 
      The Beginner's Guide to CBD, Part 4: Why Does CBD Work?
People areΒ using CBD to support a variety of healthΒ conditionsΒ and some are calling it aΒ modern-dayΒ panacea. While we at Lily Hill wouldn't go quite that far, there are multipleΒ clinical trialsΒ showing that CBDΒ can be used to supportΒ anxiety, chronic pain,Β epilepsy, schizophrenia,Β cancer and so much more.Β
How can one little molecule help with such a wide range ofΒ conditions?Β Science is helping us figure that out, with studies showingΒ thatΒ CBD has more than 65 molecular targets (i.e., the molecules in the body with which CBD interacts).Β Of these,Β scientists believe the followingΒ areΒ the most important targets for CBDβsΒ therapeutic potential:Β
- The endocannabinoid systemΒ (ECS)
- Serotonin receptorsΒ
- Pain receptorsΒ
- Gene activation receptorsΒ
- Other receptorsΒ
- EnzymesΒ
WeΒ covered theΒ ECS in PartsΒ 2Β &Β 3Β of this series and will therefore be exploring someΒ of the otherΒ targetsΒ in this post.Β
SerotoninΒ ReceptorsΒ
You likely know thatΒ serotonin is aΒ neurotransmitter thatΒ plays aΒ large role in mood and emotions. What you may not know is that serotoninΒ isΒ alsoΒ used forΒ digestion, bone synthesis and cardiovascular function.Β Β
So,Β whatβs the link between CBD and serotonin?Β CBD can mimic serotonin in the brain (I know, amazing!).
CBDΒ can bind and activate your body's 5-HT1A serotonin receptors. The 5-HT1A serotonin receptorΒ is what many anti-anxiety and anti-depressant medications target. ThisΒ is likely the reason for CBDβs anti-anxietyΒ properties.Β These effectsΒ have alsoΒ contributed to the view that CBD holds potentialΒ to be used as aΒ tool for addiction recoveryΒ because this serotonin receptor has also been shown to inhibit drug-seeking behavior.
Pain ReceptorsΒ
An important pain receptor with which CBD interacts isΒ TRPV1. These receptors are found throughout your body and can detect temperature.Β They are essentialΒ for helping us to respond quickly to situations that could damage your body.Β For example, if you put your hand on a wood stove, these receptors willΒ tell you itβsΒ hot by causing pain (and you'll move your hand--fast!).
When the body isΒ dealingΒ withΒ inflammation or injury, chemicalsΒ in the body are released and can increase the sensitivity to the TRPV1 receptors, thereby causing you to have pain. CBD works by desensitizingΒ these receptors.Β The effect that CBD has onΒ TRPV1 receptorsΒ isΒ considered pivotal toΒ itsΒ usefulness in treating epilepsy and arthritic pain.
Gene Activation ReceptorsΒ
AnotherΒ class of receptors thatΒ CBDΒ activatesΒ is calledΒ peroxisome proliferator-activated receptor Ξ³Β (PPARΞ³). When activated, it changes which genes in your DNAΒ canΒ be expressed.Β PPARΞ³βsΒ main function is to help regulate metabolism, but it also reduces production of inflammatory molecules in the body while increasing its production of antioxidants.
CBD's activation ofΒ PPARΞ³ may be the keyΒ to CBDβs anti-inflammatory and neuroprotective functions. This effect onΒ PPARΞ³Β has also been linked to CBD's therapeutic potential for ulcerative colitis, multiple sclerosis and Alzheimerβs disease.Β Β
Other ReceptorsΒ Β
CBD interacts with other receptors that have less definedΒ roles in the body,Β such asΒ GPR55 (G-protein-coupled receptor 55).Β Even though there is much more to learn about this receptor, itΒ has been connectedΒ toΒ appetite, insulin secretion, bone density, and (most significantly) cancer proliferation.Β
Instead of activating the GPR55 receptor, CBD actually seems to block this receptor from activating. GPR55Β activates cancer cell growth, so it is thought thatΒ CBDβsΒ blockingΒ of this receptor is why CBD appears to protect against cancer cell proliferation.
With the public's growing knowledgeΒ ofΒ CBD,Β itΒ is becoming a popular supplement for aΒ broad spectrum of uses.Β Although CBD is not a panacea for all modern ills, it does haveΒ scientifically provenΒ anti-anxiety, anti-inflammatory, anti-seizure, antioxidant, and anti-tumor activities.Β The good news is that the number of studies in the works does not appear to be slowing down.Β Β I have experienced some of these effects myself and amΒ excited to seeΒ what elseΒ science will tell us about CBD!
Sources:
- IbeasΒ Bih, C., Chen, T., Nunn, A.V.W.Β et al.Β Molecular Targets of Cannabidiol in Neurological Disorders.Β Neurotherapeutics.Β 12, 699β730 (2015).
- Russo, E.B., Burnett, A., Hall, B.Β et al.Β Agonistic Properties of Cannabidiol at 5-HT1a Receptors.Β Neurochem Res.Β 30, 1037β1043 (2005).
- Jay B. Cohn, Karl Rickels & John F. Steege.Β A Pooled, Double-blind Comparison of the effects of Buspirone, Diazepam and Placebo in Women with Chronic Anxiety. Current Medical Research and Opinion.Β 11:5.Β 304-320.Β (1989).
- JF Cryan, A.M. Redmond, J.P. Kelly and B.E. Leonard.Β The effects of the 5-HT1A agonistΒ flesinoxan, in three paradigms for assessing antidepressant potential in the rat. European Neuropsychoparmacology. 7:2,Β 109-114.Β (1997).Β
- ChristianΒ P. MΓΌller, RobertΒ J. Carey, JosephΒ P. Huston, MariaΒ A. DeΒ Souza Silva. Serotonin and psychostimulant addiction: Focus on 5-HT1A-receptors.Β Progress in Neurobiology. 81:3,Β 133-178. (2007)
- Tsuji, Fumio, and Hiroyuki Aono. βRole of transient receptor potential vanilloid 1 in inflammation and autoimmune diseases.βΒ Pharmaceuticals (Basel, Switzerland)Β 5:8 837-52. (2012)
- Fabio Arturo Iannotti, Charlotte L. Hill, Antonio Leo,Β AhlamΒ Alhusaini, CamilleΒ Soubrane, Enrico Mazzarella, Emilio Russo, Benjamin J. Whalley, Vincenzo DiΒ Marzo, and Gary J. Stephens.Β NonpsychotropicΒ Plant Cannabinoids,Β CannabidivarinΒ (CBDV) and Cannabidiol (CBD), Activate and Desensitize Transient Receptor Potential Vanilloid 1 (TRPV1) Channels in Vitro: Potential for the Treatment of Neuronal Hyperexcitability.Β ACS ChemicalΒ NeuroscienceΒ Β 5:11Β 1131-1141Β (2014)
- Kapadia, Ramya et al. Mechanisms of anti-inflammatory and neuroprotective actions of PPAR-gamma agonists. Frontiers in bioscience: a journal and virtual library.Β 13.Β 1813-26. (2008)
- Ferro R et al.Β GPR55Β signallingΒ promotes proliferation of pancreatic cancer cells andΒ tumourΒ growth in mice, and its inhibition increases effects of gemcitabine. Oncogene.Β 37:49.Β 6368-6382.Β (2018).
 
            