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Spartacus's avatar

I've given this some thought. A few things:

-SARS-CoV-2's E and 3a proteins act as calcium ion channels. Intracellular calcium influx is an essential part of the life cycle of coronaviruses, and basically all severely-ill COVID-19 patients have noticeable hypocalcemia. This is very likely why Vitamin D repletion seems to help; it pumps calcium back out of cells. If Vitamin K is taken as well, it fixes the excess calcium in bone and teeth.

-SARS-CoV-2's disruption of ACE2 also disrupts the kallikrein-kinin system. ACE2 normally breaks down des-arg9-bradykinin (DABK). As SARS-CoV-2 fuses with ACE2, the DABK starts building up, and when it acts upon the bradykinin receptor, it promotes arachidonic acid release and intracellular calcium pathway activity, which leads to isoprostane formation, superoxide release, and severe oxidative stress.

-COVID-19 causes intussusceptive angiogenesis:

https://www.sciencedirect.com/science/article/pii/S2531043721001604

Look up how SARS-CoV-2 uses neuropilin-1 as a secondary host factor:

https://www.science.org/doi/10.1126/science.abd2985

Then, look at the relationship between neuropilin-1 and transforming growth factor beta, and the relationship between TGF-β and vascular endothelial growth factor (VEGF):

https://pubmed.ncbi.nlm.nih.gov/18436584/

https://www.nature.com/articles/s41467-021-22210-3

As for radiation injury, I have spoken with PhD biologists and virologists on this, including a guy who works for NASA, analyzing the effects of cosmic radiation on the health of astronauts, and he straight-up admitted to me, well over a year ago, that the pathways of COVID-19 injury, as I'd described them to him, resembled the effects of radiation injury. Walter is on the right track.

Basically everyone who suffers from severe COVID-19 has a noticeable dip in nitric oxide and an increase in nitrotyrosine:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8106525/

Nitrotyrosine is mostly formed when peroxynitrite nitrates tyrosine to make it. It's basically proof positive that nitric oxide is being consumed in a reaction with superoxide. This has a very close relationship to what Martin L. Pall terms as "NO/ONOO- Disease":

https://www.clinicaleducation.org/resources/reviews/how-can-we-cure-noonoo-cycle-diseases-a-review/

This is a vicious cycle where peroxynitrite (ONOO-) uncouples endothelial nitric oxide synthase (eNOS) by destroying the BH4 cofactors needed for eNOS to synthesize nitric oxide. Uncoupled eNOS produces more superoxide instead of nitric oxide, which reacts with any available nitric oxide to form peroxynitrite, which uncouples more eNOS enzymes, which produce more superoxide. This goes in a loop until all the nitric oxide is gone.

In COVID-19, this is a bad thing, because SARS-CoV-2's replication is directly inhibited by nitric oxide. It is as if the virus is trying to force cells to form radicals to get the nitric oxide out of its way. This is also true of SARS-CoV:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7111989/

Peroxynitrite has no beneficial effect against the Spike. As soon as the nitric oxide is all gone, the virus starts replicating even faster. This is the fundamental reason why SARS-CoV-2 affects people with pre-existing endothelial dysfunction (obese, diabetic, hypertensive, and/or aged, etc.) before everyone else. Their vascular endothelial tissue is already teetering on the edge. COVID-19 comes along and pushes them off the cliff.

To make matters worse, SARS-CoV-2 actively inhibits the Nrf2 pathway:

https://www.nature.com/articles/s41423-022-00887-w

When I had COVID-19, I took NAC, curcumin, resveratrol, quercetin, Vitamin D, Benadryl, and Pepcid. The latter two are not just histamine blockers, they're powerful antioxidants and inhibitors of the Fenton reaction. I'm basically fine.

There is a very significant rationale here for antioxidants and Nrf2 activators to be a standard part of every COVID-19 treatment regimen.

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Aion's avatar

Do you have some recipes you'd like to share?

I'm trying to build a cookbook from different sources.

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