IRON DEFICIENCY IN CHILDREN
Cleghorn GJ
Department of Paediatrics and Child Health,
University of Queensland, Royal Children’s Hospital, Brisbane, Queensland,
Australia
In
1968, Dobbing suggested that there were vulnerable periods of neurological
development that coincided with times of maximal brain growth. These periods
began during fetal development at around 25 weeks gestation and continued for
the first two years of postnatal life. He went on to suggest that nutrient
deficiencies occurring during these vulnerable periods may well have some
impact upon brain growth and hence neurological and psychomotor development.
This has since shown to be the case. These nutrient deficits have been shown to
result in functional deficiencies rather than physical abnormalities. One area
that appears to be involved in this process is the process of myelination.
Myelination in particular appears to be vulnerable to malnutrition. In humans,
the myelin sheath begins to appear around the fourth month of fetal development
and first appears in the spinal cord before spreading to the medulla, pons and
the higher centres. It is assumed that myelination precedes functional
activity. In children with marasmus, myelination is reduced with a reduction in
quantity but with no aberration in composition.
Iron is directly involved in myelination as a
co-factor for cholesterol and lipid biosynthesis and indirectly with its
involvement in oxidative metabolism that is highest in the brain in the
oligodendrocytes. The oligodendrocytes are the iron containing cells
in the brain and their only known function is myelin production. The
oligodendrocytes also contain transferrin and ferritin, both of which are
essential for normal iron homeostasis. The ferritin in the oligodendrocytes is in
the form of H-ferritin that is the heavy chain form and which is associated
with high iron usage and low iron storage7. H-chain ferritin is only
seen in the oligodendrocytes in early development at the time of maximal myelin
deposition. Hence it is very clear that iron deprivation occurring during this
time period may have an adverse effect upon myelination and hence psychomotor
development. A number of studies have demonstrated this and have also suggested
that deficiencies occurring during these vulnerable periods of development
result in permanent disability. It has also been shown that iron deficiency
does have a negative effect upon nerve conduction and hence myelination with
studies of auditory evoked potentials showing an increase in central conduction
time with a change in amplitude of the waves and a longer interwave latent
period.
Iron is essential for brain development. Brain iron is stored preferentially in the extra pyramidal tracts and is laid down in the first twelve months of life. Once the blood brain barrier closes very little iron can be deposited in the CNS and hence the dietary intake of iron is essential during this deposition period. Iron also appears to be an integral part of the synthesis, uptake and degradation of the neurotransmitter dopamine and iron deficient animals have been shown to have dopamine deficiency. Several studies have now shown that iron deficient anaemic infants can score lower on tests of mental development compared to non-iron deficient controls. Furthermore, at least one study has shown that these deficits appear to be permanent. These infants appeared to have reproducible deficits in body balance and coordination and in language skills which could be interpreted as implying problems with nerve conduction and hence myelination.