Guided by principles from life-history theory, theories of adaptive calibration provide an overarching theoretical framework for understanding the developmental roots of impulsivity and externalizing psychopathology. The current research provides evidence for robust associations between perceptions of childhood unpredictability, delay discounting (Studies 1a and 1b), and adult externalizing traits and behaviors (Study 2). Both associations were observed while controlling for perceptions of the harshness of childhood environments, as well as a range of demographic characteristics. The association with externalizing traits and behavior was observed over and above current mood and depressive symptoms. Study 2 also replicated a previously documented association between changes in maternal employment, residence, and cohabitation during childhood and externalizing behavior and, furthermore, suggested that this association was mediated by perceptions of unpredictability. These studies provided no evidence for links between perceived childhood unpredictability and basic forms of risk-taking (Studies 1a and 1c). This research adds to a growing body of work leveraging principles from life-history theory to demonstrate links between childhood experiences, impulsivity, and potentially debilitating forms of mental illness. This work also highlights the value of assessing people’s perceptions of their childhood environments.

Prospective longitudinal studies of idiopathic autism spectrum disorder (ASD) have provided insights into early symptoms and predictors of ASD during infancy, well before ASD can be diagnosed at age 2–3 years. However, research on the emergence of ASD in disorders with a known genetic etiology, contextualized in a developmental framework, is currently lacking. Using a biobehavioral multimethod approach, we (a) determined the rate of ASD in N = 51 preschoolers with fragile X syndrome (FXS) using a clinical best estimate (CBE) procedure with differential diagnoses of comorbid psychiatric disorders and (b) investigated trajectories of ASD symptoms and physiological arousal across infancy as predictors of ASD in preschoolers with FXS. ASD was not diagnosed if intellectual ability or psychiatric disorders better accounted for the symptoms. Our results determined that 60.7% of preschoolers with FXS met the Diagnostic and Statistical Manual of Mental Disorders (fifth edition) (DSM-5) criteria for ASD using the CBE procedure. In addition, 92% of these preschoolers presented with developmental delay and 45.4% also met criteria for psychiatric disorders, either anxiety, ADHD, or both. ASD diagnoses in preschoolers with FXS were predicted by elevated scores on traditional ASD screeners in addition to elevated autonomic arousal and avoidant eye contact from infancy.

Gene × Environment interaction contributes to externalizing disorders in childhood and adolescence, but little is known about whether such effects are long lasting or present in adulthood. We examined gene–environment interplay in the concurrent and prospective associations between antisocial peer affiliation and externalizing disorders (antisocial behavior and substance use disorders) at ages 17, 20, 24, and 29. The sample included 1,382 same-sex twin pairs participating in the Minnesota Twin Family Study. We detected a Gene × Environment interaction at age 17, such that additive genetic influences on antisocial behavior and substance use disorders were greater in the context of greater antisocial peer affiliation. This Gene × Environment interaction was not present for antisocial behavior symptoms after age 17, but it was for substance use disorder symptoms through age 29 (though effect sizes were largest at age 17). The results suggest adolescence is a critical period for the development of externalizing disorders wherein exposure to greater environmental adversity is associated with a greater expression of genetic risk. This form of Gene × Environment interaction may persist through young adulthood for substance use disorders, but it appears to be limited to adolescence for antisocial behavior.

Childhood maltreatment has lasting negative effects throughout the life span. Early intervention research has demonstrated that these effects can be remediated through skill-based, family-centered interventions. However, less is known about plasticity during adolescence, and whether interventions are effective many years after children experience maltreatment. This study investigated this question by examining adolescent girls' ability to make advantageous decisions in the face of risk using a validated decision-making task; performance on this task has been associated with key neural regions involved in affective processing and executive functioning. Maltreated foster girls (n = 92), randomly assigned at age 11 to either an intervention designed to prevent risk-taking behaviors or services as usual (SAU), and nonmaltreated age and socioeconomic status matched girls living with their biological parent(s) (n = 80) completed a decision-making task (at age 15–17) that assessed risk taking and sensitivity to expected value, an index of advantageous decision making. Girls in the SAU condition demonstrated the greatest decision-making difficulties, primarily for risks to avoid losses. In the SAU group, frequency of neglect was related to greater difficulties in this area. Girls in the intervention condition with less neglect performed similarly to nonmaltreated peers. This research suggests that early maltreatment may impact decision-making abilities into adolescence and that enriched environments during early adolescence provide a window of plasticity that may ameliorate these negative effects.

Social cognitive deficits can have many negative consequences, spanning social withdrawal to psychopathology. Prior work has shown that child maltreatment may associate with poorer social cognitive skills in later life. However, no studies have examined this association from early childhood into adolescence. Using data from the Avon Longitudinal Study of Parents and Children (ALSPAC; n = 4,438), we examined the association between maltreatment (caregiver physical or emotional abuse; sexual or physical abuse), assessed repeatedly (every 1–3 years) from birth to age 9, and social cognitive skills at ages 7.5, 10.5, and 14 years. We evaluated the role of both the developmental timing (defined by age at exposure) and accumulation of maltreatment (defined as the number of occasions exposed) using a least angle regression variable selection procedure, followed by structural equation modeling. Among females, accumulation of maltreatment explained the most variation in social cognitive skills. For males, no significant associations were found. These findings underscore the importance of early intervention to minimize the accumulation of maltreatment and showcase the importance of prospective studies to understand the development of social cognition over time.

Lexical processing deficits in children with developmental language disorder (DLD) have been postulated to arise as sequelae of their grammatical deficits (either directly or via compensatory mechanisms) and vice versa. We examined event-related potential indices of lexical processing in children with DLD (n = 23) and their typically developing peers (n = 16) using a picture–word matching paradigm. We found that children with DLD showed markedly reduced N400 amplitudes in response both to auditorily presented words that had initial phonological overlap with the name of the pictured object and to words that were not semantically or phonologically related to the pictured object. Moreover, this reduction was related to behavioral indices of phonological and lexical but not grammatical development. We also found that children with DLD showed a depressed phonological mapping negativity component in the early time window, suggesting deficits in phonological processing or early lexical access. The results are partially consistent with the overactivation account of lexical processing deficits in DLD and point to the relative functional independence of lexical/phonological and grammatical deficits in DLD, supporting a multidimensional view of the disorder. The results also, although indirectly, support the neuroplasticity account of DLD, according to which language impairment affects brain development and shapes the specific patterns of brain responses to language stimuli.

This study compared a group of 18 high-functioning children with autism (9–16 years of age) and a group of 14 normally developing children (9–14 years of age) on their abilities to take the perceptual perspective of someone else and to seriate objects based on length, size, weight, and color. Results indicated that the high-functioning children with autism were as able as the normally developing children to seriate the various objects. In contrast, significant differences emerged on the perceptual perspective-taking tasks with the high-functioning children with autism as a group performing less well than the normally developing children. However, the majority of autistic children showed good perspective-taking ability. The implications of these results to our understanding of autism are discussed.

In utero exposure to maternal psychological distress is a risk factor for developmental psychopathology, and these effects are believed to partially occur via dysregulation of the maternal and fetal hypothalamus–adrenal–pituitary axes. Nevertheless, only a few human studies have directly assessed the effects of prenatal cortisol exposure on infant cortisol reactivity, and none have investigated sex differences or potential interactions between prenatal cortisol and psychological distress. Here we report on a prospective longitudinal investigation (N = 236) of in utero exposure to maternal cortisol and distress in a relatively high socioeconomic status and low-risk population to determine whether these exposures interact in their effects on infant (M age = 3.0 months, range = 2.3–5.0 months, 51.9% male) cortisol reactivity and whether there are sex differences in these effects. Results revealed both sexually dimorphic and interactive effects of prenatal cortisol and distress, even after controlling for postnatal distress. In general, blunted reactivity in females was associated with exposure to high maternal distress and flattened patterns of diurnal maternal cortisol, whereas blunted reactivity in males was associated with exposure to steeper morning increases and daytime decreases in maternal cortisol. The findings suggest that sex differences in the effects of prenatal cortisol and distress on infant cortisol reactivity are a plausible mechanism by which maternal experiences during pregnancy contribute to sex differences in the development of psychopathology.

Psychosocial stress during childhood and adolescence is associated with alterations in the hypothalamic–pituitary–adrenal (HPA) axis and with heightened inflammation, both of which are implicated in poor health; however, factors that may protect against these effects relatively early in life are not well understood. Thus, we examined whether psychosocial resources protect against stress-related alterations in the HPA axis and heightened inflammation in a sample of 91 late adolescents. Participants completed measures of various stressors (major life events, daily interpersonal stress, early adversity), and psychosocial resources (mastery, optimism, self-esteem, and positive reappraisal). They also completed the Trier Social Stress Test and provided saliva and blood samples for the assessment of cortisol and interleukin-6 reactivity. Each of the stressors was associated with lower cortisol reactivity. Additionally, associations with major life events and daily stress were moderated by psychological resources, such that more life events and daily stress were associated with decreased HPA reactivity among adolescents with lower levels of psychological resources, but not among those with higher levels of psychological resources. This pattern of findings was observed only for cortisol reactivity and not for interleukin-6 reactivity. Findings suggest that psychological resources may counteract the effects of certain adversity-related decreases in cortisol reactivity.

The origins of individual differences in social development are examined in relation to early stress (immune challenge) and social milieu (maternal behavior) in a genetic–developmental analysis using an animal model. Neonatal male mice (5 or 6 days of age) from two lines of mice selectively bred for high versus low levels of inter-male aggressive behavior received a standard immune challenge (i.p. injections of 0.05 mg/kg endotoxin or saline). Animals were reared by their line-specific biological dam or by a foster dam from a line bred without selection. Adult levels of social behaviors were assessed in a dyadic test (age 45–50 days). Mice from the high-aggressive line show more developmental sensitivity to immune challenge than mice from the low-aggressive line, and line differences persist regardless of the early maternal environment. As adults, endotoxin-treated mice from the high-aggressive line have lower levels of aggressive behavior, longer latency to attack, and higher rates of socially reactive and inhibited behaviors compared to saline controls. Developmental effects of endotoxin in the low-aggressive line are minimal: endotoxin increases socially reactive behaviors, compared to saline controls, but only for mice reared by their biological dams. Rearing by foster dams increases social exploration in the low-aggressive line. The findings raise novel questions regarding the openness of behavioral systems to effects of nonobvious but omnipresent features of the environment, such as antigenic load, how these effects are integrated to affect social development and psychopathology, and the nature of intrinsic factors that contribute to individual differences in sensitivity to early stressors.

The relations of children's coping strategies and coping efficacy to parent socialization and child adjustment were examined in a sample of school-age children that included families in which some of the grandparents and/or parents had an alcoholism diagnosis. Parents and older children reported on the children's coping strategies; parents reported on their parenting behavior; and teachers reported on children's externalizing and internalizing problems. Measures of parent socialization were associated with parents' and children's reports of active coping strategies and parents' reports of both support-seeking coping and coping efficacy. Some of these relations were moderated by familial alcohol status. Children higher in parent-reported active/support-seeking coping and coping efficacy were rated lower in teacher-reported externalizing and internalizing adjustment problems. The findings were consistent with the view that active/support-seeking coping and coping efficacy mediated the association of parent socialization to children's psychological adjustment and that this relation was sometimes moderated by parental alcohol status.This research was supported by a grant from the National Institute of Drug Abuse (DA05227; Laurie Chassin, Principle Investigator, Nancy Eisenberg, Co-Principal Investigator).

The goal of the study was to examine several factors that may explain the development of anxiety symptoms in middle childhood. Using data from the NICHD Study of Early Child Care (n = 1,364 families), we examined mother–child relationships, other aspects of family context, and child characteristics as predictors of anxiety in preadolescence. Latent growth curve analyses revealed that children who were more anxious at the beginning of middle childhood had been more behaviorally inhibited as preschoolers, and in middle childhood lived in families who experienced more negative life events and had mothers who were more anxious. Children who became more anxious across middle childhood were less behaviorally inhibited as preschoolers and in middle childhood perceived less security in their attachments to their mothers, experienced more negative life events, and had mothers who were more anxious. The findings illustrate the need to include a broad set of risk factors in etiological models of anxiety. In addition, the evidence for cumulative effects suggests several possible points of intervention with anxious children and their parents.

Accumulating evidence indicates that the fetal environment plays an important role in brain development and sets the brain on a trajectory across the life span. An abnormal fetal environment results when factors that should be present during a critical period of development are absent or when factors that should not be in the developing brain are present. While these factors may acutely disrupt brain function, the real cost to society resides in the long-term effects, which include important mental health issues. We review the effects of three factors, fetal alcohol exposure, teratogen exposure, and nutrient deficiencies, on the developing brain and the consequent risk for developmental psychopathology. Each is reviewed with respect to the evidence found in epidemiological and clinical studies in humans as well as preclinical molecular and cellular studies that explicate mechanisms of action.

The extent to which indices of maternal physiological arousal (skin conductance augmentation) and regulation (vagal withdrawal) while parenting predict infant attachment disorganization and behavior problems directly or indirectly via maternal sensitivity was examined in a sample of 259 mothers and their infants. Two covariates, maternal self-reported emotional risk and Adult Attachment Interview attachment coherence were assessed prenatally. Mothers' physiological arousal and regulation were measured during parenting tasks when infants were 6 months old. Maternal sensitivity was observed during distress-eliciting tasks when infants were 6 and 14 months old, and an average sensitivity score was calculated. Attachment disorganization was observed during the Strange Situation when infants were 14 months old, and mothers reported on infants' behavior problems when infants were 27 months old. Over and above covariates, mothers' arousal and regulation while parenting interacted to predict infant attachment disorganization and behavior problems such that maternal arousal was associated with higher attachment disorganization and behavior problems when maternal regulation was low but not when maternal regulation was high. This effect was direct and not explained by maternal sensitivity. The results suggest that maternal physiological dysregulation while parenting places infants at risk for psychopathology.

This short-term longitudinal study examined the associations between relational and physical victimization and depressive symptoms, and the moderating role of school-aged children's relational-interdependent self-construals in these associations. The participants were 387 children (51.8% boys) who were in the fifth grade (M = 10.48 years, SD = 0.55) in Taiwan and followed at two time points (a 6-month interval) during a calendar year. A multiple-informant approach was used where forms of peer victimization, depressive symptoms, and relational-interdependent self-construals were assessed via peer nominations, teacher reports, and child reports, respectively. All measures had favorable psychometric properties. The results of a multigroup cross-lagged model demonstrated that relational victimization (not physical victimization) was positively predictive of subsequent depressive symptoms, and the effect was evidenced for highly interdependent children only. The opposite link was also significant, such that depressive symptoms predicted subsequent relational victimization (not physical victimization) for children who exhibited low and high levels of relational-interdependent self-construals. In contrast, physical victimization predated a lower level of depressive symptoms for highly interdependent children. These effects were unaffected by the gender of the child. The findings, especially the interactive effects of relational victimization (as a contextual factor) and relational-interdependent self-construals (as an individual vulnerability) on depressive symptoms, are discussed from a developmental psychopathology perspective.

This study examines the intergenerational effects of caregivers' unresolved loss and abuse on children's behavior problems from middle childhood to early adolescence in an economically disadvantaged sample. One hundred twenty-four caregivers completed the Adult Attachment Interbiew (AAI) and a lifetime trauma interview during the age 13 wave of the study. Child behavior problems were assessed at four time points (ages 6, 8, 10, and 13) with teacher-reported Child Behavior Checklist total problem scales. The children of insecure caregivers with unresolved loss showed a consistent pattern of increased behavior problems from middle childhood to early adolescence. Caregivers' AAI status accounted for more variance in child behavior problems than did an alternative model of caregiver psychopathology (depression and dissociation). The results extend the literature on the effects of caregiver unresolved states of mind beyond infancy to older children and adolescents.

The link between parental depressive history and parenting styles is well established, as is the association of parenting with child psychopathology. However, little research has examined whether a depressive history in one parent predicts the parenting style of the other parent. As well, relatively little research has tested transactional models of the parenting–child psychopathology relationship in the context of parents' depressive histories. In this study, mothers and fathers of 392 children were assessed for a lifetime history of major depression when their children were 3 years old. They then completed measures of permissiveness and authoritarianism and their child's internalizing and externalizing symptoms when children were 3, 6, and 9 years old. The results showed that a depressive history in one parent predicted the other parent's permissiveness. Analyses then showed that child externalizing symptoms at age 3 predicted maternal permissiveness and authoritarianism and paternal permissiveness at age 6. Maternal permissiveness at age 6 predicted child externalizing symptoms at age 9. No relationships in either direction were found between parenting styles and child internalizing symptoms. The results highlight the importance of considering both parents' depressive histories when understanding parenting styles, and support transactional models of parenting styles and child externalizing symptoms.

This study was designed to investigate a genetic moderation effect of dopamine receptor 4 gene (DRD4) alleles that have seven or more repeats (long alleles) on an intervention to deter drug use among rural African American adolescents in high-risk families. Adolescents (N = 291, M age = 17) were assigned randomly to the Adults in the Making (AIM) program or to a control condition and were followed for 27.5 months. Adolescents provided data on drug use and vulnerability cognitions three times after pretest. Pretest assessments of caregiver depressive symptoms, disruption in the home, and support toward the adolescent were used to construct a family risk index. Adolescents living in high-risk families who carried at least one DRD4 long allele and were assigned to the control condition evinced greater escalations in drug use than did (a) adolescents who lived in high-risk families, carried the DRD4 long allele, and were assigned to AIM, or (b) adolescents assigned to either condition who carried no DRD4 long alleles. AIM-induced reductions in vulnerability cognitions were responsible for the Family Risk × AIM × DRD4 status drug use prevention effects. These findings support differential susceptibility predictions and imply that prevention effects on genetically susceptible individuals may be underestimated.