# Do GLP-1 Drugs Cause Gout? The Study Everyone Cites Cannot Say | This GLP

Do GLP-1 drugs cause gout? A 295,907-person comparison, a randomized urate analysis in 2,539 adults, and why an active-comparator design cannot answer it.

Publisher: This GLP Editorial Team
Canonical: https://thisglp.com/research/do-glp1-drugs-cause-gout
Updated: 2026-09-17
Published: 2026-09-16

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Evidence

# Do GLP-1 Drugs Cause Gout? The Study Everyone Cites Cannot Say

A 295,907-person comparison put gout at 7.8 events per 1,000 person-years on a GLP-1 against 4.9 on an SGLT2 inhibitor. Both arms were treated, so neither rate has a baseline to sit against.

[This GLP Editorial Team](https://thisglp.com/about)September 20269 min readUpdated September 2026

Gout, events per 1,000 person-years · SGLT2 inhibitor · 4.9 · GLP-1 agonist · 7.8 · no treatment · not in the study · Without the third bar, neither rate can be called high or low.

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Nobody has run the study that could answer that. The comparison everyone cites followed 295,907 adults with type 2 diabetes and found gout at 7.8 events per 1,000 person-years on a GLP-1 drug against 4.9 on an SGLT2 inhibitor [\[1\]](https://thisglp.com/research/do-glp1-drugs-cause-gout#ref-1). Both arms were taking something, so the study establishes a difference between two treated rates and nothing about where either one sits against no treatment. Meanwhile the thing that produces gout moved the other way: across 2,539 adults in SURMOUNT-1, serum uric acid fell up to 0.95 mg/dL on tirzepatide against 0.18 on placebo [\[2\]](https://thisglp.com/research/do-glp1-drugs-cause-gout#ref-2).

## Key takeaways

-   In 295,907 adults with type 2 diabetes, gout occurred at 4.9 events per 1,000 person-years on SGLT2 inhibitors and 7.8 on GLP-1 agonists.
-   The hazard ratio was 0.64 (95% CI 0.57 to 0.72) in favor of the SGLT2 inhibitor, with a rate difference of 2.9 events per 1,000 person-years.
-   The study's conclusion is about SGLT2 inhibitors possibly reducing gout risk. It is routinely cited as though it showed GLP-1 drugs raising it.
-   ⛔ There was no untreated comparison group, so the study cannot say whether the GLP-1 rate is high, normal or low.
-   In SURMOUNT-1, serum uric acid fell 0.69 to 0.95 mg/dL on tirzepatide against 0.18 on placebo, with 72.7% of that attributed to weight loss.
-   That analysis counted no gout flares, no new diagnoses and no urate-lowering prescriptions.

A study comparing two drugs produces one number and two possible readings, and only one of them is supported. This is a clean example, and it is worth working through because the misreading circulates. A reader who has heard that these drugs raise gout risk has probably met this study wearing the wrong label, the same way a composite gets over-heard in [what a composite endpoint hides](https://thisglp.com/research/tirzepatide-heart-failure-composite).

## What was compared

Researchers identified 295,907 adults with type 2 diabetes newly prescribed either an SGLT2 inhibitor or a GLP-1 receptor agonist. Gout occurred at 4.9 events per 1,000 person-years in the SGLT2 group and 7.8 in the GLP-1 group. That is a hazard ratio of 0.64 (95% CI 0.57 to 0.72) and a rate difference of 2.9 events per 1,000 person-years (95% CI 2.1 to 3.6).

The authors’ conclusion is that SGLT2 inhibitors may reduce the risk of gout, and they say further studies are needed to confirm it. SGLT2 inhibitors have a known mechanism for this: they increase urinary excretion of uric acid, which is what causes gout.

The bar that is missing

⛔ Everyone in the study was taking something. There is no arm of comparable patients taking neither drug, which means the study establishes the difference between two rates and nothing about where either sits.

If the untreated rate were 8 per 1,000 person-years, the GLP-1 result would be unremarkable and the SGLT2 result protective. If it were 5, the reading would change entirely. The study does not contain the information to choose between those, and neither does this page.

## What happened to uric acid itself

The mechanism runs through urate, and that has been measured inside a randomized trial. A post hoc analysis of SURMOUNT-1 tracked serum uric acid in 2,539 adults with obesity or overweight across 72 weeks [\[2\]](https://thisglp.com/research/do-glp1-drugs-cause-gout#ref-2). It fell by 0.69, 0.92 and 0.95 mg/dL on the 5, 10 and 15 mg tirzepatide doses, against 0.18 mg/dL on placebo, all at P < .001.

A mediation analysis attributed 72.7% of that reduction to weight loss, leaving roughly a quarter attributed to something else about the drug. The fall did not differ by baseline uric acid quartile (P = .610) or by baseline BMI (P = .362), which is unusual in this literature. The full reading, including why a mediation split is a model output rather than a measurement, is in [the SURMOUNT-1 urate analysis](https://thisglp.com/research/uric-acid-fell-and-most-of-it-was-weight).

Uric acid is a blood test. Gout is an attack.

That analysis measured a laboratory value. It reports no gout flares, no new gout diagnoses and no change in urate-lowering prescriptions, because those were not among the outcomes. Lowering serum urate is how gout treatment works, so the direction is encouraging — but a 0.95 mg/dL drop is not a count of attacks avoided.

## The same design problem, in a second condition

Kidney stones were compared the same way and produced the same trap. A new-user study matched 358,203 pairs starting an SGLT2 inhibitor or a GLP-1 receptor agonist and followed them a median of 192 days [\[3\]](https://thisglp.com/research/do-glp1-drugs-cause-gout#ref-3). Nephrolithiasis occurred at 14.9 events per 1,000 person-years in the SGLT2 arm against 21.3 in the GLP-1 arm, a hazard ratio of 0.69 (95% CI 0.67 to 0.72).

That is again a study about SGLT2 inhibitors, with the GLP-1 arm as the thing they were measured against. It cannot say whether a GLP-1 raises the stone rate above no treatment at all, because no untreated group was followed. The same reading is set out in [the kidney stone comparison](https://thisglp.com/research/do-glp1-drugs-cause-kidney-stones).

## Why the misreading is easy

Because an active-comparator design is a good way to answer a clinical question — which of two drugs should this patient take — and a bad way to answer a safety question about either one alone. The output is a ratio, ratios have a numerator and a denominator, and a reader who cares about the denominator will read the ratio as being about it.

The same structure appears throughout this literature. A result reported against another drug, or against people who were prescribed nothing for reasons nobody recorded, is answering a narrower question than its sentence suggests. That thread runs through [what the semaglutide trials are worth](https://thisglp.com/research/semaglutide-cochrane-review) and [the suicidal ideation cohorts](https://thisglp.com/research/glp1-and-suicidal-ideation).

## What this does and does not change

If you have gout and type 2 diabetes and a choice between these two classes, the first study is directly relevant and points one way. If you have gout and are considering a GLP-1 drug for weight, it tells you almost nothing, because the population is different and the comparison you care about is absent. Your urate is likely to fall, which is the direction gout treatment aims for, and the trial that would count flares rather than measure blood has not been done.

That is worth knowing before a seller’s page cites a study at you. Most storefronts tracked here publish no evidence summary at all, and the ones that do rarely name the comparator. It is a gap in the same family as the ones counted in [what sellers will not tell you](https://thisglp.com/research/what-glp1-sellers-do-not-publish) and [what happens outside a trial](https://thisglp.com/research/glp1-weight-loss-in-ordinary-care).

## Frequently asked

Do GLP-1 drugs cause gout?

No study has tested that. The comparison usually cited found 7.8 gout events per 1,000 person-years on a GLP-1 against 4.9 on an SGLT2 inhibitor, with no untreated arm to say whether either rate is high or normal.

What does the study actually show?

That SGLT2 inhibitors came with fewer gout events than GLP-1 drugs in people with type 2 diabetes. The authors' own conclusion is about SGLT2 inhibitors possibly reducing risk.

Do these drugs lower uric acid?

In SURMOUNT-1, serum uric acid fell 0.69 to 0.95 mg/dL on tirzepatide against 0.18 mg/dL on placebo over 72 weeks. A mediation analysis attributed 72.7% of that to weight loss.

Does lower uric acid mean fewer gout attacks?

That analysis counted none. It reports no flares, no new diagnoses and no change in urate-lowering prescriptions, because those outcomes were not measured.

Does the same problem affect the kidney stone comparison?

It does. A 358,203-pair study found 21.3 stone events per 1,000 person-years on a GLP-1 against 14.9 on an SGLT2 inhibitor, again with no untreated group followed.

## Sources

1.  \[1\] Fralick M, et al. (2020). Assessing the Risk for Gout With Sodium-Glucose Cotransporter-2 Inhibitors in Patients With Type 2 Diabetes: A Population-Based Cohort Study Annals of Internal Medicine. [PMID 31931526](https://pubmed.ncbi.nlm.nih.gov/31931526/)
2.  \[2\] Sattar N, Scilletta S, Stefanski A, Wang H, Daly JW, Linetzky B (2026). Tirzepatide and change in uric acid and its association with weight reduction: post hoc analyses of the SURMOUNT-1 randomised placebo-controlled trial Annals of the Rheumatic Diseases. [PMID 41198460](https://pubmed.ncbi.nlm.nih.gov/41198460/)
3.  \[3\] Paik JM, et al. (2024). Sodium-Glucose Cotransporter 2 Inhibitors and Nephrolithiasis Risk in Patients With Type 2 Diabetes JAMA Internal Medicine. [PMID 38285598](https://pubmed.ncbi.nlm.nih.gov/38285598/)

## Where to get it

### Best GLP-1 injections

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