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Extending Supplementary Nutrition in Malnutrition: More Is Better?

Forbes, David A.*; Brewster, David R.

Journal of Pediatric Gastroenterology and Nutrition: April 2015 - Volume 60 - Issue 4 - p 424–425
doi: 10.1097/MPG.0000000000000727
Invited Commentaries

*School of Paediatrics & Child Health, University of Western Australia, Perth, Australia

RACS ATLASS Programme, Hospital Nacional Guido Valadares, Dili, Timor-Leste.

Address correspondence and reprint requests to David A. Forbes, MBBS, FRACP, School of Paediatrics & Child Health, University of Western Australia, GPO Box D184, Perth, WA 6840, Australia (e-mail:

Received 30 November, 2014

Accepted 14 January, 2015

The authors report no conflicts of interest.

See “Extending Supplementary Feeding for Children Younger Than 5 Years With Moderate Acute Malnutrition Leads to Lower Relapse Rates” by Trehan et al on page 544.

A frustrating constraint of clinical practice guidelines (CPGs) has been the paucity of good-quality studies to guide the management of childhood malnutrition. The study in this issue of the Journal by Trehan et al in Malawi is a welcome addition to the evidence base on malnutrition (1). Trehan et al assessed anthropometric endpoints for community supplementary feeding of children with moderate acute malnutrition (MAM), comparing supplements for a fixed period of 12 weeks with stopping supplements when the weight-for-height z score (WHZ) reached −2 (approximately the third centile). The higher mean WHZ (−1.14 ± 0.67) and mid-upper arm circumference (MUAC; 13.0 ± 0.8 cm) achieved after 12 weeks of supplements for MAM resulted in significantly more children remaining well nourished (71% vs 63%) during 12 months of follow-up.

CPGs based on the best available evidence aim to standardize the management of clinical problems. Some guidelines, such as the World Health Organization's (WHO's) updates on the management of severe acute malnutrition (SAM) in infants and children, are also designed to be used in a variety of settings, including by health workers with limited training (2). In paediatric practice in low- to middle-income countries, CPGs work well for malnutrition based on classification by a simple MUAC or more complex WHZ, both indicators of degrees of wasting (3). Of course, it is also important to diagnose underlying conditions such as tuberculosis, human immunodeficiency virus infection, and developmental delay (including syndromes with growth failure). The application of CPGs to other conditions in low- and middle-income countries, however, has proven problematic (4).

Present recommendations are that children with SAM should be discharged from treatment only at a WHZ ≥−2 or MUAC ≥125 mm (depending on which admission criterion was used), providing that oedema has resolved for at least 2 weeks (1). This is different from the WHO 1999 recommendations of discharge only when the WHZ had reached −1 (3). Although the Malawian study dealt with only MAM in the community instead of SAM, their findings support increasing the anthropometric endpoints of supplementation to WHZ ≥−1.5 and MUAC ≥13.0 to decrease the subsequent relapse rate.

The authors are appropriately cautious in their recommendations because of issues of feasibility and cost-effectiveness, which may require local answers. The importance of this Malawian study is that it provides evidence about anthropometric endpoints of treatment and outcomes such as remaining well nourished, relapsing, and dying during the following 12 months. This is crucial information for donor agencies and health ministries running supplementary feeding and other nutritional rehabilitation programmes, some of which may operate without considering available evidence. It is also consistent with robust findings that all of the degrees of anthropometric deficits in children younger than 5 years of age increase the risks of dying from respiratory infections and diarrhoeal diseases (5,6). Improved nutritional status is likely to be associated with improved immune and mucosal function, both of which decrease the risks of MAM-associated infection (7,8). We now have evidence that children with even moderate degrees of wasting should be supplemented until they reach higher WHZ and MUAC endpoints than those recommended by WHO (1).

Recent Cambodian data on anthropometric screening of malnutrition complement the Malawian study (9). In this study, the MUAC cutoffs for diagnosing acute malnutrition (MUAC <125 mm), MAM (115 mm ≤ MUAC < 125 mm), and SAM (MUAC <115 mm) had poor correlations with the same categories as defined by WHZ, with low κ scores and sensitivities. Using receiver operator characteristic curves, Laillou et al calculated optimal MUAC cutoffs of 138 mm to detect acute malnutrition and of 133 mm to detect SAM using WHZ criteria. These screening MUAC values are higher than recommended endpoints in the Malawi study and would identify too many children in many settings, raising the question of whether single anthropometric cutoffs can be applied globally.

The Cambodian study (9) argues that MUAC and WHZ identify different subgroups of children with acute malnutrition at risk of death, with neither index functioning reliably as a sole criterion. This may be because MUAC is strongly related to fat mass in children, whereas WHZ reflects both fat mass and lean body mass. The advantage of MUAC and WHZ over other anthropometric indices is that wasting is a stronger determinant of mortality than stunting or being underweight. In a pooled analysis of 10 studies, the mortality hazard ratio for severe wasting was 11.6 (95% confidence interval 9.8–13.8) compared with 5.5 (4.6–6.5) for severe stunting (6). The main advantage of MUAC is that it is an easier and more robust screening tool at community level than WHZ (9), although the use of MUAC changes as an indicator of recovery during nutritional rehabilitation, particularly using a single cutoff value to indicate recovery, has not been validated.

In addition to the question of endpoints for supplementation addressed by the Malawi study (1), more research is needed on related issues of seasonal vulnerability, stunting, and the implications of the developmental origins hypothesis. Seasonal variations of paediatric disease prevalence are one of the most striking features in low- and middle-income countries, and this is especially true for malnutrition (10). The same WHZ and MUAC may carry different risks going into the rainy or hungry season than at the end of it. Second, in spite of the high global prevalence of stunting, we do not understand clearly either the pathogenesis underlying linear growth failure or the most effective interventions for preventing it (11). It is notable that no research study has ever been able to promote normal linear growth among disadvantaged children living in developing countries. Finally, the “developmental origins of health and disease” hypothesizes that nutritional deprivation during pregnancy or infancy causes permanent epigenetic changes in metabolism and organ function. Although these changes may provide some survival benefit, they increase the risks of hypertension, cardiovascular disease, and type 2 diabetes mellitus, especially when aggravated by rapid weight gain and obesity after 2 years of age. We need to be sure that by supplementing children to a MUAC ≥130 mm, we do not promote obesity and cardiovascular disease in later life.

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