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BACKGROUND: Iron and folic acid supplementation have been recommended in pregnancy for anaemia prevention, and may improve other maternal, pregnancy, and infant outcomes. OBJECTIVES: To examine the effects of daily oral iron supplementation during pregnancy, either alone or in combination with folic acid or with other vitamins and minerals, as an intervention in antenatal care. SEARCH METHODS: We searched the Cochrane Pregnancy and Childbirth Trials Registry on 18 January 2024 (including CENTRAL, MEDLINE, Embase, CINAHL, ClinicalTrials.gov, WHO's International Clinical Trials Registry Platform, conference proceedings), and searched reference lists of retrieved studies. SELECTION CRITERIA: Randomised or quasi-randomised trials that evaluated the effects of oral supplementation with daily iron, iron + folic acid, or iron + other vitamins and minerals during pregnancy were included. DATA COLLECTION AND ANALYSIS: Review authors independently assessed trial eligibility, ascertained trustworthiness based on pre-defined criteria, assessed risk of bias, extracted data, and conducted checks for accuracy. We used the GRADE approach to assess the certainty of the evidence for primary outcomes. We anticipated high heterogeneity amongst trials; we pooled trial results using a random-effects model (average treatment effect). MAIN RESULTS: We included 57 trials involving 48,971 women. A total of 40 trials compared the effects of daily oral supplements with iron to placebo or no iron; eight trials evaluated the effects of iron + folic acid compared to placebo or no iron + folic acid. Iron supplementation compared to placebo or no iron Maternal outcomes: Iron supplementation during pregnancy may reduce maternal anaemia (4.0% versus 7.4%; risk ratio (RR) 0.30, 95% confidence interval (CI) 0.20 to 0.47; 14 trials, 13,543 women; low-certainty evidence) and iron deficiency at term (44.0% versus 66.0%; RR 0.51, 95% CI 0.38 to 0.68; 8 trials, 2873 women; low-certainty evidence), and probably reduces maternal iron-deficiency anaemia at term (5.0% versus 18.4%; RR 0.41, 95% CI 0.26 to 0.63; 7 trials, 2704 women; moderate-certainty evidence), compared to placebo or no iron supplementation. There is probably little to no difference in maternal death (2 versus 4 events, RR 0.57, 95% CI 0.12 to 2.69; 3 trials, 14,060 women; moderate-certainty evidence). The evidence is very uncertain for adverse effects (21.6% versus 18.0%; RR 1.29, 95% CI 0.83 to 2.02; 12 trials, 2423 women; very low-certainty evidence) and severe anaemia (Hb < 70 g/L) in the second/third trimester (< 1% versus 3.6%; RR 0.22, 95% CI 0.01 to 3.20; 8 trials, 1398 women; very low-certainty evidence). No trials reported clinical malaria or infection during pregnancy. Infant outcomes: Women taking iron supplements are probably less likely to have infants with low birthweight (5.2% versus 6.1%; RR 0.84, 95% CI 0.72 to 0.99; 12 trials, 18,290 infants; moderate-certainty evidence), compared to placebo or no iron supplementation. However, the evidence is very uncertain for infant birthweight (MD 24.9 g, 95% CI -125.81 to 175.60; 16 trials, 18,554 infants; very low-certainty evidence). There is probably little to no difference in preterm birth (7.6% versus 8.2%; RR 0.93, 95% CI 0.84 to 1.02; 11 trials, 18,827 infants; moderate-certainty evidence) and there may be little to no difference in neonatal death (1.4% versus 1.5%, RR 0.98, 95% CI 0.77 to 1.24; 4 trials, 17,243 infants; low-certainty evidence) or congenital anomalies, including neural tube defects (41 versus 48 events; RR 0.88, 95% CI 0.58 to 1.33; 4 trials, 14,377 infants; low-certainty evidence). Iron + folic supplementation compared to placebo or no iron + folic acid Maternal outcomes: Daily oral supplementation with iron + folic acid probably reduces maternal anaemia at term (12.1% versus 25.5%; RR 0.44, 95% CI 0.30 to 0.64; 4 trials, 1962 women; moderate-certainty evidence), and may reduce maternal iron deficiency at term (3.6% versus 15%; RR 0.24, 95% CI 0.06 to 0.99; 1 trial, 131 women; low-certainty evidence), compared to placebo or no iron + folic acid. The evidence is very uncertain about the effects of iron + folic acid on maternal iron-deficiency anaemia (10.8% versus 25%; RR 0.43, 95% CI 0.17 to 1.09; 1 trial, 131 women; very low-certainty evidence), or maternal deaths (no events; 1 trial; very low-certainty evidence). The evidence is uncertain for adverse effects (21.0% versus 0.0%; RR 44.32, 95% CI 2.77 to 709.09; 1 trial, 456 women; low-certainty evidence), and the evidence is very uncertain for severe anaemia in the second or third trimester (< 1% versus 5.6%; RR 0.12, 95% CI 0.02 to 0.63; 4 trials, 506 women; very low-certainty evidence), compared to placebo or no iron + folic acid. Infant outcomes: There may be little to no difference in infant low birthweight (33.4% versus 40.2%; RR 1.07, 95% CI 0.31 to 3.74; 2 trials, 1311 infants; low-certainty evidence), comparing iron + folic acid supplementation to placebo or no iron + folic acid. Infants born to women who received iron + folic acid during pregnancy probably had higher birthweight (MD 57.73 g, 95% CI 7.66 to 107.79; 2 trials, 1365 infants; moderate-certainty evidence), compared to placebo or no iron + folic acid. There may be little to no difference in other infant outcomes, including preterm birth (19.4% versus 19.2%; RR 1.55, 95% CI 0.40 to 6.00; 3 trials, 1497 infants; low-certainty evidence), neonatal death (3.4% versus 4.2%; RR 0.81, 95% CI 0.51 to 1.30; 1 trial, 1793 infants; low-certainty evidence), or congenital anomalies (1.7% versus 2.4; RR 0.70, 95% CI 0.35 to 1.40; 1 trial, 1652 infants; low-certainty evidence), comparing iron + folic acid supplementation to placebo or no iron + folic acid. A total of 19 trials were conducted in malaria-endemic countries, or in settings with some malaria risk. No studies reported maternal clinical malaria; one study reported data on placental malaria. AUTHORS' CONCLUSIONS: Daily oral iron supplementation during pregnancy may reduce maternal anaemia and iron deficiency at term. For other maternal and infant outcomes, there was little to no difference between groups or the evidence was uncertain. Future research is needed to examine the effects of iron supplementation on other maternal and infant health outcomes, including infant iron status, growth, and development.

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Background: The effects of coronavirus disease 2019 (COVID-19) remain a global public health emergency because of the ensuing economic burden and death. With robust research into vaccines, antibody treatments, and antiviral drugs for COVID-19, there is still a dearth of evidence on the role of an individual's nutritional status on the severity of COVID-19. Objective: This study aimed to investigate the association between selenium (Se) and zinc (Zn) status and COVID-19 severity among individuals diagnosed with COVID-19 in North Carolina. Methods: Subjects (n = 106) were recruited remotely as part of the Nutrition and COVID-19 in North Carolina (NC-NC) study and filled out online screening questionnaires and dietary surveys. Toenail samples from 97 participants were analyzed to determine Se and Zn concentrations. To assess the severity of severe acute respiratory coronavirus (SARS-CoV)-2 infection, subjects were asked about the presence and duration of 10 commonly reported symptoms. These responses were used to calculate a COVID-19 severity index (CSI). The relationship between Se and Zn status (intake and toenail concentrations) and CSI was explored using a regression analysis. Results: Our results showed that the median (25th, 75th percentiles) dietary Se and Zn intake from selected food sources were 65.2 µg (43.2, 112.9) and 4.3 mg (1.8, 8), respectively. Headache, cough, loss of smell or taste, and fever were reported by at least half of the participants. In stepwise regression analysis, among individuals with low Se and Zn intake (below the median), Se intake was inversely associated with increasing CSI (ß = -0.66; 95% CI: -1.21, -0.11; P = 0.02). Conclusions: Findings from this study support a potential benefit of increasing the intake of dietary Se to mitigate the severity of SARS-CoV-2 infection.

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Chronic, systemic inflammation, which is associated with obesity and numerous other diseases, impairs iron status by increasing hepcidin concentration. Inflammation also decreases the concentration of transferrin, the main iron transport protein and a negative acute phase protein, which is indirectly assessed by measuring total iron binding capacity (TIBC). However, the contribution of diet-induced inflammation has not been studied. Data from two studies, namely Diet and Inflammation and Selenium and Inflammation Studies (total n=98) were used to assess the associations among Dietary Inflammatory Index (DII®) scores derived from three-day dietary records, body mass index (BMI=weight[kg]/height[m]2), inflammatory and hematological markers among young adults with normal-weight, overweight or obesity. Subjects' diets were also categorized as less inflammatory diets (LID) and inflammatory diets (ID) using cluster analysis. Independent t-test and regression analyses were used to assess associations in the data. Intakes of iron, proteins, fat, fiber, and calories were higher in the LID group compared to the ID group (p<0.05). Demographic characteristics and concentrations of C-reactive protein (CRP) and iron status biomarkers did not differ significantly between the two groups (p>0.05). Higher DII score was associated with increasing CRP (ß+SE=0.23+0.07, p=0.002) and lower TIBC (ß+SE=-8.46+3.44, p=0.02), independent of BMI category. The LID diet was associated with higher TIBC (ß+SE=29.87+10.75, p=0.007) compared to the ID diet. In conclusion, inflammatory diets may impair iron status by reducing the iron binding capacity of transferrin.

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Manganese (Mn) is found in many commonly consumed foods and therefore its deficiency is rare. However, excessive exposure to Mn from contaminated drinking water as well as occupational exposure can result in toxic accumulation in the brain, which has been associated with impaired neurological function. The objective of this study was to examine the NHANES 2013 - 2014 cycle focusing on the relationship between whole blood Mn concentrations and cognitive tests including working memory, word recall and sustained attention in elderly adults (aged 60 years and older). The different cognitive function test scores were used in principal component analysis to develop a composite score. The relationship between blood Mn concentration and cognitive function (principal component score and Digit Symbol Substitution Test (DSST)) were investigated using regression analysis. Median (95% CI) concentrations of blood Mn, serum copper, and serum iron were 8.76 (8.5, 9.1) µg/L, 114.9 µg/dL (110.3, 118.1), and 80 (78, 83) µg/dL, respectively. We found that among individuals in the highest quartile of blood Mn concentration (>11.18 µg/L), there was an inverse association between blood Mn and cognitive function as assessed using DSST (ß (95% CI) = -0.76 (-1.19 to -0.33); p = 0.003), while the inverse relationship with the composite score trended towards significance (ß (95% CI) = -0.04 (-0.08 to 0.00); p = 0.053). These findings suggest that having elevated blood Mn ay be associated with cognitive decline in aging and warrants further studies on how the different sources of Mn may contribute to this outcome.

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Phytate, an antioxidant, may improve cognition by inhibiting iron catalyzed hydroxyl radical formation. Particularly in the elderly, this provides a potential dietary approach for mitigating age-related brain neuronal dysfunction and loss. In this study, we investigated the relationship between phytate intake and cognitive function in the elderly. We used data from the 2013-2014 National Health and Nutrition Examination Survey (NHANES) and the corresponding Food Patterns Equivalents Database (FPED). Phytate content of food groups from published data were merged with the appropriate FPED data to estimate the total phytate intake for each subject. Principal component analysis was used to develop a composite score from four cognitive function scores in NHANES data, and regression analysis was used to determine the relationship between this score and phytate intake. Median phytate intake was 0.65 (0.61, 0.71) g/day. It was low among females, non-Hispanic blacks, and people with history of at least one chronic disease (p < 0.05). In regression analysis adjusted for confounders, phytate intake was positively associated with cognitive function (ß (95% CI) = 1.90 (0.73-3.07); p = 0.015). These results suggest that phytate may be associated with improved cognition, hence the need to consider including phytate-rich foods in the diet among the elderly.