Iron as Mineral – Rich Food Sources, Functions, Deficiency & Daily Requirements for Children, Men & Women

Health Care Guide on Iron (Fe) functions in Human Body, Absorption, Excretion, Regulation facts & disease (Anemia) in word/ .doc / ppt / .pdf format


Iron is present in all organisms and in all cells. It is a transient metal capable of being present in Fe2+ (ferrous) and Fe3+ (ferric) forms. Iron is essential for the formation of haemoglobin in RBCs, transport of oxygen and oxido-reduction reactions of the electron transport chain.


Food iron can be classified as haem iron and nonhaem iron (iron-porphyrin complexes are referred to haem compounds while nonhaem iron refers to substances which have iron in the prosthetic group but no porphyrin).

  • Haeme iron in the body is constituted by Hb (85%), Mb (5%) and heame enzymes (10%) such as cytochromes, cytochrome oxidase and peroxidase. 40% of total food iron is heame iron. It is obtained from organ meats, fish etc.
  • Nonhaeme iron is present in Fe-S proteins such as ferredoxin, adrenodoxin, flavoproteins, succinate dehydrogenase transferrin, ferritin, haemosiderin. The food sources of nonhaeme protein are vegetables, fruits, legumes and nuts 60% of total food iron is nonhaeme iron.  

Daily requirement:

-          Adult man and postmenopausal women : 10 mg.
-          Premenopausal women : 15-20 mg.
-          Pregnant women: 30-60 mg.Serum level 11-32umol/L.
-          1 g of haemoglobin contains –3.4 mg iron.
-          - 30 mg iron loss occurs in menstruation.


  • Mainly occurs in gastrointestinal mucosal cells.
  • Vit.C, calcium, gastric HCL, tissue needs have positive influence.
  • Tissue saturation, high pH, high phosphates, phytates and oxalates have negative influence.

Haem iron:

-          Generally, haeme iron is in combination with globin.
-          Proteolytic enzymes release the globin part.
-          Haeme iron enters the mucosal cells. it is transferred via transferrin.

Nonhaeme iron:

  • Haeme uptake is enhanced by vitamin C, succinic acid, sugars, sulphur containing amino acids and increased calcium levels. Calcium chelates with phytates.
  • Phosphates, phytates, tannic acid found in tea and antacid preparations inhibit absorption.
  • Absorption of iron takes place largely in the upper part of the small intestine.
  • Most foods contain iron in the ferric state.
  • The acid medium frees the bound iron.
  • Reducing substances such as vitamin C, glutathione help to convert ferric iron to ferrous iron, this is then absorbed.
  • Ferrous iron forms chelates with vitamin C, amino acids and sugars.
  • These chelates remain soluble in the jejunum and duodenum.
  • Absorption occurs by passive diffusion.
  • The iron combines with apoferritin of form ferritin.

Conservation of iron:

  • Body reutilizes iron to compensate for the low capability of iron absorption.
  • Iron is called a “one way” substance. Only 10% is absorbed but once absorbed, little is excreted.

Applied aspects:

  • In pregnancy, more iron is needed. Milk contains low amounts of iron.
  • Foetus uses maternal iron. Approximately 600 mg is transferred to the foetus.
  • Foetal Hb levels are 22-23 mg/dl.

Storage and transport forms of iron:

  • Ferritin is made up of a protein part (apoferritin) and iron. 4300 iron atoms are present in one molecule of apoferritin.
  • Haemosiderin is the form of brownish granules, which are large aggregates of ferritin molecules. Iron content is high. Increased levels cause haemosiderosis.
  • Both these molecules are storage forms of iron.
  • The following are transport forms of iron.
  • Lactoferrin is present in milk, tears, cervical mucous, seminal plasma, bile, saliva.
  • Transferrin binds two atoms of Fe3+ iron.

Transferring plays a dual role-

Accepts iron from                Delivers iron to
a) Intestinal tract                a) Bone for synthesis of Hb
b) Sites of storage                b) Reticulo-endothelial system for storage
c) Hb destruction                c) Placenta

Excretion of iron:

  • Faeces.
  • Desquamation of skin increases iron loss with sweating.
  • Urinary loss is negligible.
  • Menstrual loss is large.
  • In pregnancy, iron is transferred to the foetus.
  • In lactation, 1.5 mg/day of iron is lost.

Clinical manifestations:

  • Increased amounts of iron are excreted in haematuria and haemoglobinuria.
  • Iron deficiency leads to low plasma bound protein, increase in total iron binding capacity (TIBC) and decrease in iron and Hb levels.
  • In women, there is poor intake and absorption of iron. There is loss during menstruation, sometimes due to multiple pregnancies.


It can be classified as follows:

  • Dyshaemopoietic. Insufficient blood formed due to inadequate intake, absorption and utilization of iron. Factors required in adequate amounts are:
  • Minerals – iron, traces of cobalt and copper.
  • Proteins.
  • Vitamin, B12, vitamin C and folic acid.
  • Haemorrhagic. Occurs due to blood loss caused by piles, ulcers, bleeding and anti-inflammatory drugs.
  • Haemolytic. Occurs due to excessive intravascular blood destruction caused by red cell destruction and sensitizing of glucose 6-phosphate dehydrogenase.
  • Iron deficiency anaemia. In its severest form, it is characterized by hypochromic, microcytic red cells. defective synthesis of haem-complex and iron-containing metalloenzymes is responsible for fatigue and epithelial changes. It is a public health problem resulting in substandard performance of millions of people. Causes include :
  • Poor intake, absorption, loss of iron during menstruation, repeated pregnancies, prolonged lactation, parasitic infection. Blood donors may develop iron deficiency.
  • Diseases of bone marrow diminish RBC production, e.g.,  ionizing radiation, “crowding out” of red cell precursors. This condition occurs in leukemia, multiple myeloma and Hodgkin’s disease.
  • Treatment of iron deficiency anemia includes fortified food, doses of ferrous sulphate, Fe2+ gluconate and rarely intramuscular injections.

Iron excess or overload:

  • Idiopathic hemochromatosis, a genetically determined disease, is caused by increased iron absorption over years.
  • In Bantu tribes, haemosiderosis occurs.
  • Thalassemia patients receiving repeated blood transfusion and have defective Hb show accumulation of iron.
  • Refractory anaemia occurs due to high-iron diet intake. Interestingly, patients with iron overload can trigger and alarm at the airport when they go through metal detector.
  • In treatment, iron chelating agent, viz., desferrioxamine is used.

Bronze diabetes:

It is a disease that leads to :

  • Increased deposits of haemosiderin.
  • Degeneration of cardiac muscle, congestive heart failure and hepatic fibrosis. Pancreatic damage results in diabetes mellitus.

Iron toxicity:

  • Results in hepatic failure, diabetes, testicular atrophy, arthritis, cardiomyopathy, peripheral neuropathy and hyperpigmentation.
  • The following are the laboratory tests for assessing patients with iron disorders :
-          RBC count and estimation of Hb.
-          Determination of plasma iron, TIBC and percentage of transferrin.
-          Ferritin by RIA.
-          Prussian blue stain of tissue.
-          Amount of iron (mg/dl) in tissue biopsy.

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