The phenomenon of limited cellular division was first observed by Leonard Hayflick, and is now referred to as the Hayflick limit. Significant discoveries were made by the team led by Professor Elizabeth Blackburn at the University of California, San Francisco (UCSF).
Advocates of human life extension promote the idea of lengthening the telomeres in certain cells through temporary activation of telomerase (by drugs), or possibly permanently by gene therapy. They reason that this would extend human life. So far these ideas have not been proven in humans.
However, it has been hypothesized that there is a trade-off between cancerous tumor suppression and tissue repair capacity, in that lengthening telomeres might slow aging and in exchange increase vulnerability to cancer (Weinstein and Ciszek, 2002).
A study done with the nematode worm species Caenorhabditis elegans indicates that there is a correlation between lengthening telomeres and a longer lifespan. Two groups of worms were studied which differed in the amount of the protein HRP-1 their cells produced, resulting in telomere lengthening in the mutant worms. The worms with the longer telomeres lived 24 days on average, about 20 percent longer than the normal worms.
Techniques to extend telomeres could be useful for tissue engineering, because they might permit healthy, noncancerous mammalian cells to be cultured in amounts large enough to be engineering materials for biomedical repairs.
However, there are several issues that still need to be cleared up. First, it is not even certain whether the relationship between telomeres and aging is causal. Changing telomere lengths are usually associated with changing speed of senescence. This telomere shortening, however, might be a consequence of, and not a reason for, aging.
That the role of telomeres is far from being understood is demonstrated by two recent studies on long-lived seabirds. In 2003, scientists observed that the telomeres of Leach's Storm-petrel (Oceanodroma leucorhoa) seem to lengthen with chronological age, the first observed instance of such behaviour of telomeres. In 2006, Juola et al. reported that in another unrelated, long-lived seabird species, the Great Frigatebird (Fregata minor), telomere length did decrease until at least c.40 years of age (i.e. probably over the entire lifespan), but the speed of decrease slowed down massively with increasing ages, and that rates of telomere length decrease varied strongly between individual birds. They concluded that in this species (and probably in frigatebirds and their relatives in general), telomere length could not be used to determine a bird's age sufficiently well. Thus, it seems that there is much more variation in the behavior of telomere length than initially believed.
The telomere length varies in cloned animals. Sometimes the clones end up with shorter telomeres since the DNA has already divided countless times. Occasionally, the telomeres in a clone's DNA are longer because they get "reprogrammed". The clone's new telomeres combine with the old ones, giving it abnormally long telomeres.
In 2008, UCLA and Sierra Sciences confirmed two different small molecule compounds that activated Telomerase. Sierra Sciences, a biotechnology company in Reno, NV, has discovered a small-molecule, drug-like compound that turns on the expression of telomerase in human cells. Their scientists are presently characterizing its mechanism of action. While UCLA confirmed a small-molecule extract from a plant, that turns on the expression of telomerase in human cell.
In 2008, Dr. Dean Ornish of the Preventive Medicine Research Institute (Sausalito, CA) and colleagues at the University of California at San Francisco conducted a study of 30 men with low-risk prostate cancer on the possible effects of lifestyle changes on telomeres. The findings of the study were published in The Lancet Oncology. The men were asked to make several lifestyle changes, including attending a three-day retreat; eating a diet low in refined sugars and rich in whole foods, fruits, and vegetables, with only 10 percent of calories derived from fat; and engaging in several other activities, such as moderate aerobic exercise, relaxation techniques and breathing exercises. Telomerase levels were measured at baseline, and again after three months, when researchers discovered that, in the 24 participants with sufficient data for analysis, telomerase in the blood had increased by 29 percent. The authors commented that "The implications of this study are not limited to men with prostate cancer. Comprehensive lifestyle changes may cause improvements in telomerase and telomeres that may be beneficial to the general population as well." In a cautionary note due to the limited nature of the pilot study, the authors indicated the link between lifestyle changes and increases in telomerase activity was reported as "significant association rather than inferring causation" until wider studies are completed.