My "agenda" doesn't influence the validity of my assertions. Regardless I state my motive in the first paragraph of my post.
"I agree about the risk of inconsistent physical reactions to NBOMe chemicals. I also believe there are many wonderful chemicals that elicit a more consistent physical response. Both things should be highlighted in some simple, attention grabbing, and lucid way."
I also restate my motive later in my post.
"My recommendation is we suggest people unfamiliar with how their body responds to 5ht2a agonist consider lsd or psilocybin instead."
And still, what you achieved in this thread already, was making more "naive" people wonder, "gosh, maybe 25B isn't that unsafe after all, scientists are using it for human experiments. And that smart scienceguy posted links that prove it".
That's why I ask to know your agenda.
Your assertions don't have any validity, they are just
that, assertions (because you are not Hansen or Nichols in disguise, are you?) But still you want to make them sound like more than what they are. In my opinion you should choose your words and assertions more wisely in the future, if your aim posting here really is harm reduction.
That the scientists mapping the serotonin receptor in the human body considers 25B-NBOMe safe to inject in pigs, which they then kill right after, basically means fuck all. So why bring it up here in the way you do? it has the absolute opposite effect of what this thread is meant for.
Humans aren't pigs in a lab, and when they gave 1,5 ug 25B-NBOMe to a human, it had nothing, what so ever to do with the psychedelic activity that that drug has. It's not psychedelic research.
You have to keep things seperate. That's the whole problem with the whole NBOMe debate. People think that we know a lot about them because we know the Ki affinities, due to them being made and used for real legit research. Well we don't know all about them.
And to my knowledge, no real research has been made what so ever, as to these drugs safety as legal highs. If they had, we wouldn't need this thread.
And likening NBOMe's and DOx's therapeutic indices is also just wrong for so many reasons. Even though many DOx's are almost as potent as the NBOme's, longer lasting, just as stimulating
and orally active, they still have caused surprisingly few deaths.
Maybe some one can answer me these questions:
1.What is the pharmacological cause behind the NBOMe deaths?
2.What is the complete pharmacological mechanism of the various NBOMe's?
3.What is the mechanism behind psychedelic activity? (and no, it's not
just 5HT2a agonism)
4. And, are all 5HT2a agonists psychedelics?
No? Okay, I thought not. Thanks.
Peace,
and light.
Rant over
)