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Subject:
From:
"Jeffrey P. Krabbe" <[log in to unmask]>
Date:
Wed, 2 Apr 1997 01:20:02 EDT
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Frieda Wallace writes:

PA>What evidence actually exists that high-protein diets cause acidosis?  In
PA>what groups has this ever actually been observed?  The Inuit eat remarkable
PA>amounts of meat and don't seem to have trouble with acidosis.  Do they have
PA>some kind of special buffering that other humans do not?

            By high-protein diets we need to delineate them as either
ketogenic or anti-ketogenic.  On a ketogenic diet, irrespective of the
levels of the two main macronutrients (fat and protein) ketoacidosis by
definition CAN NOT occur in normal healthy human beings on this type of
diet for the following reasons:
            1. Ketoacidosis envelops due to a total lack of insulin
            on a ketogenic diet, insulin's levels are indeed low, but the
sensitivity of tissues to insulin's anti-ketogenic nature is vastly
increased, i.e. less insulin but greater sensitivity to it.  Contrast this
to a type I diabetic (IDDM) in which they are insulin deficient and are
also ketoacidosis-prone. Type II diabetics are NOT ketoacidosis prone due
to higher systemic insulin, but less tissue sensitivity, thus insulin's
antiketogenic effect is in place.
            2. Ketoacidosis occurs due to a competition between fuels.
            Ketoacidosis only occurs in IDDM and alcoholics.  In IDDM
ketosis occurs with hyperglycemia (high blood glucose levels).  Since the
body is accustomed to using carbohydrates are a fuel (especially the brain)
the ketones are not used and accumulate in the bloodstream, bring down pH,
and a coma will shortly ensue.
            3. Ketones are self-regulating.
            The most amazing thing about ketosis as on a low-carb diet is
the ability of ketone bodies to limit their production so as to never cross
the maximal threshold.  They accomplish this mighty task by feedback
regulation which includes the secretion of insulin to limit overproduction.
In IDDM with the lack of insulin this negative feedback inhibition is no
longer present, and insulin is unable to reprise it's role in limiting over
production.  In fact hyperketonemia, and the uncontrolled production of
ketone bodies is accepted among the other above statements as one the
central reasons this will occur in IDDM.

            There are other factors, but they require a working knowledge
of interconversion rates between AcAc (acetoacetate) and BHB
(beta-hydroxybutyrate), and the normal ratios of these two substrates in
the body in normal vs. IDDM subjects.

            Don't be fooled by anyone though.  A ketogenic diet will lower
pH some, but that only reflects the dietary intake of a ketogenic diet, the
products of metabolism, and the compensatory mechanisms at work like
bi-carb reabsorption, ammonia to glutamine, and the like.  If you are
referring to non-ketogenic diet, that I highly doubt there would be any
acidosis, and even then the protein intake would have to be substantial and
far above any reasonable and prudent intake, i.e. excessive.

            JPK

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