| Literature DB >> 33619371 |
John Muthii Muriuki1,2, Alexander J Mentzer3,4, Ruth Mitchell5, Emily L Webb6, Anthony O Etyang7, Catherine Kyobutungi8, Alireza Morovat9, Wandia Kimita7, Francis M Ndungu7, Alex W Macharia7, Caroline J Ngetsa7, Johnstone Makale7, Swaib A Lule10, Solomon K Musani11, Laura M Raffield12, Clare L Cutland13, Sodiomon B Sirima14, Amidou Diarra14, Alfred B Tiono14, Michal Fried15, Moses Gwamaka16,17,18, Seth Adu-Afarwuah19, James P Wirth20, Rita Wegmüller20, Shabir A Madhi13, Robert W Snow7,21, Adrian V S Hill3,22, Kirk A Rockett3,23, Manjinder S Sandhu23, Dominic P Kwiatkowski3,4,23, Andrew M Prentice24, Kendra A Byrd25, Alex Ndjebayi26, Christine P Stewart27, Reina Engle-Stone27, Tim J Green28,29, Crystal D Karakochuk30, Parminder S Suchdev31, Philip Bejon7,21, Patrick E Duffy15, George Davey Smith5, Alison M Elliott10,32, Thomas N Williams7,21,33, Sarah H Atkinson34,35,36.
Abstract
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%.Entities:
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Year: 2021 PMID： 33619371 PMCID： PMC7610676 DOI： 10.1038/s41591-021-01238-4
Source DB: PubMed Journal: Nat Med ISSN： 1078-8956 Impact factor: 53.440