The research over four decades concerning coconut oil in the diet and heart disease is quite clear: coconut oil has been shown to be beneficial. This research leads us to ask the question, "should coconut oil be used to both prevent and treat coronary heart disease?"
This statement is based on several reviews of the scientific literature concerning the feeding of coconut oil to humans. Blackburn et al (1988) have reviewed the published literature of "coconut oil's effect on serum cholesterol and atherogenesis" and have concluded that when "...[coconut oil is] fed physiologically with other fats or adequately supplemented with linoleic acid, coconut oil is a neutral fat in terms of atherogenicity."
After reviewing this same literature, Kurup and Rajmohan (1995) conducted a study on 64 volunteers and found "...no statistically significant alteration in the serum total cholesterol, HDL cholesterol, LDL cholesterol, HDL cholesterol/total cholesterol ratio and LDL cholesterol/HDL cholesterol ratio of triglycerides from the baseline values..." A beneficial effect of adding the coconut kernel to the diet was noted by these researchers.
Kaunitz and Dayrit (1992) have reviewed some of the epidemiological and experimental data regarding coconut-eating groups and noted that the "available population studies show that dietary coconut oil does not lead to high serum cholesterol nor to high coronary heart disease mortality or morbidity." They noted that in 1989 Mendis et al reported undesirable lipid changes when young adult Sri Lankan males were changed from their normal diets by the substitution of corn oil for their customary coconut oil. Although the total serum cholesterol decreased 18.7% from 179.6 to 146.0 mg/dl and the LDL cholesterol decreased 23.8% from 131.6 to 100.3 mg/dl, the HDL cholesterol decreased 41.4% from 43.4 to 25.4 mg/dl (putting the HDL values very much below the acceptable lower limit of 35 mg/dl) and the LDL/HDL ratio increased 30% from 3.0 to 3.9. These latter two changes are considered quite undesirable. Mendis and Kumarasunderam (1990) also compared the effect of coconut oil and soy oil in normolipidemic young males, and again the coconut oil resulted in an increase in the HDL cholesterol, whereas the soy oil reduced this desirable lipoprotein. As noted above, Kurup and Rajmohan (1995), who studied the addition of coconut oil alone to previously mixed fat diets, had reported no significant difference from baseline.
Previously, Prior et al (1981) had shown that islanders with high intakes of coconut oil showed "no evidence of the high saturated fat intake having a harmful effect in these populations." When these groups migrated to New Zealand, however, and lowered their intake of coconut oil, their total cholesterol and LDL cholesterol increased, and their HDL cholesterol decreased. Statements that any saturated fat is a dietary problem is not supported by evidence (Enig 1993).
Studies that allegedly showed a "hypercholesterolemic" effect of coconut oil feeding, usually only showed that coconut oil was not as effective at lowering the serum cholesterol as was the more unsaturated fat to which coconut oil was being compared. This appears to be in part because coconut oil does not "drive" cholesterol into the tissues as does the more polyunsaturated fats. The chemical analysis of the atheroma shows that the fatty acids from the cholesterol esters are 74% unsaturated (41% of the total fatty acids is polyunsaturated) and only 24% are saturated. None of the saturated fatty acids were reported to be lauric acid or myristic acid (Felton et al 1994).
There is another aspect to the coronary heart disease picture. This is related to the initiation of the atheromas that are reported to be blocking arteries. Recent research shows that there is a causative role for the herpes virus and cytomegalovirus in the initial formation of atherosclerotic plaques and the reclogging of arteries after angioplasty. (New York Times 1991) What is so interesting is that the herpes virus and cytomegalovirus are both inhibited by the antimicrobial lipid monolaurin, but monolaurin is not formed in the body unless there is a source of lauric acid in the diet. Thus, ironically enough, one could consider the recommendations to avoid coconut and other lauric oils as contributing to the increased incidence of coronary heart disease.
Chlamydia pneumoniae, a gram-negative bacteria, is another of the microorganisms suspected of playing a role in atherosclerosis by provoking an inflammatory process that would result in the oxidation of lipoproteins with induction of cytokines and production of proteolystic enzymes, a typical phenomena in atherosclerosis (Saikku 1997). Some of the pathogenic gram-negative bacteria with an appropriate chelator have been reported to be inactivated or killed by lauric acid and monolaurin as well as capric acid and monocaprin (See above, Bergsson et al 1997 and Thormar et al 1999).
However, the microorganisms most frequently identified as probable causative infecting agents are in the herpes virus family and include cytomegalovirus, type 2 herpes simplex (HSV-2), and Coxsackie B4 virus. The evidence for a causative role for cytomegalovirus is the strongest (Ellis 1997, Visseren et al 1997, Zhou et al 1996, Melnick et al 1996, Epstein et al 1996, Chen & Yang 1995), but a role for HSV-2 is also shown (Raza-Ahmad et al 1995). All members of the herpes virus family are reported to be killed by the fatty acids and monoglycerides from saturated fatty acids ranging from C-6 to C-14 (Isaacs et al 1991), which include approximately 80% of the fatty acids in coconut oil.
In spite of what has been said over the past four or more decades about the culpability of the saturated fatty acids in heart disease, they are ultimately going to be held blameless. More and more research is showing the problem to be related to oxidized products. One protection man has against oxidized products is the naturally saturated fats such as coconut oil.