The Double Burden of Child Malnutrition: Molecular Mechanisms and Policy Implications of Concurrent Stunting and Obesity

Abstract

Lower-middle income countries (LMICs) are experiencing a double burden of malnutrition. In these countries, the prevalence of undernutrition remains high while that for overweight and obesity is increasing rapidly as a result of a nutrition transition. In addition, a new form of malnutrition in which children are found to be both stunted, a form of undernutrition, and obese has started to become more prevalent. This thesis investigates and evaluates the literature regarding the molecular mechanisms that explain the association between stunting and subsequent obesity as well as nutritional policies that would be able to address this unique form of malnutrition. First, this thesis explores the key causes and consequences of both stunting and obesity in order to attain a deeper understanding on how each of these conditions independently develops, and to convey the double burden stunted-obese individuals suffer from. Although the genetic contribution to the development of obesity is significant, environmental factors, characterized by the nutritional transition, plays a more significant role in explaining the rapid increases in the rate of obesity in LMICs. Meanwhile, stunting occurs most commonly while an individual is in utero or in infancy, critical periods of time in which the programming of set points for metabolic pathways occurs. Stunted individuals have a greater tendency to accumulate fat and have impaired fat oxidation. Second, in order to elucidate the physiological and molecular mechanisms that would explain how undernutrition and stunting leads to the development of obesity, this thesis explores two novel avenues of molecular biology research, namely epigenetic mechanisms and the gut microbiota. Individuals who were undernourished while in utero have altered expression of particular candidate genes, pdx 1, glut 4, nr3c1, and pomc, that lead to increased feeding behavior and insulin resistance. Stunted individuals also have a lower representation of species from the Bacterioidetes phylum in their gut microbiota, which results in decreased expression of factors responsible for fat oxidation. Third, this thesis makes recommendations for policies and interventions that are able to target both problems of stunting and obesity, given the established link between these two forms of malnutrition and the collective burden they place on LMICs. Policies and interventions must match the nutritional profile of the populations they serve. In conclusion, I propose that the causal link between undernutrition and obesity proposed by molecular biology research would suggest that policies targeting the first 1000 days of life will be most effective in addressing the double burden of malnutrition.