On Wed, 13 Sep 2000 09:04:59 -0400, Todd Moody
<[log in to unmask]>
wrote:

>Amadeus, I have been doing some research on the matter of MUFAs
>competing with EFAs for D6D.  What I have learned is that D6D
>*preferentially* acts on EFAs, and in fact D6D action on MUFA is
>rare and only occurs in cases of EFA deficiency.
> Therefore, if
>one's EFA intake is adequate, MUFAs should not interfere.
>Similarly, since SFAs are converted to MUFAs by D9D, they also
>should not interfere.

That sounds interesting. Could you tell, what you found and where?

This questions parts of the EFA to MUFA *ratio* problem.
Particularly the pathways that lead to prostaglandin precursors
and long chain FAs (EPA and DHA).
I also recall a study, that resulted in the the conclusion that
varying
(high) EFA-levels do *not* change the levels of DHA.
There seems to be a regulative somewhere in this pathway.

However, you only mention D6D, the first stage of conversion.
Competition can occur at all later levels (elongases, D5D) and at all
other places of usage of LNA and LA (cell membranes, triglycerides).

Do you have any indication in *which way* D6D preferes EFAs over
MUFAs? If it is built in D6D to prefer EFAs (always in the same rate
of preferance) then a very high excess of oleic acid (compared to
EFAs)
will still diminish porper prostaglandin formation.

This is at last, what the one study referenced by WestonAPrice (and
Erasmus)
sais:
  http://www.westonaprice.org/tripping.htm :
  "There is some evidence that an excess of
  oleic acid (found chiefly in olive oil and nuts) may inhibit
prostaglandin
  production. (Reference to Horrobin, David F, Prostaglandins:
Physiology,
  Pharmacology and Clinical Significance The Book Press, Brattleboro,
  Vermont, 1978, p 20, 35)"
And exactely this is what also concerns beef fat.

Erasmus goes more into detail, listing exactely the critical ratio at
which
"EFA activity" ceases, 65:15 of OA to LN/LNA.

Then the w-3 to w-6 ratio is of concern, in addition.
Obviously excess w-6 outcompetes w-3.
This concerns animal fats (but only of farmed animals) as well as
certain widespread plant fats, particularly sunflower, but also olive.

>
>What matters is not the ratio of MUFAs to EFAs, but the adequacy
>of the absolute amounts of EFAs available.

This is the statement you rise.

But why then are very small EFA amounts sufficient in the absence of
other
fats? (e.g. like with other primates)?
Maybe, because they work more efficient in the absence of competing
fats.

>So how much is
>adequate?  Opinions vary widely, but Simopoulos seems to think
>that a gram/day of EPA+DHA is enough, plus a comparable amount of
>LA or even twice that, but not more.  Siguel, on the other hand,
>argues for a much higher EFA intake.
>

EPA+DHA are only end products of the w-3 pathway. Very useful in brain
and
eyes. But not one prostaglandin molecule is made out of them.

At last we try to be thinking paleo here.
What is the healthy diet adapted over the yearmillions?
I couldn't name a diet in any timeframe that was as low in EFAs as
beef fat is. Also not concurrent hunter/gatherer diets.
They all have *very* high EFAs in their diet. With more than 30% EFA.
This is how LA and LNA could become essential.
How could a source with only 5% EFA be considered similar to paleo
nutrition, which had about 30% EFA? In animals and in most plants.

Amadeus S.

(I don't know Siguel. Could you tell about the book?)