Maybe you should do the work before you speculate, I definitely got higher, maybe better also I will admit.
-SamS
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Scrutinizing Strains with Science : An Objective Discussion
- Thread starter MyGreenToe
- Start date
Maybe you should do the work before you speculate, I definitely got higher, maybe better also I will admit.
-SamS
CannaBo- You might have a point thru a novice eye. Seasoned smokers can tell the nuances of the effects of different "strains". People that dont smoke alot tend to get "blown away" high when they do, which is why you cant tell the difference. For many of us cannabis doesn't effect us like that anymore, smoke everyday for, hell, I hate to say it but 20 years, then tell us how it effects you. It takes different strokes, different strokes, different strokes to move the world......
Speculation, or better yet, a true hypothesis, comes before a study, not after; unless during the course of the study one finds more questions.
In everything I have been able to find, none of the terpenoids from cannabis are psychoactive in terms of getting a person 'high'. However, they seem able to affect the 'high' from cannabinoid(s) like THC. Sorry to say, but that is what I have found so far, and that is what I used for my speculation. If you have studies or scientific (analytical) evidence to the contrary please post the info, however, your subjective smoke tests do not fit the bill as scientific evidence. That said, I think there could be terpenoid(s) that have psychoactive proprieties from cannabis (as found from Saliva divinorum), even though none have yet to be found, as far as I know.
No problem,
I did a lot of speculating for years until I did the work myself to answer at least some of the questions. And I did try maybe a dozen Terpenoids by their selves with and with out THC. None of them got me high at all without THC. That does not mean that none of the 130+ Terpenoids found in Cannabis will be found to be psychoactive by itself, but not yet.
BTW, if you do the work then I suspect we would not be having this discussion, as I believe that you would then agree with me, as all who tried did. THC+the right Terpenoids for sure makes you higher, either by allowing more THC to bind to the CB1 receptors, or faster binding, or otherwise modifying THC's effects, of that I have no doubt. I have not done blood plasma THC levels to see if that would help answer if more THC reaches the blood with the right Terpenoids present. But that is not my real interest to be honest.
-SamS
I did a lot of speculating for years until I did the work myself to answer at least some of the questions. And I did try maybe a dozen Terpenoids by their selves with and with out THC. None of them got me high at all without THC. That does not mean that none of the 130+ Terpenoids found in Cannabis will be found to be psychoactive by itself, but not yet.
BTW, if you do the work then I suspect we would not be having this discussion, as I believe that you would then agree with me, as all who tried did. THC+the right Terpenoids for sure makes you higher, either by allowing more THC to bind to the CB1 receptors, or faster binding, or otherwise modifying THC's effects, of that I have no doubt. I have not done blood plasma THC levels to see if that would help answer if more THC reaches the blood with the right Terpenoids present. But that is not my real interest to be honest.
-SamS
hops, a close relative of cannabis, has psychoactive properties. i'm not sure if it's caused by terpenoids though, i dont think so.
I'm just stopping in to say "Hi." I work for a research lab that is hoping to offer analytical services to the medical cannabis community in Arizona. We are waiting until we are sure of out legal situation before proceeding to offer any services. We do have the equipment and staff to handle this sort of thing. The potential snag really is the state government, but we are working on that. Currently we are planning to use an HPLC method for potency testing. We haven't yet decided on how to proceed with pesticide or other contaminant testing.
More later, folks.
(BTW I've been here before, but under my own, personal account. Actually it's weird working for a company with what might turn out to be a government sanctioned interest in all of this. Down the rabbit hole!)
More later, folks.
(BTW I've been here before, but under my own, personal account. Actually it's weird working for a company with what might turn out to be a government sanctioned interest in all of this. Down the rabbit hole!)
FlowerTops
Member
It would be cool to buy pot that not only labels the thc% but also the terpenoid profile.
BTW which terpenoids are associated with that great sativa high, and is it possible to brreed them into peaking with earlier flowering strains?
BTW which terpenoids are associated with that great sativa high, and is it possible to brreed them into peaking with earlier flowering strains?
- I haven't read that paper in a long time
- I should have explained better when I said “kind of high” and “all pot”… Because I agree other Cannabinids and Terpenes will modulate the effects, which I notice absolutely, but for me, those effects are typically much more subtle with most commercial strains I find on the market.
- I should further qualify my previous statement by saying that for me, and tolerance I am sure is a factor too, even seemly good pot tends to appear mostly the same in terms of general feeling, which makes sense to me because most of what is effecting us (me) is THC and that will always have a “baseline” experience;
- Onset has distinct general physical alterations, like slight pressure on the temples, forehead, or other areas of the body. Smoking will procure a speedy “rush” effect as the compounds within the plant take hold, and as the “high” wanes, drowsiness ensues. Tolerance builds to a strain over time. The time from rush to drowsy (and the strength and presence or lack of either of these), I attribute to varying Cannabinoid and Terpenoid levels in the strains I am smoking (and tolerance).
- Very rarely there will be strains that are mostly all rush (or is that rather simply lack of a "down"), and am I mistaking "rush" for psychedelic, and the similarities and differences between the two (as some pot is certainly on the psychedelic side, like ak-47, and northern lights has this bonkers side to it, I don't know if I would say it had that "rush" though.. More like "blackout" or "blinkout"), and others too with no appreciable tolerance effect (afgooey haze), or both (mostly rush and no tolerance buildup, bubblegum seems to have this). But usually the effects with most pot are extremely subtle and subjective, which is why I made a point that I could better tell a strain by smell and taste than how it makes me feel from the “high”.
-What I really should have done is proofread better, I was rushed in my last round of posts, and had posted a lot, which I should have gone over more, but I had been wanting to get responses back out in some timely fashion.
- I think, further thinking this through, is that what I mean with saying “all pot” has a “kind of high” that “is the same”, is that in general, all pot puts me in that same general place, and has distinct feelings as compared to other drugs and entheogens that have their own set of reactions and associated feelings. Terpeniods modulate these effects, but the effect is still one of being under Cannabis, I can typically always tell the difference between a Cannabis "high" and a "high" from any other drug, no matter the varying constituents in the Cannabis (like for instance, Cannabis versus alcohol or Salvia).
- This is all a large part of my ongoing lifelong study, I am happy to find out new things and change my ideas as I go along; that’s the beauty of ideas, they are malleable. I am much more apprehensive of beliefs.
- See how much trouble I get in for one little sentence
- For me the difference in terpenoids, the speedy feeling or couchlock, is more subtle. I tend to feel speedy upon onset, and as time goes on, I will become drowsy. But there are more feelings being influenced by the other Cannabinoids and terpenoids than just "speedy" and "couchlock" I agree, though they are generally much more difficult to pin point and put a finger on, feelings of clarity of thought, rush of thoughts, pain relief, psychedelic qualities, feelings of pressure, etc. are difficult to describe because of their subjectivity.
- My best clarification is that all pot is the same to me, in that all pot brings me to this.. Place… No.. Rather its like a connect and disconnect. All pot dissolves a veil existing somewhere between my perception and reality that typically is unseen, from whence I can feel the flow of all the universe around me again, when usually not under the effects, I cannot feel such... That pressure, from all angles flowing back inward and outward, a subtle touch, a tickle reminding me my place within this place. Yeah, right
- That is more what I meant, and also too, it is those really elite strains that seasoned smokers can set apart from the generic commercial bud they encounter, even though that pot may be very good, it still doesn't have that "beyond" quality that is found with some strains. Any new strain will give a new effect as compared to another strain previously smoked and grown tolerant too, but that strain too will generally procure tolerance and thus the cycle for better and better weed continues
swimming_whale
New member
I stumbled upon a rather insightful review regarding cannabinoids produced by plants not belonging to the Cannabaceae. Most interesting are the sections about terpenes and polyphenols. Forgive me if it was mentioned earlier, but my current workload doesn't allow me to read through the whole post.
By the way Sam, I hope you have your experiments well documented, because as anecdotal as it may be, the could contain very valuable data. Do you have tested beta-caryophyllene?
Gertsch, Pertwee, Di Marzo: Phytocannabinoids beyond the Cannabis plant – do they exist?. British Journal of Pharmacology (2010), 160, 523–529
"The bicyclic sesquiterpene, b-caryophyllene (trans-isomer)
(Table 2), which is a plant volatile very frequently found in
plants, has been shown to selectively target the CB2 receptor
at nM concentrations (Ki = 155 nM) and to act as a full agonist
(Gertsch et al., 2008). Remarkably, b-caryophyllene is also a
major compound in Cannabis sativa L. essential oil. Thus,
Cannabis produces two entirely different chemical scaffolds
able to differentially target CB receptors. While studies on the
pharmacokinetics of b-caryophyllene are still ongoing, it is
already clear that this cyclobutane-ring containing terpene is
readily bioavailable, and, unlike many polyphenolic natural
products, is not metabolized immediately but shows a Tmax
>1 h after one single oral administration (J.G., unpublished
data). Orally administed b-caryophyllene (<5 mg·kg-1
) produces strong anti-inflammatory and analgesic effects in wild-
type mice but not in CB2 receptor knockout mice, which is a
clear indication that it may be a functional CB2 ligand.
Ongoing studies show that b-caryophyllene is effective at
reducing neuropathic pain in a CB2 receptor-dependent
manner (Zimmer et al., 2009). Therefore, the FDA approved
food additive b-caryophyllene has the potential to become an
attractive candidate for clinical trials targeting the CB2 receptor (Gertsch, 2008). Interestingly, the diterpene salvinorin A
from Salvia divinorum Epling & Jativa-M (Table 1) has been
reported to be a selective high-affinity kappa-opioid receptor
(KOP) agonist, but recent data also suggest that itmay interact
with a putative CB receptor/KOP heterodimer which may be
formed during inflammatory conditions (Fichna et al., 2009)."
By the way Sam, I hope you have your experiments well documented, because as anecdotal as it may be, the could contain very valuable data. Do you have tested beta-caryophyllene?
Gertsch, Pertwee, Di Marzo: Phytocannabinoids beyond the Cannabis plant – do they exist?. British Journal of Pharmacology (2010), 160, 523–529
"The bicyclic sesquiterpene, b-caryophyllene (trans-isomer)
(Table 2), which is a plant volatile very frequently found in
plants, has been shown to selectively target the CB2 receptor
at nM concentrations (Ki = 155 nM) and to act as a full agonist
(Gertsch et al., 2008). Remarkably, b-caryophyllene is also a
major compound in Cannabis sativa L. essential oil. Thus,
Cannabis produces two entirely different chemical scaffolds
able to differentially target CB receptors. While studies on the
pharmacokinetics of b-caryophyllene are still ongoing, it is
already clear that this cyclobutane-ring containing terpene is
readily bioavailable, and, unlike many polyphenolic natural
products, is not metabolized immediately but shows a Tmax
>1 h after one single oral administration (J.G., unpublished
data). Orally administed b-caryophyllene (<5 mg·kg-1
) produces strong anti-inflammatory and analgesic effects in wild-
type mice but not in CB2 receptor knockout mice, which is a
clear indication that it may be a functional CB2 ligand.
Ongoing studies show that b-caryophyllene is effective at
reducing neuropathic pain in a CB2 receptor-dependent
manner (Zimmer et al., 2009). Therefore, the FDA approved
food additive b-caryophyllene has the potential to become an
attractive candidate for clinical trials targeting the CB2 receptor (Gertsch, 2008). Interestingly, the diterpene salvinorin A
from Salvia divinorum Epling & Jativa-M (Table 1) has been
reported to be a selective high-affinity kappa-opioid receptor
(KOP) agonist, but recent data also suggest that itmay interact
with a putative CB receptor/KOP heterodimer which may be
formed during inflammatory conditions (Fichna et al., 2009)."
Hey swimming whale, yeah I am pretty sure I posted up that study earlier. No worries though
It was pretty formal, with an organoleptic survey with about 100 questions filled in before and after each test, only one test per day, before any subject smoked anything that day, more then a dozen subjects. Everything was weighed to .1 mg. accuracy. Tested in a Volcano.
It was double blind, neither the subjects or the testers knew what was being tried. We tried about a dozen Terpenes, and 6 pure Cannabinoids alone, and in combinations. No one involved in the tests doubted that terpenes changed, modified, and in some cases improved THC by modifying the effects and making it stronger. Yes we tried beta-caryophyllene.
The most surprising to most subjects was that 25 mg 100% pure THC is not as good or as strong as 25 mg of great resin rich in terpenes but only 50% THC by weight.
-SamS
It was double blind, neither the subjects or the testers knew what was being tried. We tried about a dozen Terpenes, and 6 pure Cannabinoids alone, and in combinations. No one involved in the tests doubted that terpenes changed, modified, and in some cases improved THC by modifying the effects and making it stronger. Yes we tried beta-caryophyllene.
The most surprising to most subjects was that 25 mg 100% pure THC is not as good or as strong as 25 mg of great resin rich in terpenes but only 50% THC by weight.
-SamS
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D
decarboxylator
it should be no surprise that natural medicine has greater efficacy. I think you meant 25 mg (not ml) for both.
madscientist81
Member
Hello all. I'm not sure if anyone is still adding to this thread since the last post was in March. Either way though, I really love the general idea of this thread and the topics and content that has been specifically discussed. Being a neuroscience and pharmacology researcher, I could provide a few thoughts/references regarding a couple things. Naturally, and in the spirit of the thread, if I have made any errors please feel free to point out. If I have added anything redundant or already posted, my apologies. Here we go...
1.)Some non-CB1/non-CB2 receptor effects of certain cannabinoids can be non-receptor mediated (i.e THC and CBD being antioxidants) but as far as other important receptors for Endo/Phyto/Synthetic cannabinoids, one that has only recently been investigated is GPR55. Important for our discussion, THC binds to GPR55 and I believe CBD may be a GPR55 antagonist. GPR55 is an orphan GPCR(G protein coupled receptor) that was discovered by Big Pharma when fishing for novel ligands with medical applications. I have kept a vigilent eye on pubmed for any new papers on this receptor's role in physiology and there have thus far only been a few which I will post below.
Then of course there is TRPV1, which is mainly a CBD thing.
Also as far as a correlation between neurochemistry and subjective effects of cannabis/cannabinoids etc, there is a lot of crosstalk between the cannabinoid system and the opioid system. In certain systems, THC can augment opiate function of the u-opiate receptor (the euphoric one) and in other instances can augment the K-opiate receptor (the dysphoric one). This effect is dose dependent and biphasic (as are many of the effects of cannabis). Low doses may be more anxiolytic/euphoric which would relate to the u-opiate system, and higher doses with potential anxiety/paranoia may be related to K-opiate system. As far as terpenes and opiates, I believe that Myrcene has shown some mild opiate activity in vivo and in vitro.
Another biphasic effect neurochemically (and perhaps also cognitive/subjective wise) is the cholinergic system. Low doses of THC augment the release of acetylcholine in the hippocampus, while high doses inhibit release. Related to terpenes, many of them (such as a-pinene) are acetylcholinesterase inhibitors.
Ok I have a few refs posted below, the rest I'm still looking for(but I know I have them all).
1.)Some non-CB1/non-CB2 receptor effects of certain cannabinoids can be non-receptor mediated (i.e THC and CBD being antioxidants) but as far as other important receptors for Endo/Phyto/Synthetic cannabinoids, one that has only recently been investigated is GPR55. Important for our discussion, THC binds to GPR55 and I believe CBD may be a GPR55 antagonist. GPR55 is an orphan GPCR(G protein coupled receptor) that was discovered by Big Pharma when fishing for novel ligands with medical applications. I have kept a vigilent eye on pubmed for any new papers on this receptor's role in physiology and there have thus far only been a few which I will post below.
Then of course there is TRPV1, which is mainly a CBD thing.
Also as far as a correlation between neurochemistry and subjective effects of cannabis/cannabinoids etc, there is a lot of crosstalk between the cannabinoid system and the opioid system. In certain systems, THC can augment opiate function of the u-opiate receptor (the euphoric one) and in other instances can augment the K-opiate receptor (the dysphoric one). This effect is dose dependent and biphasic (as are many of the effects of cannabis). Low doses may be more anxiolytic/euphoric which would relate to the u-opiate system, and higher doses with potential anxiety/paranoia may be related to K-opiate system. As far as terpenes and opiates, I believe that Myrcene has shown some mild opiate activity in vivo and in vitro.
Another biphasic effect neurochemically (and perhaps also cognitive/subjective wise) is the cholinergic system. Low doses of THC augment the release of acetylcholine in the hippocampus, while high doses inhibit release. Related to terpenes, many of them (such as a-pinene) are acetylcholinesterase inhibitors.
Ok I have a few refs posted below, the rest I'm still looking for(but I know I have them all).
frikn squirrel
Member
Great Thread! Thanks to all who contributed!
G
Godless
This amazing thread begs the question: what is the vaporization temperature of the terpines in cannabis?
-Edit-
Smoked a bowl of and the implications incremented exponentially!
Allow me to revise:
This amazing thread begs a million questions
Some prominent ones for me now:
What are the vaporization temperatures of the various terpines in cannabis? Is this known?
Is it possible for the "common man" to to acquire isolated terpines?
Sam, have you added non-cannabis generated, but cannabis present and prominent terpines to pure THC? If so, Same effect?
THC + terpines/cannaboids consumed simultaneously = high modified by the terpine. Have you examined the effect of pure THC from different plants? Specifically looking at differences like picking early/late, using early maturing/late maturing strains? Or maybe those details just modify the cannaboids and terpines?
Sam, immense respect for your explorations and even more for your willingness to share costly information - truly first class!
-Edit-
Smoked a bowl of and the implications incremented exponentially!
Allow me to revise:
This amazing thread begs a million questions
Some prominent ones for me now:
What are the vaporization temperatures of the various terpines in cannabis? Is this known?
Is it possible for the "common man" to to acquire isolated terpines?
Sam, have you added non-cannabis generated, but cannabis present and prominent terpines to pure THC? If so, Same effect?
THC + terpines/cannaboids consumed simultaneously = high modified by the terpine. Have you examined the effect of pure THC from different plants? Specifically looking at differences like picking early/late, using early maturing/late maturing strains? Or maybe those details just modify the cannaboids and terpines?
Sam, immense respect for your explorations and even more for your willingness to share costly information - truly first class!
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Sam_Skunkman: your comment on THC and THC mixed with other stuff.
I do hexane extractions. The wash time for optimum THC (85%) is 45 seconds at -10 degrees F. But many years back I started using 120 seconds at room temp, giving 60% THC and more "stuff". I would think about it occasionally and come up with all sorts of reasons I was diluting my drug. Never occurred to me that other fragments would enhance or change the effect of the THC. But it always just felt better at 60% and now I know it isn't me being mental, thanks for the post.
:kitty:
I do hexane extractions. The wash time for optimum THC (85%) is 45 seconds at -10 degrees F. But many years back I started using 120 seconds at room temp, giving 60% THC and more "stuff". I would think about it occasionally and come up with all sorts of reasons I was diluting my drug. Never occurred to me that other fragments would enhance or change the effect of the THC. But it always just felt better at 60% and now I know it isn't me being mental, thanks for the post.
:kitty:
there is a process where you separate, to an extent, certain cannabinoids using a specific temperature for each individual group.
Steam-distillation I know, protects them from boiling. Boil, as in a nucleated bubble, which hot air would do in normal pressure.
Therefore the function of the pressure and temperature would be key in separation also, of course.
Steam-distillation I know, protects them from boiling. Boil, as in a nucleated bubble, which hot air would do in normal pressure.
Therefore the function of the pressure and temperature would be key in separation also, of course.
greenpenguin
Active member
Thanks to everyone who has contributed to this thread, it's an incredibly interesting and informative read.
I have a few questions based on some topics brought up throughout this thread, and note I'm a layman and have no scientific background so please be nice
I've always understood (or possibly misunderstood) that curing cannabis after drying will:
* allow the slow escape of moisture.
* allow chlorophyll to break down for a smoother smoke.
* allow for decarboxylation of THCA to THC where COOH is removed.
* allow chemical changes in terpenoids/flavonoids to occur to refine the effect and flavor.
All in the name of creating a better product. I've also known that heating the THCA during consumption (either vaporization or burning) will covert it to THC via immediate decarboxylation so do we really care about that aspect of curing?
I always assumed that maybe by burning/vaporizing we don't decarboxylate all of it so curing allows more of it to be readily available thus increasing potency. Am I completely wrong?
Also has anyone done GC tests before and after curing to see changes in levels of THCA and THC? How about terpenoid profile before and after?
SamS, I'm curious since you mention that only THC got you "high", I'm curious since you tested pure forms of various cannabinoids and terpenoids, can you comment on the effects felt if any from the other cannabinoids/terpenoids in their pure forms?
Also there's been some discussion on about CBD and counteractive effects on THC. I've long used high cbd or mellow cultivars (see that spurr?), which I assumed have higher CBD:THC ratios, to counteract ill effects of high anxiety and stressful cultivars. I've always wondered about doing the same to counteract effects of edibles when they're too potent. I believe it should work the same but whenever I have edibles that are tripping me out bad I'm too scared to try it even though I feel like it will help.
I heard that with edibles the liver converts the delta-9 THC to delta-11 THC which affects you differently than delta-9, if this is true does the different delta bond somehow change the effect?
Also, I don't quite understand the mechanism in which THC and CBD affect us differently, and this is probably due to my lack of knowledge in neurochemistry. Lets say you have a bunch of CB1 and CB2 recepters and introduce THC or CBD. Someone here said CBD doesn't bind well to CB1 recepters and better to CB2, so is it the different recepters that they bind to that changes their effects in the brain? Or if THC binded to the same recepter as CBD would they have the same effects?
I've read lots of misinformation out there and i'm hoping get some information.
I have a few questions based on some topics brought up throughout this thread, and note I'm a layman and have no scientific background so please be nice
I've always understood (or possibly misunderstood) that curing cannabis after drying will:
* allow the slow escape of moisture.
* allow chlorophyll to break down for a smoother smoke.
* allow for decarboxylation of THCA to THC where COOH is removed.
* allow chemical changes in terpenoids/flavonoids to occur to refine the effect and flavor.
All in the name of creating a better product. I've also known that heating the THCA during consumption (either vaporization or burning) will covert it to THC via immediate decarboxylation so do we really care about that aspect of curing?
I always assumed that maybe by burning/vaporizing we don't decarboxylate all of it so curing allows more of it to be readily available thus increasing potency. Am I completely wrong?
Also has anyone done GC tests before and after curing to see changes in levels of THCA and THC? How about terpenoid profile before and after?
SamS, I'm curious since you mention that only THC got you "high", I'm curious since you tested pure forms of various cannabinoids and terpenoids, can you comment on the effects felt if any from the other cannabinoids/terpenoids in their pure forms?
Also there's been some discussion on about CBD and counteractive effects on THC. I've long used high cbd or mellow cultivars (see that spurr?), which I assumed have higher CBD:THC ratios, to counteract ill effects of high anxiety and stressful cultivars. I've always wondered about doing the same to counteract effects of edibles when they're too potent. I believe it should work the same but whenever I have edibles that are tripping me out bad I'm too scared to try it even though I feel like it will help.
I heard that with edibles the liver converts the delta-9 THC to delta-11 THC which affects you differently than delta-9, if this is true does the different delta bond somehow change the effect?
Also, I don't quite understand the mechanism in which THC and CBD affect us differently, and this is probably due to my lack of knowledge in neurochemistry. Lets say you have a bunch of CB1 and CB2 recepters and introduce THC or CBD. Someone here said CBD doesn't bind well to CB1 recepters and better to CB2, so is it the different recepters that they bind to that changes their effects in the brain? Or if THC binded to the same recepter as CBD would they have the same effects?
I've read lots of misinformation out there and i'm hoping get some information.
