Methodology

How we calculate inflammation scores

Every Inflamous score is grounded in peer-reviewed research. Here is exactly how we translate published evidence into the number you see on each food page.

Scientific foundation

Our scoring methodology builds on three pillars of published research:

Pillar 1

Dietary Inflammatory Index (DII)

Developed by Shivappa et al. at the University of South Carolina (2014), the DII quantifies the inflammatory potential of 45 food parameters by scoring each against six inflammatory biomarkers (CRP, IL-1B, IL-4, IL-6, IL-10, TNF-alpha) drawn from 1,943 peer-reviewed articles.^[1]

Pillar 2

NOVA Processing Classification

The degree of food processing is a strong independent predictor of inflammatory biomarker elevation. We incorporate the NOVA framework (Monteiro et al., 2019) to weight processing level in our scores. Ultra-processed foods consistently elevate CRP and IL-6 across populations.^[8][9]

Pillar 3

Nutrient-Pathway Mapping

Specific nutrients activate or suppress known inflammatory pathways (NF-kB, MAPK, NLRP3 inflammasome). We use evidence from Minihane et al. (2015) and Calder et al. (2011) to weight individual ingredients by their molecular mechanism of action.^[5][6]

Scoring methodology

Each food in our database is scored through a four-step process:

Ingredient decomposition

Each food is parsed into its constituent ingredients and their approximate proportions. For example, a granola bar might decompose into: oats (30%), honey (15%), almonds (12%), canola oil (8%), brown rice syrup (10%), dried cranberries (10%), whey protein (8%), salt (0.5%), natural flavors (1%), and other components.

Ingredient-level impact scoring

Each ingredient receives an inflammation impact score based on its documented effect on inflammatory biomarkers. This scoring draws from DII parameter weights^[1], nutrient-pathway evidence^[5][6], and processing-level data^[8]. Key factors include:

Omega-3 fatty acids (EPA, DHA, ALA): strongly anti-inflammatory, suppress NF-kB and reduce IL-6 production
Dietary fiber: feeds beneficial gut bacteria that produce short-chain fatty acids (SCFAs), which suppress systemic inflammation
Polyphenols (flavonoids, anthocyanins, curcuminoids): inhibit COX-2 and NF-kB pathways
Refined sugars: trigger post-prandial inflammatory spikes via advanced glycation end products (AGEs) and oxidative stress
Trans and excessive saturated fats: activate toll-like receptor 4 (TLR4), triggering pro-inflammatory cytokine cascades
Processing additives (emulsifiers, artificial colors, preservatives): disrupt gut barrier integrity and promote endotoxemia

Weighted aggregation

Ingredient impact scores are weighted by their proportion in the food and aggregated into a single composite score. The weighting accounts for dose-response relationships: a food containing 2% added sugar has a different inflammatory profile than one containing 30%. The composite is then normalized to our -5 to +5 scale.

Band classification

The final score is classified into three bands:

-5 to -1: Anti-Inflammatory-1 to +1: Neutral+1 to +5: Pro-Inflammatory

Inflammatory biomarkers

The DII was validated against six biomarkers measured in blood samples across 11 countries^[1][2]. These markers are the standard in clinical inflammation research:

C-Reactive Protein (CRP)

Produced by the liver in response to IL-6. The most widely used clinical marker of systemic inflammation. Levels above 3 mg/L indicate elevated cardiovascular risk.

Interleukin-6 (IL-6)

Pro-inflammatory cytokine that drives the acute-phase response. Elevated by refined carbohydrates, saturated fat, and visceral adiposity. Reduced by omega-3s and polyphenols.

TNF-alpha

Tumor necrosis factor alpha. A master regulator of inflammatory cascades. Chronically elevated levels are associated with insulin resistance, atherosclerosis, and autoimmune conditions.

Interleukin-1 beta (IL-1B)

Activates the NLRP3 inflammasome pathway. Elevated by saturated fat and ultra-processed food. Suppressed by fiber-derived short-chain fatty acids.

Interleukin-10 (IL-10)

An anti-inflammatory cytokine. Higher IL-10 levels are protective. Omega-3 fatty acids and fermented foods promote IL-10 production.

Interleukin-4 (IL-4)

An anti-inflammatory cytokine that counterbalances Th1-driven inflammation. Promoted by dietary patterns rich in fruits, vegetables, and whole grains.

The 45 DII food parameters

The original DII^[1] evaluates dietary intake across 45 parameters. Each parameter was scored as pro-inflammatory (+1), anti-inflammatory (-1), or null (0) based on its effect on the six biomarkers above. The parameters include:

Anti-inflammatory parameters

Fiber, omega-3 (EPA + DHA), beta-carotene, vitamin A, vitamin C, vitamin D, vitamin E, vitamin B6, folic acid, magnesium, zinc, selenium, niacin, thiamin, riboflavin, iron, turmeric, garlic, ginger, onion, green/black tea, flavan-3-ol, flavones, flavonols, flavonones, anthocyanidins, isoflavones, rosemary, oregano, pepper, saffron, and alcohol (moderate).

Pro-inflammatory parameters

Saturated fat, trans fat, cholesterol, total fat (in excess), vitamin B12 (in excess), carbohydrate (refined), protein (in excess of needs), and total energy (caloric surplus). The DII also accounts for the ratio of omega-6 to omega-3 fatty acids.

Pro-inflammatory mechanisms

NF-kB activation: Saturated fat and refined sugar activate nuclear factor kappa-B, the master switch for inflammatory gene expression
AGE formation: High-heat cooking of sugary or fatty foods produces advanced glycation end products that bind RAGE receptors and trigger cytokine release
Gut barrier disruption: Emulsifiers (polysorbate-80, carboxymethylcellulose) thin the intestinal mucus layer, allowing bacterial endotoxins (LPS) into the bloodstream
Omega-6 excess: Excess arachidonic acid from omega-6 rich seed oils feeds the production of pro-inflammatory prostaglandins and leukotrienes

Anti-inflammatory mechanisms

SCFA production: Dietary fiber is fermented by gut bacteria into butyrate, propionate, and acetate, which suppress NF-kB and strengthen the gut barrier
Resolvin synthesis: EPA and DHA from omega-3s are converted into resolvins and protectins that actively resolve inflammation
Polyphenol inhibition: Curcumin, quercetin, and EGCG directly inhibit COX-2 and iNOS enzymes, reducing prostaglandin and nitric oxide production
Microbiome diversity: Fermented foods and prebiotic fibers increase microbial diversity, which correlates with lower systemic CRP levels

Limitations and disclaimers

Inflamous scores are estimates based on published population-level evidence. Individual inflammatory responses vary significantly based on genetics, gut microbiome composition, and metabolic health^[10].
Scores reflect the food as typically consumed. Preparation method, portion size, and meal context (what else you eat with it) can shift real-world inflammatory impact.
This is not a diagnostic or clinical tool. It is an educational resource for understanding the relative inflammatory potential of foods.
The DII was designed to score total dietary patterns, not individual foods. Our ingredient-level adaptation is an extension of DII principles, not a direct DII calculation.
We update scores as new research is published. Nutrition science evolves, and our methodology evolves with it.

Frequently asked questions

How is the Inflamous inflammation score calculated?

Each food is broken into its ingredient components. Each ingredient receives a weighted inflammation impact score based on its effect on biomarkers like CRP, IL-6, and TNF-alpha, derived from peer-reviewed DII research. These ingredient scores are aggregated into a single food-level score on a -5 (strongly anti-inflammatory) to +5 (strongly pro-inflammatory) scale.

What is the Dietary Inflammatory Index (DII)?

The DII is a literature-derived scoring system developed by Shivappa et al. (2014) that quantifies the inflammatory potential of diets based on 45 food parameters. It was validated against blood biomarkers (CRP, IL-6) across 11 countries and has been cited in over 1,000 peer-reviewed studies.

What biomarkers does the DII measure against?

The DII was developed using six inflammatory biomarkers: C-reactive protein (CRP), interleukin-1-beta (IL-1B), interleukin-4 (IL-4), interleukin-6 (IL-6), interleukin-10 (IL-10), and tumor necrosis factor-alpha (TNF-alpha). These markers are widely used in clinical research to assess systemic inflammation.

How is Inflamous different from the original DII?

The original DII scores an entire diet based on 45 nutrient parameters. Inflamous adapts this evidence to score individual foods at the ingredient level, making it practical for everyday food choices. We also incorporate processing level (NOVA classification) and food matrix effects, which the original DII does not account for.

Why do you score at the ingredient level instead of the food level?

The same food can have vastly different inflammatory profiles depending on its ingredients. For example, yogurt with live cultures and no added sugar is anti-inflammatory, while yogurt loaded with high-fructose corn syrup and artificial colors is pro-inflammatory. Ingredient-level scoring captures these differences.

Is this a medical diagnostic tool?

No. Inflamous is an educational tool that translates published nutrition research into practical food scores. It is not a substitute for medical advice, blood tests, or clinical diagnosis. Always consult a healthcare provider for personalized dietary guidance.

References

Shivappa N, Steck SE, Hurley TG, Hussey JR, Hébert JR. “Designing and developing a literature-derived, population-based dietary inflammatory index.” Public Health Nutrition 17(8):1689-1696 (2014). DOI: 10.1017/S1368980013002115. PMID: 23941862.
Original DII methodology paper. Defines the 45 food parameters, inflammatory effect scores, and global dietary reference database.
Shivappa N, Steck SE, Hurley TG, Hussey JR, Hébert JR. “A population-based dietary inflammatory index predicts levels of C-reactive protein in the SEASONS study.” Public Health Nutrition 17(8):1825-1833 (2014). DOI: 10.1017/S1368980013002565. PMID: 24107546.
Validation study showing DII scores correlate with CRP levels in a US cohort.
Tabung FK, Smith-Warner SA, Chavarro JE, et al.. “Development and validation of an empirical dietary inflammatory index.” Journal of Nutrition 146(8):1560-1570 (2016). DOI: 10.3945/jn.115.228718. PMID: 27358416.
Empirical Dietary Inflammatory Index (EDII) developed from Nurses' Health Study data linking food groups directly to IL-6, CRP, and TNF-alpha receptor 2.
Marx W, Veronese N, Kelly JT, et al.. “The Dietary Inflammatory Index and Human Health: An Umbrella Review of Meta-Analyses.” Advances in Nutrition 12(5):1681-1690 (2021). DOI: 10.1093/advances/nmab037. PMID: 33873204.
Umbrella review of 12 meta-analyses confirming DII association with cardiovascular disease, cancer, all-cause mortality, and depressive symptoms.
Calder PC, Ahluwalia N, Brouns F, et al.. “Dietary factors and low-grade inflammation in relation to overweight and obesity.” British Journal of Nutrition 106(S3):S5-S78 (2011). DOI: 10.1017/S0007114511005460. PMID: 22133051.
Comprehensive review of how specific nutrients (omega-3, fiber, polyphenols, saturated fat, trans fat, refined carbohydrates) modulate inflammatory biomarkers.
Minihane AM, Vinoy S, Russell WR, et al.. “Low-grade inflammation, diet composition and health: current research evidence and its translation.” British Journal of Nutrition 114(7):999-1012 (2015). DOI: 10.1017/S0007114515002093. PMID: 26228057.
Maps specific dietary components to inflammatory pathways (NF-kB, MAPK, NLRP3 inflammasome) at the molecular level.
Schulze MB, Martínez-González MA, Fung TT, Lichtenstein AH, Forouhi NG. “Food based dietary patterns and chronic disease prevention.” BMJ 361:k2396 (2018). DOI: 10.1136/bmj.k2396. PMID: 29898951.
Evidence that food-based patterns (Mediterranean, DASH) consistently reduce inflammatory markers across populations.
Monteiro CA, Cannon G, Levy RB, et al.. “Ultra-processed foods: what they are and how to identify them.” Public Health Nutrition 22(5):936-941 (2019). DOI: 10.1017/S1368980018003762. PMID: 30744710.
NOVA classification framework. Processing level is a key input to our scoring since ultra-processed foods consistently elevate CRP and IL-6.
Lane MM, Gamage E, Du S, et al.. “Ultra-processed food exposure and adverse health outcomes: umbrella review of epidemiological meta-analyses.” BMJ 384:e077310 (2024). DOI: 10.1136/bmj-2023-077310. PMID: 38418082.
Umbrella review of 45 meta-analyses linking ultra-processed food to 32 adverse health outcomes including inflammatory biomarker elevation.
Berry SE, Valdes AM, Drew DA, et al.. “Human postprandial responses to food and potential for precision nutrition.” Nature Medicine 26:964-973 (2020). DOI: 10.1038/s41591-020-0934-0. PMID: 32528151.
PREDICT study showing significant individual variation in post-meal inflammatory responses, supporting ingredient-level rather than food-group-level analysis.

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