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Early life adversity (ELA) is associated with sexual risk, but ELA dimensions—and potential mechanisms—have been less examined. We evaluated associations between threat and deprivation—two key ELA dimensions—and sexual behaviors in adolescents. Secondary analyses investigated age at menarche as a mechanism linking ELA with sexual outcomes in girls. We predicted associations between threat and sexual behaviors, with younger age at menarche as a pathway. Data were from the National Comorbidity Survey, Adolescent Supplement. Adolescents and caregivers reported on youths' ELA experiences, which were categorized as threat- or deprivation-related. Adolescents reported if they engaged in sex (N = 9,937) and on specific sexual risk indicators, including age at first sex, number of past-year sexual partners, and condom use consistency ("always" vs. "not always" used). Girls reported age at menarche. Threat (odds ratio [OR] = 1.76 [95% confidence interval [CI], 1.62–1.92]) and deprivation (OR = 1.51 [95% CI, 1.24–1.83]) were each linked with engagement in sex, p s<.05. Threat-related experiences were associated with multiple sexual risk markers, even when accounting for deprivation: earlier age at first sex (b = −0.20 [95% CI, −0.27 to 0.13]), greater number of partners (b = 0.17 [95% CI, 0.10–0.25]), and inconsistent condom use (OR = 0.72 [95% CI, 0.64–0.80]), p s <.001. Deprivation was not associated with sexual risk when adjusting for threat. We observed no significant indirect effects through age at menarche. Although threat and deprivation were related to engagement in sexual activity, threat-related experiences were uniquely associated with sexual risk. Screening for threat-related ELA may identify adolescents at-risk for poor sexual health. [ABSTRACT FROM AUTHOR]

We investigate whether neural, cognitive, and psychopathology phenotypes that are more strongly related to genetic differences are less strongly associated with family- and state-level economic contexts (N = 5374 individuals with 1KG-EUR-like genotypes with 870 twins, from the Adolescent Behavior and Cognitive Development study). We estimated the twin- and SNP-based heritability of each phenotype, as well as its association with an educational attainment polygenic index (EA PGI). We further examined associations with family socioeconomic status (SES) and tested whether SES-related differences were moderated by state cost of living and social safety net programs (Medicaid expansion and cash assistance). SES was broadly associated with cognition, psychopathology, brain volumes, and cortical surface areas, even after controlling for the EA PGI. Brain phenotypes that were more heritable or more strongly associated with the EA PGI were not, overall, less related to SES, nor were SES-related differences in these phenotypes less moderated by macroeconomic context and policy. Informing a long-running theoretical debate, and contra to widespread lay beliefs, results suggest that aspects of child brain development that are more strongly related to genetic differences are not, in general, less associated with socioeconomic contexts and policies. [ABSTRACT FROM AUTHOR]

Previously institutionalized adolescents show increased risk for psychopathology, though placement into high-quality foster care can partially mitigate this risk. White matter (WM) structure is associated with early institutional rearing and psychopathology in youth. Here we investigate associations between WM structure and psychopathology in previously institutionalized youth. Adolescent psychopathology data were collected using the MacArthur Health and Behavior Questionnaire. Participants underwent diffusion MRI, and data were processed using fixel-based analyses. General linear models investigated interactions between institutionalization groups and psychopathology on fixel metrics. Supplementary analyses also examined the main effects of psychopathology and institutionalization group on fixel metrics. Ever–Institutionalized children included 41 randomized to foster care (Mage=16.6), and 40 to care-as-usual (Mage=16.7)). In addition, 33 participants without a history of institutionalization were included as a reference group (Mage=16.9). Ever–Institutionalized adolescents displayed altered general psychopathology–fixel associations within the cerebellar peduncles, inferior longitudinal fasciculi, corticospinal tract, and corpus callosum, and altered externalizing–fixel associations within the cingulum and fornix. Our findings indicate brain–behavior associations reported in the literature may not be generalizable to all populations. Previously institutionalized youth may develop differential brain development, which in turn leads to altered neural correlates of psychopathology that are still apparent in adolescence. [ABSTRACT FROM AUTHOR]

Schools provide access to mental health services for traditionally underserved youth. However, there is variability in the types of school-based services students receive (e.g., school counseling, services in separate classrooms, or schools serving students with psychiatric disorders). Prior research has typically not distinguished among these different types of school-based services. The present study examines sociodemographic characteristics and disorders associated with the types of services received in schools. Data were analyzed from a sample of adolescent–parent pairs in the U.S. National Comorbidity Survey Adolescent Supplement who received school mental health services (N = 1,204). DSM-IV diagnoses were based on the Composite International Diagnostic Interview administered to adolescents and questionnaires self-administered to parents. Adolescents (aged 13–18 years) and parents also responded to questions about lifetime school-based mental health service receipt. Among those receiving school-based mental health services, almost one-third (29.7%) received services in a separate classroom and almost one-fourth (22.3%) in a separate school. Increased likelihood of lifetime placement in a separate classroom or school was detected among older youth, males, blacks, Latinos, youth with learning disabilities, those whose parents had fewer years of education, and those who received community-based mental health services. Oppositional defiant disorder was associated with increased lifetime placement in a separate school. The results advance the evidence base by indicating that racial/ethnic minority youth and those whose parents have fewer years of education were more likely to receive school-based mental health services in separate settings. These results provide more context to studies of school-based mental health service receipt. [ABSTRACT FROM AUTHOR]

• Hippocampus-dependent associative learning deficits may increase risk for PTSD. • Meta-analysis provides preliminary support for this novel conceptual model. • Identification of new mechanisms could inform development of PTSD interventions. • Offers a complementary perspective to prevailing threat models of PTSD. 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. [ABSTRACT FROM AUTHOR]

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. • Several clear developmental pathways link childhood adversity with psychopathology. • These include threat and reward processing and emotional reactivity and regulation. • We suggest intervention approaches to target these mechanisms. • Knowledge of learning mechanisms linking adversity and psychopathology is limited. • Emotional learning mechanisms provide clear targets for behavioral interventions. [ABSTRACT FROM AUTHOR]

Abstract 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 < 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 < 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. Highlights • Non-Latino Whites most likely to have 12-month disorders, even with SES controls. • Link between race/ethnicity and mood disorder varied by nativity among Whites. • Race/ethnicity interacted with education, but not income, to predict prevalence. • Racial/ethnic minority groups had more persistent mood disorders than Whites. • Observed links to persistent mood and substance disorders varied by education level. [ABSTRACT FROM AUTHOR]

Abstract The human brain is remarkably plastic. The brain changes dramatically across development, with ongoing functional development continuing well into the third decade of life and substantial changes occurring again in older age. Dynamic changes in brain function are thought to underlie the innumerable changes in cognition, emotion, and behavior that occur across development. The brain also changes in response to experience, which raises important questions about how the environment influences the developing brain. Longitudinal functional magnetic resonance imaging (fMRI) studies are an essential means of understanding these developmental changes and their cognitive, emotional, and behavioral correlates. This paper provides an overview of common statistical models of longitudinal change applicable to developmental cognitive neuroscience, and a review of the functionality provided by major software packages for longitudinal fMRI analysis. We demonstrate that there are important developmental questions that cannot be answered using available software. We propose alternative approaches for addressing problems that are commonly faced in modeling developmental change with fMRI data. [ABSTRACT FROM AUTHOR]

Background Earlier age of pubertal maturation in females is associated with increased risk for mental health problems in adolescence, compared with on-time or later maturation. However, most investigations of pubertal timing and mental health consider risk for individual disorders and fail to account for comorbidity. A latent-modeling approach using a large, nationally representative sample could better explain the transdiagnostic nature of the consequences of early-onset puberty. Methods Data on age of menarche and mental disorders were drawn from a population-representative sample of adolescents (n = 4925), ages 13–17. Confirmatory factor analysis was used to fit four latent disorder categories: distress, eating, and externalizing, and fear disorders. Timing of menarche included those with earlier (age ≤ 10, age 11) and later age of onset (age 13, 14 +), relative to those with average timing of menarche (age 12). Associations between timing of menarche and latent disorders were estimated in a structural equation model (SEM), adjusted for age, income, race, parent marital status, BMI, and childhood adversity. Results The measurement model evidenced acceptable fit (CFI = 0.91; RMSEA = 0.02). Onset of menarche before age 11 was significantly associated with distress disorders (coefficient = 0.096; p < 0.0001), fear disorders (coefficient = 0.09; p < 0.0001), and externalizing disorders (coefficient = 0.039; p = 0.049) as compared to on-time or late menarche. No residual associations of early menarche with individual disorders over and above the latent disorders were observed. Conclusion The latent modeling approach illuminated meaningful transdiagnostic psychiatric associations with early timing of menarche. Biological processes initiated at puberty can influence cognitive and affective processes as well as social relationships for adolescents. Under developmentally normative conditions, these changes may be adaptive. However, for those out of sync with their peers, researchers and clinicians should recognize the potential for these processes to influence liability to a broad array of psychopathological consequences in adolescence. [ABSTRACT FROM AUTHOR]

The human brain requires a wide variety of experiences and environmental inputs in order to develop normally. Children who are neglected by caregivers or raised in institutional environments are deprived of numerous types of species-expectant environmental experiences. In this review, we articulate a model of how the absence of cognitive stimulation and sensory, motor, linguistic, and social experiences common among children raised in deprived early environments constrains early forms of learning, producing long-term deficits in complex cognitive function and associative learning. Building on evidence from animal models, we propose that deprivation accelerates the neurodevelopmental process of synaptic pruning and limits myelination, resulting in age-specific reductions in cortical thickness and white matter integrity among children raised in deprived early environments. We review evidence linking early experiences of psychosocial deprivation to reductions in cognitive ability, associative and implicit learning, language skills, and executive functions as well as atypical patterns of cortical and white matter development—domains that should be profoundly influenced by deprivation through the learning and neural mechanisms we propose. These patterns of atypical development are difficult to explain with existing models that emphasize stress pathways and accelerated limbic system development. A learning account of how deprived early environments influence cognitive and neural development provides a complementary perspective to stress models and highlights novel pathways through which deprivation might confer risk for internalizing and externalizing psychopathology. We end by reviewing evidence for plasticity in cognitive and neural development among children raised in deprived environments following interventions that improve caregiving quality. [ABSTRACT FROM AUTHOR]

Heterotypic continuity, whereby individuals transition from one disorder to another, is common; however, longitudinal studies examining transdiagnostic predictors of heterotypic continuity are lacking. The current study examined whether trauma exposure during childhood (maltreatment) and adulthood (interpersonal and non-interpersonal trauma) is associated with heterotypic continuity in a national sample. Men and women (N = 34,653) who participated in Waves 1 (2001–2002) and 2 (2004–2005) of the National Survey of Alcohol and Related Conditions (NESARC) completed face-to-face interviews about trauma exposure and psychopathology. Risk ratios and population attributable risk proportions (PARPs) quantified the effects of childhood maltreatment and interpersonal and non-interpersonal trauma exposure between Waves 1 and 2 on risk for incident disorders and transitions between specific types of disorders. Twenty percent of respondents reported a Wave 2 incident disorder. Those with any Wave 1 disorder were at increased risk of incident mood (RR range = 1.2–2.1) and anxiety (RR = 1.5–2.7) disorders at Wave 2. Child maltreatment and interpersonal trauma exposure since Wave 1 were associated with roughly 50% of the risk for disorder transitions (RR range = 1.2–2.7); non-interpersonal trauma was associated with 30% of the risk for disorder transitions (RR range = 1.0–1.7). Findings suggest that new onset disorders were common in U.S. adults and trauma exposure explained a large proportion of disorder incidence as well as progression from one disorder to another. Universal prevention efforts that begin early in life, rather than those targeted at specific disorders, would be fruitful for reducing the burden of population mental health and preventing a cascade of mental disorders over the life course. [ABSTRACT FROM AUTHOR]

Earlier pubertal development appears to be one pathway through which childhood trauma contributes to psychopathology in adolescence. Puberty-related changes in neural networks involved in emotion processing, namely the amygdala-medial prefrontal (mPFC) circuit, may be a potential mechanism linking trauma and adolescent psychopathology. Our participants were 227 youth between 10 and 13 years of age who completed assessments of threat and deprivation-related experiences of adversity, pubertal stage, and internalizing and externalizing symptoms. A subset (n = 149) also underwent a functional MRI scan while passively viewing fearful and calm faces. Potential mechanisms linking childhood trauma with psychopathology, encompassing earlier pubertal timing and neural response to aversive stimuli were explored. Earlier pubertal development was associated with childhood trauma as well as increased externalizing symptoms in boys only. Earlier pubertal timing in males and females was negatively associated with activation in bilateral amygdala, hippocampal, and fusiform regions when comparing fearful and calm faces. However, amygdala-mPFC connectivity showed no association with pubertal timing or psychopathology symptoms. These findings do not support accelerated amygdala-mPFC development as a mechanism linking childhood trauma and psychopathology, but instead provide support for the role of pubertal development in normative decreases in limbic activation across development. • Earlier puberty mediates the link between trauma and externalizing problems in males. • Earlier puberty relates to reduced activation in amygdala, hippocampus, and fusiform gyrus to aversive stimuli. • Pubertal timing was not related to amygdala-mPFC connectivity. • These neural patterns are not a mechanism linking trauma and psychopathology. [ABSTRACT FROM AUTHOR]

The dimensional model of adversity proposes that experiences of threat and deprivation have distinct neurodevelopmental consequences. We examined these dimensions, separately and jointly, with brain structure in a sample of 149 youth aged 8–17—half recruited based on exposure to threat-related experiences. We predicted that greater threat would be uniquely associated with reduced cortical thickness and surface area in brain regions associated with salience processing including ventromedial prefrontal cortex (vmPFC), anterior cingulate cortex (ACC), and insula, and that deprivation experiences would be uniquely associated with reductions in cortical thickness and surface area in frontoparietal areas associated with cognitive control. As predicted, greater threat was associated with thinner cortex in a network including areas involved in salience processing (anterior insula, vmPFC), and smaller amygdala volume (particularly in younger participants), after controlling for deprivation. Contrary to our hypotheses, threat was also associated with thinning in the frontoparietal control network. However, these associations were reduced following control for deprivation. No associations were found between deprivation and brain structure. This examination of deprivation and threat concurrently in the same sample provided further evidence that threat-related experiences influence the structure of the developing brain independent of deprivation. • Threat-related experiences were associated with thinner cortex in multiple areas. • Threat-related thinning spanned salience, default, and somatomotor networks. • This thinning was robust to control for deprivation experiences. • Younger, threat-exposed participants had smaller amygdala volumes. [ABSTRACT FROM AUTHOR]

While most measures of working memory (WM) performance have been shown to plateau by mid-adolescence and developmental changes in fronto-parietal regions supporting WM encoding and maintenance have been well characterized, little is known about developmental variation in WM filtering. We investigated the possibility that the neural underpinnings of filtering in WM reach maturity later in life than WM function without filtering. Using a cued WM filtering task ( McNab and Klingberg, 2008 ), we investigated neural activity during WM filtering in a sample of 64 adults and adolescents. Regardless of age, increases in WM activity with load were concentrated in the expected fronto-parietal network. For adults, but not adolescents, recruitment of the basal ganglia during presentation of a filtering cue was associated with neural and behavioral indices of successful filtering, suggesting that WM filtering and related basal ganglia function may still be maturing throughout adolescence and into adulthood. [ABSTRACT FROM AUTHOR]

Understanding of human brain development has advanced rapidly as the field of developmental cognitive neuroscience (DCN) has matured into an established scientific discipline. Despite substantial progress, DCN lags behind other related disciplines in terms of diverse representation, standardized reporting requirements for socio-demographic characteristics of participants in pediatric neuroimaging studies, and use of intentional sampling strategies to more accurately represent the socio-demographic, ethnic, and racial composition of the populations from which participants are sampled. Additional efforts are needed to shift DCN towards a more inclusive field that facilitates the study of individual differences across a variety of cultural and contextual experiences. In this commentary, we outline and discuss barriers within our current scientific practice (e.g., research methods) and beliefs (i.e., what constitutes good science, good scientists, and good research questions) that contribute to under-representation and limited diversity within pediatric neuroimaging studies and propose strategies to overcome those barriers. We discuss strategies to address barriers at intrapersonal, interpersonal, community, systemic, and structural levels. Highlighting strength-based models of inclusion and recognition of the value of diversity in DCN research, along with acknowledgement of the support needed to diversify the field is critical for advancing understanding of neurodevelopment and reducing health inequities. • Understanding how cultural and contextual diversity shape neurodevelopment is critical. • Developmental cognitive neuroscience studies lack socio-demographic diversity. • We review barriers to increasing representation in pediatric neuroimaging studies. • A range of potential solutions to overcome barriers are presented. [ABSTRACT FROM AUTHOR]

Objective The strong associations between child maltreatment and psychopathology have generated interest in identifying neurodevelopmental processes that are disrupted following maltreatment. Previous research has focused largely on neural response to negative facial emotion. We determined whether child maltreatment was associated with neural responses during passive viewing of negative and positive emotional stimuli and effortful attempts to regulate emotional responses. Method A total of 42 adolescents aged 13 to 19 years, half with exposure to physical and/or sexual abuse, participated. Blood oxygen level–dependent (BOLD) response was measured during passive viewing of negative and positive emotional stimuli and attempts to modulate emotional responses using cognitive reappraisal. Results Maltreated adolescents exhibited heightened response in multiple nodes of the salience network, including amygdala, putamen, and anterior insula, to negative relative to neutral stimuli. During attempts to decrease responses to negative stimuli relative to passive viewing, maltreatment was associated with greater recruitment of superior frontal gyrus, dorsal anterior cingulate cortex, and frontal pole; adolescents with and without maltreatment down-regulated amygdala response to a similar degree. No associations were observed between maltreatment and neural response to positive emotional stimuli during passive viewing or effortful regulation. Conclusion Child maltreatment heightens the salience of negative emotional stimuli. Although maltreated adolescents modulate amygdala responses to negative cues to a degree similar to that of non-maltreated youths, they use regions involved in effortful control to a greater degree to do so, potentially because greater effort is required to modulate heightened amygdala responses. These findings are promising, given the centrality of cognitive restructuring in trauma-focused treatments for children. [ABSTRACT FROM AUTHOR]

Background Although only a few people exposed to a traumatic event (TE) develop posttraumatic stress disorder (PTSD), symptoms that do not meet full PTSD criteria are common and often clinically significant. Individuals with these symptoms sometimes have been characterized as having subthreshold PTSD, but no consensus exists on the optimal definition of this term. Data from a large cross-national epidemiologic survey are used in this study to provide a principled basis for such a definition. Methods The World Health Organization World Mental Health Surveys administered fully structured psychiatric diagnostic interviews to community samples in 13 countries containing assessments of PTSD associated with randomly selected TEs. Focusing on the 23,936 respondents reporting lifetime TE exposure, associations of approximated DSM-5 PTSD symptom profiles with six outcomes (distress-impairment, suicidality, comorbid fear-distress disorders, PTSD symptom duration) were examined to investigate implications of different subthreshold definitions. Results Although consistently highest outcomes for distress-impairment, suicidality, comorbidity, and PTSD symptom duration were observed among the 3.0% of respondents with DSM-5 PTSD rather than other symptom profiles, the additional 3.6% of respondents meeting two or three of DSM-5 criteria B–E also had significantly elevated scores for most outcomes. The proportion of cases with threshold versus subthreshold PTSD varied depending on TE type, with threshold PTSD more common following interpersonal violence and subthreshold PTSD more common following events happening to loved ones. Conclusions Subthreshold DSM-5 PTSD is most usefully defined as meeting two or three of DSM-5 criteria B–E. Use of a consistent definition is critical to advance understanding of the prevalence, predictors, and clinical significance of subthreshold PTSD. [ABSTRACT FROM AUTHOR]

A growing body of research has examined the impact of childhood adversity on neural structure and function. Advances in our understanding of the neurodevelopmental consequences of adverse early environments require the identification of dimensions of environmental experience that influence neural development differently and mechanisms other than the frequently-invoked stress pathways. We propose a novel conceptual framework that differentiates between deprivation (absence of expected environmental inputs and complexity) and threat (presence of experiences that represent a threat to one's physical integrity) and make predictions grounded in basic neuroscience principles about their distinct effects on neural development. We review animal research on fear learning and sensory deprivation as well as human research on childhood adversity and neural development to support these predictions. We argue that these previously undifferentiated dimensions of experience exert strong and distinct influences on neural development that cannot be fully explained by prevailing models focusing only on stress pathways. Our aim is not to exhaustively review existing evidence on childhood adversity and neural development, but to provide a novel framework to guide future research. [ABSTRACT FROM AUTHOR]

Over the past decade, a growing area of research has focused on adverse childhood experiences (ACEs) and their impacts on neural and developmental outcomes. Work in the field to-date has generally conceptualized ACEs in terms of exposure to stress while overlooking the underlying dimensions of environmental experience that may distinctly impact neural development. Here, we propose a novel framework that differentiates between deprivation (absence of expected cognitive and social input) and threat (presence of a threat to one's physical integrity). We draw support for the neural basis of this distinction from studies on fear learning and sensory deprivation in animals to highlight potential mechanisms through which experiences of threat and deprivation could affect neural structure and function in humans. [ABSTRACT FROM AUTHOR]

Background Children exposed to early-life psychosocial deprivation associated with institutional rearing are at markedly elevated risk of developing attention-deficit/hyperactivity disorder (ADHD). Neurodevelopmental mechanisms that explain the high prevalence of ADHD in children exposed to institutionalization are unknown. We examined whether abnormalities in cortical thickness and subcortical volume were mechanisms explaining elevations in ADHD among children raised in institutional settings. Methods Data were drawn from the Bucharest Early Intervention Project, a cohort of children raised from early infancy in institutions in Romania ( n = 58) and age-matched community control subjects ( n = 22). Magnetic resonance imaging data were acquired when children were aged 8 to 10 years, and ADHD symptoms were assessed using the Health and Behavior Questionnaire. Results Children reared in institutions exhibited widespread reductions in cortical thickness across prefrontal, parietal, and temporal regions relative to community control subjects. No group differences were found in the volume of subcortical structures. Reduced thickness across numerous cortical areas was associated with higher levels of ADHD symptoms. Cortical thickness in lateral orbitofrontal cortex, insula, inferior parietal cortex, precuneus, superior temporal cortex, and lingual gyrus mediated the association of institutionalization with inattention and impulsivity; additionally, supramarginal gyrus thickness mediated the association with inattention and fusiform gyrus thickness mediated the association with impulsivity. Conclusions Severe early-life deprivation disrupts cortical development resulting in reduced thickness in regions with atypical function during attention tasks in children with ADHD, including the inferior parietal cortex, precuneus, and superior temporal cortex. These reductions in thickness are a neurodevelopmental mechanism explaining elevated ADHD symptoms in children exposed to institutional rearing. [ABSTRACT FROM AUTHOR]

Summary: This study examined the contributions of a polymorphism of the corticotropin-releasing hormone receptor type I (CRHR1) gene (rs110402) and a history of child maltreatment—alone and in interaction—to patterns of cortisol reactivity in adolescents. Adolescents between the age of 13 and 17 years with (n =61) and without (n =97) a history of child maltreatment were exposed to the Trier Social Stress Test (TSST). Salivary cortisol was assessed at baseline, and 15 and 30min after the start of the speech portion of the TSST. Saliva samples for genotyping rs110402 also were collected. Adolescents with one or more G alleles of rs110402, relative to A allele homozygotes, and those exposed to maltreatment, relative to non-exposed adolescents, exhibited blunted cortisol reactivity to the TSST (although these associations approached, but did not reach, the level of statistical significance when accounting for underlying population structure in our racially and ethnically diverse sample). There was also a trend for a stronger child maltreatment association with cortisol hypo-reactivity among G allele carriers, but this association was not statistically significant. Findings suggest that CRHR1 variation may moderate the downstream effects of child maltreatment on HPA axis function, and implications for understanding mechanisms of risk associated with early adversity are discussed. [ABSTRACT FROM AUTHOR]

The COVID-19 pandemic has introduced widespread societal changes that have required ongoing adaptation. Unsurprisingly, stress-related psychopathology has increased during the pandemic, in both children and adults. We review these patterns through the lens of several leading conceptual models of the link between stress and psychopathology. Some of these models focus on characteristics of environmental stressors—including cumulative risk, specific stressor types, and stress sensitization approaches. Understanding the specific aspects of environmental stressors that are most likely to lead to psychopathology can shed light on who may be in most need of clinical intervention. Other models center on factors that can buffer against the onset of psychopathology following stress and the mechanisms through which stressors contribute to emergent psychopathology. These models highlight specific psychosocial processes that may be most usefully targeted by interventions to reduce stress-related psychopathology. We review evidence for each of these stress models in the context of other widescale community-level disruptions, like natural disasters and terrorist attacks, alongside emerging evidence for these stress pathways from the COVID-19 pandemic. We discuss clinical implications for developing interventions to reduce stress-related psychopathology during the pandemic, with a focus on brief, digital interventions that may be more accessible than traditional clinical services. • Stress-related psychopathology has increased during the COVID-19 pandemic. • Models of stressor types, buffers, and mechanisms can shed light on these patterns. • We review evidence for these models of stress during the pandemic. • Implications for interventions to reduce stress-related psychopathology are discussed. [ABSTRACT FROM AUTHOR]

Objective: Although exposure to potentially traumatic experiences (PTEs) is common among youths in the United States, information on posttraumatic stress disorder (PTSD) risk associated with PTEs is limited. We estimate lifetime prevalence of exposure to PTEs and PTSD, PTE-specific risk of PTSD, and associations of sociodemographics and temporally prior DSM-IV disorders with PTE exposure, PTSD given exposure, and PTSD recovery among U.S. adolescents. Method: Data were drawn from 6,483 adolescent-parent pairs in the National Comorbidity Survey Replication Adolescent Supplement (NCS-A), a national survey of adolescents aged 13 through 17 years. Lifetime exposure to interpersonal violence, accidents/injuries, network/witnessing, and other PTEs was assessed along with DSM-IV PTSD and other distress, fear, behavior, and substance disorders. Results: A majority (61.8%) of adolescents experienced a lifetime PTE. Lifetime prevalence of DSM-IV PTSD was 4.7% and was significantly higher among females (7.3%) than among males (2.2%). Exposure to PTEs, particularly interpersonal violence, was highest among adolescents not living with both biological parents and with pre-existing behavior disorders. Conditional probability of PTSD was highest for PTEs involving interpersonal violence. Predictors of PTSD among PTE-exposed adolescents included female gender, prior PTE exposure, and pre-existing fear and distress disorders. One-third (33.0%) of adolescents with lifetime PTSD continued to meet criteria within 30 days of interview. Poverty, U.S. nativity, bipolar disorder, and PTE exposure occurring after the focal trauma predicted nonrecovery. Conclusions: Interventions designed to prevent PTSD in PTE-exposed youths should be targeted at victims of interpersonal violence with pre-existing fear and distress disorders, whereas interventions designed to reduce PTSD chronicity should attempt to prevent secondary PTE exposure. [ABSTRACT FROM AUTHOR]

Background: Emerging evidence from general population studies suggests that lesbian, gay, and bisexual (LGB) adults are more likely to experience adverse cardiovascular outcomes relative to heterosexuals. No studies have examined whether sexual orientation disparities exist in biomarkers of early cardiovascular disease risk. Purpose: To determine whether sexual orientation disparities in biomarkers of early cardiovascular risk are present among young adults. Methods: Data come from Wave IV (2008–2009) of the National Longitudinal Study for Adolescent Health (N=12,451), a prospective nationally representative study of U.S. adolescents followed into young adulthood (mean age=28.9 years). A total of 520 respondents identified as lesbian, gay, or bisexual. Biomarkers included C-reactive protein, glycosylated hemoglobin, systolic and diastolic blood pressure, and pulse rate. Analyses were conducted in 2012. Results: In gender-stratified models adjusted for demographics (age, race/ethnicity); SES (income, education); health behaviors (smoking, regular physical activity, alcohol consumption); and BMI, gay and bisexual men had significant elevations in C-reactive protein, diastolic blood pressure, and pulse rate, compared to heterosexual men. Despite having more risk factors for cardiovascular disease, including smoking, heavy alcohol consumption, and higher BMI, lesbians and bisexual women had lower levels of C-reactive protein than heterosexual women in fully adjusted models. Conclusions: Evidence was found for sexual orientation disparities in biomarkers of cardiovascular risk among young adults, particularly in gay and bisexual men. These findings, if confirmed in other studies, suggest that disruptions in core physiologic processes that ultimately confer risk for cardiovascular disease may occur early in the life course for sexual-minority men. [ABSTRACT FROM AUTHOR]

Objective: Although schools are identified as critical for detecting youth mental disorders, little is known about whether the number of mental health providers and types of resources that they offer influence student mental health service use. Such information could inform the development and allocation of appropriate school-based resources to increase service use. This article examines associations of school resources with past-year mental health service use among students with 12-month DSM-IV mental disorders. Method: Data come from the U.S. National Comorbidity Survey Adolescent Supplement (NCS-A), a national survey of adolescent mental health that included 4,445 adolescent-parent pairs in 227 schools in which principals and mental health coordinators completed surveys about school resources and policies for addressing student emotional problems. Adolescents and parents completed the Composite International Diagnostic Interview and reported mental health service use across multiple sectors. Multilevel multivariate regression was used to examine associations of school mental health resources and individual-level service use. Results: Nearly half (45.3%) of adolescents with a 12-month DSM-IV disorder received past-year mental health services. Substantial variation existed in school resources. Increased school engagement in early identification was significantly associated with mental health service use for adolescents with mild/moderate mental and behavior disorders. The ratio of students to mental health providers was not associated with overall service use, but was associated with sector of service use. Conclusions: School mental health resources, particularly those related to early identification, may facilitate mental health service use and may influence sector of service use for youths with DSM disorders. [ABSTRACT FROM AUTHOR]

The article discusses research into the correlation between food insecurity in U.S. adolescents and mental disorders validated by the "Diagnostic and Statistical Manual of Mental Disorders," fourth edition (DSM-IV). It comments on adolescent-parent comorbidity and children's socioeconomic status (SES) as factors contributing to perceptions of food safety.

Abstract: The aim of the study was to examine the social networks of sexual minority youths and to determine the associations between social networks and depressive symptoms. Data were obtained from the National Longitudinal Study of Adolescent Health (Add Health), a nationally representative cohort study of American adolescents (N = 14,212). Wave 1 (1994–1995) collected extensive information about the social networks of participants through peer nomination inventories, as well as measures of sexual minority status and depressive symptoms. Using social network data, we examined three characteristics of adolescents'' social relationships: (1) social isolation; (2) degree of connectedness; and (3) social status. Sexual minority youths, particularly females, were more isolated, less connected, and had lower social status in peer networks than opposite-sex attracted youths. Among sexual minority male (but not female) youths, greater isolation as well as lower connectedness and status within a network were associated with greater depressive symptoms. Moreover, greater isolation in social networks partially explained the association between sexual minority status and depressive symptoms among males. Finally, a significant 3-way interaction indicated that the association between social isolation and depression was stronger for sexual minority male youths than non-minority youths and sexual minority females. These results suggest that the social networks in which sexual minority male youths are embedded may confer risk for depressive symptoms, underscoring the importance of considering peer networks in both research and interventions targeting sexual minority male adolescents. [Copyright &y& Elsevier]

Objectives: Lesbian, gay, and bisexual (LGB) populations exhibit elevated rates of psychiatric disorders compared to heterosexuals, and these disparities emerge early in the life course. We examined the role of exposure to early-life victimization and adversity—including physical and sexual abuse, homelessness, and intimate partner violence—in explaining sexual orientation disparities in mental health among adolescents and young adults. Methods: Data were drawn from the National Longitudinal Study of Adolescent Health, Wave 3 (2001–2002), a nationally representative survey of adolescents. Participants included gay/lesbian (n =227), bisexual (n =245), and heterosexual (n =13,490) youths, ages 18–27. We examined differences in the prevalence of exposure to child physical or sexual abuse, homelessness or expulsion from one's home by caregivers, and physical and sexual intimate partner violence according to sexual orientation. Next we examined the associations of these exposures with symptoms of psychopathology including suicidal ideation and attempts, depression, binge drinking, illicit drug use, tobacco use, alcohol abuse, and drug abuse. Finally, we determined whether exposure to victimization and adversity explained the association between sexual orientation and psychopathology. Results: Gay/lesbian and bisexual respondents had higher levels of psychopathology than heterosexuals across all outcomes. Gay/lesbian respondents had higher odds of exposure to child abuse and housing adversity, and bisexual respondents had higher odds of exposure to child abuse, housing adversity, and intimate partner violence, than heterosexuals. Greater exposure to these adversities explained between 10 and 20% of the relative excess of suicidality, depression, tobacco use, and symptoms of alcohol and drug abuse among LGB youths compared to heterosexuals. Exposure to victimization and adversity experiences in childhood and adolescence significantly mediated the association of both gay/lesbian and bisexual orientation with suicidality, depressive symptoms, tobacco use, and alcohol abuse. Conclusions: Exposure to victimization in early-life family and romantic relationships explains, in part, sexual orientation disparities in a wide range of mental health and substance use outcomes, highlighting novel targets for preventive interventions aimed at reducing these disparities. [Copyright &y& Elsevier]

Abstract: Introduction: Exposure to child maltreatment is associated with elevated risk for behavioral disorders in adulthood. One explanation for this life-course association is that child maltreatment increases vulnerability to the effects of subsequent stressors; however, the extent to which maltreatment increases sensitivity to social context has never been examined. We evaluated whether the association between neighborhood physical disorder and binge drinking was modified by child maltreatment exposure. Methods: Data were drawn from the Detroit Neighborhood Health Study, a prospective representative sample of predominately African Americans in the Detroit population. Neighborhood physical disorder was measured via systematic neighborhood assessment. Child maltreatment indicators included self-reported physical, sexual, and emotional abuse. Incident binge drinking was defined as at least one episode of ≥5 drinks (men) or ≥4 drinks (women) in the past 30-day period among those with no binge drinking at baseline (N =1013). Results: Child maltreatment and neighborhood physical disorder interacted to predict incident binge drinking (B =0.16, p =0.02) and maximum number of past 30-day drinks (B =0.15, p =0.04), such that neighborhood physical disorder predicted problematic alcohol use only among individuals with high exposure to child maltreatment. Conclusion: The results add to the growing literature that African Americans in the US are exposed to an array of stressors that have pernicious consequences for problematic alcohol use. Our results document the need for increased attention to the potential for at-risk alcohol use among populations with a high degree of stress exposure. [Copyright &y& Elsevier]

Background: Children raised in institutional settings experience marked deprivation in social and environmental stimulation. This deprivation may disrupt brain development in ways that increase risk for psychopathology. Differential hemispheric activation of the frontal cortex is an established biological substrate of affective style that is associated with internalizing psychopathology. Previous research has never characterized the development of frontal electroencephalogram asymmetry in children or evaluated whether adverse rearing environments alter developmental trajectories. Methods: A sample of 136 children (mean age = 23 months) residing in institutions in Bucharest, Romania, and a sample of community control subjects (n = 72) participated. Half of institutionalized children were randomized to a foster care intervention. Electroencephalogram data were acquired at study entry and at ages 30, 42, and 96 months. A structured diagnostic interview of psychiatric disorders was completed at 54 months. Results: Children exhibited increases in right relative to left hemisphere frontal activation between the second and fourth years of life, followed by an increase in left relative to right hemisphere activation. Children reared in institutions experienced a prolonged period of increased right hemisphere activation and a blunted rebound in left frontal activation. Foster care placement was associated with improved developmental trajectories but only among children placed before 24 months. The development trajectory of frontal electroencephalogram asymmetry in early childhood predicted internalizing symptoms at 54 months. Conclusions: Exposure to adverse rearing environments can alter brain development, culminating in heightened risk for psychopathology. Interventions delivered early in life have the greatest potential to mitigate the long-term effects of these environments. [ABSTRACT FROM AUTHOR]

Abstract: Although significant associations between childhood socio-economic status (SES) and adult mental disorders have been widely documented, SES has been defined using several different indicators often considered alone. Little research has examined the relative importance of these different indicators in accounting for the overall associations of childhood SES with adult outcomes. Nor has previous research distinguished associations of childhood SES with first onsets of mental disorders in childhood, adolescence, and adulthood from those with persistence of these disorders into adulthood in accounting for the overall associations between childhood SES and adult mental disorders. Disaggregated data of this sort are presented here for the associations of childhood SES with a wide range of adult DSM-IV mental disorders in the US National Comorbidity Survey Replication (NCS-R), a nationally-representative sample of 5692 adults. Childhood SES was assessed retrospectively with information about parental education and occupation and childhood family financial adversity. Associations of these indicators with first onset of 20 DSM-IV disorders that included anxiety, mood, behavioral, and substance disorders at different life-course stages (childhood, adolescence, early adulthood, and mid-later adulthood) and the persistence/severity of these disorders were examined using discrete-time survival analysis. Lifetime disorders and their ages-of-onset were assessed retrospectively with the WHO Composite International Diagnostic Interview. Different aspects of childhood SES predicted onset, persistence, and severity of mental disorders. Childhood financial hardship predicted onset of all classes of disorders at every life-course stage with odds-ratios (ORs) of 1.7–2.3. Childhood financial hardship was unrelated, in comparison, to disorder persistence or severity. Low parental education, although unrelated to disorder onset, significantly predicted disorder persistence and severity, whereas parental occupation was unrelated to onset, persistence, or severity. Some, but not all, of these associations were explained by other co-occurring childhood adversities. These specifications have important implications for mental health interventions targeting low-SES children. [Copyright &y& Elsevier]

Abstract: Background: Emotion regulation deficits have been consistently linked to psychopathology in cross-sectional studies. However, the direction of the relationship between emotion regulation and psychopathology is unclear. This study examined the longitudinal and reciprocal relationships between emotion regulation deficits and psychopathology in adolescents. Methods: Emotion dysregulation and symptomatology (depression, anxiety, aggressive behavior, and eating pathology) were assessed in a large, diverse sample of adolescents (N =1065) at two time points separated by seven months. Structural equation modeling was used to examine the longitudinal and reciprocal relationships between emotion dysregulation and symptoms of psychopathology. Results: The three distinct emotion processes examined here (emotional understanding, dysregulated expression of sadness and anger, and ruminative responses to distress) formed a unitary latent emotion dysregulation factor. Emotion dysregulation predicted increases in anxiety symptoms, aggressive behavior, and eating pathology after controlling for baseline symptoms but did not predict depressive symptoms. In contrast, none of the four types of psychopathology predicted increases in emotion dysregulation after controlling for baseline emotion dysregulation. Conclusions: Emotion dysregulation appears to be an important transdiagnostic factor that increases risk for a wide range of psychopathology outcomes in adolescence. These results suggest targets for preventive interventions during this developmental period of risk. [Copyright &y& Elsevier]

Abstract: The high rate of comorbidity among mental disorders has driven a search for factors associated with the development of multiple types of psychopathology, referred to as transdiagnostic factors. Rumination is involved in the etiology and maintenance of major depression, and recent evidence implicates rumination in the development of anxiety. The extent to which rumination is a transdiagnostic factor that accounts for the co-occurrence of symptoms of depression and anxiety, however, has not previously been examined. We investigated whether rumination explained the concurrent and prospective associations between symptoms of depression and anxiety in two longitudinal studies: one of adolescents (N = 1065) and one of adults (N = 1317). Rumination was a full mediator of the concurrent association between symptoms of depression and anxiety in adolescents (z = 6.7, p < .001) and was a partial mediator of this association in adults (z = 5.6, p < .001). In prospective analyses in the adolescent sample, baseline depressive symptoms predicted increases in anxiety, and rumination fully mediated this association (z = 5.26, p < .001). In adults, baseline depression predicted increases in anxiety and baseline anxiety predicted increases in depression; rumination fully mediated both of these associations (z = 2.35, p = .019 and z = 5.10, p < .001, respectively). These findings highlight the importance of targeting rumination in transdiagnostic treatment approaches for emotional disorders. [Copyright &y& Elsevier]

Background: More than half a million U.S. women and more than 100,000 men are treated for injuries from intimate partner violence (IPV) annually, making IPV perpetration a major public health problem. However, little is known about causes of perpetration across the life course. Purpose: This paper examines the role of “stress sensitization,” whereby adult stressors increase risk for IPV perpetration most strongly in people with a history of childhood adversity. Methods: The study investigated a possible interaction effect between adulthood stressors and childhood adversities in risk of IPV perpetration, specifically, whether the difference in risk of IPV perpetration associated with past-year stressors varied by history of exposure to childhood adversity. Analyses were conducted in 2010 using de-identified data from 34,653 U.S. adults from the 2004–2005 follow-up wave of the National Epidemiologic Survey on Alcohol and Related Conditions. Results: There was a significant stress sensitization effect. For men with high-level childhood adversity, past-year stressors were associated with an 8.8 percentage point (pp) increased risk of perpetrating compared to a 2.3 pp increased risk among men with low-level adversity. Women with high-level childhood adversity had a 14.3 pp increased risk compared with a 2.5 pp increased risk in the low-level adversity group. Conclusions: Individuals with recent stressors and histories of childhood adversity are at particularly elevated risk of IPV perpetration; therefore, prevention efforts should target this population. Treatment programs for IPV perpetrators, which have not been effective in reducing risk of perpetrating, may benefit from further investigating the role of stress and stress reactivity in perpetration. [ABSTRACT FROM AUTHOR]

The article presents a study on serious emotional disturbance (SED) among youths who are exposed to hurricane Katrina. It says that more than 1,000 persons were killed by the hurricane and caused property damage of 100 billion dollars. It states that 80% of individuals in hurricane-affected areas are experiencing psychological problems effect among children and adolescents. It mentions that traumatic stress disorder and aggressive behavior among children and adolescents were found.

Background: Children raised in institutional settings are exposed to social and environmental circumstances that may deprive them of expected environmental inputs during sensitive periods of brain development that are necessary to foster healthy development. This deprivation is thought to underlie the abnormalities in neurodevelopment that have been found in previously institutionalized children. It is unknown whether deviations in neurodevelopment explain the high rates of developmental problems evident in previously institutionalized children, including psychiatric disorders. Methods: We present data from a sample of children raised in institutions in Bucharest, Romania (n = 117) and an age- and sex-matched sample of community control subjects (n = 49). Electroencephalogram data were acquired following entry into the study at age 6 to 30 months, and a structured diagnostic interview of psychiatric disorders was completed at age 54 months. Results: Children reared in institutions evidenced greater symptoms of attention-deficit/hyperactivity disorder, anxiety, depression, and disruptive behavior disorders than community controls. Electroencephalogram revealed significant reductions in alpha relative power and increases in theta relative power among children reared in institutions in frontal, temporal, and occipital regions, suggesting a delay in cortical maturation. This pattern of brain activity predicted symptoms of hyperactivity and impulsivity at age 54 months, and significantly mediated the association between institutionalization and attention-deficit/hyperactivity disorder symptoms. Electroencephalogram power was unrelated to depression, anxiety, or disruptive behaviors. Conclusions: These findings document a potential neurodevelopmental mechanism underlying the association between institutionalization and psychiatric morbidity. Deprivation in social and environmental conditions may perturb early patterns of neurodevelopment and manifest as psychiatric problems later in life. [Copyright &y& Elsevier]

The article presents a study which assesses the prevalence of serious emotional disturbance (SED) among youths who were exposed to Hurricane Katrina. In this study, a survey among the residents of areas affected by the hurricane was conducted to assess hurricane-related stressors, the lifetime history of psychopathology of the respondents as well as the SED in their children. Results reveal a 14.9% prevalence rate of SED among youths exposed to Hurricane Katrina.

Abstract: Preliminary evidence supports the role of emotion-related deficits in generalized anxiety disorder (GAD), including heightened emotional intensity, poor understanding of emotion, negative cognitive reactivity to emotions, and maladaptive emotion management. However, questions remain concerning the specificity of these emotion-related deficits compared to highly comorbid conditions such as social anxiety disorder (SAD). In the current study, 113 undergraduate students were administered measures of GAD, SAD, and emotion-related factors in order to clarify relationships among these variables. In univariate analyses, presence of SAD did not significantly impact the association between GAD and the emotion-related measures. Further, a discriminant function analysis revealed that emotional intensity and impaired regulation strategies provided the greatest discrimination between groups and best predicted a diagnosis of GAD (regardless of SAD comorbidity). Although their discriminatory ability was weaker, poor emotional understanding best predicted a diagnosis of SAD (regardless of GAD comorbidity), and non-acceptance of emotions best predicted comorbid GAD and SAD. [Copyright &y& Elsevier]

Abstract: Purpose: Stressful life events represent potent risk factors for the development of internalizing symptoms among adolescents. However the mechanisms linking stress to adolescent psychopathology remain inadequately understood. This study examined the role of emotion dysregulation as a mechanism linking stress to changes in internalizing symptoms among adolescents. Methods: This study used a short-term longitudinal design. Stressful life events were assessed in a large diverse sample of adolescents (N = 1065), and emotion dysregulation and symptomatology outcomes were assessed at two subsequent time points. Structural equation modeling was used to examine the role of emotion dysregulation as a mediator of the association between stress and subsequent changes in internalizing symptoms. Results: Emotion dysregulation mediated the relationship between stressful life events and changes in internalizing symptoms over time. Sobel''s test indicated a significant indirect effect of stressful life events on subsequent symptoms of depression (z = 5.05, p < .001) and anxiety (z = 4.95, p < .001) through emotion dysregulation. Conclusions: Stressful life events appear to disrupt the adaptive processing of emotion among adolescents. Emotion dysregulation represents an intrapersonal mechanism linking stress to poor mental health outcomes. The implications for preventive interventions are discussed. [Copyright &y& Elsevier]

Abstract: The role of worry in generalized anxiety disorder (GAD) has been posited to serve as an avoidance of emotional experience, and emotion regulation deficits in GAD have been found in several previous studies. It remains unclear whether those with GAD experience more dysregulated emotions during periods of euthymia and positive affect or whether these deficits occur only during periods of worry. Individuals with GAD (with and without co-occurring dysphoria) and non-anxious controls were randomly assigned to receive a worry, neutral, or relaxation induction. Following the induction, all participants viewed a film clip documented to elicit sadness. Intensity of emotions and emotion regulation were examined following the induction period and film clip. The results revealed that, regardless of co-occurring dysphoria, individuals with GAD in the worry condition experienced more intense depressed affect than GAD participants in the other conditions and controls participants. In contrast, presence of worry appeared to have less impact on indices of emotion dysregulation, which were greater in participants with GAD compared to controls, but largely insensitive to contextual effects of worry or of relaxation. Following film viewing, both GAD participants with and without dysphoria displayed poorer understanding, acceptance, and management of emotions than did controls. However, acceptance and management deficits were most pronounced in individuals with both GAD and co-occurring dysphoria. Implications for the role of emotions in conceptualization and treatment of GAD are discussed. [Copyright &y& Elsevier]

The effects of worry and rumination on affective states and mentation type were examined in an unselected undergraduate sample in Study 1 and in a sample of individuals with high trait worry and rumination, high rumination, and low worry/rumination in Study 2. Participants engaged in worry and rumination inductions, counterbalanced in order across participants to assess main and interactive effects of these types of negative thinking. During mentation periods, the thought vs. imaginal nature and the temporal orientation of mentations were assessed 5 times. Following mentation periods, negative and positive affect, relaxation, anxiety, and depression were assessed. Both worry and rumination produced increases in negative affect and decreases in positive affect. Worry tended to generate greater anxiety, and rumination tended to generate greater depression. Interactive effects were also found indicating that worry may lessen the anxiety experienced during subsequent rumination. Moreover, worry lessened the depressing effects of rumination. Worry was associated with significantly greater thought than imagery, compared to rumination. Rumination involved a progression from mentation about the past to mentation about the future over time. Implications for understanding the generation of negative affect and comorbid anxiety and depression are discussed. [ABSTRACT FROM AUTHOR]

Children from low-socioeconomic status (SES) households on average exhibit lower academic achievement than their higher-SES peers. We investigated a novel hypothesis that differences in early-developing sensory networks—specifically the ventral visual stream (VVS), which is involved in processing visual stimuli—contribute to SES-related disparities in executive functions (EF) and academic outcomes. We used fMRI to investigate SES-related differences in neural function in children (6–8 years, n = 62) during two attentional tasks involving attention to visual information: cued attention and memory-guided attention. Recruitment of VVS during both tasks was associated with EF and academic achievement, and SES-related differences in VVS activation during cued attention were marginally explained by differences in cognitive stimulation. VVS activation during cued attention mediated SES-related differences in academic achievement. Finally, the link between VVS activation during both tasks and academic achievement was mediated by differences in EF. We extend previous work by highlighting that: (i) early-developing visual processing regions play a role in supporting complex attentional processes, (ii) childhood SES is associated with VVS function, which is explained in part by SES-related differences in cognitive stimulation and (iii) provide preliminary evidence that individual differences in VVS function may play a role in the emergence of the income-achievement gap. • The neural mechanisms explaining the income-academic achievement gap remain poorly understood. • We have proposed that early-developing visual processing may play an important role. • Ventral visual stream (VVS) activation was a mechanism in the income-achievement gap. • Cognitive stimulation marginally mediated the association between income and VVS activation. • Executive function (EF) mediated the link between VVS activation and academic achievement. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

• Processing of emotional facial expressions is important for social functioning. • Low socio-economic status impacts processing of emotional faces. • Exposure to violence impacts processing of emotional faces. • Amygdala response to angry faces positively correlated with both. • Multiple pathways to increased amygdala responsiveness exist. 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. [ABSTRACT FROM AUTHOR]