Adverse Experiences, Psychopathology, and Brain Morphology in Longitudinal Cohort Studies

Abstract

Exposure to adverse experiences in childhood, including trauma and poverty, is linked to increased risk for psychopathology, such as depression and posttraumatic stress disorder (PTSD) in adolescence and adulthood. While the long-term negative consequences of severe and chronic adversity on child development are well documented, there are still gaps in the literature about the underlying mechanisms or specific pathways that help explain childhood adversity’s impact on mental health outcomes in adolescence. More recently, especially with the availability of large cohort studies with imaging data, researchers have explored the role of brain structure. This dissertation investigates the associations between adverse childhood experiences, brain structure, and psychopathology using a large, longitudinal cohort study consisting of adolescents from the general population. Additionally, with the goal of understanding ways to prevent the development of posttraumatic psychopathology, I examine multilevel resiliency factors in the aftermath of trauma. In Chapter 1, I use the Adolescent Brain Cognitive Development (ABCD) Study to examine whether childhood poverty, measured by income-to-needs ratio, is associated with change in internalizing or externalizing problems over two years. Then, I use vertex-wise analyses to investigate the association between childhood poverty and cortical surface area, volume, and thickness. I test whether structural differences in cortical regions mediate the association between poverty and change in psychopathology in early adolescence. I show that indeed, childhood poverty is associated with structural differences in widespread regions. The association between poverty and increased externalizing problems was mediated by cortical regions that support executive functioning, decision making, visual and auditory processing, and emotion regulation. I find no evidence of poverty and change in internalizing problems over two years. In Chapter 2, I use the ABCD Study to investigate whether childhood trauma is related to change in psychopathology in early adolescence, and whether brain structure mediates this association. I define trauma in two ways; trauma defined broadly as adverse events, and violent trauma which consists of interpersonal threat-related events. Both measures of trauma were associated with increased internalizing and externalizing symptoms, but only violent trauma was associated with increase in psychotic-like experiences. While both measures of trauma were associated with structural differences in brain regions important for emotion regulation, pain, language, and more, after accounting for family income and material deprivation, only hippocampal volume remained associated with trauma. There was no evidence of mediation in the relationship between trauma and psychopathology by hippocampal volume. Finally in Chapter 3, I use data from the Advancing Understanding of RecOvery after trauma (AURORA) Study, which is comprised of adults who were presented to the emergency department after an acute traumatic event. The study uses two approaches to examine first the relative contributions of higher-order resiliency domains (individual vs. social) and second, more granular associations between specific resiliency factors within the domains and posttraumatic psychopathology. I found that higher-level social resiliency domain (consisting of emotional support, social engagement, and social network) was associated with lower depressive symptoms after 3 months, whereas the individual resiliency domain (consisting of trait resilience, mindfulness, and self-efficacy) was not. Within the social resiliency domain, emotional support and social network were protective against depression and PTSD. Within the individual resiliency domain, trait resilience and self-efficacy were protective, whereas mindfulness was associated with higher depressive and PTSD symptoms.