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podgaj | 4 years ago
> while it can lead to more robust synthesis of endocannabinoids, really has nothing to do with the study at hand. Generally we use drugs because they have different or greater degrees of their mechanism than the endogenous compounds.
You can either excite these receptors or not. Exciting the receptor more than needed, which is what these overly high levels of exogenous cannabinols do, leads to degraded receptor sensitivity (dependance) and probably a rebound effect when the drug is stopped. It is not that I feel the drugs do not work, but they are not needed and are lacking the sensitivity.
> Not to mention we don't know if endocannabinoids such as anandamide or 2-AG even have the same effect as high doses of CBD shown in this study. Also the concentrations of the endogenous molecules are likely nowhere near high enough
The arachidonic acid (Omega 6) derivatives (anandamide) are known to not be as anti-inflammatory and is more in line with THC, not CDB, in its action. Which is my point of having to get the 3/6 ratio much higher, and has nothing to do with this study other than showing that we need LESS anandamide and more docosahexaenoyl and eicosapentaenoyl ethanolamides.
If someone has enough omega 3 endocannabinoids it is likely that they would not need the heavy hammer of CBD to get them out of the inflammation. I am not saying CBD does not work, but endocannabinoids are more than just one molecule, and CBD cannot compare.
For a overall robust immune system we should be studying Omega 3's/Omega 6 balance more deeply.
netizen-936824|4 years ago
We also don't know the mechanism of CBD preventing infection, this is only a preliminary study which shows that CBD has some effect through some mechanism. CBD's receptor profile has not been fully characterized afaik
You seem to be jumping to an awful lot of conclusions