What is the difference between CBD and CBD-A?

CBD-A is a precursor to CBD

There are many steps in cannabinoid synthase. The compounds in hemp flowers form cannabigerolic acid (CBGA), from which various cannabinoid acids are formed, such as cannabidiol acid (CBDA). In general, CBDA is considered inactive and decarboxylated CBD is active, but current research shows that CBDA is not as useless as previously thought. As it warms up and ages, cannabinoid acids break down into cannabinoids. This process is called decarboxylation. Acidic cannabinoids are specified in the -a (acid) appendix. Raw hemp is non-decarboxylated.

CBD-A (cannabidiol acid) possibly more effective than CBD (cannabidiol)?

Raw hemp inflorescence is an excellent dietary supplement suitable for foods, groceries and skin care products.

In the light of current research, the health effects of raw hemp compounds are multidimensional and holistic, as the endocannabinoid system receiving these compounds has been found to regulate, inter alia, pain, inflammation, appetite, digestive (34, 35).

From raw hemp, the body can utilize larger amounts of cannabinoids (1), for this reason, Dr. William Courtney, a doctor specializing in the benefits of juicing raw hemp, suggests that CBD-A would be more effective than CBD when it comes to its antioxidant, anti-inflammatory, anti-diabetic and ischemia effects . Courtney says she has found health benefits in many of her patients using hemp raw. Patents have also been issued in the United States for the medicinal effects of cannabinoid acids (11, 3, 38).

As it warms up and ages, cannabinoid acids break down into cannabinoids. This process is called decarboxylation. Acidic cannabinoids are specified in the -a (acid) appendix. Raw hemp is non-decarboxylated (2, 16).

CBD-A becomes used in the body differently than CBD. Both work in multiple ways, producing a wide range of effects. To date, more research has been done on the effects of CBD.

CBD-A has been found to be anti-inflammatory, anti-nausea, antioxidant, analgesic, antiproliferative, anti-cancer, and antibacterial and antimicrobial (2, 3, 12, 15).

CBD-A has a stronger tendency to bind to the 5-HT1A receptor than CBD. 5-HT1A belongs to the serotonin receptors. These receptors elicit a wide variety of intracellular communications that produce either an excitatory (accelerating) or inhibitory (retarding) effect, depending on the chemical content of the message (13). Binding of CBD to 5-HT1A receptors provides antianxiety and depression-relieving effects (17). CBD-A has been shown to have antiemetic (nausea-reducing) effects that are even more potent than CBD or THC (17).

CBD-A can bind to GPR55, TRPA1, TRPV1, and TRPM8 receptors at doses of 1-10 μm. At higher concentrations, the compound may slow the degradation of enzymes in the endocannabinoid system via COX-1 and COX-2 receptors (29, 30).

Eating cannabinoids and cannabinoid acids may be key in the treatment of chronic diseases caused by endocannabinoid system deficiencies (9), such as migraine, irritable bowel syndrome, glaucoma, fibromyalgia, and potentially many other diseases (10).

CBD has been found to relieve pain, reduce inflammation, be a more effective antioxidant than vitamin C or E, and have antiemetic, antipsychotic, and antiepileptic effects that act through, among others, 5-HT1A, GPR55, GPR18, TRPV1, and other TRP receptors. The United States even has a patent on cannabinoids as antioxidants (31, 32, and 33).

CBD has been found to slow the natural degradation of anandamide and thus increase the amount of endocannabinoids in brain synapses. This increase in endocannabinoids may be a significant factor in the neuroprotective and other disorders of CBD. health effects (18).

In addition, CBD has been studied to increase the amount of the neurotransmitter adenosine, which regulates the activity of adenosine receptors. A1A and A2A receptors play an important role in the cardiovascular system, regulating myocardial oxygen uptake and blood flow in the coronary artery. These receptors also have broad anti-inflammatory effects in the body (20).

CBD also acts as a so-called positive allosteric modulator for the GABA-A receptor, i.e. it can enhance or inhibit the conduction of signals at these receptors. In other words, CBD increases the ability of the natural agonist of the GABA-A receptor to bind aminobutyric acid. Aminobutyric acid is one of the most important neurotransmitters in mammals. This increased butyric acid binding has sedative and anxiolytic effects (19). CBD also has a similar negative effect on the CB1 receptor, which reduces the psychoactive effects of THC (21).

CBD is associated with the TRPV1 receptor, which is known to affect pain, inflammation, and body temperature (22).

According to some studies, CBD affects the so-called as an agonist that blocks or deactivates the GPR55 receptor. The GPR55 receptor is found especially in the cerebellum. It is involved in blood pressure, bone density, etc. in the regulation of physiological processes. When it is overactive, osteoporosis occurs, which can potentially be treated with CBD. It has also been found to have antiproliferative effects, i.e., to reduce the proliferation of cancer cells. The GPR55 receptor causes the proliferation of cancer cells and is manifested in several types of cancer (23).

CBD also potentially creates cancer-reducing effects by activating PPA receptors that are expressed in cell nuclei. Studies have shown that PPA receptor activation has anti-proliferative effects as well as the ability to regress cancer (25, 26). In addition, its activation has been found to degrade amyloid-beta plaque, one of the major causes of Alzheimer’s. Therefore, the PPA receptor agonist CBD may be useful in Alzheimer’s patients (24). PPA receptors also regulate genes involved in energy homeostasis, lipid uptake, insulin sensitivity, and the like. in metabolic processes. Thus, CBD may also potentially help in the treatment of diabetes (27, 28)

Repeated experiments on animals and cells illustrate that cannabinoids have the potential to maintain health and prevent several diseases. On the other hand, more human studies are needed (2, 7, 12, 13, 14).

CBD-A et al. unexplored potential of cannabinoids

The endocannabinoid system was not understood until 1990. Subsequent studies have found that endocannabinoids and their receptors are found throughout the body, such as in the brain, organs, connective tissues, glands, central nervous system, and immune cells.

Thus, hemp cannabinoids may have more health and medicinal potential than we currently understand, as research is young and accelerating. (34, 35, 36, 37)

Thus, CBD-A may also have more latent effects than have been observed, as current studies have focused primarily on CBD and THC.

Calcium channel blockers, blood thinners, and other medications used to treat high blood pressure and arrhythmias may cause unwanted side effects in combination with CBD. CBD can reduce or prevent the breakdown of drugs. e.g for warfarin (Marevan), CBD has been shown to potentiate the effect of the drug. (39)

Finally, in addition to research data and user experience, there are already several patents in the United States for the medicinal and health effects of hemp:

“According to the invention, cannabinoid acids can be used to relieve pain and / or prevent inflammation, as well as to reduce nausea.”

– AAJ Korthout and others. Medicinal acidic cannabinoids. United States Patent. 2010

“Cannabinoids have been found to have antioxidant effects, which may make their use useful in the treatment of several inflammatory diseases.”

– Aidan J. Hampson et al. Cannabinoids as antioxidants and neuroprotectants. Google Patents. 2003

This essay is part of my dissertation on cannabinoids.

Tommi Saltiola

Agrologist AMK

Hemp researcher⎟Hemp entrepreneur

Sources:

1. D. Butterfield. Top 10 Cannabinoids And What They Do. http://herb.co/2016/02/06/top-10-cannabinoids/ . 2016.
2. D. Butterfield. Cannabidiolic Acid (CBD -A): The Raw Cannabinoid That Fights Inflammation. http://herb.co/2017/05/20/cbda/ . 2017
3. Dr. Courtney. Raw Cannabis Advantages. Patients Out of Time. Interview during the Seventh National Clinical Conference at Cannabis Therapeutics in Tucson, AZ. https://www.youtube.com/watch?v=IlsBGXNxJYU . 2012.
4. D. Butterfield. Cannabidiolic Acid (CBD -A): The Raw Cannabinoid That Fights Inflammation. Herb.co. 2017
5. N. Smith. Transdermal cannabinoid patch. https://www.google.com/patents/US20160022627 . 2016.
6. CJ Dibble and IB Cole. Methods for obtaining purified cannabis extracts and THCA crystals. https://www.google.com/patents/US20170008870 . 2016.
7. A. Izzo, F. Borreli, R. Capasso, V. Di Marzo and R. Mechoulam. Proposed Molecular mechanisms of the actions of non-psychotropic phytocannabinoids. Non-psychotropic plant cannabinoids: new Therapeutic opportunities from an ancient herb. 2009.
8. S. Takeda, K. Misawa, I. Yamamoto and K. Watanabe. Cannabidiolic Acid (CBD -A) as a Selective Cyclooxygenase-2 Inhibitory Component in Cannabis. Drug Metabolism and Disposition. http://dmd.aspetjournals.org/content/36/9/1917.long . 2008.
9. EB Russo. Clinical endocannabinoid deficiency (CECD): can this concept explain Therapeutic benefits of cannabis in migraine, fibromyalgia, irritable bowel syndrome and other treatment-resistant conditions? https://www.ncbi.nlm.nih.gov/pubmed/15159679 . 2004.
10. EB Russo. Clinical endocannabinoid deficiency (CECD): can this concept explain Therapeutic benefits of cannabis in migraine, fibromyalgia, irritable bowel syndrome and other treatment-resistant conditions? https://www.ncbi.nlm.nih.gov/pubmed/18404144 . 2008.
11. Dr. Courtney. Why You Should Be Eating Raw Weed. http://herb.co/2016/02/13/eating-raw-weed/ . 2016.
12. Radosevic. The Composition of Hemp Seed Oil and Its Potential as an Important Source of Nutrition. http://www.davoil.ro/documente/the-composition-of-seed-oil-and-its-potential-as-an-important-source-nutrition.pdf . 2000.
13. D. Bolognini et al. Cannabidiolic acid (CBD -A) prevents vomiting in Suncus murinus and nausea-induced behavior in rats by Enhancing 5-HT1A receptor activation. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3596650/ . 2013.
14. AJ. Hampson Ym. Neuroprotective antioxidants from marijuana. https://www.ncbi.nlm.nih.gov/pubmed/10863546 . 2000.
15. S. Takeda Ym. Cannabidiolic acid (CBD -A) mediated selective down-regulation of c-fos in highly aggressive breast cancer MDA-MB-231 cells: possible involvement of its down-regulation in the abrogation of aggressiveness. https://www.ncbi.nlm.nih.gov/pubmed/27530354 . 2017.
16. Dr. I Hunt. Decarboxylation. Department of Chemistry, University of Calgary.
17. M. Schier et al. Antidepressant-like and anxiolytic-like effects of cannabidio (CBS) l: a chemical compound of Cannabis sativa. Institute of Psychiatry – Federal University of Rio de Janeiro and others. 2014.
18. Deutsch DG. A Personal Retrospective: Elevating Anandamide (AEA) by Targeting Fatty Acid Amide Hydrolase (FAAH) and the Fatty Acid Binding Proteins (FABPs). Department of Biochemistry and Cell Biology, Stony Brook University Stony Brook, NY, USA. 2016.
19. Bakas T. et al. The direct actions of cannabidiol (CBD) and 2-arachidonoyl glycerol at GABAA receptors. Faculty of Pharmacy, The University of Sydney et al. 2017.
20. Ribieiro A. Cannabidiol (CBD), a non-psychotropic plant-derived cannabinoid, decreases inflammation in a murine model of acute lung injury: role for the adenosine A (2A) receptor. Neuroimmunomodulation Research Group et al. 2012.
21. RB Laprairie. Cannabidiol (CBD) is a negative allosteric modulator of the cannabinoid CB1 receptor. British Journal of Pharmacology. 2015.
22. B. Costa et al. The vanilloid TRPV1 receptor mediates the antihyperalgesic effect of the nonpsychoactive cannabinoid, cannabidiol (CBD), in a rat model of acute inflammation. British Journal of Pharmacology. 2004.
23. G. Hu et al. Oncogene – The putative cannabinoid receptor GPR55 promotes cancer cell proliferation. Key Laboratory of Stem Cell Biology et al. 2010.
24. G. Esposito et al. Cannabidiol (CBD) in vivo blunts β-amyloid induced neuroinflammation by suppressing IL-1β and iNOS expression. British Journal of Pharmacology. 2007.
25. McAllister SD. Cannabidiol (CBD) as a novel inhibitor of Id-1 gene expression in aggressive breast cancer cells. California Pacific Medical Center and others. 2007.
26. R. Ramer et al. COX-2 and PPAR-γ Confer Cannabidiol-Induced (CBD) Apoptosis of Human Lung Cancer Cells. American Association for Cancer Research. 2013.
27. JN Feige. Transcriptional coregulators in the control of energy homeostasis. Institute of Genetics and Biological Sciences Molecular and Cellular. 2007.
28. Y. Sun et al. Cannabinoids: A New Group of Agonists of PPARs. School of Biomedical Sciences, University of Nottingham Medical School. 2007.
29. P. Pacher et al. Modulating the endocannabinoid system in human health and disease: successes and failures. Laboratory of Physiologic Studies et al. 2013.
30. D. Kendall and S. Alexander. Cannabinoid Pharmacology. Advances in Pharmacology. 2017.
31. EB Russo. Cannabidiol (CBD) claims and misconceptions. Trends in Pharmacological Sciences.
32. AJ Hampson. Cannabidiol (CBD) and (-) Δ9-tetrahydrocannabinol are neuroprotective antioxidants. Laboratory of Cellular and Molecular Regulation et al. 1998.
33. Aidan J. Hampson et al. Cannabinoids as antioxidants and neuroprotectants. Google Patents. 2003.
34. Martin A. Lee. The Discovery of the Endocannabinoid System. The Prop 215 Era. 2012
35. Bradley E. Alger, Ph.D. Getting High on the Endocannabinoid System. Cerebrum. 2013.
36. L. Matsuda et al. Structure of a cannabinoid receptor and functional expression of the cloned cDNA. Letters to Nature. 1990.
37. R. Mechoulam et al. Isolation and structure of a brain constituent that binds to the cannabinoid receptor. Science. 1992
38. HAAJ Korthout et al. Medicinal acidic cannabinoids. United States Patent. 2010.
39. Kerstin Iffland and Franjo Grotenhermen. An Update on Safety and Side Effects of Cannabidiol: A Review of Clinical Data and Relevant Animal Studies
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5569602/ . 2017.

Questions and answers about CBDa and CBD in general