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Genes, Behavior, and the Social Environment: Moving Beyond the Nature/Nurture Debate C Social Environmental and Genetic Influences on Obesity and Obesity-Promoting Behaviors: Fostering Research Integration Myles S. Faith, Ph.D. and Tanja V. E. Kral, Ph.D.* Weight and Eating Disorders Program SECTION 1: INTRODUCTION Obesity is one of the most pressing public health disorders in the United States and other westernized societies. Its prevalence is increasing worldwide and it is associated with concerning medical comorbidities, most notably the metabolic syndrome and type 2 diabetes [1-4]. Hence, innovative research that elucidates the causes of obesity has become an increasingly important focus for the National Institutes of Health. A challenge to this mission, however, is that fact that obesity is a “complex disorder.” For most individuals in the population, obesity results from multiple genetic and environmental factors that may interact with, or may be correlated with, each other. Genes operate additively and through gene-gene interactions to influence body weight . The topic of genetic and social environmental influences on obesity, and how they interact, is a unique topic for which conceptual frameworks are scarce. Research within each domain appears to have advanced largely within independent “camps,” each of which has undergone major advances in the past decade. Research into the genetics of human obesity has become increasingly sophisticated with respect to molecular technologies, biostatistics, and efficient design strategies; however, as illustrated in this report, these studies generally did not measure specific aspects of the social environment. Research into social environmental influences on obesity has expanded its scope * University of Pennsylvania School of Medicine.
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Genes, Behavior, and the Social Environment: Moving Beyond the Nature/Nurture Debate of coverage from interpersonal variables to potential consequences of a broader “toxic environment;” however, these studies generally did not collect DNA or use genetically informative designs. Hence, there appears to be room for greater scientific synergy between the domains. There are two overarching aims to the present report: (a) to review evidence for genetic and social-environmental influences on obesity, respectively, and the types of methodologies used to establish these associations, and (b) to consider opportunities for greater methodological synergy between the two domains. The report strives to foster ideas for new research that bridge genetic and social-environmental research, as they relate to obesity and obesity-promoting behaviors. Conceptual frameworks that posit potential interactions or covariation among genetic and social environmental factors are proposed. SECTION 2: ORGANIZATIONAL FRAMEWORK OF THIS REPORT Figure C-1 presents the conceptual framework around which the present report is organized. The model posits that genetic and social-environmental factors promote obesity through their independent influences on intermediary behavioral variables. These intermediary phenotypes may induce a positive energy balance (i.e., greater energy intake than expenditure) that, when sustained, promotes obesity. Although physiological variables are not depicted in the model, they clearly are central to energy balance regulation and the putative behavior phenotypes listed in the figure. The model is intended to reflect much of the current literature, in that correlations or interactions among the social environment and genetic factors are not explicitly posited. However, as reviewed in this report, certain studies challenge this assumption and suggest that expansions of this model may help guide future research. The final section of this report suggests additional research that would test interactions and correlations among genetic and social-environmental variables. The following section of the report, Section 3, addresses putative social-environmental influences on obesity-promoting behaviors and obesity, corresponding to pathways b and c in Figure C-1. Section 4 addresses evidence for selected refined behavioral traits that have been associated with obesity in some studies, corresponding to the “putative behavioral phenotypes” noted in the figure. Section 5 addresses putative genetic influences on obesity-promoting behaviors and obesity, corresponding to pathways a and c in the figure. Section 6 addresses evidence for potential interactions among genetic, social, environmental, and behavioral influences on obesity. The data presented in this section challenge the premise that genetic and environmental factors do not interact or cannot influence each other. Section 7 suggests additional research questions and designs that
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Genes, Behavior, and the Social Environment: Moving Beyond the Nature/Nurture Debate FIGURE C-1 Conceptual model relating genetic and social-environmental factors to obesity. In this figure, the effects of genetic and social-environmental factors, respectively, are posited to operate through putative behavioral phenotypes that promote positive energy balance. Although not depicted, genetic and social-environmental factors are posited to impact on physiological variables as well. might test new questions concerning the interplay between genes, social environment, behavior, and obesity. It should be noted that the term “obesity,” used throughout this report, was not necessarily measured in the same way across all the reviewed studies. Most studies defined obesity based on the body mass index (BMI; kg/m2), which is a reasonable proxy measure of total body fat, at least in population studies. Guidelines by the National Heart, Lung, and Blood Institute stipulate a BMI between 25.0 and 29.9 as “overweight,” and greater than 30.0 as “obese.” More refined body composition measures were used in some studies. Given the range of topics covered in this report, a table of contents for the major report sections and subsections is provided for the reader (Table C-1). SECTION 3: SOCIAL-ENVIRONMENTAL INFLUENCES ON OBESITY AND OBESITY-PROMOTING BEHAVIORS For the purposes of this report, a broad definition of “social environment” is used. Specifically, as defined by Barnett and Casper , “Human social environments encompass the immediate physical surroundings, social relationships, and cultural milieus within which defined groups of
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Genes, Behavior, and the Social Environment: Moving Beyond the Nature/Nurture Debate TABLE C-1 Organizational Sections of Summary Report and Accompanying Pages Section Number and Topic Starting Page Number 1. Introduction 236 2. Organizational Framework of This Report 237 3. Social-Environmental Influences on Obesity and Obesity-Promoting Behaviors 238 3a. Macroenvironmental Influences 240 3b. Microenvironmental Influences 242 4. Refined Behavioral Traits Associated with Obesity 245 4a. Eating Traits 245 4b. Physical Activity and Sedentary Behavior 251 5. Genetic Influences on Obesity and Obesity-Promoting Behaviors 253 5a. Genetic Influences on BMI and Fat Mass 253 5b. Genetic Influences on Food Intake 257 6. Evidence for Interactions Among Social Environmental, Genetic, and Behavioral Factors as They Relate to Obesity 262 6a. Social Environment as a Potential Moderator Variable 263 7. Opportunities for Future Research That Would Enlighten Relationships Between Genetics and the Social Environment 266 8. Conclusion 272 people function and interact. Components of the social environment include built infrastructure; industrial and occupational structure; labor markets; social and economic processes; wealth; social, human, and health services; power relations; government; race relations; social inequality; cultural practices; the arts; religious institutions and practices; and beliefs about place and community. [ … ] Social environments can be experienced at multiple scales, often simultaneously, including households, kin networks, neighborhoods, towns and cities, and regions.” This section reviews evidence for potential social-environmental influences on obesity and obesity-promoting behaviors, corresponding to paths b and c in Figure C-1. The social-environmental variables include two “macroenvironmental” variables and two “microenvironmental” variables. Macroenvironmental factors operate across larger communities or populations, specifically, exposure to components of the “toxic environment” and socioeconomic status (SES); “microenvironmental” factors, on the other hand, refer to smaller groups of individuals or family members, specifically, the “social facilitation” of overeating that occurs in group settings and parent-child feeding dynamics. The social-environmental variables reviewed below are not necessarily independent of each other, but are presented individually for ease of presentation.
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Genes, Behavior, and the Social Environment: Moving Beyond the Nature/Nurture Debate 3a. Macroenvironmental Influences The two macroenvironmental factors reviewed below are (i) exposure to the “toxic environment” and (ii) SES. These particular factors are reviewed because there is a reasonable database providing information on these variables and because of their potential relevance for obesity prevention. i. Exposure to the “Toxic Environment” Brownell coined the term “toxic environment” [7, 8], referring to a pervasive series of social and economic changes that have occurred in the United States during in the past several decades. Brownell argues that these changes have caused the rising obesity prevalence, even though strong causal inferences cannot be easily made from these observational trends. These changes are outlined in detail elsewhere [9-12], but include the increased portion sizes and the “super-sizing” of commercially available foods, the proliferation of fast-food restaurants, the reduced cost of fast-food products, the increasing access to energy-dense foods in schools, the increased use of labor saving devices that reduce physical activity, and reduced opportunities for physical activity in schools and at safe playgrounds. Data have been published that are consistent with the notion that some of these changes may have contributed to the rising obesity prevalence. As reviewed elsewhere , for example, data on national food supply and utilization from the U.S. Marketing System indicate that the overall energy availability per capita in the United States increased by 15 percent between 1970 and 1994, a period during which there was also an increase in per capita availability of dietary fat, increased consumption of added fats (commonly found in snack or confectionary foods), reduced milk intake, and increased soft-drink intake. During this period, there was an increased number of households with two or more television sets, home video recorders, and home computers. Despite these findings, several caveats are warranted. First, although these aforementioned findings are consistent with a causal influence (i.e., pathways b and c in Figure C-1), evidence for a causal relationship per se is limited . Much of the evidence comes from observational studies that could not control for potential confounding factors or did not directly test associations between participant weight status and exposure to putative environmental risk factors. Second, specific aspects of the “toxic environment” that have the greatest impact on obesity are unknown . Third, findings from certain studies did not support expected predictions. For example, in a cohort of over 7,000 children who were 36 to 59 months of age and from low-income families, child obesity status was not associated
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Genes, Behavior, and the Social Environment: Moving Beyond the Nature/Nurture Debate with access to playgrounds, proximity to fast-food restaurants, or neighborhood crime level . Finally, it has not been tested whether exposure to the toxic environment is related to genotype. That is, individuals with obesity-predisposing genes may be particularly responsive to the effects of such a “toxic” environment. In addition, certain individuals may be more likely to seek out or expose themselves to aspects of the toxic environment. The topic of gene-environment correlations as a topic for additional research is discussed further in Section 7. ii. Socioeconomic Status (SES) Several studies (e.g., [15-17]) have documented an inverse relationship between SES and obesity in previous years. In a recent review, Ball and colleagues  examined 34 articles to test the hypothesis that persons from lower SES strata are at increased risk of weight gain. Their hypothesis was supported for predominantly non-African American samples, but not for African American samples. Reviewing relevant studies, they found little support for a relationship between SES and weight gain among African Americans. In contrast, depending on the particular indicator for SES that was used (i.e., occupational status, education, and income), they found that lower SES was associated with an increased risk of weight gain in non-African American individuals. Specifically, the authors found an inverse association between occupational status and weight gain for men and women. When SES was assessed using education as the indicator, the relationship became less strong (particularly among men). Using income level as the particular indicator for SES, findings for associations between weight gain and SES were inconsistent for both men and women. Finally, the authors noted a differential rate of weight gain by SES and attributed that finding to an early onset of weight gain in a person’s life, when parental SES may still be influential. Prospective analyses of the National Longitudinal Survey of Youth  found that children from lower SES families were more likely to have been overweight during the prior year than children from higher SES families. Negative associations between obesity status and household income and parental education were found even when controlling for ethnicity and other demographic variables. Several mechanisms could underlie the link between low SES and obesity. Factors such as limited access to resources, poor knowledge of nutrition and health, increased exposure to fast-food outlets, and limited physical activity due to deprived or unsafe neighborhoods [20, 21] have been suggested to influence energy intake and energy expenditure and, consequently, body weight. For instance, in an ecological study of 267 postal districts in Melbourne, Australia, families living in the poorest SES strata
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Genes, Behavior, and the Social Environment: Moving Beyond the Nature/Nurture Debate had 2.5 times the exposure to fast-food outlets and thus increased access to relatively inexpensive, calorically dense foods compared to families from the wealthiest SES strata . The relationship between SES and obesity may also be influenced by differential costs of less or more nutritious foods. For instance, in a series of elegant analyses, Drewnowski documented that the cost of healthy, nutrient-dense foods such as fruits and vegetables were reliably more expensive than more energy-dense, less nutritious foods [23-25]. Possibly for this reason, the availability of fruits and vegetables in adolescents’ homes was shown to be greater among families from high compared to low SES strata . These data suggest that families from lower SES strata have overall fewer monetary resources to purchase more nutrient-dense, healthy foods [23, 25, 27]. Reduced access to recreational facilities or parks in deprived neighborhoods also may contribute to diminished energy expenditure and thus increased body weight in individuals of lower SES . In summary, lower SES may contribute to the onset of obesity in that it provides an environment which promotes the intake of calorically dense foods while it reduces the need or the opportunity for physical activity. 3b. Microenvironmental Influences The two microenvironmental influences reviewed in this section are social facilitation of eating and parental feeding practices. These particular factors are reviewed because there is a reasonable database providing information on these variables and, in regards to feeding practices, because of its potential relevance for obesity prevention. i. Social Facilitation of Eating There is reliable evidence that total energy intake at meals is increased significantly when eating in the presence of other people, a phenomenon termed “social facilitation” . This phenomenon would be represented by pathway b in Figure C-1. De Castro  studied 63 adults who maintained a 7-day continuous food diary and recorded the number of people present at each meal. Results indicated that energy intake during meals that were eaten alone was significantly lower compared to energy intake during meals that were consumed in the presence of others. This was observed for total energy intake (410 vs. 591 kcals), carbohydrate intake (190 vs. 241 kcals), fat intake (157 vs. 230 kcals), and protein intake (65 vs. 100 kcals). Satiety ratings were 30 percent greater following meals eaten with others compared to meals eaten alone. Additional analyses of de Castro’s data indicated that the social facili-
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Genes, Behavior, and the Social Environment: Moving Beyond the Nature/Nurture Debate tation effect was greater for meals consumed in the presence of a spouse, family member, or friend compared to less familiar or unknown companions, suggesting that enhanced social interactions and discussions were the underlying mechanisms . Indeed, de Castro and de Castro  argued that physiological signals that relate to appetite and meal size can be overridden by social interactions. Specifically, they found that reported total energy intake at meals was positively correlated with time since prior meal consumption, but only for meals eaten alone. When others were present at meals, there was no longer a significant association, suggesting that post-prandial meal regulation may be “disrupted by the presence of other people” (p. 246). Laboratory studies have also demonstrated this social facilitation phenomenon. Edelman et al.  showed that overweight and normal-weight subjects consumed more lasagna when eating in groups of 4 or 5 persons compared to when eating alone, and that there was no significant difference between the weight groups in terms of this phenomenon. Klesges et al. documented the social facilitation effect in a restaurant setting, with the effect being more pronounced for women than men. Kimm and Kissileff  also demonstrated the social facilitation of eating in a cafeteria setting. The mechanism underlying social facilitation of eating has been termed “time-extension” [29, 34] and has received the most empirical support. Specifically, the presence of people at a meal serves to lengthen meal time which, in turn, promotes further energy intake. The point is important to the present paper because, as presented in Section 5, there is evidence that the tendency to eat with others may be genetically influenced. Thus, the fact that some individuals are more likely to eat in the presence of others may not be a random event; rather, eating in the presence of others may be a trait that is influenced by genes that indirectly promote social facilitation of eating at meals. ii. Parental Feeding Practices: Breast-Feeding vs. Bottle-Feeding An area of active research concerns parental feeding practices and parent-child feeding dynamics that might promote a positive energy balance and overweight in young children. Review of this literature reveals two specific feeding practices that are prospectively associated with increased body weight and weight gain in infants and children. These practices are, first, bottle-feeding as opposed to breast-feeding, and, second, parental use of restrictive child feeding practices. With respect to breast-feeding practices, prospective epidemiology studies have shown that childhood and adolescent obesity rates were reduced among infants who were breast-fed as opposed to never breast-fed  and among infants who were breast-fed for longer compared to shorter durations [36, 37]. In one seminal study, the prevalence
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Genes, Behavior, and the Social Environment: Moving Beyond the Nature/Nurture Debate of overweight was studied in 8,186 girls and 7,155 boys, 9 to 14 years of age, who were participating in a national growth and development study . Among children who were mostly or exclusively breast-fed during the first 6 months of life, compared to children who were mostly or exclusively formula-fed, the odds ratio for being overweight was 0.78. This held true when controlling for maternal BMI and other variables reflecting SES and lifestyle activities. It should be noted that not all studies replicated this significant association , and that one study found the association to be true in non-Hispanic white families but not African American families . The mechanisms for the apparent protective effect of breast-feeding on overweight development were unknown, although recent data implicate parental feeding patterns as a possible factor. Specifically, mothers who breast-fed their infants were less restrictive in their feeding practices (as measured by self-report questionnaire) than mothers who bottle-fed their infants . As discussed in the next section, restriction of child eating may impede a child’s ability to self-regulate food intake and instead teach a child to eat in response to external cues . Whether or not this is the actual mechanism needs to be clarified in future research. iii. Parental Feeding Practices: Restrictive Feeding Practices An extensive literature has examined which parental feeding practices, if any, are associated with increased child food intake during meals and increased weight status . Investigators have measured feeding practices by parent-report questionnaires, direct observation, or analysis of videotapes, with the most common assessment tool being the parent-report Child Feeding Questionnaire . A recent review of this literature concluded that, across the range of parental feeding domains that have been studied, only restriction of child eating was consistently associated with increased child total energy intake and weight status . Parents who restrict their children’s access to foods tend to have heavier children. No other feeding domains were associated with childhood obesity, including use of food to calm infants and children, feeding on schedule, pushing child to eat more, and provision of structure during feeding, or using food as a reward [45, 46]. Several mechanisms by which parental restriction may promote increased child energy intake and body weight have been proposed. First, restrictive feeding practices may impede on a child’s ability to adhere to internal hunger and satiety cues (i.e., impaired self-regulation) and thereby teach children to eat in response to external cues (e.g., portion size, time of day). Among preschool children, the ability to self-regulate food and energy intake across meals was poorer among children whose parents reported elevated efforts to control child eating . Second, restricting children’s
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Genes, Behavior, and the Social Environment: Moving Beyond the Nature/Nurture Debate access to foods may have the counterproductive effect of making those “forbidden” foods more desirable . Third, restriction of foods may teach children to eat in the absence of hunger, that is, to continue eating despite being full when food is available . At the same time, the body of evidence suggests that parental restriction of child eating is elicited, at least in part, by a child’s increased body weight [43, 49]. Indeed, in one study, the association between restrictive feeding practices and increased child weight gain was only seen in children who were born at high risk for obesity . As in other realms of child development, there appears to be a bidirectional association such that parental restriction of child eating partially is elicited by child’s weight, which in turn may exacerbate further child weight gain. This also suggests a possible gene-environment correlation such that genes and environmental conditions that promote childhood obesity are interrelated. The topic of gene-environment correlations is discussed in Section 7. 4. REFINED BEHAVIORAL TRAITS ASSOCIATED WITH OBESITY This section reviews refined behavioral traits that have been associated with obesity in cross-sectional or prospective investigations. As such, it addresses the putative behavioral phenotypes listed in Figure C-1. Obesity results from an imbalance between energy input and energy output. The daily energy surplus that is necessary to promote weight gain is small; specifically, Hill et al.  estimated that a sustained daily energy surplus above a person’s daily energy requirements as small as 100 kcal/day is sufficient to promote weight gain. For this reason, it is desirable to identify refined behavioral traits that are related to positive energy balance and obesity. Identifying such intermediary traits may help elucidate the pathways through which the social environment and/or genes promote obesity. 4a. Eating Traits In the 1970s and early 1980s there was much interest in identifying an “obese eating style” [51-57] which differentiates lean and obese individuals’ eating behavior. It has been argued that intraindividual differences in various eating behaviors may underlie the disparity in energy intake and body weight among both groups. In light of the recent obesity epidemic, the search for distinctive patterns of food intake among individuals with differing body sizes continues to be of great importance. Following is a description of selected eating traits which may represent behavioral phenotypes of obesity.
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Genes, Behavior, and the Social Environment: Moving Beyond the Nature/Nurture Debate i. Externality and Dietary Disinhibition During the late 1960s results from a series of experiments conducted by Schachter and colleagues [58-60] suggested that the eating behavior of obese individuals is greatly influenced by the immediate (food) environment. In particular, the eating behavior of obese individuals was believed to be controlled by external cues related to the perception of time, taste and sight of food, and the number of highly palatable food cues present [53, 60, 61], rather than by internal physiological cues of hunger. Subsequent studies [62, 63] failed to replicate consistent differences between lean and obese individuals in their responsiveness to external food-related and non-food-related cues. These studies found large intraindividual variability among individuals across all weight groups in their response to external cues. However, this early research on “external eating” developed into a more promising line of research on the trait of dietary “disinhibition.” Disinhibition refers to the loss of self-imposed cognitive control of eating behavior in response to external or emotional stimuli, and is the behavioral trait that most consistently differentiates between obese and nonobese individuals . Obese subjects show greater disinhibition scores than do nonobese individuals [65, 66] and degree of disinhibition is strongly associated with energy intake [64, 67], weight status and weight gain [68, 69], weight fluctuations , binge eating , and body fat . In summary, dietary disinhibition, a characteristic that associated with external eating, may represent a behavioral phenotype which is relevant to obesity and obesity-related traits. ii. Impaired Satiation In recent years there has been much debate over whether obesity is the result of impairment in the regulation of energy intake. One way to study food and energy intake in individuals is to examine satiation (or intrameal satiety). Satiation refers to the process leading to the termination of eating. It is assessed by measuring food and energy intake during a single meal which subjects consumed ad libitum. To date only a limited number of studies is available that investigated the effects of dietary manipulation on satiation in both normal-weight and overweight/obese subjects. A study conducted by Bell and Rolls  was designed to examine the effects of energy density across three levels of dietary fat on intake in both lean and obese women. Results demonstrated that the energy density of the meals significantly affected subjects’ energy intake across all levels of dietary fat. The response to the dietary manipulation was similar between lean and obese women. All women consumed approximately 20 percent less energy in the condition of low energy density compared to high energy density.
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Genes, Behavior, and the Social Environment: Moving Beyond the Nature/Nurture Debate FIGURE C-4 Gene-environment interaction model, with genotype as moderator. In this model, the effects of social-environmental influences on obesity and obesity-promoting behaviors depend on genotype. signs, in which MZ and DZ twins are used to estimate the heritability of response to an experimental manipulation; or candidate gene designs, in which participants are selected based on specific genotypes. In all cases, pertinent outcome variables could be behavioral and/or physiological measures, as well as changes in body weight if the manipulation is sustained over time. Additional research that evaluates gene-environment correlations. Genetic studies of obesity most commonly used BMI or body fat as the primary phenotype, followed by metabolic and physiological measures, and, least commonly, behavioral measures. However, in principle, obesity-promoting genes may operate by influencing the environments into which individuals place themselves. Such a scenario is depicted in Figure C-5. That is, social-environmental measures might be conceptualized as the phenotype in a genetics study, especially if genes influence whether certain individuals will seek out “obesity-promoting” environments (e.g., fast-food restaurants). As noted in Section 3, there is evidence that obese individuals may be more likely to attend restaurants than nonobese individuals on the days that buffets are served, which would be suggestive of a gene-environment correlation. Plomin et al.  provide a more detailed dis-
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Genes, Behavior, and the Social Environment: Moving Beyond the Nature/Nurture Debate cussion of such “active” gene-environment correlations, in which genes influence people’s tendencies to create their own environments. The issue of gene-environment correlations is also relevant to the domain of child development and, in recent years, there has been increasing interest in the “genetics of parenting” [178-180]. Data suggest that certain parenting behaviors towards children are, in fact, elicited by child attributes and behavioral patterns that are probably genetically influenced. This may be a useful framework for studying parent-child feeding dynamics as they relate to obesity onset. As noted Section 3, there is evidence that parental restriction of child eating is elicited by child weight characteristics  and this in turn may exacerbate further weight gain by the child. Additional genetics studies could evaluate whether parental feeding restriction, or other parenting domains, are associated with specific candidate genes for obesity. Additional research that builds upon existing conceptual models for “organism-environment interactions.” Conceptual models that explicitly address the integration of genetic and social-environmental influences on behavioral traits may help guide future studies. The field of developmental behavioral genetics has addressed this issue, although not in regards to obesity per se. Several pertinent books have been published [181-186]. In addition, several longitudinal behavioral genetics studies measured specific FIGURE C-5 Gene-environment correlation model. In this model, there is a correlation among genes and social-environmental factors that influence obesity and obesity-promoting behaviors.
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Genes, Behavior, and the Social Environment: Moving Beyond the Nature/Nurture Debate aspects of the social environment and genetic factors and may provide useful models for obesity research. De Castro [187-189] has one of the few proposed models that integrates genetic and environmental influences on food intake. Additional institutional and/or funding mechanisms to support integrative research projects or interdisciplinary training for scientists. Interdisciplinary research of the sort reviewed in this report would likely require new collaborative relationships that bring together investigators from different “camps.” Institutional and/or funding initiatives that encourage such collaborations may help advance such efforts, given the economic and logistical challenges of such research. Initial collaboration of this sort could be exemplars for other institutions and investigators. SECTION 8: CONCLUSION This report set out to highlight two distinct areas of research that share the common goal of identifying factors that contribute to weight gain and obesity in the population. The areas reviewed in this report included research on (social-) environmental factors, as well as the genetic factors, that may be associated with obesity or the onset thereof. Despite their unique focuses, the literature reviewed in this report shows that the two areas have the potential to complement each other and to stimulate future collaborations among investigators. The pathways that lead to obesity are complex and multivariate for most individuals in the population. Additional research that addresses how the genetics of obesity impacts on environmental choices made by certain individuals, and how certain environments moderate the expression of obesity-promoting genes, may advance the current state of knowledge and provide new insights for the prevention and the treatment of obesity. LITERATURE CITED 1. Pi-Sunyer, F.X., Health implications of obesity. Am J Clin Nutr, 1991. 53(6 Suppl): p. 1595S-1603S. 2. Zhu, S., et al., Race-ethnicity-specific waist circumference cutoffs for identifying cardiovascular disease risk factors. Am J Clin Nutr, 2005. 81(2): p. 409-15. 3. Zhu, S., et al., Combination of BMI and waist circumference for identifying cardiovascular risk factors in whites. Obes Res, 2004. 12(4): p. 633-45. 4. Park, Y.W., et al., The metabolic syndrome: prevalence and associated risk factor findings in the US population from the Third National Health and Nutrition Examination Survey, 1988-1994. Arch Intern Med, 2003. 163(4): p. 427-36. 5. Dong, C., et al., Interacting genetic loci on chromosomes 20 and 10 influence extreme human obesity. Am J Hum Genet, 2003. 72(1): p. 115-24.
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Representative terms from entire chapter: