"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,
Correct, you also need to lower Omega 6 fats dramatically, and probably focus on long chain Omega 3.
> 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.
Endocannabinoids have been known for a while, but how Endocannabinoids are made in the human body is a newer discovery (~2016).
What should be being broadcast is how important Omega 3 is for increasing CB1R and CB2R activity to reduce inflammation and disease. This has everything to do with COVID and learning to live with SARS2 without people dropping dead or having to stay home from work. This is something everyone can do now, without waiting for legalization, working about dosing, or giving money to yet another 3rd party.
Why is there so little talk about Omega 3 and lowering COVID complications?
Because people are trained by the media everyday that drugs are the answer to everything and diet does not matter.
The global cannabidiol market size was valued at $2.8 billion in 2020 and is expected to expand at a compound annual growth rate of 21.2% from 2021 to 2028. Do you think these people want you to know that the same anti-inflammatory action can be achieved by lowering Omega 6 and increasing Omega 3 in your diet?
> You're overlooking the somewhere between 1% and 30% chance of becoming disabled from Long Covid.
As a Daoist how can I not see the good in this? Maybe now now that everyone knows they can suffer a chronic disease they will find a cure for those of us suffering with ME/CFS for all these years?
This is the arrogance that amazes me. Suddenly everyone cares about chronic disease. the ME/CFS community has been crying for help for years. Am I glad this happened to you or anyone? No. But as I said, maybe some good will come out of it.
By the way, if you want to get out of your situation the only answer is nutrition.