We can all argue until we are blue in the face until we have the actual data.
Until then experience tells me I enjoy terpenoid-associated fractions with my cannabinoid fraction.
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10 years ago people would suggest mangos and lemongrass would provide enough myrcene to help thc penetrate the blood brain barrier further than without. It seems pretty obvious to me that terpenes act as a vehicle to help deliver the cannabinoids to different places it couldn’t travel as a solid state vs a solution.
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Ditto.
Real world experience definitely points toward magnification of effects with both present.
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Good bot
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Terpenes are the primary constituents of essential oils and are responsible for the aroma characteristics of cannabis. Together with the cannabinoids, terpenes illustrate synergic and/or entourage effect and their interactions have only been speculated in for the last few decades. Hundreds of terpenes are identified that allude to cannabis sensory attributes, contributing largely to the consumer’s experiences and market price . Terpenes Flavors to The People!
Research changes every day and anyone that claims to have all the answers is a quack doctor. The research experiment done about a year and change ago that “disproved” the entourage effect was fully debunked. University of Arizona claims just the opposite
Study shows Cannabis terpenes provide pain relief, contribute to 'entourage effect' -- ScienceDaily.
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This one too
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Until we have receptor binding studies AND protein pathway activation studies we won’t have the full picture.
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beta-Caryophyllene preferentially binds the CB2 receptor and activates it. (It does not do this to the CB1 receptor.). This is well documented in the scientific literature, e.g. binding affinity, reversibility, and where on the CB2 receptor this terpene binds.
This leads one to believe that the relative amount of “head high” and “body high/effects” is partly a function of the (relative) amounts of this terpene in different cannabis products.
If interested, start your literature search here:
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I’ll repost my last “huh” paper regarding this, posted in another thread.
“Terps” loosely termed here including other aromatics, are a major factor, and they do absolutely have effects on the CB receptors.
If they didn’t effect mood, I’d figure we wouldn’t use them in aroma therapy.
Sit with some trippy kids and have them blast rose water in your face, bet you’ll find it quite soothing and relaxing.
There’s certainly something there.
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i think this is the most fair statement on where we’re at in our understanding of this theory/phenomenon/thing.
a few terpenes are confirmed to actually bind to cannabinoid receptors; hard to say they wouldn’t have something to do with modulation of experience.
a lot of terpenes don’t bind to cannabinoid receptors; however it’s likely they play a role in influencing the ‘set’ of the user, and then the cannabinoid effect has a different canvas to play on; less of a direct effect but an effect nonetheless.
some terpenes do neither, but appear to increase the absorption of other compounds.
the conception the user has that ‘this strain is an indica/sativa or is known to make me feel this/that way bc leafly or the budtender said it would’ will influence the perceived experience, because the mind is a powerful thing.
we haven’t even begun to understand the role that all those minor cannabinoids at >1%, that we don’t even see on most COAs, play when in this ratio vs. in that ratio vs. combined with this or that terpene profile.
then, the way these play out person to person, and things like the fact that long time cannabis consumers tend to notice a difference in the effect cannabis has on them when they first started vs. 10 years later (how many people do you know ‘dont smoke anymore cuz it makes me too anxious’)
i realize i’m not stating anything that hasn’t been stated already. i just think that given we’re just cracking a lot of this open, and given the incredibly complexity of testing the effects of so many variables on so many different physiologies, i don’t understand how anyone can claim that the theory as we currently conceive it be completely true or untrue. we have some clues but far from anything resembling a true understanding. it’s somewhere in between, and we should adjust the theory to fit the ongoing research. we’re just not there yet and won’t be for awhile, and that’s why it’s called a ‘theory’
hard to argue that
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Ooo-oooo-oooo-oooo.
(Opinion alert)
(Like seriously subjective)
(Like, the grain of salt you need could salt roads)
So!
The #1 grievance I hear most commonly is “it makes me anxious”. My hypothesis regarding this has to do with one of two factors. Either it’s too high in THC, unfamiliar to the consumer, or a terpene profile so heavily layered thanks to the great “hybridization”.
If you give a person a dosage of something more so than one is accustomed to, then the likelihood of their body responding negatively could theoretically go up.
I have noticed with the older, more mild strains, I haven’t observed negative reactions, even when consuming beyond their normal means, or consuming in ways that isn’t normative to them.
My theory is as follows, THC by itself, tends to let the mind race, too layered a terpene and other active compound profile, and your body gets overwhelmed.
(I know this is entirely subjective, but this is the theorem I tend to go by after observing hundreds of consumers of various age ranges personally.)
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Terpenes do not bind to cb1 or cb2… Polyphenols do though.
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from the paper posted by @TheGooMan:
‘studies have shown that a gavage of β-caryophyllene activated CB2 [5] and topical application of it up-regulated TRPM1, TRPM6, TRPV4, and TRPV6 of the TRP channels [2]. These studies indicate that β-caryophyllene activates at least three types of receptors: olfactory receptors, TRPs, and CB2.’
it would appear that at least one of them does
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another relevant paper https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7246407/
–which actually seems to classify β-caryophyllene as ‘a sesquiterpene alkene and atypical dietary cannabinoid’
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Huh … I keep finding contrary evidence. As well as personal experimentation. Pretty sure alot of links in this thread are cross reffed in the below study as well.
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right on, frankly i love it when this happens, thanks for posting
fave part so far: ‘All terpenes were purchased from True Terpenes’
’ Importantly, this study cannot rule out the existence of an entourage effect for terpenoids. However, in combination with Santiago et al. (2019), there is likely now sufficient data to rule out direct interactions with either cannabinoid receptor as being the mechanism by which an entourage effect is mediated, so attention must move to other types of effect. Within the endocannabinoid system, this would mean investigating the effect of terpenoids on metabolism or synthesis of the endocannabinoids’
seems that this does have a lot of evidence to disprove ‘direct’ interactions with the cannabinoid system/receptors, and β-caryophyllene’s binding to CB2 appears to be a weak one. doesn’t discount that they may modulate in other ways, and i think important to keep in mind, only studied 5 terpenes.
very fun to think about where these studies overlap and where they disprove each other’s findings
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My prediction that CB1 and CB2 are not the whole story still stands.
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It could have something to do with like isoprenylation with protiens or some other kind of pharmacological interaction. Like I’ve said above, I really think we should be looking more at polyphenols as far as “modulating” the cb receptors…
A point the guest makes on the Hamilton podcast also talks about how much terpenes(very small), the route of ingestion(typically inhaled), and degradation(smoke and vaporization) by the time the body can metabolise them(are they still terpenes?). It’s important information we all forget to think about.
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