When the telomerase enzyme is not active the telomere shortens every time the cell duplicates leading to a reproductive limit (Hayflicks limit). On one hand this is a believed reason for aging. On the other hand this makes a mutated cell more difficult to acquire cancer, since in order to become cancerous, it would need to mutate such that the telomere enzyme becomes active.

The telomere enzyme is not active in most human cells. Therefore activating the telomerase enzyme in somatic (body) cells could theoretically decrease aging but would also increase the risk of cancer.

Am I right to assume that in order to avoid aging of humans one would first need to "solve cancer"?

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    $\begingroup$ I've put an answer explaining why aging shouldn't be avoided in first place. It got an upvote, then it was closed by moderators, saying this is not a group about ethics, but about biology. If biology can be done without ethics, than we are able to watch yet some great nightmares. $\endgroup$
    – Rodrigo
    Feb 22, 2014 at 11:37
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    $\begingroup$ @Rodrigo I agree that avoiding aging is a highly ethical question. That said, my question targets the biology aspect and not the ethical aspect. Feel free to ask a question on the ethical/moral stackexchange $\endgroup$
    – brillout
    Feb 23, 2014 at 13:22
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    $\begingroup$ OK. I only wanted you to know what I think about this. $\endgroup$
    – Rodrigo
    Feb 23, 2014 at 18:37

3 Answers 3


Interesting question. My answer is no, but it requires a rather science-fiction style answer - at least it's beyond current technology, but here goes:

My Assumptions

I make the simplifying assumption that ageing is only related to telomere length. Thus by "avoid ageing" I assume you mean "avoid telomere shortening". Also to clarify things for others, I'll clear up the role of telomeres in aging and cancer:

Telomeres in cancer - it has been hypothesised that telomeres act as "mitotic clocks" - keeping track of how many times a cell can divide before it stops. This "time limit" is supposed to put a halt to cancerous cells before becoming malignant.

Telomeres in aging - Since telomeres set a limit to the number of times a cell can divide this essentially sets a time limit for the organism as a whole - those cells that divide faster (e.g. hair and skin cells) go out first (grey hair and wrinkles) etc.

Short answer


Long answer

All we need to do is come up with a way to somehow "maintain" average telomere length at some "safe" length, i.e. we keep them at a length that is long enough to prevent us from aging but short enough so that a cancerous cell will not be able to proliferate to dangerous numbers.

For example, every now and then we provide "telomere length booster jabs" (this is some abstract fictional idea of course). This is like adding more time to our lives when we are about to run out: "Oh look, I only have three months left!", "Don't you worry, with our new telomere booster jab you will have an extra 3 months!"...

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    $\begingroup$ Interesting answer. You give this assumption: "aging is only related to telomere length". Does is seem a reasonable assumption to you? What part of the variance in senecense in the human population has to be accounted to telomere length? (There are certainly not known answer !) $\endgroup$
    – Remi.b
    Dec 8, 2013 at 12:55
  • $\begingroup$ Great point you make, indeed it is murky waters for whether telomere length and aging are related to a significant degree. Here's the related discussion on stack: bit.ly/18tkAhp. I guess how relevant my answer here is, depends on the validity of the assumption of telomere length and aging I made. $\endgroup$ Dec 8, 2013 at 13:07

In short, yes.

The best way to think about ageing is as an accumulation of age-related disorders. Telomere loss is one of many cellular defects that accumulate with age. Other defects include oxidative stress, accumulation of amyloid proteins and metabolic dysfunction. While these are all likely related in some way, there is no evidence that specifically preventing telomere shortening would stop ageing. In fact, while telomere length is roughly correlated with age, it is not well correlated with such age-related disorders as Alzheimer's disease.

However, it is clear that loss of telomeres is a problem. Therapies that restore telomerase function will always run the risk of causing cancer. Most cells in the human body do not express telomerase, and those that do often do so transiently during times of replication. Introducing functional telomerase into new cells could only increase the risk of developing cancer. A generalized cure for cancer would make designing anti-telomere shortening therapies much easier, because listing cancer as a side effect would not be as ridiculous as it is today.

The way I see it is that cancer is just one of those many age-related disorders that comprises the term "ageing." Especially colorectal cancers have a strong association between onset and age, hence all the colonoscopies recommended after age 50. If colorectal cancer is so well associated with age, and there is a mechanism that ties the formation of cancer to the passage of time (the build up of deleterious mutations during the many divisions that occur in colonic crypts), then I think its safe to consider it a part of ageing.

In order to stop ageing, you have to stop all of the age-related disorders, and that includes cancer.


Not exactly. However, assuming that we will eventually be able to reverse the effects of aging, cancer formation will become much more rare as a by-product. The explanation for this is a bit involved, due to the complexity of the subject.

One of the most fundamental processes that drive human aging is the irreversible accumulation of genomic (and mitochondrial) DNA mutations. The reason for this is simply because it is extremely unlikely for DNA damage to get repaired by chance; DNA is the most complex molecule in any organism, and once information in it is lost for good, there is little hope that it will be reconstructed by random chemical reactions alone.

Other important forms of aging-associated degeneration include atherosclerosis, the formation of advanced glycation end-products, the accumulation of indigestible waste products within lysosomes as well as proteinopathies (although these can be caused by DNA mutations; see below) such as Alzheimer's disease. Telomere shortening can also be considered to be a form of aging-associated degeneration, but it is almost certainly not a central mechanism underlying any of the more noticeable aspects of the symptomatology of physiological aging due to its easily reversible nature (i.e. otherwise we would already have seen "immortals" appear due to random germline mutations causing overexpression of telomerase within stem cells).

While the accumulation of genomic DNA mutations eventually leads to carcinogenesis, cancer is actually a relatively unlikely consequence of this process, since multiple key mutations in several oncogenes/tumor suppressor genes tend to be necessary for transformation. As such, a much more likely (initial) consequence of the accumulation of DNA mutations would be the random inhibition of cellular functions by knock-out and modification of actively transcribed genes (or random activation of silent genes). This would explain why in old age, the body tends to be 'worn out' in general; if nearly all cells have some degree of dysfunction, we would naturally expect to see the body as a whole to perform poorly as well.

Also, even when enough mutations have accumulated to potentially cause cancer, usually, this ends up triggering the anti-cancer defenses of a cell and turn them senescent. When stem cells become senescent, they stop dividing. This would neatly explain why wounds and infections heal much slower in older individuals. In fact, it has been shown that hematopoietic stem cells lose their regeneration capacity over time, and that this is correlated with the accumulation of DNA mutations (Rossi et al. 2007).

In addition, random DNA mutations can also conceivably trigger proteopathies (e.g. Alzheimer's disease or idiopathic prion disease), since for many of these you only need one gene producing a 'bad version' of a protein to cause aggregation and cell death. Both prion proteins and amyloid-beta tend to be infectious (Jaunmuktane et al. 2015), so it is entirely possible that a single mutation in a single cell could trigger large-scale degeneration.

So, to stop aging, you would at least need to fix DNA damage periodically, and this would more or less prevent cancer as a by-product. However, I imagine it would be hard to repair the DNA damage in each and every cell in the body with a single treatment (e.g. with some kind of a viral correction therapy where the treatment is administered by intravenous injection, it would be extremely unlikely for the therapeutic agent to reach all cells every time, since there is a limit to how concentrated you can make it). As such, it would still be possible for a cancer to arise at some point, and in this sense, it is entirely possible for us to end up in a situation where we are able to reverse all aspects of biological aging, and yet people still die of aggressive cancers every now and then.


Jaunmuktane, Zane, et al. "Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy." Nature 525.7568 (2015): 247.

Rossi, D.J., Bryder, D., Seita, J., Nussenzweig, A., Hoeijmakers, J. and Weissman, I.L., 2007. Deficiencies in DNA damage repair limit the function of haematopoietic stem cells with age. Nature, 447(7145), p.725.


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