The vitamin C–kidney stone controversy is another example of bias in scientific and medical research, as well as in media reporting. The media play an important role in communicating health information to the public at large, yet they often do so without taking responsibility for being accurate or presenting balanced facts. Various media platforms frequently raise expectations about the efficacy of pharmaceutical drugs while being negatively prejudiced toward nutritional supplements. This is not surprising, considering the media’s well-known financial dependence on pharmaceutical advertisers and the strong influence of the pharmaceutical industry on the medical profession. Many years ago, Dr. Marcia Angell, former editor-in-chief of the New England Journal of Medicine, even declared that it is “no longer a science journal.”

It is unfortunate that many doctors, having been trained to believe that vitamin C causes kidney stones, do not scrutinize this topic further. By advising their patients against vitamin C intake, they may inadvertently deprive them of the health benefits of this essential nutrient—without actually reducing their risk of kidney stones.

In this article, we evaluate in more detail the scientific evidence available on the vitamin C–kidney stone connection, including our own commentary on the topic, so that our readers can gain a better understanding of the nature of this controversy and make informed health decisions.

Closer look at the origins of perception linking vitamin C to kidney stones.
The controversy surrounding the risk of kidney stones associated with vitamin C intake has persisted for many decades. In a 1998 review article published in the Journal of the American Medical Association (JAMA), medical doctors Goodwin and Tangum scrutinized the scientific references cited in various research papers that claimed a causative link between vitamin C and kidney stones.

Among other sources, they examined a scientific review titled "The Toxic Effects of Water-Soluble Vitamins," published in Nutrition Reviews in 1984. This article supported the claim that vitamin C promotes kidney stones by citing seven references. But what were these references?

One of them was not a clinical study but a letter to the editor published in a medical journal The Lancet in 1973, which described a few case reports based on individual observations. Another reference was entirely unrelated to the topic and included in error. The remaining five references came from books, not from experimental data. Moreover, only two of those five books actually cited a reference to support the claim that high doses of vitamin C can cause kidney stones. Of those two, one referred to a chapter in another book, while the other relied on the 1973 letter to the editor.

This analysis illustrates that, upon closer examination, there was no solid scientific basis for the far-reaching conclusion that vitamin C intake causes kidney stones. Nevertheless, the claim found fertile ground in the media and was easily propagated.

Importance of Understanding What Are Kidney Stones

Kidney stones are crystals of mineral or organic origin that precipitate in the kidneys. They can range in size from the diameter of a grain of rice to the width of a golf ball. Kidney stones may remain in the kidneys or travel along the urinary track. During their passage, large or irregularly shaped crystals can cause significant pain.

Main Types of Kidneys Stones

1. Stones Made of Mineral Salts

• Calcium phosphate stones are quite common and can dissolve easily in acidified urine. Since ascorbic acid (vitamin C) can make urine more acidic, it helps dissolve existing phosphate stones and prevents their formation.
o Incidence: 24–30% in children, 8–18% in adults, and 75% in pregnant women.

• Magnesium ammonium phosphate (struvite) stones are less common and often develop after a urinary tract or kidney infection. They can grow very large and may damage the kidneys more than other types of stones. These stones also dissolve in urine acidified by vitamin C. Both the infections and the stones are largely preventable with daily consumption of vitamin C in amounts significantly higher than the Recommended Dietary Allowance (RDA).
o Incidence: 7–13% in children, 2–4% in adults. These stones are more common in women than in men.

2. Stones That Combine Mineral and Organic Molecules

• Calcium oxalate stones are composed of the organic molecule oxalic acid and the mineral calcium. These are the most common type of kidney stones, accounting for about 60% of all cases. They do not dissolve completely in acidic urine, while more alkaline urine promotes the formation of insoluble complexes between oxalic acid and minerals like calcium. This type of stone is more likely to form in individuals with chronic bowel inflammation or those who have undergone intestinal bypass surgery or stoma surgery.
o Incidence: 45–65% in children, 56–61% in adults.

3. Stones Made of Organic Molecules Only

• Uric acid stones result from issues in metabolizing chemical compounds called purines (adenine, xanthine, theobromine [found in chocolate], and uric acid). The risk increases in individuals with gout.
o Incidence: 2–4% in children, 9–17% in adults.

• Cystine stones are caused by a hereditary inability to reabsorb an amino acid - cystine. Cystine stones often appear in children, though they are rare overall.
o Incidence: 5–8% in children, 1% in adults.

How Common Are Kidney Stones?
Kidney stones are less prevalent than heart disease, cancer, or diabetes, but they still affect 5–10% of the population in various countries. Generally, people of white ethnicity are more prone to developing kidney stones than Black individuals, with men being more frequently affected than women.
In men, the incidence of kidney stones begins to rise in their 40s and continues to increase into their 70s. In women, the prevalence peaks in their 50s. However, kidney stone formation has become increasingly common among younger people. Today, about 13% of all male and nearly 20% of all female stone-formers experience their first stone before the age of 20—compared to just 4.7% and 4.0%, respectively, in 1975.
Pregnancy increases the risk of kidney stones, with a threefold higher likelihood of developing calcium phosphate stones compared to oxalate stones. Once a person has had more than one kidney stone, they are more likely to develop additional stones in the future.

A Closer Look at Calcium Oxalate Stones
Since stones made of calcium and oxalic acid are more common than other types of kidney stones, it is important to learn more about sources of oxalate in the body. Most oxalate in urine originates from our diet and metabolic processes occurring in our body, with only a small fraction coming from the metabolic conversion of vitamin C.

1. Dietary Oxalate

Oxalic acid is present in many common foods, including:
• Spinach: 100–200 mg of oxalate per 28 g
• Rhubarb: 570–1900 mg per 100 g
• Almonds: 122 mg per 3 g
• Beets: One cup provides 152 mg
• Wheat bran: 220 mg per 100 g

Tea and coffee are considered the largest sources of dietary oxalate for many people, providing up to 150–300 mg per day. Typically, daily oxalate intake for an adult can range from 80–150 mg, but in individuals who consume a typical Western diet it can vary from 44–1000 mg per day.
This is significantly more than the 20–30 mg of oxalate that would likely be generated from taking 1000 mg of vitamin C daily.
Early Interventions to Decrease Dietary Oxalate Absorption
Dietary oxalic acid is readily absorbed from the intestine into the bloodstream, with an estimated 2–15% of oxalic acid absorbed from different foods. One way to reduce the amount of oxalate entering the bloodstream and reaching the kidneys is to bind it in the intestinal tract with calcium. This process results in forming insoluble calcium oxalate crystals that are eliminated in the stool.
The preferred form of calcium for this purpose is calcium citrate, taken with meals. Calcium citrate not only binds oxalate but also inhibits its absorption in the intestinal tract.
Probiotics may also help reduce oxalate absorption by promoting its degradation in the intestine. In addition to Oxalobacter bacteria strain, Bifidobacterium lactis and Lactobacillus acidophilus have enzymes that degrade oxalates. Individuals with low levels of these bacteria are more susceptible to kidney stone formation.

2. Metabolic Oxalate Present in Blood and Urine
It is estimated that blood reaching the kidneys contains approximately 0.4–0.9 mg/dL of oxalate, derived from both dietary sources and our body metabolic processes.
Oxalate Formed in the Liver
The liver is the main site of oxalate production in the body. From there oxalate enters the bloodstream and is then excreted in the urine. Oxalate comes from the metabolic conversion of:

• Amino acids (e.g., glycine, hydroxyproline, tryptophan)
• Sugars (e.g., glucose, fructose, pentose sugars)
• Vitamin C
• Glyoxal (a breakdown product of carbohydrates, proteins, and fats)

Glyoxal can be further converted into glyoxylate, a direct precursor to oxalate (J. Knight, 2010). Notably, both glyoxal and oxalate synthesis are associated with oxidative stress.
Contribution of Vitamin C Metabolism to Oxalate Formation
Only a small portion (1–1.5%) of vitamin C in the body cells is converted into oxalate. In practice, it is unlikely that vitamin C significantly contributes to oxalate stone formation. Several factors support this:

• Vitamin C in urine tends to bind calcium, reducing calcium’s availability to bind with oxalate.
• Vitamin C acidifies urine, which also decreases calcium-oxalate binding.
• Its diuretic effect increases urine flow, reducing the stagnation necessary for stone formation. As the saying goes: “Fast-moving rivers deposit little silt.”

Oxalate Triggered by Infections
Some oxalate may be generated in individuals affected by fungal infections, such as those caused by Aspergillus species.

Types of Evidence Used in Evaluating the Risk of Kidney Stones from Vitamin C Intake

The connection between vitamin C and kidney stones remains inconclusive. There are no large, well-controlled studies directly demonstrating that regular intake of a specific amount of vitamin C leads to the development of kidney stones. Most evidence—both supporting and opposing such a connection—comes from retrospective epidemiological studies. These studies involve individuals monitored over long periods (several years). Vitamin C intake is typically assessed through self-reported questionnaires, submitted at various intervals (often every few years), which ask the individuals to recall lifestyle factors, dietary habits, supplement use, etc. Such methods are subject to bias and reporting errors.
Other studies provide indirect evidence, such as increased oxalate excretion in the urine of some individuals consuming vitamin C. However, this is not direct evidence of kidney stone formation.

1. Clinical Evidence Showing That Vitamin C Intake Is Not Linked to Kidney Stone Formation
• In the large Harvard Prospective Health Professionals Follow-Up Study (HPFS), which included 45,251 men, those with a vitamin C intake greater than 1,500 mg/day had a lower risk of kidney stones than those with the lowest intake (Curhan et al., 1996).
• A meta-analysis of results from the Nurses’ Health Study (NHS) and the HPFS found that vitamin C intake up to 1 g/day was not associated with kidney stones in women. However, in men, there was a 19% increased risk (Ferraro et al., 2016). These conclusions were based on food frequency questionnaires and did not account for the composition of the kidney stones. Additionally, the study in men had low statistical significance.
• Another large-scale prospective study involving 85,557 women followed over 14 years found no evidence that vitamin C increases the risk of kidney stones. There was no difference in the incidence of stones between those consuming less than 250 mg/day and those consuming 1.5 g/day or more. The authors of these large studies concluded that restricting higher doses of vitamin C due to concerns about kidney stones is unwarranted (Curhan et al., 1999; Curhan et al., 1996).
• Tsao and Salimi (Tsao et al., 1984) evaluated oxalate levels in urine samples in healthy individuals taking 10 g of vitamin C daily for at least two years. Of the six subjects, five showed no significant change in urinary oxalate excretion. One individual had an elevated level, but it was still within the normal range expected from a consuming typical diet.
• Gerster (Gerster, 1997) concluded that vitamin C does not contribute to the formation of oxalate-type kidney stones.

2. Studies Linking Vitamin C Intake to Kidney Stone Formation
• A prospective study in men, published in JAMA Internal Medicine in 2013, claimed that vitamin C supplements increased the risk of developing kidney stones. The study suggested that the stones were most likely of oxalate type, which could be formed from vitamin C metabolic conversion. However, it did not analyze the kidney stones of the participants directly. Instead, it relied on a separate study on kidney stones in which ascorbate was not tested.
This type of poorly structured study does little to help the medical profession or the public and instead contributes to confusion. The authors acknowledged that accurate information on vitamin C dosage was unavailable and that the results required confirmation through further research.
• Another study followed 23,355 Swedish men over a decade. Participants were divided into two groups: one that did not take any supplements (22,448 men) and a smaller group (907 men) that took vitamin C. While the average diet for each group was recorded, the details were limited. It appeared that the group taking vitamin C had a slightly higher risk of developing kidney stones. However, this additional risk was very low—147 cases per 100,000 person-years, or just 0.15% per year.
This was an observational study, not a randomized controlled trial in which vitamin C would be administered to a randomly selected group. Observational studies have inherent limitations that make their conclusions less reliable. Moreover, the correlation between vitamin C supplementation and kidney stones could not be accurately determined due to the lack of detailed information on the patient’s diet and the absence of chemical analysis of the stones, which could have helped identify their cause. Drawing firm conclusions from such a study is hardly a strong example of "evidence-based medicine."
• Massey’s study (Massey et al., 2005) included 29 stone formers and 19 non-stone formers who were supplemented with 2 grams of vitamin C. After five days on a low-oxalate diet, participants consumed 136 mg of oxalate, including 18 mg of oxalic acid, and remained on a low-oxalate diet for the rest of the day. At the end of the study, 12 stone formers and 7 non-stone formers showed more than a 10% increase in oxalate excretion following supplementation. Interestingly, seven of the individuals with increased oxalate levels were non-stone formers. The crucial question of why some people are prone to forming kidney stones while others are not, was notably overlooked.
The only clear finding from this study was that "the absorption of dietary oxalate" increased with a 2 g vitamin C supplement. While the authors were eager to suggest that vitamin C increases the risk of kidney stones, the study itself did not report a single case of kidney stone formation.
Ironically, in 1946, physician William McCormick used vitamin C to prevent and eliminate kidney stones, stating: "There is no evidence that vitamin C causes kidney stones. Indeed, in some cases, high doses may be curative" (McCormick, 1946).

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Practical Aspects in Preventing Kidney Stones
Kidney stones are an example of a multifactorial disease with no single factor defined as fully responsible for their formation. Even though a portion of oxalate in urine derives from metabolized vitamin C, this does not mean that vitamin C causes calcium oxalate kidney stones. It is important to state that vitamin C—an essential nutrient not produced by our bodies—is critical for health and survival, playing a key role in collagen formation, antioxidant defense, immune function, iron absorption, and many other biological processes.

1. Known Risk Factors for Kidney Stones That You Can Control
• Low fluid intake is inversely associated with the risk of kidney stones. Studies show a relative risk of 0.71 in men and 0.61–0.68 in women.
• A diet high in animal protein may increase the risk of uric acid kidney stones due to its association with increased urinary calcium and reduced urinary citrate. Although proteins in dairy food products increase calcium excretion, they promote excretion of citrate and reduce oxalate and uric acid in the urine.
• Foods rich in oxalate (e.g., spinach, rhubarb, nuts, and beets) can elevate oxalate levels in urine.
• Fructose consumption should be monitored. High-fructose syrups and sodas have been linked to increased risk of kidney stone formation, as fructose raises urinary excretion of calcium, oxalate, and uric acid, reduces magnesium, and alters acidity of urine (Johnson et al., 2018). Intravenous fructose infusion increased urinary oxalate excretion by 60% compared to glucose infusion (Nguyen et al., 1995). Individuals with metabolic syndrome or those exposed to heat stress may be especially affected by fructose. The association between fructose intake and kidney stone risk has also been confirmed in a meta-analysis of several prospective studies in men and women (Taylor et al., 2008).
• Inflammatory bowel disease (IBD), such as Crohn's disease, is associated with excessive urinary oxalate excretion and magnesium malabsorption. Kidney stones are also more common in patients who have undergone resection or bypass of the small bowel.
• Metabolic conditions can also contribute to stone formation. For example, hyperparathyroidism involves excessive secretion of parathyroid hormone (PTH), leading to elevated calcium levels in the blood and urine. Kidney-related conditions, such as medullary sponge kidney (present in 3–20% of stone formers), also increase risk.

2. What You Can Do to Decrease Your Risk of Kidney Stones
• Be aware and manage the controllable risk factors outlined above.
• Stay hydrated. Maintaining diluted urine is a key strategy in kidney stone prevention. High fluid intake is associated with a 40% reduction in recurrence risk.
• Choose beverages wisely. A study of 45,289 men aged 40–75 with no history of kidney stones followed for six years found:
o Coffee consumption reduced stone risk by 10%
o Tea by 14%
o Beer by 21%
o Wine by 39%
o However, the risk of stone formation increased by 35% for apple juice and 37% for grapefruit juice (Curhan et al., 1996)
• Ensure sufficient intake of essential nutrients
o Potassium promotes urinary citrate, which inhibits crystal formation.
o Magnesium, from foods like buckwheat, green vegetables, beans, and nuts, or from supplements, is also an inhibitor of urinary crystal formation. A daily intake of at least 300–400 mg is recommended (more may be needed to maintain 1:1 balance of magnesium to calcium). Well absorbable magnesium forms include citrate, chelate, malate, and chloride. Magnesium oxide is inexpensive but poorly absorbed (around 5%) and mainly acts as a laxative.
o Calcium binds with oxalate in the gut, reducing its absorption and preventing it from reaching the kidneys. Calcium citrate is preferred, as it also increases excretion of urinary citrate. Calcium supplements should be taken with meals.
o B-complex vitamins, especially B6, can be helpful in preventing kidney stones, particularly calcium oxalate stones, by reducing the amount of oxalate in the urine.
o Probiotics containing oxalate-degrading bacteria, such as Oxalobacter formigenes, may help patients with high oxalate levels. Studies have shown a 96% reduction in oxalate secretion with Oxalobacter supplementation (Hatch et al., 2006; Hoppe et al., 2005). A recent case-controlled study involving 58 patients and 29 controls also demonstrated a significant decrease in urinary oxalate with this probiotic (Tavasoli et al., 2020).
Note: Many antibiotics—including sulfonamides, ampicillin, amoxicillin, quinolones, furans, and pyridines—can destroy many types of beneficial bacteria including Oxalobacter formigenes.

REFERENCES
J. Knight et al. Metabolism of fructose to oxalate and glycolate, Hormone and Metabolic Research, 2010, 42, 868-873.
Curhan G.C. Willett W.C. Rimm E.B. Stampfer M.J. (1996) A prospective study of the intake of vitamins C and B6, and the risk of kidney stones in men, J Urology, 155(6), 1847-1851.
Ferraro PM, Curhan GC, Gambaro G, Taylor EN. Total, Dietary, and Supplemental Vitamin C Intake and Risk of Incident Kidney Stones. Am J Kidney Dis. 2016; 67(3):400-7. doi: 10.1053/j.ajkd.2015.09.005.
Curhan, G. C., Willett, W. C., Speizer, F. E., Stampfer, M. J. (1999) Megadose Vitamin C consumption does not cause kidney stones. Intake of vitamins B6 and C and the risk of kidney stones in women, J Am Soc Nephrol., Apr, 10, 4, 840-845.
Curhan G.C. Willett W.C. Rimm E.B. Stampfer M.J. (1996) A prospective study of the intake of vitamins C and B6, and the risk of kidney stones in men, J Urology, 155(6), 1847-1851.
Tsao CS, Salimi SL. Effect of large intake of ascorbic acid on urinary and plasma oxalic acid levels. Int J Vitam Nutr Res. 1984;54(2-3):245-9.
Gerster H, No contribution of ascorbic acid to renal calcium oxalate stones, Ann Nutr Metab. 1997;41(5):269-82. (http://orthomolecular.org/resources/omns/v01n07.shtml)
Massey LK, Liebman M, Kynast-Gales SA. Ascorbate increases human oxaluria and kidney stone risk. J Nutr. 2005;135(7):1673-7. doi: 10.1093/jn/135.7.1673.
McCormick W.J. (1946) Lithogenesis and hypovitaminosis, Medical Record, 159, 410-413.
Johnson RJ, Perez-Pozo SE, Lillo JL, Grases F, Schold JD, et al., Fructose increases risk for kidney stones: potential role in metabolic syndrome and heat stress. BMC Nephrol. 2018, 19(1):315. doi: 10.1186/s12882-018-1105-0.
Nguyen, N.U, Dumoulin, G, Henriet, M.T. Increase in urinary calcium and oxalate after fructose infusion, Horm Metab Res. 1995; 27:155-158
Taylor EN, Curhan GC. Fructose consumption and the risk of kidney stones. Kidney Int. 2008 Jan;73(2):207-12. doi: 10.1038/sj.ki.5002588.
Hatch M, Cornelius J, Allison M, Sidhu H, Peck A, Freel RW. Oxalobacter sp. reduces urinary oxalate excretion by promoting enteric oxalate secretion. Kidney Int. 2006; 69(4):691-8. doi: 10.1038/sj.ki.5000162.
Hoppe B, von Unruh G, Laube N, Hesse A, Sidhu H. Oxalate degrading bacteria: new treatment option for patients with primary and secondary hyperoxaluria? Urol Res. 2005; 33(5):372-5. doi: 10.1007/s00240-005-0497-z.
Tavasoli S, Alebouyeh M, Naji M, Shakiba Majd G, et al., Association of intestinal oxalate-degrading bacteria with recurrent calcium kidney stone formation and hyperoxaluria: a case-control study. BJU Int. 2020;125(1):133-143. doi: 10.1111/bju.14840.
Curhan GC, Willett WC, Rimm EB, Spiegelman D, Stampfer MJ. Prospective study of beverage use and the risk of kidney stones. Am J Epidemiol. 1996;143(3):240-7. doi: 10.1093/oxfordjournals.aje.a008734.

 

 Dr. Aleksandra Niedzwiecki