From: NetSurfer (netsurf@pixi.com)
Date: Wed Apr 09 1997 - 00:11:28 MDT
Many thanks for the info and pointers!
-
James Wilson
http://www.pixi.com/~netsurf
----------
From: Crosby_M <Crosby_M@bls.gov>
To: 'extropians@extropy.org'
Subject: DMAE availability
Date: Tuesday, April 08, 1997 12:09 PM
Well, the list seems to be working again now so I'll try sending this
again...
NetSurfer wrote:
<Please excuse my ignorance but what are the benefits of
centrophenoxine or of DMAE?>
In case you're unable to do a Web search here are some summaries:
>From http://www.naturallife.com/DMAE.html
<DMAE The memory stimulant ... Choline is the usual precursor of
acetylcholine, but it does not cross the blood-brain barrier very
well. The body makes acetylcholine from choline as it is needed. DMAE
is basically a choline molecule with one methyl group missing from the
nitrogen. DMAE is more able to cross the blood-brain barrier than
choline. Once inside the brain, an enzyme performs a methylation that
converts DMAE into choline. So, taking DMAE increases the brain's
potential to make neurotransmitters. Dean and Morgenthaler's book
reports the following effects for DMAE: mood elevation, improvement of
memory and learning, intelligence increases, and increases in the life
span of laboratory animals.>
>From http://www.damicon.fi/sd/centrophenoxine.html
<Lipofuscin is the material centrophenoxine is said to remove or scour
from the glial cells or neurons. It is the waste or residue of
digestion by lysosomes of effete organelles and bacteria.... The data
demonstrate that centrophenoxine-induced inhibition of lipofuscin
accumulation has a positive influence on the cell metabolism and the
mitotic division capacity and causes a delay of the cellular aging of
the human glia cells in vitro. (Rodemann and Bayreuther, 1979)
Concomitant with the reduction of the accumulated lipofuscin,
centrophenoxine- treated glia cells show enhanced rates of RNA
synthesis, protein synthesis and glucose uptake. Most likely the
utilization of glucose is shifted from glycolysis to the pentose
phosphate pathway. Data suggest reduction of lipofuscin by
centrophenoxine has a positive effect on cell metabolic functions and
causes a delay of the cellular aging of the human glia cells in vitro.
(1983)>
As for what Morris Johnson was referring to (BTW, I didn't see any
reference by Max More to centrophenoxine) when saying
<I was astonished at the similarity between the combination of DMAE
plus the common herbicide 2,4-D and centrophenoxine. The only
difference is the 2, chloro of the 2,4-D. Would people exposed to
minimal amounts of 2,4-d while also consuming DMAE have similar
effects to those of centrophenoxine?>
I haven't a clue - interaction of neurochemicals in the brain is an
EXTREMELY complex subject.
Mark Crosby
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