BackgroundDietary and illness factors affect risk of growth faltering; the role of enteropathogens is less clear. As part of the Etiology, Risk Factors and Interactions of Enteric Infections and Malnutrition and the Consequences for Child Health and Development (MAL-ED) study, we quantify the effects of enteropathogen infection, diarrhoea and diet on child growth.MethodsNewborns were enrolled and followed until 24 months. Length and weight were assessed monthly. Illnesses and breastfeeding practices were documented biweekly; from 9 to 24 months, non-breast milk intakes were quantified monthly. Routinely collected non-diarrhoeal stools were analysed for a broad array of enteropathogens. A linear piecewise spline model was used to quantify associations of each factor with growth velocity in seven of eight MAL-ED sites; cumulative effects on attained size at 24 months were estimated for mean, low (10th percentile) and high (90th percentile) exposure levels. Additionally, the six most prevalent enteropathogens were evaluated for their effects on growth.ResultsDiarrhoea did not have a statistically significant effect on growth. Children with high enteropathogen exposure were estimated to be 1.21±0.33 cm (p<0.001; 0.39 length for age (LAZ)) shorter and 0.08±0.15 kg (p=0.60; 0.08 weight-for-age (WAZ)) lighter at 24 months, on average, than children with low exposure. Campylobacter and enteroaggregativeEscherichia coli detections were associated with deficits of 0.83±0.33 and 0.85±0.31 cm in length (p=0.011 and 0.001) and 0.22±0.15 and 0.09±0.14 kg in weight (p=0.14 and 0.52), respectively. Children with low energy intakes and protein density were estimated to be 1.39±0.33 cm (p<0.001; 0.42 LAZ) shorter and 0.81±0.15 kg (p<0.001; 0.65 WAZ) lighter at 24 months than those with high intakes.ConclusionsReducing enteropathogen burden and improving energy and protein density of complementary foods could reduce stunting.

Environmental enteropathy (EE) is a syndrome of altered small intestine structure and function hypothesized to be common among individuals lacking access to improved water and sanitation. There are plausible biological mechanisms, both inflammatory and non-inflammatory, by which EE may alter the cardiometabolic profile. Here, we test the hypothesis that EE is associated with the cardiometabolic profile among young children living in an environment of intense enteropathogen exposure. In total, 156 children participating in the Peruvian cohort of a multicenter study on childhood infectious diseases, growth and development were contacted at 3-5 years of age. The urinary lactulose:mannitol ratio, and plasma antibody to endotoxin core were determined in order to assess intestinal permeability and bacterial translocation. Blood pressure, anthropometry, fasting plasma glucose, insulin, and cholesterol and apolipoprotein profiles were also assessed. Extant cohort data were also used to relate biomarkers of EE during the first 18 months of life to early child cardiometabolic profile. Lower intestinal surface area, as assessed by percent mannitol excretion, was associated with lower apolipoprotein-AI and lower high-density lipoprotein concentrations. Lower intestinal surface area was also associated with greater blood pressure. Inflammation at 7 months of age was associated with higher blood pressure in later childhood. This study supports the potential for a relationship between EE and the cardiometabolic profile.

Abstract Objective: To estimate the total energy and micronutrient intakes of children 9–24 months of age and evaluate the probability of adequacy (PA) of the diet in seven MAL-ED sites. Design: Cohort study. Food intake was registered monthly using 24-h recalls beginning at 9 months. We estimated PA for thirteen nutrients and overall mean PA (MPA) by site and 3-month periods considering estimated breast milk intake. Setting: Seven sites in Asia, Africa and Latin America. Participants: 1669 children followed from birth to 24 months of age. Results: Median estimated %energy from breast milk ranged from 4 to 70 % at 9–12 months, and declined to 0–39 % at 21–24 months. Iron bioavailability was low for all sites, but many diets were of moderate bioavailability for zinc. PA was optimal for most nutrients in Brazil and South Africa, except for iron and vitamin E (both), calcium and zinc (South Africa). PA for zinc increased only for children consuming a diet with moderate bioavailability. MPA increased 12–24 months as the quantity of complementary foods increased; however, PA for vitamin A remained low in Bangladesh and Tanzania. PA for vitamins D and E and iron was low for most sites and age groups. Conclusions: MPA increased from 12 to 24 months as children consumed higher quantities of food, while nutrient density remained constant for most nutrients. Ways to increase the consumption of foods containing vitamins D, E and A, and calcium are needed, as are ways to increase the bioavailability of iron and zinc.