30 Apr How Does Cannabidiol (CBD) Work?
Before making the decision to buy CBD oil, I strongly recommend you to take the time to learn more about this product and to get familiar with the numerous benefits of cannabinoids on the human body. We’ve already discussed some of these benefits in previous articles, so right now it’s time to take a closer look at how CBD works inside the human body.
CBD’s action inside the body
CBD or cannabidiol is the main active compound in hemp, and unlike THC, it is not psychoactive, so it doesn’t make people high. As you know, inside the human body there’s the endocannabinoid system, with receptors spread throughout the brain and body. THC activates the CB1 and CB2 receptors, while CBD does not directly stimulate these receptors.
The CB1 and CB2 receptors
Cannabinoid receptors are involved in a series of processes inside the human body, including the regulation of mood, pain sensation, appetite and memory.
These receptors can be activated by endocannabinoids (produced by the human body) as well as by plant cannabinoids (like those found in hemp or cannabis), and they’re grouped in two main categories: CB1 and CB2.
CB1 receptors are found mostly in the central nervous system, and in smaller numbers in the liver, kidneys and lungs, while CB2 receptors are part of the immune system and found in the hematopoietic blood cells as well . CB1 play a role in the production and release of neurotransmitters, cannabis products that exert psychoactive effects stimulating these receptors .
At the same time, CB1 receptors are involved in the lipogenesis process that takes place inside the liver, and seem to play a role in the maintenance of homeostasis (body’s internal equilibrium). Various studies suggest that CB1 also influence pleasure, concentration and appetite, memory and pain tolerance .
CB2 receptors on the other hand affect the immune system, being involved in a variety of functions like immune suppression or apoptosis (programmed cell death). Studies suggest that CB2 modulate the pain sensation and could play a role in various diseases, from liver and kidney problems to neurodegenerative diseases [4, 5].
CBD’s effects inside the body
CBD does not stimulate these two receptors; instead, it activates other receptors, like the vanilloid, adenosine and serotonin receptors. Then, CBD inhibits the FAAH enzyme, a compound that activates the CB1 receptor. By doing so, CBD minimizes the activation of CB1 by THC, reducing its psychoactive effects.
Adenosine receptors are also involved in the release of dopamine and glutamate, two neurotransmitters that play major roles inside the body. Dopamine is involved in cognition, motor control, motivation and reward mechanisms, while glutamate is one of the major mediators of excitatory signals, being involved in memory, learning and cognition.
High concentrations of CBD have been shown to activate the 5-HT1A serotonin receptor, exerting anti-depressant effects. The same receptor is involved in a series of processes from pain perception, appetite, nausea and anxiety to sleep and addiction mechanisms.
As previously said, CBD blocks the psychoactive action of THC, this being one of the reasons it’s generally considered advantageous to combine CBD and THC when for treatment purposes.
- Pertwee RG., Pharmacology of cannabinoid receptor ligands, Current medical chemistry, 1999, 6(8):635-64;http://www.ncbi.nlm.nih.gov/pubmed/10469884
- Ashton JC, Wright JL, McPartland JM, Tyndall JD, Cannabinoid CB1 and CB2 receptor ligand specificity and the development of CB-2 selective antagonists, Current medical chemistry, 2008, 15(14):1428-43;http://www.ncbi.nlm.nih.gov/pubmed/18537620
- Racz I, Nadal X, Alferink J et al., Crucial role of CB2 cannabinoid receptor in the regulation of central immune responses during neuropathic pain, The Journal of Neuroscience, 2008, 28(46):12125-35; http://www.jneurosci.org/content/28/46/12125.long
- Costa B., Giagnoni G. et al., Vanilloid TRPV1 receptor mediates the antihyperalgesic effect of the nonpsychoactive cannabinoid, cannabidiol, in a rat model of acute inflammation, British Journal of Pharmacology, 2004, 143(2):247-50; http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1575333/