Thanks Kofi, interesting stuff.
CB 2 agonists demonstrate remarkable anti inflammatory properties but your
idea of receptor attraction has some merit, at least with respect to the CB
1 receptor. I recall an old study wherein they found that cannabis tolerance
was proportional to the level of receptor retraction from the cell surface.
This does raise some worrying questions with respect to the chronic
ingestion of the same but the studies tend to find little ill effects.
Cannabidol, the non-psychoactive form, strikes me as an excellent target for
therapeutic potential.
A recent news release about some research indicated that topical application
of THC, which does ligand to the CB 2, had strong anti-allergic effects,
sufficient to warrant clinical trials. This is entirely concordant with
other studies showing that CB 2 activation down regulates excessive
inflamation being driven by innate immune responses.
Thanks,
John.
"Kofi" <kofi from anon.un> wrote in message
news:kofi-59A74F.20025514062007 from news.east.earthlink.net...
> Cannabinoid receptors are partly regulated by the mu opioid pathway.
> You might want to check some of my previous posts on the subject in
> sci.med.cannabis and alt.support.crohns-colitis. In particular, I
> theorize that low-dose cannabinoid receptor *antagonists* might be able
> to enhance anti-inflammatory cannabinoid signaling by upregulating
> cannabinoid receptors similar to the way low-dose naltrexone upregulates
> mu opioid receptors. It's on my list of things to try if my helminths,
> butyrate and vitamin D3 injections don't achieve the remission for which
> I'm hoping.
>> On a slightly separate note, given that cathelicidin per se has
> anti-allergic effects, I'd bet that cannabinoids are regulators of the
> innate immune system.
