potassium bicarbonate to cure gout

[Charles Weber]

Potassium Bicarbonate to Ameliorate Gout

By Mr. Charles Weber
Corresponding Author Mr. Charles Weber
Self Employed, – United States of America
Submitting Author Mr. Charles Weber
Subject Category : NEPHROLOGY

Keywords : Gout, Potassium, Bicarbonate, Uric, Urate

How to cite the article: Weber C. Potassium Bicarbonate to Ameliorate Gout. WebmedCentral NEPHROLOGY 2013;4(4):WMC004217
doi: 10.9754/journal.wmc.2013.004217

Copyright: This is an open-access article distributed under the terms of the Creative Commons Attribution License(CC-BY), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
WebmedCentral Peer Reviewed: No
Submitted on: 24 Apr 2013 02:07:37 PM GMT
Published on: 25 Apr 2013 05:47:09 AM GMT
Abstract
It has been found that potassium bicarbonate supplements make the urine sufficiently alkaline that uric acid can be efficiently kept soluble and thus successfully excreted. This will prevent the destructive effects associated with gout. Some of the circumstances causing gout are discussed as well as some other ameliorators such as cherries, coffee, and orotic acid.
Introduction
One of the arthritic diseases is known as gouty arthritis in which sodium urate crystals are deposited in cartilage, especially in the feet. 90% of victims are men, perhaps because men are more likely to come in contact with lead, a kidney poison. The crystals are thought to be ingested by white blood cells and produce inflammation by rupture of the lysosome sacs and release of their contents [Turner]. Urate is the major end product of purine (nucleoproteins) degradation in higher primates in contrast to most other mammals because of the genetic silencing of hepatic oxidative enzyme uricase [from Wikipedia]. The kidney plays the dominant role in urate excretion, with the intestines accounting for about one third as much. The kidney excretes 70% of the daily urate production [Naohiko].. The medical profession currently almost exclusively uses chemical based medicines to cope with gout or palliatives.
Discussion
Lin has statistical evidence linking gout to lead poisoning [Lin 2002]. The lead poisoning makes the aldosterone system insensitive to potassium concentration and increases the potassium content of the blood plasma [Gonzalex]. The blood lead content is no indicator of toxicity and the status must be obtained with an EDTA mobilization test [Batuman]. Lead level in the body is significantly correlated with urate excretion and gout [Lin 2002]. Ethylenediaminetetraacetic acid chelator of lead has successfully increased uric acid excretion [Lin 2001]. Fluoride has been suggested to increase lead intake [Masters]. Other poisons than lead may move one a little closer to gout also, such as timalol (Blocadran) combined with hydrochlorothiazide and amiloride (a diuretic [Greenly]). I also suspect that toluol or some other chemical in acrylic automobile enamel may be able to trigger gout, from personal experience and I also suspect echinacea herb.
The initiating factor is probably usually lead poisoning though [Wright] [Batuman]. There is an association in peoples minds between gout and rich foods and lifestyle, probably because people with gout have trouble excreting nitrogen in a soluble form, which nitrogen is high in meat, and perhaps also because wine bottles and plumbing used to contain lead, which last were only available to affluent people in the distant past. Until such time as the matter is elucidated, it would be a good idea to stop eating lead, eat less proteins (especially purines), and not allow any potassium to be lost from one’s food at least if you have gout. It may be that proteins from low fat dairy products may not exaggerate gout.
POTASSIUM and GOUT
I have heard of a doctor who gave his patients potassium losing diuretics and thus triggered an attack of gout. By adding a potassium supplement he was able to remove the gout. A medical doctor respondent has used potassium supplements for years for gout [private communication]. Gout can be triggered by the same agents that cause potassium losses such as fasting, surgery, and potassium losing diuretics [Rodman]. A potassium deficiency can increase urate levels in the blood [Davis] so there is a circumstantial connection. Urate kidney stones form during gout in a 10-30% of cases [Colton]. Making the urine less acid with potassium citrate or sodium bicarbonate is a current treatment for kidney stones [Shekarriz] [Rodman]. Potassium citrate has been successfully used to eliminate urate stones and sodium bicarbonate did not prevent their formation [Pak]. I suspect that potassium bicarbonate or citrate would be preferable to potassium chloride. Potassium chloride added to a junk food diet should be equivalent to adding hydrochloric acid to a nutritious diet. I have rapidly removed gout symptoms by large potassium bicarbonate supplements several times. By rapidly I mean several days. 1000 milligrams per day should be enough for adults and will bring a junk food diet almost up to normal (3500 milligrams per day). If it is a diet as eaten by black people in Georgia [Grim], 2000 or more would be necessary. If the patient?s kidneys are damaged such as not retaining potassium well, more than the above may be necessary. Potassium bicarbonate may be obtained from organizations selling it as a wine additive. Research to determine this hypothesis would be very desirable.
Cherries have been shown to decrease urate in the urine of healthy women [Jacob], so they may have some therapeutic value. Some support to this possibility is that one half pound of cherries relieved the gout in 12 people [Blau]. It is possible that there is a substance in cherries that retards potassium excretion. There is some anecdotal evidence that celery and lettuce will relieve gout. If so, their high potassium content is probably what is involved. One would think that people with kidney failure that causes potassium retention would not have gout, but I know of no evidence for such a correlation.
OTHER FACTORS
Uric acid itself is not a factor in heart disease because uric acid does not correlate with mortality from heart disease when damage to the heart and kidneys is taken into account [Lazzeri]. Orotic acid has been recommended for gout since it decreases uric acid. A dosage of 4,000 mg of Orotic Acid ((Pyrimidinecarboxylic acid, also known as vitamin B13, Animal Galactose Factor, Oro, Orodin, Oropur, Orotonin, Oroturic, Orotyl or whey factor. Vitamin B13 is not really recognized as a vitamin. It is manufactured in the body by intestinal flora and is normally used for a maximum of six days in Gout patients. Orotic acid is not necessarily always good in excess since it is said to bind zinc to a non-biologically active state and can damage the liver, but I would think that the 50 to 100 milligrams that has been recommended for normal supplementation should be safe. Sources of oratate are whey, yogurt, beetroot, carrots, and jerusalem artichoke.
Drinking coffee but not tea has been found to lower uric acid in the serum so this effect is not likely to be from caffeine [Kiyohara] or the potassium.
Conclusions
Potassium bicarbonate dissolved in juice or sprinkled on food is a safe and effective way to ameliorate gout. Other substances that have evidence of ameliorating gout should be safe to use with potassium bicarbonate. They had better be because there is potassium in almost all food. However, until more research is performed, it would be wise not to use them on the same day or at least in the same meal. I am convinced that potassium bicarbonate should be used to cure gout and chemicals never should be and that this procedure would eliminate gout from our society.
References
1. Batuman V Maesaka JK Landy E Haddad B Wedeen P Tepper E 1981 The role of lead in gout nephropathy. New England Journal of Medicine 304; 520-3.
2. Blau LW. Cherry diet control for gout and arthritis. Tex Rep Biol Med 1950;8:309-11.
3. Colton RS Ward LE 1966 Uric acid gout and the kidney. The Medical Clinics of North America. 50(4); 1031-1042.
4. Davis WH 1970 Does potassium deficiency hold a clue to metabolic disorders associated with liability to heart disease?. South African Med. Journal 44; 1297.
5. Folis RH. Myocardial necroses in rats on a potassium low diet prevented by thiamine deficiency. Bulletin Johns Hopkins Hosp. 1942; 71: 235-241
6. Gonzalez JJ et al 1979 Renin aldosterone system and potassium levels in chronic lead intoxication. South Med. Journal 72; 433436.
7. Greenly L 2003 An overview of antihypertensive medications and assessing blood pressure using the latest guidelines. Journal of Chiropractic Medicine 2; 117-123.
8. Grim CE, Luft FC, Miller JZ, Meneely GR, Battarbee HD, Hames CG, Dahl LK 1980 Racial differences in blood pressure in Evans County, Georgia: relationship to sodium and potassium intake and plasma renin activity. J Chronic Dis. 33(2):87-94.
9. Jacob RA, Spinozzi GM, Simon VA, Kelley DS, Prior RL, Hess-Pierce B, Kader AA. 2003 Consumption of cherries lowers plasma urate in healthy women. J Nutr. 2003 Jun;133(6); 1826-9.
10. Kiohara C, et al 1999 Inverse association between coffee drinking and serum uric acid concentration in middle – aged Japanese males. British Medical Journal 82; 125-130.
11. Lin JL, Yu C.C, Lin-Tan D.T, Ho H.H. 2001 Lead chelation therapy and urate excretion in patients with chronic renal diseases and gout. Kidney Int. Jul;60(1):266-71.
12. Lin JL, Tan D.T, Ho H.H, Yu CC 2002 Environmental lead exposure and urate excretion in the general population. . Am J Med. 2002 Nov;113(7):563-8.
13. Lazzeri C. Valente S. Chlostri M. Picariello C. Gencini G.F. 2010 Uric acid in the early risk stratification of ST-elevation myocardial infarction. Internal and Emergency Medicine published online Jan. 15.
14. Masters R.D. and Coplan M. 1998 Water Treatment with Silicofluorides and enhanced lead uptake, Fluoride, Vol. 31, No. 3, Aug.
15. Naohiko Anzai, Atsushi Enomoto and Hitoshi Endou 2005 Renal Urate Handling: Clinical Relevance of Recent Advances. Current Rheumatology Reports 7; 227-234.
16. Pak C.Y Sakhaee K. Fuller C. 1986 Successful management of uric acid nephrolithiasis with potassium citrate. Clinical Investigation 30; 422-428. doi:10.1038/ki986.201.
17. Rodman J.S. 2002 Intermittent versus continuous alkaline therapy for uric acid stones and uretal stones of uncertain composition. Urology 60; 378-382.
18. Shekarriz B, Stoller M.L. 2002 Uric acid nephrolithiasis: current concepts and controversies. J Urol. 2002 Oct;168(4 Pt 1):1307-14.
19. Turner RA Counts G.B. Treadway W.J. Holt D.A. Agudelo C.A. 1981 Rheumatoid factor and monosodium urate crystal-neutrophil interactions in gouty inflammation. Inflammation 5; 353-361
20. Wright, L.F.; Saylor, R.P.; Ceere, F.A. 1984 Occult lead intoxication in patients with gout and kidney disease. Journal of Rheumatology. 11, no. 4; 517-520.
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[Keith Taylor]

GoutPal readers should note that, though this view of potassium bicarbonate for gout has been presented as scientific research, it has not actually been reviewed according to the original source.

I’m far from convinced that adding potassium bicarbonate is an effective gout cure. If you have potassium imbalance, it is through bad diet, or through other illness, as well as diuretics in some circumstances, as described above.

In the case of illness, the you need treatment for that illness. Illnesses likely to lead to potassium shortage include prolonged diarrhea, prolonged vomiting, and hormone problems such as over-production of aldosterone by the adrenal glands.

In the case of diet, you can improve potassium intake from my High Potassium Foods List at Foodary. Note that the key to potassium management is to get the right balance of sodium and potassium. That list at Foodary is part of a series of articles about alkaline diets. Diets that alkalize the body will help gout sufferers, by making uric acid more soluble. I have more information at Alkalizing Gout Diet Menu .

Note that dietary improvements can help gout, but they might not be enough. You must always get uric acid tested at least once per year, and ensure it never rises above 5mg/dL

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