“By Spring 2021 reports began to trickle in describing a rash of clotting disorders, both arterial and venous, occurring days to weeks following vaccination. Such events also occur in COVID-19 infections. Arterial thromboses present as heart attack or stroke. In addition to the more common venous thromboses in the lower extremities, vaccine-related clotting occurs in atypical locations like cerebral sinuses and intestinal veins. (Figure 1) Venous thrombosis, in turn, leads to a higher incidence of pulmonary embolism. (Figure 2) Such events prompted the temporary withdrawal of the J & J vaccine in Europe and the US.
Laboratory data pointed toward an immune-mediated process. Thrombosis is associated with low blood platelet levels suggesting a consumptive process. Vaccine-induced thrombosis and thrombocytopenia (VITT) is strikingly similar to heparin-induced thrombocytopenia (HIT) in which administered heparin induces autoantibody formation against platelet factor-4 (PF4). The heparin-PF4-immune complex triggers release of pro-thrombotic substances by platelets that induce clot formation throughout the vascular tree. In the process platelets are consumed which, subsequently, increases the risk for bleeding.
Platelet-activating antibodies against PF4 are present in VITT. The same hypercoagulable conditions, with or without PF4 autoantibodies, are present in COVID-19 infections. Besides triggering platelets to release pro-clotting factors, anti-PF4 antibodies induce neutrophils to release NETs which promote inflammation, immune-mediated thrombosis, and end-organ damage associated with both COVID-19 infection and HIT. And, not surprisingly, NET formation also occurs in VITT. The common thread that ties VITT and COVID-19-related thrombosis together is endothelial inflammation, diastolic dysfunction and impaired energy generation.
Given such evidence, we are again led to question the logic behind mRNA vaccines. Why would scientists continue to employ an agent that induces inflammation, immune dysfunction, and vascular thrombosis, the same pathophysiological effects as viral infection, while at the same time conferring only temporary protection that is qualitatively inferior to natural infection? One can only wonder.”
© 2022 K. E. Thorp, James A. Thorp, Elise M. Thorp. This is an Open Access article distributed under the Creative Commons Attribution License, which permitsunrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. use, distribution, and reproduction in any medium, provided theoriginal work is properly cited.