What causes ulcerative colitis

When I was diagnosed with Crohn's disease in 2015, the first question I asked my gastroenterologist was simple: why? Why did I get this? What caused it? He looked at me, paused, and said something along the lines of: we don't really know. Bad luck, probably. Genetics. These things just happen.

That answer didn't sit well with me. I was 30 years old, and for most of my twenties I'd been living on fast food, beer, and late nights. My stress levels were through the roof, I barely slept, and the idea that my gut just randomly decided to attack itself felt incomplete. So I started reading. Everything I could find. And what I learned over the following months changed not only how I understood my own illness, but how I eventually recovered from it — without medication, within six months. I've been symptom-free for more than eight years now.

Ulcerative colitis and Crohn's disease are different conditions, but they share most of their underlying mechanisms. What I'm going to lay out here applies to both, and it's backed by a growing body of research that's finally catching up with what many of us suspected all along: UC doesn't come out of nowhere. It builds up, layer by layer, until something tips the balance.

Genetics load the gun, but they don't pull the trigger

About 20% of people with ulcerative colitis have a close family member with some form of inflammatory bowel disease. That's a real genetic component, and it would be dishonest to ignore it. Certain gene variants affect how your immune system responds to bacteria in the gut, how well your gut lining repairs itself, and how efficiently you process inflammation.

But genetics alone don't explain why UC rates have been rising sharply in countries that are industrialising rapidly, or why identical twins — who share the same DNA — often don't share the same diagnosis. Something in the environment activates what the genes make possible. And that something, in most cases, is a combination of the factors I'll describe below.

Your gut bacteria are not passive residents

For decades, researchers treated gut bacteria as a kind of background noise. They were there, they helped with digestion, and that was about it. That picture has changed dramatically in the past few years.

In 2026, a team at the Helmholtz Centre in Munich published a study in Nature Microbiology that showed something remarkable: ordinary gut bacteria — not invaders, not pathogens, but the bacteria that live in your colon every day — use specialised injection systems to pump proteins directly into your cells. These are called Type III secretion systems, and until recently scientists thought only disease-causing bacteria used them. It turns out that your commensal bacteria are actively communicating with your immune cells, and in people with Crohn's disease, the genes for these injection proteins appear more frequently. Your bacteria aren't sitting quietly. They're shaping how your immune system behaves.

Around the same time, researchers at Cambridge identified a specific bacterial species — provisionally called CAG-170 — that appears to be a universal marker of gut health. It's consistently lower in people with IBD, Crohn's, and obesity. What's striking is that this bacterium belongs to what scientists call the "hidden microbiome": roughly two-thirds of all gut species that we didn't even know existed until advanced sequencing made them visible. We've been studying the gut microbiome for years, and we were only seeing a third of the picture.

What this means in practical terms is that the bacterial ecosystem in your gut is far more complex and far more actively involved in your immune regulation than anyone appreciated even five years ago. When that ecosystem is disrupted — through antibiotics, poor diet, stress, or environmental chemicals — your immune system loses its calibration. And in the colon, where bacterial density is highest, that miscalibration shows up as chronic inflammation.

Leaky gut: the gateway

Your gut lining is a single layer of cells, held together by structures called tight junctions. When those junctions work properly, they allow nutrients through while keeping bacteria, undigested food particles, and other large molecules on the inside of the gut where they belong. When the tight junctions loosen — a condition researchers call increased intestinal permeability, and the rest of us call leaky gut — things start passing through that shouldn't.

Once bacterial fragments and food proteins reach the tissue beneath the gut lining, your immune system reacts. It's supposed to react, because those molecules aren't meant to be there. The problem is that the reaction doesn't stop. Your immune system keeps attacking, inflammation becomes chronic, and over time the tissue itself starts to break down. In ulcerative colitis, this happens specifically in the colon and rectum. In Crohn's, it can happen anywhere in the digestive tract.

Leaky gut isn't the cause of UC by itself, but it's the mechanism through which most of the other causes do their damage. Fix the permeability, and you take away the trigger for the immune overreaction. That's why so much of the work we do in our practice starts with the gut lining.

Diet: the factor doctors rarely ask about

In 2026, roughly 61% of the average Dutch diet consists of ultra-processed food. In the UK and the US, the numbers are similar or higher. About 70% of what's on supermarket shelves is ultra-processed — meaning it contains ingredients you wouldn't find in a home kitchen: emulsifiers, artificial sweeteners, modified starches, flavour enhancers, and preservatives.

These substances matter because many of them directly damage your gut bacteria and your gut lining. A 2025 study from Cambridge tested 1,076 common industrial chemicals — pesticides, flame retardants, plasticisers — and found that 168 of them damage gut bacteria at concentrations people are regularly exposed to. Some of those chemicals also cause bacteria to become antibiotic-resistant, which compounds the problem. You don't need to work in a chemical plant to be exposed. These compounds are in food packaging, non-stick pans, cleaning products, and the residues on conventionally grown produce.

Then there's the dietary pattern itself. A diet heavy in refined sugar, alcohol, and processed grains feeds the wrong bacteria and starves the ones that produce short-chain fatty acids — the compounds your colon cells depend on for energy and repair. Over months and years, this shifts the entire bacterial population in your gut toward a profile associated with inflammation. Researchers call it dysbiosis, and it's one of the most consistent findings in UC patients.

I can speak to this personally. Before my diagnosis, I was living on takeaway food, white bread, pasta, beer, and sugary snacks. I didn't think twice about it. And when I finally got a food poisoning episode from a dodgy meal, my gut didn't recover the way it should have. That single infection, landing on years of accumulated damage, triggered a massive flare-up. Looking back, the food poisoning was the match, but the diet had been soaking everything in petrol for years.

Stress and the gut-brain connection

Your gut and your brain communicate constantly through the vagus nerve, through hormones, and through the immune system itself. When you're under chronic stress, your body produces cortisol, which directly affects the composition of your gut bacteria, slows down gut motility, and weakens the tight junctions in your gut lining. It's not just that stress makes your stomach feel uncomfortable — stress physically changes the environment inside your gut.

A large study presented at Digestive Disease Week in 2026, based on over 11,000 participants from the US National Health and Nutrition Examination Survey, found that the combination of psychological stress and late eating — eating within two hours of going to sleep — increased the risk of constipation and diarrhoea by 1.7 to 2.5 times. The same combination was associated with significantly reduced microbiome diversity. Not stress alone, and not late eating alone, but the two together, which is exactly how most people under pressure actually live: stressed all day and eating their biggest meal right before bed.

This matters because stress isn't just a trigger for flare-ups. It's a contributing cause. Chronic stress changes your gut in measurable, structural ways, and those changes make everything else — the dietary damage, the bacterial shifts, the leaky gut — worse.

Geography, sunlight, and the hygiene hypothesis

UC is far more common in Northern Europe, Canada, and the northern United States than in equatorial regions. The further you live from the equator, the higher your statistical risk. Part of this is almost certainly vitamin D: people in northern latitudes produce less of it, and vitamin D plays a direct role in maintaining the gut barrier and regulating immune responses in the gut wall.

But geography also correlates with something else — the hygiene hypothesis. In highly industrialised countries, children grow up in cleaner environments with less microbial exposure. They're more likely to be born by caesarean section (which means they miss the first major bacterial transfer from their mother — research shows that about 58.5% of an infant's gut bacteria come directly from the mother during natural birth). They're less likely to play in soil, less likely to be around farm animals, and more likely to receive multiple courses of antibiotics in early childhood.

The first three years of life are when your gut microbiome is established. What happens during that window — how you're born, whether you're breastfed, what infections you encounter, what antibiotics you receive — shapes the bacterial community that will regulate your immune system for the rest of your life. When that foundation is thin or unbalanced, the risk of autoimmune conditions like UC rises. It's not a guarantee, but it's a pattern that shows up consistently in the data.

The infection trigger

Many people with UC can point to a specific moment when their symptoms started: a bout of food poisoning, a stomach virus, a course of antibiotics for something unrelated. That's not a coincidence. A viral or bacterial infection can trigger an immune response that, in a gut that's already compromised — already permeable, already dysbiotic, already genetically primed — simply doesn't switch off.

Your immune system is designed to ramp up during an infection and then stand down once the threat is gone. But when the gut lining is damaged and bacterial fragments keep leaking through, the immune system never gets the all-clear signal. The infection resolves, but the inflammation becomes self-sustaining. That's the transition from an acute gut infection to a chronic inflammatory condition, and it's the story I hear from clients again and again.

It's never just one thing

If there's one message I want you to take from this article, it's that UC is not caused by a single factor. It's the accumulation of several: a genetic predisposition, a depleted microbiome, a damaged gut lining, years of dietary stress, environmental chemical exposure, chronic psychological pressure, and often an acute infection that tips everything over the edge. Remove enough of these layers, and the inflammation can subside. That's not theory — it's what I've seen in practice, over and over, with the clients we work with.

In our practice, we start by investigating what's actually going on inside your gut. Through stool analysis, we can see which bacteria are present and which are missing. Through food intolerance testing, we identify which foods are driving inflammation for you specifically (because it's different for everyone). And from there, we build a personalised programme that addresses the root causes rather than masking the symptoms with medication.

If you want to understand what's happening in your gut, that's always the first step. Not a pill, not a diet you found online, but a clear picture of what your body is actually dealing with — and a plan to address it.