Abstract
BackgroundEnvironmental enteric dysfunction (EED) is commonly defined as an acquired subclinical disorder of the small intestine, characterized by villous atrophy and crypt hyperplasia. EED has been proposed to underlie stunted growth among children in developing countries. A collection of biomarkers, organized into distinct domains, has been used to measure different aspects of EED. Here, we examine whether these hypothesized relationships, among EED domains and between each domain and stunting, are supported by data from recent studies.MethodologyA systematic literature search was conducted using PubMed, MEDLINE, EMBASE, Web of Science, and CINAHL between January 1, 2010 and April 20, 2017. Information on study objective, design, population, location, biomarkers, and results were recorded, as well as qualitative and quantitative definitions of EED. Biomarkers were organized into five EED domains, and the number of studies that support or do not support relationships among domains and between each domain with stunting were summarized.ResultsThere was little evidence to support the pathway from intestinal permeability to microbial translocation and from microbial translocation to stunting, but stronger support existed for the link between intestinal inflammation and systemic inflammation and for intestinal inflammation and stunting. There was conflicting evidence for the pathways from intestinal damage to intestinal permeability and intestinal damage to stunting.ConclusionsThese results suggest that certain EED biomarkers may require reconsideration, particularly those most difficult to measure, such as microbial translocation and intestinal permeability. We discuss several issues with currently used biomarkers and recommend further analysis of pathogen-induced changes to the intestinal microbiota as a pathway leading to stunting.
Highlights
One-quarter of children under the age of 5 years are stunted, defined as a height-for-age > 2 standard deviations below the median as defined by the World Health Organization growth standards
There was little evidence to support the pathway from intestinal permeability to microbial translocation and from microbial translocation to stunting, but stronger support existed for the link between intestinal inflammation and systemic inflammation and for intestinal inflammation and stunting
These results suggest that certain enteric dysfunction (EED) biomarkers may require reconsideration, those most difficult to measure, such as microbial translocation and intestinal permeability
Summary
One-quarter of children under the age of 5 years are stunted, defined as a height-for-age > 2 standard deviations below the median as defined by the World Health Organization growth standards. Studies have focused predominantly on nutrition-specific interventions for stunting; previous systematic reviews highlight that neither food quantity nor quality fully explains impaired linear growth in children [14,15]. While diarrheal episodes in the first few months after birth lead to increased prevalence of stunting at 24 months [20], catch-up growth between diarrheal episodes can be sufficient for linear growth recovery in some children [21]. EED has been proposed to underlie stunted growth among children in developing countries. We examine whether these hypothesized relationships, among EED domains and between each domain and stunting, are supported by data from recent studies
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