The present study has examined the relationship between biological ageing, SES and disease in participants in Glasgow, with documented health issues associated with social deprivation. Interestingly, in the light of possible confounders MK-1775 inhibitor relating to the veracity of SES data, employment status was reported to associate significantly with shorter telomeres, in a large cross sectional study from an overlapping demographic area. Surprisingly, despite the prevalence of CVD in this cohort and its proven association with SES, there were no other associations found with other markers of SES. Our data are not incongrous with previous reports, as we observed no associations with area based deprivation and employment. However, we have demonstrated a direct link between accelerated biological ageing, low income and poor diet. Furthermore, we have observed a relationship with a measure of adiposity, namely waist/hip ratio, a predictive measure for CVD and diabetes as well as all cause mortality in prospective studies. These observations are intuitive and in keeping with the Marmot findings who indicated that relative health inequalities are associated with SES. It is reasonable to assume that a low relative income means a decreased likelihood of being able to afford a good quality diet, leading to an acceleration in biological ageing. Poorer quality, fat and sugar rich diets, are known to result in the production of more reactive oxygen species, which directly cause DNA breaks that lead to gene malfunction, telomere attrition and disease. Notably, these observations indicating an interaction between biological ageing and SES are reinforced by the finding that telomere length, in the pSoBid cohort, associates positively with LDL cholesterol levels, a strong and unambiguous causal risk factor in CVD. In our study, telomere attrition was associated with increasing IL-6 levels, an emerging risk factor for CVD, which may predict fatal events more strongly than non-fatal events. The association of IL-6 with biological age is in keeping with recent observations indicating that senescent cells up-regulate and secrete IL-6. It would be expected, as a consequence of increased telomere attrition, that this group would have more senescent cells present and thus higher IL-6 levels and have an elevated risk of a range of conditions, if indeed IL-6 is causally related to CVD and diabetes. The association between accelerated biological ageing and increased IL-6 levels has been previously been reported to be linked with disease, general health and social deprivation.