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1) RETWEET!!!!!! THE SPIKE PROTEIN OF SARS-CoV-2 IS A "SUPERALLERGEN"!!!!!!! WE ARE "ALLERGIC" TO IT!!!
The curious case of MIS-C brings an important concept to mind. Children that present with MIS-C, they have mild/asymp COVID before developing the condition weeks later, most
The curious case of MIS-C brings an important concept to mind. Children that present with MIS-C, they have mild/asymp COVID before developing the condition weeks later, most
2) likely when neutralizing antibodies wear off. Is the first exposure to the spike protein for most sensitization? Note that what works against severe allergic reactions, works against severe COVID! Long COVID is the persistence of the Spike Protein. The body is creating
3) constant antihistamines. Side effects of antihistamines include anticholinergic effects, such as drowsiness, dry mouth, blurred vision, constipation, difficulty with urination, confusion, and light-headedness (particularly after a person stands up), as well as drowsiness.
4) The spike protein vaccines MUST be stopped instantly, as we are sensitizing ourselves to the Spike Protein. The reaction is similar to INSECT VENOM! NOTE THE TREATMENTS THAT WORK AGAINST SEVERE ALLERGIC RESPONSES:
Mast cell stabilizers
Corticosteroids
Leukotriene modifiers
Mast cell stabilizers
Corticosteroids
Leukotriene modifiers
5) Omalizumab
THE SPIKE PROTEIN IS AN ENGINEERED SUPERALLERGEN.
THE SPIKE PROTEIN IS AN ENGINEERED SUPERALLERGEN.
It explains sudden cardiac deaths/collapses by athletes, etc:
Cardiovascular symptoms can be the sole manifestation of exercise-induced food allergies, in which case death may mimic sudden cardiac death during exertion due to other pathologic causes. https://pubmed.ncbi.nlm.nih.gov/15171174/
Cardiovascular symptoms can be the sole manifestation of exercise-induced food allergies, in which case death may mimic sudden cardiac death during exertion due to other pathologic causes. https://pubmed.ncbi.nlm.nih.gov/15171174/
The doctor in Florida's death was indeed an allergic reaction to the vaccine:
https://rarediseases.org/rare-diseases/immune-thrombocytopenia/
The exact cause of Schonlein-Henoch purpura is not fully understood, although research suggests that it may be an autoimmune disease, e.g. a severe allergic reaction...
https://rarediseases.org/rare-diseases/immune-thrombocytopenia/
The exact cause of Schonlein-Henoch purpura is not fully understood, although research suggests that it may be an autoimmune disease, e.g. a severe allergic reaction...
I am certainly correct. Allergens work via IgE cross linking and mast cell activation, although it is possible to activate mast cells directly in other ways and this is what happens with Pfizer vaccine. Some extracts:
Much of Covid-19 hyperinflammation is consistent with
Much of Covid-19 hyperinflammation is consistent with
mast-cell-driven inflammation. Prevalence of severe Covid-19 is similar to that of mast cell activation syndrome (MCAS). Drugs inhibiting mast cells (MCs) and their mediators show promise in Covid-19. The pulmonary pathological findings associated with COVID-19 seems to result
from the release of multiple proinflammatory cytokines, especially interleukin (IL)-6, that can damage the lungs. A key source of such cytokines and chemokines is the mast cells, which are ubiquitous in the body, especially the lungs, and are critical for allergic and pulmonary
diseases. In fact, activated mast cells were recently detected in the lungs of deceased patients with COVID-19 and were linked to pulmonary edema, inflammation, and thromboses.
Mast cells are typically activated by allergic triggers, but they can also be triggered by
Mast cells are typically activated by allergic triggers, but they can also be triggered by
pathogen-associated molecular patterns via activation of Toll-like receptors. In addition, mast cells express the renin-angiotensin system, the ectoprotease angiotensin-converting enzyme 2 required for SARS-CoV-2 binding, and serine proteases, including TMPRSS2, required for
priming of the corona spike protein.3 Such triggers could lead to secretion of multiple proinflammatory mediators selectively, without release of histamine or tryptase, as we had previously reported in the Journal of Immunology for release of IL-6 in response to IL-1β from
cultured human mast cells. Moreover, we recently reported in the Proceedings of the National Academy of Sciences of the United States of America that human mast cells can be synergistically stimulated by the peptide substance P and IL-33 to release impressive amounts of
vascular endothelial growth factor, IL-1β or tumor necrosis factor again without secretion of histamine or tryptase.
