This chapter presents a developmental psychopathology perspective on the emergence of major depression in children and adolescents. We highlight neurobiological, psychological, and social developmental processes that are involved in the etiology of child and adolescent depression and examine how the development of these systems is shaped by the social and environmental contexts in which children are embedded across time. We focus specifically on family, peer, and school contexts as well as broader social and ecological factors that can alter the developmental trajectories of these systems in ways that increase risk of depression during three specific developmental stages: early childhood, middle childhood, and adolescence.
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.
Early environmental experiences profoundly shape children's cognitive and neural development. In particular, cognitive stimulation, defined as environmental inputs that engage the senses and provide learning opportunities for children, fosters acquisition of knowledge across various cognitive domains. In humans, cognitive stimulation varies as a function of socioeconomic status that, on average, creates disparities in children's access to enriching experiences that provide the foundation for learning. Low levels of cognitive stimulation in early life restrict learning opportunities, resulting in lasting consequences for neural development and later academic and occupational achievement. This review delves into the role of cognitive stimulation on neural development and related cognitive performance, available tools for measuring cognitive stimulation in various settings, and offers insights into potential future research directions. We also leverage evidence from intervention studies to illustrate the importance of cognitive stimulation for children's outcomes. Investigating the influence of cognitive stimulation on children's brain and behavior development is crucial for developing effective intervention strategies to foster the healthy development of all children and unlocking their full potential.
Post-traumatic stress disorder (PTSD) should be one of the most preventable mental disorders, since many people exposed to traumatic experiences (TEs) could be targeted in first response settings in the immediate aftermath of exposure for preventive intervention. However, these interventions are costly and the proportion of TE-exposed people who develop PTSD is small. To be cost-effective, risk prediction rules are needed to target high-risk people in the immediate aftermath of a TE. Although a number of studies have been carried out to examine prospective predictors of PTSD among people recently exposed to TEs, most were either small or focused on a narrow sample, making it unclear how well PTSD can be predicted in the total population of people exposed to TEs. The current report investigates this issue in a large sample based on the World Health Organization (WHO)'s World Mental Health Surveys. Retrospective reports were obtained on the predictors of PTSD associated with 47,466 TE exposures in representative community surveys carried out in 24 countries. Machine learning methods (random forests, penalized regression, super learner) were used to develop a model predicting PTSD from information about TE type, socio-demographics, and prior histories of cumulative TE exposure and DSM-IV disorders. DSM-IV PTSD prevalence was 4.0% across the 47,466 TE exposures. 95.6% of these PTSD cases were associated with the 10.0% of exposures (i.e., 4,747) classified by machine learning algorithm as having highest predicted PTSD risk. The 47,466 exposures were divided into 20 ventiles (20 groups of equal size) ranked by predicted PTSD risk. PTSD occurred after 56.3% of the TEs in the highest-risk ventile, 20.0% of the TEs in the second highest ventile, and 0.0-1.3% of the TEs in the 18 remaining ventiles. These patterns of differential risk were quite stable across demographic-geographic sub-samples. These results demonstrate that a sensitive risk algorithm can be created using data collected in the immediate aftermath of TE exposure to target people at highest risk of PTSD. However, validation of the algorithm is needed in prospective samples, and additional work is warranted to refine the algorithm both in terms of determining a minimum required predictor set and developing a practical administration and scoring protocol that can be used in routine clinical practice.
Abstract Background Altered DNA methylation (DNAm) may be one pathway through which early-life adversity (ELA) contributes to adverse mental and physical health outcomes. This study investigated whether the presence versus absence of ELA experiences reflecting the dimensions of threat and deprivation were associated with epigenome-wide DNAm cross-sectionally and longitudinally in a community-based sample of children and adolescents. Methods In 113 youths aged 8–16 years with wide variability in ELA, we examined associations of abuse (physical, sexual, emotional; indicating threat-related experiences) and neglect (emotional, physical; indicating deprivation-related experiences) with DNAm assessed with the Illumina EPIC BeadChip array, with DNA derived from saliva. In cross-sectional epigenome-wide analyses, we investigated associations of lifetime abuse and neglect with DNAm at baseline. In longitudinal epigenome-wide analyses, we examined whether experiencing abuse and neglect over an approximately 2-year follow-up were each associated with change in DNAm from baseline to follow-up. Results In cross-sectional analyses adjusting for lifetime experience of neglect, lifetime experience of abuse was associated with DNAm for four cytosine-phosphodiester-guanine (CpG) sites (cg20241299: coefficient = 0.023, SE = 0.004; cg08671764: coefficient = 0.018, SE = 0.003; cg27152686: coefficient = − 0.069, SE = 0.012; cg24241897: coefficient = − 0.003, SE = 0.001; FDR < .05). In longitudinal analyses, experiencing neglect over follow-up was associated with an increase in DNAm for one CpG site, adjusting for abuse over follow-up (cg03135983: coefficient = 0.036, SE = 0.006; FDR < .05). Conclusions In this study, we identified examples of epigenetic patterns associated with ELA experiences of threat and deprivation that were already observable in youth. We provide novel evidence for change in DNAm over time in relation to ongoing adversity and that experiences reflecting distinct ELA dimensions may be characterized by unique epigenetic patterns.
Objective. Low socioeconomic status (SES) during childhood is associated with higher levels of youth psychopathology. However, limited longitudinal work has examined the role of both household and neighborhood SES in shaping mental health trajectories over time using large population-based data. The goal of the present study was to characterize associations between SES and changes in mental health problems during early adolescence.Methods. We investigated independent and joint associations of household income-to-needs ratio, parent educational attainment, material hardship, and neighborhood disadvantage with internalizing, externalizing, and attention symptom trajectories using longitudinal data from the Adolescent Brain Cognitive Development Study. Youth-reported mental health was assessed across six time-points from age 10 to 13 years (M=10.4, SD=0.63 years at T1, N=9,488) and SES was assessed six months prior to T1.Results. Main effects indicated that high SES was associated with lower mental health symptoms. However, longitudinally, higher SES was associated with greater increases in mental health problems over time. A higher income-to-needs ratio predicted greater increases in internalizing, externalizing, and attention problems. Two-way interactions between SES indicators predicting changes in symptoms were non-significant.Conclusion. Our finding that youth from higher-SES backgrounds exhibited greater increases in mental health problems during early adolescence contrasts with findings from prior cross-sectional studies. However, mental health problems are on the rise and the landscape of risk for psychopathology is changing. More research is needed to understand how childhood SES contributes to risk and resilience for psychopathology during the transition to adolescence.
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