Jul 17, 2022Liked by Walter M Chesnut

Walter, my deepest concerns lie with the fact that most doctors, do not know any of this. Because if they did, they would be prescribing alternative treatments from those currently being used such as covid boosters, remdesivir, paxlovid, intubation. Living in the UK. Majority of people here, brainwashed and believe more covid vaxx is better, mask mandates must be brought back, would be thrilled to see a return of lockdowns. And while we were distracted most recently with the resignation of Boris, and fearmongering about hot weather and told to stay indoors, the ONS published stats showing 91% of those who died in the UK between Jan and May ‘22, were triple vaxxed. I have an autoimmune disease. I requested a medical exemption. It was denied. My faith in the medical profession is zero.

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So basically, don’t catch it and don’t get vaccinated for it….it maybe too late for some, so moving forward,

A. if you’re not vaccinated but you’ve had covid and recovered…what should you do?

B. If you’re vaccinated but haven’t had covid…what should you do?

C. If you’re vaccinated and had covid…..what should you do?

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I’ll have to study this. Thank you. Just a thought, vaccine induced viral immune escape variants x vaccine induced cytokine storm x down regulation of the immune system and DNA repair x ADE. Gain of function spike protein in virus and vaccine. They knew all along.

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Jul 17, 2022Liked by Walter M Chesnut

Walter - This reminds me of the Mast cell connection to Covid or more accurately the PGE2-EP2-mast cell axis.

“Role of Janus kinase 3 in mast cell-mediated innate immunity against gram-negative bacteria”




Because TLR2 is involved in mast cell activation against infections - “TLR2 Regulates Mast Cell IL-6 and IL-13 Production During Listeria monocytogenes Infection”


EP2 is involved in inflammation

Eg. UVB -

PGE2-EP2/EP4 signaling is mandatory in UV-induced acute skin inflammation


EP2 reduces fibrosis - “Activation of the prostaglandin E2 EP2 receptor attenuates renal fibrosis”


EP2 is involved in amyloidosis -“Prostaglandin E2 Stimulates the Production of Amyloid-β Peptides”


EP2 reduces ferroptosis - “COX-2/PGE2 Pathway Inhibits the Ferroptosis Induced by Cerebral Ischemia Reperfusion”


EP2 acute and chronic inflammation - “PGE2 induces acute inflammation through mast cell activation via the EP3 receptor. PGE2 also induces chronic inflammation and various autoimmune diseases through T helper 1 (Th1)-cell differentiation, Th17-cell proliferation and IL-22 production from Th22 cells via the EP2 and EP4 receptors”


EP2 - immunosuppression - “PGE 2-EP2/EP4 signaling elicits immunosuppression by driving the mregDC-Treg axis in inflammatory tumor microenvironment”


EP2 - senescence/ageing - “The cyclooxygenase-2-prostaglandin E2 pathway maintains senescence of chronic obstructive pulmonary disease fibroblasts”



Autoimmunity via EP2 regulation of Th17 - “Prostaglandin E2 regulates Th17 cell differentiation and function through cyclic AMP and EP2/EP4 receptor signaling”



The actions of PGE2 and EP2 can be viewed as physiologically protective as they help to reduce DRP1 mitochondrial fission


“EP2 prostanoid receptor agonism coupled with protein kinase A activation attenuated mitochondrial fission in PAH PASMCs by inhibiting the activating phosphorylation of DRP1 whilst inducing its inhibitory phosphorylation”

But, they can also be pathological - eg cancer

PGE2 regulates fever, kidney function, pain, mucosal integrity, blood vessel homeostasis, and inflammation. In pathological conditions, as in cancer, PGE2 is produced by cancerous stromal cells and enhances tumor cell proliferation and survival, promotes angiogenesis, and induces metastasis


And neurodegenerative

“PGE2 directly induces neuronal death through activation of the E-prostanoid (EP) 2”


And also as an alternative pathway for ADE - “Infants with multisystem inflammatory syndrome in children (MIS-C) associated with COVID-19 may also have ADE caused by maternally acquired SARS-CoV-2 antibodies bound to mast cells.”


So, how does this link in with FcγRIIB?

FcγRIIB is expressed on Mast cells along with other cells of the immune system and (excluding B cells) reduces phagocytosis and pro-inflammatory cytokine release.

and it is thought -

“This diversity of its expression and function underlies the importance of FcγRIIB in regulating defence against infection and susceptibility to autoimmune disease”.


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In a recent interview, Paul Marik (FLCCC) noted that the spike protein inhibited/interfered with autophagy (eating of the cells to process the debris). Some other research shows that the PASC (long covid via infection or vax) is likely the result of the persistence of spike protein.

Marik suggested that early treatment and nutraceuticals, as well as intermittent fasting, stimulate autophagy and promote viral cleanup.

All in all, it seems to me that, outside of living in a bubble, the best thing one can do is promote one's innate immune system, possibly with the of use nasal washes to limit viral load (thus minor exposures will train the innate aspect without overloading it).

Everyone's reaction is going to be different, though. I, personally had a sucky case of it (technically mild/moderate), but got early treatment (well, a little delayed) but it cleared up nicely. My second full exposure, half a year later, from 2 vaxxed coworkers (with their 2nd and worsened infection) resulted in no more than a slight sniffle for me and feeling not so great for one day. I have returned to using the iodine nasal rinse, here and there after a full day, just to tamp things down but I'm not going to live in a bubble or wear a respirator (or a cloth mask). That's just not worth it, to me.

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FC Receptor binds Antibody--Infected cell complex -----> Antibody-mediated Phagocytosis , also of brain

In other words, self-cannibalism

Cannibalism -- Prion / Amyloid

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So basically, all but the 5% who’ve never been exposed to the spike protein are doomed? Would one of you brilliant folks translate for those of us who are not in the scientific/medical field, please?

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Some heavy duty biology here -

Ok JJ ( Couey ), can you help all us layfolk out here, please ?

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Walter, what do you think about getting monoclonal antibodies then? Likely bad news from what I’m reading. What to do to try and remedy this?

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Nice work Walter!

Niacin would be quite promising here. Be well.

"niacin treatment remarkably reduced the expression levels of these MPO, IL-1β, IL-6, and TNF-α

Activation of GPR109A significantly promoted the formation of autophagic lysosomes

These results indicate that GPR109A mainly promotes autophagy through AMPK"


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Thanks, Walter for your written every word since early of 2020! It has been helping me a huge for understanding the spike protein as a major toxin. So far, antidotes are the only way for either infected or vaccinated person, I think.

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Thanks Walter! 💕 Are all the viral spike immune complexes also on the mRNA injection spike?

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practical implications. how to influence T helper 1 vs T helper 2 immune response. lactoferion?, licorice?, path to the stimulation of early interferon response? All I understand says says avoid the development of antibodies. Simple protocols, few realize, salt, iodine, baby shampoo, baking soda, ethanol, licorice, dandelion, basic eye protection and eye wash and eye anti-viral, sprays and nebulization real N95+ "masking" keep it out kill what gets in. tragedy for the many

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Adam Gaertner spoke a lot about prion disease early on. He has a lot of info on treatments including vitamin D2, nattokinase, methylene blue, etc

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Saw a report that Johns Hopkins claims we can be vaccinated 'without our knowledge' by the PCR test. Can they be trusted? Who knows.

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