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Prostaglandins, Leukotrienes and Essential Fatty Acids ] (]]]]) ]]]–]]]
Contents lists available at ScienceDirect
Prostaglandins, Leukotrienes and
Essential Fatty Acids
journal homepage: www.elsevier.com/locate/plefa
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 redu-
cing 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.
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
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.
References
[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 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 supplemen-
tation 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.
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[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 Malmö diet and cancer cohort?, Int.
J. Cancer 123 (7) (2008) 1637–1643.
[16] A.C. Thiébaut, V. Chajès, 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: etribole@gmail.com