Why Anti-Inflammatory Foods Aren’t Anti-Inflammatory for Everyone

Search “anti-inflammatory foods” and you’ll get the same list everywhere: olive oil, blueberries, salmon, turmeric — all good. “Pro-inflammatory foods” gets you the mirror image: sugar, red meat, gluten, dairy — all bad. These lists aren’t wrong, exactly. They’re averages. And why anti-inflammatory foods don’t work for everyone comes down to one simple fact the lists leave out: your inflammatory response to a food and someone else’s response to that same food can be completely different.

After 25+ years in clinical practice and my own MRT/LEAP journey, I’ve come to see chronic, low-grade inflammation as the common thread running through nearly every chronic condition I treat — and food as one of its most powerful, most individual triggers. Here’s the research behind that, why the generic “anti-inflammatory diet” is an educated guess rather than a personalized answer, and what to do instead.

In this article: Inflammation as the root of chronic disease · Where the Dietary Inflammatory Index falls short · Why your response to food is unique · Why the labels mislead · MRT vs. IgG, IgE allergy testing, and hs-CRP · Test, don’t guess: MRT · FAQ

Inflammation Is the Shared Mechanism Behind Most Chronic Disease

Acute inflammation is protective — it’s how your body responds to a cut, an infection, an injury. The problem is chronic, low-grade inflammation: a smoldering immune response that never fully resolves. A 2025 review in Physiology describes this state as a shared mechanism strongly associated with obesity, cancer, and cardiovascular disease, and identifies a low-quality diet high in ultra-processed foods, refined sugar, and industrial fats as one of the primary drivers.

That’s not an isolated finding. A 2024 editorial in Frontiers in Medicine ties inflammation directly to cardiovascular disease, chronic kidney disease, diabetes, fatty liver disease, cancer, autoimmune conditions, and neurodegenerative and behavioral health disorders. In cardiology specifically, the American College of Cardiology’s 2025 scientific statement now treats residual inflammation — measured by hs-CRP — as a risk factor that predicts cardiac events even in patients whose cholesterol is already well controlled.

Cancer, autoimmune disease, cardiovascular disease, kidney disease, mood disorders — vastly different diagnoses, one recurring biological thread underneath. That’s why I tell clients that treating inflammation isn’t a “gut health thing” or a “heart thing.” It’s foundational.

Where the Dietary Inflammatory Index Falls Short

Most anti-inflammatory food lists are built on the Dietary Inflammatory Index (DII), a scoring system that ranks foods and nutrients by their average effect on inflammatory biomarkers like CRP, IL-6, and TNF-α across large populations. It’s a genuinely useful research tool — it’s how we know that, on average, saturated fat trends pro-inflammatory and fiber trends anti-inflammatory.

But “on average” is the operative phrase. The DII describes what a food does across thousands of people pooled together. It says nothing about what a specific food does inside your immune system. Two people can eat the same DII-friendly salad and walk away with opposite inflammatory outcomes, because the index was never built to measure individual reactivity — only population trends.

Food Is a Major Trigger — And Your Response Isn’t Like Anyone Else’s

This is where most nutrition advice quietly falls apart. The assumption baked into every “eat this, not that” list is that a food’s inflammatory effect is a fixed property of the food itself. The research says otherwise.

The PREDICT study out of King’s College London, published in Nature Medicine, tracked postprandial responses in over 1,000 healthy adults eating identical meals. The finding: inflammation triggered by the same food varied up to ten-fold between individuals. A follow-up analysis of that same cohort found that postprandial inflammatory markers were highly variable between people, and that gut microbiome diversity and visceral fat mass — not the meal’s nutrient composition alone — helped explain who reacted and who didn’t.

A 2025 review in Food & Function reinforces the same pattern across multiple studies: people eating the exact same food show markedly different glycemic, lipid, and inflammatory responses, shaped by genetics, metabolic profile, gut microbiome, circadian rhythm, and behavior. Even glucose-monitoring research designed to find reliable “good food / bad food” patterns for individuals has struggled — one study found that repeated responses to the identical meal, within the same person, are far less consistent than assumed, which is exactly why a static list can’t do the job a functional test can.

The KCL researchers put it plainly: the proportion of nutrients in a meal explains less than 25% of our response to it. Genetics, sleep, timing, stress, and — in my clinical experience, above all — individual immune reactivity to specific foods make up the rest.

Why “Anti-Inflammatory” and “Pro-Inflammatory” Labels Mislead

Here’s the distinction that almost never makes it into mainstream nutrition content: a food’s population-level anti-inflammatory reputation and its effect on your immune system are two entirely different things. Olive oil dampens inflammatory markers on average. Salmon does the same. But if your immune system has flagged either one as a trigger, the antioxidants and omega-3s inside it don’t cancel that reaction out — they’re working against the tide.

I see this constantly in my MRT food sensitivity testing work. Foods that show up on every “eat more of this” list — olive oil, legumes, sunflower oil, mustard — are reactive foods for plenty of my clients. They’re reactive foods for me. My own MRT panel flagged sunflower oil, soy, mustard, and several legumes as inflammatory triggers, foods that sit comfortably at the top of nearly every anti-inflammatory diet chart on the internet. Once I removed them, my seasonal allergies — which I’d managed for years — resolved completely.

What surprises people most is that this isn’t limited to clients who come in already unwell. Even in my otherwise healthy clients — people with no diagnosed condition, good labs, and a genuinely clean diet — I see a high rate of reactivity to foods widely considered healthy. Being fit, symptom-free, or careful about what you eat doesn’t exempt you from this; it just means the reactive foods have been hiding in plain sight, disguised as the “good” choices.

I regularly see clients test reactive to broccoli, onions, and garlic — foods practically synonymous with “anti-inflammatory” in the popular imagination — while pork, which almost never appears on an approved list and is often treated as an inflammatory villain, turns out to be one of their least reactive proteins. Rice and quinoa, two of the “safest” base foods in almost any elimination or anti-inflammatory plan, can test highly reactive too. So can ginger, turmeric, and cinnamon — the three spices that appear in nearly every anti-inflammatory food list on the internet, turmeric especially. There’s nothing wrong with the DII or the popular lists as population-level guidance; the problem is applying them to an individual without checking first, because the exceptions are common enough that they aren’t really exceptions at all.

The most common offender I see in practice is dairy — often recommended specifically for its anti-inflammatory, gut-supporting probiotic content in fermented forms like yogurt and kefir. In my clinical experience, it’s one of the most frequently reactive foods on MRT panels. My mentor, who has run this testing with clients for more than 30 years, has observed the same thing over an even longer career: dairy is consistently the single most inflammatory food she sees, probiotic reputation notwithstanding.

That’s not an argument against the Mediterranean diet or population nutrition research; that research is genuinely useful for identifying broad patterns and public health guidance. It’s an argument against applying population averages to an individual body without checking first. As I’ve written elsewhere, a diet that shows statistical significance for reducing inflammation across a study population remains an educated guess for any one person — and educated guesses are exactly what functional testing exists to replace.

How MRT Compares to IgG, IgE Allergy Testing, and hs-CRP

“Food sensitivity testing” isn’t one thing — the tests on the market measure fundamentally different biology, which is exactly why they produce different results and different reputations. Here’s how the main options actually compare.

IgE allergy testing is the gold standard for true, immediate food allergies, but it isn’t built to catch delayed food sensitivities at all. It’s also notoriously prone to false positives — one food allergy resource estimates that 50–60% of positive skin prick tests don’t reflect a true allergy. Major allergy guidance bodies are explicit that these tests should only be ordered when a person’s history already points to a specific food, because indiscriminate screening produces high sensitivity and negative predictive value but poor specificity and low positive predictive value. It answers “is this a true allergy?” — a different, narrower question than “is this food driving my chronic inflammation?”

IgG testing only captures one immune pathway (antibody production), and a growing body of allergy literature notes that elevated food-specific IgG is common and doesn’t reliably distinguish clinical reactivity from ordinary dietary exposure, which is part of why mainstream allergy guidelines don’t endorse it for diagnosing food sensitivity. It measures whether your immune system has been exposed to a food, not whether that food is triggering an inflammatory cascade.

hs-CRP is a genuinely useful marker — it’s the same one the American College of Cardiology now uses to flag residual cardiovascular risk — but it’s a thermometer, not a map. It tells you systemic inflammation is present; it can’t tell you which of the dozens of foods you eat in a week is responsible.

MRT takes a different approach entirely: rather than testing for one antibody or mechanism, it measures the actual functional endpoint — white blood cell mediator release — that all of these different immune pathways converge on. A blinded, peer-reviewed study reported 94.5% sensitivity and 91.8% specificity, figures cited widely by MRT-affiliated clinical resources; I’d note this comes from a single study rather than the large replication base that IgE testing has behind it, which is worth knowing even as someone who relies on it clinically. What it offers that the others don’t is a direct, food-by-food functional readout, rather than an antibody proxy or a general inflammation thermometer.

Test, Don’t Guess: How MRT Identifies Your Personal Inflammatory Triggers

The Mediator Release Test (MRT) is the tool I rely on clinically and used on myself. It measures white blood cell reactivity — the release of cytokines, histamine, leukotrienes, and prostaglandins — after your blood is exposed to up to 176 individual foods and food chemicals. Pro-inflammatory mediator release from white blood cells is the common denominator across diet-induced inflammatory reactions, regardless of which food triggers it or which symptoms show up downstream.

From there, the LEAP (Lifestyle, Eating, and Performance) protocol builds a phased reintroduction plan starting with your least-reactive foods — not a generic “anti-inflammatory” template, but a map of your own immune system’s actual responses. It’s the difference between guessing which foods are working against you and testing for the answer.

What I see clinically, over and over, is what happens once that inflammation actually comes down. Clients who spent years following textbook “anti-inflammatory” diets — cutting red meat, adding turmeric, loading up on olive oil and leafy greens — with little or nothing to show for it, start losing weight effortlessly once we’ve identified and removed their specific triggers via MRT. Not through a new calorie rule or more exercise. Their motivation comes back. Their mood lifts. That pattern shows up so consistently in practice because it isn’t really about willpower or the “right” foods in the abstract — it’s about finally removing the specific foods that were keeping their immune system, and by extension their metabolism and hormones, in a constant low-grade fight.

I run this testing with the majority of my clients, and in all that time, I have yet to have a single one tell me they wish they hadn’t done it. They don’t just feel better physically — their cravings for their own reactive, inflammatory foods fall away on their own, without a battle of willpower. That’s usually the moment clients realize those cravings were never really about lack of discipline in the first place; they were the body asking, in the only language it has, for less of what was harming it.

If you want the fuller picture of how food sensitivity-driven inflammation shows up in the body, my Ultimate Gut Health Guide and my MRT testing overview go deeper into both the science and the practical process.

Frequently Asked Questions

Is inflammation really the root cause of chronic disease?
Chronic, low-grade inflammation is a shared underlying mechanism linked to cardiovascular disease, type 2 diabetes, cancer, autoimmune disease, chronic kidney disease, fatty liver disease, and neurodegenerative and mood disorders. It’s not the sole cause of every disease, but it’s a common pathway across most of the leading chronic conditions worldwide.

Can the same food be anti-inflammatory for one person and pro-inflammatory for another?
Yes. The PREDICT study from King’s College London found that inflammation triggered by identical meals varied up to ten-fold between individuals. A food’s population-level anti-inflammatory reputation reflects an average, not a guarantee for any one immune system.

What is the Dietary Inflammatory Index, and is it useful?
The DII scores foods and nutrients by their average effect on inflammatory biomarkers across large study populations. It’s a useful research and public-health tool, but it can’t tell you how a specific food affects your own body — only functional testing can do that.

Why do generic anti-inflammatory diets sometimes not work?
Generic anti-inflammatory diets are built from population-level research and don’t account for individual food sensitivities. A food widely labeled anti-inflammatory, such as olive oil or legumes, can still provoke a measurable inflammatory response if your immune system has flagged that specific food as a trigger.

What is MRT testing and how does it identify personal food triggers?
The Mediator Release Test (MRT) measures white blood cell reactivity to up to 176 individual foods and food chemicals, detecting the release of inflammatory mediators like cytokines, histamine, leukotrienes, and prostaglandins. Results build a personalized LEAP (Lifestyle, Eating, and Performance) reintroduction plan starting with your least-reactive foods.

How is a personalized anti-inflammatory diet different from the Mediterranean diet?
The Mediterranean diet is built on population-level evidence and works well for many people, but it isn’t individualized. A personalized anti-inflammatory diet starts with your own MRT results, so it reflects your immune system’s actual reactive and safe foods rather than a generic pattern.

The Bottom Line

Chronic inflammation sits underneath a striking range of the chronic diseases we treat individually — cardiovascular disease, autoimmune conditions, cancer, metabolic disease, even mood disorders. Food is one of the biggest levers we have over it. But the research is now clear that inflammatory food response is highly individual, not a fixed property you can read off a chart or a DII score. The next time you see a food confidently labeled “anti-inflammatory” or “pro-inflammatory,” the honest answer is: it depends entirely on whose body is eating it. Testing — not guessing — is how you find out which side of that list you’re actually on.

I write about this in much more depth, alongside the cortisol-inflammation connection, in Cortisol Fix.