CBD or CBDa? THC or THCa?

[danut]

Sirs ..

I have a test subject to work with. My wife.

She is a registered mmj patient. Yet she doesn't consume.

She uses my topical extensively on her back.

She also works in the lab at the hospital.

After repeated use of the topical oil, she tested her urine at work. THC was able to be detected, but well below the threshold defined as a positive.

I fed her a solid block of a BHO that likely contained a usable amount of CBD. I had a batch of RSO from the same starting materials. The RSO tested at 17.8%CBD. So I think it was likely the BHO also had a similar CBD content.

However, the BHO had substantially less heat applied to it.

She ate about 1/3 gram of the BHO.

Think about it. Someone that never smokes or eats brownies, takes down 1/3 gram of some VERY nice BHO as one single hit ...

It suddenly turned into mass fall cleanup day. I got drafted for the effort It helped that I ate some also.

It's nice to think that you can bring someone up to a therapeutic dose level at day one.

One gram of Simpson oil, more so with the newby, in one gulp is a tad much. They usually aren't awake for dose number two.

Next, my wife tested her urine. In the hospital lab.

It tested one single tick below the positive line.

Tell me .. if you smoke a quarter gram of BHO, would your urine test any where near that clean? No .. it could take a couple of weeks before it hit that clean line.

 

[danut]

I put the same size block of the same BHO in a Vapor Cone and share it for a week.

 

[danut]

All of her body aches and pain completely went away.

We completely gutted the garage and a couple other areas of the house. Sorted, stacked and organized the whole mess.

And she was mad as a wet hornet at me. Yes, there is a psychoactive effect. Much less that the neutral form, but still some.

By observation, the vast majority of what was excreted from her body was not the metabolite that turns urine dirty. That means the actions are not based on how much of the acid form is converted.

 

[danut]

Exposure of GPR55 to the cannabinoids THC and JWH015 in dorsal root ganglion neurons and in receptor-transfected HEK293 cells correlates with increases of intracellular Ca2+ (11). In contrast, GPR55 is insensitive to the CB1 inverse agonist AM281 and the potent cannabinoid agonist WIN55212-2 but is antagonized by the marijuana constituent CBD (9, 10). However, Oka et al. (13) reported that GPR55 is not a typical cannabinoid receptor, as numerous endogenous and synthetic cannabinoids, including many mentioned above, had no effect on GPR55 activity.

From here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2785612/

 

[danut]

Scanning this one here:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2095107/

I'm not seeing THC v THCa being illustrated.

 

[danut]

Interesting:

Cancer

D9-THC, CBD, CBG, CBC, D9-THCA and CBDA have been shown to exert anti-proliferative/pro-apoptotic effects (IC50 in the range 5–25 mM) in a panel of tumor cell lines: human breast carcinoma, human prostate carcinoma, human colorectal carcinoma, human gastric adeno carcinoma, C6 rat glioma, rat basophilic leukemia and transformed thyroid cells. CBD exhibited the highest potency with IC50 values between 6 mM and 10.6 mM, and maximal efficacy at 25 mM, followed by CBG and CBC [11]. CBDA was the least effective compound, being active against only breast, thyroid and glioma cells. Furthermore, prostate carcinoma cells were found to be quite resistant to the action of phytocannabinoids, with only CBD and CBG exerting anti-proliferative effects [11]. More in-depth studies showed that CBD inhibited glioma, leukaemia and breast cancer, as detailed below.

1) CBD exerted cannabinoid-independent anti-metastatic and pro-apoptotic effects on human glioma cells and tumor regression in vivo [1,7,27]. CBD-induced apoptosis of human glioma cells involves early production of ROS and concomitant activation of initiator caspase-8 and caspase-9, converging into the activation of the downstream effector caspase-3 [27]. In vivo, CBD induced glioma growth inhibition through specific modulation of the pro-carcinogenic LOX pathway [69].

2) CBD induced a CB2-mediated reduction in viability and apoptosis in leukemia cells, and reduced tumor burden and increased the number of apoptotic tumours in EL-4-bearing mice in vivo; the effect was associated with increased production of ROS, which was mediated through regulation of Nox4 and p22phox [70].

3) CBD inhibited the growth of xenograft tumours obtained by subcutaneous injection of human breast carcinoma cells into athymic mice [11]. Studies investigating the mode of action showed that CBD down-regulated the expression of Id-1 (a key regulator of the metastatic potential of breast and other carcinomas) in metastatic human breast cancer cells, leading to reduction of tumour aggressiveness [71].

Phytocannabinoids have been shown to inhibit ATPbinding cassette (ABC) transporters, which play a part in the multi-drug resistance of tumor cells. Specifically, P-glycoprotein (ABCB1) was inhibited by CBD, but not by D9-THCV, D9-THCA or CBN [72]; multi-drug resistance related protein 1 (ABCC1/MRP1) and breast cancer resistance protein were inhibited by CBD, CBN and D9-THC (order of potency: CBD > CBN > D9-THC) [73].

CBD was shown to attenuate oxidative/nitrosative stress, inflammation, and cell death induced by the anticancer drug cisplatin in the mouse kidney [74]. Nephrotoxicity is a common complication of cisplatin chemotherapy, which limits its clinical use. In summary, the phytocannabinoidsCBD,CBGandCBC have shown interesting pro-apoptotic properties in cancer
cell lines. The most studied phytocannabinoid is CBD. CBD induces increases in [Ca2+]i, thereby stimulating ROS production
and causing apoptosis. In vivo, CBD inhibits glioma growth and experimental breast carcinoma.

Taken from http://www.advancedholistichealth.org/PDF_Files/cannbiniods therapeutic chart article.pdf

 

[SeaMaiden]

All of her body aches and pain completely went away.

We completely gutted the garage and a couple other areas of the house. Sorted, stacked and organized the whole mess.

And she was mad as a wet hornet at me. Yes, there is a psychoactive effect. Much less that the neutral form, but still some.

By observation, the vast majority of what was excreted from her body was not the metabolite that turns urine dirty. That means the actions are not based on how much of the acid form is converted.

May I inquire as to your wife's issues and reasons/need for MMJ? I would love to be able to eliminate the pain in my knees, it's taking more out of me than the back injury ever did. I love smoking, but would be happy to work with topicals.

 

[danut]

Chronic back pain. Not sure of the source.

re topical oil. I can't figure out how to talk about it here without triggering threads being deleted.

 

[madscientist81]

Scanning this one here:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2095107/

I'm not seeing THC v THCa being illustrated.

In the last paragraph of the section GPR55 binds and is activated by cannabinoid ligands they say the following...

We next tested Δ9-THC, the psychoactive component of the cannabis plant C. sativa, for its activity at GPR55. Δ9-THC activated GTPγS binding with an EC50 of 8nM (Figure 5a and Table 1)

THCA may be an agonist at GPR55 but the review article by Mechoulam et al. I just posted seems to suggest this is not likely. Check the article out and let me know if you find it at all intersting or helpful.

So I see that the link I tried to put in my previous post to the thread here on ICmag that discussed neutral and acidic CB's is not posted. Perhaps this is a no no, or just an error. At any rate it should be listed in the medical section with the title Decarboxylation and medical properties???

After repeated use of the topical oil, she tested her urine at work. THC was able to be detected, but well below the threshold defined as a positive.

I fed her a solid block of a BHO that likely contained a usable amount of CBD. I had a batch of RSO from the same starting materials. The RSO tested at 17.8%CBD. So I think it was likely the BHO also had a similar CBD content.

However, the BHO had substantially less heat applied to it.

Danut- you mentioned your wife working in the hospital and testing her urine. What method was she using if I may ask? You said just below the cut-off so that made me wonder if she was using the "higher end" type of testing like GC/MS etc (vs cheap dip stick immuno-staining type tests).

So was your stuff tested with HPLC or some other analytical method that would show both neutral and acidic cannabinoids? Was the topical she has been using the RSO?

Thanks

 

[danut]

Danut- you mentioned your wife working in the hospital and testing her urine. What method was she using if I may ask? You said just below the cut-off so that made me wonder if she was using the "higher end" type of testing like GC/MS etc (vs cheap dip stick immuno-staining type tests).

So was your stuff tested with HPLC or some other analytical method that would show both neutral and acidic cannabinoids? Was the topical she has been using the RSO?

Thanks

Tested with GC. More precise information than the dip stick.

Topical: diluted RSO. Olive oil base. 1 ml RSO per 8 oz of olive oil.

The RSO was tested via a GC method. It had been subjected to about 220 f for about eight hours.

The BHO .. showed what would be expected as a result of consuming the acid form. Clean urine test.

 

[MattMatt]

Interesting:



Taken from http://www.advancedholistichealth.org/PDF_Files/cannbiniods therapeutic chart article.pdf

One thing I find strange with this article, and with many other sources, is that THCA is mentioned as having anti proliferative effects, along with many other cannabinoids and acids, yet when they break down the specific studies proving anti proliferative effects of various cannabinoids and cannabinoid acids THCA is not mentioned. Has anyone found the clinical basis for the anti cancer effects of THCA. I find it strange that THCA is promoted as anti cancer more than any other cannabinoid (neutral or acidic) yet seems the least supported by clinical data

 

[Bongstar420]

Your on the right track, but I wouldn't be taking lessons from Rick Simpson as the guy doesn't seem to be the brightest bulb in the box. He is only popular because of the IQ and educational distribution of the population.

Moisture will do nothing but increase oxidation rates. The drops of water would be better experimented with as H2 gas since water wont give up its hydrogen without releasing O-.

I'm thinking something like that also.

Current wisdom says it's UV and heat. Then they store it dark and cool to prove it. WTF????

enzymes .. That makes sense. As time is a factor in the process.

Adding heat doesn't seem to speed up the process ..

Moisture .. THAT has been a haunting thought for a few years now. That is something that Simpson does that is different than most in his extraction process. He adds a few drops of water at the end. I have two samples that I collected today. Both from the same collection of resin. This is supposed to be a cannatonic strain with about a 1:1 ratio of THC:CBD. I took out a couple grams of the oil for the additional step. Added a couple of drops of RO water to the hot oil. (~230F) Cooked it until all the water was gone. I'll post the tests when I get the results.

So that would be the combination of water and heat.

Oxygen. Could be tested by storing bud material in Nitrogen. The oxygen may be supplied by the plant material as it ages.