How do exposures to stress affect biobehavioral development and, through it, psychiatric and biomedical disorder? In the health sciences, the allostatic load model provides a widely accepted answer to this question: stress responses, while essential for survival, have negative long-term effects that promote illness. Thus, the benefits of mounting repeated biological responses to threat are traded off against costs to mental and physical health. The adaptive calibration model, an evolutionary–developmental theory of stress–health relations, extends this logic by conceptualizing these trade-offs as decision nodes in allocation of resources. Each decision node influences the next in a chain of resource allocations that become instantiated in the regulatory parameters of stress response systems. Over development, these parameters filter and embed information about key dimensions of environmental stress and support, mediating the organism's openness to environmental inputs, and function to regulate life history strategies to match those dimensions. Drawing on the adaptive calibration model, we propose that consideration of biological fitness trade-offs, as delineated by life history theory, is needed to more fully explain the complex relations between developmental exposures to stress, stress responsivity, behavioral strategies, and health. We conclude that the adaptive calibration model and allostatic load model are only partially complementary and, in some cases, support different approaches to intervention. In the long run, the field may be better served by a model informed by life history theory that addresses the adaptive role of stress response systems in regulating alternative developmental pathways.

The co-occurrence of child conduct problems (CPs) and callous–unemotional (CU) traits confers risk for psychopathy. The oxytocin (OXT) system is a likely candidate for involvement in the development of psychopathy. We tested variations in the OXT receptor gene (OXTR) in CP children and adolescents with varying levels of CU traits. Two samples of Caucasian children, aged 4–16 years, who met DSM criteria for disruptive behavior problems and had no features of autism spectrum disorder, were stratified into low versus high CU traits. Measures were the frequencies of nine candidate OXTR polymorphisms (single nucleotide polymorphisms). In Sample 1, high CU traits were associated with single nucleotide polymorphism rs1042778 in the 3′ untranslated region of OXTR and the CGCT haplotype of rs2268490, rs2254298, rs237889, and rs13316193. The association of rs1042778 was replicated in the second rural sample and held across gender and child versus adolescent age groups. We conclude that polymorphic variation of the OXTR characterizes children with high levels of CU traits and CPs. The results are consistent with a hypothesized role of OXT in the developmental antecedents of psychopathy, particularly the differential amygdala activation model of psychopathic traits, and add genetic evidence that high CU traits specify a distinct subgroup within CP children.

Child conduct problems (CPs) are a robust predictor of adult mental health; the concurrence of callous–unemotional (CU) traits confers specific risk for psychopathy. Psychopathy may be related to disturbances in the oxytocin (OXT) system. Evidence suggests that epigenetic changes in the OXT receptor gene (OXTR) are associated with lower circulating OXT and social–cognitive difficulties. We tested methylation levels of OXTR in 4- to 16-year-old males who met DSM criteria for a diagnosis of oppositional–defiant or conduct disorder and were stratified by CU traits and age. Measures were DNA methylation levels of six CpG sites in the promoter region of the OXTR gene (where a CpG site is a cytosine nucleotide occurs next to a guanine nucleotide in the linear sequence of bases along its lenth, linked together by phosphate binding), and OXT blood levels. High CU traits were associated with greater methylation of the OXTR gene for two cytosine nucleotide and guanine nucleotide phosphate linked sites and lower circulating OXT in older males. Higher methylation correlated with lower OXT levels. We conclude that greater methylation of OXTR characterizes adolescent males with high levels of CU and CPs, and this methylation is associated with lower circulating OXT and functional impairment in interpersonal empathy. The results add genetic evidence that high CU traits specify a distinct subgroup within CP children, and they suggest models of psychopathy may be informed by further identification of these epigenetic processes and their functional significance.

Evidence for the intergenerational transmission of posttraumatic stress disorder (PTSD) is documented in the literature, although the underlying mechanisms are poorly understood. Attachment theory provides a framework for elucidating the ways in which maternal PTSD may increase offspring PTSD vulnerability. The current study utilized two independent prospective data sets to test the hypotheses that (a) maternal PTSD increases the probability of developing an insecure mother–infant attachment relationship and (b) an insecure mother–infant attachment relationship increases the risk of developing PTSD following trauma exposure in later life. In the first study of urban, primarily low-income ethnic/racial minority mothers and infants (N = 45 dyads), elevated maternal PTSD symptoms at 6 months were associated with increased risk for an insecure, particularly disorganized, mother–infant attachment relationship at 13 months. In the second birth cohort of urban, low-income mothers and children (N = 96 dyads), insecure (avoidant or resistant) attachment in infancy was associated in a dose–response manner with increased lifetime risk for a diagnosis of PTSD by adolescence. A history of disorganized attachment in infancy predicted severity of PTSD symptoms, including reexperiencing, avoidance, hyperarousal, and total symptoms, at 17.5 years. In both studies, associations between attachment and PTSD were not attributable to numerous co-occurring risk factors. The findings suggest that promoting positive mother–child relationships in early development, particularly in populations at high risk for trauma exposure, may reduce the incidence of PTSD.

Children who were maltreated and enter foster care are at risk for maladjustment and relationship disturbances with foster carers. A popular hypothesis is that prior attachment relationships with abusive birth parents are internalized and carried forward to impair the child's subsequent attachment relationships. However, the empirical base for this model is limited, especially in adolescence. We examined the attachment patterns of 62 adolescents with their birth parents and their foster parents; we compared them to a comparison sample of 50 adolescents in normal-risk families. Attachment was assessed using the Child Attachment Interview; adolescent–parent interaction quality was assessed from direct observation; disruptive behavior symptoms were assessed from multiple informants. Whereas nearly all of the adolescents in foster families exhibited insecure attachments to their birth mothers (90%) and birth fathers (100%), nearly one-half were classified as having a secure attachment with their foster mother (46%) and father (49%); rates of secure attachment toward foster parents did not differ significantly from the rate in comparison families. Within the foster care sample, attachment security to the foster mother was predicted from current observed relationship quality and the duration of current placement. In addition, attachment quality in foster adolescents was associated with fewer disruptive behavior symptoms, and this association was equally strong in foster and comparison families. Our findings demonstrate that there is substantial potential for maltreated children to change and develop subsequent secure attachments in adolescence.

Child maltreatment is a reliable predictor of posttraumatic stress disorder (PTSD) symptoms. However, not all maltreated children develop PTSD symptoms, suggesting that additional mediating variables explain how certain maltreated children develop PTSD symptoms and others do not. The current study tested three potential mediators of the relationship between child maltreatment and subsequent PTSD symptoms: (a) respiratory sinus arrhythmia reactivity, (b) cortisol reactivity, and (c) experiential avoidance, or the unwillingness to experience painful private events, such as thoughts and memories. Maltreated (n = 51) and nonmaltreated groups (n = 59) completed a stressor paradigm, a measure of experiential avoidance, and a semistructured interview of PTSD symptoms. One year later, participants were readministered the PTSD symptoms interview. Results of a multiple mediator model showed the set of potential mediators mediated the relationship between child maltreatment and subsequent PTSD symptoms. However, experiential avoidance was the only significant, specific indirect effect, demonstrating that maltreated children avoiding painful private events after the abuse were more likely to develop a range of PTSD symptoms 1 year later. These results highlight the importance of experiential avoidance in the development of PTSD symptoms for maltreated children, and implications for secondary prevention and clinical intervention models are discussed.

Parent–child relationships are critical in development, but much remains to be learned about the mechanisms of their impact. We examined the early parent–child relationship as a moderator of the developmental trajectory from children's affective and behavioral responses to transgressions to future antisocial, externalizing behavior problems in the Family Study (102 community mothers, fathers, and infants, followed through age 8) and the Play Study (186 low-income, diverse mothers and toddlers, followed for 10 months). The relationship quality was indexed by attachment security in the Family Study and maternal responsiveness in the Play Study. Responses to transgressions (tense discomfort and reparation) were observed in laboratory mishaps wherein children believed they had damaged a valued object. Antisocial outcomes were rated by parents. In both studies, early relationships moderated the future developmental trajectory: diminished tense discomfort predicted more antisocial outcomes, but only in insecure or unresponsive relationships. That risk was defused in secure or responsive relationships. Moderated mediation analyses in the Family Study indicated that the links between diminished tense discomfort and future antisocial behavior in insecure parent–child dyads were mediated by stronger discipline pressure from parents. By indirectly influencing future developmental sequelae, early relationships may increase or decrease the probability that the parent–child dyad will embark on a path toward antisocial outcomes.

This study examined individual differences in how mothers' depressive symptoms affect children's early adjustment. It tested whether problematic development among children high in negative emotionality is accentuated by (a) maternal reactivity, the negative reactivity of mothers with depressive symptoms to difficult child characteristics; and (b) child vulnerability, the susceptibility of negatively emotional children to the negative parenting of mothers with depressive symptoms. Based on 1,364 participants from the NICHD Study of Early Child Care, results showed that mothers' depressive symptoms predicted greater risk for adjustment problems at age 3 among children who as infants were high rather than low in negative emotionality. Increased risk was evident for behavior problems, low responsiveness, high separation distress, and low social competence. Mediational tests suggested that increased risk reflected maternal reactivity: the stronger mothers' depressive symptoms, the more they responded with negative parenting to children high in negative emotionality. The proposal that child vulnerability mediates the greater impact of mothers' depressive symptoms on negatively emotional children was verified only for separation distress. The results support the proposal that, when mothers are high in depressive symptoms, aversive characteristics of children and their behavior increasingly influence early adjustment and do so because they elicit negative parent behavior.

This study examined developmentally salient risk and protective factors of adolescent substance use assessed during early childhood and early adolescence using a sample of 310 low-income boys. Child problem behavior and proximal family risk and protective factors (i.e., parenting and maternal depression) during early childhood, as well as child and family factors and peer deviant behavior during adolescence, were explored as potential precursors to later substance use during adolescence using structural equation modeling. Results revealed that early childhood risk and protective factors (i.e., child externalizing problems, mothers' depressive symptomatology, and nurturant parenting) were indirectly related to substance use at the age of 17 via risk and protective factors during early and middle adolescence (i.e., parental knowledge and externalizing problems). The implications of these findings for early prevention and intervention are discussed.

We utilized a longitudinal twin study (N = 2,510) to identify the child characteristics present prior to initiation of substance use that best predicted later substance use disorders. Two independent traits accounted for the majority of premorbid risk: socialization (conformity to rules and conventional values) and boldness (sociability and social assurance, stress resilience, and thrill seeking). Low socialization was associated with disruptive behavior disorders, parental externalizing disorders, and environmental adversity and exhibited moderate genetic (0.45) and shared environmental influences (0.30). Boldness was highly heritable (0.71) and associated with less internalizing distress and environmental adversity. In combination, these traits exhibited robust associations with adolescent and young adult substance use disorders (R = .48 and .50, respectively) and incremental prediction over disruptive behavior disorders, parental externalizing disorders, and environmental adversity. The results were replicated in an independent sample. Socialization and boldness offer a novel conceptualization of underlying risk for substance use disorders that has the potential to improve prediction and theory with implications for basic research, prevention, and intervention.

Emotion knowledge in childhood has been shown to predict social functioning and psychological well-being, but relatively little is known about parental factors that influence its development in early childhood. There is some evidence that both parenting behavior and maternal depression are associated with emotion recognition, but previous research has only examined these factors independently. The current study assessed auditory and visual emotion recognition ability among a large sample of preschool children to examine typical emotion recognition skills in children of this age, as well as the independent and interactive effects of maternal and paternal depression and negative parenting (i.e., hostility and intrusiveness). Results indicated that children were most accurate at identifying happy emotional expressions. The lowest accuracy was observed for neutral expressions. A significant interaction was found between maternal depression and negative parenting behavior: children with a maternal history of depression were particularly sensitive to the negative effects of maladaptive parenting behavior on emotion recognition ability. No significant effects were found for paternal depression. These results highlight the importance of examining the effects of multiple interacting factors on children's emotional development and provide suggestions for identifying children for targeted preventive interventions.

The long-term sequelae of adolescent depressive symptoms were examined in a multimethod, multireporter study of a diverse community sample of 179 adolescents followed from age 14 to 24. Mild to moderate levels of early adolescent depressive symptoms were found to predict lower maternal relationship quality, less positive interactions with romantic partners, and greater loneliness in adulthood even after accounting for prior levels of social functioning and for concurrent levels of adult depressive symptoms. Predictions were partially mediated via late adolescent avoidance of social interactions and poor maternal relationship quality. Results are interpreted as suggesting the potential impact of depressive symptoms on adolescent social development and the need to consider treatment for even mild symptoms and their social concomitants.

In this study, we prospectively examined developmental trajectories of five anxiety disorder symptom dimensions (generalized anxiety disorder, panic disorder, school anxiety, separation anxiety disorder, and social anxiety disorder) from early to late adolescence in a community sample of 239 adolescents, assessed annually over 8 years. Latent growth modeling indicated different developmental trajectories from early into late adolescence for the different anxiety disorder symptoms, with some symptoms decreasing and other symptoms increasing over time. Sex differences in developmental trajectories were found for some symptoms, but not all. Furthermore, latent class growth analysis identified a normal developmental profile (including a majority of adolescents reporting persistent low anxiety disorder symptoms over 8 years) and an at-risk developmental profile (including a minority of adolescents reporting persistent high anxiety disorder symptoms over 8 years) for all of the anxiety disorder symptom dimensions except panic disorder. Additional analyses longitudinally supported the validity of these normal and at-risk developmental profiles and suggested differential associations between different anxiety disorder symptom dimensions and developmental trajectories of substance use, parenting, and identity development. Taken together, our results emphasize the importance of examining separate dimensions of anxiety disorder symptoms in contrast to a using a global, one-dimensional approach to anxiety.

The purpose of this study was to extend the literature on the ontogeny of autism spectrum disorder (ASD) by examining early attainment and loss of specific sociocommunicative skills in children with autism (AUT; n = 125), pervasive developmental disorder not otherwise specified (PDD-NOS; n = 42), nonspectrum developmental delays (n = 46), and typical development (n = 31). The ages of skill attainment and loss were obtained from a caregiver interview. The findings indicated that children with AUT, PDD-NOS, and developmental delays diverged from typically developing children in attainment of sociocommunicative skills early in the first year of life. Loss of at least one skill was reported in a majority of children with AUT and PDD-NOS. Significant delays in attainment of skills were also reported in children who lost skills. The wide variation in skill attainment and loss reported across children indicates that symptom onset and regression may be best represented continuously, with at least some early delay and loss present for a great majority of children with ASD.

Autobiographical memory (AM) was assessed in 63 children (aged 8–17 years) with an autism spectrum disorder (ASD) and compared with 63 typically developing children matched for age, gender, IQ, and verbal ability. A range of methodologies was employed for eliciting past experience with particular focus on the ability to recall (a) specific events, (b) the recent and remote past, and (c) semantic versus episodic memories across different lifetime periods. Results indicated that the ASD group manifested difficulties in retrieving specific memories to word cues and had poorer access to the remote past. Deficits were found in the context of intact recent memory and preserved general memory abilities, with some impairment of visual memory. Problems in retrieving episodic and semantic AMs across the life span were also evident. Qualitative analysis of memory reports suggested that the ASD group was less likely to refer to emotion in their remote memories but more likely to describe emotions in their recent memories. Important predictors of AM performance in the ASD group were central executive abilities, in particular cognitive flexibility and verbal fluency.

Behavioral inhibition, a temperament identifiable in infancy, is associated with heightened withdrawal from social encounters. Prior studies raise particular interest in the striatum, which responds uniquely to monetary gains in behaviorally inhibited children followed into adolescence. Although behavioral manifestations of inhibition are expressed primarily in the social domain, it remains unclear whether observed striatal alterations to monetary incentives also extend to social contexts. In the current study, imaging data were acquired from 39 participants (17 males, 22 females; ages 16–18 years) characterized since infancy on measures of behavioral inhibition. A social evaluation task was used to assess neural response to anticipation and receipt of positive and negative feedback from novel peers, classified by participants as being of high or low interest. As with monetary rewards, striatal response patterns differed during both anticipation and receipt of social reward between behaviorally inhibited and noninhibited adolescents. The current results, when combined with prior findings, suggest that early-life temperament predicts altered striatal response in both social and nonsocial contexts and provide support for continuity between temperament measured in early childhood and neural response to social signals measured in late adolescence and early adulthood.

It is unclear whether the concepts and findings of the underlying neurobiology of adult psychopathy apply to youths as well. If so, a life span approach to treatment should be taken. Because youths’ brains are still developing, interventions at an early age may be far more effective in the long run. The aim of this systematic review is to examine whether the neurocognitive and neurobiological factors that underlie juvenile psychopathy, and specifically callous–unemotional (CU) traits, are similar to those underlying adult psychopathy. The results show that youths with CU traits show lower levels of prosocial reasoning, lower emotional responsivity, and decreased harm avoidance. Brain imaging studies in youths with CU traits are still rare. Available studies suggest specific neural correlates, such as a reduced response of the amygdala and a weaker functional connectivity between the amygdala and the ventromedial prefrontal cortex. These findings are largely in line with existing theories of adult psychopathy, such as the dual-hormone serotonergic hypothesis and the integrated emotions systems theory. We recommend that future studies investigate the role of oxytocin, invest in the study of neural mechanisms, and study the precursors, risk factors, and correlates of CU traits in early infancy and in longitudinal designs.

Investigating etiological processes early in the life span represents an important step toward a better understanding of the development of personality pathology. The current study evaluated the interaction between an individual difference risk factor (i.e., temperament) and a biological risk factor for aggressive behavior (i.e., atypical [larger] rightward hippocampal asymmetry) in predicting the emergence of borderline personality disorder (BPD) and antisocial personality disorder symptoms during early adolescence. The sample consisted of 153 healthy adolescents (M = 12.6 years, SD = 0.4, range = 11.4–13.7) who were selected from a larger sample to maximize variation in temperament. Interactions between four temperament factors (effortful control, negative affectivity, surgency, and affiliativeness), based on the Early Adolescent Temperament Questionnaire—Revised, and volumetric measures of hippocampal asymmetry were examined as cross-sectional predictors of BPD and antisocial personality disorder symptoms. Boys were more likely to have elevated BPD symptoms if they were high on affiliation and had larger rightward hippocampal asymmetry. In boys, low affiliation was a significant predictor of BPD symptoms in the presence of low rightward hippocampal asymmetry. For girls, low effortful control was associated with elevated BPD symptoms in the presence of atypical rightward hippocampal asymmetry. This study builds on previous work reporting significant associations between atypical hippocampal asymmetry and poor behavioral regulation.