Folic acid supplements challenged - L-methylfolate better?
Cruiser
about the bioavailability of folic acid supplements.
This appears similar to the questions I raised about the cyanocobalamin
supplements, but without the cyanide poisoning issue.
I switched to methylcobalamin sublingual. Now I am wondering about the folic
acid supplement that I am using.
It is the same deal. The active form in the body for B12 is methylcobalamin
and now they are saying that the active form of folic acid in the body is
L-methylfolate. In both cases, the body's ability to convert the regular
supplement to the methylated form is being questioned.
http://www.hsfolate.com/folate_not_folic.htm
http://store.yahoo.com/iherb/metafolin.html
Cruiser
Cruiser
It looks like Merck released this product in 2001 and there has been slow
market uptake by supplement makers.
Most of the products using it are mixes of supplements and not straight
metafolin. Most of those products contain cyanocobalamin, which I get in my
regular vitamin supplements. Unfortunately, if I want a couple pills that
provide a host of nutrients, I have to put up with it. However, I don't
want anymore of that crap in me than I already get.
From what I am reading regular folic acid supplement may not be very usable
and may inhibit absorption of usable methyfolate from dietary sources.
As a side note, I started eating crab and seafood delis from Subway, for
lunch a few years ago, and I found that psoriasis reduced considerably. I
attributed this change to other things that I was doing. I would get a heap
of lettuce every day, and often drank a V8 juice, which is made with leafy
green vegetables. I was eating more salads at the time. I am not fond of
salad and rarely eat it. I wonder if folic acid has been the chemical
process limiter for me, in reducing homocysteine levels. When I stopped
eating at subway and also strayed from eating salads, the psoriasis stopped
improving, and it has even started to get worse lately.
I have supplemented all this time with folic acid in adequate amounts, but I
am beginning to believe that folic acid supplements are not well utilized in
the body. I am trying to source some Source Naturals metafolin supplement,
but it does not seem to be available at any of the health stores around.
I can get it from the WEB, but that will take weeks.
http://www.metafolin.com/
http://www.metafolin.com/pdfs/metafolin2004_merck.pdf
I started drinking a 340ml can of V8 juice at lunch, a couple weeks ago, and
I have sent a note to Campbell, requesting information on the methyfolate
content of a can of V8. It is made with the juice of leafy green vegetables,
and should contain at least some folate.
Maybe, I should start gobbling spinach and orange juice.
Hmmmm.....
Cruiser
cruiser
Just found a very good reference on Folic Acid. Tons of really good
information.
Here is a sampling.
polyglutamate - form in food
monglutamate - in plasma, the only form that can pass membranes
tetrahydrofolic acid (THFA) - active form in body
500-20,000 mcg of folate in body stores
Within the plasma, folate is present, mostly in the 5-methyltetrahydrofolate
(5-methyl THFA) form, and is loosely associated with plasma albumin in
circulation. The 5-methyl THFA enters the cell via a diverse range of folate
transporters with differing affinities and mechanisms (ie, adenosine
triphosphate [ATP]-dependent H+ cotransporter or anion exchanger). Once
inside, 5-methyl THFA may be demethylated to THFA, the active form
participating in folate-dependent enzymatic reactions. Cobalamin (B-12) is
required in this conversion, and in its absence, folate is "trapped" as
5-methyl THFA.
From then on, folate no longer is able to participate in its metabolic
pathways, and megaloblastic anemia results. Large doses of supplemental
folate can bypass the folate trap, and megaloblastic anemia will not occur.
However, the neurologic/psychiatric abnormalities associated with B-12
deficiency ensue progressively.
The biologically active form of folic acid is tetrahydrofolic acid (THFA),
which is derived by the 2-step reduction of folate involving dihydrofolate
reductase. THFA plays a key role in the transfer of 1-carbon units (such as
methyl, methylene, and formyl groups) to the essential substrates involved
in the synthesis of DNA, RNA, and proteins. More specifically, THFA is
involved with the enzymatic reactions necessary to synthesis of purine,
thymidine, and amino acid. Manifestations of folate deficiency thereafter,
not surprisingly, would involve impairment of cell division, accumulation of
possibly toxic metabolites such as homocysteine, and impairment of
methylation reactions involved in the regulation of gene expression, thus
increasing neoplastic risks.
---snip--
Mechanistically speaking, current theory proposes that folate is essential
for synthesis of S-adenosylmethionine, which is involved in numerous
methylation reactions. This methylation process is central to the
biochemical basis of proper neuropsychiatric functioning.
---snip---
People with alcoholism can have very active alcohol dehydrogenase that binds
up folate and thus interferes with folate with folate utilization.
---snip----
Increased requirement: Factors that increase the metabolic rate can increase
the folic requirement. Infancy (a period of rapid growth), pregnancy (rapid
fetal growth), lactation (uptake of folate into breast milk), malignancy
(increased cell turnover), concurrent infection (immunoproliferative
response), and chronic hemolytic anemia (increased hematopoiesis) all can
result in an increased folate requirement.
---snip---
Increased excretion/loss: Increased excretion of folate can occur subsequent
to vitamin B-12 deficiency. During the course of vitamin B-12 deficiency,
methylene THFA is known to accumulate in the serum, which is known as the
folate trap phenomenon. In turn, large amounts of folate filter through the
glomerulus, and urine excretion occurs. Another mechanism of excess
excretion occurs in people with chronic alcoholism who can have increased
excretion of folate into the bile. Patients undergoing hemodialysis also
have been known to have excess folate loss during procedures.
---snip---
Increased destruction: Superoxide, an active metabolite of ethanol
metabolism, is known to inactivate folate by splitting the folate molecule
in half between the C9 and N10 position. The relationship between cigarette
smoking and low folate levels has been noted as possibly due to folate
inactivation in exposed tissue.
---snip---
resistance to treatment may occur in patients with alcoholism and
deficiencies of other vitamins; adverse effects include anorexia, nausea,
abdominal pain, flatulence, altered sleep pattern, irritability,
overactivity, erythremia, rash, and itching.
Cruiser
randall
Ok as to your list of things that folate is good for. Good info to make
one think.
Let's try to get a clearer picture via pubmed of the role of P and
folic acid.
Here's the first hit, that speaks to me. The majority of hits of course
are for
MTX and folic acid as mtx inhibits it.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=9420019
Folate and antifolate pharmacology.
Kamen B.
Department of Pediatrics, The University of Texas Southwestern Medical
Center, Dallas 75235-9063, USA.
Folic acid is a water-soluble vitamin associated with the other B
vitamins. In its fully reduced form (tetrahydrofolate), folate serves
as a 1-carbon donor for synthesis of purines and thymidine as well as
in the remethylation cycle of homocysteine to methionine. Folate is
essential for normal cell growth and replication. It therefore is not
surprising that folate analogues have served and continue to serve well
as antibiotics and cytotoxic drugs in the treatment of cancer,
autoimmune diseases, psoriasis, and bacterial and protozoal infections.
During the past 50 years, many of the enzymes requiring folate as a
co-factor (ie, thymidylate synthase), and molecules critical in folate
homeostasis (ie, the reduced folate carrier, folylpolyglutamate
synthase), have been purified and even crystallized. The genes have
been cloned, sequenced, and mapped, providing detailed knowledge of
their regulation and three-dimensional structure. This has, in part,
led to the rational synthesis of a large number of folate analogues
that differ from methotrexate, the "classical antifolate," in
transport, metabolism, and intracellular targets. Currently, several
new folate analogues with unique biochemical properties and clinical
applications are being tested. The goals of this brief review are to
review folate homeostasis, to highlight the similarities and
differences between natural folate and antifolates with respect to
biochemistry and metabolism, and to present the pharmacology of
methotrexate and several next-generation folate analogues, such as
trimetrexate and raltritrexed, with an emphasis on mechanisms of drug
resistance.
PMID: 9420019
The major theme on the P group also seems to be the anti folic acid
MTX,
http://groups.google.com/groups?q=folic+acid+psoriasis&qt_s=Search
Next, look what else is on that list now.
The antifolate activity of tea catechins.
Navarro-Peran E, Cabezas-Herrera J, Garcia-Canovas F, Durrant MC,
Thorneley RN, Rodriguez-Lopez JN.
Grupo de Investigacion de Enzimologia, Departamento de Bioquimica y
Biologia Molecular A, Facultad de Biologia, Universidad de Murcia,
Spain.
A naturally occurring gallated polyphenol isolated from green tea
leaves, (-)-epigallocatechin gallate (EGCG), has been shown to be an
inhibitor of dihydrofolate reductase (DHFR) activity in vitro at
concentrations found in the serum and tissues of green tea drinkers
(0.1-1.0 micromol/L). These data provide the first evidence that the
prophylactic effect of green tea drinking on certain forms of cancer,
suggested by epidemiologic studies, is due to the inhibition of DHFR by
EGCG and could also explain why tea extracts have been traditionally
used in "alternative medicine" as anticarcinogenic/antibiotic agents or
in the treatment of conditions such as psoriasis. EGCG exhibited
kinetics characteristic of a slow, tight-binding inhibitor of
7,8-dihydrofolate reduction with bovine liver DHFR (K(I) = 0.109
micromol/L), but of a classic, reversible, competitive inhibitor with
chicken liver DHFR (K(I) = 10.3 micromol/L). Structural modeling showed
that EGCG can bind to human DHFR at the same site and in a similar
orientation to that observed for some structurally characterized DHFR
inhibitor complexes. The responses of lymphoma cells to EGCG and known
antifolates were similar, that is, a dose-dependent inhibition of cell
growth (IC50 = 20 micromol/L for EGCG), G0-G1 phase arrest of the cell
cycle, and induction of apoptosis. Folate depletion increased the
sensitivity of these cell lines to antifolates and EGCG. These effects
were attenuated by growing the cells in a medium containing
hypoxanthine-thymidine, consistent with DHFR being the site of action
for EGCG.
PMID: 15781612
So green tea and mtx both inhibit DHFR. Do we need more folate then, if
taking green tea caps? I'm thinking of you know who right now.
You cruiser! Your taking a bomber load of Green tea, right?
You need it then. But,
It really hasn't made much difference over the years that i'm aware of.
Not
like many many other things i've taken. Even curcumin gives a better
punch for
the buck and that's not much.
This next one has the B12 link to folates,
Anemia, serum vitamin B12, and folic acid in patients with rheumatoid
arthritis, psoriatic arthritis, and systemic lupus erythematosus.
Segal R, Baumoehl Y, Elkayam O, Levartovsky D, Litinsky I, Paran D,
Wigler I, Habot B, Leibovitz A, Sela BA, Caspi D.
Department of Geriatrics, Shmuel-Harofeh Geriatric Medical Center, Baer
Yaakov, Israel. shm...@netvision.net.il
OBJECTIVE:Although anemia is frequent in inflammatory rheumatic
diseases, data regarding vitamin B12 status is scarce. The purpose of
this study was to analyze the incidence and nature of B12 and folic
acid (FA) deficiencies in a cohort of rheumatic patients with
rheumatoid arthritis (RA), psoriatic arthritis (PsA), and systemic
lupus erythematosus (SLE). METHODS: Levels of B12, FA, and parameters
of anemia were recovered or examined in 276 outpatients. In those with
recent findings of low serum B12 levels, further studies of serum
homocysteine (Hcy) and urine methylmalonic acid (MMA) levels were
performed. RESULTS: The incidence of anemia was high: 49%, 46%, and
35%, in RA, SLE, and PsA, respectively. Low levels of serum B12 were
also frequent (24%), with almost similar occurrence in the three
disease groups. Deficiency in FA was rare (<5%). Mean levels of both
vitamins did not differ significantly among the three groups. No
correlation between serum B12 levels and anemia was found. In the 15
patients with recently detected low B12 levels, Hcy and MMA were
evaluated before and following B12 therapy. In ten of them, baseline
Hcy levels were high, while MMA was increased in one patient only.
Response to B12 administration, i.e., a decrease in Hcy and/or MMA
levels, was noticed in four patients only, suggesting that only 26% of
the low-serum-B12 patients had true B12 deficiency. CONCLUSIONS: The
incidences of anemia and decreased serum B12 levels were high in these
three groups of rheumatic patients. However, true tissue deficiency
seems to be much rarer.
PMID: 12720045
Yet, I see no magic here or when I take them.
As to all the B vits used in synergy i really only see YELLOW pee.
And the same old other P.
randall
cruiser
> Mechanistically speaking, current theory proposes that folate is essential
> for synthesis of S-adenosylmethionine, which is involved in numerous
> methylation reactions.
This struck me as interesting.
I have been curious abou the methylization of cobalamin, and folic acid. I
hav e also been curious about the homcysteine cycle. This information seems
to tie it all up.
---------------------------------------------------------
http://www.healingdaily.com/conditions/sam-e-1.htm
SAM-E (also known as SAM or AdoMet) is a derivative of the amino acid,
methionine. It's formed when methionine combines with adenosine triphosphate
(ATP), a nucleotide present in all living cells. ATP is the major source of
cellular energy. The liver uses this process to make SAM-E, as much as 8
grams of it every day, when the liver is perfectly healthy. Liver disease,
osteoarthritis and the overuse of prescription drugs or over-the-counter
medications can diminish the body's production of SAM-E. A small amount of
SAM-E is found in food, but it is highly unstable and an unreliable means of
increasing blood levels.
As a methyl donor, SAM-E "donates" units called methyl groups, which contain
hydrogen and carbon atoms, to other substances. This process is called
methylation, and it is one way in which the body protects itself from damage
on the cellular level.
SAM-E facilitates the manufacture of brain neurotransmitters
Methyl donors help to protect against cancer, heart disease, neurological
disorders, and many age-related problems, and facilitate the manufacture of
DNA and brain neurotransmitters. SAM-E is involved in more than 50
methylation reactions in the body, including the regulation of various
hormones and neurotransmitters such as serotonin, melatonin, and dopamine.
Once SAM-E donates its methyl group to choline, creatine, carnitine, DNA,
RNA, epinephrine, and other compounds, it is transformed into
S-adenosyl-homocysteine, (SAH). SAH donates its sulfur molecule to
sulfur-containing amino acids such as cysteine, from which glutathione is
formed. SAH then gives up its adenosine molecule to yield homocysteine.
Homocysteine is a potentially toxic amino acid and an independent risk
factor for coronary disease. Folic acid, choline, or betaine can change
homocysteine back to methionine in the presence of vitamin B12, or convert
homocysteine into cysteine and glutathione in the presence of vitamin B6.
For this reason, it is recommended to supplement your diet with vitamin B12
and B6 when taking SAM-E.
SAM-E is particularly important for the liver because glutathione is
synthesized from it. Glutathione is crucial for liver function. A good
portion of liver SAM-E is turned into glutathione. Glutathione is the
liver's natural antioxidant.
SAM-E has many other beneficial uses for several wide-ranging conditions.
For best results it is recommended to also take TMG (trimethylglycine)
500mg-2000mg twice a day (which increases the metabolism of SAM-E), as well
as co-factors such as folic acid up to 1mg/day, vitamin B6 up to 100mg/day,
and vitamin B12 1mg/day.
These nutrients will prevent SAM-E from being metabolized into harmful
homocysteine and will help re-methylate homocysteine back to SAM-E, so they
may be useful in those who want to reduce the dose of SAM-E, and still get
the full benefits.
randall
cruiser wrote:
> Randall,
>
> > Mechanistically speaking, current theory proposes that folate is essential
> > for synthesis of S-adenosylmethionine, which is involved in numerous
> > methylation reactions.
>
> This struck me as interesting.
>
> I have been curious abou the methylization of cobalamin, and folic acid. I
> hav e also been curious about the homcysteine cycle. This information seems
> to tie it all up.
> ---------------------------------------------------------
> http://www.healingdaily.com/conditions/sam-e-1.htm
>
> SAM-E (also known as SAM or AdoMet) is a derivative of the amino acid,
> methionine. It's formed when methionine combines with adenosine triphosphate
> (ATP), a nucleotide present in all living cells. ATP is the major source of
> cellular energy. The liver uses this process to make SAM-E, as much as 8
> grams of it every day, when the liver is perfectly healthy. Liver disease,
> osteoarthritis and the overuse of prescription drugs or over-the-counter
> medications can diminish the body's production of SAM-E. A small amount of
> SAM-E is found in food, but it is highly unstable and an unreliable means of
> increasing blood levels.
>
The cheapest i've found and haven't look hard as the price is high,
http://www.costco.com/Browse/Product.aspx?prodid=10043335&whse=BC&topnav=&cat=3283&hierPath=589*3283*
Doesn't it make sense to get the liver working better? So it can make
those 8 grams (8,000 mg's) per day?
Look at what it would cost you to buy that much per day!
NoPe, not for me. Your liver is your friend. Do unto him as you want
from you.
And haven't you given it enough to work with by now?
If sam-e was uwe's magic suPPlement, what would the loading dose be?
40 grams?
If I believed this was his big X, i'd try to find the precursor's
instead.
randall
cruiser
Check this out.
http//www.lef.org/magazine/mag99/sept99_review2.html
choline and trimethylglycine. While choline does contain three methyl
groups, for methylation purposes it needs to be converted to
trimethylglycine (TMG ), which in turn is a very efficient methylator.
Choline has many vital functions in the body, including serving as a
precursor for the production of the neurotransmitter acetylcholine. One
animal study indicated that coffee strongly potentiates the action of
choline in raising the levels of acetylcholine.
TMG, on the other hand, is very effective at raising the levels of SAMe and
lowering homocysteine. Seafood, beets and spinach contain TMG, but for the
methyl-deficient older people, supplements are highly recommended.
Interestingly, moderate alcohol intake together with TMG can result in
higher levels of SAMe than TMG alone.
Methionine is the dietary amino acid that is the precursor of SAMe. Too much
methionine, however, can result in elevated homocysteine, particularly if
methyl nutrients are insufficient. Unfortunately we do not know the optimal
levels of methionine in relation to the levels of methylators such as folic
acid. Cooney strongly warns against taking methionine supplements,
especially if you regularly eat meat and other animal protein. Taking
methionine in addition to eating meat could lead to abnormally high
methionine levels, with resulting higher SAMe but also high homocysteine,
with both compounds rising and falling in spikes.
Cooney is particularly concerned about body builders who use protein mixes,
and hence are in effect supplementing thionine. Possibly taking methyl
supplements with methionine might make methionine supplementation safe, but
we simply do not know what doses of methyl supplements it would take.
Folic acid and vitamin B12 are vital for remethylating homocysteine back to
methionine. A coenzyme form of vitamin B12, methylcobalamin, is necessary
for the enzyme methionine synthase, which catalyzes the methylation of
homocysteine to methionine.
Vitamin B6 (pyridoxine) helps convert homocysteine to cysteine. Cooney warns
that too much B6 (over 200mg) may result in too much conversion to cysteine
rather than methionine, and consequently in impaired methylation.
Selenium participates in methylation as selenomethionine. Animal studies
have shown that selenomethionine raises the levels of SAMe.
Zinc is part of various enzymes that help methylate homocysteine. The enzyme
DNA methyltransferase also contains zinc.
Inositol facilitates the action of many methyl agents.
Cruiser
Cruiser
I am looking to target homocycteine.
Why?
It appears that elevated homocysteine may cause an inflammtory cascade
through stimulating the AT1 receptor.
I have elevated cholesterol, and blood pressure on the high side.
I am fairly certain that Hayek is using B12 in his formula. The best
complement for B12 seems like it could be
TMG, since in combination they will raise SAM-e levels and drop homocysteine
levels.
At one point Hayek bragged about curing someone's cirrhosis of the liver.
Cirrhosis of the liver is related to scaring of the liver tissue. SAM-e is
supposed to reduce scarring of the liver tissue.
Here are a whole bunch of studies related to TMG.
http://www.lef.org/prod_hp/abstracts/php-ab112a.html
Cheers, Cruiser
Cruiser
http://www.enzymestuff.com/methylation.htm
Methylation
Copyright August 2002. Kd.
This is a discussion which tries to outline the points of methylation and
establish some relationships that will result in the practical application
of the information. Special thanks to andrew who contributed many links and
much understanding to this discussion.
This link has a nice picture of what this process looks like. You may want
to refer to it often during the following discussion.
http://www.nutriwest.com/articles/homovmsm.htm
The issue of a person being an under or over methylator can be confusing. It
may not be one of the all time critically defining issues, but it may help
in the general sense. Several common supplements often recommended for those
with autism spectrum conditions are involved in this process (this is just
one of the processes these supplements may help with).
A "methyl" group is simply one carbon connected to three hydrogen atoms. It
may be written as CH3 with the 3 being a subscript.
"Methylation" is not just one specific reaction. There are hundreds of
"methylation" reactions in the body. Methylation is simply the adding or
removal of the methyl group to a compound or other element.
So why do we care about methylation at all? In general, when some compounds
receive a methyl group, this "starts" a reaction (such as turning a gene on
or activating an enzyme). When the methyl group is "lost" or removed, the
reaction stops (or a gene is turned off or the enzyme is deactivated). Some
of the more relevant methylation reactions would be:
1. getting methyl groups "turns on" detox reactions that detox the body of
chemicals, including phenols. So if you are phenol sensitive, and you
increase your methylation, then theoretically your body can process more
phenols and you can eat fruits without enzymes!
2. getting methyl groups "turns on" serotonin, and thus melatonin,
production. Therefore, if you are a under-methylator, you can increase your
methylation and have higher more appropriate levels of serotonin and
melatonin. This means you may not have to take SSRIs, or may have improved
sleep.
3. if you are an over-methylator you can take certain supplements to
decrease methylation and perhaps turn off reactions that need to be off.
This may decrease aggression or hyperness, for example.
This is the general idea. To what extent this actually works in real life
for any individual is back to "every one is different." But this is one
thing that the Pfeiffer Treatment Center really looks at. I hope this
explanation helps.
Something to note is that everyone is not EITHER an over OR under
methylator. There are more groups than that, and you may be just fine in
regards to methylation. Even if the Pfeiffer statistic is exactly correct
when they say 45% are under-methylators and 15% are over-methylators, that
totals 60%, so almost half the people are
neither.
Where this MIGHT be helpful would be in picking supplements. So someone may
do badly on the high B6 protocol. If that person does badly on TMG or DMG
too this may be a clue that they will do poorly on ALL the methylation
precursors so they can steer clear of that group in high doses. And vice
versa, if they did really well with one, then they may also do well with
others in the group. Of course, they may not see additional benefit if the
methylation process is fixed with the first supplement, but it is something
that might help a person know why they or their child is consistently doing
well or poorly with a group of supplements.
Is there any evidence to support this? Well, I am looking at the ARI data
gathered from over 18,500 parent surveys. Let's say Pfeiffer is exactly
correct and under-methylators are about 45% of the "autism" population.
These are the values for the precursors for methylation:
- calcium 39% saw improvement
- DMG 43% saw improvement
- Folic acid 44% saw improvement
- B6/mag (both of these are precursors) 46% saw improvement
- Zinc 43% saw improvement
So if you look at any of the precursors, really, most are around that 45%
mark of under-methylators (calcium was a little low, but it is a supporting
element). So we have a mark of consistency here. SAMe, methionine, and B12
were not choices. What this does NOT point out is which came first. Was zinc
low for some reason not related to methylation and because it was low,
methylation dropped? or are you a genetically low-methylator to begin with
and do not utilize the nutrients at hand well? Or was folic acid the
bottle-neck? or
magnesium deficiency? Or an injured gut which cannot adequately absorb any
of the nutrients? or....
This is how I see it, just as a general guideline that may be helpful, not a
cast in stone type of thing.
Where do SAMe, methionine, folate, depression,
and all that other stuff fit in?
Please refer to the diagram at the link given:
http://www.nutriwest.com/articles/homovmsm.htm
The basic cycle works like this. Methionine is an amino acid that occurs
naturally with all protein foods. Meats and dairy are especially high in
Methionine (as they are higher in protein and thus, all amino acids).
Methionine enters the body. Notice that this amino acid contains a methyl
group as indicated in the name - METHionine.
At some point, the methionine gets in touch with some energy in the form of
ATP and magnesium, and becomes SAMe. SAMe travels throughout the body
delivering a methyl group to any number of reactions (at least over 400
identified ones). The methyl group allows other metabolic pathways to "go"
or work properly. [We will skip the SAH part of the diagram.]
~ So, methionine + ATP/magnesium = SAMe
After SAMe delivers the methyl group, it becomes homocysteine.
~ SAMe minus methyl group = homocysteine.
Homocysteine is ready to accept another methyl group which transforms it
back into methionine.
~ homocysteine + methyl = methionine
Remember that methionine + ATP/MG = SAMe. And this is how methyl groups are
transported throughout the body.
However, if there are not enough methyl groups to add to homocysteine, then
the homocysteine levels build-up in the body. This is bad. Very bad.
Elevated homocysteine levels are associated with heart disease, poor
circulation, degenerative illnesses, and other unpleasant conditions. So we
must get homocysteine levels down.
Where can homocysteine get some methyl groups so it can transform into
methionine? One pathway is from folate+B12. A different pathway is from TMG
(or betaine, DMG). Either of these pathways can give a methyl group to
homocysteine. Some people may make better use of one pathway over another so
this is why several of these precursors are often recommended together.
Choline is another possible methyl donor. MSM MAY be a methyl donor but
research has not confirmed this.
An alternate way to keep homocysteine from building up is with B6/magnesium.
This is a transsulfation pathway that converts homocysteine to cysteine.
~ Homocysteine + B6/magnesium = cysteine
Some more conversions happen in this pathway including making glutathione
and taurine. One step is adding molybdenum and continuing on to convert
toxic sulfite molecules to really helpful sulfate molecules. The sulfate
then goes throughout the body doing both wonderful building up work, and
detoxing harmful chemicals (such as heavy metals and phenols).
Cysteine is real interesting. It is a thiol (meaning it contains sulfur) and
its side chain is used on enzymes and it is also responsible for the
3-dimensional stability of enzymes.
http://micro.magnet.fsu.edu/aminoacids/pages/cysteine.html
Over-methylator and Under-methylator
The Pfeiffer Treatment Center identifies two different supplement regimes
depending on if you are an "over-methylator" or an "under- methylator."
These are VERY rough estimations and nothing concrete...they may not be
accurate either; further research is needed.
Q: How can you find out if you are over or under?
A: Histamine levels may be a good indicator of whether someone is an over or
under-methylator.
Low histamine points to over-methylator: If your histamine level is low you
are probably an over-methylator (according to Pfeiffer research). This means
that many supplements would be detrimental to him (those containing methyl).
These would include taurine, GABA [both precursors to methyl activity in the
brain], folic acid, B12, B6, DMG, TMG (and SAMe) - to name a few.
Q: What test checks histamine levels?
A: There is a blood test to measure histamine. Your pediatrician can do it.
Q: How can I lower the histamine level, and the results of a histamine
reaction?
A: Some people who have trouble converting sulfur to sulfate (PST issue),
and who have a sensitivity to certain foods and chemicals because of this,
often times develop a high histamine level. My son develops a runny nose as
a reaction to this problem. Benadryl helps my son with this, and anything
else that lowers histamine would help him, also. I think the Feingold Diet,
No-Fenol, or avoiding certain phenolic and high salicylate foods may help
the sulfation problem and subsequently lower the high histamine level.
Benadryl and Pepcid AC are histamine blockers. This might explain why Pepcid
AC is so effective on some kids. A few parents have reported that a
histamine reaction with certain foods did not happen when No-Fenol was given
with those foods. MSM or Epsom salts also supply sulfur to the system and
may be helpful. Some people cannot convert the sulfur in MSM to the needed
sulfate form although other people can. Epsom salts supply sulfur in the
sulfate form directly. Taking MSM or Epsom salts may alleviate a histamine
reaction.
Q: What amount of B6 is considered "high"?
A: From the site http://www.methylmagic.com/faq.html
Some supplements have lots of B6 (e.g. 100mg) and the author usually aims
for between 20 and 50mg per day of B6. Excess niacin (B3) is metabolized by
methylation and thus uses up methyl groups. Also aim for 50 mg or less.
These values are likely for an adult so a child needs much less.
According to Pfeiffer, "Actually excess niacin (B3) is metabolized by
methylation and thus uses up methyl groups." So if you are an
over-methylator, meaning you have extra, then B3 is good because it uses
them up, but if you are an under-methylator, meaning deficient, then giving
extra B3 is bad because it drains an already poor supply.
Frequently Asked Questions
http://www.methylmagic.com/faq.html
Q: What do we really need for methylation to prevent or treat depression? -
vitamins, TMG or SAMe?
A: People need folate, B12, B6, TMG and zinc whether or not they use SAMe.
SAMe will not replace all the actions of any of these. All SAMe provides are
methyl groups (expensive but also direct and efficient methyl groups),
adenosine and methionine. Many people who "need" SAMe actually are low in
precursors (e.g. methionine, folate, B12, B6, TMG and zinc). If you take
SAMe, these precursors will help you recycle it, and should reduce the
amounts of SAMe you need to take. (extra methionine is probably unnecessary
as long as you have good protein sources in your diet and as long as your
digestion is good).
Also note that for depression several aspects of biochemistry come into play
and a depressed person should want to handle all of these. Three key areas:
1. Fatty acids, e.g. fish oil for membrane fluidity this helps receptors,
etc. to function.
2. Methyls, e.g. folic acid, B12, B6, zinc and TMG (and SAMe) for membrane
fluidity as well as for dopamine metabolism, acetylcholine and epinephrine
production etc.
3. Amino acids, e.g. protein or supplements such as 5- hydroxytryptophan
(5-HTP) for the starting material for neurotransmitters including dopamine,
serotonin, epinephrine etc.
Q: What about MSM (methyl-sulfonyl-methane) as a methyl donor?
A: Despite having looked in the literature, the Methyl Magic manufacturers
have not yet found out if MSM acts as a methyl donor. It may be fine and
just that no one has done the experiments. Some of MSM's properties may be
due to methylation but we just don't know. MSM is apparently a good source
of organic sulfur. TMG (betaine) is a good methyl source - TMG works and is
inexpensive.
Q: How does high dose niacin (vitamin B3) fit in with methylation?
A: Actually excess niacin is metabolized by methylation and thus uses up
methyl groups. One source suggests to aim for under 75mg (usually ~50mg) of
niacin+niacinamide per day from supplements. If you are taking large
quantities of B3, please get your homocysteine and SAM checked to make sure
this niacin isn't excessively taxing the methyl metabolism. Likewise some
supplements have lots of B6 (e.g. 100mg) and between 20 and 50mg per day of
B6, or less, might be better.
Q: Why would someone necessarily be deficient in methylation other than a
lack of the proper nutrients? Is there a genetic variation serious enough
that a person with sufficient vitamins would still suffer from insufficient
methylation?
A: There are genetic variations that make some people especially deficient
or "slow methylators". There are several kinds of such people and variations
i.e. several genes and the enzymes they produce that can be inefficient or
even missing altogether. In extreme cases these can cause homocysteinuria.
Usually these can be handled with a combination of folic acid, B12, B6 and
TMG. With some, but not all of these variations, extra amounts of the
cofactor (e.g. folate) will compensate for the inefficient enzyme. Other
times you need to rely on the other pathways e.g. TMG, and B6 pathways when
the folate+B12 pathway is missing. Today we know that zinc should also be in
this supplement combination. For people with these more serious deficiencies
very high levels of folic acid (e.g. 5 milligrams/day) and TMG (e.g. 6
grams/day) are usually needed. There are some types of genetic deficiencies
where SAMe is the specific needed supplement although these are less common
(according to conventional wisdom) than those needing B6, folic acid, TMG
etc.
Contradiction with information from Pfeiffer Treatment Center
There is a contradiction between the majority of the information on
methylation and the description on the Pfeiffer Treatment Center web site.
The precursors that go into the methylation cycle for
SAMe/neurotransmitters/dopamine/serotonin are methionine, folate, B12, B6,
TMG and zinc, and maybe some calcium and magnesium.
So, logic follows that if the one of the precursors is limiting (low), then
methylation would be limiting (low) and the neurotransmitters and resulting
pathways would be limited (low). This also supports the use of SAMe and the
precursors as being effective for depression (because they increase
neurotransmitters which improve mood).
But the Pfeiffer information does not follow this. From the Pfeiffer site
http://www.hriptc.org/BioTreatment.html in regards to depression and
neurotransmitters, one sentence says: "Over- Methylation: Many persons who
suffer from anxiety and depression are over-methylated which results in
excessive levels of dopamine, norepinephrine and serotonin."
Over-methylation would result in excessive levels of the neurotransmitters
listed, but this is not necessarily consistent with depression (I don't know
about anxiety). The other references say that under-methylation results in
depression.
The next sentence from Pfeiffer says:
"Typical symptoms include chemical and food sensitivities, underachievement,
upper body pain, and an adverse reaction to serotonin-enhancing substances
such as Prozac, Paxil, Zoloft, St. John's Wort, and SAMe."
It would seem that over-methylation would be adversely affected by MORE
serotonin, SAMe, etc, because the body already has too much of that stuff.
However, I could also associate the food sensitivities and underachievement
with depression.
Continuing with Pfeiffer: "They have a genetic tendency to be very depressed
in folates, niacin, and Vitamin B-12, and biochemical treatment focuses on
supplementation of these nutrients."
This part is the opposite of other references. The folates and vitamin B-12
would be precursors, so an over-methylator should not be deficient in precur
sors. A person deficient in precursors should be low in methylation.
Pfeiffer may have different information...or it may be more complicated and
the short summary on their web site is not conveying things right. So,
either something is missing, one of these is not quite right, or something
else is going on, but at least this explains the inconsistency between
Pfeiffer and other sources.
Pfeiffer is saying that B6, TMG, DMG, SAMe and SSRIs (medications that
increase serotonin such as Zoloft and Prozac) are good for those with low
methylation, but B12 and folic acid is not (even though folic acid and B12
are precursors too). However, the other sites say that ALL of those
nutrients listed are precursors or otherwise aid in increasing methylation.
Pfeiffer is splitting out the folic acid and B12 from the others for some
reason. Andy Cutler made a comment at one point saying that Pfeiffer may be
using these terms differently and may be referring to specific aspects of
the methylation cycle
I called the Pfeiffer office and the answer was that they would be happy to
answer the methylation question and discuss it for $90. I explained the
situation, and the receptionist said no problem, but it would cost $90 up
front. If someone is currently a patient of Pfeiffer, then maybe they could
ask at their next visit or conference call.
This is the question that needs to be answered by Pfeiffer:
"If folate (folic acid) and B12 are two of the precursors (as are B6, TMG,
and maybe zinc, magnesium and calcium) why would a deficiency of folate and
B12 indicate OVER-methylation. Wouldn't a deficiency of the precursors also
mean a deficiency of the end products or low/under methylation?"
So what does this have to do with enzymes or
autism conditions/neurology?
If you are GFCF this probably becomes much more of a concern because you
loose primary sources of the B vitamins including folate and B12, amino
acids and minerals; then you get into adding all that stuff back in
individually as supplements. By taking enzymes, you can eat the whole grains
and dairy which are excellent sources of those things plus anything you eat
will likely be better digested and absorbed with enzymes. So you get more
actual nutrition from your food and any supplements you take. This is not
about some mythical function but taking advantage of rate limiting processes
and providing a nutrient that removes the rate limit. There is quite high
B12 in milk. If you have an injured gut by any means, you sharply reduce
your ability to absorb B12. If you go grain and dairy free in addition to
this, you are very likely to be B12 deficient.
This explains why some people do so much better on enzymes as well. Enzymes
are supplying better nutrition and correcting multiple pathway hurdles
throughout the body all at the same time. Many of the treatments and
supplements recommended to those with autism conditions are targeted to one
pathway at a time, or aim to correct a pathway by supplying all the needed
precursors individually.
One technique of giving high doses of taurine (as done by Dr. Bradstreet)
has an effect of improving digestion. Taurine is needed in bile
production.bile improves fat digestion and digestion in general. If you take
enzymes to do this digestion, then you are more directly accomplishing the
same thing as the taurine supplementation. You also get the added bonus of
improving all nutrient uptake at the same time, including better uptake of
taurine from food. So you improve the faulty pathway in both directions.
Other commonly suggested supplements include NAC (cysteine), glutathione,
molybdenum, sulfur/sulfate, melatonin, and serotonin. If you can get the
methylation working properly, you may not need to add in all these
components separately. The melatonin and serotonin come from SAMe function.
Too much B6 may deplete this. Having a good source of methyl groups plus
methionine in the diet is a good way to improve serotonin and melatonin
supplies.
Why do we see the constant trend of people with phenol intolerances having
bad reactions to high B6 supplements?
This seems to go back to the methylation cycle. If you look at the diagram
at the link given above, you see that B6/magnesium converts homocysteine to
cysteine. However, in order for the cysteine to be converted on you need
sulfation to be working properly. Those with faulty sulfation processes are
not able to do this well and too much cysteine accumulates. Cysteine has
excitatory properties and can even be toxic in high amounts. So supplying B6
increases the cysteine supply where it gets stuck in the pathway and
accumulates.
This also explains why if someone did okay with high B6 or even TMG and then
started enzymes, they may start to see problems with those supplements over
time. Or if they take Peptizyde and go off a GFCF diet (thereby adding in
more B vitamins). The enzyme therapy is adding in more B vitamins, so now
there is a greater supply of B6. The increase in B6 "pulls" the methylation
cycle into producing more cysteine.maybe too much cysteine accumulates. So
ending the high B vitamins lets this cycle settle into a more balanced
state. The high cysteine levels are reduced and the adverse reactions
subside. Someone may be very well on a "regular" recommended daily allowance
of B6, but only sees adverse reactions at the higher doses.
Here are some links that explain the problems with too much cysteine.
http://www.cfsn.com/sulph.html
http://www.mercola.com/1999/apr/4/secretin_autism.htm
http://www.mercola.com/1999/apr/11/l_cysteine_for_autism_caution.htm
What is the health risk of too much vitamin B6 ?
Too much vitamin B6 can result in nerve damage to the arms and legs. This
neuropathy is usually related to high intake of vitamin B6 from supplements,
(28) and is reversible when supplementation is stopped. According to the
Institute of Medicine, "Several reports show sensory neuropathy at doses
lower than 500 mg per day". As previously mentioned, the Food and Nutrition
Board of the Institute of Medicine has established an upper tolerable intake
level (UL) for vitamin B6 of 100 mg per day for all adults. "As intake
increases above the UL, the risk of adverse effects increases."
[Institute of Medicine. Food and Nutrition Board. Dietary Reference Intakes:
Thiamin, riboflavin, niacin, vitamin B6, folate, vitamin B12, pantothenic
acid, biotin, and choline. National Academy Press. Washington, DC, 1998. ]
http://www.cc.nih.gov/ccc/supplements/vitb6.html#risk
How does mercury toxicity affect methylation?
Mercury toxicity may disrupt this cycle making it practically unsolvable
until the metals are removed.
Mercury is highly attracted to sulfur. If there is mercury floating around,
it will gravitate to sulfur compounds and tie them up. Any or all of the
sulfur reactions will be faulty, and it will be hard to fix unless (or
until) you remove the mercury or other metals. If you are mercury toxic and
you do anything to increase methylation, you may increase cysteine. So if a
child responds badly to high B6, mercury toxicity is a possibility because
it more directly increases cysteine. Instead of this increase being
beneficial, it may very likely attract mercury, and thus increase mercury
movement and cause further damage.so you just can't win. You need to
increase the sulfur compounds to detox the mercury (and other things), but
these same sulfur compounds also start to float the mercury and cause worse
problems as it moves around....
One interpretation is if you respond well to B6 and possibly TMG then you
may be an under-methylator and may not have severe mercury toxicity. This is
what cysteine is about, if you are severely mercury toxic then you are
caught since you need more cysteine to function since the mercury takes it
out, but if you have more cysteine you mobilize the mercury and you get more
doing damage.
Mercury is involved in defeating so many pathways. Mercury may lead to the
problems with phenol intolerance too. The mercury disrupts the cysteine
pathway, so sulfate is limited and is not supplied for detoxing the phenol
compounds (or other compounds).
Selenium binds with mercury and parks it in the liver in an insoluble form,
as well as aiding the manufacture of glutathione which is a mercury detox
pathway. So by adding Selenium you may start making some ground in
correcting the pathways. So selenium gives a lot of effect for minimal
hassle provided you don't take too much. Look for the selenomethionine form
(a source of selenium and methionine). This is not chelation but may help
while you are looking at chelation or in the process of chelating.
This methylation stuff may be more complex than is obvious. It is an
intertwined process. Remember also that amino acids such as tryptophan and
tyrosine may be involved in this more directly. I don't know what the
relationship is between the levels of methylation and amino acids, but that
may outweigh all this other stuff. Biochemistry gets very complex very
rapidly.
About B12 and Increasing Methylation
There is a "newer" interest in vitamin B12. This is supplemented in two
forms. One is called Cyanocobalamin. The other is Methylcobalamin and is the
methylated, coenzyme form of B-12 (cobalamin) active in the brain and
central nervous system. The cyanocobalamin form needs to be converted to the
methylcobalamin form, so the latter is preferable if possible. B12 is needed
to work with folate (folic acid or vitamin B9). B6, B12, and folate have a
synergistic effect when given together. The B12 working with the others is
needed for good nervous system working and myelin integrity. High folate
levels or taking high amounts of folate without B12 can mask a B12
deficiency. There is lots of information by doing a search for B12. The
following is from the Vitamin Research Products site:
"For memory, some subjects improved some in memory and cognition with: 750
mcg of folate, 15 mcg of vitamin B12, and 75 mg of vitamin B6 daily for 35
days."
[New Study: B Vitamins Affect Memory, www.vrp.com]
"Recently a flurry of interesting articles from the medical newswires and
lay press have focused on B vitamins--specifically vitamins B6, B12, and
folic acid. Some articles are simple reiterations of research from the past.
Methyl Caps includes vitamin B6, B12, folic acid, and betaine
(trimethylglycine). VRP was one of the first supplement companies to
recognize the damaging effects of high levels of homocysteine, and how
homocysteine could be easily controlled by the simple nutrients found in
Methyl Caps."
[Provocative New Findings on Vitamins B6, B12 and Folic Acid Link Discovered
Between Homocysteine, Alzheimer's and Diabetes]
Besides just trying to supplement the individual precursors to increase
methylation, there are a few products just for increasing methylation. They
contain most of the precursors (a couple listed below). Most of the sites
suggested adding the precursors rather than the SAMe or methionine as being
a good corrective measure. I thought the ratios of B6 to B12 were
interesting - the B6 is usually quite under 25 mg:
http://www.integrisnutrition.com/methylate.shtml
http://www.gaines.com/html/Source/SN1038info.html
http://www.gaines.com/html/product_info/ARG/ARG72580info.html
Here are the ingredients of Methyl Caps sold by www.vrp.com
Name: Methyl Caps, 180 capsules
Serving Size: 1 Capsule
Amount Per Serving % Daily Value
Vitamin B6 (pyridoxine HCl) 17 mg 850%
Folic Acid 267 mcg 67%
Vitamin B12 (cyanocobalamin) 17 mcg 283%
Betaine (trimethylglycine or TMG) 400 mg *
Three capsules each day of VRP's Methyl Caps provide a synergistic
mix of methyl donors which work quickly to convert homocysteine into
a harmless amino acid.
What is a 'good' amount of B12 versus a therapeutic amount. Some companies
sell B12 supplements in amounts up to 1000 mcg even though the RDA value is
between 2 and 6 mcg/day for an adult. That is quite a range!
Here is a description from NOW brand used therapeutically:
Brain B-12 - 1000 mcg Methylcobalamin - 100 Lozenges
"Vitamin B12, plays an important role in the metabolism of nerve tissue,
protein, fats and carbohydrates. It also aids in the production of DNA/RNA
and red blood cells. It also plays a role in the health of the spinal cord.
A lack of adequate levels of Vitamin B12 may lead to pernicious anemia, lack
of energy, weakness, muscle soreness, mental and nervous disorders, poor
reflexes, speaking difficulty and nerve degeneration. As a dietary
supplement, take one lozenge 1 to 2 times daily by holding under the tongue
until dissolved."
Of course there were much lower strengths of B12 too. This was at a site
called GreenCanyon.com that had lots of name brand supplements discounted by
20% or more.
Some other places said that those most likely to be deficient in B12 are
those "Individuals with stomach and small intestinal disorders may not
absorb enough vitamin B12 from food to maintain healthy body stores" Also,
vitamin B12 can not be manufactured by any plants, and therefore is only
found in animal products. So, vegetarians may not consume dairy products or
meat which are good sources of B12, and they need to take care not to become
deficient. Older people are also likely to become deficient. B12 is getting
more recent press because of how it might aid in Alzheimers. Fortified
breakfast cereals or foods were suggested for vegetarians or older people.
There are sublingual dots you can buy too as well as in other supplements.
(one place to read quick summaries about vitamins is www.anyvitamins.com)
B12 does not come from plants, only animal products. Strict vegetarians need
to be aware of this and supplement it. B12 is stored in the liver and a few
other spots. B12 toxicity is very hard to achieve and the main problems have
been associated with B12 injections. This has even been attributed to some
of the "other stuff" in the injection and may not be the B12. Or there are a
few rare conditions that the injections may be contraindicated for.
B12 is released from proteins by stomach acid and digestion. Older people
and those with low stomach acid or faulty digestion may develop B12
deficiencies (along with other nutrient deficiencies) because of this.
Enzymes, particularly the proteases, digest the proteins and may make more
B12 available (along with other nutrients). If you take anything that
inhibits digestion or stomach acid, then you are inhibiting B12 release and
absorbtion: like calcium carbonate with meals, Tums, Rolaids, and certain
medications which affect stomach acid.
B12 combines with something called Intrinsic Factor in order to work. The
stomach acid issues can affect the Intrinsic Factor availability too.
B12 is absorbed in the ileum, the very last part of the small intestine.
Most everything else is absorbed before that in earlier parts of the
intestine. For this reason, people with colon problems may be B12 deficient
but not as deficient in other nutrients because the ileum is followed by the
colon (so when problems "backup" from the colon into the small intestine,
the B12 is affected first).
B12 may be deficient in people with injured guts because something called
Intrinsic Factor is necessary to bind with the B12 in the stomach to
"protect" it in the upper small intestine and from the stomach acid. Then
the Intrinsic Factor attaches to some receptors at the end of the small
intestine in the ileum aiding the B12 uptake. So at times it is the
Intrinsic Factor and the fact it cannot attach to the receptors to
facilitate transport and absorption into the body that is the problem and
the cause of B12 deficiency. The sublingual B12 is highly preferred for this
reason because it gets the B12 into the system and bypasses the entire
Intrinsic Factor mechanism.
B12 deficiency can affect the nerves (as other nutrients can). The recent
popular idea of getting more folic acid in the diet can mask a B12 problem,
and too much folic acid (over 800 mcg a day for an adult) can lead to B12
deficiency if it is not in balance. So when people read folic acid is
necessary and run out and start wolfing down folic acid without balancing
it, this can provoke a B12 deficiency.
B12 is needed in incredibly small amounts like 2-6 mcg a day for an adult,
kids need less. However, the therapeutic amount is between 100-1000 or more
mcg a day for an adult for a couple of months. When the therapeutic amount
should be used is open for debate with no clear cut evidence except for
pernicious anemia (which is chronic B12 deficiency). The Alzheimers, MS,
AIDS, etc issues are speculative at the moment. Some people say it may help,
but others say not.
So it appears to me that healing the gut, taking enzymes (particularly
proteases), and eating at least some animal foods go a long way to resolving
this issue. Additional B12 for awhile may be helpful - a "try it and see"
sort of thing - for mental and nerve function. Give at least a little bit of
other Bs and folic acid along with it.
Here are a few more easier to understand yet thorough explanations. One has
a picture of how B12 and folic acid affect the cycle of methylation, and B6
acts on another part. The precursors are much cheaper than the SAMe. It says
that methylation is enhanced by estrogen and this may point to gender
differences....anyway, more to explore.
http://www.lef.org/magazine/mag98/aug98-report2.html
http://www.lef.org/magazine/mag99/sept99_review.html
http://www.lef.org/magazine/mag99/sept99_review2.html
Here is a link on the interrelationships of these things. It gives different
amounts of B12 and folate for increasing methylation:
http://www.miami-dade-online.com/MethylManual2.htm
http://www.miami-dade-online.com/MethylManual1.htm
This one mentions that one form of B12 may be more effective than another:
http://www.lef.org/magazine/mag2001/jan2001_qanda.html
Part 2: Histamine
I spent a ton of time looking into this. Here are some of the results.
Please take all of this in context of everything else, these biochemical
reactions are all intertwined and complex.
I was wondering WHY would histamine levels tell you about methylation
function?
Methionine is a methyl carrying amino acid + ATP/magnesium = SAMe.
SAMe goes throughout the body delivering methyl groups to over 400 different
reactions.
One way histamine is de-activated (eliminated) is by receiving a methyl
group from SAMe. So if there is low methylation, there is low SAMe, and the
histamine levels are higher because of the lack of methyl groups to
deactivate it. If there is high methylation, there is higher amounts of
SAMe, and lots of histamine can be deactivated.
Where does this histamine come from?
One source is when the amino acid histidine looses a carboxyl group. Some
bacteria can faciliate this conversion too. So if you have a bacteria
overgrowth, it may be using up histidine and converting it to more
histamine. Another big source is directly from foods. Some people may have a
problem eliminating histamine from their foods and this causes reactions
which LOOK LIKE allergies, but are not true IgE mediated allergies. You may
see a histamine reaction which is just too high levels of histamine and not
because an antigen caused an immune reaction to something.
What are histamine containing foods?
Here is a great site on what foods contain what chemicals. The first link
tells about "histamine intolerance" and amine foods:
http://users.bigpond.net.au/allergydietitian
Notice that many of the foods are often considered "phenol" foods even
though they are not high in salicylates or phenols. They are high in
amines/histamine. There are also foods that trigger a histamine reaction.
This means that they directly cause a release of histamine - in some people,
this includes the natural salicylates or other common additives:
Egg, strawberries, cocoa, chocolate, bananas, citrus, pineapple, pork, soy,
benzoates, sulfites, nitrates, BHA, BHT, food colors, MSG.
The similarity with this and the Feingold program is very interesting.
If someone has low methylation (maybe B12 deficiency or metal interference,
etc.) then you may have high histamine levels and a problem eliminating the
additional histamine from foods. You would also have more chemical running
around in the body triggering histamine reactions.
What lowers histamine?
Taking an antihistamine is one way. Antihistamines typically work by either
inhibiting the release of histamine (like during an immune reaction) or
blocking the uptake of histamine (like from food). Magnesium and vitamin C
are natural anti-histamines. Vitamin C can destroy histamine directly. This
is why these supplements are recommended when you are sick for any reason.
Another way to reduce histamine levels is to supply antioxidants. Free
radicals are produced from both external sources and internal natural
biochemical reactions. Too many free radicals provoke histamine reactions.
Natural "phenols" in foods such as polyphenols, flavenoids, bioflavenoids,
beta-caroteine and all those other things that No-Fenol appears to make more
available to the body act as antihistamines. These natural phenols are also
the trendy "antioxidants" for eliminating free radicals in the body which
many places are advertising now. They neutralize the free radicals which
cause histamine reactions. Less free radicals, less histamine reaction.
These phenols coming from the fruits and vegetables lower histamine by 2 or
3 different mechanisms. Again, it gets complicated and there is no ONE
definitive pathway.
Salicylates occur in most foods as a mean to "protect" the plant from
injury. When the surface of the fruit is damaged (disease, injury, bugs,
something taking a bite out of it), the food comes into contact with oxygen,
and starts to break down via oxidation. The salicylates/phenol in the food
are an anti-oxidant which preserves the food. This is why if you take a bite
out of an apple, the "bite-mark" starts to turn brown. The apple is
ttempting to heal the injury like applying a bandaid and slow or stop the
rotting oxidation.
Remember that "phenols" are a huge category of compounds. Some are
beneficial from natural foods, but others may be a problem. Saying something
has "phenol" is like saying something contains "nitrogen". It could be
anything.
A main mechanism of lowering histamine is by an enzyme produced in the gut
mucosa. So if you have an injured gut for whatever reason, less enzyme may
be produced, and this may mean you have a lower ability to eliminate
histamine (especially from food sources). If you have multiple chemical
allergies, you may want to consider a "histamine intolerance" or that you
have histamine levels that run high. Inability to get rid of too much
histamine would make you reactive to many foods, and overreactive to many
things in the environment. Common additives such as artificial colorings,
sulfites, BHA, BHT, benzoates, etc, can all inhibit this histamine degrading
enzyme. Another way these can be problematic.
see Feingold Program
What does histamine do?
Histamine is located throughout the entire body. In many instances, it
causes inflammation, runny nose, itching, hives, sore throat, coughing,
flushing, headache and all those other typical allergy reactions. In the
gut, it signals the production of gastric acid. This is why some remedies
for acid stomach are really antihistamines. In the brain, it functions like
a neurotransmitter. A couple of functions include affecting hunger or
feeding, and also sleep/wake cycles (the circadian rhythm). A bit more
histamine keeps you awake, and lower histamine levels help you sleep. This
is why many antihistamines make you drowsy. Some newer antihistamines have
been developed to get around this issue.
http://www.thedietdoctor.com/incl/571.cfm
The role of antioxidants in the immune system is multifaceted as they can
serve to either suppress or enhance the immune response. Depending on the
desired response, different antioxidants can play different roles in
balancing the immune response effectively in an individual. Beta-carotene,
selenium, vitamin C, and vitamin E are all examples of exogenous
antioxidants. In addition to these that come from our diet, the body also
has a system of enzymes, which form the endogenous antioxidants. Together,
they work to eliminate free radicals from the body.
As andrew pointed out, if the immune system is under-reactive, this is a
problem, but if it is over-reactive it is a problem. People may have any
assortment of these things going on at a time.
randall
Cruiser wrote:
> Randall,
>
> I am looking to target homocycteine.
>
> Why?
>
> It appears that elevated homocysteine may cause an inflammtory cascade
> through stimulating the AT1 receptor.
>
Ok. Then your back to lowering arginine,
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15521698
> I have elevated cholesterol, and blood pressure on the high side.
>
I suggest you starve yourself some.
> I am fairly certain that Hayek is using B12 in his formula. The best
> complement for B12 seems like it could be
> TMG, since in combination they will raise SAM-e levels and drop homocysteine
> levels.
>
> At one point Hayek bragged about curing someone's cirrhosis of the liver.
> Cirrhosis of the liver is related to scaring of the liver tissue. SAM-e is
> supposed to reduce scarring of the liver tissue.
>
Why not let your body cure it self without having to put things in?
> Here are a whole bunch of studies related to TMG.
>
> http://www.lef.org/prod_hp/abstracts/php-ab112a.html
I do eat beets and take TMG, betaine once in awhile.
Have never lowered P with it. But staying alive longer has been
a benefit of most of what i've done. With the exception of my present
trial. Eating the flare foods and using high C and IP6.
Btw, how are you doing with IP6/Vitamin C?
randall
>
> Cheers, Cruiser
randall
Ok got it.
But what if you don't need it?
Simply by taking MSM you burn up your molybdenum and then
you have a rube goldberg machine like depletion thing going
on. If it isn't broke don't fix it.
But what if you are taking vitamin depleters? Like mtx?
If your on MTx you most likely do need folic acid (as mentioned many
times in
the P ng),
(plus there must be a 100 abstracts in pubmed about derm's giving folic
acid
to there mtx'ers)
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=8765212
DNA hypomethylation in inflammatory arthritis: reversal with
methotrexate.
Kim YI, Logan JW, Mason JB, Roubenoff R.
University of Toronto, Ontario, Canada.
This study investigated whether methotrexate, by interrupting the
methyl transfer function of folate, can induce genomic DNA
hypomethylation in patients with inflammatory arthritis. Consecutive
subjects with inflammatory arthritis (rheumatoid or psoriatic), who
were taking methotrexate (n = 7) or other medications (n = 6), and
control subjects, either healthy or with osteoarthritis and taking
nonsteroidal anti-inflammatory agents only (n = 9) were recruited. The
methylation status of genomic DNA from peripheral blood mononuclear
cells was determined. Plasma levels of folate, B12, and
pyridoxal-5'-phosphate (PLP), all of which are involved in biologic
methylation, were also examined. The extent of genomic DNA methylation
was lowest in subjects with inflammatory arthritis who were not taking
methotrexate, highest in subjects with inflammatory arthritis who were
taking methotrexate, and intermediate in control subjects (p < 0.05).
Plasma levels of folate and B12 were similar among the three groups.
The mean plasma PLP level in subjects with inflammatory arthritis was
33% lower than that in control subjects (p = 0.04). No significant
correlation between genomic DNA methylation and folate, B12, and PLP
levels was observed. These data do not support the hypothesis that
methotrexate induces genomic DNA hypomethylation. However, these data
indicate that inflammatory arthritis is associated with genomic DNA
hypomethylation that is reversed with methotrexate. Future studies
using a larger number of subjects are warranted to confirm these
findings.
PMID: 8765212
>
> Methylation
Will hypermethylation do anything positive?
What if the P problem here is CPG DNA methylation?
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12934112
Analysis of 14-3-3sigma expression in hyperproliferative skin diseases
reveals selective loss associated with CpG-methylation in basal cell
carcinoma.
Lodygin D, Yazdi AS, Sander CA, Herzinger T, Hermeking H.
Molecular Oncology, Max-Planck-Institute of Biochemistry, Am
Klopferspitz 18A, D-82152 Martinsried near Munich, Germany.
The p53-regulated 14-3-3sigma gene encodes an inhibitor of cell cycle
progression essential for senescence and clonal evolution of
keratinocytes in vitro. Here we analysed the in vivo expression of
14-3-3sigma protein in several skin diseases, which are characterized
by hyperproliferative keratinocytes. Unexpectedly, the 14-3-3sigma
protein was expressed at high levels in psoriasis (11 of 11 patients),
condylomata acuminata (11/11), actinic keratoses (11/11) and squamous
cell carcinomas (SCC) (11/11). However, keratinocytes that had
undergone transformation to basal cell carcinoma (BCC) showed partial
(10 of 41; 24.4%) or complete (19 of 41; 46.3%) loss of 14-3-3sigma
protein expression. BCC (5/5), SCC (6/6) and actinic keratoses (7/7)
concomitantly expressed the p53-homolog p63 and 14-3-3sigma at high
levels, ruling out potential inhibitory effects of p63 isoforms on
14-3-3sigma transcription as the basis for loss of 14-3-3sigma
expression. Of 41 BCC samples isolated by laser-capture
microdissection, 28 (68.3%) showed CpG-hypermethylation of the
14-3-3sigma promoter combined with reduced or absent 14-3-3sigma
protein levels in 22 cases (78.6%). Since it has been reported that BCC
retain wild-type p16(INK4A) and here BCC with CpG-methylation of
14-3-3sigma did not show CpG-methylation of p16(INK4A) (0/17),
silencing of 14-3-3sigma may contribute to evasion of senescence in
BCC. As experimental removal of 14-3-3sigma sensitizes to DNA damage,
silencing of 14-3-3sigma may explain the high efficacy of radiation
therapy in the treatment of BCC.
PMID: 12934112
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15857576
The crystal structure of the non-liganded 14-3-3sigma protein: insights
into determinants of isoform specific ligand binding and dimerization.
Benzinger A, Popowicz GM, Joy JK, Majumdar S, Holak TA, Hermeking H.
Molecular Oncology Group, Max-Planck-Institute for Biochemistry,
Martinsried, Germany.
Seven different, but highly conserved 14-3-3 proteins are involved in
diverse signaling pathways in human cells. It is unclear how the
14-3-3sigma isoform, a transcriptional target of p53, exerts its
inhibitory effect on the cell cycle in the presence of other 14-3-3
isoforms, which are constitutively expressed at high levels. In order
to identify structural differences between the 14-3-3 isoforms, we
solved the crystal structure of the human 14-3-3sigma protein at a
resolution of 2.8 Angstroms and compared it to the known structures of
14-3-3zeta and 14-3-3tau. The global architecture of the 14-3-3sigma
fold is similar to the previously determined structures of 14-3-3zeta
and 14-3-3t: two 14-3-3sigma molecules form a cup-shaped dimer.
Significant differences between these 14-3-3 isoforms were detected
adjacent to the amphipathic groove, which mediates the binding to
phosphorylated consensus motifs in 14-3-3-ligands. Another specificity
determining region is localized between amino-acids 203 to 215. These
differences presumably select for the interaction with specific
ligands, which may explain the different biological functions of the
respective 14-3-3 isoforms. Furthermore, the two 14-3-3sigma molecules
forming a dimer differ by the spatial position of the ninth helix,
which is shifted to the inside of the ligand interaction surface, thus
indicating adaptability of this part of the molecule. In addition, 5
non-conserved residues are located at the interface between two
14-3-3sigma proteins forming a dimer and represent candidate
determinants of homo- and hetero-dimerization specificity. The
structural differences among the 14-3-3 isoforms described here
presumably contribute to isoform-specific interactions and functions.
PMID: 15857576
Cpg methylation has been mentioned in the groups (h'mm-- billi and I),
http://groups.google.com/groups?q=cpg+methylation+psoriasis&qt_s=Search
It has to be on the web, yep,
http://www.google.com/search?q=cpg%20methylation%20psoriasis&qt_s=Search&sa=N&tab=gw
How about images? yep,
http://images.google.com/images?q=methylation%20dna&hl=en&lr=&sa=N&tab=wi
&
http://images.google.com/images?svnum=10&hl=en&lr=&q=methylation+dna+cpg&btnG=Search
or
http://images.google.com/images?svnum=10&hl=en&lr=&q=methylation+cpg&btnG=Search
Yet,
What if this is compensatory to stop other diseases?
We may have a gene to protect one thing like p53 which may be
overexpressed
but yet benefit us in counterintuitive ways,
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=16180010
And btw, i don't know how bad that cyanocobalamin could be, as vrp.com
products has it on their site.
Look at methyl caps, the supplement and open the ingredients box.
If vrp is selling it, you must have been spun by someone else?
I mean they've been on the vanguard of health since 1979. Back when
they were in Mountain View Ca.
I guess they went to carson to save taxes.
Which means they understand business as well?
Well, well... staying ahead of the TAX man.
But is it something in us that's being taxed or not?
If uwe has a magic X that will make the immune system work better,
they why wouldn't it simply make more psoriasis?
Answer:: Because you believe that it's a bacterial or some other kind
of
bug infection.
And once again. If you want to make your entire body work better you
need to change the terrain of your gut to slightly acidic.
And that brings me back to vrp. I see they sell culturelle for good gut
flora.
Maybe their crazy? No matter how good the stuff is, 1 zillion live
bacteria
in each ounce or not, it still doesn't make it thru the acid in the
stomach.
Has VRP sold out?
randall... revelations are a B---- itch. <sigh>
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> MF<R9S*;*\+*RLM?7U__,F:VID/___P``````````````````````````````
> M`````````````````````````"'Y! ``````+ ````#,`0P```6T8"2.9&F>
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> MON"P>$PNF\_HM'K-;KO?\'A[`$$D`/B P `('/8$<H*#A(6&AXB"78N,20,%
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> I6W0`!P4""KB]QL?(R4./P@W%RM#1TM,K`PX%S]3:V]S&`]G=X3PA`#L`
> `
> end
Cruiser
Here's the thing. I live in a resort area. It is kinda party time, most of
the time. I have friends that come to my door univited and want to party. My
wife has guests too and we both get invited with to party with friends. We
have bon fires, hang by the pool, sit on screen porches, or sit by the water
and watch the sunset. Usually there is drink involved.
I have gotten into the bad habit of drinking a bottle of wine or two with
neighbours, or a few beers with my buddies. It seems like most weekends and
evenings.
When I drink a bit, the next morning my nails look pretty ugly. Then they
seem to improve during the day, since starting all the supplements. I really
did not notice much difference before.
I also have a P spot on my leg that I got rid of a year or two ago. It has
returned. In addition I have been getting a few small spots here and there
since the beginning of September.
All these spots act much llike my nails and get worse after an evening of
indulgence.
So, last night I barricaded myself indoors. The fact that is was raining
helped. I did not drink.
Today things looked better in the morning. I am going to try to avoid the
booze for a couple weeks to see if I can get cleared. The party will have to
go on without me.
Otherwise there is really no difference yet. All spots are still there and
nothing has cleared. I might even have a couple new ones. The only
difference seems to be the crustiness. More crusty after a night of
indulgence.
However, the little aches and pains are gone from sites of many old joint
injuries. My joints feel all loosy-goosy. I feel too like I am emerging from
an extended mental funk.
I picked up some TMG and zinc to add to the supplements trial.
If there is a cure in this somewhere, I am determined to find it!
I will be running out of many of the things I have been supplementing,
before the end of this week.
So, I am going to drop some things.
At his point, I think the DHEA, DHA, GLA, glutathione & NAC can all be
tossed.
Boron should do in place of DHEA. I had to get the DHEA under the table
anyway, since it is not legal here.
The TMG should cover off the glutathione and NAC, by re-methylizing the
homocysteine to SAM-e, which will provide the same thing.
The DHA and GLA were tossed in for the heck of it, just in case. I will drop
them and see what happens. I am curious to see if my nails still have the
same shine after dropping these. They are definitely more shiny now than
before (except some morning after days)
I will stick with my normal B100, multivitamin, Lysine, green tea, and now
boron.
I will extend with Ascorbic Acid, IP6/Inositol, B12, folic acid, TMG, and
Zinc trial going forward.
The B12, Zinc, folic acid, and TMG should effectively cover off lowering
homocysteine and raising SAM-e.
Cruiser
randall
Cruiser wrote:
> Randall,
>
> Here's the thing. I live in a resort area.
That's nice. I grew up in southern california during the 60's and 70's.
> It is kinda party time, most of
> the time. I have friends that come to my door univited and want to party. My
> wife has guests too and we both get invited with to party with friends. We
> have bon fires, hang by the pool, sit on screen porches, or sit by the water
> and watch the sunset. Usually there is drink involved.
>
Then your very lucky you didn't onset earlier. But maybe not.
> I have gotten into the bad habit of drinking a bottle of wine or two with
> neighbours, or a few beers with my buddies. It seems like most weekends and
> evenings.
>
Dial it down to a glass and you may live to 100.
> When I drink a bit, the next morning my nails look pretty ugly.
Not the nails themselves? But you mean the fungal components?
> Then they
> seem to improve during the day, since starting all the supplements. I really
> did not notice much difference before.
>
And i would suspect your visiting your barber more often as well.
> I also have a P spot on my leg that I got rid of a year or two ago. It has
> returned. In addition I have been getting a few small spots here and there
> since the beginning of September.
>
Cruiser, do you know the story of my family involvement?
My father and older brother both onset in their late 40's.
Could you be looking at it finally taking off?
> All these spots act much llike my nails and get worse after an evening of
> indulgence.
>
OK. And if i induced guttate right now, i'd see the same exact thing
on me. I do happen to know what your talking about. I have my fair
share
of spots due to the ethanol in my current trial.
> So, last night I barricaded myself indoors. The fact that is was raining
> helped. I did not drink.
>
LOok, friends are true friends if they give you your sPace.
Mine do.
When i whiPPed out my bare leg in a four star restuarant recently, they
sceptically said, are you on steroids.
I said nope. Its all due to IP6. Now their off riPPing me off selling
a secret formula on the net. His name is uwe. lol
Sorry couldn't resist.
> Today things looked better in the morning. I am going to try to avoid the
> booze for a couple weeks to see if I can get cleared. The party will have to
> go on without me.
>
YOu most likely can do a glass of cab if thats all you do. Nurse it.
Be in the moment and they will expand and fill your consciousness at
the same time.
> Otherwise there is really no difference yet. All spots are still there and
> nothing has cleared. I might even have a couple new ones. The only
> difference seems to be the crustiness. More crusty after a night of
> indulgence.
>
As if i didn't go to 70% plus in my dirty thirties? lol
> However, the little aches and pains are gone from sites of many old joint
> injuries. My joints feel all loosy-goosy. I feel too like I am emerging from
> an extended mental funk.
>
Brain fog is gone? Wow you had symptoms i didn't realize.
> I picked up some TMG and zinc to add to the supplements trial.
>
Can't hurt and may help to avoid the obvious stuff already making the
rounds.
Those kids go back to school and bingo. The bugs all get mixed back
into
society.
> If there is a cure in this somewhere, I am determined to find it!
>
As well you must. I'm here to make that happen.
> I will be running out of many of the things I have been supplementing,
> before the end of this week.
>
> So, I am going to drop some things.
>
> At his point, I think the DHEA, DHA, GLA, glutathione & NAC can all be
> tossed.
>
I'd keep the nac. I've used it many many times to more clearings then
almost
anything. till the gut- colon fix came along.
> Boron should do in place of DHEA. I had to get the DHEA under the table
> anyway, since it is not legal here.
>
Dhea didn't do anything but make my libido go crazy.
That's no help.
> The TMG should cover off the glutathione and NAC, by re-methylizing the
> homocysteine to SAM-e, which will provide the same thing.
>
Ok, and i'd still hold on to the nac for later.
> The DHA and GLA were tossed in for the heck of it, just in case. I will drop
> them and see what happens. I am curious to see if my nails still have the
> same shine after dropping these. They are definitely more shiny now than
> before (except some morning after days)
>
> I will stick with my normal B100, multivitamin, Lysine, green tea, and now
> boron.
>
If you do the green tea, which is more helpful for cancer then
psoriasis, i'd
want to add a little extra folic acid.
> I will extend with Ascorbic Acid, IP6/Inositol, B12, folic acid, TMG, and
> Zinc trial going forward.
>
Sounds good to me. If you don't see anything you may be just like the
other two makes in my immediate family.
Your going to accelerate towards more severe psoriasis. You had a
very mild form of P and now the dragon is out of the closet.
Or the IP6 is going to mask this process.
YOu could stop everything and wait and see.
Then after your either more severe or not rework your trials.
You have to remember i have decades more P on you. I mean me. :(
> The B12, Zinc, folic acid, and TMG should effectively cover off lowering
> homocysteine and raising SAM-e.
>
> Cruiser
Whatever. Either go cold turkey on all of it or fiddle around till you
actually know whats going on.
randall... been there done that and now am the same.
Cruiser
"randall" <ranh...@aol.com> wrote in message
news:1127778488.0...@g49g2000cwa.googlegroups.com...
> > However, the little aches and pains are gone from sites of many old
joint
> > injuries. My joints feel all loosy-goosy. I feel too like I am emerging
from
> > an extended mental funk.
> >
>
> Brain fog is gone? Wow you had symptoms i didn't realize.
>
Not only that, but it has been raining and I haven't felt even a twinge, in
my
joints.
> > Boron should do in place of DHEA. I had to get the DHEA under the table
> > anyway, since it is not legal here.
> >
>
> Dhea didn't do anything but make my libido go crazy.
>
> That's no help.
>
Well I think the Boron is involved in what's happening. Here is my theory.
Boron
is a limiter in cell division. So, it stops or diminishes T-Cell
replication, due to a
shortage. That is its relation to RA. It seems I had a touch of RA starting
and have
disposed of it with the boron.
So maybe a boron shortage also stops or slows psoriatic skin replication for
the
same reason. Now, that I have boron, my immune system in working better, but
also the skin cells can replicate more and so I am getting more spots and
flaking.
The good news is that beating off the RA must have killed off some sort of
infection. So, I am hopefully rid of that, at least. However, I do not think
that
was the only infection. I think there is more. Maybe I killed some
myoplasmas,
and or some candida, but there is still more going.
>
> > The TMG should cover off the glutathione and NAC, by re-methylizing the
> > homocysteine to SAM-e, which will provide the same thing.
> >
>
> Ok, and i'd still hold on to the nac for later.
>
I am worried about developing an over abundance of cysteine, which is also
supposed to be problematic. Taking all the NAC and glutathione has dumped a
bunch of cysteine into my system at various stages of the glutathione,
SMA-e,
and homocysteine cycle. The ascorbic acid, B12, folic acid, zinc, and TMG
supplements should turn over the the glutathione/vitamin C and
homocysteine/SAM-e cycles, making more supplement unecessary. I should
have plenty now, since I have been gobbling it for a couple weeks.
>
> If you do the green tea, which is more helpful for cancer then
> psoriasis, i'd
> want to add a little extra folic acid.
>
Yes, and if you read the last article which I posted, there are some B
vitamins
that I am taking in quantities that use up methyl groups. So, this can
contribute
to under-methylization.
BTW, if you did not read that article, please do. It is really a very good
and
very informative read. Excellent stuff. I cannot recommend it strongly
enough.
I am taking 10mg methyl-cobalamin (B12) sublingual, and about 10-12mg folic
acid, per day. The folic acid is not methylized and so is another methyl
group
robber. It is supposed to convert homocysteine to SAM-e by donating a methyl
group. Instead it takes a methyl group to build methylfolate from the folic
acid.
It steals methyl groups instead of donating them.
The TMG does not need folic acid or methylfolate to convert homocycteine to
SAM-e. It is tri-methyl-glycine, with three methyl groups. It can do the job
with
the help of some zinc and B12. Folic acid not required.
The methylcobalamin sublingual bypasses any gastric absorption problems,
and delivers the B12 in already active form. The TMG provides methyl donors
to activate folic acid, and it bypasses the need for folic acid for
converting
homocysteine. Folic acid absorption and/or conversion problems become
non-issues.
This seems like an excellent way to knock down elevated homocysteine and
boost low SAM-e.
FYI. I am using TMG instead of betaineHCl, since I get acid reflux once in
awhile, have tested my body acidity as high, and do not need any more acid.
The ascorbic acid is problably boosting my acidity way up too.
>
> > I will extend with Ascorbic Acid, IP6/Inositol, B12, folic acid, TMG,
and
> > Zinc trial going forward.
> >
>
> Sounds good to me. If you don't see anything you may be just like the
> other two makes in my immediate family.
>
> Your going to accelerate towards more severe psoriasis. You had a
> very mild form of P and now the dragon is out of the closet.
>
>
> Or the IP6 is going to mask this process.
>
> YOu could stop everything and wait and see.
>
> Then after your either more severe or not rework your trials.
>
I am concerned that the boron will now just make the P get worse, if I don't
find the answer. The boron is a blessing, in that it has cleared me of RA,
and probably has had other good affects, but it is likely worsening the P,
by removing a cell division limiter.
In a way that is good since, I can now get a better sense of how my body
in reacting to supplements.
Cruiser
randall
Cruiser wrote:
> "randall" <ranh...@aol.com> wrote in message
> news:1127778488.0...@g49g2000cwa.googlegroups.com...
>
> Not only that, but it has been raining and I haven't felt even a twinge, in
> my
> joints.
>
And since you did two dozen new supplements it's hard to ferret out the
one that did the most? Could be nac as far as you know.
I have tested single supplements like nac many times.
>
> Well I think the Boron is involved in what's happening. Here is my theory.
> Boron
> is a limiter in cell division. So, it stops or diminishes T-Cell
> replication, due to a
> shortage. That is its relation to RA. It seems I had a touch of RA starting
> and have
> disposed of it with the boron.
>
> So maybe a boron shortage also stops or slows psoriatic skin replication for
> the
> same reason. Now, that I have boron, my immune system in working better, but
> also the skin cells can replicate more and so I am getting more spots and
> flaking.
>
Yet if I use some and it does nothing then your faced with the OTHER
supplements as at effect.
I may pick up some. Any suggestions? Brands?
Yours has other trace minerals in it?
> The good news is that beating off the RA must have killed off some sort of
> infection. So, I am hopefully rid of that, at least. However, I do not think
> that
> was the only infection. I think there is more. Maybe I killed some
> myoplasmas,
> and or some candida, but there is still more going.
>
Ok if you believe so.
I try to think in terms of the bubble boy in these situations.
What is the immune system up to.
And scid mice with P are in that bubble now.
And the real scientists are using them to our favor.
Check new P news for a good abstract on them.
(9/27/2005 P news)
>
> I am worried about developing an over abundance of cysteine, which is also
> supposed to be problematic. Taking all the NAC and glutathione has dumped a
> bunch of cysteine into my system at various stages of the glutathione,
> SMA-e,
> and homocysteine cycle. The ascorbic acid, B12, folic acid, zinc, and TMG
> supplements should turn over the the glutathione/vitamin C and
> homocysteine/SAM-e cycles, making more supplement unecessary. I should
> have plenty now, since I have been gobbling it for a couple weeks.
>
Then you should have positive results by now? Yet any progression in
your
P is now suspect because you don't know if it may have been worse
without
the current regime.
> >
> > If you do the green tea, which is more helpful for cancer then
> > psoriasis, i'd
> > want to add a little extra folic acid.
> >
>
> Yes, and if you read the last article which I posted, there are some B
> vitamins
> that I am taking in quantities that use up methyl groups. So, this can
> contribute
> to under-methylization.
>
> BTW, if you did not read that article, please do. It is really a very good
> and
> very informative read. Excellent stuff. I cannot recommend it strongly
> enough.
>
Ok i'll give it more time.
> I am taking 10mg methyl-cobalamin (B12) sublingual, and about 10-12mg folic
> acid, per day. The folic acid is not methylized and so is another methyl
> group
> robber. It is supposed to convert homocysteine to SAM-e by donating a methyl
> group. Instead it takes a methyl group to build methylfolate from the folic
> acid.
> It steals methyl groups instead of donating them.
>
> The TMG does not need folic acid or methylfolate to convert homocycteine to
> SAM-e. It is tri-methyl-glycine, with three methyl groups. It can do the job
> with
> the help of some zinc and B12. Folic acid not required.
>
> The methylcobalamin sublingual bypasses any gastric absorption problems,
> and delivers the B12 in already active form. The TMG provides methyl donors
> to activate folic acid, and it bypasses the need for folic acid for
> converting
> homocysteine. Folic acid absorption and/or conversion problems become
> non-issues.
>
> This seems like an excellent way to knock down elevated homocysteine and
> boost low SAM-e.
>
> FYI. I am using TMG instead of betaineHCl, since I get acid reflux once in
> awhile, have tested my body acidity as high, and do not need any more acid.
> The ascorbic acid is problably boosting my acidity way up too.
>
Ok and linus pauling lived and worked till 93. He took 20 plus grams a
day.
> >
> > > I will extend with Ascorbic Acid, IP6/Inositol, B12, folic acid, TMG,
> and
> > > Zinc trial going forward.
> > >
> >
> > Sounds good to me. If you don't see anything you may be just like the
> > other two ___males___(*was makes) in my immediate family.
(*correction... makes changed to males)
> >
> > Your going to accelerate towards more severe psoriasis. You had a
> > very mild form of P and now the dragon is out of the closet.
> >
> >
> > Or the IP6 is going to mask this process.
> >
> > YOu could stop everything and wait and see.
> >
> > Then after your either more severe or not rework your trials.
> >
>
> I am concerned that the boron will now just make the P get worse, if I don't
> find the answer. The boron is a blessing, in that it has cleared me of RA,
> and probably has had other good affects, but it is likely worsening the P,
> by removing a cell division limiter.
>
Or you miscalculated on something else. LIke why p gets worse to begin
with.
And any alcohol will exacerbate that situation. Which is the reason why
i'm so surprised by my current results.
I'm going to have to go back and reconsider some of my LPS thoughts.
Or are those beliefs at fault?
> In a way that is good since, I can now get a better sense of how my body
> in reacting to supplements.
>
Well, you are going in a direction regardless of what happens next.
Please keep us posted. Your results should/may help others to find a
direction too.
randall
> Cruiser