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.
The Latest On the Trans Fatty Acids
Both the United States and Canada will soon require labeling of the trans fatty acids, which will put coconut oil in a more competitive position than it has been in the past decade. A fear of the vegetable oil manufacturers has always been that they would have to label trans fatty acids. The producers of trans fatty acids have relied on the anti-saturated fat crusade to protect their markets. However, the latest research on saturated fatty acids and trans fatty acids shows the saturated fatty acids coming out ahead in the health race.
It has taken this last decade, from 1988 to 1998, to see changes in perception. During this period, the trans fatty acids have taken a deserved drubbing. Research reports from Europe have been emerging since the seminal report by Mensink and Katan in 1990 that the trans fatty acids raised the low density lipoprotein (LDL) cholesterol and lowered the high density lipoprotein (HDL) cholesterol in serum. This has been confirmed by studies in the U.S. (Judd et al 1994, Khosla and Hayes 1996, Clevidence 1997).
In 1990, the lipids research group at the University of Maryland published a paper (Enig et al 1990) correcting some of the erroneous data sponsored by the food industry in the 1985 review by the Life Sciences Research Office of Federation of American Societies for Experimental Biology (LSRO-FASEB) (Senti 1985) of the trans fatty acids.
Also, in 1993, a group of researchers at Harvard University, led by Professor Walter Willett, reported a positive relationship between the dietary intake of the trans fatty acids and coronary heart disease in a greater than 80,000 cohort of nurses who had been followed by the School of Public Health at Harvard University for more than a decade.
Pietinen and colleagues (1997) evaluated the findings from the large cohort of Finnish men who were being studied for a cancer prevention study. After controlling for the appropriate variables including several coronary risk factors, the authors observed a significant positive association between the intake of trans fatty acids and the risk of death from coronary disease.
There was no association between intakes of saturated fatty acids, or dietary cholesterol and the risk of coronary deaths.
This is another example of the differences between the effects of the trans fatty acids and the saturated fatty acids and further challenge to the dietary cholesterol hypothesis.
The issue of the trans fatty acids as a causative factor in remains underexplored, but recent reports have found a connection. Bakker and colleagues (1997) studied the data for the association between breast-cancer incidence and linoleic acid status across European countries since animal and ecological studies had suggest a relationship.
They found that the mean fatty acid composition of adipose did not show an association with omega-6 linoleic acid and breast, colon or prostate cancer. However, cancers of the breast and colon were positively associated with the trans fatty acids. Kohlmeier and colleagues (1997) also reported that data from the EURAMIC study showed adipose tissue concentration of trans fatty acids having a positive association with postmenopausal breast cancer in European women.
In 1995 a British documentary on the trans fatty acids aired on a major television station in the U.K. This documentary included an expose of the battle between the edible oil industry and some of the major researchers of the trans fatty acids. Just this year, this same documentary has been aired on television in France where it was requested by a major television station.
Several of the early researchers into the trans problems, Professor Fred Kummerow and Dr. George Mann, have continued their research and/or writing (Mann 1994). The popular media has continued to press the issue of the amounts of trans in the foods, for which there are still no comprehensive government data bases, and a recent published paper from a U.S. Department of Agriculture researcher states:
"Because trans fatty acids have no known health benefits and strong presumptive evidence suggests that they contribute markedly to the risk of developing CHD, the results published to date suggest that it would be prudent to lower the intake of trans fatty acids in the U.S. diet."(Nelson 1998).
Professor Meir Stampfer from Harvard University refers to trans fats as "one of the major nutritional issues of the nation," contending that "they have a large impact" and "...we should completely eliminate hydrogenated fats from the diet" (Gottesman 1998).
Lowering the trans fatty acids in the foods in the U.S. can only be done by returning to the use of the natural unhydrogenated and more saturated fats and oils.
Predictions can be made regarding the future of the trans fatty acids. Our ability to predict has been pretty good; for example when Enig Associates started producing the marketing newsletter Market Insights written by Eric Enig, we predicted that trans fatty acids would eventually be swept out of the market. It appears that this prediction may be close to coming true.
Also in the early 1990s, Market Insights predicted that CSPI would change its mind about the trans fatty acids, which it had spent years defending. CSPI did change its mind, and in fact went on the attack regarding the trans, but CSPI never admitted that it had originally been promoting the trans or that the high levels of trans found in the fried foods in the fast food and other restaurants and in many other foods are directly due to CSPI lobbying.
While its change was welcome, CSPI's revisionist version of its own history of support of partially hydrogenated oils and trans fatty acids would have fit perfectly into George Orwell's "1984"
Comparison Of Saturated Fats With The Trans Fats
The statement that trans fatty acids are like saturated fatty acids is not correct for biological systems. A listing of the biological effects of saturated fatty acids in the diet versus the biological effects of trans fatty acids in the diet is in actuality a listing of the good (saturated) versus the bad (trans).
When one compares the saturated fatty acids and the trans fatty acids, we see that:
|saturated fatty acids raise HDL cholesterol, the so-called good cholesterol, whereas the trans fatty acids lower HDL cholesterol (Mensink and Katan 1990, Judd et al 1994);|
|saturated fatty acids lower the blood levels of the atherogenic lipoprotein |
|saturated fatty acids conserve the elongated omega-3 fatty acids (Gerster 1998), whereas trans fatty acids cause the tissues to lose these omega-3 fatty acids (Sugano and Ikeda 1996);|
|saturated fatty acids do not inhibit insulin binding, whereas trans fatty acids do inhibit insulin binding;|
|saturated fatty acids are the normal fatty acids made by the body, and they do not interfere with enzyme functions such as the delta-6-desaturase, whereas trans fatty acids are not made by the body, and they interfere with many enzyme functions such as delta-6-desaturase;|
|some saturated fatty acids are used by the body to fight viruses, bacteria, and protozoa, and they support the immune system, whereas trans fatty acids interfere with the function of the immune system.|
What About The Unsaturated Fats?
The arteries of the heart are also compromised by the unsaturated fatty acids. When the fatty acid composition of the plaques (atheromas) in the arteries has been analyzed, the level of saturated fatty acids in the cholesterol esters is only 26 percent compared to that in the unsaturated fatty acids, which is 74 percent.
When the unsaturated fatty acids in the cholesterol esters in these plaques are analyzed, it is shown that 38 percent are polyunsaturated and 36 percent are monounsaturated. Clearly the problem is not with the saturated fatty acids.
As an aside, you need to understand that the major role of cholesterol in heart disease and in cancer is as the body's repair substance, and that cholesterol is a major support molecule for the immune system, an important antioxidant, and a necessary component of neurotransmitter receptors. Our brains do not work very well without adequate cholesterol. It should be apparent to scientists that the current approach to cholesterol has been wrong.
The pathway to cholesterol synthesis starts with a molecule of acetyl CoA that comes from the metabolism of excess protein forming ketogenic amino acids and from the metabolism of excess carbohydrate, as well as from the oxidation of excess fatty acids.
Grundy in 1978 reported that the degree of saturation of the fat in the diet did not affect the rate of synthesis of cholesterol. Research reported in 1997 (Jones 1997), however, showed that the polyunsaturated fatty acids in the diet increase the rate of cholesterol synthesis relative to other fatty acids. Furthermore, research reported in 1993 (Hodgsons et al 1993) had shown that dietary intake of the omega-6 polyunsaturated fatty acid linoleic acid was positively related to coronary artery disease.
Thus, those statements made by the consumer activists in the United States to the effect that the saturated fatty acids increase cholesterol synthesis is without any foundation.
What happens when there is an increase or a decrease of cholesterol in the serum is more like a shift from one compartment to another as the body tries to rectify the potential damage from the excess polyunsaturated fatty acids. Research by Dr. Hans Kaunitz reported in 1978 clearly showed the potential problems with excess polyunsaturated fatty acids.