On Thu, 3 Aug 2000 09:35:06 -0400, Todd Moody <[log in to unmask]>
wrote:

>I understand this, in principle, and find it plausible.  But
>lately I am having some misgivings.  For one thing, EFAs are
>PUFAs, and highly oxidizable.  A high concentration of PUFAs in
>cell membranes must make them more susceptible to oxidation
>damage, and I doubt this is a good thing.

I think, eather the EFAs are required, then they have to be protected
by the antioxidants (namely Vitamin E,C).
The main reason for tocopherol to be a vitamin (E).
If SFA was the right for cell membranes, why would the body try to pick
out the PUFAs? If very much SFAs are present?
Why should the body bother then to convert SFAs by desaturating them?

Much of what is written over diseases of blood vessels (and heart valves)
blames their hardening. This is what i would expect to happen in an
environment of lacking EFAs.

I also find the paleo view important.
Saturated fat intake is obviously very unpaleo because never, anyplace
anytime in history man (or predecessors) has been exposed to amounts of
saturated fats.

Not in savannah yearmillions , assuming heavy game eating: wild game fat is
very unsaturated and overall low in fat.

Not in savannah times, eating tubers (low fat) or nuts (high
polyunsaturated).

Not in ice shield times: wild game was high fat, but probably is very
unsaturated.

Not in rain forest time- fruit is low fat and nuts are polyunsaturated.

There's no time and reason for human bodies to be prepared prepare for much
dietary saturated fats. The dietary saturated fat attack come only since
mass meat and dairy production. Less than 100 years. After refrigeration was
available.

Just an idea by the way:
I would be a reason for the body *not* to dissolve its fat depots
if saturated fat in the blood is deleterious, and body fat consists of such.

>Second, we *do* have the enzymes for turning SFAs into MUFAs as
>needed.  So buildup of SFAs in membranes shouldn't be a problem,
>if these enzymes are working.

Some is turned to MUFA, but not to EFAs.
However SFA AND MUFA, both were reported to work against EFA in concert.
Erasmus put it in
page 225 "Test showed that....... above certain parts of OA compared to EFA
 EFA activity is totally suppressed..."
For beef this ratio is reached even with only the OA (monounsaturated) part.
But the SFAs are turned to more OA too.

>I am very skeptical.  For one thing, arteriosclerosis is not
>correlated with fat intake or cholesterol levels *at all*.

In my memory i recall totally different.
Wasn't it that each 50mg of cholesterol elevation doubles the risk of heart
death? I've to take a look. Could you mention matching studies?

I find the explanation of Erasmus (of "Omega Diet" i think, and others too)
very plausible, that cholesterol was used to strenghten (but unfortunately
also otherwise narrow) unflexible blood vessels.

> And I'm sure you've considered that many fowl, such as
>ducks, also have substantial amounts of fat, a good deal of which
>is saturated.  I think water fowl would have been an important
>food source.  For example, pheasant is about 9.3% fat, almost a
>third of which is saturated.  Wild duck is about 15% fat, about a
>third of which is saturated.  In fact, the fat composition of
>wild duck is similar to that of feedlot beef.

Honestly i didn't think of water fowl. They have bigger fat amounts
(although 15% still is way below beef and pig) and it's saturated (for
waterproof surface).
However i doubt ducks to have been an important food source.
They can fly away.
Bows and arrows are a recent invention of only 40k years.
I don't expect them in glaciation nor in savannah.

>Now consider organ meats: liver, pancreas, spleen.  If you do a
>bit of checking you will find that in almost every case the SFA
>content of these foods is greater than the MUFA or PUFA content.
>In a few cases, the SFA and MUFA are about equal.  So I'm not
>seeing any particular scarcity of SFAs in paleo animal foods.

How much is liver, pancreas, spleen of an animal?
It's not about scarcity. SFA+MUFA in beef (and dairy) is 95%.

>
>> Not only saturated, but also monounsaturated fats compete with EFAs
>> on enzymes, but to a lesser degree. Then its a matter of EFA compared to
>> total fat.
>
>Again, I'd like to see evidence that this competition is a
>*problem*.

I looked it up (page 225) and only found "Tests have shown..." but not the
reference. Could we write to Udo for the reference???

However in understanding that the enzymes work on various FA it's plausible.
And who's haveing the paleo-view of exposition time. Who but us?

>...
>Masai, Samburu, and Jamaican people.  The first two eat almost
>exclusively meat and dairy (and some blood); the Jamaicans use
>large amounts of coconut oil, which is more saturated than any
>animal fat.  All have extremely low rates of diabetes and heart
>disease.  This isn't what you'd expect if their cell membranes
>are turning to stone, is it?
>
That's true.
Healthy eaters of masses of saturated fat don't match.
Concerning the african pastoralists (Massai): The kind of cattle *they* have
("Zebu" cattle) have a excellent fat composition (listed by Erasmus).
If milk fat resembles the food of the animals, then the truely grass fed and
lean zebus may have a more adequate fat.
But coconut... they have exceptionally saturated fat.
Udo Erasmus mentiones the paradox too, and assumes a "local factor", which
leads to healthy consumers in the tropics, as opposed to consumers of the
same oils in other countries (and processed form).

I looked at coconut. Only ripe meat was available at usda, not the "tender"
ones (part ripe), which are locally eaten. I personally loved them tender
and got too much soon from ripe ones.
What catched my attention is that the SFA of coconut is mainly 12:0 instead
of more long chain 16:0 and 18:0 of beef.

some traces to that puzzle

cheers and no coconut tonight ...

Amadeus