Title: Iron Fortification of Foods

Key words: Iron intake, LRNI, haemoglobin, cytochrome, haemosiderin, dietary reference values, haem iron, non-haem iron, absorption, bioavailability

Date: Nov 1998

Category: 4. Food Data

Type: Article

Author: Dr van Rhijn


Iron Fortification of Foods

An Assessment of the Desirability of Such a Policy


Nationally representative surveys in the UK suggest that iron intake among certain population groups is inadequate. Younger women (16-18 years) are particularly at risk, where up to a third have intakes below the Lower Recommended Nutrient Intake (LRNI). This led to the supplementation of processed foods with iron as a preventative measure against iron deficiency. However, in recent years there has been speculation about a potential association between high levels of iron stores in the body and certain chronic diseases. This has raised enough concern to warrant caution regarding intensifying fortification programmes, although the exact mechanisms are still unknown.

Current Iron function and Requirements

Iron (3-4 g in an adult body) is a component of haemoglobin (65% - oxygen transport), myoglobin (5% - oxygen storage) and many cytochrome & enzymes (energy production). Iron is transported by transferrin and stored in the reticulo-endothelial system as ferritin (20% - storage protein) and haemosiderin (10%). Iron stores are influenced by long-term nutrition, and can account for up to 30% of total body iron. Dietary Reference Values (DRVs in mg/day) for Fe is set at LRNI (4.7), EAR (6.7) and RNI (8.7) for adult males. Women of childbearing age require twice as much, teenagers 1 times and children below the age of 7 only 50% of these values.

Absorption and Bioavailability of Iron

The major sources of iron in the UK are cereals (50%), meat products (18%), vegetables (16%), and fortified wheat flour and breakfast cereals (10%). The average diet in the UK provides 12 mg of non-haem iron a day. The absorption and utilisation of iron is influenced by numerous factors, including genetic. In general, haem iron (Ferrous - Fe2+), from meat is readily absorbed (30 %) and relatively less affected by the dietary and physiological factors that influence the absorption of non-haem iron (Ferric - Fe3+).

A diet rich in animal protein and vitamin C enhance, whilst a high content of polyphenols & phytic acid inhibits, the bioavailability of non-haem iron. Other influences from riboflavin, zinc, copper, calcium and manganese share absorptive pathways with iron and may interfere with its absorption. On average only 15% of iron is generally absorbed from a mixed diet. Iron is efficiently re-utilised from blood corpuscles and the amount of iron in the body is almost entirely controlled by the amount of absorption. Absorption increases when the body’s stores are depleted and when there is a greater demand, as in children and women of childbearing age.

Iron Excess

Excessive iron status is currently diagnosed by measuring increased serum transferrin saturation, and high serum ferritin and iron levels, TIBC, Hb and MCV. Unfortunately these tests do give false positive results (acute phase effect) and fail to identify patients in the early stages of iron accumulation where treatment can still prevent tissue damage. Transcutaneous liver biopsy can confirm parenchymal iron overload (elevated hepatic iron index). The two oxidation states of iron (Ferrous Fe 2+ and Ferric Fe 3+) act as catalysts in redox (free-radical) reactions, and cause the formation of the destructive hydroxyl radical OH-. Iron also catalyses the breakdown of lipid peroxides to produce more radicals (starting chain reactions) or cytotoxic aldehydes. High levels of iron, in the presence of oxygen free radicals, can therefor cause severe damage to cellular components if not modulated by antioxidants or iron binding proteins.

Iron Toxicity

Growing evidence exists that iron supplementation may be harmful.

Acute and chronic "over-exposure" to iron may lead to the following health hazards:

This is rare and occurs mainly among young children, and requires ingestion of large doses of therapeutic iron. The lethal dose of iron is 200-250 mg/kg. (Therapeutic dose = 2-5mg/kg/day). These large doses result in local haemorrhagic necrosis of the gastrointestinal tract with vomiting and bloody diarrhoea due to hyperchlorhydria, along with systemic coagulation defects and metabolic acidosis.

Haemolytic anaemia, due to preoxidative damage, among preterm infants deficient in vitamin E, receiving iron-fortified formula or oral supplements.

Long term excessive accumulation of iron result in haemosiderosis and haemochromatosis, which is one of the most common autosomal recessive inherited conditions in Europe, resulting in excess absorption of iron from the diet. Studies have demonstrated that most homozygous individuals (0.4% of Northern Europeans) will have phenotypical expression of the disease with very high absorption of iron and that even heterozygous individuals (1% of Northern Europeans) absorb iron significantly more than normal control individuals. Although the condition has a wide range of expression, studies have suggested that a large proportion of homozygotes remain undetected in the community who could be in the preclinical stages of haemochromatosis, with the consequences of parenchymal tissue damage, fibrosis, diabetes and a shortened life expectancy.

High iron levels promote carcinogenesis (experimental studies), greater incidence of cancer mortality (epidemiological cohort study) and an increased risk of hepatocellular carcinoma. Excess iron could also be implicated in the high incidence of colorectal cancer (case-control studies) in the developed countries. High levels of dietary iron may increase the production of free radicals in the colon, producing potential carcinogens.

The association between high iron status and coronary heart disease and heart failure has not been substantiated, due to contradictory research results. Excess iron is known to increase plasma viscosity (predictor of coronary risk) and promote oxidation of lipids in the arterial wall. However, studies have shown that there is an association between blood donations and a reduced risk of acute myocardial infarction.

Pre-eclampsia in pregnancy (proteinuria, hypertension, oedema, clotting disturbances) cause serious risk to the lives of mothers and babies in 1% of pregnancies, and affects 10% of all pregnancies to some degree. Pre-eclamptic women have significantly higher serum levels of total iron and ferritin saturation (decreased iron binding reserve), resulting in lipid peroxidation. The clinical features are due to damaged endothelial cells caused by free radicals and lipid peroxides, produced as a result of placental ischaemia.

Sudden infant death syndrome (SIDS) may be associated with high ferritin levels in post-mortem serum samples, as well as increased liver iron concentrations. Studies suggest that the excess iron was acquired after birth and the readily available iron then enhances free radical damage, which may be implicated in SIDS.


More information is needed on the Fe status of different groups of the population. This should be coupled with reliable measures of intake and losses. Iron supplementation should not be given to women at risk of pre-eclampsia, unless they are iron deficient. The extra iron required during the 2nd and 3rd trimester of pregnancy is compensated for by a normal physiological adaptation (9 fold increase of iron absorption), rendering fortification of food obsolete and providing no clinical benefit.


There is increasing concern about iron overnutrition following epidemiological observations of associations between elevated levels of transferrin or transferrin saturation and cancer or coronary heart disease. Although the validity of these associations is still obscure, it cannot be ignored, for these two disease groups account for most deaths in developed countries. Further studies to investigate the impact of high iron stores on health should be encouraged, and fortification should not be further enhanced until there is a better understanding about the exact causes of these chronic diseases. In the interim, awareness of the other factors that enhance iron absorption should suffice.


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