Re: Estrogen increases the dietary requirement for choline.

mjw...@googlemail.com

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Jun 13, 2014, 9:44:10 AM6/13/14

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On Wednesday, 10 April 2013 10:57:53 UTC+1, John H. Gohde wrote:
> On Apr 10, 2:48 am, None Given <trigonometry1...@gmail.com> wrote:
>
>
>
> > Aw but it is you who is bitching, female dog state of mind.
>
> > It does a lot to discredit the other thread on the related topic.
>
> > It has content. You buried your content where on the web.
>
> >
>
> > Anyway this dog only bites the tires of parked subcompacts.......Trig
>
>
>
>
>
>
>
> To whom it may concern, I am talking to myself.
>
>
>
> YOU guys are NOT fooling anybody.
>
>
>
> The addictive personality types, otherwise known as Dick-Heads, will
>
> do anything to justify their Bad habits whether it be eating meat,
>
> fat, salt, sugar, fastfood, junk food, etc.
>
>
>
> Moi on the other other hand uses his brain and corrects his previously
>
> OFF lifestyle towards one That makes a heck of a lot more sense.
>
>
>
> Life-Extension crap is just pure Bull used as an excuse to be a Dick-
>
> Head and go full speed ahead with the insane lifestyles of the Science
>
> Psychos.
>
>
>
> The Dick-Head addictive personality types have my condolences.

Why does it trouble you so? Why concern yourself? You seem angry. Perhaps you need to consider whether something is the root cause of your anger because your responses seems a little dramatic!

Olafur Pall Olafsson

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Jul 27, 2007, 9:32:23 AM7/27/07

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Phosphatidylcholine (PC) is synthesized endogenously in the liver in
the human body by the enzyme phosphatidylethanolamine N-
methyltransferase (PEMT). Estrogen induces expression of the PEMT gene
resulting in increased PC synthesis in premenopausal women because of
their higher estrogen levels compared to males and postmenopausal
women.

The obvious implications of this is that males and postmenopausal
women may need more dietary/supplementary choline than premenopausal
women, at least to prevent deficiency. And this is exactly what the
second abstract below demonstrates. On the other hand because of the
high demand PC synthesis has for methyl groups (PMID: 16400042), this
also implies that due to their increased endogenous synthesis, choline
supplementation may be more effective as a homocysteine lowering agent
in premenopausal women compared to males and postmenopausal women.
Also because they synthesize more choline endogenously, premenopausal
women may need a higher dose of choline to fully replace all the
endogenously synthesized PC which is needed to get maximum
homocysteine lowering benefits from the choline.

IUBMB Life. 2007 Jun;59(6):380-7. Related Articles, Links
Click here to read
Gene response elements, genetic polymorphisms and epigenetics
influence the human dietary requirement for choline.

Zeisel SH.

Nutrition Research Institute, Department of Nutrition, School of
Public Health and School of Medicine, University of North Carolina at
Chapel Hill. North Carolina. USA.

Recent progress in the understanding of the human dietary
requirement for choline highlights the importance of genetic variation
and epigenetics in human nutrient requirements. Choline is a major
dietary source of methyl-groups (one of choline's metabolites,
betaine, participates in the methylation of homocysteine to form
methionine); also choline is needed for the biosynthesis of cell
membranes, bioactive phospholipids and the neurotransmitter
acetylcholine. A recommended dietary intake for choline in humans was
set in 1998, and a portion of the choline requirement can be met via
endogenous de novo synthesis of phosphatidylcholine catalyzed by
phosphatidylethanolamine N-methyltransferase (PEMT) in the liver.
Though many foods contain choline, many humans do not get enough in
their diets. When deprived of dietary choline, most adult men and
postmenopausal women developed signs of organ dysfunction (fatty
liver, liver or muscle cell damage, and reduces the capacity to handle
a methionine load, resulting in elevated homocysteine). However, only
a portion of premenopausal women developed such problems. The
difference in requirement occurs because estrogen induces expression
of the PEMT gene and allows premenopausal women to make more of their
needed choline endogenously. In addition, there is significant
variation in the dietary requirement for choline that can be explained
by common polymorphisms in genes of choline and folate metabolism.
Choline is critical during fetal development, when it alters DNA
methylation and thereby influences neural precursor cell proliferation
and apoptosis. This results in long term alterations in brain
structure and function, specifically memory function. IUBMB Life, 59:
380 - 387, 2007.

PMID: 17613168 [PubMed - in process]

Paul Antonik Wakfer

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Jul 27, 2007, 2:37:00 PM7/27/07

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> for adult males and 425mg for adult females (http://lpi.oregonstate.edu/infocenter/othernuts/choline/). The

> primary criterion used to estimate the AI for choline is the
> prevention of liver damage. Clearly this level is too low since 19 out
> of 57 subjects in the study below developed signs of organ dysfunction
> when consuming 550mg of choline per day. And this is just the AI, not
> the optimal intake, the latter of course would be even higher for most
> people.
>
> I haven't done much research on choline in the past and I just
> realized that, depending on what I eat, on some days I do not even get
> the AI for males. I have been getting 125mg a day of choline from a
> multi vitamin and a B complex supplement I take. I also get a few
> hundred milligrams a day of choline from my diet, most of which comes
> from eating at least one egg every day. In addition I get 720mg of PC
> from a lecithin supplement, but since PC is only about 13,2% choline

I am not sure how you arrived at your 13.2%. The molecular weight of
choline is 104.17 and the site www.jenabioscience.com/images/5103fef174/LI-004.pdf
states that the molecular weight of their chicken egg PC is 760.09
which would make the percentage 13.7% instead. In any case, since PC
is not a pure substance, all such percentages are only approximate,
because the molecular weight of PC can vary somewhat depending on
which fatty acids are attached to the other two positions on the
glycerol backbone of the molecule (choline is attached to a phosphate
group at only one of the three positions). A diagram of a typical PC
molecule in included in the above note pdf.

> this only gives me extra 95mg of choline daily. So all in all I am
> only getting 220mg daily from supplements plus a a few hundred
> milligrams from my diet. On days I happen to not eat an egg my total
> choline intake can get as low as 300mg.
>
> As a result of this research I have decided to up my supplementary
> intake of lecithin considerably and also take some extra choline
> separately. Just like the AI for choline the optimal intake of choline
> will of course vary between people based on many factors and as I've
> explained the AI isn't even adequate for a large part of the
> population, let alone optimal. Because of this I've decided to aim for
> a choline intake well above the AI so my total daily choline intake
> will be close to a gram daily. Chances are this is more than I need,
> but given the individual variation in choline requirement I think it
> is wise to aim a little high on the dose as long I stay well below the
> tolerable upper intake level, which for choline has been defined as
> 3,5g per day.

Taking some choline bitartrate daily (41% choline) is probably the
simplest/best way to achieve your desired intake.

-Paul Wakfer

MoreLife for the rational - http://morelife.org
Reality based tools for more life in quantity and quality
The Self-Sovereign Individual Project - http://selfsip.org
Self-sovereignty, rational pursuit of optimal lifetime happiness,
individual responsibility, social preferencing & social contracting

Olafur Pall Olafsson

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Jul 27, 2007, 9:09:09 PM7/27/07

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In my files I had written down that the molecular mass of
phosphatidylcholine is 790,09. I also saved a link to the source from
which I got this number. However examining the source again I see that
this number is incorrect since the source gives the same molar mass
you gave above (it gives 760,076). So it appears that I have either
misread or mistyped 790 instead of 760. Thanks for the correction. BTW
here's the source from which I got the number:
http://pubchem.ncbi.nlm.nih.gov/summary/summary.cgi?cid=5497103
I just recently discovered and started using PubChem and I find it
very useful.

> In any case, since PC
> is not a pure substance, all such percentages are only approximate,
> because the molecular weight of PC can vary somewhat depending on
> which fatty acids are attached to the other two positions on the
> glycerol backbone of the molecule (choline is attached to a phosphate
> group at only one of the three positions). A diagram of a typical PC
> molecule in included in the above note pdf.

Thanks for the additional information. Being so used to looking up the
molar mass of chemicals whose name only applies to a single molecular
formula it did not occur to me that the name phosphatidylcholine
applied to more than one chemical. The name of course does not specify
the exact fatty acids attached to the glycerol backbone. Here is the
definition of phosphatidylcholines taken from the link I gave above:

"Derivatives of phosphatidic acids in which the phosphoric acid is
bound in ester linkage to a choline moiety. Complete hydrolysis yields
1 mole of glycerol, phosphoric acid and choline and 2 moles of fatty
acids."

The fatty acids are not specified in the definition, for the other
compounds there is only a single molecular formula to which the name
of each of them applies. This matches with your statement that the
fatty acid attached can vary.

BTW the PubChem link I gave above displays a nice diagram of
phosphatidylcholine. It is just like the one in the pdf. file you
linked to but it shows additional details, such as the kink in one of
the fatty acid chains at the double bond.

> > this only gives me extra 95mg of choline daily. So all in all I am
> > only getting 220mg daily from supplements plus a a few hundred
> > milligrams from my diet. On days I happen to not eat an egg my total
> > choline intake can get as low as 300mg.
>
> > As a result of this research I have decided to up my supplementary
> > intake of lecithin considerably and also take some extra choline
> > separately. Just like the AI for choline the optimal intake of choline
> > will of course vary between people based on many factors and as I've
> > explained the AI isn't even adequate for a large part of the
> > population, let alone optimal. Because of this I've decided to aim for
> > a choline intake well above the AI so my total daily choline intake
> > will be close to a gram daily. Chances are this is more than I need,
> > but given the individual variation in choline requirement I think it
> > is wise to aim a little high on the dose as long I stay well below the
> > tolerable upper intake level, which for choline has been defined as
> > 3,5g per day.
>
> Taking some choline bitartrate daily (41% choline) is probably the
> simplest/best way to achieve your desired intake.

That's exactly what I've been doing for the past few days. I
immediately went out to a nearby health food store the next day and
bought some choline bitartrate as soon as I realized that my choline
intake was probably below optimal. I take one capsule containing 650mg
of choline bitartrate with my breakfast, providing me with additional
260mg of choline. I also doubled my supplemental lecithin intake and
will increase it even further when an order I recently placed
(containing plenty of lecithin) arrives. So right now I'm getting
around 200mg of choline from lecithin, 125mg from a multivitamin and a
B complex and 260mg from choline bitartrate. A total of ~585mg of
choline from supplements. On days I eat one egg I should get at least
200mg of choline from my diet giving me a total of around 800mg of
choline daily. I might start taking two capsules of the choline
bitartrate though, at least on days I happen to not eat an egg.

trigonom...@gmail.com

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Jul 28, 2007, 5:22:54 AM7/28/07

to

>
> > Taking some choline bitartrate daily (41% choline) is probably the
> > simplest/best way to achieve your desired intake.
>
> That's exactly what I've been doing for the past few days. I
> immediately went out to a nearby health food store the next day and
> bought some choline bitartrate as soon as I realized that my choline
> intake was probably below optimal. I take one capsule containing 650mg
> of choline bitartrate with my breakfast, providing me with additional
> 260mg of choline. I also doubled my supplemental lecithin intake and
> will increase it even further when an order I recently placed
> (containing plenty of lecithin) arrives. So right now I'm getting
> around 200mg of choline from lecithin, 125mg from a multivitamin and a
> B complex and 260mg from choline bitartrate. A total of ~585mg of
> choline from supplements. On days I eat one egg I should get at least
> 200mg of choline from my diet giving me a total of around 800mg of
> choline daily. I might start taking two capsules of the choline
> bitartrate though, at least on days I happen to not eat an egg.

I will suggest a different view. Choline chloride and I think
bitratrate are subject to breakdown in the GI tract such
that you don't get the full amount and the dimethylamine
and related chemicals are formed which under certain circumstances can
lead to
the formation of nitrosamines. Nor is lecithin an ideal source
for other reasons. First with lecithin one gets a large
dose of phosphate as you clearly know. Second lecithin may also
have methylamine content.

I'll suggest betaine aka N,N,N-trimethylgylcine maybe
a better way to go for a methyl group contributor supplement.
It is less prone to methylamine formation in the
GI tract.
=======================
Here are some randomly arranged abstracts
on the issue.

J Nutr. 1989 May;119(5):800-4.

Conversion of dietary choline to trimethylamine and dimethylamine in
rats:
dose-response relationship.

Zeisel SH, daCosta KA, Youssef M, Hensey S.

Department of Pathology, Boston Unversity School of Medicine, MA
02118.

Trimethylamine (TMA) and dimethylamine (DMA) are normal components of
human
urine and are precursors of dimethylnitrosamine, a potent carcinogen.
In part,
DMA and TMA are products of the metabolism of dietary choline by
intestinal
bacteria. Most TMA formed in the intestinal tract is later oxidized
and excreted
as trimethylamine oxide (TMAO). Humans treated with large doses of
choline smell
"fishy" (the odor of TMA). Humans ingest choline as part of foods, and
yet
rarely smell fishy, suggesting that TMA formation must depend upon the
dose of
choline ingested. We found that, in adult rats, at low doses of
choline (1.5
mmol/kg body wt) only 9 mumol choline (6% of the dose) reached the
part of the
intestine which is colonized by bacteria (the cecum and colon). After
administration of 15 mmol choline/kg body wt, 237 mumol (16% of the
dose)
reached the cecum and colon. At both doses, 64-65% of the administered
choline
was absorbed from the intestine by 3 h after the dose. We found that
orally
administered choline slightly increased TMA and TMAO excretion at
doses of
choline smaller than 7 mmol/kg body wt, but that there was a
disproportionately
large increase in TMA excretion per 24 h when larger doses were
administered
(from 11 mumol TMA and 100 mumol TMAO per kg body wt in controls to
226 mumol
TMA and 3617 mumol TMAO per kg body wt in rats treated with 15 mmol
choline/kg
body wt).(ABSTRACT TRUNCATED AT 250 WORDS)

PMID: 2723829

===============================

J. Pharmacol. Exp. Ther. 1983 May;225(2):320-4.

Formation of methylamines from ingested choline and lecithin.

Zeisel SH, Wishnok JS, Blusztajn JK.

Humans ingest substantial amounts of choline and lecithin as part of
common
foods. Physicians have recently begun administering large doses of
these
compounds to individuals with neurological diseases. A significant
fraction of
ingested choline is destroyed by enzymes within gut bacteria, forming
trimethylamine (TMA), dimethylamine (DMA) and monomethylamine (MMA).
Some of
these methylamines are eventually excreted into the urine, presumably
after being
absorbed and carried to the kidneys via the bloodstream. The
methylamines formed
after choline is eaten could be substrates for the formation of
nitrosamines,
which have marked carcinogenic activity. Twenty-seven millimoles of
choline
chloride, choline stearate or lecithin were administered to healthy
human
subjects. It was found that these treatments markedly increased the
urinary
excretion of TMA, DMA and MMA, with choline chloride having the
greatest effect.
Rats were treated with 2 mmol/kg b.wt. of choline chloride or
lecithin, and it
was found that these treatments significantly increased urinary TMA
excretion and
did not alter DMA or MMA excretion. Our choline chloride preparation
contained no
MMA, DMA or TMA; however, it was found that our choline stearate and
all the
commercially available lecithins tested were contaminated with
methylamines.
Prior removal of methylamines from our lecithin preparation minimized
the effect
of oral administration of this compound on methylamine excretion in
urine of rats
and humans.

Publication Types:
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.

PMID: 6842395
==============================

J Toxicol Environ Health. 1991 Mar;32(3):319-30.

Developmental toxicity of methylamines in mice.

Guest I, Varma DR.

Department of Pharmacology and Therapeutics, McGill University,
Montreal, Canada.

Monomethylamine (MMA), dimethylamine (DMA), and trimethylamine (TMA)
are
endogenous substances as well as metabolites of methyl isocyanate, the
chemical
involved in the 1984 accident at Bhopal, India. Although methylamines
exert
several toxic effects including inhibition of protein turnover and
oocyte RNA
synthesis, their reproductive toxicity has not been investigated. We
therefore
studied the possible developmental toxicity of these amines using
pregnant CD-1
mice and mouse embryo culture as experimental models. Intraperitoneal
injections
(daily from d 1 to 17 of gestation) of TMA at 2.5 and 5 mmol/kg/d
significantly
(p less than .001) decreased fetal body weight but not the placental
weight or
maternal body weight gain; however, 5 of 11 mice treated with 5 mmol/
kg TMA died.
Similar treatment with DMA and MMA did not exert any obvious maternal
or fetal
effects. All three methylamines, when added to embryos in culture,
caused
dose-dependent decreases in size, DNA, RNA, and protein content as
well as embryo
survival; the order of toxicity was TMA greater than DMA greater than
MMA. The
ability of methylamines to adversely affect fetal development suggests
that these
amines, especially trimethylamine, may act as endogenous teratogens
under certain
conditions.

Publication Types:
Research Support, Non-U.S. Gov't

PMID: 2002514
=====================

J. Nutr. 1989 May;119(5):800-4.

Conversion of dietary choline to trimethylamine and dimethylamine in
rats:
dose-response relationship.

Zeisel SH, daCosta KA, Youssef M, Hensey S.

Department of Pathology, Boston Unversity School of Medicine, MA
02118.

Trimethylamine (TMA) and dimethylamine (DMA) are normal components of
human urine
and are precursors of dimethylnitrosamine, a potent carcinogen. In
part, DMA and
TMA are products of the metabolism of dietary choline by intestinal
bacteria.
Most TMA formed in the intestinal tract is later oxidized and excreted
as
trimethylamine oxide (TMAO). Humans treated with large doses of
choline smell
"fishy" (the odor of TMA). Humans ingest choline as part of foods, and
yet rarely
smell fishy, suggesting that TMA formation must depend upon the dose
of choline
ingested. We found that, in adult rats, at low doses of choline (1.5
mmol/kg body
wt) only 9 mumol choline (6% of the dose) reached the part of the
intestine which
is colonized by bacteria (the cecum and colon). After administration
of 15 mmol
choline/kg body wt, 237 mumol (16% of the dose) reached the cecum and
colon. At
both doses, 64-65% of the administered choline was absorbed from the
intestine by
3 h after the dose. We found that orally administered choline slightly
increased
TMA and TMAO excretion at doses of choline smaller than 7 mmol/kg body
wt, but
that there was a disproportionately large increase in TMA excretion
per 24 h when
larger doses were administered (from 11 mumol TMA and 100 mumol TMAO
per kg body
wt in controls to 226 mumol TMA and 3617 mumol TMAO per kg body wt in
rats
treated with 15 mmol choline/kg body wt).(ABSTRACT TRUNCATED AT 250
WORDS)

Publication Types:
Research Support, U.S. Gov't, P.H.S.

PMID: 2723829

============================

1: Food Chem. Toxicol. 1999 May;37(5):515-20.

Dietary precursors of trimethylamine in man: a pilot study.

Zhang AQ, Mitchell SC, Smith RL.

Molecular Toxicology, Division of Biomedical Sciences, Imperial
College School of
Medicine, South Kensington, London, UK.

An increased urinary excretion of trimethylamine and its N-oxide were
observed in
man following the oral intake (15 mmol) of choline (63% dose as
trimethylamine
and its N-oxide), D,L-carnitine (31% dose) and trimethylamine N-oxide
(78% dose).
Similar ingestion of betaine, creatinine or lecithin failed to elicit
any
significant increases. Of 46 different foods investigated, only fish
and other
sea-products gave rise to significant increases in urinary
trimethylamine and
N-oxide. Ingestion of fruits, vegetables, cereal and dairy produce,
and meats had
no measurable effects. Reasons for the apparent lack of trimethylamine
provision
by foods previously thought to be precursors are given and the role of
gut
microflora highlighted.

Publication Types:
Clinical Trial
Research Support, Non-U.S. Gov't

PMID: 10456680 [

Paul Antonik Wakfer

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Jul 28, 2007, 1:29:36 PM7/28/07

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Thanks for posting the interesting reply and supporting abstracts. I
had not thought of and was not aware of the possibility of choline
producing nitrosamine precursors by bacterial GI processing.
I don't know about Olafur, but I also supplement lots of TMG (betaine)
specifically to supply methyl groups. However, the question remains of
whether or not choline supplies benefits that cannot be met through
TMG supplementation. I will leave it to Olafur to research and resolve
this question.

BTW, the low rat dose of 1.5 mmol/kg body wt was still a hefty amount
since it would be equivalent to a dose of about 3 grams for a 70 kg
human using the standard rat to human dosage scaling. Since I also
take my choline bitartrate on an empty stomach (first thing in the AM
about 6 hours before my one daily meal) I think the chances of any of
it getting to my cecum or colon unabsorbed are minimal (besides which,
it is not clear whether your posted abstract will apply equally to the
bitartrate form).

Even so, I do thank you for the additional new information, which I
will certainly keep in mind (particularly if I start smelling fishy :)

Finally, it would be nice to have a name attached to your cryptic
handle.

--Paul Wakfer

MoreLife for the rational - http://morelife.org
Reality based tools for more life in quantity and quality
The Self-Sovereign Individual Project - http://selfsip.org
Self-sovereignty, rational pursuit of optimal lifetime happiness,
individual responsibility, social preferencing & social contracting

Tom

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Aug 1, 2007, 11:55:10 AM8/1/07

to

Paul Antonik Wakfer wrote:
> Finally, it would be nice to have a name attached to your cryptic
> handle.

like Tom Matthews over the years past?

Olafur Pall Olafsson

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Aug 2, 2007, 8:16:36 AM8/2/07

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On Jul 28, 9:22 am, trigonometry1...@gmail.com wrote:
> > > Taking some choline bitartrate daily (41% choline) is probably the
> > > simplest/best way to achieve your desired intake.
>
> > That's exactly what I've been doing for the past few days. I
> > immediately went out to a nearby health food store the next day and
> > bought some choline bitartrate as soon as I realized that my choline
> > intake was probably below optimal. I take one capsule containing 650mg
> > of choline bitartrate with my breakfast, providing me with additional
> > 260mg of choline. I also doubled my supplemental lecithin intake and
> > will increase it even further when an order I recently placed
> > (containing plenty of lecithin) arrives. So right now I'm getting
> > around 200mg of choline from lecithin, 125mg from a multivitamin and a
> > B complex and 260mg from choline bitartrate. A total of ~585mg of
> > choline from supplements. On days I eat one egg I should get at least
> > 200mg of choline from my diet giving me a total of around 800mg of
> > choline daily. I might start taking two capsules of the choline
> > bitartrate though, at least on days I happen to not eat an egg.
>
> I will suggest a different view. Choline chloride and I think
> bitratrate are subject to breakdown in the GI tract such
> that you don't get the full amount and the dimethylamine
> and related chemicals are formed which under certain circumstances can
> lead to
> the formation of nitrosamines.

Thanks for an interesting post. I was not aware of this potential of
choline to form methylamines and nitrosamines in the digestive tract.

> Nor is lecithin an ideal source
> for other reasons. First with lecithin one gets a large
> dose of phosphate as you clearly know.

Yes, that is one of the downsides of taking lecithin that I am taking
into account when deciding how much to take. As I recently posted on
the group increased dietary phosphate may negatively effect expression
of the anti-aging gene Klotho. Another downside is all the extra
calories you get from taking lecithin as a choline source compared to
taking e.g. choline bitartrate. But on the positive, lecithin also
contains phosphatidylinositol and phosphatidylethanolamine both of
which have been shown to be beneficial.

> Second lecithin may also
> have methylamine content.

According to PMID: 11580915 exogenous sources (dietary or
supplementary) only contribute minimally to urinary methylamines. The
main source appears to be endogenous. So as long as one takes a
moderate dose of lecithin it's effect on urinary methylamines is
likely minimal.

> I'll suggest betaine aka N,N,N-trimethylgylcine maybe
> a better way to go for a methyl group contributor supplement.
> It is less prone to methylamine formation in the
> GI tract.

Thanks for the tip. I already take a gram of betaine daily as a methyl
donor;-) With respect to methyl groups, it's effect of sparing methyl
groups is not the main reason I take lecithin. I consider it only as
one more additional measure to lower homocysteine. I prefer to attack
homocysteine from all angles. The main reason I take lecithin is to
provide me with choline, phosphatidylinositol and
phosphatidylethanolamine.

In the above abstract, not only was the lowest dose used very large as
Paul already mentioned, but according to the full text they used
choline chloride. In the abstract you posted below choline chloride
resulted in a greater increase in urinary methylamines than did an
equimolar amount of choline stearate or lecithin. This suggests that
lecithin would be even safer in this regard. The difference appears to
be caused by differences in absorption. Choline from lecithin has been
shown to be much more effective at raising serum choline concentration
in humans than choline from choline chloride (PMID: 69151).

In the abstract above all the commercially available lecithins tested
were contaminated with methylamines. However the abstract is from
1983. Most lecithin products available today probably contain lower
amounts of methylamines due to improvements in processing techniques.

> PMID: 10456680 [

In the above abstract 2,1g of choline increased urinary excretion of
trimethylamine and its N-oxide while 11,65g of lecithin did not do so
to any significant extent. This suggests that supplementary lecithin
does not significantly increase urinary methylamines when consumed at
moderate doses. Here is a quote from the full text that shows the
doses used:

"They were then given oral doses (15 mmol) of betaine (1.76 g),
carnitine (2.97 g), choline (2.10 g), creatinine (1.70 g), lecithin
(11.65 g, mol. wt 776.7) and trimethylamine N-oxide (1.67 g) on six
different and separate occasions, at least 2 wk apart. After each
ingestion, urine was again collected daily for the following 3 days."

My conclusion from this is that choline from lecithin will not cause
any significant formation of nitrosamines unless perhaps one consumes
very large amounts of it or if one suffers from impared absorption of
fat. Choline chloride is more likely to result in significant
formation of nitrosamines although one would generally need to take
pretty high doses of it for the effect to be significant.

Olafur Pall Olafsson

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Aug 2, 2007, 8:19:23 AM8/2/07

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On Jul 28, 5:29 pm, Paul Antonik Wakfer <p...@morelife.org> wrote:
> Thanks for posting the interesting reply and supporting abstracts. I
> had not thought of and was not aware of the possibility of choline
> producing nitrosamine precursors by bacterial GI processing.
> I don't know about Olafur, but I also supplement lots of TMG (betaine)
> specifically to supply methyl groups.

I take a gram of TMG daily. I do it specifically to supply methyl
groups, but also because TMG is particularily effective at lowering
postprandial homocysteine levels which evidence indicates is more
important than fasting homocysteine levels.

> However, the question remains of
> whether or not choline supplies benefits that cannot be met through
> TMG supplementation. I will leave it to Olafur to research and resolve
> this question.

I assume you are refering specifically to it's effect on homocysteine
levels in comparsion to betaine, since choline of course has other
benefits in addition to lowering homocysteine that betaine has not. My
immediate thought is that in an individual taking a sufficiently large
dose of TMG, choline supplementation will not lower homocysteine
levels further. But a detailed look into how each of the compounds
affects the methionine cycle is needed to solve this question.

TMG's role in the methionine cycle is simple. It donates a methyl
group to homocysteine leading to it's conversion to methionine, a
reaction catalized by the enzyme betaine homocysteine methyl
transferase (BHMT). See this figure for clarification:
http://www.ajcn.org/cgi/content/full/80/3/539/F1
Choline on the other hand does not directly participate in the
methionine cycle. But it effects it indirectly in two ways:

1) First of all choline effects the methyl cycle by being oxidized to
TMG in the liver or kidneys. The TMG produced can then lower
homocysteine by the mechanism I described before.

2) There is only one endogenous biosynthesis pathway for choline
biosynthesis in mammals. It involves the conversion of
phosphatidylethanolamine (PE) into phosphatidylcholine (PC) by the
enzyme phosphatidylethanolamine N-methyltransferase (PEMT). In this
reaction SAMe acts as a methyl donor, requiring three molecules of
SAMe for every molecule of PC synthesized. In the process SAMe gets
converted to S-adenosylhomocysteine. Since SAMe is one of the main
compounds in the methionine cycle choline affects the methionine cycle
indirectly. Ingesting choline will reduce the body's need to
synthesize choline endogenously. Since choline synthesis requires SAMe
taking choline will consequently make more SAMe available in the body.

Clearly choline does not offer any advantage over betaine by the first
mechanism above. One could simply take TMG rather than trying to
increase it's synthesis with choline supplementation. But choline may
have additional benefits when it comes to the second mechanism. This
can be seen if one looks at the methionine cycle. As I explained
earlier TMG acts on the methionine cycle by converting homocysteine to
methionine. Choline does the same thing through increasing betaine
concentration. In addition, by mechanism number 2 above, choline
reduces the conversion of SAMe to S-adenosylhomocysteine. This is
important since S-adenosylhomocysteine may be even more harmful than
homocysteine (PMID: 11722952). Furtheremore during the next step in
the cycle S-adenosylhomocysteine gets converted to homocysteine. The
important difference here is that while TMG helps speed up the
conversion of homocysteine to methionine, in contrast to exogenously
supplied choline it does nothing to reduce the conversion of SAMe to S-
adenosylhomocysteine. This is a benefit of choline that cannot be met
through increased TMG supplementation and is one reason I would
recommend taking choline in addition to taking TMG.

> BTW, the low rat dose of 1.5 mmol/kg body wt was still a hefty amount
> since it would be equivalent to a dose of about 3 grams for a 70 kg
> human using the standard rat to human dosage scaling. Since I also
> take my choline bitartrate on an empty stomach (first thing in the AM
> about 6 hours before my one daily meal) I think the chances of any of
> it getting to my cecum or colon unabsorbed are minimal (besides which,
> it is not clear whether your posted abstract will apply equally to the
> bitartrate form).

As I I have shown choline from lecithin has a much better absorption
than choline chloride. I am not sure about the absorption of choline
bitartrate though, I did not find any studies on it's absorption. But
I agree with you that unless it is poorly absorbed it is unlikely that
any of it gets to your cecum or colon unabsorbed when you take it on
an empty stomach.

> Even so, I do thank you for the additional new information, which I
> will certainly keep in mind (particularly if I start smelling fishy :)
>
> Finally, it would be nice to have a name attached to your cryptic
> handle.

I second this last.

> --Paul Wakfer
>
> MoreLife for the rational -http://morelife.org

> Reality based tools for more life in quantity and quality

> The Self-Sovereign Individual Project -http://selfsip.org

Jefferson

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Aug 2, 2007, 1:52:34 PM8/2/07

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Hi Olafur:

> TMG's role in the methionine cycle is simple. It donates a methyl
> group to homocysteine leading to it's conversion to methionine, a
> reaction catalized by the enzyme betaine homocysteine methyl
> transferase (BHMT). See this figure for clarification:
> http://www.ajcn.org/cgi/content/full/80/3/539/F1

The full article has been cited in quite a few subsequent articles.
Have you reviewed any of these articles?

Betaine in human nutrition - http://www.ajcn.org/cgi/content/full/80/3/539

Frank

Olafur Pall Olafsson

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Aug 2, 2007, 7:59:21 PM8/2/07

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On Aug 2, 5:52 pm, Jefferson <fw...@adelphia.netxeopheno> wrote:
> Hi Olafur:
>
> > TMG's role in the methionine cycle is simple. It donates a methyl
> > group to homocysteine leading to it's conversion to methionine, a
> > reaction catalized by the enzyme betaine homocysteine methyl
> > transferase (BHMT). See this figure for clarification:
> >http://www.ajcn.org/cgi/content/full/80/3/539/F1
>
> The full article has been cited in quite a few subsequent articles.
> Have you reviewed any of these articles?

Yes, I have reviewed a few of these in the past, in addition to
reviewing the full text article. This one f.ex. is a good one:
http://www.ajcn.org/cgi/content/full/83/1/5

Paul Antonik Wakfer

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Aug 3, 2007, 12:27:11 AM8/3/07

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Olafur Pall Olafsson wrote:
> On Jul 28, 5:29 pm, Paul Antonik Wakfer <p...@morelife.org> wrote:
> > Thanks for posting the interesting reply and supporting abstracts. I
> > had not thought of and was not aware of the possibility of choline
> > producing nitrosamine precursors by bacterial GI processing.
> > I don't know about Olafur, but I also supplement lots of TMG (betaine)
> > specifically to supply methyl groups.
>
> I take a gram of TMG daily. I do it specifically to supply methyl
> groups, but also because TMG is particularily effective at lowering
> postprandial homocysteine levels which evidence indicates is more
> important than fasting homocysteine levels.
>
> > However, the question remains of
> > whether or not choline supplies benefits that cannot be met through
> > TMG supplementation. I will leave it to Olafur to research and resolve
> > this question.
>
> I assume you are refering specifically to it's effect on homocysteine
> levels in comparsion to betaine, since choline of course has other
> benefits in addition to lowering homocysteine that betaine has not.

No, I was specifically meaning benefits of choline which are not
obtained from TMG since the previous poster was suggesting that
choline intake should be kept low (because of potential nitrosamine
production) and that TMG should be used instead. I knew that choline
has benefits additional to supplying methyl groups, but I wanted
someone else to do the research and justification of what those are
and how important they are.

> My
> immediate thought is that in an individual taking a sufficiently large
> dose of TMG, choline supplementation will not lower homocysteine
> levels further. But a detailed look into how each of the compounds
> affects the methionine cycle is needed to solve this question.

I agree with your "immediate thought" and I think that no more
research is necessary than to remember that there is a direct
enzymatic pathway to use TMG to change homocysteine into methionine
(as you describe in detail below).

>
> TMG's role in the methionine cycle is simple. It donates a methyl
> group to homocysteine leading to it's conversion to methionine, a
> reaction catalized by the enzyme betaine homocysteine methyl
> transferase (BHMT). See this figure for clarification:
> http://www.ajcn.org/cgi/content/full/80/3/539/F1
> Choline on the other hand does not directly participate in the
> methionine cycle. But it effects it indirectly in two ways:
>
> 1) First of all choline effects the methyl cycle by being oxidized to
> TMG in the liver or kidneys. The TMG produced can then lower
> homocysteine by the mechanism I described before.
>
> 2) There is only one endogenous biosynthesis pathway for choline
> biosynthesis in mammals. It involves the conversion of
> phosphatidylethanolamine (PE) into phosphatidylcholine (PC) by the
> enzyme phosphatidylethanolamine N-methyltransferase (PEMT). In this
> reaction SAMe acts as a methyl donor, requiring three molecules of
> SAMe for every molecule of PC synthesized. In the process SAMe gets
> converted to S-adenosylhomocysteine. Since SAMe is one of the main
> compounds in the methionine cycle choline affects the methionine cycle
> indirectly. Ingesting choline will reduce the body's need to
> synthesize choline endogenously. Since choline synthesis requires SAMe
> taking choline will consequently make more SAMe available in the body.

And at the same time require less SAMe per molecule of PE and PC
produced.

>
> Clearly choline does not offer any advantage over betaine by the first
> mechanism above. One could simply take TMG rather than trying to
> increase it's synthesis with choline supplementation. But choline may
> have additional benefits when it comes to the second mechanism. This
> can be seen if one looks at the methionine cycle. As I explained
> earlier TMG acts on the methionine cycle by converting homocysteine to
> methionine. Choline does the same thing through increasing betaine
> concentration. In addition, by mechanism number 2 above, choline
> reduces the conversion of SAMe to S-adenosylhomocysteine. This is
> important since S-adenosylhomocysteine may be even more harmful than
> homocysteine (PMID: 11722952). Furtheremore during the next step in
> the cycle S-adenosylhomocysteine gets converted to homocysteine. The
> important difference here is that while TMG helps speed up the
> conversion of homocysteine to methionine, in contrast to exogenously
> supplied choline it does nothing to reduce the conversion of SAMe to S-
> adenosylhomocysteine. This is a benefit of choline that cannot be met
> through increased TMG supplementation and is one reason I would
> recommend taking choline in addition to taking TMG.

Agreed.

TP

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Aug 3, 2007, 2:45:29 PM8/3/07

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"Olafur Pall Olafsson" <olafu...@yahoo.com> wrote in message
news:1186057163.4...@k79g2000hse.googlegroups.com...

>
> I take a gram of TMG daily. I do it specifically to supply methyl
> groups, but also because TMG is particularily effective at lowering
> postprandial homocysteine levels which evidence indicates is more
> important than fasting homocysteine levels.
>

I take 6 grams a day of TMG for sleep. I suffered a severe insomnia problem
a few years ago, read about TMG, immediately went to a vitamin store,
purchased some and took 5 gm at a time every 15 minutes while sitting in my
car. By the time an hour was over, I had fallen asleep for 6 hours. After
getting fully awake again I went back into the store, stocked up, drove off.
I kept taking TMG, only now 2 grams. t.i.d. iHerb and I are very good
friends <G>.

None Given

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Apr 9, 2013, 2:15:36 AM4/9/13

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Its time for this thread to spring to life.

John H. Gohde

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Apr 9, 2013, 3:27:52 AM4/9/13

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On Apr 9, 2:15 am, None Given <trigonometry1...@gmail.com> wrote:
>
> Its time for this thread to spring to life.

Old threads died for a reason.

ged...@gmail.com

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Apr 9, 2013, 10:30:17 AM4/9/13

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But TMG can elevate bp and heart rate. Any other suggestions for methyl donors?

None Given

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Apr 9, 2013, 1:11:57 PM4/9/13

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I'd add in magnesium for the BP (to keep it down). Understand I've not
made the correlation between TMG and blood pressure. Is there something
published on the topic? Guess, I'll have to check.

Perhaps its the context? Perhaps beets instead of eggs? Beets have a
heavy load of sugar so I'll stick with eggs yolks and isolated TMG.
Interestingly, it fish not red meat that was most suspect if you read
the last abstract I posted in my long posting from some years ago.

Frankly, we will likely find this new concern is over-blown or flat
out wrong. Sometimes, I suspect all foods kill even the healthy ones.
Perhaps that why calorie restriction tends to work? LOL.
Don't make dietary choices per newspaper headlines unless it
some frank contamination issue, IHMO.

time for both steak and some fish and
then a run or bicycle ride.......Trig

John H. Gohde

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Apr 9, 2013, 6:34:48 PM4/9/13

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> > >http://lpi.oregonstate.edu/infocenter/othernuts/choline/). The

YOU really need to STOP reply to THREADS started and ended in 2007.

You are like a dog who likes to bark at passing cars. NOT cute at
all. Just annoying and stupid, IMHO.

None Given

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Apr 10, 2013, 2:48:29 AM4/10/13

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John H. Gohde

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Apr 10, 2013, 5:54:59 AM4/10/13

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On Apr 10, 2:48 am, None Given <trigonometry1...@gmail.com> wrote:

> Aw but it is you who is bitching, female dog state of mind.
> It does a lot to discredit the other thread on the related topic.
> It has content. You buried your content where on the web.
>
> Anyway this dog only bites the tires of parked subcompacts.......Trig

My REPLY was posted on the other Dumb-ASS THREAD.

Okay numb-nuts, obey the social conventions of Usenet and STOP
replying to OLD, DEAD Threads, Moron!

Am, I communicating numb-nuts?

John H. Gohde

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Apr 10, 2013, 5:57:53 AM4/10/13

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On Apr 10, 2:48 am, None Given <trigonometry1...@gmail.com> wrote:

> Aw but it is you who is bitching, female dog state of mind.
> It does a lot to discredit the other thread on the related topic.
> It has content. You buried your content where on the web.
>
> Anyway this dog only bites the tires of parked subcompacts.......Trig

Taka

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Jun 13, 2014, 11:03:21 PM6/13/14

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This personality disorder happens when you supplement 3+ years with steroids like he does ... It rises his testosterone and hence aggression. Together with starring at the blue light computer screens day and night it puts him in an eternal summer breeding mode. But because he is already too old and damaged to find a receptive mate and doesn't run miles to let some steam off by exercise it results in hostility, aggression and narcissism. If the social Obumacare and the likes system didn't protect him and he lived in our natural evolutionary environment, he would be already taken out by younger peers as soon as his teeth started rotting. The human aging is all about the reproduction and competition, that's how we have been wired by the Gods ...

Taka