X-Message-Number: 7786
From:  (Thomas Donaldson)
Subject: Re: Mr. Coetzee's comments and cloning
Date: Sat, 1 Mar 1997 11:22:26 -0800 (PST)

To Mr. Coetzee:

If I am to "keep up with the present state of knowledge" it would help if
you were to state just what that state is.

In any case, it's far from obvious that DNA damage (other than damage occurring
during the actual process) led to failures of cloning. One very basic fact
about our gametes (eggs and sperm) is that unlike our normal body cells, they
have whatever mechanisms which tone down DNA repair turned OFF. Before I would
simply conclude that the failed clones in the Scottish experiment failed
due to previous DNA damage, I'd want to know if the egg produced in these
experiments had normal DNA repair mechanisms FOR EGGS. It seems to me that
experiments to find that out should be quite possible.

Furthermore, so far as I understand it, gerontologists HAVE looked at the
lifespans of children born to their parents at high ages, and found at best
a very small shortening of lifespan: nothing that could be explained simply
by postulating that they had been created with aged, damaged DNA.

Telomeres do seem to play a role in this repair; but I would agree with Dr.
Strout that this role does not of itself mean that they bear on aging.

As for cloning, I can think of indirect ways it might bear on our study of
aging, but it will probably do very little directly. The major problem is
that our brains (and glands such as the pineal gland, together with the
hypothalamus (which is part of our brain)) play much more of a controlling
role than any changes to our body. This is shown by the results Pierpaoli
had when he transplanted old pineal glands into young mice: it shortened
their lives a good deal. Our hypothalamus, entirely part of our brain,
also puts out guiding hormones which activate/deactivate other glands,
but since it is a part of our brain its removal and replacement become
that much harder. Even for our pineal glands, our brain gets in the way
of the surgery Pierpaoli could do on mice.

In terms of the Hayflick theory, I personally think that there is a cascade
of different kinds of damage, not just one kind. For instance, even with
transplanted pineal glands, the recipient mice lived much longer but still
died. I doubt that the Hayflick theory bears on our PRESENT problems with
aging, but we may eventually find, once we can all live to 150, that we
bump up against IT, too. Not that we won't have means to deal with it by
then, but that it simply doesn't bear on earlier kinds of damage. And if
we really want to think about aging, it's quite pertinent that the genetic
experiments which produced long-lived animals have not produced animals for
which aging has been turned off completely.

Why do I believe in a cascade rather than one single explanation? Basically
because I doubt that aging results from any special trait promoted by
evolution. We age, and our caged lab animals age, because we and they have
lived beyond the ages at which most members of our species would have been
dead for other reasons in the wild. Mice, for instance, will only live for
a few months in the wild. Even for human beings, it has not been many
generations at all since (say before 1850) most people lived under conditions
which caused them to die before reaching age 60. The tiny upper class
(economically and politically) had no genetic impact on the rest of humanity.

If we believe this evolutionary explanation, then it would be very unlikely
that any one gene or process would account for our aging. Well, I believe
this evolutionary explanation.

			Best and long long life,

				Thomas Donaldson


Rate This Message: http://www.cryonet.org/cgi-bin/rate.cgi?msg=7786