"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 Astrophan@att.net 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 http://www.subtleenergies.com/ormus/ormus/ormus4.htm . 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 http://www.subtleenergies.com/ormus/tw/Radiatio.htm and http://www.subtleenergies.com/ormus/presentations/tampaout.htm.

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 particles of gold after she took MSM) there are no known episodes of spontaneous deposition of precious metals in the body. But there is plenty of evidence for the accumulation of toxic levels of non-precious metals in association with certain diseases, such as copper in amyotrophic lateral sclerosis, iron in Parkinson's disease, and mercury in a large number of different disorders including Alzheimer's disease, chronic fatigue syndrome/fibromyalgia and autism.

To take one example, is it possible that some of the mercury in our bodies doesn't come from dental amalgams, vaccinations or trace amounts in the diet, but from transmutation of Ormus into mercury and subsequent "pinning" of m-state mercury to metal? Mercury accumulation is notoriously difficult to clear. One reason may be that under certain pathological circumstances our bodies manufacture more of it. It is interesting that mercury occurs at the end of the list of known Ormus elements. Perhaps it can arise as the terminal product of a series of transmutations in which protons are successively fused with Ormus; elevated acidity (an increased number of protons) in tissues could help drive the reactions.

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. Alkalinity does appear to play a role in Ormus biochemistry. It has previously been suggested on the Forum that maintaining an alkaline pH facilitates the absorption of Ormus; my suspicion is that alkalinity facilitates the proper utilization of Ormus rather than its absorption. Thus, mercury accumulation in tissues could arise as the result of a combination of pathological factors, including acid pH, oxidation/reduction imbalance, and the presence of one of more of Hudson's "substances"--or equivalently, the absence of a nutrient that could counteract those substances. That's where B12 and molybdenum (Mo) come in.

One final remark before discussing the Ormus-preserving effects of B12 and Mo. What I have suggested above is not a complete theory, only a sketch for a theory. It will raise more questions than answers and, hopefully, suggest new directions for research. For example, I have evidence for the exacerbation of mercury toxicity in some people following intake of Ormus. Other reports, however, have suggested that Ormus intake can help clear mercury toxicity. 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. For another example, I have suggested that copper toxicity in ALS and iron toxicity in Parkinson's *may* be due in part to altered Ormus metabolism. If this is indeed true it may be that a different transmutation mechanism (fission rather than fusion) is at work in such cases. Perhaps these conditions are related to excess alkalinity rather than excess acidity. These are all questions for future research.

Let's return now to Hudson's substances that can pin Ormus to metal. Leaving carbon aside for later discussion, the other chemical substances are nitric oxide (NO), carbon monoxide (CO) and sulfites. The term "sulfites" can be taken to mean any form of sulfur in the +4 oxidation state, including sulfite (SO3--), metabisulfite (S2 O5--), hydrogensulfite (HSO3 -), and the atmospheric pollutant sulfur dioxide (SO2). Collectively I will write them all as SO3--, since this is the typical form in which they ultimately appear in the body.

In one form or another, sulfites are often added to food and drink as preservatives and antioxidants and to breads and pastries as dough conditioners. Our bodies also make sulfite as part of the process of degrading or catabolizing sulfur amino acids, including cysteine, methionine and taurine, as well as other natural sources of organic sulfur such as MSM. White blood cells known as neutrophils produce sulfite (and also nitric oxide) in response to bacterial infection, which makes sense in view of the pro-inflammatory and antibacterial nature of sulfite. 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), but we should also remember that it has a natural and beneficial role to play in immune defense. Only when our bodies get out of alignment does sulfite become a problem.

However, the fact is that many people are sensitive to sulfites, especially to those used as food additives. I'm one of these people since I tend to get headaches from drinking sulfite-treated wine. Fortunately I don't come down with other more severe reactions to sulfites, such as hives, rosacea, facial swelling or throat constriction. Sulfites can also trigger bronchospasm in people with asthma. Other diseases complicated by sulfites include chronic fatigue syndrome, fibromyalgia and arthritis, irritable bowel syndrome, heart arrhythmia, irregular blood pressure and Behcet's vasculitis. Some people with extreme sensitivity to sulfites cannot tolerate any form of organic sulfur, including MSM, biotin and even garlic or onions. See http://members.aol.com/nosulfites/chronic.htm for a discussion of sulfite intolerance and its relationship to chronic disease as outlined above.

Sulfite is detoxified by conversion to sulfate by the enzyme sulfite oxidase. A genetic impairment of sulfite oxidase will of course lead to sulfite intolerance, but so will a deficiency of Mo, a trace metal central to the functioning of the enzyme. 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, and that chelation therapy plus Mo supplements can improve sulfite tolerance; see http://members.aol.com/nosulfites/therapy.htm.

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. Molybdopterin holds on to the Mo ion through a pair of thiol groups. (A thiol group is a piece of a molecule consisting of a sulfur atom linked to a hydrogen.) Guess what--mercury loves to grab hold of thiols and bind them tightly. My suggestion is that mercury displaces Mo from molybdopterin and hence inactivates it, resulting in an effective deficiency of this coenzyme. The same could be true of lead, which also has an affinity for thiol groups. Mercury and lead can also interact directly with thiol groups on the enzyme itself and impair its function. Thus, chelation therapy plus Mo supplements make sense for decreasing sulfite intolerance. An even better idea would be to supplement with Mo bound to molybdopterin rather than Mo alone, but so far as I know this product is not commercially available anywhere.

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. In such a scenario the accumulation of mercury (e.g., initiated by dental amalgams) would impair the function of sulfite oxidase, leading to increased levels of sulfite which could in turn convert m-state mercury to metal a la Hudson, which would in turn lead to an even greater impairment of sulfite oxidase, and so on. Thus, a little mercury could eventually result in a lot of mercury in the body. The process would be slow to start at first but would abruptly accelerate as a runaway feedback loop in the later stages. More generally, the same mechanism could be at work in causing the pathological accumulation of other transition metals such as copper. I will not discuss the ramifications of this interesting idea any further here since we have much additional ground to cover.

Like sulfites, both nitric oxide and carbon monoxide are naturally produced in our bodies. Both can be toxic, but surprisingly both have been found to play roles as signaling molecules in the nervous system. Nitric oxide, produced from the breakdown of the amino acid arginine, is known to regulate blood pressure and inflammation. Too little NO in your body can result in high blood pressure or even male impotence (that's what Viagra corrects, since it's a nitric oxide donor). On the other hand, too much NO in your system is associated with pathologically low blood pressure and is one of the main causes of mortality in shock. 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. The toxic effects of NO seem mostly associated with the production of peroxynitrite. Excess NO released in the brain is neurotoxic, typically through the formation of peroxynitrite.

Carbon monoxide is produced by the action of heme oxidase on heme to release CO and bilirubin. Bilirubin is a powerful antioxidant and CO can have beneficial blood vessel relaxing effects similar to those of NO. However, too much CO, from breathing auto exhaust or natural gas, can cause death because CO inhibits the oxygen-carrying function of hemoglobin through the formation of carboxyhemoglobin.

Now, 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, what do SO 3--, NO and CO all have in common?

The answer is vitamin B12, as you may have already guessed. B12 binds each of these substances and can help ameliorate their toxic effects. Surely this is no coincidence. Therefore B12 must play an important role in Ormus metabolism.

1) SulfitoB12 is a form of B12 found naturally in the body. It is believed to arise from the scavenging of sulfite by B12. Both cyanoB12 and hydroxoB12 have been used to treat sulfite-sensitive asthma because of this scavenging action. CyanoB12 is the form most familiar to us as vitamin B12 in vitamin pills. When cyanoB12  is ingested, the body clips off the cyano group and generates aquoB12, essentially the same thing as hydroxoB12. In addition, I have found information suggesting that B12 can facilitate the oxidation of sulfite to sulfate and not merely scavenge sulfite, so in this sense B12 may be able to act as a nonenzymatic equivalent of sulfite oxidase.

Earlier I mentioned that neutrophils (white blood cells) generate both sulfite and NO for immune defense. It's interesting that of all blood cells, neutrophils also contain the largest amount of B12. 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. Conversely, B12 deficiency and/or mercury toxicity should be associated with persistent inflammatory conditions, which does in fact seem to be the case.

A sensitive radioassay for sulfites in food has been developed using hydroxoB12. 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. Both cysteine and sulfites are used as dough conditioners in bread and pastry, although some bakeries are reluctant to admit the use of sulfites for this purpose. I suspect this is a large hidden problem and another reason for avoiding mass-produced baked goods. I also think that Ormus depletion via exposure to sulfites and to nitric oxide should be considered in the pathogenesis of Parkinson's disease. Sulfite is known to worsen the neurotoxic effects of peroxynitrite (formed from nitric oxide), and neurodegeneration in Parkinson's disease has been linked with peroxynitrite formation. 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, massive doses of B12 are sometimes used as a treatment for clearing mercury. This has always puzzled me because B12 also generates more methylB12, which in turn converts inorganic mercury to methylmercury (the toxic organic form of mercury). 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. There's also another mechanism whereby B12 stimulates the production of glutathione; glutathione is a thiol that binds mercury and can move it out of tissues. The mercury-clearing effects of B12 are probably caused by both mechanisms, sequestration of sulfite by B12 and increased production of glutathione leading to sequestration of mercury. 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, but other forms of B12 work too, especially at higher doses.

2) NitrosylB12 has also been found in the body as a natural form of B12 combined with nitric oxide. It has tumor-killing effects. HydroxoB12 is known to scavenge excess NO and has been used as a treatment for experimental septic shock, where the primary cause of mortality is hypotension caused by massive release of nitric oxide.

3) In some anaerobic bacteria B12 binds CO and helps oxidize it to CO 2. This is similar to the oxidation of sulfite to sulfate thought to be promoted by B12. The inverse reaction can also be demonstrated nonenzymatically in the laboratory, whereby B12 can convert CO 2 into CO under the right conditions. B12 binds CO and CO 2 (and also O2 and NO) the same way that heme in hemoglobin can, because in some ways B12 is chemically very similar to heme.

In summary, vitamin B12 can interact with and sequester SO3 --, NO and CO, three of the physical substances mentioned by Hudson as pinning Ormus to metal. This phenomenon is likely to be relevant to Ormus retention in the body and to human health. I know for myself that taking Ormus with CBX (the enhanced-uptake B12 formulation I helped develop) improves the quality of the Ormus experience. I have heard similar remarks from others who have taken Ormus with ordinary B12. CyanoB12 is fine for this purpose unless you have elevated levels of cyanide in your body, e.g., from smoking or from diseases such as Leber's hereditary optic neuropathy (LHON) or amyotrophic lateral sclerosis (ALS). In such cases it would be preferable to take hydroxoB12 instead of cyanoB12.

As for molybdenum, 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. By the same token, these Mo supplements may enhance the retention of Ormus or the quality of the Ormus experience. I have not personally experimented with Mo, although I think it will work well with B12 for counteracting sulfite toxicity.

It is intriguing that some bacteria also use Mo as a cofactor in the enzyme carbon monoxide oxidase, a relative of sulfite oxidase, which converts CO to CO2. Plants, bacteria and fungi use Mo as a cofactor for nitrate reductase, another relative of sulfite oxidase, which is part of the apparatus for converting nitrate to NO. It may be that there a much deeper connection between vitamin B12 and Mo (or Mo-bound molybdopterin), since each is involved with similar pathways metabolizing SO3--, CO and perhaps NO. This is not too surprising because both B12 and molybdopterin can facilitate oxidation and reduction reactions, enzymatically or otherwise.
 
There's at least one other aspect of B12 and Ormus that needs clarification. Hudson also mentioned carbon (as in burned food) as capable of pinning Ormus to metal. What could he have meant and why did he specify burned food rather than, say, charcoal? There are in fact suggestions that the interstitial spaces in charcoal can trap Ormus; see Hudson's 1995 Dallas lecture. Barry has remarked about something similar occurring with his friend Jim's ozone generator. But to me burned food suggests something more than just charcoal.

It's known that carbonized or pyrolized proteins, as in burned food, generate cyanide and that hydroxoB12 is unexcelled at scavenging cyanide. That's why massive doses of hydroxoB12 are administered to smoke inhalation victims, to purge their bodies of cyanide. In fact, that's also why cyanoB12 is the most widely used form of B12, even though not much of it occurs naturally in the body under normal circumstances. That we call cyanoB12 "vitamin B12" is really an accident of history, since the early researchers who first isolated the natural forms of B12 filtered their samples through charcoal; traces of cyanide in the charcoal converted all of the biological forms of B12 (such as aquo-, methyl- and adenosylB12) into cyanoB12. Interestingly, 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.

Some tentative conclusions:

1) Vitamin B12 helps retain Ormus in the body by counteracting Hudson's "substances"--sulfites, nitric oxide, carbon monoxide and (in my interpretation) cyanide--that pin Ormus to metal.

2) Molybdenum can do the same insofar as counteracting sulfite is concerned. Because increased molybdenum intake can result in copper depletion, copper supplements may eventually become necessary. Consult with a nutritional professional before taking extra copper.

3) Mercury toxicity is intimately linked with sulfite sensitivity and the two may arise together. It's possible that sulfites help create more mercury in the body by pinning m-state mercury to metal. Vitamin B12 plus molybdenum can interrupt the cycle and simultaneously treat mercury intoxication and sulfite sensitivity.

4) Contrary to what the Essene has suggested, I believe that organic sources of sulfur such as onions and garlic can impair Ormus metabolism, but only in individuals with extreme sulfite sensitivity.

5) MSM is not likely to interfere with Ormus retention except in people with untreated sulfite sensitivity.

6) Most people supplementing with B12 and/or molybdenum can safely take MSM--or any other source of organic sulfur, including DMSO, taurine, cysteine, methionine and biotin--without interfering with Ormus retention. However, caution is advised for anyone with a history of mercury toxicity or severe sulfite sensitivity, since even with supplemental B12 and molybdenum it may take the body a while to readjust its threshold of sensitivity to sulfites.

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. My initial instinct was that there aren't any biologically relevant redox couples that could provide potentials in the range we're interested in. Typically the potentials for redox couples like GSSG/2GSH or NADP+/NADPH tend to run to a few hundred millivolts; for example, for the NADP+/NADPH system, it's about 320 mV.

After thinking a bit more about, 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, e.g., Fe, Mn, Co or Cu. Of course, my favorite transition metal is Co because it's at the heart of B12, which many bacteria in fact do use as well as mammalian cells. Cobalt has three oxidation states. The redox couple Co(III)/Co(II) generates a potential of 1.83 V in the presence of 2 M H2SO4; compare this to the standard electrochemical potential of 0.771 V for the Fe(III)/Fe(II) redox couple or 0.153 V for Cu(II)/Cu(I).

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). B12 is known to be capable of catalyzing a number of electron transfer reactions, including the reduction of molecular oxygen, alkyl halides and nitric oxide, as well as the oxidation of nitric oxide, cysteine, glutathione, mercaptoethanol and hydrazine to name a few. I have no idea what the corresponding ORPs for the redox couples based on B12 would be, although my guess is that the potentials would be smaller than that generated by the Co(III)/Co(II) system in H2 SO4. Next time I'm at the science library I'll look up a few papers to check on B12-related ORPs. Maybe you can get a biologically relevant redox process occurring at something like 1000 mV or above, but I still don't see anything coming close to Hudson's 2.5 V.

There are other possibilities, however. I asked a friend who has consulted for Patrick Flanagan in the development of Microhydrin for his opinion. (His background is in electrical engineering so he talks about EMF rather than ORP.) 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, but I have heard several hypothesized, including a simple chain battery mediated by some kind of clathrate or even a charge carrier.  However, I suspect that the questioners may be limiting themselves unnecessarily in looking primarily for evidence of such large EMFs (as 1.776 V or 2.5 V) as a necessary precondition for biological transmutation.  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, or where such would become secondary or inconsequential.

Thanks for stimulating my interest in a new direction. I'll comment further if I come up with any relevant data from a literature search.

Regards,
Astrophan