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The Issue of Dietary Omega-6 Fatty Acids:What Happened to Do No Harm?

The Issue of Dietary Omega-6 Fatty Acids:What Happened to Do No Harm?

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A critical look at public health and the impact of dietary omega-6 fat consumption. Omega-6 fatty acids are the most commonly consumed polyunsaturated fats in industrialized countries. Top sources are soybean oil, cottonseed oil and corn oil. www.Omega-6-News.org
A critical look at public health and the impact of dietary omega-6 fat consumption. Omega-6 fatty acids are the most commonly consumed polyunsaturated fats in industrialized countries. Top sources are soybean oil, cottonseed oil and corn oil. www.Omega-6-News.org

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Published by: Evelyn Tribole, MS, RD on Jul 14, 2009
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Letter to the editor
 What happened to do no harm? The issue of dietary omega-6fatty acids
In 1999, scientists from around the globe gathered to addressdietary recommendations for omega-3 and omega-6 fatty acids[1]. Their recommendation emphasized the importance of redu-cing omega-6 fatty acids in order to reduce adverse health effectsof excesses of arachidonic acid (AA) and its eicosanoid products.Therefore, they set an upper limit for linoleic acid (LA), to no morethan 6.67g/day, based on a 2000kcal diet of 3.0% of energy. Yet,based on the current series of papers published on LA[2–4], onemight be led to believe there has been a substantial body of evidence to refute the recommendation, which is not the case. Theresearch cited is taken outof context and/or is based on verysmallstudies, many of which were published over a decade ago, asdescribed below.
Comments on three papers published in PLEFA September 2008(vol. 79, issue 3)
The health implications of changing linoleic acid intakes by JayWhelan (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? byKevin 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 eatingtoo much LA. Subjects with the highest quartile of plasmaarachidonic acid levels had lower pro-inflammatory markers andhigher anti-inflammatory markers. But an important detail fromthis study is ignored
the subjects from this Mediterraneanregion eat a low LA diet, averaging 7g/day. In this context, it isnot surprising that plasma AA was associated with beneficialinflammation biomarkers
because it does so in the presenceof eating a balanced proportion of omega-6 and omega-3 fattyacids. The results of this study support the benefits of eating alower LA diet!Harris[3]concludes that, ‘‘Reducing LA intakes to less than 5%energy would be more likely to increase, not decrease, risk forCHD’’. Yet, that is not what the research shows. The Lyon DietHeart Study[6]put their subjects on a low omega-6 fat diet, witha maximum 7g (
4.6% calories), which resulted in a strikingreduction in all-cause mortality, including sudden cardiac deathand cancer. Notably, studies have demonstrated harm from eatinghigh LA diets on cardiovascular health[7–9].Whelan[4]states that a number of studies fail to linkenrichment of AA in tissues with deleterious outcomes. Yet fourout of five of these studies[10–13]were performed on only10 healthy men! He also says that there is no adverse effect fromeating dietary LA intake on breast cancer. Large studies from theUSA, France and Sweden indicate otherwise[14–16]. For example,in a case-control study on nearly 1700 women[14], researchersdemonstrated that women with a genotype influencing the LOXenzyme, had a two-fold increase in breast cancer risk if they atehigh levels of LA (
17.4g/day). Yet, this genotype had noinfluence on breast cancer risk, if these women ate a lower LA diet.
: At best, these papers[2–4]serve as editorialsreflecting opinions of individual scientists. And at worst, thesepapers are disservice to the scientific process and public health, asthey have been published without counterpoint or a serious reviewof the literature. The issue of an optimal level of dietary omega-6fats is far from settled. But a plethora of papers published in thelast decade[17]merit a serious discussion on the public healthissue of dietary omega-6 fats; the most commonly consumedpolyunsaturated fat in industrialized countries.
[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 inflamma-tory 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 cardiovascularcomplications after myocardial infarction: final report of The Lyon Diet HeartStudy, Circulation 99 (1999) 779–785.[7] J.H. Dwyer, H. Allayee, K.M. Dwyer, et al., Arachidonate 5-lipoxygenasepromoter 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 acidsmodulates effect of apolipoprotein A5 gene on plasma fasting triglycerides,remnant lipoprotein concentrations, and lipoprotein particle size: TheFramingham Heart Study, Circulation 113 (2006) 2062–2070.[9] H. Allayee, A. Baylin, J. Hartiala, et al., Nutrigenetic association of the5-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 supplemen-tation enhances synthesis of eicosanoids without suppressing immunefunctions 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 dietaryarachidonic acid on platelet function, platelet fatty acid composition, andblood coagulation in humans, Lipids 32 (1997) 421–425.
Contents lists available atScienceDirectjournal homepage:www.elsevier.com/locate/plefa
Prostaglandins, Leukotrienes andEssential Fatty Acids
0952-3278/$-see front matter
2008 Elsevier Ltd. All rights reserved.doi:10.1016/j.plefa.2008.12.004Prostaglandins, Leukotrienes and Essential Fatty Acids

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