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B12 Deficiency vs Dependency

Discussion in 'Detox: Methylation; B12; Glutathione; Chelation' started by Adster, Apr 20, 2011.

  1. Adster

    Adster Senior Member

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    Fred, Rich I wonder if it is worth talking about b12(or overall methylation support) deficiency vs dependency. My understanding is that a deficiency can be rectified through supplementation then if all else is functioning and the diet is sufficient, supplementation can be ceased.

    With dependency, the supplementation may have to continue for ever, as a separate issue is causing the dependency and until that is resolved equilibrium cannot be sustained "naturally". This might be genetic, viral or due to heavy metals or toxins etc.

    I guess an initial deficiency could cause a lifelong dependency if left too long? I sometimes think about the time I spent as a vegetarian, I doubt that was a wise move in regards to my health.

    I'd be keen to hear any thoughts anyone has on this.
  2. richvank

    richvank Senior Member

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    Hi, Adster.

    If my hypothesis is valid, there is a functional B12 deficiency in ME/CFS that is caused by glutathione depletion. We know from lab testing that lifting the partial methylation cycle block restores glutathione automatically. Therefore, the B12 protection by glutathione should be restored, and the need to supplement B12 at high dosage should end. I've heard from at least one person who reports full recovery, back to work, ability to handle exercise and stress, and she forgets to take supplements and still does O.K. An N of one is not much to go on, and I wish I had more data, but there it is.

    Best regards,

    Rich
  3. Freddd

    Freddd Senior Member

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    Hi Adster,

    I have had 8 years experience in this so far and talked with thousands of people.

    My understanding is that a deficiency can be rectified through supplementation then if all else is functioning and the diet is sufficient, supplementation can be ceased.

    First, there is the idea that "if all else is functioning". If that were the case most people, other than vegetarians would never have become deficient in the first place. So there is that problem. Second there is zero research evidence that the entero hepatic recirculation loop ever gets re-established. There is a LOT of assumption that it does, repeated over and over, but there is zero evidence either in research or in practice. Third, as people approach 50 the percent showing b12 deficiency symptoms approaches 50% as stomach acid falls off and who knows what other problems. As many people on a b12 deficiency forum found out no cause of deficiency is ever found in the majority of cases. IF problems are quite rare. As it turns out, folate deficiency whether naturally come by or induced by glutathione or paradoxical folate deficiency caused by folic/folinic acid can also induce b12 deficiency as a sort of double whammy. Fourth, as those with CSF/FMS along with MS, Parkinsons's, Alzheimer's, ALS etc also have LOW CNS/CSF cobalamin, and that is probably genetic, that propensity probably doesn't change no matter how long one takes mb12/adb12. Fifth, after damage occurs it appears that a higher level is needed to heal the damage or if the damge is severe, to maintain functional gains and to keep the damage from progressing.

    So far of people I know taking mb12/adb12, those who were caught early on before damage and before the entero-hepatic recirculation runs dry, can get by on occasional doses to supplement the dietary b12. Those who deplete their body levels to the point of exhausting the entero-hepatic loop and have damage, especially neurological damage, appear to need to take it to prevent the return of symptoms. As mb12 affects 200 more symptoms than hydroxycbl that gives 200 more chances for symptoms to return upon cessation of mb12, which they typically start to do in 3 days following the last dose. However, when healing is completed a reduced dose appears possible to maintain. For instance, I always had folate and b12 deficiency symptoms, even in childhood. They were not as severe as they became later, but given the choice, I would not choose to return to "only" that level of malfunction. I was sick a lot. I've had 8 years of not being sick all the time not to mention many worse things. If I am willing to be in a wheelchair, in diapers, unable to read or think and let my damaged nervous system go as a writeoff then I could get by on probably 1-5mg a day sublingual and stay alive. If I had never had the CNS damage in the first place a once a week preventive injection probably would have done the trick at keeping my CNS healthy.

    So I have no condition of "former health" to return to. Does that make me dependent? That "dependency" was existent from birth. I am as dependent upon mb12/adb12/Metafolin as a person on insulin is dependent upon it. That is NOT the same as being dependent upon morphine for instance, by reason of accommodation. A person can taper morphine easily and only have return of pain.

    So I and many others are healthy and able to return to work and play, doing roof, hiking in the mountains, aerobic exercise, have memory and cognitive abilities for having done the active b12 protocol. However, all that I know of who were disabled have damage that requires continued doses. I consider "dependency" to be the wrong word to describe the situation. I am also dependent upon eating and breathing.
  4. Adster

    Adster Senior Member

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    Sorry for the delay in getting back to this. I certainly didn't use the word "dependency" with any negative connotations, apologies if that was how it came across.

    The other thing I've been wondering about is whether or not some people need to increase their dose to maintain the improved level of functioning. Have you come across this?
  5. Richard Lee

    Richard Lee

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    I would very much like to believe this. I feel uneasy at having to rely on B12 pills indefinitely. But Dr Joseph Chandry, with 30 years of treating B12 deficiency (admittedly on a restricted protocol), believes that

    Dr Chandry does not spell out the precise nature of the damage, and I guess we don't know enough to be more precise. Rich, what level of serum B12 does your fully recovered subject maintain?

    Dr Chandry goes on to speculate that not only is there no going back to a supplement-free state, but the attempt to go back is likely to return you to the decrepit state you would have been in if you'd had never been rescued by supplements in the first place.

    This depressing notion reminds me of those film-clips where you see someone who has swallowed the elixir of youth suddenly age before your eyes because he cannot renew his dose.

    I would prefer to imagine that you feel worse than ever if you stop supplementation only because your partly-healed nerves are more sensitive to the remaining damage, but that might be wishful thinking.
  6. richvank

    richvank Senior Member

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    Hi, Richard.

    I think that whether there will be a continuing need for high-dosage B12 depends on what a particular person's disorder actually is. I focus on ME/CFS. It is defined as an acquired disorder. That is, it is defined as something that is not present at birth, but develops later in life. I think this rules out quite a few of the more serious genetic issues involved with B12 absorption, transport and utilization by the cells. I have offered the hypothesis that ME/CFS develops when a vicious circle mechanism becomes established, due to a variety of possible causes. This vicious circle includes a functional deficiency, rather than an absolute deficiency, in B12. The serum B12 level is commonly normal or higher than normal in ME/CFS, because there is not an absolute B12 deficiency. The problem is that the cells are not able to utilize the B12 to perform its normal functions, so they export it back to the blood, bound to haptocorrin, and this is the dominant fraction of B12 in a conventional B12 serum test, even in normal, healthy people. So this measurement is not meaningful in functional B12 deficiency.
    A urine methylmalonate measurement will detect most functional B12 deficiencies. This is included in urine organic acids panels, such as the Genova Diagnostics Metabolic Analysis Profile, available from some doctors, or without a doctor's order from www.directlabs.com. An elevated MMA level in the urine with a normal serum B12 level suggests a functional B12 deficiency.

    Freddd is dealing with B12 issues across the board, not only functional deficiencies. The treatment he suggests bypasses all the normal B12 absorption, transport, and intracellular processing of B12, and as such, it is effective in both absolute and functional B12 deficiency states of all sorts. His views on the level of continuing need for B12 are based on his own experience. The question is, how generalizable is his experience to most cases of ME/CFS, which are more likely due to acquired functional deficiencies, rather than to inborn errors of metabolism, as evidenced by the fact that the people experienced good health earlier in their lives, which Freddd reports that he did not? As I've written before, I very much appreciate Freddd's contribution to the whole area of treating B12 deficiencies, and I'm glad especially for his own sake and the sakes of people who cannot be helped in any other way, that he found a treatment that works for him and other cases of inborn B12 metabolic abnormalities. However, my concern is that I think we need to be careful in extrapolating his experience to cases that may be very different in terms of the details of the abnormalities in B12 absorption, transport and utilization.

    Best regards,

    Rich
    Lotus97 likes this.
  7. Freddd

    Freddd Senior Member

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  8. Freddd

    Freddd Senior Member

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    Hi Rich,

    I think that whether there will be a continuing need for high-dosage B12 depends on what a particular person's disorder actually is.

    I suppose what that would mean would depend on what "high dosage b12" means. Otherwise, As there are 4 different forms of b12 deficiencies and several forms of folate processing (ie tendency to have paradoxical folate deficiency involving folic acid and/or folinic acid and/or food folate) a full definition of the matrix is not yet possible. So there are a lot of different possible faces this disorder may wear.


    I focus on ME/CFS. It is defined as an acquired disorder. That is, it is defined as something that is not present at birth, but develops later in life. I think this rules out quite a few of the more serious genetic issues involved with B12 absorption, transport and utilization by the cells.

    I think that ME/CFS is not the "acquired" disorder you may think. Perhaps the word "triggered" may be a more appropriate word. I suspect that the tendency to have low CSF cobalamin level as measured in studies of CFS/FMS (mostly USA studies which generally doesn't recognize ME) compared to body serum cobalamin levels puts it squarely in the genetic predisposition arena. Then when other circumstances occur, ie certain viral or bacterial infections, traumatic injuries, toxic injuries or other things that strain the physical system in certain ways, a marginal, but coping, equilibrium situation, something breaks and shifts balance to a lower level and stays there without intervention. The body may have sufficient b12 but the CSF and hence CNS doesn't have sufficient mb12 and/or adb12. The second generation of studies on these matters is ongoing. They are finding in the diseases that had a generally "low" CSF cobalamin level with normal or high body serum cobalamin level; CFS, FMS, Alzheimers, Parkinson's, ALS, MS and others, specific markers for dramatically low levels of either of the two active b12s - adb12 and mb12 - in the form of elevated MMA and/or Hcy in the CSF. This appears to proceed disease diagnosis by 20+ years. These depressed CSF cobalamin levels have non-specific and at first, quite subtle and apparently unconnected symptoms, with different symptom sets for mb12, adb12 and the combination. Further out of that universe of symptoms, most people only have some fraction of them, possibly connected to how they use folic acid, folinic acid and food folate, among other things.


    I have offered the hypothesis that ME/CFS develops when a vicious circle mechanism becomes established, due to a variety of possible causes. This vicious circle includes a functional deficiency, rather than an absolute deficiency, in B12. The serum B12 level is commonly normal or higher than normal in ME/CFS, because there is not an absolute B12 deficiency.

    You continue to ignore the effects of LOW CSF cobalamin.

    A urine methylmalonate measurement will detect most functional B12 deficiencies.

    This is not even close to accurate. It is completely wrong. First, it can detect only one of four forms of b12 deficiency, and it doesnt do that well. A lack of elevated MMA doesnt demonstrate sufficiency. It is a common oft repeated fallacy and one reason why 99% of b12 deficiency is invisible, a stealth deficiency disease. An elevated urine MMA will indicate that SPECIFCALLY adenosylb12 is very low, so low as to cause system failure. The other test that specifically identifies low levels of mb12 SPECIFICALLY (and possibly methylfolate and/or P-5-P) is for elevated Homocysteine. By the time a person has elevated uMMA and/or Hcy they are already damaged, they have already fallen off the cliff. Finding elevated MMA in the CSF appears to indicate the ongoing damage that leads to Parkinsons. Finding elevated Hcy in the CSF appears to indicate the damage leading to MS. Finding elevated Hcy and MMA in the CSF appears to indicate the damage leading to ALS.

    Trying to define your way out of the logical conundrum by differentiating between functional or absolute deficiency is based on a flawed definition of deficiency. Deficiency is not a statistical abstraction based on averages from a group in which half are deficient. So half the people in this country are functionally deficient as defined by standards based on inactive cobalamin and pernicious anemia. Such a deficiency being so normal it is invisible, a stealth deficiency disease. Serum cobalamin level doesnt indicate amount of active b12s available to the cells. The serum levels were set in reference to pernicious anemia and very enlarged red blood cells, the final breakdown leading to death if it continues long. They were NEVER set with the entire range of body active b12 deficiency symptoms in mind. A realistic lower limit for being asymptomatic is probably in the area of 3000-6000pg/ml. Further, even a serum level of 6000pg/ml might very well not be sufficient to correct the low cobalamin in the CSF/CNS. Whether it is enough to prevent neurological breakdown and differentiation into multiple diseases would require a 20-30 year trial depending upon a host of factors.

    An elevated MMA level in the urine with a normal serum B12 level suggests a functional B12 deficiency.

    The definition of normal b12 level is based on a population of which 50% are chronically deficient of b12 and totally unrecognized. The normal serum level is an oxymoron. It is a near worthless definition that can point out deficiencies of a certain extreme nature but CANT indicate sufficiency. Deficiency has become normal via the miracle of statistics. This definition of normal serum level is one of the items corrupted by 60 years of research on inactive cobalamin. As MANY researchers have pointed out over and over in many articles I have read is that the ONLY definitive test of b12 deficiency is an actual trial of b12 and I would amend that to read mb12 and adb12 instead of simply b12. There is absolutely no combination of tests that can assure sufficiency for all needs. B12 research has 60 years of trying to prove that pigs can fly by looking at them the instant they are thrown off the diving board without ever pulling back and looking at the whole picture. It is the most corrupt set of research I have ever seen. The results are filled with unsupportable assumptions and weasel words sanctified by repetition going back to original speculations and assumptions. This whole body of research goes back to a Nobel prize for an inactive lab mistake. It ought to be the biggest medical research and treatment scandal ever. Instead if Codex Alimentarius is passed the whole thing will be buried out of reach of ever revealing the truth killing millions and making hundreds of millions ill with mysterious stealth deficiency diseases. Ive been part of the mainstream medical delivery system since the early 80s. Never have I been more disgusted with it. Now it comes down to two inactive vitamins, inactive cobalamin and inactive folates, replacing the real things, both causing stealth deficiency diseases. Both were sanctified with Nobel prizes and both leave a substantial number of people to rot without relief possible. Both have created millions and millions of people who are writeoffs. We all know what it is like being resented by the medical profession for these imaginary diseases we suffer from through no fault of our own. After all, the most profitable forms of cobalamin and folate are those that keep them coming back forever since they are at best incompletely effective creating a huge market for drugs at high prices to treat all the mysterious stealth deficiency diseases and because they are the most stable forms, the twinkies of the vitamin world. That doesnt mean they are the best or even adequate forms for people actually using them.


    Freddd is dealing with B12 issues across the board, not only functional deficiencies. The treatment he suggests bypasses all the normal B12 absorption, transport, and intracellular processing of B12, and as such, it is effective in both absolute and functional B12 deficiency states of all sorts

    I appear to have several problem areas, most of which I share with others with CSF/FMS. Based on pragmatic trials I appear to have lower CSF/CNS levels of both mb12 and adb12, which is consistent with the finding that those with FMS/CFS have lowered CNS/CSF cobalamin levels. I appear to have difficulty using folates from the folic- acid/folinic-acid/food-folate set of folates causing paradoxical folate deficiency otherwise known as detox which I too experienced over and over for decades. From the results of switching to Metafolin and discontinuing folic/folinic acids so far it appears that quite a few people have this characteristic to one degree or another. Its taken me two years to chase this down after seeing it in concentrated form the first time I came to this forum. I find Metafolin far more effective than folic acid and/or folinic acid as do many people here. I find that mb12 and adb12 are far more effective for far more symptoms than hycbl and/or cycbl as do almost everybody on this forum. I have distinctly different effects from adb12 and mb12 as do many people on this forum. I HAD the same symptoms most everybody here has or had, just more of them except for the sickest. Except for your fixation on my possible genetics I was indistinguishable from the general group of folks here, especially the sickest longest duration of illness subset.


    His views on the level of continuing need for B12 are based on his own experience.

    Actually they are not based on my own personal experience. My experience is included in with that of many others for this. I am still in the continuing healing category, of sub acute combined degeneration. And the healing I am doing is the most difficult and least known about, neurological. It is difficult to just keep it from progressing. Damage of any kind, when not healed to completion, starts breaking down almost immediately upon cessation of the active b12s and active folate. Until recently I was never completely out of folate deficiency. Its effect upon completeness of healing may be critical in all this. Good health is a very subjective thing.




    The question is, how generalizable is his experience to most cases of ME/CFS, which are more likely due to acquired functional deficiencies, rather than to inborn errors of metabolism, as evidenced by the fact that the people experienced good health earlier in their lives, which Freddd reports that he did not?

    Good health is a very subjective thing. During my entire child raising period I was able to buy scads of preferred non-smoker rate term life insurance in large quantities because my health was good. They didnt care that I had night terrors as a child, heard noises under the bed or in the closet at bedtime, had sleep disturbances, had more streps than usual, delayed speech, growing pains, missed 6-8 weeks of school a year due to illness, Osgood Schlaters disease, hypothyroid, was considered a hypochondriac by mother, was considered a serious underachiever by mother, was a good athlete or a near straight A student much of the time. After all, most of my medical records were lost. Those that were carried forward indicated I used a lot of antibiotics and had a lot of normal childhood problems. I had only one procedure, tonsillectomy at age 6, and one expensive test, Basal Metabolism, and a couple of broken bones from ordinary traumatic injuries. As medical records are mostly a record of drugs prescribed, tests and procedures performed, there was nothing there. When the characteristics of a problem are not recognized and treated, they leave no significant trace. On the other hand, the spinal fractures, damaged nerves and disks, which the auto insurance company denied could possibly be caused by a side collision were reason to deny me medical insurance for the rest of my life to this point because of anticipated future morbidity from those same impossible injuries. Those are my on record health problems.

    No doctor ever was able to diagnose my problems except by knowing what cured them. They were all totally blind to them because of the belief system fostered by decades of research on inactive folates and inactive cobalamin. The typical physician and researcher wouldnt recognize 99% of b12 and folate deficiencies if it hit them smack between the eyes like a 2x4. When they see it a few tests based on inactive cobalamin and folic acid convince them that they are wrong.

    There are all sorts of reasons, perhaps 20 reasons, caused by methylfolate deficiency, and each variation of mb12 deficiency and adb12 deficiency, perhaps 400 combinations in all. I could list them ad nauseum but what they amount to is that the methylation crash is impossible when mb12 and Metafolin are being taken in the first place. Low glutathione appears to be a marker for broken methylation cycle. It cant happen ion the first place if the two active forms are being taken in the absence of NAC, whey, glutathione and maybe some other food products or supplements, food extracted folate, folic acid and folinic acid.

    Mitochiondrial crash can often be prevented by again taking Metafolin and adb12 in the absence of NAC, whey, glutathione and maybe some other food products or supplements, food extract folate, folic acid and folinic acid.

    These possible combinations are all complicated by the multitude of genetic variations around the processing of the forms of b12 and inactive folates. Either a methyfolate deficiency, absolute or functional and/or an mb12 deficiency of any form can cause the break in the methylation cycle accounting for perhaps 1/3 of the b12 deficiency symptoms. The rest of the symptoms are not methylation related or are only partially so related.

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