Eico-sa-what's?

What are eicosanoids? And more importantly, how do I even pronounce that word? Eicosanoids are chemicals that are created within the body to control a multitude of reactions. But first let's discuss how and why they are created.

Within the human body there are needs for different forms of fats (or lipids). A "healthy" diet should include a combination of polyunsaturated, monounsaturated and saturated fats, with little-to-no trans fat. The percentages of Poly - Mono - Saturated fat vary from person-to-person, but one thing is certain, all are necessary. Without getting into the biochemistry of how each of these lipids are constructed, with regard to eicosanoids, the most important fats are the polyunsaturated.

There are 2 essential fatty acids (fatty acids are the simplest fat substances with regard to the human body) that the human body can not create, and thus needs to ingest. These two fatty acids are 20-Carbon long molecules named :

- alpha linolenic acid; &

- linoleic acid.

The difference between these two molecules is in the number of specific bonds, as the alpha linolenic acid is termed an Omega-3 fatty acid, whereas linoleic acid is termed an Omega-6 fatty acid. Typically the latter, the O-6 fatty acids, are INFLAMMATORY in nature and O-3 are ANTI-INFLAMMATORY. A "healthy" ratio within the diet should be O-6:O-3 - 4:1. The standard american diet has a typical ratio of 20:1, so extremely inflammatory. 

Linoleic Acid, through a series of chemical reactions becomes arachadonic acid, a metabolite from which eicosanoids are born. These eicosanoids are shown in the pink box above. The blue box to the left represents the omega-3-derived eicosanoids. 

Eicosanoids are then grouped into 4 different families: the protaglandins, prostacyclins, leukotrienes and thromboxanes. Each of these substances is involved in numerous chemical reactions, including:

 - cause constriction or dilation in vascular smooth muscle cells

 - cause aggregation or disaggregation of platelets

 - sensitize spinal neurons to pain

 - induce labor

 - decrease intraocular pressure

 - regulate inflammatory mediation.

For the purpose of this discussion, that's as far as we'll go about their function. Once these four families are created, there are enzymes that are utilized by the body to create the eicosanoids. The two enzyme pathways that are responsible for this conversion are the:
 - Cyclooxygenase (COX) Pathway; and

 - Lipoxygenase Pathyway.

The COX pathway is inhibited by non-steroidal anti-inflammatory drugs, such as aspirin and ibuprofen. The classical COX inhibitors are not selective and inhibit all types of COX. The resulting inhibition of prostaglandin and thromboxane synthesis has the effect of reduced inflammation, as well as antipyretic, antithrombotic and analgesic effects. The most frequent adverse effect of NSAIDs is irritation of the gastric mucosa as prostaglandins normally have a protective role in the gastrointestinal tract. Some NSAIDs are also acidic which may cause additional damage to the gastrointestinal tract.

Selectivity for COX-2 is the main feature of celecoxib, rofecoxib, and other members of this drug class. Because COX-2 is usually specific to inflamed tissue, there is much less gastric irritation associated with COX-2 inhibitors, with a decreased risk of peptic ulceration. The selectivity of COX-2 does not seem to negate other side-effects of NSAIDs, most notably an increased risk of renal failure, and there is evidence that indicates an increase in the risk for heart attack, thrombosis, and stroke through an increase of thromboxane unbalanced by prostacyclin (which is reduced by COX-2 inhibition). Rofecoxib (brand name Vioxx) was withdrawn in 2004 because of such concerns. Some other COX-2 selective NSAIDs, such as celecoxib, and etoricoxib, are still on the market.


There are various other natural COX inhibitors such as culinary mushrooms, like Maitake, a variety of flavonoids, fish oils and hyperforin.