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Relationships between psychological factors and immune dysregulation in context: a life-course approach -PhD thesis-


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The thesis provides evidence about relationships between adverse exposures, psychological responses to them and immune dysregulation. The approach taken is informed by theories about the life-course, the stress process, the stress response and the inflammatory theory of depression. The first two empirical chapters provide evidence about the contribution of psychosocial factors to immune dysregulation. Immune dysregulation is measured by onsets of asthma and rheumatoid arthritis during adulthood. Comprehensive life-course data are used to provide valuable evidence about the epidemiology of each disease. More specifically, new evidence is provided about the psychosocial pathways that lead to disease onset. After adjustment for material adversities, social adversities predict onsets of each disease. Chronic as opposed to acute adversities are salient for rheumatoid arthritis onset, which is consistent with existing theory that chronic stress contributes to immune dysregulation. Depressive symptoms mediate an association between childhood adversity and asthma onset decades later. A small but consistent association between depressive symptoms and asthma onset soon afterwards may reflect psychological consequences of chronic inflammation preceding asthma diagnosis. The third empirical chapter tests prospective associations between chronic inflammation and depressive symptoms. It finds that chronic inflammation predicts depressive symptoms and provides new evidence that these associations are mediated by factors associated with sickness behaviours. Findings indicate the relevance of psychosocial pathways to the development of immune-mediated diseases and the potential involvement of immune behaviours in psychological symptoms. Practitioners and policy makers working with people who have conditions characterised by immune dysregulation should consider the psychological predictors and consequences of immune dysregulation. More research in this area is needed and this would be facilitated by the development and inclusion in surveys of well-validated measures of psychological and biological stress and of the psychological and behavioural correlates of sickness behaviours thought to be induced by inflammation.


Psychology, Well Being, Health, Life Course Analysis, and Biology


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