Xemnoraq
Member
- Joined
- Oct 3, 2016
- Messages
- 266
- Age
- 27
So Peat has spoken of this before, many have critisized me for pointing this out as well, ive recieved alot of backlash regarding this virus when it goes against someones ideas they cling to.
Many people have told me things like, “its a new virus we dont have immunity to it”
Or
“SARS caused by corona virus is different than other causes, or pneumonia caused by corona virus is different”
However none of them have EVER once provided any resources/studies to back up those mainstream medicine ideologies,
This is just a copy and paste from a post i made about this on facebook, but these studies point towards immunity likely being a matter of being able to produce enough ACE2 to degrade angiotensin because the virus decreases the availability of the ACE2 enzyme which degrades angiotensin.
Young and healthy people have been quoted to produce more ACE2, which outlines why some dont suffer symptoms,
Also as @haidut has shared in one of his threads, the evidence we have right now suggests SARS (regardless of trigger) may be due to elevated lipolysis from PUFA.
COVID-19/SARS May Be Due Simply To Serum PUFA And Its Peroxidation
Which implies As the study mentioned, SARS may be just an inflammatory disorder driven largely by the peroxidation of PUFA.
“Thus, the serum acyl ratio may not only prospectively identify and facilitate the assessment of new treatments in patients at highest risk for developing ARDS, but may also lead to new insights about the pathogenesis of ARDS."
Which would dismiss the empty claims that people have made suggesting SARS caused by COVID-19 is completely different, because so far there has been no evidence to support that.
We do have evidence however, suggesting SARS is caused by elevated FFA, where the virus is just the stress trigger (which would explain why drugs that inhibit lipolysis have been so effective in SARS and viral infections)
It seems Dr. Peat is on the right track again and may be correct on this,
I had someone critisize Peat implying he didnt do his research which i thought was comical,
This is the original post i made and theres 3 studies that support the idea of using angiotensin blockers/ACE2 promoters as treatment/protection from this pandemic as we like to call it.
———————————————————————
So its been known for quite some time now that this COVID-19 and the previous strains cause respiratory failure through a modulation of the ACE2 enzyme that degrades angiotensin with something called the spike protein in the virus.
The ACE2 enzyme is produced in larger amounts in younger and healthier people which would provide an explanation as to why some people are asymptomatic or able to handle the infection fine with no symptoms.
The virus, has been cited to attach so to speak to the ACE2 enzyme and decrease the bioavailability of it,
The ACE2 enzyme has been implicated in protecting from fibrosis and lung failure which is known to be the main causes of death in SARS/COVID-19
Therapies that increase the production of ACE2 (so it outweighs what the virus is doing) has been suggested along with angiotensin inhibitors, which have a very good history of success in SARS from many viral infections including the corona virus types.
—————————————————————
“Some studies have reported an increased inflammatory responses due to AT1 activated by AngII. In some pathological conditions, overactivation of AT1 may lead to damaging events such as fibrosis in different organs (eg, liver and lungs), perhaps through increasing TGF-β expression. Other studies have indicated that ACE2 has a protective effect on the fibrogenesis and inflammation of different organs, as well as the liver and the lungs. Taking these studies together, the ACE–AngII–AT1 axis in the RAS system shows a predominant role in organ fibrosis, par- ticularly in the lungs and liver.
(Which we also know serotonin plays a huge part)
“According to some recent studies, ACE2 has a regulatory effect on innate immunity and gut microbiota composition. Moreover, ACE2 has a determinant antifibrotic role in the lung injury induced by sepsis, acid aspiration, SARS, and lethal avian influenza A H5N1 virus.”
“Accordingly, losartan is a selective antagonist of AT1 receptor that exerts an inhibitory effect on the ACE–AngII–AT1 axis in the RAS system, a known molecular pathway for end-organ fibrosis. Thus, losartan may be suggested as a potential agent of protection from lung damage induced by COVID-19. Losartan may also have a protective function against lung fibrosis through other molecular mechanisms such as the downregulation of TGF-β1. This hypothesis need to be verified through in vitro and in vivo investigations.”
https://www.cambridge.org/core/serv...n_against_coronavirus_induced_lung_damage.pdf
—————————————————————
“These results show that SARS CoV spike protein can directly affect the development of severe acute lung failure through ACE2”
Taken together our data show that SARS CoV spike can exaggerate acute lung failure through the deregulation of the renin-angiotensin system. Moreover SARS CoV spike-mediated lung failure can be rescued by the inhibition of AT1R.”
https://www.researchgate.net/public..._ACE2_in_SARS_coronavirus-induced_lung_injury
—————————————————————
“The risk model established upon IL-6, CRP and hypertension had the highest predictability in this study. Besides, IL-6 played a pivotal role in the severity of COVID-19 and had a potential value for monitoring the process of severe cases.”
https://www.researchgate.net/public...sess_the_severity_of_coronavirus_disease_2019
—————————————————————
I had first heard that this COVID-19 virus initiated its negative effects through the angiotensin system from Dr. Ray Peat who was doing his own research on the virus and suggested losartan and ACE2 promoters as a possible treatment for this virus.
When i looked it up for my myself i came across various studies such as these supporting that claim so it seems Dr. Peat is on the right track,
As we already know the people highest at risk for COVID-19 are those with hypertention,
This matches what these studies suggest that the virus elicits its negative effects by decreasing the availability of the ACE2 (angiotensin degrading enzyme) through the CoV spike protein.
These studies have claimed angiotensin blockers, and ACE2 promoting substances as a potential for the main line of treatment (which have already shown wide success is respiratory ailments)
Something Dr. Peat has mentioned already and also suggested ACE2 promoters such as progesterone, vitamin B1, aspirin (things that are already known to have powerful anti-viral effects)
The recent studies have suggested that resistance to the virus has more to do with overall health and the ability to produce enough ACE2 to offset what the virus is doing, rather than the general idea of immunity.
(Along with oxidative metabolism/FFA levels etc.)
Many have claimed we dont have immunity but none of them have defined what immunity really is relative to this specific virus,
Based on these various studies, we can start to shift towards the conclusion that immunity, or (resistance) is largely dependant on the ability to degrade angiotensin through the ACE2 enzyme, something healthy people, and people with low risk of hypertension have good cappability of doing,
(And the metabolic rate/ thyroid function)
Supporting the idea that this virus (like every other virus in history) generally affects those who are already have compromised health and who are already at high risk of pulmonary disorders and hypertension among other things.
Concluding this it would be interesting to see some trials with the approach of addressing ACE2 and blocking angiotensin with angiotensin receptor antagonists,
And ACE2 promoters.
Many people have told me things like, “its a new virus we dont have immunity to it”
Or
“SARS caused by corona virus is different than other causes, or pneumonia caused by corona virus is different”
However none of them have EVER once provided any resources/studies to back up those mainstream medicine ideologies,
This is just a copy and paste from a post i made about this on facebook, but these studies point towards immunity likely being a matter of being able to produce enough ACE2 to degrade angiotensin because the virus decreases the availability of the ACE2 enzyme which degrades angiotensin.
Young and healthy people have been quoted to produce more ACE2, which outlines why some dont suffer symptoms,
Also as @haidut has shared in one of his threads, the evidence we have right now suggests SARS (regardless of trigger) may be due to elevated lipolysis from PUFA.
COVID-19/SARS May Be Due Simply To Serum PUFA And Its Peroxidation
Which implies As the study mentioned, SARS may be just an inflammatory disorder driven largely by the peroxidation of PUFA.
“Thus, the serum acyl ratio may not only prospectively identify and facilitate the assessment of new treatments in patients at highest risk for developing ARDS, but may also lead to new insights about the pathogenesis of ARDS."
Which would dismiss the empty claims that people have made suggesting SARS caused by COVID-19 is completely different, because so far there has been no evidence to support that.
We do have evidence however, suggesting SARS is caused by elevated FFA, where the virus is just the stress trigger (which would explain why drugs that inhibit lipolysis have been so effective in SARS and viral infections)
It seems Dr. Peat is on the right track again and may be correct on this,
I had someone critisize Peat implying he didnt do his research which i thought was comical,
This is the original post i made and theres 3 studies that support the idea of using angiotensin blockers/ACE2 promoters as treatment/protection from this pandemic as we like to call it.
———————————————————————
So its been known for quite some time now that this COVID-19 and the previous strains cause respiratory failure through a modulation of the ACE2 enzyme that degrades angiotensin with something called the spike protein in the virus.
The ACE2 enzyme is produced in larger amounts in younger and healthier people which would provide an explanation as to why some people are asymptomatic or able to handle the infection fine with no symptoms.
The virus, has been cited to attach so to speak to the ACE2 enzyme and decrease the bioavailability of it,
The ACE2 enzyme has been implicated in protecting from fibrosis and lung failure which is known to be the main causes of death in SARS/COVID-19
Therapies that increase the production of ACE2 (so it outweighs what the virus is doing) has been suggested along with angiotensin inhibitors, which have a very good history of success in SARS from many viral infections including the corona virus types.
—————————————————————
“Some studies have reported an increased inflammatory responses due to AT1 activated by AngII. In some pathological conditions, overactivation of AT1 may lead to damaging events such as fibrosis in different organs (eg, liver and lungs), perhaps through increasing TGF-β expression. Other studies have indicated that ACE2 has a protective effect on the fibrogenesis and inflammation of different organs, as well as the liver and the lungs. Taking these studies together, the ACE–AngII–AT1 axis in the RAS system shows a predominant role in organ fibrosis, par- ticularly in the lungs and liver.
(Which we also know serotonin plays a huge part)
“According to some recent studies, ACE2 has a regulatory effect on innate immunity and gut microbiota composition. Moreover, ACE2 has a determinant antifibrotic role in the lung injury induced by sepsis, acid aspiration, SARS, and lethal avian influenza A H5N1 virus.”
“Accordingly, losartan is a selective antagonist of AT1 receptor that exerts an inhibitory effect on the ACE–AngII–AT1 axis in the RAS system, a known molecular pathway for end-organ fibrosis. Thus, losartan may be suggested as a potential agent of protection from lung damage induced by COVID-19. Losartan may also have a protective function against lung fibrosis through other molecular mechanisms such as the downregulation of TGF-β1. This hypothesis need to be verified through in vitro and in vivo investigations.”
https://www.cambridge.org/core/serv...n_against_coronavirus_induced_lung_damage.pdf
—————————————————————
“These results show that SARS CoV spike protein can directly affect the development of severe acute lung failure through ACE2”
Taken together our data show that SARS CoV spike can exaggerate acute lung failure through the deregulation of the renin-angiotensin system. Moreover SARS CoV spike-mediated lung failure can be rescued by the inhibition of AT1R.”
https://www.researchgate.net/public..._ACE2_in_SARS_coronavirus-induced_lung_injury
—————————————————————
“The risk model established upon IL-6, CRP and hypertension had the highest predictability in this study. Besides, IL-6 played a pivotal role in the severity of COVID-19 and had a potential value for monitoring the process of severe cases.”
https://www.researchgate.net/public...sess_the_severity_of_coronavirus_disease_2019
—————————————————————
I had first heard that this COVID-19 virus initiated its negative effects through the angiotensin system from Dr. Ray Peat who was doing his own research on the virus and suggested losartan and ACE2 promoters as a possible treatment for this virus.
When i looked it up for my myself i came across various studies such as these supporting that claim so it seems Dr. Peat is on the right track,
As we already know the people highest at risk for COVID-19 are those with hypertention,
This matches what these studies suggest that the virus elicits its negative effects by decreasing the availability of the ACE2 (angiotensin degrading enzyme) through the CoV spike protein.
These studies have claimed angiotensin blockers, and ACE2 promoting substances as a potential for the main line of treatment (which have already shown wide success is respiratory ailments)
Something Dr. Peat has mentioned already and also suggested ACE2 promoters such as progesterone, vitamin B1, aspirin (things that are already known to have powerful anti-viral effects)
The recent studies have suggested that resistance to the virus has more to do with overall health and the ability to produce enough ACE2 to offset what the virus is doing, rather than the general idea of immunity.
(Along with oxidative metabolism/FFA levels etc.)
Many have claimed we dont have immunity but none of them have defined what immunity really is relative to this specific virus,
Based on these various studies, we can start to shift towards the conclusion that immunity, or (resistance) is largely dependant on the ability to degrade angiotensin through the ACE2 enzyme, something healthy people, and people with low risk of hypertension have good cappability of doing,
(And the metabolic rate/ thyroid function)
Supporting the idea that this virus (like every other virus in history) generally affects those who are already have compromised health and who are already at high risk of pulmonary disorders and hypertension among other things.
Concluding this it would be interesting to see some trials with the approach of addressing ACE2 and blocking angiotensin with angiotensin receptor antagonists,
And ACE2 promoters.
Ray Peat right again. haidut right again!!!
