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; or3. by checking for oedema in the lower legs

or feet Chronic1. 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

maternal/ prenatal

20%Diar-rhoea 10%

Feeding 30%

EE 40%

Potential causes of stunting

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)

StuntingImpaired 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 coli

E coli/ per gram

Average E Coil Per “ serving size”

Infant Food 0% 0 0

Drinking Water

54% 2 800

Soil in laundry area

60-80% 70 2,100

Chicken feces 100% 10,000,000 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