Peer-reviewed article
Environmental enteric dysfunction pathways and child stunting: A systematic review
Kaitlyn M. Harper, Maxine Mutasa, Andrew J. Prendergast, Jean H. Humphrey, Amee R. Manges ·
Summary
Written by AI, not yet AICS's view · claude-haiku-4-5-20251001This systematic review examines how environmental enteric dysfunction (EED), a subclinical intestinal disorder, contributes to child stunting in developing countries. The authors reviewed studies from 2010-2017 to evaluate whether proposed biological pathways linking EED biomarkers to stunting are supported by evidence. The review finds strong evidence that intestinal inflammation relates to both systemic inflammation and stunting, but weak evidence for other proposed pathways like microbial translocation. The authors recommend reconsidering how EED is measured and studied.
Key points
- Little evidence supports the pathway from intestinal permeability to microbial translocation to stunting
- Stronger support exists for links between intestinal inflammation and systemic inflammation, and between intestinal inflammation and stunting
- Conflicting evidence exists for pathways from intestinal damage to intestinal permeability and intestinal damage to stunting
- Biomarkers such as microbial translocation and intestinal permeability are difficult to measure and may require reconsideration
- Further analysis of pathogen-induced changes to intestinal microbiota is recommended as a pathway to stunting
Limitations
This is a systematic review that synthesizes existing studies; it cannot directly measure the mechanisms by which EED affects child growth. The review is limited to studies published between 2010-2017 and cannot evaluate the quality of evidence from individual studies in detail.
Abstract
BACKGROUND: Environmental 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. METHODOLOGY: A 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. RESULTS: 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. There was conflicting evidence for the pathways from intestinal damage to intestinal permeability and intestinal damage to stunting. CONCLUSIONS: These 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.