The ability to identify and label one’s emotions is associated with effective emotion regulation, rendering emotional awareness important for mental health. We evaluated how emotional awareness was related to psychopathology and whether low emotional awareness was a transdiagnostic mechanism explaining the increase in psychopathology during the transition to adolescence and as a function of childhood trauma—specifically, violence exposure. In Study 1, children and adolescents (N = 120, age range = 7–19 years) reported on emotional awareness and psychopathology. Emotional awareness was negatively associated with psychopathology (p-factor) and worsened across age in females but not males. In Study 2 (N = 262, age range = 8–16 years), we replicated these findings and demonstrated longitudinally that low emotional awareness mediated increases in p-factor as a function of age in females and violence exposure. These findings indicate that low emotional awareness may be a transdiagnostic mechanism linking adolescent development, sex, and trauma with the emergence of psychopathology.

{OBJECTIVE: Exposure to violence in childhood is associated with increased risk for multiple forms of internalizing and externalizing psychopathology. We evaluated how exposure to violence in early life influences neural responses to neutral and threat-related stimuli in childhood and adolescence, developmental variation in these associations, and whether these neural response patterns convey transdiagnostic risk for psychopathology over time. METHOD: Participants were 149 youth (75 female youth), ages 8 to 17 (M =12.8

Executive functions (EF), including working memory, inhibition, and cognitive flexibility, vary as a function of socioeconomic status (SES), with children from economically disadvantaged backgrounds having poorer performance than their higher SES peers. Using observational methods, we investigated cognitive stimulation in the home as a mechanism linking SES with EF. In a sample of 101 children aged 60–75 months, cognitive stimulation fully mediated SES-related differences in EF. Critically, cognitive stimulation was positively associated with the development of inhibition and cognitive flexibility across an 18-month follow-up period. Furthermore, EF at T1 explained SES-related differences in academic achievement at T2. Early cognitive stimulation—a modifiable factor—may be a desirable target for interventions designed to ameliorate SES-related differences in cognitive development and academic achievement.

Exposure to childhood adversity is common and associated with a host of negative developmental outcomes. The most common approach used to examine the consequences of adversity exposure is a cumulative risk model. Recently, we have proposed a novel approach, the dimensional model of adversity and psychopathology (DMAP), where different dimensions of adversity are hypothesized to impact health and well-being through different pathways. We expect deprivation to primarily disrupt cognitive processing, whereas we expect threat to primarily alter emotional reactivity and automatic regulation. Recent hypothesis-driven approaches provide support for these differential associations of deprivation and threat on developmental outcomes. However, it is not clear whether these patterns would emerge using data-driven approaches. Here we use a network analytic approach to identify clusters of related adversity exposures and outcomes in an initial study (Study 1: N = 277 adolescents aged 16–17 years; 55.1% female) and a replication (Study 2: N = 262 children aged 8–16 years; 45.4% female). We statistically compare our observed clusters with our hypothesized DMAP model and a clustering we hypothesize would be the result of a cumulative stress model. In both samples we observed a network structure consistent with the DMAP model and statistically different than the hypothesized cumulative stress model. Future work seeking to identify in the pathways through which adversity impacts development should consider multiple dimensions of adversity.

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.