Guest guest Posted July 6, 2007 Report Share Posted July 6, 2007 Penny Houle <pennyhoule@...> wrote: " It's already happening with near epidemic proportions in children with ear infections and skin infections (staph). " Hi Penny, I believe that's happening precisely due to the over–prescribing of antibiotics for the last 20-30 years. We have to ask ourselves: Why can't we seem to get over these bugs that nearly everyone has antibodies to, yet their infections resolve in a matter of weeks? Of course it's very complex, and there are many issues to confront, but I think the answers lie mainly in restoring our immune function so that it will work like most people's. To me, that's the only obvious difference. We all carry a variation of the same collection of critters...but we stay sick while others recover much faster. This methylation block issue may be a critical piece of the puzzle... ??? Best, Dan > > 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 > > > > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted July 6, 2007 Report Share Posted July 6, 2007 "I believe that's happening precisely due to the over–prescribing of antibiotics for the last 20-30 years." Over prescribing of the WRONG antibiotics, with no regard for using the correct ones or understanding of the bugs abilities. This approach seems a bit silly to me when we don't have a prayer of adapting our immune systems as quickly as the bugs do. It doesn't take 30 years for a bug to become resistant to the latest new pharmaceutical, more like 30 hours. Again, I'm not against strengthening the immune system, but you just illustrate my point. You accept what the docs tell you, that the problem lies strictly in patients using antibiotics unnecessarily, when in fact, the problem lies with docs who don't diagnose or prescribe properly. The only way that is going to change is when understanding of the bugs increases and docs are required to test and treat properly... not just throw the latest abx at you with no regard for whether your bugs may already be resistant to it making them stronger than ever, ready to decimate the next unfortunate victim who happens to get in the way. Why is there so much resistance to learning how to treat the bugs properly? And why are patients so complacent about this serious issue? Why isn't everybody demanding better from the docs? WHY???? penny kdrbrill <kdrbrill@...> wrote: Penny Houle <pennyhoule@...> wrote:"It's already happening with near epidemic proportions in children with ear infections and skin infections (staph). "Hi Penny, I believe that's happening precisely due to the over–prescribing of antibiotics for the last 20-30 years.We have to ask ourselves: Why can't we seem to get over these bugs that nearly everyone has antibodies to, yet their infections resolve in a matter of weeks? Of course it's very complex, and there are many issues to confront, but I think the answers lie mainly in restoring our immune function so that it will work like most people's. To me, that's the only obvious difference. We all carry a variation of the same collection of critters...but we stay sick while others recover much faster. This methylation block issue may be a critical piece of the puzzle... ???Best,Dan>> 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> > >> >> Quote Link to comment Share on other sites More sharing options...
Guest guest Posted July 6, 2007 Report Share Posted July 6, 2007 Why? Because that would require people to take responsibility for their own health. It's ever so much easier to just go to some guru and say, "please tell me what to do" or "just give me a pill. You get to pick which one." We have met the enemy, and he is us. People on this list are necessarily more proactive about their health because the alternatives are, for them, too terrible to contemplate. Proving once again that when the pain of change is less than the pain of not changing, people can and do change. --Bob Penny Houle wrote: "I believe that's happening precisely due to the over–prescribing of antibiotics for the last 20-30 years." Over prescribing of the WRONG antibiotics, with no regard for using the correct ones or understanding of the bugs abilities. This approach seems a bit silly to me when we don't have a prayer of adapting our immune systems as quickly as the bugs do. It doesn't take 30 years for a bug to become resistant to the latest new pharmaceutical, more like 30 hours. Again, I'm not against strengthening the immune system, but you just illustrate my point. You accept what the docs tell you, that the problem lies strictly in patients using antibiotics unnecessarily, when in fact, the problem lies with docs who don't diagnose or prescribe properly. The only way that is going to change is when understanding of the bugs increases and docs are required to test and treat properly... not just throw the latest abx at you with no regard for whether your bugs may already be resistant to it making them stronger than ever, ready to decimate the next unfortunate victim who happens to get in the way. Why is there so much resistance to learning how to treat the bugs properly? And why are patients so complacent about this serious issue? Why isn't everybody demanding better from the docs? WHY???? penny kdrbrill <kdrbrill > wrote: Penny Houle <pennyhoule@...> wrote: "It's already happening with near epidemic proportions in children with ear infections and skin infections (staph). " Hi Penny, I believe that's happening precisely due to the over–prescribing of antibiotics for the last 20-30 years. We have to ask ourselves: Why can't we seem to get over these bugs that nearly everyone has antibodies to, yet their infections resolve in a matter of weeks? Of course it's very complex, and there are many issues to confront, but I think the answers lie mainly in restoring our immune function so that it will work like most people's. To me, that's the only obvious difference. We all carry a variation of the same collection of critters...but we stay sick while others recover much faster. This methylation block issue may be a critical piece of the puzzle... ??? Best, Dan > > 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 > > > > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted July 6, 2007 Report Share Posted July 6, 2007 Ear infections may just as likely be due to lack of breastfeeding. Indeed, if you read the studies on non-denatured whey perhaps we are all sicker because of the pasteurization of milk. a Carnes > > " It's already happening with near epidemic proportions in children with ear infections and > skin infections (staph). " > > Hi Penny, > > I believe that's happening precisely due to the over–prescribing of antibiotics for the last > 20-30 years. > > We have to ask ourselves: Why can't we seem to get over these bugs that nearly everyone > has antibodies to, yet their infections resolve in a matter of weeks? > > Of course it's very complex, and there are many issues to confront, but I think the answers > lie mainly in restoring our immune function so that it will work like most people's. To me, > that's the only obvious difference. > > We all carry a variation of the same collection of critters...but we stay sick while others > recover much faster. This methylation block issue may be a critical piece of the > puzzle... ??? > > Best, > > Dan > > > > > > > > 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 > > > > > > > > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted July 6, 2007 Report Share Posted July 6, 2007 > > > > > > > > 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 > > > > > > > > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted July 7, 2007 Report Share Posted July 7, 2007 Dan Thanks for the lead on an alternate antibiotic. I hadn't heard of it. Here's a recent PubMed paper on it: http://tinyurl.com/yvba7e PubMed also has at least one article saying that Triphala works against tumor cells, which makes me think that the concentrations of the extracts that have been tested against bacteria may also be toxic to host cells, though there's some evidence that the tetracyclines inhibit tumor cells in culture, so there's precedent for a safe antibiotic having a bit of anti-cancer properties. Anti- fungal, too? I get more skeptical about a drug when the number of positive attributes it is given exceeds two. I'm too sick, though, not to at least investigate a lead like this and to thank anyone who provides it. I haven't had time to investigate Triphala. Do you take it orally? Is it absorbed systemically after oral ingestion? Or could this be a luminal agent that is treating undiagnosed small intestinal bacterial overgrowth? Do you notice any side effects? You say that you can't take antibiotics due to concurrent fungal infections. Aside from a furry tongue or colonies of candida in the mouth, I've never been clear about how people decide that they have fungal infections that are more than bystanders. What's the evidence in your case? Has Triphala worked against the fungus? You indicate that you get normal infections, but are abnormal in your ability to clear them. Are you one of those people who get colds/flus often and for protracted periods? Matt > > > I'm finding help using old " drugs " -- in my case, the ayurvedic herbal formula called > Triphala. One of the three ingredients is called Harataki (sp?) also known as Terminalia > chebula. > > I was recently diagnosed with a pseudomonas infection, and found this extract was > recently shown to completely kill off the stubborn buggers. Antibiobiotics have become > resistant in many cases, plus, in my case, I can't take them due to a concurrent fungal > infection (which triphala treats as well). > > Here's an article about the 17 year old med student who discovered it's effectiveness: > > http://cfvancouver.ca/cms/index.php? option=com_content & task=view & id=63 & Itemid=38 > > > Take care, > > Dan > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted July 7, 2007 Report Share Posted July 7, 2007 I like the pseudonomas diagnosis. Whjat made thedoc make an effort to diagnose this bug? 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 > > > > > > > > > > > > > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted July 7, 2007 Report Share Posted July 7, 2007 Your post certainly is not seen as an attack. I'm especially glad you cited a possibly effective treatment. My problem is this constant focus by most on strengthening the immune system as being more critical than recognizing the inherent strength of the bugs. People always ask why some get sick and others don't. My view is that the ones who aren't sick haven't reached their tipping point. They're still one bug short. Or perhaps they have reached critical mass, but disease manifests differently, such as diabetes or cancer or who knows what other illness, so many of which have been linked to bacteria. I'm all for strengthening our immune systems. Become an iron man if you wish, but don't forget how tough the bugs are. Otherwise, we'll never get our immune systems strong enough no matter how hard we try. Not to mention the handicap the illness creates in us in the first place. Since bugs attack the immune system and actually turn it against us in some ways, it only seems sensible to me to try to weaken the bugs just as much as we try to strengthen (and heal) our immune systems. pennykdrbrill <kdrbrill@...> 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. 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> > > >> > >> >> Quote Link to comment Share on other sites More sharing options...
Guest guest Posted July 7, 2007 Report Share Posted July 7, 2007 Matt, this is such a good point. If my immune system is so weak, why is it that after getting full blown CFS, I didn't have a single cold or flu for over 7 years? Because the bacteria are in charge. And they can shut down viruses as easily as they can ward off my immune system. And I know I'm not alone in that. So many pwc stop getting colds for long periods of times. There are a few exceptions of course, but if all these people would just do a little digging, they'd see that most of our symptoms are from overactive immune systems, not underactive ones. Inflammation is rapidly becoming known as the cause of so many illnesses. So what is inflammation? The immune system of course! penny phagelod <mpalmer@...> wrote: DanThanks for the lead on an alternate antibiotic. I hadn't heard of it. Here's a recent PubMed paper on it:http://tinyurl.com/yvba7ePubMed also has at least one article saying that Triphala works against tumor cells, which makes me think that the concentrations of the extracts that have been tested against bacteria may also be toxic to host cells, though there's some evidence that the tetracyclines inhibit tumor cells in culture, so there's precedent for a safe antibiotic having a bit of anti-cancer properties. Anti-fungal, too? I get more skeptical about a drug when the number of positive attributes it is given exceeds two. I'm too sick, though, not to at least investigate a lead like this and to thank anyone who provides it.I haven't had time to investigate Triphala. Do you take it orally? Is it absorbed systemically after oral ingestion? Or could this be a luminal agent that is treating undiagnosed small intestinal bacterial overgrowth? Do you notice any side effects?You say that you can't take antibiotics due to concurrent fungal infections. Aside from a furry tongue or colonies of candida in the mouth, I've never been clear about how people decide that they have fungal infections that are more than bystanders. What's the evidence in your case? Has Triphala worked against the fungus?You indicate that you get normal infections, but are abnormal in your ability to clear them. Are you one of those people who get colds/flus often and for protracted periods?Matt>> > I'm finding help using old "drugs" -- in my case, the ayurvedic herbal formula called > Triphala. One of the three ingredients is called Harataki (sp?) also known as Terminalia > chebula. > > I was recently diagnosed with a pseudomonas infection, and found this extract was > recently shown to completely kill off the stubborn buggers. Antibiobiotics have become > resistant in many cases, plus, in my case, I can't take them due to a concurrent fungal > infection (which triphala treats as well).> > Here's an article about the 17 year old med student who discovered it's effectiveness:> > http://cfvancouver.ca/cms/index.php?option=com_content & task=view & id=63 & Itemid=38> > > Take care,> > Dan> > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted July 7, 2007 Report Share Posted July 7, 2007 As far as I know, most new mothers have been breastfeeding for the past 20+ years. It's considered very uncool to not breast feed, especially for the first few weeks of life, and most people do it for at least a couple months and more. All the studies show that the immunity is developed in those first weeks anyway. So the argument doesn't seem at all relevant to the current explosion of pediatric ear and skin infections. It's this kind of mythology that keeps us stuck in reverse I'm afraid. penny pjeanneus <pj7@...> wrote: Ear infections may just as likely be due to lack of breastfeeding. Indeed, if you read the studies on non-denatured whey perhaps we are all sicker because of the pasteurization of milk.a Carnes> > "It's already happening with near epidemic proportions in children with ear infections and > skin infections (staph). "> > Hi Penny, > > I believe that's happening precisely due to the over–prescribing of antibiotics for the last > 20-30 years.> > We have to ask ourselves: Why can't we seem to get over these bugs that nearly everyone > has antibodies to, yet their infections resolve in a matter of weeks? > > Of course it's very complex, and there are many issues to confront, but I think the answers > lie mainly in restoring our immune function so that it will work like most people's. To me, > that's the only obvious difference. > > We all carry a variation of the same collection of critters...but we stay sick while others > recover much faster. This methylation block issue may be a critical piece of the > puzzle... ???> > Best,> > Dan> > > > > >> > 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> > > >> > >> >> Quote Link to comment Share on other sites More sharing options...
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