A unique profile of fatty acids
- Modulate the body's production of eicosanoids
- A more effective nutritional support than conventional fish oils.
- Extract of Perna canaliculus, the New Zealand green-lipped mussel

Omega-3 fatty acids are now well-known inflammation fighters. Controlled clinical trials clearly show that they fight inflammation, reducing and in some cases eliminating the need for anti-inflammatory drugs with their disturbing short and long-term side effects. Both omega-3 fatty acids, and nearly all anti- inflammatory drugs, work through their effects on a group of local, cellular "hormones" called eicosanoids.

Eicosanoids are messengers that cells use to communicate with one another, coordinating their activities. Some ("bad") eicosanoids promote inflammation, while other ("good") eicosanoids have potent anti-inflammatory functions. Thus, the body's inflammatory response rests in large part on the balance of "good" and "bad" eicosanoids produced by your cells when they hear the immune system's inflammatory call.

"Bad" eicosanoids are made from an omega-6 fatty acid called arachidonic acid. Most drug approaches to inflammation, from aspirin and the older NSAIDs (Non-Steroidal Anti-Inflammatory Drugs, like ibuprofen) to the new "COX-2 inhibitor" drugs, like celecoxib [Celebrex®] and rofecoxib [Vioxx®]), work by inhibiting the formation of the series-2 prostanoid group of "bad" eicosanoids. Prostanoids are formed from arachidonic acid by an enzyme called cyclooxygenase, or COX. (AA).

But while these drugs certainly provide symptomatic relief in the short term, COX-2 inhibitors can actually accelerate the underlying inflammatory disease in the long term, by diverting arachidonic acid into another, slower-acting, and ultimately more destructive pathway: the lipoxygenase (LOX) enzyme pathway, which produces the ravaging series-4 leukotrienes. Leukotrienes are the eicosanoids released by immune cells involved in the body's inflammatory responses, and are more responsible for the long-term consequences of inflammation, which can result when a deranged immune system attacks the very body that it was designed to defend.

Therefore, blocking the COX pathway alone results in an imbalance - an imbalance that ultimately trades short¬term gain for long-term pain. What people suffering with autoimmune disorders most need is a "dual pathway inhibitor:" a molecule which will shut down COX-2 and LOX alike, preventing the formation of all "bad" eicosanoids.

Transnational pharmaceutical giants are racing to create such drugs. But Nature is already waiting for them at the finish line, with two rare omega-3 fatty acids.

Introducing ETA and SDA
Eicosatetraenoic acid (ETA) and its precursor stearidonic acid (SDA), are omega-3 fatty acids you probably haven't heard much about. Because ETA and SDA are so rare in food sources, there's been little study of their role in the effects of diet on chronic disease (unlike eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), which are commonly found in fatty fish and in regular fish-oil supplements).

While ETA is very rare in the normal Western diet, it is found in significant amounts in the fatty acids of the green¬lipped mussel (Perna canaliculus). Many early studies in humans and animals found that crude extracts of Perna were effective in reducing inflammation, and in relieving the symptoms of rheumatoid and osteoarthritis - but other studies found no effect.

The reason, as later studies confirmed, was that the anti-inflammatory properties of the green-lipped mussel were due to their content of SDA and ETA. Most green-lipped mussel supplements are not stable fatty acid extracts, but are crude concentrates or are based on mucopolysaccharides. When seven commercially-available green mussel products were put to the test by comparing them with a stable fatty extract rich in ETA and SDA, the fatty acid extract revealed strong anti-inflammatory powers, while the other extracts were found to vary wildly in strength. Great variations were even revealed in different batches of the same product.

More tellingly, when the inflammation-fighting powers of a stable ETA- and SDA-rich extract were compared with crude
P. canaliculus extracts whose fatty acid content had been deliberately removed, the fatty acid extract of the mussel exhibited potent anti-inflammatory effects, while the ETA-depleted preparation was found to be completely ineffective.