Sep 16 2016
Numerous clinical studies and scientific papers are reporting successful therapy with CBD cannabinoids. The greatest attention is in the field of auto-immune diseases. Recent research, including clinical, has confirmed that the CBD is as important as THC, in some cases even more so.
What is CBD or cannabidiol?
CBD or cannabidiol is one of 85 active phytocannabinoids identified in cannabis resin which are located on the hairs of bracts and in flowers of hemp (1). CBD is a lipophilic molecule and has no noticeable psychoactive effects. CBD represents over 40% of phytocannabinoids in the extract of plants and is present in almost all varieties of cannabis, mostly in hemp (Cannabis sativa).
Are cannabinoids only present in hemp?
Cannabinoid molecules are not only present in hemp and other plants, but are also found in the human body and the bodies of all vertebrates, called endocannabinoids. Cannabinoids serve as intercellular “fat messengers” and are signaling molecules which are released from a cell membrane and activate cannabinoid receptors in other nearby cell membranes. Their signals are retrograde, which means that they move in the opposite direction to the normal intercellular signals or the exchange of materials and communication. Their signals communicate inhibiting, reducing, stabilising and triggering different cell changes and are involved in regulating a variety of physiological processes in the body (2-5).
Why is CBD so effective in autoimmune diseases?
Animal and plant cannabinoids can only be effective if they bind to the cannabinoid receptors in cells and are then degraded by enzymes. Receptors are small proteins that are embedded into each cell membrane. When a specific molecule binds itself as a key to these receptors, cellular changes (3-6) begin to happen. CBD molecule binds to GPR55, CB2, TRPV4 receptors and a little less to the CB1 receptors in the cell. The secret to successful CBD activity is the fact that most of the cannabinoid CB2 receptors are located in the lymphoid organs (tonsils, thymus gland, spleen, lymphatic glands and lymph nodes) and can signal a reduced reaction of the immune system (6). You can also find cannabinoid receptors in skin cells, thus the functioning of CBD is also active locally via dermal routes (7).
How does CBD work in treating acne and psoriasis?
The endocannabinoid system (ECS) regulates many physiological processes in the body, including the growth of skin cells and their differentiation (diversity). EKS is affected by a CBD plant molecule, which has been used in a number of clinical studies without major side-effects (8) and a number of further second and third phases of studies attempt to explore its future therapeutic potential. Recent research in the field of skin diseases, is detecting the potential of CBD molecules in the treatment of acne and psoriasis (9,10). Acne and psoriasis are the most common human skin diseases, affecting the life quality of millions of people around the world.
Acne is caused by the excessive production of sebum (fat secreted by the sebaceous glands), inflammation and rapid proliferation of cells (sebocyte), which form sebaceous glands and secrete sebum. Fast reproduction of skin cells (keratinocytes which produce keratin protein) results in scaly skin or psoriasis. Clinical studies have shown that the CBD molecule reduces lipogenesis of sebocytes (accumulation of fat in the sebaceous gland) through activation of the receptor cell membrane TRPV4 and nuclear receptor protein-1 (NRIP1), which affects the level of glucose (sugar) and fat metabolism, thereby inhibiting sebocytes (9).
CBD also performs a complex anti-inflammatory action, as has already been demonstrated in a number of other experimental studies of diabetes, rheumatoid arthritis and the like (11). In order to confirm the alleged universal anti-inflammatory effect of CBD on human sebocytes the study included modelling of both Gram-negative and Gram-positive bacterial infections. The results showed that the CBD fully prevented Gram-positive bacterial infection (9, 12, 13, 14).
A slower division of sebaceous glands cells and cells producing keratin results from the oral and dermal application of hemp CBD resin extract, which can effectively treat psoriasis and acne with an appropriate dosage (10, 15, 20).
Based on these findings it can be claimed that phytocannabinoids from hemp, mimic the endocannabinoid system in our body and therefore have a great potential for the development of new, natural therapies for the treatment of many diseases (16, 17, 18, 19).
How is the legislation in the field of potential application of CBD regulated?
Cannabidiol or CBD is not a psychoactive substance and as such is not prohibited and is not on the list of narcotic drugs, nor is it otherwise legally regulated. Slovenian legislation allows the possibility to grow hemp (less than 0.2 percent of THC and a high content of CBD).
Clinical studies and scientific articles
3.Abood ME, Sorensen RG, Stella N, eds.endoCANNABINOIDS.New York, New York, USA: Springer Science+Business Media New York; 2013.
5.Russo EB. Taming THC: potential cannabis synergy and phytocannabinoid-terpenoid entourage effects.Br J Pharmacol.2011;163(7):1344–1364. doi: 10.1111/j.1476-5381.2011.01238.x.[PMC free article][PubMed][Cross Ref]
6. Thomas A, Baillie GL, Phillips AM, Razdan RK, Ross RA, Pertwee RG. Cannabidiol displays unexpectedly high potency as an antagonist of CB1 and CB2 receptor agonist.Br J Pharmacol.2007;150:613–623.[PMC free article][PubMed]
7. Lodzki M, et al. Cannabidiol-transdermal delivery and anti-inflammatory effect in a murine model. J Control Release. 2003;93(3):377–387. doi: 10.1016/j.jconrel.2003.09.001. [PubMed] [Cross Ref]
8. Pertwee RG. Cannabinoid pharmacology: the first 66 years. Br J Pharmacol.2006;147(suppl 1):S163–S171. [PMC free article] [PubMed]
9. Attila Oláh, Balázs I. Tóth, [...], and Tamás Bíró. Cannabidiol exerts sebostatic and antiinflammatory effects on human sebocytes. J Clin Invest. 2014 Sep;124(9):3713-24. doi: 10.1172/JCI64628. Epub 2014 Jul 25.
10.Wilkinson JD, Wiliamson EM. Cannabinoids inhibit human keratinocyte proliferation through a non-CB1/CB2 mechanism and have a potential therapeutic value in the treatment of psoriasis.J Dermatol Sci.2007;45(2):87–92. doi: 10.1016/j.jdermsci.2006.10.009.[PubMed][Cross Ref]
11.Booz GW. Cannabidiol as an emergent therapeutic strategy for lessening the impact of inflammation on oxidative stress.Free Radic Biol Med.2011;51(5):1054–1061. doi: 10.1016/j.freeradbiomed.2011.01.007.[PMC free article][PubMed][Cross Ref]
12. Klein TW. Cannabinoid-based drugs as anti-inflammatory therapeutics.Nat Rev Immunol.2005;5:400-411. PubMed
13. Tubaro A, et al. Comparative topical anti-inflammatory activity of cannabinoids and cannabivarins. Fitoterapia. 2010;81(7):816–819. doi: 10.1016/j.fitote.2010.04.009. [PubMed] [Cross Ref]
14.Ribeiro A, et al. Cannabidiol, a non-psychotropic plant-derived cannabinoid, decreases inflammation in a murine model of acute lung injury: role for the adenosine A(2A) receptor.Eur J Pharmacol.2012;678(1–3):78–85.PubMed
16. Hill AJ, Williams CM, Whalley BJ, Stephens GJ. Phytocannabinoids as novel therapeutic agents in CNS disorders. Pharmacol Ther. 2012a;133:79–97.[PubMed]
17. Mariangela Pucci, Cinzia Rapino, [...], and Mauro Maccarrone. Epigenetic control of skin differentiation genes by phytocannabinoids. 2013 Oct;170(3):581-91. doi: 10.1111/bph.12309.Br J Pharmacol.
18.Kupczyk P, Reich A, Szepietowski JC. Cannabinoid system in the skin - a possible target for future therapies in dermatology.Exp Dermatol.2009;18(8):669–679. doi: 10.1111/j.1600-0625.2009.00923.x.PubMedCross Ref
19.Bíró T, et al. The endocannabinoid system of the skin in health and disease: novel perspectives and therapeutic opportunities.Trends Pharmacol Sci.2009;30(8):411–420. doi: 10.1016/j.tips.2009.05.004.PMC free articlePubMedCross Ref
20.Tóth BI, et al. Endocannabinoids modulate human epidermal keratinocyte proliferation and survival via the sequential engagement of cannabinoid receptor-1 and transient receptor potential vanilloid-1.J Invest Dermatol.2011;131(5):1095–1104. doi: 10.1038/jid.2010.421.PubMedCross Ref