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.

An overview of the literature pertaining to the construct of emotional availability is presented, illustrated by a sampling of relevant studies. Methodological, statistical, and conceptual problems in the existing corpus of research are discussed, and suggestions for improving future investigations of this important construct are offered.

The past decade has witnessed an exponential growth in studies that have attempted to identify the genetic polymporphisms that moderate the influence of environmental risks on mental disorders. What tends to be neglected in these Gene × Environment (G × E) interaction studies has been a focus on resilience, which refers to a dynamic pattern of positive adaptation despite the experience of a significant trauma or adversity. In this article, we argue that one step toward advancing the field of developmental psychopathology would be for G × E research to consider resilience instead of focusing almost exclusively on mental disorders. After providing an up-to-date summary on the expanding definitions and models of resilience, and the available evidence regarding measured G × E studies of childhood maltreatment, we discuss why resilience would be a worthwhile phenotype for studies of measured G × E. First, although G × E hypotheses require that there be an environmental risk (e-risk) involved in a causal process that leads to psychopathology, e-risks are typically not included in the diagnostic criteria for most psychiatric disorders. In contrast, resilience by definition includes an e-risk. Second, G × E hypotheses require that there is evidence of variability in response to an environmental stressor, and resilience often represents the positive end on this continuum of adaptation. Third, both resilience and G × E are best understood from a developmental perspective. Fourth, although resilient outcomes are not public health concerns, the types of adversities (e.g., childhood maltreatment, poverty, or exposure to natural disasters) that are often investigated in studies of resilience certainly are. Understanding how some individuals, perhaps because of their genetic makeup, are able to withstand such adversities can inform prevention and intervention efforts to improve mental health.

The emerging adulthood years, commonly defined as the late teens and twenties, represent a period of significant variability and change for much of the population. Thus, it is important for the field to consider pathways of at-risk youth as they move through this key window of development. We review research on positive outcomes in the transition to adulthood following a history of experienced adversity, including both investigations focused on resilience in diverse specific populations as well as broader longitudinal studies. There is compelling evidence for major protective and promotive factors identified in younger age periods continuing to exert an influence at this stage of development, along with evidence for new factors unique to this developmental time and/or to specific populations. We conclude by noting recommendations for future work in this area, emphasizing Garmezy's call for the testing of competing models.

This study examined the significance of childhood Big Five personality traits for competence and resilience in early adulthood. Resilience was defined in terms of adaptive success in age-salient developmental tasks despite significant adversity throughout childhood/adolescence. The Project Competence Longitudinal Study tracked 205 young people from childhood (around age 10) to emerging adulthood (EA, age 20) and young adulthood (YA, age 30; 90% retention). Multimethod composites were created for personality traits, adversity exposure, and adult outcomes of academic achievement, work, rule-abiding conduct, friendship, and romantic relationships. Regressions showed significant main effects of childhood personality predicting adult outcomes, controlling for adversity, with few interaction effects. In person-focused analyses, the resilient group in EA and YA (high competence, high adversity) showed higher childhood conscientiousness, agreeableness, and openness and lower neuroticism than the maladaptive group (low competence, high adversity). The competent (high competence, low adversity) and resilient groups showed similar childhood traits. Turnaround cases, who changed from the maladaptive group in EA to the resilient group in YA, exhibited higher childhood conscientiousness than persistently maladaptive peers. Findings suggest that children on pathways to success in adulthood, whether facing low or high adversity, have capacities for emotion regulation, empathy and connection, dedication to schoolwork, and mastery and exploration.

Based on attachment theory, the construct of emotional availability and its assessment goes beyond attachment in important ways. Its origins in clinical experience and emotions research are discussed as well as the prospects for continuing advances in knowledge stimulated by the contributions in the Special Section. This is especially so in terms of developmental variations and the biological underpinnings of emotional availability. A major need and opportunity also exists concerning research related to psychopathology, clinical interventions, and training.

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.

Despite the substantial heritability of nearly all psychological traits, it has been difficult to identify specific genetic variants that account for more than a tiny percentage of genetic variance in phenotypes. Common explanations for this “missing heritability” include massive polygenicity, rare variants, epigenetics, epistasis, and gene–environment interactions. Gene–trait (G × T) interaction is another concept useful for understanding the lack of obvious genetic main effects. Both genes and environments are distal contributors to human behavior, but the brain is the proximal driver of behavior. The effect of any single genetic variant is dependent on the configuration of the brain in which it is expressed. One method to begin studying how single genes interact with variations in the rest of the brain is to investigate G × T interactions. A psychological trait reflects a characteristic pattern of psychological function (and, therefore, of brain function), which has its origin in the cumulative effects of both the genome and the environment. A trait therefore describes variation in the broad organismic context in which any single gene operates. We describe the nature and significance of G × T interactions for understanding psychopathology and normal trait variation, which are illustrated with empirical examples.

A wide range of developmental disorders present with characteristic psychopathologies and behaviors, with diagnoses including, inter alia, cognitive disorders and learning disabilities, epilepsies, autism, and schizophrenia. Each, to varying extent, has a genetic component to etiology and is associated with cytogenetic abnormalities. Technological developments, particularly array-based comparative genome hybridization and single nucleotide polymorphism chips, has revealed a wide range of rare recurrent and de novo copy number variants (CNVs) to be associated with disorder and psychopathology. It is surprising that many apparently similar CNVs are identified across two or more disorders hitherto considered unrelated. This article describes the characteristics of CNVs and current technological restrictions that make accurately identifying small events difficult. It summarizes the latest discoveries for individual diagnostic categories and considers the implications for a shared neurobiology. It examines likely developments in the knowledge base as well as addressing the clinical implications going forward.

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.

The commentary opens by highlighting the contribution of the Emotional Availability Scales (EAS) in providing developmental researchers with a clinically sensitive and reliable assessment of the emotional quality of caregiver–child interactions that takes into consideration their coregulated nature. The numerous studies that have used the EAS attest to their usefulness and to the way they balance complexity and attention to emotional nuances with clarity. Several issues with regard to the EAS are discussed subsequently. First, I propose that looking at patterns of the EA scales might be a way to capture the quality of each dyad's emotional dialogue. Second, I suggest that the description of attachment research as concerned almost exclusively with the regulation of distress is inaccurate, in light of Ainsworth's broad assessment of naturalistic home observations. Third, I raise the possibility that additional specialized coding systems beyond the EAS may be needed for predicting certain specific psychopathological outcomes (e.g., disorganized attachment). Fourth, I propose that it is important to explore cross-culturally the meaning of the behaviors on which the EAS focus, rather than assume cross-cultural equivalence. Fifth and finally, I point out the importance of placing the EAS in the context of the existing literature on early intervention and treatment.

Cognitive deficits in schizophrenia are increasingly accepted as core features of this disorder that play a role as vulnerability indicators, as enduring abnormalities during clinical remission, and as critical rate-limiting factors in functional recovery. This article demonstrates the lasting influence of Norman Garmezy through his impact on one graduate student and then through his later collaborative research with colleagues. The promise of core cognitive deficits as vulnerability indicators or endophenotypes was demonstrated in research with children born to a parent with schizophrenia as well as with biological parents and siblings of individuals with schizophrenia. In studies of patients with a recent onset of schizophrenia, cognitive deficits were found to endure across psychotic and clinically remitted periods and to have a strong predictive influence on likelihood of returning successfully to work or school. Converging lines of evidence for the enduring core role of cognitive deficit in schizophrenia have led in recent years to a burgeoning interest in developing new interventions that target cognition as a means of improving functional recovery in this disorder.

This article reviews past research on the parenting characteristics of childhood sexual abuse survivors and presents the results of a qualitative study exploring the women's perspectives on mothering as a survivor. Grounded theory was used in the collection and analysis of the data. Data sources included the narrative responses of 79 women (mean age = 38.2 years) and in-depth interviews of a purposive sample of 15 women (mean age = 39 years). They had an average of 2.2 children, ranging in age from 5 months to young adulthood. The theoretical model identified through analysis of data using the constant comparison method was entitled “The Hard Work of Mothering as a Survivor.” Processes emerged that described the ways participants managed the work of mothering in light of memories of the abuse and attempts to heal from this earlier trauma. The conditions for committing to the work included becoming aware of and accepting the reality of the abuse and how it affected one's life, and taking on the hard work of developing a mothering self. This included expanding awareness, developing and evaluating a personal model of mothering, navigating typical and abuse salient parenting challenges, mothering through the pain of recovery, and battling for balance. The findings highlighted the dynamic, multifaceted nature of recovery and resilience for these mothers and the need for an increased focus on parenting in counseling with childhood sexual abuse survivors. Provision of anticipatory guidance regarding commonly experienced stressors at varying stages of the child's development and the mother's stage of recovery and methods for coping with these challenges, would benefit these mothers and promote parenting competence. Specific implications for psychotherapy and directions for future research are discussed.

We appreciate both the opportunity to co-edit this Special Section of Development and Psychopathology and the thoughtful commentaries provided by Marjorie Beeghly, Marc Bornstein, Robert Emde, and David Oppenheim. Their commentaries review historical perspectives, provide new insights, and suggest future horizons for the study of emotional availability (EA) within a developmental psychopathology framework. Along with the collection of empirical studies in this Special Section, they begin to chart a course for further growth and integration of EA into the field of developmental psychopathology. Taking stock of the research on EA, we realize that there is now a sufficient corpus to suggest that research focusing on this construct, as operationalized by the EA Scales (Biringen, Robinson, & Emde, 1998) is entering a more mature phase of inquiry. In the last 14 years, research on EA, including several special journal issues on the topic (see Biringen & Easterbrooks, 2008; Easterbrooks & Biringen, 2000, 2005, 2009), has explored the methodological concerns, reliability, and validity of the EA Scales and application across different samples and ages. This “critical mass” of knowledge (more than 100 peer-reviewed publications) supports the current focus on asking incisive questions for the field of developmental psychopathology (Cicchetti & Toth, 1995, 2009).

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.

Copy number variants (CNVs) are submicroscopic deletions and duplications of genomic material that were previously thought to be rare phenomena. They have now been robustly associated with a variety of disorders such as autism, schizophrenia, and attention-deficit/hyperactivity disorder through an emerging research base in affective disorders. A complex picture is emerging of a polygenic, heterogeneous model of disease, with CNVs conferring broad susceptibility to a variety of neurodevelopmental disorders, rather than specific disorders per se. Although the insights gleaned thus far only represent a small piece of a much larger puzzle, progress has been rapid and new technologies promise even more insights into these hitherto opaque brain disorders. We will discuss CNVs, the current state of evidence for their role in the pathogenesis of classical psychiatric disorders, and the application of such knowledge in clinical settings.

Based on numerous suggestions in the literature, we evaluated lexical decision (LD) as a putative endophenotype for reading comprehension by investigating heritability estimates and segregation analyses parameter estimates for both of these phenotypes. Specifically, in a segregation analysis of a large sample of families, we established that there is little to no overlap between genes contributing to LD and reading comprehension and that the genetic mechanism behind LD derived from this analysis appears to be more complex than that for reading comprehension. We conclude that in our sample, LD is not a good candidate as an endophenotype for reading comprehension, despite previous suggestions from the literature. Based on this conclusion, we discuss the role and benefit of the endophenotype approach in studies of complex human cognitive functions.

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 article reviews and reflects on studies that have explored the effects of war on children around the world. Most are cross-sectional and based on self-reports. They describe a range of mental health problems, related to dose effects and to the negative impact of being a victim or witness of violent acts, threats to and loss of loved ones, prolonged parental absence, and forced displacement. The more recent the exposure to war, and the older the child, the higher was the likelihood of reported posttraumatic stress disorder symptoms. Especially vulnerable to long-term emotional distress were child soldiers, children who were raped, and children who had been forcibly displaced. In adulthood, war-traumatized children displayed significantly increased risks for a wide range of medical conditions, especially cardiovascular diseases. Among protective factors that moderated the impact of war-related adversities in children were a strong bond between the primary caregiver and the child, the social support of teachers and peers, and a shared sense of values. Among the few documented intervention studies for children of war, school-based interventions, implemented by teachers or locally trained paraprofessionals, proved to be a feasible and low-cost alternative to individual or group therapy. More longitudinal research with multiple informants is needed to document the trajectories of risk and resilience in war-affected children, to assess their long-term development and mental health, and to identify effective treatment approaches.

Previous studies with nonhuman species have shown that animals exposed to early adversity show differential DNA methylation relative to comparison animals. The current study examined differential methylation among 14 children raised since birth in institutional care and 14 comparison children raised by their biological parents. Blood samples were taken from children in middle childhood. Analysis of whole-genome methylation patterns was performed using the Infinium HumanMethylation27 BeadChip assay (Illumina), which contains 27,578 CpG sites, covering approximately 14,000 gene promoters. Group differences were registered, which were characterized primarily by greater methylation in the institutionalized group relative to the comparison group, with most of these differences in genes involved in the control of immune response and cellular signaling systems, including a number of crucial players important for neural communication and brain development and functioning. The findings suggest that patterns of differential methylation seen in nonhuman species with altered maternal care are also characteristic of children who experience early maternal separation.