In July, the Summit Supercomputer at Oak Ridge National Laboratory in Tennessee crunched data on forty-thousand-plus genes associated with nearly twenty-thousand genetic samples of COVID-19. The results were more than interesting.
Scientists have known for a few months that the SARS-CoV-2 virus attacks the ACE2 (Angiotensin-Converting Enzyme 2) receptors in the human body (nose, intestines, kidneys, lungs, and heart). After attaching to the ACE2 receptors, the virus controls the immune system causing it to upregulate the ACE2 receptors which allow more virus molecules to enter the body.
Our blood pressure and fluid balance are controlled by the Renin-Angiotensin-Aldosterone System (RAAS or sometimes RAS). It is made up of three hormones. Within the control of the RAS is a chemical called bradykinin.
Last week, The Scientist (https://bit.ly/2QY3tQB) published an article predicting a COVID-19 bradykinin-storm like the COVID-19 cytokine storm we have heard about since early summer – or was it misdiagnosed?
Bradykinin is a vasodilator which can lower blood pressure. The SARS-CoV-2 virus causes bradykinin to be created in such great levels so that the body cannot control its production. It becomes a bradykinin storm which is theorized as the genesis of the deadly effects of COVID-19.
The current theory is that both the bradykinin and cytokine storms act in concert to create havoc within our bodies. Some studies suggest that the cytokine storm is the primary cause of COVID-19 pathologies and other stories point to the bradykinin storm. Could all the studies be correct?
Vascular permeability (or leaking) occurs as bradykinin levels rise in the body. Studies identifying COVID-19 as a vascular disease point to the rise in bradykinin levels. It is hard to fully understand the true pathology since the rise in vascular permeability caused increased leaking of the blood vessels in the lungs resulting in a build-up of fluid.
Complications now arise as the SARS-CoV-2 virus causes an increase in hyaluronic acid in the lungs. Hyaluronic acid absorbs more than one thousand times its weight in fluid. Inside the lungs, a hydrogel is formed by the combination of hyaluronic acid with the excessive leakage of the lung’s blood vessels.
Breathing through this gel-like substance is nearly impossible, even on a ventilator. Patients can suffocate when air is force-fed into the lungs because the alveoli are contaminated with the hydrogel substance.
Many healthy people after being treated for COVID-19 exhibit heart problems that they did not have previously. It is summarized in this study that the heart damage is due to the RAS destabilization of cardiac contractions and blood pressure. The bradykinin storm manifests a low blood pressure condition that creates arrhythmias.
Other COVID-19 symptoms that a bradykinin storm can create are dizziness, seizures, delirium, and stroke. There is a French study that shows blood vessel leakage in the brain of COVID-19 patients. The suspect for this condition is extremely high levels of bradykinin which pass through the blood-brain-barrier. WebMD posted an article a couple of months back identifying neurological symptoms as a prelude to COVID-19 (https://wb.md/3bww219).
What options are available now that more information is known about the pathological pathways the virus disrupts the body? Increased bradykinin levels act as if they were an ACE inhibitor – a drug used to lower high blood pressure.
Side effects of an ACE inhibitor are a dry cough, fatigue, increased blood potassium levels, and more – symptoms commonly found in COVID-19 patients. Additionally, some ACE inhibitors cause the loss of both smell and taste! Some scientists are convinced that COVID-19 toes are a direct result of increased levels of bradykinin.
Drugs Already Approved That Might Help
Several of the pathologies defined can be addressed by drugs already present and approved by the FDA in the marketplace. Danazol, stanozolol, ecallantide, and icatibant reduce the production of and signaling processes of bradykinin.
Several studies have suggested that vitamin D can be effective in treating COVID-19 development (https://bit.ly/3lS06c9). Vitamin D downregulates the levels of renin which inhibits bradykinin production. It is speculated by medical professionals familiar with COVID-19 that deficiency of vitamin D exacerbates the severity of COVID-19 symptoms.
Hymecromone reduces hyaluronic acid levels that could reduce or stop the hydrogel formation in the lungs. Timbetasin is another drug that has great potential to combat the effects of increased levels of bradykinin.
None of these drugs mentioned can be applied willy-nilly to COVID-19 patients. There are protocols that must be used to introduce ‘off-label’ approval of existing drugs to treat new diseases.
More is known about the pathways that the SARS-CoV-2 virus enters the body and disrupts the normal operation of our internal organs. There are good hypotheses that can now be tested in clinical trials to verify the efficacy of the intended results.
Scientists are learning about how COVID-19 infects and disrupts the body and how to combat it.
Live Longer & Enjoy Life! – Red O’Laughlin – RedOLaughlin.com