Prostaglandins, Leukotrienes and Essential Fatty Acids ] (]]]]) ]]]–]]]

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Prostaglandins, Leukotrienes and Essential Fatty Acids
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Letter to the editor
What happened to do no harm? The issue of dietary omega-6 fatty acids In 1999, scientists from around the globe gathered to address dietary recommendations for omega-3 and omega-6 fatty acids [1]. Their recommendation emphasized the importance of reducing omega-6 fatty acids in order to reduce adverse health effects of excesses of arachidonic acid (AA) and its eicosanoid products. Therefore, they set an upper limit for linoleic acid (LA), to no more than 6.67 g/day, based on a 2000 kcal diet of 3.0% of energy. Yet, based on the current series of papers published on LA [2–4], one might be led to believe there has been a substantial body of evidence to refute the recommendation, which is not the case. The research cited is taken out of context and/or is based on very small studies, many of which were published over a decade ago, as described below. out of five of these studies [10–13] were performed on only 10 healthy men! He also says that there is no adverse effect from eating dietary LA intake on breast cancer. Large studies from the USA, France and Sweden indicate otherwise [14–16]. For example, in a case-control study on nearly 1700 women [14], researchers demonstrated that women with a genotype influencing the LOX enzyme, had a two-fold increase in breast cancer risk if they ate high levels of LA (417.4 g/day). Yet, this genotype had no influence on breast cancer risk, if these women ate a lower LA diet. Conclusion: At best, these papers [2–4] serve as editorials reflecting opinions of individual scientists. And at worst, these papers are disservice to the scientific process and public health, as they have been published without counterpoint or a serious review of the literature. The issue of an optimal level of dietary omega-6 fats is far from settled. But a plethora of papers published in the last decade [17] merit a serious discussion on the public health issue of dietary omega-6 fats; the most commonly consumed polyunsaturated fat in industrialized countries.

Comments on three papers published in PLEFA September 2008 (vol. 79, issue 3) The health implications of changing linoleic acid intakes by Jay Whelan (pp. 165–167). Linoleic acid and coronary heart disease by William S. Harris (pp. 169–171). Too much linoleic acid promotes inflammation—doesn’t it? by Kevin L. Fritsche (173–175). Comments by: Evelyn Tribole—1100 Quail Street, Suite 111, Newport Beach, CA 92660, USA. Fritsche [2] describes the CHIANTI study by Ferrucci et al. [5], as an example of no adverse impact on inflammation from eating too much LA. Subjects with the highest quartile of plasma arachidonic acid levels had lower pro-inflammatory markers and higher anti-inflammatory markers. But an important detail from this study is ignored—the subjects from this Mediterranean region eat a low LA diet, averaging 7 g/day. In this context, it is not surprising that plasma AA was associated with beneficial inflammation biomarkers—because it does so in the presence of eating a balanced proportion of omega-6 and omega-3 fatty acids. The results of this study support the benefits of eating a lower LA diet! Harris [3] concludes that, ‘‘Reducing LA intakes to less than 5% energy would be more likely to increase, not decrease, risk for CHD’’. Yet, that is not what the research shows. The Lyon Diet Heart Study [6] put their subjects on a low omega-6 fat diet, with a maximum 7 g (4.6% calories), which resulted in a striking reduction in all-cause mortality, including sudden cardiac death and cancer. Notably, studies have demonstrated harm from eating high LA diets on cardiovascular health [7–9]. Whelan [4] states that a number of studies fail to link enrichment of AA in tissues with deleterious outcomes. Yet four
0952-3278/$ - see front matter & 2008 Elsevier Ltd. All rights reserved. doi:10.1016/j.plefa.2008.12.004

[1] A.P. Simopoulos, A. Leaf, N. Salem, Workshop statement on the essentiality of and recommended dietary intake for omega-6 and omega-3 fatty acids, Prostaglandins Leukot. Essent. Fatty Acids 63 (2000) 119–121. [2] K.L. Fritsche, Too much linoleic acid promotes inflammation—doesn’t it?, Prostaglandins Leukot. Essent. Fatty Acids 79 (2008) 173–175. [3] W.S. Harris, Linoleic acid and coronary heart disease, Prostaglandins Leukot. Essent. Fatty Acids 79 (2008) 169–171. [4] J. Whelan, The health implications of changing linoleic acid intakes, Prostaglandins Leukot. Essent. Fatty Acids 79 (2008) 165–167. [5] L. Ferrucci, A. Cherubini, S. Bandinelli, B. Bartali, A. Corsi, F. Lauretani, et al., Relationship of plasma polyunsaturated fatty acids to circulating inflammatory markers, J. Clin. Endocrinol. Metab. 91 (2006) 439–446. [6] M. de Lorgeril, P. Salen, J.-L. Martin, I. Monjaud, J. Delaye, N. Mamelle, Mediterranean diet, traditional risk factors, and the rate of cardiovascular complications after myocardial infarction: final report of The Lyon Diet Heart Study, Circulation 99 (1999) 779–785. [7] J.H. Dwyer, H. Allayee, K.M. Dwyer, et al., Arachidonate 5-lipoxygenase promoter genotype, dietary arachidonic acid, and atherosclerosis, N. Engl. J. Med. 350 (2004) 29–37. [8] C.Q. Lai, D. Corella, S. Demissie, et al., Dietary intake of n-6 fatty acids modulates effect of apolipoprotein A5 gene on plasma fasting triglycerides, remnant lipoprotein concentrations, and lipoprotein particle size: The Framingham Heart Study, Circulation 113 (2006) 2062–2070. [9] H. Allayee, A. Baylin, J. Hartiala, et al., Nutrigenetic association of the 5-lipoxygenase gene with myocardial infarction, Am. J. Clin. Nutr. 88 (2008) 934–940. [10] D.S. Kelley, P.C. Taylor, G.J. Nelson, B.E. Mackey, Arachidonic acid supplementation enhances synthesis of eicosanoids without suppressing immune functions in young healthy men, Lipids 33 (1998) 125–130. [11] D.S. Kelley, P.C. Taylor, G.J. Nelson, P.C. Schmidt, B.E. Mackey, D. Kyle, Effects of dietary arachidonic acid on human immune response, Lipids 32 (1997) 449–456. [12] G.J. Nelson, P.C. Schmidt, G. Bartolini, D.S. Kelley, S.D. Phinney, D. Kyle, et al., The effect of dietary arachidonic acid on plasma lipoprotein distributions, apoproteins, blood lipid levels, and tissue fatty acid composition in humans, Lipids 32 (1997) 427–433. [13] G.J. Nelson, P.C. Schmidt, G. Bartolini, D.S. Kelley, D. Kyle, The effect of dietary arachidonic acid on platelet function, platelet fatty acid composition, and blood coagulation in humans, Lipids 32 (1997) 421–425.

2 Letter to the editor / Prostaglandins, Leukotrienes and Essential Fatty Acids ] (]]]]) ]]]–]]]

[14] J. Wang, et al., 5-Lipoxygenase and 5-lipoxygenase-activating protein gene polymorphisms, dietary linoleic acid, and risk for breast cancer, Cancer Epidemiol. Biomarkers Prev. 10 (2008) 2748–2754. [15] E. Sonestedt, U. Ericson, B. Gullberg, et al., Do both heterocyclic amines and omega-6 polyunsaturated fatty acids contribute to the incidence of breast ¨ cancer in post-menopausal women of the Malmo diet and cancer cohort?, Int. J. Cancer 123 (7) (2008) 1637–1643. ´ ` [16] A.C. Thiebaut, V. Chajes, M. Gerber, et al., Dietary intakes of omega-6 and omega-3 polyunsaturated fatty acids and the risk of breast cancer, Int. J. Cancer (2008) published online: 9 September 2008.

[17] A.P. Simopoulous, The importance of the omega-6/omega-3 fatty acid ratio in cardiovascular disease and other chronic diseases, Exp. Biol. Med. 233 (6) (2008) 674–688.

Evelyn Tribole 1100 Quail Street, Suite 111, Newport Beach, CA 92660, USA E-mail address:

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