A Neuroecological Approach to Examining the Effects of Early Life Adversity on Adolescent Drug Use Vulnerabilities Using the ABCD Dataset

Early life adversity (ELA) is a multidimensional and potent risk factor for neurocognitive risk, downstream drug use vulnerabilities, and adolescent drug use and misuse. The effects of ELA on youth’s drug use risk depend on multiple dynamic family, peer, school, community, and demographic risk and protective contexts. Yet, a significant knowledge base is missing to further our understanding of the contexts in which neural biomarkers affect drug risk vulnerabilities and behaviors in adolescence. Emerging research and theory implicate neuroregulatory systems that underpin emotion and behavioral regulation as a powerful focus for adolescent drug use risk investigations. We focus on individual differences in neuroregulatory systems whereby cognitive control networks become more effective over time in modulating emotion processing networks, including the emotion/salience and reward salience networks. According to this dual system view, a neuroregulatory imbalance between the socioemotional network (or ERSN, comprised of the emotional, reward, and salience networks) and CCN ushers in diminished self-regulation abilities that underlie drug risk behaviors in adolescence. This developmental mechanism and subsequent risk behaviors may be differentially affected by youth’s dimensional stress. Extant developmental studies have cataloged psychosocial risk and protective processes that moderate the impact of ELA and the development of drug use vulnerabilities in adolescence. Yet ecological approaches remain rare in neuroscience approaches. Using a developmental ecological neuroscience approach, we propose to investigate neurocognitive mechanisms that mediate, and the contextual factors that moderate, the effect of ELA on drug-related vulnerabilities and drug use. We will focus on the impact of ELA on developmental changes in functional activation and communication (i.e., functional connectivity; FC) between the ERSN and CCN networks and its mechanistic role in leading to adolescent drug use vulnerabilities and later drug use. We propose to use a large, longitudinal dataset: the Adolescent Brain Cognitive Development Study (ABCD; N=11,883; ages 9-10 at baseline and 11.5-12.5 at wave 6). We aim to test (a) the developmental cognitive mechanisms that mediate the effect of ELA on drug use vulnerabilities and attendant drug use and misuse (b) the moderating influence of family, peer, school, community, and developmental contexts on the neurocognitive processes that lead to drug use vulnerabilities. Modeling multilevel latent change in ecological, behavioral, and neuroimaging data is critical to further the precision and specificity of developmental models and preventative intervention programs for drug addiction resilience in adolescence.