On Wed, 23 Aug 2000 09:59:37 -0400, Todd Moody <[log in to unmask]>
wrote:

>The following abstracts of the research of lipidologist ML Garg
>contradict Udo Erasmus's claim that SFAs interfere with EFA
>utilization.

Thanks for the new puzzlestones to the EFA metabolism.
Before looking at them in depth, I'd like to mention some
points in the texts that don't fit very good to the fatcs I've
collected so far. Though I am not a professional fat researcher.

>Anti-thrombotic effects of omega-3 (n-3) fatty acids are believed
>to be due to their ability to reduce arachidonic acid levels.

I thought we are attributing the main health advantages of essential FA
oils to their effect on prostaglandin formation.
PG-1 have the most positive effects (particularly PGE1),
PG-2 have the deteriorating effects (in excess)
PG-3 are down-modulating PG-2 effects.

As PG-2 are made of AA and PG-3 out of w-3 LNA and EPA.
So the goal should be at first to boost PG-1 and then
to downregulate PG-2 by whatever. In this order.
Not only to reduce AA levels.
AA is not only formed, it is also eaten.
You have provided reasons, that AA is also regulated by storage
modulators (e.g. red blood cells).
So this above text looks a little simple, humbly said.

>... The effect of diet on the
>rate-limiting enzyme of arachidonic acid biosynthesis (delta
>6-desaturase) and on the lipid composition of hepatic microsomal
>membrane was determined. Both linseed oil- or fish oil-containing
>diets inhibited conversion of linoleic acid to gamma-linolenic
>acid.

Why should we want *this*? GLA is the precursor for all the good PG-1's.
Inhibiting this step would rob away the positive PG-1 at first....
D6d inhibition indeed is a major problem, because trans-fats,
alcohol and some more substances inhibit d6d, disabling *all*
EFA aktivity. We should *want* d6d activity. On EFAs w-3 and w-6.

>Inhibition was greater with fish oil than with linseed oil,
>only when fed with saturated fat.

Makes sense, that SFA does this, because SFA and linseed both compete for
D6D. But "greater"?  SFA  *alone* can inhibit d6d activity on EFAs.
I can't see why fish oil (containing end product EFA) should influence D6D
rate (it influences PG-2 formation out of AA).

This all makes sense with the stamements of Erasmus (or better his ref).

> Arachidonic acid content of serum lipids and
>hepatic microsomal phospholipids was lower when n-3 fatty acids
>were fed in combination with beef tallow but not when fed with
>safflower oil.

This is to be expected. n-3 (linseed, LNA ) and SFA (tallow) competes
with n-6 (safflor). Of course safflor doesn't interfere with itself.
The question is if the same amount of w-3 (linseed) as SFA (tallow)
would equally downregulate d6d availability for w-6.

However the advantage of w-3 only against w-3 with SFA would be that
1. it is made to EPA, which downregulates PG-2 (bad) making out of AA.
2. it is made to DHA - for the nerves.

> Similarly, n-3 fatty acids (18:3n-3, 20:5n-3,
>22:5n-3, and 22:6n-3) accumulated to a greater extent when n-3
>fatty acids were fed with beef tallow than with safflower oil.

Nothing is said about the amounts.
If both LA 18:2 and SFA 18:0 supress w-3 conversion by competition,
then more of SFA would be burnt, leading to less competition
*if* SFA (tallow) and LA (safflog) were given in similar amounts.

But if you look at natural fat sources (green plants,wild game)
then w-3 comes in amounts comparable to both SFA and w-6.
Unlike safflor (w-6 predominating) and tallow (SFA dominating).
(For the wild game I'm always thinking on the whole animal fat, not only
the storage fat)

>These observations indicate that the efficacy of n-3 fatty acids
>in reducing arachidonic acid level is dependent on the linoleic
>acid to saturated fatty acid ratio of the diet consumed.

We want more PG-1 out of DGLA and less PG-2 out of AA.
But DGLA is only one step away from AA and both are w-6 series.
So we'd want to promote prostaglandin(-1) formation of DGLA and
downregulate PG-2 formation out of AA.
The latter is done by EPA, which comes from w-3 LNA.
This may be the main and missing function of LNA in this picture.

We also might want to limit the conversion of DGLA to AA.
But the same enzyme is making EPA too, so we shouldn't want to limit *this*.

Are we speaking about the same thing here, Todd?

What spoke against the SFAs was different:
As SFAs (only long chain 18 and 16:0) compete at all formation levels
against EFA activity, the point was that *all* EFA activity is diminished.

So the relative part of EFAs to SFAs is to be raised to percentages
as they are found in any natural source and where EFA activity begins again.
*If* EFA activity begins, then the relative amount of w-3 against w-6
begins to count and w-3 helps downregulating PG-2 from AA.

This all cannot be tested in studies of high EFA diets may it be linseed
or safflor.

The point against beef fat was
1. To much saturated fat compared to very few total EFAs
2. only then: too few w-3 in relation to w-6 EFAs.

And paleo: where is the nature world fat source similar to the
fat in a cows muscle.

regards

Amadeus Schmidt