On Wed, 9 Aug 2000 08:48:24 -0400, Todd Moody <[log in to unmask]>
wrote:
>Look at the GJ Nelson et al. studies in _Lipids_, vol. 32 (1997).
>These studies involved *massive* supplementation of dietary AA in
>normal people -- the equivalent of about 25 eggs per day.  The
>additional AA was well tolerated, and the researchers found that
>dietary AA is preferentially taken by red blood cells, which lack
>the enzyme (cyclo-oxidase, I think) needed to produce the
>inflammatory prostaglandins.  This is an area where Barry Sears
>made a mistake.  While *endogenous* AA may be your "worst
>biological nightmare," as he puts it, dietary AA in amounts
>likely to be encountered in an ordinary diet is not.
>

And On Thu, 24 Aug:
>When
>AA is eaten, it has little effect on PG2 production because it is
>taken up by red blood cells, which lack cyclooxygenase, the
>enzyme needed to convert AA to PG2.

Dietary AA is a point that came into my focus recently.
I found the above explanations from you.
Basically you conclude that the dietary AA wents into red blood cells for
storage, where they don't harm, as long as enough EPA takes care for it not
to be released.

Ok, but the amount of red blood cells is limited and red blood cells die.
They are recycled, not excreted.
The AA is still there, it will show up at some time.

In the article (from JohnX) Simopoulos states: "..increasing dietary ALA
increases EPA concentrations in plasma phospholipids after both 3 and 6 wk
of intervention. Dihomo--linolenic acid (20:3n-6) concentrations were
reduced but AA concentrations were not altered."

I think that shows that AA storage is of long term character.
Like burying atomar waste.

Opinions?
What would happen if dietary AA would be stopped for some time?
What happens if dietary AA intake is higher that the amount necessary
for inflammatory prostaglandins, on the long term?
What if a lot of red blood cells die (running, smoking)?

regards, Amadeus