title: Environmental Enteric Dysfunction and Growth Failure/Stunting in Global Child Health.
abstract: Approximately 25% of the world's children aged <5 years have stunted growth, which is associated with increased mortality, cognitive dysfunction, and loss of productivity. Reducing by 40% the number of stunted children is a global target for 2030. The pathogenesis of stunting is poorly understood. Prenatal and postnatal nutritional deficits and enteric and systemic infections clearly contribute, but recent findings implicate a central role for environmental enteric dysfunction (EED), a generalized disturbance of small intestinal structure and function found at a high prevalence in children living under unsanitary conditions. Mechanisms contributing to growth failure in EED include intestinal leakiness and heightened permeability, gut inflammation, dysbiosis and bacterial translocation, systemic inflammation, and nutrient malabsorption. Because EED has multiple causal pathways, approaches to manage it need to be multifaceted. Potential interventions to tackle EED include: (1) reduction of exposure to feces and contact with animals through programs such as improved water, sanitation, and hygiene; (2) breastfeeding and enhanced dietary diversity; (3) probiotics and prebiotics; (4) nutrient supplements, including zinc, polyunsaturated fatty acids, and amino acids; (5) antiinflammatory agents such as 5-aminosalicyclic acid; and (6) antibiotics in the context of acute malnutrition and infection. Better understanding of the underlying causes of EED and development of noninvasive, practical, simple, and affordable point-of-care diagnostic tools remain key gaps. "Omics" technologies (genomics, epigenomics, transcriptomics, proteomics, and metabolomics) and stable isotope techniques (eg,13C breath tests) targeted at children and their intestinal microbiota will enhance our ability to successfully identify, manage, and prevent this disorder.
authors.affiliation: International Atomic Energy Agency, Vienna, Austria; v.owino@iaea.org.
authors.forename: Victor
authors.initials: V
authors.lastname: Owino
authors.affiliation: International Centre for Diarrhoeal Research, Bangladesh, Dhaka, Bangladesh.
authors.forename: Tahmeed
authors.initials: T
authors.lastname: Ahmed
authors.affiliation: Division of Pediatric Endocrinology, Duke University Medical Center, Durham, North Carolina.
authors.forename: Michael
authors.initials: M
authors.lastname: Freemark
authors.affiliation: University of Zambia, Lusaka, Zambia.|Blizard Institute, Queen Mary University of London, London, United Kingdom.
authors.forename: Paul
authors.initials: P
authors.lastname: Kelly
authors.affiliation: Department of Microbiology and Ecosystem Science, Research Network "Chemistry meets Microbiology," University of Vienna, Vienna, Austria; and.
authors.forename: Alexander
authors.initials: A
authors.lastname: Loy
authors.affiliation: Washington University, St Louis, Missouri.
authors.forename: Mark
authors.initials: M
authors.lastname: Manary
authors.affiliation: International Atomic Energy Agency, Vienna, Austria.
authors.forename: Cornelia
authors.initials: C
authors.lastname: Loechl
mesh_terms: D002648:Child; D000067576:Child Health; D002675:Child, Preschool; D004777:Environment; D005183:Failure to Thrive / Q000175:diagnosis / Q000453:epidemiology*; D005260:Female; D000069196:Gastrointestinal Microbiome; D014943:Global Health; D006130:Growth Disorders / Q000453:epidemiology* / Q000209:etiology* / Q000503:physiopathology; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D007410:Intestinal Diseases / Q000175:diagnosis* / Q000453:epidemiology / Q000382:microbiology; D008286:Malabsorption Syndromes / Q000175:diagnosis / Q000453:epidemiology*; D008297:Male; D044342:Malnutrition / Q000453:epidemiology*; D009752:Nutritional Status; D015995:Prevalence; D018570:Risk Assessment; D006113:United Kingdom