Elisa M Holmlund-Suila1, Helena H Hauta-Alus2, Maria Enlund-Cerullo3, Jenni Rosendahl4, Saara M Valkama5, Sture Andersson6, Outi Mäkitie7. 1. Children's Hospital, Pediatric Research Center, University of Helsinki and Helsinki University Hospital, Biomedicum 2 C, P.O. Box 705, 00020 HUS, Helsinki, Finland; Research Program for Clinical and Molecular Metabolism, Faculty of Medicine, University of Helsinki, Biomedicum 1, P.O. Box 63, 00014, Helsinki, Finland. Electronic address: elisa.holmlund-suila@hus.fi. 2. Children's Hospital, Pediatric Research Center, University of Helsinki and Helsinki University Hospital, Biomedicum 2 C, P.O. Box 705, 00020 HUS, Helsinki, Finland; Research Program for Clinical and Molecular Metabolism, Faculty of Medicine, University of Helsinki, Biomedicum 1, P.O. Box 63, 00014, Helsinki, Finland; Finnish Institute for Health and Welfare (THL), Population Health Unit, P.O. Box 30, FI-00271, Helsinki, Finland; PEDEGO Research Unit, Oulu University Hospital and University of Oulu, P.O. Box 8000, FI-90014, Oulu, Finland. Electronic address: helena.hauta-alus@helsinki.fi. 3. Children's Hospital, Pediatric Research Center, University of Helsinki and Helsinki University Hospital, Biomedicum 2 C, P.O. Box 705, 00020 HUS, Helsinki, Finland; Research Program for Clinical and Molecular Metabolism, Faculty of Medicine, University of Helsinki, Biomedicum 1, P.O. Box 63, 00014, Helsinki, Finland; Folkhälsan Institute of Genetics, Helsinki, Finland. Electronic address: maria.enlund@helsinki.fi. 4. Children's Hospital, Pediatric Research Center, University of Helsinki and Helsinki University Hospital, Biomedicum 2 C, P.O. Box 705, 00020 HUS, Helsinki, Finland; Research Program for Clinical and Molecular Metabolism, Faculty of Medicine, University of Helsinki, Biomedicum 1, P.O. Box 63, 00014, Helsinki, Finland. Electronic address: jenni.rosendahl@hus.fi. 5. Children's Hospital, Pediatric Research Center, University of Helsinki and Helsinki University Hospital, Biomedicum 2 C, P.O. Box 705, 00020 HUS, Helsinki, Finland; Research Program for Clinical and Molecular Metabolism, Faculty of Medicine, University of Helsinki, Biomedicum 1, P.O. Box 63, 00014, Helsinki, Finland. Electronic address: saara.valkama@hus.fi. 6. Children's Hospital, Pediatric Research Center, University of Helsinki and Helsinki University Hospital, Biomedicum 2 C, P.O. Box 705, 00020 HUS, Helsinki, Finland. Electronic address: sture.andersson@hus.fi. 7. Children's Hospital, Pediatric Research Center, University of Helsinki and Helsinki University Hospital, Biomedicum 2 C, P.O. Box 705, 00020 HUS, Helsinki, Finland; Research Program for Clinical and Molecular Metabolism, Faculty of Medicine, University of Helsinki, Biomedicum 1, P.O. Box 63, 00014, Helsinki, Finland; Folkhälsan Institute of Genetics, Helsinki, Finland; Department of Molecular Medicine and Surgery, Karolinska Institutet, and Clinical Genetics, Karolinska University Laboratory, Karolinska University Hospital, SE-17176, Stockholm, Sweden. Electronic address: outi.makitie@helsinki.fi.
Abstract
BACKGROUND & AIMS: During early childhood the risk of iron deficiency (ID) is high. Serum ferritin serves as a marker of iron status. We explored prevalence of ID and iron deficiency anemia (IDA), and identified determinants of iron status in infants and toddlers. METHODS: We performed a secondary analysis of the Vitamin D intervention in infants (VIDI) study in Finnish healthy term infants. According to study protocol, at 12- and 24-months of age iron status, growth and dietary intakes were evaluated. ID was defined as serum ferritin <10 μg/L and IDA as serum ferritin <10 μg/L and Hb <112 g/L. For the present study, altogether 766 children provided data (N = 498 infants at 12 months, N = 508 toddlers at 24 months). RESULTS: ID prevalence increased from 14% in infants to 20% in toddlers. IDA prevalence was 3% at both time points. In infants, ID and IDA were more common in boys than in girls (19% vs. 9%, p = 0.001 and 5% vs. 1%, p = 0.039) but no sex-difference in toddlers was observed. Of infants, 30% had daily iron intake below average requirement of 5 mg/day. Higher daily iron intake per body weight (mg/kg) independently associated with higher infant serum ferritin (B (95% CI) 0.30 (0.04, 0.56), p = 0.026). Correlation between iron intake and ferritin was stronger in infants with ID than in infants without ID. Breastfeeding was more common (63% vs. 35%, p < 0.001) among ID infants than in infants without ID. In toddlers, frequent consumption of milk products independently associated with lower ferritin (B (95% CI) -0.03 (-0.05, -0.01), p = 0.001). Consumption of meat and fish associated with better iron status. Serum ferritin at both time points associated with duration of gestation and growth. The association of growth and ferritin was age-dependent in boys, while in girls, faster growth associated consistently with lower ferritin. CONCLUSIONS: In Northern European healthy infants and toddlers ID is common. The intake of iron remains below recommendations and food consumption and iron intake associate with iron status. Further studies are warranted to assess significance of ID on child development and clinical health outcomes. The project protocol is registered at ClinicalTrials.gov: NCT01723852.
BACKGROUND & AIMS: During early childhood the risk of iron deficiency (ID) is high. Serum ferritin serves as a marker of iron status. We explored prevalence of ID and iron deficiency anemia (IDA), and identified determinants of iron status in infants and toddlers. METHODS: We performed a secondary analysis of the Vitamin D intervention in infants (VIDI) study in Finnish healthy term infants. According to study protocol, at 12- and 24-months of age iron status, growth and dietary intakes were evaluated. ID was defined as serum ferritin <10 μg/L and IDA as serum ferritin <10 μg/L and Hb <112 g/L. For the present study, altogether 766 children provided data (N = 498 infants at 12 months, N = 508 toddlers at 24 months). RESULTS: ID prevalence increased from 14% in infants to 20% in toddlers. IDA prevalence was 3% at both time points. In infants, ID and IDA were more common in boys than in girls (19% vs. 9%, p = 0.001 and 5% vs. 1%, p = 0.039) but no sex-difference in toddlers was observed. Of infants, 30% had daily iron intake below average requirement of 5 mg/day. Higher daily iron intake per body weight (mg/kg) independently associated with higher infant serum ferritin (B (95% CI) 0.30 (0.04, 0.56), p = 0.026). Correlation between iron intake and ferritin was stronger in infants with ID than in infants without ID. Breastfeeding was more common (63% vs. 35%, p < 0.001) among ID infants than in infants without ID. In toddlers, frequent consumption of milk products independently associated with lower ferritin (B (95% CI) -0.03 (-0.05, -0.01), p = 0.001). Consumption of meat and fish associated with better iron status. Serum ferritin at both time points associated with duration of gestation and growth. The association of growth and ferritin was age-dependent in boys, while in girls, faster growth associated consistently with lower ferritin. CONCLUSIONS: In Northern European healthy infants and toddlers ID is common. The intake of iron remains below recommendations and food consumption and iron intake associate with iron status. Further studies are warranted to assess significance of ID on child development and clinical health outcomes. The project protocol is registered at ClinicalTrials.gov: NCT01723852.