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CBD: The Facts About Cannabidiol

CBD, or Cannabidiol, and THC are two of the main components of marijuana and hemp plants, although there are “over 85 cannabinoids” in total (Medical Marijuana Inc). THC is the well-known psychoactive component of cannabis plants that causes the ‘high’ sensation popular for recreational use. CBD, on the other hand, is a non-psychoactive component, meaning it does not produce the ‘high’ sensation. This means that any medicinal benefits that marijuana offers can be gotten from CBD without the side effect that concerns medical professionals.

In order to most efficiently produce the desired results from CBD, the component is extracted from the cannabis plant via a CO2 extraction process, leaving the cannabidiol separated from the rest of the components. CO2 is known as a ‘tunable’ solvent, meaning extracting CBD with CO2 makes the process as fine-tuned as possible (edenlabs.com).  Then, the cannabidiol is mixed with substances like coconut oil or vegetable glycerine to make CBD oil, the form that CBD is most often consumed as. All CBD oil can be taken sublingually, meaning under the tongue, and CBD oil with vegetable glycerine can be vaped as well. Different amounts of CBD can be added in order to create different strengths of CBD oil. Prof. Whyte’s CBD Oil comes in strengths from 150-1500 milligrams per bottle, and is also sold as a crumble, within candy or vegan edibles, and in a body lotion for topical use.


Where Does Our CBD Oil Come From?

Prof. Whyte’s CBD Oil is extracted from domestically sourced industrial hemp, which naturally contains high
levels of CBD and only trace amounts of THC. Industrial hemp is used for a plethora of things, including medicine, rope/cords, building materials, textiles, dynamite/TNT, plastics, and fuels (hempaware.com).

Why Use CBD?

There are many reasons why someone might use CBD, just as there are many potential benefits of CBD. During the 2015 Senate Caucus on International Drug Control, Nora D. Volkow, director at the National Institute on Drug Abuse, spoke about the science behind therapeutic uses for CBD as well as ongoing research on the subject.  Her address begins by reassuring the caucus on the safety of CBD, just like we have done previously in this article. She shifts then to provide “An overview of what the science tells us about the therapeutic potential of CBD and the ongoing research” on the substance. Volkow  address the myriad benefits of CBD one at a time, we’ll attempt to summarize below!


Volkow’s address, as well as other articles on the subject, stress a lack of clinical trials on CBD and seizures. That being said, Volkow and others also point out the positive findings of studies done on animal models where seizure activity was reduced with CBD. On top of these studies, Volkow and groups like CURE, focused on promoting epilepsy research, acknowledge anecdotal evidence from parents of and people with seizures that have benefited from the use of CBD. While these testimonials aren’t steadfast proof of CBD’s anti-seizure properties, they do show that people have found success here when they found it nowhere else. These testimonials have not infrequently become news stories, like Wired magazine’s article “Boy, Interrupted” which details one father’s turn to CBD after countless attempts to ease his son’s seizures ended fruitlessly.

In this case, the boy in question, Sam, was experiencing up to 100 seizures a day, and had visited “six neurologists at four hospitals in three states,” with little success. At the end of their rope, Sam’s family took him to London’s Great Ormond Street Hospital where they had set up CBD pills to be made specifically for their son. The day before treatment started Sam had 68 seizures, by the next day it was already down to 10. At the time the article was written, he was “between zero and five seizures a day,” and “living like a normal boy.” (Vogelstein, Wired). The hurdles Sam’s family had to jump through in order for him to receive this treatment were extreme, but the results can hardly be questioned.
There are many articles and testimonials like this one, and they make a compelling case for further research on CBD’s anti-seizure properties. As the article notes, “about 1 percent of the US population has epilepsy, and about a third of that 1 percent has epilepsy that can’t be cured by medication… 1 million Americans with uncontrolled seizures,” and it’s startling to consider that CBD could be a potential solution if it weren’t for government restrictions on research (Vogelstein, Wired). Perhaps one day restrictions will be lifted, until then families like Sam’s will have to jump through similar hoops to try a potentially life changing treatment.

Neuroprotective (aiding neurodegenerative diseases like Parkinson’s, Multiple Sclerosis, Alzheimer’s, Stroke)

Another area of research on CBD is it’s potential neuroprotective properties, which Volkow stated could be beneficial for neurodegenerative diseases such as Alzheimer’s, Parkinson’s, multiple sclerosis, stroke, and neurodegeneration due to alcohol abuse. An article on NORML.org goes further in depth on these properties, citing “a recent preclinical study” that showed cannabinoids reduced alcohol related cell death in the brain by “up to 60%,” as well as several other studies throughout the years with similar findings on neuroprotective properties (Armentano, NORML.org). Volkow ends her section on neuroprotective properties by noting a double-blind study in “patients with Parkinson’s disease [that] found the CBD improved quality-of-life scores,” which means at the very least, CBD can improve life for patients of neurodegenerative diseases, if not more (Volkow, drugabuse.gov).


Inflammation can lead to a variety of problems in the body. CBD is noted for it’s anti-inflammatory properties, and Volkow briefly touches on this in her address. Things that could be alleviated with an anti-inflammatory are conditions such as arthritis, asthma, ulcerative colitis, and others where inflammation is involved.

Pain relief

Unfortunately, most research on cannabinoids and pain relief focus on THC rather than CBD, but Volkow postulates that the known anti-inflammatory aspects of CBD alone would potentially mean that CBD is pain relieving as well. Nabiximols, a drug containing roughly equivalent amounts of THC and CBD, is approved in Canada to treat pain in some MS and cancer patients, however it’s unclear whether these effects are due to the THC, CBD, or both.


An article from NORML.org mentioned earlier also contains a section on the possibility of cannabinoids having anti-tumor properties. It mentions research done in Italy that found CBD had the ability to inhibit cancer cell growth, specifically glioma cells, as well as other studies that saw CBD help “halt the progression of lung carcinoma, leukemia, skin carcinoma, colorectal cancer, prostate cancer and breast cancer.” (Armentano, NORML.org). Volkow’s testimony noted that CBD might be tumor-reducing as well, though further testing on human subjects would be needed before this could be said conclusively.


While Volkow quickly points out that marijuana as a whole has been linked in several studies to increased risk of psychosis, she observes that THC is the probable culprit, and that a few “small scale clinical trials” reported positive results when psychosis was treated  with CBD. More research and larger studies would be needed for these findings to be supported, but it seems as though CBD could be an anti-psychotic.


Perhaps the benefit that Volkow is most certain of is CBD’s anti-anxiety properties. Because CBD’s anti-anxiety properties have been tested on both animals and humans, Volkow sees the evidence as more fully corroborated than other effects we’ve discussed. CBD’s ability to improve PTSD symptoms in a laboratory model is a promising sign, as well as another study where CBD was shown to improve stage fright in people with social anxiety. While the exact mechanism of how CBD reduces anxiety is unknown, it seems fairly certain that CBD’s anti-anxiety properties are effective.

Further Possibilities

Volkow ends her address by noting areas of CBD research that are just being looked into, including treating substance abuse disorders, cognitive deficits caused by THC, and neuropathic pain from a spinal cord injury.

In-article References:


Volkow’s list of references:

• i Welty et al. Cannabidiol: promise and pitfalls. Epilepsy Curr. 14(5):250-2. (2014).
• ii Borgelt et al. The pharmacologic and clinical effects of medical cannabis. Pharmacotherapy (Review) 33 (2): 195–209 (2013).
• iii Martin-Santos et al. Acute effects of a single, oral dose of d9-tetrahydrocannabinol (THC) and cannabidiol (CBD) administration in healthy volunteers. Curr Pharm Des. 2012;18(32):4966-79.
• iv Fusar-Poli et al. Distinct Effects of Δ9-Tetrahydrocannabinol and Cannabidiol on Neural Activation During Emotional Processing. Arch Gen Psychiatry. 2009;66(1):95-105.
• v Winton-Brown et al. Modulation of Auditory and Visual Processing by Delta-9-Tetrahydrocannabinol and Cannabidiol: an fMRI Study. Neuropsychopharmacology. 2011 Jun;36(7):1340-8.
• vi Jones et al. Cannabidiol exerts anti-convulsant effects in animal models of temporal lobe and partial seizures. Seizure. 2012 Jun;21(5):344-52.
• vii Consroe P and Wolkin A. Cannabidiol–antiepileptic drug comparisons and interactions in experimentally induced seizures in rats. J Pharmacol Exp Ther. 1977 Apr;201(1):26-32.
• viii Porter BE and Jacobson C. Report of a parent survey of cannabidiol-enriched cannabis use in pediatric treatment-resistant epilepsy. Epilepsy & Behavior 29 (2013) 574–577.
• ix Press et al. Parental reporting of response to oral cannabis extracts for treatment of refractory epilepsy. Epilepsy & Behavior 45 (2015) 49–52.
• x Hussain et al. Perceived efficacy of cannabidiol-enriched cannabis extracts for treatment of pediatric epilepsy: A potential role for infantile spasms and Lennox-Gastaut syndrome. Epilepsy Behav. 2015 Apr 29. pii: S1525-5050(15)00157-2.
• xi Gloss and Vickrey B. Cannabinoids for epilepsy. Cochrane Database Syst Rev. 3:CD009270. (2014).
• xii Esposito G et al. The marijuana component cannabidiol inhibits beta-amyloid-induced tau protein hyperphosphorylation through Wnt/beta-catenin pathway rescue in PC12 cells. J Mol Med (Berl). 84(3):253-8. (2006).
• xiii Martín-Moreno et al. Cannabidiol and Other Cannabinoids Reduce Microglial Activation In Vitro and In Vivo: Relevance to Alzheimer’s Disease. Molecular Pharmacology. 79(6):964-973. (2011).
• xiv Iuvone et al.Neuroprotective effect of cannabidiol, a non-psychoactive component from Cannabis sativa, on beta-amyloid-induced toxicity in PC12 cells. J Neurochem. 89(1):134-41. (2004).
• xv Pazos et al. Mechanisms of cannabidiol neuroprotection in hypoxic-ischemic newborn pigs:role of 5HT(1A) and CB2 receptors. Neuropharmacology. 71:282-91. (2013).
• xvi Hampson et al. Cannabidiol and (-)Delta9-tetrahydrocannabinol are neuroprotective antioxidants. Proc Natl AcadSci U S A.95(14):8268-73. (1998).
• xvii Pryce et al. Neuroprotection inExperimental Autoimmune Encephalomyelitis and Progressive Multiple Sclerosis by Cannabis-Based Cannabinoids. J Neuroimmune Pharmacol. 2014 Dec 24. [Epub ahead of print]
• xviii García-Arencibia et al. Evaluation of the neuroprotective effect of cannabinoids in a rat model of Parkinson’s disease: importance of antioxidant and cannabinoid receptor-independent properties. Brain Res. 1134(1):162-70. (2007).
• xix Hamelink et al. Comparison of cannabidiol, antioxidants, and diuretics in reversing binge ethanol-induced neurotoxicity. J Pharmacol Exp Ther. 2005 Aug;314(2):780-8.
• xx Di Marzo and Centonze . Placebo effects in a multiple sclerosis spasticity enriched clinical trial with the oromucosal cannabinoid spray (THC/CBD): dimension and possible causes. CNS Neurosci Ther. 21(3):215-21. (2015).
• xxi Flachenecker et al. Nabiximols (THC/CBD oromucosal spray,Sativex®) in clinical practice–results of a multicenter, non-interventional study (MOVE 2) in patients with multiple sclerosis spasticity. Eur Neurol.71(5-6):271-9. (2014)
• xxii Chagas et al. Effects of cannabidiol in the treatment of patients with Parkinson’s disease: an exploratory double-blind trial. J Psychopharmacol. 28(11):1088-98. (2014).
• xxiii Russo EB. Cannabinoids in the management of difficult to treat pain. Therapeutics and Clinical Risk Management. 4(1):245-259.(2008).
• xxiv Iskedjian et al. Meta-analysis of cannabis based treatments for neuropathic and multiple sclerosis-related pain. Curr Med Res Opin. 23(1):17-24.(2007).
• xxv Svendsen et al. Does the cannabinoid dronabinol reduce central pain in multiple sclerosis? Randomised double blind placebo controlled crossover trial. BMJ. 2004 Jul 31;329(7460):253.
• xxvi Portenoy et al. Nabiximols for opioid-treated cancer patients with poorly-controlled chronic pain: a randomized, placebo-controlled, graded-dose trial. J Pain. 2012 May;13(5):438-49.
• xxvii Neelakantan et al. Distinct interactions of cannabidiol and morphine in three nociceptive behavioral models in mice. Behav Pharmacol. 26(3):304-14. (2015).
• xxviii McAllister et al. The Antitumor Activity of Plant-Derived Non-Psychoactive Cannabinoids. J Neuroimmune Pharmacol. 2015 Apr28. [Epub ahead of print]
• xxix McAllister et al. The Antitumor Activity of Plant-Derived Non-Psychoactive Cannabinoids. J Neuroimmune Pharmacol. 2015 Apr28. [Epub ahead of print].
• xxx Massi et al. 5-Lipoxygenase and anandamide hydrolase (FAAH) mediate the antitumor activity of cannabidiol, a non-psychoactive cannabinoid. J Neurochem. 2008 Feb;104(4):1091-100.
• xxxi Wilkinson et al. Impact of Cannabis Use on the Development of Psychotic Disorders. Curr Addict Rep. 2014 Jun 1;1(2):115-128.
• xxxii Iseger and Bossong. A systematic review of the antipsychotic properties of cannabidiol in humans. Schizophr Res. 162(1-3):153-61. (2015).
• xxxiii Guimaraes et al. Antianxiety effect of cannabidiol in the elevated plus-maze. Psychopharmacology (Berl) 100:558–559 (1990).
• xxxiv Lemos et al. Involvement of the prelimbic prefrontal cortex on cannabidiol-induced attenuation of contextual conditioned fear in rats. Behav Brain Res 207:105–111(2010).
• xxxv Bergamaschi et al. Cannabidiol reduces the anxiety induced by simulated public speaking in treatment-naive social phobia patients. Neuropsychopharmacology 2011;36:1219–1226.
• xxxvi Das et al. Cannabidiol enhances consolidation of explicit fear extinction in humans. Psychopharmacology (Berl). 2013 Apr;226(4):781-92.
• xxxvii Campos et al. Involvement of serotonin-mediated neurotransmission in the dorsal periaqueductal gray matter on cannabidiol chronic effects in panic-like responses in rats. Psychopharmacology (Berl). 2013 Mar;226(1):13-24.
• xxxviii Katsidoni et al. Cannabidiol inhibits the reward-facilitating effect of morphine: involvement of 5-HT1A receptors in the dorsal raphe nucleus. Addict Biol. 2013;18(2):286–96.
• xxxix Ren et al. Cannabidiol, a nonpsychotropic component of cannabis, inhibits cue-induced heroin seeking and normalizes discrete mesolimbic neuronal disturbances. J Neurosci. 2009;29(47):14764–9.
• xl Pertwee RG. The diverse CB1 and CB2 receptor pharmacology of three plant cannabinoids: Δ9-tetrahydrocannabinol, cannabidiol and Δ9-tetrahydrocannabivarin. Br J Pharmacol. 2008 Jan; 153(2): 199–215.
• xli Bergamaschi et al. Safety and side effects of cannabidiol, a Cannabis sativa constituent. Curr Drug Saf. 2011 Sep 1;6(4):237-49