Re: TH1-TH2 balancer

[Guest guest]

Hi, .

" Du Pre " <isaiah40@...> wrote:

>

> Hello,

> My friend has this question and I do also:

> what natural product was it to balance TH1/2?

> That wasn't the undenatured whey was it?

> I know that was for glutathione,but couldn't recall if if it did the TH thing

too.

***NONdenatured whey is the product for shifting and creating Th1/Th2 balance,

at least it is the best, barring CBS SNP upregulation sulfur side-effects, for

CFS. But any effective means for building glutathione can do this given

glutathione is the basis of intracellular(Th1) immunity.

***In CFS one's immunity has become shifted or unbalance in favor of Th2

immunity, so strengthening Th1 immunity by methods for improving glutathione

status can balance this. This is the science and my personal experience as

well.

[Guest guest]

Hi, .

I agree with what said about this. To really get the Th1 and

Th2 immune responses back into stable balance, it's necessary to

stabilize glutathione back up in the normal range. and a few

others have been able to do this with nondenatured whey protein, and

I think that's wonderful.

I suspect, however, that this won't work for everyone, and

mentioned in particular the issue of the people with CBS

upregulation SNPs. In cases such as this, and perhaps in some other

subsets as well, it looks as though these SNPs must be dealt with

more directly in order to correct the methylation cycle block and

restore the glutatione level. Inherent in all of this is restoring

the folate metabolism, too, since it is linked to the methylation

cycle, and the folate metabolism is necessary to enable the

synthesis of new DNA and RNA, which in turn is required for the

cloning of T lymphocytes, and essential step in the Th1 immune

response.

There have also been temporary fixes attempted using immune

modulators, and some people have benefited from them. I'm referring

to things like Isoprinosine. I don't think they bring about a

permanent correction for most people. To fix this problem

permanently, I think you have to get at the root of it, which

appears to be the glutathione depletion and the methylation cycle--

folate metabolism block.

Rich

>

> Hello,

> My friend has this question and I do also:

> what natural product was it to balance TH1/2?

> That wasn't the undenatured whey was it?

> I know that was for glutathione,but couldn't recall if if it did

the TH thing too.

> Thanks,

> Du Pre

> Poetry website:

http://www.angelfire.com/poetry/soareagle/index.html

> " By words the mind is winged. " Aristophanes

> Website for National Alliance for Myalgic Encephalomyelitis:

http://www.name-us.org

>

>

[Guest guest]

I have read that folate (and I don't know if this includes folinic acid and

folic acid as well) contribute (or become) glutamate. Also, that folinic

acid has calcium in it, which aparently contributes to glutamate (I really

don't understand the mechanism for this; I knew that casein, milk protein

contained a lot of gluatmate, but am not understanding how all calcium

increases glutamate levels. I also didn't know that folinic acid, by

itself, had calcium in it, without calcium being added to it in a

supplement)

So those of us who have hi glutamate/glutamic acid levels (or who are very

sensitive to glutamate), yet need the folate to help with methylation - what

can we use? If folic acid, being the most inactive form of all three of

them, would be the 'safest' to use so as not to experience a 'direct hit',

what if this also means that its comparative lack of bioavailability is not

'reaching' the person's methylation cycle?

Are these people in a catch 22 situation? (I feel a bit more brain dead

than usual today, so sorry if the above is not making sense) Les

Re: TH1-TH2 balancer

> Hi, .

>

> I agree with what said about this. To really get the Th1 and

> Th2 immune responses back into stable balance, it's necessary to

> stabilize glutathione back up in the normal range. and a few

> others have been able to do this with nondenatured whey protein, and

> I think that's wonderful.

>

> I suspect, however, that this won't work for everyone, and

> mentioned in particular the issue of the people with CBS

> upregulation SNPs. In cases such as this, and perhaps in some other

> subsets as well, it looks as though these SNPs must be dealt with

> more directly in order to correct the methylation cycle block and

> restore the glutatione level. Inherent in all of this is restoring

> the folate metabolism, too, since it is linked to the methylation

> cycle, and the folate metabolism is necessary to enable the

> synthesis of new DNA and RNA, which in turn is required for the

> cloning of T lymphocytes, and essential step in the Th1 immune

> response.

>

> There have also been temporary fixes attempted using immune

> modulators, and some people have benefited from them. I'm referring

> to things like Isoprinosine. I don't think they bring about a

> permanent correction for most people. To fix this problem

> permanently, I think you have to get at the root of it, which

> appears to be the glutathione depletion and the methylation cycle--

> folate metabolism block.

>

> Rich

>

>

>>

>> Hello,

>> My friend has this question and I do also:

>> what natural product was it to balance TH1/2?

>> That wasn't the undenatured whey was it?

>> I know that was for glutathione,but couldn't recall if if it did

> the TH thing too.

>> Thanks,

>> Du Pre

>> Poetry website:

> http://www.angelfire.com/poetry/soareagle/index.html

>> " By words the mind is winged. " Aristophanes

>> Website for National Alliance for Myalgic Encephalomyelitis:

> http://www.name-us.org

>>

>>

[Guest guest]

Hi, Les.

" Masland " <lmas@...> wrote:

>

> I have read that folate (and I don't know if this includes folinic acid and

> folic acid as well) contribute (or become) glutamate.

***This doesn't seem to me to be accurate information. Would you tell us your

source and perhaps a brief direct quote from the text making this claim.

Also, that folinic acid has calcium in it, which aparently contributes to

glutamate (I really don't understand the mechanism for this; I knew that casein,

milk protein

> contained a lot of gluatmate, but am not understanding how all calcium

> increases glutamate levels.

***Me either. It does'nt make sense to my understanding of both folinic as well

as calcium.

I also didn't know that folinic acid, by itself, had calcium in it, without

calcium being added to it in a supplement) So those of us who have hi

glutamate/glutamic acid levels (or who are very sensitive to glutamate), yet

need the folate to help with methylation - what can we use?

***I am very sensitive to glutamate also, but I take both folinic acid and

calcium every day. I experiece no problems at all from these like when I've

known I was ingesting actual glutamate.

If folic acid, being the most inactive form of all three of them, would be the

'safest' to use so as not to experience a 'direct hit', what if this also means

that its comparative lack of bioavailability is not 'reaching' the person's

methylation cycle?

***You are right that folic acid is good but not the most active form like

folinic acid is. I sort of doubt that it would cause a problem, but if you or

some others fear this you can always use folapro as effective alternative.

Are these people in a catch 22 situation? (I feel a bit more brain dead than

usual today, so sorry if the above is not making sense) Les

***Got it. Maybe your confusing these things with something else that can

increase glutamate to toxic levels. I know the guy at cfsn.com has a

glutathione percursor product with l-glutamate in it which caused me immediate

problems when I took it.

I took heed and moved on to somethine else that had l-glutamine instead and this

solved the problem.

> From: " rvankonynen " <richvank@...>

>

>

> > Hi, .

> >

> > I agree with what said about this. To really get the Th1 and

> > Th2 immune responses back into stable balance, it's necessary to

> > stabilize glutathione back up in the normal range. and a few

> > others have been able to do this with nondenatured whey protein, and

> > I think that's wonderful.

> >

> > I suspect, however, that this won't work for everyone, and

> > mentioned in particular the issue of the people with CBS

> > upregulation SNPs. In cases such as this, and perhaps in some other

> > subsets as well, it looks as though these SNPs must be dealt with

> > more directly in order to correct the methylation cycle block and

> > restore the glutatione level. Inherent in all of this is restoring

> > the folate metabolism, too, since it is linked to the methylation

> > cycle, and the folate metabolism is necessary to enable the

> > synthesis of new DNA and RNA, which in turn is required for the

> > cloning of T lymphocytes, and essential step in the Th1 immune

> > response.

> >

> > There have also been temporary fixes attempted using immune

> > modulators, and some people have benefited from them. I'm referring

> > to things like Isoprinosine. I don't think they bring about a

> > permanent correction for most people. To fix this problem

> > permanently, I think you have to get at the root of it, which

> > appears to be the glutathione depletion and the methylation cycle--

> > folate metabolism block.

> >

> > Rich

[Guest guest]

>> I have read that folate (and I don't know if this includes folinic

>> acid and folic acid as well) contribute (or become) glutamate.

>

> ***This doesn't seem to me to be accurate information. Would you tell us

> your source and perhaps a brief direct quote from the text making this

> claim.

http://www.food.gov.uk/multimedia/pdfs/evm0018p.pdf#page=36

" folic acid is used to indicate the parent compound, pteroylglutamic acid,

whilst folate is used in a generic sense to indicate one or a mixture of

pteroylglutamates, with various levels of reduction of the pteridine ring,

one-carbon substitutions, and numbers of glutamate residues. "

[Guest guest]

Hi, Tensevern(Les?).

Tensevern <tensevern@...> wrote:

http://www.food.gov.uk/multimedia/pdfs/evm0018p.pdf#page=36

***This link doesn't seem to work.

> " folic acid is used to indicate the parent compound, pteroylglutamic acid,

> whilst folate is used in a generic sense to indicate one or a mixture of

> pteroylglutamates, with various levels of reduction of the pteridine ring,

> one-carbon substitutions, and numbers of glutamate residues. "

***Pteroylglutamic is an alternative systematic name for folic acid according to

http://en.wikipedia.org/wiki/Folic_acid

It's not l-glutamic acid nor acts like it, though this quote suggests glutamic

acid is included among many entities some categorize in general as a folate.

***Glutamic acid alone(aspartate and MSG included) I think is the problem for

many PWCs as it readily crosses the blood-brain barrier(BBB) in people(PWCs)

that already have a permiable BBB as part of their illness to start.

[Guest guest]

davidhall2020 wrote:

> Tensevern <tensevern@...> wrote:

> <http://www.food.gov.uk/multimedia/pdfs/evm0018p.pdf#page=36>

>

> ***This link doesn't seem to work.

Hmmm... Works fine for me, I've just checked. It's also an authoritative piece

- the UK government's Expert Group on Vitamins and Minerals - Review of Folic

Acid, 2002.

Sue

[Guest guest]

> > <http://www.food.gov.uk/multimedia/pdfs/evm0018p.pdf#page=36>

> >

> > ***This link doesn't seem to work.

>

> Hmmm... Works fine for me, I've just checked. It's also an

authoritative piece

> - the UK government's Expert Group on Vitamins and Minerals -

Review of Folic

> Acid, 2002.

>

> Sue

>

Short-term oral administration of ginseng extract induces type-1

cytokine production.

Author: Liou CJ , Huang WC , Tseng J

Source: Immunopharmacol Immunotoxicol, 28(2): 227-40 2006

Service Fee: $12.00 ; Copyright Royalties: $28.00

Abstract: Ginseng radix (Panax ginseng C.A. Meyer) is a popular

herbal medicine used as a major ingredient in tonic recipes in

eastern Asian countries. In our study, male BALB/c mice were treated

orally with various doses of ginseng root extract for 5 consecutive

days. The extract reduced the serum level of IgG but elevated the

level of IgA. Under in vitro condition, the lipopolysaccharide-

stimulated spleen cells from the ginseng-treated mice also showed a

significant decrease in IgG production but an increase in IgA

production. The serum level and production of IgM was unaffected. The

interleukin-2, interferon-gamma (Th1-type cytokines), and interleukin-

10 (Tr1-type cytokine) production by Con A-stimulated spleen cells

from the ginseng-treated mice showed an upregulation relative to the

control group. However, the production of interleukin-4 (Th2-type

cytokine) showed no significant change. The activity of natural

killer cells was increased in the ginseng group, but the percentages

of T-lymphocytes (CD3+) and CD4+8-, CD4-8+ subset were reduced. Thus,

short-term oral administration of ginseng extract appears to enhance

Th1-type cytokine production.

Language: eng

[Guest guest]

> > > <http://www.food.gov.uk/multimedia/pdfs/evm0018p.pdf#page=36>

> > >

> > > ***This link doesn't seem to work.

> >

> > Hmmm... Works fine for me, I've just checked. It's also an

> authoritative piece

> > - the UK government's Expert Group on Vitamins and Minerals -

> Review of Folic

> > Acid, 2002.

> >

> > Sue

> >

> Short-term oral administration of ginseng extract induces type-1

> cytokine production.

Title: Reduced levels of antiinflammatory cytokines in patients with

chronic widespread pain.

Author: Uçeyler N , Valenza R , Stock M , Schedel R , Sprotte G ,

Sommer C

Source: Arthritis Rheum, 54(8): 2656-2664 2006

Service Fee: $12.00 ; Copyright Royalties: $30.00

Abstract: OBJECTIVE: The term chronic widespread pain refers to a

group of painful diseases of poorly understood pathophysiology. One

major subgroup is fibromyalgia (FM), as defined by the criteria of

the American College of Rheumatology. Among other hypotheses, a

potential pathophysiologic role of cytokines in chronic widespread

pain has been proposed. We undertook this study to investigate

whether cytokine profiles differ in patients with chronic widespread

pain and controls. METHODS: We analyzed cytokine expression patterns

in 40 patients with chronic widespread pain (26 of whom had FM), 40

age- and sex-matched healthy controls, and an additional 15 patients

with chronic widespread pain who were recruited from a different

center. Expression of messenger RNA (mRNA) for interleukin-2 (IL-2),

IL-4, IL-8, IL-10, tumor necrosis factor alpha (TNFalpha), and

transforming growth factor beta1 (TGFbeta1) in peripheral blood was

analyzed using quantitative real-time polymerase chain reaction

(PCR). Serum protein levels were measured by enzyme-linked

immunosorbent assay. RESULTS: We found significantly lower relative

gene expression (P < 0.0001 for IL-4; P = 0.03 for IL-10) and lower

levels of serum protein concentrations (P < 0.0001 for IL-4; P = 0.04

for IL-10) of the Th2 cytokines IL-4 and IL-10 in patients with

chronic widespread pain than in the control group. This finding was

corroborated in an additional group of 15 patients with chronic

widespread pain. There were no significant differences between the

groups in levels of mRNA for IL-2, IL-8, TNFalpha, or TGFbeta1.

Protein data paralleled the real-time PCR results. CONCLUSION:

Chronic widespread pain is associated with a lack of antiinflammatory

and analgesic Th2 cytokine activity, which may contribute to its

pathogenesis.

Language: ENG

[Guest guest]

Hi, Sue.

The link provided does not work. Nothing is wrong with my browser, so I don't

know what's up. Also, it's just very strange, the comment on folinic acid, given

that Dr Cheney, the DAN! group, Dr Yasko and Rich on this list all recommend it

to PWCs and autistics they are attempting to help, never noting excitoxicity

problems from those who have previously used it.

So, I seriously doubt what appears to be an irrational fear that it can do this.

I thank you for the quote, but it also doesn't say anything about toxicity from

folic acid, never mind folinic acid.

If this UK Government group is in fact making such a claim, I would want to see

what evidence they base it upon as well as see it corroborated by another

independent source, outside the UK. You know any commentary that is medical or

medical related has a tremendous credibility gap to overcome when it comes from

the UK Government, right?

Lack of integrity, deception and downright stupidity have been the calling cards

of UK health insitutions most poingnantly when it comes to ME/CFS and no doubt

other health concerns. They are not to be trusted.

Tensevern <tensevern@...> wrote:

>

> davidhall2020 wrote:

> > Tensevern <tensevern@> wrote:

> > <http://www.food.gov.uk/multimedia/pdfs/evm0018p.pdf#page=36>

> >

> > ***This link doesn't seem to work.

>

> Hmmm... Works fine for me, I've just checked. It's also an authoritative

piece

> - the UK government's Expert Group on Vitamins and Minerals - Review of Folic

> Acid, 2002.

>

> Sue

[Guest guest]

- thanks for posting that link - VERY interesting! (the entire site

is interesting!)

In Section 144, it states: " the neurotoxic effects of folates '(and at the

end of the article it is stated that 'the term folate is used generically

to describe the various deriatives of pteroglutamic acid (PGA, folic acid)')

'may be due to the liberation of glutatmate residues from the polyglutatmate

tail of folate polyglutamic species'.

In my simplistic mind (I do not know chemistry at all, and was having

trouble deciphering this statement), it seems to me that, if the 'glutamate

residues are liberated', that means they are more able to float freely in

the blood (and therefore more bioavailable?)

And, altho I know that glutamate, glutamine, and glutamic acid are not the

same thing, my body/brain has trouble with all of them; I get increased

neurological symptoms, insomnia, etc, if I ingest them (even the glutamine,

which I think is not supposed to do this, right?)

In section 145 of the same article, there is cited a possible association

between folates and increased seizure activity: " Anticonvulsant drugs " (and

Klonopin and Neurontin would be included in that grouping, correct? And

possibly anything that inhibits NMDA excitation?) 'interfere with folate

metabolism, possibly causing low folate. Treatment to correct folate

deficiency has been assoicated with precipitaiton of seizures or increased

seizure frequency'.

So this possibly could explain increased neurological symptoms , right? It

certainly could worsen insomnia-

Which still puts those of us , who are sensitive to folates (folate, folinic

acid, and folic acid), in a bind, if we are working to restore folic acid

'synthesis ' (if that is the right word), in our methylation pathways, yet

we are making our symptoms worse by doing so (and possibly counteracting

some of the meds we are taking) - Les

Re: TH1-TH2 balancer

> Hi, Tensevern(Les?).

>

>

>

> Tensevern <tensevern@...> wrote:

> http://www.food.gov.uk/multimedia/pdfs/evm0018p.pdf#page=36

>

>

>

> ***This link doesn't seem to work.

>

>

>

>> " folic acid is used to indicate the parent compound, pteroylglutamic

>> acid,

>> whilst folate is used in a generic sense to indicate one or a mixture of

>> pteroylglutamates, with various levels of reduction of the pteridine

>> ring,

>> one-carbon substitutions, and numbers of glutamate residues. "

>

>

>

> ***Pteroylglutamic is an alternative systematic name for folic acid

> according to http://en.wikipedia.org/wiki/Folic_acid

> It's not l-glutamic acid nor acts like it, though this quote suggests

> glutamic acid is included among many entities some categorize in general

> as a folate.

>

>

>

> ***Glutamic acid alone(aspartate and MSG included) I think is the problem

> for many PWCs as it readily crosses the blood-brain barrier(BBB) in

> people(PWCs) that already have a permiable BBB as part of their illness to

> start.

>

>

>

>

>

>

>

>

>

>

> This list is intended for patients to share personal experiences with each

> other, not to give medical advice. If you are interested in any treatment

> discussed here, please consult your doctor.

>

[Guest guest]

> >

Title: Circadian rhythms: glucocorticoids and arthritis.

Author: Cutolo M , Sulli A , Pizzorni C , Secchi ME , Soldano S ,

Seriolo B , Straub RH , Otsa K , Maestroni GJ

Source: Ann N Y Acad Sci, 1069(): 289-99 2006

Service Fee: $12.00 ; Copyright Royalties: $10.00

Abstract: Circadian rhythms are driven by biological clocks and are

endogenous in origin. Therefore, circadian changes in the metabolism

or secretion of endogenous glucocorticoids are certainly responsible

in part for the time-dependent changes observed in the inflammatory

response and arthritis. More recently, melatonin (MLT), another

circadian hormone that is the secretory product of the pineal gland,

has been found implicated in the time-dependent inflammatory reaction

with effects opposite those of cortisol. Interestingly, cortisol and

MLT show an opposite response to the light. The light conditions in

the early morning have a strong impact on the morning cortisol peak,

whereas MLT is synthesized in a strictly nocturnal pattern. Recently,

a diurnal rhythmicity in healthy humans between cellular (Th1 type)

or humoral (Th2 type) immune responses has been found and related to

immunomodulatory actions of cortisol and MLT. The interferon (IFN)-

gamma/interleukin (IL)-10 ratio peaked during the early morning and

correlated negatively with plasma cortisol and positively with plasma

MLT. Accordingly, the intensity of the arthritic pain varies

consistently as a function of the hour of the day: pain is greater

after waking up in the morning than in the afternoon or evening. The

reduced cortisol and adrenal androgen secretion, observed during

testing in rheumatoid arthritis (RA) patients not treated with

glucocoticoids, should be clearly considered as a " relative adrenal

insufficiency " in the presence of a sustained inflammatory process,

and allows Th1 type cytokines to be produced in higher amounts during

the late night. In conclusion, the right timing (early morning) for

the glucocorticoid therapy in arthritis is fundamental and well

justified by the circadian rhythms of the inflammatory mechanisms.

Language: eng

re: previous post on biphasic use of cortef and book by jeffries

[Guest guest]

Hi, Les.

I didn't provide the link, Sue did. For what it's worth, I consider it

misleading and incorrect in what one might infer from it about any of the folic

acid supplements one might purchase these days.

Under its UK Government characterization of folates, all PWCs and autistics

would have folate sensitivity and toxicity issues. Their exceedling broad

definition of folate necessarily includes the molecule L-glutamate, aspartame

and monosodium glutamate(MSG), known to toxic in many people and especially

PWCs.

These clearly are NOT folic acid, folinic acid or folapro nor related in how

they act within our bodies, though these too are included as folates by this UK

Government group. There is no evidence nor reported clinical experience from

these when taken by PWCs or autistics that suggest they lead to glutamate

toxicity.

In fact, these may help calm your brain and upregulated side of your immune

system down, quite the opposite of excitotoxicity that too much glutamate can

induce.

" Masland " <lmas@...> wrote:

>

> - thanks for posting that link - VERY interesting! (the entire site

> is interesting!)

> In Section 144, it states: " the neurotoxic effects of folates '(and at the

> end of the article it is stated that 'the term folate is used generically

> to describe the various deriatives of pteroglutamic acid (PGA, folic acid)')

> 'may be due to the liberation of glutatmate residues from the polyglutatmate

> tail of folate polyglutamic species'.

> In my simplistic mind (I do not know chemistry at all, and was having

> trouble deciphering this statement), it seems to me that, if the 'glutamate

> residues are liberated', that means they are more able to float freely in

> the blood (and therefore more bioavailable?)

> And, altho I know that glutamate, glutamine, and glutamic acid are not the

> same thing, my body/brain has trouble with all of them; I get increased

> neurological symptoms, insomnia, etc, if I ingest them (even the glutamine,

> which I think is not supposed to do this, right?)

> In section 145 of the same article, there is cited a possible association

> between folates and increased seizure activity: " Anticonvulsant drugs " (and

> Klonopin and Neurontin would be included in that grouping, correct? And

> possibly anything that inhibits NMDA excitation?) 'interfere with folate

> metabolism, possibly causing low folate. Treatment to correct folate

> deficiency has been assoicated with precipitaiton of seizures or increased

> seizure frequency'.

> So this possibly could explain increased neurological symptoms , right? It

> certainly could worsen insomnia-

> Which still puts those of us , who are sensitive to folates (folate, folinic

> acid, and folic acid), in a bind, if we are working to restore folic acid

> 'synthesis ' (if that is the right word), in our methylation pathways, yet