Iron is unique among all minerals in that humans have no regulatable excretory pathway to eliminate excess iron after it is absorbed. Iron deficiency anemia occurs when absorbed iron is not sufficient to meet body iron demands, whereas iron overload and subsequent deposition of iron in key organs occur when absorbed iron exceeds body iron demands. Over time, iron accumulation in the body can increase risk of chronic diseases, including cirrhosis, diabetes, and heart failure. To date, only ∼30% of the interindividual variability in iron absorption can be captured by iron status biomarkers or iron regulatory hormones. Much of the regulation of iron absorption may be under genetic control, but these pathways have yet to be fully elucidated. Genome-wide and candidate gene association studies have identified several genetic variants that are associated with variations in iron status, but the majority of these data were generated in European populations. The purpose of this review is to summarize genetic variants that have been associated with alterations in iron status and to highlight the influence of ethnicity on the risk of iron deficiency or overload. Using extant data in the literature, linear mixed-effects models were constructed to explore ethnic differences in iron status biomarkers. This approach found that East Asians had significantly higher concentrations of iron status indicators (serum ferritin, transferrin saturation, and hemoglobin) than Europeans, African Americans, or South Asians. African Americans exhibited significantly lower hemoglobin concentrations compared with other ethnic groups. Further studies of the genetic basis for ethnic differences in iron metabolism and on how it affects disease susceptibility among different ethnic groups are needed to inform population-specific recommendations and personalized nutrition interventions for iron-related disorders.

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Background Based on limited data, it is estimated that the placenta retains 90 mg of iron (Fe). Little is known about determinants of placental Fe content. Animal data indicate that the placenta prioritizes Fe for its own needs, but this hypothesis has not been evaluated in humans. Objectives To characterize placental Fe content and placental Fe concentration (p[Fe]) in pregnant women at risk of Fe insufficiency and identify determinants of p[Fe]. Methods Placentae were collected from 132 neonates born to teens carrying singletons (≤18 y) and 101 neonates born to 48 women carrying multiples (20–46 y). Maternal and neonatal Fe status indicators (hemoglobin, SF, sTfR, serum Fe, TBI) and hormones (erythropoietin, hepcidin) were measured. P[Fe] was measured using ICP-MS. Correlation analyses and mixed-effects models were constructed to identify determinants of p[Fe]. Results Mean placental Fe content was 23 mg per placenta [95%CI 15–33] in the multiples and 40 mg [95%CI 31–51] in the teens (P = 0.03). Mean p[Fe] did not differ between the cohorts. P[Fe] was higher in anemic (175 [95%CI 120–254] μg/g) compared to non-anemic (46 [95%CI 26–82] μg/g) women carrying multiples (P = 0.009), but did not differ between anemic (62 [95%CI 40–102] μg/g) and non-anemic (73 [95%CI 56–97] μg/g) teens. In women carrying multiples, low maternal Fe status [lower SF (P = 0.002) and lower TBI (P = 0.01)] was associated with higher p[Fe], while in teens, improved Fe status [lower sTfR (P = 0.03) and higher TBI (P = 0.03)] was associated with higher p[Fe]. Conclusions Placental Fe content was ∼50% lower than previously estimated. P[Fe] is significantly associated with maternal Fe status. In women carrying multiples, poor maternal Fe status was associated with higher p[Fe], while in teens, improved Fe status was associated with higher p[Fe]. More data are needed to understand determinants of p[Fe] and the variable Fe partitioning in teens compared to mature women. Clinical Trial Registry: These clinical trials were registered at clinicaltrials.gov as NCT01019902 (https://clinicaltrials.gov/ct2/show/NCT01019902) and NCT01582802 (https://clinicaltrials.gov/ct2/show/NCT01582802).

Seguir una dieta saludable proporciona muchos beneficios a lo largo del ciclo de la vida. Mantener buenos hábitos de alimentación a medida que envejecemos puede ser especialmente útil para preservar la salud cognitiva―la capacidad de recordar, aprender y tomar decisiones. This is the Spanish-language version of FSHN17-9/FS304, Diet and Brain Health. This 4-page document provides tips for healthful eating that may help to maximize brain health in older adults. Written by Wendy J. Dahl and published by the UF/IFAS Department of Food Science and Human Nutrition, April 2018. http://edis.ifas.ufl.edu/fs307

Objectives Murine data suggest that the placenta prioritizes iron (Fe) for its own needs when Fe is limited by upregulating transferrin receptor 1 (TFR1) and downregulating the Fe exporter ferroportin (FPN). Human data on the impact of maternal and neonatal Fe status on placental FPN are conflicting. The study aims were to identify determinants of placental FPN protein abundance in women at risk of Fe insufficiency and to assess the utility of the placental Fe deficiency index (PIDI), which is the FPN/TFR1 ratio, as a measure of maternal/fetal Fe insufficiency. Methods FPN and TFR1 protein abundance was measured by semi-quantitative western blots in placentae collected from 43 neonates born to teens (17.4 ± 1.1 y) carrying singletons (39.9 ± 1.3 weeks of gestation at birth) and from 57 neonates born to 26 women (31.3 ± 6.3 y) carrying multiples (35.5 ± 2.7 weeks of gestation at birth). Fe status biomarkers (Hb, SF, sTfR, TBI) and hormones (hepcidin, EPO, ERFE) were assessed in maternal and cord blood. Results FPN and TFR1 were detected in all samples analyzed between 30.4–41.7 weeks of gestation. In both cohorts, FPN protein abundance was associated with neonatal but not maternal factors. Higher FPN was associated with lower cord Hb (p = 0.03) in the multiples cohort and with higher cord EPO (p = 0.002) in the teens. In contrast, TFR1 was inversely associated with maternal Fe status; multiples cohort (SF, p = 0.01; sTfR, p = 0.01; TBI, p = 0.003; hepcidin p = 0.01), teens (SF, p = 0.01). The PIDI was predicted by maternal and neonatal Fe status but in opposite directions. In the multiples cohort, Fe deficient women (mid-gestation sTfR > 8.5 mg/L, delivery SF < 12 μg/L or TBI < 0 mg/kg) had a lower PIDI (p = 0.02, p = 0.003, p = 0.04) but lower cord Hb was associated with a higher PIDI (p = 0.004). In the teens, lower mid-gestation hepcidin was associated with a lower PIDI (p = 0.009) but higher cord EPO was associated with a higher PIDI (p = 0.006). Conclusions Placental FPN protein was inversely associated with neonatal Fe status. The PIDI captures fetal and maternal regulation of placental Fe trafficking as it reflects Fe export to the fetus relative to Fe import from maternal circulation. More data are needed to assess the utility of the PIDI as an indicator of Fe insufficiency during pregnancy and how it relates to neonatal outcomes that are driven by placental health. Funding Sources USDA, Gerber Foundation, NIH NICHD.