Admittedly, this is a bit of a paradox which can be answered in six words. “Because we can’t talk about it.”
Here is their page on cannabinoids for health practitioners.
The Dietary Supplementation Health Education Act (DSHEA) prevents dietary supplement manufacturers from talking about research that indicates their products may treat, or even PREVENT, any kind of disease or health condition. Cancer definitely falls under that category.
So lets say, hypothetically, that you are a manufacturer of dietary supplements who is releasing a new product that is made of the natural Cannabis sativa cannabinoid CBD (cannabidiol). Wouldn’t you want to tell the world if there was information that indicated that your product could address cancer? We know from other countries where CBD (and even THC which is illegal in 48 of 50 states) is sold as a prescription drug for conditions such as epilepsy, pediatric seizure disorder, anxiety, severe nausea and lack of appetite, that it can be a versatile natural substance. Helping to prevent cancer might be something folks would want to know about? Well, you, if you were a manufacturer of dietary supplements you wouldn’t be able to say that, or else risk the legal ramifications of being cited by the government’s Food and Drug Administration. Of course in most cases in order to BE a manufacturer, you’d have to believe in Corporate_personhood because most supplement manufacturers are corporations. As well it should be.
I am not a manufacturer of dietary supplements, although I work with many companies that are and have for a long time, none of which I personally consider people. I am an American citizen with first ammendment rights guaranteed by the constitution. So I can tell you what that link I posted to above says, just in case you haven’t clicked on it yet.
“CBD, in particular, is thought to have significant analgesic and anti-inflammatory activity without the psychoactive effect (high) of delta-9-THC.”
One study in mice and rats suggested that cannabinoids may have a protective effect against the development of certain types of tumors.[3] During this 2-year study, groups of mice and rats were given various doses of THC by gavage. A dose-related decrease in the incidence of hepatic adenoma tumors and hepatocellular carcinoma (HCC) was observed in the mice. Decreased incidences of benign tumors (polyps and adenomas) in other organs (mammary gland, uterus, pituitary, testis, and pancreas) were also noted in the rats. In another study, delta-9-THC, delta-8-THC, and cannabinol were found to inhibit the growth of Lewis lung adenocarcinoma cells in vitro and in vivo .[4] In addition, other tumors have been shown to be sensitive to cannabinoid-induced growth inhibition.[5–8]
Cannabinoids may cause antitumor effects by various mechanisms, including induction of cell death, inhibition of cell growth, and inhibition of tumor angiogenesis invasion and metastasis.[9–12] Two reviews summarize the molecular mechanisms of action of cannabinoids as antitumor agents.[13,14] Cannabinoids appear to kill tumor cells but do not affect their nontransformed counterparts and may even protect them from cell death. These compounds have been shown to induce apoptosis in glioma cells in culture and induce regression of glioma tumors in mice and rats. Cannabinoids protect normal glial cells of astroglial and oligodendroglial lineages from apoptosis mediated by the CB1 receptor.[15]
An in vitro study of the effect of CBD on programmed cell death in breast cancer cell lines found that CBD induced programmed cell death, independent of the CB1, CB2, or vanilloid receptors. CBD inhibited the survival of both estrogen receptor–positive and estrogen receptor–negative breast cancer cell lines, inducing apoptosis in a concentration-dependent manner while having little effect on nontumorigenic, mammary cells.[19]
CBD has also been demonstrated to exert a chemopreventive effect in a mouse model of colon cancer.[20] In the experimental system, azoxymethane increased premalignant and malignant lesions in the mouse colon. Animals treated with azoxymethane and CBD concurrently were protected from developing premalignant and malignant lesions. In in vitro experiments involving colorectal cancer cell lines, the investigators found that CBD protected DNA from oxidative damage, increased endocannabinoid levels, and reduced cell proliferation. In a subsequent study, the investigators found that the antiproliferative effect of CBD was counteracted by selective CB1 but not CB2 receptor antagonists, suggesting an involvement of CB1 receptors.[21]
Another investigation into the antitumor effects of CBD examined the role of intercellular adhesion molecule-1 (ICAM-1).[12] ICAM-1 expression has been reported to be negatively correlated with cancer metastasis. In lung cancer cell lines, CBD upregulated ICAM-1, leading to decreased cancer cell invasiveness.
In an in vivo model using severe combined immunodeficient mice, subcutaneous tumors were generated by inoculating the animals with cells from human non-small cell lung carcinoma cell lines.[22] Tumor growth was inhibited by 60% in THC-treated mice compared with vehicle-treated control mice. Tumor specimens revealed that THC had antiangiogenic and antiproliferative effects. However, research with immunocompetent murine tumor models has demonstrated immunosuppression and enhanced tumor growth in mice treated with THC.[23,24]
In addition, both plant-derived and endogenous cannabinoids have been studied for anti-inflammatory effects. A mouse study demonstrated that endogenous cannabinoid system signaling is likely to provide intrinsic protection against colonic inflammation.[25] As a result, a hypothesis that phytocannabinoids and endocannabinoids may be useful in the risk reduction and treatment of colorectal cancer has been developed.[26–29]
CBD may also enhance uptake of cytotoxic drugs into malignant cells. Activation of the transient receptor potential vanilloid type 2 (TRPV2) has been shown to inhibit proliferation of human glioblastoma multiforme cells and overcome resistance to the chemotherapy agent carmustine.[30] In an in vitro model, CBD increased TRPV2 activation and increased uptake of cytotoxic drugs, leading to apoptosis of glioma cells without affecting normal human astrocytes. This suggests that coadministration of CBD with cytotoxic agents may increase drug uptake and potentiate cell death in human glioma cells.
The page also covers very well the research on appetitie stimulation and analgesia (pain relief). Neither of which the makers of dietary supplements will let you know about it. “Because we can’t talk about it.”
God bless America.
