On Thu, 6 Feb 2003 09:38:00 -0500, Darko Mrakovcic <[log in to unmask]> wrote:

 >While I also find that Rohde's explanation (which I read a long time ago)
 >of the interrelationship of all the above concepts is excellent, my
 >understanding of it is very different from yours.
 >It seems to me there is an obvious contradiction in your assertions that
 >ammonia is acidic and that at the same time "excreting ammonia lets the
 >body get rid of some excess acid", which is why Rohde calls protein a very
 >basic food. Indeed, if ammonia were acidic, excreting it would only add to
 >PRAL, rather than reducing it. I believe that Rohde implies that ammonia
 >(or, to be more precise, ammonium hydroxide NH4OH) is alkaline and thus
 >enables excretion of acids, e.g. ketones (since the NH4+ cation forms a
 >salt with the anion from the acid). If I am wrong, could you please provide
 >a reference about acidity of ammonia?

Hi Darko,

thank you for your thoughtful response.
You are right, ammonia of course is very basic (pH11) not acidic.
Is misinterpreted Roland's paragraph about blood pH and protein beeing a
basic food item so that excreting ammonia would lower blood pH directely
(like the kidney can make the urin acidic until ph 3).
It's like you said, ammonia is basic, but helps the kidney excrete more
acids.

However, the problem is (similar to my postulation) that ammonia production
can't be risen very much because it is so toxic (by "unsure" mechanisms, but
you mentioned some).
Indeed blood ammonia is very little - 10-40mmol/L, compared to urea
(~10-fold). Thanks god - considering it's toxicity.
I think that's the reason why additional 100g protein can *not* be excreted
as ammonia resulting in less blood acidity. The metabolic swith shuts down
ammonia production at an early stage.
For smaller amounts of protein - in the dimensions like can be made to
ammonia and buffered by the blood - Rolands equation should work.

Therefore the protein ceiling should be determined by the capacity to make
and excrete urea. You wrote that increasing fat intake itself would rise the
protein ceiling, due to "less need of gluconeugenesis and higher ketosis".
But what occurs to say 100g amino acids which were eaten and cannot be built
into new tissue? I think (correct me if I'm wrong) that there is no way to
avoid gluconeugenesis for this extra protein. By with else pathway should
the body get rid of it, once it's eaten?

More ketosis makes more ketone bodies and these are acidic.
This would even reduce the ammonia (and acid) excretion, because the
metabolic switch to urea occured earlier. Right?
If the trigger for the switch (from ammonia to urea) is indeed blood acidity
as you write, and not the level of ammonia,
then higher ketosis could rather lift the protein ceiling
because less ammonia is produced (less toxicity for the brain) -
if ammonia is the reason for rabbit starvation.

 > (See U.C. Davis lecture notes on metabolism
 >at http://www.zonehome.com/met/metprotnit.htm).

Great reading, all of the parts.

 >In my interpretation Rohde essentially says that acid-base balance is
 >irrelevant in the context of a low-carb high protein diet owing to
 >neutralization of excess acid in kidney by ammonia. Furthermore, it is my
 >understanding that this ammonia is generated in the first step of
 >gluconeogenesis in kidney (from glutamine), thus gluconeogenesis does
 >definitely not cause excess acidity.

I think the acid-base balance *is* important in a low-carb and high-protein
environment, and it has to do with the information in Roland's posting.

He writes very interesting about the effects of blood acidity
on the K+ levels. Acidity in the blood depletes cells from K+.
Which impairs several cell functions (insulin sensitivity, nerve working).
That's a way how blood acid *is* toxic.

Now has protein a high PRAL or not?
The net acid/base load of protein -after digestion, excretion and all- is
described as acidic in literature.
Roland mentions the HCl production in the stomach *before* digestion as
lowering the blood acidity. That's fine, but how long does it last? And in
sum? Also the ammonia production (makes basic) is limited.
At least big protein amounts should be considered with the PRAL.

Does ketosis increase the need of K+ (potassium) to replenish the K+ loss
from blood acidity? (low-carbers think of endive ;-)
Does a high intake of high-PRAL food increase potash demands as well?
It looks so.

At last Roland recommends "avoid metabolic acidosis".
How is this accomplished best?
Cordaine's answer is to add low PRAL, basic food items (vegetables and
fruit). What's Roland's, what is yours?

Where are the blood tests after eating of one day meat and fat only?
Could be done easily. Inhowfar is raw meat different that cooked meat?
David karas mentioned he had low acidity after eating raw meat.

It comes to my mind that this could be because you won't be able to eat as
much meat raw as cooked. Less protein could indeed work basic because of the
ammonia connection we discussed about.

What is the best way to increase K+ intake (as Roland recommends too)?

regards

Amadeus S.