Montgomery, et al. Publish an Article Supporting What I Hypothesized Two Years Ago – SARS-CoV-2 Causes Demyelination

This article provides additional evidence supporting my hypothesis that demyelination may be a reason behind the staggering increase in Sudden Cardiac Deaths.

It was early in the pandemic, and it was a hunch. I had known that human coronaviruses could be neurotropic – and that the Spike was to blame.

The respiratory involvement of HCoV has been clearly established since the 1960s. In addition, for almost three decades now, the scientific literature has also demonstrated that HCoV are neuroinvasive and neurotropic and could induce an overactivation of the immune system, in part by participating in the activation of autoreactive immune cells that could be associated with autoimmunity in susceptible individuals. Furthermore, it was shown that in the murine CNS, neurons are the main target of infection, which causes these essential cells to undergo degeneration and eventually die by some form of programmed cell death after virus infection. Moreover, it appears that the viral surface glycoprotein (S) represents an important factor in the neurodegenerative process.

Neuroinvasive and Neurotropic Human Respiratory Coronaviruses: Potential Neurovirulent Agents in Humans
https://pmc.ncbi.nlm.nih.gov/articles/PMC7121612/

This is obvious and goes without saying – why were we so repeatedly reassured that SARS-CoV-2 was, overall, a “mild respiratory” disease?

From Day One, I was absolutely certain this virus was from the Wuhan lab, and that it was almost certainly part of a bioweapons research program. Therefore, I assumed the worst from it. As readers of this Substack know, I never gave it a Planck length.

I believed the virus was neurotropic and its Spike could eventually invade the brainstem. So, I began searching for sudden deaths in Italy and later the United States during the summer of 2020. What I found was astounding. So many individuals under thirty Dying Suddenly. I posted lists of the death notices on X. Of course, this was not talked about...

Then, in August of 2022, I was finally able to concretely determine a mechanism by which the Spike Protein could cause Sudden Cardiac Death by an assault on the brainstem. This was through demyelination. I arrived at this finding by studying Multiple Sclerosis.

Cardiovascular autonomic dysfunction is not uncommon in multiple sclerosis (MS) and is related to the involvement of the vegetative areas of cardiac innervations in the medulla oblongata. It has been suggested that this may contribute to the occurrence of sudden death in MS. In this case report, we present a patient with active relapsing–remitting MS who died unexpectedly due to the sudden onset of cardiac arrythmias. Post-mortem examination showed the presence of active demyelinating lesions in the medulla oblongata. As far as we know, this is the first case report clearly linking sudden cardiac death to active MS on the histopathological level.

Sudden cardiac death in multiple sclerosis caused by active demyelination of the medulla oblongata
https://journals.sagepub.com/doi/10.1177/1352458511408476

This would fit, as the Spike had been found in the brainstem at autopsy.

More convincingly, in another autopsy study of deceased COVID-19 patients, SARS-CoV-2 RNA and proteins (nucleocapsid or spike) were detected in 50% and 40% of brainstem samples, respectively.36 Similarly, another autopsy study has found SARS-CoV-2 RNA and spike proteins in the olfactory mucosal-neuronal junction and brainstem’s medulla in 67% and 19% of samples, respectively.37 In sum, these autopsy studies have provided evidence for SARS-CoV-2 tropism from the olfactory system into the brainstem.

Persistent Brainstem Dysfunction in Long-COVID: A Hypothesis
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7874499/

But this was all hypotheses. I needed evidence that the virus was actually causing demyelination. A paper published on November 29^th definitively shows a direct causal association between SARS-CoV-2 infection and demyelination. It has arrived.

There is evidence from this study of associations of SARS-CoV-2 infection with CNS demyelination (the extent to which this is a causal association requires more evidence), but there is a question over whether the pandemic will have an influence on future risk beyond what is reported here. There is typically a 10–20-year duration between exposure to an environmental risks factor, including acute infections6-8 and other exposures,24,25 and a multiple sclerosis diagnosis. It should however be noted that the vast majority of those who go on to develop multiple sclerosis do not have a diagnosed demyelinating event or other evidence of early multiple sclerosis onset in the years immediately following infections or other environmental exposures linked with multiple sclerosis risk.6,8,25 Given the possible CNS involvement in SARS-CoV-2 infection,26 there may be a possibility of future demyelinating disease diagnoses, but perhaps this will be largely among those with more severe COVID-19, as shown previously for other infections with direct or indirect access to the CNS.6,8,22

SARS-CoV-2 infection and risk of subsequent demyelinating diseases: national register–based cohort study
https://academic.oup.com/braincomms/article/6/6/fcae406/7909395?login=false

The authors rightly point out that for most, MS develops over a period of 10-20 years. Perhaps only a very susceptible few present with rapid demyelination while the process may be slowly developing in a larger (much?) number.

This fits in with a larger observation of mine. That we should not dismiss SARS-CoV-2 and its Spike quickly. I see it as potentially being a Short-, Medium- and Long-Term devastator.

CODED TO KILL: A SHORT-RANGE, MID-RANGE AND LONG-RANGE CELLULAR WEAPON
https://wmcresearch.substack.com/p/coded-to-kill-a-short-range-mid-range

Indeed, we are confronted with significant obstacles by this virus and its proteins. That does not mean they are insurmountable. We continually find therapeutics. I will continue to search for them.

As always, thank you for your readership, dialogue and support. I will continue to study and report back to you so we may all understand and find paths to healing.