On Wed, 9 Aug 2000 08:48:24 -0400, Todd Moody <[log in to unmask]>
wrote:

>No.  Wolfgang Lutz, for example, specifically urges his patients
>to eat fatty meats.  And dairy fats, as we already saw, are
>loaded with long-chain saturates.  In the Hays study, 90% of the
>fat consumed by the patients was saturated fat.  Their overall
>protein:fat:carb ratio was 30:50:20.  Main fat sources were meat
>and cheese. ...long-term study ..

Your point and the Lutz study betrays especially improvements
with glucose intolerance. As I reasoned before, I would expect
the change the main energy source to fat to have major improvements.
And so showed the study.
And IMO this is the main working mechanism of neanderthin in helping
against the widespread glucose intolerance and blood glucose swings.

As the major reason for this i consider the partly disabled carbohydrate
mechanism. Disabled IMO by lack of mayor breakdown steps by insufficient
available coenzymes which depend on some B-Enzymes.
The most fragile factor here is thiamin, which is very sensible to heating,
storage, leaching and which is missing in sweets and white-flour-products
(this is supporting the raw-foodist and enzyme-eating theories).

Primates in general have no problem to rely in 99% or 95% on carbohydrate
only, as is shown by the fruit nutrition of rain forest times and
the cereal based nutrition in neolithic (but pre-industrial) times.
The carbohydrates then were fresh and unmodified, and we have hardly ever
heard of any diabetic symptoms from roman authors, middle age authors
or from rural populations > 100 years ago.

You may remember that thiamin (in pyruvate decarboxylase) governs the entry
of carbohydrates to the Citric Acid Cycle and can inhibit its use for
energetic usage.

This explains also, why body tissues don't intake more glucose despite high
insulin levels. This is how glucose intolerance is described.
Glucose dams up at the level of pyruvate (also reported) and the cells
have to reduce glucose intake from blood, where it piles up.

Changing the energy pattern to 30:50:20 (Lutz) circumvents
the pyruvate stage by using fat, and the meat eaten in volume has
some thiamin (and probably other enzyme complexes like aplha lipoic acids
which *are* assimilated undigested from the gut).

You write:
>> >But if your theory is right, animal fats should interfere with
>> >glucose tolerance, by making membranes less permeable to glucose.
>> >Why isn't that so?

Permeability of membranes to glucose if governed by insulin, or insulin
resistance, not by a general inability to let that molecule pass.

>So, theory says that people on these high-fat diets with lots of
>saturates should be getting sicker.  The actual facts point in a
>different direction.  This suggests that the theory needs work.

If they have glucose intolerance *this* disease will improve.
If the diet is high in 16:0 or 1 and 18:0 or 1 (long chain) saturates
*in relation to EFAs* other diseases and quicker aging will result.
According to my reading and understanding. And as shown in many studies
(most generally blaming SFAs or "red mead" which is assiciated with
such stearate type fat in western sources).

In the long term I'd expect other problems to arise but just like average
affluent diets, where 40% die from CVD and 40% from cancer.
The ratio in beef fat isn't changed by volume, what counts is ratio.
IMO.

The ratio of P:S (PUFA to SFA) as is often mentioned, but the ratio
of P:(M+LCS) is what should more meaningful.

yours

Amadeus