Ed,
nothing could be farther from me than separating protein from potassium.
In fact, I used their ratio for my calculations.
Nor dit I want to establish new dietary ratios.
What I simply wanted to show is that it's not necessary to explain
the deleterious effects of potassium deficiency by acid/base calculations.
Actually they are physiologically not very relevant, to say the least.
The kidneys (and the lungs, CO2) are responsible for the acid/base
balance. Most relevant is the question, wether the excreted acids can be
compensated by an appropriate amount of bases to keep the pH-value
in a "normal" range. Whether these bases are fixed or more volatile
is not so important. In case of protein it's pretty
clear that it always brings more potential NH4+ with it than is needed to
compensate for the sulphur content. By the way, your literature [2]
explicitely confirms this. I cite from the abstract:
"In the bodybuilders renal ammonium excretion was higher at any given
value of urine pH than in the controls. In a regression analysis
protein intake proved to be an independent factor modulating the ratio
between urine-pH and renal ammonium excretion.The
concomitant increase of renal net acid excretion and maximum renal
acid excretion capacity in periods of high protein intake appears
to be a highly effective response of the kidney to a specific food
intake leaving a large renal surplus capacity for an additional renal
acid load."
A newer one [1] from the same author:
Further analyses of the interrelation between diet and acid-base
status revealed that increasing protein intake (despite its potential
to increase NAE) also significantly improves the capacity for renal
net acid excretion by stimulating urinary ammonium excretion.
... protein itself moderately improves the renal capacity to excrete
net acid by increasing the endogenous supply of ammonia which is the
major urinary hydrogen ion acceptor."
As everything that we ingest has to pass our vascular system before it is
metabolized within the cells, I further tried to direct your attention to
the well known fact that K+ is one of the most critical food constituents,
critical for the appropriate function of many excitable organs, like the
heart. A high potassium concentration (in the blood, not in the cells)
can kill you within one single heart beat. This ion is closely tied to
glucose metabolism, a substance that in a paleolithic diet is mainly a
metabolic intermediate sourcing from and stoichiometrically coupled to
protein uptake. Carbs as the essentally new neolithic nutritional factor
can thus disturb this delicate electrolyte balance. The 10g K+ per 100g
carb ratio is merely a theoretical one and was mentioned to get an idea of
the K+ gap in western diets if we assume a stoichiometric relation between
cellular K+- and glucose-uptake, independently of the glucose source (food
or gluconeogenesis). Grain is especially deleterious, because it is
accompanied by about only 0,6 grams of K+ per 100g starch, even if one
eats all parts of the grain. White flour has even half of that, i.e. 3%
of what it should have. It's a little bit strange that many of the
mentioned K+ -facts are well accepted in classical medical sciences like
pharmacology, intensive care medicine, and anesthesiology because they are
relevant for the survival of their patients. But there seem to be no
consequences for every day life of the general population. Many
nutritionists talk about the "empty calories" of sugar and fat. But they
are not aware of the emptiness of grain and even many fruits in this
respect. Assuming that man is so very strongly adapted to meat that he
will not really thrive on a diet that is composed very differently, a K+
-imbalance could well be one possible additional factor for diabetes and
other diseases. One factor, not the sole one and not even necessarily the
pivotal one.
Especially the omega-3 connection is very promising. The cited paper [3]
is in so far not untypical as it uses not a pure omega-3 fatty acid but
fish oil, that surely contains a lot of other active metabolites, like
vitamins A and D. In my recent posting "lions & dogs" you can find two
papers [4,5] about phytanic acid (PA). This is a new star on the fatty
acid scene. It is already proven to positively influence the glucose
metabolism [5] in rat liver cells. It acts as a vitamin-hormone, very
similar to vitamin A [literature in 4]. And it is hormonally necessary as
a coactivation partner for the so called ppar-receptors that mediate the
effects of many of those fatty acids like omega-3. It is most exciting
that PA not only is ocurring in the same fats that have good omega-3/6
ratios, fish oil [6] and the fat of grass fed animals, it even comes from
the same primary sources, namely grass or algae that contain chlorophyll.
Even nematodae and insects have receptors for it!
There is no contradiction between potassium and fatty acids as causative
factors in diabetes development. Diseases like diabetes can't be
monocausal from a non-paleo point of view, otherwise we would know the
cause since a long time.
Roland
[1] Remer, T. Influence of nutrition on acid-base balance--metabolic
aspects.
Eur J Nutr 2001 Oct;40(5):214-20
[2] Manz F, Remer T, Decher-Spliethoff E, Hohler M, Kersting M, Kunz C,
Lausen B. Effects of a high protein intake on renal acid excretion in
bodybuilders. Z Ernahrungswiss 1995 Mar;34(1):10-5
[3] Somova L, Moodley K, Channa ML,
Nadar A. Dose-dependent effect of
dietary fish-oil (n-3) polyunsaturated fatty acids on in vivo insulin
sensitivity in rat.
Methods Find Exp Clin Pharmacol 1999 May;21(4):275-8
[4] McCarty M, The chlorophyll metabolite phytanic acid is a natural
rexinoid--potential for treatment and prevention of diabetes.
Med Hypotheses 2001 Feb;56(2):217-9.
[5] Heim M, Phytanic acid, a natural peroxisome proliferator-activated
receptor agonist, regulates glucose metabolism in rat primary
hepatocytes. FASEB J 2002 May;16(7):718-20
[6] Ratnayake WM, Olsson B, Ackman RG. Novel branched-chain fatty
acids in certain fish oils. Lipids 1989 Jul;24(7):630-7.
roro
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