Can Antacids Increase Uric Acid? The Connection for Your Nutrition Diet

October 10, 2025 •

4 min read

According to a 2018 study published in Biomedicine & Pharmacotherapy, certain acid-inhibitory drugs, commonly known as antacids, were shown to cause a transient but significant elevation in serum uric acid levels. For individuals already managing their diet for conditions like hyperuricemia, understanding the direct impact of these common over-the-counter medications is crucial. This article answers the question: Can antacids increase uric acid?

Quick Summary

Some acid-inhibiting medications, including certain H2 blockers, can cause a temporary rise in serum uric acid by affecting the body's ATP metabolism. This can pose a risk for individuals with pre-existing hyperuricemia or gout.

Key Points

Antacids Can Elevate Uric Acid: Certain antacid types, particularly H2 blockers and PPIs, have been shown to cause a transient increase in serum uric acid levels by affecting the body's ATP metabolism.
Risk for Hyperuricemia/Gout Patients: The effect of antacids on uric acid levels is most concerning for individuals with pre-existing hyperuricemia or gout, as it can potentially trigger a gout flare.
Mechanism Involves ATP Turnover: Antacids can slow the ATP turnover rate, leading to an increase in adenosine metabolites, which are eventually converted to uric acid.
Long-Term Aerobic Exercise Helps: The same research indicating antacids' effect also found that long-term aerobic exercise helps lower serum uric acid by accelerating ATP turnover.
Not All Antacids Are the Same: Traditional antacids containing calcium, magnesium, or aluminum can pose different risks, such as electrolyte imbalance for those with kidney disease, and high doses can interfere with certain gout medications.
Consult a Doctor: Patients with a history of gout should consult their healthcare provider about their antacid use and consider alternatives or dietary management strategies.

Understanding Uric Acid and Its Regulation

Uric acid is a waste product formed from the breakdown of purines, chemical compounds found in many foods and also produced naturally by the body. Normally, the body regulates uric acid levels by excreting it through the kidneys and urine. When the body produces too much uric acid or fails to excrete it efficiently, it can lead to a condition called hyperuricemia. High levels of uric acid are the primary risk factor for developing gout, a painful form of inflammatory arthritis. The painful gout flares are caused by the formation of uric acid crystals in the joints.

For many years, the primary focus for controlling uric acid has been dietary management and specific urate-lowering medications. However, emerging research has shed light on other factors, including the potential side effects of common medications like antacids.

The Surprising Link Between Antacids and Uric Acid

A pivotal 2018 study revealed a direct link between the administration of certain antacids and an increase in serum uric acid levels. Researchers found that acid-inhibitory drugs significantly increased serum uric acid levels in patients with pre-existing hyperuricemia. While the increase was transient and might not be clinically significant for a healthy individual, it was notable enough to trigger gout flares in susceptible patients.

The Mechanism: Impact on ATP Metabolism

So how exactly do antacids raise uric acid? The study points to an impact on adenosine triphosphate (ATP) turnover. Here's a breakdown of the biochemical mechanism:

ATP Turnover: ATP is the primary energy currency of the cell. Its turnover rate affects the concentration of its breakdown products. One of these products, adenosine, is further metabolized into hypoxanthine and then, ultimately, uric acid.
Slower Turnover: The 2018 study discovered that antacids slow down the ATP turnover rate.
Uric Acid Elevation: By slowing the ATP turnover, antacids cause an increase in serum ATP, adenosine, and hypoxanthine, which subsequently leads to a rise in serum uric acid.

This finding is crucial because it identifies a metabolic pathway by which these seemingly harmless medications can affect uric acid balance, especially in those with already compromised metabolic function. This is distinct from interactions with urate-lowering drugs like lesinurad, where high doses of antacids have been shown to reduce the drug's effectiveness.

Which Antacids Are Involved?

The 2018 study focused on certain acid-inhibitory drugs, including H2 blockers like ranitidine and PPIs like famotidine and omeprazole. It's important to differentiate these from traditional calcium carbonate (e.g., Tums) or magnesium/aluminum hydroxide-based antacids (e.g., Maalox), which can also pose risks for those with kidney issues but operate via different mechanisms related to electrolyte balance. The specific impact of newer antacids on ATP turnover is less understood and requires more research.

Comparison Table: Antacid Types and Uric Acid Effects


Antacid Type	Common Examples	Primary Mechanism	Effect on Uric Acid	Considerations for High Uric Acid/Gout
H2 Blockers	Ranitidine, Famotidine	Blocks histamine receptors to reduce stomach acid production.	Associated with transient uric acid elevation by affecting ATP metabolism.	Potential risk for gout flares in predisposed individuals, especially with chronic use.
Proton Pump Inhibitors (PPIs)	Omeprazole, Esomeprazole	Blocks the enzyme responsible for the final step of acid production.	Cited in the 2018 study as acid-inhibitory drugs that increase uric acid.	Exercise caution, especially for those with existing hyperuricemia.
Calcium-Based	Calcium Carbonate (Tums)	Neutralizes stomach acid directly.	High doses can potentially interact with urate-lowering drugs like lesinurad.	Long-term excessive use can lead to hypercalcemia and kidney issues, but direct link to uric acid increase is less prominent.
Aluminum/Magnesium-Based	Maalox, Mylanta	Neutralizes stomach acid directly.	High doses can potentially interact with urate-lowering drugs like lesinurad.	Avoid in cases of severe renal impairment due to risk of aluminum or magnesium toxicity.

Managing Your Diet and Medications for Gout Risk

When considering your nutrition diet and medication use, especially if you have hyperuricemia or gout, a holistic approach is best. Here are some key steps:

Discuss Medications with Your Doctor: Always inform your healthcare provider about all medications and supplements you take, including over-the-counter antacids. They can help evaluate the risk versus benefit, especially if you have a history of gout.
Prioritize Dietary Management: A purine-controlled diet remains the cornerstone of uric acid management. This involves limiting red meat, seafood, and alcohol while focusing on fruits, vegetables, and whole grains.
Consider Alternatives to Antacids: For chronic acid reflux, discuss alternative management strategies with your doctor, such as dietary modifications, lifestyle changes, or different medications that don't carry this specific uric acid risk.
Stay Active: The 2018 study also highlighted the benefits of long-term aerobic exercise, which was found to help reduce serum uric acid levels by accelerating the ATP turnover rate. This is a natural and effective way to help balance uric acid production.

Conclusion

The answer to the question, can antacids increase uric acid?, is a qualified "yes." While the effect is typically transient, certain acid-inhibitory drugs like H2 blockers and PPIs have been shown to elevate serum uric acid by slowing down ATP metabolism. This is particularly concerning for individuals with pre-existing hyperuricemia or a history of gout, where even a temporary increase could trigger a painful flare-up. Rather than discontinuing necessary medications, the key is awareness, communication with a healthcare professional, and integrating smart dietary and lifestyle choices to manage overall uric acid levels effectively. For those interested in the scientific details, the full study, "Antacids' side effect hyperuricaemia could be alleviated by long-term aerobic exercise via accelerating ATP turnover rate," is available on ScienceDirect(https://www.sciencedirect.com/science/article/abs/pii/S075333221736290X).

Frequently Asked Questions

Yes, for individuals with pre-existing hyperuricemia or gout, studies have shown that taking certain antacids can cause a transient spike in uric acid, which is enough to potentially trigger a gout attack.

The primary medications identified are H2 blockers like ranitidine and famotidine, as well as proton pump inhibitors (PPIs) such as omeprazole. The effect was specifically studied on these acid-inhibitory drugs.

You should first consult your doctor about potential antacid alternatives or dosages. Lifestyle changes, including a low-purine diet and regular aerobic exercise, can also help lower and manage overall uric acid levels.

No, the increase in serum uric acid levels from antacid use was found to be transient in the reported studies, returning to baseline levels after discontinuation. However, chronic use can maintain elevated levels.

While high doses of certain antacids (including those with calcium, magnesium, and aluminum) can affect the effectiveness of some urate-lowering drugs, they primarily cause issues related to electrolyte balance or toxicity for individuals with kidney disease, rather than elevating uric acid through the ATP mechanism.

Diet is a cornerstone of uric acid management, and a low-purine nutrition plan is highly effective. However, some people may have underlying metabolic issues or may require medication to control their uric acid levels, especially if they have gout.

Antacids were found to slow down the body's ATP turnover rate. This process leads to an accumulation of ATP metabolites, including hypoxanthine and uric acid, ultimately raising serum uric acid concentrations.