I took a gout tablet every day for twenty-four years. One tablet. Every morning. So automatic I barely noticed I was doing it anymore. And then, in February 2024, I stopped.
Not dramatically. Not impulsively. I stopped because the data said something had shifted, and I wanted to find out whether the medication was still doing a job — or whether it had become a habit I’d inherited from a version of me that no longer existed.
What happened over the following eighteen months surprised me more than I expected. No attacks. No swelling. And one afternoon last summer, on day 24 of an extended fast, I looked at my big toe and noticed something I hadn’t seen in years. The uric acid crystal buildup — the lumpy, slightly swollen knuckle I’d accepted as permanent — was nearly gone. I put on a pair of Birkenstocks and walked four miles. Without flinching.
That’s what this post is about.
[Note to Neil: Add YouTube embed once video is published]
Twenty-Four Years on a Tablet That Wasn’t Actually Working
The first gout attack came in 1999. Mid-thirties. Big toe. I woke up at three in the morning convinced something had broken in the night. Couldn’t put weight on it. Couldn’t wear a shoe. Couldn’t walk to the bathroom without gripping the wall.
My GP sent me for bloods. Urate: elevated. “You’ve got gout,” she said. “We’ll start you on allopurinol.” And that was that. One tablet a day, for the next two and a half decades.
Here’s what I didn’t understand at the time — and this took an embarrassingly long time to figure out — the allopurinol wasn’t fixing anything. It was targeting one number: uric acid levels. Managing a symptom. The assumption was that lower uric acid meant fewer crystals, fewer attacks. That’s the theory. Except my uric acid levels were still outside the reference range for most of those twenty-four years, despite taking the tablet daily.
August 2014: 0.53 mmol/L. Outside range. On medication. October 2014: 0.51 mmol/L. Still outside. January 2015: 0.44 mmol/L. Slightly better, still elevated. March 2015: 0.46 mmol/L. Back up. Four tests across one year. All outside the reference range. All while taking a medication specifically designed to bring that number down.
By August 2020, the reading had climbed to 502 µmol/L. The notes flagged it as “above high reference limit — make an appointment to see the doctor.” Twenty years in. Still not controlled.
The question I wasn’t asking at any point during those two decades: why is my body producing too much uric acid in the first place? I was asking whether the tablet worked. I should have been asking what was driving the problem. Those are very different questions.
Boxing Day 2023 — and What Came Next
I’ve told the Boxing Day story before. Eighteen stone. Couldn’t get up the stairs without getting winded. Looked in the mirror and something snapped. Started fasting. Stopped eating ultra-processed food. Within two months the weight was moving and the energy was returning.
By February 2024 — roughly ten weeks after that decision — I stopped all my medications. Not on a whim. I’d been tracking my bloods closely and the data was moving in the right direction. I spoke to my GP. We reviewed the numbers together. And I stopped the allopurinol.
I want to be honest about what I was expecting: a gout attack, probably within a few weeks. Anyone who’s had gout knows what those attacks feel like. Not background ache. Not stiffness. White-hot, can’t-sleep, can’t-put-your-foot-down pain. I’d been through it dozens of times over twenty-four years. So I stopped the tablet, and I waited.
Summer 2024. First summer without allopurinol in nearly a quarter of a century. At a client dinner. A massive ribeye on the table — the kind of steak old Neil would have eyed nervously. Red meat and gout have always had a complicated relationship; high purine foods, your body converts purines to uric acid, that’s the received wisdom. I’d been cautious around red meat for years. That evening I ate the steak.
Went to bed waiting. Woke up the next morning: fine. Day two: fine. Day three: still fine. A week later: nothing. No attack. No swelling. No pain.
Then, around day 24 of an extended fast in summer 2025, I noticed the crystal buildup on my big toe knuckle had all but disappeared. A lumpy, slightly swollen joint I’d accepted as permanent — gone, or near enough gone that I had to look twice. That same afternoon I put on Birkenstocks that had been sitting in the cupboard for years — too much pressure on the joint before, not possible — and walked four miles. Without flinching.
Twenty-four years. And a change in how I was eating had done something that two decades of daily medication hadn’t managed.
What I Think Was Actually Going On
I want to be clear: this is my reading of my own N=1 data alongside some science I’ve looked into. Not a diagnosis. Not a prescription for anyone else. But it makes sense to me.
Professor Janet Lord at the University of Birmingham researches inflammation and ageing. She describes something called inflammaging — chronic low-level inflammation that grumbles along for years, running two to three times higher in older adults than in younger people. It’s quietly linked to heart disease, dementia, and metabolic dysfunction. The kind of thing that accumulates over decades without obvious symptoms.
Gout isn’t separate from that picture. Gout is an inflammatory condition. Your body produces excess uric acid, it forms crystals in the joints, those crystals trigger an inflammatory response, and the result is the attack you know about. The allopurinol was targeting the uric acid number. What it wasn’t touching was the systemic inflammation underneath — the environment in which the uric acid was being overproduced in the first place.
Professor Lord also discusses intermittent fasting and inflammation. She describes autophagy — the body’s cellular clean-up process, activated during fasting — as a kind of internal hoover, clearing out damaged cells and cellular debris. Her point: fasting stimulates that process and drops inflammation down.
That’s what I think happened in my case. Eighteen months of consistent fasting, switching away from ultra-processed food — those changes reduced the systemic inflammation that had been driving the problem. Not managing the number. Changing the environment that was producing the number.
The allopurinol was managing the symptom. The fasting and the food changes addressed the cause. And once the cause shifted, the body regulated itself. That’s a big claim for an N=1. I can’t say it would work for everyone. I’m not saying stop your medication — I’d never say that. What I’m saying is that in my case, after twenty-four years, the thing that actually shifted the problem wasn’t the tablet. It was changing the inputs that were driving the problem in the first place.
What to Do With This If It Sounds Familiar
If you’re already managing gout with medication and your urate readings are stubbornly outside the reference range despite taking it daily — that’s worth a conversation with your GP. Not about stopping the medication. About whether the underlying inflammation is being addressed. Ask specifically about insulin resistance. Ask about dietary changes. Ask what they’d expect to see if the root cause was being addressed, not just the number. The number matters. But the environment producing the number matters more.
If you’re earlier in the picture — morning joint stiffness, one gout attack and a “watch your diet and come back if it happens again,” elevated urate on your bloods but not yet on medication — that early window is worth paying attention to. Not to panic. To be curious.
Elevated urate is often a sign that something else is happening systemically: insulin resistance, diet-driven metabolic load, chronic low-level inflammation. That conversation is worth having before the first tablet, not after twenty-four years of them.
If I were starting this over, I’d have asked the question much sooner: why is this happening, not just how do I manage it? That’s not a criticism of the doctors I saw. They were doing what the system does — manage the number, keep the patient functional. But I wish I’d been more curious earlier.
🎯 Key Takeaways
- Managing a number isn’t the same as fixing a problem — Allopurinol targets uric acid levels; it doesn’t address the systemic inflammation that drives excess production in the first place
- The data was clear for over a decade — Four consecutive readings outside the reference range while on daily medication; the tablet wasn’t controlling the condition
- Fasting may reduce the inflammatory environment — Professor Janet Lord’s research links intermittent fasting and autophagy to reduced chronic inflammation; this matches what happened in my case
- N=1, not a prescription — What happened when I stopped medication is personal and documented; it is not a recommendation for anyone else to do the same
- Ask the earlier question — “Why is this happening?” is more useful than “how do I manage it?” — and it’s worth asking before twenty-four years pass
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🔽 Read the Video Transcript
I’d taken gout pills for twenty-four years. I couldn’t remember who I was without them.
I’m Neil. I spent two decades believing I’d always need medication, until one day I didn’t.
In the next eight minutes: why I decided to test stopping | what my GP said | what happened in the twelve months after. Let’s start with 1999.
- I was in my mid-thirties. First gout attack. Big toe. Woke up at three in the morning thinking something had broken in the night. Couldn’t put weight on it. Couldn’t wear a shoe. Couldn’t walk to the bathroom without gripping the wall.
GP sent me for bloods. Urate: elevated. “You’ve got gout,” she said. “We’ll start you on allopurinol.”
And that was that.
One tablet a day. Every day. For the next twenty-four years.
Here’s what I thought at the time: fair enough. Gout is gout. It’s a condition. You manage it. That’s what medication is for. I wasn’t questioning the system — I was relieved there was a tablet that made the pain go away.
Except. The pain didn’t entirely go away.
Because what I didn’t understand then — and this took me an embarrassingly long time to figure out — is that the allopurinol wasn’t fixing anything. It was lowering my uric acid numbers. Those are different things.
Two years in. 2014. Blood tests still showing elevated urate. Still outside the reference range. I was on the medication, and the medication wasn’t even getting the numbers right. Let alone fixing the joints. Let alone fixing the reason my body was producing too much uric acid in the first place.
I just… kept taking the tablet. Because I didn’t know there was another option.
Let me give you the numbers. Because this is where it gets interesting.
August 2014. Urate: 0.53 mmol/L. Outside the reference range. On allopurinol. October 2014. Urate: 0.51 mmol/L. Still outside. Still on the medication. January 2015. Urate: 0.44 mmol/L. Slightly better. Still elevated. March 2015. Urate: 0.46 mmol/L. Back up again.
Four tests across one year. All outside the reference range. All while taking a tablet specifically designed to bring that number down.
By August 2020, the number had gone to 502 micromoles per litre. That’s when they flag it in the notes as “above high reference limit — make an appointment to see the doctor.” Twenty years in. Still not controlled.
Now here’s the thing I wasn’t asking at any point in those twenty years: why is my body producing too much uric acid?
I was asking: “does the tablet work?” I should have been asking: “what’s driving this in the first place?”
Those are very different questions.
Fast forward to Boxing Day 2023. The decision. I’ve told that story before — eighteen stone, couldn’t get up the stairs without getting winded, looked in the mirror and something snapped. Started fasting. Stopped eating ultra-processed food. Within two months the weight was moving. The energy was coming back.
And in February 2024 — roughly ten weeks after Boxing Day — I stopped all my medications. Not impulsively. I’d been tracking my bloods closely. The data was moving in the right direction. I stopped the allopurinol.
I want to be honest about what I was expecting. I was expecting a gout attack. Probably within a few weeks. Those attacks are painful in a way that’s hard to describe unless you’ve had one — not background ache, not stiffness, but white-hot, can’t-sleep, can’t-put-your-foot-down pain. I’d been through it dozens of times over twenty-four years. I knew what it felt like.
So I stopped the tablet, and I waited.
Summer 2024. First summer without allopurinol in nearly a quarter of a century.
I was at a client dinner. They’d ordered a massive ribeye — the kind of steak that old Neil would’ve looked at nervously. Red meat and gout have always had a complicated relationship. High purine foods, your body converts purines to uric acid — that’s the received wisdom. That’s why I’d been cautious around red meat for years.
I ate the steak. Grass-fed, properly cooked, no nonsense.
Went to bed that night waiting. Woke up the next morning. Fine. Day two. Fine. Day three. Still fine. A week later. Nothing.
No attack. No swelling. No pain.
I ate that steak — and nothing happened.
Then around Day 24 of my extended fast — this was summer 2025, so about eighteen months after stopping the medication — something else happened. I looked at my big toe. The crystals. I’d had visible uric acid crystal buildup on that joint for years. A lumpy, slightly swollen knuckle that I’d just accepted as part of who I was.
They were gone. Or near enough gone that I had to look twice.
That same day I put on a pair of Birkenstocks. If you’ve ever had gout in your toe, you know why that matters. Birkenstocks have been sitting in the cupboard for years. Too much pressure on the joint. Not possible.
I walked four miles in them. Without flinching.
Twenty-four years. And a change in how I was eating and fasting had done something that two decades of daily medication hadn’t managed.
Everything here is tracked against real blood tests — not a protocol I read, not something I’m selling, just what actually happened when I did this and documented all of it. If that matters to you, subscribe. New video every Monday, Wednesday and Friday.
So what was actually going on?
Here’s what I think happened — and I want to be clear, this is my reading of my own N=1 data alongside some science I’ve looked into. Not a diagnosis. Not a prescription for anyone else. But it makes sense to me.
Professor Janet Lord — she’s a researcher at the University of Birmingham who studies inflammation and ageing — describes something called inflammaging. Her description: chronic low-level inflammation that grumbles along for years. It’s two to three times higher in older adults than in young people. And it drives disease. Heart disease, dementia, metabolic dysfunction. The kind of stuff that accumulates quietly for decades.
Gout isn’t separate from that picture. Gout is an inflammatory condition. Your body produces excess uric acid, it forms crystals in the joints, those crystals trigger an inflammatory response, and the result is the attack you know about.
The allopurinol was targeting one number: uric acid levels. Lower the uric acid, fewer crystals, fewer attacks. That’s the theory. Except my uric acid levels were still outside the reference range for most of those twenty-four years, despite taking the tablet daily.
What the medication wasn’t touching was the systemic inflammation underneath. The environment in which uric acid was being overproduced.
Professor Lord also talks about intermittent fasting reducing inflammation. Her words, not mine: fasting stimulates autophagy — she describes it as “a little hoover going around the body, hoovering everything up and getting rid of the rubbish” — and it drops inflammation down.
That’s what I think happened. Eighteen months of consistent fasting, switching away from ultra-processed food — those changes reduced the systemic inflammation that had been driving the problem. Not just managing the number. Changing the environment.
The allopurinol was managing the symptom. The fasting and the food changes addressed the cause. And once the cause shifted, the body regulated itself.
That’s a big claim for an N=1, I know. I can’t say it would work for everyone. I’m not saying stop your medication — I’d never say that. What I’m saying is that in my case, after twenty-four years, the thing that actually shifted the problem wasn’t the tablet I was taking. It was changing the inputs that were driving the problem in the first place.
If I were starting this over, I’d have asked the question much sooner: why is this happening, not just how do I manage it?
Twenty-four years on a tablet without once sitting down with someone and asking what was causing my body to produce too much uric acid. That’s not a criticism of the doctors I saw — they were doing what the system does. Manage the number. Keep the patient functional. But I wish I’d been more curious earlier.
If you’re tracking your own urate readings and they’re stubbornly outside the reference range despite medication — that’s worth a conversation with your GP. Not about stopping the medication. About whether the underlying inflammation is being addressed. Ask specifically about insulin resistance. Ask about dietary changes. Ask what they’d expect to see if the root cause was being addressed, not just the number.
The number matters. But the environment producing the number matters more.
If your joints are stiff in the morning. If you’ve had one gout attack and you’ve been told to just watch your diet and come back if it happens again. If you’ve noticed your blood tests flagging elevated urate and you’re not yet on medication — that early window is worth paying attention to.
Not to panic. To be curious.
Elevated urate is often a sign that something else is happening systemically — insulin resistance, inflammation, diet-driven metabolic load. That’s worth asking about before the first tablet, not after twenty-four years of them.
If you want to start tracking your own patterns the way I track mine, I’ve put a link in the description to the free 7-Day Fasting Blueprint. It’s where I’d start — not because fasting is the only tool, but because it’s the one that shifted my data fastest and most clearly.
Link below. Free. No email sequence pressure — just the guide.
And the important bit: everything I’ve shared today is educational content, not medical advice. Gout is a medical condition. Stopping medication is something you do with your GP, not instead of your GP. All my biomarker changes were supervised. My GP knew what I was doing and we tracked it closely. Speak to your GP before changing your fasting pattern, your diet, or your medication. Always.
Next Monday: a different pattern from the data. Same detective process.
⚠️ Important: This is educational content based on evidence and personal experience. It is not medical advice. Speak to your GP before making changes to your fasting pattern, diet, or medication.
Questions? Email hello@waymorethanweightloss.com
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