On Wed, 13 Dec 2000 07:55:47 -0500, Todd Moody <[log in to unmask]>
wrote:

>.. Sears calls elevated AA your
>"worst biological nightmare" and urges caution in consumption of
>eggs and beef (fat).

I'm presently trying to make a quick outline for my friends, why omega-3
fats and EFAs are good for health and why i eat so much.
So i again retraced the whole reasoning.
Most (but not all) good EFA effects are attributed to the actions of the
prostaglandins. There are the nightmare-prostaglandins with a list of
effects that read like a inventory of degenerative diseases. And there are
the nice ones, which are nice but mainly oppose the nightmare PG's.

OK if no EFA's are eaten PG's cannot be made at all - that's obvious.
Further we assume that dietary composition (ratios) influence the PG-making.
But Sears reported some kind of "back-adjustment" after some weeks (of
Borage).....

I reread some of the stuff, and really it appears to me that AA is the
gateway to the nightmares.
(now i hope for counterarguments as far as I'm wrong):
1. All bad PG's are made of AA (series 2 PG, omega-6 series)
2. good PG's from omega-3 mainly work in inhibiting AA-release from cells
3. The good series-1 PG's are also omega-6 descendants, made of DGLA, which
   is the predecessor of AA.

It appears that both, good and bad are made of omega-6 EFA's (LA or GLA or
DGLA). Shouldn't it be the worst case scenario to add AA to the system and
imbalancing it therefore?

> However, studies show that *dietary* AA is
>not a problem, because it is *not* converted to the series 2
>eicosanoids.
Can i read this?
What is the difference then? why is the one converted, the other not?
So far i understood that the body counterreacts against dietary AA by
producing less own AA(like with cholesterol)
And dietary AA is tolerable for *that* reason.

Some thoughts on the system and the assumptions we share:
Omega-3 fats work (e.g. anti inflammatory) by beeing converted to EPA, which
 slows AA release from cell walls. Only that?
Wouldn't it be wiser to eat less AA (which in turn could be "released"
later).

The ZONE diets's main tool turned out to be reducing insulin-high phases
to emphasize the good PG's. He (Sears) wants to achieve it by adding protein
to every meal. Where's the reference that protein does this (undoubted but
possibly not the best way). Adding fat to a meal does the same job of
slowing carb digestion. Eating slow carb/glucose elevators may be even
better. Or fighting the insulin spikes by normalizing carb metabolism, best.

Eating GLA (ev.primrose, hemp, borage) improves  availability of all PGs
(good and bad, s.1 and s.2).
But how to reduce conversion of PG-2's from AA, without reducing AA?

Reading Erasmus again impresses with the benefits of LNA in addition to the
prostaglandin effect.

regards, Amadeus