Etiology of IDA:

Iron deficiency results when insufficient amount of iron is available to meet body's requirements. This can occur because of:

• Decreased supply of iron due to :
  

  • Inadequate intake of iron,
  • Reduced bioavailability of dietary iron.
• Decreased absorption of iron : Cause of iron malabsorption includes chronic diarrhea, malabsorption syndromes, milk allergy, sprue, partial or total gastrectomy and rarely genetically determined absorptive defect specific for iron. Pica though may be a manifestation of iron deficiency, is also considered to be a predisposing factor for poor iron absorption.
  
  
• Increased requirement of iron as seen in premature babies during first few months (as they have a rapid growth) and during the periods of growth as in infancy and adolescence, lactation, pregnancy.
  
  
• Chronic blood loss
  
  

Gastrointestinal bleeding : The chronic loss of few milliliters of blood daily is sufficient to deplete iron stores and lead to iron deficiency. Often these bleeds are occult and unsuspected. In the western world, milk induced enteropathy is the commonest cause of occult G.I. bleeding seen in approximately more than 50% of infants with IDA. Hookworm infestation is the other important cause of intestinal blood loss, particularly in developing countries. 450 million people all over the world harbor this parasite and about 0.2 cc of blood/worm of ankylostoma per day may be lost and with necator-infestation each worm accounts for loss of about 0.1-0.5 ml/day. Female subjects harboring more than 100 worms (5 ml/day blood loss) and male subjects harboring more than 250 worms (12.5 ml/day blood loss) tend to become anemic. The daily blood loss may be as great as 250 cc/day.

Feto-maternal bleed: is one of the important causes of anemia in newborn. In about 50% of all pregnancies, there is some degree of feto-maternal hemorrhage of which 8% are significant (0.5 - 40 cc fetal blood loss) and 1% severe (> 100 cc fetal blood loss). Repeated venepunctures for investigations, hemodialysis, and regular blood donations are important iatrogenic causes of iron deficiency due to chronic blood loss.

Decreased supply
Breast milk, the primary source of infant nutrition is poor in iron, containing 0.28-0.73 mg/lit. However, the iron in breast milk has a very high bioavailability (20-80%) and hence iron deficiency rarely occurs in exclusively breast fed infants till the age of 4-6 months. Breast-feeding does not protect against iron deficiency after the age of 6 months, unless iron containing weaning foods are introduced. During adolescence false concern about the body figure, food fads, ignorance, particularly in girls lead to iron deficiency.

Table 1 : ETIOLGICAL FACTORS IN IRON DEFICIENCY ANEMIA

Decreased iron assimilation	Blood loss	Increased physiologic requirement
Iron Poor Diet & poor bioavailability of Fe in the food Iron malabsorption Chronic diarrhea & malabsorption syndrome Sprue Pica	G.I. bleeding Hookworm infestation Peptic ulcer Diverticulitis Milk induced enteropathy Aspirin & other drugs G.I.surgery Feto-maternal transfusion Early clamping of cord-Bleeding disorders	Period of growth Prematurity Infancy Adolescence

An average adult has about 3-5 gm of iron and children have 55 mg/kg/body weight of iron in the body. It is more in males as compared to females. 70% of iron in the body is in the form of Hb, 26% constitutes the stores and 3.9% is incorporated in myoglobin and various other iron containing enzymes. Plasma iron forms only 0.1% of the body iron.

Iron balance in the body is achieved mainly by control of absorption of iron rather than its excretion. Body iron remains fixed within relatively narrow limits. Most of the iron is recirculated in the body. Only 1-1.5 mg of iron is excreted daily. Thus daily requirement is minimum. Absorption of iron mainly depends upon dietary content of iron.

Table 2 : IRON CONTENT OF FOOD ARTICLES

Class of Food	Iron content mg/100 g	Articles rich in iron > 10 mg / 100 g
Cereals	2.5 - 14.0	Bajra, Wild Barley, Kang Ragi, Rice flakes, whole wheat Flour, Kodra (Harik)
Pulses & Legumes	2.7 - 11.0	Bengal gram, Cow gram, Soya bean
Leafy Vegetables	0.9 - 40.0	Amaranth, Beet, Greens,Bengal gram leaves, Coriander, Alu leaves, Pudina, Neem, Radish top, Rajgira leaves, Turnip greens, all types of green bhajis. (Spinach, methi, lettuce, etc.)
Roots & tubers	0.4 - 13.9
Other Vegetables	0.2 - 22.2	Amaranth seeds, Daincha seeds
Nuts & oil seeds	2.5 - 10.0	Garden cress, Gingelly, mustard, Pistachio
Fruits	0.1 - 10.0	Dates, Karwanda, Raisins
Sea food	1.0 - 11.5	Most Indian fish, crab
Meat	2.0 - 18.8	Beef
Milk	0.2 - 0.8
Miscellaneous		Jaggery, Yeast

Bioavailability of iron: Ultimate absorption of iron into mucosal cells mainly depends upon bioavailability of iron in the various foodstuffs. The non-vegetarian foods have iron (heme) with very high bioavailability and the absorption of this is not affected by any other factor in the lumen including various food ingredients. Absorption of iron from vegetarian sources is affected by various factors as shown in following Table 3

Table 3: FACTORS AFFECTING THE BIOAVAILABILITY OF THE DIETARY NON- HEME IRON

Enhance	Ascorbic acid, meat, fish, poultry
Inhibit	Tannates (tea, coffee), Bran, Egg Yolk, Calcium Phosphate,EDTA, Antacids, phytates, cholestyramine, clay, starch.

Mucosal cell control: Appropriate iron balance in the body is achieved by mucosal cell control through transferrin and apoferritin receptors. When the serum iron is normal and adequate, the iron gets incorporated into apoferritin in the mucosal cell and this is ultimately excreted after 3-4 days, when lifespan of mucosal cells is over. However, if iron deficiency state exists in the body, transferrin is utilized to combine with iron and is transported and stored at storage site.

Iron transport and storage:
Transferrin helps in transport of iron from the intestine to the site of its utilization. Iron is stored in the body in the form of ferritin and hemosiderin.

Transport of iron across the placenta:
The transport of iron across placenta occurs against a gradient, thereby protecting fetus against iron deficiency. However, this effective fetal parasitism is limited in cases of severe maternal iron deficiency. Thus babies with low iron stores may be born to mothers who are severely iron deficient during pregnancy. It is important to remember that most of the placental transfer of the iron occurs during the 3rd trimester of pregnancy. As a consequence of this, all preterm babies invariably develop anemia unless supplemented by iron and conversely iron deficiency in the mother may cause preterm labor.