Potential candidate Gene × Environment interactions in the etiology of childhood attention-deficit/hyperactivity disorder (ADHD) are examined between the dopamine receptor D2 gene (DRD2) and putative family environmental risk factors that reflect mothers' marital stability. Specifically, interactions were tested between DRD2 and mothers' marital status, number of marriages or cohabiting relationships, and age at first marriage. Moderate relations were found among the marital stability measures, and mother's marital status and number of marriages or cohabiting relationships (but not age at first marriage) were risk factors for their children's ADHD. All three mother's marital stability variables were associated with either the child's or mother's DRD2 genotypes. Gene × Environment interactions were found for children's ADHD diagnoses between children's DRD2 genotypes and mother's marital status and number of marriages or cohabiting relationships. It is of interest that these interactions were strengthened with the progressive addition of sets of covariates intended to control for alternative causal pathways that represent background genetic and environmental context confounds. The present findings highlight the importance of considering both the nexus of putative environmental risk factors and whether their etiology and effects are truly environmental in future Gene × Environment interaction research.

Biological parents pass on genotypes to their children, as well as provide home environments that correlate with their genotypes; thus, the association between the home environment and children's temperament can be genetically (i.e., passive gene–environment correlation) or environmentally mediated. Furthermore, family environments may suppress or facilitate the heritability of children's temperament (i.e., gene–environment interaction). The sample comprised 807 twin pairs (mean age = 7.93 years) from the longitudinal Wisconsin Twin Project. Important passive gene–environment correlations emerged, such that home environments were less chaotic for children with high effortful control, and this association was genetically mediated. Children with high extraversion/surgency experienced more chaotic home environments, and this correlation was also genetically mediated. In addition, heritability of children's temperament was moderated by home environments, such that effortful control and extraversion/surgency were more heritable in chaotic homes, and negative affectivity was more heritable under crowded or unsafe home conditions. Modeling multiple types of gene–environment interplay uncovered the complex role of genetic factors and the hidden importance of the family environment for children's temperament and development more generally.

Adoption provides a unique opportunity for the study of child development. Because adopted children are raised in families in which they have no genetic relationship with their parents, and possibly none with their siblings, they provide a rare opportunity to study the relative importance of genetic, shared environmental, and nonshared environmental influences on the development of child characteristics and behaviors. Because children are adopted from a variety of circumstances and at a wide range of ages, studies of adopted children and their families provide researchers the opportunity to examine the short- and long-term influences of a wide range of environments on children's development. Because children are adopted into homes with a range of characteristics (e.g., multiracial homes), adoption provides the opportunity to study the range of influences of these homes on child development. Adoption research that focuses on each of these areas is reviewed in this article. We present conclusions about the value of adoption in psychological research and some reasons why many psychologists ignore the opportunities presented by studying adoptive families, as well as potential useful directions for future research with adopted children and their families.

Extensive research has established a positive association between caregiver-child behavioral synchrony and child developmental functioning. Burgeoning research examining physiological synchrony has yet to elucidate its impact for children’s developing self-regulation. The objectives of this systematic review were to: 1) determine whether there is evidence that caregiver-child physiological synchrony promotes positive child development, 2) examine developmental differences in physiological synchrony and its correlates, and 3) explore whether context, risk, and/or stress influence patterns of synchrony. Sixty-nine studies met the following criteria on PubMed and PsycINFO: 1) peer-reviewed empirical articles in English that 2) examine autonomic, hypothalamic-pituitary-adrenocortical, and/or central nervous system activity 3) for caregivers and children 4) in response to a task and 5) directly examine the association between caregiver and child physiology. Findings varied based on developmental period and current behavioral context. Functional differences may exist across physiological systems and contexts. Synchrony may have different developmental consequences for dyads with and without certain risk factors. Few studies examine physiological synchrony across multiple systems or contexts, nor do they measure child characteristics associated with synchrony. Statistical and methodological challenges impede interpretation. Findings generally support the idea that physiological synchrony may support children’s developing self-regulation. Longitudinal research is needed to examine child developmental outcomes over time.

To determine if drinking behavior in adolescence provides a “gateway” leading to the misuse of other psychoactive substances and antisocial behavior, we genotyped 180 Asian adolescent adoptees to determine if they inherited the deficient from of the aldehyde dehydrogenase 2 (ALDH2) enzyme that is important in the metabolism of alcohol. Based on the gateway model, we hypothesized that those with normal enzyme activity (70% of the sample) who began to misuse alcohol would also misuse other drugs and display antisocial tendencies. Those with the enzyme deficiency (30%), because they experience unpleasant side effects associated with drinking, were expected to show less evidence of alcohol misuse and thus be less likely to progress to the misuse of other substances or engage in antisocial acts. Consistent with previous research, we found that ALDH2 deficiency was significantly associated with lower rates of drinking and getting drunk but not with ever having tried alcohol. Contrary to the gateway model, we found no evidence that ALDH2 deficiency was associated with lower rates of nonalcohol substance use or antisociality. Finally, in an examination of factors that may moderate the impact of the metabolic protection because of ALDH2 deficiency, we identified siblings rather than parents as the major source of familial environmental effect on adolescent drinking.

To examine the effects of risk on infant development within cultural contexts, 141 dual-earner Israeli and Palestinian couples and their first-born child were observed at 5 months and again at 34 months. Eight ecological determinants were examined as potential risk factors, including the infant's observed and parent-reported difficult temperament; the mother's depressive symptoms, work–family interference, and experience of childbirth; the parents' marital satisfaction and social support; and observed maternal and paternal sensitivity. Symbolic play and behavior problems were assessed at 34 months. Culture-specific effects of risk and protective factors were found. Parent sensitivity facilitated symbolic competence to a greater extent in the Israeli group. Culture moderated the effects of maternal depression and family social support on toddlers' behavior problems. Maternal depressive symptoms had a negative impact on the behavior adaptation of Israeli children and social support buffered against behavior problems in the Arab group. Implications for research on risk and resilience and the role of culture in moderating the effects of ecological risk are discussed.The Israeli–Palestinian Project was supported by the New-Land Foundation. The study is dedicated to the memory of the late professor Donald Cohen, MD, whose vision and support enabled this project.

To identify types of families, latent-class analysis was applied to (reported) marriage and (observed) parenting measures obtained during the infancy, toddler, and/or preschool years for 828 two-parent families participating in the NICHD Study of Child Care. Five types of families were identified: Consistently Supportive (i.e., good parenting, good marriage, 15% of sample), Consistently Moderate (i.e., moderate marriage, moderate parenting, 43%), Consistently Risky (i.e., poor parenting, poor marriage, 16%), Good Parenting/Poor Marriage (19%), and Poor Parenting/Good Marriage (7%). When groups were compared in terms of contextual antecedents (measured at child age 1 month) and child cognitive–academic and socioemotional functioning in first grade, results indicated (a) that contextual risks increased linearly and children's functioning decreased linearly as one moved across the first three aforementioned groups; and after controlling for group differences in background factors (b) that children in the Good-Parenting/Poor-Marriage families outperformed those in the Poor Parenting/Good Marriage; (c) that there was evidence of “added value” developmentally when children experienced two sources of support (i.e., good marriage and good parenting) rather than just one (i.e., good marriage or good parenting); but (d) that there was only modest evidence of protective buffering whereby children experiencing just good parenting (but not just good marriages) outperformed children experiencing poor parenting and poor marriages. Results are discussed in terms of the relative influence of marriage and parenting on child development and the potential benefits of applying typological approaches to the study of marriage–parenting family subsystems.The research described herein was supported by a cooperative agreement with the National Institute of Child Health and Human Development (U10-HD25420). The authors express their appreciation to all collaborating investigators of the NICHD Study of Early Child Care.

The participants (originally 196 boys and 173 girls) in an ongoing longitudinal study were examined using peer nomination and teacher rating at ages 8 and 14 years. Criminal records were collected at age 27 years. The results showed that (a) criminal offenses were best predicted if the accumulation of behavior problems over the school years was considered; (b) the risk for different types of offenses was highest for boys who exhibited escalating conduct problems and school failure over the school years; (c) norm-breaking behavior in early adolescence was strongly related to a propensity to later criminal offenses; (d) childhood aggressiveness did not predict arrests without the presence of other problems. When followed by norm-breaking in early adolescence, it predicted violent offenses, and when followed by poor school success, it predicted property offenses; (e) interestingly, low prosociality turned out to have a significant independent relationship to arrests; and (f) the distinction between an early-onset path and a late-onset path proved to be valid.

This article reviews major issues of a developmental psychopathology understanding of youth violence and related insights gained from violence prevention efforts to date. Based in a perspective that emphasizes three areas of knowledge, epidemiology, risk factors and models, and developmental trajectories, findings are reviewed that help clarify theoretical propositions about the developmental patterns, influences, and pathways related to youth violence. Extant research is able to support several major contentions of basic developmental psychopathology theories of youth violence. Support is most robust for risk factors central to prevailing models of the development of youth violence. In addition to noting current knowledge contributions, the review suggests areas of needed additional analytic progress and theoretical extension to refine knowledge and expand understanding of the development of violence risk and its prevention.

The mechanisms through which early life stress leads to psychopathology are thought to involve allostatic load, the “wear and tear” an organism is subjected to as a consequence of sustained elevated levels of glucocorticoids caused by repeated/prolonged stress activations. The allostatic load model described this phenomenon, but has been criticized as inadequate to explain alterations associated with early adverse experience in some systems, including behavior, which cannot be entirely explained from an energy balance perspective. The reactive scope model has been more recently proposed and focuses less on energy balance and more on dynamic ranges of physiological and behavioral mediators. In this review we examine the mechanisms underlying the behavioral consequences of early life stress in the context of both these models. We focus on adverse experiences that involve mother–infant relationship disruption, and dissect those mechanisms involving maternal care as a regulator of development of neural circuits that control emotional and social behaviors in the offspring. We also discuss the evolutionary purpose of the plasticity in behavioral development, which has a clear adaptive value in a changing environment.

The interaction between childhood maltreatment and the serotonin transporter (5-HTT) gene linked polymorphic region has been associated with increased risk to develop major depression. This Gene × Environment interaction has furthermore been linked with increased levels of anxiety and glucocorticoid release upon exposure to stress. Both endophenotypes are regulated by the neuropeptide corticotropin-releasing factor (CRF) or hormone, which is expressed by the paraventricular nucleus of the hypothalamus, the bed nucleus of the stria terminalis, and the central amygdala (CeA). Therefore, we hypothesized that altered regulation of the expression of CRF in these areas represents a major neurobiological mechanism underlying the interaction of early life stress and 5-HTT gene variation. The programming of gene transcription by Gene × Environment interactions has been proposed to involve epigenetic mechanisms such as DNA methylation. In this study, we report that early life stress and 5-HTT genotype interact to affect DNA methylation of the Crf gene promoter in the CeA of adult male rats. Furthermore, we found that DNA methylation of a specific site in the Crf promoter significantly correlated with CRF mRNA levels in the CeA. Moreover, CeA CRF mRNA levels correlated with stress coping behavior in a learned helplessness paradigm. Together, our findings warrant further investigation of the link of Crf promoter methylation and CRF expression in the CeA with behavioral changes that are relevant for psychopathology.

This article reviews memory-related impairments in trauma survivors with posttraumatic stress disorder and their possible association to neuroendocrine alterations seen in this disorder. The neuroendocrine profile in PTSD first described in chronically ill combat veterans is characterized by lower basal cortisol levels, higher glucocorticoid receptor number, enhanced sensitivity to exogenous steroids, and increased variation in basal cortisol levels over the diurnal cycle. The generalizability and time course of these neuroendocrine alterations are explored in longitudinal studies and studies in other traumatized populations. These studies suggest that at least some aspects of this neuroendocrine profile can also be seen in other populations, including women, children, and victims of childhood trauma. Additionally, the alterations may be present early in the course of illness, perhaps even in the immediate aftermath of trauma, and may continue to be manifest in elderly trauma survivors. The mechanisms by which these neuroendocrine alterations may influence the formation and processing of traumatic memories are discussed.

Sociometric status differences in children's social competence were examined in a sample of elementary school-aged children using teacher ratings and peer nominations. Rejected children evinced significantly fewer competencies (e.g., peer group entry, responses to provocation) than popular, average, or neglected children but differed from controversial children only with respect to their inability to meet established social norms for cooperative behavior and teachers' expectations for classroom behavior. An examination of the heterogeneity of peer-rejected children revealed that rejected-aggressive children were deficient in all aspects of social competence assessed and were most disliked by their peers. Rejected-withdrawn children were seen by peers as most unhappy, whereas rejected-undifferentiated children (i.e., rejected children who were neither highly aggressive nor highly withdrawn) had problems with social withdrawal, disruptive behavior, and socially appropriate behavior. Rejected-aggressive and rejected-withdrawn children had more difficulties with reactive aggression combined with an inability to respond positively to peers than their nonrejected agemates. The need for further research on the heterogeneity of peer-rejected children and the long-term implications for these children are discussed.

This article highlights the defining principles, progress, and future directions in epigenetics research in relation to this Special Issue. Exciting studies in the fields of neuroscience, psychology, and psychiatry have provided new insights into the epigenetic factors (e.g., DNA methylation) that are responsive to environmental input and serve as biological pathways in behavioral development. Here we highlight the experimental evidence, mainly from animal models, that factors such as psychosocial stress and environmental adversity can become encoded within epigenetic factors with functional consequences for brain plasticity and behavior. We also highlight evidence that epigenetic marking of genes in one generation can have consequences for future generations (i.e., inherited), and work with humans linking epigenetics, cognitive dysfunction, and psychiatric disorder. Though epigenetics has offered more of a beginning than an answer to the centuries-old nature–nurture debate, continued research is certain to yield substantial information regarding biological determinants of central nervous system changes and behavior with relevance for the study of developmental psychopathology.

This longitudinal study examined antecedents of substance use behavior among 176 (53% male) adolescents. Adolescents were classified as (a) abstainers (n = 19), (b) experimenters (n = 65), (c) at-risk youth (n = 63), and (d) abusers (n = 29) based on their reported substance use behavior at age 17.5. Parental behavior, peer competence, and problem behavior, measured from early childhood through age 16, were examined as predictors of substance use patterns. Multinomial logistic regression models revealed that early maternal hostility, externalizing behavior problems in first grade and at age 16, internalizing behavior in first grade and at age 16, and parental monitoring at age 16 significantly differentiated substance use groups. The study provides evidence that experiences occurring early in development, in addition to those that occur later in development, can play a pivotal role in setting the stage for late adolescent substance use behavior.Preparation of this work and the research described herein were supported by a grant from the National Institute of Mental Health (R01MH40864-18). We acknowledge the participants and their families for their continued participation in this research. Special thanks to Judy Cook, W. Andrew Collins, and the numerous graduate and undergraduates who made this project possible.

This paper integrates the work of Stern on affect regulation, Ainsworth on quality of attachment, Piaget on cognitive development, Tulving on memory systems, and Bowlby on internal representational models around the issue of promoting secure attachment. It is proposed that procedural models of the self and attachment figures develop in infancy, are maintained throughout the life span, and are accessed preconsciously to regulate everyday behavior. In the preoperational period, semantic models of generalizations regarding the self and others are constructed (often from parents' words), encoded, and accessed linguistically when the expectations implied by procedural models are discrepant with outcomes; that is, semantic models are used for problem solving. Episodic models, encoded by multiple means (e.g., verbally, auditorially, visually) develop last and consist of episodes of experience that can be accessed unconsciously and regulate behavior when individuals are emotionally aroused. Of interest is the relation among these emerging models, the patterns of information processing contained in them, and the means of guiding their development in children experiencing distorted relationships. Treatment approaches drawn from social learning theory, family systems theory, cognitive therapy, and psychodynamic theory are associated with the memory systems and integrated into an approach to treatment.

While many studies focus on the association between early life adversity and the later risk for psychopathology, few simultaneously explore diverse forms of environmental adversity. Moreover, those studies that examined the cumulative impact of early life adversity focus uniquely on postnatal influences. The objective of this study was to focus on the fetal period of development to construct and validate a cumulative prenatal adversity score in relation to a wide range of neurodevelopmental outcomes. We also examined the interaction of this adversity score with a biologically informed genetic score based on the serotonin transporter gene. Prenatal adversities were computed in two community birth cohorts using information on health during pregnancy, birth weight, gestational age, income, domestic violence/sexual abuse, marital strain, as well as maternal smoking, anxiety, and depression. A genetic score based on genes coexpressed with the serotonin transporter in the amygdala, hippocampus, and prefrontal cortex during prenatal life was constructed with an emphasis on functionally relevant single nucleotide polymorphisms, that is, expression quantitative trait loci. Prenatal adversities predicted a wide range of developmental and behavioral alterations in children as young as 2 years of age in both cohorts. There were interactions between the genetic score and adversities for several domains of the Child Behavior Checklist (CBCL), with pervasive developmental problems remaining significant adjustment for multiple comparisons. Scores combining different prenatal adverse exposures predict childhood behavior and interact with the genetic background to influence the risk for psychopathology.

The clinical characteristics and adaptive functioning of preschoolers who met DSM-IV criteria for bipolar disorder versus psychiatric and healthy comparison groups were investigated. A community-based sample of 303 preschoolers (3–6 years of age) and their caregivers was ascertained. Diagnostic classification based on parent report of mania symptoms was made using an age-appropriate psychiatric interview. Results indicated that 26 preschoolers met DSM-IV criteria for bipolar disorder who could be identified based the presence of 13 core age-adjusted mania items. These children could be clearly differentiated from children in two psychiatric groups (DSM-IV disruptive disorders, and major depressive disorder) and a “healthy” comparison group based on a specific symptom constellation. Findings indicated that preschoolers in the bipolar group were significantly more (p < .05) impaired than the two psychiatric and healthy groups based on independent measures. Further, even after controlling for comorbid attention-deficit/hyperactivity disorder (81% comorbidity rate), the bipolar group remained significantly (p < .05) more impaired in multiple domains compared to preschoolers with DSM-IV disruptive disorders and healthy controls. Findings suggested that children as young as 3 years can manifest DSM-IV bipolar disorder when age adjusted symptom descriptions are employed, and that these children can be distinguished from healthy and disruptive disordered preschoolers. Recommendations for future research in this area that integrates developmental and mental health models are made.We gratefully acknowledge Edward Spitznagel for his statistical consultation. We are also grateful to the The Early Emotional Development Program staff, our preschool participants and their parents, and community recruiting sites whose participation and cooperation made this research possible. Funding for the study of preschool depression was provided by NIMH Grant NIMH R01 MH64769-01 (to J.L.).

Children reared in impoverished environments are at risk for enduring psychological and physical health problems. Mechanisms by which poverty affects development, however, remain unclear. To explore one potential mechanism of poverty's impact on social–emotional and cognitive development, an experimental examination of a rodent model of scarcity-adversity was conducted and compared to results from a longitudinal study of human infants and families followed from birth (N = 1,292) who faced high levels of poverty-related scarcity-adversity. Cross-species results supported the hypothesis that altered caregiving is one pathway by which poverty adversely impacts development. Rodent mothers assigned to the scarcity-adversity condition exhibited decreased sensitive parenting and increased negative parenting relative to mothers assigned to the control condition. Furthermore, scarcity-adversity reared pups exhibited decreased developmental competence as indicated by disrupted nipple attachment, distress vocalization when in physical contact with an anesthetized mother, and reduced preference for maternal odor with corresponding changes in brain activation. Human results indicated that scarcity-adversity was inversely correlated with sensitive parenting and positively correlated with negative parenting, and that parenting fully mediated the association of poverty-related risk with infant indicators of developmental competence. Findings are discussed from the perspective of the usefulness of bidirectional–translational research to inform interventions for at-risk families.

Motivational ideas in psychology and their relation to causes are reviewed. Key ideas include hedonism, arousal, rational decision-making, reinforcement, and impulsivity. Motivations proposed for different acts classified as conduct disorder or delinquency are discussed as well as motivational constructs in delinquency theories. It is concluded that theories should include energizing, directing, inhibiting, and decision-making stages at a minimum. Empirical studies of motivations for delinquency that involve asking youth to give reasons for their acts are also reviewed. The most common motivations reported are utilitarian (seeking money or material goods) and hedonistic (seeking excitement or pleasure). It is pointed out that the validity of motivational theories is a separate issue from the validity of verbal reports of motivations. People may be aware of immediate situational motivations but unaware of longer term biological, psychological, or social factors. A program of research on the energizing, directing, and inhibiting of antisocial behavior is recommended and on the relative effectiveness, in reducing conduct disorder and delinquency, of programs targeting these different stages.