I believe this moment in history marks the beginning of a new era in our understanding of human metabolism and human physiology. COVID-19 is a fascinating and complex disease, but there is an army of researchers intent on figuring out what is happening in severe cases, and collectively they are making important discoveries. Here, I will develop the argument that deuterium is central to the disease process.
As you will see, I believe that proper deuterium fractionation is crucial for metabolism to work properly in the mitochondria. I am coming to the realization that the water accumulating in the lungs - a common feature of COVID-19 – is actively participating in a plan to restore mitochondrial health to the immune cells and beyond. This may even be a general feature of edema anywhere in the body.
This article will take you through a whirlwind tour of several factors in health and disease, and space does not permit more than a brief introduction to each of them. If you want to explore deeper, a good place to start is to look up any of the papers referenced at the end.
1 Deuterium
I first became aware of the role deuterium plays in health in December 2019, when Prof. László Boros reached out to me and explained the remarkably damaging effects that deuterium has on mitochondria [5]. Deuterium is the heavy isotope of hydrogen. Hydrogen is the smallest atom, with just one proton and one electron. Deuterium is the same, except that it also has an extra neutron. This makes it about twice as heavy as hydrogen, which gives it distinct physical and chemical properties. Deuterium is pervasive in nature - it is present in 155 parts per million in seawater. Mitochondria are small organelles contained in large numbers in most eukaryotic cells, and they are responsible for producing ATP (adenosine triphosphate), the energy currency of the cells. When they make ATP, they also combine protons with oxygen to make water, in the famous oxidative phosphorylation reaction that takes place across a mitochondrial membrane.
Systemic mitochondrial deterioration is a primary marker of the aging process [6]. Mitochondrial dysfunction has been linked to many neurological, metabolic, and oncological diseases, as aged mitochondria spew out more tissue-damaging reactive oxygen species (ROS) and produce ATP less efficiently. Mitochondria depend upon a “proton motive force” to produce ATP, which involves pumping huge numbers of protons across a membrane through the ATPase pump. Deuterons, being larger and heavier, disrupt the smooth flow and decrease the efficiency of the pump, much like putting sugar in the gas tank.
Biological organisms have developed a remarkable and sophisticated system for making sure that the protons in the mitochondria are not deuterons. There are two main parts to their strategy - trapping deuterium in gelled water and selecting for hydrogen over deuterium in catalytic reactions involved in supplying protons to the pump.
Most of the water in the body is trapped in a gel that is maintained by a “glycocalyx,” through the synthesis of large complex amino-sugar chains called glycosaminoglycans (GAGs). Crucial to maintenance of the gel are sulfate anions that are attached to these GAGs. The glycocalyx lines all the blood vessels of the body, and as described eloquently by Gerry Pollack in his book, “Cells, Gels and the Engines of Life,” the gel pushes protons out and maintains a negative charge within its interior, essentially creating a battery that can be used as an energy source. Because deuterons are heavier and they form stronger covalent bonds, they tend to be left behind in the gel [7]. I proposed in a TEDx Talk that these protons are ushered into the cell along cytoskeletal channels and delivered to the mitochondrial intermembrane space to be used in ATP synthesis [8].