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WHY HYDROXYCBL MIGHT NOT WORK

Discussion in 'Detox: Methylation; B12; Glutathione; Chelation' started by Freddd, Jan 5, 2012.

  1. Freddd

    Freddd Senior Member

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    I would like to combine several things that have come to my attention recently to once again discuss why hydroxycobalamin might not work to start a methylation cycle that is either blocked or depleted.

    As I have mentioned multiple times through the years, in any given study on the use of hydroxycbl for the relief of several b12 deficiency symptoms and signs, approximately 1/3 of people in the study have zero effectivness on the symptoms or signs being studied. As the study symptoms are selected only from the list of those items KNOWN TO RESPOND to some extent to cyanocbl and hydroxycbl, about 1/3 of the total of all active mb12/adb12 deficincy symptoms, there are clearly some issues that prevent 1/3 of the people from responding.

    So let's consider first several chains of reactions. Assume sufficiency of other needed items such as magnesium, l-carnitine and folate for this discussion.

    methylb12 yields SAM-e
    methylb12 yields glutathione
    adenosylb12 yields ATP


    hydroxycbl with assumed glutathione and assumed ATP and assumed SAM-e yields methylb12 and adenosylb12 in processes

    The flaws in this are that these reactions can be deadlocked. It takes ATP produced by adb12 to produce adb12 and mb12. It takes glutathione to produce mb12 to produce glutathione. It takes ATP and mb12 to produce SAM-e to produce mb12


    Without enough adb12 to produce ATP hydroxcbl doesn't produce adb12.
    Without enough mb12 to produce glutathione, hydroxycbl doesn't produce glutathione.
    Without enough SAM-e to produce mb12 hydroxycbl doesn't produce mb12 to produce SAM-e.
    Without enough adb12 to produce ATP hydroxcbl doesn't produce mb12


    Each of these are classic deadlock situations. The reactions are dependent upon sufficiency of the items or related items to be produced. In other words this has to act like a biochemical perpetual motion machine.

    All of this happens because hydroxcbl competes for methyl groups instead of providing them and needs energy (ATP) to complete these up hill energy transactions. In each case hydroxcbl needs one or more of the items it is supposed to produce in order to produce the items.

    Any ONE of these is enough to cripple hydroxycbl.

    Methylb12 and adenosylb12 and Methylfolate start methylation and cell reproduction almost immediately and confirms it by depleting potassium within 3 days and epithelial tissues obviously starting healing in 10 days.

    Adenosylb12 often starts mitochondrial functioning to improve starting within 10 minutes.

    Hydroxycbl and folinic acid can take days to never to start methylation and cell reproduction, and then only paritally. This can be demonstrated as no duration of Hydroxcbl usage prevents mb12 startup responses. Hydroxycbl almost never adequately causes mitochondria to function fully. This can be demonstrated by no duration of hydroxycbl use preventing adb12 startup reponses.

    After a period of hydroxycbl and folinic acid usage startup response of mb12 and adb12 tend to be more intense than if nothing at all had been taken. Many deficiency symptoms tend to worsen while these are taken.

    Hydroxycbl usually needs lab tests to show effectiveness.
    Adb12 and mb12 provide naked eye results almost always.


    http://forums.phoenixrising.me/show...nversion-of-OH-B12-to-methyl-B12-new-evidence

    Will Marsden recently called my attention to a recent paper from Prof. Richard Deth's group (abstract below) that provides evidence from a rat experiment that major glutathione depletion blocks the conversion of hydroxocobalamin to methylcobalamin.

    This has been one of the main propositions of the pathogenesis model that I have proposed for ME/CFS, i.e. the Glutathione Depletion--Methylation Cycle Block hypothesis. So far, this model has continued to be supported as more research is being completed.

    One of the things this has brought home to me is that in cases in which glutathione or SAMe are extremely low, it will be difficult to get the methylation cycle going using hydroxocobalamin as the form of B12. This is the form included in the simplified protocol I have suggested, and it was found to be helpful for more than two-thirds of the people in our clinical study, but this may explain why some of the people did not receive benefit from this protocol.

    Note that the protocol recommended by Freddd uses methylcobalamin as one of the forms of B12. Methylcobalamin is also used by Dr. Amy Yasko in some cases, depending on genomic polymorphisms. It is also used by Dr. Neubrander and other physicians participating in the DAN! project for treating autism.

    Recently I have been suggesting that if the simplified protocol does not produce benefits within three months, either testing should be performed to determine why, or a change should be made in the protocol used. One possibility would be to add methylcobalamin, starting at low dosage and working up, as tolerated.

    Best regards,

    Rich



    Alcohol Clin Exp Res. 2011 Feb;35(2):277-83. doi: 10.1111/j.1530-0277.2010.01343.x. Epub 2010 Dec 1.

    Ethanol lowers glutathione in rat liver and brain and inhibits methionine synthase in a cobalamin-dependent manner.

    Waly MI, Kharbanda KK, Deth RC.
    Source

    Department of Food Science and Nutrition, Sultan Qaboos University, Muscat, Sultanate of Oman.
    Abstract
    BACKGROUND:

    Methionine synthase (MS) is a ubiquitous enzyme that requires vitamin B12 (cobalamin) and 5-methyl-tetrahydrofolate for the methylation of homocysteine to methionine. Previous studies have shown that acute or chronic ethanol (ETOH) administration results in the inhibition of MS and depletion of glutathione (GSH), and it has been proposed that GSH is required for the synthesis of methylcobalamin (MeCbl).
    METHODS:

    We measured GSH levels and investigated the ability of different cobalamin cofactors [cyano- (CNCbl), glutathionyl- (GSCbl), hydroxo- (OHCbl), and MeCbl] to support MS activity in liver and brain cortex from control and ETOH-treated rats.
    RESULTS:

    In control animals, MS activity was higher in liver than in cortex for all cobalamins and MeCbl-based activity was higher than for other cofactors. S-adenosylmethionine (SAM) was required for OHCbl, CNCbl, and GSCbl-based activity, but not for MeCbl. Feeding an ETOH-containing diet for four weeks caused a significant decrease in liver MS activity, in a cobalamin-dependent manner (OHCbl ? CNCbl > GSCbl > MeCbl). In brain cortex, OHCbl, CNCbl, and GSCbl-based activity was reduced by ETOH treatment, but MeCbl-based activity was unaffected. GSH levels were reduced by ETOH treatment in both liver and cortex homogenates, and addition of GSH restored OHCbl-based MS activity to control levels. Betaine administration had no significant effect on GSH levels or MS activity in either control or ETOH-fed groups.
    CONCLUSIONS:

    The ETOH-induced decrease in OHCbl-based MS activity is secondary to decreased GSH levels and a decreased ability to synthesize MeCbl. The ability of MeCbl to completely offset ETOH inhibition in brain cortex, but not liver, suggests tissue-specific differences in the GSH-dependent regulation of MS activity.

    Copyright 2010 by the Research Society on Alcoholism.

    PMID:
    21121936
    kurt likes this.
  2. kurt

    kurt Senior Member

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    Logically if a person has problems with B12, then the hydroxy form is less likely to be helpful. This is because we get hydroxy form in some foods already, and ordinary bacteria in the digestive system (including in the mouth) also produce hydroxy form. So most CFS patients probably already are getting hydroxy, but if we still have problems with methylation, then the logical conclusion is that our digestion, absorption, and/or conversion to active form is impaired. However, that said, I have noticed different benefits from all the forms of B12. So I really think the only logical pathway is to try them out, singly and in combinations, and at various doses, and with important co-factors, then see what results.
  3. Freddd

    Freddd Senior Member

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    Hi Kurt,

    we get hydroxy form in some foods already, and ordinary bacteria in the digestive system (including in the mouth) also produce hydroxy form

    Can you provide some references for these two statements. In reading over 1000 papers on the subject over 9 years I have never seen either of these things suggested. The bacteria in our intestines below the level of the areas in which b12 is absorbed produces mb12. Fermented animal manures contains more mb12 than fresh manure. YUM YUM. Our mitochondria that are suspected as starting out as a symbiotic organism in some simple organism early on, molds and bacteia produce mb12 and a few convert it to adb12 as well, and the entire animal kingdom uses mb12 and adb12. Hydroxycbl exists as a breakdown product all the way up and down the tree of life. What is found in saliva is transcobalmin 1 which is a transport protein that binds with some food cobalamin for protection and transport and handoff to intrinsic factor for absorbtion in the upper part of the small intestine. When it is carrying cobalamin it is call holotranscobalamin 1. It is picked up by transcobalmin 2 which then becomes holotranscobalamin 2.

    As hycbl has no known actual function in the body as the b12 vitamin except to be converted to the two active b12s, it does combine with cyanide for instance but that is purely chemical, not a vitamin effect, what effects are you attributing to it?


    It could modify the effects of the active b12s as suggested in the quote below. For a person finding ATP generation intolerable perhaps it impairs the theraputic response sufficiently that very little ATP gets made thereby feeling "better".
    http://forums.phoenixrising.me/showt...iewed-research

    Methylmalonic acidemia is generally the result of an inherited metabolic defect, although it is possible to have elevated levels of this metabolite due to a functional deficiency of AdeCbl in the absence of an inherited defect. Bhatt et al have suggested a transient response to OH-Cbl might be misleading and might subsequently impair the therapeutic response to AdeCbl. They further suggest AdeCbl be the cobalamin therapy of choice for individuals with biochemically uncharacterized methylmalonic
  4. snowathlete

    snowathlete

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    Is there any known genetic marker to show whether hydroxycdl does or doesnt work for an individual?
  5. Freddd

    Freddd Senior Member

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    Hi Snowathlete,

    I don't know. These genetic things would be rare and many of the children die as infants. However, that would be an "absolute" thing as Rich has pointed out. These impairments in conversion are functional things. The involve the substances that get made by active b12 to make active b12 out of inactive b12. It's the endless mink farm in which the cats eat the skinned minks and then become food for the next generation of minks that become the food for the next generation of cats ... A biological perpetual motion machine. I have a perpetual motion machine sitting on the counter next to me. It serves as reminder to look for circular reasoning. In can confound a child for hours, until they find the battery compartment.

    http://en.wikipedia.org/wiki/Circular_reasoning
    Circular reasoning, or in other words, paradoxical thinking, is a type of formal logical fallacy in which the proposition to be proved is assumed implicitly or explicitly in one of the premises. For example:

    "Only an untrustworthy person would run for office. The fact that politicians are untrustworthy is proof of this."

    Such an argument is fallacious, because it relies upon its own proposition "politicians are untrustworthy" in order to support its central premise. Essentially, the argument assumes that its central point is already proven, and uses this in support of itself.


    It's a toy and of course a fake. It is of the variety known as magnetic rotational motor. The only catch is that it is a disguised and open electric motor. The perpetual motion machines of old always had hidden wires or hidden compressed air channels or whatever to add that increment of energy needed to keep it going.

    So with hycbl we have a substance that can be converted in small quantity, reclaimed from broken down active b12, back to active b12s. For those in whom it works at all, it works for at most about 1/3 of symptoms and then not very completely. It's a similar situation for cyanocbl. For me, it served to keep my MCV below 100. That is actually as well as mb12 worked for me too in that symptom. For me the thing was that folic acid and vegetable folate didn't work at all. So my MCV didn't come down until Metafolin came along. Cycbl also worked in a barely noticable extent for burning red tongue. I could feel the difference it made if I abstained for 3 months, which I tried, and then took cycbl and b-complex. The burning pain came down one small notch and then no further change. That is the problem with these inactive cobalamins, when they work they only work partially. The size of that "partial" effect varies consideably.

    These possible deadlocks COULD be the explanation I have been looking for that would explain why it is so difficult for people to get out of the b12 hole once they are in it. It would explain why hycbl doesn't work an any studied symptom for 1/3 of persons. Rich always said that "missing factors" would explain it. I had just assumed it would be other nutritional factors, loke Metafolin. Instead, the missing factors appear to be just those things made by active b12s, BOTH of them.

    If cycbl and hycbl work best at replenishing the b12 because to do so there needs to be a certain level of active b12s to make the substances needed to process the hycbl back to active. As the active ones leak away the inactive ones become less and less effective. If you look at a person with pernicious anemia being maintained on an injection once each 1-3 months, they are not well. They may have hundreds of symptoms. They just are not going to die of macrocytic anemia, they are just sick with all these symptoms we all know so well.
  6. Freddd

    Freddd Senior Member

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    accidental duplicated post
  7. richvank

    richvank Senior Member

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    Freddd,

    Are you able to eat sauerkraut without having what you have called a paradoxical folate deficiency? I'm getting very interested in Annesse's sauerkraut treatment (see her recent posts). I know sauerkraut contains folate, but I don't know if it contains folinic acid or if it is all 5-MTHF.

    Best regards,

    Rich
  8. kurt

    kurt Senior Member

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    The source of that info was a website that I did not save, sorry. That site, (I'll keep looking) claimed that the bacteria that produce hB12 are found in our mouths, and I presume from that are pretty ubiquitous. Anyway, I've looked again for that ref but not found it.

    But if hydroxy is not the form found in foods, then what form of B12 is in foods, such as listed on the NIH website?

    http://ods.od.nih.gov/factsheets/vitaminb12

    IF the bacteria produce mB12 only, then that website was wrong.
  9. Freddd

    Freddd Senior Member

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    Hi Kurt,

    But if hydroxy is not the form found in foods, then what form of B12 is in foods, such as listed on the NIH website?

    The types of b12 found in meats, eggs, dairy products, insects, insect egges and all such is basically the same cross-section we have in our flesh. We have in muscle meat mostly adb12 with some mb12 amounting to perhaps 98% of the total and a dozen or more intermediate stage, detox product, breakdown product etc cobalamin forms. In liver it is more mb12 and less adb12 with a larger percentage of misc mixed cobalamins because that is where they are accumulated for excretion by the liver in the bile. Muscles, clams and oysters likely have a larger percentage of mb12 because they feed on all that bacteria and so on that produces primarily mb12. Adb12 creeps in too in some bacteria.

    The only exception on that list is "enriched" cerials that usually contain cyanocbl or maybe hydroxcbl in some countries.

    If you ever go into an old house with "Paris Green" wall paper and the wall is water damaged and moldy and you smell garlic, or from old fashioned pressure treated wood, the garlic smell comes form arsenic forming any of several volitile methyl-arsenate gases. If a person has arsenic in their body and takes mb12 you will smell garlic on their breath as it is flushed out of their system via the lungs.

    claimed that the bacteria that produce hB12 are found in our mouths, and I presume from that are pretty ubiquitous

    I have seen such claims and many others on vegan websites. A non-animal source of human usable b12 is the holy grail in that context and has been announced over and over and been wrong over and over, 100% wrong so far. Having to have a vitamin that only comes from animal source foods irks a lot of vegans as it demonstrates that we must eat meat to survive when supplements are not available. Many of the best mb12 producing bacteria are diease causing bacteria, which is no problem in commercial fermentation vats but a big problem in our bodies. The research coming out of India is very focused on the endemic b12 deficiencies of their population and the reproductive problems it casues.

    The historic "Tantric" meal in these societies includes beef and fish. The theory was that overcoming taboos gave great power to the person allowing them to do the sexual and energetic (Kundalini) acts of Tantra. The meal included adb12, mb12, omega3 oils, methylfolate, high quality protein and a whole grain dish with b-vitamins as a minimum. This allowed spiritual and sexual experiences that were often not otherwise available. Consider the reputation of Oysters as an aphrodesiac. Filterfeeding shellfish are by far the most potent food sources of b12. Some studies indicate that beef in the USA only has 5% of the b12 it used to have before feed supplemented with cyanocbl. A New Zealand study indicates that 6 week lambs injected with 5mg of mb12 once have 20% more meat produced at slaughter.

    If you look at patent applications there are a lot claiming infusing plants with 12bacteria that produce mb12 so that one can get b12 from veggies. So far nobody has succeeded and it is all proposed wishful thinking.

  10. Freddd

    Freddd Senior Member

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    Hi Rich,

    I am totaly unable to eat sauerkraut without retching violently. My body says "spoiled - expell immediately". I can't tolerate the taste or smell of lactic acid either. For some reason I am quite hypersensitive to these things. I eat small amounts of cabbage in eggrolls and strifry without a problem but that is my limit. Can you point me at one of her posting with the info?
  11. richvank

    richvank Senior Member

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    Hi, Freddd.

    Annesse has been posting on several threads, and has also written a book entitled "Autoimmune, the Cause and the Cure." She suffered from lupus herself, with earlier diagnoses of CFS and FM. After trying lots of things, she found that raw, organic sauerkraut caused her to recover. She reports that this also works for other autoimmune diseases, and she also includes CFS and FM. Her hypothesis is that these disorders are caused by a lack of protease enzymes, and that sauerkraut and other fermented foods can supply these enzymes. Like you, she builds her arguments on observation of symptoms and comparison of symptoms between different disorders. She acknowledges the involvement of B12 deficiency in these disorders.

    Here are some threads on which Annesse has been posting:

    http://forums.phoenixrising.me/show...ifference-between-MS-and-ME&highlight=annesse

    http://forums.phoenixrising.me/show...-causes-sjogrens-syndrome&highlight=sjogren's

    http://forums.phoenixrising.me/show...es)-and-the-symptoms-of-CFS&highlight=annesse

    Best regards,

    Rich
  12. Freddd

    Freddd Senior Member

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    Hi Rich,

    I honestly can't find anything in saurkraut to account for much of anything. It has enough Vitamin C to prevent scurvy. In order of % of mdr sodium, vit C, vit K. Folate is down at 34mcg , 9%, for 1 cup. There isn't enough folate of any kind here to make any significant difference. High lactic acid content is it's most outstanding feature.

    I have read much of those 3 threads and will finish them soon. Here is the thing I see. Digestive problems, lesions in the epithelial tissues of the entire digestive track, inflammation, damage of the mucous tissues drying everything out, stomach damage causing less acid and less ability to digest portein, etc. The catch is that this damage can be kicked off by, you've got it, FOLATE deficiency. This whole business of digestive system damage results whether the cause of the b12 deficiency is a result of vegetarianism or anything else. It doesn't need any body problem at all. They are all caused by the b12 deficiencies. It appears to be a positive feedback loop, including nutrient specific (b12) anorexia, that ends in death. In a primative condition, once a person's body starts breaking down in this way, they die rapidly leaving scarce resources for others. In my reading I have frequently come across the phrase "Continued folate deficiency inevitably leads to b12 deficincy" or similar phrases meaning the same thing. It is always tossed off in an offhand "everybody knows" manner.

    B12 deficiency causes hyper-reactivity in the nurological zsystem and immune system and is supected as a cause in many autoimmune disorders. hashimoto's throiditis appears to actually reverse if damage isn't too far along when mb12 is started.

    MS, now there is an interesting question. In my very limited experience, it can go into significant remission with CNS penetrating injections of mb12 and adb12. Also, l-carnitine fumarate and methylfolate appear essential in that. What results in an MS diagnosis is ruling out b12 deficiency (160pg/ml) and lack of Hcy/MMA, but the CSF is not tested. When the CSF is tested MS patients are low in CSF cobalamin and have elevate CSF HCY. That sure doesn't sound like a valid ruling out of b12 deficincy. Also, the neurological damage of subacute combined degeneration is more bi-lateral than MS (that sounds like an almost meaningless distinction to me). People with MS (very small sample) have way more fear to try mb12,adb12, carnitine, methyfolate, more like I see here than it was at WD.

    She makes the same faulty assumptions I generally see. She considers b12 deficiency to be all one thing rather than 4 distinct deficiency syndromes. Mb12 deficiency also damages endothelial tissue. I haven't posted it yet, I'm still getting it ready. ME, CFS and FMS can all be differentiated by how much the four different b12 deficiencies and folate deficiency play into each of them. Also, as the 5 deficiencies cause over 600 malfunctions in every system and every enzyme and hormone system, every neurotransmitter system etc, chasing each of these as a cause is like 600 dogs chasing their tails. Instead, with the correction of the b12 and folate deficiencies virtually all of these systems rebalance and are fixed.

    She also ignores the distribution of b12 by diffusion bypassing 100% of the distribution system, and all the assumptions surrounding it, which is damaged by the lack of the b12s and folate themselves. Without the methylfolate b12 is flushed from the body. Adding methylfolate makes an immediate visible difference for anybody taking enough b12, a difference folic acid and folinic acid don't appear to make. Of course maybe everybody who can't utilize folic acid and/or folinic acid are the only ones that see that effect. Then that would be a very simple diagnostic test to detect who can't convert folic/folinic acid. There is insufficient data so far to say either way. That also could account of one mechansim for folate deficiency ny any casue to then quickly cause the b12 deficiencies merely by allowing it to be flushed out 5x as fast or whatever the rate is. Even a doubling, and it is more than that, possibly lots more would completely screw the pooch on a system that is always on the edge of a disaster. There is no redundency or margin in the b12 accumulation and retention system. At best it's on the edge of disaster. It appears to be the most frequently lacking massively limiting factor with no work around. In that sense while it is an extraorinarily complex system it is also extremely fragile with a multitude of vulnerabilities that can crash it usually irretrivably. Wthout the mb12 I'd be 7 years dead and buried. Based on my biological birthday I'm 64. Based on my adoptive birthday I'm weeks away from that. I turn 65 just before midnight on Dec 21, 2012. At 11:50 pm on that day I have decreed a mandatory toast with Grand Marnier in lieu of the end of the world. So everybody do that toast and save the world.

    The more of these RESULTANT abnormalities a person tries to chase down the more complex this whole thing looks. Occam never looked better than making a choice between 600 separate causes or 1 cause (1-5 related deficiencies) with 600 results. That appears to be the reasons so many people have been so wrong for so long about this whole set of problems, one resultant defect gets blamed for causing the problems. That is putting the cart before the horse, over and over.

    Another factor is one that I have been trying to find info on for some years. My internist says that all anybody talks about at conventions is the explosion in all these diseases the past 30 years. This includes the explosion of allergies in school children, the explosion of nerological diseases in the middle aged and older, including CFS/FMS, Parkinson's, MS, Autism, Alzheimer's (only 20% as much in Japan using mb12 and 550pg/ml as low), SupraNuclear Palsy all tied together by low CSF cobalamin. There are more and more children every year showing up with early stage CFS/FMS. Interestingly the upward curves of all these things appears to match the folic acid and cyanocbl tonnage that is being put into the diet via flour and food fortification and vitamin consumption with some lag depending upon disease of as much as 20 years or more. Even if the folic acid effect is limited to 20% of the poplation unable to convert folic acid to methylfolate that is a lot of US. And that ignores all those who arrive at their problems via any of several other pathways.

    Most of this has come about because the of the focus on pernicious anemia to the exclusion of hundreds of other problems because that is one of the only things that cyanocbl and hydroxcbl actually morfe or less work against for 2/3 of people. The other third are writeoffs who are not even told that they could take mb12 and never were told. CFS and FMS were garbage diagnoses in which people were belittled, called liars, hypochondriac, lazy, imaginary diseases, yuppie flu and so on and kicked out of practices if the dared to insist that they had a real problem and need effective treatment and denied insurance for these imaginary disease becasue they cost so much to pretend to treat with things that don't work enriching the drug companies and financially destroying millions of people. Is there any part of the medical establishment that wants to see that this is a man caused set of deficiency diseases? I say that from working inside that establishment almost my entire working life.

    I identified these problems, lack of adb12 and mb12, in 1978 the first time I tried to find the cause of my problems. The only thing I didn't spot was folic acid. And since then there are now 10x as many people affected, too many to ignore. And yet the establishment is tring to shut down uncontrolled access to all these vitamin forms we use so that what, maybe they won't have to be embarrassed by folks like us finding the real causes? Or is it purely about being able to charge 20 times more for them since they work.

    Sorry for the rant, but we are on a very tight time schedule before they take away forever our ability to run tests uncontrolled by the industy and for unauthorized healing. We are on the edge of that disaster right now if certain US laws are enforced the way the FDA wants to enforce them or Codex alimetarus gets implimented and enforced.


    Rich, I'm adding this in at the end. The big mystery is why is it that some folks, those who end up with these many neurological and metabolic diseases, can't get the b12 into the CSF and/ort retain it adequately. Is it hereditary? Is it the lack of something that disappears, either unconnected to body level of b12s/folate or when serum cobalamin falls below 1500pg/ml or so or maybe it all traces back to lack of methylfolate for some reason or maybe, some enzyme or something. How does cobalamin get into the CSF in the first place? What is the mechanism. As everything else involved with b12s involves active abcorbtion and transport systems, it is liokely to be one at that level too. That it takes 7.5mg SC to get the serum level high enough long enough to allow diffusion into the CSF indicates that it is broken in me and any others who require that size injection to get it in there. In myself, the lack of CSF/CNS cobalamin manifested as delayed myelination (probably both mb12 and adb12 not getting in) when I was a young child. I didn't have the body manifestations then. It appears that ME specifically has a strong component of low mb12 and maybe low adb12 in the CSF if I am understanding the "pure case" ME symptoms correctly, and I'm not yet finished mapping all this out.

    Maybe this is where Annesse's hypothesis actually fits in. There is a missing piece right there.


  13. Freddd

    Freddd Senior Member

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    Hi Kurt,


    IF the bacteria produce mB12 only, then that website was wrong

    I'm making another pass at that NIH website.

    IN FIRST PARAGRAPH
    Vitamin B12 exists in several forms and contains the mineral cobalt [1-4], so compounds with vitamin B12 activity are collectively called "cobalamins". Methylcobalamin and 5-deoxyadenosylcobalamin are the forms of vitamin B12 that are active in human metabolism [5].

    Vitamin B12, bound to protein in food, is released by the activity of hydrochloric acid and gastric protease in the stomach [5]. When synthetic vitamin B12 is added to fortified foods and dietary supplements, it is already in free form and, thus, does not require this separation step. Free vitamin B12 then combines with intrinsic factor, ...Approximately 56% of a 1 mcg oral dose of vitamin B12 is absorbed, but absorption decreases drastically when the capacity of intrinsic factor is exceeded (at 1-2 mcg of vitamin B12) [8].

    Dietary supplements
    In dietary supplements, vitamin B12 is usually present as cyanocobalamin [5], a form that the body readily converts to the active forms methylcobalamin and 5-deoxyadenosylcobalamin. Dietary supplements can also contain methylcobalamin and other forms of vitamin B12.

    Strict vegetarians and vegans are at greater risk than lacto-ovo vegetarians and nonvegetarians of developing vitamin B12 deficiency because natural food sources of vitamin B12 are limited to animal foods [5]. Fortified breakfast cereals are one of the few sources of vitamin B12 from plants and can be used as a dietary source of vitamin B12 for strict vegetarians and vegans.


    I read every word and can't find anything on that site saying anything about what kind of b12 bacteria produce. CDan you quote the paragraph please and tell me where it is? Thankyou


  14. Lotus97

    Lotus97 Senior Member

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    Dr. Nathan and Rich conducted a methylation study in 2009 using hydroxocobalamin and found it to be effective for the vast majority of CFS patients in the study.
    http://www.mecfs-vic.org.au/sites/w...Article-2009VanKonynenburg-TrtMethylStudy.pdf
    Based on Methylation Pathways Panel Results significant improvements were documented in all of these categories:

    Glutathione (plasma)
    Oxidized glutathione (plasma)
    Adenosine (plasma)
    S-adenosylmethionine (RBC)
    S-adenosylhomocysteine (RBC)
    5-methyl tetrahydrofolate (plasma)
    10-formyl tetrahydrofolate (plasma)
    5-formyl tetrahydrofolate (plasma)
    Tetrahydrofolate (plasma)
    Folic acid (plasma)
    Folinic acid (whole blood)
    Folic acid (RBC)

    In response to the question asking for a subjective estimate of percentage of improvement after 6 months of treatment, 15 out of 21 (71%) reported improvement, 5 reported no improvement
    (24%), and one did not respond. Of those who reported a percentage of improvement, the
    percentages ranged from 5 to 98%, with a mean value of 47.5% and a standard deviation of 25%.

    In response to the symptoms checklist, twenty out of 21 patients (95%) reported a decrease in
    their number of symptoms at 6 months, compared to their number at the start of treatment, and
    one reported an increase from 19 to 20 symptoms.

    In the self-rating of outcome measures at 6 months, 16 of 21 (76%) reported improvement in
    energy, 16 of 21 (76%) reported improvement in sleep, 15 of 21 (71%) reported improvement in
    mental clarity, 15 of 21 (71%) reported greater freedom from pain, and 14 of 21 (67%) reported
    improvement in their overall feeling of wellbeing
  15. Xara

    Xara Senior Member

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    The vast majority... They started with 30 patients, not much is being said about the situation, improvement or deterioration, of the 9 left out in the presented results. And as for the rest of the figures you quoted:

    Aaron Levenstein:
    “Statistics are like a bikini. What they reveal is suggestive, but what they conceal is vital.”
    In case you're interested: The problem with statistics:
    http://public.wsu.edu/~taflinge/evistats.html
    Not meaning to be disrespectful here; what Rich and Nathan did was certainly interesting.

    I just don't understand why, in this thread, you repeat the results of a four year old, limited study done to test a hypothesis proposed in 2007. Especially since this is a thread where Rich himself responded, in January 2012. But here you are, simply repeating his (older) words.

    Science progresses and the man who could tell us which parts, if any, of that specific study are outdated or not, is no longer here, alas.

    If you're trying to convince Freddd his theory is wrong, entirely or partially, by simply repeating what Rich has said and done in the past: I fear there's a big chance Freddd has already seen Rich's earlier postings, so please say something new, add something of yourself, if you want to help.

    If you're trying to inform others about the cons of Freddd's protocol and the pros of Rich's protocol, please start a new thread and repeat over there things that were once said and done by Freddd and once said and done by Rich. An overview, a summory, would be more helpful to newcomers/oldcomers than having to look into all sorts of different threads with all sorts of repeated info.


    Nothing new beneath this line.
    ------------------------------

    In response to your quotation I'd like to quote from that same study:

    "Limitations of this Study
    The principal limitations of this study, being a preliminary, open label study, were that it was not blinded, randomized or placebo-controlled, it was limited in size to 21 patients (who met the strict selection criteria) in a single practice, and the duration of uniform treatment was limited to 6 months.

    Because they funded their own office visits and supplements, the patients may have been biased toward achieving a positive outcome.

    (...) self-evaluation of symptoms
    (..) relatively modest statistical power.

    Additional, more controlled study will be necessary to determine whether these improvements will continue to stand when possible sources of bias that are inherent in a preliminary study of this type are subject to control, and also to determine to what degree the results can be generalized to the CFS population as a whole.

    It is not possible to determine from this study what the ultimate degree of improvement might be from this treatment, or how long a duration of treatment would be required before either no further improvement (or, more optimistically, even complete recovery) would be observed.*
    (..)
    It should also be pointed out that this treatment has not been optimized for CFS, and it is therefore likely that it could be improved by controlled studies."

    Xara: * Did all 30 improve? If there was any deterioration for any of those 30 cases what kind of deterioration was that?
    ahmo likes this.
  16. Lotus97

    Lotus97 Senior Member

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    I could care less what Freddd thinks. There a lot of other people trying to learn about methylation. I've never criticized Freddd's protocol so I don't understand what you're getting at. I never even mentioned Freddd's protocol in my post (or Rich's protocol for that matter). I'm surprised you can so easily dismiss a methylation study done on CFS patients. It sounds like you're the one trying to prove something, not me.
  17. Xara

    Xara Senior Member

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    The study had its limitations. You seem to dismiss those limitations.
    Also, simply quoting Rich does not tell me how Rich would have thought about the subject on hand anno 2013.
    Again, if you'd like to simply repeat Rich's words why don't you start a new thread with a summary? Then I would know what to expect.
    Reading an entire thread only to learn that at the end nothing new is said and things are simply repeated is rather irritating, sorry.
  18. ahmo

    ahmo Senior Member

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    Lotus, I agree w/ Xara. It might not have been your intention, but you seem hostile to Freddd's contributions. I've spent many hours here in the last few months, trying to get these protocols clear. Hydroxy was useless for me, but I'd started it thinking it was the next step. Whereas methyl and adeno B12 are proving v helpful. that's just me. I also agree that starting a new thread specifically to make your point would be useful. ahmo
  19. Lotus97

    Lotus97 Senior Member

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    What exactly are you referring to when you mention 2013?
  20. Xara

    Xara Senior Member

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    First of all I think of Rich as a researcher who was open to evolvement, who was eager to learn new things and ready to adapt (improve) theories when presented with new data, new experiences and new groundbreaking thoughts. (I am not saying you see him differently, I am merely trying to explain myself. I am hoping you'll see what's troubling me, and I am hoping you will understand.)

    When you are quoting him... because the man was very active on this forum I start wondering:
    1. Was this indeed the last thing he said - or thought - about the subject?
    2. Would he himself still have said the thing you're quoting had he been alive today, in 2013? To me, when reading words Rich wrote down, words taken out of history, being repeated in the present in a different setting, it feels like Rich is tied down to a specific opinion, to an opinion that would have been his no matter what.

    You see, I think there lies my problem with you quoting Rich in reaction to threads or postings where Freddd (or anybody else) has a different opinion - Freddd (or anybody else) is alive and is able to grow, to change - has changed, opinion wise, because every day he is learning new things. Rich does not, can not, alas, a huge loss. But you Lotus, you give Rich a say: the same, unchanged answer. To me, that goes against Richs character. (not saying I'm the expert in this)
    Understand?

    Now, don't get me wrong, I definitely don't think quoting Rich is a bad idea. In some cases it could be enlightening, in some cases it IS enlightening. But when in a conflict situation, when using Richs words to point the finger at something that is not in line with what (you think) Rich once (or a hundred times had) said... I'd prefer to see you use your own words, Lotus, for you/I don't know if he'd be on your side, if he had agreed with you, or if he'd even agreed with him, himself, had he lived now. In 2013.

    In the above I hope I did not step on your toes, or anybodys toes. I also hope I was capable of making myself clear and answering your question. I am sure I would have done a better job if I had written it in Dutch. :) Please, learn Dutch. :)

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