Applying the social cognitive and sociological models of stigma to student attitudes towards major depression and bipolar disorder

Suzanne Brans

Research output: ThesisDoctoral Thesis

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The aims of the current research program were to examine the social-cognitive and sociological models of stigma in relation to student attitudes towards an individual experiencing a mood disorder. Two experiments (Studies 1 and 2) sought to empirically distinguish between controllability and responsibility, both constructs of the attribution model which is subsidiary to the social-cognitive model of stigma. Despite manipulating controllability, participants were reluctant to attribute controllability of cause to individuals experiencing depression or bipolar disorder. The stability of beliefs about the controllability of cause for condition onset was consistent with research suggesting that the Australian public increasingly conceptualise mental disorders in terms of biochemical and genetic causal factors. These findings, in combination with past research linking biogenetic beliefs to negative attitudes, resulted in a change in focus of investigation in Studies 3, 4, 5 and 6 to explain why, contrary to the prediction of the attribution model, biogenetic explanations of mental disorders are associated with the proliferation of stigma. To measure causal beliefs, the Causal Belief Inventory (CBI) was developed in Study 3 and refined in Study 4. The correlational results examined in Studies 4, 5 and 6 found that genetic and biochemical causal beliefs were associated with a number of positive attitudes towards individuals experiencing a mood disorder and that genetic cause was associated with a reduced implicit bias against major depression. Furthermore, each study pointed to the centrality of judgments of differentness in determining affective responses and direct and proxy measures of behaviour. In contrast, manipulation of genetic and psychosocial cause in Study 5 found that causal condition largely failed to impact upon student attitudes. Mediator analysis did, however, find that beliefs about the stability of the vignette actor's condition fully mediated the relationship between the negative influence of genetic cause on proxy helping behaviour. Manipulation of psychosocial, genetic and biochemical cause with the inclusion of a non-depressed control in Study 6 resulted in more ambiguous findings. The combination of findings from Studies 1 to 6 suggest that focusing on the impact of the controllability of cause of depression onset on student attitudes is unwarranted. Instead researchers and public health educators should be examining models which facilitate the examination of the cognitive factors that mediate these relationships. Two such models, namely the social-cognitive and sociological models of stigma, were found to adequately fit the data. Recommendations for integrating these two models of stigma are discussed.
Original languageEnglish
QualificationDoctor of Philosophy
Publication statusUnpublished - 2008


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