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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. [ABSTRACT FROM AUTHOR]

Whether or not there is a form of healthy obesity remains controversial. Contemporary imaging techniques might help answer this question. It is proposed that low levels of visceral adipose tissue and ectopic adipose tissue combined with a preferential accumulation of gluteal and femoral adipose tissue might define a 'super healthy obesity' phenotype. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Fibrinogen has been prospectively found to correlate with coronary heart disease (CHD) but a similar association has not been well established for lipoprotein (a) (Lp(a)). Plasma lipids, Lp(a), and fibrinogen levels were measured in 2,125 men (aged 47 to 76 years) who were free of clinical CHD. During a 5-year follow-up period, 116 first CHD events were documented. Men with CHD were older, smoked more, had a higher prevalence of diabetes, and higher levels of systolic blood pressure, cholesterol, low-density lipoprotein cholesterol, Lp(a), and fibrinogen, and lower plasma high-density lipoprotein cholesterol levels. Only fibrinogen levels in the upper tertile of the distribution compared with the lower tertiles were associated with a significant risk of CHD (adjusted risk ratio 2.5; 95% confidence interval [CI] 1.4 to 4.2; p = 0.0010). Such an association was not observed with Lp(a). To assess a possible relation between fibrinogen and Lp(a) to the risk of CHD events, men were assigned to 1 of 4 groups according to fibrinogen median levels and a Lp(a) cut-off level of 300 mg/L: group 1: fibrinogen <4.05 g/L and Lp(a) <300 mg/L; group 2: fibrinogen <4.05 g/L and Lp(a) ≥300 mg/L; group 3: fibrinogen ≥4.05 g/L and Lp(a) <300 mg/L; and group 4: fibrinogen ≥4.05 g/L and Lp(a) ≥300 mg/L. Using group 1 as a reference, a significant risk ratio was only documented in group 4 (2.5; 95% CI 1.2 to 5.1; p = 0.0132). In this population, high fibrinogen levels associated with high Lp(a) levels significantly increased the risk of CHD. [Copyright &y& Elsevier]

COVID-19 has been described as a syndemic of COVID-19 and chronic diseases. Obesity has been identified as a contributing factor to morbidity and mortality associated with COVID-19; however, sedentary behaviours and lack of physical activity should also be targeted by health authorities to reduce the risk of severe COVID-19 outcomes. [ABSTRACT FROM AUTHOR]

In 1994, we reported in The American Journal of Cardiology that a simple anthropometric measurement, waist circumference, was related to the amount of abdominal visceral adipose tissue measured by computed tomography. An elevated waist circumference was also found to be associated with several features of the cardiometabolic risk profile such as glucose intolerance, hyperinsulinemia, and an atherogenic dyslipidemic profile that included hypertriglyceridemia and reduced high-density lipoprotein cholesterol levels. Although a linear relation was found between waist circumference and these metabolic alterations, we reported that a waist circumference value of about 100 cm was associated with a high probability of finding diabetogenic and atherogenic abnormalities. The present short report provides a brief update of issues that have been raised regarding the measurement of waist circumference and its clinical use over a period of 20 years since the original publication. [ABSTRACT FROM AUTHOR]

Abstract: Adipose tissue, which has been considered mainly as a site of energy storage and mobilization, is found in many depots throughout the body. Adipose depots may have structural properties such as, for instance, the fat pads located in the hands and feet and the periorbital fat supporting the eyes. Adipose tissue also shows remarkable regional heterogeneity. For instance, substantial differences have been reported in the metabolic properties of visceral (intra-abdominal) vs. subcutaneous adipose depots. Visceral adipose tissue (VAT) has active endocrine and paracrine functions with the secretion of various pro-inflammatory chemokines potentially contributing to the progression of atherosclerosis related with obesity. In addition, adipose depots surrounding the heart, such as epicardial (EAT) and perivascular adipose tissues (PAT) may also exert important roles in the pathogenesis of cardiovascular disease beyond the contribution of VAT due to their close anatomic relationships with vascular structures and myocardium. The purpose of the present review is to outline the current understanding of the pathophysiological links between EAT, PAT and atherosclerotic cardiovascular disease. Also, we discuss the current investigative methods for PAT quantification and discuss the potential impact of PAT on cardiovascular risk prediction. Finally, potential clinical implications of these notions are discussed. [Copyright &y& Elsevier]

Excess intra- abdominal adipose tissue accumulation, often termed visceral obesity, is part of a phenotype including dysfunctional subcutaneous adipose tissue expansion and ectopic triglyceride storage closely related to clustering cardiometabolic risk factors. Hypertriglyceridemia; increased free fatty acid availability; adipose tissue release of proinflammatory cytokines; liver insulin resistance and inflammation; increased liver VLDL synthesis and secretion; reduced clearance of triglyceride-rich lipoproteins; presence of small, dense LDL particles; and reduced HDL cholesterol levels are among the many metabolic alterations closely related to this condition. Age, gender, genetics, and ethnicity are broad etiological factors contributing to variation in visceral adipose tissue accumulation. Specific mechanisms responsible for proportionally increased visceral fat storage when facing positive energy balance and weight gain may involve sex hormones, local cortisol production in abdominal adipose tissues, endocannabinoids, growth hormone, and dietary fructose. Physiological characteristics of abdominal adipose tissues such as adipocyte size and number, lipolytic responsiveness, lipid storage capacity, and inflammatory cytokine production are significant correlates and even possible determinants of the increased cardiometabolic risk associated with visceral obesity. Thiazolidinediones, estrogen replacement in postmenopausal women, and testosterone replacement in androgen-deficient men have been shown to favorably modulate body fat distribution and cardiometabolic risk to various degrees. However, some of these therapies must now be considered in the context of their serious side effects. Lifestyle interventions leading to weight loss generally induce preferential mobilization of visceral fat. In clinical practice, measuring waist circumference in addition to the body mass index could be helpful for the identification and management of a subgroup of overweight or obese patients at high cardiometabolic risk. [ABSTRACT FROM AUTHOR]

The article focuses on the risks of cardiovascular diseases due to accumulation of body fat. It mentions the decreased mortality rate through coronary heart diseases due to proper focus on the risk factors including smoking, hypertension and high cholesterol level. It discusses the harmful effects of obesity causing several health problems.

The global prevalence of obesity is increasing at a rapid pace and is likely to have an impact on the prevalence of Type 2 diabetes and cardiovascular disease (CVD). Identifying individuals carrying a high-risk obesity phenotype, such as those patients with an accumulation of visceral or intra-abdominal fat, goes beyond the assessment of the BMI and even waist circumference. An increasing amount of population-based studies have shown that the hypertriglyceridemic waist phenotype (the combination of an elevated waist girth and triglyceride levels) could identify individuals with increased amounts of visceral fat that are characterized by a concomitant deteriorated cardiometabolic risk profile and prospectively, with an increased risk of developing both Type 2 diabetes and CVD. Our objective is to review the evidence on the relationship between the hypertriglyceridemic waist phenotype and the risk of CVD and Type 2 diabetes as well as to discuss how to identify and manage individuals who have this high-risk obesity phenotype. [ABSTRACT FROM AUTHOR]

The article examines the epidemiology of obesity and its related co-morbidities. The methods available for assessing adiposity in adults, and some of the challenges and issues associated with assessing adiposity, are discussed. It also provides recommendations for the clinician in practice, with an aim of identifying more at-risk overweight/obese individuals.

Background Although the total to high-density lipoprotein cholesterol ratio (TC ⁄ HDL-C) has been used for decades to identify individuals at risk for coronary heart disease (CHD), apolipoprotein-based (apolipoprotein B⁄ apolipoprotein A-I [apoB ⁄ apoA-I]) and nuclear magnetic resonance spectroscopy (NMR)-based lipoprotein concentrations (low-density lipoproteinNMR ⁄ high-density lipoproteinNMR [LDLNMR ⁄HDLNMR]) may also be useful for CHD risk stratification. Materials and methods In a case–control study conducted within the European Prospective Investigation into Cancer and Nutrition (EPIC)-Norfolk study population, 870 individuals who developed CHD during a 6-year follow-up were matched to 1659 controls on the basis of gender, age and enrolment time. LDLNMR and HDLNMR were measured by proton NMR spectroscopy. Results After adjusting for traditional CHD risk factors, men in the top quintile of the various lipoprotein ratios proved to be at increased CHD risk (OR = 2Æ59 [95% IC, 1Æ76–3Æ83] for TC ⁄ HDL-C ratio, 2Æ59 [1Æ75–3Æ83] for apo- B⁄ apoA-I ratio and 2Æ78 [1Æ86–4Æ17] for LDLNMR ⁄HDLNMR ratio) compared with men in the bottom quintile. Similar associations were observed in women (OR = 2Æ86 [1Æ71–4Æ80] for TC ⁄ HDL-C ratio, 2Æ94 [1Æ74–4Æ97] for apoB ⁄ apoA-I ratio and 2Æ03 [1Æ21–3Æ43] for LDLNMR ⁄HDLNMR ratio). Compared with participants with only one component of the metabolic syndrome, those who had five had an increased TC ⁄ HDL-C ratio (73Æ0% and 80Æ4% in men and women respectively), apoB ⁄ apoA-I ratio (58Æ0% and 62Æ9% in men and women respectively) and for LDLNMR ⁄HDLNMR ratio (52Æ6% and 54Æ1% in men and women respectively). Conclusion In this European study population, the TC ⁄ HDL-C, apoB ⁄ apoA-I and LDLNMR ⁄HDLNMR ratios were similarly associated with components of the metabolic syndrome and CHD risk. [ABSTRACT FROM AUTHOR]

Abstract: Objective: To examine the long-term relationship between sleep duration and type 2 diabetes or impaired glucose tolerance (IGT). Methods: Body composition measurements and self-reported sleep duration were determined in a longitudinal sample of 276 individuals aged 21 to 64 years followed for a mean of 6 years. Risk factors of type 2 diabetes/IGT over the follow-up were determined and relative risks (RRs) calculated for the development of type 2 diabetes/IGT by sleep duration group. Results: Independent risk factors of type 2 diabetes/IGT over the follow-up included age, obesity, sleep duration, and glucose/insulin homeostasis indicators. Using adults with 7-8h of sleep as a reference, the adjusted RR for the development of type 2 diabetes/IGT was 2.78 (1.61-4.12) for those with ⩽6h of sleep and 2.54 (1.42-3.53) for those with ⩾9h of sleep. These elevated RRs remained significant after adjustment for body mass index, waist circumference or percent body fat. Conclusion: Short and long sleeping times are associated with a higher risk of developing type 2 diabetes/IGT, independent of several covariates. These results suggest that sleep duration may represent a novel risk factor for type 2 diabetes/IGT. [Copyright &y& Elsevier]

Adipose tissue synthesizes and secretes a wide range of biologically active molecules considered as inflammatory markers whose dysregulation in obesity plays a role in the development of insulin resistance and vascular disorders. Thus, finding genes that influence circulating levels of inflammatory biomarkers may provide insights into the genetic determinants of obesity-related metabolic diseases. We performed linkage analyses for fasting plasma levels of adiponectin, C-reactive protein (CRP), interleukin-6 (IL-6) and tumor-necrosis factor-alpha (TNF-α) in 764 subjects enrolled in the Quebec family study (QFS). A maximum of 393 pairs of siblings from 211 nuclear families were available for analyses. A total of 443 markers spanning the 22 autosomal chromosomes with an average inter-marker distance of 6.24 Mb were genotyped. Linkage was tested using both allele-sharing (SIBPAL) and variance component linkage methods (MERLIN). We showed suggestive evidence of linkage for plasma adiponectin levels on chromosome 15q21.1 [D15S659; logarithm of the odds (LOD) score = 2.23], 3q13.33 (D3S3023; LOD = 2.09), 20q13.2 (D20S197; LOD = 1.96) and 14q32.2 (D14S1426; LOD = 1.79). Evidence of linkage (SIBPAL) was also found for CRP on 12p11.23 ( P = 0.001) and 12q15 ( P = 0.0005) and for IL-6 on 14q12 ( P = 0.002). None of these linkages remained significant after adjustment for body mass index. No evidence of linkage was found for TNF-α plasma levels. These results suggest that several QTLs can influence plasma levels of adiponectin and CRP, partly via their effects on adiposity. [ABSTRACT FROM AUTHOR]

Abstract: Cholesterol ester transfer protein (CETP) plays a key role in remodeling triglyceride-rich particles and high-density lipoproteins (HDL). We investigated CETP sequence variants in response to long-term overfeeding (100 days) in 12 pairs of male monozygotic twins (mean age±S.D.: 21±2 years). Body fat mass (FM), abdominal subcutaneous (ASF) and visceral fat (AVF), and plasma lipoproteins were determined. The CETP variants C>T/In9 (rs289714) and G>A/Ex14 (rs5882, or I405V) were investigated by RFLP-PCR methodologies. Before overfeeding, the CETP CC/In9 (n =18) genotype was associated with lower FM compared to the C>T/In9 heterozygotes. Overfeeding induced more FM and ASF accretion in C>T/In9 carriers (P ≤0.05). CETP V405V homozygotes (n =8) had lower BMI, FM, and ASF before overfeeding than those with the I405I (n =6) or I405V (n =10) genotypes. However, V405V subjects had the largest gain in AVF with overfeeding (P =0.02). Decreases from baseline were significantly different across the I405V genotypes for HDL-C, HDL-Apo AI, HDL2, and HDL3 (P ≤0.05). Our data suggests that CETP sequence variation contributes to the undesirable changes in adiposity and HDL-C levels when exposed to excessive calorie consumption and may be potentially helpful to identify individuals with the metabolic syndrome who are at higher risk of cardiovascular disease. [Copyright &y& Elsevier]

Metabolic syndrome is associated with abdominal obesity, blood lipid disorders, inflammation, insulin resistance or full-blown diabetes, and increased risk of developing cardiovascular disease. Proposed criteria for identifying patients with metabolic syndrome have contributed greatly to preventive medicine, but the value of metabolic syndrome as a scientific concept remains controversial. The presence of metabolic syndrome alone cannot predict global cardiovascular disease risk. But abdominal obesity — the most prevalent manifestation of metabolic syndrome — is a marker of 'dysfunctional adipose tissue', and is of central importance in clinical diagnosis. Better risk assessment algorithms are needed to quantify diabetes and cardiovascular disease risk on a global scale. [ABSTRACT FROM AUTHOR]

Twelve pairs of male monozygotic (MZ) twins (mean age±S.D.: 21±2 years) were subjected to an overfeeding protocol of 4.2 MJ (1000 kcal) above their pre-established individual daily energy needs, 6 days a week, over a period of 100 days. Body weight increased significantly (gain of 8.1 kg, P<0.001), as did fat mass (5.4 kg, P<0.001) after overfeeding. Plasma triacylglycerol (TG) levels significantly increased (P<0.05) without change in plasma cholesterol (CHOL). Plasma very-low-density-lipoprotein (VLDL)–TG, VLDL–Apoprotein (Apo) B, low-density-lipoprotein cholesterol (LDL-C) and LDL–Apo B (P≤0.05) rose, whereas high-density-lipoprotein cholesterol (HDL-C) levels fell (P<0.05) raising the CHOL/HDL-C ratio (20%) (P<0.001). Considerable individual differences occurred in plasma lipoprotein responses to overfeeding. However, these changes were not random; significant within-pair resemblance registered for the response of plasma CHOL, TG, VLDL–TG, VLDL-C, LDL–TG, HDL-C, HDL–Apo A–I, HDL2-C, HDL3-C to overfeeding (0.48≤ri≤0.85). Furthermore, a high within-pair resemblance was found for changes in ratios of CHOL/HDL-C (ri=0.86, P<0.0001) and HDL2-C/HDL3-C (ri=0.69, P<0.01). These results strongly suggest that the response of plasma lipoproteins to chronic energy surplus has a significant genetic component as does the detrimental effect of chronic caloric affluence on CHD risk. [Copyright &y& Elsevier]

The prevalence of type 2 diabetes has substantially increased in North America largely due to the fact that obesity has reached epidemic proportions in our society. Although obesity increases the likelihood of developing type 2 diabetes, hypertension and coronary heart disease (CHD), not every obese patient is characterized by these complications, emphasizing the fact that obesity is a heterogeneous condition. Evidence reviewed in this short paper supports the notion that body fat distribution, especially visceral adipose tissue accumulation, is a critical correlate of a cluster of diabetogenic, atherogenic, thrombotic and inflammatory metabolic abnormalities. This “dysmetabolic cluster”, referred to as the insulin resistance or metabolic syndrome, is associated with a substantially increased risk of CHD, even in the absence of hyperglycemia or elevated LDL cholesterol concentrations. From a risk assessment standpoint, we have reported that the “hypertriglyceridemic waist” phenotype (waist circumference ≥90 cm combined with triglycerides ≥2.0 mmol/l) was associated with a high likelihood (80%) of finding the cluster of metabolic abnormalities of abdominal obesity. Since waist circumference has been suggested to be a useful index of abdominal visceral obesity and of related metabolic complications, it is suggested that waist girth should be systematically measured in all patients. Finally, it is proposed that until abdominal obesity is identified as a therapeutic target, clinicians will not optimally manage cardiovascular disease risk in abdominally obese patients with type 2 diabetes or the metabolic syndrome. [Copyright &y& Elsevier]

Evaluates data on the effects of fenofibrate on plasma high density lipoprotein cholesterol (HDL-C) levels. Characterization of typical dyslipidemia in patients with type 2 diabetes by moderate hypertriglyceridemia and reduced HDL-C levels; Finding that all fibrates are not equal in their ability to alter HDL-C concentration and composition.

The HERITAGE Family Study: A Review of the Effects of Exercise Training on Cardiometabolic Health, with Insights into Molecular Transducers. Med. Sci. Sports Exerc., Vol. 54, No. 5, pp. S1-S43, 2022. The aim of the HERITAGE Family Study was to investigate individual differences in response to a standardized endurance exercise program, the role of familial aggregation, and the genetics of response levels of cardiorespiratory fitness and cardiovascular disease and diabetes risk factors. Here we summarize the findings and their potential implications for cardiometabolic health and cardiorespiratory fitness. It begins with overviews of background and planning, recruitment, testing and exercise program protocol, quality control measures, and other relevant organizational issues. A summary of findings is then provided on cardiorespiratory fitness, exercise hemodynamics, insulin and glucose metabolism, lipid and lipoprotein profiles, adiposity and abdominal visceral fat, blood levels of steroids and other hormones, markers of oxidative stress, skeletal muscle morphology and metabolic indicators, and resting metabolic rate. These summaries document the extent of the individual differences in response to a standardized and fully monitored endurance exercise program and document the importance of familial aggregation and heritability level for exercise response traits. Findings from genomic markers, muscle gene expression studies, and proteomic and metabolomics explorations are reviewed, along with lessons learned from a bioinformatics-driven analysis pipeline. The new opportunities being pursued in integrative -omics and physiology have extended considerably the expected life of HERITAGE and are being discussed in relation to the original conceptualmodel of the study. [ABSTRACT FROM AUTHOR]

The aim of the HERITAGE Family Study was to investigate individual differences in response to a standardized endurance exercise program, the role of familial aggregation, and the genetics of response levels of cardiorespiratory fitness and cardiovascular disease and diabetes risk factors. Here we summarize the findings and their potential implications for cardiometabolic health and cardiorespiratory fitness. It begins with overviews of background and planning, recruitment, testing and exercise program protocol, quality control measures, and other relevant organizational issues. A summary of findings is then provided on cardiorespiratory fitness, exercise hemodynamics, insulin and glucose metabolism, lipid and lipoprotein profiles, adiposity and abdominal visceral fat, blood levels of steroids and other hormones, markers of oxidative stress, skeletal muscle morphology and metabolic indicators, and resting metabolic rate. These summaries document the extent of the individual differences in response to a standardized and fully monitored endurance exercise program and document the importance of familial aggregation and heritability level for exercise response traits. Findings from genomic markers, muscle gene expression studies, and proteomic and metabolomics explorations are reviewed, along with lessons learned from a bioinformatics-driven analysis pipeline. The new opportunities being pursued in integrative -omics and physiology have extended considerably the expected life of HERITAGE and are being discussed in relation to the original conceptual model of the study. [ABSTRACT FROM AUTHOR]

The Look AHEAD trial did not show that a lifestyle modification programme aimed at weight loss could reduce the incidence of cardiovascular disease events. We attempt to address why this trial was 'negative', and emphasize that further randomized lifestyle modification trials focusing on the effects of physical activity and exercise are needed. [ABSTRACT FROM AUTHOR]

The article discusses several studies published in 2012 which highlighted the role of high-density lipoprotein (HDL) particles and HDL cholesterol in cardiovascular risk. The ILLUMINATE trial has found that torcetrapib, the first cholesteryl ester transfer protein (CETP), was not able to reduce the size of atherosclerotic plaques in imaging trials. Another CETP inhibitor, dalcetrapib, has been found to increase HDL-concentration in the DAL-OUTCOME study.

Studies published in 2012 in the field of HDL research have provided further evidence suggesting that a low HDL-cholesterol level, in the absence of related lipid or nonlipid risk factors, is not associated with increased risk of coronary heart disease. [ABSTRACT FROM AUTHOR]

The article discusses the association of body mass index (BMI), a commonly used anthropometric index of adiposity, with risk for death. Topics discussed include the use of BMI to document the growth in prevalence of overweight and obesity, optimal BMI associated with the lowest risk for death and a research which showed that overweight as defined by a single baseline BMI was not linked with increased risk for death.

Aims: To evaluate the clinical safety, tolerability, and pharmacokinetic and pharmacodynamic profile of the novel cannabinoid receptor‐1 (CB1R) inverse agonist, INV‐202, in adults with features of metabolic syndrome. Materials and Methods: This was a multicentre, randomized, double‐blind, placebo‐controlled, 28‐day repeat‐dose (INV‐202 [25 mg] or placebo, once‐daily oral tablet), parallel‐group study in 37 participants aged 18 to 65 years (46% female, mean age 55 years, glycated haemoglobin 5.7% [39 mmol/mol], body mass index [BMI] 38.1 kg/m2) with features of metabolic syndrome and glucose intolerance. An oral glucose tolerance test (OGTT) was performed at baseline and at the end of the study. Lipid profiles, weight, waist circumference and biomarkers were assessed weekly. Statistical comparisons were performed post hoc. Results: INV‐202 was well tolerated with no serious or severe treatment‐emergent adverse events; the most common events related to known effects of CB1R blockade in the gastrointestinal tract. INV‐202 produced a significant mean weight loss of 3.5 kg (3.3% compared with placebo participants who gained a mean 0.6 kg [0.5%]). INV‐202 also exhibited significant reductions in waist circumference and BMI (P ≤ 0.03). There was no significant difference in OGTT 0‐ to 3‐hour area under the curve for INV‐202 versus placebo: least squares mean 29.38 versus 30.25 h*mmol/L, with an INV‐202: placebo ratio of 97.1% (95% confidence interval 90.2, 105.6; P = 0.43). Conclusions: INV‐202 was well tolerated, producing a signal for rapid weight loss with improvements in other metabolic syndrome markers in this population. These findings support further exploration and long‐term assessment of cardiometabolic effects. [ABSTRACT FROM AUTHOR]

A letter to the editor is presented in response to the article on usefulness of measuring body mass index and waist circumference for the estimation of visceral adiposity and related cardiometabolic risk by J.A. Nazare and others in the 2015 issue and a response from the authors is also presented.

A growing appreciation of the pathophysiological interrelatedness of metabolic risk factors such as obesity and diabetes, chronic kidney disease, and cardiovascular disease has led to the conceptualization of cardiovascular-kidneymetabolic syndrome. The confluence of metabolic risk factors and chronic kidney disease within cardiovascular-kidney-metabolic syndrome is strongly linked to risk for adverse cardiovascular and kidney outcomes. In addition, there are unique management considerations for individuals with established cardiovascular disease and coexisting metabolic risk factors, chronic kidney disease, or both. An extensive body of literature supports our scientific understanding of, and approach to, prevention and management for individuals with cardiovascular-kidney-metabolic syndrome. However, there are critical gaps in knowledge related to cardiovascular-kidney-metabolic syndrome in terms of mechanisms of disease development, heterogeneity within clinical phenotypes, interplay between social determinants of health and biological risk factors, and accurate assessments of disease incidence in the context of competing risks. There are also key limitations in the data supporting the clinical care for cardiovascular-kidney-metabolic syndrome, particularly in terms of early-life prevention, screening for risk factors, interdisciplinary care models, optimal strategies for supporting lifestyle modification and weight loss, targeting of emerging cardioprotective and kidney-protective therapies, management of patients with both cardiovascular disease and chronic kidney disease, and the impact of systematically assessing and addressing social determinants of health. This scientific statement uses a crosswalk of major guidelines, in addition to a review of the scientific literature, to summarize the evidence and fundamental gaps related to the science, screening, prevention, and management of cardiovascular-kidneymetabolic syndrome. [ABSTRACT FROM AUTHOR]

The concept that raising HDL-cholesterol level will uniformly translate into cardiovascular risk reduction has been challenged by genetic epidemiology studies and large-scale, randomized clinical trials. Studies suggest that we should go beyond HDL cholesterol, and consider emerging biomarkers of HDL concentration, composition, and functionality as surrogates for cardiovascular risk reduction. [ABSTRACT FROM AUTHOR]

The article focuses on the results of the Justification for Use of Statins in Prevention: An Intervention Trial Evaluating Rosuvastatin (JUPITER) and the Heart Protection Study (HPS) on the clinical benefits of rosuvastatin in patients with high C-reactive protein (CRP). HPS negates the belief that stratification of patients based on CRP concentrations predicts the relative vascular benefits of simvastatin. A comparison of the patients involved in the study is presented. Also cited is the importance of constructive criticism to CRP.

The authors comment on the study by Ridker and colleagues that examined the benefits of statins in participants in the trial Justification for the Use of Statins in Prevention: An Intervention Trial Evaluating Rosuvastatin (JUPITER). They believe Ridker and colleagues need to put their work into a clinical and public health perspective. They explain that the JUPITER trial results show that better global cardiovascular disease risk assessment is needed.

Purpose: The aim was to compare the anthropometric and metabolic profiles and lifestyle behaviours of yogurt consumers and non-consumers and to determine if the observed differences persisted after adjustment for diet quality and related variables.Methods: Using cross-sectional and follow-up data from the Québec Family Study, men and women were classified into yogurt consumers (n = 269; 96 men and 173 women) and non-consumers (n = 570; 279 men and 291 women), and their anthropometric measurements, metabolic profiles, and lifestyle factors were compared.Results: Men yogurt consumers had a lower body weight, BMI, % body fat, waist circumference and lower plasma insulin, and C-peptide concentrations in response to oral glucose, while women yogurt consumers had lower waist circumference, BMI, % body fat, plasma glucose, insulin, and C-peptide compared with non-consumers (P < 0.05). After adjustment for the Nutrient-Rich Foods (NRF) index, a marker of diet quality, these differences persisted in men and only for glycemic variables in women. Additional adjustment for physical activity participation and % body fat did not abolish the significant differences observed between yogurt consumers and non-consumers for plasma glucose, insulin, and C-peptide responses to oral glucose in women only (P < 0.05). Analyses of data after a 6-year follow-up reinforced these observations, since both men and women yogurt consumers maintained a better metabolic profile compared with non-consumers after adjustments for age and NRF (P < 0.05). In addition, an interaction between group and time for % body fat in men suggests a benefit of yogurt consumption over time on body composition.Conclusion: Yogurt consumption is associated with body composition and metabolic health benefits that are not entirely explained by a global effect of diet quality. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

An introduction to the journal is presented in which the editor discusses the 3rd International Congress on Abdominal Obesity hosted by the International Chair on Cardiometabolic Risk (ICCR) in partnership with "MD Conference Express ®" that was held in Quebec City on July 9-12, 2012.

The article discusses the approach that targets abdominal obesity and metabolic syndrome in managing the risk of cardiovascular disease. It examines the pathophysiology of obesity where people are more prone to gather extra fat which could lead to complications. It mentions that despite the genetic susceptibility differences of individuals to body fat collection, it is obvious that the outbreak ratios hit by obesity is partially the result of a marked decrease in daily physical activity.

A letter to the editor is presented in response to the article "Efficacy and Safety of the Weight-Loss Drug Rimonabant," published in the November 17, 2007 issue.

Dr. Denis Richard, a renowned physiologist, passed away in December 2023, leaving a significant impact on academia and those who knew him. He received his Ph.D. in Physiology from Université Laval in 1982 and made important contributions to the field of the central control of energy balance. Dr. Richard was a pioneer in the neurobiology of obesity and focused on understanding the role of the central nervous system in regulating metabolism. He organized numerous international symposia and was known for his mentorship and visionary leadership. His legacy will continue to influence the fields of physiology and neuroendocrinology. [Extracted from the article]

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. [Display omitted] • Body mass index, the most commonly used metric to diagnose obesity, has major limitations. • Several studies have highlighted the remarkable inter-individual differences in the way humans store energy as body fat. • Approaches advising people to eat less and move more are not sustainable for most people for long-term weight loss. • Emphasis should be placed on improving diet quality and increasing physical activity levels in the general population. • We highlight ten limitations of body mass index as a measure in medicine. [ABSTRACT FROM AUTHOR]

Abstract: Objective: The objective of this study was to investigate the association between self-reported sleep duration and the incidence of features of the metabolic syndrome in adults. Methods: A longitudinal analysis from the Quebec Family Study (Canada) was conducted on 293 participants, aged 18 to 65years, followed for a mean of 6years (until 2001). Participants were categorized as short (≤6h), adequate (7–8h) or long (≥9h) sleepers. The metabolic syndrome was defined according to the American Heart Association/National Heart, Lung, and Blood Institute's criteria. The hypertriglyceridemic waist phenotype was defined as high waist circumference (≥90cm in men and ≥85cm in women) combined with high fasting triglyceride level (≥2.0mmol/L in men and ≥1.5mmol/L in women). Results: The incidence rates of metabolic syndrome and hypertriglyceridemic waist phenotype were 9.9% and 7.5%, respectively. Short sleepers were significantly more at risk of developing the metabolic syndrome (relative risk (RR): 1.74; 95% confidence interval (CI): 1.05–2.72) and the hypertriglyceridemic waist phenotype (RR: 1.82; 95% CI: 1.16–2.79), compared to those sleeping 7 to 8h per night after adjusting for covariates. However, long sleep duration was not associated with an increased risk of developing the metabolic syndrome or the hypertriglyceridemic waist phenotype (either unadjusted or adjusted models). Conclusion: Short sleep duration is associated with an increased risk of developing features of the metabolic syndrome in adults. [Copyright &y& Elsevier]

Background: Previous studies looking at the relationship between sleep duration and the metabolic syndrome have only used a dichotomous approach (presence/absence) and failed to adjust for important confounding factors. The objective of the present study was to examine the association between self-reported sleep duration and features of the metabolic syndrome in adults. Methods: A cross-sectional analysis from the Quebec Family Study (Canada) was conducted on 810 participants aged 18 to 65 years. Participants were categorized as short (≤6 h), adequate (7–8 h) or long (≥9 h) sleepers. The metabolic syndrome was defined according to the American Heart Association/National Heart, Lung, and Blood Institute’s criteria. Results: Overall, 24.6% of the sample had the metabolic syndrome. A U-shaped relationship between sleep duration and the prevalence of metabolic syndrome (33.3%, 22.0% and 28.8% in short, adequate and long sleepers, respectively) was observed (P<0.01). Only short sleepers had a significant increase in the odds of having the metabolic syndrome (OR = 1.76, 95% CI = 1.08–2.84) compared to adequate sleepers after adjustment for age, sex, smoking habits, highest education level, total annual family income, alcohol consumption, coffee intake, menopausal status, daily caloric intake, and moderate-to-vigorous physical activity. Likewise, the clustered cardiometabolic risk score (i.e. continuous risk score based on the metabolic syndrome components) was significantly higher in short sleepers compared to adequate sleepers after adjustment for covariates (P<0.05). Conclusion: Sleeping ≤6 h per night is associated with an elevated cardiometabolic risk score and an increase in the odds of having the metabolic syndrome after adjusting for possible confounders. These results strongly suggest that short sleep duration is a risk factor for the metabolic syndrome. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Abstract: The objective of this cross-sectional study was to examine the association between sleep duration and alcohol consumption in adults (301 men and 402 women aged 18–64years) from the greater Quebec City area. Sleep duration (self-reported), alcohol consumption (3-day food record and questions on drinking habits), and disinhibition eating behavior trait (score⩾6 on the Three-Factor Eating Questionnaire) were assessed. Participants were categorized as short- (⩽6h), average- (7–8h) or long- (⩾9h) duration sleepers. Overall, short-duration sleepers consumed significantly more alcohol than the two other sleep-duration groups. After adjusting for relevant covariates, short sleep duration was associated with an increase in the odds of exceeding the recommendations for sensible weekly alcohol intake of 14 drinks for men and 7 drinks for women compared to those sleeping between 7 and 8h (OR 1.87, 95%CI 1.03–3.54, both sexes combined). In both men and women, daily alcohol intake was significantly higher in short-duration sleepers having a high disinhibition eating behavior trait. However, the prevalence of a binge drinking occasion (i.e. ⩾5 drinks on one occasion) was more common in men than women. Men sleeping less than 6h per night with a disinhibited eating behavior were more likely to report binge drinking (41% of them). In summary, the combination of short sleep duration with disinhibited eating behavior is associated with greater alcohol intake in adults. [Copyright &y& Elsevier]

Background: Screening for increased waist circumference and hypertriglyceridemia (the hypertriglyceridemic-waist phenotype) has been proposed as an inexpensive approach to identify patients with excess intra-abdominal adiposity and associated metabolic abnormalities. We examined the relationship between the hypertriglyceridemic-waist phenotype to the risk of coronary artery disease in apparently healthy individuals. Methods: A total of 21 787 participants aged 45-79 years were followed for a mean of 9.8 (standard deviation 1.7) years. Coronary artery disease developed in 2109 of them during follow-up. The hypertriglyceridemic-waist phenotype was defined as a waist circumference of 90 cm or more and a triglyceride level of 2.0 mmol/L or more in men, and a waist circumference of 85 cm or more and a triglyceride level of 1.5 mmol/L or more in women. Results: Compared with participants who had a waist circumference and triglyceride level below the threshold, those with the hypertriglyceridemic-waist phenotype had higher blood pressure indices, higher levels of apolipoprotein B and C-reactive protein, lower levels of high-density lipoprotein cholesterol and apolipoprotein A-I, and smaller low-density lipoprotein particles. Among men, those with the hypertriglyceridemic- waist phenotype had an unadjusted hazard ratio for future coronary artery disease of 2.40 (95% confidence interval [CI] 2.02-2.87) compared with men who did not have the phenotype. Women with the phenotype had an unadjusted hazard ratio of 3.84 (95% CI 3.20-4.62) compared with women who did not have the phenotype. Interpretation: Among participants from a European cohort representative of a contemporary Western population, the hypertriglyceridemic- waist phenotype was associated with a deteriorated cardiometabolic risk profile and an increased risk for coronary artery disease. [ABSTRACT FROM AUTHOR]