Both Tom Matthews and James seem to think that research into calorie/dietary
restriction,(CR), is the better way to proceed in the search for longevity.
I'm willing to take an analytical look at this research to see if there is
some potential benefits deserving of it having the highest funding priority.
I'll play the devil's advocate here and apply the same criteria to this
research as we have tried to apply to the telomeric theory. That is how
effective is it, what does the research show, and how does it address any
First I've seen numerous posts, (but not from Tom), that state that CR is one
of the very few methods of extending any organisms life span. This is
patently not the case. The appropriate way to phrase this phenomena is that
"Caloric restriction has been demonstrated to retard aging processes and
extend *maximal* life span in some species."
While CR mice do live longer than mice whose diet is not restricted they live
no longer than than other mice on CR. Their life span has not been increased
by CR only their life expectancy has been increased.
This relegates this research to the same class as vaccines, antibiotics,
hormonal replacement and dietary supplements. It is valid research and could
possibly achieve some significant increases in human life expectancy but has
little if any relation to extending the human life span.
That said let's look at some of the other problems with this research. From
the research I've looked at it appears that CR is primarily effective when
started very early in the life cycle. Lipman RD, et al., in Aging (Milano)
1995 Apr;7(2):136-139T, said "The data suggest there may be a level of
maturity, or a stage in the aging process, after which caloric restriction no
longer increases longevity."
Most of the studies have used a 60% reduction in food intake as the
approximate amount necessary to achieve maximal life expectancy extension.
As Tom has pointed out this would be close to the starvation level in a human
diet. Lesser dietary restrictions have increasingly lesser beneficial
effects on the aging processes and longevity.
So I do agree that an alternative method of mimicking these effects would
have to be found. And as Tom also pointed out we first have to "discover its
mechanism in detail".
Dr. E.J. Masoro, a major researcher in the field of CR at The University of
Texas Health Science Center at San Antonio, has suggested two possible
mechanisms. The first is "the altered metabolic characteristics of glucose
fuel use and of oxidative metabolism" and the second "relates to the enhanced
ability of the rodents restricted in food intake to cope with challenges,
which in turn has been linked to the glucocorticoid system and to the
heat-shock protein system".
Any suggestions on how to proceed?
Thomas Mahoney, Pres.
Lifeline Laboratories, Inc.