THE ANATOMY OF COCONUT OIL
Beliefs about the value of coconut oil cross the whole spectrum of possibility. Some call it a health villain and indeed coconut oil is strictly prohibited in many heart-healthy hospital-administered diets. Others call it a fountain of youth because of its MCFA (medium chain fatty acid) components with claimed benefits in fighting cancer; battling viruses and bacteria including HIV; reducing diabetes, heart disease, kidney disease, digestive problems, insomnia and osteoporosis; and promoting weight loss. Most of these claims are not backed by solid scientific evidence. They originate from personal accounts; small, often uncontrolled animal studies or human studies that feed one component of coconut oil rather than the whole food (1). However the effect of coconut oil on cardiovascular health has been closely scrutinized and its effects on weight loss, diabetes, Alzheimer’s Disease and the immune system have also been delved into.
It has been known since the 1950s, when the first study came out showing that substituting coconut oil with soybean oil resulted in a 25% drop in blood cholesterol level, that coconut oil is one of the most potent substances for elevating cholesterol in the blood (2). Coconut oil causes a larger increase in total blood cholesterol level than beef fat (4) although it creates somewhat less of an increase compared with butter (5). This cholesterol augmenting effect happens quickly, within six hours of eating the coconut oil (3). A meal high in coconut oil or even coconut milk also impairs the anti-inflammatory action of HDL and reduces the amount of blood flow through the arteries (impairs endothelial function) at 3 hours and 6 hours after eating the meal (8,9). A randomized crossover study completed in 2017 looked at the impact of adding two tablespoons of virgin coconut oil to the daily diet and found that, compared to safflower oil, coconut oil caused a 14% higher rise in blood cholesterol levels, an effect that occurred within one month (6). A review of studies on coconut oil, including twenty-one pertinent research papers, shows that coconut oil generally raises both total cholesterol and LDL cholesterol significantly more than does unsaturated plant oil (7).
This first article on coconut oil is all about what coconut oil is made of because this is helpful in understanding the effects of this oil on human beings. If you are not interested in the “anatomy” of coconut oil, feel free to skip right over to part two for a review of coconut oil’s place in a healthy diet.
MEDIUM CHAIN FATTY ACIDS (MCFAs)
LONG CHAIN FATTY ACIDS (LCFAs)
A quick chemistry primer: Saturated fatty acids form straight chains, allowing them to pack together very tightly for efficient energy storage. Fatty acids are categorized by the number of carbon atoms in their chain and the number of double bonds between the carbon atoms. Saturated fatty acids do not have any double bonds. So when you see a symbol such as 10:0, this means that this fatty acid has ten carbon atoms in its chain with no double bonds. Medium chain fatty acids are generally considered to be those with carbon chains of between seven and ten or twelve atoms (7,11). Scientific research on medium-chain fatty acids focuses mainly on 8:0 and 10:0 fatty acids (7). Lauric acid, one important component of coconut oil, has twelve carbon atoms in its chain and can be classified as either a medium-chain or long-chain fatty acid. It behaves more like a long-chain fatty acid because it must be broken up and absorbed with chylomicrons while 95% of true medium-chain fatty acids are absorbed completely and directly into the portal vein which then feeds them into the liver where they are quickly oxidized into energy. Medium-chain fatty acids are more soluble than long-chain fatty acids which also hastens their absorption. Research has found that higher dietary intake of longer chain fatty acids, including 12:0, 14:0, 16:0 and 18:0 is associated with increased risk of coronary heart disease, whereas intake of shorter chain 4:0 to 10:0 fatty acids is not (12).
Let’s look at the type of fats that make up coconut oil. Coconut oil is 99% fat with about 90% of that fat being the saturated type. Half of the saturated fat in coconut oil is in the form of MCFAs (medium chain fatty acids) while the other half is LCFAs (long chain fatty acids), the same fats found in red meat, chicken and pork. (Some cold-pressed virgin coconut oils may have a slightly higher percentage of MCFAs). Even if you don’t include the theoretically beneficial MCFAs (which we’ll discuss in Part Two) you’re still left with an oil containing 44% LCFAs making it higher in cholesterol-raising saturated fat than lard which contains 43% LCFAs.
The MCFAs and their relative concentrations found in coconut oil are 8% caprylic acid (8:0) and 7% capric acid 10:0.
Lauric acid (12:0) is present at a level of 48% and lands somewhere between MCFAs and LCFAs.
LCFAs in coconut oil are 16% myristic acid (14:0), 9% palmitic acid (16:0) and 2% stearic acid (18:0).
Unsaturated fatty acids in coconut oil are 7% oleic acid (18:1 n-9) and 2% linoleic acid (18:2 – n-6) with 1% being other types of fatty acids (10,14).
The fatty acids in coconut oil that are known to raise LDL-cholesterol levels are lauric acid, myristic acid and palmitic acid. Lauric acid also raises HDL (“good” cholesterol), enough that the ratio of total to HDL cholesterol remains in the favourable range. Myristic and palmitic acid do not raise HDL.
Stearic acid has a neutral effect on blood cholesterol levels, perhaps because it is converted to oleic acid, an 18-carbon monounsaturated fat, by the liver (13). For this reason people are often advised that the stearic acid in foods such as coconut oil or beef can be disregarded as a threat to health. However, cholesterol is not the only marker for heart disease and stearic acid shows other adverse effects. One study found that stearic acid increases the risk for coronary artery disease more than lauric, myristic and palmitic acid, both by lowering HDL and by increasing levels of Lp(a) (lipoprotein a), another important marker for the risk of developing heart disease. Current medical thinking is that stearic acid should not be separated from other saturated fatty acids when it comes to dietary advice (12).
Now that you have some familiarity with the “anatomy” of coconut oil, you’ll be all set for Part Two of this article which discusses the effects of coconut oil on health.
1 Lockyer, S., Stanner, S. Facts Behind the Headlines: Coconut oil – a nutty idea? Nutrition Bulletin – British Nutrition Foundation February 2016; 41 (1): 42-54.
2 Wright I.S. Editorial: Cardiovascular diseases-guidelines for prevention and care resources. Circulation. 1974 Mar; 49(3):387-9.
3 Myhrstad, M.C., Narverud, I., Telle-Hansen, V.H., Karhu, T. et al. Effect of the fat composition of a single high-fat meal on inflammatory markers in healthy young women. Br J Nutr. 2011 Dec; 106(12):1826-1835.
4 Reiser, R., Probstfield, J.L., Silvers, A., Scott, L.W., Shorney, M.L. et al. Plasma lipid and lipoprotein response of humans to beef fat, coconut oil and safflower oil. Am J Clin Nutr. 1985 Aug; 42(2):190-197.
5 Cox, C., Sutherland, W., Mann, J., de Jong, S., Chisholm ,A., Skeaff, M. Effects of dietary coconut oil, butter and safflower oil on plasma lipids, lipoproteins and lathosterol levels. Eur J Clin Nutr. 1998 Sep; 52(9):650-654.
6 Harris, M., Hutchins, A., Fryda, L. The Impact of Virgin Coconut Oil and High-Oleic Safflower Oil on Body Composition, Lipids, and Inflammatory Markers in Postmenopausal Women. J Med Food. 2017 Apr; 20(4):345-351.
7 Eyres, L., Eyres, M.F., Chisholm, A., Brown, R.C. Coconut oil consumption and cardiovascular risk factors in humans. Nutr Rev. 2016 Apr; 74(4):267-280.
8 Nicholls, S.J., Lundman, P., Harmer, J.A., Cutri, B., Griffiths, K.A., Rye, K.A., Barter, P.J., Celermajer, D.S. Consumption of saturated fat impairs the anti-inflammatory properties of high-density lipoproteins and endothelial function. J Am Coll Cardiol. 2006 Aug 15; 48(4):715-720.
9 Ng, C.K., Chan, A.P., Cheng, A. Impairment of endothelial function–a possible mechanism for atherosclerosis of a high-fat meal intake. Ann Acad Med Singapore. 2001 Sep; 30(5):499-502.
10 Gunstone, F.D. (Author); Fatty acid and lipid chemistry. London: Blackie Academic and Professional, 1996.
11 Schönfeld, P., Wojtczak, L. Short- and medium-chain fatty acids in energy metabolism: the cellular perspective. The Journal of Lipid Research June 2016; 57: 943-954.
12 Hu, F.B., Stampfer, M.J., Manson, J.E., et al. Dietary saturated fats and their food sources in relation to the risk of coronary heart disease in women. Am J Clin Nutr. 1999; 70: 1001–1008.
13 Mensink, R.P., Zock, P.L., Kester, A.D., Katan, M.B. Effects of dietary fatty acids and carbohydrates on the ratio of serum total to HDL cholesterol and on serum lipids and apolipoproteins: a meta-analysis of 60 controlled trials. Am J Clin Nutr. 2003 May; 77(5) :1146-1155.
14 Gunstone, F.D. (Author); Fatty acid and lipid chemistry. London: Blackie Academic and Professional, 1996.
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