If people are suffering (either from diarrhoea or via environmental enteric dysfunction) due to poor disposal of faecal matter, then this will undo much of the good that improved diet and care does for growth.
To assess whether growth and biomarkers of environmental enteric dysfunction in infancy are related to health outcomes in midchildhood in Tanzania.
A major cause of child stunting and anemia is environmental enteric dysfunction (EED).
Recently, environmental enteric dysfunction (EED) has been hypothesized as a primary mediator of the association between fecally contaminated environments, stunting, and anemia [ 1– 3].
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].
SHINE is motivated by the premise that environmental enteric dysfunction (EED) is a major underlying cause of stunting and anemia and that EED is primarily caused by infant ingestion of fecal microbes due to living in conditions of poor WASH.
We hypothesize that protection from fecal microbes will prevent environmental enteric dysfunction (EED) [ 3] and systemic inflammation and thereby remove constraints on the growth hormone insulin-like growth factor 1 (IGF-1) axis that governs linear growth [ 4, 5].
Environmental enteric dysfunction (EED) is a virtually ubiquitous, but poorly defined, disorder of the small intestine among people living in conditions of poverty, which begins early in infancy and persists.
The Sanitation Hygiene Infant Nutrition Efficacy (SHINE) trial is motivated by a 2-part premise [ 26]: A major cause of child stunting and anemia is environmental enteric dysfunction (EED).
A key hypothesis of the Sanitation Hygiene Infant Nutrition Efficacy (SHINE) trial is that environmental enteric dysfunction (EED), a subclinical disorder of the small intestine, is a major cause of child stunting [ 1].
A recent working group proposed the term environmental enteric dysfunction to better capture the functional, as well as structural, abnormalities associated with this condition [ 17]; however, the disorder remains poorly characterized [ 9].
