Prenatal supplementation with daily iron are effective to reduce the risk of low birthweight, and to prevent maternal anaemia and iron deficiency in pregnancy. Associated maternal side effects and particularly high Hb concentrations during pregnancy at currently used doses suggest the need to update recommendations on doses and regimens for routine iron supplementation.

Universal prenatal supplementation with iron or iron+folic acid provided either daily or weekly is effective to prevent anaemia and iron deficiency at term. We found no evidence, however, of the significant reduction in substantive maternal and neonatal adverse clinical outcomes (low birthweight, delayed development, preterm birth, infection, postpartum haemorrhage). Associated side effects and particularly haemoconcentration during pregnancy may suggest the need for revising iron doses and schemes of supplementation during pregnancy and adjust preventive iron supplementation recommendations.

Pregnancy, mostly because of the mitochondria-rich placenta, is a condition that favors oxidative stress. Transitional metals, especially iron, which is particularly abundant in the placenta, are important in the production of free radicals. Protective mechanisms against free radical generation and damage increase throughout pregnancy and protect the fetus, which, however, is subjected to a degree of oxidative stress. Oxidative stress peaks by the second trimester of pregnancy, ending what appears to be a vulnerable period for fetal health and gestational progress. Conditions restricted to pregnancy, such as gestational hypertension, insulin resistance and diabetes, exhibit exaggerated indications of free radical damage. Antioxidants as well as avoidance of iron excess ameliorate maternal and early fetal damage. In rats both iron deficiency and excess result in free radical mitochondrial damage. Estimates of gestational iron requirements and of the proportion of iron absorbed from different iron supplemental doses suggest that with present supplementation schemes the intestinal mucosal cells are constantly exposed to unabsorbed iron excess and oxidative stress. Unpublished work carried out in Mexico City with nonanemic women at midpregnancy indicates that 60 mg/d of iron increases the risk of hemoconcentration, low birth weight and premature birth and produces a progressive decline in plasma copper. These risks are not observed in women supplemented with 120 mg iron once or twice per week. Studies on the influence of iron supplementation schemes on oxidative stress are needed.

Approximately two billion people, mainly women and children, are iron deficient. Two studies examined the effects of iron deficiency and supplementation on rats. In study 1, mitochondrial functional parameters and mitochondrial DNA (mtDNA) damage were assayed in iron-deficient (<5 g͞day) and iron-normal (800 g͞day) rats and in both groups after daily high-iron supplementation (8,000 g͞day) for 34 days. This dose is equivalent to the daily dose commonly given to iron-deficient humans. Iron-deficient rats had lower liver mitochondrial respiratory control ratios and increased levels of oxidants in polymorphonuclear-leukocytes, as assayed by dichlorofluorescein (P < 0.05). Rhodamine 123 fluorescence of polymorphonuclear-leukocytes also increased (P < 0.05). Lowered respiratory control ratios were found in daily high-iron-supplemented rats regardless of the previous iron status (P < 0.05). mtDNA damage was observed in both iron-deficient rats and rats receiving daily high-iron supplementation, compared with ironnormal rats (P < 0.05). Study 2 compared iron-deficient rats given high doses of iron (8,000 g) either daily or every third day and found that rats given iron supplements every third day had less mtDNA damage on the second and third day after the last dose compared to daily high iron doses. Both inadequate and excessive iron (10 ؋ nutritional need) cause significant mitochondrial malfunction. Although excess iron has been known to cause oxidative damage, the observation of oxidant-induced damage to mitochondria from iron deficiency has been unrecognized previously. Untreated iron deficiency, as well as excessive-iron supplementation, are deleterious and emphasize the importance of maintaining optimal iron intake.

Further studies are needed to assess the effects of routine antenatal supplementation with iron or a combination of iron and folic acid on clinically important maternal and infant outcomes.

The iron status of a national sample of adults living in France and participating in the SU.VI.MAX cohort, was assessed using serum ferritin and hemoglobin concentrations. Complete data were obtained for 6648 women 35 ± 60 y old and for 3283 men 45 ± 60 y old. Assessment of iron dietary intakes was realized on a subsample of 3111 women and 2337 men who reported six 24 h dietary records during a one-year period; 22.7% of menstruating women and 5.3% of post-menopausal women presented a total depletion of iron stores (serum ferritin`15 mgal). Iron-de®cient anemias were found in, respectively, 4.4% and less than 1% of these women. Three-quarters of the anemias were related to iron de®ciency in menstruating women. In men, iron depletion and iron de®ciency anemia were very rare. Post-menopausal women had much higher serum ferritin levels than menstruating women. In menstruating women, those using intrauterine devices had signi®cantly lower serum ferritin levels than those without contraception, and much lower than those using oral contraception. The frequency of iron depletion reached 28.1% in women using intrauterine devices, but only 13.6% in those using oral contraceptives. The mean iron intake was 16.7 AE 5.7 mgad in men and 12.3 AE 3.4 mgad in women. Heme iron represented respectively, 11.1 and 10.4% of iron intake. Ninety-three percent of menstruating women had dietary iron intakes lower than recommended dietary allowances (RDA); 52.6% consumed less than two thirds of these RDA. In post-menopausal women and men, respectively 27.7% and 3.6% had dietary intakes lower than RDA. Serum ferritin was positively correlated with meat, ®sh and total iron intake, and negatively correlated with dietary products consumption, calcium and ®ber intake.

Background: Genetically modified, low-phytic acid strains of maize were developed to enhance mineral absorption, but have not been tested previously in humans. Objectives: We evaluated the mineral and phytic acid contents of a low-phytic acid "flint" maize (LPM, the lpa-1-1 mutant) and its parent, wild-type strain (WTM) and measured iron absorption from tortillas prepared with each type of maize and from a reference dose of ferrous ascorbate. Design: Proximate composition and mineral and phytic acid contents were measured by standard techniques. Iron absorption from tortillas was evaluated by using the extrinsic tag method and was measured as the incorporation of radiolabeled iron into the red blood cells of 14 nonanemic men 2 wk after intake. Results: The phytic acid content of LPM was 3.48 mg/g, Ϸ35% of the phytic acid content of WTM; concentrations of macronutrients and most minerals were not significantly different between strains. Iron absorption results were adjusted to 40% absorption of ferrous ascorbate. Iron absorption was 49% greater from LPM (8.2% of intake) than from WTM (5.5% of intake) tortillas (P < 0.001, repeated-measures analysis of variance). Conclusion: Consumption of genetically modified, low-phytic acid strains of maize may improve iron absorption in human populations that consume maize-based diets.Am J Clin Nutr 1998;68:1123-7. KEY WORDSIron, iron absorption, iron deficiency, phytic acid, corn, maize, tortilla, men INTRODUCTIONNonheme iron from cereals and other plant sources is poorly absorbed because of the presence of inhibitors of iron absorption, such as phytic acid, tannins, and selected dietary fibers, which irreversibly bind iron in the intestinal lumen (1-3). One possible approach to improving iron absorption is to reduce the phytic acid content of foods by genetically modifying their capacity to synthesize phytic acid (4; V Raboy et al, unpublished observations, 1994). Recent experiments indicate that much of the phytic acid in maize and other cereals can be removed through genetic engineering without affecting the total phosphorus content of the grain or the health of the plant (V Raboy, K Young, P Gerbasi, unpublished observations, 1994). This offers great promise for human trace mineral nutrition, especially in populations that are primarily dependent on plantderived diets.Before promoting the large-scale production of low-phytic acid grain for human consumption, it is necessary that we determine whether a reduction in phytic acid content affects other components of the grain and whether low-phytic acid mutants do indeed have the expected effect on mineral absorption from mixed diets consumed by humans. We therefore conducted several laboratory analyses of the nutrient content of low-phytic acid and unmodified strains of maize and completed a clinical study of the effect of substituting the low-phytic acid maize on the absorption of nonheme iron from maize tortillas. The studies were conducted with maize tortillas because this is the most common form in which maize is ...

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