Strange Clots
Since mid-2021, unusual, lengthy blood clots found in the vessels of COVID-19 patients and jab recipients have been reported across the world.“We as embalmers are seeing some strange clots since the COVID outbreak. These clots are very rubbery feeling and very long as they exit the veins that we use during the embalming procedure. They really appear to be like earthworms. I have never seen this in my career until now,” Larry Mills, a licensed embalmer and funeral director in the State of Alabama, told The Epoch Times.
Other embalmers confirmed similar findings and spoke on the condition of anonymity.
Richard Hirschman, Alabama funeral director and embalmer since 2001, was one of the first to bring attention to this phenomenon. He said that prior to COVID perhaps 5 to 10 percent of people had these clots. Now more than half of the bodies he sees have them.
One embalmer, licensed since 2001, said in an interview, “I can tell you with certainty that the clots Richard has shown online are a phenomenon that I have not witnessed until probably the middle of last year. That is pretty much all I have to say about it. I have no knowledge as to what is causing the clots, but they did seemingly start showing up around the middle of 2021.”
A Condition With Over 200 Symptoms
Doctors have realized, since the early days of the pandemic, that COVID-19 is not just a lung disease, but also an endothelial and vascular disease.This is perhaps the largest number of symptoms reported with a medical condition so far.
The most frequent symptoms include breathlessness, fatigue, brain fog, cognitive dysfunction, muscle aches and pains (myalgia), sleeping difficulties, and anxiety or depression.
Blood Clots Causing Symptoms
In November 2020, a report with findings of increased microclots in COVID-19 patients versus healthy or diabetic patients could reasonably explain the breathlessness, fatigue, and post-exertional malaise syndrome.An artery clot is the kind that could cause a heart attack or ischemic stroke by blocking blood flow to the heart or brain.
Even though that risk drops sharply to less than four times higher than someone without COVID in the second week, it remains high (2x) even up to 49 weeks after the initial diagnosis. This is especially so in regards to the risk of deep vein thrombosis. These are clots that form in large veins.
Spike Protein: The First Domino Toppled
Blood is a liquid that circulates under pressure through the blood vessels in our whole body, like the water flowing through the house that you then use to shower, do the dishes, and so on.Following a vascular injury, any blood “leaking out” must rapidly be converted into a gel (a “clot”) to fill in the hole and minimize further blood loss.
Unfortunately, the blood clotting mechanism can also lead to unwanted blood clots inside blood vessels (pathologic thrombosis), e.g. heart attack or stroke, both of which are a leading cause of disability and death in the world.
It appears that the virus’s unique spike protein triggers the cascade via many “non-traditional” pathways.
The spike protein’s direct invasion of the epithelium cells is the first domino toppled.
Spike Protein Impairs Epithelium Cells
SARS-CoV-2 enters our cells via a protein receptor called the angiotensin-converting enzyme 2 (ACE2).Endothelial cells (ECs), express an abundance of ACE2. ECs reside on the inner surface of every blood vessel across our entire body, making them a direct target of the virus infection.
Subsequently, the release of cytokines initiates the switch-like molecule (E-selectin) on the endothelial cell membrane, allowing them to attach with immune cells, thereby initiating subsequent disease processes.
Cytokines are small proteins secreted by cells (mainly T cells and macrophages). They have many specific names, and serve as a communicator between cells (cell signaling) for further action. Cytokines are the “mailmen” of the body that connect and communicate between cells.
Spike Proteins Trigger the Clotting Cascade
Many other cells, including lung epithelial cells, enterocytes lining the small intestines, and cardiac pericytes, all express ACE2.Spike proteins don’t only activate epithelial cells (EC) and promote localized inflammation. They also promote systemic inflammation as ACE2 is almost everywhere inside our major organs and tissues.
Consequently, more pro-inflammatory genes are expressed. More and more immune cells are attracted and sent to the injured or infected tissues (vessels in the lung, heart, gut, etc).
- Complement-mediated inflammation of epitheliums (endothelialitis): Spike proteins docking on ACE2 ECs activates the complement pathway and coagulation cascade, resulting in a systemic endothelialitis (lung injury) and procoagulant state (tendency to develop blood clots).
- As the complement destroys the endothelium, the procoagulant von Willebrand factor (vWF) and FVIII are released. A significant increase of vWF can form multimers that promote thrombus growth. vWF is secreted mainly from endothelial cells and from a-granules of platelets (megakaryocytes derived). This is comparable to the string in the “beads and string” of a necklace where the beads represent platelets.
- Platelet storm: Platelets are a small fragment of the megakaryocytes. The complement anaphylatoxins C3a and C5a activate platelets and increase the production of tissue factor further promoting a clotting forming state. ACE2 receptors are present on platelets, and this may contribute to the massive platelet aggregation, which is a characteristic of severe COVID-19 infection.
- Activation of neutrophils leads to formation of neutrophil extracellular traps (NETs), a process sometimes referred to as NETosis, which contributes to thrombosis.
- EC injury is compounded by toll-like receptor (TLR) activation by viral RNA recognition, with resulting increased reactive oxidative species (ROS) production. The increased ROS further upregulates the expression of vWF.
- Spike protein can induce expression and secretion of a series of clotting proteins which cascades into the clotting process, including factor (F)-V, thrombin, and fibrinogen to promote clotting process.
Spike Protein Dysregulates RAAS, Worsening the Clotting State
Due to the spike protein directly interacting with ACE2 expression, COVID-19 patients showed an elevated level of serum angiotensin II indicating a dysregulation of the RAA system (renin angiotensin aldosterone system, or RAAS).Traditionally, people think angiotensin II is a neurohormone that stimulates the constriction of vascular smooth muscle cells and is responsible for salt and water balance.
In a regulated and self-limited immune response, these mechanisms help to calm down the local injury, with subsequent healing and returning to a resting EC state.
Here is a short summary of the first scene of the clot story: spike induced endothelial disruption, massive amounts of vWF released, a subsequent platelet storm, hypoxia induced upregulation and activation of vWF, fibrous network from neutrophil extracellular traps (NETs), as well as increased angiotensin II level, all adding up to initiate thrombogenesis.
This is how the clotting mechanism comes to be. Furthermore, the upcoming second scene takes another pivotal part in the whole story.
A COVID vaccine instructs the cells to produce large quantities of spike proteins. Normal biochemical and physiological processes are “hijacked” in order to make an abnormal amount of these spike proteins.
Spike Proteins Directly Disrupt the Clot Dissolving Mechanism
In a normal healthy person, the body will, in the presence of a blood clot, break it down by a process of fibrinolysis. This is a natural healing and balancing mechanism to prevent an abundance of blood clots.During this process, Tissue Plasminogen activator (TPA, coming from the endothelium) helps plasminogen change into plasmin and then generate d-dimer (a small protein fragment left when a blood clot dissolves).
It has been discovered that fibrinogen in blood can clot into an abnormal “amyloid” form of fibrin that (like other β-rich amyloids and prions) is relatively resistant to proteolysis (fibrinolysis).
This is strongly manifested in the platelet-poor plasma (PPP) of individuals with long COVID. The extensive fibrin amyloid microclots can persist.
When spike protein S1 was added to healthy PPP, it resulted in structural changes to β and γ fibrin(ogen), complement 3, and prothrombin. These proteins were substantially resistant to trypsinization in the presence of spike protein S1.
Hence, the results suggest that the presence of spike protein in circulation may contribute to the hyper clotting status, and may cause substantial impairment of the clot dissolving process.
Such lytic impairment may result in the persistent large microclots that people have reported and which have been found in plasma samples of COVID-19 patients.
Spike Proteins Form Amyloid-Like Substance
Furthermore, to everyone’s surprise again, spike proteins are identified to present seven amyloidogenic sequences and are able to form amyloid-like substances.In other words, these spike proteins are similar to those beta-amyloid or tau or alpha-synuclein like substances which may cause neuronal loss in Alzheimer’s or Parkinson’s disease patients.
Their structure makes it easy to form tighter string-like bonded structures with longitudinal twisting as well as cross binding, forming a fibrous-like structure visible under the microscope.
After a second trypsinization, the persistent pellet deposits (microclots) were solubilized. Various inflammatory molecules substantially increased in both the supernatant and trapped in the solubilized pellet deposits of COVID-19, versus that of the control samples.
Of particular interest was a substantial increase in α(2)-antiplasmin (α2AP), various fibrinogen chains, as well as Serum Amyloid A (SAA) that were trapped in the solubilized fibrinolytic-resistant pellet deposits.
Spike Protein Inhibits Another Anti-Clot Mechanism
Spike protein is just one surprise after another.SARS-CoV-2 spike proteins at a similar concentration (~10 μg/mL) as the viral load in critically ill patients can directly cause blood coagulation and thrombosis in the zebrafish model.
Spike Protein Is the Smoking Gun
There is clinical evidence that the SARS-CoV-2 spike protein has been detected in clots retrieved from COVID-19 patients with acute ischemic stroke and myocardial infarction.Recent research conducted by cardiologists from the University of Colorado sheds light on the crucial role of spike protein in the pathology of COVID and COVID vaccine-related injuries.
In other words, regardless of whether the myocarditis was caused by the virus or vaccine, the expression of genes responsible for prothrombotic state in response to spike protein, inflammation, and myocardial dysfunction, exhibited similar changes.
Based on gene analysis, COVID-19 and post-mRNA vaccine injury have a common molecular mechanism.
The altered genes pattern includes down-regulation in ACE2, ACE2/ACE ratio, AGTR1, and ITGA5, and up-regulation in ACE and F3 (tissue factor).
Tip of the Iceberg
Based on the causal relation between ChAdOx1-S vaccines (the AstraZeneca adenovirus COVID vaccine) and thrombosis with thrombocytopenia syndrome, the product information for ChAdOx1-S has been updated to include thrombosis with thrombocytopenia syndrome as a very rare side effect.These unusual blood clots in combination with thrombocytopenia were reported predominantly in women aged under 60 years. Accordingly, several European countries restricted the use of adenovirus vaccines in younger age groups.
However this may be only the tip of the iceberg. There are many more events that could be attributed to the clotting issues including sudden death, cardiovascular events, cardiac death, stroke, disabilities, thrombotic events, etc.
Blood vessels are in all our organs. The vessel problems could explain a wide range of symptoms from the dysfunction to mild decline of our brain, heart, lung, and extremities.