-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.
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):
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:
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":
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:
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:
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.
Wonderful, thanks! "Covid19" does seem to be 5G related.
Regarding the neuropilin-1 - I will have to add to my list of receptors spike can mess with - I likened it to a master key that can break into two master keys. Pomegranate peel would be helping this issue then too by preventing the furin cleavage.
"Infection of these cell lines by the WT, but not the mutant, virus increased in the presence of NRP1, providing further evidence that NRP1 requires a furin-cleaved substrate for its effects (Fig. 2, E and F). " https://www.science.org/doi/10.1126/science.abd2985 *still reading
Martin L. Pall also believes that EMF can open voltage-gated calcium ion channels, which kind of makes this something like a binary bioweapon. Someone who is being blasted by a MASER experiences more rapid cellular calcium influx and a more severe infection. In short, EMF aids the virus:
The theme of the book is to be a sort of white magic compendium to combat the dark magic cast upon us.
The idea is to compile simple (or not) recipes to help people suffering through this (everyone). The idea would be to have a footing explaining the rationale behind the ingredients and any extra considerations.
My tapioca pudding at this stage of development is so good I shouldn't call it tapioca pudding because it is unlike the standard milky type. It is good for gut pain or colitis issues.
You are a load of information! Thanks! Curious would being suntanned be bad for few months in summer..( not burned red) and is using topical retinol for skin few times a week bad?
I think moderate exposure would be fine unless really sun sensitive, which you do learn whether you are or not. Too much sun leaves me feeling flu-ish later on. But I was tan last summer with no problem, I never got sunburnt maybe. My yard is very shady. I only get too much sun when errands on sunny days. The Retinoid Toxicity issue does not seem to happen to everyone but if you do have ME/CFS I would strong suspect it.
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.
Wonderful, thanks! "Covid19" does seem to be 5G related.
Regarding the neuropilin-1 - I will have to add to my list of receptors spike can mess with - I likened it to a master key that can break into two master keys. Pomegranate peel would be helping this issue then too by preventing the furin cleavage.
"Infection of these cell lines by the WT, but not the mutant, virus increased in the presence of NRP1, providing further evidence that NRP1 requires a furin-cleaved substrate for its effects (Fig. 2, E and F). " https://www.science.org/doi/10.1126/science.abd2985 *still reading
Martin L. Pall also believes that EMF can open voltage-gated calcium ion channels, which kind of makes this something like a binary bioweapon. Someone who is being blasted by a MASER experiences more rapid cellular calcium influx and a more severe infection. In short, EMF aids the virus:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3780531/
Yes, EMF can open voltage gated calcium channels. I've written about EMF risks before CoV - 2017. Magnesium would be protective. It is a calcium channel blocker. Nrf2 would help to. Rereading my posts is a trail of breadcrumbs about when I first learned something - Nrf2 is protective. https://transcendingsquare.com/2017/12/22/emfs-and-intracellular-calcium-magnesium-is-natures-calcium-channel-blocker/
Do you have some recipes you'd like to share?
I'm trying to build a cookbook from different sources.
I have some recipes on some of my sites. Not here on Substack necessarily.
What type of theme cookbook?
The theme of the book is to be a sort of white magic compendium to combat the dark magic cast upon us.
The idea is to compile simple (or not) recipes to help people suffering through this (everyone). The idea would be to have a footing explaining the rationale behind the ingredients and any extra considerations.
Oh, perfect. That has been part of my goal too, but I just haven't gotten that far yet. Adding recipes to my protocol I mean.
My tapioca pudding at this stage of development is so good I shouldn't call it tapioca pudding because it is unlike the standard milky type. It is good for gut pain or colitis issues.
You are a load of information! Thanks! Curious would being suntanned be bad for few months in summer..( not burned red) and is using topical retinol for skin few times a week bad?
I think moderate exposure would be fine unless really sun sensitive, which you do learn whether you are or not. Too much sun leaves me feeling flu-ish later on. But I was tan last summer with no problem, I never got sunburnt maybe. My yard is very shady. I only get too much sun when errands on sunny days. The Retinoid Toxicity issue does not seem to happen to everyone but if you do have ME/CFS I would strong suspect it.
Here's another one that's right up your alley
Human gut bacteria produce Τ Η 17-modulating bile acid metabolites
https://www.nature.com/articles/s41586-022-04480-z
good stuff Jennifer, thanks!
found this one the other day you might find interesting
PMID: 33254555
COVID-19: Endogenous Retinoic Acid Theory and Retinoic Acid Depletion Syndrome