Abstract
Advances in DNA sequencing technology now allow us to explore the dynamics and functions of the microbes that inhabit the human body, the microbiota. Recent studies involving experimental animal models suggest a role of the gut microbiota in growth. However, the specific changes in the human gut microbiota that contribute to growth remain unclear, and studies investigating the gut microbiota as a determinant of environmental enteric dysfunction (EED) and child stunting are lacking. In this article, we review the evidence for a link between the developing infant gut microbiota, infant feeding, EED, and stunting, and discuss the potential causal pathways relating these variables. We outline the analytic approaches we will use to investigate these relationships, by capitalizing on the longitudinal design and randomized interventions of the Sanitation Hygiene Infant Nutrition Efficacy trial in Zimbabwe.
Highlights
A key hypothesis of the Sanitation Hygiene Infant Nutrition Efficacy (SHINE) trial is that a subclinical intestinal pathology, termed environmental enteric dysfunction (EED), underlies child stunting [1]
In a substudy of the SHINE trial, we will examine how the gut microbiota contributes to linear growth between 0 and 18 months of age among human immunodeficiency virus (HIV)–unexposed infants
We hypothesize that the developing infant gut microbiota may impact child growth via 2 potential pathways: (1) a nutrition pathway, through which the gut microbiota can make nutrients and energy available to the infant; and (2) an EED pathway, through which the gut microbiota drives subclinical changes in intestinal morphology, leading to increased intestinal permeability, allowing passage of microbes and/or their byproducts across a compromised intestinal barrier, which results in chronic systemic inflammation, suppression of insulin-like growth factor 1 (IGF-1), and redirection of nutrients and energy away from growth (Figure 1)
Summary
A key hypothesis of the Sanitation Hygiene Infant Nutrition Efficacy (SHINE) trial is that a subclinical intestinal pathology, termed environmental enteric dysfunction (EED), underlies child stunting [1]. We hypothesize that the developing infant gut microbiota may impact child growth via 2 potential pathways: (1) a nutrition pathway, through which the gut microbiota can make nutrients and energy available to the infant (or decrease their availability); and (2) an EED pathway, through which the gut microbiota drives subclinical changes in intestinal morphology, leading to increased intestinal permeability, allowing passage of microbes and/or their byproducts across a compromised intestinal barrier (microbial translocation), which results in chronic systemic inflammation, suppression of insulin-like growth factor 1 (IGF-1), and redirection of nutrients and energy away from growth (Figure 1)
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
