Walter M Chesnut Profile picture
Mar 19, 2022 14 tweets 4 min read Read on X
1) BUILDING: MY MOST IMPORTANT FINDING TO DATE: DIED UNEXPECTEDLY SOLVED
SUDEP AND “DIED UNEXPECTEDLY” – THE SPIKE PROTEIN, FIBROSIS AND THE BRAINSTEM
PART I “A SILENT ENTRANCE”
As you recall, the original spike caused a loss of the sense of smell, the medical term is Anosmia. ImageImageImage
2) The olfactory (sense of smell) system happens to be a DIRECT ROUTE TO THE BRAINSTEM.
Indeed, when we look at autopsies, the Spike Protein is a very frequent “guest” in the Brainstem. Pathological immune responses or SARS-CoV-2 invasion of the brainstem is suspected.
3) An autopsy study has isolated 32 brain sections from 16 victims of COVID-19 and found concentrated SARS-CoV-2 RNA (>5 copies/mm3) in three sections from the olfactory nerves and the brainstem’s MEDULLA. More convincingly, in another autopsy study of deceased COVID-19 patients,
4) SARS-CoV-2 RNA and proteins (nucleocapsid or SPIKE) were detected in 50% and 40% of brainstem samples, respectively. Similarly, another autopsy study has found SARS-CoV-2 RNA and SPIKE PROTEINS in the olfactory mucosal-neuronal junction and brainstem’s MEDULLA in 67% and 19%
5) of samples, respectively. In sum, these autopsy studies have provided evidence for SARS-CoV-2 tropism FROM THE OLFACTORY SYSTEM INTO THE BRAINSTEM.
OK. We know the Spike Protein invades the Medulla of the Brainstem. So, what does this mean? Well, those who suffer from Epilepsy
6) are prone to sudden death. In fact, it is because of PATHOLOGIC CORRELATIONS IN THE MEDULLA that they suffer what is known as SUDEP- Sudden Unexpected Death in Epilepsy.
Sudden unexpected death in epilepsy (SUDEP) likely arises as a result of AUTONOMIC DYSFUNCTION around the
7) time of a seizure. In vivo MRI studies report volume reduction in the MEDULLA and other brainstem autonomic regions. Rostro-caudal alterations of medullary volume in SUDEP localize with regions containing respiratory regulatory nuclei. They may represent seizure-related
8) alterations, relevant to the pathophysiology of SUDEP.
PART II “FIBROSIS AND SUDEP”
Now, this heretofore rare event is now becoming all too common. The “One-Two Punch” of aberrant spike protein brainstem signaling (remodeling) combined with spike protein cardiac remodeling
9) has virtually recreated the EXACT ENVIRONMENT OF SUDEP!
The histologic evaluation was possible in 65% of the cases (15/23) whose death was attributed to SUDEP and in 71% (15/21) of controls. Forty percent of the SUDEP cases (6/15) presented several foci of fibrotic changes in
10) the deep and subendocardial myocardium in contrast to 1 control (6.6%, P = 0.03). None of the subjects from the SUDEP group showed fibrotic changes in their conduction system as compared with 1 control (6.6%). The quantitative evaluation of fibrosis demonstrated a trend
11) toward more fibrosis in the deep and subendocardial myocardium of the SUDEP cases. Forty percent of cases in the SUDEP group were men (6/15), characteristically young at time of death (mean age 38 years) and with a late epilepsy onset (mean age 21 years). Antemortem, 73% of
12) the SUDEP patients (11/15) had experienced infrequent seizures (self-reported). We conclude that the SUDEP cases displayed significant fibrosis of the myocardium when this was assessed by qualitative means. This fibrosis may be the consequence of myocardial ischemia as a
13) direct result of repetitive epileptic seizures, which, associated with the ictal sympathetic storm, may lead to lethal arrhythmias.
And frontiersin.org/articles/10.33…, the Spike Protein’s induction of Iron Overload plays into this.
14) I implore all public health authorities: The Spike Protein Accelerants must be stopped this instant.
researchgate.net/publication/22…
pubmed.ncbi.nlm.nih.gov/32559314/
pubmed.ncbi.nlm.nih.gov/15897710/
frontiersin.org/articles/10.33…
https://t.co/gx1CEQcgcs

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More from @Parsifaler

Jan 23, 2023
1) Although decreased translation fidelity causes protein misfolding and aggregation in both cardiomyocytes and Purkinje cells, the downstream pathways that lead to cell death in the two cell types may be quite different. Interestingly, a point mutation in the editing domain of
2) human mitochondrial AlaRS (AARS2) has been associated with infantile mitochondrial cardiomyopathy, suggesting increased errors in either cytoplasmic or mitochondrial protein synthesis can lead to cell death in the heart. In summary, our data show that a global reduction in
3) translational fidelity, rather than disruption of a specific protein, can induce defects in proteostasis in numerous cell types in the mouse. It is thus possible that proteinopathy can occur in the brain, heart, or even other tissues as a combination of genetic and/or
Read 4 tweets
Jan 3, 2023
On Damar Hamlin and Dr. Sutterer's "diagnosis" of Commodio Cordis
I am shocked that Commodio Cordis (CC) is named as the cause. Please examine the images carefully. In CC Ventricular fibrillation can be triggered by chest wall IMPACT ONLY OVER THE HEART, and predominantly occurs
with impact over the center of the left ventricle. Although CC usually involves impact from a baseball, it has also been reported during hockey, softball, lacrosse, karate, and other sports activities in which a relatively hard and compact projectile or bodily contact caused
impact to the person's precordium. Are we to believe that with the padding that professional football players wear, the location of the heart and the location of the impact, that this was actually CC?

Nonsense. Rapidly stated, narrative, ARRANT NONSENSE.
Read 6 tweets
Apr 11, 2022
1) UPDATED SYNTHESIS: EXTREMELY URGENT
IT’S COMPLICATED, BUT CLEAR – LOOKING ONE MOVE DEEPER
THE SPIKE PROTEIN PATHOGENIC ALGORITHM – DUAL PATHS TO TERMINAL SYSTEMIC FIBROSIS: IMMEDIATE FOR THOSE WITH SIGNIFICANT COMORBIDITIES, INDUCED FOR THOSE WITHOUT
The Spike Protein is Image
2) inducing terminal systemic fibrosis of all organs, including the blood, via two principal mechanisms.
The first is a direct, immediate path via binding to RGD-binding integrins, which includes several TGF-β -activating integrins. This this activates Myofibroblasts which ImageImageImage
3) induces Fibrosis. Indeed, in autopsies of COVID-19 patients with advanced disease, 38% collagen deposition was found in their lungs.
This is a rapid and certainly fatal circumstance.
But, this is not limited to the lungs. In a series of cardiac autopsies conducted in
Read 12 tweets
Apr 8, 2022
1) MORE THAN AMYLOIDOSES. ALL HUMAN TISSUES ARE BEING TRANSFORMED INTO FIBROUS MASSES. INCLUDING. THE. BLOOD.
AMYLOIDOSIS. FIBROSIS. | AUTOPSIES. INCREASED ORGAN WEIGHT. | CLOTS. AMYLOIDS.
The tissues of the body, INCLUDING THE BLOOD, are being either DEPOSITED WITH FIRBILS OR ImageImage
2) BEING TRANSFORMED INTO FIBRILS. Amyloidosis > Deposition of Fibrils. Fibrosis > Transformation into Fibrils.
The Spike Protein is transforming (at least) all human tissue (perhaps other species?) into non-functioning fibrous masses.
I was reading papers in the solarium after
3) dinner while having a cigar. And I kept thinking about Amyloidosis and Fibrosis. I have seen both. Is it one? Is it the other? After reading more papers – AND SOME AUTOPSY REPORTS - I came to a startling and incredibly disturbing conclusion. It is BOTH!
THE CLOTS WE ARE
Read 9 tweets
Apr 8, 2022
1) THE SPIKE PROTEIN IS THE “AMYLOID” BEING DEPOSITED AND INDUCING AMYLOIDOSES: A MAJOR FINDING MISSED
SEVERE COVID MAY BE DUE TO THE ADDED DEPOSITION OF COMPLEMENT WITH THE SPIKE
The paper “The histologic and molecular correlates of COVID-19 vaccine-induced changes in the skin” ImageImageImage
2) made a case for the immune response to the Spike Protein causing self-limited hypersensitivity reactions to the vaccine. However, if you study the paper carefully, you notice that the authors have missed a far more important finding.
The biopsy specimens of normal skin post
3) vaccine and of skin affected by the post-vaccine eruption showed rare deep microvessels positive for spike glycoprotein with no complement deposition contrasting with greater vascular deposition of spike protein and complement in skin biopsies from patients experiencing severe
Read 6 tweets
Apr 4, 2022
1) PLEASE READ THIS ENTIRE THREAD. IT IS URGENT.
Building on all recent work. By far my most important synthesis:
A NEW KIND OF CANCER: THE MARRIAGE OF ONCOGENESIS AND PRIONOPATHY
THE PROGRESSIVE DESTRUCTION OF TISSUE AND ORGANS BY THE AMYLOIDOGENIC AND OLIGOMERIC PROPERTIES OF Image
2) THE SARS-CoV-2 SPIKE PROTEIN
It has been proposed that Alzheimer's disease might be a 'whole body' problem, as amyloid-beta can travel, cancer-like, to brain from other parts of body.
Normal mice that had been joined (via bloodstreams) to genetically modified partners for a
3) year "contracted" Alzheimer's disease. The researcher song says the amyloid-beta traveled from the genetically-modified mice to the brains of their normal partners, where it accumulated and began to inflict damage.
Not only did the normal mice develop plaques, but also a
Read 11 tweets

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