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, such as income, which may be confounded by undeclared income. The present study has examined the relationship between biological ageing, SES and disease in participants in Glasgow, a city with an extreme socioeconomic gradient, with documented health issues associated with social deprivation.
Interestingly, in the light of possible confounders relating to the veracity of SES data, employment status (men who reported being out of work) was reported to associate significantly with shorter telomeres 
, in a large cross sectional study from an overlapping demographic area (the WOSCOPS cohort). 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 (including educational attainment, employment status, area-based deprivation and physical stature measured as a proxy for early life social circumstances).
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 
. These observations are congruent with more extant inflammatory conditions in the most deprived, a situation exacerbated by increasing age.
Our findings suggest the unadjusted association between telomere length and IL-6 is strong, and it is still marginally significant with adjustment for age and gender. This association is only partially weakened by further adjusting for smoking but subsequent addition of deprivation, income and diet does not appear to weaken the IL-6-telomere association further (). In simple terms, these observations suggest that varying upstream factors drive both telomere shortening and elevated IL-6 levels. However, we cannot exclude the possibility that part of the mechanism for elevated IL-6 is via telomere shortening. Future studies need to explore this potential further, particularly as IL-6 is attracting increasing interest in the diabetes and CVD arenas 
Of the four previous studies in this field 
only two have indicated an association with SES. These comprised an analysis of female twins, where non manual workers had longer telomere lengths than manual workers 
. However, in analyses in which the authors used a more comprehensive range of SES categories, no evidence of a relationship was observed with biological age. The other, analysed Chinese men and indicated men with higher self-rated socioeconomic status have shorter telomeres 
. This was postulated as possibly being mediated through psychosocial, rather than lifestyle factors, or the presence of chronic disease. These authors also argue that there may be significant cultural, ethnic and age-related differences in social determinants of health.
The Q-PCR methodology employed in the present study yielded similar telomere length data in keeping with other reports 
using the same methodology. Our observations must also be viewed with reference to the fact that any differences reflect that PBL telomere length is neither an absolute, nor precise measure of biological ageing. The telomere lengths measured are an average and reflect a range of lengths in cells. A better measure may be an absolute marker of cellular growth arrest, such as CDKN2A 
. The use of such a marker would avoid the potentially confounding effects of differences in telomere length measurement methodology, that currently beset the field 
The difference in observations using telomere length as a marker of biological ageing, that have been reported by different groups have been elegantly summarised by Nordfjall et al 
. Our observations find consensus with those using a similar methodology, when applied to age, BMI, smoking, insulin, triglycerides and glucose. Our observations on the effect of smoking, however, maybe limited by lack of detailed information on smoking history.
We differ in the detections of associations with total and LDL cholesterol, though these have previously been reported to be associated with telomere length in a disease setting 
, along with IL6 
. These observations were also in keeping with concomitant elevation of DNA damage (as measured by 8-0H dG levels) in a specific disease cohort. However, our observations are consistent with previous biochemical analysis of the pSoBid cohort 
, which demonstrated that total cholesterol and LDL were inversely associated with deprivation. This is congruent with more extant inflammatory conditions in the most deprived, a situation exacerbated by increasing age. It is thus also in keeping with the observed elevation of IL-6 correlating with short telomeres.
Our observations provide an intuitive link between proven socio-economic drivers of disease 
and a biological phenomenon underlying any predisposition, or extant disease, namely cellular ageing. The tendency of our data to show faster ageing in those with lower socio-economic status, is indicative of this and reflects ‘more miles on the clock’ for these individuals.
This study may be limited by its size and cross sectional nature. Indeed, the social gradient in Glasgow is so extreme that a ‘survivor effect’ among the most deprived cannot be excluded. This merits a larger, longitudinal study to look at the relative impacts of further markers of SES and potential SE and lifestyle interventions. Such interventions are not without precedence and appear to show direct benefit to biological ageing. A recent intervention study in men with prostate cancer, reported that changing lifestyle, primarily via better diet and increased exercise leads to increased telomerase activity and deceleration of telomere attrition rate 
. A similar result in the pSoBid cohort would be expected to have significant health benefits.
In summary, we show convincingly that factors associated with lower socio-economic status and poor diet are relevant to accelerated biological ageing in a cohort representing extremes of social class. Our findings also suggest potential associations of elevated circulating IL-6, a measure known to predict CVD and diabetes, with biological ageing, observations which require further study to tease out potential mechanistic links.