On Wed, 23 Aug 2000, Amadeus Schmidt wrote:

> First of all on saturated fat I'd like to correct my last posting - or add
> to it:
> The competitors for the enzymes working on EFAs are the *monounsaturated*
> fats 18:1 and 16:1.
> Saturated fats compete as well, but only after one stage of processing by a
> desaturase (D9D), which makes them monounsaturated.
> Adding the 18/16-C monounsaturated and 18/16-c saturated fats is what totals
> beef fat to such a small part of EFAs.

Why are you assuming that all the SFAs are converted to MUFAs?
Do you have specific information about how much SFA is converted?
Is there a feedback mechanism that regulates the conversion on an
as-needed basis?

> Other animal slaughter fats like pig fat are somewhat less EFA suppressing,
> according to Erasmus' reference.

What is this reference, anyway?

> Other saturated fats (< length of 16 , like most of butter and coconut)
> are also not converted to competitors or at least more slowly.

According to Horrobin, lauric acid increases activity in the w-6
pathway.

> Weston Price has some good articles.
> Some I've seen erraneous - as in the critic about the book of Udo Erasmus
> it's stated that hemp (promoted by Erasmus) wouldn't have a history of
> usage. That's wrong. Hemp is a most nutritious nut with superb properties
> and in use by humans since many thousands of years in China.

Hemp is a nut?  I don't doubt that hemp seed is nutritious, but I
doubt that it played a major role in paleolithic diets.

> However I like their enthusiasm on nourishing traditions, which emphasizes
> diets as proven at least over several centuries.

But you are not enthusiastic about their discovery that there are
*no* vegetarian traditional diets.

> Saturated fats *are* of course important in the body - but not essential.
> The body makes them as needed. Where's the reference (above) that they would
> "enhance the body’s use of essential fatty acids"?

The references are to Garg.

> Also shorter chain SFAs are neutral on EFAs - as far as i know.

And long-chain are used as fuel for heart muscle.

> That's true. Cholersterol is not the *cause* of artery diseases  it's just
> the repair substance *indicating* that artery repair is necessary.
> 
> But *why is* the repair necessary after all? This is the (CHD) question.
> There are indications that exactely the lack of EFAs to be incorporated
> into membranes (to keep them elastic) causes the demand for repair.

What indications?  What evidence is there that vascular damage is
caused by insufficient EFA in arterial cells?

Todd Moody
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