Skip to main content
ARS Home » Plains Area » Houston, Texas » Children's Nutrition Research Center » Research » Publications at this Location » Publication #242662

Title: Protein metabolism in severe childhood malnutrition

item Jahoor, Farook - Children'S Nutrition Research Center (CNRC)
item Badaloo, Asha - University Of The West Indies
item Reid, Marvin - University Of The West Indies
item Forrester, Terrence - University Of The West Indies

Submitted to: Annals of Tropical Paediatrics: International Child Health
Publication Type: Review Article
Publication Acceptance Date: 3/8/2008
Publication Date: 6/6/2008
Citation: Jahoor, F., Badaloo, A., Reid, M., Forrester, T. 2008. Protein metabolism in severe childhood malnutrition. Annals of Tropical Paediatrics. 28(2):87-101.

Interpretive Summary:

Technical Abstract: The major clinical syndromes of severe childhood malnutrition (SCM) are marasmus (non-oedematous SCM), kwashiorkor and marasmic-kwashiorkor (oedematous SCM). Whereas treatment of marasmus is straightforward and the associated mortality is low, kwashiorkor and marasmic-kwashiorkor are difficult to treat and have high morbidity and mortality rates. Despite extensive research, the pathogenic factors that cause a child to develop the oedematous instead of the non-oedematous form of SCM in response to food deprivation are still not clear. Over the years, two attractive hypotheses have been put forward. The first proposed that a dysadaptation in protein metabolism was involved, and the second proposed that free radical damage of cellular membranes might be involved. To address aspects of these hypotheses, in this article we have reviewed work done by our group and by others on protein metabolism and pro-oxidant/anti-oxidant homeostasis in children with the oedematous and non-oedematous syndromes of SCM. A significant finding is that when there is chronic food deprivation children with non-oedematous SCM can maintain body protein breakdown at the same rate as when they are well nourished, but children with oedematous SCM cannot. The slower protein breakdown rate of children with oedematous SCM reduces the supply of most amino acids, resulting in decreased availability for the synthesis of plasma proteins involved in nutrient transport and the acute phase response to infection. Another consistent finding is that children with oedematous SCM have oxidative stress as there is evidence of oxidant-induced cellular damage and impaired synthesis of the primary cellular anti-oxidant glutathione.