Jul 8, 2022·edited Jul 8, 2022Liked by Modern Discontent
This is a great, thoughtful post. Just like you, I was wondering, how come a brand new variant, without anything intermediate, appeared out of nowhere?
I did, and still do, have doubts as to mildness of Omicron. For example, Ba1 and Ba2 appeared at almost the same time. But it took Ba1 to "bust the gates" open for Ba2 to take hold some months later and start reinfecting people.
What exactly did Ba1 do, to make people more susceptible to Ba2? Nobody knows. There is a lot of mysteries in Covid-19 that people are not even perceiving as mysteries.
Is Covid mild if each reinfection kills 20% of lymphocytes andmonocytes?
In addition, there are several narratives. The "lab origin" narrative says that Covid and many variants all come from a lab. Another says that Covid is undergoing natural evolution and "Omicron proved Geert was right". Well if they all came from a lab, there is no evolution!
The truth is probably somewhere in the middle.
Nowadays, Geert and many people say that "Covid is regaining virulence". But perhaps it is reinfections that make people sicker and sicker, as opposed to innately higher vorulence. Lots of stuff to think about.
P.S. I and my son did NOT have Omicron despite zero preventative measures. We are both unvaxed and had Covid earlier (Nov 2020 for me and Apr 2021 for him)
Thanks Igor, I do remember that you wrote about it. I couldn't remember and it's rather difficult to fish through older articles on Substack so I gave up on that.
So, there's a few reasons and I have a working idea that I'm trying to figure out so it's very hypothetical at the moment.
If we consider that, at the point of Delta, that the world generally had a Delta/Wuhan immune landscape, we may have a landscape that encourages any variant that can overcome this immune landscape. Omicron emerges with both Ba.1 and Ba.2 (we'll leave Ba.4/Ba.5 out of the discussion for now), and the virus with the best fitness to overcome the Delta/Wuhan immune landscape would be the one that wins, which appears to have been Ba.1. Afterwards, there was a general Ba.1 immune landscape that may have then allowed Ba.2 to take over as it had the capabilities to overcome this landscape. Then eventually Ba.4/Ba.5 were able to come in next. I think it's a matter of all of these Omicron variants likely coming onto the scene at the same time versus variants such as Alpha -> Beta -> Delta slowly emerging through mutation and immune escape. So maybe this explained why we cycled through the Omicron variants so quickly.
It's interesting that the 69-70 deletion was seen in both Ba.1 and Ba.4/Ba.5, as well as the Q493 reversion. Also, the L452R mutation which was seen in Delta and likely played a role in its virulence is now seen in Ba.4/Ba.5, so it's almost like we went full circle. In some ways, maybe the emergence of Omicron caused our immune system to undergo some sort of immunological round-about.
I'm not sure about the lymphocytes and monocytes, but we may want to look at other viruses and see if that is also a factor in those infections as well. Also, if those deaths are longterm or only temporary. Remember that just as we are learning about Omicron we're also learning about other viruses as well. The field of science is nowhere near the end- there's plenty of things that have not been figured out, and there are plenty more things that are likely to be corrected. Therefore, we shouldn't expect to see things in COVID and assume that these are unique only to COVID- it could very well be that these are how other viruses behave, yet science never took time to fully look into it beforehand.
Also, Omicron and the apparent L452R mutation in the Ba.4/Ba.5 variant are some of the reasons why I am skeptical of Geert's hypothesis. His hypothesis relies on the idea that Ba.1 was less virulent because that's how immune escape starts before it picks up in virulence. It just feels like one of those things that fits way too coincidentally with the model. Until Geert rectifies the gap with Omicron rather than just incorporate it into his working model I will remain skeptical.
There's likely to be poeple who did not have Omicron, the same way many people didn't get prior variants. I think as Omicron moves on we are likely to come across it at some point, but that also requires that we confirm symptoms with some sort of test.
69-70del could be a recurrent artifact of lab conditions, similar to how the furin cleavage site often drops during serial passage in cell culture. Such drops could be physio/mechanically favored by the polymerase or the RNA molecule, in other words the polymerase “likes” to hop over these bits when replicating the RNA molecule, or the molecule has more stable packing with the N protein in that region if those nucleotides are deleted, conferring fitness. So del on BA.1 favors the idea that BA.1 (either with BA.2 or after isolation) was cooked in similar lab conditions to the 2020 fall VOCs and del on 4/5 favors my idea that all the Omicron siblings were cooked together.
Another piece of food for thought RE GvdB: The whole idea of immune escape, even though so much of our immunology and vaccinology understanding leans completely on it, is more or less an untested hypothesis. It stems from the failure of Francis’ first mid-40s flu vaxxes, which were cultured from a 30s isolate. Well, maybe Francis just sucked at vaccines. Maybe the egg culture serial passaged the virus into something unrelated to the infectious strain. Maybe a billion other things. It could be the case that antigenic drift is not relevant to natural selection for viruses that do not rely on a viremia pathway like measles. A notable example is polio which doesn’t antigenically shift: well, how did it survive vs human immunity all this time?
That's interesting Brian. The 69-70 del has been more of a supposition, as the argument for its compensatory mechanism is based on its presence more than any causative analysis.
As to immune escape, I suppose this is one area where I concede to the consensus for now. I think there's far too many things to consider that at this point, and so I'd rather consider this point somewhere I won't lose my mind over!
"Remember that just as we are learning about Omicron we're also learning about other viruses as well. The field of science is nowhere near the end- there's plenty of things that have not been figured out, and there are plenty more things that are likely to be corrected. Therefore, we shouldn't expect to see things in COVID and assume that these are unique only to COVID- it could very well be that these are how other viruses behave, yet science never took time to fully look into it beforehand."
I've thought about this many times. SARS-CoV-2 has received an unprecedented amount of scientific attention. Is it really such a weird virus, or do other viruses share many of the same traits, but we never looked hard enough? I think it likely is an oddball, but I bet a lot of other viruses have quirks that we haven't discovered yet.
Yes I think it's working both ways. Brian Mowrey of Unglossed have made remarks that maybe the long storage of antigens in lymph nodes may just be what antigen presenting cells do, and maybe we just don't know much about the matter.
I think there's been a general issue of having the term "novel" override many of our faculties so that we are suddenly believing that many of these things that are happening from a SARS-COV2 infection are unique to SARS-COV2. This really should tell people that much of science is not settled, and we should be mindful not to box ourselves into biases.
The first thing to do for those infected with COVID-19, or who have sepsis, Kawasaki disease, MIS-C or any other clinital emergency is to get their circulating 25-hydroxyvitamin D up to at least 50 ng/mL 125 nmol/L. Any less than this and their immune system cannot work as effectively as it should against viral, bacterial and fungal pathogens. Low 25-hydroxyvitamin D levels also increase the risk of wildly dysregulated hyper-inflammatory responses, which kill cells indiscriminately. This drives sepsis, severe COVID-19, KD and MIS-C. In severe COVID-19, inflammation damages the endothelial cells in the lungs (which line the blood vessels and capillaries). This causes the blood to become hyper-coagulative. The resulting microembolisms worsen the hypoxia caused by the inflammation and damage the lungs, brain, spinal cord, heart and all other organs.
The best approach to COVID-19 and numerous other health problems is proper vitamin D3 supplementation so all people have at least 50 ng/mL 25-hydroxyvitamin D all year round. Without proper supplementation, most people have 1/10th to 1/2 of this. If this is not done, then those infected need a 4 hour boost of 25-hydroxyvitamin D by ingesting a single oral dose of calcifediol (which _is_ 25-hydroxyvitamin D: 0.014 mg per kg body-weight, which is 1 mg for 70 kg 154 lb average adult body-weight. If calcifediol is not available, bolus vitamin D3 should be used, such as a single dose of 10 mg 400,000 IU. This takes about 4 days to boost 25-hydroxyvitamin D safely over 50 ng/mL, due to the delays inherent in it being hydroxylated in the liver to 25-hydroxyvitamin D.
Except for those few people today who have 50 ng/mL or more 25-hydroxyvitamin D, no other treatment matters more than calcifediol or bolus vitamin D3 to attain this level. Magnesium, zinc, vitamin C, B vitamins and probably vitamin A are also important early nutritional interventions: https://c19early.com . Ivermectin, quercetin and other early treatments are also likely to be helpful, safe and easy to obtain.
Only then should anyone bother to fuss about monoclonal antibodies, or any of the other patented, profitable, treatments. None of them are more urgently important than meeting the immune system's nutritional needs.
Jul 8, 2022·edited Jul 9, 2022Liked by Modern Discontent
Yes. My wife, a retired family practice doc, 20 years ago always recommended 100,000 iu Vitamin D for three days to boost D for ANY respiratory infection or flu like symptoms. It works. She was harassed by her colleagues about it, but who can argue with success. Research, as you say, is there and easy to find.
There you go with that Vitamin D Robin! Jokes aside, it's the summer time in the Northern Hemisphere so we should really be encouraging people to go outside and get some natural sunlight! Especially if we are so concerned about more cases we should be outdoors more and really soak in all of that natural goodness that we can.
Yes - but it takes months to raise 25-hydroxyvitamin D levels. COVID-19 is not the worst of it - sepsis kills 10 million people a year worldwide, and this would be rare if everyone had 50 ng/mL 25-hydroxyvitamin D, instead of their usual, unsupplemented, maybe some UV-B from sunshine in summer, levels of 5 to 25 ng/mL.
Sepsis could be treated much better with a single oral dose of 1 mg calcifediol (for 70 kg BW - and many with sepsis are twice this weight)) to boost 25-hydroxyvitamin D over 50 ng/mL in 4 hours or so.
Instead, not understanding anything about this, and being fascinated with all their complex, pseudo-sophisticated, narrowly-targeted, drugs, vaccines and other treatments, legions of doctors and nurses work their guts out trying to save millions of people from lasting harm and death, while almost all of these people's immune system cannot work properly due to lack of 25-hydroxyvitamin D.
We are having this great global health emergency with COVID-19, but we have always had disastrous levels of sepsis and other acute and chronic illness which would be very much reduced if everyone had 50 ng/mL or more 25-hydroxyvitamin D.
For most people it all sounds too simple to be true - not worth looking at the research. How could all those highly trained doctors not know this? The answer is complex and long - I haven't totally got to the bottom of it. Major contributors are corruption, groupthink and (for some doctors, certainly not all) fancying themselves as heroic priestly figures dealing out special, complex, difficult treatments no-one else could understand or reliably use. Vitamin D is far to simple to be attractive to people who think this way.
Paul R's wife had no such problems! See the groupthink he reports "harassed by her colleagues". Her colleague doctors were arguing against success and so actively arguing for harming and killing people in the guise their priestly divinations and dispensations.
“Remember that these strains are all derived from similar geographical regions”
This point is especially important. We have to bear in mind that if human transmission were responsible for BA.4 and 5, why hasn’t the hugely higher amount of transmission outside of “Omicron ground zero” led to a 6 and 7 and so on? So 4 and 5 were in the original release, variants produced by the serial passage conditions that also produced 1 and 2.
I would like to see more evidence about 4 and 5, but based on 1 and 2 I really wouldn't be surprised if there was some Omicron "big bang" moment or something of the like to have the emergence of all of these variants at the same time.
I honestly checked out in examining these variants as soon as Omicron came. I took it as everyone is getting sick, so let's just move on with our lives. Looking into it I see now how there are so many crucial features of Omicron that have not been factored or properly included into analyses but so many people are just continuing to move forward with their models anyways. I think this is really making me wonder about hypotheses such as Vanden Bossche's which relies so heavily on Omicron to validate the hypothesis.
Right, that’s where I was going with my post last month RE 4 and 5 being blamed for reinfections. I’ll prolly do a follow up post with a cross-post of my comments on your other post...
The best Antibody strategy is to have multiple mono-colonels targeting multiple sites. Then get testing that can identify specific variants. So you get sick, get tested, find the variant - then pick a combination of monoclonals that could work. You know - like physicians have done for 100's of years....
Multiple monoclonals targeting multiple sites? Like, having many antibodies target the spike? If only that were a thing! I can't put my finger on who or what can conduct such a feat!
Okay, jokes aside I do wonder why most monoclonals have included only up to two antibodies. I suppose there are concerns over autoimmune disorders, or maybe something with respect to EUA approval and some loophole needed.
There is a general issue of the R&D required to examine which monoclonals are needed. Considering that this virus is mutating pretty rapidly that would mean going back to conduct research every few months, or just have a cocktail of 5 and hope for the best.
Sequencing also takes a lot of time and money. Think up to a few thousand dollars to sequence one sample. Sequencing would also take several days and at that time it may be too difficult to deploy monoclonals, especially if timing is important.
Excuse me Rob, you have committed a sin! Which sin? Not sure, but A sin! I'll look at the post and see what I can find.
However, I don't want to impugn anyone because I believe these people are far more intelligent than myself, but I will be frank and say that many of my recent posts have been somewhat in response to a few of the articles I'm seeing floating around.
I believe Jessica is extremely intelligent, yet there have been a few times where I have questioned her analyses. I wrote my LNP articles because of her remarks that somehow the LNP in Moderna's formulation is carcinogenic based on the SDS. My remarks were that the SDS was horrible updated after they changed their formulation from chloroform to alcohol. I even used the Wayback Machine as suggested by a commenter and that appears to be the case.
There is also the hydrogel study published in the ACS which was being used to tie into amyloidosis, yet the peptide used in the study was found in seasonal human coronaviruses. I don't see anyone remarking about seasonal colds and amyloidosis, but apparently we need to be concerned about SARS-COV2, the vaccines and amyloidosis. The concerns don't parallel the studies being cited.
There's also that Moderna patent paper floating around suggesting that the insertion within the furin cleavage site may be due to some serial passage Moderna was studying, or it was associated to an MSH3 mutation that may lead to cancer. In reality, the authors of that paper would never conceivably have been able to come across the Moderna patent based on how they outlined their data. There was absolutely no tie to the MSH3 protein but because of this improper methodology, yet everyone latched onto that paper to relate spike protein to cancer.
There's also that immune imprinting paper from science to which has many, many flaws! It didn't even include any naturally immunized participants, and so the reference was to triple-vaccinated, uninfected individuals. In no ways can we extrapolate that immune imprinting is not occurring in those who are naturally infected, if we intend on arguing that OAS/immune imprinting are a thing.
So this is a bit long-winded, but I am a bit concerned that so many people are being riled up when there hasn't been a proper reading of the science. I don't know what's going on, and to be honest a lot of this becomes very tiring, mostly because I'm not making much on this Substack and spending hours upon hours trying to piece together information when I can just yell about the sky falling or we're all going to die may get more attention makes me rather disheartened.
So I tried reading the post. I'll be candid and say that I am terrible at statistics and so this may be something I need to look at a few times.
Like you stated, it appears the issue is related to the grey zone of relating vaccinated to injected. Jessica has taken some liberties, which means we should probably analyze the data with those caveats. Her perspective is that those who have gotten the two shots should be considered "injected" while hospitals would consider them to be "unvaccinated", and correcting that data would mean that more injected individuals are being hospitalized than uninjected.
I'll state that I don't think I have the knowledge right now to fully dissect the data, but from this alone I think we should be concerned about data manipulation. It's very easy to make statistics say what you want it to, and generally biases should be left outside of the analysis. This could be an issue of confounding variables just adding onto one another.
I am concerned that people may just take this information at face value and just extrapolate what they want to see.
No, I believe the data was only based on up to the 2nd dose, so anyone past 2nd dose and 14 days would likely be considered vaccinated irrespective of booster situation.
So generally there's an argument as to how to categorize those within that 14 day window after the 2nd dose. Generally those people would be considered vaccinated. Jessica believes it would be more appropriate to categorize them under "injected" and to instead measure hospitalization rates based on injection status. So I believe from this argument it's believed that if you shuffle these select people over from "unvaccinated" to "injected" then the data will indicate that hospitalization is occurring more within the injected group than the uninjected.
Edit: I believe Jessica is counting "partially vaccinated" as uninjected in her analysis as well? I would have to look over the data again and see.
This is making a lot of assumptions, and all of this is based on whether the categories used are accurate in the first place. Also, it boils down to what we can use with that data. It requires us to ask "why" this may be occurring, not that it just appears to be the case.
I think this is a general problem where people are looking at charts and just extrapolating that we can tell what's going on with these people when we really can't. It's why I generally avoid charts such as those because it lacks any context and nuance.
Apologies if I did not make it clear. I suppose, based on Jessica's assumptions, I have problems because it does require far too many suppositions. I don't know if her starting numbers are correct, and to then extrapolate to get a model that fits the original intent (i.e. injected individuals are ending up in the hospital at greater rates than uninjected ones) has a bit of a leap for me.
I think that's what your original concern was, such that it seems like several liberties were taken to come to those conclusions, but how those liberties came about and whether they were accurate/valid liberties is where the concerns lie?
Honestly, it's a pretty damn shame that Substack is becoming a place no different than Twitter or other social medial platforms. How can we consider ourselves to be greater thinkers when we shut out open discourse? Why is it that I can be someone who was heavily against vaccinations, lost my job over it, and am trying to piece together information yet have to consider censoring myself lest I run afoul for those who I should play nice with? It may be a bold comment to make, but we should all hope to encourage good-faith criticisms in order for us to grow as both individuals and as publishers. There's no good in having people follow along within an echo chamber to the degree that appears to be happening.
I absolutely feel you Rob. It's a strange state of affairs where I'm seeing so many concerning things and I just want people to follow the science (note, not "the" science which vaccine proponents have been pushing) rather than bastardize the science to come to the conclusions that they want.
I wish more commenters would speak out and provide a little pushback. I suppose one of the reasons is that many readers may not quite understand what they are reading. However, if I throw in some pathos, such as suggesting why "I" am scared, why you should be scared, or why we are all doomed then that immediately overrides those faculties needed for logic and reason so that people only know to respond through emotion.
I could not agree with you more! And I give you credit for actively trying to sort out the confusion; Unlike you, I just take the passive approach and rely on the comments section to help.
That being said, thanks — I just piggy backed on your search for clarity. 😊
Honestly, you should never be scared to comment that you don't understand. We won't ever know if someone doesn't understand something unless they tell us. I think there is a duty for readers to provide feedback.
There should be a general discussion that provides dialogue both ways, not just an avenue to lecture into the echo chamber.
Yeah, so the main problem is that the spikes are occurring during the Omicron waves, and that I believe is intended to be the main thing that is supposed to be taken away. But like you said, it's a strange argument to make that 14 day windows from all across the year would account for what's seen during the Omicron waves.
Generally speaking, there's far too many variables happening, including the most critical one which is that no one was protected from Omicron (what I was arguing above), so really it's generally a moot point to look at this data and try to make an argument.
So these always raise questions as to whether the data may be manipulated in such a way to get the results that were wanted.
This is a great, thoughtful post. Just like you, I was wondering, how come a brand new variant, without anything intermediate, appeared out of nowhere?
I wrote an article on Dec 3 and then another:
https://igorchudov.substack.com/p/urgent-omicron-variant-likely-to
https://igorchudov.substack.com/p/omicron-as-a-bioweapon-thoughts-and
I did, and still do, have doubts as to mildness of Omicron. For example, Ba1 and Ba2 appeared at almost the same time. But it took Ba1 to "bust the gates" open for Ba2 to take hold some months later and start reinfecting people.
What exactly did Ba1 do, to make people more susceptible to Ba2? Nobody knows. There is a lot of mysteries in Covid-19 that people are not even perceiving as mysteries.
Is Covid mild if each reinfection kills 20% of lymphocytes andmonocytes?
In addition, there are several narratives. The "lab origin" narrative says that Covid and many variants all come from a lab. Another says that Covid is undergoing natural evolution and "Omicron proved Geert was right". Well if they all came from a lab, there is no evolution!
The truth is probably somewhere in the middle.
Nowadays, Geert and many people say that "Covid is regaining virulence". But perhaps it is reinfections that make people sicker and sicker, as opposed to innately higher vorulence. Lots of stuff to think about.
P.S. I and my son did NOT have Omicron despite zero preventative measures. We are both unvaxed and had Covid earlier (Nov 2020 for me and Apr 2021 for him)
Thanks Igor, I do remember that you wrote about it. I couldn't remember and it's rather difficult to fish through older articles on Substack so I gave up on that.
So, there's a few reasons and I have a working idea that I'm trying to figure out so it's very hypothetical at the moment.
If we consider that, at the point of Delta, that the world generally had a Delta/Wuhan immune landscape, we may have a landscape that encourages any variant that can overcome this immune landscape. Omicron emerges with both Ba.1 and Ba.2 (we'll leave Ba.4/Ba.5 out of the discussion for now), and the virus with the best fitness to overcome the Delta/Wuhan immune landscape would be the one that wins, which appears to have been Ba.1. Afterwards, there was a general Ba.1 immune landscape that may have then allowed Ba.2 to take over as it had the capabilities to overcome this landscape. Then eventually Ba.4/Ba.5 were able to come in next. I think it's a matter of all of these Omicron variants likely coming onto the scene at the same time versus variants such as Alpha -> Beta -> Delta slowly emerging through mutation and immune escape. So maybe this explained why we cycled through the Omicron variants so quickly.
It's interesting that the 69-70 deletion was seen in both Ba.1 and Ba.4/Ba.5, as well as the Q493 reversion. Also, the L452R mutation which was seen in Delta and likely played a role in its virulence is now seen in Ba.4/Ba.5, so it's almost like we went full circle. In some ways, maybe the emergence of Omicron caused our immune system to undergo some sort of immunological round-about.
I'm not sure about the lymphocytes and monocytes, but we may want to look at other viruses and see if that is also a factor in those infections as well. Also, if those deaths are longterm or only temporary. Remember that just as we are learning about Omicron we're also learning about other viruses as well. The field of science is nowhere near the end- there's plenty of things that have not been figured out, and there are plenty more things that are likely to be corrected. Therefore, we shouldn't expect to see things in COVID and assume that these are unique only to COVID- it could very well be that these are how other viruses behave, yet science never took time to fully look into it beforehand.
Also, Omicron and the apparent L452R mutation in the Ba.4/Ba.5 variant are some of the reasons why I am skeptical of Geert's hypothesis. His hypothesis relies on the idea that Ba.1 was less virulent because that's how immune escape starts before it picks up in virulence. It just feels like one of those things that fits way too coincidentally with the model. Until Geert rectifies the gap with Omicron rather than just incorporate it into his working model I will remain skeptical.
There's likely to be poeple who did not have Omicron, the same way many people didn't get prior variants. I think as Omicron moves on we are likely to come across it at some point, but that also requires that we confirm symptoms with some sort of test.
69-70del could be a recurrent artifact of lab conditions, similar to how the furin cleavage site often drops during serial passage in cell culture. Such drops could be physio/mechanically favored by the polymerase or the RNA molecule, in other words the polymerase “likes” to hop over these bits when replicating the RNA molecule, or the molecule has more stable packing with the N protein in that region if those nucleotides are deleted, conferring fitness. So del on BA.1 favors the idea that BA.1 (either with BA.2 or after isolation) was cooked in similar lab conditions to the 2020 fall VOCs and del on 4/5 favors my idea that all the Omicron siblings were cooked together.
Another piece of food for thought RE GvdB: The whole idea of immune escape, even though so much of our immunology and vaccinology understanding leans completely on it, is more or less an untested hypothesis. It stems from the failure of Francis’ first mid-40s flu vaxxes, which were cultured from a 30s isolate. Well, maybe Francis just sucked at vaccines. Maybe the egg culture serial passaged the virus into something unrelated to the infectious strain. Maybe a billion other things. It could be the case that antigenic drift is not relevant to natural selection for viruses that do not rely on a viremia pathway like measles. A notable example is polio which doesn’t antigenically shift: well, how did it survive vs human immunity all this time?
That's interesting Brian. The 69-70 del has been more of a supposition, as the argument for its compensatory mechanism is based on its presence more than any causative analysis.
As to immune escape, I suppose this is one area where I concede to the consensus for now. I think there's far too many things to consider that at this point, and so I'd rather consider this point somewhere I won't lose my mind over!
"Remember that just as we are learning about Omicron we're also learning about other viruses as well. The field of science is nowhere near the end- there's plenty of things that have not been figured out, and there are plenty more things that are likely to be corrected. Therefore, we shouldn't expect to see things in COVID and assume that these are unique only to COVID- it could very well be that these are how other viruses behave, yet science never took time to fully look into it beforehand."
I've thought about this many times. SARS-CoV-2 has received an unprecedented amount of scientific attention. Is it really such a weird virus, or do other viruses share many of the same traits, but we never looked hard enough? I think it likely is an oddball, but I bet a lot of other viruses have quirks that we haven't discovered yet.
Yes I think it's working both ways. Brian Mowrey of Unglossed have made remarks that maybe the long storage of antigens in lymph nodes may just be what antigen presenting cells do, and maybe we just don't know much about the matter.
I think there's been a general issue of having the term "novel" override many of our faculties so that we are suddenly believing that many of these things that are happening from a SARS-COV2 infection are unique to SARS-COV2. This really should tell people that much of science is not settled, and we should be mindful not to box ourselves into biases.
The first thing to do for those infected with COVID-19, or who have sepsis, Kawasaki disease, MIS-C or any other clinital emergency is to get their circulating 25-hydroxyvitamin D up to at least 50 ng/mL 125 nmol/L. Any less than this and their immune system cannot work as effectively as it should against viral, bacterial and fungal pathogens. Low 25-hydroxyvitamin D levels also increase the risk of wildly dysregulated hyper-inflammatory responses, which kill cells indiscriminately. This drives sepsis, severe COVID-19, KD and MIS-C. In severe COVID-19, inflammation damages the endothelial cells in the lungs (which line the blood vessels and capillaries). This causes the blood to become hyper-coagulative. The resulting microembolisms worsen the hypoxia caused by the inflammation and damage the lungs, brain, spinal cord, heart and all other organs.
The best approach to COVID-19 and numerous other health problems is proper vitamin D3 supplementation so all people have at least 50 ng/mL 25-hydroxyvitamin D all year round. Without proper supplementation, most people have 1/10th to 1/2 of this. If this is not done, then those infected need a 4 hour boost of 25-hydroxyvitamin D by ingesting a single oral dose of calcifediol (which _is_ 25-hydroxyvitamin D: 0.014 mg per kg body-weight, which is 1 mg for 70 kg 154 lb average adult body-weight. If calcifediol is not available, bolus vitamin D3 should be used, such as a single dose of 10 mg 400,000 IU. This takes about 4 days to boost 25-hydroxyvitamin D safely over 50 ng/mL, due to the delays inherent in it being hydroxylated in the liver to 25-hydroxyvitamin D.
Except for those few people today who have 50 ng/mL or more 25-hydroxyvitamin D, no other treatment matters more than calcifediol or bolus vitamin D3 to attain this level. Magnesium, zinc, vitamin C, B vitamins and probably vitamin A are also important early nutritional interventions: https://c19early.com . Ivermectin, quercetin and other early treatments are also likely to be helpful, safe and easy to obtain.
Only then should anyone bother to fuss about monoclonal antibodies, or any of the other patented, profitable, treatments. None of them are more urgently important than meeting the immune system's nutritional needs.
Please read the research articles cited at: https://vitamindstopscovid.info/00-evi/ , the list of early treatments (with only the expensive ones FDA approved) at: https://nutritionmatters.substack.com/p/the-fda-cdc-and-most-other-western and the calcifediol or bolus D3 treatment at: https://nutritionmatters.substack.com/p/calcifediol-to-boost-25-hydroxyvitamin .
All sound too simple? Read the research!
Yes. My wife, a retired family practice doc, 20 years ago always recommended 100,000 iu Vitamin D for three days to boost D for ANY respiratory infection or flu like symptoms. It works. She was harassed by her colleagues about it, but who can argue with success. Research, as you say, is there and easy to find.
There you go with that Vitamin D Robin! Jokes aside, it's the summer time in the Northern Hemisphere so we should really be encouraging people to go outside and get some natural sunlight! Especially if we are so concerned about more cases we should be outdoors more and really soak in all of that natural goodness that we can.
Yes - but it takes months to raise 25-hydroxyvitamin D levels. COVID-19 is not the worst of it - sepsis kills 10 million people a year worldwide, and this would be rare if everyone had 50 ng/mL 25-hydroxyvitamin D, instead of their usual, unsupplemented, maybe some UV-B from sunshine in summer, levels of 5 to 25 ng/mL.
Sepsis could be treated much better with a single oral dose of 1 mg calcifediol (for 70 kg BW - and many with sepsis are twice this weight)) to boost 25-hydroxyvitamin D over 50 ng/mL in 4 hours or so.
Instead, not understanding anything about this, and being fascinated with all their complex, pseudo-sophisticated, narrowly-targeted, drugs, vaccines and other treatments, legions of doctors and nurses work their guts out trying to save millions of people from lasting harm and death, while almost all of these people's immune system cannot work properly due to lack of 25-hydroxyvitamin D.
We are having this great global health emergency with COVID-19, but we have always had disastrous levels of sepsis and other acute and chronic illness which would be very much reduced if everyone had 50 ng/mL or more 25-hydroxyvitamin D.
For most people it all sounds too simple to be true - not worth looking at the research. How could all those highly trained doctors not know this? The answer is complex and long - I haven't totally got to the bottom of it. Major contributors are corruption, groupthink and (for some doctors, certainly not all) fancying themselves as heroic priestly figures dealing out special, complex, difficult treatments no-one else could understand or reliably use. Vitamin D is far to simple to be attractive to people who think this way.
Paul R's wife had no such problems! See the groupthink he reports "harassed by her colleagues". Her colleague doctors were arguing against success and so actively arguing for harming and killing people in the guise their priestly divinations and dispensations.
“Remember that these strains are all derived from similar geographical regions”
This point is especially important. We have to bear in mind that if human transmission were responsible for BA.4 and 5, why hasn’t the hugely higher amount of transmission outside of “Omicron ground zero” led to a 6 and 7 and so on? So 4 and 5 were in the original release, variants produced by the serial passage conditions that also produced 1 and 2.
I would like to see more evidence about 4 and 5, but based on 1 and 2 I really wouldn't be surprised if there was some Omicron "big bang" moment or something of the like to have the emergence of all of these variants at the same time.
I honestly checked out in examining these variants as soon as Omicron came. I took it as everyone is getting sick, so let's just move on with our lives. Looking into it I see now how there are so many crucial features of Omicron that have not been factored or properly included into analyses but so many people are just continuing to move forward with their models anyways. I think this is really making me wonder about hypotheses such as Vanden Bossche's which relies so heavily on Omicron to validate the hypothesis.
Right, that’s where I was going with my post last month RE 4 and 5 being blamed for reinfections. I’ll prolly do a follow up post with a cross-post of my comments on your other post...
I'll have to check on that post again. Boy, all of these cross-posts are occurring more frequently than these cross-reactive antibodies!
The best Antibody strategy is to have multiple mono-colonels targeting multiple sites. Then get testing that can identify specific variants. So you get sick, get tested, find the variant - then pick a combination of monoclonals that could work. You know - like physicians have done for 100's of years....
Multiple monoclonals targeting multiple sites? Like, having many antibodies target the spike? If only that were a thing! I can't put my finger on who or what can conduct such a feat!
Okay, jokes aside I do wonder why most monoclonals have included only up to two antibodies. I suppose there are concerns over autoimmune disorders, or maybe something with respect to EUA approval and some loophole needed.
There is a general issue of the R&D required to examine which monoclonals are needed. Considering that this virus is mutating pretty rapidly that would mean going back to conduct research every few months, or just have a cocktail of 5 and hope for the best.
Sequencing also takes a lot of time and money. Think up to a few thousand dollars to sequence one sample. Sequencing would also take several days and at that time it may be too difficult to deploy monoclonals, especially if timing is important.
Excuse me Rob, you have committed a sin! Which sin? Not sure, but A sin! I'll look at the post and see what I can find.
However, I don't want to impugn anyone because I believe these people are far more intelligent than myself, but I will be frank and say that many of my recent posts have been somewhat in response to a few of the articles I'm seeing floating around.
I believe Jessica is extremely intelligent, yet there have been a few times where I have questioned her analyses. I wrote my LNP articles because of her remarks that somehow the LNP in Moderna's formulation is carcinogenic based on the SDS. My remarks were that the SDS was horrible updated after they changed their formulation from chloroform to alcohol. I even used the Wayback Machine as suggested by a commenter and that appears to be the case.
There is also the hydrogel study published in the ACS which was being used to tie into amyloidosis, yet the peptide used in the study was found in seasonal human coronaviruses. I don't see anyone remarking about seasonal colds and amyloidosis, but apparently we need to be concerned about SARS-COV2, the vaccines and amyloidosis. The concerns don't parallel the studies being cited.
There's also that Moderna patent paper floating around suggesting that the insertion within the furin cleavage site may be due to some serial passage Moderna was studying, or it was associated to an MSH3 mutation that may lead to cancer. In reality, the authors of that paper would never conceivably have been able to come across the Moderna patent based on how they outlined their data. There was absolutely no tie to the MSH3 protein but because of this improper methodology, yet everyone latched onto that paper to relate spike protein to cancer.
There's also that immune imprinting paper from science to which has many, many flaws! It didn't even include any naturally immunized participants, and so the reference was to triple-vaccinated, uninfected individuals. In no ways can we extrapolate that immune imprinting is not occurring in those who are naturally infected, if we intend on arguing that OAS/immune imprinting are a thing.
So this is a bit long-winded, but I am a bit concerned that so many people are being riled up when there hasn't been a proper reading of the science. I don't know what's going on, and to be honest a lot of this becomes very tiring, mostly because I'm not making much on this Substack and spending hours upon hours trying to piece together information when I can just yell about the sky falling or we're all going to die may get more attention makes me rather disheartened.
So I tried reading the post. I'll be candid and say that I am terrible at statistics and so this may be something I need to look at a few times.
Like you stated, it appears the issue is related to the grey zone of relating vaccinated to injected. Jessica has taken some liberties, which means we should probably analyze the data with those caveats. Her perspective is that those who have gotten the two shots should be considered "injected" while hospitals would consider them to be "unvaccinated", and correcting that data would mean that more injected individuals are being hospitalized than uninjected.
I'll state that I don't think I have the knowledge right now to fully dissect the data, but from this alone I think we should be concerned about data manipulation. It's very easy to make statistics say what you want it to, and generally biases should be left outside of the analysis. This could be an issue of confounding variables just adding onto one another.
I am concerned that people may just take this information at face value and just extrapolate what they want to see.
No, I believe the data was only based on up to the 2nd dose, so anyone past 2nd dose and 14 days would likely be considered vaccinated irrespective of booster situation.
So generally there's an argument as to how to categorize those within that 14 day window after the 2nd dose. Generally those people would be considered vaccinated. Jessica believes it would be more appropriate to categorize them under "injected" and to instead measure hospitalization rates based on injection status. So I believe from this argument it's believed that if you shuffle these select people over from "unvaccinated" to "injected" then the data will indicate that hospitalization is occurring more within the injected group than the uninjected.
Edit: I believe Jessica is counting "partially vaccinated" as uninjected in her analysis as well? I would have to look over the data again and see.
This is making a lot of assumptions, and all of this is based on whether the categories used are accurate in the first place. Also, it boils down to what we can use with that data. It requires us to ask "why" this may be occurring, not that it just appears to be the case.
I think this is a general problem where people are looking at charts and just extrapolating that we can tell what's going on with these people when we really can't. It's why I generally avoid charts such as those because it lacks any context and nuance.
Apologies if I did not make it clear. I suppose, based on Jessica's assumptions, I have problems because it does require far too many suppositions. I don't know if her starting numbers are correct, and to then extrapolate to get a model that fits the original intent (i.e. injected individuals are ending up in the hospital at greater rates than uninjected ones) has a bit of a leap for me.
I think that's what your original concern was, such that it seems like several liberties were taken to come to those conclusions, but how those liberties came about and whether they were accurate/valid liberties is where the concerns lie?
Honestly, it's a pretty damn shame that Substack is becoming a place no different than Twitter or other social medial platforms. How can we consider ourselves to be greater thinkers when we shut out open discourse? Why is it that I can be someone who was heavily against vaccinations, lost my job over it, and am trying to piece together information yet have to consider censoring myself lest I run afoul for those who I should play nice with? It may be a bold comment to make, but we should all hope to encourage good-faith criticisms in order for us to grow as both individuals and as publishers. There's no good in having people follow along within an echo chamber to the degree that appears to be happening.
I absolutely feel you Rob. It's a strange state of affairs where I'm seeing so many concerning things and I just want people to follow the science (note, not "the" science which vaccine proponents have been pushing) rather than bastardize the science to come to the conclusions that they want.
I wish more commenters would speak out and provide a little pushback. I suppose one of the reasons is that many readers may not quite understand what they are reading. However, if I throw in some pathos, such as suggesting why "I" am scared, why you should be scared, or why we are all doomed then that immediately overrides those faculties needed for logic and reason so that people only know to respond through emotion.
I could not agree with you more! And I give you credit for actively trying to sort out the confusion; Unlike you, I just take the passive approach and rely on the comments section to help.
That being said, thanks — I just piggy backed on your search for clarity. 😊
Honestly, you should never be scared to comment that you don't understand. We won't ever know if someone doesn't understand something unless they tell us. I think there is a duty for readers to provide feedback.
There should be a general discussion that provides dialogue both ways, not just an avenue to lecture into the echo chamber.
Yeah, so the main problem is that the spikes are occurring during the Omicron waves, and that I believe is intended to be the main thing that is supposed to be taken away. But like you said, it's a strange argument to make that 14 day windows from all across the year would account for what's seen during the Omicron waves.
Generally speaking, there's far too many variables happening, including the most critical one which is that no one was protected from Omicron (what I was arguing above), so really it's generally a moot point to look at this data and try to make an argument.
So these always raise questions as to whether the data may be manipulated in such a way to get the results that were wanted.