Arthritis inflammation.

Unfortunately, almost every week we speak to someone with Arthritis inflammation or Rheumatoid arthritis.  Sufferers are always looking for treatments that firstly, reduce their pain and inflammation and secondly don’t have a list of adverse effects as long as your arm.

I recently came across two very detailed studies showing how Beta Caryophyllene (BCP) has the potential to help arthritis sufferers both with their pain and inflammation and no contraindications.  Below is a summary of the first study.

What is Arthritis inflammation

Rheumatoid arthritis (RA) is a chronic, relapsing inflammatory and autoimmune multi-system illness that affects the joints and is characterised by synovial membrane inflammation, pain, and limited joint movement.
RA is a systemic inflammatory disease in which articular cartilage destruction causes bone deformity, loss of joint function, and, eventually, severe pain.  It is the most common inflammatory arthritis, affecting 1-2 percent of the global population, or approximately 20 million people.

While there are many treatments available for Arthritis inflammation, such as nonsteroidal anti-inflammatory drugs (NSAIDs) and disease-modifying antirheumatoid arthritic drugs (DMARDs), up to 30% of patients do not respond to treatment. Aside from the high cost, long-term use of many of these drugs is associated with severe adverse reactions such as gastric and duodenal ulcers, complications in the small intestine and colon that cause colitis, bleeding, perforation, stricture, and chronic problems such as iron deficiency anaemia, protein loss, and toxicity.

Recently, there has been an increasing interest in natural food for scavenging the free radicals because of their wide acceptance. Some constituents of plants, particularly terpenoids, have been reported to be useful in the management of inflammatory diseases. Among the terpenoids, Beta Caryophyllene is a sesquiterpene present in very large amounts in natural products e.g. clove oil, cinnamon leaves, and copaiba balsam, all of which have been used as natural remedies. Beta Caryophyllene is also known to be anti-microbial, anti-oxidant, and anti-carcinogenic and to possess skin penetration-enhancing properties.

The conclusion of this study stated:
The Beta-Caryophyllene is an effective anti-arthritic agent experimentally and holds prospect in future Arthritis inflammation treatment. In conclusion, this study has verified that Beta Caryophyllene suppressed the joint inflammation and destruction in adjuvant arthritic rats. We are confident that our data provide mechanistic evidence for anti-arthritic appliance of Beta Caryophyllene as a promising candidate for novel therapeutic agent of Rheumatoid arthritis.
Source: https://bone.imedpub.com/antiarthritic-and-anti-inflammatory-activity-of-beta-caryophyllene-against-freunds-complete-adjuvant-induced-arthritis-in-wistar-rats.php?aid=7220


The second study stated:
Our study, for the first time, clearly shows that BCP ameliorates the clinical signs of arthritis. This beneficial effect was associated with a marked reduction in several inflammatory biomarkers and with a clear-cut reduction in histological joint damage.

BCP administration significantly ameliorated the signs and the clinical symptoms associated with the development of arthritis. The severity of the disease, analyzed by the means of the clinical and histological scores, was markedly reduced by the treatment with the natural CB2 agonist. This finding represents the first clear-cut experimental evidence in support of an anti-arthritic effect of BCP.

Interestingly, the cannabinoid receptor agonist reduced pro-inflammatory cytokines such as TNF-α, IL-6, Il-1β and increased the anti-inflammatory cytokine IL-13. BCP also suppressed joint expression of TNF-α, IL-6, Il-1β and of MMP 3 and MMP9.

BCP administration dampened the augmented activity of both inflammatory molecules. This effect is the consequence of the intracellular signaling cascade initiated by the BCP-induced triggering of the CB2 receptors, which leads to a blunting of NF-ĸB activation.

Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6723248/