On Mon, 31 Jul 2000, Amadeus Schmidt wrote:

> >Can you explain how beef fat "deletes" EFAs from some other
> >source?
>
> You challenge my ability to remember Erasmus' details..
>
> Basically, the enzymes, which work on EFAs activating them in the various
> ways (longer chain, prostaglandins, cell membrans) also work on saturated or
> monounsaturated fats.
> In this way they drive the "attention" of this enzymes (may be elongases and
> desaturase) and therefore disable necessary pathway for the EFAs.

So the idea is that the saturates are competing for the same
enzymes?  I'd need to see more.  For one thing, the absolute
amounts of EFAs needed to make prostglandins is very, very small.
Second, according to references in the Allan and Lutz book that I
just read, SFAs are the *preferred fuel* of the heart, but
endogenous SFAs are not a significant source of energy for the
heart, which entails that the main source would be dietary.  They
provide references to two textbooks on lipids for this, which I
haven't verified yet.  So, given that the heart likes to have
plenty of free SFAs around for fuel, I somehow doubt that this
would cause problematic competition for the enzymes needed to
make minute quantities of prostaglandins.

> A deadline of percentage is given, below which EFAs' effects are discarded
> from too much saturates. Beef fat is much beyond even this line.
> (This as result of a study).

Hmm... and I wonder if the study controlled for carbohydrate
intake, since insulin downregulates some of those enzymes
(delta-6 desaturase in particular).  If Sears is right, this is
also why the results of fish oil studies are equivocal.

> My own thoughts:
> Some of the enzymes drawn away, necessary for prostaglandin formation may be
> equaled out by eating already ready elongated and desaturated EFAs,
> namely EPA (or unheated DHA, if the backconverting enzyme to EPA is
> available). Means fish oil supplements of course, or brain.

Yes.  Or DHA from algae.

> EPA beeing the source of PGE3 (good) prostaglandins could support this path.
> PGE1 (good) protaglandins (sounding even better) however have a different
> fate.

But the same desaturase enzymes are involved, as well as some
others.

If I can find it, at least one study suggests that the benefits
of fish oil depend on adequate levels of SFAs.  Here it is...


J Lipid Res 1990 Feb;31(2):271-277

Interactions of saturated, n-6 and n-3 polyunsaturated fatty
acids to modulate arachidonic acid metabolism.

Garg ML, Thomson AB, Clandinin MT

Nutrition and Metabolism Research Group, University of Alberta,
Edmonton, Canada.

Anti-thrombotic effects of omega-3 (n-3) fatty acids are believed
to be due to their ability to reduce arachidonic acid levels.
Therefore, weanling rats were fed n-3 acids in the form of
linseed oil (18:3n-3) or fish oil (containing 20:5n-3 and
22:6n-3) in diets containing high levels of either saturated
fatty acids (hydrogenated beef tallow) or high levels of linoleic
acid (safflower oil) for 4 weeks. 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. Inhibition was greater with fish oil than with linseed oil,
only when fed with saturated fat. delta 6-Desaturase activity was
not affected when n-3 fatty acids were fed with high levels of
n-6 fatty acids. 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. 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.
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.