Average telomere length in at least some tissues makes a good marker for general health, but the progressive shortening of telomeres may or may not be a root cause of aging. Telomere length results from a dynamic system of lengthening and shortening processes, which seems more likely to be a reflection of underlying function and dysfunction: "In an ongoing study of almost 20,000 Danes, a team of researchers [have] isolated each individual's DNA to analyse their specific telomere length - a measurement of cellular aging. ... The risk of heart attack or early death is present whether your telomeres are shortened due to lifestyle or due to high age ... The recent Copenhagen General Population Study involved almost 20,000 people, some of which were followed during almost 19 years, and the conclusion was clear: If the telomere length was short, the risk of heart attack and early death was increased by 50 and 25 per cent, respectively. ... That smoking and obesity increases the risk of heart disease has been known for a while. We have now shown, as has been speculated, that the increased risk is directly related to the shortening of the protective telomeres - so you can say that smoking and obesity ages the body on a cellular level, just as surely as the passing of time. ... one in four Danes has telomeres with such short length that not only will they statistically die before their time, but their risk of heart attack is also increased by almost 50 per cent. Future studies will have to reveal the actual molecular mechanism by which the short telomere length causes heart attacks. Does one cause the other or is the telomere length and the coronary event both indicative of a third - yet unknown - mechanism?" I lean towards the latter hypothesis, that both risk of catastrophic failure in bodily systems and telomere length reflect levels of accumulated damage at the level of cells and macromolecules in the body.