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Too many free methyl groups

Discussion in 'Detox: Methylation; B12; Glutathione; Chelation' started by retireddpm, Aug 26, 2010.

  1. retireddpm

    retireddpm

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    Is it possible to have too many free methyl groups. I started methyl b12 for a deficiency state with sublingual as Freddd protocol. Did fine for first 3-4 weeks then seemed to go downhill, with tinnitus and arm and foot paresthesias worse. some say this is a sign of recovery but I am not so sure of this.
    Any thoughts appreciated.

    Thanks
     
  2. richvank

    richvank Senior Member

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    Hi, Ron.

    I do think that a person can become overloaded with methyl groups from taking high dosages of methylcobalamin sublingually or by injection. This is an unnatural way of supplying B12 to the cells, which bypasses the normal ability of the cells to control how much methylcobalamin they make. For a person who has inborn errors of metabolism in the intracellular B12 processing enzymes, as freddd has posted that he does, this is the only way to supply enough of the active, coenzyme forms of B12 to the cells. But for people who have CFS as a result of a partial block in their methylation cycle, but otherwise normal B12 processing enzymes, I prefer using hydroxocobalamin. This allows the cells to control the production of methylcobamin. It may be necessary to use fairly large dosages of hydroxocobalamin to overcome the problem of hijacking of B12 by toxins, until glutathione comes up enough to be able to protect the B12, as it normally does, but this will still not overmethylate the cells.

    I might add that freddd has different views than I do about these things, and some people do seem to benefit from his approach, so I think there can be differences from one person to another. Anyway, that's my take on it, and if you want to find out more about my thinking, you can find it at www.cfsresearch.org by clicking on CFS/M.E. and then on my name.

    Best regards,

    Rich
     
  3. retireddpm

    retireddpm

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    Rich

    Thanks so much for the reply. I have switched to the perque hydroxo b12 sublingual. Since my main goal is to raise my b12 levels and try to reverse the peripheral neuropathy symptoms, my biggest question is how much hydroxo b12 is converted to the active forms especially methyl. I can find no references anywhere about this. Freddd states that the body can only convert 10 mcg a day of hydroxo or cyano forms regardless of amounts taken due to conversion limitations and what he calls the keyhole effect. He then states that you can absorb and use 15-20 % of a good methyl sublingual.
    I would appreciate any comments or references regarding this.

    Thanks again

    Ron
     
  4. Freddd

    Freddd Senior Member

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    Hi Ron,

    As regards things changing after a few weeks this is quite normal in the recovery process. If things come to a halt, it is usually because one isn't taking the other needed cofactors, most often Metafolin, adb12, b-complex, or some other things. However, neurological healing takes months. The symptoms are often experienced backwards from the sequence when they were coming on from the latest forms of the symptoms to the earliest forms.

    In my years of reading b12 research I have come across multiple items specifying conversion rates of inactiove to active forms. This is only mentioned in passing usually and is always very vague in how it is stated. The indefinite fuzzy statements are open to much interpretation. So I usually give the 10-30mcg range for conversion as some researchers indicate it is "per day" and others suggest that is is "per incident" for the 10 mcgs. Intentional fuzziness in statements in papers, and there is a lot of that in b12 papers, to me indicates that they don't really have anything terribly concrete. There is a lot of repetition and quoting of earlier fuzzy statements. The statements that are quite clear are that the conversion rate is very limited and approximately matches the rate of IF mediated absorbtion. That is that the interconversion capacity approximately matches the ability to absorb the b12 from food. Another definite statement about cobalamin injections (all forms) is that approximately 99% is excreted by the kidneys unchanged from a dose of 1000mcg. That means that about 10mcg (1% of 1000mcg dose) is retained from the typical dose. That would look like it puts an upper limit on the amount of an hycbl dose that can be converted. If it is excreted unchanged, then it can't be in the body in any form. If 10 mcg is retained and made useful and all of it ends up in serum then serum level would go up by 2000pg/ml. Research on the binding of cobalamin to the transport system suggests that 6mcg will fully saturate the TC2 converting it to HTC2. Other research suggests that it takes up to a dose of 100mcg of inactive cobalamin to supply the bound 6mcg.

    Dose proportionate response is something to look at here. For instance for a long time there was thought to be no dose proportionate response to cycbl or hycbl. It turns out that there is dose proportionate response over the dose range of 1-100mcg according to newer research. For methylb12 the dose proportionality is established for 1-5000mcg by a variety of research. The Japanese research extends that dose proportionality to 50,000mcg of mb12 daily when one includes the central nervous system response.

    Since the dose proportionality of hycbl is limited to what the transport system can provide it is limited to the 6mcg that saturate the system and the number of times that can occur before the Hycbl is excreted. As mb12 and adb12 are not limited by having to fit through ther keyhole of binding to the transport system they have a much higher top end to their dose proportionality.

    Then let's look at this based on the bringing the b12 levels of the body, inclusive of all tissues and serum, up to snuff. This is all a theoretical matter as only cadavers can be fully tested in this way. Let us use 3mg as the total body accumulation of b12. If a person has been deficient for a long time, the body level goes down and down. When there is not enough to maintain the krebs cycle the MMA increases. Then there is the lack in the CNS and the effects on the nervous system, lack of metrhylation and homocystein, cell replication and all the rest. It is not unreasonable to think that the body accumulation is down some amount. Let's use 1mg as a convienient number. If the body needs the 6mcg gotten from food to maintain the levels and cover the days losses via the usual paths, how long does it take to bring the body level up to normal if 10 mcg are actually retained per day? If the backlog can be filled at 4mcg per dose, that would take 250 doses. However, as experience demonstrates, there is no duration of takning hycbl that actually can demonstrate that effectivness. After a year or two years or whatever of taking Hycbl, a person who then takes a dose of mb12 after years of hycbl, will still have startup responses for their remaining still worsening b12 deficiency symptoms. So hycbl demonstrates that it is NEVER sufficient. It never fills the b12 needs of the body to the point that there is nothing left to demonstrate startup responses for either mb12 or adb12.

    Consider the treatment of Pernicious Anemia. Once a month injections of inactive cobalamins stop a person from dying from it but by no means does it make them healthy. It corrects a few symptoms but not the 300 or so that originate with mb12.adb12 defciencies.

    And for the past 50 years, the more widespread hycbl and cycbl become in food and drinks, the more widespread and severe these mysterious stealth diseases, especially neurological, has become. This doesn't establish causality. However, the increasingly high MCV that has become "normal" should be a clue that the population as a whole have inadequate methylfolate and/or mb12. And this increase is occurring despite or maybe becasue of the increasingly widespread usage of inactive folate and inactive cobalamin. Did anybody ever here of MCS (multiple chemical sensitivity) in 1950 or 1960? Lot's of people have it now and it appears that mb12 and methylfolate are effective, with cofactors, at reducing or correcting that. And of course we all knew lots of people with CFS and FMS in the 50s and 60s, RIGHT? And of course autism was as widespread in the 50s as it is now, RIGHT? And there are a whole lot more that could be ennumerated.

    Finally consider that no body is actually deficient of hycbl or cycbl. The body does not use that except in starvation mode for the real thing, and then it can limp along and survive for most. There are 4 b12 deficiencies; body-mb12, body-adb12, brain/cord-mb12, brain/cord-adb12.

    Rich likes to make a big deal out of my reduced ability to use the inactive cobalamins. The thing is as long as I ate meat I was doing ok, not great, but ok. I was a professional ski patrolman. I could ski 2600 vertical feet non stop all day. I could jog 5 miles in 40 minutes every day for years. I didn't have CFS from birth. After the CFS onset, I had trouble walking 500 feet on the level. I didn't almost die of overt b12 deficiency as a young child so my problem wasn't so severe that it couldn't help but be discovered. I developed FMS after being broken in half sideways in a car wreck. This is the same type of post injury trigger half the people here have for FMS. I didn't develop CFS until after 7 years as a vegetarian, of systematically starving my body of mbn12/adb12. Sure I took cycbl, but that turned out to be ineffective. For most taking cycbl and hycbl it doesn't start out ineffective. It becomes ineffective when the person's body can no longer methylate it. In other words the good old methyl block. Cycbl was infamous for having startup effects the first time its taken and then doing a fast fade, giving non duplicatable effects as it exhausts the methylation ability of the body and aquiring the reputation of the startup effects being "placebo" effect.

    So Ron, after 6 months or a year on hycbl, recording how all your symptoms change for the duration, try the mb12/adb12/methylfolate again and compare how it is different from the first time and from the Hycbl for you. I'm sure it will be an interesting comparison.

    As far as reversing peripheral neuropathy with Hycbl I would be very surprised if it does so. Your odds are far better with the mb12/adb12/methylfolate plus cofactors. Keep track of the symptoms and try some A-B crossover periods. With peripheral neuropathy in my experience 75% of all the healing will happen in the first year you get the right combination of needed factors. If the symptoms are actually coming from the cord breakdown of myelin the odds of healing are far worse than if the problem is with the peripheral nerves themselves. Neurological healing is one of those things that mb12 research has shown that mb12 is far superior of inactive cobalamins at doing.

    One other thing to remember, in my experience of giving mb12 and/or adb12 to over 1000 people, people without the symptoms on the list don't have startup responses; none at all generally. Those that originally say they don't have symptoms and then have startup responses then modify their statement to "Oops, I forgot about those symptoms since the doctor told me they were nonspecific and didn't mean a thing years ago." If mb12 were able to force responses on non deficient people via "overmethylation or something one would expect some sort of response from nonsymptomatic people. Instead there is a great big nothing.

    As regards the 15-25% of some sublinguals being absorbed, that comes from my own series of tests compared to injections by urine colorimetry and effectiveness, backed up by similar responses from others.
    Good luck.
     
  5. Joopiter76

    Joopiter76 Senior Member

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    Hi to all,

    Ive been taking Oh-B12 for about a year now as injection (1500 to 3000mcg per day) But instead of going down Methylmalonic acid raised! It has gone a little down while I was taking methyl-B12 drops but didnt go down as much as it should. So as raised MMA is a sign of A-B12 deficiency I have now added A-B12 and M-B12 per injection an sublingual tablets. Now my MCV went up. maybe this is a sign of folate deficiency. My doc told me several times when I take large amounts of B12 I need to take alos large amounts of folic acid otherwise I will run into deficiency. I now another person where the MCV also raised (up to the top of the norm, borderline to raised) So I wonder if this would be the case. On the onset of my illness I had an MCV that was lower and didnt take anything, then during treatment MCV was always in the middle of the norm. Now that I take much more B12 and not the same amount more folate, its going up. So as Im starting to tolerate folate better I will increase this, and if MCV goes down this will have been the reason.

    I wonder if all those who improve on Valcyte or Valtrex take additional some methylation supps. And I wonder if glutathione also goes up with the beginning of the improvement after 6 moths. It would be very interesting to have methylation panel results before and after treatment from this patients.
     
  6. aquariusgirl

    aquariusgirl Senior Member

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    Joopiter

    Some of us have posted before and after vitamin diagnostics labs over at the cfs_yasko site in the files section.

    Of course, most of us/those folks were on hydroxocobalamin.

    I did high dose hydroxy for several years & my MMA was still elevated.

    I was doing a shot of 25mg/ml and some sublinguals too.

    My most recent MMA was 10.4 (figlu was 4.3).

    I don't see much response at 3-4000 mcg of methyl a day.

    So the other day I took 15 mg in one day and got horrendous detox the following day. Felt bad for 3 days. Brain felt demyelinated.

    A couple of days after that, I took 5mg methyl & for a brief period I felt like someone had switched the lights back on.

    I"m wondering if that feeling was due to the cumulative effect.? You would think the earlier methyl B12 had washed out by then, huh?.

    I think the pay-off with hydroxy--if there is any -- is finite & we do need methyl.

    At this point, I just wonder how I can get enough methyl to have healing w/out going thru nasty detox that mobilises more toxins than I can excrete and demyelinates my brain.. (if I'm interpreting that correctly....which I think I am... been down that road before.)
     
  7. aquariusgirl

    aquariusgirl Senior Member

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    Rich

    You talk about overmethylating the cells. But is there any risk of over methylation if one has an elevated MMA? IN teh 10 and above range?

    How do you square your concerns with the large doses of methyl the DAN docs are giving the autistic kids?

    This is tricky. I obviously need methyl, just not sure how to supplement.

    It seems the low doses I can tolerate are completely inadequate for neurological healing.

    Thanks
    AQ
     
  8. markmc20001

    markmc20001 Guest

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    Rich, freddd, and all FYI:

    I use my doctors reccomendations, Freddd's protocol, and alot of trial and error.

    I take all kinds of stuff, but recently started taking much more zinc (150 a day) and Malic acid(3 capsules). Not sure if it was one or the other or both that have made the changes to my system. However For some reason I seem to require less Methyl-b12 losenges. I was taking 3x jarrow 5000mcg a day and now seem to get by on one or two 5000mcg a day. not sure if the zinc or the malic acid changing my requirements. or if I have just lost my bearings on this journey.

    My requirements for p5p seems to have changed, I get wired from the p5p lately. not sure if I have taken too much, or the mailc acid doing it, or if it is the p5p and the zinc interacting(I thought read that is a problem) The malic acid seems to have a noticable effect on my ability to use certain vitamins.
     
  9. aquariusgirl

    aquariusgirl Senior Member

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    Mark

    You've been sick a long time right?
    Did you get sick (nausea,detox) when you first started supplementing 15000 mcg a day of methyl b12?
    how could you tolerate that much?
    That blows me away.

    Sorry, can't comment on the recent changes.
    I did just read you need zinc to heal the gut wall, & 200 processes in the body but anway ...
     
  10. markmc20001

    markmc20001 Guest

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    Yes, 1985. I think I worked up to that point over time like 1 or 2 years. probably the sauans, the vitamin D, the ABX, then the NAC, then adding the ALA, then adding the hydroxy shots, then finally freddd's high dose methyl cobalamin. I started with 1000 and made my way to 15000 over a couple months. So I guess the answer is very slow. In the beginning I probably couldn;t have tolerated so much. Even vitamin D was hard on me in the beginning.

    I don;t take NAC anymore and seem to have a have a difficult time without the ABX.

    Taking the mb12 is kind of like taking M&M's at this point, but I did have detox in the beginning. Slept ALOT when starting the lsoenges and alls kinds of extra brain dyfunction from detox. I don;t get nausea though.
     
  11. Joopiter76

    Joopiter76 Senior Member

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    when I get 5mg M-B12 per injection I get tired and feel more poisoned than usual. I usually feel poisoned but dont know why. The most improvement on strength came from folinic acid, but now Im a little concerned about the paraesthesia like feeling in my legs because I dont know where it comes from. I take 5mg M-B12 and 5mg A-B12 every second day as well as 6000mcg OH-B12 two times a weeks. Additionally I take 2 times daily 5mg M-B12 as sublinguals as well as 3mg Adenosyl-b12 sublinguals. So this isnt that much Freddds talking about and I wonder where does the paraesthesia like feeling come from. It concerns me.

    aquariusgirl: MMA is a marker for Adenosyl-B12 so if you take Oh-B12 or Methyl-B12 it doesnt mean you have enough A-B12. A-B12 works in the mitochondria and if you have massive oxidative or nitrosative stress inside them A-B12 will become depleted faster than it can be generated from M-B12 or Oh-B12. So check for nitric oxide stress, Oh_b12 works best against nitric oxide stress, and OH-B12 is the only one that scavanges H2S. So if you have high H2S levels as many have, OH-B12 should also be taken.
    my doc told me not to take that large amounts of B12 without taking enough folic acid. But folic acid isnt tolerated very well by myself. I guess from detox or reaktivation of partial methylation block.
     
  12. aquariusgirl

    aquariusgirl Senior Member

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    thanks mark
    I'm sure you've said on other threads.. but how many years of abx?
    yes, I think fatigue is a sign of healing.. at least the kind that makes you want to sleep during the day.

    @joopiter: are u doing anything for the poisoned feeling? Very important to bind or chelate metals if you're mobilising them and then replenish minerals IMO.

    I was watching a presentation by Dietrich Klinghardt (link is on the KPU thread on this site) & he says to throw the kitchen sink at that problem when it happens.

    he's talking about how KPU releases loads of metals, and he says to take DMSA, OSR,Microsilica, cilantro to bind up the metals.

    I just offer this up for what it's worth. .. Of course chelation is a controversial subject. Most people agree you shouldn't use mercury chelators if you've still got amalgams. Dr amy yasko doesn't like chlorella because of all the copper. Etc. Etc. Do yr own diligence etc.

    Is there a test for NO?

    I wasn't aware hydroxy scavenged H2S. I will google this, but do you have any links?

    Folic acid: amy yasko says it can accumulate in some people, (possibly because of conversion problems...can't remember the specifics....) and generate increased glutmate which is an excitotoxin, which is bad for the brain.

    Can't you just switch to L5 methyl and folinic acid same as the autitistic kids use?
     
  13. aquariusgirl

    aquariusgirl Senior Member

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    Joopiter

    where do you get the sublingual Adb12? are you talking about the country life brand?
    Very hard to find pure adb12. I guess a compounding pharmacy can make it.
    There's source naturals dibencozide sublinguals... Not sure about their potency.
    Amy Yasko sells drops...Kinda expensive.
    So i'm still looking.
    TIA for any information.
     
  14. aquariusgirl

    aquariusgirl Senior Member

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  15. richvank

    richvank Senior Member

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    Hi, AQ, freddd, and the group.

    As has already been noted, an elevated MMA usually indicates that the cells do not have enough adenosylcobalamin. If a person takes dosages of methylcobalamin in the milligrams range either sublingually or by injection, significant amounts of it are apparently able to diffuse into the cells of the body in general, and are thus available directly to support methionine synthase. However, if this is the only form of B12 that is taken, there may still be a shortage of adenosylcobalamin in the cells, because some of the methylcobalamin would need to be converted to adenosylcobalamin in order to lower the MMA. This pathway depends on having enough glutathione in the cells to protect the cobalamin at an intermediate stage in the pathway to make adenosylcobalamin. In CFS, glutathione is depleted, so that can be a problem.

    freddd's protocol overcomes this problem by including supplemental adenosylcobalamin at milligrams dosages, also.

    In freddd's case, combined high-dose methyl- and adenosylcobalamin is apparently the only option that will work in a really good way, because he has an inherited defect in his B12 processing enzymes. Based on his disastrous experience with supplementing glutathione, I think we can narrow this down to an enzyme that normally acts beyond the step of formation of glutathionylcobalamin in the cells. Normally, this can be converted respectively to both methylcobalamin and adenosylcobalamin. However, in freddd's case, his cells are apparently not able to convert glutathionylcobalamin to methylcobalamin and adenosylcobalamin, so that when he built up glutathione in his cells, this trapped the B12 in a form that his cells could not access.

    It is my view that this type of metabolic defect is not present in the vast majority of PWCs. Their basic problem is that their glutathione is depleted, so that their B12 is not protected from toxins. We have lab test data that shows that glutathione is depleted in PWCs, and also that it is increased as a result of treating the partial methylation cycle block. In PWCs, glutathione is not an enemy, it is a friend. It's a fundamentally different problem at the genetic and biochemical levels between freddd and the vast majority of PWCs. It happens that freddds' treatment protocol also works for many PWCs, because it bypasses the problem of insufficient glutathione, while it also helps him because it bypasses his problem of glutathione binding B12 in a form his cells cannot use. So I think his protocol works for him and for the PWCs for different biochemical reasons.

    My concerns about overdriving the methylation cycle are first that if methionine synthase is driven too fast by high levels of 5-methyl THF and methylcobalamin, too much of the homocysteine is converted rapidly back to methionine, so that not enough is available to go down the transsulfuration pathway to form glutathione. I've seen results of organic acids and amino acids testing on people who were taking high dosages of methylcobalamin, and I think this concern was born out. I think this will slow the progress of recovery, and slow the detox of stored toxins. Second, I'm concerned about the possible effects of overmethylating the DNA. I don't know what the effects of this might be. DNA methylation controls gene expression, and the methylation capacity is normally tightly controlled in the body. Taking high dosages of methylcobalamin might override this normal control, and I think we should be cautious about doing that.

    Though freddd has discounted the possibility that high methylcobalamin will methylate inorganic mercury, I still remember the people who reported serious neurological symptoms right after getting high-dose I.V. methylcobalamin. I realize that freddd does not advocate I.V. methylcobalamin.

    The DAN! doctors give methylcobalamin subcutaneously. I think this limits the rate of release of methylcobalamin to the blood stream, from the subcutaneous fat layer, especially prominent in babies.

    All I can suggest is to come up slowly on the dosage, if you find that you need methylcobalamin. As you know, Amy Yasko recommends methylcobalamin for people whose genetics indicates that they do not have enough methyl groups to do the conversion from hydroxocobalamin. Other ways of dealing with this might be to supplements some SAMe directly, or to boost the alternative BHMT pathway to make SAMe with betaine (trimethylglycine), making sure that there is also enough methionine to feed this pathway, so that more SAMe can be produced.

    freddd has argued that the ability of the body to utilize hydroxocobalamin is limited to microgram levels per day. I think that is only true if the hydroxocobalamin is taken orally, so that its absorption is limited by the intrinsic factor mechanism. If it is taken sublingually or by injection in milligram quantities, I don't think this limit applies, because it is capable of diffusing into the cells of the body in general in the same way that methylcobalamin and adenosylcobalamin do in his treatment protocol. Once the hydroxocobalamin gets inside the cells, I think that the normal B12 processing pathways have a greater capacity than the limit posed by the intrinsic factor absorption pathway in the gut. Of course, if there is an inborn error of metabolism in these B12 processing enzymes, which freddd has reported having, and which is also evidenced by his negative response to building up glutathione, then I agree with him that hydroxocobalamin would not be very effective. But again, I don't think that's an issue in the vast majority of PWCs, and I think that the widespread positive response to hydroxocobalamin treatment in the CFS population is evidence of that. For documentation of this, see the reports on our clinical study at www.cfsresearch.org. We have measured data that shows that hydroxocobalamin works well in a cohort that is documented to actually have CFS by the international definition. When freddd speaks of his 1,000 people, I continue to wonder how many of them actually had CFS, as opposed to B12 deficiencies from a variety of possible causes, including the one he has, as well as those with pernicious anemia, poor B12 absorption because of gastrectomy or gut disorders, transcobalamin deficiency, etc. freddd's treatment protocol will work for a wide variety of B12-related problems, but for different reasons in each cohort, and I object to applying his personal results directly to explaining what goes on in everyone who has CFS. I don't doubt that it will also work for many PWCs, but I think that some caution should be used, for the reasons I have given. And to tell people with CFS that they should avoid glutathione because it produced problems for freddd just does not make sense, in my opinion, based on the documented lab evidence. I would love to see some measurements run on freddd so that we could better understand these differences. The methylation pathways panel, together with urine organic acids (a Genova MAP panel) and plasma and urine amino acids tests would be very instructive, I think. Handwaving arguments can be interesting, but there is nothing like some hard data to figure out what is actually going on.

    Best regards,

    Rich
     
  16. Joopiter76

    Joopiter76 Senior Member

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    Thanks rich for this explanation, I wonder what it indicates in my case as I took daily Oh-B12 inj. for over a year and MMA raised !! I guess I have a converting problem or the A-b12 is oxidized faster than it can be synthesized. So how can I check this? How can the b12 converting enzymes be checked. genetic testing? How do are these enzymes/genes called?

    How much M-b12 and A-b12 do you think Rich is orally and how much is o.K. per injection?? Are 5mg inj. three times per week too much?

    I guess the question is how much active b12 is immedeately distroyed. As the strength of oxidative and nitrosative stress is very different in PWCs.

    thanks.
     
  17. aquariusgirl

    aquariusgirl Senior Member

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    Well, that made a lot of sense to me.

    I was struggling to understand Fredd's rational for not using glutathione, esp. since don't some of the Alzheimer's folks mix up glutathione and B12 precisely so they can get some glutathionylcobalamin to boost their b12?

    It would be nice to nail this all down, because it's tough enough to do these protocols w/out all the apparent contradictions.

    Anyway, I'd like to thank you both for the time and effort you've put in. I hope you can work out all the bugs.
     
  18. aquariusgirl

    aquariusgirl Senior Member

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    I was wondering the same thing Joopiter.
    How much methyl is safe?
    And if ppl have a high H2S level for example, won't they need a higher dose of hydroxy because it's being used up scavenging sulfite?
    My cystathionine is 230 on my last UAA (top of the range is 50), & I feel like my brain function has been even worse recently.
    I took 2ccs of 25mg/ml hydroxy today and 5mg of methyl & I feel pretty good.
    I think my cystathionine is high because I am doing amino acid IVs and a lack of B6 is holding up the transamination reactions...but I'm not sure.
    Sorry.. so my point is ..maybe I need lots of hydroxy to scavenge the sulfite created by the H2S generated by the cystathionine..and of course that leaves less to drive the methylation cycle, even assuming most of it isn't vaporised by toxins.

    How do you figure out how much is enough?
     
  19. Joopiter76

    Joopiter76 Senior Member

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    I can say that Adenosyl-B12 together with Mg Injections helped me a lot, I dont need Mg injections actually.
    I can state as most PWCs get adverse reaktions when starting detoxing that the earlier you begin the better it is. So as I started with ALA and vit C Glutathione all as Infusion and all every day, directly after I became bedbound within 3 months after illness onset I tolerated this well when I then stopped this treatment after some months everything became worse, as the nitric oxide stress wasnt gone. So 4 months after stopping I restarted with Glutathione injections and became headache, but I didnt stop and after some weeks this was gone. Sometimes I felt a little worse after GSH but within a few months this improved an everytime I got GSH I felt better. So there is evidence that if the cells suffer from oxidative stress and get additionally depleted from GSH the apoptoic rate increases about 80% and ATP production falls. So why should GSH be bad, the only thing is because GSSG is toxic but what is more toxic peroxynitrite, superoxide not working metabolism?? I think the answer is clear.

    @AQ: usually Cystathione is high because of B6 deficiency, maybe try P5P but I dont know if your CBS suggests this. Maybe you also run out of zinc?
     
  20. aquariusgirl

    aquariusgirl Senior Member

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    What's the zinc connection?
    Yes, I have 2 CBS upregulations.
     

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