The Entourage: One Of The Many Missing Pieces To The Puzzle

[in vivo]

Amnesia (haze x nl) Review:

 

Method of consumption being reviewed: Smoked

 

The period of the day you use this strain the most: Day or Evening

 

List of some of the effects that I feel feel describe this strain:

 

Anxious, Creative, Disorientating, Dizzy, Dry Eyes, Energetic, Euphoric, Expectorant, Focused, Giggly, Happy, Paranoid, Positive, Talkative Tingly, Therapeutic (depression?), Uplifted

 

List of aromas that I associate with this strain:

 

Pungent, Super Sweet, Flowery, Slightly Astringent, with just a hint of skunk.

 

Amnesia (haze x nl) is claimed to be "90% sativa". This was my first round with it. It's currently a daytime favorite amongst patients. I'd say it sort of gets the creative juices flowing, but doesn't cause a 'nap crash' like many strains seem to after the initial peak stabilizes. I often find that strains have what I would refer to as stages or layers in relation to the psychoactive effects. Many times a strain can be 'headie' initially, but then fades into a more sedative like effect, which I associate with good pain relief and muscle relaxation. That's one of the reasons I like the hindu so much, because it has a 'layered effect' that isn't too extreme in any regard, but is really enjoyable. Amnesia seems more headie overall. I wouldn't recommend it to a non seasoned  patient. It'd be the kind of strain that might cause a person to have a panic attack, imo. 

 

Let's look at why that may be: 

 

 

 

 

Edited March 13, 2014 by in vivo

[Restorium2]

What method of ingestion are you speaking of?  Makes all the difference.

[in vivo]

You are absolutely correct. My apologies (reviews and methods added). I'm rather lazy and don't like the hassle of vapes, and I'm more of a bubble guy than oil, so I primarily smoke. We should setup a format like erowid, or other similar sites to more accurately account for variables. I think that will help a great deal in terms of associating effects to individual, or combinations of compounds. I wish i was better at providing descriptions, but I seem to struggle with it. I just got off the phone with another patient that has many of these genetics as well. They agreed to come into this thread and provide their reports on the psychoactive and therapeutic effects of these strains. I might encourage other patients to do so as well. I'm just as interested in that as I am in learning how to take a more systematical approach to cannabinoid based therapies.  

 

What I find interesting about this profile is that the second most prominent cannabinoid is CBC, then CBG, but moreso that it was over 20% delta9 in combination with what seems like a particularly low CBD content. CBD is a CB1 and CB2 agonist blocker. The theory is that the higher CBD ratio, the lower the psychoactive effect. Maybe that's partly why it's what I consider 'headie'.

 

The terpenes might offer another explanation. It looks like it's primarily limonene and myrcene. I had guessed that there was linalool in it. I was wrong. It's limonene instead of linalool. My being wrong about that was of little surprise to me, but the high levels of myrcene are. That's supposed to add to the 'couch lock', or muscle fatigue/relaxation effect. It's a sedative on its own. That makes me wonder if limonene can counter that. I believe it does. It also makes me wonder if breeders overseas know more about terpenes than they let on. Have they already recognized that limonene might add to the 'sativa' like effect, saw some chemotypes close to 90% limonene, and call it 90% sativa? I'm not saying they did mind you. This is simply what comes to mind.

 

I will say that some muscle fatigue seems noticeable after smoking amnesia all day, but the same can be said about any strain.  

Edited March 13, 2014 by in vivo

[in vivo]

DOSE:

T+ 0:00 200mg oral m. extract powder

T+ 1:05 cup of coffee oral  caffeine (liquid)

T+ 1:10 bowl of amnesia smoked  profile above dried flowers

T+ 1:24 other meds        etc  etc

T+ 2:53 etc        

T+ 6:00        

 

Here's an example of what might help with descriptions.

 

(It was a table, but that apparently got lost when it was posted.)

Edited March 5, 2014 by in vivo

[in vivo]

CBC is a TRPA1 agonist

 

 

Background and Purpose

The non-psychotropic cannabinoid cannabichromene is known to activate the transient receptor potential ankyrin-type1 (TRPA1) and to inhibit endocannabinoid inactivation, both of which are involved in inflammatory processes. We examined here the effects of this phytocannabinoid on peritoneal macrophages and its efficacy in an experimental model of colitis.

Experimental Approach

Murine peritoneal macrophages were activated in vitro by LPS. Nitrite levels were measured using a fluorescent assay; inducible nitric oxide (iNOS), cyclooxygenase-2 (COX-2) and cannabinoid (CB₁ and CB₂) receptors were analysed by RT-PCR (and/or Western blot analysis); colitis was induced by dinitrobenzene sulphonic acid (DNBS). Endocannabinoid (anandamide and 2-arachidonoylglycerol), palmitoylethanolamide and oleoylethanolamide levels were measured by liquid chromatography-mass spectrometry. Colonic inflammation was assessed by evaluating the myeloperoxidase activity as well as by histology and immunohistochemistry.

Key Results

LPS caused a significant production of nitrites, associated to up-regulation of anandamide, iNOS, COX-2, CB₁ receptors and down-regulation of CB₂ receptors mRNA expression. Cannabichromene significantly reduced LPS-stimulated nitrite levels, and its effect was mimicked by cannabinoid receptor and TRPA1 agonists (carvacrol and cinnamaldehyde) and enhanced by CB₁ receptor antagonists. LPS-induced anandamide, iNOS, COX-2 and cannabinoid receptor changes were not significantly modified by cannabichromene, which, however, increased oleoylethanolamide levels. In vivo, cannabichromene ameliorated DNBS-induced colonic inflammation, as revealed by histology, immunohistochemistry and myeloperoxidase activity.

Conclusion and Implications

Cannabichromene exerts anti-inflammatory actions in activated macrophages – with tonic CB₁ cannabinoid signalling being negatively coupled to this effect – and ameliorates experimental murine colitis.

 

http://onlinelibrary.wiley.com/doi/10.1111/bph.12120/full

 

 

It's got anti-inflammatory properties not associated with CB1 or TRPA1.

 

 

Abstract

BACKGROUND AND PURPOSE Cannabichromene (CBC) is a major non-psychotropic phytocannabinoid that inhibits endocannabinoid inactivation and activates the transient receptor potential ankyrin-1 (TRPA1). Both endocannabinoids and TRPA1 may modulate gastrointestinal motility. Here, we investigated the effect of CBC on mouse intestinal motility in physiological and pathological states.

 

EXPERIMENTAL APPROACH Inflammation was induced in the mouse small intestine by croton oil. Endocannabinoid (anandamide and 2-arachidonoyl glycerol), palmitoylethanolamide and oleoylethanolamide levels were measured by liquid chromatography-mass spectrometry; TRPA1 and cannabinoid receptors were analysed by quantitative RT-PCR; upper gastrointestinal transit, colonic propulsion and whole gut transit were evaluated in vivo; contractility was evaluated in vitro by stimulating the isolated ileum, in an organ bath, with ACh or electrical field stimulation (EFS).

 

KEY RESULTS Croton oil administration was associated with decreased levels of anandamide (but not 2-arachidonoyl glycerol) and palmitoylethanolamide, up-regulation of TRPA1 and CB₁ receptors and down-regulation of CB₂ receptors. Ex vivo CBC did not change endocannabinoid levels, but it altered the mRNA expression of TRPA1 and cannabinoid receptors. In vivo, CBC did not affect motility in control mice, but normalized croton oil-induced hypermotility. In vitro, CBC reduced preferentially EFS- versus ACh-induced contractions. Both in vitro and in vivo, the inhibitory effect of CBC was not modified by cannabinoid or TRPA1 receptor antagonists.

 

CONCLUSION AND IMPLICATIONS CBC selectively reduces inflammation-induced hypermotility in vivo in a manner that is not dependent on cannabinoid receptors or TRPA1.

 

http://onlinelibrary.wiley.com/doi/10.1111/j.1476-5381.2012.01879.x/full

 

And we may have a winner:

 

 

 

Abstract

In contrast to the numerous reports on the pharmacological effects of Δ⁹-tetrahydrocannabinol (THC), the pharmacological activity of another substituent of Cannabis sativa, cannabichromene (CBC) remains comparatively unknown. In the present study, we investigated whether CBC elicits cannabinoid activity in the tetrad assay, which consists of the following four endpoints: hypomotility, antinociception, catalepsy, and hypothermia. Because cannabinoids are well documented to possess anti-inflammatory properties, we examined CBC, THC, and combination of both phytocannabinoids in the lipopolysaccharide (LPS) paw edema assay. CBC elicited activity in the tetrad that was not blocked by the CB₁ receptor antagonist, rimonabant. Moreover, a behaviorally inactive dose of THC augmented the effects of CBC in the tetrad that was associated with an increase in THC brain concentrations. Both CBC and THC elicited dose-dependent anti-inflammatory effects in the LPS-induced paw edema model. The CB₂ receptor, SR144528 blocked the anti-edematous actions of THC, but not those produced by CBC. Isobolographic analysis revealed that the anti-edematous effects of these cannabinoids in combination were additive. Although CBC produced pharmacological effects, unlike THC, its underlying mechanism of action did not involve CB₁ or CB₂ receptors. In addition, there was evidence of a possible pharmacokinetic component in which CBC dose-dependently increased THC brain levels following an i.v. injection of 0.3 mg/kg THC. In conclusion, CBC produced a subset of behavioral activity in the tetrad assay and reduced LPS-induced paw edema through a noncannabinoid receptor mechanism of action. These effects were augmented when CBC and THC were co-administered.

 

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2967639/

 

That's awesome. CBC might increase the bioavailability of THC. I'm gonna have to read that one more closely. (Looks like it competes with THC and potentially pushes more of it into the brain. Highlighted in quote below.)

Edited March 5, 2014 by in vivo

[in vivo]

“drug type” marijuana primarily contained higher concentrations of CBC than CBD, while “fiber type” marijuana contained higher concentrations of CBD than CBC. This classification of “drug type” or “fiber type” marijuana is related to some strains of marijuana that have more potent psychotropic effects compared to other strains that cultivated as hemp for their fiber. While CBC is the second most abundant cannabinoid in some strains of marijuana growing in the United States (Brown et al., 1990), it represents 0.3% of the constituents from confiscated cannabis preparations (Mehmedic, et al., 2010).

 

CBC was shown to have analgesic properties and potentiated the analgesic effects of THC in the mouse tail-flick assay (Davis et al., 1983). It also was found to prolong hexabarbital-induced hypnosis (Hatoum et al., 1981). In addition, it potentiated bradycardia caused by THC, though it did not induce bradycardia on its own (O'Neil et al., 1979)

 

Dunnett’s post hoc analysis (p<0.05) revealed that THC (3 and 10 mg/kg) and CBC (100 mg/kg) produced significant locomotor suppression, catalepsy, and hypothermia compared to vehicle control mice. However, in this experiment, CBC did not elevate tail-flick latencies, though THC (1, 3, and 10 mg/kg) produced significant antinociception.

 

In contrast, there were no significant main effects of rimonabant or interactions between CBC and rimonabant for any of the four dependent ³ measures, indicating that CBC produces these pharmacological effects through a non CB₁ receptor mechanism of action.

 

In order to test whether the enhanced pharmacological results occurred because of a pharmacokinetic interaction, we quantified blood and brain levels of CBC and THC given in combination. Although the behaviorally inactive dose of THC did not significantly alter CBC blood or brain concentrations, 30 or 100 mg/kg CBC led to significantly elevated THC levels in brain, but did not quite achieve statistical significance in affecting THC blood levels (p<0.07). These results suggest that THC had distributed out of the blood and into lipophilic matrices, such as brain, which is consistent with the reported pharmacokinetics of THC and its rapid distribution phase (Grotenhermen, 2003). About 90% of THC in blood is bound to plasma (10% to red blood cells) and 95 – 99% of plasma THC is bound to lipoproteins (Hunt et al., 1980; Widman et al., 1974). A high dose of CBC (30 or 100 mg/kg) may compete with THC (0.3 mg/kg) for the lipoprotein binding sites, which ultimately leads to the distribution of THC out of the blood and into lipophilic tissue such as the brain. Subsequently, the higher concentrations of THC in brain tissue might have interacted with CB₁ receptors to elicit significant tetrad activity. It is noteworthy that these same doses of CBC produced enhanced pharmacological effects when given in combination with the threshold dose of THC. Thus, it is plausible that a pharmacokinetic interaction between the two cannabinoids contributed to the leftward shift in the CBC dose response in the presence of 0.3 mg/kg THC. Taken together, these data suggest that high doses of CBC may augment a threshold dose of THC to produce significant cannabinoid activity in the tetrad.

 

However, neither rimonabant nor SR144528 ameliorated the anti-inflammatory effects of CBC, suggesting that the anti-edematous effects of this phytocannabinoid do not involve either CB₁ or CB₂ receptors.

 

 

4. Discussion

The degree to which constituents other than THC contribute to the overall pharmacological effects of marijuana, have pharmacological effects of their own, and interact with the pharmacological effects of THC remain important questions. Few of the phytocannabinoids present in marijuana have been extensively evaluated in established in vivo models indicative of cannabinoid activity, such as the mouse tetrad, which consists of four in vivo assays: locomotor activity, catalepsy, antinociception, and hypothermia (Fride, 2006). CBC is a phytocannabinoid found in most common strains of marijuana but can also occur in concentrations equal to that of THC (Brown et al., 1990; Holley et al., 1975; Turner et al., 1980)...

 

CBC produced significant pharmacological effects only when administered at a high dose (i.e., 100 mg/kg), which consistently produced locomotor suppression, catalepsy, and hypothermia, but only occasionally produced a small magnitude of antinociception. The observation that CBC sporadically produced antinociception may indicate that there is a different threshold dose needed to produce this effect compared to the other three indices. Other cannabinoids have been shown to have different thresholds or potencies within each measure that make up the tetrad assay. For example, anandamide, which is an endogenous cannabinoid, had similar ED₅₀ values for hypomotility, catalepsy, and hypothermia, but was 3 – 4 fold less potent in producing antinociception than the other measures after i.v. administration in wild type mice (Smith et al., 1994). In contrast, THC dose-dependently produced significant effects for each of the four measures, with high efficacy. These findings are consistent with previously reported tetrad effects of THC (Fan et al., 1994; Martin et al., 1991).

 

Considering the great disparity between mean percentages of THC (i.e., 8.8%) and CBC (i.e., 0.3%) from confiscated cannabis preparations seized in 2008 (Mehmedic, et al., 2010) as well as our observation that CBC is substantially less potent than THC in the tetrad, it is unlikely that CBC by itself relevantly contributes to the psychoactive effects of marijuana. This conclusion is in agreement with a previous study that reported the tetrad effects of marijuana were primarily accounted for by its THC content and not by the other constituents of this plant (Varvel et al., 2005). Another study that utilized human subjects varied the concentration of CBC in marijuana cigarettes and found that the CBC concentration in their cigarettes (0.01 – 2.31%) did not affect behavioral (cognitive tasks) or neurophysical measures (EEG, ERP) in the study (Ilan et al., 2005).

 

The CB₁ receptor antagonist, rimonabant failed to block the tetrad activity of CBC, indicating a non CB₁ receptor mechanism of action. These results are consistent with the observation that CBC possesses poor affinity to the CB₁ receptor (i.e., K_i value > 10,000 nM; Booker et al., 2009). In comparison, rimonabant has been reported to have a K_i value of 2 nM and has been shown to block the tetrad effects of THC and other cannabinoids (Compton et al., 1996; Rinaldi-Carmona et al., 1994; Wiley et al., 1998). Various noncannabinoid classes of drugs have also been shown to have partial tetrad effects including central nervous system depressants and anti-psychotics that were not blocked by rimonabant (Wiley et al., 2003). Because the tetrad effects of CBC were not blocked by a CB₁ receptor antagonist, the mechanism by which CBC elicited tetrad effects remains to be established in future studies.

 

Another objective of the present study was to examine whether a threshold dose of THC would modify the pharmacological actions of CBC in the tetrad. An inactive dose of THC (i.e., 0.3 mg/kg) was selected based on a dose-response study of this compound in the tetrad assay. Administration of this dose of THC produced leftward shifts in the CBC dose-response relationship for catalepsy, antinociception, and hypothermia; however it did not enhance CBC-induced locomotor suppression. In order to test whether the enhanced pharmacological results occurred because of a pharmacokinetic interaction, we quantified blood and brain levels of CBC and THC given in combination. Although the behaviorally inactive dose of THC did not significantly alter CBC blood or brain concentrations, 30 or 100 mg/kg CBC led to significantly elevated THC levels in brain, but did not quite achieve statistical significance in affecting THC blood levels (p<0.07). These results suggest that THC had distributed out of the blood and into lipophilic matrices, such as brain, which is consistent with the reported pharmacokinetics of THC and its rapid distribution phase (Grotenhermen, 2003). About 90% of THC in blood is bound to plasma (10% to red blood cells) and 95 – 99% of plasma THC is bound to lipoproteins (Hunt et al., 1980; Widman et al., 1974). A high dose of CBC (30 or 100 mg/kg) may compete with THC (0.3 mg/kg) for the lipoprotein binding sites, which ultimately leads to the distribution of THC out of the blood and into lipophilic tissue such as the brain. Subsequently, the higher concentrations of THC in brain tissue might have interacted with CB₁ receptors to elicit significant tetrad activity. It is noteworthy that these same doses of CBC produced enhanced pharmacological effects when given in combination with the threshold dose of THC. Thus, it is plausible that a pharmacokinetic interaction between the two cannabinoids contributed to the leftward shift in the CBC dose response in the presence of 0.3 mg/kg THC. Taken together, these data suggest that high doses of CBC may augment a threshold dose of THC to produce significant cannabinoid activity in the tetrad.

 

^^ They say it doesn't likely effect most strains, but they're basing that on 8.8% delta9 and .3% CBC samples. I wonder at which point the CBC and THC ratio/variable really play into one another.?  

 

 

In summary, CBC produced a subset of effects in the mouse tetrad assay and significantly reduced LPS-induced paw edema. Moreover, both of these effects were enhanced when CBC was given in combination with THC. The tetrad effects of CBC were not CB₁ receptor mediated and its anti-inflammatory effects were not CB₁ or CB₂ receptor mediated. In contrast, we determined that THC produced its anti-inflammatory effects in the LPS-induced paw edema model via CB₂ receptor activation, a finding that had not been previously reported in this assay. Isobolographic analysis indicated an additive relationship between the anti-inflammatory effects of CBC and THC. A threshold dose of THC augmented the tetrad effects of CBC. However, the observation that high doses of CBC led to increased brain levels of THC suggests a potential pharmacokinetic interaction for the augmented tetrad effects of the two drugs given in combination.

 

In conclusion, CBC produced a subset of behavioral activity in the tetrad assay and reduced LPS-induced paw edema through a noncannabinoid receptor mechanism of action. Moreover, combination of CBC and THC leads to enhanced tetrad and anti-inflammatory actions.

Edited March 5, 2014 by in vivo

[in vivo]

I'm not sure if I've linked this already, but it should be so I'm going to do it again. This is a study by Bedrocan examining plasma levels after smoking/vaping. That's not what I'm trying to point out though. They have very complete profiles of their chemotypes, and they expected to see a variance in the binding of cannabinoids based on the terpenes present. They didn't. That suggests that this isn't as much about unknown 'entourage variables' as it is additive effects of these terpenes via independent mechanisms. Many of these terpenes are highly researched. Now we just need to try and put the pieces of the puzzle together.  

 

Cannabinoid Receptor 1 Binding Activity and Quantitative Analysis of Cannabis sativa L. Smoke and Vapor

 

Conclusions
Our CB1 binding results verify previous reports in humans
which showed that the subjective psychoactive effects of
cannabis are primarily due to D9-THC content.28,29) Our results
demonstrate that any non-D9-THC components in
cannabis smoke and vapor are too dilute to have any significant
effects in vitro on CB1 binding. However there still exists
evidence that other components in cannabis extracts play
a role in the plants overall therapeutic effects.30—35) There has

even been considerable controversy over this issue.36,37) We
propose that any additional beneficial effects observed by patients
using cannabis are due to effects other then CB1 agonism.
Such benefits could come from other components in
cannabis that interact with the CB2 receptors or new potential
cannabinoid receptors such as the transient receptor potential
vanilloid 1.38)

Quantitative comparison of cannabis smoke and vapor
shows that vaporizing cannabis with the Volcano® is a more
reliable and safer administration form for the delivery of D9-
THC due to the lack of pyrolytic degradation and more efficient
D9-THC volatilization. Analysis of cannabis smoke and
vapor showed for the first time in a quantitative manner that
terpenoids are major components of the smoke and vapor of
3 medicinal cannabis varieties. Myrcene has analgesic and
anti-inflammatory properties which may contribute to the
medical benefits of cannabis. Other compounds identified in
our samples terpineol, terpinene-4-ol, g -terpinene, limonene
and a -pinene are acetylcholine esterase inhibitors that may
act by reducing acetylcholine deficits in the hippocampus induced
by D9-THC.39) Further research should be done to determine
whether or not terpenoids and other non-D9-THC
components of cannabis are contributing to the overall medical
benefits of herbal cannabis.

 

http://cpb.pharm.or.jp/cpb/201002/c02_0201.pdf?origin=publication_detail

Edited March 5, 2014 by in vivo

[in vivo]

Limonene

 

There's a slew of research on limonene, it's in a lot of citrus products. It looks like a considerable amount of the research on it is cancer related. I've got some citrus and I think grapefruit essential oil both of which the primary constituent is limonene. I liked the smell of those essential oils. After I read that thesis I went out and bought one of the essential oil infusers that you plug into the wall. That didn't work all that well, it dries out quickly and didn't permeate the room like some other oils. I probably still have one plugged in that's dry. 

 

I need to find it, but I believe I have a patent that uses limonene to increase the bioavailability of poorly water soluble lipids.

 

Safety evaluation and risk assessment of d-limonene

 

D-Limonene modulates T lymphocyte activity and viability

 

d-limonene suppresses doxorubicin-induced oxidative stress and inflammation via repression of COX-2, iNOS, and NFκB in kidneys of Wistar rats

 

D-Limonene modulates inflammation, oxidative stress and Ras-ERK pathway to inhibit murine skin tumorigenesis

 

Citrus aurantium L. essential oil exhibits anxiolytic-like activity mediated by 5-HT1A-receptors and reduces cholesterol after repeated oral treatment

 

Limonene inhibits methamphetamine-induced locomotor activity< i> via</i> regulation of 5-HT neuronal function and dopamine release

 

 

 

Here's one below that looks interesting.

 

Monoterpenes with analgesic activity—a systematic review

 

 

I'm gonna read that more closely. I can't link the full pdf, but if search that title on Google Scholar you can get the pdf. Same with some of those other ones. 

 

I'd like to make clear that I'm not suggesting current methods aren't efficient, or safe. They clearly are by in large. I'm saying we should be careful not to sell this plant short. The ECS is fundamental to health and disease, so much so that it seems laughable that it wasn't previously unraveled. This might be the biggest blunder in medical history that seems to be a direct result of political policies/agendas that aren't scientifically based at all. I don't want to get into politics here, but I thought I should make my position clear.   

Edited March 5, 2014 by in vivo

[earthling]

For being so chock-full of data, research, and other quantifiable, objective information, the responses to this thread in the last couple pages have unexpectedly veered toward anecdote and psuedoscience.  It may be that some of this information has hit too close to home, threatening deeply held beliefs, but when people's health is involved, it is incredibly important to keep conversations like this based in quantifiable, repeatable, experiments and evidence.

 

Yes this is my first post, and that first paragraph is quite bold, but this is real life.  People's lives and wellbeings are at stake.  The information they find here, if refined, can lead them to more effective treatment, or, if we rely on anecdote and hearsay they will be lost down a rabbit hole of home remedies based on old wives tales and technophobia. 

 

Yes, it is possible a certain aromatic bouquet may indicate certain medicinal qualities to an individual who has years of experience, but claiming this to be a reliable means of finding an effective treatment for someones debilitating illness is extraordinary, and we can all agree: The more extraordinary the claim being made, the more extraordinary the evidence must be in order for the claim to be considered worthy of further investigation.  Claims like these are where hypothesies are born, the clay they are molded from. These claims are the beginning, not the conclusion.

 

For me, this conversation is about elucidating the pharmacological functions of lesser known cannabis constituents, particularly terpenes, to increase the effectiveness of treatments based on medical marijuana.  If you can smell what works for you, great!  The fact you believe it is going to work will increase the therapy derived due solely to the placebo effect.  I for one am a huge fan of the placebo effect, since I generally have positive expectations.  Unfortunately for patients who are new to cannabis therapies, this is unlikely to be an easy skill to learn.

 

If we are to find effective and repeatable therapies, we need to use the tools of science.  It is important to remember that we are conversating through means that would seem magical if it were not based on repeatable, objective, science based concepts.  Science works.

 

One main reason science works is it gets around the tricks our brains play on themselves.  These tricks are known as cognitive biases(link).  We are not perfect biological computers, our noses are not highly precise analytical devices, microwaves do not emit black-magic death rays, and only through experiementation can we approach fact.  I try to perceive fact as unnobtainable so as to avoid false conclusions. 

 

I came here to give my own flimsy anecdotes regarding the strains in-vivo has been mentioning, and will do just that, beginning tomorrow. 

[in vivo]

edit

Edited March 12, 2014 by in vivo

[in vivo]

Ha!

 

Good to see you here. I'm not convinced about the microwaves.

[in vivo]

Apparently Sour OG is gonna have to wait. I can't get the cannabinoid ratio jpeg from their site. I'll have to hit them up tomorrow.

[in vivo]

I don't understand the seemingly adversarial positions. Perhaps whereas others may see a double edged sword, I see our only chance in the fight that is yet to come. 

 

 

earthling, on 05 Mar 2014 - 18:30, said:

Yes this is my first post, and that first paragraph is quite bold, but this is real life.  People's lives and wellbeings are at stake.  The information they find here, if refined, can lead them to more effective treatment, or, if we rely on anecdote and hearsay they will be lost down a rabbit hole of home remedies based on old wives tales and technophobia. 

This is also not true. If patients were to wait on science to tell them how to find relief with cannabis, they would be lost down a rabbit hole of unsubstantiated and incomplete, albeit fascinating, scientific papers. No relief in that, but lots of relief in old wives tales, so to speak.

 

I may be wrong on this. Perhaps reading these papers has really led a large number of patients to better results with their cannabis therapy. But I don't think so.

 

I believe it was the science behind the medicine that paved the way for prop 215. That and a heart wrenching story. To use the history of cannabis use as the argument seems odd. I mean, they used to chew and brew willow bark. Now we've developed new methods.

 

As to whether reading papers has helped patients, well, is the science used as justification to enact these laws? Yes. Bedrocan, GW Pharm, clinical trials for a number of phyto and synthetic cannabinoids. So yea, I'd say it has helped. Maybe my rambling hasn't done much good. But I'm some wook from the woods. I'd say those that have dedicated their lives to this field have helped a great deal.

 

Cannabis is a tremendous resource that's easily manipulated in short periods of time to develop specific chemotypes tailored to ones needs. That's the advantage over the machine. I don't care if they have 1000 chemotypes to chose from. It will never compare to the number of variations that can be created in the hands of the people. 

Edited March 6, 2014 by in vivo

[in vivo]

   I am just not of the opinion that the science is quite ready to fully explain what the whole plant can do for certain conditions, and that patients and their experience with the plant are crucial to the full understanding.

 

I like to think that's what this thread is all about.

 

I also do not believe that understanding of this material is crucial to using cannabis as medicine or a supplement.

 

That seems to imply that the majority of the therapeutic value that will ever be derived from cannabis is associated with high levels of delta9, and can be directly correlated to the psychoactive effects that have been bred into cannabis over the past 50 years. I simply don't see it that way. I think the plant is so valuable that it wouldn't matter which cannabinoid is most prominent, they all 'work'. It's knowing how they work that makes the difference. Can cannabis be used safely without knowing any of this? Absolutely. Is THC good for a number of ailments? Yes. But we've been breeding for psychoactivity not therapeutics. Do I believe that reading any of this makes me "know" how to approach a treatment? No. But I do believe it makes me a better guesser. The same can be true for anyone.

Edited March 6, 2014 by in vivo

[in vivo]

Cannatonic #4 Review:

 

I can't really give this a decent review. This was my first run with it. I smoked one bowl from the plant before extracting the rest. I had broken of a small branch about a week prior to cutting her down. When I went to harvest her I found it and it smelled delicious. I won't try to describe it without it right in front of me. I had already been smoking some amnesia, but I decided to fill a bowl of the cannatonic to see what it was like. I remember thinking that I liked the taste. It felt almost like a Vicodin coming on for maybe five minutes. It seemed pleasant. Then that turned to a sensation that's difficult to describe, I felt a little uncomfortable. Within about 30-45min I started to get a headache.

 

I wouldn't put too much stock into this review. The headache could have been a coincidence. I'll be able to provide a more complete review in a few weeks. It would be beneficial to see other reviews on this chemotype.

 

Here's the cannatonic 4 concentrate ratios:

 

 

 

I don't have a whole lot to say about it. The cannabinoids seem in line with what was expected. Some of the minors are a little higher than I've seen previous. I wish I would have had the flowers tested. I'd like to know the difference in ratios between an extract and the flowers it comes from. I'd also like to get some bubble tested. The ratios of terpenes seem even more likely to shift. The cannabinoid ratio overall appears similar to other results posted in MI, and on a site in CA I've been searching. The one thing I have noticed though is that in almost all of the other high CBD cannatonic strains, posted with terpene results in CA, are high in linalool. Linalool has anticonvulsant characteristics. This concentrate is high in maaliene. I can't find much info on it. I'll have to dig deeper.

 

Then equal parts phytol and beta-caryophyllene

 

Anticonvulsant effect of phytol in a pilocarpine model in mice

 

Anxiolytic-< i> like</i> effects of phytol: Possible involvement of GABAergic transmission

 

There's also anti-inflammatory and antioxidant characteristics. If these flowers are high in maaliene as well, I'd like to breed some linalool into this line. The Charolettes Web is also very high in linalool.  

Edited March 13, 2014 by in vivo

[in vivo]

Back in the day people used to think that every once in a while when cracking beans you'd get a 'dud'. You'd grow it out, it looks good, it smells good, but if it doesn't elicit the response you were seeking you'd call that a waste of time. Not because the individual thought that it just didn't 'work' for them, but because they didn't think it would 'work' for anybody. Today if I got a 'dud' I'd call that exciting. Not because I don't value delta9, but because I value all of it, and now have the means of differentiating between them so that I might identify what ailments it could be best suited for.

 

I guess I'd use cannatonic 4 as my example. Prior to knowing about the medicinal value of CBD, that plant would have never made into my flower twice. Now I know better.

Edited March 6, 2014 by in vivo

[in vivo]

Something I'm interested in doing is procuring concentrate high in CBC. Sessile trichomes are high in CBC and CBG. It's been shown that any plant high in delta9 can be taken out of veg, extracted via bubble bags to get a concentrate high in CBC and CBG. Nothing special to it. You run all the bags and capture only the 25. That's where all the little sessile trichomes add up.

 

I was looking for the plant with the highest delta9 content to do this. Now that I see the Amnesia is over 20% delta9 and the second highest is CBC at 1.64%, I've decided to use that one instead.

 

This was discussed previously in these threads:

http://michiganmedicalmarijuana.org/topic/44032-gw-pharmaceuticals-supported-thesis-on-growing/?hl=thesis

http://michiganmedicalmarijuana.org/topic/44323-gw-pharma-cbc-patent/?view=findpost&p=458980&hl=thesis

[Restorium2]

CBC's relatively high boiling point could be used to isolate it in an oil. In other words, take any extract that has CBC and cook it at just under 428 F and you will have an extract that has a high ratio of CBC.

[in vivo]

I'm sorry that it seems so difficult for you to accept facts that contradict your worldview. It's a part of life. You can learn to accept that and continue to evolve, or continue displaying the type of behavior that you have here. I just ask that you please refrain from trolling my threads.

 

For anyone reading please disregard anything Rev says. He apparently has taken issue to me, and this thread, and seems intent on derailing it. Fortunately for you, I see his display as an example of why this thread is so important. 

[trichcycler]

can we ignore the fact that every test conducted from different areas of every plant will report varying amounts of compounds? I know that one garden can produce a rotten meat fuely skunky profiled plant while the same plant in another garden could show none of those traits, depending on environmental factors and grow habits? I've smelled and tasted samples that smelled and tasted just like the dank basement they were grown in, and a clone of it smells of sexy goodness grown elsewhere, surely reporting different terpenes and very likely many differing compounds.

Something I'm interested in doing is procuring concentrate high in CBC. Sessile trichomes are high in CBC and CBG. It's been shown that any plant high in delta9 can be taken out of veg, extracted via bubble bags to get a concentrate high in CBC and CBG. Nothing special to it. You run all the bags and capture only the 25. That's where all the little sessile trichomes add up.

 

I was looking for the plant with the highest delta9 content to do this. Now that I see the Amnesia is over 20% delta9 and the second highest is CBC at 1.64%, I've decided to use that one instead.

 

This was discussed previously in these threads:

http://michiganmedicalmarijuana.org/topic/44032-gw-pharmaceuticals-supported-thesis-on-growing/?hl=thesis

http://michiganmedicalmarijuana.org/topic/44323-gw-pharma-cbc-patent/?view=findpost&p=458980&hl=thesis

[Restorium2]

I'm sorry that it seems so difficult for you to accept facts that contradict your worldview. It's a part of life. You can learn to accept that and continue to evolve, or continue displaying the type of behavior that you have here. I just ask that you please refrain from trolling my threads.

 

For anyone reading please disregard anything Rev says. He apparently has taken issue to me, and this thread, and seems intent on derailing it. Fortunately for you, I see his display as an example of why this thread is so important.

Why don't you just tell me why I'm wrong instead of going into these dramatic personal attacks?

[Restorium2]

CBC's relatively high boiling point could be used to isolate it in an oil. In other words, take any extract that has CBC and cook it at just under 428 F and you will have an extract that has a high ratio of CBC.

[in vivo]

can we ignore the fact that every test conducted from different areas of every plant will report varying amounts of compounds? I know that one garden can produce a rotten meat fuely skunky profiled plant while the same plant in another garden could show none of those traits, depending on environmental factors and grow habits? I've smelled and tasted samples that smelled and tasted just like the dank basement they were grown in, and a clone of it smells of sexy goodness grown elsewhere, surely reporting different terpenes and very likely many differing compounds.

 

Here are some quotes from the other thread:

 

One thing that stands out at me is being able to identify high CBG plants by viewing the trichomes of plants in veg. High CBG plants had cloudy trichome heads after the first few weeks of veg. 

 

 

 

Quote

sessile trichomes, which have been shown to have a higher proportion of CBC to capitate stalked trichomes of the same age

 

^^ They caught a higher percentage of CBC in their 25um screen.

 

Quote

>The trichome on this sieve contained a higher proportion developed within the first weeks of growth when the proportion of CBC within the whole plant was much higher

 

^^ This might be a feasible way of procuring CBC. (Find a strain with a large number of sessile trichomes in the first few weeks of veg, then use bubble bags to concentrate.) 

 

Cannabinoid profiles of younger plants will also have higher percentages of CBG.

 

Quote

from this test it was important to note that separating trichomes with sieves appeared to offer a means of producing phytopharmaceutical feedstocks with a favorably altered cannabinoid profiles

 

This one below is what I was looking for to address your statement. 178 plants from a variety of sources. I think we can disregard variance to a point. We can identify CBG in plants in veg with a loop. We can also identify sessile trichomes. This gives us a way, without testing, to procure these cannabinoids. The guy that wrote the thesis linked in the other thread seemed to have figured this out while writing it, and GW rushed to patent the process. I don't much care about that, it's a free market. But the thesis and patent are both available describing this simple process, and they're linked above.  

 

They took 178 plants from a "variety of sources" and extracted CBC from them in veg. They found that CBC was the highest cannabinoid in 4.5% of samples, and the second in 78%.

 

This might add another cannabinoid to my medicine cabinet.

[Restorium2]

[trichcycler]

got it, thanks !

Here are some quotes from the other thread:

 

 

 

 

^^ This might be a feasible way of procuring CBC. (Find a strain with a large number of sessile trichomes in the first few weeks of veg, then use bubble bags to concentrate.) 

 

Cannabinoid profiles of younger plants will also have higher percentages of CBG.
 

Quote

 

This one below is what I was looking for to address your statement. 178 plants from a variety of sources. I think we can disregard variance to a point. We can identify CBG in plants in veg with a loop. We can also identify sessile trichomes. This gives us a way, without testing, to procure these cannabinoids. The guy that wrote the thesis linked in the other thread seemed to have figured this out while writing it, and GW rushed to patent the process. I don't much care about that, it's a free market. But the thesis and patent are both available describing this simple process, and they're linked above.