breeding for terpenes

[MiMedicineMan]

And thank you for the longview Joe. not all of us have been as up on this as we should be

Thank you also to alterego, therealhash OO and in vivo for making me think.


Now another question arises in my brain...

Can any terpene combination be bred from any cannabis strain (lineage) or does a strain (lineage) have a finite amount of terpenes it can produce. IE Can you take thai weed and through selective breeding get oaxacan? And through the generations does the palate of terpenes get more plentiful or less or either?

The more I learn and the more cannabis I see, it seems everything I like comes from afghani

 

[Only Ornamental]

I believe to remember having read about two publications (by Hillig maybe?) on that subject. Now, the following is out of my memory and may be wrong, so don't hang me if there are some twisted facts stated!
One publication used used PCA to analyse whether it is possible to attribute the origin of cannabis to a certain location. They were successful. But a PCA does often look at absolute and relative amounts as well as relations between constituents than just presence or absence thereof.
The other tried focussed on the genetic diversity to prove/refute the current nomenclature of Cannabis. All they saw was that some species, I don't remember if it was only WLD or all C. indica, contained additional sesquiterpenes absent in C. sativa. Pretty sure this publication was from Hillig et al.
Cannabis by itself contains the basic tools for terpene synthesis like most higher plants. It's like most men have an axe and access to wood; they theoretically have the tools to build a house (rather log cabin) but if they do and how depends not only on predisposition (skill, genes) but also environmental factors (law, culture, money).
Taken together with my knowledge about other plants I'd say that many varieties of drug type cannabis have the ability to synthesise a good part or even the whole range of known cannabis terpenes. But as said genetics is only one part; which terpenes are produced and at what amount heavily depends on environmental factors, epigenetic regulation, and also common enzymes not directly related to terpene synthesis.
I suppose (but may be terribly wrong) that with enough skill, time, money, luck and diagnostic tools one could selectively breed varieties which express more or less of at least the dominant terpenes. Dealing with the dozen of minor constituents will be tricky because several aren't directly regulated or form semi-haphazardly.

Likely, you see that it will be a lot faster to get the oaxacan smell from an oaxacan variety than by trying to change a thai variety.

 

[in vivo]

Joe,

Either you're in luck or I'm in luck, because I jack off to way more than Russo. But I don't deny that I'm a half retard.

The 2002 argument seems moot and almost reads like hurt feelings, imo. They used crappy 4% shake with minimal amounts of stems and seeds in it. I can't imagine what their THC free shake (placebo) tasted like. But okay the point you seem to be making is that there is no scientific evidence. I'd disagree. It really comes down to the endocannabinoid system (ECS) and G Protein-Coupled Receptors (GPCRs). About 40% of all clinically available drugs target GPCRs. Cannabinoid receptors are the most highly expressed of any GPCR. GPCR's do not have a singular mechanisms of action. They modulate one another in a variety of ways. Some relevant examples might be:

VI. Glossary
• Ago-allosteric modulator. Ligand that is both an
allosteric modulator and allosteric agonist.
*
• Allosteric agonist. Ligand that possesses efficacy
and that binds to a site distinct from the orthosteric
site.
*
• Allosteric binding site. A ligand binding site distinct
to the orthosteric binding site. Can be ontarget
or off-target.
*
• Allosteric modulator. An exogenous or endogenous
molecule that binds to a distinct and nonoverlapping
site to influence binding or signaling at
another, usually orthosteric, site.
*
• Cooperativity. The effect(s) of multiple equivalents
of the same ligand binding to multiple (generally)
identical sites.
*
• Functional selectivity. Selective activation of a
subset of the signaling pathways available to a receptor
by a ligand.
*
• GPCR allosterism. The reciprocated effect(s) of
binding two (or more) distinct ligands at different
sites on a receptor monomer, homomer or heteromer.
Such effects can be positive or negative.
*
• Heteromeric receptor. A signaling unit composed
of two or more GPCR protomers that by themselves
are nonfunctional.
*
• Negative allosteric modulator. Reduces binding or
activity.
*
• Orphan receptor. A GPCR for which the endogenous
ligand remains to be discovered.
*
• Orthosteric binding site. The primary binding site
of the receptor, usually where the endogenous ligand
binds and elicits a signal.
*
• Positive allosteric modulator. Enhances binding
or activity.
*
• Receptor heteromers. Two or more molecularly distinct
and individually functional GPCRs that combine to
form a molecular entity with distinct pharmacology.
*
• Receptor homomers. Two or more molecularly
equivalent and functional GPCRs that combine to
form a molecular entity with distinct pharmacology.

http://pharmrev.aspetjournals.org/content/62/4/701.long

http://pharmrev.aspetjournals.org/content/62/4/588.short


As you can see there is much more in play here than CB1 (more accurately CB1, CB1a, and CB1b). Activation of one receptor can turn another one down or up. Two receptors activated at the same time can perform a function dissimilar to either of the parent receptors, etc.

I'm not sure if THC or its metabolites measured in plasma tell the whole story. Hell, it might even mean that there is less in the brain. There is considerable research into the pharmacokenetics of botanical extracts vs isolated cannabinoids.

I guess I'd be interested to hear your thoughts on Taming THC which was published in 2011 by Russo. He claims to 'scientifically demonstrate' the relevance of minor cannabinoids and terpenoids in that paper. The amount of information in regards to the synergistic characteristics of terpenoids is extensive beyond Russo or even cannabis. When inhaled levels as low as 0.05% are believed to be pharacologically relevant.

I'd also argue about whether or not other cannabinoids are present in relevant amounts. I haven't even had all of mine analyzed yet and I've already found a hindu kush with 8% CBG.

I haven't steamed flowers, but I have added essential oils (with GC/MS and distill date) on top and smoked them. I don't doubt the impact that they have. My problem was that I didn't care for the taste at all. That god damn pine taste will linger. My other issue was that I never got an essential oil that had myrcene as the primary constituent, some hops extracts supposedly have it in them but I couldn't find a vendor that offered GC/MS or a distilled date. I did play around with beta-caryophyllene, limonene, alpha/beta-pinene, linalool, and a few others. I've used aromatics international for the essential oils. You can search by the constituents and they provide GC/MS and distill dates on everything. It's also interesting to look at previous batches to identify the level of variation. If I was interested in really exploring that idea again I would likely use the little aroma sticks (like a vics inhaler) as my delivery method, or I'd pull the vaporizer out of the closet. Smoking them was lame and more often than not I'd end up just dumping out the bowl and trashing it.

I would never be willing to give flowers to patients with essential oils on top, however one of the reasons I settled on the essential oils was due to an interest in topical applications. That line of research is ongoing, but really very interesting. I haven't been able to post about it on my local board out of fear that a patient would see it. I highly doubt they'll be on here. I played around with different aromas from various mixtures of essential oils. I focused primarily on CB2 direct activation, and skin penetrants, and worked the aroma around that. I also used phytocannabinoids from sources other than cannabis for additional CB2 activation. I fused 4mg/ml of cannabis concentrate to this mixture and had a friend that's a caregiver give bottles to five patients that were believed to potentially benefit from a topical application. In order to be a part of the trial they had to use a number of pain management sheets. Consistently across the board their was indication of improvements on a 10 point scale. As was expected patients with pain and inflammation towards the surface area of their skin indicated the most benefit. I wasn't sure what to make of it. I was excited but also fully aware of the concept of placebo. For round two I decided to make two new batches. One doubled the cannabis concentrate and left the rest. The other had no cannabis concentrate and pretty much doubled the rest. The one with no cannabis showed better results across the board. Now I'm in the process of doing a third round where I'm going to create a pleasant aroma but not consisting of the constituents I believe to be providing the benefit along with another cannabis concentrate free version similar to the previous one. I'm not sure if these people are just getting benefit from massaging their skin and muscles (applying the topical) or if it's the concoction we've whipped up, but it's certainly got my interest.

I can also offer my own anecdotal experiences with CBD, I grow a cannatonic that's about a 15:1 ratio. I've only smoked it once, I didn't like it. I was already stoned and it was a total buzz kill. That's likely because even though CBD doesn't have much binding affinity for CB1 or CB2, it is an effective CB1 and CB2 agonist blocker, but like other cannabinoids it's also been shown to push more THC into the brain (like the study you linked). All of my CBD ended up going to a cancer patient, or I'd be able to offer more input. It won't be long until I have some more to play with.

A good thesis on terpenes:
https://openaccess.leidenuniv.nl/bitstream/handle/1887/20608/04.pdf?sequence=10

Ornamental,

I'd like to hear you input on:
http://www.researchgate.net/publica...Cannabis_sativa_L/file/d912f5112790e434cb.pdf

Terpenes are strongly inherited and little influenced by environmental factors and, therefore, have been widely used as biochemical marker in chemosystematic studies to characterize
plant species, provenances, clones, and hybrids.

 

[G.O. Joe]

It really comes down to the endocannabinoid system (ECS) and G Protein-Coupled Receptors (GPCRs).

I am like many persons my age exceptionally familiar with the 2-4% THC cannabis unloved by Russo, aka Mexibrick. I've grown their bagseed and modern creations like BOG's. It's pot. If anything, the brickweed was more pleasant than anything I've smoked in years, but it would not be logical to say that the soaring highs it produced were the result of anything other than my fresh inexperienced brain cells, so I don't jump to conclusions about the terpene content of Mexican, or the effects of curing the green out of it. I've brought up the hash analogy before, if CBD blocks THC, how do people get high from hash? Oh wait, CBD actually modifies THC by taking away anxiety. I've smoked a lot of pot nearly free of CBD, and it's never made me anxious. Nor have I heard reports from people over the years saying how different the high from hash is. Aren't these molecular, computer model, petri dish, knockout mice studies of the same sort that say that aspirin and ibuprofen block the effects of THC, and they have definitive (non-live-human, non-smoked MJ) proof? And, in the real world?

Pick something out of Russo and look up the reference, and judge how definitive it is. People are doing lots of work and writing, but mostly for the work and writing - real world usefulness is rare in highly technical work, whether math, chemistry, biology, whatever, though the author naturally makes it the most important thing ever. Taking bits and pieces from other work that you probably don't understand and assembling it to try to make your own publishable work is popular in the journals these days, but it isn't science. The scientific method is finding a way to prove your hypotheses. Russo for example avoids scientific method while criticizing work that's pure scientific method. This alone tells me everything I need to know. My point is, if you're going to say this gets you higher, that brings you down, this relieves whatever, someone else's cytometic bead array analyses aren't going to cut it as proof.

 

[in vivo]

I've brought up the hash analogy before, if CBD blocks THC, how do people get high from hash? Oh wait, CBD actually modifies THC by taking away anxiety. I've smoked a lot of pot nearly free of CBD, and it's never made me anxious. Nor have I heard reports from people over the years saying how different the high from hash is.

THC has a high affinity for CB1 and more appears to be pushed into the brain when consumed with other cannabinoids like CBD and CBC.

I have strains that are likely to make a non experienced smoker very anxious, and an experienced smoker very happy. It's likely a matter of the expression level of CB1 receptors.

The hash comment kinda makes the point. If you're talking about most oil that's had the majority of the terpenes essentially cooked of them I agree. Not much difference between the majority of them. If we're talking about good oil or bubble with a high terpene content, I'd again have to disagree. There seems to be a significant difference.

the same sort that say that aspirin and ibuprofen block the effects of THC,

This comment tells me that you're not paying attention, or that you don't believe in the science of pharmacology. Do you not believe that ibuprofen modulates endocannabinoids? You must not have caught the recent patent to diagnose autism simply by giving a person some acetaminophen and observing the degree of modulation of AEA and 2-AG.

I don't believe that COX-2 is believed to prevent a person from getting high. Inhibiting COX-2 with ibuprofen simply cancels out the increase of COX-2 in the hippocampus which aids in memory.

It seems easy to criticize a paper without having even read it.

 

[G.O. Joe]

This comment tells me that you're not paying attention

https://www.icmag.com/ic/showthread.php?t=275613

Post 7 is mine. I'm perfectly sure ibuprofen doesn't do anything for me related to MJ, just as I'm sure that pistachios are not a cannabis antidote, and that no bags I tried did anything for my acne in high school.

 

[in vivo]

So you're willing to make an unfounded claim like the British Journal of Pharmacology isn't a legitimate scientific source, and that hundreds of citations from Taming THC are all "non scientific" (which implies that every peer review publication that published them are bogus) but you're not willing to so much as read or comment on the piece that you attempt to discredit. If you're not willing to learn then why even post?

The fact that you've taken ibuprofen every four hours for years might not make you an authority on the potentially subtle pharmacological interactions between it and cannabis (not at CB1 mind you and I'm sorry that you chose to read an editorial rather than the actual paper itself, if you had you'd realize it has nothing to do with the "buzz"). I question whether an individual can be that objective, but I'll take note of your experience. It should be noted that a number of papers have subsequently shown that acidic forms of cannabinoids (also COX-2 inhibitors) can also inhibit particular mechanisms of action of the neutrals. Truly the idea that you can't buy into it means that you don't buy into the endocannabinoid system, and quite honestly I don't blame you. I'm in awe at how they could have missed such an enormous piece to the puzzle myself. That being said it doesn't make it any less real.

Terpenes don't get you high? I thought that's what we're talking about here. Why not buy some essential oils and you tell me?

 

[Only Ornamental]

British Journal of Pharmacology
...
Terpenes don't get you high? I thought that's what we're talking about here. Why not buy some essential oils and you tell me?

Do you have the link or author and issue/year?

Terpenes don't make you high (well, camphor, thujone and salvinorin A do ). The trick is to mix them with THC and somehow modulate the perceived effect...
I also wonder why nobody adds essential oil but desperately seeks this or that monoterpene in a strain because they believe it gives them the best buzz. Many would be served quick&nicely with some essential oil added .

 

[in vivo]

Here's Taming THC:
http://onlinelibrary.wiley.com/doi/10.1111/j.1476-5381.2011.01238.x/full

Here's are just a few others unrelated to cannabis:
http://www.jnronline.com/index.php/jnr/article/download/28918/25048

http://imsear.hellis.org/bitstream/123456789/144960/1/ijeb2010v48n3p208.pdf

http://www.sciencedirect.com/science/article/pii/S0944711304700586?cc=y

Google Scholar pulls like 25k hits.

 

[in vivo]

MMM,

Here's a link to a study you might find interesting:

The inheritance of chemical phenotype in Cannabis sativa L. (IV): cannabinoid-free plants

 

[G.O. Joe]

So you're willing to make an unfounded claim like the British Journal of Pharmacology isn't a legitimate scientific source, and that hundreds of citations from Taming THC are all "non scientific" (which implies that every peer review publication that published them are bogus) but you're not willing to so much as read or comment on the piece that you attempt to discredit. If you're not willing to learn then why even post?

You've cleared up much, about yourself. I hope we haven't strayed too far off topic.

Terpenes don't get you high? I thought that's what we're talking about here. Why not buy some essential oils and you tell me?

Finally! The question isn't why I have not done so, it's why Russo et al. hasn't.

 

[in vivo]

There is plenty of research into botanical extracts vs isolated compounds. Much of it done by GW Pharma.. There are also plenty of patents that show the differences between isolated compounds vs botanical extracts. So what are you talking about? You say he Russo hadn't published another paper, he did. You say there is no evidence that terpenoids are pharmacologically active, I pointed some out to you. You claim minor cannabinoids aren't relevant, I have at least one strain with 8% CBG. You make plenty of claims..

I have preconceived notions as well, but none that I'm not willing to scrap based on new evidence.

 

[Only Ornamental]

...
Google Scholar pulls like 25k hits.

...There are also plenty of patents that show the differences between isolated compounds vs botanical extracts...

Thanks (although, it's 'just' a review...)! I asked exactly because of too much hits . Although, I prefer Pubmed, ScienceDirect and SciFinder for that purpose.

Most patents claim things but actually don't prove anything (don't have to) or allegedly do so but not in a scientific enough way (again, no need to). Many state actual publications but there's no regulations if and how those have to correspond to the claim. You can literally file a patent for ANYTHING and base it on no matter what you like; question is, if it won't be contested and how/if you can defend it...
That's why I really dislike patents (and for other reasons too, but that's beside the point) and always opt for the actual publication or scientific finding.

 

[G.O. Joe]

So what are you talking about?

Random lab facts can't be offered as proof of anything other than the random lab facts. Critical thinking is the very heart of scientific method. You can't just say that caryophyllene reacts with your body, therefore, it gets you high, or prevents you from getting high. The critical thinker might ask:
Is this amount of caryophyllene actually present in the amount of vapor inhaled in a typical cannabis dosage?
Is this amount actually transported to the receptors?
Does this receptor binding actually happen in the presence of the other things in cannabis?
Does any actual binding that happens have an actual effect noted by the user, instead of the technician?
before being concerned with whatever methodology was used to obtain the random lab facts.

The critical thinker might suggest that there is a limited number of ways to prove these entourage hypotheses, all of which involve double-blind studies of smoked cannabis preparations in humans. Wachtel et al. saw this and did it. Point us to something else similar.

 

[Only Ornamental]

Random lab facts can't be offered as proof of anything other than the random lab facts. Critical thinking is the very heart of scientific method. You can't just say that caryophyllene reacts with your body, therefore, it gets you high, or prevents you from getting high. The critical thinker might ask:
Is this amount of caryophyllene actually present in the amount of vapor inhaled in a typical cannabis dosage?
Is this amount actually transported to the receptors?
Does this receptor binding actually happen in the presence of the other things in cannabis?
Does any actual binding that happens have an actual effect noted by the user, instead of the technician?
before being concerned with whatever methodology was used to obtain the random lab facts.

The critical thinker might suggest that there is a limited number of ways to prove these entourage hypotheses, all of which involve double-blind studies of smoked cannabis preparations in humans. Wachtel et al. saw this and did it. Point us to something else similar.

Usually, RANDOM lab results aren't considered facts and won't (at least shouldn't) be published.
Why did you chose caryophyllene as an example? It's a rather selective CB2 ligand and scientific findings indicate that, depending on the diet (it's present in more than cannabis), it may have a pharmacological effect. Like many pharmacological effects (apart from hallucinations amongst others), they are not always perceived by a healthy 'test subject' and sometimes not even by real patients.
It may be a matter of debate or 'scientific philosophy' if and to what extent human trials truly prove a mode of action or a molecular mechanism. They do prove efficiency and hopefully show absence of toxicity... till shown otherwise. You're right concerning the limitations of entourage effects. They are often as complex as the system they affect and most of the times we don't even know (I say 'we' because I'm one of those guys) which compounds in a plant preparation cause them when we start with the first in vitro assays. That's often the reason for failing to publish (and not the lack of methods/skill/money used) synergistic effects of plant constituents and especially extracts in more than Planta Medica.
Testing in mice can give indications but the metabolism is not the same than in humans and not knowing which constituents to measure and what outcome to determine limits these tests. That leaves us with human trials which have their own limitations (like laws and ethics committees)... and they may not prove anything. Can't make a dose-response without knowing what you dosed, can you?

 

[Sam_Skunkman]

I am like many persons my age exceptionally familiar with the 2-4% THC cannabis unloved by Russo, aka Mexibrick. I've grown their bagseed and modern creations like BOG's. It's pot. If anything, the brickweed was more pleasant than anything I've smoked in years, but it would not be logical to say that the soaring highs it produced were the result of anything other than my fresh inexperienced brain cells, so I don't jump to conclusions about the terpene content of Mexican, or the effects of curing the green out of it. I've brought up the hash analogy before, if CBD blocks THC, how do people get high from hash?

IF YOU SMOKE 100MG PURE CBD BEFORE ANY THC YOU DO NOT GET HIGH FROM THE THC FOR SEVERAL HOURS AT LEAST.
IF YOU SMOKE A CBD/THC HASH, LIKE ALMOST ALL IMPORTED SIFTED HASH, LIKE AFGHAN, PAKISTANI, LEBANESE, YOU DO GET HIGH BUT THE HIGH IS QUITE DIFFERENT THEN HASH THAT IS HAND RUBBED FROM NEPAL FROM NLD PLANTS ALSO GROWN FOR GANJA AND WITH LITTLE CBD. ALSO ALL SIFTED AND HAND RUBBED IS MADE FROM SEEDED PLANTS AND THE RESIN IS NOT AS GOOD AS THE SAME PLANT SINSEMILLA. ALL IMPORTED SIFTED HASH HAS UPTO HALF CBD.

Oh wait, CBD actually modifies THC by taking away anxiety. I've smoked a lot of pot nearly free of CBD, and it's never made me anxious.

MAYBE YOU NEED THC, NO CBD AND THE RIGHT TERPENES WITH THE THC? MAYBE?

Nor have I heard reports from people over the years saying how different the high from hash is.

I ASSURE YOU IF YOU SMOKE 100% PURE DRY SIFTED RESIN YOU WILL NOTICE HOW DIFFERENT.

Aren't these molecular, computer model, petri dish, knockout mice studies of the same sort that say that aspirin and ibuprofen block the effects of THC, and they have definitive (non-live-human, non-smoked MJ) proof? And, in the real world?

Pick something out of Russo and look up the reference, and judge how definitive it is.

MOST OF WHAT HE SAYS IS RIGHT ON, YOU NEED TO TRY 100% PURE THC WITH AND WITHOUT A TERPENE LIKE LIMONENE OR MYRCENE, AND SEE FOR YOUR SELF THE DIFFERENCES. OR YOU CAN TRY 25 mg 100% PURE THC THEN TAKE SOME TAKE REAL GOOD NATURALLY TERPENE RICH DRY SIFT SAY 50% THC AND ADD 12.5mg OF IT TO 12.5mg 100% PURE THC SO YOU HAVE 25mg MIXTURE OF THC/DRY SIFT WITH A THC % OF ABOUT 75%, TRY IT AND TELL ME WHAT YOU THINK.
THIS HAS BEEN CONFIRMED BY HUNDREDS OF PEOPLE NOW, NO ONE THAT HAS TRIED IT HAS DENIED THE EFFECTS OF TERPENES
TO MODIFY THC. WHY IS THAT? YOU NEED TO TRY IT.
I KNOW RUSSO, YOU ARE WRONG ABOUT YOUR FEELINGS.
HE IS A SCIENCE JUNKIE.
-SamS

People are doing lots of work and writing, but mostly for the work and writing - real world usefulness is rare in highly technical work, whether math, chemistry, biology, whatever, though the author naturally makes it the most important thing ever. Taking bits and pieces from other work that you probably don't understand and assembling it to try to make your own publishable work is popular in the journals these days, but it isn't science. The scientific method is finding a way to prove your hypotheses. Russo for example avoids scientific method while criticizing work that's pure scientific method. This alone tells me everything I need to know. My point is, if you're going to say this gets you higher, that brings you down, this relieves whatever, someone else's cytometic bead array analyses aren't going to cut it as proof.

What about human trials with me, Rob Clarke, and 10 more experienced volunteers?
Done a decade ago...
Double blind, a 100 question organoleptic survey filled in pre and post testing, only one test a day done early before any Cannabis use that day. Weighed all samples to .001 gram. Vaporized all samples.
Had a dozen pure Cannabinoids and a dozen terpenes to try alone or in combinations with THC or other Cannabinoids.
Does that count?
That is when I found that 100mg pure CBD vaporized before THC will block the effects of THC for 6-8 hours. Everyone noticed this.
Funny how everyone that has attempted anything like this kind of terpene/THC testing has reported it works, including many of the top laboratories testing Cannabis, where are the reports from people that tried and found no success? I have not heard of one!
-SamS

 

[Only Ornamental]

...
Funny how everyone that has attempted anything like this kind of testing has reported it works, including most of the laboratories testing Cannabis, where are the reports from people that tried and found no success? I have not heard of one!
-SamS

Unfortunately, it's difficult if not impossible to publish findings which aren't or of things which don't work. Mostly every lab has wasted money by redoing the mistakes of others because of that. There should be a database of failures for those looking for it... but no one would waist money and time on writing them down in an acceptable form.
And then there is the problem that not all trials are publicly available (as you very well know )...

 

[in vivo]

it seems like a critical thinker might review the available evidence, explore these compounds themselves, analyze their current strains to become familiar with the most prominent compounds present, and not simply draw a line in the sand which seems tantamount to waiting for clinically available cannabis.

There's plenty of double blind studies. They're just not focusing on the psychoactive characteristics. It's not as if GW Pharma hasn't studied their area of expertise extensively. I wonder why there isn't more research into the psychoactive effects, I heard they're passing out licenses like candy. I also wonder how so many pharmaceutical companies can still be in business basing their businesses on such quasi scientific approaches.

The Wachtel study seems to fall short of anything remotely close to conclusive. It's not much of a placebo if you can identify a difference based on taste. Also the lack of less prominent cannabinoids, and unknown levels of terpenoids seem like a significant issue when attempting to identify ways in which they might modulate THC.

It's not difficult to order some essential oil and prove anecdotally to oneself that terpenes matter. Nobody said that beta-caryophyllene gets you high. It is a full CB2 agonist that has been shown to displace other cannabinoids. It's also been proven that CB1 and CB2 form functional heteromers and negatively modulate one another. Therefor it's not much of a leap of faith to assume that beta-caryophyllene present in high enough amounts modulates THC in at least those two ways. That's just one example. Are we better off remaining in the dark age until the gatekeepers provide clinically available cannabis?

Does it make sense to claim that all of the scientific evidence is worthless and that these compounds simply aren't relevant, even though there is absolutely no evidence to support that?

 

[Sam_Skunkman]

Actually it is no harder to report that certain terpenes had no effect to modulate THC then to report they do. Either way first you try and understand 100% pure THC's effects by trying 25mg vaporized first thing in a morning, then wait a bit and try 25mg pure THC spiked with the smallest amount of limonene or Myrcene you can add.
Or Try 12.5mg 100% pure THC with a little 12.5mg naturally terpene rich dry sifted resin added, if it can melt and bubble it is good enough to add. Then smoke or vaporize the mixture and say if it effects the pure THC or not, you will have no doubt if it does. The 100% pure THC is pretty flat and boring with little to no individuality like herbal Cannabis has. Terpenes are the individuality!
That is why there are no reports that terpenes do not modify THC's effects, because they do....
Unless you try one like beta-caryophyllene that does not seem to modify the psychoactive effects of THC, it is active at the CB2 receptor, so it is modifying, just not the high....

-SamS

Unfortunately, it's difficult if not impossible to publish findings which aren't or of things which don't work. Mostly every lab has wasted money by redoing the mistakes of others because of that. There should be a database of failures for those looking for it... but no one would waist money and time on writing them down in an acceptable form.
And then there is the problem that not all trials are publicly available (as you very well know )...

 

[G.O. Joe]

Well I have smoked THCA and found it no different than the NL5xHaze buds it came from, and said so here. It's the foundation of my doubt. I don't think there's anything for me to be wrong about Russo since all I said was he hasn't produced anything like Wachtel, and he hasn't as far as anyone is saying. That's all I've said in all of my posts, but Only Ornamental and especially in vivo seem intent on putting words and thoughts that I didn't say in my mouth. There might be enough material to try another THCA extraction in a few weeks, but there is a scheduled UA after that, so it might be a while. Essential oils - perhaps hemp oil itself - could be arranged. What if it's the same result again? Am I totally fucked up? Lying? Crazy? This is why something definitive on the terpene subject such as addressing Russo's concerns on Wachtel et al. is necessary. This whole pharmacological basis that needn't have even come up here is built up and ready to go, yet it's the cart before the horse.