It seems to hold promise for reducing inflammation, which could alleviate pain caused by autoimmune diseases such as rheumatoid arthritis, says Dr. Cannabis, it doesn't actually produce THC or CBD. The plant produces all the cannabinoids in acid form. Instead of producing THC and CBD directly, it synthesizes tetrahydrocannabinolic acid (THCA) and cannabidiolic acid (CBDA) from their precursor, cannabigerolic acid (CBGA).
THCA is generally administered together with other components of cannabis in the form of a tincture using a dropper or spray to be placed under the tongue. Sulak's article states that higher doses of THCA generally did not improve the response, and one patient worsened after increasing the dose of THCA. Sulak also discovered that specific terpenes, together with THCA, in a given strain of cannabis can contribute significantly to the antiepileptic effect. Linalool, in this case, was necessary for the antiepileptic effect.
Goldstein told Project CBD that daily consumption of 10 to 20 mg of THCA was effective in reducing pain in some of his patients with arthritis and irritable bowel syndrome. In a patient with Alzheimer's disease, THCA improved cognitive symptoms and allowed the patient to reduce the use of other drugs. In this edition of Cannabis Conversations, the director of the CBD Project, Martin A. Lee, analyzes the benefits of CBD, the “entourage effect” and the microbiome with Dr.
Neither THCA-A nor THCA-B should be confused with THC-COOH (11-nor-9-carboxy-THC), which is a metabolic degradation product of THC in the human body. It's possible that the anti-nausea effect of smoking cannabis is partly due to the small amount of THCA that remains when cannabis is burned. In states where cannabis is legal for recreational or medical purposes, you should be able to buy CBD. They can be combined with each other or with the brand's full-spectrum Rare Hawaiian CBD oil to achieve an entourage effect.
Another explanation could result from an inconsistency between two molecular isoforms of THCA, THCA-A and THCA-B, which could result in different results (see sidebar). Interestingly, the effect of THCA in the Guelph study was prevented by blocking the CB1 cannabinoid receptor. A study conducted by Rosenthaler and a group of Austrian scientists assumed that THCA has a higher binding affinity to the CB1 receptor than THC. If so, a cannabis smoker could inhale the small amount of remaining THCA, which could also have a therapeutic effect.
The properties of THCA indicated by preclinical research may be relevant to cannabinoid medicine in the future, but they do not explain the remarkable results currently achieved by patients with low doses of THCA. Two studies on inflammation revealed that THCA does not inhibit COX-2, an inflammatory enzyme blocked by ibuprofen and aspirin, and that high doses of THCA were needed to obtain an anti-inflammatory effect. One possible explanation for this finding is that rimonabant, the experimental drug they used to block the CB1 receptor, could have inhibited the effects of THCA through a different channel or receptor, such as GPR55 (which is activated by Rimonabant).
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