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Methylation for Lyme Disease (Immune System and Glutathione Depletion) Rich Vank's Posts

Discussion in 'Lyme Disease and Co-Infections' started by Lotus97, Jan 27, 2013.

  1. Lotus97

    Lotus97 Senior Member

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    I was wondering how many people here with Lyme Disease or another type of infection/virus are also following a methylation protocol? I thought I'd share some of Rich Vank's posts on the subject. The first is a forum post by Rich and the second looks like it's a speech he gave at a conference or maybe just a paper he submitted for the conference.
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    http://forums.phoenixrising.me/inde...-van-konynenburg-parts-1-7.11488/#post-198779
    Helen, golden, Lala and 1 other person like this.
  2. Lotus97

    Lotus97 Senior Member

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    So having Lyme Disease could cause depleted Cysteine levels, but I was reading that having mercury toxicity could cause elevated Cysteine levels. What do I do if I suspect I have both Lyme and Mercury? I don't know if I feel like paying for tests and I don't think my doctor would even have me tested since she's not familiar with either condition.
  3. Lotus97

    Lotus97 Senior Member

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    I've been coming across some information about a relationship between mercury and Lyme. I know not everyone with Lyme has mercury problems, but I thought I'd mention it here since methylation can be both useful and also pose certain challenges for those who have mercury issues. Methylation initiates detoxification which can cause problems for those who are especially toxic. Some people with mercury or other heavy metal toxicity might need to do chelation before or along with methylation treatment. I am just newly learning about this so I hope someone more knowledgeable can share their experiences.
  4. Lotus97

    Lotus97 Senior Member

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    I came across a question and answer article by Dr. Neil Nathan who has used Rich's methylation protocol on some of his CFS/Fibromyalgia patients. There were some things he said about Lyme which I thought I'd share. I would like to hear some thoughts on this because I've been struggling with what order to do things (especially since I might also be dealing with metal toxicity in addition to Lyme)
    * * * *
    Q: Would the Methylation Protocol be of any benefit for individuals with Lyme disease? Would the vitamin B-12 and folic acid be good for it? My girlfriend has had Lyme disease for the past 7 years. She was diagnosed 5 years ago and has been on antibiotics for the past 4 years as of June 2011. Do you have any suggestions or directions regarding the continued use of antibiotics for the treatment of chronic Lyme disease? Any help would be much appreciated. She has been through hell and is better but not cured of the Lyme.

    A: We treat a large number of patients with Lyme disease, and we have found that most of them (as with patients chronically ill with virtually any condition) do not methylate properly. Many of them do respond to a methylation protocol, but again, I must warn you that most of our Lyme patients wrestle with problems of toxicity and are at high risk of reacting to the protocol, initially. So I would go VERY slowly and carefully, work with someone who understands this.
    * * * *
    Q: For someone with a diagnosis of Lyme pathogens, would you recommend treating the Lyme first or doing the Methylation Protocol first?

    A: Treat the Lyme first. If you try the methylation protocol first, you will release toxins that the individual cannot handle and you have a high risk of making them worse.
    * * * *
    Q: My Lyme doctor put me on the Methylation Protocol (I have had chronic fatigue for more than 10 years)… It made me feel like I was on speed. Any insights on this
    A: Yes. It was too strong for you. You may need to cut it way back for it to be of benefit.
    * * * *
    Q: Rich Van Konynenburg wrote several years ago in the ProHealth ME/CFS/FM message board that he had a hypothesis that “Lyme disease is one route of entry into CFS for people who are genetically susceptible.” What is your current thinking on whether ME/CFS and Lyme may sometimes be linked or otherwise associated?

    A: As we continue to study this, it becomes clear that many patients who have been diagnosed with ME/CFS have Lyme disease that hadn't been looked for or diagnosed. The numbers are much higher than we had thought, so that some Lyme specialists think most patients with "CFS" actually have Lyme. I would not take it that far, but I would agree that we should check all CFS patients for Lyme disease. We don't want to realize three years down the road that we missed a treatment component.
    Helen likes this.
  5. juniemarie

    juniemarie Senior Member

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    I have lyme and have been on Rich's protocol for over 2 yrs. I have not started lyme treatment yet. I hope addressing methylation first will help my body respond better to lyme treatments.
  6. Lotus97

    Lotus97 Senior Member

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    Hi, juniemarie. Thanks for your response. So I assume the methylation protocol has helped since you've been doing it for two years? I am actually hoping the same thing about methylation strengthening my body for the lyme treatments. I don't think Dr. Neil Nathan who I quoted earlier is necessarily correct (at least not for everyone) in saying to treat Lyme first. Although it is true methylation can be hard on a person's body either through detoxing or overmethylation (both of which can be minimized by starting on low doses), treating Lyme can often be more brutal from what I've heard. If you take antibiotics they cause a lot of toxins to be released through die-off/herxing/Herxheimer Effect. In addition, they kill the probiotics in your body which further weaken your system.
  7. Lala

    Lala Senior Member

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    I do not see why these two treatments could not be used together very slowly. I am on heavy antibiotic treatment longterm and adding methylation supps very slowly. Dr. Stratton and Wheldon suggest supporting methylation along with atb treatment. Waiting few years after one or either treatment is done can be too long and moreover how can we know treatment is done when we still suffer from symptoms.
  8. Lotus97

    Lotus97 Senior Member

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    Yeah, it really depends on the individual. I know for myself I'm not able to tolerate either treatments very well right now, but during a period last year when I was making a recovery I think I could have been able to do both of treatments at the same time without too much trouble.
  9. Lotus97

    Lotus97 Senior Member

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    This from Rich talking about potential adverse reactions to watch out for during methylation treatment.
    One physician I know gives all his patients the methylation treatment, and then watches the response. If they experience some symptoms that appear to be caused by detox, but they are able to tolerate them, he continues with this treatment. If they have intolerable symptoms that appear to be related to mobilization of toxins, then he stops the methylation treatment and works on improving the status of the gut. When that is working better, he moves on to supporting the liver. His thinking is that the toxins that were being mobilized were being reabsorbed by the gut and sent back to the liver. In order to properly process and excrete the toxins, the gut and liver must both be functioning well enough to handle them.

    My guess is that when there is an inflammation response to methylation cycle treatment, there is an infection. If the inflammation continues without resolution, then my guess is that the immune system has been reactivated, but is not capable of defeating an existing infection. In such cases, I think that treating to support the immune system would be one approach. Another would be to test to determine what pathogen is causing the infection, and then treating it with an antibiotic, antiviral or antifungal, depending on the pathogen.

    I think it's important to note that a healthy person would not have any reaction to the supplements used in the methylation protocols, because their methylation cycle, detox system and immune system would already be functioning normally. So the fact that there is a response, even though it may seem to be deleterious, means that the methylation cycle was partially blocked and that these supplements were needed. However, the way one should proceed from that point on probably depends on the type of response that the individual person has.

    So far, I'm pretty sure that if the following are present, they will need specific treatment, in addition to treating the methylation cycle partial block: biotoxin (including mold) illness, Lyme disease and its coinfections, well-entrenched viral infections, and high body burdens of toxic heavy metals, such as mercury. There may be others of which I'm not aware, but there is some experience with these, at least, which people have reported

    I believe that the partial methylation cycle block is the pivotal abnormality in the pathogenesis and pathophysiology. With respect to the root cause or causes (etiology) of ME/CFS, I have suggested that this disorder arises from a combination of a genetic predisposition and some combination of a variety of stressors, which can be physical. chemical, biological, or psychological/emotional. I've suggested that this combination leads to glutathione depletion, which leaves B12 unprotected, which causes a decreased production of methylacobalamin, which inhibits methionine synthase, which forms a vicious circle with glutathione depletion, making ME/CFS a chronic condition. The retroviruses would fit within the biological stressors in my hypothesis, and certainly could be a root cause. If effective treatment of the retroviruses ends up bringing about recovery from ME/CFS, that will be very convincing as to its role as an etiologic agent. I hope that turns out to be the case for at least some of the PWMEs/PWCs. It may not be true for all of them, though, because this population seems to be very heterogeneous.

    The reason I have included the variety of stressors as etiologic agents is that I have studied the published "risk factor" studies, and have also queried quite a few PWMEs/PWCs as to the events that preceded their onset, and I've found a variety of precursors. The common factor seems to be that they are all things that would be dealt with by the body's nonspecific stress response systems, and these in turn are known to place demands on glutathione.

    In addition to this, there are now many PWMEs/PWCs who have taken the Health Diagnostics methylation pathways panel, and nearly all of them show evidence of a partial methylation cycle block or glutathione depletion, and usually both.

    And when treatment was given in our clinical study that is directed toward lifting the partial methylation cycle block, we observed by testing that this does in fact occur, and that glutathione also comes up automatically. This was accompanied by improvement in symptoms in at least two-thirds of those who were treated.

    Putting all of this together, I think the GD-MCB hypothesis is consistent with the observations and with known biochemistry and physiology. That doesn't mean that I believe that it is scientifically proven, which is a very high standard to meet, and requires considerable investment in time, money and effort, but that it is a valid working hypothesis. I'm hoping to interest researchers and fundors in this model so that it can be more thoroughly tested.

    The methylation cycle is at the beginning of the sulfur metabolism. It is fed by methionine, which comes in as part of protein in the diet. Homocysteine is produced from methionine (via SAMe and SAH) in the methylation cycle, and then methionine synthase "decides" how much should be converted back to methionine, to stay in the methylation cycle. In the liver and kidneys, the BHMT reaction also converts some homocysteine back to methionine. The rest of the homocysteine enters the transsulfuration pathway, which is downstream.

    The way that methionine synthase does its "deciding" is that the cobalt ion in the cobalamin that is its cofactor gets oxidized at a rate that depends on the state of oxidative stress in the cells. The more oxidizing this state is, the more often the cobalt ion gets oxidized, and that temporarily shuts down the methionine synthase reaction and diverts the homocysteine flow into the transsulfuration pathway, which helps to make more glutathione, which counters the oxidative stress. Unfortunately, in ME/CFS this delicate mechanism gets overwhelmed, and the oxidative stress becomes more severe, so that glutathione doesn't recover and get control of it. The result is that methionine synthase becomes partially blocked, and the sulfur metabolites drain down the transsulfuration pathway, into sulfoxidation, and get excreted too much as taurine and sulfate, which depletes methionine. The whole sulfur metabolism becomes dysfunctional, and that takes down the cell-mediated immune response as well as the detoxication system. As well, everything that depends on methylation reactions is affected, including gene expression, synthesis of several needed substances, and the neurotransmitter metabolism. Also, this drains the folates from the cells via the methyl trap mechanism, and that affects things that depend on folate, such as synthesis of new RNA and DNA. The latter is what cause the red blood cells to be too big and too few in number.

    The methylation cycle is so fundamental to so many parts of the body's biochemistry that when it becomes dysfunctional, it causes a host of problems, and this is why people experience so many symptoms, involving so many body systems and organs, in this disorder.
    Helen likes this.
  10. Branston

    Branston

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    Lala... can you tell me where you found the Stratton/Wheldon references to methylation support? I have Chronic CPn/Lyme, MTHFR C677T +/+ MTRR A66G +/+ I know the CPn is supposed to produce antibodies to B12 and therefore supplementation with B12 is advised......
  11. Lala

    Lala Senior Member

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    You can read about their treatment on cpnhelp.org. I think I read about methylation support in Stratton´s patent on the net. Sorry I can not be more specific like pointing out to specific page as it is very long time I read this info.
  12. Lotus97

    Lotus97 Senior Member

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    In another thread, Rich was talking about how methylation and restoring glutathione levels can be useful in improving immune function. These quotes are actually from multiple posts by Rich in that thread. I've tried to include the most important parts, but I would also recommend checking out the thread if you have time since there are more posts by Rich as well as many other posts by other members who add additional information to this subject and raise questions about the theory and other alternatives.
    http://forums.phoenixrising.me/inde...lls-perforin-and-glutathione-depletion.17603/
    As many of you know, the most reliable immune-related marker for ME/CFS is probably the low cytotoxic (cell-killing) activity of the natural killer cells.

    As you may also know, natural killer cells normally kill cells that are infected with viruses. They do this by secreting a substance called perforin, which makes a hole in the cell membrane, and then injecting granzymes, which induce the cell to undergo apoptosis (programmed cell death). The CD8 cytotoxic T cells operate in the same way in terms of their killing mechanism.

    Some years ago, Dr. Kevin Maher, who was in Dr. Nancy Klimas's group, reported that the natural killer cells in PWMEs are low in perforin. It was also found that the CD8 cytoxic T lymphocytes were also low in perforin. This would, of course, inhibit their cytotoxic activity.

    The question then became "Why are the NK and CD8 cells in ME/CFS low in perforin?

    In 2007, when I proposed the Glutathione Depletion-Methylation Cycle Block (GD-MCB) hypothesis, I noted that the perforin molecule has a large number (20) of cysteine residues in its protein structure. It is known that in order for a cell to be able to synthesize a protein that contains cysteine residues, it must have sufficient glutathione and a high enough ratio of reduced to oxidized glutathione to keep the cysteine molecules in the cytosol of the cell in their chemically reduced state as cysteine, and not oxidized as cystine. Otherwise, the cell cannot assemble the chain of amino acids properly and join the cysteine residues to their proper partners to form the proper tertiary structure of the molecule. I therefore proposed then that the perforin deficit in NK cells and CD8 cells in ME/CFS is due to glutathione depletion in these cells. If this is true, one would expect that the gene expression of the perforin gene (as measured by the level of messenger RNA corresponding to the PRF1 gene) would not be below normal, because the glutathione deficit would impact the protein synthesis process downstream of gene expression.

    Recently, a group at Bond University in Australia (lead author Ekua W. Brenu) published a paper entitled "Immunological abnormalities as potential biomarkers in Chronic Fatigue Syndrome/Myalgic Encephalomyelitis":

    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3120691/pdf/1479-5876-9-81.pdf

    In this paper, together with a following one:

    http://www.translational-medicine.com/content/pdf/1479-5876-10-88.pdf

    they reported that the NK cell and CD8 cell cytotoxic activities were consistently low in ME/CFS patients, but the messenger RNA for the perforin gene PRF1 was significantly higher in both cell types in the PWMEs than in the normal control subjects.

    I suggest that this new result is consistent with the mechanism I have proposed for low perforin in ME/CFS. It indicates that the NK cells and CD8 cells are "trying hard" to produce perforin by boosting the transcription of the PRF1 gene to messenger RNA, but the protein synthesis process is at least partially blocked and cannot respond. If glutathione is somewhat depleted in the NK cells and CD8 cells, the protein synthesis process would indeed be partially blocked.

    I continue to propose, as I did in 2007, that other features of the observed immune dysfunction in ME/CFS can also be explained by the GD-MCB hypothesis. These include the shift to Th2 immune response, the elevated RNase-L and formation of the low-molecular-weight RNase-L, the elevated inflammation, the failure of lymphocytes to proliferate when stimulated with mitogens, the reactivation of viruses and intracellular bacteria, and the accumulation of pathogens over time.

    Here's a brief outline of the whole GD-MCB hypothesis, as it currently stands (always subject to modification as we learn more):


    1. Genetic predisposition is present (perhaps including SNPs in genes coding for enzymes related to glutathione that cause it to be more easily depleted, as reported in autism by Bowers et al., 2011).

    2. Stressors (physical, chemical, biological and/or psychological/emotional, the mix varying from one case to another, based on patient histories) deplete glutathione by various means, some by oxidative stress, some by conjugation, some by lowering its rate of synthesis. The depletion of glutathione is demonstrated by the methylation pathways panel.

    3. The state of oxidative stress worsens as a result of the depletion of glutathione, and peroxynitrite rises, due to reaction of rising superoxide with existing nitric oxide.

    4. Glutathione depletion lowers the affinity of the CblC complementation group for cobalamin (as reported by Jeong and Kim, 2011), producing a functional B12 deficiency, thus lowering intracellular methylcobalamin and adenosylcobalamin. Anecdotal observations of elevated urine methylmalonate in the presence of normal or elevated serum B12 in ME/CFS patients confirm the presence of a functional B12 deficiency.

    5. The lowered methylcobalamin inhibits the methionine synthase reaction, since it is the necessary coenzyme for this reaction.

    6. The methyl trap mechanism continues the conversion of other forms of folate into methylfolate, but the lowered rate of the methionine synthase reaction decreases the demand for it.

    7. The elevated peroxynitrite catabolizes methylfolate, preventing its rise in the plasma.

    8. The above process depletes the intracellular folates in general (as inferred from measurements with the methylation pathways panel).

    9. Homocysteine drains into the transsulfuration pathway, since its conversion to methionine is inhibited, and over time, methionine therefore becomes depleted (as found by Bralley and Lord,1994), leading to dysregulation and depletion of the sulfur metabolism in general.

    10. The above combination of steps produces a stable vicious circle mechanism, and this is the reason ME/CFS is chronic.
    11. Treatment must include a high dosage (relative to the RDA) of a form of vitamin B12 delivered to the bloodstream, such as sublingually or by injection, together with an RDA-level dosage of folate, which can be given orally. The high dosage of B12 is necessary to compensate for the greatly lowered affinity for cobalamin of the CblC complementation group, so as to overcome the functional B12 deficiency, and the oral route is not adequate to supply this necessary high dosage (first reported by Lapp and Cheney, 1993 and 1999). The folate is necessary to compensate for the loss of methylfolate from the cells due to the peroxynitrite catabolism reaction. The B12 is best given as hydroxocobalamin or methylcobalamin. The folate is best given as methylfolate, though folinic acid works for some patients. There are individual differences in genetic polymorphisms that determine the best forms of B12 and folate for individual patients. If there are deficiencies in cofactor vitamins and minerals or in necessary amino acids, these must be supplemented in addition. Replacement of oxidatively damaged essential fatty acids is also needed. If toxic metals levels are high enough to significantly block enzymes in this part of the metabolism, chelation may be necessary before this treatment will be successful.

    12. This treatment is directed at the core of the pathophysiology. However, it does not directly treat the etiologies ("stressors" in step #2 above) that brought about this pathophysiology, nor does it directly treat pathogens and toxins that may have accumulated since the onset of ME/CFS, while the body's immune and detoxication systems have been dysfunctional as a result of the dysfunction of the sulfur metabolism. Additional treatments are needed in most cases to deal with them directly, to work toward achieving full recovery, because even though the immune system and the detoxification system may be largely restored, they are often not able to overcome these etiologies and accumulated factors on their own. Some of the etiologies and accumulated factors in various cases are Lyme disease and its coinfections, biotoxin illness, entrenched viral infections (and perhaps retroviral infections), and high body burdens of toxins.

    I don't know how many of the cysteines are involved in sulfide bridges, but I suspect that quite a few, and maybe all of them, are. And yes, glutathione depletion will likely cause misfolding of the protein structure. I should note that there is a quality control system built into the endoplasmic reticulum of cells, so that many of the misfolded proteins are detected and recycled via disassembly of the amino acids in the proteasomes, but some are probably released, and yes, they might have low activity.

    Incidentally, I have invoked this same mechanism to explain why some other secretory proteins, such as some of the peptide hormones, are deficient in ME/CFS. I think that vasopressin and oxytocin are in this category, and I think that ACTH is, also. All of these have cysteine residues that have to form particular disulfide bonds to produce the proper tertiary structure of their molecules. Any secretory protein that normally has disulfide bonds and is formed in a cell that is depleted in glutathione will have this problem. I think the hypothalamus and pituitary are depleted in glutathione. On the other hand, it's likely that the pancreas is not, so insulin is properly formed in ME/CFS. The reason the pancreas is not likely to be depleted in glutathione is that it is one of the few vital organs that have a complete transsulfuration pathway, and thus are able to make cysteine from methionine, so that they can maintain glutathione synthesis when the body as a whole is having problems maintaining its glutathione inventory.

    I also think it's possible that some of the autoimmune activity in ME/CFS may result from the immune system trying to clean up these misshapen proteins. To go a step further, that may be why Rituximab helped some people. By knocking out the B lymphocytes, the antibodies will be decreased over time, and that should lower the autoimmune reactions and the accompanying inflammation with its oxidative stress. Maybe that allows glutathione to come back up and restore things.

    To try to respond to your questions, I think I should first summarize how the immune system normally responds to viral infections, then discuss what I think the dysfunction in ME/CFS involves, and then comment on your questions:

    So first, how does the immune system normally respond to viral infections? There are basically four types of responses, listed here in roughly the chronological order in which they normally occur:

    1. Type I interferon (interferons alpha and beta) responses
    2. Natural killer cell response
    3. Virus-specific cytotoxic T lymphocyte (CD-8 "killer" T cell) response.
    4. Antibody response

    Type I interferons are secreted by infected cells, to alert nearby cells, and hopefully prevent them from becoming infected. The Interferon responses include the PKR, the 2,5-OAS RNase-L, and the Mx responses, among others. The PKR response inhibits the synthesis of viral proteins inside host cells. The 2,5-OAS RNase-L response degrades viral RNA inside host cells. The Mx response inhibits viral gene expression and assembly of the virions inside host cells.

    The natural killer cells recognize virally infected cells in which the viruses are attempting to hide from the immune system by shutting off the Class I HLA mechanism that the CD-8 cells use to recognize virally infected cells. If the Class I HLA molecules are not displayed on the cell surface, the NK cell kills the cell.

    The CD-8 killer T cells kill cells that are displaying viral antigens by means of the Class I HLA molecules.

    Antibodies against viral antigens are made by B lymphocytes and plasma cells, and they bind to viruses that are outside the host cells, as when an infection is beginning or when viruses are spreading from one host cell to another.
    This neutralizes the viruses, so that they cannot enter new host cells, and it can also "mark" them for attack by other cells of the immune system, such as macrophages.

    O.K., now what happens to these responses in ME/CFS?

    Well, the Type I interferon responses continue to work, and even though they are intended to be short term responses to hold back the viral infection until the "cavalry" in the form of the CD-8 killer cells arrives, and the CD-8 cells, together with the NK cells, knock out the viral infection, in ME/CFS the interferon responses continue to work overtime (and even become dysregulated in the case of the RNase-L) because the CD-8 killer cells are not able to take over. Sadly, the "cavalry" never arrives, leaving the "civilians" to battle the "Indians" in an ongoing guerrilla war.
    What causes the formation of the dysregulated low-molecular-weight RNase-L molecules? I propose that glutathione depletion is responsible. It activates calpain, and calpain cleaves the normal RNase-L molecules. The cleaved parts join together, forming the unregulated LMW RNase-L.

    Both the NK cells and the CD-8 killer T cells are rendered impotent by their inability to make perforin and granzymes in normal amounts. Furthermore, the CD-8 killer T cells are not able to multiply to outnumber the "bad guys" as they should. Why does this happen? I propose that it is a result of glutathione depletion and depletion of folates, respectively, which are part of the GD-MCB vicious circle mechanism that I believe is at the basis of the pathogenesis of ME/CFS.

    Antibody production continues, and in fact may be increased, because of the shift toward the Th2 immune response in ME/CFS, which favors humoral immunity, i.e. the production of antibodies by B lymphocytes and plasma cells. What causes this shift? Again, I have proposed that glutathione depletion is responsible, in this case in the "naive" T cells.

    So what we have are heightened interferon and antibody responses, but failure of the main "kill" mechanisms. The result is that latent viruses in the body (such as EBV, CMV and HHV6) are able to reactivate, and the immune system continues to fight with the weapons it has left, confining the viruses and keeping the host alive, but not winning the war against the viruses by completely knocking them out or putting them back into latency.

    Now, what about your questions?

    Would interferon treatment work? Well, to some degree, but without the other dysfunctional immune responses to help them, they cannot completely knock out the viruses.

    Why don't PWMEs get colds and flus? I think it's because of the constantly elevated interferon responses. This produces what has been called the "antiviral state." With this going on, it's difficult for a newly introduced virus to get a foothold.

    Does this have anything to do with the elevated cytokines in ME/CFS? Yes. The immune system is well aware that there are enemies inside the perimeter, and it is sounding the alarm, trying to organize the defense. The cells of the immune system are sending chemical messages back and forth to each other in the form of cytokines. However, because the NK cells and the CD-8 cells are impotent, even though the trumpet sounds, they don't respond, because they are not able to, so the messages just keep flying back and forth, unheeded.

    Beyond that, because viruses that are well-entrenched have various ways of foiling the immune system, even though the immune system is restored, other measures will likely also be needed. One interesting one is GcMAF, which overcomes one of the strategies used by viruses to foil the immune system, i.e. nagalase. Antivirals are another possibility, especially in view of some success using them, as in Dr. Lerner's experience.

    So what's the solution to this problem? How do we win the war? Well, I'm still working on that, but I think that a big part of it will be to restore glutathione, folates and methylation, and that will probably require a methylation protocol.

    Best regards,

    Rich
    Helen likes this.
  13. Lotus97

    Lotus97 Senior Member

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    Does anyone know what Rich means by "the immune system has been reactivated"? Does this have to do with Th1/Th2, cytokines, or...? And how are we supposed to be "treating to support the immune system"?
  14. Sushi

    Sushi Moderator and Senior Member Albuquerque

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    Lotus97

    I think he means that the immune system is on hyper alert but shooting blanks--can't actually kill much off. He could have meant immune modulators like LDN or other forms of immune therapy. He was familiar with LDN.

    Sushi
    Lotus97 likes this.
  15. PhoenixBurger

    PhoenixBurger Senior Member

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    Quercetin has given me tons of relief with a reactivated immune system that is shooting blanks.
    Lotus97 likes this.
  16. Lotus97

    Lotus97 Senior Member

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    Hmm, that seems to sort of tie in to what he said about natural killers cells and glutathione depletion or this a separate issue? I've started taking nucleotides which among other things is supposed to raise CD4, CD8, cytoxic and NK cells, but is it going to work if I'm depleted of glutathione and my methylation cycle is blocked?
    --------
    Does this have anything to do with the elevated cytokines in ME/CFS? Yes. The immune system is well aware that there are enemies inside the perimeter, and it is sounding the alarm, trying to organize the defense. The cells of the immune system are sending chemical messages back and forth to each other in the form of cytokines. However, because the NK cells and the CD-8 cells are impotent, even though the trumpet sounds, they don't respond, because they are not able to, so the messages just keep flying back and forth, unheeded.

    Beyond that, because viruses that are well-entrenched have various ways of foiling the immune system, even though the immune system is restored, other measures will likely also be needed. One interesting one is GcMAF, which overcomes one of the strategies used by viruses to foil the immune system, i.e. nagalase. Antivirals are another possibility, especially in view of some success using them, as in Dr. Lerner's experience.

    So what's the solution to this problem? How do we win the war? Well, I'm still working on that, but I think that a big part of it will be to restore glutathione, folates and methylation, and that will probably require a methylation protocol.

    Best regards,

    Rich
  17. Sushi

    Sushi Moderator and Senior Member Albuquerque

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    Lotus97

    Re: the GcMAF, that and some other "killing strategies" have definitely helped--nagalase has slowly gone down and the immune system is working better (both according to my perception and as measured by tests).

    Sushi
  18. Prema

    Prema

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    Austria
    Hi Lotus,
    what comes to my mind is what I heard and read from Dr.Klinghardt and Dr. Yasko: viruses and intracellular bacteria like borrelia add to Your DNA there own and that way deprogramme it so that the immune-systeme thinks the pathogens are good part of Your body and does not react anymore to them. Normally methyl-groups are added to the DNA to prevent that, or do reprogramming. But the cells would use up methyl-donors to produce glutathion first, if there is too much toxicity, which is said to be the case in lyme-disease. Then there might be no methyl-donors left over to attach to DNA. When You give methyl-donors doing the protocol, the cells can add them to the DNA and release the block of the IS and the IS reacts to the pathogenes again.

    Then also say that pathogenes attach to the toxic metals in the cells. then You have a problem to get the metals out (trying with DMSA with alphaliponic acid or whatever). You have to adress the infection when it flares up after having supported with methyl-donors to get the toxins out as well...

    I am also wondering how we should "treat to support the immune-system"...

    I have ordered quercetin now, because boswellia or curcumin&peperin have not really helped with inflammation.

    Thanks for posting the texts from Rich vK about lyme and methylation-protocol!
    Prema :)
  19. Prema

    Prema

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    Austria
    I have been diagnosed with slightly active lyme-disease by LTT (Elispot) and testing CD57. An other lyme-doctor was doing westernblot last year and said I don't have lyme. My symptoms are mainly inflammation and fatigue in the brain since five year. (before I got DMPS, I also had brain fog and dementia-symptoms). So far I wanted to avoid antibiotics and used only herbal antibiotics, and now I am going for the methylation protocol, because I am stuck with the treatments I had so far.

    I am heaving strong Inflammation-reactions to Hydroxy-B12 with really low Dosis of methyl-B9 and -B6 with phosphatidylcholine/serine as well as little pain in the liver-area, which makes me worrying and provokes some doubts.

    I would be interested in other people's experiences with lyme having started the methylation-protocol.
    (I am in Europe and guess here is no doctor available who knows about the genetic testing and methylation)

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