The obesity epidemic and associated chronic diseases are often attributed to modern lifestyles. The term “lifestyle” however, ignores broader social, economic, and environmental determinants while inadvertently “blaming the victim.” Seen more eclectically, lifestyle encompasses distal, medial, and proximal determinants. Hence any analysis of causality should include all these levels. The term “anthropogens,” or “…man-made environments, their by-products and/or lifestyles encouraged by these, some of which may be detrimental to human health” provides a monocausal focus for chronic diseases similar to that which the germ theory afforded infectious diseases. Anthropogens have in common an ability to induce a form of chronic, low-level systemic inflammation (“metaflammation”). A review of anthropogens, based on inducers with a metaflammatory association, is conducted here, together with the evidence for each in connection with a number of chronic diseases. This suggests a broader view of lifestyle and a focus on determinants, rather than obesity and lifestyle per se as the specific causes of modern chronic disease. Under such an analysis, obesity is seen more as “a canary in a mineshaft” signaling problems in the broader environment, suggesting that population obesity management should be focused more upstream if chronic diseases are to be better managed.
The prevalence of childhood obesity has increased rapidly during the last three decades in the Netherlands. It is assumed that mainly environmental factors have contributed to this trend. Parental overweight and low social economic status are risk factors for childhood obesity. Childhood obesity affects self-esteem and has negative consequences on cognitive and social development. Obese children tend to become obese adults, which increases the risk for developing cardiovascular complications, type 2 diabetes mellitus, and psychosocial problems. Additionally, the secretion of several gastrointestinal hormones, responsible for appetite and food intake, is impaired in obese subjects. Weight reduction through lifestyle changes in order to change health risks is, until now, suggested as the preferred treatment for childhood obesity.
The objective of this study is the effect evaluation of a family-based cognitive behavioral multidisciplinary lifestyle treatment. The intervention aims to establish long-term weight reduction and stabilization, reduction of obesity-related health consequences and improvement of self-image by change of lifestyle and learning cognitive behavioral techniques.
In this randomized clinical trial newly presented children with obesity (8-17 years old) are divided, by randomization, in an intervention and control group, both consisting of 40 obese children. The intervention is carried out in groups of 8-11 children, and consists of respectively 7 and 5 separate group meetings for the children and their parents and 1 joint group meeting of 2 ½ hours. Main topics are education on nutrition, self-control techniques, social skills, physical activity and improvement of self-esteem. The control group is given advice on physical activity and nutrition. For normal data comparison, data were collected of 40 normal-weight children, 8-17 years old.
Because of the increasing prevalence of childhood obesity and the impact on the individual as well as on society, prevention and treatment of obesity in children is of great importance. For evaluation of short- and long-term effects of the treatment, measurements are taken before and after 3 months of treatment, and after 12 and 24 months follow-up. During these visits clinical and biochemical data are determined, cardiovascular fitness tests are performed and quality of life questionnaires are completed.
International Standard Randomised Controlled Trial Number Register ISRCTN36146436
The prevalence of obesity, which is a heritable trait that arises from the interactions of multiple genes and lifestyle factors, continues to increase worldwide, causing serious health problems and imposing a substantial economic burden on societies. For the past several years, various genetic epidemiological approaches have been utilized to identify genetic loci for obesity. Recent evidence suggests that development of obesity involves hormones and neurotransmitters (such as leptin, cocaine- and amphetamine-regulated transcript (CART), and ghrelin) that regulate appetite and energy expenditure. These hormones act on specific centers in the brain that regulate the sensations of satiety. Mutations in these hormones or their receptors can lead to obesity. Aberrant circadian rhythms and biochemical pathways in peripheral organs or tissues have also been implicated in the pathology of obesity. More interestingly, increasing evidence indicates a potential relation between obesity and central nervous system disorders (such as cognitive deficits). This paper discusses recent advances in the field of genetics of obesity with an emphasis on several established loci that influence obesity. These recently identified loci may hold the promise to substantially improve our insights into the pathophysiology of obesity and open up new therapeutic strategies to combat growing obesity epidemic facing the human population today.
Rising and epidemic rates of obesity in many parts of the world are leading to increased suffering and economic stress from diverting health care resources to treating a variety of serious, but preventable, chronic diseases etiologically linked to obesity, particularly type 2 diabetes mellitus and cardiovascular diseases. Despite decades of research into the causes of the obesity pandemic, we seem to be no nearer to a solution now than when the rise in body weights was first chronicled decades ago. The case is made that impediments to a clear understanding of the nature of the problem occur at many levels. These obstacles begin with defining obesity and include lax application of scientific standards of review, tenuous assumption making, flawed measurement and other methods, constrained discourse limiting examination of alternative explanations of cause, and policies that determine funding priorities. These issues constrain creativity and stifle expansive thinking that could otherwise advance the field in preventing and treating obesity and its complications. Suggestions are made to create a climate of open exchange of ideas and redirection of policies that can remove the barriers that prevent us from making material progress in solving a pressing major public health problem of the early 21st century.
In this study we assessed the potential effects of climate variability and change on population health in Cuba. We describe the climate of Cuba as well as the patterns of climate-sensitive diseases of primary concern, particularly dengue fever. Analyses of the associations between climatic anomalies and disease patterns highlight current vulnerability to climate variability. We describe current adaptations, including the application of climate predictions to prevent disease outbreaks. Finally, we present the potential economic costs associated with future impacts due to climate change. The tools used in this study can be useful in the development of appropriate and effective adaptation options to address the increased climate variability associated with climate change.
climate change; climate indices; climate variability; human health; impacts
Obesity is a significant global public health problem and the main cause of many chronic diseases in both developed and developing countries. The increase in obesity in different populations worldwide cannot be explained solely by metabolic and genetic factors; environmental and social factors also have a strong association with obesity. Thus, it is believed that the current obesity epidemic is the result of a complex combination of genetic factors and an obesogenic environment .The purpose of this study was to evaluate individual variables and variables within the built and social environment for their potential association with overweight and obesity in an urban Brazilian population.
Cross-sectional study was carried out in a sample of 3404 adults living in the urban area of the city. Information from the surveillance system for chronic diseases of Brazilian Ministry of Health was used and individual data was collected by telephone interviews. The database was geocoded using the Brazilian System of Postal Codes for participant residences. An updated, existing list based on the current addresses of supermarkets and hypermarkets in the city was used as an indicator variable of the availability and access to food. Georeferenced information on parks, public squares, places for practicing physical activity and the population density were also used to create data on the built environment. To characterize the social environment, we used the health vulnerability index (HVI) and georeferenced data for homicide locations.
The prevalence was 44% for overweight, poisson regression was used to create the final model. The environment variables that independently associated with overweight were the highest population density, very high health vulnerability index and the homicide rate adjusted for individuals variables. The results of the current study illustrate and confirm some important associations between individual and environmental variables and overweight in a representative sample of adults in the Brazilian urban context.
The social environment variables relating to the socioeconomic deprivation of the neighborhood and the built environment variables relating to higher walkability were significantly associated with overweight and obesity in Belo Horizonte.
Obesity is a global health problem that is gradually affecting each continent of the world. Obesity is a heterogeneous disorder, and the biological causes of obesity are complex. The rapid increase in obesity prevalence during the past few decades is due to major societal changes (sedentary lifestyle, over-nutrition) but who becomes obese at the individual level is determined to a great extent by genetic susceptibility. In this review, we evidence that obesity is a strongly heritable disorder, and provide an update on the molecular basis of obesity. To date, nine loci have been involved in Mendelian forms of obesity and 58 loci contribute to polygenic obesity, and rare and common structural variants have been reliably associated with obesity. Most of the obesity genes remain to be discovered, but promising technologies, methodologies and the use of “deep phenotyping” lead to optimism to chip away at the ‘missing heritability’ of obesity in the near future. In the longer term, the genetic dissection of obesity will help to characterize disease mechanisms, provide new targets for drug design, and lead to an early diagnosis, treatment, and prevention of obesity.
Candidate gene; childhood obesity; copy number variation; gwas; heritability; linkage; monogenic; polygenic.
Obesity is a worldwide problem with increasing prevalence and incidence in both developed and developing countries. In older adults, excess weight is associated with a higher prevalence of cardiovascular disease, metabolic disease, several important cancers, and numerous other medical conditions. Obesity has been also associated with increased functional limitations, disability, and poorer quality of life. Additionally, obesity has been independently associated with all-cause mortality. The obesity epidemic has important social and economic implications, representing an important source of increased public health care costs. The aim of this review is to report the epidemiology of obesity world-wide and the implications of obesity on disability and chronic diseases.
Obesity; Older Adults; Disability; Chronic Disease
Cardiovascular disease is the leading cause of mortality in Cuba. Lifestyle risk factors for coronary heart disease (CHD) in Cubans have not been compared to risk factors in Cuban Americans. Articles spanning the last 20 years were reviewed. The data on Cuban Americans are largely based on the Hispanic Health and Nutrition Examination Survey (HHANES), 1982–1984, while more recent data on epidemiological trends in Cuba are available. The prevalence of obesity and type 2 diabetes mellitus remains greater in Cuban Americans than in Cubans. However, dietary preferences, low physical activity, and tobacco use are contributing to the rising rates of obesity, type 2 diabetes mellitus, and CHD in Cuba, putting Cubans at increased cardiovascular risk. Comprehensive national strategies for cardiovascular prevention that address these modifiable lifestyle risk factors are necessary to address the increasing threat to public health in Cuba.
Data suggest that hyperpalatable foods may be capable of triggering an addictive process. Although the addictive potential of foods continues to be debated, important lessons learned in reducing the health and economic consequences of drug addiction may be especially useful in combating food-related problems.
In the current paper, we review the potential application of policy and public health approaches that have been effective in reducing the impact of addictive substances to food-related problems.
Corporate responsibility, public health approaches, environmental change, and global efforts all warrant strong consideration in reducing obesity and diet-related disease.
Although there exist important differences between foods and addictive drugs, ignoring analogous neural and behavioral effects of foods and drugs of abuse may result in increased food-related disease and associated social and economic burdens. Public health interventions that have been effective in reducing the impact of addictive drugs may have a role in targeting obesity and related diseases.
Food; obesity; addiction; public health
Obesity, a growing health problem worldwide, has been associated with the metabolic syndrome, diabetes, cardiovascular disease, hypertension, and other chronic diseases. Recently, the obesity–cancer link has received much attention. Epidemiological studies have shown that obesity is also associated with increased risk of several cancer types, including colon, breast, endometrium, liver, kidney, esophagus, gastric, pancreatic, gallbladder, and leukemia, and can also lead to poorer treatment and increased cancer-related mortality. Biological mechanisms underlying the relationship between obesity and cancer are not well understood. They include modulation of energy balance and calorie restriction, growth factors, multiple signaling pathways, and inflammatory processes. Key among the signaling pathways linking obesity and cancer is the PI3K/Akt/mTOR cascade, which is a target of many of the obesity-associated factors and regulates cell proliferation and survival. Understanding the molecular and cellular mechanisms of the obesity–cancer connection is important in developing potential therapeutics. The link between obesity and cancer underscores the recommendation to maintain a healthy body weight throughout life as one of the most important ways to protect against cancer.
obesity; cancer; mechanisms; recommendations; prevention
Obesity, a growing health problem worldwide, has been associated with the metabolic syndrome, diabetes, cardiovascular disease, hypertension, and other chronic diseases. Recently, the obesity–cancer link has received much attention. Epidemiological studies have shown that obesity is also associated with increased risk of several cancer types, including colon, breast, endometrium, liver, kidney, esophagus, gastric, pancreatic, gallbladder, and leukemia, and can also lead to poorer treatment and increased cancer-related mortality. Biological mechanisms underlying the relationship between obesity and cancer are not well understood. They include modulation of energy balance and calorie restriction, growth factors, multiple signaling pathways and inflammatory processes. Key among the signaling pathways linking obesity and cancer is the PI3K/Akt/mTOR cascade, which is a target of many of the obesity-associated factors and regulates cell proliferation and survival. Understanding the molecular and cellular mechanisms of the obesity–cancer connection is important in developing potential therapeutics. The link between obesity with cancer underscores the recommendation to maintain a healthy body weight throughout life as one of the most important ways to protect against cancer.
obesity; cancer; mechanisms; recommendations; prevention
Worldwide, obesity trends are causing serious public health concern and in many countries threatening the viability of basic health care delivery. It is an independent risk factor for cardiovascular diseases and significantly increases the risk of morbidity and mortality. The last two decades have witnessed an increase in health care costs due to obesity and related issues among children and adolescents. Childhood obesity is a global phenomenon affecting all socio-economic groups, irrespective of age, sex or ethnicity. Aetiopathogenesis of childhood obesity is multi-factorial and includes genetic, neuroendocrine, metabolic, psychological, environmental and socio-cultural factors. Many co-morbid conditions like metabolic, cardiovascular, psychological, orthopaedic, neurological, hepatic, pulmonary and renal disorders are seen in association with childhood obesity. The treatment of overweight and obesity in children and adolescents requires a multidisciplinary, multi-phase approach, which includes dietary management, physical activity enhancement, restriction of sedentary behaviour, pharmacotherapy and bariatric surgery. A holistic approach to tackle the childhood obesity epidemic needs a collection of activities including influencing policy makers and legislation, mobilizing communities, restructuring organizational practices, establishing coalitions and networks, empowering providers, imparting community education as well as enriching and reinforcing individual awareness and skills. The implications of this global phenomenon on future generations will be serious unless appropriate action is taken.
Adolescents; children; dietary management; obesity; overweight
The prevalence of obesity among children, adolescents and adults has been dramatically increasing worldwide during the last several decades. The obesity epidemic has been recognized as one of the major global health problems, because its health hazard is linked to a number of common diseases including breast and prostate cancers. Obesity is caused by combination of genetic and environmental factors. While genetic contribution to obesity has been known to be significant, the genetic factors remain relatively unchanged. Recent studies have highlighted the involvement of environmental “obesogens”, i.e. the xenobiotic chemicals that can disrupt the normal development and homeostatic control over adipogenesis and energy balance. Several lines of evidence suggest that increasing exposure to chemicals with endocrine-disrupting activities (endocrine disrupting chemicals, EDCs) contributes to the increased obesity. The cellular and molecular mechanisms underlying obesogen-associated obesity are just now being appreciated. In this paper, we comprehensively reviewed current knowledge about the role of estrogen receptors alpha and beta (ERα and ERβ) in regulation of energy metabolism pathways, including glucose transport, glycolysis, tricarboxylic acid (TCA) cycle, mitochondrial respiratory chain (MRC adenosine nucleotide translocator (ANT) and fatty acid β-oxidation and synthesis, by estrogens and then examined the disturbance of E2/ER-mediated energy metabolism pathways by environmental obesogens; and finally, we discussed the potential implications of disturbance of energy metabolism pathways by obesogens in obesity and pointed out several key aspects of this area that need to be further explored. A better understanding of the cellular and molecular mechanisms underlying obesogen-associated obesity will lead to new approaches for slow down and/or prevention of the increased trend of obesity associated with exposure to obesogens.
Adenosine nucleotide translocase (ANT); Estrogens; Estrogen receptor alpha and beta; Endocrine disrupting chemicals; Glucose transport; Glycolysis; Mitochondrial respiratory chain; Obesity; Tricarboxylic acid cycle
Pancreatic cancer (PC) is one of the most lethal malignant diseases with the worst prognosis. It is ranked as the fourth leading cause of cancer-related deaths in the United States. Many risk factors have been associated with PC. Interestingly, large numbers of epidemiological studies suggest that obesity and diabetes, especially type-2 diabetes, are positively associated with increased risk of PC. Similarly, these chronic diseases (obesity, diabetes and cancer) are also a major public health concern. In the U.S. population, 50 percent are overweight, 30 percent are medically obese and 10 percent have diabetes mellitus (DM). Therefore, obesity and DM have been considered as potential risk factors for cancers; however, the focus of this article is restricted to PC. Although the mechanisms responsible for the development of these chronic diseases leading to the development of PC are not fully understood, the biological importance of the activation of insulin, insulin like growth factor-1 (IGF-1) and its receptor (IGF-1R) signaling pathways in insulin resistance mechanism and subsequent induction of compensatory hyperinsulinemia has been proposed. Therefore, targeting insulin/IGF-1 signaling with anti-diabetic drugs for lowering blood insulin levels and reversal of insulin-resistance could be useful strategy for the prevention and/or treatment of PC. A large number of studies have demonstrated that the administration of anti-diabetic drugs such as metformin and thiazolidinediones (TZD) class of PPAR-γ agonists decreases the risk of cancers, suggesting that these agents might be useful anti-tumor agents for the treatment of PC. In this review article, we will discuss the potential roles of metformin and TZD anti-diabetic drugs as anti-tumor agents in the context of PC, and will further discuss the complexities and the possible roles of microRNAs (miRNAs) in the pathogenesis of obesity, diabetes and PC.
obesity; diabetes mellitus; pancreatic cancer; metformin; and TZD
Colorectal cancer (CRC) is one of the leading causes of cancer and cancer-related mortality worldwide. The disease has been traditionally a major health problem in industrial countries, however the CRC rates are increasing in the developing countries that are undergoing economic growth. Several environmental risk factors, mainly changes in diet and life style, have been suggested to underlie the rise of CRC in these populations. Diet and lifestyle impinge on nuclear receptors, on the intestinal microbiota and on crucial molecular pathways that are implicated in intestinal carcinogenesis. In this respect, the epidemiological transition in several regions of the world offers a unique opportunity to better understand CRC carcinogenesis by studying the disease phenotypes and their environmental and molecular associations in different populations. The data from these studies may have important implications for the global prevention and treatment of CRC.
Colorectal cancer; Developing countries; Environment; Diet; Nuclear receptors; Gut microbiota
Overweight and obesity have reached epidemic proportions in many Asian
countries. These countries also face a grave burden of obesity-related disorders such as diabetes, hypertension, and cardiovascular diseases, which develop at a younger age than in Western populations. These disorders are also manifested in childhood. The major causative factors are related to the lifestyle changes occurring due to rapid socioeconomic transition. Asian populations show several differences in genetic factors when compared with the white population, and they also have lower cut points for environmental risk factors. National programmes targeting public awareness, education and improved structural facilities to facilitate healthy lifestyle are the keys to alleviate the economic and health care burden of the obesity-related disorders.
The rapid rise in the incidence of obesity has emerged as one of the most pressing global public health issues in recent years. The underlying etiological causes of obesity, whether behavioral, environmental, genetic, or a combination of several of them, have not been completely elucidated. The obesity epidemic has been attributed to the ready availability, abundance, and overconsumption of high-energy content food. We determined here by Pearson's correlation the relationship between food type consumption and rising obesity using the loss-adjusted food availability data from the United States Department of Agriculture (USDA) Economic Research Services (ERS) as well as the obesity prevalence data from the Behavioral Risk Factor Surveillance System (BRFSS) and the National Health and Nutrition Examination Survey (NHANES) at the Centers for Disease Control and Prevention (CDC). Our analysis showed that total calorie intake and consumption of high fructose corn syrup (HFCS) did not correlate with rising obesity trends. Intake of other major food types, including chicken, dairy fats, salad and cooking oils, and cheese also did not correlate with obesity trends. However, our results surprisingly revealed that consumption of corn products correlated with rising obesity and was independent of gender and race/ethnicity among population dynamics in the U.S. Therefore, we were able to demonstrate a novel link between the consumption of corn products and rising obesity trends that has not been previously attributed to the obesity epidemic. This correlation coincides with the introduction of bioengineered corns into the human food chain, thus raising a new hypothesis that should be tested in molecular and animal models of obesity.
Obesity; food trend; corn product; genetically modified; bioengineered
A strong analogy exists between over/under consumption of energy at the level of the human body and of the industrial metabolism of humanity. Both forms of energy consumption have profound implications for human, environmental, and global health. Globally, excessive fossil-fuel consumption, and individually, excessive food energy consumption are both responsible for a series of interrelated detrimental effects, including global warming, extreme weather conditions, damage to ecosystems, loss of biodiversity, widespread pollution, obesity, cancer, chronic respiratory disease, and other lethal chronic diseases. In contrast, data show that the efficient use of energy—in the form of food as well as fossil fuels and other resources—is vital for promoting human, environmental, and planetary health and sustainable economic development. While it is not new to highlight how efficient use of energy and food can address some of the key problems our world is facing, little research and no unifying framework exists to harmonize these concepts of sustainable system management across diverse scientific fields into a single theoretical body. Insights beyond reductionist views of efficiency are needed to encourage integrated changes in the use of the world’s natural resources, with the aim of achieving a wiser use of energy, better farming systems, and healthier dietary habits. This perspective highlights a range of scientific-based opportunities for cost-effective pro-growth and pro-health policies while using less energy and natural resources.
Obesity is a leading risk factor for impaired glucose tolerance and type 2 diabetes (T2D). Although the cause of the obesity epidemic is multi-factorial and not entirely clear, the recent acceleration in incidence is too rapid to be accounted for only by genetics, the wide availability of calorie-rich foods, and increasingly sedentary lifestyles. Accumulating data suggest that the important causes of the obesity epidemic may be related to developmental and early life environmental conditions. The concept of the developmental origins of health and disease (DOHaD) suggests that adverse influences early in development, particularly during intrauterine life, may result in permanent changes in the physiology and metabolism of the infant, which in turn result in an increased risk of non-communicable diseases in adulthood. For example, undernutrition during pregnancy and rapid postnatal weight gain are associated with obesity and T2D in the adult offspring. Moreover, increasing evidence suggests that early-life exposure to a wide range of chemicals has a significant impact on the causes of metabolic disorders. Although the underlying molecular mechanisms remain to be determined, these factors can affect epigenetic processes, such as DNA methylation, allowing the developmental environment to modulate gene transcription. The objective of this review article was to summarize recent progress in the biomedical implications of the DOHaD concept, focusing on the pathogenesis of obesity and T2D, and to discuss a future direction for preventive strategies from a public health perspective.
Chemicals; Developmental origins of health and disease; Epigenetics; Obesity; Type 2 diabetes
In recent years, there has been a marked change in life-style of South Asian countries caused by economic growth, affluence, urbanization and dietary westernization. Few studies on the prevalence of obesity, hypertension and diabetes in the Indian population have been reported. However, there has been scarce literature on the study of prevalence of type 2 diabetes mellitus (DM) and Hypertension in overweight and obese people in India with criteria suggested by World Health Organization (WHO) for Asians. Information on such public health issues would provide evidence based data to develop guidelines and policies on this subject.
The aim of this article is to determine the prevalence of hypertension and type 2 DM in overweight and obese people.
Setting and Design:
A cross-sectional study consisted of people selected from the out-patient department and indoors of a large defense hospital in a semi urban area of Assam.
Materials and Methods:
Patients with overweight and obesity, reporting for consultation and medical examination were taken into the study. The data collected was analyzed using the criteria for overweight, obesity, diabetes and hypertension defined by WHO, Joint National Committee VII and International Diabetes Federation, American Diabetes Association. A descriptive statistical analysis has been carried out in the study.
A total of 300 people were the subject population of this study. Among the subject population, there were 97 overweight and 203 obese. The 56 subjects were found to be diabetic. The prevalence of type 2 DM in overweight subjects was 15.5% and in obese was 20.2% and overall was 18.7%. Prevalence of hypertension in the overweight population was 8.2% and in obese was 22.2% and overall found to be 17.7%.
The prevalence of type 2 DM, hypertension in the obese group of the study population were found to be 20.2%, 22.2% and in the overweight population were 15.5% and 8.2%, respectively. This indicates that the prevalence of type 2 DM and hypertension increases with increasing weight of the individuals. The prevalence of type 2 DM and hypertension were relatively higher compared with other studies in India and abroad.
Hypertension; obesity; overweight; type 2 diabetes mellitus
Obesity is a serious international health problem that increases the risk of several diet-related chronic diseases. The genetic factors predisposing to obesity are little understood. Rcan2 was originally identified as a thyroid hormone-responsive gene. In the mouse, two splicing variants that harbor distinct tissue-specific expression patterns have been identified: Rcan2-3 is expressed predominately in the brain, whereas Rcan2-1 is expressed in the brain and other tissues such as the heart and skeletal muscle. Here, we show that Rcan2 plays an important role in the development of age- and diet-induced obesity. We found that although the loss of Rcan2 function in mice slowed growth in the first few weeks after birth, it also significantly ameliorated age- and diet-induced obesity in the mice by causing a reduction in food intake rather than increased energy expenditure. Rcan2 expression was most prominent in the ventromedial, dorsomedial and paraventricular hypothalamic nuclei governing energy balance. Fasting and refeeding experiment showed that only Rcan2-3 mRNA expression is up-regulated in the hypothalamus by fasting, and loss of Rcan2 significantly attenuates the hyperphagic response to starvation. Using double-mutant (Lepob/ob Rcan2−/−) mice, we were also able to demonstrate that Rcan2 and leptin regulate body weight through different pathways. Our findings indicate that there may be an Rcan2-dependent mechanism which regulates food intake and promotes weight gain through a leptin-independent pathway. This study provides novel information on the control of body weight in mice and should improve our understanding of the mechanisms of obesity in humans.
Obesity is a public health problem that has become epidemic worldwide. Substantial literature has emerged to show that overweight and obesity are major causes of co-morbidities, including type II diabetes, cardiovascular diseases, various cancers and other health problems, which can lead to further morbidity and mortality. The related health care costs are also substantial. Therefore, a public health approach to develop population-based strategies for the prevention of excess weight gain is of great importance. However, public health intervention programs have had limited success in tackling the rising prevalence of obesity. This paper reviews the definition of overweight and obesity and the variations with age and ethnicity; health consequences and factors contributing to the development of obesity; and critically reviews the effectiveness of current public health strategies for risk factor reduction and obesity prevention.
obesity; prevention; public health
Two-thirds of American adults are overweight or obese, 75 million have hypertension and another 25 million have diabetes. Cardiovascular disease is the leading cause of morbidity and mortality and a major driver of health care costs in patients with type 2 diabetes. Observational studies suggest that insulin resistance, hypertension and hyperglycemia independently predict cardiovascular disease and chronic kidney disease. Indeed, coexisting hypertension appears to be a most powerful determinant of cardiovascular disease risk in diabetic patients. This update explores recent investigation which sheds light on our understanding of various metabolic and hemodynamic factors which promote vascular disease, as well as strategies to lessen cardiovascular disease in patients with diabetes.
Economic changes and policy reforms, consistent with economic globalization, in New Zealand in the mid-1980s, combined with the recent global demand for dairy products, particularly from countries undergoing a 'nutrition transition', have created an environment where a proportion of the New Zealand population is now experiencing financial difficulty purchasing milk. This situation has the potential to adversely affect health.
Similar to other developed nations, widening income disparities and health inequalities have resulted from economic globalization in New Zealand; with regard to nutrition, a proportion of the population now faces food poverty. Further, rates of overweight/obesity and chronic diseases have increased in recent decades, primarily affecting indigenous people and lower socio-economic groups. Economic globalization in New Zealand has changed the domestic milk supply with regard to the consumer and may shed light on the link between globalization, nutrition and health outcomes. This paper describes the economic changes in New Zealand, specifically in the dairy market and discusses how these changes have the potential to create inequalities and adverse health outcomes. The implications for the success of current policy addressing chronic health outcomes is discussed, alternative policy options such as subsidies, price controls or alteration of taxation of recommended foods relative to 'unhealthy' foods are presented and the need for further research is considered.
Changes in economic ideology in New Zealand have altered the focus of policy development, from social to commercial. To achieve equity in health and improve access to social determinants of health, such as healthy nutrition, policy-makers must give consideration to health outcomes when developing and implementing economic policy, both national and global.