. Bicarbonate supplementation slows progression of CKD and improves nutritional status. J Am Soc Nephrol. 2009 Sep;20(9):2075-84. doi: 10.1681/ASN.2008111205. Epub 2009 Jul 16.
[PMID: 19608703] [PMCID: 2736774] [DOI: 10.1681/ASN.2008111205]
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Baking soda (also known as sodium bicarbonate or sodium hydrogen carbonate) taken with water has been used for shortness of breath, kidney immunopathologyA temporary increase in disease symptoms experienced by Marshall Protocol patients that results from the release of cytokines and endotoxins as disease-causing bacteria are killed., as well as many other intolerable or bothersome symptoms reported by members on the Marshall protocolA curative medical treatment for chronic inflammatory disease. Based on the Marshall Pathogenesis.. Not everyone can tolerate it but many have found it to be helpful. Be sure not to confuse baking powder with baking soda.
In one study it was found to slow progression of chronic kidney disease for those patients who could tolerate it.1) In this study, the patients were given very small doses (600 mg) of oral sodium bicarbonate tablets daily for two years. (600 mg is a just little over 1/2 a gram. A very small amount considering some athletes are reported as taking multiple grams prior to events.)
It is not dangerous, but it tastes appalling and can make you want to retch. It can make some people nauseous when it hits their stomach and a few suffer an upset stomach or diarrhoea when they take it.
Dr. Folland, Times Online
It was summer here when I determined that I really needed to drink 'Jigsaw water' everyday. I made and stored in the freezer a series of bottles with a very little bicarb in each, I did not know it was supposed to taste terrible, for me it had no taste until cold weather set in and I drank some at room temperature …ugh! Sallie Q
A daily dose of baking soda may help reduce the destructive inflammationThe complex biological response of vascular tissues to harmful stimuli such as pathogens or damaged cells. It is a protective attempt by the organism to remove the injurious stimuli as well as initiate the healing process for the tissue. of autoimmune diseases like rheumatoid arthritis, scientists say. 2)
They have some of the first evidence of how the cheap, over-the-counter antacid can encourage our spleen to promote instead an anti-inflammatory environment that could be therapeutic in the face of inflammatory disease.
Many members posting on the MP site have had kidney tests, particularly serum creatinine levels (with derived eGFRs), and been told they face kidney failure. The basis of this conclusion is the use of serum creatinine an indicator of kidney function. High values are assumed to indicate that the kidneys are not effectively performing their function of filtering unwanted compounds from the blood and so may be failing. This can be alarming to patient and medical professional alike because kidney disease is known to be progressive. Hence, chronic kidney disease or CKD. The first thing to note, for those on the MP, is that their kidneys are not as bad as the test results may suggest. Several factors contribute to this conclusion:
Creatinine is not an indicator of toxic uremic metabolites.
OlmesartanMedication taken regularly by patients on the Marshall Protocol for its ability to activate the Vitamin D Receptor. Also known by the trade name Benicar. raises creatinine by mechanisms independent of kidney function.
IP appears to raise creatinine, and certainly urea.
Olmesartan, and other ARBs, reversibly reduce kidney function by limiting the up- regulatory actions of angiotensin II.
It is sensible to assume that the last factor may be operating as an important contributor to high serum creatinine values because it implies that the kidneys are dependent on being spurred by angiotensinII. This leaves them open to progressive damage if left unprotected from the spur. It is well known that actions of Angiotensin II and the RAAS are major factors in progressive kidney damage in CKD. The best form of protection is high dose olmesartan as used in the MP..
It is also wise to make this assumption because olmesartan is known to affect serum electrolyte levels controlled through kidney function. Table 2, posted below from this publication, showed that olmesartan (sufficient to lower BP to <130/80 or to reduce proteinuria) significantly decreased GFR (measured as 24 hour creatinine clearance) and sodium re-absorption in patients with mild kidney disease (CKD1 or 2)
| <html>Baseline</html> | P Value | .A.R.B. | |
|---|---|---|---|
| SNa, mmol/l | 142 ± 2 | 0.3 | 142 ± 2 |
| GFR, ml/min | 82 ± 42 | 0.0006 | 68 ± 35 |
| Tubular Na load, mmol/day | 16,726 ± 8,604 | 0.0005 | 13,861 ± 7,169 |
| TNa, mmol/day | 16,619 ± 8,598 | 0.0005 | 13,744 ± 7,167 |
| UNaV, (mmol/day) | 82 ± 42 | 0.7 | 118 ± 36 |
table values are: means ± SD (n = 41). SNa, serum sodium concentration; GFR, glomerular filtration rate; TNa, tubular sodium reabsorption; UNaV, urinary sodium excretion rate.
The affect of olmesartan in suppressing tubular sodium re-absorption is a reason why MP members should, and can safely, maintain a high salt intake. With more severe kidney disease, effects extend to decreased acid and potassium excretion, leading to the possibilities of serum acidosis and hyperkalemia. These conditions should be watched for because they have potential for adverse effects: but are simply corrected..
Critical processes for serum electrolyte regulation occur in the distal region of nephrons under the influence of angiotensin II plus aldosterone . The latter is also dependent on angiotensin II for its secretion. So blocking angiotensin II will weaken these processes. Overall the mechanisms involved include :
With diminished kidney capacity in CKD and and further limitation by the blocking of angiotensin II these processes may become inadequate. The result is a tendency to serum acidosis and hyperkalemia. Production of ammonia in the proximal tubule of nephrons is also involved in the neutralisation of excreted acid. This provides an additional factor contributing towards a linkage between hyperkalemia and acidosis because high potassium inhibits the ammonia production, potentially initiating a vicious circle.
Most of the reports of hyperkalemia by MP members have shown accompanying acidosis. Acidosis is indicated by subnormal levels of serum bicarbonate, reported as CO2 by US pathology labs. Members reporting these conditions have found that the aberrant values can be moderated by
For one MP member a serum potassium test level of 6.5 mmol/L was down to 4.5 mmol/L within 6 days, with earlier symptomatic relief, using the following regime:
Immediately take 1/2 teaspoon of sodium bicarbonate (baking soda) sub-lingually (let it dissolve and disappear in your mouth). Then take 1/2 teaspoon (2g) of sodium bicarbonate (baking soda) and 1/2 tsp (3g) of sodium chloride (cooking salt) in 1.5 litres of drinking water daily for a few days. Then drop back to 1/4 tsp baking soda and 1/3 tsp salt. If you get an upset gut you may take the baking soda sub-lingually.
Patients are also using this to help with many different symptoms of immunopathology.
Several members have found that some variant of these regimes has been adequate to keep sodium, potassium and bicarbonate (CO2) tests within range. And for some to allow relaxation of strict avoidance of high potassium foods.
slows progression of CKD3)
A study making a comparison of treating metabolic acidosis in CKD stage 4 hypertensive kidney disease with fruits and vegetables or sodium bicarbonate showed similar positive results.5)
Current guidelines recommend Na(+)-based alkali for CKD with metabolic acidosis and plasma total CO2 (PTCO2) < 22 mM. Because diets in industrialized societies are typically acid-producing, we compared base-producing fruits and vegetables with oral NaHCO3 (HCO3) regarding the primary outcome of follow-up estimated GFR (eGFR) and secondary outcomes of improved metabolic acidosis and reduced urine indices of kidney injury.
One year of fruits and vegetables or NaHCO3 in individuals with stage 4 CKD yielded eGFR that was not different, was associated with higher-than-baseline PTCO2, and was associated with lower-than-baseline urine indices of kidney injury. The data indicate that fruits and vegetables improve metabolic acidosis and reduce kidney injury in stage 4 CKD without producing hyperkalemia.