On Thu, 3 Aug 2000, Amadeus Schmidt wrote:

> >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).

Since only E is fat-soluble, that would be the main one, I think.

> The main reason for tocopherol to be a vitamin (E).

I think not.  Vitamin E's primary point of importance was in
preventing or curing certain cases of sterility.  In fact the
etymology of the word "tocopherol" refers to child-bearing.

> If SFA was the right for cell membranes, why would the body try to pick
> out the PUFAs? If very much SFAs are present?

I suspect that a combination of both are used.

> Why should the body bother then to convert SFAs by desaturating them?

To maintain a balance.  I do not believe that cell membranes are
supposed to consist entirely of SFAs.

> 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.

Hardening of blood vessels (arteriosclerosis) is a result of
calcification, not SFAs in cell membranes.  Lack of EFAs may
contribute to this, but an abundance of SFAs does not equal a
lack of 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.

But if you look at the fats in organ meats and marrow, which are
predominantly saturated, and accept that these were the
*preferred* edible portions, then it appears that significant
amounts were eaten.

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

Again, you are only counting muscle fat.  Organ, structural and
marrow fats are highly saturated.  And you are ignoring water
fowl.

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

Probably?  Storage fats are highly saturated.

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

But tropical oils are very saturated.

> 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.

So why would the body *make* saturates from glucose?

> 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..."

What is OA?  Is that oleic acid?  What does he mean by "EFA
activity"?  Is that prostaglandin synthesis?

> >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?

You were talking about hardening of the arteries, which is
arteriosclerosis.  There is no correlation with cholesterol.  But
maybe you were thinking of atherosclerosis, which is something
different from hardening.  In any case, now you're talking about
cholesterol, not SFAs.  The relation between SFAs and cholesterol
is itself very loose.  And atherosclerotic plaques contain
substantial amounts of PUFAs as well as cholesterol.

If you haven't already read
http://home2.swipnet.se/~w-25775/index.htm, you should.  Also
read Mary Enig's comments on Paleodiet.  She has a new book on
this subject, but I haven't read it yet.  One important point,
based on recent research is that lipoprotein(a) levels are an
important risk factor for heart disease, and *only* SFAs reduce
Lp(a).  This is probably post-Erasmus research.

> 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.

You're kidding, right?  Spears can be thrown; rocks can be
thrown.  Dogs are pretty good at catching them too.

> >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%.

I'm saying that if these were the preferred edible parts, as
evidence suggests, then they were getting good amounts of SFAs.

> >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).

Well, there could be such a "local factor" or he could be just
wrong about the alleged dangers of SFAs to begin with.

One of the interesting things in the Allan/Lutz book is the way
in which Dr. Lutz kept detailed records of many, many patients,
over a long time.  He typically recommended a diet low in carbs
and high in animal fats.  He also did periodic insulin resistance
checks, by means of a glucose challenge.  He found that after
some months on his diet, the blood glucose response to the
glucose challenge *normalized*.  This is the opposite of what we
would expect if cell membranes were becoming less and less
permeable to insulin.

I know that I have more than once posted studies that purport to
show that SFAs cause insulin resistance.  Ken Stuart pointed out
that they were all epidemiological, and it is a mistake to put
too much weight on epidemiological studies.  Controlled clinical
studies are more significant, since it's easier to keep track of
the variables.

Last year James Hays, an endocrinologist in Delaware, presented
his results of a year-long study of a low-carb diet in which
almost all the fat was animal fat.  The results were improved
glucose tolerance and improved lipids.  There's something going
on here...

Todd Moody
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