History of DCA
Many mitochondrial diseases have been treated with Sodium Dichloroacetate (DCA) since its first in 1973. It prevents lactate from building up in cells and inhibits pyruvate dehydrogenase kinase. Several U.S. and Canadian medical and research facilities utilize it to this day because of its proven efficacy in treating lactic acidosis.
Those who have tried DCA are mostly newborns born with mitochondrial diseases. In addition to preventing future neurological damage, mental incapacity, microcephaly, blindness, and mobility abnormalities, the medicine might restore the normal activity of the cellular enzymes. For quite some time prior to the speculation that dichloroacetate may aid people with cancer, its safety had already been established.
Otto Warburg, a German scientist working in the 1920s, discovered that cancer cells had atypical metabolisms. Normally, cells oxidize glucose for energy, a process that requires the presence of oxygen. Glycolysis is a vital process for cancer cells because it allows them to generate energy even in the absence of oxygen, however it does need the presence of sugar. Even when there is enough oxygen for oxidative phosphorylation to occur, cancer cells still prefer glycolysis, which results in a ravenous need for glucose. Because of this observation, Warburg hypothesized that dysfunction in the mitochondria was the root cause of cancer. As a result of blocking the “Warburg Effect,” sodium dichloroacetate (DCA) has therapeutic value.
DCA triggers apoptosis, or cell death, and causes cancer cells to forsake their favored metabolic pathway. Cancer cells may avoid apoptosis and proliferate even in the absence of oxygen because their mitochondria have been rendered inactive. It’s the DCA that flips this. Direct cytotoxic activity (DCA) directly induces apoptosis in cancer cells and enhances the efficacy of other cancer treatments.
• Dr. Evangelos Michelakis of Canada’s University of Alberta presented a study in 2007 that sparked fresh interest in dynamic causal analysis. A decrease in tumor size was seen, suggesting that DCA may be useful in treating cancer. DCA was given to rats that had tumor cells injected into them (brain, breast and lung). DCA was able to eradicate cancer cells while having no effect on normal cells. After three weeks of therapy with DCA, tumors in the rats shrank by up to 70 percent:
Restoring a normal level of activity along the mitochondria-K channel axis promotes apoptosis and suppresses tumor growth, which is suppressed in cancer.
The cancer-fighting properties of DCA have been verified by further studies. However, the vast majority of research has been conducted on laboratory cell cultures rather on actual cancer patients. However, there is a high degree of consistency amongst studies, showing DCA is beneficial against a broad range of cancers.
• Dichloroacetate (DCA) Phase 1 clinical trials were completed in Canada in 2013. Using the dosage range defined for metabolic illnesses, it shown that DCA is viable and well tolerated in patients with recurrent malignant gliomas and other cancers with brain metastases:
Adults with recurring malignant brain tumors were included in a phase 1 study with dichloroacetate (DCA).
• Oral DCA was used to treat five patients with glioblastoma multiforme for up to 15 months in a separate research. In four of the five patients, the study demonstrated clinically encouraging results:
Diethylacetate’s role in glioblastoma metabolism
DCA therapy is currently being offered to patients at the Canadian cancer clinic Medicor Cancer Center. Case reports demonstrating DCA’s efficacy and safety have been published on multiple occasions. Access to its Observational DCA patient data, gathered from actual clinical practice, is open to the general public. Many pre-clinical studies and clinical trials are still ongoing at this time. DCA has been shown to be effective on its own, but it has been found that when used in combination with other drugs, the benefits last much longer.