Neighborhood conditions, neural circuits, and substance use behaviors across the early life course.

The etiology of substance use disorders (SUD, i.e., alcohol, cannabis, cocaine, opioids) are multifactorial, with risk factors including adverse social conditions, clinical comorbidities, neurodevelopmental influences, and genetic liabilities. However, little research has integrated data across these domains to study pathways of SUD risk. Given the changing landscape of cannabis legalization, the ongoing opioid crisis, and the decrease in life expectancy related to SUD, it is essential that we understand the etiologic pathways to SUD. While prior research shows a complex relationship, findings suggest that lower individual socioeconomic status, or SES (income, education, and employment), and contexts related to neighborhood SES (e.g., neighborhood disadvantage, residential segregation) are associated with greater risk of SUD, and that associations vary across sociodemographic characteristics and genetic vulnerabilities. Therefore, research utilizing sophisticated, longitudinal methods in representative samples is needed to examine the nature of the associations and interactions between individual and neighborhood social contexts and SUD. Atypical cognitive processing and development of neural communication have been widely documented both among those with SUD and those facing socioeconomic adversity. Our preliminary studies have used measures of EEG oscillatory activity (e.g., EEG functional connectivity, event-related oscillations during response inhibition) to demonstrate atypical neural networks in the resting state and during inhibitory control among individuals with SUD who have experienced early life adversity, with findings most prominent frontally in alpha frequency (8-12 Hz) and theta (3-7 Hz) frequency bands. Our data also established the first association with SUD polygenic scores and EEG connectivity, as well as differences by sex and throughout adolescence and young adulthood. However, it remains unclear how individual, family and neighborhood-level context influences neural communication and substance misuse across adolescent and young adult development, and how the associations may differ by genetic risk. This project will curate new neighborhood data to integrate alongside existing social, neurodevelopmental and genomic data from the Collaborative Study on the Genetics of Alcoholism (COGA)’s longitudinal, developmental study of adolescent and young adult offspring from families densely affected with SUD, to improve understanding of whether individual, family and neighborhood-level socioeconomic context influences neural communication across development and increases risk for SUD. Adding neighborhood-level data to COGA’s demographically and SUD enriched sample (DSM-5 alcohol use disorder: 40%, nicotine use disorder: 22%, cannabis use disorder: 32%, cocaine use disorder: 5%, opioid use disorder: 5%) with detailed assessments of individual-level social and economic adversity, EEG functional connectivity, and substance use behaviors/disorders, we will examine the influence of SES on trajectories of EEG activity and SUD from ages 12-34 in participants at high-risk for SUD, and the roles that sociodemographic characteristics and polygenic scores may play.