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by netizen-936824 1615 days ago
As I stated before, the receptor binding profile of CBD has not been fully characterized. That means that its binding to other proteins and we don't know what they are yet

While its possible that its a downstream effect of CBR 1/2 we can't jump to that conclusion, the pharmacology of CBD is absurdly complex and biochemical inflammation pathways may be tangential to IRE1α which is part of the ER stress response

>Mounting evidence suggests that there are novel cannabinoid receptors[10] that is, non-CB1 and non-CB2, which are expressed in endothelial cells and in the CNS. In 2007, the binding of several cannabinoids to the G protein-coupled receptor GPR55 in the brain was described.[11]

>The existence of additional cannabinoid receptors has long been suspected, due to the actions of compounds such as abnormal cannabidiol that produce cannabinoid-like effects on blood pressure and inflammation, yet do not activate either CB1 or CB2.[25][26]

https://en.m.wikipedia.org/wiki/Cannabinoid_receptor

>Cannabidiol may be an antagonist of GPR55, a G protein-coupled receptor and putative cannabinoid receptor that is expressed in the caudate nucleus and putamen in the brain.[70][71] It also may act as an inverse agonist of GPR3, GPR6, and GPR12.[72] CBD has been shown to act as a serotonin 5-HT1A receptor partial agonist.[73] At higher concentrations, CBD acts as an inverse agonist of 5-HT1A receptors.[74] It is an allosteric modulator of the μ- and δ-opioid receptors as well.[75] The pharmacological effects of CBD may involve PPARγ agonism, inhibition of voltage-gated cation channels, and intracellular calcium release.[14]

https://en.m.wikipedia.org/wiki/Cannabidiol

On a discussion of ~65 possible protein targets for CBD:

>Some CBD effects at these targets in in vitro assays only manifest at high concentrations, which may be difficult to achieve in vivo, particularly given CBD’s relatively poor bioavailability.

https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC4604182/?r...

Here's an alternative receptor for your inflammation theory: A2

https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC2588644/?r...

1 comments

But in the same breath you can dismiss what the human body can do given a sufficient balance of omega-3 to omega 6?

Did you even try to see if omega 3 endocanibinols effected the g coupled protein receptors as well?

Absolutely, until there is evidence for it that's my stance. Different compounds interact with different proteins due to differences in electronic structure, sterics, and varying topology. We simply cannot jump to conclusions.

There is evidence for CBD causing activation of ER stress pathways in conjunction with viral infection, if you can point out studies of endogenous compounds doing this I'm more than happy to read and consider them