Making detection of significant effects of age-related diseases more difficult: it may be unclear how much of the residual variance is explained by the disease and how much is attributable to error in the estimate of an age effect. This has been discussed in detail eleswhere. Recent human data have now established telomere attrition as a major risk factor for numerous diseases, including cardiovascular disease, hypertension, diabetes and end stage renal disease as well as being associated with elevated psychological stresses. Many such pathologies, showing an association with increased telomere attrition rates, are predominant in deprived communities where there is a higher prevalence of classical risk factors for disease, but this explanation does not account totally for these variations in disease incidence. One hypothesis for the increased disease prevalence in these communities is underlying chronic inflammation, a known component and predictor of CVD and diabetes, that is linked to a diverse range of pathologies. A possible contributory factor to generating an increased CPI-613 pro-inflammatory state, is accelerated biological ageing. Both telomere attrition and CDKN2A expression have been reported to show association with IL-6 levels in disease and ostensibly ‘healthy’ populations. Such associations are intuitive, as senescent cells upregulate and secrete pro-inflammatory cytokines as part of the senescent secretosome. A link between accelerated biological ageing and socioeconomic status has previously been reported by some, but not by others. The reasons for this equivocacy remain to be proven, but may be attributable to methodological differences. Any putative link, however, may be weak and open to multiple confounders, such as parental telomere length and epigenetic effects. We have chosen to evaluate the contribution of socio-economic factors to biological age, as measured by telomere length, in the extreme setting of the pSoBid cohort, to determine to what extent this in turn affects risk factors for ill health. It has been hypothesized that socio-economic deprivation can accelerate biological ageing, resulting in shorter telomeres in deprived individuals in comparison to more affluent-aged matched controls. Five previous studies examining this relationship report positive, null and negative associations. The equivocacy between these reports is possibly due to methodological differences, variations inherent in individual cohorts and in the veracity of subject answers relating to SES data.