From: Robert J. Bradbury (bradbury@aeiveos.com)
Date: Fri Dec 06 2002 - 11:26:34 MST
On Thu, 5 Dec 2002, Reason wrote:
> ---> Joao Magalhaes
>
> > aging, the way I see it, aging is programmed into the genes--how else can
> > we explain the 25-fold difference in rate of aging between mice and
> > humans?
I wouldn't say "aging" is programmed into the genes but genomes are
programmed with other features that result in aging. So citing
some other examples in this thread -- mice have hair and are primarily
nocturnal animals so they do not really need extensive UV-damage DNA
repair systems (compared with humans who are primarily active in the
daytime). Lacking such systems might tend to increase their cancer rate
(if say there are environmental toxins cause damages similar to UV
radiation -- pure speculation) and thus tend to shorten their lifespans.
> Just to be contrarian, how about aging being a function of damage due to
> rate of energy processing? That doesn't have to be particularly genetic. I
> seem to recall that most mammals go through the same number of heartbeats in
> a lifetime (ballpark) irrespective of size.
It is much more complex than simple heartbeats. As Joao points out the
rate-of-living theory has some significant flaws.
I think I've pointed this out in a previous message, but in case people
haven't read it, I'll point it out again.
One of the major problems is double-strand-breaks corrupting the genetic code.
Both radiation and free radicals can produce DNA double strand breaks.
When this happens you have 2 possible repair paths. The first, homologous
recombination (HR), copies the genetic code from the sister chromosome and
can result in the copying of mutated/defective alleles or even incorrect
code (because of all of the similarity in the junk DNA in the genome).
This results in what is known as "gene conversion" and leads to cancer.
The second, non-homologous-end-joining (NHEJ), involves deleting, or in some
cases inserting, random amounts of DNA, and sticking the broken chromosome
back together. When this happens in the middle of a gene one is likely
to get a "broken" gene. This produces a protein which will not fold
properly and as these accumulate in the cell an increasing amount of
the cells energy is devoted to producing and breaking down these
defective proteins. I call this the "Energy catastrophe" hypothesis
of aging.
For the programmers on the list its simple --
"The code becomes corrupted".
The only way we are going to solve this is to find ways to introduce
greater redundancy and/or ECC into the code maintenence processes.
Robert
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