I've seen a few other people covering this, and so I finally decided to look at the paper. Just as you stated, it seems entirely confusing how they got their results.
For instance, when considering VAP did they differentiate pneumonia from SARS-COV2 vs VAP? The methods suggest that at least 48 hours on a ventilator with bacterial culturing were used to suggest a VAP episode:
". By definition, VAP was considered to be an incident pneumonia that was diagnosed by a BAL performed after at least 48 hours of mechanical ventilation (39); only VAP episodes that were adjudicated to be due to bacteria were included in the analysis. "
They don't provide any evidence of what bacteria they cultured, and the study does not appear to use SARS-COV2 ICU patients without ventilation as a frame of reference (the 190 included appeared to have had SARS-COV2-related pneumonia, although one can argue that the design of SCRIPT would inherently focus only on pneumonia so this group should be assumed to not be included).
So I'm struggling to see how they were able to fully differentiate SARS-COV2 pneumonia from VAP, but I suppose that's an issue with any VAP study. They also don't indicate specific timepoints for when BAL samples were collected, just stating they did "serial collection".
I tried skimming through the supplemental section but it doesn't seem to indicate the number of BAL samples collected. This sentence in the methods makes it seem as if they only collected samples at the time of a suspected episode of pneumonia, but does that mean they continued to take samples throughout the course of the infection:
"ICU physicians at NMH routinely obtain bronchoscopic or non-bronchoscopic BAL samples
from mechanically ventilated patients whenever pneumonia is suspected (47)."
Given that all of the correlations made by their software are dependent upon the data they provide it, I would assume that there's an inherent bias in these results that should be taken into great account.
I think the last thing I noticed so far is that they never mentioned anything related to actual quantitation of cytokine profiles. Their limitations actually mentions that they did not quantitate any inflammatory biomarkers, but rather it appears that they are making assumptions about a "cytokine storm" with respect to the transitions into worse groups. This would seem like a non-answer for anything for or against the cytokine storm argument. It just looks like they didn't take any approach at all and are just making qualitative assumptions.
I haven't spent more time with this paper but it seems like so much was left up to how the AI interpreted the results that I can't help but consider this a fishing expedition.
May 12, 2023ยทedited May 12, 2023Liked by Brian Mowrey
So, the virus caused lung damage, which we can infer because their O2sats got real low, but that was likely because they were denied any meds to treat the virus.
Then they were hooked up to ventilators and lots of them developed secondary infections which then killed them.
These people have no idea what they're talking about. Look at CRP of severe covid sufferers, driven predominantly by IL-6, TNF-alpha, and IL-1แบ. I experienced it first-hand. Thank God for colchicine.
Years ago, they were doing a study on ARDS (acute respiratory distress syndrome.) I don't know the difference with the SARS supposedly caused by the sars virus.
It was about high-dose intravenous vitamin c treatment.
Brian, do you know anything about this?
In particular, to your current knowledge, is it possible to stop viral replication by using megadoses of ascorbic acid or sodium ascorbate directly on the bloodstream?
One last question, if you don't mind. to your knowledge, is it possible to prevent the progression of the disease by the mechanism of preventing viral entry to non-infected cells?
Basically even in the sickest and most comorbid of patients who actually died from covid, true myocarditis was a factor in less than 2% of deaths, whereas cardiac clotting and inflammation was a factor in ~50% of deaths.
I take this to mean that spike protein is basically bad for you, whatever the source. ๐ค
Does it matter what you call it? High levels of inflammation and very elevated markers of inflammatory cytokines/chemokines are characteristics of the early variants of SARS-CoV-2.
The first autopsies on COVID deaths uniformly revealed major blood clotting (micro & macro clots) in the lungs, quite capable of being the cause of the severe hypoxia observed in those patients. They didn't even need secondary bacterial infections/pneumonia. They suffocated to death because of severely impaired perfusion from the blocked circulation.
Cytokine storm is real and has been discussed in ICU's before Covid. Release of chemicals in massive amounts causing massive inflammation. Inhalation breathing treatments greatly reduced the inflammatory response and kept many out of the hospital. Those who were hospitalized were usually past the massive viral replication phase and into the cytokine release phase but were not given high enough doses of steroids and the less effective steroids to boot.
Another take that seems more reasonable:
https://popularrationalism.substack.com/p/missed-bacterial-pneumonia-cases
It seems very hard to get to the truth, or is it the case that so many are interested in muddying the waters?
https://peterhalligan.substack.com/p/denis-rancourt-there-was-no-c19-respiratory
Another interesting speculation about suddenly:
https://geoffpain.substack.com/p/atrial-fibrillation-is-the-most-common
However, this article suggests to me that there are multiple mechanisms relating to vaccinations and suddenly: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10166549/pdf/pone.0283988.pdf
I've seen a few other people covering this, and so I finally decided to look at the paper. Just as you stated, it seems entirely confusing how they got their results.
For instance, when considering VAP did they differentiate pneumonia from SARS-COV2 vs VAP? The methods suggest that at least 48 hours on a ventilator with bacterial culturing were used to suggest a VAP episode:
". By definition, VAP was considered to be an incident pneumonia that was diagnosed by a BAL performed after at least 48 hours of mechanical ventilation (39); only VAP episodes that were adjudicated to be due to bacteria were included in the analysis. "
They don't provide any evidence of what bacteria they cultured, and the study does not appear to use SARS-COV2 ICU patients without ventilation as a frame of reference (the 190 included appeared to have had SARS-COV2-related pneumonia, although one can argue that the design of SCRIPT would inherently focus only on pneumonia so this group should be assumed to not be included).
So I'm struggling to see how they were able to fully differentiate SARS-COV2 pneumonia from VAP, but I suppose that's an issue with any VAP study. They also don't indicate specific timepoints for when BAL samples were collected, just stating they did "serial collection".
I tried skimming through the supplemental section but it doesn't seem to indicate the number of BAL samples collected. This sentence in the methods makes it seem as if they only collected samples at the time of a suspected episode of pneumonia, but does that mean they continued to take samples throughout the course of the infection:
"ICU physicians at NMH routinely obtain bronchoscopic or non-bronchoscopic BAL samples
from mechanically ventilated patients whenever pneumonia is suspected (47)."
Given that all of the correlations made by their software are dependent upon the data they provide it, I would assume that there's an inherent bias in these results that should be taken into great account.
I think the last thing I noticed so far is that they never mentioned anything related to actual quantitation of cytokine profiles. Their limitations actually mentions that they did not quantitate any inflammatory biomarkers, but rather it appears that they are making assumptions about a "cytokine storm" with respect to the transitions into worse groups. This would seem like a non-answer for anything for or against the cytokine storm argument. It just looks like they didn't take any approach at all and are just making qualitative assumptions.
I haven't spent more time with this paper but it seems like so much was left up to how the AI interpreted the results that I can't help but consider this a fishing expedition.
On a related subject, a paper was published suggesting that the S1 protein contains a nuclear localization signal and that the mRNA piggy backs on it.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9536038/
So, the virus caused lung damage, which we can infer because their O2sats got real low, but that was likely because they were denied any meds to treat the virus.
Then they were hooked up to ventilators and lots of them developed secondary infections which then killed them.
It that the real story?
These people have no idea what they're talking about. Look at CRP of severe covid sufferers, driven predominantly by IL-6, TNF-alpha, and IL-1แบ. I experienced it first-hand. Thank God for colchicine.
This must be a bit of a joke, The cytokine storm is not real but covid is? Come on. How can anyone take this article seriously?
Off-topic but related.
Years ago, they were doing a study on ARDS (acute respiratory distress syndrome.) I don't know the difference with the SARS supposedly caused by the sars virus.
It was about high-dose intravenous vitamin c treatment.
Brian, do you know anything about this?
In particular, to your current knowledge, is it possible to stop viral replication by using megadoses of ascorbic acid or sodium ascorbate directly on the bloodstream?
One last question, if you don't mind. to your knowledge, is it possible to prevent the progression of the disease by the mechanism of preventing viral entry to non-infected cells?
Thhanks!
The lungs were injured by the ventilators - hence the urgency to have more ventilators at the beginning of 2020
It was increased lung pressure and
oxygen toxicity that resulted in
Alveoli damage in 90%
Read my article
We breathe air not oxygen
And youโll see lung physiology has no thing to do with oxygen and carbon dioxide gaseous exchange - and this gaseous belief retards medicine!
Research oxygen toxicity!
The lungs are hydrating the RBCs with salt water.
The oxygen red light monitoring is really just recording RBC hydration with light penetration
Dehydrated: contracted dense RBCs
Hydrated: plump bright RBCs
80% oxygenation is really 80% hydration or 20% dehydrated
Salt is the sponge
Water then follows
Reminds me of this study which got no attention attention in the media whatsoever:
Myocarditis is rare in COVID-19 autopsies: cardiovascular findings across 277 postmortem examinations
https://pubmed.ncbi.nlm.nih.gov/33132119/
Basically even in the sickest and most comorbid of patients who actually died from covid, true myocarditis was a factor in less than 2% of deaths, whereas cardiac clotting and inflammation was a factor in ~50% of deaths.
I take this to mean that spike protein is basically bad for you, whatever the source. ๐ค
Does it matter what you call it? High levels of inflammation and very elevated markers of inflammatory cytokines/chemokines are characteristics of the early variants of SARS-CoV-2.
The first autopsies on COVID deaths uniformly revealed major blood clotting (micro & macro clots) in the lungs, quite capable of being the cause of the severe hypoxia observed in those patients. They didn't even need secondary bacterial infections/pneumonia. They suffocated to death because of severely impaired perfusion from the blocked circulation.
Cytokine storm is real and has been discussed in ICU's before Covid. Release of chemicals in massive amounts causing massive inflammation. Inhalation breathing treatments greatly reduced the inflammatory response and kept many out of the hospital. Those who were hospitalized were usually past the massive viral replication phase and into the cytokine release phase but were not given high enough doses of steroids and the less effective steroids to boot.