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BUILDING BLOCKS OF A DISORDER

Discussion in 'Detox: Methylation; B12; Glutathione; Chelation' started by Freddd, May 15, 2012.

  1. Freddd

    Freddd Senior Member

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    Eight years and 51 weeks ago I put that first mb12 "Under my tongue ..." (As sung by the Stones). I knew my life was changed in 1 hour flat. Over the next year I learned there are 4 b12 deficiencies, not one, and a whole lot more. Things separate out into components that have some at least logical discreteness.

    1. Indentification of effectiveness of current form of b12. When evaluated against the list of symptoms for which both active b12s are near 100% effective with suitable cofactors the identification of cyanocbl and hydrocbl goes like this. Cyanocbl was noticably but slightly effective for 6 of 300 symptoms. Hydroxycbl caused rapid onset of skin lesions that continued to spread as long as I took it. Hydroxcbl could not be continued long enough to determine if it had any effectiveness because of epithelial lesions and rapid neurological breakdown. A combination of methylb12 and adenosylb12 were effective for 175 of the 200 symptoms I had. Results will vary by person. However, hysdroxycbl and cyanocbl are not full effective for anybody. The degree of partial effectiveness varies considerably from 1 to maybe a dozen or two dozen symptoms affected partially.
    2. Idenitifcation of BODY - mb12 deficiency
    3. Identification of BODY - adb12 deficiency
    4. Identification of CNS/CSF- mb12 deficiency - large dose required to penetrate CNS
    5. Identification of CNS/CSF - adb12 - large dose required to penetrate CNS
    6. Indtification of sudden low potassium casued by methylation (healing) startup
    7. Idenitification of folate insufficiency
    8. Identification of paradoxical folate deficiency - folic acid
    9. Identification of paradoxical folagte deficiency - folinic acid
    10. Identification of paradoxical folate deficiency - vegetable food source folate
    11. Identification of paradoxical folate deficiency/insufficiency on small doses of Metafolin
    12. Identification of CNS/CSF - adb12 - normal dose or micro dose required to penetrate CNS coupled with neurological hypersensitivity to l-carnitine fumarate in limbic system all tied into neuronal ATP hypersensitivity and and increased sensitivity to dopamine variations some with Benzo side effects affecting dopamine receptors causing "Tolerance withdrawal".
    13. Hypothesized - CNS hypersensitivity to mb12 with microdoses but not to adb12. As some mb12 converts to adb12 to test this one would need to saturate on adb12 first and see what the mb12 response is after that. There is some indication that after adb12 and carnintine are in place that mb12 hypersensitivity may appear as it needs the functioning mitochondria as a prerequisite.
    Basically hydroxycbl, like cyanocbl, will affect some small percentage of the 300 symptoms, maybe limited to a number that can be counted on your fingers. Item 12 above is the only one about which there is any question of whether it can be substantially healed.


    So out of all of these building blocks and probably a few more not yet identified we can build the follwoing. Remember, there can be comodbidities and otehr complications that are not related and DON'T respond to the active b12 protocol.
    1. ME - Active b12 protocol 90% effective against these symptoms
    2. CFS - Active b12 protocol 90% effective against these symptoms
    3. FMS - Active b12 protocol 90% effecrtive against these symtpoms
    4. Pre-parkinson's leading to (hypothesized) Parkinson's - Carefully titratrated active b12 protocol affects this hugely, whether this leads to effectivbe healing or not is currently unknon.
    5. Pre- MS (hypothesized) leading to (hypothesized) MS (MS may not be anything really different from SubAcute Combined Degeneration except the specif-c nerves affected.
    6. Pre- ALS (hypothesized) leading to (hypothesized) ALS
    7. Pre- Alzheimer's (hypothesized) leading to (hypothesized) Alzheimer's
    8. Pre- SupraNuclearPalsy (hypothesized) leading to (hypothesized) SupraNuclearPalsy
    As these identifications are pragmatic, they also suggest possible treatment by correcting the funtional and/or absolute deficiencies. The first 3 can be reasonably well healed in a year with several more years to rehabilitate and finish healing. The question is what about these others, Item 4 for instance which is up right now. Does correcting the deficiencies in the end correct the problem? When does it become too late for repair and the disease becomes inevitable. Can it be moderated? Should it be treated even if the treatment is unpleasant or should the person simply take the path of avoidance of unpleasentness into the full blown illness? Can it be effectively treated any other way than ending the deficiencies?

    Lack of methylation happens with the lack of methylb12 and Methylfolate though these are not generally enough in themsleves and are recycled many times receiving methyl groups from Choline, TMG and other donors. SAM-e is a product of having methylb12 in the body and unless added as a separate item is part of a zero sum situation. I don't think there can be broken methylation in the presence of methylfolate and methyb12. This abnormal condition only occurs when the body is being starved for the real thing by being given pseudo vitamins like folic acid, cyanocbl and hydoxycbl or has paradoxical folate deficiency or other dietary and/or heriditary processing conditions. These three pseudo vitamins do not allow the body to normalize. Adenosylb12, methylb12 and Methylfolate allow the body to normalize. The intial stage of the body normalizing is for cell reproduction to turn on allowing general healing. 50mcg of methylb12 (1/4 of a sublingual 1mg ET or Jarrow) and 50mcg of adenosylb12 appear sufficient for widespread body healing but may not be enough for CNS normalization. As healing with mb12 and adb12 appears dose proportionate more of these allow somewhat more widespread healing to occur at the same time.

    ATP startup is often by far the "stronger" startup. It can independently trigger enough healing that didn't happen with mb12/metafolin that it can casue an increased need for potassium and additional Metafolin and additional mb12.
  2. Freddd

    Freddd Senior Member

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    I would also like to add to the above that most all of these diseases have had (cyanocbl OR hydroxycbl) AND folic acid AND b6 tested as a treatment and/or preventive because other people can read the research and see that low csf cobalamin and elevated MMA and/or HCY sure seems to indicate a b12/folate/b6 deficiency. Since they automatically use the inactive forms of all the vitamins they have had no results. It is not conjecture on my part that the inactive hydroxcbl, cyanocbl, folic aicd and b6 don't work. Reserarch as already demostrated if not proven in all cases that they don't. Based on our collective experiences with mb12 and adb12 and metafolin and p5p it is clear that a lack of response to the inactive forms in no way predicts what the active forms might do. Also, they leave out all sorts of other important and even essential items. The tests with just the cyanocbl/hydroxycbl preceded the 3 item tests usually so these are gnerally 2nd generation tests. The active b12 protocol has been through in excess of 30 generations of variations getting to be effective. If you include all the side trials pinning down what brands of b12 work and how sublingual relates to injection, why all sorts of variations don't work, micro titration trials, combinations trials and all that, there are well over 100 generations of active b12 protocol, hundreds of years if done sequentially on the usual type of research cycle, to get from hydroxycbl-cyanocbl & folic acid and b6 with doesn't work to the active b12 protocol which works on some of the listed diseases and might help for the hypothesized ones.
  3. alex3619

    alex3619 Senior Member

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    Logan, Queensland, Australia
    This active/inactive issue goes beyond B vitamins too. Vitamin E has a range of versions with different activity (gamma or mixed tocopherols are better) and much of the CoEnzyme Q in the diet is Q9 (from vegetables, meat has Q10). As we get older we lose the ability to convert Q9 to Q10, so for older people an increase in meat intake is required for good health.

    I am currently trialing Thorne Research B Complex which has mb12 and adb12, as well as methyl folate and folinic acid (and I am aware that not everyone tolerates folinic acid). This has currently (only out to two weeks so far) reversed my circadian dysfunction. I get up shortly after dawn every day now, though I do have to nap once or twice in the day. Based on past experiences this might well stop working at some point, but then again it might continue. Side effects include slight fevers and a general higher body temperature (though I was never particularly cold unlike some). I also have an increase in allergic effects, though I wonder if this is due to increased mast cell activity as my immune system has had a boost?

    Testing inappropriate vitamins is a big problem. So is testing vitamins in isolation. Vitamins work in combination with each other and cofactors - highly reductionist experimentation can be expected to fail on occasion for this reason alone.

    What is the basis for your claim that this is helpful in Parkinson's Freddd, if you can say? I ask this because apparently an uncle of mine died from it, or at least died in the advanced stages.

    On the precautionary principle I think every B complex and every mutivitamin should do away with the common drug forms of any vitamin. I am aware they use these for two reasons - they are cheap and they are stable and so do not degrade much over time. The natural forms will reduce the shelf life, but they will also be much more effective. This includes vitamin E. Every vegetarian formula must also include CoEnzyme Q10. There may be other vitamins similarly effective but I am not up to date on vitamin research.

    Bye, Alex
    SickOfSickness likes this.
  4. Freddd

    Freddd Senior Member

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    Hi Alex,

    What is the basis for your claim that this is helpful in Parkinson's Freddd, if you can say? I ask this because apparently an uncle of mine died from it, or at least died in the advanced stages.

    I have no idea if it will be helpful in Parkinson's. What I have identified is the symptoms characteristic of a specific one of 4 b12 deficiencies with limbic system damage and symptoms that look like Parkinson's symptoms (which damages the limbic system, and which are exaggerated by benzos which change the dopamine receptor making them less sensitive giving a preview of characteristics after dopamine reduces for other causes.

    These folks are hypersensitive to adenosylb12, l-carnitine fumarate and possibly mb12. They tend to develop "tolerance withdrawal" on benzos and anxiety is a major characteristic. When the neurons turn on from mitochondrial function it triggers intolerable anxiety, panic, fear and in succession sometimes rage and even murderous rage without provocation. One can get quite a tour through the behaviors of the limbic system.

    I posted a more complete description in the past few days on this same methylation menu.
    Some questions exist:
    1. At what point does it cease being a vitamin deficiency and begin to be Parkinson's?
    2. When does the damage become irreversible.
    3. How much can be reversed at any given point?
    4. Is the actual damage the same as in Sub Acute Combined Degeneration and MS, that is to say demyelinations that can be healed to some extent or something different?
    5. Can further damage be stopped by reversing the deficiencies even if existing damage can't be healed.
    Many b12 deficiencies are thought to be hereditary. My kids all have similar b12 and folate characteristics as I have. I also had a CNS-CSF adb12 deficiency of a moderately extreme nature as well as a marching mb12 deficiency as well as both body deficiencies. I went though two 6 month CNS healing periods that were quite emotionally volatile and unpleasant.
    Michael likes this.

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