By Kirsten West ND, Lac

Typically, when one hears the word telomere, one thinks of aging. At least those in the medical field. If you did not think of aging when you heard the word telomere- now you will.

Telomeres are involved not only in aging, our general health and longevity but also, in the development of cancer. It is easiest to think of telomeres as hats on our DNA. They protect our chromosomes from wear and tear, from the “weather” of the physiological environment.[i] Oxidative stress is one of the largest storms telomeres must withstand. The production of free radicals, byproducts of natural physiological processes, result in daily oxidative stress. Environmental stressors are also significant causes and these consists of (and are not limited to): smoking, obesity, lack of exercise (or too much exercise), and poor dietary habits.[ii] [iii] [iv] Of note, these things all promote inflammation. The more telomeres become taxed (shorten)- aging accelerates.[v] [vi] While our chronological age is measured by years, our biological age is measured by the length of our telomeres. I would consider the latter, the best representation of just how old we are.[vii] [viii] In other words, “How old would you be if you didn’t know how old you are?

If telomeres become damaged so too do our chromosomes, the very essence of our DNA.[ix] The fields of aging and focused longevity research have given great focus to telomeres. This is because the bigger and more protective our DNA hats/helmets (telomeres) are, the greater protection provided, the longer our chromosomes survive and so too, our lives and health. It makes sense that telomeres are seemingly the key to anti-aging. Unfortunately, with each cell division and replication, telomeres shorten.[x] Those telomeres of a 5yo look different than those of an 80yo and accordingly, those of a 30-year-old smoker, will look much different than those of a 30-year-old non-smoker. The more we age and the more oxidative stress our bodies undergo, the shorter the telomere. Notably, the immune system is one of the systems most sensitive to this (which is why the elderly are so prone to age related illness and disease). [xi] Bottom-line, when our telomeres are gone, we are gone.

Several supplements have been touted to extend the length and therefore lives, of telomeres. How well any of them actually work is the question and in many cases, there are likely differences on a case by case basis. As we continue to learn and be mindful of- what works for one does not necessarily work for another. One thing that seems to hold true across the board is the role of stress reduction and telomere longevity. The less stress the more protected and longer the telomeres.[xii] Meditation and gentle exercise may hold a true and very real physiological therapeutic advantage.

The key question becomes: what else can we do to help protect our telomeres and subsequently our ability to live longer and healthier lives? This of course, is desired. However, there is a caveat here. While telomere lengthening and protection may be a good thing in healthy cells, it is the very opposite, a very bad thing, in cancer cells. The longevity of cancer cells is obviously, not desirable. In fact, the lengthening of telomeres is one of the ways in which cancer cells become immortal. [xiii]

There has been considerable research in the world of telomeres and cancer. A recent study elucidates the additional roles telomeres may play in tumorigenesis (the creation and maintenance of a tumor cell). As noted above, oxidative stress has been shown to accelerate telomere shortening. However, when researchers decided to actually study what happens to telomeres when damaged by oxidative stress they found that instead of shortening, telomeres became longer. In fact, in an environment of oxidative stress, they found that the enzyme which is responsible for lengthening telomeres, Telomerase, continued to add more telomere building blocks in cancer cells. The question became, why did this happen? Especially when so much research has elucidated the role free radicals play in telomere demise.

In an effort to understand the primary components in telomere lengthening and the effect of oxidative stress on each one of these individually, the researchers isolated telomerase and the telomere building blocks. When the building blocks were exposed to oxidative stress (not telomerase) the telomeres were unable to lengthen. In other words, the actual telomere substrates (bricks and mortar) were too damaged. This may be the key to understanding just how oxidative stress causes aging AND most importantly, may offer a key to inhibiting telomere growth in cancer cells. If the building blocks can be damaged, cancer cells could become MORTAL.

As is seemingly obvious, more research is needed. Researchers are now trying to discover how to successfully manipulate oxidative stress and its target. Additional studies will involve the use of a photosensitizer which elicits damage directly to telomere substrates (the building blocks). If this can be accomplished, the ability to direct oxidative stress to specific cellular components may offer a novel therapeutic advantage in the treatment of cancer.

Not only does this research offer a new therapeutic tool, it also provides continued elucidation of the role global environmental stressors plays on our cells. This oxidative stress not only leads to telomere shortening (aging) but also the development of cancer. It is the “terrain” we must continually be mindful of.

The more we learn about what makes cancer and how these cells survive, we are offered continued and greater awareness to its prevention. It seems that quest for immortality may be overrated and the attention to the “terrain,” imperative.


[i] Blackburn EH, Epel ES. Comment: Too toxic to ignore. Nature. 2012;490:169-171.

[ii] Blackburn EH, Epel ES. Comment: Too toxic to ignore. Nature. 2012;490:169–171.

[iii] Aubert G, Lansdorp PM. Telomeres and aging. Physiological Reviews. 2008;88:557–579.

[iv] 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.

[v] Jaskelioff M, et al. Telomerase reactivation reverses tissue degeneration in aged telomerase-deficient mice. Nature. 2011;469:102-107.

[vi] Sahin E, DePinho RA. Linking functional decline of telomeres, mitochondria and stem cells during ageing. Nature. 2010;464:520-528.

[vii] Sahin E, DePinho RA. Linking functional decline of telomeres, mitochondria and stem cells during ageing. Nature. 2010;464:520–528.

[viii] Jaskelioff M, et al. Telomerase reactivation reverses tissue degeneration in aged telomerase-deficient mice. Nature. 2011;469:102–107.

[ix] Blackburn EH, Epel ES. Comment: Too toxic to ignore. Nature. 2012;490:169-171.

[x] 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.

[xi] Kaszubowska L. Telomere shortening and ageing of the immune system. Journal of Physiology and Pharmacology. 2008;59(Suppl 9):169-186.

[xii] Doheny K. (2011) Stress Reduction in Cancer Patients May Pay Off. WebMD. Retrieved from: http://www.webmd.com/cancer/news/20110401/stress-reduction-in-cancer-patients-may-pay-off?src=RSS_PUBLIC#1

[xiii] Fouquerel E, Lormand J, Bose A, Lee H, Kim G, Li J, Sobol R, Freudenthal B, Myong S, Opresko P. Oxidative guanine base damage regulates human telomerase activity Nature Structural & Molecular Biology. (2016). doi:10.1038/nsmb.3319. Published online 07 November 2016