Benson Steven Ku

Based on the social disorganization theory, Chapters 2 and 3 empirically investigate measured area-level social fragmentation and psychosis-related outcomes. Chapter 2 provides an extension of prior research on the social determinants of psychosis, showing that childhood exposure to socially fragmented neighborhoods plays a causal role in psychotic disorders. The impact might not be immediate but surfaces later in life, affecting school adaptation in childhood and leading to poor social functioning in adulthood. Such association is greater among those who are at clinical high risk for psychosis (CHR-P) compared to healthy controls. Chapter 2 establishes a notable framework that disrupted social functioning might be a key factor linking social fragmentation and the onset and risk for psychosis. Youth at CHR-P might struggle to connect with others. Living in socially fragmented neighborhoods might hinder or delay the development of social skills, potentially resulting in poor school adaptation. These early signs may act as social stressors, initiating social withdrawal, marginalization, and poor social skill development during adolescence, closer to the onset of psychosis.

From a neurobiological perspective, Chapter 3 shows that area-level residential instability is associated with reduced gray matter volumes in brain areas involving exposure to social stress. The fact that residential instability likely impacts these brain regions among both CHR-P individuals and healthy controls indicates that this detrimental social-environmental factor is generalized and not only specific to the development of psychosis. These two chapters demonstrate that exposure to cumulative social stressors from area-level social fragmentation might impact social functioning through chronic adverse social experiences and lead to neurobiological changes in the brain.

Chapters 4, 5, and 6 investigate the potential protective role of social engagement in the development of psychosis in the CHR-P cohort (Chapters 4 and 5) and a large national sample of children (Chapter 6). Chapter 4 provides novel evidence of the role of social engagement in moderating the relationship between neighborhood poverty and reduced hippocampal volume among individuals at CHR-P. In particular, no association between neighborhood poverty and hippocampal volume was found among those with high levels of social engagement. In contrast, the association was pronounced among those with low levels of social engagement. These results suggest that the adverse effects of neighborhood poverty on brain morphology might be especially prominent among some but not others. Perhaps social engagement may mitigate the detrimental effects of neighborhood poverty on brain morphology, especially for those at CHR-P, which may inform potential interventions.

Chapter 5 investigates neurobiological correlates of exposure to ethnoracial minority density during childhood. In this study, I found that lower levels of childhood ethnoracial minority density, indexed as the proportion of residents who did not identify as White non-Hispanics in the neighboring area, were associated with lower cortical thickness of critical regions implicated in social cognitive functioning (right fusiform gyrus and right insula). Furthermore, I demonstrated the potential moderating role of social engagement, such that this association is only significant among youth with low social engagement, suggesting that high social engagement may reduce the effect of ethnoracial minority density on cortical thinning among minority youth at CHR-P.

Chapter 6 presents another line of evidence of the moderating role of social-physical activities in the association between polygenic risk score for schizophrenia (PRS-SCZ) and the trajectories of distressing psychotic-like experiences (PLE) using a large national longitudinal dataset. PRS-SCZ was positively associated with persistently distressing PLE at 3-year follow-up, and levels of social-physical activities (those that involve teamwork and social interactions), as opposed to non-social-physical activities, were significantly associated with lower risk for persistently distressing PLE. Findings from Chapter 6 demonstrate a potential gene X environment interaction such that positive social interactions might attenuate psychotic-like experiences among youth who are genetically vulnerable to psychosis.