Thanks for the article. I hadn't noticed the paper and will have to give it a read.
Disequilibrium between pro-inflammatory and anti-inflammatory cytokine cascades is one of the mechanisms, along with telomere length, by which you might get the outcome of increased tissue healing at the expense of increased tendency towards cancer. I'm glad you pointed to Bret here. I immediately thought of his dissertation work when I read your title. I'm sure you know, but I'll point out that the same forces which caused this outcome in lab mice would be present in any laboratory animal, including these primates.
It would be interesting to know to what extent primates are compromised in this way. Since their lifespans are longer these evolutionary pressures have had fewer generations to affect them. Having said that, one could argue that the pressure would be stronger in primates. As primates are more expensive to maintain and have fewer children, there is a greater need to get as many offspring as possible from them while they're young. This is of course the same pattern that lead to the observed healing and cancer outcome in mice. My guess is that they wouldn't be as affected as mice, but that the economics of lab animals would be pushing them in a similar direction.
From my experience, the degree to which different control genotypes vary is shocking. I worked with drosophila as an undergraduate and several times had to run comparison experiments with flies from the same genotype from separate labs across the US. There were *always* significant differences between groups. This in a genetic lab that was very serious and thorough about the genetic background. Mouse labs are terrible with genetic controls in comparison. Unfortunately, this is only one of the major flaws undermining the foundation of scientific research.
You're ranked in my book "Heroes and Villains: The COVID-19 Book of Lists" available at heroesandvillainsbooks.com Get the e book. If you want to do a post on it, let me know.
I would forward this to my genetic engineer son, but he has already made it clear that anything I send him is worthless and probably written by a "used car salesman type".
This article goes in line with your previous work looking at in vitro cell lines. All this tells us that there's so much nuance to the cells and animals we use more than the clear-cut results of whether things are dying off if no critical molecular/biochemical assessment is done.
It becomes more clear that many of these animal studies miss out on creating robust profiles for the mice. So researchers use mice because they provide quick turnaround time without looking at all the little details.
As to the LNPs, it's been a while but I believe Pfizer and Moderna's ionizable lipid only differs by the length of one of their sidechains which I believe differs by 2-4 carbons, so I wouldn't think that would create such a large difference in inflammatory response. It'd be nice if researchers actually compared different LNPs and done a comparative analysis.
It seems that this difference between certain mouse sub/species being more adept at cellular reparation than humans, or even their wild mouse cousin is important in an other aspect. This would seem to make it possible to game a study to produce a more favorable outcome by selecting the "right" mouse strain. Am I crazy, or is that possible?
Joomi, please stop being so clear and intelligent. You are making the big pharma companies, the CDC and the FDA look stupid or malevolent or both.
Thanks for the article. I hadn't noticed the paper and will have to give it a read.
Disequilibrium between pro-inflammatory and anti-inflammatory cytokine cascades is one of the mechanisms, along with telomere length, by which you might get the outcome of increased tissue healing at the expense of increased tendency towards cancer. I'm glad you pointed to Bret here. I immediately thought of his dissertation work when I read your title. I'm sure you know, but I'll point out that the same forces which caused this outcome in lab mice would be present in any laboratory animal, including these primates.
It would be interesting to know to what extent primates are compromised in this way. Since their lifespans are longer these evolutionary pressures have had fewer generations to affect them. Having said that, one could argue that the pressure would be stronger in primates. As primates are more expensive to maintain and have fewer children, there is a greater need to get as many offspring as possible from them while they're young. This is of course the same pattern that lead to the observed healing and cancer outcome in mice. My guess is that they wouldn't be as affected as mice, but that the economics of lab animals would be pushing them in a similar direction.
From my experience, the degree to which different control genotypes vary is shocking. I worked with drosophila as an undergraduate and several times had to run comparison experiments with flies from the same genotype from separate labs across the US. There were *always* significant differences between groups. This in a genetic lab that was very serious and thorough about the genetic background. Mouse labs are terrible with genetic controls in comparison. Unfortunately, this is only one of the major flaws undermining the foundation of scientific research.
Incredibly valuable and timely research. Thank you for bringing this important data into the critical conversation about vaccine harms!
Thank you for bringing this to our attention, it is important especially if mice are going to pass for human tests.
Joomi:
You're ranked in my book "Heroes and Villains: The COVID-19 Book of Lists" available at heroesandvillainsbooks.com Get the e book. If you want to do a post on it, let me know.
I would forward this to my genetic engineer son, but he has already made it clear that anything I send him is worthless and probably written by a "used car salesman type".
This article goes in line with your previous work looking at in vitro cell lines. All this tells us that there's so much nuance to the cells and animals we use more than the clear-cut results of whether things are dying off if no critical molecular/biochemical assessment is done.
It becomes more clear that many of these animal studies miss out on creating robust profiles for the mice. So researchers use mice because they provide quick turnaround time without looking at all the little details.
As to the LNPs, it's been a while but I believe Pfizer and Moderna's ionizable lipid only differs by the length of one of their sidechains which I believe differs by 2-4 carbons, so I wouldn't think that would create such a large difference in inflammatory response. It'd be nice if researchers actually compared different LNPs and done a comparative analysis.
It seems that this difference between certain mouse sub/species being more adept at cellular reparation than humans, or even their wild mouse cousin is important in an other aspect. This would seem to make it possible to game a study to produce a more favorable outcome by selecting the "right" mouse strain. Am I crazy, or is that possible?