Sodium Dichloroacetate has recently come to the forefront after Cardiologist Evangelos D. Michelakis, MD, FACC, FAHA, Associate Professor of Medicine working at the Department of Medicine, University of Alberta Canada discovered that DCA a relatively non-toxic, odourless and colourless small molecule caused regression in several types of cancer.
http://www.thedcasite.com/index.html
http://www.dca.med.ualberta.ca/Home/Updates/2010-05-12_Update.cfm
Anyone tried it?
Hi, Frank.
I have been following the DCA work since it was first announced, and I think it is an exciting development for cancer treatment. This is an old drug for which the patent has run out, and it has been used for treating mitochondrial disorders. There was a company in Sonora, CA, USA, producing it "for veterinary use," but it was shut down by the FDA. I don't know how available it is in Europe.
This drug works by blocking an enzyme that inhibits the pyruvate dehydrogenase complex in the mitochondria. This stimulates flow of pyruvate to form acetyl CoA and feed the Krebs cycle, promoting oxidative metabolism. As you may know, cancer cells were found by Otto Warburg to operate by anaerobic metabolism. Apparently, this drug forces the cancer cells to become aerobic, like normal cells, and then they have a normal lifetime and die, just as normal cells do, rather than being immortal, which is the problem with cancer cells. I think this is a very promising approach for treating cancer, and I hope it will survive the probable opposition from economic interests supporting the current crude cancer treatments that stand to lose if it is successful. Please note that I am a cancer survivor, and am grateful for the treatment I received, but am also aware from personal experience that surgery, chemo and radiation are rather crude and brutal treatments that could really stand to be improved.
With regard to whether DCA would help in CFS, I am not optimistic. If my GD--MCB hypothesis is valid, the problem in the mitochondria in CFS is somewhat downstream from the pyruvate dehydrogenase complex, at the aconitase enzyme in the Krebs cycle, due to glutathione depletion. If this is correct, boosting the pyruvate dehydrogenase activity would likely have the effect of converting more carbohydrates to stored fat, rather than improving the function of the mitochondria.
I would be happy to be proven wrong if it would mean an effective treatment for CFS, but I am not optimistic, for the reason given. If anyone is interested in finding more information about the GD--MCB hypothesis for CFS, it is available at
www.cfsresearch.org which is operated by Nico Van den Eynde in Belgium.
Best regards,
Rich