Iron is an essential element required for the correct function of the haemoglobin and myoglobin molecules. In its role as a cofactor with these molecules, iron is integral in the transport of oxygen in the body and its therefore of major importance to cellular respiration and energy production. As well as its role in oxygen transport, iron is also a cofactor in a number of enzymes, most notably tyrosine hydroxylase, the rate limiting step in catecholamine synthesis. Iron therefore has a pivotal role in energy metabolism and motivational behaviour. Like most vitamin and mineral deficiencies, iron deficiency was first described in animals. In the 1920’s, red blood cell removal from dogs caused changes in the way that foods affected blood regeneration, and the liver was identified as being pivotal in their process, largely due to its considerable store of iron. However it took 40 years for these ideas to be developed into the understanding that iron from food was required to maintain iron status in the blood for correct transport of oxygen.
During pregnancy, the placenta is highly efficient at transferring iron to the growing foetus, through transfer from the maternal ferritin stores. Around 300 mg of iron are accumulated in the growing foetus during gestation in this way. It is only after birth that the iron status of the infant may be compromised and in this regard the diet of both the mother initially, and later the infant as it grows to adulthood are pivotal in supplying adequate dietary iron. Iron balance in humans and other animals is highly regulated mainly through changes in the rates of absorption, but excretion rates do play a small role. Periods of growth require higher iron intakes and so early infancy and adolescence are times when iron balance may become negative if diet is poor. This is particularly true for females who have an increased requirement for iron following adolescence. The additional requirement for iron in females is thought to be around 0.5 mg per day, and pregnancy can increase requirements further due to the sequestration of maternal iron by the foetus.
The extra demands of growth and blood loss can cause an increase in the absorption of iron from the small intestine that might amount to as much as 3 mg per day iron. Feedback mechanisms regulate the absorptive capacity of the small intestine to iron stores, such that as stores decrease, iron absorption increases. However, the iron in the diet can have an influence on the amount of iron absorbed, because two forms of dietary iron exist. Haem iron is present in molecules of haemoglobin and myoglobin in animals tissue, and this form of iron has much higher absorption rates when compared to non-haem iron from plants. Haem iron has superior absorption because it has a separate absorption route in the small intestine. In this regard, haem iron is absorbed intact and processed within the intestinal mucosa, whereas non-haem iron can pass through the intestinal mucosa intact or may be absorbed attached to proteins such as transferrin. Non-haem iron is affected by substances within the gut such as phytates from cereal grains and tannins from tea.
Maximum iron absorption in non-anaemic subjects equates to around 3.5 mg per day iron, and the iron content of food is around 6 mg per 1000 kcal. Iron deficiency is diagnosed clinically based on three biochemical parameters, plasma ferritin, transferrin saturation and red cell protoporphyrin. In these test it is assumed that 1 microgram of ferritin is equivalent to 120 micrograms of iron per kg body weight, that below 16 % transferrin saturation normal erythropoiesis is impaired and that an increase in red blood cell protoporphyrin indicates an inadequate iron supply to the red blood cells. Use of these three measurements, along with the haemoglobin concentration allows clinicians to diagnose different types and stages of iron deficiency. Decreased ferritin signifies iron depletion, decreases ferritin and transferrin saturation with increased red cell protoporphyrin signifies iron deficiency without anaemia, and decreased ferritin and transferrin saturation with increased red cell protoporphyrin and a decrease in haemoglobin signifies iron deficient anaemia.