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.

Previous research supports gene–environment interactions for polymorphisms in the corticotropin hormone receptor 1 gene (CRHR1) and the serotonin transporter gene linked polymorphic region (5-HTTLPR) in predicting depression, but it has rarely considered genetic influences on stress sensitization processes, whereby early adversities (EA) increase depressive reactivity to proximal stressors later in life. The current study tested a gene–environment–environment interaction (G × E × E; specifically, gene–EA–proximal stress interaction) model of depression in a 20-year longitudinal study. Participants were assessed prospectively for EA up to age 5 and recent chronic stress and depressive symptoms at age 20 and genotyped for CRHR1 single nucleotide polymorphism rs110402 and 5-HTTLPR. EA predicted stronger associations between recent chronic stress and depression, and the effect was moderated by genes. CRHR1 A alleles and 5-HTTLPR short alleles were associated with greater stress sensitization (i.e., greater depressive reactivity to chronic stress for those also exposed to high levels of EA). The results are consistent with the notion that EA exposure results in neurobiological and cognitive–emotional consequences (e.g., altered hypothalamic–pituitary–adrenal axis functioning), leading to emotional distress in the face of recent stressors among those with certain genetic characteristics, although further research is needed to explore explanatory mechanisms.

Attention control plays an important role in the development of internalizing symptoms in children. We explored the degree to which infants' genetic and environmentally based risk moderated the link between attention control and internalizing problems during toddlerhood. These associations were examined within a prospective adoption design, enabling the disentanglement of genetic and environmental risk for internalizing problems. Attention control in adopted infants was observed during periods of distress at age 9 months. Birth parents' anxiety symptoms were used as an index of genetic risk, while adoptive parents' anxiety symptoms were used as an index of environmental risk. Adoptive mothers and fathers reported on children's internalizing problems when children were 18 and 27 months old. Greater attention control in infancy appeared to mitigate genetically based risk for internalizing problems during toddlerhood when children were raised by adoptive parents who were low in anxiety. Findings suggest that for genetically susceptible children who are raised in low-risk environments, attention control may provide a protective factor against developing internalizing problems across early life.

Autism spectrum disorders (ASDs) are characterized by social impairments, including inappropriate responses to affective stimuli and nonverbal cues, which may extend to poor face-emotion recognition. However, the results of empirical studies of face-emotion recognition in individuals with ASD have yielded inconsistent findings that occlude understanding the role of face-emotion recognition deficits in the development of ASD. The goal of this meta-analysis was to address three as-yet unanswered questions. Are ASDs associated with consistent face-emotion recognition deficits? Do deficits generalize across multiple emotional expressions or are they limited to specific emotions? Do age or cognitive intelligence affect the magnitude of identified deficits? The results indicate that ASDs are associated with face-emotion recognition deficits across multiple expressions and that the magnitude of these deficits increases with age and cannot be accounted for by intelligence. These findings suggest that, whereas neurodevelopmental processes and social experience produce improvements in general face-emotion recognition abilities over time during typical development, children with ASD may experience disruptions in these processes, which suggested distributed functional impairment in the neural architecture that subserves face-emotion processing, an effect with downstream developmental consequences.

Adolescents' peer experiences may have significant associations with biological stress-response systems, adding to or reducing allostatic load. This study examined relational victimization as a unique contributor to reactive hypothalamic–pituitary–adrenal (HPA) axis responses as well as friendship quality and behavior as factors that may promote HPA recovery following a stressor. A total of 62 adolescents (ages 12–16; 73% female) presenting with a wide range of life stressors and adjustment difficulties completed survey measures of peer victimization and friendship quality. Cortisol samples were collected before and after a lab-based interpersonally themed social stressor task to provide measures of HPA baseline, reactivity, and recovery. Following the stressor task, adolescents discussed their performance with a close friend; observational coding yielded measures of friends' responsiveness. Adolescents also reported positive and negative friendship qualities. Results suggested that higher levels of adolescents' relational victimization were associated with blunted cortisol reactivity, even after controlling for physical forms of victimization and other known predictors of HPA functioning (i.e., life stress or depressive symptoms). Friendship qualities (i.e., low negative qualities) and specific friendship behaviors (i.e., high levels of responsiveness) contributed to greater HPA regulation; however, consistent with theories of rumination, high friend responsiveness in the context of high levels of positive friendship quality contributed to less cortisol recovery. Findings extend prior work on the importance of relational victimization and dyadic peer relations as unique and salient correlates of adaptation 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.

Theories of borderline personality disorder (BPD) postulate that high-risk transactions between caregiver and child are important for the development and maintenance of the disorder. Little empirical evidence exists regarding the reciprocal effects of parenting on the development of BPD symptoms in adolescence. The impact of child and caregiver characteristics on this reciprocal relationship is also unknown. Thus, the current study examines bidirectional effects of parenting, specifically harsh punishment practices and caregiver low warmth, and BPD symptoms in girls aged 14–17 years based on annual, longitudinal data from the Pittsburgh Girls Study (N = 2,451) in the context of child and caregiver characteristics. We examined these associations through the use of autoregressive latent trajectory models to differentiate time-specific variations in BPD symptoms and parenting from the stable processes that steadily influence repeated measures within an individual. The developmental trajectories of BPD symptoms and parenting were moderately associated, suggesting a reciprocal relationship. There was some support for time-specific elevations in BPD symptoms predicting subsequent increases in harsh punishment and caregiver low warmth. There was little support for increases in harsh punishment and caregiver low warmth predicting subsequent elevations in BPD symptoms. Child impulsivity and negative affectivity, and caregiver psychopathology were related to parenting trajectories, while only child characteristics predicted BPD trajectories. The results highlight the stability of the reciprocal associations between parenting and BPD trajectories in adolescent girls and add to our understanding of the longitudinal course of BPD in youth.

Multiple behavioral and health outcomes, including internalizing symptoms, may be predicted from prenatal maternal anxiety, depression, or stress. However, not all children are affected, and those that are can be affected in different ways. Here we test the hypothesis that the effects of prenatal anxiety are moderated by genetic variation in the child's brain-derived neurotrophic factor (BDNF) gene, using the Avon Longitudinal Study of Parents and Children population cohort. Internalizing symptoms were assessed from 4 to 13 years of age using the Strengths and Difficulties Questionnaire (n = 8,584); a clinical interview with the adolescents was conducted at age 15 years (n = 4,704). Obstetric and psychosocial risk and postnatal maternal symptoms were included as covariates. Results show that prenatal maternal anxiety predicted internalizing symptoms, including with the diagnostic assessment at 15 years. There was a main effect of two BDNF polymorphisms (rs6265 [val66met] and rs11030104) on internalizing symptoms up to age 13. There was also genetic moderation of the prenatal anxiety effect by different BDNF polymorphisms (rs11030121 and rs7124442), although significant effects were limited to preadolescence. The findings suggest a role for BDNF gene–environment interactions in individual vulnerability to the effects of prenatal anxiety on child internalizing symptoms.

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.

Children with histories of disorganized attachment exhibit diverse problems, possibly because disorganization takes at least two distinctive forms as children age: controlling–punitive and controlling–caregiving. This variation in the developmental legacy of disorganization has been attributed primarily to variations in children's rearing experiences. Here an alternative explanation of these divergent sequelae of disorganization is evaluated: one focused on genotype. Structural equation modeling was applied to data on 704 Norwegian children to test whether the catechol-O-methyltransferase Val158Met genotype moderates the effect of disorganized attachment, which was measured dimensionally at 4 years of age using the Manchester Child Attachment Story Task, on changes in aggressive behavior and social competence from ages 4 to 6. Children who scored high on disorganization and were homozygous for the valine allele displayed significantly greater increases in aggression and decreases in self-oriented social skills (e.g., self-regulation and assertiveness) over time than did their disorganized counterparts carrying the methionine allele, whereas disorganized children carrying the methionine allele increased their other-oriented social skill (e.g., cooperation and responsibility) scores more than did valine-homozygous children. These results are consistent with the controlling–punitive and controlling–caregiving behaviors observed in disorganized children, suggesting that the children's genotype contributed to variations in the social development of disorganized children.

This study had two goals. The first goal was to examine the association between two indicators of negative bias in children and their associations with children's aggression. The second goal was to examine a possible dual role of social status, operationalized as popularity, as a concurrent correlate of negative bias and as a moderator of the effect of negative bias on children's aggression. The roles of gender and type of aggression were also examined. Participants were 366 fifth- and sixth-grade children (49% girls; Mage = 11.07 years, SD = 0.85 year) who completed peer- and self-report measures in their classrooms. The results showed that the two indicators of negative bias were associated with each other and with children's aggression. Popularity was weakly associated with negative bias. However, popularity did moderate the association of hostile attributions with aggression. The associations of both measures of negative bias with aggression also varied by gender, with stronger associations for boys than for girls. Theoretical and practical implications are discussed.

Childhood depressive symptoms may arise from genetic and environmental risks, which act to bias the ways in which children process emotional information. Previous studies show that several “cognitive biases” are heritable and share genetic and environmental risks with depressive symptoms. Past research suggests that many cognitive biases only reflect genetic risks for depressive symptoms from adolescence. The present study sought to identify (a) when interpersonal cognitions mature as risk factors for depressive symptoms by examining whether these factors are stable and predict symptoms across time in childhood, and (b) the extent to which interpersonal cognitions reflect inherited/environmental risks on children's depressive symptoms. Results showed that there was some stability for interpersonal cognitive biases from age 8 to 10 years (rs = .32–.43). Only the absence of positive self/other perceptions, and negative peer and mother expectations at age 8 predicted depressive symptoms at age 10 (after controlling for depressive symptoms at age 8). The absence of positive self/other perceptions shared genetic influences with depressive symptoms within and across time. Across middle to late childhood, interpersonal cognitions begin to operate as vulnerability-trait factors for depressive symptoms, gradually reflecting distal genetic risks on symptoms.

Early biobehavioral regulation, a major influence of later adaptation, develops through dyadic interactions with caregivers. Thus, identification of maternal characteristics that can ameliorate or exacerbate infants’ innate vulnerabilities is key for infant well-being and long-term healthy development. The present study evaluated the influence of maternal parenting, postpartum psychopathology, history of childhood maltreatment, and demographic risk on infant behavioral and physiological (i.e., salivary cortisol) regulation using the still-face paradigm. Our sample included 153 women with high rates of childhood maltreatment experiences. Mother–infant dyads completed a multimethod assessment at 7 months of age. Structural equation modeling showed that maternal positive (i.e., sensitive, warm, engaged, and joyful) and negative (i.e., overcontrolling and hostile) behaviors during interactions were associated with concurrent maternal depressive symptoms, single parent status, and low family income. In turn, positive parenting predicted improved infant behavioral regulation (i.e., positive affect and social behaviors following the stressor) and decreased cortisol reactivity (i.e., posttask levels that were similar to or lower than baseline cortisol). These findings suggest increased risk for those women experiencing high levels of depressive symptoms postpartum and highlight the importance of maternal positive interactive behaviors during the first year for children's neurodevelopment.

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.

Despite widespread recognition that the physiological systems underlying stress reactivity are well coordinated at a neurobiological level, surprisingly little empirical attention has been given to delineating precisely how the systems actually interact with one another when confronted with stress. We examined cross-system response proclivities in anticipation of and following standardized laboratory challenges in 664 4- to 14-year-olds from four independent studies. In each study, measures of stress reactivity within both the locus coeruleus-norepinephrine system (i.e., the sympathetic and parasympathetic branches of the autonomic nervous system) and the corticotrophin releasing hormone system (i.e., the hypothalamic–pituitary–adrenal axis) were collected. Latent profile analyses revealed six distinctive patterns that recurred across the samples: moderate reactivity (average cross-system activation; 52%–80% of children across samples), parasympathetic-specific reactivity (2%–36%), anticipatory arousal (4%–9%), multisystem reactivity (7%–14%), hypothalamic–pituitary–adrenal axis specific reactivity (6%–7%), and underarousal (0%–2%). Groups meaningfully differed in socioeconomic status, family adversity, and age. Results highlight the sample-level reliability of children's neuroendocrine responses to stress and suggest important cross-system regularities that are linked to development and prior experiences and may have implications for subsequent physical and mental morbidity.

The complex interplay between bullying/victimization and defending was examined using a longitudinal social network approach (stochastic actor-based models). The (co)evolution of these relations within three elementary schools (Grades 2–5 at Time 1, ages 8–11, N = 354 children) was investigated across three time points within a year. Most bullies and defenders were in the same grade as the victims, although a substantial number of bullies and defenders were in other grades (most often one grade higher). Defenders were usually of the same gender as the victims, whereas most bullies were boys, with boys bullying both boys and girls. In line with goal-framing theory, multiplex network analyses provided evidence for the social support hypothesis (victims with the same bullies defended each other over time) as well as the retaliation hypothesis (defenders run the risk of becoming victimized by the bullies of the victims they defend). In addition, the analysis revealed that bullies with the same victims defended each other over time and that defenders of bullies initiated harassment of those bullies' victims. This study can be seen as a starting point in unraveling the relationship dynamics among bullying, victimization, and defending networks in schools.

The present study incorporates a person-based approach to identify spillover and compartmentalization patterns of interpartner conflict and maternal parenting practices in an ethnically diverse sample of 192 2-year-old children and their mothers who had experienced higher levels of socioeconomic risk. In addition, we tested whether sociocontextual variables were differentially predictive of theses profiles and examined how interpartner-parenting profiles were associated with children's physiological and psychological adjustment over time. As expected, latent class analyses extracted three primary profiles of functioning: adequate functioning, spillover, and compartmentalizing families. Furthermore, interpartner-parenting profiles were differentially associated with both sociocontextual predictors and children's adjustment trajectories. The findings highlight the developmental utility of incorporating person-based approaches to models of interpartner conflict and maternal parenting practices.

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.

Developmental or fetal programming has emerged as a major model for understanding the early and persisting effects of prenatal exposures on the health and development of the child and adult. We leverage the power of a 14-year prospective study to examine the persisting effects of prenatal anxiety, a key candidate in the developmental programming model, on symptoms of behavioral and emotional problems across five occasions of measurement from age 4 to 13 years. The study is based on the Avon Longitudinal Study of Parents and Children cohort, a prospective, longitudinal study of a large community sample in the west of England (n = 7,944). Potential confounders included psychosocial and obstetric risk, postnatal maternal mood, paternal pre- and postnatal mood, and parenting. Results indicated that maternal prenatal anxiety predicted persistently higher behavioral and emotional symptoms across childhood with no diminishment of effect into adolescence. Elevated prenatal anxiety (top 15%) was associated with a twofold increase in risk of a probable child mental disorder, 12.31% compared with 6.83%, after allowing for confounders. Results were similar with prenatal depression. These analyses provide some of the strongest evidence to date that prenatal maternal mood has a direct and persisting effect on her child's psychiatric symptoms and support an in utero programming hypothesis.

Evidence now implicates inflammatory proteins in the neurobiology of internalizing disorders. Genetic factors may influence individual responses to maltreatment; however, little work has examined inflammatory genetic variants in adults and none in children. The present study examined the role of an interleukin 1B gene (IL1B) variant in preschoolers exposed to maltreatment and other forms of adversity in internalizing symptom development. One hundred ninety-eight families were enrolled, with one child (age 3–5 years) from each family. Adversity measures included child protective service documentation of moderate–severe maltreatment in the last 6 months and interview-assessed contextual stressors. Internalizing symptoms were measured using the Child Behavior Checklist and the Diagnostic Infant and Preschool Assessment. Maltreated children had higher major depressive disorder (MDD) and posttraumatic stress disorder symptoms and marginally higher internalizing symptoms on the Child Behavior Checklist. Controlling for age, sex, and race, IL1B genotype was associated with MDD symptoms (p = .002). Contextual stressors were significantly associated with MDD and posttraumatic stress disorder and marginally with internalizing symptoms. The IL1B genotype interacted with contextual stress such that children homozygous for the minor allele had more MDD symptoms (p = .045). These results suggest that genetic variants of IL1B may modulate the development of internalizing symptoms in the face of childhood adversity.