On Mon, 31 Jul 2000 13:13:41 -0400, Todd Moody <[log in to unmask]>
wrote:

>So the idea is that the saturates are competing for the same
>enzymes?  I'd need to see more.

I don't have the book at hand, i will reread and note if i missed some
details. It was in the small meat chapter, where the FA compositions of the
various animals from wild game over nature pastoralist to farmed animals are
listed.

> For one thing, the absolute
>amounts of EFAs needed to make prostglandins is very, very small.

That's true, so in a diet of some greens only the few well balanced EFAs
may be enough. But in an environment of very much different dietary fats,
the enzymes may well be lost amoung so many competitors.
I think this doesn't only betray prostaglandins.
Cell membranes and other EFA functions (in brain and nerves) similarily need
converting enzymes, which could be crowded out by SFAs.

From the paleo point of view , i find it also important to consider the
evolutionary probability of such saturated fat amounts in the human food.

And high saturated fat intake is very unprobable in any savannah
yearmillion. Because wild game is very lean. And wild game is high in EFAs.
Arctic animals, which are fat are very rich of EFAs of marine source
(Erasmus notes that too).
This leaves the human years in ice-environments, like glaciated europe.
Hunting mammouths. Mammouth *were* fat, but how rich in EFAs/SFAs was their
fat? Such animals would use the short ice-age summer to eat tons of herbs
(no trees were available). This hints to a fat rather high in EFAs. Maybe
one of the mammouth dig out or a caribou analysis can tell...

I'd say, even if mammouth had saturated fat like beef: The timeframe
CroMagnon humans were exposed to it was small (max. 30k years). And we can't
tell how healthy humans mastered to survive in *this* areas.

Conclusion:
Beef which isn't grasfed only (nor fattened on grain) is unpaleo.
And its unpaleoness implies well documented health dangers.

Sorry to say. And i know that this questions the paleofood implementation
how the most practice it and how neanderthin promotes it (as a "allowable"
trade off in the modern world).  But so it is. Use unfarmed wild game.

>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.

That makes sense for the heart, which is a very constant energy demanding
organ, without much variation. It uses fat, as the most reliable and long
term - low impact fuel. It can spare glucose for the brain in this way.
It also makes sense to have this motor use fuels, which are otherwise not so
valuable. Of course saturated fats are burned first to spare EFAs.
For this purpose heart muscle has a quite special composition.

>> Means fish oil supplements of course, or brain.
>
>Yes.  Or DHA from algae.

I experiment with algae, in search of a natural iodide source.
I have seen how much alge were lying on the beaches and can imagine it
as a savannah time food.
Algae have DHA? which? I use to rely on my *desaturase and elongas enzymes
to make it. After what i know now of saturated fats, i tend more to exclude
saturated and even lower monounsaturated sources (a little less of olive).

>
>> 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.

Do you mean the same enzymes, which make PGE3s out of EPA?
Anyway, according to the research EPA from certain fish or perhaps brain
can help in a hampered prostaglandin situation by suppressing
AA release and therefore decreasing the ("bad") PGE2 pruduction.

>from:
>Nutrition and Metabolism Research Group, University of Alberta,
>Edmonton, Canada.
>
>Anti-thrombotic effects of omega-3 (n-3) fatty acids...
>.. 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.....
> 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.

This sounds not as when that saturated fats were especially helpful, but
worked when they *replaced* w-6 safflor oil.

This is logical because LA and LNA (w-6 or w-6) compete for the same enzymes
in prostaglandin (and cell membrane) synthesis.
High w-6 (safflor) outcompetes the LNA.
This is why the w-3 to w-6 ratio is relevant.

And it's also logical that supplying EPA, which is some steps further in
the w-3 pathway, works better in the competition against w-6.

But w-6 LA is also an essential substance. I don't consider it helpful
to totally stop w-6 intake. We need both pathways and both EFAs.

I don't want to argue against saturated fats as whole. A lower percentage
occurs in natural food too. Just a very high percentage will crowd out EFAs
like w-3 and w-6 compete one against the other.

Amadeus Schmidt