This article reviews the research on resilience in order to delineate its significance and potential for understanding normal development. Resilience refers to the process of, capacity for, or outcome of successful adaptation despite challenging or threatening circumstances. Three resilience phenomena are reviewed: (a) good outcomes in high-risk children, (b) sustained competence in children under stress, and (c) recovery from trauma. It is concluded that human psychological development is highly buffered and that long-lasting consequences of adversity usually are associated with either organic damage or severe interference in the normative protective processes embedded in the caregiving system. Children who experience chronic adversity fare better or recover more successfully when they have a positive relationship with a competent adult, they are good learners and problem-solvers, they are engaging to other people, and they have areas of competence and perceived efficacy valued by self or society. Future studies of resilience will need to focus on processes that facilitate adaptation. Such studies have the potential to illuminate the range and self-righting properties of, constraints on, and linkages among different aspects of cognitive, emotional, and social development.

The circumplex model of affect proposes that all affective states arise from cognitive interpretations of core neural sensations that are the product of two independent neurophysiological systems. This model stands in contrast to theories of basic emotions, which posit that a discrete and independent neural system subserves every emotion. We propose that basic emotion theories no longer explain adequately the vast number of empirical observations from studies in affective neuroscience, and we suggest that a conceptual shift is needed in the empirical approaches taken to the study of emotion and affective psychopathologies. The circumplex model of affect is more consistent with many recent findings from behavioral, cognitive neuroscience, neuroimaging, and developmental studies of affect. Moreover, the model offers new theoretical and empirical approaches to studying the development of affective disorders as well as the genetic and cognitive underpinnings of affective processing within the central nervous system.This work was supported in part by NIMH Grants MH01232, MH59139, MH36197, MHK02-74677, and MH068318; a grant from the National Alliance for Research in Schizophrenia and Affective Disorders (NARSAD); NSF Grant BSC-0421702; and funding from the Thomas D. Klingenstein and Nancy D. Perlman Family Fund and the Suzanne Crosby Murphy Endowment at Columbia University.

Biological reactivity to psychological stressors comprises a complex, integrated, and highly conserved repertoire of central neural and peripheral neuroendocrine responses designed to prepare the organism for challenge or threat. Developmental experience plays a role, along with heritable, polygenic variation, in calibrating the response dynamics of these systems, with early adversity biasing their combined effects toward a profile of heightened or prolonged reactivity. Conventional views of such high reactivity suggest that it is an atavistic and pathogenic legacy of an evolutionary past in which threats to survival were more prevalent and severe. Recent evidence, however, indicates that (a) stress reactivity is not a unitary process, but rather incorporates counterregulatory circuits serving to modify or temper physiological arousal, and (b) the effects of high reactivity phenotypes on psychiatric and biomedical outcomes are bivalent, rather than univalent, in character, exerting both risk-augmenting and risk-protective effects in a context-dependent manner. These observations suggest that heightened stress reactivity may reflect, not simply exaggerated arousal under challenge, but rather an increased biological sensitivity to context, with potential for negative health effects under conditions of adversity and positive effects under conditions of support and protection. From an evolutionary perspective, the developmental plasticity of the stress response systems, along with their structured, context-dependent effects, suggests that these systems may constitute conditional adaptations: evolved psychobiological mechanisms that monitor specific features of childhood environments as a basis for calibrating the development of stress response systems to adaptively match those environments. Taken together, these theoretical perspectives generate a novel hypothesis: that there is a curvilinear, U-shaped relation between early exposures to adversity and the development of stress-reactive profiles, with high reactivity phenotypes disproportionately emerging within both highly stressful and highly protected early social environments.The research on which this paper was based was supported by grants from the John D. and Catherine T. MacArthur Foundation's Research Network on Psychopathology and Development, the National Institute of Child Health and Human Development (1RO1 HD 24718), and by the Division of Intramural Research of NICHD. The first author is particularly indebted to Dr. Steve Suomi and Dr. Jan Genevro for a series of conversations that directly influenced the ideas upon which this paper is based. We also thank Dr. Jay Belsky and Dr. David Bjorklund for their helpful comments on an earlier draft of this paper.

The focus of this article is on the interface between research on resilience—a construct representing positive adaptation despite adversity —and the applications of this work to the development of interventions and social policies. Salient defining features of research on resilience are delineated, as are various advantages, limitations, and precautions linked with the application of the resilience framework to developing interventions. For future applied efforts within this tradition, a series of guiding principles are presented along with exemplars of existing programs based on the resilience paradigm. The article concludes with discussions of directions for future work in this area, with emphases on an enhanced interface between science and practice, and a broadened scope of resilience-based interventions in terms of the types of populations, and the types of adjustment domains, that are encompassed.

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.

The paper traces the relationship between attachment processes and the development of the capacity to envision mental states in self and others. We suggest that the ability to mentalize, to represent behavior in terms of mental states, or to have “a theory of mind” is a key determinant of self-organization which is acquired in the context of the child's early social relationships. Evidence for an association between the quality of attachment relationship and reflective function in the parent and the child is reviewed and interpreted in the context of current models of theory of mind development. A model of the development of self-organization is proposed which has at its core the caregiver's ability to communicate understanding of the child's intentional stance. The implications of the model for pathological self-development are explored, with specific reference to the consequences of maltreatment.

During the past 10 years nearly 80 studies on disorganized attachment involving more than 6,000 infant–parent dyads have been carried out. The current series of meta-analyses have established the reliability and discriminant validity of disorganized infant attachment. Although disorganized attachment behavior is necessarily difficult to observe and often subtle, many researchers have managed to become reliable coders. Furthermore, disorganized attachment shows modest short- and long-term stability, in particular in middle class environments, and it is not just a concomitant of constitutional, temperamental, or physical child problems. The predictive validity of disorganized attachment is established in terms of problematic stress management, the elevated risk of externalizing problem behavior, and even the tendency of disorganized infants to show dissociative behavior later in life. In normal, middle class families, about 15% of the infants develop disorganized attachment behavior. In other social contexts and in clinical groups this percentage may become twice or even three times higher (e.g., in the case of maltreatment). Although the importance of disorganized attachment for developmental psychopathology is evident, the search for the mechanisms leading to disorganization has just started. Frightening parental behavior may play an important role but it does not seem to be the only causal factor involved in the emergence of disorganized attachment.

Two extant evolutionary models, biological sensitivity to context theory (BSCT) and differential susceptibility theory (DST), converge on the hypothesis that some individuals are more susceptible than others to both negative (risk-promoting) and positive (development-enhancing) environmental conditions. These models contrast with the currently dominant perspective on personal vulnerability and environmental risk: diathesis stress/dual risk. We review challenges to this perspective based on emerging theory and data from the evolutionary, developmental, and health sciences. These challenges signify the need for a paradigm shift in conceptualizing Person × Environment interactions in development. In this context we advance an evolutionary–neurodevelopmental theory, based on DST and BSCT, of the role of neurobiological susceptibility to the environment in regulating environmental effects on adaptation, development, and health. We then outline current thinking about neurogenomic and endophenotypic mechanisms that may underpin neurobiological susceptibility, summarize extant empirical research on differential susceptibility, and evaluate the evolutionary bases and implications of BSCT and DST. Finally, we discuss applied issues including methodological and statistical considerations in conducting differential susceptibility research; issues of ecological, cultural, and racial–ethnic variation in neurobiological susceptibility; and implications of differential susceptibility for designing social programs. We conclude that the differential susceptibility paradigm has far-reaching implications for understanding whether and how much child and adult development responds, for better and for worse, to the gamut of species-typical environmental conditions.

This article reports a comparison on childhood risk factors of males and females exhibiting childhood-onset and adolescent-onset antisocial behavior, using data from the Dunedin longitudinal study. Childhood-onset delinquents had childhoods of inadequate parenting, neurocognitive problems, and temperament and behavior problems, whereas adolescent-onset delinquents did not have these pathological backgrounds. Sex comparisons showed a male-to-female ratio of 10:1 for childhood-onset delinquency but a sex ratio of only 1.5:1 for adolescence-onset delinquency. Showing the same pattern as males, childhood-onset females had high-risk backgrounds but adolescent-onset females did not. These findings are consistent with core predictions from the taxonomic theory of life-course persistent and adolescence-limited antisocial behavior.

In the last decade, cardiac vagal tone has emerged as a psychophysiological marker of many aspects of behavioral functioning in both children and adults. Research efforts during this time have produced an extensive list of vagal tone correlates that includes temperamental variables as well as both anxious/internalizing and disruptive/externalizing behaviors. This potentially confusing state of affairs is compounded by developmental shifts in vagal tone–behavior relations that to date have not been elucidated. In this paper, the vagal tone literature is reviewed, and discrepancies, including the lack of specificity of vagal tone as a psychophysiological marker, are clarified. Such clarification requires that we (a) view vagal tone–behavior relations in developmental context, (b) juxtapose vagal tone–behavior relations in typical and atypical samples, and (c) consider the parasympathetic underpinnings of vagal tone as but one component in a broader model of autonomic nervous system functioning. Such a model is provided by combining Gray's motivational theory with Porges's polyvagal theory. Together these models account for behavioral and emotional differences in a diverse range of psychological disorders that are not differentiated by either model alone. Moreover, use of the integrated model offers a theory-driven approach to the study of autonomic nervous system–behavior relations.

The concept of resilience has as its starting point the recognition that there is huge heterogeneity in people's responses to all manner of environmental adversities. Resilience is an inference based on evidence that some individuals have a better outcome than others who have experienced a comparable level of adversity; moreover, the negative experience may have either a sensitizing effect or a strengthening “steeling” effect in relation to the response to later stress or adversity. After noting the crucial importance of first testing for the environmental mediation of risk through “natural experiments,” findings are reviewed on “steeling effects” in animal models and humans. Gene–environment interaction findings are considered, and it is noted that there is some evidence that the genetic influences concerns responsivity to all environments and not just bad ones. Life course effects are reviewed in relation to evidence on turning point effects associated with experiences that increase opportunities and enhance coping. Attention is drawn to both research implications and substantive findings as features that foster resilience.

Child development involves both reactive and self-regulatory mechanisms that children develop in conjunction with social norms. A half-century of research has uncovered aspects of the physical basis of attentional networks that produce regulation, and has given us some knowledge of how the social environment may alter them. In this paper, we discuss six forms of developmental plasticity related to aspects of attention. We then focus on effortful or executive aspects of attention, reviewing research on temperamental individual differences and important pathways to normal and pathological development. Pathologies of development may arise when regulatory and reactive systems fail to reach the balance that allows for both self-expression and socially acceptable behavior. It remains a challenge for our society during the next millennium to obtain the information necessary to design systems that allow a successful balance to be realized by the largest possible number of children.

The clinical concept of psychopathy (“psychopathic personality”) is generally considered to entail persistent behavioral deviancy in the company of emotional–interpersonal detachment. However, longstanding debates continue regarding the appropriate scope and boundaries of the concept. Here, we review alternative historic descriptions of the disorder together with empirical findings for the best-established assessment instruments in use with adolescents and youth as a basis for formulating an integrative, triarchic model of psychopathy. The essence of the triarchic model is that psychopathy encompasses three distinct phenotypic constructs: disinhibition, which reflects a general propensity toward problems of impulse control; boldness, which is defined as the nexus of social dominance, emotional resiliency, and venturesomeness; and meanness, which is defined as aggressive resource seeking without regard for others (“dysaffliated agency”). These differing phenotypic components are considered in terms of relevant etiologic and developmental pathways. The triarchic conceptualization provides a basis for reconciling and accommodating alternative descriptive accounts of psychopathy, and a framework for coordinating research on neurobiological and developmental processes contributing to varying manifestations of the disorder.

There is a growing acceptance of a holistic, interactionistic view in which the individual is seen as an organized whole, functioning and developing as a totality. This view emphasizes the importance of patterns of operating factors. Within this framework, a standard variable-oriented approach, focusing on the variable as the main theoretical and analytical unit, has limitations. A person-oriented approach would often be preferable, where the main theoretical and analytical unit is the specific pattern of operating factors. Such an approach is presented here, focusing on individual development and psychopathology. A brief theoretical and methodological overview is given and a classification approach is emphasized. Empirical examples concerning the longitudinal study of adjustment problems illustrate a number of issues believed to be important to development and psychopathology: problem gravitation, the significance of single variables and of patterns, the developmental study of syndromes (=typical patterns), and the detection of “white spots” in development.

Increasing evidence supports the view that the interaction of perinatal exposure to adversity with individual genetic liabilities may increase an individual's vulnerability to the expression of psycho- and physiopathology throughout life. The early environment appears to program some aspects of neurobiological development and, in turn, behavioral, emotional, cognitive, and physiological development. Several rodent and primate models of early adverse experience have been analyzed in this review, including those that “model” maternal separation or loss, abuse or neglect, and social deprivation. Accumulating evidence shows that these early traumatic experiences are associated with long-term alterations in coping style, emotional and behavioral regulation, neuroendocrine responsiveness to stress, social “fitness,” cognitive function, brain morphology, neurochemistry, and expression levels of central nervous system genes that have been related to anxiety and mood disorders. Studies are underway to identify important aspects of adverse early experience, such as (a) the existence of “sensitive periods” during development associated with alterations in particular output systems, (b) the presence of “windows of opportunity” during which targeted interventions (e.g., nurturant parenting or supportive–enriching environment) may prevent or reverse dysfunction, (c) the identity of gene polymorphisms contributing to the individual's variability in vulnerability, and (d) a means to translate the timing of these developmental “sensitive periods” across species.

Advances in the fields of cognitive and affective developmental neuroscience, developmental psychopathology, neurobiology, genetics, and applied behavior analysis have contributed to a more optimistic outcome for individuals with autism spectrum disorder (ASD). These advances have led to new methods for early detection and more effective treatments. For the first time, prevention of ASD is plausible. Prevention will entail detecting infants at risk before the full syndrome is present and implementing treatments designed to alter the course of early behavioral and brain development. This article describes a developmental model of risk, risk processes, symptom emergence, and adaptation in ASD that offers a framework for understanding early brain plasticity in ASD and its role in prevention of the disorder.

The precise nature and etiopathogenesis of borderline personality disorder (BPD) continues to elude researchers and clinicians. Yet, increasing evidence from various strands of research converges to suggest that affect dysregulation, impulsivity, and unstable relationships constitute the core features of BPD. Over the last two decades, the mentalization-based approach to BPD has attempted to provide a theoretically consistent way of conceptualizing the interrelationship between these core features of BPD, with the aim of providing clinicians with a conceptually sound and empirically supported approach to BPD and its treatment. This paper presents an extended version of this approach to BPD based on recently accumulated data. In particular, we suggest that the core features of BPD reflect impairments in different facets of mentalization, each related to impairments in relatively distinct neural circuits underlying these facets. Hence, we provide a comprehensive account of BPD by showing how its core features are related to each other in theoretically meaningful ways. More specifically, we argue that BPD is primarily associated with a low threshold for the activation of the attachment system and deactivation of controlled mentalization, linked to impairments in the ability to differentiate mental states of self and other, which lead to hypersensitivity and increased susceptibility to contagion by other people's mental states, and poor integration of cognitive and affective aspects of mentalization. The combination of these impairments may explain BPD patients' propensity for vicious interpersonal cycles, and their high levels of affect dysregulation and impulsivity. Finally, the implications of this expanded mentalization-based approach to BPD for mentalization-based treatment and treatment of BPD more generally are discussed.

This paper examines interrelations between biological and social influences on the development of self-regulation in young children and considers implications of these interrelations for the promotion of self-regulation and positive adaptation to school. Emotional development and processes of emotion regulation are seen as influencing and being influenced by the development of executive cognitive functions, including working memory, inhibitory control, and mental flexibility important for the effortful regulation of attention and behavior. Developing self-regulation is further understood to reflect an emerging balance between processes of emotional arousal and cognitive regulation. Early childhood educational programs that effectively link emotional and motivational arousal with activities designed to exercise and promote executive functions can be effective in enhancing self-regulation, school readiness, and school success.