All DAMPS are not created equal. Some are more inflammatory than others. What DAMPS are released depend on the type of cell death. A healthy person will have 50 billion cells die each day, mostly via apoptosis which is relatively not inflammatory. Besides apoptosis you have necrosis/necroptosis and pyroptosis, which release more inflammatory DAMPS
As for the viral kinetics. The virus is gone in most immunocompetent patients within 10 days. There are other studies showing the same.
Remdesivir helps a bit with viral clearance, but is not required
“Model-based simulations predict that remdesivir reduced time to viral clearance by 0.7 days compared with SoC, ...Remdesivir had a larger impact in patients with high viral load at randomization, reducing viral production by 5-fold on...and median time to viral clearance by 2.4 days l”
“I could counter that 80% of ICU patients were PCR positive vs. only 25% of immunocompromised.”
The 25% were from the LTACH cohort who had been transferred from ICU for prolonged treatment. They were not all immunosuppressed
I am in favor of preventing lung damage and treating it effectively when it occurs. We should be making Ivermectin available OTC for early treatment and encouraging use of Vit D/C.
That said, no treatment is going to work for everyone
I remember John Paul wrote an interesting sub stack on bacteria binding to subunits of the spike protein.
"the Spike Protein interacted with (bacterial) LPS to form aggregates of Spike Protein",
"While using different pathways, a lot of the recent deaths directly from vaccination (as per the pathologists analysis) and from the infection since early 2020 have something in common. Bacterial overgrowth, excessive presence of bacteria in the blood."
Thanks for the trigger warning! With so much concern about long-term side effects of these injections, I've also kept in mind that they seem to have a short-term benefit on the very low risk of severe infection.
Some people seemingly cannot understand that if you survive the first shot (with few side-effects) you have a good chance of surviving subsequent shots.
“it sounds like the virus is perfectly capable of destroying lots of lung cells on its own, unchecked, thanks to suppression of antiviral innate immunity.”
I agree with this. However, Cell death promotes inflammatory response.
“Microbes-infected stressed or dying cells can also release Damage-associated molecular patterns (DAMPs),that can modulate immune sensing of infected cells. However, cytokines or chemokines have received more attention in the context of infection-associated cell death rather than DAMPs “
[I agree with you on Cytokine storm being the sole cause of excess inflammation]
“In his review article , W.G. Land surveyed the current literature on respiratory viruses (including, coronavirus disease-19 [COVID-19]) and found that DAMPs-driven immune responses also dominated respiratory virus pathology together with cytokine-associated responses. This review concludes that DAMPs might have an underappreciated role in the pathogenesis of acute respiratory distress syndrome and systemic inflammatory response syndrome (including COVID-19). The review also high- lights how DAMPs might serve the purpose of diagnostic or prognostic biomarkers for such infections.
A recent single-cell resolution analyses of lung- associated bronchoalveolar fluid from patients with severe COVID- 19, found that COVID-19 associated lung pathology was associated with considerable release of extracellular ATP . Accordingly, genetic signatures of purinergic and inflammasome signalling (that is downstream of extracellular ATP) were enriched across various lung-associated immune compartments “
“Replication-competent virus was detected in 4 of 11 (36.3%) immunocompromised patients up to 45 days after symptom onset and in 1 of 67 (1.5%) immunocompetent patients 10 days after symptom onset (P = .001). “
So the virus in immunocompetent people is defeated by the immune system in 10 days. No more replicating virus, but most people develop symptoms of serious disease as the virus is being defeated.
The immune response to the cell damage caused by the virus is what kills patients. Cytokine storm may well be overstated, but inflammation from inflammatory IgG (present in noticeable amounts by day 7-10) as well as immune cells responding to cell death also cause problems
Steroids
The Recovery Trial showed benefit of steroids. Clinicians argue it would show more at higher doses. Giving steroids during viral replication phase is non-sensible. As is giving kidney killing antivirals [Remdesivir] after viral replication phase is over. Its all about timing.
Most cases don’t become serious until 7-10 days after symptoms began because this is when the immune system goes into overdrive dealing with the lung cell damage and it also coincided with igG antibody production which is inflammatory (especially afucosylated antibodies).
Disease severity is correlated with higher levels of antibodies than those with mild disease. Thats because by the time antibodies are at a high level there is no virus to neutralize, but plenty of viral debris to latch onto , and this signals an army of Immune cells to clean the mess up
One of the great myths is that antibodies are the first line of defense. Most new antibodies created during infection of a virus for the first time are created after the innate immune cells and T-cells have all but knocked out the infection. The purpose of serum antibodies is to help prevent a reinfection in a short period of time and let the victorious immune system to recharge its batteries, and also as antibodies wane and reinfection occurs the memory B-Cells cant quick start antibody production and join the fight earlier allowing milder disease
As for milder disease in Omicron, Omicron does not replicate as well in the lungs as did earlier variants. Less cell death, so less inflammation. Besides, almost everyone has either been infected or vaxxed, so new IgG antibodies are all fucosylated (less inflammation)
As for the Paxlovid study. Its likely those with an early antibody response already had natural immunity due to earlier infection and had memory B cells which ramped up fucosylated antibodies early, while naive infected antibodies came later and were afucosylated. Remember, this is a Pfizer trial. Not to be trusted. They give Paxlovid out like candy in Taiwan and we are having 60 COVID DEATHS a day (equivalent to 900 in US)
I just followed a chain of links to previous articles and came across a reference to a paper from 2015 about Resident Memory T-Cells. Damn, I get a lot of value from your writing, so thank you very much.
That brought up a thought. To what extent would Trms from prior exposure to Corona viruses provide cross-reactive protection against SARS-CoV-2? Is there any research on this?
Feb 12, 2023·edited Feb 14, 2023Liked by Brian Mowrey
I agree it's a numbers game. If you can shut down replication of the virus fast enough you will be fine.
I am surprised, or maybe not, that you didn't mention Ivermectin. I think there is strong evidence that it functions as a protease inhibiter and also binds to the N protein and thus acts against the virus in multiple ways.
However, IMO, the strongest case that Ivermectin is effective against SARS-CoV-w is the fact that a fake paper was submitted to the Lancet that claimed it was dangerous, and was quickly published, only to be retracted after about a month when it was discovered to be fake.
Update. I was mistaken. It was HCQ that the fake paper was submitted to the Lancet about. So, that tells me HCQ was effective. However, the various trials of Ivermectin all used subterfuges to provide a negative result, like using too little or dosing it too late.
I appreciate that you're taking a nuanced perspective. Even if we argue that the vaccines come with serious concerning side effects they are still producing immunity, just not something that may be worth the risk for a very good deal of the population.
The same with the other therapeutics. I think we should remember that the initial argument about PAXLOVID and Molnupiravir weren't that they were not effective, but that we were essentially told nothing is approved for use against COVID UNTIL the vaccines and these outpatient treatments came about. Even monoclonals received limited use in certain parts, but it's also interesting to see how people turned against that when you just show a simple ADE paper that raises more questions than actually affirming ADE.
It'd be interesting to see if the pause with PAXLOVID may actually help give the immune system a head start. It'd be hard to measure if the symptom rebound would be less severe because...That would be hard to model 🤷♂️.
I think the biggest issue with many of these therapeutics were that they were offered disjointed when most antivirals are given as cocktails so this itself was new territory.
The rest of the article is something that makes me curious about the lung dynamics. I think it's true that the cytokines are elevated, but I'm really curious about this actual "cytokine storm" effect since it does seem like maybe a lot of this got ahead and was part of the fear dynamics. I'd probably have to look into this information more myself and parse the information.
I have a simpler explanation that does not require more complicated models of days, adjusted-days, adjusted-health samples, sero-immunal prelavance of antigens, expressed upregulation of proteins or proxy indicators which are all factually weaker signals of chronic/acute damage than just diagnosing your 'physical' health.
1. Do you notice an increase, decrease or no-change in every-day life of normal deaths.
2. Do you notice an increase, decrease, or no-change in every-day life of sudden deaths.
3. If 1 or 2 applies, did you care.
4. If not, stop worrying over it.
5. If you did notice 1 or 2, was it because you paid more attention to it or you just casually inferred from your circle of friends, family, etc and not because of age-related increases in mortality.
6. If the frequency of X was observed to be over Y expectancy, then it can be attributable to external causes, which can be increased stress, lack of alternative treatment, the 'virus' itself, decreased immunity, or medical interventions like the injection.
Now knowing 1-6, what other things in life can kill you at an augmented rate?
-- So are you presently optimizing your sunshine input, exercise, diet?
No? Then it's irrational to worry about something that has a lower potential negative effect (some random thing which has a lower rate of possible infection and lower possible rate of mortality than the flu) than all the possible negative environmental disturbances to homeostasis (i.e. radiation, sun damage, household pollutants, eating poor foods, inflammation from sedentary lifestyle, not releasing enough endorphins/good hormones from lack of friends, etc).
Get a fitness tracker, HR monitor, etc, monitor your HRV, blood-pressure, sleep cycles. skin temperature, HRV, BMI, fat proportion % and notice the trends overtime. If something is out of 'parameters', then you know you have a 'valid' signal and do routine pre-check ups at mid-late age for potential cancers. Keep time metrics on how long it takes you to do X, your mental performance to do Y tasks. Else, skip all the non-sense tests.
Reality is.
Antigens is *not* all there is. There is your gut biome. Your virome. Distinguishing noise from signal is the *key* to health. Even if there is antigens, there can be UPregulation or DOWNregulation of hormones, genes, epigenetic controls, expression of genes, confirmational changes, change of distribution of fats, lipids, sugars, hGh. All of which are known to have more effect than the possibility of a detectance of one antigen in your body.
Pneuomia can also come from other bacterial infections. Wheeze more polluted air or irritants, and you also increase your susceptibility to *other things*. So always take the absolute risk of something and weight it all *other* risks in life else you are spending $999,999,999 and 99,999,999 calories over caring about something stupidenously small. Models are *not* reality, they are *potential* approximations. Same with *causal pathways* and *mechanisms*. An AI with statistical inferences can black-box engineer your probabilities of being X or having Y better than an academic in some tower can posit X->Y->Z pathways because it is *accumulating data* from large populations and analyzing it without bias * as long as the labels are proper (i.e. knowing what haplotype someone belongs to from a simple 4x4 pixel image of low-resolution).
Also let me get this clear it is not *viral* or *bacterial* or whatever that is *causing* harm. It is always the BODY's response to *X* foreign agent which is VARIABLE with respect to the demographic, and medication is also VARIABLE response to *X* agent as well as *Y* body (sometimes downregulating immune responses) which are symptoms *XYZ* that people dislike. The majority of sub-50 population do not have *XYZ* symptoms long as long as they are not in a *negative* environment like wheezing in coal ashes or abestos, because they have *adaptive resilience* Things that are *lethal* or *chronic* are *USUALLY* dose-dependent on RECURRING *exposure* to foreign things, we know BODIES *the human population* responds favourably well because it has adapted to FOREIGN things of nature constantly to survive. We also know that CELL DEATH and APTOSIS* is programmed and the genetic material that floats around if not *cleaned* up can also be harmful and is sometimes MISREPRESENTED as *viral material*. We also have siRNA to degrade sequences of floating code. Let's be real, the *absolute* risk does not warrant this much scientific energies to administer anything to the majority of the populace. MERs, SARS, Swine flu were just the *testing A/B control measures* to see how much compliance one can force the population with *theoretical* daily number charts. Even if 1 in 100 people die, you would *not notice it*. Considering already 1 in 50 have some form of autism when 2 decades ago it was 1 in 1,000 or 1 in 20,000.. *lol*
I never got thru the article...so I probably missed a lot.
Based on what I did read...(and I bailed at your commotio)....but it would appear you must be jabbed and boosted?
Maybe not...but if I was shilling for the jab and paxlovid...I would now be triple boosted...making sure I got the extra special bi-valent potion...and I would be in the black-market hunt for Paxlovid and Remdesivir. I would avoid vitamin D and eggs...stay out of the dirt...and try to breathe less.
As it stands...I remain unjabbed and have horsepaste in storage.
Just another tinfoil hatter I am.
I should follow the science like that chick on MSNBC and join her with peri and miocarditis from a common cold.
I remember that happening all the time when I grew up. Kids were getting cardiac arrest every cold season when I was a kid. It was just what we expected.
1) Ivermectin has been shown to rapidly turn around cases of low blood ox.. and the mechanism proposed is reversal of hemagglutination within blood. You are proposing (or the authors you quote are proposing) another mechanism leading to low blood ox in Covid-19 patients. Which is it, or both?
2) You talk about antibodies protecting the lungs. As you are probably aware, the prolific tweeter Dr. Lee holds that antibodies don't get to this location. How do you answer Dr. Lee?
3) In all the discussion of antibiotics, and specifically macrolides, in early treatment protocols or otherwise used, why is nobody mentioning their anti-viral properties?
"Azithromycin, but not erythromycin or telithromycin, significantly increased rhinovirus 1B- and rhinovirus 16-induced interferons and interferon-stimulated gene mRNA expression and protein production. Furthermore, azithromycin significantly reduced rhinovirus replication and release. Rhinovirus induced IL-6 and IL-8 protein and mRNA expression were not significantly reduced by azithromycin pre-treatment."
Some of the IVM/HCQ studies were designed with late administration or overdosing, etc. Ultimately, if the trials for IVM/HCQ were designed exactly like the Pax study(ies) (or, if we only look at the IVM/HCQ studies that were designed similarly to the Pax studies) would we likely get a similar effect: reduced viral replication?
I'm pretty sure there a quite a few ivermectin users who would agree with the Brian theory.
After my daughter's 2nd covid (Oct 2020) her legs no longer worked and she became incontinent....among other horrid symptoms like intense pain. No doctors would treat her for this apparently psychiatric illness....yeah
Ok. So after 8 months of being bedridden, with the help of a kind soul, we found ivermectin. My daughter was walking again in two days.
I don't believe cytokine storm, immune dysfunction, or psychosis can explain that.
I do believe if we'd had ivermectin much sooner than over a year after 1st infection and 8 months after 2nd infection, that she wouldn't be a long hauler. It was too little too late, but still a miracle.
As it was her only med, it must have acted directly on the virus.
If people could speak of ivermectin...or actually USE it, there'd be that much greater understanding of the virus. But the censors/overlords can't have that happening.
Why use a safe med like ivermectin when you can kill and maim with a shot?
Makes sense. My guess is genetics combined with pre-existing. Jibes with this https://www.nature.com/articles/s41564-021-00961-5
All DAMPS are not created equal. Some are more inflammatory than others. What DAMPS are released depend on the type of cell death. A healthy person will have 50 billion cells die each day, mostly via apoptosis which is relatively not inflammatory. Besides apoptosis you have necrosis/necroptosis and pyroptosis, which release more inflammatory DAMPS
As for the viral kinetics. The virus is gone in most immunocompetent patients within 10 days. There are other studies showing the same.
Remdesivir helps a bit with viral clearance, but is not required
“Model-based simulations predict that remdesivir reduced time to viral clearance by 0.7 days compared with SoC, ...Remdesivir had a larger impact in patients with high viral load at randomization, reducing viral production by 5-fold on...and median time to viral clearance by 2.4 days l”
https://pubmed.ncbi.nlm.nih.gov/35233617/
“I could counter that 80% of ICU patients were PCR positive vs. only 25% of immunocompromised.”
The 25% were from the LTACH cohort who had been transferred from ICU for prolonged treatment. They were not all immunosuppressed
I am in favor of preventing lung damage and treating it effectively when it occurs. We should be making Ivermectin available OTC for early treatment and encouraging use of Vit D/C.
That said, no treatment is going to work for everyone
I remember John Paul wrote an interesting sub stack on bacteria binding to subunits of the spike protein.
"the Spike Protein interacted with (bacterial) LPS to form aggregates of Spike Protein",
"While using different pathways, a lot of the recent deaths directly from vaccination (as per the pathologists analysis) and from the infection since early 2020 have something in common. Bacterial overgrowth, excessive presence of bacteria in the blood."
https://hiddencomplexity.substack.com/p/spike-protein-as-a-endotoxin-delivery
Thanks for the trigger warning! With so much concern about long-term side effects of these injections, I've also kept in mind that they seem to have a short-term benefit on the very low risk of severe infection.
Joel Smalley on an insurance analyst's presentation on excess deaths:
https://metatron.substack.com/p/josh-stirling-dissecting-excess-death
Some people seemingly cannot understand that if you survive the first shot (with few side-effects) you have a good chance of surviving subsequent shots.
“it sounds like the virus is perfectly capable of destroying lots of lung cells on its own, unchecked, thanks to suppression of antiviral innate immunity.”
I agree with this. However, Cell death promotes inflammatory response.
“Microbes-infected stressed or dying cells can also release Damage-associated molecular patterns (DAMPs),that can modulate immune sensing of infected cells. However, cytokines or chemokines have received more attention in the context of infection-associated cell death rather than DAMPs “
[I agree with you on Cytokine storm being the sole cause of excess inflammation]
“In his review article , W.G. Land surveyed the current literature on respiratory viruses (including, coronavirus disease-19 [COVID-19]) and found that DAMPs-driven immune responses also dominated respiratory virus pathology together with cytokine-associated responses. This review concludes that DAMPs might have an underappreciated role in the pathogenesis of acute respiratory distress syndrome and systemic inflammatory response syndrome (including COVID-19). The review also high- lights how DAMPs might serve the purpose of diagnostic or prognostic biomarkers for such infections.
A recent single-cell resolution analyses of lung- associated bronchoalveolar fluid from patients with severe COVID- 19, found that COVID-19 associated lung pathology was associated with considerable release of extracellular ATP . Accordingly, genetic signatures of purinergic and inflammasome signalling (that is downstream of extracellular ATP) were enriched across various lung-associated immune compartments “
https://www.nature.com/articles/s41435-022-00184-6.pdf
“Replication-competent virus was detected in 4 of 11 (36.3%) immunocompromised patients up to 45 days after symptom onset and in 1 of 67 (1.5%) immunocompetent patients 10 days after symptom onset (P = .001). “
https://academic.oup.com/cid/article/76/3/e416/6590994?login=false
So the virus in immunocompetent people is defeated by the immune system in 10 days. No more replicating virus, but most people develop symptoms of serious disease as the virus is being defeated.
The immune response to the cell damage caused by the virus is what kills patients. Cytokine storm may well be overstated, but inflammation from inflammatory IgG (present in noticeable amounts by day 7-10) as well as immune cells responding to cell death also cause problems
Steroids
The Recovery Trial showed benefit of steroids. Clinicians argue it would show more at higher doses. Giving steroids during viral replication phase is non-sensible. As is giving kidney killing antivirals [Remdesivir] after viral replication phase is over. Its all about timing.
Most cases don’t become serious until 7-10 days after symptoms began because this is when the immune system goes into overdrive dealing with the lung cell damage and it also coincided with igG antibody production which is inflammatory (especially afucosylated antibodies).
Disease severity is correlated with higher levels of antibodies than those with mild disease. Thats because by the time antibodies are at a high level there is no virus to neutralize, but plenty of viral debris to latch onto , and this signals an army of Immune cells to clean the mess up
One of the great myths is that antibodies are the first line of defense. Most new antibodies created during infection of a virus for the first time are created after the innate immune cells and T-cells have all but knocked out the infection. The purpose of serum antibodies is to help prevent a reinfection in a short period of time and let the victorious immune system to recharge its batteries, and also as antibodies wane and reinfection occurs the memory B-Cells cant quick start antibody production and join the fight earlier allowing milder disease
As for milder disease in Omicron, Omicron does not replicate as well in the lungs as did earlier variants. Less cell death, so less inflammation. Besides, almost everyone has either been infected or vaxxed, so new IgG antibodies are all fucosylated (less inflammation)
As for the Paxlovid study. Its likely those with an early antibody response already had natural immunity due to earlier infection and had memory B cells which ramped up fucosylated antibodies early, while naive infected antibodies came later and were afucosylated. Remember, this is a Pfizer trial. Not to be trusted. They give Paxlovid out like candy in Taiwan and we are having 60 COVID DEATHS a day (equivalent to 900 in US)
I just followed a chain of links to previous articles and came across a reference to a paper from 2015 about Resident Memory T-Cells. Damn, I get a lot of value from your writing, so thank you very much.
That brought up a thought. To what extent would Trms from prior exposure to Corona viruses provide cross-reactive protection against SARS-CoV-2? Is there any research on this?
I agree it's a numbers game. If you can shut down replication of the virus fast enough you will be fine.
I am surprised, or maybe not, that you didn't mention Ivermectin. I think there is strong evidence that it functions as a protease inhibiter and also binds to the N protein and thus acts against the virus in multiple ways.
However, IMO, the strongest case that Ivermectin is effective against SARS-CoV-w is the fact that a fake paper was submitted to the Lancet that claimed it was dangerous, and was quickly published, only to be retracted after about a month when it was discovered to be fake.
Update. I was mistaken. It was HCQ that the fake paper was submitted to the Lancet about. So, that tells me HCQ was effective. However, the various trials of Ivermectin all used subterfuges to provide a negative result, like using too little or dosing it too late.
I appreciate that you're taking a nuanced perspective. Even if we argue that the vaccines come with serious concerning side effects they are still producing immunity, just not something that may be worth the risk for a very good deal of the population.
The same with the other therapeutics. I think we should remember that the initial argument about PAXLOVID and Molnupiravir weren't that they were not effective, but that we were essentially told nothing is approved for use against COVID UNTIL the vaccines and these outpatient treatments came about. Even monoclonals received limited use in certain parts, but it's also interesting to see how people turned against that when you just show a simple ADE paper that raises more questions than actually affirming ADE.
It'd be interesting to see if the pause with PAXLOVID may actually help give the immune system a head start. It'd be hard to measure if the symptom rebound would be less severe because...That would be hard to model 🤷♂️.
I think the biggest issue with many of these therapeutics were that they were offered disjointed when most antivirals are given as cocktails so this itself was new territory.
The rest of the article is something that makes me curious about the lung dynamics. I think it's true that the cytokines are elevated, but I'm really curious about this actual "cytokine storm" effect since it does seem like maybe a lot of this got ahead and was part of the fear dynamics. I'd probably have to look into this information more myself and parse the information.
Do you have convincing science to show how and where Paxlovid "works"?
How much gets to the lung replicating Virus?
Are there any 19F NMR studies to show its biodistribution, metabolism and excretion after swallowing the magic pills?
I have a simpler explanation that does not require more complicated models of days, adjusted-days, adjusted-health samples, sero-immunal prelavance of antigens, expressed upregulation of proteins or proxy indicators which are all factually weaker signals of chronic/acute damage than just diagnosing your 'physical' health.
1. Do you notice an increase, decrease or no-change in every-day life of normal deaths.
2. Do you notice an increase, decrease, or no-change in every-day life of sudden deaths.
3. If 1 or 2 applies, did you care.
4. If not, stop worrying over it.
5. If you did notice 1 or 2, was it because you paid more attention to it or you just casually inferred from your circle of friends, family, etc and not because of age-related increases in mortality.
6. If the frequency of X was observed to be over Y expectancy, then it can be attributable to external causes, which can be increased stress, lack of alternative treatment, the 'virus' itself, decreased immunity, or medical interventions like the injection.
Now knowing 1-6, what other things in life can kill you at an augmented rate?
Respiratory diseases, cardiovascular diseases, etc...
-- So are you presently optimizing your sunshine input, exercise, diet?
No? Then it's irrational to worry about something that has a lower potential negative effect (some random thing which has a lower rate of possible infection and lower possible rate of mortality than the flu) than all the possible negative environmental disturbances to homeostasis (i.e. radiation, sun damage, household pollutants, eating poor foods, inflammation from sedentary lifestyle, not releasing enough endorphins/good hormones from lack of friends, etc).
Get a fitness tracker, HR monitor, etc, monitor your HRV, blood-pressure, sleep cycles. skin temperature, HRV, BMI, fat proportion % and notice the trends overtime. If something is out of 'parameters', then you know you have a 'valid' signal and do routine pre-check ups at mid-late age for potential cancers. Keep time metrics on how long it takes you to do X, your mental performance to do Y tasks. Else, skip all the non-sense tests.
Reality is.
Antigens is *not* all there is. There is your gut biome. Your virome. Distinguishing noise from signal is the *key* to health. Even if there is antigens, there can be UPregulation or DOWNregulation of hormones, genes, epigenetic controls, expression of genes, confirmational changes, change of distribution of fats, lipids, sugars, hGh. All of which are known to have more effect than the possibility of a detectance of one antigen in your body.
Pneuomia can also come from other bacterial infections. Wheeze more polluted air or irritants, and you also increase your susceptibility to *other things*. So always take the absolute risk of something and weight it all *other* risks in life else you are spending $999,999,999 and 99,999,999 calories over caring about something stupidenously small. Models are *not* reality, they are *potential* approximations. Same with *causal pathways* and *mechanisms*. An AI with statistical inferences can black-box engineer your probabilities of being X or having Y better than an academic in some tower can posit X->Y->Z pathways because it is *accumulating data* from large populations and analyzing it without bias * as long as the labels are proper (i.e. knowing what haplotype someone belongs to from a simple 4x4 pixel image of low-resolution).
Also let me get this clear it is not *viral* or *bacterial* or whatever that is *causing* harm. It is always the BODY's response to *X* foreign agent which is VARIABLE with respect to the demographic, and medication is also VARIABLE response to *X* agent as well as *Y* body (sometimes downregulating immune responses) which are symptoms *XYZ* that people dislike. The majority of sub-50 population do not have *XYZ* symptoms long as long as they are not in a *negative* environment like wheezing in coal ashes or abestos, because they have *adaptive resilience* Things that are *lethal* or *chronic* are *USUALLY* dose-dependent on RECURRING *exposure* to foreign things, we know BODIES *the human population* responds favourably well because it has adapted to FOREIGN things of nature constantly to survive. We also know that CELL DEATH and APTOSIS* is programmed and the genetic material that floats around if not *cleaned* up can also be harmful and is sometimes MISREPRESENTED as *viral material*. We also have siRNA to degrade sequences of floating code. Let's be real, the *absolute* risk does not warrant this much scientific energies to administer anything to the majority of the populace. MERs, SARS, Swine flu were just the *testing A/B control measures* to see how much compliance one can force the population with *theoretical* daily number charts. Even if 1 in 100 people die, you would *not notice it*. Considering already 1 in 50 have some form of autism when 2 decades ago it was 1 in 1,000 or 1 in 20,000.. *lol*
I never got thru the article...so I probably missed a lot.
Based on what I did read...(and I bailed at your commotio)....but it would appear you must be jabbed and boosted?
Maybe not...but if I was shilling for the jab and paxlovid...I would now be triple boosted...making sure I got the extra special bi-valent potion...and I would be in the black-market hunt for Paxlovid and Remdesivir. I would avoid vitamin D and eggs...stay out of the dirt...and try to breathe less.
As it stands...I remain unjabbed and have horsepaste in storage.
Just another tinfoil hatter I am.
I should follow the science like that chick on MSNBC and join her with peri and miocarditis from a common cold.
I remember that happening all the time when I grew up. Kids were getting cardiac arrest every cold season when I was a kid. It was just what we expected.
1) Ivermectin has been shown to rapidly turn around cases of low blood ox.. and the mechanism proposed is reversal of hemagglutination within blood. You are proposing (or the authors you quote are proposing) another mechanism leading to low blood ox in Covid-19 patients. Which is it, or both?
2) You talk about antibodies protecting the lungs. As you are probably aware, the prolific tweeter Dr. Lee holds that antibodies don't get to this location. How do you answer Dr. Lee?
https://twitter.com/leelasik/status/1624185237164142592
3) In all the discussion of antibiotics, and specifically macrolides, in early treatment protocols or otherwise used, why is nobody mentioning their anti-viral properties?
https://erj.ersjournals.com/content/36/3/646
"Azithromycin, but not erythromycin or telithromycin, significantly increased rhinovirus 1B- and rhinovirus 16-induced interferons and interferon-stimulated gene mRNA expression and protein production. Furthermore, azithromycin significantly reduced rhinovirus replication and release. Rhinovirus induced IL-6 and IL-8 protein and mRNA expression were not significantly reduced by azithromycin pre-treatment."
Some of the IVM/HCQ studies were designed with late administration or overdosing, etc. Ultimately, if the trials for IVM/HCQ were designed exactly like the Pax study(ies) (or, if we only look at the IVM/HCQ studies that were designed similarly to the Pax studies) would we likely get a similar effect: reduced viral replication?
I'm pretty sure there a quite a few ivermectin users who would agree with the Brian theory.
After my daughter's 2nd covid (Oct 2020) her legs no longer worked and she became incontinent....among other horrid symptoms like intense pain. No doctors would treat her for this apparently psychiatric illness....yeah
Ok. So after 8 months of being bedridden, with the help of a kind soul, we found ivermectin. My daughter was walking again in two days.
I don't believe cytokine storm, immune dysfunction, or psychosis can explain that.
I do believe if we'd had ivermectin much sooner than over a year after 1st infection and 8 months after 2nd infection, that she wouldn't be a long hauler. It was too little too late, but still a miracle.
As it was her only med, it must have acted directly on the virus.
If people could speak of ivermectin...or actually USE it, there'd be that much greater understanding of the virus. But the censors/overlords can't have that happening.
Why use a safe med like ivermectin when you can kill and maim with a shot?
Covid pneumonia and no mention of Azithromycin? Midazolam?
“Experimental gene transfection injection protects as well”
There you lost me.
“One has to belong to the intelligentsia to believe things like that: no ordinary man could be such a fool.”
— George Orwell