Yet another reason why blanket mandates that every single person get vaccinated were insane. If individual responses are genetically based and can vary so widely, there's no way to know how individuals will react. I hope that in the future we'll figure out some way to get care tailored to each person's genetic makeup.
It would be nice to get that personalized of a medical profile but that would be very difficult on a population-wide scale. This may just be an unfortunate consequence of there lacking any research into infection-related TT so researchers probably didn't even consider this as a possible adverse event, then it happens after millions of people get the injections and then they scramble to figure out why. The biggest issue is that it is taking so long for research to come out when it seems like initial hypotheses should direct towards looking at differences/similarities between the vaccines and adverse events to start testing for. I mean if this model is accurate why did it take 3 years when it could have just taken months to formulate and test?
As of now no- J&J had their EUA revokes last year and AstraZeneca was just removed from the market, but at this point it honestly doesn't matter because people who have wanted the vaccines have already gotten it (most people really don't seem to want anymore at this point) and so what matters more is helping people who may be suffering from VITT or other adverse events.
When pushing one-size-fits-all medicine for the sake of "efficiency" there's DISincentive to acknowledge that people are not all the same, and cannot be made so.
COVID policies absolutely bulldozed the field of pharmacogenomics.
Significant losses among the elites will eventually reverse this trend.
This excellent article is a window into why adenovirus based COVID jabs are being abandoned. The mechanisms by which the mRNA jabs are inducing clotting disorders are equally of vital significance.
Thanks for the link! It helps to solidify the idea that viral infections can induce TT, but again it's strange that this came within the second half of 2023- again two years after vaccination occurred? It's strange that such research took so long to come out.
1. If adenoviruses from vaccines bind to platelets, shouldn’t all adenoviruses exhibit the same behavior? Unless this is something specific to the engineered variant from AstraZeneca.
2 I thought blood clots happened in mRNA vaccines too. I don’t know if it is VITT with mRNA. Since all these vaccines dump spike protein into the blood stream, I was thinking that either spike or some complex from it was scratching the endothelial cells, which in turn started the cascade that led to thrombosis. Are you aware if this is a possible hypothesis,
Thanks for the questions! I'll try to answer as best as possible:
1. So the adenovirus isn't binding to platelets themselves- they are binding to PF4. This is released from platelets but isn't platelets themselves, and hence the paradoxical disease of thrombosis with thrombocytopenia (thrombocytopenia is low platelet count). It's also why initial findings drew parallels to heparin-induced thrombocytopenia as heparin is a blood thinner that reduces platelet count and yet still results in clots in some individuals- in the form of anti-PF4 antibodies.
With respect to if all adenoviruses exhibiting this behavior the general idea would be a hypothetical "yes" as it appears that it's the structure of the adenovirus itself that affords the binding to PF4. We should expect that structures that deviate from the pockets of negative charges would likely not show the same degree of binding, and I believe the in-silica model from the study shows that binding isn't consistent across the vaccines and the virus itself.
We also have to remember that not much research was conducted prior to COVID to look into this phenomenon- remember that absence of evidence is not evidence of absence, and so researchers may have gone in blind or started with an assumption that the viral structure is not to be considered (which would be a ridiculous assumption).
This also comes with questions of variability. Many people have viral infections which just appear as flu-like illness so many people may be exposed to adenoviruses but unaware. Given that this disease (VITT) is autoimmune in nature it operates similar to any adaptive immune-related event whereby initial sensitization comes before the autoimmune response- acknowledgement before action. So this raises a question if some people may have been sensitized towards anti-PF4 antibodies from prior infections. But that also raises the question if those who take heparin may also be sensitized- why didn't researchers look into seeing if some of these people who experienced VITT also had prior heparin exposure? I think that's one thing I brought up before since that would also provide a direction to look into.
This also has to be paired with the fact that most of the adenoviral vaccines were on a strange 2-dose regimen- at least I believe AstraZeneca's was. This means that you're already setting people up for a sensitizing event followed by the autoimmune response, and therefore may explain why VITT appears to occur mostly after the second dose.
Now, why this may be more sporadic in infected individuals (and therefore why it wasn't researched) may be due to the fact that it may require the adenovirus to make its way into the bloodstream, and it may be here where the autoimmune action is more likely given that this is where PF4 will likely reside. In that case it's possible that mistakes in vaccination which led to intravenous rather than intramuscular injections could also make people more prone to formation of adenovirus/PF4 complexes and causing the autoimmune response.
2. We have to remember that clotting is a general term that may manifest from different mechanisms. Again, the pathology for VITT is that it is not related to platelets and therefore doesn't manifest in a similar way as typical blood clots. I haven't kept up with the discussion of blood clots related to the mRNA vaccines, and personally I'm not really swayed by the white clots as of now. Findings in coroner reports may not translate to actual events in people. But from what I can recall it does appear that some of the issues may relate to endothelial damage possibly from spike protein causing ACEII-related events. I believe there was some suggestion that any structural findings may be cellular debris caused from endothelial damage, and therefore may cause clot formation of aggregated.
The main question is asking how much spike is enough spike, and how would spike appear in the blood. I think there's a lot of gaps in knowledge on this front. Some evidence suggests that people still have spike circulating months afterwards although I can't recall how much spike is quantified in those cases. In children it does appear that processing of spike is different than adults and therefore it's possible that children can't deal with spike-in-the-blood as sufficiently as adults and may be the reason for some of the myocarditis and other cardiovascular-related events that appear more in children relative to adults.
So for now it's possible that spike-in-the-blood is a problem, it's likely causing damage systemically, but the degree of the damage is the question, and how long this persists and whether the body can manage the damage is worth considering.
Sorry for not providing as thorough as a response to the 2nd question. I personally find that when an area gets covered extensively it's hard to come at it unbiased. The clots have been covered a lot and some of the information seems interesting but then it seems like some reports just help to muddy the waters more for talking points such as "clot shots" or "died suddenly".
From what you wrote, children would form an interesting group vs adults when it comes to spike action in blood. This is because children don’t have ace2 receptors everywhere as do adults — that’s my understanding . I don’t know but I’d surmise that they’ve ace2 in heart cells. If so, this would imply the spike goes around the body and finds a receptor to bind in the heart. Is this why young adults and children show up with myocarditis?
If the ace2 binding hypothesis is correct adults should have a concentration of them in stomach vs children. May be autopsies will tell.
So there has been some research where it appeared that children didn't appear to process spike from the vaccines in the same way adults did whereby children had more intact spike proteins as well as antibodies that didn't appear to bind to spike as well.
One of the challenges is that the presentation of adverse events are so multifaceted that we may not be able to pin down one causative explanation. I find that I keep coming back to the endothelial-based hypothesis but in some sense I believe that it's not the spike directly targeting tissues and organ but that it could be that disruption of typical endothelial function may affect nearby environments and cause inflammation and other pathologies that are harmful.
The ace2 hypothesis or at least the endothelial hypothesis would generally be backed by some sort of uptick in hypertension or similar diseases. I tried looking into it a while back when Dr. Campbell mentioned that he needed to be on hypertension medications following his vaccines but there didn't appear to be much research out there. It may be something worth revisiting if I can fit it into my schedule:
Yet another reason why blanket mandates that every single person get vaccinated were insane. If individual responses are genetically based and can vary so widely, there's no way to know how individuals will react. I hope that in the future we'll figure out some way to get care tailored to each person's genetic makeup.
It would be nice to get that personalized of a medical profile but that would be very difficult on a population-wide scale. This may just be an unfortunate consequence of there lacking any research into infection-related TT so researchers probably didn't even consider this as a possible adverse event, then it happens after millions of people get the injections and then they scramble to figure out why. The biggest issue is that it is taking so long for research to come out when it seems like initial hypotheses should direct towards looking at differences/similarities between the vaccines and adverse events to start testing for. I mean if this model is accurate why did it take 3 years when it could have just taken months to formulate and test?
Self centered researchers, can only look in their very tiny microscopes... no awareness of anything outside of that... or its consequences.
Are there any adeno vaxes still being given?
As of now no- J&J had their EUA revokes last year and AstraZeneca was just removed from the market, but at this point it honestly doesn't matter because people who have wanted the vaccines have already gotten it (most people really don't seem to want anymore at this point) and so what matters more is helping people who may be suffering from VITT or other adverse events.
When pushing one-size-fits-all medicine for the sake of "efficiency" there's DISincentive to acknowledge that people are not all the same, and cannot be made so.
COVID policies absolutely bulldozed the field of pharmacogenomics.
Significant losses among the elites will eventually reverse this trend.
This excellent article is a window into why adenovirus based COVID jabs are being abandoned. The mechanisms by which the mRNA jabs are inducing clotting disorders are equally of vital significance.
Interesting. I also came across this article:
Adenovirus-Associated Thrombocytopenia, Thrombosis, and VITT-like Antibodies:
https://www.nejm.org/doi/full/10.1056/NEJMc2307721
Thanks for the link! It helps to solidify the idea that viral infections can induce TT, but again it's strange that this came within the second half of 2023- again two years after vaccination occurred? It's strange that such research took so long to come out.
and surprising it was allowed to come out.
Thank you. This was very informative.
Two questions.
1. If adenoviruses from vaccines bind to platelets, shouldn’t all adenoviruses exhibit the same behavior? Unless this is something specific to the engineered variant from AstraZeneca.
2 I thought blood clots happened in mRNA vaccines too. I don’t know if it is VITT with mRNA. Since all these vaccines dump spike protein into the blood stream, I was thinking that either spike or some complex from it was scratching the endothelial cells, which in turn started the cascade that led to thrombosis. Are you aware if this is a possible hypothesis,
Thank you.
Thanks for the questions! I'll try to answer as best as possible:
1. So the adenovirus isn't binding to platelets themselves- they are binding to PF4. This is released from platelets but isn't platelets themselves, and hence the paradoxical disease of thrombosis with thrombocytopenia (thrombocytopenia is low platelet count). It's also why initial findings drew parallels to heparin-induced thrombocytopenia as heparin is a blood thinner that reduces platelet count and yet still results in clots in some individuals- in the form of anti-PF4 antibodies.
With respect to if all adenoviruses exhibiting this behavior the general idea would be a hypothetical "yes" as it appears that it's the structure of the adenovirus itself that affords the binding to PF4. We should expect that structures that deviate from the pockets of negative charges would likely not show the same degree of binding, and I believe the in-silica model from the study shows that binding isn't consistent across the vaccines and the virus itself.
We also have to remember that not much research was conducted prior to COVID to look into this phenomenon- remember that absence of evidence is not evidence of absence, and so researchers may have gone in blind or started with an assumption that the viral structure is not to be considered (which would be a ridiculous assumption).
This also comes with questions of variability. Many people have viral infections which just appear as flu-like illness so many people may be exposed to adenoviruses but unaware. Given that this disease (VITT) is autoimmune in nature it operates similar to any adaptive immune-related event whereby initial sensitization comes before the autoimmune response- acknowledgement before action. So this raises a question if some people may have been sensitized towards anti-PF4 antibodies from prior infections. But that also raises the question if those who take heparin may also be sensitized- why didn't researchers look into seeing if some of these people who experienced VITT also had prior heparin exposure? I think that's one thing I brought up before since that would also provide a direction to look into.
This also has to be paired with the fact that most of the adenoviral vaccines were on a strange 2-dose regimen- at least I believe AstraZeneca's was. This means that you're already setting people up for a sensitizing event followed by the autoimmune response, and therefore may explain why VITT appears to occur mostly after the second dose.
Now, why this may be more sporadic in infected individuals (and therefore why it wasn't researched) may be due to the fact that it may require the adenovirus to make its way into the bloodstream, and it may be here where the autoimmune action is more likely given that this is where PF4 will likely reside. In that case it's possible that mistakes in vaccination which led to intravenous rather than intramuscular injections could also make people more prone to formation of adenovirus/PF4 complexes and causing the autoimmune response.
2. We have to remember that clotting is a general term that may manifest from different mechanisms. Again, the pathology for VITT is that it is not related to platelets and therefore doesn't manifest in a similar way as typical blood clots. I haven't kept up with the discussion of blood clots related to the mRNA vaccines, and personally I'm not really swayed by the white clots as of now. Findings in coroner reports may not translate to actual events in people. But from what I can recall it does appear that some of the issues may relate to endothelial damage possibly from spike protein causing ACEII-related events. I believe there was some suggestion that any structural findings may be cellular debris caused from endothelial damage, and therefore may cause clot formation of aggregated.
The main question is asking how much spike is enough spike, and how would spike appear in the blood. I think there's a lot of gaps in knowledge on this front. Some evidence suggests that people still have spike circulating months afterwards although I can't recall how much spike is quantified in those cases. In children it does appear that processing of spike is different than adults and therefore it's possible that children can't deal with spike-in-the-blood as sufficiently as adults and may be the reason for some of the myocarditis and other cardiovascular-related events that appear more in children relative to adults.
So for now it's possible that spike-in-the-blood is a problem, it's likely causing damage systemically, but the degree of the damage is the question, and how long this persists and whether the body can manage the damage is worth considering.
Sorry for not providing as thorough as a response to the 2nd question. I personally find that when an area gets covered extensively it's hard to come at it unbiased. The clots have been covered a lot and some of the information seems interesting but then it seems like some reports just help to muddy the waters more for talking points such as "clot shots" or "died suddenly".
Thanks for the detailed response.
From what you wrote, children would form an interesting group vs adults when it comes to spike action in blood. This is because children don’t have ace2 receptors everywhere as do adults — that’s my understanding . I don’t know but I’d surmise that they’ve ace2 in heart cells. If so, this would imply the spike goes around the body and finds a receptor to bind in the heart. Is this why young adults and children show up with myocarditis?
If the ace2 binding hypothesis is correct adults should have a concentration of them in stomach vs children. May be autopsies will tell.
So there has been some research where it appeared that children didn't appear to process spike from the vaccines in the same way adults did whereby children had more intact spike proteins as well as antibodies that didn't appear to bind to spike as well.
https://moderndiscontent.substack.com/p/circulating-spike-in-post-vaccinated
One of the challenges is that the presentation of adverse events are so multifaceted that we may not be able to pin down one causative explanation. I find that I keep coming back to the endothelial-based hypothesis but in some sense I believe that it's not the spike directly targeting tissues and organ but that it could be that disruption of typical endothelial function may affect nearby environments and cause inflammation and other pathologies that are harmful.
The ace2 hypothesis or at least the endothelial hypothesis would generally be backed by some sort of uptick in hypertension or similar diseases. I tried looking into it a while back when Dr. Campbell mentioned that he needed to be on hypertension medications following his vaccines but there didn't appear to be much research out there. It may be something worth revisiting if I can fit it into my schedule:
https://moderndiscontent.substack.com/p/overlooked-adverse-reactions-hypertension
https://moderndiscontent.substack.com/p/overlooked-adverse-reactions-hypertension-f20