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B Emerging Issues in Early Childhood Obesity Prevention T here is growing interest in the potential role of exogenous agents— including chemical pollutants, drugs, and microorganisms—that may dis- turb metabolism in a manner that promotes obesity in young children. These agents are generally thought to be potentially influential through prenatal exposures, but could also be associated with exposures to the child. The com- mittee does not view the evidence linking these agents to childhood obesity as sufficient to influence policy, but it is important to monitor the evidence in this area and promote research whose results could indicate that curtailing these exposures would reduce the risk of early childhood obesity. Endocrine-disrupting chemicals in the environment have been hypoth- esized to increase the risk of obesity (Heindel and vom Saal, 2009; Newbold et al., 2008). This hypothesis suggests that these chemicals cause biologic changes in the systems that control adipose tissue development, ultimately causing offspring to be of higher body weight. The mechanisms, though poor- ly understood, are thought to be parallel to the pathways by which maternal metabolism during pregnancy and tobacco smoke are believed to program the fetus toward having a higher risk of obesity. A range of drugs have been used in the livestock industry to enhance growth of farm animals (Heindel and vom Saal, 2009). The list of contenders for chemical “obesogens” is extensive, including drugs such as diethylstilbes- trol and antithyroid medications and pollutants such as bisphenol A (BPA), phthalates, organophosphates, carbamates, PCBs (polychlorinated biphenyls), 153

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DDT (dichlorodiphenyltrichloroethane), cadmium, and lead (Heindel and vom Saal, 2009; Newbold et al., 2008). Pollutants that act as endocrine disruptors include agents that are known to alter metabolism in experimental settings and may have analogous effects in adult humans, although there is no direct evidence of effects on infants or children. In one study of participants in the National Health and Nutrition Examination Survey, evidence was found linking levels of phthalates in blood to waist circumference and levels of insulin resistance in adults (Stahlhut et al., 2007). An analogous study in the National Health and Nutrition Examination Survey of polyfluoroalkyls did not find an association of blood levels with body mass index (BMI) or insulin resistance (Nelson et al., 2010). In 2006, a paper published in Nature reported that microbial populations in the gut differ between obese and lean people, and that when obese people lost weight, the state of their microflora reverted back to that observed in a lean person, suggesting that obesity may have a microbial component (Turnbaugh et al., 2006). In a more recent study, Turnbaugh showed that the microbiota in the human gut can be transferred successfully to germ-free mice; that in germ-free mice transplanted with human fecal microbiota, a high-fat, high-sugar diet dura- bly changes the transplanted microbiome; and that this diet-altered microbiome promotes obesity (Turnbaugh et al., 2009). The chemicals of concern have a range of endocrine effects and are therefore of health concern independently of whether they influence obesity in children in particular. Regulation needs to take into account the full array of health concerns and target the most sensitive endpoints as the limiting factor in defining acceptable exposure levels. Reducing human exposure to these agents would have no known detrimental effects on health. Enhanced efforts are warranted to determine whether such agents make a contribution to the marked changes seen in the occurrence of childhood obesity. Such efforts include further mechanistic research, as well as observational stud- ies, to determine whether such exposures during gestation and early childhood are related to increased weight and elevated risk of obesity. REFERENCES Heindel, J. J., and F. S. vom Saal. 2009. Role of nutrition and environmental endocrine disrupting chemicals during the perinatal period on the aetiology of obesity. Molecular and Cellular Endocrinology 304(1-2):90-96. Early Childhood Obesity Prevention Policies 154

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Nelson, J. W., E. E. Hatch, and T. F. Webster. 2010. Exposure to polyfluoroalkyl chemicals and cholesterol, body weight, and insulin resistance in the general U.S. population. Environmental Health Perspectives 118(2):197-202. Newbold, R. R., E. Padilla-Banks, W. N. Jefferson, and J. J. Heindel. 2008. Effects of endocrine disruptors on obesity. International Journal of Andrology 31(2):201-207. Stahlhut, R. W., E. van Wijngaarden, T. D. Dye, S. Cook, and S. H. Swan. 2007. Concentrations of urinary phthalate metabolites are associated with increased waist circumference and insulin resistance in adult U.S. males. Environmental Health Perspectives 115(6):876-882. Turnbaugh, P. J., R. E. Ley, M. A. Mahowald, V. Magrini, E. R. Mardis, and J. I. Gordon. 2006. An obesity-associated gut microbiome with increased capacity for energy harvest. Nature 444(7122):1027-1031. Turnbaugh, P. J., V. K. Ridaura, J. J. Faith, F. E. Rey, R. Knight, and J. I. Gordon. 2009. The effect of diet on the human gut microbiome: A metagenomic analysis in humanized gnotobiotic mice. Science Translational Medicine 1(6). 155 Appendix B

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