So far as I know, we never had RDA values set for omega-3 and omega-6 fatty acids, but now that we've switched to the Dietary Reference Intake they've added softer recommendations for the nonessentials. This pdf (linked to by the USDA here) lists the Adequate Intake for lenoleic (omega-6) fatty acids in the 14-17 g/day range for adult men, 11-12 g/day for adult women, while for alpha-linolenic (omega-3) the numbers are 1.6 g/day for adult men, 1.1 g/day for adult women.

Which fatty acids are 'essential'?

The essential fatty acids were described by Burr and Burr in 1930 as those fatty acids which cured the deficiency disease brought on by a lack of fat in the diet. Arachidonic acid was one of the fatty acids which they tested and found to be effective. Further work has shown that any of the common ω-3 or-6 fatty acids will work. And the common usage in the field is that the term essential fatty acid comprises all the ω-3 or-6 fatty acids (or at least the polyunsaturated, straight-chain methylene-interrupted ones; there are some conjugated oddities like calendic acid that aren't.) Authorative sources include the whole families, without qualification. ^{[1] [2] [3]} The human body can make some long-chain PUFA (arachidonic acid, EPA and DHA) from lineolate or lineolinate. Some writers therefore hold that the LC-PUFA are not essential. But is not how the field has generally used the term.

EPA but not other LC ω-3 or -6 decrease natural killer cells in folks 55+. ^[4]

Muskiet

1. Higher LCP contents in fetal than in maternal circulation ["biomagnification" (15)] suggests that nature has determined a major role for transplacental transport and to a lesser extent fetal LCP synthesis.
2. The poor conversion of labeled ALA to DHA, but not to EPA and its elongation product 22:5(n-3), in young men, but better conversion to DHA in women of childbearing age (16–18) suggests that the DHA synthesis machinery becomes somewhat upregulated in conditions of high DHA demands.
3. The relation between fetal and maternal LCP status and depletion of maternal stores during pregnancy and lactation suggests that the maternal diet should contain higher LCP contents (19).
4. The LCP status of newborns is lower in those receiving formula with LA and ALA, but not LCP, compared with counterparts receiving human milk or formula with LCP (20,21).
5. The predominant ß-oxidation of orally administered stable isotopically labeled parent EFA is opposed to the predominant tissue incorporation of orally administered LCP (22–24).
6. The inability of dietary ALA supplements to augment DHA status in vegans has been observed despite their low baseline DHA status (25).
7. A highly increased EPA and its elongation product, 22:5(n-3), with DHA within the reference range, follows the administration of 12 g ethyl-EPA daily for 16 mo (14). ^[5]

Obtusilic acid, 14:1 ω-3, is a monounsaturated ω-3 oil found in the seed oil of Lindera obtusiloba. ^[6]

What is an encosanoid, anyhow? Who sez?

• De Catrina and Basta include hydroxy- and epoxy-FAs, lipoxins (LX) and isoprostanes.
• These guys say its just the prostanoids and LT
  • Nishimura K, Tsumagari H, Morioka A, Yamauchi Y, Miyashita K, Lu S, Jisaka M, Nagaya T, Yokota K. "Regulation of apoptosis through arachidonate cascade in mammalian cells". Appl Biochem Biotechnol. 102–103 (1–6): 239–50. PMID  12396127.{{ cite journal}}: CS1 maint: multiple names: authors list ( link)
• Dorlands sez eicosanoid (ei·co·sa·noid) (i-ko´sə-noid) any of the biologically active substances derived from arachidonic acid, including the prostaglandins and leukotrienes.
• These guys sez anything formed by COX or any of the lipoxygenases. Later, they add in the Cytochrome P450 products.
  • Nathoo N, Barnett G, Golubic M (2004). "The eicosanoid cascade: possible role in gliomas and meningiomas". J Clin Pathol. 57 (1): 6–13. PMID  14693827.{{ cite journal}}: CS1 maint: multiple names: authors list ( link)
• MeSH terms say TX, PG, LT and HETEs. They include PGI within PG. OTOH, their indented structure (same page) includes Lipoxins but not the LT. Oddly, they say that eicosanoids come from the eicosanoic acids, which they define as the unsaturated C20.
• Soberman says it's pretty much any oxygenated derivative of AA. List prostanoids, leuokotrienes, EETs, lipoxins, isoprostanes, anything produced by any lipoxygenase or peroxidation.
• The U Kansas document says any of the oxygenated derivatives of EFAs. They only mention the prostanoids and leukotrienes by name, but show hepoxillans in the diagram.

Complexity of pathways

Eicosanoid signaling paths are complex. It is therefor difficult to characterize the action any particular eicosanoid. For example, PGE₂ binds four receptors, dubbed EP1–4. Each is coded by a separate gene, and some exist in multiple isoforms. Each EP receptor in turn couple to a G protein. EP₂, EP₄ and one isoform of the EP₃ receptors couple to G_s. This increases intracellular cAMP and is anti-inflammatory. EP₁ and other EP₃ isoforms couple to G_q. This leads to increased intracellular calcium and is pro-inflammatory. Finally, yet another EP₃ isoform couples to G_i, which both decreases cAMP and increases calcium. Many immune-system cells express multiple receptors that couple these apparently opposing pathways. Presumably, EPA-derived PGE3 has a somewhat different effect of on this system, but it is not well-characterized.

Eicosanoids and arteriosclerosis

Fish oil feedings make small effect on humans with low eicosanoid output, but make marked effect on the TX in urine in those with chronic inflammation. ^[7]

Interesterification can be used to add EPA to vegetable oils. ^[8]

References