For years I filed celiac disease under solved. Cut the gluten, the gut heals, the antibodies drop, you move on. I believed the tidy version, and it turns out I was trusting the wrong half of it.

The half I trusted was the blood test. If you have celiac disease and you have been good about your diet, your doctor draws blood, checks your anti-tissue-transglutaminase antibodies (the famous tTG), sees a nice low number, and tells you you are doing great. That falling number is supposed to mean your small intestine is knitting itself back together. Here is the part no one had told me: once you are on a gluten-free diet, that reassuring result catches only about half of the people whose guts are still inflamed. A team at the University of Oslo and Oslo University Hospital has now gone looking for something that catches the other half.

Their study, published in Gastroenterology and described this month by News-Medical, ran 264 blood and tissue samples through targeted serum proteomics, a method that reads the levels of many proteins at once instead of hunting for a single antibody. The samples came from people with celiac disease, drawn before treatment and again after a year on a gluten-free diet, plus people without the disease as controls. The researchers pulled out 24 proteins that tracked with the disease, and 9 that tracked specifically with how badly the intestine was damaged. Untreated patients carried the highest levels of inflammatory proteins. Healthy controls carried the lowest. And the patients a year into a strict gluten-free diet still sat higher than the healthy group. So if the diet is working and the antibodies have gone quiet, why is the blood still carrying a signature of inflammation?

The answer is in what the antibody test actually measures, and it humbled me a little once I saw it. The tTG antibody is your immune system’s reaction to gluten. Take the gluten away and the reaction winds down, so the antibody number falls. But the villi, those fingerlike projections lining the small intestine that pull nutrients out of your food, do not recover on the same schedule. They can stay blunted and inflamed for months while the antibody that was supposed to stand in for them quietly normalizes. We were reading the smoke alarm and assuming it told us the state of the house. Lead author Jostein Holen Ibsen said the old blood test “simply does not work as well once patients have started treatment with a gluten-free diet.”

This is not a lone complaint. A write-up from ADLM’s Clinical Laboratory News on a 2017 Gastroenterology meta-analysis pooled 26 studies and found that in patients on a gluten-free diet, tTG IgA caught persistent villous atrophy with a sensitivity of 0.50, and the related EMA antibody managed 0.45. In plain terms, these tests miss roughly half the people whose guts are still damaged. Both are highly specific, so a positive result means something, but a reassuring negative means much less than patients are led to believe. The authors’ own conclusion was blunt: until a sensitive noninvasive marker exists, a follow-up biopsy stays the only appropriate way to confirm the gut has healed. A biopsy. As in another endoscopy, another tube, another day you do not eat. That is the choice the field has quietly lived with, and it is why researchers have spent years hunting for a blood marker that tracks recovery instead.

So what the Oslo group is chasing is a way to read the gut lining without going down into it. Nine proteins that rise and fall with the actual extent of intestinal damage would let a clinician watch healing happen, or fail to happen, from a single blood draw. And the finding that treated patients still run slightly hot points at something the gluten-free-diet-as-cure story tends to gloss over: strict avoidance does not always buy you a fully quiet gut. “The findings therefore suggest that patients have some inflammation in the gut even when they follow the diet,” Ibsen said. If you have ever gone painfully strict and still not felt right, that sentence might land hard.

I want to be careful about what this is, because the temptation to oversell a biomarker is real and I am not going to do it. This is a profiling study, not a clinic-ready test. Two limits matter most: the team says it needs more patients before anything reaches a clinic, and even the researchers frame the panel as a complement to existing tests, not a replacement. Senior author Knut Lundin put the ceiling on it plainly, saying only that there is “potential for tests based on these new biomarkers to be used alongside serology, which is the test used today and which does not distinguish clearly enough between ongoing intestinal damage and healing.” Worth noting too: the work was funded by the South-Eastern Norway Regional Health Authority, a public body rather than a diagnostics company with a test to sell. That does not make the result true, but it does mean the obvious commercial thumb was off the scale.

The open question is whether those nine proteins hold up in a bigger, messier population than one Oslo cohort, and whether any of them are specific enough to celiac healing to build a real test around. Until that lands, here is what I would do. If I had celiac disease, I would stop treating a normal antibody result as proof my gut had healed, because for persistent gut damage the old antibody tests miss too much to count as proof. I would ask my doctor directly whether my recovery had ever actually been confirmed, I would take lingering symptoms seriously even with clean bloodwork, and I would keep watching this line of work, because a blood test that reads the lining itself is the thing I have quietly wanted all along.

Sources

  1. News-Medical – Blood biomarkers help track gut pathology in celiac disease (2026)
  2. Gastroenterology – Ibsen et al., “Targeted Serum Proteomics Reveals Profiles Associated With Gut Pathology in Celiac Disease” (2026)
  3. Clinical Laboratory News / ADLM – on the 2017 Gastroenterology meta-analysis of tTG and EMA for persistent villous atrophy
  4. Journal of Gastrointestinal and Liver Diseases – “Celiac Disease: Promising Biomarkers for Follow-Up” (2023)