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Any thoughts on Dichloroacetic acid?

Discussion in 'Detox: Methylation; B12; Glutathione; Chelation' started by markmc20001, Jul 29, 2011.

  1. markmc20001

    markmc20001 Guest

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  2. richvank

    richvank Senior Member

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    Hi, Mark.

    DCA works by stimulating flow through the pyruvate dehydrogenase complex, by blocking an enzyme that slows this flow. The pyruvate dehydrogenase complex is the enzyme complex that connects the glycolysis pathway in the cytosol of cells with the Krebs cycle in their mitochondria. It converts pyruvate from glycolysis idiabetes and Alzheimer's,nto acetyl-CoA to feed the Krebs cycle. For disorders in which this complex is blocked or partially blocked, which can include some mitochondrial diseases and cancer, DCA can be helpful. There is some evidence that it will also help in type 2 diabetes, and based on the observation that this complex is blocked in Alzheimer's, I suspect it might help there, also.

    In my opinion, it is not likely to help in ME/CFS, because the fundamental issue in the pathogenesis is that there is a chronic vicious circle mechanism that includes glutathione depletion, B12 functional deficiency, a partial block in the methylation cycle, and folate draining from the cells. The mitochondria are impacted in ME/CFS, but in my view this is a secondary effect of the more fundamental vicious circle mechanism. Namely, glutathione depletion causes a partial block of the enzyme aconitase, which operates just beyond citric acid in the cycle, and it also inhibits at least one enzme in the respiratory chain. Furthermore, the methylation cycle partial block causes depletion of at least three substances needed by the mitochondria, namely carnitine, creatine and coenzyme Q10. All of these problems impact the energy metabolism downstream of the pyruvate dehydrogenase complex, so that speeding up this complex will not help them, but instead will increase the pileup of citric acid. I predict that this will have the effect of increasing the rate of conversion of carbohydrates to stored fat in a person with ME/CFS, because when citric acid goes high, it is shunted out of the mitochondria and is converted to fatty acids (particularly palmitic acid) and that is put into triglycerides that are stored in adipose (fat) cells.

    I do believe that DCA is a real breakthrough for cancer treatment, though, and I applaud the efforts of Dr. Michelakis at the University of Alberta, who is trying to get it through Phase 3 trials. Like Bursynski's antineoplastons, high-dose IV ascorbate (shown to work by Mark Levine's group at the NIH), and some other alternative cancer treatments, it is very promising, but very difficult to get through the approval process. Note that there a strong economic forces behind maintaining the status quo in cancer treatment. These treatments are not patentable, so there is no opportunity to get a monopoly, raise the price high, and make a tidy profit after funding the FDA-required trials and the promotion of the treatment to physicians. Try to see the movie "Burzynski, the Movie," if you can find it. I think our best hope is for more people to find out and understand what goes on in the cancer therapy business.

    Best regards,

    Rich
  3. MDL

    MDL

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    Hi Rich,
    Your post made me think about something I wrote in "Hypothesis: Chronic Fatigue Syndrome, Mitochondrial Hypo-function and Hydrogen Sulfide a few years back:
    "The traditional explanation of the toxic effects of hydrogen sulfide is based on its property as a chemical asphyxiate; it binds to the mitochondrial enzyme cytochrome c oxidase (iron-containing protein), blocking oxidative phosphorylation and ATP production. In rats, the gas causes an increase of blood lactate concentration and the lactate/pyruvate ratio, leading to anaerobic glycolysis and inhibition of lipid peroxidation."

    I am wondering if you see any common themes here. Do you think that H2S plays a role in what you are describing above? As you know, hydroxycobalamin is an antidote to H2S poisoning: http://www.ncbi.nlm.nih.gov/pubmed/21396232 What are your thoughts?

    All best,
    Marian
  4. richvank

    richvank Senior Member

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    Hi, Marian.

    Anything that causes mitochondrial dysfunction can cause a rise in lactic acid, because the cells are not able to complete the oxidative metabolism of carbohydrates, and pyruvate is then converted to lactate. This includes a block in the pyruvate dehydrogenase complex, which is located upstream of the Krebs cycle and the respiratory chain, and which I have discussed here. It also includes a block in cytochrome C oxidase, which is located at the end of the respiratory chain, which can be caused by hydrogen sulfide or cyanide or carbon monoxide (note that CO also binds to hemoglobin and myoglobin, interfering with oxygen transport as well as acceptance of electrons by oxygen). Some of the various genetic mitochondrial diseases can also cause a rise in lactic acid.

    Best regards,

    Rich
  5. MDL

    MDL

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    Thank you, Rich. Yes, I did know about carbon monoxide, which only adds to the reasons why we should look more carefully at cytochrome c oxidase. As they say, in for a nickel, in for a dime...

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