[podgaj]

Yes, it is. They are not explaining HOW IRE1a is triggered by CDB, and it is because CDB triggers the CB1/2 receptor which activates these pathways.

https://journals.plos.org/plosone/article?id=10.1371/journal...

"Overall, our study investigates for the first time the effects of the endocannabinoid AEA on primary human T-lymphocytes, demonstrating that it is a powerful modulator of immune cell functions. In particular, not only we clarify that CB2R mediates the immunosuppressive activity of AEA, but we are the first to describe such an immunosuppressive effect on the newly identified Th-17 cells. These findings might be of crucial importance for the rational design of new endocannabinoid-based immunotherapeutic approaches."

The only way CBD can trigger these pathways is by effecting a cell receptor The only cell receptors for CBD are CB1r and CB2R. There is literally no other way this can happen.

If y9ou can explain how CBD increases IRE1α activity any other way I am all ears,

[netizen-936824]

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...

[podgaj]

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?