High Rates of Obesity and Non-Communicable Diseases Predicted across Latin America

Non-communicable diseases (NCDs) such as cardiovascular disease and stroke are a major public health concern across Latin America. A key modifiable risk factor for NCDs is overweight and obesity highlighting the need for policy to reduce prevalence rates and ameliorate rising levels of NCDs. A cross-sectional regression analysis was used to project BMI and related disease trends to 2050. We tested the extent to which interventions that decrease body mass index (BMI) have an effect upon the number of incidence cases avoided for each disease. Without intervention obesity trends will continue to rise across much of Latin America. Effective interventions are necessary if rates of obesity and related diseases are to be reduced.     

特定人群超重及肥胖与相关疾病患病分析

目的：分析特定人群超重患病率,以及超重与高血压、糖尿病、血脂异常、脂肪肝等相关疾病的关系,为及早预防慢性非传染性疾病奠定基础。方法：对平房地区采取长效避孕措施的603名户籍农村已婚育龄妇女进行健康体检,按体重指数（BMI）分为正常组、超重组和肥胖组,比较各组间高血压、高血糖、高血脂、脂肪肝等相关疾病检出率的差异。结果：特定人群超重发病率及超重相关疾病检出率的差异均具有统计学意义（P〈0．01）。结论：平房地区特定人群超重及肥胖发病率未明显高于国内平均水平及全市水平。但超重及肥胖与高血压、糖尿病、血脂异常、脂肪肝等疾病存在较大相关关系,为了进一步降低心脑血管高危因素和死亡率。需采取早期、有效的措施控制超重和肥胖倾向。     

Mitochondrial oxidative stress and inflammation: an slalom to obesity and insulin resistance

Mitochondria, in addition to energy transformation, play a role in important metabolic tasks such as apoptosis, cellular proliferation, heme/steroid synthesis as well as in the cellular redox state regulation. The mitochondrial phosphorylation process is very efficient, but a small percentage of electrons may prematurely reduce oxygen forming toxic free radicals potentially impairing the mitochondria function. Furthermore, under certain conditions, protons can reenter the mitochondrial matrix through different uncoupling proteins (UCPs), affecting the control of free radicals production by mitochondria. Disorders of the mitochondrial electron transport chain, overgeneration of reactive oxygen species (ROS) and lipoperoxides or impairments in antioxidant defenses have been reported in situations of obesity and type-2 diabetes. On the other hand, obesity has been associated to a low degree pro-inflammatory state, in which impairments in the oxidative stress and antioxidant mechanism could be involved. Indeed, reactive oxygen species have been attributed a causal role in multiple forms of insulin resistance. The scientific evidence highlights the importance of investigating the relationships between oxidative stress and inflammation with obesity/diabetes onset and underlines the need to study in mitochondria from different tissues, the interactions of such factors either as a cause or consequence of obesity and insulin resistance.     

Clinical Considerations Regarding the Use of Obesity Pharmacotherapy in Adolescents with Obesity

A growing number of youth suffer from obesity and in particular severe obesity for which intensive lifestyle intervention does not adequately reduce excess adiposity. A treatment gap exists wherein effective treatment options for an adolescent with severe obesity include intensive lifestyle modification or metabolic and bariatric surgery while the application of obesity pharmacotherapy remains largely underutilized. These youth often present with numerous obesity‐related comorbid diseases, including hypertension, dyslipidemia, prediabetes/type 2 diabetes, obstructive sleep apnea, nonalcoholic fatty liver disease, musculoskeletal problems, and psychosocial issues such as depression, anxiety, and social stigmatization. Current pediatric obesity treatment algorithms for pediatric primary care providers focus primarily on intensive lifestyle intervention with escalation of treatment intensity through four stages of intervention. Although a recent surge in the number of Food and Drug Administration‐approved medications for obesity treatment has emerged in adults, pharmacotherapy options for youth remain limited. Recognizing treatment and knowledge gaps related to pharmacological agents and the urgent need for more effective treatment strategies in this population, discussed here are the efficacy, safety, and clinical application of obesity pharmacotherapy in youth with obesity based on current literature. Legal ramifications, informed consent regulations, and appropriate off‐label use of these medications in pediatrics are included, focusing on prescribing practices and prescriber limits.     

State- and payer-specific estimates of annual medical expenditures attributable to obesity

The goal of this study is to expand prior analyses by presenting current state-level estimates of the costs of obesity in total and separately for Medicare and Medicaid. Quantifying current Medicare and Medicaid expenditures attributable to obesity is important because high public sector costs of obesity have been a primary motivation for publicly funded obesity prevention efforts at the state level. We also present estimates of the obesity-attributable fraction (OAF) of total, Medicare, and Medicaid expenditures and the percentage of total obesity costs within each state that is funded by the public sector. We used the 2006 Medical Expenditure Panel Survey, nationally representative data that include information on obesity and medical expenditures, to generate an equation that predicts annual medical expenditures as a function of obesity status. We used the 2006 Behavioral Risk Factor Surveillance System, state representative data, and the equation generated from the national model to predict state (and payer within state) expenditures and the fraction of expenditures attributable to obesity for each state. Across states, annual medical expenditures would be between 6.7 and 10.7% lower in the absence of obesity. Between 22% (Virginia) and 55% (Rhode Island) of the state-level costs of obesity are financed by the public sector via Medicare and Medicaid. The high costs of obesity at the state level emphasize the need to prevent and control obesity as a way to manage state medical costs.     

Determinants of obesity in transition economies: The case of Russia

This paper examines human obesity, measured as weight and body mass index (BMI), and its determinants in Russia. Obesity increased dramatically during transition from a planned to a market economy, by 38%. We determine the factors contributing to rising obesity using individual level data from the Russia Longitudinal Monitoring Survey for 1994 and 2004. We find a strong positive effect of diet/caloric intake and a strong negative effect of smoking on weight and BMI. Gender, education, and income are other major determinants of obesity. Our analysis provides information on dietary patterns and other determinants of obesity in Russia which is essential for formulation and implementation of effective policies designed to reduce the problem and improve the health of the population.     

Contingent valuation analysis of willingness to pay to reduce childhood obesity

Several recent surveys have asked Americans whether they support policies to reduce childhood obesity. There is reason for skepticism of such surveys because people are not confronted with the tax costs of such policies when they are asked whether they support them. This paper uses contingent valuation (CV), a method frequently used to estimate people's willingness to pay (WTP) for goods or services not transacted in markets, applied to unique survey data from New York State to estimate the willingness to pay to reduce childhood obesity. The willingness to pay data correlate in predictable ways with respondent characteristics. The mean WTP for a 50% reduction in childhood obesity is $46.41 (95% CI: $33.45, $59.15), which implies a total WTP by New York State residents of $690.6 million (95% CI: $497.7, $880.15), which is less than that implied by previous surveys that did not use CV methods but greater than current spending on policies to reduce childhood obesity and greater than the estimated savings in external costs. The findings provide policymakers with useful information about taxpayers' support for, and preferred budget for, anti-obesity policies.     

Obesity reduction within a generation: the dual roles of prevention and treatment

In 2010, the White House Task Force on Childhood Obesity provided benchmark goals for reducing childhood obesity. We evaluated the balance of prevention and treatment required for achieving Task Force goals in benchmark years 2015, 2020, and 2030. We created a simulation of US birth cohorts (2-19 years) born 2008-2030. For each year, we assumed "old" birth cohorts (part of previous benchmark obesity estimates) would benefit from obesity treatment strategies, and "new" birth cohorts would benefit from obesity prevention strategies. We assessed obesity prevalence that must be achieved through prevention strategies, under varying assumptions of treatment effectiveness. When we assumed a 1% absolute reduction in prevalence through treatment, we found that prevention strategies would need to achieve an obesity prevalence of 12% by 2015, 8% by 2020, and 0.3% by 2030. Because of higher obesity prevalence among minority children, prevention strategies would need to achieve a negative prevalence by 2030, which is implausible. Under more generous assumptions of treatment effectiveness, estimates became positive but remained low. Task Force goals are more difficult to achieve with each benchmark year. Policies must focus on obesity treatment interventions, particularly targeted to racial/ethnic minority children, to make progress in stemming the epidemic.     

Liraglutide modulates gut microbiota and reduces NAFLD in obese mice

Metabolic disorders such as insulin resistance and diabetes are associated with obesity and nonalcoholic fatty liver disease (NAFLD). The aggressive form of a fatty liver disease may progress to cirrhosis and hepatocellular carcinoma. Furthermore, recent studies demonstrated that there is a dysbiosis in the gut microbiota associated with early stages of metabolic disease. Therefore, the identification and repurposing of drugs already used to treat insulin resistance may be an excellent option for other disorders. We evaluated the effect of liraglutide on obesity, NAFLD and gut microbiota modulation in two different animal models of obesity: the ob/ob mice and the high-fat diet (HFD)-fed mice. Liraglutide treatment induced significant weight loss in both obesity models, showed improvements in glycemic parameters and reduced inflammatory cell infiltration in the cecum and the liver. In ob/ob mice, the liraglutide treatment was able to reduce the accumulation of liver fat by 78% and reversed steatosis in the HFD mice. The gut microbiota analysis showed that liraglutide changed the overall composition as well as the relative abundance of weight-relevant phylotypes such as a reduction of Proteobacteria and an increase of Akkermansia muciniphila in the treated HFD group. We show that liraglutide can lead to weight loss and gut microbiota modulations, and is associated with an improvement of NAFLD. Furthermore, by generating a profile of the intestinal microbiota, we compiled a list of potential bacterial targets that may modulate metabolism and induce a metabolic profile that is considered normal or clinically controlled.     

Food and emotion

The relationship between eating and emotion has always interested researchers of human behavior. This relationship varies according to the particular characteristics of the individual and according to the specific emotional state. We consider findings on the reciprocal interactions between, on the one hand, emotions and food intake, and, on the other, the psychological and emotional consequences of losing weight and dieting. Theories on the relationship between emotions and eating behaviors have their origin in the literature on obesity. The psychosomatic theory of obesity proposes that eating may reduce anxiety, and that the obese overeat in order to reduce discomfort. The internal/external theory of obesity hypothesizes that overweight people do not recognize physiological cues of hunger or satiety because of faulty learning. It thus predicts that normal weight people will alter (either increase or decrease) their eating when stressed, while obese people will eat regardless of their physiological state. The restraint hypothesis postulates that people who chronically restrict their food intake overeat in the presence of disinhibitors such as the perception of having overeaten, alcohol or stress. These theories are examined in the light of present research and their implications on eating disorders are presented.     

Implications of Odera Oruka's ethics of consumerism for reducing globesity

In this paper, I advance Odera Oruka's insights on the ethics of consumerism in order to draw relevant implications of his thoughts on rethinking the problem of obesity. I argue that Oruka's ethics of consumerism and his right to human minimum theory entail some salient ideas that might serve as a better ethical model for reducing the global obesity prevalence. Though Oruka's African moral philosophy is yet to receive universal attention it arguably deserves, the interests of the international and ‘globesity’ community would be better served learning from the contributions of an African moral theory to contemporary bioethical discourse on obesity. Oruka's moral thoughts are by constitution, a deontological and cosmopolitan call for reducing hunger in globalized world, while also indirectly, addressing obesity of the poor. I show the limitations of his ethics of consumerism, and the shortcomings of such ethics in the context of obesity of the poor. Consequently, I develop a neo‐Orukan virtue based ethics that is worthy of attention in efforts towards addressing the obesity tide. No such perspective currently exists in the context of obesity; yet the exigent need for one is necessitated by the defects of the libertarian and harm principle approaches in Western bioethical discourse.     

Bioactive Compounds and Adipocyte Browning Phenomenon

Overweight and obesity have become worldwide health issues in most countries. Current strategies aimed to prevent or reduce overweight and obesity have mainly focused on the genes and molecular mechanisms that give the functional characteristics to different types of adipose tissue. The Browning phenomenon in adipocytes consists of phenotypic and metabolic changes within white adipose tissue (WAT) activated by thermogenic mechanisms similar to that occurring in brown adipose tissue (BAT); this phenomenon has assumed great relevance due to its therapeutic potential against overweight and obesity. In addition, the study of inflammation in the development of overweight and obesity has also been included as a relevant factor, such as the pro-inflammatory mechanisms promoted by M1-type macrophages in adipose tissue. Studies carried out in this area are mainly performed by using the 3T3-L1 pre-adipocyte cell line, testing different bioactive compound sources such as plants and foods; nevertheless, it is necessary to standardize protocols used in vitro as well to properly scale them to animal models and clinical tests in order to have a better understanding of the mechanisms involved in overweight and obesity.     

Narrative review of ferroptosis in obesity

Obesity is widely recognized as a major global health problem caused by a chronic energy imbalance resulting from a combination of excess caloric intake and insufficient energy expenditure. Excessive energy intake and physical inactivity are traditional risk factors for obesity. Obesity is a risk factor for many diseases, including hypertension, diabetes and tumours. Recent studies have found a strong link between ferroptosis and obesity. Ferroptosis is an iron-dependent regulated cell death caused by iron overload and reactive oxygen species-dependent excessive accumulation of lipid peroxidation. Ferroptosis is involved in many biological processes, such as amino acid metabolism, iron metabolism and lipid metabolism. Some potential strategies to reduce the adverse effects of ferroptosis on obesity are suggested and future research priorities are highlighted.     

The role of oxidative stress in the development of obesity and obesity-related metabolic disorders

Obesity is a serious medical condition, defined as excessive accumulation of fat. Abdominal fat is recognized as the major risk for obesity related diseases such as: hypertension, dyslipidemia, type 2 diabetes mellitus, coronary heart disease, stroke, non-alcoholic fatty liver disease etc. Fat accumulation is also related to pro-oxidant and pro-inflammatory states. Recently published articles suggest that oxidative stress may be a link between obesity and related complications. Adiposity leads to increased oxidative stress via several multiple biochemical processes such as superoxide generation through the action of NADPH oxidase, glyceraldehyde auto-oxidation, oxidative phosphorylation, protein kinase C (PKC) activation, and polyol and hexosamine pathways. On the other hand, oxidative stress plays a causative role in the development of obesity, by stimulating the deposition of adipose tissue, including preadipocyte proliferation, adipocyte differentiation and growth. Exercise-induced weight loss can improve the redox state by modulating both oxidative stress and antioxidant promoters, which reduce endothelial dysfunction and inflammation.     

Topical application of capsaicin reduces visceral adipose fat by affecting adipokine levels in high‐fat diet‐induced obese mice

Objective:

Visceral obesity contributes to the development of obesity‐related disorders such as diabetes, hyperlipidemia, and fatty liver disease, as well as cardiovascular diseases. In this study, we determined whether topical application of capsaicin can reduce fat accumulation in visceral adipose tissues.

Methods and Results:

We first observed that topical application of 0.075% capsaicin to male mice fed a high‐fat diet significantly reduced weight gain and visceral fat. Fat cells were markedly smaller in the mesenteric and epididymal adipose tissues of mice treated with capsaicin cream. The capsaicin treatment also lowered serum levels of fasting glucose, total cholesterol, and triglycerides. Immunoblot analysis and RT‐PCR revealed increased expression of adiponectin and other adipokines including peroxisome proliferator‐activated receptor (PPAR) α, PPARγ, visfatin, and adipsin, but reduced expression of tumor necrosis factor‐α and IL‐6.

Conclusions:

These results indicate that topical application of capsaicin to obese mice limits fat accumulation in adipose tissues and may reduce inflammation and increase insulin sensitivity.     

Bariatric surgery to unload the stressed heart: a metabolic hypothesis

Obesity is an independent risk factor for cardiovascular disease. Data from the Framingham Study have reported a higher incidence of heart failure in obese individuals compared with a normal cohort. The body initially copes with the abundance of fuel present in an obese milieu by storing it in adipose tissue. However, when the storage capacity is exceeded, the excess energy is taken up and stored ectopically as fat in vital organs such as the heart. Indeed, intramyocardial lipid overload is present in hearts of obese patients, as well as in hearts of animal models of obesity, and is associated with a distinct gene expression profile and cardiac dysfunction. By imposing a metabolic stress on the heart, obesity causes it to hypertrophy and ultimately to fail. Conventional measures to treat obesity include diet, exercise, and drugs. More recently, weight loss surgery (WLS) has achieved increasing prominence because of its ability to reduce the neurohumoral load, normalize metabolic dysregulation, and improve overall survival. The effects of WLS on systemic metabolic, neurohumoral, and hemodynamic parameters are well described and include an early normalization of serum glucose and insulin levels as well as reduction in blood pressure. WLS is also associated with reverse cardiac remodeling, regression of left ventricular hypertrophy, and improved left ventricular and right ventricular function. By targeting the source of the excess energy, we hypothesize that WLS improves contractile function by limiting exogenous substrate availability to the metabolically overloaded heart. These changes have also been found to be associated with increased levels of adiponectin and improved insulin sensitivity. Taken together, the sustained beneficial effects of WLS on left ventricular mass and function highlight the need to better understand the mechanism by which obesity regulates cardiovascular physiology.     

Portrayals of canine obesity in English-language newspapers and in leading veterinary journals, 2000-2009: implications for animal welfare organizations and veterinarians as public educators

In industrialized societies, more than 1 in 3 dogs and people currently qualify as overweight or obese. Experts in public health expect both these figures to rise. Although clinical treatment remains important, so are public perceptions and social norms. This article presents a thematic analysis of English-language mass media coverage on canine obesity from 2000 through 2009 and compares these results with a thematic analysis of articles on canine obesity in leading veterinary journals during the same time period. Drawing on Giddens's theory of structuration, this study identified articles that emphasized individual agency, environmental structure, or both as contributors to canine obesity. Comparisons with weight-related health problems in human populations were virtually absent from the veterinary sample. Although such comparisons were almost always present in the media sample, quotations from veterinarians and other spokespeople for the welfare of nonhuman animals emphasized the agency of individual caregivers (owners) over structural influences. Now that weight gain and obesity have been established as a pressing animal welfare problem, these results suggest a need for research and for interventions, such as media advocacy, that emphasize intersections between animal-owner agency, socioenvironmental determinants, and connections between animal welfare and human health.     

Obesity and cancer: pathophysiological and biological mechanisms

Excess body weight (overweight and obesity) is characterized by chronic hyperinsulinaemia and insulin resistance, and is implicated both in cancer risk and cancer mortality. The list of cancers at increased risk of development in an "obesogenic" environment include common adult cancers such as endometrium, post-menopausal breast, colon and kidney, but also less common malignancies such as leukaemia, multiple myeloma, and non-Hodgkin's lymphoma. The pathophysiological and biological mechanisms underpinning these associations are only starting to be understood. Insulin resistance is at the heart of many, but there are several other candidate systems including insulin-like growth factors, sex steroids, adipokines, obesity-related inflammatory markers, the nuclear factor kappa beta (NF-kappa B) system and oxidative stresses. With such as diversity of obesity-related cancers, it is unlikely that there is a "one system fits all" mechanism. While public health strategies to curb the spread of the obesity epidemic appear ineffective, there is a need to better understand the processes linking obesity and cancer as a pre-requisite to the development of new approaches to the prevention and treatment of obesity-related cancers.     

Chronic intake of proanthocyanidins and docosahexaenoic acid improves skeletal muscle oxidative capacity in diet-obese rats

Obesity has become a worldwide epidemic. The cafeteria diet (CD) induces obesity and oxidative-stress-associated insulin resistance. Polyunsaturated fatty acids and polyphenols are dietary compounds that are intensively studied as products that can reduce the health complications related to obesity. We evaluate the effects of 21 days of supplementation with grape seed proanthocyanidins extract (GSPE), docosahexaenoic-rich oil (DHA-OR) or both compounds (GSPE+DHA-OR) on skeletal muscle metabolism in diet-obese rats. The supplementation with different treatments did not reduce body weight, although all groups used more fat as fuel, particularly when both products were coadministered; muscle β-oxidation was activated, the mitochondrial functionality and oxidative capacity were higher, and fatty acid uptake gene expressions were up-regulated. In addition to these outcomes shared by all treatments, GSPE reduced insulin resistance and improved muscle status. Both treatments increased 5’-AMP-activated protein kinase (AMPK) phosphorylation, which was consistent with higher plasma adiponectin levels. Moreover, AMPK activation by DHA-OR was also correlated with an up-regulation of peroxisome proliferator-activated receptor alpha (Pparα). GSPE+DHA-OR, in addition to activating AMPK and enhancing fatty acid oxidation, increased the muscle gene expression of uncoupling protein 2 (Ucp2). In conclusion, GSPE+DHA-OR induced modifications that improved muscle status and could counterbalance the deleterious effects of obesity, and such modifications are mediated, at least in part, through the AMPK signaling pathway.     

What Is the Economic Case for Treating Obesity?

From both societal and payer perspectives, the economic effect of obesity in the United States is substantial, estimated at approximately 6% of our national health expenditure and cost of care in a major health maintenance organization. The number of physician visits related to obesity has increased 88% in a 6-year period. The morbidity cost (lost productivity) and functional capability of the patient with obesity is increasing rapidly (50% increase in lost productivity, 36% increase in restricted activity, and 28% increase in number of bed-days). Cost savings of treating obesity are comparable to those of treating other chronic diseases such as coronary heart disease and diabetes. Most studies indicate that most of the direct health care costs of obesity are from type 2 diabetes, coronary heart disease and hypertension. To date, however, there have been no published reports of the cost effectiveness of the medical management of obesity treatment. In conclusion, the cost of obesity is comparable to that of other chronic diseases, yet it receives disproportionately less attention. Cost effectiveness studies need to be initiated promptly.