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. 1. Introduction The object of this review is to show how there could be no possible expectation of general patient benefit with prophylactic fish oil use. It will be shown that the amount of EPA/DHA from routine fish oil recommendations is 20Xs–500Xs more than the body would naturally produce on its own from alpha-linolenic acid (ALA)—Parent omega-3. Advances in quantitative analysis have been made in the 21st century which are not yet disseminated in the medical community; that is, the delta-6/-5 enzymes are not impaired in the general patient population, and the amount of EPA/DHA required on a daily basis by the brain is now known to be less than 7.2？mg/day. Neither extremely important fact was known in the 20th century. Lipid physiology makes the following clear: (a) Marine oil’s EPA/DHA spontaneously oxidizes at room temperature and more rapidly at normal body temperature—no level of antioxidants can stop this deleterious effect. (b) Fish oil blunts the insulin response and raises resting blood glucose levels. (c) Fish oil decreases critical prostacyclin (PGI2) in patients with atherosclerosis—a very bad outcome. (d) Fish oil rapidly decreases arterial compliance—increasing “hardening of the arteries.” (e) In contrast to researcher’s expectations, fish oil accelerates metastases in animals. (g) Fish oil’s
References
[1]
The Risk and Prevention Study Collaborative Group, “n-3 fatty acids in patients with multiple cardiovascular risk factors,” The New England Journal of Medicine, vol. 368, no. 19, pp. 1800–1808, 2013.
[2]
E. Topol and Heartwire, No Benefit of Fish Oil in High Risk Patients, 2013.
[3]
T. M. Brasky, A. K. Darke, X. Song, et al., “Plasma phospholipid fatty acids and prostate cancer risk in the SELECT trial,” Journal of the National Cancer Institute, vol. 105, no. 15, pp. 1132–1141, 2013.
[4]
T. M. Brasky, C. Till, E. White et al., “Serum phospholipid fatty acids and prostate cancer risk: results from the prostate cancer prevention trial,” American Journal of Epidemiology, vol. 173, no. 12, pp. 1429–1439, 2011.
[5]
F. L. Crowe, N. E. Allen, P. N. Appleby et al., “Fatty acid composition of plasma phospholipids and risk of prostate cancer in a case-control analysis nested within the European Prospective Investigation into Cancer and Nutrition,” American Journal of Clinical Nutrition, vol. 88, no. 5, pp. 1353–1363, 2008.
[6]
AREDS2 Research Group, “Lutein + Zeaxanthin and Omega-3 fatty acids for age-related macular degeneration: the Age-Related Eye Disease Study 2 (AREDS2) Randomized Clinical trial,” Journal of the American Medical Association, vol. 309, no. 19, pp. 2005–2015, 2013.
[7]
S. M. Kwak, S. K. Myung, Y. J. Lee, and H. G. Seo, “Efficacy of Omega-3 fatty acid supplements (eicosapentaenoic acid and docosahexaenoic acid) in the secondary prevention of cardiovascular disease: a meta-analysis of randomized, double-blind, placebo-controlled trials,” Archives of Internal Medicine, vol. 172, no. 9, pp. 686–694, 2012.
[8]
E. C. Rizos, E. E. Ntzani, E. Bika, M. S. Kostapanos, and M. S. Elisaf, “Association between Omega-3 fatty acid supplementation and risk of major cardiovascular disease events: a systematic review and meta-analysis,” The Journal of the American Medical Association, vol. 308, no. 10, pp. 1024–1033, 2012.
[9]
F. M. Sacks, F. H. Stone, C. Michael Gibson, D. I. Silverman, B. Rosner, and R. C. Pasternak, “Controlled trial of fish oil for regression of human coronary atherosclerosis,” Journal of the American College of Cardiology, vol. 25, no. 7, pp. 1492–1498, 1995.
[10]
I. M. Campbell, D. N. Crozier, and R. B. Caton, “Abnormal fatty acid composition and impaired oxygen supply in cystic fibrosis patients,” Pediatrics, vol. 57, no. 4, pp. 480–486, 1976.
[11]
B. S. Peskin and M. J. Carter, “Chronic cellular hypoxia as the prime cause of cancer: what is the de-oxygenating role of adulterated and improper ratios of polyunsaturated fatty acids when incorporated into cell membranes?” Medical Hypotheses, vol. 70, no. 2, pp. 298–304, 2008.
[12]
R. S. Chapkin, V. A. Ziboh, C. L. Marcelo, and J. J. Voorhees, “Metabolism of essential fatty acids by human epidermal enzyme preparations: evidence of chain elongation,” Journal of Lipid Research, vol. 27, no. 9, pp. 945–954, 1986.
[13]
A. Andersson, A. Sj？din, A. Hedman, R. Olsson, and B. Vessby, “Fatty acid profile of skeletal muscle phospholipids in trained and untrained young men,” American Journal of Physiology: Endocrinology and Metabolism, vol. 279, no. 4, pp. E744–E751, 2000.
[14]
S. G. Young and S. Parthasarathy, “Why are low-density lipoproteins atherogenic?” Western Journal of Medicine, vol. 160, no. 2, pp. 153–164, 1994.
[15]
G. Spiteller, “The relation of lipid peroxidation processes with atherogenesis: a new theory on atherogenesis,” Molecular Nutrition and Food Research, vol. 49, no. 11, pp. 999–1013, 2005.
[16]
U. N. Das, “A defect in the activity of Δ6 and Δ5 desaturases may be a factor in the initiation and progression of atherosclerosis,” Prostaglandins Leukotrienes and Essential Fatty Acids, vol. 76, no. 5, pp. 251–268, 2007.
[17]
A. J. Hulbert, “Metabolism and longevity: is there a role for membrane fatty acids?” Integrative and Comparative Biology, vol. 50, no. 5, pp. 808–817, 2010.
[18]
A. J. Hulbert, R. Pamplona, R. Buffenstein, and W. A. Buttemer, “Life and death: metabolic rate, membrane composition, and life span of animals,” Physiological Reviews, vol. 87, no. 4, pp. 1175–1213, 2007.
[19]
K. Gopakumar and M. Rajendranathan Nair, “Fatty acid composition of eight species of Indian marine fish,” Journal of the Science of Food and Agriculture, vol. 23, no. 4, pp. 493–496, 1972.
[20]
L. A. Piche, H. H. Draper, and P. D. Cole, “Malondialdehyde excretion by subjects consuming cod liver oil vs a concentrate of n-3 fatty acids,” Lipids, vol. 23, no. 4, pp. 370–371, 1988.
[21]
C. Hamilton and D. Kirstein, Does Rancidity, as Measured by Peroxide Value, Affect Animal Performance, Darling International Inc., 2008.
[22]
J. V. Higdon, J. Liu, S.-H. Du, J. D. Morrow, B. N. Ames, and R. C. Wander, “Supplementation of postmenopausal women with fish oil rich in eicosapentaenoic acid and docosahexaenoic acid is not associated with greater in vivo lipid peroxidation compared with oils rich in oleate and linoleate as assessed by plasma malondialdehyde and F2-isoprostanes,” American Journal of Clinical Nutrition, vol. 72, no. 3, pp. 714–722, 2000.
[23]
S. Sethi, O. Ziouzenkova, H. Ni, D. D. Wagner, J. Plutzky, and T. N. Mayadas, “Oxidized omega-3 fatty acids in fish oil inhibit leukocyte-endothelial interactions through activation of PPARα,” Blood, vol. 100, no. 4, pp. 1340–1346, 2002.
[24]
S. G. Kaasgaard, G. Holmer, C.-E. Hoy, W. A. Behrens, and J. L. Beare-Rogers, “Effects of dietary linseed oil and marine oil on lipid peroxidation in monkey liver in vivo and in vitro,” Lipids, vol. 27, no. 10, pp. 740–745, 1992.
[25]
G. Stix, “A malignant flame,” Scientific American, vol. 297, no. 1, pp. 60–67, 2007.
H. Yang, Z. Rivera, S. Jube et al., “Programmed necrosis induced by asbestos in human mesothelial cells causes high-mobility group box 1 protein release and resultant inflammation,” Proceedings of the National Academy of Sciences of the United States of America, vol. 107, no. 28, pp. 12611–12616, 2010.
[28]
F. Balkwill, K. A. Charles, and A. Mantovani, “Smoldering and polarized inflammation in the initiation and promotion of malignant disease,” Cancer Cell, vol. 7, no. 3, pp. 211–217, 2005.
[29]
C. E. Lewis and J. W. Pollard, “Distinct role of macrophages in different tumor microenvironments,” Cancer Research, vol. 66, no. 2, pp. 605–612, 2006.
[30]
K. E. de Visser, A. Eichten, and L. M. Coussens, “Paradoxical roles of the immune system during cancer development,” Nature Reviews Cancer, vol. 6, no. 1, pp. 24–37, 2006.
[31]
I. B. King, A. R. Kristal, S. Schaffer, M. Thornquist, and G. E. Goodman, “Serum trans-fatty acids are associated with risk of prostate cancer in β-carotene and retinol efficacy trial,” Cancer Epidemiology Biomarkers and Prevention, vol. 14, no. 4, pp. 988–992, 2005.
[32]
J. C. Umhau, W. Zhou, R. E. Carson et al., “Imaging incorporation of circulating docosahexaenoic acid into the human brain using positron emission tomography,” Journal of Lipid Research, vol. 50, no. 7, pp. 1259–1268, 2009.
[33]
P. L. L. Goyens, M. E. Spilker, P. L. Zock, M. B. Katan, and R. P. Mensink, “Conversion of α-linolenic acid in humans is influenced by the absolute amounts of α-linolenic acid and linoleic acid in the diet and not by their ratio,” American Journal of Clinical Nutrition, vol. 84, no. 1, pp. 44–53, 2006.
[34]
N. Hussein, E. Ah-Sing, P. Wilkinson, C. Leach, B. Griffin, and D. Millward, “Physiological compartmental analysis of alpha-linolenic acid metabolism in adult humans,” Journal of Lipid Research, vol. 46, pp. 269–280, 2005.
[35]
G. Barceló-Coblijn, E. J. Murphy, R. Othman, M. H. Moghadasian, T. Kashour, and J. K. Friel, “Flaxseed oil and fish-oil capsule consumption alters human red blood cell n-3 fatty acid composition: a multiple-dosing trial comparing 2 sources of n-3 fatty acid,” American Journal of Clinical Nutrition, vol. 88, no. 3, pp. 801–809, 2008.
[36]
M. Plourde and S. C. Cunnane, “Extremely limited synthesis of long chain polyunsaturates in adults: implications for their dietary essentiality and use as supplements,” Applied Physiology, Nutrition and Metabolism, vol. 32, no. 4, pp. 619–634, 2007.
[37]
A. A. Welch, S. Shakya-Shrestha, M. A. H. Lentjes, N. J. Wareham, and K.-T. Khaw, “Dietary intake and status of n-3 polyunsaturated fatty acids in a population of fish-eating and non-fish-eating meat-eaters, vegetarians, and vegans and the precursor-product ratio of α-linolenic acid to long-chain n-3 polyunsaturated fatty acids: results from the EPIC-Norfolk cohort,” American Journal of Clinical Nutrition, vol. 92, no. 5, pp. 1040–1051, 2010.
[38]
F. Gao, H.-W. Kim, M. Igarashi et al., “Liver conversion of docosahexaenoic and arachidonic acids from their 18-carbon precursors in rats on a DHA-free but α-LNA-containing n-3 PUFA adequate diet,” Biochimica et Biophysica Acta, vol. 1811, no. 7-8, pp. 484–489, 2011.
[39]
B. S. Peskin, “SELECT trial results explained: why fish oil, DHA and “Oily Fish” are more inflammatory than harmful trans fats-expect increased prostate cancer, epithelial cancers and CVD,” Food and Nutrition Sciences, vol. 4, no. 11, pp. 1128–1144, 2013.
[40]
B. S. Peskin and A. Habib, The Hidden Story of Cancer, Pinnacle Press, Houston, Tex, USA, 6th edition, 2011.
[41]
H. M. Sinclair, “Deficiency of essential fatty acids and atherosclerosis, etcetera,” The Lancet, vol. 270, no. 6919, pp. 381–383, 1956.
[42]
M. B. Katan, J. P. Deslypere, A. P. van Birgelen, M. Penders, and M. Zegwaard, “Kinetics of the incorporation of dietary fatty acids into serum cholesteryl esters, erythrocyte membranes, and adipose tissue: an 18-month controlled study,” Journal of Lipid Research, vol. 38, no. 10, pp. 2012–2022, 1997.
[43]
M. I. Gurr, “Dietary fatty acids with trans unsaturation,” Nutrition Research Reviews, vol. 9, pp. 259–279, 1996.
[44]
S. K. Abbott, P. L. Else, and A. J. Hulbert, “Membrane fatty acid composition of rat skeletal muscle is most responsive to the balance of dietary n-3 and n-6 PUFA,” British Journal of Nutrition, vol. 103, no. 4, pp. 522–529, 2010.
[45]
J. Delarue, F. Labarthe, and R. Cohen, “Fish-oil supplementation reduces stimulation of plasma glucose fluxes during exercise in untrained males,” British Journal of Nutrition, vol. 90, no. 4, pp. 777–786, 2003.
[46]
P. E. Wainwright, Y. S. Huang, B. Bulman-Fleming et al., “The effects of dietary n-3/n-6 ratio on brain development in the mouse: a dose response study with long-chain n-3 fatty acids,” Lipids, vol. 27, no. 2, pp. 98–103, 1992.
[47]
W. E. M. Lands, A. Morris, and B. Libelt, “Quantitative effects of dietary polyunsaturated fats on the composition of fatty acids in rat tissues,” Lipids, vol. 25, no. 9, pp. 505–516, 1990.
[48]
B. Alberts, D. Bray, J. Lewis, M. Raff, K. Roberts, and J. Watson, Molecular Biology of the Cell, Garland Science, New York, NY, USA, 3rd edition, 1994.
[49]
R. Murray Jr., D. K. Granner, P. A. Mayes, and P. A. Rodwell, Harper’s Illustrated Biochemistry, McGraw-Hill, New York, NY, USA, 26th edition, 2003.
[50]
C. Guyton and J. E. Hall, in Textbook of Medical Physiology, pp. 861–862, WB Saunders, Philadelphia, Pa, USA, 9th edition, 1996.
[51]
H. Esterbauer, H. Puhl, M. Dieber-Rotheneder, G. Waeg, and H. Rabl, “Effect of antioxidants on oxidative modification of LDL,” Annals of Medicine, vol. 23, no. 5, pp. 573–581, 1991.
[52]
H. M. Sinclair, “Essential fatty acids in perspective,” Human Nutrition, vol. 38, no. 4, pp. 245–260, 1984.
[53]
C. Guyton and J. E. Hall, in Textbook of Medical Physiology, pp. 872–873, WB Saunders, Philadelphia, Pa, USA, 9th edition, 1996.
[54]
K. M. Bothem and P. A. Mayes, “Cholesterol synthesis, transport, and excretion,” in Harper’s Illustrated Biochemistry, R. Murray Jr., D. K. Granner, P. A. Mayes, and V. W. Rodwell, Eds., p. 235, McGraw-Hill, New York, NY, USA, 26th edition, 2003.
[55]
W. B. Zhang, P. B. Addis, and T. P. Krick, “Quantification of 5α-cholestane-3β, 5, 6β-triol and other cholesterol oxidation products in fast food French fried potatoes,” Journal of Food Science, vol. 56, no. 3, pp. 716–718, 1991.
[56]
W. Korytowski, G. J. Bachowski, and A. W. Girotti, “Photoperoxidation of cholesterol in homogeneous solution, isolated membranes, and cells: comparison of the 5 alpha- and 6 beta-hydroperoxides as indicators of singlet oxygen intermediacy,” Photochemistry and Photobiology, vol. 56, no. 1, pp. 1–8, 1992.
[57]
G. Spiteller, “Is atherosclerosis a multifactorial disease or is it induced by a sequence of lipid peroxidation reactions?” Annals of the New York Academy of Sciences, vol. 1043, pp. 355–366, 2005.
[58]
G. Spiteller, “Peroxyl radicals: inductors of neurodegenerative and other inflammatory diseases. Their origin and how they transform cholesterol, phospholipids, plasmalogens, polyunsaturated fatty acids, sugars, and proteins into deleterious products,” Free Radical Biology and Medicine, vol. 41, no. 3, pp. 362–387, 2006.
[59]
B. S. Peskin, D. Sim, and M. J. Carter, “The failure of vytorin and statins to improve cardiovascular health: bad cholesterol or bad theory?” Journal of American Physicians and Surgeons, vol. 13, no. 3, pp. 82–87, 2008.
[60]
B. S. Peskin, “Why fish oil fails to prevent or improve CVD: a 21st century analysis,” Food and Nutrition Sciences, vol. 4, no. 9A, pp. 76–85, 2013.
[61]
H. Esterbauer, G. Jurgens, O. Quehenberger, and E. Koller, “Autoxidation of human low density lipoprotein: loss of polyunsaturated fatty acids and vitamin E and generation of aldehydes,” Journal of Lipid Research, vol. 28, no. 5, pp. 495–509, 1987.
[62]
A. A. Spector, “Plasma free fatty acid and lipoproteins as sources of polyunsaturated fatty acid for the brain,” Journal of Molecular Neuroscience, vol. 16, no. 2-3, pp. 159–165, 2001.
[63]
C. Weiss, S. Regele, T. Velich, P. B？rtsch, and T. Weiss, “Hemostasis and fibrinolysis in patients with intermittent claudication: effects of prostaglandin E1,” Prostaglandins Leukotrienes and Essential Fatty Acids, vol. 63, no. 5, pp. 271–277, 2000.
[64]
C. P. Burns and A. A. Spector, “Effects of lipids on cancer therapy,” Nutrition Reviews, vol. 48, no. 6, pp. 233–240, 1990.
[65]
B. A. Nassar, M. S. Manku, and Y. S. Huang, “The influence of dietary marine oil (Polepa) and Evening Primrose Oil (Efamol) on prostaglandin production by the rat mesenteric vasculature,” Prostaglandins Leukotrienes and Medicine, vol. 26, no. 3, pp. 253–263, 1987.
[66]
M. Stones, “China to Overtake Western Europe in EPA & DHA Oil Consumption,” June 2011, http://www.nutraingredients.com/Industry/China-to-over-take-Western-Europe-in-EPA-DHA-oil-consumption.
[67]
B. E. Karlstr？m, A. E. J？rvi, L. Byberg, L. G. Berglund, and B. O. H. Vessby, “Fatty fish in the diet of patients with type 2 diabetes: comparison of the metabolic effects of foods rich in n-3 and n-6 fatty acids,” American Journal of Clinical Nutrition, vol. 94, no. 1, pp. 26–33, 2011.
[68]
H. Glauber, P. Wallace, K. Griver, and G. Brechtel, “Adverse metabolic effect of omega-3 fatty acids in non-insulin-dependent diabetes mellitus,” Annals of Internal Medicine, vol. 108, no. 5, pp. 663–668, 1988.
[69]
P. W. Stacpoole, J. Alig, L. Ammon, and S. E. Crockett, “Dose response effects of dietary marine oil on carbohydrate and lipid metabolism in normal subjects and patients with hypertriglyceridemia,” Metabolism, vol. 38, no. 10, pp. 946–956, 1989.
[70]
J. F. Quinn, R. Raman, R. G. Thomas et al., “Docosahexaenoic acid supplementation and cognitive decline in Alzheimer disease: a randomized trial,” Journal of the American Medical Association, vol. 304, no. 17, pp. 1903–1911, 2010.
[71]
V. Bertele, C. Cerletti, and G. de Gaetano, “Pathophysiology of critical leg ischaemia and mode ofaction of prostaglandins,” in Proceedings of the 5th International Symposium on Prostaglandins in the Cardiovascular System, pp. 18–26, Vienna, Austria, September 1991.
[72]
H. R. Knapp, I. A. G. Reilly, P. Alessandrini, and G. A. Fitzgerald, “In vivo indexes of platelet and vascular function during fish-oil adminstration in patients with atherosclerosis,” The New England Journal of Medicine, vol. 314, no. 15, pp. 937–942, 1986.
[73]
M. R. Buchanan, S. J. Brister, and M. C. Bertomeu, “Eicosanoids, other fatty acid metabolites and the cardiovascular system: are the present antithromobtic approaches rational?” in Proceedings of the 5th International Symposium on Prostaglandins in the Cardiovascular System, pp. 18–26, Vienna, Austria, September 1991.
[74]
G. Heisenberg and W. H. Simmons, Principles of Medical Biochemistry, Mosby, St. Louis, Mo, USA, 1998.
[75]
C. Guyton and J. E. Hall, in Textbook of Medical Physiology, p. 12, WB Saunders, Philadelphia, Pa, USA, 9th edition, 1996.
[76]
M. B. Veirord MB, D. S. Tjelle, and P. Laake, “Diet and risk of cutaneous malignant melanoma: a prospective study of 50, 757 Norwegian men and women,” International Journal of Cancer, vol. 71, no. 4, pp. 600–604, 1997.
[77]
J. Cody, “Link between fish oil and increased risk of colon cancer in mice,” Medical News Today, October 2010, http://www.medicalnewstoday.com/releases/203683.php.
[78]
H. L. Woodworth, S. J. McCaskey, D. M. Duriancik et al., “Dietary fish oil alters T lymphocyte cell populations and exacerbates disease in a mouse model of inflammatory colitis,” Cancer Research, vol. 70, no. 20, pp. 7960–7969, 2010.
[79]
A. Mannini, N. Kerstin, L. Calorini, G. Mugnai, and S. Ruggieri, “Dietary n-3 polyunsaturated fatty acids enhance metastatic dissemination of murine T lymphoma cells,” British Journal of Nutrition, vol. 102, no. 7, pp. 958–961, 2009.
[80]
V. R. Fantin, J. St-Pierre, and P. Leder, “Attenuation of LDH-A expression uncovers a link between glycolysis, mitochondrial physiology, and tumor maintenance,” Cancer Cell, vol. 9, no. 6, pp. 425–434, 2006.
[81]
M. A. Kiebish, X. Han, H. Cheng, J. H. Chuang, and T. N. Seyfried, “Cardiolipin and electron transport chain abnormalities in mouse brain tumor mitochondria: lipidomic evidence supporting the Warburg theory of cancer,” Journal of Lipid Research, vol. 49, no. 12, pp. 2545–2556, 2008.
[82]
J. J. R. Krebs, H. Hauser, and E. Carafoli, “Asymmetric distribution of phospholipids in the inner membrane of beef heart mitochondria,” The Journal of Biological Chemistry, vol. 254, no. 12, pp. 5308–5316, 1979.
[83]
O. Warburg, The Metabolism of Tumours: Investigations from the Kaiser Wilhelm Institute for Biology, Constable & Co Ltd., 1930, Translated by Frank Dickens.
[84]
O. Warburg, “The metabolism of carcinoma cells,” The Journal of Cancer Research, vol. 9, pp. 148–163, 1925.
[85]
O. Warburg, “On the origin of cancer cells,” Science, vol. 123, no. 3191, pp. 309–314, 1956.
[86]
C. D. Malis, P. C. Weber, A. Leaf, and J. V. Bonventre, “Incorporation of marine lipids into mitochondrial membranes increases susceptibility to damage by calcium and reactive oxygen species: evidence for enhanced activation of phospholipase A2 in mitochondria enriched with n-3 fatty acids,” Proceedings of the National Academy of Sciences of the United States of America, vol. 87, no. 22, pp. 8845–8849, 1990.
[87]
A. Turaka, M. K. Buyyounouski, A. L. Hanlon, E. M. Horwitz, R. E. Greenberg, and B. Movsas, “Hypoxic prostate/muscle pO2 (P/M pO2) ratio predicts for biochemical failure in patients with localized prostate cancer: long-term result,” Journal of Clinical Oncology, vol. 27, no. 15, p. 5136, ASCO Annual Meeting Proceedings, 2009.
[88]
G. Spiteller, “Furan fatty acids: occurrence, synthesis, and reactions. Are furan fatty acids responsible for the cardioprotective effects of a fish diet?” Lipids, vol. 40, no. 8, Article ID L9447, pp. 755–771, 2005.
[89]
A. Teixeira, R. C. Cox, and M. R. Egmond, “Furan fatty acids efficiently rescue brain cells from cell death induced by oxidative stress,” Food & Function, vol. 4, no. 8, pp. 1209–1215, 2013.
[90]
T. Wakimoto, H. Kondo, H. Nii et al., “Furan fatty acid as an anti-inflammatory component from the green-lipped mussel Perna canaliculus,” Proceedings of the National Academy of Sciences of the United States of America, vol. 108, no. 42, pp. 17533–17537, 2011.
[91]
S. D. Anton, K. Heekin, C. Simkins, and A. Acosta, “Differential effects of adulterated versus unadulterated forms of linoleic acid on cardiovascular health,” Journal of Integrative Medicine, vol. 11, no. 1, pp. 2–10, 2013.
