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Rubbery Blood Clots
Another form of Spike Protein Disease
We have seen pictures of blood clots that have been pulled from the veins of cadavers. Mike Adams produced one of the largest collections of these rubbery strings. He wrote this on NaturalNews.com:
“We don’t yet know what all these structures are. We know what they are not, however: They are not simply clotted blood cells. If they were, then at the 1500x magnification shown in the last photo, above, we would be able to see individual blood cells. These are not blood cells, they are protein structures.”
Here is an interview with Richard Hirschman, if you’d like to hear what he has to say.
What is causing this? Like the other 20+ Mechanisms of Injury (MOI) that I identified and published in May/July 2021, are these rubber-like clots something that can be directly attributed to the COVID-19 injections?
A very recent study (published May 2022) may shed some light and give an explanation for these unusual and horrific clots.
SARS-CoV-2 infection is associated with a surprising number of morbidities. Uncanny similarities with amyloid-disease associated blood coagulation and fibrinolytic disturbances together with neurologic and cardiac problems led us to investigate the amyloidogenicity of the SARS-CoV-2 spike protein (S-protein).... Our data propose a molecular mechanism for potential amyloidogenesis of SARS-CoV-2 S-protein in humans...
REF: Sofie Nyström and Per Hammarström. “Amyloidogenesis of SARS-CoV-2 Spike Protein.” J. Am. Chem. Soc. 2022, 144, 20, 8945–8950. May 17, 2022 - LINK
As you can see from the REF (reference) the title of this article is “Amyloidogenesis of SARS-CoV-2 Spike Protein.”
What the heck is amyloidogenesis? (pronounced am-uh-loi-doe-genesis)
What does this have to do with rubbery blood clots found by Richard Hirschman, a mortician who found a large number of strange blood and tissue clots in cadavers after the COVID shots?
Let’s take a step back and explain a few terms.
What is amyloid and what is amyloidosis?
Amyloid is an abnormal protein; it is not found in the body under healthy conditions. It occurs when a protein is damaged and begins to fold abnormally on itself. Amyloidosis (am-uh-loi-DOE-sis) is the term given when the abnormal amyloid proteins accumulate in organs and throughout the body, interfering with normal function.
Amyloids are thread-like, fibrous strands that look like strings. These tiny structures are typically 7–13 nanometers in diameter and can be many microns in length. To understand how microscopically small that is, one inch is 25,400,000 nanometers.
When thousands of amyloids aggregate together, they twist into fibrils with a sheet-like appearance. This is called a β-sheet. Amyloid fibrils can also be bound tightly together by horizontal fibers known as cross-β strands. These abnormal proteins can fold, unfold and refold into different configurations, each time increasing their stability and tinsel strength. The fibrils are usually highly organized, with consistent lengths and a tensile strength that approaches that of steel (Fabrizio, pg13)
As of 2017, at least 25 amyloid proteins have been associated with human diseases: Seven are associated with neurodegenerative conditions, such as Alzheimer and Parkinson diseases and 15 have been found to aggregate the heart, spleen, liver, pancreas and kidney. The remaining are miscellaneous findings, often associated with rare genetic diseases. When organs are filled with amyloid proteins, this condition is called systemic amyloidosis. The severity of systemic amyloidosis can range from non-symptomatic deposition to localized cell death to complete impairment of specific organs.
REF: Fabrizio Chiti and Christopher M. Dobson. “Protein Misfolding, Amyloid Formation, and Human Disease.” Annual Review of Biochemistry Vol. 86:27-68 (May 12, 2017) LINK
Researchers asked the question: Does the spike protein induce the formation of amyloid, leading to blood clots?
To study this premise, researchers took a selection of spike protein sequences and in vitro, added substances known to induce amyloid fibrils. Almost all of the spike proteins formed amyloid fibrils within a few hours after they combined the spike proteins with neutrophil elastase, an enzyme released during an infection.
REF: Sofie Nyström and Per Hammarström. “Amyloidogenesis of SARS-CoV-2 Spike Protein.: J. Am. Chem. Soc. 2022, 144, 20, 8945–8950. May 17, 2022. LINK
So, yes, the spike protein can lead to the formation of amyloid in serum. If you want to see a few pictures of what this looks like under the microscope and in the blood, go here.
The problem is, plasmin, which usually regulates clot formation to prevent “over-clotting” is not capable of breaking down and removing these spike-amyloid clots.
Spikes and Clots
Researchers demonstrated this phenomenon a second way. Plasma was taken from healthy, unvaccinated donors. When the spike protein was added to their blood, extensive microclots formed leading to hypercoagulation.
The spike protein also interacts with platelets and fibrinogen, interfering with blood flow, also leading directly to hypercoagulation. When the spike protein was mixed with other blood proteins, the combined amyloid-like structure was resistant to the enzymes that would normally break down the clot (called impaired fibrinolysis). This leads to the persistence of a voluminous number of microclots in small blood vessels throughout the body called capillaries. Millions of these tiny clots effectively block the passage of red blood cells into tissues, decreasing oxygen exchange and leading to multiorgan system failure.
spike proteins + fibrin -> amyloid proteins -> large, rubbery clots -> death
While the recent findings in the blood may seem bizarre, even other worldly, it appears the answer is coming directly through that needle. Spike protein disease, leading to the deposition of amyloid in organs and filling up arteries and veins is certainly one more MOI for the books.
Articles/References (no particular order)
SARS-CoV-2 spike protein S1 induces fibrin(ogen) resistant to fibrinolysis: implications for micro clot formation in COVID-19: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8380922/
A central role for amyloid fibrin microclots in long COVID/PASC: origins and therapeutic implications https://pubmed.ncbi.nlm.nih.gov/35195253/
The bloody path of amyloids and prions: https://onlinelibrary.wiley.com/doi/10.1111/j.1538-7836.2007.02575.x