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Anti-Inflammatory Effects of a Vegan Diet Versus the American Heart Association-Recommended Diet in Coronary Artery Disease Trial.
Shah, B, Newman, JD, Woolf, K, Ganguzza, L, Guo, Y, Allen, N, Zhong, J, Fisher, EA, Slater, J
Journal of the American Heart Association. 2018;7(23):e011367
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Inflammation plays a central role in the progression of atherosclerosis and is associated with adverse cardiovascular events. The aim of this study was to determine the effects of a vegan versus American Heart Association (AHA)-recommended diet on high-sensitivity C-reactive protein (hsCRP) [a type of protein found in blood plasma], as well as other markers of inflammation, glucometabolic markers, and lipid profiles in patients with established coronary artery disease (CAD) on guideline-directed medical therapy. This study is a prospective, randomized, open-label, blinded end point study design. The active study duration was 8 weeks, with an interim visit at 4 weeks and a final visit at 8 weeks. Results show: - a significantly greater reduction in hsCRP with a vegan versus AHA-recommended diet in patients with established CAD on guideline-directed medical therapy. - that the degree of weight loss, as measured by both body mass index and waist circumference, did not significantly differ between the 2 diet groups. - that markers of glycaemic control and lipid profiles, overall, also did not significantly differ in the vegan diet group when compared with the AHA-recommended diet group. Authors conclude that in patients with CAD and an elevated hsCRP, despite guideline-directed medical therapy, a vegan diet may be considered to further lower the parameters of inflammation.
Abstract
Background Dietary interventions may play a role in secondary cardiovascular prevention. hsCRP (High-sensitivity C-reactive protein) is a marker of risk for major adverse cardiovascular outcomes in coronary artery disease. Methods and Results The open-label, blinded end-point, EVADE CAD (Effects of a Vegan Versus the American Heart Association-Recommended Diet in Coronary Artery Disease) trial randomized participants (n=100) with coronary artery disease to 8 weeks of a vegan or American Heart Association-recommended diet with provision of groceries, tools to measure dietary intake, and dietary counseling. The primary end point was high-sensitivity C-reactive protein. A linear regression model compared end points after 8 weeks of a vegan versus American Heart Association diet and adjusted for baseline concentration of the end point. Significance levels for the primary and secondary end points were set at 0.05 and 0.0015, respectively. A vegan diet resulted in a significant 32% lower high-sensitivity C-reactive protein (β, 0.68, 95% confidence interval [0.49-0.94]; P=0.02) when compared with the American Heart Association diet. Results were consistent after adjustment for age, race, baseline waist circumference, diabetes mellitus, and prior myocardial infarction (adjusted β, 0.67 [0.47-0.94], P=0.02). The degree of reduction in body mass index and waist circumference did not significantly differ between the 2 diet groups (adjusted β, 0.99 [0.97-1.00], P=0.10; and adjusted β, 1.00 [0.98-1.01], P=0.66, respectively). There were also no significant differences in markers of glycemic control between the 2 diet groups. There was a nonsignificant 13% reduction in low-density lipoprotein cholesterol with the vegan diet when compared with the American Heart Association diet (adjusted β, 0.87 [0.78-0.97], P=0.01). There were no significant differences in other lipid parameters. Conclusions In patients with coronary artery disease on guideline-directed medical therapy, a vegan diet may be considered to lower high-sensitivity C-reactive protein as a risk marker of adverse outcomes. Clinical Trial Registration URL http://www.clinicaltrials.gov . Unique identifier: NCT 02135939.
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Glucotypes reveal new patterns of glucose dysregulation.
Hall, H, Perelman, D, Breschi, A, Limcaoco, P, Kellogg, R, McLaughlin, T, Snyder, M
PLoS biology. 2018;16(7):e2005143
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One in 10 individuals is affected by diabetes, a condition involving abnormal regulation of blood glucose. Currently, diabetes is assessed using single-time or average measurements of blood glucose, without consideration for how blood glucose fluctuates over time. This study used continuous glucose monitoring (CGM) technology to evaluate how blood glucose fluctuates in individuals over time. The authors found that many individuals considered nondiabetic by standard measures experienced frequent elevations in blood glucose levels into the pre-diabetic or diabetic range (15% and 2% of the time, respectively). The authors developed a model for determining the “glucotype” (low, moderate or severe variability) of an individual, a more comprehensive measure of glucose patterns than the standard tests currently used. The authors argue that CGM should become an important tool in early identification of those at risk for type 2 diabetes.
Abstract
Diabetes is an increasing problem worldwide; almost 30 million people, nearly 10% of the population, in the United States are diagnosed with diabetes. Another 84 million are prediabetic, and without intervention, up to 70% of these individuals may progress to type 2 diabetes. Current methods for quantifying blood glucose dysregulation in diabetes and prediabetes are limited by reliance on single-time-point measurements or on average measures of overall glycemia and neglect glucose dynamics. We have used continuous glucose monitoring (CGM) to evaluate the frequency with which individuals demonstrate elevations in postprandial glucose, the types of patterns, and how patterns vary between individuals given an identical nutrient challenge. Measurement of insulin resistance and secretion highlights the fact that the physiology underlying dysglycemia is highly variable between individuals. We developed an analytical framework that can group individuals according to specific patterns of glycemic responses called "glucotypes" that reveal heterogeneity, or subphenotypes, within traditional diagnostic categories of glucose regulation. Importantly, we found that even individuals considered normoglycemic by standard measures exhibit high glucose variability using CGM, with glucose levels reaching prediabetic and diabetic ranges 15% and 2% of the time, respectively. We thus show that glucose dysregulation, as characterized by CGM, is more prevalent and heterogeneous than previously thought and can affect individuals considered normoglycemic by standard measures, and specific patterns of glycemic responses reflect variable underlying physiology. The interindividual variability in glycemic responses to standardized meals also highlights the personal nature of glucose regulation. Through extensive phenotyping, we developed a model for identifying potential mechanisms of personal glucose dysregulation and built a webtool for visualizing a user-uploaded CGM profile and classifying individualized glucose patterns into glucotypes.
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Enhanced cortisol production rates, free cortisol, and 11beta-HSD-1 expression correlate with visceral fat and insulin resistance in men: effect of weight loss.
Purnell, JQ, Kahn, SE, Samuels, MH, Brandon, D, Loriaux, DL, Brunzell, JD
American journal of physiology. Endocrinology and metabolism. 2009;296(2):E351-7
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Excess abdominal fat in men is a risk factor for both type 2 diabetes and cardiovascular disease. The aim of this study was to test the hypothesis that increased cortisol levels contribute to increased abdominal fat and insulin resistance in men. Twenty-four healthy men aged 18-70 took part in the study. Eight of the participants, who were obese, were put on a calorie-controlled weight loss diet. Cortisol production rate (CPR) and free cortisol (FC) were correlated with increased intra-abdominal fat (IAF) and decreased insulin sensitivity (Si). Cortisol levels were not correlated with subcutaneous fat (SQF). CPR and FC did not change with weight loss, suggesting that cortisol levels could influence the distribution of body fat upon weight regain. The authors concluded that their findings support a role for activation of the HPA axis and abnormal cortisol secretion in determining body fat distribution and predisposing these men to type 2 diabetes.
Abstract
Controversy exists as to whether endogenous cortisol production is associated with visceral obesity and insulin resistance in humans. We therefore quantified cortisol production and clearance rates, abdominal fat depots, insulin sensitivity, and adipocyte gene expression in a cohort of 24 men. To test whether the relationships found are a consequence rather than a cause of obesity, eight men from this larger group were studied before and after weight loss. Daily cortisol production rates (CPR), free cortisol levels (FC), and metabolic clearance rates (MCR) were measured by stable isotope methodology and 24-h sampling; intra-abdominal fat (IAF) and subcutaneous fat (SQF) by computed tomography; insulin sensitivity (S(I)) by frequently sampled intravenous glucose tolerance test; and adipocyte 11beta-hydroxysteroid dehydrogenase-1 (11beta-HSD-1) gene expression by quantitative RT-PCR from subcutaneous biopsies. Increased CPR and FC correlated with increased IAF, but not SQF, and with decreased S(I). Increased 11beta-HSD-1 gene expression correlated with both IAF and SQF and with decreased S(I). With weight loss, CPR, FC, and MCR did not change compared with baseline; however, with greater loss in body fat than lean mass during weight loss, both CPR and FC increased proportionally to final fat mass and IAF and 11beta-HSD-1 decreased compared with baseline. These data support a model in which increased hypothalamic-pituitary-adrenal activity in men promotes selective visceral fat accumulation and insulin resistance and may promote weight regain after diet-induced weight loss, whereas 11beta-HSD-1 gene expression in SQF is a consequence rather than cause of adiposity.