CHRONIC MALNUTRITION (STUNTING) Presenters: Dr Nkhoma, Dr Zimba Moderator: Dr Amadi
ACUTE MALNUTRITION Acute malnutrition Diarrhoea
MALNUTRITION Acute 1. by weighing a child and measuring his or her height (wasting); 2. by measuring the circumference of the mid-upper arm; or 3. by checking for oedema in the lower legs or feet Chronic 1. by takina height of child against his or her age (stunting)
STUNTING MAGNITUDE Of the 555 million children in developing countries: 32% stunted Consequences > 20 % of all <5 year mortality Fewer years of school and poorer performance while there Long-term cognitive defects Lower adult productivity For girls: increased risk of stunted children
WHAT CAUSES STUNTING? Malnourished mothers? Meta-analysis shows 20-30% of stunting is due to intra-uterine factors Poor feeding? The average deficit in African children is -2 HAZ but the best studies of complementary feeding improve growth only 0.7 HAZ (about 30% of the deficit) Diarrhea? Five studies suggest that 5% to 20% of stunting is associated with diarrhea Environmental enteropathy? A study from the Gambia showed that all young children are affected and attributed 40-60% of stunting to this condition
ENVIRONMENTAL ENTEROPATHY (EE) EE also called tropical enteropathy is a subclinical disorder that occurs among inhabitants of environments with poor sanitation and hygiene, such as those often found in developing countries Chronic exposure to faecal pathogens is hypothesized to cause inflammation and structural changes in the small bowel, which ultimately result in functional changes
IMPACT AND COURSE OF EE EE explained 43% of growth faltering in the Gambia with a range from ~40-60% based on different measures – No association with frequency of diarrhoea – Little impact of supplementary feeding on growth EE first occurs at ~2 mo; affects 50% of infants at 6 mo; and 96% at 10 mo During the first yr of life, EE present >75% of the time compared with diarrhoea for 7-10% of the time Of over 400 infants studied, all had EE at some point before 15 mo of age (Lunn PG. Proceedings of Nutr Society, 2000)
PATHOPHYSIOLOGY OF EE Flattening of villi in gut mucosa –villous atrophy – modest malabsorption – Reduced lactase enzyme – functional lactose intolerance – Increased permeability, absorption of pathogens and chronic inflammation Measuring EE – Decreased mannitol uptake & increased lactulose uptake measured by ratio of the two in a 5 hr urine sample
MECHANISM OF EE Chronic immune activation ↑ pro-inflammatory cytokines Immunosenescence (premature aging) of adaptive cell- mediated immune system Anemia ↑ Hepcidin ↓ Growth Factor (IGF-1) Stunting Impaired response to vaccines and infections
TODDLERS CONSUME POULTRY FECES Peruvian shantytown families: – Households who owned free-range poultry: Average ingestion of poultry faeces by toddlers per 12-hour observation period was 3.9 times – Marquis GM et al., Am J Public Health 1990 Rural Zimbabwe: – Not selected for poultry ownership: 3 of 7 toddlers directly ate chicken faeces during a 6- hour observation period. – Ngure F et al., submitted, 2012
MICROBIAL CONTENT OF CHILD EXPOSURES:ZIMBABWE %HH with E coliE coli/ per gramAverage E Coil Per “ serving size” Infant Food0%00 Drinking Water54%2800 Soil in laundry area 60-80%702,100 Chicken feces100%10,000,000
Baby WASH: Potential Interventions to Prevent EE Protective play space Limit child exposure in high risk areas Keep animals out of house Latrines/safe disposal of feces (adult & infant) Infant handwashing Clean water Community developed solutions
Thank you for Listening