Re: Lyme Disease: Wiped out by Vitamin C

[Guest guest]

Hi, Penny and all.

A well-founded hypothesis for the biochemical mechanism by which high-

dose intravenous vitamin C works in cancer treatment has been proposed

by Dr. Mark Levine and coworkers at the NIH. I suspect that the same

mechanism might be effective where pathogens are involved, the idea

being that the pathogens or the cells they are occupying are not able

to cope with the additional oxidative stress, while normal, healthy

cells have enough antioxidant capacity to tolerate it. In the case of

Lyme disease, there is published work indicating that the Borrelia

bacteria deplete glutathione and inhibit glutathione peroxidase.

Perhaps the vitamin C kills the cells they are occupying because the

bacteria have already put them under oxidative stress.

The abstract of the Levine et al. study is below, and the full paper is

available free at PubMed.

I suspect that the MiracleMineral Supplement, if it indeed works,

probably works by a somewhat similar mechanism, i.e. that mixing sodium

chlorite and citric acid in a water solution produces some chlorine

dioxide. Being a neutral species, some chlorine dioxide is able to

diffuse across cell membranes and enter cells. Once inside, it reacts

as a highly oxidizing species, and the additional oxidative stress

pushes cells over the edge if they are already suffering from oxidative

stress. It is claimed that MMS works on malaria. In that case, the

malaria parasite produces oxidative stress in the red blood cell it

occupies when it consumes the hemoglobin, releasing iron, which

catalyzes the Fenton reaction. The extra oxidative stress perhaps

kills the infected cells, while the uninfected cells are able to cope

with it. The difference between the high-dose vitamin C treatment and

the MMS treatment would then be that the diffusing and oxidizing

species in the former is hydrogen peroxide, while in the latter it is

chlorine dioxide. But the kill mechanism may be the same.

Rich

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[Guest guest]

Hi, Penny and all.

Sorry, I forgot to post the abstract. Here it is:

Proc Natl Acad Sci U S A. 2007 May 22;104(21):8749-54. Epub 2007 May

14.

Ascorbate in pharmacologic concentrations selectively generates

ascorbate radical and hydrogen peroxide in extracellular fluid in

vivo.Chen Q, Espey MG, Sun AY, Lee JH, Krishna MC, Shacter E, Choyke

PL, Pooput C, Kirk KL, Buettner GR, Levine M.

Molecular and Clinical Nutrition Section, National Institute of

Diabetes and Digestive and Kidney Diseases, National Institutes of

Health, Bethesda, MD 20892, USA.

Ascorbate (ascorbic acid, vitamin C), in pharmacologic concentrations

easily achieved in humans by i.v. administration, selectively kills

some cancer cells but not normal cells. We proposed that

pharmacologic ascorbate is a prodrug for preferential steady-state

formation of ascorbate radical (Asc(*-)) and H(2)O(2) in the

extracellular space compared with blood. Here we test this hypothesis

in vivo. Rats were administered parenteral (i.v. or i.p.) or oral

ascorbate in typical human pharmacologic doses ( approximately 0.25-

0.5 mg per gram of body weight). After i.v. injection, ascorbate

baseline concentrations of 50-100 microM in blood and extracellular

fluid increased to peaks of >8 mM. After i.p. injection, peaks

approached 3 mM in both fluids. By gavage, the same doses produced

ascorbate concentrations of <150 microM in both fluids. In blood, Asc

(*-) concentrations measured by EPR were undetectable with oral

administration and always <50 nM with parenteral administration, even

when corresponding ascorbate concentrations were >8 mM. After

parenteral dosing, Asc(*-) concentrations in extracellular fluid were

4- to 12-fold higher than those in blood, were as high as 250 nM, and

were a function of ascorbate concentrations. By using the synthesized

probe peroxyxanthone, H(2)O(2) in extracellular fluid was detected

only after parenteral administration of ascorbate and when Asc(*-)

concentrations in extracellular fluid exceeded 100 nM. The data show

that pharmacologic ascorbate is a prodrug for preferential steady-

state formation of Asc(*-) and H(2)O(2) in the extracellular space

but not blood. These data provide a foundation for pursuing

pharmacologic ascorbate as a prooxidant therapeutic agent in cancer

and infections.

PMID: 17502596 [PubMed - indexed for MEDLINE]

Rich

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[Guest guest]

In high doses Vitamin C works as an antioxidant, probably denaturing

the toxins released by bugs that paralyze the immune system and cause

a cytokine storm as well.

If you look in Levine's classic book on Antioxidants

(available through Allergy Research) you will find a table at the back

that he dubs the " morbidity index. " The amount of OXIDIZED vitamin C

went up in those who were the most ill or dying from infections. As

those with severe infections began to recover, the amount of Vitamin C

in antioxidant form recovered. The body was obviously, in severe

infection, using up the antioxidant form and unable to generate more,

and the oxidized form was building up.

That may be the mechanism by which it helps infection. There may be

others too. There was also some research last year on a discovery as

to how it helps in hypoxic tissue in cancer but it was complex and

I've completely forgotten it. Not what you'd expect.

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[Guest guest]

Well- not in my case- but in my case I couldn't find anyone to IV it

into me..

I had bowel intolerance at oral levels >8g ...

But I always wanted to try IV C when I was ill and didn't know what I

had.

Barb

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wiped_out_ by_vitamin_ c.htm

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