Research on the use of dichloroacetate (DCA) for treating cancer has been conducted on experimental animals and human cells.

Research on the use of dichloroacetate (DCA) for treating cancer has been conducted on experimental animals and human cells.

For a long time, the use of dichloroacetate (DCA) to treat children with congenital lactic acidosis has been understood. Recently, its potential in the therapy of cancer has been made apparent. This disease, which Warburg first described in 1932, is due to an issue with the mitochondria.

DCA is able to inhibit or put an end to these interruptions. Therefore, it can be used as an option to chemotherapy or as an addition to it.

In 2007, Bonnet discussed mitochondrial malfunctions in malignant cells and explored how the utilization of DCA could reverse them (Cancer Cell 11, 37-51, Jan. 2007).

He supposes that the absence of oxygen in the glycolysis that is usual in tumor cells might inhibit apoptosis in the cells due to an amelioration of the mitochondria membrane potential. The compound of dichloroacetate for cancer stops mitochondrial pyruvate dehydrogenase kinase that is formed in swollen levels in the tumor cells, culminating in the obstruction of the division of pyruvate. Nevertheless, pyruvate is required for glucose oxidation and the general metabolic and respiratory function of healthy cells.

Pyruvate degradation being heightened by PDK causes the metabolic process to switch from optimal aerobic ATP generation to inefficient anaerobic glycolysis in the mitochondria. DCA stimulates potassium channels in the mitochondria membrane, restoring the cell membrane potential. Additionally, DCA induces apoptosis, stops cell growth, and impedes tumor growth with negligible harm.

In 2008, Wengang Cao of Florida (as reported in The Prostate, April 2008) looked into what happens when DCA is used with radiation treatment for prostate cancer. He observed that DCA suppressed an oncogene called Bcl-2, which prevents apoptosis in prostate cancer cells. When exposed to DCA, the apoptosis process in these cells began to function again, the growth of the tumors slowed down.  Additionally, the utilization of DCA was found to make tumor cells more sensitive to radiation.

Michaelakis from Canada researched the effect of Warburg’s anaerobic glycolysis on cell apoptosis and published his findings in the British Journal of Cancer in 2008 (British Journal of Cancer, 2008, 99(7), 989-994). He identified this as a key cause of the various abnormalities seen in cancer cells and noted that it seemed to be accompanied by an inhibition of mitochondrial function, which may be reversible. It was further demonstrated that inhibition of PDK with DCA encourages the movement of pyruvate into mitochondria, thus favoring mitochondrial respiration instead of fermentation. This process has been seen to inhibit tumour growth both in vitro and in vivo.

Ramon C. Sun, publishing in Breast Cancer Res. Treat in June 2009, conducted an experimental study on the use of DCA for treating breast cancer in rats. In his in vitro and in vivo trials, he discovered that DCA inhibited the growth of multiple breast cancer cell lines without causing any cell death. Additionally, he noticed a 58% decrease in lung metastases in rats that were given DCA compared to those without treatment. The dose of DCA seemed related to the amount of growth inhibition based on Sun’s research.

In rodents, positive effects were seen when 280 mg of DCA per kilogram of body mass was administered. Phase 1 and 2 toxicity trials of DCA have been ended in people. Shangraw had detailed the involvement of DCA in liver transfers to keep intraoperative pH balance in 2008, with a dose of 80 mg/kg body mass taken intravenously with no difficulties. Sun suggests a daily dosage of 25 mg per kilogram of body mass in humans based on the DCA levels experienced in rat experiment and seen during the procedure.

In comparison to the standard cancer treatment medications, the reactions to DCA are insignificant. Using DCA for an extended period of time, over the course of several weeks, could cause slight damage to the nerves, but this can be reversed once it is no longer taken.

In a study released by Michaelakis in the journal Science Translational Medicine from May 12, 2010, it was found that glioblastoma, a type of malignant brain tumor, could be treated with DCA. When the mitochondrial membrane was hyperpolarized in the glioblastoma tissue, it was able to be neutralized when DCA was added in vitro. Furthermore, the formation of cancerous vessels in the tumor was diminished.

In the study, five people diagnosed with glioblastoma took oral DCA (starting with 12.5 mg/kg of body weight 2 times daily and increasing to 25mg/kg twice daily after 1 month) for 15 months. The adverse effects experienced with the medication were peripheral neuropathies that depended solely on the dose and there were no noteworthy problems with the heart, blood, liver, or kidneys. Patients who took the drug without having serious peripheral neuropathy saw some helpful results.

The available data from test tube, animal, and human experiments suggest DCA for cancer is helpful in controlling tumors. Its easy availability with no adverse effects makes it a valuable tool for cancer treatments.

We suggest combining DCA infusions with localized deep thermal therapy in order to make this treatment much more successful.

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