Telomeres are protective lengths of material at the end of your chromosomes. Telomere length and aging are correlated, as are telomere length and health - in both cases the worse your situation, the shorter your telomeres:
Telomeres - the terminal caps of chromosomes - become shorter as individuals age, and there is much interest in determining what causes telomere attrition since this process may play a role in biological aging. The leading hypothesis is that telomere attrition is due to inflammation, exposure to infectious agents, and other types of oxidative stress, which damage telomeres and impair their repair mechanisms. Several lines of evidence support this hypothesis, including observational findings that people exposed to infectious diseases have shorter telomeres.
There are hints that shortened telomeres might be caused by damage to mitochondria, which is in turn a known root cause of many aspects of degenerative aging. In a recently published study, researchers found that telomere length in the oldest humans is still strongly correlated with health - suggesting that perhaps aging is not the primary correlation here.
Prior animal model studies have demonstrated an association between telomere length and longevity. Our study examines telomere length in centenarians in good health versus poor health. Using DNA from blood lymphocytes, telomere length was measured by quantitative polymerase chain reaction in 38 sex- and age-matched centenarians (ages 97-108).
"Healthy" centenarians (n = 19) with physical function in the independent range and the absence of hypertension, congestive heart failure, myocardial infarction, peripheral vascular disease, dementia, cancer, stroke, chronic obstructive pulmonary disease, and diabetes were compared to centenarians with physical function limitations and >/=2 of the above conditions (n = 19).
Healthy centenarians had significantly longer telomeres than did unhealthy centenarians (p =.0475). Our study demonstrated that investigations of the association between telomere length and exceptional longevity must take into account the health status of the individuals. This raises the possibility that perhaps it is not exceptional longevity but one's function and health that may be associated with telomere length.
This makes more sense if you think of aging as less of a process and more of an accumulation of biochemical damage. Telomere length seems to be a marker for your personal level of damage, possibly by virtue of its connections to one or more of the primary modes of damage. Many questions remain, however, as to where exactly it fits in the grand scheme of cause and effect.