I spent six years chasing food sensitivities while navigating my own lichen sclerosus diagnosis. Six years of IgG and IgA panels, rotating eliminations, and getting nowhere. Not because I wasn't trying. Because the tests I was using were measuring the wrong thing.

That experience is what eventually pushed me toward a completely different approach - both to testing and to what food reactivity actually means in the context of autoimmune and chronic inflammatory conditions like LS. What I learned changed how I practice, and it's what this article is about.
QUICK REFERENCE
- The Problem with Most Food Sensitivity Tests
- Allergies, Sensitivities, and Intolerances - They Are Not the Same Thing
- What White Blood Cell Testing Actually Measures
- These Tests Go Beyond Food
- How I Read the Results - and Why it Matters
- The Foods that Flag Most Often - and What That Actually Tells You
- The Oxalate Conversation Needs to Expand
- Elimination Diets are Still the Gold Standard - Here is Where Testing Fits
- The Elimination Trap - and Why it is a Real Clinical Risk
- A Specific Word on Carnivore
- Your Genes Matter - a Brief Introduction to Nutrigenomics
- Sensitivities Can Shift - with the Right Work
- How to Access MRT and KBMO Testing
- FAQs
- Discussion
The Problem with Most Food Sensitivity Tests
Most people who have done food sensitivity testing have done IgG or IgA panels. These are the tests your functional medicine doctor ordered, the ones you found online, the ones that came back with a long list of foods and sent you into a months-long elimination spiral.
Here is the core problem: IgG and IgA tests measure antibody levels-specifically, whether your immune system has produced antibodies against certain foods. But the presence of antibodies does not reliably tell you whether a food is actively driving inflammation in your body right now.
Think of it this way. Your immune system produces antibodies as a record of exposure - like a filing system that logs everything you have come into contact with. IgG, in particular, is primarily a marker of exposure, not of reaction. You can test high for a food you tolerate perfectly well, and test clean on a food that is quietly loading your immune system every time you eat it.
There is another layer to this that made six years of my life significantly harder than it needed to be. When your gut lining is compromised - which is extremely common in autoimmune conditions - your immune system starts producing antibodies to whatever you are eating regularly. It does not mean those foods are the problem. It means your gut isn't doing its job of keeping food particles from entering the bloodstream in the first place. The result is an ever-shifting list of flagged foods, rotating eliminations, and no real resolution.
IgG and IgA testing are also heavily influenced by what you are currently eating. If you have already eliminated a food for several months, it may not show up on the test even if it was a significant driver of inflammation. You can get a falsely clean result and add a problematic food back in with false confidence.
Standard allergy panels - the kind an allergist runs - have an entirely different limitation. They are designed to catch true allergic responses: the immediate, histamine-driven reactions that cause hives, swelling, and anaphylaxis. That is not the same thing as the slow, low-grade immune activity that drives symptoms in conditions like LS. A clean allergy panel tells you almost nothing useful about whether food is contributing to your inflammatory load.
Allergies, Sensitivities, and Intolerances - They Are Not the Same Thing
Before going further, it is worth being clear about what these terms actually mean, because they are used interchangeably in most online spaces, and that causes real confusion.
A true food allergy is an IgE-mediated immune response. It involves mast cells, immediate histamine release, and fast-onset symptoms - sometimes severe and life-threatening. This is what an allergist tests for. It is the narrowest category and the one most people are familiar with.
A food sensitivity is a broader, delayed immune response. It involves white blood cells, cytokines (chemical signals that coordinate immune activity), and a range of inflammatory compounds beyond histamine. Reactions can take hours to days to show up, which is part of why they are so difficult to identify without testing. Sensitivities are dose-dependent - small amounts may be fine; larger or repeated exposure tips the scale - and are highly individual.
A food intolerance is a non-immune response, usually involving an enzyme deficiency or a problem with how the digestive system processes a specific compound. Lactose intolerance is the classic example: the issue is a lack of the enzyme lactase, not an immune reaction to dairy.
The critical thing to understand about food sensitivities specifically is this: they are not a root problem - they are a symptom of deeper dysfunction. When the gut barrier is compromised, when the body's stress load is high, when the immune system is chronically activated - food sensitivities are what you get. Addressing the food without addressing the underlying terrain is like mopping the floor while the pipe is still leaking. It brings some relief. It does not change the underlying picture.
What White Blood Cell Testing Actually Measures
The MRT (Mediator Release Test) and the KBMO FIT Test take fundamentally different approaches. Rather than measuring whether antibodies to a food are present, they measure white blood cell activity directly.
Here is why that matters. When your immune system reacts to a food, white blood cells release chemical compounds called mediators - cytokines, histamine, leukotrienes, and prostaglandins. These mediators are what cause your symptoms. The primary immune pathways involved in food reactivity converge on this same endpoint: mediator release. That is what these tests are measuring - the actual process, not a downstream record of it.
Because MRT and KBMO measure white blood cell activity rather than antibody levels, they are not affected by what you are currently eating. A food does not need to be in active rotation to trigger a white blood cell response. This makes them significantly more reliable as clinical tools - especially for people who are already partway through an elimination process and worried about getting inaccurate results.
The two tests differ slightly in methodology. MRT measures the physical change in white blood cells after antigen exposure - when cells release mediators, they shrink, and the test measures that change. KBMO's FIT test uses a multi-pathway approach that measures both IgG antibodies and immune complexes, improving accuracy over IgG-only testing. The FIT 132 and FIT 176 panels now include a Gut Barrier Panel that measures intestinal permeability alongside food reactivity - particularly useful for understanding how much gut compromise may be driving the sensitivity picture.
Both panels test over 170 foods and food chemicals. Which brings me to the part most people do not know.
A Note on Evidence: Research on MRT demonstrates it can distinguish between symptomatic and asymptomatic populations and that MRT-guided dietary protocols correlate with meaningful symptom reduction. Neither MRT nor KBMO has large-scale randomized trial evidence specific to LS or most autoimmune conditions - much of the validation data is manufacturer-sponsored. These tests represent a meaningfully better clinical tool than IgG/IgA panels, but they are a starting point, not a definitive diagnosis. One additional note: if you are currently using topical or systemic corticosteroids or other immunosuppressants - common in the LS population - your results may be affected by the suppressed immune response. Raise this with your practitioner before ordering.
These Tests Go Beyond Food
One of the most underappreciated features of both MRT and KBMO is that they test synthetic food chemicals directly - not just whole foods. Dyes, preservatives, flavor enhancers, stabilizers. Compounds such as FD&C Red 40, sodium benzoate, carrageenan, BHA, BHT, aspartame, titanium dioxide, and more are listed on the panels as testable items.
This matters enormously in the LS population. Carrageenan - a thickener found in dairy alternatives, canned goods, and many "clean" packaged foods - has a substantial body of research behind its capacity to drive gastrointestinal inflammation and disrupt the gut lining. It is worth knowing about regardless of your test results.
More broadly: the majority of synthetic food dyes and many common preservatives are potent histamine liberators - meaning they trigger histamine release from mast cells independent of any food protein. In my clinical experience at Soil to Soul Nutrition, histamine is the single most prevalent reactant category in people navigating LS. Many of my clients have diligently eliminated high-histamine whole foods and still not improved - because they were still consuming synthetic dyes and preservatives in packaged foods, condiments, medications, and supplements without realizing those chemicals were driving their histamine load.
If you have done everything right on paper and are still symptomatic, food chemicals are a primary suspect. Managing this requires reading labels, not just changing ingredients.
How I Read the Results - and Why it Matters
Getting better testing is only half the equation. The other half is what you do with the results.
Most practitioners look at a food-sensitivity panel and build an elimination list based on whatever is flagged. I do not work that way. When I receive MRT or KBMO results for a client at Soil to Soul Nutrition, I sort the reactive foods by irritant category before making any recommendations. This is where the clinical picture becomes genuinely useful - and where pattern-based interpretation, which requires clinical training to execute accurately, separates useful guidance from a simple elimination list.
The categories I look at include histamine, other biogenic amines, glutamates, oxalates, lectins, phytates, salicylates, tannins, trypsin inhibitors, saponins, nightshades, phytoestrogens, goitrogens, sulfur compounds, mold and mycotoxins, gluten and gliadin, copper-rich foods, FODMAPs, and food dyes and preservatives. The interactive graphic below covers each category in detail - what it is, why it triggers immune responses, and where it appears in food.
Select a category to see the mechanism, common sources, and why it matters in the context of immune reactivity. MRT and KBMO panels include food chemicals directly - not just whole foods.
When reactive foods cluster within a category, that is a pattern - and patterns tell you something a list of individual foods cannot. A cluster of peanuts, corn, dried fruit, and coffee is a mycotoxin pattern: the immune system is not reacting to those foods themselves but to the mold toxins that commonly contaminate them. Broad nightshade reactivity across tomatoes, peppers, and eggplant points to solanine and lectin burden rather than individual protein reactions. A dense cluster of histamine-containing foods alongside reactive food dyes suggests histamine is the primary driver, and that managing chemical exposure is as important as managing dietary sources.
This approach also protects against over-elimination. When you understand why a food is flagging, you can prioritize intelligently rather than removing everything reactive and ending up with a diet of five foods.
The Foods that Flag Most Often - and What That Actually Tells You
In clinical practice, the most commonly reactive foods I see across this population are dairy, gluten, soy, eggs, peanuts, tree nuts, corn, and nightshades. If you have been in the LS community for any length of time, you have probably already eliminated several of these.
Here is what matters: many people restricting these foods are still symptomatic because they are reactive to something else entirely. Someone can be completely dairy- and gluten-free and still be driving significant immune reactivity through histamine-liberating food dyes, high-oxalate intake, or a mycotoxin pattern they have never identified. The common eliminations are a reasonable starting point, but they are not the complete picture - treating them as such is a significant reason people plateau.
This is also why blanket elimination of the usual suspects without testing leaves so much clinical information on the table. You may be avoiding a food that was never your problem, while continuing to consume the actual drivers.
The Oxalate Conversation Needs to Expand
Oxalates deserve specific mention because they have become the dominant dietary narrative in the LS community, and that framing is too narrow.
Oxalates are real. They bind minerals like calcium, magnesium, iron, and zinc - meaning those minerals cannot be absorbed and used properly. In a compromised gut, oxalate crystals can drive localized tissue inflammation, including in the vulvar region. For some people, reducing oxalate load makes a meaningful difference.
But in my clinical experience, histamine is a more prevalent and significant reactant in this population than oxalates. Research has found elevated numbers of mast cells - the cells that store and release histamine - in LS tissue biopsies. Histamine receptors have been identified in vulvar tissue. The biological mechanism for histamine's role in LS symptom burden is there. The community just has not caught up to it yet.
And there are 17 other irritant categories in this article that rarely figure in the conversation. Chasing oxalates while ignoring histamine burden, lectin load, nightshade reactivity, or mycotoxin patterns is a common reason people do significant dietary work and still do not improve. The oxalate conversation is not wrong. It is just not enough.
Elimination Diets are Still the Gold Standard - Here is Where Testing Fits
A well-designed elimination diet remains the most reliable way to identify food reactivity. No test replaces it. If you have the time, support, and capacity to work through a structured elimination-and-reintroduction protocol, that remains the most direct path to understanding your individual picture.
What food sensitivity testing does is cut through the trial and error. A properly interpreted MRT or KBMO result can tell you where to focus your elimination effort rather than removing everything at once and spending months in a dietary guessing game. For people who have already done multiple rounds of elimination without resolution, testing often reveals the pattern that has been missed.
Evidence Note:Â There are currently no head-to-head randomized controlled trials comparing testing-guided versus elimination-guided approaches specifically for LS or most autoimmune conditions. The case for white blood cell testing over traditional elimination rests on mechanistic rationale and clinical observation. That is still meaningful - it is the basis of most functional medicine practice - but it is worth knowing.
The Elimination Trap - and Why it is a Real Clinical Risk
There is a problem I see consistently in clinical practice that does not get talked about enough: people who find relief on a strict elimination diet and then never leave it.
AIP (Autoimmune Protocol) is the most common example. Someone eliminates a long list of foods, symptoms improve, and they are so relieved that they stay on the elimination phase indefinitely - afraid that reintroducing any of those foods will bring symptoms back, or stuck in a cycle where every attempted reintroduction triggers a flare. The same pattern shows up with carnivore diets.
This is a problem, and not only for reasons of nutritional adequacy. When you exclude a food from your diet for an extended period without addressing the underlying terrain that made you reactive in the first place, you are at risk of losing oral tolerance to that food entirely. Your immune system, no longer regularly exposed, can mount an increasingly aggressive response on reintroduction. The prolonged elimination meant to protect you can worsen your food reactivity over time.
What drives this pattern is often not a lack of information. For many people in the LS community, years of not being believed, being dismissed by medical providers, and searching alone for answers mean that the restricted diet became the one thing they could control that seemed to work. It became evidence of agency in a situation that had offered almost none. The nervous system learns this pattern - relief from symptoms is a powerful signal - and reintroduction activates a real fear response, not just an intellectual concern. Knowing that reintroduction is important does not automatically override that.
Giving people the intellectual case for reintroduction without acknowledging the somatic experience of doing it - the physical anxiety, the anticipatory dread - is where most advice falls short. If you have been on a strict elimination diet long past its clinical usefulness and every attempt to expand your diet triggers fear, working with a practitioner who understands the behavioral and nervous system dimension of dietary change is as important as the clinical interpretation of test results.
The goal of elimination is not to find a restricted diet you can tolerate indefinitely. It is to reduce immune burden enough to stabilize your terrain while you address the deeper factors driving reactivity. Then reintroduction - done methodically, with support, one food at a time - is the path forward.
A Specific Word on Carnivore
Carnivore diets have genuine advocates in the autoimmune community, and for some people, removing all plant foods provides real relief. The reduction in lectins, oxalates, salicylates, and other plant-based irritants can meaningfully lower immune burden in the short term. That is a legitimate clinical observation.
Where carnivore can backfire - and where I see it backfire specifically in the LS population - is in the context of estrogen metabolism.
Estrogen dominance is a relevant terrain factor in LS. A fully carnivore diet is high in animal protein and fat and devoid of the fiber and phytonutrients that support the body's natural estrogen clearance process. This matters for two reasons.
First, the gut microbiome directly influences estrogen metabolism through a community of bacteria known as the estrobolome. These bacteria regulate whether used estrogens get cleared from the body or recirculated back into the bloodstream. A carnivore diet substantially alters this microbial community in ways that tend to favor recirculation over excretion.
Second: some people carry genetic variants - particularly in genes such as CYP1B1, COMT, and glucuronidation pathways - that already slow the liver's ability to process and clear estrogen. In someone with these variants, a diet that simultaneously reduces estrogen clearance through the gut and taxes the liver's detox capacity can worsen estrogen-dominant symptoms even as other inflammatory markers improve.
This is not an argument against carnivore as a short-term therapeutic tool. It is an argument for understanding your individual genetic terrain before committing to it long-term. Which brings me to nutrigenomics.
Your Genes Matter - a Brief Introduction to Nutrigenomics
Nutrigenomics is the study of how your genetic variants - small differences in your DNA - influence the way your body responds to food, nutrients, and environmental inputs. It is the difference between a general dietary recommendation and understanding why a particular food or nutrient pattern works for some people and not others.
In practical terms: knowing that you carry a variant that impairs your ability to clear sulfur compounds explains why garlic and cruciferous vegetables - universally promoted as health foods - make you feel worse. Knowing your estrogen metabolism variants changes how you think about a carnivore diet. Knowing how well your body clears histamine changes how aggressively you need to manage histamine sources in your food.
On the histamine point specifically: two enzymes are responsible for breaking down histamine in the body - DAO (diamine oxidase), which works in the gut, and HNMT (histamine N-methyltransferase), which works inside cells. Genetic variants in either can reduce your baseline capacity to clear histamine. But here is what most people miss: even with good genetics, these enzymes need specific nutrients to function - copper, B6, vitamin C, and zinc for DAO; a methyl donor called SAMe for HNMT. In a population with chronic gut dysfunction and high stress load, these nutrients are frequently depleted. This is why someone can diligently eliminate high-histamine foods and still struggle: the enzyme machinery that should be clearing histamine is not getting the raw materials it needs to work.
Nutrition Genome is the tool I use and recommend for nutrigenomic analysis. It provides actionable reporting at the SNP (gene variant) level that integrates directly with the pattern analysis I do from MRT and KBMO results. Understanding what you are currently reacting to and why your body responds the way it does gives a significantly more complete picture than either alone.
Sensitivities Can Shift - with the Right Work
One of the questions I get most often is whether food sensitivities are permanent. The answer is: it depends, and the nuance matters.
Many food sensitivities will shift and improve as terrain work progresses. Some will resolve entirely. But this is not simply a matter of following a gut-healing supplement protocol - and I want to be direct about that because the gut health industry has created the impression that leaky gut is a condition you fix with a stack of L-glutamine and probiotics.
That is not how it works in complex chronic illness.
My mentor, Dr. Nasha Winters, ND, FABNO, speaks about the importance of "removing the barrier to cure" before any protocol can take hold. That barrier is different for every person. For some, it is a chronic toxic burden - heavy metals, mold exposure, chemical accumulation. For others, it is chronic nervous system dysregulation, unresolved trauma, or survival patterns that keep the body in a state of threat response that no dietary intervention can override.
This last point matters more than most people realize. The autonomic nervous system - the part that governs whether you are in a state of safety or threat - directly controls gut lining integrity, immune signaling in the gut, and the body's capacity to tolerate and process food. A person with chronic sympathetic activation (fight-or-flight) cannot repair their gut lining, regardless of what they eat or supplement with. For many people navigating LS - particularly those who have experienced years of medical dismissal, chronic pain, or the specific shame this condition can carry - nervous system capacity is not one factor among several. It is often the primary reason dietary interventions do not land the way they should.
The foundational terrain inputs that most directly support a shift in food reactivity over time are: consistent sleep and circadian rhythm, blood sugar stabilization, reduction in toxic burden, adequate hydration (DAO enzyme activity and mucosal integrity are both hydration-dependent in ways that are consistently underestimated), stress reduction, and the nervous system work that enables the body to move out of chronic threat response. The habits have to change. The nervous system needs a reason to feel safe. The underlying contributors to allostatic load - the cumulative stress burden on the body's systems - have to be identified and addressed. Not just the foods.
Retesting after a period of meaningful terrain work - typically six months to a year of substantive change for straightforward cases, and two or more years when chronic mold exposure, heavy metal burden, or significant trauma history is part of the picture - will often show a meaningful shift. Fewer flags, lower reactivity levels, a cleaner pattern. That is information worth having. If reactivity has not shifted after genuine terrain work, that is also important information pointing to factors that have not yet been addressed.
Some sensitivities will not fully resolve regardless of terrain work. The goal is not a perfect test result. The goal is a body with enough adaptive capacity to tolerate a wider range of foods without triggering the immune system - and a diet that supports that process rather than constantly loading it.
How to Access MRT and KBMO Testing
Both tests have direct-order pathways, though both are significantly more useful with practitioner support for interpretation. Working through results without that background risks building an incomplete or incorrect elimination strategy - and in a population already managing high allostatic load, inappropriate elimination carries real cost.
MRT is licensed through Oxford Biomedical Technologies and can be ordered directly at nowleap.com or through a practitioner. The full panel of 176 foods and chemicals runs approximately $695 and is not covered by insurance, though HSA and FSA cards can be used.
KBMO FIT testing is available through practitioners and through platforms like Rupa Health. The FIT 176 is the most comprehensive panel and now includes the Gut Barrier Panel, measuring intestinal permeability alongside food reactivity. A bloodspot version is available for at-home collection.
If you are working with a practitioner trained in pattern-based interpretation - not just elimination list building - you will get significantly more clinical value from either test. The result itself is a starting point. What you do with the pattern is where the work actually happens.
Six years of elimination spirals taught me that the question was never just "which foods are the problem." It was always "what is happening in the terrain that is making so many things a problem."
The testing described in this article gives you a better map. But the map is only useful if you are willing to address the territory - the gut barrier, the toxic burden, the nervous system, the habits, the unresolved load. That is where the real shift happens. And for most people navigating LS, it is also where the most meaningful reclamation of a life not defined by a restricted list of foods becomes possible.
Living with cancer, autoimmunity, or complex chronic illness? Check out these success stories from clients who addressed the root-cause contributors that were disrupting their terrain, leaving them vulnerable to disease, and are now thriving!
FAQs
Standard IgG and IgA food sensitivity tests are not reliable tools for people with lichen sclerosus because they measure antibody exposure rather than active immune reactivity - and compromised gut integrity, which is common in autoimmune conditions, causes false positives that shift constantly. White blood cell tests such as MRT and KBMO measure the underlying inflammatory process and are significantly more clinically useful in this population.
A food allergy is an immediate IgE-mediated immune response involving histamine that can cause life-threatening reactions. A food sensitivity is a delayed immune response involving white blood cells and inflammatory mediators that can take hours or days to show up. A food intolerance is a non-immune response, typically an enzyme deficiency - lactose intolerance being the most common example. Food sensitivities are often a symptom of deeper dysfunction in the gut or immune system rather than a primary problem.
A low-oxalate diet helps some people with lichen sclerosus, but oxalates are one of nineteen irritant categories that can drive immune reactivity - not the primary driver for most people. In clinical practice, histamine is the most prevalent reactant category in the LS population, and many people who plateau on a low-oxalate approach still consume a significant histamine load from food dyes, preservatives, and other overlooked sources.
The most commonly reactive foods in the LS population include dairy, gluten, soy, eggs, peanuts, tree nuts, corn, and nightshades. However, many people who restrict these foods remain symptomatic because they are reacting to something else entirely - histamine-liberating food dyes and preservatives, mycotoxin-containing foods, or high-FODMAP foods are frequent culprits. Blanket elimination of common trigger foods without testing leaves significant clinical information on the table.
The MRT (Mediator Release Test) measures white blood cell activity in response to foods and food chemicals rather than antibody levels. Unlike IgG tests, MRT is not affected by current dietary rotation - a food does not need to be actively consumed to trigger a white blood cell response - making it more reliable for people already partway through an elimination process. MRT tests over 170 foods and food chemicals, including synthetic dyes and preservatives that standard panels do not include.
Many food sensitivities improve or resolve as underlying terrain factors are addressed, but this requires more than a gut-healing supplement protocol. Reducing toxic burden, stabilizing blood sugar, improving sleep, and - critically - supporting nervous system regulation are foundational to any shift in food reactivity. Some sensitivities will not fully resolve regardless of terrain work. The goal is to build enough adaptive capacity that the immune system is no longer chronically triggered by a wide range of foods.
AIP can provide real symptom relief for people with lichen sclerosus by reducing lectins, nightshades, and other immune irritants, but staying on the elimination phase indefinitely carries clinical risk. Extended elimination without addressing the underlying terrain that created reactivity in the first place increases the risk of losing oral tolerance - where the immune system mounts increasingly aggressive responses to foods it has not encountered in a long time. AIP is a tool, not a long-term dietary identity.
Histamine intolerance occurs when the body cannot break down histamine fast enough - typically due to reduced DAO or HNMT enzyme activity - causing symptoms ranging from itching and flushing to joint pain and brain fog. In clinical practice with LS populations, histamine is the single most prevalent food reactivity category. Synthetic food dyes and many preservatives are potent histamine liberators and are a frequently overlooked source of histamine load, even in people who believe they are already managing a low-histamine diet.
References:
- Bhattacharyya S, et al. Carrageenan-induced innate immune response is modified by enzymes that hydrolyze distinct galactosidic bonds. Gut. 2008;57(4):488-495.
- Bonaz B, et al. The vagus nerve at the interface of the microbiota-gut-brain axis. Frontiers in Neuroscience. 2018;12:49.
- GĂĽnthert AR, et al. Mast cells and lichen sclerosus: findings and clinical implications. Journal of Reproductive Medicine. 2014;59(1-2):29-34.
- Maintz L, Novak N. Histamine and histamine intolerance. American Journal of Clinical Nutrition. 2007;85(5):1185-1196.
- Plottel CS, Blaser MJ. Microbiome and malignancy. Science Translational Medicine. 2011;3(98):98ps30.
- Stapel SO, et al. Testing for IgG4 against foods is not recommended as a diagnostic tool. Allergy. 2008;63(7):793-796.
- AAAAI Board of Directors. Unproven diagnostic tests for food allergy. Journal of Allergy and Clinical Immunology. 2012;130(4):1030.





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