[ProtectOurFreedom]

Coronavirus Pandemic Update 61: Blood Clots & Strokes in COVID-19; ACE-2 Receptor; Oxidative Stress, April 27, 2020

Thrombosis (blood clots), strokes, and myocardial infarctions are mysterious complications for some patients with COVID-19. Dr. Seheult discusses a recent case study involving a 72-year-old with elevated d-dimer and plasma Von Willebrand factor, and goes on to illustrate a hypothesis for how downregulation of ACE-2 may result in oxidative stress. This process may put patients with underlying elevated levels of oxidative stress (cardiovascular diseases, diabetes, obesity, etc.) at the greatest risk for severe COVID-19 infection.

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Coronavirus Update 120: Anticoagulants (Blood Thinners) Improve Hospital Outcomes (Full Dose), January 24, 2021

Professor Roger Seheult, MD explains new data from large trials that demonstrate full dose anticoagulants may improve outcomes for patients hospitalized with COVID 19. This is important news because we've learned over the past year that thromboembolic (blood clot) complications from COVID-19 contribute significantly to morbidity (pulmonary embolism, stroke, myocardial infarction, etc.) and mortality

[ransomnote]

In the video, Dr. Hoffe explains that he performs the D-Dimer test on patients within 7 days of ‘vaccination’ so these aren’t people with Covid-19.

However, a whistleblower has said the ‘vaccine’ is a more concentrated version of Covid-19 hence they have similar side effects and symptoms.

[Ragnar54]

Not surprising, since people who get the Chinese Flu are generally low in vitamin D. From an article in 2019:

Emerging Role of Vitamin D and its Associated Molecules in Pathways Related to Pathogenesis of Thrombosis

“A recent study demonstrated the association of low vitamin D levels with the development of deep venous thromboembolic (DVT) events in patients with ischemic stroke [51]. Likewise, a case-control study observed that the concentration of 25(OH)D was significantly lower in 82 participants with idiopathic lower-extremity DVT as compared to 85 sex and age-matched healthy participants [50]. Further, Blondon et al. [56] found a protective effect of vitamin D supplementation on the risk of unprovoked venous thromboembolism (VTE) and women with low vitamin D concentrations. This finding suggests that vitamin D deficiency could be treated as an undiagnosed risk factor for unprovoked VTE that constitutes around 40% cases of all VTE [56].”

“Furthermore, VDR has recently been found in human platelets and a megakaryocyte lineage [63]. Platelets are critically important mediators of the coagulation pathway, activating the TF-mediated processes and contact-arms of the coagulation cascade [64,65]. Larger platelets are shown to be more reactive and have greater pro-thrombotic potential. The elevated mean platelet volume (MPV) is associated with increased risk for DVT and MI in a large sample size study, supporting the concept that platelet reactivity is indispensable in the pathogenesis of venous thromboembolism [66]. Furthermore, a recent study has associated the increase in MPV with a decrease in serum 25(OH)D concentrations in patients with stable coronary artery disease, suggesting further linkage of vitamin D to thrombosis and hemostasis [55]. They concluded that there exists a negative correlation between MPV and serum 25(OH)D concentration, with MPV highest in group of patients with 25(OH)D concentration <10 ng/mL, moderate in group with the concentration of 10–20 ng/mL, and lowest in group with the concentration >20 ng/mL.”