Technically speaking, its THC—the cannabinoid that gets you high—which is illicit. When you take a drug test, the aim is to detect THC in your body, not “cannabis.” If you possessed weed without any THC in it, technically you wouldn’t be in violation of the law. Because “weed” without THC has a different name: hemp. And the rules governing hemp are quite different from the restrictions placed on cannabis.
In addition to the research on the use of cannabinoids in palliative treatments for cancer—reducing pain and nausea and in increasing appetite—there are also several pre-clinical reports showing anti-tumor effects of CBD in cell culture and in animal models.xxviii These studies have found reduced cell viability, increased cancer cell death, decreased tumor growth, and inhibition of metastasis (reviewed in McAllister et al, 2015).xxix These effects may be due to the antioxidant and anti-inflammatory effects of CBD;xxx however these findings have not yet been explored in human patients. There are multiple industry sponsored clinical trials underway to begin to test the efficacy of CBD in human cancer patients.
Success stories like Oliver’s are everywhere, but there’s not a lot of data to back up those results. That’s because CBD comes from cannabis and, like nearly all other parts of the plant, is categorized by the Drug Enforcement Agency (DEA) as a Schedule 1 drug—the most restrictive classification. (Others on that list: heroin, Ecstasy, and peyote.) This classification, which cannabis advocates have tried for years to change, keeps cannabis-derived products, including CBD, from being properly studied in the U.S.
Cannabidiol has low affinity for the cannabinoid CB1 and CB2 receptors, although it can act as an antagonist of CB1/CB2 agonists despite this low affinity. Cannabidiol may be an antagonist of GPR55, a G protein-coupled receptor and putative cannabinoid receptor that is expressed in the caudate nucleus and putamen in the brain. It also may act as an inverse agonist of GPR3, GPR6, and GPR12. CBD has been shown to act as a serotonin 5-HT1A receptor partial agonist. It is an allosteric modulator of the μ- and δ-opioid receptors as well. The pharmacological effects of CBD may involve PPARγ agonism and intracellular calcium release. cannabidiol