Malaria is a cause of iron deficiency in African children

Malaria and iron deficiency (ID) are common and interrelated public health problems in African children. Observational data suggest that interrupting malaria transmission reduces the prevalence of ID1. To test the hypothesis that malaria might cause ID, we used sickle cell trait (HbAS, rs334), a genetic variant that confers specific protection against malaria2, as an instrumental variable in Mendelian randomization analyses. HbAS was associated with a 30% reduction in ID among children living in malaria-endemic countries in Africa (n = 7,453), but not among individuals living in malaria-free areas (n = 3,818). Genetically predicted malaria risk was associated with an odds ratio of 2.65 for ID per unit increase in the log incidence rate of malaria. This suggests that an intervention that halves the risk of malaria episodes would reduce the prevalence of ID in African children by 49%

Mild riboflavin deficiency is highly prevalent in school-age children but does not increase risk for anaemia in Cote d'Ivoire

There are few data on the prevalence of riboflavin deficiency in sub-Saharan Africa, and it remains unclear whether riboflavin status influences the risk for anaemia. The aims of this study were to: (1) measure the prevalence of riboflavin deficiency in children in south-central Côte d'Ivoire; (2) estimate the riboflavin content of the local diet; and (3) determine if riboflavin deficiency predicts anaemia and/or iron deficiency. In 5- to 15-year-old children (n 281), height, weight, haemoglobin (Hb), whole blood zinc protoporphyrin (ZPP), erythrocyte glutathione reductase activity coefficient (EGRAC), serum retinol, C-reactive protein (CRP) and prevalence of Plasmodium spp. (asymptomatic malaria) and Schistosoma haematobium (bilharziosis) infections were measured. Three-day weighed food records were kept in twenty-four households. Prevalence of anaemia in the sample was 52%; 59% were iron-deficient based on an elevated ZPP concentration, and 36% suffered from iron deficiency anaemia. Plasmodium parasitaemia was found in 49% of the children. Nineteen percent of the children were infected with S. haematobium. Median riboflavin intake in 5- to 15-year-old children from the food records was 0.42 mg/d, approximately 47% of the estimated average requirement for this age group. Prevalence of riboflavin deficiency was 65%, as defined by an EGRAC value > 1.2. Age, elevated CRP and iron deficiency were significant predictors of Hb. Riboflavin-deficient children free of malaria were more likely to be iron deficient (odds ratio; 3.07; 95% CI 1.12, 8.41). In conclusion, nearly two-thirds of school-age children in south-central Côte d'Ivoire are mildly riboflavin deficient. Riboflavin deficiency did not predict Hb and/or anaemia, but did predict iron deficiency among children free of malaria

The effect of zinc-biofortified rice on zinc status of Bangladeshi preschool children: a randomized, double-masked, household-based, controlled trial

Background Zinc biofortification of rice could sustainably improve zinc status in countries where zinc deficiency is common and rice is a staple, but its efficacy has not been tested. Fatty acid desaturases (FADS) are putative new zinc status biomarkers. Objectives Our objective was to test the efficacy of zinc-biofortified rice (BFR) in preschool-aged children with zinc deficiency. Our hypothesis was that consumption of BFR would increase plasma zinc concentration (PZC). Methods We conducted a 9-mo, double-masked intervention trial in 12–36-mo-old rural Bangladeshi children, most of whom were zinc-deficient (PZC <70 µg/dL) and stunted (n = 520). The children were randomly assigned to receive either control rice (CR) or BFR provided in cooked portions to their households daily, with compliance monitoring. The primary outcome was PZC. Secondary outcomes were zinc deficiency, linear growth, infection-related morbidity, FADS activity indices, intestinal fatty acid binding protein (I-FABP) and fecal calprotectin. We applied sparse serial sampling for midpoint measures and analyzed data by intention-to-treat using mixed-effects models. Results At baseline, median (IQR) PZC was 60.4 (56.3–64.3) µg/dL, 78.1% of children were zinc deficient, and 59.7% were stunted. Mean ± SD daily zinc intakes from the CR and BFR during the trial were 1.20 ± 0.34 and 2.22 ± 0.47 mg/d, respectively (P 0.05). There was a time–treatment interaction for height-for-age z-scores (P < 0.001) favoring the BFR group. The morbidity longitudinal prevalence ratio was 1.08 (95% CI: 1.05, 1.12) comparing the BFR and CR groups, due to more upper respiratory tract illness in the BFR group. Conclusions Consumption of BFR for 9 mo providing ∼1 mg of additional zinc daily to Bangladeshi children did not significantly affect PZC, prevalence of zinc deficiency, or FADS activity. The trial was registered at clinicaltrials.gov as NCT03079583.ISSN:0002-9165ISSN:1938-320

Malaria is a cause of iron deficiency in African children

Malaria and iron deficiency (ID) are common and interrelated public health problems in African children. Observational data suggest that interrupting malaria transmission reduces the prevalence of ID1. To test the hypothesis that malaria might cause ID, we used sickle cell trait (HbAS, rs334), a genetic variant that confers specific protection against malaria2, as an instrumental variable in Mendelian randomization analyses. HbAS was associated with a 30% reduction in ID among children living in malaria-endemic countries in Africa (n = 7,453), but not among individuals living in malaria-free areas (n = 3,818). Genetically predicted malaria risk was associated with an odds ratio of 2.65 for ID per unit increase in the log incidence rate of malaria. This suggests that an intervention that halves the risk of malaria episodes would reduce the prevalence of ID in African children by 49%