Understanding Fibrinous Clots and Coagulation

When I look at what we're seeing with the clots,

we're seeing a mixture of the fibrinous and the traditional clot,

but when you look at the fibrinous clot,

it tends to be one long strand,

and you've got clots attached to it,

natural clots attached to it.

So you've got two processes, Philip.

You've got the fibrinous structures that are forming,

and you've got those fibrinous structures causing turbulence in blood flow,

which actually causes normal clotting around it.

So what I think is happening,

if I were to put it into a framework,

a little bit of understanding, I think that,

imagine a streamer in the lumen of the vessel,

and it's not including blood flow,

but it's stuck to the vessel wall,

and that streamer's growing.

So what happens is you've got some process that's on a nidus

on the vessel wall, triggering a process, a catalytic process,

that's going to cause this fibrinous clot to constantly elongate.

As that fibrinous clot elongates,

it doesn't occlude the lumen.

It's flapping around like a streamer in the lumen wall,

and the blood is flowing past it,

so you don't see it.

It's there, and it keeps growing,

but it keeps causing more and more normal coagulation around it.

And the longer it grows, the longer the clot,

but it hasn't occluded the vessel.

And because it needs this turbulence to have coagulation around it,

it will occur in slow flowing areas of the body,

and in vessels with bigger lumen, with more stasis of blood.

So in the venous system, in the bigger vessels.

So as this fibrinous clot grows through a polymerization process,

where it keeps getting proteins from your system,

sticking onto it and growing it,

it also acts as a foreign body in the vessel, creating turbulence.

And it's that turbulence that causes the blood to start to clot around it,

until eventually the pressure cannot push through,

and it eventually just blocks up.

So depending on when it blocks up,

you can get a short strand of it,

or you can get a very long,

like they're pulling out two feet clots from patients' leg veins and things like that.

So it couldn't have occluded it at a short piece.

It had to be a two foot clot

that was still allowing blood flow through,

for it not to have been detected at two feet.

Right, exactly. And the polymerization is the key.

You know, the contents that are in these clots are not normal blood products,

as you know.

When you look at the polymerization process,

when they looked at the content of the fibrinous clot,

they found a lot of things that weren't normal constituents of blood.

You didn't find the high levels of ferritin and things.

But one thing that they found that was strange was

they found a high content of tin.

They found a spike in tin.

Now if you look at tin,

tin is used as a catalyst in the making of PVC pipes.

And so all our water supply is PVC pipes,

and so a lot of people have tin in their system.

So tin being a catalyst, and of course in the lipid nanoparticles,

you've got phosphates and sulfates,

which actually act as polymers as well, catalysts to a polymerization process.

So all you need is one trigger event on a vessel wall,

and all the proteins in blood act as monomers.

And this is a magnet for them,

and they keep sticking on,

and the end of them is always sticky and it sticks another one on.

So it's like putting a drop of catalyst into fiberglass,

that one drop just spreads and hardens the entirety.

So you've got this one fibrinous structure growing inside the vessel through a polymerization process.

And when you look at it,

the polymerization process creating the cross-linking will give it its structure

and elasticity and its tenaciousness,

because it's not just stuck on, it's cross-linked like polymerization does.

So if you look at the fibrinous structure,

you'd say it's almost like polyurethane foaming in the center of the vessel.

But because it's flapping around as blood flows past,

it's creating a needless for normal coagulation to take place around it

until it eventually just blocks up.

End of transcript · 719 words

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