The Institute’s work on Telomeres bis DRAFT..

Telomeres shorten as we get older causing

aging in our cells.1,4,6

We inherit telomeres from our parents, but no matter the length of our telomeres at birth, everyone’s get shorter as they age.4,6

Shorter telomeres have a negative effect on our health.4,8

Telomere shortening is the main cause of age-related break down of our cells.2

When telomeres get too short, our cells can no longer reproduce, which causes our tissues to degenerate and eventually die.1,4

Some cells, like those found in the skin, hair and immune system, are most affected by telomere shortening because they reproduce more often.4,6

Short telomeres have been connected to premature cellular aging3,8

Mounting evidence shows a strong connection between short telomeres and aging in our cells3,4,5

There is scientific evidence that telomeres can be lengthened

An enzyme called telomerase can slow, stop or perhaps even reverse the telomere shortening that happens as we age.2,5 The amount of telomerase in our bodies declines as we age.4

Telomerase maintains and may even lengthen telomeres.2,5,6 Exposing human cells to telomerase slows cell aging and allows cells to begin copying again2 and longer telomeres cause gene expression to change to a younger phenotype which makes cells function as though they were younger.

There are other things we can do that might help restore telomere length or at least slow the loss of telomere length: reduce stress, stop smoking, lose weight, exercise more and eat a healthier diet.3,7,11



  1. Jaskelioff M, et al. Telomerase reactivation reverses tissue degeneration in aged telomerase-deficient mice. Nature. 2011;469:102–107.
  2. Sahin E, DePinho RA. Linking functional decline of telomeres, mitochondria and stem cells during ageing. Nature. 2010;464:520–528.
  3. Blackburn EH, Epel ES. Comment: Too toxic to ignore. Nature. 2012;490:169–171.
  4. Eisenberg DTA. An evolutionary review of human telomere biology: the thrifty telomere hypothesis and notes on potential adaptive paternal effects. American Journal of Human Biology. 2011;23:149–167.
  5. Oeseburg H, et al. Telomere biology in healthy aging and disease. Pflügers Archiv – European Journal of Physiology. 2010;459:259–268.
  6. Aubert G, Lansdorp PM. Telomeres and aging. Physiological Reviews. 2008;88:557–579.
  7. Ornish D. Effect of comprehensive lifestyle changes on telomerase activity and telomere length in men with biopsy-proven low-risk prostate cancer: 5-year follow-up of a descriptive pilot study. The Lancet Oncology. 2013;14(11):1112–1120.
  8. Armanios M, Blackburn EH. The telomere syndromes. Nature Reviews Genetics. 2012;13:693–704.
  9. Kaszubowska L. Telomere shortening and ageing of the immune system. Journal of Physiology and Pharmacology. 2008;59(Suppl 9):169–186.
  10. Valdes AM, et al. Telomere length in leukocytes correlates with bone mineral density and is shorter in women with osteoporosis. Osteoporosis International. 2007;18(9)1203–1210.
  11. Valdes AM, et al. Obesity, cigarette smoking, and telomere length in women. The Lancet. 2005;366(964)662–664.

The phenomenon of limited cellular division was first observed by Leonard Hayflick, and is now referred to as the Hayflick limit. In this perspective, significant discoveries were made by the team led by Professor Elizabeth Blackburn at the University of California (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”.

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.


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Disclaimer. This blog is educational and nothing therein should be construed to be medical advise.

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