Different patterns of emotional reactivity characterize proactive and reactive functions of aggressive behavior, and theory also suggests a link of both types with narcissism. How people with narcissistic traits respond emotionally to competitive scenarios could influence their aggressiveness. Participants were 85 adolescent boys from a detention center. Several indices of emotional functioning were assessed, including attentional bias to negative emotional stimuli and psychophysiological responding. In addition, we included self-report and laboratory measures of aggression and measures of psychopathy-linked narcissism, callous–unemotional traits, and impulsivity. Psychopathy-linked narcissism was uniquely related to unprovoked aggression (i.e., proactive aggression) and to heightened attention to pictures depicting others’ distress. Compared with those scoring low on narcissism, those high on narcissism, who were the least physiologically reactive group, evinced greater proactive aggression, whereas those showing a pattern of coactivation (i.e., sympathetic and parasympathetic autonomic reactivity) evinced greater reactive aggression. Results are consistent with descriptions of narcissistic individuals as being hypervigilant to negative cues and exhibiting poor emotion regulation. These characteristics may lead to aggressive and violent behavior aimed at maintaining dominance over others.

Genetic factors can play a key role in the multiple level of analyses approach to understanding the development of child psychopathology. The present study examined gene–environment correlations and Gene × Environment interactions for polymorphisms of three target genes, the serotonin transporter gene, the D4 dopamine receptor gene, and the monoamine oxidase A gene in relation to symptoms of anxiety, depression, and oppositional behavior. Saliva samples were collected from 175 non-Hispanic White, 4-year-old children. Psychosocial risk factors included socioeconomic status, life stress, caretaker depression, parental support, hostility, and scaffolding skills. In comparison with the short forms (s/s, s/l) of the serotonin transporter linked polymorphic repeat, the long form (l/l) was associated with greater increases in symptoms of oppositional defiant disorder in interaction with family stress and with greater increases in symptoms of child depression and anxiety in interaction with caretaker depression, family conflict, and socioeconomic status. In boys, low-activity monoamine oxidase A gene was associated with increases in child anxiety and depression in interaction with caretaker depression, hostility, family conflict, and family stress. The results highlight the important of gene–environment interplay in the development of symptoms of child psychopathology in young children.

A model examining the effects of an increasing number of maltreatment subtypes experienced on antisocial behavior, as mediated by impulsivity and moderated by a polygenic index of dopaminergic genotypes, was investigated. An African American sample of children (N = 1,012, M age = 10.07) with and without maltreatment histories participated. Indicators of aggression, delinquency, and disruptive peer behavior were obtained from peer- and counselor-rated measures to form a latent variable of antisocial behavior; impulsivity was assessed by counselor report. Five genotypes in four dopaminergic genes (dopamine receptors D4, D2, known as DRD4, DRD2; dopamine active transporter 1, known as DAT1; and catechol-O-methyltransferase, known as COMT) conferring heightened environmental sensitivity were combined into one polygenic index. Using structural equation modeling, a first-stage, moderated-mediation model was evaluated. Age and sex were entered as covariates, both as main effects and in interaction with maltreatment and the gene index. The model had excellent fit: χ2 (32, N = 1,012) = 86.51, p < .001; comparative fit index = 0.982, Tucker–Lewis index = 0.977, root mean square error of approximation = 0.041, and standardized root mean square residual = 0.022. The effect of maltreatment subtypes on antisocial behavior was partially mediated by impulsivity (β = 0.173, p < .001), and these relations were moderated by the number of differentiating dopaminergic genotypes. Specifically, a significant Gene × Environment interaction (β = 0.016, p = .013) indicated that the relation between maltreatment and impulsivity was stronger as children evinced more differentiating genotypes, thereby strengthening the mediational effect of impulsivity on antisocial behavior. These findings elucidate the manner by which maltreated children develop early signs of antisocial behavior, and the genetic mechanisms involved in greater vulnerability for maladaptation in impulse control within the context of child maltreatment.

A general theory of personality and its development is described in terms of four quantitative dimensions of temperament and three quantitative dimensions of character. The four temperament dimensions (harm avoidance, novelty seeking, reward dependence, and persistence) are moderately heritable, moderately stable throughout life, and invariant despite sociocultural influences. The three character dimensions (self-directedness, cooperativeness, and self-transcendence) mature in a stepwise manner from early childhood throughout adulthood. Transitions between levels of maturity are nonlinear functions of temperament, specific genetic influences, social learning, and random life events. Personality development is quantitatively formulated in terms of nonlinear dynamics of a complex adaptive system. The psychosocial interpretation of personality as a fitness-optimizing process is described and illustrated in terms of available data about the development of different personality configurations. Several quantitative predictions of this theory of personality development are tested, including the sequence of emergence of the different character dimensions, individual differences in the development of stable temperament configurations, and the effects of sociocultural influences. The theoretical predictions agree with available empirical data and suggest many hypotheses for future developmental research, including etiological, dynamic, and therapeutic studies.

The present review revisits three hypothesized models that potentially could explain how prenatal maternal stress influences fetal development, birth outcomes, and subsequent developmental psychopathology. These models were mostly based on animal models, and new evidence for these models from human studies is evaluated. Furthermore, divergent trajectories from prenatal exposure to adversities to offspring affected outcomes are reviewed, including the comparison of studies on prenatal maternal stress with research on maternal substance use and maternal malnutrition during pregnancy. Finally, new directions in research on the mechanism underlying prenatal stress effects on human offspring is summarized. While it is concluded that there is abundant evidence for the negative associations between prenatal maternal stress and offspring behavioral, brain, and psychopathological outcomes in humans, there is no consistent evidence for specific mechanisms or specific outcomes in relation to stress exposure in utero. Rather, principles of multifinality and equifinality best describe the consequences for the offspring, suggesting a generic vulnerability and different pathways from prenatal adversities to developmental psychopathology, which complicates the search for underlying mechanisms. New and promising directions for research are provided to get a better understanding of how prenatal stress gets under the skin to affect fetal development.

Borderline personality disorder (BPD) is considered as a disorder of autonomy, and is related to both predisposing vulnerabilities and social relationships that fail to support basic psychological needs. Autonomy, which is defined within the self-determination theory as the capacity for self-endorsed action based on integrative, reflective awareness, is discussed as a developmental line that is dependent on specific supports from caregivers. Unresponsiveness, invalidation, or abuse by caregivers is argued to impair the capacity for autonomy and to catalyze an array of processes, both biological and psychological, which impact subsequent development and, in vulnerable individuals, can lead to BPD. Aspects of treatment, including the emphases on validation and acceptance of the patient's experience, and the cultivation of more reflective or mindful regulation of behavior, can be deduced from this analysis of autonomy disturbance, and these in turn have appeared as the cornerstones of effective treatments for BPD.

Adolescent internalizing and externalizing psychopathology is strongly associated with adult psychiatric morbidity, including psychotic disorders. This study examined whether internalizing or externalizing trajectories (continuity/discontinuity of symptoms) from middle childhood were associated with adolescent psychotic-like experiences (PLEs). Prospective data were collected from a community sample of 553 children (mean age = 10.4 years; 50% male) and their primary caregivers. Participants completed questionnaire reports of internalizing and externalizing psychopathology and PLEs at baseline, and again approximately 2 years later. Logistic regression was used to examine the association of adolescent PLEs with four trajectories of internalizing and externalizing psychopathology (persistent, incident, remitting, and none), controlling for a range of potential confounders and sampling bias. Significant associations were identified between adolescent PLEs and the incident internalizing (adjusted odds ratio [adj. OR] = 2.96; 95% confidence interval [CI] = 1.60–5.49) and externalizing psychopathology (adj. OR = 2.14; 95% CI = 1.11–4.14) trajectories, as well as the persistent internalizing (adj. OR = 1.90; 95% CI = 1.13–3.18) and externalizing (adj. OR = 1.81, 95% CI = 1.02–3.19) trajectories. Children with remitting psychopathology trajectories were no more likely to present later PLEs than those who never experienced psychopathology. While for many individuals symptoms and illness remit during development without intervention, this study provides important insights regarding potential targets and timing for delivery of early intervention and prevention programs.

Evidence suggests that the left frontal region is specialized for the expression of positive emotions, such as joy, whereas the right frontal region is specialized for certain negative emotions, such as distress. We previously reported that infants of mothers with depressive symptoms exhibited atypical patterns of frontal electroencephalographic (EEG) activity. We now extend these findings by examining the combined influence of maternal depression and attachment security on the infant's behavior and brain activity. Participants were 26 infants, 11–17 months of age, and their mothers. Twelve mothers reported elevated levels of depressive symptoms. Attachment behavior was observed in the traditional Strange Situation. While left and right, frontal and parietal EEG was recorded, infants were exposed to a baseline and three emotion-eliciting conditions (play with mother, stranger approach, maternal separation). During baseline and the condition designed to elicit positive emotion (play with mother), securely attached infants of symptomatic mothers exhibited reduced left frontal brain activity, compared to securely attached infants of nonsymptomatic mothers. During maternal separation, the most robust finding was that infants of symptomatic mothers, regardless of their attachment classification, exhibited reduced right frontal activity and lower levels of behavioral distress. The results suggest that both the mother's emotional well-being and her attachment relationship with her infant can influence infant frontal brain activity and affective behavior.

A history of research on gene–environment interaction (G × E) is provided in this article, revealing the fact that there have actually been two distinct concepts of G × E since the very origins of this research. R. A. Fisher introduced what I call the biometric concept of G × E (G × EB), whereas Lancelot Hogben introduced what I call the developmental concept of G × E (G × ED). Much of the subsequent history of research on G × E has largely consisted of the separate legacies of these separate concepts, along with the (sometimes acrimonious) disputes that have arisen time and again when employers of each have argued over the appropriate way to conceptualize the phenomenon. With this history in place, more recent attempts to distinguish between different concepts of G × E are considered, paying particular attention to the commonly made distinction between “statistical interaction” and “interactionism,” and Michael Rutter's distinction between statistical interaction and “the biological concept of interaction.” I argue that the history of the separate legacies of G × EB and G × ED better supports Rutter's analysis of the situation and that this analysis best paves the way for an integrative relationship between the various scientists investigating the place of G × E in the etiology of complex traits.

While maltreatment is known to impact social and emotional functioning, threat processing, and neural structure, the potentially dimorphic influence of sex on these outcomes remains relatively understudied. We investigated sex differences across these domains in a large community sample of children aged 10 to 14 years (n = 122) comprising 62 children with verified maltreatment experience and 60 well-matched nonmaltreated peers. The maltreated group relative to the nonmaltreated comparison group exhibited poorer social and emotional functioning (more peer problems and heightened emotional reactivity). Cognitively, they displayed a pattern of attentional avoidance of threat in a visual dot-probe task. Similar patterns were observed in males and females in these domains. Reduced gray matter volume was found to characterize the maltreated group in the medial orbitofrontal cortex, bilateral middle temporal lobes, and bilateral supramarginal gyrus; sex differences were observed only in the supramarginal gyrus. In addition, a disordinal interaction between maltreatment exposure and sex was found in the postcentral gyrus. Finally, attentional avoidance to threat mediated the relationship between maltreatment and emotional reactivity, and medial orbitofrontal cortex gray matter volume mediated the relationship between maltreatment and peer functioning. Similar mediation patterns were observed across sexes. This study highlights the utility of combining multiple levels of analysis when studying the “latent vulnerability” engendered by childhood maltreatment and yields tentative findings regarding a neural basis of sex differences in long-term outcomes for maltreated children.

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.

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.

Child maltreatment has been established as a risk factor for borderline personality disorder (BPD), yet few studies consider how maltreatment influences the development of BPD features through childhood and adolescence. Subtype, developmental timing, and chronicity of child maltreatment were examined as factors in the development of borderline personality features in childhood. Children (M age = 11.30, SD = 0.94), including 314 maltreated and 285 nonmaltreated children from comparable low socioeconomic backgrounds, provided self-reports of developmentally salient borderline personality traits. Maltreated children had higher overall borderline feature scores, had higher scores on each individual subscale, and were more likely to be identified as at high risk for development of BPD through raised scores on all four subscales. Chronicity of maltreatment predicted higher overall borderline feature scores, and patterns of onset and recency of maltreatment significantly predicted whether a participant would meet criteria for the high-risk group. Implications of findings and recommendations for intervention are discussed.

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.

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 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.

Disorganized attachment is associated with a host of negative developmental outcomes, leading to a growing interest in preventative interventions targeting the attachment relationship in infancy. The objective of this meta-analysis was to assess the effectiveness of interventions that aimed to prevent or reduce rates of disorganization among children at risk. We performed a literature search using PsycINFO, MEDLINE, and ProQuest databases for studies published between January 1989 and August 2016. All 16 studies (N = 1,360) included a control condition and reported postintervention rates of organized and disorganized attachments assessed by the Strange Situation Procedure. Results showed that, overall, interventions were effective in increasing rates of organized attachment compared to control conditions (d = 0.35, 95% CI [0.10–0.61]). Moderator analyses demonstrated that interventions were more effective (a) in more recently published studies than in older studies, (b) for maltreated samples than nonmaltreated samples, and (c) as children increased in age. These results have important implications for future development, tailoring, and implementation of attachment-based intervention programs.

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.

This investigation examined transactional relations across contextual strain, parenting quality, and child adjustment in 209 mothers and children at 24, 42, and 72 months of age. Independent ratings of mothers' stressful life events, social support, and relationship quality provided an objective measure of maternal contextual strain. Observers evaluated parenting quality during parent–child interactions at each time point. Child regulatory functioning during laboratory tasks at 24 and 42 months was evaluated by independent observers based on both behavioral (e.g., noncompliance, distractibility) and emotional (e.g., frustration, anger) indices. At 72 months, teachers reported on children's externalizing behaviors, and children completed objective measures of academic achievement. Nested path analyses were used to evaluate increasingly complex models of influence, including transactional relations between child and parent, effects from contextual strain to parenting and child adaptation, and reciprocal effects from child and parent behavior to contextual strain. Over and above stability within each domain and cross-sectional cross-domain covariation, significant paths emerged from maternal contextual strain to subsequent child adjustment. Bidirectional relations between parenting and child adjustment were especially prominent among boys. These findings counter unidirectional models of parent-mediated contextual effects by highlighting the direct influences of contextual strain and parent–child transactions on early childhood behavioral and academic adjustment, respectively.

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.