First case of postmortem study in a patient vaccinated against SARS-CoV-2

[md_a]

Thanks for this @md_a! I haven’t spoken to you in a while but you have always got such great finds. I for one appreciate the help in understanding.
So what I am getting from this (and please do correct if I am wrong as an expert on this I am not by any stretch of the imagination this is what I feel I am contributing to the forum the average guy who knows very little but is not afraid to ask questions)
Cascara segrada would provide a source of emotion which would help prevent the spike proteins spread via transmission bind to the ACE2 receptor and perhaps detox (for lack of a better term) it from our system or at least help move it on the ejection side of things?
Is there a reference to possibly the pine needle tea mentioned earlier in another thread the word polygonaceae seems familiar but I could be wrong.

Your reasoning is correct. Emodin can also be obtained from aloe vera, as a drink without side effects. I gave this example with emodin, but there are several substances in their natural state that have this effect. The sun, vitamin B1, cocoa, ... decrease Ang II. I don't know anything about pine needle tea.

The most common complication leading to the CoV-induced mortality can be justified through ACE-AngII-AT1-Spike protein overactivation caused by virus / toxin / antiviral drugs

The spikes protein have high affinity to ACE2, uses ACE2 to enter a cell.
It is suggested that this “occupation” of the virus of ACE2 might reduce the ability of Ang II to bind to ACE2.

Accumulated Ang II result in an increased activation of AT1.

Activation of AT1 results in vasoconstriction, increased pro-inflammatory response.


.........

Ray:
The virus uses ACE2 (angiotensin converting enzyme 2) as receptor and enters cells by the angiotensin receptor. Losartan (recommended in China), an angiotensin blocker, is effective protection, and has many other antiinflammatory effects. The Chinese also have good results with cinanserin, a serotonin blocker. I think cyproheptadine might help, too. Progesterone lowers the angiotensin receptor, but doesn’t act immediately as losartan does.

“The virus activates the angiotensin receptor (AT1), so the receptor blockers are protective—losartan, telmisartan, etc. Progesterone is a natural inhibitor of that receptor. Also the usual antiinflammatory things, aspirin, eggnog, orange juice would be helpful.” Ray Peat


...the angiotensin converting enzyme is one of the early parts of our immune system that sets up an inflammatory reaction that will set in action a whole chain of events, if the pathogen gets trough and is actually a treat, then you activate this proteolytic protein that create angiotensin witch is like a transmitter of a panic reaction to the organism, and it happens this coronavirus is able to bind to one of this angiotensin converting enzymes, there is one with is only pro-inflammatory and the other one that backs that up, which undoes, inhibits the inflammatory damage done by the first angiotensin producing enzyme, this is called ACE2, and ACE2 happens to be attacked by this particular virus witch binds to that enzyme, and that’s receptor its vulnerable point of organism as far this fire is concern, and binding to that ACE2 means that it leaves the ACE1 which produces angiotensin, it leaves that free to act, and ACE2 is capable in inactivating angiotensin breaking down to the first seven amino acids, they call it angiotensin 1-7, and this is a defensive anti-inflammatory peptide, so if your ACE2 is knocked out, angiotensin has a free range to cause damage, so the virus increases the inflammatory reaction by sticking to the defensive enzyme, and that enzyme combined with the virus, than acts to enter the cell by way of the angiotensin receptor which is called the AT1, that are two known receptors by which angiotensin can do damage. Angiotensin 1 is strictly an inflammation producing system, the angiotensin 2 produces somewhat defensive reactions, but it happens that the virus enzyme combination entering the cell by way of angiotensin receptor 1, AT1, and that turns on a whole range of destructive processes, nitric oxide, serotonin for example. And, so, just looking at the effects, its obvious you can defend by anything that defends you against nitric oxide and serotonin, so anti-inflammatory things are the known treatment for this kind of virus that Chinese for years have been using, cinanserin which is a serotonin blocker for other treatments, and they find that is helpful for people with the established respiratory corona infection, and losartan witch is high blood pressure drug is the most well-known blocker of angiotensin 1 receptor.. losartan is cheap and widely available. - Ray Peat
...........

The mechanistic overview of SARS-CoV-2 using angiotensin-converting enzyme 2 to enter the cell for replication: possible treatment options related to the renin–angiotensin system

Abstract

The SARS-CoV-2 pandemic is a healthcare crisis caused by insufficient knowledge applicable to effectively combat the virus. Therefore, different scientific discovery strategies need to be connected, to generate a rational treatment which can be made available as rapidly as possible. This relies on a solid theoretical understanding of the mechanisms of SARS-CoV-2 infection and host responses, which is coupled to the practical experience of clinicians that are treating patients. Because SARS-CoV-2 enters the cell by binding to angiotensin-converting enzyme 2 (ACE2), targeting ACE2 to prevent such binding seems an obvious strategy to combat infection. However, ACE2 performs its functions outside the cell and was found to enter the cell only by angiotensin II type 1 receptor (AT1R)-induced endocytosis, after which ACE2 is destroyed. This means that preventing uptake of ACE2 into the cell by blocking AT1R would be a more logical approach to limit entry of SARS-CoV-2 into the cell. Since ACE2 plays an important protective role in maintaining key biological processes, treatments should not disrupt the functional capacity of ACE2, to counterbalance the negative effects of the infection. Based on known mechanisms and knowledge of the characteristics of SARS-CoV we propose the hypothesis that the immune system facilitates SARS-CoV-2 replication which disrupts immune regulatory mechanisms. The proposed mechanism by which SARS-CoV-2 causes disease immediately suggests a possible treatment, since the AT1R is a key player in this whole process. AT1R antagonists appear to be the ideal candidate for the treatment of SARS-CoV-2 infection. AT1R antagonists counterbalance the negative consequences of angiotesnin II and, in addition, they might even be involved in preventing the cellular uptake of the virus without interfering with ACE2 function. AT1R antagonists are widely available, cheap, and safe. Therefore, we propose to consider using AT1R antagonists in the treatment of SARS-CoV-2.

Conclusion

Because SARS-CoV-2 enters the cell bound to ACE2, which induces ACE2 deficiency at the cell membrane, AngII is persistently activated. Increased AngII induces activation of AT1R, causing more uptake of SARS-CoV-2 and increasing ACE2 deficiency, thus maintaining and exacerbating a non-specific immune response, consisting of cytokine-induced inflammation. This non-specific immune response is an attempt to reduce the viral load, while the specific immune response is mounted. Unrestrained AngII eventually causes death by respiratory distress induced by excessive inflammation and its deleterious effects on other organs. Therefore, SARS-CoV-2-induced mortality is promoted by three mechanisms: (i) increased AngII induces endocytosis of ACE2-bound SARS-CoV-2, leading to ACE2 deficiency and viral replication; (ii) ACE2 deficiency prevents the priming of an adaptive immune response by lack of NO; and (iii) Ang II induces an increase in viral load leading to an increased innate immune response and a further increase in AngII levels. Therefore, treatments should aim at preventing the AngII ‘storm’ in an early phase of the infection, restoring the modulation of NO, and preventing the entry of SARS-CoV-2 into the cell. All these mechanisms are targeted by AT1R antagonists. They may reduce morbid inflammatory distress and provide an environment to facilitate an effective, virus-specific adaptive immune response.

The mechanistic overview of SARS-CoV-2 using angiotensin-converting enzyme 2 to enter the cell for replication: possible treatment options related to the renin–angiotensin system



………


[6]-gingerol: a novel AT₁ antagonist for the treatment of cardiovascular disease

Abstract

Considering the prevalence of cardiovascular disease in public health and the limited validated therapeutic options, this study aimed to find novel compounds targeting the angiotensin II type 1 receptor, accepted as a therapeutic target in cardiovascular disease. A small library consisting of 89 compounds from 39 Chinese herbs was profiled using a cell-based calcium mobilization assay which was developed and characterized for high-throughput screening. [6]-Gingerol derived from Zingiber officinale Roscoe (ginger) was identified as a novel angiotensin II type 1 receptor antagonist, with an IC50 value of 8.173 µM. The hit was further tested by a specificity assay indicating that it had no antagonistic effects on other evaluated GPCRs, such as endothelin receptors. The major ingredient of ginger, [6]-gingerol, could inhibit angiotensin II type 1 receptor activation, which partially clarified the mechanism of ginger regulating blood pressure and strengthening heart in the cardiovascular system.

[6]-gingerol: a novel AT₁ antagonist for the treatment of cardiovascular disease - PubMed

……….

Molecular docking study of potential phytochemicals and their effects on the complex of SARS-CoV2 spike protein and human ACE2

Hesperidin is a major flavonoid compound, present in orange and lemon fruits. 470–761 mg/L of Hesperidin is normally present in orange juice31. This phytochemical exhibit various medicinal properties. According to oral toxicity study of hesperidin, it can be concluded that this phytochemical can be safely used in herbal formulations with its LD50 value more than 2000 mg/kg31. This flavanone glycoside, has a long medicinal history in both Indian and Chinese herbal medications32. This phytochemical alone or in combination with other chemicals, is often used to treat various diseases.

Emodin is a polyphenol found in the roots, bark and leaves of several plants including aloe vera, cascara, rhubarb, senna etc. In traditional medicine, emodin has been used for cardiovascular diseases and osteoporosis. It has been suggested earlier that emodin can inhibit influenza A virus replication33 via several cell signaling pathways.

Chrysin a natural flavonoid, is commonly found in propolis and honey. As reported earlier, chrysin can act as an inhibitor during enterovirus 71 (EV71) growth and replication34. Similarly, Song et al.35described antiviral activity of chrysin against coxsackievirus B3 (CVB3).

Considering the results obtained from molecular docking studies, phytochemicals hesperidin, emodin and chrysin can be used for COVID-19 treatment, after in-silico mutagenesis study and experimental verification. These phytochemicals have shown comparable spike protein inhibiting efficacy as that of known inhibitors such as chloroquine and hydroxychloroquine. From the molecular dynamics and QSAR study, it can be concluded that for ACE2 receptor protein, ligand binding activity of spike protein fragment, will be decreased noncompetitively by modulator hesperidin. So, this natural compound can show antiviral activity by destabilizing spike protein binding with human host ACE2 receptor. The modulation of hesperidin of ACE2 protein try to prevent its interaction with spike protein. It has been proved by a simple in silico experiment and the result of this experiment in shown in Supplementary Information S3.

Molecular docking study of potential phytochemicals and their effects on the complex of SARS-CoV2 spike protein and human ACE2

.........

Methylene Blue Inhibits the SARS-CoV-2 Spike–ACE2 Protein-Protein Interaction–a Mechanism that can Contribute to its Antiviral Activity Against COVID-19

As far as clinical applications, one promising indication comes from a report of a cohort of 2,500 French patients treated with MeBlu as part of their cancer care none of whom developed influenza like illness during the COVID-19 epidemics (Henry et al., 2020). MeBlu has also been explored in one Phase one clinical trial (NCT04370288) for treatment of critically ill COVID-19 patients in Iran as part of a three-drug last therapeutic option add-on cocktail (MeBlu 1 mg/kg, vitamin C 1500 mg/kg, and N-acetyl cysteine 2000 mg/kg) based on the hypothesis that this combination could rebalance NO, methemoglobin, and oxidative stress. Four of the five patients responded well to treatment (Alamdari et al., 2020).

In conclusion, screening of our organic dye-based library identified MeBlu as a low-micromolar inhibitor of the interaction between SARS-CoV-2 spike protein and its cognate receptor ACE2, a PPI that is the first critical step initiating the viral entry of this coronavirus. While MeBlu shows strong polypharmacology and might be a somewhat promiscuous PPI inhibitor, its ability to inhibit this PPI could contribute to the antiviral activity of MeBlu against SARS-CoV-2 even in the absence of light making this inexpensive and widely available drug potentially useful in the prevention and treatment of COVID-19 as an oral or inhaled medication.

Methylene Blue Inhibits the SARS-CoV-2 Spike–ACE2 Protein-Protein Interaction–a Mechanism that can Contribute to its Antiviral Activity Against COVID-19

 

[J.R.K]

Dandelion tea works too, even for variants:

Common dandelion (Taraxacum officinale) efficiently blocks the interaction between ACE2 cell surface receptor and SARS-CoV-2 spike protein D614, mutants D614G, N501Y, K417N and E484K in vitro

On 11th March 2020, coronavirus disease 2019 (COVID-19), caused by the SARS-CoV-2 virus, was declared as a global pandemic by the World Health Organization (WHO). To date, there are rapidly spreading new “variants of concern” of SARS-CoV-2, the United Kingdom (B.1.1.7), the South African...

www.biorxiv.org

Wow! This would probably help in transmission scenarios as well. I better tell my vaccinated mother not to look so dimly on the yellow flowers that irritate her idea of a pristine lawn. It might be a lifesaver for her. But I am going to grab some before they get a going over with malathion,such is the level of her disdain for the offensive yellow!

 

[J.R.K]

Your reasoning is correct. Emodin can also be obtained from aloe vera, as a drink without side effects. I gave this example with emodin, but there are several substances in their natural state that have this effect. The sun, vitamin B1, cocoa, ... decrease Ang II. I don't know anything about pine needle tea.

The most common complication leading to the CoV-induced mortality can be justified through ACE-AngII-AT1-Spike protein overactivation caused by virus / toxin / antiviral drugs

The spikes protein have high affinity to ACE2, uses ACE2 to enter a cell.
It is suggested that this “occupation” of the virus of ACE2 might reduce the ability of Ang II to bind to ACE2.

Accumulated Ang II result in an increased activation of AT1.

Activation of AT1 results in vasoconstriction, increased pro-inflammatory response.


.........

Ray:
The virus uses ACE2 (angiotensin converting enzyme 2) as receptor and enters cells by the angiotensin receptor. Losartan (recommended in China), an angiotensin blocker, is effective protection, and has many other antiinflammatory effects. The Chinese also have good results with cinanserin, a serotonin blocker. I think cyproheptadine might help, too. Progesterone lowers the angiotensin receptor, but doesn’t act immediately as losartan does.

“The virus activates the angiotensin receptor (AT1), so the receptor blockers are protective—losartan, telmisartan, etc. Progesterone is a natural inhibitor of that receptor. Also the usual antiinflammatory things, aspirin, eggnog, orange juice would be helpful.” Ray Peat


...the angiotensin converting enzyme is one of the early parts of our immune system that sets up an inflammatory reaction that will set in action a whole chain of events, if the pathogen gets trough and is actually a treat, then you activate this proteolytic protein that create angiotensin witch is like a transmitter of a panic reaction to the organism, and it happens this coronavirus is able to bind to one of this angiotensin converting enzymes, there is one with is only pro-inflammatory and the other one that backs that up, which undoes, inhibits the inflammatory damage done by the first angiotensin producing enzyme, this is called ACE2, and ACE2 happens to be attacked by this particular virus witch binds to that enzyme, and that’s receptor its vulnerable point of organism as far this fire is concern, and binding to that ACE2 means that it leaves the ACE1 which produces angiotensin, it leaves that free to act, and ACE2 is capable in inactivating angiotensin breaking down to the first seven amino acids, they call it angiotensin 1-7, and this is a defensive anti-inflammatory peptide, so if your ACE2 is knocked out, angiotensin has a free range to cause damage, so the virus increases the inflammatory reaction by sticking to the defensive enzyme, and that enzyme combined with the virus, than acts to enter the cell by way of the angiotensin receptor which is called the AT1, that are two known receptors by which angiotensin can do damage. Angiotensin 1 is strictly an inflammation producing system, the angiotensin 2 produces somewhat defensive reactions, but it happens that the virus enzyme combination entering the cell by way of angiotensin receptor 1, AT1, and that turns on a whole range of destructive processes, nitric oxide, serotonin for example. And, so, just looking at the effects, its obvious you can defend by anything that defends you against nitric oxide and serotonin, so anti-inflammatory things are the known treatment for this kind of virus that Chinese for years have been using, cinanserin which is a serotonin blocker for other treatments, and they find that is helpful for people with the established respiratory corona infection, and losartan witch is high blood pressure drug is the most well-known blocker of angiotensin 1 receptor.. losartan is cheap and widely available. - Ray Peat
...........

The mechanistic overview of SARS-CoV-2 using angiotensin-converting enzyme 2 to enter the cell for replication: possible treatment options related to the renin–angiotensin system

Abstract

The SARS-CoV-2 pandemic is a healthcare crisis caused by insufficient knowledge applicable to effectively combat the virus. Therefore, different scientific discovery strategies need to be connected, to generate a rational treatment which can be made available as rapidly as possible. This relies on a solid theoretical understanding of the mechanisms of SARS-CoV-2 infection and host responses, which is coupled to the practical experience of clinicians that are treating patients. Because SARS-CoV-2 enters the cell by binding to angiotensin-converting enzyme 2 (ACE2), targeting ACE2 to prevent such binding seems an obvious strategy to combat infection. However, ACE2 performs its functions outside the cell and was found to enter the cell only by angiotensin II type 1 receptor (AT1R)-induced endocytosis, after which ACE2 is destroyed. This means that preventing uptake of ACE2 into the cell by blocking AT1R would be a more logical approach to limit entry of SARS-CoV-2 into the cell. Since ACE2 plays an important protective role in maintaining key biological processes, treatments should not disrupt the functional capacity of ACE2, to counterbalance the negative effects of the infection. Based on known mechanisms and knowledge of the characteristics of SARS-CoV we propose the hypothesis that the immune system facilitates SARS-CoV-2 replication which disrupts immune regulatory mechanisms. The proposed mechanism by which SARS-CoV-2 causes disease immediately suggests a possible treatment, since the AT1R is a key player in this whole process. AT1R antagonists appear to be the ideal candidate for the treatment of SARS-CoV-2 infection. AT1R antagonists counterbalance the negative consequences of angiotesnin II and, in addition, they might even be involved in preventing the cellular uptake of the virus without interfering with ACE2 function. AT1R antagonists are widely available, cheap, and safe. Therefore, we propose to consider using AT1R antagonists in the treatment of SARS-CoV-2.

Conclusion

Because SARS-CoV-2 enters the cell bound to ACE2, which induces ACE2 deficiency at the cell membrane, AngII is persistently activated. Increased AngII induces activation of AT1R, causing more uptake of SARS-CoV-2 and increasing ACE2 deficiency, thus maintaining and exacerbating a non-specific immune response, consisting of cytokine-induced inflammation. This non-specific immune response is an attempt to reduce the viral load, while the specific immune response is mounted. Unrestrained AngII eventually causes death by respiratory distress induced by excessive inflammation and its deleterious effects on other organs. Therefore, SARS-CoV-2-induced mortality is promoted by three mechanisms: (i) increased AngII induces endocytosis of ACE2-bound SARS-CoV-2, leading to ACE2 deficiency and viral replication; (ii) ACE2 deficiency prevents the priming of an adaptive immune response by lack of NO; and (iii) Ang II induces an increase in viral load leading to an increased innate immune response and a further increase in AngII levels. Therefore, treatments should aim at preventing the AngII ‘storm’ in an early phase of the infection, restoring the modulation of NO, and preventing the entry of SARS-CoV-2 into the cell. All these mechanisms are targeted by AT1R antagonists. They may reduce morbid inflammatory distress and provide an environment to facilitate an effective, virus-specific adaptive immune response.

The mechanistic overview of SARS-CoV-2 using angiotensin-converting enzyme 2 to enter the cell for replication: possible treatment options related to the renin–angiotensin system



………


[6]-gingerol: a novel AT₁ antagonist for the treatment of cardiovascular disease

Abstract

Considering the prevalence of cardiovascular disease in public health and the limited validated therapeutic options, this study aimed to find novel compounds targeting the angiotensin II type 1 receptor, accepted as a therapeutic target in cardiovascular disease. A small library consisting of 89 compounds from 39 Chinese herbs was profiled using a cell-based calcium mobilization assay which was developed and characterized for high-throughput screening. [6]-Gingerol derived from Zingiber officinale Roscoe (ginger) was identified as a novel angiotensin II type 1 receptor antagonist, with an IC50 value of 8.173 µM. The hit was further tested by a specificity assay indicating that it had no antagonistic effects on other evaluated GPCRs, such as endothelin receptors. The major ingredient of ginger, [6]-gingerol, could inhibit angiotensin II type 1 receptor activation, which partially clarified the mechanism of ginger regulating blood pressure and strengthening heart in the cardiovascular system.

[6]-gingerol: a novel AT₁ antagonist for the treatment of cardiovascular disease - PubMed

……….

Molecular docking study of potential phytochemicals and their effects on the complex of SARS-CoV2 spike protein and human ACE2

Hesperidin is a major flavonoid compound, present in orange and lemon fruits. 470–761 mg/L of Hesperidin is normally present in orange juice31. This phytochemical exhibit various medicinal properties. According to oral toxicity study of hesperidin, it can be concluded that this phytochemical can be safely used in herbal formulations with its LD50 value more than 2000 mg/kg31. This flavanone glycoside, has a long medicinal history in both Indian and Chinese herbal medications32. This phytochemical alone or in combination with other chemicals, is often used to treat various diseases.

Emodin is a polyphenol found in the roots, bark and leaves of several plants including aloe vera, cascara, rhubarb, senna etc. In traditional medicine, emodin has been used for cardiovascular diseases and osteoporosis. It has been suggested earlier that emodin can inhibit influenza A virus replication33 via several cell signaling pathways.

Chrysin a natural flavonoid, is commonly found in propolis and honey. As reported earlier, chrysin can act as an inhibitor during enterovirus 71 (EV71) growth and replication34. Similarly, Song et al.35described antiviral activity of chrysin against coxsackievirus B3 (CVB3).

Considering the results obtained from molecular docking studies, phytochemicals hesperidin, emodin and chrysin can be used for COVID-19 treatment, after in-silico mutagenesis study and experimental verification. These phytochemicals have shown comparable spike protein inhibiting efficacy as that of known inhibitors such as chloroquine and hydroxychloroquine. From the molecular dynamics and QSAR study, it can be concluded that for ACE2 receptor protein, ligand binding activity of spike protein fragment, will be decreased noncompetitively by modulator hesperidin. So, this natural compound can show antiviral activity by destabilizing spike protein binding with human host ACE2 receptor. The modulation of hesperidin of ACE2 protein try to prevent its interaction with spike protein. It has been proved by a simple in silico experiment and the result of this experiment in shown in Supplementary Information S3.

Molecular docking study of potential phytochemicals and their effects on the complex of SARS-CoV2 spike protein and human ACE2

.........

Methylene Blue Inhibits the SARS-CoV-2 Spike–ACE2 Protein-Protein Interaction–a Mechanism that can Contribute to its Antiviral Activity Against COVID-19

As far as clinical applications, one promising indication comes from a report of a cohort of 2,500 French patients treated with MeBlu as part of their cancer care none of whom developed influenza like illness during the COVID-19 epidemics (Henry et al., 2020). MeBlu has also been explored in one Phase one clinical trial (NCT04370288) for treatment of critically ill COVID-19 patients in Iran as part of a three-drug last therapeutic option add-on cocktail (MeBlu 1 mg/kg, vitamin C 1500 mg/kg, and N-acetyl cysteine 2000 mg/kg) based on the hypothesis that this combination could rebalance NO, methemoglobin, and oxidative stress. Four of the five patients responded well to treatment (Alamdari et al., 2020).

In conclusion, screening of our organic dye-based library identified MeBlu as a low-micromolar inhibitor of the interaction between SARS-CoV-2 spike protein and its cognate receptor ACE2, a PPI that is the first critical step initiating the viral entry of this coronavirus. While MeBlu shows strong polypharmacology and might be a somewhat promiscuous PPI inhibitor, its ability to inhibit this PPI could contribute to the antiviral activity of MeBlu against SARS-CoV-2 even in the absence of light making this inexpensive and widely available drug potentially useful in the prevention and treatment of COVID-19 as an oral or inhaled medication.

Methylene Blue Inhibits the SARS-CoV-2 Spike–ACE2 Protein-Protein Interaction–a Mechanism that can Contribute to its Antiviral Activity Against COVID-19

This is fantastic md_a. Just verifying my original thoughts on your highly informed thread. The spike protein binds to the ACE2 receptor and effectively depletes it thereby opening up the ACE1 receptor through which the virus gains entry into the cell to begin replication.
So in reality if one were to follow (and I hesitate to use this phrase) a “Ray Peat diet” if such a thing exists. But including orange juice, niacinamide, some cascara segrada, honey and some propolis, methylene blue, and marmalade which is rich in all the flavonoids due to the peel being included, as well as Nemos dandelion tea suggestion one might already be resistant or more resilient to the transmission dangers of the vaccinated’s spike protein by product, and the virus. Provided that one was not on an ACE inhibitor which puts you ACE2 in a depleted position already.
Again please feel free to correct anything I am misunderstanding.
These seem like some easy things to help (at least to me as most of these things I am doing already, but for someone new this could be very overwhelming.
But I think that it would be prudent to take into account the use of the medical drugs to help clean out the system but again just like supplements you need to test one at a time to see how they affect you. Otherwise you do not know which did what. Dr Fleming had even mentioned that in his Dallas Texas conference.
Fantastic stuff md_a and Nemo. I appreciate you both taking the time to help the slow guy at the back of the class!!

 

[md_a]

This is fantastic md_a. Just verifying my original thoughts on your highly informed thread. The spike protein binds to the ACE2 receptor and effectively depletes it thereby opening up the ACE1 receptor through which the virus gains entry into the cell to begin replication.
So in reality if one were to follow (and I hesitate to use this phrase) a “Ray Peat diet” if such a thing exists. But including orange juice, niacinamide, some cascara segrada, honey and some propolis, methylene blue, and marmalade which is rich in all the flavonoids due to the peel being included, as well as Nemos dandelion tea suggestion one might already be resistant or more resilient to the transmission dangers of the vaccinated’s spike protein by product, and the virus. Provided that one was not on an ACE inhibitor which puts you ACE2 in a depleted position already.
Again please feel free to correct anything I am misunderstanding.
These seem like some easy things to help (at least to me as most of these things I am doing already, but for someone new this could be very overwhelming.
But I think that it would be prudent to take into account the use of the medical drugs to help clean out the system but again just like supplements you need to test one at a time to see how they affect you. Otherwise you do not know which did what. Dr Fleming had even mentioned that in his Dallas Texas conference.
Fantastic stuff md_a and Nemo. I appreciate you both taking the time to help the slow guy at the back of the class!!

I think that if everyone understood the correct mechanism that you stated the treatment or prevention would be very easy to do. For me, the virus represents environmental toxins, radiation, pesticides, polluting nanoparticles, which reach the cells on a stressed body with the help of unsaturated fats. I don't think the virus has any effect but the spike protein and the toxins listed. A healthy / high metabolism has the ability to pass without problems but one that has accumulated a lot of unsaturated fats has a hard time fighting.

 

[J.R.K]

Dandelion tea works too, even for variants:

Common dandelion (Taraxacum officinale) efficiently blocks the interaction between ACE2 cell surface receptor and SARS-CoV-2 spike protein D614, mutants D614G, N501Y, K417N and E484K in vitro

On 11th March 2020, coronavirus disease 2019 (COVID-19), caused by the SARS-CoV-2 virus, was declared as a global pandemic by the World Health Organization (WHO). To date, there are rapidly spreading new “variants of concern” of SARS-CoV-2, the United Kingdom (B.1.1.7), the South African...

www.biorxiv.org

I think that if everyone understood the correct mechanism that you stated the treatment or prevention would be very easy to do. For me, the virus represents environmental toxins, radiation, pesticides, polluting nanoparticles, which reach the cells on a stressed body with the help of unsaturated fats. I don't think the virus has any effect but the spike protein and the toxins listed. A healthy / high metabolism has the ability to pass without problems but one that has accumulated a lot of unsaturated fats has a hard time fighting.

That is very true my friend. I am feeling like I am putting pieces of a jigsaw puzzle together. But I don’t have all the pieces nicely contained in one box and it is just a matter of sorting it out. But rather I have to look for answers and ask questions of those who have more knowledge on well all these topics that are part of our very complex biological and biochemical makeup.
It took me years to find the one huge piece of the puzzle that being PUFA being bad, here I was eating nuts by the pound. Then I had to start eliminating that out of my system. But as you said that is only one component,the environment, our lifestyle (the rat race), pollution in the air, our food and water. Add to that political systems that push us to do things they know (or at least I am pretty sure they know) are not conducive to happiness and longevity such as using us as guinea pigs for a from what I can see is a huge experiment. It does make finding a desert island with an abundance of fruit, freshwater and some chickens and a few cows seem quite appealing.
If memory serves you are from Spain, correct?

 

[Mito]

What dose are we telling people?

That could be a problem, from the study “The ability of MeBlu to inhibit the SARS-CoV-2-S–ACE2 PPI could be a mechanism of action contributing to such activity especially as we also showed MeBlu to inhibit the entry of SARS-CoV-2 pseudovirus into ACE2-expressing cells with low micromolar IC50 (Figure 4). If this PPI inhibitory activity of MeBlu is retained at similar levels in vivo as found here (IC50 ≈ 3 μM), it is within a range that can be obtained in blood following typical doses (e.g., 200 mg/day) as indicated by pharmacokinetic studies in humans.”

 

[J.R.K]

That could be a problem, from the study “The ability of MeBlu to inhibit the SARS-CoV-2-S–ACE2 PPI could be a mechanism of action contributing to such activity especially as we also showed MeBlu to inhibit the entry of SARS-CoV-2 pseudovirus into ACE2-expressing cells with low micromolar IC50 (Figure 4). If this PPI inhibitory activity of MeBlu is retained at similar levels in vivo as found here (IC50 ≈ 3 μM), it is within a range that can be obtained in blood following typical doses (e.g., 200 mg/day) as indicated by pharmacokinetic studies in humans.”

Wow! 200 mg per day! That seems like a lot but I could be wrong.

 

[Nemo]

That could be a problem, from the study “The ability of MeBlu to inhibit the SARS-CoV-2-S–ACE2 PPI could be a mechanism of action contributing to such activity especially as we also showed MeBlu to inhibit the entry of SARS-CoV-2 pseudovirus into ACE2-expressing cells with low micromolar IC50 (Figure 4). If this PPI inhibitory activity of MeBlu is retained at similar levels in vivo as found here (IC50 ≈ 3 μM), it is within a range that can be obtained in blood following typical doses (e.g., 200 mg/day) as indicated by pharmacokinetic studies in humans.”

Thank you, Mito.

 

[md_a]

That is very true my friend. I am feeling like I am putting pieces of a jigsaw puzzle together. But I don’t have all the pieces nicely contained in one box and it is just a matter of sorting it out. But rather I have to look for answers and ask questions of those who have more knowledge on well all these topics that are part of our very complex biological and biochemical makeup.
It took me years to find the one huge piece of the puzzle that being PUFA being bad, here I was eating nuts by the pound. Then I had to start eliminating that out of my system. But as you said that is only one component,the environment, our lifestyle (the rat race), pollution in the air, our food and water. Add to that political systems that push us to do things they know (or at least I am pretty sure they know) are not conducive to happiness and longevity such as using us as guinea pigs for a from what I can see is a huge experiment. It does make finding a desert island with an abundance of fruit, freshwater and some chickens and a few cows seem quite appealing.
If memory serves you are from Spain, correct?

I live in Romania, the city of Constanta. I would like to live in Spain. Unfortunately, I live in the city and depend on the mafia political class that receives orders directly from abroad on the Biden security chain. Living on a farm in a mountainous area offers protection from the plandemic wave.

 

[Nemo]

Covid mortality rates are 40x higher in Israel since mass vaxxing started and it's all because of the soaring mortality rate in the vaxxed. For people under age 65, the Covid death rate is 260x times higher among the vaxxed.

That's ADE. Vax-created antibodies enhancing the disease, making it more deadly. The vax spike protein facilitates entry of wild Covid into your cells. Plus the vax disables several critical chunks of your immune system.

Didn't happen among Palestinians because they didn't get the shot. There's actually been a decrease in new cases among the unvaxxed Palestinians as the Israeli vaxxed case numbers soared.

So it doesn't protect you from infection. It doesn't protect you from transmitting the infection to others. It doesn't protect you from the worst symptoms, instead it makes them more likely. And it increases your chance of dying.

But don't imagine this is the total death toll from the vax. With every exposure to wild Covid the ADE will get worse. Plus we have more clotting events and autoimmune deaths and prion disease deaths yet to come.

The scientists who put the study together say, "This is a new holocaust."


View: https://twitter.com/heidegger79/status/1404424631558213633

 

[Peatness]

The one thing about this plandemic that shocks me and surprises is why Israel used these injections, mostly pfizer, on it’s population. I would have thought the Israel’s doctors/politicians would have known of the potential dangers? What deal was done with Pfizer? And why did Israel not see this coming? These are genuine questions in case anyone has an answer.

 

[Nemo]

The one thing about this plandemic that shocks me and surprises is why Israel used these injections, mostly pfizer, on it’s population. I would have thought the Israel’s doctors/politicians would have known of the potential dangers? What deal was done with Pfizer? And why did Israel not see this coming? These are genuine questions in case anyone has an answer.

Was Netanyahu Trump-like, trusting evil people and thinking he'd be rewarded by the people for doing a good thing?

Or was he blackmailed and an enemy of his own people, as it seems clear the U.S. government is?

 

[Peatness]

Was Netanyahu Trump-like, trusting evil people and thinking he'd be rewarded by the people for doing a good thing?

Or was he blackmailed and an enemy of his own people, as it seems clear the U.S. government is?

Perhaps both.

 

[J.R.K]

Covid mortality rates are 40x higher in Israel since mass vaxxing started and it's all because of the soaring mortality rate in the vaxxed. For people under age 65, the Covid death rate is 260x times higher among the vaxxed.

That's ADE. Vax-created antibodies enhancing the disease, making it more deadly. The vax spike protein facilitates entry of wild Covid into your cells. Plus the vax disables several critical chunks of your immune system.

Didn't happen among Palestinians because they didn't get the shot. There's actually been a decrease in new cases among the unvaxxed Palestinians as the Israeli vaxxed case numbers soared.

So it doesn't protect you from infection. It doesn't protect you from transmitting the infection to others. It doesn't protect you from the worst symptoms, instead it makes them more likely. And it increases your chance of dying.

But don't imagine this is the total death toll from the vax. With every exposure to wild Covid the ADE will get worse. Plus we have more clotting events and autoimmune deaths and prion disease deaths yet to come.

The scientists who put the study together say, "This is a new holocaust."


View: https://twitter.com/heidegger79/status/1404424631558213633

The tip of the iceberg, this is the scary part. I keep coming back to @Lollypop2s quote from Jacques Atoli wherein he said ,”they will go willingly to the slaughter”. If this is true with each exposure to the wild version the ADE will be increased in it’s virulence we are in for some rough times ahead. The court ruling in Texas today saying that it was illegal for health care workers in that Houston hospital to refuse the vaccine, this I fear will cause a precedent worldwide and rights and freedoms could become words that come after the phrase. “Do you remember when?”
Let us hope the death toll does not have to become to great before our leaders wisen up or feel some level of compassion.

 

[Nemo]

The tip of the iceberg, this is the scary part. I keep coming back to @Lollypop2s quote from Jacques Atoli wherein he said ,”they will go willingly to the slaughter”. If this is true with each exposure to the wild version the ADE will be increased in it’s virulence we are in for some rough times ahead. The court ruling in Texas today saying that it was illegal for health care workers in that Houston hospital to refuse the vaccine, this I fear will cause a precedent worldwide and rights and freedoms could become words that come after the phrase. “Do you remember when?”
Let us hope the death toll does not have to become to great before our leaders wisen up or feel some level of compassion.

That judge in Texas is the most-frequently overturned judge on the entire 5th Circuit Court of Appeals. That ruling will never stand. It's against federal law to mandate an experimental drug or use any kind of threat or coercion to get someone to take it.

But they assigned the case deliberately to that judge because the full court won't be able to hear the case for another five months, so it gives them another five months to break the law to get the shots into people.

In five months, the data will be too clear for them too hide but it will be too late for many more millions of people.

 

[J.R.K]

Covid mortality rates are 40x higher in Israel since mass vaxxing started and it's all because of the soaring mortality rate in the vaxxed. For people under age 65, the Covid death rate is 260x times higher among the vaxxed.

That's ADE. Vax-created antibodies enhancing the disease, making it more deadly. The vax spike protein facilitates entry of wild Covid into your cells. Plus the vax disables several critical chunks of your immune system.

But don't imagine this is the total death toll from the vax. With every exposure to wild Covid the ADE will get worse. Plus we have more clotting events and autoimmune deaths and prion disease deaths yet to come.

The scientists who put the study together say, "This is a new holocaust."


View: https://twitter.com/heidegger79/status/1404424631558213633

I am curious on the mechanism of mortality with ADE. In COVID 19 one usually dies as a result of the cytokine storm gone wild,and/or blood clotting finally asphyxiation if my understanding is correct.
But in a vaccinated person that has immunosuppression does the cytokine storm happen at all? Or at any point do the T cells and B cells come into play or are they to sidelined as the virus enters cells more freely and reproduces without opposition. Thus the person then just succumbs to viral overload and possibly endotoxin as a result of the relationship that the spike protein has with activation of the TLR 4 receptor.
My presumption would be that vaccine created antibodies are in the game and they would react to the spike protein and this would create the bleeding and deep veinous thrombosis (blood clotting) until the clotting agents are exhausted and death would occur as a result of either a clot reaching the lungs or heart given that the spike protein is widespread throughout the entire vascular system as Dr Bhakdi has mentioned. Or if this does not happen the mortality could possibly due to exsanguination or just massive internal trauma due to all of the above contributing.
Is this hypothesis even close? All insights are appreciated greatly?

That judge in Texas is the most-frequently overturned judge on the entire 5th Circuit Court of Appeals. That ruling will never stand. It's against federal law to mandate an experimental drug or use any kind of threat or coercion to get someone to take it.

But they assigned the case deliberately to that judge because the full court won't be able to hear the case for another five months, so it gives them another five months to break the law to get the shots into people.

In five months, the data will be too clear for them too hide but it will be too late for many more millions of people.

Sounds like you are close to the situation Nemo. Clever strategy on the Empire’s side.
More needles into more arms and more carnage like in Israel.

 

[Nemo]

I am curious on the mechanism of mortality with ADE. In COVID 19 one usually dies as a result of the cytokine storm gone wild,and/or blood clotting finally asphyxiation if my understanding is correct.
But in a vaccinated person that has immunosuppression does the cytokine storm happen at all? Or at any point do the T cells and B cells come into play or are they to sidelined as the virus enters cells more freely and reproduces without opposition. Thus the person then just succumbs to viral overload and possibly endotoxin as a result of the relationship that the spike protein has with activation of the TLR 4 receptor.
My presumption would be that vaccine created antibodies are in the game and they would react to the spike protein and this would create the bleeding and deep veinous thrombosis (blood clotting) until the clotting agents are exhausted and death would occur as a result of either a clot reaching the lungs or heart given that the spike protein is widespread throughout the entire vascular system as Dr Bhakdi has mentioned. Or if this does not happen the mortality could possibly due to exsanguination or just massive internal trauma due to all of the above contributing.
Is this hypothesis even close? All insights are appreciated greatly?

Sounds like you are close to the situation Nemo. Clever strategy on the Empire’s side.
More needles into more arms and more carnage like in Israel.

I do not know about the cytokine storm since no one is yet admitting there is ADE.

They claimed that 86-year-old man in the postmortem study died of organ failure. That's what Dolores Cahill said they would say about ADE cases, that it would all be called sepsis and organ failure. He had lung crackles and other Covid symptoms but I believe he died from the T cells killing off his organs in an autoimmune attack.

Clearly you are right there are plenty of clotting deaths too. How would an autoimmune attack on your endothelial cells work? What would that look like?

 

[J.R.K]

I do not know about the cytokine storm since no one is yet admitting there is ADE.

They claimed that 86-year-old man in the postmortem study died of organ failure. That's what Dolores Cahill said they would say about ADE cases, that it would all be called sepsis and organ failure. He had lung crackles and other Covid symptoms but I believe he died from the T cells killing off his organs in an autoimmune attack.

Clearly you are right there are plenty of clotting deaths too. How would an autoimmune attack on your endothelial cells work? What would that look like?

I do not know what an autoimmune attack on the endothelial cells would look like, but I imagine it would be akin to the old execution style of ,”death by a thousand cuts, only internally, given that the spike protein is spread throughout the entire vascular network and a hoard of antibodies coursing throughout the network attacking not only each cell with a spike protein attached to it but also cells that mimic a spike protein.
I cannot say how it would look but for those whom this might be their fate, I would hope that it would be over quickly and with as little pain as possible.

 

[J.R.K]

The one thing about this plandemic that shocks me and surprises is why Israel used these injections, mostly pfizer, on it’s population. I would have thought the Israel’s doctors/politicians would have known of the potential dangers? What deal was done with Pfizer? And why did Israel not see this coming? These are genuine questions in case anyone has an answer.

Do you remember back in February or Maybe March when Palestine was complaining they could not get access to any vaccines and Israel had more than they needed?
This being the Holy land it reminds me that God answers all prayers, while yes is an answer that is preferred.As we see here sometimes no is also a very good and acceptable answer.

 

[Nemo]

I do not know what an autoimmune attack on the endothelial cells would look like, but I imagine it would be akin to the old execution style of ,”death by a thousand cuts, only internally, given that the spike protein is spread throughout the entire vascular network and a hoard of antibodies coursing throughout the network attacking not only each cell with a spike protein attached to it but also cells that mimic a spike protein.
I cannot say how it would look but for those whom this might be their fate, I would hope that it would be over quickly and with as little pain as possible.

Great way of putting it. I remember one of the scientists, I think Dr. Bhakdi, speaking about the effects on the lungs, saying the first dose of vax would be like someone cutting your lung tissue, the second would be like someone taking a razor blade to the tissue to completely shred it. He wouldn't say what a third dose would be like.

I think you're correct that we'd essentially be seeing death by a thousand cuts.