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At a population level, engagement in healthy lifestyle behaviors is suboptimal in the United States. Moreover, marked disparities exist in healthy lifestyle behaviors and cardiovascular risk factors as a result of social determinants of health. In addition, there are specific challenges to engaging in healthy lifestyle behaviors related to age, developmental stage, or major life circumstances. Key components of a healthy lifestyle are consuming a healthy dietary pattern, engaging in regular physical activity, avoiding use of tobacco products, habitually attaining adequate sleep, and managing stress. For these health behaviors, there are guidelines and recommendations; however, promotion in clinical settings can be challenging, particularly in certain population groups. These challenges must be overcome to facilitate greater promotion of healthy lifestyle practices in clinical settings. The 5A Model (assess, advise, agree, assist, and arrange) was developed to provide a framework for clinical counseling with consideration for the demands of clinical settings. In this science advisory, we summarize specific considerations for lifestyle-related behavior change counseling using the 5A Model for patients across the life span. In all life stages, social determinants of health and unmet social-related health needs, as well as overweight and obesity, are associated with increased risk of cardiovascular disease, and there is the potential to modify this risk with lifestyle-related behavior changes. In addition, specific considerations for lifestyle-related behavior change counseling in life stages in which lifestyle behaviors significantly affect cardiovascular disease risk are outlined. Greater attention to healthy lifestyle behaviors during every clinician visit will contribute to improved cardiovascular health.

The American Heart Association criteria for cardiovascular health include overall diet quality (DQ). The present study evaluated the effect of a workplace health promotion program targeting DQ and physical activity on features of cardiometabolic risk (CMR). Before and after the 3-month intervention, 2260 employees (1462 men and 798 women) completed a health and fitness evaluation including assessment of DQ using a validated food-based questionnaire. After the 3-month lifestyle modification program, DQ increased significantly in both sexes (p &lt, 0.0001) as well as physical activity level (p &lt, 0.0001). A reduction in waist circumference (p &lt, 0.0001) and improved lipid levels were also observed. Significant associations were found between changes in DQ index and changes in CMR variables in both men (standardized regression coefficients ranged from −0.19 (95% confidence interval: −0.26 to −0.12) to −0.29 (95% confidence interval: −0.34 to −0.25)) and women (standardized regression coefficients ranged from −0.18 (95% confidence interval: −0.25 to −0.11) to −0.27 (95% confidence interval: −0.41 to −0.13)). Multiple linear regression analyses showed a significant contribution of changes in the DQ index to the variation in some CMR variables, independent from changes in physical activity level and cardiorespiratory fitness. This study provides evidence that targeting DQ at the workplace is relevant to improve cardiometabolic health.

High overall nutritional quality (NQ) is an important component of ideal cardiovascular health, a concept introduced in 2010 by the American Heart Association. However, data on the independent contribution of overall NQ to the variation in the cardiometabolic risk (CMR) profile are limited. This observational study aimed to investigate the association between overall NQ and the CMR profile in 4785 participants (65⋅4 % of men, age 43⋅3 (sd 10⋅8) years) who underwent a cardiometabolic health evaluation, including lifestyle habits, anthropometric measurements, blood pressure, lipid profile and HbA1c concentrations. In addition, a submaximal exercise test was conducted to assess cardiorespiratory fitness (CRF). Using a standardised NQ questionnaire (twenty-five items food-based questionnaire), participants were classified into three subgroups: (1) low, (2) moderate or (3) high NQ and variance and multiple linear regression analyses were performed. Results showed that less than 15 % of participants presented a high NQ. A high NQ was associated with a healthier lifestyle habits and a more favourable CMR profile (lower values of waist circumference and cholesterol:HDL-cholesterol ratio, lower concentrations of non-HDL-cholesterol, TAG and HbA1c). Some of these associations were independent of age, physical activity level (PAL) and CRF. A better NQ was also associated with a lower proportion of participants presenting the hypertriacylglycerolaemic waist phenotype independently of both PAL and CRF. The present study suggests that overall NQ can be assessed with a short food-based questionnaire and should be considered in clinical practice as a new ‘vital sign’ associated with other health behaviours and cardiometabolic health.

PURPOSE Low-attenuation muscle (LAM) area at mid-thigh, a computed tomography (CT)-derived index of intramuscular lipids, is associated with insulin resistance, obesity, and type 2 diabetes. The present study aimed at testing the hypothesis that changes in LAM area in trunk muscles from a single abdominal scan could provide relevant information to evaluate the effects of a lifestyle intervention without the use of a mid-thigh CT scan. METHODS Cardiometabolic risk variables, including waist circumference, lipoprotein-lipid profile, glucose tolerance, and cardiorespiratory fitness, were assessed in a sample of 102 dyslipidemic viscerally obese men at baseline and after a 1-yr lifestyle intervention. Abdominal (L4-L5) and mid-thigh CT scans were performed and abdominal muscles classified as psoas and core muscles. Scans were segmented to calculate muscle areas, LAM areas, and mean attenuation values. RESULTS All muscle groups showed a decrease in LAM areas (P < 0.0001) in response to the lifestyle intervention. Changes in LAM areas were significantly associated with changes in triglycerides, high-density lipoprotein (HDL) cholesterol, cholesterol/HDL cholesterol ratio and log triglycerides/HDL cholesterol ratio (mid-thigh, 0.20 ≤ |r| ≤ 0.29; psoas, 0.28 ≤ |r| ≤ 0.38; core, 0.29 ≤ |r| ≤ 0.34, P < 0.05). Changes in core LAM area were significantly associated with changes in 2-h glucose levels, glucose area measured during the oral glucose tolerance test and homeostasis model assessment of insulin resistance (0.21 ≤ r ≤ 0.34, P < 0.05). Stepwise regression analyses showed that changes in LAM psoas area were associated with changes in HDL cholesterol and the cholesterol/HDL cholesterol ratio independently from changes in visceral adiposity. CONCLUSIONS Changes in trunk LAM areas are useful indices of changes in mid-thigh LAM area observed with a 1-yr lifestyle intervention. Thus, an additional mid-thigh scan is not necessary to evaluate muscle lipid content by CT when an abdominal CT scan is available.

Obesity has been associated with elevated leptinemia and vitamin D deficiency. To date, whether there is an association between vitamin D and leptin levels independent from adiposity remains uncertain. Our objective was to investigate the associations between changes in 25(OH) vitamin D levels, changes in adiposity variables, and changes in leptin levels produced by a 1-year lifestyle intervention program. Sedentary men (n = 113) with abdominal obesity, dyslipidemic, and non-vitamin D supplemented were involved in a 1-year lifestyle modification program. Subjects were individually counseled by a kinesiologist and a nutritionist once every 2 weeks during the first 4 months with subsequent monthly visits in order to elicit a 500 kcal daily energy deficit and to increase physical activity/exercise habits. Adiposity mapping by computed tomography and cardiometabolic biomarkers, as well as vitamin D measurements were performed at baseline and at the 1-year visit. The 1-year intervention resulted in a 26% decrease in visceral adipose tissue volume (from 1951 ± 481 to 1463 ± 566 cm3), a 27% decrease in leptin levels (from 12.0 ± 8.1 to 8.5 ± 7.8 ng/mL) and a 27% increase in plasma 25(OH) vitamin D concentrations (from 50 ± 18 to 60 ± 18 nmol/L, p

To assess the effectiveness of exercise and pharmacotherapy interventions in reducing visceral adipose tissue (VAT).A systematic search of Ovid MEDLINE, Scopus, Web of Science, Cochrane Library, ClinicalTrials.gov, New York Academy of Science Grey Literature Report, and OpenGrey was combined with hand searches of existing literature. A total of 2515 titles and abstracts were reviewed. Only randomized controlled trials evaluating the effectiveness of monitored exercise or pharmacological interventions in reducing VAT by using computed tomography or magnetic resonance imaging during a sustained intervention period (≥6 months) were included. Data were independently extracted by reviewers according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines and assessed for quality and risk of bias. Separate analyses for each intervention were performed using random effect models, with pooled estimates of the change in VAT area (in centimeters squared) from baseline to follow-up reported as standardized mean difference (SMD; with 95% CI).A total of 3602 participants from 17 randomized controlled trials were included in the final analysis. Both exercise and pharmacological interventions were associated with significant reductions in VAT: small reduction with pharmacological interventions (SMD, -0.27; 95% CI, -0.47 to -0.07; P=.02) and more substantial reductions with exercise interventions (SMD, -0.54; 95% CI, -0.63 to -0.46; P.001). The mean absolute VAT reduction was greater in pharmacological trials than in exercise trials. Meta-regression exhibited a linear correlation between VAT and weight loss (RExercise interventions resulted in greater reduction in VAT relative to weight loss than did pharmacological interventions. A preferential reduction in VAT may be clinically meaningful when monitoring success of interventions because weight loss alone may underestimate benefits.

Recent transversal studies have associated insulin-like growth factor binding protein (IGFBP)-2 levels with glucose tolerance and parameters of the lipoprotein-lipid profile. Here, we aimed at determining the longitudinal effects of a one-year lifestyle modification program on IGFBP-2 levels and to identify specific metabolic improvements impacted by the changes in IGFBP-2.99 middle-aged Caucasian men were involved in a lifestyle modification program consisting in personalized healthy eating and physical activity counseling, combined to elicit a daily 500 kcal deficit. Anthropometric and metabolic parameters as well as circulating IGFBP-2 levels were measured before and after one year of the lifestyle modification program.The intervention triggered positive changes in many metabolic parameters and a 43% (p 0.0001) increase of IGFBP-2 levels. Subjects with the most substantial increases in IGFBP-2 also experienced the most important metabolic improvements. Changes in IGFBP-2 levels (both absolute and relative) were correlated with markers of body fat distribution and lipoprotein-lipid profile, and independently associated with changes in LDL apolipoprotein (apo) B but not VLDL apo B concentrations. Further analyses showed that for similar changes in BMI, waist circumference and visceral adipose tissue volume, large changes in IGFBP-2 levels were required to observe improvements in LDL apo B levels.The 1-year lifestyle modification program was associated with increased IGFBP-2 concentrations. Increases in IGFBP-2 levels were closely associated with reduced LDL apo B concentrations and independently of the modifications in fat mass and insulin sensitivity. Further mechanistic studies are required to assess the effects of IGFBP-2 levels on LDL metabolism.

With the global epidemics of obesity and associated conditions, including type 2 diabetes, metabolic dysfunction-associated fatty liver disease, chronic kidney disease, hypertension, stroke, cardiovascular disease, osteoporosis, cancer, and cognitive changes, the prevalence of multimorbidity is rapidly increasing worldwide. In this Review, a panel of international experts from across the spectrum of metabolic diseases come together to identify the challenges and provide perspectives on building a framework for a virtual primary care-driven, patient-centred, multidisciplinary model to deliver holistic care for patients with metabolic dysfunction-associated fatty liver disease and associated metabolic diseases. We focus on clinical care and innovative trial design for metabolic dysfunction-associated fatty liver disease and associated metabolic diseases. This work represents a call to action to promote collaboration and partnerships between stakeholders for improving the lives of people with, or at risk of, metabolic dysfunction-associated fatty liver disease and associated metabolic diseases.

We assessed the reliability and validity of a Salty Food Frequency Questionnaire for Sodium (FFQ-Na) and a Discretionary Salt Questionnaire (DSQ) developed for the French-Canadian population. The reliability was evaluated according to temporal stability over a 7&ndash, 15 day interval (n = 36). Validity was evaluated by testing the tools against a 24-h urine sodium excretion (24 h Uri-Na) and a 3-day food record, and this at individual and group levels (n = 164). The intra-class coefficients (ICC) values for the test-retest of the DSQ, the FFQ-Na and the two questionnaires combined were 0.73, 0.97 and 0.98 respectively. Correlations of the FFQ-Na with the 24 h Uri-Na and the 3-day food record were 0.3 (p &lt, 0.001) and 0.35 (p &lt, 0.001) respectively. The DSQ showed no significant correlation with the reference measures. The correlation between the two methods combined were 0.29 (p &lt, 0.001) with the 24 h Uri-Na and 0.31 (p &lt, 0.001) with the 3-day food record. The results of Bland&ndash, Altman indicated that for the combined questionnaires, there was a bias of measurement (underestimation of intake), but it was constant for every level of intake according to the reference measures. Finally, the cross-classification indicated an acceptable proportion of agreement, but a rate between 20% and 30% of classification in the opposite quartile. In conclusion, the developed tools are reliable and showed some facets of validity.

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 under-addressed modifiable risk factor remains a challenge. In this review, we emphasize that the tendency among healthcare 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 two 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.

Background Although abdominal adiposity is associated with an altered cardiometabolic risk profile, the specific contribution of abdominal adipose tissue distribution remains not fully understood. Computed tomography (CT) is a well-established and precise method to measure abdominal adipose tissue distribution. The present study investigated abdominal adiposity assessed by CT in a large-scale Chinese population. Method A total of 59,429 adults who underwent a low dose chest CT for lung cancer screening at one of 13 health checkup centers throughout China were evaluated. Abdominal visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) areas were measured at the center of the 2nd lumbar vertebra with Mindways quantitative CT software using the existing CT dataset without any additional radiation exposure. The ratio of visceral to total adipose tissue (TAT) areas (VAT/TAT ratio) was calculated and expressed as a percentage. Anthropometric indices including body mass index (BMI) and waist circumference were also obtained. Results BMI, waist circumference, VAT area, SAT area, and the VAT/TAT ratio were 25.0 ± 3.0 kg/m2, 90 ± 8 cm, 194 ± 77 cm2, 85 ± 41 cm2, and 69.5 ± 9.1%, respectively, in men and 23.3 ± 3.1 kg/m2, 79 ± 8 cm, 120 ± 57 cm2, 123 ± 53 cm2, and 48.9 ± 9.7% in women. With increasing age, VAT area and the VAT/TAT ratio increased in both sexes whereas SAT area decreased in men (P Conclusion In a nationwide study conducted in China, distributions of CT-derived measures of visceral and subcutaneous adiposity were found to vary significantly between sex and age groups. Our study also revealed that the proportion of VAT (an important driver of cardiometabolic risk) could not be predicted from BMI in a Chinese population.

International audience; 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.

Despite decades of unequivocal evidence that waist circumference provides both independent and additive information to BMI for predicting morbidity and risk of death, this measurement is not routinely obtained in clinical practice. This Consensus Statement proposes that measurements of waist circumference afford practitioners with an important opportunity to improve the management and health of patients. We argue that BMI alone is not sufficient to properly assess or manage the cardiometabolic risk associated with increased adiposity in adults and provide a thorough review of the evidence that will empower health practitioners and professional societies to routinely include waist circumference in the evaluation and management of patients with overweight or obesity. We recommend that decreases in waist circumference are a critically important treatment target for reducing adverse health risks for both men and women. Moreover, we describe evidence that clinically relevant reductions in waist circumference can be achieved by routine, moderate-intensity exercise and/or dietary interventions. We identify gaps in the knowledge, including the refinement of waist circumference threshold values for a given BMI category, to optimize obesity risk stratification across age, sex and ethnicity. We recommend that health professionals are trained to properly perform this simple measurement and consider it as an important ‘vital sign’ in clinical practice., In this Consensus Statement, the International Atherosclerosis Society and International Chair on Cardiometabolic Risk Working Group on Visceral Obesity recommend that waist circumference be included routinely as a measurement in clinical practice. They summarize the evidence that waist circumference and BMI together can provide improved assessments of cardiometabolic risk compared with either measurement alone.

Background/objectives Thigh muscle attenuation measured by computed tomography (CT) has been shown to be a reliable and useful index of skeletal muscle fat infiltration. Thigh muscle fat content assessed by CT has been linked to obesity and type 2 diabetes and is a correlate of insulin resistance in sedentary individuals. However, as measurement of mid-thigh fat content requires the assessment of another region of interest beyond the usual abdominal scan required to measure levels of visceral and subcutaneous abdominal adipose tissue, this study aimed at testing the hypothesis that skeletal muscle fat measured from a single abdominal scan (L4-L5) would also provide information relevant to the estimation of muscle fat infiltration as it relates to cardiometabolic risk. Methods Abdominal (L4-L5) and mid-thigh CT scans were performed in a sample of 221 sedentary men covering a wide range of adiposity values. Trunk muscles on the L4-L5 scan were classified into 2 groups: 1) psoas and 2) core muscles. The two scans were segmented to calculate muscle areas, mean attenuation values as well as low-attenuation muscle (LAM) areas, the latter being considered as an index of skeletal muscle fat infiltration. Body mass index (BMI), body composition and waist circumference were assessed and a 75 g oral glucose tolerance test (OGTT) was performed. Results Mid-thigh, psoas and core LAM areas were all significantly associated with body composition indices (0.46 ≤ r ≤ 0.71, p Conclusion Our results suggest that CT-imaging derived indices of trunk muscle quality are related to glucose tolerance and visceral adiposity. However, the relationship between skeletal muscle fat and insulin resistance appears to be largely mediated by the concomitant variation in visceral adiposity. Finally, our results suggest that a single CT scan performed at L4-L5 is adequate to assess skeletal muscle fat content related to cardiometabolic risk.

This study examined the relationship between yogurt consumption, family history of obesity (FHO), and health determinants. Youth (n = 198; mean age: 20 ± 0.5 years) from the Quebec Family Study were first classified based on their FHO, defined as the presence or absence of at least one obese (BMI ≥30 kg/m2) 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. 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. 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.

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. 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 Malmo Preventive Project cohort were analyzed. 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 Malmo 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). 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.

BACKGROUND: Low-risk limits recommended for alcohol consumption vary substantially across different national guidelines. To define thresholds associated with lowest risk for all-cause mortality and cardiovascular disease, we studied individual-participant data from 599 912 current drinkers without previous cardiovascular disease.METHODS: We did a combined analysis of individual-participant data from three large-scale data sources in 19 high-income countries (the Emerging Risk Factors Collaboration, EPIC-CVD, and the UK Biobank). We characterised dose–response associations and calculated hazard ratios (HRs) per 100 g per week of alcohol (12·5 units per week) across 83 prospective studies, adjusting at least for study or centre, age, sex, smoking, and diabetes. To be eligible for the analysis, participants had to have information recorded about their alcohol consumption amount and status (ie, non-drinker vs current drinker), plus age, sex, history of diabetes and smoking status, at least 1 year of follow-up after baseline, and no baseline history of cardiovascular disease. The main analyses focused on current drinkers, whose baseline alcohol consumption was categorised into eight predefined groups according to the amount in grams consumed per week. We assessed alcohol consumption in relation to all-cause mortality, total cardiovascular disease, and several cardiovascular disease subtypes. We corrected HRs for estimated long-term variability in alcohol consumption using 152 640 serial alcohol assessments obtained some years apart (median interval 5·6 years [5th–95th percentile 1·04–13·5]) from 71 011 participants from 37 studies.FINDINGS: In the 599 912 current drinkers included in the analysis, we recorded 40 310 deaths and 39 018 incident cardiovascular disease events during 5·4 million person-years of follow-up. For all-cause mortality, we recorded a positive and curvilinear association with the level of alcohol consumption, with the minimum mortality risk around or below 100 g per week. Alcohol consumption was roughly linearly associated with a higher risk of stroke (HR per 100 g per week higher consumption 1·14, 95% CI, 1·10–1·17), coronary disease excluding myocardial infarction (1·06, 1·00–1·11), heart failure (1·09, 1·03–1·15), fatal hypertensive disease (1·24, 1·15–1·33); and fatal aortic aneurysm (1·15, 1·03–1·28). By contrast, increased alcohol consumption was log-linearly associated with a lower risk of myocardial infarction (HR 0·94, 0·91–0·97). In comparison to those who reported drinking >0–≤100 g per week, those who reported drinking >100–≤200 g per week, >200–≤350 g per week, or >350 g per week had lower life expectancy at age 40 years of approximately 6 months, 1–2 years, or 4–5 years, respectively.INTERPRETATION: In current drinkers of alcohol in high-income countries, the threshold for lowest risk of all-cause mortality was about 100 g/week. For cardiovascular disease subtypes other than myocardial infarction, there were no clear risk thresholds below which lower alcohol consumption stopped being associated with lower disease risk. These data support limits for alcohol consumption that are lower than those recommended in most current guidelines.FUNDING: UK Medical Research Council, British Heart Foundation, National Institute for Health Research, European Union Framework 7, and European Research Council.

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 (sd5·7) years were randomly assigned to a control (10–15, 55–60 and 30 % energy as protein, carbohydrate and lipid, respectively;n34) or satiating (20–25, 45–50 and 30–35 % energy as protein, carbohydrate and lipid, respectively;n35) diet for 16 weeks, and were classified as having a low (LSP) or high (HSP) satiety phenotype. Both diets were consumedad 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 (sd2·1) %;Psd2·5) %;Psd2·5) % and HSP: −1·3 (sd2·6) %) (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 (sd2·9) to +7·2 (sd5·5)), flexible control (+0·9 (sd1·4) to +2·3 (sd2·7)), rigid control (+2·2 (sd1·5) to +2·5 (sd2·8)), disinhibition (−2·8 (sd3·7) to −3·2 (sd2·6)) and susceptibility to hunger (−2·7 (sd4·1) to −4·6 (sd3·9)) 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.

Prediction of coronary events remains elusive. Carotid atherosclerosis may be a surrogate for coronary risk, as carotid and coronary diseases occur simultaneously — albeit at times with a weak association — depending on clinical presentation. We investigated carotid and coronary atherosclerosis in men with new-onset unstable coronary artery disease (CAD) presenting with acute ST-segment elevation myocardial infarction (STEMI) vs. long-standing severe chronic stable angina (CSA). Bilateral carotid artery and 3-vessel coronary artery atherosclerosis burdens were measured within 1 month, respectively, by 3D-volumetric carotid magnetic resonance imaging and coronary angiography-derived modified CASS-50 score. Men with STEMI (n = 50) and long-standing CSA (n = 50), matched for age, were enrolled (58.6 ± 8.8 years). All of them had carotid atherosclerosis. Atherosclerosis burden was greater in the carotid arteries of STEMI vs. CSA (wall volume: 196.2 ± 44.4 vs. 169.2 ± 38.0 mm3/4 mm, p = 0.002), but greater in the coronary arteries of CSA vs. STEMI (modified CASS-50 score: 3 vs. 1, p < 0.0001). Normalized wall index (NWI) of internal carotid was associated with modified CASS-50 score in STEMI (ρ = 0.40, p = 0.022) and in CSA (ρ = −0.39, p = 0.031). Carotid atherosclerosis was observed in all CAD patients, and atherosclerosis burden in carotid and in coronary arteries varied according to clinical presentation.

Background Overconsumption of dietary sugars, fructose in particular, is linked to cardiovascular risk factors such as type 2 diabetes, obesity, dyslipidemia and nonalcoholic fatty liver disease. However, clinical studies have to date not clarified whether these adverse cardiometabolic effects are induced directly by dietary sugars, or whether they are secondary to weight gain. Objectives To assess the effects of fructose (75 g day−1), served with their habitual diet over 12 weeks, on liver fat content and other cardiometabolic risk factors in a large cohort (n = 71) of abdominally obese men. Methods We analysed changes in body composition, dietary intake, an extensive panel of cardiometabolic risk markers, hepatic de novo lipogenesis (DNL), liver fat content and postprandial lipid responses after a standardized oral fat tolerance test (OFTT). Results Fructose consumption had modest adverse effects on cardiometabolic risk factors. However, fructose consumption significantly increased liver fat content and hepatic DNL and decreased β-hydroxybutyrate (a measure of β-oxidation). The individual changes in liver fat were highly variable in subjects matched for the same level of weight change. The increase in liver fat content was significantly more pronounced than the weight gain. The increase in DNL correlated positively with triglyceride area under the curve responses after an OFTT. Conclusion Our data demonstrated adverse effects of moderate fructose consumption for 12 weeks on multiple cardiometabolic risk factors in particular on liver fat content despite only relative low increases in weight and waist circumference. Our study also indicates that there are remarkable individual differences in susceptibility to visceral adiposity/liver fat after real-world daily consumption of fructose-sweetened beverages over 12 weeks.

Background and aims: Incretin hormones glucagon-like peptide (GLP)-1 and glucose-dependent insulinotropic polypeptide (GIP) are affected early on in the pathogenesis of metabolic syndrome and type 2 diabetes. Epidemiologic studies consistently link high fructose consumption to insulin resistance but whether fructose consumption impairs the incretin response remains unknown. Methods and results: As many as 66 obese (BMI 26-40 kg/m(2)) male subjects consumed fructose-sweetened beverages containing 75 g fructose/day for 12 weeks while continuing their usual lifestyle. Glucose, insulin, GLP-1 and GIP were measured during oral glucose tolerance test (OGTT) and triglycerides (TG), GLP-1, GIP and PYY during a mixed meal test before and after fructose intervention. Fructose intervention did not worsen glucose and insulin responses during OGTT, and GLP-1 and GIP responses during OGTT and fat-rich meal were unchanged. Postprandial TG response increased significantly, p = 0.004, and we observed small but significant increases in weight and liver fat content, but not in visceral or subcutaneous fat depots. However, even the subgroups who gained weight or liver fat during fructose intervention did not worsen their glucose, insulin, GLP-1 or PYY responses. A minor increase in GIP response during OGTT occurred in subjects who gained liver fat (p = 0.049). Conclusion: In obese males with features of metabolic syndrome, 12 weeks fructose intervention 75 g/day did not change glucose, insulin, GLP-1 or GIP responses during OGTT or GLP-1, GIP or PYY responses during a mixed meal. Therefore, fructose intake, even accompanied with mild weight gain, increases in liver fat and worsening of postprandial TG profile, does not impair glucose tolerance or gut incretin response to oral glucose or mixed meal challenge. (C) 2017 The Italian Society of Diabetology, the Italian Society for the Study of Atherosclerosis, the Italian Society of Human Nutrition, and the Department of Clinical Medicine and Surgery, Federico II University. Published by Elsevier B.V. All rights reserved.

Our objective was to examine the respective contributions of changes in visceral adiposity, subcutaneous adiposity, liver fat, and cardiorespiratory fitness (CRF) to the improvements in cardiometabolic risk markers in response to a 3-yr healthy eating/physical activity lifestyle intervention. Ninety-four out of 144 viscerally obese healthy men completed a 3-yr lifestyle intervention. Body weight, body composition, and fat distribution were assessed by anthropometry and DEXA/computed tomography. CRF, adipokines, lipoprotein/lipid profile, and 75 g of oral glucose tolerance were assessed. CRF and visceral and subcutaneous adiposity significantly improved over the 3-yr intervention, with a nadir in year 1 and a partial regain in year 3. Liver fat (estimated by insulin hepatic extraction) stabilized from year 1 to year 3, whereas HOMA-IR, ISI-Matsuda index, and adiponectin continued to improve. Multivariate analysis revealed that both visceral adiposity and estimated liver fat reductions contributed to the improved ISI-Matsuda index observed over 3 yr ( r2= 0.28, P < 0.001). Three-year changes in fat mass and CRF were independently associated with changes in visceral fat (adjusted r2= 0.40, P < 0.001), whereas only changes in CRF were associated with changes in estimated liver fat (adjusted r2= 0.18, P < 0.001). A long-term (3 yr) healthy eating/physical activity intervention in men improves several cardiometabolic risk markers over the long term (3 yr) despite a partial body weight regain observed between year 1 and year 3. The improvement in CRF contributes to visceral and estimated liver fat losses over the long term, which in turn explain the benefits of the lifestyle intervention on cardiometabolic risk profile.

Mickaël Martin,1 Natalie Almeras,1 Jean-Pierre Després,1 Harvey O Coxson,2 George R Washko,3 Isabelle Vivodtzev,4 Emiel FM Wouters,5 Erica Rutten,6 Michelle C Williams,7 John T Murchison,8 William MacNee,7 Don D Sin,2 François Maltais1 On behalf of the Evaluation of COPD Longitudinally to Identify Predictive Surrogate Endpoints (ECLIPSE) Study Group 1Research Centre, Institut universitaire de cardiologie et de pneumologie de Québec, Université Laval, Québec, QC, 2Department of Radiology, University of British Columbia, Vancouver, BC, Canada; 3Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA, USA; 4Hypoxia Pathophysiology Laboratory, Grenoble University Hospital, Grenoble, France; 5Department of Respiratory Medicine, Maastricht University Medical Center, Maastricht, 6Research and Development, CIRO, Horn, the Netherlands; 7Department of Respiratory Medicine, University of Edinburgh, 8Department of Radiology, Royal Infirmary of Edinburgh, Edinburgh, UK Background: Obesity is increasingly associated with COPD, but little is known about the prevalence of ectopic fat accumulation in COPD and whether this can possibly be associated with poor clinical outcomes and comorbidities. The Evaluation of COPD Longitudinally to Identify Predictive Surrogate Endpoints (ECLIPSE) substudy tested the hypothesis that COPD is associated with increased ectopic fat accumulation and that this would be associated with COPD-related outcomes and comorbidities.Methods: Computed tomography (CT) images of the thorax obtained in ECLIPSE were used to quantify ectopic fat accumulation at L2–L3 (eg, cross-sectional area [CSA] of visceral adipose tissue [VAT] and muscle tissue [MT] attenuation, a reflection of muscle fat infiltration) and CSA of MT. A dose–response relationship between CSA of VAT, MT attenuation and CSA of MT and COPD-related outcomes (6-minute walking distance [6MWD], exacerbation rate, quality of life, and forced expiratory volume in 1second [FEV1] decline) was addressed with the Cochran–Armitage trend test. Regression models were used to investigate possible relationships between CT body composition indices and comorbidities.Results: From the entire ECLIPSE cohort, we identified 585 subjects with valid CT images at L2–L3 to assess body composition. CSA of VAT was increased (P

Purpose Fatty liver disease is associated with cardiometabolic disorders and represents a potential key comorbidity in Chronic Obstructive Pulmonary Disease (COPD). Some intermediary mechanisms of fatty liver disease (including its histological component steatosis) include tissue hypoxia, low-grade inflammation and oxidative stress that are key features of COPD. Despite these shared physiological pathways, the effect of COPD on the prevalence of hepatic steatosis, and the association between hepatic steatosis and comorbidities in this population remain unclear. Liver density measured by computed tomography (CT)-scan is a non-invasive surrogate of fat infiltration, with lower liver densities reflecting more fat infiltration and a liver density of 40 Hounsfield Units (HU) corresponding to a severe 30% fat infiltration. Patients and Methods We took advantage of the international cohort ECLIPSE in which non-enhanced chest CT-scans were obtained in 1554 patients with COPD and 387 healthy controls to analyse the liver density at T12-L1. Results The distribution of liver density was similar and the prevalence of severe steatosis (density

Aims Cardiovascular risk factors are used for risk stratification in primary prevention. We sought to determine if simple cardiac risk scores are associated with magnetic resonance imaging (MRI)-detected subclinical cerebrovascular disease including carotid wall volume (CWV), carotid intraplaque haemorrhage (IPH), and silent brain infarction (SBI). Methods and results A total of 7594 adults with no history of cardiovascular disease (CVD) underwent risk factor assessment and a non-contrast enhanced MRI of the carotid arteries and brain using a standardized protocol in a population-based cohort recruited between 2014 and 2018. The non-lab-based INTERHEART risk score (IHRS) was calculated in all participants; the Framingham Risk Score was calculated in a subset who provided blood samples (n = 3889). The association between these risk scores and MRI measures of CWV, carotid IPH, and SBI was determined. The mean age of the cohort was 58 (8.9) years, 55% were women. Each 5-point increase (∼1 SD) in the IHRS was associated with a 9 mm3 increase in CWV, adjusted for sex (P < 0.0001), a 23% increase in IPH [95% confidence interval (CI) 9–38%], and a 32% (95% CI 20–45%) increase in SBI. These associations were consistent for lacunar and non-lacunar brain infarction. The Framingham Risk Score was also significantly associated with CWV, IPH, and SBI. CWV was additive and independent to the risk scores in its association with IPH and SBI. Conclusion Simple cardiovascular risk scores are significantly associated with the presence of MRI-detected subclinical cerebrovascular disease, including CWV, IPH, and SBI in an adult population without known clinical CVD.

ObjectiveThis study assessed whether apolipoprotein CIII-lipoprotein(a) complexes (ApoCIII-Lp(a)) associate with progression of calcific aortic valve stenosis (AS).MethodsImmunostaining for ApoC-III was performed in explanted aortic valve leaflets in 68 patients with leaflet pathological grades of 1–4. Assays measuring circulating levels of ApoCIII-Lp(a) complexes were measured in 218 patients with mild–moderate AS from the AS Progression Observation: Measuring Effects of Rosuvastatin (ASTRONOMER) trial. The progression rate of AS, measured as annualised changes in peak aortic jet velocity (Vpeak), and combined rates of aortic valve replacement (AVR) and cardiac death were determined. For further confirmation of the assay data, a proteomic analysis of purified Lp(a) was performed to confirm the presence of apoC-III on Lp(a).ResultsImmunohistochemically detected ApoC-III was prominent in all grades of leaflet lesion severity. Significant interactions were present between ApoCIII-Lp(a) and Lp(a), oxidised phospholipids on apolipoprotein B-100 (OxPL-apoB) or on apolipoprotein (a) (OxPL-apo(a)) with annualised Vpeak(all ppeak(pConclusionApoC-III is present on Lp(a) and in aortic valve leaflets. Elevated levels of ApoCIII-Lp(a) complexes in conjunction with Lp(a), OxPL-apoB or OxPL-apo(a) identify patients with pre-existing mild–moderate AS who display rapid progression of AS and higher rates of AVR/cardiac death.Trial registrationNCT00800800.

Although the first description of a syndrome defined by the co-existence of atherogenic and diabetogenic metabolic abnormalities is debated in the literature, it was Gerald Reaven who proposed, in his landmark 1988 Banting award lecture, that a significant proportion of individuals (with diabetes or not) were characterised by insulin resistance causing prejudice to cardiovascular health. However, Reaven was influenced by seminal observations made more than 50 years earlier by Himsworth who proposed that there were two forms of diabetes (insulin resistant v. insulin sensitive). Reaven went further in proposing the theory that insulin resistance was the most prevalent cause of CVD associated with metabolic abnormalities that he named syndrome X. Because there was a syndrome X documented in cardiology, the term evolved to insulin resistance syndrome. As Reaven could also find insulin-resistant individuals in non-obese subjects, he did not include obesity as a feature of syndrome X. Imaging studies then revealed that excess adipose tissue in the abdominal cavity, a condition described as visceral obesity, was the form of overweight/obesity associated with insulin resistance and its related abnormalities. As obesity risk assessment and management remain largely based on body weight (BMI) and weight loss, it is proposed that our clinical approaches and public health messages should be revisited. First, patients should be educated about the importance of monitoring their waistline as a crude index of abdominal adiposity. Secondly, public health approaches focussing on ‘lifestyle vital signs’ including achieving healthy waistlines rather than healthy body weights should be developed.

Targeting metabolic determinants of exercise performance with pharmacological agents that would mimic/potentiate the effects of exercise represents an attractive clinical alternative to counterbalance the poor exercise capacity in patients with type 2 diabetes mellitus (T2DM). We examined the effect of 1-yr treatment with the insulin sensitizer peroxisome proliferator-activated receptor (PPAR)γ agonist rosiglitazone on aerobic exercise capacity and body fat composition/distribution in men with T2DM and stable coronary artery disease (CAD). One-hundred four men (age: 64 ± 7 yr; body mass index: 30.0 ± 4.4 kg/m2) with T2DM and CAD were randomized to receive rosiglitazone or placebo for 1 yr. Aerobic exercise capacity (exercise duration) was assessed with a maximal treadmill test, and body composition/distribution were assessed by dual-energy X-ray absorptiometry/computed tomography scans. At 1 yr, patients with T2DM under PPARγ agonist treatment showed a reduction in aerobic exercise capacity compared with the control group (exercise duration change, −31 ± 8 versus 7 ± 11 s, P = 0.009). Significant increases in body fat mass (3.1 ± 0.4 kg, 12%), abdominal and mid-thigh subcutaneous adipose tissue (AT) levels, and mid-thigh skeletal muscle fat were found (all P < 0.01), whereas no effect on visceral AT levels was observed ( P > 0.05) under treatment. Subcutaneous fat mass gained under PPARγ agonist was the strongest predictor of the worsening in aerobic exercise capacity ( P > 0.0001); no association was found with skeletal muscle fat infiltration nor visceral AT. Treatment with the insulin sensitizer PPARγ agonist rosiglitazone in patients with T2DM and CAD is associated with a worsening in aerobic exercise capacity, which seems to be mainly attributable to weight gain and subcutaneous fat mass expansion.

BACKGROUND: Despite their important clinical value, second generation antipsychotics (SGAs) are known to induce weight gain, insulin resistance, and dyslipidemia. However, the extent of these metabolic alterations differs among patients, and there is a current lack of knowledge about the factors that influence this inter-variability. Circulating levels of insulin-like growth factor binding protein (IGFBP)-2 below 220ng/mL have been proposed as a potential integrative biomarker negatively associated with features of the metabolic syndrome, including waist circumference and hypertriglyceridemia. Thus, we tested the hypothesis that the metabolic alterations developed upon the use of SGAs are impacted by circulating IGFBP-2 levels. METHODS: In order to assess metabolic risk factors in schizophrenic patients using SGAs on the basis of their plasma IGFBP-2 levels, a cross-sectional study was performed in 97 young Caucasian men newly diagnosed with schizophrenia and treated with olanzapine or risperidone for approximately 20 months. Plasma glucose, insulin and IGFBP-2 levels, anthropometric data, as well as lipid-lipoprotein profiles were determined at the end of the treatments. RESULTS: Body weight, waist circumference and fasting insulin levels were similar between patients on olanzapine or risperidone. Plasma IGFBP-2 levels were also not different between the two groups (173 ± 15 vs 199 ± 16 ng/mL, respectively). As expected, IGFBP-2 concentrations were negatively correlated with BMI, waist circumference, insulin sensitivity, and plasma triglyceride levels in the entire cohort. However, the proportion of schizophrenic patients with a hypertriglyceridemia and large waist circumference ranged from 43% for olanzapine and 12% for risperidone users with IGFBP-2 levels lower than 220 ng/mL, compared to 8% and 0%, respectively for patients with plasma IGFBP-2 above this threshold (p = 0.0178). DISCUSSION: Our findings suggest that circulating levels of IGFBP-2 may underlie the inter-variability on metabolic risk in schizophrenic patients using SGAs. Longitudinal studies are required to evaluate whether IGFBP-2 levels can predict the development of a hypertriglyceridemic waist phenotype in this population.

To assess the benefits of a 1-year lifestyle modification program on exercise capacity and diastolic function in men with left ventricular (LV) diastolic dysfunction (LVDD) and coronary artery disease (CAD), according to glucose tolerance status.Fifty-three men (62 ± 8 years; BMI: 27.3 ± 3.5 kg/mThe 1-year lifestyle modification program was associated with reductions in body weight, and visceral and cardiac fat levels (all P 0.05). CRF increased by 13% (24.9 ± 4.1 vs. 28.2 ± 4.8 mL OIrrespective of glucose tolerance status, a 1-year lifestyle modification program in men with LVDD and CAD is associated with significant improvements in exercise capacity and LV diastolic function in more than half of patients.

No abstract available.

Purpose of review Low vitamin D levels have been extensively reported in obesity. Thus, the pandemic of obesity has been paralleled by a high prevalence of low vitamin D status. Given the well documented associations linking poor vitamin D status to adverse health outcomes (diabetes, cardiovascular disease, cancers, all-cause mortality), a proper understanding of the mechanisms linking excess adiposity to low vitamin D status is key to identify and implement effective interventions to replenish vitamin D levels in obese individuals. In this review, we will discuss recent literature investigating the effects of adipose tissue volume loss through energy restriction and/or physical activity on circulating 25-hydroxyvitamin D [25(OH)D] levels. Recent findings Improvements of circulating 25(OH)D levels with adiposity loss through lifestyle interventions without supplementation is being reported by a growing number of studies, including recent randomized controlled trials. Summary Low 25(OH)D is one of the metabolic disturbances associated with excess adiposity, particularly visceral adiposity. Recommendations for the treatment of obesity-related vitamin D deficiency should emphasize the role of visceral adiposity loss through healthy lifestyle habits, in conjunction with weight-adjusted vitamin D supplementation, not only to replenish 25(OH)D levels but also to address other visceral adiposity-related disturbances, such as insulin resistance, inflammation, hypertension, and dyslipidemia.

Author(s): Writing Group Members; Mozaffarian, Dariush; Benjamin, Emelia J; Go, Alan S; Arnett, Donna K; Blaha, Michael J; Cushman, Mary; Das, Sandeep R; de Ferranti, Sarah; Despres, Jean-Pierre; Fullerton, Heather J; Howard, Virginia J; Huffman, Mark D; Isasi, Carmen R; Jimenez, Monik C; Judd, Suzanne E; Kissela, Brett M; Lichtman, Judith H; Lisabeth, Lynda D; Liu, Simin; Mackey, Rachel H; Magid, David J; McGuire, Darren K; Mohler, Emile R; Moy, Claudia S; Muntner, Paul; Mussolino, Michael E; Nasir, Khurram; Neumar, Robert W; Nichol, Graham; Palaniappan, Latha; Pandey, Dilip K; Reeves, Mathew J; Rodriguez, Carlos J; Rosamond, Wayne; Sorlie, Paul D; Stein, Joel; Towfighi, Amytis; Turan, Tanya N; Virani, Salim S; Woo, Daniel; Yeh, Robert W; Turner, Melanie B; American Heart Association Statistics Committee; Stroke Statistics Subcommittee

Severe obesity is often characterized by ectopic fat deposition, which is related to development of type 2 diabetes (T2D). Thus, resolution of T2D may not be linearly associated with weight loss. The importance of ectopic fat reduction after bariatric surgery and T2D resolution is uncertain.The aim of this pilot study is to compare body composition and body fat distribution in severely obese patients with or without T2D after biliopancreatic diversion with duodenal switch (BPD-DS) surgery in relation to diabetes resolution.Sixty-two severely obese patients were evaluated at baseline, 6, and 12 months. Of these, 40 patients underwent BPD-DS surgery. Anthropometric measurements and abdominal and mid-thigh computed tomography scans were performed at each visit.Before BPD-DS surgery, obese patients with T2D had higher weight as well as greater ectopic fat deposition in the abdomen and mid-thigh level than obese patients without T2D (p 0.05). Resolution of T2D was 65 and 90 % at 6 and 12 months, respectively. No difference in body composition changes at 6 and 12 months could be found between patients without T2D, patients with T2D resolution, and patients who remained T2D. Resolution of T2D was associated with a greater absolute loss of visceral adipose tissue (VAT) in comparison to patients without T2D (-1175 ± 570 cm(3) vs. -729 ± 394 cm(3) at 6 months and -1647 ± 816 cm(3) vs. -1103 ± 422 cm(3) at 12 months; all p ≤ 0.05).Ectopic fat mobilization, particularly the absolute loss of VAT, may play a major role in T2D resolution following BPD-DS surgery, regardless of the amount of weight loss.

Objective The goal was to examine lipoprotein subclass responses to regular exercise as measured in 10 exercise interventions derived from six cohorts. Methods Nuclear magnetic resonance spectroscopy was used to quantify average particle size, total and subclass concentrations of very low-density lipoprotein, low-density lipoprotein, and high-density lipoprotein particles (VLDL-P, LDL-P, and HDL-P, respectively) before and after an exercise intervention in 1555 adults from six studies, encompassing 10 distinct exercise programs: APOE (N = 106), DREW (N = 385), GERS (N = 79), HERITAGE (N = 715), STRRIDE I (N = 168) and II (N = 102). Random-effects meta-analyses were performed to evaluate the overall estimate of mean change across the unadjusted and adjusted mean change values from each exercise group. Results Meta-analysis of unadjusted data showed that regular exercise induced significant decreases in the concentration of large VLDL-P, small LDL-P, and medium HDL-P and mean VLDL-P size, with significant increases in the concentration of large LDL-P and large HDL-P and mean LDL-P size. These changes remained significant in meta-analysis with adjustment for age, sex, race, baseline body mass index, and baseline trait value. Conclusions Despite differences in exercise programs and study populations, regular exercise produced putatively beneficial changes in the lipoprotein subclass profile across 10 exercise interventions. Further research is needed to examine how exercise-induced changes in lipoprotein subclasses may be associated with (concomitant changes in) cardiovascular disease risk.

Valérie Coats,1 Jean-Pierre Després,1 Natalie Alméras,1 Mickaël Martin,1 Don D Sin,2 Rémi Rabasa-Lhoret,3 Éric Larose,1 Wan C Tan,2 Jean Bourbeau,4 François Maltais1On behalf of the CanCOLD Collaborative Research Group and the Canadian Respiratory Research Network 1Centre de recherche, Institut universitaire de cardiologie et de pneumologie de Québec, Université, Laval, QC, Canada; 2University of British Columbia, Vancouver, BC, Canada; 3Institut de Recherches Cliniques de Montréal, Département de Nutrition et Service d’Endocrinologie, Centre Hospitalier de l’Université de Montréal, Montréal, QC, Canada; 4Respiratory Epidemiology and Clinical Research Unit, Research Institute of the McGill University Health Centre, Montreal, QC, CanadaRationale: 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

Introduction: Visceral adiposity increases the level of atherogenic lipoproteins and is linked to sex-related differences in cardiovascular risk. Hypothesis. Atherogenic lipoproteins could mediate the relationship between visceral fat and sex-related differences in atherosclerosis burden and composition, including the lipid-rich necrotic core (LRNC). Methods: This study included 294 women (39.4 ± 15.0 years) and 324 men (39.5 ± 13.8 years), matched for age and risk factors (hypertension, dyslipidemia, obesity, diabetes, smoking). Carotid atherosclerosis, visceral abdominal fat (VAT) and cardiac fat (CAT) were studied by magnetic resonance imaging. Results: For similar age and risk profile, women had less VAT ( p p p p p =0.23), men had a greater LRNC volume ( p p =0.025). There was also an interaction between sex, VAT, and total cholesterol/high-density lipoprotein cholesterol ratio (TC/HDL-C) on LRNC volume ( p =0.012), beyond age and risk factors ( p =0.011). Only 8.6% of men and none of the women were classified at high risk (presence of LRNC) by the Framingham Risk Score while 35.4% of men and 14.0% of women were classified at high risk by the Pathobiological Determinants of Atherosclerosis in Youth (PDAY) risk score (risk of advanced atherosclerosis). Elevated TC/HDL-C (≥3) and/or WHR (≥0.8 in women, ≥0.9 in men) were superior to the PDAY risk score, identifying 62.2% of women (Net Reclassification Improvement [NRI]=1.85, p p Conclusions: Women had less visceral adiposity, carotid atherosclerosis burden and LRNC volume, independently of age and risk profile. Carotid LRNC volume varied with sex, VAT, and atherogenic lipoproteins. WHR and TC/HDL-C improved the identification of high-risk carotid atherosclerosis features in women as well as men. This evidence supports the clinical potential of the atherogenic lipoprotein profile and of adiposity distribution in atherosclerosis risk evaluation of both women and men.

In the United States, 32% of beverages consumed by adults and 19% of beverages consumed by children in 2007 to 2010 contained low-calorie sweeteners (LCSs). Among all foods and beverages containing LCSs, beverages represent the largest proportion of LCS consumption worldwide. The term LCS includes the 6 high-intensity sweeteners currently approved by the US Food and Drug Administration and 2 additional high-intensity sweeteners for which the US Food and Drug Administration has issued no objection letters. Because of a lack of data on specific LCSs, this advisory does not distinguish among these LCSs. Furthermore, the advisory does not address foods sweetened with LCSs. This advisory reviews evidence from observational studies and clinical trials assessing the cardiometabolic outcomes of LCS beverages. It summarizes the positions of government agencies and other health organizations on LCS beverages and identifies research needs on the effects of LCS beverages on energy balance and cardiometabolic health. The use of LCS beverages may be an effective strategy to help control energy intake and promote weight loss. Nonetheless, there is a dearth of evidence on the potential adverse effects of LCS beverages relative to potential benefits. On the basis of the available evidence, the writing group concluded that, at this time, it is prudent to advise against prolonged consumption of LCS beverages by children. (Although water is the optimal beverage choice, children with diabetes mellitus who consume a balanced diet and closely monitor their blood glucose may be able to prevent excessive glucose excursions by substituting LCS beverages for sugar-sweetened beverages [SSBs] when needed.) For adults who are habitually high consumers of SSBs, the writing group concluded that LCS beverages may be a useful replacement strategy to reduce intake of SSBs. This approach may be particularly helpful for persons who are habituated to a sweet-tasting beverage and for whom water, at least initially, is an undesirable option. Encouragingly, self-reported consumption of both SSBs and LCS beverages has been declining in the United States, suggesting that it is feasible to reduce SSB intake without necessarily substituting LCS beverages for SSBs. Thus, the use of other alternatives to SSBs, with a focus on water (plain, carbonated, and unsweetened flavored), should be encouraged.

Findings from epidemiological studies over the past 30 years have shown that visceral adipose tissue, accurately measured by CT or MRI, is an independent risk marker of cardiovascular and metabolic morbidity and mortality. Emerging evidence also suggests that ectopic fat deposition, including hepatic and epicardial fat, might contribute to increased atherosclerosis and cardiometabolic risk. This joint position statement from the International Atherosclerosis Society and the International Chair on Cardiometabolic Risk Working Group on Visceral Obesity summarises the evidence for visceral adiposity and ectopic fat as emerging risk factors for type 2 diabetes, atherosclerosis, and cardiovascular disease, with a focus on practical recommendations for health professionals and future directions for research and clinical practice. We discuss the measurement of visceral and ectopic fat, pathophysiology and contribution to adverse health outcomes, response to treatment, and lessons from a public health programme targeting visceral and ectopic fat. We identify knowledge gaps and note the need to develop simple, clinically applicable tools to be able to monitor changes in visceral and ectopic fat over time. Finally, we recognise the need for public health messaging to focus on visceral and ectopic fat in addition to excess bodyweight to better combat the growing epidemic of obesity worldwide.

BACKGROUND Early identification of individuals at increased cardiometabolic risk is an essential step to improve primary preventive interventions. Excessive maximal exercise blood pressure (EBP) has been associated with several adverse outcomes. We examined how submaximal EBP could help us to identify individuals with a deteriorated cardiometabolic risk profile. METHODS Data from an observational study of 3,913 participants from a convenience sample were used. Subjects included in the analyses completed a comprehensive cardiometabolic health assessment (resting blood pressure [BP]; waist circumference; lipid profile; HbA1c; submaximal treadmill exercise test including a standardized stage [3.5 mph and 2% slope] with BP and heart rate measurements). Participants were classified on BP response at the standardized stage (Normal or Excessive Response). Excessive response was defined as systolic BP ≥ 80th percentile or diastolic BP ≥ 90 mmHg. Subjects were also classified into five resting BP subgroups according to current guidelines. RESULTS The Excessive Response group had more deteriorated cardiometabolic and cardiorespiratory profiles than the Normal Response group (P ≤ 0.01). The Excessive Response group also showed a greater proportion of carriers of the hypertriglyceridemic waist phenotype in most resting BP subgroups (P ≤ 0.05). Finally, excessive BP response to submaximal exercise showed an independent contribution on cardiometabolic and cardiorespiratory factors beyond age, sex, and resting BP. CONCLUSIONS This study demonstrates that an excessive BP response to a submaximal exercise is associated with a deteriorated cardiometabolic risk profile beyond resting BP profile. Therefore, submaximal EBP represents a simple screening tool to better identify at-risk individuals requiring aggressive preventive lifestyle interventions.

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.

Cholesterol efflux capacities (CECs) are negatively associated with cardiovascular disease risk, irrespective of plasma high-density lipoprotein (HDL) cholesterol levels. Whether interventions targeting lifestyle improve HDL-CECs is unknown. Our objective was to determine whether improving dietary quality and increasing physical activity levels improves HDL-CECs in men with abdominal obesity and dyslipidemia. Our study sample included men (48 ± 8.5 yr) with an elevated waist circumference (≥90 cm) associated with dyslipidemia (triglycerides ≥1.69 and/or HDL cholesterol 3H]cholesterol-labeled J774 macrophages and HepG2 hepatocytes. The lifestyle modification program led to an overall improvement in the cardiometabolic risk profile, increases in J774-HDL-CEC by 14.1% (+0.88 ± 1.09%, P < 0.0001), HepG2-HDL-CEC by 3.4% (+0.17 ± 0.75%, P = 0.01), and HDL cholesterol and apolipoprotein A-1 levels (13.5%, P < 0.0001 and 14.9%, P < 0.0001, respectively). J774-HDL-CECs and HepG2-HDL-CECs did not change in the control group. The best predictor for changes in HDL-CEC was apolipoprotein A-1 level. The lifestyle modification program also improved HDL-CEC response in postprandial lipemia during an OLTT. HDL-CEC did not change during the OLTT. Our results suggest that increasing physical activity levels and improving diet quality can have a positive impact on both HDL quantity and quality in men with abdominal obesity and dyslipidemia.

Background Our objective was to identify the determinants of high‐density lipoprotein cholesterol efflux capacity ( HDL ‐ CEC ) changes in patients with coronary artery disease who participated in a lifestyle modification program aimed at increasing physical activity levels and improving diet quality. Methods and Results A total of 86 men with coronary artery disease aged between 35 and 80 years participated in a 1‐year lifestyle modification program that aimed to achieve a minimum of 150 minutes of aerobic physical activity weekly and improve diet quality. HDL ‐ CEC s were measured before and after the 1‐year intervention using 3 H‐cholesterol–labeled J774 and HepG2 cells. Visceral, subcutaneous, and cardiac adipose tissue levels were assessed before and after the intervention using magnetic resonance imaging. Lipoprotein particle size and concentrations were measured by proton nuclear magnetic resonance spectroscopy and a complete lipoprotein‐lipid profile was obtained. At baseline, the best correlate of HDL ‐ CEC s were apolipoprotein AI ( R 2 =0.35, P R 2 =0.21, P HDL ‐ CEC s and HepG2‐ HDL ‐ CEC s, respectively. Baseline and longitudinal changes in HDL ‐ CEC s were associated with several lipoprotein size and concentration indices, although high‐density lipoprotein cholesterol was the best predictor of longitudinal changes in J774‐ HDL ‐ CEC s ( R 2 =0.18, P =0.002) and apolipoprotein AI was found to be the best predictor of longitudinal changes in HepG2 cholesterol efflux capacities ( R 2 =0.21, P =0.002). Conclusions Results of this study suggest that increases in high‐density lipoprotein cholesterol and apolipoprotein AI levels typically observed in patients with coronary artery disease undergoing healthy lifestyle modification therapy may be indicative of higher plasma concentrations of functional high‐density lipoprotein particles.

Background Subclinical atherosclerosis identification remains challenging; abdominal visceral adiposity may improve risk stratification beyond traditional cardiovascular risk factors. Hypertriglyceridemic waist, a visceral adiposity marker combining elevated triglycerides (≥2 mmol/L) and waist circumference (≥90 cm), has been related to carotid atherosclerosis, although associations with high‐risk features, including lipid‐rich necrotic core (LRNC), remain unknown. We tested the hypothesis that hypertriglyceridemic waist is an independent marker of high‐risk atherosclerosis features. Methods and Results In this cross‐sectional study including 467 white men (mean age, 45.9±14.8 years; range 19.4–77.6 years), carotid atherosclerosis characteristics were examined by magnetic resonance imaging and associations with hypertriglyceridemic waist and benefits beyond Framingham Risk Score (FRS) and Pathobiological Determinants of Atherosclerosis in Youth (PDAY) were determined. Subclinical carotid atherosclerosis was present in 61.9% of participants, whereas 50.1% had LRNC. Hypertriglyceridemic waist was associated with carotid maximum wall thickness ( P =0.014), wall volume ( P =0.025), normalized wall index ( P =0.004), and Carotid Atherosclerosis Score (derived from wall thickness and LRNC; P =0.049). Hypertriglyceridemic waist was associated with carotid LRNC volume beyond FRS ( P =0.037) or PDAY ( P =0.015), contrary to waist circumference alone (both P >0.05). Although 69.7% and 62.0% of participants with carotid atherosclerosis and/or LRNC were not high‐risk by FRS or PDAY, respectively, hypertriglyceridemic waist correctly reclassified 9.7% and 4.5% of them, respectively. Combining hypertriglyceridemic waist with FRS (net reclassification improvement=0.17; P P =0.003) was superior to each score alone in identifying individuals with carotid atherosclerosis and/or LRNC. Conclusions Hypertriglyceridemic waist is an independent marker of carotid high‐risk atherosclerosis features in men, improving on FRS and PDAY risk score.

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.

Background Previous studies reported that middle‐aged patients with atherogenic lipoprotein‐lipid profile exhibit faster progression of aortic valve stenosis ( AS ). The ratio of apolipoprotein B/apolipoprotein A‐I (apoB/apoA‐I) reflects the balance between atherogenic and anti‐atherogenic lipoproteins. The aim of this study was to examine the association between apoB/apoA‐I ratio and AS hemodynamic progression and to determine whether this association varies according to age. Methods and Results A total of 159 patients (66±13 years, 73% men) with AS were prospectively recruited in the PROGRESSA (Metabolic Determinants of the Progression of Aortic Stenosis) study. Hemodynamic progression of AS was determined by the change in peak aortic jet velocity (V peak ) measured by Doppler‐echocardiography between baseline and 2‐year follow‐up. Patients in the top tertile of apoB/apoA‐I ratio (≥0.62) had a faster progression rate of AS compared with those in the bottom/mid tertiles (V peak progression: 0.30 [0.09˗0.49] versus 0.16 [0.01˗0.36] m/s, P =0.02). There was a significant interaction ( P =0.007) between apoB/apoA‐I ratio and age. Among younger patients (ie, aged AS progression compared with those in the bottom/mid tertiles (V peak progression: 0.34 [0.13˗0.69] versus 0.10 [−0.03˗0.31] m/s, P =0.002), whereas there was no significant difference between tertiles in the subgroup of older patients ( P =0.83). After comprehensive adjustment, higher apoB/apoA‐I ratio was significantly associated with faster AS progression in the subset of younger patients (all, standardized β≥0.36; P ≤0.01). Conclusions Higher apoB/apoA‐I ratio is significantly associated with faster hemodynamic progression of AS in the younger patients. These findings suggest that atherogenic lipid factors may play a crucial role in the pathogenesis of AS in younger patients, but may be are less important in older patients. Clinical Trial Registration URL : https://www.clinicaltrials.gov . Unique identifier: NCT 01679431.