Background. Disturbed immune activity and vascular inflammation are associated both with clinical depression and coronary atherogenesis, and may constitute a mechanism through which depression contributes to coronary heart disease. If this is the case, then non-clinical depressive symptoms and psychological distress should be associated with immune activation and vascular inflammation. We tested this hypothesis in a healthy middle-aged sample.
Method. Measures of depressive symptoms and hopelessness were obtained from 226 volunteers (122 men, 104 women) aged 47–59 years, drawn from the Whitehall II epidemiological cohort. C-reactive protein, fibrinogen, plasma interleukin-6, tumour necrosis factor alpha, interleukin-1 receptor antagonist, and T- and B-lymphocyte, and natural killer cells numbers and percentages were assessed.
Results. There were no associations between measures of depressive symptoms or hopelessness and markers of immune activation or inflammatory response.
Conclusions. Factors such as the measures of depressive symptoms, the choice of inflammatory and immune indices, and sample size, are unlikely to be responsible for these null effects. Associations may be confined to clinically depressed or older age populations, but there are problems of confounding by co-morbidity and health compromising behaviours in this literature. We conclude that disturbances of immune function and inflammatory processes are unlikely to be primarily responsible for the associations between depressive symptoms and coronary heart disease described in the literature, and that other pathways are involved.