Invest in ME Conference 12: First Class in Every Way
OverTheHills wraps up our series of articles on this year's 12th Invest in ME International Conference (IIMEC12) in London with some reflections on her experience as a patient attending the conference for the first time.
Discuss the article on the Forums.


Discussion in 'Detox: Methylation; B12; Glutathione; Chelation' started by Freddd, Feb 7, 2013.

  1. Dreambirdie

    Dreambirdie work in progress

    N. California

    Really good points, Sushi. (my bolds)

    I have been really concerned about Freddd puttting himself exclusively "in charge" of the methylation threads. In my personal experience, his protocol is extreme, and his style of working with people does not account for individual differences or individual LIMITS, something that Rich was very very careful to consider.

    I had *SEVERE* detoxification symptoms (heart palpitations, dizziness, and shortness of breath, that immobilized me completely) after just 10 days on Freddd's active B12 protocol. Freddd predictably dismissed and reduced my symptoms to a "START-UP REACTION." In time, I saw him do this regularly to other people as well. In fact, START-UP REACTION and INDUCED PARADOXICAL FOLATE DEFICIENCY were his standard responses for almost every problem someone had on his protocol. And yeah, the hypokalemia was thrown in there in good time as well.

    As for DETOXIFICATION symptoms, in my case Freddd argued, rather prolifically, that I couldn't possibly be having a detox reaction. It was start-up, start-up, start-up (in so MANY words). Fortunately I was able to procure a fecal metals test at the peak of my crisis. Sure enough, the results showed that I had been detoxing several toxic heavy metals, which had been mobilized while taking the methyl and ad B12, in doses that I now know were much too high for me.

    Rather than encourage me to slow down the pace of methylation, and lower my doses, in order to minimize the severity of my reactions, FReddd encouraged me to UP my doses and push through. That was the point where I stopped his protocol completely and focused on Rich's protocol instead. My body is too fragile and my nervous system is much too sensitive, to blast it into crisis with high dose methylation supps.

    I hope people take what Freddd says with a very BIG grain of salt. He is not a medical health professional, and according to my understanding of th forum rules, he should not be prescribing treatments and doling out medical advice on this forum. Given his track record with pushing his agenda and pushing high doses, I think a high deal of caution is warranted here.
    Valentijn, brenda, Sushi and 2 others like this.
  2. Freddd

    Freddd Senior Member

    Salt Lake City
    Things change.

    Before 1800 an estimated 2,000,000 seamen died of scurvy despite the best medical knowledge.

    In 1890 90% of modern women going to hospitals for childbirth died of childbed fever, passed by doctors who didn't believe in disease micorbes and unintentionally killed their patients.

    In 1870-1930 or so millions of people were diesased, confined in mental asylums and died from beriberi (B1) and pellagra (B3) becasue of the best of science giving them perfect white flour that didn't go rancid.

    In the 40s and 50s the heart attack express was that little stick of transfats that medical science said we should eat instead of real fats. Transfats don't go rancid qucikly.

    Sushi said:

    Also, the phenomenon of "detoxification" is widely accepted by researchers and medical practitioners and is often associated with an increase in glutathione. I think very few who worked with the Simplified Methylation Protocol were confused between detox and hypokalemia. Those I know were aware of an increased need for potassium (as was Rich) and acted accordingly with supplementation.
    And they too are quite wrong. An appeal to authority doesn't matter. I've been evaluating journal articals for decades and many of them would flunk high school chemistry lab reports for poor proof reading and simple mistakes, not to mention outright tilting the results and even imaginary but necesary data points to prove their case. A lot of it looks custom made for marketing departments wanting to stretch claims. The sum total of 60 years of research on CyCbl, HyCbl and folic acid don't add up to a working system. That might not mean anything to you. To me it means one big belly flop as far as understanding everything based on it Since those items work so poorly producing glutathione, it is no wonder they don't see that. As the low serum potassium symptoms happen as high as 4.3 at least in me and others who have reported it to me, it is dangerous for people to not know that. While real "detox" as they believe it to be may exist, believeing that Glutathione produces that is just plain wrong. AS there were two things that often occurred in turns it could be very confusing, folate deficiency alternating with low SERUM potassium which can happen very quickly becasue the bufferring of potassium out of tissue is slow. I don't care what their qualications are, I was misdiagnosed and mistreated by the best.I could find for decades, with theories of all kinds including detox theory. It was all the helpful folks here on this board who make it so clear. An increase in glutathione is related to an increase as methylation. You are speaking of another effect, not a cause. Glutathione isn't at the root of things. It is a result, an effect, blocking and unblocking methylation. I take this very seriously. If we don't exchange this information and get it out from behind the faulty research and beliefs my family and a lot of other families won't survive. Figuring out the way through the individual maze we each have can be done with method and effectiveness if a person can follow the clues and succeeds in interpreting them properly, they can heal reasonably quickly. I agree with Rich., three months is plenty long to tell if the exact program one is doing is working or not. I tried hundreds of things, with minor hints that eventually came into play, before I hit 10 bingoes in a row. I tried lots of things over and over again in different amounts and different combinations and different timings. Most people told me "too complcated". I'll tell you now, I don't think it can be simple until the researchers figure out why these things work and even then it might not get easy. There are lots of variations. I'm working on screening questionaires that can identify subtypes. So far only several main types are identifiable specifically.

    ascorbicacid likes this.
  3. dbkita

    dbkita Senior Member

    Fair enough. I am always open to discussion :)

    Just to clarify I have been taking FolaPro 800-1600 mcg for over two years. Folinic acid was used in the first year. I have not used it for a long time. I have not used folic acid or consumed ANY folic acid in my diet for several years now. I am have been taking exclusively methyl b12 sublinguals (Jarrow until Aug 2012, Enzymatic Therapy since then) for 4-5 years. I started adb12 (Source Naturals) only about 9 months ago. I do not take a B-complex, I take all b-vitamins as separate pills to carefully balance them and to avoid too much B6 or B5, and any folic acid. I do take 500 mg of niacinamide and 100 mg riboflavin and B1 per day since they really seem to help me feel better. I used TMG 500 mg for about 18 months and I used SAMe for about six months starting Spring 2012 and had to discontinue both TMG and SAMe due to bad side-effects and harsh potassium balance issues.Of the deadlock quarter I have not taken L-carnitine in any form for some time. That I will freely admit.

    Note borderline hypokalemia has been around for about 2 years and was really bad when I added the SAMe and despite 10+ grams per day I was routinely tested below 3.3 or so after a fast in the morning (of course it does oscilate over the course of the day I am sure). Bigger concern was (and to some extent is) my enormous excretion and my routinely low RBC values for intracellular K (low for many years even prior to methylation)

    Your point about half-life is intriguing. I am not sure I have the stones to take 5mthf at bed time. But taking all in one dose with my other meds and supplements + food probably leaves something to be desired in terms of absorption and effectiveness. I know B3 will tend to mop up extra SAMe, but vitamin C (especially ascorbic acid) will actually destabilize methylfolate in the gut as I have found by trial and error the hard way.

    Ok I agree with many of your points. I think #10 is a very valid and often overlooked point.

    Where I am not sure is #7, especially if the two are taken apart given the very different ways the intestinal lumen works with the two forms (i.e. folinic acid can be converted to 5,10 methylene THF to 5MTHF in the lumen without recourse to the liver, unlike folic acid ... provided a person's folate machinery is operational of course).

    Where I disagree is #8.

    Folinic acid is a 5-formyl derivative of THF. The folates in vegetables are not folinic or folic acid (a fully oxidized synthetic folate, i.e. pteroylmonoglutamic acid). This is a notorious misconception in the research community. The folates in food are metabolites of THF packed within polyglutamates. In the intestinal lumen these polyglutmate dietary forms are broken down into monoglutamate variants which can then be converted to DHF and then THF by their respective enzymes. The DHFR enzyme is not present in humans for the synthetic folic acid it is present for processing dietary folates. Folinic acid is readily converted to 5,10 methylene THF without use of DHFR. That being said dietary folates parallel more with folic acid than with folinic acid with one crucial difference ... they can be processed in the intestinal lumen and the liver. Folic acid (I am pretty sure) being fully oxidized must be converted in the liver.

    I don't think this changes the fact that high dietary folates could be an issue for some people who can not make use of them, have intestinal wall damage, or critical needs for 5mthf but let's be honest while maybe garden feasts are not a good idea, it is not wise probably to eschew vegetables entirely as a general rule. My bigger exclusion on vegetables is to limit high thiol containing ones for other reasons.

    Then again as I stated above and in my former post, I don't consume folic acid nor any folinic acid for some time now. And my diet is heavily slanted to animal protein and fats with relatively low carbs and moderate vegeatables. I am also gluten, dairy, corn, and soy free.

    I don't disagree. I think genes have some importance but it is often overstated. Especially focusing on heterozygote mutations that say 20-40% of the population have anyways. I tend to favor more epigenetic effects, events like infections, etc., or habits like diet, stress, etc. I do think a ensemble of key mutations can lead to certain undesirable fall back patterns when exposed to certain stressors, infections, etc. I only mentioned A1298C heterozygote since unlike most on here I do not have the C677 mutation in any way so my MTHFR production is not handicapped by genetics. I do have a track record of low BH4 levels but instead of blaming that on a heterozygote A1298C that is likely a product of inflammation in the body.

    I would be interested if you could point me to a list of which medications have this effect. I tend to avoid most herbs since they often have broad spectrum selectivity issues.

    At one point before methylation treatment was started, I was put on glutathione IVs. And yes I did react very badly to them. But not in the ways you listed. I had hideous reflux, excitotoxicity, and pain. Only later did I figure out what was going on. Glutathione cannot enter the cell unless broken back down and reassembled inside. For this reason most glutathione taken even by IV at best is absorbed in the liver and kidneys. But I was so low on ATP that reassembly was not possible at the GCL stage. Hence I was swimming in glutamate. Given that I have very low GABA production for other reasons, I was overloaded in the CNS (not fun). Even after enduring 8 such treatments over 2 months or so, my RBC glutathione levels were the lowest Rich Vank had ever seen. The solution turned out to be a combination of antioxidatns (vitamin C, etc.), ATP support (d-ribose, creatine, etc.), and later methylation treatment. Within a year my glutathione RBC levels had tripled to high normal. Personally I think glutathione supplementation (of any type) is a bit of a sham given the complicated absorption issues at the cell membrane.

    I would say that for the last two years I have primarily been in some form of group 1 with occasional flirtations with group 2b. I was in group 3 back in 2008 and 2009 and briefly in 2010 when given glutathione IVs as mentioned above. The problem is when I peaked in terms of 5MTHF, TMG, R5P / P5P, meb12 and adb12, and then added SAMe, the hypokalemia just skyrocketed and I had to eat 4000 calories a day of high potassium food to hit a 10-11 grams target since extended release KCL was suicidal on my GI tract at levels above 2 grams. By dropping the TMG, lowering P5p and r5p, removing SAMe, better balanced meb12 and adb12, and chopped 5mthf in half, suddenly not only did I need less potassium (like now 6-7 grams per day) but a LOT of other things got better. By not doing a proper titration when I started out, I think I had unwittingly overshot the mark for a couple of years and was stuck there suffering many things needlessly. And I am sorry but after two plus years, I was way beyond startup effects.

    Thank you for the decision tree.

    I selected the three that are relevant potentially to me. The first two I have definitely experienced as already outlined before.

    For the third branch, I have taken all of the aforementioned (D, A, C, E, etc.) for several years now. I take 1000 mg magnesium per day in various forms. For a long time I took at Rich Vank's suggestion high dose vitamin C for a while, but have now opted for Na ascorbate 3 grams per day. I take 2500 IU vitamin D now, in the past took higher levels. Sadly both D and A in the gut can elevate inflammation and norepinephrine. For 18 months I was on vitamin A 20000 IU per day and as high as 50 K IU 3 times per week. Those had distinctly different effects than what you listed. I no longer supplement A since I get 5000 IU per day in diet generally. My vitamin D levels are lowish, but the active form 1,25 calcitriol is quite good due probably to the high magnesium.

    Could you explain how the third branch (" IF adding or increasing any of Vitamins D, A, E, or C, magnesium, zinc (perhaps 10%)" leads to Paradoxical Folate problems?

    Not sure I understand the connection here. Why is the body making its own glutathione a bad thing? Making my own did wonders to help with my autoimmune symptoms.

    I routinely take glutamine to prevent muscle catabolism and aid muscle recovery. But glutamine is the most abundant amino acid in the body and I get 230-250 grams of protein anyways. NAC is a different matter and I avoid it (makes me to mentally fogged since the glutamate drop to make glutathione is too mentally fatiguing for me to do scientific research). I figure the body should be left to its own devices to make glutathione as it needs provided there are no nasty blocks. I do not accept glutathione deficit as the central defect in most chronic disorders. But maybe that is just me.

    Yes my MCV is higher than I would desire but that has been true for 10+ years and the methylation protocol has not changed that number (always high 90s). Actually looking at my labs, my MCV peaked near 100 for the six months I was at the highest methylation support level. So not sure what to say there (at least for me personally).

    Anyways sorry for the lengthy reply.

    P.S. I agree that detox is a way over used concept on these forums. But I also think for some of us we are way beyond startup effects when we are deep into the protocols.

    P.S.S. I still don't buy the cell growth depletion theory of potassium for the methylation. I do not believe the numbers add up nor can they explain high excretion.
    Sidereal and Valentijn like this.
  4. brenda

    brenda Senior Member

    I tried Freddd`s protocol too and ran into trouble but it was not detox. I am very sure it was mobilisation of mercury due to it being methalysed by methylco b12. The problem was that I was NOT detoxing it. Freddd did the same thing to me too and encouraged me to continue denying that it could be anything other than `start-up`. Quite a significant number of others went through this too and were implied to be `softies` who would not cope with a bit of discomfort.

    He argued the toss repeatedly and would not tolerate the idea that he could be wrong despite many people telling him the same thing but eventually he conceeded to say one should go slower but this took a lot of time for him to get there and to listen to those who said he should have a disclaimer on his posts which have since disappeared saying these were just his own ideas and he was not able to give medical advice which he was doing as DB says, breaking forum rules .

    This is not to deny that he has helped people but he has also harmed people and I see he is still arguing the toss just the same, this time saying he has changed. He has not changed this part.

    This is experimental work and not without risk and it should be made clear on every one of Freddd`s posts.
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  5. Xara

    Xara Senior Member

    The Netherlands
    I think all(!) that is mentioned here on this subforum of Phoenixrising is experimental work, we are guinea pigs experimenting on ourselves and learning from each other.

    Where I live doctors in regular medicine laugh when the word detox is mentioned, doctors in regular medicine point to psychological treatments when confronted with a patient having ME/CFS, and they are being backed by official treatment guidelines (it's the same in the UK, I've read).

    I was diagnosed B12 deficiency, and therefore got HyB12 injections - hydrocobalamine, that's the standard in my country. I was lucky, at last: serious attention and serious (though in my case insufficient) treatment after more than twenty years of illness and being labeled 'ME/CFS'.

    For years and years regular medicine in my country thought that stomach ulcers were caused by stress, not an ordinary bacteria.
    Recent medical history is full of researchers not doing the right research and doctors (and patients) rigidly rejecting other suggested possibilities.

    Please, all here is unknown territory, isn't it?

    Freddd's theory's no different? Let the man speak out. I for one am eager to read his views. I too have questions though.
    For instance when it comes to folinic acid (man has been eating greens for centuries, for me it's hard to believe folinic acid is capable of blocking so much of essential methylfolate), or when it comes to the difference in sensitivity when taking different amounts of methylfolate (no reaction to big amounts, symptoms when getting low amounts).

    Freddd is obviously helping some, he may help others. Don't gag him, please, do give him the same respect and approach as others get on these forums who share their (hypothetical) views.

    Since all mentioned on this forums is experimental and based on few data no one can blame someone else for things going wrong.
    There is no official protocol, there are no official dummy proof standard practices. If it was regular medical science we would not be here trying all sorts of things, we would be following up on doctors orders.

    I too have my own responsibilty, so doing it slowly and starting at low doses is wise I think, but if things do go wrong I can only blame myself. And If things do go wrong I will definitely not try to silence or attack the one that was only trying to help - I will inform him and others, in a respectful way, so that my suffering might lead to a/some change in the advised protocol. But yes, I understand, exceptions do not make the rule, exceptions do not change the big view - it's the same in the professional world: the pharma industrie gathers information about abnormal reactions to their medicine, but they need big amounts of data before they will change the instruction given.

    If I do not like responsibility and dealing with the consequences myself, the alternative is going to my GP and staying ill, probably getting worse.

    Please Freddd, do go on, share your theory and views.
  6. Lotus97

    Lotus97 Senior Member

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

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

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

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

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

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

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

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

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

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

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

    The methylation cycle is so fundamental to so many parts of the body's biochemistry that when it becomes dysfunctional, it causes a host of problems, and this is why people experience so many symptoms, involving so many body systems and organs, in this disorder.
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  7. Red04

    Red04 Senior Member

    I second this. I don't have to tell you because your personality probably won't allow anything different, but please go on. Upon my wifes 95% recovery two years ago, her career (and our financial situation) has blossomed, our relationship is an actual relationship, we have a 6 month old son, and are doing great. Please let me know if there is someway I can help you or assist you in your efforts.

    It's obvious that some people were not able to get through the "startup" symptoms. Some people can push through them or adjust the protocol accordingly. Other's are not able to get through it. So there is likely either a titration problem or an unknown limiting factor or perhaps a toxin problem. My wife had startup symptoms. There is NO WAY she could have gotten through it without my help. I kept pushing her. We know a lot more about folic acid now, so that could have been the startup issue. We will learn more about startup moving forward. Freddd's approach is to hit the root cause and let the body heal itself. Other's want to get things in place first. Like toxins or gut problems. These problems are likely caused by a methylation breakdown. To test the theory of detox seems like an uphill battle.

    I would play with microtitration attempting to let the body cure itself, before trying to clear toxins first. If you have some difinitive proof or hunch about why you are toxic, and know what you might do about it, it may be worth a look. But trying to decipher toxin symptoms seems overwhelming without significant resources and testing. Perhaps, an easier first step would be to work with what is known. Potassium and Methylfolate. This is not working for everyone, as expressed above and this is also mostly my personal opinion.

    My wife's startup symptoms included hives, erratic emotions, muscle cramping, IBS fluctuations, tingling and other nervous system oddities, sleep changes. She got a massage and had to pull over on the way home, because her entire body completely cramped up. I don't remember what else. It was pretty crazy and scary. The only thing scarrier was remaining sick the rest of her life and returning to the doctors for more colonoscopys or endoscopys or MRI's or get back on prozac or klonopin or wellbutrin, or whatever else.
  8. Lotus97

    Lotus97 Senior Member

    United States
    You make it sound as if the people following Freddd's protocol are the first people to ever try methylation. For years Rich, Dr. Yasko, and Dr. Nathan have used methylation on many of their patients and run countless scientific tests. And I mean actual scientific tests and not just "how do you feel".
    Valentijn likes this.
  9. Red04

    Red04 Senior Member

    I think maybe you are over-estimating the "actual scientific tests" going into Yasko and Rich's work and under-estimating Freddds. Yasko regards treatment over research and Rich's info was largely based on other studies, collaborations, and theory....Not too long ago, Rich was reccomending glutathione injections based on actual scientific testing. Early on, my wife endured this treatment from Dr. Salvato in Houston. It caused negative effects on my wifes wellness. The irony is that 2 years later I found a cure with Freddd and Rich's info as it had evolved from gultathione injections.

    I think most would agree that all the protocols are in their early stages and will require years of evolution and learning and experimenting (collaborative, empirical, theoretical, and clinical) before they are finalized. I think that was much of Xara's point. If Freddd started everything with "it is my opinion" or "the data tells me" or "in my experience" this really wouldn't change anything.

    Can you imagine the disclaimer outside a MD's office? "The chemicals I give you will likely be considered dangerous in a few years. You and your family may profit from a class action drug lawsuit in the near future. I have a limited understanding of the human body, nutrition is a foreign concept to me, understanding what is wrong with you is largely out of my job description, and my hands are mostly tied with malpractice insurance and gov't regulations. etc...etc...etc...."
  10. Lotus97

    Lotus97 Senior Member

    United States
    Your timeline is way off
    I encouraged people to boost gltutathione directly from about 1999 through 2004. It gave temporary help to some, but was not a permanent way to raise glutathione. In late 2004 I read the work of S.Jill James et al. in autism. They found that glutathione was also low in autism, but that it could be raised by lifting the partial methylation cycle block that is upstream of glutathione synthesis in the sulfur metabolism. I encouraged people with ME/CFS to try this, since the biochemistry in autism and ME/CFS are quite similar. It turned out to work for most people who tried it. The simplified methylation protocol is designed to lift this partial block.

    There are two types of tests that people are getting involving methylation. One is the Yasko panel, available (or using a panel to get most of the results of the Yasko panel). This is a genetic polymorphism panel, and it tells you what your tendencies are, based on the genes you have inherited.

    The other type is the methylation pathways panel that is offered by the Health Diagnostics and Research Institute in New Jersey, or the European Laboratory of Nutrients in the Netherlands. This is a biochemical panel that tells you what is actually going on in the biochemistry of the methylation cycle, the folate metabolism and glutathione (you have to order glutathione separately at the European lab).

    They can both be helpful, but I favor use of the biochemical panel, because it gives more direct information about what is going on, and can lead to treatment with the simplified methylation protocol. For those who want to follow the full Yasko treatment program, the Yasko genetics panel is necessary. This program is more complex and also more expensive, but it deals with the issues that show up in the genetics results in more detail. There hasn't been a direct clinical comparison of the outcomes of the two approaches, but both have been found to be helpful.

    I will paste the contact info for the Health Diagnostics lab below, as well as an interpretive guide for the methylation pathways panel.

    Best regards,


    Methylation Pathways Panel

    This panel will indicate whether a person has a partial methylation cycle block and/or glutathione depletion. I recommend that this panel be run before deciding whether to consider treatment for lifting the methylation cycle block. I am not associated with the lab that offers this panel.

    The panel requires an order from a physician or a chiropractor. The best way to order the panel is by fax, on a clinician’s letterhead.

    Available from:

    Health Diagnostics and Research Institute540 Bordentown Avenue, Suite 2300
    South Amboy, NJ 08879 USA
    Phone: (732) 721-1234
    Fax: (732) 525-3288


    Lab Director: Elizabeth Valentine, M.D.

    Dr. Tapan Audhya, Ph.D., is willing to help clinicians with interpretation of the panel by phone, or you can use the interpretive guide below:

    March 25, 2012

    Interpretation of Results of the Methylation Pathways Panel

    Richard A. Van Konynenburg, Ph.D.
    Independent Researcher

    Disclaimer: The Methylation Pathways Panel is offered by the European Laboratory of Nutrients in the Netherlands and the Health Diagnostics and Research Institute in New Jersey, USA. I am not affiliated with these laboratories, but have been a user of this panel, and have written these suggestions at the request of Tapan Audhya, Ph.D., Director of Research for the Health Diagnostics lab, for the benefit of physicians who may not be familiar with this panel. My suggestions for the interpretation of results of the panel are based on my study of the biochemistry involved, on my own experience with interpreting panel results as part of the analysis of a fairly large number of cases of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) over the past four years, and on discussion of some of the issues with Dr. Audhya. I am a researcher, not a licensed physician. Treatment decisions based on the results of applying this panel and its interpretation to individual cases are the responsibility of the treating physician.

    Application: In addition to being useful in analyzing cases of ME/CFS, this panel can also be usefully applied to cases of autism and other disorders that involve abnormalities in glutathione, methylation and the folate metabolism.

    The panel includes measurement of two forms of glutathione (reduced and oxidized), S-adenosylmethionine (SAMe), S-adenosylhomocysteine (
    SAH), adenosine, and seven folate derivatives.

    According to Dr. Audhya (personal communication), the reference ranges shown on the lab reports for each of these metabolites were derived from measurements on at least 120 healthy male and female volunteer medical students from ages 20 to 40, non-smoking, and with no known chronic diseases. The reference ranges extend to plus and minus two standard deviations from the mean of these measurements.

    Glutathione (reduced): This is a measurement of the concentration of the
    chemically reduced (active) form of glutathione (abbreviated
    GSH) in the blood
    plasma. The reference range is 3.8 to 5.5 micromoles per liter.

    Glutathione plays many important roles in the biochemistry of the body, including serving as the basis of the antioxidant enzyme system, participating in the detoxication system, and supporting the cell-mediated immune response, all of which exhibit deficits in CFS. The level of GSH in the plasma is likely to be more reflective of tissue intracellular glutathione status than the more commonly and more easily measured red blood cell or (essentially equivalent) whole blood glutathione level, which is about three orders of magnitude greater, because red blood cells are normally net producers of glutathione. Also, knowledge of the level of the reduced form, as distinguished from total (reduced plus oxidized) glutathione, which is more commonly measured, is more diagnostic of the status of glutathione function.

    In order to be able to approximate the in vivo level of reduced glutathione when blood samples must be shipped to a lab, it is necessary to include special enzyme inhibitors in the sample vials, and these are included in the test kit supplied by these two laboratories.

    Most people with chronic fatigue syndrome (PWCs), but not all, are found to have values of GSH that are below the reference range*. This means that they are suffering from glutathione depletion. As they undergo treatment to lift the partial methylation cycle block, this value usually rises into the normal range over a period of a few months. I believe that this is very important, because
    glutathione normally participates in the intracellular metabolism of vitamin B12, and if it is low, a functional deficiency of vitamin B12 results, and insufficient methylcobalamin is produced to support methionine synthase in the methylation cycle. In my view, this is the mechanism that causes the onset of ME/
    CFS. This functional deficiency is not detected in a conventional serum B12 test, but will produce elevated methylmalonate in a urine organic acids test. In my opinion, many of the abnormalities and symptoms in ME/CFS can be traced directly to glutathione depletion.

    Anecdotal evidence suggests that PWCs who do not have glutathione depletion do have abnormalities in the function of one or more of the enzymes that make use of glutathione, i.e. the glutathione peroxidases and/or glutathione transferases. This may be due to genetic polymorphisms or DNA adducts on the genes that code for these enzymes, or in the case of some of the glutathione peroxidases, to a low selenium status.

    Glutathione (oxidized): This is a measurement of the concentration
    of the oxidized form of glutathione (abbreviated GSSG) in the blood
    plasma. The reference range is 0.16 to 0.50 micromoles per liter.

    Normally, oxidized glutathione in the cells is recycled back to reduced glutathione by glutathione reductase, an enzyme that requires vitamin B2 and NADPH. If this reaction is overwhelmed by oxidative stress, the cells export excess GSSG to the plasma. In some (but not all) PWCs, GSSG is elevated above the normal
    range, and this represents oxidative stress. It is more common in CFS to see this level in the high-normal range. This value may increase slightly under initial treatment of a partial methylation cycle block.*

    Ratio of Glutatione (reduced) to Glutathione (oxidized): This is not shown explicitly on the panel results, but can be calculated from them. It is a measure of the redox potential in the plasma, and reflects the state of the antioxidant system in the cells. The normal mean value is 14. PWCs often have a value slightly more than half this amount, indicating a state of glutathione depletion and oxidative stress. This ratio has been found to increase during treatment of a partial methylation cycle block, but other types of treatment may be necessary to bring it to normal.*

    S-adenosymethionine (
    RBC): This is a measure of the concentration of S-adenosylmethionine (SAMe) in the red blood cells. The reference range is 221 to 256 micromoles per deciliter.

    SAMe is produced in the methylation cycle and is the main supplier of methyl (CH3) groups for a large number of methylation reactions in the body, including the methylation of DNA and the biosynthesis of creatine, carnitine, phosphatidylcholine, coenzyme Q10, melatonin and epinephrine. This measurement is made in the red blood cells because the level there reflects an average over a longer time and is less vulnerable to fluctuations than is the plasma level of SAMe.

    Most PWCs have values below the reference range, and treatment raises the value.* A low value for SAMe represents a low methylation capacity, and
    in CFS, it usually appears to result from an inhibition or partial block of the enzyme methionine synthase in the methylation cycle. Many of the abnormalities in CFS can be tied to lack of sufficient methylation capacity.

    S-adenosylhomocysteine (RBC): This is a measure of the
    concentration of S-adenosylhomocysteine (SAH) in the red blood cells. The reference range is 38.0 to 49.0 micromoles per deciliter.

    SAH is the product of the many methyltransferase reactions that utilize SAMe as a source of methyl groups. In CFS, its value ranges from below the reference range to above the reference range. Values appear to converge toward the reference range with treatment.

    Sum of
    SAM and SAH: When the sum of SAM and SAH is below about 268
    micromoles per deciliter, it appears to suggest the presence of
    upregulating polymorphisms in the cystathionine beta synthase (CBS)
    enzyme, though this may not be true in every case. For those considering following the Yasko treatment program, this may be useful information.

    Ratio of
    SAM to SAH: A ratio less than about 4.5 represents low
    methylation capacity. Both the concentration of
    SAM and the ratio of
    concentrations of
    SAM to SAH are important in determining the
    methylation capacity, because they affect the rates of the methyltransferase reactions.

    Adenosine: This is a measure of the concentration of adenosine in the
    blood plasma. The reference range is 16.8 to 21.4 x 10(-8) molar.

    Adenosine is a product of the reaction that converts SAH to homocysteine. It is also exported to the plasma when mitochondria develop a low energy charge, so that ATP drops down to ADP, AMP, and eventually, adenosine. Adenosine in the plasma is normally broken down to inosine by the enzyme adenosine deaminase.

    In some PWCs adenosine is found to be high, in some it is low, and in some it is in the reference range. I don't yet understand what controls the adenosine level in these patients, and I suspect that there is more than one factor involved. In most PWCs who started with abnormal values, the adenosine level appears to be moving into the reference range with methylation cycle treatment, but more data are needed.

    5-CH3-THF: This is a measure of the concentration of 5L-methyl
    tetrahydrofolate in the blood plasma. The reference range is 8.4 to 72.6 nanomoles per liter.

    This form of folate is present in natural foods, and is normally the most abundant form of folate in the blood plasma. It is the form that serves as a reactant for the enzyme methionine synthase, and is thus the important form for the methylation cycle. It is also the only form of folate that normally can enter the brain. Its only known reactions are the methionine synthase reaction and reaction with the oxidant peroxynitrite.

    When there is a partial block in methionine synthase, the other forms of folate continue to be converted to 5L-CH3-THF by the so-called “methyl trap” mechanism. Some of the 5L-CH3-THF is broken down by reaction with peroxynitrite, which results from the condition of oxidative stress that is usually concomitant with glutathione depletion.

    Many PWCs have a low value of 5L-CH3-THF, consistent with a partial block in the methylation cycle. Most methylation treatment protocols include supplementation with 5L-CH3-THF, which is sold over-the-counter as Metafolin, FolaPro, or MethylMate B (trademarks), as well as the newer Quatrefolic (trademark) and in the prescription “medical foods” supplied by PamLab, including Deplin, CerefolinNAC and Metanx. There are some others on the market that include both racemic forms (5L and 5R) of this folate.

    When methylation treatment is used, the level of 5-CH3-THF rises in nearly every PWC. If the concentration of 5-CH3-THF is within the reference range, but either SAM or the ratio of SAM to SAH is below the reference values, it suggests that there is a partial methylation cycle block and that it is caused by inavailability of sufficient bioactive B12, rather than inavailability of sufficient folate. A urine organic acids panel will show elevated methylmalonate if there is a functional deficiency of B12. I have seen this combination frequently, and I think it demonstrates that the functional deficiency of B12 is the immediate root cause of most cases of partial methylation cycle block. Usually glutathione is low in these cases, which is consistent with such a functional deficiency. As the activity of the methylation cycle becomes more normal, the demand for 5-CH3-THF will likely increase, so including it in the treatment protocol, even if not initially low, will likely be beneficial.

    10-Formyl-THF: This is a measure of the concentration of 10-formyl
    tetrahydrofolate in the blood plasma. The reference range is 1.5 to 8.2 nanomoles per liter.

    This form of folate is involved in reactions to form purines, which form part of RNA and DNA as well as ATP. It is usually on the low side in PWCs, likely as a result of the methyl trap mechanism mentioned above. This deficiency is likely the reason for some elevation of mean corpuscular volume (MCV) and mean corpuscular hemoglobin (MCH) often seen in PWCs. This deficit may also impact replacement of cells lining the gut, as well as white blood cells.

    Rarely, 10-formyl-THF is found to be much higher than the normal reference range. If this is found, the patient should be examined for cancer, since cancer cells upregulate this form of folate in order to make purines more rapidly to support their rapid cell division.

    5-Formyl-THF: This is a measure of the concentration of 5-formyl
    tetrahydrofolate (also called folinic acid) in the blood plasma. The reference range is 1.2 to 11.7 nanomoles per liter.

    This form is not used directly as a substrate in one-carbon transfer reactions, but it can be converted into other forms of folate, and may serve as a buffer form of folate. Most but not all PWCs have a value on the low side. It is one of the
    supplements in some methylation protocols. It can be converted to 5L-CH3-THF in the body by a series of three reactions, one of which requires NADPH, and it may also help to supply other forms of folate to the cells until the methionine synthase reaction comes up to more normal activity.

    THF: This is a measure of the concentration of tetrahydrofolate in
    the blood plasma. The reference range is 0.6 to 6.8 nanomoles per liter.

    This is the fundamental chemically reduced form of folate from which several other reduced folate forms are synthesized, and thus serves as the “hub” of the folate metabolism. THF is also a product of the methionine synthase reaction, and participates in the reaction that converts formiminoglutamate (figlu) into glutamate in the metabolism of histidine. If figlu is found to be elevated in a urine organic acids panel, it usually indicates that THF is low. In PWCs it is lower than the mean normal value of 3.7 nanomoles per liter in most but not all PWCs.

    Folic acid: This is a measure of the concentration of folic acid in
    the blood plasma. The reference range is 8.9 to 24.6 nanomoles per liter.

    Folic acid is a synthetic form of folate, not found in nature. It is added to food grains in the U.S. and some other countries in order to lower the incidence of neural tube birth defects, including spina bifida. It is the oxidized form of folate, and therefore has a long shelf life and is the most common commercial folate supplement. It is normally converted into THF by two sequential reactions catalyzed by dihydrofolate reductase (DHFR), using NADPH as the reductant. However, some people are not able to carry out this reaction well for genetic reasons, and PWCs may be depleted in NADPH, so folic acid is not the best supplemental form of folate for these people.

    Low values suggest folic acid deficiency in the current diet. High values, especially in the presence of low values for THF, may be associated with inability to convert folic acid into reduced folate readily, such as because of a genetic polymorphism in the DHFR enzyme. They may also be due to high supplementation of folic acid.

    Folinic acid (WB): This is a measure of the concentration of folinic acid in the whole blood. The reference range is 9.0 to 35.5 nanomoles per liter.

    See comments on 5-formyl-THF above. Whole blood folinic acid usually tracks with the plasma 5-formyl-THF concentration. They are the same substance.

    Folic acid (
    RBC): This is a measure of the concentration of folic acid in the red blood cells. The reference range is 400 to 1500 nanomoles per liter.

    The red blood cells import folic acid when they are initially being formed, but during most of their lifetime, they do not normally import, export, or use it. They simply serve as reservoirs for it, giving it up when they are broken down.

    Many PWCs have low values of this parameter. This can be caused by a low folic acid status in the diet over the previous few months, since the population of RBCs at any time has ages ranging from zero to about four months. However, in CFS it can also be caused by oxidative damage to the cell membranes, which allows folic acid to leak out of the cells. Dr. Audhya reports that treatment with omega-3 fatty acids has been found to raise this value over time in one cohort.

    If anyone finds errors in the above suggestions, I would appreciate being notified at

    * Nathan, N., and Van Konynenburg, R.A., Treatment Study of Methylation Cycle Support in Patients with Chronic Fatigue Syndrome and Fibromyalgia, poster paper, 9th International IACFS/ME Conference, Reno, Nevada, March 12-15, 2009. (

  11. Red04

    Red04 Senior Member

    Well I guess that depends on your definition of not too long ago. My wife received the treatment in 2009. I even requested that Rich reach out to her.

    I think saying it worked for most of the poeple who tried it is wrong as well.

    You brought in a good quote though. Rich used a largely unrelated autism study and some assumptions and one measurement of glutathione to reccomend a treatment back in 1999. Experimental and mostly theoretical. And it potentially harmed several people as well. This was exactly my point. He waivered and changed his SMP based on how people felt in his latest revisions as well. In addition, he selected supplements that were readily available and affordable and that why it's called "simplified".

    I am very familiar with these tests. I have been on this forum and the wrong diagnosis forum for several years. I don't think this necessarily validates the SMP, or even attempts to validate it. It is more of a diagnostic and an experimental diagnostic that will likely evolve as well. Xara's original point and my emphasis was that all of this is experimental and evolving and should be treated accordingly and everyone here is self diagnosing and treating to some degree. And everyone here should take responisibility for their self treatment. Also, the testing is largely empirical as clinical testing (not diagnostic) is difficult and expensive and the broad nature of MTHFR symptoms are hard to classify. How do you get an MCS patient, Fibro, a manic depressant, and someone with one of the other 14 "syndromes" under one clinical test?
  12. Adster

    Adster Senior Member

    Personally, I'd love Freddd to keep posting here and I really appreciate how hard he works for people. I just want to see more acknowledgement of the experimental nature of the work(such as a disclaimer to this effect in his signature line that will appear in every post he makes) and less of the "in the style of a proper clinical study" writing. It's blatantly misleading.
    CedarHome, ahmo, brenda and 3 others like this.
  13. Lotus97

    Lotus97 Senior Member

    United States
    Rich has said that some people need methylcobalamin, but most people improve with hydroxocobalamin.
    To my delight, 70% of my patients had improved within 3 months, and 20% reported that they were much better, occasionally to the point of feeling cured.
    BTW, for anyone who does read this article (and I hope everyone does) when he says folic acid he is referring to folinic acid and methylfolate.
  14. Lou

    Lou Senior Member

    southeast US

    Having had this illness for twenty-eight years I long ago had to choose --after seeing nearly twenty doctors and undergoing untold number of their tests and unburdening myself of a lot of cash-- 'how I felt' over their tests as a better 'barometer' of what was actually going on with me health-wise. The other option was believing as they did, that I was 'fit as a fiddle'. I wasn't, but their scientific tests did not show it.

    I first tried Yasko's method. Went from low bp to high bp. Felt worse. Abandoned it. Next, I tried Rich's protocol for several months. It did little or no good in the beginning and made me worse toward the end.

    Then, I began Fredd's protocol while on an extended trip abroad. Though initially I got in trouble (low K, and difficulty balancing folate and mb12), I knew, whether good or bad, this was indeed a powerful therapy. This was evident from fleeting periods of crystal clear thought, something I completely thought impossible to experience again, from seeing my muscles regain their tone and strength almost weekly, from more energy and better mood, and finally from people asking what had I been doing while away to make me look and act so much healthier.

    Sadly, I plateaued after about three months, but it was a great ride while it lasted. Haven't been able to figure out how to restart the healing (no longer require even a small amount of extra K) and the complexity of Fredd's method is probably its biggest shortcoming. But it is what it is, and nobody is being forced to try it.
    SJB944 likes this.
  15. Lotus97

    Lotus97 Senior Member

    United States
    No one can design a perfect methylation protocol. Some people don't do well on Rich's, but same thing with Freddd's. I'm not trying to say Freddd's protocol doesn't work, but Rich's protocol works for a lot of people too. I'm sorry it didn't work some of the people in this thread. Of course Rich's protocol is more flexible in that it allows either hydroxocobalamin or methylcobalamin to be used. When you're dealing with sick people it's good to be cautious.
    For people who do not get a response from the SMP within a couple of months, switching to methylcobalamin would be an option to try. Another option would be to try adding some adenosylcobalamin (dibencozide). However, I do not favor raising the overall dosage of B12 very much above 2,000 micrograms per day, and especially not when it is combined with dosages of methyfolate that are much above the RDA range of 400 to 800 micrograms per day. This combination can overdrive the methylation cycle and hinder the rise of glutathione.
    SJB944 likes this.
  16. Red04

    Red04 Senior Member

    Right, the Simplified Methylation Protocol improved 70% of people. All largely based on how they were feeling.

    However, your original Rich quote stated that the glutathione injections from 1999-2004 worked for most people and I think it's well documented that this isn't true.
  17. SJB944

    SJB944 Senior Member

    As with all protocol's: they are brilliant if they work.

    Arguably even if you don't benefit from Fred's protocol, there is much to be said for his structured and logical approach. The blockage, or limiting factor, could be anything.

    Fred's ability to identify and interpret his own symptoms and determine what is causing what is nothing short of exceptional -- particularly in light of how sick he was. The difficulty is that many of us just don't have his ability to analyse our own symptoms and interpret them whilst in the mire of such a barrage of cognitive dysfunction.

    Not only that, it's wading through the conflicting advice and philosophical differences -- one person's detox is another's potassium deficiency.

    Fred does come across as very definitive, but then again maybe it is this that has helped him get to where he is today.

    The stakes are high: this is our life. But, I like to think that all we can do is continue to make decisions the best we can. To do and try nothing, seems to be giving in.
    helen1, Victronix, Xara and 1 other person like this.
  18. Linda828


    I am very aware that Freddd has come up with many non-standard ways of explaining the empirical evidence he has seen in himself and others that are not necessarily supported by research. My biochemical comprehension is very limited, though, so I can’t follow much of this debate. With my limited mental resources what I can follow is that Freddd healed himself. Others have been helped and some hurt. I want to know how Freddd did it and experiment with that on myself.

    My approach is to never push myself into uncomfortable reactions. A week ago I went through a totally uncharacteristic period of anxiety. Normally I am peaceful. I stopped all supplements. The mood subsided in a day and I added them back one at a time in gradually increasing doses. My body is always my first guide, and other input, including Freddd’s, is measured against that ruler.

    I didn’t notice start up effects because there was no lower to go by the time I realized I was B12 deficient. At that point I couldn’t sit for more than a few minutes due to my heart hurting so badly and the pins and needles throughout my extremities. Methylcobalamin saved my life. Perhaps I am a simpler case than most.

    Now I’m increasing the MTHF. The way I take it is the same way as the dibencoplex. I pour some of the capsule between my lower lip and gum and let it sit there. Most of the day, either dibencoplex or MTHF is dissolving in that space. That was helpful information, Freddd, about the 3 hour half-life and encourages me to continue my “time release” technique. I’m hoping that in this fashion 15 mg a day will do the job. 30 mg would cost me $6 a day, and thus gets cost prohibitive.

    I use Thorne 5-MTHF 5 mg. Thorne binds the MTHF with glucosamine rather than calcium. That was for purposes of getting around Merk’s patent. Otherwise it is exactly the same (i.e.not a racemic form), Thorne products don’t contain magnesium stearates and other fillers and additives, so I prefer it. I’d be curious if anyone else out there is using Thorne or has a sense of it’s effectiveness versus the metafolin. The sulpher in glucosamine could be a problem for some people.

    Cutting back on the vegetables is something I need to try for awhile. I eat a diet very high in fresh fruits and vegetables. If food folate blocks the MTHF in my body, almost no supplemented amount would counteract the quantities I eat. Your detailed explanation of folates in food was very informative, dbkita.

    A few questions. Freddd, when you talk about muscle spasms from low potassium, is that the same as a cramp or Charlie horse? I’ve always assumed that to be low calcium. I had a lot more of those before starting B12. Now when I get them, I respond by upping the calcium (and magnesium).

    One odd side affect of the B12 protocol is that when I get up in the mornings, I have the sensation of deep achiness that feels like it resides deep in the bones of my feet and lower legs. If I exercise it is worse. It’s not like the pleasant achiness of a used muscle after exercise. Years ago when chronic fatigue was my primary symptom, this sensation was constant and much stronger, but that has been thirty years. It started again to a minor degree with B12 injections. Anyone have any ideas about that?

    Regarding the MCS, I often wonder whether it is not due to structural damage that occurred from years of B12 deficiency, either demylination, or breaking down of the lipid blood brain barrier. A metabolic dysfunction, like low levels of functional MTHF would sure be a lot quicker to heal than one that is structural.

    One more minor thought. I had read that most CnCbl and some MeCbl is produced by GMO strains of bacteria. Anyone else heard this? I checked with my pharmaceutical compounder, and mine is not. I wonder if that could account for some of the variability in effectiveness between batches.
    I appreciate all the thoughts and debates in this thread,

    helen1 likes this.
  19. dbkita

    dbkita Senior Member

    When you say restart the healing what do you mean? Do you expect that the process is supposed to continue forever as a non-equilibrium phenomena and the body should always require high amounts of potassium? Have you had improvement in your symptoms? Has those improvements remained? Or by restart do you mean you take the same doses but now you relapsed? Just curious.
  20. dbkita

    dbkita Senior Member

    Glutathione injections certainly messed me up. Those were in early 2010 and ironically Rich Vank while not necessarily recommending them to me via private communications was hopeful they would help. They were in fact a disaster since as I have outlined in another post on this thread I simply could not reassemble the component amino acids back into glutathione within the cell after transport across the membrane.

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