A dimensional model of personality disturbance is presented that is defined by extreme values on interacting subsets of seven major personality traits. Being at the extreme has marked effects on the threshold for eliciting those traits under stimulus conditions: that is, the extent to which the environment affects the neurobiological functioning underlying the traits. To explore the nature of development of extreme values on these traits, each trait is discussed in terms of three major issues: (a) the neurobiological variables associated with the trait, (b) individual variation in this neurobiology as a function of genetic polymorphisms, and (c) the effects of environmental adversity on these neurobiological variables through the action of epigenetic processes. It is noted that gene–environment interaction appears to be dependent on two main factors: (a) both genetic and environmental variables appear to have the most profound and enduring effects when they exert their effects during early postnatal periods, times when the forebrain is undergoing exuberant experience–expectant dendritic and axonal growth; and (b) environmental effects on neurobiology are strongly modified by individual differences in “traitlike” functioning of neurobiological variables. A model of the nature of the interaction between environmental and neurobiological variables in the development of personality disturbance is presented.

A developmental–evolutionary perspective is used to synthesize basic research from the neurosciences, ethology, genetics, and developmental psychology into a unified framework for understanding the nature and origins of social anxiety and avoidant personality disorder. Evidence is presented that social anxiety disorder (social phobia) and avoidant personality disorder may be alternate conceptualizations of the same disorder because they have virtually the same symptoms and genetic basis, and respond to the same pharmacologic and psychotherapeutic interventions. A functionalist perspective on social anxiety is formulated to (a) explain the origins of normative states of anxiety, (b) outline developmental pathways in the transition from normative anxiety to social anxiety and avoidant personality disorders, and (c) account for the processes leading to gender-differentiated patterns of anxiety-related disorders after puberty.

The present longitudinal study investigated cascade effects linking the longitudinal trajectories of shyness and aggressiveness between age 4 and 23 and individual differences in this longitudinal relationship. Results demonstrated that there were cascade effects from shyness to adjacent measures of aggressiveness at three moments in time, and that the dynamics of these relationships changed over time. Children who were shy at age 6 became less aggressive at age 7 and the same effect was found between age 8 and age 10. From adolescence to early adulthood, the direction of the relationship changed and shy adolescents at age 17 became increasingly aggressive 5 years later. Interindividual differences were found in the latter cascade effect in that shyness at age 17 only predicted an increase in aggressiveness at age 23 for adolescents receiving low levels of support from their parents and for adolescents spending little time in part-time work. Together, findings suggest the importance of examining the development of normal variations in personality and personality disorders from a developmental perspective and taking into account person–environment interactions.

Early antisocial behavior has its origins in childhood behavior problems, particularly those characterized by aggressive and destructive behavior. Deficits in self-regulation across multiple domains of functioning, from the physiological to the cognitive, are associated with early behavior problems, and may place children at greater risk for the development of later antisocial behavior. Data are presented from a longitudinal study of early self-regulation and behavior problems, the RIGHT Track Research Project, demonstrating that children at greatest risk for early and persistent problem behavior display patterns of physiological and emotional regulation deficits early in life. Parenting behavior and functioning have also been examined as predictors of trajectories of early problem behavior, and some data support the interaction of parenting and self-regulation as significant predictors of patterns of problematic behavior and ongoing problems with the regulation of affect. Peer relationships also affect and are affected by early self-regulation skills, and both may play a role in academic performance and subsequent school success. These data provide evidence that the social contexts of early family and peer relationships are important moderators of the more proximal mechanism of self-regulation, and both types of processes, social and biobehavioral, are likely implicated in early antisocial tendencies. Implications of these findings on self-regulation and early behavior problems are discussed in terms of future research and treatment approaches.

This paper reviews research on chronic patterns of antisocial behavior and places this research into a developmental psychopathology framework. Specifically, research suggests that there are at least three important pathways through which children and adolescents can develop severe antisocial behaviors. One group of youth shows antisocial behavior that begins in adolescence, and two groups show antisocial behavior that begins in childhood but differ on the presence or absence of callous–unemotional traits. In outlining these distinct pathways to antisocial behavior, we have tried to illustrate some key concepts from developmental psychopathology such as equifinality and multifinality, the importance of understanding the interface between normal and abnormal development, and the importance of using multiple levels of analyses to advance causal theories. Finally, we discuss how this development model can be used to enhance existing interventions for antisocial individuals.

The current diagnostic system suggests that personality disorder categories be applied to children and adolescents in rare circumstances because of expected changes in personality pathology across development. The present study examined the stability in personality pathology, specifically psychopathy, across childhood and adolescence. Using a short form of the CPS and mixed models incorporating fixed and random effects, we examined the reliability, individual stability, mean-level stability, and predictive utility of juvenile psychopathy as a function of age (i.e., from 7 to 17 years old) in over 1,500 boys from the three cohorts of the Pittsburgh Youth Study. If adolescent development contributes to instability in personality pathology, large age-related fluctuations in reliability, stability, and predictive utility should be observed, particularly in the latter part of adolescence when normative changes are hypothesized to influence levels of psychopathy. Such fluctuations were not observed. In general, juvenile psychopathy could be reliably assessed beginning in childhood, was fairly stable across short and long intervals, showed little mean-level fluctuation, and predicted delinquency across adolescence. These results suggest that concerns about large changes in personality pathology across childhood and adolescence may be overstated. Implications and future directions are discussed.

Research suggests that depressive personality (DP) disorder may represent a persistent, trait-based form of depression that lies along an affective spectrum ranging from personality traits to diagnosable clinical disorders. A significant gap in this area of research concerns the development of DP and its applicability to youth. The present research explored the construct of DP traits in youth. Specifically, this study examined the reliability, stability, and validity of the construct, potential origins of DP traits, and the developmental consequences of DP traits. A sample of 143 youth (mean age = 12.37 years, SD = 1.26) and their caregivers completed semistructured interviews and questionnaires on two occasions, separated by a 12-month interval. The measure of DP traits was reliable and moderately stable over time. Providing evidence of construct validity, DP traits were associated with a network of constructs, including a negative self-focus, high-negative and low-positive emotionality, and heightened stress reactivity. Moreover, several potential origins of DP traits were identified, including a history of family adversity, maternal DP traits, and maternal depression. Consistent with hypotheses regarding their developmental significance, DP traits predicted the generation of stress and the emergence of depression (but not nondepressive psychopathology) during the pubertal transition. Finally, depression predicted subsequent DP traits, suggesting a reciprocal process whereby DP traits heighten risk for depression, which then exacerbates these traits. These findings support the construct of DP traits in youth, and suggest that these traits may be a useful addition to developmental models of risk for youth depression.

This study examined the childhood history of maltreatment, peer relations, and externalizing problems among individuals who manifested low, moderate, or high symptom levels of paranoid personality disorder (PPD) in adolescence. Participants included 174 children who attended a longitudinal summer camp research program between the ages of 9 to 12. Multiple sources of information (self-, peer, and counselor reports) were utilized. Subsequently, they participated in a personality disorder assessment during adolescence (mean age = 15.30). The results indicated that children who manifested higher levels of PPD symptoms in adolescence had higher odds of having a history of child maltreatment. Children who manifested high levels of PPD symptoms in adolescence showed a faster growth rate for peer bullying and externalizing problems in childhood. In addition, their peers rated them as less cooperative, less likely to be leaders, and more likely to initiate fights. These findings suggested that children who manifested elevated PPD symptoms in adolescence had shown early signs of behavioral disturbances in childhood, some of which gradually worsened as they approach adolescence.

Schizophrenia has come to be viewed as a neurodevelopmental disorder that is characterized by genetic vulnerability, stressors during the prenatal period that may be marked by minor physical anomalies and neurobehavioral deficits that emerge in early development. Less is known about the neurodevelopmental origins of schizotypal personality symptoms. The present study examines schizotypal symptoms in Israeli adolescents (mean age = 16.79 years) who have not yet reached the developmental period during which first schizophrenic episode is most likely to emerge: 39 adolescent offspring of parents with schizophrenia, 39 offspring of parents with other psychiatric disorders, and 36 offspring of parents with no history of mental illness. The Semi-Structured Kiddie Interview for Personality Syndromes was used to assess cognitive–perceptual, interpersonal, and disorganized schizotypal symptoms. Interpersonal schizotypal symptoms were more prevalent in the schizophrenia offspring group than in the no-mental-illness offspring group. Among the schizophrenia offspring group, interpersonal, but not cognitive–perceptual, schizotypal symptoms were associated with minor physical anomalies, fine motor dyscoordination, and deficits in executive functioning during adolescence. Among young people whose parents did not have schizophrenia, cognitive–perceptual schizotypal symptoms were correlated with deficits in executive functioning. Adolescent schizotypal symptoms were associated with neurobehavioral symptoms measured during middle childhood in a subgroup of the sample that had been assessed prospectively. Finally, young people who had genetic risk for schizophrenia, minor physical anomalies, and neurobehavioral signs together were at markedly increased risk for symptoms of interpersonal schizotypal symptoms, compared to young people with one or none of these risk factors.

Personality disorders (PDs) have been thought historically to be enduring, inflexible, and set in psychological stone relatively firmly; however, empirical findings from recent prospective multiwave longitudinal studies establish otherwise. Nearly all modern longitudinal studies of personality disorder have documented considerable change in PDs over time, suggesting considerable flexibility and plasticity in this realm of psychopathology. The factors and mechanisms of change in the PDs remain essentially opaque, and this area of PD research is just beginning to be probed using candidate predictors of change, such as personality systems. In this report, we investigate whether change in temperament dimensions (emotionality, activity, and sociability) predicts change in schizoid personality disorder. We present a latent growth framework for addressing this question and provide an illustration of the approach using data from the Longitudinal Study of Personality Disorders. Schizoid personality disorder was assessed using two different methodologies (structured psychiatric interview and self-report) and temperament was assessed using a well-known psychometric measure of temperament. All constructs were measured at three time points over a 4-year time period. To analyze these panel data, we fitted a covariance structure model that hypothesized simultaneous relationships between initial levels and rates of change in temperament and initial levels and rates of change in schizoid personality disorder. We found that rates of change in the core temperament dimensions studied do not predict rates of change in schizoid personality over time. We discuss the methodological advantages of the latent growth approach and the substantive meaning of the findings for change in schizoid personality disorder.

Narcissism is a dynamic form of personality characterized by a pervasive sense of grandiosity and self-importance, and by a need to obtain continuous self-validation from others. Very little is known about its etiology and development. What factors (e.g., temperament, parenting experiences) and processes (e.g., transactions between these factors over time) cause some children to become more narcissistic than others? When does narcissism first emerge, and how does narcissism develop over time? This article describes a framework for research on the etiology and development of narcissism, and recommends ten research priorities. This research should yield fundamental knowledge and should inform intervention efforts to minimize the negative impact narcissistic individuals have on themselves and on others.

A multisample, multistudy project aimed at understanding how individual differences in narcissism during early adolescence are related to distortions in the aggression, and the reactivity of the hypothalamic–pituitary–adrenal axis to negative and positive experiences. The findings indicate that individual differences in narcissism are a remarkably stable aspect of personality during early adolescence. It is predictably related to an inflated view of the self that is not warranted by objective indices of social functioning. Further evidence shows that it promotes the continuity of aggressive behavior and is more strongly related to reactive aggression than to proactive aggression and more strongly related to relational aggression than to physical aggression. Finally, there is evidence that distortions in the self may derive from the inadequate functioning of the hypothalamic–pituitary–adrenal axis, one of the body's main response system for dealing with stress. These findings are discussed in terms of the processes by which early adolescents react to threats and arousal in their daily functioning.

Although research has been conducted on the course, consequences, and correlates of borderline personality disorder (BPD), little is known about its emergence in childhood, and no studies have examined the extent to which theoretical models of the pathogenesis of BPD in adults are applicable to the correlates of borderline personality symptoms in children. The goal of this study was to examine the interrelationships between two BPD-relevant personality traits (affective dysfunction and disinhibition), self- and emotion-regulation deficits, and childhood borderline personality symptoms among 263 children aged 9 to 13. We predicted that affective dysfunction, disinhibition, and their interaction would be associated with childhood borderline personality symptoms, and that self- and emotion-regulation deficits would mediate these relationships. Results provided support for the roles of both affective dysfunction and disinhibition (in the form of sensation seeking) in childhood borderline personality symptoms, as well as their hypothesized interaction. Further, both self- and emotion-regulation deficits partially mediated the relationship between affective dysfunction and childhood borderline personality symptoms. Finally, results provided evidence of different gender-based pathways to childhood borderline personality symptoms, suggesting that models of BPD among adults are more relevant to understanding the factors associated with borderline personality symptoms among girls than boys.

Emotional instability and poor emotional awareness are cardinal features of the emotional dysregulation associated with borderline personality disorder (BPD). Most models of the development of BPD include child negative emotional reactivity and grossly inadequate caregiving (e.g., abuse, emotional invalidation) as major contributing factors. However, early childhood emotional reactivity and exposure to adverse family situations are associated with a diverse range of long-term outcomes. We examine the known effects of these risk factors on early childhood emotional functioning and their potential links to the emergence of chronic emotional instability and poor emotional awareness. This examination leads us to advocate new research directions. First, we advocate for enriching the developmental assessment of children's emotional functioning to more closely capture clinically relevant aspects. Second, we advocate for conceptualizing children's early family experiences in terms of the proximal emotional environment to which young children may be or become sensitive. Such approaches should contribute to our ability to identify risk for BPD and guide preventive intervention.

The antecedents and developmental course of borderline personality disorder symptoms were examined prospectively from infancy to adulthood using longitudinal data from a risk sample (N = 162). Borderline personality disorder symptom counts were derived from the Structured Clinical Interview for DSM Disorders diagnostic interview at age 28 years. Correlational analyses confirmed expected relations between borderline symptoms and contemporary adult disturbance (e.g., self-injurious behavior, dissociative symptoms, drug use, relational violence) as well as maltreatment history. Antecedent correlational and regression analyses revealed significant links between borderline symptoms in adulthood and endogenous (i.e., temperament) and environmental (e.g., attachment disorganization, parental hostility) history in early childhood and disturbance across domains of child functioning (e.g., attention, emotion, behavior, relationship, self-representation) in middle childhood/early adolescence. Process analyses revealed a significant mediating effect of self-representation on the relation between attachment disorganization on borderline symptoms. The findings are discussed within a developmental psychopathology framework in which disturbance in self-processes is constructed through successive transactions between the individual and environment.

Although personality disorders are best understood in the context of lifetime development, there is a paucity of work examining their longitudinal trajectory. An understanding of the expected course and the genetic and environmental contributions to these disorders is necessary for a detailed understanding of risk processes that lead to their manifestation. The current study examined the longitudinal course and heritability of borderline personality disorder (BPD) over a period of 10 years starting in adolescence (age 14) and ending in adulthood (age 24). In doing so, we built on existing research by using a large community sample of adolescent female twins, a sensitive dimensional measure of BPD traits, an extended follow-up period, and a longitudinal twin design that allowed us to investigate the heritability of BPD traits at four discrete ages spanning midadolescence to early adulthood. Results indicated that mean-level BPD traits significantly decline from adolescence to adulthood, but rank order stability remained high. BPD traits were moderately heritable at all ages, with a slight trend for increased heritability from age 14 to age 24. A genetically informed latent growth curve model indicated that both the stability and change of BPD traits are highly influenced by genetic factors and modestly by nonshared environmental factors. Our results indicate that as is the case for other personality dimensions, trait BPD declines as individuals mature from adolescence to adulthood, and that this process is influenced in part by the same genetic factors that influence BPD trait stability.

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.