Neil5585's list is rather comprehensive. Avoiding all those may be a major challenge for arachidonic acid supplementation. To be fair, all the agents on that list are not equally potent in arachidonic-acid inhibition. Furthermore, the dosages used can also make a difference. Finally, a more potent arachidonic-acid inhibition response is obtained when more than one of those are used at effective dosages, because herbs display considerable potency when combined versus when used singly.
A certain book, Beyond Aspirin (Newmark et al. 2000), discusses naturally-occuring cyclooxygenase-2 (COX-2) inhibitors. Some might find this useful.
By the way, while discussing arachidonic-acid (AA) inhibition, it might help to recall that its complete inflammatory cascade includes COX-1, COX-2, and 5-Lipooxygenase (5-LOX).
5-LOX is an enzyme that is produced in higher amounts by the body in response to an overload of arachidonic acid. 5-LOX functions to degrade arachidonic acid. However, 5-LOX directly stimulates the propagation of cancer cells. Furthermore, 5-LOX produces breakdown products from arachidonic acid. These products, leukotriene B4, 5-HETE, and hydroxylated fatty acids, motivate tissue destruction, chronic inflammation, as well as the increased resistance of tumor cells to apoptosis or programmed cell destruction.
Apart from 5-LOX, the body produces other dangerous enzymes such as cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) that participate in the breakdown of arachidonic acid.
COX-1 leads to the production of thromboxane A2. Thromboxane can enhance abnormal arterial blood clotting or thrombosis, leading to heart attack and stroke. Yet, COX-1, in base quantities, are required in many metabolic processes. This is why non-steriodal anti-inflammatory drugs (NSAIDs) that quench COX-1 also trigger certain health problems in our body, including bowel distress, amongst others. (NSAIDs express their pharmacological action via COX and prostaglandin synthase inhibition).
COX-2 participates directly in cancer cell propagation. Its breakdown product, prostaglandin E2 fosters chronic inflammation.
It is useful to note that when COX-2 is inhibited, arachidonic acid expresses itself through 5-LOX, so a complete strategy would involve both COX-2 and 5-LOX inhibition.
Lastly, I would like to add one or tow things to Neil5585's post.
1) Sesamin/Sesame lignans are direct arachidonic-acid inhibitors.
2) Silymarin/Silibinin, actives in Milk Thistle, also COX-2 inhibitors.
3) High insulin levels trigger the conversion of arachidonic acid into inflammatory prostaglandins.
4) CLA has a dose-dependent ability to suppress aracidonic acid, and is sometimes used as chemopreventive (because arachidonic acid triggers inflammatory mediators that can support cancer initiation and progression).
5) Curcumin inhibits COX-2 and thromboxane A2, a highly unstable, but biologically active compound created by COX from AA. Furthermore, curcumin also effectively inhibits 5-LOX and HETE.
6) Gamma tocopherol is a dose-dependent COX-2 inhibitor.
7) Ginger not only suppresses COX-2, it also supports the positive effects of COX-1.
8) Feverfew contains apigenin and melatonin, both COX-2 inhibitors. Besides, Feverfew also possesses 5-LOX-inhibiting properties.
9) Berberine and berberine-containing herbs (goldenseal, barberry, goldthread, oregon grape) not only inhibit COX-2, but also support the beneficial actions of COX-1.
10) Green Tea's COX-2-inhibiting actions occur via two pathways. 1) Salicylic acid, the main anti-inflammatory component of aspirin, naturally occurs in Green Tea, giving it its COX-2 inhibition abilities; 2) The polyphenols and flavonoids in Green Tea also exhibit COX-2 inhibition.
11) A special extract of the Boswellia plant known as AKBA (3-O-acetyl-11-keto-ß-boswellic acid) is one of the most potent selective 5-LOX inhibitors around.