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Mitochondrial damage and viral infection different symptoms in different people

Discussion in 'General ME/CFS News' started by Gerwyn, Apr 17, 2010.

  1. WillowJ

    WillowJ Senior Member

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    most fascinating, Rich. Thanks for explaining. I knew not to take the Vermeulen et al. study seriously, but I didn't know all the reasons why not. :cool::cool:

    Willow
     
  2. richvank

    richvank Senior Member

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    Hi, Cort, Willow and the group.

    I just received word from Dr. Howard that he and Dr. Booth have been working on a "structured reply" to the Vermeulen et al. paper. He said that they agree with most of my concerns, but also have some of their own. He also said that he also thinks that there are some things that can be learned from this paper, though, particularly concerning oxygen utilization. I'll be interested to read their "structured reply." I presume that they will send it to the journal that published the Vermeulen et al. paper.

    Best regards,

    Rich
     
  3. surfbh

    surfbh

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    I've read several studies where most CFS/FM sufferers are iron deficient. I also read that iron deficiency is very common in hypothyroidism. I have high TSH and T4 that is a tenth over the low cutoff. I found that iron is responsible for activating the enzyme that makes T4 from iodine and tyrosine. I know I am iodine sufficient, I have been taking 1-2 iodoral for at least 6 months + sometimes lugol's and lugol's off and on for several years. I also take tyrosine everyday. Anyways, after researching Iron and finding a safe form I bought Source Naturals Advanced Ferrochel. 45 minutes after taking the first one, my energy skyrocketed. Same for my wife. I no longer have cold hands or feet and we both are waking up at night hot. This is unusual. This tells me that our T4 is most likely rising. Also my never ending flatulence is 90% gone, after years. It has only been a few days and this has happened. It usually takes weeks for energy levels to rise from iron supplementation. Oh, and of course the standard iron tests are worthless unless you are severely anemic. Iron storage aka ferritin levels need to be checked. I also read that 30% of the world is deficient and women are WAY more likely to be than men. Since iron is partially responsible for making blood cells and them holding oxygen I thought this would be relavent here. Ferrochel is an extremely safe form of Iron and quite cheap, wouldn't hurt to try it and see if your energy levels increase.
     
  4. Cort

    Cort Phoenix Rising Founder

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    Thanks Rich, I look forward to the reply and reading the rest of your reply but about this

    Can you really say for sure that diastolic dysfunction is caused by insufficient ATP production?

    Why not fibrous areas in the heart muscle? How about improper signaling from the nervous system? Or ??? Are you sure that ATP production is at cause here?
     
  5. Cort

    Cort Phoenix Rising Founder

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    This is from Wikipedia on pulse oximetry. I could be way off but I thought I put this out. The problem is that I don't really trust Cheney!

     
  6. richvank

    richvank Senior Member

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    Hi, Cort.

    I can’t say that a low ATP production rate by the heart muscle cell mitochondria is scientifically proven as the cause of diastolic dysfunction in ME/CFS. However, I do currently think it is the most likely explanation. Here is why I believe this:

    1. I think it is generally agreed that oxidative stress is present in CFS. There are quite a few studies that reach this conclusion. I think it is about the best established feature of the abnormal biochemistry of CFS. I have also seen evidence for it in lab test results that I have received from many PWCs over the past few years.

    2. Because the balance between reduced and oxidized glutathione normally maintains the redox potential inside the cells, it is to be expected that this balance will be shifted toward the oxidized form when oxidative stress is present, and this is observed in CFS. You and I have discussed the published data on glutathione in CFS in the past, and I have discussed the reasons why the published results in some cases do not support this expectation. The main reason is that the published results usually report measurement of whole blood or red blood cell total glutathione, and this does not reflect muscle tissue cell glutathione levels well, because the red blood cells are normally net producers and exporters of glutathione, while the muscle cells are net users. These measurements also do not distinguish between reduced and oxidized glutathione. The red blood cells are able to maintain their total glutathione levels in the early phase of CFS, because of their ability to produce it. In more serious cases, however, the red blood cell levels also drop, and I have seen quite a few lab test results from Acumen Lab that demonstrate this. The Health Diagnostics methylation pathways panel measures reduced and oxidized glutathione in the blood plasma, which is more difficult to do, because the concentrations are about a factor of a thousand lower, but these levels are more reflective of tissue cell levels, because they represent levels in the concentration gradient at a point lying between the sources (red blood cells and the liver) and the sinks (muscle tissue and other net users of glutathione), and they do correspond to what would be expected in the presence of oxidative stress. I have seen hundreds of these results now.

    3. Although there have not been many publications about it, I have seen evidence in lab tests from many PWCs that the body burdens of toxins, including the heavy metals, are elevated. I think there is abundant experience from individual PWCs that supports this.

    4. It is well established that oxidative stress, glutathione ratios shifted toward the oxidizing side, and elevated toxin concentrations have deleterious effects on the ability of the mitochondria to produce ATP. This constitutes mitochondrial dysfunction, and it would therefore be expected to occur in CFS, given these observed biochemical abnormalities.

    5. In the heart muscle as well as the skeletal muscles, ATP is used during the phase when the muscle relaxes, both to pump calcium back into the sarcoplasmic reticulum, and to “cock” the muscle fibers so that they are ready to contract when they receive the signal to do so. The diastolic phase of the heart’s cycle is the phase during which muscle relaxation occurs. There is a limited time during which this is allowed to occur, because the heart must continue beating to preserve life. If insufficient ATP is available during this brief time interval, the heart muscle’s relaxation, and hence the filling of the left ventricle with blood, will be lower than normal. This constitutes diastolic dysfunction.

    6. Thus, my first argument in support of mito dysfunction causing the diastolic dysfunction in CFS is that it flows naturally from what we know about the biochemistry of this disorder.

    7. My second argument is that in CFS we see both skeletal muscle deficit (physical fatigue) and heart muscle deficit (diastolic dysfunction). Both can be explained by mitochondrial dysfunction, and both would be expected, given the biochemical abnormalities. Thus, this hypothesis would conform to an Ockham’s razor approach to hypothesis development. While this is not a hard and fast requirement for hypothesis development, it is usually a good guide.

    8. Beyond these arguments, I think that it’s helpful to examine other possible hypotheses, such as the two you’ve suggested. First, fibrosis in the heart muscle. It’s true that in some diseases, such as multiple myeloma and sarcoidosis, this has been found. However, if the heart muscle is fibrotic, I think we would expect fibrosis elsewhere as well, and there is no evidence for this in CFS. In addition, if the muscle were fibrotic, I would expect that its response during the systolic phase would be affected as well, and this should show up as a lowered ejection fraction. According to Dr. Cheney, he does not observe this, and in fact, he often sees an elevated ejection fraction in PWCs, which he interprets as the sympathetic nervous system attempting to compensate for the low blood volume in the ventricle as a result of the diastolic dysfunction, by squeezing it harder, to put out more blood, i.e. to raise the stroke volume.

    9. You also suggested improper signaling by the nervous system as a possible cause of diastolic dysfunction. If this were the case, I would expect that it could be seen on the electrocardiogram as lower intensity signals or other abnormalities in the PR segment. Although other abnormalities in the EKGs of PWCs have been reported (oscillating or flattened T waves by Dr. Lerner, and shortened QT interval by Naschitz et al.) I have not seen any reports of abnormalities in the PR segment. Thus, it does not appear that improper signaling by the nervous system can be the cause of the diastolic dysfunction in CFS. (Note that the IVRT, which Dr. Cheney reports to be increased, represents a small part of the QT interval, which Naschitz et al. find to be decreased in CFS, so these observations are not in conflict.)

    10. It would be very nice to have data for IVRT before and after the methylation treatment, which corrects the oxidative stress, and also causes excretion of toxins, but so far, we don’t have any. I think Dr. Cheney is the only one measuring this parameter in CFS, and so far he has not bought into my hypothesis, although recently he suggested that correcting the methylation deficit may help to silence the expression of the genes for the retroviruses, which he is taking seriously. So maybe some day we will have this type of data.

    In summary, no, I can’t say that it is proven that mitochondrial dysfunction is responsible for the diastolic dysfunction reported in CFS, but it does seem to me to be the most likely cause. I use what are called a “systems approach” in engineering and “gedanken” experiments in physics to the development of hypotheses. I realize that this approach has not been commonly used in the biomedical sciences in the past, and I think the reason is that they are relatively young sciences. However, in my opinion there is now a large enough body of knowledge in these fields that these approaches can be productively used in them now, too.

    In the “systems approach” one looks at the whole system from start to finish, and develops a hypothesis with a cause and effect tree that is self-consistent, agrees with all of what is accepted as “known” science, and also agrees with all the observables in the system that is being studied. Even though there are not enough observed data to test every step of the hypothesis, if it agrees at the observable “peg points” that are available and is self-consistent in its logic, then the unproven parts can be “bridged” temporarily, and it can be viewed as a good working hypothesis, subject of course to additional testing as new observed data become available. Using such an approach, it is possible to make faster advances in understanding than one can make using the older reductionist approach, which takes only one step at a time. (I see this as being analogous to the difference between trench warfare, as used in WW I, and General Patton’s tank assaults, as used in WW II.) The important thing is to acknowledge, of course, that one is still dealing with an unproven hypothesis, and I do acknowledge that. I’m sorry if I do not always make that clear in my posts. However, I do think that the GD-MCB hypothesis, of which mitochondrial dysfunction is a part, is the only one that has been offered that has the capability of explaining all the observed abnormalities and symptoms of CFS in a logical and straightforward manner, with a minimum of “hand-waving” arguments. It is also capable of meshing well with the retrovirus involvement, if this is shown to be present, since methylation suppresses viral expression, and glutathione depletion inhibits the cell-mediated immune response that is needed to combat viral infections in general. Thus, this hypothesis could incorporate the retrovirus infections as either causes or effects, depending on what is learned by future research.

    Best regards,

    Rich
     
  7. richvank

    richvank Senior Member

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    ***Hi, Cort.

    ***My responses are at the asterisks below:

    This is from Wikipedia on pulse oximetry. I could be way off but I thought I put this out.

    ***Great. I think it’s good information.

    The problem is that I don't really trust Cheney!

    ***I’m sorry about this. Of course, everyone has to make their own judgments about whom to trust. For what it’s worth, I believe that Dr. Cheney is an honest person, and that he tries to report his observations accurately. Of course, like all of us, he is subject to making errors in his measurements, and that’s why it’s helpful for the scientific community to review the methods used and to see if the results can be duplicated. I realize that Dr. Cheney has not been publishing his results in peer reviewed journals in recent years, but he does interact with other researchers and clinicians. The scarcity of research funding for CFS has made replication of results difficult, but perhaps this is changing. When it comes to interpretation of his observations, I do not always agree with Dr. Cheney, and have shared my differing views with him many times. He has also noted publicly that he does not agree with all of my hypotheses, and I think that is a healthy situation, because we are both still trying to establish what is true.

    Pulse oximetry data is necessary whenever a patient's oxygenation may be unstable, as in intensive care, critical care, and emergency department areas of a hospital. Data can also be obtained from pilots in unpressurized aircraft,[2] and for assessment of any patient's oxygenation in primary care. A patient's need for oxygen is essential to life; no human life thrives in the absence of oxygen (cellular or gross). Although pulse oximetry is used to monitor oxygenation, it cannot determine the metabolism of oxygen, or the amount of oxygen being used by a patient.

    ***This is true. Single, one-time pulse oximetry measurements (without breath holding, which Dr. Cheney does) will only tell to what degree the hemoglobin that is in the arterial blood is saturated with oxygen. However, if pulse oximetry is done continuously during breath holding, it will give an indication of oxygen utilization by the body, because during breath holding, no new oxygen is added to the blood. Therefore the rate at which the degree of oxygen saturation drops is a measure of how rapidly the cells are using it.

    Pulse oximetry measures solely of oxygenation, not ventilation, and it is not a substitute for blood gases checked in a laboratory because it gives no indication of base deficit, carbon dioxide levels, blood pH, or bicarbonate HCO3- concentration. The metabolism of oxygen can be readily measured by monitoring expired CO2.

    ***This is also true. I’m aware of one published paper reporting measurement of ventilation in CFS, and it was found to be normal. Dr. Cheney has also carried out blood gases measurements on CFS patients.



    Oximetry is not a complete measure of respiratory sufficiency. A patient suffering from hypoventilation (poor gas exchange in the lungs) given 100% oxygen can have excellent blood oxygen levels while still suffering from respiratory acidosis due to excessive carbon dioxide.

    ***This is also true. Poor respiratory sufficiency does not appear to be a problem in most CFS patients, however. In most cases of CFS, the lungs are working well.

    It is also not a complete measure of circulatory sufficiency. If there is insufficient bloodflow or insufficient hemoglobin in the blood (anemia), tissues can suffer hypoxia despite high oxygen saturation in the blood that does arrive.

    ***This is a relevant point in CFS. Anemia is usually not present, in the sense that complete blood counts usually do not show low hemoglobin or low red blood cell count. However, complete blood counts look only at these values on the basis of per unit volume of blood. It is known from the late Dr. Streeten’s work that many people with CFS have low total blood volume. I have suggested that this results from diabetes insipidus (not the same as diabetes mellitus), which appears to be present in many PWCs. Basically, because of insufficient secretion of antidiuretic hormone (observed), too much water is excreted in the urine, lowering the total blood volume. Apparently the kidneys adjust their secretion of erythropoietin to keep the red blood cell count normal in the presence of this diuresis. If they didn’t, the blood viscosity would rise, which would be problematic, but this is not observed.

    ***Dr. Peckerman and Dr. Cheney have also reported low cardiac output in PWCs. Both low total blood volume and low cardiac output could cause a deficit in oxygen delivery to the cells, even though the hemoglobin that is present was sufficiently saturated with oxygen. That’s why it’s important to measure both arterial and venous blood gases levels, and to look particularly at the venous oxygen level. Dr. Cheney has done this. He finds that in PWCs, the venous oxygen level is lower than normal. This suggests that the cells are drawing down the blood oxygen level more than normal, which does suggest that the low blood volume and/or low cardiac output may be causing insufficient delivery of blood to the cells.

    ***However, when Dr. Cheney gives supplemental oxygen to PWCs, he finds that they go into severe hypoventilation, and some stop breathing entirely, and their IVRT increases, which represents more severe diastolic dysfunction. This does not occur in healthy, normal people when given supplemental oxygen. He refers to this as oxygen toxicity in PWCs. This suggests that even though the blood may not be delivering enough oxygen to the cells, if the oxygen supply is increased too much, the respiratory center in the brain lowers the rate and depth of breathing. My interpretation of what is going on here is that the additional oxygen worsens the state of oxidative stress in the mitochondria of the body’s cells, and this causes more severe mitochondrial dysfunction, which further lowers the carbon dioxide production of the mitochondria. Since the respiratory center responds to the carbon dioxide level in the blood, when the CO2 level goes lower, the respiratory center lowers the rate and depth of breathing.

    ***So what do I conclude from all of this? Well, I think that when all the observed data are considered, there is evidence for both mitochondrial dysfunction and for lower than normal capacity for oxygen delivery to the cells. However, the mitochondrial dysfunction appears to be the dominant effect. In my view, if the mito dysfunction is corrected by lifting the partial methylation cycle block, which in turn causes glutathione levels to return to normal, the diastolic dysfunction will also be corrected, as will the insufficient secretion of antidiuretic hormone. The result will be restoration of normal cardiac output and total blood volume.

    ***I will grant you that this is a hypothesis that is not completely proven at this point, but I believe that it is logically consistent and that it is also consistent with the clinical observations. I look forward to the day when we have enough data to test it more completely.

    ***Best regards,

    ***Rich
     
  8. serg1942

    serg1942 Senior Member

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    Thanks so much Cort for your pertinent questions, and Rich, thanks a lot for your so detailed and comprehensive replies!

    I look forward to read Dr. Howard's response to Vermeulen paper, if this finally happens!

    Rich, let me take the advantage to ask you something, a bit off-topic:

    As I have told you a few times in the past, it seems incredible to me that a theory so well designed and built (GD-MCB theory), that is able to incorporate almost everything --even the new discoveries!--, from a Hg poisoning to a retrovirus infection in order to explain CFS, is not giving the expected results when brought to practice...On paper it is utterly brilliant, so, what occurs in practice?

    Which are in your opinion the most feasible "pitfalls" where the body is not able to recover and repair on its own, as it should do in theory?

    From your scientific and very knowledgeable perspective on CFS, do you think we can be missing some essential things to decipher the CFS puzzle, or could it be more a matter of finding the right order for the known pieces?

    Thanks in advance and best wishes,
    Sergio
     
  9. richvank

    richvank Senior Member

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    Hi, Sergio.

    Thank you for your kind comments. With regard to why treatment based on this hypothesis does not bring all PWCs to full recovery, let me start with what I wrote last July. which you probably already read:

    "About two-thirds of the people report that the treatment gives them significant benefit, but only a few have been brought to what seems like full recovery from it.

    "About a third of the people have reported either that they could not tolerate the treatments, or that they have not experienced any benefit from them.

    "Among those who have not been able to tolerate the treatments, it appears that excitotoxicity has been one of the main problems. This leads to insomnia, anxiety, hypersensitivity of the senses, and a constantly "wired" feeling.

    "In recent months I have been trying to understand how to improve this situation, and I want to share some more thoughts on that.

    "First, for the people who can tolerate the treatments but do not experience benefits from them, I suspect that the likely causes are that the methylation cycle and related pathways do not have all the nutrients they need to come back up to normal operation. These include amino acids (especially methionine, serine, glycine, glutamine, and cysteine), vitamins (especially the other B vitamins and vitamin C), and certain minerals (especially zinc, copper, magnesium, manganese, selenium and molybdenum). These deficiencies could be at least partly caused by dysfunction of the digestive system, and I think that there is a lot of potential in working to fix the gut problems. I think the biofilm treatments and Dr. de Meirleir's most recent gut work are things we should pay attention to here. I think the KPU or HPU that Dr. Klinghardt has emphasized comes in here, too, in some cases, depleting zinc, B6 and other nutrients.

    "For people who experience severe excitotoxicity and thus cannot tolerate the treatments, I suspect that this is caused by a temporary further depletion of glutathione as more of the homocysteine is converted back to methionine, and less is available for making cysteine and glutathione.

    "I recently read Dr. Amy's article on excitotoxicity in the publications section of her website. She has some interesting ideas there, and I think that her discussion of the metabolism of glutamate in the brain shows where the main cause of excitotoxicity on this type of treatment lies. Normally, glutamate is secreted by neurons into their synapse with other neurons, serving as an excitatory neurotransmitter. The astrocytes are then supposed to import the glutamate, convert it to glutamine, and send it back to the neurons to be converted to glutamate and to be used again as a neurotransmitter. But this importation and conversion requires energy in the form of ATP, and I think that's where the problem arises. If glutathione becomes more depleted, the mitochondria of the astrocytes will be less able to produce ATP at normal rates, because of the oxidative stress that will arise, partially blocking the Krebs cycle and the respiratory chain. So I think there is a good basis for suspecting that the temporary glutathione depletion that occurs when this treatment is used is what is responsible for the rise in excitotoxicity.

    "If this is true, then it would seem that boosting glutathione while doing the methylation cycle treatments would help this situation. There are lots of ways to try to do this. I know that some people have been nebulizing glutathione, and some have been using liposomal forms of glutathione. There are other ways as well. For people who can tolerate glutathione boosting, this may help to calm the excitotoxicity when doing methylation cycle treatments.

    "For people who have experienced some benefits, but have then plateaued and have not had much improvement for a long time, I suspect that the problem is that there are factors that are preventing glutathione from coming up, or are preventing the methylation cycle from coming up, or both. So far, the people in this situation who have repeated the methylation pathways panel offered by Health Diagnostics and Research Institute (formerly Vitamin Diagnostics) have reported that their results on this panel have still not normalized. That's why I suspect that something is preventing recovery of this part of the metabolism in these people.

    "So what is it? I think the major suspects are things known to deplete glutathione. These include mold toxins, Borrelia bacteria (Lyme disease), and heavy metals, such as mercury. We don't know yet about how important XMRV is in CFS, but this may also be a possibility.

    "If these factors are indeed holding down glutathione, then I suspect that they will need to be dealt with directly before the methylation cycle treatments will be successful in restoring the methylation cycle and the folate and glutathione levels.

    "I have just heard from Lisa (slayadragon) that when she and another person have dealt with other issues, including mold toxins, they have then found that the methylation treatments have been much more effective in helping them to detox. Again, I think this suggests that other impediments to raising glutathione may need to be dealt with first.

    "Along this same line, the women who were treated in the study that Dr. Neil Nathan and I carried out had already been treated for a variety of other issues before starting the methylation treatments. These issues included mold illness, Lyme disease, and heavy metal toxicity.

    "In addition, the people who have reported essentially complete recovery from these treatments have also reported that they did a number of other treatments beforehand, some of them being antiviral treatments.

    "So I think there are bits and pieces of evidence that support this line of thinking.

    "One other thing that occurs to me is that this may be a major difference between CFS in adults and autism in children. The children with autism are of course much younger, in general. This being the case, they have had much less time to accumulate toxins and infections than have the adults. They also don't have amalgam fillings in their baby teeth. The really young ones have probably not had as much possible exposure to tick bites as the adults. The point is that the adults (especially those who have been ill with CFS for many years) may have many more impediments to the success of these treatments than the young children with autism, and they may need more additional treatments to address them specifically."


    I think that the only thing I can think of to add is that perhaps the GD-MCB hypothesis does not extend far enough in time to describe everything that goes on in a person's body after they have developed the partial methylation cycle block, glutathione depletion, B12 hijacking, and draining of folate metabolites. I do think that this combination is the decisive thing in the development of CFS, but perhaps I should put more emphasis on what happens after that. For a person who has had CFS for an extended time, during which their defenses against oxidative stress, buildup of toxins, and infection with a variety of pathogens are deficient because of this combination, unfortunately a great deal more could happen. I am speculating here, because you have asked me what the pitfalls may be that the body might not be able to recover from on its own.

    Oxidative stress over time might produce accumulating damage to the mitochondria, much as is seen in normal ageing, but on a faster timescale. I have suggested to Dr. Cheney that one of the beneficial effects of stem cell therapy might be that the person is infused with cells that have "young" mitochondria. Normally, new mitochondria are formed from the previous ones, and if there is damage to the mitochondrial DNA, the new ones will also have this damage.

    Buildup of toxins over time might reach levels that are sufficiently high that the detox system itself is impaired, so that it cannot work down the backlog of toxins on its own. It is known that toxins can block enzymes, and the detox system depends on many enzymes to do its job. In this situation, additional measures to support detox, such as chelation, may be the answer.

    Buildup of pathogens may become great enough that even if the immune system is operating completely normally, it will not be able to conquer the pathogens by itself. Pathogens have ways of frustrating the immune system so that they can survive. In this situation, the answer may be to add antimicrobials, i.e. antibiotics, antivirals, and/or antifungals. And now with the prospect of retroviruses being involved in CFS, perhaps antiretrovirals or things like GcMAF and Nexavir, as Dr. de Meirleir is using, will be needed.

    I think it's possible that there could also be combined effects of oxidative stress, toxins and pathogens, so that they interact to produce more problems than each could by itself. I note that Amy Yasko has suggested that pathogens and metal toxins interact with each other.

    As you can see, all I can do is speculate about this at this point, and the answer may well be different for different PWCs, depending on what has accumulated in their bodies. I note that in the study that Dr. Nathan and I did on the methylation treatment, he added some additional individualized treatments after the initial uniform treatment for 6 months, which were based on testing for heavy metals, mold illness, and Lyme disease, and in a couple of cases the results were very good. So I think it may be that all PWCs share a common core pathogenesis initially, but then each individual may accumulate different toxins or pathogens, depending on what they are exposed to, after the vicious circle involving the partial methylation cycle block has been established.

    Again, I'm speculating here, based on the little evidence I have available. Maybe you have some thoughts on this.

    I still believe that the GD-MCB hypothesis is essentially valid, as far as it goes, but I may not have carried it far enough.



    Best regards,

    Rich
     
  10. serg1942

    serg1942 Senior Member

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    Hi Rich,

    Thanks for putting all this info together, and adding some new thoughts. I read very carefully this message of yours a few months ago. Let me give you my opinion on some things, as a patient who has followed most of these techniques without much success. This is just my impression, and I’d really like to know other’s.

    1- The lack of key nutrients:
    Those of us who were following the full Dr. Yasko's approach I think were covering this problem, by taking a good background of general supplementation, and also by satisfying the individual needs as shown by aminoacids and organic acids tests results. We (PWCs following this protocol for CFS) usually modified the protocol in those points you suggested (because of the differences between CFS and autism), like taking normal-high amount of protein and/or taking B6. However, my impression from PWCs who were or still are following this protocol, is that most of them improve to some extent, and then, they either plateau or became intolerant to the supplements.

    2- Accumulated toxins:
    This is for sure a problem, but in practice, the measures that should work (chelations, saunas, supplementation for the detox routes, etc.), are not giving the expected outcomes. I know better the mercury poisoning issue, and, to put this as an example, although it is very likely that Hg has been in many cases the trigger of CFS, most of people don’t improve by removing this toxic from the body…It’s clear that the damage is done, so the question would be: what’s the damage? Of course the chronic block on the methylation cycle would explain this, as would the accumulation of other toxins and chronic infections (or all of this together!).

    3- Damaged mitochondria and DNA: This is one of the main concerns many people have. If this were so decisive in determine the recovery from CFS, one should expect to see great recoveries in people who has not been sick for long. Although it is true that the later are the PWCs with best prognosis, it seems to me that after 2-3 years of disease, people response to treatment is quite similar to other patients who have being ill much more time…

    4- Chronic Infections:
    I remember you expressing your concern about this –especially for viruses that enter into the brain like HHV-6--. It is curios that XMRV is this kind of viruses, and that it is so dependent on methylation. However, I cannot avoid to compare it with HIV in AIDS, where, it seems that it is not as simple as “VIH=AIDS”, in the sense that it could be necessary a predisposed body (depressed immune system, low selenium…) in order for the body to be chronically infected. In this sense, we’d need to treat the infections together with the rest of the issues…

    In sum, I agree with you in all the points, and I really hope XMRV (or other MLVs) is the key for many of us who don’t improve with the therapies that should work on paper…This is why I am going to focus on it as well as on restoring the methylation cycle, and hopefully, if I recover enough to work, I’d like to follow a therapy with stem cells afterwards, because of the reasons you have pointed out.

    It is just very frustrating not to be able to improve with treatments that do make sense…Let’s hope the retroviruses turn out to be important in this disease, or that we find other missing pieces of the puzzle soon...

    Thanks for your wholehearted support,
    Sergio

    PS. Pardon the English...I am very tired today:In bed:
     
  11. richvank

    richvank Senior Member

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    Hi, Sergio.

    I wish you the best with the things you are trying now, and will be very interested to hear how the retrovirus treatment goes.

    I very much appreciate kicking ideas around with you, and learn a lot from doing so.

    Best regards and Merry Christmas!

    Rich
     

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