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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 world- wide and it is associated with concerning medical comorbidities, most nota- bly 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 interac- tions to influence body weight [5]. 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 increas- ingly 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. Re- search into social environmental influences on obesity has expanded its scope *University of Pennsylvania School of Medicine. 236

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237 APPENDIX C 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, respec- tively, and the types of methodologies used to establish these associations, and (b) to consider opportunities for greater methodological synergy be- tween 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 environmen- tal 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 intermedi- ary behavioral variables. These intermediary phenotypes may induce a posi- tive energy balance (i.e., greater energy intake than expenditure) that, when sustained, promotes obesity. Although physiological variables are not de- picted 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 ex- plicitly posited. However, as reviewed in this report, certain studies chal- lenge 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 obe- sity, 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 influ- ences on obesity-promoting behaviors and obesity, corresponding to path- ways a and c in the figure. Section 6 addresses evidence for potential inter- actions among genetic, social, environmental, and behavioral influences on obesity. The data presented in this section challenge the premise that ge- netic and environmental factors do not interact or cannot influence each other. Section 7 suggests additional research questions and designs that

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238 Genetic a Risk/Genes c Obesity b Social Environment Putative Behavioral Phenotypes Food Intake: Physical Activity: • Increased TV Viewing • Increased Disinhibition • Decreased Non-Exercise • Impaired Satiation and Satiety Activity Thermogenesis • Enhanced Reinforcing Value of Food • Differences in Food Preferences (NEAT) • Increased Rate of Eating and Sucking Avidity 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 environ- ment” is used. Specifically, as defined by Barnett and Casper [6], “Human social environments encompass the immediate physical surroundings, so- cial relationships, and cultural milieus within which defined groups of

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239 APPENDIX C 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 253 Behaviors 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 266 Relationships Between Genetics and the Social Environment 8. Conclusion 272 xx people function and interact. Components of the social environment in- clude built infrastructure; industrial and occupational structure; labor mar- kets; social and economic processes; wealth; social, human, and health services; power relations; government; race relations; social inequality; cul- tural 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 net- works, neighborhoods, towns and cities, and regions.” This section reviews evidence for potential social-environmental influ- ences 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 popula- tions, 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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240 GENES, BEHAVIOR, AND THE SOCIAL ENVIRONMENT 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 prod- ucts, the increasing access to energy-dense foods in schools, the increased use of labor saving devices that reduce physical activity, and reduced op- portunities 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 [13], 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 (com- monly 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 record- ers, 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 [13]. 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 environ- ment” that have the greatest impact on obesity are unknown [13]. 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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241 APPENDIX C with access to playgrounds, proximity to fast-food restaurants, or neigh- borhood crime level [14]. Finally, it has not been tested whether exposure to the toxic environ- ment is related to genotype. That is, individuals with obesity-predisposing genes may be particularly responsive to the effects of such a “toxic” envi- ronment. 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 [18] 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 sup- port for a relationship between SES and weight gain among African Ameri- cans. 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 [19] 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 obe- sity. Factors such as limited access to resources, poor knowledge of nutri- tion and health, increased exposure to fast-food outlets, and limited physi- cal activity due to deprived or unsafe neighborhoods [20, 21] have been suggested to influence energy intake and energy expenditure and, conse- quently, 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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242 GENES, BEHAVIOR, AND THE SOCIAL ENVIRONMENT 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 [22]. 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, nutri- ent-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 [26]. 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 neighbor- hoods also may contribute to diminished energy expenditure and thus in- creased body weight in individuals of lower SES [28]. 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 infor- mation 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” [29]. This phenomenon would be represented by pathway b in Figure C-1. De Castro [30] studied 63 adults who main- tained 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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243 APPENDIX C tation effect was greater for meals consumed in the presence of a spouse, family member, or friend compared to less familiar or unknown compan- ions, suggesting that enhanced social interactions and discussions were the underlying mechanisms [31]. Indeed, de Castro and de Castro [30] argued that physiological signals that relate to appetite and meal size can be over- ridden 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 phe- nomenon. Edelman et al. [32] 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 [33] 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 spe- cific 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 [35] 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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244 GENES, BEHAVIOR, AND THE SOCIAL ENVIRONMENT 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 [38]. 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 signifi- cant association [39], and that one study found the association to be true in non-Hispanic white families but not African American families [40]. 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 [41]. 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 [42]. 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 [43]. Investigators have measured feeding practices by parent-report questionnaires, direct observation, or analysis of video- tapes, with the most common assessment tool being the parent-report Child Feeding Questionnaire [44]. A recent review of this literature con- cluded 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 [43]. 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 in- creased 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 [42]. Second, restricting children’s

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245 APPENDIX C access to foods may have the counterproductive effect of making those “forbidden” foods more desirable [47]. 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 [48]. 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 [49]. As in other realms of child develop- ment, 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 condi- tions 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. [50] 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 path- ways 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 individu- als’ 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 differ- ing body sizes continues to be of great importance. Following is a descrip- tion of selected eating traits which may represent behavioral phenotypes of obesity.

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246 GENES, BEHAVIOR, AND THE SOCIAL ENVIRONMENT 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) environ- ment. 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 be- tween 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 [64]. 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 [65], binge eating [70], and body fat [71]. 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 [72] 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 manipula- tion 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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270 GENES, BEHAVIOR, AND THE SOCIAL ENVIRONMENT Moderator: Genetic Risk/Genes b a Social Obesity Environment Selected Putative Behavioral Phenotypes Food Intake: Physical Activity: • Increased TV Viewing • Increased Disinhibition • Decreased Non-Exercise • Impaired Satiation and Satiety • Enhanced Reinforcing Value of Food Activity Thermogenesis (NEAT) • Differences in Food Preferences • Increased Rate of Eating and Sucking Avidity 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 mea- sures, 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 pheno- type in a genetics study, especially if genes influence whether certain indi- viduals 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. [177] provide a more detailed dis-

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271 APPENDIX C 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 do- main 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 [43] 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 Genetic Risk/Genes Obesity Social Environment Selected Putative Behavioral Phenotypes Food Intake: Physical Activity • Increased T VViewing • Increased Disinhibition • Impaired Satiation and Satiety • Decreased Non-Exercise • Enhanced Reinforcing Value of Food Activity Thermogenesis (NEAT) • Differences in Food Preferences • Increased Rate of Eating and Sucking Avidity 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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272 GENES, BEHAVIOR, AND THE SOCIAL ENVIRONMENT 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 inte- grative research projects or interdisciplinary training for scientists. Interdis- ciplinary research of the sort reviewed in this report would likely require new collaborative relationships that bring together investigators from dif- ferent “camps.” Institutional and/or funding initiatives that encourage such collaborations may help advance such efforts, given the economic and lo- gistical 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 re- search 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 collabora- tions among investigators. The pathways that lead to obesity are complex and multivariate for most individuals in the population. Additional re- search that addresses how the genetics of obesity impacts on environmental choices made by certain individuals, and how certain environments moder- ate 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 car- diovascular 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 cardiovas- cular 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 Examina- tion 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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274 GENES, BEHAVIOR, AND THE SOCIAL ENVIRONMENT 29. Herman, C.P., D.A. Roth, and J. Polivy, Effects of the presence of others on food intake: a normative interpretation. Psychol Bull, 2003. 129(6): p. 873-86. 30. de Castro, J.M. and E.S. de Castro, Spontaneous meal patterns of humans: influence of the presence of other people. Am J Clin Nutr, 1989. 50(2): p. 237-47. 31. de Castro, J.M., Family and friends produce greater social facilitation of food intake than other companions. Physiol Behav, 1994. 56(3): p. 445-5. 32. Edelman, B., et al., Environmental effects on the intake of overweight and normal- weight men. Appetite, 1986. 7(1): p. 71-83. 33. Kim, J.Y. and H.R. Kissileff, The effect of social setting on response to a preloading manipulation in non-obese women and men. Appetite, 1996. 27(1): p. 25-40. 34. de Castro, J.M., et al., Social facilitation of the spontaneous meal size of humans occurs regardless of time, place, alcohol or snacks. Appetite, 1990. 15(2): p. 89-101. 35. Kramer, M.S. and B. Moroz, Do breast-feeding and delayed introduction of solid foods protect against subsequent atopic eczema? J Pediatr, 1981. 98(4): p. 546-50. 36. Armstrong, J. and J.J. Reilly, Breastfeeding and lowering the risk of childhood obesity. Lancet, 2002. 359(9322): p. 2003-4. 37. Liese, A.D., et al., Inverse association of overweight and breast feeding in 9 to 10-y-old children in Germany. Int J Obes Relat Metab Disord, 2001. 25(11): p. 1644-50. 38. Gillman, M.W., et al., Risk of overweight among adolescents who were breastfed as infants. JAMA, 2001. 285(19): p. 2461-7. 39. Wadsworth, M., et al., Breast feeding and obesity. Relation may be accounted for by social factors. BMJ, 1999. 319(7224): p. 1576. 40. Grummer-Strawn, L.M. and Z. Mei, Does breastfeeding protect against pediatric over- weight? Analysis of longitudinal data from the Centers for Disease Control and Pre- vention Pediatric Nutrition Surveillance System. Pediatrics, 2004. 113(2): p. e81-6. 41. Taveras, E.M., et al., Association of breastfeeding with maternal control of infant feeding at age 1 year. Pediatrics, 2004. 114(5): p. e577-83. 42. Johnson, S.L. and L.L. Birch, Parents’ and children’s adiposity and eating style. Pediat- rics, 1994. 94(5): p. 653-61. 43. Faith, M.S., et al., Parent-child feeding strategies and their relationships to child eating and weight status. Obes Res, 2004. 12(11): p. 1711-22. 44. Birch, L.L., et al., Confirmatory factor analysis of the Child Feeding Questionnaire: a measure of parental attitudes, beliefs and practices about child feeding and obesity proneness. Appetite, 2001. 36(3): p. 201-10. 45. Wardle, J., et al., Parental feeding style and the inter-generational transmission of obesity risk. Obes Res, 2002. 10(6): p. 453-62. 46. Baughcum, A.E., et al., Maternal feeding practices and beliefs and their relationships to overweight in early childhood. J Dev Behav Pediatr, 2001. 22(6): p. 391-408. 47. Birch, L.L. and J.A. Fisher, Appetite and eating behavior in children. Pediatr Clin North Am, 1995. 42(4): p. 931-53. 48. Fisher, J.O. and L.L. Birch, Eating in the absence of hunger and overweight in girls from 5 to 7 y of age. Am J Clin Nutr, 2002. 76(1): p. 226-31. 49. Faith, M.S., et al., Parental feeding attitudes and styles and child body mass index: prospective analysis of a gene-environment interaction. Pediatrics, 2004. 114(4): p. e429-36. 50. Hill, J.O., et al., Obesity and the environment: where do we go from here? Science, 2003. 299(5608): p. 853-5. 51. Adams, N., et al., The eating behavior of obese and nonobese women. Behav Res Ther, 1978. 16(4): p. 225-32. 52. Dodd, D.K., H.J. Birky, and R.B. Stalling, Eating behavior of obese and normal-weight females in a natural setting. Addict Behav, 1976. 1(4): p. 321-5.

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276 GENES, BEHAVIOR, AND THE SOCIAL ENVIRONMENT 77. Heitmann, B.L. and L. Lissner, Dietary underreporting by obese individuals—is it specific or non-specific? BMJ, 1995. 311(7011): p. 986-9. 78. Westerterp-Plantenga, M.S., et al., Energy intake adaptation of food intake to extreme energy densities of food by obese and non-obese women. Eur J Clin Nutr, 1996. 50(6): p. 401-7. 79. Meyer, J.E. and V. Pudel, Experimental studies on food-intake in obese and normal weight subjects. J Psychosom Res, 1972. 16(4): p. 305-8. 80. Westerterp-Plantenga, M.S., L. Wouters, and F. ten Hoor, Restrained eating, obesity, and cumulative food intake curves during four-course meals. Appetite, 1991. 16(2): p. 149-58. 81. Matsuda, M., et al., Altered hypothalamic function in response to glucose ingestion in obese humans. Diabetes, 1999. 48(9): p. 1801-6. 82. Del Parigi, A., et al., Neuroimaging and obesity: mapping the brain responses to hun- ger and satiation in humans using positron emission tomography. Ann N Y Acad Sci, 2002. 967: p. 389-97. 83. Kissileff, H.R., Satiating efficiency and a strategy for conducting food loading experi- ments. Neurosci Biobehav Rev, 1984. 8(1): p. 129-35. 84. Rolls, B.J., et al., Satiety after preloads with different amounts of fat and carbohydrate: implications for obesity. Am J Clin Nutr, 1994. 60(4): p. 476-87. 85. Fricker, J., et al., Effect of a covert fat dilution on the spontaneous food intake by lean and obese subjects. Appetite, 1995. 24(2): p. 121-37. 86. Roe, L.S., et al., A meta-analysis of factors predicting energy compensation in preloading studies. FASEB Journal, 1999. 13: p. A871. 87. Faith, M.S., et al., Familial aggregation of energy intake in children. Am J Clin Nutr, 2004. 79(5): p. 844-50. 88. Epstein, L.H. and B.E. Saelens, Behavioral economics of obesity: food intake and en- ergy expenditure, in Reframing Health Behavior Change with Behavioral Economics, W.K. Bickel and R.E. Vuchinich, Editors. 2000, Lawrence Erlbaum: Mahwah, NJ. p. 293-311. 89. Epstein, L.H.S., B.E, Behavioral economics of obesity: Food intake and energy expen- diture, in Reframing health behavior change with behavioral economics, W.K.V. Bickel, R.E, Editor. 2000, Lawrence Erlbaum: Mahwah, NJ. p. 293-311. 90. Saelens, B.E. and L.H. Epstein, Reinforcing value of food in obese and non-obese women. Appetite, 1996. 27(1): p. 41-50. 91. Lappalainen, R. and L.H. Epstein, A behavioral economics analysis of food choice in humans. Appetite, 1990. 14(2): p. 81-93. 92. Ferster, C.B., J.I. Nurnberger, and E.B. Levitt, The control of eating. J Mathematics, 1962. 1: p. 87-109. 93. Spiegel, T.A., E.E. Shrager, and E. Stellar, Responses of lean and obese subjects to preloads, deprivation, and palatability. Appetite, 1989. 13(1): p. 45-69. 94. Kissileff, H.R. and J. Thornton, Facilitation and inhibition in the cumulative food intake curve in man, in Changing Concepts of the Nervous System, A.J. Morrison and P. Stick, Editors. 1982, Academic Press: New York. p. 585-605. 95. Stunkard, A.J., et al., Energy intake, not energy output, is a determinant of body size in infants. Am J Clin Nutr, 1999. 69(3): p. 524-30. 96. Stunkard, A.J., et al., Predictors of body size in the first 2 y of life: a high-risk study of human obesity. Int J Obes Relat Metab Disord, 2004. 28(4): p. 503-13. 97. Spiegel, T.A., et al., Bite size, ingestion rate, and meal size in lean and obese women. Appetite, 1993. 21(2): p. 131-45. 98. Spiegel, T.A., Rate of intake, bites, and chews—the interpretation of lean-obese differ- ences. Neurosci Biobehav Rev, 2000. 24(2): p. 229-37.

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