1) THE CONTINUOUS PRESENCE OF SPIKE PROTEIN WILL ALMOST CERTAINLY CAUSE MALE STERILITY VIA m6A METHYLATION. METFORMIN SUPPRESSES m6A METHYLATION!
COVID-19 IS NOT A BLOOD VESSEL DISEASE. IT IS A DISEASE OF IMPAIRED METABOLISM AND AUTOPHAGY (INDUCING SENESCENCE) CAUSED BY THE SPIKE
2) PROTEIN’S MASSIVE UPREGULATION OF m6A METHYLATION. THE ENDOTHELIAL DYSFUNCTION IS FROM THE SPIKE PROTEIN’S SUPPRESSION OF AUTOPHAGY AND SIMULTANEOUS ATTACK ON ACE2 RECEPTORS. EPIGENETIC CHANGES ARE REVERSIBLE. A CONSTANT PRESENCE OF SPIKE PROTEIN WILL MAINTAIN THE DELETERIOUS
3) ENVIRONMENT.
Once again, the medical establishment is completely incorrect as to the origins of the bioweapon that is SARS-CoV-2 and the disease that it causes. We are dealing with a VERY sophisticated bioweapon that impairs autophagy, metabolism and ion channels. I believe
4) the hypercoagulation being observed is from the body being unable to clear the massive number of dead cells caused by the spike protein. THE SPIKE PROTEIN BOTH CAUSES MASSIVE DAMAGE AND PREVENTS ITS “CLEANUP. “
It has been determined that SARS-CoV-2 infection triggers a global
5) increase in host m6A methylome, exhibiting altered localization and motifs of m6A methylation in mRNAs. M6A Methylation is also a hallmark of aging and is involved STERILITY. m6A modification could alter testosterone synthesis and develop oligospermia or azoospermia. These
6) findings emphasize the essential role of m6A RNA modification in the regulation of autophagy and testosterone synthesis. THIS MAY RENDER MALES STERILE.
As a result of increased m6A, m6A levels are increased on the mRNAs of ATG genes, and the transcripts of these genes became
7) highly susceptible to degradation. Hence autophagy is suppressed. Recent research reveals that both m6A demethylases (FTO and ALKBH5) could positively regulate autophagy and showed that m6A modification is inversely associated with the autophagy process.
Several studies have
8) suggested that there is a correlation between autophagy and the endothelial NO function. It has been shown that autophagy induction is associated with increased eNOS expression, whereas decreased autophagy is accompanied by down-regulation of the eNOS expression. It has been
9) observed that in COVID-19 pathophysiological alterations lead to an imbalance NO production. Also, reduction of eNOS-derived NO production causes endothelial dysfunction, which represents a risk factor for severe COVID-19.
It is without a doubt that repeated exposure to the

• • •

Missing some Tweet in this thread? You can try to force a refresh
 

Keep Current with Walter M Chesnut

Walter M Chesnut Profile picture

Stay in touch and get notified when new unrolls are available from this author!

Read all threads

This Thread may be Removed Anytime!

PDF

Twitter may remove this content at anytime! Save it as PDF for later use!

Try unrolling a thread yourself!

how to unroll video
  1. Follow @ThreadReaderApp to mention us!

  2. From a Twitter thread mention us with a keyword "unroll"
@threadreaderapp unroll

Practice here first or read more on our help page!

More from @Parsifaler

30 Sep
1) Let’s tie some more loose ends together, shall we?
METHYLATION, FIBROSIS, SENESCENCE, COVID-19 AND THE SPIKE PROTEIN
What percent of deaths worldwide do you think are due to fibrotic disease? Please sit down. Before COVID, worldwide, fibrotic diseases cause over 800,000 deaths Image
2) per year, accounting for ~FORTY-FIVE PERCENT of total deaths.
One of the most concerning aspects of COVID-19 is the appearance of organ fibrosis post infection. This is NOT limited to lung fibrosis. Let us look at the results of a preliminary six-month study of cardiac
3) involvement in COVID-19 patients. The preliminary 6-month follow-up study with a limited number of patients revealed persistent cardiac involvement in 29.6% (8/27) of recovered patients from COVID-19 after discharge. Patients with cardiac injury during hospitalization were
Read 14 tweets
29 Sep
1) DNA METHYLATION DRIVES COVID. Please read this entire post. Once you understand a concept, you must always ask yourself if there is something greater behind it. Such is the study of COVID. Therefore, I keep finding broader and deeper mechanisms for what is occurring in the Image
2) disease.
SENESCENCE IS A HISTONE CODE!
Here we provide an overview of the most relevant histone modifications, which characterize senescence, aging and the activation of a prolonged DNA damage response.
LET ME BE CLEAR. THIS IS NOT A RESPIRATORY VIRUS. IT IS A MILD RESPIRATORY Image
3) VIRUS WITH A BIOWEAPON SPIKE PROTEIN DESIGNED TO KILL IMMEDIATELY OR DRAMATICALLY REDUCE LIFE EXPECTANCY BY AT LEAST 50%.
COVID-19 IS A DISEASE OF HISTONE METHYLATION/DESTRUCTION INDUCING EPIGENETIC CHANGES RESULTING IN THE GENETIC LANDSCAPE AND DISEASES OF THE VERY OLD. Image
Read 11 tweets
27 Sep
1) THE SPIKE PROTEIN MAY SEVERELY IMPAIR MULTIPLE SYSTEMS AND MAY BE RESPONSIBLE FOR THE ENTIRETY OF LONG COVID.
IS CRAC CHANNELOPATHY INDUCED BY INTERACTIONS OF THE SARS-CoV-2 SPIKE PROTEIN AND TRANSIENT RECEPTOR POTENTIAL (TRP) CHANNELS AN EXPLANATION FOR THE SUDDEN DRAMATIC
2) INCREASE IN EXCESS DEATHS DUE TO INFECTIOUS DISEASES OTHER THAN COVID AND THE SUDDEN APPEARANCE OF AUTOIMMUNE DISEASE?
Excess deaths have skyrocketed in the past few months. These deaths are not due to COVID. In the UK, acute and chronic respiratory infections were also up
3) with 3,416 more mentions on death certificates than expected since the start of July, while there have been 1,234 extra urinary system disease deaths, 324 with cirrhosis and liver disease and 1,905 with diabetes.
The Spike Protein and SARS-CoV-2 is known to interact with TRP
Read 11 tweets
26 Sep
1) Please sit down before you read this post and then please review the graphic observing how much we have previously discussed is apparent.
First, please review the following:
Immunization with neuronal nicotinic acetylcholine receptor induces neurological autoimmune disease
2) jci.org/articles/view/…
Next, please review this paper:
A potential interaction between the SARS-CoV-2 spike protein and nicotinic acetylcholine receptors
ncbi.nlm.nih.gov/pmc/articles/P…
This interaction with the receptors is triggering toxification, which is creating antibodies
3) against achrs. This is documented.
In a recent study, Restivo et al. presented three patients who newly developed MG 5–7 days after onset of COVID-19 (13). Clinical manifestations of Myasthenia Gravis were mild in all three patients (13). In all three patients, MG was due to
Read 13 tweets
25 Sep
1) AGING, SENESCENCE, FIBROSIS, THE SPIKE PROTEIN AND COVID-19: HOW STUDYING CYSTIC FIBROSIS REVEALS THAT COVID-19 IS AN ION TRANSPORT DISEASE. I BELIEVE TREATMENT AS A RESPIRATORY INFECTION WILL CERTAINLY HARM THE PATIENT.
Cystic Fibrosis is the most common lethal genetic
2) disorder. However, most people are not aware of the mechanism that causes cystic fibrosis (CF). CF is a disease of ION TRANSPORT DYSREGULATION. A genetic misfolding prevents the body from forming the correct ion channels to transport sodium and chlorine across the cell
3) membrane.
The relation of CF to COVID-19 is not that it IS a form of CF, but rather that it CAUSES ION TRANSPORT DYSREGULATION. This is most likely accomplished by the orf3a gene directly, and the Spike Protein via antagonism of nAChR receptors and perhaps other yet unknown
Read 16 tweets
24 Sep
REQUIEM.

And so the cells, aged and tired, must choose. Between cancer and fibrosis.



Aging is an important predisposing factor for fibrotic heart and respiratory diseases. Age-related processes such as senescence and inflammaging diminish the
regenerative capacity of damaged cardiac and pulmonary tissue, increasing the likelihood of pathological fibrosis following injury or challenge. What is interesting about these two processes is that at low levels, they mediate beneficial effects, but as you age and the level
increases, they become deleterious. This is most evident with senescence, which protects the organism from cancer but which, in excess, can promote aging and the hallmark features of fibrosis.
Read 4 tweets

Did Thread Reader help you today?

Support us! We are indie developers!


This site is made by just two indie developers on a laptop doing marketing, support and development! Read more about the story.

Become a Premium Member ($3/month or $30/year) and get exclusive features!

Become Premium

Too expensive? Make a small donation by buying us coffee ($5) or help with server cost ($10)

Donate via Paypal Become our Patreon

Thank you for your support!

Follow Us on Twitter!

:(