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In inner cities in the UK, iron deficiency anaemia (IDA) occurs in infants with the same frequency as in developing countries. Evidence is now accumulating to show that IDA is associated with developmental delay, and that the association is causal. IDA is readily preventable, even in a profoundly socially disadvantaged population, by the provision of an iron supplemented formula in place of unmodified cows’ milk. In the United States there has been a substantial reduction over the last 20 years in the prevalence of IDA among infants and young children from low income families.1-3 None the less there is no evidence of a similar downward trend in the UK.4 The lack of urgency in dealing with this problem in the UK is puzzling. We have therefore summarised the existing data on the epidemiology of IDA in the UK and on its causes and consequences. We also suggest some strategies for prevention. The special needs of preterm infants are well recognised, and have been specifically excluded.
Definitions
After release from a relatively hypoxic intrauterine environment, mean haemoglobin concentration falls by 30% to 110 g/1 by the eighth postnatal week, followed by a rise to 125 g/1 at 4 months. Mean haemoglobin then increases gradually to 135 g/1 in preadolescents.5 The lower 95% limit of the reference range from 6 months to 4 years for haemoglobin is 110 g/1, with corresponding values of 32% for packed cell volume, and 72 fl for mean corpuscular volume (MCV). Iron deficiency without anaemia implies that haemoglobin synthesis is impaired, but that haemoglobin concentration has not fallen sufficiently to meet the definition of anaemia. It is usually recognised on the basis of criteria other than haemoglobin concentration: serum ferritin (<l0 μg/l), erythrocyte protoporphyrin (>2.5 μg/g haemoglobin), MCV <72 fl, or a response to oral …