There are over 80 known phytocannabinoids in the marijuana plant. One of these is delta‐9‐tetrahydrocannabinol (THC), and one of these is Cannabidiol (CBD). These two phytocannabinoids have very different stories.
THC is the psychoactive component of marijuana and gets you high. Cannabidiol is NOT psychoactive and does not get you high. In fact, when CBD is combined with THC it mitigates some of the psychoactive component of THC (it can mitigate some of unpleasant symptoms of THC like paranoia, or anxiety).
Indeed, these two compounds are each unique. While some research suggests THC may increase risk for schizophrenia in particular if consumed before the brain is matured, CBD appears to have zero side effects.
For instance, a review of potential side effects in humans found that CBD was well tolerated across a wide dose range, up to 1500 mg/day (orally).
Note: this is huge, clinical doses are in the range of 300-600mg, with no reported psychomotor slowing, negative mood effects, or vital sign abnormalities noted.[i]
Other extensive safety reviews have been conducted which found no adverse effects.[ii] Furthermore, unlike THC, CBD does not trigger withdrawal effects or tolerance.[iii],[iv]
CBD is very different than THC in the brain.
THC is a partial agonist at the CB1 (cannabinoid receptor type 1) and CB2 (cannabinoid receptor type 2) receptors in the endogenous cannabinoid system, and exerts its psychoactive and pain modulatory effects via CB1 agonism.
Think of receptors as a lock for a key, agonism means the key “activates the lock”.
Contrary to popular belief, CBD has low affinity for the CB1R (cannabinoid 1 receptor). [v],[vi] This means it does not “activate this lock”. I see people incorrectly claim this all the time. In other words, the majority of the time CBD will NOT act through the CB1R, and when it does, it does so indirectly meaning it doesn’t actually bind to it.
A more likely target of CBD is Seratonin receptors (5-HT). In vivo studies (studies done in the LIVING animal brain) are more consistent with CBD acting as an allosteric modulator (indirect), or facilitator of 5-HT1A signaling.[vii],[viii]
There are other possibilities, like adenosine A2A receptors.
Lastly, CBD possesses antipsychotic, analgesic, neuroprotective, anticonvulsant, antiemetic, antioxidant, anti-inflammatory, antiarthritic, and antineoplastic properties.[ix],[x],[xi]
It has shown potential in animal models to treat everything from Irritable Bowel Syndrome (IBS), to Epilepsy, Multiple Schlerosis, to Alzheimer’s Disease, and Concussion. This is because (for 4 of the 5 examples here) neuroinflammation is a contributor to basically every brain disorder. And no anti inflammatory meds cannot do the same because they prevent inflammation by BLOCKING other biological mechanisms important for survival. Meanwhile CBD seems to facilitate our natural anti inflammatory mechanisms.
CBD for Athletic Performance
I’m calling it now. This is going to be the next big sports supplement.
How the hell could a cannabinoid with anti inflammatory potential be a sports supplement?
Because the one attribute that is consistent across ALL sports, that is key to maintaining a high level of performance is the athlete’s ability to RECOVER AS FAST AS POSSIBLE. Think of professional sports where athletes are playing upwards of 4-5 games per week! Throw in practices and off ice training and that is some HIGH VOLUME.
Any former athlete can appreciate that the body would take some serious absue from this.
When you break down muscle tissue during a game and generate energy to fuel those muscles, you create inflammation. Sore muscles the next day? That’s inflammation (not lactic acid), marked by increased levels of proinflammatory cytokines like IL-6 and sometimes TNF-alpha.
Waking up after a gruelling road trip feeling mentally drained? This is also very likely due to inflammation (and neuroinflammation in the brain). I wrote an article on the roles of neuroinflammation on mental fatigue after training, you can check it out here at the athlete daily.
These are just two examples of where CBD would improve recovery and therefore improve performance. Joint pain is another one. This is inevitable during a long hockey season. I didn’t even mention cold/sickness and digestion which also have HUGE inflammatory components.
CBD for concussions are a whole other story that I will be sure to address in a separate post.
So maybe you were unfamiliar with CBD, maybe you weren’t. Either way, we are going to start hearing alot more about this stuff so do your homework, and if you hear anyone clumping CBD and THC together into the same category you can let them know!
[i] Blessing et al., “Cannabidiol as a Potential Treatment for Anxiety Disorders.”
[ii] “European Industrial Hemp Association (EIHA) Review on: Safety and Side Effects of Cannabidiol – A Review of Clinical Data and Relevant Animal Studies,” accessed June 7, 2018, http://eiha.org/media/2016/10/16-10-24-Safety-and-Side-Effects-of-CBD.pdf.
[iii] J. Pérez, “Combined Cannabinoid Therapy via an Oromucosal Spray,” Drugs of Today 42, no. 8 (2006): 495, https://doi.org/10.1358/dot.2006.42.8.1021517.
[iv] David J. Rog, Turo J. Nurmikko, and Carolyn A. Young, “Oromucosal Δ9-Tetrahydrocannabinol/Cannabidiol for Neuropathic Pain Associated with Multiple Sclerosis: An Uncontrolled, Open-Label, 2-Year Extension Trial,” Clinical Therapeutics 29, no. 9 (September 1, 2007): 2068–79, https://doi.org/10.1016/j.clinthera.2007.09.013.
[v] Esther M. Blessing et al., “Cannabidiol as a Potential Treatment for Anxiety Disorders,” Neurotherapeutics 12, no. 4 (October 1, 2015): 825–36, https://doi.org/10.1007/s13311-015-0387-1.
[vi] E. M. Rock et al., “Cannabidiol, a Non-Psychotropic Component of Cannabis, Attenuates Vomiting and Nausea-like Behaviour via Indirect Agonism of 5-HT1A Somatodendritic Autoreceptors in the Dorsal Raphe Nucleus,” British Journal of Pharmacology 165, no. 8 (n.d.): 2620–34, https://doi.org/10.1111/j.1476-5381.2011.01621.x.
[vii] Rock et al.
[viii] Raquel Linge et al., “Cannabidiol Induces Rapid-Acting Antidepressant-like Effects and Enhances Cortical 5-HT/Glutamate Neurotransmission: Role of 5-HT1A Receptors,” Neuropharmacology 103 (April 2016): 16–26, https://doi.org/10.1016/j.neuropharm.2015.12.017.
[ix] Tabitha A. Iseger and Matthijs G. Bossong, “A Systematic Review of the Antipsychotic Properties of Cannabidiol in Humans,” Schizophrenia Research 162, no. 1–3 (March 2015): 153–61, https://doi.org/10.1016/j.schres.2015.01.033.
[x] Eva M. Marco et al., “Endocannabinoid System and Psychiatry: In Search of a Neurobiological Basis for Detrimental and Potential Therapeutic Effects,” Frontiers in Behavioral Neuroscience 5 (2011), https://doi.org/10.3389/fnbeh.2011.00063.
[xi] Orrin Devinsky et al., “Cannabidiol: Pharmacology and Potential Therapeutic Role in Epilepsy and Other Neuropsychiatric Disorders,” Epilepsia 55, no. 6 (n.d.): 791–802, https://doi.org/10.1111/epi.12631.