The interplay between social factors and psychotic symptoms : Cognitive vulnerability and affective pathway in focus

Abstract

Psychotic disorder is a disabling mental disorder listed as the 8th leading cause of living with disability for people between the age of 15 and 44 according to the World Health Report by WHO in 2001. The question of what are the causes of psychotic disorder, however, remains elusive. Drawing from classic twin studies, psychotic disorder has been suggested to be highly heritable, but recent findings from genome wide association studies imply that this may have been overestimated. More recently, evidence has accumulated demonstrating the importance of environmental factors, particularly social factors. However, despite the numerous studies showing associations between various social factors and psychotic disorder, the mechanism that explains this relationship remains unclear. The present dissertation aimed to address these research gaps by testing hypotheses drawn mainly from two theoretical frameworks, the social defeat hypothesis and cognitive model of psychosis. The social defeat hypothesis argues that the common denominator of various apparently different social risk factors is the negative experience of being excluded from the majority group, and that this social defeat experience has a causal influence on psychosis. The first study in this dissertation tested this hypothesis by investigating whether various social adversities can be summed up into one latent common factor, and whether this factor has an effect on psychotic symptoms while controlling for its effect on depression and anxiety. Competing hypotheses arguing for the reverse effect were also tested. This first study was a cross-sectional survey in a community sample (N = 2350) from Germany (n = 786), Indonesia (n = 844), and the United States (n = 720). Confirmatory factor analysis (CFA) and path analysis with structural equation modeling were used to test the hypotheses. In the CFA two latent factors reflecting current and past experiences of social defeat could be identified with acceptable model fit. Path analysis indicated acceptable fit for both social defeat and reverse models, and both the path from current social defeat to psychotic symptoms and the reverse path were significant, although the reverse path was weaker. Interestingly, the current but not the past social defeat factor was significantly associated with psychotic symptoms. Overall, the results indicate that postulates derived from the social defeat hypothesis fit the data. The second study aimed to discover the psychological mechanisms explaining the association between social defeat and psychosis found in the first study. Drawing from cognitive model of psychosis, several putative mediators indicating cognitive vulnerability were tested. Specifically, based on the sample of the first study, low perceived social rank, negative schemas related to self-and other, and loneliness were tested as plausible mediators. Mediation path analysis with structural equation modeling was used. Social rank, negative schemas, and loneliness significantly mediated the relationship between social defeat and negative symptoms and the models explained a large amount of the variance (R2 = .43 - .44). For positive symptoms, only negative schemas were a significant mediator (R2 = .27). The results support the assumption that cognitive vulnerability is a relevant translating mechanism as postulated by cognitive models of psychosis. After discovering that negative-self schemas were the most important mediator, in the third study the postulate from cognitive models of psychosis that negative-self beliefs both cause and maintain psychotic symptoms via negative affect was examined. A longitudinal cohort design in a community sample (N = 962) from Germany, Indonesia, and the United States was used. Negative-self schema, negative affect, and psychotic symptoms were measured repeatedly every four months (baseline, 4-, 8-, and 12-months-follow-up). Cross-lagged panel and longitudinal mediation analyses with structural equation modeling were used. Independent cross-lagged panel models showed a significant unidirectional longitudinal path from negative-self schema to psychotic symptoms and bidirectional longitudinal associations between negative-self schema to negative affect, suggesting a vicious cycle of schema and affect. Furthermore, there was a significant indirect effect pathway of negative schema (baseline) via negative affect (4-months-follow-up), maintained over the course of eight months (8-months-follow-up) to psychotic symptoms (12-months-follow-up) suggesting mediation. Our findings support the postulated affective pathway from negative-self schema to symptoms. Specifically, negative-self schema and affect formed a vicious cycle building up over the course of several months, before impacting upon psychotic symptoms. Overall, the results contribute to extending the theoretical framework of social defeat hypothesis and cognitive models of psychosis. Importantly, psychological mechanisms of the relationship between social defeat and psychosis derived from cognitive models of psychosis were empirically found. In this regard, negative schemas were the most important mediator that transmitted its effect onto psychotic symptoms via negative affect. One clinical implication is that breaking the vicious cycle by targeting negative-self schema and negative affect in populations vulnerable to social defeat may be a viable prevention strategy. This approach may be guided by CBT techniques such as cognitive restructuring for negative schema and improving emotion regulation skills for negative affect.