>Amadeus Schmidt <[log in to unmask]> wrote:
>>Darko Mrakovcic <[log in to unmask]> wrote:
>>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.
IMO acid-base bala
nce is indeed important in generak and usually easily
achieved by several mechanisms, and in low-carb high-protein enviroment it
is even more easily achieved owing to an additional mechanism, namely acid-
base metabolic switch mechanism (which can be thought of as proper
redistribution of gluconeogenesis between the two sites, i.e. liver and
kidney). In other enviroments the main long-term mechanism is buffering by
calcium from bone, and in all enviroments the main short-term mechanism is
adjustment of carbonic acid concentration in blood simply by exhaling
carbon dioxide at different rates. I believe this is essentially what
Roland Rohde http://maelstrom.stjohns.edu/CGI/wa.exe?
A2=ind0209&L=paleodiet&F=&S=&P=456 says - cf. the following quotation from
his other post
http://maelstrom.stjohns.edu/CGI/wa.exeA2=ind0209&L=paleodiet&F=&S=&P=932 :
"The kidneys 8and 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. ... 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."
Rohde goes on to quote from abstracts of two articles by those authors
(Manz et alii):
"In the bodybuilders renal ammonium excretion was higher at any given
value of urine pH than in the controls.....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 additio
nal renal
acid load....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."
>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.
Here our interpretations of Rohde post coincide - higher blood acidity
(=higher concentration of hydrogen ions in blood) is also reduced by
transfer of th
ese ions (which are simply protons) into cells, and this
requires simultaneous transfer of potassium ions from cells into blood to
maintain balance of electric charges. This extracellular potassium is
readily excreted in kidneys (to keep serum potassium concentration within
tight bounds), and this leads in long term to intracellular potassium
depletion, which according to Rohde is an important contributing factor in
insulin resistance. In my interpretation of Rohde this could happen on LOW
PROTEIN ketogenic diet, i.e. low-carb diet with too high fat-protein
ratio. However, a more widespread cause of an even more drastic potassium
depletion (through a different mechanism) and resulting insulin resistance
is according to Rohde the typical grain-based (or other nearly vegetarian)
diet.
>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.
These questions are more or less answered by the above quotations from
Rohde and Manz et al. The fact that net potential renal acid load of
protein is positive IMO simply means that high protein results in higher
acidity of urine relative to blood. What Manz et al. say is (again IMO)
that urine acidity can be kept within a bound (which is much higher than
for blood) if the high-PRAL food consumed is protein, owing to the acid-
base metabolic switch mechanism.
>Does ketosis increase the need of K+ (potassium) to replenish the K+ loss
>from blood acidity? (low-carbers
think of endive ;-)
Yes, if ketosis is induced by low-protein ketogenic diet.
>Does a high intake of high-PRAL food increase potash demands as well?
>It looks so.
No, in my opinion, if the high-PRAL food is protein.
>At last Roland recommends "avoid metabolic acidosis".
>How is this accomplished best?
High protein diet, according to my interpretation of Rohde's views.
>Cordaine's answer is to add low PRAL, basic food items (vegetables and
>fruit). What's Roland's, what is yours?
My answer is based on the above (hopefully correct) interpretation of
Rohde's posts. In fact, even before reading Rohde - Thompson debate in
Paleodiet archives, I thought that Cordain perhaps failed to give the most
cogent argument, namely the acid-base metabolic switch, in his lengthy
explanation of the "paradoxically" high bone mineral density in
paleolithic hunter-gatherers. I was pleasantly surprised to see that Rohde
(and Manz and others), whom I found no less competent than Cordain,
apparently does not think there is a paradox at all. I am curious about
why that spurt of activity on Paleodiet list in 1992 was so short-lived -
I wouldn't be surprised if Rohde's ideas about acid-base balance and
protein ceiling were perceived as heretical by what "Ravnskov Camp"
(thincs.org) would call "Cordain Camp". (I regret Rohde did not get to
state his views on the Lipid Hypothesis/saturated fat controversy; I guess
that would have helped me finally formulate my own view; currently I am
totally undecided, perhaps slightly closer to "Cordain Camp".)
>Where are the blood tests after eating of one day meat and fat only?
>Could be done easily.
I have no idea. Of course, there exists anecdotal evidence about long-term
all-meat
diets (Stefansson, Anderson, some members of this list and
thincs. I will soon post my own blood test results, which look almost as
bad as Anderson's unless you look at cholesterol breakdown.)
>Inhowfar is raw meat different that cooked meat?
>David karas mentioned he had low acidity after eating raw meat.
Again, I do not have a strong opinion on this. My naive speculation would
be that dried meat is healthiest, followed by cooked. (That is at least
what I eat.)
>It comes to my mind that this could be because you won't be able to eat as
>much meat raw as cooked.
Perhaps. However, I would speculate this is because we don't have predator-
carnivore instincts, but only instincts of (unusually delicate) scavenger-
carnivores. (This explains why hominids became the only carnivores who
felt bad about being carnivores once the transition from scavenging to
hunting occurr
ed, i.e. once they became uniquely non-instinctive, i.e.
rational, predators. It also explains why many members of this list, e.g.
myself, used to be vegetarians, and why some, like you, still are.)
Less protein could indeed work basic because of the
>ammonia connection we discussed about.
I do not agree.
>What is the best way to increase K+ intake (as Roland recommends too)?
All-meat diet, according to Rohde (if I interpret him correctly).
Regards
Darko
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