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From:
Darko Mrakovcic <[log in to unmask]>
Reply To:
Paleolithic Eating Support List <[log in to unmask]>
Date:
Mon, 14 Jul 2003 10:44:31 -0500
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On Fri, 11 Jul 2003 12:45:26 EDT, Adrienne Smith <[log in to unmask]> wrote:

>What do you define as high protein ie how many grams? How would one
determine
>the requisite grams of protein for a high protein regime.  Also  what
>proportion of fat to protein would you consider ideal?

My messages in this thread were entirely based on Roland Rohde's messages
in Paleodiet list. This seems to be the only quantitative info he gives
regarding your question:

"An important additional factor for the cellular K+ -content is the blood
pH. If blood becomes more acidic, this leads to a H+ -shift from blood to
cells and a reverse K+ -shift. The K+ shifted to the extracellular space
is excreted by the kidneys and thus lost. In a low carb diet, this danger
always is present (Ketosis! See recently [6]). This is not a question of
acid-base-balance! Additional 100g protein contains additional 16g
nitrogen = 1,14 mol that could be excreted as positively charged ammonia
instead of neutral urea by the kidneys, sparing 1,14 * 39g = 45g K+, if
necessary! A person eating 280 g of protein instead of 80g theoretically
may excrete 2280 mVal more basic equivs as NH4+. This is often not
considered by those acid-base-balance people. Protein is the most basic
nutrient one can find!"

Thus, Rohde only quantifies the protein required to "theoretically" save a
given amount of intracellular potassium, but not the protein required to
prevent depletion (and its consequences like IR) in practical terms.
(Incidentaly, this depletion is not caused by the same mechanism as  the
well-known ketosis-induced hypokalemia, ie. depletion of only
extracellular potassium, which results from increased diuresis and absence
of potassium retention  in kidneys, and which is easily corrected simply
by potassium supplementation; absence of potassium retention mechanism is
due to abundance of potassium - unlike sodium - in paleo food.) An obvious
confounding variable here is correction of acidosis through another
mechanism, namely mobilization of calcium carbonate from bones; this would
IMO mean that a smaller quantity of protein would be required since
plentiful potassium has higher priority than bone mineral density; thus
you might avoid IR with a much smaller quantity of protein than Rohde's
280 g, but the price payed could be osteoporosis.

The most likely reason you felt the worst on a higher protein and lower
fat diet is IMO protein toxicity, despite of of your statement to the
contrary. The main symptom of mild hyperammonemia is lethargy, rather than
nausea and vomiting (which would be a more severe form, and which on this
list seems to be identified with protein toxiciity). Lethargy usually
means drowsiness (which was my main symptom at protein intake higher than
yours almost by an order of magnitude), but a milder version could be
sluggishness, indifference, laziness, or possibly what you call
exhaustion. (If I am right about this, your urea cycle is probably
somewhat defective, since your protein intake was not very high by any
standards.) Another contributing factor to your exhaustion could be simply
the simultaneous stress of ketosis (under rather extreme caloric
restriction, at least from my perspective) and of exercise. IIRC Ray Peat
says that very high level of stress hormones can cause hypothyriodism, or
at least reduce the metabolic rate.

Even if your present objective is still weight loss (which does not seem
prudent to me given your objective of 49 kg), I believe you should raise
again your protein intake to boost your metabolism (this is not very
contorversial since Peat and Cordain agree about this) and simultaneously
keep or raise further your high saturated fat intake; this should
eliminate protein toxicity (a well-known effect which is in my opinion due
to translocation of gluconeogenesis to kidney, i.e. acid-base switch -
does anyone have any other explanation?), reduce renal acid load (which is
according to Cordain another cause of diet-induced hypothyroidism), and,
according to Peat, eliminate the main cause of diet-induced
hyperthyriodism, namely high unsaturated vs saturated ratio. I know this
would up your total calories, but it might result in no weight gain if it
really raises your metabolism, especially if the coconut oil people are
right about MCTs.

I am doing a similar experiment these days: after six years of calorically
restricted paleo ketogenic diet, I have been on a strict all-meat higher
calorie diet for 6 months continuously (+ 3 months last summer), and I had
my blood tested recently. Since my TC is comparable to Anderson's, namely
347, I have now introduced some minor changes. After geting my results, I
have studied blood profiles of people on this list, and I found out yours
seems to be about the best (was that before you introduced coconut oil and
perhaps a result of your higher protein diet?). Incidentally, my TG vs HDL
ratio is almost as enviable as yours, namely 41/99 ~ 0.4 (this is
according to Sears a surrogate for fasting insulin, and generally regarded
as the most important indicator), and also my TC/HDL of 347/99 ~ 3.5 is
actually good: it officially puts me at half the average risk for CVD.
Even the astronomical LDL of 239 could coceivably be a good thing if the
small dense LDL theory is correct: my VLDL is quite low at 8 (normal range
5 - 40), and this according to Cordain is most likely the source of small
dense LDL.

In any case, I have decided to give Peat's recommendations a chance,
although I have not formed an opinion of his theories yet. (It was from
you that I first heard about him; do you know why he is not a member of
thincs?) According to him, my (and your) high  HDL is actually a bad thing
(hopefully he is totally wrong here - there seems to be too much
contradicting evidence), namely "practically a diagnosis of
hypothyroidism". More importantly, he says that TC builds up since it is
not used for production of steroids, and this is caused by hypothyroidism
To correct this, one should supposeddly reduce unsaturated vs saturated
ratio. Since my diet has indeed been relatively low in sat fats (although
not absolutely because of shere quantity of meat - well over 3 pounds a
day), I have decided to try coconut oil since MCTs seem to have all these
nice properties (they supposedly efficiently boost metabolism without
spending carnitine and yet, like sat fats in general, they don't burn your
mitochondria - no lipid peroxides, and perhaps they are less atherogenic
than palmitic acid - although there is a lot of evidence to the contrary).
I had to overcome my all-meat paleo religiousness to include coconut oil,
but now I am adding at least twice the amount of it you do. I hope my
total calories remain reasonably low (less than 2500?) since i have
signifiacantly reduced the quantity of meat as a result of adding oil. I
suppose you are aware that 3 tablespoons of any oil is a mere 300
calories, and that your sat fat and caloric intake could actually be quite
low. My objective is not weight loss - at 183 cm  (6 ft) height, I am
still underweight even after my weight has crept up from 64 kg to 68 kg
(=150 lb) in the past 6 months, but I would prefer to remain underweight.
I hope Peat is right when he says that they stopped feeding farm animals
coconut oil in the fifties sice they were getting leaner. I still have
some serious questions about the paleo-correctness of MCTs (due to their
plant origin and exotic nature) and this experiment will probably not last
long. I find Peat does not address that aspect of MCTs sufficiently, and I
would appreciate any information on that.

Darko

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