Exposure to early life adversity (ELA) is associated with increased rates of psychopathology and poor physical health. The present study builds on foundational work by Megan Gunnar identifying how ELA results in poor long-term outcomes through alterations in the stress response system, leading to major disruptions in emotional and behavioral regulation. Specifically, the present study tested the direct effects of ELA against the role of parent socialization to shed light on the mechanisms by which ELA leads to emotion regulation deficits. Children ages 4–7 years (N = 64) completed interviews about their experiences of deprivation and threat, a fear conditioning and extinction paradigm, and an IQ test. Parents of the children completed questionnaires regarding their own emotion regulation difficulties and psychopathology, their children's emotion regulation, and child exposure to adversity. At the bivariate level, greater exposure to threat and parental difficulties with emotion regulation were associated with poorer emotion regulation in children, assessed both via parental report and physiologically. In models where parental difficulties with emotion regulation, threat, and deprivation were introduced simultaneously, regression results indicated that parental difficulties with emotion regulation, but not deprivation or threat, continued to predict children's emotion regulation abilities. These results suggest that parental socialization of emotion is a robust predictor of emotion regulation tendencies in children exposed to early adversity.

We examined maternal depression and maternal sensitivity as mediators of the association between maternal childhood adversity and her child's temperament in 239 mother–child dyads from a longitudinal, birth cohort study. We used an integrated measure of maternal childhood adversity that included the Childhood Trauma Questionnaire and the Parental Bonding Index. Maternal depression was assessed with the Edinburgh Postnatal Depression Scale at 6 months postpartum. Maternal sensitivity was assessed with the Ainsworth maternal sensitivity scales at 6 months. A measure of “negative emotionality/behavioral dysregulation” was derived from the Early Childhood Behaviour Questionnaire administered at 36 months. Bootstrapping-based mediation analyses revealed that maternal depression mediated the effect of maternal childhood adversity on offspring negative emotionality/behavioral dysregulation (95% confidence interval [0.026, 0.144]). We also found a serial, indirect effect of maternal childhood adversity on child negative emotionality/behavioral mediated first by maternal depression and then by maternal sensitivity (95% confidence interval [0.031, 0.156]). Results suggest the intergenerational transmission of the effects of maternal childhood adversity to the offspring occurs through a two-step, serial pathway, involving maternal depression and maternal sensitivity.

Self-directed speech is considered an important developmental achievement as a self-regulatory mediator of thinking and behavior. Atypical self-directed speech is often implicated in the self-regulatory challenges characteristic of children with neurodevelopmental disorders. A growing body of evidence provides snapshots across age-levels and diagnoses, often presenting conflicting results. This systematic review is undertaken to impose clarity on the nature, extent, and self-regulatory implications of self-directed speech interruption in children with developmental language disorder (DLD), autism spectrum disorder (ASD), and attention deficit hyperactivity disorder (ADHD).

A rigorous search process of relevant databases (i.e., PsychInfo, PubMed, CINAHL, ERIC) uncovered 19 relevant peer-reviewed articles that investigate self-directed speech in children with neurodevelopmental disorders. Consistent across the research, children with DLD, ASD, and ADHD present with differential development and use of self-directed speech.

In its synthesis of findings, this systematic review clearly explicates the differential ontogenesis of self-directed speech in neurodevelopmental disorders and interprets the self-regulatory implications for children with DLD, ASD, and ADHD. Furthermore, the review spotlights important future research directions to better understand the mechanistic relationship between self-directed speech and self-regulation.

Cognitive strategies that adolescents use to cope with negative emotions might show distinct profiles of cognitive emotion regulation strategies, which could be differentially associated with depressive symptoms. In total, 411 Dutch adolescents who had experienced at least one stressful life event that required some coping strategy participated in this study, including 334 nonclinical and 77 clinically depressed adolescents (12–21 years). A person-centered approach with Latent Profile Analysis was used to identify underlying profiles of cognitive emotion regulation based on the adolescents’ reports of their use of cognitive emotion regulation strategies when they were confronted with stressful life events. Nine different strategies, five adaptive and four maladaptive, were used as indicators. Four profiles with distinct features were found in the nonclinical sample, as well as in the combined sample of nonclinical and clinically depressed adolescents: Low Regulators, High Regulators, Maladaptive Regulators, and Adaptive Regulators. In both samples, the High Regulators profile was most commonly used, followed by the Adaptive, Maladaptive, and Low Regulators profile. Maladaptive Regulators endorsed higher levels of depressive symptoms relative to Low, High, and Adaptive Regulators. The findings underscore the utility of using a person-centered approach in order to identify patterns of cognitive emotion regulation deficits in psychopathology.

Although child maltreatment is a major public health concern, which adversely affects psychological and physical development, we know relatively little concerning psychophysiological and personality factors that may modify risk in children exposed to maltreatment. Using a three-wave, short-term prospective design, we examined the influence of individual differences in two disparate psychophysiological measures of risk (i.e., resting frontal brain electrical activity and respiratory sinus arrhythmia) on the trajectories of extraversion and neuroticism in a sample of female adolescents (N = 55; M age = 14.02 years) exposed to child maltreatment. Adolescents exposed to child maltreatment with relatively higher left frontal absolute alpha power (i.e., lower brain activity) at rest exhibited increasing trajectories of extraversion, and adolescents exposed to child maltreatment with relatively lower respiratory sinus arrhythmia at rest displayed increasing trajectories of neuroticism over 1 year. Individual differences in psychophysiological measures indexing resting central and peripheral nervous system activity may therefore differentially influence personality characteristics in adolescent females exposed to child maltreatment.

Sleep disturbance is a symptom of and a well-known risk factor for depression. Further, atypical functioning of the HPA axis has been linked to the pathogenesis of depression. The purpose of this study was to examine the role of adolescent HPA axis functioning in the link between adolescent sleep problems and later depressive symptoms. Methods: A sample of 157 17–18 year old adolescents (61.8% female) completed the Pittsburgh Sleep Quality Inventory (PSQI) and provided salivary cortisol samples throughout the day for three consecutive days. Two years later, adolescents reported their depressive symptoms via the Center for Epidemiological Studies Depression Scale (CES-D). Results: Individuals (age 17–18) with greater sleep disturbance reported greater depressive symptoms two years later (age 19–20). This association occurred through the indirect effect of sleep disturbance on the cortisol awakening response (CAR) (indirect effect = 0.14, 95%CI [.02 -.39]). Conclusions: One pathway through which sleep problems may lead to depressive symptoms is by up-regulating components of the body’s physiological stress response system that can be measured through the cortisol awakening response. Behavioral interventions that target sleep disturbance in adolescents may mitigate this neurobiological pathway to depression during this high-risk developmental phase.

Parents serve important functions in regulating children's responses to stress and challenge. However, the parental characteristics that modulate the effectiveness of parents as stress buffers remain to be fully characterized. To address this gap, this study examined parental characteristics and behaviors that may explain variation in parents’ ability to buffer cortisol responses to acute stress of 180 children (ages 9–11 years old, M = 9.9 years, SD = .58). Children were randomly assigned to either participate in a public speaking task, the Trier Social Stress Test – modified for children (TSST-M) or a control condition. Children in the TSST-M condition were randomly assigned to prepare for the public speaking task either with their parent (N = 59) or alone (N = 60), whereas 61 children were assigned to the control condition (no TSST-M). We found that parental education moderated the effect of condition on children's responses to acute stress. Children whose parents had lower levels of education exhibited reduced cortisol responses in the parent condition compared to the alone condition, showing a buffered pattern of reactivity. In contrast, children of parents with high levels of education displayed higher cortisol reactivity in the parent condition compared to the alone and control conditions. Parental education was also positively associated with higher levels of state anxiety within the parent condition. These results suggest that highly educated parents may emphasize performance over comfort, amplifying their children's state anxiety and cortisol responses to a public performance.

Social withdrawal and social anxiety are believed to have a bidirectional influence on one another, but it is unknown if their relationship is bidirectional, especially within person, and if peer experiences influence this relationship. We investigated temporal sequencing and the strength of effects between social withdrawal and social anxiety, and the roles of peer victimization and acceptance in the pathways. Participants were 2,772 adolescents from the population-based and clinically referred cohorts of the Tracking Adolescents' Individual Lives Survey. Self- and parent-reported withdrawal, and self-reported social anxiety, peer victimization, and perceived peer acceptance were assessed at 11, 13, and 16 years. Random-intercept cross-lagged panel models were used to investigate within-person associations between these variables. There was no feedback loop between withdrawal and social anxiety. Social withdrawal did not predict social anxiety at any age. Social anxiety at 11 years predicted increased self-reported withdrawal at 13 years. Negative peer experiences predicted increased self- and parent-reported withdrawal at 13 years and increased parent-reported withdrawal at 16 years. In turn, self-reported withdrawal at 13 years predicted negative peer experiences at 16 years. In conclusion, adolescents became more withdrawn when they became more socially anxious or experienced greater peer problems, and increasing withdrawal predicted greater victimization and lower acceptance.

Emotion regulation dysfunction is characteristic of psychotic disorders, but little is known about how the use of specific types of emotion regulation strategies differs across phases of psychotic illness. This information is vital for understanding factors contributing to psychosis vulnerability states and developing targeted treatments. Three studies were conducted to examine emotion regulation across phases of psychosis, which included (a) adolescent community members with psychotic-like experiences (PLEs; n = 262) and adolescents without PLEs (n = 1,226); (b) adolescents who met clinical high-risk criteria for a prodromal syndrome (n = 29) and healthy controls (n = 29); and (c) outpatients diagnosed with schizophrenia or schizoaffective disorder (SZ; n = 61) and healthy controls (n = 67). In each study, participants completed the Emotion Regulation Questionnaire and measures of psychiatric symptoms and functional outcome. The three psychosis groups did not differ from each other in reported use of suppression; however, there was evidence for a vulnerability-related, dose-dependent decrease in reappraisal. Across each sample, a lower use of reappraisal was associated with poorer clinical outcomes. Findings indicate that emotion regulation abnormalities occur across a continuum of psychosis vulnerability and represent important targets for intervention.

The current study examined whether social status and social integration, two related but distinct indicators of an adolescent's standing within a peer network, mediate the association between risky symptoms (depressive symptoms and deviant behavior) and substance use across adolescence. The sample of 6,776 adolescents participated in up to seven waves of data collection spanning 6th to 12th grades. Scores indexing social status and integration were derived from a social network analysis of six schools and subsequent psychometric modeling. Results of latent growth models showed that social integration and status mediated the relation between risky symptoms and substance use and that risky symptoms mediated the relation between social standing and substance use during the high school transition. Before this transition, pathways involving deviant behavior led to high social integration and status and in turn to substance use. After this transition, both deviant behavior and depressive symptoms led to low social integration and status and in turn greater substance use. These findings suggest that the high school transition is a risky time for substance use related to the interplay of increases in depressive symptoms and deviant behavior on the one hand and decreases in social status and integration on the other.

There is an extensive literature describing the detrimental effects of adverse childhood experiences (ACE; e.g., abuse, neglect, and household dysfunction) on physical and mental health. However, few large-scale studies have explored these associations longitudinally in urban minority cohorts or assessed links to broader measures of well-being such as educational attainment, occupation, and crime. Although adversity and resilience have long been of interest in developmental psychology, protective and promotive factors have been understudied in the ACE literature. This paper investigates the psychosocial processes through which ACEs contribute to outcomes, in addition to exploring ways to promote resilience to ACEs in vulnerable populations. Follow-up data were analyzed for 87% of the original 1,539 participants in the Chicago Longitudinal Study (N = 1,341), a prospective investigation of the impact of an Early Childhood Education program and early experiences on life-course well-being. Findings suggest that ACEs impact well-being in low-socioeconomic status participants above and beyond the effects of demographic risk and poverty, and point to possible mechanisms of transmission of ACE effects. Results also identify key areas across the ecological system that may promote resilience to ACEs, and speak to the need to continue to support underserved communities in active ways.

The parent-child relationship undergoes substantial reorganization over the transition to adolescence. Navigating this change is a challenge for parents because teens desire more behavioral autonomy as well as input in decision-making processes. Although it has been demonstrated that changes in parental socialization approaches facilitates adolescent adjustment, very little work has been devoted to understanding the underlying mechanisms supporting parents’ abilities to adjust caregiving during this period. Guided by self-regulation models of parenting, the present study examined how parental physiological and cognitive regulatory capacities were associated with hostile and insensitive parent conflict behavior over time. From a process-oriented perspective, we tested the explanatory role of parents’ dysfunctional child-oriented attributions in this association. A sample of 193 fathers, mothers, and their early adolescent (ages 12–14) participated in laboratory-based research assessments spaced approximately 1 year apart. Parental physiological regulation was measured using square root of the mean of successive differences during a conflict task; cognitive regulation was indicated by set-shifting capacity. Results showed that parental difficulties in vagal regulation during parent-adolescent conflict were associated with increased hostile conflict behavior over time; however, greater set-shifting capacity moderated this association for fathers only. In turn, father's dysfunctional attributions regarding adolescent behavior mediated the moderating effect. The results highlight how models of self-regulation and social cognition may explain the determinants of hostile parenting with differential implications for fathers during adolescence.

Impaired cognitive functioning constitutes an important symptom of major depressive disorder (MDD), potentially associated with elevated cortisol levels. Adverse childhood experiences (ACE) enhance the risk for MDD and can contribute to disturbances in the stress systems, including cortisol and cognitive functions. In healthy participants, cortisol administration as well as acute stress can affect cognitive performance. In the current study, we tested cognitive performance in MDD patients with (N = 32) and without (N = 52) ACE and healthy participants with (N = 22) and without (N = 37) ACE after psychosocial stress induction (Trier Social Stress Test, TSST) and a control condition (Placebo-TSST). MDD predicted lower performance in verbal learning and both selective and sustained attention, while ACE predicted lower performance in psychomotoric speed and working memory. There were no interaction effects of MDD and ACE. After stress, MDD patients were more likely to show lower performance in working memory as well as in selective and sustained attention compared with participants without MDD. Individuals with ACE were more likely to show lower performance in verbal memory after stress compared with individuals without ACE. Our results indicate negative effects of MDD and ACE on distinct cognitive domains. Furthermore, MDD and/or ACE seem to enhance susceptibility for stress-related cognitive impairments.

Institutionally deprived young children often display distinctive patterns of attachment, classified as insecure/other (INS/OTH), with their adoptive parents. The associations between INS/OTH and developmental trajectories of mental health and neurodevelopmental symptoms were examined. Age 4 attachment status was determined for 97 Romanian adoptees exposed to up to 24 months of deprivation in Romanian orphanages and 49 nondeprived UK adoptees. Autism, inattention/overactivity and disinhibited-social-engagement symptoms, emotional problems, and IQ were measured at 4, 6, 11, and 15 years and in young adulthood. Romanian adoptees with over 6 months deprivation (Rom>6) were more often classified as INS/OTH than UK and Romanian adoptees with less than 6 months deprivation combined. INS/OTH was associated with cognitive impairment at age 4 years. The interaction between deprivation, attachment status, and age for autism spectrum disorder assessment was significant, with greater symptom persistence in Rom>6 INS/OTH(+) than other groups. This effect was reduced when IQ at age 4 was controlled for. Age 4 INS/OTH in Rom>6 was associated with worse autism spectrum disorder outcomes up to two decades later. Its association with cognitive impairment at age 4 is consistent with INS/OTH being an early marker of this negative developmental trajectory, rather than its cause.

Maternal antenatal depression strongly influences child mental health but with considerable inter-individual variation that is, in part, linked to genotype. The challenge is to effectively capture the genotypic influence. We outline a novel approach to describe genomic susceptibility to maternal antenatal depression focusing on child emotional/behavioral difficulties. Two cohorts provided measures of maternal depression, child genetic variation, and child mental health symptoms. We constructed a conventional polygenic risk score (PRS) for attention-deficit/hyperactivity disorder (ADHD) (PRSADHD) that significantly moderated the association between maternal antenatal depression and internalizing problems at 60 months (p = 2.94 × 10−4, R2 = .18). We then constructed an interaction PRS (xPRS) based on a subset of those single nucleotide polymorphisms from the PRSADHD that most accounted for the moderation of the association between maternal antenatal depression and child outcome. The interaction between maternal antenatal depression and this xPRS accounted for a larger proportion of the variance in child emotional/behavioral problems than models based on any PRSADHD (p = 5.50 × 10−9, R2 = .27), with similar findings in the replication cohort. The xPRS was significantly enriched for genes involved in neuronal development and synaptic function. Our study illustrates a novel approach to the study of genotypic moderation on the impact of maternal antenatal depression on child mental health and highlights the utility of the xPRS approach. These findings advance our understanding of individual differences in the developmental origins of mental health.

There is evidence that individuals with Williams syndrome (WS) show an attention bias toward positive social-perceptual (happy) faces. Research has not yet considered whether this attention bias extends beyond social-perceptual stimuli to perceptually neutral stimuli that are paired with positive (trustworthy) biographical information. Fourteen participants with WS (mean age = 21 years, 1 month) learned to associate perceptually neutral faces with trustworthy (positive), neutral, or untrustworthy (negative) biographical information, before completing a dot-probe task where the same biographical faces were presented. The performance of the WS group was compared to two typically developing control groups, individually matched to the WS individuals on chronological age and mental age, respectively. No between-group bias toward untrustworthy characters was observed. The WS group displayed a selective attention bias toward trustworthy characters compared to both control groups (who did not show such a bias). Results support previous findings that indicate WS individuals show a preference for positive social-perceptual stimuli (happy faces) at the neurological, physiological, and attentional levels. The current findings extend this work to include a “top-down” positive bias. The implications of a positive bias that extends beyond social-perceptual stimuli (or “bottom-up” processes) in this syndrome are discussed.

This is the first review to rigorously examine the mediating role of cognitive factors in the relationship between childhood trauma and subsequent adult psychopathology, and highlight areas for future research. A database search (Child Development & Adolescent Studies, ERIC, Global Health, PsycARTICLES, and PsycINFO) was conducted to identify empirical studies on cognitive factors, explaining the relationship between different types of adverse childhood experiences and adult psychopathology across clinical and nonclinical populations. A narrative synthesis and appraisal of the methodological quality of the studies was conducted. Ninety-eight mediation studies were identified, comprising 4,137 clinical and 28,228 nonclinical participants. Despite great variation in methodological quality of the studies, our narrative synthesis suggests that cognitive factors mediate the relationship between early trauma and later psychopathology. This finding is consistent across different measures of traumatic experiences, psychopathology, and cognitive mediators. Cognitive mediators represent potentially valuable intervention targets for (non)clinical patients who have experienced childhood adversity. Future studies are needed to (a) establish longitudinal causal connections, and (b) assess the effect of interventions that specifically target cognitive change in patients with different levels and types of pathology.

The Young Adolescent Project (YAP) is an ongoing longitudinal study investigating the effects of abuse and neglect on adolescent development. It is a multidisciplinary study guided by a developmental, ecological perspective, and designed to consider the physical, social, and psychological effects of childhood maltreatment through the transition from childhood to adolescence. Four waves of data collection have been completed, ranging from early (Mean age = 10.95) to late adolescence (Mean age = 18.24). Members of the maltreated group (n = 303) were selected from new cases that had been opened by the Department of Child and Family Services, whereas the comparison group (n = 151) were not involved with child welfare but lived in the same neighborhoods as the maltreated group. The study assessed a wide variety of domains including physical development (e.g., height, weight, body mass, pubertal development); physiological reactivity (e.g., cortisol); cognitive abilities; mental health (e.g., symptoms of depression, anxiety, trauma, and aggression); risk behavior (e.g., sexual activity, delinquency, or substance use); social development (e.g., self-esteem, competence, and social support); family environment; and exposure to community violence. Overall, our findings demonstrated the pervasive and persistent adverse effects of child maltreatment both within and across domains, but they also identified maltreated youth with positive functioning. Our hope is that this work will help move us toward identifying targets for intervention to cultivate resilience and positive adaptation after early maltreatment experiences.

We conducted signal detection analyses to test for curvilinear, U-shaped relations between early experiences of adversity and heightened physiological responses to challenge, as proposed by biological sensitivity to context theory. Based on analysis of an ethnically diverse sample of 338 kindergarten children (4–6 years old) and their families, we identified levels and types of adversity that, singly and interactively, predicted high (top 25%) and low (bottom 25%) rates of stress reactivity. The results offered support for the hypothesized U-shaped curve and conceptually replicated and extended the work of Ellis, Essex, and Boyce (2005). Across both sympathetic and adrenocortical systems, a disproportionate number of children growing up under conditions characterized by either low or high adversity (as indexed by restrictive parenting, family stress, and family economic condition) displayed heightened stress reactivity, compared with peers growing up under conditions of moderate adversity. Finally, as hypothesized by the adaptive calibration model, a disproportionate number of children who experienced exceptionally stressful family conditions displayed blunted cortisol reactivity to stress.

Stress associated with caring for a mentally ill spouse can adversely affect the health status of caregivers and their children. Adding to the stress of caregiving is the stigma often placed against spouses and children of people with mental illness. Contrary to mental illness, many physical disorders such as cancer may be less stigmatized (expect pulmonary cancer). In this study, we measured externalized and internalized stigma, as well as psychological (depressive symptoms and stressful life events) and physiological (basal salivary cortisol levels) markers of stress in 115 spouses and 154 children of parents suffering from major depressive disorder, cancer, or no illness (control group). The results show that spouses and children from families with parental depression present significantly more externalized stigma than spouses and children from families with parental cancer or no illness, although we find no group differences on internalized stigma. The analysis did not show a significant group difference either for spouses or their children on depressive symptomatology, although spouses from the parental depression group reported greater work/family stress. Finally, we found that although for both spouses children the awakening cortisol response was greater on weekdays than on weekend days, salivary cortisol levels did not differ between groups. Bayes factor calculated on the null result for cortisol levels was greater than 100, providing strong evidence for the null hypothesis H0. Altogether, these results suggest an impact of stigma toward mental health disorder on psychological markers of stress but no impact of stigma on physiological markers of stress. We suggest that these results may be due to the characteristics of the families who participated in the present study.