Overwhelming success writing in plainer language and refreshing change from struggling with sentences so full of confusing terms and acronyms. It's also my first encounter with the naming and function of ACE2 beyond knowing it as a binding domain imagining weaponized viral bits sticking like the partner sides of Velcro. I can't offer any thoughts on the theory but the biology lesson was wonderful and makes me happy that you smart folks are riddling these questions! <3
I find it refreshing that hypotheses come along that don't insert themselves as the dominant explanation, but rather add to the ever expanding story of the mechanism of covid-19. There's more than one way to skin a cat. Also, thank you for explaining it in terms a layman can understand. I must admit, reading about it felt more comprehensible than hearing about it on the podcast, as a person who doesn't science.
Interesting- I didn't know much about this pathway before. Something I was wondering though was do we know whether vax encoded spike (which is supposed to be locked in a prefusion conformation) can bind to ACE2?
From what I can tell, the evidence isn't what I would call conclusive. FWIW, there are in silico experiments that suggest pre-fusion locked states favor ACE2 binding over non-modified states. I take it with a grain of salt. My understanding from reading a paper using SCV1 is that pre-fusion locked conformation can dock to ACE2 but resists subsequent modification. An experiment that would give us a lot of info on this would be to check serum Ang II levels after vaccination at different time points compared to control. Could even have LNP/AVV only control and maybe n-protein group to compare. If one didn't see an increase in Ang II in Spike group that implies that tax Spike can't bind to ACE2 and is evidence that this mechanism isn't a major source of post-vaccination damage. Complicating factors: it would be hard to test for localized jumps in Ang II which might not show up well in serum and your group size would have to be pretty big to make sure to catch the events if it only happens in certain people.
This is really, really good; it was a pleasure to read! I looked at some of your references also. I was very interested in the comorbidity paper; I think some of their findings are the result of analyzing such a massive database. I'm kinda surprised no cancer comorbidity category was analyzed, but maybe it didn't occur in 10% of the study subjects. The aplastic anemia is a little surprising to me too; it is not common. I wonder if it could have been caused by the infection. I don't really buy that thyroid disorders increase adverse Covid outcomes and am pretty skeptical about the "anxiety and fear-related disorders" too. Coding bias is a real thing in these databases of hospital data; coders will make sure as many conditions as are present are coded, which is why some things looked "protective", like hypertension and controlled diabetes. I am looking forward to more writing by you!!!
oddly enough, was just looking at AGE-RAGE today and trying to see if there were any herbal allies. Don't know if this formula is sourceable, but may look more into the plants that were most promising. Baical Skullcap comes up a lot in COVID herbal discussions, so that's a good one to study.
Only understanding maybe 70% of this type of material this seems to fit what I've read. To me it fits in will with the pathophsyiology paper Dr. Paul Marik wrote perhaps offering a specific mechanism of how some cases become uncontrollable. He indicated that in the more severe cases the worst of the symptoms happen after the virus cleared....(but what about remaining spike). https://covid19criticalcare.com/wp-content/uploads/2021/09/Covid-Pathophysiology.pdf
And wouldn't this hypothesis also dovetail with some of the theoretical mechanisms of action of HCQ and Ivermectin? Probably best to leave those taboo terms out of the article because some people wouldn't be able to look past it. But the dots are there to be connected.
Overwhelming success writing in plainer language and refreshing change from struggling with sentences so full of confusing terms and acronyms. It's also my first encounter with the naming and function of ACE2 beyond knowing it as a binding domain imagining weaponized viral bits sticking like the partner sides of Velcro. I can't offer any thoughts on the theory but the biology lesson was wonderful and makes me happy that you smart folks are riddling these questions! <3
I find it refreshing that hypotheses come along that don't insert themselves as the dominant explanation, but rather add to the ever expanding story of the mechanism of covid-19. There's more than one way to skin a cat. Also, thank you for explaining it in terms a layman can understand. I must admit, reading about it felt more comprehensible than hearing about it on the podcast, as a person who doesn't science.
Interesting- I didn't know much about this pathway before. Something I was wondering though was do we know whether vax encoded spike (which is supposed to be locked in a prefusion conformation) can bind to ACE2?
From what I can tell, the evidence isn't what I would call conclusive. FWIW, there are in silico experiments that suggest pre-fusion locked states favor ACE2 binding over non-modified states. I take it with a grain of salt. My understanding from reading a paper using SCV1 is that pre-fusion locked conformation can dock to ACE2 but resists subsequent modification. An experiment that would give us a lot of info on this would be to check serum Ang II levels after vaccination at different time points compared to control. Could even have LNP/AVV only control and maybe n-protein group to compare. If one didn't see an increase in Ang II in Spike group that implies that tax Spike can't bind to ACE2 and is evidence that this mechanism isn't a major source of post-vaccination damage. Complicating factors: it would be hard to test for localized jumps in Ang II which might not show up well in serum and your group size would have to be pretty big to make sure to catch the events if it only happens in certain people.
This is really, really good; it was a pleasure to read! I looked at some of your references also. I was very interested in the comorbidity paper; I think some of their findings are the result of analyzing such a massive database. I'm kinda surprised no cancer comorbidity category was analyzed, but maybe it didn't occur in 10% of the study subjects. The aplastic anemia is a little surprising to me too; it is not common. I wonder if it could have been caused by the infection. I don't really buy that thyroid disorders increase adverse Covid outcomes and am pretty skeptical about the "anxiety and fear-related disorders" too. Coding bias is a real thing in these databases of hospital data; coders will make sure as many conditions as are present are coded, which is why some things looked "protective", like hypertension and controlled diabetes. I am looking forward to more writing by you!!!
We'll have to discuss the implications of this at some point. Thanks for the review.
oddly enough, was just looking at AGE-RAGE today and trying to see if there were any herbal allies. Don't know if this formula is sourceable, but may look more into the plants that were most promising. Baical Skullcap comes up a lot in COVID herbal discussions, so that's a good one to study.
https://www.sciencedirect.com/science/article/abs/pii/S1043661821002346
Reading this versus watching the RTE video probably got me from about 60% to 70% understanding it. Thanks. The video link in case others missed it. https://rumble.com/v1meqze-rte-discussion-9-the-age-rage-pathway-and-covid-19-with-cody-porter.html
Only understanding maybe 70% of this type of material this seems to fit what I've read. To me it fits in will with the pathophsyiology paper Dr. Paul Marik wrote perhaps offering a specific mechanism of how some cases become uncontrollable. He indicated that in the more severe cases the worst of the symptoms happen after the virus cleared....(but what about remaining spike). https://covid19criticalcare.com/wp-content/uploads/2021/09/Covid-Pathophysiology.pdf
And wouldn't this hypothesis also dovetail with some of the theoretical mechanisms of action of HCQ and Ivermectin? Probably best to leave those taboo terms out of the article because some people wouldn't be able to look past it. But the dots are there to be connected.