Sensitivity Categories
Overview
Foods are classified into sensitivity categories based on their chemical content. A food can belong to multiple categories with different severity levels (low/medium/high). This classification powers the hypothesis engine and informs meal plan design.
For the biochemistry underlying these categories, see the Mast Cell Education wiki — particularly Dietary Histamine, Histamine Liberators, Salicylates, and Oxalates.
The Categories
Histamine
Mechanism: Histamine is a biogenic amine involved in immune function, neurotransmission, and digestion. Intolerance arises either from excess dietary histamine or deficiency of the DAO (diamine oxidase) enzyme that breaks it down. See Histamine Intolerance for the full mechanism. Symptoms are systemic — skin flushing, hives, headache, nasal congestion, heart palpitations, GI distress.
Key foods:
- Fermented foods (wine, beer, vinegar, sauerkraut, kimchi, kombucha, sourdough)
- Aged cheeses
- Cured and smoked meats
- Leftover meat (histamine rises with storage time)
- Shellfish and certain fish (especially canned, smoked, or not fresh)
- Avocado, spinach, eggplant, tomatoes
- Alcohol (also blocks DAO)
Histamine liberators — foods that trigger histamine release even if low in histamine themselves:
- Citrus fruits, strawberries, papaya
- Tomatoes, spinach
- Chocolate, nuts, wheat germ
DAO blockers — impair histamine breakdown:
- Alcohol, black tea, green tea, energy drinks
Clinical note: DAO enzyme level testing exists (blood test, see DAO Serum Levels). Low DAO = histamine intolerance is highly probable. This is one of the lab integration targets.
Symptom signature: Systemic — skin, respiratory, cardiovascular, neurological. Distinguished from FODMAP by lack of pure GI dominance. See Symptom Mapping for the mediator-to-symptom biochemistry.
Temporal profile: Onset within 15-60 minutes of ingestion. Peak at 1-2 hours. Resolution within 4-12 hours for most people. A biphasic pattern is possible — see late-phase response.
FODMAPs
Mechanism: Fermentable Oligosaccharides, Disaccharides, Monosaccharides and Polyols — short-chain carbohydrates poorly absorbed in the small intestine. In sensitive individuals (especially IBS), they ferment rapidly in the large intestine producing gas and drawing water osmotically, causing bloating, cramping, and altered motility.
Subcategories:
| FODMAP type | Examples |
|---|---|
| Fructans (O) | Wheat, onion, garlic, leek, asparagus |
| GOS (O) | Legumes, chickpeas, lentils |
| Lactose (D) | Milk, soft cheeses, yogurt |
| Fructose (M) | Honey, high-fructose corn syrup, some fruits |
| Polyols (P) | Sorbitol (stone fruits, apples), mannitol (mushrooms, cauliflower) |
Important: Not all FODMAPs trigger all FODMAP-sensitive people. Identifying the specific subtype matters. The reintroduction protocol should test each subcategory separately.
Symptom signature: Predominantly gut — bloating, cramping, diarrhea/constipation, flatulence. Fatigue and reflux can occur. Unlikely to cause systemic symptoms (skin, respiratory) without gut symptoms.
Temporal profile: Onset 2-6 hours (dependent on transit time to colon). Peak at 6-24 hours. Resolution within 24-48 hours.
Salicylates
Mechanism: Naturally occurring in many plants as a defense compound. Sensitivity (not allergy) causes dose-dependent symptoms via arachidonic acid pathway interference — salicylates inhibit COX enzymes, shunting more substrate toward leukotriene production. Often missed because the foods involved seem “healthy” — fruits, vegetables, spices.
Key foods (high salicylate):
- Most spices (especially mint, oregano, thyme, cumin, paprika)
- Many fruits (berries, grapes, stone fruits, citrus)
- Some vegetables (tomatoes, peppers, cucumbers)
- Tea, coffee, wine
- Almonds, peanuts
- Honey, jam
Low salicylate foods (safe):
- Pears, bananas, papaya, mango
- Cabbage, Brussels sprouts, leeks, celery
- Most meats, fish, eggs, dairy
- Rice, oats, most legumes
Clinical note: Aspirin sensitivity is a marker for salicylate intolerance — aspirin is acetylsalicylic acid. If someone reacts to aspirin or NSAIDs, salicylate testing is high priority.
Symptom signature: Overlaps with histamine — skin (urticaria, eczema), respiratory (asthma, nasal polyps), headaches. GI symptoms also occur. The overlap with histamine makes differential testing important.
Temporal profile: Onset 2-6 hours. Effects can persist 24-72 hours due to COX enzyme kinetics and downstream leukotriene-mediated inflammation.
Cross-category note: Many high-salicylate foods are also high-histamine (wine, citrus, tomatoes). This is why the hypothesis engine checks across categories when multiple suspects share overlap.
Oxalates
Mechanism: Oxalic acid binds minerals (calcium, magnesium) forming oxalate crystals. In sensitive individuals, high oxalate intake causes GI symptoms, joint pain, kidney stones, and potentially neurological symptoms. The proposed connection to mast cell activation is through mechanical crystal irritation of tissue-resident mast cells — see Oxalates for the honest evidence assessment. Common in popular “clean eating” foods — people don’t suspect them.
Key foods (high oxalate):
- Spinach (very high — 600-750mg/100g)
- Swiss chard, beet greens
- Nuts (especially almonds, cashews, peanuts)
- Chocolate and cocoa
- Beets
- Certain grains (wheat bran, quinoa)
- Tea (black and green)
Low oxalate alternatives:
- Kale (surprisingly low)
- Bok choy, broccoli, cabbage
- Most animal proteins
- Rice, corn, oats
Clinical note: 24-hour urine oxalate testing exists. Elevated urinary oxalate = hyperoxaluria, a measurable marker. Lab integration target.
Symptom signature: Joint pain, kidney pain, fatigue, GI symptoms, urinary symptoms. Less systemic than histamine, less purely GI than FODMAP.
Temporal profile: Highly variable. Acute GI symptoms within hours. Crystal deposition effects are cumulative over days-weeks and don’t map well to individual meals — this makes oxalate harder to test with the single-exposure model.
Lectins
Mechanism: Plant proteins that bind to carbohydrates. In susceptible individuals (particularly autoimmune presentations), lectins may increase intestinal permeability, trigger immune responses, and interfere with nutrient absorption.
Controversy note: The evidence for lectin sensitivity in the general population is weaker than for histamine, FODMAP, or salicylate sensitivity. However, in autoimmune and MCAS-adjacent populations, clinical reports are consistent enough to warrant testing.
Key foods:
- Legumes (beans, lentils, peanuts, soy) — especially raw or undercooked
- Grains (wheat, corn, rice — especially in the bran)
- Nightshades (tomatoes, peppers, eggplant, potatoes)
- Dairy (A1 casein specifically, not all dairy)
Mitigation: Soaking, sprouting, fermenting, and pressure cooking substantially reduce lectin content. This is why sourdough (fermented) and properly prepared legumes are often tolerated better. The app should track preparation method for lectin-category foods — a pressure-cooked bean is a fundamentally different exposure than a slow-cooked bean.
Symptom signature: GI symptoms, joint pain, fatigue, brain fog. Often delayed (12-48 hours) compared to histamine reactions. Overlap with gluten sensitivity is significant for grains.
Temporal profile: 6-48 hours onset. Peak at 12-48 hours. Resolution 24-96 hours. This long delay makes lectin reactions the hardest to attribute correctly without structured testing — the symptom appears a day or two after the exposure, by which time multiple other meals have occurred.
Glutamates
Mechanism: Glutamic acid is a naturally occurring amino acid and the primary excitatory neurotransmitter in the brain. Free glutamate in food (as opposed to protein-bound glutamate) is absorbed rapidly and can produce dose-dependent symptoms in susceptible individuals.
The MSG evidence landscape
The “Chinese Restaurant Syndrome” narrative — that MSG uniquely causes headaches and other symptoms — has been largely debunked by blinded controlled studies. When MSG is given in capsules or mixed into food without subjects knowing, most self-reported MSG-sensitive individuals cannot reliably distinguish it from placebo. However, this does NOT mean glutamate sensitivity doesn’t exist. What the research suggests is:
- The effect is dose-dependent, not binary. Large bolus doses of free glutamate (>3g on an empty stomach) can produce symptoms in some individuals.
- MSG is not unique — all sources of free glutamate (aged cheese, soy sauce, tomato paste, mushrooms) deliver the same molecule.
- The susceptible population is smaller than commonly believed but not zero.
- The mechanism may involve glutamate’s excitatory neurotransmitter role and/or peripheral effects on gut-expressed glutamate receptors.
For the app, glutamate is worth tracking as a category but should be flagged as having weaker individual-attribution evidence than histamine, FODMAP, or salicylate. The hypothesis engine should require a higher threshold (≥3 suspected foods, not 2) before generating glutamate-category suggestions.
Key foods (high free glutamate):
- MSG (monosodium glutamate, additive)
- Parmesan and aged cheeses
- Tomatoes (especially concentrated — paste, sun-dried)
- Soy sauce, fish sauce, miso
- Mushrooms (especially dried/concentrated)
- Nutritional yeast
- Anchovies, sardines
- Bone broth (long-cooked)
Symptom signature: Neurological — headaches, migraines, brain fog, flushing. Less GI than other categories.
Temporal profile: Onset 15-60 minutes. Resolution within hours. Fast onset and resolution make this category relatively easy to test if symptoms match.
Capsaicin
Mechanism: Capsaicin and related capsaicinoid compounds activate TRPV1 (transient receptor potential vanilloid 1) channels on sensory nerve endings in the gut mucosa. This triggers substance P release, which produces pain signaling and — importantly for the MCAS population — is a direct mast cell activator. This creates a nerve-mast cell-nerve feedback loop: capsaicin → nerve activation → substance P release → mast cell degranulation → mediator release → nerve sensitization.
Key foods:
- Hot chili peppers (jalapeño, serrano, habanero, cayenne) — capsaicin content roughly tracks Scoville rating
- Paprika, chili powder, hot sauce
- Bell peppers — contain capsaicinoid compounds but at much lower concentrations than hot peppers (~0.0-0.01% vs ~0.1-0.5% in jalapeños). Whether bell peppers contain enough capsaicin to trigger symptoms in sensitive individuals or whether reactions to bell peppers are driven by other mechanisms (salicylates, lectins as nightshades) is unclear.
Bell pepper attribution
Bell peppers appear on multiple category lists (capsaicin, lectin/nightshade, salicylate). If a user reacts to bell peppers, the hypothesis engine should consider all three categories rather than defaulting to capsaicin. The capsaicin content in bell peppers is genuinely low — reactions may be driven by the nightshade/lectin or salicylate pathways.
Symptom signature: GI — cramping, urgency, diarrhea, burning. Fast onset (15-60 min). Strongly dose-dependent.
Temporal profile: Onset 15-60 minutes. Resolution 2-6 hours for acute GI symptoms. TRPV1 desensitization with repeated exposure means capsaicin tolerance develops — a pattern of decreasing reactivity with consistent exposure is evidence for capsaicin as the mechanism.
Cross-Category Foods
Several common foods belong to multiple categories, making them high-priority test candidates:
| Food | Categories |
|---|---|
| Avocado | High histamine + Medium salicylate |
| Tomatoes | High histamine + High glutamate + Medium salicylate + Lectin (nightshade) |
| Spinach | High histamine + High oxalate + Medium salicylate |
| Red wine | High histamine + High salicylate + DAO blocker |
| Citrus | Histamine liberator + High salicylate |
| Almonds | High oxalate + High salicylate + Lectin |
| Chocolate | High histamine + High oxalate + High salicylate + Glutamate |
| Eggplant | High histamine + Lectin (nightshade) |
| Peppers (hot) | Capsaicin + Lectin (nightshade) + Medium salicylate |
| Bell peppers | Low capsaicin + Lectin (nightshade) + Medium salicylate |
Multi-category foods are strong signals in the hypothesis engine — if someone suspects avocado and tomatoes, the overlap in histamine AND salicylate suggests both categories warrant investigation. The total mediator load concept from mast cell biology explains why multi-category foods are more likely to trigger reactions — each category contributes to the same overflowing bucket.
Connection to Lab Testing
| Category | Lab Marker | Test Type | Evidence Quality |
|---|---|---|---|
| Histamine | DAO enzyme level | Blood | Good — low DAO correlates with HIT |
| Histamine | Plasma histamine | Blood | Poor — half-life ~1-20 min, impractical |
| Histamine | 24hr urine N-methylhistamine | Urine | Moderate — captures cumulative output |
| MCAS-related | 24hr urine 11β-PGF2α | Urine | Good — relatively mast cell-specific |
| MCAS-related | Serum tryptase | Blood | Limited for MCAS — often normal |
| MCAS-related | Nasal mast cell reactivity | Home kit (future) | Experimental |
| Oxalate | 24hr urinary oxalate | Urine | Good — directly measures oxalate burden |
IgG food antibody testing is NOT included
An earlier version of this document listed IgG food antibodies as a lab integration target. This has been removed. Food-specific IgG testing is not supported by evidence for diagnosing food allergy, intolerance, or sensitivity. Position statements from CSACI (2012), EAACI (2008), and AAAAI all recommend against it. The research consensus is that food-specific IgG reflects exposure and tolerance, not sensitivity — IgG levels rise to foods you eat regularly, including foods you tolerate perfectly well. Including IgG testing would undermine Confidente’s scientific credibility and could lead to unnecessary dietary restriction.
The app’s value proposition is structured behavioral testing (controlled exposure + symptom correlation) — which is the approach actually supported by evidence for identifying non-IgE food reactions. Lab markers that ARE useful (DAO, tryptase, urine mediators) inform the interpretation of behavioral data, not replace it.
These lab markers are lab integration targets for future versions. They complement the behavioral testing by providing biochemical context: a strong histamine-category correlation in someone with confirmed low DAO tells a clearer mechanistic story than either data point alone.