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Immune system and co-factors of Freddd's protocol

Discussion in 'Detox: Methylation; B12; Glutathione; Chelation' started by Red04, May 20, 2013.

  1. Red04

    Red04 Senior Member

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    I was always a little skeptical of all the cofactors listed in the protocols. In an effort to reduce the overall number of vitamins my wife takes, I have tried several ways to eliminate co-factors on Freddd's protocol after my wife saw an initial 95% recovery some 2.5 years ago.

    It hasn't worked. The deadlock quartet + multi B seems to reliably keep the depression/fatigue/CFS/Fibro/IBS/sleeping disorders away, but her immune system gets compromised without the cofactors. Some combination of A,D,E,C, Omega 3, Calcium, Magnesium, Zinc, are necessary for her to have a healthy immune system. Without them, she gets a chronic sore throat and other lingering upper-respiratory symptoms. As soon as we realize that it isn't just a standard cold, returning to the full protocol relieves the symptoms in maybe 7-14 days. This has been repeated reliably maybe 4 times.

    Stop the cofactors => cold/sore throat for several weeks => restart co-factors => 7-14 day period and return to good health for months as long as cofactors are continued.

    Tracking reactions to the co-factors is tricky as the reaction is really slow and even 100% healthy people may get a cold a few times a year. I had a cold over the winter that lingered for 2 weeks, so until my wife was sick for a month, I thought she was having a normal immune response. I think we will continue to work on reducing the co-factors on a slower, strategic approach to try and pinpoint the cofactors that are immune response related.
     
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  2. Freddd

    Freddd Senior Member

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    Hi Red04

    Tracking reactions to the co-factors is tricky as the reaction is really slow

    You can say that again. Very interesting post. I wouldn't be surprised if every one of the cofactors listed for a healthy immune system. I don't believe that those can be cut out. The question perhaps is why isn't diet able to supply enough for good health as is claimed by so many or maybe why so deficient on so many items? Could be any number questions that could shed light on this.

    I would look at all noticeable changes, not just immune system. But then again, the immune system may respond as a separate layer and I certainly have not pinned that one down in order of healing or anything.

    Look for patterns of change or maybe changing patterns. Look for indirect indicators which might be more obvious than the immune changes themselves. An early immune indicator for me is infected follicles or other small skin infections.

    Good luck.
     
  3. Red04

    Red04 Senior Member

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    Good point. I wasn't thinking big picture. It is really a question of why is she not absorbing or utilizing the vitamins in our nutrient rich diets like the rest of us.

    I guess our options are:

    1. Try to streamline the "bypass" by taking just the necessary supplements as I have been trying to do.
    2. Look for underlying absorption or other big picture issues.
     
  4. Valentijn

    Valentijn WE ARE KINA

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    I recall a study I was looking at where they were testing and supplementing some substances in ME/CFS patients ... basically the supplementation raised controls and ME/CFS patients by about the same amount, and the ME/CFS patients ended up with normal levels due to the supplementation.

    No explanation for why it happens, but it seems to happen for a lot of things with us - we're low even though we have normal intake, and supplementation can then raise us to normal levels.
     
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  5. Red04

    Red04 Senior Member

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    So, from a big picture, maybe a genetic mutation paired with a stressor isn't necessarily a root trigger of me/cfs. It just gets "expressed" because of some digestion issue that causes problems with the conversion/absoprtion of methyl vitamins and several others. I would guess there are a lot of people with the MTHFR mutations that never get symptoms. Could this be why?

    Otherwise, why would my wife need all these other vitamins?

    Like a gluten allergy or other unknown condition....
     
  6. Freddd

    Freddd Senior Member

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    Back in the 50s, before folic acid and CyCbl became commonplace, people ate liver. The vitamin takers also regularly warned of "induced deficiencies" when only taking 1 or two vitamins. The popular multivitamins became popular in that period perhaps because of the warnings against taking a couple of isolated vitamins. I'm just throwing out some ideas. I may be the only person here that read essentially all the PREVENTION magazine articles of the 50s getting a pretty good feel for the contemporary vitamin taking community of that period. I also became aware of all the alternative health ideas and theories I suffered through in the 70s, 80s, and 90s to absolutely zero effectiveness.

    What type of transit time for instance dose your wife have, < =12hr, > =36hr or somewhere in between? Any IBS or similar blatant signs of inflammation or something.
     
  7. Red04

    Red04 Senior Member

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    My wife still has a little IBS symptoms, but not where they get in the way of life or anything, shes just not perfect. It's not anything you would visit a doctor over. IBS is where we started with all this ME/CFS. And its still one of the last lingering symptoms. A couple dozen doctor later and we were on the B12 trail.

    I would say her IBS has improved 70%. She gets the full range of symptoms. Just light and intermittent. I always attributed it to skipping vitamins, or stress or poor diet, but I certainly don't have it. And we have the same basic diet. Her rentention time seems to vary from several days to less than 12 hours. I think that was a qualifier for IBS.
     
  8. Freddd

    Freddd Senior Member

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    Hi Red,

    There are three types of IBS more or less, " retention time seems to vary from several days to less than 12 hours" is one kind. Does she have ANY other epithelial symptoms?. That includes lining of lungs, digestive tract, vaginal lining. skin, bladder. False positive PAP tests can result from the epithelial malfunction. Watch for other things that coordinate in timing with the changes of IBS phase, such as low or high urine volume, dropping potassium, other skin problems, allergies, asthma, hypersensitivity to food, etc. I believe this is solvable too.

    Sometimes this pattern can happen from food sensitivities from a tissues that haven't yet recovered. It took me 3 years to get my intestines healed up enough that I could "cheat' with a little cheese or ice cream or cheesecake or whatever once each 2-3 weeks without penalty. Twice could start problems, 3 cheats always did. Low folate can be cause IBS. Too much (relative?) B2. After a couple of months of severe IBS, that has finally healed to 24 hours transit time which has only been my norm for some months here and there. Normally 12 hours has been it since elementary school. I also had angular cheilitis for all the same decades. Good luck.
     
  9. Victronix

    Victronix Senior Member

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    IBS is where we started with all this ME/CFS.

    Indeed. It would be nice to have a better handle on this. Are you aware of a resource for what percentage of ME/CFS have significant digestive issues? Has there been a poll on here? Seems like most do.

    I know the conventional wisdom has been "heal the gut issues first", but of course if they are due to a deficiency of the protocol, that won't be possible. And I know that people on here have found a variety of gut problems via the testing. It would be interesting to take a closer look at those who have healed gut issues, and what changed.

    I think your wife's case is very important, in part because of her overall success but also the unique loss of the need for potassium that others continue to struggle with.
     
  10. Freddd

    Freddd Senior Member

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    Hi Victronix,

    IBS is a major set of symptoms in FMS at least. As it can turn on and off in days with folate problems, like paradoxical folate insufficiency or donut hole folate insufficiency, it can come and go a lot and has been one of my primary symptoms I use in evaluation my epithelial health. It usually comes on before allergies, asthma and hypersensitivity of all kinds when the folate insufficiency gets worse and continues.

    "heal the gut issues first",

    The deadlock quartet is a key factor in healing the gut. I don't know ANY way to heal the gut that doesn't supply these essential nutrients, or at least those that are deficient.

    I have my gut issues 95% healed. The hypokalemia symptoms go away as fast as the potassium can be corrected. The IBS takes 5 days to become non-manifest after the vitamins are in place for it to heal but appears to take months to heal all the way from long term inflammation. All of this is based on my own 55 years of experience.
     
  11. 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
     
  12. Red04

    Red04 Senior Member

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    I think most understand that correcting methylation improves immune function. My wife's immune system can function better than mine when on freddds protocol and all the cofactors. The thread was more in reference to why the need for cofactors with a supplemented methylation.

    Why does someone need vitamin c when taking all the methylation supplements? If methylation is the root cause, why the need for co-factors. A healthy person doesn't need vitamins.
     
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  13. Red04

    Red04 Senior Member

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    She has some light body acne and probably more facial acne than a 28 year old should have and small bumps on her scalp. I get those small bumps on my scalp too though. I've never tracked it concurrently with her IBS. Or tracked it at all they are all mild symptoms and pretty constant.
     
  14. Lotus97

    Lotus97 Senior Member

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    Perhaps, but maybe some people would actually want to know WHY.
    First of all, this thread is about the immune system and it's in the methylation/glutathione forum. I'm sorry you don't find this relevant, but a lot of people here have viruses and infections and would like to learn about this. Did you know that on Phoenix Rising there are
    -174 threads with either Valcyte, Valtrex, Famvir, or antiviral in the title
    -180 threads with virus or viral in the title
    -100 threads with infection in the title
    -97 threads with Lyme in the title

    Second of all, there are a lot of cofactors in the multivitamin that Rich recommends. Freddd doesn't have a monopoly on ideas.

    Vitamin C recycles glutathione and improves GSH/oxidized glutathione ratio. Selenium and molybdenum are cofactors for glutathione. B2 and B3 recycle glutathione. Supplements such as carnitine, lipoic acid, D ribose and coenzyme Q10/ubiquinol that support the Krebs cycle and/or improve mitochondrial function will also increase glutathione. So yes, there is a connection to glutathione so not only is your response to me insulting, but it's also wrong.
    Whoever said methylation was the root cause? I have no idea if Freddd claimed that, but Rich certainly did not claim that. This is from Rich (he's talking about Dr. Pall's theories) where he clearly states that methylation isn't adressing the "root cause"
    I should note that both Marty's model and mine are focused on the pathophysiology of ME/CFS. Neither deals in much detail with the etiology (or etiologies), i.e. the root causes. I think Marty and I basically agree on the general categories of the etiologies, though. I call them stressors, and within that I include physical, chemical, biological and psychological/emotional stressors. The toxins are included within the chemical stressors, and the infectious pathogens are included within the biological stressors. I believe that the combination of stressors that bring the onset of ME/CFS differ from one person to another. I am very gratified to see the increased research effort by several groups now to look at the infectious pathogens as possible etiological agents for ME/CFS.

    As far as I know, the improvements people have experienced when treating on the basis of the GD-MCB model have exceeded the improvements when treatment has been based on the NO-ONOO model. I don't disagree that antioxidants can help to lessen the oxidative stress in ME/CFS, but I have not found that the core of the pathophysiology, which I believe lies at a partial block in methionine synthase, can be addressed effectively with antioxidants.

    Best regards,

    Rich
     
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  15. Freddd

    Freddd Senior Member

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    Hi Red,

    By definition a person has to have all the vitamins to be healthy, however they happen to get them. If they stop getting enough vitamins they stop being healthy. Lots of animals make their own vitamin C, humans can't.
     

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