LAUSR

A healthy adult requires about 25–30 mg iron per day for synthesis of red blood cells and iron-containing enzymes. Most of this iron requirement (20–25 mg) is needed to synthesize hemoglobin for the daily production of new erythrocytes [1] and the rest, about 20% of the total, is needed to supply the tissues that are constantly regenerating [2]. The need for absorbed dietary iron, however, is only 1–2 mg iron/day. This is because there is no active mechanism for iron excretion, and because blood and tissue iron is continually recycled and re-used (Fig. 1). Erythrocytes have an average life span of around 120 days after which they are phagocytosed by macrophages in the spleen and liver. The recovered iron is then released into the blood stream and transported by transferrin for re-use. Any dietary or recycled iron in excess of immediate need is stored as ferritin in the liver, spleen and bone marrow, and a typical storage amount maybe 1000 mg in an adult male. Dietary iron is needed mainly to replace iron losses from skin, intestinal cells, and blood (especially during menstruation), although at certain stages of the life cycle (infancy, childhood, pregnancy), there is an additional iron requirement for growth and increased blood volume. Iron homeostasis is maintained by regulating intestinal iron absorption. Absorption is low when iron supply is adequate but can be increased when dietary supply is low or when physiological needs are increased. When the combined iron supply from food and recycled red cells is insufficient, iron stores are utilized and gradually depleted, resulting ultimately in iron deficiency (ID) defined as lack of iron stores but normal red cell hemoglobin levels. Erythrocyte hemoglobin eventually decreases below normal ranges and iron deficiency anemia (IDA) results. Globally, 1.6 billion people are estimated to be anemic. These are mainly women and children living in the developing countries of Africa, Asia, and South America [3]. Anemia, however. has multiple origins and IDA due to low dietary iron absorption is estimated to account for only about 50% of global anemia, with infection/inflammation and hemoglobinopathies being the other major causes. In Sub Saharan Africa, low dietary iron bioavailability and infection/ inflammation are equally important causes of anemia [4] that can affect 50% or more of the women and young children living in resource-poor populations. The negative health consequences of ID and IDA caused by low dietary iron absorption or infection/inflammation are reported to include poor brain development in fetus and young child, poor iodine utilization, reduced work capacity, and poor pregnancy outcome, including decreased survival of a child born with low iron status [5]. Public health interventions to control IDA have traditionally been based on increasing dietary supply through iron-fortified foods or by providing iron supplements. Iron absorption from fortified foods is markedly influenced by meal composition and by the iron status of the consumer. Diet influences the passage of iron from the gastrointestinal (GI) tract into the intestinal cell, whereas iron status controls iron exit from the intestinal cell into the blood stream. Meal composition can either restrict or facilitate passage of iron into the intestinal cell by influencing access of iron to the iron transporter DTM1. Phytic acid, common in cereals and legume foods, and phenolic compounds from tea or green leafy vegetables, bind iron in insoluble and/or nonabsorbable complexes. Ascorbic acid from fruits and vegetables and peptides from partly digested muscle tissue convert ferric to ferrous iron and/or bind iron in soluble * Richard F Hurrell [email protected]