Take the 2-minute tour ×
Biology Stack Exchange is a question and answer site for biology researchers, academics, and students. It's 100% free, no registration required.

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"?

share|improve this question
    
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. –  Rodrigo Feb 22 at 11:37
    
@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 –  brillout.com Feb 23 at 13:22
    
OK. I only wanted you to know what I think about this. –  Rodrigo Feb 23 at 18:37

2 Answers 2

up vote 7 down vote accepted

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

No.

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!"...

share|improve this answer
1  
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 !) –  Remi.b Dec 8 '13 at 12:55
    
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. –  hello_there_andy Dec 8 '13 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.

share|improve this answer

Your Answer

 
discard

By posting your answer, you agree to the privacy policy and terms of service.

Not the answer you're looking for? Browse other questions tagged or ask your own question.