Feb 23, 2023·edited Feb 24, 2023Liked by Brian Mowrey
I posted about IGY antibodies before, but an important thing to be aware of is that those IGY antibodies will only be useful if the chickens have been challenged with SARS-CoV-2:
He suggests that what is going on is that if the person doing the injection does not aspirate then they inject shit-loads into the vasculature and this can have varying effect:
1. pericardial or myocardial cells take up the LNP encapsulated mRNA and produce spike and the person's immune system kills those cells for their efforts,
2. Vasculature epithelial cells take up the LNP encapsulated mRNA and produce lots of spike which gets into the blood all over the place and leads to thrombotic thrombocytopenia or pulmonary embolisms or strokes etc.
3. When people do a blood draw they find up to 638 billion free-floating spike proteins
In those cases where aspiration was used the side-effects are likely to be less severe.
I still maintain that no one needs that shit but we need to figure out what is going on and hiding it under the carpet is not useful.
Returning to the mRNA gene-therapy generated Spike protein and the claims that it is LOCKED into the prefusion conformation.
Do we know for sure, 100% that this is absolutely true?
Since the mRNA is generated in a bacterial soup using plasmids it seems like there are opportunities for this to go wrong and I have read elsewhere that Pfizer and Moderna can only manage something like 60% intact and or correct mRNA in the shots.
However, the second issue is: What are all the error modes when our ribosomes are presented with mRNA that has pseudo-uridine in it? I have seen claims that they only recognize stop codons with pseudo-uridine about 60% of the time. However, could there be other error modes were they generate spike protein that can fully fuse to ACE2 bearing cells and thus form syncytia if they manage to migrate to the surface of the cell they were created in?
I doubt anyone actually knows what all the possible outcomes are and JikkyLeaks claims there can be up to 436B spikes circulating in the serum so there may well be many studded in the surfaces of cells where they were created.
Proline doesn't depend on any uridines - the third nucleotide is irrelevant. And Pfizer and Moderna probably defaulted to C or G for the third nucleotide. So there is no reason to think that the stabilizing prolines will be a hotspot for mistranslation.
Yes, cells will probably be studded with spike protein - Which is why the immune system will kill them, whether they have fused or not, until you start getting IgG4, which switches that off
I don't see how these concerns top the generic fact that no one knows if cell fusion occurs after injection or not.
i.e., why worry about whether the prolines get installed correctly if we don't even know if the prolines work all the time? Moreover, the error rate in general is going to impact fusion more than it impacts the stabilization thereof; i.e., fusion requires function of the spike protein's many parts. In nature the S2 unit, which contains the fusion machinery, is extremely conserved, because fusion is a delicate mechanical process.
So RNA infidelity is more likely to break fusion than to cause it. Just as you're less likely to die in a car that was made with no technical expertise vs. one made with technical expertise, because the former can't even get out of the driveway -- so it doesn't matter how often an airbag accelerometer is upside down.
Thus, the proline failure rate is almost certainly greater than the "get all the other translation correct but mess up only the prolines" rate. Either way what you really want to know is how often does it actually happen, and no one is looking at that.
Are there any papers that look at whether or not the mRNA gene-therapy treatments cause clotting (perhaps because of the sialic acid on the S protein) or syncytia?
Off the top of my head, none of the handful of in vitro experiments using actual vaccine product report anything about cell fusion, and there's nothing about what goes on in vivo. As with everything else, there was no attempt before authorization to figure out what these products actually do in the body https://unglossed.substack.com/p/pfizer-did-not-know-what-the-covid and there's been little progress since. I'm not hyper familiar with the Bhakdi/Burkhardt autopsy results but I haven't heard anything about cell fusion associated with those.
If you mean looking at clotting systematically, as opposed to just trying to detect patterns from healthcare visits, I am not aware of any. But we know that S1 / spike cause clotting alone, so why wouldn't transfection-induced spike do the same (at least before antibodies come around)
Hmmm, I think my question about syncytia was not well thought out. The mRNA gene-therapy treatment is supposed to generate S protein locked in the pre-fusion conformation, but is there any evidence that it can actually cause fusion with other cells?
If I've read Horne et al correctly (and damn this is a stretch for someone not immersed in this stuff!), what I'm seeing is a genuine comparison between those with no injections and those with two, i.e. concerns about miscategorization do not apply. Is this generally the case with studies of vax efficacy (and safety), or do some studies play around with 'unvaxxed' in a muddying-the-water kind of way, e.g. including 14 days post 1st shot in the category? Or is this oft-mentioned concern just misguided? I do recall that the definition of 'unvaxxed' in some (most) jurisdictions (i.e. govt-posted data) *did* include that initial period, and that sometimes the data presentation was fudged even more by lumping the un-injected in with one-shotters in a 'not fully vaxxed' group. Data malfeasance on the part of governments everywhere, it seems.
Unrelated (I think?): again from Horne et al: "Rates of non-covid-19 related death were consistently lower among fully vaccinated than unvaccinated people." How is this even possible? What magical properties does this stuff have so as to reduce all-cause non-Covid mortality? Within a few weeks of 2 shots, the vaxxed are something like 60% less likely to experience a non-Covid death than the unvaxxed. The effect wanes, as with all the other effects measured, but I don't understand why there would be an effect in the first place.
The "playing around" with vaccination status does happen, but the concern over it is excessive. My next post will be finishing a series I started last month rebutting this trope; but basically there's nothing really interesting going on in the "worry window." When studies do report on this period, you have ~12 days of background similar PCR+ rates after dose 1, and then a drop. So if anything, lumping the people who are between 1 and ≥14 days post-dose-2 makes the "unvaccinated" look microscopically better as case rates. And when you compare studies that use these problematic windows with ones that are more precise, the results are similar - again, because there's nothing actually going on in the window.
As in my annotation to the graph, there could be some lumping of previously infected into the unvaccinated group despite the fact that anyone who was in the system as infected was excluded from the study. That's a hypothetical.
More well-established is that there is a "not on deathbed" bias operating in the UK data. Older adults tend to have deaths preceded by declines which make the same deaths apparent in advance. At any given moment if you agree to exclude these from an intervention then deaths in the intervention-having-group are going to only include those whose deaths are not predicted in advance. This makes a big impact on the death rate, and this is why it is so low in all older ≤21 days post-dose-X groups in the ONS data
But weren't the vulnerable targeted first? The language is contradictory on this, but it supports exclusion of people who were near death (and excluding this people just makes sense, why protect those who are dying anyway?)
"In line with WHO guidance, first up are care home residents and health workers, then older and clinically extremely vulnerable people. Among those excluded from the mass vaccination plan at present are pregnant women, children under 16, and those with health conditions that put them at very high risk of serious outcomes."
Thanks for the clarification, Brian. It's still surprising to me that the "not on deathbed" bias would have such a huge impact on the non-clinically vulnerable 40-64 year olds. Surely the percentage of that cohort 'on the deathbed' at any given time is miniscule. But perhaps I'm still missing something.
Not unrelated: sad and frustrating that public health agencies are not assessing interventions by rigorously tracking excess mortality in a transparent way. Severe efficacy is meaningless if it only applies to Covid outcomes while side effects are ignored. It's like the industry gets to define the rules of the game ('only look HERE and definitely not over THERE') and then declares victory, which is simply accepted by regulators. For another, very different take on the UK data: https://www.preprints.org/manuscript/202301.0204/v3
"The extent of waning of vaccine effectiveness against severe covid-19 is less clear: studies have found no evidence of waning,91017 modest waning,511 or substantial waning.12"
Waning is itself evidence of both infection efficacy and severe efficacy - i.e., you can't lose what you don't have to begin with. So you know infection efficacy isn't a data artifact because you can see it totally disappear in the same data set after 4 months post-dose.
What you want to know is does the waning flatten out, and where - above 0, at 0, or below 0. For infection efficacy it wanes to 0 over and over after every shot - it's clearly temporary, not real immunity. Maybe it even would wane lower but boosters keep preventing a clear view of what happens here.
For severe efficacy it wanes to above 0 (in adults; for kids it wanes to 0 because there were virtually no severe outcomes to prevent). But both end-points could be influenced by bias, especially healthy user bias for severe efficacy.
And this is where I am fine with people making that assertion, or even debating the case though I think it's not strong for the UK (probably much stronger in the US, but US data is garbage and propaganda anyway).
My issue with all of this is that: The disease the shots were designed to treat no longer exists.
No one in any of these tests has the symptom cluster that was diagnostic of Covid in 2020. We might as well argue whether or not the shots prevent severe outcomes from gunshot wounds. I don't pretend to be a virologist(I sometimes pretend to be a gynecologist or a breastologist but neither of those is relevant) but my understanding is that the Omicron spike is substantially different from the spike that the mRNA codes for. Before(you are late to the party for that Jonboy) we get excited looking at numbers and arguing probabilities, is it even mechanistically reasonable that this shot would produce immune reactions to the Omicron spike? Or do any effects we see need to be referred to another mechanism of action?
There are three aspects to this, the virus, the mRNA potions, and B Cells.
The virus didn't change that much in 2021. The VOCs which all emerged "out of nowhere" were not immune-evasive to any great extent. Even though they had extreme mutation signatures (nonsynonymous/synonymous mutations in spike S1 suggesting crazy selection pressure) they didn't set off any reinfections and don't seem to be explained by immune evasion. Hence why I proposed they were lab made though I dropped the case in the end https://unglossed.substack.com/p/the-2020-variants-not-guilty
Additionally, the mRNA shots might be front-loading "variant antibodies" because the modified nature of the RNA causes errors in protein synthesis.
And in general, immunity to any "antigen" is not a monolith, it is a distributed process where multiple germinal centers target different "interesting bits" of the spike protein and different B Cells compete to bind to it. So you wind up with this pool of B Cells trained to different targets and they can all expand to make a lot of clones or scale back. So if one part of the spike protein changes and said changed-spike-having variant shows up to start an infection then the B Cells for the parts that don't change can just expand, and antibodies scale up accordingly. https://unglossed.substack.com/p/b-cells-anonymous
At the same time, previous B Cells for the changed part can re-enter germinal centers to mutate their receptor/antibody design to restore binding to the changed part. So your original B Cell response is both protective and reactive to variants. You end up with a strong cross-reactive response.
It was never a big secret that the trials were sham rush-jobs that then tanked the control group. So if you are asking my opinion on whether we can still assess the real-world evidence carefully and find abundant examples that suggest severe efficacy in different locales, then my opinion is yes, we can. I don't believe there is anything in the rulebook about dogs not playing efficacy ball.
Those who disagree, of course, can assert that everything must be too biased to judge. Of course that isn't what most denialists are actually saying.
Feb 15, 2023·edited Feb 15, 2023Liked by Brian Mowrey
My stats understanding is too rusty to understand the validity of observations made in the real world re: vaccination effectiveness when there is no control.
My question is along the lines of: if everyone (essentially) is vaccinated, how do you prove efficacy? Of any type?
If everyone is special, noone is.
Not sure if I am making sufficient sense.
Analogy: if we all wear the anti-EMF badge I see advertised on FB - about the size of a 50C piece, worn around the neck (:-/) and nobody dies of 5G radiation, does that prove severe efficacy of the anti-EMF badges?
IMO it doesn't (duh comment incoming) as without a control with no EMF badge, we can't tell if it's the badge or the fact there's no actual danger from the 5G radiation.
The typical rubric humans use is that if you can't tell if something is working, keep doing it. Most human strategy is just practical. "Fence keeps cows here" and "sword hurts enemy" never had a RCT.
Exceptions to the rule - culture X does this, why? a la Weber's Protestant Work Ethic - are just that, and the notion of different cultures might now be obsolete with the exception of Globalist West vs Russia vs Globalist China.
Vaccines have always worked that way: 1) Everyone scared 2) Inject / scrape something 3a) Move on / 3b) Revolt. But 3b stopped happening much after Cutter. Questioning vaccines has rarely been centered on efficacy rather than injury. If there were no injuries, we would just keep vaxxing for everything the same way we do anything, until someone came along and made a persuasive argument that the net effect is negative. But can you really persuade a species that defaults to interventionism that the non-interventioned immune system *is* the intervention?
My grandmother in rural Indiana had a conch shell with the end cut off, which you could blow like a trumpet. She blew the conch shell every two weeks, explaining to us kids that it kept elephants away. Worked like a charm.
Regarding the chronic infection. I'm intrigued, I admit, but there is the pesky thing called evidence of course. I've only vaguely heard of chronic covid infections. I did hear frequently about reinfections, but those inherently are defined as periods in which you hence test negative.
(As we discussed I'm also highly skeptical about these, as I suggested many of them are not re-infections but only re-exposures, and that co-infections with other illnesses will explain even a significant portion of testing positive with symptoms. But I guess that re-exposure and re-infections, the difference defined as with or without symptoms, are a gliding scale.)
But what would be the mechanism in which COVID-19 would hide detection using even 43 rounds of PCR amplification? I mean, at 33-35 one stops typically detecting virus that can replicate, so testing negative suggests not even a fragment is left?
For herpes it is clear how and where the virus family hides, but a shimmering COVID-19 infection would in my view lead to chronic symptoms and also chronic destruction. I can image the body pausing its full on attack, allowing tissue to heal, but not really stopping its attack. I'd image such shimmering infection can drag itself on for weeks or perhaps even months, but not without symptoms? Unless of course we identify a spot where COVID-19 can shimmer outside the respiratory tract. E.g. like typhoid shows it is possible, but where then would that be?
This was exactly my thinking, coronaviruses are smash and grabbers and are too selected-for-replication-amplification to have tolerable persistent infection. And so when autopsies show late post-acute stage PCR+ in tissues, you can say, "well that just goes to show persistent infections are not survivable, so when they happen you die and that's rare obviously." But I'm coming around to the alternate interpretation that these autopsies are showing something that happens a bit more than it seems, and maybe in a lot of Long Covid.
Feb 14, 2023·edited Feb 14, 2023Liked by Brian Mowrey
Maybe 'severe efficacy' would better be interpreted as 'significant reduction of high absolute risk' or 'highly protective of the most vulnerable'.
Otherwise 'Most individual people therefore cannot benefit from severe efficacy' seems a bit counter intuitive? Plus efficacy usually relates to RCT outcomes which in Pfizers case only covered symptomatic illness.
It's kinda like saying 'not jumping out of planes is severely efficacious in preventing death', whereas the risk of such is around 1:100000 for a trained skydiver:
Doing anything to "avoiding risk" is a bet that you would have experienced the negative outcome for which you were at risk. So as long as 60% don't experience the negative outcome, most people doing something to avoid the risk of 40% negative outcome lose the bet.
If the bet is costless, then obviously it's still a no-brainer to upgrade from 60% chance of being fine to 100% chance of being fine.
If the bet has any cost >nothing, right away - and this is obviously counter-intuitive - you are probably going to lose by making the bet. You probably would have been fine, so you paid for protection for nothing.
This doesn't apply for repeated risk, i.e. seatbelts and driving, where it doesn't matter if you are 99.9% safe per drive because you know you are going to take enough drives to eventually pool total likelihood of a crash >50%.
But for a one-time risk - Novel Bioweapon / Virus Thing - the chance of severe outcomes for every group is small. Delta + intentional hospital mistreatment obviously compounds the risk but for the most part, no individual on Earth was really "made more likely to die" because this virus came about. So no one can become "more likely to live" by artificial protection. I mean sure, as a group, the numbers move a few percentage points; but a few percentage points is not most people. For the most part we are all just fine regardless.
I also wonder how this argument for extreme efficacy interacts with the research by people like Sasha Latypova on good manufacturing practices, or I forget her name, a Canadian pharmacologist who looked into the nitty-gritty of the likelihood that the vials could actually contain the mRNA that the official research articles claim they do. Latypova says that it's impossible to deliver what they claim, particularly at scale, and that no one checks, either. So not only does no one know what's actually in the vials, but when they've attempted, they (Pfizer/BioNTech) have actually been unable to characterize the content of their product (the fake Western Blots, the leaked EMA scandal) So how can there be "extreme efficacy" (unless it's just about the ideal of the technology that actually cannot be made a reality) if what is claimed is practically impossible.
The "how" would be that the target dose was total overkill. So even if your injection is mostly garbage, you get a little foothold on immune response, and that is all that is required to head off the immune suppression / delayed response that leads to (rare!) severe outcomes in infection to a degree that affects rates of hospitalization.
Mind you, I emphatically endorse Latypova and Gutschi's remarks on the implausibility of scaling up manufacture without quality dropping to "0 sigma." In fact I think this probably spared a lot of people the worst harms. With that said, none of the post-injection antibody response studies I've seen show any evidence of people getting total "blanks" (despite McCairn finding a vial with no phosphorous). Ultimately this is an area where things are very ambiguous.
"I would like to remind readers once again that Pfizer is not instrumental in the development or deployment of the Covid vaccines"
I see it more as a bribe than a handout. But I think it would be great if corporations were exempt from paying taxes on the bribes they receive. Same for individuals.
That would help people who are still blind to see what is really going on here. That's a lot of hopium, I admit.
Anyway, they earned that money, and will be suffering the same calamitous world as everyone else. Their money is there to remind them they won't escape the chaos. So the more money they have, the greater the punishment.
Second, free-thinkers can sometimes be confused with shills by people who live in fear and are under a strong influenze of propaganda. Also, free-thinking is not the same as reaching correct conclusions. And being wrong is not the same as being a shill.
You've been putting out a lot of thought-provoking posts that have strayed from the consensus on both sides which is always needed.
I think the biggest issue is that new information tends to override older information, and instead it's the weighing of each evidence that's important.
The biggest problem with the vaccines weren't efficacies but uncertainties in adverse reactions which became more apparent after more time. It was only later that we gained more evidence of the vaccines not being sterile even though that probably should have been the assumption from the start.
The same goes for PAXLOVID. We didn't have to argue that PAXLOVID didn't work. Instead, the argument was that there was a message other treatments did not work, and therefore you can only rely on PAXLOVID and Molnupiravir for at-home treatment. In this case it was the inability for doctors to prescribe things that was the issue.
Then take that into monoclonal antibodies which everyone assumed was the best thing that should have been used widely, then a little study comes showing very low dosage of monoclonals may induce ADE in very specific cell lines (inherently a very limited study) and all of a sudden people are suggesting that monoclonals were always evil.
I think a lot of this may be more reflective that many people are being exposed to information but aren't quite parsing or reconciling with it constructive manner. Just throw information at some people and it can become the new narrative.
"I think a lot of this may be more reflective that many people are being exposed to information but aren't quite parsing or reconciling with it constructive manner. Just throw information at some people and it can become the new narrative." - careful, soon you're going to have to change your handle to "post-modern discontent"!
I posted about IGY antibodies before, but an important thing to be aware of is that those IGY antibodies will only be useful if the chickens have been challenged with SARS-CoV-2:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7608017/
This woman reports that her S-protein antibody levels seem really high 15 months after her last booster:
https://twitter.com/anettefri/status/1627372509174661121
Greater than 25,000 kBAU/L. They stopped counting at 25,000, it seems.
Seems like something is going wrong there.
Still searching for explanations for the injuries that some experience from the unnecessary mRNA gene-therapy treatment for the common cold.
Came across this: https://live2fightanotherday.substack.com/p/returning-to-free-floating-s-spikes
He suggests that what is going on is that if the person doing the injection does not aspirate then they inject shit-loads into the vasculature and this can have varying effect:
1. pericardial or myocardial cells take up the LNP encapsulated mRNA and produce spike and the person's immune system kills those cells for their efforts,
2. Vasculature epithelial cells take up the LNP encapsulated mRNA and produce lots of spike which gets into the blood all over the place and leads to thrombotic thrombocytopenia or pulmonary embolisms or strokes etc.
3. When people do a blood draw they find up to 638 billion free-floating spike proteins
In those cases where aspiration was used the side-effects are likely to be less severe.
I still maintain that no one needs that shit but we need to figure out what is going on and hiding it under the carpet is not useful.
Also came across this: https://t.co/l2mrQ8cEl9
SARS-CoV-2 Spike protein binds to bacterial lipopolysaccharide and boosts proinflammatory activity.
Returning to the mRNA gene-therapy generated Spike protein and the claims that it is LOCKED into the prefusion conformation.
Do we know for sure, 100% that this is absolutely true?
Since the mRNA is generated in a bacterial soup using plasmids it seems like there are opportunities for this to go wrong and I have read elsewhere that Pfizer and Moderna can only manage something like 60% intact and or correct mRNA in the shots.
However, the second issue is: What are all the error modes when our ribosomes are presented with mRNA that has pseudo-uridine in it? I have seen claims that they only recognize stop codons with pseudo-uridine about 60% of the time. However, could there be other error modes were they generate spike protein that can fully fuse to ACE2 bearing cells and thus form syncytia if they manage to migrate to the surface of the cell they were created in?
I doubt anyone actually knows what all the possible outcomes are and JikkyLeaks claims there can be up to 436B spikes circulating in the serum so there may well be many studded in the surfaces of cells where they were created.
Proline doesn't depend on any uridines - the third nucleotide is irrelevant. And Pfizer and Moderna probably defaulted to C or G for the third nucleotide. So there is no reason to think that the stabilizing prolines will be a hotspot for mistranslation.
Yes, cells will probably be studded with spike protein - Which is why the immune system will kill them, whether they have fused or not, until you start getting IgG4, which switches that off
That addresses translation but what about transcription during the manufacturing process.
How sure can we be that evil shit is not escaping into the vials?
I don't see how these concerns top the generic fact that no one knows if cell fusion occurs after injection or not.
i.e., why worry about whether the prolines get installed correctly if we don't even know if the prolines work all the time? Moreover, the error rate in general is going to impact fusion more than it impacts the stabilization thereof; i.e., fusion requires function of the spike protein's many parts. In nature the S2 unit, which contains the fusion machinery, is extremely conserved, because fusion is a delicate mechanical process.
So RNA infidelity is more likely to break fusion than to cause it. Just as you're less likely to die in a car that was made with no technical expertise vs. one made with technical expertise, because the former can't even get out of the driveway -- so it doesn't matter how often an airbag accelerometer is upside down.
Thus, the proline failure rate is almost certainly greater than the "get all the other translation correct but mess up only the prolines" rate. Either way what you really want to know is how often does it actually happen, and no one is looking at that.
So, it's worse than I thought.
More on Paxlovid double pill bonanza
https://geoffpain.substack.com/p/trifluoroacetate-from-pfizer-nirmatrelvir
Are there any papers that look at whether or not the mRNA gene-therapy treatments cause clotting (perhaps because of the sialic acid on the S protein) or syncytia?
Off the top of my head, none of the handful of in vitro experiments using actual vaccine product report anything about cell fusion, and there's nothing about what goes on in vivo. As with everything else, there was no attempt before authorization to figure out what these products actually do in the body https://unglossed.substack.com/p/pfizer-did-not-know-what-the-covid and there's been little progress since. I'm not hyper familiar with the Bhakdi/Burkhardt autopsy results but I haven't heard anything about cell fusion associated with those.
If you mean looking at clotting systematically, as opposed to just trying to detect patterns from healthcare visits, I am not aware of any. But we know that S1 / spike cause clotting alone, so why wouldn't transfection-induced spike do the same (at least before antibodies come around)
Hmmm, I think my question about syncytia was not well thought out. The mRNA gene-therapy treatment is supposed to generate S protein locked in the pre-fusion conformation, but is there any evidence that it can actually cause fusion with other cells?
If I've read Horne et al correctly (and damn this is a stretch for someone not immersed in this stuff!), what I'm seeing is a genuine comparison between those with no injections and those with two, i.e. concerns about miscategorization do not apply. Is this generally the case with studies of vax efficacy (and safety), or do some studies play around with 'unvaxxed' in a muddying-the-water kind of way, e.g. including 14 days post 1st shot in the category? Or is this oft-mentioned concern just misguided? I do recall that the definition of 'unvaxxed' in some (most) jurisdictions (i.e. govt-posted data) *did* include that initial period, and that sometimes the data presentation was fudged even more by lumping the un-injected in with one-shotters in a 'not fully vaxxed' group. Data malfeasance on the part of governments everywhere, it seems.
Unrelated (I think?): again from Horne et al: "Rates of non-covid-19 related death were consistently lower among fully vaccinated than unvaccinated people." How is this even possible? What magical properties does this stuff have so as to reduce all-cause non-Covid mortality? Within a few weeks of 2 shots, the vaxxed are something like 60% less likely to experience a non-Covid death than the unvaxxed. The effect wanes, as with all the other effects measured, but I don't understand why there would be an effect in the first place.
The "playing around" with vaccination status does happen, but the concern over it is excessive. My next post will be finishing a series I started last month rebutting this trope; but basically there's nothing really interesting going on in the "worry window." When studies do report on this period, you have ~12 days of background similar PCR+ rates after dose 1, and then a drop. So if anything, lumping the people who are between 1 and ≥14 days post-dose-2 makes the "unvaccinated" look microscopically better as case rates. And when you compare studies that use these problematic windows with ones that are more precise, the results are similar - again, because there's nothing actually going on in the window.
As in my annotation to the graph, there could be some lumping of previously infected into the unvaccinated group despite the fact that anyone who was in the system as infected was excluded from the study. That's a hypothetical.
More well-established is that there is a "not on deathbed" bias operating in the UK data. Older adults tend to have deaths preceded by declines which make the same deaths apparent in advance. At any given moment if you agree to exclude these from an intervention then deaths in the intervention-having-group are going to only include those whose deaths are not predicted in advance. This makes a big impact on the death rate, and this is why it is so low in all older ≤21 days post-dose-X groups in the ONS data
But weren't the vulnerable targeted first? The language is contradictory on this, but it supports exclusion of people who were near death (and excluding this people just makes sense, why protect those who are dying anyway?)
https://www.bmj.com/content/372/bmj.n421
"In line with WHO guidance, first up are care home residents and health workers, then older and clinically extremely vulnerable people. Among those excluded from the mass vaccination plan at present are pregnant women, children under 16, and those with health conditions that put them at very high risk of serious outcomes."
Thanks for the clarification, Brian. It's still surprising to me that the "not on deathbed" bias would have such a huge impact on the non-clinically vulnerable 40-64 year olds. Surely the percentage of that cohort 'on the deathbed' at any given time is miniscule. But perhaps I'm still missing something.
Not unrelated: sad and frustrating that public health agencies are not assessing interventions by rigorously tracking excess mortality in a transparent way. Severe efficacy is meaningless if it only applies to Covid outcomes while side effects are ignored. It's like the industry gets to define the rules of the game ('only look HERE and definitely not over THERE') and then declares victory, which is simply accepted by regulators. For another, very different take on the UK data: https://www.preprints.org/manuscript/202301.0204/v3
What to make of this from one of your cites?
"The extent of waning of vaccine effectiveness against severe covid-19 is less clear: studies have found no evidence of waning,91017 modest waning,511 or substantial waning.12"
Waning is itself evidence of both infection efficacy and severe efficacy - i.e., you can't lose what you don't have to begin with. So you know infection efficacy isn't a data artifact because you can see it totally disappear in the same data set after 4 months post-dose.
What you want to know is does the waning flatten out, and where - above 0, at 0, or below 0. For infection efficacy it wanes to 0 over and over after every shot - it's clearly temporary, not real immunity. Maybe it even would wane lower but boosters keep preventing a clear view of what happens here.
For severe efficacy it wanes to above 0 (in adults; for kids it wanes to 0 because there were virtually no severe outcomes to prevent). But both end-points could be influenced by bias, especially healthy user bias for severe efficacy.
And this is where I am fine with people making that assertion, or even debating the case though I think it's not strong for the UK (probably much stronger in the US, but US data is garbage and propaganda anyway).
My issue with all of this is that: The disease the shots were designed to treat no longer exists.
No one in any of these tests has the symptom cluster that was diagnostic of Covid in 2020. We might as well argue whether or not the shots prevent severe outcomes from gunshot wounds. I don't pretend to be a virologist(I sometimes pretend to be a gynecologist or a breastologist but neither of those is relevant) but my understanding is that the Omicron spike is substantially different from the spike that the mRNA codes for. Before(you are late to the party for that Jonboy) we get excited looking at numbers and arguing probabilities, is it even mechanistically reasonable that this shot would produce immune reactions to the Omicron spike? Or do any effects we see need to be referred to another mechanism of action?
There are three aspects to this, the virus, the mRNA potions, and B Cells.
The virus didn't change that much in 2021. The VOCs which all emerged "out of nowhere" were not immune-evasive to any great extent. Even though they had extreme mutation signatures (nonsynonymous/synonymous mutations in spike S1 suggesting crazy selection pressure) they didn't set off any reinfections and don't seem to be explained by immune evasion. Hence why I proposed they were lab made though I dropped the case in the end https://unglossed.substack.com/p/the-2020-variants-not-guilty
Additionally, the mRNA shots might be front-loading "variant antibodies" because the modified nature of the RNA causes errors in protein synthesis.
And in general, immunity to any "antigen" is not a monolith, it is a distributed process where multiple germinal centers target different "interesting bits" of the spike protein and different B Cells compete to bind to it. So you wind up with this pool of B Cells trained to different targets and they can all expand to make a lot of clones or scale back. So if one part of the spike protein changes and said changed-spike-having variant shows up to start an infection then the B Cells for the parts that don't change can just expand, and antibodies scale up accordingly. https://unglossed.substack.com/p/b-cells-anonymous
At the same time, previous B Cells for the changed part can re-enter germinal centers to mutate their receptor/antibody design to restore binding to the changed part. So your original B Cell response is both protective and reactive to variants. You end up with a strong cross-reactive response.
As noted in my posts tracking "breakthrough" Omicron responses, this is what seems to be happening for all the vaxxed, which means they are stuck with the IgG4 converting B Cell pool forever. https://unglossed.substack.com/p/omicron-infections-might-be-of-little
Can efficacy be proven without a control? I would have thought no.
Please don't waste time answering if you have already done so in this series, I have not read them all.
It was never a big secret that the trials were sham rush-jobs that then tanked the control group. So if you are asking my opinion on whether we can still assess the real-world evidence carefully and find abundant examples that suggest severe efficacy in different locales, then my opinion is yes, we can. I don't believe there is anything in the rulebook about dogs not playing efficacy ball.
Those who disagree, of course, can assert that everything must be too biased to judge. Of course that isn't what most denialists are actually saying.
My stats understanding is too rusty to understand the validity of observations made in the real world re: vaccination effectiveness when there is no control.
My question is along the lines of: if everyone (essentially) is vaccinated, how do you prove efficacy? Of any type?
If everyone is special, noone is.
Not sure if I am making sufficient sense.
Analogy: if we all wear the anti-EMF badge I see advertised on FB - about the size of a 50C piece, worn around the neck (:-/) and nobody dies of 5G radiation, does that prove severe efficacy of the anti-EMF badges?
IMO it doesn't (duh comment incoming) as without a control with no EMF badge, we can't tell if it's the badge or the fact there's no actual danger from the 5G radiation.
The typical rubric humans use is that if you can't tell if something is working, keep doing it. Most human strategy is just practical. "Fence keeps cows here" and "sword hurts enemy" never had a RCT.
Exceptions to the rule - culture X does this, why? a la Weber's Protestant Work Ethic - are just that, and the notion of different cultures might now be obsolete with the exception of Globalist West vs Russia vs Globalist China.
Vaccines have always worked that way: 1) Everyone scared 2) Inject / scrape something 3a) Move on / 3b) Revolt. But 3b stopped happening much after Cutter. Questioning vaccines has rarely been centered on efficacy rather than injury. If there were no injuries, we would just keep vaxxing for everything the same way we do anything, until someone came along and made a persuasive argument that the net effect is negative. But can you really persuade a species that defaults to interventionism that the non-interventioned immune system *is* the intervention?
Yeah inertia, like gravity, is a bitch.
My grandmother in rural Indiana had a conch shell with the end cut off, which you could blow like a trumpet. She blew the conch shell every two weeks, explaining to us kids that it kept elephants away. Worked like a charm.
Regarding the chronic infection. I'm intrigued, I admit, but there is the pesky thing called evidence of course. I've only vaguely heard of chronic covid infections. I did hear frequently about reinfections, but those inherently are defined as periods in which you hence test negative.
(As we discussed I'm also highly skeptical about these, as I suggested many of them are not re-infections but only re-exposures, and that co-infections with other illnesses will explain even a significant portion of testing positive with symptoms. But I guess that re-exposure and re-infections, the difference defined as with or without symptoms, are a gliding scale.)
But what would be the mechanism in which COVID-19 would hide detection using even 43 rounds of PCR amplification? I mean, at 33-35 one stops typically detecting virus that can replicate, so testing negative suggests not even a fragment is left?
For herpes it is clear how and where the virus family hides, but a shimmering COVID-19 infection would in my view lead to chronic symptoms and also chronic destruction. I can image the body pausing its full on attack, allowing tissue to heal, but not really stopping its attack. I'd image such shimmering infection can drag itself on for weeks or perhaps even months, but not without symptoms? Unless of course we identify a spot where COVID-19 can shimmer outside the respiratory tract. E.g. like typhoid shows it is possible, but where then would that be?
This was exactly my thinking, coronaviruses are smash and grabbers and are too selected-for-replication-amplification to have tolerable persistent infection. And so when autopsies show late post-acute stage PCR+ in tissues, you can say, "well that just goes to show persistent infections are not survivable, so when they happen you die and that's rare obviously." But I'm coming around to the alternate interpretation that these autopsies are showing something that happens a bit more than it seems, and maybe in a lot of Long Covid.
Maybe 'severe efficacy' would better be interpreted as 'significant reduction of high absolute risk' or 'highly protective of the most vulnerable'.
Otherwise 'Most individual people therefore cannot benefit from severe efficacy' seems a bit counter intuitive? Plus efficacy usually relates to RCT outcomes which in Pfizers case only covered symptomatic illness.
It's kinda like saying 'not jumping out of planes is severely efficacious in preventing death', whereas the risk of such is around 1:100000 for a trained skydiver:
https://britishskydiving.org/how-safe/
To get it in perspective, the lifetime fatality risk from a road accident is around 1:100 in the US (IIRC) and 1:240 in the UK:
http://www.bandolier.org.uk/booth/Risk/trasnsportpop.html
So for a lot of us, the 'severely effective' vaxx may be handily beaten by driving less or at least more carefully :-)
Doing anything to "avoiding risk" is a bet that you would have experienced the negative outcome for which you were at risk. So as long as 60% don't experience the negative outcome, most people doing something to avoid the risk of 40% negative outcome lose the bet.
If the bet is costless, then obviously it's still a no-brainer to upgrade from 60% chance of being fine to 100% chance of being fine.
If the bet has any cost >nothing, right away - and this is obviously counter-intuitive - you are probably going to lose by making the bet. You probably would have been fine, so you paid for protection for nothing.
This doesn't apply for repeated risk, i.e. seatbelts and driving, where it doesn't matter if you are 99.9% safe per drive because you know you are going to take enough drives to eventually pool total likelihood of a crash >50%.
But for a one-time risk - Novel Bioweapon / Virus Thing - the chance of severe outcomes for every group is small. Delta + intentional hospital mistreatment obviously compounds the risk but for the most part, no individual on Earth was really "made more likely to die" because this virus came about. So no one can become "more likely to live" by artificial protection. I mean sure, as a group, the numbers move a few percentage points; but a few percentage points is not most people. For the most part we are all just fine regardless.
I also wonder how this argument for extreme efficacy interacts with the research by people like Sasha Latypova on good manufacturing practices, or I forget her name, a Canadian pharmacologist who looked into the nitty-gritty of the likelihood that the vials could actually contain the mRNA that the official research articles claim they do. Latypova says that it's impossible to deliver what they claim, particularly at scale, and that no one checks, either. So not only does no one know what's actually in the vials, but when they've attempted, they (Pfizer/BioNTech) have actually been unable to characterize the content of their product (the fake Western Blots, the leaked EMA scandal) So how can there be "extreme efficacy" (unless it's just about the ideal of the technology that actually cannot be made a reality) if what is claimed is practically impossible.
The "how" would be that the target dose was total overkill. So even if your injection is mostly garbage, you get a little foothold on immune response, and that is all that is required to head off the immune suppression / delayed response that leads to (rare!) severe outcomes in infection to a degree that affects rates of hospitalization.
Mind you, I emphatically endorse Latypova and Gutschi's remarks on the implausibility of scaling up manufacture without quality dropping to "0 sigma." In fact I think this probably spared a lot of people the worst harms. With that said, none of the post-injection antibody response studies I've seen show any evidence of people getting total "blanks" (despite McCairn finding a vial with no phosphorous). Ultimately this is an area where things are very ambiguous.
"I would like to remind readers once again that Pfizer is not instrumental in the development or deployment of the Covid vaccines"
I see it more as a bribe than a handout. But I think it would be great if corporations were exempt from paying taxes on the bribes they receive. Same for individuals.
That would help people who are still blind to see what is really going on here. That's a lot of hopium, I admit.
Anyway, they earned that money, and will be suffering the same calamitous world as everyone else. Their money is there to remind them they won't escape the chaos. So the more money they have, the greater the punishment.
Second, free-thinkers can sometimes be confused with shills by people who live in fear and are under a strong influenze of propaganda. Also, free-thinking is not the same as reaching correct conclusions. And being wrong is not the same as being a shill.
"Also, free-thinking is not the same as reaching correct conclusions."
Well in that case I hereby "free" myself to ignore this fact!
That's what happens when one is not skeptical about skepticism itself.
Are you sure?
I'm only sure on even days of the month that are also even days of the week, but never on a full moon day, that would be dangerous.
Thank you for playing, I realise sarcasm / attempted wit is difficult to ascertain online, and your answer is appreciated.
You've been putting out a lot of thought-provoking posts that have strayed from the consensus on both sides which is always needed.
I think the biggest issue is that new information tends to override older information, and instead it's the weighing of each evidence that's important.
The biggest problem with the vaccines weren't efficacies but uncertainties in adverse reactions which became more apparent after more time. It was only later that we gained more evidence of the vaccines not being sterile even though that probably should have been the assumption from the start.
The same goes for PAXLOVID. We didn't have to argue that PAXLOVID didn't work. Instead, the argument was that there was a message other treatments did not work, and therefore you can only rely on PAXLOVID and Molnupiravir for at-home treatment. In this case it was the inability for doctors to prescribe things that was the issue.
Then take that into monoclonal antibodies which everyone assumed was the best thing that should have been used widely, then a little study comes showing very low dosage of monoclonals may induce ADE in very specific cell lines (inherently a very limited study) and all of a sudden people are suggesting that monoclonals were always evil.
I think a lot of this may be more reflective that many people are being exposed to information but aren't quite parsing or reconciling with it constructive manner. Just throw information at some people and it can become the new narrative.
"I think a lot of this may be more reflective that many people are being exposed to information but aren't quite parsing or reconciling with it constructive manner. Just throw information at some people and it can become the new narrative." - careful, soon you're going to have to change your handle to "post-modern discontent"!