Hi Amadeus

I apologize for not replying to your message
http://maelstrom.stjohns.edu/CGI/wa.exe?A2=ind0302&L=paleofood&P=R5514
from last February - I was rather busy at the time, and I thought your
questions required lengthy answers, so I kept postponing my reply
indefinitely.

Amadeus Schmidt <[log in to unmask]> wrote:

>You are right, ammonia of course is very basic (pH11) not acidic.


>Is (I?) 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).

I am not sure I understand
what you were saying here.

>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).

I disagree with your statement about the upper bound on ammonia
production: as I said in my post, http://maelstrom.stjohns.edu/CGI/wa.exe?
A2=ind0302&L=paleofood&P=R5206 , due to its toxicity, ammonia is not
produced in significant amounts anywhere except at the site of excretion,
namely in the kidney. In particular, it does not have to be present in the
blood in order to be excreted.

>Indeed blood ammonia is very little - 10-40mmol/L, compared to urea
>(~10-fold). Thanks god - considering it's toxicity.

Yes, but this does no
t imply your next statement:

>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.

The metabolic acid-base switch actually results (according to the source
that I had given and that you found a great reading) in MORE ammonia
production. (As I said in my post, which you probably did not read
carefully, the main purpose of the switch is the gradual translocation of
gluconeogenesis from liver to kidney as the liver capacity for urea
production is approached or as rising blood acidity requires more ammonia
production. Gluconeogenesis in liver and in kidney has different
substrates - alanine resp. glutamine, thus ammonia needs to be produced in
the first stage of gluconeogenesis only in kidney.)


>For smaller amounts of protein - in the dimens
ions like can be made to
>ammonia and buffered by the blood - Rolands equation should work.

As I have just explained, I don't agree with this.

>Therefore the protein ceiling should be determined by the capacity to make
>and excrete urea.

Yes, except that Roland Rohde seems to say that protein ceiling is not
absolute at all (since gluconeogenesis in kidney does not require urea
production).

You wrote that increasing fat intake itself would rise the
>protein ceiling, due to "less need of gluconeugenesis and higher ketosis".

You misquoted me here - I said "less need for gluconeogenesis IN LIVER due
to higher ketosis and resultant acid-base metabolic switch".

>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
.

I think that is correct (at least for glucogenic amino acids).

By with else pathway should
>the body get rid of it, once it's eaten?
>

Gluconeogensis (in kidney).

>More ketosis makes more ketone bodies and these are acidic.

Yes.

>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.
>

I do not understand your reasoning competely, but you obviously
misunderstood the purpose of the metabolic switch: the direction of the
switch is FROM alanine-urea TO glutam
ine-ammonia. I was saying that higher
ketosis implies higher blood acidity, and this in turn implies greater
need for ammonia production (in kidney; ammonia reduces blood acidity
although it is not present in blood - it simply enables excretion of acids
in the kidney).

I am running out of time - I'll try to answer the remaining questions as
soon as I can.

Regards

Darko