On Fri, 4 Aug 2000, Amadeus Schmidt wrote:

> Todd, i think this thread digs up interesting things.

Yes, but I also think we are reaching the limit of what we have
to say.  Let me try to summarize my view.

1. I recognize some of the evidence that persuades you that
saturates, in significant amounts, are not good.  I have
sometimes been persuaded of the same thing myself.  I am
cautioned, however, by the tension between that evidence and the
real-world experience of those who eat lots of SFAs but enjoy
good health.  I mentioned the Masai, Samburu, Jamaicans, and
patients of Dr. Lutz and Dr. Hays (see
http://www.pslgroup.com/dg/10786a.htm), as well as the anecdotal
evidence of the many people who have improved their health
through diets high in animal fats.  Dr. Lutz's work is especially
interesting, since he has studied the effect of this sort of diet
on glucose tolerance, which is just the thing that a high SFA
diet should make *worse*.  But it makes it better.

2. You are concerned about the inhibition of desaturase enzymes,
since this, and only this, would cause an excess of SFAs in cell
membranes.  But from what I have read the most potent inhibitor
of desaturase enzymes is *insulin*, not SFA.  And the most potent
stimulator of desaturase enzymes is glucagon.  The best way to
keep insulin low and to produce glucagon is to eat a low-carb,
high-protein diet.  I believe that in the context of such a diet,
and perhaps *only* in that context, the body handles SFAs well.
If you simply add animal fat to a diet that is already high in
carbs, as many studies do, you have problems, because the
carb+fat combination is a very potent stimulator of insulin
release.

3. Between 1910 and 1970 (in the U.S.) consumption of animal fats
went down somewhat, while overall fat intake went up.  In 1910,
84% of fat eaten was animal fat, the remainder coming from nuts
and the natural oils in vegetables.  By 1970 we were eating more
fat, but only about half of it was coming from animals.  The
reason, of course, was the large-scale introduction of vegetable
cooking oils, both hydrogentated and not, i.e., massive amounts
of PUFA.  During this same time, heart disease rates soared.  I
think we'll agree that this has a lot to do with the trans fats
in hydrogenated oils (which also, incidentally, raise Lp(a)
levels).  But the main point is that prior to the introduction of
these oils, the animal fats were apparently not causing trouble.

4. Although absolute amounts available vary quite a bit, most
edible animal tissues have substantial amounts of SFAs, compared
to MUFAs and PUFAs.  Even brains have about twice as much SFA as
they have either MUFA or PUFA.  Note also that Drs. Eades, in
conjuntion with Dr. Cordain, are in the process of re-studying
whole-carcass fat composition of wild game and, according to
their book, preliminary results suggest that the numbers will be
much higher than previously estimated.  This research is supposed
to be published later this year.

5. Ecologically, I expect animals in warm climates to have less
fat, while those in cooler climates have more.  Also, in warmer
climates a greater variety of plant foods are available for a
larger part of the year.  Natural diets, I believe, will reflect
these principles.  Human beings have flourished (not just
survived) in both kinds of climates.  This supports the dietary
principle that fat and carbohydrate intake should be inversely
proportional to each other.  If this principle is adhered to, I
doubt that SFAs present a problem.

Todd Moody
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