slayadragon
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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/
*
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/
*
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].
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/
*
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/
*
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].