EXCLUSIVE: The Mechanism For Myocarditis

The best hypothesis for why it affects males and how

As seen previously, we have gone over how LNPs end up in the liver and trigger clotting, and how LNPs are gene silencing monstrosities with nasty PEG tricks up their sleeve, The Daily Beagle has pieced together enough to understand the likely mechanism by which myocarditis works.

As for a thank you for paying members financing cutting edge research who understand time is not free, resources cost money, and most work is actually worth more than $7 a month (McDonalds employees make $10 an hour), they’ll get an inside look on our best hypothesis on how myocarditis occurs and why, and we think you’ll agree, it is extremely compelling given the evidence.

The model is quite complex, and as a result of the complexity it is difficult to be 100% sure on accuracy, but it’s arguably the best model so far and aligns with a lot of the datasets we’ve seen so far.

First port of call we must re-examine the immune triggering effects of PEG. Our first clue of why it disproportionately affects males is in the rat study showing inhaled PEG 3350 causes neutrophil numbers to increase by 50% in male rats. It is likely injected PEG causes something worse. We also see that it triggers Basophil white cells and anti-PEG antibodies as well.

To deduce a reverse-engineered pathway as to why neutrophils would cause myocarditis, we asked the AI GPT-3 if it thought neutrophils could cause myocarditis.

This isn’t as absurd as it might sound, as GPT-3 is trained on a lot of public datasets, including open source studies, and is a bit like a ‘sentient database’. Whilst AI can be wrong, it is an extremely good first port of call on testing theories as it can mention obscure connecting pathways or highlight discrepencies.

It’s not perfect as it doesn’t have access to closed source information, but it does a decent job in research by giving clues, which then have to be manually hunting down in papers, collated and verified.

Reactive Oxygen Species

It proposed that the ‘Reactive Oxygen Species’ (which is a real thing) generated by neutrophils could trigger myocarditis. It turns out neutrophils do indeed generate Reactive Oxygen Species (ROS), and ROS is used in clotting.

For example, in this study of damage to the heart’s endothelium (a different part of the heart, the inner cell wall lining), ROS was shown to invoke ‘micro-clotting’, and quotes pretty much exactly what we’re looking for (bolded):

[…] the endothelium senses an acute loss of preexisting isometric tension, and that downstream of this biomechanical signal, the ensuing recovery response generates reactive oxygen species (ROS), which are responsible for coordinating the micro-wound closure process […]

Damage To The Endothelium Can Lead To Myocarditis

The study then goes on to note that damage to the heart’s endothelium possibly leads to ‘myocardial infarction’ (the most commonly seen amongst those that received the COVID-19 poison shot) and ‘subsequent heart failure’:

Damage to the endothelium contributes to the development of atherosclerosis, and hence to possible myocardial infarction and subsequent heart failure.

So immediately we know that the Reactive Oxygen Species can trigger myocardial infarction. But neutrophils can end up anywhere, why do they end up in the heart specifically?

ACE-2 Receptors In The Heart

This is the part where the mRNA comes into play. A great many people have solely blamed LNPs, however even if we assume the PEGylated LNPs trigger a rise in white cells, it does not naturally follow they will attack the body itself. They might attack the PEG, but not the body.

The mRNA codes for the SARS-CoV-2 spike protein. These spike proteins have a strong affinity for binding to ACE-2 receptors. That means they won’t typically try to enter any other type of cell.

Where are ACE-2 receptors found? In a variety of places, including the spleen and liver. This might sound familiar because we discovered LNPs were found in the spleen and liver. There’s one other, very crucial, ‘aha’ moment area…

[…] the presence of ACE2 in vascular endothelium […]

‘Vascular’ for those not up to speed on medical jargon, means the blood system (you will have most likely heard it from the term ‘cardiovascular’, cardio referring to the heart). So ACE-2 receptors are expressed everywhere in the vascular system — including in the heart.

That’s right, the endothelium, of which we’ve established if it gets damaged will likely lead to myocardial infarction — or myocarditis.

Like Unwrapping Layers From Within

It helps to have a bit of understanding of the heart. It has these main layers, working from inner to outer:

• Endocardium (inner)

• Myocardium (middle)

• Epicardium (outer layer of the heart, inner layer of the serous visceral pericardium)

• Pericardium (basically a sac that surrounds the heart).

The endocardium is composed of endothelial cells (part of the body’s wider endothelium). You can imagine the endocardium as the ‘protective inner layer’ shielding the muscle myocarditis from exposure. If the endocardium gets shredded, torn, injured or opened, then the myocarditis underneath is exposed.

Naturally, the ACE-2 binding spike proteins start causing damage to the endothelium, which in turn prompts a response from the immune system…

Neutrophils Are First To The Party

Neutrophils are eager beavers. They want to get to the site first. And they sure do. They get there even before platelets (AKA thrombocytes, basically the blood clotting cells) do:

[…] neutrophils have been shown to be the first cells at the site of damage, even preceding platelets […]

So, now you’ve got this unnaturally high, 50% increased neutrophil count in males, and they’re all arriving at the scene of the crime of the damaged endothelium that has been attacked by the Moderna/Pfizer/AstraZeneca/Johnson&Johnson/Sputnik V/CureVac/Sinovac spike protein.

The unstable mRNA is going to make the immune system reaction worse because it will seem like a wide variety of foreign proteins are invading, rather than just one, causing the immune system to kick into override (hence the ‘auto-immunity’ trigger for myocarditis).

So neutrophils turn up to the scene, and start killing off damaged endothelium cells that have been polluted with the toxic mRNA (white cells basically operate ‘scorched earth’). It’s what they do. As a result, large segments of the blood vessels are damaged, which signals for clotting via Reactive Oxygen Species.

The neutrophils also release the aforementioned ‘Reactive Oxygen Species’, which in turn encourages clotting to occur along entire stretches of the blood vessels (this is why you get such long clots).

[…] neutrophils are able to activate platelets via production of ROS […]

Unsurprisingly, neutrophils have a preference for endothelium, and reducing their ability to bind reduces their ability to perform coagulation (yet another fancy word that means ‘clotting’).

[…] inhibition of neutrophil binding to the endothelium at the site of damage reduced the presence of tissue factor (TF, or FIII), the main initiator of the extrinsic coagulation cascade. […]

Meanwhile, the liver, under attack from the LNPs from the shots, is producing increased levels of fibrinogen — a fibrin generator — at absurdly high levels (+2.6x), a clotting agent that promotes fibrin based clots.

They All Combine To Form The Perfect Storm

The nearly tripled in number fibrinogen chemicals travel from the liver to meet the doubled in number neutrophils (in males) at a scene of complete chaos along the blood vessels being attacked by all sorts of weird, foreign malformed mRNA spike proteins.

The fibrinogen reacts with the Reactive Oxygen Species produced by both the endothelium and the neutrophils and the thrombocytes and produces vast amounts of clotting along entire stretches of the blood vessels where all the now damaged or destroyed ACE-2 receptors are.

This produces the extremely long, fibrous clots of which you see in the blood vessels, and once they clot together, blood is completely unable to move. You’d might call them a “super clot”, or more accurately a ‘lengthways clot’.

The impeded blood flow cuts off oxygen to the heart and brain, leading either to strokes (if it cuts of blood supply to the brain) or heart failure (if it cuts off supply to the heart). Males get myocarditis worse than females because their neutrophil count is much higher due to the PEG in their bloodstream, thus they incur much greater amounts of neutrophil-induced damage to the endothelium, which in turn leads to a higher probability of myocardial infarction.