Dichloroacetic acid, which is occasionally referred to as bichloroacetic acid, is composed of the elements CHCl2 (BCA).
Two chloroacetic acid, denoted as 2COOH, has a chemical makeup similar to acetic acid but with two of its methyl group hydrogens substituted by chlorine atoms. Various types of dichloroacetates, its salts and esters, possess numerous potential applications. In addition, research has recently been conducted to explore the potential of dichloroacetates as a prospective medicine due to their ability of inhibiting pyruvate dehydrogenase kinase.
Research on creatures and in lab samples imply that DCA could delay the advancement of certain cancers, yet there isn’t sufficient proof right now to suggest utilizing it to treat cancer.
A language built on the divisions of the northern and southern hemispheres and characterized by an element of unpredictability.
Dichloroacetic acid belongs to the group of halogenated organic acids and produces the dichloroacetate ion when diluted with water. It has a pretty strong pKa of 1.35 and unfortunately, can inflict serious injuries if inhaled, like affecting the respiratory tract’s mucous membranes and airway passageways.
It has been found that Asparagopsis taxiformis seaweed contains a trace amount of dichloroacetic acid (DCA). This material is created through the process of chlorinating drinking water, and is also a by-product of the metabolism of chlorine-based drugs and substances. DCA is generally created by reducing trichloroacetic acid. Another way to form the material is to mix chloral hydrate with calcium carbonate, sodium cyanide, water, and then add hydrochloric acid. Alternatively, hypochlorous acid can be used in combination with acetylene to make DCA.
In a lab setting, DCA and TCA are usually used as agents to move macromolecules such as proteins from a fluid to a solid state.
The effectiveness of therapy delivered through local vaporization of chemicals is demonstrated by the use of DCA and TCA for both medical treatments like genital wart chemoablation and aesthetic purposes such as chemical peels and tattoo removal. Additionally, these chemicals can be used to target and destroy healthy cells.
Although DCA was found to be safe in a randomized study, it failed to have a positive effect on newborns with congenital lactic acidosis. When tested on 15 children who had MELAS (a disorder of decreased mitochondrial activity that causes lactic acidosis), the drug caused significant neurological damage without any notable benefit, forcing the trial to be ended early. DCA for cancer was seen to lower blood lactic acid levels in adult patients, but it had no real advantages for patient well-being and did not lengthen survival.
Consequently, multiple tests with direct comparison have demonstrated that DCA has no documented positive effect with regard to this particular situation, despite some initial reports and lab experiments that suggested it might be of benefit with regards to lactic acidosis. Moreover, drug toxicity levels increased to the point where patients could no longer safely continue using it for trial purposes.
In 2007, researchers from the University of Alberta, Evangelos Michelakis and his team, disclosed that taking sodium dichloroacetate (which is the sodium version of dichloroacetic acid) had decreased tumours in rats and did away with cancerous cells in laboratory testing. Consequently, a recent article in New Scientist sparked unprecedented attraction among readers by introducing a valued and straightforward therapeutic approach which is also recognized to be reasonably risk-free and has the capability to remedy many different malignancies.
In the accompanying editorial of the study, it was stated that without the power to legally protect it through patenting, pharmaceutical companies have no incentive to pursue its approval as a cancer remedy. In a later instalment in the same journal, possible adverse reactions like nerve destruction were explored. It is currently prohibited in the US to offer chemicals that are presented as cancer cures without receiving prior authorization from the Federal Drug Administration.
In 2012, the American Cancer Society mentioned that there wasn’t enough evidence to suggest that DCA ought to be utilized in cancer treatment. According to medical specialists, taking measures of caution prior to utilizing DCA is a must and it should not be used outside of a managed clinical trial.
If you are interested in obtaining the chemical, you may face difficulties. A scam artist was convicted to spending 33 months in jail due to the fact that he deceived cancer patients by claiming the white powder he sold contained the drug DCA, however, it was just basic starch.
Despite this, only a handful of people with glioblastoma were part of the single study using DCA with live participants; it was not designed to measure its effectiveness against this illness. The goal was to decide if a particular dose could be given with no adverse effects, such as neuropathy.
The five individuals who participated in the research were all receiving other treatments. The results from experiments in a lab setting and with animals suggest that DCA may be able to rid the body of glioblastoma by forcing their altered mitochondria to become depolarized, resulting in the malignant cells’ self-destruction. Tests conducted in laboratory settings with neuroblastomas, which are deficient in their mitochondrial structure, showed that DCA was effective against malignant, ageless cells.
In 2016, a case report looked into the possibility of using DCA as a way of managing cancers that affect the central nervous system. Two years later, a study was conducted that demonstrated that DCA was capable of making tumor cells shift their metabolism from glycolysis to mitochondrial OXPHOS (the Warburg effect) and heightening the levels of oxidative stress. This augmented reaction wasn’t seen in regular cells.
Neuropathy was the reason why certain DCA clinical studies were terminated, but in 2008 an article in the British Journal of Clinical Pharmacology discovered that no such issue appeared in other DCA trials. The mechanism by which DCA causes neuropathy is still not known.
Studies conducted on neurons cultured in a laboratory setting have shed light on how DCA can cause neuropathic side effects. These studies have established that DCA can cause a dose- and time-dependent demyelination of neurons (taking off the layer around the nerve cells) that is somewhat reversible after the medication is no longer taken. However, a 2008 analysis of the same data indicated that the nerve damage resembled a length-dependent nerve condition that affected the axons of sensory neurons and had no demyelination. A 2006 research effort by Kaufman et al. is cited in support.
Investigations have been performed to discover if DCA could be an advantageous treatment for people with long-term cardiac failure due to blockage of the blood vessels. Another benefit of using DCA is that it accelerates metabolism by raising NADH levels, although when there is enough oxygen present, NADH could be depleted. https://www.dcaguide.org/
