We often hear about the importance of eating polyunsaturated fatty acids (PUFAs) for heart health. Almost all studies agree that eating PUFAs can reduce the incidence of cardiovascular disease. However, different types of PUFAs have very different effects on the body, some of which of are beneficial and others which are deleterious. In this article, I will go over a several studies that discuss the different types of PUFAs and how they affect health.
There are three main categories of PUFAS: omega-3, omega-6, and omega-9. Omega-3’s are found most prominently in fish, flax seeds, and walnuts. Omega-6’s are found in nuts and processed seed oils such as corn oil, soybean oil, safflower oil, and sunflower oil. Omega-9’s are predominately found in olive oil. This article will not focus on omega-9’s, but I will say that the literature varies on the benefits of omega-9’s for health. Some studies show protective effects against heart disease, while others show no effect. At the very least, they don’t seem to be deleterious to health.
PUFAs have variety of roles in the body. One major role is as a structural component of cell membranes (the outer layer that holds a cell’s components together). PUFAs also help form the brain and nervous system and serve as signaling molecules, which act as intermediaries in a wide range of functions (Patterson et al 2011).
Before the modern era of industrialized food, the ratio of omega-6 to omega-3 in the diet was roughly 1:1. Today, the ratio in the Western diet is about 16:1 (Simopoulos 2006). This increase is largely due to the effect of grain in the diet. Seed oils are cheap, so they are used as the primary fat in virtually all processed foods. In addition, animals that were designed to eat grass, such as cows, are now fed grain due to it’s cheap cost, ability to put fat on the animal, and quicker finishing times versus grass-fed animals. The consumption of grain by cows increases the amount of omega-6 present in their fat (Daley et al 2010). Contributing to the change in ratios, intake of omega-3 fatty acids has dropped due to reduced fish consumption in the Western diet (Simopoulos 2006).
Our genetics were selected for in an environment with a 1:1 omega-6 to omega-3 ratio. The drastic increase in the omega-6 to omega-3 ratio over the last 100 years has alarming health consequences. High omega-6 to omega-3 ratios are associated with increased total mortality, cardiovascular disease, growth of colorectal tumors, breast cancer, autoimmune diseases, inflammation, neurological degeneration, and asthma (Simopolous 2006, Hayakawa et al 2012, Lorgeril and Salen 2012, Dyall and Michael-Titus 2008).
Omega-6 Fatty Acids
The reason that health deteriorates when omega-6:omega-3 ratios increase is because omega-6’s produce inflammatory effects in the body. One type of omega-6 fatty acid is arachidonic acid (AA). AA is converted in the body to a group of compounds called eicosanoids. Eicosanoids are biologically active compounds that produce strong physiological effects. When omega-6’s are ingested in large amounts as in the Western diet, eicosanoids cause formation of thrombus (blood clots) and atheromas (swelling of arterial walls), allergic and inflammatory disorders, as well as proliferation of cells (as in tumor formation) (Simopoulos 2006, Allayee et al 2012).
In addition to causing inflammation, high omega-6 intake can increase oxidation of low-density lipoprotein (LDL) cholesterol. Oxidation increases the atherogenicity (the ability to form arterial plaques) of LDL cholesterol. Some believe that it is not the total amount of LDL that causes an increased risk of heart disease, but rather the amount of oxidized LDL. The most common omega-6 fatty acid, linoleic acid (LA), increases the oxidation rate of LDL (Parthasarathy et al 1990, Reaven et al 1991, Berry et al 1991, Bonanome et al 1992, Abbey et al 1993, Reaven et al 1993). When higher amounts of LA are present in the diet, higher amounts are incorporated into LDL molecules, and a greater percentage of LDL molecules become oxidized (Reaven et al 1994, Louheranta et al 1996). In addition, LA can be converted in the body to AA, and exacerbate the inflammation issues discussed in the previous paragraph (Patterson et al 2012).
There is strong evidence that a high intake of omega-6 fatty acids can increase the incidence of breast cancer, especially in genetically susceptible individuals. First, animal studies have shown that omega-6 fatty acids increase tumor formation in mammary tissues (Braden and Carroll 1986, Hubbard and Erickson 1987). Several epidemiological studies have correlated increased omega-6 intake with increased breast cancer risk in women (Wang et al 2008, Sonestedt et al 2008, Gago-Dominguez et al 2003, Chajes et al 2012, Murff et al 2011, Thiebaut et al 2009). Women with a genetic defect in their lysyl oxidase (LOX) gene are particularly susceptible to breast cancer when they consume a large amount of omega-6 fatty acids, but women with the same genetic defect eating a diet low in omega-6 have no greater risk of developing breast cancer than women without the genetic defect (Wang et al 2008).
Omega-3 Fatty Acids
In contrast to omega-6 fatty acids, omega-3 fatty acids have beneficial health effects. The most prevalent health effect of omega-3’s is its impact on the heart. Omega-3 fatty acids exert a protective effect against heart disease through a number of mechanisms including lowering triglycerides, and producing antithrombotic (preventing blot clots), anti-inflammatory and antihypertensive effects (Sudheendran et al 2010). Omega-3’s have been reported to be beneficial in preventing coronary heart disease (Sudheendran et al 2010). In addition, one study showed supplementation of omega-3’s after a cardiac event increased survival by 20% (Marchioli et al 2002).
Omega-3 fatty acids may have preventative effects against stroke. Populations eating a Western diet with low levels of omega-3 seem to have a reduced incidence of stroke when they increase omega-3 in their diet, however populations eating diets with already high levels of omega-3, such as those in Japan and Sweden, do no seem to benefit from increased omega-3 intake in relation to stroke (Mayurasakorn et al 2011). Perhaps these populations already have the 1:1 omega-6 to omega-3 ratio for which our genetics are adapted, therefore a further increase in omega-3 does not provide beneficial effects.
Omega-3 also has beneficial effects on the brain. In studies with mice exposed to mild stressors, supplementation with omega-3 has been shown to increase serotonin (the “feel good” hormone) (Vancassel et al 2008). Epidemiological studies correlate high intake of omega-3’s with less cognitive decline and dementia in middle and old aged people (Kalmijn et al 1997, 2004, Johnson and Schaefer 2006). Omega-3 fatty acids are an important component of the brain and a decrease in omega-3 in the brain has been correlated with Alzheimer’s disease (Skinner et al 1989, Soderberg et al 1991, Corrigan et al 1998). Studies have indicated that increased omega-3 may help prevent or improve symptoms of other neurodegenerative diseases including Parkinson’s disease, Huntington’s disease, and multiple sclerosis (Dyall and Michael-Titus, 2008).
First, it is important to note that both omega-3 and omega-6 fatty acids are absolutely needed in the body and both perform a variety of vital functions. Without either of these fatty acids, we would not live. The negative health consequences arise when omega-6 is present in great excess of omega-3.
It’s easy to think of omega-6’s as being “bad” and omega-3’s as being “good” but I don’t think this view is accurate. I believe that the negative health effects of omega-6’s are due to the fact that they are out of balance with omega-3’s in the Western diet and our body does not adapt well to the omega-6 overload. It’s quite possible that if we had an overload of omega-3 fatty acids in the diet we might be talking about the benefits of supplementation with omega-6 and the deleterious effects of omega-3.
As far as sources of omega-3, cold-water fish seem to be the best source. Eating fish with a high fat content will help boost omega-3 intake. Unfortunately, many people do not like fatty fish such as sardines. For those who do not like the taste of fish, supplementation with fish or krill oil may be wise. Some people use flax seed oil as an omega-3 supplement, but this is not a great source because our body is inefficient at converting the omega-3 found in flax into the biologically active omega-3 fatty acids, EPA and DHA. Most importantly, in order to reduce the ratio of omega-6 to omega-3, it is essential to limit intake of omega-6 fats by reducing consumption of seed oils.
Abbey M, Belling GB, Noakes M, Hirata F, Nestel PJ. Oxidation of low-density lipoproteins: intraindividual variability and the effect of dietary linoleate supplementation. Am J Clin Nutr 1993;57:391–8.
Allayee, H. Roth, N., Hodis, H. N. (2009). Polyunsaturated fatty acids and cardiovascular disease: implications for nutrigenics. J Nutrigenomics 2: 140-148.
Berry EM, Eisenberg S, Haratz D. Effects of diets rich in monounsatu- rated fatty acids on plasma lipoproteins—the Jerusalem Nutrition Study: high MUFAs vs. high PUFAs. Am J Clin Nutr 1991;53:899–907.
Bonanome A, Pagnan A, Biffanti S. Effect of dietary monounsaturated and polyunsaturated fatty acids on the susceptibility of plasma low den- sity lipoproteins to oxidative modification. Arterioscler Thromb 1992; 12:529–33.
Braden LM, Carroll KK: Dietary polyunsaturated fat in relation to mammary carcinogenesis in rats. Lipids 1986, 21:285-288.
Chajès V, Torres-Mejia G, Biessy C, Ortega-Olvera C, Angeles-Llerenas A, Ferrari P, Lazcano- Ponce E, Romieu I: ω-3 and ω-6 polyunsaturated fatty acid intakes and the risk of breast cancer in Mexican women: impact of obesity status. Cancer Epidemiol Biomarkers Prev 2012, 21:319-326.
Corrigan, F. M., Horrobin, D. F., Skinner, E. R., Besson, J. A. O., & Cooper, M. B. (1998). Abnormal content of n-6 and n-3 long-chain unsaturated fatty acids in the phosphoglycerides and cholesterol esters of parahippocampal cortex from Alzheimer’s disease patients and its relationship to acetyl CoA content. The International Journal of Biochemistry & Cell Biology, 30(2), 197–207.
Deckelbaum, R. J., Torrejon, C. (2011). The omega-3 fatty acid nutritional landscape: health benefits and sources. Journal of Nutrition 587S-591S.
Dyall, S. C., Michael-Titus, A. T. (2008). Neurological benefits of omega-3 fatty acids. Neuromol Med 10: 219-35.
Gago-Dominguez M, Yuan JM, Sun CL, Lee HP, Yu MC: Opposing effects of dietary n-3 and n-6 fatty acids on mammary carcinogenesis: The Singapore Chinese Health Study. Br J Cancer 2003, 89:1686-1692.
Hayakawa, S., Yoshikawa, D., Ishii, H, et al. (2012). Association of plasma omega-3 to omega-6 polyunsaturated fatty acid ratio with complexity of coronary artery lesion. International Medicine 51: 1009-1014.
Hubbard NE, Erickson KL: Enhancement of metastasis from a transplantable mouse mammary tumor by dietary linoleic acid. Cancer Res 1987, 47:6171-6175.
Johnson, E. J., & Schaefer, E. J. (2006). Potential role of dietary n-3 fatty acids in the prevention of dementia and macular degeneration. American Journal of Clinical Nutrition, 83(6 Suppl), 1494S–1498S.
Kalmijn, S., Launer, L. J., Ott, A., Witteman, J. C., Hofman, A., & Breteler, M. M. (1997). Dietary fat intake and the risk of incident dementia in the Rotterdam Study. Annals of Neurology, 42(5), 776–782.
Kalmijn, S., van Boxtel, M. P., Ocke, M., Verschuren, W. M., Kromhout, D., & Launer, L. J. (2004). Dietary intake of fatty acids and fish in relation to cognitive performance at middle age. Neurology, 62(2), 275–280.
Lorgeril, M., Salen, P. (2012) New Insights into the health effects of saturated and omega-6 and omega-3 polyunsaturated fatty acids. BMC Medicine 10:50.
Louheranta AM, Porkkala-Sarataho EK, Nyyssonen MK, Salonen RM,
Salonen JT. Linoleic acid intake and susceptibility of very-low-density and low-density lipoproteins to oxidation in men. Am J Clin Nutr 1996; 63:698–703.
Marchioli R, Barzi F, Bomba E, Chieffo C, Di Gregorio D, Di Mascio R, Franzosi MG, Geraci E, Levantesi G, Maggioni AP, et al. Early protection against sudden death by n-3 polyunsaturated fatty acids after myocardial infarction: time-course analysis of the results of the Gruppo Italiano per lo Studio della Sopravvivenza nell’Infarto Miocardico (GISSI)-Prevenzione. Circulation. 2002;105:1897–903.
Mayurasakorn K, Williams JJ, Ten VS, Deckelbaum RJ. Docosahexaenoic acid: brain accretion and roles in neuroprotection after brain hypoxia and ischemia. Curr Opin Clin Nutr Metab Care. 2011;14:158–67.
Murff HJ, Shu XO, Li H, Yang G, Wu X, Cai H, Wen W, Gao YT, Zheng W: Dietary polyunsaturated fatty acids and breast cancer risk in Chinese women: a prospective cohort study. Int J Cancer 2011,128:1434-1441.
Parthasarathy S, Khoo JC, Miller E, Barnett J, Witztum JL, Steinberg D. Low density lipoprotein rich in oleic acid is protected against oxida- tive modification: implications for dietary prevention of atherosclerosis. Proc Natl Acad Sci USA 1990;87:3894–8.
Reaven P, Parthasarathy S, Grasse BJ. Feasibility of using an oleate-rich diet to reduce the susceptibility of low density lipoprotein to oxidative modification in humans. Am J Clin Nutr 1991;54:701–6.
Reaven P, Parthasarathy S, Grasse BJ, Miller E, Steinberg D, Witz- tum JL. Effects of oleate-rich and linoleate-rich diets on the susceptibility of low density lipoprotein to oxidative modification in mildly hypercholesterolemic subjects. J Clin Invest 1993;91:668–76.
Reaven PD, Grasse BJ, Tribble DL. Effects of linoleate-enriched and oleate-enriched diets in combination with α-tocopherol on the suscept- ibility of LDL and LDL subfractions to oxidative modification in humans. Arterioscler Thromb 1994;14:557–66.
Simopolous, A. P. (2006) Evolutionary aspects of diet, the omega-6/omega-3 ratio and genetic variation: nutritional implications for chronic diseases. Biomedicine and Pharmacotherapy 60: 502-507.
Skinner, E. R., Watt, C., Besson, J. A. O., & Best, P. V. (1989). Lipid composition of different regions of the brain in patients with Alzheimer’s disease. Biochemical Society Transactions, 17, 213–214.
Soderberg, M., Edlund, C., Kristensson, K., & Dallner, G. (1991). Fatty acid composition of brain phospholipids in aging and Alzheimer’s disease. Lipids, 26(6), 421–425.
Sonestedt E, Ericson U, Gullberg B, Skog K, Olsson H, Wirfält E: Do both heterocyclic amines and omega-6 polyunsaturated fatty acids contribute to the incidence of breast cancer in postmenopausal women of the Malmö diet and cancer cohort? Int J Cancer 2008, 123:1637- 1643.
Sudheendran S, Chang CC, Deckelbaum RJ. N-3 vs. saturated fatty acids: effects on the arterial wall. Prostaglandins Leukot Essent Fatty Acids. 2010;82:205–9.
Thiébaut AC, Chajès V, Gerber M, Boutron-Ruault MC, Joulin V, Lenoir G, Berrino F, Riboli E, Bénichou J, Clavel-Chapelon F: Dietary intakes of omega-6 and omega-3 polyunsaturated fatty acids and the risk of breast cancer. Int J Cancer 2009, 124:924-931.
Vancassel, S., Leman, S., Hanonick, L., Denis, S., Roger, J., Nollet, M., et al. (2008). N-3 polyunsaturated fatty acids supplementation reverses stress-induced modifications on brain monoamine levels in mice. Journal of Lipid Research, 49, 340–348.
Wang J, John EM, Ingles SA: 5-lipoxygenase and 5-lipoxygenase-activating protein gene polymorphisms, dietary linoleic acid, and risk for breast cancer. Cancer Epidemiol Biomarkers Prev 2008, 17:2748-2754.