What is CBD?
POTENTIAL THERAPEUTIC BENEFITS OF CBD
Cannabidiol, commonly known as CBD, is one phytocannabinoid under investigation for its anxiolytic and anti-inflammatory effects, as well as its ability to reduce symptom severity with insomnia and chronic pain.
Lacking the widely known, and often controversial, psychoactive effects of ∆9-tetrahydrocannabinol (THC), research on cannabidiol has demonstrated symptom relief for a wide range of disorders.
This is due in no small part to its effects on activity in limbic and paralimbic areas of the brain and receptors throughout the body.
CBD has an excellent safety profile with limited adverse effects compared with other available treatments. However, while popular belief holds that CBD is a relatively benign substance, clinical evidence shows that there is a potential for drug-drug interactions. Given the wide availability of products containing CBD on the market today, from tinctures to coffee additives, this underscores the necessity for medical supervision of CBD intake and formulation-specific clinical research.
Cannabidiol exerts its effects primarily through the endocannabinoid system or ECS. The endocannabinoid system was identified in the 1992 by Raphael Mechoulam, an Israeli organic chemist and professor of Medicinal Chemistry at the Hebrew University of Jerusalem in Israel.
Studying the effects of cannabis since the 60’s, Dr. Mechoulam ascertained that THC (tetrahydrocannabinol) interacts with the largest receptor system in the human body, the endocannabinoid system (ECS). He then found that the human brain produces its very own Cannabis-like substance, a chemical they named "anandamide" after the Sanskrit word ananda, meaning “bliss”.
Anandamide exerts positive effects on mood, memory, brain function and pain, but it is rapidly inactivated by an enzyme (FAAH) making its effect short lived. CBD actually inhibits the action of the FAAH enzyme so that the body’s naturally made anandamide continues to be active, prolonging the positive effect on mood, memory, brain function and pain relief.
Our body’s ECS has at least two major receptors, CB1 and CB2, and also produces other endocannabinoids beside anandamide. The CB1 receptors are typically found in the brain and throughout the nervous system while CB2 receptors are primarily found in the immune system. Consequently, we can see why CBD oil is touted to treat illnesses from A to Z…acne, allergy, anxiety, epilepsy, pain, etc.
CBD oil extract naturally contains a number of different cannabinoids, as well as essential vitamins, minerals, fatty acids, and amino acids, but may also contain other active components such as flavonoids and terpenes. THC, the psychoactive component in hemp, is found in higher concentrations in products designed for use such as medical marijuana. However, all full spectrum products available outside of medical and recreational marijuana, by law have less than 0.3% THC and therefore have no psychoactive effects on a person, though may possibly result in a positive THC drug screen.
STUDIES ON CBD
Attenuation of the dopaminergic impairment in vivo; neuroprotection; improvement of psychiatric rating and reduction of agitation, nightmare and aggressive behavior in patients.
Lastres-Becker et al. (2005), Zuardi et al. (2009), Chagas, Eckeli, et al. (2014)
Improved signs of EAE in mice, anti-inflammatory and immunomodulatory properties.
Buccellato et al. (2011), Kozela et al. (2011, 2015), Mecha et al. (2013), Giacoppo et al. (2015)
Anticonvulsant in vitro and in vivo; reduced seizures frequency in children and adults with treatment-resistant epilepsy.
Pertwee (2008), Devinsky et al. (2016)
Short term neuroprotective effects; inhibition of excitotoxicity, oxidative stress, and inflammation in vitro and in rodent models.
Pazos et al. (2012, 2013), Hayakawa et al. (2007, 2009), Valdepefias et al. (2011)
Analgesic effect in patients with neuropathic pain resistant to other treatments.
Petzke et al. (2016), Boychuk et al.
Reduction of muscular tension, restlessness, fatigue, problems in concentration, improvement of social interactions in rodent models of anxiety and stress; reduced social anxiety in patients.
Lemos et al. (2010), Almeida et al. (2013), Moreira et al. (2006), de Mello Schier et al. (2014), Bergamaschi et al. (2011), Marinho et al. (2015)
Antidepressant effect in genetic rodent model of depression.
El-alfy et al. (2010), Hsiao et al. (2012), Shoval et al. (2016)
Anti-inflammatory properties in several in vitro and in vivo models; inhibition of inflammatory cytokines and pathways.
Ribeiro et al. (2012, 2015), Kozela et al. (2010, 2011), Mecha et al. (2012, 2013)
Inhibition of TNF-α in an animal model.
Malfait et al. (2000)
Activity gains against methicillin-resistant Staphylococcus aureus.
Appendino et al. (2008)
IBS and Crohn’s Disease
Inhibition of macrophage recruitment and TNF-α secretion in vivo and ex vivo; reduction in disease activity index in Crohn’s patients.
Sacerdote et al. (2005), De Filippis et al. (2011), Naftali et al. (2011)
Reduced infarct size through anti-oxidant and anti-inflammatory properties in vitro and in vivo.
Durst et al. (2007), Booz (2011), Stanley et al. (2013)