Spike protein accelerates aging

at 21.12.2021
Reconstructing a complex puzzle consisting of numerous recent and older scientific articles and studies, it can be concluded that long-term exposure to the action of Spike protein, through repeated illness or vaccinations, annihilates the "longevity protein", Sirtuin 6, and progressively reduces telomers on our chromosomes. This phenomenon is responsible for the aggravation and intensification of existing pathologies or the generation of new ones, especially cancers and neurodegenerative diseases, inevitably leading to reduced life expectancy.
Sirtuin 6, or "longevity Sirtuin" [1], is a protein with essential functions in stopping and repairing DNA damage caused by oxidation. It recruits and mobilizes PARP1s [2], enzymes that give a "first response" role in the regeneration process, which detects damaged DNA and then chooses the optimal path to repair it. This avoids genetic instability and mutations. SIRT6 is also important in energy production, as it plays a role in oxygen consumption and ATP production and, as a result, in maintaining the integrity of telomeres. However, the ability to repair DNA decreases with age but can be improved by stimulating the SIRT6 protein. In fact, a recent study [3] by a team of Israeli researchers shows that by applying genetically engineered procedures, Sirtuin 6 can become a real fountain of youth, leading to a 30% increase in longevity.
On the contrary, disrupting its function can significantly reduce our lifespan. Without reliable Sirtuins 6, our body can no longer repair the DNA damage that we experience every day and which, in the disease states, intensifies enormously, especially in the case of SARS-CoV-2 disease. Recent studies suggest that the Spike protein, generated by SARS-CoV-2 or anti-COVID vaccination, epigenetically annihilates the SIRT6 protein, making our body unable to regenerate.

Sirtuin 6
Responsible for regulating vital biological processes associated with multiple senescences - including oxidative stress, glucose and fat homeostasis [4], inflammatory responses, autophagy, genome integrity, and telomere homeostasis [5] - Sirtuin 6 is essential for prolonging life. For this reason, its dysfunctions are involved in many types of aging-related diseases, such as neurodegenerative diseases, cancer, or cardiovascular disease. A recent study showed that SIRT6-deficient cynomolgus monkeys are delayed in development [6]. Another study shows that in Alzheimer's patients, SIRT6 exerts a protective function against the disease by maintaining genomic stability and preventing damage to brain DNA [7]. But SIRT6 is not only a key role in brain development. Moreover, its dysfunctions determine the appearance of neurodegenerative diseases.
In the case of cancer, SIRT6 is like a double-edged sword, playing a dual role - suppressing or stimulating the tumor, according to its type [8]. Protects against tumor growth by controlling the functions of DNA damage repair, genomic stability, cellular metabolic homeostasis, and apoptosis, and is also associated with poor clinical results through its enzymatic activity that regulates cancer progression (in hepatocellular and colon cancers) [9].
In the cardiovascular system, SIRT6 plays a protective role by ameliorating vascular endothelial dysfunction, delaying the formation of atherosclerotic plaques, and inhibiting cardiac hypertrophy and heart failure [10]. In addition, several studies have shown that SIRT6 is a major regulator of glucose metabolism homeostasis [11]. Thus, stimulation of this protein may be a promising strategy for attenuating diabetic cardiomyopathy and reducing myocardial vulnerability to ischemia-reperfusion injury in diabetic patients [12].
In contrast, SIRT6 protein dysfunction induces chronic inflammation, autophagy disorder, and telomere instability - cellular processes that can lead to the onset and progression of cardiovascular diseases, such as atherosclerosis, hypertrophic cardiomyopathy, and heart failure.

Transfection with Spike protein
Endothelial cells have been shown to become senescent when transfected with Spike protein. The phenomenon is not completely elucidated, but it is certain that it occurs, and the result is the epigenetic annihilation of Sirtuin 6 since the Spike protein of coronavirus can induce simultaneous double-stranded DNA ruptures by the massive formation of hydroxyl radicals, subsequently preventing their repair. The phenomenon may be related to the continued presence of Spike protein in the body by chronic SARS-CoV-2 disease or by injection with messenger RNA-based vaccines, which lead to the production of the full-length Spike protein. One consequence of this phenomenon is the inability of the body to repair the random DNA damage that we experience daily and that increases enormously in disease states, especially in SARS-CoV-2. Thus, there is a risk of cancer or neurodegenerative disease suddenly occurring.
An in-vitro study [13] by three American researchers in Missouri, published in the Journal of Virology this September, supports this hypothesis, showing that human epithelial cells infected with SARS-CoV-2 virus or transfected with Spike protein showed increased paracrine senescence and leukocyte adhesion in epithelial cells, with the release of inflammatory molecules related to the secretory phenotype associated with senescence.


In conclusion, corroborating the results of these studies, it appears that the persistent presence of Spike protein in the body may aggravate existing pathologies or generate new ones, especially cancers and neurodegenerative diseases, annihilating the body's ability to regenerate, which inevitably leads to an accelerating the aging process and shortening the lifespan.















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