Re: Re: Methylation cycle block treatment stops heavy urination in CFS

[Guest guest]

Rich, the problem is the genetics camp ignores the bugs and their innate adaptability. This is a much bigger problem than individual human susceptibilities. Before long everyone could be "genetically susceptible" because our genetics can't keep pace with the bug's genetics (ability to adapt). It's already happening with near epidemic proportions in children with ear infections and skin infections (staph). Meanwhile, almost no one's concerned with figuring out how to slow the bugs down and the pharmaceutical companies are giving up. In fact, all medicine is currently doing is contributing to the bugs increased resistance by using the wrong drugs based on ignorance of the organisms, and pumping our food supply full of antibiotics. 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 rvankonynen <richvank@...> wrote: 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]

Funny, but an infected cut in my foot that I got at a community pool also was the beginning of the end for me. The foot wouldn't heal and then I got the sinus infection from hell that lasted for about 3 months. From then on it was nothing but downhill. That's when the migraines started. The dental trouble, everything. I believe the pool and the combination of a bad dental experience pushed me over the edge into the CFS abyss. It got so bad that for a while I was afraid I had a terminal illness. That was 20 years ago. I yo-yo'd up and down but was never the same since. penny <usenethod@...> wrote: > Your talking to someone that got ill by visiting a community pool. Evidence = ?

[Guest guest]

I find it interesting that in an area of topical interest in Australia at the moment, Aboriginal health, one of the really significant markers for improved children's health outcomes was the introduction of chlorinated community swimming pools. The "bang for bucks" was increased by the introduction of a policy of "no school, no pool" . This markedly reduced school absenteeism by dropping truancy rates and reducing absences due to illness..

Go figure

Regards

R

Re: [infections] Re: Methylation cycle block treatment stops heavy urination in CFS

Funny, but an infected cut in my foot that I got at a community pool also was the beginning of the end for me. The foot wouldn't heal and then I got the sinus infection from hell that lasted for about 3 months. From then on it was nothing but downhill. That's when the migraines started. The dental trouble, everything. I believe the pool and the combination of a bad dental experience pushed me over the edge into the CFS abyss. It got so bad that for a while I was afraid I had a terminal illness. That was 20 years ago. I yo-yo'd up and down but was never the same since.

penny <usenethod > wrote:

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