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      The effect of the apolipoprotein E genotype on response to personalized dietary advice intervention: findings from the Food4Me randomized controlled trial

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          Abstract

          The apolipoprotein E (APOE) risk allele (ɛ4) is associated with higher total cholesterol (TC), amplified response to saturated fatty acid (SFA) reduction, and increased cardiovascular disease. Although knowledge of gene risk may enhance dietary change, it is unclear whether ɛ4 carriers would benefit from gene-based personalized nutrition (PN).

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          Most cited references33

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          Cardiovascular disease in Europe 2014: epidemiological update.

          This paper provides an update for 2014 on the burden of cardiovascular disease (CVD), and in particular coronary heart disease (CHD) and stroke, across the countries of Europe. Cardiovascular disease causes more deaths among Europeans than any other condition, and in many countries still causes more than twice as many deaths as cancer. There is clear evidence in most countries with available data that mortality and case-fatality rates from CHD and stroke have decreased substantially over the last 5-10 years but at differing rates. The differing recent trends have therefore led to increasing inequalities in the burden of CVD between countries. For some Eastern European countries, including Russia and Ukraine, the mortality rate for CHD for 55-60 year olds is greater than the equivalent rate in France for people 20 years older.
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            Apolipoprotein E polymorphism and cardiovascular disease: a HuGE review.

            This review examines the association between the apolipoprotein (apo) var epsilon gene polymorphism (or its protein product (apo E)), metabolic regulation of cholesterol, and cardiovascular disease. The apo var epsilon gene is located at chromosome 19q13.2. Among the variants of this gene, alleles (*) epsilon2, (*) epsilon3, and (*) epsilon4 constitute the common polymorphism found in most populations. Of these variants, apo (*) epsilon3 is the most frequent (>60%) in all populations studied. The polymorphism has functional effects on lipoprotein metabolism mediated through the hepatic binding, uptake, and catabolism of chylomicrons, chylomicron remnants, very low density lipoprotein (VLDL), and high density lipoprotein subspecies. Apo E is the primary ligand for two receptors, the low density lipoprotein (LDL) receptor (also known as the B/E receptor) found on the liver and other tissues and an apo E-specific receptor found on the liver. The coordinate interaction of these lipoprotein complexes with their receptors forms the basis for the metabolic regulation of cholesterol. Allelic variation in apo var epsilon is consistently associated with plasma concentrations of total cholesterol, LDL cholesterol, and apo B (the major protein of LDL, VLDL, and chylomicrons). Apo var epsilon has been studied in disorders associated with elevated cholesterol levels or lipid derangements (i.e., hyperlipoproteinemia type III, coronary heart disease, strokes, peripheral artery disease, and diabetes mellitus). The apo var epsilon genotype yields poor predictive values when screening for clinically defined atherosclerosis despite positive, but modest associations with plaque and coronary heart disease outcomes. In addition to genotype-phenotype associations with vascular disease, the alleles and isoforms of apo var epsilon have been related to dementias, most commonly Alzheimer's disease.
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              Apolipoprotein E polymorphism and atherosclerosis

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                Author and article information

                Journal
                The American Journal of Clinical Nutrition
                American Society for Nutrition
                0002-9165
                1938-3207
                September 01 2016
                September 01 2016
                : 104
                : 3
                : 827-836
                Affiliations
                [1 ]on behalf of the Food4Me Study
                Article
                10.3945/ajcn.116.135012
                27510539
                828d0016-18e4-4bb9-927d-e07481040b20
                © 2016
                History

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