[11][12][13] Environmental enteropathy is believed to result in chronic malnutrition and subsequent growth stunting (low height-for-age measurement) as well as other child development deficits.

[citation needed] Reports of "poor appetite" by caregivers in LMICs,[19] and restriction of complementary foods during illness[20] is common.

Appetite may be reduced both by pro-inflammatory cytokines and leptin[21] and low zinc status,[22] and may be continuous in children with environmental enteropathy.

[23] Meanwhile, there seems to be agreement that successful interventions to improve complementary feeding practices[33] and reduce stunting[34][35] must encompass both immediate and underlying causes.The development of environmental enteropathy (EE) is multifactorial, but predominantly associated with chronic exposure to contaminated food and water.

Chronic inflammation leads to both functional and structural changes which alter gut permeability and ability of the intestine to absorb nutrients.

[2] In an effort to identify simple, accurate diagnostic tests for EE, the Bill and Melinda Gates Foundation (BMGF) has established an EE biomarkers consortium as part of their Global Grand Challenges initiative (specifically, the Discover Biomarkers of Gut Function challenge).

[11] EE is described as a reversible[41][42] condition which is probabilistically associated with poor development, but is neither a necessary nor a sufficient cause and may lead to no observable clinical outcomes.

In the 1960s, researchers reported a syndrome of non-specific histopathological and functional changes to the small intestine in individuals living in unsanitary conditions.

[13][6] Another important factor responsible for EE is contaminated soil in child play spaces, often caused by the presence of livestock such as chicken in the household.

[2] Some potential interventions to improve symptoms associated with EE are: The role of nutrition in environmental enteropathy is increasingly being recognized.

Mice fed a moderately energy- and protein deficient diet who are exposed to intestinal pathogens show traits similar to environmental enteropathy.

[51] The intestinal mucosa turnover is dynamic, nutrient-dependent and rapid,[52] and malnourished children have rate-limiting stores for repairing mucosal damage.

[24] The nutrients known to contribute to intestinal regeneration and improved barrier function are sulphur containing amino acids,[53] glutamine, vitamin A and zinc.

[citation needed] Environmental enteropathy (EE) primarily affects children living in low- and middle-income countries (LMICs).

[72] The geographic distribution of environmental enteropathy has shown an increase in incidence in such areas of poor sanitation and hygiene.

[72] Participants experienced symptoms of chronic enteric infection during and shortly after returning from their placement in low- and middle-income countries.

[73] The exact causes and consequences of EE have been difficult to establish due, in part, to the lack of a clear disease definition.

[70] Preexisting conditions such as micronutrient deficiencies, diarrheal diseases, and various chronic infections all serve as risk factors for EE.