On Thu, 10 Aug 2000, Amadeus Schmidt wrote:

> >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.

But you *shouldn't* expect it if the high percentage of
long-chain saturates in these diets is causing havoc in cell
membranes and prostaglandin.  Note also that Dr. Lutz has
recorded significant improvements in *many* disease processes,
including cardiac function and many gastrointestinal disorders (a
specialty of his, I believe).

Can you find any empirical evidence that a low-carb diet causes
any health problem?'

> 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).

Well, I agree with this to some extent, but it is still an open
question whether this is and adequate explanation of the problems
of high carb consumption.  One would expect, for example, that
people who eat lots of whole grains and fresh vegetables would
not experience these problems, but I don't think that's the case.

> 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.

Diabetes known in the ancient world and described in medical
writings.  Also, I am suspicious of "primates in general" as a
reference class.  Humans have adapted to a way of life that is
strikingly different from that of other primates.  I don't think
it is warranted to suppose that all primates are metabolically
equal.

> 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.

Yes.

> 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.

If so, then it is this, and not the SFAs in cell membranes, that
is causing insulin resistance.  This suggests an easy test.  A
small amount of brewer's yeast with high-carb meals ought to cure
insulin resistance, since brewer's yeast probably has more
thiamin and other relevant sugar-processing enzymes than any
other substance.

> 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).

Makes sense.

> 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.

Okay, good.  So that's one less reason to be concerned about
SFAs.

> >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.

But what about the many other improvements that are seen?  For
example, in my own case the most remarkable one was the curing of
long-term periodontitis.  I lost three molars because of this
disease, even with frequent flossing and occasional deep
"scraping" treatments.  This condition almost disappeared when I
switched to low-carb diet, and did disappear when I added some
vitamin C (which would have been present in the organ meats I
wasn't eating).

> 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.

Caused by what?  The saturates are less oxidizable and therefore
less likely to cause free radical damage.  Lower glucose levels
also mean reduced incidence of glycation reactions.  Free radical
damage and glycation reactions are believed to be important
contributors to aging processes.

> 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.

There is simply no evidence that low-carb diet contributes to CVD
or cancer, so why would you expect it?

That ratio is supposed to be related to prostaglandin function,
but we already know that insulin plays a large role.  Therefore
any fat ratio that does not also control for insulin levels is
going to give a distorted picture.

There is evidence that fasting insulin levels are an important
risk factor for heart disease.  Given what we know about
prostaglandin function, this shouldn't be surprising at all.  On
a low-carb diet, even high in long-chain saturates, fasting
insulin levels tend to drop.  It makes sense that under these
conditions the desaturase enzymes work properly and the saturated
fats are handled and don't cause trouble.

Now if you want to argue that under the right conditions -- i.e.,
with plenty of intact thiamin, niacin, and other co-factors
available -- a high-carb diet can be tolerated without raising
that fasting insulin level significantly, thus avoiding insulin
resistance and prostaglandin disturbances, then I agree that it
may be a healthy option.  I'm not sure, because I'm not familiar
with any body of evidence for that sort of diet, but I certainly
don't rule it out.  I've mentioned before that my grandmother was
a vegetarian (except for *very* occasional fish-- once or twice a
year) who ate beans and rice every day, with brewer's yeast.  She
lived a long and healthy life, with no heart problems or cancer.
She did experience tinnitus.  Someone posted a study yesterday on
lowcarb-tech linking tinnitus with hyperinsulinemia, oddly
enough.  But other than that she was healthy.  And in her last
years she had to rely more on processed food anyway.

Todd Moody
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