Dear Cancer Coach: I am post op stage 2 endometrial and uterine cancer, estrogen hormone positive, grade 1. I have read that T-H-C can cause hormonally driven cancers to spread.
I have seen conflicting advice on this. One site recommended 4:1 CBD to thc. Do u agree with this? I may need a coach.
Several things. I am sorry to learn of your endo/uterine cancer. Regarding your question about CBD/THC, my experience, based on the article linked below, is that CBD/THC has anti-endometrial properties. While the study below does not specifically address the issue of “hormonlly driven cancer to spread”, the article does say that C-B-D/T-H-C has:
“Selective targeting of TPRV1 by AEA, CBD, or other stable analogues may be an attractive research area for the treatment of estrogen-dependent endometrial carcinoma.”
As for the specific strain and/or ratio, I think the most important factor (according to studies) is the percentage of cannabinoids IN the CBD oil. In other words, the CBD oil that you reference may have only 1 or 2 percent of cannabinoids in the oil and therefore do very little for you. My understanding is that the CBD oil should have upwards of 20% cannabinoids content.
I have read studies that cite at least some T-H-C as enhancing the anti-cancer activity of C-B-D but some people just don’t like the psychotropic feeling of T-H-C. This is your call.
Lastly, I think it is important to add additional evidence-based, non-conventional therapies to your regimen. Therapies such as nutrition, nutritional supplements, frequent moderate exercise, etc.
Let me know if you have any other questions.
Among a variety of phytocannabinoids, Δ9-tetrahydrocannabinol (THC) and cannabidiol (CBD) are the most promising therapeutic compounds. Besides the well-known palliative effects in cancer patients, cannabinoids have been shown to inhibit in vitro growth of tumor cells. Likewise, the major endocannabinoids (eCBs), anandamide (AEA) and 2-arachidonoylglycerol (2-AG), induce tumor cell death.
The purpose of the present study was to characterize cannabinoid elements and evaluate the effect of cannabinoids in endometrial cancer cell viability.
The presence of cannabinoid receptors, transient receptor potential vanilloid 1 (TRPV1), and endocannabinoid-metabolizing enzymes were determined by qRT-PCR and Western blot. We also examined the effects and the underlying mechanisms induced by eCBs and phytocannabinoids in endometrial cancer cell viability. Besides TRPV1, both EC cell lines express all the constituents of the endocannabinoid system.
We observed that at concentrations higher than 5 μM, eCBs and CBD induced a significant reduction in cell viability in both Ishikawa and Hec50co cells, whereas THC did not cause any effect. In Ishikawa cells, contrary to Hec50co, treatment with AEA and CBD resulted in an increase in the levels of activated caspase -3/-7, in cleaved PARP, and in reactive oxygen species generation, confirming that the reduction in cell viability observed in the MTT assay was caused by the activation of the apoptotic pathway. Finally, these effects were dependent on TRPV1 activation and intracellular calcium levels.
These data indicate that cannabinoids modulate endometrial cancer cell death. Selective targeting of TPRV1 by AEA, CBD, or other stable analogues may be an attractive research area for the treatment of estrogen-dependent endometrial carcinoma. Our data further support the evaluation of CBD and CBD-rich extracts for the potential treatment of endometrial cancer, particularly, that has become non-responsive to common therapies.