Discussion:
For Three Years, Every Bite Organic
(too old to reply)
Tim Campbell
2008-12-02 18:14:10 UTC
Permalink
By TARA PARKER-POPE New York Times - Published: December 1, 2008

Fruits, vegetables and animals can be 100 percent organic. What about
people?In a fascinating experiment — on himself — Dr. Alan Greene, a
pediatrician and author in Danville, Calif., decided to find out. For
the last three years, Dr. Greene has eaten nothing but organic foods,
whether he’s cooking at home, dining out or snacking on the road. He
chose three years as a goal because that was the amount of time it
took to have a breeding animal certified organic by the Department of
Agriculture. While food growers comply with organic regulations every
day, Dr. Greene wondered whether a person could meet the same
standards.It hasn’t been easy."This isn’t a way of eating I could
recommend to anybody else because it’s so far off the beaten food
grid," said Dr. Greene, 49, the founder of a popular Web site about
children’s health, drgreene.com. "It was much more challenging than I
thought it would be, and I thought it would be tough. There were
definitely days where there was nothing I could find that was
organic."

Other writers have ventured off the traditional food grid, notably
Barbara Kingsolver in "Animal, Vegetable, Mineral" and Michael Pollan
in "The Omnivore’s Dilemma." But what makes Dr. Greene’s experiment
remarkable is the length of time he devoted to it, and his effort to
incorporate organic eating into the routines of everyday living. His
findings offer new insight into the challenges facing the organic food
industry and those of us who want to patronize it. Organic farmers
don’t use conventional methods to fertilize the soil, control weeds
and pests, or prevent disease in livestock.

Organic methods often lead to higher costs, and consumers can pay
twice as much for organic foods as for conventional products. Last
week, the financial advice Web site SmartMoney.com reported that to
feed eight people an organic meal of traditional Thanksgiving foods, a
shopper would pay $295.36 — a premium of $126.35, or 75 percent, over
a nonorganic holiday spread.To cut back on the cost of an organic
diet, Dr. Greene said he had to cut back on meat. "Whenever you go up
the food chain, the costs pile up," he said. "If you don’t eat meat at
every meal, if meat becomes more of a side dish than a centerpiece,
you can fill the plate with healthy organic food for about the same
price."Questions remain about whether organic foods are really better
for you. The data are mixed. This fall, researchers from the
University of Copenhagen reported on a two-year experiment in which
they grew carrots, kale, peas, potatoes and apples using both organic
and conventional growing methods. The researchers found that the
growing methods made no difference in the nutrients in the crops or
the levels of nutrients retained by rats that ate them, according to
the study, published in The Journal of the Science of Food and
Agriculture.But other research suggests that organic foods do contain
more of certain nutrients — almost twice as many, in the case of
organic tomatoes studied for a 2007 report in The Journal of
Agricultural and Food Chemistry.Dr. Greene said he was inspired to go
all-organic after talking to a dairy farmer who noted that livestock
got sick less after a switch to organic practices. He wondered if
becoming 100 percent organic might improve his own health.Three years
later, he says he has more energy and wakes up earlier. As a
pediatrician regularly exposed to sick children, he was accustomed to
several illnesses a year. Now, he says, he is rarely ill. His urine is
a brighter yellow, a sign that he is ingesting more vitamins and
nutrients. At home, he said, the organic routine was relatively easy.

Organic food is widely available, not just at stores like Whole Foods
but at traditional supermarkets. He also shopped at farmer’s markets
and joined a local community-supported agriculture group, or C.S.A.
Because he bought less meat, the costs tended to balance out. And his
family (two of his four children still live at home) largely went
along with the experiment.On the road, though, life was more
challenging. In corporate cafeterias and convenience stores, he looked
for stickers that began with the number 9 to signify organic; stickers
on conventionally grown produce begin with 4.

When dining out, he called ahead; high-end restaurants were willing to
accommodate his all-organic request. He also found a few lines of
organic backpacking food that he could carry with him.Dr. Greene
reached the three-year milestone in October, but his diet is still
organic. He hasn’t decided whether to keep going full tilt or to ease
up in the interest of cost and convenience. In his latest book,
"Raising Baby Green: The Earth-Friendly Guide to Pregnancy, Childbirth
and Baby Care" (Jossey-Bass), he advocates a "strategic" approach,
urging parents to insist on organic versions of a few main foods, like
milk, potatoes, apples and baby food.The biggest surprise of the whole
experience, he says, was that many people still don’t know what
"organic" means."It’s surprising to me how few people know that
organic means without pesticides, antibiotics or hormones," he said.
"In stores or restaurants around the country, I would ask, ‘Do you
have anything organic?’ Half the time they would say, ‘Do you mean
vegetarian?’ "***@nytimes.com
g***@gmail.com
2008-12-02 20:02:38 UTC
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m***@lycos.com
2008-12-02 20:29:43 UTC
Permalink
It might help a little, but if you are eating a PUFA-rich diet, you
are "playing with fire" no matter what the other food items are. I
was a vegan who ate nearly all organic food for a dozen years, and
that didn't prevent me from almost dying (apparently of not being able
to produce enough stomach acid) before the age of 40.
N***@aol.com
2008-12-03 02:18:47 UTC
Permalink
Post by m***@lycos.com
It might help a little, but if you are eating a PUFA-rich diet, you
are "playing with fire" no matter what the other food items are.  I
was a vegan who ate nearly all organic food for a dozen years, and
that didn't prevent me from almost dying (apparently of not being able
to produce enough stomach acid) before the age of 40.
Who diagnosed that your vegan/organic diet was the cause that led to
you almost dying/not able produce enough stomach acid?

Patrick
m***@lycos.com
2008-12-03 06:06:41 UTC
Permalink
Nobody, which is why I almost died. One doctor wanted me to take anti-
acid medication. It was only when I took large amounts of Betaine HCl
with meals that things started to get better (2 grams or more per
meal, but now I don't need to take any). I took those supplements for
about two years, gradually taking less about a year into it. The
gastroenterologist I saw didn't even know what Betaine HCl was !
trigonometry1972@gmail.com |
2008-12-03 08:29:36 UTC
Permalink
Nobody, which is why I almost died.  One doctor wanted me to take anti-
acid medication.  It was only when I took large amounts of Betaine HCl
with meals that things started to get better (2 grams or more per
meal, but now I don't need to take any).  I took those supplements for
about two years, gradually taking less about a year into it.  The
gastroenterologist I saw didn't even know what Betaine HCl was !
I certainly agree with you on the merits of betaine HCL. The PPI meds
the doctors offer made me sick. The effects of betaine HCL
is profound. I will add supplemental melatonin also may have played
role
in getting me to 100 percent. Betaine either in the acidic or base
form
is a good methyl group contributor.

Trig
Richard Schultz
2008-12-03 10:25:08 UTC
Permalink
In misc.health.alternative ***@gmail.com | <***@gmail.com> wrote:

: Betaine either in the acidic or base form
: is a good methyl group contributor.

<scratches head>

When did methyl group deficiency suddenly become a major health issue?
Do you even know what a methyl group is?

-----
Richard Schultz ***@mail.biu.ac.il
Department of Chemistry, Bar-Ilan University, Ramat-Gan, Israel
Opinions expressed are mine alone, and not those of Bar-Ilan University
-----
"You don't even have a clue about which clue you're missing."
m***@lycos.com
2008-12-03 20:04:22 UTC
Permalink
I've never heard of "methyl group deficiency" either. Is this the
kind of thing you are referring to, trigonometry1972?

Clin Nutr. 2008 Dec;27(6):895-9. Epub 2008 Oct 9.

Lack of effect of diet-induced hypomethylation on endothelium-
dependent relaxation in rats.

Hirsch S, Ronco AM, Pinardi G, Montequin MJ, Leiva L, de la Maza MP,
Llanos M, Bunout D.

Aging and chronic diseases program, INTA, University of Chile, PO Box
138-11, Santiago, Chile. ***@inta.cl

BACKGROUND: Endothelial dysfunction is a key process in
atherosclerosis. Hypomethylation is one of the postulated mechanisms
involved in atherogenesis and is mainly secondary to a decrease in
essential factors such as, folate and vitamin B12 for the biosynthesis
of S-adenosylmethionine (SAM), the main methyl-group donor for
methylation reactions. AIM: To investigate in an animal model, whether
hypomethylation, secondary to folate or vitamin B12 deficiency,
affects endothelium-dependent relaxation (EDR) induced by
acetylcholine (ACh). METHODS: Adult male Wistar rats were divided into
4 groups of 12 rats each: folate and B12 deficiency (FB12D 0mg folate/
kg, 0 microg/kg B12), folate deficiency (FD 0mg folate/kg and 50
microg/kg B12), B12 deficiency (B12D: 8 mg/kg folate and 0 microg/kg
B12 and control diet (CD)). After eight weeks the animals were killed
and thoracic aorta and liver removed. Serum concentration of
homocysteine, folate and vitamin B12 were determined. Hepatic levels
of SAM and S-adenosylhomocysteine (SAH) were measured, as indicator of
hypomethylation. ACh-induced EDR and sodium nitroprusside (SNP)-
induced endothelium-independent relaxation (EIR), in isolated aorta
rings were evaluated. RESULTS: Hcy concentrations were significantly
increased in the folate and B12 deficient groups. SAM and the SAM/SAH
ratio were lower in the FD and FB12D than in the control and B12D
group. Folate, B12 deficiency, serum Hcy levels and hepatic SAM/SAH
ratio did not affect EDR neither EIR. CONCLUSIONS: In adult Wistar
rats, chronic folate or folate plus vitamin B12 deficiency generates
hypomethylation which is not related to an alteration of endothelial
function.

My comment: I have heard of these kinds of things before, such as
glutathione deficiency. It seems that these are usually if not always
"downstream" affects, often due to "chronic inflammation" and/or a
great deal of oxidative or nitrosative stress.
trigonometry1972@gmail.com |
2008-12-03 21:05:20 UTC
Permalink
Post by Richard Schultz
: Betaine either in the acidic or base form
: is a good methyl group contributor.
<scratches head>
When did methyl group deficiency suddenly become a major health issue?
Do you even know what a methyl group is?
-----
Department of Chemistry, Bar-Ilan University, Ramat-Gan, Israel
Opinions expressed are mine alone, and not those of Bar-Ilan University
-----
What does anyone know? It seems the
depth of your knowledge on this specific is not so deep
given your comment. Perhaps you can make me
say "wow" and disabuse me this opinion with a
further comment.

Please consider the following examples.

Nonalcoholic fatty liver disease is a fairly common chronic
liver condition in many parts of the world. And
betaine and choline should and can have a role its prevention
and treatment.

Homocysteine levels can be lowered rather directly
by an increased intake of choline sources and betaine.
Elevated levels of homocysteine correlates with most
declines in cognition of the aging brain. Indeed, the standard
approach of taking additional folic acid has shortcomings
which maybe addressed by increasing the level choline and betaine
thus providing methyl group to be loaded on to folic acid to
form folinic acid.

Further, if one looks at the evidence an ample intake
by pregnant women for the fetus, neonates and young children
is good for brain development by helping with glycine
levels among other things.

Moreover, shortage of methyl group contributers correlates
with increased breast cancer. Plus animal models indicate
the such a shortage can result in both hypomethylation
and hypermethylation of the epigenetic controls on the
DNA.

That should be enough of an answer. The examples are just
what came randomly to mind. If you want citations, get your own.
And yes my standards of evidence maybe lower than yours.
But at least I am off the figurative crapper unlike so many who choose
willful uncertainty and then seek to enforce inaction.
See WWW.PUBMED.gov

Sneering comments are easy to make...........Trig
Richard Schultz
2008-12-04 05:37:16 UTC
Permalink
In misc.health.alternative ***@gmail.com | <***@gmail.com> wrote:
: On Dec 3, 2:25?am, ***@mail.biu.ack.il (Richard Schultz) wrote:
:> In misc.health.alternative ***@gmail.com | <***@gmail.com> wrote:

:> : Betaine either in the acidic or base form
:> : is a good methyl group contributor.

:> <scratches head>
:>
:> When did methyl group deficiency suddenly become a major health issue?
:> Do you even know what a methyl group is?

: What does anyone know?

People who have studied can be assumed to know what a methyl group is.
You, apparently, do not.

: Homocysteine levels can be lowered rather directly
: by an increased intake of choline sources and betaine.
: Elevated levels of homocysteine correlates with most
: declines in cognition of the aging brain. Indeed, the standard
: approach of taking additional folic acid has shortcomings
: which maybe addressed by increasing the level choline and betaine
: thus providing methyl group to be loaded on to folic acid to
: form folinic acid.

You might be interested in the article found at
http://www.nature.com/ki/journal/v59/n1/full/4492021a.html, or the
abstract found at http://cat.inist.fr/?aModele=afficheN&cpsidt=980776, or
the paper found at http://ndt.oxfordjournals.org/cgi/content/full/17/5/865.

All of them conclude that folinic acid is no better than folic acid in
the reduction of serum homocysteine levels.

That you don't get folinic acid by methylating folic acid (as anyone with
access to the CRC Handbook, the Merck Index, or Wikipedia can tell you)
seems to me a minor point, although it does tend to illustrate your
basic ignorance of chemistry, I suppose.

-----
Richard Schultz ***@mail.biu.ac.il
Department of Chemistry, Bar-Ilan University, Ramat-Gan, Israel
Opinions expressed are mine alone, and not those of Bar-Ilan University
-----
"You don't even have a clue about which clue you're missing."
Richard Schultz
2008-12-04 09:33:23 UTC
Permalink
In misc.health.alternative Richard Schultz <***@mail.biu.ack.il> wrote:

: :> When did methyl group deficiency suddenly become a major health issue?
: :> Do you even know what a methyl group is?
:
: : What does anyone know?
:
: People who have studied can be assumed to know what a methyl group is.

I realize that it's bad form to follow up to one's own posts, but since
it is unlikely that the editing error will be apparent to our three-sided
friend, I will point out that the above sentence should have read
"People who have studied chemistry can be assumed to know what a
methyl group is."

-----
Richard Schultz ***@mail.biu.ac.il
Department of Chemistry, Bar-Ilan University, Ramat-Gan, Israel
Opinions expressed are mine alone, and not those of Bar-Ilan University
-----
"Logic is a wreath of pretty flowers which smell bad."
trigonometry1972@gmail.com |
2008-12-04 09:52:32 UTC
Permalink
Post by Richard Schultz
:> : Betaine either in the acidic or base form
:> : is a good methyl group contributor.
:> <scratches head>
:>
:> When did methyl group deficiency suddenly become a major health issue?
:> Do you even know what a methyl group is?
: What does anyone know?
People who have studied can be assumed to know what a methyl group is.
You, apparently, do not.
: Homocysteine levels can be lowered rather directly
: by an increased intake of choline sources and betaine.
: Elevated levels of homocysteine correlates with most
: declines in cognition of the aging brain. Indeed, the standard
: approach of taking additional folic acid has shortcomings
: which maybe addressed by increasing the level choline and betaine
: thus providing methyl group to be loaded on to folic acid to
: form folinic acid.
You might be interested in the article found athttp://www.nature.com/ki/journal/v59/n1/full/4492021a.html, or the
abstract found athttp://cat.inist.fr/?aModele=afficheN&cpsidt=980776, or
the paper found athttp://ndt.oxfordjournals.org/cgi/content/full/17/5/865.
All of them conclude that folinic acid is no better than folic acid in
the reduction of serum homocysteine levels.
That you don't get folinic acid by methylating folic acid (as anyone with
access to the CRC Handbook, the Merck Index, or Wikipedia can tell you)
seems to me a minor point, although it does tend to illustrate your
basic ignorance of chemistry, I suppose.
-----
Department of Chemistry, Bar-Ilan University, Ramat-Gan, Israel
Opinions expressed are mine alone, and not those of Bar-Ilan University
-----
Of course, I am ignorant, I only have a minor in chemistry and it is
long
forgotten as that was a generation ago and since it wasn't my bread
and butter.
I should have ♦refreshed memory rather than giving you an on the spot
response. Having said that, you're still avoiding the primary point
that
methyl contributors have an importance in public health.
Indeed, my comment which started this was simply saying
extra present and maybe helpful.

Nor was I saying that folinic acid was best way to lower homocysteine.
Rather I was suggesting betaine and choline also work to lower
homocysteine and by in part a different pathway from the one
the uses folic acid.

And yes I missed a couple of steps in the pathway so you get to gloat.
FA is converted by reduction in two steps into its coenzyme
form tetrahydrofolic acid (FH4). FH4 serves as the
immediate carrier of hydrooxymethyl (-CH2OH), formyl
(-CHO) and methyl (-CH3) in a large number of
enzymatic reactions.

Yes, I know a methyl group is a -CH3 group.

So go be happy your Master's degree (?) has put a person (me)
with a rusty minor in his place. I just googled you
and your name and email address didn't popup at the university.


But l'll be the one to benefit from the extra methyl groups
if there is a benefit to be had.................Trig
Richard Schultz
2008-12-04 11:18:52 UTC
Permalink
In misc.health.alternative ***@gmail.com | <***@gmail.com> wrote:
: On Dec 3, 9:37??pm, ***@mail.biu.ack.il (Richard Schultz) wrote:
:> In misc.health.alternative ***@gmail.com | <***@gmail.com> wrote:
:> : On Dec 3, 2:25?am, ***@mail.biu.ack.il (Richard Schultz) wrote:
:> :> In misc.health.alternative ***@gmail.com | <***@gmail.com> wrote:

:> : Homocysteine levels can be lowered rather directly
:> : by an increased intake of choline sources and betaine.
:> : Elevated levels of homocysteine correlates with most
:> : declines in cognition of the aging brain. Indeed, the standard
:> : approach of taking additional folic acid has shortcomings
:> : which maybe addressed by increasing the level choline and betaine
:> : thus providing methyl group to be loaded on to folic acid to
:> : form folinic acid.

:> You might be interested in the article found at
:> http://www.nature.com/ki/journal/v59/n1/full/4492021a.html, or the
:> abstract found athttp://cat.inist.fr/?aModele=afficheN&cpsidt=980776, or
:> the paper found athttp://ndt.oxfordjournals.org/cgi/content/full/17/5/865.
:>
:> All of them conclude that folinic acid is no better than folic acid in
:> the reduction of serum homocysteine levels.
:>
:> That you don't get folinic acid by methylating folic acid (as anyone with
:> access to the CRC Handbook, the Merck Index, or Wikipedia can tell you)
:> seems to me a minor point, although it does tend to illustrate your
:> basic ignorance of chemistry, I suppose.

: Of course, I am ignorant,

Then why did you take the trouble to imply that you are less ignorant than
I am -- and why do you refuse to make use of the opportunity to learn
something?

: I should have refreshed memory rather than giving you an on the spot
: response. Having said that, you're still avoiding the primary point
: that methyl contributors have an importance in public health.

You have yet to provide any evidence for that claim.

: Nor was I saying that folinic acid was best way to lower homocysteine.
: Rather I was suggesting betaine and choline also work to lower
: homocysteine and by in part a different pathway from the one
: the uses folic acid.

Why don't you reread your own words, which I have quoted above? You made
the explicit claim that folic acid reacts with betaine to form folinic
acid, which is ridiculous on the face of it. And it's irrelevant, since,
as I pointed out to you, folinic acid (which is a metabolite of folic
acid in any case) is no better at reducing homocysteine than folic acid is.

: And yes I missed a couple of steps in the pathway so you get to gloat.

You didn't miss "a couple of steps in the pathway." You missed (and continue
to miss) that folinic acid is *not obtained from folic acid by methylation*.


-----
Richard Schultz ***@mail.biu.ac.il
Department of Chemistry, Bar-Ilan University, Ramat-Gan, Israel
Opinions expressed are mine alone, and not those of Bar-Ilan University
-----
"You don't even have a clue about which clue you're missing."
trigonometry1972@gmail.com |
2008-12-04 14:55:02 UTC
Permalink
Post by Richard Schultz
:> : Homocysteine levels can be lowered rather directly
:> : by an increased intake of choline sources and betaine.
:> : Elevated levels of homocysteine correlates with most
:> : declines in cognition of the aging brain. Indeed, the standard
:> : approach of taking additional folic acid has shortcomings
:> : which maybe addressed by increasing the level choline and betaine
:> : thus providing methyl group to be loaded on to folic acid to
:> : form folinic acid.
:> You might be interested in the article found at
:>http://www.nature.com/ki/journal/v59/n1/full/4492021a.html, or the
:> abstract found athttp://cat.inist.fr/?aModele=afficheN&cpsidt=980776, or
:> the paper found athttp://ndt.oxfordjournals.org/cgi/content/full/17/5/865.
:>
:> All of them conclude that folinic acid is no better than folic acid in
:> the reduction of serum homocysteine levels.
:>
:> That you don't get folinic acid by methylating folic acid (as anyone with
:> access to the CRC Handbook, the Merck Index, or Wikipedia can tell you)
:> seems to me a minor point, although it does tend to illustrate your
:> basic ignorance of chemistry, I suppose.
: Of course, I am ignorant,
Then why did you take the trouble to imply that you are less ignorant than
I am -- and why do you refuse to make use of the opportunity to learn
something?
Because you seemed worthy. I was reflecting what I see
in your postings, IMO. The link was nice. Thanks.
Post by Richard Schultz
: I should have refreshed memory rather than giving you an on the spot
: response. Having said that, you're still avoiding the primary point
: that methyl contributors have an importance in public health.
You have yet to provide any evidence for that claim.
OK, I'll assemble separate posting and put it in
the 5 usenet forums this thread is using.
Post by Richard Schultz
: Nor was I saying that folinic acid was best way to lower homocysteine.
: Rather I was suggesting betaine and choline also work to lower
: homocysteine and by in part a different pathway from the one
: the uses folic acid.
Why don't you reread your own words, which I have quoted above?  You made
the explicit claim that folic acid reacts with betaine to form folinic
acid, which is ridiculous on the face of it.  And it's irrelevant, since,
as I pointed out to you, folinic acid (which is a metabolite of folic
acid in any case) is no better at reducing homocysteine than folic acid is.
: And yes I missed a couple of steps in the pathway so you get to gloat.
You didn't miss "a couple of steps in the pathway."  You missed (and continue
to miss) that folinic acid is *not obtained from folic acid by methylation*.
Yes, I was WRONG about folic to methyl yielding folinic, I've already
said as much.
However, betaine lowers homocysteine in part by ANOTHER biochemical
pathway that does not use FH4. And no I don't have the reference at
hand.
My focus was not supplemental folic acid or folinic acid
but rather supplemental betaine and choline.


Trig
Post by Richard Schultz
-----
Department of Chemistry, Bar-Ilan University, Ramat-Gan, Israel
Opinions expressed are mine alone, and not those of Bar-Ilan University
-----
"You don't even have a clue about which clue you're missing."
Richard Schultz
2008-12-04 16:51:25 UTC
Permalink
In misc.health.alternative ***@gmail.com | <***@gmail.com> wrote:
: On Dec 4, 3:18?am, ***@mail.biu.ack.il (Richard Schultz) wrote:

:> : Of course, I am ignorant,

:> Then why did you take the trouble to imply that you are less ignorant than
:> I am -- and why do you refuse to make use of the opportunity to learn
:> something?

: Because you seemed worthy. I was reflecting what I see
: in your postings, IMO. The link was nice. Thanks.

Since what my postings demonstrate is that I am far less ignorant than
you, I'd say that you should have your eyeglasses checked. Did you
notice that the three links that I posted tend to refute the claim that
you originally made?

:> : I should have refreshed memory rather than giving you an on the spot
:> : response. Having said that, you're still avoiding the primary point
:> : that methyl contributors have an importance in public health.

:> You have yet to provide any evidence for that claim.

: OK, I'll assemble separate posting and put it in
: the 5 usenet forums this thread is using.

Don't forget to tell us about the health benefits of methyl alcohol.

:> : And yes I missed a couple of steps in the pathway so you get to gloat.

: Yes, I was WRONG about folic to methyl yielding folinic, I've already
: said as much.

No, you said that you "missed a couple of steps in the pathway." That
means that you were continuing to claim that you had the essence of
the chemical pathway from folic to folinic acid correct, and made
the mistake of leaving out intermediate steps.

: My focus was not supplemental folic acid or folinic acid
: but rather supplemental betaine and choline.

Apparenly, you did not take the trouble to read what you wrote. You
made one demonstrably false claim about betaine and one that may be
true but for which you have to bring any evidence.

-----
Richard Schultz ***@mail.biu.ac.il
Department of Chemistry, Bar-Ilan University, Ramat-Gan, Israel
Opinions expressed are mine alone, and not those of Bar-Ilan University
-----
"You don't even have a clue about which clue you're missing."
marcia
2008-12-04 19:41:14 UTC
Permalink
Post by Richard Schultz
:> : Of course, I am ignorant,
:> Then why did you take the trouble to imply that you are less ignorant than
:> I am -- and why do you refuse to make use of the opportunity to learn
:> something?
: Because you seemed worthy. I was reflecting what I see
: in your postings, IMO. The link was nice. Thanks.
Since what my postings demonstrate is that I am far less ignorant than
you, I'd say that you should have your eyeglasses checked. Did you
notice that the three links that I posted tend to refute the claim that
you originally made?
:> : I should have refreshed memory rather than giving you an on the spot
:> : response. Having said that, you're still avoiding the primary point
:> : that methyl contributors have an importance in public health.
:> You have yet to provide any evidence for that claim.
: OK, I'll assemble separate posting and put it in
: the 5 usenet forums this thread is using.
Don't forget to tell us about the health benefits of methyl alcohol.
:> : And yes I missed a couple of steps in the pathway so you get to gloat.
: Yes, I was WRONG about folic to methyl yielding folinic, I've already
: said as much.
No, you said that you "missed a couple of steps in the pathway." That
means that you were continuing to claim that you had the essence of
the chemical pathway from folic to folinic acid correct, and made
the mistake of leaving out intermediate steps.
: My focus was not supplemental folic acid or folinic acid
: but rather supplemental betaine and choline.
Apparenly, you did not take the trouble to read what you wrote. You
made one demonstrably false claim about betaine and one that may be
true but for which you have to bring any evidence.
I don't know why they bother to argue chemistry with you; you're in
your element. (heh.)
trigonometry1972@gmail.com |
2008-12-04 21:18:56 UTC
Permalink
Post by marcia
Post by Richard Schultz
:> : Of course, I am ignorant,
:> Then why did you take the trouble to imply that you are less ignorant than
:> I am -- and why do you refuse to make use of the opportunity to learn
:> something?
: Because you seemed worthy. I was reflecting what I see
: in your postings, IMO. The link was nice. Thanks.
Since what my postings demonstrate is that I am far less ignorant than
you, I'd say that you should have your eyeglasses checked.  Did you
notice that the three links that I posted tend to refute the claim that
you originally made?
:> : I should have refreshed memory rather than giving you an on the spot
:> : response. Having said that, you're still avoiding the primary point
:> : that methyl contributors have an importance in public health.
:> You have yet to provide any evidence for that claim.
: OK, I'll assemble separate posting and put it in
: the 5 usenet forums this thread is using.
Don't forget to tell us about the health benefits of methyl alcohol.
:> : And yes I missed a couple of steps in the pathway so you get to gloat.
: Yes, I was WRONG about folic to methyl yielding folinic, I've already
: said as much.
No, you said that you "missed a couple of steps in the pathway."  That
means that you were continuing to claim that you had the essence of
the chemical pathway from folic to folinic acid correct, and made
the mistake of leaving out intermediate steps.
: My focus was not supplemental folic acid or  folinic acid
: but rather supplemental betaine and choline.
Apparenly, you did not take the trouble to read what you wrote.  You
made one demonstrably false claim about betaine and one that may be
true but for which you have to bring any evidence.
I don't know why they bother to argue chemistry with you; you're in
your element. (heh.)
And the fan club member speaks above.

Anyway we'll see if he'll puts out. And just because I get an
important
point wrong does not prove everything I say is wrong.
And note that his citations aren't especially relevant
whereas those I cite are.

Don't you go and put out there marcia.....................Trig
Richard Schultz
2008-12-04 21:57:06 UTC
Permalink
In misc.health.alternative ***@gmail.com | <***@gmail.com> wrote:

: Anyway we'll see if he'll puts out. And just because I get an
: important point wrong does not prove everything I say is wrong.

That you got an important point wrong and clearly failed to understand
*why* it was wrong indicates that you post material without knowing (or,
it seems, caring) whether or not it is correct. One might conclude from
that observation that anything that you post must necessarily be
considered suspect.

: And note that his citations aren't especially relevant
: whereas those I cite are.

Once again, I will quote you your own words, which you seem not to have
bothered reading:
(from <65e9ea8b-b2cc-4df8-96e7-***@s9g2000prm.googlegroups.com>)

### Indeed, the standard approach of taking additional folic acid has
### shortcomings which maybe addressed by increasing the level choline and
### betaine thus providing methyl group to be loaded on to folic acid to
### form folinic acid.

You make a claim that converting folic acid to folinic acid addresses
the "shortcomings" of taking folic acid alone. I provided three references
to investigations that appear to show that there is no benefit of taking
folinic acid relative to taking folic acid. Since those citations provide
a direct refutation of a claim that you made, anyone who actually read what
you wrote -- a category that doesn't seem to include you -- would understand
their relevance.

-----
Richard Schultz ***@mail.biu.ac.il
Department of Chemistry, Bar-Ilan University, Ramat-Gan, Israel
Opinions expressed are mine alone, and not those of Bar-Ilan University
-----
"You don't even have a clue about which clue you're missing."
trigonometry1972@gmail.com |
2008-12-04 21:10:25 UTC
Permalink
Post by Richard Schultz
:> : Of course, I am ignorant,
:> Then why did you take the trouble to imply that you are less ignorant than
:> I am -- and why do you refuse to make use of the opportunity to learn
:> something?
: Because you seemed worthy. I was reflecting what I see
: in your postings, IMO. The link was nice. Thanks.
Since what my postings demonstrate is that I am far less ignorant than
you, I'd say that you should have your eyeglasses checked.  Did you
notice that the three links that I posted tend to refute the claim that
you originally made?
The links are on the topic of folic acid, variious B vitamins, and
the lowering
of homocysteine not on betaine and choline and the lowering of
homocysteine.

If you want to draw out attention to specific line, please quote it.
Do a cut and paste of the line.
Post by Richard Schultz
:> : I should have refreshed memory rather than giving you an on the spot
:> : response. Having said that, you're still avoiding the primary point
:> : that methyl contributors have an importance in public health.
:> You have yet to provide any evidence for that claim.
OK here we go.

Nonalcoholic fatty liver disease is a fairly common chronic
liver condition in many parts of the world. And
betaine and choline should and can have a role its prevention
and treatment.


1: J Nutr Biochem. 2007 Mar;18(3):184-95.

Nonalcoholic fatty liver disease:
predisposing factors and the role of nutrition.

Cave M, Deaciuc I, Mendez C, Song Z, Joshi-Barve S,
Barve S, McClain C.

Department of Medicine,
University of Louisville Medical Center,
Louisville, KY
40292, USA.

More than 20% of Americans have nonalcoholic fatty
liver disease (NAFLD), and this is, by far, the leading
cause of abnormal liver enzymes in the United States.
Nonalcoholic steatohepatitis (NASH), a more serious
form of NAFLD, can proceed to cirrhosis and even
hepatocellular carcinoma. These liver diseases represent
the hepatic component of the metabolic syndrome, and
this spectrum of liver disease represents a major
health problem both in the United States and worldwide.
Hepatic steatosis is closely linked to nutrition,
including obesity, possibly high-fructose corn
syrup consumption and consumption of certain types of
fats. There are a variety of second insults or "hits"
that appear to transform simple steatosis into NASH,
with some of these second hits including certain
proinflammatory cytokines, oxidative stress and
possibly industrial toxins. In certain underdeveloped
countries, it appears likely that industrial toxins
play a role in NASH, and there is increasing interest
in the potential interaction of industrial toxins
and nutrients. Moreover, optimal therapy for NAFLD
appears to include lifestyle modification with
exercise, diet and weight loss. Certain nutrients
may also be of benefit. Important areas for future
research are the effect(s) of nutritional supplements
on NAFLD/NASH and the effects of industrial
toxins.


PMID: 17296492


1: J Gastroenterol Hepatol.
2008 Mar;23 Suppl 1:S16-24.

Dissection of endoplasmic reticulum stress signaling
in alcoholic and non-alcoholic liver injury.

Ji C.

USC-UCLA Research Center for Alcoholic Liver and
Pancreatic Diseases,
Department of Medicine,
Keck School of Medicine,
University of Southern California,
Los Angeles, California
90033, USA.
***@usc.edu

Accumulation of unfolded or malfolded proteins induces
endoplasmic reticulum (ER) stress which elicits a
complex network of interacting and parallel responses
that dampen the stress. The ER stress response in the
liver is controlled by intrinsic feedback effectors
and is initially protective. However, delayed or insufficient
responses or interplay with mitochondrial dysfunction
may turn physiological mechanisms into pathological
consequences including apoptosis, fat accumulation
and inflammation all of which have an important role
in the pathogenesis of liver disorders such as
genetic mutations, viral hepatitis, insulin resistance,
ischemia/reperfusion injury, and alcoholic and
non-alcoholic steatosis. In both alcohol and
non-alcohol-induced ER stress, a common candidate is
hyperhomocysteinemia. Betaine supplementation and/or
expression of betaine-homocysteine methyltransferase
(BHMT) promote removal of homocysteine and alleviate
ER stress, fatty accumulation and apoptosis in
cultured hepatocytes and mouse models. The rapidity
and magnitude of homocysteine-induced activation of
each of the main ER resident transmembrane sensors
including inositol requiring enzyme 1 (IRE-l alpha),
activating transcription factor 6 (ATF-6) and
RNA-activated protein kinase (PKR)-like ER kinase
(PERK) appear different in different experimental models.
Dissection and differentiation of ER stress signaling
may reveal clues on the specific importance of the ER
stress response in contributing to liver injury and
thus provide better strategies on prevention
and treatment of liver disease.

PMCID: PMC2491335
PMID: 18336657

The full article is available by way of link on
Pubmed.


Homocysteine levels can be lowered rather directly
by an increased intake of choline sources and betaine.
Elevated levels of homocysteine correlates with most
declines in cognition of the aging brain.
<snipped my mistake due to brain rot>

The second article I referred to mentions
the none folic acid related pathway to
the regeneration of homocysteine to
methionine by way of BHMT.


Further, if one looks at the evidence an ample intake
by pregnant women for the fetus, neonates and young children
is good for brain development by helping with glycine
levels among other things.

1: J Nutr. 2007 Dec;137(12):2641-6.

Relationship of dimethylglycine, choline,
and betaine with oxoproline in plasma
of pregnant women and their newborn infants.

Friesen RW, Novak EM, Hasman D, Innis SM.

Nutrition Research Program,
Child and Family Research Institute,
University of British Columbia,
Vancouver, Canada V5Z 4H4.

Choline and glycine are inter-related through their
roles in methyl metabolism. Choline is metabolized
to betaine, which donates a methyl group to homocysteine
to form methionine, also generating dimethylglycine,
which is further metabolized to glycine. Choline
is transported across the placenta and is higher
in fetal than maternal plasma. Placental glycine
transfer, however, is limited and poor glycine
status has been suggested in preterm infants.
Insufficient glycine for glutathione (GSH) synthesis
results in increased metabolism of gamma-glutamyl
cysteine to 5-oxoproline. We measured plasma
5-oxoproline as a metabolic indicator to address
whether choline, via dimethylglycine, contributes
physiologically relevant amounts of glycine in
pregnancy. Blood was collected from healthy term
pregnant women and their newborn infants at delivery
(n = 46) and nonpregnant healthy women (n = 19) as
a reference group. Plasma choline, betaine,
dimethylglycine, homocysteine, methionine, and
5-oxoproline were quantified by HPLC-tandem MS.
Plasma choline was 45% higher, but betaine was 63%
lower and dimethylglycine was 28% lower in
pregnant than nonpregnant women (P < 0.01).
Higher white blood cell choline dehydrogenase
messenger RNA levels in a random subset of
pregnant (n = 8) than nonpregnant women (n = 7)
(P < 0.01) suggest increased betaine and
dimethylglycine turnover rather than decreased
synthesis. Plasma choline, betaine, and
dimethylglycine were higher (P < 0.001)
in fetal plasma (36.4 +/- 13, 29.4 +/- 1.0,
and 2.44 +/- 0.12 micromol/L, respectively)
than maternal plasma (15.3 +/- 0.42, 14.1 +/- 0.6
and 1.81 +/- 0.12 micromol/L, respectively).
Concentrations of 5-oxoproline and dimethylglycine
were inversely (P < 0.05) correlated in maternal
(Spearman rho = -0.35) and fetal plasma
(Spearman rho = -0.32), suggesting that choline,
via dimethylglycine, contributes glycine
for GSH synthesis in human development.


PMID: 18029477

http://jn.nutrition.org/cgi/content/full/137/12/2641

"dimethylglycine, and its choline and betaine precursors,
may play an important role in generating glycine,
an amino acid potentially limiting in early human development."


Moreover, shortage of methyl group contributers correlates
with increased breast cancer. Plus animal models indicate
the such a shortage can result in both hypomethylation
and hypermethylation of the epigenetic controls on the
DNA.

1: FASEB J. 2008 Jun;22(6):2045-52.
Epub 2008 Jan 29.

Choline metabolism and risk of breast cancer
in a population-based study.

Xu X, Gammon MD, Zeisel SH, Lee YL, Wetmur JG,
Teitelbaum SL, Bradshaw PT, Neugut AI, Santella RM, Chen J.

Department of Community and Preventive Medicine,
Mt. Sinai School of Medicine,
One Gustave L. Levy Place,
New York, NY 10029, USA.

Choline is an essential nutrient required for methyl
group metabolism, but its role in carcinogenesis
and tumor progression is not well understood.
By utilizing a population-based study of 1508 cases
and 1556 controls, we investigated the
associations of dietary intake of choline
and two related micronutrients, methionine and
betaine, and risk of breast cancer.
The highest quintile of choline consumption was
associated with a lower risk of breast cancer
[odds ratio (OR): 0.76; 95% confidence interval
(CI): 0.58-1.00] compared with the lowest quintile.
Two putatively functional single nucleotide
polymorphisms of choline-metabolizing genes,
PEMT -774G>C (rs12325817) and CHDH +432G>T (rs12676),
were also found be related to breast cancer risk.
Compared with the PEMT GG genotype, the variant CC
genotype was associated with an increased risk
of breast cancer (OR: 1.30; 95% CI: 1.01-1.67).
The CHDH minor T allele was also associated
with an increased risk (OR: 1.19; 95% CI: 1.00-1.41)
compared with the major G allele. The BHMT rs3733890
polymorphism was also examined but was found not to be
associated with breast cancer risk. We observed a
significant interaction between dietary betaine
intake and the PEMT rs7926 polymorphism
(P(interaction)=0.04). Our findings suggest
that choline metabolism may play an important role in breast
cancer etiology.

PMCID: PMC2430758
PMID: 18230680


And Yes I am aware other reseachers have done
work yeilding null results. See PMID: 18086790
Post by Richard Schultz
Don't forget to tell us about the health benefits of methyl alcohol.
Err I'll leave that mostly for you. Though I suspect some overstate
the threat of low levels of free methanol. And I have the impression
the choline and betaine derived methyl groups rather carefully
controlled but then again what do I know?
There is of course the Aspartame methanol controversy some
are quite exercised about. But also recall there are other
proposed mechanisms for toxicity.

http://en.wikipedia.org/wiki/Aspartame_controversy
Post by Richard Schultz
:> : And yes I missed a couple of steps in the pathway so you get to gloat.
: Yes, I was WRONG about folic to methyl yielding folinic, I've already
: said as much.
No, you said that you "missed a couple of steps in the pathway."  That
means that you were continuing to claim that you had the essence of
the chemical pathway from folic to folinic acid correct, and made
the mistake of leaving out intermediate steps.
: My focus was not supplemental folic acid or  folinic acid
: but rather supplemental betaine and choline.
Apparenly, you did not take the trouble to read what you wrote.  You
made one demonstrably false claim about betaine and one that may be
true but for which you have to bring any evidence.
That is the danger of the Usenet for all of us. It is too easy, not
like pen to paper.

Trig
Post by Richard Schultz
-----
Richard Schultz                              
Richard Schultz
2008-12-05 06:31:35 UTC
Permalink
In misc.health.alternative ***@gmail.com | <***@gmail.com> wrote:

:> Since what my postings demonstrate is that I am far less ignorant than
:> you, I'd say that you should have your eyeglasses checked. Did you
:> notice that the three links that I posted tend to refute the claim that
:> you originally made?

: The links are on the topic of folic acid, variious B vitamins, and
: the lowering of homocysteine not on betaine and choline and the lowering of
: homocysteine.

No, the links are on the topic of whether folinic acid is any better than
folic acid at reducing homocysteine levels.

: If you want to draw out attention to specific line, please quote it.
: Do a cut and paste of the line.

I have already explained to you -- more than once -- the relevance of the
three studies I cited to the text that you wrote but apparently did not read.
My patience for continuing to do so is at an end.

:> :> : I should have refreshed memory rather than giving you an on the spot
:> :> : response. Having said that, you're still avoiding the primary point
:> :> : that methyl contributors have an importance in public health.

: Moreover, optimal therapy for NAFLD appears to include lifestyle
: modification with exercise, diet and weight loss. Certain nutrients
: may also be of benefit.

Not a word about methyl contributors.

: Betaine supplementation and/or expression of betaine-homocysteine
: methyltransferase (BHMT) promote removal of homocysteine

Finally, an article that mentions a biological pathway in which
betaine acts as a methyl donor. The question I don't see answered is whether
betaine supplementation is of any use to people who do not already have
elevated levels of homocysteine, or whether it can prevent the development
of elevated levels of homocysteine.

: Choline is an essential nutrient required for methyl
: group metabolism,

Are you aware that betaine is a metabolite of choline?

:> Don't forget to tell us about the health benefits of methyl alcohol.
:
: Err I'll leave that mostly for you. Though I suspect some overstate
: the threat of low levels of free methanol. And I have the impression
: the choline and betaine derived methyl groups rather carefully
: controlled but then again what do I know?

I was just kidding -- methanol is not a methyl group donor (it is
metabolized via alcohol dehydrogenase and aldehyde dehydrogenase to formic
acid, which is why methanol is much more poisonous than ethanol).

-----
Richard Schultz ***@mail.biu.ac.il
Department of Chemistry, Bar-Ilan University, Ramat-Gan, Israel
Opinions expressed are mine alone, and not those of Bar-Ilan University
-----
"You don't even have a clue about which clue you're missing."
trigonometry1972@gmail.com |
2008-12-06 13:33:33 UTC
Permalink
$:> Since what my postings demonstrate is that I am far less ignorant
than
$:> you, I'd say that you should have your eyeglasses checked. Did
you
$:> notice that the three links that I posted tend to refute the claim
that
$:> you originally made?

$: The links are on the topic of folic acid, variious B vitamins, and
$: the lowering of homocysteine not on betaine and choline and the
lowering of
$: homocysteine.

$ No, the links are on the topic of whether folinic acid is any better
than
$ folic acid at reducing homocysteine levels.


The articles cover both folic and folinic and they don't
cover betaine or choline as a means of lowering homocysteine.
Though the authors of one of the papers are aware
there are other pathways related to lowering homocysteine.
"(These findings) also suggest that the reduction of plasma
homocysteine clearance may be due to multiple abnormalities
of the remethylation pathway that may not be related to folate alone"

You apparently see folic acid and B12 as "the only game in town"?

Consider this work in animals:

: J Nutr. 1989 Apr;119(4):618-21.

Effect of dietary methyl group deficiency on folate
metabolism in rats.

Horne DW, Cook RJ, Wagner C.

Department of Biochemistry,
Vanderbilt University School of Medicine,
Nashville, TN 37212.

The carcinogenic effects of methyl-deficient, amino
acid-defined diets have been attributed to alterations
in cellular methylation reactions. These diets contain
no choline, and methionine is replaced by homocysteine.
Hence, all methyl groups needed for methionine biosynthesis
with subsequent formation of S-adenosylmethionine and
polyamines must be formed de novo utilizing folate-dependent
reduction of one-carbon units. In rats fed the methyl-deficient
diet, there was a marked decrease in total liver folate
levels. This decrease was apparent in the levels of
the individual forms of folate: 10-HCO-H4folate,
5-HCO-H4folate, 5-CH3-H4folate and H4folate.
The percent of the total folate pool made up
by 5-CH3-H4folate did not change, however, until
after the rats had been fed the methyl-deficient diet
for 4 wk, and then an increase was seen. After the
methyl-deficient rats were switched to a nutritionally
adequate control diet containing methionine and choline,
all values rapidly reversed. Increased use of
folate for methyl group biosynthesis may be
responsible for the loss of folates
from the liver.


PMID: 2784833


$: If you want to draw out attention to specific line, please quote
it.
$: Do a cut and paste of the line.

$ I have already explained to you -- more than once -- the relevance
of the
$ three studies I cited to the text that you wrote but apparently did
not read.
$ My patience for continuing to do so is at an end.

You didn't address betaine and choline as a means of lowering
homocysteine or of it having health benefits.

Yes of course I've read the articles, I've reread them by
this point in time. Nor are the articles
incompatible with my view that betaine and Choline
have important roles in the recycling of homocysteine.
See the final sentence in Oxford journal paper you
cited which says:
"They also suggest that the reduction of plasma homocysteine
clearance may be due to multiple abnormalities of
the remethylation pathway that may not be related to folate alone."

Moreover, the research in your cited works is on
hyperhomocysteinemia in hemodialysis patients
which are just one group with clearly elevated homocysteine levels and
hopefully not yet the largest. Nor should it be
assumed they are representative for the other groups.



$:> :> : I should have refreshed memory rather than giving you an on
the spot
$:> :> : response. Having said that, you're still avoiding the primary
point
$:> :> : that methyl contributors have an importance in public
health.

$: Moreover, optimal therapy for NAFLD appears to include lifestyle
$: modification with exercise, diet and weight loss. Certain
nutrients
$: may also be of benefit.

Note the first comment in the Objectives section in
the next abstract found below: "No effective
therapy currently exists........."

$ Not a word about methyl contributors.

The point is that betaine can benefit NAFLD. And it
is going to do that by way of methyl contribution
as that is what it does.

Recall the first abstract stated "Certain nutrients
may also be of benefit. Important areas for future
research are the effect(s) of nutritional supplements
on NAFLD/NASH and the effects of industrial
toxins."

Moreover read the following:

: Am J Gastroenterol. 2001 Sep;96(9):2711-7.

Comment in:
Am J Gastroenterol. 2001 Sep;96(9):2534-6.

Betaine, a promising new agent for patients with
nonalcoholic steatohepatitis: results of a pilot study.

Abdelmalek MF, Angulo P, Jorgensen RA, Sylvestre PB,
Lindor KD.

Divisions of Gastroenterology and Hepatology and Surgical Pathology,
Mayo Clinic and Foundation,
Rochester, Minnesota 55905, USA.

OBJECTIVES:
No effective therapy currently exists for patients
with nonalcoholic steatohepatitis (NASH).

Betaine, a naturally occurring metabolite of choline,
has been shown to raise S-adenosylmethionine (SAM)
levels that may in turn play a role in decreasing
hepatic steatosis.

Our aim was to determine the safety and
effects of betaine on liver biochemistries and
histological markers of disease
activity in patients with NASH.

METHODS:
Ten adult patients with NASH were
enrolled. Patients received betaine anhydrous
for oral solution (Cystadane) in two divided
doses daily for 12 months. Seven out of 10 patients
completed 1 yr of treatment with betaine.

RESULTS:
A significant improvement in serum levels of
aspartate aminotransferase (p = 0.02) and ALAT
(p = 0.007) occurred during treatment. Aminotransferases
normalized in three of seven patients, decreased by
50% in three of seven patients, and remained unchanged
in one patient when compared to baseline values.
A marked improvement in serum levels of
aminotransferases (ALT -39%; AST -38%) also occurred
during treatment in those patients who did not
complete 1 yr of treatment. Similarly, a marked improvement
in the degree of steatosis, necroinflammatory grade,
and stage of fibrosis was noted at 1 yr of treatment
with betaine. Transitory GI adverse events that did
not require any dose reduction or discontinuation of
betaine occurred in four
patients.

CONCLUSIONS:
Betaine is a safe and well tolerated drug that leads to a
significant biochemical and histological improvement
in patients with NASH. This novel agent deserves
further evaluation in a randomized, placebo-controlled
trial.

-----------------------------
And yet again consider the following:

: Semin Liver Dis. 2007 Nov;27(4):367-77.

Endoplasmic reticulum stress and liver injury.

Kaplowitz N, Than TA, Shinohara M, Ji C.

Department of Medicine,
USC-UCLA Research Center for Alcoholic and Pancreatic
Diseases and USC Research Center for Liver Diseases,
Keck School of Medicine
University of Southern California,
Los Angeles, California CA 90033, USA.
***@usc.edu

Endoplasmic reticulum stress, initiated by protein overload
or malfolding, activates a complex network of interacting
and parallel responses that dampen the
stress. However, when the protective response is
insufficient, a set of responses leads to apoptosis.
Coupled with the latter are promotion of lipid synthesis
and proinflammatory responses. Evidence has been mounting
for an important role of the endoplasmic reticulum (ER)
stress response in the pathogenesis of chronic
viral hepatitis, insulin resistance and nonalcoholic
fatty liver disease, ischemia-reperfusion injury,
genetic disorders of protein malfolding, and
alcoholic liver disease. In the latter,
a key candidate for inducing ER stress is
hyperhomocysteinemia.

Betaine treatment promotes removal of homocysteine and
prevents ER stress, fatty liver, and
apoptosis in a mouse model of alcohol-induced
liver disease. With increasing interest
in the potential role of ER stress in liver
disease, greater understanding of pathophysiology,
prevention, and treatment of liver disease is anticipated.


PMID: 17979073
-------------------------

Note the sentence that I set apart from the others
in the following abstract.


1: Metab Syndr Relat Disord. 2003 Jun;1(2):159-70.

Management of hyperhomocysteinemia.

Chan E, Fonseca VA.

Section of Endocrinology, Department of Medicine,
Tulane University Medical
School, New Orleans, Louisiana.

Hyperhomocysteinemia is an established risk factor
for cardiovascular disease. The modification of
traditional cardiovascular risk factors has resulted in
better morbidity and mortality outcomes,
so the treatment of hyperhomocysteinemia
is explored for a similar benefit.
Vitamin B(6), vitamin B(12) and folate, as
co-factors in the metabolism of homosyteine, are used in the treatment
of
hyperhomocysteinemia.

Betaine, a methyl-donor in a separate homocysteine
metabolism pathway, is also used to treat hyperhomocysteinemia.

These supplements
have been used in various doses and combinations
for different periods of time, with favorable outcomes.
There is still no concensus whether hyperhomocysteinemia
can be treated with folic acid alone, or
in combination with vitamin B(6) and vitamin B(12).
The dose of the supplements required to normalize fasting
homocysteine remains to be determined, especially
in diabetic nephropathy, hemodialysis and renal
transplant patients. The benefits from lowering
homocysteine levels have mainly been demonstrated
in surrogate cardiovascular outcomes.
The treatment of hyperhomocysteinemia cannot be
firmly advocated until there are trials that
demonstrate a beneficial clinical endpoint.
In patients who have cardiovascular disease
in the absence of more established risk factors,
investigation and treatment of hyperhomocysteinemia
should be considered.


PMID: 18370637


$ : Betaine supplementation and/or expression of betaine-homocysteine
$ : methyltransferase (BHMT) promote removal of homocysteine

$ Finally, an article that mentions a biological pathway in which
$ betaine acts as a methyl donor. The question I don't see answered
is whether
$ betaine supplementation is of any use to people who do not already
have
$ elevated levels of homocysteine, or whether it can prevent the
development
$ of elevated levels of homocysteine.

It will vary some according to the MTHFR genotype of
a person or group. Logically if it can treat then it can be used
to prevent especially given its practical nontoxicity.
Further, the additional betaine and choline
may come from not from supplements but from
different dietary choices as well i.e. eggs, lecithin
(assuming you don't see lecithin as supplement, LOL.)
So the issue is do you give dietary advice or supplements
to all to benefit a subset of the population?
Or does most of the population have a span of
life come into a boichemical range that might benefit
from additional methyl donors from betaine and choline
as opposed to adding more schuttles for the
transfer of methyl group? As the methyl
groups transfered from 5-methyltetrahydrofolate
to homocysteine they didn't come on the folic
acid but come from somewhere else in
the metabolism. Whereas betaine brings it
own methyl groups.

And there is the question as to what is needed
to optimize genomic stability and optimize
epigenetic control of the genome. Some already
suggest the current recommendations for
folic acid and cobalamin
PMID: 15705599 full review available by link on Pubmed
PMID: 11506798
are suboptimal in this reguard
and by extension I think fair to suspect that it is
possible an increase in methyl donors by way
of that use betaine which in turn serves as feed
stock for the remethylation of homocysteine
by way of betaine homocysteine methyltransferase
could have important results if
maintained over the decades.

Am J Clin Nutr. 2008 Sep;88(3):685-92.

"CONCLUSIONS: These data suggest that 550 mg choline/d is
sufficient for preventing elevations in serum markers of liver
dysfunction in this population under the conditions of this study;
higher intakes may be needed to optimize other endpoints."

PMID: 18779284
------------------

: Am J Clin Nutr. 2008 Mar;87(3):577-85.

Dietary and supplementary betaine: acute effects on
plasma betaine and homocysteine concentrations
under standard and postmethionine load conditions in
healthy male subjects.

Atkinson W, Elmslie J, Lever M, Chambers ST, George PM.

Clinical Biochemistry Unit,
Canterbury Health Laboratories,
Christchurch, New Zealand.

BACKGROUND:
Betaine comes from the diet and from choline,
and it is associated with vascular disease in some
patient groups. Betaine supplementation lowers
plasma total homocysteine.

OBJECTIVE:
We compared the acute effects of dietary
and supplementary betaine and choline on plasma
betaine and homocysteine under standard conditions
and after a methionine load.

DESIGN:
In a randomized crossover study,
8 healthy men (19-40 y)
consumed a betaine supplement (approximately 500 mg),
high-betaine meal (approximately 517 mg),
choline supplement (500 mg),
high-choline meal (approximately 564 mg),
high-betaine and
-choline meal (approximately 517 mg betaine,
approximately 622 mg choline), or a
low-betaine and -choline control meal under
standard conditions
or postmethionine load. Plasma betaine, dimethylglycine,
and homocysteine concentrations were
measured hourly for 8 h and at 24 h after treatment.

RESULTS:
Dietary and supplementary betaine raised plasma betaine
concentrations relative to control (P
< 0.001) under standard conditions. This was
not associated with raised plasma
dimethylglycine concentration, and
no significant betaine appeared in the urine.
A small increase in dimethylglycine excretion
was observed when either betaine or
choline was supplied (P = 0.011 and < 0.001).
Small decreases in plasma
homocysteine 6 h after ingestion under standard
conditions (P < or = 0.05) were
detected after a
high-betaine meal and after a high-betaine and
high-choline meal. Dietary betaine and choline
and betaine supplementation attenuated the
increase in plasma homocysteine at both 4 and 6 h a
fter a methionine load (P < or
= 0.001).

CONCLUSIONS:
Dietary betaine and supplementary betaine acutely increase
plasma betaine, and they and choline attenuate the
postmethionine load rise in homocysteine concentrations.


PMID: 18326594




$ : Choline is an essential nutrient required for methyl
$ : group metabolism,

$ Are you aware that betaine is a metabolite of choline?

Yes. Choline has a OH functional group instead of
an COOH functional that is on Betaine but otherwise it is
the same molecule.

'Test on Thursday'....;-)


$ :> Don't forget to tell us about the health benefits of methyl
alcohol.
$ :
$ : Err I'll leave that mostly for you. Though I suspect some
overstate
$ : the threat of low levels of free methanol. And I have the
impression
$ : the choline and betaine derived methyl groups rather carefully
$ : controlled but then again what do I know?

$ I was just kidding -- methanol is not a methyl group donor
$ (it is metabolized via alcohol dehydrogenase and aldehyde
$ dehydrogenase to formic acid, which is why methanol is
$ much more poisonous than ethanol).

Yes of course. You were "leaving bait" as I saw it.

-----
$ Richard Schultz
$ Department of Chemistry


consuming betaine in multiple grams daily.........Trig
Richard Schultz
2008-12-07 05:58:32 UTC
Permalink
In misc.health.alternative ***@gmail.com | <***@gmail.com> wrote:

: You apparently see folic acid and B12 as "the only game in town"?

No, I made the mistake of assuming that you had read your own posts, a
mistake that I shall make every effort to refrain from making in the future.

-----
Richard Schultz ***@mail.biu.ac.il
Department of Chemistry, Bar-Ilan University, Ramat-Gan, Israel
Opinions expressed are mine alone, and not those of Bar-Ilan University
-----
"You don't even have a clue about which clue you're missing."
trigonometry1972@gmail.com |
2008-12-07 11:53:45 UTC
Permalink
Post by Richard Schultz
: You apparently see folic acid and B12 as "the only game in town"?
No, I made the mistake of assuming that you had read your own posts, a
mistake that I shall make every effort to refrain from making in the future.
-----
Department of Chemistry, Bar-Ilan University, Ramat-Gan, Israel
Opinions expressed are mine alone, and not those of Bar-Ilan University
-----
"You don't even have a clue about which clue you're missing."
I noticed your full name doesn't show on the list professors,
postgrads and etc
at the U.

Anyway, this thread seems to be ended.

not the last word though........................Trig
marcia
2008-12-07 15:49:09 UTC
Permalink
Post by ***@gmail.com |
Post by Richard Schultz
: You apparently see folic acid and B12 as "the only game in town"?
No, I made the mistake of assuming that you had read your own posts, a
mistake that I shall make every effort to refrain from making in the future.
-----
Department of Chemistry, Bar-Ilan University, Ramat-Gan, Israel
Opinions expressed are mine alone, and not those of Bar-Ilan University
-----
"You don't even have a clue about which clue you're missing."
I noticed your full name doesn't show on the list professors,
postgrads and etc
at the U.
Funny, because after you wrote this, I FOUND plenty of evidence that
he is a professor in the Department of Chemistry of Bar-Ilan
University, but I'm not going to share the information with you
because of the potential for misuse.

I hope you're not planning to stalk or harass him, because that would
be ill-advised.

Suffice it to say, he is genuine, as is his PhD and expertise in
chemistry.
trigonometry1972@gmail.com |
2008-12-07 17:17:52 UTC
Permalink
Post by marcia
Post by ***@gmail.com |
Post by Richard Schultz
: You apparently see folic acid and B12 as "the only game in town"?
No, I made the mistake of assuming that you had read your own posts, a
mistake that I shall make every effort to refrain from making in the future.
-----
Department of Chemistry, Bar-Ilan University, Ramat-Gan, Israel
Opinions expressed are mine alone, and not those of Bar-Ilan University
-----
"You don't even have a clue about which clue you're missing."
I noticed your full name doesn't show on the list professors,
postgrads and etc
at the U.
Funny, because after you wrote this, I FOUND plenty of evidence that
he is a professor in the Department of Chemistry of Bar-Ilan
University, but I'm not going to share the information with you
because of the potential for misuse.
I hope you're not planning to stalk or harass him, because that would
be ill-advised.
Suffice it to say, he is genuine, as is his PhD and expertise in
chemistry.
No he quite safe, but I did feel compelled to take a brief look given
that he put up his "shingle" (sign) so
to speak. I don't recall that he claimed having a Ph D so he
maybe further down to totem pole, he might even be an
undergrad for all I know.

enough...................Trig
Richard Schultz
2008-12-07 20:43:56 UTC
Permalink
In misc.health.alternative ***@gmail.com | <***@gmail.com> wrote:

: I don't recall that he claimed having a Ph D so he
: maybe further down to totem pole, he might even be an
: undergrad for all I know.

I have a Ph.D. in physical chemistry from the University of California
at Berkeley. It's also unlikely that an undergrad would have been posting
to usenet for more than 20 years.

-----
Richard Schultz ***@mail.biu.ac.il
Department of Chemistry, Bar-Ilan University, Ramat-Gan, Israel
Opinions expressed are mine alone, and not those of Bar-Ilan University
-----
"Logic is a wreath of pretty flowers which smell bad."
Richard Schultz
2008-12-07 20:42:18 UTC
Permalink
In misc.health.alternative marcia <***@gmail.com> wrote:

: Suffice it to say, he is genuine, as is his PhD and expertise in
: chemistry.

One can always look for the record of my dissertation in the UC library
catalog (http://melvyl.cdlib.org) -- an author search for "Schultz, Richard"
limited to dissertations at UC-Berkeley turns it up without too much
difficulty.

-----
Richard Schultz ***@mail.biu.ac.il
Department of Chemistry, Bar-Ilan University, Ramat-Gan, Israel
Opinions expressed are mine alone, and not those of Bar-Ilan University
-----
"Logic is a wreath of pretty flowers which smell bad."
marcia
2008-12-07 23:43:14 UTC
Permalink
Post by Richard Schultz
: Suffice it to say, he is genuine, as is his PhD and expertise in
: chemistry.
One can always look for the record of my dissertation in the UC library
catalog (http://melvyl.cdlib.org) -- an author search for "Schultz, Richard"
limited to dissertations at UC-Berkeley turns it up without too much
difficulty.
Guided-ion beam studies of thermochemistry, reactions, and electronic
effects in N+2, N+4, Ligated Fe+-alkane reaction systems / by Richard
Hersch Schultz ?

I made the mistake of typing in your last name only, and had to
waaaaiiiiiitttttttt while the computer located all the Schultz
dissertations written since the late 19th-century (and I did narrow to
UC-Berkeley). Unfortunately, the only chemistry term I'm familiar with
from the title is Fe. :)

RF
2008-12-03 04:12:21 UTC
Permalink
Post by m***@lycos.com
It might help a little, but if you are eating a PUFA-rich diet, you
are "playing with fire" no matter what the other food items are. I
was a vegan who ate nearly all organic food for a dozen years, and
that didn't prevent me from almost dying (apparently of not being able
to produce enough stomach acid) before the age of 40.
Hi Monty,

What PUFA amounts would you consider safe?
m***@lycos.com
2008-12-03 06:04:46 UTC
Permalink
I think it's more about reading food labels. I eat things like
cookies if the fat content is well over 50% SFAs. I prefer 70% or
more. Basically, these kinds of food items are made to last, whereas
with PUFA-rich oils used for cooking you're dealing with something
that's going to be generating free radicals as soon as you open up the
bottle (and cooking with it makes it worse). Cooked meat can also be
very rich in PUFAs, and the PUFA-rich oils/cooked meat combination is
especially bad (generating lots of HCAs). I also don't avoid more
than very small amounts of cholesterol in such food items (but I eat
full fat butter and cheese, though I don't heat them up). Eggs are
okay if boiled.

I can't say what caused the stomach acid problem, but I avoided
everything said to be "bad," such as salt, and you need salt to make
stomach acid, so that could have been a major issue. However, I was
doing fine until the Fall, 2000, then things rapidly went bad, with
little digestion taking place. I started to take omega 3 supplements
in mid 1998, so that could have played a role too (I don't take any
omega 3 supplement and avoid all omega 3-rich food items).
N***@aol.com
2008-12-04 02:14:03 UTC
Permalink
I think it's more about reading food labels.  I eat things like
cookies if the fat content is well over 50% SFAs.  I prefer 70% or
more.  Basically, these kinds of food items are made to last, whereas
with PUFA-rich oils used for cooking you're dealing with something
that's going to be generating free radicals as soon as you open up the
bottle (and cooking with it makes it worse).   Cooked meat can also be
very rich in PUFAs, and the PUFA-rich oils/cooked meat combination is
especially bad (generating lots of HCAs).  I also don't avoid more
than very small amounts of cholesterol in such food items (but I eat
full fat butter and cheese, though I don't heat them up).  Eggs are
okay if boiled.
A high-fat diet doesn't leave much caloric room for the good things.
I can't say what caused the stomach acid problem,
So why completely change your diet? Sounds like you were doing things
right (vegan and organics), though I would have added some meat, eggs
and little dairy.
but I avoided
everything said to be "bad," such as salt, and you need salt to make
stomach acid,
No one says salt is bad. Only that salt in excess can be bad. What
other "bad" things did you avoid?
so that could have been a major issue.  However, I was
doing fine until the Fall, 2000, then things rapidly went bad, with
little digestion taking place.  I started to take omega 3 supplements
in mid 1998, so that could have played a role too (I don't take any
omega 3 supplement and avoid all omega 3-rich food items).
Why supplements? (Just eat some fish, walnuts or flax.) Nothing
beats getting it from food.

Patrick
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