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Iron deficiency is the most common nutritional deficiency
worldwide. Iron depletion and deficiency and, less commonly,
iron-deficiency anaemia (defined in the Box) are prevalent in all age
groups, but particularly in infants, the elderly and women after the
onset of menses, and also in socioeconomically deprived
populations, such as refugees and recent migrants.
Infancy is the critical period for brain growth, and nutrient
deficiencies during this time may affect psychomotor development
and neurocognition. Iron-deficient infants are often apathetic,
listless, irritable and anorexic. These symptoms resolve rapidly
with iron supplementation, but less well known is the fact that long
term neurocognitive impairment may persist.1,2 Young children with
iron-deficiency anaemia have been found to score 12 to 15 points lower
on the Bayley infant development scale than their iron-sufficient
peers.3 Prolonged iron
supplementation improved these scores and other performance
parameters, such as fine motor and discriminative skills, but did not
produce complete resolution despite an excellent haematological
response.4 Persisting
deficits in a variety of psychometric tests have also been shown both
in five-year-olds in Chile and 10-year-olds in Costa Rica who were
iron deficient in infancy,1,5 but there are no
convincing data on long term outcome in adult life. In older children
with iron deficiency (eg, teenage girls), iron supplementation can
also improve neurocognitive performance.6
Therefore, although no studies have established a direct causal
relationship between iron deficiency and performance, it is prudent
to prevent iron depletion and, if present, to treat it until iron
status is normal.
Australian paediatricians have long been aware that populations who
have recently migrated, such as the Vietnamese, as well as refugees
from most of the world's troublespots and Indigenous populations,
have a high prevalence of iron deficiency. In this issue of the
Journal, Karr and colleagues report on the iron status of a group of
Sydney children whose mothers were born in an Arabic-speaking
country.7 In this
group of 403 children aged 12-38 months, prevalence of
iron-deficiency anaemia was 6%, iron deficiency without anaemia 9%,
and iron depletion 23%. These levels are disturbing. Similar results
have been found among children of South East Asian descent in
Adelaide, South Australia.8 Although most children with
iron depletion will suffer no long term harm, they should be viewed as
part of a continuum, with children with iron-deficiency anaemia at
greatest risk of not achieving their full intellectual potential.
Most of these children have no other nutritional deficiency and,
indeed, are often obese.
The risk factors for impaired iron status identified by Karr
and colleagues were similar to those seen in other countries, and
include prematurity, excessive consumption of cows' milk and recent
maternal immigration. However, the mechanisms by which these risk
factors contribute to iron depletion are explored only
superficially by Karr and colleagues, and no convincing strategies
to correct iron depletion were espoused other than provision of
Arabic interpreters at early childhood health centres.
Some of the reasons the identified risk factors contribute to iron
depletion are as follows. Prematurity results in inadequate iron
accrual. Cows' milk is deficient in iron and in young infants causes
occult microscopic blood loss from the colon. Recent maternal
immigration may be linked to poverty, and these children may consume
excessive amounts of cows' milk because it is cheap and readily
available. Recent immigrant mothers may also have inadequate iron
stores, resulting in diminished iron stores in their babies. Once
children become iron deficient, they become very restricted in the
range of foods they will accept. Appetite and tolerance of new or
previously discarded foods improves with iron
repletion.9
Furthermore, maternal iron deficiency results in large placental
size and small babies whose iron stores are insufficient to sustain
them through rapid early growth.10 The currently
fashionable "Barker hypothesis" states that health outcomes in
later life are programmed by intrauterine events. Infants who are
small for gestational age tend to have worse adult outcomes and are
more likely to develop insulin resistance and hypertension.
Maternal iron deficiency may conceivably result in yet to be
recognised consequences in adult life.
Medical practitioners should try to ensure that children and women of
childbearing age are iron replete. Commonsense dictates that,
because of the concern over persisting neurocognitive deficits, it
is much better to prevent iron deficiency in the community than to
treat it case by case. Although it is tempting to view iron depletion as
a problem of disadvantage, many other children are at risk.
We therefore recommend that:
- Young children of
high-risk ethnic groups, survivors of prematurity and children with
excessive cows' milk consumption or prolonged breast-feeding
(breast milk is very low in iron) should have a full blood examination
and iron studies, including measurement of ferritin levels.
- Any developmentally delayed child should be screened for iron
status. In addition, children with breath holding may be iron
deficient, and breath holding may improve substantially following
iron supplementation.11
- Iron-depleted children should receive full supplementation of
elemental iron at a dose of 6 mg/kg per day for about two to three months,
when the iron studies should be repeated. Commercial iron
preparations are relatively unpalatable, and it is often difficult
to enforce prolonged therapy. Iron absorption is enhanced if
supplements are administered with a vitamin C source, such as orange
juice. Parents should be warned that bowel motions are often black and
that this does not denote ill-health. Dietary advice about iron-rich
foods should also be offered.
- Protocol advice for iron deficiency should be incorporated into the
early years program currently being promoted by the Commonwealth
Department of Health and Aged Care and the Royal Australasian College
of Physicians, which concentrates on optimising intellectual and
social outcomes with interventions aimed at infants.
Some countries, not including Australia, recommend iron
supplementation in infancy. The most effective measure on a global
scale to prevent iron deficiency has been fortification of infant
formula with iron, and currently all breast-milk substitute
formulas in Australia are iron fortified. This intervention is most
effective in the first year of life, but does not address the problem of
infants who are exclusively breastfed and children with a large
intake of cows' milk. All infants should have iron-rich foods,
particularly red meat, introduced shortly after six months of age.
A dietary program aimed at improving iron status in Australian
mothers and children would benefit both individuals and society as a
whole. The high incidence of iron-deficiency anaemia in this cohort
of Australian children of Arabic background and its known
association with persisting neurocognitive deficits should
provide Australian health planners with food for thought.
Richard T L Couper
Senior Paediatric Gastroenterologist
University of Adelaide, Women's and Children's Hospital, Adelaide,
SA
Karen N Simmer
Associate Professor and Staff Neonatologist Flinders University
and Flinders Medical Centre, Adelaide, SA
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infants with iron deficiency. N Engl J Med 1991; 325: 687-694.
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De Andraca I, Walter T, Castillo M, et al. Iron deficiency anaemia
and its effects upon psychological development at preschool age: a
longitudinal study. Nestlé Foundation Nutritional Annual Report.
Lausanne: Nestlé Foundation, 1990; 53-62.
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Oski FA, Honig AS. The effects of therapy on the developmental
scores of iron deficient infants. J Pediatr 1978; 92: 21-25.
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Lozoff B, Wolf AW, Jimenez E. Iron deficiency anaemia and infant
development: effects of extended oral iron therapy. J Pediatr
1996; 129: 382-385.
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Lozoff B, Jimenez E, Hagen J, et al. Poorer behavioural and
developmental outcome more than 10 years after treatment for iron
deficiency in infancy. Pediatrics 2000; 105: ES1.
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Bruner AB, Joffe A, Duggan AK, et al. Randomized study of cognitive
effects of iron supplementation in non-anaemic iron deficient
adolescent girls. Lancet 1996; 348: 992-996.
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Karr MA, Mira M, Alperstein G, et al. Iron deficiency in
Australian-born children of Arabic background in central Sydney.
Med J Aust 2001; 174: 165-168.
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Oti-Boateng P, SeshadTi R, Petrick S, Gibson RA, Simmer K. Iron
status and dietary iron intake of 6-24 month old children in Adelaide.
J Paediatr Child Health 1998; 34: 250-253.
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Stockman JA. Microcytic anaemias. In: Behram RE, editor. Nelson
textbook of paediatrics. 14th ed. Philadelphia: WB Saunders, 1992;
1239-1241.
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Hindmarsh PC, Geary NIPP, Rodeck CH, et al. Effects of early
maternal iron stores on placental weight and structure.
Lancet 2000; 356: 719-723.
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Mocan H, Yildiran A, Orhan F, Erduran E. Breath holding spells in 91
children and response to treatment with iron. Arch Dis Child
1999; 81: 361-362.
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© 2001 Medical Journal of Australia.
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