- Chronic metabolic acidosis exists normally in humans eating ordinary diets that yield normal net rates of EAP (endogenous acid production). The diets have an excess of noncarbonic acids (sulfuric acid) instead of a base (bicarbonate)
- These diets have been linked to nephrolithiasis and osteoporosis
- Low grade Acidosis increases with age resulting from kidney function declining with age
- This acidosis contributes to the loss of skeletal muscle mass that occurs with aging
- Chronic metabolic acidosis induces muscle protein breakdown but when the acidosis is corrected the effects are reversed
- This leads to stimulation of ATP and ubiquitin-dependent proteolytically released branch chain amino acid (valine, leucine and isoleucine) preventing reuptake for protein synthesis
- Nonbranched chain amino acids, especially glutamine, are released and are made available to the kidney
- The kidney excretes ammonium ( releasing H ions to balance ph from acid diet and eliminates muscle N
- The degradation in muscle increases the production of nitrogen (N) end products that are eliminated in urine
- N loss occurs when endogenous acid production is abnormally high (i.e. chronic ketoacidosis) or when acid excretory and/or bicarbonate reabsorpitve capacity of kidney is impaired (i.e. advanced renal insufficiency)
- N metabolism is a direct result of the acidosis.
- Releasing increased amounts of amino acids (glutamine) can increase excretion of acid (ammonium getting rid of the H ions ) mitigating the severity of the acidosis
- KHCO3 can potentially prevent continuing age-related loss of muscle mass and restore previous deficits. It reduces the net endogenous acid production and corrects previous low grade metabolic acidosis state
- Administration of ammonium chloride or increased dietary protein intake leads to urinary calcium excretion which results in inhibition of net renal tubular calcium reabsorption, lack of intestinal calcium absorption and stimulation of bone resorption leading to negative calcium balance
- KHCO3 but not NaHCO3 reduce urinary Ca excretion no matter what their dietary Ca intake is
- Ca retention during KHCO3 administration occurred without changes in net intestinal Ca absorption indicating it was the result of renal Ca retention or enhanced Ca retention in bone or a combination of the two
- Potassium, independent of HCO3 could reduce urinary Ca excretion
- KHCO3 could stimulate renal tubular Ca reabsorption
- Intermittently higher serum K+ levels during KHCO3 administration might enhance tubular K+ entry in ascending loop of Henle resulting in a more positive luminal voltage which enhances tubular Ca and Mg reabsorption
- Failure of NaHCO3 to reduce urinary Ca excretion could be a consequence of natriuresis
- Both NaHCO3 and KHCO3 administration resulted in more positive Na or K balances and a more negative acid balance (this is why one may consideration of the Alka seltzer Gold )
- Alka Seltzer Gold Ingredients
- Anhydrous citric acid 1000mg
- Antacid-Potassium bicarbonate 344 mg
- Antacid-Sodium bicarbonate 1050 mg
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- Both NaHCO3 and KHCO3 administration likely resulted in deposition of the salts into the bones
- Metabolic acidosis, high protein diets and animal proteins result in increased urinary Ca excretion but ingesting a diet containing more vegetables and fruits or supplementing KHCO3 and less protein can enhance Ca retention and protect skeletal mass
- Lower dietary NaCl content would minimize urinary Ca excretion and protect bone
Take away points from the Beverly Hills Mastermind 6
- Normal pH in the body is between 7.35-7.45 but even the slightest change in pH (even in the normal range) can have a significant effect on your metabolism
- When the body is trying to keep an acid/alkaline balance there is an increase in protons. This increase in protons will go to the muscle and pull-out amino acids. The kidney then converts the amino acid into ammonia and excretes it. This process is the start of sarcopenia and proteolysis
- Increase in protons leads to mitochondria backing up and building up ROS and free radicals which leads to lipid peroxidation, carbonalyation of proteins and DNA damage which sets the cell up for senescence
- Low grade acidosis sends a message to your pituitary gland to force a release of cortisol. This is not a direct affect on the adrenal gland, this is indirect from the pituitary with ACTH release.
- NADPH production is increased in acidosis and works on 11 B-hydroxysteroid dehydrogenase-1 which causes cortisone to convert to cortisol
- NADPH needs to work with an antioxidant to prevent unfavorable changes in cellular redox
- Chronic acidosis leads to osteoporosis because the body is pulling out Ca and Mg from the bone to try to balance the low grade acidosis . Osteoclast are activated by NFK-B/RANKL which then sets off an inflammatory cascade.
- Citrate is metabolized into HCO3. The cell is trying to compensate the acidosis by keeping citrate in the cell. Under a stable Acid/Base state , Ca is excreted by the kidneys and citrate follows. Ca oxalate without citrate is less soluble resulting in formation of kidney stones
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Here is a great resource that goes discusses Potassium bicarbonate, but not sodium bicarbonate, reduces urinary calcium excretion and improves calcium balance in healthy men that is worth the read: Lemann, Jacob, Richard W. Gray, and Joan A. Pleuss. “Potassium Bicarbonate, but Not Sodium Bicarbonate, Reduces Urinary Calcium Excretion and Improves Calcium Balance in Healthy Men.” Kidney International 35, no. 2 (February 1989): 688–95. https://doi.org/10.1038/ki.1989.40.
Here is another great resource that discusses Potassium Bicarbonate Reduces Urinary Nitrogen Excretion in Postmenopausal Women: Frassetto, L, R Curtis Morris, and A Sebastian. “Potassium Bicarbonate Reduces Urinary Nitrogen Excretion in Postmenopausal Women” 82, no. 1 (1997): 6.
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