We present an analysis of the role of emotions in normal and abnormal development and preventive intervention. The conceptual framework stems from three tenets of differential emotions theory (DET). These principles concern the constructs of emotion utilization; intersystem connections among modular emotion systems, cognition, and action; and the organizational and motivational functions of discrete emotions. Particular emotions and patterns of emotions function differentially in different periods of development and in influencing the cognition and behavior associated with different forms of psychopathology. Established prevention programs have not emphasized the concept of emotion as motivation. It is even more critical that they have generally neglected the idea of modulating emotions, not simply to achieve self-regulation, but also to utilize their inherently adaptive functions as a means of facilitating the development of social competence and preventing psychopathology. The paper includes a brief description of a theory-based prevention program and suggestions for complementary targeted interventions to address specific externalizing and internalizing problems. In the final section, we describe ways in which emotion-centered preventions can provide excellent opportunities for research on the development of normal and abnormal behavior.

In light of evidence that the effects of attachment security on subsequent development may be contingent on the social context in which the child continues to develop, we examined the effect of attachment security at age 15 months, cumulative contextual risk from 1 to 36 months, and the interaction of attachment and cumulative risk to predict socioemotional and cognitive linguistic functioning at age 3 years, using data from the National Institute of Child Health and Human Development Study of Early Child Care. Results indicated that early attachment predicts both socioemotional development and language skills, but not cognitive functioning as indexed by a measure of school readiness, and that the effect of attachment on socioemotional development and expressive language varied as a function of social-contextual risk. Insecure–avoidant infants proved most vulnerable to contextual risk, not children classified as secure or insecure more generally, although in one instance security did prove protective with respect to the adverse effects of cumulative contextual risk. Findings are discussed in terms of risk and resilience and in light of the probabilistic nature of the relation between early attachment and later development.

Externalizing behavior problems of 124 adolescents were assessed across Grades 7–11. In Grade 9, participants were also assessed across social-cognitive domains after imagining themselves as the object of provocations portrayed in six videotaped vignettes. Participants responded to vignette-based questions representing multiple processes of the response decision step of social information processing. Phase 1 of our investigation supported a two-factor model of the response evaluation process of response decision (response valuation and outcome expectancy). Phase 2 showed significant relations between the set of these response decision processes, as well as response selection, measured in Grade 9 and (a) externalizing behavior in Grade 9 and (b) externalizing behavior in Grades 10–11, even after controlling externalizing behavior in Grades 7–8. These findings suggest that on-line behavioral judgments about aggression play a crucial role in the maintenance and growth of aggressive response tendencies in adolescence.

The study of brain development and that of behavioral development have historically proceeded independently of one another. This is an unfortunate set of circumstances, given that the disciplines concerned with development—for example, developmental psychology, pediatrics, psychiatry, clinical psychology, and the neurosciences—have much to learn from each other. Drawing on recent advances in the developmental brain and behavioral sciences, we illustrate the transdisciplinary approach our group has adopted in the service of uniting the research on brain and behavior in the context of development. We specifically report on our nonhuman primate and human studies that collectively illustrate our “genes to behavior” approach to the study of development. Our goal in summarizing our research in this fashion is to promote discussion about promising templates for how research on brain, behavior, and development might proceed into the 21st century.

This study examined the relation of negative emotionality in infancy to child social and cognitive developmental outcomes among low birth weight (LBW) preterm infants participating in the Infant Health and Development Program (IHDP), a comprehensive compensatory education intervention beginning in infancy and lasting through age 3 years. In this analysis, intervention effects at age 36 months on maternal report of child behavior as assessed by the Child Behavior Checklist externalizing and internalizing scales and on intelligence as measured by the Stanford–Binet scale were largest among children characterized by higher levels of negative emotionality in infancy. Findings indicate that for LBW preterm infants characterized by negative emotionality at age 12 months the intervention was associated with a twofold decrease in the occurrence of clinically meaningful levels of behavior problems at age 3 years and a fourfold decrease in the occurrence of a high-risk profile in which both internalizing and externalizing scores are in the clinically meaningful range. The intervention was also associated with a fivefold decrease in the occurrence of IQ ≤ 75 at age 3 years among children with higher levels of negative emotionality and heavier LBW (2001–2500 g). However, specific aspects of temperamental difficulty such as fearfulness and anger were related to internalizing and externalizing, respectively, in both the intervention and control groups. Findings are consistent with research linking negative emotionality in infancy with social and cognitive developmental outcomes in early childhood among normal birth weight infants. Results suggest the need for further attention to child temperament in early intervention research.

To date, research involving functional neuroimaging of typical and atypical development has depended on several assumptions about the postnatal maturation of the brain. We consider evidence from multiple levels of analysis that brings into question these underlying assumptions and advance an alternative view. This alternative view, based on an “interactive specialization” approach to postnatal brain development, indicates that there is a need to: obtain data from early in development; focus more on differences in interregional interactions rather than searching for localized, discrete lesions; examine the temporal dynamics of neural processing; and move away from deficits to image tasks in which atypical participants perform as well as typically developing participants.

Observed parent–adolescent autonomy struggles were assessed as potential predictors of the development of peer-rated hostility over a decade later in young adulthood in both normal and previously psychiatrically hospitalized groups of adolescents. Longitudinal, multireporter data were obtained by coding family interactions involving 83 adolescents and their parents at age 16 years and then obtaining ratings by close friends of adolescents' hostility at age 25 years. Fathers' behavior undermining adolescents' autonomy in interactions at age 16 years were predictive of adolescents-as-young-adults' hostility, as rated by close friends at age 25 years. These predictions contributed additional variance to understanding young adult hostility even after accounting for concurrent levels of adolescent hostility at age 16 years and paternal hostility at this age, each of which also significantly contributed to predicting future hostility. Results are discussed as highlighting a pathway by which difficulties attaining autonomy in adolescence may presage the development of long-term difficulties in social functioning.

Intervention research with children and adolescents has suffered from a dearth of relevant theoretical grounding and from the lack of a reciprocal “feedback” mechanism by which clinical trials can inform relevant theorizing and conceptualization. There are hopeful signs, however, of increasing confluence between clinical efforts and theoretical models. Indeed, the key issue I discuss is how intervention studies can yield information about developmental and clinical theory as well as mechanisms related to psychopathology. Specific research examples in the field, particularly those emanating from the Multimodal Treatment Study of Children with attention deficit/hyperactivity disorder (MTA study), reveal that probes of moderator and mediator variables can clearly enhance our knowledge of relevant processes and mechanisms. In fact, recent MTA findings have relevance for models of genetic and epigenetic influence on symptomatology related to attentional deficits and hyperactivity. It would be overzealous, however, to make premature claims regarding etiologic variables from intervention research, as treatment studies typically address variables that are causally far “downstream” from primary causal factors and most clinical trials have statistical power that is barely sufficient for main outcome questions, much less mediational linkages. Overall, the field has severely underutilized experimental intervention research to subserve the dual ends of improving the lives of youth and advancing theoretical conceptualization regarding development and psychopathology.

With advancements in the technology of prevention and treatment of childhood anxiety disorders, information regarding our understanding of normal and abnormal child development can be enriched. Typically, research has focused on developing efficacious and effective interventions with less attention devoted to the impact this information may have on the field of developmental psychopathology. By reviewing the results of both treatment and prevention studies, several potential contributions of intervention research to the field can be explored. Results from wait-list or monitoring control groups will be reviewed, providing valuable information regarding the normal trajectory of the anxious child. Outcomes of children receiving the intervention prove that this pathway can be altered and is not impermeable. Furthermore, a review of long-term follow-up studies addresses the question of whether intervention can change the long-term trajectory of an anxiety-disordered child and prevent disorders in later life. Contributions to the etiological understanding of the anxiety disorders will also be reviewed: changes in variables considered important in the etiology and maintenance of disorder can be examined in synchronicity with changes in symptomatology following intervention. An examination of potential developmental predictors of treatment outcome will also contribute to this review, with a focus on the limitations of the current research in gaining a complete understanding of the relationship between developmental level and outcome. Directions regarding future research in the study of interventions for child and adolescent anxiety disorders will be discussed with the aim of promoting further communication between intervention research and the field of developmental psychopathology.

Research suggests that disruptions in early caretaking can have long-term effects on the hypothalamic–pituitary–adrenal (HPA) axis, which mediates the stress response. Children of depressed mothers are at increased risk for developing internalizing problems in part because of disruptions in their caretaking environment. The present study investigated whether children of depressed mothers exhibit elevated salivary cortisol levels. Salivary cortisol samples were collected from 45 7- to 8-year-old children of mothers with a history of depression and 29 children of nondepressed mothers. Samples were collected soon after arrival to the laboratory and after a mild laboratory stressor and at home after wakeup and before bedtime. Children who had elevated levels of internalizing symptoms and whose mothers had a history of depression showed elevated laboratory baseline cortisol levels. Children who were reported to have clinically significant internalizing symptoms were also more likely to show an elevated stress response to a mild laboratory stressor. When the longitudinal history of maternal depression was examined, maternal depression during the child's first 2 years of life was the best predictor of elevations in baseline cortisol at age 7 years. This study provides evidence that internalizing symptoms exist in conjunction with a more reactive hormonal stress system in children of depressed mothers. The results also provide preliminary evidence that exposure to maternal depression in the first 2 years of life may be related to children's cortisol levels later in life.

The hypothesis that brain stem injury plays a role in the autism spectrum disorders was suggested by evidence that exposure to thalidomide during the earliest stages of brain development increases the risk of autism spectrum disorders. The implications for the embryological origin of autism first led to studies of neuroanatomy in a human case and an animal model and then to examinations of minor craniofacial features in autism. But the general hypothesis had much broader implications. It has now generated studies of the behavioral and neurological symptoms of human patients, of human molecular genetics and population genetics, and of animal behavioral teratology and molecular pharmacology. The collection of this range of data was made possible by adding experts from many fields to the research team. They worked both independently and collaboratively to try to unravel the etiology of autism.

Although they have received little empirical attention, departures from the parental home play a significant role in demarcating the transition from adolescence to young adulthood. The current study examined the extent to which various features of young adults' experiences of leaving home differed for children of alcoholic (COAs) versus nonalcoholic parents, what adolescent precursors might account for noted differences and what indicators of young adult adjustment are related to the leaving home experience. A total of 227 young adults drawn from a high-risk, community sample of COAs and matched controls were interviewed at ages 18–23 years regarding their prior leaving home experiences. COAs showed greater difficulties in negotiating this transition, fewer positive feelings about the transition, and different reasons for leaving home as compared to participants without an alcoholic parent. Moreover, adolescent risk behaviors, family conflict, and family disorganization (assessed prior to this transition) each partly accounted for COAs' risk for difficulty in the leaving home transition. Although certain aspects of the leaving home transition were uniquely related to young adult adjustment, future research is still needed to more comprehensively understand the implications for young adult development associated with such individual differences in the leaving home transition.

All children who enter foster care have experienced disruptions in their relationships with caregivers, and many have experienced maltreatment. Studying the effects of these adverse early experiences can inform developmental theory. In particular, insight can be provided regarding sensitive periods in the development of attachment and self-regulatory capabilities. The quality of surrogate caregivers varies as a function of both the intervention services provided and foster parent characteristics. Studying the effects of foster parent quality can suggest which aspects of child functioning are more or less canalized at various developmental periods. This paper considers salient developmental issues of infancy, preschool years, middle childhood, and adolescence and examines ways in which these issues may present special difficulties for foster children. Across development, foster care is associated with difficulties regulating behaviors, emotions, and physiology. Thus, conditions associated with foster care placement (e.g., disruptions in care, maltreatment) appear to affect very basic and fundamental regulatory processes. Interventions have been designed that target developmentally specific manifestations of regulatory difficulties. Although the literature regarding evidence-based interventions for foster parents is quite limited, preliminary findings provide some evidence that nurturing, responsive care can serve to partially remediate early deficits. These findings suggest that stable and nonfrightening care is essential for normal development. Nonetheless, even in the case of quite adverse early experience that results in problematic child outcomes, there is some evidence that the development of many systems remains relatively plastic.

This paper uses a latent class modeling approach to examine gender related variations in offending trajectories from adolescence to young adulthood. This approach is applied to data gathered over the course of a longitudinal study of 896 New Zealand children studied from birth to age 21 years. The analysis identified five trajectory groups: a group of low-risk offenders, three groups of adolescent-limited offenders who varied in the timing of the onset of offending (early, intermediate, and late onset), and a group of chronic offenders. Identical offending trajectories applied for males and females. However, probabilities of trajectory group membership varied with gender, with females being more likely to exhibit low-risk or early onset adolescent-limited offending and males later onset and chronic offending. Examination of social, family, and individual factors associated with these trajectories suggested the presence of a series of common etiological factors relating to family functioning and early adjustment that discriminated between trajectory groups. These risk factors appeared to operate in a similar fashion for both males and females. Implications of these findings for trajectory theories of offending are discussed.

Smoking during pregnancy is associated with adverse consequences for children. Most recently, it has been established as a risk factor for developmental psychopathology, specifically Conduct Disorder (CD). Although this association has been shown to be robust, developmental pathways from exposure to CD have not been established. We examined how prenatal exposure to cigarettes interacts with child and family factors to increase risk of CD symptoms in a longitudinal study of 10-year-old urban, African-American youth (N = 77). The effects of prenatal exposure at school age were moderated by child sex. Boys whose mothers smoked during pregnancy were significantly more likely to develop CD symptoms, but exposure did not increase risk in girls. A similar trend was found during infancy: prenatal smoking was associated with low sociability/negative emotionality only for boys. The effects of smoking during pregnancy were also moderated by the quality of the early caregiving environment. Exposed boys whose mothers were unresponsive during infancy were at increased risk of CD symptoms, but exposed boys with early responsive mothers were not. Prospective studies, with developmentally based measures of behavior across time, are critical for further elucidating pathways from prenatal exposure to cigarettes to the development of clinical disorder. The identification of a potentially modifiable, prenatal risk factor for early onset developmental psychopathology has important implications for prevention.

Developmental language learning impairments (LLI) are one of the most prevalent of all developmental disabilities, can occur in children for a wide variety of reasons, and have been shown to co-occur frequently with other developmental social, emotional and behavioral disorders, as well as with academic achievement problems. Research pertaining to developmental LLI of unknown origin, with an emphasis on the continuum between oral and written language impairment, is the focus of this review. Given the complexity of language learning, research has focused on multiple levels of analysis, including linguistic, neuropsychological, genetic, neurobiological, and remediation studies. To date, the vast majority of data on LLI derive from studies focused on a single level of analysis. Although attempts have been made to integrate data across studies and multiple levels of analysis, this has proven to be problematic, given the heterogeneity of the subject populations used to study LLI, as well as the differences in ages, degree of impairment, and types of impairment included in each study. Given that LLI is a complex developmental disability, it is suggested that future research would benefit from taking a multiple levels of analysis approach with the same individuals, incorporating mathematical models designed to analyze dynamically changing complex systems, and studying individual differences in language learning, prospectively and longitudinally, throughout the most dynamic stages of the process.

Achieving progress in understanding the cause, nature, and treatment of autism requires an integration of concepts, approaches, and empirical findings from genetic, cognitive neuroscience, animal, and clinical studies. The need for such integration has been a fundamental tenet of the discipline of developmental psychopathology from its inception. It is likely that the discovery of autism susceptibility genes will depend on the development of dimensional measures of broader phenotype autism traits. It is argued that knowledge of the cognitive neuroscience of social and language behavior will provide a useful framework for defining such measures. In this article, the current state of knowledge of the cognitive neuroscience of social and language impairments in autism is reviewed. Following from this, six candidate broader phenotype autism traits are proposed: (a) face processing, including structural encoding of facial features and face movements, such as eye gaze; (b) social affiliation or sensitivity to social reward, pertaining to the social motivational impairments found in autism; (c) motor imitation ability, particularly imitation of body actions; (d) memory, specifically those aspects of memory mediated by the medial temporal lobe–prefrontal circuits; (e) executive function, especially planning and flexibility; and (f) Language ability, particularly those aspects of language that overlap with specific language impairment, namely, phonological processing.

This article reports a comparison on outcomes of 26-year-old males who were defined several years ago in the Dunedin longitudinal study as exhibiting childhood-onset versus adolescent-onset antisocial behavior and who were indistinguishable on delinquent offending in adolescence. Previous studies of these groups in childhood and adolescence showed that childhood-onset delinquents had inadequate parenting, neurocognitive problems, undercontrolled temperament, severe hyperactivity, psychopathic personality traits, and violent behavior. Adolescent-onset delinquents were not distinguished by these features. Here followed to age 26 years, the childhood-onset delinquents were the most elevated on psychopathic personality traits, mental-health problems, substance dependence, numbers of children, financial problems, work problems, and drug-related and violent crime, including violence against women and children. The adolescent-onset delinquents at 26 years were less extreme but elevated on impulsive personality traits, mental-health problems, substance dependence, financial problems, and property offenses. A third group of men who had been aggressive as children but not very delinquent as adolescents emerged as low-level chronic offenders who were anxious, depressed, socially isolated, and had financial and work problems. These findings support the theory of life-course-persistent and adolescence-limited antisocial behavior but also extend it. Findings recommend intervention with all aggressive children and with all delinquent adolescents, to prevent a variety of maladjustments in adult life.

There is growing recognition that traditional strategies, such as pullout special education programs and on-site casework and guidance, are no longer sufficient to address the staggering needs of a growing number of troubled children entering U.S. schools. This paper introduces a school-based prevention and intervention method for young adolescents called Responsive Advocacy for Life and Learning in Youth (RALLY). Prevention practitioners, a new role developed by the program, work in classrooms and after-school settings to provide nonstigmatizing support to students. Using a three-tiered prevention model, practitioners integrate a mental health and educational focus to foster students' academic, social, and emotional success. The intervention involves all children of an age cohort in middle schools. The practitioners are developmental specialists who create relationships with youth, teachers, and families in high-risk environments and serve triage functions to existing community and health care institutions. The RALLY intervention builds on normative developmental and developmental psychopathology theory, especially a risk and resilience framework. The paper describes the principles behind the practice and how the work in this field has created innovations in theory and a new impetus for research.

This study investigated the correlates of childhood depressive symptoms in an African American sample. We included processes that are likely to operate for all children, regardless of race or ethnicity, as well as events and circumstances that are largely unique to children of color. These various constructs were assessed at both the individual and community level. The analyses consisted of hierarchical linear modeling with a sample of 810 African American families living in Iowa and Georgia. Three individual-level variables were associated with childhood depressive symptoms: uninvolved parenting, racial discrimination, and criminal victimization. At the community level, prevalence of both discrimination and criminal victimization were positively related and community ethnic identification was negatively related to depressive symptoms. Further, there was evidence that community ethnic identification and neighborhood poverty serve to moderate the relationship between criminal victimization and depressive symptoms. Overall, the findings underscore the importance of considering factors unique to the everyday lives of the cultural group that is the focus of study, while demonstrating the dangers of a “one model fits all” approach to studying children of color.