SIRT6 – THE SPIKE PROTEIN’S MASTER TARGET

October 30, 2021

EXECUTION BY NATURAL DEATH

SIRT6 – THE SPIKE PROTEIN’S MASTER TARGET: THE ULTIMATE GOAL BEING TO STOP DNA REPAIR, RESULTING IN A MASSIVELY ACCELERATED (RANDOM AND UNTRACEABLE) NATURAL DEATH

One may view the actions of the spike protein by reversing a well-worn saying:

“If you give a man a fish, you feed him for a day. If you teach a man to fish, you feed him for a lifetime.”

The Spike prefers:

“If you stop a cell from repairing itself, it just dies. If you teach the host to stop repairing itself, you rob it of its lifetime.”

On May 31st of this year, researchers in Israel discovered the Fountain of Youth. They observed that SIRT6 controls the rate of healthy aging. If you increase this, the mice live for an average of THIRTY PERCENT LONGER. So, imagine 130 being the new 100. SIXTY being the new THIRTY! LITERALLY!

An interesting observation was also made by the team: “If we can determine how to activate it in humans, we will be able to prolong life, and this could have enormous health and economic implications."

Enormous implications, indeed. Clearly there are those who certainly DO NOT want Seven Billion people living an extra thirty years…

So, what happens if you REMOVE SIRT6? You guessed it. Very, very bad things happen. Especially death.

Without SIRT6 your body is unable to repair the DNA damage that we experience every day, and which is ENORMOUSLY increased in states of disease, particularly so in the case of SARS-CoV-2.

THE ENDOTHELIAL SENESCENCE CONNECTION

It has been established that endothelial cells become senescent when transfected with the Spike Protein. They have not determined WHY it happens, just that it DOES HAPPEN and the effects it has. I now know why it happens. The Spike Protein is epigenetically silencing SIRT6.

What does SIRT6 do, in addition to controlling DNA repair?

DNA Repair, Gene Expression, Telomeric Maintenance, Mitosis and Meiosis, Stem Cell Pluripotency and Differentiation (how cells obtain their specific functionality), Metablic Diseases (Diabetes, for example), Cancer, Immune Regulation, Stress Response, Senescence and Aging.

Everything COVID and Long COVID.

It has already been hypothesized that Sirtuins are implicated in COVID. In a paper on COVID and related Sepsis it was determined that Metformin may improve metabolic derangements, improve mitochondrial function, and decrease cytokine production. NAD+ boosters such as resveratrol, a naturally occurring polyphenol, found in red grapes and blueberries, activate Sirtuin activity and attenuate the NF-ĸB activity, improve endothelial function, and decrease microvascular inflammation.

SIRT1 is also implicated in COVID: COVID-19: NAD+ deficiency may predispose the aged, obese and type2 diabetics to mortality through its effect on SIRT1 activity

But, what are the possible long term implications? Organisms that are deprived of their natural SIRT6 have very, very short lifespans. Mice, for example, die within four weeks without SIRT6.

The Spike Protein may simultaneously induce dsDNA breaks through massive hydroxyl radical formation, and then prevent its repair. This rinse/repeat activity MAY be dependent on the CONTINUAL PRESENCE OF THE SPIKE PROTEIN. Does the Spike Protein cause a genome wide SIRT6 silencing on one exposure? Two? Need it be present to silence SIRT6? Or, will it eventually cause the certain silencing of SIRT6 over multiple exposures.

Is there a hormetic dynamic?

What would this potentially look like? The body unable to repair random damage. A fatal cancer or neurodegenerative disease would be induced completely untraceable to the Spike Protein, as it would be a “natural death.” Of course, we know better.

I conclude this post with an article from the Fourth Military Medical University, Xi’an, China:

SIRT6 in Senescence and Aging-Related Cardiovascular Diseases

Referenced/Related Papers

SIRT6 in Senescence and Aging-Related Cardiovascular Diseases

https://www.frontiersin.org/articles/10.3389/fcell.2021.641315/full

SIRT6, a Mammalian Deacylase with Multitasking Abilities

https://journals.physiology.org/doi/full/10.1152/physrev.00030.2018

Characterization of physiological defects in adult SIRT6-/- mice

https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0176371

SARS-CoV-2 Spike Protein Induces Paracrine Senescence and Leukocyte Adhesion in Endothelial Cells

https://journals.asm.org/doi/10.1128/JVI.00794-21?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%20%200pubmed

The sirtuins, oxidative stress and aging: an emerging link

https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC3629286/

SIRT6 protects human endothelial cells from DNA damage, telomere dysfunction, and senescence

https://academic.oup.com/cardiovascres/article/97/3/571/276051?login=true

Enfermedad del coronavirus(covid-19) y las sirtuinas

https://revistas.unc.edu.ar/index.php/med/article/view/28196/29899

Is nuclear sirtuin SIRT6 a master regulator of immune function?

https://journals.physiology.org/doi/abs/10.1152/ajpendo.00483.2020?journalCode=ajpendo

DNA double strand break repair, aging and the chromatin connection

https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC4887314/

Coronavirus (Covid-19) sepsis: revisiting mitochondrial dysfunction in pathogenesis, aging, inflammation, and mortality

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7410962/

SARS-CoV-2 Mediated Endothelial Dysfunction: The Potential Role of Chronic Oxidative Stress

https://www.frontiersin.org/articles/10.3389/fphys.2020.605908/full

The unbalanced p53/SIRT1 axis may impact lymphocyte homeostasis in COVID-19 patients

https://pubmed.ncbi.nlm.nih.gov/33578018/

COVID-19: NAD+ deficiency may predispose the aged, obese and type2 diabetics to mortality through its effect on SIRT1 activity

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7322475/

Israeli researchers increase life expectancy of mice by average of 30%

https://www.jpost.com/health-science/israeli-researchers-increase-life-expectancy-of-mice-by-average-of-30-percent-669723