Eicosanoids, Other Fatty Acid Metabolites and the Cardiovascular System: Are the Present Antithrombotic Approaches Rational?

Buchanan, Ian; Brister, SJ; Bertomeu, MC

doi:10.1007/978-3-0348-7262-1_38

Cited by 3 publications

(2 citation statements)

References 54 publications

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“…Synthesis of the platelet agonist thromboxane A2 (produced in the platelets) declined by 58% (good outcome). This may first appear to be a reasonably successful intervention, but that analysis would be incorrect for the following reason: atherosclerotic patients require increased intimal PGI2 output, as vessel wall thrombogenicity, and not reduced platelet adhesion, is a much more significant factor for minimizing thrombosis [ 73 ]. Furthermore, template-bleeding times were significantly prolonged in all fish-oil-consuming patients (bad outcome).…”

Section: Physiologic Excess Of Omega-3 Series Fatty Acids Is Harmmentioning

confidence: 99%

Why Fish Oil Fails: A Comprehensive 21st Century Lipids-Based Physiologic Analysis

Peskin¹

2014

Journal of Lipids

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The medical community suffered three significant fish oil failures/setbacks in 2013. Claims that fish oil's EPA/DHA would stop the progression of heart disease were crushed when The Risk and Prevention Study Collaborative Group (Italy) released a conclusive negative finding regarding fish oil for those patients with high risk factors but no previous myocardial infarction. Fish oil failed in all measures of CVD prevention—both primary and secondary. Another major 2013 setback occurred when fish oil's DHA was shown to significantly increase prostate cancer in men, in particular, high-grade prostate cancer, in the Selenium and Vitamin E Cancer Prevention Trial (SELECT) analysis by Brasky et al. Another monumental failure occurred in 2013 whereby fish oil's EPA/DHA failed to improve macular degeneration. In 2010, fish oil's EPA/DHA failed to help Alzheimer's victims, even those with low DHA levels. These are by no means isolated failures. The promise of fish oil and its so-called active ingredients EPA / DHA fails time and time again in clinical trials. This lipids-based physiologic review will explain precisely why there should have never been expectation for success. This review will focus on underpublicized lipid science with a focus on physiology.

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Section: Physiologic Excess Of Omega-3 Series Fatty Acids Is Harmmentioning

confidence: 99%

Why Fish Oil Fails: A Comprehensive 21st Century Lipids-Based Physiologic Analysis

Peskin¹

2014

Journal of Lipids

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“…This may first appear a reasonably successful intervention, but that analysis is naï ve and very wrong. Atherosclerotic patients require increased intimal PGI 2 output, as vessel wall thrombogenecity and not reduced platelet adhesion, is a much more significant factor for minimizing thrombosis [39]. Template bleeding times were significantly prolonged in all patients [bad outcome].…”

Section: Fish Oil Causes Decreased Prostacyclin Productionmentioning

confidence: 99%

RETRACTED: SELECT Trial Results Examined: Why Fish Oil, DHA and “Oily Fish” Are Inflammatory, Leading to Increases in Prostate Cancer, Epithelial Cancers and CVD

Peskin¹

2013

FNS

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Dietary modulation of phospholipid fatty acid composition and lipoxygenase products in mouse lung homogenates

Zhang

German

1996

Lipids

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This study investigated the potential of dietary fats to modulate the arachidonic acid content of mouse lung phospholipids and the formation of lipoxygenase products from arachidonic and eicosapentaenoic acids. Prior to breeding, female mice were fed for five months diets with 10 wt% of either olive oil, safflower oil, fish oil, or linseed oil. The same diets were fed to the females during gestation and to the pups from day 18 to day 42 postpartum. On day 42, the phospholipids were extracted from fresh lung tissue and separated into classes [phosphatidylethanolamine (PE), phosphatidylserine (PS), phosphatidylcholine (PC), and phosphatidylinositol (Pl)] by thin‐layer chromatography. Methyl esters of phospholipid fatty acids and unesterified fatty acids were analyzed by gas chromatography. At comparable dietary n‐3/n‐6 ratios, arachidonic acid was reduced 85 and 75% in lungs from mice fed linseed oil and fish oil, respectively, compared to lungs of safflower oil‐fed mice. Dietary fats affected the proportion of arachidonic acid in phospholipids in the order: PE>PS>PS>Pl. Following incubation of homogenized lung tissue, the total amount of 12‐lipoxygenase products was lowest in lungs from mice fed olive oil, and 12‐hydroxyeicosatetraenoic acid was lowest in incubated lungs from mice fed linseed oil. Comparison of the amounts of lipoxygenase substrate fatty acids in the individual phospholipids with the lipoxygenase products suggested that the major substrate pool for the 12‐lipoxygenase pathway in mouse lung homogenates was PC.

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Eicosanoids, Other Fatty Acid Metabolites and the Cardiovascular System: Are the Present Antithrombotic Approaches Rational?

Cited by 3 publications

References 54 publications

Why Fish Oil Fails: A Comprehensive 21st Century Lipids-Based Physiologic Analysis

Why Fish Oil Fails: A Comprehensive 21st Century Lipids-Based Physiologic Analysis

RETRACTED: SELECT Trial Results Examined: Why Fish Oil, DHA and “Oily Fish” Are Inflammatory, Leading to Increases in Prostate Cancer, Epithelial Cancers and CVD

Dietary modulation of phospholipid fatty acid composition and lipoxygenase products in mouse lung homogenates

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