Iron status of breastfed infants is improved equally by medicinal iron and iron-fortified cereal
Ziegler EE, et al.
Am J Clin Nutr. 2009; 90(1):76-87.
(AA) Although uncommon, iron deficiency (ID) occurs in breastfed infants. The regular provision of iron may prevent ID. The objective was to test the feasibility and effectiveness of 2 modalities of providing iron (medicinal iron or iron-fortified cereal) to breastfed infants. The study tested the hypothesis that regular provision of iron improves iron status of breastfed infants without adverse effects. In this prospective, randomized, open-label trial, breastfed infants received on a regular basis either medicinal iron (n = 48) or an iron-fortified fruit-cereal combination (n = 45) from 4 to 9 mo or no intervention (control group; n = 59). The interventions provided 7.0-7.5 mg ferrous sulfate/d. Infants were enrolled at 1 mo and were followed to 2 y. Iron-status indicators were determined periodically, stool characteristics were recorded, and growth was monitored. The regular provision of iron led to improved iron status during and for some months after the intervention. Both sources of iron were about equally effective. Iron affected stool color but had no effect on feeding-related behavior. However, medicinal iron was associated with a small but significant reduction in length gain and a trend toward reduced weight gain. ID anemia was observed in 4 infants (2.3%), most of whom had a low birth iron endowment. Mild ID was common in the second year of life. Regular provision of medicinal iron or iron-fortified cereal improves the iron status of breastfed infants and may prevent ID. Both modalities are equally effective, but medicinal iron leads to somewhat reduced growth.
Optimization of a phytase-containing micronutrient powder with low amounts of highly bioavailable iron for in-home fortification of complementary foods
Troesch B, et al.
Am J Clin Nutr. 2009; 89(2):539-44.
(AA) In-home fortification of complementary foods with micronutrient powders containing low amounts of iron may be potentially safer than powders containing high amounts of iron. However, low iron doses have little nutritional effect, unless iron absorption is high. The objective was to maximize iron absorption from a low-iron micronutrient powder for in-home fortification by testing combinations of iron as NaFeEDTA, ascorbic acid, and a microbial phytase active at gut pH. In addition, a recently proposed enhancer of iron absorption, L-alpha-glycerophosphocholine (GPC), was tested. In 6 separate iron-absorption studies using a crossover design, women (n = 101) consumed whole-maize porridge fortified with 3 mg stable isotope-labeled FeSO4 or NaFeEDTA with different combinations of enhancers added to the meals at the time of consumption. Incorporation of iron isotopes into erythrocytes 14 d later was measured. The addition of phytase when iron was present as either NaFeEDTA or FeSO4, with or without ascorbic acid, significantly increased iron absorption. The combined addition of phytase, ascorbic acid, and NaFeEDTA resulted in an absorption of 7.4%, compared with an absorption of 1.5% from FeSO4 without enhancers in the same meal (P < 0.001). The addition of ascorbic acid did not significantly increase iron absorption from NaFeEDTA, and the addition of calcium did not significantly inhibit iron absorption from NaFeEDTA in the presence of ascorbic acid. The addition of L-alpha-glycerophosphocholine did not significantly increase iron absorption. Optimization of the micronutrient powder increased iron absorption from a highly inhibitory meal approximately 5-fold. This approach may allow for effective, untargeted in-home fortification of complementary foods with low amounts of highly bioavailable iron
Serum hepcidin is significantly associated with iron absorption from food and supplemental sources in healthy young women
Young MF, et al.
Am J Clin Nutr. 2009; 89(2):533-8.
(AA) Hepcidin is a key regulator of iron homeostasis, but to date no studies have examined the effect of hepcidin on iron absorption in humans. Our objective was to assess relations between both serum hepcidin and serum prohepcidin with nonheme-iron absorption in the presence and absence of food with the use of dual stable-iron-isotope techniques. The study group included 18 healthy nonpregnant women. Women received in random order a supplemental iron source (7.6 mg FeSO4 providing 0.9 mg 58Fe as FeSO4) and 6.8 mg 57Fe ferrous sulfate tracer administered with a nonheme food source [orange-fleshed sweet potato (OFSP): 1.4 mg native Fe]. Iron absorption was determined by analyzing blood samples taken 14 d after dosing with the use of magnetic sector thermal ionization mass spectrometry. Serum hepcidin was assessed by a new competitive serum enzyme-linked immunosorbent assay (ELISA) specific for the refolded, mature 25-amino acid form, and serum prohepcidin was assessed by an ELISA specific for amino acids 28-47 of the hepcidin prohormone. In these women, iron absorption averaged 14.71 +/- 10.7% from the supplemental iron compared with 3.63 +/- 6.5% from the OFSP. Absorption of nonheme iron assessed in the presence (P = 0.038) and absence (P = 0.0296) of food was significantly associated with serum hepcidin but was not significantly related to serum prohepcidin. Serum hepcidin, but not prohepcidin, was inversely associated with iron absorption from supplemental and food-based nonheme-iron sources in iron-replete healthy women.
Copper deficiency alters the neurochemical profile of developing rat brain
Gybina AA, et al.
Nutr Neurosci. 2009; 12(3):114-22.
(AA) Copper deficiency is associated with impaired brain development and mitochondrial dysfunction. Perinatal copper deficiency was produced in Holtzman rats. In vivo proton NMR spectroscopy was used to quantify 18 cerebellar and hippocampal metabolites on postnatal day 21 (P21). Copper status was evaluated in male copper-adequate (CuA) and copper-deficient (CuD) brothers at P19 and at P23, 2 days following NMR experiments, by metal and in vitro metabolite data. Compared to CuA pups, CuD pups had lower ascorbate concentration in both brain regions, confirming prior HPLC data. Both regions of CuD rats also had lower N-acetylaspartate levels consistent with delayed development or impaired mitochondrial function similar to prior work demonstrating elevated lactate and citrate. For other metabolites, the P21 neurochemical profile of CuD rats was remarkably similar to CuA rats but uniquely different from iron-deficient or chronic hypoxia models. Further research is needed to determine the neurochemical consequences of copper deficiency.
Iron status and oxidative stress biomarkers in adults: a preliminary study
Mendes JF, et al.
Nutrition. 2009; 25(4):379-84.
(AA) Although essential to many vital processes, iron catalyzes reactions that produce reactive oxygen species, which are associated with the increased risk of non-communicable chronic diseases and precocious aging. This study investigated whether ferritin, hemoglobin concentration, and dietary iron consumption are related to oxidative stress biomarkers in adults. Data were collected from 134 allegedly healthy subjects >18 y of age who were randomly selected to participate in a cross-sectional study as part of the pilot project Prevalence of Risk Factors for Non-communicable Chronic Diseases in the Federal District, Brazil (VIVA Saúde-DF). Serum ferritin, malondialdehyde (MDA) and protein carbonyl concentrations, hemoglobin, and dietary iron consumption were analyzed. A weak positive correlation (r = 0.189, P = 0.032) and association (P = 0.046) was observed for serum ferritin and MDA. Hemoglobin concentrations were positively associated with serum MDA (P = 0.040). Dietary iron intake and serum protein carbonyl concentrations showed a weak positive correlation (r = 0.173, P = 0.046) for all subjects. Iron intake by women was positively associated with serum protein carbonyl (P = 0.03). A lower serum MDA concentration was found in ferritin-deficient subjects (P = 0.015) and men with anemia (P = 0.011). These results suggest that low levels of iron may reduce oxidative stress.
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