Different outcomes for omega-3 heart trials: why?
aDepartment of Pediatrics, Institute of Human Nutrition, Columbia University Medical Center, New York, New York, USA bHuman Development and Health Academic Unit, Institute of Human Nutrition, Faculty of Medicine, University of Southampton, Southampton, UK.Current opinion in clinical nutrition and metabolic care 12/2011; 15(2):97-8. DOI: 10.1097/MCO.0b013e32834ec9e5
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ABSTRACT: Fatty acid research began about 90 years ago but intensified in recent years. Essential fatty acids (linoleic and α-linolenic) must come from diet. Other fatty acids may come from diet or may be synthesized. Fatty acids are major components of cell membrane structure, modulate gene transcription, function as cytokine precursors, and serve as energy sources in complex, interconnected systems. It is increasingly apparent that dietary fatty acids influence these vital functions and affect human health. While the strongest evidence for influence is found in cardiovascular disease and mental health, many additional conditions are affected. Problematic changes in the fatty acid composition of human diet have also taken place over the last century. This review summarizes current understanding of the pervasive roles of essential fatty acids and their metabolites in human health.Journal of Evidence-Based Complementary & Alternative Medicine. 10/2013; 18(4):268-289.
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ABSTRACT: Objective Effects of progressive substitution of dietary n-3 fatty acids (FA) for saturated FA (SAT) on modulating risk factors for atherosclerosis have not been fully defined. Our previous reports demonstrate that SAT increased, but n-3 FA decreased, arterial lipoprotein lipase (LpL) levels and arterial LDL-cholesterol deposition early in atherogenesis. We now questioned whether incremental increases in dietary n-3 FA can counteract SAT-induced pro-atherogenic effects in atherosclerosis-prone LDL-receptor knockout (LDLR-/-) mice and have identified contributing mechanisms. Methods and results Mice were fed chow or high-fat diets enriched in SAT, n-3, or a combination of both SAT and n-3 in ratios of 3:1 (S:n-3 3:1) or 1:1 (S:n-3 1:1). Each diet resulted in the expected changes in fatty acid composition in blood and aorta for each feeding group. SAT-fed mice became hyperlipidemic. By contrast, n-3 inclusion decreased plasma lipid levels, especially cholesterol. Arterial LpL and macrophage levels were increased over 2-fold in SAT-fed mice but these were decreased with incremental replacement with n-3 FA. n-3 FA partial inclusion markedly decreased expression of pro-inflammatory markers (CD68, IL-6, and VCAM-1) in aorta. SAT diets accelerated advanced atherosclerotic lesion development, whereas all n-3 FA-containing diets markedly slowed atherosclerotic progression. Conclusion Mechanisms whereby dietary n-3 FA may improve adverse cardiovascular effects of high-SAT, high-fat diets include improving plasma lipid profiles, increasing amounts of n-3 FA in plasma and the arterial wall. Even low levels of replacement of SAT by n-3 FA effectively reduce arterial lipid deposition by decreasing aortic LpL, macrophages and pro-inflammatory markers.Atherosclerosis 06/2014; · 3.97 Impact Factor
- Current opinion in clinical nutrition and metabolic care. 01/2014;
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