Food Allergy or Food Intolerance?

An allergy and an intolerance are not the same thing, and the difference is bigger than a bad afternoon. One is your immune system misidentifying a threat. The other is your digestion struggling with a job. Here is how to tell them apart — and where celiac disease and wheat allergy fit, because neither is either.

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Food is not just fuel. It is culture, celebration, memory, and the thing that puts people around the same table. Which is exactly why an adverse reaction to it is so disruptive — it is never only about the sandwich.

The words get used loosely, and the looseness has consequences. Which label applies determines which test you get, which foods you have to avoid, and whether you need to carry epinephrine. So it is worth a careful walk through all four.

How common is this, really?

Food allergy does appear to be genuinely increasing in industrialized countries. Some of the apparent rise is better awareness and more testing rather than more disease — in one national US survey, nearly twice as many adults believed they had a food allergy (19.0%) as met clinical criteria for one (10.8%).^1,2 But the underlying trend is real, and it is not only a childhood story.

The current US numbers:

• 10.8% of US adults have a food allergy meeting clinical symptom criteria — roughly 1 in 9.¹
• 7.6% of US children — roughly 1 in 13.²
• 6.7% of adults and 5.3% of children have a physician-diagnosed food allergy, per CDC’s 2024 National Health Interview Survey.³
• 48% of food-allergic adults developed at least one allergy as an adult.¹ You do not age out of the risk of acquiring one.

Food intolerance is considerably more common than food allergy — European survey work puts non-immune food intolerance at roughly 15–20% of the population.⁴ The single biggest contributor is lactose malabsorption, which we will get to.

Food allergy: the immune system gets it wrong

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The NIAID expert panel definition is refreshingly plain: a food allergy is "an adverse health effect arising from a specific immune response that occurs reproducibly on exposure to a given food."⁵

Notice what that definition does not require. It does not require IgE antibodies, and it does not require the reaction to be systemic or life-threatening. Most of what people picture — hives, swelling, anaphylaxis — is IgE-mediated allergy. But there are others:

• IgE-mediated: allergen-specific IgE antibodies; reactions within minutes to about two hours. Peanut, tree nut, shellfish, milk, egg. This is the category that causes anaphylaxis.⁵
• Non-IgE-mediated: cell-mediated, delayed by hours to days. FPIES (food protein-induced enterocolitis syndrome), food protein-induced proctocolitis, food protein-induced enteropathy — and celiac disease.⁵
• Mixed: both mechanisms at once. Eosinophilic esophagitis is the main example.⁵

The practical consequence: not every true food allergy shows up on a skin-prick test or an IgE blood panel, and not every one is immediately life-threatening. A negative IgE test does not rule out a food allergy — it rules out one type.

What anaphylaxis actually looks like

Breathing difficulty or wheeze. Throat tightness or swelling. Hives and flushing. A drop in blood pressure, dizziness, collapse. Those are the signs most people can list, and all of them are real. Two more belong on the list and rarely make it there.

Intramuscular epinephrine into the outer thigh is the first-line treatment. It is not one option among several — it is the treatment.⁶

Antihistamines do not treat anaphylaxis. They have, in WAO’s words, "a limited role," useful mainly for relieving skin symptoms.⁶ The NIAID panel is blunter about why this matters: reaching for an antihistamine is "the most common reason reported for not using epinephrine, and may place a patient at significantly increased risk for progression toward a life-threatening reaction."⁵ Evidence for steroids in acute anaphylaxis is also weak enough that their routine use has become controversial.⁶

If this section applies to you or someone you feed, this is a conversation for an allergist, not a blog post. Get the prescription. Carry it. Two of them.

The Big Nine — not the Big Eight

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You have probably heard of "the Big 8." That list is retired.

The FASTER Act of 2021 (Public Law 117-11, signed 23 April 2021) declared sesame the ninth major food allergen recognized in the United States, and the labeling requirement took effect on 1 January 2023.^7,8 FDA’s current list of major food allergens reads, verbatim: "milk, eggs, fish, Crustacean shellfish, tree nuts, peanuts, wheat, soybeans, and sesame."⁷

• Milk
• Eggs
• Fish
• Crustacean shellfish
• Tree nuts
• Peanuts
• Wheat
• Soybeans
• Sesame — added 2023

These nine must be plainly declared on US food labels. Plenty of material still in circulation says eight — including pages that have since been quietly replaced. The School Nutrition Association, for one, now publishes a page titled "Major Allergens: The Big Nine."⁹ If a source still says eight, check its date before you trust the rest of it.

About that "90%" figure

The line you will see everywhere is that the major allergens account for about 90% of food allergies. FDA’s actual wording is more careful than the version in circulation: "At the time of FALCPA’s passage, the eight major allergens accounted for 90 percent of food allergies and serious allergic reactions in the U.S."⁷

That is a 2004 legislative-findings estimate, stated in the past tense, and attached to the original eight. FDA does not currently assert that the nine account for 90%. It is a reasonable rule of thumb. It is not a live measurement.

The most common individual culprits in US adults, by prevalence: shellfish 2.9%, milk 1.9%, peanut 1.8%, tree nut 1.2%, fin fish 0.9%. In children: peanut 2.2%, milk 1.9%, shellfish 1.3%, tree nut 1.2%, egg 0.9%.^1,2

For comparison, the European Union requires declaration of fourteen allergens, adding celery, mustard, lupin, molluscs and sulphites to the US list.¹⁰ If you are traveling, that difference cuts both ways.

Food intolerance: no immune system involved

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An intolerance is a non-immune adverse reaction to food. It is usually dose-dependent — a splash of milk in coffee may be fine where a glass is not — and the symptoms are mostly digestive: bloating, gas, cramping, diarrhea, nausea. It does not cause anaphylaxis.

Zopf and colleagues sort these into four mechanisms, and the four-way split is more useful than the usual two:⁴

• Enzymatic — a missing or reduced enzyme. Lactose intolerance is the classic.
• Transport — the sugar cannot be absorbed efficiently. Fructose and sorbitol malabsorption work this way, through the GLUT5 transporter. No enzyme is involved.
• Pharmacological — the food contains something with drug-like activity. Biogenic amines such as histamine and tyramine, and caffeine.
• Undefined or pseudoallergic — reactions to some additives, where the mechanism is not established.

Worth noticing: histamine, caffeine and food dyes all sit in the last two branches. They are not digestive failures at all. They are your body responding to a compound the food happens to contain.

Lactose intolerance is the human default

The small intestine stops making enough lactase to break down milk sugar. But framing that as a defect gets the biology backwards. Lactase production normally declines after weaning in mammals, humans included. The ability to keep digesting lactose into adulthood is the derived trait — it comes from variants in a regulatory region of the MCM6 gene sitting next to the lactase gene LCT, and it spread in populations with a long history of dairying.¹¹

About 65% of adults worldwide have a reduced ability to digest lactose after infancy. The variation by ancestry is enormous: roughly 5% of people of Northern European descent, against 70–100% of people of East Asian descent.¹¹

Two other forms exist and are worth distinguishing. Congenital lactase deficiency is a rare genetic condition — about 1 in 60,000 newborns, concentrated in Finland — causing severe diarrhea from birth.¹¹ Secondary lactose intolerance is temporary, following damage to the intestinal lining from gastroenteritis, Crohn’s disease or untreated celiac disease. That last one links this section to the next one, and it is a common reason people think they are lactose intolerant when the real problem is something else.

Gluten sensitivity: real symptoms, contested label

Non-celiac gluten sensitivity is a diagnosis of exclusion. There is no biomarker and no validated test — it is defined as celiac-like symptoms triggered by gluten in someone who does not have celiac disease or wheat allergy.

When it has been tested blind, the results have not been kind to the name. In a randomized double-blind placebo-controlled crossover trial, 59 people on self-instituted gluten-free diets, with celiac excluded, were given concealed muesli bars containing gluten, fructans, or placebo. Fructans produced significantly worse symptoms than placebo. Gluten did not differ from placebo.¹² An earlier crossover trial had already found no gluten-specific effect once background FODMAPs were reduced.¹³

Fructans are a FODMAP carbohydrate, and wheat happens to be one of the largest sources of them in the Western diet. So people who feel better off wheat are frequently right about the food and wrong about the molecule.

Histamine, sulfites, dyes and caffeine

Histamine intolerance is widely discussed and poorly established. In a placebo-controlled histamine challenge study of 59 people with suspected histamine intolerance, 63% reacted to placebo, and the diagnosis was ultimately excluded in 85% of them. The authors also found that serum DAO (diamine oxidase) testing — the test most often sold for this — "is not specific enough for diagnosis."¹⁴

Histamine in food is a genuine phenomenon, though. Biogenic amine content ranges from under 20 mg/kg in most beverages, fermented vegetables and soy products up to several hundred mg/kg in some aged cheeses and fermented sausages.¹⁵ The gap between "this food contains histamine" and "I have histamine intolerance" is where the evidence runs out.

Sulfites are real and specific. Used as preservatives in wine, dried fruit and some processed foods, they can trigger bronchoconstriction in a minority of asthmatics — the best estimate is under 3.9% of asthmatic patients, with steroid-dependent asthmatics at highest risk.¹⁶ Reactions in people without asthma are rare. US law requires sulfites to be declared at 10 ppm or above, and FDA banned their use on raw fruits and vegetables in 1986 after deaths in sulfite-sensitive asthmatics. Note that sulfites are a declarable allergen in the EU but are not one of the nine US major food allergens.

Food dyes are having a regulatory moment, and the details matter. The 2007 Southampton trial linked certain synthetic colors to hyperactive behavior in children, which led the EU to require the warning "may have an adverse effect on activity and attention in children" on six specific colors — a labeling requirement, not a ban.¹⁷ In the US, FDA revoked authorization for FD&C Red No. 3 on 15 January 2025, with compliance deadlines of 15 January 2027 for food and 18 January 2028 for ingested drugs.¹⁸

Two precision points, because this gets garbled constantly. The Red No. 3 revocation was made under the Delaney Clause on the basis of cancer in male rats, through a hormonal mechanism specific to that species — FDA states plainly that "there is no evidence showing FD&C Red No. 3 causes cancer in humans."¹⁸ And the six further dyes announced in April 2025 are a voluntary industry phase-out, not a ban.¹⁹

Caffeine sensitivity is pharmacological, not digestive — it is about how your body processes a drug, not about failing to break down a food. Variation in the CYP1A2 gene affects how fast you clear caffeine, and variation in ADORA2A, the adenosine receptor caffeine acts on, is associated with caffeine-related anxiety and sleep disturbance.²⁰ Which is why the same espresso is unremarkable for one person and ruins the night for another.

Celiac disease is a third thing entirely

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Celiac disease does not fit in either box, and that is not a technicality.

It is not a food intolerance, because the immune system is central to it. It is not a classic food allergy, because it is not IgE-mediated and does not cause anaphylaxis. It is an autoimmune reaction to a food — the immune response damages your own intestinal tissue, not merely the gluten.

What is actually happening

Nearly everyone with celiac disease carries HLA-DQ2 (about 95%) or HLA-DQ8 (about 5%).²¹ But 30–40% of the general population carries those genes and almost none of them develop celiac disease, so the genes are necessary and nowhere near sufficient. That asymmetry is why HLA typing is used to rule out celiac rather than to diagnose it.

When gluten is eaten, an enzyme called tissue transglutaminase modifies gluten peptides in a way that makes them bind far more tightly to those HLA molecules, provoking a T-cell response. The immune system attacks the lining of the small intestine, producing villous atrophy — the flattening of the finger-like projections that do the absorbing. First-line testing is tissue transglutaminase IgA, which has better than 95% sensitivity and specificity, confirmed by duodenal biopsy.²¹

Celiac disease affects roughly 1% of the US population. In a national survey, about 83% of cases were undiagnosed.²² The only established treatment is a strict, lifelong gluten-free diet.

What untreated celiac disease does

Iron deficiency, first and hardest. The damage in celiac disease concentrates in the duodenum, which happens to be exactly where iron is absorbed. Iron deficiency anemia is present in a substantial share of adults at diagnosis, and deficiencies of folate, B12, vitamin D, calcium and zinc are also common.²³ This runs both ways — current ACG guidance lists unexplained iron deficiency anemia as a reason to test for celiac disease.²¹

Neurological problems are well documented. Gluten neuropathy is reported in 4–23% of adults with celiac disease, and gluten ataxia in 0–6% of general celiac populations, rising to 19–41% among those with neurological symptoms. Both often improve on a strict gluten-free diet, though ataxia less consistently.²⁴

Gallbladder function also turns up on complication lists, and it deserves a smaller mention than it usually gets. Celiac disease can disturb cholecystokinin signaling and slow gallbladder emptying — but the evidence base is thin and mostly predates 2005, the effect appears reversible on a gluten-free diet in most cases, and people with celiac disease do not appear more prone to actual gallbladder disease.²⁶ It is a measurable motility finding, not something to lose sleep over.

And then there is wheat allergy

Three wheat-related conditions get confused constantly, and telling them apart determines what you have to avoid:

• Wheat allergy — IgE-mediated, a true food allergy, can cause anaphylaxis. The reaction is to wheat proteins. Diagnosed by specific IgE, skin-prick testing or oral challenge.⁵
• Celiac disease — autoimmune, non-IgE, does not cause anaphylaxis. Triggered by gluten. Diagnosed by tTG-IgA plus duodenal biopsy.²¹
• Non-celiac gluten sensitivity — mechanism unknown and contested, no biomarker, diagnosed only by exclusion.¹²

The practical asymmetry: someone with a wheat allergy may be perfectly fine with barley and rye. Someone with celiac disease must avoid all three. There is also a subtype called wheat-dependent exercise-induced anaphylaxis, where a reaction only occurs when wheat is eaten close to exercise, alcohol or NSAIDs — a food allergy that is invisible on ordinary days.

Living with it

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• Get a diagnosis before you eliminate. This is the single most useful thing on this list. Self-diagnosis leads to unnecessarily narrow diets, and in celiac disease it actively destroys your ability to be tested.
• Read labels, and re-read familiar ones. Formulations change, and the sesame requirement is recent enough that some products you have eaten for years now declare it. Sesame has to be listed by name.⁷
• Know that "may contain" is voluntary. Precautionary allergen labeling is not regulated the way ingredient declarations are, and its absence is not a guarantee.
• Carry epinephrine if you have been prescribed it, and carry two. Given that only a quarter of allergic adults have a current prescription, the more common failure is not having it at all.¹
• Dose matters for intolerance, not for allergy. Many people with lactose intolerance handle small amounts, hard cheeses and yogurt without trouble. Do not apply that logic to an allergy.
• Watch for the secondary case. If a new intolerance appears out of nowhere, especially lactose, it can be a downstream sign of something else going on in the small intestine.¹¹
• Use the patient organizations. For celiac disease in particular, the Celiac Disease Foundation is a solid starting point for practical, day-to-day support — the kind of information a guideline document is not written to give you.³⁰

Where Flourish fits — and where it does not

Flourish is not a treatment for food allergy, food intolerance or celiac disease. Starting there, because it is the only claim that matters in an article on this subject.

The research is clear on the point. In the best direct test — a randomized trial of peanut oral immunotherapy given with or without an added probiotic in children — the immunotherapy did the work and the probiotic added nothing to efficacy: 46% sustained unresponsiveness with the probiotic, 51% without it, a difference that was not statistically significant.²⁷ The World Allergy Organization’s prevention guidelines make conditional, very-low-certainty recommendations for eczema, and list food allergy as an open research question rather than a supported use.²⁸ For celiac disease, a meta-analysis of six trials found a symptom signal on one scale that did not hold up across combined scales, with the authors noting their confidence was limited by the low quality of the evidence.²⁹ Probiotics do not restore villi, reverse the autoimmune process, or make gluten safe.

What Flourish can tell you is what is not in the bottle. It is made in a facility dedicated to probiotic production, and incoming ingredients go to an independent third-party lab that confirms they are free of peanuts, tree nuts, dairy, eggs, soy, gluten, shellfish, carrageenan, glyphosate, artificial colors, GMOs and artificial sweeteners. That is the panel we test against, and it is the list we state. Third-party testing has also reported histamine as undetectable in our formulations.

The short version

• Allergy = immune system. Can be life-threatening. Epinephrine, not antihistamines.
• Intolerance = no immune system involved. Uncomfortable, dose-dependent, not dangerous.
• Celiac disease = autoimmune. Neither of the above. Strict lifelong gluten-free diet, and get tested before you quit gluten.
• Wheat allergy = a fourth thing, and a real IgE allergy.
• Nine major allergens in the US, not eight. Sesame joined in 2023.

If you react to food, the label you give it determines the test you get, the diet you follow, and whether you need to carry epinephrine. It is worth getting right.

Important information

This article is for general education and is not a substitute for professional medical advice, diagnosis, or treatment. Food allergy, celiac disease and anaphylaxis are medical conditions requiring diagnosis and management by a qualified clinician — always seek the advice of your physician or another qualified health provider, and never delay or discontinue prescribed treatment based on what you read here. If you have been prescribed epinephrine, carry it and use it as directed. Guideline recommendations are summarized here in brief; the linked documents carry the full wording and the strength of each recommendation. Probiotic effects are specific to the strain, the dose and the population studied, and evidence for one product does not transfer to another. These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease.

Sources

1. Gupta, R. S., Warren, C. M., Smith, B. M., Jiang, J., Blumenstock, J. A., Davis, M. M., Schleimer, R. P., & Nadeau, K. C. (2019). Prevalence and severity of food allergies among US adults. JAMA Network Open, 2(1), e185630 — n=40,443; 10.8% convincing food allergy, 19.0% self-reported, 51.1% with a severe reaction, 24.0% with a current epinephrine prescription. Source
2. Gupta, R. S., Warren, C. M., Smith, B. M., Blumenstock, J. A., Jiang, J., Davis, M. M., & Nadeau, K. C. (2018). The public health impact of parent-reported childhood food allergies in the United States. Pediatrics, 142(6), e20181235 — n=38,408; 7.6% convincing food allergy, 42.3% with severe-allergy symptoms, 40.7% with a current auto-injector prescription. Source
3. National Center for Health Statistics, Centers for Disease Control and Prevention. Almost a Third of U.S. Adults and Children Have at Least One Allergy (8 January 2026) — NHIS 2024; diagnosed food allergy in 6.7% of adults and 5.3% of children. Source
4. Zopf, Y., Baenkler, H.-W., Silbermann, A., Hahn, E. G., & Raithel, M. (2009). The differential diagnosis of food intolerance. Deutsches Ärzteblatt International, 106(21), 359–370 (PMID 19547751) — the four-mechanism classification of non-immunological food intolerance. Figures in this paper describe industrialized countries and the German population. Source
5. Boyce, J. A., Assa’ad, A., Burks, A. W., et al. (2010). Guidelines for the diagnosis and management of food allergy in the United States: summary of the NIAID-sponsored expert panel report. Journal of Allergy and Clinical Immunology, 126(6), 1105–1118. Source
6. Cardona, V., Ansotegui, I. J., Ebisawa, M., et al. (2020). World Allergy Organization anaphylaxis guidance 2020. World Allergy Organization Journal, 13(10), 100472 — diagnostic criteria including severe gastrointestinal symptoms and presentations without skin involvement; intramuscular epinephrine as first-line. Source
7. U.S. Food and Drug Administration. Food Allergies — the nine major food allergens; the FASTER Act declaring sesame the 9th; and the FALCPA-era "90 percent" wording in its original past-tense framing. Source
8. Food Allergy Safety, Treatment, Education, and Research (FASTER) Act of 2021, S.578, 117th Congress, Public Law 117-11 — signed 23 April 2021; sesame labeling effective 1 January 2023. Source
9. U.S. Department of Agriculture, Food Safety and Inspection Service. Food Allergies: The "Big 9". See also School Nutrition Association, Major Allergens: The Big Nine. Source
10. Regulation (EU) No 1169/2011, Annex II — the 14 allergens requiring declaration in the European Union, adding celery, mustard, lupin, molluscs and sulphites to the US list. Source
11. MedlinePlus Genetics, U.S. National Library of Medicine. Lactose intolerance — approximately 65% of the human population has reduced lactase after infancy; LCT/MCM6 genetics; congenital lactase deficiency; secondary lactose intolerance. Source
12. Skodje, G. I., Sarna, V. K., Minelle, I. H., et al. (2018). Fructan, rather than gluten, induces symptoms in patients with self-reported non-celiac gluten sensitivity. Gastroenterology, 154(3), 529–539 — randomized double-blind placebo-controlled crossover, n=59; fructans worsened symptoms, gluten did not differ from placebo. Source
13. Biesiekierski, J. R., Peters, S. L., Newnham, E. D., Rosella, O., Muir, J. G., & Gibson, P. R. (2013). No effects of gluten in patients with self-reported non-celiac gluten sensitivity after dietary reduction of fermentable, poorly absorbed, short-chain carbohydrates. Gastroenterology, 145(2), 320–328. Source
14. Bent, R. K., Kugler, C., Faihs, V., Darsow, U., Biedermann, T., & Brockow, K. (2023). Placebo-controlled histamine challenge disproves suspicion of histamine intolerance. Journal of Allergy and Clinical Immunology: In Practice, 11(12), 3724–3731 — n=59; 62.7% reacted to placebo; histamine intolerance excluded in 84.7%; serum DAO not specific enough for diagnosis. Source
15. Barbieri, F., Montanari, C., Gardini, F., & Tabanelli, G. (2019). Biogenic amine production by lactic acid bacteria: a review. Foods, 8(1), 17 — biogenic amine content by food category; decarboxylase activity is strain-specific rather than species- or genus-specific. Source
16. Bush, R. K., Taylor, S. L., Holden, K., Nordlee, J. A., & Busse, W. W. (1986). Prevalence of sensitivity to sulfiting agents in asthmatic patients. American Journal of Medicine, 81(5), 816–820 — best estimate 3.9% of asthmatic patients studied, less than that in the asthmatic population as a whole. Source
17. McCann, D., Barrett, A., Cooper, A., et al. (2007). Food additives and hyperactive behaviour in 3-year-old and 8/9-year-old children in the community: a randomised, double-blinded, placebo-controlled trial. The Lancet, 370(9598), 1560–1567 — the basis for the EU warning-label requirement under Regulation (EC) No 1333/2008, Annex V. Source
18. U.S. Food and Drug Administration. FD&C Red No. 3 — authorization revoked 15 January 2025 under the Delaney Clause; compliance 15 January 2027 (food) and 18 January 2028 (ingested drugs); "there is no evidence showing FD&C Red No. 3 causes cancer in humans." Source
19. Covington & Burling LLP (22 April 2025). FDA Announces Steps to Phase Out Synthetic Color Additives — revocation of Citrus Red No. 2 and Orange B, and a voluntary industry phase-out of six further dyes by end of 2026. Source
20. Kapellou, A., King, A., Graham, C. A. M., Pilic, L., & Mavrommatis, Y. (2023). Genetics of caffeine and brain-related outcomes: a systematic review of observational studies and randomized trials. Nutrition Reviews, 81(12), 1571–1598 — CYP1A2 and ADORA2A variation. Source
21. Rubio-Tapia, A., Hill, I. D., Semrad, C., Kelly, C. P., Greer, K. B., Limketkai, B. N., & Lebwohl, B. (2023). American College of Gastroenterology guidelines update: diagnosis and management of celiac disease. American Journal of Gastroenterology, 118(1), 59–76. Source
22. Rubio-Tapia, A., Ludvigsson, J. F., Brantner, T. L., Murray, J. A., & Everhart, J. E. (2012). The prevalence of celiac disease in the United States. American Journal of Gastroenterology, 107(10), 1538–1544 — NHANES 2009–2010; 0.71% prevalence, and most cases undiagnosed. Source
23. Montoro-Huguet, M. A., Santolaria-Piedrafita, S., Cañamares-Orbis, P., & García-Erce, J. A. (2021). Iron deficiency in celiac disease: prevalence, health impact, and clinical management. Nutrients, 13(10), 3437 — the duodenum is both the site of maximal mucosal damage and the site of maximal iron absorption. Source
24. Mearns, E. S., Taylor, A., Thomas Craig, K. J., et al. (2019). Neurological manifestations of neuropathy and ataxia in celiac disease: a systematic review. Nutrients, 11(2), 380 — gluten neuropathy in 4–23% of adults; gluten ataxia in 0–6% of general celiac populations. Source
25. Elfström, P., Sundström, J., & Ludvigsson, J. F. (2014). Systematic review with meta-analysis: associations between coeliac disease and type 1 diabetes. Alimentary Pharmacology & Therapeutics, 40(10), 1123–1132 — shared HLA-DQ2/DQ8 risk; approximately 6% of people with type 1 diabetes have celiac disease. Source
26. Poddighe, D., Dossybayeva, K., Abdukhakimova, D., Akhmaltdinova, L., & Ibrayeva, A. (2022). Celiac disease and gallbladder: pathophysiological aspects and clinical issues. Nutrients, 14(20), 4379 — cholecystokinin-related dysmotility, reversible on a gluten-free diet in most cases; no clear predisposition to gallbladder complications. Source
27. Loke, P., Orsini, F., Lozinsky, A. C., et al. (2022). Probiotic peanut oral immunotherapy versus oral immunotherapy and placebo in children with peanut allergy in Australia (PPOIT-003): a multicentre, randomised, phase 2b trial. Lancet Child & Adolescent Health, 6(3), 171–184 — 46% versus 51% sustained unresponsiveness; "addition of a probiotic did not improve efficacy of OIT." Source
28. Fiocchi, A., Pawankar, R., Cuello-Garcia, C., et al. (2015). World Allergy Organization–McMaster University guidelines for allergic disease prevention (GLAD-P): probiotics. World Allergy Organization Journal, 8(1), 4 — conditional recommendations on very low quality evidence, for eczema; food allergy listed as a research priority. Source
29. Seiler, C. L., Kiflen, M., Stefanolo, J. P., et al. (2020). Probiotics for celiac disease: a systematic review and meta-analysis of randomized controlled trials. American Journal of Gastroenterology, 115(10), 1584–1595 — six trials, 279 participants; no significant difference across combined symptom scales; authors note low quality of evidence. Source
30. Celiac Disease Foundation. What is Celiac Disease? — a practical patient resource. Mechanism, prevalence and comorbidity statements above are sourced to the ACG guideline and the primary literature. Source

A note on sources. Prevalence figures for the United States come from the national survey data at references 1 to 3; Zopf 2009 (reference 4) is a German paper and is used here for its classification of food intolerance rather than for US prevalence. A widely circulated 2017 global estimate of lactose malabsorption was retracted in December 2024 and has been avoided; the figures above come from the NIH instead.