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Methylation

Discussion in 'Detox: Methylation; B12; Glutathione; Chelation' started by Cort, Aug 10, 2009.

  1. Jody

    Jody Senior Member

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    Sushi,

    You nailed it for me.

    I second this.:D

    I'm on board with you, jen, Wayne and Lisa.

    Gotta love this place. :D
  2. R**

    R** Senior Member

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    Questions

    Not as gifted as some of you with the science, but I will tread forward.

    Yep, Joey, Dr. K did say something to that effect. I cant remember his exact words, but I felt doomed. I didnt see him correct that implication in the DVD series. I have heard it passed on from a patient of his that he believes that KPU has to be treated for life. He is basing that on a test for pyrolles (however you spell that) in urine not a genetic test, so how do we know its permanent? Dr. Yasko thinks lead could be interfering with the heme cycling making heme somethings bind B6 and zinc. (her board) There is a cascade effect with other nutrients from there (from Depression Free Naturally).

    I'm not sure DNA cant change. Im confused on that point. I also wonder about the 95% of genes that we dont use and their roles. I get the impression from the books I have read that we can epigentically change the expression of genes in many different ways as have been listed by you all. Bruce Lipton seems to indicate DNA can, but I could be misunderstanding. He said something about cells in a perti dish lacking enzyme to digest lactose. they are given only lactose and they develop the enzyme.. so maybe that is more epigenetic than a change in DNA? maybe those hidden genes pop out llike little angels and do this stuff. :D ???

    You raise mice without nuturing, their genes express "badly." You raise them with nuturing, they dont express "badly." You switch them.. place unnurtured mice with nurturing mice, the expression switches and visa versa. One example of how expression can change. (The Genie in Your Genes)

    What I dont get is if my methylation gene, lets say the MTRR which is involved with B12 absorption or recycling.. I forget.. if that gene is "defective" .. and expressing or not expressing.. what does that mean? If it does not express, seems to me it is not working at all. If it is expressing, then it is working "badly?" ???

    I am either experiencing detox or just more flares on the yasko methylation protocol. Urine test this weekend to see if there are clues there. I think the ammonia protocol and gluatmate/gaba balancing has been helpful. I am still not doing well. But just started and have not ramped up to full simplified (which I am taking with yasko support for other genetics). I get the impression that the methylation protocol simplified has helped some people and others the full yasko is more helpful.. maybe it is the magic key for some and just some help for others.

    I am just seeing that there are so many gene "defects" that could get us into trouble.. if they were all "expressing" we would all be doomed. I looke dup cancer genes and was floored. Which leads me back to one of my questions above.. which genes are just on the side and express or dont and when not expressing dont have any action or role in the body and which ones do we always need to act and you cant unexpress them without losing their function? Does that make any sense at all?
  3. R**

    R** Senior Member

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    Woo Woo

    I must be center left (or would that be right? since woo woo is probably more of a right brained phenomenum) on the woo woo. I wish I was less skeptic sometimes. Placebo can account for 35% of all healing including those under the allopathic umbrella.
  4. jenbooks

    jenbooks Guest

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    Sometimes you just don't have the correct functioning gene. The clearest example of this would be the "one gene" diseases like cystic fibrosis or SCIDS (severe combined immunodeficiency syndrome). There are several causes of SCIDS--which leads to "bubble baby" syndrome with no functioning immune system. Several have recently been cured with gene therapy--to insert the correct functioning gene.

    If you don't HAVE a good functioning gene, you ain't never gonna have one...

    Most conditions are not that simple. There are polymorphisms--variations in genes. They might be a benefit in one environment (gene for sickle cell anemia which protects against malaria because the red blood cells are misshapen and don't host the malaria parasites well--you'd benefit from that in Africa with lots of malaria, but you aren't too happy with that gene here in America...) and be a problem in another. Moderately okay methylators might do fine if not poisoned with a mouthful of amalgams. Nature usually doesn't present us with that severe kind of mercury poisoning, so those genes generally sufficed, and natural selection did not pressure them out of existence.

    Some genes can be upregulated and downregulated by diet fairly easily. For instance, the genes that regulate the 3 types of estrogen you produce as a woman. We all have them. And they are responsive to diet. You can eat a lot of broccoli for 3 weeks and the gene activity for the estrogens will shift that quickly.

    Its complex so not easily simplified.

    Don't take Lipton to heart. He plays fast and loose. He has a good scientific background but he likes being a mystic guru and so he makes all kinds of leaps and claims that don't have backup.

    The environment, and life's happenstance, has a big role to play. I remember reading about two elderly identical twins. One was healthy as an ox, the other had all kinds of debilitating health problems. Not much difference in how they lived. Obviously one had exposure to viruses or toxins that the other didn't.
  5. Sushi

    Sushi Moderator and Senior Member Albuquerque

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    Jirtle Genetics Lab Duke

    I am crossing a bit into another subject area, but it follows on from recent posts. Here is an interesting place to watch: http://www.geneimprint.com/lab/intro/

    I wrote to Dr. Jirtle (asking if he might get interested in us, and he actually replied in a very nice manner, though we are not on the current research menu. Here is a bit from the Intro to the lab. If you poke around this site, you may find interesting stuff--I did!

    "Welcome to the laboratory of Randy Jirtle in the Department of Radiation Oncology at Duke University. Extensive human epidemiological studies and experimental animal results support the early origins of adult disease hypothesis [Jirtle and Skinner]. This theory proposes the intriguing idea that the evolution of developmental epigenetic plasticity, which enables an organism to adapt to environmental signals during early life, can also increase the risk of developing chronic diseases when there is a mismatch between the perceived environment and that which is encountered in adulthood. Moreover, these environmentally-induced epigenetic modifications can leave a transgenerational legacy because they are not always completely erased during egg and sperm formation. The overall objective of our research is to define those targets in humans that are epigenetically labile, so that we can better diagnose, prevent, and treat human diseases and neurological disorders."
  6. R**

    R** Senior Member

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    I wish I understood that, Sushi...

    Jenbrooks, I think thats where I get a confused. I think he does play loose (which I like on the one hand), and maybe he has made some intuitive leap as well.. I dont know.

    What I am dealing with are the methylation genes. So they are what they are and until some load hit them hard or a continual load finally broke their backs in a sense, I was fine enough and functioning.

    I am not sure what any one factor was, but I am betting stress and infection along with compounding toxins from poorly functioning methylation.

    So yasko and others propose a nutrigenomic way to bypass I think the methylation pathway. Once it is broken it has to be fixed. I am getting with the help of your comment that possibly the gene expression could be upregulated or downregulated to extremes in this internal environment.
  7. jenbooks

    jenbooks Guest

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    Sushi, Randy Jirtle has done wonderful work.

    R**, not exactly fixed, but bolstered up so it can handle its overload.
  8. JanisB

    JanisB Senior Member

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    When I had a practice, I had two people with ME-CFS work with a practitioner using the Bio Meridian, and then, on the basis of their individual energetic readings, she made homeopathic detox drops. Since they were super-sensitive individuals, they put one drop on their skin. Well, neither could tolerate the detox. One became so angry she couldn't sleep, the other sick and faint.

    The point I'm making is that homeopathics can be quite potent, but if the detox pathways aren't open, some individuals can't tolerate even the most gentle detox push.

    I hope you get well with homeopathy. I got rid of hyperthyroid once in the past with a talented classical homeopath, and saw remedies work wonders on my daughter, but I personally couldn't get too far with it on this illness.

    Janis
  9. R**

    R** Senior Member

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    jenbrooks

    Bolstered up is perfect. Thank you for filling in the pieces for me.
  10. aquariusgirl

    aquariusgirl Senior Member

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    yasko/methylation

    Very interesting about Klinghardt's remark about how long it would take to recover by supporting methylation only.
    Sort of rings true to me.
    I have been on yasko or simplified methylation support for 30 months approx.
    I would say I am about 35 percent improved. I would say my energy envelope runs to 4-5 hours a day.
    Acumen labs show I am only making modest amounts of energy (ATP tests), which is better than the energy deficit I was running for about 15 years.
    But I still have only a modest methylation capacity,as measured by that Vitamin Diagnostics panel, and at this rate it could be several more years before I could get back to some type of work.
    I'm told one of the bottlenecks is methyl B12 and I haven't been using that up to now.
    I just started experimenting and I got too high a dosage and it really did a number on my brain, so I'm gonna have to back down and try a lower dose and build up. But, this just seems like it's going to take years.
    Dont' get me wrong, methylation support turned everything around but it's been a long, hard slog, and if Rich Van K is right and excretion is the rate limiting factor, then it seems like you would have to add other therapies to speed it up.
    Question is what's safe? I wonder about IVIG. Haven't heard much about that on here. I know some of the autistic kids are going that route and having some positive results.
    Any adults here tried IVIG?
  11. JanisB

    JanisB Senior Member

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    So glad you hear you are making progress. :) I've been doing the methylation for less than a year and I realized yesterday that I have nearly eliminated all the symptoms of a pounding heart. Plus, I am often sleeping soundly without the need for sleep medicine. But I still can't walk, bike, or stand on my feet much.

    Fortunately, I'm going to see a Doc who does neural therapy and acupuncture (like Mike Dessin did) and hope to get off this home pharmacy of supplements and regain an active life. Keeping my fingers crossed and the prayers flowing.

    Janis
  12. jenbooks

    jenbooks Guest

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    If people have a chance, could they put on their profile page what their supplement regimen is? Then when we see posts about improvement we can correlate that...Janis, I think you're on something like the Simplified Protocol, right? And Aquarius, too?

    I'm interested to start with either hydroxy & folapro and/or Fredd's approach with the adenysol and methyl b12.
  13. Tony

    Tony Still working on it all..

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    Agreed Jen. I also think we need to show what our particular illness looks like (as much as possible anyway) as we are so diverse as a group.
    It's impossible to compare with others if we only know they have a diagnosis of ME/CFS. What does that look like? High viral load tested? Gut dysbiosis, hormones, sleep dysfunction tested? etc. It sure isn't the same for us all.
  14. Freddd

    Freddd Senior Member

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    On the subject of detox I have a few things to say. Order of starting and combinations of supplements appear to have a profound effect on this. Some folks have hinted at the effects they experienced when having to discontinue some things until later and so on. I don't think that this order of supplements has been at all explored generally.

    Many of the symptoms being chalked up to detox also happen to be b12 deficiency symptoms, quite possible being intensified by the toxins without the protective and healing effects of the actual active b12s. The incidence of these detox reactions appears to be something like 100x more frequent when methylators are started with hydroxycoblamin rather than some months AFTER methylb12 and adenosylb12 are started, by which time many of the reported symptoms would have healed and no lponger be a factor. As this is observational I can't be sure of all the details.

    I don't know how to make the switchover. I suspect that quitting the hydroxyb12 and backing off on the methylators and then titrating the active b12s, possibly starting with adenosylb12 then methylb12 and then later after those effects diminish, starting up one methylator at a time as the effects diminish after each addition may just be the way to do it. I have cautioned against starting them all at once because of overwhelming effects. With methylb12 there is a rapid falloff of startup effects as the intensified symptoms actually heal and go away and stay away so that each added item of a group has less and less effect generally. What they don't tend to do is stay around for months at high intensity. For instance, methylfolate, when added after methylb12 and SAM-e has no particular startup effects of any note at all for most people. It's a non event. I was surprised to read of all the startup effects attributed to it methylfolate when hydroxycobalamin is taken. In hundreds of people starting methylfolate NONE have had to titrate or reduce the dose because of startup effects of any kind.

    In the six years I have been at this the ONLY people showing up at other sites where I have been active with "detox" symptoms are those on inactive cobalamins such as cyanocoblamin and hydroxycobalamin and typically a lot of methylators. With what I have heard here it is becoming increasingly clear that these "detox" symptoms which look an awful lot like methylb12 deficiency symptoms, are characteristic of hydroxycobalamin based protocols and not methylb12/adenosylb12 based protocols. It had been apparant previously that the people with the most and most intense reactions to methylb12 were those previously long established on inactive cobalamins. Now it is evident that they have these same reactions for much much longer while on hydroxycobalamin.

    It is my OPINION that the hypothetical and theoretical basis for using hydroxycoblamin instead of methylcoblamin is just plain wrong in practice. Fear of the methylb12 briar patch makes people jump into the hydroxycobalamin tar pit instead with far worse results, metaphorically speaking.

    I'm going to go ask around of some people who have hopefully sucessfully made the transition from hydroxycobalamin with "detox" symptoms to methylb12/adenosylb12 without those symptoms and see what I can find.
  15. Marylib

    Marylib Senior Member

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    Hydroxy vs. the other ones

    Not sure where this post is fitting in, but I was wanting to ask something of Freddd and whoever else has a good brain: I am so unclear about all this. Is it Rich K who advises the hydroxy injections, rather than the kind of B12 Freddd uses? Have both these fellas compared notes at any time? That would be useful, eh?
    I would like to give Freddd's or Rich K's protocol a try, but at this point I am confused.
    Please help someone, if you can. My brain needs a bit of help here.

    Thanks!
  16. richvank

    richvank Senior Member

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    To freddd (and the group).

    Hi, freddd.

    I'm the guy who (about two and a half years ago) extracted (with the help of a person who has CFS) part of step 2 of Amy Yasko's treatment program (primarily used in autism), called it the "Simplified Treatment Approach," and suggested that it be tried as a treatment for CFS. This protocol includes five supplements. The main B12 supplement is sublingual hydroxocobalamin. It also includes both 5-methyl tetrahydrofolate and folinic acid.

    I've studied the extensive posts that you've made to this forum, and I'm aware of your position on which forms of B12 should be used, and which should not.

    Let me just say up front that I find what you've done very impressive, and I imagine that it has helped (and expect that it will help) a lot of people.

    Since quite a few people have been raising questions about our apparent differences, I think it behooves me to make some comments here, for what they are worth.

    I want to acknowledge that I realize that I have a lot to learn about all of this, and I want to say that my goal is to try to find the truth, and to use it to help as many people as I can to recover from CFS. I'm not motivated to try to defend a hypothesis for the sake of trying to be "right."
    So I hope you will view what I say in that light.

    The first thing I would like to clarify is the distinction between an inborn error of metabolism (IEM), which stems from a rare and serious inherited genetic mutation, and an acquired syndrome. Chronic fatigue syndrome, by its case definition, is an acquired syndrome. In the words of the Fukuda et al. case definition, the fatigue must be "of new or definite onset (has not been lifelong)". An IEM, on the other hand, is by definition "inborn," i.e. lifelong. There is evidence for a genetic component to the predisposition to developing CFS, but the syndrome itself is not apparent in the first part of the person's life. I realize that this is just a consensus definition, and it has many problems, but nevertheless, this is what it says, and people who have been diagnosed on the basis of this definition do not have a lifelong illness.

    From what you have posted, Fred, I understand that you have an IEM that involves the genes that code for one or more of the cobalamin processing enzymes. On the other hand, the people to whom I proposed the "Simplified Treatment Approach" have chronic fatigue syndrome.

    As you may know, while this number varies depending on which definition of CFS is used, and is the subject of current debate, the prevalence of CFS as defined by the Fukuda et al. definition has been estimated at about 0.4% of the population by Jason et al., which would amount to over a million people in the U.S. alone.

    I have not been able to find published data on the prevalence of the cobalamin processing-related IEMs. I've read that cblC is the most common of them, and that it is "rare." I'm not sure how rare. One source, dated in 2006, reported that there were a total of 250 known cases.

    My point here is that only a very small fraction of people with CFS can possibly have the IEM that you inherited.

    In pointing this out, I am in no way trying to minimize the severity or the importance of your condition. As you pointed out, you are fortunate to be alive, given the experience of many people who inherited the IEM that you have. I do want to suggest, though, that these two are different, and that there is not much comorbidity between these two disorders. As such, though much of what you have learned in treating your IEM may apply to the treatment of CFS, there are likely also some differences.

    You have emphasized that in the treatment of your disorder, it has been necessary to use large dosages of methylcobalamin and adenosylcobalamin, and that other forms of cobalamin, such as hydroxocobalamin, are not useful. According to my understanding of the IEM that you have, you are absolutely right about that, and the fact that you have found this out is vital to your regaining your life.

    However, for those who do not have these IEMs, which as I've indicated above would include the vast majority of those who have CFS, other forms of B12 are useful. In fact, recent research (PMID: 19447654) indicates that whatever the form of cobalamin, when it enters a cell in the normal way, the first thing that happens is that the beta ligand (whether cyano- hydroxo-, aquo-, methyl-, or adenosyl-) is removed from the cobalamin molecule by the cblC enzyme, before the cobalamin goes on to be converted to either methylcobalamin or adenosylcobalamin. So in the case of a person who does not have these IEMs, any form of cobalamin can be used to produce the two active coenzyme forms. These researchers did find, however, that the initial form of the cobalamin did have an effect on the relative amounts of methyl- and adenosylcobalamin that were formed. Based on this, I do not think it is valid to state that hydroxocobalamin cannot be used in the treatment of CFS.

    You have made the point that use of methylcobalamin and adenosylcobalamin should, however, suffice for treating any of these B12-related conditions, including the IEMs and CFS. I agree that this is true, but I have one concern with use of high dosages of methylcobalamin in CFS. It relates to the fact that many people who have CFS have had amalgam fillings in their teeth during many years of illness, during which glutathione has been depleted in their bodies. It is likely (and there is evidence to support this) that these people have significant body burdens of inorganic (mercuric) mercury. It has been shown that methylcobalamin has the capability of converting mercuric mercury into methylmercury, and it has also been shown that methylmercury is able to cross the blood-brain barrier readily, thus delivering a major neurotoxin into the brain. I am concerned about this. I have heard of two cases in which high dosages of methylcobalamin were applied intravenously in the presence of significant apparent body burdens of mercury, and in both cases, the people reported what seemed to me to be symptoms of neurotoxicity shortly afterward.

    Do I have quantitative evidence to show that this is a problem? No, I don't. Methylcobalamin is used a lot in autism, as advocated and practiced by Dr. James Neubrander. However, babies and young children do not usually have amalgam fillings. The bulk of the mercury they have received, such as from thimerosol in vaccinations, has been organic ethylmercury, which unfortunately has already had a chance to enter the brain.

    When sufficiently large dosages of methylcobalamin are given, as you have noted, the carrying capacity of the transcobalamin carrier protein in the blood plasma is saturated, and the excess methylcobalamin exists for a time in the blood as free molecules. It is this methylcobalamin that concerns me, in terms of its capability to react with mercury. I realize that you need to do this to get enough methylcobalamin into your cells, given your IEM, but this is not true for the majority of people with CFS, and I think there is a risk in doing it this way if there is much inorganic mercury present. I can't prove that this is a problem, but I'm concerned that it might be.

    Incidentally, I am not a fan of using large dosages of cyanocobalamin, either. I know of one case where the person developed cyanide toxicity from the use of milligrams-level daily dosages of cyanocobalamin in the presence of depletion of all of the body's mechanisms for detoxing cyanide.

    I would also like to comment on glutathione. You have emphasized that adding glutathione torpedoes your ability to make use of methylcobalamin. I can understand this, since it will react to form glutathionylcobalamin, and given your IEM, your body is not able to convert this back to methylcobalamin. However, for the great majority of people who have CFS, this is not a problem, and in fact, if my hypothesis is correct, the lack of enough glutathione to form glutathionylcobalamin, which normally protects cobalamin from reacting with toxins at an intermediate stage of its processing in the cell, is at the root of the pathogenesis of CFS. As I noted in an earlier post that was relayed to this board, glutathione is not part of the Simplified Treatment Approach, but some people have added it and found that it has been beneficial. Others report that they cannot tolerate it. I'm not sure why, but suspect that it raises either cysteine or sulfite too much in some people. Adding molybdenum has helped some people, suggesting that sulfite was the problem in those cases.

    Well, I just wanted to make those points. It is not my desire to be argumentative, and I certainly do not want to discourage you from helping a lot of people. I'm willing to listen, and hopefully learn, from any response you might want to offer on these issues. I just wanted to try to clear up differences, to the degree possible.

    I wish you the best.

    Rich Van Konynenburg
  17. aquariusgirl

    aquariusgirl Senior Member

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    How much methyl B12 is too much?

    Hi Rich

    Do you think that the risk of neurotoxicity from methyl B12 supplementation in PWCs with a body burden of mercury is seen at any dose or is there a threshold (dosage level) at which it becomes a concern?

    I'm guessing some of the adverse effects seen with very small dosages of methyl B12 could be demyelination.. as the brain dumps metals.....and not necessarily mercury being moved into the brain or whatever?

    Thanks
  18. Freddd

    Freddd Senior Member

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    Hi Aquariusgirl,

    I'm going to chime in here too with an opinion from a different basis, while my more complete answer is under preparation for Rich. First, as demyelination is a methylb12 deficiency symtom how would one ever tell the difference? And second, as 80% of mercury's neurological effects are those of b12 deficiency and since mercury appears to sit there disabling the methylb12 and preventing it's functioning and thereby contributing to b12 deficiency symptoms while it sits in the brain especially or anywhere in the body possibly how would one ever be able to tell the difference? I don't really have an answer to this, just a consideration that is not often brought up about mercury. When mercury steals the methyl group from methylb12 , the cobalamin becomes deactivated and ceases acting as b12. It appears that as mercury mops up methyl groups from any convienient methyl donor the cobalamin remains disabled. Without active b12 demyelination occurs.

    I know this isn't an answer, just a consideration that needs explaining if your question can be answered.
    .
  19. richvank

    richvank Senior Member

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    Hi, Freddd.

    I'm afraid I have to take issue with your statement quoted below:

    Research has shown that mercuric mercury can accept methyl groups only from methylcobalamin and related corrinoid molecules. The reason is that mercuric ion has two positive charges, and it can accept only a negatively charged methyl group (that is, a carbanion). Methylcobalamin and related corrinoid molecules are the only methyl donors that can supply carbaniions.
    This was shown by Wood et al. back in the 70s.

    The bacteria in the aquatic environment that methylate mercury use these molecules to do it, and this is apparently a protective mechanism to move mercury out of the bacterial cells. The mercury in the environment comes primarily from coal-fired power plants, and rains out of the atmosphere to enter the waterways, where certain bacteria methylate it. It has been shown that the sulfate-reducing bacteria are the ones that produce most of the methylmercury in the aquatic environment. The methylmercury then moves up the food chain, and that's how the larger fish, such as tuna, end up containing enough methylmercury that the EPA has put limits on its consumption.

    With the recent attention given to sulfate-reducing bacteria in the gut of PWCs (as evidenced by positive responses on the urine H2S test), I'm wondering how much methylation of mercury is also going on in the gut in these people. If this is a significant process, it really points to the importance of giving a high priority to fixing the gut problems in CFS.

    Best regards,

    Rich
  20. richvank

    richvank Senior Member

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    Hi, aquariusgirl.

    Sorry, I don't have a good answer to your question. My concern is based on theoretical considerations and a very small amount of observation.

    As I mentioned in my earlier post, I'm concerned that unbound methylcobalamin may react with mercuric mercury.

    The dosage required to produce unbound methylcobalamin is pretty small. The instantaneous carrying capacity of all the transcobalamin II in the blood plasma is only a few micrograms. If more than this is put in in a short time, there will be unbound methylcobalamin. The lifetime of transcobalamin-B12 is thought to be somewhere between one and 12 hours, and the amount of transobalamin II can be increased somewhat by the presence of free cobalamin. So if the methylcobalamin is put in more slowly, more of it will be carried by transcobalamin II.

    But there's also a rate-of-reaction dependence. Reaction rates increase as the concentration of the reactants are raised. So going to higher concentrations of unbound methylcobalamin can be expected to increase the rate of reaction with mercury.

    As you probably know, methylcobalamin is used a lot in autism, both by the DAN! doctors and by Amy Yasko (the latter depending on genetic polymorphisms in the patient). Dr. James Neubrander puts in enough to make the urine turn pink, which means that there is a significant amount of unbound methylcobalamin in the blood. They don't seem to worry about methylating mercury, but as I noted before, I don't think the autistic kids have the amounts of inorganic mercury in their bodies that adults with CFS have.

    Some PWCs report that they use significant dosages of methylcobalamin (milligram-levels) and don't have neurological problems. But how much inorganic mercury do they have on board?

    I wish I had the answers to these questions. Maybe I'm being overly cautious. I really don't want people to become more ill as they are trying to get better, though.

    Best regards,

    Rich

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