DichloroAcetate or DCA is an organic substance derived from TCE, chemically known as trichloroethylene. It is a very inexpensive (because is not patented yet), simple drug that has shown the ability to kill cancer cells. It has been previously used in certain metabolic disorders and appears to have a good safety profile.
It was a 2007 study published by scientists for the University of Alberta, which showed the anti-cancer qualities of DCA. In this study, dichloroacetate decreased the size of cancerous tumors in rats and also inhibited the growth of cultured human cancer cells. Thus, DCA may be able to change a cancerous cell back to a normal cell.
Evangelos Michelakis, MD, lead researcher along with his team from the University of Alberta, Edmonton, Canada, evaluated DCA on human cells cultured outside the body (in test tubes) and found that this substance had the ability to kill lung, breast and brain cancer cells, while leaving the healthy cells intact. Cancerous tumors induced in laboratory rats (these tumors were a result of infecting the animals with human cancer) also shrank significantly when they were fed with a diet including DCA for several weeks.
How DCA works?
During this study, scientists learned that DCA alters cancer cell metabolism in which the cancer cells make their energy in the main body of the cell (cytoplasm), rather than in distinct cellular components called mitochondria (mitochondria is the powerhouse of the cells). During this process, medically known as glycolysis, a significant amount of sugar is used with large amounts of lactic acid produced.
Previously, it was believed that cancer cells use this process (glycolysis) because the mitochondria is permanently damaged when it is transformed from a healthy cell into a cancerous cell. However, the Canadian researchers found that DCA has the ability to heal the mitochondria in cancerous cells. The now active mitochondria activate a process called apoptosis (cell death). Apoptosis causes the cancer cells to become weak and eventually die.
Now it appears that the switch to glycolysis as a cell’s energy source occurs when cells in the middle of an abnormal but benign tumor don’t get enough oxygen for their mitochondria to function properly. In order to survive, these cancerous cells would turn off their mitochondria and start producing energy necessary for the cell through glycolysis. Mitochondrial metabolism requires oxygen. Glycolysis does not require oxygen. This process of turning off the mitochondria stops the normal process of apoptosis.
Interestingly, mitochondria have another important role in the cellular function. They activate the process of cellular (programmed) self destruction, medically known as apoptosis. As a result, when these cells turn off the mitochondria they become immortal. When mitochondria are reactivated by DCA, apoptosis would be activated and cancerous cells would be programmed to die.
DCA Safety
Some patients reported pain, numbness and gait abnormalities while taking this drug, however the benefits of killing cancerous cells are more important than these minor adverse reactions. In addition, current conventional chemo drugs have many more (and much more serious) side effects. A new Canadian clinical study is being done that will further evaluate the effects of DCA for cancer, and will also test for safety in humans, as well as the proper dosage to be effective against cancer. Don’t take DCA on your own, talk to a healthcare professional to learn more about this drug.
References:
http://www.thedcasite.com
http://www.drweil.com/drw/u/QAA400338/DCA-Hope-or-Hype.html
http://www.newscientist.com/article/dn10971-cheap-safe-drug-kills-most-cancers.html
http://www.cell.com/cancer-cell/retrieve/pii/S1535610806003722
A Mitochondria-K+ Channel Axis Is Suppressed in Cancer and Its Normalization Promotes Apoptosis and Inhibits Cancer Growth; Sébastien Bonnet, Stephen L. Archer, Joan Allalunis-Turner, Alois Haromy, Christian Beaulieu, Richard Thompson, Christopher T. Lee, Gary D. Lopaschuk, , Lakshmi Puttagunta, Sandra Bonnet, Gwyneth Harry, Kyoko Hashimoto, Christopher J. Porter, Miguel A. Andrade, Bernard Thebaud and Evangelos D. Michelakis: Cancer Cell, Volume 11, Issue 1, 37-51, 1 January 2007; http://www.cell.com/cancer-cell/retrieve/pii/S1535610806003722
