Does Sugar Cause Kidney Stones?

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The idea that sugar, especially fructose, increases your risk of forming kidney stones has been widely accepted. However, is there any proof that supports this claim?

Fructose is a naturally occurring sugar in fruits. But it’s also a component of table sugar (sucrose). So that means we actually use fructose in many ways in our foods every day.

Also, fructose is contained in many processed foods and beverages. For instance, high-fructose corn syrup (HFCS) is a common sweetener in colas, pastries, ice creams, canned goods like fruits, vegetables, soups, and meats.

FRUCTOSE CONSUMPTION

The average fructose consumption of Americans in the 1800s and early 1900s was just about 15 grams, primarily from consuming fruits and vegetables. However, we saw a rapid spike in fructose consumption when food processing rose in popularity.

Today, Americans take an average of 55 grams of fructose daily, with adolescents consuming as much as 73 grams. This increase appears to be related to the rise in metabolic disorders, obesity, diabetes, hypertension, and non-alcoholic fatty liver and kidney diseases. And it could be a risk factor for certain types of kidney stones.

A normal kidney can filter about 180 liters of blood per day. That means the kidneys in healthy individuals would ideally filter between 4 and 25 grams of fructose daily. Before and after meals, blood fructose concentrations typically range between 2mg/dL (0.11 millimolar) and 14mg/dL (0.77 millimolar).

Usually, a low to moderate fructose consumption (≤ 50g) would not be a problem for most people unless they have fructose malabsorption issues. But if consumption exceeds 100g per day, it may cause problems for some individuals. That includes impacting four urinary parameters:

• uric acid

• calcium

• oxalates

• urine pH

All of these are risk indicators for kidney stones.

HOW DOES FRUCTOSE INCREASE URIC ACID IN THE BODY?

Compared to other carbohydrates, fructose may increase the production of uric acid. When fructose is metabolized in the liver, it depletes phosphate stores and prevents a compound called adenosine triphosphate (ATP) from regenerating. This results in high levels of another compound called adenosine monophosphate (AMP). AMP is then converted to uric acid by an enzyme called xanthine oxidase.

Blood uric acid is considered normal when it ranges from 2.6 to 6.0 mg/dL for women and 3.5-7.0 mg/dL for men. Anything over these numbers can pose risks for many diseases. But note that values may differ a bit depending on the measurement used by your lab.

The amount of uric acid produced by fructose can vary depending on several factors, including metabolic differences.

A study of 33 males that were given 200g of fructose daily for two weeks, found an increase of 1.01mg/dL serum uric acid. This is already a significant rise given the normal ranges mentioned above. The subjects were healthy nonsmoking males without a history of fructose intolerance and other metabolic disorders.

Nevertheless, high uric acid levels alone don’t necessarily increase uric acid stone risk unless urine pH is low (<5.5).

FRUCTOSE CONSUMPTION MAY LEAD TO LOW URINE PH

The magic ingredient for uric acid kidney stones is low urine pH (<5.5). Without low urine pH, uric acid stones will not form.

The bad news is excessive fructose consumption leads to acidic urine.

In the same study above, involving 33 men, urine pH went down by 0.26 to 0.61, from about 5.78 before the experiment to about 5.52 after two weeks of 200g daily fructose. These are striking numbers!

Too much fructose consumption (over 100g/day) may cause metabolic disorders, such as insulin resistance. The reason is that high uric acid levels may impair the body’s insulin-signaling mechanism. Also, fructose metabolism leads to fatty acid synthesis, which, in an excess manner, may interfere with insulin signaling.

Insulin resistance may cause proximal tubule (main reabsorption unit of the kidney) dysfunction. A direct result can be a decrease in ammonium ion excretion in the urine. Ammonium ions are essential for maintaining acid-base balance in the body. In turn, this leads to an increased acid load and results in a low urine pH. This condition is known as tubular acidosis.

FRUCTOSE CONSUMPTION INCREASES URINARY CALCIUM

The truth is, the direct mechanism of how fructose intake increases urinary calcium is unknown. And so, it is quite unreliable to believe this claim. Some studies tried to correlate fructose consumption to reduced calcium absorption in the nephron (basic functional part of the kidney), but no conclusive evidence can prove this.

But suppose high fructose intake really increases calcium in the urine. It is important to know that high calcium levels alone don’t mean you’ll end up with nasty calcium-based stones. For example, calcium-oxalate stones form when calcium and oxalates bind. So if you already kicked oxalates out of your diet, nothing will bind with calcium, so no stones will form.

CAN FRUCTOSE INTAKE INCREASE OXALATE PRODUCTION?

Using cultured HepG2 cells (human liver cancer cell line) in one study showed that prolonged exposure to high levels of fructose caused more oxalate production. This is compared to prolonged exposure to glucose. However, the difference in amounts is insignificant.

Both glucose and fructose produce an acid called glyoxylate, a precursor for oxalate synthesis. However, less oxalates are synthesized from glucose because fructose is metabolized more efficiently in the liver.

The enzyme fructokinase convert a small portion of fructose to an acid called glycolate, which will be further broken down to, glyoxylate, then to oxalate through a complex process in the liver.

However, no known pathway would give a significant conversion of fructose to oxalates. Nor is there proof that fructose will significantly increase oxalate levels.

CONCLUSION

High fructose intake (>100g daily) may cause an increased stone risk for some individuals since it increases uric acid in the body and lowers urine pH. These two are a perfect match for uric acid stones. Regarding calcium and oxalates, no significant evidence directly links these two to fructose.

But a low to moderate fructose consumption up to 50g should be fine for the general population. That would mean eating 9-10 small bananas (less than 6 inches long) or five medium-sized apples (about 182 grams). Nevertheless, fruits differ in fructose, so it is better to check with your dietitian or an app.

Check out our Coaching Program to create the best diet plan and make sure that you are not putting yourself at risk of kidney stones in any way.

References

1. Fructose Ingestion: Dose-Dependent Responses in Health Research
2. Fructose increases risk for kidney stones: potential role in metabolic syndrome and heat stress
3. The Epidemiology of Uric Acid and Fructose
4. Is it time to revise the normal range of serum uric acid levels?
5. Renal Tubular Handling of Glucose and Fructose in Health and Disease