Nutrition and Ormus Retention

"What is the most effective way to keep Ormus in your body?" Apologies for the length of this post. I could have put in even more information but chose not to in the interest of keeping things somewhat manageable. In particular I have left out citations to the scientific literature; anyone interested in this level of detail should contact me directly at for more info. Finally, if you don't have the patience to go through the entire document and would like to cut to the chase, please see the conclusions at the bottom of the page. Halfway through writing this post I received an email from Barry asking for my comment on a related question from Mic. So, yes, Mic, in my opinion you are correct--genetic defects in the enzyme sulfite oxidase can lead to an intolerance for MSM (as well as other sources of organic sulfur), resulting in an impairment of Ormus function or retention in the body. See the discussion of sulfites below. However, any genetic defect that leads to complete inactivation or total deficiency of the enzyme is invariably fatal early in life. For sulfite sensitivities that are not quite so severe, some nutritional solutions are fortunately available. In my view there are specific nutrients that can facilitate the optimal use of Ormus. In this post I will discuss two such nutrients that help retain Ormus and keep it in its active (i.e., nonmetallic) state, namely vitamin B12 and molybdenum. In a later post I'll present the results of my research on other nutrients that can counteract potentially negative side effects of Ormus. You may recall my discussion of the spiritual nature of vitamin B12 and its relationship to Ormus from my posts to the Forum four or five months ago. Since then I've discovered a much deeper connection between Ormus and B12. This connection also suggests a definitive answer to the perennial question about whether Ormus can be taken with sulfur compounds and MSM in particular. In his 1996 interview with Binga, David Hudson stated that there are several substances that can drop Ormus to its metallic state. Leaving aside short wavelength UV, which is not a physical substance, the others he mentioned are nitric oxide, sulfites, carbon, and carbon monoxide. See . Note to Barry: In the web page cited above, "sulfites" is misspelled as "sulfides" and the formula given (SO3) should really be written as SO3--. The spelling , but not the chemical formula, is given correctly at and Hudson gives no basis for his statement and for all we know he simply intuited this information. But let's take it at face value and see what the implications are. Since all of the substances that Hudson mentions are found naturally in the body or can be taken in through eating food or breathing air, the first and most obvious implication is that it must be possible for some Ormus to be converted to metal within the body. This is a startling implication at first glance, because (aside of exceptional events such as the stories about Barry's friend Jim excreting gold through his skin or the woman whose tears contained

For another example. It has previously been suggested on the Forum that maintaining an alkaline pH facilitates the absorption of Ormus. But there is plenty of evidence for the accumulation of toxic levels of non-precious metals in association with certain diseases. One final remark before discussing the Ormus-preserving effects of B12 and Mo. sulfites are often added to food and drink as preservatives and antioxidants and to breads and pastries as dough conditioners. since this is the typical form in which they ultimately appear in the body. chronic fatigue syndrome/fibromyalgia and autism. the absence of a nutrient that could counteract those substances. including sulfite (SO3--). my suspicion is that alkalinity facilitates the proper utilization of Ormus rather than its absorption. only a sketch for a theory. carbon monoxide (CO) and sulfites. however. One must remember that Louis Kervran originally proposed biological transmutation--for example. transmutation of sodium to magnesium or potassium to calcium via proton transfer-as a means of regulating pH balance. What I have suggested above is not a complete theory. is it possible that some of the mercury in our bodies doesn't come from dental amalgams. Alkalinity does appear to play a role in Ormus biochemistry. In one form or another. These cases need to be analyzed retrospectively to determine whether pathological mechanisms--such as acidic pH or impaired antioxidant status--were present in cases of mercury accumulation and absent in cases of mercury clearance. It will raise more questions than answers and. have suggested that Ormus intake can help clear mercury toxicity. Leaving carbon aside for later discussion. I have evidence for the exacerbation of mercury toxicity in some people following intake of Ormus. and mercury in a large number of different disorders including Alzheimer's disease. Our bodies also make sulfite as . metabisulfite (S2 O5--). vaccinations or trace amounts in the diet. If this is indeed true it may be that a different transmutation mechanism (fission rather than fusion) is at work in such cases. hydrogensulfite (HSO3 -). It is interesting that mercury occurs at the end of the list of known Ormus elements. the other chemical substances are nitric oxide (NO). These are all questions for future research. iron in Parkinson's disease. To take one example. Collectively I will write them all as SO3-. hopefully. elevated acidity (an increased number of protons) in tissues could help drive the reactions. Other reports. Thus. One reason may be that under certain pathological circumstances our bodies manufacture more of it. The term "sulfites" can be taken to mean any form of sulfur in the +4 oxidation state. Perhaps these conditions are related to excess alkalinity rather than excess acidity. such as copper in amyotrophic lateral sclerosis. including acid pH.particles of gold after she took MSM) there are no known episodes of spontaneous deposition of precious metals in the body. suggest new directions for research. Let's return now to Hudson's substances that can pin Ormus to metal. mercury accumulation in tissues could arise as the result of a combination of pathological factors. but from transmutation of Ormus into mercury and subsequent "pinning" of m-state mercury to metal? Mercury accumulation is notoriously difficult to clear. and the presence of one of more of Hudson's "substances"--or equivalently. That's where B12 and molybdenum (Mo) come in. Perhaps it can arise as the terminal product of a series of transmutations in which protons are successively fused with Ormus. I have suggested that copper toxicity in ALS and iron toxicity in Parkinson's *may* be due in part to altered Ormus metabolism. oxidation/reduction imbalance. For example. and the atmospheric pollutant sulfur dioxide (SO2).

heart arrhythmia. initiated by dental amalgams) would impair the function of sulfite oxidase. which would in turn lead to an even greater impairment of sulfite oxidase. Molybdopterin holds on to the Mo ion through a pair of thiol groups. and so on. Sulfite is detoxified by conversion to sulfate by the enzyme sulfite oxidase. resulting in an effective deficiency of this coenzyme. (A thiol group is a piece of a molecule consisting of a sulfur atom linked to a hydrogen.htm. including cysteine. but so far as I know this product is not commercially available anywhere. biotin and even garlic or onions.. irritable bowel syndrome. The same could be true of lead.part of the process of degrading or catabolizing sulfur amino acids. Only when our bodies get out of alignment does sulfite become a problem. which also has an affinity for thiol groups.htm for a discussion of sulfite intolerance and its relationship to chronic disease as outlined above. rosacea. such as hives. Mercury and lead can also interact directly with thiol groups on the enzyme itself and impair its function. Most interesting is the suggestion that accumulation of heavy metals such as lead and mercury can displace Mo from sulfite oxidase or otherwise impair the function of this enzyme. It's easy to think of sulfite as a villain because it's a pollutant and a preservative that can cause toxic reactions (see below). An even better idea would be to supplement with Mo bound to molybdopterin rather than Mo alone. leading to increased levels of sulfite which could in turn convert m-state mercury to metal a la Hudson. The process would be slow to start at first but would abruptly accelerate as a runaway feedback loop in the later stages. Other diseases complicated by sulfites include chronic fatigue irregular blood pressure and Behcet's vasculitis. as well as other natural sources of organic sulfur such as More generally. the same mechanism could be at work in causing the pathological accumulation of other transition .) Guess what--mercury loves to grab hold of thiols and bind them tightly. facial swelling or throat constriction. but we should also remember that it has a natural and beneficial role to play in immune defense. and that chelation therapy plus Mo supplements can improve sulfite tolerance. which makes sense in view of the pro-inflammatory and antibacterial nature of sulfite. including MSM. methionine and taurine. chelation therapy plus Mo supplements make sense for decreasing sulfite intolerance.g. especially to those used as food additives. However. Sulfites can also trigger bronchospasm in people with asthma. see http://members. White blood cells known as neutrophils produce sulfite (and also nitric oxide) in response to bacterial infection. a little mercury could eventually result in a lot of mercury in the body. I'm one of these people since I tend to get headaches from drinking sulfitetreated wine. A genetic impairment of sulfite oxidase will of course lead to sulfite intolerance. a trace metal central to the functioning of the enzyme. Some people with extreme sensitivity to sulfites cannot tolerate any form of organic sulfur. but so will a deficiency of Mo. My suggestion is that mercury displaces Mo from molybdopterin and hence inactivates it. The poisoning of sulfite oxidase by mercury suggests that a catalytic feedback loop could suddenly bring on the symptoms of both severe sulfite sensitivity and mercury toxicity. Thus. Fortunately I don't come down with other more severe reactions to sulfites. the fact is that many people are sensitive to sulfites. See http://members. In such a scenario the accumulation of mercury ( How could such a pathological displacement of molybdenum occur? It is known that Mo attaches to sulfite oxidase in the form of a complex with a "coenzyme" or enzymatic cofactor known as molybdopterin. fibromyalgia and arthritis.

B12 deficiency and/or mercury toxicity should be associated with persistent inflammatory conditions. the body clips off the cyano group and generates aquoB12. Therefore B12 must play an important role in Ormus metabolism. Carbon monoxide is produced by the action of heme oxidase on heme to release CO and bilirubin. Nitric oxide. I will not discuss the ramifications of this interesting idea any further here since we have much additional ground to cover. 1) SulfitoB12 is a form of B12 found naturally in the body. The toxic effects of NO seem mostly associated with the production of peroxynitrite. Conversely. Too little NO in your body can result in high blood pressure or even male impotence (that's what Viagra corrects. Both cyanoB12 and hydroxoB12 have been used to treat sulfite-sensitive asthma because of this scavenging action. Excess NO released in the brain is neurotoxic. Both can be toxic. too much NO in your system is associated with pathologically low blood pressure and is one of the main causes of mortality in shock. Earlier I mentioned that neutrophils (white blood cells) generate both sulfite and NO for immune defense. I suspect this is a large hidden problem and another reason for avoiding mass-produced baked goods. CyanoB12 is the form most familiar to us as vitamin B12 in vitamin pills. NO and CO all have in common? The answer is vitamin B12. Bilirubin is a powerful anti oxidant and CO can have beneficial blood vessel relaxing effects similar to those of NO. both nitric oxide and carbon monoxide are naturally produced in our bodies. produced from the breakdown of the amino acid arginine. The role of NO in immunity is more complicated since it can both contribute to joint destruction in arthritis and help quell the inflammatory response. Both cysteine and sulfites are used as dough conditioners in bread and pastry. It's interesting that of all blood cells. from breathing auto exhaust or natural gas. is known to regulate blood pressure and inflammation. as you may have already guessed. However. so in this sense B12 may be able to act as a nonenzymatic equivalent of sulfite oxidase. since it's a nitric oxide donor).metals such as copper. too much CO. B12 binds each of these substances and can help ameliorate their toxic effects. Surely this is no coincidence. Now. essentially the same thing as hydroxoB12. neutrophils also contain the largest amount of B12. When cyanoB12 is ingested. but surprisingly both have been found to play roles as signaling molecules in the nervous system. Like sulfites. although some bakeries are reluctant to admit the use of sulfites for this purpose. which does in fact seem to be the case. what do SO 3--. The researcher found that sulfites and cysteine (which gets metabolized to sulfite) were capable of exacerbating symptoms of Parkinson's disease in susceptible individuals who ate pastry. I have found information suggesting that B12 can facilitate the oxidation of sulfite to sulfate and not merely scavenge sulfite. can cause death because CO inhibits the oxygen-carrying function of hemoglobin through the formation of carboxyhemoglobin. In addition. On the other hand. It is believed to arise fr om the scavenging of sulfite by B12. A sensitive radioassay for sulfites in food has been developed using hydroxoB12. The B12 must be present both to protect the neutrophil itself and to help rein in the cytotoxic effects of sulfite so that the immune response doesn't get out of control. aside of the fact that they're all naturally produced in the body and that too much of any of them can be a bad thing. typically through the formation of peroxynitrite. I also think that .

whereby B12 can convert CO 2 into CO under the right conditions. This is similar to the oxidation of sulfite to sulfate thought to be promoted by B12. HydroxoB12 is known to scavenge excess NO and has been used as a treatment for experimental septic shock. Sulfite is known to worsen the neurotoxic effects of peroxynitrite (formed from nitric oxide). In summary. which is part of the apparatus for converting nitrate to NO. This phenomenon is likely to be relevant to Ormus retention in the body and to human health. The inverse reaction can also be demonstrated nonenzymatically in the laboratory. glutathione is a thiol that binds mercury and can move it out of tissues. e. I am of course prejudiced in favor of my own company's B12 product because of its enhanced oral uptake and increased ability for promoting glutathione synthesis. Plants. I have not personally experimented with Mo. By the same token. It may be that there a much deeper connection . from smoking or from diseases such as Leber's hereditary optic neuropathy (LHON) or amyotrophic lateral sclerosis (ALS). and neurodegeneration in Parkinson's disease has been linked with peroxynitrite formation. because in some ways B12 is chemically very similar to heme. which in turn converts inorganic mercury to methylmercury (the toxic organic form of mercury). although I think it will work well with B12 for counteracting sulfite toxicity. three of the physical substances mentioned by Hudson as pinning Ormus to metal.g. but other forms of B12 work too. But if sulfite toxicity and mercury toxicity are deeply intertwined--and in particular if sulfites help deposit more inorganic mercury in the body from Ormus--then it makes sense that B12 can interrupt this pathological cycle. As for molybdenum. I know for myself that taking Ormus with CBX (the enhanced-uptake B12 formulation I helped develop) improves the quality of the Ormus experience. a relative of sulfite oxidase. There's also another mechanism whereby B12 stimulates the production of glutathione. these Mo supplements may enhance the retention of Ormus or the quality of the Ormus experience. vitamin B12 can interact with and sequester SO3 --. 3) In some anaerobic bacteria B12 binds CO and helps oxidize it to CO 2. where the primary cause of mortality is hypotension caused by massive release of nitric oxide. bacteria and fungi use Mo as a cofactor for nitrate reductase. especially at higher doses. another relative of sulfite oxidase. there are various forms of this element such as sodium molybdate or molybdenum picolinate that may be useful in counteracting sulfite sensitivity and mercury toxicity. B12 binds CO and CO 2 (and also O2 and NO) the same way that heme in hemoglobin can. 2) NitrosylB12 has also been found in the body as a natural form of B12 combined with nitric oxide. It has tumor-killing effects.Ormus depletion via exposure to sulfites and to nitric oxide should be considered in the pathogenesis of Parkinson's disease. It is intriguing that some bacteria also use Mo as a cofactor in the enzyme carbon monoxide oxidase. The mercury-clearing effects of B12 are probably caused by both mechanisms. This has always puzzled me because B12 also generates more methylB12. I have heard similar remarks from others who have taken Ormus with ordinary B12. There is a great deal of promise for the use of B12 to treat Parkinson's and other neurodegenerative diseases such as Alzheimer's. By the way. In such cases it would be preferable to take hydroxoB12 instead of cyanoB12. which converts CO to CO2. massive doses of B12 are sometimes used as a treatment for clearing mercury.. sequestration of sulfite by B12 and increased production of glutathione leading to sequestration of mercury. CyanoB12 is fine for this purpose unless you have elevated levels of cyanide in your body. NO and CO.

generate cyanide and that hydroxoB12 is unexcelled at scavenging cyanide. that's also why cyanoB12 is the most widely used form of B12. cysteine. This is not too surprising because both B12 and molybdopterin can facilitate oxidation and reduction reactions. 3) Mercury toxicity is intimately linked with sulfite sensitivity and the two may arise together. CO and perhaps NO. Consult with a nutritional professional before taking extra copper. What could he have meant and why did he specify burned food rather than. Vitamin B12 plus molybdenum can interrupt the cycle and simultaneously treat mercury intoxication and sulfite sensitivity. 6) Most people supplementing with B12 and/or molybdenum can safely take MSM--or any other source of organic sulfur. Some tentative conclusions: 1) Vitamin B12 helps retain Ormus in the body by counteracting Hudson's "substances"-sulfites. Interestingly. caution is advised for anyone with a history of mercury toxicity or severe sulfite sensitivity. 4) Contrary to what the Essene has suggested. see Hudson's 1995 Dallas lecture. copper supplements may eventually become necessary. methionine and biotin-without interfering with Ormus retention. as in burned food. It's possible that sulfites help create more mercury in the body by pinning m-state mercury to metal. since even with supplemental B12 . since the early researchers who first isolated the natural forms of B12 filtered their samples through charcoal. There's at least one other aspect of B12 and Ormus that needs clarification. nitric oxide. enzymatically or otherwise. even though not much of it occurs naturally in the body under normal circumstances. However. but only in individuals with extreme sulfite sensitivity. That we call cyanoB12 "vitamin B12" is really an accident of history. carbon monoxide and (in my interpretation) cyanide--that pin Ormus to metal. Because increased molybdenum intake can result in copper depletion. 2) Molybdenum can do the same insofar as counteracting sulfite is concerned. Hudson also mentioned carbon (as in burned food) as capable of pinning Ormus to metal. charcoal? There are in fact suggestions that the interstitial spaces in charcoal can trap Ormus. including DMSO. taurine.and adenosylB12) into cyanoB12. methyl. Barry has remarked about something similar occurring with his friend Jim's ozone generator. I believe that organic sources of sulfur such as onions and garlic can impair Ormus metabolism. Hudson's "heap leach" process for recovering gold--where he first discovered what we're now calling Ormus--made use of both cyanide and charcoal. In fact. 5) MSM is not likely to interfere with Ormus retention except in people with untreated sulfite sensitivity. say. to purge their bodies of cyanide. since each is involved with similar pathways metabolizing SO3--. It's known that carbonized or pyrolized proteins. traces of cyanide in the charcoal converted all of the biological forms of B12 (such as aquo-. That's why massive doses of hydroxoB12 are administered to smoke inhalation victims. But to me burned food suggests something more than just charcoal.between vitamin B12 and Mo (or Mo-bound molybdopterin).

compare this to the standard electrochemical potential of 0. Typically the potentials for redox couples like GSSG/2GSH or NADP+/NADPH tend to run to a few hundred millivolts. e. B12 itself has reversible redox properties (meaning that it can participate in either oxidation or reduction depending on the direction in which the electrons are being transferred) and it can also participate in sequential reactions involving Co(III)/Co(II) and Co(II)/Co(I). chain or otherwise. Cobalt has three oxidation states.. There are other possibilities. it's about 320 mV. Co or Cu. for example. cysteine. I asked a friend who has consulted for Patrick Flanagan in the development of Microhydrin for his opinion. I suspect that there are dozens of pathways by which a cell or organism might accomplish transmutation which would be independent of a localized EMF differential.771 V for the Fe(III)/Fe(II) redox couple or 0. He may be right with regard to the last two sentences. or where such would become secondary or inconsequential. (His background is in electrical engineering so he talks about EMF rather than ORP. The redox couple Co(III)/Co(II) generates a potential of 1. Of course. including a simple chain battery mediated by some kind of clathrate or even a charge carrier. Fe. however.153 V for Cu(II)/Cu(I). although my guess is that the potentials would be smaller than that generated by the Co(III)/Co(II) system in H2 SO4. I realized that one way you might be able to get a high enough ORP in bacteria would be if you had a redox system involving a transition metal. which many bacteria in fact do use as well as mammalian cells.83 V in the presence of 2 M H2SO4. for the NADP+/NADPH system. Maybe you can get a biologically relevant redox process occurring at something like 1000 mV or above. as proposed at the beginning of his remarks. I have no idea what the corresponding ORPs for the redox couples based on B12 would be. After thinking a bit more about. Next time I'm at the science library I'll look up a few papers to check on B12-related ORPs. but I have to admit I like the idea of a battery.g. Mn. but I still don't see anything coming close to Hudson's 2. as well as the oxidation of nitric oxide.and molybdenum it may take the body a while to readjust its threshold of sensitivity to sulfites.) Here's what he wrote: I know of no rock-solid means by which bacteria or animal/plant cells might achieve a potential of over -320 mv.5 V) as a necessary precondition for biological transmutation. my favorite transition metal is Co because it's at the heart of B12.776 V or 2. glutathione.5 V. including the reduction of molecular oxygen. I suspect that the questioners may be limiting themselves unnecessarily in looking primarily for evidence of such large EMFs (as 1. B12 is known to be capable of catalyzing a number of electron transfer reactions. mercaptoethanol and hydrazine to name a few. What sort of voltage potentials are involved in bacterial life processes? Could their ability to organize water molecules generate clusters of this size and thus the necessary potential? Could this be the basis of biological transmutation? This is a very valuable question. Some researchers . alkyl halides and nitric oxide. but I have heard several hypothesized. My initial instinct was that there aren't any biologically relevant redox couples that could provide potentials in the range we're interested in. However.

In a different context. Astrophan . Perhaps the other side of the coin is also true--that B12 actually helps create Ormus from metal as well as protect it. But intuitively I like the concept of a complex built on B12 plus a battery that could play a role in boosting metal to m-state.have constructed a molecular complex consisting of a B12 derivative covalently attached to 5 viologen units which act as a 10-electron battery. I believe that B12 plays an important role in protecting Ormus from being dropped to its metallic state. There's also an intriguing connection between Arthur's comment about organized water molecules and my friend's comment about clathrate structures. Thanks for stimulating my interest in a new direction. The resulting complex behaves as an electron trap with regard to the Co(III)/Co(II) couple. my partner and I once lookeded at (noncovalent) complexes of B12 which can organize water and perhaps also act as molecular batteries. I'll comment further if I come up with any relevant data from a literature search. by sequestering and interacting with SO3-. Perhaps it's time to take another look at these strcuutures.and NO in redox reactions. I'll have to look up the paper to get an idea of the potential(s) involved. After all. as I have stated previously. Regards.