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Effect of improved vitamin A status on response to iron supplementation in Pakistani infants
C A Northrop-Clewes1, P I Paracha, U J McLoone
1Department of Biomedical Sciences, University of Ulster, Coleraine, United Kingdom. c.clewes@ulst.ac.uk
Insights
Vitamin A may protect infants receiving iron supplements. Increased vitamin A status was linked to reduced inflammation and infection markers, suggesting a protective role against potential iron toxicity in developing countries.
Area of Science:
- Nutritional Immunology
- Pediatric Nutrition
- Micronutrient Interactions
Background:
- Iron supplementation is crucial for preventing anemia in infants.
- Potential adverse effects of iron supplementation, such as increased infection risk, are a concern.
- Vitamin A plays a vital role in immune function and has anti-infective properties.
Purpose of the Study:
- To investigate the potential protective effect of vitamin A in infants receiving iron supplements.
- To explore the relationship between vitamin A status, iron status, and inflammatory markers in infants.
Main Methods:
- Observational study in infants receiving iron supplements or placebo for 3 months.
- Monitoring of hemoglobin, ferritin, and acute-phase proteins (e.g., alpha 1-antichymotrypsin).
- Assessment of plasma vitamin A (retinol) and other nutrient levels, including immunoglobulins.
Main Results:
- Iron supplementation increased hemoglobin and ferritin levels.
- Both groups showed improved vitamin A status, likely due to seasonal dietary changes.
- In iron-supplemented infants, increased vitamin A was associated with reduced markers of inflammation (ACT) and infection (immunoglobulins A and M).
Conclusions:
- Vitamin A status may influence the effects of iron supplementation in infants.
- Even small increases in dietary vitamin A could mitigate potential adverse effects of iron, possibly by reducing infection.
- Further intervention studies are needed to confirm the role of vitamin A in reducing infection and its benefits on iron status.
Abstract:
We report an apparently protective effect of vitamin A in infants who received iron supplements (15 mg/d) for 3 mo. Those receiving iron showed increases in hemoglobin (8 g/L), ferritin (3.7 micrograms/L), and the acute-phase protein alpha 1-antichymotrypsin (ACT; 0.06 g/L). In both the placebo and iron-supplemented groups there were increases in plasma retinol, lutein, alpha-tocopherol, immunoglobulin A, and immunoglobulin G. The improvement in vitamin A status could only have been from a seasonal increase in dietary sources of vitamin A, eg, breast milk and early weaning foods, and there were no obvious effects on iron utilization (hemoglobin concentrations). However, in the infants receiving iron, those whose retinol concentrations increased also showed reductions in ACT, ferritin, immunoglobulin A, and immunoglobulin M. Vitamin A is well known for its antiinfective properties and we suggest that these observations illustrate the importance of even small increases in dietary vitamin A or differences in vitamin A status in reducing the potentially toxic effects of iron supplements in persons in developing countries. These conclusions should now be confirmed with an intervention study to show that the benefits of vitamin A on iron status are due to reduced levels of infection.