Deadly Substitution, and Farewell to Andrew
New article shed more light on the problematic usage of N1-methylpseudouridine in the mRNA experimental gene therapy ("vaccine"). Here is a summary of the article, plus a farewell to one of my heroes.
Hi everyone,
Due to complex personal situation I’m in I’ve been very quiet, but I wanted to write a quick summary of an article that just been published and comment on it, as the points raised in it are of extreme importance because they provide more information on the problematic usage of codon optimisation, which I covered in my previous writing on the topic (#Coptigate, as well as variantology).
The article “Report: Effects of N1-methyl-pseudouridine in the Pfizer mRNA Vaccine”, was written by Daniel B. Demers, who has a PhD in pathology, and has spent more than 30 years working in DNA diagnostics and forensic genetics. I highly recommend reading it when you can.
As you might know, the mRNA experimental gene therapy (AKA "vaccines") is using a modified uridine (N1-methylpseudouridine) to replace uridine (U) which appears in the original spike protein. They used N1-methylpseudouridine to eliminate the “wobble” properties of the pseudouridine. N1-methylpseudouridine has an added methyl group (CH3) in comparison to pseudouridine.
There is not a lot of knowledge about the way pseudouridine impact biological systems, and much less on the impact of N1-methylpseudouridine.
As the author has written, to date, there has been nothing even close in nature that resembles the Pfizer modified mRNA.
Our immune system has two major elements, an innate and an adaptive immunity, where the innate is the 1st line of defence, using the production of interferon, cytokines, and chemokines. This mechanism has stopped traditional mRNA vaccines from working because such mRNA gene therapy has led to increase interferon production which is associated with inflammation and potentially autoimmunity, edema, blood coagulation and thrombosis, as well as increasing cytotoxicity.
A modified RNA, which is containing pseudouridine or N1-methylpseudouridine has been shown to suppress the innate immunity, and this is why for Pfizer used it in its BNT162b2 product. However, using such strategy is extremely problematic as suppression of the innate immune system is leading to downregulating critical systems related to cancer surveillance, infection control and cellular homeostasis.
When Ivanova et al. (2021) looked at the immune response of patients who had severe COVID19 vs those who received the Pfizer BNT162b2, they noticed a clear distinction: those who got COVID19 had an augmented interferon signalling and upregulation of genes associated with cytotoxicity, while those who received the Pfizer BNT162b2 didn’t, and the COVID19 patients had an elevated levels of IgA and IgM antibodies compared to those who got the Pfizer BNT162b2 . Also, Jain et al. (2021) reported on a study of 63 patients with “coronavirus disease 2019 vaccination-associated myocarditis (C-VAM)”, where all the patients were less than 21 years of age, 92% were male, all had an mRNA vaccine and except for one patient, all presented after the second dose, which can be explained by the toxicity of the spike protein and the suppression of the innate immune system.
Another problem of using N1-methylpseudouridine in an mRNA experimental gene therapy is the fact that by doing so it extends the mRNA half-life and, as a result, increases the spike protein production. This can explain why Röltgen et al. (2022) has reported that mRNA was found in germinal centers (secondary lymphoid organs including lymph nodes and spleen which are important for B-cell activation) two months after it was introduced to the body.
Last point that was raised in the article was the fact that using N1-methylpseudouridine substitution leads to what is known as enhanced translation, or over production (as reported by McKernan et al., 2022; Morais et al., 2021; Nance et al., 2021; Parr et al., 2020; Mauger et al 2019; Svitkin et al., 2017; Kariko et al., 2008). This excess translation is leading to a phenomenon known as MicroRNAs (miRNAs), which are being exported out of the cells via exosomes and are transported to distant tissues and organs, including the brain and central nervous system. Since the SARS-CoV-2 genome, including the spike protein mRNA, have been shown to encode their own miRNAs, and since some of which interact with human miRNAs (Liu et al., 2020), the exosomes distribution of the miRNAs can lead to long term impact on our DNA which was neither mentioned nor investigated by Pfizer.
In conclusion, the author has stated that while the usage of N1-methylpseudouridine has “solved” the problem of the activation of the innate immune system as a result of introducing a mRNA experimental gene therapy, it has created a set of new problems and introduced new risks which we have little ability to measure or estimate due to the fact there is practically no scientific knowledge what is the impact of using N1-methylpseudouridine. Since Pfizer has not conducted any studies on this issue, nor is conducting any studies, we have no ability to quantify the real impact of the introduction of N1-methylpseudouridine.
My final comments on the article,
As I’ve written in COPTIGATE - THE WORST DESIGN FLAW IN HUMAN HISTORY THAT IS IMPACTING YOUR HEALTH, the answer to the question “If an engineering design flaw exists and no one measures it, can it really injure people or kill them?” is no, because no one from the regulatory authorities which are supposed to perform these measurements are doing what they are supposed to do.
Not only the codon optimisation technology used in the experimental gene therapy was known to be problematic and yet was not evaluated for the risk it introduced, the decision to use N1-methylpseudouridine as uridine (U) substitution has introduced more risks which the medical regulators across the world seems to have decided they don’t need to measure.
For me, as someone who spent his whole professional career managing risks, I find the medical regulators behaviour to be nothing short of criminal. The institutes that are supposed to protect us from pharmaceutical products that can harm us has made a conscious decision to ignore risks which can harm human lives, and this makes them not fit for purpose. No one should trust any statement that comes from them, especially when these statements are about the safety and efficiency of pharmacological products.
Farewell, Andrew
Allow me to end this post by saying goodbye to one of my musical heroes, Andrew Woolfolk, the legendary saxophonist of Earth Wind and Fire, who has passed to a better world on the 24th of April 2022, at the age of 71, after battling for 6 years with an illness.
Andrew Paul Woolfolk II was born on October 11, 1950, in Denver, Colorado. He was a year older than Philip Bailey (the lead singer of Earth Wind and Fire), and like Larry Dunn, the legendary keyboardist of Earth Wind and Fire, all three has studied in Denver’s East High School.
While Philip Bailey joined EWF in the early stage of the band, Andrew joined later, when the band’s original horn player, Ronnie Laws, wanted to pursue a solo career. His contribution to the unique sound of the band will forever echo in the hearts of anyone who ever heard its music.
If you want to understand what a genius Andrew Woolfolk was, just listen to this EXTREMELY RARE live recording from 1976, which starts with words of the late Maurice White, the man who created Earth Wind and Fire:
"This is a song all about the world; all about you and I; all of us. THIS SONG CAN SET YOU FREE, so we're going to ask you to sing along, with a feelin’. Right now, we'd like to feature mister Andrew Woolfolk, check him out…"
Andrew’s solo sax solo starts straight after that. It was never captured in any other recording of the band. I invite you to open your heart, close your eyes, listen, and allow the music to set you free…
REST IN PEACE Andrew Woolfolk.
That’s it for today. Until the next now…
I am the LOVE that is YOU.
Ehden
Savour the real percussion. No drum machines which, so soon after this, displaced rhythm in so many bands.
Love the sax, but I first noticed the human in the rhythm syncopation.
How do incomplete RNA fragments (comprising about 40% of the total RNA) in the jabs interact with microRNAs?
Do these RNA fragments generate shorter proteins, and what's their effect?