It has been established that a chemical called dichloroacetate (DCA) can aid in the treatment of congenital lactacidosis in children for quite a while. Its blocking of lactic acid production in cells is the reason behind it. But lately, it has also been seen as having prospective uses for treating cancer too, and research from Warburg (1932) has observed that cancer is a malfunction of the mitochondria.
DCA has the power to stop or get rid of these issues. As a result, this is either an alternative to taking chemo medication or added to it.
A report from Bonnet in 2007 discussed how certain dysfunctions in the mitochondria of cancerous cells can be addressed using DCA, as published in Cancer Cell 11 from January 2007 (37-51).
He thinks the lack of oxygen (anaerobic) glucose usage generally seen in cancerous cells may disrupt the regular cell death process, due to a modification in the electric potential of the mitochondria. The best suppliers of Dichloroacetate for cancer used obstructs the mitochondrial pyruvate dehydrogenase kinase (PDK) that is present in high levels in cancerous cells, consequently halting the breakdown of pyruvate. However, pyruvate is needed for normal cell functioning, oxidizing glucose, and respiratory chain action.
Pyruvate degradation is increased due to PDK, meaning that aerobic ATP production is decreased in favor of anaerobic glycolysis inside the mitochondria. DCA also activates potassium channels in the mitochondria’s membrane to stabilize the cell membrane potential. He stated that DCA has been proven to inhibit cellular proliferation, tumor growth, and promote apoptosis yet show virtually no toxicity.
In 2008, Wengang Cao of Florida (The Prostate, April 2008) explored how DCA combined with radiation therapy affected prostate cancer. He found that DCA inhibited an oncogene (Bcl-2) which suppresses the self-destructive apoptosis process in prostate cancer cells. This led to a diminishment of the tumor size. Moreover, his research showed that DCA increased the susceptibility of the tumor cells to radiation.
Michaelakis’ paper which was published in the British Journal of Cancer in September 2008 describes that the Warburg effect, also known as anaerobic glycolysis, has the ability to suppress cell apoptosis. (British Journal of Cancer, 2008, 99(7), 989-994).
He suggested that this effect is mainly responsible for the different faults in a cancer cell and noted that it seems to be linked to the blockage, possibly able to be reversed, of mitochondrial functions. Research has shown that when DCA stops PDK, pyruvate slips into mitochondria and this encourages respiratory functions in mitochondria as opposed to fermentation. There appears to be a decrease in tumor growth both inside a cell and living bodies.
In June 2009, Ramon C. Sun conducted an experiment researching the effectiveness of DCA on breast cancer treatments in rats. Through observation, it was reported that DCA greatly inhibited the development of different breast cancer cell lines in the laboratory.
He documented that, when administered to rats, DCA inhibited glycolysis in cells without causing any fatalities. Additionally, he found a 58% decrease in lung metastases in rats injected with breast cancer cells and treated with DCA as opposed to an untreated group. When he ran further trials both in vivo and in vitro, it became evident that the inhibitory effects of DCA were reliant upon the dose administered.
Rats that were administered dosages of 280 mg DCA per kilogram of body weight had a positive outcome. Human trials in Phase 1 and Phase 2 have been completed and the results of its toxicity levels are known. In 2008, Shangraw discovered DCA in the use of liver transplants to remain within a certain acid-base balance and administered a dosage of 80 mg/kg of body weight intravenously without difficulty.
Sun suggests that for humans, 25 milligrams of the substance should be taken per kilogram of body weight on a daily basis, depending on the plasma concentrations from the DCA rat model and the concentrations achieved during the procedure.
In relation to regular drugs used in chemotherapy, the side effects of DCA are insignificant. With prolonged use over a number of weeks, there may be a slight weakening of the peripheral nerves, however, it will go back to normal after stopping taking the medication.
In a new document published in www.scienceTranslationalMedicine.org on 12 May 2010 (Vol 2 Issue 31 31ra34), Michaelakis talks about the potential of employing DCA in glioblastoma cases – a harmful cancerous brain tumor. Additionally, analysis of polarized mitochondrial membranes within glioblastoma tissues and its subduing when DCA was introduced in vitro was detected. The angiogenesis (formulation of fresh vessels) of the tumor was also observed to recede.
FIVE individuals with glioblastoma received oral DCA treatment (beginning at 12.5mg/kg bw 2 times daily, going up to 2 x 25mg/kg bw daily after the first four weeks) for a time period of fifteen months. Peripheral neuropathy was the dose-limiting toxicity, however no haematologic, hepatic, renal or cardiological side effects were seen. Positive effects were noticed at doses that did not result in peripheral neuropathy.
The tests and trials suggest that DCA has the potential to be a beneficial part of tumor treatment. What’s more, its low toxicity and ease of use make it a very valuable element of cancer therapy, as it doesn’t come with any unfavorable effects.
We suggest combining DCA infusions with local deep hyperthermia as a way to enhance the potency of this treatment.
