SARS-CoV-2 Spike Protein Impairs Endothelial Function via Downregulation of ACE2

So the study indicates that the Spike Protein binds to ACE2 that is found in the membranes of cells located in the lungs, arteries, heart, kidney, and intestines, and down regulates them to the point where it damages your mitochondria in those organs. So according to the research they did, it's not just the virus that can hurt you but the mechanism (Spike Protein) the virus uses to attach to your cells and replicate that can cause this damage.

It is likely that the vaccine itself which holds the mRNA and not the actual Spike Protein or Virus (just the instructions on how to make the Spike Protein) is administered in a intramuscular area of the body (Shoulder Area), never able to live long enough (mRNA dies off quickly) to enter these areas where ACE2 is found (Heart, Lungs, Kidneys, etc). The muscle tissue/cells in the upper arm create some Spike Protein and your immune system basically say WTF is that and kills it long before it can ever reach these organs or areas of the body.

The real Virus typically enters the body through the nose and mouth and heads directly into the sinuses and can spread very quickly to lungs and then move on from there into other organs. If you're someone who is one of the folks (Metabolic Disease, severe autoimmune dysfunction) who might be susceptible to what this study suggests, the vaccine is the way to go since it might give you a better chance to avoid the negative outcome from the Spike Protein affecting ACE2 and then damaging the mitochondria in your Organs cells.

However, their metric was IIRC "within 3 days of first or second dose"; so 6 days worth of myocarditis compared to your full year number, so a factor of 60 (assuming uniform distribution over the year) to put on same scale.

Corona viruses have been with us for a few thousand (millions?) of years. It is estimated 25% or so of colds are caused by corona viruses. And not surprisingly, they can also cause really, really bad outcomes in the sick and elderly -- in fact, there is some speculation that before they became endemic, they were as virulent as sars-cov-2.

And there definitely have been attempts; not as focused, of course, but nevertheless over many years. The most focused attempts were at SARS-Cov-1 and MERS - and both burned out quickly - but also all failed spectacularly at the animal testing stage.

> This isn't a mechanistic explanation of how you've arrived at a stronger level of comfort with earlier safety trials, unless your evaluation criteria is literally just that they took longer.

(a) animal testing (skipped entirely in this case, which would have shown perhaps that targeting the spike protein may be an issue, and

(b) yes, more time. some signals take time to surface - do read the pandermix papers I linked to. Whatever is happening now is just too close for comfort, and I sincerely hope it will end better.

What more can you ask for, when I show you a horrible experiment from 2009, which matches in almost every possible way except we're now using now technology? With articles from science and the BMJ? Is there anything that can satisfy your request for reasonable doubt?

A little bit of spike trains your body to identify it and neutralize it.

A whole lot of spike is toxic to your organs and damages them.

To downregulate ACE2 you need a whole lot of receptor activation and a lot of ligands floating around in your system binding to it to cause that. The dose of spike protein matters.