endlessness said:
do you know anything about harmalas efect on cytokine production?
No, but I'm looking into the literature. There must exist further work on the mechanism behind the reported antiviral properties of harmalas.
If anyone knows anything about the mechanism of peyote' reported cytokine
induction, I'd be delighted to hear. There's a fair possibility that isoquinolines might be responsible for this, seeing how isoquinolines are to phenethylamines as betacarbolines are to tryptamines. Just as a thought.
Edit: I see you've updated your post.
Tbh, I'm feeling a bit out of my depth now! The factors that this subject hinges on have become highly technical, and also I would point you back to my first post in this thread, where the diversity of the group loosely called cytokines was noted. Not all cytokines are inflammatory.
I'm just attempting to interpret and share information that appears important but am considering now just not saying anything at all instead. Maybe I should reduce the font size in the middle of that last post?
Really, we need to know which substance was used in the in vitro test Nichols was referring to, and what exactly was meant by "ramps up the virus". To answer your question about my reasoning, it applies to the initial stages of infection that
inflammatory cytokine supression would weaken the immune response to the virus. Once a patient reached the stage where cytokine storm it seems unlikely they'd be in a position to consider being administered a classical psychedelic.
When it comes to the latter stages of a severe case, ramping down the inflammatory cytokines could prove to be a lifesaver. This appears to be the rationale behind the use of tocilizumab that you mentioned. However, tocilizumab is a monoclonal antibody and as such treatment would be
fairly expensive. This would be quite advantageous to those who produce the stuff, to have it pushed as the lifesaver for severe CoVID19 cases. Thus, I can quite understand the appeal of a potential cheap, orally active alternative such as harmalas, especially given that "no randomized prospective trial has provided direct evidence of IL-6R blockade reducing incidence or severity of CRS."
(This is also making me wonder how the observed age-related decline in cytokine production correlates with the age-related increase in mortality rate. Such a lot of reading to do now!)