Disorganized attachment is an important early risk factor for socioemotional problems throughout childhood and into adulthood. Prevailing models of the etiology of disorganized attachment emphasize the role of highly dysfunctional parenting, to the exclusion of complex models examining the interplay of child and parental factors. Decades of research have established that extreme child birth weight may have long-term effects on developmental processes. These effects are typically negative, but this is not always the case. Recent studies have also identified the dopamine D4 receptor (DRD4) as a moderator of childrearing effects on the development of disorganized attachment. However, there are inconsistent findings concerning which variant of the polymorphism (seven-repeat long-form allele or non–seven-repeat short-form allele) is most likely to interact with caregiving in predicting disorganized versus organized attachment. In this study, we examined possible two- and three-way interactions and child DRD4 polymorphisms and birth weight and maternal caregiving at age 6 months in longitudinally predicting attachment disorganization at 36 months. Our sample is from the Maternal Adversity, Vulnerability and Neurodevelopment project, a sample of 650 mother–child dyads. Birth weight was cross-referenced with normative data to calculate birth weight percentile. Infant DRD4 was obtained with buccal swabs and categorized according to the presence of the putative allele seven repeat. Macroanalytic and microanalytic measures of maternal behavior were extracted from a videotaped session of 20 min of nonfeeding interaction followed by a 10-min divided attention maternal task at 6 months. Attachment was assessed at 36 months using the Strange Situation procedure, and categorized into disorganized attachment and others. The results indicated that a main effect for DRD4 and a two-way interaction of birth weight and 6-month maternal attention (frequency of maternal looking away behavior) and sensitivity predicted disorganized attachment in robust logistic regression models adjusted for social demographic covariates. Specifically, children in the midrange of birth weight were more likely to develop a disorganized attachment when exposed to less attentive maternal care. However, the association reversed with extreme birth weight (low and high). The DRD4 seven-repeat allele was associated with less disorganized attachment (protective), while non–seven-repeat children were more likely to be classified as disorganized attachment. The implications for understanding inconsistencies in the literature about which DRD4 genotype is the risk direction are also considered. Suggestions for intervention with families with infants at different levels of biological risk and caregiving risk are also discussed.

Children born preterm are at risk for experiencing significant deleterious developmental outcomes throughout their childhood and adolescence. However, individual variation and resilience are hallmarks of the preterm population. The present study examined pathways to resilience across multiple domains (e.g., social activities, peer relations, attention-deficit/hyperactivity disorder symptomology, externalizing and internalizing behavior, and sleep quality) as children born preterm reached school age. The study also examined early child and family predictors of resilience. Using a prospective longitudinal design, 173 infants born preterm and without significant neurological complications were assessed at five time points: neonatal intensive care unit discharge, 9 months, 16 months, 24 months, and 6 years. Three pathways of adaptation emerged at 6 years: children who were resilient, those who remained at-risk, and children who exhibited significant difficulties. Resilient children were less likely to have experienced negative parenting at 9 and 16 months, more likely to delay gratification at 24 months, and more likely to experience neonatal health complications than nonresilient children.

Prenatal cocaine exposure may affect developing stress response systems in youth, potentially creating risk for substance use in adolescence. Further, pathways from prenatal risk to future substance use may differ for girls versus boys. The present longitudinal study examined multiple biobehavioral measures, including heart rate, blood pressure, emotion, and salivary cortisol and salivary alpha amylase (sAA), in response to a stressor in 193 low-income 14- to 17-year-olds, half of whom were prenatally cocaine exposed (PCE). Youth's lifetime substance use was assessed with self-report, interview, and urine toxicology/breathalyzer at Time 1 and at Time 2 (6–12 months later). PCE × Gender interactions were found predicting anxiety, anger, and sadness responses to the stressor, with PCE girls showing heightened responses as compared to PCE boys on these indicators. Stress Response × Gender interactions were found predicting Time 2 substance use in youth (controlling for Time 1 use) for sAA and sadness; for girls, heightened sadness responses predicted substance use, but for boys, dampened sAA responses predicted substance use. Findings suggest distinct biobehavioral stress response risk profiles for boys and girls, with heightened arousal for girls and blunted arousal for boys associated with prenatal risk and future substance use outcomes.

Childhood maltreatment represents a complex stressor, with the developmental timing, duration, frequency, and type of maltreatment varying with each child (Barnett, Manly, & Cicchetti, 1993; Cicchetti & Manly, 2001). Multiple brain regions and neural circuits are disrupted by the experience of child maltreatment (Cicchetti & Toth, in press; DeBellis et al., 2002; McCrory & Viding, 2010; Teicher, Anderson, & Polcari, 2012). These neurobiological compromises indicate the impairment of a number of important cognitive functions, including working memory and inhibitory control. The present study extends prior research by examining the effect of childhood maltreatment on neurocognitive functioning based on developmental timing of maltreatment, including onset, chronicity, and recency, in a sample of 3- to 9-year-old nonmaltreated (n = 136) and maltreated children (n = 223). Maltreated children performed more poorly on inhibitory control and working-memory tasks than did nonmaltreated children. Group differences between maltreated children based on the timing of maltreatment and the chronicity of maltreatment also were evident. Specifically, children who were maltreated during infancy, and children with a chronic history of maltreatment, exhibited significantly poorer inhibitory control and working-memory performance than did children without a history of maltreatment. The results suggest that maltreatment occurring during infancy, a period of major brain organization, disrupts normative structure and function, and these deficits are further instantiated by the prolonged stress of chronic maltreatment during the early years of life.

Asthma is a chronic respiratory disorder that affects over 7 million children in the United States. Evidence indicates that family stressors are associated with worsening of asthma symptoms, and some research suggests that these stressful experiences engender changes in children's immune systems in ways that exacerbate airway inflammation and contribute to both acute and chronic asthma symptoms. We examined the association between observed experiences of parent–child conflict and the expression of signaling molecules involved in the transduction of anti-inflammatory signals that regulate airway inflammation and obstruction. Fifty-seven children and their parents participated in a conflict task, and coders rated interactions for evidence of harsh and supportive behaviors. Children reported on their perceptions of parental support and reported on their daily asthma symptoms for 2 weeks. We collected peripheral blood in children to measure leukocyte expression of messenger RNA for the glucocorticoid receptor and the β2-adrenergic receptor. Analyses revealed that harsh conflict behaviors were associated with decreased expression of both messenger RNAs and more severe asthma symptoms. Neither supportive behaviors nor perceived parental support was associated with gene expression or asthma symptoms. These findings suggest that harsh interactions with parents are associated with downregulation of key anti-inflammatory signaling molecules and difficulties breathing in children with asthma. Children with asthma who are also victims of maltreatment may be particularly susceptible to transcriptional changes in immune cells that could worsen asthma over time.

The current study investigated the influential role of infant avoidance on links between maternal caregiving behavior and trajectories at risk for psychopathology. A sample of 153 children, selected for temperamental reactivity to novelty, was followed from infancy through early childhood. At 9 months, infant avoidance of fear-eliciting stimuli in the laboratory and maternal sensitivity at home were assessed. At 36 months, maternal gentle discipline was assessed at home. Children were repeatedly observed in the lab with an unfamiliar peer across early childhood. A latent class growth analysis yielded three longitudinal risk trajectories of social reticence behavior: a high-stable trajectory, a high-decreasing trajectory, and a low-increasing trajectory. For infants displaying greater avoidance, 9-month maternal sensitivity and 36-month maternal gentle discipline were both positively associated with membership in the high-stable social reticence trajectory, compared to the high-decreasing social reticence trajectory. For infants displaying lower avoidance, maternal sensitivity was positively associated with membership in the high-decreasing social reticence trajectory, compared to the low-increasing trajectory. Maternal sensitivity was positively associated with the high-stable social reticence trajectory when maternal gentle discipline was lower. These results illustrate the complex interplay of infant and maternal behavior in early childhood trajectories at risk for emerging psychopathology.

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.

Magnetic resonance imaging studies of maltreated children with posttraumatic stress disorder (PTSD) suggest that maltreatment-related PTSD is associated with adverse brain development. Maltreated youth resilient to chronic PTSD were not previously investigated and may elucidate neuromechanisms of the stress diathesis that leads to resilience to chronic PTSD. In this cross-sectional study, anatomical volumetric and corpus callosum diffusion tensor imaging measures were examined using magnetic resonance imaging in maltreated youth with chronic PTSD (N = 38), without PTSD (N = 35), and nonmaltreated participants (n = 59). Groups were sociodemographically similar. Participants underwent assessments for strict inclusion/exclusion criteria and psychopathology. Maltreated youth with PTSD were psychobiologically different from maltreated youth without PTSD and nonmaltreated controls. Maltreated youth with PTSD had smaller posterior cerebral and cerebellar gray matter volumes than did maltreated youth without PTSD and nonmaltreated participants. Cerebral and cerebellar gray matter volumes inversely correlated with PTSD symptoms. Posterior corpus callosum microstructure in pediatric maltreatment-related PTSD differed compared to maltreated youth without PTSD and controls. The group differences remained significant when controlling for psychopathology, numbers of Axis I disorders, and trauma load. Alterations of these posterior brain structures may result from a shared trauma-related mechanism or an inherent vulnerability that mediates the pathway from chronic PTSD to comorbidity.

Although infants born at extremely low birth weight (ELBW; birth weight < 1000 g) are at increased risk for developing later psychopathology, the mechanisms contributing to this association are largely unknown. In the present study, we examined a putative cognitive link to psychopathology in a cohort of ELBW survivors. These individuals were followed up prospectively at age 8 and again at ages 22–26. At 8 years, participants completed measures of fluid and general intelligence. As young adults, a subset of ELBW survivors free of major neurosensory impairments provided self-reports of personality characteristics related to psychopathology. Data from 66 participants indicated that, as predicted, the association between ELBW and externalizing behaviors was moderated by fluid intelligence. Specifically, ELBW individuals with poor fluid intelligence who were born small for gestational age (birth weight < 10th percentile for gestational age) showed the highest level of externalizing behaviors. These findings provide support for a cumulative risk model and suggest that fluid intelligence might be a cognitive mechanism contributing to the development of psychopathology among nonimpaired individuals who were born at ELBW and small for gestational age.

The aim of the study was to examine possible influences on individual differences in adolescence in response to early institutional care in infancy not involving either generalized privation or subnutrition. Fifty-two adopted adolescents aged 13 years who received institutional care in infancy at the Metera Babies Centre and 36 adolescents of the same age who were raised in their biological families participated in the study. Adolescents' attachment relationships, cognition, behavioral adjustment and use of psychological services were assessed. Marked heterogeneity in outcomes was found. No predictive effects were found for preinstitutional features or for adoptive circumstances. By contrast a large effect was found for institutional care extending beyond the age of 2 years and for quality of institutional care as experienced at an individual level. There was a close association between prolonged institutional care and disorganized attachment while in the institution, but the main institutional effect derived from the length of time in the institution.

In this study, we employed an eye-gaze paradigm to explore whether children (ages 8–12) and adolescents (ages 12–18) with autism spectrum disorders (ASDs) are able to use prosodic cues to determine the syntactic structure of an utterance. Persons with ASD were compared to typically developing (TD) peers matched on age, IQ, gender, and receptive language abilities. The stimuli were syntactically ambiguous but had a prosodic break that indicated the appropriate interpretation (feel the frog … with the feather vs. feel … the frog with the feather). We found that all groups were equally sensitive to the initial prosodic cues that were presented. Children and teens with ASD used prosody to interpret the ambiguous phrase as rapidly and efficiently as their TD peers. However, when a different cue was presented in subsequent trials, the younger ASD group was more likely to respond in a manner consistent with the initial prosodic cue rather than the new one. Eye-tracking data indicated that both younger groups (ASD and TD) had trouble shifting their interpretation as the prosodic cue changed, but the younger TD group was able to overcome this interference and produce an action consistent with the prosodic cue.

Childhood maltreatment is a serious individual, familial, and societal threat that compromises healthy development and is associated with lasting alterations to emotion perception, processing, and regulation (Cicchetti & Curtis, 2005; Pollak, Cicchetti, Hornung, & Reed, 2000; Pollak & Tolley-Schell, 2003). Individuals with a history of maltreatment show altered structural and functional brain development in both frontal and limbic structures (Hart & Rubia, 2012). In particular, previous research has identified hyperactive amygdala responsivity associated with childhood maltreatment (e.g., Dannlowski et al., 2012). However, less is known about the impact of maltreatment on the relationship between the amygdala and other brain regions. The present study employed an emotion processing functional magnetic resonance imaging task to examine task-based activation and functional connectivity in adults who experienced maltreatment as children. The sample included adults with a history of substantiated childhood maltreatment (n = 33) and comparison adults (n = 38) who were well matched on demographic variables, all of whom have been studied prospectively since childhood. The maltreated group exhibited greater activation than comparison participants in the prefrontal cortex and basal ganglia. In addition, maltreated adults showed increased amygdala connectivity with the hippocampus and prefrontal cortex. The results suggest that the intense early stress of childhood maltreatment is associated with lasting alterations to frontolimbic circuitry.

Reduced supportive parenting and elevated negative parenting behaviors increase risks for maladaptive social adjustment during early childhood (e.g., Campbell, Shaw, & Gilliom, 2000). However, the magnitude of these risks may vary according to children's individual characteristics, such as sex and temperament. The current study examines whether children's sex and fear reactivity moderate the associations between mothers’ observed parenting and children's behavior problems 1 year later. The sample consists of 151 predominantly African American, low-income families with one sibling who is approximately 2 years old and the closest aged older sibling who is approximately 4 years old. Results from fixed-effects within-family models indicate that fear distress (i.e., fearfulness) moderated associations between mothers’ observed negative parenting and children's increased behavior problems, such that only those children with mean or higher observed fear distress scores showed increased behavior problems when exposed to mother's negative parenting. Child sex moderated associations between fear approach reactivity (i.e., fearlessness) and mothers’ observed supportive parenting. Specifically, low fear approach combined with supportive parenting was associated with fewer behavior problems for boys only. Implications of these findings for preventive intervention are discussed.

By 18 months children demonstrate a range of social–cognitive skills that can be considered important precursors to more advanced forms of social understanding such as theory of mind. Although individual differences in social cognition have been linked to neurocognitive maturation, sociocultural models of development suggest that environmental influences operate in the development of children's social–cognitive outcomes. In the current study of 501 children and their mothers, we tested and found support for a model in which distal environmental risk, assessed when children were newborns, was indirectly associated with children's social–cognitive competency at 18 months through mothers' responsivity at 18 months. Part of this effect also operated through children's concomitant language skills, suggesting both a language-mediated and a language-independent mechanism of social–cognitive development. These findings are discussed with respect to the Vygotskian themes of internalization and semiotic mediation.

Prior research has found inconsistent evidence regarding the association among childhood adversity, inflammation, and internalizing symptoms, perhaps because previous studies have yet to adequately integrate important factors such as the timing of the adversity, genetic variation, and other relevant processes such as neuroendocrine regulation. The aims of the present study were threefold: (a) to determine whether the effect of the timing of child maltreatment on C-reactive protein (CRP), an inflammatory marker, varies by CRP gene variation; (b) to explore whether links between salivary CRP and childhood internalizing symptoms depend on the presence and timing of maltreatment experiences; and (c) to investigate the role of CRP in the relations between child neuroendocrine regulation and internalizing symptoms and examine whether these associations are moderated by the presence and timing of child maltreatment. Participants included a sample of 267 maltreated and 222 nonmaltreated children (M age = 9.72, SD = 0.99; 52.4% male; 66% African American) who attended a summer day camp research program designed for school-aged low-income children. Department of Human Services records were examined to determine the onset and recency of maltreatment for children in the maltreated group. The results indicated that among children with recent onset maltreatment, those with at least one A allele from CRP single nucleotide polymorphism rs1417938 evidenced significantly higher CRP levels compared to recently maltreated children carrying the TT genotype. Moreover, higher levels of CRP were associated with higher levels of internalizing symptoms only for recently maltreated children. Finally, we did not find support for salivary CRP as a mechanism in the relation between neuroendocrine regulation and childhood internalizing symptoms. Our findings highlight the importance of the timing of child maltreatment and have important implications for characterizing variability in inflammation and internalizing symptoms among youth.

The present study examined the impact of children's maltreatment experiences on the emergence of externalizing problem presentations among children during different developmental periods. The sample included 788 youth and their caregivers who participated in a multisite, prospective study of youth at-risk for maltreatment. Externalizing problems were assessed at ages 4, 8, and 12, and symptoms and diagnoses of attention-deficit/hyperactivity disorder, oppositional defiant disorder, and conduct disorder were assessed at age 14, during interviews with youth and caregivers. Information about maltreatment allegations was coded from official records. Latent transition analysis identified three groups of youth with similar presentations of externalizing problems (“well adjusted,” “hyperactive/oppositional,” and “aggressive/rule-breaking”) and transitions between groups from ages 4, 8, and 12. A “defiant/deceitful” group also emerged at age 12. Girls were generally more likely to present as well adjusted than boys. Children with recent physical abuse allegations had an increased risk for aggressive/rule-breaking presentations during the preschool and preadolescent years, while children with sexual abuse or neglect allegations had lower probabilities of having well-adjusted presentations during middle childhood. These findings indicate that persistently severe aggressive conduct problems, which are related to the most concerning outcomes, can be identified early, particularly among neglected and physically and sexually abused children.

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.

How infants shape their own development has puzzled developmentalists for decades. Recent models suggest that infant dispositions, particularly negative reactivity and regulation, affect outcome by determining the extent of parental effects. Here, we used a microanalytic experimental approach and proposed that infants with varying levels of negative reactivity will be differentially impacted by parent–infant synchrony in predicting physiological and behavioral regulation of increasing social stress during an experimental paradigm. One hundred and twenty-two mother–infant dyads (4–6 months) were observed in the face-to-face still face (SF) paradigm and randomly assigned to three experimental conditions: SF with touch, standard SF, and SF with arms’ restraint. Mother–infant synchrony and infant negative reactivity were observed at baseline, and three mechanisms of behavior regulation were microcoded; distress, disengagement, and social regulation. Respiratory sinus arrhythmia baseline, reactivity, and recovery were quantified. Structural equation modeling provided support for our hypothesis. For physiological regulation, infants high in negative reactivity receiving high mother–infant synchrony showed greater vagal withdrawal, which in turn predicted comparable levels of vagal recovery to that of nonreactive infants. In behavioral regulation, only infants low in negative reactivity who received high synchrony were able to regulate stress by employing social engagement cues during the SF phase. Distress was reduced only among calm infants to highly synchronous mothers, and disengagement was lowest among highly reactive infants experiencing high mother–infant synchrony. Findings chart two pathways by which synchrony may bolster regulation in infants of high and low reactivity. Among low reactive infants, synchrony builds a social repertoire for handling interpersonal stress, whereas in highly reactive infants, it constructs a platform for repeated reparation of momentary interactive “failures” and reduces the natural tendency of stressed infants to disengage from source of distress. Implications for the construction of synchrony-focused interventions targeting infants of varying dispositions are discussed.

Within a longitudinal study of 1,005 adolescents, we investigated how exposure to childhood psychosocial adversities was associated with the emergence of depressive symptoms between 14 and 17 years of age. The cohort was classified into four empirically determined adversity subtypes for two age periods in childhood (0–5 and 6–11 years). One subtype reflects normative/optimal family environments (n = 692, 69%), while the other three subtypes reflect differential suboptimal family environments (aberrant parenting: n = 71, 7%; discordant: n = 185, 18%; and hazardous: n = 57, 6%). Parent-rated child temperament at 14 years and adolescent self-reported recent negative life events in early and late adolescence were included in models implementing path analysis. There were gender-differentiated associations between childhood adversity subtypes and adolescent depressive symptoms. The discordant and hazardous subtypes were associated with elevated depressive symptoms in both genders but the aberrant parenting subtype only so in girls. Across adolescence the associations between early childhood adversity and depressive symptoms diminished for boys but remained for girls. Emotional temperament was also associated with depressive symptoms in both genders, while proximal negative life events related to depressive symptoms in girls only. There may be neurodevelopmental factors that emerge in adolescence that reduce depressogenic symptoms in boys but increase such formation in girls.

Exposure to early life adversity is linked to impaired affective, cognitive, and behavioral functioning and increases risk for various psychiatric and medical conditions. Stress-induced increases in pro-inflammatory cytokines may be a biological mechanism of these effects. Few studies have examined cytokine levels in children experiencing early life adversity, and very little research has investigated cytokines or other markers of inflammation in saliva. In the present study, we examined salivary interleukin (IL)-1β and C-reactive protein (CRP) levels in relation to stress exposure in 40 children aged 3 to 5 years who were enrolled in a larger study of early life adversity. Childhood maltreatment status was assessed via review of child welfare records. Contextual stress exposure, traumatic life event history, and symptoms of psychopathology were assessed via caregiver interviews at a home visit. In a subsequent visit, salivary IL-1β and CRP were obtained before and after participation in four emotion-eliciting tasks. The number of past-month contextual stressors, lifetime contextual stressors, and traumatic life events each demonstrated a significant main effect on IL-1β. Baseline IL-1β was positively associated with each of the significant main-effect adversities. Postchallenge IL-1β displayed positive associations with each adversity variable, but these were not significant. CRP was not significantly associated with any of the adversity variables. Given the evidence suggesting the involvement of IL-1β in the neuropathology of psychiatric conditions, these results may have important implications for developmental outcomes.