HOW'S YOUR TELOMERES - THE PRIMARY CAUSE OF PANDEMIC DEATHS IGNORED BY GOVERNMENTS

It's strange how life has a way of circling back. Some twenty, twenty-five years ago, when I was exploring business opportunities, I zoomed in to two specific areas -- nanotechnology and vanity products. Both now seem to feature in my current interest in trying to understand the global mess of the pandemic and vaccines. I mentioned in some older blogs my earlier understanding of nanotechnology helped me speed up my understanding of the novel genetic vaccines. In vanity products I wasn't searching for the plain vanilla types, but novel nanotechnology-based ones. There were several products which were just breaking into the markets, but lack of capital fundings eventually derailed my efforts.

In vanity products, I was searching for some new approach to anti-ageing. That got me on the trail of the fountain of youth, which I understood at the time, to be any breakthrough technology that can lengthen our telomeres.

First, let me bore you with some simple backgrounder on cell biology which is a prerequisite. DNA (Deoxyribonucleic acid) is a string-like molecule packed into a structure called chromosomes. DNA is a polymer composed of two polynucleotide chains that coil around each other to form a double helix. The DNA carries 4 nucleotide bases that form the genetic code of a person. The telomeres are the compounds at the end of the DNA chain. Look at telomere as the metal clips at the end of a shoe string. The telomeres protect the DNA chain from snipping off or fusing with the ends of other DNA strains and corrupting both. The chromosome lies in the nucleus of a cell. There are 46 chromosomes in each cell, half inherited from mom and half from dad.

We are all made up of cells. There are about 37.2 trillion cells in each person. Old cells die off and are replaced by new cells all the time. Cells replicate by division. One cell will divide itself into two exactly similar cells. We are growing when more new cells are created than cells replaced. We begin to age when our body stop producing new cells.

In cell duplication process, telomeres play a very important role in ensuring integrity of genetic code. With each replication, the telomeres get shortened until it is no longer able to divide. The cell is then said to reach a state of senescence. That is when a cell ages and permanently stops dividing but does not die. Over time, large numbers of old (or senescent) cells can build up in tissues throughout the body. It is the process of growing old. That as a person ages, the telomeres are shortened is not up for argument. It is an established fact. Telomeres is like our biological clock. It will run out one day.

So the fountain of youth rests with a product that will continue to restore telomeres and thus stops or slows down the aging process. The good news is there is a natural enzyme produced by our body called telomerase. This restores telomeres to the DNA chain which then helps cell division again. The bad news is telomerase does not express in somatic (body) cells but in reproductive cells. On the other hand telomerase expresses in cancerous somatic cells thus promotes the runaway multiplication of malign cells.

Shorter telomeres, more diseases

The length of telomeres sort of establishes a person's biological age. Actually, the biological age of a person's specific organ, depending on what type of cells are impacted. With ageing, comes lots of associated diseases. Many studies and tests have long since established shortened telomeres to various diseases. For example :

- People with shortened telomeres have lower life expectancy and higher risks of contracting infectious diseases, ie they have diminished immune system. Richard M Cawthon et el 2003 (Ref #1).
- People with hypertension has shorter telomeres. This proves a relationship of shortening telomeres to cardiovascular and heart diseases. Zhiwei Yan et el 2009 (Ref #2)
- People with short telomeres are more predisposed to myocardial infarction and vascular disorder. Robert Zee et el 2009 (Ref #3)
- Short telomeres is also a marker of bone aging. People with low telomeres are more inclined to develop osteoporosis.  A. M. Valdes et el 2009 (Ref #4).
- Shortened telomeres lead to dysfunction in cell division, genetic instability, cell damage and cancer development. Subjects with shortened telomeres develop significant cancers. Xifeng Wu et el 2003 (Ref #5)
- When the length of telomeres reaches the critical limit while cell division is still going one, the automatic activation of the DNA repair mechanism in the cell leads to genomic instability conducive to oncogenesis (formation of cancer). Joo-Shik Shin et el 2006 (Ref #6)

What has telomere shortening got to do with Covid 19?

Now to bring all these home to the pandemic and mRNA vaccines.

In this pandemic, we are introduced to the spike proteins which comes naturally from the SARS-Cov2 virus and artificially from the mRNA and modified adenovirus vaccines. We are also seeing (1) 'blood clots', (2) excess deaths, and (3) Sudden Death Syndrome.

The high incidence of massive clots reported by morticians are not actually blood clots, but some goovy protein built-up as byproducts of the lipids in the delivery systems of the vaccines. There is evidence of  self-assembly of nano-particles of the delivery system. Scary stuff.

Excess deaths have increased all over the world, and SDS incidents have accelerated. Governments argue over the medico-legal ramifications and the framing of numbers to fit official narratives of dying 'from' or 'with' covid, and no one cares about the elephant in the room. There is a pot pourri of causes of deaths. But what is glaring whether dying with or from Covid, all the causes seem to be diseases of old age. We see young people dying of heart attacks, accelerated cancers, neurodegenerative diseases or other numerous diseases due to weakened immune systems of old age. Millions of older persons down with Covid are diagnosed with comorbidities when they reported not knowing having had such diseases.  

Many studies have long shown links between shortened telomeres with common respiratory viral diseases and infection risks. As early as Nov 2020 Manar Ahmed Kamal1 et el (Ref #7) has shown that Sars-Cov2  affect more males than females (women has longer telomeres less prone to attrition) and amongst men, those above 50 are more susceptible. 

Antoine Froidure et el in Oct 2020 (Ref #8) uncovered a link between telomere length and COVID-19 outcome.  A control group of 500 patients without Covid had longer telomeres. 70 Covid patients had shortened telomeres and the presence of very short telomeres (of size less than the 10th percentile for age) was associated with a significantly higher risk. admission to ICU or death.

In Jan 2021 oncologist Maria Blasco (Ref #9) confirmed Froidure et el's findings. They measured telomere length in peripheral blood lymphocytes from Covid patients aged 29 to 85 and found that shorter telomeres are associated with increased disease severity. 

The best confirmation came from  Carlo Gaetano et el in June 2021 (Ref #10) that proved the link between telomere shortening in Covid patients and the acceleration of biological age. The study measured the biological age of 117 Covid survivors and 144 uninfected volunteers. There was a significant increase in the biological age of patients who had Covid. A significant shortening of telomeres is observed in the post-covid cohort. ACE2 expression was decreased by 73% in post-covid patients. From the evidence they hypothesized that certain epigenetic alterations (means underlying changes in the cells) are associated with the post-covid state, especially in younger patients  (< 60 years old).

The question is, has the spike protein of SARS-Cov2 anything to do with this?

"I believe the Spike Protein is acting as a Progeria Drug – delivered via the Endothelium to all organs. I don’t know, yet, what to do. I am deeply saddened, and numb. No matter what evidence or hypothesis is presented – the band plays on….. And it is playing a funeral march." Walter M Chesnut (Researcher)

A Chinese medical team Yuyang Lei et el (Ref #11) showed in Mar 2021 that the main pathogen of the Covid-19 virus is its spike protein. The researchers isolated spike protein of the virus by installing it on an empty nucleus, then inoculated it into guinea pigs. The animals showed lesions in the lungs and arteries associated with inflammation of endothelial cells. But what about human beings? The team reproduced the in vitro experiment on healthy human endothelial cells. The result -- spike proteins bound to ACE2 receptors, damaging the cells' mitochondria, causing micro-thrombosis and endothelitis. Endothelial cells are the main type of cells found in the inside lining of blood vessels, lymph vessels, and the heart. The conclusions are clear: the Spike protein alone causes most of the symptoms of Covid-19.

This begs the question. How does the spike protein shorten the telomeres?

In our bodies are proteins called cytokine which are messengers running between cells to manage inflammation. A Covid infection activates massive cytokines, thus the term "cytokine storm'. Excessive cytokines cause oxidative stress. In simple terms, there is much bio-chemical work going on in our tissues and the body is stressed out trying to detoxify a lot of harmful reactive products. 

These two closely linked phenomena (chronic inflammation and oxidative stress) are the basis of most cardiovascular diseases (atherosclerosis, thrombosis, etc.), neurodegenerative diseases (Alzheimer's, Parkinson's, etc.), cancers, and also ageing. That means the telomeres are shortened. 

The link between oxidation and shortening of telomeres has long been established. There have been many studies and reports on this, eg Thomasvon Zglinicki 2002 (Ref #12). 

The spike proteins of SARs-Cov2 cause inflammation and associated oxidative stress. Oxidation is carried out by free radicals which are oxygen carrying molecules with uneven numbers of electrons. In the oxidation process, certain chemical bases are attacked, particularly guanines. If you refer to the feature image above, the GGG codes in the telomere refers to 3 consecutive guanines. The telomeres are rich in guanines, thus they are targeted, corrupted and shortened.

SARS-CoV2 infection results in the Covid syndrome which is characterized, in the worst case, by severe respiratory distress, pulmonary and cardiac fibrosis, release of inflammatory cytokines and immunosuppression. In the end, it is chronic inflammation which activates the coagulation phenomenon that ultimately causes death in patients with Covid. In effect, Covid is an inflammation and oxidative stress disease.

The $ million the question - do spike proteins of the vaccines shorten the telomeres?

In an opinion piece,  Luc Montagnier et el 2021 (Ref #13) published in France Soir on 30 Aug 2021, made a strong case that the spike proteins of mRNA and adenovirus vaccines are causing exactly the same inflammation and oxidative stress as the virus.

Luc Montagnier was a French virologist and joint recipient, with Françoise Barré-Sinoussi and Harald zur Hausen, of the 2008 Nobel Prize in Physiology or Medicine for his discovery of the human immunodeficiency virus (HIV). He had been a proponent of SARS-Cov2 being man-made from the very beginning and had been vocal in calling out the risks of the novel vaccines. It is no surprise his voice was shut out and testimony to the crusade against anti-vaccine voices is to be seen in the Wikipedia page on Montagnier which ends with "There is no evidence that SARS-CoV-2 was genetically engineered".  Montagnier passed away on 8 Feb 2022.

The spike proteins of the vaccines are made to be genetically similar to spikes of SARS-Cov2 and it is to be expected our body reacts similarly to them, causing the same inflammation and oxidative stress and shortening the telomeres. Vaccine manufacturers lied about the short life span of the spike proteins and that they remain in the vicinity of the deltoid region. Since then, it is known the spike proteins travel to various organs and remain in the body for months. It may jolly well be that millions in hospitals and thought to be down with Covid infection never had the virus but were suffering the same symptoms brought about by the vaccine spike proteins.

The evidence is clear that there is a primary cause for the high mortality brought about by both the Covid and vaccines. Yet governments all over the world choose to get lost in the pot pourri of causes, missing the wood for the trees. They stick to the narratives of big pharma-sponsored voices, turning a blind eye to those that show we are dealing with an approved toxic drug that kills with the inflammatory and oxidative stress diseases, and which shortens telomeres.

Progeria, also known as Hutchinson-Gilford syndrome, is an extremely rare, progressive genetic disorder that causes children to age rapidly. There is growing concern among scientists that the spike protein is causing accelerated ageing. A person may be 26 years old and looks like one, but walking around with a a biologically 90 year old heart, 60 year old kidneys, 50 year old uterus......  Walter M Chesnut is right. The novel vaccines are progeria drugs and governments are listening to the band playing a funeral march.

References :

#1      Association between telomere length in blood and mortality in people aged 60 years or olde by Richard M Cawthon et el (2003)

#2      Short telomeres and prognosis of hypertension in a  Chinese population by Zhiwei Yang et el (2009)

#3      Association of shorter mean telomere length with risk of incident myocardial infarction: a prospective, nested case-control approach by Robert Y L Zee 1, Sherri E Michaud, Soren Germer, Paul M Ridker (2009)

#4      Telomere length in leukocytes correlates with bone mineral density and is shorter in women with osteoporosis by A.M. Valdes et el (2007)

#5      Telomere dysfunction: a potential cancer predisposition factor by Xifeng Wu et el (2003)

#6      The role of telomeres and telomerase in the pathology of human cancer and aging by Joo-Shik Shin, Angela Hong, Michael J Solomon, C Soon Lee (2006)

#7      Sex and Age Differences in Telomere Length and Susceptibility to COVID-19  by Manar Ahmed Kamal1, Kareem Reda Alamiry and Mahmoud Zaki (N0v 2020)

#8     Short telomeres increase the risk of severe COVID-19  by Antoine Froidure et el (Oct 2020) 

#9     Shorter telomere lengths in patients with severe COVID-19 disease  by Maria A Blasco et el (Jan 2021)

#10    Evidence for Biological Age Acceleration and Telomere Shortening in COVID-19 Survivors  by  Carlo Gaetano et el (Jun 2021) 

#11    SARS-CoV-2 Spike Protein Impairs Endothelial Function via Downregulation of ACE 2 by Yuyang Lei et el 31 Mar 2021

#12    Oxidative stress shortens telomeres  by Thomasvon Zglinicki (Jul 2002)

#13    SARS-COV2 would accelerate biological age by Xavier Azalbert, Luc Montagnier et el 30 Aug 2021

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