Fish oil

About: Fish oil is a research topic. Over the lifetime, 9887 publications have been published within this topic receiving 367953 citations. The topic is also known as: fish oils & Fish oil.

Importance of maintaining a low omega–6/omega–3 ratio for reducing inflammation

Abstract: The consumption of seed oils high in the omega-6 polyunsaturated fat (PUFA) linoleic acid (LA) contributes to low-grade inflammation, oxidative stress, endothelial dysfunction and atherosclerosis.1 Moreover, dietary LA significantly increases cyclooxygenase-2 (COX-2) expression in the aorta,2 converting arachidonic acid (AA) to proinflammatory eicosanoids. This may explain why increasing LA intake can actually lower AA levels due to an increased breakdown into harmful proinflammatory metabolites. Additionally, there is an AA-independent pathway of inflammation promoted by the intake of omega-6 seed oils such as increased production of oxidised linoleic acid metabolites (OXLAMs) and proinflammatory LA CYP-eicosanoids.3–5 OXLAMs formed from LA activate NF-kB and increase proinflammatory cytokines, endothelial adhesion molecules, as well as chemokines, all of which are paramount in the formation of atherosclerosis.5–8 LA also induces an inflammatory environment in endothelial cells that may increase the risk of coronary heart disease (CHD).8 OXLAMs are found at a 50-fold higher concentration in plasma than AA metabolites, suggesting that they are more consequential in CHD and other chronic diseases,2 3 9 and lowering dietary LA reduces OXLAMs in the body.3 By inhibiting COXs and lipoxygenases (LOXs), marine omega-3s can reduce inflammation caused by the metabolism of AA. Indeed, compared with high-oleic sunflower oil (3.5 g/day), fish oil (3.5 g/day) reduces acute phase reactants (haptoglobin precursor, haemopexin, alpha-1-antitrypsin precursor and serum amyloid P component). The authors concluded, ‘The alterations in serum proteins… imply that fish oil activates anti-inflammatory mechanisms believed to impede the early onset of CHD’.10 In human atherosclerotic lesions, as the atherosclerotic lesion becomes more advanced, the ratio between oxidised LA and unoxidised LA increases.11 Moreover, rats fed LA have a significant increase in tumour necrosis factor (TNF)-alpha (p<0.05) in plasma, and higher levels of vascular cell adhesion molecule-1 (VCAM-1), intracellular adhesion molecule-1 (ICAM-1) …

Ingestion of Fish Oil or a Derived n-3 Fatty Acid Concentrate Containing Eicosapentaenoic Acid (EPA) Affects Fatty Acid Compositions of Individual Phospholipids of Rat Brain, Sciatic Nerve and Retina

Abstract: The effect of feeding redfish (Sebastes marinus or mantella) oil or a derived n-3 fatty acid concentrate containing eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) on the fatty acid compositions of individual phospholipids in selected neural tissues was studied in growing male rats. Control animals were given sunflower oil in the diet for the 5-wk feeding trial. Lipid analyses revealed that EPA (20:5n-3) became significantly enriched in all phospholipid fractions (phosphatidylcholine, phosphatidylethanolamine, phosphatidylserine and phosphatidylinositol) in the tissues studied (brain, retina and sciatic nerve) in the two n-3 fatty acid dietary groups relative to controls. Corresponding changes were also found in the 22:5n-3 contents of these tissues, whereas little or no significant elevation in DHA (22:6n-3) was found. In contrast, the percentages by weight of the n-6 fatty acids including 18:2n-6, 20:4n-6 (arachidonic acid, AA), 22:4n-6 and 22:5n-6 were generally lower in the various phospholipids/tissues of the animals given fish oil or the n-3 fatty acid concentrate; the levels of 22:5n-6 and 22:4n-6 were markedly affected in this regard. These results indicate that dietary n-3 fatty acids (as EPA plus DHA) can greatly affect the fatty acid compositions of the various membrane phospholipids in nervous tissues within a relatively short time. These biochemical alterations may be important for functional changes including altered membrane fluidity, cellular responses, ion transport and the biosyntheses of AA- and EPA-derived prostaglandins and leukotrienes.

Oral fish oil supplementation raises blood omega-3 levels and lowers C-reactive protein in haemodialysis patients—a pilot study

Abstract: Background. We previously reported that haemodialysis patients have suboptimal blood levels of the cardioprotective omega-3 polyunsaturated fatty acids (n-3 PUFA) eicosapentaenoic (EPA) and docosahexaenoic (DHA) acids. In the present pilot study, we tested the hypothesis that supplementing haemodialysis patients for 12 weeks with the American Heart Association (AHA)-recommended fish oil dose would be well tolerated and efficacious in boosting blood n-3 PUFA levels and improving cardiovascular risk biomarkers. Methods. Twenty-seven subjects were randomized in a 2 : 1 ratio to either 1.3 g of EPA þ DHA daily or placebo. Results. At baseline, 83% of subjects consumed inadequate dietary fish and had the following erythro

Dietary fish oil dose- and time-response effects on cardiac phospholipid fatty acid composition.

Abstract: Fish consumption is associated with reduced cardiovascular mortality, and elevated myocardial long-chain n-3 polyunsaturated FA (PUFA) content is implicated in this cardioprotection. This study examined the dose and time responses for incorporation of n-3 PUFA into cellular membranes in rats fed fish oil (FO)-containing diets. For the time course study, rats were fed a 10% FO diet for periods ranging from 0 to 42 d, after which myocardial and erythrocyte membrane fatty acid composition was determined. For the dose response study, rats (n = 3) were fed 0, 1.25, 2.5, 5, or 10% FO for 4 wk, with myocardial, erythrocyte, and skeletal muscle membrane FA determined. Myocardial DHA (22:6n-3) levels doubled in 2 d, stabilizing at levels approximately 200% higher than control after 28 d feeding with 10% FO. By comparison, DHA levels doubled after 4 wk of 1.25% FO feeding. In myocardium and skeletal muscle, EPA (20:5n-3) levels remained low, but in erythrocytes EPA levels reached 50% of DHA levels. The n-3 PUFA were incorporated at the expense of n-6 PUFA in myocardium and skeletal muscle, whereas erythrocytes maintained arachidonic acid levels, and total n-3 PUFA incorporation was lower. This study shows that low doses of FO produce marked changes in myocardial DHA levels; maximal incorporation takes up to 28 d to occur; and while erythrocytes are a good indicator of tissue n-3 incorporation in stable diets, they vary greatly in their time course and pattern of incorporation.