Laboratory evidence indicated that cannabidiol may reduce THC clearance, increasing plasma concentrations which may raise THC availability to receptors and enhance its effect in a dose-dependent manner. In vitro, cannabidiol inhibited receptors affecting the activity of voltage-dependent sodium and potassium channels, which may affect neural activity. A small clinical trial reported that CBD partially inhibited the CYP2C-catalyzed hydroxylation of THC to 11-OH-THC. Little is known about potential drug interactions, but CBD-mediates a decrease in clobazam metabolism.
The vast majority of CBD oils come in bottles measuring either 15 milliliters (mL), or 0.5 ounces; or 30 mL, or 1 ounce. However, CBD concentration is more important than bottle size. Concentration refers to the ratio of hemp oil solution (measured in mL) compared to the amount of CBD cannabinoid (measured in milligrams, or mg). A 15-mL bottle may contain 100 mg of CBD, 300 mg, 500 mg, or more. The higher the mg amount, the stronger the CBD oil will be. For this reason, the ‘mg’ measurement is also referred to as the oil’s strength; i.e., 400-mg oil might be called 400-strength oil.
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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