Dichloroacetic acid (DCA), also referred to as bichloroacetic acid, has a molecular structure of CHCl2 (BCA). This compound is similar to acetic acid, but two of the hydrogens in the methyl group have been replaced by chlorine atoms. It has a variety of potential uses and its salts and esters are referred to as dichloroacetates. Furthermore, DCA salts have been investigated as possible medications since they have the ability to impede pyruvate dehydrogenase kinase.
Research into the effects of dichloroacetic acid (DCA) on animals and in laboratory testing has indicated that it may have the potential to slow the growth of certain types of cancer, however no definitive evidence has been found to support its use as a cancer treatment. This organic acid, which is a member of the family of chloroacetic acids, is highly potent when it is in its pure form, with a pKa of 1.35. Inhalation of this acid could cause considerable harm to the delicate mucous membranes and airways of the upper respiratory tract.
Investigations have revealed that Asparagopsis taxiformis seaweed contains traces of DCA. DCA is made when drinking water is chlorinated and is a byproduct of the metabolism of drugs and substances containing chlorine. DCA can be produced by reacting trichloroacetic acid with calcium carbonate, sodium cyanide, water, and hydrochloric acid, or alternatively by combining hypochlorous acid with acetylene. In the laboratory, DCA and TCA are used to solidify macromolecules such as proteins from a solution. The efficacy of this process is greatly enhanced by local chemical vaporization.
DCA and TCA can be employed for both eliminating genital warts via chemical means and for cosmetic purposes (e.g. chemical peels and tattoo removal). It can even be used to destroy healthy cells.
Acid buildup in the body resulting in lactic acidosis
Despite DCA being found to be tolerable in a randomized control trial, there was no improvement in clinical outcomes for newborns with congenital lactic acidosis. A second trial of DCA for MELAS showed that all 15 children that were tested suffered from significant nerve damage without any benefit from the drug, which caused the study to be terminated early. DCA was able to lower blood lactate levels in adults with lactic acidosis, however, it had no therapeutic effect and did not improve the patients’ hemodynamics or survival rate.
Despite DCA being found to be tolerable in a randomized control trial, there was no improvement in clinical outcomes for newborns with congenital lactic acidosis. A second trial of DCA for MELAS showed that all 15 children that were tested suffered from significant nerve damage without any benefit from the drug, which caused the study to be terminated early. DCA was able to lower blood lactate levels in adults with lactic acidosis, however, it had no therapeutic effect and did not improve the patients’ hemodynamics or survival rate.
In 2007, researchers at the University of Alberta, Evangelos Michelakis and his team, reported that sodium dichloroacetate (the sodium salt of dichloroacetic acid) had the ability to reduce tumors in rats and kill cancer cells in a laboratory. A story about this “cheap and straightforward therapy” in New Scientist sparked a lot of interest in the public and the accompanying editorial noted that the chemical could not be patented, meaning that no pharmaceutical company was willing to pursue it as a potential treatment for cancer. A subsequent study in the same journal highlighted the potential side effects, like nerve damage. It is now illegal in the US to market chemicals as cancer cures without FDA approval.
In 2012, when asked if dichloroacetate (DCA) should be used in cancer treatment, the American Cancer Society cautioned against it, as there was not enough evidence to support its use. Numerous medical experts have put forward the need to be vigilant before using DCA and have cautioned against using it outside of a controlled clinical trial. Obtaining the chemical could be a challenge, as demonstrated by a 33-month jail sentence given to a fraudster who sold cancer patients a white powder claiming it was DCA, when it was actually just starch.
Even so, the only trial involving humans who were administered DCA involved only five people with glioblastoma, and the intent of the experiment was not to see if the drug could work against the condition. The point of the research was to figure out if it was safe to give a certain dosage without causing any adverse effects (i.e. neuropathy). Additionally, the five participants were all undergoing other forms of treatment.
It looks like DCA has the potential to eliminate glioblastoma cancer cells by causing their irregular mitochondria to lose their electrical charge, which leads to the cells destroying themselves (programmed cell death). In vitro studies of neuroblastomas, which have unidentified mitochondrial abnormalities, have revealed that DCA is effective against cancerous, undifferentiated cells.
In a paper released in 2016, the use of DCA in treating cancer in the central nervous system was assessed. Two years later, research showed that DCA could cause tumor cells to move away from glycolysis and toward mitochondrial OXPHOS (the Warburg effect), and result in an increase of reactive oxygen stress. This outcome was not witnessed in healthy cells.
Several DCA trials were discontinued due to the development of neuropathy; however, a 2008 study published in the British Journal of Clinical Pharmacology found that this did not occur in other DCA trials. It is not yet understood how DCA causes this side effect. Studies conducted in vitro on neurons have suggested that DCA leads to the demyelination of neurons, which can be partially reversed after the removal of the drug. However, a review of the same data by researchers in 2008 concluded that the neurotoxicity matched the pattern of length-dependent axonal sensory polyneuropathy without demyelination. The study by Kaufman et al. from 2006 was referenced in this regard.
Investigations have been conducted to see if DCA might be useful in treating long-term heart failure due to ischemia. Additionally, DCA increases metabolism by stimulating NADH production, although an excess of oxygen can cause NADH to run out.
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