Could the Geometry of Blood Vessel Wounds Be the True Trigger Behind Vaccine-induced Thrombosis?

Unnaturally long wound borders triggered by a Bolus of particles running down the vascular system necessarily stimulate unmanageable levels of coagulation factor we never evolved for.

This article addresses Pathology #3 of the Unified Bolus Theory: Thrombosis & Thrombocytopenia. Hopefully, you will appreciate the breakthrough proposed herein. It’s a sensible and perfectly logical explanation of the thrombosis phenomenon which was never about biochemistry, but more about biophysics…

Thrombosis and Thrombocytopenia Explained

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The main biological hypothesis around thrombosis to date has been anti-platelet antibodies. In other words, your body would start generating antibodies that cross-react with a coagulation factor. Frankly, that theory never made any sense to me for two main reasons:

1. Evolution would have pruned out these individuals very quickly. Imagine if each time we catch a virus, we start clotting and having thrombosis…we die. The pruning evolutionary process has done its work that’s a certainty. Possibly the immune system has a correction mechanism to avoid such disasters, possibly its maturing antibody process is more effective.

2. Almost all IV vaccine injections on rabbits¹ and on mice² create systematically thrombosis when injecting intravenously with a bolus, frankly the coincidence is improbable. Something else is at play.

And indeed, a recent study³ from Greifswald Medicine University in Germany showed that the immune responses to coagulation factor PF4 and to the spike protein are independent of one another, and that they are not the cause of thrombotic events.

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One of the last remaining mysteries of the vaccine injuries I still held in the back of my mind was:

Why on Earth did people dying of arterial ruptures - 4 or 5 months after their injection - didn’t develop thrombosis during that timeframe?

After all, the most damaging wounds had to happen when the Bolus is the most concentrated post-lungs. For example, the Bolus⁴ of lidocaine⁵ reaches the aorta in a sheep in 30 seconds and the heart in 54 seconds. By that time the dose was diluted respectively by 1.6 and by 13.7, which means the surface concentration was reduced by 27% in the aorta and divided by 6⁶ when it reached the heart.

Source: “A model of the first pass passage of drugs from i.v. injection site to the heart—parameter estimates for lignocaine in the sheep” by R. N. Upton

If we applied these dilution numbers to an inadvertent IV injection of a full dose of Pfizer vaccine on a human (I know it’s not rigorous, but it’s very indicative) :

• Aorta: 75,600 lipid nanoparticles (LNPs) would face the surface⁷ of a 1 sq.mm. of endothelium. That's equivalent to a destruction potential of 100 times!

• Heart: 17,607 LNPs would face the surface of 1 sq.mm. of endothelium, with a destruction potential of 23 times!

All within the first minute after the injection!

Even, if we are off by a factor of 10, the risk of concentrated transfection remains extremely high, and it is quite evident that the aorta and the arteries directly downstream are most at risk of a “carpet bombing scenario” than organs and veins downstream.

Obviously, autopsies show they are being hit by a large concentrated Bolus of vaccine particles followed by a massive immune attack that strips the endothelial layer. As per the photos showed notably by Pr Burkhardt, the wounds are very substantial versus the typical size of blood vessels: At least equivalent to a coin-size cut in one’s arteries. This has to trigger a very forceful - illusory - request for coagulation. But, how could a more diluted damage trigger these thrombosis and none be triggered by this massive wound? Something didn’t add up.

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Let’s go back to basics. Endothelial damage triggers coagulation by exposing the underlying tissue factor, which initiates a series of events known as the coagulation cascade. Bordering endothelial cells release von Willebrand factor, which binds to exposed collagen and recruits platelets to the site of injury. The platelets then release further factors that activate the coagulation cascade.

The coagulation cascade involves a series of enzymatic reactions that result in the conversion of prothrombin to thrombin, which in turn converts fibrinogen to fibrin, leading to the formation of a blood clot. Several coagulation factors are involved in this process, including factor VIII, factor IX, factor X, and factor XII.

In normal patients, the levels of these coagulation factors are tightly regulated to maintain the delicate balance between coagulation and anticoagulation. Several inhibitors of the coagulation cascade exist to prevent excessive clotting. These include antithrombin III, protein C, and protein S, which are produced by the liver and endothelial cells.

However, in patients with thrombosis, there clearly is an imbalance in favour of coagulation, leading to the formation of blood clots, in other words the coagulation factor overwhelms the inhibitor factor in the healthy part of the body…

The disbalance can originate either in an over-expression of coagulation factor, or in an under-expression of coagulation inhibitors. It seems reasonable to favour the over-expression hypothesis, simply because coagulation inhibitors are produced in the liver and across the endothelium, and the endothelial cells and liver of healthy vaccinated continue to produce those in spite of the vaccine. It is therefore more reasonable to investigate coagulation factor over-expression…

What could cause an unnatural expression of von Willebrand factor such that the body cannot cope with it?

The most natural hypothesis for an unnatural expression of coagulation factor has to be tied to the number of endothelial cells (EC) signalling the need for coagulation. In other words, the longer the wound borders; the more ECs expressing coagulation factor. The more coagulation factor; the higher the probability of a thrombotic event.

Could it be that - as the bolus rapidly disseminates downstream in the vascular system - the aggregate length of all the wound borders is actually significantly higher than that of the arterial rupture wound? In other words, is it the geometry or the topology - of a thousand cuts triggering a significantly higher dose of coagulation factor? How can we verify that conjecture? With a little virtual experiment…

Imagine a coin-size hole in the aorta. The surface required to poke that hole is roughly 60,000 lipid nanoparticles uptaken by an equal number of ECs. The estimated number of ECs expressing coagulation would be the periphery of that hole, a circle of 524 ECs [3.1cm in length] by my estimate. Let’s imagine serendipitously, the same 60,000 LNPs end up transfecting 1,000 holes of 60 ECs each. In aggregate, around 16,560 ECs [nearly 1m in length] will express coagulation factor, that’s 32 times the aortal rupture scenario with just 60,000 LNPs out of a total of 10-50 billion. In this scenario, the coagulation factor demanded would be 32 times the base case coin-size scenario, and an overwhelming flood of coagulation factor coagulation inhibitor bio-processes were never dimensioned to handle.

It is very obvious - based on this simplified scenario - and calculation that these vaccines have the potential - when not properly disseminated - to inflict unnatural wounds to our endothelium, and that we never evolved to survive such dramatic wounds, and therefore our coagulation inhibitors can very easily be overwhelmed by the enormous number of LNPs each with cytotoxic capacity.

Once again, biophysics explain perfectly vaccine adverse effects. People have been extremely aggressive towards me and my work, stating with certainty: “Physics have no play in biology!”. Seems that’s a preconceived idea that’s been slowing down biology for a very long time.

Once again this demonstration underlines that “There’s no Magic, only Logic!”. Only by using the scientific approach strictly with observation, questioning, hypothesis ideation, testing and (in)validation can we help solve what has evaded us for centuries.

Hope you enjoyed this new piece of insight on the mystery of Thrombosis.

Love, Marc

If you haven’t seen my discussion with John Campbell. Here it is again:

1. “Intravenous administration of recombinant adenoviruses causes thrombocytopenia, anemia and erythroblastosis in rabbits” by Cichon et al - Reference

2. “Induction of Shock After Intravenous Injection of Adenovirus Vectors” by Xu et al - Reference

3. “Anti-platelet factor 4 antibodies causing VITT do not cross-react with SARS-CoV-2 spike protein” by Greinacher et al - Reference

4. A Bolus is a concentrated dose of a drug or particles that permits the rapid delivery to an organ of those particles, briefly bypassing the disseminating function of the vascular system.

5. “A model of the first pass passage of drugs from i.v. injection site to the heart—parameter estimates for lignocaine in the sheep” by R. N. Upton - British Journal of Anaesthesia 1996 - Reference

6. 3D to 2D concentration calculation: (22.1/35.7)^(2/3) = 72.6% & (2.6/35.7)^(2/3)=17%

7. Note: the dilution might look smaller because it is a 2D concentration versus a 3D dilution.