Field notes · Food & eating · An eating disorder psychiatrist's perspective

Gluten is (usually) not the enemy. What the evidence actually says about celiac disease, gluten sensitivity, and the food rules we keep prescribing by accident.

A 20-minute read, with five interactive tools · Reid Robison, MD · adapted from a continuing-education talk for eating disorder professionals

This isn't gluten apologetics. Celiac disease is real, serious and under-diagnosed. The argument here is narrower: for the roughly 99 in 100 people who don't have celiac disease, a gluten-free diet is a restriction worth scrutinizing like any other food rule. In my field, eating disorders, a food rule that comes with a medical alibi is the hardest kind to challenge, and clinicians are sometimes the ones who hand it over.

TL;DR

Three different things people call "gluten problems"

Celiac diseaseWheat allergyNon-celiac gluten sensitivity
MechanismAutoimmune; damages the small-intestine liningIgE allergy (the "fire alarm" branch of immunity)Unknown. No established mechanism.
TesttTG-IgA blood test plus intestinal biopsySkin prick or specific IgENone. No biomarker exists.
How common~0.7–1%~0.2–0.5%Self-reported 6–13%; confirmed far lower
What exposure doesGut damage, malabsorption, long-term risksAcute allergic reaction within minutesSymptoms only. No known tissue injury.

Sources:2,9

Celiac disease is a body-wide autoimmune disease in genetically susceptible people. It's the only autoimmune disease with a fully identified environmental trigger: gluten, the storage protein of wheat, rye and barley. Untreated, it raises the risk of osteoporosis, iron-deficiency anemia, infertility, thyroid disease and small-bowel lymphoma. The only treatment is a strict, lifelong gluten-free diet: not just bread, but vigilance about malt, sauces, shared fryers and cross-contact in any kitchen you don't control2. Hold that thought. Every one of those vigilance behaviors is also, in a different person, a symptom.

What gluten actually is, and why it's in everythingA plain-language sidebar

Gluten is the protein pantry a wheat, rye or barley seed packs for its seedling. Two protein families, gliadin and glutenin, tangle into an elastic web when flour meets water. That web is why dough stretches, bread rises and pizza crust chews.

Gluten is hard for everyone to digest. Its fragments are rich in the amino acid proline, which our enzymes struggle to cut, so pieces reach the gut partly intact in all of us. For 99% of people that's completely uneventful. Celiac disease is what happens when the immune system decides those fragments are an enemy10.

Because it binds and thickens, gluten also hides in soy sauce, malt vinegar, gravies, dressings, some deli meats and even some medication coatings. That's why a truly gluten-free life means reading every label.

A short history

The link was discovered in a famine. During the Dutch Hunger Winter of the 1940s, bread disappeared from Dutch diets. Most children got sicker, but pediatrician Willem-Karel Dicke noticed a small group of chronically ill children who got dramatically better, then relapsed when relief bread arrived11. A dietary trigger became visible only when the food was taken away from everyone at once. That's the standard to hold everything else to: what happens when you remove the thing, and what happens when you put it back without telling anyone.

By the 1980s, celiac disease was understood as an immune reaction tied to the HLA-DQ2 gene12. In 2003, a screening study of more than 13,000 Americans found celiac disease in 1 in 133 people with no risk factors, about ten times more common than US medicine had believed13.

Tool · the gap

Out of 100 Americans.

0.7%have celiac disease and medically need a gluten-free diet1
~25%reported eating gluten-free in 2015 consumer surveys14
Between those two numbers sits almost everyone this post is about.

US national survey data tell the same story. From 2009–10 to 2013–14, the share of Americans with celiac disease held steady while gluten avoidance without celiac disease more than tripled15. In consumer surveys, about a quarter of gluten avoiders cite weight loss as the reason. In any other context we'd call that a diet. This one arrives with a medical vocabulary attached. Each decade seems to get a dietary villain (fat in the 1980s, carbs in the 2000s, gluten in the 2010s, seed oils now), usually with a bestselling book and a product line that costs two to four times more than what it replaced16.

What happens when you blind it

2011 · n = 34NCGS is named

People with IBS who felt better off gluten had more symptoms on gluten than placebo. But the background diet wasn't controlled for FODMAPs17.

2013 · n = 37The same team checks itself

After a low-FODMAP run-in, symptoms rose equally on high gluten, low gluten and placebo. "Absolutely no specific response to gluten"18.

2015 · n = 35Can people tell?

Only 12 of 35 correctly identified the gluten flour. 17 were sure they'd had gluten when they hadn't, and felt worse on the gluten-free flour19.

2018 · n = 59It was the fructans

Muesli bars hid gluten, fructan or placebo. Fructans caused more symptoms than gluten; gluten and placebo were indistinguishable4.

Credit to the Australian group that coined "non-celiac gluten sensitivity" in 2011: they were the ones who went back and tried to break their own finding. That's what good science looks like.

Average gastrointestinal symptom score (GSRS-IBS; higher is worse) after each blinded challenge in 59 people on self-chosen gluten-free diets. Fructan scored significantly higher than gluten. Of the 59, 24 felt worst on fructan, 22 on placebo, and only 13 on gluten4.
FODMAPs and fructans, decodedWhy a gluten-free diet is secretly a lower-FODMAP diet

FODMAP stands for fermentable oligosaccharides, disaccharides, monosaccharides and polyols: carbohydrates that are poorly absorbed, pull water into the gut and get fermented by bacteria into gas. Stretch plus gas in a sensitive gut equals bloating and pain, with no tissue damage20.

Fructans are chains of fructose that no human enzyme can cut, so they reach the colon intact. In most people that's fine, even beneficial: fructans feed friendly bacteria, which is why inulin is sold as a fiber supplement. In a gut whose nerves are "turned up too loud" (the core feature of IBS), the same gas registers as pain.

Wheat is the biggest source of fructans in Western diets. So cutting gluten also cuts fructans, and people credit the wrong molecule.

Tool · where fructans live

The low-FODMAP diet helps roughly half to three-quarters of people with IBS, but it's designed as a three-phase tool, not a lifestyle: restrict for 2–6 weeks, reintroduce systematically, then personalize. The goal is the most liberal diet that controls symptoms21. Fructan reactions are dose-dependent: a sprinkle of onion may be fine where a garlicky pasta dinner isn't. And long sourdough fermentation pre-digests much of wheat's fructan, which may be why so many people say they tolerate "bread in Europe"22.

Pooling the blinded trials

Tool · 100 people who say gluten makes them sick
16relapse on gluten specifically under double-blind challenge
40have equal or worse symptoms on placebo (a nocebo response)
44no clear response to either

Approximate shares from a pooled analysis of double-blind, placebo-controlled gluten challenge trials3. Both groups are real. Neither supports population-wide gluten avoidance.

Nocebo isn't calling anyone a liar

A nocebo effect is a negative outcome produced by expectation rather than by the substance: the mirror image of placebo, and just as physiological23. Your gut has its own nervous system in constant conversation with the brain, and the brain sets the volume on gut sensations. Calm turns it down; threat and vigilant attention turn it up, so the same stretch arrives as pain24. Think of blushing: a pure thought producing a real, visible change in blood flow. The gut blushes too.

The pain is real. The bloating is real. The attribution is the part that's wrong, and the attribution is what builds the food rule. Eat the feared food, feel awful, the rule is confirmed, the rule widens. That's the same learning loop that drives avoidance in anxiety disorders and ARFID, and we know how to treat it.

Gluten-free has a cost

Why this belongs in an eating disorder conversation

Gluten avoidance and eating disorders meet in three ways:

  1. They travel together. About 9% of people with celiac disease have an eating disorder; people with celiac disease have about 1.5 times the risk of anorexia, and people with anorexia about 2.4 times the risk of celiac disease7. A Swedish nationwide study found elevated anorexia risk both before and after a celiac diagnosis25. Some of this is detection bias, but the takeaway stands: people with anorexia and persistent GI symptoms or poor weight restoration should be screened.
  2. The treatment can become the disorder. Across published cohorts, 14–57% of people with celiac disease screen positive for ARFID (avoidant/restrictive food intake disorder). In one tertiary clinic, those with ARFID weren't more adherent and didn't heal better: they were restricting beyond what the disease required, with no medical benefit8,26.
  3. Gluten-free supplies a vocabulary for "clean eating." Orthorexic thinking needs a pure category, a contaminating category and a moral reward for staying on the right side. Gluten-free supplies all three off the shelf. Orthorexia isn't a DSM diagnosis and its screening tools are weak, so treat the data as a signal, not a rate27,28.
Two people refuse the bread. Only one of them is being treated.
Medically necessary
Eating-disorder-driven
Origin
Positive blood test and biopsy; a clinician's diagnosis
Self-diagnosis, an app, an elimination diet, a practitioner selling the test
Over time
Stable. One well-defined rule, unchanged for years
Expanding: gluten, then dairy, sugar, nightshades, "processed"
After exposure
Annoyance, inconvenience, physical symptoms
Anxiety, shame, guilt, compensatory behavior
Flexibility
Eats freely within the rule and enjoys food
Volume and variety shrink alongside the rule
Social life
Plans around it; still eats with people
The rule becomes a reason not to eat with others
If offered a cure
Relief
Ambivalence or resistance

Seven questions that sort necessity from disorder

These ask what the restriction does, not what it excludes. Clinicians can ask them; anyone on a gluten-free diet without celiac disease can ask them of themselves.

  1. Who first told you gluten was a problem, and what test were they looking at?
  2. Were you eating gluten at the time you were tested?
  3. What else has come off the list since gluten did?
  4. When you eat gluten by accident, what's the worst part: the symptoms, or the feeling that you slipped?
  5. Are you eating less overall since going gluten-free, or just differently?
  6. What have you stopped doing socially because of the diet?
  7. If a gastroenterologist called tomorrow and said the tests were clear and you could eat anything, what would that be like?

Listen for relief versus dread. Dread is the finding.

Test before anyone goes gluten-free

Tool · the celiac testing path

A simplified version of the 2023 American College of Gastroenterology approach for adults. Work through it with your clinician; this doesn't replace one.

The four tests, translatedWanted posters, printer ink, shag carpet and a dealt hand

tTG-IgA: the wanted poster. Antibodies against an enzyme your own gut uses. High levels mean the immune system has put up wanted posters for your own tissue. Better than 95% accurate while you're eating gluten; stop eating it and the posters come down within months.

Total IgA: checking the printer has ink. A few people in every thousand make almost no IgA, so their tTG-IgA reads falsely normal. If total IgA is low, IgG-based tests are used instead.

Biopsy: looking at the carpet. Healthy intestinal villi look like shag carpet; untreated celiac looks like tile. Still the confirming step in adults2.

HLA-DQ2/DQ8: the dealt hand. About a third of people carry these genes; virtually everyone with celiac does. So a negative result rules celiac out permanently, while a positive result alone means very little.

The trap: ruling celiac out requires eating gluten, typically 1–3 grams a day (one or two slices of bread) for 2–8 weeks before testing2,29. For someone whose eating disorder is organized around avoiding exactly that food, that isn't a lab order. It's a structured exposure, and it deserves planning: decide together whether the answer is worth it (HLA typing is sometimes the kinder route), involve the dietitian, expect early nocebo symptoms, and agree on the end date before day one.

And never base a diagnosis on IgG food-sensitivity panels, hair analysis, applied kinesiology or "leaky gut" tests. None are validated, and all of them manufacture restrictions people then have to live inside2.

What to say instead

Arguing with the belief rarely works, because the person's evidence is their own body. Validate the symptom, move the attribution, and offer a small, testable next step.

Instead of"Gluten sensitivity isn't a real thing."
Try"I believe your symptoms are real. I want to find out what's actually causing them, because I don't think we've proven it's gluten yet."
Instead of"You need to start eating bread again."
Try"Let's test one food, once, and see what happens. You keep control of what and when."
Instead of"That's just the eating disorder talking."
Try"I notice the list has gotten longer this year and you're eating less overall. What do you make of that?"

The reframe that works: "In the best studies, the thing causing the bloating wasn't gluten. It was a carbohydrate that travels with it. That means the answer probably isn't less food. It might be different food, and more of it." You're replacing a wide rule with a narrow, testable one, and a narrow rule is one an eating disorder can't live inside.

A word to clinicians

"Just try cutting it out and see if you feel better" is a prescription. It costs us nothing to say. It costs the patient a whole category of food, a diagnostic test we can no longer interpret, and a rule with our authority behind it. An unblinded elimination trial in someone with an eating disorder will nearly always "work," thanks to expectation, fewer FODMAPs and less food overall30. Before suggesting one: screen for celiac first while they're still eating gluten, ask whether this person can hold a restriction lightly, define the trial and its end date, and build reintroduction into the plan from the start.

Five things to remember

  1. Celiac disease is serious, under-diagnosed and worth screening for, especially with anorexia, persistent GI symptoms, iron deficiency or poor weight restoration.
  2. Non-celiac gluten sensitivity is real in a small minority. Under blinding, the trigger is more often fructans or expectation than gluten.
  3. A gluten-free diet has real costs: nutritional, financial, social and psychological. It's a treatment, and it needs an indication.
  4. Test before stopping gluten. You can't get those months back.
  5. When restriction isn't medically required, treat it as what it is (a food rule) and ask what it's doing for the person before trying to take it away.

For about one person in a hundred, gluten genuinely is the enemy, and they deserve a fast, accurate diagnosis and a lifetime of support. For the rest, the enemy was never the protein. It was the certainty that something in the food was doing this, and how good it felt to finally have a name for it.

Related: No one chooses this, for families of people with eating disorders, and Sugar & Shadow, on placebo and nocebo. More on the food & eating topic page.

Sources

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  2. Rubio-Tapia A, Hill ID, Semrad C, et al. American College of Gastroenterology guidelines update: diagnosis and management of celiac disease. Am J Gastroenterol. 2023;118(1):59–76.
  3. Molina-Infante J, Carroccio A. Suspicion of not-celiac gluten sensitivity confirmed in few patients after gluten challenge in double-blind, placebo-controlled trials. Clin Gastroenterol Hepatol. 2017;15(3):339–348.
  4. Skodje GI, Sarna VK, Minelle IH, et al. Fructan, rather than gluten, induces symptoms in patients with self-reported non-celiac gluten sensitivity. Gastroenterology. 2018;154(3):529–539.
  5. Melini V, Melini F. Gluten-free diet: gaps and needs for a healthier diet. Nutrients. 2019;11(1):170.
  6. Lebwohl B, Cao Y, Zong G, et al. Long term gluten consumption in adults without celiac disease and risk of coronary heart disease: prospective cohort study. BMJ. 2017;357:j1892.
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  8. Published cohorts of ARFID in celiac disease: scoping review (Nutrients, 2025), adult tertiary celiac clinic survey (Gastro Hep Advances, 2022;1:361–364), consecutive celiac/NCGS referrals (Nutrients, 2026), and a pediatric cross-sectional cohort of 101 children (2026).
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  10. Shan L, Molberg Ø, Parrot I, et al. Structural basis for gluten intolerance in celiac sprue. Science. 2002;297(5590):2275–2279.
  11. van Berge-Henegouwen GP, Mulder CJJ. Pioneer in the gluten free diet: Willem-Karel Dicke 1905–1962, over 50 years of gluten free diet. Gut. 1993;34(11):1473–1475.
  12. Sollid LM, Markussen G, Ek J, Gjerde H, Vartdal F, Thorsby E. Evidence for a primary association of celiac disease to a particular HLA-DQ alpha/beta heterodimer. J Exp Med. 1989;169(1):345–350.
  13. Fasano A, Berti I, Gerarduzzi T, et al. Prevalence of celiac disease in at-risk and not-at-risk groups in the United States: a large multicenter study. Arch Intern Med. 2003;163(3):286–292.
  14. Bulka CM, Davis MA, Karagas MR, Ahsan H, Argos M. The unintended consequences of a gluten-free diet. Epidemiology. 2017;28(3):e24–e25.
  15. Choung RS, Unalp-Arida A, Ruhl CE, Brantner TL, Everhart JE, Murray JA. Less hidden celiac disease but increased gluten avoidance without a diagnosis in the United States: findings from the National Health and Nutrition Examination Surveys from 2009 to 2014. Mayo Clin Proc. 2017;92(1):30–38.
  16. Niland B, Cash BD. Health benefits and adverse effects of a gluten-free diet in non-celiac disease patients. Gastroenterol Hepatol. 2018;14(2):82–91.
  17. Biesiekierski JR, Newnham ED, Irving PM, et al. Gluten causes gastrointestinal symptoms in subjects without celiac disease: a double-blind randomized placebo-controlled trial. Am J Gastroenterol. 2011;106(3):508–514.
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  19. Zanini B, Baschè R, Ferraresi A, et al. Randomised clinical study: gluten challenge induces symptom recurrence in only a minority of patients who meet clinical criteria for non-coeliac gluten sensitivity. Aliment Pharmacol Ther. 2015;42(8):968–976.
  20. Gibson PR, Shepherd SJ. Evidence-based dietary management of functional gastrointestinal symptoms: the FODMAP approach. J Gastroenterol Hepatol. 2010;25(2):252–258.
  21. Halmos EP, Power VA, Shepherd SJ, Gibson PR, Muir JG. A diet low in FODMAPs reduces symptoms of irritable bowel syndrome. Gastroenterology. 2014;146(1):67–75.
  22. Loponen J, Gänzle MG. Use of sourdough in low FODMAP baking. Foods. 2018;7(7):96.
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  27. Wąsowicz M, et al. Dietary behavior and risk of orthorexia in women with celiac disease. Nutrients. 2022;14:904.
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  29. Leffler D, Schuppan D, Pallav K, et al. Kinetics of the histological, serological and symptomatic responses to gluten challenge in adults with coeliac disease. Gut. 2013;62(7):996–1004.
  30. Harer KN. Irritable bowel syndrome, disordered eating, and eating disorders. Gastroenterol Hepatol. 2019;15(5):280–282.

Educational only. This isn't medical advice and isn't a substitute for care. If you think you might have celiac disease, ask for testing before changing your diet.