Todd Moody wrote:

> The thing that I find strange is that more than one study has shown that
> supposedly "heart-healty" MUFA increases Lp(a) substantially, and Lp(a)
> is known to be an independent risk factor for heart disease.

Tis is consistent with the EFA-Suppressing effect of MUFA if it's in a
proportion of 69 : 3.5  (MUFA to EFA) or bigger. As found in one study
mentioned by Udo Erasmus and by Weston A Price.

Logical as the enzymes d6d , d5d, elongases work on MUFA as well as on
EFAs, therefore compete for the enzymes and could make EFAs stop working
if MUFAs were too much.

Suppressing EFA activity would mean only prostaglandins from readymade
LC-fatty acids (AA, EPA) would be available. This would in turn mean
nearly only "bad" prostaglandins (from AA) a little good ones from EPA
(if any was eaten). But missing the major good series-1 ones from DGLA.
Bad prostaglandins are known to rise Lp(a) which is known to be a major
risk factor for heart diseases.

MUFAs would be heart healthy only protortions of < 50% or so of total
fat, therefore reducing the total part of SFA (with the effects
described in this thread) but not yet influencing EFA activity.

regards

Amadeus S.