We examined whether maltreatment experienced in childhood and/or adolescence prospectively predicts young adult functioning in a diverse and well-characterized sample of females with childhood-diagnosed attention-deficit/hyperactivity disorder (N = 140). Participants were part of a longitudinal study and carefully evaluated in childhood, adolescence, and young adulthood (Mage = 9.6, 14.3, and 19.7 years, respectively), with high retention rates across time. A thorough review of multisource data reliably established maltreatment status for each participant (Mκ = 0.78). Thirty-two (22.9%) participants experienced at least one maltreatment type (physical abuse, sexual abuse, or neglect). Criterion variables included a broad array of young adult measures of functioning gleaned from multiple-source, multiple-informant instruments. With stringent statistical control of demographic, prenatal, and family status characteristics as well as baseline levels of the criterion variable in question, maltreated participants were significantly more impaired than nonmaltreated participants with respect to self-harm (suicide attempts), internalizing symptomatology (anxiety and depression), eating disorder symptomatology, and well-being (lower overall self-worth). Effect sizes were medium. Comprising the first longitudinal evidence linking maltreatment with key young adult life impairments among a carefully diagnosed and followed sample of females with attention-deficit/hyperactivity disorder, these findings underscore the clinical importance of trauma experiences within this population.

The present study examined the impact of children's maltreatment experiences on the emergence of externalizing problem presentations among children during different developmental periods. The sample included 788 youth and their caregivers who participated in a multisite, prospective study of youth at-risk for maltreatment. Externalizing problems were assessed at ages 4, 8, and 12, and symptoms and diagnoses of attention-deficit/hyperactivity disorder, oppositional defiant disorder, and conduct disorder were assessed at age 14, during interviews with youth and caregivers. Information about maltreatment allegations was coded from official records. Latent transition analysis identified three groups of youth with similar presentations of externalizing problems (“well adjusted,” “hyperactive/oppositional,” and “aggressive/rule-breaking”) and transitions between groups from ages 4, 8, and 12. A “defiant/deceitful” group also emerged at age 12. Girls were generally more likely to present as well adjusted than boys. Children with recent physical abuse allegations had an increased risk for aggressive/rule-breaking presentations during the preschool and preadolescent years, while children with sexual abuse or neglect allegations had lower probabilities of having well-adjusted presentations during middle childhood. These findings indicate that persistently severe aggressive conduct problems, which are related to the most concerning outcomes, can be identified early, particularly among neglected and physically and sexually abused children.

Autism spectrum disorder (ASD) is associated with pervasive social deficits as well as marked emotion dysregulation across the life span. Decreased social motivation accounts in part for social difficulties, but factors moderating its influence are not fully understood. In this paper, we (a) characterize social and emotional functioning among children and adolescents with ASD, (b) explore contributions of social motivation and emotion dysregulation to social skill, and (c) consider biological sex and intellectual functioning as moderators of these associations. In a sample of 2,079 children and adolescents with ASD from the Simons Simplex Collection, we document direct effects of social motivation, internalizing symptoms, aggression, attention problems, irritability, and self-injurious behavior on children's social skills. Furthermore, dysregulation in several domains moderated the association between social motivation and social skill, suggesting a blunting effect on social motivation in the context of emotional difficulties. Moreover, when considering only individuals with intellectual skills in the average range or higher, biological sex further moderated these associations. Findings add to our understanding of social–emotional processes in ASD, suggest emotion dysregulation as a target of intervention in the service of social skill improvements, and build on efforts to understand sources of individual difference that contribute to heterogeneity among individuals with ASD.

Children who grow up in poverty are more likely to experience chronic stressors that generate “wear” on stress regulatory systems including the hypothalamus–pituitary–adrenal (HPA) axis. This can have long-term consequences for health and well-being. Prior research has examined the role of proximal family and home contributions to HPA axis functioning. However, there is evidence to suggest that more distal levels of context, including neighborhoods, also matter. Prior evidence has primarily focused on adolescents and adults, with little evidence linking the neighborhood context with HPA activity in infancy and toddlerhood. We tested whether neighborhood disadvantage (indexed by US Census data) was associated with basal salivary cortisol levels at 7, 15, and 24 months of child age in a large sample of families (N = 1,292) residing in predominately low-income and rural communities in the United States. Multilevel models indicated that neighborhood disadvantage was positively associated with salivary cortisol levels and that this effect emerged across time. This effect was moderated by the race/ethnicity of children such that the association was only observed in White children in our sample. Findings provide preliminary evidence that the neighborhood context is associated with stress regulation during toddlerhood, elucidating a need for future work to address possible mechanisms.

Relations between restricted and repetitive behavior at age 26 months and children's concurrent (N = 203) and later (n = 161) social cognition and language development were investigated. Restricted and repetitive behavior was assessed using two scales: sensory and motor repetitive behaviors and rigidity/routines/restricted interests. Language was assessed at ages 26 and 51 months; social cognition was assessed at ages 26 (symbolic play) and 51 and 61 months (theory of mind). Sensory and motor repetitive behavior was negatively related to children's (a) language performance at 26 and 51 months, (b) instructed symbolic play at 26 months, and (c) theory of mind performance at 51 and 61 months. Path analyses showed that children's sensory and motor repetitive behavior at age 26 months was related to lower receptive verbal ability and theory of mind at 51 months, which led to lower theory of mind at 61 months. Rigidity/routines/restricted interests at 26 months were unrelated to concurrent and later social cognition and language. These results are discussed in terms of the pathways via which sensory and motor repetitive behavior might impact negatively on development.

The transition to young adulthood is both a time when risky health behaviors such as substance misuse peak and a time of opportunity for growth and development through the acquisition of adult roles. In this transition, coping styles include responses to the stressors and opportunities associated with the emergence of adulthood. The extent to which such coping styles are skillfully employed in part determines adjustment into adulthood. The current study used a high-risk, longitudinal design to examine the development of coping styles over adolescence, continuity in these coping styles from adolescence to adulthood, the impact of coping on adult stress and substance misuse, the ability of coping to buffer effects of stress on substance use, and differences in coping between at-risk youth (i.e., children of alcoholics [COAs]) and their peers. A sample of 340 adolescents completed four assessments over ages 11–23. We used latent trajectory models to examine interindividual and intraindividual change in coping over time. Evidence for both change and continuity in the development of coping from adolescence to adulthood was found, although adolescent coping had limited impact on stress and substance use in adulthood. Support was also found for complex stress-buffering and stress-exacerbating effects of coping on the relations between major life events and adult drug use and between stress associated with the new roles of adulthood and heavy alcohol use. Implications of these findings for development and adjustment in the transition to adulthood are discussed.

The current study tested the impact of the transition to parenthood on growth in alcohol consumption from early adolescence through emerging adulthood. We measured age-related discontinuity in trajectories of alcohol consumption associated with timing of the parenthood transition, above and beyond the effects of accrued educational status, gender, and time-varying marital status. We also examined the impact of a familial selection factor for the transmission of alcohol use problems, family history density of alcoholism (FHD), on both risk for adolescent parenthood and risk for adolescent parents' continuity in alcohol consumption after the parent transition within a mediation structural equation model. Premature timing of parenthood had a distinct effect on emerging adult alcohol trajectories. Although participants who became parents as emerging adults showed role-related decline in alcohol consumption, those who became parents during adolescence showed a role-related rise in emerging adult alcohol consumption. Gender moderated adolescent parents' role-related growth in emerging adult alcohol consumption. Adolescent fathers showed an adverse rise in alcohol consumption after becoming parents, whereas adolescent mothers' alcohol consumption did not change significantly. FHD was related to high adolescent alcohol consumption, which mediated risk for the incidence of early parenthood. Finally, the adverse effect of FHD on trajectories of emerging adult alcohol use was mediated by a dual pathway: (a) developmental continuity of conduct problems and (b) early transition to parenthood.

Longitudinal bidirectional effects between parents and children are usually studied in samples of typically developing children, but remain understudied in families with a child with autism spectrum disorder. This three-wave longitudinal study examined how parents and children with autism spectrum disorder influence one another, relying on parent reports of parenting behaviors and children's problem behaviors across 9 years, in a sample of 139 youngsters (M age Time 1 = 10.2 years, 83% boys). Cross-lagged analyses indicated that children's externalizing problems at Time 1 predicted negative controlling parenting 6 years later (Time 2) that in turn predicted externalizing problems 3 years later (Time 3). Negative parental control at Time 1 also increased the risk for internalizing problems at Time 2. It was surprising that externalizing problems at Time 2 also predicted positive parental involvement at Time 3. Thus, although results indicate that externalizing problems generally elicit maladaptive reactions in parents, this study also suggests that parents adjust their way of reacting to externalizing child problems as their child reaches adolescence/emerging adulthood. Implications for future research on parenting dynamics in families with a child with autism spectrum disorder are discussed.

A considerable body of evidence suggests that early caregiving may affect the short-term functioning and longer term development of the hypothalamic–pituitary–adrenocortical axis. Despite this, most research to date has been cross-sectional in nature or restricted to relatively short-term longitudinal follow-ups. More important, there is a paucity of research on the role of caregiving in low- and middle-income countries, where the protective effects of high-quality care in buffering the child's developing stress regulation systems may be crucial. In this paper, we report findings from a longitudinal study (N = 232) conducted in an impoverished periurban settlement in Cape Town, South Africa. We measured caregiving sensitivity and security of attachment in infancy and followed children up at age 13 years, when we conducted assessments of hypothalamus–pituitary–adrenocortical axis reactivity, as indexed by salivary cortisol during the Trier Social Stress Test. The findings indicated that insecure attachment was predictive of reduced cortisol responses to social stress, particularly in boys, and that attachment status moderated the impact of contextual adversity on stress responses: secure children in highly adverse circumstances did not show the blunted cortisol response shown by their insecure counterparts. Some evidence was found that sensitivity of care in infancy was also associated with cortisol reactivity, but in this case, insensitivity was associated with heightened cortisol reactivity, and only for girls. The discussion focuses on the potentially important role of caregiving in the long-term calibration of the stress system and the need to better understand the social and biological mechanisms shaping the stress response across development in low- and middle-income countries.

The central question addressed in this study was whether upper class, suburban teenagers can engage in various problem behaviors and still maintain adequate academic grades, because of environmental safety nets, unlike their low-income, inner-city counterparts. Three problem behavior dimensions were assessed among tenth graders, that is, substance use, delinquency, and low school engagement. Academic achievement was assessed in terms of grades across four major subjects. Variable-based analyses indicated unique links with grades for self-reported delinquency and school disengagement in high- and low-income samples, but for substance use only among the former. Person-based analyses showed that in both schools, grades were clearly compromised among youth with disturbances in all three problem domains. In addition, in the suburban school only, grades were low in the cluster characterized chiefly by high substance use. Results are discussed in terms of stereotypes regarding risks (or lack thereof) stemming from families' socioeconomic status; implications for theory and interventions are also considered.Preparation of this manuscript was funded in part by grants from the National Institutes of Health (RO1-DA10726, RO1-DA11498, R01-DA14385), the William T. Grant Foundation, and the Spencer Foundation.

In contrast to victimization, prior research on the antecedents and outcomes of bullying perpetration has provided little conclusive knowledge. Some adolescent bullies may be well adjusted and popular among peers, while other bullies are rejected and lack self-control. There is also great variation in the outcomes, with a number of studies (but not all) showing increased risk for externalizing and internalizing problems. We used a developmental framework and data from 2,230 participants of the Dutch Tracking Adolescents’ Individual Lives Survey (TRAILS) to examine bullying perpetration across adolescence, to test the links with various antecedents in preadolescence, and to elucidate the outcomes in early adulthood. Latent growth models indicated significant variance in initial bullying perpetration levels and an overall decrease between pre- and late adolescence. Individual, family, and peer factors were associated with initial levels and partially associated with bullying development over time. Bullying perpetration was linked to later maladjustment and substance use, although only in girls. Finally, bullying perpetration appears to function as an intermediate variable between preadolescent individual, family, and peer risk and substance use more than 10 years later. These results have important implications for understanding the gender-specific nature of bullying perpetration and its outcomes and for demonstrating that bullying carries early risk into adulthood.

Psychotic disorders continue to be among the most disabling and scientifically challenging of all mental illnesses. Accumulating research findings suggest that the etiologic processes underlying the development of these disorders are more complex than had previously been assumed. At the same time, this complexity has revealed a wider range of potential options for preventive intervention, both psychosocial and biological. In part, these opportunities result from our increased understanding of the dynamic and multifaceted nature of the neurodevelopmental mechanisms involved in the disease process, as well as the evidence that many of these entail processes that are malleable. In this article, we review the burgeoning research literature on the prodrome to psychosis, based on studies of individuals who meet clinical high risk criteria. This literature has examined a range of factors, including cognitive, genetic, psychosocial, and neurobiological. We then turn to a discussion of some contemporary models of the etiology of psychosis that emphasize the prodromal period. These models encompass the origins of vulnerability in fetal development, as well as postnatal stress, the immune response, and neuromaturational processes in adolescent brain development that appear to go awry during the prodrome to psychosis. Then, informed by these neurodevelopmental models of etiology, we turn to the application of new research paradigms that will address critical issues in future investigations. It is expected that these studies will play a major role in setting the stage for clinical trials aimed at preventive intervention.

Differences in mothers' and fathers' relationships with siblings and children's behavior problems were studied in a sample of 63 8-year-olds and their families. Mothers and fathers independently provided information about their relationships with siblings, and mothers rated children's adjustment and temperament. Children whose relationships with mothers and fathers were more conflictual and less close than their siblings' relationships had more emotional temperaments and more behavior problems than did other children in the sample. Mothers' and fathers' differential relationships with children were examined in combination. Children had the fewest behavior problems if both parents were closer to them than to their sibling, and they had the most behavior problems if both parents were closer to their sibling than to them. In families in which the mother was closer to one sibling and the father was closer to the other sibling, children had adjustment outcomes that fell in between the other two groups but did not differ significantly from them.

We used a longitudinal twin design to examine selection effects of personality traits at age 11 on high-risk environmental contexts at age 14 and the extent to which these contexts mediated risk for substance abuse at age 17. Socialization at age 11 (willingness to follow rules and endorse conventional values) predicted exposure to contextual risk at age 14. Contextual risk partially mediated the effect of socialization on substance abuse, though socialization also had a direct effect. In contrast, boldness at age 11 (social engagement and assurance, thrill seeking, and stress resilience) also predicted substance abuse directly but was unrelated to contextual risk. There was substantial overlap in the genetic and shared environmental influences on socialization and contextual risk, and genetic risk in socialization contributed to substance abuse indirectly via increased exposure to contextual risk. This suggests that active gene–environment correlations related to individual differences in socialization contributed to an early, high-risk developmental trajectory for adolescent substance abuse. In contrast, boldness appeared to index an independent and direct genetic risk factor for adolescent substance abuse.

Building upon methods and research utilized with normative populations, we examine extant assumptions regarding the effects of child maltreatment on memory. The effects of stress on basic memory processes is examined, and potential neurobiological changes relevant to memory development are examined. The impact of maltreatment-related sequelae (including dissociation and depression) on basic memory processes as well as false memories and suggestibility are also outlined. Although there is a clear need for additional research, the investigations that do exist reveal that maltreated children's basic memory processes are not reliably different from that of other, nonmaltreated children.Preparation of this article was supported by a grant from the National Institute of Mental Health to the authors.

There is considerable evidence that the development of joint attention and pretend play skills are impaired in children with autism. Some accounts of autistic psychopathology give a crucial role to early impairments in joint attention and suggest that these lead to impoverished development of the representational abilities that underlie the later emerging impairments in pretend play and theory of mind. Other accounts of impairments in joint attention and pretend play see them merely as symptoms of a more basic underlying cognitive deficit, in attention or executive function. This review examines the evidence for the possible relationships that may exist between joint attention and pretend play and the later development of a theory of mind. It also suggests directions for future work to clarify the relationship between the two skills and to identify the nature of the underlying primary deficit in autism.

The Young Adolescent Project (YAP) is an ongoing longitudinal study investigating the effects of abuse and neglect on adolescent development. It is a multidisciplinary study guided by a developmental, ecological perspective, and designed to consider the physical, social, and psychological effects of childhood maltreatment through the transition from childhood to adolescence. Four waves of data collection have been completed, ranging from early (Mean age = 10.95) to late adolescence (Mean age = 18.24). Members of the maltreated group (n = 303) were selected from new cases that had been opened by the Department of Child and Family Services, whereas the comparison group (n = 151) were not involved with child welfare but lived in the same neighborhoods as the maltreated group. The study assessed a wide variety of domains including physical development (e.g., height, weight, body mass, pubertal development); physiological reactivity (e.g., cortisol); cognitive abilities; mental health (e.g., symptoms of depression, anxiety, trauma, and aggression); risk behavior (e.g., sexual activity, delinquency, or substance use); social development (e.g., self-esteem, competence, and social support); family environment; and exposure to community violence. Overall, our findings demonstrated the pervasive and persistent adverse effects of child maltreatment both within and across domains, but they also identified maltreated youth with positive functioning. Our hope is that this work will help move us toward identifying targets for intervention to cultivate resilience and positive adaptation after early maltreatment experiences.

Prenatal inflammation is an established risk factor for schizophrenia. However, the specific inflammatory pathways that mediate this association remain unclear. Potential candidate systems include inflammatory markers produced by microglia, such as cytokines and complement. Accumulating evidence suggests that these markers play a role in typical neurodevelopmental processes, such as synapse formation and interneuron migration. Rodent models demonstrate that altered marker levels during the prenatal period can cause lasting deficits in these systems, leading to cognitive deficits that resemble schizophrenia. This review assesses the potential role of prenatal cytokine and complement elevations on the etiology of schizophrenia. The current neurobiological understanding of the development of schizophrenia is reviewed to identify candidate cellular mechanisms that may be influenced by prenatal inflammation. We discuss the functions that cytokines and complement may play in prenatal neurodevelopment, review evidence that links exposure to these factors with risk for schizophrenia, and consider how these markers may interact with genetic vulnerabilities to influence the neurodevelopment of schizophrenia. We consider how prenatal inflammatory exposure may influence childhood and adolescent developmental risk trajectories for schizophrenia. Finally, we identify areas of further research needed to support the development of anti-inflammatory treatments to prevent the development of schizophrenia in at-risk neonates.

The momentum of genomic science will carry it far into the future and into the heart of research on typical and atypical behavioral development. The purpose of this paper is to focus on a few implications and applications of these advances for understanding behavioral development. Quantitative genetics is genomic and will chart the course for molecular genomic research now that these two worlds of genetics are merging in the search for many genes of small effect. Although current attempts to identify specific genes have had limited success, known as the missing heritability problem, whole-genome sequencing will improve this situation by identifying all DNA sequence variations, including rare variants. Because the heritability of complex traits is caused by many DNA variants of small effect in the population, polygenic scores that are composites of hundreds or thousands of DNA variants will be used by developmentalists to predict children's genetic risk and resilience. The most far-reaching advance will be the widespread availability of whole-genome sequence for children, which means that developmentalists would no longer need to obtain DNA or to genotype children in order to use genomic information in research or in the clinic.

Childhood adversity can negatively impact development across various domains, including physical and mental health. Adverse childhood experiences have been linked to aggression and substance use; however, developmental pathways to explain these associations are not well characterized. Understanding early precursors to later problem behavior and substance use can inform preventive interventions. The aim of the current study was to examine neurobiological pathways through which childhood adversity may lead to early adolescent problem behavior and substance use in late adolescence by testing two prospective models. Our first model found that early adolescent externalizing behavior mediates the association between childhood adversity and alcohol, cigarette, and marijuana use in late adolescence. Our second model found that activation in the anterior cingulate cortex (ACC) during an inhibitory control task mediates the association between childhood adversity and early adolescent externalizing behavior, with lower ACC activation associated with higher levels of adversity and more externalizing behavior. Together these findings indicate that the path to substance use in late adolescence from childhood adversity may operate through lower functioning in the ACC related to inhibitory control and externalizing behavior. Early life stressors should be considered an integral component in the etiology and prevention of early and problematic substance use.