The Beginner's Guide to CBD, Part 4: Why Does CBD Work?

People are using CBD to support a variety of health conditions and some are calling it a modern-day panacea. While we at Lily Hill wouldn't go quite that far, there are multiple clinical trials showing that CBD can be used to support anxiety, chronic pain, epilepsy, schizophrenia, cancer and so much more. 

How can one little molecule help with such a wide range of conditions? Science is helping us figure that out, with studies showing that CBD has more than 65 molecular targets (i.e., the molecules in the body with which CBD interacts)Of these, scientists believe the following are the most important targets for CBD’s therapeutic potential: 

  • The endocannabinoid system (ECS)
  • Serotonin receptors 
  • Pain receptors 
  • Gene activation receptors 
  • Other receptors 
  • Enzymes 

We covered the ECS in Parts 2 & 3 of this series and will therefore be exploring some of the other targets in this post. 

Serotonin Receptors 

You likely know that serotonin is a neurotransmitter that plays a large role in mood and emotions. What you may not know is that serotonin is also used for digestion, bone synthesis and cardiovascular function.  

So, what’s the link between CBD and serotonin? CBD can mimic serotonin in the brain (I know, amazing!).

CBD can bind and activate your body's 5-HT1A serotonin receptors. The 5-HT1A serotonin receptor is what many anti-anxiety and anti-depressant medications target. This is likely the reason for CBD’s anti-anxiety properties. These effects have also contributed to the view that CBD holds potential to be used as a tool for addiction recovery because this serotonin receptor has also been shown to inhibit drug-seeking behavior.

Pain Receptors 

An important pain receptor with which CBD interacts is TRPV1. These receptors are found throughout your body and can detect temperature. They are essential for helping us to respond quickly to situations that could damage your body. For example, if you put your hand on a wood stove, these receptors will tell you its hot by causing pain (and you'll move your hand--fast!).

When the body is dealing with inflammation or injury, chemicals in the body are released and can increase the sensitivity to the TRPV1 receptors, thereby causing you to have pain.CBD works by desensitizing thesereceptors. The effect that CBD has on TRPV1 receptors is considered pivotal to its usefulness in treating epilepsy and arthritic pain.

Gene Activation Receptors 

Another class of receptors that CBD activates iscalled peroxisome proliferator-activated receptor γ (PPARγ). When activated, it changes which genes in your DNA can be expressed. PPARγ’s 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 of PPARγ may be the key to CBD’s anti-inflammatory and neuroprotective functions. This effect on PPARγ has also been linked to CBD's therapeutic potential for ulcerative colitis, multiple sclerosis and Alzheimer’s disease.  

Other Receptors  

CBD interacts with other receptors that have less defined roles in the body, such as GPR55 (G-protein-coupled receptor 55). Even though there is much more to learn about this receptor, it has been connected to appetite, insulin secretion, bone density, and (most significantly) cancer proliferation. 

Instead of activating the GPR55 receptor, CBD actually seems to block this receptor from activating. GPR55 activates cancer cell growth, so it is thought that CBD’s blocking of this receptor is why CBD appears to protect against cancer cell proliferation.

With the public's growing knowledge of CBD, iis becoming a popular supplement for a broad spectrum of uses. Although CBD is not a panacea for all modern ills, it does have scientifically proven anti-anxiety, anti-inflammatory, anti-seizure, antioxidant, and anti-tumor activities. The good news is that the number of studies in the works does not appear to be slowing down.  Ihave experienced some of these effects myself and am excited to see what else science will tell us about CBD!

Sources:

  1. Ibeas Bih, C., Chen, T., Nunn, A.V.W. et al. Molecular Targets of Cannabidiol in Neurological Disorders. Neurotherapeutics. 12, 699–730 (2015).
  2. Russo, E.B., Burnett, A., Hall, B. et al. Agonistic Properties of Cannabidiol at 5-HT1a Receptors. Neurochem Res. 30, 1037–1043 (2005).
  3. Jay B. Cohn, Karl Rickels & John F. Steege.  A Pooled, Double-blind Comparison of the effects of Buspirone, Diazepam and Placebo in Women with Chronic Anxiety. Current Medical Research and Opinion. 11:5. 304-320(1989).
  4. JF Cryan, A.M. Redmond, J.P. Kelly and B.E. Leonard. The effects of the 5-HT1A agonist flesinoxan, in three paradigms for assessing antidepressant potential in the rat. European Neuropsychoparmacology. 7:2, 109-114. (1997). 
  5. Christian P. Müller, Robert J. Carey, Joseph P. Huston, Maria A. De Souza Silva. Serotonin and psychostimulant addiction: Focus on 5-HT1A-receptors. Progress in Neurobiology. 81:3, 133-178. (2007)
  6. Tsuji, Fumio, and Hiroyuki Aono. “Role of transient receptor potential vanilloid 1 in inflammation and autoimmune diseases.” Pharmaceuticals (Basel, Switzerland) 5:8 837-52. (2012)
  7. Fabio Arturo Iannotti, Charlotte L. Hill, Antonio Leo, Ahlam Alhusaini, Camille Soubrane, Enrico Mazzarella, Emilio Russo, Benjamin J. Whalley, Vincenzo Di Marzo, and Gary J. Stephens. Nonpsychotropic Plant Cannabinoids, Cannabidivarin (CBDV) and Cannabidiol (CBD), Activate and Desensitize Transient Receptor Potential Vanilloid 1 (TRPV1) Channels in Vitro: Potential for the Treatment of Neuronal Hyperexcitability. ACS Chemical Neuroscience  5:11 1131-1141 (2014)
  8. Kapadia, Ramya et al. Mechanisms of anti-inflammatory and neuroprotective actions of PPAR-gamma agonists.Frontiers in bioscience: a journal and virtual library13. 1813-26. (2008)
  9. Ferro R et al. GPR55 signalling promotes proliferation of pancreatic cancer cells and tumour growth in mice, and its inhibition increases effects of gemcitabine. Oncogene. 37:496368-6382. (2018).

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