On 4 Sep 1998 13:41:51 GMT, ag24 at mole.bio.cam.ac.uk (Aubrey de Grey)
>I wouldn't yet go quite so far as "because", but certainly there is a
>consensus that this is a large part of the reason.
You are correct. It might not be the only reason caloric restriction
lengthens life span but it may be one of the more important reasons.
>>I don't really agree. I think what would be much more interesting
>is to find out why (or how) caloric restriction reduces free radical
>damage. We haven't been very successful in reducing free radical
>damage by antioxidant therapy, for example; caloric restriction may
>be doing something we haven't thought of but which we could emulate.
I did not think that caloric restriction did anything to reduce free
radical damage except to make cells produce fewer free radicals. In my
opinion if we found out that CR was doing something else to actually
PREVENT the damage then that would be very interesting.
>>Certainly, masses. And yes, there is -- especially in the non-dividing
>cells and the ones that use a lot of oxygen.
Ok. Cool. Thanks for the info.
Here is a question that just popped in my mind: There is a lot of Free
Radical damage in human cells that accumilate over time. So, what
would it take to REPAIR all of this damage that has accumilated?
>>A fine theory except for the size of its gaps. We don't yet have any
>plausible, *detailed* hypothesis for a mechanism whereby short-telomered
>cells would produce more free radicals in such a way as to harm cells
>that aren't dividing. We're not exactly spoilt for detailed hypotheses
>whereby a small number of mitochondrially defunct cells would do this,
>either, but at least there's one (in my JAAM article). The importance
>of detail, of course, is that it gives both easier testability and more
>opportunity to design interventions.
Cool. Thanks for all the information.
>>Aubrey de Grey