Coronary artery disease (CAD) is a condition in which the blood supply to the heart muscle is partially or completely blocked. The most deadly presentation of CAD is acute myocardial infarction (AMI), where heart muscle cells are dead. Atherosclerosis is characterized by accumulation of lipids and cholesterol within the inside covering of the vessel wall, along with a component of vascular inflammation.   

Increased risk for CAD is attributed to elevated levels of serum cholesterol, which in turn is due to increased intake of saturated fats. However, a fear complex has been created among the general public that consumption of coconut oil results in elevated cholesterol levels. This “myth” is primarily due to equating coconut oil with saturated fat; without knowing that saturated fat in coconut oil are of the short chain and medium chain fatty acids.  Fats that cause heart disease are saturated fats with long chain fatty acids. Nearly 50 % of the fat in coconut oil is Lauric acid (medium chain fatty acid). These medium chain fatty acids directly enter into the cells and are metabolized immediately. On the other hand, long-chain fatty acids (of other oils) require the help of lipoproteins, which are eventually deposited into various organs, including heart vessels.  

People in Kerala State in India were using coconut oil from time immemorial. However, due to the attack against coconut oil in general press, the per capita coconut oil consumption has been reduced to 1/3 during the last 50 years. However, during the same period, the rate of heart attack has been increased to 3 times in the same population. This alone will be sufficient to show that coconut oil has nothing to do with heart attacks.   

We have conducted a large scale study at Kochi, India. Serum samples were analysed from 302 normal healthy persons, out of which 152 were consuming coconut oil and 150 were using sunflower oil for the past 2 years or more. There were no statistically significant differences in the cholesterol, HDL or LDL levels in coconut oil consuming population versus sunflower oil consuming population. Further, lipid profile in serum was analysed in 76 coronary artery disease patients, out of which 41 were used to take coconut oil and 35 were used to take sunflower oil atleast for the past 2 years. There were no differences in cholesterol levels in these two groups. Thus plasma fatty acid composition reflected no changes with dietary fat source.

Our own studies on animals at Kochi, India showed that coconut oil intake did not cause hypercholesterolemia or oxidative stress in rats. There are many animal and human studies in world literature to disprove allegations about coconut oil enhancing the risk of a CAD.  At the same time, there is not even one paper in the whole literature, directly showing that coconut oil increases cardiac diseases.  Studies that were wrongly interpreted as hyper- cholesterolemic effect of coconut oil feeding, in fact, have only shown that coconut oil was not as effective at lowering the serum cholesterol as compared with the unsaturated fat. Without any evidence, the wrong publicity is still going on to spoil the name of coconut oil. 

Further, at Amrita Institute of Medical Sciences, Kochi, India, we have analysed the fatty acid composition of the plaques taken from diseased arteries. A total of 71 samples of plaques were analysed, of which 48 persons were using coconut oil and 23 persons were using sunflower oil routinely. Plaques did not contain significant amounts of Lauric acid or Myristic acid (fatty acids from coconut oil). Instead, palmitic acid and stearic acid (long chain saturated fatty acids) were the main ingredients of these plaques. Fatty acid content of plaques from coconut oil consuming group and sunflower consuming group were the same.  This clearly shows that coconut oil does not have any action on plaque formation or heart disease.