Re: Methylation cycle block treatment stops heavy urination in CFS

[Guest guest]

Rich

We want you to post here. And the methylation cycle block hypothesis

isn't a problem with most here.IT'S THE GENETICALLY SUSCEPTABLE STUFF

THAT MAKES US ANGRY.I believe that everything in this disease process

needs to be understood, BUT you must try and understand the picture

more completely instead of taking bits and pieces. The first thing

you may notice when falling ill with cfs/fibromyalgia is your urine

CHANGES. Your pissing INFLAMMATION URINE, which is different to

normal urine. You also notice a change at the other end - your stools

are loose or even constipated, the formation is never the same.

cheers tony

>

> Hi, all.

>

> I know that some folks here would prefer that I not post things

about

> the methylation cycle block treatment on this list, but please

> forgive me for this one. I think it's a biggie, and I think

> everybody here should hear about it.

>

> A woman on the ImmuneSuppport CFS discussion board who is on the

> simplified treatment approach for lifting the methylation cycle

block

> just reported that she was able to stop

> her use of desmopressin (which she had been using since last

> September to control her heavy urine volume), and her urine volume

> did not jump back up, as it formerly did when she stopped the

> desmopressin. I think this agrees with Hall's report some time

> ago that restoring his glutathione level corrected his diabetes

> insipidus, too. Here is the response I wrote to this woman. I took

> her name off to protect her privacy, but she posted to a public

> discussion board, and you can read her post there.

>

> Rich

>

>

> Hi, _______.

>

> This is wonderful! It's wonderful both for you and for me and for

the

> whole CFS community, because it provides more observational support

> for the GD-MCB hypothesis.

>

> As you probably know (but I want to make sure other readers are

aware

> of it, too), part of this hypothesis says that the low production of

> antidiuretic hormone (also called arginine vasopressin) in CFS

> results from low glutathione in the hypothalamus. This results in a

> (usually mild) case of diabetes insipidus, not to be confused with

> diabetes mellitus, which involves high blood sugar and low insulin.

>

> " Diabetes " means you have a lot of urine. " Mellitus " means your

urine

> tastes sweet, because it has elevated blood sugar or glucose in

> it. " Insipidus " means that your urine tastes insipid, i.e. it isn't

> sweet. Not many people like to diagnose these by tasting the urine

> these days, but it's much quicker than doing the lab tests! (:-)).

>

> Diabetes insipidus produces high urine volume and low total blood

> volume, as well as constant thirst. This is the phenomenon in CFS

> that Dr. Teitelbaum refers to as " Pee like a racehorse, drink like a

> fish. "

>

> The simplified treatment approach, among other things, is designed

to

> allow glutathione levels to come up to normal. When this happens, we

> should expect that the diabetes insipidus will disappear, and you

> have verified that it did in your case.

>

> I should make a small correction to what you wrote, in that while

> this does involve the hypothalamus, it doesn't actually say that the

> HPA (hypothalamus-pituitary-adrenal) axis has been restored to

normal

> operation. I expect that that will occur as well, but the

> disappearance of the diabetes insipidus does not prove that.

Evidence

> for improvement in the HPA axis would include things like blood

> pressure coming up to normal, decrease in symptoms of hypoglycemia,

> cortisol and DHEA levels restored to normal, disappearance of

> orthostatic problems such as problems with blood pressure or heart

> rate when standing, better ability to cope with stress of all sorts,

> and other cortisol-related things. If you are observing those things

> as well, then I would agree that your HPA axis is doing better, too.

> I fully expect that to happen for you, too, if it hasn't already,

> because the same basic mechanism in the biochemistry that restored

> ADH should also restore ACTH, which I think will bring the HPA axis

> back to normal operation.

>

> At the biochemical level, I think this observation also supports my

> more fundamental suggestion that secretory proteins that contain

> cysteine double bonds are not being made well in CFS because of

> glutathione depletion in the cells in which they are made. If this

is

> true, it also provides support for my hypotheses to explain low

> levels of some of the other secretory proteins in CFS, including

> human growth hormone, ACTH, oxytocin, perforin, and probably some

> others as well. So this is big, from my point of view!

>

> Thank you so much for posting this, and keep on keeping on!

>

> Rich

>

[Guest guest]

Speaking for myself, I don't mind at all. This is discussion of an

experimental treatment and its results - I don't know what could be more

relevant.

On 7/4/07, rvankonynen <richvank@...> wrote:

>

> Hi, all.

>

> I know that some folks here would prefer that I not post things about

> the methylation cycle block treatment on this list, but please

> forgive me for this one. I think it's a biggie, and I think

> everybody here should hear about it.

>

> A woman on the ImmuneSuppport CFS discussion board who is on the

> simplified treatment approach for lifting the methylation cycle block

> just reported that she was able to stop

> her use of desmopressin (which she had been using since last

> September to control her heavy urine volume), and her urine volume

> did not jump back up, as it formerly did when she stopped the

> desmopressin.

[Guest guest]

However, this person has also added a lot of other remedies during the

same period, so it's unknown what actually helped her urination problem.

From her 5/22/07 message:

" I recently added DHEA, pregnenolone, estrogen cream, progesterone

cream, adrenal glandular and dexamethasone to help with hormones and

adrenal support. "

http://www.immunesupport.com/chat/forums/message.cfm?id=1092068 & B=FM#110\

4831

<http://www.immunesupport.com/chat/forums/message.cfm?id=1092068 & B=FM#11\

04831>

> >

> > Hi, all.

> >

> > I know that some folks here would prefer that I not post things

about

> > the methylation cycle block treatment on this list, but please

> > forgive me for this one. I think it's a biggie, and I think

> > everybody here should hear about it.

> >

> > A woman on the ImmuneSuppport CFS discussion board who is on the

> > simplified treatment approach for lifting the methylation cycle

block

> > just reported that she was able to stop

> > her use of desmopressin (which she had been using since last

> > September to control her heavy urine volume), and her urine volume

> > did not jump back up, as it formerly did when she stopped the

> > desmopressin.

>

>

>

[Guest guest]

Hi, Mark.

Those other things she added don't impact ADH production to eliminate

CFS related diabetes insipidus(low water retention/heavy urination),

low blood volume, low bp, POTS and likely better thyroid function she

got too like the methylation cycle block treatment he created is

showing can correct. In fact, what she added are downstream issues to

ADH production as far as I can tell and well may have been corrected

with methylation cycle block treatment anyway.

She may not have needed to add them given her measured improvement on

Rich's treatment and I think he is just using her case as one

illustration, the most recent example among several reports he's

received that this issue is clearly ameliorated by addressing

methylation cycle blocks. I should know, the same thing happened with me.

I think Rich just used her recent report of<mrl@...> wrote:

>

>

> However, this person has also added a lot of other remedies during the

> same period, so it's unknown what actually helped her urination problem.

> From her 5/22/07 message:

>

> " I recently added DHEA, pregnenolone, estrogen cream, progesterone

> cream, adrenal glandular and dexamethasone to help with hormones and

> adrenal support. "

>

>

http://www.immunesupport.com/chat/forums/message.cfm?id=1092068 & B=FM#110\

> 4831

>

<http://www.immunesupport.com/chat/forums/message.cfm?id=1092068 & B=FM#11\

> 04831>

>

>

> > >

> > > Hi, all.

> > >

> > > I know that some folks here would prefer that I not post things

> about

> > > the methylation cycle block treatment on this list, but please

> > > forgive me for this one. I think it's a biggie, and I think

> > > everybody here should hear about it.

> > >

> > > A woman on the ImmuneSuppport CFS discussion board who is on the

> > > simplified treatment approach for lifting the methylation cycle

> block

> > > just reported that she was able to stop

> > > her use of desmopressin (which she had been using since last

> > > September to control her heavy urine volume), and her urine volume

> > > did not jump back up, as it formerly did when she stopped the

> > > desmopressin.

> >

>

[Guest guest]

Exactly. See my posts on CFS-Yasko the last few days. I went onto

immunesupport and looked at the posts. Each person has a different

protocol. One took the simplified protocol, stopped, did Famvir which

helped, then resumed it. Another handles her viruses with virastop and

other enzymes. Another felt much worse after she stopped her b12 shots

and better when she started them again--having nothing to do with the

simplified protocol.

I really like Rich and he is sincere in his intentions but the posting

he made the other day was imo not useful. At least we should have an

" N " from which he's speaking (he can count the people he's actually in

contact with) how long they've each been doing it, and what percentage

have typical improvements. just to list them anonymously, without

knowing their distribution (improved sleep, improved urination etc)

gives us no information. And then to imply it's a potential cure, I

assume with the hope of getting folks' attention and having them try

it too, I'm not sure this is useful for us either.

In general the simplified protocol IS a good idea as the full Yasko

program is so expensive.

Sorry for discussing it here but I've made multiple postsi n this

regard on the other list.

> > >

> > > Hi, all.

> > >

> > > I know that some folks here would prefer that I not post things

> about

> > > the methylation cycle block treatment on this list, but please

> > > forgive me for this one. I think it's a biggie, and I think

> > > everybody here should hear about it.

> > >

> > > A woman on the ImmuneSuppport CFS discussion board who is on the

> > > simplified treatment approach for lifting the methylation cycle

> block

> > > just reported that she was able to stop

> > > her use of desmopressin (which she had been using since last

> > > September to control her heavy urine volume), and her urine volume

> > > did not jump back up, as it formerly did when she stopped the

> > > desmopressin.

> >

> >

> >

[Guest guest]

Hi, Jill.

I don't think Mark is making as good a point as you think given the

downstream supplements to ADH production that improved with Rich's

treatment in this woman. Yours and Marks point is valid, but it is

not a new revelation as Rich has already addressed this issue straight

on.

Rich has on several occassions noted that the kind of pilot study this

methylation treat is won't be able to completely eliminate

augmentations PWCs have always done on informal experiments as well as

formal ones with lots of financial investment put like Ampligen, which

from personal experience I can tell you PWCs on it were augmenting

with other things quite a lot.

This is the way studies often happen for serious chronic illnesses yet

they still get published. Nevertheless and despite this lack of

purity we ideally prefer, it's still possible to discern and

accurately attribute benefits people are receiving from the treatment

being studied.

<jenbooks13@...> wrote:

>

> Exactly. See my posts on CFS-Yasko the last few days. I went onto

> immunesupport and looked at the posts. Each person has a different

> protocol. One took the simplified protocol, stopped, did Famvir which

> helped, then resumed it. Another handles her viruses with virastop and

> other enzymes. Another felt much worse after she stopped her b12 shots

> and better when she started them again--having nothing to do with the

> simplified protocol.

[Guest guest]

Hi, Tony.

I'm glad to hear that you don't have a problem with the methylation

block hypothesis.

I'm not sure why genetic susceptibility bothers you. The human

genome codes for about 25,000 to 30,000 genes. In the total genome,

there are estimated to be about 10 million different genetic

variations (polymorphisms or SNPs) in the entire human population.

We all have a unique set of SNPs. That's what makes you so good

looking and me so homely!(:-) It shouldn't be such a stretch of the

imagination that some of us inherit a set of SNPs that could make us

more vulnerable to a toxin or to a pathogen, and there is plenty of

research evidence coming in every day now that supports this notion,

not only in CFS, but in a growing number of other diseases and

conditions. This has become a very active field of research with the

completion of the Human Genome Project and the development of less

expensive technology for characterizing SNPs, such as the Affymetrix

gene chips.

In CFS itself, there are already several SNPs that have been found to

be present in PWCs at significantly higher rates than in people who

don't have CFS. I reviewed the data on this that was available in

January in my IACFS poster paper. There is also evidence from twin

studies and from family tree studies that show that there is a

genetic component to developing CFS. I hope you understand that this

is not totally determinate. It is only a predisposition. In order

to develop CFS, other things have to happen. If they don't happen to

a person, he or she can go through their entire life and not develop

CFS.

I've been writing here primarily about the socalled sporadic cases of

CFS, which seem to be most of what we are seeing nowadays. As you

know, there have also been epidemic clusters, such as the one in the

area around Incline Village, Nevada, in the 1980s. In these

clusters, since such a large fraction of the people in certain

locations developed CFS, it seems clear that genetics did not play as

big a role as in the sporadic cases. In the clusters, it seems most

likely that a very virulent pathogen was involved, so that people

with a range of genetic makeups were all vulnerable.

I hope this clarifies my views on genetics in CFS somewhat, and I

hope we can continue to find common ground in our understanding of

this disorder.

Best regards,

Rich

> >

> > Hi, all.

> >

> > I know that some folks here would prefer that I not post things

> about

> > the methylation cycle block treatment on this list, but please

> > forgive me for this one. I think it's a biggie, and I think

> > everybody here should hear about it.

> >

> > A woman on the ImmuneSuppport CFS discussion board who is on the

> > simplified treatment approach for lifting the methylation cycle

> block

> > just reported that she was able to stop

> > her use of desmopressin (which she had been using since last

> > September to control her heavy urine volume), and her urine volume

> > did not jump back up, as it formerly did when she stopped the

> > desmopressin. I think this agrees with Hall's report some

time

> > ago that restoring his glutathione level corrected his diabetes

> > insipidus, too. Here is the response I wrote to this woman. I took

> > her name off to protect her privacy, but she posted to a public

> > discussion board, and you can read her post there.

> >

> > Rich

> >

> >

> > Hi, _______.

> >

> > This is wonderful! It's wonderful both for you and for me and for

> the

> > whole CFS community, because it provides more observational

support

> > for the GD-MCB hypothesis.

> >

> > As you probably know (but I want to make sure other readers are

> aware

> > of it, too), part of this hypothesis says that the low production

of

> > antidiuretic hormone (also called arginine vasopressin) in CFS

> > results from low glutathione in the hypothalamus. This results in

a

> > (usually mild) case of diabetes insipidus, not to be confused with

> > diabetes mellitus, which involves high blood sugar and low

insulin.

> >

> > " Diabetes " means you have a lot of urine. " Mellitus " means your

> urine

> > tastes sweet, because it has elevated blood sugar or glucose in

> > it. " Insipidus " means that your urine tastes insipid, i.e. it

isn't

> > sweet. Not many people like to diagnose these by tasting the urine

> > these days, but it's much quicker than doing the lab tests! (:-)).

> >

> > Diabetes insipidus produces high urine volume and low total blood

> > volume, as well as constant thirst. This is the phenomenon in CFS

> > that Dr. Teitelbaum refers to as " Pee like a racehorse, drink

like a

> > fish. "

> >

> > The simplified treatment approach, among other things, is

designed

> to

> > allow glutathione levels to come up to normal. When this happens,

we

> > should expect that the diabetes insipidus will disappear, and you

> > have verified that it did in your case.

> >

> > I should make a small correction to what you wrote, in that while

> > this does involve the hypothalamus, it doesn't actually say that

the

> > HPA (hypothalamus-pituitary-adrenal) axis has been restored to

> normal

> > operation. I expect that that will occur as well, but the

> > disappearance of the diabetes insipidus does not prove that.

> Evidence

> > for improvement in the HPA axis would include things like blood

> > pressure coming up to normal, decrease in symptoms of

hypoglycemia,

> > cortisol and DHEA levels restored to normal, disappearance of

> > orthostatic problems such as problems with blood pressure or heart

> > rate when standing, better ability to cope with stress of all

sorts,

> > and other cortisol-related things. If you are observing those

things

> > as well, then I would agree that your HPA axis is doing better,

too.

> > I fully expect that to happen for you, too, if it hasn't already,

> > because the same basic mechanism in the biochemistry that restored

> > ADH should also restore ACTH, which I think will bring the HPA

axis

> > back to normal operation.

> >

> > At the biochemical level, I think this observation also supports

my

> > more fundamental suggestion that secretory proteins that contain

> > cysteine double bonds are not being made well in CFS because of

> > glutathione depletion in the cells in which they are made. If

this

> is

> > true, it also provides support for my hypotheses to explain low

> > levels of some of the other secretory proteins in CFS, including

> > human growth hormone, ACTH, oxytocin, perforin, and probably some

> > others as well. So this is big, from my point of view!

> >

> > Thank you so much for posting this, and keep on keeping on!

> >

> > Rich

> >

>

[Guest guest]

> Those other things she added don't impact ADH production to eliminate

> CFS related diabetes insipidus(low water retention/heavy urination),

> low blood volume, low bp, POTS and likely better thyroid function she

> got too like the methylation cycle block treatment he created is

> showing can correct. In fact, what she added are downstream issues to

> ADH production as far as I can tell and well may have been corrected

> with methylation cycle block treatment anyway.

First, we don't know what 's actual problem is, because her doctor

didn't diagnose that she actually had diabetes insipidus. Excess

urination, or polyuria, can have many causes:

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

<http://en.wikipedia.org/wiki/Polyuria>

Secondly, if you read 's messages over the last 6 months, you will

see that she was constantly changing her supplements and remedies that

she was taking, so that even by anecdotal standards, she has had too

many variables to make any conclusions of what caused what. For

example, she had cut out a lot of her older supplements and herbs. It's

possible that perhaps one or more of those supplements were actually

contributing to her problem, possibly acting as diuretics, or containg

the anti-caking material that the above web page mentions.

IMHO, if you want to make an anecdotal claim of the usefulness of a

protocol, you need to avoid changing any variables while you are testing

the protocol, before pronouncing that it is useful.

- Mark

[Guest guest]

Hi --I noted your post that you also lost your diabetes

insipidus. I found that useful.

You've seen my criticisms of Rich--I would much prefer the effort to

collate everybody's experience. I'd like to view it myself. It can be

anonymous or not, ie male 28, CFIDS 11 years, major symptoms before

protocol x y and z, previous protocols tried that helped, previous

protocols tried that failed, improvements on methylation protocol, is

that person only on the simplified protocol or other things as well. I

know it takes a bit of time but then I could find out myself what the

patterns were.

> >

> > Exactly. See my posts on CFS-Yasko the last few days. I went onto

> > immunesupport and looked at the posts. Each person has a different

> > protocol. One took the simplified protocol, stopped, did Famvir which

> > helped, then resumed it. Another handles her viruses with virastop and

> > other enzymes. Another felt much worse after she stopped her b12 shots

> > and better when she started them again--having nothing to do with the

> > simplified protocol.

>

[Guest guest]

Hi, Mark.

<mrl@...> wrote:

>

>

> <david-hall@> wrote:

> > Those other things she added don't impact ADH production to eliminate

> > CFS related diabetes insipidus(low water retention/heavy urination),

> > low blood volume, low bp, POTS and likely better thyroid function she

> > got too like the methylation cycle block treatment he created is

> > showing can correct. In fact, what she added are downstream issues to

> > ADH production as far as I can tell and well may have been corrected

> > with methylation cycle block treatment anyway.

>

First, we don't know what 's actual problem is, because her

doctor didn't diagnose that she actually had diabetes insipidus.

Excess urination, or polyuria, can have many causes:

>

> http://en.wikipedia.org/wiki/Polyuria

> <http://en.wikipedia.org/wiki/Polyuria>

***Well, we most docs don't check for diabetes insipidus, they'd find

a lot of it in PWCs if they did, and we do have a very good indication

this is what she had given her CFS diagnosis and the symptoms that

abated. It's very unlikely she got it from these other causes, which

are rare.

>

> Secondly, if you read 's messages over the last 6 months, you will

> see that she was constantly changing her supplements and remedies that

> she was taking,

***This is typical PWC behavior, you'd find a lot of it among many

PWCs if you check or ask them about it in depth. It doesn't discount

Rich's observation and this behavior even takes place in quite formal

studies like it did in ampligen where accurate assessments of efficacy

or lack of it were still discernible.

so that even by anecdotal standards, she has had too

> many variables to make any conclusions of what caused what.

***This is your assumption and your not taking her comments into

consideration with the all important context of Rich's other cases of

diabetes insipidus clearing up on methylation cycle block treatment

and how these all fit his hypothesis for CFS pathogensis. Explain how

this all happened and how they fit so well if you're not buying this

particular part of his hypothesis?

could For

> example, she had cut out a lot of her older supplements and herbs. It's

> possible that perhaps one or more of those supplements were actually

> contributing to her problem, possibly acting as diuretics, or containg

> the anti-caking material that the above web page mentions.

***This is reaching, she doesn't mention any diuretic or diuretic

potentialed supplements and you'd have to explain to me better how

filler material in such supplements would affect ADH production, the

primary mechanism that would need to be knocked down to produce DI.

Some PWCs seem to clearly have sensitivities to fillers, but that's a

different subject.

>

> IMHO, if you want to make an anecdotal claim of the usefulness of a

> protocol, you need to avoid changing any variables while you are

testing the protocol, before pronouncing that it is useful.

***You're talking about an ideal that is preferrable, but does not

ordinarily happen in the real world even when measures have been taken

to do so, particularly with people and even more particularly with

people doing internet experimental protocols. Nevertheless, PWCs

quite often accurately deduce what is doing what in their bodies and

are able to judge effects despite the fact they are doing an internet

experiment with all the variables, both known and unknown, that may be

there.

***We wouldn't all be on these lists if we hadn't experienced that in

fact through these conversations and despite mistakes happening

accurate observations and practical assessments of efficacy can be made.

>

> - Mark

>

>

***

>

[Guest guest]

Hi, Jill.

<jenbooks13@...> wrote:

>

> Hi --I noted your post that you also lost your diabetes

> insipidus. I found that useful.

***Yes, it's one of two parts of his hypothesis for CFS pathogenisis,

the other part being his theory that glutathione enhancement can

reverse CFS related hypothyroidism, that I happen to know are fact.

I'm still waiting for the major brain pain and inflammation to clear

in my case, but so far treatment consistent with his theory are

producing these other clear and tangible results and make it worth

continuing to persue.

>

> You've seen my criticisms of Rich--I would much prefer the effort to

> collate everybody's experience. I'd like to view it myself. It can be

> anonymous or not, ie male 28, CFIDS 11 years, major symptoms before

> protocol x y and z, previous protocols tried that helped, previous

> protocols tried that failed, improvements on methylation protocol, is

> that person only on the simplified protocol or other things as well. I

> know it takes a bit of time but then I could find out myself what the

> patterns were.

>

***I understand. We all want as much certainty about this treatment

path as possible. I just don't know if he'll go for what your asking

given what he's stated to you already, your request seems to fly in

the face of his sensibilities for the purpose of this pilot study

treatment and it would take a level of effort and time to implement

that he presently isn't willing or able to give.

***

[Guest guest]

Meant to say the associated section on diabetes insipidus(DI) with

that links other causes for it are rare. Also, urinary urge frequency

can be part of heavy urination over the course of a day, but it is the

heavy urination itself being discussed when talking DI.

> > <david-hall@> wrote:

most docs don't check for diabetes insipidus, they'd find

> a lot of it in PWCs if they did, and we do have a very good indication

> this is what she had given her CFS diagnosis and the symptoms that

> abated. It's very unlikely she got it from these other causes, which

> are rare.

>

[Guest guest]

Rich

Your talking to someone that got ill by visiting a community pool.

Your also avoiding the way in which the majority of people with

these conditions get ill. I also believe that genetic

susceptability, is scienctists playing with there DICKS- next time

you visit a supermarket have a look around at how about 50 plus

percent of the population don't look so healthy and look like they

are capable of joining any one of the many autoimmune groups if they

just get hit with one more insult to there body..

So NO I can't sit here and like that part of your science.You avoided

UNDERSTANDING that we have got problems with our urine, it's no

longer the same when your suffering long term inflammation. You also

must understand your stools are also no longer what they where and

I'm sure genetics ain't in the picture when you have bad poop.When

you have bad poop your also likeley to have encephalitis because

expelling it thru having a hose stiuck up your arse is the norm in

liver disease.

> > >

> > > Hi, all.

> > >

> > > I know that some folks here would prefer that I not post things

> > about

> > > the methylation cycle block treatment on this list, but please

> > > forgive me for this one. I think it's a biggie, and I think

> > > everybody here should hear about it.

> > >

> > > A woman on the ImmuneSuppport CFS discussion board who is on the

> > > simplified treatment approach for lifting the methylation cycle

> > block

> > > just reported that she was able to stop

> > > her use of desmopressin (which she had been using since last

> > > September to control her heavy urine volume), and her urine

volume

> > > did not jump back up, as it formerly did when she stopped the

> > > desmopressin. I think this agrees with Hall's report some

> time

> > > ago that restoring his glutathione level corrected his diabetes

> > > insipidus, too. Here is the response I wrote to this woman. I

took

> > > her name off to protect her privacy, but she posted to a public

> > > discussion board, and you can read her post there.

> > >

> > > Rich

> > >

> > >

> > > Hi, _______.

> > >

> > > This is wonderful! It's wonderful both for you and for me and

for

> > the

> > > whole CFS community, because it provides more observational

> support

> > > for the GD-MCB hypothesis.

> > >

> > > As you probably know (but I want to make sure other readers are

> > aware

> > > of it, too), part of this hypothesis says that the low

production

> of

> > > antidiuretic hormone (also called arginine vasopressin) in CFS

> > > results from low glutathione in the hypothalamus. This results

in

> a

> > > (usually mild) case of diabetes insipidus, not to be confused

with

> > > diabetes mellitus, which involves high blood sugar and low

> insulin.

> > >

> > > " Diabetes " means you have a lot of urine. " Mellitus " means your

> > urine

> > > tastes sweet, because it has elevated blood sugar or glucose in

> > > it. " Insipidus " means that your urine tastes insipid, i.e. it

> isn't

> > > sweet. Not many people like to diagnose these by tasting the

urine

> > > these days, but it's much quicker than doing the lab tests! (:-

)).

> > >

> > > Diabetes insipidus produces high urine volume and low total

blood

> > > volume, as well as constant thirst. This is the phenomenon in

CFS

> > > that Dr. Teitelbaum refers to as " Pee like a racehorse, drink

> like a

> > > fish. "

> > >

> > > The simplified treatment approach, among other things, is

> designed

> > to

> > > allow glutathione levels to come up to normal. When this

happens,

> we

> > > should expect that the diabetes insipidus will disappear, and

you

> > > have verified that it did in your case.

> > >

> > > I should make a small correction to what you wrote, in that

while

> > > this does involve the hypothalamus, it doesn't actually say

that

> the

> > > HPA (hypothalamus-pituitary-adrenal) axis has been restored to

> > normal

> > > operation. I expect that that will occur as well, but the

> > > disappearance of the diabetes insipidus does not prove that.

> > Evidence

> > > for improvement in the HPA axis would include things like blood

> > > pressure coming up to normal, decrease in symptoms of

> hypoglycemia,

> > > cortisol and DHEA levels restored to normal, disappearance of

> > > orthostatic problems such as problems with blood pressure or

heart

> > > rate when standing, better ability to cope with stress of all

> sorts,

> > > and other cortisol-related things. If you are observing those

> things

> > > as well, then I would agree that your HPA axis is doing better,

> too.

> > > I fully expect that to happen for you, too, if it hasn't

already,

> > > because the same basic mechanism in the biochemistry that

restored

> > > ADH should also restore ACTH, which I think will bring the HPA

> axis

> > > back to normal operation.

> > >

> > > At the biochemical level, I think this observation also

supports

> my

> > > more fundamental suggestion that secretory proteins that contain

> > > cysteine double bonds are not being made well in CFS because of

> > > glutathione depletion in the cells in which they are made. If

> this

> > is

> > > true, it also provides support for my hypotheses to explain low

> > > levels of some of the other secretory proteins in CFS, including

> > > human growth hormone, ACTH, oxytocin, perforin, and probably

some

> > > others as well. So this is big, from my point of view!

> > >

> > > Thank you so much for posting this, and keep on keeping on!

> > >

> > > Rich

> > >

> >

>

[Guest guest]

> Your talking to someone that got ill by visiting a community pool.

Evidence = ?

[Guest guest]

Rich

The last post was written before I read all your post. Too much

science is VERY DANGEROUS in many ilnesses. Many people go out to

prove something and often they get there fraudulently, so your

enthusiasm for genetic markers and the like doesn't do anything for

me because it just gives you this false sense of you can't get back

to what you were the last week, before you fell over ill.

tony

> > >

> > > Hi, all.

> > >

> > > I know that some folks here would prefer that I not post things

> > about

> > > the methylation cycle block treatment on this list, but please

> > > forgive me for this one. I think it's a biggie, and I think

> > > everybody here should hear about it.

> > >

> > > A woman on the ImmuneSuppport CFS discussion board who is on the

> > > simplified treatment approach for lifting the methylation cycle

> > block

> > > just reported that she was able to stop

> > > her use of desmopressin (which she had been using since last

> > > September to control her heavy urine volume), and her urine

volume

> > > did not jump back up, as it formerly did when she stopped the

> > > desmopressin. I think this agrees with Hall's report some

> time

> > > ago that restoring his glutathione level corrected his diabetes

> > > insipidus, too. Here is the response I wrote to this woman. I

took

> > > her name off to protect her privacy, but she posted to a public

> > > discussion board, and you can read her post there.

> > >

> > > Rich

> > >

> > >

> > > Hi, _______.

> > >

> > > This is wonderful! It's wonderful both for you and for me and

for

> > the

> > > whole CFS community, because it provides more observational

> support

> > > for the GD-MCB hypothesis.

> > >

> > > As you probably know (but I want to make sure other readers are

> > aware

> > > of it, too), part of this hypothesis says that the low

production

> of

> > > antidiuretic hormone (also called arginine vasopressin) in CFS

> > > results from low glutathione in the hypothalamus. This results

in

> a

> > > (usually mild) case of diabetes insipidus, not to be confused

with

> > > diabetes mellitus, which involves high blood sugar and low

> insulin.

> > >

> > > " Diabetes " means you have a lot of urine. " Mellitus " means your

> > urine

> > > tastes sweet, because it has elevated blood sugar or glucose in

> > > it. " Insipidus " means that your urine tastes insipid, i.e. it

> isn't

> > > sweet. Not many people like to diagnose these by tasting the

urine

> > > these days, but it's much quicker than doing the lab tests! (:-

)).

> > >

> > > Diabetes insipidus produces high urine volume and low total

blood

> > > volume, as well as constant thirst. This is the phenomenon in

CFS

> > > that Dr. Teitelbaum refers to as " Pee like a racehorse, drink

> like a

> > > fish. "

> > >

> > > The simplified treatment approach, among other things, is

> designed

> > to

> > > allow glutathione levels to come up to normal. When this

happens,

> we

> > > should expect that the diabetes insipidus will disappear, and

you

> > > have verified that it did in your case.

> > >

> > > I should make a small correction to what you wrote, in that

while

> > > this does involve the hypothalamus, it doesn't actually say

that

> the

> > > HPA (hypothalamus-pituitary-adrenal) axis has been restored to

> > normal

> > > operation. I expect that that will occur as well, but the

> > > disappearance of the diabetes insipidus does not prove that.

> > Evidence

> > > for improvement in the HPA axis would include things like blood

> > > pressure coming up to normal, decrease in symptoms of

> hypoglycemia,

> > > cortisol and DHEA levels restored to normal, disappearance of

> > > orthostatic problems such as problems with blood pressure or

heart

> > > rate when standing, better ability to cope with stress of all

> sorts,

> > > and other cortisol-related things. If you are observing those

> things

> > > as well, then I would agree that your HPA axis is doing better,

> too.

> > > I fully expect that to happen for you, too, if it hasn't

already,

> > > because the same basic mechanism in the biochemistry that

restored

> > > ADH should also restore ACTH, which I think will bring the HPA

> axis

> > > back to normal operation.

> > >

> > > At the biochemical level, I think this observation also

supports

> my

> > > more fundamental suggestion that secretory proteins that contain

> > > cysteine double bonds are not being made well in CFS because of

> > > glutathione depletion in the cells in which they are made. If

> this

> > is

> > > true, it also provides support for my hypotheses to explain low

> > > levels of some of the other secretory proteins in CFS, including

> > > human growth hormone, ACTH, oxytocin, perforin, and probably

some

> > > others as well. So this is big, from my point of view!

> > >

> > > Thank you so much for posting this, and keep on keeping on!

> > >

> > > Rich

> > >

> >

>

[Guest guest]

" " " Until the human genetics/immune system people start looking at

both sides of this serious issue, and not only at the human side, I

will continue to find the rationale for strengthening the immune

system inadequate and only partially viable. " " " "

Penny anyone dealiung with infectious disease will tell you a healthy

immune system is often what get's hijacked to make one ill. The

scientists at CDC in atlanta, following and understanding many years

of disease- will all tell you this..

tony

> > >

> > > Hi, all.

> > >

> > > I know that some folks here would prefer that I not post things

> > about

> > > the methylation cycle block treatment on this list, but please

> > > forgive me for this one. I think it's a biggie, and I think

> > > everybody here should hear about it.

> > >

> > > A woman on the ImmuneSuppport CFS discussion board who is on the

> > > simplified treatment approach for lifting the methylation cycle

> > block

> > > just reported that she was able to stop

> > > her use of desmopressin (which she had been using since last

> > > September to control her heavy urine volume), and her urine

volume

> > > did not jump back up, as it formerly did when she stopped the

> > > desmopressin. I think this agrees with Hall's report some

> time

> > > ago that restoring his glutathione level corrected his diabetes

> > > insipidus, too. Here is the response I wrote to this woman. I

took

> > > her name off to protect her privacy, but she posted to a public

> > > discussion board, and you can read her post there.

> > >

> > > Rich

> > >

> > >

> > > Hi, _______.

> > >

> > > This is wonderful! It's wonderful both for you and for me and

for

> > the

> > > whole CFS community, because it provides more observational

> support

> > > for the GD-MCB hypothesis.

> > >

> > > As you probably know (but I want to make sure other readers are

> > aware

> > > of it, too), part of this hypothesis says that the low

production

> of

> > > antidiuretic hormone (also called arginine vasopressin) in CFS

> > > results from low glutathione in the hypothalamus. This results

in

> a

> > > (usually mild) case of diabetes insipidus, not to be confused

with

> > > diabetes mellitus, which involves high blood sugar and low

> insulin.

> > >

> > > " Diabetes " means you have a lot of urine. " Mellitus " means your

> > urine

> > > tastes sweet, because it has elevated blood sugar or glucose in

> > > it. " Insipidus " means that your urine tastes insipid, i.e. it

> isn't

> > > sweet. Not many people like to diagnose these by tasting the

urine

> > > these days, but it's much quicker than doing the lab tests! (:-

)).

> > >

> > > Diabetes insipidus produces high urine volume and low total

blood

> > > volume, as well as constant thirst. This is the phenomenon in

CFS

> > > that Dr. Teitelbaum refers to as " Pee like a racehorse, drink

> like a

> > > fish. "

> > >

> > > The simplified treatment approach, among other things, is

> designed

> > to

> > > allow glutathione levels to come up to normal. When this

happens,

> we

> > > should expect that the diabetes insipidus will disappear, and

you

> > > have verified that it did in your case.

> > >

> > > I should make a small correction to what you wrote, in that

while

> > > this does involve the hypothalamus, it doesn't actually say

that

> the

> > > HPA (hypothalamus-pituitary-adrenal) axis has been restored to

> > normal

> > > operation. I expect that that will occur as well, but the

> > > disappearance of the diabetes insipidus does not prove that.

> > Evidence

> > > for improvement in the HPA axis would include things like blood

> > > pressure coming up to normal, decrease in symptoms of

> hypoglycemia,

> > > cortisol and DHEA levels restored to normal, disappearance of

> > > orthostatic problems such as problems with blood pressure or

heart

> > > rate when standing, better ability to cope with stress of all

> sorts,

> > > and other cortisol-related things. If you are observing those

> things

> > > as well, then I would agree that your HPA axis is doing better,

> too.

> > > I fully expect that to happen for you, too, if it hasn't

already,

> > > because the same basic mechanism in the biochemistry that

restored

> > > ADH should also restore ACTH, which I think will bring the HPA

> axis

> > > back to normal operation.

> > >

> > > At the biochemical level, I think this observation also

supports

> my

> > > more fundamental suggestion that secretory proteins that contain

> > > cysteine double bonds are not being made well in CFS because of

> > > glutathione depletion in the cells in which they are made. If

> this

> > is

> > > true, it also provides support for my hypotheses to explain low

> > > levels of some of the other secretory proteins in CFS, including

> > > human growth hormone, ACTH, oxytocin, perforin, and probably

some

> > > others as well. So this is big, from my point of view!

> > >

> > > Thank you so much for posting this, and keep on keeping on!

> > >

> > > Rich

> > >

> >

>

[Guest guest]

> ***Well, we most docs don't check for diabetes insipidus, they'd

find

> a lot of it in PWCs if they did, and we do have a very good

indication

> this is what she had given her CFS diagnosis and the symptoms that

> abated. It's very unlikely she got it from these other causes,

which

> are rare.

But she is also taking dilantin (phenytoin) for seizures, and

apparently phenytoin is capable of suppressing ADH (vasopressin). It

has been used to suppress excess ADH production:

http://www.nature.com/jp/journal/v22/n3/abs/7210657a.html

<http://www.nature.com/jp/journal/v22/n3/abs/7210657a.html>

And here's a case report of phenytoin induced diabetes insipidus:

http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve & db=PubMed & list_uid\

s=10778541 & dopt=Citation

<http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve & db=PubMed & list_ui\

ds=10778541 & dopt=Citation>

Perhaps taking dilantin made her susceptible to diabetes insipidus,

and it became a full blown problem when it was combined with other

factors, such as diet, supplements, or herbs that she was taking at

the time. Or perhaps emotional stress can also be a factor. See

this study:

" Suppressive vasopressin response to emotional stress "

http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve & db=PubMed & list_uid\

s=1337126 & dopt=Citation

<http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve & db=PubMed & list_ui\

ds=1337126 & dopt=Citation>

Not only that, but phenytoin is also capable of reducing cortisol

levels, decreasing glutathione levels, and decreasing folic acid

levels , leading to increased homocysteine. See here for a list of

possible negative effects:

http://dermatology.cdlib.org/93/reviews/dilantin/scheinfeld.html

<http://dermatology.cdlib.org/93/reviews/dilantin/scheinfeld.html>

While dilantin is probably not the root cause of her problems, it

could be significantly contributing to it, so that her condition is

possibly unique, and her response to any treatment might be totally

different compared to other people. - Mark

[Guest guest]

Taking the methylation supps of Folinic acid, Folapro,

IntrinsiB12/Folate all increased my thirst, as well as disrupted my

sleep. I would go to bed and not be able to fall asleep, as well as

wake up earlier in the day and not be able to fall back asleep, which

totally wrecks my sleep deprived body.

On the plus side, my mental clarity did improve, as well as my

activity levels. But combined with the thirst and disrupted sleep,

I'm just compromising and taking the supps when I feel my head start

to get cloudy, around once every week or two. Also an intense rage

that makes me feel like I'm the fucking Hulk or a Transformer or

something. Like 'roid rage or some such.

So I do congratulate and thank Rich on his find, as well as the

effort it took in order to get here, but as for a cure, it doesn't

seem to be one for me.

I'm not doing the whole protocol either. No multivite or serine. Just

the Folapro and IntrinsiB12/Folate, although I have since switched to

folinic acid and homocysteine calm, since I can find them without

mag. stearate/stearic acid.

> > ***Well, we most docs don't check for diabetes insipidus, they'd

> find

> > a lot of it in PWCs if they did, and we do have a very good

> indication

> > this is what she had given her CFS diagnosis and the symptoms that

> > abated. It's very unlikely she got it from these other causes,

> which

> > are rare.

>

> But she is also taking dilantin (phenytoin) for seizures, and

> apparently phenytoin is capable of suppressing ADH (vasopressin).

It

> has been used to suppress excess ADH production:

>

> http://www.nature.com/jp/journal/v22/n3/abs/7210657a.html

> <http://www.nature.com/jp/journal/v22/n3/abs/7210657a.html>

>

> And here's a case report of phenytoin induced diabetes insipidus:

>

> http://www.ncbi.nlm.nih.gov/sites/entrez?

cmd=Retrieve & db=PubMed & list_uid\

> s=10778541 & dopt=Citation

> <http://www.ncbi.nlm.nih.gov/sites/entrez?

cmd=Retrieve & db=PubMed & list_ui\

> ds=10778541 & dopt=Citation>

>

> Perhaps taking dilantin made her susceptible to diabetes insipidus,

> and it became a full blown problem when it was combined with other

> factors, such as diet, supplements, or herbs that she was taking at

> the time. Or perhaps emotional stress can also be a factor. See

> this study:

>

> " Suppressive vasopressin response to emotional stress "

> http://www.ncbi.nlm.nih.gov/sites/entrez?

cmd=Retrieve & db=PubMed & list_uid\

> s=1337126 & dopt=Citation

> <http://www.ncbi.nlm.nih.gov/sites/entrez?

cmd=Retrieve & db=PubMed & list_ui\

> ds=1337126 & dopt=Citation>

>

> Not only that, but phenytoin is also capable of reducing cortisol

> levels, decreasing glutathione levels, and decreasing folic acid

> levels , leading to increased homocysteine. See here for a list of

> possible negative effects:

>

> http://dermatology.cdlib.org/93/reviews/dilantin/scheinfeld.html

> <http://dermatology.cdlib.org/93/reviews/dilantin/scheinfeld.html>

>

> While dilantin is probably not the root cause of her problems, it

> could be significantly contributing to it, so that her condition is

> possibly unique, and her response to any treatment might be totally

> different compared to other people. - Mark

>

>

>

>

>

>

[Guest guest]

Hi, J.

<mascis_j@...> wrote:

>

> Taking the methylation supps of Folinic acid, Folapro,

> IntrinsiB12/Folate all increased my thirst, as well as disrupted my

> sleep.

***That's interesting. It could be you're overmethylating on it, but

I'm not sure. I got severe thirst problems on SAMe in the past, so

left this option out. Sleep disruption probably is from glutamate

excitation which can become upregulated during detox, tough to avoid

completely though GABA, lower calcium diet and Yasko's step 1 stuff

can help calm it some.

I would go to bed and not be able to fall asleep, as well as

> wake up earlier in the day and not be able to fall back asleep, which

> totally wrecks my sleep deprived body.

>

> On the plus side, my mental clarity did improve, as well as my

> activity levels. But combined with the thirst and disrupted sleep,

> I'm just compromising and taking the supps when I feel my head start

> to get cloudy, around once every week or two. Also an intense rage

> that makes me feel like I'm the fucking Hulk or a Transformer or

> something. Like 'roid rage or some such.

***Yup, we're freakin' super heroes. Glutamate excitation again is

what I think is happening in you from detox. So, the treatment sounds

like it's doing what it's supposed to do, though your right amygdala

is momentarily more pissed and hissing and ready for war.

>

> So I do congratulate and thank Rich on his find, as well as the

> effort it took in order to get here, but as for a cure, it doesn't

> seem to be one for me.

***How long we're you willing to give it before drawing the conclusion

of its curative capability or not?

>

> I'm not doing the whole protocol either. No multivite or serine.

***There is something special to HHCs multi neuro health formula. It

could increase benefits for you, might be worth a shot.

Just

> the Folapro and IntrinsiB12/Folate, although I have since switched to

> folinic acid and homocysteine calm, since I can find them without

> mag. stearate/stearic acid.

***

[Guest guest]

Does anyone wonder if the fillers are bothering them?

Folapro has fillers.

So does SAME.

> >

> > Taking the methylation supps of Folinic acid, Folapro,

> > IntrinsiB12/Folate all increased my thirst, as well as disrupted my

> > sleep.

>

>

>

> ***That's interesting. It could be you're overmethylating on it, but

> I'm not sure. I got severe thirst problems on SAMe in the past, so

> left this option out. Sleep disruption probably is from glutamate

> excitation which can become upregulated during detox, tough to avoid

> completely though GABA, lower calcium diet and Yasko's step 1 stuff

> can help calm it some.

>

>

>

> I would go to bed and not be able to fall asleep, as well as

> > wake up earlier in the day and not be able to fall back asleep, which

> > totally wrecks my sleep deprived body.

> >

> > On the plus side, my mental clarity did improve, as well as my

> > activity levels. But combined with the thirst and disrupted sleep,

> > I'm just compromising and taking the supps when I feel my head start

> > to get cloudy, around once every week or two. Also an intense rage

> > that makes me feel like I'm the fucking Hulk or a Transformer or

> > something. Like 'roid rage or some such.

>

>

>

> ***Yup, we're freakin' super heroes. Glutamate excitation again is

> what I think is happening in you from detox. So, the treatment sounds

> like it's doing what it's supposed to do, though your right amygdala

> is momentarily more pissed and hissing and ready for war.

>

> >

> > So I do congratulate and thank Rich on his find, as well as the

> > effort it took in order to get here, but as for a cure, it doesn't

> > seem to be one for me.

>

>

>

> ***How long we're you willing to give it before drawing the conclusion

> of its curative capability or not?

>

> >

> > I'm not doing the whole protocol either. No multivite or serine.

>

>

>

> ***There is something special to HHCs multi neuro health formula. It

> could increase benefits for you, might be worth a shot.

>

>

> Just

> > the Folapro and IntrinsiB12/Folate, although I have since switched to

> > folinic acid and homocysteine calm, since I can find them without

> > mag. stearate/stearic acid.

>

>

> ***

>

[Guest guest]

Hi, Mark.

<mrl@...> wrote:

>

>

<david- hall@>

> > ***Well, most docs don't check for diabetes insipidus, they'd

> find

> > a lot of it in PWCs if they did, and we do have a very good

> indication

> > this is what she had given her CFS diagnosis and the symptoms that

> > abated. It's very unlikely she got it from these other causes,

> which

> > are rare.

>

> But she is also taking dilantin (phenytoin) for seizures, and

> apparently phenytoin is capable of suppressing ADH (vasopressin). It

> has been used to suppress excess ADH production:

>

> http://www.nature.com/jp/journal/v22/n3/abs/7210657a.html

> <http://www.nature.com/jp/journal/v22/n3/abs/7210657a.html>

***If she's still taking it and what you found here is true, it makes

Rich's inclusion of her reported elimination of DI more profound since

his treatment seems to be what did it anyway despite something in her

working in opposition. On the other hand, if she also stopped this

drug recently and then found her DI had gone, this would call into

question her example being used aside the others to illustrate his point.

>

> And here's a case report of phenytoin induced diabetes insipidus:

>

>

http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve & db=PubMed & list_uid\

> s=10778541 & dopt=Citation

>

<http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve & db=PubMed & list_ui\

> ds=10778541 & dopt=Citation>

>

> Perhaps taking dilantin made her susceptible to diabetes insipidus,

> and it became a full blown problem when it was combined with other

> factors, such as diet, supplements, or herbs that she was taking at

> the time. Or perhaps emotional stress can also be a factor. See

> this study:

>

> " Suppressive vasopressin response to emotional stress "

>

http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve & db=PubMed & list_uid\

> s=1337126 & dopt=Citation

>

<http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve & db=PubMed & list_ui\

> ds=1337126 & dopt=Citation>

***All possibilities, but given her CFS diagnosis and the fact that

her very likely DI symptoms abated after starting to use his treatment

and others with CFS have experienced the same, consistent with his

well supported hypothesis that predicts this could happen, I tend to

give this explanation more weight. It could be wrong, it certainly

isn't an ideal way to conduct a study, but I'm sensing Rich is drawing

the correct conclusion in her case nevertheless.

Not only that, but phenytoin is also capable of reducing cortisol

> levels, decreasing glutathione levels, and decreasing folic acid

> levels , leading to increased homocysteine. See here for a list of

> possible negative effects:

>

> http://dermatology.cdlib.org/93/reviews/dilantin/scheinfeld.html

> <http://dermatology.cdlib.org/93/reviews/dilantin/scheinfeld.html>

>

> While dilantin is probably not the root cause of her problems, it

> could be significantly contributing to it, so that her condition is

> possibly unique, and her response to any treatment might be totally

> different compared to other people.

***Yes, these issues are potentially true and you're being very

rigorous with every turn of the coin here. This is really fine with

me and I think it's smart, but it just so happens for this instance

and for the point about it with her there is greater rigor in counter

analysis, other real world examples with the same benefit and these

all fitting Rich's comprehensive hypothesis for CFS pathogensis(2007

IACFS poster) being key.

***

[Guest guest]

Bothering them how? Almost everything has fillers of one sort or the

other. I remember reading the labels on the Folapro and didn't notice

anything out of the ordinary. One thing that is not out of the

ordinary is the inclusion of magnesium stearate and/or stearic acid,

which I have noticed along with partially hydrogenated vegetable oils

give me severe brainfog and concurrant headache, so I refrain as much

as possible from taking supps that contain them and go out of my way

to find alternatives that don't have them.

> > >

> > > Taking the methylation supps of Folinic acid, Folapro,

> > > IntrinsiB12/Folate all increased my thirst, as well as

disrupted my

> > > sleep.

> >

> >

> >

> > ***That's interesting. It could be you're overmethylating on it,

but

> > I'm not sure. I got severe thirst problems on SAMe in the past,

so

> > left this option out. Sleep disruption probably is from glutamate

> > excitation which can become upregulated during detox, tough to

avoid

> > completely though GABA, lower calcium diet and Yasko's step 1

stuff

> > can help calm it some.

> >

> >

> >

> > I would go to bed and not be able to fall asleep, as well as

> > > wake up earlier in the day and not be able to fall back asleep,

which

> > > totally wrecks my sleep deprived body.

> > >

> > > On the plus side, my mental clarity did improve, as well as my

> > > activity levels. But combined with the thirst and disrupted

sleep,

> > > I'm just compromising and taking the supps when I feel my head

start

> > > to get cloudy, around once every week or two. Also an intense

rage

> > > that makes me feel like I'm the fucking Hulk or a Transformer

or

> > > something. Like 'roid rage or some such.

> >

> >

> >

> > ***Yup, we're freakin' super heroes. Glutamate excitation again

is

> > what I think is happening in you from detox. So, the treatment

sounds

> > like it's doing what it's supposed to do, though your right

amygdala

> > is momentarily more pissed and hissing and ready for war.

> >

> > >

> > > So I do congratulate and thank Rich on his find, as well as the

> > > effort it took in order to get here, but as for a cure, it

doesn't

> > > seem to be one for me.

> >

> >

> >

> > ***How long we're you willing to give it before drawing the

conclusion

> > of its curative capability or not?

> >

> > >

> > > I'm not doing the whole protocol either. No multivite or serine.

> >

> >

> >

> > ***There is something special to HHCs multi neuro health

formula. It

> > could increase benefits for you, might be worth a shot.

> >

> >

> > Just

> > > the Folapro and IntrinsiB12/Folate, although I have since

switched to

> > > folinic acid and homocysteine calm, since I can find them

without

> > > mag. stearate/stearic acid.

> >

> >

> > ***

> >

>

[Guest guest]

I take folapro, no problem. I've taken SAMe, which likely has the

similar fillers as folapro, but had a problem. So, fillers don't

seem to be much if any issue in me.

>

> Does anyone wonder if the fillers are bothering them?

> Folapro has fillers.

> So does SAME.

[Guest guest]

> <david- hall@>

> > > ***Well, most docs don't check for diabetes insipidus, they'd

> > find

> > > a lot of it in PWCs if they did, and we do have a very good

> > indication

> > > this is what she had given her CFS diagnosis and the symptoms

that

> > > abated. It's very unlikely she got it from these other causes,

> > which

> > > are rare.

> >

> > But she is also taking dilantin (phenytoin) for seizures, and

> > apparently phenytoin is capable of suppressing ADH

(vasopressin). It

> > has been used to suppress excess ADH production:

> >

> > http://www.nature.com/jp/journal/v22/n3/abs/7210657a.html

> > <http://www.nature.com/jp/journal/v22/n3/abs/7210657a.html>

>

>

> ***If she's still taking it and what you found here is true, it

makes

> Rich's inclusion of her reported elimination of DI more profound

since

> his treatment seems to be what did it anyway despite something in

her

> working in opposition. On the other hand, if she also stopped this

> drug recently and then found her DI had gone, this would call into

> question her example being used aside the others to illustrate his

point.

She is still on the drug. But as I said, you would also have to

examine every other change that's she made in the last few months.

For example, she recently added Dexamethasone, and Dexamethasone is

known to reduce serum levels of phenytoin, which in theory would then

reduce her diabetes insipidus symptoms:

http://www.smw.ch/dfe/set_archiv.asp?target=2002/29/smw-10085

Btw, it's not clear to me if she was actually diagnosed with CFS by a

CFS knowledgable person. For example, one common side effect from

phenytoin is fatigue, severe enough that I read of one person who was

prescribed provigil to offset the fatigue. It would be interesting

to find out has long she has been on that drug.

- Mark

[Guest guest]

Hi, Mark.

> > <mrl@> wrote:

> She is still on the drug. But as I said, you would also have to

> examine every other change that's she made in the last few months.

> For example, she recently added Dexamethasone, and Dexamethasone is

> known to reduce serum levels of phenytoin, which in theory would then

> reduce her diabetes insipidus symptoms:

>

> http://www.smw.ch/dfe/set_archiv.asp?target=2002/29/smw-10085

>

> Btw, it's not clear to me if she was actually diagnosed with CFS by a

> CFS knowledgable person. For example, one common side effect from

> phenytoin is fatigue, severe enough that I read of one person who was

> prescribed provigil to offset the fatigue. It would be interesting

> to find out has long she has been on that drug.

>

> - Mark

***I agree more in depth analysis would render better qualified

assessments and judgement calls on what's happening in her or any

case. As far as her CFS diagnosis goes and whether it is accurate for

her, that's a whole other can of worms.

***It seems to me there at about 30 distinct and established diagnosis

that could come under the CFS umbrella that even someone like Dr

Cheney could have trouble teasing apart despite the enormous amount of

time he gives each case in person(from my observation half the time

and half the tests he does are directed toward narrowing this field of

possibilities). Not everyone and perhaps only a few can get to a Dr

Cheney.

***But for the most part, FWIW, it seems to me most on these lists

have a fairly well qualified diagnosis, as it goes, and I seem to

identify with most of what they're experiencing and have some common

test results contrasted to what they report. Nevertheless, the CFS

diagnosis is a mess, the heterogenenous population(many subsets) makes

it radioactive, a repulsion to most main stream researchers.

***I think some researchers are good at getting at and studying what

seems to be the largest or one of the larger subsets of CFS, but the

CFS diagnosis itself continues to be a problem.

***