Why do you think you have to infuse again in 12 hours instead of 24?

That's great HP! Perhaps others who are taking sodium chlorite could try adding swimming to their repertoire to see if they get any benefit.

I noticed on your PLM profile that on June 1 you also started taking 1000 mg taurine daily. Does this include infusion days as well, or do you only take it on your off-days?

Mike

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"If I have seen a little further it is by standing on the shoulders of Giants." - Isaac Newton

Oh I definitely agree that sodium chlorite is most likely the principal reason for your recent improvements.

However, I am also of the opinion that a majority of the benefits reported by pALS while taking sodium chlorite are not actually due to the direct action of chlorite on the body, but rather to the action of the N-chlorotaurine (NCT) that is generated when chlorite reacts with taurine within/around macrophages. Though I've been unable to confirm it, I suspect that NCT itself is not able to cross the blood-brain barrier, and if not then the prospect of experiencing ongoing benefits from sodium chlorite treatment rests entirely upon the availability of taurine on the other side of the BBB.

Therefore, as Olly already pointed out, deficiency and/or depletion of taurine could compromise the effectiveness of sodium chlorite, while daily taurine supplementation could likewise bolster chlorite's effectiveness.

(It's also quite possible that taurine plays other significant roles regarding sodium chlorite treatment, such as a connection between taurine depletion and dehydration.)

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"If I have seen a little further it is by standing on the shoulders of Giants." - Isaac Newton

Nem posted this earlier on:

'
I found this alternative perspective on chlorite to be a bit interesting, both from a historical and chemical perspective.

It is a cheap alternative with a clinical utility in the 3rd world as well as for those who no one cares for in the 1st.'

This is the link:
http://www.waisenmedizin.org/Waisenmedizin/RSS-Feed/Eintrage/2011/3/18_DVD_International_Workshop_files/K_W_Stahl_Na-chlorsum_LEICO.pdf

I looked through this presentation again and what I found interesting is that it states concerning DAC N055, a chlorite drug used for wound healing:

Properties of DAC N-055
•(i) in situ disinfection due to ClO2 (= free radical oxidant, oxidative strength 0.95 V in solution) discharge at pH <6 1O2 discharge at UV A light exposure
•(ii) immune modulation is due to in vivo formation of Compound I at pH 7.4 which can be detected by oxidative ethylene split from ACC


Now NPOO1 is supposed to work by immune modulation if I have been reading correctly?

There is some chemical data in this presentation, slide 15, that may show how this occurs?

Would any resident chemist or researcher with a chemical background care to explain how this occurs in simple English so as to open a possible new research path for us in the uses of chlorite?

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Into the heart, an air that kills, from yon far country blows.
What are those blue remembered hills, what sphires what farms are those.
That is the land of lost content,I see it shining plain,
The happy highways where I went and cannot come again

Hello Olly,

I believe they are looking at possible reactions involved with topical wounds. The reactions inside the body are probably different.

I found this interesting comment on TCDO

http://www.nationmaster.com/discussion/encyclopedia/Oxoferin

Does this mean that formation of TCDO is a hoax?

Tom

Well, here are my initial impressions regarding DAC N-055:

- Based on the information pertaining to DAC N-055, the link provided by Tom, and the TCDO patent application, it appears that the formation of a TCDO complex is indeed a hoax. The TCDO "complex," such as it were, appears to be the product of the peroxychlorite dimer photolysis reaction presented on line 2 of slide 13 in the DAC N-055 presentation. TCDO therefore consists only of some extra residual oxygen dissolved in a sea of sodium chlorite, making it no more effective than pure sodium chlorite itself.

- On the other hand, the peroxychlorite dimer in DAC N-055 is purported to cause immunomodulation activity seemingly beyond that provided by chlorite alone. However, my first impression is that the nature of this additional immunomodulation is fundamentally different from that produced by chlorite. Whereas chlorite is often believed to both up- and down-regulate certain aspects of immunoresponse, slides 16 and 18 seem to indicate that the peroxychlorite dimer immunomodulation results from indiscriminate attacking of cell membranes leading entirely to up-regulation of certain immunoresponses. As a result, for pALS this additional activity could very well exacerbate rather than ameliorate their issues.

(Please be mindful however that, being purely a chemist, I have only a rudimentary understanding of immunomodulation compared to others writing on this forum, so when it comes to assessing the implications of the DAC N-055 chemistry I would largely defer to their analyses. Moreover, it seems that actual infusions of DAC N-055 are currently only used regularly to treat radiation exposure, so my next focus will be examining the literature on this usage to see what clues it may offer as to the general immunomodulation activity of DAC N-055.)

Mike

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"If I have seen a little further it is by standing on the shoulders of Giants." - Isaac Newton

Hello Olly,

With a wound to the skin, the lymph and blood have a slightly alkaline pH. Sodium chlorite also has an alkaline pH. In order to release chlorine dioxide from sodium chlorite you need to reduce the pH.

The white blood cells respond to the infections present in a wound. They usually destroy pathogens by engulfing them and using hypochlorous acid produced from hydrogen peroxide to kill the pathogen. When there is a large area, the white blood cells clump together and surround the bacteria.

The invading bacteria produce acid waste and the infected area forms an abscess. The pus in an abscess is acidic.

Now we have an acid to activate the sodium chlorite to produce chlorine dioxide.

Some of the white blood cells seem to be capable of operating in an acidic environment. Otherwise an abscess would never heal. However if the wound is large, the body may not be able to produce white blood cells fast enough to stop the bacteria from spreading. In this case the wound doesn't heal.

When topically used for something like this, the chlorite has some oxidative properties, but the major oxidation is done by the forming of chlorous acid and chlorine dioxide. Chlorite not only supplies the chlorine dioxide through activation, but also uses up the acids produced by the bacteria. This "cleans up" the wound area and allows the body to heal.

If you drink sodium chlorite, it will do something similar when it meets the stomach acid. However, if you adjust the pH of the chlorite solution to slightly acidic, more of the chlorite will be able to pass through the stomach acid. In this case the sodium chlorite is transformed to chlorous acid. Chlorous acid seems to hold on to the chlorite in solution and prevent it from freely releasing chlorine dioxide when it contacts the stomach acid. In the duodenum the pH is adjusted to alkaline and the chlorite is ready to be absorbed into the body. Any chlorine dioxide produced in the stomach that makes it into the duodenum may also partially convert back to chlorite in the duodenum.

The topical use of sodium chlorite is much different than the oral use of it. With topical use there is direct access to the problem area. With oral use the blood stream needs to carry the chlorite to the problem area. Compound I and II are more likely to form when chlorite contacts pus and exposed blood and lymph fluid, according to the medical professionals I have discussed this with. It seems that some oxidation is needed before the formation of those compounds can even be considered. Chlorous acid with an oxidation strength of around 1.57 volts can do that, but chlorite only has a strength of around 0.78. This is lower than oxygen that comes in at around 1.2 volts.

I am not trained in medicine, but I do take good notes. This is how it was explained to me. As you know there isn't a lot of research on this, so consider this a "best guess."

On a side note...

Chlorite is known to react with some minerals like magnesium, phosphorus, and sulfur. These minerals are critical to body function. I am just starting research on this, but it could be that a reduction of sulfur in the body could contribute to hypoxia. IF there is anything to this, it could start to explain why chlorite starts off very beneficial, then the benefits seem to fade over extended use of it. Right now this only qualifies as a "wild ass guess," but I am working on it. In the meantime, those who are using chlorite should review their diet to make sure they are getting generous amounts of sulfur. You can check the sulfur content of food by putting "sulfur diet" into a search engine.

Tom

Just my 2 cents.

If one wishes to raise their serum or RBC magnesium levels, epsom salt foot baths are not going to cut it. The best way of course, is using intravenous magnesium sulfate, if someone has lab values that clearly show a magnesium deficiency. However, oral Magnesium Glycinate is very effective, with Magnesium Taurate and Magensium Citrate coming a close second, in order to help prevent potential deficiency. (Magnesium is also great for other things like muscular (skeletal and smooth muscle) relaxation and vasodilation, but that's for another thread . . .)

It's pretty difficult to be sulfur deficient, especially if the protein content of the diet is good, and even if the protein in the diet is inadequate, it's still pretty much uncommon. Then again, a good protein diet is high in ALCAR, Taurine, L-arginine, L-lysine, but that's for another thread too . . .

The other thing I wanted to ask, is this: are those who are taking OSC, WF10 or home made IV SC, having regular CBC and lytes done? I had never heard of OCS for use in medicine until I started reading this site. With no safety data regarding this substance, is anyone concerned about hemolysis? or at least the need to monitor for this possible (?) side effect?

There may indeed be something to this idea (along the same lines as the potential importance of taurine supplementation). Cysteine in particular plays a very important role in the body’s oxidative defenses. Not only does cysteine behave as an anti-oxidant on its own, but it is also required for the synthesis of glutathione, the body’s primary anti-oxidant. (Interestingly, glutathione is also capable of regenerating oxidized taurine in the body.)

Also, from one of the early animal studies on sodium chlorite:

“Sodium chlorite induced haemolysis, decreased haemoglobin concentrations and loss of packed cell volume in the blood of male Sprague- Dawley rats treated for 30 and 60 days with 100-500 mg/l chlorite in drinking-water but did Dot induce methaemoglobinaemia at concentrations up to 500 mg/l chlorite. After 90 days of treatment, red blood cell counts and haemoglobin concentrations returned to normal; however, red blood cell glutathione concentrations remained significantly depressed and 2,3-diphosphoglycerate levels elevated in animaIs treated with concentrations of chlorite as low as 50 mg/l.”

Elevated diphosphoglycerate levels may also serve as an indication of that some degree of hypoxia.

Mike

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"If I have seen a little further it is by standing on the shoulders of Giants." - Isaac Newton

Hello Mike,

I took the time to duplicate the tests to make sure I haven't missed something or corrupted the test results...

I am coming from an industrial perspective. There may be a difference of definitions between industrial use and the concepts used in chemistry.

Let me see if I can explain what I understand to be going on, and you can explain it from a chemistry perspective. I don't know if there is any protection involved, but it is an interesting concept. Perhaps TCDO was an attempt to explore this.

I am starting with sodium chlorite and adding an acid. This gives me acidified sodium chlorite. A period of time passes and the acidified sodium chlorite forms chlorous acid. This is what I am referring to as activation.

In use, acidified sodium chlorite has different properties than chlorous acid. They are related, but different.

The activation time is dependent on the concentration of the chemicals used and the type of acid used. Temperature is another variable.

At low concentrations there is a minimum of chlorous acid produced initially, but the reaction will continue over time forming more chlorous acid. A by product of chlorous acid formation is chlorine dioxide.

The method of mixing and the activation time depends on how you intend to use the solution.

Some examples...

To disinfect drinking water you need the activation time to be as small as possible and you want all of the available chlorine dioxide from the chlorite released as free chlorine dioxide. To do this the feed chemicals are higher concentrations, the chlorous acid is formed in a reaction chamber and then the chlorine dioxide gas is metered into the water stream.

In this case the activation time is fractions of a second.

Another application is to keep water that is stored free of any biological growth. Water treatment does a good job with water that is rapidly used, but in storage some of the microbes that remain after the initial disinfection can continue to grow in the water. To treat this water small amounts of sodium chlorite are added to the water to protect it for a period of 2 - 5 years. Adding the sodium chlorite to water reduces the pH of the sodium chlorite and this begins its activation.

In this case the activation time is 2 - 5 years.

In food processing acidified sodium chlorite is used. When the solution is mixed there is less than 2 PPM free chlorine dioxide produced. With 1200 - 1500 PPM available chlorine dioxide, there is not much chlorous acid produced. In some cases the activation continues until the package is opened for use.

In this case the solution is used before activation can take place with the exception of the residual left that continues to work during transit.

When dealing with mold and mildew you need some chlorine dioxide to kill off anything that is left over after cleaning, then you need a residual that can continue to work over a period of time. This application involves mixing concentrated chemicals and letting them activate for 10 minutes, then diluting them for use. The solution is then fogged or sprayed and in something like a walk in cooler. This solution continues to work for about two weeks.

In this case the activation is 10 minutes.

ALS people reported some side effects from taking oral sodium chlorite. By lowering the pH of the solution and letting it activate for 24 hours, the side effects were minimized. I am not sure of what biological process is going on here, but it does seem to be effective.

In this case the activation is 24 hours.

I hope this clarifies how I am using the term "activation."

I agree that when an acid comes into contact with chlorite a reaction takes place. The question I have is what happens when an acid contact chlorous acid? This reaction may be different than simply the reaction between an acid and chlorite. You have also brought up the question of additional compounds being formed. With citric acid activation some sodium citrate is formed. This may serve as a buffer during further acidification.

You stated...

"In fact, I can state categorically that there is NO possible way that simply having small amounts of chlorous acid in solution with chlorite could protect either species from further reaction when mixed with a strong acid. The reason for this is that all H+ ions are equivalent to one another in every way, which means that the chlorite/chlorous acid molecules in the solution can't distinguish between H+ from the so-called "activation" step and H+ from the strong acid. Therefore, the reaction must ultimately proceed the exact same way as would an "unactivated" solution mixed with strong acid."

Yet actual testing doesn't support your categorical statement... Well, it does and it doesn't depending upon the concentration of chemicals used.

I believe stomach acid can be duplicated by using 0.1M HCl.

To test this you can mix up a sodium chlorite solution that gives 300 PPM available chlorine dioxide and then add the simulated stomach acid to it. The 300 PPM available chlorine dioxide concentration is representative of what people are taking in the oral sodium chlorite experiment.

When I run tests on this I find that a 300 PPM solution has a pH of 8+. Adding 0.1M HCl to bring the pH down to 2.5 and giving it time to activate I end up with about 180 PPM free chlorine dioxide.

When I start with a 300 PPM solution and add citric acid to adjust the pH from 8 down to around 5, let it sit for 24 hours to activate, and then add the HCl, I end up with about 25 PPM free chlorine dioxide.

On one hand when simulated stomach acid is added to sodium chlorite we get a reaction that uses up most of the chlorite to form chlorine dioxide. On the other hand if the sodium chlorite solution is combined with a small amount of citric acid and the solution is given time to activate, the addition of the simulated stomach acid has little effect on the chlorite. With ALS the goal is to maximize the amount of chlorite that makes it through the stomach for later absorption.

As you can see, prior activation seems to stabilize the chlorite when additional acid is added. Theoretically you should be correct, but actual tests done with the concentrations of chemicals that are being used show something different. I am not sure what other compounds are formed that would protect the chlorite from additional acidification, but something is going on here.

Now, if you run the same tests using 12M HCl instead of 0.1M HCl and 50000 PPM sodium chlorite instead of 300 PPM sodium chlorite, you comments are absolutely correct. The previously formed chlorous acid has very little effect on stopping the conversion of chlorite to chlorine dioxide.

Run the tests for yourself and see if you get similar results. At high concentrations of chemicals you are absolutely correct, but things seem to change a little at lower concentrations. The industrial perspective is that chlorous acid doesn't begin until the pH of sodium chlorite is dropped below 4. Most of the applications in food processing involve a pH range of 2 - 3. Within that range the sanitizing capability of acidified sodium chlorite and chlorous acid are at a peak. The downside is corrosion. In an effort to deal with corrosion efforts exploring chlorous acid production in the pH range of 4 - 6 are being looked at. Other research is looking at adding chlorous acid to an alkaline system. This is very interesting because the chlorous acid reverts back to chlorite in the alkaline system while the chlorine dioxide circulates freely killing active pathogens. Biofilms in the system produce acid waste and the chlorite reacts with that acid to form chlorine dioxide and that keeps the biofilm in check.

All right, it's grill time. No chlorite involved. Just sear the meat and lock those juices in... :)

Tom