Unless you're changing the topic, irrelevant.
flavonoids, CBD, grapefruit juice, may inhibit p450. but that has nothing to do with the metabolism of THC that's inhaled.
oral THC gets absorbed through the small intestine and absorbed via the liver, and metabolism is affected by p450 enzymes. So a p450 antagonist is a multiplier. It's then converted into 11-OH-THC, which is also a multiplier, it has about twice the potency.
I try to avoid 11-OH-THC myself.
interesting that CBD antagonizes p450.
However inhaled THC bypasses the implicated metabolism mechanism entirely. Period.
THC as a mimetic to anandamide is both an agonist of CB1 and CB2... thc agonizes directly cb1 and indirectly cb2 through the peripheral actions... so- @ cb2 thc can have effect on CBD albeit differently but ... isn't entourage all about this mingling of compounds? None of the cannabinoids are exact specific agonists but rather weak agonists/antagonists with low binding affinity
Quote
"
The CB1 receptor was originally considered to be mainly a CNS receptor, but it is now known to be present in many tissues and organs and its activation leads to both central and peripheral effects [
10,
49]. Its best known effect is psychoactivity; its activation and the resulting ‘high’ are the most popular upshot. Its specific effects – in the nervous, cardiovascular, gastrointestinal, reproductive etc. systems – are of paramount importance in vertebrate and invertebrate physiology.
The CB2 receptor has recently been bestowed the title of a ‘cannabinoid receptor with an identity crisis’ [
50]. Initially it was presumed to be absent in the central nervous system. High levels of CB2 mRNA were found in the spleen. However, more recently it was found in microglia, particularly during neuroinflammation, which causes activation of the microglia and enhancement of CB2 levels [
13,
50]. Its presence in neurons [
51] is still controversial – hence the ‘identity crisis’. CB2 is coupled to a Gi/o protein receptor and inhibits adenylyl cyclase, which is similarly affected by the CB1 receptor, but the latter can also be coupled with other G proteins such as Gs and Gq/11 [
49]. It modulates Ca2+ channels, though less than the CB1 receptor, promotes MAPK activation and ceramide production among many other effects [
13,
50]. Interestingly, stimulation of CB2 receptors in immune cells after initial decrease in cAMP production may lead to a sustained, more pronounced increase in cAMP levels, which results in suppression of T cell receptor signaling through a cAMP/PKA/Csk/Lck pathway [
52]. "
taken from
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3062638/
