Iron is an essential trace mineral required for oxygen transport, cellular energy metabolism, DNA synthesis and numerous enzymatic reactions. Most body iron is incorporated into haemoglobin within red blood cells, where it allows oxygen to bind reversibly and be transported from the lungs to tissues. Additional iron is present in myoglobin in muscle and in enzymes involved in electron transfer and other metabolic processes.
The body has no major physiological pathway for actively excreting excess iron, so iron balance is controlled principally through regulation of intestinal absorption. This differs fundamentally from minerals that can be more readily eliminated in urine. Iron exists in different chemical forms, with haem iron associated with animal tissues and non-haem iron occurring in plant foods and many fortified products. Iron deficiency is among the most common nutritional deficiencies worldwide, while excessive iron accumulation can also cause serious tissue damage.
Dietary iron absorption is regulated largely by the hormone hepcidin, which controls the activity of ferroportin, a protein responsible for exporting iron from intestinal cells and storage cells into the circulation. When body iron stores are adequate or inflammation is present, higher hepcidin levels reduce iron release and intestinal absorption. When iron demand is increased or stores are depleted, hepcidin can decrease, permitting greater iron availability.
This regulatory mechanism explains why iron absorption changes according to physiological circumstances rather than remaining constant. Iron is transported through the blood bound principally to transferrin and stored within cells in proteins including ferritin. The liver, spleen and bone marrow are particularly important in iron storage and recycling. A large proportion of daily iron needs is met not by new dietary absorption but by recycling iron from ageing red blood cells through macrophage activity.
Haemoglobin is the central iron-containing protein for oxygen transport. Each haemoglobin molecule contains haem groups whose iron atoms bind oxygen reversibly, enabling red blood cells to load oxygen in the lungs and release it in tissues. Iron is also present in myoglobin, which facilitates oxygen handling in muscle, and in mitochondrial proteins involved in electron transport and energy production. Iron-containing enzymes participate in a wide variety of oxidation-reduction reactions, DNA synthesis and other biochemical pathways.
Consequently, iron deficiency can affect more than red-cell production. When iron stores become depleted, the body prioritises essential functions, but prolonged deficiency can eventually impair haemoglobin synthesis and produce iron-deficiency anaemia. The resulting reduction in oxygen-carrying capacity can contribute to fatigue, weakness, reduced exercise tolerance and impaired concentration.
Iron deficiency can arise through inadequate intake, impaired absorption, increased physiological requirements or blood loss. Menstruating individuals can have increased requirements because of recurring blood loss, while pregnancy increases iron demand because of expansion of maternal red-cell mass and development of the fetus and placenta. Infants and adolescents also have increased needs during rapid growth. Gastrointestinal blood loss can be an important cause of iron deficiency in adults and may require investigation rather than being attributed automatically to diet. Conditions affecting the stomach or intestine can reduce absorption, while certain dietary components influence non-haem iron availability. Iron deficiency progresses through stages, beginning with depletion of storage iron and potentially progressing to impaired production of haemoglobin and overt anaemia.
Haem iron and non-haem iron behave differently nutritionally. Haem iron, found mainly in meat and fish, is generally absorbed more efficiently and is less affected by many meal components. Non-haem iron, found in legumes, grains, nuts, seeds, vegetables and fortified foods, has more variable absorption. Vitamin C can enhance non-haem iron absorption by promoting chemical reduction and maintaining iron in a more absorbable form. Conversely, certain compounds in foods and beverages can reduce absorption under particular circumstances.
This does not make plant-based diets inherently incapable of providing adequate iron; rather, it means that total intake, dietary composition and individual physiology determine effective iron availability. The body can also adapt to low iron stores by increasing absorption, although this compensatory mechanism has limits.
Iron deficiency is assessed using a combination of clinical information and laboratory measures. Haemoglobin identifies anaemia but does not by itself establish its cause. Ferritin is widely used as a marker of iron stores, although it can rise during inflammation because it is also an acute-phase reactant. Transferrin saturation and other iron-related measures can provide additional information. A low mean corpuscular volume can occur in iron-deficiency anaemia, but microcytosis has other causes and is not diagnostic on its own. In suspected deficiency, identifying the reason for iron loss or inadequate absorption is as important as replacing the iron. This is particularly important in adults with unexplained iron-deficiency anaemia, where gastrointestinal blood loss or another underlying condition may require assessment.
Excess iron can be harmful because the body has limited mechanisms for eliminating it. Hereditary haemochromatosis is an inherited condition in which inappropriate iron absorption can cause progressive accumulation in tissues, potentially damaging the liver, heart, pancreas and other organs. Excessive supplemental iron can also cause acute toxicity, particularly in children who accidentally ingest concentrated preparations. Iron supplementation therefore differs from taking a general multivitamin: unnecessary high-dose iron can create real risks. Iron supplements can also cause gastrointestinal side effects such as constipation, nausea and abdominal discomfort. Different preparations vary in elemental iron content and tolerability, so treatment should be selected according to the cause and severity of deficiency rather than simply maximising the dose.
Iron is therefore best understood as a tightly regulated trace mineral whose central roles include oxygen transport, cellular respiration and enzyme activity. Its physiology depends on a balance between dietary absorption, hepcidin regulation, transferrin transport, ferritin storage and extensive recycling of iron from ageing red blood cells. Deficiency is common and can progress to anaemia, but unexplained deficiency may indicate blood loss or impaired absorption rather than simply inadequate food intake. Excess iron is also dangerous because the body cannot readily excrete it. Distinguishing haem from non-haem iron, dietary intake from bioavailability, iron stores from haemoglobin concentration, and nutritional deficiency from disease-related iron disturbance is essential for understanding Iron accurately.
