X-Message-Number: 10617
Date: Tue, 20 Oct 1998 10:23:00 -0400
From: Thomas Donaldson <>
Subject: CryoNet #10610 - #10615

Hi everyone!

To Peter Merel:
It is a fundamental tenet of economics, with which I agree, that there
will ALWAYS be scarcity in some form or another. No technology will
change that tenet, it will simply modify what is scarce and what is
not. As an example, suppose we really could duplicate any piece of
matter at all. What would be scarce? The design of a new kind of
object ie. to be simple, we can easily duplicate our 1998 model cars,
but what about the next model? Someone will have to design it first.
And so we would have an economy in which the first model of anything
could be duplicated indefinitely --- but the scarcity would consist
of the lack of new things to duplicate.

Even Nanotechnology as believed in by its proponents will have this
particular problem, plus the problem of getting the necessary raw
materials, to. And probably the issue of where to put these things,
also (even a nanosized X takes up some space, after all). Yes, it 
would not look like our present economy, but there would definitely
be scarcity.

Finally, you raise another problem which is important to cryonics:
who would revive you. This comes down to another kind of scarcity:
we will never know how to make ourselves live literally forever.
Therefore there will continue to be risks of death, for which 
some form of cryonics (however far evolved from our present ideas
and methods) will continue. You will be revived by other cryonicists,
who will revive you as one means of eventually insuring their own
revival. How can that happen? Well, after all, we are NOT all
powerful, nor will we ever be. Hence there will be accidents, and
not just the kind of accidents with which we are familiar but
completely new kinds, too. Your nanotechnological thingamajig may
go badly wrong and mess you up in new and unforeseen ways --- which
will (almost by definition) not be among those the people of the
time will know how to fix. So they will store you until they work
out how to fix you. And the name for that is "cryonics".

To Brian Delaney:
I won't argue about who is most familiar with the aging literature;
I'm sure that you have read papers which I've not read, and vice
versa. HOWEVER I was quite definitely NOT claiming that the drugs
I listed produced a squaring of the lifespan curve. If you look up
the actual studies you will see that they do NOT do that --- they
actually show some animals in the treated group living longer than
ANY animal in the nontreated group. For L-Dopa, cf G Cotzias, S Miller
et al, SCIENCE 196(1977) 549551. For melatonin, W Pierpaoli,
IMMUNOLOGY LETTERS 16(1987) 355-362 and ANNALS NY ACAD SCIENCES 621
(1991) 291-313 (there were other authors than Pierpaoli for both of
these papers). For dilantin (phenytoin) VM Dilman, VN Anisimov
GERONTOLOGY 26(1980) 241-246. For CoQ10, EG Bliznakov, MECHANISMS
OF AGEING AND DEVELOPMENT 7(1978) 189-197 (there is a second 
experiment by LS Coles and HB Harris in RM Klatz (ed) ADVANCES IN
ANTIAGING MEDICINE, 1996, pp. 205-215 which did not show an increase
in maximal lifespan of the treated animals compared to controls).
Finally, for HGH, DN Khansari, T Gustad MECHANISMS OF AGEING AND
DEVELOPMENT 57(1991) 87-100.

Regardless of what the authors of these articles say, a 
scrutiny of the lifespan curves they give shows that treated animals
clearly outlived those that were not treated.

As for the issue of lifespans of different strains, you are correct
that at one time for one set of different strains of mice statistics
were published on their lifespan. These statistics did not include
lifespans on crosses between these, nor on strains developed later.
Furthermore a serious read of the literature on drugs which may
increase lifespan (however that effect is defined) will show that
such studies have often been done with quite different strains and
dosages. That is why I say that it is hard to form a unified idea
on this issue: the only recipe for resolving the question of whether
or not a drug will increase maximal lifespan is to do more experiments.

AS I said in my original message, I do not doubt that calorie restriction
will increase the lifespan of mice, and probably human lifespan too.
Moreover, lots more experiments have been done with it than with, say,
dilantin or deprenyl. And the worst problem with CR studies is not
so much design of experiments verifying CR, but the failure among
almost all of those doing them to ask just exactly why CR works. It's
easy to produce a THEORY of why it works, the real issue is to 
find out the truth here. What does CR do to the hormonal state of
the animal, and can we modify that state in the same way to get the
same effect? Not only that, but any serious attempt to work out how
to prolong lifespans should hardly stop with CR. After all, compared
to 1000 years, even a 50% lifespan increase is small. So where do we
go then?

			Best and long long life,

				Thomas Donaldson

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