On Wed, 13 Dec 2000, Amadeus Schmidt wrote:

> 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?

That would be the case if dietary AA were directed to the
production of series 2 prostaglandins, but apparently that is not
the case.

> > However, studies show that *dietary* AA is
> >not a problem, because it is *not* converted to the series 2
> >eicosanoids.
> Can i read this?

I don't know if I still have the studies, but I posted the
abstracts here a few years ago.  At the time I was engaged in a
dispute on this list when I thought Sears had it right.  At any
rate the studies were by GJ Nelson, in 1997.  If I can find them
around here I'll post them again.

> What is the difference then? why is the one converted, the other not?

It turns out that dietary AA is preferentially taken up by red
blood cells, which lack an enzyme (cyclo-oxygenase, I think)
necessary to turn them into series 2 eicosanoids.  So they have
little effect on prostaglandin balance.

> 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).

Wiser than what?

Todd Moody
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