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      Effects of a DASH-like diet containing lean beef on vascular health

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          Abstract

          A DASH (dietary approaches to stop hypertension) dietary pattern rich in fruits and vegetables and low-fat dairy products with increased dietary protein provided primarily from plant protein sources decreases blood pressure. No studies, however, have evaluated the effects of a DASH-like diet with increased dietary protein from lean beef on blood pressure and vascular health. The aim of this study was to study the effect of DASH-like diets that provided different amounts of protein from lean beef (DASH 28 g beef per day; beef in an optimal lean diet (BOLD) 113 g beef per day; beef in an optimal lean diet plus additional protein (BOLD+) 153 g beef per day) on blood pressure, endothelial function and vascular reactivity versus a healthy American diet (HAD). Using a randomized, crossover study design, 36 normotensive participants (systolic blood pressure (SBP), 116±3.6 mm Hg) were fed four isocaloric diets,: HAD (33% total fat, 12% saturated fatty acids (SFA), 17% protein (PRO), 20 g beef per day), DASH (27% total fat, 6% SFA, 18% PRO, 28 g beef per day), BOLD (28% total fat, 6% SFA, 19% PRO, 113 g beef per day) and BOLD+ (28% total fat, 6% SFA, 27% PRO, 153 g beef per day), for 5 weeks. SBP decreased ( P<0.05) in subjects on the BOLD+ diet (111.4±1.9 mm Hg) versus HAD (115.7±1.9). There were no significant effects of the DASH and BOLD diets on SBP. Augmentation index (AI) was significantly reduced in participants on the BOLD diet (−4.1%). There were no significant effects of the dietary treatments on diastolic blood pressure or endothelial function (as measured by peripheral arterial tonometry). A moderate protein DASH-like diet including lean beef decreased SBP in normotensive individuals. The inclusion of lean beef in a heart healthy diet also reduced peripheral vascular constriction.

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          Cross-sectional relations of digital vascular function to cardiovascular risk factors in the Framingham Heart Study.

          Digital pulse amplitude augmentation in response to hyperemia is a novel measure of peripheral vasodilator function that depends partially on endothelium-derived nitric oxide. Baseline digital pulse amplitude reflects local peripheral arterial tone. The relation of digital pulse amplitude and digital hyperemic response to cardiovascular risk factors in the community is unknown. Using a fingertip peripheral arterial tonometry (PAT) device, we measured digital pulse amplitude in Framingham Third Generation Cohort participants (n=1957; mean age, 40+/-9 years; 49% women) at baseline and in 30-second intervals for 4 minutes during reactive hyperemia induced by 5-minute forearm cuff occlusion. To evaluate the vascular response in relation to baseline, adjusting for systemic effects and skewed data, we expressed the hyperemic response (called the PAT ratio) as the natural logarithm of the ratio of postdeflation to baseline pulse amplitude in the hyperemic finger divided by the same ratio in the contralateral finger that served as control. The relation of the PAT ratio to cardiovascular risk factors was strongest in the 90- to 120-second postdeflation interval (overall model R(2)=0.159). In stepwise multivariable linear regression models, male sex, body mass index, ratio of total to high-density lipoprotein cholesterol, diabetes mellitus, smoking, and lipid-lowering treatment were inversely related to PAT ratio, whereas increasing age was positively related to PAT ratio (all P<0.01). Reactive hyperemia produced a time-dependent increase in fingertip pulse amplitude. Digital vasodilator function is related to multiple traditional and metabolic cardiovascular risk factors. Our findings support further investigations to define the clinical utility and predictive value of digital pulse amplitude.
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            Treatment of hypertension in the prevention and management of ischemic heart disease: a scientific statement from the American Heart Association Council for High Blood Pressure Research and the Councils on Clinical Cardiology and Epidemiology and Prevention.

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              Modelling the decline in coronary heart disease deaths in England and Wales, 1981-2000: comparing contributions from primary prevention and secondary prevention.

              To investigate whether population based primary prevention (risk factor reduction in apparently healthy people) might be more powerful than current government initiatives favouring risk factor reduction in patients with coronary heart disease (CHD) (secondary prevention). The IMPACT model was used to synthesise data for England and Wales describing CHD patient numbers, uptake of specific treatments, trends in major cardiovascular risk factors, and the mortality benefits of these specific risk factor changes in healthy people and in CHD patients. Between 1981 and 2000, CHD mortality rates fell by 54%, resulting in 68,230 fewer deaths in 2000. Overall smoking prevalence declined by 35% between 1981 and 2000, resulting in approximately 29,715 (minimum estimate 20 035, maximum estimate 44,675) fewer deaths attributable to smoking cessation: approximately 5035 in known CHD patients and approximately 24,680 in healthy people. Population total cholesterol concentrations fell by 4.2%, resulting in approximately 5770 fewer deaths attributable to dietary changes (1205 in CHD patients and 4565 in healthy people) plus 2135 fewer deaths attributable to statin treatment (1990 in CHD patients, 145 in people without CHD). Mean population blood pressure fell by 7.7%, resulting in approximately 5870 fewer deaths attributable to secular falls in blood pressure (520 in CHD patients and 5345 in healthy people) plus approximately 1890 fewer deaths attributable to antihypertensive treatments in people without CHD. Approximately 45,370 fewer deaths were thus attributable to reductions in the three major risk factors in the population: some 36 625 (81%) in people without recognised CHD and 8745 (19%) in CHD patients. Compared with secondary prevention, primary prevention achieved a fourfold larger reduction in deaths. Future CHD policies should prioritise population-wide tobacco control and healthier diets.
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                Author and article information

                Journal
                J Hum Hypertens
                J Hum Hypertens
                Journal of Human Hypertension
                Nature Publishing Group
                0950-9240
                1476-5527
                October 2014
                19 June 2014
                : 28
                : 10
                : 600-605
                Affiliations
                [1 ]Department of Nutritional Sciences, Pennsylvania State University , University Park, PA, USA
                [2 ]Department of Statistics, Pennsylvania State University , University Park, PA, USA
                [3 ]Department of Biobehavioral Health, Pennsylvania State University , University Park, PA, USA
                [4 ]Department of Medicine, Pennsylvania State University , University Park, PA, USA
                [5 ]Department of Veterinary and Biomedical Sciences, Pennsylvania State University , University Park, PA, USA
                [6 ]New Jersey Institute for Food, Nutrition and Health, Rutgers, The State University of New Jersey , New Brunswick, NJ, USA
                Author notes
                [* ]Department of Nutritional Sciences, 119 Chandlee Lab, The Pennsylvania State University , University Park, PA 16802, USA. E-mail: pmk3@ 123456psu.edu
                [7]

                Current address: Division of Health Sciences, University of South Australia, Adelaide, South Australia, Australia.

                [8]

                Current address: Department of Statistics, Carnegie Mellon University, Pittsburgh, PA, USA.

                Article
                jhh201434
                10.1038/jhh.2014.34
                4160562
                24943285
                939f3169-c330-41e8-b31a-8c2792494e31
                Copyright © 2014 Macmillan Publishers Limited

                This work is licensed under a Creative Commons Attribution 3.0 Unported License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/3.0/

                History
                : 13 November 2013
                : 24 February 2014
                : 05 March 2014
                Categories
                Original Article

                Cardiovascular Medicine
                Cardiovascular Medicine

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