Children reared in impoverished environments are at risk for enduring psychological and physical health problems. Mechanisms by which poverty affects development, however, remain unclear. To explore one potential mechanism of poverty's impact on social–emotional and cognitive development, an experimental examination of a rodent model of scarcity-adversity was conducted and compared to results from a longitudinal study of human infants and families followed from birth (N = 1,292) who faced high levels of poverty-related scarcity-adversity. Cross-species results supported the hypothesis that altered caregiving is one pathway by which poverty adversely impacts development. Rodent mothers assigned to the scarcity-adversity condition exhibited decreased sensitive parenting and increased negative parenting relative to mothers assigned to the control condition. Furthermore, scarcity-adversity reared pups exhibited decreased developmental competence as indicated by disrupted nipple attachment, distress vocalization when in physical contact with an anesthetized mother, and reduced preference for maternal odor with corresponding changes in brain activation. Human results indicated that scarcity-adversity was inversely correlated with sensitive parenting and positively correlated with negative parenting, and that parenting fully mediated the association of poverty-related risk with infant indicators of developmental competence. Findings are discussed from the perspective of the usefulness of bidirectional–translational research to inform interventions for at-risk families.

Epigenetic DNA modifications in genes related to the hypothalamic–pituitary–adrenal (HPA) axis are discussed as a mechanism underlying the association between prenatal depression and altered child HPA activity. In a longitudinal study, DNA methylation changes related to prenatal depressive symptoms were investigated in 167 children aged 6 to 9 years. At six candidate genes, 126 cytosine–guanine dinucleotides were considered without correcting for multiple testing due to the exploratory nature of the study. Further associations with the basal child HPA activity were examined. Children exposed to prenatal depressive symptoms exhibited lower bedtime cortisol (p = .003, ηp2 = 0.07) and a steeper diurnal slope (p = .023, ηp2 = 0.06). For total cortisol release, prenatal exposure was related to lower cortisol release in boys, and higher release in girls. Furthermore, prenatal depressive symptoms were associated with altered methylation in the glucocorticoid receptor gene (NR3C1), the mineralocorticoid receptor gene (NR3C2), and the serotonin receptor gene (SLC6A4), with some sex-specific effects (p = .012–.040, ηp2 = 0.03–0.04). In boys, prenatal depressive symptoms predicted bedtime cortisol mediated by NR3C2 methylation, indirect effect = –0.07, 95% confidence interval [–0.16, –0.02]. Results indicate relations of prenatal depressive symptoms to both child basal HPA activity and DNA methylation, partially fitting a mediation model, with exposed boys and girls being affected differently.

The proopiomelanocortin (POMC) molecule has been implicated in models of self-injurious behavior (SIB) in neurodevelopmental disorders, but it has never been specifically sequenced in search of base specific polymorphisms. The empirical focus of this preliminary study was to sequence the POMC gene in 11 children (mean age = 41.8 months, range = 12–60 months; 73% male) with clinical concerns regarding global developmental delay, 5 with reported self-injury. Genomic DNA was extracted from blood samples, and the POMC gene was amplified by specific oligonucleotide primers via polymerase chain reaction. The amplified gene products were sequenced by the University of Minnesota Genomic Center, and the results were analyzed using Sequencher software. A single nucleotide polymorphism (SNP), 1130 C>T, was found in the 3’ untranslated region (UTR) of two samples (one of whom had SIB). The program TargetScanHuman was used to predict the function of this mutation. Variant c.1130 C<T was predicted to be located in the target site of two microRNAs (miRNAs; hsa-mir-3715 and hsa-mir-1909), and the variant allele T may result in an increased minimum free energy for the two miRNAs. Further work with much larger samples is needed to continue the investigation of POMC’s possible function as a risk factor for the development of SIB in children with developmental delay/disability. The findings presented in this study show that the SNP found in the 3’ UTR could alter the binding of miRNAs to POMC 3'UTR, thus, increasing POMC expression and affecting several biological systems with high relevance to the biology of self-injury. There was a significant difference in β-endorphin levels between SIB (M = 169.25 pg/mL) and no SIB (M = 273.5 pg/mL, SD = 15.2) cases (p < .01). Intervention implications are tied to prior observations of individual differences among SIB responders and nonresponders to treatment with the opioid antagonist naltrexone. Stratifying individuals with SIB by POMC mutation status may provide a potential tailoring-like variable to guide the selection of who is more (or less) likely to respond to opiate antagonist treatment. Currently, opioid antagonistic treatment for SIB is empiric (trial and error).

A recent article in this journal reported a number of gene × environment interactions involving a serotonin transporter–gene network polygenic score and a composite index of prenatal adversity predicting several problem behavior outcomes at 48 months (e.g., anxious/depressed, pervasive developmental problems) and at 60 months (e.g., withdrawal, internalizing problems), yet did not illuminate the nature or form these genetic × environment interactions took. Here we report results of six additional analyses to evaluate whether these interactions reflected diathesis–stress or differential–susceptibility related processes. Analyses of the regions of significance and proportion of interaction index are consistent with the diathesis–stress model, seemingly because of the truncated nature of the adversity score (which did not extend to supportive/positive prenatal experiences/exposures); in contrast, the proportion (of cases) affected index favors the differential–susceptibility model. These results suggest the need for future studies to extend measurement of the prenatal environment to highly supportive experiences and exposures.

This study used a structural equation mixture model to examine associations between child maltreatment, polygenic risk, and indices of adaptive functioning. Children aged 6 to 13 years (N = 1,004), half maltreated, half nonmaltreated, were recruited to attend a research day camp. Multi-informant indicators of prosocial behavior, antisocial behavior, withdrawn behavior, and depression were collected and used in a latent class analysis. Four classes emerged, characterizing “well-adjusted,” “externalizing,” “internalizing,” and “socially dominant” groups. Twelve genetic variants, previously reported in the Gene × Environment literature, were modeled as one weighted polygenic risk score. Large main effects between maltreatment and adaptive functioning were observed (Wald = 35.3, df = 3, p < .0001), along with evidence of a small Gene × Environment effect (Wald = 13.5, df = 3, p = .004), adjusting for sex, age, and covariate interaction effects.

Using a large and nationally representative sample, we examined how adolescents’ 5-HTTLPR genotype and perceived parenting quality independently and interactively associated with trajectories of alcohol use from early adolescence to young adulthood and whether/how gender may moderate these associations. The sample for this study included 13,749 adolescents (53.3% female; 56.3% non-Hispanic White, 21.5% Black, 16.0% Hispanic, and 6.1% Asian) followed prospectively from adolescence to young adulthood. Using growth mixture modeling, we identified four distinct trajectories of alcohol use (i.e., persistent heavy alcohol use, developmentally limited alcohol use, late-onset heavy alcohol use, and non/light alcohol use). Results indicated that the short allele of 5-HTTLPR was associated with higher risk of membership in the persistent and the late-onset heavy alcohol use trajectories. Parenting quality was associated with lower likelihoods of following the persistent heavy and the developmentally limited alcohol use trajectories but was not associated with risk of membership for the late-onset heavy drinking trajectory. 5-HTTLPR interacted with parenting quality to predict membership in the persistent heavy alcohol use trajectory for males but not for females. Findings highlighted the importance of considering the heterogeneity in trajectories of alcohol use across development and gender in the study of Gene Environment interactions in alcohol use.

According to the developmental psychopathology framework, adverse childhood experiences, including child sexual abuse (CSA), may alter the course of normal development in children. Attachment security has been identified as a protective factor against psychopathology and may thus play a critical role in predicting victims’ adaptation. The main objective of the present study was to investigate the mediating effect of attachment representations in the relation between CSA and behavior problems over a 1-year period. The sample consisted of 391 children (251 sexually abused) aged 3.5 to 6 years. The Attachment Story Completion Task and the Child Behavior Checklist were used. Disorganized attachment partially mediated the relation between CSA and children's internalizing and externalizing behavior problems 1 year following the initial assessment. This mediation effect was not found for ambivalent nor secure attachment dimensions. Child gender was found to moderate the association between CSA and disorganization, with larger effects of CSA among boys. These findings underscore the importance of considering attachment representations in treatment programs for preschool victims. Evidence-based practice focusing on trauma could be combined with an attachment-based intervention targeting the parent–child relationship. Moreover, interventions should be gender sensitive, as CSA appears to affect boys and girls differently.

Efforts to differentiate between the developmental sequelae of childhood emotional abuse and childhood emotional neglect are critical to both research and practice efforts. As an oft-identified mechanism of the effects of child maltreatment on later adjustment, emotion dysregulation represents a key potential pathway. The present study explored a higher order factor model of specific emotion regulation skills, and the extent to which these skill sets would indicate distinct developmental pathways from unique emotional maltreatment experiences to multidomain adjustment. A sample of 500 ethnoracially diverse college students reported on their experiences. A two-factor model of emotion regulation skills based on subscales of the Difficulties in Emotion Regulation Scale was revealed. Significant indirect effects of childhood emotional abuse on psychopathology and problems in social relationships were found through response-focused difficulties in emotion regulation, whereas a significant indirect effect of childhood emotional neglect on problems in social relationships was found through antecedent-focused difficulties in emotion regulation. These results are consistent with theoretical models and empirical evidence suggesting differential effects of childhood emotional abuse and emotional neglect, and provide an important indication for developing targeted interventions focusing on specific higher order emotion dysregulation skill clusters.

There is a relative consensus about the detrimental impact of childhood maltreatment on later mental health problems and behavioral difficulties. Prior research suggests that neurophysiological stress mechanisms may partly mediate this association. However, inconsistent findings regarding hypothalamic-pituitary-adrenal axis and sympathetic responses to stress complicate this investigation. Furthermore, the concordance in these two stress systems is not well understood. We tested whether the severity of maltreatment affected the association between maltreatment and cortisol and heart rate (HR) stress responses and the symmetry of these responses. Participants were 155 males (56 maltreated and 99 controls) aged 18 to 35 years. Cortisol and HR were measured in response to the Trier Social Stress Test. Childhood maltreatment, sociodemographic factors, and health-related factors were measured using self-reported questionnaires. Maltreated participants had higher cortisol responses to stress in comparison to controls. However, a shift from moderate to lower to higher cortisol responses was noted as the severity of the experiences increased. Participants exposed to more experiences of maltreatment also showed a greater symmetry between cortisol and HR stress responses. Our findings provide further support for persistent dysregulation of the HPA axis following childhood maltreatment, of which the expression and symmetry with the sympathetic system may change according to the severity of experiences.

Research suggests that early adversity places individuals at risk for psychopathology across the life span. Guided by concepts of allostasis and allostatic load, the present study examined whether early adversity contributes to the development of subsequent internalizing symptoms through its association with traitlike individual differences in hypothalamic–pituitary–adrenal axis regulation. Early adolescent girls (n = 113; M age = 12.30 years) provided saliva samples at waking, 30 min postwaking, and bedtime over 3 days (later assayed for cortisol). Objective contextual stress interviews with adolescents and their mothers were used to assess the accumulation of nine types of early adversity within the family environment. Greater early adversity predicted subsequent increases in internalizing symptoms through lower levels of latent trait cortisol. Traitlike individual differences in hypothalamic–pituitary–adrenal axis activity may be among the mechanisms through which early adversity confers risk for the development of psychopathology.

As approximately one-third of peer-victimized children evidence heightened aggression (Schwartz, Proctor, & Chien, 2001), it is imperative to identify the circumstances under which victimization and aggression co-develop. The current study explored two potential moderators of victimization–aggression linkages: (a) attentional bias toward cues signaling threat and (b) attentional bais toward cues communicating interpersonal support. Seventy-two fifth- and sixth-grade children (34 boys; Mage = 11.67) were eye tracked while watching video clips of bullying. Each scene included a bully, a victim, a reinforcer, and a defender. Children's victimization was measured using peer, parent, and teacher reports. Aggression was measured using peer reports of overt and relational aggression and teacher reports of aggression. Victimization was associated with greater aggression at high levels of attention to the bully. Victimization was also associated with greater aggression at low attention to the defender for boys, but at high attention to the defender for girls. Attention to the victim was negatively correlated with aggression regardless of victimization history. Thus, attentional biases to social cues integral to the bullying context differentiate whether victimization is linked to aggression, necessitating future research on the development of these biases and concurrent trajectories of sociobehavioral development.

The development of executive function (EF) in autism spectrum disorder (ASD) has been investigated using only “cool”-cognitive EF tasks while there is limited knowledge regarding the development of “hot”-affective EF. Although cool EF development and its links to theory of mind (ToM) have been widely examined, understanding of the influence of hot EF to ToM mechanisms is minimal. The present study introduced a longitudinal design to examine the developmental changes in cool and hot EF of children with ASD (n = 45) and matched (to age and IQ) controls (n = 37) as well as the impact of EF on ToM development over a school year. For children with ASD, although selective cool (working memory and inhibition) and hot (affective decision making) EF domains presented age-related improvements, they never reached the performance level of the control group. Early cool working memory predicted later ToM in both groups but early hot delay discounting predicted later ToM only in the ASD group. No evidence was found for the reverse pattern (early ToM predicting later EF). These findings suggest that improvements in some EF aspects are evident in school age in ASD and highlight the crucial role that both cool and hot EF play in ToM development.

Child maltreatment is a major cause of pediatric posttraumatic stress disorder (PTSD). Previous studies have not investigated potential differences in network architecture in maltreated youth with PTSD and those resilient to PTSD. High-resolution magnetic resonance imaging brain scans at 3 T were completed in maltreated youth with PTSD (n = 31), without PTSD (n = 32), and nonmaltreated controls (n = 57). Structural covariance network architecture was derived from between-subject intraregional correlations in measures of cortical thickness in 148 cortical regions (nodes). Interregional positive partial correlations controlling for demographic variables were assessed, and those correlations that exceeded specified thresholds constituted connections in cortical brain networks. Four measures of network centrality characterized topology, and the importance of cortical regions (nodes) within the network architecture were calculated for each group. Permutation testing and principle component analysis method were employed to calculate between-group differences. Principle component analysis is a methodological improvement to methods used in previous brain structural covariance network studies. Differences in centrality were observed between groups. Larger centrality was found in maltreated youth with PTSD in the right posterior cingulate cortex; smaller centrality was detected in the right inferior frontal cortex compared to youth resilient to PTSD and controls, demonstrating network characteristics unique to pediatric maltreatment-related PTSD. Larger centrality was detected in right frontal pole in maltreated youth resilient to PTSD compared to youth with PTSD and controls, demonstrating structural covariance network differences in youth resilience to PTSD following maltreatment. Smaller centrality was found in the left posterior cingulate cortex and in the right inferior frontal cortex in maltreated youth compared to controls, demonstrating attributes of structural covariance network topology that is unique to experiencing maltreatment. This work is the first to identify cortical thickness-based structural covariance network differences between maltreated youth with and without PTSD. We demonstrated network differences in both networks unique to maltreated youth with PTSD and those resilient to PTSD. The networks identified are important for the successful attainment of age-appropriate social cognition, attention, emotional processing, and inhibitory control. Our findings in maltreated youth with PTSD versus those without PTSD suggest vulnerability mechanisms for developing PTSD.

Fathers are a crucial source of support for children following the birth of an infant sibling. This study examined whether fathers were more vulnerable to the effects of interparental conflict than mothers, and whether there was a subsequent spillover cascade from interparental conflict to children's externalizing behavior problems. We followed 241 families after the birth of a second child. Mothers and fathers reported on interparental conflict and parental efficacy at 1 and 4 months postpartum and punitive discipline and firstborn children's externalizing behavior problems across a longitudinal investigation (prenatal and 4, 8, and 12 months postpartum). For both mothers and fathers, interparental conflict prenatally predicted decreased parental efficacy following the birth. Fathers’ lower parental efficacy was significantly associated with increased punitive discipline toward the older sibling at 4 months, whereas mothers’ lower parental efficacy was not. Coercive family processes were present between mothers’ and fathers’ punitive discipline and older siblings’ externalizing behavior problems. Results were inconsistent with the father vulnerability hypothesis in that both mothers and fathers were vulnerable to interparental conflict, which in turn spilled over to create coercive family processes that exacerbated children's externalizing behavior problems in the year following the birth of a second child.

The aim of the current research was to disentangle four theoretically sound models of externalizing behavior etiology (i.e., attachment, language, inhibition, and parenting) by testing their relation with behavioral trajectories from early childhood to adolescence. The aim was achieved through a 10-year prospective longitudinal study conducted over five waves with 111 referred children aged 3 to 5 years at the onset of the study. Clinical referral was primarily based on externalizing behavior. A multimethod (questionnaires, testing, and observations) approach was used to estimate the four predictors in early childhood. In line with previous studies, the results show a significant decrease of externalizing behavior from early childhood to adolescence. The decline was negatively related to mothers’ coercive parenting and positively related to attachment security in early childhood, but not related to inhibition and language. The study has implications for research into externalizing behavior etiology recommending to gather hypotheses from various theoretically sound models to put them into competition with one another. The study also has implications for clinical practice by providing clear indications for prevention and early intervention.

We studied the pattern of personality development in a longitudinal population-based sample of 752 American adolescents. Personality was assessed reliably with the Junior Temperament and Character Inventory at 12, 14, and 16 years of age. The rank-order stability of Junior Temperament and Character Inventory traits from age 12 to 16 was moderate (r = .35). Hierarchical linear modeling of between-group variance due to gender and within-group variance due to age indicated that harm avoidance and persistence decreased whereas self-directedness and cooperativeness increased from age 12 to 16. Novelty seeking, reward dependence, and self-transcendence increased from age 12 to 14 and then decreased. This biphasic pattern suggests that prior to age 14 teens became more emancipated from adult authorities while identifying more with the emergent norms of their peers, and after age 14 their created identity was internalized. Girls were more self-directed and cooperative than boys and maintained this advantage from age 12 to 16. Dependability of temperament at age 16 was mainly predicted by the same traits at earlier ages. In contrast, maturity of character at age 16 was predicted by both temperament and character at earlier ages. We conclude that character develops rapidly in adolescence to self-regulate temperament in accord with personally valued goals shaped by peers.

A need to identify early infant markers of later occurring inattentive and hyperactive/impulsive behaviors has come to the fore in the current attention-deficit/hyperactivity disorder literature. The purpose of such studies is to identify driving mechanisms that could enable early detection of attention-deficit/hyperactivity disorder liability and thus facilitate early intervention. Here we study independent and interactive effects of cognitive regulation (inhibition and sustained attention), temperament (reactive and regulatory aspects), and maternal sensitivity (as external regulation) in a sample of 112 typically developing 10-month-old infants (59 boys, 52.7%), in relation to inattentive and hyperactive/impulsive behavior at 3 years. The results showed that infant temperamental regulation and maternal sensitivity made independent contributions to both inattention and hyperactivity/impulsivity, in that higher levels of temperamental regulation and maternal sensitivity were related to less inattentive and hyperactive/impulsive behavior. In addition, the temperamental factor positive affectivity/surgency made a significant contribution to later hyperactivity/impulsivity, in that higher levels of positive affectivity/surgency were related to more hyperactive/impulsive behavior. No interaction effects were found. Our findings suggest temperament and parental regulation as potential and independent markers of later inattentive and hyperactive/impulsive behavior.

Maternal elaborative reminiscing supports preschool children's autobiographical memory, self-concept, and emotion understanding. What are the factors contributing to mothers' elaborative style of reminiscing? In a longitudinal community sample (n = 170 at the final data point), this study explored the role of maternal depression (8–44 months), maternal sensitivity and maternal mind-mindedness (8 months), as well as child factors of joint attention (15 months), attachment security (15 months), and language (26 months) for mother–child reminiscing about a positive (happy) and a negative (scared) event at 44 months. Mothers could be classed into two groups of low versus increasing depression from 8 to 44 months, yet maternal depression did not uniquely predict mother–child reminiscing after accounting for maternal sensitivity and other factors. Instead, maternal sensitivity, children's joint attention, and language uniquely predicted children's elaborations about the scared event at 44 months, and maternal sensitivity uniquely predicted mothers' elaborations about the scared event at 44 months. Mothers who are more sensitive in early interactions may later be better at engaging their children when reminiscing about negative emotions. These findings have implications for the design of interventions targeted at supporting mothers to engage in elaborative reminiscing with their preschool children.

Researchers are becoming increasingly interested in linking specific forms of early life stress (ELS) to specific neurobiological markers, including alterations in the morphology of stress-sensitive brain regions. We used a person-centered, multi-informant approach to investigate the associations of specific constellations of ELS with hippocampal and amygdala volume in a community sample of 211 9- to 13-year-old early adolescents. Further, we compared this approach to a cumulative risk model of ELS, in which ELS was quantified by the total number of stressors reported. Using latent class analysis, we identified three classes of ELS (labeled typical/low, family instability, and direct victimization) that were distinguished by experiences of family instability and victimization. Adolescents in the direct victimization class had significantly smaller hippocampal volume than did adolescents in the typical/low class; ELS classes were not significantly associated with amygdala volume. The cumulative risk model of ELS had a poorer fit than did the person-centered model; moreover, cumulative ELS was not significantly associated with hippocampal or amygdala volume. Our results underscore the utility of taking a person-centered approach to identify alterations in stress-sensitive brain regions based on constellations of ELS, and suggest victimization is specifically associated with hippocampal hypotrophy observed in early adolescence.

Recent proposals suggest early adversity sets in motion particularly chronic and neurobiologically distinct trajectories of internalizing symptoms. However, few prospective studies in high-risk samples delineate distinct trajectories of internalizing symptoms from preschool age onward. We examined trajectories in a high-risk cohort, oversampled for internalizing symptoms, several preschool risk/maintenance factors, and school-age outcomes. Parents of 325 children completed the Strengths and Difficulties Questionnaire on up to four waves of data collection from preschool (3–5 years) to school age (8–9 years) and Preschool Age Psychiatric Assessment interviews at both ages. Multi-informant data were collected on risk factors and symptoms. Growth mixture modelling identified four trajectory classes of internalizing symptoms with stable low, rising low-to-moderate, stable moderate, and stable high symptoms. Children in the stable high symptom trajectory manifested clinically relevant internalizing symptoms, mainly diagnosed with anxiety disorders/depression at preschool and school age. Trajectories differed regarding loss/separation experience, maltreatment, maternal psychopathology, temperament, and stress-hormone regulation with loss/separation, temperament, maternal psychopathology, and stress-hormone regulation (trend) significantly contributing to explained variance. At school age, trajectories continued to differ on symptoms, disorders, and impairment. Our study is among the first to show that severe early adversity may trigger a chronic and neurobiologically distinct internalizing trajectory from preschool age onward.