Iron is a vital component of hemoglobin, which transports oxygen to the various tissues of the body. Life and iron are inseparable: with the sole exception of lactic acid bacteria, all living organisms require iron as an essential element for growth and multiplication. Iron deficiency is the most common nutritional problem in the world.
Free ionic iron hardly exists in the body. All the intracellular iron is either in hemoglobin or in the iron-storage protein ferritin.
Iron is rather unique in that nature regulates its absorption, because there is no mechanism that enables excretion of excess iron1 The precise mechanisms and control of iron absorption are not clear.
The duodenum is the main site of iron absorption. Small intestinal iron absorption is by a process of diffusion. The amount of iron absorbed is 1%-5% of the dietary iron in a normal man, studied using a radioactive isotope.
Because of the multiplicity of factors affecting iron absorption, it is not possible to make a valid estimate of iron absorption from a meal. The absorption varies with foods, being higher with a rice-based diet and lower with millets. Germination and baking increase absorption, while it is reduced with tannins, tea, tamarind, phytate and cereals. Food analysis reveals considerable tannin in cereals, pulses, soybeans, and condiments like tamarind, turmeric and chillies. Absorption from soybean is enhanced when taken with meat or vitamins. Prolonged warming of meals decreases their vitamin C content, and hence, iron absorption. The amino acid cysteine enhances iron absorption from vegetables, animal foods, and iron salts.
Iron in meat and liver is better absorbed than that in eggs and leafy vegetables. With animal foods, the mean iron absorption ranges from 7% from ferritin to 22% from veal muscle, with intermediate values of 11 % from fish and 13% from liver. Animal protein in beef, pork, chicken or fish (but not egg and milk) increases absorption of non-heme iron from vegetable sources. On a rice-based diet, iron absorption increases with the addition of 40 g fish.
Iron absorption on a cereal diet is decreased because phosphate and phytates precipitate ionised iron. Soya protein is a major inhibitory factor of iron absorption due to its phytate content.4Fiber in wheat and maize decreases iron absorption. Tea and coffee form insoluble iron tannate that is not absorbed. Coconut milk, used extensively in cooking in Thailand and southern India, inhibits iron absorption.
Iron absorption increases with iron-deficiency anemia, low plasma iron, increased red blood cell activity in the bone marrow, pancreatic deficiency, and in women. Increased iron absorption occurs in normal persons during menstruation, pregnancy, puberty, and after blood loss. Iron absorption is increased if iron body stores are depleted.
Inorganic ferrous and ferric salts are both absorbed, but ferrous iron is absorbed better. There is no difference in the absorption of the inexpensive ferrous sulphate and the more expensive slow-release iron tablets. Hemoglobin iron is absorbed intact as heme, even at neutral pH, and is not affected by dietary phosphate or phytate.
Gastric acidity maintains the solubility of inorganic iron, which aids the formation of small molecu les with ascorbic acid, citrate, fructose, and amino acids. Citrate and ascorbate, being soluble, are more easily absorbed, while tannate (from tannic acid in tea), phytate and phosphate are not so readily absorbed.
Vitamin C reduces ferric iron to ferrous iron which. remains soluble even at neutral pH and is better absorbed. Even when the diet is poor in iron, vitamin C supplement with each meal enhances iron absorption.? Vitamin C taken in divided doses with each meal will increase iron absorption to a greater extent than a single large dose with breakfast.
Calcium inhibits iron absorption. Radio-iron absorption tests in human volunteers show decreased absorption with cimetidine and antacids.
PLASMA IRON :- Normal plasma iron level is 60-160 micrograms per 100 ml (10.74-28.6 micromol/l); the total plasma iron-binding capacity (TIBC) is 280-400 microgram per 100 ml (50.1-71.6 micromol/l), of which about one-third is normally saturated.
The iron-binding proteins are transferrin (siderophilin), lactoferrin (found in milk, tears, saliva, bile, seminal secretions, and cervical mucus), and desferrioxamine (a fungal product). Mucosal transferrin binds iron in the lumen of the gut to transport it across the brush border of the intestinal mucosa. Plasma transferrin transports protein and binds two atoms of iron; its half-life is eight days, but varies widely because iron deficiency itself is a stimulus to transferrin formation.
The total body iron is 3-5 g (54-90 mmol), the bulk of which is in hemoglobin. The sites of storage are the liver, spleen, and bone marrow, where iron is stored as ferritin or hemosiderin.
Ferritin, derived from the reticuloendothelial tissue of the liver, spleen, and bone marrow, is a spherical storage iron protein which binds up to 4000 atoms of iron per molecule. It has 24 subunits arranged in a cluster like a raspberry, and contains 20% iron. Ferritin represents the soluble, readily mobilizable fraction of storage iron; its estimation, by radioimmunoassay, helps in diagnosing iron deficiency or overload. This estimation is less expensive than that of serum iron and TIBC. The normal values range from 12 to 250 micrograms per litre; values less than 10 micrograms per litre denote iron deficiency.
One microgram per litre of serum is equivalent to 80 mg (1.4 mmol) storage iron. Storage iron is about 980 mg (17.5 mmol) in normal men and 450 mg (8 mmol) in women. In iron overload, the values are higher; in acute liver cell damage, too, release of ferritin gives abnormally high values.
The structure of hemosiderin is not well understood, but it is believed to be a degradation product of ferritin. Hemosiderin iron is not readily released.
Desferrioxamine is a chelating agent that binds iron and excretes it in the urine. The urinary excretion of iron is thus easily measured, and this method is utilized to estimate iron stores. Injection of desferrioxamine in patients with decreased iron stores results in diminished urinary iron excretion.
Transferrin is a glycoprotein synthesized mainly by the liver. It can bind two ferric iron molecules and is responsible for the total iron-binding capacity of the serum, which is 250-370 micrograms per 100 ml.
Absorbed iron is tenaciously bound to protein. The little excretion that occurs, as with shedding of the inner lining of the digestive tract (desquamation of the epithelium of the mucous membrane), cannot be correctly assessed. Iron passed in stool is mostly unabsorbed dietary iron; some iron is also -lost through the bile. Desquamation of the skin increases iron loss with sweating in the hot, humid climate of the tropics. The urinary loss of iron is negligible.
IRON Loss IN WOMEN
A woman loses additional iron during her reproductive life: (i) during each menstrual cycle 30-60 ml of blood is lost, which involves a monthly loss of 15-30 mg (269-537 micromol) iron; (ii) during pregnancy the fetus, placenta, and loss during parturition drain the mother of over 500 mg (9 mmol) iron, which would require an increase in the daily absorption by 2 mg (36 micromol); and (iii) during lactation, there is an additional daily loss of 1.5 mg (27 micromol) iron. Owing to such losses, women–even in Western countries-have low iron stores.
Anemia are the most common and widespread nutrition problems. A vast majority of cases are due to iron deficiency. On a global basis, 2.15 billion persons are anemic or iron-deficient.
Iron is also utilized by the brain. Iron uptake is maximum during rapid brain growth in the fetus 15 Iron-deficient infants are below par in mental and physical development. Iron intervention can reverse these development delays.
A post-cricoid web is often associated with iron deficiency; when followed up, some of these developed cancer in that region. Lowered levels of intestinal disaccharidases occur with iron deficiency anemia; this’ is corrected by oral iron supplement.
Serum ferritin radioimmunoassay is the most reliable test for iron-deficiency anemia. Little additional information is gained from other noninvasive tests.