Til Death Do You Part: The Spike Protein and Chronic Stress: The Key Behind the Observed Accelerated Aging?

More than ever, we must determine not Viral Load, but Spike Load in the population – and is the Spike retrotranscribing?

This is my most important work to date.

A Tweet sent by a doctor I greatly admire caused me to go into a deep think. He gave a Sympathetic Ganglion Block to two related individuals who experienced loss of taste and smell post Delta. The treatment restored 95% of function – INSTANTANEOUSLY. This rang bells on two fronts. First, confirmation that the effects of the disease (read Spike) are genetic. And second, more importantly, the instantaneous response I believe indicates that there is a Chronic Stress Response being induced by the Spike Protein. I am concerned that the Block may be covering a chronic stress response. Not to take away from the curative actions of the treatment, but I believe we need to look at this phenomenon very closely.

The reason for this concern is that Sympathetic Nerve Blocks are used in treating pain and chronic stress responses.

The sympathetic autonomic nervous system (SANS) is spatially and pathophysiologically related to both acute and chronic pain. Acute generalized sympathetic activation, as occurs with the stress response, can temporarily increase the nociceptive threshold via a combination of neural and endocrine effects.

Sympathetic Nerve Block
https://www.ncbi.nlm.nih.gov/books/NBK557637/

There is ample evidence that the Spike Protein induces a tremendous stress response. In fact, this was known about the Spike Protein of SARS-CoV back in 2007!

In this study, it is demonstrated that lytic MHV and SARS-CoV infection can induce ER stress responses and Cxcl2 mRNA induction. We hypothesize that CoV spike protein-mediated ER stress can initiate the transcription of chemokine genes based on the following observations: (i) MHV and SARS-CoV induced ER stress and upregulated chemokine mRNA levels during infection; (ii) ER stress and chemokine mRNA upregulation were both induced only by spike expression, and their expression occurred simultaneously; (iii) ER-retained MHV spike was sufficient to induce Cxcl2 transcription.

The Coronavirus Spike Protein Induces Endoplasmic Reticulum Stress and Upregulation of Intracellular Chemokine mRNA Concentrations
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2045536/

Indeed, it is also true for the Spike Protein of SARS-CoV-2.

When dissecting the corresponding networks, we identified significant changes primarily in genes associated with the cellular stress response. This includes metal ion homeostasis, the cellular oxidation–reduction process, and NF-κB signaling-associated genes.

Long-lived macrophage reprogramming drives spike protein-mediated inflammasome activation in COVID-19
https://www.embopress.org/doi/full/10.15252/emmm.202114150

Then everything came into focus. And this fits in perfectly with everything else myself and others have discovered about Spike Protein pathology. All the mechanisms and pathways are intimately associated with the Stress Response. And it really does make sense.

People exposed to chronic stress age rapidly. The telomeres in their cells of all types shorten faster. Inflammation is another important feature of stress that, along with aging, accounts for the phenomenon of inflammaging. In addition to aging itself, inflammaging can contribute to the development of several pathologies, including atherosclerosis, diabetes, hypertension, and others. Oxidative stress is one of the main mechanisms related to stress. Oxidative stress is caused by the over-production of reactive oxygen species (ROS) that can damage various tissues. The main source of ROS is mitochondria. Being suppressed by mitochondrial mutations, mitophagy can aggravate the situation. In this case, the aging-specific pro-inflammatory changes are amplified. It happens because of the inability of cells to maintain the normal state of mitochondria. Macrophages are the crucial element of the innate immunity associated with the chronic inflammation and, subsequently, with the inflammaging. In this review, we focus on the therapy approaches potentially reducing the deleterious effects of oxidative stress. These include stimulation of mitophagy, activation of mitochondrial uncoupling, induction of the expression of the telomerase catalytic component gene, and use of antioxidants. Any method reducing oxidative stress should improve post-traumatic stress disorder.

The Link between Chronic Stress and Accelerated Aging
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7400286/

We MUST determine circulating Spike in those with COVID, Long COVID, Vaccinated, Unvaccinated and the Healthy. It is absolutely critical. Also, we must determine if the Spike is retrotranscribing itself. If so, we need to find effective therapeutics. At the very least, we need to find a way to clear the Spike in those that have it circulating. If not, it will almost certainly be there – til death do you part.