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B12 and Mycotoxins

Discussion in 'Detox: Methylation; B12; Glutathione; Chelation' started by slayadragon, Jan 25, 2012.

  1. slayadragon

    slayadragon Senior Member

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    Here are a couple of articles suggesting a connection between B12 deficiency and mycotoxins (biotoxins made by certain species of mold). Freddd, Rich or others, do you have any thoughts about that?


    Anyanwu EC, Kanu I. Biochemical impedance on intracellular functions of vitamin B12 in chronic toxigenic mold exposures. ScientificWorldJournal. 2007 Oct 12;7:1649-57. PMID: 17982599

    A majority of patients with neurological disorders with chronic exposures to toxigenic molds and mycotoxins has vitamin B12 deficiency that is unrelated to dietary insufficiency. Vitamin B12 is a source of coenzymes, and participates in intracellular recycling of methionine, and in methionine synthase reactions. The biochemical processes that lead to B12 depletion and deficiency are not fully understood. This paper examines and assesses various most likely biochemical reasons that could impede upon the normal intracellular functions of vitamin B12 that lead to neurological manifestations. By biochemical implications and derivations, it is most likely that mycotoxins interrupt the structure and function of vitamin B12 through reactive interference with the normal One-Carbon metabolism leading to the observed clinical neurological manifestations such as nerve damage and, demyelination, degeneration of PNS leading to paralysis, progressive peripheral neuropathy, and spinal degeneration.

    http://www.tswj.com/2007/923182/abs/

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    Anyanwu EC, Morad M, Campbell AW. Metabolism of mycotoxins, intracellular functions of vitamin B12, and neurological manifestations in patients with chronic toxigenic mold exposures. A review. ScientificWorldJournal. 2004 Aug 26;4:736-45. PMID: 15349513

    This paper evaluates the possible reasons for consistent vitamin B12 deficiency in chronic toxigenic mold exposures and the synergistic relationships with the possible mycotoxic effects on one-carbon metabolism that lead to the manifestations of clinical neuropathological symptomology. Vitamins are first defined in general and the nutritional sources of vitamin B12 are evaluated in particular. Since patients with chronic exposures to toxigenic molds manifest vitamin B12 deficiencies, the role of mycotoxins in vitamin B12 metabolism is assessed, and since vitamin B12 plays important biochemical roles in one-carbon metabolism, the synergistic effects with mycotoxins on humans are reviewed. An outline of the proposed mechanism by which mycotoxins disrupt or interfere with the normal functions of vitamin B12 on one-carbon metabolism is proposed. The overall functions of vitamin B12 as a source of coenzymes, in intracellular recycling of methionine, in methionine synthase reaction, in the prevention of chromosome breakage, in methylation, and in maintaining a one-carbon metabolic balance are reviewed. Signs, symptoms, and clinical neurological indications of vitamin B12 deficiency are also cited. By implication and derivation, it is likely that the interruption of the structure and function of vitamin B12 would in turn interfere with the one-carbon metabolism leading to the neurological manifestations. This review is an attempt to formulate a basis for an ongoing research investigation on the subject.

    http://www.tswj.com/2004/957412/abs/

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    Anyanwu EC. The validity of the environmental neurotoxic effects of toxigenic molds and mycotoxins. The Internet Journal of Toxicology. 2008 Volume 5 Number 2.

    The problems and controversies about the validity of environmental neurotoxic health effects of toxigenic mold and mycotoxin exposures have taken a center stage in scientific, legal, social, and political discourse to which important basic scientific truth has been misrepresented by subjective double talk in recent years. Fortunately, the scientific truth is characterized by objectivity and systematic organization based on compelling pieces of evidence. This paper reviews the relevant, most recent peer reviewed literatures that support the validity of the environmental risks and adverse neurotoxic health effects of chronic exposures to toxigenic molds and mycotoxins. The structures of typical mycotoxins are cited to show the relevance of functional groups, and how their biochemical activities may contribute to adverse health effects in relation to signs, symptoms, and mechanisms. The proven interactions between the biological system and the molecular functional groups of mycotoxins are evaluated to explain how they may lead to neurotoxic health effects in terms of carcinogenic, biochemical, immunological, neurophysiological and behavioral properties. Based on all the relevant affect factors, there are huge compelling pieces of evidence derived by exposure conditions, clinical presentations, scientific laboratory investigations, and the development of science of nanotoxicology, that support the validity of adverse environmental neurotoxic health effects of toxigenic mold and mycotoxins.

    The overall functions of vitamin B12 as a source of coenzymes, in intracellular recycling of methionine, in methionine synthase reaction, in the prevention of chromosome breakage, in methylation, and in maintaining a one-carbon metabolic balance are well established. Signs, symptoms, and clinical neurological indications of vitamin B12 deficiency are also been known [28. Consistent vitamin B12 deficiency in chronic toxigenic mold exposures has been observed in patients exposed to chronic toxigenic molds and mycotoxins [11]. It is possible that the synergistic mycotoxic effects on one-carbon metabolism will lead to the manifestations of clinical neuropathological symptomology. Since patients with chronic exposures to toxigenic molds manifest vitamin B12 deficiencies, the role of mycotoxins in vitamin B12 metabolism is recognized. Since vitamin B12 plays important biochemical roles in one-carbon metabolism, the synergistic effects with mycotoxins on humans are apparently possible. By implication and derivation, it is likely that the interruption of the structure and function of vitamin B12 would in turn interfere with the one-carbon metabolism leading to the neurological manifestations [28].
     
  2. Freddd

    Freddd Senior Member

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    Salt Lake City

    Hi Lisa,

    I am going to SPECULATE here as I don't know. Consider that these molds likely need mb12 as much as we do. Some molds create their own and some live with others that generate mb12. So if they are actually living and growing in the body they could be outright stealing the mb12 for their own use. Let's consdier toxins. Mb12 does destroy many toxins and in the process is deactivated or desroyed itself, depending upon whether the toxin combines with the cobalamin portion. An example of such a toxin is cyanide. It combines with mb12 to make cyanocobalamin which is the body's preferred excretion form. A treatment for cyanide poisoning is 35 gram (35,000,000mcg) infusions one after another of mb12, adb12 or hycbl until all cyanide is flushed from the system. CN has a molecular mass of 26. Mb12 has a mass of 1335 or so of which the methyl group (CH3) is 18. So 1mg of cyanide destroys 50mg of mb12 APPROXIMATELY. On the other hand let's look at arsenic. Each atom of arsenic reacts with 3 or 4 methyl groups forming a volitle gas that is exhaled smelling of garlic. So 1mg of arsenic (about 75) deactivates appox 60 to 80 mg of mb12.

    So if mb12 is either being destroyed or deactivated by the mycotoxins it will take very little mycotoxin to interfer with many multiples of the entire body content of mb12 causing a very rapid onset of b12 deficiency which will then casue the methyl trap reaction of flushing folate from the cells causong onset of problems in minutes to hours. Either or both could well be considered as "interferring" with one carbon metabolism. There might be other causes as well. Nitrous oxide combines with cobalamin to make nitrocobalamin or some such very rapidly and can cause onset of b12 deficiency crisis in the brain in the duration of a dental procedure for susceptable people.
     
  3. Rosebud Dairy

    Rosebud Dairy Senior Member

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    As I like to think........
    knowing your own genetics helps when dealing with these on a personal level.

    that would be HLA DR/DBQ - Human Leukocyte Antigen, I think.

    Dr. Ritchie Shoemaker has his own analysis posted at survivingmold.com.

    If you have a mold susceptible (or, mycotoxin susceptible HLA) AND an MTHFR.........WATCH OUT!

    Those are the people who may have it the worst as far as chemical sensitivity goes, then you have to look at VIP. vasoactive intestinal polypeptide.

    So, fit the B12 into the genetic picture, if possible, to see how it fits for you.
     

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