The goalRecipes scored for the iron you actually absorb
Scores are a transparent model built on this tool's evidence, applied to recipes sourced from the sites credited on each card. They rate absorbed-iron potential, not taste or total nutrition, and don't replace the original recipe's full method or medical advice. Built on the cited, peer-reviewed and government sources listed under each section; last reviewed 18 June 2026.
Category 1Iron-rich is not the same as high in usable iron
"Iron-rich" = total iron
The figure on a label or database. It counts every milligram of iron in the food, regardless of whether your gut can take it up.
Plant foods carry only non-heme iron, absorbed at roughly 2–20% and easily blocked by phytate, polyphenols and calcium.
"High usable iron" = absorbed iron
Total iron adjusted for how much actually crosses into the blood. Heme iron from animal flesh and blood is absorbed at ~15–35% and largely shrugs off meal inhibitors.
This is why organ meats, blood products and shellfish punch far above their label weight.
Category 2The top 100 foods that block iron — how much, and how
Bars show the peak single-meal reduction reported where a figure exists; phytate-dominant foods are dose-dependent and shown by potency tier. Both overstate real-diet impact.
Category 3The top 100 foods that drive inflammation
Bars show strength of evidence that the food or group raises inflammation, not a dose. Inflammation tracks the overall pattern and quantity; an occasional portion of any single item matters little.
The overrideInflammation, hepcidin & why the tables are conditional
Hepcidin is a liver hormone — the master switch for iron. Everything in Categories 1 and 2 happens in the gut. Hepcidin acts one step later, at the gate that lets iron out of cells into the blood.
Inflammation
Infection, injury or chronic disease raises the cytokine IL-6.
Hepcidin rises
IL-6 drives the liver to pump out more hepcidin.
Ferroportin closes
Hepcidin degrades ferroportin, the only iron-export gate on gut and storage cells.
Absorption falls
Dietary iron is taken up but can't pass into blood; stored iron stays locked away.
The consequence is anaemia of inflammation: low blood iron despite normal or high stores. It's also why a perfectly built iron-rich, vitamin-C-paired meal can still deliver little during active inflammation — high hepcidin overrides the dietary levers. The system runs both ways: iron deficiency, blood loss and low oxygen suppress hepcidin and ramp absorption up.
Beyond dietOther reasons iron deficiency happens
Iron-deficiency anaemia is usually a sign of an underlying process, not a diet problem alone. Causes frequently coexist, and even a full workup finds no cause in about a third of cases.
Blood loss
GI bleeding (ulcers, cancer, NSAIDs), heavy periods, childbirth, frequent donation. Unexplained cases warrant GI investigation.
Malabsorption
Coeliac disease, IBD, H. pylori and atrophic gastritis, gastric or bariatric surgery. A classic cause of iron that won't respond to tablets.
Drugs
PPIs and H2 blockers cut absorption (less acid, more hepcidin); NSAIDs and aspirin cause GI bleeding; anticoagulants worsen loss.
Increased demand
Pregnancy, infancy and childhood growth, adolescence and lactation outrun a normal diet's supply.
Low intake
Genuinely low-iron diets and poorly planned vegetarian or vegan eating — usually a contributor rather than the sole cause.
Parasites & infection
Worldwide the largest driver: hookworm and schistosomiasis cause chronic gut blood loss.
Chronic disease
Inflammation locks iron away in chronic kidney disease (plus dialysis loss, low EPO) and heart failure.
Intravascular haemolysis
PNH and mechanical heart valves shed iron in the urine, draining stores over time.
Genetic (IRIDA)
TMPRSS6 mutations cause inappropriately high hepcidin and iron deficiency refractory to oral iron.
The clinical distinction between true iron deficiency and anaemia of inflammation is made with tests (ferritin, transferrin saturation, CRP), because they need opposite management.