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