More on the danger of the spike protein

More on the danger of the spike protein

Rewrite: Let’s tag team this until everybody understands

The modified spike protein is dangerous and for very specific reasons.

To my readers: Pertaining to the article and photos previously linked to this article – I was unable to verify the validity of the photos of the magnified tissues and therefore, I do not feel comfortable using them. Time always tells.

The take home message of this article still holds.

The structures inducing arterial embolisms in post-injected individuals are not blood clots.

Here’s a screenshot1 of pathologist Ryan Cole holding up a sample (courtesy of Richard Hirschman) of strange proteinaceous structures extracted from embalming/autopsies. I am waiting on some first-hand pathology results from Ryan now so stay tuned! This article will be MUCH stronger with them. And I do love pretty pictures.

Kind of looks like a tapeworm, no?

A blood vessel can change its inner diameter via vasoconstriction (see RAAS) but it would be safe to say, that for any selected blood vessel, the diameter would be somewhere between between 8 um-25 mm, depending on what type you pick and if its vasoconstricted.

So let’s assume our white lengthy, stringy bits in the above glass sample vials were extracted from 4 mm arteries. That seems about right, yes? So, I am not an embalmer, but I hear that clots ‘normally’ show up in veins and not so much in arteries. By the way, when a vein is blocked from a clot, this is called a venous thrombosis is and when an artery is blocked by a clot, this is called an arterial thrombosis. Is it a thrombotic bus or an embolic bus, House MD would ask? Well I would say these people died suddenly from arterial embolisms caused by these fibrous structures. The following photo shows what a gelatinous, ‘normal’ blood clot looks like in a big artery (heart-proximal?). It looks exactly like red current jelly.

Arterial Embolism. Causes, symptoms, treatment Arterial Embolism

So, now us non-embalmer laymen can rest assured that these strange white fibrous proteinacious structures are not blood clots. The structures did, however, obstruct the flow of blood in the arteries of these individuals and likely is what killed them.

Amyloidosis, amyloid or beta-amyloid plaque formation is known to be associated with the brain and neurons. But what if these spike-related amyloidogenic proteins didn’t have a neural preference?

Below is case of Cardiac amyloidosis from C. Michael Gibson, M.S., M.D. and Cafer Zorkun, M.D., PhD.

This is a higher-power photomicrograph of the heart tissue from this case. Note the amyloid deposition throughout the myocardium (1) as well as deposition in the wall of the blood vessel (2).

To quote some smart people:

Follow a theory, spend loads of [money] trying find a drug and then, if it doesn’t work or produces serious side effects, dump the programme. What is needed is a much more holistic approach to the whole disease, rather than trying to compartmentalise it neatly within an ‘amyloid hypothesis,’ a ‘Tau hypothesis’ or anything else.2

This is what severe atherosclerosis looks like, by the way. Not the same as our strange long strands.

I think we are dealing with a devilishly insipid hand-crafted (modified) RNA whose protein by-products (that appear to be multi-dimensional), following either translation, or digestion for MHC presentation, are amyloidogenic. Clinical presentation = systemic plaques/proteination of affected areas/tissues/vessels.

The location of the plaque formation/proteination would depend on many factors such as:

  1. whether or not the injection was intra-muscular or into the blood,
  2. the initial bio-distribution of the LNPs,
  3. the efficiency of delivery of the modified RNA payload,
  4. the integrity of the modified RNA template,
  5. the rate and efficacy of translation,
  6. the products of translation (which would depend on template(s),
  7. the immune response to the presence of the foreign proteins,
  8. the immune state of the individual prior to injection (chronic low level inflammation?)

just to name a few.

I think it is possible that the myocarditis cases being reported are due to Cardiac Amyloidosis. The primary symptoms of Cardiac Amyloidosis are shortness of breath, fatigue, swelling in the legs, heart palpitations, lightheadedness – pretty much the same as myocarditis (breathing difficulties, chest pain, fatigue, swelling in the legs, rapid heartbeat, lightheadedness and flu-like symptoms).3 4 These lists are pretty identical and I got them from 2 different sources.

I leave it here for now.


Taken from an interview Ryan Cole did with Steve Kirsch.



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