How CBD works is just as complicated, even or more so.
As with caffeine, CBD oil has different mechanisms of actions as an isolate alone. Below is a peak of some of the various receptors CBD oil has been found to “hit” in the body from various sources.
Imagine, all that impact with one tiny molecule!
5-HT, 5-hydroxytryptamine; AEA, N-arachidonoylethanolamine; CB1 and CB2, cannabinoid receptor type 1 and 2; eCB, endocannabinoid; FAAH, fatty acid amide hydrolase; PPAR?, peroxisome proliferator-activated receptor gamma; modulation of THC, ?9-tetrahydrocannabinol; TRPA1, transient receptor potential cation channel A1; TRPM8, transient receptor potential cation channel M8; TRPV1 and TRPV2, transient receptor potential cation channel V1 and V2.
CBD acts as agonist of the receptors TRPV1, PPARy, and 5-HT1A, and as antagonist of the receptor GPR55. CBD is an inverse agonist of the receptors GPR3, GPR6, and GPR12. Moreover, CBD antagonizes the action of CB1 and CB2 receptors agonists, and is suggested to act as an inverse agonist and a negative allosteric modulator of these receptors. CBD also inhibits FAAH, which results in increased anandamide levels. Anandamide activates CB1, CB2, and TRPV1 receptors. By acting on mitochondria, CBD increases the activity of mitochondrial complexes. In addition, CBD displays antioxidant and anti-inflammatory effects—that are partially mediated by CBD’s actions on TRPV1, mitochondria and PPAR?. 5-HT1A, serotonin receptor 1A; CB1, cannabinoid receptor type 1; CB2, cannabinoid receptor type 2; FAAH, fatty acid amide hydrolase; GPR3, G-protein-coupled receptor 3; GPR6, G-protein-coupled receptor 6; GPR12, G-protein-coupled receptor 12; GPR55, G-protein-coupled receptor 55; PPARy, peroxisome proliferator-activated receptor gamma; ROS, reactive oxygen species; TRPV1, transient receptor potential vanilloid type 1.
Another review demonstrates multiple effects of CBD, and the authors also give us a glance at the difference between it and another cannabis compound, THC (delta9-tetrahydrocannabinol):
Cannabidiol (CBD) is a phytocannabinoid with therapeutic properties for numerous disorders exerted through molecular mechanisms that are yet to be completely identified. CBD acts in some experimental models as an anti-inflammatory, anticonvulsant, anti-oxidant, anti-emetic, anxiolytic and antipsychotic agent, and is therefore a potential medicine for the treatment of neuroinflammation, epilepsy, oxidative injury, vomiting and nausea, anxiety and schizophrenia, respectively. The neuroprotective potential of CBD, based on the combination of its anti-inflammatory and anti-oxidant properties, is of particular interest and is presently under intense preclinical research in numerous neurodegenerative disorders. In fact, CBD combined with delta9-tetrahydrocannabinol is already under clinical evaluation in patients with Huntington’s disease to determine its potential as a disease-modifying therapy. The neuroprotective properties of CBD do not appear to be exerted by the activation of key targets within the endocannabinoid system for plant-derived cannabinoids like delta9-tetrahydrocannabinol, i.e. CB1 and CB2 receptors, as CBD has negligible activity at these cannabinoid receptors, although certain activity at the CB2 receptor has been documented in specific pathological conditions (i.e. damage of immature brain). Within the endocannabinoid system, CBD has been shown to have an inhibitory effect on the inactivation of endocannabinoids (i.e. inhibition of FAAH enzyme), thereby enhancing the action of these endogenous molecules on cannabinoid receptors, which is also noted in certain pathological conditions. CBD acts not only through the endocannabinoid system, but also causes direct or indirect activation of metabotropic receptors for serotonin or adenosine, and can target nuclear receptors of the PPAR family and also ion channels.
Then, There’s Your Own…Endogenous Cannabinoids Actions
Add this complexity of CBD’s actions to the fact that CBD modulates the use of our own endocannabinoids (eCBs), and now you’ve multiplied its multifactorial effects. This article states:
“In addition to CB1 and CB2, cannabinoids and eCBs can exert their effects engaging other non-CB receptors, including the transient receptor potential vanilloid 1 (TRPV1) channel, expressed mainly in peripheral tissues, including peripheral sensory neurons, epithelial and endothelial cells as well as immune cells (Xia et al., 2011). Other targets are peroxisome proliferator-activated receptors (PPAR) a and y (Pistis and Melis, 2010) that belong to a family of nuclear receptors whose role is mainly to control lipid metabolism; and orphan G protein-coupled receptor GPR55 (Moriconi et al., 2010).”(source)