Abstract
The provision of iron- fortified foods is a common strategy to prevent iron deficiency; however, ensuring adequate iron absorption is a challenge. Iron bioavailability depends on the choice of iron compound, the presence enhancers and inhibitors of absorption in the food matrix, and the physiological state of the consumer, including iron status, other nutritional deficiencies and inflammatory disorders. Inflammation associated with infections and inflammatory disorders would be expected to decrease iron absorption and reduce the efficacy of iron- fortified foods. The decreased absorption is due to an increase in circulating hepcidin in response to inflammatory cytokines. Hepcidin degrades ferroportin and blocks the passage of iron from the intestinal cell to the plasma. This is the innate immune response to infections and aims to restrict pathogen growth by restricting iron supply. Stable isotope studies have reported women and children with chronic malaria parasitemia or febrile malaria to have increased inflammatory cytokines, increased hepcidin and much decreased iron absorption. No studies have specifically investigated the efficacy of iron- fortified foods in the absence and presence of infections. In contrast, inflammation and increased hepcidin associated with adiposity in overweight have been linked to both lower iron absorption and the decreased efficacy of iron- fortified foods.