I see Canibis oil touted on the internet as capable of killing cancer.....anyone have results from its use?
Canibis: I see Canibis oil touted on... - Advanced Prostate...
Canibis
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michaeland
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I looked into that, too. I found no evidence anywhere beyond some anecdotes, like the guy from Cheach and Chong. I also read that it kills cancer cells in petri jars, but, if you google lots of different things, there are lots of cancer cell killers that work in petri jars. I think marijuana may be helpful for relaxation and stress relief, which is supposed to fight cancer. And, I read that it is helpful for nausea from chemo, etc.
In fact, I think if there were a simple answer, given the speed of the internet, we would all know about it by now. Of course, if you are smoking or using the oil, etc, then you probably think it is keeping you alive. I think the same for myself as for my mediterranean style diet.
I do and will start a discussion soon about it.
Short answer- the treatment makes sense from a theoretical perspective and there is sound " bench science " to support its use.
I used a rigorous single subject experimental design to evaluate the effects of an accepted protocol involving ingestion of 62 grams of cannabinoid oil derived from 50/50 mixture of Sativa ( for THC) and Indica( for CBD) strains.
My " resting/ steady state THC level during the trial was over 260 ng/ml so I have external validation that the protocoll delivered it's intended results- prolonged exposure to the desired chemical preparation.
A fine-grained analysis of PSA kinetics throughout the trial, in the context of an equally thorough comparison of changes documented during the trial vs changes documented before and immediately after surgery, as well as after salvage radiation treatment, all indicated that the last PSA value obtained was almost exactly on the projectory documented during the previous phase of treatment.
More on the experimental design later.
I have been doing about a Tble spoon of hemp oil a day for 5 months now....my psa is still rising slowly
Hemp oil is not cannabis oil--- you need the THC and CBD from cannabis, extracted and concentrated.
What keeps my interest in this topic alive, is the presence of cannabinoid receptors in the prostate, particularly CB1.
Incidentally, the natural ligand that binds to CB1 & CB2 is anandamide. The body doesn't make much & it is cleared quickly. It was discovered ~25 years ago. A synthetic analog of anandamide is methanandamide.
The discovery [3] [4] that CB1 is upregulated in PCa cells, coupled with research showing that CB1 could be an attractive therapeutic target, seems almost too good to be true. However, PCa also upregulates FAAH (fatty acid amide hydrolase), the enzyme that metabolizes cannabinoids. It looks as though a FAAH inhibitor will be needed, for CB1/CB2 agonists to be effective. [8]
Almost all of the patient interest in cannabinoids is confined to cannabis sativa. There is an assumption that the psychoactive THC (tetrahydrocannabinol) must be the only active ingredient. However, CBD (cannabidiol) shouldn't be ignored, particularly since there are hemp oil companies that mail CBD products to every U.S. state. Seemingly, legally at the moment. [6]
Ultimately, we might see a synthetic therapeutic cannabinoid with a strong affinity for binding to CB1/CB2, without the psychoactivity of THC. Some PCa studies have used WIN 55,212-2, which is a much more powerful CB1 agonist than THC. It is banned in the UK, so presumably is not without psychoactivity.
For a 2013 review of the literature, see [7].
{The vanilloid receptors in the prostate are also of interest, since there is some overlap with the cannabinoid receptors, in terms of the ligands that bind to them. The most well-known vanilloid receptor ligand is capsaicin, from cayenne.}
Studies:
[1] (2003) "Both mRNA for CB(1) and the corresponding protein are expressed in the human prostate gland at a level comparable with the receptor expressed in cerebellum. ... Immunohistochemical studies show that CB(1) is preferentially expressed in the epithelia of the prostate."
[2] (2003) "The potent anti-proliferative and cytotoxic effects of {Anandamide} on metastatic prostatic cancer cells might provide basis for the design of new therapeutic agents for effective treatment of recurrent and invasive prostatic cancers."
[3] (2005) "... expression of both CB1 and CB2 receptors was significantly higher in prostate cancer cells LNCaP, DUI45, PC3 ... as compared with normal prostate cells ..."
[4] (2009) In biopsies from Swedish men "... the tumour CB(1)IR score and the Gleason score were independent prognostic variables. It is concluded that a high tumour CB(1)IR score is associated with prostate cancer severity and outcome."
[5] (2009) "This study defines the involvement of CB(2)-mediated signalling in the in vivo and in vitro growth inhibition of prostate cancer cells and suggests that CB(2) agonists have potential therapeutic interest and deserve to be explored in the management of prostate cancer."
[6] (2013) "Cannabidiol (CBD) significantly inhibited cell viability."
"Two standard drugs for the treatment of prostate cancer, bicalutamide and docetaxel, were tested on either LNCaP or DU-145 cells, cultured in the presence of serum, with or without different concentrations of CBD. Given alone, docetaxel did not markedly affect the proliferation of LNCaP cells (IC50 > 25 µM), however, when tested in combination with pure CBD, a greater effect was observed, even though this appeared to be due to an additive effect (Figure S3A). Docetaxel was more effective at inhibiting DU-145 cell growth, and CBD (only at the lowest concentration tested) potentiated the effect of this compound (Figure S3C). Finally, CBD significantly enhanced the efficacy of bicalutamide (10 µM) on LNCaP cells, although only at the highest dose tested (Figure S3B)."
"We carried out studies in vivo on the effects of docetaxel, bicalutamide and CBD–BDS on xenograft tumours obtained in athymic mice with LNCaP and DU-145 cells. CBD–BDS dose-dependently inhibited the growth of xenografts from LNCaP, but not DU-145, cells. At the highest dose tested (100 mg·kg−1, i.p.), the extract exerted an effect on LNCaP xenografts, quantitatively similar to that of docetaxel (5 mg·kg−1, i.v.), although it reduced the tumour growth inhibitory effect of this agent (Figure 2A). In DU-145 cell xenografts, CBD–BDS significantly potentiated docetaxel (Figure 2B). In a second experiment with xenograft tumours from LNCaP cells, two doses (25 and 50 mg·kg−1, p.o.) of bicalutamide alone or CBD–BDS alone (100 mg·kg−1, i.p.) produced little effect on tumour weight and volume at the end of the treatment, possibly because this experiment was interrupted after only 35 days. However, co-administration of bicalutamide at 25 mg·kg−1 and CBD–BDS significantly inhibited xenograft growth (Figure 2C). In a third experiment, survival was assessed by Kaplan–Meier analysis. After 47 days of treatment, CBD–BDS plus bicalutamide significantly prolonged survival as compared with bicalutamide or CBD–BDS alone (Figure 2D)."
-Patrick
[1] ncbi.nlm.nih.gov/pubmed/124...
[2] ncbi.nlm.nih.gov/pubmed/127...
[3] cancerres.aacrjournals.org/...
[4] ncbi.nlm.nih.gov/pubmed/190...
[5] ncbi.nlm.nih.gov/pubmed/196...
[6] ncbi.nlm.nih.gov/pmc/articl...
Online sources for CBD are very iffy. Most have little to none CBD. You really need a concentrate from a reliable source.
