Children reared in orphanages typically experience the lack of stable, reliable caregivers and are at increased risk for deficits in regulatory abilities including difficulties in inhibitory control, attention, and emotion regulation. Although adoption results in a radical shift in caregiving quality, there remains variation in postadoption parenting, yet little research has examined postadoption parenting that may promote recovery in children experiencing early life adversity in the form of institutional care. Participants included 93 postinstitutionalized children adopted between 15 and 36 months of age and 52 nonadopted same-aged peers. Parenting was assessed four times during the first 2 years postadoption (at 2, 8, 16, and 24 months postadoption) and children's regulation was assessed at age 5 (M age = 61.68 months) and during kindergarten (M age = 71.55 months). Multiple parenting dimensions including sensitivity/responsiveness, structure/limit setting, and consistency in routines were examined. Both parental sensitivity and structure moderated the effect of preadoption adversity on children's emotion regulation while greater consistency was associated with better inhibitory control and fewer attention problems. Results support the notion that postadoption parenting during toddlerhood and the early preschool years promotes better regulation skills following early adversity.

Very little work has examined potential moderating effects in the link between prenatal intimate partner violence (IPV) and infant adjustment, especially in the first critical weeks following delivery. The current study evaluated the protective role of breastfeeding in the relationship between prenatal IPV and infant temperament at 4 months. Pregnant women (n = 82) were interviewed during pregnancy and at 6 weeks and 4 months postpartum. It was hypothesized that (a) prenatal IPV would predict infant temperament outcomes at the 4-month postpartum visit, and (b) breastfeeding continuation at 6 weeks acts as a protective factor such that breastfed infants will be less affected by the risk posed by prenatal IPV. Results indicated direct and negative effects of prenatal IPV on positive affectivity/surgency and orienting/regulatory capacity at 4 months. A significant moderating effect of breastfeeding at 6 weeks postpartum was identified. Mothers who were not breastfeeding at 6 weeks postpartum demonstrated the expected negative relationship between prenatal IPV exposure and infant adjustment, but if mothers were breastfeeding at 6 weeks postpartum, the relationship between IPV exposure and infant positive affectivity/surgency and orienting/regulatory capacity was not significantly different from zero. Results indicate a significant protective effect of breastfeeding in the intergenerational transmission of risk for infants born to mothers exposed to IPV.

Associations between prenatal maternal psychological distress and offspring developmental outcomes are well documented, yet relatively little research has examined links between maternal distress and development in utero, prior to postpartum influences. Fetal heart rate (FHR) parameters are established indices of central and autonomic nervous system maturation and function which demonstrate continuity with postnatal outcomes. This prospective, longitudinal study of 149 maternal–fetal pairs evaluated associations between prenatal maternal distress, FHR parameters, and dimensions of infant temperament. Women reported their symptoms of psychological distress at five prenatal visits, and FHR monitoring was conducted at the last three visits. Maternal report of infant temperament was collected at 3 and 6 months of age. Exposure to elevated prenatal maternal psychological distress was associated with higher late-gestation resting mean FHR (FHRM) among female but not male fetuses. Higher late-gestation FHRM was associated with lower infant orienting/regulation and with higher infant negative affectivity, and these associations did not differ by infant sex. A path analysis identified higher FHRM as one pathway by which elevated prenatal maternal distress was associated with lower orienting/regulation among female infants. Findings suggest that, for females, elevated maternal distress alters fetal development, with implications for postnatal function. Results also support the notion that, for both sexes, individual differences in regulation emerge prenatally and are maintained into infancy. Collectively, these findings underscore the utility of direct assessment of development in utero when examining if prenatal experiences are carried forward into postnatal life.

During South Africa's first two decades as a democracy, the Western Cape Province has undergone radical changes to its healthcare system in an effort to address the extensive socioeconomic inequities that remain in the aftermath of the apartheid era. Although progress has been made, there is a clear need for interventions that support parents and children receiving health services in the public sector who are vulnerable to multiple psychosocial risks associated with extreme poverty. In this mixed-method study, we examined the feasibility and acceptability of adapting an evidence-based parenting intervention called Mothering from the Inside Out that was developed for mothers who are vulnerable to similar risks in the United States. Using qualitative methods, we documented the collaborative process that was guided by principles of community-based participatory research and examined themes in the Western Cape collaborators’ perspectives about the feasibility and acceptability of the intervention. Using quantitative methods, we tested the preliminary efficacy of the adapted version of Mothering from the Inside Out for improving maternal reflective functioning and mother–child interactions. Although findings from both study components indicated preliminary promise, a number of obstacles and challenges at multiple levels underscore the need for (a) flexibility and contextual support for intervention research conducted in under-resourced communities, (b) clinical sensitivity to the unique experiences of parents rearing children in highly stressful, under-resourced environments, and (c) equal partnerships that allow the expertise of local providers to inform the design proposals of consulting investigators.

Anxiety disorders are common in autism spectrum disorder (ASD) and associated with social–communication impairment and repetitive behavior symptoms. The neurobiology of anxiety in ASD is unknown, but amygdala dysfunction has been implicated in both ASD and anxiety disorders. Using resting-state functional magnetic resonance imaging, we compared amygdala–prefrontal and amygdala–striatal connections across three demographically matched groups studied in the Autism Brain Imaging Data Exchange (ABIDE): ASD with a comorbid anxiety disorder (N = 25; ASD + Anxiety), ASD without a comorbid disorder (N = 68; ASD-NoAnx), and typically developing controls (N = 139; TD). Relative to ASD-NoAnx and TD controls, ASD + Anxiety individuals had decreased connectivity between the amygdala and dorsal/rostral anterior cingulate cortex (dACC/rACC). The functional connectivity of these connections was not affected in ASD-NoAnx, and amygdala connectivity with ventral ACC/medial prefrontal cortex (mPFC) circuits was not different in ASD + Anxiety or ASD-NoAnx relative to TD. Decreased amygdala–dorsomedial prefrontal cortex (dmPFC)/rACC connectivity was associated with more severe social impairment in ASD + Anxiety; amygdala–striatal connectivity was associated with restricted, repetitive behavior (RRB) symptom severity in ASD-NoAnx individuals. These findings suggest comorbid anxiety in ASD is associated with disrupted emotion-monitoring processes supported by amygdala–dACC/mPFC pathways, whereas emotion regulation systems involving amygdala–ventromedial prefrontal cortex (vmPFC) are relatively spared. Our results highlight the importance of accounting for comorbid anxiety for parsing ASD neurobiological heterogeneity.

Given high rates of co-occurring conditions in youth and adults with autism spectrum disorder (ASD), it is critical to examine the developmental trajectories of these symptoms of psychopathology. Using data from a cohort of participants (n = 194), most of whom were first assessed for ASD in very early childhood, we investigated the trajectories of co-occurring depressive, anxiety, and attention-deficit hyperactivity disorder (ADHD) symptoms from late childhood to adulthood. Additionally, childhood predictors and adult outcomes associated with these symptom trajectories were examined. Using group-based trajectory modeling, we found two distinct classes of individuals exhibiting each of these co-occurring symptom patterns: one class exhibited fairly low symptoms across time, and one class with elevated symptoms with varied fluctuation across time (ADHD symptoms starting high but decreasing, anxiety symptoms high and stable, and depressive symptoms fluctuating but peaking at clinically significant levels in young adulthood). All high trajectory classes were associated with age 9 adaptive skills; verbal IQ predicted higher anxiety and depressive symptom classes. After accounting for verbal IQ, all high symptom trajectory classes were negative predictors of objective adult outcomes. These findings call for wide-ranging considerations of the needs of individuals across ability levels, autism symptoms, and behavioral and emotional challenges.

Early behaviors that differentiate later biomarkers for psychopathology can guide preventive efforts while also facilitating pathophysiological research. We tested whether error-related negativity (ERN) moderates the link between early behavior and later psychopathology in two early childhood phenotypes: behavioral inhibition and irritability. From ages 2 to 7 years, children (n = 291) were assessed longitudinally for behavioral inhibition (BI) and irritability. Behavioral inhibition was assessed via maternal report and behavioral responses to novelty. Childhood irritability was assessed using the Child Behavior Checklist. At age 12, an electroencephalogram (EEG) was recorded while children performed a flanker task to measure ERN, a neural indicator of error monitoring. Clinical assessments of anxiety and irritability were conducted using questionnaires (i.e., Screen for Child Anxiety Related Disorders and Affective Reactivity Index) and clinical interviews. Error monitoring interacted with early BI and early irritability to predict later psychopathology. Among children with high BI, an enhanced ERN predicted greater social anxiety at age 12. In contrast, children with high childhood irritability and blunted ERN predicted greater irritability at age 12. This converges with previous work and provides novel insight into the specificity of pathways associated with psychopathology.

Environmental adversity increases child susceptibility to disrupted developmental outcomes, but the mechanisms by which adversity can shape development remain unclear. A translational cross-species approach was used to examine stress-mediated pathways by which poverty-related adversity can influence infant social development. Findings from a longitudinal sample of low-income mother–infant dyads indicated that infant cortisol (CORT) on its own did not mediate relations between early-life scarcity-adversity exposure and later infant behavior in a mother-child interaction task. However, maternal CORT through infant CORT served as a mediating pathway, even when controlling for parenting behavior. Findings using a rodent “scarcity-adversity” model indicated that pharmacologically blocking pup corticosterone (CORT, rodent equivalent to cortisol) in the presence of a stressed mother causally prevented social transmission of scarcity-adversity effects on pup social behavior. Furthermore, pharmacologically increasing pup CORT without the mother present was not sufficient to disrupt pup social behavior. Integration of our cross-species results suggests that elevated infant CORT may be necessary, but without elevated caregiver CORT, may not be sufficient in mediating the effects of environmental adversity on development. These findings underscore the importance of considering infant stress physiology in relation to the broader social context, including caregiver stress physiology, in research and interventional efforts.

Theory of mind, the ability to represent the mental states of others, is an important social cognitive process, which contributes to the development of social competence. Recent research suggests that interactions between gene and environmental factors, such as oxytocin receptor gene (OXTR) polymorphisms and maternal parenting behavior, may underlie individual differences in children's theory of mind. However, the potential influence of DNA methylation of OXTR remains unclear. The current study investigated the roles of OXTR methylation, maternal behavior, and their statistical interaction on toddlers’ early emerging theory of mind abilities. Participants included a community sample of 189 dyads of mothers and their 2- to 3-year-old children, whose salivary DNA was analyzed. Results indicated that more maternal structuring behavior was associated with better performance, on a battery of three theory of mind tasks, while higher OXTR methylation within exon 3 was associated with poorer performance. A significant interaction also emerged, such that OXTR methylation was related to theory of mind among children whose mothers displayed less structuring, when controlling for children's age, sex, ethnicity, number of child-aged siblings, verbal ability, and maternal education. Maternal structuring behavior may buffer the potential negative impact of hypermethylation on OXTR gene expression and function.

In this article, we describe the results of the second phase of a randomized controlled trial of Minding the Baby (MTB), an interdisciplinary reflective parenting intervention for infants and their families. Young first-time mothers living in underserved, poor, urban communities received intensive home visiting services from a nurse and social worker team for 27 months, from pregnancy to the child's second birthday. Results indicate that MTB mothers' levels of reflective functioning was more likely to increase over the course of the intervention than were those of control group mothers. Likewise, infants in the MTB group were significantly more likely to be securely attached, and significantly less likely to be disorganized, than infants in the control group. We discuss our findings in terms of their contribution to understanding the impacts and import of intensive intervention with vulnerable families during the earliest stages of parenthood in preventing the intergenerational transmission of disrupted relationships and insecure attachment.

Identifying developmental endophenotypes on the pathway between genetics and behavior is critical to uncovering the mechanisms underlying neurodevelopmental conditions. In this proof-of-principle study, we explored whether early disruptions in visual attention are a unique or shared candidate endophenotype of autism spectrum disorder (ASD) and attention-deficit/hyperactivity disorder (ADHD). We calculated the duration of the longest look (i.e., peak look) to faces in an array-based eye-tracking task for 335 14-month-old infants with and without first-degree relatives with ASD and/or ADHD. We leveraged parent-report and genotype data available for a proportion of these infants to evaluate the relation of looking behavior to familial (n = 285) and genetic liability (using polygenic scores, n = 185) as well as ASD and ADHD-relevant temperament traits at 2 years of age (shyness and inhibitory control, respectively, n = 272) and ASD and ADHD clinical traits at 6 years of age (n = 94).

Results showed that longer peak looks at the face were associated with elevated polygenic scores for ADHD (β = 0.078, p = .023), but not ASD (β = 0.002, p = .944), and with elevated ADHD traits in mid-childhood (F(1,88) = 6.401, p = .013, $\eta _p^2$=0.068; ASD: F (1,88) = 3.218, p = .076), but not in toddlerhood (ps > 0.2). This pattern of results did not emerge when considering mean peak look duration across face and nonface stimuli. Thus, alterations in attention to faces during spontaneous visual exploration may be more consistent with a developmental endophenotype of ADHD than ASD. Our work shows that dissecting paths to neurodevelopmental conditions requires longitudinal data incorporating polygenic contribution, early neurocognitive function, and clinical phenotypic variation.

Early adversity has been shown to sensitize individuals to the effects of later stress and enhance risk of psychopathology. Using a longitudinal randomized trial of foster care as an alternative to institutional care, we extend the stress sensitization hypothesis to examine whether early institutional rearing sensitizes individuals to stressful events in adolescence engendering chronic low-grade inflammation. At baseline, institutionalized children in Romania (ages 6–31 months) were randomly assigned to foster care or to remain in usual care within institutions. A group of never-institutionalized children was recruited as an in-country comparison sample. At ages 12 and 16, participants reported stressful events. At age 16, Interleukin-6 (IL-6) and C-reactive protein (CRP) were derived from blood spots. Among children assigned to care as usual, more stressful events at age 12, but not age 16, were associated with higher IL-6. In the same group, stressful events at age 16 were associated with higher CRP, though these effects attenuated after adjusting for covariates. These associations were not observed in the foster care or never-institutionalized groups. The findings suggest that heightened inflammation following stress exposure is one pathway through which early neglect could compromise physical health. In contrast, early family care might buffer against these risks.

Relational victimization typically emerges first during the elementary school period, and has been associated with increased levels of internalizing symptoms in children. Individual differences in autonomic nervous system functioning have been suggested as a potential factor linking social stressors and internalizing symptoms. The aim of this study was therefore to examine whether heart rate and heart rate variability mediated the association between relational victimization and internalizing symptoms in 373 mainstream elementary school children. Children were assessed in 2015 (T0; Grades 3–5, M age = 9.78 years, 51% boys) and reassessed in 2016 (T1). Heart rate and heart rate variability were assessed during a regular school day at T1. A multi-informant (teacher and peer report) cross-time measure of relational victimization, and a multi-informant (self- and teacher report) measure of internalizing problems at T1 was used. Results showed that heart rate variability, but not heart rate, mediated the association between relational victimization and internalizing symptoms. This study provides tentative support that in children from a general population sample, a psychobiological factor may mediate the association of relational victimization with internalizing symptoms.

This study examined whether the interaction between parenting and inhibitory control predicts hyperactivity-impulsivity and inattention in 195 children. Observation data of positive parenting were collected at 4 years, and mother reports of coercive parenting at 5 years, inhibitory control at 6 years, and hyperactivity-impulsivity/inattention at 7 years were obtained. The common and unique variance of hyperactivity-impulsivity and inattention symptoms were examined as outcomes using a bifactor model. Results indicated that positive parenting practices predicted lower levels of hyperactivity-impulsivity/inattention behaviors at age 7 only when children's inhibitory control was high. These results support the vantage sensitivity model, which posits that some individuals show an increased sensitivity to positive experiences exclusively, and support the appropriateness of a targeted prevention approach in early childhood.

It is unclear how individual differences in parenting and brain development interact to influence adolescent mental health outcomes. This study examined interactions between structural brain development and observed maternal parenting behavior in the prediction of adolescent depressive symptoms and psychological well-being. Whether findings supported diathesis-stress or differential susceptibility frameworks was tested. Participants completed observed interactions with their mothers during early adolescence (age 13), and the frequency of positive and aggressive maternal behavior were coded. Adolescents also completed structural magnetic resonance imaging scans at three time points: mean ages 13, 17, and 19. Regression models analyzed interactions between maternal behavior and longitudinal brain development in the prediction of late adolescent (age 19) outcomes. Indices designed to distinguish between diathesis-stress and differential susceptibility effects were employed. Results supported differential susceptibility: less thinning of frontal regions was associated with higher well-being in the context of low levels of aggressive maternal behavior, and lower well-being in the context of high levels of aggressive maternal behavior. Findings suggest that reduced frontal cortical thinning during adolescence may underlie increased sensitivity to maternal aggressive behavior for better and worse and highlight the importance of investigating biological vulnerability versus susceptibility.

Autism spectrum disorder (ASD) and attention-deficit/hyperactivity disorder (ADHD) are believed to share partially overlapping causal mechanisms suggesting that early risk markers may also overlap. Using latent profile analysis (LPA) in a sample of infants enriched for ASD and ADHD, we first examined the number of distinct groups of 3-year-old children, based on ADHD and ASD symptomatology. To investigate early predictors of ASD and ADHD symptom profiles, we next examined differences in trajectories of infant behaviors among the LPA classes spanning general development, negative affect, attention, activity level, impulsivity, and social behavior. Participants included 166 infants at familial risk for ASD (n = 89), ADHD (n = 38), or low-risk for both (n = 39) evaluated at 12, 18, 24, and 36 months of age. A three-class solution was selected reflecting a Typically Developing (TD) class (low symptoms; n = 108), an ADHD class (high ADHD/low ASD symptoms; n = 39), and an ASD class (high ASD/ADHD symptoms; n = 19). Trajectories of infant behaviors were generally suggestive of a gradient pattern of differences, with the greatest impairment within the ASD class followed by the ADHD class. These findings indicate a mixture of overlapping and distinct early markers of preschool ASD- and ADHD-like profiles that can be difficult to disentangle early in life.

We examined time-ordered associations between children's compliance behavior and maternal respiratory sinus arrhythmia (RSA) in a sample of 127 child-maltreating (physical abuse, physical neglect, emotional abuse) and 94 non-maltreating mothers and their preschool-aged children. Child prosocial and aversive compliance behaviors and maternal RSA were continuously collected during a joint challenge task. Child behavior and mother RSA were longitudinally nested within-person and subjected to multilevel modeling (MLM), with between-person child maltreatment subtype and level of inconsistent parenting modeled as moderators. Both child maltreatment type and inconsistent parenting moderated the effects of child compliance on maternal RSA. Increases in children's prosocial compliance behaviors led to decreasing RSA in physically abusive mothers 30s later (i.e., increasing arousal), but predicted increases in non-maltreating mothers’ RSA (i.e., increasing calm). Inconsistent parenting (vacillating between autonomy-support and strict control) also moderated the effects of children's compliance behavior on maternal physiology, weakening the effects of child prosocial compliance on subsequent maternal RSA. These findings highlight variations in mothers’ physiological sensitivity to their children's prosocial behavior that may play a role in the development of coercive cycles, and underscore the need to consider individual differences in parents’ physiological sensitivity to their children to effectively tailor interventions across the spectrum of risk.

While child self-regulation is shaped by the environment (e.g., the parents’ caregiving behaviors), children also play an active role in influencing the care they receive, indicating that children's individual differences should be integrated in models relating early care to children's development. We assessed 409 children's observed temperamental behavioral inhibition (BI), effortful control (EC), and the primary caregiver's parenting at child ages 3 and 5. Parents reported on child behavior problems at child ages 3, 5, and 8. Mediation analyses were conducted to examine relations between child temperament and parenting in predicting child problems. BI at age 3 was positively associated with structured parenting at age 5, which was negatively related to child internalizing and attention-academic problems at age 8. In contrast, parenting at child age 3 did not predict child BI or EC at age 5, nor did age 3 EC predict parenting at age 5. Findings indicate that child behavior may shape the development of caregiving and, in turn, long-term child adjustment, suggesting that studies of caregiving and child outcomes should consider the role of child temperament toward developing more informative models of child–environment interplay.

Although disaster-related posttraumatic stress symptoms (PTSS) typically decrease in intensity over time, some youth continue to report elevated levels of PTSS many years after the disaster. The current study examines two processes that may help to explain the link between disaster exposure and enduring PTSS: caregiver emotion socialization and youth recollection qualities. One hundred and twenty-two youth (ages 12 to 17) and their female caregivers who experienced an EF-4 tornado co-reminisced about the event, and adolescents provided independent recollections between 3 and 4 years after the tornado. Adolescent individual transcripts were coded for coherence and negative personal impact, qualities that have been found to contribute to meaning making. Parent–adolescent conversations were coded for caregiver egocentrism, a construct derived from the emotion socialization literature to reflect the extent to which the caregiver centered the conversation on her own emotions and experiences. Egocentrism predicted higher youth PTSS, and this association was mediated by the coherence of adolescents’ narratives. The association between coherence and PTSS was stronger for youth who focused more on the negative personal impacts of the tornado event during their recollections. Results suggest that enduring tornado-related PTSS may be influenced in part by the interplay of caregiver emotion socialization practices and youth recollection qualities.

Exposure to child maltreatment increases the risk for psychiatric and physical diseases. Inflammation has been proposed as a mechanism through which early adverse experiences become biologically embedded. However, most studies providing evidence for the link between early adverse exposures and inflammation have been retrospective or cross-sectional in design, or did not assess inflammation immediately after maltreatment in young children. In the present study we investigated the association between childhood maltreatment and salivary C-reactive protein (CRP) concentrations in a population of N = 173 children, 3–5 years of age, who were recruited in the immediate aftermath of maltreatment and followed-up longitudinally every 6 months over a period of 2 years. We found that the association between maltreatment and CRP concentrations was significantly moderated by child sex, such that in girls, CRP concentrations were higher in the maltreated compared to the control group, and this difference was stable across the 2-year follow-up-period, while in boys, there was no association between maltreatment and CRP. Our findings suggest that the effect of maltreatment on inflammation may already emerge right after exposure at a very young age in girls and manifest over time. Our study provides important evidence for the development of personalized, early interventions strategies targeting the early-life period.