Neither do I have any idea, but it seems reasonable to draw that
conclusion. If you read into the study I provided in the initial
posting, you see that phosphatidylcholine, or lecithin, creates an
environment gastroenterologically that we are trying to avoid, and
that also choline supplementation on its own has a similar effect.
(See section "Dietary choline or TMAO promotes atherosclerosis".) This
means that even Citicoline supplementation, which happens to be
hydrolyzed to choline and cytadine or choline and uridine (I'm not
positive) before absorption, should theoretically have a similarly
deleterious effect on health, and should probably be kept to a
minimum. Because dimethylaminoethanol (DMAE) is not metabolized in the
same way, and because the literature suggests (though cannot prove
definitively) that it upregulates acetylcholine levels in the brain,
it may be an effective work around. I've looked around and I cannot
find any where any thing that suggests that DMAE is metabolized into
choline, or into TMAO, or into betaine, leading me to draw this
conclusion, but please take it with a grain of salt because my
training is not in Biology. I should also point out that the
elimination of choline or lecithin from the diet is probably
unreasonable, and I only brought this up to bring it to the attention
of the group.
On Jun 18, 4:47 pm, Mike <
mikebk...@gmail.com> wrote:
> Your right, but after gut flora produces bacteria with substances, the
> bacteria moves to the liver.
> ==
> bacteria aren't usually able
> to cross the intestinal wall at whim, one of the jobs of the
> intestinal wall is to prevent bacterial invasion.
> ==
>
> If the gut bacteria never reaches the liver, and DMAE gets transformed into
> choline in the liver or the brain (according to wikipedia below), DMAE could
> be bypassing this supposed danger of choline metabolism in the gut?
>
> maybe DMAE could be a safer route to increasing acetylcholine in the brain?
> anyone can confirm this? I have absolutely no idea whether this is true.
>
> ==
> Biochemical precursor
>
> Dimethylaminoethanol is related to
> choline<
http://en.wikipedia.org/wiki/Choline>and may be a biochemical
> precursor to the neurotransmitter
> acetylcholine <
http://en.wikipedia.org/wiki/Acetylcholine>, although this
> conclusion has been
> disputed.[3]<
http://en.wikipedia.org/wiki/DMAE#cite_note-Zahniser-2>It
> is believed that dimethylaminoethanol is
> methylated <
http://en.wikipedia.org/wiki/Methyl> to produce choline in the
> brain.[3] <
http://en.wikipedia.org/wiki/DMAE#cite_note-Zahniser-2> It is
> known that dimethylaminoethanol is processed by the
> liver<
http://en.wikipedia.org/wiki/Liver>into choline; however, the
> choline molecule is charged and cannot pass the blood-brain
> barrier <
http://en.wikipedia.org/wiki/Blood-brain_barrier>.[3]<
http://en.wikipedia.org/wiki/DMAE#cite_note-Zahniser-2>
> [edit<
http://en.wikipedia.org/w/index.php?title=Dimethylethanolamine&action...>
> ] Research
>
> Short-term studies have shown an increase in vigilance and alertness with a
> positive influence on
> mood<
http://en.wikipedia.org/wiki/Mood_%28psychology%29>following
> administration of DMAE, vitamins, and minerals.
> [4] <
http://en.wikipedia.org/wiki/DMAE#cite_note-3> Research for attention
> deficit hyperactivity
> disorder<
http://en.wikipedia.org/wiki/Attention_deficit_hyperactivity_disorder>(ADHD)
> has been promising, though inconclusive.
> [5] <
http://en.wikipedia.org/wiki/DMAE#cite_note-4> Long-term studies are
> equivocal. Some showed dimethylaminoethanol to increase the lifespan of
> animals in which it was tested, while others indicate a possible reduction
> in the average life span <
http://en.wikipedia.org/wiki/Average_life_span> of
> quail <
http://en.wikipedia.org/wiki/Quail>.[6]<
http://en.wikipedia.org/wiki/DMAE#cite_note-5>