Methylation cycle block treatment stops heavy urination in CFS

[Guest guest]

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