Widespread dietary iron deficiency exists in Australia. Estimates suggest that 40% of females 12 - 50 years old receive less than the RDA, and 45% of infants 1- 5 years old receive less than the RDA. Reasons for inadequate iron (or increased requirements) include dietary insufficiency, pregnancy and lactation, heavy menstrual loss, malabsorption states, and decreased stomach acidity. Iron deficiency can produce a wide range of clinical symptoms before the onset of diagnostic anaemia.

Clinical applications

Technical information

Nutritional anaemia is the most common aberration in erythropoiesis. Nutritional anaemia is defined as a drop in haemoglobin to a level below normal and a reduced content of one or more essential erythopoietic factors.1

One of the most well known erythropoietic factors is iron. Iron deficiency is the most prevalent worldwide nutritional deficiency, being almost universal in some countries.2 Iron deficiency is thought to be the most frequent cause of anaemia.3 It has been estimated that at least 20 million people in the United States are iron deficient.3 Recently, the USDA published the results of a nationwide food consumption survey that was taken in 1977 to 1978.4 The following findings were reported in relation to iron intake in the United States1: average iron intakes of females 12 to 50 years old were 35% to 40% below the RDA.2 The iron intake of infants in 1977 was more than twice the intake in 1965. However, the average intake of one to two year olds was much lower, about 454% below the 1974 RDA. It is apparent that problems do exist with regard to iron nutrition in the United States.

Iron deficiency produces a number of different clinical conditions or symptoms. In early stages of iron deficiency anaemia, patients may have vague symptoms of tiring easily, headache, irritability, or depression.2,3 Tachycardia, shortness of breath, angina pain, equilibrium disturbances, tinnitus and a tendency to faint may develop later.2 Other symptoms include gastrointestinal discomfort, loss or perversion of appetite, flatulence, nausea, abdominal cramping, constipation or diarrhoea, dryness and soreness of mouth and tongue.2

Physical examination may reveal dry or rough skin, vertical and horizontal ridges on the nail of the thumb, brittle, thinning, greying hair, dry and cracked lips and reddening of the tip of the tongue.2

Iron deficiency can be caused by chronic blood loss, malabsorption of iron, inadequate dietary iron intake, pregnancy, lactation, intravascular haemolysis or a combination of these factors.2,3

Oral iron supplementation is the preferred form of therapy.3 Its supportive effects have been reported by such ancient peoples as the Egyptians, Greeks and Romans.2 Oral iron supplementation is safe and inexpensive.2,3 Although a diversified diet is encouraged, it must be emphasised that no individual food contains enough iron to be useful therapeutically.3

Malabsorption of iron is not only a causal factor in iron deficiency but also a concern in oral iron supplementation. To ensure iron assimilation, factors promoting its absorption should be utilised while avoiding those that are inhibitory.

Iron diglycinate

The form of iron is an important consideration for efficient correction of iron abnormalities. A true mineral chelate is one where the mineral has been covalently bound to one or more organic molecules. Salt forms of iron are not chelates, and form free ions (dissociate) in solution. The absorption of free ions is a difficult and inefficient process which also causes gastrointestinal upsets like nausea, diarrhoea, and typically with iron, constipation.

Iron covalently bound to two molecules of the smallest amino acid (glycine) provides absorption benefits above any other orally administered iron known. The iron molecule is carried through the gut mucosa by glycine, through the very efficient amino acid uptake pathways and is released into the cell directly. Research shows that the diglycinate form of iron is able to correct iron deficiency signs as effectively as iron sulphate, although only
1/4 as much diglycinate was required as sulphate.

Vitamin B6 responsive anaemias have also been reported in the medical literature.27,28,29,30 The classic form is an anaemia that is usually severe and hypochromic, microcytic in type.27 Its remission is totally dependent upon the administration of supplemental vitamin B6.27 Other usual haematinics such as iron, vitamin B12 and folic acid have no effect. Withdrawal of B6 results in a full relapse of the anaemia.27 Paradoxically, no other evidences of systemic B6 deficiency are discernible and dietary intake appears to be adequate.27

Iron supplementation has little effect in people who are deficient in vitamin A. Haematological indexes were improved only when vitamin A and iron were administered together. As a safe, and independently therapeutic precursor to vitamin A, beta-carotene represents a useful adjunct to the haematologically relevant nutrients.

A number of other studies have demonstrated a significant positive relationship exists between serum vitamin A levels and biochemical indicators of iron status.37,38

Both calcium and vitamin C are helpful in erythropoeisis. Ascorbate keeps iron in the Fe2+ state, which is beneficial for both absorption and utilisation of the iron molecule.