Designer schools: the role of school space and architecture in obesity prevention

Spatial features of obesogenic environments studied on a broad community level have been associated with childhood overweight and obesity, but little research has focused on the effects of the design of micro spaces, such as schools, on individual health behaviors. This article aims to generate thinking and research on the link between school space and architecture and obesity prevention by reviewing and synthesizing available literature in architecture, environmental psychology, and obesity research, in an effort to propose promising ideas for school space design and redesign. The school environment is defined through 5 dimensions: physical, legal, policy, social, and cultural domains. Theories underlying environmental interventions and documented associations between the environment and health behaviors and outcomes are reviewed to illustrate how existing environmental research could translate to obesity prevention. Design strategies aimed at promoting physical activity and healthful eating are proposed, with particular emphasis on the design of cafeterias, activity spaces, connectivity with the larger community, and student health centers.     

Genetic associations with temporal shifts in obesity and severe obesity during the obesity epidemic in Norway: A longitudinal population-based cohort (the HUNT Study)

BackgroundObesity has tripled worldwide since 1975 as environments are becoming more obesogenic. Our study investigates how changes in population weight and obesity over time are associated with genetic predisposition in the context of an obesogenic environment over 6 decades and examines the robustness of the findings using sibling design.Methods and findingsA total of 67,110 individuals aged 13–80 years in the Nord-Trøndelag region of Norway participated with repeated standardized body mass index (BMI) measurements from 1966 to 2019 and were genotyped in a longitudinal population-based health study, the Trøndelag Health Study (the HUNT Study). Genotyping required survival to and participation in the HUNT Study in the 1990s or 2000s. Linear mixed models with observations nested within individuals were used to model the association between a genome-wide polygenic score (GPS) for BMI and BMI, while generalized estimating equations were used for obesity (BMI ≥ 30 kg/m²) and severe obesity (BMI ≥ 35 kg/m²).The increase in the average BMI and prevalence of obesity was steeper among the genetically predisposed. Among 35-year-old men, the prevalence of obesity for the least predisposed tenth increased from 0.9% (95% confidence interval [CI] 0.6% to 1.2%) to 6.5% (95% CI 5.0% to 8.0%), while the most predisposed tenth increased from 14.2% (95% CI 12.6% to 15.7%) to 39.6% (95% CI 36.1% to 43.0%). Equivalently for women of the same age, the prevalence of obesity for the least predisposed tenth increased from 1.1% (95% CI 0.7% to1.5%) to 7.6% (95% CI 6.0% to 9.2%), while the most predisposed tenth increased from 15.4% (95% CI 13.7% to 17.2%) to 42.0% (95% CI 38.7% to 45.4%). Thus, for 35-year-old men and women, respectively, the absolute change in the prevalence of obesity from 1966 to 2019 was 19.8 percentage points (95% CI 16.2 to 23.5, p < 0.0001) and 20.0 percentage points (95% CI 16.4 to 23.7, p < 0.0001) greater for the most predisposed tenth compared with the least predisposed tenth, defined using the GPS for BMI. The corresponding absolute changes in the prevalence of severe obesity for men and women, respectively, were 8.5 percentage points (95% CI 6.3 to 10.7, p < 0.0001) and 12.6 percentage points (95% CI 9.6 to 15.6, p < 0.0001) greater for the most predisposed tenth. The greater increase in BMI in genetically predisposed individuals over time was apparent after adjustment for family-level confounding using a sibling design. Key limitations include a slightly lower survival to date of genetic testing for the older cohorts and that we apply a contemporary genetic score to past time periods. Future research should validate our findings using a polygenic risk score constructed from historical data.ConclusionsIn the context of increasingly obesogenic changes in our environment over 6 decades, our findings reveal a growing inequality in the risk for obesity and severe obesity across GPS tenths. Our results suggest that while obesity is a partially heritable trait, it is still modifiable by environmental factors. While it may be possible to identify those most susceptible to environmental change, who thus have the most to gain from preventive measures, efforts to reverse the obesogenic environment will benefit the whole population and help resolve the obesity epidemic.

In a longitudinal population-based cohort study in Norway, Maria Brandkvist and colleagues investigate how genetic predisposition relates to changes in BMI and obesity over the past six decades.     

Central obesity and health-related factors among middle-aged men: a comparison among native Japanese and Japanese-Brazilians residing in Brazil and Japan

The objective of this study was to investigate the influence of different cultural environments on the development of obesity by examining the association of central obesity, lifestyle, and selected coronary risk factors among people with identical Japanese genetic backgrounds living in Japan and Brazil. One hundred and four native Japanese and 286 Japanese-Brazilians residing in Brazil and Japan aged 35 years or over were studied. Obesity, metabolic risk factors for coronary disease, and history of regular sports activity, daily physical activity, and eating habits were assessed. The results showed Japanese-Brazilians residing in Brazil with significantly higher waist circumference values, and greater prevalence of central obesity compared to native Japanese and Japanese-Brazilians residing in Japan. The risk of developing central obesity was found to be 2.8 times higher among Japanese-Brazilians residing in Brazil. However, this association was no longer found to be significant after adjusting for lifestyle factors in the logistic model. Additionally, waist circumference was found to be significantly associated with metabolic risk factors for coronary disease. These findings suggest substantial variation in measures of central obesity among the three groups of Japanese ancestry, and underscore the heterogeneity of risk factors among communities of Japanese ancestry living in different cultural environments. The results also suggest that immigrant men exposed to the Brazilian cultural environment are more susceptible to the development of central obesity, and it seems to be associated with various lifestyle items and metabolic risk factors for coronary disease.     

Culture as a stressor: A revised model of biocultural interaction

Contemporary urban societies display in high relief the action of social stratification on human biology. Recent studies of biological responses to urban environments and of socioeconomically disadvantaged people indicate that culture allocates risks disproportionately to some individuals and groups within society through its constituent values and related patterns of behavior. Although risk allocation is present in all societies, it is very clear in urban environments within stratified societies where high exposure to harmful materials is many times more likely for some segments of society. In urban environments, culture may be seen as adding stressors to the environment by concentrating naturally occurring materials to levels that are toxic to humans and through the creation of new toxic materials. In stratified societies the risk of exposure to these new stressors is focused on the socioeconomically disadvantaged. This exposure has consequences that increase the likelihood of more exposure and more socioeconomic disadvantage, thereby increasing social stratification. This suggests that models of biocultural interaction include a feedback relationship in which biological factors influence the sociocultural system in addition to the usual action of the sociocultural system on biological features and responses. This model strongly reinforces the view that stressors can originate from cultural arrangements. Am J Phys Anthropol 102:67–77, 1997 © 1997 Wiley-Liss, Inc.     

Culture and the evolution of obesity

Human predispositions to fatness and obesity are best understood in the context of cultural and biological evolution. Both genes and cultural traits that were adaptive in the context of past food scarcities play a role today in the etiology of maladaptive adult obesity. The etiology of obesity must account for the social distribution of the condition with regard to gender, ethnicity, social class, and economic modernization. This distribution, which has changed throughout history, undoubtedly involves cultural factors. A model of culture is presented that has advantages over an undifferentiated concept of the “environment” for hypothesis generation. Cultural predispositions to obesity are found in the productive economy, the mode of reproduction, social structure, and cultural beliefs about food and ideal body size. Cross-cultural comparison can contribute to an understanding of the prevalence of obesity in some modern affluent societies.     

The evolution of human fatness and susceptibility to obesity: an ethological approach

Human susceptibility to obesity is an unusual phenomenon amongst animals. An evolutionary analysis, identifying factors favouring the capacity for fat deposition, may aid in the development of preventive public health strategies. This article considers the proximate causes, ontogeny, fitness value and evolutionary history of human fat deposition. Proximate causes include diet composition, physical activity level, feeding behaviour, endocrine and genetic factors, psychological traits, and exposure to broader environmental factors. Fat deposition peaks during late gestation and early infancy, and again during adolescence in females. As in other species, human fat stores not only buffer malnutrition, but also regulate reproduction and immune function, and are subject to sexual selection. Nevertheless, our characteristic ontogenetic pattern of fat deposition, along with relatively high fatness in adulthood, contrasts with the phenotype of other mammals occupying the tropical savannah environment in which hominids evolved. The increased value of energy stores in our species can be attributed to factors increasing either uncertainty in energy availability, or vulnerability to that uncertainty. Early hominid evolution was characterised by adaptation to a more seasonal environment, when selection would have favoured general thriftiness. The evolution of the large expensive brain in the genus Homo then favoured increased energy stores in the reproducing female, and in the offspring in early life. More recently, the introduction of agriculture has had three significant effects: exposure to regular famine; adaptation to a variety of local niches favouring population-specific adaptations; and the development of social hierarchies which predispose to differential exposure to environmental pressures. Thus, humans have persistently encountered greater energy stress than that experienced by their closest living relatives during recent evolution. The capacity to accumulate fat has therefore been a major adaptive feature of our species, but is now increasingly maladaptive in the modern environment where fluctuations in energy supply have been minimised, and productivity is dependent on mechanisation rather than physical effort. Alterations to the obesogenic environment are predicted to play a key role in reducing the prevalence of obesity.     

Stemming the obesity epidemic: a tantalizing prospect

Objective: Obesity is a growing problem worldwide, but there are no good methods to assess the future course of the epidemic and the potential influence of interventions. We explore the behavior change needed to stop the obesity epidemic in the U.S. Research Methods and Procedures: We modeled the population distribution of BMI as a log‐normal curve of which the mean shifts upward with time due to a positive population energy balance. Interventions that decrease food intake or increase physical activity result in more favorable trends in BMI. Results: The recently observed trend in average BMI implies that the average U.S. adult over‐consumes by ～10 kcal/d. If this trend continues unaltered, obesity prevalence will exceed 40% for men and 45% for women in 2015. To stop the epidemic, it suffices to decrease caloric consumption by ～10 kcal or walk an extra 2 to 3 minutes per day, on average. Discussion: This leads to a paradox: little behavior change seems sufficient to halt the epidemic, but in practice this proves hard to achieve. The obesogenic environment is the likely culprit. Individuals trying to maintain a healthy weight need to be supported by environments that stimulate physical activity and do not encourage over‐consumption. Research should show what measures are effective.     

Impact of diet-induced obesity on the mouse brain phosphoproteome

Obesity is closely associated to several diseases such as type 2 diabetes, cardiovascular disease, hepatic steatosis, airway disease, neurodegeneration, biliary diseases and certain cancers. It is, therefore, of importance to assess the role of nutrition in disease prevention as well as its effect in the course of such pathologies. In the present study, we addressed the impact of the exposure to different obesogenic diets in the mice brains phosphoproteome. To analyze if the obesity could be able to modify the protein pattern expression of brain neurons, obesity was induced in two different groups of mice. One group of mice was fed with hyperglycemic diet (HGD) and the other one was fed with high-fat diet (HFD), both for 12 weeks. A control group of lean mice was fed with a standard diet (SD). Metabolic parameters were measured before sacrifice, and brains were harvested for label-free phosphoproteomic analysis. Mice brains were analyzed to find differences, if any, in protein phosphorylation. Interestingly, the changes were independent of the obesogenic diet as no changes were detected between the two obese groups. Dephosphorylation of proteins involved in neuronal development (among others SYNGAP1 and PPP1R9B), in vesicle trafficking (for example SNAP91 and AMPH) and in cytoskeletal functions (for example, CLASP2 and GSK3B) was identified, while increased phosphorylation was detected for microtubule proteins (such as MAP2 and MAPT). Phospho site analysis of the mouse brain proteome reveals important changes that point to a connection between diet-induced obesity and impairment of neuronal functions and signaling.     

Information is not knowledge: Cooking and eating as skilled practice in Australian obesity education

This paper examines the relationship between obesity, knowledge and education in a South Australian community setting. In public health circles and public understandings it is commonly assumed that obesity is the result of lack of knowledge about the right things to eat or how to take care of oneself. It is thought that education will fill this knowledge lacunae and most public health campaigns have education as the main platform of information dissemination to enact behavioural change. Based on long‐standing ethnographic work in a community targeted as obesogenic, I explore the limits of mainstream nutrition education, and how constructing people as having deficit knowledge has the unwarranted effect of implying ignorance. Key to the analysis is Ingold's articulation of different modalities of education, one dominant mode which inducts people into rules and regulations of already pre‐formed knowledge, and another which sees education as learning that goes on in the doing of everyday environments.     

Diabetes, the ice free corridor, and the Paleoindian settlement of North America

Since the 1940s, many Amerindian populations, including some with mixed Amerindian ancestry, have experienced an epidemic of obesity and adult-onset diabetes (NIDDM). Obesity and NIDDM were apparently rare among Amerindian populations prior to that time. Though the evidence is equivocal, obesity and NIDDM seem to be rare today among Athapaskan Amerindians of the North American Arctic, sub-Arctic, and Southwest. It is hypothesized that the Amerindian genotype(s) susceptible to obesity and NIDDM arose from selection favoring "thrifty" genes during the peopling of North America south of the continental glaciers. "Thrifty" genes (Neel: Am. J. Hum. Genet. 14:353-362, 1962) allowed a more efficient food metabolism as hunter-gatherers from an unusually harsh mid-latitude tundra environment (the "ice free" corridor) adapted to more typical mid-latitude environments to the south. The early Paleoindian settlement pattern from Wyoming to Arizona and Texas indicates a relatively brief period of reliance on unpredictable big game resources in lower elevations and smaller game and gathered resources in higher elevations. This unusual "specialist" settlement pattern may have resulted from the early Paleoindian's unfamiliarity with gathered foods and small game in lower elevations. Athapaskan populations evidently moved south from Beringia sometime after the Paleoindian migration when the "ice free" corridor had widened and contained environments and resources more typical of subarctic latitudes. Thus, Athapaskan hunter-gatherers could gradually adapt to the resources of lower latitudes such that "thrifty" genes would not have been as advantageous. The interaction of recently introduced "western" diets and "thrifty" genes have evidently led to today's epidemic of obesity and NIDDM among Amerindians of Paleoindian ancestry.     

Fetal Sex Modulates Developmental Response to Maternal Malnutrition

The incidence of obesity and metabolic diseases is dramatically high in rapidly developing countries. Causes have been related to intrinsic ethnic features with development of a thrifty genotype for adapting to food scarcity, prenatal programming by undernutrition, and postnatal exposure to obesogenic lifestyle. Observational studies in humans and experimental studies in animal models evidence that the adaptive responses of the offspring may be modulated by their sex. In the contemporary context of world globalization, the new question arising is the existence and extent of sex-related differences in developmental and metabolic traits in case of mixed-race. Hence, in the current study, using a swine model, we compared male and female fetuses that were crossbred from mothers with thrifty genotype and fathers without thrifty genotype. Female conceptuses evidence stronger protective strategies for their adequate growth and postnatal survival. In brief, both male and female fetuses developed a brain-sparing effect but female fetuses were still able to maintain the development of other viscerae than the brain (mainly liver, intestine and kidneys) at the expense of carcass development. Furthermore, these morphometric differences were reinforced by differences in nutrient availability (glucose and cholesterol) favoring female fetuses with severe developmental predicament. These findings set the basis for further studies aiming to increase the knowledge on the interaction between genetic and environmental factors in the determination of adult phenotype     

Adipositas – eine Bürde der Evolution?

Obesity – a consequence of evolution? The high obesity rates are the result of a dramatic mismatch between current environment and a human body evolved in the environment of our evolutionary adaptedness. Various evolutionary hypotheses try to explain this relationship. Natural and sexual selection shaped our gene pool towards an optimal adaptation to these environments and life circumstances. Our recent obesogenic environment differs dramatically from that in which we evolved.     

Amerindians show no association of PC-1 gene Gln121 allele and obesity: a thrifty gene population genetics

PC-1 Gln121 gene is a risk factor for type 2 diabetes, obesity and insulin resistance in European/American Caucasoids and Orientals. We have aimed to correlate for the first time this gene in Amerindians with obesity and their corresponding individuals genotypes with obesity in order to establish preventive medicine programs for this population and also studying the evolution of gene frequencies in world populations. Central obesity was diagnosed by waist circumference perimeter and food intake independent HDL-cholesterol plasma levels were measured. HLA genes were determined in order to more objectively ascertain participants Amerindians origin. 321 Amerindian blood donors who were healthy according to the blood doning parameters were studied. No association was found between PC-1 Gln121 variant and obesity. Significant HDL-cholesterol lower values were found in the PC-1 Lys121 bearing gene individuals versus PC-1 Gln121 bearing gene ones (45.1 ± 12.7 vs. 48.7 ± 15.2 mg/dl, p < 0.05). Population analyses showed a world geographical gradient in the PC-1 Gln121 allele frequency: around 9% in Orientals, 15% in European Caucasoids and 76% in Negroids. The conclusions are: (1) No association of PC-1 Gln121 gene is found with obesity in Amerindians when association is well established in Europeans. (2) PC-1 Gln121 gene is associated to higher levels of HDL-cholesterol than the alternative PC-1 Lys121 allele. This may be specific for Amerindians. (3) Amerindians have an intermediate frequency of this possible PC-1 Gln121 thrifty gene when compared with Negroid African Americans (78.5%) or Han Chinese (7.5%, p < 0.0001). Historical details of African and other groups may support the hypothesis that PC-1 Gln121 is indeed a thrifty gene.     

How copying affects the amount, evenness and persistence of cultural knowledge: insights from the social learning strategies tournament

Darwinian processes should favour those individuals that deploy the most effective strategies for acquiring information about their environment. We organized a computer-based tournament to investigate which learning strategies would perform well in a changing environment. The most successful strategies relied almost exclusively on social learning (here, learning a behaviour performed by another individual) rather than asocial learning, even when environments were changing rapidly; moreover, successful strategies focused learning effort on periods of environmental change. Here, we use data from tournament simulations to examine how these strategies might affect cultural evolution, as reflected in the amount of culture (i.e. number of cultural traits) in the population, the distribution of cultural traits across individuals, and their persistence through time. We found that high levels of social learning are associated with a larger amount of more persistent knowledge, but a smaller amount of less persistent expressed behaviour, as well as more uneven distributions of behaviour, as individuals concentrated on exploiting a smaller subset of behaviour patterns. Increased rates of environmental change generated increases in the amount and evenness of behaviour. These observations suggest that copying confers on cultural populations an adaptive plasticity, allowing them to respond to changing environments rapidly by drawing on a wider knowledge base.     

Escalating coverage of obesity in UK newspapers: the evolution and framing of the "obesity epidemic" from 1996 to 2010

Obesity is one of the fastest growing and most serious public health challenges facing the world in the 21st century. Correspondingly, over the past decade there has been increased interest in how the obesity epidemic has been framed by the media. This study offers the first large-scale examination of the evolution and framing of the obesity epidemic in UK newspapers, identifying shifts in news coverage about the causal drivers of and potential solutions to the obesity epidemic. Seven UK newspapers were selected and 2,414 articles published between 1 January 1996 and 31 December 2010 were retrieved from electronic databases using keyword searches. The thematic content of articles was examined using manifest content analysis. Over the 15-year period there was an increase in media reporting on obesity and in particular on childhood obesity. There was evidence of a trend away from a focus on individuals towards a greater level of reporting on societal solutions such as regulatory change, with the greatest shift in reporting occurring in mid-market and serious newspapers. Given that the media have a huge influence in shaping public opinion, this shift in reporting might be an early indicator to policymakers of a growing public discourse around a need for regulatory change to tackle the obesogenic environment.     

Placing Well-Being: A Maori Case Study of Cultural and Environmental Specificity

Studies of well-being have been dominated by perspectives that stem from Western, health-science notions of individual’s health and psychological development. In recent times, however, there has been a developing sensitivity to the cultural and place-specific contexts affecting the health and well-being of contrasting populations in different environments. Drawing on these advances, this article explores the potential in conceptualizing a place-based notion of well-being that recognizes the cultural and environmental specificity of well-being for specific populations in a given setting. We argue that a geographical approach to well-being enables the linking of culture and environment for future indigenous research into both ecosystems and human health. Taking the case of an indigenous population, we identify the contexts that affect Maori well-being and we argue that key sociocultural and environmental dimensions need to be integrated for a culturally appropriate approach to Maori well-being.     

Pathophysiology and genetics of obesity

Obesity, a global problem, is a multifactorial disorder. The factors are environmental, metabolic and genetic and their interaction with each other regulates the body weight. Imbalance in either of the factors may be responsible for weight gain. With advancement of research techniques in the last decade, genetic studies have been undertaken for several different causative mutations involving obesity loci on different chromosomes. Monogenic and polygenic obesity has been observed however, polygenic forms are more common. So far more than 200 genes in mouse and more than 100 genes in humans have been identified which result in phenotypes that affect body weight regulation. In spite of this knowledge, the field of obesity has still not been explored extensively. There remain a lot of lacuna regarding causes and treatment of obesity. Challenges are still there to identify the exact cause of weight gain and the use of current knowledge for development of anti-obesity drugs targeted for body weight regulation. In this review, we have explained neuropathophysiologic regulation of feeding behaviour and some aspects of obesity-genetics especially with single nucleotide polymorphism of selected candidate genes and their functional aspects mainly in monogenic obesity.     

中国藏缅语族成人的超重与肥胖

运用人体测量学的方法,研究组从2015年到2019年在贵州、云南、四川、西藏、湖北、湖南6省区调查藏缅语族17个少数民族成人的体质指标。测量指标包括体质量、身高与皮褶厚度。计算指标包括身体质量指数、体密度和体脂率。藏缅语族民族的身体质量指数与人均GDP呈正相关。藏缅语族民族的肥胖与超重率受社会经济因素和历史文化因素影响。藏缅语族男女的肥胖与超重率都较高,迫切需要采取积极的措施来应对和预防。     

Neighborhood health‐promoting resources and obesity risk (the multi‐ethnic study of atherosclerosis)

Objective:

While behavioral change is necessary to reverse the obesity epidemic, it can be difficult to achieve and sustain in unsupportive residential environments. This study hypothesized that environmental resources supporting walking and a healthy diet are associated with reduced obesity incidence.

Design and Methods:

Data came from 4,008 adults aged 45‐84 at baseline who participated in a neighborhood ancillary study of the Multi‐Ethnic Study of Atherosclerosis. Participants were enrolled at six study sites at baseline (2000‐2002) and neighborhood scales were derived from a supplementary survey that asked community residents to rate availability of healthy foods and walking environments for a 1‐mile buffer area. Obesity was defined as BMI ≥ 30 kg/m². Associations between incident obesity and neighborhood exposure were examined using proportional hazards and generalized linear regression.

Results:

Among 4,008 nonobese participants, 406 new obesity cases occurred during 5 years of follow‐up. Neighborhood healthy food environment was associated with 10% lower obesity incidence per s.d. increase in neighborhood score. The association persisted after adjustment for baseline BMI and individual‐level covariates (hazard ratio (HR) 0.88, 95% confidence interval (CI): 0.79, 0.97), and for correlated features of the walking environment but CIs widened to include the null (HR 0.89, 95% CI: 0.77, 1.03). Associations between neighborhood walking environment and lower obesity were weaker and did not persist after adjustment for correlated neighborhood healthy eating amenities (HR 0.98, 95% CI: 0.84, 1.15).

Conclusions:

Altering the residential environment so that healthier behaviors and lifestyles can be easily chosen may be a precondition for sustaining existing healthy behaviors and for adopting new healthy behaviors.