Iron is important in neurodevelopment and cognitive function, and globally preventing iron deficiency and iron deficiency anemia remains a high priority. Term breast-fed infants and infants fed an iron-fortified formula usually have a satisfactory iron status during the first 6 months of life, but there are still ambiguities in assessing iron status in infants and how to properly meet their iron requirements. This is particularly evident for preterm infants, who are born with low iron stores, and for whom recommendations for iron provision vary considerably. In part, this may be due to immaturity in the regulation of iron homeostasis in young infants.
Whereas 9-month-old infants appear to be able to downregulate iron absorption when being iron replete, 6-month-old infants cannot do this. Iron may be provided as drops or in iron-fortified products, but the forms provided may be metabolized differently, and excess iron in drops may cause adverse effects, possibly due to a limited ability to regulate iron absorption in young infants. Adverse effects are manifested by decreased growth: in well-nourished infants by reduced gain in length, in poorly nourished populations by lower gain in weight. The mechanism behind the decreased growth is not known, but it may involve free radical-mediated effects of iron or an interaction with zinc absorption/homeostasis. It therefore seems that iron drops should not be given to iron-replete infants.
The main causes of iron deficiency (ID) are briefly discussed, followed by the examination of studies of ID and child cognitive and motor development and behaviour for evidence of a causal link, classifying them by study design. Iron deficiency anaemia (IDA) is associated with many psychosocial and economic disadvantages that can affect child development and could explain the frequently demonstrated relationship between IDA and poor development and behavioural differences.
There is evidence of changes to brain function in infants with IDA. Many treatment trials lack statistical power due to small samples, including children without ID in the sampling or iron treatment resulting in little or no differences in iron status between placebo and treated groups. In children with IDA under 3 years, randomized trials indicate that iron supplementation is usually beneficial to motor development, but the effect on mental development is inconsistent.
Iron supplementation also has a beneficial effect on cognitive function in school-aged children with IDA. Evidence for a threshold level of ID at which child development is affected is inconsistent, but children with IDA are most likely to benefit from iron supplementation. Possible harmful effects of iron supplementation in iron-replete children on growth and morbidity have to be considered when developing programmes and policy.
Iron deficiency (ID) is prevalent in infants, children and adolescents worldwide due to their high iron requirements during growth, low dietary iron intake and low-bioavailability diet. Low iron status is associated with adverse health consequences throughout childhood. Prevention measures should be initiated early and include iron supplementation of pregnant women, delayed cord clamping at delivery and exclusive breast-feeding for 6 months. Iron needs to increase sharply after the first 4-6 months of life and high iron content of complementary foods is critical. Iron fortification of infant formulas and infant cereals, addition of micronutrient powders to home-prepared complementary foods, or provision of iron drops are the most effective prevention strategies in weaning infants, but early introduction of meat and delayed introduction of cow’s milk are also important.
Prevention strategies in older children involve dietary approaches which increase iron content and bioavailability of the diet, and consumption of iron-fortified foods. In areas of extensive ID, iron supplementation may be required. If malaria is prevalent, large supplementation doses should only be given to children with confirmed ID. All interventions to control pediatric ID should be integrated into larger national and global health programs for pregnant women and children, including health education, malaria prevention and deworming. The impact of ID prevention strategies on iron status and the prevalence of ID should be monitored by measuring iron status periodically in the population.
Infantile iron deficiency anemia (IDA) reduces maximal lifetime cognitive capacity and can threaten the life of an adolescent mother in childbirth. Administration of iron is a component of strategies for preventing or reversing iron deficiency (ID) and iron can be given parenterally or as oral supplements or fortified food. Safety issues can arise at the point of administration, i.e. in the gut lumen, and as a consequence of excessive iron stores arising from the interventions.
Recent improvements in the pharmacology of parenteral iron compounds open the way to greater consideration of the intravenous route in pediatric therapy, and even public health. Oral iron supplementation, usually with folic acid, is the main treatment of IDA in the clinical setting. It is often combined with multiple micronutrients and is also used for resolution of severe anemia at the community level and for prophylaxis in the nonanemic population. Fortification of staple food (such as flour), or age-specific foods (infant formula, complementary foods) and beverages are the usual methods for ID prophylaxis. Special iron-rich preparations (powders, crushable tablets, edible spreads) are available for home fortification. Biofortification, i.e. enriching the iron content of crops during cultivation, is a novel approach, yet to be fully implemented or evaluated for children. Side effects and toxicity after oral iron intake are seen in the gut lumen.
After oral and parenteral iron intake, the rise in circulating iron can increase the risk of complications from coexisting infections, notably with malaria, and when individual iron status is adequate. Growth impairment occurs with exposure of iron-sufficient children to iron interventions, so that targeting of iron to ID individuals seems advisable.
Numerous adverse consequences from accumulation of excessive total body iron stores show up as a consequence of iron-mediated oxidative stress. Incomplete maturation of iron homoeostasis may permit higher iron absorption before 6 months of age.