On Mon, 23 Jul 2001 20:09:06 -0700, Peter Brandt <[log in to unmask]>
wrote:

>Amadeus:
> >ALA can outcompete d5d witch produces the bad AA.
>
>The position that AA is "bad" has been challenged on many
>occasions on this list.  It has been my understanding that AA is
>only a problem with inadequate amounts of ALA in the diet.

Maybe it has been challenged that *dietary* AA was "bad".
It can be stored in cell membranes, and there is some regulative, which
stores it there.
I'm not shure about this (I am not concerned, I never eat AA).
I think what is stored will be released some time.
Sears' suggestion is to decrease dietary AA intake anyway.

Sears main approach is, and I think that's right, to regulate
AA *synthesis* in the body.
That AA is a major culprit in making bad eicosanoids
is no question, as I understand the topic.
Low insulin levels decrease AA making by lowering d5d activity.
High ALA levels decrease AA making by outcompeting d5d AND by the influence
of the resulting EPA.

I noted that Sears gave up the hope to influence the production of the one
good series 2 eicosanoid, PGI2.
I've found a web article that concentrates much on the topic how to
influence PGI2 in contrast to all the other bad eicos:
http://geocities.com/bsy53/dn/neuropat.html

Definitely interesting for diabetics and insulin resistant.

Amadeus