Have you been given the advice to substitute vegetables oils high in polyunsaturated fatty acids (PUFAs) for animal fats high in saturated fats? Sure you have—if you have been listening to worldwide dietary guidelines since the 1960s. The basis of this advice relates to studies that found diets high in PUFAs are associated with lower levels of cholesterol. So a diet high in PUFAs has long been recommended as a heart-healthy diet.
There are two main types of PUFAs—omega-6 and omega-3 PUFAs (both are not made by the body and must be taken as food or supplements). When these widespread dietary guidelines were made, people switched from animals fats (primarily butter and lard) to omega-6 PUFAs (primarily vegetable oils). The result of this switch was a drastic change in the omega-6 to omega-3 ratio. People were eating much more omega-6, but the same amount of omega-3 (which for most people was, and still is, very little). And saturated fats ended up taking the blame for poor heart health.
While some scientists questioned the reasoning behind these recommendations, industry and government charged ahead spreading the message that PUFAs were good and animal fats were bad. And somehow, omega-3 fats were marginalized.
In 1978, the Sydney Diet Heart Study (SDHS) brought some light to this topic, however.1 Researchers evaluated data on a group of people who replaced animal fats with safflower oil. Because safflower oil is a PUFA high in omega-6 with no omega-3, this study provided a clear look at what happens when omega-6 PUFAs are increased, yet omega-3 PUFAs are not. The people who replaced saturated animal fats with polyunsaturated omega-6 safflower oil were found to be at increased risk of death from all causes (all-cause mortality).
You would think that might have raised the red flag, but for some reason, people went right on recommending the replacement of saturated fat with vegetable oils. And we listened.
A recent study published in the British Medical Journal will hopefully help change this story, and be an eye-opener to nutrition, dietary, and medical professionals worldwide. Researchers obtained the original data from the SDHS study and used modern statistical methods to compare rates of all-cause death as well as cardiovascular and coronary heart disease death by group.2 As suspected, they found that increasing omega-6 PUFA from safflower oil increased death rates from cardiovascular disease, coronary heart disease, and all-cause mortality when compared to a diet rich in saturated fats from animal fats.
This study also opens up questions about previous studies that have found cardiovascular benefit by replacing animal fats with PUFAs—those studies did not control for the fact that people were also increasing omega-3 PUFAs. They state, “Therefore, benefits previously attributed to greater intake of total PUFA might be specifically attributable to omega-3 PUFAs, and are not necessarily generalizable to omega-6, or PUFAs in general.”
Here the plot thickens. It is known that increasing omega-6 fats in the diet lowers total cholesterol, mostly by reducing LDL-cholesterol (also known as “bad” cholesterol). Traditional recommendations to reduce saturated fat are based on the assumption that this decrease in LDL-cholesterol will result in reduced risk of coronary heart disease and improve survival. In this new study, total cholesterol levels were decreased as expected, but—and this is important—these reductions were not associated with reduced risk of cardiovascular death.
They stated, “These observations, combined with recent progress in the field of fatty acid metabolism, point to a mechanism of cardiovascular disease pathogenesis independent of our traditional understanding of cholesterol lowering.” This is just the point that Brenda and I make in our latest book, Heart of Perfect Health: there is more to the story than simply lowering cholesterol levels. In fact, an entire chapter is dedicated to this topic, entitled, “Cholesterol is Not All Bad.”
The paper goes on to talk about the importance of the state in which cholesterol is found (just as our book does). They recognize that oxidized omega-6 linoleic acid metabolites (OXLAMs) are the most abundant oxidized fatty acids found in oxidized LDL-cholesterol. And oxidized LDL (which is, essentially, damaged LDL that creates oxidative stress and inflammation) is a significant marker of plaque buildup in the arteries.
The good news is that we can reverse the damage we’ve done. The same researchers recently performed another study showing that by lowering dietary omega-6 linoleic acid for 12 weeks, they were able to reduce omega-6 linoleic acid and their oxidized metabolites in circulation, and increase omega-3 EPA and DHA.3 This is most likely due to the fact that omega-6 linoleic acid (LA) competes with omega-3 alpha-linolenic acid (ALA) for the same enzymes (enlongase and desaturase). If there is too much omega-6 LA, then omega-3 ALA will not be able to convert into EPA and DHA. As we know, higher amounts of EPA and DHA are associated with better heart health.
The results of this study, in combination with a few previous studies that have been helping to build the evidence against the current widespread dietary recommendations, will hopefully get the attention they deserve. Indeed, the paper concludes, “These findings could have important implications for worldwide incorrect dietary advice to substitute omega-6 linoleic acid, or PUFAs in general, for saturated fats.” Let’s hope everyone is listening.
- J.M. Woodhill, et al., “Low fat, low cholesterol diet in secondary prevention of coronary heart disease.” Adv Exp Med Biol. 1978;109:317-30.
- C.E. Ramsden, D. Samora, et al., “Use of dietary linoleic acid for secondary prevention of coronary heart disease and death: evaluation of recovered data from the Sydney Diet Heart Study and updated meta-analysis.” BMJ. 2013;346:e8707.
- C.E. Ramsden, et al., “Lowering dietary linoleic acid reduces bioactive oxidized linoleic acid metabolites in humans.” Prostaglandins Leukot Essent Fatty Acids. 2012 Oct-Nov;87(4-5):135-41.