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Where are we on understanding and treating ME/CFS today?

Discussion in 'General ME/CFS News' started by richvank, Apr 4, 2012.

  1. Gavman

    Gavman Senior Member

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    Rich,

    I think one of the most effective tools that methylation seems to help with is balancing the neurochemicals, keeping mood stable and assisting in sleep. Balancing an out of balance system is very important. I do love the work you are doing, Richvank and definately like your open-minded approach.

    I seem to go quite hyper on the b12 and folic acid mix. And mostly benefit from b6, zinc and on the other side, tmg and l-methionine. As your approach tends to favor b12 and folic acid, might it be that mine is high and that this cycle is working, its the other cycles that are out on me. And might adding niacin be effective with this due to its ability to help balance adrenaline?

    Cheers,
    Gavin
     
  2. Don Quichotte

    Don Quichotte Don Quichotte

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    A possible explanation, in my opinion, for the lack of response or even worsening in some patients is that the low levels of glutathione are beneficial and the result of a beneficial oxidation reaction.

    changes in the red-ox potential is a regulatory mechanism, and as such it may be beneficial or detrimental depending on the circumstances.

    The same is true for methylation.

    Many excellent theories and even some which showed promising results in cell cultures , were eventually found to be too simplistic. The main reason for that is the complexity of the human body and regulation mechanisms, which involve complex and interlaced biochemical reactions that are orchestrated in a fascinating spatial and timely manner.

    Also, many times in medicine, correcting an abnormality without understanding the underlying mechanism, can have unwanted effects.

    An excellent example is TTP (thrombotic thrombocytopenic purpra).
    Patients with this disease may present with severe bleeding and their blood tests will show very low platelet counts. Yet, if you correct this by giving them platelets (as you would intuitively do) you are going to make them much worse. The reason for that is that their platelets are low because they have too much clotting (and not too little) so by giving them platelets you add fuel to the fire.

    That being said, many effective and even curative treatments were found empirically or with partial understanding of their mechanism.

    Possibly your (no doubt interesting) theory is correct in some patients, but not in others.

    The major questions regarding your treatment approach (as is true for every medical intervention) is how many patients benefit from it, how many are harmed from it, how significant is the benefit and does it justify the potential harm, is there any way in which you can know (or prevent/correct) the harm. And those answers in my opinion can only be given in some form of clinical trial (which could possibly be patient initiated).

    I believe that the main reason for the lack of significant progress, as yet, in the understanding of CFS is the complex nature of this disease, the large clinical variability (which probably also reflects biological variability) and abnormalities that are not usually seen (or at least not routinely tested for) in other diseases that are well known and relatively easy to diagnose.

    This combined with the (very wrong assumption) of many clinicians that normal or non-specific tests rule out a serious illness. And the other (very wrong assumption) that what we can not explain by our current understanding and knowledge, is due to "emotional problems". (which is a very poorly defined entity, that basically requires that a person would have emotions, in order to fit into it).

    I personally think that a better and more accurate clinical definition (and possibly sub-classification) of the disease and a development of a reliable clinical severity index score combined with a definition of clinical response is the first step.
     
    Tito and WillowJ like this.
  3. nanonug

    nanonug Senior Member

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    Are you really taking folic acid?
     
  4. richvank

    richvank Senior Member

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    ***Hi, Don.

    A possible explanation, in my opinion, for the lack of response or even worsening in some patients is that the low levels of glutathione are beneficial and the result of a beneficial oxidation reaction.

    changes in the red-ox potential is a regulatory mechanism, and as such it may be beneficial or detrimental depending on the circumstances.

    The same is true for methylation.

    ***I understand your point. This is the main issue between Dr. Cheney and myself concerning the treatment of ME/CFS, and has been for several years. It's certainly true that the body has built-in mechanisms for dealing with its problems by itself, and in many cases is able to heal itself. However, there are limits to what the body can deal with, as evidenced by chronic illnesses and death. The challenge is to determine whether something that is going on in the body is a built-in mechanism that is actually beneficial and is involved in healing or is a response to a disease that is helping to preserve life, but is not helping to achieve recovery. I agree that it is not always easy to tell, and that's why I have tried to develop a comprehensive hypothesis that encompasses what appear to be the causes as well as how the disorder develops and how the symptoms are produced. I think that if one has a thoroughgoing hypothesis that includes all of this, one has a better chance to understand what is a beneficial effect and what is not. But I agree that we need to intervene at the root cause and not downstream in the pathophysiology only. I do think that if we are treating at the root cause, downstream support in addition to this can be helpful, but the downstream support by itself will likely not bring recovery, and as you point out, can sometimes make things worse instead of better.

    Many excellent theories and even some which showed promising results in cell cultures , were eventually found to be too simplistic. The main reason for that is the complexity of the human body and regulation mechanisms, which involve complex and interlaced biochemical reactions that are orchestrated in a fascinating spatial and timely manner.

    ***I agree. I think that developing a comprehensive hypothesis that starts at the beginning, matches all the observables and is logically self-consistent and consistent with known biochemistry and physiology is the best way to make sure that we are not "coming in at the middle of the movie" so to speak.

    Also, many times in medicine, correcting an abnormality without understanding the underlying mechanism, can have unwanted effects.

    ***True.

    An excellent example is TTP (thrombotic thrombocytopenic purpra).
    Patients with this disease may present with severe bleeding and their blood tests will show very low platelet counts. Yet, if you correct this by giving them platelets (as you would intuitively do) you are going to make them much worse. The reason for that is that their platelets are low because they have too much clotting (and not too little) so by giving them platelets you add fuel to the fire.

    ***Definitely bad news.

    That being said, many effective and even curative treatments were found empirically or with partial understanding of their mechanism.

    ***True, but I prefer trying to understand the whole picture before figuring out how to treat, rather than just hoping to get lucky. Of course, that's not easy.

    Possibly your (no doubt interesting) theory is correct in some patients, but not in others.

    ***I think that's true. That's why I recommend that people run the methylation pathways panel before trying the treatment, to see if the GD-MCB hypothesis does in fact fit their case.
    So far, for people who meet the case definitions for ME/CFS, very few turn out not to have a partial methylation cycle block and glutathione depletion.

    The major questions regarding your treatment approach (as is true for every medical intervention) is how many patients benefit from it, how many are harmed from it, how significant is the benefit and does it justify the potential harm, is there any way in which you can know (or prevent/correct) the harm. And those answers in my opinion can only be given in some form of clinical trial (which could possibly be patient initiated).

    ***Very true. We have been able to do only a simple open-label clnical trial so far. The report on it is here:

    http://www.mecfs-vic.org.au/sites/w...Article-2009VanKonynenburg-TrtMethylStudy.pdf

    ***It would of course be wonderful to have the results of a full-blown randomized, double-blind, placebo-controlled, statistically significant clinical trial with objective outcome measures, but that costs money and needs the right setting. In the meantime, about two-thirds of the people in the small clinical trial did report significant benefit, and the lab testing indicated that the treatment did improve the status of methylation and glutathione.

    I believe that the main reason for the lack of significant progress, as yet, in the understanding of CFS is the complex nature of this disease, the large clinical variability (which probably also reflects biological variability) and abnormalities that are not usually seen (or at least not routinely tested for) in other diseases that are well known and relatively easy to diagnose.

    ***These definitely do make it challenging!

    This combined with the (very wrong assumption) of many clinicians that normal or non-specific tests rule out a serious illness. And the other (very wrong assumption) that what we can not explain by our current understanding and knowledge, is due to "emotional problems". (which is a very poorly defined entity, that basically requires that a person would have emotions, in order to fit into it).

    ***Yes, these do muddy the waters!

    I personally think that a better and more accurate clinical definition (and possibly sub-classification) of the disease and a development of a reliable clinical severity index score combined with a definition of clinical response is the first step.

    ***I agree that better definition would help. I have suggested that the methylation pathways panel be used as a diagnostic. I agree that objective measures of clinical response would also help a lot (such as actimetry, cardiopulmonary exercise testing (though it's kind of brutal for PWMEs), sleep monitoring with a pulse oximeter, dolimetry for pain threshold monitoring, neuropsychological testing for brain function, immune system testing, such as by cytokine measurements, and HPA axis testing, such as 24-hour saliva cortisol testing).

    ***I don't know if you would be interested in looking into the GD-MCB hypothesis in more detail, but if so, there is a video and a set of slides (blue print below the video) available here:

    http://iaomt.media.fnf.nu/2/skovde_2011_me_kroniskt_trotthetssyndrom/$%7Bweburl%7D

    ***Thank you for your comments.

    ***Best regards,

    ***Rich
     
    WillowJ likes this.
  5. richvank

    richvank Senior Member

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    Hi, Gavman.

    Thanks for your response. I'm sorry that the B12 and (I presume you mean the reduced folates rather than folic acid) make you hyper. This could be due to excitotoxicity. A lot of people
    have reported symptoms like feeling hyper or wired or nervous, having insomnia, and/or having anxiety. These can be caused by excitotoxicity. I continue to work on finding treatments that will help with this.

    With regard to zinc and B6, these can be depleted in HPU, which some PWMEs seem to have, and if so, they need to be supplemented before the methylation cycle can operate normally.
    TMG helps to activate the BHMT pathway in the liver and kidneys, which is the alternate methylation pathway. That can help to build up SAMe initially, but ultimately it is necessary to get methionine synthase up and running properly. Methionine is important because it is the feed material for the methylation cycle, and many PWMEs are low in it, because their sulfur metabolism has drained out and been excreted, owing to the partial block in methionine synthase. Niacin can also be deficient, and when it is, too much of the tryptophan is diverted into making niacin, so that not enough goes into making serotonin.

    If it's feasible to do lab testing to see if there are deficiencies in the supporting nutrients, that can be very helpful. Otherwise, it's kind of a hit-or-miss process to figure out what to supplement.

    Thanks again.

    Best regards,

    Rich
     
  6. caledonia

    caledonia

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    Rich,
    What lab tests would you suggest?
     
  7. kiteman

    kiteman

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    Hi Rich,

    I have been reading some of your theories with great interest. I recently had a test done for Urinary Kryptopyrrol (HPU) and it showed that it was elevated , normal range 0 - 200 ng/ml and mine was 395.870 ng/ml. I have been supplementing with Zinc , Selenium, Cortico B5 B6 (metagenics) and now need to introduce non flush niacin. 2 weeks ago i was to take 2 tablets of Spirulina and 2 tablets of Chlorella twice a day - this caused me to get very bad muscle pain throughout my body to the point that even my intestines were aching. I have now stopped taking the chlorella and spiralina and after a few days the muscle pain has almost gone, it seems i was having some sort of reaction to these supplements. I have been considering trying your treatment to see if i can get some improvement, I am just worried about having the same sort of reaction as i did to the spiralina and chlorella. In the past i have been very sensitive to taking B Vitimans. I noticed that you mentioned Glutamine in a previous post - this is the one thing that did help me with regards to energy. If i did excercie i would normally need to replace with a lot of food afterwards as i felt drained, but when i introduced L-Glutamine i didn't get that energy dump directly afterwards and felt that my body was functioning a lot better. One last question what are your views on supplementing with Reduced Glutathione as i read an article about Recancostat and was wondering if this is at all beneficial ? Please excuse the spelling.
     
  8. Don Quichotte

    Don Quichotte Don Quichotte

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    Hi Rich,

    Thanks for your reply.

    No doubt that the major advantage of studies like yours is that there are no hidden conflicts of interest, and it is clear that you are only interested in truly gaining a better understanding of this illness and finding the optimal management approach.

    I think this is important, because unfortunately this is not so for many clinical studies nowadays, which are driven by egos, academic achievements and other clearly obvious or hidden profits.

    At the same time such studies are more prone to a placebo effect. So, mostly measuring relatively vague subjective clinical parameters is problematic.

    The objective biochemical parameters that have changed are mostly what you would expect in someone receiving a large dose of those nutrients, regardless if this has a beneficial clinical effect or not.
    It would be the equivalent of measuring a drug level in the blood, as evidence of clinical response.

    There are clinical situations in which gluthathione depletion is beneficial, even if it carries a price. For example:

    http://www.ncbi.nlm.nih.gov/pubmed/18574029

    http://www.ncbi.nlm.nih.gov/pubmed/22215096

    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2643723/

    Or in other words gluthathione depletion may be a marker of another process, such as fighting a viral infection or even a malignant process.

    I am not saying that this is the case, but this possibility should be taken into account.
    Correcting the gluthathione depletion in such a patient, may be equivalent to giving platelets to a patient with TTP.

    Red-ox regulation is a very complex and not yet well-understood process which is important in numerous cellular functions both in normal and malignant cells.

    No doubt that diseases happen when our normal healing processes have failed, no doubt that there are effective treatments that can enable the body restore the impaired function or altered repair mechanisms.
    At the same time diseases make us much more vulnerable to further insults and what may initially seem beneficial may in fact be detrimental. Or what is beneficial in one person may not be so in another with a very similar illness.

    I think that your thoughts and ideas are definitely worth perusing. I think that there is quite a lot of proof in your data that altered red-ox regulation is significant in this illness.

    I was also impressed in another post of yours by the fact that you are one of the few who seriously addressed the relatively low CO2 levels seen in some patients and did not attribute it to the ridiculous explanation of "hyperventilation/anxiety" (this is by the way a good example of how errors can be made when lab values are interpreted without understanding the complexity of the process causing them).

    I hope you see my suggestions and comments as constructive criticism.
    As I have said I have found your work very interesting and thought provoking.
     
  9. richvank

    richvank Senior Member

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    Hi, Caledonia.

    There are two approaches to this. One is to do direct measurements of the concentrations of the various supporting nutrients (in most cases in the blood, but the EXAtest from Intracellular Diagnostics, Inc. on cells swabbed from the mouth is best for magnesium), and the other is to do a set of biochemical tests to get an overall picture of the function of the metabolism. In the first category, Health Diagnostics and Research Institute (formerly Vitamin Diagnostics, Inc.) in New Jersey offers tests for the whole range of vitamins, essential elements and amino acids, and some other labs offer some of these tests, also. In the second category, combined panels such as the Metametrix ION profile with 40 plasma amino acids and the Genova Diagnostics NutrEval Profile can be very helpful. They can be ordered from some physicians, or can be obtained without a doctor's order from www.directlabs.com.

    Best regards,

    Rich
     
  10. richvank

    richvank Senior Member

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    Hi, kiteman.

    Sounds like testing for HPU was a good idea in your case. As I understand it, manganese and biotin are two other nutrients that are depleted in HPU.

    I'm sorry to hear about your reaction to spirulina and chlorella, but glad it seems to be clearing up after stopping them.

    It's true that most people who do the methylation treatment do have some symptom exacerbation at first, and I encourage starting low and slow to see how it goes.

    I'm glad that you responded well to glutamine. Some people do well with this, and others don't tolerate it, presumably because too much gets converted to glutamate and doesn't get recycled properly. When it is tolerated, it is helpful particularly for the gut and for the lymphocytes of the immune system.

    Oral reduced glutathione hasn't been very helpful in ME/CFS. Most of it is broken down in the gut. It probably does help the cells lining the gut, and some of the amino acids must get to the liver, and that is probably somewhat helpful, but this approach does not raised glutathione levels in the cells of the body in general. Lifting the partial methylation cycle block has been the most effective way to do that. Acetyl glutathione and liposomal glutathione are probably able to do that, too, but probably only on a temporary basis.

    Best regards,

    Rich
     
  11. richvank

    richvank Senior Member

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    ***Hi, Don.

    Thanks for your reply.

    ***Likewise!

    No doubt that the major advantage of studies like yours is that there are no hidden conflicts of interest, and it is clear that you are only interested in truly gaining a better understanding of this illness and finding the optimal management approach.

    I think this is important, because unfortunately this is not so for many clinical studies nowadays, which are driven by egos, academic achievements and other clearly obvious or hidden profits.

    ***Well, I'm human, and I'm sure I have an ego, too, but I do try to focus on the objective.

    At the same time such studies are more prone to a placebo effect. So, mostly measuring relatively vague subjective clinical parameters is problematic.

    ***True.

    The objective biochemical parameters that have changed are mostly what you would expect in someone receiving a large dose of those nutrients, regardless if this has a beneficial clinical effect or not.
    It would be the equivalent of measuring a drug level in the blood, as evidence of clinical response.

    ***Well, we did measure methylfolate, and that was part of the treatment, so yes, that would be like measuring a drug that you are giving. However, we also measured SAMe and glutathione. The focus of the treatment was on lifting the activity of methionine synthase, which appears to have happened, but seeing glutathione come up when we weren't supplementing it directly (other than a pretty small dosage of NAC) does go a bit beyond what you would expect to happen directly.

    I understand your point. This is the main issue between Dr. Cheney and myself concerning the treatment of ME/CFS, and has been for several years. It's certainly true that the body has built-in mechanisms for dealing with its problems by itself, and in many cases is able to heal itself. However, there are limits to what the body can deal with, as evidenced by chronic illnesses and death.
    There are clinical situations in which gluthathione depletion is beneficial, even if it carries a price. For example:

    http://www.ncbi.nlm.nih.gov/pubmed/18574029

    http://www.ncbi.nlm.nih.gov/pubmed/22215096

    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2643723/

    ***Right. Note, though, that all three of these examples involved interaction of glutathione with chemotherapy agents.

    Or in other words gluthathione depletion may be a marker of another process, such as fighting a viral infection or even a malignant process.

    ***I agree that the viral infections lower glutathione. They are definitely a factor in ME/CFS, and they do place demands on glutathione. The herpes family benefits by glutathione depletion, in terms of being able to form disulfide bonds in their glycoprotein B. But if glutathione can be brought back up, these viruses cannot propagate. We do have to watch for malignancies. I have found what I think was one of them. The 10-formyl tetrahydrofolate on the methylation pathways panel is a marker for cancer. Cancer cells raise it by shutting down the enzyme that normally catabolizes it, in order to be able to make purines faster, so that they can carry out cell division faster.

    I am not saying that this is the case, but this possibility should be taken into account.
    Correcting the gluthathione depletion in such a patient, may be equivalent to giving platelets to a patient with TTP.

    ***As I say, so far I've seen only one case that looked like cancer was involved, but I agree that it's important to be on the lookout for that. I think it's still debatable whether antioxidant treatment during chemotherapy or radiation treatment for cancer is beneficial or detrimental. When I had these treatments for colorectal cancer, I took a hefty nutritional supplement formula that was rich in antioxidants, including NAC to make glutathione. My oncologists thought it was O.K., and my N=1 study in this case came out well! :)-) (We also prayed a lot!)

    Red-ox regulation is a very complex and not yet well-understood process which is important in numerous cellular functions both in normal and malignant cells.

    ***True.

    No doubt that diseases happen when our normal healing processes have failed, no doubt that there are effective treatments that can enable the body restore the impaired function or altered repair mechanisms.
    At the same time diseases make us much more vulnerable to further insults and what may initially seem beneficial may in fact be detrimental. Or what is beneficial in one person may not be so in another with a very similar illness.

    I think that your thoughts and ideas are definitely worth perusing.

    ***I appreciate that!

    I think that there is quite a lot of proof in your data that altered red-ox regulation is significant in this illness.

    ***Yes, and there are now a large number of published studies showing oxidative stress in ME/CFS.

    I was also impressed in another post of yours by the fact that you are one of the few who seriously addressed the relatively low CO2 levels seen in some patients and did not attribute it to the ridiculous explanation of "hyperventilation/anxiety" (this is by the way a good example of how errors can be made when lab values are interpreted without understanding the complexity of the process causing them).

    ***I'm glad you liked that.

    I hope you see my suggestions and comments as constructive criticism.

    ***Yes, I do, and I appreciate your making the effort to give them to me.

    As I have said I have found your work very interesting and thought provoking.

    ***I find your comments the same!

    ***Best regards,

    ***Rich
     
  12. Little Bluestem

    Little Bluestem Senescent on the Illinois prairie, USA

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    I know I am speaking out if my class here, but I found this interesting. The gluthathione depletion may have been "worth it" when my body was fighting the sledgehammer virus 26 years ago, but I am sceptical that it still is today.
     
  13. alex3619

    alex3619 Senior Member

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    A little philosophy of mine in response to Rich's good comments on asking the right questions:

    A good answer to a poor question might tell you something but its not very useful.

    A poor answer to a good question is at least a step toward really understanding things.

    Questions are the key to good science and understanding. Good questions eventually lead to very useful answers. Bad questions can head the research toward dogma - like BPS/CBT/GET.

    I am still not convinced the methylation issues are causal, but its very probable they drive at least some of our symptoms. Over time I hope to see more of it mapped out and the model integrated into others. We are all blind people describing the elephant, we all describe the bit we feel and so it sounds different from different sources. Of course there is no guarantee we are all studying the same elephant either.

    In particular if the Rituximab studies are fully validated over time and lead to complete remissions, then all models are going to have to explain how all the symptoms are mediated by B cell activity.

    Bye, Alex
     
  14. richvank

    richvank Senior Member

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    Hi, Alex.

    Thanks for the philosophy!

    Best regards,

    Rich
     
  15. lampkld2

    lampkld2

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    Hi Rich,

    Thanks for your excellent (As always) and encouraging thoughts!

    Just another thing to add to your initial post (sorry, did not read through the thread).

    Another issue people face with opening back up the methylation cycle is increased inflammation. In some with autoimmune disorders, specific or not, it becomes too much to handle.

    Do we know the mechanism for this?

    MTHFR.net remarks on this phenomenon that I and others have experienced. He reccomends liposomal curcumin, but I see that as just a stopgap that some cannot tolerate.

    Lamp
     
  16. richvank

    richvank Senior Member

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    Hi, Lamp.

    One of the first adverse effect cases that surfaced in July, 2007 involved a person who had a history of autoimmune disorders. Apparently lifting the partial methylation cycle block and raising the folates and glutathione activated the immune system is a way that was not helpful. She developed autoimmune scleritis and had to have steroid drops for her eye.

    We do know that ME/CFS involves a shift to the Th2 immune response. It's likely that methylation treatment raises the Th1 response. I know that some autoimmune conditions do involve Th1, so that may be the explanation.

    Best regards,

    Rich
     
  17. lnester7

    lnester7 Seven

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    Too much b12

    Rich,

    I can feel the difference on B12 (love it) but my Dr asked me to stopped because it was b12 levels were too high (3,000). So how does one break the block if b12 keep increasing when supplementing? or does it mean I have no block??

    Currently taking: coq10 200mg twice a day, Vit C 2,000/d, Fish Oil 4,000 /day, Imunovir + equillibrant.

    Viral reactivation: ParvoVirus, Coaksakie, Roseola.
    b cells results: 21 Range: 8-18 High
    NK CD3-CD56+ results:1.27 Range: 5-16 Low
    CD5+ results:67 Range: 68-82 Low
    CD5+CD19+ results:0.78 Range: 1-9 Low
    CD8+CD95+ results:1.46 ..

    Thank you,
    7
     
    K2 for Hope likes this.
  18. nanonug

    nanonug Senior Member

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    Do you not take a multivitamin with all the B's? The B's all need each other to work properly. In particular, you may need plenty of methylfolate. And if your body is in a state of oxidative stress, all that B12 in your blood stream could all be oxidised and essentially useless. In this latter case, it would probably be appropriate to raise glutathione levels.
     
  19. lnester7

    lnester7 Seven

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    I used from fatigue to fantastic powder, has all Bs in it. But problem started when I tried to do the simplified protocol, I started the methylfolate and folic acid or one of the other bottles when I was asked to stop. How does one raise glutathione levels without using B vitamins????
     
  20. lampkld2

    lampkld2

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    Rich,

    Thank you for your reply.

    This is actually what I suspected!

    I seem to get worse on other TH1 stimulants (Zinc, Vit E).

    The problem is, when I take TH2 stimulants to balance this TH1 dominance out, I get sick ( Tonsils hurt). I got a tonsilectomy, so I will be trying the immune modulation again with the hope that whatever pathogen is keeping me TH1 shifted, was localized to the tonsils. (may do an antiviral trial first)

    Perhaps those that experience excessive TH1 flareup after starting the protocol can try to take TH2 shifters to balance it out? (curcuming, quercitan, vit a, GSE, Resveratrol etc).

    Another question is this: Is this TH1 shift permanent/ a "feature", or just a temporary hump that one has to get through in the beggining untill the body achieves homeostasis?
     

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