One of the most common uses for CBD is undoubtedly pain.
This is not new. Hua Tho, a second-century Chinese physician invented mafeisan, ‘hemp boiling powder’ which dissolved in wine. It was the first recorded general anaesthesia employed during a surgical procedure.
Back to the modern day, there’s a good body of emerging evidence suggesting that CBD may be useful for all kinds of pain. Pain is usually differentiated into:
– neuropathic (originating in nerves)
– visceral (originating in an organ eg. menstrual cramps)
– somatic (musculoskeletal or the skin)
– psychogenic (the experience of a panic attack or tension headache for example).
CBD is an incredible plant compound, because it can have many different effects in the body all at one time – its impact is ubiquitous. Mechanistically speaking, CBD pushes a lot of buttons that help reduce pain.
- CBD increases Anandamide, which is anti-inflammatory and analgesic upon activation of the CB1 receptor within the nervous system (Huang et al., 2016)..
- CBD turns down the volume at mu (μ) and delta (δ) opioid receptors to reduce pain signalling (Kathmann et al., 2006)
- CBD turns down the volume at Glycine receptors to reduce pain signalling (Xiong et al., 2012)
- CBD increases the signalling at GABA receptors to overcome the sensation of pain (Bakas., et al 2017)
- CBD activates TRPV1 and TRPA1 receptors to reduce pain signalling (Muller et al., 2018)
- CBD promotes adenosine A2A signalling which may reduce pain (Pandolfo et al., 2011)
Clinical trials with CBD have also found it to be effective for managing pain. CBD (2.5mg per actuation) have been shown to significantly reduce neuropathic pain compared to placebo (Wade et al., 2002), (Notcutt et al., 2004).
Bakas, T. et al. (2017) ‘The direct actions of cannabidiol and 2-arachidonoyl glycerol at GABAA receptors’, Pharmacological Research. Academic Press, 119, pp. 358–370. doi: 10.1016/j.phrs.2017.02.022.
Huang, W. J., Chen, W. W. and Zhang, X. (2016) ‘Endocannabinoid system: Role in depression, reward and pain control (Review)’, Molecular Medicine Reports. Spandidos Publications, pp. 2899–2903. doi: 10.3892/mmr.2016.5585.
Kathmann, M. et al. (2006) ‘Cannabidiol is an allosteric modulator at mu- and delta-opioid receptors’, Naunyn-Schmiedeberg’s Archives of Pharmacology, 372(5), pp. 354–361. doi: 10.1007/s00210-006-0033-x.
Muller, C., Morales, P. and Reggio, P. H. (2019) ‘Cannabinoid ligands targeting TRP channels’, Frontiers in Molecular Neuroscience. Frontiers Media S.A. doi: 10.3389/fnmol.2018.00487.
Notcutt, W. et al. (no date) Initial experiences with medicinal extracts of cannabis for chronic pain: Results from 34 ‘N of 1’ studies.
Pandolfo, P. et al. (2011) ‘Cannabinoids inhibit the synaptic uptake of adenosine and dopamine in the rat and mouse striatum’, European Journal of Pharmacology. Elsevier B.V., 655(1–3), pp. 38–45. doi: 10.1016/j.ejphar.2011.01.013.
Wade, D. T. et al. (2003) ‘(No Title)’, Clinical Rehabilitation, 1, pp. 21–29. doi: 10.1191/0269215503cr581oa.
Xiong, W. et al. (2012) ‘Cannabinoids suppress inflammatory and neuropathic pain by targeting α3 glycine receptors’, Journal of Experimental Medicine, 209(6), pp. 1121–1134. doi: 10.1084/jem.20120242.