Gout treatment has recently changed, and I'm tired of seeing it mishandled in the clinic. It came into sharp focus for me again last week, when a patient's whole gout treatment plan was just completely wrong. So here's how to actually treat gout and prevent it — without the pain, and without following a restrictive diet.
Table of Contents
- What Actually Happens in Gout
- What Raises Uric Acid
- The Old Approach: Diet and Allopurinol
- What's Changed: GLP-1 Medications
- Why Starting Treatment Can Trigger an Attack
- How to Start Treatment Safely
- The Bottom Line
What Actually Happens in Gout
Gout happens when urate in the blood — also called uric acid — climbs past a level of about 0.36 mmol/L. Once you cross that point, urate crystals can start to form in the joints. The urate effectively moves out of the bloodstream and settles into the joint.
From there, it's almost like a bomb sitting in the joint. If something triggers inflammation, those crystals set off an intense inflammatory reaction — and that is a gout attack. So the whole game is about keeping urate low enough that the crystals never get the chance to form in the first place.
What Raises Uric Acid
The next question is what actually pushes uric acid levels up in the blood. Uric acid comes from the breakdown of purine. Everything we eat contains DNA, and purine is one of the building blocks of DNA. When that DNA is broken down, it releases a lot of purine, and that's what raises uric acid levels.
That's why certain foods are notorious for gout: they're especially high in purine. Organ meats and shellfish are classic examples, and even beer can push uric acid really, really high.
So one lever has always been obvious: eat less of the high-purine foods, and uric acid tends to come down. The problem, as we'll see, is that this lever doesn't work equally well for everyone.
The Old Approach: Diet and Allopurinol
Previously, doctors like me worked to a set target: get urate below roughly 0.36 mmol/L in the blood, because at that level we can prevent gout from happening. There were a couple of ways to get there.
The first was to put someone on a restrictive diet. For some patients that works well, but realistically it hasn't been that effective for a lot of people — because they don't want to give up their organ meats, their shellfish, or the occasional beer, and honestly, that's fine.
So instead we'd typically reach for a medication, most commonly allopurinol. Allopurinol tells the kidneys to pee out more uric acid, which lowers blood levels and reduces the chance of those crystals forming in the joints. For decades, that was the mainstay.
What's Changed: GLP-1 Medications
Here's where things have changed massively: the arrival of GLP-1 medications. If we can reduce the amount of food — and therefore purine — that a person is eating, we reduce the amount of uric acid in their blood.
The patient I saw the other week is a perfect example. They'd been on a GLP-1 medication for about a year and were seeing great results, steadily losing weight. When I looked back through their blood work over that year, I could see their uric acid dropping, and dropping, and dropping.
That's obviously great — but their allopurinol dose hadn't changed at all. And that annoyed me. This might sound strange coming from a doctor, but I'm firmly of the view that less medicine is better: we should only put patients on drugs when they genuinely need them. This person's urate had fallen to around 0.12 mmol/L, which is very, very low, and they were still on 600 mg of allopurinol. Their urate dropped because they were eating less on the GLP-1 — which is wonderful — so what we should have done is reduce the allopurinol dose. We want the level just under 0.36, not way down at 0.12. Left as it was, we were simply overmedicating them.
So this is the real shift in gout management. Some patients still respond beautifully to a restrictive diet. But for the many who don't, GLP-1 therapies have started to supersede what we used to do with allopurinol, because the weight loss alone often brings urate down. If that's still not enough, allopurinol absolutely still has a role — but it's no longer the automatic first and only move.
Why Starting Treatment Can Trigger an Attack
Here's the critical point whenever you start these medications or make any change: initiating treatment can itself trigger a gout attack. Let me explain why.
If you already have urate crystals sitting in a joint, then lowering your blood uric acid pulls some of those crystals back out of the joint and into the bloodstream, where the kidneys can flush them away. During that process you get a big flux of urate moving across the joint membrane — and it's that movement across the membrane that can set off an attack.
It's the same mechanism going the other way. If you suddenly eat a lot of shellfish and beer, you drive uric acid from the bloodstream into the joint, and that movement across the joint membrane is what triggers the attack. So whether urate is rushing in or rushing out, it's the rapid shift that causes the problem.
How to Start Treatment Safely
Because of that, when we do need to start allopurinol, we start low — typically around 100 mg — and hold there for about four weeks. Just as important, we introduce an anti-inflammatory alongside it to reduce the chance of triggering an attack.
What I typically add in the clinic is low-dose colchicine, around 500 micrograms — a very low dose. The idea is that while the urate crystals are being pulled out of the joint, the colchicine is there as an anti-inflammatory to stop an acute attack from firing off. Then every four weeks we increase the allopurinol by roughly 100 mg at a time, until the blood level drops below that magic 0.36 mark.
And this is exactly where the GLP-1 picture matters again. When someone is losing significant weight and eating less on a GLP-1, their urate falls on its own — so we need to be actively adjusting the allopurinol dose down, rather than leaving them on a dose that's now far too high.
The Bottom Line
The reason I wanted to lay this out is that there's so much misinformation online about restrictive diets, with people still suffering painful gout attacks — and a lot of that is wholly unnecessary. We understand very well now how to treat gout and how to prevent it. One of the biggest changes to that playbook is the arrival of GLP-1 therapies, which let us support patients to keep living the way they want to while still keeping attacks at bay.
One disclaimer I should have made at the very start: yes, I'm a physician, but I'm not your physician. Before you make any change to your gout management — or anything else about your health plan — please discuss it with your own doctor.
