Food Sensitivity Testing: IgG, MRT, and the Elimination Diet

Three Different Animals

The language around food reactions is imprecise in popular culture, and that imprecision kills clinical accuracy. There are three fundamentally different mechanisms at work, and conflating them leads to misdiagnosis, unnecessary restriction, and missed root causes.

Food allergy (IgE-mediated): Immediate hypersensitivity. Minutes to two hours. The immune system produces IgE antibodies against a food protein. Mast cells degranulate. Histamine floods the system. Hives, throat swelling, anaphylaxis. Peanut allergy, shellfish allergy, tree nut allergy — these are IgE reactions. Tested by skin prick or serum specific IgE. This is not what we are discussing here.

Food sensitivity (IgG/IgA-mediated and cell-mediated): Delayed hypersensitivity. Twenty-four to seventy-two hours after ingestion. The immune system mounts a slower, subtler response — IgG and IgA antibody complexes, complement activation, cytokine cascading. Symptoms are diffuse and chronic: headaches, fatigue, joint pain, brain fog, skin eruptions, mood changes, sinus congestion, bloating. Because the reaction is delayed, patients almost never connect the food to the symptom. They ate the eggs on Tuesday and the migraine arrives on Thursday.

Food intolerance (enzyme deficiency): No immune involvement. The body lacks an enzyme to digest a food component. Lactose intolerance (lactase deficiency), fructose malabsorption (GLUT5 transporter issue), and histamine intolerance (DAO enzyme deficiency) are the primary examples. Testing: hydrogen breath test (lactose, fructose), serum DAO level (histamine intolerance).

In the IFM Matrix, food reactions sit at the intersection of the Assimilation and Immune/Inflammation nodes. Chronic food sensitivity drives intestinal permeability (leaky gut), systemic inflammation, and immune dysregulation — creating a self-perpetuating cycle where gut damage increases reactivity, and increased reactivity damages the gut further.

IgG Food Panels

What They Measure

IgG food sensitivity panels test serum IgG antibody levels against a panel of food proteins — typically 96 to 190 or more foods. The patient draws blood (or in some panels, a finger prick), and the lab quantifies IgG response to each food. Results are reported as a heat map: green (low/no reactivity), yellow (moderate), red (high).

Major companies include US BioTek, Genova Diagnostics, and Cyrex Laboratories (Array 10). Each uses slightly different methodology and food panels.

The Controversy

IgG food sensitivity testing is the most debated topic in functional medicine diagnostics. The criticism: IgG antibodies to food may simply represent exposure, not pathology. You eat wheat every day — of course you have IgG antibodies to wheat. The American Academy of Allergy, Asthma, and Immunology (AAAAI) has formally stated that IgG testing should not be used for food allergy diagnosis.

The counterargument from functional medicine: IgG4 may represent tolerance, but IgG1, IgG2, and IgG3 subclasses activate complement and drive inflammation. The clinical evidence, while imperfect, shows that elimination diets guided by IgG panels produce symptomatic improvement in IBS, migraine, and eczema in multiple studies. The Bentz 2010 study in Gut showed that IgG4-guided elimination improved symptoms in Crohn’s disease patients.

The practical approach: use IgG panels as a guide, not a gospel. High IgG to a food that correlates with a patient’s symptoms is actionable. High IgG to a food the patient eats daily with no symptoms may represent exposure. Always confirm with elimination and reintroduction.

Cyrex Array 10

Cyrex brings sophistication to IgG testing. Array 10 tests reactivity to both raw and cooked food proteins — critical because cooking denatures proteins, changing their immunogenic profile. A patient may tolerate raw tomato but react to cooked tomato (or vice versa). Array 10 also tests food additives, gums (xanthan, carrageenan, guar), lectins, and artificial colorings.

Cyrex Array 4: Gluten Cross-Reactivity

A patient goes gluten-free and still feels terrible. Why? Molecular mimicry. Certain food proteins share amino acid sequences with gluten peptides — the immune system mistakes them for gluten and attacks.

Cyrex Array 4 tests for these cross-reactive foods: dairy proteins (casein, whey, milk butyrophilin), oats (even certified gluten-free), yeast, coffee (instant and regular), chocolate, corn, rice, potato, soy, millet, hemp, amaranth, quinoa, tapioca, teff, and sorghum. This test explains why some celiac and non-celiac gluten sensitivity patients plateau on a standard gluten-free diet — they are cross-reacting to their replacement foods.

MRT: Mediator Release Test

The MRT, developed by Oxford Biomedical, takes a fundamentally different approach. Instead of measuring antibodies, it measures the end result of all immune-mediated food reactions: mediator release.

When white blood cells encounter a reactive food antigen, they release inflammatory mediators — histamine, cytokines, prostaglandins, leukotrienes. The MRT measures the change in cell volume that occurs when these mediators are released. A large volume change indicates significant mediator release — the cells are reacting strongly.

This approach captures all pathways of food sensitivity — IgG-mediated, IgA-mediated, complement-mediated, T-cell-mediated, and cell-mediated reactions that IgG testing misses entirely. The MRT panel tests 170 items including foods, food chemicals (MSG, tyramine, solanine, capsaicin), artificial sweeteners (aspartame, sucralose), food dyes (FD&C Yellow #5, Red #40), and preservatives (sodium benzoate, BHA, BHT, sulfites).

The MRT is paired with the LEAP protocol (Lifestyle, Eating, And Performance) — a structured elimination and reintroduction program designed by certified LEAP therapists. Phase 1 eliminates all reactive and moderately reactive items, building meals from the lowest-reactive foods. Phases 2 and 3 systematically reintroduce items and expand the diet.

Many functional medicine clinicians consider the MRT the most clinically useful food sensitivity test available. Its limitation is cost and the requirement for a trained LEAP therapist to properly interpret and implement results.

The Alcat Test

The Alcat Test measures leukocyte cellular reactivity — a concept similar to the MRT (changes in white blood cell size and volume upon food antigen exposure). It tests up to 450 items. The Alcat has less published research supporting its clinical utility compared to the MRT, and reproducibility studies have shown variable results. Some clinicians use it; most functional medicine practitioners prefer MRT or IgG panels.

The IFM Elimination Diet: The Gold Standard

No test replaces the elimination diet. It remains the most reliable method for identifying food sensitivities because it tests the entire organism — not just one immune pathway in a lab.

Phase 1: Removal (21-28 Days)

Remove completely: gluten (all sources — wheat, barley, rye, spelt, kamut, triticale, and hidden sources in sauces, dressings, processed foods), dairy (all forms — milk, cheese, yogurt, butter, whey, casein), eggs, corn, soy, peanuts, refined sugar, alcohol, caffeine, processed and packaged foods.

Optional additional removals for more sensitive patients or autoimmune presentations: nightshades (tomatoes, peppers, eggplant, white potatoes), citrus, tree nuts, shellfish, and beef.

Eat freely: all vegetables (excluding nightshades if removed), rice, quinoa, millet, buckwheat, sweet potatoes, quality meats (chicken, turkey, lamb, wild game), wild-caught fish (salmon, cod, sardines), all fruits, nuts and seeds (except peanuts), olive oil, coconut oil, avocado, ghee (if tolerating), herbs and fresh spices, herbal teas.

Twenty-one days is the minimum. Antibodies have a half-life of approximately 21 days — it takes this long for immune complexes to clear and inflammation to settle. Twenty-eight days is preferred. Many patients report that their symptoms do not fully resolve until days 18-24, only to experience dramatic improvement in the final week.

Phase 2: Reintroduction (Methodical, Patient)

This is where clinical rigor matters. One food group every three to five days. On Day 1 of reintroduction, eat two to three generous servings of the test food. Then remove it again and monitor for 72 hours.

Reactions to track: digestive symptoms (bloating, gas, diarrhea, constipation, pain), energy level, mood and cognition (brain fog, irritability, anxiety, depression), pain (joint pain, headache, migraine, muscle aches), skin (acne, eczema flares, hives, rashes), sleep quality, nasal congestion or sinus symptoms, and heart rate (resting pulse increase of 10+ BPM after eating can indicate reactivity).

If any reaction occurs: remove that food for a minimum of three months, then retry. If no reaction: that food is cleared. Add it back to the diet and move to the next food group.

Recommended reintroduction order: start with the foods most likely to be tolerated (rice, legumes, citrus, eggs), then progress to the more common triggers (dairy, gluten, soy, corn). This builds confidence and expands the diet early while saving the most reactive foods for last.

The Symptom Tracking Journal

Daily ratings on a 1-10 scale for: energy, digestion, mood, pain, sleep quality, brain fog, and skin clarity. This creates an objective record that reveals patterns invisible to memory alone. A patient may not connect Friday’s joint pain to Wednesday’s reintroduction of dairy without the journal.

Histamine Intolerance: The Special Case

Histamine intolerance is not a food sensitivity — it is a processing deficiency. Diamine oxidase (DAO) is the enzyme that breaks down histamine in the gut. When DAO is deficient, histamine from food accumulates in the bloodstream.

Symptoms

The symptom picture is remarkably broad: headaches and migraines (histamine is vasodilatory), hives and flushing, nasal congestion and runny nose, rapid heart rate and palpitations, anxiety and panic (histamine is excitatory in the brain), GI symptoms (abdominal pain, diarrhea, nausea), menstrual irregularity (estrogen stimulates histamine release, histamine stimulates estrogen — a bidirectional amplification loop that explains premenstrual migraines), and hypotension or dizziness.

Testing

Serum DAO level: below 10 U/mL suggests deficiency. Whole blood histamine: elevated levels confirm histamine excess. The OAT does not directly test histamine, but elevated markers of gut dysbiosis on the OAT may indicate a histamine-producing microbiome.

High-Histamine Foods

Fermented foods top the list: sauerkraut, kimchi, kombucha, wine (especially red), beer, aged cheese, vinegar, soy sauce, miso. Also: cured and smoked meats (salami, bacon, smoked fish), canned fish (histamine accumulates in improperly stored fish — fresh is far lower), spinach, avocado, eggplant, tomatoes, and leftovers. Histamine in food increases with time and temperature — a freshly cooked chicken breast has minimal histamine, but the same chicken breast reheated after two days in the fridge has substantially more.

Histamine liberators (trigger mast cells to release endogenous histamine even though the food itself is not high in histamine): citrus fruits, strawberries, pineapple, papaya, chocolate, alcohol, egg whites, and shellfish.

Treatment Protocol

DAO enzyme supplements: Take before histamine-containing meals. Brands like Seeking Health (Histamine Block) and Ancestral Supplements (kidney-derived DAO) provide exogenous enzyme support.

Quercetin: 500mg twice daily. A natural mast cell stabilizer — inhibits histamine release from mast cells. Works synergistically with vitamin C.

Vitamin C: 1-2g daily. Degrades histamine enzymatically and supports DAO production.

B6 as P5P: 50mg daily. Cofactor for DAO synthesis.

Low-histamine diet: Strict for 4-6 weeks, then gradual reintroduction. Cook fresh, eat fresh, freeze leftovers immediately.

Address the root cause: Histamine intolerance is often secondary to SIBO (histamine-producing bacteria in the small intestine), gut dysbiosis (certain bacteria — Morganella, Klebsiella, Citrobacter — produce histamine), impaired methylation (HNMT enzyme methylates histamine intracellularly — requires SAMe), or hormonal imbalance (estrogen dominance amplifies histamine).

Treating histamine intolerance without addressing the underlying gut or methylation dysfunction is symptomatic management. The DAO supplements and low-histamine diet buy time and relief while you find and fix the root.

Integrating Testing with Clinical Practice

The optimal approach combines testing with elimination. Run an MRT or IgG panel to identify likely reactive foods. Use those results to design a targeted elimination diet — removing the identified reactives plus the standard IFM elimination foods. This gives you the speed of testing (you know what to remove on day one) with the reliability of elimination (you confirm the reactions with real-world exposure).

After three to six months of avoidance and gut healing (5R protocol: Remove, Replace, Reinoculate, Repair, Rebalance), many food sensitivities resolve. The reactivity was driven by intestinal permeability, not a permanent immune defect. Heal the gut, fix the permeability, and the immune system stops overreacting to food proteins. Retest or reintroduce to confirm — a food that triggered IgG antibodies six months ago may now be tolerated.

This is the IFM approach in action. Do not just identify sensitivities — ask why the sensitivities exist. Fix the terrain, and the reactivity resolves.