From: Robert J. Bradbury (bradbury@aeiveos.com)
Date: Sat Apr 29 2000 - 04:27:33 MDT
On Fri, 28 Apr 2000, Al Villalobos wrote:
>
> All of the above work implicates high insulin levels as the likely culprit
> in a host of age-related diseases and (dare I say?) the ageing process
> itself.
>
Al, I believe you may be misinterpreting the results. Studies with
diabetics have consistently shown that maintenance of proper insulin
levels extends lifespan.
More correctly, I believe you want to say that high *glucose* levels or
perhaps high *glucose* level "spikes" (before insulin can be produced
to bring the levels down to normal) correspond to diminished lifespan.
There is a path, probably highly genetic, involving "insulin resistance"
that may lead to a failure of the body to respond to the production
of insulin. That allows circulating glucose levels to remain higher
longer, most likely causing more extensive damage. The primary culprit
here *is* the glucose and not the insulin.
This is due to the fact that glucose leads to protein glycosylation
(though the Amadori reaction pathway). I believe it is Alteon that
currently has drugs undergoing trials that have the ability to reverse
protein glycosylation (and therefore potentially some of the consequences
of high sugar levels).
Given the genetic components in this pathway (I've seen estimates as high
as 10-20 genes involved in diabetes), it is likely that any "one-size fits
all" dietary recomendations *will* be wrong. For example, people with the
"Milan mutation" in their apolipoprotein genes can eat dozens of eggs a day
and never get heart disease.
Robert
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