Red Blood Cells of Long-Haul Covid-19 Patients Are Smaller Than Normal; Explains Blood Clotting Risk

If the public is to believe all of the unusual and atypical symptoms caused by COVID-19, uncharacteristic of any of the other seven types of coronaviruses, one might conclude this isn’t a virus at all.  It must be something else.  In particular, modern medicine is perplexed over patients with long-term symptomology, what has now been called long-haul COVID-19.

Researchers at the Max Planck Institute For Physical Medicine in Germany find red blood cells from recovered long-haul COVID-19 patients to be enlarged which they say may explain the phenomenon of oxygen deprivation and other symptoms among these patients.

Writing in The Biophysical Journal, investigators assessed 4 million red blood cells from healthy, infected and recovering COVID-19 patients.  Actively-infected patients have larger red blood cells, and 7 months after hospitalization their red blood cells are smaller (see graphic).

Investigators say these deformed cells could explain the increased risk for blood clots or embolisms (blood clot released to another organ like the lungs or brain).

According to one report, Both COVID-19 infection and vaccination increase the risk for blood clots, though in hard numbers the risk is small, a few in a million.  Active infection increases the risk 8-10 times more than vaccination however.  Clots were 100 times more common among COVID-19 infected patients than healthy adults.  But long-term data isn’t available regarding the risk for blood clots upon reinfection with a coronavirus.

Researchers at the Michigan Medicine Frankel Cardiovascular Center believe this COVID-19 blood clotting problem emanates from antiphospholipid antibodies.  Surprisingly, half of hospitalized COVID-19 patients were positive for these auto-antibodies   and also had super-activated neutrophils, a type of white blood cell that can potentially be destructive if overactivated.  These investigators say there are clueless as to what is causing this.

Meanwhile, researchers reporting in the CRITICAL CARE Journal may have an answer to this perplexing problem.  They employed 200 milligrams of daily vitamin B1 (thiamine) intravenously and achieved a 75% reduction in absolute risk for mortality among hospitalized COVID-19 patients compared to non-B1-treated patient.  Additionally, B1 therapy reduced risk for thrombosis (blood clots) by 81%!  This vitamin is not known for having anti-blood clotting properties.  It does not make blood platelets less sticky and prone to clot.

The lack of thiamine may induce megaloblastic anemia where there are fewer red blood cells and remaining cells are larger than normal.

Women with COVID-19 report cases of abnormal menstrual bleeding.  So far, the reason for this is unknown.  But we do not that the provision of Thiamine B1 is reported to reduce abnormal menstrual bleeding.

In living tissues, the lack of oxygen (hypoxia) increases thiamine transporters by 31-fold and a 2-fold net increased delivery of oxygen to tissues.  The lack of thiamine impairs the production of nitric oxide, a transient intra-arterial gas that dilates (widens) arteries to facilitate delivery of oxygen-carrying red blood cells and regulate blood pressure.  A shortage of thiamin B1 promotes a protein called hypoxia inducing factor.

An underlying environmental factor may set up human populations for oxygen starvation by COVID-19 patients.  The herbicide Roundup/glyphosate (Monsanto) contains arsenic that can set the stage of oxygen starvation diseases.  Arsenic is a toxic mineral that is widely found in water and other environmental sources and may induce pseudo-hypoxia.

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