First, everybody is different; your age, gender, weight, metabolism, eating habits, and severity of your leukemia symptoms will all influence your effective dosage range. According to some researchers, a low dose of CBD ranges from less than 1 mg to 50 mg/kg/day.
CBD oil has a dense nutritional content that may help ease the symptoms of leukemia among other health conditions. Full-spectrum hemp extracts contain particularly high levels of antioxidants, vitamins, proteins, and essential fatty acids on top of terpenes, terpenoids, and minerals. All these compounds may promote optimal health.
There are several types of leukemia depending on the type of white blood cells affected and the rate at which it deteriorates.
CBD Dosage for Leukemia
If you’re thinking of adding CBD oil to your anti-leukemia regime, consult this idea with a holistic doctor experienced in cannabis use. Doing so will help you determine the effective dose and avoid the aforementioned CBD-drug interactions.
Before recommending a treatment protocol for leukemia, doctors run several examinations to diagnose the condition. Usually, a complete blood count and tissue biopsy from your bone marrow are performed.
CBD might also have anti-cancer effects that have the potential to stop the growth of malignant cells. However, it’s important to remember that there’s a lack of clinical trials in this area, and the majority of the research comes from animal models and human case reports.
Studies have found that CBD oil packs potent anti-cancer properties that may help reduce the rate at which the malignant cells spread. Moreover, CBD signals the body’s endocannabinoid system (ECS) to produce more of its therapeutic messengers (endocannabinoids) to restore the state of homeostasis. Through apoptosis, CBD is able to eliminate cancer cells in human leukemia (1).
Saw an online site that sell cannabis oil with THC, which is not only illegal but goodness knows what additives they contain.
I have read of miraculous cures contributing to the us of cannabis oil, and have been told many times by friends that I should be using this.
If one is on chemotherapy it’s hugely dangerous to take any medication, herbal or otherwise without checking with your Consultant.
Dont be fooled!! Trust your medical team.
Every single medication has unwanted side effects, even over the counter drugs. I have to check with the clinic before I take anything apart from paracetamol.
I am not at all convinced, I have Myelodisplastic Syndrome RAEB2 which will eventually deteriorate into
Acute Myeloid leukaemia. I am being treated successfully for over three years with Azacitidine which is not a cure but is keeping my blood levels reasonably stable although I have a degree of neutropenia.
Sensitivity of Jurkat leukemia cells towards THC after selective CB1-, resp. CB2, CRISPR knockdown. (A) Cells are transfected using standard protocols of the manufacturer (Santa Cruz) using a selective CB1, respectively CB2, CRISPR Double Nickase plasmid. GFP transfection efficiency control by flow cytometry after puromycin selection is shown. EV, empty vector negative control. (B) Validation of CRISPR knockdown of CB1, resp. CB2 protein expression using a flow cytometry approach. (C) Sensitivity of Jurkat cells towards THC (40 μM) after selective CB1, resp. CB2, interference (CB1i/CB2i) with regard to induction of apoptosis. Mean data of 3-5 independent annexin V/PI-based experiments are provided. (*-**) statistical significance at p < 0.05 (Student’s t-test). EV, empty vector. (TIFF 237 kb)
Despite numerous reports on the anti-cancerous efficacy of THC the mechanisms of action as well as defined responder populations still remain unclear. Our data demonstrating antiproliferative as well as proapoptotic efficacy in defined acute leukemia models as well as ex vivo patient samples thereby aims to define a patient sample cohort potentially profiting from dronabinol therapy. The observation that lymphoid blasts or myeloid samples expressing lymphatic markers are more sensitive towards THC is extremely valuable for therapeutic decisions and the observed lineage-dependency might explain the controversial results observed for cannabinoid activation in acute leukemia models in the past. But studies on a larger patient cohort are necessary to verify our observation and future studies will have to address the underlying mechanisms.
We established an assay to specifically block the CB1 or CB2 receptor prior to exposure of leukemia cells to THC and used MOLM13 or Jurkat cells as a myeloid, respective lymphoid leukemia model:
Notably, correlation of CB-expression levels with responders to THC (defined as an apoptosis rate of at least 20 % upon treatment with THC for 48 h) revealed that expression of the cannabinoid receptors is a definite prerequisite to achieve any proapoptotic effect in native leukemia blasts.
Additional annexin V-staining data is provided in Additional file 1: Figure S1, demonstrating dose-dependent induction of early apoptosis in Jurkat cells treated with THC for 10 h.
Delta9-Tetrahydrocannabinol is the major psychoactive constituent of Cannabis sativa and signals through G-protein-coupled cannabinoid receptors (CB).
Kerstin Kampa-Schittenhelm no conflicts. Olaf Salitzky no conflicts. Figen Akmut no conflicts. Barbara Illing no conflicts. Lothar Kanz no conflicts. Helmut Salih no conflicts. Marcus Schittenhelm no conflicts.