On Mar 19, 2012 1:33 AM POOKIETRAIN wrote:
RJ, I have seen this publicized on TV a few years ago and sort of forgot about it. Thanks for reminding us. Pharma-DCA.com "" target="_blank" rel="nofollow">http://Pharma-DCA.com " target="_blank" rel="nofollow">Pharma-DCA.com seems to supply this molecule, however it doesn't recommend what quantity and frequency an individual should be taking. Any further information would be helpful. By the way, thanks for the apricot pit suggestion. I have been taking about 15 a day for a week now.
I can get it here in Australia But I think For a few years now DCA been band by the FDA in the USA. But you can still get it in some of the other countries around the world And you don't have to be good at chemistry to make it your self DCA and the Warburg effect
DCA is a very simple molecule, deceptively simple. Basically, it is an analog of acetic acid in which two of the three hydrogen atoms of the methyl group have been replaced by chlorine atoms. Interestingly, it is only one chlorine atom off from trichloroacetic acid (TCA), a chemical we routinely use in the laboratory to precipitate nucleic acids and proteins from solution.
DCA has been around for a long time (which is why is it no longer under patent) and has primarily been used for inherited diseases of mitochondrial metabolism. Mitochondria are often (and correctly) referred to as the "powerhouses" or the "batteries" of the cell, because it is in the mitochondria that the main energy-containing molecule, ATP, is produced using byproducts of glycolysis and the Krebs citric acid cycle to generate a proton gradient across the mitochondrial membrane, which supplies the energy for the enzyme ATP synthase, which, true to its name, synthesizes ATP for use in the cell as a chemical source of energy. The key thing to remember about oxidative phophorylation is that it requires oxygen, whereas glycolysis does not. When there is insufficient oxygen, the end products of glycolysis end up being turned into lactic acid, which is one of the things that make muscles feel tired after a rapid workout that exceeds the capacity of the body to deliver oxygen to the tissues. The primary activity of DCA in cells is to inhibit the enzyme pyruvate dehydrogenase kinase. The result, to boil it down (and not to have to stress my knowledge of the basic biochemistry of glycolosis, the Krebs cycle, and oxidative phosphorylation too much) is to shift the metabolism of pyruvate from glycolysis towards oxidation in the mitochondria. To boil it down even further, DCA shifts the cell's metabolism from anaerobic to aerobic metabolism.
Why, then, would such an activity be useful as an anticancer therapy?
It all boils down to something known as the Warburg effect, which Otto Warburg first described way back in 1928 and reported inScienceback in 1956. Over the last five years or so, cancer researchers have been increasingly coming to appreciate the role of abnormalities in metabolism, in particular the mitochondria, in cancer. To put it briefly, many cancers (approximately 60-90%) favor glycolysis, even in the presence of adequate oxygen for oxidative phosphorylation, leading to a voracious appetite for glucose. Indeed, it is this very avidity of cancer cells for glucose that is the basis of the PET scan, which detects the high uptake of a radiolabeled form of glucose by cancer cells relative to the surrounding normal cells.
Over the last few years, there has been a sort of "chicken or the egg" argument about what is more important and what is the first abnormality leading to cancer. The traditional view has long been that mutations in DNA lead to the activation of protooncogenes into cancer-initiating and causing oncogenes and to the shutdown of tumor suppressor genes. Under this model, mutations leading to cancer also lead to the observations of abnormalities in metabolism. In the wake of the DCA furor, there have been data reported suggesting that the metabolic derangements may actually occur first or simultaneously with the mutations. p53, for instance, the granddaddy of tumor suppressor genes,can trigger the Warburg effectwhen mutated. Whatever the case, it is now fairly clear that abnormalities in cancer cell metabolism are very important in driving cancer growth and could well represent targets for cancer therapy. AS a result of these new data, studying the metabolism of cancer cells has become a much hotter topic of research than it has been in the past. Everything old is new again, it seems. Why cancer cells might have an advantage due to the Warburg effect is a matter of debate, although, given how tumors frequently outgrow their blood supply, being able to maintain themselves in low oxygen situations would be advantageous.
This fascinating basic science met the public in January 2007, when Michelakis and his colleagues at the University of Alberta in Edmonton published a seminal paper inCancer Cell. In the study, DCA was tested in multiple cell culture and rodent models of cancer. In rats, tumor weights in animals treated with DCA were approximately 60% lower than the tumors in the untreated control groups. The drug increased apoptosis, decreased proliferation, and inhibits tumor growth by acting on a critical enzyme that controls the switch between aerobic and anaerobic metabolism without harming non-cancerous cells. Even better, DCA had already been FDA-approved for mitochondrial disorders, meaning that using it in humans would be an "off-label" use of an already existing drug to test it in humans. Thus, the regulatory requirements were considerably easier to meet for early drug trials in cancer.
http://scienceblogs.com/insolence/2010/05/dichloroacetate_dc