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
Interesting. Still, 62% had viral culture negative. Most of the positive cultures were only about a week longer than expected . Given this is South Africa I wonder about immune deficiency due to HIV or other reasons. We know from a NIH study virus replication can persist for weeks or more in some immunocompromised patients.
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.
Feb 12, 2023·edited Feb 12, 2023Liked by Brian Mowrey
Clutching at straws here, but just today I saw a recent video from a Youtube creator where he gets some random virus from his kid (non Covid, non flu), kid is fine but he gets severe fever and ends up in hospital with significant myocarditis:
So I wonder exposure to mRNA spike protein can make you much more vulnerable to other non Covid illnesses thorough some mechanism that isn't necessarily inflammation related?
I believe that there's probably generic immune suppression, and maybe this explains the weird waves of infections going around the last two years (with kids in turn also getting hit by higher quantity of infections passed on from adults). This seemed to be the signal across the board in the Swedish teens study https://unglossed.substack.com/i/82178933/findings-safety
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.
"What you see when you analyze this data is that although the vaccinated appear to have had lower mortality in the year 2021 in general and aggregate across all ages, in 2022, generally the vaccinated have had much higher mortality than the unvaccinated."
Er... basically just a two little pigs effect. The straw is blown away first, then the sticks. It doesn't mean the sticks got "more blown away."
Are you saying that those who were more susceptible to the #ClotShot died early, or that the #ClotShot does not really protect you from death, so those who died in 2021 were mostly the unvaccinated because there were few unvaccinated, but because the idiots flocked to the #ClotShot, from 2022 there were more vaccinated dying (but not at a higher rate)?
My comment is in reaction to the portion I quoted. As mentioned in my American excess deaths posts, I don't think vaccine-induced deaths are having any detectable effect on excess deaths to date. Excess deaths are from the virus. So the virus was hitting the unvaccinated in 2021, with deaths also driven of course from denial of treatment. It can't hit them again in 2022, they all have natural immunity.
So it's the other little piggy that is dying now. But it's still the virus driving deaths. This may be what starts happening in the ONS data after the May blackout - maybe weekly per-100k deaths finally went red in the "any dose any time" combined group. Supposedly they will put it back online in a few days so we'll see. The problem is that contra most rumors, "Covid deaths" do not appear to be overcounted. The excess deaths are higher than official Covid deaths in a way that doesn't seem related to the vaccine (because otherwise you would have spikes in places without viruses, eg Northeast US during Delta wave, but you don't have any spikes there).
“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)
DAMPS are not unique to SARS-CoV-2. They are universal to cell death. The response cannot therefore be meaningfully characterized as an over-reaction if it is proportionate to the amount of cell death.
The headline result you quoted from Kim, et al. is misleading.
1 - The "immunocompentent" group was exclusively ICU patients. So it makes sense that the sole positive culture was in day 10 - but likewise, most people are still experiencing "day 10" out of the ICU. They are out there with the virus still destroying lung and driving them toward higher respiratory distress. Maybe up to day 11,12,13, etc. But they aren't being sampled until they hit the ICU. What if I want to prove inflammation has no role at all? I know, I'll just wait and only check on dead people. Using an excessively dire disease benchmark is not going to show causation of that dire state. You aren't looking at what led up to X.
2 - 92% remdesivir use in same group is going to confound viral kinetics. But 1 is more important here. We don't know if the days before ICU are being spent out of the hospital or not, and therefore how much remdesivir treatment precedes ICU, so we can't infer anything about the role of the virus from inefficacy of antivirals after hospitalization.
3 - I could counter that 80% of ICU patients were PCR positive vs. only 25% of immunocompromised. Yes, the latter seem to have been lower cycle / higher culture+ when PCR-positive, but this may be due to confounding with remdesivir.
Overall it's essentially a "rigged" design that isn't going to let you see a lot of virus.
Let's say it's still reflective of viral kinetics. The reason severe disease develops "after" the virus goes through the lungs, per the Brian Mowrey theory, is that it has already burned through all the fuel. Your lungs have been destroyed. I see this as fundamentally a dogma in medicine that blames inflammation for injury because it only cares about what can be treated. Except here there is a chance to prevent the injury which has been ignored. This matters tremendously. Are you for example suggesting people are better off with doctors hyper-focusing on fine-tuning steroids to capture that extra 1% of prevented deaths (leaving 20+% to still die) or focusing on preventing the injury that leads to inflammation? If you aren't suggesting the former then you don't actually believe your own case that inflammation is the causative agent.
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 have never regarded the evidence on ivermectin clear enough to write about. If I was out personally treating people with it and seeing results that would be one thing. And I don't discourage anyone from listening to those same people, or from using it, and I even have my own box though I decided to just tough the virus out in the end -- but I can't add value by saying "I believe X because Y says so and he smiles nice," so, I don't discuss it much.
Had "THE VIRUS" about 12 months ago. Decided to tough it out also as I do with all other viruses I catch. Took nothing for it except 2 nights aspirin to help sleep. Felt bad about 3 days w the usual aches & pains but not awful. 4th day much better about 70% normal. 5th day about 95% normal. Losing taste/smell was a bit strange. Have had much worse colds/ flu. 68 years old.
Glad you had a mostly uneventful recovery (though sorry to hear about the taste/smell loss, hopefully that was temporary). I had brain fog for two days, it was pretty wild.
Partially, my decision was based on the FLCCC switching back to HCQ for Omicron (but I didn't have any) and based on wanting "moar immunity" ie what if limiting viral replication diminishes immune response. I went with a no pain no gain strategy in the end.
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’m not up to date on this but I thought that it was always the consensus view that Paxlovid works in the unvaccinated but not in those who got the shots?
It is my understanding that the whole point of the drug was to pause viral replication and let the immune system catch up.... but it was found not to work properly in those who were vaccinated...... leading to a relapse.
There were signs of rebound in the trial as well. They claimed it was in both treatment and control, but when you apply cycle count standards from other studies that PCR people over multiple days it's clear that Paxlovid recipients are doing something unique.
The impression that it doesn't work in the vaxxed is based mainly on the Israel paper which had obvious confounders (ie compared low risk not-takers to at-risk takers, at which point you might as well compare it to people who don't even have the virus). As I say in footnote 12, confounders also apply to the papers that show a better result. So I don't think we can say one way or the other whether it "works" in the vaxxed, but I think rebound is universal.
I did cite two post-auth studies - footnote 12 - though acknowledged signs of healthy user bias in the Wales one. If you have any other objections to those studies, I'm all ears. Otherwise they show lower severe outcomes in treatment. The Mass General one doesn't show the same bias and still achieves better outcomes:
"During the study period, 12 541 (28.1%) patients were prescribed nirmatrelvir plus ritonavir, and 32 010 (71.9%) were not. Patients prescribed nirmatrelvir plus ritonavir were more likely to be older, have more comorbidities, and be vaccinated. The composite outcome of hospitalization or death occurred in 69 (0.55%) patients who were prescribed nirmatrelvir plus ritonavir and 310 (0.97%) who were not "
And of course the trial. You can allege the trial is fraud, but I have to wonder why molnupiravir couldn't pull off nearly as impressive a result if all these trials are fraud.
Thanks very much. I should have been more specific, as Paxlovid is actually 2 quite different molecules. Nirmatrelvir is the super nasty hazard from my perspective. I will have to read more about the 2 drug combo versus each nasty separately.
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*
Why does any word not fit into where you put "virus," e.g. "tooth-brushing, being bit by cobras," "driving" etc.? People still care about those things. I have said ad nauseam that the virus did not meaningfully change what it means to go through life. Everybody dies, big deal. But I can't say that every time I talk about the virus anymore than I could run a car blog saying that about driving.
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.
I never got through the comment. Based on what I did read... Thanks so much, kind remarks like this are why I keep working hard (or is it hardly working😹)!
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."
The mechanism in Archer et al. (V/Q mismatch) is supported by other studies including Heiss et al. (which is for mild infections! still hopefully some kind of bias going on there). Lots of viruses cause hemagglutination, so I'm not sure that can account for the low O2 problem (though it's true that flu is associated with cyanosis too). Which would tend to make me think there should already be other drugs for stopping hemagglutination if to do so can turn around hypoxia? Overall I think the in vivo evidence for ivermectin is unfortunately not strong enough to learn how it's really working, but maybe there are mechanistic studies I am not aware of.
2 IgG transudation is pretty well recognized and I provided citation for the RSV example. I am not sure how anyone else would explain temporary infection efficacy, and we know temporary infection efficacy is tied to serum IgG levels since it goes away when those drop. So the serum IgG is getting into the respiratory tract. As far as I would guess, it could just be breathed into the lower lungs from the upper tract.
3 As shown in part 1.5, hospitalized patients were prescribed antibiotics very heavily. However, this doesn't tell us whether they would have had an antiviral benefit if given earlier, same as HCQ being too late to act as an antiviral at that point (so it's too late to show impact on my "virus causes injury" theory, but not too late to show impact on the "immune over-reaction causes injury"). However, antibiotic promotion of innate antiviral immunity is a very interesting tidbit that I did not know about, ty
Thank you Brian. I do believe that the power of macrolide antibiotics in early treatment cocktails is likely synergistic anti-viral for the most part, prophylactic against bacterial secondarily. As Arkmedic states in his previous comment you highlighted in this piece, it doesn't really matter, and it's not possible to deconvolute... but again, I think it's important to recognize that the benefit could be mostly anti-viral in nature. Don't throw out the baby with the bathwater.. or something like that.
Regarding reversal of Hemagglutination by Ivermectin, the reference is here;
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?
HCQ research is more Mathew Crawford's thing, but my impression is that yes there was universal mis-application i.e. sabotage. Whereas I've seen more regarding ivermectin and am not convinced it's been sabotaged per se. But I think doctors should use it if they think it works, and people should be able to buy it OTC like is the case in many places.
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?
"If people could speak of ivermectin...or actually USE it, there'd be that much greater understanding of the virus." I agree. I think that's why there's still so much confusion around the etiology of the disease - doctors weren't actually treating patients, so they didn't actually see the disease. This applies to things like CT scans which were discouraged because it increased contact with patients (!)
The drs where I live in Texas have said that they've been threatened with loss of licensure if they even speak the "i" word. If they prescribe it, they'll lose their license.
Drs saw the disease and sent everyone home to suffer and deteriorate....to die a slow painful death as their bodies become more and more debilitated over time.
I'm based in the US and don't have a strong interest in the midazolam theory. Maybe it happened in the UK. We seem to kill patients a different way here in the US (wait plus ventilate plus remdesivir) which implies we like the virus to do the work.
He made it very clear it is short term protection followed by the Price is Right cliff of doom. The point was that "Covid pneumonia" didn't seem to be as bad a problem when anti-viral of some sort was used - suggesting that in this case it is a spike effect since it also wasn't as bad a problem for Omicron. I had an Omicron maybe illness from a nursing home exposure and it was different. Extreme fatigue for days and migraines, but not much respiratory symptoms.
What helps spike CoV lung issues a lot is citrus peel or hesperidin as an extract probably also would help in early stages. Once the damage is too great, that itself is a problem. And of course, pomegranate peel blocks spike in many ways. The citrus peel is a direct anti-asthmatic though, so has more symptom immediate relief for the lung symptoms. It opens airways, thins mucus, helps move it up and out - within 20 minutes the effect is noticeable. Cheap, available, and I have been pitching it since March 2020. People don't want treatment though; they want a magic pill - from someone in a white coat or on a talk show circuit.
The “short-term protection” is a mirage created by the shenanigans of defining the injected as “unvaccinated” the first 14 days after each injection.
It seems to me Brian is clinging on to the belief that these synthetic mRNA injectable *countermeasures* ought to have some protective effect – despite the overwhelming evidence pointing to the contrary.
Indeed, there are fortunately plenty of natural remedies that can actually help you fight off the disease/virus/spike protein: zink, vitamin D, curcumin (from turmeric), quercetin, black seed oil, N-acetylcysteine (NAC), bromelain (from pineapple) and olive leaf extract to mention a few. Citrus bioflavonoids like hesperidin could very well have similar beneficial effects although I haven't read any studies demonstrating it myself.
Yes, unfortunately the relentless 5th generation warfare propaganda has been very effective on most people (speaking of effectiveness).
You cannot win the cost-benefit argument against the experimental gene transfections if you just deny the benefit. "One does not win arguments with fantasy" - me
Labeling people "deniers" of a non-existent benefit seems like a poor strategy of winning an argument, although it's apparently an effective propaganda strategy.
The “short-term benefit” is effectively a mirage created by the shenanigans of defining the injected as “unvaccinated” the first 14 days after each injection (probably in conjunction with other data manipulations).
You are clearly a clever and educated man, Brian, but with a tendency of sometimes missing the forest for the trees (weeds).
When discussing severe efficacy, the much-hyped "shenanigans" of classification time lags are irrelevant. The worry window is not real, and almost no one is getting infected after day 12 post-first injection until another four months go by and infection efficacy goes away. So you look at the severe outcome rate per infection there.
This is what I am. I have run a blog since mid-2021 that could gain 100 subscribers a post if I could prove that severe efficacy isn't real. But I can't prove that because it is real. In the same period I have observed the pathetic attempts by other people running blogs in the same ecosystem to "prove" it isn't real by making up imaginary stories about the worry window, "secret unvaccinated deaths" etc. And I have been harassed endlessly by the people still falling for that idiotic argument. Because why? Because the people who see through it stop paying attention to the issue because they realize that everyone pretending to actually care about the Covid vaccines is just making stuff up to appease readers.
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'm scrounging up a follow-up post hence revisiting these comments. Of note, deep lung tissue of fatal cases have robust culture positivity rates even at 15 days https://www.medrxiv.org/content/10.1101/2023.03.06.23286834v1
Interesting. Still, 62% had viral culture negative. Most of the positive cultures were only about a week longer than expected . Given this is South Africa I wonder about immune deficiency due to HIV or other reasons. We know from a NIH study virus replication can persist for weeks or more in some immunocompromised patients.
Good news for Remdesivir though
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.
Clutching at straws here, but just today I saw a recent video from a Youtube creator where he gets some random virus from his kid (non Covid, non flu), kid is fine but he gets severe fever and ends up in hospital with significant myocarditis:
https://www.youtube.com/watch?v=qQV7KHUo6VU
So I wonder exposure to mRNA spike protein can make you much more vulnerable to other non Covid illnesses thorough some mechanism that isn't necessarily inflammation related?
I believe that there's probably generic immune suppression, and maybe this explains the weird waves of infections going around the last two years (with kids in turn also getting hit by higher quantity of infections passed on from adults). This seemed to be the signal across the board in the Swedish teens study https://unglossed.substack.com/i/82178933/findings-safety
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.
"What you see when you analyze this data is that although the vaccinated appear to have had lower mortality in the year 2021 in general and aggregate across all ages, in 2022, generally the vaccinated have had much higher mortality than the unvaccinated."
Er... basically just a two little pigs effect. The straw is blown away first, then the sticks. It doesn't mean the sticks got "more blown away."
OK, I don't understand the analogy.
Are you saying that those who were more susceptible to the #ClotShot died early, or that the #ClotShot does not really protect you from death, so those who died in 2021 were mostly the unvaccinated because there were few unvaccinated, but because the idiots flocked to the #ClotShot, from 2022 there were more vaccinated dying (but not at a higher rate)?
My comment is in reaction to the portion I quoted. As mentioned in my American excess deaths posts, I don't think vaccine-induced deaths are having any detectable effect on excess deaths to date. Excess deaths are from the virus. So the virus was hitting the unvaccinated in 2021, with deaths also driven of course from denial of treatment. It can't hit them again in 2022, they all have natural immunity.
So it's the other little piggy that is dying now. But it's still the virus driving deaths. This may be what starts happening in the ONS data after the May blackout - maybe weekly per-100k deaths finally went red in the "any dose any time" combined group. Supposedly they will put it back online in a few days so we'll see. The problem is that contra most rumors, "Covid deaths" do not appear to be overcounted. The excess deaths are higher than official Covid deaths in a way that doesn't seem related to the vaccine (because otherwise you would have spikes in places without viruses, eg Northeast US during Delta wave, but you don't have any spikes there).
“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)
DAMPS are not unique to SARS-CoV-2. They are universal to cell death. The response cannot therefore be meaningfully characterized as an over-reaction if it is proportionate to the amount of cell death.
The headline result you quoted from Kim, et al. is misleading.
1 - The "immunocompentent" group was exclusively ICU patients. So it makes sense that the sole positive culture was in day 10 - but likewise, most people are still experiencing "day 10" out of the ICU. They are out there with the virus still destroying lung and driving them toward higher respiratory distress. Maybe up to day 11,12,13, etc. But they aren't being sampled until they hit the ICU. What if I want to prove inflammation has no role at all? I know, I'll just wait and only check on dead people. Using an excessively dire disease benchmark is not going to show causation of that dire state. You aren't looking at what led up to X.
2 - 92% remdesivir use in same group is going to confound viral kinetics. But 1 is more important here. We don't know if the days before ICU are being spent out of the hospital or not, and therefore how much remdesivir treatment precedes ICU, so we can't infer anything about the role of the virus from inefficacy of antivirals after hospitalization.
3 - I could counter that 80% of ICU patients were PCR positive vs. only 25% of immunocompromised. Yes, the latter seem to have been lower cycle / higher culture+ when PCR-positive, but this may be due to confounding with remdesivir.
Overall it's essentially a "rigged" design that isn't going to let you see a lot of virus.
Let's say it's still reflective of viral kinetics. The reason severe disease develops "after" the virus goes through the lungs, per the Brian Mowrey theory, is that it has already burned through all the fuel. Your lungs have been destroyed. I see this as fundamentally a dogma in medicine that blames inflammation for injury because it only cares about what can be treated. Except here there is a chance to prevent the injury which has been ignored. This matters tremendously. Are you for example suggesting people are better off with doctors hyper-focusing on fine-tuning steroids to capture that extra 1% of prevented deaths (leaving 20+% to still die) or focusing on preventing the injury that leads to inflammation? If you aren't suggesting the former then you don't actually believe your own case that inflammation is the causative agent.
I'll return to read/respond to other sections
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?
At best, as far as the current available research, you could take circulating T Cell responses as a proxy for resident T Cell protection. https://www.nature.com/articles/s41467-021-27674-x https://www.nature.com/articles/s41586-021-04186-8
My impression is that we aren't measuring tissue immunity at all, we only know it's probably there because of animal studies
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 have never regarded the evidence on ivermectin clear enough to write about. If I was out personally treating people with it and seeing results that would be one thing. And I don't discourage anyone from listening to those same people, or from using it, and I even have my own box though I decided to just tough the virus out in the end -- but I can't add value by saying "I believe X because Y says so and he smiles nice," so, I don't discuss it much.
Had "THE VIRUS" about 12 months ago. Decided to tough it out also as I do with all other viruses I catch. Took nothing for it except 2 nights aspirin to help sleep. Felt bad about 3 days w the usual aches & pains but not awful. 4th day much better about 70% normal. 5th day about 95% normal. Losing taste/smell was a bit strange. Have had much worse colds/ flu. 68 years old.
Glad you had a mostly uneventful recovery (though sorry to hear about the taste/smell loss, hopefully that was temporary). I had brain fog for two days, it was pretty wild.
Partially, my decision was based on the FLCCC switching back to HCQ for Omicron (but I didn't have any) and based on wanting "moar immunity" ie what if limiting viral replication diminishes immune response. I went with a no pain no gain strategy in the end.
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’m not up to date on this but I thought that it was always the consensus view that Paxlovid works in the unvaccinated but not in those who got the shots?
It is my understanding that the whole point of the drug was to pause viral replication and let the immune system catch up.... but it was found not to work properly in those who were vaccinated...... leading to a relapse.
There were signs of rebound in the trial as well. They claimed it was in both treatment and control, but when you apply cycle count standards from other studies that PCR people over multiple days it's clear that Paxlovid recipients are doing something unique.
The impression that it doesn't work in the vaxxed is based mainly on the Israel paper which had obvious confounders (ie compared low risk not-takers to at-risk takers, at which point you might as well compare it to people who don't even have the virus). As I say in footnote 12, confounders also apply to the papers that show a better result. So I don't think we can say one way or the other whether it "works" in the vaxxed, but I think rebound is universal.
That can't be the case because the claim is that Paxlovid stops viral replication.
Apparently it does in the unvaccinated.
Are they still trying to claim that it works in the vaccinated?
Every vaccinated person that I’ve ever heard taking it has suffered a rebound bout of Covid.....
I did cite two post-auth studies - footnote 12 - though acknowledged signs of healthy user bias in the Wales one. If you have any other objections to those studies, I'm all ears. Otherwise they show lower severe outcomes in treatment. The Mass General one doesn't show the same bias and still achieves better outcomes:
"During the study period, 12 541 (28.1%) patients were prescribed nirmatrelvir plus ritonavir, and 32 010 (71.9%) were not. Patients prescribed nirmatrelvir plus ritonavir were more likely to be older, have more comorbidities, and be vaccinated. The composite outcome of hospitalization or death occurred in 69 (0.55%) patients who were prescribed nirmatrelvir plus ritonavir and 310 (0.97%) who were not "
And of course the trial. You can allege the trial is fraud, but I have to wonder why molnupiravir couldn't pull off nearly as impressive a result if all these trials are fraud.
Mechanism: It causes dramatic symptom and antigen / PCR test relapses https://www.medrxiv.org/content/10.1101/2022.11.14.22282195v1 - no other drug does that. The reason is because nsp5 / 3CL-pro is auto-cleaving and gains efficiency after dimerization https://unglossed.substack.com/p/unfinished-business. So the relapses show it is working as advertised (binding to pre-cleaved 3CL-pro) unless someone can offer a different theory for relapse.
Thanks very much. I should have been more specific, as Paxlovid is actually 2 quite different molecules. Nirmatrelvir is the super nasty hazard from my perspective. I will have to read more about the 2 drug combo versus each nasty separately.
https://en.wikipedia.org/wiki/Nirmatrelvir
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*
Why does any word not fit into where you put "virus," e.g. "tooth-brushing, being bit by cobras," "driving" etc.? People still care about those things. I have said ad nauseam that the virus did not meaningfully change what it means to go through life. Everybody dies, big deal. But I can't say that every time I talk about the virus anymore than I could run a car blog saying that about driving.
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.
I never got through the comment. Based on what I did read... Thanks so much, kind remarks like this are why I keep working hard (or is it hardly working😹)!
😂😂😂
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."
The mechanism in Archer et al. (V/Q mismatch) is supported by other studies including Heiss et al. (which is for mild infections! still hopefully some kind of bias going on there). Lots of viruses cause hemagglutination, so I'm not sure that can account for the low O2 problem (though it's true that flu is associated with cyanosis too). Which would tend to make me think there should already be other drugs for stopping hemagglutination if to do so can turn around hypoxia? Overall I think the in vivo evidence for ivermectin is unfortunately not strong enough to learn how it's really working, but maybe there are mechanistic studies I am not aware of.
2 IgG transudation is pretty well recognized and I provided citation for the RSV example. I am not sure how anyone else would explain temporary infection efficacy, and we know temporary infection efficacy is tied to serum IgG levels since it goes away when those drop. So the serum IgG is getting into the respiratory tract. As far as I would guess, it could just be breathed into the lower lungs from the upper tract.
3 As shown in part 1.5, hospitalized patients were prescribed antibiotics very heavily. However, this doesn't tell us whether they would have had an antiviral benefit if given earlier, same as HCQ being too late to act as an antiviral at that point (so it's too late to show impact on my "virus causes injury" theory, but not too late to show impact on the "immune over-reaction causes injury"). However, antibiotic promotion of innate antiviral immunity is a very interesting tidbit that I did not know about, ty
Thank you Brian. I do believe that the power of macrolide antibiotics in early treatment cocktails is likely synergistic anti-viral for the most part, prophylactic against bacterial secondarily. As Arkmedic states in his previous comment you highlighted in this piece, it doesn't really matter, and it's not possible to deconvolute... but again, I think it's important to recognize that the benefit could be mostly anti-viral in nature. Don't throw out the baby with the bathwater.. or something like that.
Regarding reversal of Hemagglutination by Ivermectin, the reference is here;
https://www.mdpi.com/1422-0067/23/24/15480
Title: SARS-CoV-2 Spike Protein Induces Hemagglutination: Implications for COVID-19 Morbidities and Therapeutics and for Vaccine Adverse Effects
Published: 7 December 2022
" IVM blocked HA when added to RBCs prior to spike protein and reversed HA when added afterward."
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?
HCQ research is more Mathew Crawford's thing, but my impression is that yes there was universal mis-application i.e. sabotage. Whereas I've seen more regarding ivermectin and am not convinced it's been sabotaged per se. But I think doctors should use it if they think it works, and people should be able to buy it OTC like is the case in many places.
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?
"If people could speak of ivermectin...or actually USE it, there'd be that much greater understanding of the virus." I agree. I think that's why there's still so much confusion around the etiology of the disease - doctors weren't actually treating patients, so they didn't actually see the disease. This applies to things like CT scans which were discouraged because it increased contact with patients (!)
The drs where I live in Texas have said that they've been threatened with loss of licensure if they even speak the "i" word. If they prescribe it, they'll lose their license.
Drs saw the disease and sent everyone home to suffer and deteriorate....to die a slow painful death as their bodies become more and more debilitated over time.
Covid pneumonia and no mention of Azithromycin? Midazolam?
See pt. 1.5 for discussion of the antibiotic withholding myth as mentioned. There was no withholding of antibiotics, patients hospitalized for "Covid-19" were given antibiotics like candy https://unglossed.substack.com/p/the-myth-of-secondary-infection-in
I'm based in the US and don't have a strong interest in the midazolam theory. Maybe it happened in the UK. We seem to kill patients a different way here in the US (wait plus ventilate plus remdesivir) which implies we like the virus to do the work.
“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
He made it very clear it is short term protection followed by the Price is Right cliff of doom. The point was that "Covid pneumonia" didn't seem to be as bad a problem when anti-viral of some sort was used - suggesting that in this case it is a spike effect since it also wasn't as bad a problem for Omicron. I had an Omicron maybe illness from a nursing home exposure and it was different. Extreme fatigue for days and migraines, but not much respiratory symptoms.
What helps spike CoV lung issues a lot is citrus peel or hesperidin as an extract probably also would help in early stages. Once the damage is too great, that itself is a problem. And of course, pomegranate peel blocks spike in many ways. The citrus peel is a direct anti-asthmatic though, so has more symptom immediate relief for the lung symptoms. It opens airways, thins mucus, helps move it up and out - within 20 minutes the effect is noticeable. Cheap, available, and I have been pitching it since March 2020. People don't want treatment though; they want a magic pill - from someone in a white coat or on a talk show circuit.
The “short-term protection” is a mirage created by the shenanigans of defining the injected as “unvaccinated” the first 14 days after each injection.
It seems to me Brian is clinging on to the belief that these synthetic mRNA injectable *countermeasures* ought to have some protective effect – despite the overwhelming evidence pointing to the contrary.
Indeed, there are fortunately plenty of natural remedies that can actually help you fight off the disease/virus/spike protein: zink, vitamin D, curcumin (from turmeric), quercetin, black seed oil, N-acetylcysteine (NAC), bromelain (from pineapple) and olive leaf extract to mention a few. Citrus bioflavonoids like hesperidin could very well have similar beneficial effects although I haven't read any studies demonstrating it myself.
Yes, unfortunately the relentless 5th generation warfare propaganda has been very effective on most people (speaking of effectiveness).
You cannot win the cost-benefit argument against the experimental gene transfections if you just deny the benefit. "One does not win arguments with fantasy" - me
Labeling people "deniers" of a non-existent benefit seems like a poor strategy of winning an argument, although it's apparently an effective propaganda strategy.
The “short-term benefit” is effectively a mirage created by the shenanigans of defining the injected as “unvaccinated” the first 14 days after each injection (probably in conjunction with other data manipulations).
You are clearly a clever and educated man, Brian, but with a tendency of sometimes missing the forest for the trees (weeds).
You say label, I say description.
When discussing severe efficacy, the much-hyped "shenanigans" of classification time lags are irrelevant. The worry window is not real, and almost no one is getting infected after day 12 post-first injection until another four months go by and infection efficacy goes away. So you look at the severe outcome rate per infection there.
This is what I am. I have run a blog since mid-2021 that could gain 100 subscribers a post if I could prove that severe efficacy isn't real. But I can't prove that because it is real. In the same period I have observed the pathetic attempts by other people running blogs in the same ecosystem to "prove" it isn't real by making up imaginary stories about the worry window, "secret unvaccinated deaths" etc. And I have been harassed endlessly by the people still falling for that idiotic argument. Because why? Because the people who see through it stop paying attention to the issue because they realize that everyone pretending to actually care about the Covid vaccines is just making stuff up to appease readers.