In Haitian women and preschool children, iron absorption from wheat flour-based meals fortified with sodium iron EDTA is higher than that from meals fortified with ferrous fumarate, and is not affected by Helicobacter pylori infection in children.

Fe fortification of wheat flour was proposed in Haiti to combat Fe deficiency, but Fe bioavailability from fortificants has never been investigated in Haitian women or preschool children, two key target groups. We aimed to investigate the bioavailability of ferrous fumarate (FeFum), NaFeEDTA and their combination from fortified wheat flour. We recruited twenty-two healthy mother-child pairs in Port au Prince, Haiti, for an Fe-absorption study. We administered stable Fe isotopes as FeFum or NaFeEDTA individually in low-extraction wheat flour bread rolls consumed by all participants in a randomised, cross-over design. In a final, identical meal, consumed only by the women, FeFum+NaFeEDTA was administered. We measured Fe absorption by using erythrocyte incorporation of stable isotopes 14 d after consumption of each meal, and determined Fe status, inflammatory markers and Helicobacter pylori infection. Fe absorption (geometric mean was 9·24 (95 % CI 6·35, 13·44) and 9·26 (95 % CI 7·00, 12·31) from FeFum and 13·06 (95 % CI 9·23, 19·10) and 12·99 (95 % CI 9·18, 18·39) from NaFeEDTA in mothers and children, respectively (P<0·05 between compounds). Fe absorption from FeFum+NaFeEDTA was 11·09 (95 % CI 7·45, 17·34) and did not differ from the other two meals. H. pylori infection did not influence Fe absorption in children. In conclusion, in Haitian women and children, Fe absorption from NaFeEDTA was 40 % higher than from FeFum, and the combination FeFum+NaFeEDTA did not significantly increase Fe absorption compared with FeFum alone. In the context of Haiti, where the high costs of NaFeEDTA may not be affordable, the use of FeFum at 60 mg Fe/kg flour may be a preferable, cost-effective fortification strategy.

Sharply higher rates of iron deficiency in obese Mexican women and children are predicted by obesity-related inflammation rather than by differences in dietary iron intake.

BACKGROUND: Obese individuals may be at increased risk of iron deficiency (ID), but it is unclear whether this is due to poor dietary iron intakes or to adiposity-related inflammation. OBJECTIVE: The aim of this study was to examine the relations between body mass index (BMI), dietary iron, and dietary factors affecting iron bioavailability, iron status, and inflammation [C-reactive protein (CRP)] in a transition country where obesity and ID are common. DESIGN: Data from the 1999 Mexican Nutrition Survey, which included 1174 children (aged 5-12 y) and 621 nonpregnant women (aged 18-50 y), were analyzed. RESULTS: The prevalence of obesity was 25.3% in women and 3.5% in children. The prevalence of ID was significantly (P < 0.05) higher in obese women and children compared with normal-weight subjects [odds ratios (95% CIs): 1.92 (1.23, 3.01) and 3.96 (1.34, 11.67) for women and children, respectively]. Despite similar dietary iron intakes in the 2 groups, serum iron concentrations were lower in obese women than in normal-weight women (62.6 ± 29.5 compared with 72.4 ± 34.6 µg/dL; P = 0.014), and total-iron-binding capacity was higher in obese children than in normal-weight children (399 ± 51 compared with 360 ± 48 µg/dL; P < 0.001). CRP concentrations in obese women and children were 4 times those of their normal-weight counterparts (P < 0.05). CRP but not iron intake was a strong negative predictor of iron status, independently of BMI (P < 0.05). CONCLUSIONS: The risk of ID in obese Mexican women and children was 2-4 times that of normal-weight individuals at similar dietary iron intakes. This increased risk of ID may be due to the effects of obesity-related inflammation on dietary iron absorption. Thus, ID control efforts in Mexico may be hampered by increasing rates of adiposity in women and children.

Does obesity increase risk for iron deficiency? A review of the literature and the potential mechanisms.

Increasing obesity is a major global health concern while at the same time iron-deficiency anemia remains common worldwide. Although these two conditions represent opposite ends of the spectrum of over- and under-nutrition, they appear to be linked: overweight individuals are at higher risk of iron deficiency than normal-weight individuals. Potential explanations for this association include dilutional hypoferremia, poor dietary iron intake, increased iron requirements, and/or impaired iron absorption in obese individuals. Recent evidence suggests obesity-related inflammation may play a central role through its regulation of hepcidin. Hepcidin levels are higher in obese individuals and are linked to subclinical inflammation; this may reduce iron absorption and blunt the effects of iron fortification. Thus, low iron status in overweight individuals may result from a combination of nutritional (reduced absorption) and functional (increased sequestration) iron deficiency. In this review, we focus on subclinical inflammation in obesity, and its effect on hepcidin levels, as the most plausible explanation for the link between iron deficiency and obesity.