A brief paper appearing in The New England Journal of Medicine, shook the belief of a multitude of people who since time immemorial rested their hopes and looked towards anitioxidant supplements to curb the development of cancer.
Authors David Tuveson, MD, PhD, Cold Spring Harbor Laboratory Professor and Director of Research for the Lustgarten Foundation, and Navdeep S. Chandel, PhD, of the Feinberg School of Medicine at Northwestern University, suggest the reasons behind the failure of antioxidant supplements in reducing cancer development.They also attempted to explain why they can cause harm than good.
This paper was based on the developments made in the study of the system in our cells that naturally strike a balance between the oxidising and anti-oxidising compounds. Oxidants like hydrogen peroxide are crucial to the body in small quantities, and they are produced with the cell itself. A large amount can be toxic and dangerous, and for this reason, the cell itself manufactures anti-oxidants to fight and neutralise them. Antioxidant supplements, for this reason, are consumed in large quantities to destroy these oxidants, hydrogen peroxide and similar toxic "reactive oxygen species" or ROS that are generated excessively by cancer cells to boost and feed their growth.
Drawing on all of this, David and Chandel propose that the consumption of antioxidant rich food or supplements are not beneficial because they do not function in the regions where ROS is produced, which is the mitochondria. Instead they accumulate at scattered distant regions away from the ROS-producing areas, "leaving tumor-promoting ROS relatively unperturbed," the researchers say.
A higher level of anti-oxidants ironically increases the cancer cells production of oxidants and ROS to counter them, and there is a high probability of the growth to continue. Referring to the radiation therapy that increases the oxidant level in the body to kill these toxic oxidants and ROS, they state that an increase in the level of oxidants in the body will do the patients good.
The authors suggest "genetic or pharmacologic inhibition of antioxidant proteins." A tried and tested concept that was successful on rodent models with lung and pancreatic cancers, they state it may be a useful therapeutic approach in humans as well. According to them, the biggest challenge would be to identify antioxidant proteins and the pathways in the cells that are used only by cancer cells and not by healthy cells. Hampering the production of antioxidants in healthy cells will upset the delicate redox balance upon which normal cellular function depends.
The authors propose a new research on it.