Endocannabinoids Mediate Racial/Ethnic Discrimination Prediction of Post-Traumatic Stress Disorder Symptoms Moderated by Resting-State Functional Connectivity in Black and African American Individuals.

Abstract

Background: Individuals from marginalized ethnoracial groups face higher risk for posttraumatic stress disorder (PTSD) symptoms, exacerbated by experiencing racial/ethnic discrimination. Prior work separately explored the endocannabinoid (eCB) system and functional connectivity response to stress/trauma, and suggests that experiences of chronic minority stress, such as racial discrimination, contribute to eCB tone and resting state functional connectivity. We explored how circulating eCB tone, in conjunction with resting-state connectivity, contributes to increased risk for PTSD symptoms following trauma among individuals experiencing discrimination.

Methods: Black/African Americans (n=74, Mage=33.81) were recruited from a Level 1 trauma center. Correlational and linear models explored whether experiences of racial/ethnic discrimination (PEDQ), eCB (AEA, 2-AG) concentrations, default mode network (DMN), or salience network (SN) functional connectivity were associated with PTSD symptoms (PCL-5). We then explored moderated mediation models where discrimination predicted PTSD symptoms with eCB concentration as a mediator and functional connectivity as a moderator.

Results: Discrimination was correlated with PTSD symptoms (r=0.50), serum AEA concentration (r=0.43), and DMN connectivity (r=0.23). When including urine THC, lifetime trauma, age, and sex as covariates, AEA concentration was associated with PTSD symptoms (r=0.30) and DMN connectivity (r=0.24). AEA mediated the relationship between discrimination and PTSD symptoms, and SN connectivity moderated this mediation (B=52.46).

Conclusions: Our findings highlight how racial/ethnic discrimination impacts neurobiological systems that may lead to increased vulnerability for PTSD symptoms following an injury. Future work should continue to explore biological factors associated with the social-ecological model of health as mechanisms of risk for adverse outcomes following trauma.