Iron !

Iron carries oxygen in haemoglobin and moves electrons in mitochondria; the body has no way to excrete it, so it controls absorption.

Updated 2026-11-01

Key facts

About two thirds of body iron is in haemoglobin; the rest is in ferritin (storage), myoglobin and enzymes (cytochromes, catalase).
There is no regulated excretion route: balance is set at duodenal absorption, and liver hepcidin is the brake.
Low serum ferritin is the most specific sign of iron deficiency; ferritin rises with inflammation.
Iron deficiency is the world's most common nutritional deficiency and the leading cause of anaemia.

Sources: heme iron (meat, organ meats, fish), which is well absorbed, and non-heme iron (legumes, leafy greens, fortified cereals), which is poorly absorbed. Vitamin C helps; phytates, tea, coffee and calcium hinder.
Absorption in the duodenum: ferrireductase (duodenal cytochrome b) reduces Fe³⁺ to Fe²⁺; DMT1 brings it into the enterocyte; ferroportin exports it to blood; hephaestin (a copper enzyme) oxidises it back to Fe³⁺.
Transport and storage: transferrin carries two Fe³⁺; cells take it up via the transferrin receptor; it is stored in ferritin (and haemosiderin) in the liver, spleen and marrow.
Regulation: hepcidin binds ferroportin and destroys it, closing the exit of iron from gut and macrophages. It rises with high iron and inflammation (IL-6); it falls with anaemia, hypoxia and active erythropoiesis.
Deficiency: losses (heavy periods, gut bleeding, parasites), pregnancy and growth, poor diet, malabsorption (coeliac disease, gastrectomy). Microcytic hypochromic anaemia, fatigue, pica, spoon nails, cheilitis.
Excess: hereditary haemochromatosis (low hepcidin, HFE gene), repeated transfusions, tablet poisoning in children; damages liver, pancreas, heart and joints.
Lab: ferritin, serum iron, transferrin or total iron-binding capacity (TIBC), transferrin saturation; blood count with low MCV and MCH and high RDW.

Iron deficiency: low ferritin, high TIBC, low saturation. Anaemia of inflammation: normal or high ferritin, low TIBC, because hepcidin is high.
In iron deficiency anaemia in an adult (especially a man or a postmenopausal woman) gut bleeding is sought, including colorectal cancer.
Iron poisoning in children who swallow tablets is an emergency: bloody vomiting, shock and liver failure; the chelator is deferoxamine.

Think of the answer, then tap the question to see it.

Which hormone controls iron absorption, and how?

Hepcidin, from the liver: it binds ferroportin and degrades it, so iron cannot leave enterocytes or macrophages.

Which lab pattern separates iron deficiency from anaemia of inflammation?

Deficiency: low ferritin and high TIBC. Inflammation: normal or high ferritin and low TIBC.

Why does vitamin C improve non-heme iron absorption?

It reduces Fe³⁺ to Fe²⁺, the form the DMT1 transporter carries into the enterocyte.

Why is copper needed for iron metabolism?

Hephaestin and ceruloplasmin are copper ferroxidases that oxidise Fe²⁺ to Fe³⁺ so it can load onto transferrin.

Educational information, not medical advice. For any symptom, see a health professional.

Sources: Iron in diet: MedlinePlus Medical Encyclopedia (MedlinePlus, US National Library of Medicine, 2026); Iron Tests: MedlinePlus Medical Test (MedlinePlus, US National Library of Medicine, 2026); Ferritin Blood Test: MedlinePlus Medical Test (MedlinePlus, US National Library of Medicine, 2026); HAMP gene: MedlinePlus Genetics (MedlinePlus, US National Library of Medicine, 2026); SLC40A1 gene: MedlinePlus Genetics (MedlinePlus, US National Library of Medicine, 2026); Anaemia (World Health Organization, 2026); Textbook of Biochemistry for Medical Students, 6th ed. (Jaypee Brothers Medical Publishers (Vasudevan DM, Sreekumari S, Vaidyanathan K), 2011).

Spotted a mistake?We are always improving for the community. Tell us what is wrong and our team will review it.Report a mistake

Representative model, for educational purposes only.