X-Message-Number: 10656
Date: Thu, 29 Oct 1998 07:02:40 -0500
From: Thomas Donaldson <>
Subject: CryoNet #10650 - #10654

To Brin Deela
To Brian Delaney:
I gave a partial answer to Jan Coetzee on the question you ask.

I too have read these various experiments. I am not impressed by
the depth of thinking that lay behind them. (I'll add, too, that
you have not disposed of the "developmental program" explanation
simply by the observation that CR works after puberty. We develop
after puberty, too. Some authors claim that even aging comes under
that heading).

So here are some MORE suggestions, just to add to those I gave for 
Jan Coetzee. We note that CR restriction causes the CR animal to
have a variety of metabolic differences from a normal animal. You
suggest, for instance, that improved glucose regulation plays
an important role in the effects of CR. Well, the obvious experiment
is to take a population of NON-calorie restricted animals and try
with drugs (chromium picolinate comes to mind, but aminoguanidine
is worth trying too. And a good search is likely to find still
others). Do these drugs produce similar effects to that of CR?
If not, why not? Among other questions such a hypothesis suggests
is simply that of finding the point at which the improved glucose
regulation occurs --- after all, our cells deal with glucose
using quite complicated metabolic machinery, especially our
brain cells. 

It may or may not be of interest here that chromium picolinate
does cause an increase in lifespan. I did not list it among
those drugs for which an experiment shows an increase in maximal
lifespan because the experiment showing an increase only provided
a table of the number of animals surviving 1000 days, experimental
versus controls. That chromium PICOLINATE worked while 2 other forms
of chromium did not is also interesting.

The aim of such an experiment is not just to decide that CR causes
better regulation of glucose metabolism, but to work out in much
more detail just how it does that. For that matter, if we did find
a drug which reproduced the lifespan effects of CR in adult mice,
the next step would be to see what it did to prepubertal mice, too.
If it doesn't cause the same effects there, then the hypothesis is

CR most certainly causes lots of metabolic changes. The only way to
work out exactly which of these is primary and which is secondary
is NOT to work only with CR mice, but instead to produce similar
changes by other methods and see just what they do to the treated
animals. That can be done by drugs or genetic manipulation of the
mice, both of which are very well developed techniques. Repeated
repetition of CR experiments, in which some new variable is 
measured, just isn't going to tell us very much at all. 

			Best and long long life,

				Thomas Donaldson

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