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B-12 - The Hidden Story

Discussion in 'Detox: Methylation; B12; Glutathione; Chelation' started by Cort, Jul 26, 2009.

  1. dmholmes

    dmholmes Senior Member

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    Hi Rich, in the interest of gauging effectiveness I'd be willing to switch from mb12/adb12 to hb12 for a period of time. It would be nice to have the methylation panel done first, but I don't think it is available yet. Any value in trying that?
     
  2. This is weird. I took the same dosage of B12 an hour and a half ago (added the methyl-folate on a empty stomach this morning), and don't feel any shift???? Could a temporary plateau be reached after one dose???

     
  3. maryb

    maryb iherb code TAK122

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    Thank you so much Rich for your detailed reply. I have ordered the basic supplements. so maybe I will just try starting very slowly with them.
     
  4. Freddd

    Freddd Senior Member

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    Hi Rich,


    Rich said:

    freddd has reported that in his case, he found glutathione or its precursors to be deleterious. He has also reported information suggesting that he has inherited a mutation or inborn error of metabolism in his B12 processing enzymes. I suggest that based on his experience with glutathione, this mutation must be located in an enzyme that is involved in a step beyond the use of glutathione to remove the methyl group from cobalamin. Apparently, his cells are not able to replace the methyl group on cobalamin after it has been removed, or to add an adenosyl group to cobalamin. Thus, he has found that the only way his cells can get enough methylcobalamin and adenosylcobalamin is to supply these active, coenzyme forms directly as supplements, taken in large dosages. This is what might be referred to in the physical sciences as a "brute force" approach. I can understand that it is the only thing that works in a case like his, and I'm glad that he discovered it.

    I do agree with most eveything in this paragraph in general. However, I disagree with calling it a brute force approach. I consider it to be a particularly elegant approach. I'm a systems analyst in the healthcare field and have been for about 30 years now. I'm also a philosopher though not professionally. This approach is as a result of solving a serious problem via massive reading of the literature, not via throwing enough mud on the way and see what sticks. I was misdiagnosed and mistreated by approximately 100 practioners of many varieties through the decades. The question that came to my mind was WHY. I dissected the reasoning of the many practitioners by the results of what they said and did. I looked for "practice patterns". This is something I did for years in my consulting and software business, analyzed practice patterns for all sorts of reasons from fraud detection to finding the best docs for second opinions and the ones with the worst outcomes to ellminate from a PPO. When one doc misdiagnoses and mistreats a condition that is not unusual, that can happen for all sorts of reasons. When 100 docs from many disiplines, specialties, areas of practice and the like all do it there is something more fundamental going on. I spent 10 years intensively seeking diagnosis and treatment. My "traveling collection" as I called my collection of reports, lab results, MRIs, etc was several inches thick. After 10 years I knew no more than I had learned with the very first one, that the docs actually had no idea what was going on or how to treat it and some of them reached back to 19th century psychiatry, 60 years before b12 was discovered, to justify their diagnosis and treatment. That itselof was a clue.

    Deriving that more fundamental thing is one way of solving a problem. I did not assume that they were all "bad" docs. I did my best to select the best availble when possible. What I found out from my reading was that there are certain assumptions underlying their 100% failure rate. Those assumptions are in the literature and textbooks. I was given stacks of old textbooks by various docs, photocopies of journal articles. I spent weeks at the public library and medical school library and later on line. I came up with all the assumptions, some of which Rich describes about how things are "supposed" to work. I say supposed to because the cumulative failure rate is high, much higher than I think Rich has any idea.

    If one reads many articles clear pattrerns emerge. One of those patterns is that 1/3 or so of people in these various studies fail to respond to inactive cobalamins for one reason or another. Sure, perhaps only some fraction of 1% of those are due to genetic causes such as I appear to have so that is not the high sensitivity factor, in fact it hardly figures in at all. In adults doctors almost NEVER recognize it. However that does not eliminate the well demonstrated failure of the inactive cobalamins to do the jobs of active b12. Cumulatively then when one has one assumption stacked upon another stacked upon another perhaps 10 deep there is plenty of room for an accumulated failure rate of 33%. If my software had that kind of failure rate nobody would have used it.

    I set out to determine what I would have to do to elliminate all those assumptions. The first time I attempted this was in the late 70s and there was no solution possilbe. None of the real b12s or folates were available to test my hypothesis. I did the best I could with dessicated liver, 100 tablets a day, and had a very slight hint of confimation. When I approached it again, with the failure of many docs as data, and had the internet available, databases and other such tools, and 20 years experience in consulting, analysis and design to help organize and analyze the data, I came up with the same answer and understood it much better.

    I set out to design a program that got around 100% of the traditional assumptions and depended upon only one assumption, diffusion. The Japanese research on methylb12 indicated that would be a sure bet. They had demonstrated it over and over by that time even though that wasn't the goal of their research. I make my own interpretations of the research. When the researchers are focused on the cellular structure of the leaves they can't see the tree much less the forest. In all this I also came up with the folic acid problem though that had to wait for a solution until methylfolate became available.





    However, I want to emphasize that this biochemical behavior is unusual, and it is not likely to be the case in most people who have CFS, because the mutations that can cause this are rare in the human population.

    Yes, my mutations are rare, they probably account for less than 1% of the 33% failure rate of inactive cobalamins in study after study.


    Many people with CFS have reported that they have found glutathione to be beneficial to them.

    I offer you a clue on this. In doing reading on this whole "over/under" methylation situation I came upon several statements that some people appeared to benefit from a folate antagonist. As the glutathione (precursors) acted strongly as a folate antagonist perhaps that is one way such apparant benefit comes about.



    There are also some who have not reacted well to it. It isn't clear that this is because of interference with B12 utilization, as in freddd's case, however.

    Again, in reading I found a multitude of people who reacted poorly to it. In every case of "glutathione detox reaction" the people appeared to be sufferring from a hard folate deficiency primarily that once started continued indefinitely even when discontinuing the glutathione (precursors) and even if taking folic acid or 800mcg doses of methylfolate. Any b12 problems in them and in myself appeared secondary to the folate deficiency. A few people decided to test this hypothesis at my suggestion and they found that they could indeed stop the "glutathione detox reaction" in a few days starting within hours with 4800mcg of Metafolin and then normal sublingual doses of both active b12s in 5 star brands. Not one of them who tested the hypothesis failed to respond to Metafolin & active b12s to my knowledge. Active b12s alone were NOT effective.

    It may result from utilization of glutathione by yeasts in the gut, mobilization of toxins into the blood by improved operation of the detox system, stimulation of the immune system, producing a Herxheimer effect, or breakdown of some of the glutathione to form sulfite, which is more than the sulfite oxidase enzyme can handle. I don't think we know which of these mechanisms could be involved in a given case.

    These may certainly have a play in it but the induced folate deficiency might be at the root of it.


    In order for freddd's approach to work, it must be true that by putting large concentrations of the coenzyme forms of B12 into the blood, enough of each of them diffuses into the cells and survives removal of their ligands to give the cells enough methyl B12 and adenosyl B12 directly to satisfy their needs for them. As far as I know, this is not described in the current research literature.

    I haven't been able to find anything direct on this either. However, most all of the in vitro cell culture work with various b12s just add the b12 to the medium and voila! it is absorbed into the cells. And again the Japanese high dose mb12 research implies it. It is a very visible hole in the reasearch. When my associates and I would come across a hole like this in the data we described it as " a hole big enough to drive a loaded Brinks truck through". It is a money shot all the way. Consider "The Dog that Didn't Bark". It is in this hole that most of the answers to the mysteries of active b12s are situated. It is the area that has most studiously been avoided by the work being done mostly on inactive cobalamins or based on assumptions growing out of inactive cobalamin research. It is an excellent example of corrupted thinking growing out of inactive b12 research.

    I suggest that the reason it did not work for nearly a third of them is not that hydroxocobalamin is not effective for them, but that they have had other issues that have prevented the methylation cycle function from being restored, such as depletion of vitamin and mineral cofactors for this part of the metabolism (such as zinc, magnesium, or other B-vitamins) or depletion of amino acids, including methionine, or high body burdens of toxic metals that block the enzymes in this part of the biochemistry.

    I suggest that your assumptions here are partially correct. Inactive b12s don't work for 1/3 of people. However, both active b12s with methylfolate brings that up to about 95% (estimate) effective. The other 5% respond following the introduction of various cofactors. However, almost all respond better with more consistancy with the necessary cofactors. The problem is that even for the 2/3 who have some degree of response to hydoxyb12 it is a weak and partial response at best. It leaves the majority of active b12 responsive symptoms untouched with some considerably worsened. People who responded to hydroxyb12 at all will even a year or two or three later have even more response to both active b12s. Hydroxyb12 never produces sufficiency in either active b12 much less both. A large percentage of people right here who have tried both find that they have separate responses to both mb12 and adb12 at a rate far far higher than could possibly be suggested by presumably rare genetics like mine.

    I want to reiterate that according to the literature, mutations in the intracellular B12 processing enzymes are rare. The most recent paper I've found reports that only about 400 people have been identified worldwide as having these mutations.

    I've never been identified, neither have my children. There are lot's like me with some sort of problem that have never been identified. You need to read the early cyanob12 research showing why they considered the effects such as we routinely see here in response to active b12s as "placebo" effect. That is another takeoff point for clues into what is going wrong. I'll tell you one place it leads, to the blocked/depleted methylator. The people would respond a few times to cb12 injections and then cease repsonding. That was normal therefore the "placebo" effect designation. What is the mechanism? So again, one approach I took was "what was required to reliably produce such "placebo" effects. I looked in another data hole. All possibilites exist in the void.

    Look at it this way. The active b12 protocol, which I did not develop, but merely took from many places and refined it to remove many uncertainties, works well enough that I could walk into an insurance plan and tell them who to extract from the database based on symtoms and medication profiles and guarantee x results in one year followed by significant pharmacy, disability and medical savings. What I need is a controled study to "prove" it.

    The refinements I made to remove uncertainties were practical things, like brands and cofactor groupings, with food or without food. My object was to come up with something that worked to the greatest extent for the maximum percentage of symptoms in the most people possible. I wanted something you could bet the bank on. I wanted something that worked for the worst afflicted with the highest costs, like me. Any "solution" that didn't include me and my children, that is willing to write us off and watch us die according to protocol is no solution that I find acceptable. That comes down to "solve the problem for the worst 1% and the problem is solved". Solving it for the easiest 1% isn't a solution. Of course there is overkill. You get more ducks with a shotgun than a BB gun, and they don't even have to be lined up in a row. The active b12 protocol works pretty well for most people for whom it is suited in a year with some years of rehabilitation and fine tuning after that. Inactive b12 and trying to pick off each thing that crops up, layer upon layer, with a BB gun can take the rest of a persons life to work that well.

    When cyanob12 cost $50 for a 1mg injection ($250 in todays dollars) of course one looks for the minimum resource path. When sublingual methylb12/adb12 cost $0.05 per mg that is penny wise and pound foolish. A reduction of 99.98% in cost should cause a reevaluation of therapies.

    Rich, come over to http://forums.wrongdiagnosis.com/showthread.php?p=219396#post219396 and talk to people there. Ask questions of people who have been doing these things for years. There are certainly those with comorbidities that have had some symptomatic relief but are not healed. On the other hand there are an awful lot that stop in to say hi who are not around much becasue they are back at work or whatever. One posted today said "I've been absent from the forum for a while because, REJOICE, I have been feeling excellently well and been able to be mad busy."










     
  5. Freddd

    Freddd Senior Member

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    Hi Michael,

    It is pretty usual to only feel a difference from methylfolate once. It isn't unusual to only feel an effect from mb12 a couple of times either. In fact these are more common than the big responses day after day. Be glad you don't have the problems that lead to those big responses. On the other hand they might come along with any of a number of cofactors that you may not yet be taking.

    Elsewhere I was criticized for "overplaying" the strong repeating responses. Sometimes you just can't win.
     
  6. Fred: I promise not to complain! Thanks
     
  7. Freddd

    Freddd Senior Member

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    Hi Michael,

    One of my favorite Mayor Daly quotes is "I have been villified. I have been crucified. Yes, I have even been criticized".

    Another -

    "Get this straight gentlemen. The police are not here to create disorder. The police are here to preserve disorder".

    Of course being from Chicago maybe in all fairness he was saying "dis order" instead of "disorder".
     
  8. Fred: Spoke to soon! I have a question about the B12 test results I just got, so I still may have to complain (but not to you, unless you want me to).

    Homocysteine was 10 (down from 20 a year ago).
    MMA was 0.15 (I think that was the measurement? He said normal. Never been tested before for that).
    B12 > 1,000 (that's the only data the test provides -- not the exact figure. Last year it was 900).
    MCV was 103 last month (it has risen steadily the last eight months from about 98).

    So, wondering if the type of serum B12 could effect homocysteine and MMA to normalize, but not the the MCV? Perhaps all of that whey I had every morning and glulathione was good for some of my blood work (-: Now, as I've expressed, I seemed to have some strong responses to the addition of the methylB12, so something could be different in how the body is utilizing this type and not needing to convert?? Of course, hematologist wants to determine the "differential" -- he likes to say that alot -- to see what is going on via a biopsy. Just tell me "the good news", please.
     
  9. Sunday

    Sunday Senior Member

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    oh my, michaeldf, I'm so jealous of you! You're doing this protocol the easy way!
     
  10. Freddd

    Freddd Senior Member

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    Hi Michael,

    By all means speak up, I was just saying that taken all together there are lots of contradictions amongst people. The only thing that brought my MCV down was methylfolate. Mb12 would be used for making blood cells and bringling down Hcy. MMA is brought down by adb12. These two items can fall rapidly. MCV falls slowly becasue of the 90-120 day turnover rate of red blood cells even if corrected ones startt right up. It is the sudden surge of matured red cells of normal size that happens when whichever deficiency causes it that causes the hypokalemia. B6/p5p is also required in the Hcy reduction. Other b components are also incloved in just about everything.

    You demonstrate diffrerent effects from the two forms of active b12 despite you not likely having the genetic situation I have.

    All that whey might have impacted your folate status selectively and thereby cause increased MCV.
     
  11. Freddd

    Freddd Senior Member

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    Hi Rich,

    The item I didn't address in my long reply to you is that of cerebral spinal fluid cobalamin level. Since a substantially reduced CSF cobalamin level has been detected in both FMS/CFS and Alzheimer's so far regardless of serum level , that is not addressed at all by small amounts of hydroxyb12 or mb12 or adb12 for that matter. The Japanese mb12 research with high doses does address that. Also, the high dose form of the active b12 protocol does address that. Whether that is a genetic concern I do have in common with most CFS/FMS patients or of some other causality is unanswered. And once again, there is a differential effect of adb12 and mb12 in some people at high CSF/CNS penetrating doses, once again presumed by diffusion. This can be easily demonstrated but only after a person has already become accomodated and equilibrium reached at body levels. There is a sudden threshold (indicated by Japanese research) effect when the dose gets high enough and it can happen with either adb12 or mb12 or both separately. The effects of the two active b12s are distinctly different. This does not appear to have anything at all to do with genetic lack of certain enzymes. Other research appears to indicate that there are two potentially different problems, a hinderence in absorbtion into the CSF and an overly rapid clearance of cobalamins. Some people may have both. This low CSF cobalamin level may turn out to be a smoking gun for CSF/FMS/Alzheimer's.
     
  12. Hi Sunday: If I could, I'd send you the blessing of peace and comfort! I was so relieved the other day when the effects of the B12 wore off and I felt human. I was in quite a state. So I won't be disappointed I didn't feel any discomfort today.

    For me, this whole health thing is a spiritual quest -- to try and keep my composure in the face of the fear of the body not working as I would like it to!

    I felt good enough to go downstairs just now and jump on my rebounder. Listening through my fairly expensive stereo while rebounding to Santana, Crosby Stills Nash & Young (I'm the same age as Fred, a 60's guy), Barbara Stresiand and Barry Gibbs, and finally Michael Buble, I laughed and jumped for joy. Seems to me, the joy is a good part of any healing if you can summon it up. A few good tunes did it for me and I'm grateful.

     
  13. Thk u 4 my healing

    Thk u 4 my healing

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    Hi fredd and all,
    Don't know where to post so posting at the end of this thread. I had a great improvement using your b-12's protocol. I stuck with ad-12 only as the mb was too strong for me even in minute amounts. So i had been wanting to thank you Fredd! Started in November and was telling everyone i was 80% better during January!
    The only problem now is to figure out how to proceed. I have been crashed for about 3 weeks now... After reading some entries of others, I thought to increase my protocol titration to add in a little B-Right B complex and some mb12. But cut it out againafter about a week... I can't afford to be sitting around feeling totally useless and sick. ( I have to find some place free to live, move out and am stressed enough). Any way will add the factors back in one by one this time. Coffee enemas by the way everybody, is my cure-all. feel better imediatly!!
    More later, Best to you, Cristina
     
  14. Thank you Fred. I was thinking. If folate deficiency can also create higher MCV's, I should probably ask the hematologist to do a serum and red blood cell folate level before a biopsy? He was relying on folate tests a year old. Assume the the higher B12 (from 900 to above 1000) could be caused by the supplement I've been taking since last April, Brainstorm -- Vitamin B12 (as Dibencaside) 25 micrgrams 420% times three a day. It also has some form of folic acid -- Folic Acid 50 micrgrams 13% times three a day.

    What is the possible mechanism of whey disrupting folate uage? Any reason, besides skewing folate blood tests, to not start the increased methylfolate dosage you described in your own case to effect MCV?

    Why I started having neurological feet and hand tingling and sensations about a month ago is another question if B12 is sufficient, yes?. Could be heavy metals, as these started after some DMSA and ALA chelation I did one weekend after a year of being off that protocol,.



     
  15. Freddd

    Freddd Senior Member

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    REASONS WHY B12 THERAPIES DON'T WORK FOR MANY PEOPLE
    Version 1.0 - 07/19/09
    Version 1.1 - 03/03/10


    1. They take an inactive b12, either cyanob12 or hydroxyb12. The research “validating” their use was primarily for reducing blood cell size in Pernicious Anemia, keeping the serum b12 level over 300pg/ml at the end of the period between injections. They make a statistically significant effect that can be seen in lab tests in a significant percentage of people compared to placebo. They do not heal most damage done by active b12 deficiencies and have little or no effect on the vast majority of symptoms. They may even block active b12 from receptor sites hindering the effects of real b12. They both cause a keyhole effect of having only a very limited amount (estimated at 10-30mcg/day) that can actually be bound and converted to active forms. They in no way increase the level of unbound active cobalamins which appear required for most healing. They do nothing beneficial in a substantial percentage of people (20-40%) while giving the illusion that the problem is being treated and if it doesn’t work, oh well, that’s the accepted therapy. There is no “dose proportionate” healing with these inactive b12s because it all has to go through this keyhole. Some people are totally incapable of converting these to active forms because they lack the enzyme



    2. They take active b12 as an oral tablet reducing absorbtion to below 1%. A 1000mcg active b12 oral tablet might bind as much as 10-30mcg of b12. Again the b12 has to be squeezed through a keyhole that limits the amount and is subject to binding problems in the person whether genetic or acquired.



    3. They take a sublingual tablet of active b12 and chew it or slurp it down quickly reducing absorbtion back to that same 1% and limited to binding capacity. With sublingual tablets absorbtion is proportionate to time in contact with tissues. I performed a series of absorbtion tests comparing sublingual absorbtion to injection via hypersensitive response and urine colorimetry.



    4. Of the many brands of sublingual methylb12 only some are very effective. Some are completely ineffective and some have a little effect.



    5. For injectable methylb12, if it is exposed to too much light (very little light actually is too much) it breaks down. Broken down methylb12 is hydroxyb12. It doesn’t work at healing brain/cord problems of those who have a presumed low CSF cobalamin level. That requires a flood of unbound methylb12 and adenosylb12 (2 separate deficiencies) that can enter by diffusion. Adenosylb12 from sublinguals can ride along with injected methylb12.


    6.They don’t take BOTH active b12s.


    7. They don’t take enough active b12s for the purpose. Active b12s have a dose proportionate activity. There is a threshold effect at high levels of dosage when the cerebral spinal fluid is penetrated for some people, espcially with CFS/FMS/Alzheimer's and subacute combined degeneration.


    8. Lack of methylfolate - This is the number one lack after right b12s are in place.



    9. Lack of other critical cofactors. Lack limits healing with most people to some degree, fully prevents effectiveness to a lesser extent.



    10. Lack of basic cofactors. Lack limits healing in most people to some degree and fully prevents effectiveness to a lesser extent.


    These reasons are all still the same as when I first wrote this.

    These represent the actual order, more or less I go though these items with people when they say "I'm taking b12, why don't I get better?" Taking the wrong kind and/or wrong brand and/or wrong method turns out to be the BINGO factor in most people.
     
  16. enough_is_enough

    enough_is_enough One day I will run and not get weary.

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    I tried hydroxocobalamin extreme from prohealth a few days ago, it dissolves under your tongue, what a strange reaction it had on me, for a few minutes I felt "this is it, I found something els that work!!" Then wam it hits me the "horrible feeling" I only slept an hour that night. As I think back I had the same reaction with mercury chelation a few years back.
    '
     
  17. markmc20001

    markmc20001 Guest

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    I'm not a pro, but here is my opinion. dumping metals can make me loose sleep and make me feel brain foggy and tired. When I do the chelation I can loose motility and loose sleep becuase of metals (I have been told). My doctor reccomends fiber with oil(away from supplements), milk thistle, probioitcs, anything to help keep the gut healthy and eliminate the metals. Sauna can help too. But try and figure out a way to catch the metals instead of absorbing them back into your blood. I think there is some stuff in the gut forum section that may help (metal detox). good luck. I take zinc on an empty stomach to help displace the lead and stuff that comes out. lead and zinc can bond to the same places in the body I think. Everybody has different issues and things that work. so it helps to do one thing at a time and listen to your body and figure out what works for you.
     
  18. Freddd

    Freddd Senior Member

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    Hi Widaisy,

    1. Jarrow Formulas B-right, working up to one twice a day. Also, take NOW Foods, Gamma E complex. When comfortable with this...

    I would also prefer to see you start with all the basics first; a, d, c, magnesium, calcium, potassium, omega3 oils in addition to the b-right and Gamma E complex. ALL of these are really needed for healing and making new tissue. Taking at least modest quantities of all of these.

    2. Country Life Dibencozide, working up to 3 a day (sublingual)

    One of these a day is quite sufficient for most people, especially until everything else is started and you get started with the fine tuning for what your body needs which you can't tell until everything is started and stable. Then your body will either be working much better or you will know what isn't working right and can start targeting what needs adjustment.

    3. Jarrow methyl B-12, 5mg, working up to 25mg a day (sublingual)

    I would suggest starting withj 1 x 1000mcg Jarrow sublingual a day for 45-120+ minutes per day, increasing to 5 or 6 per day one at a time and then go to two at a time, then 3 at a time several times a day and then switch to the 5mg and increase by one at a time. Do them serially at first then increase dose size until an additional tablet makes no additional difference. When you are up to 3mg daily add 1 Metafolin (Solgar methylfolate or other Metafolin brand).

    There may be hard startup responses. I had them. They did not stop until I flooded my body with methylb12 after 3 months of 5mg or less daily. However, many folks seem to turn a corner after about 3 months so maybe that is how long it takes. My impression is however that it showed no tendency to slow down until I just basically took one subnlingual methylb12 after another all day.

    Mb12 affects the nerves. All the symptoms are suddenly sensed far more clearly and intensely. Whether they actually are more intense or are only sensed more intensely I can't tell you. Also they can start changing rapidly and reverting to early forms you may have forgotten about. Mine progressed backwards through the same symptoms as when they started only 30 times faster. Some people attribute the startup reposnses to other effects of many varieties. Mb12 mostly can affect hundreds of different things throughout the body and adb12 affects energy generation in all mitochondria so lots and lots of things can be affected in all sorts of different ways. The people who keep going get though it. The things that heal first are usually the things affected immediately. Some people attribute the startup to all sorts of potentially terrible things and find it intolerable to keep going. There is little proof either way as to what is actually happening. Both Lena and Sunday had a lot of difficulty with startup and both have posted recently that they are doing better now. It is better to reduce dose but keep going than to stop and start over and over. That appears to get a very unstable seesaw going and increase the intensity.

    Later, after things have stabilized is the time to start adding critical cofactors. Read about all this on the first few pages of this set of posts. The potassium is needed for your protection because there is one dangerous startup effect for sure, hypokalemia, caused by a lack of sufficient potassium and it can hit hard and nasty within a few days of starting. Goods luck. Feel free to ask about anything that occurs while starting and so on. Pay attention to brands as there can be all the difference in the world.
     
  19. Freddd

    Freddd Senior Member

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    Hi Enough_is_enough,

    Consider the active b12s instead, say as detailed in the previous post. Consider taking the basics with b-Right for the first month or 2 to get yourself up off the bottom with a minimal amount of mb12 as contained in the B-right. Any of these b-12s can energize you immensly at first when you ar very deficiencty and can cause sleep problems. Over the longer run methylb12 generates melatonin and relieves sleep disorders caused by b12 deficiencies. Be careful not to scare ourself. The way out is through. An excess energizing is pretty normal for startup and passes in time and seems to be required for normalization. The more deficient a person is the more intense the startup usually and especially the energized feeling.
     
  20. Freddd

    Freddd Senior Member

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    Hi Michael,


    What is the possible mechanism of whey disrupting folate uage? Any reason, besides skewing folate blood tests, to not start the increased methylfolate dosage you described in your own case to effect MCV?

    To the extent that whey acts as an effective glutathione precursor, gthe glutathione can act as a methylfolate antagonist rtapidly inducing folate deficiency symptoms. Some people had this effect with whey.

    I don't give a single hoot much less 2 hoots about skewing folate blood tests, completely irrelevant. The problem was for me taking the glutathione precursors was that no amount of folate worked while taking the precursors and after stopping it took 4800 mcg daily to correct the problem. A year after stopping the precursors I still haven't been able to drop back to the formerly effective level of methylfolate.


    Vitamin B12 (as Dibencaside) 25 micrgrams 420% times three a day. It also has some form of folic acid -- Folic Acid 50 micrgrams 13% times three a day.

    These are miniscule doses.
     

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