Cognitive stimulation as a mechanism linking socioeconomic status and neural function supporting working memory: a longitudinal fMRI study.

Childhood experiences of low socioeconomic status are associated with alterations in neural function in the frontoparietal network and ventral visual stream, which may drive differences in working memory. However, the specific features of low socioeconomic status environments that contribute to these disparities remain poorly understood. Here, we examined experiences of cognitive deprivation (i.e. decreased variety and complexity of experience), as opposed to experiences of threat (i.e. violence exposure), as a potential mechanism through which family income contributes to alterations in neural activation during working memory. As part of a longitudinal study, 148 youth between aged 10 and 13 years completed a visuospatial working memory fMRI task. Early childhood low income, chronicity of low income in early childhood, and current income-to-needs were associated with task-related activation in the ventral visual stream and frontoparietal network. The association of family income with decreased activation in the lateral occipital cortex and intraparietal sulcus during working memory was mediated by experiences of cognitive deprivation. Surprisingly, however, family income and deprivation were not significantly related to working memory performance, and only deprivation was associated with academic achievement in this sample. Taken together, these findings suggest that early life low income and associated cognitive deprivation are important factors in neural function supporting working memory.

Foster care leads to sustained cognitive gains following severe early deprivation.

This study examined longitudinal data from the Bucharest Early Intervention Project, a randomized controlled trial of foster care as an alternative to institutional care following exposure to severe psychosocial deprivation. We report data from 135 participants assessed in early adulthood (age 18 y). We find that 16 y after randomization occurred, those who had been randomized to high-quality foster care had significantly higher IQ scores (9 points, 0.6 SD) than those randomized to care as usual. Mediation analyses provide evidence that the causal effect of the intervention on cognitive ability in early adulthood could be explained, in part, by higher-quality caregiving and attachment security. These findings indicate that early investment in family care as an alternative to institutional care leads to sustained gains in cognitive ability. Fostering caregiving relationships is a likely mechanism of the intervention. In addition, exploratory analyses indicate that stable placements throughout childhood are associated with the greatest long-term gains in cognitive ability. Whether early interventions for infants and young children lead to lasting change has significant implications for decisions to invest in programs aimed at improving children's developmental outcomes.

Alterations in fear learning as a mechanism linking childhood exposure to violence with PTSD symptoms: a longitudinal study.

BACKGROUND: Fear learning is a core component of conceptual models of how adverse experiences may influence psychopathology. Specifically, existing theories posit that childhood experiences involving childhood trauma are associated with altered fear learning processes, while experiences involving deprivation are not. Several studies have found altered fear acquisition in youth exposed to trauma, but not deprivation, although the specific patterns have varied across studies. The present study utilizes a longitudinal sample of children with variability in adversity experiences to examine associations among childhood trauma, fear learning, and psychopathology in youth. METHODS: The sample includes 170 youths aged 10-13 years (M = 11.56, s.d. = 0.47, 48.24% female). Children completed a fear conditioning task while skin conductance responses (SCR) were obtained, which included both acquisition and extinction. Childhood trauma and deprivation severity were measured using both parent and youth report. Symptoms of anxiety, externalizing problems, and post-traumatic stress disorder (PTSD) were assessed at baseline and again two-years later. RESULTS: Greater trauma-related experiences were associated with greater SCR to the threat cue (CS+) relative to the safety cue (CS-) in early fear acquisition, controlling for deprivation, age, and sex. Deprivation was unrelated to fear learning. Greater SCR to the threat cue during early acquisition was associated with increased PTSD symptoms over time controlling for baseline symptoms and mediated the relationship between trauma and prospective changes in PTSD symptoms. CONCLUSIONS: Childhood trauma is associated with altered fear learning in youth, which may be one mechanism linking exposure to violence with the emergence of PTSD symptoms in adolescence.

Identifying cognitive, affective, and developmental mechanisms linking threat and deprivation with adolescent psychopathology.

BACKGROUND: The mechanisms linking early-life adversity with psychopathology over the life-course are complex. In this prospective study, we collectively examined cognitive, affective, and developmental mediators previously found to individually link childhood threat and deprivation experiences to adolescent psychopathology to identify the most potent mechanisms. METHODS: Data came from a community sample of 227 children (mean child age 11.5 ± 0.5 years, 48.5% female) from the Seattle metro area with recruitment designed to reflect diversity in family income. Candidate mechanisms included self-rated pubertal development and task-measured attention bias to threat, emotion regulation, theory of mind, fear learning, inhibitory control, language ability, reasoning, and reward sensitivity. Using a high-dimensional mediation approach, we determined which mediating pathways linking threat and deprivation to psychopathology persisted after controlling for all candidate mechanisms associated with psychopathology. Models additionally controlled for the child's age, sex, early-childhood emotional and behavioral symptoms, poverty, and maternal depression. RESULTS: Blunted reward sensitivity mediated the prospective relationship between threat and internalizing psychopathology, explaining 17.25% (95% CI 1.08%, 69.96%) of this association. Advanced pubertal development was associated with increases in internalizing and externalizing symptoms (standardized associations of 0.16 (95% CI 0.03, 0.29) and 0.17 (95% CI 0.05, 0.29), respectively), but not with adversity. Although deprivation was strongly related to psychopathology, no mechanisms were empirically identified. CONCLUSIONS: In a well-characterized community sample, we isolated reward sensitivity as a robust mediator of the prospective association between early-life threat and adolescent internalizing psychopathology. Interventions aimed at bolstering reward sensitivity may mitigate the impact of early-life threat experiences on internalizing problems.

Conversation disruptions in early childhood predict executive functioning development: A longitudinal study.

Conversational turn-taking is a complex communicative skill that requires both linguistic and executive functioning (EF) skills, including processing input while simultaneously forming and inhibiting responses until one's turn. Adult-child turn-taking predicts children's linguistic, cognitive, and socioemotional development. However, little is understood about how disruptions to temporal contingency in turn-taking, such as interruptions and overlapping speech, relate to cognitive outcomes, and how these relationships may vary across developmental contexts. In a longitudinal sample of 275 socioeconomically diverse mother-child dyads (children 50% male, 65% White), we conducted pre-registered examinations of whether the frequency of dyads' conversational disruption during free play when children were 3 years old related to children's executive functioning (EF; 9 months later), self-regulation skills (18 months later), and externalizing psychopathology in early adolescence (age 10-12 years). Contrary to hypotheses, more conversational disruptions significantly predicted higher inhibition skills, controlling for sex, age, income-to-needs (ITN), and language ability. Results were driven by maternal disruptions of the child's speech, and could not be explained by measures of overall talkativeness or interactiveness. Exploratory analyses revealed that ITN moderated these relationships, such that the positive effect of disruptions on inhibition was strongest for children from lower ITN backgrounds. We discuss how adult-driven "cooperative overlap" may serve as a form of engaged participation that supports cognition and behavior in certain cultural contexts.

Developmental mechanisms linking deprivation and threat to psychopathology and school outcomes.

BACKGROUND: Decades of evidence have elucidated associations between early adversity and risk for negative outcomes. However, traditional conceptualizations of the biologic embedding of adversity ignore neuroscientific principles which emphasize developmental plasticity. Dimensional models suggest that separate dimensions of experiences shape behavioral development differentially. We hypothesized that deprivation would be associated with higher psychopathology and lower academic achievement through executive function and effortful control, while threat would do so through observed, and parent reported emotional reactivity. METHODS: In this longitudinal study of 206 mother-child dyads, we test these theories across the first 7 years of life. Threat was measured by the presence of domestic violence, and deprivation by the lack of cognitive stimulation within the parent-child interaction. We used path analyses to test associations between deprivation and threat with psychopathology and school outcomes through cognition and emotional reactivity. RESULTS: We show that children who experienced more deprivation showed poor academic achievement through difficulties with executive function, while children who experienced more threat had higher levels of psychopathology through increased emotional reactivity. CONCLUSION: These observations are consistent with work in adolescence and reflect how unique adverse experiences have differential effects on children's behavior and subsequently long-term outcomes.

Child abuse and automatic emotion regulation in children and adolescents.

Child abuse is associated with elevated risk for psychopathology. The current study examined the role of automatic emotion regulation as a potential mechanism linking child abuse with internalizing psychopathology. A sample of 237 youth aged 8-16 years and their caregivers participated. Child abuse severity was assessed by self-report questionnaires, and automatic emotion regulation was assessed using an emotional Stroop task designed to measure adaptation to emotional conflict. A similar task without emotional stimuli was also administered to evaluate whether abuse was uniquely associated with emotion regulation, but not cognitive control applied in a nonemotional context. Internalizing psychopathology was assessed concurrently and at a 2-year longitudinal follow-up. Child abuse severity was associated with lower emotional conflict adaptation but was unrelated to cognitive control. Specifically, the severity of emotional and physical abuse, but not sexual abuse, were associated with lower emotional conflict adaptation. Emotional conflict adaptation was not associated with internalizing psychopathology prospectively. These findings suggest that childhood emotional and physical abuse, in particular, may influence automatic forms of emotion regulation. Future work exploring the socioemotional consequences of altered automatic emotion regulation among youth exposed to child abuse is clearly needed.

Does reward processing moderate or mediate the link between childhood adversity and psychopathology: A longitudinal study.

Childhood adversity is common and associated with elevated risk for transdiagnostic psychopathology. Reward processing has been implicated in the link between adversity and psychopathology, but whether it serves as a mediator or moderator is unclear. This study examined whether alterations in behavioral and neural reward processing function as a mechanism or moderator of psychopathology outcomes following adversity experiences, including threat (i.e., trauma) and deprivation. A longitudinal community sample of 10-15-year-old youths was assessed across two waves (Wave 1: n = 228; Wave 2: n = 206). Wave 1 assessed adverse experiences, psychopathology symptoms, reward processing on a monetary incentive delay task, and resting-state fMRI. At Wave 2, psychopathology symptoms were reassessed. Greater threat experiences were associated with blunted behavioral reward sensitivity, which, in turn, predicted increases in depression symptoms over time and mediated the prospective association between threat and depression symptoms. In contrast, reward sensitivity moderated the association between deprivation experiences and prospective externalizing symptoms such that the positive association of deprivation with increasing externalizing symptoms was absent for children with high levels of reward sensitivity.

Early life adversity and psychopathology in preschoolers: mechanisms and moderators.

Developmental theories suggest that exposure to early life adversity (ELA) alters developing emotional response systems, predicting risk for psychopathology across the life span. The present study examines whether negative emotionality (NE), a trait-like measure of emotionality that develops during early childhood, mediates the association between ELA and psychopathology in a representative sample of 917 preschoolers (Mage = 3.84). Additionally, we explored whether cognitive control, which supports attentional focusing and inhibition and has been identified as a transdiagnostic protective factor, moderates the impact of heightened emotionality following adversity on psychopathology risk. We utilized parent report of adversity, psychopathology, and NE and parent report and task-based measures of cognitive control. Structural equation modeling of cross-sectional data revealed that NE partially mediated the link between ELA and psychopathology symptoms. Moreover, parent-reported cognitive control buffered this link such that the effect of ELA on psychopathology through NE was stronger in children with low versus high cognitive control. These results identify elevated NE as one mechanism linking ELA and psychopathology, specifically among children with poorer top-down control, informing our understanding of key risk and protective factors among adversity-exposed children.

Exposure to Violence as an Environmental Pathway Linking Low Socioeconomic Status with Altered Neural Processing of Threat and Adolescent Psychopathology.

Low childhood socioeconomic status (SES) is associated with increased risk for psychopathology, in part because of heightened exposure to environmental adversity. Adverse experiences can be characterized along dimensions, including threat and deprivation, that contribute to psychopathology via distinct mechanisms. The current study investigated a neural mechanism through which threat and deprivation may contribute to socioeconomic disparities in psychopathology. Participants were 177 youths (83 girls) aged 10-13 years recruited from a cohort followed since the age of 3 years. SES was assessed using the income-to-needs ratio at the age of 3 years. At the age of 10-13 years, retrospective and current exposure to adverse experiences and symptoms of psychopathology were assessed. At this same time point, participants also completed a face processing task (passive viewing of fearful and neutral faces) during an fMRI scan. Lower childhood SES was associated with greater exposure to threat and deprivation experiences. Both threat and deprivation were associated with higher depression symptoms, whereas threat experiences were uniquely linked to posttraumatic stress disorder symptoms. Greater exposure to threat, but not deprivation, was associated with higher activation in dorsomedial pFC to fearful compared with neutral faces. The dorsomedial pFC is a hub of the default mode network thought to be involved in internally directed attention and cognition. Experiences of threat, but not deprivation, are associated with greater engagement of this region in response to threat cues. Threat-related adversity contributes to socioeconomic disparities in adolescent psychopathology through distinct mechanisms from deprivation.

Threat Responsivity Predicts Posttraumatic Stress Disorder Hyperarousal Symptoms in Children after Hurricane Florence.

Following a traumatic event, posttraumatic stress disorder (PTSD) symptoms are common. Considerable research has identified a relationship between physiological responses during fear learning and PTSD. Adults with PTSD display atypical physiological responses, such as increased skin conductance responses (SCR) to threatening cues during fear learning (Orr et al., 2000). However, little research has examined these responses in childhood when fear learning first emerges. We hypothesized that greater threat responsivity in early acquisition during fear conditioning before Hurricane Florence would predict PTSD symptoms in a sample of young children following the hurricane. The final sample included 58 children in North Carolina who completed fear learning before Hurricane Florence-a potentially traumatic event. After the hurricane, we assessed severity of hurricane impact and PTSD symptoms. We found that threat responsivity as measured by differential SCR during fear learning before the hurricane predicted PTSD hyperarousal symptoms and that hurricane impact predicted PTSD symptoms following the disaster. This exploratory work suggests that prospective associations between threat responsivity and PTSD symptoms observed in adulthood may be replicated in early childhood. Results are discussed in the context of the current COVID-19 crisis.

Altered white matter microstructural organization in posttraumatic stress disorder across 3047 adults: results from the PGC-ENIGMA PTSD consortium.

A growing number of studies have examined alterations in white matter organization in people with posttraumatic stress disorder (PTSD) using diffusion MRI (dMRI), but the results have been mixed which may be partially due to relatively small sample sizes among studies. Altered structural connectivity may be both a neurobiological vulnerability for, and a result of, PTSD. In an effort to find reliable effects, we present a multi-cohort analysis of dMRI metrics across 3047 individuals from 28 cohorts currently participating in the PGC-ENIGMA PTSD working group (a joint partnership between the Psychiatric Genomics Consortium and the Enhancing NeuroImaging Genetics through Meta-Analysis consortium). Comparing regional white matter metrics across the full brain in 1426 individuals with PTSD and 1621 controls (2174 males/873 females) between ages 18-83, 92% of whom were trauma-exposed, we report associations between PTSD and disrupted white matter organization measured by lower fractional anisotropy (FA) in the tapetum region of the corpus callosum (Cohen's d = -0.11, p = 0.0055). The tapetum connects the left and right hippocampus, for which structure and function have been consistently implicated in PTSD. Results were consistent even after accounting for the effects of multiple potentially confounding variables: childhood trauma exposure, comorbid depression, history of traumatic brain injury, current alcohol abuse or dependence, and current use of psychotropic medications. Our results show that PTSD may be associated with alterations in the broader hippocampal network.

Association of adversity with psychopathology in early childhood: Dimensional and cumulative approaches.

BACKGROUND: The association between adversity and psychopathology in adolescents and adults is characterized by equifinality. These associations, however, have not been assessed during early childhood when psychopathology first emerges. Defining adversity using both dimensional and cumulative risk approaches, we examined whether specific types of adversity are differentially associated with psychopathology in preschool-aged children. METHODS: Measures of threat, deprivation, and total adversities (i.e., cumulative risk) were calculated based on parent-reported information for 755 2- to 5-year old children recruited from pediatric primary care clinics. Logistic regression was used to estimate cross-sectional associations between type of adversity and anxiety, depression, ADHD, and behavioral disorder diagnoses. RESULTS: Threat and cumulative risk exhibited independent associations with psychopathology. Threat was strongly related to behavioral disorders. Cumulative risk was consistently related to all psychopathologies. CONCLUSIONS: Using mutually adjusted models, we identified differential associations between threat and psychopathology outcomes in preschool-aged children. This selectivity may reflect different pathways through which adversity increases the risk for psychopathology during this developmentally important period. As has been observed at other ages, a cumulative risk approach also effectively identified the cumulative impact of all forms of adversity on most forms of psychopathology during early childhood.

Why and how does early adversity influence development? Toward an integrated model of dimensions of environmental experience.

Two extant frameworks - the harshness-unpredictability model and the threat-deprivation model - attempt to explain which dimensions of adversity have distinct influences on development. These models address, respectively, why, based on a history of natural selection, development operates the way it does across a range of environmental contexts, and how the neural mechanisms that underlie plasticity and learning in response to environmental experiences influence brain development. Building on these frameworks, we advance an integrated model of dimensions of environmental experience, focusing on threat-based forms of harshness, deprivation-based forms of harshness, and environmental unpredictability. This integrated model makes clear that the why and the how of development are inextricable and, together, essential to understanding which dimensions of the environment matter. Core integrative concepts include the directedness of learning, multiple levels of developmental adaptation to the environment, and tradeoffs between adaptive and maladaptive developmental responses to adversity. The integrated model proposes that proximal and distal cues to threat-based and deprivation-based forms of harshness, as well as unpredictability in those cues, calibrate development to both immediate rearing environments and broader ecological contexts, current and future. We highlight actionable directions for research needed to investigate the integrated model and advance understanding of dimensions of environmental experience.

Measuring early life adversity: A dimensional approach.

Exposure to adversity in childhood is associated with elevations in numerous physical and mental health outcomes across the life course. The biological embedding of early experience during periods of developmental plasticity is one pathway that contributes to these associations. Dimensional models specify mechanistic pathways linking different dimensions of adversity to health and well-being outcomes later in life. While findings from existing studies testing these dimensions have provided promising preliminary support for these models, less agreement exists about how to measure the experiences that comprise each dimension. Here, we review existing approaches to measuring two dimensions of adversity: threat and deprivation. We recommend specific measures for measuring these constructs and, when possible, document when the same measure can be used by different reporters and across the lifespan to maximize the utility with which these recommendations can be applied. Through this approach, we hope to stimulate progress in understanding how particular dimensions of early environmental experience contribute to lifelong health.

Emotional maltreatment and neglect impact neural activation upon exclusion in early and mid-adolescence: An event-related fMRI study.

Child maltreatment gives rise to atypical patterns of social functioning with peers which might be particularly pronounced in early adolescence when peer influence typically peaks. Yet, few neuroimaging studies in adolescents use peer interaction paradigms to parse neural correlates of distinct maltreatment exposures. This fMRI study examines effects of abuse, neglect, and emotional maltreatment (EM) among 98 youth (n = 58 maltreated; n = 40 matched controls) using an event-related Cyberball paradigm affording assessment of both social exclusion and inclusion across early and mid-adolescence (≤13.5 years, n = 50; >13.5 years, n = 48). Younger adolescents showed increased activation to social exclusion versus inclusion in regions implicated in mentalizing (e.g., superior temporal gyrus). Individual exposure-specific analyses suggested that neglect and EM coincided with less reduction of activation to social exclusion relative to inclusion in the dorsal anterior cingulate cortex/pre-supplementary motor area (dACC/pre-SMA) among younger versus older adolescents. Integrative follow-up analyses showed that EM accounted for this dACC/pre-SMA activation pattern over and above other exposures. Moreover, age-independent results within respective exposure groups revealed that greater magnitude of neglect predicted blunted exclusion-related activity in the parahippocampal gyrus, while EM predicted increased activation to social exclusion in the precuneus/posterior cingulate cortex.

The maturation and cognitive relevance of structural brain network organization from early infancy to childhood.

The interactions of brain regions with other regions at the network level likely provide the infrastructure necessary for cognitive processes to develop. Specifically, it has been theorized that in infancy brain networks become more modular, or segregated, to support early cognitive specialization, before integration across networks increases to support the emergence of higher-order cognition. The present study examined the maturation of structural covariance networks (SCNs) derived from longitudinal cortical thickness data collected between infancy and childhood (0-6 years). We assessed modularity as a measure of network segregation and global efficiency as a measure of network integration. At the group level, we observed trajectories of increasing modularity and decreasing global efficiency between early infancy and six years. We further examined subject-based maturational coupling networks (sbMCNs) in a subset of this cohort with cognitive outcome data at 8-10 years, which allowed us to relate the network organization of longitudinal cortical thickness maturation to cognitive outcomes in middle childhood. We found that lower global efficiency of sbMCNs throughout early development (across the first year) related to greater motor learning at 8-10 years. Together, these results provide novel evidence characterizing the maturation of brain network segregation and integration across the first six years of life, and suggest that specific trajectories of brain network maturation contribute to later cognitive outcomes.

History of conditioned reward association disrupts inhibitory control: an examination of neural correlates.

The neural processes that support inhibitory control in the face of stimuli with a history of reward association are not yet well understood. Yet, the ability to flexibly adapt behavior to changing reward-contingency contexts is important for daily functioning and warrants further investigation. This study aimed to characterize neural and behavioral impacts of stimuli with a history of conditioned reward association on motor inhibitory control in healthy young adults by investigating group-level effects as well as individual variation in the ability to inhibit responses to stimuli with a reward history. Participants (N = 41) first completed a reward conditioning phase, during which responses to rewarded stimuli were associated with money and responses to unrewarded stimuli were not. Rewarded and unrewarded stimuli from training were carried forward as No-Go targets in a subsequent go/no-go task to test the effect of reward history on inhibitory control. Participants underwent functional brain imaging during the go/no-go portion of the task. On average, a history of reward conditioning disrupted inhibitory control. Compared to inhibition of responses to stimuli with no reward history, trials that required inhibition of responses to previously rewarded stimuli were associated with greater activity in frontal and striatal regions, including the inferior frontal gyrus, insula, striatum, and thalamus. Activity in the insula and thalamus during false alarms and in the ventromedial prefrontal cortex during correctly withheld trials predicted behavioral performance on the task. Overall, these results suggest that reward history serves to disrupt inhibitory control and provide evidence for diverging roles of the insula and ventromedial prefrontal cortex while inhibiting responses to stimuli with a reward history.

Alterations in neural circuits underlying emotion regulation following child maltreatment: a mechanism underlying trauma-related psychopathology.

BACKGROUND: Disruptions in neural circuits underlying emotion regulation (ER) may be a mechanism linking child maltreatment with psychopathology. We examined the associations of maltreatment with neural responses during passive viewing of negative emotional stimuli and attempts to modulate emotional responses. We investigated whether the influence of maltreatment on neural activation during ER differed across development and whether alterations in brain function mediated the association between maltreatment and a latent general psychopathology ('p') factor. METHODS: Youth aged 8-16 years with (n = 79) and without (n = 72) exposure to maltreatment completed an ER task assessing neural responses during passive viewing of negative and neutral images and effortful attempts to regulate emotional responses to negative stimuli. P-factor scores were defined by a bi-factor model encompassing internalizing and externalizing psychopathology. RESULTS: Maltreated youth had greater activation in left amygdala and salience processing regions and reduced activation in multiple regions involved in cognitive control (bilateral superior frontal gyrus, middle frontal gyrus, and dorsal anterior cingulate cortex) when viewing negative v. neutral images than youth without maltreatment exposure. Reduced neural recruitment in cognitive control regions mediated the association of maltreatment with p-factor in whole-brain analysis. Maltreated youth exhibited increasing recruitment with age in ventrolateral prefrontal cortex during reappraisal while control participants exhibited decreasing recruitment with age. Findings were similar after adjusting for co-occurring neglect. CONCLUSIONS: Child maltreatment influences the development of regions associated with salience processing and cognitive control during ER in ways that contribute to psychopathology.

Deprivation and psychopathology in the Fragile Families Study: A 15-year longitudinal investigation.

BACKGROUND: Early adversity consistently predicts youth psychopathology. However, the pathways linking unique dimensions of early adversity, such as deprivation, to psychopathology are understudied. Here, we evaluate a theoretical model linking early deprivation exposure with psychopathology prospectively through language ability. METHODS: Participants included 2,301 youth (47.5% female) enrolled in the Fragile Families and Child Wellbeing Study. We include data from assessment points at ages 1, 3, 5, 9, and 15. Latent factors for deprivation and threat were modeled from multiple indicators at ages 1 and 3. Youth language ability was assessed at Age 5. Indicators of psychopathology were assessed at ages 5, 9, and 15. A structural equation model tested longitudinal paths to internalizing and externalizing psychopathology from experiences of deprivation and threat. RESULTS: Deprivation from birth to Age 3 was associated with an indirect effect on internalizing and externalizing symptoms in early childhood (Age 5), later childhood (Age 9), and adolescence (Age 15) via language ability in early childhood (Age 5). Early threat exposure was associated with increased internalizing and externalizing psychopathology across all ages. There was no significant indirect effect from threat to psychopathology via language ability. CONCLUSIONS: The effects of deprivation on psychopathology during early childhood, late childhood, and adolescence are explained, in part, through early childhood language ability. Results provide insight into language ability as a possible opportunity for intervention.