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Given that aging is caused by the accumulation of random and pleiotropic
mutations that have not been selected against in the course of human
evolution (because until recently, humans mostly ended up dead from disease
or accident long before these mutations kicked in)...
Then, aging is not a single programmed pathway we can interfere in. It's
more like a network of interacting pathways, where the evolutionary rules
of thumb we use to make other biological puzzles tractable no longer apply.
What can be done.
1. Borrow the modelling tools and concepts from complexity theory and use
them to at least narrow the search-space for anti-aging treatments.
2. Just keep plowing ahead with the leads that look promising at the moment
and hope we get lucky. Hope that the pathways we happen to block in the
network of aging-related degenerations happen to be ones that influence a
large number of other pathways.
In the big picture, if our species manages to survive and remain civilized
long enough, there will be mild evolutionary pressure for our lifespan to
increase commensurate with our life expectancy. That's just blind evolution,
mind you. Directed evolution (i.e. continued molecular biology trial and
error) should proceed far faster. Of course I'm hoping that we don't have
to wait for the big picture, that we stumble onto a breakthrough before
it's liquid nitro time.
As for competing risks that were mentioned, Hayflick sounds pretty much
on target. Here are the mechanisms of 'death by old age' if/when cancer
and heart disease are eliminated:
1. NON-early onset Alzheimer's
2. Exhaustion of pluripotent stem cells due to Hayflick limit
- --
Terrorist Task Force 160 Randy Weaver Koresh
Why are the above words in my signature? Check out:
http://www.echelon.wiretapped.net
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This archive was generated by hypermail 2b30 : Mon May 28 2001 - 09:56:45 MDT