive behavior. However, very few studies have examined fear in infants from a multimethod and prospective longitudinal perspective. This study had the following objectives: to examine behavioral, maternal reported, and physiological indices of fearful temperament in infancy, together with their relations and stability over time; and to establish whether early indices of fear predict fear later in toddlerhood. We also examined the association between behavioral and physiological measures of fear and guilt and whether fear in infancy predicts guilt in toddlers. Finally, we investigated infant risk factors for later psychopathology. We recorded skin conductance level (SCL) and heart rate (HR) and observed children's responses during a Laboratory Temperament Assessment Battery fear paradigm across the first 3 years of life and during a guilt induction procedure at age 3 (N = 70). The results indicate that different measures of infant fear were associated across time. Observed fearlessness in infancy predicted observed fearlessness and low levels of SCL arousal to fear and guilt in toddlers. Low levels of HR and SCL to fear in infancy predicted low levels of physiological arousal to the same situation and to guilt 2 years later. Fear and guilt were significantly associated across measures. Finally, toddlers with clinically significant internalizing problems at age 3 were already notably more fearful in Year 1 as reflected by their significantly higher HR levels. The results indicated that assessments of children in infancy are predictive of how these children react 2 years later and therefore lend support to the idea that the emotional thermostat is set in the first 3 years of life. They also showed, for the first time, that infant fear is a predictor of guilt, which is an emotion that develops later. The implications of these findings for our understanding of developmental psychopathology are discussed.

The present study utilized a multilevel approach to examine developmental trajectories in risk-taking propensity. We examined the moderating role of specific executive function components, attention shifting and inhibitory control, on the link between exuberant temperament in infancy and propensity for risk taking in childhood. Risk taking was assessed using a task previously associated with sensation seeking and antisocial behaviors. Two hundred ninety-one infants were brought into the lab and behaviors reflecting exuberance were observed at 4, 9, 24, and 36 months of age. Executive function was assessed at 48 months of age. Risk-taking propensity was measured when children were 60 months of age. The results indicated that exuberance and attention shifting, but not inhibitory control, significantly interacted to predict propensity for risk taking. Exuberance was positively associated with risk-taking propensity among children who were relatively low in attention shifting but unrelated for children high in attention shifting. These findings illustrated the multifinality of developmental outcomes for temperamentally exuberant young children and pointed to the distinct regulatory influences of different executive functions for children of differing temperaments. Attention shifting likely affords a child the ability to consider both positive and negative consequences and moderates the relation between early exuberance and risk-taking propensity.

We tested for gender moderation within a multidomain model of antisocial behavior (ASB) among community youth, drawn from the Project on Human Development in Chicago Neighborhoods study. Youths (N = 1,639) were 9 to 12 years old at baseline and were followed for two additional waves, spaced approximately 2.5 years apart. We hypothesized that harsh and physically coercive parenting, a familial level risk factor, would impact individual level risk factors for ASB, such as childhood temperament ratings of emotionality and inhibitory control, and preadolescent externalizing and internalizing symptoms, as well as involvement with antisocial peers. We further hypothesized that this process and its impact on ASB would be moderated by gender. We used both multiple indicator multiple causes and multiple group analyses to test for gender moderation and a structural equation modeling multiple mediation framework to evaluate the strength of indirect effects. We tested the role of family, individual, and peer level influences on ASB, after accounting for the role of known contextual factors, including poverty, race, and neighborhood. Our overall model fit the data well for males and females, indicating harsh parenting, disinhibition, emotionality, and peers exert a strong influence on risk for ASB. Gender moderated the pathway from harsh parenting to externalizing behavior, such that this was a significant pathway for girls, but not boys. We discussed the importance of these findings with regard to intervention planning for youth at risk for ASB and future gender-informed models of ASB.

Despite the large number of studies tracing patterns of youth antisocial behavior (AB) during adolescence, few have prospective data on the developmental precursors of AB beginning during infancy. Using a cohort of 268 low-income boys first assessed at 18 months, the current study examined predictors of early- and late-starting trajectories of AB assessed during early childhood and early adolescence. Four trajectory groups were identified, including early- and late-starting groups, a low stable group, and a high decreasing group, characterized by multiple risk factors during early childhood and early adolescence. During early childhood, parenting and maternal depression discriminated two AB trajectory groups, an early-starting and a high decreasing group, who would go on to demonstrate a high preponderance of juvenile court involvement (60% to 79%) and elevated rates of clinical depression 13 to 15 years later. The results were discussed in reference to targeting malleable family risk factors during early childhood associated with patterns of AB and mental health disorders during adolescence.

Conduct problems are a general risk factor for adolescent alcohol use. However, their role in relation to alcohol-specific risk pathways of intergenerational transmission of alcohol use is not well understood. Further, the roles of alcohol-specific contextual influences on children's early alcohol use have been little examined. In a 20-year prospective, multimethod study of 83 fathers and their 125 children, we considered the predictors of child alcohol use by age 13 years. The predictors included fathers' adolescent antisocial behavior and alcohol use, both parents' adult alcohol use, norms about and encouragement of child use, parental monitoring, child-reported exposure to intoxicated adults, and parent-reported child externalizing behaviors. Path models supported an association between fathers' adolescent alcohol use and children's use (β = 0.17) that was not better explained by concurrent indicators of fathers' and children's general problem behavior. Fathers' and mothers' adult alcohol use uniquely predicted child use, and exposure to intoxicated adults partially mediated the latter path. Other family risk mechanisms were not supported. However, parental alcohol use and child alcohol use were linked in expected ways with family contextual conditions known to set the stage for alcohol use problems later in adolescence.

Gene–environment interaction effects in predicting antisocial behavior in late childhood were investigated among maltreated and nonmaltreated low-income children (N = 627, M age = 11.27). Variants in three genes were examined: tryptophan hydroxylase 1 (TPH1), serotonin transporter linked polymorphic region (5-HTTLPR), and monoamine oxidase A (MAOA) upstream variable number tandem repeat. In addition to child maltreatment status, we considered the impact of maltreatment subtypes, developmental timing of maltreatment, and chronicity. Indicators of antisocial behavior were obtained from self-, peer, and adult counselor reports. In a series of analyses of covariance, child maltreatment and its parameters demonstrated strong main effects on early antisocial behavior as assessed by all report forms. Genetic effects operated primarily in the context of gene–environment interactions, moderating the impact of child maltreatment on outcomes. Across the three genes, among nonmaltreated children no differences in antisocial behavior were found based on genetic variation. In contrast, among maltreated children specific polymorphisms of TPH1, 5-HTTLPR, and MAOA were each related to heightened self-report of antisocial behavior; the interaction of 5-HTTLPR and developmental timing of maltreatment also indicated more severe antisocial outcomes for children with early onset and recurrent maltreatment based on genotype. TPH1 and 5-HTTLPR interacted with maltreatment subtype to predict peer reports of antisocial behavior; genetic variation contributed to larger differences in antisocial behavior among abused children. The TPH1 and 5-HTTLPR polymorphisms also moderated the effects of maltreatment subtype on adult reports of antisocial behavior; again, the genetic effects were strongest for children who were abused. In addition, TPH1 moderated the effect of developmental timing of maltreatment and chronicity on adult reports of antisocial behavior. The findings elucidate how genetic variation contributes to identifying which maltreated children are most vulnerable to antisocial development.

The effects of divorce on children's behavioral development have proven to be quite varied across studies, and most developmental and family scholars today appreciate the great heterogeneity in divorce effects. Thus, this inquiry sought to determine whether select dopaminergic genes previously associated with externalizing behavior and/or found to moderate diverse environmental effects (dopamine receptors D2 and D4, catechol-O-methyltransferase) might moderate divorce effects on adolescent self-reported externalizing problems; and, if so, whether evidence of gene–environment (G × E) interaction would prove consistent with diathesis–stress or differential-susceptibility models of environmental action. Data from the first and third wave of the Dutch Tracking Adolescents' Individual Lives Survey (n = 1,134) revealed some evidence of G × E interaction reflecting diathesis–stress but not differential susceptibility. It is intriguing that some evidence pointed to “vantage sensitivity,” which are benefits accruing to those with a specific genotype when their parents remained together, the exact opposite of diathesis–stress. The limits of this work are considered, especially with regard to the conditions for testing differential susceptibility, and future directions are outlined.

This study was designed to examine the prospective relations of life stress and genetic status with increases in drug use. African Americans (N = 399) in rural Georgia (Wave 1 mean age = 17 years) provided three waves of data across 27.5 months and a saliva sample from which the dopamine receptor D4 (DRD4) gene was genotyped. Multilevel growth curve modeling analysis indicated that emerging adults manifested the highest escalations in drug use when they reported high life stress and carried an allele of DRD4 with 7 or more repeats (7 + R allele). In addition, emerging adults who reported high life stress and carried the 7 + R allele evinced the largest increases in two proximal risk factors for drug use: affiliations with drug-using companions and drug use vulnerability cognitions. Furthermore, when the Gene × Environment interaction effects on the increases in affiliations with drug-using companions and vulnerability cognitions were entered into the model forecasting drug use, the Life Stress × DRD4 Status interaction on drug use became nonsignificant in the presence of the risk mechanisms. This finding provides an example of “second generation” Gene × Environment interaction research in which the interaction's effects on proximal risk mechanisms account for its effects on outcomes.

This study examined the interplay between the influence of peers who promote alcohol use and μ-opioid receptor M1 (OPRM1) genetic variation in the intergenerational transmission of alcohol use disorder (AUD) symptoms while separating the “traitlike” components of AUD symptoms from their age-specific manifestations at three ages from emerging adulthood (17–23 years) to adulthood (29–40 years). The results for males were consistent with genetically influenced peer selection mechanisms as mediators of parent alcoholism effects. Male children of alcoholics were less likely to be carriers of the G allele in single nucleotide polymorphism A118G (rs1799971), and those who were homozygous for the A allele were more likely to affiliate with alcohol use promoting peers who increased the risk for AUD symptoms at all ages. There was evidence for women of an interaction between OPRM1 variation and peer affiliations but only at the earliest age band. Peer influences had stronger effects among women who were G-carriers. These results illustrate the complex ways in which the interplay between influences at multiple levels of analysis can underlie the intergenerational transmission of alcohol disorders as well as the importance of considering age and gender differences in these pathways.

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.

Early onset aggression precipitates a cascade of risk factors, increasing the probability of a range of externalizing and internalizing psychopathological outcomes. Unfortunately, decades of research on the etiological contributions to the manifestation of aggression have failed to yield identification of any risk factors determined to be either necessary or sufficient, likely attributable to etiological heterogeneity within the construct of aggression. Differential pathways of etiological risk are not easily discerned at the behavioral or self-report level, particularly in young children, requiring multilevel analysis of risk pathways. This study focuses on three domains of risk to examine the heterogeneity in 207 urban kindergarten children with high levels of aggression: cognitive processing, socioemotional competence and emotion processing, and family context. The results indicate that 90% of children in the high aggression group could be characterized as either low in verbal ability or high in physiological arousal (resting skin conductance). Children characterized as low verbal, high arousal, or both differed in social and emotional competence, physiological reactivity to emotion, and aspects of family-based contextual risk. The implications of this etiologic heterogeneity of aggression are discussed in terms of assessment and treatment.

During the last quarter century, developmental psychopathology has become increasingly inclusive and now spans disciplines ranging from psychiatric genetics to primary prevention. As a result, developmental psychopathologists have extended traditional diathesis–stress and transactional models to include causal processes at and across all relevant levels of analysis. Such research is embodied in what is known as the multiple levels of analysis perspective. We describe how multiple levels of analysis research has informed our current thinking about antisocial and borderline personality development among trait impulsive and therefore vulnerable individuals. Our approach extends the multiple levels of analysis perspective beyond simple Biology × Environment interactions by evaluating impulsivity across physiological systems (genetic, autonomic, hormonal, neural), psychological constructs (social, affective, motivational), developmental epochs (preschool, middle childhood, adolescence, adulthood), sexes (male, female), and methods of inquiry (self-report, informant report, treatment outcome, cardiovascular, electrophysiological, neuroimaging). By conducting our research using any and all available methods across these levels of analysis, we have arrived at a developmental model of trait impulsivity that we believe confers a greater understanding of this highly heritable trait and captures at least some heterogeneity in key behavioral outcomes, including delinquency and suicide.