by Craig Weatherby
Many scientists see signs of harm from Americans’ relatively recent shift to radically higher intake of omega-6 fatty acids.
The available evidence indicates that people thrive best on diets providing about three parts omega-6 fats to one part omega-3 fats.
Rigorous evidence review refutes the American Heart Association’s 2009 finding that Americans’ high intake of omega-6 fats poses no heart risks (Ramsden CE et al. 2010).
The AHA’s 2009 report didn’t distinguish between clinical trials that raised people’s omega-6 intake only vs. those in which omega-3 intake also rose.
Doctors and public health authorities should see this evidence and act on it.
But that intake ratio shifted dramatically over the past 150 years, and is now about 25 parts omega-6s to one part omega-3s.
Rather than lack of omega-3s—though many Americans need more of those—most of that huge shift stemmed from a flood of omega-6 fats.
Those omega-6 fats came from the polyunsaturated vegetable oils that started replacing butter and lard in the 1960’s… with the intent of reducing heart disease risks.
But growing evidence shows that America’s relatively recent turn to oils high in omega-6 fats—and the packaged and takeout foods made with them—was way too much of a good thing.
AHA addressed omega-6 fears with a flawed analysis
In response to a rising tide of concern over inflammation-related health risks associated with excess omega-6s, the American Heart Association (AHA) commissioned a scientific review of the clinical evidence.
The authors of the AHA review, published in 2009, purported to find no evidence that the country’s enormous increase in omega-6 fat intake poses a risk to heart health (Harris WS et al. 2009).
Oslo Study exemplifies the
flaws in the American Heart Association's 2009 review
One of the most striking examples of the many imprecisions in the AHA’s 2009 evidence review is the Oslo Heart Study.
In that controlled trial, people in the test group consumed as much as three times more omega-6s than the control group… but they were also getting a whopping five grams per day of omega-3s and cut their intake of trans fats drastically
Nonetheless, the AHA team counted the Oslo Heart Study as proving the heart-health powers of increased omega-6 intake!
In fact, despite their high omega-3 intake, the test group did not enjoy substantially better heart-health outcomes… possibly, as Dr. Hibbeln’s team wrote, because they were also consuming omega-6 fats to excess.
But leading fatty acid scientists had persuasively tied diets very high in omega-6 fats to greater risk for heart disease, likely due to their generally pro-inflammatory influences in the body.
(See “Report Finds Americans Need Far More Omega-3s,” whose subtitle provides the full picture: “Extremely high intake of omega-6s creates need for major increase in omega-3 intake; drastic drop in omega-6 intake would cut omega-3 requirement dramatically.”)
Some of these same scientists responded to the AHA’s exoneration of omega-6-heavy diets with some pretty compelling preliminary critiques.
Captain Joseph Hibbeln, M.D., of the National Institutes of Health (NIH) was among many leading scientists in the field to find serious flaws in the AHA’s omega-6 report.
Today, he and his colleagues published a painstaking, ground-breaking re-analysis of the evidence the Heart Association used to exonerate high omega-6 intake as a heart risk factor (Ramsden CE et al. 2010).
Editorial says prior Heart Association analysis ignored key distinctions
The new review by Dr. Hibbeln’s group reveals some remarkably obvious and deeply consequential flaws in the AHA report.
The title of an accompanying editorial by leading fatty acid researcher Philip Calder, Ph.D., says it all: “The American Heart Association advisory on n-6 fatty acids: evidence based or biased evidence?”
Professor Calder goes on to echo the key critique made by Dr. Hibbeln’s team, which is that the AHA team included many clinical trials in which people increased their intakes of omega-6 and omega-3 fats… but counted these studies as though the participants increased only their omega-6 intake.
Dr. Hibbeln’s group made some smart decisions in taking their own look at the evidence.
They evaluated studies that examined the impact of increased omega-6 intake alone… separately from those that raised people’s intakes of omega-6 and omega-3 fatty acids.
They also did extensive work to estimate as precisely as possible the overall fatty acid intakes of study participants, and even contacted the authors of some of the older studies in order to clarify uncertain points.
Professor Calder expressed an implied criticism of the AHA’s analysis, and admiration for the Hibbeln group’s painstaking efforts, in understated British fashion:
“This scholarly approach… has yielded a different conclusion from the AHA advisory... This piece of work by Ramsden and colleagues is to be applauded and will, it is hoped, open a healthy scientific debate on this important matter.”
We believe that—unlike the AHA’s review—their incisive analysis will bear up under close scrutiny.
And we hope it will help awaken public health officials and regular folks alike to one likely danger of Americans’ extremely high omega-6 intakes.
Heart Association’s analysis ignores key distinctions
Dr. Hibbeln’s team report that the review performed on behalf of the American Heart Association contains
“imprecisions” that inevitably led the AHA's analysis astray.
In short, most of these flaws flowed from the AHA team's failure to distinguish between the two kinds of polyunsaturated fats—omega-3 and omega-6—that people consumed more of in clinical trials.
When trial participants consumed diets that replaced saturated fats with omega-6 polyunsaturated fats their heart risks tended to rise.
In contrast, trials in which participants replaced saturated fats with some mix of omega-6 and omega-3 polyunsaturated fats yielded lower heart risks.
The new, more careful analysis shows that when participants increased their intake of both omega-6 and omega-3 fats, their risk of non-fatal heart attacks and/or heart-related deaths was 22 percent lower.
But, when participants increased only their intake of omega-6 fats, the combined risk of non-fatal heart attacks and/or heart-related deaths was 13 percent higher.
Overall, the risk of non-fatal heart attacks and/or heart-related deaths was significantly higher in “omega-6-only” diets compared to mixed “omega-3 + omega-6” diets.
(The term “omega-6-only” diets oversimplifies, because the people eating them did not necessarily change their usual omega-3 intake much.)
And in clinical trials where people substituted regular omega-6 fats for trans omega-6 fats and saturated fats—without simultaneously increasing omega-3 intake—the participants suffered an increase in risk of death that, as the authors said, “approached statistical significance.”
The conclusion reached by Dr. Hibbeln’s team was based on a much more careful, nuanced analysis of the data used by the AHA’s scientists:
“Advice to specifically increase n-6 PUFA [omega-6 fat] intake… is unlikely to provide the intended benefits, and may actually increase the risks of CHD [coronary heart disease] and death” (Ramsden CE et al. 2010).
As to any possible heart risks of lowering your omega-6 intake below the AHA’s recommended level—a minimum of five percent of daily calories—a large clinical study (not included either group’s statistical analyses) found big heart-health benefits among participants who went below the AHA guideline for minimum omega-6 intake.
It’s important to note that the low-omega-6 group ate a proven heart-healthful Mediterranean-style diet with ample omega-3s, based on vegetables, fruits, whole grains, dairy, nuts, fish, and olive oil, which is relatively low in omega-6s … with extra virgin grade abounding in artery-enhancing polyphenols.
So, you might ask, what are omega-6 fats, and where are they found?
The omega imbalance in American diets
Your diet must contain two kinds of essential polyunsaturated fatty acids… or you will suffer disease and eventually die.
Omega-3 fats come from seafood, leafy greens, walnuts, and flaxseed.
Omega-6 fats in Americans’ diets come from common seed oils (corn, soy, cottonseed, safflower, sunflower), grains (wheat, corn), and the flesh of factory farmed beef, chicken, and pork raised on those foods… rather than on pasture or forage with a lower (better) omega-6/omega-3 ratio.
Only three common oils—olive oil, macadamia nut oil, and “hi-oleic” sunflower oil—are comparatively low in omega-6s.
So-called “short-chain” omega-3 and omega-6 fats (called ALA and LA, respectively) compete with each other for conversion into the usable long-chain forms that our cells and bodies require to survive and thrive.
Over the past 40 years, the average American has consumed ever increasing amounts and proportions of short-chain omega-6 fats from vegetable oils.
This “omega imbalance” has made it difficult for the far smaller amounts of short-chain omega-3s in Americans’ diets to get converted to the long-chain forms (EPA and DHA) needed in cell membranes and for key brain and immune functions.
The critical functions enabled or mediated by omega-3 fats include basic brain operations and moderation or cessation of chronic, unhealthful inflammation, which is associated with increased risk of cardiovascular disease, dementia, diabetes, arthritis, and other degenerative conditions.
This massive dietary shift away from saturated animal fats (butter, red meat) in favor of vegetable oils high in polyunsaturated fats was a direct response to evidence linking diets high in saturated fats to increased risk of cardiovascular disease.
Many researchers have found flaws in the hypothesis that dietary saturated fat promotes heart disease… but there is evidence on both sides of that debate.
Regardless of the merits of reducing intake of saturated fats, this shift has had unintended consequences.
The first unintended consequence was a shift to “shelf-stable” hydrogenated vegetable oils, which are inherently high in trans-form omega-6 fats… a kind of fat proven to raise heart risks dramatically.
(In addition to rendering the omega-6 polyunsaturated fats in vegetable oils resistant to oxidation by making them more like saturated fats, hydrogenation destroys virtually all of the omega-3 fats found in the few vegetable oils that contain them. (In order of increasing omega-3 content, these are soy, canola, walnut, and flaxseed oil.)
The finding that trans omega-6 fats are much worse than saturated fats when it comes to heart health has led to a rapid societal retreat from hydrogenated oils.
That’s been a very good thing, but it hasn’t dealt with the dangers of excessive omega-6 intake, which mostly relate to the generally (though not exclusively) pro-inflammatory effects exerted by omega-6 fats.
Chronic, “silent” inflammation is a prime driver of heart disease, cancer, dementia, and more.
So overloading your cells with omega-6 fatty acids, which, in excess, tend to promote and sustain inflammation, is a very bad idea.
But this dietary trend has taken hold worldwide, thanks to well-meant but misguided medical advice… an error that has persisted due to sloppy research and a very human reluctance to admit error.
We can only hope that the new analysis by Dr. Hibbeln’s team leads to a comprehensive overhaul of dietary advice to Americans… soon.
American Heart Association. Omega-6 fatty acids: Make them a part of heart-healthy eating. Jan. 27, 2009. Accessed online at http://americanheart.mediaroom.com/index.php?s=43&item=650
de Lorgeril M et al. Mediterranean Diet, Traditional Risk Factors, and the Rate of Cardiovascular Complications After Myocardial Infarction : Final Report of the Lyon Diet Heart Study Circulation1999;99:779-785 (Free full text)
de Lorgeril M, Reanud S, Mamelle N, Salen P, Martin JL, Monjuad I, Gidolet J, Touboul P, Delaye J. Mediterranean alpha-linolenic acid-rich diet in secondary prevention of coronary heart disease. Lancet. 1994;343:1454-1459.
de Lorgeril M, Salen P, Martin JL, Monjaud I, Delaye J, Mamelle N. Mediterranean diet, traditional risk factors, and the rate of cardiovascular complications after myocardial infarction: Final report of the Lyon Diet Heart Study. Circulation. 1999;99:779-785.
Dwyer JH et al. Arachidonate 5-Lipoxygenase Promoter Genotype, Dietary Arachidonic Acid, and Atherosclerosis. N Engl J Med 2004 350: 29-37.
Ghosh S, Novak EM, Innis SM. Cardiac proinflammatory pathways are altered with different dietary n-6 linoleic to n-3 -linolenic acid ratios in normal, fat-fed pigs. Am J Physiol Heart Circ Physiol (2007)293: H2919-H2927.
Griffin BA. How relevant is the ratio of dietary n-6 to n-3 polyunsaturated fatty acids to cardiovascular disease risk? Evidence from the OPTILIP study. Curr Opin Lipidol. 2008 Feb;19(1):57-62. Review.
Harris WS, Mozaffarian D, Rimm E, Kris-Etherton P, Rudel LL, Appel LJ, Engler MM, Engler MB, Sacks F. Omega-6 fatty acids and risk for cardiovascular disease: a science advisory from the American Heart Association Nutrition Subcommittee of the Council on Nutrition, Physical Activity, and Metabolism; Council on Cardiovascular Nursing; and Council on Epidemiology and Prevention. Circulation. 2009 Feb 17;119(6):902-7. Epub 2009 Jan 26.
Hibbeln JR et al. Healthy intakes of n-3 and n-6 fatty acids: estimations considering worldwide diversity.Am J Clin Nutr 2006 83: S1483-1493. Free Full Text.
Lai CQ 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 (2006)113: 2062-2070.
Lands WE. Dietary fat and health: the evidence and the politics of prevention: careful use of dietary fats can improve life and prevent disease. Ann N Y Acad Sci. 2005 Dec;1055:179-92.
Leaf A. Dietary Prevention of Coronary Heart Disease: The Lyon Diet Heart Study.Circulation 1999;99:733-735.
Louheranta AM et al. Linoleic acid intake and susceptibility of very-low-density and lowdensity lipoproteins to oxidation in men. Am J Clin Nutr 1996 63: 698-703.
Okuyama H. Prevention of Coronary Heart Disease From the Cholesterol Hypothesis to omega-6/omega-3 Balance. World Review of Nutrition and Dietetics (2007) Vol. 96:1-158.
Ramsden CE, Hibbeln JR, Majchrzak SF, Davis JM. n-6 Fatty acid-specific and mixed polyunsaturate dietary interventions have different effects on CHD risk: a meta-analysis of randomised controlled trials. Br J Nutr (2010). doi:10.1017/S0007114510004010
Ramsden CE, Hibbeln JR, Lands WE. Letter to the Editor re: Linoleic acid and coronary heart disease. Prostaglandins Leukot. Essent. Fatty Acids (2008), by W.S. Harris. Prostaglandins Leukot Essent Fatty Acids. 2009 Jan;80(1):77; author reply 77-8. Epub 2009 Jan 14.
Ramsden CE, Faurot KR, Carrera-Bastos P, Cordain L, De Lorgeril M, Sperling LS. Dietary fat quality and coronary heart disease prevention: a unified theory based on evolutionary, historical, global, and modern perspectives. Curr Treat Options Cardiovasc Med. 2009 Aug;11(4):289-301.
Sears B. Consume more omega-6 fatty acids? They have to be kidding. February 2009. Accessed online at http://www.drsears.com/tabid/399/itemid/13303/Consume-more-omega6-fatty-acids-They-have-to-be.aspx
Simopoulos AP. The importance of the omega-6/omega-3 fatty acid ratio in cardiovascular disease and other chronic diseases.Exp Biol Med (Maywood). 2008 Jun;233(6):674-88.
Simopoulos AP, Leaf A, Salem N. Workshop on the Essentiality of and Recommended Dietary Intakes for Omega-6 and Omega-3 Fatty Acids.J Am Coll Nutr 1999 18: 487-489.
Tribole E..What happened to do no harm? The issue of dietary omega-6 fatty acids.Prostaglandins Leukot Essent Fatty Acids. 2009 Jan 13. [Epub ahead of print] .
Wang J et al. 5-Lipoxygenase and 5-Lipoxygenase-Activating Protein Gene Polymorphisms, Dietary Linoleic Acid, and Risk for Breast Cancer. Cancer Epidemiol Biomarkers Prev October 1, 2008(17): 2748-2754
Wijendran V, Hayes KC. Dietary n-6 and n-3 fatty acid balance and cardiovascular health. Annu Rev Nutr. 2004;24:597-615. Review.