Only about 10% of dietary iron is absorbed, and only as little as 1—5% of that in many plant foods. As discussed in section 188.8.131.52, iron deficiency is a serious problem; some 10—15% of women of child-bearing age have menstrual iron losses greater than can be met from a normal dietary intake. Haem iron in meat is absorbed better than is inorganic iron from plant foods, and by a separate transport system.
Inorganic iron is absorbed only in the Fe2+ (reduced) form. This means that a variety of reducing agents present in the intestinal lumen together with dietary iron will enhance its absorption. The most effective such compound is vitamin C (section 184.108.40.206) and, although intakes of 40—60 mg of vitamin C per day are more than adequate to meet requirements, an intake of 25—50 mg per meal is sometimes recommended to enhance iron absorption. Alcohol and fructose also enhance iron absorption.
Like other minerals, iron enters the mucosal cells by carrier-mediated passive diffusion and is accumulated in the cells by binding to a protein, ferritin. Once all the ferritin in the mucosal cell is saturated with iron, no more can be taken up from the gut lumen. Iron can leave the mucosal cell only if there is free transferrin in plasma for it to bind to and, once plasma ferritin is saturated with iron, any that has accumulated in the mucosal cells will be lost back into the intestinal lumen when the cells are shed at the tip of the villus (section 4.1).
The mucosal barrier to the absorption of iron has a protective function. Iron overload is a serious condition, leading to deposition of inappropriately large amounts of iron in tissues, and about 10% of the population are genetically susceptible to iron overload. Once the normal tissue iron-binding proteins are saturated, free iron ions will accumulate in tissues. As discussed in section 220.127.116.11, iron ions in solution are able to generate tissue-damaging oxygen radicals, and this may be a factor in the development of cardiovascular disease and some forms of cancer. Indeed, one of the reasons why women are less at risk of atherosclerosis than men may be that women generally have a lower iron status than men because of menstrual blood losses.
This raises the interesting problem of whether or not it is desirable to recommend high intakes of iron for women of child-bearing age in order to raise their iron reserves to the same level as seen in men. This would prevent the development of iron deficiency but might also put them at risk of iron overload and increased risk of atherosclerosis.
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