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Are genetically modified organisms contributing to obesity among americans

We review the literature with regard to the two core hypotheses in the NCS that relate to environmental origins of obesity and describe strategies that will be used to test each hypothesis.

Although it is clear that obesity in an individual results from an imbalance between energy intake and expenditure, control of the obesity epidemic will require understanding of factors in the modern built environment and chemical exposures that may have the capacity to disrupt the link between energy intake and expenditure.

Through its embrace of the life-course approach to epidemiology, the NCS will be able to study the origins of obesity from preconception through late adolescence, including factors ranging from genetic inheritance to individual behaviors to the social, built, and natural environment and chemical exposures.

It will have sufficient statistical power to examine interactions among these multiple influences, including geneenvironment and geneobesity interactions. A major secondary benefit will derive from the banking of specimens for future analysis. The prevalence of obesity in American children has trebled in the past 30 years1-3.

This great increase are genetically modified organisms contributing to obesity among americans obesity portends future increases in incidence of heart disease5, diabetes6, stroke, and possibly cancer7 and is therefore projected to produce the first decline in U. The recent explosive increase in prevalence of obesity reflects a complex interplay among a changes in individual behaviors; b changes in community structure, lifestyle, and the built environment; and c possibly exposures to certain synthetic chemicals, such as endocrine disruptors EDsthat may have the capacity to disrupt energy balance.

Control of the obesity epidemic will require understanding each of these factors and the interplay among them. This understanding will guide development of multipronged evidence-based strategies for obesity control. The goal of this review is to describe the approaches that the National Children's Study NCS will employ to develop understanding of the causes of obesity, especially with regard to environmental factors. Background Behavioral change is critical to the prevention and treatment of childhood obesity.

A successful approach to reducing obesity and its comorbidities must also embrace understanding of community-level factors including the social, built, and natural environments. These environmental influences interact with a child's diet, physical activity, genetic makeup, and metabolism10-12. An example of a multipronged approach that took careful cognizance of environmental influences is the success of the state of Arkansas in reducing obesity prevalence among school-age children.

A thoughtful redesign of the school environment, with changes to school dietary options, implementation of universal physical education programs, and reduction of access to sugary soft drinks resulted in a decline in the prevalence of overweight children from 20. Access to safe play spaces may also influence activity patterns and thus reduce risk of obesity14,15.

Direct marketing to children for example, through television ads during child-focused programming encourages consumption of high-fat and high-sugar content foods and is a negative environmental influence16,17. Unique windows of vulnerability have been identified for many of the environmental exposures linked to obesity12. Fetal are genetically modified organisms contributing to obesity among americans such as maternal nutritional deprivation and smoking can result in intrauterine growth restriction IUGR and thereby influence hypothalamicpituitary axis programming to increase future risk of obesity and diabetes10.

Infants born to women with insulin-dependent diabetes are at higher risk of obesity, and milder, diet-controlled gestational diabetes may also increase risk18,19. Maternal smoking during pregnancy is an independent risk factor for the development of childhood obesity20,21. Excess gestational weight gain has been associated with increased child adiposity at 3 years of age in at least one prospective cohort22. Exposure to endocrine-disrupting chemicals during pregnancy may enhance the risk for obesity in childhood23.

Rapid weight gain during the first year of life24 and fewer hours of sleep during infancy25 further enhance the risk for the development of childhood obesity.

Although previous cohort studies have contributed greatly to identifying many individual-level factors that contribute to the development of obesity in children and its persistence into adulthood both in the United States and in other countries11,26-38, findings from those previous longitudinal studies have several limitations: Previous studies have not fully capitalized on the life-course approach to chronic disease epidemiology39, an approach that embraces the concept that adult disease can have its origins in early life or even fetal exposures.

Barker and Osmond40 promulgated this concept to account for an association between low birth weight and adult ischemic heart disease in Britain and Wales. The concept has been adopted increasingly in the epidemiologic approach to understanding chronic conditions41 including obesity42-44 and neurodegenerative conditions45. The application of the life-course approach to identifying temporal relationships among risk factors for childhood obesity and their interaction is depicted in Figure 1.

Multiple studies have documented unique windows of vulnerability to environmental hazards that may contribute to the causation of chronic conditions such as obesity21,46, yet few studies to date have collected the scope of data depicted in this figure at multiple points in the life span.


This weakness is especially relevant in light of new knowledge from animal studies, which suggest that endocrine-disrupting chemicals may modulate response to dietary intake48,49, disrupt the hypothalamicpituitary axis50, and possibly increase risk for childhood obesity23.

Although some studies have collected genetic are genetically modified organisms contributing to obesity among americans on participants and have been able to identify polymorphisms that increase risk for obesity, they have not simultaneously collected the data on environmental exposures that are necessary to examine carefully the interactions of genetic and environmental factors with diet and physical activity.

Recent studies also suggest that obesity develops as a chronic condition much earlier than the school-age years51. Earlier cohort studies that were first initiated when obesity in the preschool years was relatively infrequent are unlikely to provide data on exposures in early life that are essential to identify prenatal and early childhood risk factors for obesity.

Many previous cohorts were limited in their capacity to identify risk factors for obesity that may be unique among Hispanics, a population for which obesity prevalence is increasing especially rapidly2,52.

Previous cohorts are limited in that they have not included sufficient numbers of children to draw contrasts between risk factors specific to rural and urban environments34. Past studies have been unable to allow accurate assessment of the role of access to parks and other places that encourage physical activity among children living in urban areas53.

Many cohort studies were begun before the tripling of childhood obesity prevalence occurred3,55,56 - a trend increasingly attributed to the collective effect of community-level factors for which policy changes may be the only effective means for preventing further increases in obesity prevalence9.

To assess the impact of these more recent community-level factors, new cohorts in which these risk factors exist are needed. Although studies from other countries, such as the Avon Longitudinal Study of Parents and Children11,12 and the Danish National Birth Cohort57, will provide important insights into the etiology of childhood obesity, the environmental factors that contribute to obesity in American children are likely to be different, and the pool of genetic polymorphisms that modify risk may be much different from that of European children.

The New Food Fights: U.S. Public Divides Over Food Science

Progress of the NCS In response to increases in the prevalence of obesity and a number of other chronic conditions, the U. Congress, through the Children's Health Act of 2000, authorized the National Institute of Child Health and Human Development NICHD "to conduct a national longitudinal study of environmental influences including physical, chemical, biological, and psychosocial on children's health and development"58.

The design of the NCS has been extensively described elsewhere59-62. Families who are enrolled in the study will participate in a minimum of 13 data collection encounters: Figure 2 depicts the timeline of visits across the complete study, and Tables 1 and 2 describe the measurements planned for preconception through 3 years of age for the seven Vanguard pilot locations.

Enrollment of women will occur in 105 primary sampling units counties or, in the case of more sparsely populated areas, clusters of counties and began in January 2009.

The mission of the NCS is to provide the federal government with a scientifically robust guide to disease prevention, and to assure scientific rigor the study has always been hypothesis-driven.

The topical working groups convened by the NCS Advisory Committee developed initial core hypotheses for the study, in consultation with thousands of scientists and representatives from community groups and professional organizations.

Childhood obesity is a lead focus of the NCS and is addressed in 6 of 30 core hypotheses. Table 3 presents the gaps of knowledge that remain with respect to four of these core hypotheses: Table 3 also presents how the NCS will address these gaps through its design. In this review, are genetically modified organisms contributing to obesity among americans highlight how the study will provide important new knowledge with regard to two core hypotheses that link factors in the chemical and built environments with childhood obesity.

Obesity-Related Hypotheses of the NCS Impact of neighborhood environment on risk of obesity and insulin resistance Built environment features such as mixed land use, increased proximity to recreational activities and green space, as well as safety e.

Decreased access to healthy eating choices in low socioeconomic status neighborhoods has been documented in at least two studies72,73. Factors such as climate and topography have been taken into account infrequently74. The effect of after school and summer adult organized programs on obesity and insulin resistance is unknown.

In the absence of such programs, parents living in urban areas may instruct their children to go directly home from school where indoor activities are largely limited to watching television and playing computer games in the security of the home. A systematic review of previous studies of the built environment and childhood obesity identified inconsistencies in measurements of the built environment across studies and cross-sectional designs as major deficits of previous studies, and noted that these studies rarely studied both diet and physical activity71.

Because of its focus on community characterization60, the NCS will allow more careful identification of those features of neighborhoods that affect physical activity and diet, such as proximity to play spaces, availability of healthy food stores, and neighborhood walkability. The NCS represents a major opportunity to explore the role of specific aspects of the neighborhood environment at different periods in a child's development.

Access to safe play spaces near a child's home, for example, may be especially protective against obesity during the early school years, but less so during adolescence. The design of the NCS capitalizes on the life-course approach and allows for separate analyses of the impact of certain factors on the development of obesity or increase in adiposity within certain time periods. Simultaneous collection of socioeconomic and genetic data as well as measures of diet and physical activity Tables 1 and 2 will permit careful distinction of the role of certain environmental risk factors during each window of vulnerability.

  1. Environmental Protection Agency; 1998. BMJ 2005; 331 7517.
  2. Pediatrics 2006; 117 2. Pesticides in the Diets of Infants and Children.
  3. Scand J Public Health 2001; 29 4.

Chemical environmental agents and the endocrine system The impact of EDs on humans was first identified by Herbst and Bern, who observed eight cases of clear cell adenocarcinoma of the vagina in young women who had been exposed in uteroto diethylstilbestrol DESa synthetic estrogen prescribed to pregnant women in the 1950s, 1960s, and 1970s to prevent miscarriage75. Prenatal exposure to DES has been found subsequently to induce obesity in an animal model23.

Identification of endocrine-disrupting chemicals has been limited by the lack of toxicity testing data available for many chemicals in widespread use76. Because so few chemicals have been tested for their toxicity, the possibility exists that other chemicals besides DES influence somatic growth and obesity48,50.

One potential endocrine-disrupting chemical, bisphenol A BPAis used to manufacture polycarbonate resin in the coatings of food and beverage containers77. Exposure to BPA, phthalates, and other EDs is widespread in American children78, and animal studies increasingly suggest the potential for toxicity at current levels of exposure79.

In vitro studies have found that BPA induces fibroblast differentiation into adipocytes80. Animal studies have found that BPA affects glucose transport in fat cells81.

Student explains link between GMO products and obesity

BPA also disrupts glucagon secretion in intact Langerhans cells at nanomolar levels82. Phthalates are used in a variety of personal care products such as shampoos and in the synthesis of polyvinyl chloride84. Phthalates have been documented consistently in animal studies to have antiandrogenic effects85-87.

Cohort studies have begun to assess for potential effects in humans and suggest susceptibility at lower levels of exposure than those documented to have effects in animals.

It is hypothesized that the most severe effects may be associated with exposures in prenatal and early postnatal life. Decreases in anogenital distance among infant males have been associated with elevated urinary phthalate levels during pregnancy88, and breast milk levels of monoester phthalates have been associated with higher serum hormone binding globulin levels and luteinizing hormone to free testosterone ratios89.

Diminished sperm motility has been identified among exposed men90-92, and low-molecular-weight phthalates have been associated with increased birth weight and longer duration of gestation in at least one birth cohort83. Although few studies have analyzed the impact of phthalate exposure on increased adiposity in children, analysis of the 1999 - 2002 National Health and Nutrition Examination Survey has identified increases in urinary phthalate levels among men with increased waist circumference and homeostatic model assessment, a measure of insulin resistance93.

Lack of accurate information on the level and timing of past exposures to EDs has been the principal limitation of most previous studies of the potential human impacts of EDs. This limitation will be directly addressed by the prospective design of the NCS. In the NCS, exposures to chemicals will are genetically modified organisms contributing to obesity among americans measured during pregnancy, in breast milk, and in the perinatal period before the appearance of health effects.

The large sample size will facilitate investigation of possible links between low-prevalence endocrine-disruptor exposures and health outcomes, and state-of-the-art laboratory assessment of chemical exposures will further sharpen the study's ability to discern effects of exposures to EDs.

The large sample size will also permit study of genetic polymorphisms and geneenvironment interactions, which may unearth individual differences in susceptibility to EDs. As new EDs are identified, specimens can be withdrawn from the NCS repository to analyze their content for appropriate biomarkers to assess whether these EDs may be risk factors in the development of obesity94. Conclusion The NCS presents previously unrealized opportunities for the identification of risk factors for childhood obesity, and for their subsequent elimination through prevention.

Just as the Are genetically modified organisms contributing to obesity among americans Heart Study provided health care providers with hitherto novel information on risk factors for cardiovascular disease that enabled them to offer evidence-based advice to limit smoking, reduce the intake of fatty foods, and control hypertension, the NCS will suggest interventions that can be used to prevent obesity by communities, policy makers, and child health providers.

A major strength of the study is that it will be representative of American children. The hypotheses presented in this review cover only a small percentage of the findings likely to emerge from the NCS. The core NCS hypotheses are dynamic, and as the study is implemented, new questions will emerge and result in modifications to the study protocol.

Others may be clearly answered through the NCS or other studies, or become outdated as the whole body of knowledge adjusts the direction of inquiry. For some areas of inquiry where the science is in relatively nascent stages, the major benefits to be gained from the study derive from its hypothesis-generating nature. The NCS will provide a major opportunity to confirm putative genetic links identified in other studies through the study of genetic sequences of children and their families95.

As new putative EDs are identified, subsamples of biospecimens stored at the NCS Specimen Repository can be rapidly analyzed to test for associations in a large-scale cohort that represents the population of U. Of course, no observational study by itself can demonstrate causality.

The NCS will identify risk factors for which causality may be suggested on the basis of strength, consistency, temporality, biological gradient, and plausibility. Findings from the NCS will prompt further interventions such as randomized controlled trials, policy interventions, and other initiatives that will confirm or refute the role of identified risk factors in the development of obesity and its associated comorbidities.

The life-course approach underlying the design of the NCS may very well lead to delineating the duration and impact of environmental, behavioral, and social exposures on risk for obesity.