Low socioeconomic status (SES) is associated with greater risk for symptoms of attention-deficit/hyperactivity disorder (ADHD). One mechanism through which SES may confer risk for ADHD is by influencing brain structure. Alterations to cortical thickness, surface area and subcortical volume have been associated with low SES and with the presence of ADHD across multiple studies. The current study examined whether cortical thickness, surface area or subcortical volume mediate the associations between SES and ADHD in youth 3–21 years old (N = 874) from the Pediatric Imaging, Neurocognition and Genetics Study. Freesurfer was used to estimate cortical thickness, surface area and subcortical volume from structural magnetic resonance imaging. Parents reported on demographics, family SES, ADHD diagnoses and the presence of child attention problems. Statistical mediation was assessed using a bootstrap resampling procedure. Controlling for parental ADHD, child age, gender, birth weight and scanner, children in low SES families were more likely to be in the ADHD group. Consistent with previous reports in this sample, low SES was associated with reduced surface area across the frontal lobe and reduced subcortical volume in the amygdala, cerebellum, hippocampus and basal ganglia. Of these regions, a significant indirect effect of SES on ADHD status through subcortical volume was observed for the left cerebellum (95% confidence interval: 0.004, 0.022), the right cerebellum (95% confidence interval: 0.006, 0.025), and the right caudate (95% confidence interval: 0.002, 0.022). Environmentally mediated changes in the cerebellum and the caudate may be neurodevelopmental mechanisms explaining elevated risk of ADHD in children in low SES families.
Decades of research have unequivocally shown that life stress is a central factor in the onset and course of almost every psychiatric disorder. However, the processes by which stress influences mental health are complex, and the integration of the myriad of biological and psychological systems involved requires a multidisciplinary perspective. Fortunately, scientists working from diverse vantage points have made huge advances in unpacking the complexities of stress-disorder relations. The Oxford Handbook of Stress and Mental Health provides a comprehensive, up-to-date overview of the science of stress and mental health. Topics covered include assessment issues, the role of stress in various mental disorders, developmental influences and individual difference factors that predict reactivity to stress, and treatment of stress-related mental health problems. Internationally recognized scholars in the field of stress and stress-related disorders have contributed their diverse expertise, providing both depth and breadth in terms of understanding stress and mental health. Chapters 1 to 4 provide a critical discussion of assessment issues in the domains of stress exposure and stress response. Chapters 5 to 14 review the relation of stress exposures to a broad range of mental health outcomes across the lifespan. Chapters 15 to 25 are concerned with understanding how the stress response unfolds at both psychological and neurobiological levels. Lastly, Chapters 26 to 33 addresses stress adaptation and resilience, as well as evidence-based treatments for stress and stress-related disorder. This volume will constitute an invaluable resource for students, established scientists, and clinicians looking for a comprehensive treatment of the topic of stress and mental health.
An extensive literature on childhood adversity and neurodevelopment has emerged over the past decade. We evaluate two conceptual models of adversity and neurodevelopment—the dimensional model of adversity and stress acceleration model—in a systematic review of 109 studies using MRI-based measures of neural structure and function in children and adolescents. Consistent with the dimensional model, children exposed to threat had reduced amygdala, medial prefrontal cortex (mPFC), and hippocampal volume and heightened amygdala activation to threat in a majority of studies; these patterns were not observed consistently in children exposed to deprivation. In contrast, reduced volume and altered function in frontoparietal regions were observed consistently in children exposed to deprivation but not children exposed to threat. Evidence for accelerated development in amygdala-mPFC circuits was limited but emerged in other metrics of neurodevelopment. Progress in charting neurodevelopmental consequences of adversity requires larger samples, longitudinal designs, and more precise assessments of adversity.
Childhood socioeconomic status (SES) is associated with numerous aspects of cognitive development and disparities in academic achievement. The specific environmental factors that contribute to these disparities remain poorly understood. We used observational methods to characterize three aspects of the early environment that may contribute to SES-related differences in cognitive development: violence exposure, cognitive stimulation, and quality of the physical environment. We evaluated the associations of these environmental characteristics with associative memory, cued attention, and memory-guided attention in a sample of 101 children aged 60–75 months. We further investigated whether these specific cognitive abilities mediated the association between SES and academic achievement 18 months later. Violence exposure was specifically associated with poor associative memory, but not cued attention or memory-guided attention. Cognitive stimulation and higher quality physical environment were positively associated with cued attention accuracy, but not after adjusting for all other environmental variables. The quality of the physical environment was associated with memory-guided attention accuracy. Of the cognitive abilities examined, only memory-guided attention contributed to SES-related differences in academic achievement. These findings suggest specificity in how particular aspects of early environmental experience scaffold different types of attention and memory subserved by distinct neural circuits and shed light on a novel cognitive-developmental mechanism underlying SES-related disparities in academic achievement.
Generational changes in IQ (the Flynn Eﬀect) have been extensively researched and debated. Within the US, gains of 3 points per decade have been accepted as consistent across age and ability level, suggesting that tests with outdated norms yield spuriously high IQs. However, ﬁndings are generally based on small samples, have not been validated across ability levels, and conﬂict with reverse eﬀects recently identiﬁed in Scandinavia and other countries. Using a well-validated measure of ﬂuid intelligence, we investigated the Flynn Eﬀect by comparing scores normed in 1989 and 2003, among a representative sample of American adolescents ages 13–18 (n = 10,073). Additionally, we examined Flynn Eﬀect variation by age, sex, ability level, parental age, and SES. Adjusted mean IQ diﬀerences per decade were calculated using generalized linear models. Overall the Flynn Eﬀect was not signiﬁcant; however, eﬀects varied substantially by age and ability level. IQs increased 2.3 points at age 13 (95% CI = 2.0, 2.7), but decreased 1.6 points at age 18 (95% CI = −2.1, −1.2). IQs decreased 4.9 points for those with IQ ≤ 70 (95% CI = −4.9, −4.8), but increased 3.5 points among those with IQ ≥ 130 (95% CI = 3.4, 3.6). The Flynn Eﬀect was not meaningfully related to other background variables. Using the largest sample of US adolescent IQs to date, we demonstrate signiﬁcant heterogeneity in ﬂuid IQ changes over time. Reverse Flynn Eﬀects at age 18 are consistent with previous data, and those with lower ability levels are exhibiting worsening IQ over time. Findings by age and ability level challenge generalizing IQ trends throughout the general population.
The purpose of this study was to: (1) examine the associations of individual-level objective socioeconomic status (OSS), subjective socioeconomic status (SSS), and area-based indicators of socioeconomic status, with 12-month DSM-IV mood, anxiety, alcohol use, and drug use disorders; and, (2) determine the extent of racial/ethnic differences in these associations across non-Latino White, non-Latino Black, Latino, and Asian participants. Data are from the Collaborative Psychiatric Epidemiology Studies dataset, a collection of three population-based surveys of mental disorders among U.S. residents aged 18 and older (n = 13,775). Among all indicators of socioeconomic status, SSS was most consistently associated with 12-month mental disorders. Income was negatively associated with mood and anxiety disorders; education was negatively associated with alcohol use and drug use disorders. Significant interactions with race/ethnicity were found for the associations of socioeconomic indicators with anxiety, alcohol use, and drug use disorders but not with mood disorders. SSS was not associated with any of the 12-month mental disorders among Blacks. Education had stronger associations with 12-month anxiety and alcohol use disorders among Whites than among other racial/ethnic groups. Among Asians, low income compared to high income was associated with a lower risk of anxiety disorders and less than high school completion compared to college or more was associated with a lower risk of alcohol use disorders. Finally, tract-level income inequality was associated with a greater risk of drug use disorders only among Blacks. The patterns and magnitudes of the associations of individual-level and area-based socioeconomic indicators differed by type of disorder and race/ethnicity.
Adverse childhood experiences have been associated with more negative coupling between the ventromedial prefrontal cortex (vmPFC) and amygdala, a brain network involved in emotion regulation in both children and adults. This pattern may be particularly likely to emerge in individuals exposed to threatening experiences during childhood (e.g., exposure to child abuse), although this has not been examined in prior research. We collected functional magnetic resonance imaging data on 57 adolescents during an emotion regulation task. Greater negative functional connectivity between vmPFC and amygdala occurred during viewing of negative compared to neutral images. This vmPFC-amygdala task-related functional connectivity was more negative in adolescents exposed to physical, sexual, or emotional abuse than those without a history of maltreatment and was associated with abuse severity. This pattern of more negative functional connectivity was associated with higher levels of externalizing psychopathology concurrently and 2 years later. Greater negative connectivity in the vmPFC-amygdala network during passive viewing of negative images may reflect disengagement of regulatory responses from vmPFC in situations eliciting strong amygdala reactivity, potentially due to stronger appraisals of threat in children exposed to early threatening environments. This pattern may be adaptive in the short term but place adolescents at higher risk of psychopathology later in life.
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.