Bill, I had the very same
question about 6 months ago.
As I had it explained to me:
Although the series II eicosanoids (maybe unfairly called bad), are needed as well as the series I, it is the exagerate production of series II what is referred as detrimental. Not that series II are unwanted, on the contrary, they are very much needed when inflammatory processes
must take place, but too much is not good. The reason why both books recommend to increase omega-3 fats consumption is to compensate the ratio omega-6 to omega-3 and bring it back to what it should be (2:1 instead of 20:1).
The problem with ALA -- and its high content in flaxseed oil (an Omega-3 oil) -- is that the fatty acid inhibits the production of delta-6-desaturase, the critical enzyme that converts linoleic acid (in borage, evening primrose, and black currant Omega-6 oils) into GLA, precursor to the "metabolically activated" fatty-acid building block of eicosanoids, DGLA.
This "blocking" action occurs in much the same way that EPA in fish oil (also an Omega-3), in a positive way, blocks some of the action of the enzyme responsible for converting activated fatty acids (DGLAs) into arachidonic acid, the building block of "bad" eicosanoids.
The reason why both books recommend increasing omega-3 fats consumption is to compensate the ratio omega-6 to omega-3. The intake of already converted products like EPA and DHA is encouraged due to the "inhibiting" effects of ALA. For those who can't/won't eat animal products (fish), then flax seed oil provides us with omega-3 fats that we wouldn't get otherwise.
HTH,
Nat