The capacity of the human body to excrete iron is severely limited as compared with most other mammals (Finch et al., 1978). Iron loss in human beings (per kg body weight) is only one-tenth that of other mammals (Dubach et al., 1955; Green et al., 1968; Finch et al., 1978) and human dietary intake only one-fiftieth to one-hundredth that of other mammals. It follows, as was originally suggested by McCance and
Widdowson (1937), that iron balance in man is primarily determined by iron absorption. There is a reciprocal relationship between iron stores and iron absorption: as stores decline, absorption increases. Similarly the rate of erythropoiesis (red cell development) is a major determinant of iron absorption: enhanced erythropoietic activity is linked to increased iron absorption. The principal site of iron absorption is the upper part of the gastrointestinal tract (the duodenum). Both the amount and bioavailability of dietary iron, together with the pH and motility of the gut lumen and other factors, influence iron absorption. These different factors do not, however, regulate iron absorption: this is thought to be carried out by the intestinal mucosa, which under normal circumstances adjusts the amount of dietary iron absorbed so that it just compensates for the iron that is lost by excretion. Since the human body lacks effective means of iron excretion, this means that only very small amounts of dietary iron are absorbed - in males about 1 mg/day to compensate for daily iron losses of about the same amount (14 ^g/kg). Two-thirds of this comes from the gastrointestinal tract by exfoliation of mucosal cells and loss of red cells, and one-third by exfoliation of cells from the skin and the urinary tract. In premenopausal women the average daily absorption is about double that in men, largely because of blood losses during menstruation (typically around 20 mg/period), resulting in a net daily iron loss of around 2 mg (30 ^g/kg). Iron absorption increases significantly during pregnancy (2.7 mg/day on average, but up to 5-6 mg/day in the last trimester) and during lactation (less than 0.3 mg/day).
Iron absorption from the diet depends not only on the iron content, but on its composition. Typical Western diets contain about 5-6 mg iron per 1000 kcal, with very little variation from meal to meal: this corresponds to a total daily intake of 12-18 mg for most subjects. There are two major pools of food iron: haem iron and non-haem iron. Haem iron is highly bioavailable and well absorbed - 20-30 %, regardless of other dietary or physiological variables (FAO/WHO, 1988). The haem iron in meat is absorbed as intact metalloporphyrin via specific, high-affinity mucosal brush-border haem-binding sites; this may be a receptor-mediated process. Haem itself is poorly absorbed, probably due to the formation of macromolecular haem polymers. In contrast, haem given as haemoglobin is well absorbed since it is maintained in its monomeric state by the primary amines released during the proteolysis of globin. Haem bioavailability can be substantially reduced by baking or prolonged frying.
Non-haem iron in food enters an exchangeable pool where it is subject to the interplay of luminal factors which both promote and inhibit its absorption. The major enhancers of non-haem iron absorption are meat and organic acids. Ascorbic acid is the most powerful promoter of these. It can, of course, reduce poorly soluble ferric iron to the more soluble ferrous state, but it could also chelate ferric chloride in the acidic pH of the stomach; this complex would remain not only stable, but soluble, at the alkaline pH prevailing in the gastrointestinal tract. Prolonged heating leads to the destruction of ascorbic acid and has a deleterious effect on the bioavailability of iron - so please don't cook the life out of green vegetables! A number of organic acids, notably citrate, malate, lactate and tartrate, also enhance non-haem iron bioavailability.
Inhibitors of non-haem iron absorption include polyphenols and phytates. The former, secondary plant metabolites rich in phenolic hydroxyl groups, are found in a high molecular form in tea (tannins) but polyphenols are also present in vegetables, legumes and condiments. Phytates, which constitute 1-2 % by weight of many cereals, nuts and legumes, also inhibit dietary iron bioavailability, probably due to the complexation of iron to form di-and tetraferric phytates, which are poor sources of iron. Other inhibitors of non-haem iron absorption are thought to be wheat bran and other components of dietary fibre complexes, calcium and phosphorus acting together, perhaps due to the formation of poorly available calcium-phosphate-iron complexes, and dietary protein particularly from soy beans, nuts and lupines.
Diets rich in enhancers such as meat and/or ascorbate have high iron bioavailability (about 3 mg absorbed/day) whereas diets with inhibitors such as polyphenols and phytates are poor sources of iron (less than 1 mg/day) (Bothwell etal., 1989). The human body is genetically adapted to haem iron absorption, a throwback to the days when man was a hunter. The progressive change in dietary habits that began with the introduction of the cultivation of grain about 10 000 years ago, has led to the replacement of well absorbed haem iron by less well absorbed non-haem iron from a cereal diet. The poor availability of dietary iron, particularly amongst the economically underprivileged, explains in large part the estimated more than 500 million persons throughout the world suffering from anaemia due to dietary iron deficiency (Chapter 9). With the current tendency in Western society to adopt a vegetarian regime, particularly among young women, we can expect a significant increase in anaemia, exacerbated by the progressive decrease in caloric intake (which of course correlates with dietary iron). Also, at the opposite extreme, an only slightly enhanced excessive mucosal iron absorption can lead to parenchymal iron overload sufficient to cause tissue damage, a condition unique to man - genetic haemochromatosis is probably the most frequent inherited disease in humans (Chapter 9).
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