Average telomere length is presently measured in white blood cells from a blood sample. Telomeres, the caps of repeating DNA sequences that protect the ends of chromosomes, tend to become shorter on average with age, but also with illness: this is probably largely a reflection of stem cell activity (delivering new cells with longer telomeres) and cell division rates (telomere length reduces with each division) in the immune system, which in turn reflects some of the present state of health and age-related decline. This is a statistical observation, however, and it is has more than enough individual variation to be a pretty terrible measure of aging for any practical use. So it isn't unexpected to see observations like this one, in which average telomere length in immune cells is shown to have little to no relationship to a specific outcome in aging:
There is great interest in developing new biomarkers of cardiovascular risk that allow a more accurate risk predication than classical risk factors such as high cholesterol, smoking, physical inactivity, and high blood pressure. An estimated half of cardiovascular disease (CVD) patients do not have a high risk profile based on classical risk factors. Moreover, many individuals who score high for these risk factors do not develop the disease. There is therefore a clear need to find new biomarkers to enable the early identification of individuals who do not yet show disease symptoms but are at high risk of developing atherosclerosis and suffering a heart attack or stroke. One possible biomarker is telomere length, but a new study suggests that leukocyte telomere length (LTL) in circulating blood does not effectively predict CVD risk in individuals without disease symptoms. "These results are rather like taking a snapshot at a single point in a person's lifetime, and we still need to determine if atherosclerosis progresses faster in people who start with shorter leukocyte telomeres, have a higher proportion of very short telomeres, or in whom telomeres shorten at a faster rate during the aging process."
Numerous studies have demonstrated that telomere DNA shortens progressively as we age, leading to genomic instability and eventually cell death, especially when the telomeres become "critically" short. Telomere DNA shortening has come to be viewed as a marker not only of aging, but also of an individual's general state of health, and this has generated great interest in the possibility that telomere length in circulating white blood cells might predict the risk of CVD. This idea is supported by epidemiological studies demonstrating shorter LTL in patients suffering coronary artery disease, heart attack, or stroke. However, the results obtained to date are inconclusive, especially in relation to subclinical atherosclerosis. Moreover, there is a lack of information about the possible association of CVD with a high proportion of very short telomeres.
The new study included 1459 volunteers participating in the PESA (Progression of Early Subclinical Atherosclerosis) clinical trial. In the study, the research team explored whether mean LTL and the proportion of critically short telomeres show an association with the presence and extent of subclinical atherosclerosis. In line with previous studies, the results show an association between increasing age and a lower mean LTL and a higher proportion of short telomeres (defined arbitrarily as those measuring less than 3 kilobases). However, none of these parameters showed any association with the presence or extent of subclinical atherosclerosis in the PESA cohort.