Multiple Myeloma an incurable disease, but I have spent the last 25 years in remission using a blend of conventional oncology and evidence-based nutrition, supplementation, and lifestyle therapies from peer-reviewed studies that your oncologist probably hasn't told you about.
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Hello David- I write with mixed feelings. Normally, one would be elated, but unfortunately, it’s not the case. I only dreamed of being able to write this, but now that the time has come, there are so many other complications that it’s not happy times. My dad’s M-protein has been at zero for 2 months now. He continues on the velcade injection treatments for his multiple myeloma (MM) (1 injection to the stomach a week for 3 weeks, and one week off).
The velcade worked well, and quickly, but the M-protein hovered at 2.0 for months. It wasn’t until we started giving my father concentrated RSO oil at night to help him sleep (he was getting up so much due to prostate issues) that we’re correlating this to possibly the difference in the M-protein. We were told by the oncologist that it’s very unusual for someone to hit zero on velcade after a relapse.
Unfortunately, we’re now querying heart issues as my Dad is so weak, he can barely walk, and only wants to be in bed. He can’t sit up at a table without resting his head on it. it’s so concerning.
The hospital seems to insist he keep up with his weekly injections, fearmongering to say if he doesn’t do so, the M-protein will go up and they might not be able to get it under control. I’m of the opposite mindset- why risk habituation to it giving it when it’s not needed, and possibly shortening the life of the usefulness of the drug?
Thought I would write to you to see if you had thoughts….
Hi Terry,
“Multiple myeloma (MM) is a plasma cell (PC) malignancy characterised by the accumulation of a monoclonal PC population in the bone marrow (BM). Cannabidiol (CBD) is a non-psychoactive cannabinoid with antitumoural activities, and the transient receptor potential vanilloid type-2 (TRPV2) channel has been reported as a potential CBD receptor.
TRPV2 activation by CBD decreases proliferation and increases susceptibility to drug-induced cell death in human cancer cells. However, no functional role has been ascribed to CBD and TRPV2 in MM.
In this study, we identified the presence of heterogeneous CD138+TRPV2+ and CD138+TRPV2- PC populations in MM patients, whereas only the CD138+ TRPV2- population was present in RPMI8226 and U266 MM cell lines.
Because bortezomib (BORT) is commonly used in MM treatment, we investigated the effects of CBD and BORT in CD138+TRPV2- MM cells and in MM cell lines transfected with TRPV2 (CD138+TRPV2+).
These results showed that CBD by itself or in synergy with BORT strongly inhibited growth, arrested cell cycle progression and induced MM cells death by regulating the ERK, AKT and NF-κB pathways with major effects in TRPV2+ cells. These data provide a rationale for using CBD to increase the activity of proteasome inhibitors in MM.