The interplay between social isolation and the immune system and the identification of underpinning mechanisms

The absence of social ties or contact with others has shown robust links with markers of inflammation but the mechanisms underpinning this link remain unidentified. Previous literature suggests that associations with inflammation and the mediating mechanisms are different for each social sphere. Stress-related processes and health behaviours have been proposed as underlying mechanisms. However, the conflation of different social spheres into a single measure of isolation and the lack of mediation studies may explain why the current body of literature is unable to identify the mechanisms that underpin isolation-inflammation links. Whilst addressing these limitations, this thesis empirically investigates the role of different mediating mechanisms in the link between isolation and immunity. In the second chapter, data from Understanding Society is used in cross-sectional pathway analysis to ascertain the role of health behaviours as a mediating mechanism. In chapter three, through the use of cross-sectional pathway analysis on data from the English Longitudinal Study of Aging (ELSA) which included cortisol data, the findings from the previous chapter were replicated and the role of stress responses as a mediator was investigated. Using data from ELSA and Understanding Society chapter four investigated the individual contribution of smoking, nutritional intake, alcohol consumption and exercise as mediators. In chapter 5 data from ELSA was used to investigate the directionality of the associations identified in the previous chapters. This thesis found that:1) health behaviours play a role in explaining the relationship between isolation and inflammation, 2) the relationship between isolation, inflammation and health behaviours varies with the social sphere missing ties and the marker of inflammation, and 3) the link between isolation and immunity made up of a network of bi-directional relationships that allow isolation to influence inflammation and vice versa. Recommended refinements to a popular social determinant of health framework are proposed.