The underlying mechanism of a promising study into cancer treatment was dissected in a scientific paper by Tico biomedical researchers years before it made headlines.

Ever since Canadian researchers at the University of Alberta announced their progress on the effects of dichloroacetate on human cells in 2007, there has been quite a bit of scientific controversy over the future of cancer research. The published results of the clinical trials in 2010 were certainly promising: dichloroacetate (DCA) alters the metabolism of cancer cells by cutting off their nutrition and weakening their stubborn resistance to existing pharmacokinetic therapies. The fact that DCA was discovered a very long time ago, and thus cannot be exclusively patented by the pharmaceutical industry, has lead to speculation about whether a cure for cancer is being snubbed by Big Pharma.

The financial support that has been given to the Canadian DCA research team has been paltry in comparison to the colossal budgets set aside by the major pharmaceuticals for research and development. One of the lead researchers, Evangelos Michelakis, went the crowdfunding route by asking for online contributions, an unceremonious and unusual step in biomedical cancer research.

One of the focus areas of the DCA research study is the mitochondria, microscopic organs in the human cells that act as cancer fighters. An anatomical mitochondrion model is pictured above. Mitochondria need to be triggered in order to perform their cancer-fighting duties, something that DCA accomplishes effectively. In cancerous cells, mitochondria should also be eliminated in order to prevent a metabolic process that would further nourish cancer cells, one of the reasons behind tumor growth. DCA also destroys mitochondria to prevent cancer from spreading.

Lack of funding may not be the only obstacle faced by DCA research. There’s also the issue of being overly optimistic of medical studies in progress. Mitochondria are subject to what Enrique Freer from the Electron Microscopy Unit and Rocío Castro Arce from the Physiology Department at UCR discussed on their December 2000 paper “El oxígeno: molécula esencial y causa de envejecimiento” (Oxygen as an Essential Molecule and Cause of Aging).

Freer and Castro Arce wrote about the Oxygen Paradox; a concept whereby mitochondria depend on oxygen to turn glucose (sugar) into energy, but which at the same time promotes the aging process. The two Tico researchers then posited that by understanding the Oxygen Paradox and manipulating our dietary and pharmacological intake, we can actually cheat the aging process, but at what cost? The paper concludes with another paradox: “To achieve longevity, should we be super-skinny, undernourished, prone to hypothermia, and obligated to ingest copious amounts of vitamins and antioxidants; or should we just eat well and live happily for about 85 years?”

The Oxygen Paradox is at the heart of DCA research. Changing cell oxidation so that it benefits mitochondria promotes the self-destruction of cancer cells, while at the same time accelerating the aging process. Getting older prematurely is certainly a small price to pay when facing the evils of cancer. Since longevity and delaying the aging process are currently areas of deep interest for Big Pharma, it’s no surprise that DCA research is not enjoying the funding it deserves.