Virginia Thornley, M.D.
April 3, 2019
Cannabidiol has been in the news lately blown up by the media as the miracle cure. You see anecdotal information that it works for various conditions. The research has been slow since it was previously a schedule 1 agent now declassified. Attention is now turned to the different conditions where It might work including dermatologic disorders. But what are the mechanisms?
Mechanisms how cannabidiol might work in dermatologic disorders.
Melanogenesis occurs as protection from dangerous factors such as UV radiation exposure. In one study, cannabidiol increases MITP or microphthalmia associated transcription factor through one pathway involved in MAPK (mitogen activating protein kinase) phosphorylation of p38 as well as p42 MAPK.
Potential effects on acne vulgaris
Cannabidiol was found to reduce the multiplication of sebocytes, the cells in the sebaceous glands by activating the TPRV channels (transient receptor potential of vanilloid). It reduces the production of the oily substances from the skin. It controls inflammation by inhibition of the NF-kB signalling
Potential effects on psoriasis
Cannabinoids are found to reduce proliferation of cancer cells in cell lines in some studies. One study sought to study reduction of keratinocytes in an inflammatory condition such as psoriasis. It was found it can reduce the proliferation but may not contribute significantly to the process.
- Kim, M.O., Kang, M., Oh, S.W., Nho, Y.H., Park, S.H., Lee, J., Cannabidiol upregulates melanogenesis through CB1 dependent pathway by activating p38 MAPK and p42/44 MAPK. Chem Biol Interact 2017, Aug;273:107-114
- Olah, A., Toth, B., Borbiro, I, Sugawara, K., Szoliosi, A.G., Czifra, G., Pal, B., Ambrus, L., Kloepper, J., Camera, E., Ludovici, M., Picardo, M., Voets, T., Zouboulis, C.C., Paus, R., Biro, T. Cannabidiol exerts sebostatic and anti-inflammatory effects on human sebocytes, J. Clin Invest. 2014 Sep; 124(9):3713-24
- Wilkinson, J.D., Williamson, E.M. Cannabinoids inhibit keratinocyte proliferation through a non-CB1/CB2 mechanism and have a potential therapeutic value in the treatment of psoriasis. J. Dermatol. Sci 2007 Feb; 45(2):87-92