Aubrey de Grey wrote:
>> Tom Matthews wrote:
>> > This is a reasonable way of looking at aging, IMO, except that we
> > *know* that mitochondrial mutations and free radical damage (and AGE
> > accumulation and many other things) *are* causal factors in normal
> > aging, whereas we do *not* know that telomere shortening is.
>> to which William wrote:
>> > Well, I believe that there is more than enough evidence to prove that
> > telomere shortening is a factor in human aging. What needs to be
> > determined is whether telomere shortening starts causing problems
> > after 100, 200, or 1000 years.
>> I'm very pleased that emphasis is being laid on the difference between
> showing that a phenomenon will eventually cause aging and showing that
> it causes aging in a currently normal lifetime. However, I'm afraid
> we do not yet know for certain that mitochondrial mutations are causal
> factors in normal aging (ie that they cause the macroscopic pathologies
> which comprise aging).
When I wrote the above statement, I knew that I might be slightly
overstating the case re mtDNA mutations. But is it not true, at least,
that mitochondrial "decline" (whether caused by mutations or not) is a
clear cause of some aging pathologies? The examples, of dimentia and
weakened hearts come to mind.
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