Do you have syphilis? Or snort cocaine, or smoke tobacco, or have a bacterial infection or periodontal disease that causes overproduction of cholesterol that accumulates in the arteries? If none of these “insults” apply to your body, the cause of chronic inflammation, and therefore the cause of atherosclerotic plaque in your arteries, is likely to be dietary.
The relationship between dietary fat and atherosclerosis, however, is a contentious field. The USDA, in its food pyramid and Dietary Guidelines for Americans, promotes a low-fat diet, based largely on the view that fat in the diet is atherogenic. The American Heart Association, the American Diabetes Association and the National Cholesterol Education Program make similar recommendations. Especially singled out are saturated fats, dietary cholesterol and trans fats. Trans fats are one of the few consensus points in nutrition as everyone thinks these are very bad for your health. But could all of these authorities be wrong about the role of saturated fats and dietary cholesterol?
In a word, “yes.” Writing in Science, multiple award-winning science writer Gary Taubes says that political considerations played into the recommendation of government bodies. Gary Taubes broke onto the scene with his 2002 exposé in the New York Times Sunday magazine cover story, “What if it’s All Been a Big Fat Lie?” Later he wrote a tome for serious readers, “Good Calories – Bad Calories” and later still a more readable “Why We Get Fat – And What to Do About It.”
Professor Walter Willett, of the Harvard School of Public Health and Principal Investigator of the second Nurse’s Health Study, recommends much higher levels of dietary fat than the public health establishment, and especially of monounsaturated and polyunsaturated fat. Once again, there is growing unanimity that monounsaturated fats, such as are found in olive oil, are healthy. But polyunsaturated fats, such as are found in vegetable and seed oils, are coming under increasing scrutiny. Soy bean oil and corn oil are the most widely used, accounting for over 90% of food oils used in the U.S.
Unfortunately, polyunsaturated fats are not particularly stable. They become damaged or oxidized very easily. Oxidized or rancid fats play a very troubling role. Feed rancid fats to lab rats and they will develop atherosclerosis. In another study, rabbits fed atherogenic diets containing various seed and grain oils showed the largest increase in oxidative susceptibility of LDL. In a study involving rabbits fed heated soybean oil, “grossly induced atherosclerosis and marked liver damage were histological and clinically demonstrated,” as per Wikipedia.
Rancid fats and oils taste and smell very bad even in small amounts and people avoid eating them. But, in the United States, the majority of oils consumed are refined, bleached, deodorized and degummed by manufacturers. The resultant oils are colorless, odorless, tasteless, and have a longer shelf life than their unrefined counterparts. This extensive processing makes fully oxidized, rancid oils much more elusive to detection via human senses.
To properly protect polyunsaturated fats (vegetable and seed oils) from oxidation, it is best to keep them cool and in a dark and oxygen free environment. And don’t overheat or use them repeatedly, such as in deep fat frying. I keep my Omega-3 fish oil capsules and Flax Oil (very high in Omega-3s) in the refrigerator. I also keep Safflower Oil, another polyunsaturated fatty acid (PUFA), which I use with olive oil and coconut oil to make mayonnaise, in the refrigerator.
So, if atherosclerosis is defined by Wikipedia as “a chronic inflammatory response in the walls of arteries, promoted by LDL…without adequate removal of fats and cholesterol…by…HDL,” then we should be concerned about the quality and quantity of LDL in our arteries – lest it become oxidized LDL. Likewise, we should be concerned if our circulating HDL in not high enough to transport any oxidized-LDL back to the liver the way it is supposed to.
Why do these two conditions (high LDL and low HDL) co-exist in so many of us today? It’s the diet of course. To avoid oxidized LDL, we can begin by eating far fewer polyunsaturated fats, especially ones that are hydrogenated, oxidized, or overheated. We can also take supplementary Omega-3s to help us regain a better Omega 6/Omega 3 balance. Then, we can significantly raise our HDL so they can do their job. See The Nutrition Debate #34 for “Foods that Raise HDL.”
The oxidized-LDL hypothesis posits that, “Once inside the vessel wall, LDL molecules become susceptible to oxidation by free radicals and become toxic to the cells.” (See The Nutrition Debate #48) Free radicals cause the oxidative stress that “triggers a cascade of immune responses which over time can produce an atheroma, the characteristic nodule in the artery wall that is the start of atherosclerosis. “Free Radicals and Oxidative Stress” is the subject of the next column.
© Dan Brown 4/21/12