Smaller hippocampal volume is associated with increased risk for PTSD following trauma, but the hippocampal functions involved remain unknown. We propose a conceptual model that identifies broad impairment in hippocampus-dependent associative learning as a vulnerability factor for PTSD. Associative learning of foreground cues and background context is required to form an integrated representation of an event. People with poor associative learning may have difficulty remembering who or what was present during a trauma, where the trauma occurred, or the sequence of events, which may contribute to PTSD symptoms. We argue that associative learning difficulties in PTSD exist for cues and context, regardless of the emotional nature of the information. This contrasts with PTSD models that focus exclusively on threat-processing or contextual-processing. In a meta-analysis, people with PTSD exhibited poor associative learning of multiple information types compared to those without PTSD. Differences were of medium effect size and similar magnitude for neutral and negative/trauma-related stimuli. We provide evidence for associative learning difficulties as a neurocognitive pathway that may contribute to PTSD.
The processing of emotional facial expressions is important for social functioning and is influenced by environmental factors, including early environmental experiences. Low socio-economic status (SES) is associated with greater exposure to uncontrollable stressors, including violence, as well as deprivation, defined as a lack or decreased complexity of expected environmental input. The current study examined amygdala and fusiform gyrus response to facial expressions in 207 early adolescents (mean age = 13.93 years, 63.3% female). Participants viewed faces displaying varying intensities of angry and happy faces during functional MRI. SES was assessed using the income-to-needs ratio (INR) and a measure of subjective social status. Cumulative exposure to violence was also assessed. When considered in isolation, only violence exposure was associated with heightened amygdala response to angry faces. When considered jointly, violence exposure and lower INR were both associated with increased amygdala response to angry faces and interacted, such that lower INR was associated with increased amygdala reactivity to anger only in those youth reporting no exposure to violence. This pattern of findings raises the possibility that greater amygdala reactivity to threat cues in children raised in low-SES conditions may arise from different factors associated with an economically-deprived environment.
Post-traumatic stress disorder (PTSD) is a common mental health problem. Here, the authors report a GWAS from the Psychiatric Genomics Consortium in which they identify two risk loci in European ancestry and one locus in African ancestry individuals and find that PTSD is genetically correlated with several other psychiatric traits.
Background The prevalence of mental disorders among Black, Latino, and Asian adults is lower than among Whites. Factors that explain these differences are largely unknown. We examined whether racial/ethnic differences in exposure to traumatic events (TEs) or vulnerability to trauma-related psychopathology explained the lower rates of psychopathology among racial/ethnic minorities. Methods We estimated the prevalence of TE exposure and associations with onset of DSM-IV depression, anxiety and substance disorders and with lifetime post-traumatic stress disorder (PTSD) in the Collaborative Psychiatric Epidemiology Surveys, a national sample (N = 13 775) with substantial proportions of Black (35.9%), Latino (18.9%), and Asian Americans (14.9%). Results TE exposure varied across racial/ethnic groups. Asians were most likely to experience organized violence – particularly being a refugee – but had the lowest exposure to all other TEs. Blacks had the greatest exposure to participation in organized violence, sexual violence, and other TEs, Latinos had the highest exposure to physical violence, and Whites were most likely to experience accidents/injuries. Racial/ethnic minorities had lower odds ratios of depression, anxiety, and substance disorder onset relative to Whites. Neither variation in TE exposure nor vulnerability to psychopathology following TEs across racial/ethnic groups explained these differences. Vulnerability to PTSD did vary across groups, however, such that Asians were less likely and Blacks more likely to develop PTSD following TEs than Whites. Conclusions Lower prevalence of mental disorders among racial/ethnic minorities does not appear to reflect reduced vulnerability to TEs, with the exception of PTSD among Asians. This highlights the importance of investigating other potential mechanisms underlying racial/ethnic differences in psychopathology.
Background Childhood adversity is strongly linked to negative mental health outcomes, including depression and anxiety. Leveraging cognitive neuroscience to identify mechanisms that contribute to resilience in children with a history of maltreatment may provide viable intervention targets for the treatment or prevention of psychopathology. We present a conceptual model of a potential neurobiological mechanism of resilience to depression and anxiety following childhood adversity. Specifically, we argue that neural circuits underlying the cognitive control of emotion may promote resilience, wherein a child’s ability to recruit the frontoparietal control network to modulate amygdala reactivity to negative emotional cues—such as during cognitive reappraisal—buffers risk for internalizing symptoms following exposure to adversity. Methods We provide preliminary support for this model of resilience in a longitudinal sample of 151 participants 8 to 17 years of age with (n = 79) and without (n = 72) a history of childhood maltreatment who completed a cognitive reappraisal task while undergoing functional magnetic resonance imaging. Results Among maltreated youths, those who were better able to recruit prefrontal control regions and modulate amygdala reactivity during reappraisal exhibited lower risk for depression over time. By contrast, no association was observed between neural functioning during reappraisal and depression among youths without a history of maltreatment. Conclusions These preliminary findings support the hypothesis that children who are better able to regulate emotion through recruitment of the frontoparietal network exhibit greater resilience to depression following childhood maltreatment. Interventions targeting cognitive reappraisal and other cognitive emotion regulation strategies may have potential for reducing vulnerability to depression among children exposed to adversity.
Variability is a fundamental feature of human brain activity that is particularly pronounced during development. However, developmental neuroimaging research has only recently begun to move beyond characterizing brain function exclusively in terms of magnitude of neural activation to incorporate estimates of variability. No prior neuroimaging study has done so in the domain of emotion regulation. We investigated how age and affective experiences relate to spatial and temporal variability in neural activity during emotion regulation. In the current study, 70 typically developing youth aged 8 to 17 years completed a cognitive reappraisal task of emotion regulation while undergoing functional MRI. Estimates of spatial and temporal variability during regulation were calculated across a network of brain regions, defined a priori, and were then related to age and affective experiences. Results showed that increasing age was associated with reduced spatial and temporal variability in a set of frontoparietal regions (e.g., dorsomedial prefrontal cortex, superior parietal lobule) known to be involved in effortful emotion regulation. In addition, youth who reported less negative affect during regulation had less spatial variability in the ventrolateral prefrontal cortex, which has previously been linked to cognitive reappraisal. We interpret age-related reductions in spatial and temporal variability as implying neural specialization. These results suggest that the development of emotion regulation is undergirded by a process of neural specialization and open a host of possibilities for incorporating neural variability into the study of emotion regulation development. (PsycINFO Database Record (c) 2019 APA, all rights reserved).
Socioeconomic status (SES) is associated with executive function (EF) and prefrontal cortex (PFC) development. However, understanding of the specific aspects of SES that influence development of EF and the PFC remains limited. We briefly review existing literature on proposed mechanisms linking SES with EF. Then, we present a novel conceptual model arguing that early cognitive stimulation shapes EF and PFC development. We propose that cognitive stimulation drives lower-level sensory and perceptual processes that may impact EF and PFC development through reciprocal connections between the ventral visual stream and PFC. We argue that caregivers guide attention and associative learning, which provides children the opportunity to regulate attention and gain semantic knowledge. This experience in turn allows for opportunities to train the PFC to resolve conflict between stimuli with overlapping features and engage in increasingly complex computations as visual processing systems develop; this may lay the groundwork for development of EF. We review existing evidence for this model and end by highlighting how this conceptual model could launch future research questions.
Associations between stressful life events (SLEs) and internalizing psychopathology are complex and bidirectional, involving interactions among stressors across development to predict psychopathology (i.e., stress sensitization) and psychopathology predicting greater exposure to SLEs (i.e., stress generation). Although stress sensitization and generation theoretical models inherently focus on within-person effects, most previous research has compared average levels of stress and psychopathology across individuals in a sample (i.e., between-person effects). The present study addressed this gap by investigating stress sensitization and stress generation effects in a multiwave, prospective study of SLEs and adolescent depression and anxiety symptoms. Depression, anxiety, and SLE exposure were assessed every 3 months for 2 years (8 waves of data) in a sample of adolescents (n = 382, aged 11 to 15 at baseline). Multilevel modeling revealed within-person stress sensitization effects such that the association between within-person increases in SLEs and depression, but not anxiety, symptoms were stronger among adolescents who experienced higher average levels of SLEs across 2 years. We also observed within-person stress generation effects, such that adolescents reported a greater number of dependent-interpersonal SLEs during time periods after experiencing higher levels of depression at the previous wave than was typical for them. Although no within-person stress generation effects emerged for anxiety, higher overall levels of anxiety predicted greater exposure to dependent-interpersonal SLEs. Our findings extend prior work by demonstrating stress sensitization in predicting depression following normative forms of SLEs and stress generation effects for both depression and anxiety using a multilevel modeling approach. Clinical implications include an individualized approach to interventions. (PsycINFO Database Record (c) 2019 APA, all rights reserved)
Difficulties with emotion regulation can take many forms, including increased sensitivity to emotional cues and habitual use of maladaptive cognitive or behavioral regulation strategies. Despite extensive research on emotion regulation and youth adjustment, few studies integrate multiple measures of emotion regulation. The present study evaluated the underlying structure of emotion regulation processes in adolescence using both task- and survey-based measures and determined whether differences in these emotion regulation latent factors mediated the association between peer victimization and internalizing psychopathology. Adolescents aged 16–17 years (n = 287; 55% female; 42% White) recruited in three urban centers in the United States completed baseline and follow-up assessments 4 months apart. Three models of emotion regulation were evaluated with confirmatory factor analysis. A three-factor model fit the data best, including cognitive regulation, behavioral regulation, and emotional reactivity latent factors. Task-based measures did not load onto these latent factors. Difficulties with behavioral regulation mediated the association between peer victimization and depression symptoms, whereas cognitive regulation difficulties mediated the association with anxiety symptoms. Findings point to potential targets for intervention efforts to reduce risk for internalizing problems in adolescents following experiences of peer victimization.
Childhood maltreatment is associated with increased risk for most forms of psychopathology. We examine emotion dysregulation as a transdiagnostic mechanism linking maltreatment with general psychopathology. A sample of 262 children and adolescents participated; 162 (61.8%) experienced abuse or exposure to domestic violence. We assessed four emotion regulation processes (cognitive reappraisal, attention bias to threat, expressive suppression, and rumination) and emotional reactivity. Psychopathology symptoms were assessed concurrently and at a 2-year longitudinal follow-up. A general psychopathology factor (p factor), representing co-occurrence of psychopathology symptoms across multiple internalizing and externalizing domains, was estimated using confirmatory factor analysis. Maltreatment was associated with heightened emotional reactivity and greater use of expressive suppression and rumination. The association of maltreatment with attention bias varied across development, with maltreated children exhibiting a bias toward threat and adolescents a bias away from threat. Greater emotional reactivity and engagement in rumination mediated the longitudinal association between maltreatment and increased general psychopathology over time. Emotion dysregulation following childhood maltreatment occurs at multiple stages of the emotion generation process, in some cases varies across development, and serves as a transdiagnostic mechanism linking child maltreatment with general psychopathology.
Little is known about how childhood adversity influences the development of learning and memory and underlying neural circuits. We examined whether violence exposure in childhood influenced hippocampus-dependent associative learning and whether differences: a) were broad or specific to threat cues, and b) exhibited developmental variation. Children (n = 59; 8–19 years, 24 violence-exposed) completed an associative learning task with angry, happy, and neutral faces paired with objects during fMRI scanning. Outside the scanner, participants completed an associative memory test for face-object pairings. Violence-exposed children exhibited broad associative memory difficulties that became more pronounced with age, along with reduced recruitment of the hippocampus and atypical recruitment of fronto-parietal regions during encoding. Violence-exposed children also showed selective disruption of associative memory for threat cues regardless of age, along with reduced recruitment of the intraparietal sulcus (IPS) during encoding in the presence of threat. Broad associative learning difficulties may be a functional consequence of the toxic effects of early-life stress on hippocampal and fronto-parietal cortical development. Difficulties in the presence of threat cues may result from enhanced threat processing that disrupts encoding and short-term storage of associative information in the IPS. These associative learning difficulties may contribute to poor life outcomes following childhood violence exposure.
Exposure to childhood adversity is common and a powerful risk factor for many forms of psychopathology. In this opinion piece, we argue for greater translation of knowledge about the developmental processes that are inﬂuenced by childhood adversity into targeted interventions to prevent the onset of psychopathology. Existing evidence has consistently identiﬁed several neurodevelopmental pathways that serve as mechanisms linking adversity with psychopathology. We highlight three domains in which these mechanisms are well-established and point to clear targets for intervention: 1) threat-related social information processing biases; 2) heightened emotional reactivity and diﬃculties with emotion regulation; and 3) disruptions in reward processing. In contrast to these established pathways, knowledge of how childhood adversity inﬂuences emotional learning mechanisms, including fear and reward learning, is remarkably limited. We see the investigation of these mechanisms as a critical next step for the ﬁeld that will not only advance understanding of developmental pathways linking childhood adversity with psychopathology, but also provide clear targets for behavioral interventions. Knowledge of the mechanisms linking childhood adversity with psychopathology has advanced rapidly, and the time has come to translate that knowledge into clinical interventions to prevent the onset of mental health problems in children who have experienced adversity.
Objective: Children exposed to institutional rearing often exhibit problems across a broad array of developmental domains. We compared the consequences of long-term, high-quality foster care versus standard institution-based care, which began in early childhood on cardio- metabolic and immune markers assessed at the time of adolescence. Methods: The Bucharest Early Intervention Project is a longitudinal investigation of children institutionalized during early childhood (ages 6 to 30 months at baseline) who were subsequently randomized to either high-quality foster care or continued institutional care. At the age of 16 years, 127 respondents participated in a biomarker collection protocol, including 44 institutionalized children randomly assigned to receive care as usual, 41 institutionalized children randomized to be removed from institutional care and placed in high-quality foster care in infancy, and a control group of 42 demographically matched children raised in biological families. Outcomes included body mass index (BMI), systolic and diastolic blood pressure, C-reactive protein, interleukin (IL)-6, IL-8, IL-10, tumor necrosis factor α, gly- cosylated hemoglobin A1c, and Epstein-Barr virus antibody titers.
Results: Early institutional rearing was not associated with differences in cardiometabolic or immune markers. Randomization to foster care and age of placement into foster care were also unrelated to these markers, with the exception of BMI z-score, where children assigned to care as usual had lower BMI z-scores relative to children assigned to foster care (−0.23 versus 0.08, p = .06), and older age at placement was associated with lower BMI (β = −0.07, p = .03).
Conclusions: The impact of institutional rearing on measures of cardiometabolic health and immune system functioning is either absent or not evident until later in development. These findings provide new insights into the biological embedding of adversity and how it varies developmentally and across regulatory systems and adversity type.
Purpose There has been no comprehensive examination of how race/ethnicity and nativity intersect in explaining differences in lifetime prevalence of mental disorders among Asian, Black, Latino, and White adults. This study aims to estimate racial/ ethnic differences in lifetime risk of mental disorders and examine how group differences vary by nativity. Methods Survival models were used to estimate racial/ethnic and nativity differences in lifetime risk of DSM-IV anxiety, mood, and substance use disorders in a nationally representative sample of over 20,000 respondents to four US surveys. Results Asians had the lowest lifetime prevalence of mental disorders (23.5%), followed by Blacks (37.0%), Latinos (38.8%), and Whites (45.6%). Asians and Blacks had lower lifetime risk than Whites for all disorders even after adjusting for nativity; Latinos and Whites had similar risk after adjusting for nativity. Risk of disorder onset was lowest for foreign-born respondents in years before migration. There were significant race/ethnicity and nativity interactions for mood and substance use disorders. Odds of mood disorder onset were higher for Whites with at least one US-born parent. Odds of substance use disorder onset among Asians were higher for US-born respondents; for Latinos, they were higher for those with at least one US-born parent. Conclusions Parental foreign-born nativity is associated with a low risk of mental disorders, but not uniformly across racial/ ethnic groups or disorders. Exposure to the US context may be associated with greater mental disorder risk for Latinos and Whites particularly. Investigations of cultural processes, including among Whites, are needed to understand group differences.
Childhood abuse is a potent risk factor for psychopathology, including posttraumatic stress disorder (PTSD). Research has shown high resting vagal tone, a measure of parasympathetic nervous system function, protects abused youth from developing internalizing psychopathology, but potential mechanisms explaining this effect are unknown. We explored fear extinction learning as a possible mechanism underlying the protective effect of vagal tone on PTSD symptoms among abused youth. We measured resting respiratory sinus arrhythmia (RSA) and skin conductance responses (SCR) during a fear conditioning and extinction task in youth with variability in abuse exposure (N = 94; aged 6–18 years). High RSA predicted lower PTSD symptoms and enhanced extinction learning among abused youths. In a moderated-mediation model, extinction learning mediated the association of abuse with PTSD symptoms only among youth with high RSA. These findings highlight extinction learning as a possible mechanism linking high vagal tone to decreased risk for PTSD symptoms among abused youth.
Early-life adversity (ELA) is strongly associated with risk for psychopathology. Within adversity, deprivation and threat may lead to psychopathology through different intermediary pathways. Specifically, deprivation, defined as the absence of expected cognitive and social inputs, is associated with lower performance on complex cognitive tasks whereas threatening experiences, defined as the presence of experiences that reflect harm to the child, are associated with atypical fear learning and emotional processes. However, distinct associations of deprivation and threat on behavioral outcomes have not been examined in early childhood. The present study examines how deprivation and threat are associated with cognitive and emotional outcomes in early childhood. Children 4-7 years old (N=63) completed behavioral tasks assessing cognitive control and fear conditioning; deprivation and threat were assessed using child interview and parent questionnaires. Regression analyses were performed including deprivation and threat scores and controls for age, gender and IQ. Because this is the first time these variables have been examined in early childhood, interactions with age were also examined. Deprivation, but not threat was associated with worse performance on the cognitive control task. Threat, but not deprivation interacted with age to predict fear learning. Young children who experienced high levels of threat showed evidence of fear learning measured by differential skin conductance response even at the earliest age measured. In contrast, for children not exposed to threat, fear learning emerged only in older ages. Children who experienced higher levels of threat also showed blunted reactivity measured by amplitude of skin conductance response to the reinforced stimuli regardless of age. Results suggest differential influences of deprivation and threat on cognitive and emotional outcomes even in early childhood. Future work should examine the neural mechanisms underlying these behavioral changes and link changes with increased risk for negative outcomes associated with adversity exposure, such as psychopathology.
Exposure to childhood adversity is common and a powerful risk factor for many forms of psychopathology. In this opinion piece, we argue for greater translation of knowledge about the developmental processes that are influenced by childhood adversity into targeted interventions to prevent the onset of psychopathology. Existing evidence has consistently identified several neurodevelopmental pathways that serve as mechanisms linking adversity with psychopathology. We highlight three domains in which these mechanisms are well-established and point to clear targets for intervention: 1) threat-related social information processing biases; 2) heightened emotional reactivity and difficulties with emotion regulation; and 3) disruptions in reward processing. In contrast to these established pathways, knowledge of how childhood adversity influences emotional learning mechanisms, including fear and reward learning, is remarkably limited. We see the investigation of these mechanisms as a critical next step for the field that will not only advance understanding of developmental pathways linking childhood adversity with psychopathology, but also provide clear targets for behavioral interventions. Knowledge of the mechanisms linking childhood adversity with psychopathology has advanced rapidly, and the time has come to translate that knowledge into clinical interventions to prevent the onset of mental health problems in children who have experienced adversity.
Background Despite equivalent or lower lifetime and past-year prevalence of mental disorder among racial/ethnic minorities compared to non-Latino Whites in the United States, evidence suggests that mental disorders are more persistent among minorities than non-Latino Whites. But, it is unclear how nativity and socioeconomic status contribute to observed racial/ethnic differences in prevalence and persistence of mood, anxiety, and substance disorders. Method Data were examined from a coordinated series of four national surveys that together assessed 21,024 Asian, non-Latino Black, Latino, and non-Latino White adults between 2001 and 2003. Common DSM-IV mood, anxiety, and substance disorders were assessed using the Composite International Diagnostic Interview. Logistic regression analyses examined how several predictors (e.g., race/ethnicity, nativity, education, income) and the interactions between those predictors were associated with both 12-month disorder prevalence and 12-month prevalence among lifetime cases. For the second series of analyses, age of onset and time since onset were used as additional control variables to indirectly estimate disorder persistence. Results Non-Latino Whites demonstrated the highest unadjusted 12-month prevalence of all disorder types (p \textless 0.001), though differences were also observed across minority groups. In contrast, Asian, Latino, and Black adults demonstrated higher 12-month prevalence of mood disorders among lifetime cases than Whites (p \textless 0.001) prior to adjustments Once we introduced nativity and other relevant controls (e.g., age, sex, urbanicity), US-born Whites with at least one US-born parent demonstrated higher 12-month mood disorder prevalence than foreign-born Whites or US-born Whites with two foreign parents (OR = 0.51, 95% CI = [0.36, 0.73]); this group also demonstrated higher odds of past-year mood disorder than Asian (OR = 0.59, 95% CI = [0.42, 0.82]) and Black (OR = 0.70, 95% CI = [0.58, 0.83]) adults, but not Latino adults (OR = 0.89, 95% CI = [0.74, 1.06]). Racial/ethnic differences in 12-month mood and substance disorder prevalence were moderated by educational attainment, especially among adults without a college education. Additionally, racial/ethnic minority groups with no more than a high school education demonstrated more persistent mood and substance disorders than non-Latino Whites; these relationships reversed or disappeared at higher education levels. Conclusion Nativity may be a particularly relevant consideration for diagnosing mood disorder among non-Latino Whites; additionally, lower education appears to be associated with increased relative risk of persistent mood and substance use disorders among racial/ethnic minorities compared to non-Latino Whites.
Background Recent conceptual models argue that early life adversity (ELA) accelerates development, which may contribute to poor mental and physical health outcomes. Evidence for accelerated development in youths comes from studies of telomere shortening or advanced pubertal development following circumscribed ELA experiences and neuroimaging studies of circuits involved in emotional processing. It is unclear whether all ELA is associated with accelerated development across global metrics of biological aging or whether this pattern emerges following specific adversity types. Methods In 247 children and adolescents 8 to 16 years of age with wide variability in ELA exposure, we evaluated the hypothesis that early environments characterized by threat, but not deprivation, would be associated with accelerated development across two global biological aging metrics: DNA methylation (DNAm) age and pubertal stage relative to chronological age. We also examined whether accelerated development explained associations of ELA with depressive symptoms and externalizing problems. Results Exposure to threat-related ELA (e.g., violence) was associated with accelerated DNAm age and advanced pubertal stage, but exposure to deprivation (e.g., neglect, food insecurity) was not. In models including both ELA types, threat-related ELA was uniquely associated with accelerated DNAm age ($\beta$ = .18) and advanced pubertal stage ($\beta$ = .28), whereas deprivation was uniquely associated with delayed pubertal stage ($\beta$ = -.21). Older DNAm age was related to greater depressive symptoms, and a significant indirect effect of threat exposure on depressive symptoms was observed through DNAm age. Conclusions Early threat-related experiences are particularly associated with accelerated biological aging in youths, which may be a mechanism linking ELA with depressive symptoms.