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DNA and aging


lucaspa

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It seems a long thing to go over it (and I'm neither interested on the subject), but I've heard that our aging and our death is to prevent cancer.

When I heard this I found it ridiculous and still do, but I've heard it far too often to be ridiculous.

 

Then what about people who already have cancer?

 

Is there any truth in it?

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It seems a long thing to go over it (and I'm neither interested on the subject),

Then why did you bother to post in this thread?

 

 

but I've heard that our aging and our death is to prevent cancer.

When I heard this I found it ridiculous and still do, but I've heard it far too often to be ridiculous.

 

Then what about people who already have cancer?

 

Is there any truth in it?

 

You should open your own thread for such a discussion, unless you can show how it relates to one or more of the articles shared in the OP. :rolleyes:

 

 

 

For those interested in the genetics of aging, a recent issue of Nucleic Acids Research is devoted to the topic. You can read the articles free online at:

http://www.oxfordjournals.org/nar/for_authors/dna_aging_collection.html

 

Thanks for the link, Lucaspa. I am looking forward to reviewing some of these. :)

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It seems a long thing to go over it

 

I posted it as a resource for those who are interested. If you are not interested, then don't read the articles.

 

but I've heard that our aging and our death is to prevent cancer.

 

Absolutely not. Some cancers -- particularly osteosarcomas -- turn up in younger people.

 

The current theory is that cancers arise from adult stem cells that have lost their growth control. Our bodies have mechanisms to eliminate cancer cells early before they multiply and actually form a cancer. Remember, a cancer that is detectable as a lump or by CT or MRI has at least a billion cells in it.

 

However, no mechanism can be perfect and prevent every cell that loses growth control from eventually multiplying. Eventually a cell will arise that can get around all the mechanisms designed to kill it. Natural selection only cared about mechanisms that were good enough to get us past the age where we have kids. Natural selection is blind to what happens after that. Which explains why most cancers happen to people > 50 years of age: they have already had kids.

 

It is not possible to have a complex machine -- and organisms can be looked at as complex biochemical machines -- that can function forever. Despite the most elaborate repair processes, eventually an essential part will fail and the repair process will fail. A completely error-free machine or error-free repair process is not possible due to the 2nd Law of Thermodynamics.

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Thanks for replying to my question lucapsa, I appreciate it!

 

And iNow: "It's better to post in an existing thread than start a new one" - you ever heard this?.

 

What I posted was related to the subject of this thread, and opening a new thread would be absolutely unnecessary!

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ut I've heard that our aging and our death is to prevent cancer.

 

Actually I was quite dumbfolded when I first read that. Why should it be advantageous to die before getting cancer (dead is dead, you cannot reproduce either way). But after re-reading I am pretty sure that this statement is based on a simple misunderstanding (or maybe misformulating?). Essentially cell division (and cell aging) are strictly regulated (best known element is probably telomere shortening). In theory deregulated cells can divide longer and faster, though, which can reduce effects of aging. The downside is that this increases the risk of cancer.

 

So essentially there is a trade-off between cell aging and cancer, with the mechanisms selected to maximize the overall reproduction efficiency of the organism. Death by aging occurs almost by definition later, when (as lucaspa pointed out) reproductive abilities were reduced (or absent), anyway.

This is an example of the so-called antagonistic pleiotropy theory of aging, which states that pleiotropic alleles (in this case those controlling cell division) that increase survival/reproduction in early life but decrease the same at late life, can accumulate in a population because the selective advantages of the former outweigh the cost of the latter.

 

Under the so-called mutation accumulation theory it is assumed that deleterious alleles can accumulate if their negative effects are confined to the old age when the selective forces are lower.

 

If the first case was true that any change in genes involved in senescence will have an impact on early-life fitness (for example, increased cancer risk), whereas according to the second theory it would not be the case. As usual the in reality probably both effects play a role.

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