Abstract
Sustainable Development Goal 2.2—to end malnutrition by 2030—includes the elimination of child wasting, defined as a weight-for-length z-score that is more than two standard deviations below the median of the World Health Organization standards for child growth1. Prevailing methods to measure wasting rely on cross-sectional surveys that cannot measure onset, recovery and persistence—key features that inform preventive interventions and estimates of disease burden. Here we analyse 21 longitudinal cohorts and show that wasting is a highly dynamic process of onset and recovery, with incidence peaking between birth and 3 months. Many more children experience an episode of wasting at some point during their first 24 months than prevalent cases at a single point in time suggest. For example, at the age of 24 months, 5.6% of children were wasted, but by the same age (24 months), 29.2% of children had experienced at least one wasting episode and 10.0% had experienced two or more episodes. Children who were wasted before the age of 6 months had a faster recovery and shorter episodes than did children who were wasted at older ages; however, early wasting increased the risk of later growth faltering, including concurrent wasting and stunting (low length-for-age z-score), and thus increased the risk of mortality. In diverse populations with high seasonal rainfall, the population average weight-for-length z-score varied substantially (more than 0.5 z in some cohorts), with the lowest mean z-scores occurring during the rainiest months; this indicates that seasonally targeted interventions could be considered. Our results show the importance of establishing interventions to prevent wasting from birth to the age of 6 months, probably through improved maternal nutrition, to complement current programmes that focus on children aged 6–59 months.
| Original language | English |
|---|---|
| Pages (from-to) | 558-567 |
| Number of pages | 10 |
| Journal | Nature |
| Volume | 621 |
| Issue number | 7979 |
| DOIs | |
| Publication status | Published - 21 Sept 2023 |
| Externally published | Yes |
| Publication type | A1 Journal article-refereed |
Funding
This research was financially supported by a global development grant (OPP1165144) from the Bill & Melinda Gates Foundation to the University of California, Berkeley. J.B.-C. acknowledges funding from the National Institute of Allergy and Infectious Diseases under award K01AI141616. J.B.-C. is a Chan Zuckerberg Biohub investigator. We would also like to thank the following collaborators on the included cohorts and trials for their contributions to study planning, data collection and analysis: M. Sharif, S. Kerio, Urosa, Alveen, S. Hussain, V. Paudel, A. Costello, B. Torun, L. M. Locks, C. M. McDonald, R. Kupka, R. J. Bosch, R. Kisenge, S. Aboud, M. Wang and all other members of the study staff and field teams. We also thank all study participants and their families for their contributions. T.N. is an employee of the Bill & Melinda Gates Foundation. K.H.B. and P.C. are former employees of the Bill & Melinda Gates Foundation. J.C., V.S., R. Hafen and J.H. work as research contractors funded by the Bill & Melinda Gates Foundation.
| Funders | Funder number |
|---|---|
| National Institute of Allergy and Infectious Diseases | K01AI141616 |
| The Bill and Melinda Gates Foundation | |
| University of California, Berkeley |
ASJC Scopus subject areas
- General
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