Dichloroacetic acid, sometimes known as bichloroacetic acid, is a unique concoction of elements fashioned into CHCl2 (BCA). It’s a bit like a cousin to acetic acid, sharing a similar chemical profile, but it dances to its own tune with two of its methyl group hydrogen atoms replaced by chlorine atoms. This chemical twist gives birth to a family of dichloroacetates, their salts, and esters, opening up a universe of potential uses. Recently, scientists have turned their gaze towards dichloroacetates, intrigued by their possible role as a future medicine due to their knack for putting a brake on pyruvate dehydrogenase kinase.
As scientists delve into the labyrinth of research, experiments with creatures and lab samples suggest that DCA, our dichloroacetic acid, might slow down the march of certain cancers. Yet, it’s like exploring an enigmatic novel where the end is not yet written. We don’t have enough evidence right now to advocate using it as a cancer treatment.
Dichloroacetic acid tells a tale that spans the northern and southern hemispheres, its narrative imbued with a dash of unpredictability that keeps us on our toes.
When dichloroacetic acid joins the halogenated organic acids club, it undergoes a transformation upon meeting water, giving birth to the dichloroacetate ion. With a remarkably robust pKa of 1.35, it unfortunately has a darker side. If breathed in, it can wage a war on the respiratory tract, assaulting the delicate mucous membranes and airway passages.
Scientists have discovered that the seaweed known as Asparagopsis taxiformis harbors tiny amounts of dichloroacetic acid (DCA). This compound can be produced during the process of making our drinking water safe, or as a side-effect when our bodies break down certain chlorine-based drugs. Typically, DCA is made by taming trichloroacetic acid. Another recipe involves mixing chloral hydrate with calcium carbonate and sodium cyanide in water, and then inviting hydrochloric acid to the party. If you’re feeling adventurous, you could also combine hypochlorous acid with acetylene to create DCA.
In the hushed environment of a lab, scientists often rely on DCA and TCA to perform a bit of molecular magic: transforming large molecules like proteins from a liquid to a solid state.
DCA and TCA have proved their worth in delivering therapy through the misty avenue of local vaporization. They’ve been the unsung heroes in medical procedures like chemoablation of genital warts, as well as in beauty rituals like chemical peels and tattoo removal. However, these chemicals can also play a darker role, attacking and destroying healthy cells.
Despite passing the safety test in a randomized study, DCA proved to be a disappointment when it came to helping newborns with a condition called congenital lactic acidosis. In another test, 15 children with MELAS (a disorder marked by reduced mitochondrial activity and lactic acidosis) were given DCA. But instead of benefits, it resulted in serious neurological harm, forcing an early end to the trial. Even in cancer treatment, DCA only managed to lower blood lactic acid levels in adults, failing to improve overall wellness or extend survival.
Despite the early promise that shone in lab experiments, suggesting that DCA could be a boon for lactic acidosis, follow-up tests painted a different picture. Time and again, DCA failed to show any real benefits in this specific circumstance. Additionally, the toxic levels of the drug escalated to a point that made it unsafe for patients to continue using it for experimental purposes.
In a tale from 2007, researchers from the University of Alberta, led by Evangelos Michelakis, shared a discovery that stirred hope. They revealed that sodium dichloroacetate for cancer, a sodium-touched version of dichloroacetic acid, had shrunk tumors in rats and erased cancer cells in lab tests. This tale echoed in a recent New Scientist article, causing a wave of excitement among its readers. The article presented an appealingly simple treatment approach that seemed to be fairly safe and might cure a variety of cancers.
However, the accompanying commentary in the study highlighted a roadblock. Without the ability to legally shield it via patenting, pharmaceutical companies lack the motivation to champion its approval as a cancer treatment. A subsequent edition of the same journal explored potential side-effects like nerve damage. As it stands now, in the US, it’s against the law to sell substances touted as cancer cures without first obtaining a green light from the Federal Drug Administration.
In 2012, the American Cancer Society voiced a note of caution, stating that there wasn’t enough proof to back the use of DCA in cancer treatment. Medical experts stress the importance of prudence when it comes to DCA, insisting that it should only be used within the safe boundaries of a controlled clinical trial.
Obtaining this chemical can be a tricky business, as illustrated by a tale of a fraudster sentenced to 33 months in prison. His crime? Duping cancer patients into believing the ordinary white powder he sold was DCA, when in fact it was just plain starch.
Nonetheless, a study involving DCA did take place with a small group of people affected by glioblastoma. However, it wasn’t designed to measure how effective DCA could be against this disease. Rather, the aim was to find out if a certain dose could be administered without causing undesirable side-effects, like nerve damage.
The five participants of this study were all receiving other treatments alongside. Lab experiments and animal studies hint that DCA might have the power to purge the body of glioblastoma by causing their rogue mitochondria to destabilize, triggering the self-destruction of these malignant cells. Lab tests with neuroblastomas, characterized by faulty mitochondrial structures, revealed that DCA could effectively combat these eternally youthful, malignant cells.
Fast forward to 2016, a case study investigated the potential of DCA as a strategy for managing cancers that target the central nervous system. Two years later, a study showed that DCA could prompt tumor cells to switch their metabolism from glycolysis to mitochondrial OXPHOS (the Warburg effect) and ramp up the levels of oxidative stress. Interestingly, this heightened reaction was not observed in normal cells.
Neuropathy, or nerve damage, was the stumbling block that led to the premature closure of some DCA clinical trials. However, a 2008 report in the British Journal of Clinical Pharmacology presented a contrasting picture, revealing no signs of neuropathy in other DCA trials. The mystery of how DCA triggers neuropathy remains unsolved.
Lab-grown neurons have provided a window into DCA’s potential to cause neuropathic side-effects. Experiments have shown that DCA can strip neurons of their protective layer in a way that’s linked to both the dosage and the duration of treatment. Interestingly, this damage appears to be somewhat reversible once the medication is stopped. But a 2008 review of the same data suggested that the nerve damage was more akin to a length-dependent nerve disorder that affected sensory neuron axons, without any loss of the protective layer. A 2006 study by Kaufman et al. was cited in support of this viewpoint.
Research efforts have been made to explore whether DCA could be a lifeline for individuals suffering from chronic heart failure caused by blockages in their blood vessels. Another feather in DCA’s cap is its ability to speed up metabolism by boosting NADH levels, although it’s worth noting that in the presence of adequate oxygen, NADH could be used up. For more information, visit https://www.dcaguide.org/.
