There are five types of kidney stones:
- Calcium phosphate stones are common and easily dissolve in urine acidified by Vitamin C.
- Calcium oxalate stones are also common but they do not dissolve in acid urine.
- Magnesium ammonium phosphate (struvite stones) are much less common, often appearing after an infection. They dissolve in vitamin C acidified urine.
- Uric acid stones result from a problem metabolizing purines (the chemical base of adenine, xanthine, theobromine [in chocolate] and uric acid). They may form in a condition such as gout.
- Cystine stones result from a hereditary inability to reabsorb cystine. Most children's stones are this type, and these are rare.
The Role of Vitamin C in Preventing and Dissolving Kidney Stones
The very common calcium phosphate stone can only exist in a urinary tract that is not acidic. Ascorbic acid (vitamin C's most common form) acidifies the urine, thereby dissolving phosphate stones and preventing their formation.
Acidic urine will also dissolve magnesium ammonium phosphate stones, which would otherwise require surgical removal. These are the same struvite stones associated with urinary tract infections. Both the infection and the stone are easily cured with vitamin C in large doses. BOTH are virtually 100% preventable with daily consumption of much-greater-than-RDA amounts of ascorbic acid. Think grams, not milligrams! A gorilla gets about 4,000 mg of vitamin C a day in its natural diet. The US RDA for humans is only 60 mg. Someone is wrong, and I don't think it's the gorillas.
The common calcium oxalate stone can form in an acidic urine whether one takes vitamin C or not. However, if a person gets adequate quantities of B-complex vitamins and magnesium, this type of stone does not form. Any common B-complex supplement twice daily, plus about 400 milligrams of magnesium, is usually adequate.
Ascorbate (the active ion in vitamin C) does increase the body's production of oxalate. Yet, in practice, vitamin C does not increase oxalate stone formation. Drs. Emanuel Cheraskin, Marshall Ringsdorf, Jr. and Emily Sisley explain in The Vitamin C Connection (1983) that acidic urine or slightly acidic urine reduces the UNION of calcium and oxalate, reducing the possibility of stones. "Vitamin C in the urine tends to bind calcium and decrease its free form. This means less chance of calcium's separating out as calcium oxalate (stones)." (page 213) Also, the diuretic effect of vitamin C reduces the static conditions necessary for stone formation in general. Fast moving rivers deposit little silt.
Furthermore, you can avoid excessive oxalates by not eating (much) rhubarb, spinach, or chocolate. If a doctor thinks that a person is especially prone to forming oxalate stones, that person should read the suggestions below before abandoning the benefits of vitamin C.
Ways for ANYONE to reduce the risk of kidney stones:
- Maximize fluid intake. Especially drink fruit and vegetable juices. Orange, grape and carrot juices are high in citrates which inhibit both a build up of uric acid and also stop calcium salts from forming. (Carper, J. "Orange Juice May Prevent Kidney Stones," Lancaster Intelligencer-Journal, Jan 5, 1994)
- Control urine pH: acidic urine helps prevent urinary tract infections, dissolves both phosphate and struvite stones, and will not cause oxalate stones.
- Eat your veggies: studies have shown that dietary oxalate is generally not a significant factor in stone formation. I would go easy on rhubarb and spinach, however.
- Most kidney stones are compounds of calcium and most Americans are calcium deficient. Instead of lowering calcium intake, reduce excess dietary phosphorous by avoiding carbonated soft drinks, especially colas. Soft drinks contain excessive quantities of phosphorous as phosphoric acid. This is the same acid that has been used by dentists to etch tooth enamel before applying sealant.
- Take a magnesium supplement of AT LEAST the US RDA of 300-350 mg/day (more may be desirable in order to maintain an ideal 1:2 balance of magnesium to calcium)
- Be certain to take a good B-complex vitamin supplement daily, which contains pyridoxine (Vitamin B-6). B-6 deficiency produces kidney stones in experimental animals. Remember:
* B-6 deficiency is very common in humans
* B-1 (thiamine) deficiency also is associated with stones (Hagler and Herman, "Oxalate Metabolism, II" American Journal of Clinical Nutrition, 26:8, 882-889, August, 1973)
- Additionally, low calcium may itself CAUSE calcium stones (L. H. Smith, et al, "Medical Evaluation of Urolithiasis" Urological Clinics of North America 1:2, 241-260, June 1974)
- For uric acid/purine stones (gout), STOP EATING MEAT! Nutrition tables and textbooks indicate meats as the major dietary purine source. Naturopathic treatment adds juice fasts and eating sour cherries. Increased Vitamin C consumption helps by improving the urinary excretion of uric acid. (Cheraskin, et al, 1983).
- Persons with cystine stones (only 1% of all kidney stones) should follow a low methionine diet and use buffered C.
- Kidney stones are associated with high sugar intake, so eat less (or no) added sugar (J. A. Thom, et al "The Influence of Refined Carbohydrate on Urinary Calcium Excretion," British Journal of Urology, 50:7, 459-464, December, 1978)
- Infections can cause conditions that favor stone formation, such as overly concentrated urine (from fever sweating, vomiting or diarrhea). Practice good preventive health care, and it will pay you back with interest.
Cheraskin, Ringsdorf Jr., and Sisley: The Vitamin C Connection, Harper and Row, 1983
Pauling, Linus "Are Kidney Stones Associated with Vitamin C Intake?" Today's Living, September, 1981
Pauling, Linus "Crystals in the Kidney," Linus Pauling Institute Newsletter, 1:11, Spring, 1981
Pauling, Linus How to Live Longer and Feel Better, Freeman, 1986
Myth/Half-Truth: ascorbate causes kidney stones:The origins of this myth are not too obscure, but its persistence is a mystery. There is no conclusive clinical evidence that high intake of ascorbate is firmly linked to oxalate kidney stones or to large increases in urinary oxalate spillage. For most people, there is simply no significant connection: M.P. Lamden & G.A. Chrystowski (Proc Soc Exp Biol Med, 85:1, 190-192, Jan 1954), K. Schmidt et al (Am J Clin Nutr 34:3, 305-311, March 1981), F. Erden et al (Acta Vitamin Enzym 7:1-2, 123-130, 1985) reported either insignificant or very low increases in urinary oxalate after taking ascorbate.
There have been scattered, sparsely-reported anecdotes of unusual stone-formers (e.g. M.H. Briggs et al, Med J Australia 2:1, 48-49, 7 July 1973) whose urinary oxalate increased unusually when taking large amounts of ascorbic acid, and a few other reports of known stone-formers whose urinary oxalate dropped when ascorbate was stopped (e.g. D.A. Roth et al J.A.M.A., 237:8, 768, 21 Feb 1977). But these patients had a history of stones before taking ascorbate, and the studies did not rule out contributions of common dietary sources of oxalate (coffee, tea, beans, spinach, oranges etc.). The tenor of most such studies seems alarmist, apparently aimed at creating panic over the “dangers” of ascorbate.
For the rare but unfortunate stone-formers out there, awareness of this biochemical peculiarity and consequent nutritional counseling by a competent practitioner should already be part of day-to-day living. Ascorbate advocates generally recommend that ascorbic acid be avoided, taking instead sodium ascorbate or other mineral-complexed ascorbate. In any case dietary ascorbate is not the biggest problem here.
Complicating matters is that the notion that high-oxalate excretors are necessarily stone-formers (and vice versa) is not borne out clinically, with inconsistencies and contradictions between hypothesis and observation.
On the one hand, there is zero clinical evidence showing that, with people who do not already have a kidney stone problem, ascorbate is even remotely associated with stone formation. On the other hand, soft water, low magnesium, excess sugar, chronic dehydration, and B1- and B6-vitamin deficiencies (L. Hagler et al, Am J Clin Nutr 26:6, 882-889, August 1973; also see Curhan 1999) definitely are associated with stones.
So maybe a lot of researchers have been barking up the wrong tree for way too long. Many people over many years have really wanted ascorbate to be the culprit here, but they just cannot prove a connection. All this obsessing over ascorbate and kidney stones is old news and should stop now. Time to move on.
Myth: ascorbate causes uric-acid urinary-tract stones and gout: This myth originated with dire speculations issued by H.B. Stein et al (Ann Internal Med 84:4, 385-388, Apr 1976), who grudgingly observed that blood uric acid levels did drop, with increased urinary excretion, after taking 4-8 gram doses of ascorbic acid. But then they warned—without evidence—that predisposed individuals could have problems with ascorbic acid-mobilized uric acid causing gout or renal calculi.
There is just no clinical evidence to support this alarmist myth. As with oxalate kidney stones, there are other dietary considerations, in this case an excess of purine-rich foods, sugars and alcohol, which are clinically far more relevant in uric-acid problems. Another ascorbate-hostile speculation down in flames.
(BTW eating a good quantity of cherries is a widely-known anecdotal but effective folk remedy for gout. Since cherries are not patentable, one does not suppose we’ll soon see any corporate research into cherries’ active anti-gout substances.)
For many years, experts have speculated that the intake of large amounts of vitamin C may contribute to the formation of oxalate-type kidney stones because of the metabolic conversion of vitamin C to oxalic acid. If the amount of oxalic acid in the urine increases as the dose of vitamin C increases, they reasoned, then a prolonged intake of large amounts of vitamin C may cause kidney stones. Some experimental evidence supports this concern. For instance, Dr. Constance Tsao, formerly with the Linus Pauling Institute of Science and Medicine, published two studies in the 1980s that investigated the relationship between vitamin C and oxalic acid. In one study, Dr. Tsao demonstrated that doses of 3-10 grams/day of vitamin C taken by ten subjects for 2-10 years did not result in abnormal levels of oxalic acid in the blood. In the other study, however, she showed that the ingestion of 10 grams/day of vitamin C by six subjects resulted in slightly elevated levels of oxalic acid in the urine, although the amount was within the range obtained by the consumption of normal diets. In contrast, a study with six subjects published in 1996 by Dr. Mark Levine and colleagues at the National Institutes of Health found that increasing the daily intake of vitamin C from 200 mg to 1,000 mg resulted in an increase in urinary oxalic acid of about 30%. Consequently, Dr. Levine suggested that the "upper safe doses of vitamin C are less than 1,000 mg daily in healthy people", although he noted that several earlier studies had not found any association between the incidence of kidney stones and the regular daily intake of 1,000 mg or more of vitamin C.
Dr. Carol Johnston of Arizona State University published an article in Nutrition Reviews in March in which she reviewed the scientific and medical evidence that might allow the establishment of an "upper intake level" for vitamin C. She examined the evidence on "rebound scurvy", kidney stones, hemolytic anemia in patients with glucose-6-phosphate dehydrogenase deficiency, enhanced iron absorption, pro-oxidant effects, and the destruction of vitamin B12. She noted that the experimental, clinical, and epidemiological evidence does not support a detrimental role for vitamin C in any of these conditions, although we still do not know the effect of large amounts of vitamin C in people with hemochromatosis, or iron-overload disease. Her analysis is in agreement with the many other reviews of the safety of supplemental vitamin C. Dr. Johnston concludes that "the available data indicate that very high intakes of vitamin C (2-4 g/day) are well tolerated biologically in healthy mammalian systems. Currently, strong scientific evidence to define and defend a UL [Tolerable Upper Intake Level] for vitamin C is not available." In other words, we cannot establish a threshold of toxicity for vitamin C.
To this evidence, we can add another recently published study by Dr. Gary Curhan and colleagues at Harvard, Brigham and Women’s Hospital, and Massachusetts General Hospital. For 14 years, Dr. Curhan et al. followed a group of 85,557 women with no prior history of kidney stones. Their intake of vitamin B6 and vitamin C was assessed and correlated with the development of stones. Daily intakes of 40 mg or more of vitamin B6 provided significant protection against the formation of stones, but there was no significant difference in stone formation between the groups with the lowest (less than 250 mg/day) and highest (1,500 mg/day or more) intake of vitamin C. In a previous study of a group of over 45,000 men followed for 6 years, the authors found a protective role for vitamin C but not for vitamin B6. They conclude, "...our findings for vitamin C, which have been consistent for women and men, do not support the practice of routine restriction of vitamin C to prevent kidney stones." Addressing previous experimental studies that associated vitamin C with increased urinary oxalate (the salt of oxalic acid), the authors point to another study from 1994, which showed that vitamin C is easily converted to oxalate during analytical procedures. Therefore, the increased amounts of oxalate observed in urine may have been artifactually produced and have no relation to what happens in the body.
The accumulated evidence demonstrates that vitamin C, even in large amounts, is a remarkably safe substance. This evidence strongly supports the role of vitamin C as an important antioxidant, not a pro-oxidant. While we know that the relatively small amount of 100-200 mg/day provides substantial protection against age-related diseases, including heart disease, cancer, and cataract, and that a still smaller amount prevents scurvy, we do not yet know the optimal amount of vitamin C (see "The Optimal Intake of Vitamin C" by Stephen Lawson, LPI Newsletter Spring/Summer 1997). Large doses of vitamin C have been shown to be of therapeutic benefit in promoting relaxation of the arteries (vasodilation), which benefits patients with heart disease and "coronary risk factors", such as diabetes, high serum cholesterol levels, and high serum homocysteine levels. Large doses of vitamin C are also useful in combating viral infections, preventing toxemia in pregnant women (possibly through vasodilation), and as an adjunct to the appropriate conventional treatment of cancer. There is also a tremendous amount of anecdotal evidence and some clinical evidence that vitamin C may be of benefit in treating other illnesses and conditions. The difficulty of determining the optimal intake of vitamin C is due to its many different functions in the body, biochemical individuality, and the impracticability of measuring the vitamin C content of various tissues and organs in healthy people in order to correlate those amounts with blood levels and optimal function.
Over twenty years ago, Linus Pauling proposed that the RDA for vitamin C should be increased to 200 mg/day. At about the same time, he mustered theoretical and experimental arguments to support his belief at that time that the optimal intake for humans is about 2 grams/day. While the merits of ingesting that much vitamin C or more each day are debatable, at least we can be confident that large doses are not harmful for healthy people and may be of therapeutic benefit in many cases. In particular, the concern about the role of vitamin C in kidney stone formation, a source of speculation for several decades, appears to be no longer justified.
He has some reassuring words for those who feel kidney stones are an automatic result of large doses of Vitamin C. He says in all cases a stasis of urine flow “and a concentrated urine appear to be the chief physiological factors.” Oxalic acid precipitates out of solution only from a neutral or alkaline solution—pH 7 to pH 10. Urine pH in those consuming ten grams of Vitamin C daily is about 6. Even in diabetics who take this large amount of C (10 grams), the urinary oxalate excretion remains relatively unchanged. “Vitamin C is an excellent diuretic. No urinary stasis; no urine concentration. The ascorbic acid/kidney stone story is a myth.” One more bon mot: “Methylene will dissolve calcium oxalate stones, if the patient is given 65 mg orally two to three times a day,” he learned from Medical World News (Smith, M.J.V., M.D.: Dec. 4, 1970).
(90% of all stones are calcium stones. Calcium is soluble in acid media. Vitamin C acidifies the urine. Acid urine discourages the growth of bacteria. Although uric acid stones are theoretically possible with high doses of C and a low urinary pH, none have been reported.)
A report in N.E.J.M. on 11 Feb, 1971 [Merton Lamden] suggested that large doses of C might cause diabetes in humans. The experiment was done in rats, but the dose translation in humans would have amounted to 5000 grams! [Paterson] Maybe there is a toxic dose. (Dr. Klenner at the time of that writing had been on 10 to 20 grams of C daily for eighteen years. No diabetes, and no kidney stones). This study has no relationship to the use of therapeutic doses of C.
Lamden found that an ingestion of 9 grams of C/day resulted in oxalate spills of 68 mg. in the urine per 24 hours. Controls without C spilled 64 mg./24 hours. Not a big difference.
Sherry Lewin wrote:It is known that some of the ingested ascorbate is metabolized to oxalate. (e.g. Lamden and Christokowski, 1954, 1971; Briggs et al., 1973), and that is mainly excreted in the urine.* It has been established that ingestion of ascorbate below 4 g daily results in average insignificant increase of oxalic acid excretion in the urine (Lamden and Christokowski, 1954). It has been inferred that the greater the quantity of oxalate excreted, the greater should be the probability of calcium calculi formation and consequently the use of mega vitamin C administration should result in detrimental effects. Further, only one case of a healthy individual developing a urinal stone after taking a short course of ascorbic acid treatment has been reported (Briggs, 1973).
However, Klenner (1971), Poser (1972) and Hoffer (1973) have concluded from their wide experience over many years of prescribing multigram daily doses of ascorbic acid - when they noted no patients who suffered calcium oxalate stone formation - that such hazards are very remote. Also Takiguchi et al. (1966) found no significant increase in urinary oxalate excretion on administration of up to 2 g daily of ascorbic acid for up to 6 months. Murphy and Zelman (1965) also concluded after 3 years of investigation that the hazard of oxalate calcuil form is not significant
Thus, the basic argument that an increase in oxalate excretion in the urine, resulting from mega intake of vitamin C, is likely to be accompanied by the formation of calcium oxalate stones is not valid; rather the reverse because of the accompanying increased acidity and increase ascorbate concentration in the urine.
(a) increased acidity: Multigram administration of ascorbic acid is often recommended (McDonald and Murphy, 1959; Murphy and Zelman, 1965) for increased acidity of the urine which effect enhances bacteriostacis. Such acidity is exponentially effective in reducing calcium oxalate precipitation. This precipitation requires that the solubility product of [Ca++][C2C4] be exceeded. Oxalic acid is a dibasic acid, and its ionization takes place in two stages. However for the sake of simplicity we can write
H2C2O4 == 2 H+ + C2O4—and therefore [C2O4—][H+]2 / [H2C2O4] = K
Hence, increase in [H+] (the pH usually drops by about 0.5 to 1 pH unites) should have an adverse effect to the second power on the [C2O4—], and correspondingly decreases the probability of calcium oxalate precipitation. Indeed, acid urine is known to solubilze calcium salts thereby reducing the hazard of stone formation (Hockaday and Smith, 1963).
(b) Diuresis.* Stone formation requires static conditions when the initial minute nuclei, capable of passing through the fairly porous membranes of the kidney tissue, grow to large sizes. Diuresis by increasing urine flow obviates the urolithiasis. Increasingly larger intakes of ascorbic acid are known to result in corresponding increases in diuresis; some physicians recommend as much as 10 g daily as a diuretic (e.g. Klenner, 1971). Increasing diuresis should therefore inhibit correspondingly the probability of stone formation.
( c ) Increased ascorbate concentration: This results in increased complexing of the Ca++ thereby decreasing the free Ca++. This decrease the probability of the solubility product of calcium oxalate being exceeded.
Hence increase ascorbic acid intake, although resulting in some increase in oxalic acid excretion in the urine, is hardly likely to increase the probability of the formation of calcium oxalate calcuil.
Sherry Lewin wrote:The warning that mega intake of vitamin C is likely to result in increased probability of formation of uric acid calculi has been voiced on several occasions. It is therefore necessary to examine the available data. Intravenous (or intramuscular) injection of 0.5 g of vitamin C on two successive days in several patients resulted in the average values of uric acid in 6-hour urine of the subjects rising from 111 to 260 mg dropping subsequently to 102 mg. The corresponding average values for uric acid in the blood were 3.9, 4.1, 4.3 and 3.8 mg% (Pena et al., 1963) (See also Pena et al., Nutritional Abstracts and Reviews, 1964). The pattern is therefore that of an increase of C. 10% uric acid concentration (following mega vitamin C administration*) together with a small increase in blood uric acid concentration; there are accompanied by approximately 1.5 times increase in the excretion of uric acid. Such a pattern suggest that any increase in vitamin C administration greatly potentates uric acid excretion to an extent significantly greater that that of its increased blood levels. Is id difficult to understand therefore how such data can reasonably be used to indicate increased probability of formation of uric acid calculi
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