From: Phil Osborn (firstname.lastname@example.org)
Date: Sat Jan 05 2002 - 16:57:28 MST
The idea that there is an inverse correlation between aging versus cancer is hardly new. I understood that correlation from 1980, when the Chinese American researcher at the first Life Extension Foundation Conference at the Disneyland Hotel discussed his findings that cancer cells were not subject to the Hayflick limit. In the next instant, I recall thinking, "Ah, and that's because the Hayflick limit is the natural brake on cancer, and why childhood cancers are so deadly." There was also an sf short story from many years before that, in which a medical research scientist discovers how to prevent cellular dieoff, and then suddenly realizes to her horror that she has just ensured that she will get cancer.
The reason that this kind of idea has taken so long to reach the forefront of research consciousness is that so many of the major researchers were locked into the idea that there could not be such a thing as genetically programmed lifespan, as most individuals never get very close to death from senesense anyway. They pass on their genes while still young, so there's no evolutionary selection against aging.
The opposing argument, as propounded by W. Donner Denkla, was that species require a genetic turnover in order to shift to adapt to changing environments. If the turnover rate is too low, the species becomes extinct.
For example, suppose you had a species that could only reproduce reliably within a certain temperature range. There are two sets of genes in the species population. One sets the optimum temp high. The other sets it low. Having both genes results in a medium level. If you have fluctuating temperatures, then the expected period of fluctuation will interact with the genes to select for one or the other. But you need both genes in the population in sufficient numbers for the species to shift according to the temperature. If individuals are too long-lived compared to the rate of fluctuation in temperature, then you reduce the rate of reproduction.
The answer I always got to this line of argument, from the LE gurus of the 60's & 70's was that evolution only selected via individuals
>>(Damien Broderick cites a recent paper indicating p53 protects against tumors
in mice at the cost of speeding aging)
>CurtAdams@aol.com writes in reply on Fri Jan 04 2002 - 01:27:51 MST :
I don't think it's gloomy news. Basic population biology indicates aging
either serves some purpose useful for the aging individual or it's really,
really hard to fix. So, I expected this kind of thing. To really fix aging,
we must step outside of the box with cyborgization or cell line replacement
(either in vivo or ex vivo via organ replacement). This result actually
brings us a bit closer to the latter in that we have a slightly better
understanding of what must be fixed in the replacement line. Further, we may
be able to manipulate related systems in people to improve quality or
quantity of life in individual people. The systems should approach
optimality for a human hunter-gatherer but may be a bit off for our lives;
plus we can adjust the systems to deal with specific problems: de-age for
broken hips and prostatectomy; age for cancer treatment. >
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