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The Vinitsky Protocol via the Thriiive Conference

Discussion in 'Detox: Methylation; B12; Glutathione; Chelation' started by soulfeast, Jun 23, 2010.

  1. soulfeast

    soulfeast Senior Member

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    http://web.mac.com/thriiive/THRiiiVE_New/Stuff/Entries/2010/6/22_The_"Vinitsky_Protocol"__.html

    This is s presentation given by Dr V as well as the pdf. Very interesting and would love to hear comments.

    He is addressing ANS imbalance by scavenging aldehydes and glutatmates with a sublingual form of hydroxy B12 and folic acid in a 5:2 ratio FA to HB12. This is called "cleaning up stress". The claims are that once the stress is cleaned up, folks can tolerate supplements and therapies they could not before. I have made it through the presentation: videos 1-12 and am still to view the question, answer session, videos 13-14.

    My Questions so far:
    (1) What about CBS upregulation and draining the transsulfuration pathway?
    (2) Is it possible to overpush methylation with the continual high doses of the 5:2 (6-30/40 a day!) and the use of methionine?
    (3) Methyalted form of FA is used for folks who are MTHFr++. Is there are potential problem with the FA forms competing in the cells for methylation? Is there a problem using only FA and when exactly does FA become methylated?
    (4) FA loses glutamates when it is methylated, I believe. How does the body determine how much FA to methylate? Dr V says first priority of the body is to clean up stress.. before methylation. Im wondering about FA losing glutamates which would create a repeating cycle of picking up and dropping.
    (5) Do you pass FA in the urine with glutatmates and aldehydes attached?
    (6) What happens to aldehydes. I think I read in another publication by Dr V that aldehydes are passed to HB12 for another purpose.. I'll look that up.
    (7) What happens to blood/serum levels of FA and cellular levels?
    (8) What are the methylation markers.. this is mentioned in the presentation and I think the measures are different from Rich's and Dr Amys.

    Thanks!!
  2. richvank

    richvank Senior Member

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    Hi, Robin.

    In response to your request, I watched Dr. Alan Vinitsky’s presentation on the Thriiive website. I had some difficulty hearing all the audio and reading the slides, but here are my comments on the parts that I think I did catch:

    First, I want to acknowledge that I think Dr. Vinitsky made a very important discovery when he found that the combination of a form of B12 and a form of folate, taken together, are effective in correcting the function of the methylation cycle. I’m not sure, but I think he may have been the first, or at least one of the first, to find that this combination is effective.

    I also want to acknowledge that it appears that he has done considerable study of the biochemistry involved, and that in my opinion he has applied a great deal of it correctly and has reached several conclusions that I believe are valid and that I agree with. In particular, he has recognized the importance of glutathione in the metabolism of vitamin B12.

    That having been said, I feel that I also need to say that I don’t believe that there is evidence to support all of his current interpretations of the biochemical mechanisms involved. I think it is important to distinguish between what he has reported to have observed clinically in his patients and what his interpretations of these observations are, and to evaluate these separately.

    He has reported that clinically he has found that the best form of B12 to use is hydroxocobalamin, and the best form of folate is folic acid. He reports that they need to be taken together, by the sublingual route, and that the dosages should be 5 milligrams of folic acid together with 2 milligrams of hydroxocobalamin. He also reports that these dosages may need to be taken as many as sixteen times per day, and that the appearance of symptoms that he interprets as an “adrenaline rush” is an indication that additional dosages of these two supplements need to be taken, and that when this is done, these symptoms subside. He acknowledges that if a patient has polymorphisms in the MTHFR enzyme, they may need to add some active folate, such as 5-methyl tetrahydrofolate, to this treatment. In addition, some other supplements may need to be added. If homocysteine is found to drop below normal, he takes this as an indication that methionine is low and must be added. He also finds that magnesium, taurine, vitamin C, vitamin B6, amino acids and/or glutathione may need to be supplemented to get good results.

    With regard to the forms of the supplements, I agree that hydroxocobalamin is a good choice. One reason is that if hydroxocobalamin is used, the production of the coenzyme forms of B12 that are actually used in the biochemical reactions in the cells (methylcobalamin and adenosylcobalamin) will be under the control of the cells themselves. I think this is desirable to prevent overdriving the methylation reaction, which I have seen evidence for (elevated sarcosine, low cystathionine) when large dosages of methylcobalamin are used. I’m concerned that this may limit flow down the transsulfuration pathway and might also impact gene expression deleteriously. Another concern I have about using large dosages of methylcobalamin is that it is known that this form of B12 is able to chemically react with inorganic mercury to produce methylmercury, which can readily cross the blood-brain barrier. Many people with CFS have elevated body burdens of inorganic mercury. I don’t have proof that this will happen in humans, but I am concerned that it might.

    I also don’t favor use of high dosages of cyanocobalamin, because of the possibility of cyanide poisoning, which was observed in one person with CFS who took large dosages of cyanocobalamin in the presence of deficits in the cyanide detox pathways.

    Adenosylcobalamin (dibencozide) may be beneficial, particularly in supporting the mitochondria, but I still prefer use of hydroxocobalamin, allowing the cells to make as much adenosylcobalamin as they need.

    Dr. Vinitsky argues that folic acid is the best form of folate to use on the grounds that it serves as a scavenger for aldehydes and glutamate. This is a place where I have to part company with him. First, I think it should be noted that folic acid is a synthetic form of folate, not found naturally in significant amounts. It is an oxidized form, preferred in commerce because of its long shelf life. It does not take part significantly in the biochemistry until it is chemically reduced twice by the dihydrofolate reductase enzyme to form tetrahydrofolate. The first of these two reactions is very slow in some people, so that their cells are not able to utilize folic acid very well (PMID: 19706381). The result is that it is absorbed into their blood and remains at fairly high levels there.

    I am aware of no evidence that folic acid or dihydrofolate bind aldehydes. According to his presentation, Dr. Vinitsky has apparently reached this conclusion on the basis of literature reports that the level of malondialdehyde varies inversely with the level of folic acid. I think he has misinterpreted the biochemistry involved in this. Malondialdehyde is a product of peroxidation of lipids due to oxidative stress. If a person is low in folate, this can impact the entire sulfur metabolism, lowering glutathione among other effects, and that will result in oxidative stress, allowing increased peroxidation of lipids. So I would argue that this is the explanation for this inverse variation, not a direct interaction between folic acid and aldehydes.

    With regard to glutamate scavenging by folic acid, I don’t believe that the evidence supports this, either. For one thing, most cell types use the reduced folate transporter to import folate, and folic acid is not a very good substrate for this transporter. For another thing, folic acid is also not a good substrate for the enzyme folyl polyglutamate synthetase, which is the enzyme that adds glutamate residues to folate molecules (PMID: 8662720). Finally, the concentrations of folates are several orders of magnitude lower than the concentration of glutamate, so the folates are not likely to have a significant impact on the glutamate concentration.

    There has been some indication reported in the medical literature that elevated folic acid might be associated with increased cancer risk, as I’ve written in the past (PMID: 19499262). This evidence is not very solid at present, and I don’t know whether this is a valid association, but I think it’s something we should keep in mind.

    With regard to taking the B12 and folate together via the sublingual route, I can understand how this might be advantageous. Some people have difficulty absorbing B12 and even folate by the normal intestinal route, for genetic reasons or because of intestinal disorders or intestinal surgery in the past. Taking them together sublingually would ensure that they both reached the bloodstream in good quantities, and at about the same time, so that they would both be available to the cells.

    With regard to dosages, the dosage of hydroxocobalamin that Dr. Vinitsky recommends is the same as the dosage I’ve suggested for the Simplified Treatment Approach, based on Dr. Amy Yasko’s treatment program. The reason for this relatively high dosage, compared to the RDA dosage for B12, in my opinion, is that because of glutathione depletion, much of the B12 is “hijacked” by reactions with toxins. I gather that Dr. Vinitsky agrees that glutathione depletion is responsible, and I note that in some cases he reports using transdermal glutathione to increase the B12 utilization.

    As I’ve mentioned in the past, it may be that the reason Dr. Vinitsky finds such large dosages of folic acid to be necessary in some cases is that the first DHFR reaction on folic acid is very slow in some people, as noted above. If folinic acid, or particularly 5-methyl tetrahydrofolate, is used instead of folic acid, smaller dosages would probably be adequate, in my opinion.

    One thing that I find very interesting is Dr. Vinitsky’s recommendation to increase the frequency of these combined supplements if symptoms that he interprets as an “adrenaline rush” occur. This is reminiscent of the recommendation by “freddd” on the aboutmecfs forum to continue with high dose treatments (though he uses different forms of B12 and folate) when symptoms occur. As you know, in the past I have recommended decreasing the dosages if the symptoms become intolerant, so as to “do no harm” and so as to make it more likely that people will continue with the treatment, so that they can eventually get some benefit from it. I don’t have the comparative clinical data that would be necessary to make a good choice between these two approaches, so this is still an open issue as far as I am concerned. Since both folate and B12 are water-soluble nutrients, it seems likely that the excesses would be readily excreted in the urine, thus preventing direct toxicity, but I don’t know what effects there may be on the body associated with the symptoms.

    I suspect that the symptoms Dr. Vinitsky attributes to an “adrenaline rush” are more likely due to excitotoxicity. His emphasis on glutamate binding by folic acid suggests that he may believe that excitotoxicity is involved, also.

    I concur with his addition of active forms of folate when there are MTHFR polymorphisms, and in fact, I think that these forms of folate are preferable in all cases, for reasons already discussed.

    Dr. Vinitsky’s addition of other supplements makes sense to me, too. I think that his use of low homocysteine during treatment as an indicator of low methionine is probably valid. I prefer direct measurement of methionine in the plasma or urine as well as running the Health Diagnostics and Research Institute methylation pathways panel to see the SAMe and SAH levels, but a conventional lab test of homocysteine might be a good marker for methionine under treatment with B12 and folate.

    I’m also interested to see that he adds glutathione transdermally in some cases, to rescue B12 from being hijacked. This is something that I think might be helpful, for those who can tolerate glutathione. As you may know, for several years I encouraged direct boosting of glutathione in CFS, and it was temporarily helpful to many people, but not a permanent fix for the glutathione depletion. When I learned about the methylation cycle dysfunction that was linked to the depletion of glutathione, I shifted my focus to the methylation cycle, and stopped recommending direct glutathione boosting. As time has gone by and we have gotten more experience, I have begun to see the merit in adding glutathione boosting to the methylation cycle treatment for those who can tolerate it. Some people don’t tolerate it well, and I’m not sure why. Perhaps it brings the immune system and/or the detox system up too fast, so that toxins are mobilized rapidly into the blood. Or perhaps too much of the glutathione is metabolized and either produces elevated cysteine, which auto-oxidizes, or produces too much sulfite for the sulfite oxidase reaction to handle. In the latter case, molybdenum supplementation might help. But for those who can tolerate it, adding glutathione by various means might help to save more of the B12, so that the methylation cycle treatment will be more effective.

    I also concur with the other additional supplements Dr. Vinitsky sometimes adds to his protocol. I have suggested that the vitamin and mineral cofactors for the enzymes in this part of the metabolism might need to be added, as well as amino acids if they are low.

    Now I’ll move on to some of Dr. Vinitsky’s other interpretations of the biochemistry associated with his protocol.

    One thing he notes is that he believes that the hydroxocobalamin and folic acid are serving as scavengers for nitric oxide and peroxynitrite, based on discussions with Prof. Marty Pall. It’s true that hydroxycobalamin will bind nitric oxide (PMID: 16990191), and that 5-methyl tetrahydrofolate (but not folic acid) will react with peroxynitrite (PMID: 16940192). However, it is not clear how significant these reactions are in the treatment effect of these supplements, in comparison to their actions in stimulating the methylation cycle.

    Dr. Vinitsky discussed effects of his protocol on the autonomic nervous system, particularly in terms of bringing the parasympathetic system operation up into balance with that of the sympathetic system. His explanation of this connection was not clear to me. My own hypothesis is that the reason for the low parasympathetic activity is that there is a deficiency in acetylcholine, which is the neurotransmitter for the parasympathetic nervous system. I think that the reason for this deficiency is that the second greatest use of methylation in the body is for the conversion of phosphatidylethanolamine to phosphatidylcholine. The partial block in the methylation cycle causes a deficit in choline production, and that impacts synthesis of acetylcholine. I think there has been a misinterpretation of choline in the CFS literature dealing with magnetic resonance spectroscopy. Because of an incorrect assumption about constancy of creatine, it has been concluded that choline is high instead of low in CFS, which I think is opposite of the actual reality.

    Dr. Vinitsky discussed methylation priorities. I agree that there is a system of priorities for methylation, as there is for all other substances and processes in the biochemistry. Whether the set of priorities he has proposed accurately represents the actual ones, I don’t know.

    He mentioned histamine and suggested that when there is high histamine, raising the intake of B12 and folic acid will overcome it. This makes sense to me, since methylation is used to metabolize histamine in at least one of the pathways.

    He suggested that hydroxocobalamin given sublingually is picked up in the blood by transcobalamin II after about three hours, and that this makes it unavailable. That doesn’t make sense to me, since transcobalamin II is the normal carrier for B12 in the blood, and the cells of the body have receptors specifically for transcobalamin II. Being picked up by this carrier should make the B12 more available to the cells, not less.

    He suggested that the reason isoleucine drops is that its metabolism via methylmalonate is blocked by the functional deficiency of B12. It’s true that its metabolism is blocked, but I think that would cause its level to rise rather than to drop. I suggest that the reason isoleucine drops is that the cells burn amino acids for fuel more than normal in CFS (or autism) because the partial block early in the Krebs cycle due to glutathione depletion inhibits the burning of carbohydrates and fats for fuel.

    Now, Robin, I’ll address the questions you asked on the aboutmecfs forum.

    1. What about CBS upregulation and draining the transsulfuration pathway?

    These are real phenomena. People who have these SNPs do experience faster draining of sulfur metabolites down the transsulfuration pathway.

    2. Is it possible to overpush methylation with the continual high doses of the 5:2 (6-30/40 a day!) and the use of methionine?

    I don’t think it’s likely, unless way too much methionine is taken. When hydroxocobalamin is the form of B12 that is used, as in Dr. Vinitsky’s protocol and the one I’ve suggested, the cells are able to control the amount of methylcobalamin that they make, and that will limit the drive on the methylation cycle.

    3. Methylated form of FA is used for folks who are MTHFR++. Is there are potential using only FA and when exactly does FA become methylated?

    I’m not totally sure I understand what you are asking here. I think you are asking whether people with MTHFR++ can benefit from using only FA, rather than adding 5-methyl tetrahydrofolate. I don’t know for sure, but I think they would do a lot better if some of the latter is used. If the person happens to have a very slow DHFR reaction in addition to MTHFR++, I think they will have a very difficult time using FA to make the active form of folate that their cells actually need. In order for FA to produce 5-methyl THF, it first has to be transported into a cell, which is difficult because most cell types use the reduced folate carrier, and FA is not a reduced form of folate. Then, there has to be a sequence of four reactions inside the cell to do the conversion: two DHFR reactions, SHMT, and MTHFR. If there are SNPs in these enzymes that slow the reactions down, this will make the conversion slower.

    4. FA loses glutamates when it is methylated, I believe. How does the body determine how much FA to methylate? Dr. V. says first priority of the body is to clean up stress, before methylation. I’m wondering about FA losing glutamates which would create a repeating cycle of picking up and dropping.

    As I noted earlier, FA has only one glutamate residue. As it goes through the first reactions in the pathway that I mentioned above, it becomes a better substrate for the folyl polygammaglutamate sythetase reaction, and picks up more glutamates. When it is converted to 5-methyl THF, it loses its glutamate tail. The folate metabolism is regulated partly by the SAMe level in the methylation cycle, and partly responds to concentrations of reactants and products. I’m not sure what Dr. V. means when he refers to “cleaning up stress markers.” That is not very precise biochemical terminology! It’s true that the folates do pick up and drop glutamate residues as they move through their pathways. That’s normal and does not cause problems. The glutamate tails are negatively charged, and they serve to prevent the folates from diffusing across the cell membrane and leaving the cell (except for 5-methyl THF, which does not have a glutamate tail, and is able to leave the cell via the so-called “methyl trap” mechanism. This is in fact what happens when there is not enough methylcobalamin being formed. 5-methyl THF piles up, and then diffuses out of the cells into the blood. In my opinion, that’s why both B12 and folate must be supplemented when treating CFS or autism.

    5. Do you pass FA in the urine with glutamates and aldehydes attached?

    As I discussed above, FA doesn’t bind glutamates and aldehydes, as far as I know. FA is usually not excreted much in the urine, unless large dosages are taken, so that the normal reabsorption of folate by the kidneys is overwhelmed.

    6. What happens to aldehydes. I think I read in another publication by Dr V that aldehydes are passed to HB12 for another purpose…I’ll look that up.

    The body has enzymes called aldehyde oxidase and aldehyde dehydrogenase, and they normally process aldehydes.

    7. What happens to blood/serum levels of FA and cellular levels?

    Because FA is not utilized very well, it tends to remain high in the blood. A person who ate only natural foods (i.e. foods not fortified with FA, as bread and some other foods are) would not have FA in their blood. The cells don’t import FA very well, because it is an oxidized form, and most cell types use the reduced folate carrier to bring in folate. Normally, 5-methyl THF is the dominant form of folate in the blood.

    8. What are the methylation markers..this is mentioned in the presentation and I think the measures are different from Rich’s and Dr. Amy’s.

    I know he mentioned measuring homocysteine. I’m not sure if he mentioned others.

    Best regards,

    Rich
  3. soulfeast

    soulfeast Senior Member

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    Hi Rich,

    Thank you so much for your comments.

    I am using the transdermal form of glutathione from Lee Silsby and so far, so good. I can determine how much each day. It comes in a syringe which can be measured. If I feel like I need to back off, I can very easily and not worry about losing product because it has a separate activator.. the glutathione itself is not activted until I add it, so its shelf stable.

    You have been very thorough, thank you. Im can grasp some of this and need to process the rest. I do have a few questions if you have the time:

    You said:

    >>3. Methylated form of FA is used for folks who are MTHFR++. Is there are potential using only FA and when exactly does FA become methylated?

    I’m not totally sure I understand what you are asking here. I think you are asking whether people with MTHFR++ can benefit from using only FA, rather than adding 5-methyl tetrahydrofolate. I don’t know for sure, but I think they would do a lot better if some of the latter is used. If the person happens to have a very slow DHFR reaction in addition to MTHFR++, I think they will have a very difficult time using FA to make the active form of folate that their cells actually need. In order for FA to produce 5-methyl THF, it first has to be transported into a cell, which is difficult because most cell types use the reduced folate carrier, and FA is not a reduced form of folate. Then, there has to be a sequence of four reactions inside the cell to do the conversion: two DHFR reactions, SHMT, and MTHFR. If there are SNPs in these enzymes that slow the reactions down, this will make the conversion slower.>>

    I meant to say: Is there a potential for a block using only FA? Where FA blocks out the methyl form? I think Ive read that once the cells take in any form of FA then they are shut down to receiving more. So if a cell takes in FA form, then shuts down then cant convert then you are kind of in a bind?

    So if you are also taking the methyl THF, that doesnt guarentee that the methyl THF is even making it to the cells because the FA could beat it to the punch so to speak?

    Also, if one is MTR++ (which i am) then you need a constant supply of the methylated form of b12, which hydroxy can supply, but... hydroxy gets its methyl donor from methyl THF.. SO... if the conversion from FA to methyl THF is slow then would there be a constant supply of methyl donors to the hydroxy b12?

    I understand this all happens so fast.. can the cells convert FA fast enough to keep up with methylation?

    Then will the FA form potentially block the methyl THF if bothe are taken?

    You said:

    >>4. FA loses glutamates when it is methylated, I believe. How does the body determine how much FA to methylate? Dr. V. says first priority of the body is to clean up stress, before methylation. I’m wondering about FA losing glutamates which would create a repeating cycle of picking up and dropping.

    As I noted earlier, FA has only one glutamate residue. As it goes through the first reactions in the pathway that I mentioned above, it becomes a better substrate for the folyl polygammaglutamate sythetase reaction, and picks up more glutamates. When it is converted to 5-methyl THF, it loses its glutamate tail. The folate metabolism is regulated partly by the SAMe level in the methylation cycle, and partly responds to concentrations of reactants and products. I’m not sure what Dr. V. means when he refers to “cleaning up stress markers.” That is not very precise biochemical terminology! It’s true that the folates do pick up and drop glutamate residues as they move through their pathways. That’s normal and does not cause problems. The glutamate tails are negatively charged, and they serve to prevent the folates from diffusing across the cell membrane and leaving the cell (except for 5-methyl THF, which does not have a glutamate tail, and is able to leave the cell via the so-called “methyl trap” mechanism. This is in fact what happens when there is not enough methylcobalamin being formed. 5-methyl THF piles up, and then diffuses out of the cells into the blood. In my opinion, that’s why both B12 and folate must be supplemented when treating CFS or autism.>>

    Well, I think he is using simple terminology so it makes sense to the masses... the glutamates and aldehydes produce stress or at least stresslike symptoms. If you can clean that up first by scavenging them out like a vacuum cleaner, I suppose, then you can handle detox, die off, supplements, treatments better.. with less side effects.

    So whe FA becomes a better substrate for folyl polygammaglutamate sythetase reaction, and picks up more glutamates, isnt it then scavenging glutamates? ??

    IF FA does scavenge glutamates (im not quite getting if so or if not.. how either way) then do they stay attached to the FA and flush out of the body or does the FA drop the glutamate tale, which it seems it will have to if converted to methyl THF... then what happens to that glutamate tail? If the theory were to be correct, then the glutamate tail is at least dropped to make methyl THF.. then has to be scavenged by something. what in the body takes care of glutamates?

    If the high doses of FA are truly acting like vaccuum cleaners for glutamates (and aldehydes), then if it is not all capable of being converted to other forms because of the DHFR, SMHT, MTHR and whatever reasons.. then would it then leave the body with glutamates attached.

    Im wondering about the adrenaline rush as well.. if the FA is scavenging and it drops, then you are recycling glutamates which will mean you will need more FA to pick up what it eventualy drops... unless it leaves the body intact with tail.

    Of course, premise being the FA is scavenging. he says it scavenges best in the di-tetrahydrofolate form.

    Arg! I am so sorry to not be getting this completely... he glutamate tail is negatively charged and this keeps it in the cell, so if it is truly scavenging glutamates which if its picking them up, it is scavenging them?? then does it stay trapped in the cell with the gluatmate tail unless it is converted to the methyl THF form?

    Then... doesnt methyl THF donate its methyl group to hydroxy ... so if so then if there is not enough hydroxy to donate TO.. thats when the methyl THF leaves the cell? What does it need methyl b12 for? Does methyl b12 remethylate folic acid once it loses its methyl group to hydroxy?

    Again. so sorry....
    Thank you Rich, esp for your time and patience.
  4. soulfeast

    soulfeast Senior Member

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    can FA even enter cells.. isnt dhfr in the liver? if taken sublingually and goes straight to blood then it has to go through liver to be broken down to di-tetrahydrofolate then to other forms... which form does the cell take in more readily?

    If methyl thf is most often found in the blood then is that after it is reduced in the cell then pushed back out?

    so confusing.

    Why do some of us have high FA levels in blood.. and what measure is this.. folate or folic acid or methyl thf? but low levels in the cells? Even after months to years of not taking ANY supplemental FA except the methyl and folinic forms? It doesnt make sense if this stuff is excreted...
  5. soulfeast

    soulfeast Senior Member

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    Are we sure about the ratio of hydroxy to methy THF? I hear there is another doc who is working on a transdermal formula at a 5:1 ratio using methyl THF (but possibly the FA form.. ahve to wait until it is out).

    If you are using hydroxy which I think needs a methyl donor from methyl THF, and there is not enough methy THF, then hows methylation supposed to be kept up at a steady rate rather than in spurts?
  6. soulfeast

    soulfeast Senior Member

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    at risk of further belaboring the point.. Neubrander uses methyl b12 only at a certain dilution subcutaneously to maintain an even and constant flow of methyl b12 to keep the methyl cycle constant, esp in the brain. He uses folinic not methy THF. This makes me further wonder about the ratio of methyl THF to HB12 if one wants a continual process of methylation unless the lower amounts of 300mcg of methyl THF are sufficient to supply up to 3-6 doses of sublingual HB12 daily. ??

    I wish all the methylation protocols would get together in a room and work it out amongst themselves. ??
  7. THRiiiVE.com

    THRiiiVE.com Guest

    Hi all...Dana here from THRiiiVE.com and I stumbled upon this thread and was blown away by the level of the thread...way over my head!
    I just wanted to let you know that I am going to pass this on to Dr Vinitsky because I think he could really be interested in not only answering some questions but learning from your perspective.

    One thing that I hope was clear is that he is specifically talking about FOLIC ACID for the purpose of this protocol because it is un-methylated. He believes that the un-methylated Folic Acid cleaves methyl donors from Formaldehyde (converting it to Aldehyce - less toxic) then transferring the methyl to the proximal HydroxoB12 making it MethylB12. The role of all the other forms of Folic are separate from this protocol.
  8. soulfeast

    soulfeast Senior Member

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    I am posting a response I made to a thread in another venue about protein loss in CFS. Any thoughts?

    I think Dr Vinitsky explains the protein issue in his presentation. Homocyestein is converted to HC-thiolactone which destroys proteins. The key is to get and keep methyaltion going.. I think..

    This along with Neubranders idea of a continual slow release supply of methyl b12 makes me wonder about how well HB12 and lower doses of methyl THF are actually working to keep methylation going.. HB12 gets its methyl group from methyl THF (only source??) and if methyl THF is not there, then what happens to methylation. .

    Also if not enough methionine.. wondering what happens.. if it is converted to homocysteine then lost to HC-thiolactone and not being convereted back to homocyseine which will then move on to make methionine.. ????

    Do I have this right???
  9. soulfeast

    soulfeast Senior Member

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    Hi Dana, Thank you for your comment and interest.

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