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      Lifestyle and Dietary Determinants of Serum Apolipoprotein A1 and Apolipoprotein B Concentrations: Cross-Sectional Analyses within a Swedish Cohort of 24,984 Individuals

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          Abstract

          Low serum apolipoprotein (Apo) A1 concentrations and high serum ApoB concentrations may be better markers of the risk of cardiovascular disease than high-density lipoprotein (HDL) and low-density lipoprotein (LDL). However, the associations between modifiable lifestyle factors and Apo concentrations have not been investigated in detail. Therefore, this study investigated the associations between Apo concentrations and education, lifestyle factors and dietary intake (macronutrients and 34 food groups). These cross-sectional associations were examined among 24,984 individuals in a Swedish population-based cohort. Baseline examinations of the cohort were conducted between 1991 and 1996. Dietary intake was assessed using a modified diet history method. The main determinants of high ApoA1 concentrations ( r between 0.05 and 0.25) were high alcohol consumption, high physical activity, non-smoking, and a low body mass index (BMI), and the main determinants of high ApoB concentrations were smoking and a high BMI. The intake of sucrose and food products containing added sugar (such as pastries, sweets, chocolate, jam/sugar and sugar-sweetened beverages) was negatively correlated with ApoA1 concentrations and positively correlated with ApoB concentrations and the ApoB/ApoA1 ratio, whereas the intake of fermented dairy products, such as fermented milk and cheese, was positively correlated with ApoA1 concentrations and negatively correlated with the ApoB/ApoA1 ratio. These results indicate that smoking, obesity, low physical activity, low alcohol consumption and a diet high in sugar and low in fermented dairy products are correlated with an unfavorable Apo profile.

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          Most cited references36

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          The Malmo Diet and Cancer Study. Design and feasibility.

          The Malmö Diet and Cancer study is a 10-year prospective case-control study in 45-64-year-old men and women (n = 53,000) living in a city with 230,000 inhabitants. One objective is to clarify whether a western diet is associated with certain forms of cancer whilst taking other life-style factors into account. Another broad question is whether oxidative stress and the activity in DNA-repairing systems influence the impact of diet on the development of all or certain forms of cancer. The study is also to act as a resource available for testing new hypotheses emanating from other studies. Initially food intake, heredity, socio-economic factors, life-style pattern, occupational situation, previous and current diseases, symptoms and medications, will be determined. Viable lymphocytes, granulocytes, erythrocytes, and plasma/serum will be stored in a biological bank together with tumour specimens gathered from cases. The incidence and mortality of all cancer forms will then be followed for 10 years by existing registries. Data from the initial examination in these cases will then be compared with those of control subjects not having developed any form of cancer. A biomarker programme, utilizing the biological bank, has been developed and is aimed at finding predictors and/or precursors of cancer. A high participation rate (> 70%) and a high quality biological bank are prerequisites for a successful project. The experience gathered so far indicates that these goals are feasible.
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            Sweetened beverage consumption, incident coronary heart disease, and biomarkers of risk in men.

            Sugar-sweetened beverage consumption is associated with weight gain and risk of type 2 diabetes mellitus. Few studies have tested for a relationship with coronary heart disease (CHD) or intermediate biomarkers. The role of artificially sweetened beverages is also unclear. We performed an analysis of the Health Professionals Follow-Up Study, a prospective cohort study including 42 883 men. Associations of cumulatively averaged sugar-sweetened (eg, sodas) and artificially sweetened (eg, diet sodas) beverage intake with incident fatal and nonfatal CHD (myocardial infarction) were examined with proportional hazard models. There were 3683 CHD cases over 22 years of follow-up. Participants in the top quartile of sugar-sweetened beverage intake had a 20% higher relative risk of CHD than those in the bottom quartile (relative risk=1.20; 95% confidence interval, 1.09-1.33; P for trend <0.01) after adjustment for age, smoking, physical activity, alcohol, multivitamins, family history, diet quality, energy intake, body mass index, pre-enrollment weight change, and dieting. Artificially sweetened beverage consumption was not significantly associated with CHD (multivariate relative risk=1.02; 95% confidence interval, 0.93-1.12; P for trend=0.28). Adjustment for self-reported high cholesterol, high triglycerides, high blood pressure, and diagnosed type 2 diabetes mellitus slightly attenuated these associations. Intake of sugar-sweetened but not artificially sweetened beverages was significantly associated with increased plasma triglycerides, C-reactive protein, interleukin-6, and tumor necrosis factor receptors 1 and 2 and decreased high-density lipoprotein, lipoprotein(a), and leptin (P<0.02). Consumption of sugar-sweetened beverages was associated with increased risk of CHD and some adverse changes in lipids, inflammatory factors, and leptin. Artificially sweetened beverage intake was not associated with CHD risk or biomarkers.
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              Atherosclerosis: Basic Mechanisms

              Circulation, 91(9), 2488-2496
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                Author and article information

                Journal
                Nutrients
                Nutrients
                nutrients
                Nutrients
                MDPI
                2072-6643
                28 February 2017
                March 2017
                : 9
                : 3
                : 211
                Affiliations
                [1 ]Diabetes and Cardiovascular Disease—Genetic Epidemiology, Department of Clinical Sciences Malmö, Lund University, Jan Waldenströms gata 35, SE-20502 Malmö, Sweden; gbi10kfr@ 123456student.lu.se (K.F.); madelene.borg.342@ 123456student.lu.se (M.B.); ulrika.ericson@ 123456med.lu.se (U.E.)
                [2 ]Cardiovascular Epidemiology, Department of Clinical Sciences Malmö, Lund University, Jan Waldenströms gata 35, SE-20502 Malmö, Sweden; yan.borne@ 123456med.lu.se
                [3 ]Hypertension and Cardiovascular Disease, Department of Clinical Sciences Malmö, Lund University, Jan Waldenströms gata 35, SE-20502 Malmö, Sweden; olle.melander@ 123456med.lu.se
                [4 ]Nutritional Epidemiology, Department of Clinical Sciences Malmö, Lund University, Jan Waldenströms gata 35, SE-20502 Malmö, Sweden
                Author notes
                [* ]Correspondence: emily.sonestedt@ 123456med.lu.se ; Tel.: +46-40-391325
                Article
                nutrients-09-00211
                10.3390/nu9030211
                5372874
                28264492
                999b44c3-c196-4281-a472-e56f38ea107c
                © 2017 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 15 December 2016
                : 22 February 2017
                Categories
                Article

                Nutrition & Dietetics
                diet,nutrition,apolipoproteins,epidemiology
                Nutrition & Dietetics
                diet, nutrition, apolipoproteins, epidemiology

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