Obesity, Health at Every Size, and Public Health Policy
Obesity, Health at Every Size, and Public Health Policy
Current public health approaches to obesity largely consist of promoting individual weight loss dieting or alterations to "obesogenic environments."
A particularly potent argument against public health's existing anti-obesity tactics is the proven ineffectiveness of weight loss attempts at an individual level. Indeed, as early as 1992, the American National Institutes of Health (NIH) released a consensus statement that dieting is an ineffective method to produce sustained weight loss. Mann et al. conducted a comprehensive review of the long-term consequences of weight loss dieting in long-term randomized trials, observational studies without a control group, and prospective studies without randomization. The studies reviewed by Mann et al. were methodologically biased to show long-term weight-loss maintenance. The effectiveness of dieting presented by the studies was likely overestimated attributed to confounding of the effects of diet and exercise, low follow-up rates, self-report of participants' weight by phone or mail, and many participants' use of subsequent diets following the studies in question. Regardless, the trials demonstrated no consistent health benefits, including sustained weight loss. Indeed, one-to-two thirds of dieters regained more weight than initially lost.
Only recently have the long-term physiological changes following weight loss begun to be illuminated. In part, this gap in knowledge arises from low numbers of weight-loss maintainers. Recent evidence on the physiological changes that follow weight loss in obese animal models and humans suggests organisms' endocrine systems actively promote weight regain. Such changes involve highly integrated alterations including reduced satiety, increased hunger, suppressed energy expenditure, a decrease in nutrient availability, enhanced metabolic flexibility, an increase in energy efficiency and storage in peripheral tissues, a decline in adipose energy depletion signaling from leptin and insulin, altered neural activity, and alterations in hepatic, adipose tissue, and skeletal muscle metabolism. Importantly, similar changes have been identified in humans for a full year after weight loss. One year following weight loss, subjective hunger, ghrelin (hunger stimulating hormone), gastric inhibitory polypeptide, and pancreatic polypeptide were all elevated among overweight and obese individuals who lost weight in an intervention. Decreases in insulin, leptin, polypeptide YY, and cholecystokinin were also observed. These findings align with the reduced rates of nonresting and resting energy expenditure and thermic effect of feeding present in individuals who have sustained a loss of at least 10% of body weight over a year. Such processes may help explain the very high rates of recidivism in weight-loss dieters. Given these rates of recidivism, it is concerning that weight regain is largely composed of fat; the weight regained does not replace bone mass or lean mass lost during weight loss. Furthermore, weight loss may not be harmless and may increase stress, release of persistent organic pollutants, and risk of osteoporosis.
Those individuals who do sustain substantial weight loss over time generally must maintain high levels of dietary restraint, physical activity, and self-monitoring behaviors. This is evident in reports from members of the National Weight Control Registry (NWCR). The NWCR is composed of individuals who have sustained a 30-pound weight loss for at least a year. The registry has been critiqued for its nonrepresentativeness of the US population, its reliance on self-reported data, and its high rates of loss to follow-up. Ogden et al. conducted a latent class cluster analysis of the NWCR to detect distinctive methods, experiences, and perspectives on weight loss and weight maintenance among successful weight losers. Although a majority of weight losers were satisfied with their weight loss and reported good health and healthy behaviors, particularly high levels of exercise, other results were more distressing. For example, more than one quarter (26.9%) of participants reported high rates of stress, depression, and dissatisfaction with their weight loss. This cluster struggles with their weight, frequently weight cycle, and compared with other members of NWCR, report poorer health. Interestingly, these individuals are trying to maintain the greatest weight loss. The cluster identified as trying to maintain the second largest weight loss (9.9%), reported low levels of physical activity, frequent skipping of meals, and the poorest levels of health apart from those who had lost more weight. The relatively poor psychological and physical health of the individuals in these 2 clusters, and their struggles to maintain weight healthily, suggest that they may be striving to maintain an overly extreme weight loss.
Current public health approaches assume that intentional weight loss is always positive and that a BMI in the range of 18.5 to 24.9 is necessarily the healthiest range for all individuals. Importantly, despite its widespread adoption, BMI is acknowledged to be a crude measurement of obesity that may not adequately account for regional body fat distribution and subsequent risk. In certain populations, BMI may not adequately measure adiposity or differentiate between populations, particularly with respect to athletes and athletic populations. Perhaps most importantly, BMI is a population-level proxy measure of obesity, and an individual's BMI may say little concerning that individual's health. Additionally, overweight status (BMI = 25–30) has been shown to be associated with decreased mortality risk in US, Canadian, and international samples. Obesity (BMI > 30) has even demonstrated a protective or neutral effect among some chronic disease or older populations. Minor (≤ 5%) intentional weight loss may reduce mortality risk in obese individuals with related comorbidities, but weight loss heightens mortality risk among healthy obese individuals. Therefore, in addition to being extraordinarily difficult to maintain, weight loss may not always be health enhancing, particularly for the large proportion of obese persons who may be cardiometabolically healthy, or whose ill health may be attributable to numerous non–weight-related confounding factors.
Aiming for a narrow "healthy" range of body size may induce individuals to engage in disordered eating practices. These behaviors may remain hidden, and these individuals may still be valorized for their "healthiness," particularly by others trying to lose weight. This is evident among members of, and in the espousal of seemingly bulimic practices in, commercial weight-loss groups. That is, weight-loss groups' weight-loss strategies may include advice similar to bulimic practices of binge eating and subsequent compensation through dietary restriction or compulsive exercising. Furthermore, a public health approach in which obese individuals are viewed as unhealthy burdens on the health care system and individually responsible for their weight may promote weight stigma. This stigma may produce ill health through direct stress-induced neuroendocrine pathways or adverse coping mechanisms. Weight bias is highly prevalent among health care professionals, and this may pose a barrier to individuals receiving adequate health care. Additionally, weight discrimination may diminish an individual's socioeconomic standing, which will have further deleterious effects on health. In summary, the efficacy and safety of weight-loss dieting is questionable, as are the health consequences of the most common forms of obesity. In addition to being ineffective, focusing on individuals as the cause and likeliest cure for obesity promotes weight stigma, which may be particularly health debilitating.
An ecological perspective on obesity causation was first proposed by Egger and Swinburn in 1997 and further developed by Swinburn, et al. in 1999. Their definition of the obesogenic environment included the micro- and macrocomponents of individuals' physical, political, economic, and sociocultural circumstances. More recently, the obesogenic environment is thought to be composed of factors such as the reduced time-cost of food, the increased availability of high-calorie, nutrient-poor food, and the increased motorization and mechanization of daily life. These factors are thought to have all simultaneously produced an energy imbalance in the daily lives of individuals and consequent population-wide weight gain.
Rectifying the obesogenic environment would require comprehensive government reforms. Existing evaluations of health interventions appear to support the notion that the most effective interventions for chronic disease prevention and health promotion focus on larger-scale interventions that make healthy choices more convenient and affordable, restrict unhealthy products, focus on community development, and support healthy social, economic, and environmental policy. The most cost-effective approaches to obesity, as determined by modeling studies, are those that include a taxation on unhealthy foods, restriction of junk food advertisement to children, and improved nutrition labeling. Targeted family-based programs for obese children and school-based campaigns to increase physical education and reduce sweetened beverage consumption and television viewing are also cost-effective in models. These modeling studies and reviews of previous public health interventions have led proponents of obesogenic environmental reforms to extrapolate that obesity prevalence could be lessened through structural modifications that would facilitate energy expenditure or inhibit caloric intake.
Appeals to the obesogenic environment may appear to be an effective and nonstigmatizing approach to obesity policy. However, a number of limitations must be considered regarding these strategies. Particularly problematic is the lack of direct empirical evidence that environments necessarily predispose individuals to developing obesity, which calls into question the validity of using obesity as a justification for environmental reforms. A recent review, for example, highlighted that all evidence used to support the obesogenic environment is observational and inconsistent, and the proposed relationship between environment and obesity must be viewed as presumptive. Models are thus based on hypothetical contributors to an overly simplistic energy balance model, rather than empirical evidence. Furthermore, obesity may not even indicate poor health, and reduced obesity prevalence may not improve population health. Kirk et al. assert that a main issue hindering effective obesogenic environment research is nonconsensus over what aspects of the environment, a necessarily complex, dynamic, and multilevel concept, should be implicated under the obesogenic environment rubric. Other issues persist in environmental obesity research. Randomized control trials are difficult to conduct, and impossible for the highest level of upstream environmental determinants given small number of units (e.g., high-end food policies). Thus the highest quality of research originates from natural experiments or quasi-experimental designs. However, the majority of environmental research remains observational. Causality is difficult to assess, as multilevel studies can only suggest causality, and cross-sectional studies may not establish causality. Difficulties arise in identifying valid, reliable, and consistent dietary, social and material resource, and spatial measures. Accounting for all individual level factors and their potential mediating and confounding effects is particularly challenging. Furthermore, there may be numerous unknown or unmeasured effects or multiple interactions of social and individual factors that may affect interpretation.
Kirk et al. conducted a scoping review on obesogenic environment research. The review determined that most studies focused on the physical microenvironment, and many studies used physical activity, rather than diet or BMI, as outcome measures. Few studies focused on the economic or political (such as household or workplace policies) microenvironment. Also limited were studies conducted on the macro level, including urban development, health and transportation systems, the media, and the food industry. Most importantly, the review found that such studies are methodologically stymied by a general inability to measure potential environmental effects appropriately and a comprehensive theoretical framework that would help conceptualize the intricate and multifaceted obesogenic environment.
Reviews of existent research suggest only limited support for the obesogenic environment. A systematic review conducted by Giskes et al. on environmental effects on fat and energy intake established there was limited evidence that environment influenced fat or energy intake and that any such evidence was produced from observational, cross-sectional studies. A more recent review on food-related environmental factors also was unable to confirm the impact of the obesogenic environment. However, some reviews have found support for an association between the built environment and BMI or obesity. Greater support is available for a relationship between physical activity accessibility and BMI or obesity than for food environments and BMI or obesity. Evidence suggests walkability, density, accessibility of recreational spaces, and attractiveness increase physical activity and may lower risk of elevated BMI. Isolated longitudinal studies have found some support for environmental factors and their effect on BMI and obesity. Accessibility to healthy food increase is associated with dietary quality, but less evidence exists to support a link to BMI or obesity. This may be an artifact of less research focusing on diet, because of dietary measures-related difficulties.
Recent independent studies also failed to confirm a basic relationship between environment and obesity. McPhail et al. found that Canadian adolescents' socioeconomic class or access to fast food did not affect their likelihood to consume fast food. Kim and Leigh established that middle-class US familes were more likely to eat at fast-food restaurants than were lower or higher income individuals, whereas higher income individuals were more likely to eat at full-service restaurants. An and Sturm found that California children and adolescents' proximity to fast-food outlets and convenience stores, and distance from larger grocery stores, is not associated with healthy food consumption or BMI. Lee determined that elementary-school children residing in poorer and minority neighborhoods in the United States had greater access to both fast-food outlets and grocery stores. Food access was also not found to independently predict weight gain in children over time. This access also did not account for socioeconomic and minority differences over time in weight gain, which disadvantaged poorer and minority students. Interestingly, higher income and White majority neighborhoods also have a greater share of fast-food outlets, of all food establishments, compared with minority or poorer neighborhoods. Junk food in schools was not a determinant in the development of obesity by the eighth grade in the United States. A recent study by the US Department of Agriculture asserted that assessments of the affordability of a healthy diet are largely dependent on the metric used to measure food prices. For example, if food is measured by portion, it appears less expensive than if food is measured by weight or calorie.
Ethical implications of broad-based antiobesogenic environmental reforms are also essential to consider. As limited interventions have been implemented, this involves considering their potential implications on target audiences based on proposed projects and deployed rhetoric. Broad alterations to the environment may increase stigma on obese individuals who do not lose weight, despite these environmental modifications. Should individuals not lose weight despite environmental reforms, this might be viewed as proof that their obesity is the result of an unwillingness to practice healthy choices. Such stigma may contribute to poorer health outcomes. Obesogenic environment approaches may contribute to a homogenizing view of lower-income lifestyles and the perception of lower-income individuals as passive and lacking in agency. Furthermore, this view may serve as a mask for gender-, race-, or socioeconomic-based discrimination and essentialist arguments, and the moralization of a health issue. The obesogenic environment rationale has also been criticized as being overly simplistic and dismissive of the role of neoliberalism, its systematic overproduction and overconsumption, and consequent societal anxieties and values. Importantly, broad-based reforms may become increasingly invasive and truly limit the freedom of choice of individuals. A compelling argument can be made for the type of environmental restructuring proposed by obesogenic environment arguments, without relying on mobilizing fear of fat to support their institution. By focusing on other measures of health and well-being, or sustainability, livability, and accessibility, valuable and legitimately effective reforms could be undertaken. In summary, limited evidence suggests that environment affects obesity prevalence in a direct, simplistic manner, and reforms based on restructuring particular environments to remedy obesity rates have important ethical implications. Furthermore, as the empirical evidence suggests, none of these actions may necessarily result in thinner populations.
Existing Approaches
Current public health approaches to obesity largely consist of promoting individual weight loss dieting or alterations to "obesogenic environments."
Weight Loss Dieting
A particularly potent argument against public health's existing anti-obesity tactics is the proven ineffectiveness of weight loss attempts at an individual level. Indeed, as early as 1992, the American National Institutes of Health (NIH) released a consensus statement that dieting is an ineffective method to produce sustained weight loss. Mann et al. conducted a comprehensive review of the long-term consequences of weight loss dieting in long-term randomized trials, observational studies without a control group, and prospective studies without randomization. The studies reviewed by Mann et al. were methodologically biased to show long-term weight-loss maintenance. The effectiveness of dieting presented by the studies was likely overestimated attributed to confounding of the effects of diet and exercise, low follow-up rates, self-report of participants' weight by phone or mail, and many participants' use of subsequent diets following the studies in question. Regardless, the trials demonstrated no consistent health benefits, including sustained weight loss. Indeed, one-to-two thirds of dieters regained more weight than initially lost.
Only recently have the long-term physiological changes following weight loss begun to be illuminated. In part, this gap in knowledge arises from low numbers of weight-loss maintainers. Recent evidence on the physiological changes that follow weight loss in obese animal models and humans suggests organisms' endocrine systems actively promote weight regain. Such changes involve highly integrated alterations including reduced satiety, increased hunger, suppressed energy expenditure, a decrease in nutrient availability, enhanced metabolic flexibility, an increase in energy efficiency and storage in peripheral tissues, a decline in adipose energy depletion signaling from leptin and insulin, altered neural activity, and alterations in hepatic, adipose tissue, and skeletal muscle metabolism. Importantly, similar changes have been identified in humans for a full year after weight loss. One year following weight loss, subjective hunger, ghrelin (hunger stimulating hormone), gastric inhibitory polypeptide, and pancreatic polypeptide were all elevated among overweight and obese individuals who lost weight in an intervention. Decreases in insulin, leptin, polypeptide YY, and cholecystokinin were also observed. These findings align with the reduced rates of nonresting and resting energy expenditure and thermic effect of feeding present in individuals who have sustained a loss of at least 10% of body weight over a year. Such processes may help explain the very high rates of recidivism in weight-loss dieters. Given these rates of recidivism, it is concerning that weight regain is largely composed of fat; the weight regained does not replace bone mass or lean mass lost during weight loss. Furthermore, weight loss may not be harmless and may increase stress, release of persistent organic pollutants, and risk of osteoporosis.
Those individuals who do sustain substantial weight loss over time generally must maintain high levels of dietary restraint, physical activity, and self-monitoring behaviors. This is evident in reports from members of the National Weight Control Registry (NWCR). The NWCR is composed of individuals who have sustained a 30-pound weight loss for at least a year. The registry has been critiqued for its nonrepresentativeness of the US population, its reliance on self-reported data, and its high rates of loss to follow-up. Ogden et al. conducted a latent class cluster analysis of the NWCR to detect distinctive methods, experiences, and perspectives on weight loss and weight maintenance among successful weight losers. Although a majority of weight losers were satisfied with their weight loss and reported good health and healthy behaviors, particularly high levels of exercise, other results were more distressing. For example, more than one quarter (26.9%) of participants reported high rates of stress, depression, and dissatisfaction with their weight loss. This cluster struggles with their weight, frequently weight cycle, and compared with other members of NWCR, report poorer health. Interestingly, these individuals are trying to maintain the greatest weight loss. The cluster identified as trying to maintain the second largest weight loss (9.9%), reported low levels of physical activity, frequent skipping of meals, and the poorest levels of health apart from those who had lost more weight. The relatively poor psychological and physical health of the individuals in these 2 clusters, and their struggles to maintain weight healthily, suggest that they may be striving to maintain an overly extreme weight loss.
Current public health approaches assume that intentional weight loss is always positive and that a BMI in the range of 18.5 to 24.9 is necessarily the healthiest range for all individuals. Importantly, despite its widespread adoption, BMI is acknowledged to be a crude measurement of obesity that may not adequately account for regional body fat distribution and subsequent risk. In certain populations, BMI may not adequately measure adiposity or differentiate between populations, particularly with respect to athletes and athletic populations. Perhaps most importantly, BMI is a population-level proxy measure of obesity, and an individual's BMI may say little concerning that individual's health. Additionally, overweight status (BMI = 25–30) has been shown to be associated with decreased mortality risk in US, Canadian, and international samples. Obesity (BMI > 30) has even demonstrated a protective or neutral effect among some chronic disease or older populations. Minor (≤ 5%) intentional weight loss may reduce mortality risk in obese individuals with related comorbidities, but weight loss heightens mortality risk among healthy obese individuals. Therefore, in addition to being extraordinarily difficult to maintain, weight loss may not always be health enhancing, particularly for the large proportion of obese persons who may be cardiometabolically healthy, or whose ill health may be attributable to numerous non–weight-related confounding factors.
Aiming for a narrow "healthy" range of body size may induce individuals to engage in disordered eating practices. These behaviors may remain hidden, and these individuals may still be valorized for their "healthiness," particularly by others trying to lose weight. This is evident among members of, and in the espousal of seemingly bulimic practices in, commercial weight-loss groups. That is, weight-loss groups' weight-loss strategies may include advice similar to bulimic practices of binge eating and subsequent compensation through dietary restriction or compulsive exercising. Furthermore, a public health approach in which obese individuals are viewed as unhealthy burdens on the health care system and individually responsible for their weight may promote weight stigma. This stigma may produce ill health through direct stress-induced neuroendocrine pathways or adverse coping mechanisms. Weight bias is highly prevalent among health care professionals, and this may pose a barrier to individuals receiving adequate health care. Additionally, weight discrimination may diminish an individual's socioeconomic standing, which will have further deleterious effects on health. In summary, the efficacy and safety of weight-loss dieting is questionable, as are the health consequences of the most common forms of obesity. In addition to being ineffective, focusing on individuals as the cause and likeliest cure for obesity promotes weight stigma, which may be particularly health debilitating.
Environmental Antiobesity Reforms
An ecological perspective on obesity causation was first proposed by Egger and Swinburn in 1997 and further developed by Swinburn, et al. in 1999. Their definition of the obesogenic environment included the micro- and macrocomponents of individuals' physical, political, economic, and sociocultural circumstances. More recently, the obesogenic environment is thought to be composed of factors such as the reduced time-cost of food, the increased availability of high-calorie, nutrient-poor food, and the increased motorization and mechanization of daily life. These factors are thought to have all simultaneously produced an energy imbalance in the daily lives of individuals and consequent population-wide weight gain.
Rectifying the obesogenic environment would require comprehensive government reforms. Existing evaluations of health interventions appear to support the notion that the most effective interventions for chronic disease prevention and health promotion focus on larger-scale interventions that make healthy choices more convenient and affordable, restrict unhealthy products, focus on community development, and support healthy social, economic, and environmental policy. The most cost-effective approaches to obesity, as determined by modeling studies, are those that include a taxation on unhealthy foods, restriction of junk food advertisement to children, and improved nutrition labeling. Targeted family-based programs for obese children and school-based campaigns to increase physical education and reduce sweetened beverage consumption and television viewing are also cost-effective in models. These modeling studies and reviews of previous public health interventions have led proponents of obesogenic environmental reforms to extrapolate that obesity prevalence could be lessened through structural modifications that would facilitate energy expenditure or inhibit caloric intake.
Evidence for the Obesogenic Environment
Appeals to the obesogenic environment may appear to be an effective and nonstigmatizing approach to obesity policy. However, a number of limitations must be considered regarding these strategies. Particularly problematic is the lack of direct empirical evidence that environments necessarily predispose individuals to developing obesity, which calls into question the validity of using obesity as a justification for environmental reforms. A recent review, for example, highlighted that all evidence used to support the obesogenic environment is observational and inconsistent, and the proposed relationship between environment and obesity must be viewed as presumptive. Models are thus based on hypothetical contributors to an overly simplistic energy balance model, rather than empirical evidence. Furthermore, obesity may not even indicate poor health, and reduced obesity prevalence may not improve population health. Kirk et al. assert that a main issue hindering effective obesogenic environment research is nonconsensus over what aspects of the environment, a necessarily complex, dynamic, and multilevel concept, should be implicated under the obesogenic environment rubric. Other issues persist in environmental obesity research. Randomized control trials are difficult to conduct, and impossible for the highest level of upstream environmental determinants given small number of units (e.g., high-end food policies). Thus the highest quality of research originates from natural experiments or quasi-experimental designs. However, the majority of environmental research remains observational. Causality is difficult to assess, as multilevel studies can only suggest causality, and cross-sectional studies may not establish causality. Difficulties arise in identifying valid, reliable, and consistent dietary, social and material resource, and spatial measures. Accounting for all individual level factors and their potential mediating and confounding effects is particularly challenging. Furthermore, there may be numerous unknown or unmeasured effects or multiple interactions of social and individual factors that may affect interpretation.
Kirk et al. conducted a scoping review on obesogenic environment research. The review determined that most studies focused on the physical microenvironment, and many studies used physical activity, rather than diet or BMI, as outcome measures. Few studies focused on the economic or political (such as household or workplace policies) microenvironment. Also limited were studies conducted on the macro level, including urban development, health and transportation systems, the media, and the food industry. Most importantly, the review found that such studies are methodologically stymied by a general inability to measure potential environmental effects appropriately and a comprehensive theoretical framework that would help conceptualize the intricate and multifaceted obesogenic environment.
Reviews of existent research suggest only limited support for the obesogenic environment. A systematic review conducted by Giskes et al. on environmental effects on fat and energy intake established there was limited evidence that environment influenced fat or energy intake and that any such evidence was produced from observational, cross-sectional studies. A more recent review on food-related environmental factors also was unable to confirm the impact of the obesogenic environment. However, some reviews have found support for an association between the built environment and BMI or obesity. Greater support is available for a relationship between physical activity accessibility and BMI or obesity than for food environments and BMI or obesity. Evidence suggests walkability, density, accessibility of recreational spaces, and attractiveness increase physical activity and may lower risk of elevated BMI. Isolated longitudinal studies have found some support for environmental factors and their effect on BMI and obesity. Accessibility to healthy food increase is associated with dietary quality, but less evidence exists to support a link to BMI or obesity. This may be an artifact of less research focusing on diet, because of dietary measures-related difficulties.
Recent independent studies also failed to confirm a basic relationship between environment and obesity. McPhail et al. found that Canadian adolescents' socioeconomic class or access to fast food did not affect their likelihood to consume fast food. Kim and Leigh established that middle-class US familes were more likely to eat at fast-food restaurants than were lower or higher income individuals, whereas higher income individuals were more likely to eat at full-service restaurants. An and Sturm found that California children and adolescents' proximity to fast-food outlets and convenience stores, and distance from larger grocery stores, is not associated with healthy food consumption or BMI. Lee determined that elementary-school children residing in poorer and minority neighborhoods in the United States had greater access to both fast-food outlets and grocery stores. Food access was also not found to independently predict weight gain in children over time. This access also did not account for socioeconomic and minority differences over time in weight gain, which disadvantaged poorer and minority students. Interestingly, higher income and White majority neighborhoods also have a greater share of fast-food outlets, of all food establishments, compared with minority or poorer neighborhoods. Junk food in schools was not a determinant in the development of obesity by the eighth grade in the United States. A recent study by the US Department of Agriculture asserted that assessments of the affordability of a healthy diet are largely dependent on the metric used to measure food prices. For example, if food is measured by portion, it appears less expensive than if food is measured by weight or calorie.
Ethical Considerations of Environmental Reforms
Ethical implications of broad-based antiobesogenic environmental reforms are also essential to consider. As limited interventions have been implemented, this involves considering their potential implications on target audiences based on proposed projects and deployed rhetoric. Broad alterations to the environment may increase stigma on obese individuals who do not lose weight, despite these environmental modifications. Should individuals not lose weight despite environmental reforms, this might be viewed as proof that their obesity is the result of an unwillingness to practice healthy choices. Such stigma may contribute to poorer health outcomes. Obesogenic environment approaches may contribute to a homogenizing view of lower-income lifestyles and the perception of lower-income individuals as passive and lacking in agency. Furthermore, this view may serve as a mask for gender-, race-, or socioeconomic-based discrimination and essentialist arguments, and the moralization of a health issue. The obesogenic environment rationale has also been criticized as being overly simplistic and dismissive of the role of neoliberalism, its systematic overproduction and overconsumption, and consequent societal anxieties and values. Importantly, broad-based reforms may become increasingly invasive and truly limit the freedom of choice of individuals. A compelling argument can be made for the type of environmental restructuring proposed by obesogenic environment arguments, without relying on mobilizing fear of fat to support their institution. By focusing on other measures of health and well-being, or sustainability, livability, and accessibility, valuable and legitimately effective reforms could be undertaken. In summary, limited evidence suggests that environment affects obesity prevalence in a direct, simplistic manner, and reforms based on restructuring particular environments to remedy obesity rates have important ethical implications. Furthermore, as the empirical evidence suggests, none of these actions may necessarily result in thinner populations.
