New information has emerged that “COVID-19 causes prolonged and progressive hypoxia (starving your body of oxygen) by binding to the heme groups in hemoglobin in your red blood cells. People are simply desaturating (losing O2 in their blood), and that’s what eventually leads to organ failures that kill them, not any form of Acute Respiratory Distress Syndrome (ARDS) or pneumonia. All the damage to the lungs you see in CT scans is from the release of oxidative iron from the hemes, this overwhelms the natural defenses against pulmonary oxidative stress and causes that nice, always-bilateral ground glass opacity in the lungs. Patients returning for re-hospitalization days or weeks after recovery suffering from apparent delayed post-hypoxic leukoencephalopathy strengthen the notion COVID-19 patients are suffering from hypoxia despite no signs of respiratory “tire out” or fatigue.” Is this true and a major factor in the morbidity and mortality?

This is insightful science being applied here and will prove to be a major factor in understanding what COVID-19 does to cause respiratory distress and fatality. It is not the whole story with regard to fatal outcomes as there are multiorgan involvements and this will also hit people in their weakest link, so to speak, but the idea this is a typical pneumonia is in fact incorrect. This is a different kind of etiology because the point of attack is not on the linings of the alveoli through an inflammatory response to viral release by infected cells alone, although that is happening as well. A major factor here is the direct interaction of the virus with the hemoglobin molecule to make it inefficient in carrying oxygen to the tissues. That competition is in some cases deadly and is reflected in the mortality statistics as a major causal sequence of events.