The bulk of the evidence suggests that this cannabimimetic compound is too weak to have noticeable effects in Kava.
Show me any evidence that suggests it's absorbed well enough, present in high enough levels or has a high enough efficacy to get around the fact that it has a VERY weak affinity. To reiterate, this is 700 TIMES WEAKER THAN JWH-018- a full agonist.
Let's pretend it's a full agonist. Doesn't exactly fit the known pharmacophore, but oh well. Pravadoline, a full agonist with a similarly weak affinity requires 20-50mg/kg for cannabimimetic effect. How much Kava do you have to eat before you reach a yangonin dose that reaches those levels? A LOT!!!
ehh not more than you have on it being non-cannabimimetic
Alright, now this is just getting fucking retarded. You can't keep saying something and have it become true.
You're going to say that all of the evidence saying:
A. Yangonin is present at levels too low to reach an active concentration
B. Is not well enough absorbed into the brain to reach an active concentration
C. Has too weak of an affinity to be meaningful at the concentrations it is present in
D. It's the kavalactone least present, the others, present at much higher concentrations with far better defined affinities for other receptors, are far better explanations for the scientifically described effects. Is Kava positive for tetrad effects? Didn't think so.
Is equal to one study with weak effects? What?
I'm the only one presenting any reasoning here. You keep pointing to one study that finds exceptionally weak effects as if that is meaningful. Perhaps if it was the primary kavalactone or present at much higher levels, sure. That might make sense. If a common Kava dose would yield doses in the hundreds of milligrams of yangonin, sure. That'd make sense.
Present one logical argument that concludes with Kava producing cannabimimetic effects.
and actually you'll find many more people comparing its effects to marijuana, as well as noting a synergy, so I do doubt its an antagonist but maybe
That's not it. Remember the old adage, "the plural of anecdote is not evidence"? Oh yeah...
Again, you have ZERO EVIDENCE that it's a full agonist. You have a hope that is, because that would (almost) support the answer you want. I don't give a fuck what the answer turns out to be, but there's A LOT of reason to suggest that ITS NOT the answer you seem so SET ON.
Could be an antagonist, agonist or partial agonist. Based on what you've got, you might as well flip a coin. But again, based on the affinity found and common doses of the compound, that weak affinity is probably completely irrelevant.
I mean, are you smoking echinacea because it contains compounds with weak affinity for CB1? I'm guessing not.
To see this level of retadery in this forum is astounding. It really is.
consider the statements synonymous; sanctioned by, from (caught up in semantics, you are)
the ncbi is a governmental organization (i'm assuming you live in the United States I do, but what relevance do that have? It was published in Italy...)
Now you're sounding like a Republican, hoping to repeat a lie so many times that your opponent just drops it because it's become so retarded. The problem is that when they do, others start to believe it.
This is the claim you were making earlier, and which I addressed earlier. I was hoping I misunderstood you, but quite obviously I did not.
You're claiming that somehow this is a study that came from or was sanctioned by (these are not synonyms) the US Government, right?
And you're talking about the NCBI because you found the abstract on PubMed, correct?
I honestly can't address this claim without insulting you. I'm actually laughing out loud right now. It is literally impossible not to, because there's no way I can point out that PubMed just collects abstracts and makes them available as a public service, and does so with all chemistry/medical/biology related abstracts and not have you look like a fool.
It has absolutely nothing to do with the production or sanctioning of those studies. It passes absolutely no judgment on the quality of the article. It's just making those abstracts available as a public service. Didn't you wonder about those studies from the 20's that are in there, long before the government got in the business of "sanctioning" any research? LOL. Based on the shear volume of articles in the PubMed database the US government would have to completely control all published research in the world. There are >22 million citations! This claim might have some merit were this published in PLoS ONE. It wasn't.
Publishers submit citations themselves.
Are there actually people out there with such limited intellectual levels that they think articles they found on PubMed are articles that the government is paying for or somehow sanctioning? LOL This is hilarious. No wonder we're in so much debt!
Look at the citation it gives. It's from an Italian journal genius. The only government that may have contributed ANY money to or "sanctioned" (in whatever convoluted sense you're going to claim you were using that word in) this study was the Italian government, but as far as I can tell, that's not even the case.
) would be to have two small test groups, one Kava and one Kava+Rimonabant. Would be surprisingly easy to do given the easy online access to both drugs. You'd just need to find a dozen people. That's not the smallest population size I've seen in a study of that sort.