On Fri, 11 Aug 2000, Amadeus Schmidt wrote:

> >This requires a liberal amount of protein, yes, but by no means a
> >toxic amount.
>
> The 500 or so kcal from protein are way below the toxic amount,
> but for kidney diseased it could be a problem.

Sure, but there is no indication that a high-protein (but
sub-toxic, obviously) diet *causes* kidney disease, and there are
some indications that the opposite is true.  The analogy is this:
If you have weak ankles, then ice-skating may not be good for
you.  But ice-skating doesn't cause weak ankles; it prevents
them.

> I know very few (actually no) vegetarian overweights - but here on the
> list I've heared about. I tend to attribute this to health dangers
> which are more likely to hit them
> - food toxin dangers by unfermented or sprouted grains (esp.phytin)
> - problems by trans fats (more likely in unconcious veg.fat consumers)
> - w-3 and w-6 imbalances (also due to  widespread w-6-only fats)

Dr. Dean Ornish is looking rather plump these days, and Dr.
Andrew Weil is just plain fat.  You may not know these guys; they
are American "celebrity doctors."  Both of them advocate avoidance
of trans-fats, whole foods, and vegetarian diets.  Perhaps they
don't practice what they preach?

> Diabetes has some implications which should show up, like "need to eat"
> (hypoglycemie) sugar cravings, loss of feet etc. after injuries,
> not healing wounds.

Yes, but I don't know whether these, especially the need to eat
and sugar cravings, would have been seen as part of the same
disease as sweet urine.

> Any volunteers? Do you know where the high carb list is?

Well, you could try http://drmcdougall.com.  The McDougall diet
is perhaps as different from what you find on this list as
anything you could imagine.

> Does fasting insulin exist anyway?

Yes.  Definitely.  And when it is higher than normal there are
problems.  Elevated fasting insulin is a direct marker for
insulin resistance. See, for example, Circulation 2000 Jul
4;102(1):42-7 Chronic subclinical inflammation as part of the
insulin resistance syndrome: the Insulin Resistance
Atherosclerosis Study (IRAS).   Festa A, D'Agostino R Jr, Howard
G, Mykkanen L, Tracy RP, Haffner SM

> At least 3 hours after a meal
> glucose should go down and insulin with it. This is glucagon time.

Right, but that doesn't mean that insulin must be zero.  It means
that it should be low enough to allow glucagon to work.  If it
isn't then there's trouble.

> Insulin works totally opposite of glucagon how could they coexist?
> Strange to me. I haven't read about fasting insulin yet.

Do a PubMed search on "fasting insulin" (don't forget quotation
marks) and you'll find quite a lot.

> Erasmus mentiones vitamin c as a strong arteries protecting factor.

I think there's little doubt about that.

> Insulin decreases d6d activity.
> Would you postulate insulin to disable d6d delectively differently for
> 18:0 (SFA) amd  18:3 (EFA) fatty acids?

I don't know.  But consider that if I am consuming my EFA in
short-chain form (EPA, DHA, and AA, for example) there's no
competition anyway, because these fats are past the D6D step.
So, if sufficient EPA, DHA, and AA are available, the D6D only
needs to work on the SFAs and MUFAs, and there's no EFA
bottleneck.

The moral of the story may be: The more LCSFA and MUFA you
consume, the more important it is to get your EFAs in
pre-desaturated form.  This presents a problem for eaters of
farmed meats; I've never denied that.  Such people really should
get their EFAs as DHA or EPA, rather than flax oil.  That means
brains or fatty fish or algae-derived DHA.

> >But the point is that these are the fats used in modern LC
> >approaches.
>
> Yes, this questions "modern" LC approaches and "modern"
> paleo-inuit-reconstructing diets.

It may question them, but the success of these approaches
suggests an answer.  In fact, my own difficulties on Neanderthin
appear to be traceable to (more than any single factor) my
enthusiastic consumption of nuts (not very Inuit).  I really
think the "magic" of the Anchell diet is just as Rachel said: It
is forcing me to adopt a disciplined approach that cuts carbs and
calories in the process.  It allows me no dietary corners to hide
in.

> And hypertension is modulated by  ... working of prostaglandins.
> Or excess salt?
> Series-2 prostaglandins increase salt retention.
> Salt increases water retention.

All of the above.  I think the prostaglandin effect is the master
switch.  This is another thing that low-carb diet cured for me.
My blood pressure had crept up to 150/100; it dropped to 120/80
or 75 after just a week of carb restriction, and has stayed there
ever since.  And as you know, I am an unrecovering salt addict.

Todd Moody
[log in to unmask]