Fish, fish oils, n-3 polyunsaturated fatty acids and cardiovascular health (original) (raw)
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Salmon-rich diet inhibits arachidonate cyclooxygenation in healthy men
The Journal of Nutritional Biochemistry, 1991
Dietary. long-chain omega-3 polyunsaturated fatty acids (PUFA influence cardiovascular and immunological parameters. Eicosanoid-mediated processes are believed to be key metabolic components of the underlying mechanisms. With a view toward developing a biochemical basis to rationalize the phenomena observed, we compared the effect of a salmon (S, w6/o93 PUFA ratio = 3.6) and of a reference (R, w6/o03 = 19.5) diet on the biosynthesis of E prostaglandins in 10 male volunteers by measuring the major urinary metabolite, PGE-M, in 24-hr urine by gas chromatography-mass spectrometry. Energy contributions (en%) from proteins, carbohydrates, and fat were virtually identical in both diets: 19, 56, and 25%, respectively. The subjects were confined in a nutrition suite at the Western Human Nutrition Research Center for 100 days. During a stabilization period of 20 days, they were placed on the R diet. Then half were fed the S diet for 40 days while the others remained on the reference diet. The two groups switched diets for the last 40-day period. The menu cycle was 5 days, and all diets were calculated to provide adequate amounts of essential nutrients. Diet S was associated with an average 24% reduction in PGE-M daily output, in comparison to diet R (P = 0.001). This reduction in the synthetic rate of E prostaglandins was attained by incorporating less than 500 [,,/day of salmon in the diet. Omega-6 PUFA were maintained constant in both diets. An alteration of PGE synthesis of this size is likely to have clinically significant repercussions on cardiovascular and immune functions. Although these effects appear to occur in a predominantly favorable direction, other physiological systems (e.g., the renal system) might be affected in ways yet to be determined.
The Journal of Lipid Research, 2010
Omega-3 fatty acids (3 FA), e.g., eikosapentaenoic acid (EPA, 20:5 3) and dokosahexaenoic acid (DHA, 22:6 3), present in marine oils, modulate infl ammatory reactions and ameliorate symptoms of several autoimmune and other infl ammatory disorders (1, 2). In addition, EPA and DHA administration reduces cardiovascular morbidity and mortality (3). Recently, high-fi sh intake or dietary supplementation with 3 FAs was linked to reductions in the risk of developing Alzheimer's disease (AD) (4-6) and to delay cognitive decline in patients with very mild AD (7). 3 FA exert the anti-infl ammatory effects on several cellular levels, including modulation of surface receptor, ion pumps, G-proteins, binding to transcription factors (e.g., NF B), and gene interactions (8-10). One prevalent hypothesis is that 3 FA, particularly EPA, give rise to prostaglandins and leukotrienes with reduced pro-infl ammatory activity compared with corresponding arachidonic acid (AA; 20:4 6) derived compounds, because the former contain one additional double bond, changing the 3D structure and, hence, the ability to bind to receptors. Moreover, an abundance of 3 FAs might reduce generation of 6 metabolites by, among other things, competing for the same enzyme systems. In addition, EPA and DHA Abstract Omega-3 fatty acids, e.g., dokosahexaenoic acid (DHA) and eikosapentaenoic acid (EPA), ameliorate infl ammatory reactions by various mechanisms, but the role of prostaglandins remains unclear. Our aim was to determine if dietary supplementation with a DHA-rich fi sh oil infl uenced the release of PGF 2 ␣ from peripheral blood mononuclear cells (PBMC). In the OmegAD study, 174 Alzheimer disease patients received either 1.7 g DHA plus 0.6 g EPA or a placebo daily for six months. PBMCs from the 21 (9 on fi sh oil and 12 on placebo) fi rst-randomized patients were stimulated with either lipopolysaccharide (LPS) or phytohemagglutinin (PHA) before and after 6 months. Our results showed that plasma concentrations of DHA and EPA increased signifi cantly at 6 months in the omega-3 group. PGF 2 ␣ release from LPS-(but not from PHA-) stimulated PBMC was signifi cantly diminished in this group; no change was noted in the placebo group. PGF 2 ␣ changes correlated inversely with changes in plasma DHA and EPA. Decreased IL-6 and IL-1  levels correlated with decreased PGF 2 ␣ levels. The stimulus-specifi c PGF 2 ␣ release from PBMC after 6 months of oral supplementation with the DHA-rich fi sh oil might be one event related to reduced infl ammatory reactions associated with omega-3 fatty acid intake .-Vedin, I.
Biochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolism, 1985
A synthetic diet preparation supplemented with 10% by weight of either safflower oil, hydrogenated coconut oil containing 3% safflower oil, or 'max EPA' fish oil was fed to rats over a &week period. Serial measurements of serum fatty acids, serum thromboxane B, and urinary prostaglandin excretion were taken during the treatment perfod to assess the rate of change in fatty acid composition and prostaglandin synthesis following dietary manipulation. There was no significant change in weight gain between the dietary groups during the treatment period. Significant changes in serum fatty acids occurred within 48 h of treatment, with the 'max EPA' oil group having arachidonic acid levels reduced by 23% (P -c 0.01) compared to the coconut oil group. Conversely, rats fed safflower oil had an 18% enhancement of arachidonic acid during the same time period. Whole blood synthesis of thromboxane IQ was significantly depressed (P < 0.01) after 48 h in rats fed 'max EPA' oil compared to the safflower oil or coconut oil groups. This suppression reached a maximum of 65% (P -C 0.001) after 7 days of dietary 'max EPA' oil treatment. The safflower oil and coconut oil-fed groups showed the same levels of serum thromboxane I$ production over the treatment period. Urinary excretion of both dketoprostaglandin F,. and prostaglandin E, varied significantly (P < 0.01) between the groups after 7 days of dietary treatment. Rats fed 'max EPA' oil had depressed urinary prostanoid excretion compared to the safflower and coconut oil groups which remained very similar to each other. After the 8-week treatment period rats were killed and the phospholipid fatty acid composition and prostaglandin-generating capacity of platelets, aorta and renal tissue was examined. Prostanoid production by kidney cortex and medulla and segments of aorta was consistently suppressed in rats fed 'max EPA' oil. These observations correlated well with changes in the phospholipid fatty acid profiles in these tissues. This study shows rapid changes in serum fatty acids and thromboxane I& generation following dietary manipulation, while changes in urinary excretion or prostanoid metabolites occur only after a longer time period.
Lipids, 1988
The effect of fish diet on 43 healthy male students was studied. They ate a fish-containing meal for 15 weeks on an average of 3.7 times per week. Twenty-one of them voluntarily restricted their lipid intake while the rest ate normally. Controls continued their usual eating habits (19 students). The meals consisted of Finnish freshwater fish (87%) (vendace, pike, perch and rainbow trout) and brackish water fish (13%) (Baltic herring) that provided about 1 g of omega-3 polyunsaturated fatty acids per day (0.25 g eicosapentaenoic acid and 0.55 g docosahexaenoic acid). During the diet, omega-3 fatty acids increased in erythrocyte ghosts and platelets at the expense of omega-6 fatty acids. The concentration of serum cholesterol diminished in those fish consumers who lowered their lipid intake. Apolipoprotein A1 and B were lowered in both fish-consuming groups. Triglyceride levels also showed a tendency to decrease. The formation of thromboxane B2 during incubation of whole blood decreased in both fish-consuming groups. The decrease of plasma 6-keto-PGF1 alpha was not statistically significant, if compared with the controls. The results obtained indicate that a moderate intake of fish-containing meals has some beneficial effects on the plasma lipid and prostanoid metabolism, when coronary heart disease risk factors are considered.
Compilation of Articles and Essays 2004-2020 on Fish Oil, Fatty Acid, CFAT
Integr Med 2019, Nutr Perspect 2004/2005/2011, conference 2020, 2004
This is a compilation of various published articles and presentation transcripts including:Integr Med (Encinitas). 2019 Feb;18(1):8-15. Concerns About The Integrity of The Scientific Research Process-Focus On Recent Negative Publications Regarding Nutrition, Multivitamins, Fish Oil And Cardiovascular Disease Alex Vasquez, Joseph Pizzorno PMID: 31341427 PMCID: PMC6601430 https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/31341427/ Reply to "role of Western diet in inflammatory autoimmune diseases" by Manzel et al. In current allergy and asthma reports (volume 14, issue 1, January 2014). Vasquez A. Curr Allergy Asthma Rep. 2014 Aug;14(8):454. doi: 10.1007/s11882-014-0454-4. PMID: 24947682 No abstract available. Mitochondrial medicine arrives to prime time in clinical care: nutritional biochemistry and mitochondrial hyperpermeability ("leaky mitochondria") meet disease pathogenesis and clinical interventions. Vasquez A. Altern Ther Health Med. 2014 Winter;20 Suppl 1:26-30. PMID: 24473983 No abstract available. The clinical importance of vitamin D (cholecalciferol): a paradigm shift with implications for all healthcare providers. Vasquez A, Manso G, Cannell J. Altern Ther Health Med. 2004 Sep-Oct;10(5):28-36; quiz 37, 94. PMID: 15478784 Review. No abstract available.
Fish and coronary artery disease
Heart, 1987
Does fish consumption protect against coronary heart disease? If so what are the mechanisms for such protection and how much fish (and of what types) would need to be consumed?
Prostaglandins, Leukotrienes and Essential Fatty Acids
… and Essential Fatty …, 2008
The innate immune system of the brain is principally composed of microglial cells and astrocytes, which, once activated, protect neurons against insults (infectious agents, lesions, etc.). Activated glial cells produce inflammatory cytokines that act specifically through receptors expressed by the brain. The functional consequences of brain cytokine action (also called neuroinflammation) are alterations in cognition, mood and behaviour, a hallmark of altered well-being. In addition, proinflammatory cytokines play a key role in depression and neurodegenerative diseases linked to aging. Polyunsaturated fatty acids (PUFA) are essential nutrients and essential components of neuronal and glial cell membranes. PUFA from the diet regulate both prostaglandin and proinflammatory cytokine production. n-3 fatty acids are anti-inflammatory while n-6 fatty acids are precursors of prostaglandins. Inappropriate amounts of dietary n-6 and n-3 fatty acids could lead to neuroinflammation because of their abundance in the brain and reduced well-being. Depending on which PUFA are present in the diet, neuroinflammation will, therefore, be kept at a minimum or exacerbated. This could explain the protective role of n-3 fatty acids in neurodegenerative diseases linked to aging.
Recent Patents on Cardiovascular Drug Discovery, 2007
ω-3 and ω-6 Polyunsaturated fatty acids (PUFA) are the major families of PUFA that can be found as components of the human diet. After ingestion, both ω-3 and ω-6 PUFA are distributed to every cell in the body where they are involved in a myriad of physiological processes, including regulation of cardiovascular, immune, hormonal, metabolic, neuronal, and visual functions. At the cell level, these effects are mediated by changes in membrane phospholipids structure, interference with eicosanoid intracellular signaling, and regulation of gene expression. Two longchain ω-3 PUFAs, the docosahexaenoic (DHA) and eicosapentaenoic (EPA) acid, are found in fatty fish and other marine sources and might be the putative dietary components thought to modify the cardiovascular risk in subjects consuming high amounts of such food. Evidence of an inverse relationship between fatty fish intake and cardiovascular risk has, in fact, emerged in studies performed more than twenty years ago in Eskimos and has been subsequently confirmed in other ethnic groups. The benefits of ω-3 PUFA might relate principally to prevention of coronary heart disease, coronary artery restenosis after angioplasty, and sudden arrhythmic death. In this brief review, we will cover the general biochemical aspects of ω-3 PUFA, summarize the evidence relating these fatty acids with control of cardiovascular risk factors and prevention of cardiovascular events, and overview the most recent and relevant patents that are related to these issues. More specifically, we will deal with the possibility to use PUFA in association with other molecules that can potentiate their antiinflammatory and antiatherogenic effects.