The association between sedentary time and the risk for CVD is nonlinear with an increased risk only at very high levels. These findings could have implications for guideline recommendations regarding the risks related to sedentary behavior.

Objective To determine the association between cardiorespiratory fitness and sedentary behavior, independent of exercise activity. Patients and Methods We included 2,223 participants (ages 12-49 years, 47% female) without known heart disease who had both cardiovascular fitness testing and at least one day of accelerometer data from NHANES 2003-2004. From accelerometer data, we quantified bouts of exercise as mean minutes per day for each participant. Sedentary time was defined as <100 counts per minute in mean minutes per day. Cardiorespiratory fitness was derived from a sub-maximal exercise treadmill test. Multivariable-adjusted linear regression analyses were performed with fitness as the dependent variable. Models were stratified by gender, adjusted for age, BMI, wear time and included sedentary and exercise time. Results An additional hour of daily exercise activity time was associated with a 0.88 (0.37 to 1.39, P<.001) MET higher fitness for men and a 1.37 (0.43 to 2.31, P=.004) MET higher fitness for women. An additional hour of sedentary time was associated with a -0.12 (-0.02 to -0.22, P=.03) and a -0.24 (-0.10 to -0.38, P<.001) MET difference in fitness for men and women, respectively. Conculsion After adjustment for exercise activity, sedentary behavior appears to have an inverse association with fitness. These findings suggest that the risk related to sedentary behavior might be mediated, in part, through lower fitness levels.

Abstract-Obesity is associated with impaired endothelial-dependent flow-mediated dilation, a precursor to hypertension and atherosclerosis. Although dieting generally improves cardiovascular risk factors, the direct effect of different dietary strategies on vascular endothelial function is not known. The purpose of this study was to test the hypothesis that a low-fat (LF) diet improves endothelial function compared with an isocaloric low-carbohydrate (LC) diet. Obese (nϭ20; body mass index: 29 to 39; mean systolic blood pressure: 107 to 125 mm Hg) and otherwise healthy volunteers were randomly assigned to either the American Heart Association modeled LF (30% fat calories) diet or an isocaloric LC Atkins' style diet (20 g of carbohydrates) for 6 weeks (4-week weight loss and 2-week maintenance phase). Brachial flow-mediated dilation and dilation to nitroglycerin were measured with ultrasound using automated edge detection technology (baseline, week 2, and week 6). Blood pressure, weight loss, and cholesterol profiles were measured throughout the study. Key Words: diet Ⅲ weight loss Ⅲ endothelium Ⅲ obesity Ⅲ blood pressure O besity is a risk factor for atherosclerosis, a major cause of morbidity and mortality throughout the world. In the United States, the incidence of obesity has risen dramatically in the past decade. Public awareness of the "obesity epidemic" has resulted in various dietary weight loss strategies, and it is estimated that 45% of American women and 30% of American men diet to lose weight. 1 However, the nutrientspecific effects of these diets on cardiovascular health are largely unknown.Mounting evidence suggests that the integrity of the vascular endothelium is critical in the prevention of atherosclerosis, likely through release of endothelial-derived factors such as NO, which confer antiproliferative, antiinflammatory, and antithrombotic properties, in addition to vasodilation. 2,3 Abnormal endothelial function marked by reduced dilation to an increase in flow (endotheliumdependent flow-mediated dilation [FMD]) is an early hallmark of cardiovascular disease and a strong prognostic factor for future cardiovascular events. 4 -9 Most risk factors for coronary artery disease are associated with reduced FMD. 10 Weight loss through conventional low-fat (LF) diets improve endothelial function 11,12 ; however, some currently popular diets emphasize low-carbohydrate (LC) intake supplemented by high dietary fat and protein. Initial reports show sustained weight loss while on LC diets without detrimental effects on serum lipid levels. 13,14 Further benefit may be derived from the reduction in arterial pressure from either LF or LC diets. However, it is unclear whether these cardiovascular benefits of weight loss on a LC diet are negated by the known detrimental effects on endothelial function of even a single high-fat meal. [15][16][17] Weight loss is similar on LC and LF diets, but effects on cardiovascular health, a major anticipated benefit of most weight-loss regimens, may diverge. Therefore, the pur...

Aims Higher parity has been associated with increased maternal risk of cardiovascular (CV) disease, but the mechanism is not well delineated. Whether the number of live births is associated with coronary and aortic subclinical atherosclerosis has not been fully evaluated. Methods and Results Women from the Dallas Heart Study, a multiethnic population-based cohort of subjects aged 30–65, were included if they had data on self-reported live births and coronary artery calcium (CAC) measured by computed tomography or aortic wall thickness (AWT) by MRI. CAC was positive if >10 Agatston Units, and AWT if greater than the 75th percentile reference point for age and gender. Among the 1644 women included in the study, the mean age was 45 years and 55% were black. Sequential multivariable models were done adjusting for age, race, traditional CV risk factors, body mass index, income, education, hormone replacement therapy, oral contraceptives, and physical activity. Using women with 2–3 live births as the reference, those with 4 or more live births had an increased prevalence of elevated CAC (OR 2.2, 95% CI 1.28–3.65) and AWT (OR 1.6, 95% CI 1.04–2.41). Women with 0–1 live births also had increased CAC (OR 1.9, 95% CI 1.16–3.03) and AWT (OR 1.5, 95% CI 1.05–2.09) after multivariable adjustment. Conclusion The number of live births is associated with subclinical coronary and aortic atherosclerosis, with an apparent U-shaped relationship. Further studies are needed to confirm this association and explore the biological underpinnings of these findings.