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The worldwide prevalence of individuals with an elevated body weight has increased steadily over the past five decades. Billions of research dollars have been invested to improve our understanding of the causes and consequences of having an elevated body weight. All this knowledge has, however, failed to influence populational body weight trajectories of most countries around the world. Research on the definition of "obesity" has also evolved. Body mass index (BMI), the most commonly used tool to make its diagnosis, has major limitations. In this review article, we will highlight evidence from observational studies, genetic association studies and randomized clinical trials that have shown the remarkable inter-individual differences in the way humans store energy as body fat. Increasing evidence also suggests that, as opposed to weight inclusive, lifestyle-based approaches, weight-centric approaches advising people to simply eat less and move more are not sustainable for most people for long-term weight loss and maintenance. It is time to recognize that this outdated approach may have produced more harm than good. On the basis of pathophysiological, genetic and clinical evidence presented in this review, we propose that it may be time to shift away from the traditional clinical approach, which is BMI-centric. Rather, emphasis should be placed on actionable lifestyle-related risk factors aiming at improving overall diet quality and increasing physical activity level in the general population., Competing Interests: Declaration of competing interests BJA is a consultant for Novartis, Eli Lilly, Editas Medicine and Silence Therapeutics and has received research contracts from Pfizer, Eli Lilly, Ionis Pharmaceuticals and Silence Therapeutics. ACC received research funding by Eli Lilly (2019 - ongoing) and NovoNordisk (2021 - ongoing) and consultation fees by Eli Lilly, HLS Therapeutics, Janssen Inc., Novartis Pharmaceuticals Canada Inc., and Novo Nordisk Canada Inc. PP received continuous medical education/consultation fees from Abbott, Amgen, Astrazeneca, Bayer, Bausch Health, Boehringer Ingelheim, Eli Lilly, GSK, HLS Therapeutics Inc, Janssen Inc, Novartis Pharmaceuticals Canada Inc, Mantra Pharma, Novo Nordisk Canada Inc, Sanofi, Servier. JPD discloses having received consulting fees from Inversago., (Copyright © 2024 The Authors. Published by Elsevier B.V. All rights reserved.)

Competing Interests: J-PD is the Scientific Director of the International Chair on Cardiometabolic Risk supported by the Fondation de l'Université Laval and is the co-chair holder of the Chaire de recherche en santé durable funded by Fonds de recherche du Québec—Santé. Research from J-PD is currently supported by the Canadian Institutes of Health Research (foundation grant FDN-167278). J-PD reports receiving consulting fees from Inversago and honoraria from Rockpointe for participation as a speaker at a Novo Nordisk sponsored symposium held at American Heart Association's annual meeting 2022.

Obesity contributes to reduced life expectancy because of its link with type 2 diabetes and cardiovascular disease. Yet, targeting this poorly diagnosed, ill-defined, and underaddressed modifiable risk factor remains a challenge. In this review, we emphasize that the tendency among health care professionals to amalgam all forms of obesity altogether as a single entity may contribute to such difficulties and discrepancies. Obesity is a heterogeneous condition both in terms of causes and health consequences. Attention should be given to 2 prevalent subgroups of individuals: 1) patients who are overweight or moderately obese with excess visceral adipose tissue; and 2) patients with severe obesity, the latter group having distinct additional health issues related to their large body fat mass. The challenge of tackling high-cardiovascular-risk forms of obesity through a combination of personalized clinical approaches and population-based solutions is compounded by the current obesogenic environment and economy., Competing Interests: Funding Support and Author Disclosures Dr Després is the Scientific Director of the International Chair on Cardiometabolic Risk supported by the Fondation de l’Université Laval. Research from Dr Després discussed in this paper has been and is currently supported by the Canadian Institutes of Health Research (Foundation grant: FDN-167278) as well as by the Fondation of the Québec Heart and Lung Institute. Dr Carpentier holds the Canada Research Chair in Molecular Imaging of Diabetes; and has received funding for consulting from Eli Lilly, HLS Therapeutics, Janssen, Novartis Pharmaceuticals Canada, and Novo Nordisk Canada. Dr Tchernof has received research funding from Johnson & Johnson Medical Companies, Medtronic, and Bodynov for studies unrelated to this work; and has received consulting fees from Bausch Health and Novo Nordisk. Dr Neeland has received a grant from National Institutes of Health/NIDDK (K23 DK106520); has received speaking and consultancy fees from Boehringer Ingelheim, Merck, and AMRA Medical; and has received a grant from Novo Nordisk. Dr Poirier has received honoraria for CME/consultant/expert events from Abbott, Amgen, AstraZeneca, Bayer, Bausch Health, Boehringer Ingelheim, Eli Lilly, HLS Therapeutics, Janssen, Merck, Novartis, Novo Nordisk, Sanofi, and Servier., (Copyright © 2021 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

The global obesity epidemic is well established, with increases in obesity prevalence for most countries since the 1980s. Obesity contributes directly to incident cardiovascular risk factors, including dyslipidemia, type 2 diabetes, hypertension, and sleep disorders. Obesity also leads to the development of cardiovascular disease and cardiovascular disease mortality independently of other cardiovascular risk factors. More recent data highlight abdominal obesity, as determined by waist circumference, as a cardiovascular disease risk marker that is independent of body mass index. There have also been significant advances in imaging modalities for characterizing body composition, including visceral adiposity. Studies that quantify fat depots, including ectopic fat, support excess visceral adiposity as an independent indicator of poor cardiovascular outcomes. Lifestyle modification and subsequent weight loss improve both metabolic syndrome and associated systemic inflammation and endothelial dysfunction. However, clinical trials of medical weight loss have not demonstrated a reduction in coronary artery disease rates. In contrast, prospective studies comparing patients undergoing bariatric surgery with nonsurgical patients with obesity have shown reduced coronary artery disease risk with surgery. In this statement, we summarize the impact of obesity on the diagnosis, clinical management, and outcomes of atherosclerotic cardiovascular disease, heart failure, and arrhythmias, especially sudden cardiac death and atrial fibrillation. In particular, we examine the influence of obesity on noninvasive and invasive diagnostic procedures for coronary artery disease. Moreover, we review the impact of obesity on cardiac function and outcomes related to heart failure with reduced and preserved ejection fraction. Finally, we describe the effects of lifestyle and surgical weight loss interventions on outcomes related to coronary artery disease, heart failure, and atrial fibrillation.

This review addresses the interplay between obesity, type 2 diabetes mellitus, and cardiovascular diseases. It is proposed that obesity, generally defined by an excess of body fat causing prejudice to health, can no longer be evaluated solely by the body mass index (expressed in kg/m 2 ) because it represents a heterogeneous entity. For instance, several cardiometabolic imaging studies have shown that some individuals who have a normal weight or who are overweight are at high risk if they have an excess of visceral adipose tissue-a condition often accompanied by accumulation of fat in normally lean tissues (ectopic fat deposition in liver, heart, skeletal muscle, etc). On the other hand, individuals who are overweight or obese can nevertheless be at much lower risk than expected when faced with excess energy intake if they have the ability to expand their subcutaneous adipose tissue mass, particularly in the gluteal-femoral area. Hence, excessive amounts of visceral adipose tissue and of ectopic fat largely define the cardiovascular disease risk of overweight and moderate obesity. There is also a rapidly expanding subgroup of patients characterized by a high accumulation of body fat (severe obesity). Severe obesity is characterized by specific additional cardiovascular health issues that should receive attention. Because of the difficulties of normalizing body fat content in patients with severe obesity, more aggressive treatments have been studied in this subgroup of individuals such as obesity surgery, also referred to as metabolic surgery. On the basis of the above, we propose that we should refer to obesities rather than obesity.

A high prevalence of intermediate cardiometabolic risk factors and obesity in chronic obstructive pulmonary disease (COPD) has suggested the existence of pathophysiological links between hypertriglyceridemia, insulin resistance, visceral adiposity, and hypoxia or impaired pulmonary function. However, whether COPD contributes independently to the development of these cardiometabolic risk factors remains unclear. Our objective was to compare ectopic fat and metabolic profiles among representative individuals with COPD and control subjects and to evaluate whether the presence of COPD alters the metabolic risk profile. Study participants were randomly selected from the general population and prospectively classified as non-COPD controls and COPD, according to the Global Initiative for Chronic Obstructive Lung Disease classification. The metabolic phenotype, which consisted of visceral adipose tissue area, metabolic markers including homeostasis model assessment of insulin resistance (HOMA-IR), and blood lipid profile, was obtained in 144 subjects with COPD and 119 non-COPD controls. The metabolic phenotype was similar in COPD and controls. The odds ratios for having pathologic values for HOMA-IR, lipids and visceral adipose tissue area were similar in individuals with COPD and control subjects in multivariate analyses that took into account age, sex, body mass index, tobacco status and current medications. In a population-based cohort, no difference was found in the metabolic phenotype, including visceral adipose tissue accumulation, between COPD and controls. Discrepancies between the present and previous studies as to whether or not COPD is a risk factor for metabolic abnormalities could be related to differences in COPD phenotype or disease severity of the study populations., Competing Interests: MM, CB, NA and VC have no conflicts of interest to declare. DV report grants from Astra Zeneca France outside the submitted work. MEP is research scholars from the Fonds de Recherche du Québec-Santé (FRQ-S) JPD reports personal fees from Abbott Laboratories, AstraZeneca, GSK, Merck and Pfizer Canada Inc. and personal fees from Abbott Laboratories, Sanofi and Torrent Pharmaceuticals Ltd. outside the submitted work. WCT reports grants from Canadian Institute of Heath Research (CIHR/Rx&D Collaborative Research Program Operating Grants-93326) with industry partners AstraZeneca Canada Ltd, Boehringer Ingelheim Canada Ltd, GlaxoSmithKline Canada Ltd, Merck, Novartis Pharma Canada Inc., Nycomed Canada Inc., Pfizer Canada Ltd, during the conduct of the study. JB reports grants from Canadian Institute of Heath Research (CIHR/Rx&D Collaborative Research Program Operating Grants-93326) with industry partners AstraZeneca Canada Ltd, Boehringer Ingelheim Canada Ltd, GlaxoSmithKline Canada Ltd, Merck, NovartisPharma Canada Inc., Nycomed Canada Inc., Pfizer Canada Ltd, during the conduct of the study. JLP report grants from Air Liquide Foundation, Agiradom, AstraZeneca, Fisher and Paykel, Mutualia, Philips, Resmed and Vitalaire outside the submitted work and personnal fees from Agiradom, AstraZeneca, Boehringer Ingelheim, Jazz pharmaceutical, Night Balance, Philips, Resmed and Sefam outside the submitted work. FM reports grants and personal fees from Boehringer Ingelheim and GSK, grants from Nycomed and grants and personal fees from Novartis outside the submitted work. All fees are pooled with other revenues of the group of pulmonologists to which FM is a member and then shared among members of the group. This does not alter our adherence to PLOS ONE policies on sharing data and materials.

Background/objectives: This study examined the relationship between yogurt consumption, family history of obesity (FHO), and health determinants., Subjects/methods: Youth (n = 198; mean age: 20 ± 0.5 years) from the Québec Family Study were first classified based on their FHO, defined as the presence or absence of at least one obese (BMI ≥30 kg/m 2 ) parent [with FHO (FHO+; n = 112) or without FHO (FHO-; n = 86)] and then on their yogurt consumption [yogurt consumers (YC+) n = 61 or non-consumers (YC-) n = 137]. A two-factor mixed ANOVA was performed to evaluate the association between FHO, YC, and their interaction with health determinant such as weight and body composition, metabolic and behavioral profiles., Results: There was a main effect of FHO, but not YC, for weight and body composition, but no interaction between YC and FHO for these measures. However, a significant interaction between YC and FHO was observed for fasting insulin (P = 0.02), insulin area under the curve (AUC) (P = 0.02), and homeostatic model assessment of insulin resistance (HOMA-IR; P = 0.03) after adjustment for studied covariates. Specifically, lower fasting plasma insulin, insulin AUC, and HOMA-IR were observed in FHO+ and YC+ youth compared to YC- youth of the same group while no differences were found between the FHO- sub-groups., Conclusions: Consuming yogurt may protect against insulin resistance more specifically among youth at risk of obesity, and this relationship appears to be independent of body composition and lifestyle factors measured in this study.

Rationale: Obesity/overweight is the most prevalent body composition abnormality in COPD. However, little is known about the impact of fat distribution on cardiometabolic health in COPD., Objective: To study the associations between ectopic adiposity, cardiometabolic health, and COPD., Methods: A total of 263 subjects (166 males; age=65±9 years) were randomly selected from the general population. Subjects were classified as non-COPD controls and COPD, according to the Global initiative for chronic Obstructive Lung Disease (GOLD) classification, and the presence of cardiometabolic comorbidities was recorded. Ectopic fat accumulation was documented from computed tomography measurements of visceral adipose tissue cross-sectional areas and muscle mean attenuation, assessed at L4-L5. Blood glucose, lipid, and adipokine profiles were also evaluated., Results: After correcting for age, sex, and tobacco exposure, visceral adipose tissue cross-sectional area was higher in GOLD 2+ compared to GOLD 1 individuals. Consistent with this, mean muscle tissue attenuation was lower in GOLD 2+ vs GOLD 1 and non-COPD controls ( P <0.001). In multiple regression models, visceral adipose tissue cross-sectional area was strongly associated with hypertension ( P <0.001) and diabetes ( P <0.001), while muscle attenuation was associated with coronary artery disease ( P <0.001). Blood glucose, lipid, and adipokine profiles were similar across groups with the exception of leptin level which was higher in GOLD 2+ subjects compared to GOLD 1 and controls., Conclusion: GOLD 2+ COPD was associated with ectopic fat accumulation which modulated cardiometabolic health., Competing Interests: Disclosure The authors report no conflicts of interest in this work.

Background: Diastolic dysfunction (DD) is increasingly common. However, its metabolic determinants are poorly known. This study aims to determine which metabolic and inflammatory features predict DD in initially healthy adults., Methods: We prospectively analyzed the association between metabolic features and DD in 728 initially healthy adults aged 30-60 from Eastern France enrolled in the STANISLAS population-based cohort. Clinical and biological cardiovascular features were collected at baseline (1994-1995). DD was assessed twenty years later (2011-2016) by echocardiography using current international guidelines. For replication purposes, 1463 subjects from the Malmö Preventive Project cohort were analyzed., Results: In the STANISLAS cohort, 191 subjects (26.2%) developed DD. In age-sex-adjusted logistic models, significant predictors of DD were body mass index (BMI, odds ratio for 1-standard-deviation increase (OR) 1.28, 95% CI 1.08-1.52), waist circumference (WC, OR 1.48, 95% CI 1.18-1.84), waist-hip ratio (OR 1.53, 95% CI 1.16-2.02), systolic blood pressure (OR 1.19, 95% CI 1.00-1.43) and triglycerides (TG, OR 1.18, 95% CI 1.00-1.40). Subjects with elevated WC (> 80th percentile) and TG (> 50th percentile) had a twofold higher DD risk (age-sex-adjusted odds ratio 2.00, 95% CI 1.20-3.31, P = 0.008), whereas no such interplay was observed for BMI. In the Malmö cohort, BMI was similarly associated with DD; participants with both elevated BMI and TG were at higher DD risk (age-sex-adjusted odds ratio 1.61, 95% CI 1.18-2.20, P = 0.002)., Conclusions: Subjects with elevated WC and TG may have a higher long-term DD risk. Prevention targeting visceral obesity may help reduce the incidence of DD.

Obesity is recognized as a heterogeneous condition in which individuals with similar body mass index may have distinct metabolic and cardiovascular risk profiles. Susceptibility to obesity-related cardiometabolic complications is not solely mediated by overall body fat mass, but is largely dependent upon individual differences in regional body fat distribution and ability of subcutaneous adipose tissue to expand. The present review will discuss to what extent the individual variation in body fat distribution is one of the clinical key variables explaining the metabolic heterogeneity of obesity and its related cardiovascular risk. We will present the evidence for the complex nature of the relationship between obesity and cardiovascular disease, outline our current understanding of the mechanisms involved, and identify future direction of research pertinent to this interaction., (Copyright © 2018 Elsevier Inc. All rights reserved.)

The prevalence of obesity has increased globally over the last 2 decades. Although the body mass index has been a convenient and simple index of obesity at the population level, studies have shown that obesity defined by body mass index alone is a remarkably heterogeneous condition with varying cardiovascular and metabolic manifestations across individuals. Adipose tissue is an exquisitely active metabolic organ engaged in cross-talk between various systems; perturbation of adipose tissue results in a pathological response to positive caloric balance in susceptible individuals that directly and indirectly contributes to cardiovascular and metabolic disease. Inadequate subcutaneous adipose tissue expansion in the face of dietary triglycerides leads to visceral and ectopic fat deposition, inflammatory/adipokine dysregulation, and insulin resistance. Conversely, preferential fat storage in the lower body depot may act as a metabolic buffer and protect other tissues from lipotoxicity caused by lipid overflow and ectopic fat. Translational, epidemiological, and clinical studies over the past 30 years have clearly demonstrated a strong link between visceral and ectopic fat and the development of a clinical syndrome characterized by atherogenic dyslipidemia, hyperinsulinemia/glucose intolerance, hypertension, atherosclerosis, and adverse cardiac remodeling/heart failure. This relationship is even more nuanced when clinical entities such as metabolically healthy obesity phenotype and the obesity paradox are considered. Although it is clear that the accumulation of visceral/ectopic fat is a major contributor to cardiovascular and metabolic risk above and beyond the body mass index, implementation of fat distribution assessment into clinical practice remains a challenge. Anthropometric indexes of obesity are easily implemented, but newer imaging-based methods offer improved sensitivity and specificity for measuring specific depots. Lifestyle, pharmacological, and surgical interventions allow a multidisciplinary approach to overweight/obesity that may improve outcomes and align with a public health message to combat the growing epidemic of obesity worldwide and to build healthier lives free of cardiovascular diseases., (© 2018 American Heart Association, Inc.)

The aim of this study was to evaluate the impact of a non-restrictive satiating diet in men displaying various degrees of satiety efficiency. In all, sixty-nine obese men aged 41·5 (sd 5·7) years were randomly assigned to a control (10-15, 55-60 and 30 % energy as protein, carbohydrate and lipid, respectively; n 34) or satiating (20-25, 45-50 and 30-35 % energy as protein, carbohydrate and lipid, respectively; n 35) diet for 16 weeks, and were classified as having a low (LSP) or high (HSP) satiety phenotype. Both diets were consumed ad libitum. Changes in body weight, BMI, percent fat mass, waist circumference, satiety responsiveness and eating behaviour traits were assessed following the intervention. Dropout rates were higher in the control diet (44·1 %) compared with the satiating diet (8·6 %). Decreases in body weight, BMI and waist circumference were significant in both groups, yet HSP individuals lost more body weight than LSP individuals (P=0·048). Decreases in % fat mass were greater in the satiating diet (LSP: -2·1 (sd 2·1) %; P<0·01 and HSP: -3·0 (sd 2·5) %; P<0·001) compared with the control diet (LSP: -1·1 (sd 2·5) % and HSP: -1·3 (sd 2·6) %) (P=0·034). Satiety responsiveness was markedly improved in the satiating diet, whereas no significant changes were observed in the control group. Changes in dietary restraint (+3·3 (sd 2·9) to +7·2 (sd 5·5)), flexible control (+0·9 (sd 1·4) to +2·3 (sd 2·7)), rigid control (+2·2 (sd 1·5) to +2·5 (sd 2·8)), disinhibition (-2·8 (sd 3·7) to -3·2 (sd 2·6)) and susceptibility to hunger (-2·7 (sd 4·1) to -4·6 (sd 3·9)) were similar between the diets. Compared with the control diet, the satiating diet favoured adherence, decreased % fat mass and improved satiety responsiveness in both HSP and LSP individuals.

Excessive fat deposition in obesity has a multifactorial aetiology, but is widely considered the result of disequilibrium between energy intake and expenditure. Despite specific public health policies and individual treatment efforts to combat the obesity epidemic, >2 billion people worldwide are overweight or obese. The central nervous system circuitry, fuel turnover and metabolism as well as adipose tissue homeostasis are important to comprehend excessive weight gain and associated comorbidities. Obesity has a profound impact on quality of life, even in seemingly healthy individuals. Diet, physical activity or exercise and lifestyle changes are the cornerstones of obesity treatment, but medical treatment and bariatric surgery are becoming important. Family history, food environment, cultural preferences, adverse reactions to food, perinatal nutrition, previous or current diseases and physical activity patterns are relevant aspects for the health care professional to consider when treating the individual with obesity. Clinicians and other health care professionals are often ill-equipped to address the important environmental and socioeconomic drivers of the current obesity epidemic. Finally, understanding the epigenetic and genetic factors as well as metabolic pathways that take advantage of 'omics' technologies could play a very relevant part in combating obesity within a precision approach.

Obesity is currently one of the greatest public health issues worldwide. However, despite its known deleterious effects on the cardiovascular system and its association with numerous cardiovascular diseases (CVD), recent findings leading to the development of concepts such as metabolically healthy obesity, the obesity paradox, and protective subcutaneous fat depots have raised a lively debate on the disparate effects of obesity on health outcomes. Regarding the concept of metabolically healthy obesity, by presumably labelling a subset of obese people as metabolically healthy, physicians may not feel pressed to curb the current obesity epidemic and prevent the next generation of people from becoming obese. Another issue is that the most commonly used anthropometric index to define obesity, the body mass index, is at the core of the controversy because of its limitations including its inability to discriminate between fat mass and muscle mass. Many recent epidemiological and metabolic studies have used other indices such as waist-hip ratio, waist circumference, and imaging (computed tomography or magnetic resonance imaging) measurements of visceral adiposity and of ectopic fat depots. In addition, emerging evidence supports the importance of cardiorespiratory fitness, skeletal muscle mass and strength in patients with obesity as useful variables to predict CVD risk beyond adiposity. In this review, we will discuss the complex and disparate effects of obesity on CVD, particularly focusing on whether, under given circumstances, it could be harmful, potentially harmless or neutral, or even possibly protective., (Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2015. For permissions please email: journals.permissions@oup.com.)

Background: Waist circumference (WC) and body mass index (BMI) are clinically used to assess adiposity. The aim of the present study was to evaluate the association of WC with postoperative morbidity and mortality in patients who underwent isolated coronary artery bypass grafting (CABG) in relation to patients' BMI category., Methods: We analyzed the associations of WC and BMI with short-term postoperative outcomes in a cohort of 7446 patients who underwent isolated CABG. We performed univariate and adjusted analyses on main postoperative outcomes after CABG for WC and BMI., Results: Adverse events researched included postoperative mortality, intensive care unit and hospital length of stay, cardiovascular and cerebrovascular events, respiratory complications, infectious, hemostasis complications, and renal complications. WC was independently associated with all postoperative outcomes except prolonged intubation and mortality. Overall, patients in the upper WC quartile in each BMI category were at increased risk of adverse events compared with patients in the lower 3 WC quartiles, with a maximal incremental risk of 1.91 (95% confidence interval, 1.23-2.95) among patients with a BMI ≥ 35. This association was observed for men and women, across all overweight and obesity categories. Neither WC nor BMI was associated with short-term postoperative mortality., Conclusions: In our large cohort of patients who underwent isolated CABG, WC was significantly associated with clinical adverse events, independently of BMI. These findings provide further evidence on the added value of measuring WC as a simple and easy to measure anthropometric marker to refine risk assessment beyond BMI among patients who undergo CABG., (Copyright © 2016 Canadian Cardiovascular Society. Published by Elsevier Inc. All rights reserved.)

Context: Glucose and lipids stimulate the gut-hormones glucagon-like peptide (GLP)-1, GLP-2 and glucose-dependent insulinotropic polypeptide (GIP) but the effect of these on human postprandial lipid metabolism is not fully clarified., Objective: To explore the responses of GLP-1, GLP-2 and GIP after a fat-rich meal compared to the same responses after an oral glucose tolerance test (OGTT) and to investigate possible relationships between incretin response and triglyceride-rich lipoprotein (TRL) response to a fat-rich meal., Design: Glucose, insulin, GLP-1, GLP-2 and GIP were measured after an OGTT and after a fat-rich meal in 65 healthy obese (BMI 26.5-40.2 kg/m(2)) male subjects. Triglycerides (TG), apoB48 and apoB100 in TG-rich lipoproteins (chylomicrons, VLDL1 and VLDL2) were measured after the fat-rich meal., Main Outcome Measures: Postprandial responses (area under the curve, AUC) for glucose, insulin, GLP-1, GLP-2, GIP in plasma, and TG, apoB48 and apoB100 in plasma and TG-rich lipoproteins., Results: The GLP-1, GLP-2 and GIP responses after the fat-rich meal and after the OGTT correlated strongly (r = 0.73, p<0.0001; r = 0.46, p<0.001 and r = 0.69, p<0.001, respectively). Glucose and insulin AUCs were lower, but the AUCs for GLP-1, GLP-2 and GIP were significantly higher after the fat-rich meal than after the OGTT. The peak value for all hormones appeared at 120 minutes after the fat-rich meal, compared to 30 minutes after the OGTT. After the fat-rich meal, the AUCs for GLP-1, GLP-2 and GIP correlated significantly with plasma TG- and apoB48 AUCs but the contribution was very modest., Conclusions: In obese males, GLP-1, GLP-2 and GIP responses to a fat-rich meal are greater than following an OGTT. However, the most important explanatory variable for postprandial TG excursion was fasting triglycerides. The contribution of endogenous GLP-1, GLP-2 and GIP to explaining the variance in postprandial TG excursion was minor.

Although obesity is generally perceived as causing prejudice to heart health, there is considerable individual metabolic heterogeneity among equally overweight or obese individuals. Such heterogeneity suggests that several factors can modulate health risk at any given body weight. In the present article, the thesis that weight loss and achieving a healthy body weight through caloric restriction might not represent optimal clinical and public health messages to combat the current obesity epidemic is defended. Rather, it is proposed that reducing waist circumference and increasing cardiorespiratory fitness through improving nutritional quality, reducing sedentary behaviours, and increasing participation to physical activity/exercise might be associated with clinical benefits, sometimes even in the absence of weight loss., (Copyright © 2015 Canadian Cardiovascular Society. Published by Elsevier Inc. All rights reserved.)

Health authorities worldwide recommend weight loss as a primary endpoint for effective obesity management. Despite a growing public awareness of the importance of weight loss and the spending of billions of dollars by Americans in attempts to lose weight, obesity prevalence continues to rise. In this report we argue that effective obesity management in today's environment will require a shift in focus from weight loss as the primary endpoint, to improvements in the causal behaviors; diet and exercise/physical activity (PA). We reason that increases in PA combined with a balanced diet are associated with improvement in many of the intermediate risk factors including cardiorespiratory fitness (CRF) associated with obesity despite minimal or no weight loss. Consistent with this notion, we suggest that a focus on healthy behaviors for the prevention of additional weight gain may be an effective way of managing obesity in the short term., (Copyright © 2014 Elsevier Inc. All rights reserved.)

Worldwide, cardiovascular diseases (CVDs) are a leading cause of mortality. While in many westernized societies there has been a decrease prevalence of smoking and that a special emphasis has been put on the urgency to control the, so called, classical risk factors, it is more and more recognized that there remains a residual risk, which contributes to the development of CVDs. Imaging studies conducted over two decades have highlighted that the accumulation of ectopic visceral fat is associated with a plethora of metabolic dysfunctions, which have complex and intertwined interactions and participate to the development/progression/events of many cardiovascular disorders. The contribution of visceral ectopic fat to the development of coronary artery disease (CAD) is now well established, while in the last several years emerging evidence has pointed out that accumulation of harmful ectopic fat is associated with other cardiovascular disorders such as calcific aortic valve disease (CAVD), atrial fibrillation and left ventricular dysfunction. We review herein the key molecular processes linking the accumulation of ectopic fat to the development of CVDs. We have attempted, whenever possible, to use a translational approach whereby the pathobiology processes are linked to clinical observations.

The prevalence of obesity has increased worldwide and is a source of concern since the negative consequences of obesity start as early as in childhood. The most commonly used anthropometric tool to assess relative weight and classify obesity is the body mass index (BMI); BMI alone shows a U- or a J-shaped association with clinical outcomes and mortality. Such an inverse relationship fuels a controversy in the literature, named the 'obesity paradox', which associates better survival and fewer cardiovascular (CV) events in patients with elevated BMI afflicted with chronic diseases compared to non-obese patients. However, BMI cannot make the distinction between an elevated body weight due to high levels of lean vs. fat body mass. Generally, an excess of body fat (BF) is more frequently associated with metabolic abnormalities than a high level of lean body mass. Another explanation for the paradox is the absence of control for major individual differences in regional BF distribution. Adipose tissue is now considered as a key organ regarding the fate of excess dietary lipids, which may determine whether or not body homeostasis will be maintained (metabolically healthy obesity) or a state of inflammation/insulin resistance will be produced, with deleterious CV consequences. Obesity, particularly visceral obesity, also induces a variety of structural adaptations/alterations in CV structure/function. Adipose tissue can now be considered as an endocrine organ orchestrating crucial interactions with vital organs and tissues such as the brain, the liver, the skeletal muscle, the heart and blood vessels themselves. Thus, the evidence reviewed in this paper suggests that adipose tissue quality/function is as important, if not more so, than its amount in determining the overall health and CV risks of overweight/obesity., (© 2013.)

Background: We evaluated the risk assessment and management patterns employed by primary care physicians in patients at elevated cardiometabolic risk., Methods: Between April 2011 and March 2012, multiple physicians from 9 Primary Care Teams (PCTs) and 88 physicians from traditional nonteam (Solo) practices completed a practice assessment on the management of 2461 patients > 40 years old with no clinical evidence of cardiovascular disease and diagnosed with at least 1 of the following: dyslipidemia, type 2 diabetes mellitus (T2DM), or hypertension., Results: Individuals with dyslipidemia, T2DM, or hypertension tended to have a body mass index ≥ 25 kg/m(2). Waist circumference measurements, obtained for only 392/829 (47.0%) Solo patients, revealed that 88.9% of these individuals were abdominally obese and that at least 52.2% of Solo patients had metabolic syndrome. Cardiovascular risk, determined by the physicians for 83.5% of all patients without T2DM and typically performed using traditional risk engines, was often miscalculated (43.2% PCTs, 58.8% Solo; P = 0.0007). Healthy behavioural modifications were infrequently recommended (< 50%). Pharmacotherapy was widely used (> 70%) but treatment targets were infrequently met. The composite outcome of guideline-recommended low-density lipoprotein cholesterol, glycemic, and blood pressure targets was met by 9.0% and 8.1% of patients managed by PCT and Solo physicians respectively., Conclusions: Obesity and cardiovascular risk were underassessed and the latter often underestimated. Patients were infrequently counselled on the benefits of healthy behavioural changes. A paradigm change in assessing and managing obesity and cardiovascular risk via aggressive lifestyle interventions is warranted in individuals at elevated cardiometabolic risk., (Copyright © 2013 Canadian Cardiovascular Society. Published by Elsevier Inc. All rights reserved.)

Objective: The aim of this study was to examine the effect of brisk walking on cardiometabolic risk profile and on the gene expression (ie, messenger RNA [mRNA] levels) of inflammatory and thrombotic markers in abdominal and femoral subcutaneous adipose tissues (SATs) among sedentary overweight to obese women with different menopause statuses., Methods: Sixteen late premenopausal (mean [SD] age, 49 [3] y; mean [SD] body mass index, 31.9 [3.0] kg/m) and 14 early postmenopausal (53 [2] y; 30.8 [1.9] kg/m) women were involved in a 16-week walking program (three sessions of 45 min/wk at 60% of heart rate reserve). Glucose-insulin homeostasis, lipid-lipoprotein profile, and inflammatory (tumor necrosis factor-α, interleukin-6 [IL-6], and adiponectin) and thrombotic (plasminogen activator inhibitor-1) SAT mRNA and plasma levels were measured before and after the intervention., Results: Glucose area under the curve was reduced in all participants (P = 0.03) after the walking program. Increases in plasma tumor necrosis factor-α were observed in both groups (P = 0.001), whereas increases in plasminogen activator inhibitor-1 levels were found in postmenopausal women only (P = 0.014). However, plasma IL-6 and adiponectin levels remained unchanged after the intervention (0.07 < P < 0.98). Although femoral SAT adiponectin mRNA levels decreased in postmenopausal women only (P = 0.008), abdominal SAT IL-6 mRNA levels were reduced in both groups (P = 0.01)., Conclusions: Taken together, our results show that, despite a reduced abdominal SAT IL-6 expression, brisk walking does not seem to exert a favorable impact on the cardiometabolic risk profile of overweight to obese women, irrespective of their menopause status.

Background: Sedentary behaviour has recently emerged as a unique risk factor for chronic disease morbidity and mortality. One factor that may explain this relationship is visceral adiposity, which is prospectively associated with increased cardiometabolic risk and mortality. The objective of the present study was to determine whether sedentary behaviour was associated with increased accumulation of visceral fat or other deleterious changes in cardiometabolic risk over a 6-year follow-up period among adult participants in the Quebec Family Study., Methods: The current study included 123 men and 153 women between the ages of 18 and 65. Total sedentary time and physical activity were assessed by self-report questionnaire. Cross-sectional areas of visceral and subcutaneous abdominal adipose tissue were assessed using computed tomography. Cardiometabolic biomarkers including fasting insulin, glucose, blood lipids, HOMA-Insulin Resistance, and oral glucose tolerance were also measured. All variables of interest were collected at both baseline and follow-up., Results: After adjustment for age, sex, baseline BMI, physical activity, energy intake, smoking, education, income and menopausal status, baseline sedentary behaviour was not associated with changes in visceral adiposity or any other marker of cardiometabolic risk. In the longitudinal model which adjusted for all studied covariates, every 15-minute increase in sedentary behaviour from baseline to follow-up was associated with a 0.13 cm increase in waist circumference (95% CI = 0.02, 0.25). However, there was no association between changes in sedentary behaviour and changes in visceral adiposity or other markers of cardiometabolic risk., Conclusion: These results suggest that neither baseline sedentary behaviour nor changes in sedentary behaviour are associated with longitudinal changes in visceral adiposity in adult men and women. With the exception of waist circumference, the present study did not find evidence of a relationship between sedentary behaviour and any marker of cardiometabolic risk in this population.

Eating behaviour traits of rigid control and disinhibition have been associated with body weight in both adults and adolescents. Moreover, adults reporting a dieting history have increased levels of unhealthy eating behaviours. Against this background, the present study aimed to examine the relationship between dieting history and eating behaviour traits in adolescents. For the purpose of this research, a total of sixty adolescents (aged 15 (sem 2·4) years) from the Québec Family Study completed the Three-Factor Eating Questionnaire (TFEQ) and a questionnaire regarding eating habits. Self-reported current and past dieting were analysed against eating behaviour traits measured by the TFEQ, including all subscales. As the results revealed, few adolescents reported currently dieting (n 3). Adolescents who reported a dieting history (23·3 %) were older (16·9 v. 14·4 years, P < 0·001), were more likely to be female (78·6 v. 41·3 %, P < 0·05) but did not have a significantly higher BMI z-score (1·5 v. 0·9, P = 0·10), although they were more likely to be either overweight or obese (P < 0·01). After correcting for sex, BMI and age, adolescents who reported a dieting history had higher levels of rigid control and disinhibition (P < 0·05-0·0001) than those reporting no dieting history. A greater proportion of adolescents characterised by high rigid control and high disinhibition were past dieters, compared to those characterised by low levels of both behaviour traits (53 v. 4 %). The study arrived at the following conclusions: as observed in adults, adolescents with a history of dieting present unfavourable eating behaviour traits. These behavioural traits may represent an additional challenge to the long-term regulation of body weight.

Bariatric surgery has gained acceptance as the only treatment with long-term efficacy for severe obesity. Recent publications emphasize the usefulness of bariatric surgery in the reduction of long-term cardiometabolic risk, cardiovascular disease incidence and mortality, and the management of uncontrolled type 2 diabetes (T2DM), an important cardiovascular risk factor in individuals with severe obesity. The present review article offers a brief overview of the literature published over the past several months relevant to cardiometabolic outcomes in bariatric surgery patients. A recent report from the Swedish Obese Subjects (SOS) study specifically reported a reduced incidence of cardiovascular events on long-term prospective follow-up after bariatric surgery. In addition, abundant studies have been recently published on gastric bypass surgery showing high T2DM remission rates as well as improved blood lipids and inflammatory markers after surgery. Sleeve gastrectomy is increasingly performed as a stand-alone operation. Recent reports on this surgery pertaining to cardiometabolic risk showed variable T2DM remission rates that may possibly be explained by age of the patients and duration of T2DM. Available data suggest a possible favorable impact of the surgery on CRP levels and improvements in the blood lipid profile. How sleeve gastrectomy compares to other surgical approaches will require further study. Biliopancreatic diversion with duodenal switch has been reported to offer some of the best long-term weight loss for obese patients. Approximately 9 out of 10 patients treated with this surgical procedure show long-term remission rates of T2DM. Significant improvements in the cardiometabolic risk profile are also observed after BPD-DS; they are especially pronounced regarding dyslipidemia. In conclusion, bariatric procedures improve the cardiometabolic risk profile, a phenomenon that appears to be only partly explained by the magnitude of the weight loss. Significant variations are observed with respect to the type of surgery and patient characteristics. More research is clearly needed on the short and long-term cardiometabolic outcome of obesity surgeries.

Heart rate variability (HRV) is affected by age, hyperglycemia and accumulation of body fat. This study compares the predictive value of four measurements of adiposity/obesity on HRV and investigates the specific role of age, metabolic contributors and degree/distribution of fat in HRV alterations. The sample consisted of 97 non-diabetic and non-medicated men with features of the metabolic syndrome (50±8 years of age, body mass index [BMI] 31±3 kg/m(2), waist circumference [WC] 107±9 cm, triglycerides 2.3±0.7 mmol/L, fasting glucose 6.0±0.5 mmol/L, insulin 156±71 pmol/L; mean±SD). WC, BMI, percent body fat (% fat, from dual energy X-ray absorptiometry) and visceral adipose tissue volume (VAT, from computed tomography) were used as measures of adiposity/obesity. HRV measures were obtained from 24-h, day- and night-time segments of Holter recordings. BMI presented no independent association with HRV. Percentage fat was the strongest obesity index to be associated with HRV: 24-h pNN50, rMSSD, HF and daytime pNN50, rMSSD, HF and LF (-0.27≤std β≤-0.20, P<.05). VAT was associated with 24-h SDNN, LF (std β=-0.25 and -0.20, P<.05, respectively) and daytime SDNN (std β=-0.24, P<.05) while WC was associated with nighttime SDNN and SDANN (std β=0.22 and 0.32, P<.05). In addition, age, fasting glucose, 2-h oral glucose tolerance test and triglycerides presented independent association with HRV. Adiposity/obesity measurements seem to be differently associated with HRV. An approach considering the combination of age, obesity and glucose metabolism factors could be helpful in the global cardiovascular risk management in abdominally obese men., (Copyright © 2012 Elsevier Inc. All rights reserved.)

Excess visceral adipose tissue (VAT) is associated with an increased cardiometabolic risk. The study examined whether changes in cardiometabolic risk markers after a 1-year lifestyle intervention in viscerally obese men were associated with changes in VAT or with changes in subcutaneous abdominal adipose tissue (SAT). The relative contributions of changes in global adiposity vs. changes in cardiorespiratory fitness to changes in VAT were also quantified. One hundred and forty four men were selected on the basis of an increased waist circumference (≥ 90 cm) associated with dyslipidemia (triglycerides ≥ 1.69 and/or high-density lipoprotein (HDL)-cholesterol <1.03 mmol/l); 117 men completed the 1-year intervention which consisted in a healthy eating, physical activity/exercise program. Body weight, body composition, and fat distribution were assessed by anthropometry and dual-energy X-ray absorptiometry (DEXA)/computed tomography. Cardiorespiratory fitness, plasma adipokine/inflammatory markers, fasting lipoprotein-lipid profile, and oral glucose tolerance test (OGTT) were assessed. VAT volume decreased by 26%, cardiorespiratory fitness improved by 20% (P < 0.0001) after 1 year. Plasma adipokine/inflammatory markers, lipids/lipoproteins, and glucose homeostasis were improved. One-year changes in triglyceride (r = 0.29), apolipoprotein B (r = 0.21), 120-min OGTT-glucose (r = 0.27), and fasting insulin (r = 0.27) levels correlated with changes in VAT (all P < 0.05) after adjustment for changes in SAT. Using a multilinear regression model, VAT reduction was independently associated with SAT reduction and with improvement in cardiorespiratory fitness (R(2) = 0.58, P < 0.0001). Therefore, this healthy eating-physical activity/exercise program improved the cardiometabolic risk profile of viscerally obese men in relation to the reduction of VAT. Furthermore, the reduction in VAT was independently related to the reduction in global adiposity and to the improvement in cardiorespiratory fitness.

Objective: Little is known about how visceral adipose tissue (VAT) influences circulating apolipoprotein B (apoB) levels, which reflect atherogenic risk. We have examined the effects of a 1-year lifestyle modification program on plasma apoB levels in viscerally obese men and compared post-intervention levels to those of a reference group of lean healthy men., Methods: Fasting plasma apoB levels were measured in 107 non-diabetic, viscerally obese men, before and after a 1-year lifestyle intervention program aiming at improving nutritional and physical activity/exercise habits., Results: After the intervention, subjects significantly decreased their volume of VAT (Δ = -26 ± 18%, p < 0.0001) measured by computed tomography and significantly, but modestly reduced their fasting apoB levels (Δ = -3 ± 14%, p = 0.04). When compared to the reference group, men in the intervention group still had higher apoB levels suggesting that they did not "normalize" their apoB concentrations to the level of the healthy non-obese reference men. To further explore the relationship between VAT and apoB, men in the intervention group were stratified according to quartiles of VAT achieved after the intervention. Only men of the lowest quartile of VAT (corresponding to 844 ± 42 cm(3), similar to the value of the reference group; 809 ± 52 cm(3) of VAT) showed plasma apoB levels which were similar to those of the reference group (0.98 ± 0.21 vs. 0.99 ± 0.24 g/L, NS, for lowest VAT quartile and reference group, respectively)., Conclusion: These results suggest that, in order to "normalize" apoB levels in response to a lifestyle modification program, viscerally obese dyslipidemic men need to achieve levels of VAT similar to healthy non-obese men., (Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.)

Obesity is the most common cause of secondary hyperlipidemia. Atherogenic dyslipidemia refers to elevated triglycerides, low HDL-cholesterol and small dense LDL associated with visceral obesity and metabolic syndrome. Obesity may also be associated with isolated low HDL-cholesterol or high triglycerides and postprandial hyperlipidemia. While some obese patients have high LDL cholesterol concentrations, obesity has a more pronounced effect on other atherogenic lipids and lipoproteins. Obesity may aggravate familial lipid disorders. Lipid disorders in obesity are responsive to weight loss, pharmacotherapy and weight loss surgery. Statins are the lipid-lowering drug of choice, together with lifestyle change. Hard clinical end point data to support combinations of statins with other drugs is lacking. After weight loss surgery, the absolute risk of cardiovascular disease should be reassessed, but tools to facilitate risk assessment need to be developed.

With the objectives of clarifying the concepts related to "cardiometabolic risk," "metabolic syndrome" and "risk stratification" and presenting practical strategies to identify and reduce cardiovascular risk in multiethnic patient populations, the Cardiometabolic Working Group presents an executive summary of a detailed analysis and position paper that offers a comprehensive and consolidated approach to the identification and management of cardiometabolic risk. The above concepts overlap and relate to the atherogenic process and development of type 2 diabetes. However, there is confusion about what these terms mean and how they can best be used to improve our understanding of cardiovascular disease treatment and prevention. The concepts related to cardiometabolic risk, pathophysiology, and strategies for identification and management (including health behaviours, pharmacotherapy, and surgery) in the multiethnic Canadian population are presented. "Global cardiometabolic risk" is proposed as an umbrella term for a comprehensive list of existing and emerging factors that predict cardiovascular disease and/or type 2 diabetes. Health behaviour interventions (weight loss, physical activity, diet, smoking cessation) in people identified at high cardiometabolic risk are of critical importance given the emerging crisis of obesity and the consequent epidemic of type 2 diabetes. Vascular protective measures (health behaviours for all patients and pharmacotherapy in appropriate patients) are essential to reduce cardiometabolic risk, and there is growing consensus that a multidisciplinary approach is needed to adequately address cardiometabolic risk factors. Health care professionals must also consider ethnicity-related risk factors in order to appropriately evaluate all individuals in their diverse patient populations., (Copyright © 2011 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Objective: To compare two traditional (high dietary lipid intake and non-participation in high-intensity physical exercise, namely the 'Big Two' factors) versus three nontraditional (short sleep duration, high disinhibition eating behavior, and low dietary calcium intake) risk factors as predictors of excess body weight and overweight/obesity development., Method: Adult participants aged 18-64 years of the Quebec Family Study were selected for cross-sectional (n = 537) and longitudinal (n = 283; 6-year follow-up period) analyses. The main outcome measure was overweight/obesity, defined as a BMI ≥ 25 kg/m(2)., Results: We observed that both the prevalence and incidence of overweight/obesity was best predicted by a combination of risk factors. However, short sleep duration, high disinhibition eating behavior and low dietary calcium intake seemed to contribute more to the risk of overweight and obesity than high dietary lipid intake and non-participation in high-intensity physical exercise. Globally, the risk of being overweight or obese was two-fold higher for individuals having the three nontraditional risk factors combined (OR 6.05; 95% CI 4.26-7.88) compared to those reporting a high percentage of lipids in their diet together with no vigorous physical activity in their daily schedule (OR 2.95; 95% CI 2.18-3.73). Furthermore, the risk of overweight/obesity was also higher for the combination of any two of the nontraditional risk factors than for the combination of the 'Big Two' factors., Conclusion: These results are concordant with previous reports showing that obesity is a multifactorial condition, and emphasize the importance of looking beyond reported measures of the 'Big Two' factors., (Copyright © 2010 S. Karger AG, Basel.)

Obesity is a major health challenge facing the modern world. Some evidence points to obesity itself as the main driver of premature mortality. We propose that this view is oversimplified. For example, high levels of physical activity and cardiorespiratory fitness are associated with lower mortality, even in those who are overweight or obese. To address this issue, we combine epidemiological and physiological evidence in a new paradigm that integrates excess calorie intake, sedentary behavior, and a maladaptive response to stress. Human physiology is optimized to allow large distances to be covered on foot every day in order to find enough food to sustain brain metabolism. Furthermore, when the body is immobilized by an injury, it triggers efficient life-saving metabolic and inflammatory responses. Both these critical adaptations are, however, confounded by a sedentary lifestyle. The implications of these issues for clinical trial design and epidemiologic data analysis are discussed in this article.

Objective: We examined the obesity phenotype most strongly associated with increased plasma concentrations of sTNFR2, and compared which of the two markers, TNF-alpha or sTNFR2, better predicts indices of plasma glucose-insulin homeostasis., Design, Patients and Measurements: Plasma sTNFR2 levels were measured in a sample of 287 healthy nondiabetic men [age: 43.9 +/- 8.0 years (mean +/- SD)], covering a wide range of adiposity values (BMI: 29.0 +/- 4.4 kg/m(2); waist girth: 100.0 +/- 11.7 cm)., Results: Plasma sTNFR2 levels correlated positively and significantly with BMI (r = 0.36; P < 0.0001), fat mass (r = 0.42; P < 0.0001), waist girth (r = 0.38; P < 0.0001) as well as with visceral (r = 0.37; P < 0.0001) and subcutaneous adipose tissue (AT) (r = 0.40; P < 0.0001) areas measured by computed tomography. Two subgroups (n = 27 in each group) of overweight men (BMI >or=25 kg/m(2)) were individually matched for similar BMI values, but with markedly different levels of visceral AT (< or >or=130 cm(2)) and then compared with a control group of 46 lean subjects (with both BMI <25 kg/m(2) and visceral AT <130 cm(2)). This analysis revealed that men characterized by high levels of visceral AT had significantly higher concentrations of sTNFR2 compared with obese men with low visceral AT (1861 +/- 457 pg/ml vs. 1722 +/- 400; P < 0.05) and with lean controls (1570 +/- 291 pg/ml; P < 0.001). Whereas subjects classified across tertiles of TNF-alpha levels showed no difference in glucose tolerance and insulin levels, subjects in the upper tertile of plasma sTNFR2 levels were characterized with the highest plasma insulin concentrations during the OGTT and had the highest area under the curve of insulin concentrations., Conclusions: These results indicate that sTNFR2 levels are more closely related to abdominal AT accumulation than to total adiposity. Furthermore, plasma concentrations of sTNFR2 are independently related to plasma glucose-insulin homeostasis beyond the known contribution of visceral adiposity.

Objective: To investigate the effect of exercise training on markers of the lipoprotein-lipid profile and inflammatory markers in post-menopausal overweight/obese women with a moderately elevated systolic blood pressure., Methods: A total of 267 women [mean body mass index (BMI)=32.0+/-5.7kg/m(2) and mean age=57.3+/-6.6 years] underwent a 6-month exercise intervention program. Exercise training was performed 3-4 times per week at a targeted heart rate corresponding to 50% of the maximal oxygen consumption., Results: Compared to baseline values, mean change in relative VO(2) max (the primary endpoint) was of 1.18+/-2.25mL/minkg (p<0.0001), mean weight loss was of 1.4+/-3.3kg (p<0.0001), mean reduction in waist circumference was of 2.4+/-6.9cm (p<0.0001) and systolic blood pressure did not change significantly (-1.2+/-13.0mmHg, NS). No changes were observed in markers of the lipoprotein-lipid profile. No changes were observed for plasma levels of C-reactive protein, interleukin-6, tumor-necrosis factor-alpha and adiponectin. Changes in VO(2) max were negatively associated with changes in body weight (r=-0.26, p<0.0001) and waist circumference (r=-0.16, p=0.01), but not with changes in cardiometabolic risk markers., Conclusion: Although exercise training significantly increased cardiorespiratory fitness in these sedentary, but metabolically healthy obese/overweight women with a moderately elevated systolic blood pressure, no significant improvements were observed in their cardiometabolic risk profile.

When compared with other modifiable cardiovascular risk factors, such as hypertension, dyslipidemia and smoking, obesity remains a surprisingly puzzling condition to prevent and treat. The history of the development of anti-obesity drugs has known more defeats than even partial victories. With very few drugs on the market, and bad publicity related to adverse events, obesity remains an almost completely unmet challenge for the pharmaceutical industry. In light of past experience with endocannabinoid-system antagonists, such as rimonabant, we propose that a major paradigm shift in clinical practice might be necessary to justify the use of pharmacotherapy for obesity. Furthermore, we suggest that the criteria currently used by regulatory authorities to evaluate and approve anti-obesity drugs should be rigorously re-examined. Finally, we discuss how pharmacological approaches that aim to counteract overactivity of the endocannabinoid system should be revisited in the future to treat visceral (intra-abdominal) obesity and its metabolic consequences.

The aim of this study was to determine the independent contribution of previously reported risk factors for adult overweight and obesity. A cross-sectional (n=537) and a longitudinal (n=283; 6-year follow-up period) analysis was performed for nine risk factors for overweight and obesity assessed in adult participants (aged 18-64 years) of the Quebec Family Study (QFS). The main outcome measure was overweight/obesity, defined as a BMI>or=25 kg/m2. Using logistic regression analysis adjusted for age, sex, and socioeconomic status, short sleep duration, high disinhibition eating behavior, low dietary calcium intake, high susceptibility to hunger behavior, nonparticipation in high-intensity physical exercise, high dietary restraint behavior, nonconsumption of multivitamin and dietary supplements, high dietary lipid intake, and high alcohol intake were all significantly associated with overweight and obesity in the cross-sectional sample. The analysis of covariance adjusted for age, socioeconomic status, and all other risk factors revealed that only individuals characterized by short sleep duration, high disinhibition eating behavior, and low dietary calcium intake had significantly higher BMI compared to the reference category in both sexes. Over the 6-year follow-up period, short-duration sleepers, low calcium consumers, and those with a high disinhibition and restraint eating behavior score were significantly more likely to gain weight and develop obesity. These results show that excess body weight or weight gain results from a number of obesogenic behaviors that have received considerable attention over the past decade. They also indicate that the four factors, which have the best predictive potential of variations in BMI, be it in a cross-sectional or a longitudinal analytical design, do not have a "caloric value" per se.

Background: The ratio of limb fat to trunk fat (LF/TF) is associated with markers of cardiometabolic risk in elderly men and women. It is unknown if LF/TF is associated with cardiometabolic risk beyond that explained by LF and TF independently., Methods: Participants included abdominally obese men (n = 58) and women (n = 78) between 60 and 80 years of age. Regional adiposity was quantified using magnetic resonance imaging. Insulin resistance, fasting glucose, high-density lipoprotein (HDL) cholesterol, plasma triglycerides, and adiponectin were determined using standard procedures., Results: After control for potential confounders, TF was positively associated with fasting glucose, insulin resistance, and plasma triglycerides and negatively associated with HDL cholesterol and adiponectin (p < or = .05). These associations were strengthened after further control for LF (p < .05), with the exception of adiponectin in men (p > .05). After control for potential confounders, LF was negatively associated with adiponectin in men (p < .05) but not with any other marker of cardiometabolic risk (p > .05). After further control for TF, LF was negatively associated with plasma triglycerides and positively associated with HDL cholesterol in both genders combined (p < .05) and with adiponectin in women (p < .05) but not in men (p > .05). LF/TF was not associated with any marker of cardiometabolic risk after control for LF and TF., Conclusion: These results suggest that it is the absolute, rather than relative, amounts of LF and TF that have the greatest influence on cardiometabolic risk in elderly men and women.

Objective: To assess the impact of a weight management program on metabolic health of second-generation antipsychotic (SGA)-treated patients., Methods: A prospective 12-week intervention program including individual exercise training and nutritional group sessions was performed as a pilot study. An intervention group of 6 SGA-treated patients (5 men and 1 woman; mean 15.0, SD 11.8 months) was compared with 10 reference patients under SGAs (8 men and 2 women; mean 14.0, SD 14.2 months), presenting similar age and baseline weekly levels of physical activity. For patients of both groups, anthropometric measurements and basic fasting lipid profile were assessed. For patients in the intervention group, an adapted Rockport Test was performed to evaluate their aerobic fitness and compliance to training sessions, and was recorded., Results: After the 12-week period, reference patients significantly gained weight (P = 0.001), whereas intervention patients showed significant weight loss and decreased body mass index (P = 0.02); interaction between groups: P < 0.01. This weight loss was accompanied by a decreased cholesterol-high-density lipoprotein cholesterol ratio (P = 0.04). Overall, the intervention patients' adherence to exercise prescription was 95.1 %, and this adherence induced a significant improvement of their aerobic fitness (P = 0.05)., Conclusion: This pilot study suggests that patients under SGAs may benefit from a weight management program and improve their metabolic health, as well as their aerobic fitness.

Background: Rimonabant, the first selective cannabinoid type 1 (CB1) receptor antagonist, improves cardiometabolic risk factors in overweight/obese patients. ADAGIO-Lipids assessed the effect of rimonabant on cardiometabolic risk factors and intraabdominal and liver fat., Methods and Results: 803 abdominally obese patients with atherogenic dyslipidemia (increased triglycerides [TG] or reduced high-density lipoprotein-cholesterol [HDL-C]) were randomized to placebo or rimonabant 20 mg/d for 1 year. HDL-C and TG were coprimary end points. Intraabdominal (visceral) and liver fat were measured by computed tomography in a subgroup of 231 patients. In total, 73% of rimonabant- and 70% of placebo-treated patients completed the study treatment. Rimonabant 20 mg produced significantly greater changes from baseline versus placebo in HDL-C (+7.4%) and TG levels (-18%; P<0.0001), as well as low-density lipoprotein (LDL) and HDL particle sizes, apolipoprotein A1 and B, HDL2, HDL3, C-reactive protein, and adiponectin levels (all P<0.05). Rimonabant decreased abdominal subcutaneous adipose tissue (AT) cross-sectional area by 5.1% compared to placebo (P<0.005), with a greater reduction in visceral AT (-10.1% compared to placebo; P<0.0005), thereby reducing the ratio of visceral/subcutaneous AT (P<0.05). Rimonabant significantly reduced liver fat content (liver/spleen attenuation ratio; P<0.005). Systolic (-3.3 mm Hg) and diastolic (-2.4 mm Hg) blood pressure were significantly reduced with rimonabant versus placebo (P<0.0001). The safety profile of rimonabant was consistent with previous studies; gastrointestinal, nervous system, psychiatric, and general adverse events were more common with rimonabant 20 mg., Conclusions: In abdominally obese patients with atherogenic dyslipidemia, rimonabant 20 mg significantly improved multiple cardiometabolic risk markers and induced significant reductions in both intraabdominal and liver fat.

Global risk calculators such as the Framingham risk score generally take into account traditional risk factors such as age, sex, blood pressure, smoking status, total cholesterol and high-density lipoprotein cholesterol levels, and the presence of diabetes which are recommended to be used in clinical practice to estimate patients' cardiovascular disease (CVD) risk. Over the last decades, the prevalence of obesity has dramatically increased all over the world. The deleterious form of obesity, visceral obesity, is the most prevalent form of the so-called metabolic syndrome, a constellation of risk factors associated with perturbations of the lipoprotein-lipid profile and of the plasma glucose-insulin homeostasis also likely to be associated with increased blood pressure and a proinflammatory and prothrombotic state. To this date, metabolic syndrome is still in need of a place in global CVD risk prediction. As the metabolic syndrome is not likely to replace currently used global risk scoring algorithms, both traditional risk factors and emerging metabolic markers associated with the metabolic syndrome should be incorporated in future risk scoring systems to be developed in order to adapt CVD risk prediction tools to the epidemic of obesity which has direct consequences on the daily life of health professionals., (Copyright 2008 S. Karger AG, Basel.)

Cardiovascular disease (CVD) is a leading cause of morbidity and death in many countries worldwide. With the help of epidemiological, metabolic and clinical studies conducted over the past decades, the key factors contributing to the development of CVD have been identified. In this regard, several modifiable (hypertension, smoking, elevated cholesterol or low-density lipoprotein-cholesterol concentrations, reduced levels of high-density lipoprotein-cholesterol, type 2 diabetes) and nonmodifiable (age, sex, genetic predisposition) CVD risk factors have been recognized. Although better acute care and chronic pharmacological management have contributed to reduce CVD mortality, CVD morbidity remains very high. It has been proposed that this situation could be the consequence of the evolving landscape of CVD risk factors, which include, among others, poor nutritional habits and a reduction in physical activity contributing to the epidemic of obesity sweeping the world. However, obesity is heterogeneous both in terms of its etiology and its metabolic complications. Body fat distribution, especially visceral adipose tissue accumulation, has been found to be a major correlate of a cluster of diabetogenic and atherogenic abnormalities that has been described as the metabolic syndrome. The importance of abdominal obesity in association with the development of CVD and type 2 diabetes has been recognized in several studies, beyond the contribution of overall obesity. Additional evidence also suggests that the CVD risk related to the hyperglycemic state observed in subjects with the metabolic syndrome or type 2 diabetes is largely explained by the high prevalence of the metabolic complications of abdominal obesity. Although the presence of the metabolic syndrome clearly increases CVD risk, its clinical diagnosis is not sufficient to classify a patient at high risk for a cardiovascular event because attention must also be paid to the presence of traditional risk factors in the calculation of global CVD risk. The additional information provided by the metabolic syndrome to the risk attributed to traditional risk factors in the calculation of global CVD risk has been defined as global cardiometabolic risk. The fight against abdominal obesity as a major cause of CVD morbidity and mortality will require major societal changes and the involvement of dieticians, kinesiologists and behaviour modification specialists in clinical practice to reshape our physical activity and dietary habits. Finally, the early prevention of overweight/obesity/abdominal obesity in children, starting as early as conception, and the identification of key drivers of unhealthy nutritional and sedentary behaviours are the cornerstone of a successful comprehensive plan to fight CVD morbidity.