Re: Telomeres and stuff

From: Robert J. Bradbury (
Date: Sun Apr 30 2000 - 22:09:28 MDT

On Sun, 30 Apr 2000, John Clark wrote:

> In the April 28 issue of "Science" ,the one about the improvement
> in cloning technology, I found the following two paragraphs, they
> seem important to me, I'd like somebody to tell me why I'm wrong.

John, its a rare day when you are "wrong"... :-)

> " Another sign that the cloning process had somehow turned back
> the clock on the animals' cells came when the team cultured
> fibroblasts, a type of connective tissue cell, from the calves' ears.
> The cells expressed high levels of a gene called EPC-1, which is
> typically found at high levels in young cells and may be involved in
> cell division and proliferation."
> An imperial result independent of telomeres that seems to indicate
> the cells really are more youthful, or rather act more youthfully.

I have absolutely no problem with the fact that they have increased
telomere length and maybe even have (accidentally) flipped a switch
favoring the maintenence and repair common in "youth" over the diversion
of resources into reproduction (common in early adults).

However, that is a *far cry* from keeping alive an organism
over many years (where background radiation plays a significant

> "In a related experiment, the team cloned five calf fetuses from adult cells
> kept in culture until senescence. They removed the fetuses at 6 weeks
> of gestation so they could compare their cells with those of normal fetal
> calves. The clones' cells divided an average of 93 times compared to
> only 61 for cells from normal calves. If this increased life-span extends
> to the whole animal, Lanes says, there is "a real possibility" that cloned
> animals might live as much as 50% longer than their normal counterparts
> --up to 180 to 200 years in the case of humans--an idea, he says, that
> "is going to raise an eyebrow or two.""
> That's even more direct evidence. I grant you it still doesn't prove the
> entire animal will live longer but it does give considerable weight to
> that idea; and a increase from 61 to 93 divisions is not small and is not
> theoretical, it's a concrete experimental result.

No argument. So I'll live to 150 with skin cells that are "pretty"
(execpt where they are malignant), and with intestinal and stomach
cells that are "pretty" (except where they are malignant) and with
a very robust immune system (except where they are malignant).

Ever since Fossil's book, everyone has thought that "aging" is
associated with telomere shortening and quite simply that is crap.

> I know Robert Bradbury has expressed some contempt for this work but
> I confess I just don't understand why. Perhaps the effect was caused
> because the telomeres got longer, perhaps it was caused by something else,
> but whatever the reason the result if true is pretty damn interesting.
> And I happen to think it probably is true, I mean It's not like the report
> came out of The National Enquirer, "Science along with "Nature" are the
> two most respected science journals in the world.

I agree that the journals are reputable and the experimental results
are valid (with the caveats previously mentioned).

When you look at aging, the way to look at it is *What makes people die?"*.
The #1 cause of death is heart disease followed by cancer. Heart disease
is usually an "overproliferation" disease (too many platelets or endothelial
cells causing clots), as is cancer. The "underproliferation" diseases
(such as poor nutritional absorption in the oldest-old due to a failure
of cell division in the gut) are a distinct minority. Stroke, is also
sometimes an "underproliferation" disease as cells at "high stress points"
in the arteries wear out their telomeres, cease division, eventually become
senescent, and presumably die or fail to maintain structural integrity
in the long term.

The essence of longevity in humans is for cells to divide enough
in situations where replacements are needed and to never divide
where local functions are sufficient.

So I view any solution that lengthens telomeres, particularly
without knowing the underlying mutational load that has been
incorporated into the genome as a very mixed blessing,

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