My interest in this product is spurred on by the multiple mechanisms in which these triterpenes seem to impact the joint: regulating cytokines, reducing TNF-a, IL-6, reducing osteocalcin, improving circulation of the joint matrix, slowing inflammatory bone loss, reducing cartilage destruction and restoring collagen.

In one randomized placebo controlled trial, 117 patients with radiographic and clinical evidence of osteoarthritis of the knee or hip were given shea nut extract or placebo for 15 weeks.[1] TNF-alpha reduced 17.9% overall and 23.9% in the group with elevated levels. IL-6 fell by 30.9%; C-reactive protein reduced by 20.6%; CTX-II, a cartilage marker fell by 28.7% in patients with elevated levels vs. an increase in placebo of 17.6%; and osteocalcin reduced by 9.2% in the elevated group indicating bone repair mechanisms.

Animal studies are also being conducted by the manufacturers of high triterpene shea nut extract showing comparable anti-inflammatory effects of ibuprofen but no adverse effects as are often seen in ibuprofen. Other studies are in development and I look forward to those publications.

I have surveyed some retailers and consumers in the natural products market who have been aware of and using high triterpene shea nut extract for several months and been pleased to hear of the consistent anecdotal, yet positive reports. For practitioners, shea nut extract yielding 70% triterpenes is available as BSP 201. I look forward to increasing my own clinical usage of this product and hope to see the same positive results in my patients. With its multiple mechanisms of actions, early research, and anecdotal reports, shea nut extract leaves me optimistic.

Reference:

[1] Cheras PA, Myers SP, Outerbridge K, & Nielsen G. Randomised Placebo Controlled Trial on the Safety and Efficacy of BSP-201 in Osteoarthritis. Australian Centre for Complementary Medicine Education and Research (ACCMER). Sept. 4, 2007

The main outcome criteria were reduction of symptoms of OA using WOMAC scores and reduction of pain using visual analogue scale (VAS). The secondary outcome was a decrease in the use of analgesics. Study subjects were randomly assigned to Pycnogenol 50 mg tid or placebo. Patients were allowed to continue with their medication with NSAIDs or analgesics if they were using them before the start of the study and were allowed to change medication as needed but then reported dosage or frequency changes at each visit. Patients were evaluated at baseline, at 3 months and 4 weeks after completing the treatment. The WOMAC questionnaire for pain, stiffness and daily activities was completed by the patient every 2 weeks during the whole study. The VAS for pain was filled in by each patient weekly during the whole study.

Results: The WOMAC-A score, summarizing pain scores, improved significantly in the Pycnogenol group (p=00004) over the time of the study. The statistical difference for pain reduction compared to baseline in the Pycogenol group was evident after weeks 8,12 and 14 (p < 0.001). The difference between treatment group and placebo was near statistical significant at week 8 (p= 0.08).

The WOMAC-B score, the stiffness score, improved statistically significant (p=0.01) in the Pycnogenol groups versus baselines after weeks 8,12 and 14. Statistically significant differences between treatment group and placebo group were observe at weeks 8 and 12 (p< 0.05).

The WOMAC score in regards to the ability to perform daily activities improved significantly versus baseline in the Pycnogenol group at weeks 8,12 and 14 (p< 0.01). The change in the placebo group was not significant and the difference between the Pycnogenol and placebo groups was not significant.

Pain scores by VAS was somewhat higher in the placebo group than the Pycnogenol group at baseline although not significant. After treatment for 4 weeks, the treatment group reported less pain when compared to the placebo and pain continued to diminish until month 3. The correlation of decreased pain over time was statistically significant (p< 0.04) for the Pycnogenol group, but the correlation was poor for the placebo group (p<0.17). Only a marginal significance was seen between Pycnogenol versus placebo was seen at weeks 4 ( p=0.08) and 8 (p=0.07).

Patients in the Pycnogenol group were able to reduce their use of analgesics or NSAIDs at a higher percentage than those in the placebo group and 10% of placebo group patients had to increase their dose of analgesics whereas no higher doses were needed in the Pycnogenol group.

Cisar P, Jany R, Waczulikova I, et al. Effect of Pine Bark Extract (Pycnogenol) on symptoms of knee osteoarthritis. Phytotherapy Research 2008;22:1087-1092

Commentary: I’m encouraged to see this study and am looking forward to using this in patients with milder to moderate OA symptoms, especially of the knees. Pycnogenol is a special standardized extract from the bark of the French maritime pine. It is composed of polyphenols, several phenolic acids, catechins, taxifolin and procyanidins. In laboratory research Pycnogenol selectively inhibits matrix metalloproteinases (MMPs). MMPs are one of the inflammatory responses in arthritic joints induced by interleukin-1. The matrix degrading activity contributes to the loss of cartilage and is associated with chronic inflammation. Other in nvitro research has shown that Pycnogenol inhibits other inflammatory cells and specifically inhibits COX1 and COX2. These previously observed anti-inflammatory effects as a background to the current study, contributes a body of information that enables us to have another viable alternative treatment in early OA of the knee as well as an approach to possibly reduce the use of analgesics and NSAIDs in pain management.