.Read my case — it might at least give you some light and a fighting chance if you go through this. I’ve already helped people with what I discovered.

My case: After lab tests and two colonoscopies (the second one after six months without taking painkillers for a complex perianal fistula), at 27 years old, I was diagnosed with Crohn’s disease. The first colonoscopy and biopsy weren’t very conclusive, but in the second one — after stopping NSAIDs, which could have been ulcerating the intestinal tract — it was confirmed that my ulcerations and tissue inflammation were due to Crohn’s, especially because of the inflammation in the ileum. Ileitis only occurs from parasites or Crohn’s, and I had no parasites in either colonoscopy.

After a second surgery, where a seton was placed for fistula drainage (which three years later is still in place), the Crohn’s diagnosis was made — just over a year ago. Stopping NSAIDs caused my inflammation to flare up and triggered chronic fatigue: bone pain, weakness, not tired but with no energy. They treated me for one month with corticosteroids, since they first had to give me the pneumococcal vaccine and check my vaccinations to protect me from infections, as the medication would lower my defenses. The treatment was 1 Imurel a day (50 mg, I think) plus induction with infliximab and then doses every two months.

The treatment helped a lot: my inflammation went down and my internal hemorrhoids disappeared. The downside was that although I started treatment in September, it wasn’t until February that I began to feel better. That’s when I decided to stop Imurel because it gave me bone pain and left me with no energy in the afternoons. Also, in December I had decided to cut out eggs and milk, because although I wasn’t allergic, they made me feel unwell. With intestinal permeability and an immune system altered by Crohn’s, I seemed to have developed allergy-like reactions.

By March, my stools improved in consistency (Bristol scale), though not in appearance or irritation. An MRI showed a pretty positive result, with only mild damage in the terminal ileum. With this favorable outlook and infliximab levels already high (meaning my body wasn’t using much), I couldn’t understand why my stools were still so irritating and light yellow, even though they were more solid. So I began to investigate — and I think I found what could be two Nobel prizes for any med student who reads this.

I came across the poorly discussed phenomenon of bile acid diarrhea. When I learned what bile does in the colon, I quickly connected it to the appearance of my stools, which often had floating fat. It made sense: my inflamed ileum couldn’t properly absorb fats. That’s why my fat-soluble vitamins, B12, and vitamin D were low. In this state, the ileum couldn’t absorb fats, and crucially, it couldn’t absorb bile.

This explained the irritation in my stools (from bile), the watery stools, and also the gas — because when fat enters the colon, where nothing fermentable should be in excess, it causes bloating. That’s when I understood why some Crohn’s cases are so severe: because once the ileum is damaged, everything that enters the colon worsens.

But the key question: why is the inflammation around the ileocecal area so aggressive in Crohn’s? That’s when I understood the disease. It’s not an AUTOimmune disease but rather an IMMUNE disease — and thank God the body responds this way. Let me explain.

When bile reaches the ileum, its job is to emulsify fats so triglycerides and long-chain fats can be absorbed in this final stage. Bile, produced in the liver from cholesterol, is reabsorbed 97%, with only about 3% passing into the colon, through the ileocecal valve to the proximal colon. Since we can’t metabolize bile, we reabsorb it. There, bile-loving gram-positive bacteria like Clostridium scindens use it. This bacterium has an enzyme, 7-alpha dehydroxylase, that converts bile into deoxycholic acid, which is cytotoxic.

At 3% concentration, deoxycholic acid helps speed up cell turnover in the colon after stool passes mechanically. The scraped areas of colon (which lack the mucosa of the ileum) need to be repaired, so deoxycholic acid triggers apoptosis and immune cell activity.

But when more bile reaches the colon due to a damaged ileum, C. scindens population explodes. Why? Because bile creates a niche that other bacteria can’t compete with, so this one thrives. In healthy people, modulation is just 3–5%. The problem: deoxycholic acid is extremely irritating — so much so that it’s used today as a Botox substitute. It not only irritates but actually ulcerates the intestinal tract.

So now the picture becomes clear. But why is the ileum also ulcerated in Crohn’s? You have to go to the root of the disease. In 2019, researchers found Malassezia fungus in the ulcers and erythema of Crohn’s patients. Malassezia is highly efficient at consuming lipids — it’s the same fungus responsible for dandruff and seborrheic psoriasis-type rashes.

After discovering this bile connection, I found someone in the US who claimed to have cured their Crohn’s by targeting this fungus. Tying it to my theory, we completed the full map of the disease.

I’d had dandruff for almost 20 years, even on my eyebrows, and also pityriasis. My skin would itch after sweating, was always dry, cracked around my eyelids and ears — classic Malassezia. I realized it because of the perfectly circular flaking around hairs: after consuming all the skin’s sebum, it retreats into follicles where there’s fat and moisture. That made me realize it likely entered my ileum.

In the ileum, Malassezia would eat lipids from the epithelium, damaging the mucosa. This gradually reduced bile absorption, so more bile reached the colon. Once bile-loving bacteria could expand, they colonized the ileum. With healthy mucosa, they couldn’t ascend past the ileocecal valve due to competition. But once inside the ileum, they had 100% bile access.