How Does Coconut Oil Affect Cholesterol Levels?

How Does Coconut Oil Affect Cholesterol Levels?
Population Studies
Coconut oil (and all saturated fats) has been blamed for many years as a cause of bad cholesterol levels, which supposedly leads to heart disease. But studies done on traditional tropical populations that consume large amounts of coconut oil show just the opposite. One of the best ways to study the affects of coconut oil on human nutrition is to look at tropical populations that get most of their caloric intake from the saturated fat of coconut oil. Logic would dictate that if the saturated fat/cholesterol theory of heart disease and obesity were correct, those populations with the highest consumption of saturated fats would be the most overweight and have the highest rates of heart disease. Such is not the case.
In a study published in 1981, the populations of two South Pacific islands were examined over a period of time starting in the 1960s, before western foods were prevalent in the diets of either culture. The study was designed to investigate the relative effects of saturated fat and dietary cholesterol in determining serum cholesterol levels. Coconuts were practically a staple in the diets, with up to 60% of their caloric intake coming from the saturated fat of coconut oil. The study found very healthy people who were relatively free from the modern diseases of western cultures, including obesity and heart disease. Their conclusion: "Vascular disease is uncommon in both populations and there is no evidence of the high saturated fat intake having a harmful effect in these populations."1
Another study was done on the Indian subcontinent comparing traditional cooking oils with modern oils in relation to prevalence of atherosclerotic heart disease and Type-II diabetes. Their conclusion: "In contrast to earlier epidemiologic studies showing a low prevalence of atherosclerotic heart disease (HAD) and Type-II dependent diabetes mellitus (Type-II DM) in the Indian subcontinent, over the recent years, there has been an alarming increase in the prevalence of these diseases in Indians--both abroad and at home, attributable to increased dietary fat intake. Replacing the traditional cooking fats condemned to be atherogenic, with refined vegetable oils promoted as 'heart-friendly' because of their polyunsaturated fatty acid (PUFA) content, unfortunately, has not been able to curtail this trend. Current data on dietary fats indicate that it is not just the presence of PUFA, but the type of PUFA that is important--a high PUFA n-6 content and high n-6/n-3 ratio in dietary fats being atherogenic and diabetogenic. The newer 'heart-friendly' oils like sunflower or safflower oils possess this undesirable PUFA content and there are numerous research data now available to indicate that the sole use or excess intake of these newer vegetable oils are actually detrimental to health and switching to a combination of different types of fats, including the traditional cooking fats like ghee, coconut oil and mustard oil, would actually reduce the risk of dyslipidaemias, HAD and Type-II DM."2 So according to this study, atherosclerotic heart disease in India INCREASED when people switched from their traditional fats like coconut oil and ghee, saturated fats, and replaced them using polyunsaturated fats like sunflower and safflower oils.
When measurements of serum cholesterol (cholesterol levels in the blood) were first done, only the total of both HDL ("good cholesterol") and LDL ("bad cholesterol") were read. Now that testing has become more sophisticated, researchers look more at the balance of these two types of cholesterol. They note whether a substance raises cholesterol levels of HDL or LDL levels. In some cases, certain foods lower total cholesterol, but only by lowering good HDL cholesterol while at the same time actually raising levels of the bad LDL cholesterol. Studies now show that coconut oil often actually increases the good HDL cholesterol, while lowering LDL. So total cholesterol levels may actually increase, but in a very favorable ratio.
Faulty Science
In a lecture given in Viet Nam in 1996, Dr. Mary Enig stated that “The problems for coconut oil started four decades ago when researchers fed animals hydrogenated coconut oil that was purposely altered to make it completely devoid of any essential fatty acids. The animals fed the hydrogenated coconut oil (as the only fat source) naturally became essential fatty acid deficient; their serum cholesterol increased. Diets that cause an essential fatty acid deficiency always produce an increase in serum cholesterol levels as well as in increase in the atherosclerotic indices. The same effect has also been seen when other highly hydrogenated oils such as cottonseed, soybean or corn oils have been fed; so it is clearly a function of the hydrogenated products, either because the oil is essential fatty acid (EFA) deficient or because of transfatty acids.”3
What about studies where animals were fed unprocessed coconut oil? Enig wrote: "Hostmark et al (1980) compared the effects of diets containing 10% coconut oil and 10% sunflower oil on lipoprotein distribution in male Wistar rats. Coconut oil feeding produced significantly lower levels (p=0.05) of pre-beta lipoproteins (VLDL) and significantly higher (p=<0.01) alpha-lipoproteins (HDL) relative to sunflower feeding.”4 She also cited a study by Awad (1981) on Wistar rats fed a diet of either 14% (natural) coconut oil or 14% safflower oil. She stated: “Total tissue cholesterol accumulation for animals on the safflower diet was six times greater than for animals fed the [unhydrogenated] coconut oil. A conclusion that can be drawn from some of the animal research is that feeding hydrogenated coconut oil devoid of essential fatty acids (EFA) potentate the formation of atherosclerosis markers. It is of note that animals fed regular coconut oil have less cholesterol deposited in their livers and other parts of their bodies.”5
Do Saturated Fats Clog Arteries?
Saturated fats are probably the most maligned fats in the popular media today. They are often blamed for "clogging arteries" and leading to heart disease. However, an examination of the research and science behind saturated fats leads one to a vastly different conclusion, suggesting that the attacks against saturated fats have been primarily political and economical, and not scientific. While we will provide a brief summary of the science behind saturated fats here, we encourage you to examine the research more closely yourself. Much of it is documented at www.coconutoil.com.
First of all, saturated fats are essential to our health. They comprise about 50% of our cell membranes, and some proportion of saturated fats are found in all fats and oils, whether plant based or animal based.
In recent years some have made claims that too much saturated fats in our diet can lead to higher cholesterol levels and clogged arteries, which leads to heart disease. So an anti-saturated fat campaign was launched in the U.S. in recent years. As a results, Americans have consumed less saturated fats than any other nation, yet the U.S. is still a world leader in deaths from heart disease. Obesity rates are also at an all-time high. Many are now questioning the "wisdom" behind the low-fat nutritional advice that has dominated the popular media (see Gary Taubes article "The Soft Science of Dietary Fat.")
Does research support the claim that saturated fats like coconut oil raise cholesterol levels and clog arteries? This "lipid theory" of heart disease, which blames high cholesterol levels as causing heart disease, is seriously being questioned by researchers and doctors. Malcom Kendrick M.D., Dr. Mary Enig Ph.D., Uffe Ravnskov M.D., Ph.D (author of The Cholesterol Myths), George Mann M.D., Sc.D, and many other top researchers have written extensively on the flaws of the “cholesterol theory” of heart disease. You can read more about the cholesterol issue at www.coconutoil.com
As to the research on "clogged arteries", a study was done at the Wynn Institute for Metabolic Research, London, examining the composition of human aortic plaques. This study found that the "artery clogging fats" in those who died from heart disease were composed of 26% saturated fat: the rest (74%) were polyunsaturated fatty acids, such as those found in vegetable oils commonly consumed in today's modern societies. Their conclusion: "No associations were found with saturated fatty acids. These findings imply a direct influence of dietary polyunsaturated fatty acids on aortic plaque formation and suggest that current trends favoring increased intake of polyunsaturated fatty acids should be reconsidered."6
Virgin Better than Refined Coconut Oil
A recent study done in India comparing refined coconut oil (CO) with Virgin Coconut Oil (VCNO) found that VCNO obtained by wet process has a beneficial effect in lowering lipid components compared to CO. It reduced total cholesterol, triglycerides, phospholipids, LDL, and VLDL cholesterol levels and increased HDL cholesterol in serum and tissues. The results demonstrated the potential beneficiary effect of virgin coconut oil in lowering lipid levels in serum and tissues and LDL oxidation by physiological oxidants. This property of VCNO may be attributed to the biologically active polyphenol components present in the oil.
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References
1. Prior IA, Davidson F, et. al. "Cholesterol, coconuts, and diet on Polynesian atolls: a natural experiment: the Pukapuka and Tokelau island studies." American Journal of Clinical Nutrition. 1981 Aug;34(8):1552-61.
2. Sircar S, Kansra U. "Choice of cooking oils--myths and realities." Journal Indian Medical Association. 1998 Oct;96(10):304-7.
3. Mary G. Enig, Ph.D. “Health and Nutritional Benefits from Coconut Oil: An Important Functional Food for the 21st Century” Presented at the AVOC Lauric Oils Symposium, Ho Chi Min City, Vietnam, 25 April 1996
4. Mary G. Enig, Ph.D
5. Mary G. Enig, Ph.D
6. Felton CV, Crook D, Davies MJ, Oliver MF. Wynn Institute for Metabolic Research, London, UK. “Dietary polyunsaturated fatty acids and composition of human aortic plaques.” .Lancet. Oct,1994; 29;344(8931):1195-6.