4 ms·
> Lets be clear here: CBD is not a CB1 or CB2 agonist (or antagonist, or anything else). CBD does act on CB1 and CB2: https://www.ncbi.nlm.nih.gov/pmc/articles
by PragmaticPulp 4y ago
> Lets be clear here: CBD is not a CB1 or CB2 agonist (or antagonist, or anything else).
CBD does act on CB1 and CB2: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2219532/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2219532/
It also binds to a number of other receptors throughout the brain, but I don't think it's accurate to reduce its effects to a singular 5-HT1A receptor. It especially doesn't match the clinical effects, as Buspirone requires weeks to show effects while high doses of CBD are active within hours.
But you're very right that the CBD dose in this study is far lower than other studies. Typical study doses are 300mg of CBD or more.
> Dosing and pricing it like THC is simply placebo. It is not THC.
The study was of a mixed CBD/THC mixture. The patients were actually receiving a total of 0.7mg of THC per day. Not enough for overt effects, but enough to do something (and also fail any drug tests they might take).
The real flaw in this study is the lack of placebo group. You can't run a real psychiatric medication study without a control group and expect useful results.
- superkuh 4y agoI appreciate the input, but did you look at the Ki binding figures for CBD in the paper you linked? ~4000 nanomolar antagonist is not nanomolar unless you're really stretching it. It is so high that there are innumberable unrelated compounds with the same very low affinity. It is true it does act as an atagonist, but it is a vacuous truth applicable to so many things that you wouldn't call CB1 or CB2 antagonist.