Dec 29, 2023·edited Dec 30, 2023Liked by Brian Mowrey
Regarding happy hypoxia: at some point when I had Covid in Nov 2020, my blood oxygen briefly dropped to 88. At this time I felt slightly dizzy, but not suffocating. Having heard about happy hypoxia and having heard bad things about hospitals, I decided to stay home. Fortunately, in a few hours the blood oxygen went above 90 and never came down again.
I do not want to comment on pneumonia because of lack of knowledge, but I had loved ones with post-viral bacterial pneumonia who were helped by strong antibiotics.
An idea the search turned up is that COVID disease harm is largely caused by nucleocapsid protein and mutations, so I guess vaxx harm (aside IGg4 tolerance) must be largely caused by manufacturing and purity issues, as nucleocapsid is absent. Therefore spike toxicity may be somewhat of a red herring. Your thoughts?
Thanks! I've always been skeptical of "spike as super-poison" just based on what is availably knowable about our biological understanding to begin with. E.g., what do we know about the ability of regular coronavirus spike proteins to disrupt vascular epithelium or clotting pathways? So there's no baseline. Spike causes abnormal clotting in the Pretorius, et al. series. That's probably not a good end-product for an mRNA transfection, then. But is it any worse than other coronavirus spikes, or other SARS-CoV-2 proteins? We have no idea.
N protein is a good example of this. Two authors plugged the (Wuhan model) spike sequence into a prion-forming domain proteomics algorithm, got a slight blip, which doesn't mean a protein has a prion-forming domain or is even likely to. And so in skeptic space this study was quoted as being the end of the world. But the N protein, as part of the normal nucleocapsid phenotype, has a much higher score across all variants. So it's obviously more hypothetically 'prion-like.' At the same time, the secondary-RNA structures of the mRNA vaccines could potentially deform natural human prion protein. So hypothetical prion risk applies to both virus and vaccine - but, not really to the spike protein itself https://unglossed.substack.com/p/spike-protein-and-prions-pt-2
But very little work has been done on N. Archer, et al. look at Nsp7, Nsp9m and M as far as causing perfusion of air-less lung regions, which is the cause of Covid-19 hypoxia https://unglossed.substack.com/p/the-virus-and-hpv A bunch of preprints have looked at other nonstructural proteins. Regarding the two studies on N you have linked to, one is about cytokine storm, which isn't something that actually happens with Covid-19. The virus pumps cells full of immune-suppressing proteins, so it isn't so relevant whether S or N are more likely to trigger innate immune alarms as whether baseline antiviral immunity is tuned up high, as it is with children but isn't with older adults. In the second, it doesn't seem to make much sense to look for associations with N protein in a combined Delta-Omicron sample since most associations are just going to be clonally fixed. I.e., Delta is red-haired Vikings and Omicron brown-haired Italians, this doesn't mean hair color is determining differences in military ferocity.
I'm trying to recall prior readings but I believe it was the N protein that was looked at in prior coronavirus vaccine studies and was one of the main culprits in ADE seen in animal models. I actually wanted to write an article a few moons ago suggesting that the N protein probably wouldn't be a good candidate for vaccination since prior history and mechanistic reasons would discount this being a viable candidate.
The patients who waited for ten days at home unattended without any testing for treatment for bacterial pneumonia and who were then given antibiotics were an unusual type of bacterial pneumonia, biased toward severe bacterial given the long duration, thus as increased risk of death even with antibiotics. Once given a pcr+ based COVID diagnosis, most were not tested again for bacterial pneumonia. They were also not given corticosteroids. Semantic argumentation does not change the clinical protocol for COVID19 diagnosis forced on hospitals by public health, which included the denial of the existence of rt-pcr false positives. I have a massive intensive report on the effects of CDCs diagnostic protocol, and we and others have the data on non-Q pcr FP rates, starting with Basil et al at 11%, matching toward 38% and now who knows due to viral evolution and regulatory complicity on lax standards for testing.
The waiting was informed by the symptoms. If they develop bacterial pneumonia, that's the symptoms. But it wasn't the symptoms. I don't see how you can assume 'prolonged bacterial pneumonia.' People would have just died at home if they spent days and days with bacterial pneumonia. Further, most pneumonia already has delay as a contributing factor in pre-hospital care - homeless, elderly people who are alone, kids who are ignored by lower income parents. This is common thing in cities, getting to the hospital late. But the result - the aggregate of symptoms seen in Covid-19 - does not follow.
Fauci told everyone if they had respiratory symptoms to stay home for ten days, and if they got sick enough to need hospitalization, go to the ER. Follow the logic, it leads to the fact that most people who died on ventilators died from bacterial pneumonia, not COVID. Even the protocolists have confessed this. https://popularrationalism.substack.com/p/you-are-not-ready-for-this-did-protocolists
There is no logic that leads to that conclusion. Only the assumption that the virus did not cause deaths leads to that conclusion. But it's just an assumption. And doesn't say anything about what Covid-19 was actually like, or even really look at the question.
I doubt anyone had "ten days" memorized. People went to the hospital, and were admitted, once they were in respiratory distress. They didn't sit at home with bacterial pneumonia. In the original paxlovid high risk trial, placebo recipients are recruited avg day 3 of symptom onset, not more than 5 per protocol. Fig 2b gives the Kaplan-Meier plot for hospitalization. By day 6, most in placebo who would be hospitalized already are. This is in multiple countries in 2021 but US is heavily represented. https://www.nejm.org/doi/full/10.1056/nejmoa2118542
Even the study claiming ventilator-associated pneumonia contributed to death doesn't support the same conclusion. Covid-19 patients spend longer on ventillation, so naturally VAP is common. But 42.6% of 190 Covid-19 ICU patients studied never had VAP, and of those, just over 40% still died, whereas deaths in the group having at least one VAP are almost the same (just under 50%). So you take away VAP and deaths are almost just as frequent. And since VAP is more frequent with longer ICU stays there's nothing obviously causal about the slightly higher death rate in the VAP group to begin with. https://www.jci.org/articles/view/170682
It's absurd to make the unwarranted generalization that none of the respiratory illnesses people experienced in home that festered for 10 days we're not bacterial pneumonia. Some percentage were also RSV some percentage for also influenza and other respiratory viruses. Starting from that necessary premise, as would be dictated by reality, your conclusions are faulty.
Is the question what killed "most people" who were reported as Covid-19 deaths or what killed a minority (perhaps 10%, perhaps 1%, etc.)?
Typical US hospitalizations for pneumonia were 1,000,000/year in 2019. Supposing that SARS-CoV-2 does not cause Covid-19, then a PCR+ does not cause "pneumonia from bacteria, RSV, influenza, other respiratory viruses." In other words, unless agreeing that SARS-CoV-2 causes Covid-19, the portion of these normal 1,000,000 that are hypothetically denied timely care due to PCR+ is simply the positivity rate for all tests from Mar 2020 to April 2021, which was somewhere between 10 and 20%. I'll see if I can get raw numbers here.
So you have 100,000 to 200,000 "regular pneumonia hospitalizations" that are delayed by PCR+. This doesn't get you to 3 million+ Covid-19 hospitalizations that occurred in the same year. At most it's 3 - 6%. You can try to model in how many hospitalizations are normally prevented by outpatient antibiotics, fine. Intuitively it doesn't seem like it would get very close.
You are discounting without evidence the horrifying fact that EVERYONE with bacterial pneumonia was denied early care... for ten days. In think now you can see the very straightforward point. Good luck.
Thankyou for your work. Dr Kory/FLCCC wrote early on that he/they were seeing Organising Pneumonia possibly caused by hypersensitivity pneumonitis. Dr Kory stated that most doctors misdiagnose Organising Pneumonia, they aren't trained to see it on X-ray and have a default setting to antibiotics.
The hypersensitivity pneumonitis fits with the comments of South African Dr Shankara Chetty, who was highly successful with his early treatment program. Dr Chetty used antihistamines as part of his protocol, he said there was an allergic response to the Spike Protein.
I will not be saying " I told you" when the whole virus theory falls apart as it has in fact for those who are willing to question as we must. Good luck with your stories.
Dec 25, 2023·edited Dec 26, 2023Liked by Brian Mowrey
I believe the virus was real, it was made in a lab but had largely the same effects as an earlier Sars-cov from 2003 (the lab alterations did make it more insidious long term). I also think bacterial pneumonia could occur in the elderly, but after the original infection, so they would get sick 10-14 days after the original viral infection. Sadly, giving out antibiotics is now being accompanied with virtue signaling- "we have to be careful giving these out because it can cause antibiotic resistance" (never mind that antibiotic resistance is mainly occurring in countries that offer antibiotics over the counter not in countries requiring prescriptions, or possibly in the widespread use of antibiotics in the animal farming industry). As a result, I do think many elderly people died when antibiotics were not given out freely. I used to live in the UK and their reluctance to give antibiotics is literally why you see still so many outrageous meningitis cases, they just refuse to give the antibiotics from the get go.
I'm with you on being skeptical of the antibiotic-resistance fearmongering. Bacteria aren't really "evolving" because *we* now also attack them with molecules that have been part of the microbial arsenal for millions of years. It's just different portions of bacteria with certain plasmids and phages with certain nasty genes becoming more prominent at a given moment. Not the end of the world.
I don't have strong intuitions regarding how likely UK deaths were to be iatrogenic. But in the US we had deaths, despite as I said smothering Covid 19 patients with antibiotics. From my original post on the issue - https://unglossed.substack.com/p/the-myth-of-secondary-infection-in
How many received steroids along with antibiotics? My asthmatic family members who tested positive for Covid19 and developed pneumonia were treated with zpack and steroids (along with prescription strength cough medications) and recovered as they had preCovid. It was a battle to get prescriptions for the steroids- they kept telling me it wasn't part of the suggested protocol- but I argued that the combo always worked in the past. The typical response was to wait until they couldn't breathe, then rush them to the ER - I said hell no, I'll follow proven protocols. But it was a huge fight to get the steroids.
My impression is that steroids were given to most if not almost all hospitalized patients. I don't think anything beyond waiting days and days to treat was necessary as far as the 'iatrogenic' element goes. Ok now this person's lungs don't work - let's start poisoning them. No, a lot will die even if you help.
I believe dexamethasone was used rather commonly, but there was the matter of some arguing that the dosage wasn't high enough to treat the hyper-immune response, although I have seen some articles suggesting that the immunosuppressive nature of the drug may be more harmful at higher dosages. It seems to have been one of those points of contention that disappeared from the discussion.
I agree with you about the hospitals and the deaths stateside- the ventilator and remdesivir did most of the damage. I meant more elderly homes (not the hospitals) where they didn’t give antibiotics after the initial infection cleared. I think that makes sense that the older patients were prone to getting a secondary infection of pneumonia and then few were prescribed the necessary antibiotics. Really terrible medical decisions were made right and left, zero common sense. Like this policy in NY and CT of- “only come to the hospital if your lips turn blue, we can’t treat you beforehand” was genuinely criminal and medical malpractice.
Thank you for so eloquently putting into words what I cannot! My simplistic way of explaining to my husband what the post that you refer to is about, can be summed up as two sides arguing
‘That car is red’ v ‘ No, that bike is blue’.
Why do people on ‘our’ side continue to tie themselves up in knots arguing over things that are not helpful. I used the above example as a reply to an Unbekoming post on whether viruses existed trying to clarify how I think the no virus people argue.
I can only hope that if there really is a secret cabal of evil-doers behind all this then they are all infighting and squabbling just as much and therefore their plans won’t come to fruition!
Thank you! - I considered quoting from or linking to your, ian, and SMS's comments for a more grounded response to the 'no novel disease' argument. At this point, I (almost) only engage with the meta - 'here is why this line of thinking is just a trap that, in fact, you could set out for any knowledge that exists...' A magic trick used to wow the crowd.
Why the need, who knows. You can totally embrace the mainstream / official numbers and say, look, this was only 1/100 as bad as the worst hype said it would be. And calling this a 'pandemic' is politically and civically caustic, it catastrophizes near-normal levels of sickness and death. But no- it is instead that last 1/100 which has to be the thing attacked at all costs (including accuracy, and knowledge).
Regarding happy hypoxia: at some point when I had Covid in Nov 2020, my blood oxygen briefly dropped to 88. At this time I felt slightly dizzy, but not suffocating. Having heard about happy hypoxia and having heard bad things about hospitals, I decided to stay home. Fortunately, in a few hours the blood oxygen went above 90 and never came down again.
I do not want to comment on pneumonia because of lack of knowledge, but I had loved ones with post-viral bacterial pneumonia who were helped by strong antibiotics.
Great article😃 Prof Carl Henegan has written a paper about this too:
https://www.cebm.net/covid-19/differentiating-viral-from-bacterial-pneumonia/
An idea the search turned up is that COVID disease harm is largely caused by nucleocapsid protein and mutations, so I guess vaxx harm (aside IGg4 tolerance) must be largely caused by manufacturing and purity issues, as nucleocapsid is absent. Therefore spike toxicity may be somewhat of a red herring. Your thoughts?
https://link.springer.com/article/10.1007/s15010-023-02142-4
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10224071/
Thanks! I've always been skeptical of "spike as super-poison" just based on what is availably knowable about our biological understanding to begin with. E.g., what do we know about the ability of regular coronavirus spike proteins to disrupt vascular epithelium or clotting pathways? So there's no baseline. Spike causes abnormal clotting in the Pretorius, et al. series. That's probably not a good end-product for an mRNA transfection, then. But is it any worse than other coronavirus spikes, or other SARS-CoV-2 proteins? We have no idea.
N protein is a good example of this. Two authors plugged the (Wuhan model) spike sequence into a prion-forming domain proteomics algorithm, got a slight blip, which doesn't mean a protein has a prion-forming domain or is even likely to. And so in skeptic space this study was quoted as being the end of the world. But the N protein, as part of the normal nucleocapsid phenotype, has a much higher score across all variants. So it's obviously more hypothetically 'prion-like.' At the same time, the secondary-RNA structures of the mRNA vaccines could potentially deform natural human prion protein. So hypothetical prion risk applies to both virus and vaccine - but, not really to the spike protein itself https://unglossed.substack.com/p/spike-protein-and-prions-pt-2
But very little work has been done on N. Archer, et al. look at Nsp7, Nsp9m and M as far as causing perfusion of air-less lung regions, which is the cause of Covid-19 hypoxia https://unglossed.substack.com/p/the-virus-and-hpv A bunch of preprints have looked at other nonstructural proteins. Regarding the two studies on N you have linked to, one is about cytokine storm, which isn't something that actually happens with Covid-19. The virus pumps cells full of immune-suppressing proteins, so it isn't so relevant whether S or N are more likely to trigger innate immune alarms as whether baseline antiviral immunity is tuned up high, as it is with children but isn't with older adults. In the second, it doesn't seem to make much sense to look for associations with N protein in a combined Delta-Omicron sample since most associations are just going to be clonally fixed. I.e., Delta is red-haired Vikings and Omicron brown-haired Italians, this doesn't mean hair color is determining differences in military ferocity.
I'm trying to recall prior readings but I believe it was the N protein that was looked at in prior coronavirus vaccine studies and was one of the main culprits in ADE seen in animal models. I actually wanted to write an article a few moons ago suggesting that the N protein probably wouldn't be a good candidate for vaccination since prior history and mechanistic reasons would discount this being a viable candidate.
Wow, thanks for the detailed explanation and have a great Christmas and New Year! 🎊🎆
The patients who waited for ten days at home unattended without any testing for treatment for bacterial pneumonia and who were then given antibiotics were an unusual type of bacterial pneumonia, biased toward severe bacterial given the long duration, thus as increased risk of death even with antibiotics. Once given a pcr+ based COVID diagnosis, most were not tested again for bacterial pneumonia. They were also not given corticosteroids. Semantic argumentation does not change the clinical protocol for COVID19 diagnosis forced on hospitals by public health, which included the denial of the existence of rt-pcr false positives. I have a massive intensive report on the effects of CDCs diagnostic protocol, and we and others have the data on non-Q pcr FP rates, starting with Basil et al at 11%, matching toward 38% and now who knows due to viral evolution and regulatory complicity on lax standards for testing.
*PCR + based COVID diagnosis*
---
Dr. James...is this accepted in the medical community as a legit diagnostic method?
The waiting was informed by the symptoms. If they develop bacterial pneumonia, that's the symptoms. But it wasn't the symptoms. I don't see how you can assume 'prolonged bacterial pneumonia.' People would have just died at home if they spent days and days with bacterial pneumonia. Further, most pneumonia already has delay as a contributing factor in pre-hospital care - homeless, elderly people who are alone, kids who are ignored by lower income parents. This is common thing in cities, getting to the hospital late. But the result - the aggregate of symptoms seen in Covid-19 - does not follow.
Fauci told everyone if they had respiratory symptoms to stay home for ten days, and if they got sick enough to need hospitalization, go to the ER. Follow the logic, it leads to the fact that most people who died on ventilators died from bacterial pneumonia, not COVID. Even the protocolists have confessed this. https://popularrationalism.substack.com/p/you-are-not-ready-for-this-did-protocolists
There is no logic that leads to that conclusion. Only the assumption that the virus did not cause deaths leads to that conclusion. But it's just an assumption. And doesn't say anything about what Covid-19 was actually like, or even really look at the question.
I doubt anyone had "ten days" memorized. People went to the hospital, and were admitted, once they were in respiratory distress. They didn't sit at home with bacterial pneumonia. In the original paxlovid high risk trial, placebo recipients are recruited avg day 3 of symptom onset, not more than 5 per protocol. Fig 2b gives the Kaplan-Meier plot for hospitalization. By day 6, most in placebo who would be hospitalized already are. This is in multiple countries in 2021 but US is heavily represented. https://www.nejm.org/doi/full/10.1056/nejmoa2118542
Even the study claiming ventilator-associated pneumonia contributed to death doesn't support the same conclusion. Covid-19 patients spend longer on ventillation, so naturally VAP is common. But 42.6% of 190 Covid-19 ICU patients studied never had VAP, and of those, just over 40% still died, whereas deaths in the group having at least one VAP are almost the same (just under 50%). So you take away VAP and deaths are almost just as frequent. And since VAP is more frequent with longer ICU stays there's nothing obviously causal about the slightly higher death rate in the VAP group to begin with. https://www.jci.org/articles/view/170682
First study supported by Pfizer.
Second one appears to be NIH/NIAAD.
I seem to recall you linking the Pfizer NEJM once before.
👍
Yes, good point. Why don't I more frequently cite "retards humping sheep"?
What an absolute dick you are.
It's absurd to make the unwarranted generalization that none of the respiratory illnesses people experienced in home that festered for 10 days we're not bacterial pneumonia. Some percentage were also RSV some percentage for also influenza and other respiratory viruses. Starting from that necessary premise, as would be dictated by reality, your conclusions are faulty.
Is the question what killed "most people" who were reported as Covid-19 deaths or what killed a minority (perhaps 10%, perhaps 1%, etc.)?
Typical US hospitalizations for pneumonia were 1,000,000/year in 2019. Supposing that SARS-CoV-2 does not cause Covid-19, then a PCR+ does not cause "pneumonia from bacteria, RSV, influenza, other respiratory viruses." In other words, unless agreeing that SARS-CoV-2 causes Covid-19, the portion of these normal 1,000,000 that are hypothetically denied timely care due to PCR+ is simply the positivity rate for all tests from Mar 2020 to April 2021, which was somewhere between 10 and 20%. I'll see if I can get raw numbers here.
So you have 100,000 to 200,000 "regular pneumonia hospitalizations" that are delayed by PCR+. This doesn't get you to 3 million+ Covid-19 hospitalizations that occurred in the same year. At most it's 3 - 6%. You can try to model in how many hospitalizations are normally prevented by outpatient antibiotics, fine. Intuitively it doesn't seem like it would get very close.
You are discounting without evidence the horrifying fact that EVERYONE with bacterial pneumonia was denied early care... for ten days. In think now you can see the very straightforward point. Good luck.
Thankyou for your work. Dr Kory/FLCCC wrote early on that he/they were seeing Organising Pneumonia possibly caused by hypersensitivity pneumonitis. Dr Kory stated that most doctors misdiagnose Organising Pneumonia, they aren't trained to see it on X-ray and have a default setting to antibiotics.
The hypersensitivity pneumonitis fits with the comments of South African Dr Shankara Chetty, who was highly successful with his early treatment program. Dr Chetty used antihistamines as part of his protocol, he said there was an allergic response to the Spike Protein.
I will not be saying " I told you" when the whole virus theory falls apart as it has in fact for those who are willing to question as we must. Good luck with your stories.
Nothing has fallen apart for you.
I believe the virus was real, it was made in a lab but had largely the same effects as an earlier Sars-cov from 2003 (the lab alterations did make it more insidious long term). I also think bacterial pneumonia could occur in the elderly, but after the original infection, so they would get sick 10-14 days after the original viral infection. Sadly, giving out antibiotics is now being accompanied with virtue signaling- "we have to be careful giving these out because it can cause antibiotic resistance" (never mind that antibiotic resistance is mainly occurring in countries that offer antibiotics over the counter not in countries requiring prescriptions, or possibly in the widespread use of antibiotics in the animal farming industry). As a result, I do think many elderly people died when antibiotics were not given out freely. I used to live in the UK and their reluctance to give antibiotics is literally why you see still so many outrageous meningitis cases, they just refuse to give the antibiotics from the get go.
I'm with you on being skeptical of the antibiotic-resistance fearmongering. Bacteria aren't really "evolving" because *we* now also attack them with molecules that have been part of the microbial arsenal for millions of years. It's just different portions of bacteria with certain plasmids and phages with certain nasty genes becoming more prominent at a given moment. Not the end of the world.
I don't have strong intuitions regarding how likely UK deaths were to be iatrogenic. But in the US we had deaths, despite as I said smothering Covid 19 patients with antibiotics. From my original post on the issue - https://unglossed.substack.com/p/the-myth-of-secondary-infection-in
Among 213,338 US Inpatients with “Covid-19”*
All, received antibiotics: 77.3%
Ventilated, received antibiotics: 95.9%
Died in hospital, received antibiotics: 91.7%
How many received steroids along with antibiotics? My asthmatic family members who tested positive for Covid19 and developed pneumonia were treated with zpack and steroids (along with prescription strength cough medications) and recovered as they had preCovid. It was a battle to get prescriptions for the steroids- they kept telling me it wasn't part of the suggested protocol- but I argued that the combo always worked in the past. The typical response was to wait until they couldn't breathe, then rush them to the ER - I said hell no, I'll follow proven protocols. But it was a huge fight to get the steroids.
My impression is that steroids were given to most if not almost all hospitalized patients. I don't think anything beyond waiting days and days to treat was necessary as far as the 'iatrogenic' element goes. Ok now this person's lungs don't work - let's start poisoning them. No, a lot will die even if you help.
I believe dexamethasone was used rather commonly, but there was the matter of some arguing that the dosage wasn't high enough to treat the hyper-immune response, although I have seen some articles suggesting that the immunosuppressive nature of the drug may be more harmful at higher dosages. It seems to have been one of those points of contention that disappeared from the discussion.
I agree with you about the hospitals and the deaths stateside- the ventilator and remdesivir did most of the damage. I meant more elderly homes (not the hospitals) where they didn’t give antibiotics after the initial infection cleared. I think that makes sense that the older patients were prone to getting a secondary infection of pneumonia and then few were prescribed the necessary antibiotics. Really terrible medical decisions were made right and left, zero common sense. Like this policy in NY and CT of- “only come to the hospital if your lips turn blue, we can’t treat you beforehand” was genuinely criminal and medical malpractice.
What he said!
Thank you for so eloquently putting into words what I cannot! My simplistic way of explaining to my husband what the post that you refer to is about, can be summed up as two sides arguing
‘That car is red’ v ‘ No, that bike is blue’.
Why do people on ‘our’ side continue to tie themselves up in knots arguing over things that are not helpful. I used the above example as a reply to an Unbekoming post on whether viruses existed trying to clarify how I think the no virus people argue.
I can only hope that if there really is a secret cabal of evil-doers behind all this then they are all infighting and squabbling just as much and therefore their plans won’t come to fruition!
Thank you! - I considered quoting from or linking to your, ian, and SMS's comments for a more grounded response to the 'no novel disease' argument. At this point, I (almost) only engage with the meta - 'here is why this line of thinking is just a trap that, in fact, you could set out for any knowledge that exists...' A magic trick used to wow the crowd.
Why the need, who knows. You can totally embrace the mainstream / official numbers and say, look, this was only 1/100 as bad as the worst hype said it would be. And calling this a 'pandemic' is politically and civically caustic, it catastrophizes near-normal levels of sickness and death. But no- it is instead that last 1/100 which has to be the thing attacked at all costs (including accuracy, and knowledge).