The development of maternal representations of the child during pregnancy guides a mother’s thoughts, feelings, and behavior toward her child. The association between prenatal representations, particularly those that are disrupted, and toddler social-emotional functioning is not well understood. The present study examined associations between disrupted prenatal representations and toddler social-emotional functioning and to test disrupted maternal behavior as a mediator of this association. Data were drawn from 109 women from a larger prospective longitudinal study (N=120) of women and their young children. Prenatal disrupted maternal representations were assessed using the Working Model of the Child Interview disrupted coding scheme, while disrupted maternal behavior was coded 12-months postpartum from mother-infant interactions. Mother-reported toddler social-emotional functioning was assessed at ages 12 and 24 months. Disrupted prenatal representations significantly predicted poorer toddler social-emotional functioning at 24 months, controlling for functioning at 12 months. Further, disrupted maternal behavior mediated the relation between disrupted prenatal representations and toddler social-emotional problems. Screening for disrupted representations during pregnancy is needed to facilitate referrals to early intervention and decrease the likelihood of toddler social-emotional problems.

Childhood maltreatment (CM) is a known risk factor for adolescent pregnancy. Sleep disturbances and psychological distress, both common negative sequelae of CM, often co-occur during pregnancy, although directionality remains unclear. Furthermore, little is known about how CM affects sleep–distress associations during pregnancy. In pregnant adolescents, we examined: (a) whether there are significant predictive associations from CM to sleep quality and distress and (b) bidirectional influences of distress and sleep quality. Healthy pregnant adolescents (n = 204) were recruited before or during the 2nd trimester. CM was assessed at enrollment; sleep quality and distress were assessed in the 2nd and 3rd trimesters. Hypotheses were tested using path analysis. Findings revealed that CM was associated with worse 2nd trimester sleep quality and distress (β = .19, p < .05 for sleep; β = .30, p < .001 for distress). Higher levels of 2nd trimester distress were associated with lower 3rd trimester sleep quality (β = .19, p < .05). Findings provide novel information about (a) associations from CM to prenatal mood and sleep in pregnant adolescents, and (b) sleep–distress directionality over the course of pregnancy. These results have implications for better understanding the ways in which CM potentially exerts influences later in life, and for targeting interventions to address physical and mental health during pregnancy.

Recent models of psychopathology suggest the presence of a general factor capturing the shared variance among all symptoms along with specific psychopathology factors (e.g., internalizing and externalizing). However, few studies have examined predictors that may serve as transdiagnostic risk factors for general psychopathology from early development. In the current study we examine, for the first time, whether observed and parent-reported infant temperament dimensions prospectively predict general psychopathology as well as specific psychopathology dimensions (e.g., internalizing and externalizing) across childhood. In a longitudinal cohort (N = 291), temperament dimensions were assessed at 4 months of age. Psychopathology symptoms were assessed at 7, 9, and 12 years of age. A bifactor model was used to estimate general, internalizing, and externalizing psychopathology factors. Across behavioral observations and parent-reports, higher motor activity in infancy significantly predicted greater general psychopathology in mid to late childhood. Moreover, low positive affect was predictive of the internalizing-specific factor. Other temperament dimensions were not related with any of the psychopathology factors after accounting for the general psychopathology factor. The results of this study suggest that infant motor activity may act as an early indicator of transdiagnostic risk. Our findings inform the etiology of general psychopathology and have implications for the early identification for children at risk for psychopathology.

Here we evaluate whether infant difficult temperament (6 months) functions as a vulnerability or more general plasticity factor when investigating effects of early-childhood parenting (8–42 months) on both positive and negative early-adolescent socioemotional development (age 8–11 years). Using data from the Avon Longitudinal Study of Parents and Children (ALSPAC, N = 14,541) and a re-parameterized model-testing approach to distinguish alternative person × environment conceptual models, results indicated that temperament × parenting interacted in predicting externalizing (i.e., hyperactivity, conduct problems), but not other behavior (i.e., emotional symptoms, peer problems), in a (weak) differential susceptibility manner. While more and less supportive parenting predicted, respectively, fewer and more behavior problems, it did so more strongly for children who were more difficult as infants.

Individual differences in two inhibitory temperament systems have been implicated as key in the development of early disruptive behaviors. The reactive inhibition system, behavioral inhibition (BI) entails fearfulness, shyness, timidity, and caution. The active inhibition system, or effortful control (EC) entails a capacity to deliberately suppress, modify, or regulate a predominant behavior. Lower scores in each system have been associated with more disruptive behaviors. We examined how the two systems interact, and whether one can alleviate or exacerbate risks due to the other. In two community samples (Study 1, N = 112, ages 2.5 to 4, and Study 2, N = 102, ages 2 to 6.5), we assessed early BI and EC, and future disruptive behaviors (observed disregard for rules in Study 1 and parent-rated externalizing problems in Study 2). Robustly replicated interactions revealed that for children with low BI (relatively fearless), better EC was associated with less disruptive behavior; for children with low EC, more BI was associated with less disruptive behavior. This research extends the investigation of Temperament × Temperament interactions in developmental psychology and psychopathology, and it suggests that reactive and active inhibition systems may play mutually compensatory roles. Those effects emerged after age 2.

The present study examined the effect of early life stress (ELS) on the glucocorticoid receptor gene (NR3C1) methylation, the associations between NR3C1 methylation and behavior problems, and the effect of the program Parents as Teachers (PAT) on NR3C1 methylation. Participants included 132 children, 72 assigned to the PAT intervention group and 60 to the PAT control group. Children were aged 3 years, and were living in psychosocially at-risk families. We assessed NR3C1 methylation of the NGFI-A binding regions of exon 1F via sodium bisulfite sequencing from saliva DNA. Results indicated that (a) children living in families receiving PAT had decreased methylation at one single cytosine–guanine dinucleotides (CpG) site; (b) current maternal depressive symptoms and parental disagreement were predictive of increased methylation of mean NGFI-A and three single CpG sites; and (c) increased methylation of mean NGFI-A and one single CpG site was significantly associated with increased internalizing and externalizing symptoms. In addition, mean NGFI-A was a mediator of the association between parental disagreement and a child's affective problems. These results suggest that PAT may contribute to preventing NR3C1 methylation in preschool children living in psychosocially at-risk situations, and confirm previous findings on the associations between ELS, NR3C1 methylation, and behavior problems.

Difficult infants are commonly considered at risk for maladaptive developmental cascades, but evidence is mixed, prompting efforts to elucidate moderators of effects of difficulty. We examined features of parents’ representations of their infants – adaptive (appropriate mind-mindedness, MM) and dysfunctional (low reflective functioning, RF, hostile attributions) – as potential moderators. In Family Study (N = 102), we tested parents’ appropriate MM comments to their infants as moderating a path from infants’ observed difficulty (negative affect, unresponsiveness) to parents’ observed power assertion at ages 2–4.5 to children's observed and parent-rated (dis)regard for conduct rules at age 5.5. In father–child relationships, MM moderated that path: for fathers with low MM, the infants’ increasing difficulty was associated with fathers’ greater power assertion, which in turn was associated with children's more disregard for rules. The path was absent for fathers with average or high MM. In Children and Parents Study (N = 200), dysfunctional representations (low RF, hostile attributions) moderated the link between child objective difficulty, observed as anger in laboratory episodes, and difficulty as described by the parent. Reports of mothers with highly dysfunctional representations were unrelated to children's observed anger. Reports of mothers with average or low dysfunctional representations aligned with laboratory observations.

To identify sources of phenotypic heterogeneity in attention-deficit/hyperactivity disorder (ADHD) accounting for diversity in developmental/ pathogenic pathways, we examined, in a large sample of youth (N = 354), (a) associations between observed temperamental emotionality at age 3, an electrocortical index (i.e., reward positivity [RewP]) of initial responsiveness to reward at age 9, and ADHD symptoms at age 12, and (b) whether the association between emotionality and ADHD symptoms is mediated by initial responsiveness to reward. Bivariate analyses indicated greater positive emotionality (PE) was associated with enhanced RewP, lower age-9ADHD and lower age-12 inattention (IA). Negative emotionality (NE) was not associated with RewP or ADHD. Mediation analyses revealed the association between PE and hyperactivity/impulsivity (H/I) was mediated by RewP; enhanced RewP was associated with greater H/I. Greater PE was associated with enhanced RewP at a trend level. These effects held accounting for age-9 ADHD, age-12 IA and age-12 oppositional defiant and conduct disorder symptoms. As such, preschool emotionality is associated with adolescent ADHD-H/I symptoms through late childhood initial responsiveness to reward. These relations indicate that individual differences in emotionality and reward responsiveness may be informative for personalizing ADHD interventions.

While previous studies suggest that both genetic and environmental factors play an important role in the development of autism-related traits, little is known about potential biological mechanisms underlying these associations. Using data from the Avon Longitudinal Study of Parents and Children (ALSPAC), we examined prospective associations between DNA methylation (DNAm: nbirth = 804, nage 7 = 877) and trajectories of social communication deficits at age 8–17 years. Methylomic variation at three loci across the genome (false discovery rate = 0.048) differentiated children following high (n = 80) versus low (n = 724) trajectories of social communication deficits. This differential DNAm was specific to the neonatal period and not observed at 7 years of age. Associations between DNAm and trajectory membership remained robust after controlling for co-occurring mental health problems (i.e., hyperactivity/inattention, conduct problems). The three loci identified at birth were not replicated in the Generation R Study. However, to the best of our knowledge, ALSPAC is the only study to date that is prospective enough to examine DNAm in relation to longitudinal trajectories of social communication deficits from childhood to adolescence. Although the present findings might point to potentially novel sites that differentiate between a high versus low trajectory of social communication deficits, the results should be considered tentative until further replicated.

DNA methylation of the elongation of very long chain fatty acids protein 2 (ELOVL2) was suggested as a biomarker of biological aging, while childhood maltreatment (CM) has been associated with accelerated biological aging. We investigated the association of age and CM experiences with ELOVL2 methylation in peripheral blood mononuclear cells (PBMC). Furthermore, we investigated ELOVL2 methylation in the umbilical cord blood mononuclear cells (UBMC) of newborns of mothers with and without CM. PBMC and UBMC were isolated from 113 mother–newborn dyads and genomic DNA was extracted. Mothers with and without CM experiences were recruited directly postpartum. Mass array spectrometry and pyrosequencing were used for methylation analyses of ELOVL2 intron 1, and exon 1 and 5′ end, respectively. ELOVL2 5′ end and intron 1 methylation increased with higher age but were not associated with CM experiences. On the contrary, overall ELOVL2 exon 1 methylation increased with higher CM, but these changes were minimal and did not increase with age. Maternal CM experiences and neonatal methylation of ELOVL2 intron 1 or exon 1 were not significantly correlated. Our study suggests region-specific effects of chronological age and experienced CM on ELOVL2 methylation and shows that the epigenetic biomarker for age within the ELOVL2 gene does not show accelerated biological aging years after CM exposure.

This study evaluated whether children with higher adverse childhood experiences (ACE) scores had alterations in immune cell gene expression profiles. RNA sequencing was conducted on dried blood spot samples from 37 generally healthy English-speaking children (age 5–11) who were recruited from well-child visits at a university-affiliated pediatric practice. The Whole Child Assessment was used to assess ACE exposure. Primary analyses examined an a priori-specified composite of 19 pro-inflammatory gene transcripts. Secondary analyses examined a 34-gene composite assessing Type I interferon response, and used Transcript Origin Analyses to identify cellular mechanisms. After controlling for age, body mass index percentile, sex, race/ethnicity, current insurance status, and household smoking exposure, pro-inflammatory gene expression was elevated by 0.094 log2 RNA expression units with each Child-ACE total score point (p = .019). Type I interferon gene expression was similarly upregulated (0.103; p = .008). Transcript origin analyses implicated CD8+ T cell as the primary sources of gene transcripts upregulated, and nonclassical (CD16+) monocytes as sources of downregulated transcripts. These preliminary analyses suggest that parent-reported ACE exposures are associated with increased expression of both inflammatory and interferon gene transcripts in children's circulating blood cells.

The aim of this project was to evaluate the relationship of matrix metalloproteinase-9 (MMP-9) genetic variation and its serum concentration with autism spectrum disorder (ASD). One hundred ASD and 120 controls were enrolled in this study. Genomic DNA was extracted from blood and MMP-9 polymorphism was determined by polymerase chain reaction restriction fragment length polymorphism and serum levels were measured by enzyme-linked immunosorbent assay. The frequencies of CC, CT, and TT genotypes were 72%, 26%, and 2% in controls and 31%, 57%, and 12% in ASD, respectively. The frequencies of C and T alleles in ASD were 59.5% and 40.5%, and controls were 86% and 14%, respectively. There is a significant increase in serum MMP-9 levels in ASD as compared to controls. We have also shown that TT genotype is significantly associated with increase serum MMP-9 levels in patients (TT, CT, and CC serum levels were 91.77 ± 10.53, 70.66 ± 7.21, and 38.66 ± 5.52 and in controls were 55.55 ± 11.39, 42.66 ± 7.85, and 30.55 ± 6.34 ng/ml, respectively). It is concluded that there is a significant association between rs3918242 MMP-9 polymorphism and its serum concentration with autism. We also suggest that TT genotype is associated with increased MMP9 expression and may be a risk factor for ASD.

Researchers face an important challenge when assessing peer victimization in children, since self-reports are often discrepant with parent-reports. A latent class analysis identified patterns of response to items assessing peer victimization, which were either divergent or convergent between the parent and the child. Classes were then compared on the child sexual abuse status and on various behavioral and social outcomes. Participants were 720 school-aged child victims of sexual abuse and a comparison group of 173 nonvictims and their caregivers. We identified two discordant subgroups (self-identified and parent-identified) and two concordant groups (nonvictims and concordant victims of peer victimization). Compared to children of the comparison group, sexually abused children were five times more likely to be identified as targets of peer victimization solely by their parent than the contrary. Sexually abused children with concordant reports of peer victimization showed the poorest adjustment on all studied outcomes assessed 6 months later. Children who discounted experiencing peer victimization while their parent reported it were also at risk of maladjustment. Results underscore the importance of supplementing self-reports with other available sources of information, especially in young and vulnerable populations who may be inclined to discount their victimization experiences.

Children differ in their response to environmental exposures, with some being more sensitive to contextual factors than others. According to theory, such variability is the result of individual differences in neurobiological sensitivity to environmental features, with some individuals generally more affected by both negative and/or positive experiences. In this exploratory study we tested whether left and right amygdala and hippocampus volumes (corrected for total brain size) account for individual differences in response to environmental influences in a sample of 62 boys. Cumulative general environmental quality, ranging from low to high, was measured across the first 9 years and child behavior was reported by teachers when boys were 12–13 years old. According to analyses, only the left amygdala volume – not any of the other brain volumes – emerged as an important brain region for sensitivity to positive environmental aspects. Boys with a larger left amygdala benefited significantly more from higher environmental quality than boys with a smaller left amygdala whilst not being more vulnerable to lower quality. Besides providing preliminary evidence for differences in environmental sensitivity due to brain structure, the results also point to the left amygdala as having a specific role regarding the response to environmental influences.

The current study assessed whether the proportion of childhood (age 0–9 years) in poverty altered the developmental trajectories (ages 9–24) of multimethodological indicators of psychological well-being. In addition, we tested whether exposure to cumulative risk over time mediated the association between poverty exposure and psychological well-being. Measures of psychological well-being included internalizing and externalizing symptoms, a behavioral index of learned helplessness (task persistence), and chronic physiological stress (allostatic load). Exposure to poverty during childhood predicted the trajectory of each development outcome: individuals with more poverty exposure during childhood showed (a) relatively high levels of internalizing symptoms that diminished more slowly with maturation, (b) relatively high levels of externalizing symptoms that increased faster over time, (c) less task persistence indicative of greater learned helplessness, and (d) higher levels of chronic physiological stress which increased faster over time relative to persons with less childhood poverty exposure. Trajectories of cumulative risk exposure from physical and psychosocial surroundings from 9–24 years accounted for the association between childhood poverty and the growth curves of internalizing and externalizing symptoms but not for learned helplessness or chronic physiological stress. Additional sensitivity analyses indicate that early childhood disadvantage is particularly problematic for each outcome, except for internalizing symptoms which seem sensitive to the combination of early and lifetime poverty exposure. We also explored whether domains of cumulative risk as well as two alternatives, maternal sensitivity or family cohesion, functioned as mediators. Little evidence emerged for any of these alternative mediating constructs.

The present study examined the developmental value of parsing different forms of children's risky involvement in interparental conflict as predictors of children's subsequent psychological adjustment. Participants included a diverse sample of 243 preschool children (Mage = 4.6 years) and their mothers across two measurement occasions spaced 2 years apart. Three forms of risky involvement (i.e., cautious, caregiving, and coercive) were identified using maternal narratives describing children's emotional and behavioral reactivity during and immediately following interparental conflict. Utilizing a multimethod, multi-informant design, findings revealed that each form of involvement prospectively predicted unique configurations of children's developmental outcomes. Greater coercive involvement was associated with higher levels of externalizing problems, callous and unemotional traits, and extraversion. Higher levels of caregiving involvement were linked with greater separation anxiety. Finally, cautious involvement predicted more separation anxiety and social withdrawal.

Impaired facial emotion recognition is a transdiagnostic risk factor for a range of psychiatric disorders. Childhood behavioral difficulties and parental emotional environment have been independently associated with impaired emotion recognition; however, no study has examined the contribution of these factors in conjunction. We measured recognition of negative (sad, fear, anger), neutral, and happy facial expressions in 135 children aged 5–7 years referred by their teachers for behavioral problems. Parental emotional environment was assessed for parental expressed emotion (EE) – characterized by negative comments, reduced positive comments, low warmth, and negativity towards their child – using the 5-minute speech sample. Child behavioral problems were measured using the teacher-informant Strengths and Difficulties Questionnaire (SDQ). Child behavioral problems and parental EE were independently associated with impaired recognition of negative facial expressions specifically. An interactive effect revealed that the combination of both factors was associated with the greatest risk for impaired recognition of negative faces, and in particular sad facial expressions. No relationships emerged for the identification of happy facial expressions. This study furthers our understanding of multidimensional processes associated with the development of facial emotion recognition and supports the importance of early interventions that target this domain.

Despite broad evidence suggesting that adversity-exposed youth experience an impaired ability to recognize emotion in others, the underlying biological mechanisms remains elusive. This study uses a multimethod approach to target the neurological substrates of this phenomenon in a well-phenotyped sample of youth meeting diagnostic criteria for posttraumatic stress disorder (PTSD). Twenty-one PTSD-afflicted youth and 23 typically developing (TD) controls completed clinical interview schedules, an emotion recognition task with eye-tracking, and an implicit emotion processing task during functional magnetic resonance imaging )fMRI). PTSD was associated with decreased accuracy in identification of angry, disgust, and neutral faces as compared to TD youth. Of note, these impairments occurred despite the normal deployment of visual attention in youth with PTSD relative to TD youth. Correlation with a related fMRI task revealed a group by accuracy interaction for amygdala–hippocampus functional connectivity (FC) for angry expressions, where TD youth showed a positive relationship between anger accuracy and amygdala–hippocampus FC; this relationship was reversed in youth with PTSD. These findings are a novel characterization of impaired threat recognition within a well-phenotyped population of severe pediatric PTSD. Further, the differential amygdala–hippocampus FC identified in youth with PTSD may imply aberrant efficiency of emotional contextualization circuits.

Childhood adversity and anxiety have been associated with increased risk for internalizing disorders later in life and with a range of brain structural abnormalities. However, few studies have examined the link between harsh parenting practices and brain anatomy, outside of severe maltreatment or psychopathology. Moreover, to our knowledge, there has been no research on parenting and subclinical anxiety symptoms which remain persistent over time during childhood (i.e., between 2.5 and 9 years old). Here, we examined data in 94 youth, divided into four cells based on their levels of coercive parenting (high / low) and of anxiety (high / low) between 2.5 and 9 years old. Anatomical images were analyzed using voxel-based morphometry (VBM) and FreeSurfer. Smaller gray matter volumes in the prefrontal cortex regions and in the amygdala were observed in youth with high versus low levels of harsh parenting over time. In addition, we observed significant interaction effects between parenting practices and subclinical anxiety symptoms in rostral anterior cingulate cortical thickness and in amygdala volume. These youth should be followed further in time to identify which youth will or will not go on to develop an anxiety disorder, and to understand factors associated with the development of sustained anxiety psychopathology.

Studies have long observed the bidirectional nature of mother–infant relationships. While behavioral studies have shown that mothers high in social avoidance tendencies can influence the development of these traits in their offspring, the neurophysiological mechanisms underlying this phenomenon, and the role that the infants play, are not well understood. Here we acquired frontal electroencephalogram asymmetry (FA) data simultaneously in 40 mother–infant dyads (Mage mother = 31.6 years; Mage infant = 9 months). Using an actor–partner interdependence model, we examined whether mother (or infant) resting-state FA predicted infant (or mother) FA during two subsequent emotion-eliciting conditions (happy and fear). Maternal social approach versus avoidance traits were assessed as moderators to examine the impact of maternal characteristics on these mother–infant FA relations. In dyads led by mothers with high social avoidance/low social approach characteristics, maternal resting-state FA predicted infant FA during both emotion-eliciting conditions. We did not observe any effects of infant FA on mothers. Therefore, we speculate that individual differences in FA patterns might be a putative brain mechanism through which socially avoidant mothers transfer affective/behavioral information to their infants.