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      Comprehensive Review of the Impact of Dairy Foods and Dairy Fat on Cardiometabolic Risk 1 2 3

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          Abstract

          Because regular-fat dairy products are a major source of cholesterol-raising saturated fatty acids (SFAs), current US and Canadian dietary guidelines for cardiovascular health recommend the consumption of low-fat dairy products. Yet, numerous randomized controlled trials (RCTs) have reported rather mixed effects of reduced- and regular-fat dairy consumption on blood lipid concentrations and on many other cardiometabolic disease risk factors, such as blood pressure and inflammation markers. Thus, the focus on low-fat dairy in current dietary guidelines is being challenged, creating confusion within health professional circles and the public. This narrative review provides perspective on the research pertaining to the impact of dairy consumption and dairy fat on traditional and emerging cardiometabolic disease risk factors. This comprehensive assessment of evidence from RCTs suggests that there is no apparent risk of potential harmful effects of dairy consumption, irrespective of the content of dairy fat, on a large array of cardiometabolic variables, including lipid-related risk factors, blood pressure, inflammation, insulin resistance, and vascular function. This suggests that the purported detrimental effects of SFAs on cardiometabolic health may in fact be nullified when they are consumed as part of complex food matrices such as those in cheese and other dairy foods. Thus, the focus on low-fat dairy products in current guidelines apparently is not entirely supported by the existing literature and may need to be revisited on the basis of this evidence. Future studies addressing key research gaps in this area will be extremely informative to better appreciate the impact of dairy food matrices, as well as dairy fat specifically, on cardiometabolic health.

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          Most cited references55

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          Inflammation in atherosclerosis: from pathophysiology to practice.

          Until recently, most envisaged atherosclerosis as a bland arterial collection of cholesterol, complicated by smooth muscle cell accumulation. According to that concept, endothelial denuding injury led to platelet aggregation and release of platelet factors which would trigger the proliferation of smooth muscle cells in the arterial intima. These cells would then elaborate an extracellular matrix that would entrap lipoproteins, forming the nidus of the atherosclerotic plaque. Beyond the vascular smooth muscle cells long recognized in atherosclerotic lesions, subsequent investigations identified immune cells and mediators at work in atheromata, implicating inflammation in this disease. Multiple independent pathways of evidence now pinpoint inflammation as a key regulatory process that links multiple risk factors for atherosclerosis and its complications with altered arterial biology. Knowledge has burgeoned regarding the operation of both innate and adaptive arms of immunity in atherogenesis, their interplay, and the balance of stimulatory and inhibitory pathways that regulate their participation in atheroma formation and complication. This revolution in our thinking about the pathophysiology of atherosclerosis has now begun to provide clinical insight and practical tools that may aid patient management. This review provides an update of the role of inflammation in atherogenesis and highlights how translation of these advances in basic science promises to change clinical practice.
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            Plasma fibrinogen level and the risk of major cardiovascular diseases and nonvascular mortality: an individual participant meta-analysis.

            Plasma fibrinogen levels may be associated with the risk of coronary heart disease (CHD) and stroke. To assess the relationships of fibrinogen levels with risk of major vascular and with risk of nonvascular outcomes based on individual participant data. Relevant studies were identified by computer-assisted searches, hand searches of reference lists, and personal communication with relevant investigators. All identified prospective studies were included with information available on baseline fibrinogen levels and details of subsequent major vascular morbidity and/or cause-specific mortality during at least 1 year of follow-up. Studies were excluded if they recruited participants on the basis of having had a previous history of cardiovascular disease; participants with known preexisting CHD or stroke were excluded. Individual records were provided on each of 154,211 participants in 31 prospective studies. During 1.38 million person-years of follow-up, there were 6944 first nonfatal myocardial infarctions or stroke events and 13,210 deaths. Cause-specific mortality was generally available. Analyses involved proportional hazards modeling with adjustment for confounding by known cardiovascular risk factors and for regression dilution bias. Within each age group considered (40-59, 60-69, and > or =70 years), there was an approximately log-linear association with usual fibrinogen level for the risk of any CHD, any stroke, other vascular (eg, non-CHD, nonstroke) mortality, and nonvascular mortality. There was no evidence of a threshold within the range of usual fibrinogen level studied at any age. The age- and sex- adjusted hazard ratio per 1-g/L increase in usual fibrinogen level for CHD was 2.42 (95% confidence interval [CI], 2.24-2.60); stroke, 2.06 (95% CI, 1.83-2.33); other vascular mortality, 2.76 (95% CI, 2.28-3.35); and nonvascular mortality, 2.03 (95% CI, 1.90-2.18). The hazard ratios for CHD and stroke were reduced to about 1.8 after further adjustment for measured values of several established vascular risk factors. In a subset of 7011 participants with available C-reactive protein values, the findings for CHD were essentially unchanged following additional adjustment for C-reactive protein. The associations of fibrinogen level with CHD or stroke did not differ substantially according to sex, smoking, blood pressure, blood lipid levels, or several features of study design. In this large individual participant meta-analysis, moderately strong associations were found between usual plasma fibrinogen level and the risks of CHD, stroke, other vascular mortality, and nonvascular mortality in a wide range of circumstances in healthy middle-aged adults. Assessment of any causal relevance of elevated fibrinogen levels to disease requires additional research.
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              2012 update of the Canadian Cardiovascular Society guidelines for the diagnosis and treatment of dyslipidemia for the prevention of cardiovascular disease in the adult.

              Many developments have occurred since the publication of the widely-used 2009 Canadian Cardiovascular Society (CCS) Dyslipidemia guidelines. Here, we present an updated version of the guidelines, incorporating new recommendations based on recent findings and harmonizing CCS guidelines with those from other Societies. The Grading of Recommendations Assessment, Development and Evaluation (GRADE) system was used, per present standards of the CCS. The total cardiovascular disease Framingham Risk Score (FRS), modified for a family history of premature coronary disease, is recommended for risk assessment. Low-density lipoprotein cholesterol remains the primary target of therapy. However, non-high density lipoprotein cholesterol has been added to apolipoprotein B as an alternate target. There is an increased emphasis on treatment of higher risk patients, including those with chronic kidney disease and high risk hypertension. The primary panel has recommended a judicious use of secondary testing for subjects in whom the need for statin therapy is unclear. Expanded information on health behaviours is presented and is the backbone of risk reduction in all subjects. Finally, a systematic approach to statin intolerance is advocated to maximize appropriate use of lipid-lowering therapy. This document presents the recommendations and principal conclusions of this process. Along with associated Supplementary Material that can be accessed online, this document will be part of a program of knowledge translation. The goal is to increase the appropriate use of evidence-based cardiovascular disease event risk assessment in the management of dyslipidemia as a fundamental means of reducing global risk in the Canadian population. Copyright © 2013 Canadian Cardiovascular Society. Published by Elsevier Inc. All rights reserved.
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                Author and article information

                Journal
                Adv Nutr
                Adv Nutr
                advances in nutrition
                advannut
                Advances in Nutrition
                American Society for Nutrition
                2161-8313
                2156-5376
                10 November 2016
                November 2016
                1 November 2017
                : 7
                : 6
                : 1041-1051
                Affiliations
                [4 ]Institute of Nutrition and Functional Foods and
                [5 ]Centre Hospitalier Universitaire de Québec, Laval University, Quebec City, Canada;
                [6 ]Institut Universitaire de Cardiologie et de Pneumologie de Québec, Quebec City, Canada; and
                [7 ]Department of Nutritional Science, Faculty of Medicine, University of Toronto, Toronto, Canada
                Author notes
                [* ]To whom correspondence should be addressed. E-mail: benoit.lamarche@ 123456fsaa.ulaval.ca .
                [1]

                This review was supported in part by an unrestricted grant from the Dairy Research Consortium (Dairy Farmers of Canada, Centre national interprofessionnel de l’économie laitière, Dairy Research Institute, Dairy Australia Ltd., Dutch Dairy Association, and Danish Dairy Research Foundation) and by the Chair of Nutrition at Laval University. J-PD-C is the recipient of doctoral scholarships from the Canadian Institute of Health Research and the Fonds de Recherche du Québec—Santé. JAC is the recipient of the Alexander Graham Bell doctoral scholarship from the Natural Sciences and Engineering Research Council of Canada. M-EL is the recipient of a Canadian Institutes of Health Research fellowship (no. MFE-140953). This is a free access article, distributed under terms ( http://www.nutrition.org/publications/guidelines-and-policies/license/) that permit unrestricted noncommercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                [2]

                Author disclosures: B Lamarche is Chair of Nutrition at Laval University. This chair is supported by unrestricted endowments from the Royal Bank of Canada, Pfizer, and Provigo/Loblaws. B Lamarche has received funding in the last 5 y for his research from the Canadian Institutes of Health Research (CIHR), Natural Sciences and Engineering Research Council of Canada, Agriculture and Agrifood Canada, the Canola Council of Canada, Dairy Farmers of Canada, Dairy Research Institute, Atrium Innovations, the Danone Institute, and Merck Frosst. B Lamarche has received speaker honoraria over the last 5 y from Dairy Farmers of Canada (DFC), Dairy Research Institute (DRI). B Lamarche is Chair of the Expert Scientific Advisory Panel of DFC, and was a member in 2015 of the ad hoc committee on saturated fat of the Heart and Stroke Foundation of Canada. P Couture has received funding in the last 5 y from the CIHR, Agriculture and Agrifood Canada, DFC, DRI, Merck Frosst, and Kaneka Corporation. S Desroches has received funding in the last 5 y from the CIHR and the Danone Institute. J-P Drouin-Chartier has received speaker honoraria in 2016 from DFC. JA Côté, M-È Labonté, D Brassard, and M Tessier-Grenier, no conflicts of interest.

                [3]

                Supplemental Material is available from the “Online Supporting Material” link in the online posting of the article and from the same link in the online table of contents at http://advances.nutrition.org.

                Article
                011619
                10.3945/an.115.011619
                5105034
                28140322
                cdc06df6-5513-407a-8a34-ab8702d77825
                © 2016 American Society for Nutrition

                This is a free access article, distributed under terms ( http://www.nutrition.org/publications/guidelines-and-policies/license/) that permit unrestricted noncommercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Page count
                Pages: 11
                Categories
                Reviews

                dairy,milk,yogurt,cheese,cholesterol,blood pressure,triglyceride,apolipoprotein b,inflammation

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