by Mary G. Enig, Ph.D., F.A.C.N.
Research Showing Beneficial Effects Of Eating The More Saturated Fats
One major concern expressed by the nutrition community is related to whether or not people are getting enough elongated omega-3 fatty acids in their diets. The elongated omega-3 fatty acids of concern are eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA).
Some research has shown that (the basic omega-3 fatty acid) -linolenic acid is not readily converted to the elongated forms in humans or animals, especially when there is ingestion of the trans fatty acids and the consequent inhibition of the delta-6-desaturase enzyme.
One recent study (Gerster 1998), which used radioisotope-labeled -linolenic acid to measure this conversion in adult humans, showed that if the background fat in the diet was high in saturated fat, the conversion was approximately 6% for EPA and 3.8% for DHA, whereas if the background fat in the diet was high in omega-6 polyunsaturated fatty acids (PUFA), the conversion was reduced 40-50%.
Nanji and colleagues (1995) report that a diet enriched in saturated but not unsaturated fatty acids reversed alcoholic liver injury in their animals, which was caused by dietary linoleic acid. These researchers conclude that this effect may be explained by the down-regulation of lipid peroxidation.
This is another example of the need for adequate saturated fat in the diet. Cha and Sachan (1994) studied the effects of saturated fatty acid and unsaturated fatty acid diets on ethanol pharmacokinetics. The hepatic enzyme alcohol dehydrogenase and plasma carnitines were also evaluated. The researchers concluded that dietary saturated fatty acids protect the liver from alcohol injury by retarding ethanol metabolism, and that carnitine may be involved.
Hargrove and colleagues (1999) noted the work of Nanji et al and postulated that they would find that diets rich in linoleic acid would also cause acute liver injury after acetaminophen injection. In the first experiment, two levels of fat (15 g/100 g protein and 20 g/100 g protein) were fed using corn oil or beef tallow.
Liver enzymes indicating damage were significantly elevated in all the animals except for those animals fed the higher level of beef tallow. These researchers concluded that "diets with high [linoleic acid] may promote acetaminophen-induced liver injury compared to diets with more saturated and monounsaturated fatty acids."
Research Showing General Beneficial Effects From Feeding Coconut Oil
Research that compares coconut oil feeding with other oils to answer a variety of biological questions is increasingly finding beneficial results from the coconut oil.
Obesity is a major health problem in the United States and the subject of much research. Several lines of research dealing with metabolic effects of high fat diets have been followed. One study used coconut oil to enrich a high fat diet and the results reported were that the "coconut-oil enriched diet is effective in...[producing]...a decrease in white fat stores." (Portillo et al 1998)
Cleary et al (1999) fed genetically obese animals high fat diets of either safflower oil or coconut oil. Safflower oil-fed animals had higher hepatic lipogenic enzyme activities than did coconut oil fed animals. When the number of fat cells were measured, the safflower oil-fed also had more fat cells than the coconut oil-fed.
Many of the feeding studies produce results at variance with the popular conception. High fat diets have been used to study the effects of different types of fatty acids on membrane phospholipid fatty acid profiles. When such a study was performed on mice, the phospholipid profiles were similar for diets high in linoleic acid from high-linoleate sunflower oil relative to diets high in saturated fatty acids from coconut oil.
However, those animals fed the diets high in oleic acid (from the high-oleate sunflower oil) or high in elongated omega-3 fatty acids (from menhaden oil) were not only different from the other two diets, but they also resulted in enlarged spleens in the animals. (Huang and Frische 1992)
Oliart-Ros and colleagues (1998), Instituto Technologico de Veracruz, Mexico, reported on effects of different dietary fats on sucrose-induced cardiovascular syndrome in rats. The most significant reduction in parameters of the syndrome was obtained by the n-3 PUFA-rich diet.
These researchers reported that the diet thought to be PUFA-deficient presented a tissue lipid pattern similar to the n-3 PUFA-rich diet (fish oil), which surprised and puzzeled them. When questioned, it turned out that the diet was not really PUFA-deficient, but rather just a normal coconut oil (nonhydrogenated), which conserved the elongated omega-3 and normalized the omega-6-to-omega-3 balance.
A recent study measured the effect of high-fat diets, fed for more than three months to the neonatal pig, on the HMG-CoA reductase enzyme's function and gave some surprises. There were two feeding protocols: one with the added cholesterol and one without added cholesterol, but both with coconut oil.
The hepatic reductase activity, which was the same in all groups at the beginning of the feeding on the third day and similar on the 42nd day, was increased with and without added cholesterol on the 13th day and then decreased on the 25th day.
The data was said to suggest that dietary cholesterol suppressed hepatic reductase activity in the young pigs regardless of their genetic background, that the stage of development was a dominant factor in its regulation, and that both dietary and endogenously synthesized cholesterol was used primarily for tissue building in very young pigs. (McWhinney et al 1996) The feeding of coconut oil did not in any way compromise the normal development of these animals.
When compared with feeding coconut oil, feeding two different soybean oils to young females caused a significant decrease in HDL cholesterol. Both soybean oils, one of which was extracted from a new mutant soybean thought to be more oxidatively stable, were not protective of the HDL levels (Lu Z et al 1997).
Trautwein et al (1997) studied cholesterol-fed hamsters on different oil supplements for plasma, hepatic, and biliary lipids. The dietary oils included butter, palm stearin, coconut oil, rapeseed oil, olive oil, and sunflowerseed oil.
Plasma cholesterol concentrations were higher (9.2 mmol/l) for olive oil than for coconut oil (8.5 mmol/l), hepatic cholesterol was highest in the olive oil group, and none of the diet groups differed for biliary lipids. Even in this cholesterol-sensitive animal model, coconut oil performed better than olive oil.
Smit and colleagues (1994) had also studied the effect of feeding coconut oil compared with feeding corn oil and olive oil in rats and measured the effect on biliary cholesterol. Bile flow was not different between the three diets, but the hepatic plasma membranes showed more cholesterol and less phospholipid from corn and olive oil feeding relative to coconut oil feeding.
Several studies (Kramer et al 1998) have pointed out problems with canola oil feeding in newborn piglets, which result in the reduction in number of platelets and the alteration in their size. There is concern for similar effects in human infants. These undesirable effects can be reversed when coconut oil or other saturated fat is added to the feeding regimen (Kramer et al 1998).
Research has shown that coconut oil is needed for good absorption of fat and calcium from infant formulas. The soy oil (47%) and palm olein (53%) formula gave 90.6% absorption of fat and 39% absorption of calcium, whereas the soy oil (60%) and coconut oil (40%) gave 95.2% absorption of fat and 48.4% absorption of calcium (Nelson et al 1996). Both fat and calcium are needed by the infant for proper growth. These results clearly show the folly of removing or lowering the coconut oil in infant formulas.
Research Showing A Role For Coconut In Enhancing Immunity And Modulating Metabolic Functions
Coconut oil appears to help the immune system response in a beneficial manner. Feeding coconut oil in the diet completely abolished the expected immune factor responses to endotoxin that were seen with corn oil feeding. This inhibitory effect on interleukin-1 production was interpreted by the authors of the study as being largely due to a reduced prostaglandin and leukotriene production (Wan and Grimble 1987).
However, the damping may be due to the fact that effects from high omega-6 oils tend to be normalized by coconut oil feeding. Another report from this group (Bibby and Grimble 1990) compared the effects of corn oil and coconut oil diets on tumor necrosis factor-alpha and endotoxin induction of the inflammatory prostaglandin E2 (PGE2) production.
The animals fed coconut oil did not produce an increase in PGE2, and the researchers again interpreted this as a modulatory effect that brought about a reduction of phospholipd arachidonic acid content. A study from the same research group (Tappia and Grimble 1994) showed that omega-6 oil enhanced inflammatory stimuli, but that coconut oil, along with fish oil and olive oil, suppressed the production of interleukin-1.
Several recent studies are showing additional helpful effects of consuming coconut oil on a regular basis, thus supplying the body with the lauric acid derivative monolaurin. Monolaurin and the ether analogue of monolaurin have been shown to have the potential for damping adverse reactions to toxic forms of glutamic acid (Dave et al 1997).
Lauric acid and capric acid have been reported to have very potent effects on insulin secretion (Garfinkel et al 1992). Using a model system of murine splenocytes, Witcher et al 1996 showed that monolaurin induced proliferation of T cells and inhibited the toxic shock syndrome toxin-1 mitogenic effects on T cells.
Monserrat and colleagues (1995) showed that a diet rich in coconut oil could protect animals against the renal necrosis and renal failure produced by a diet deficient in choline (a methyl donor group). The animals had less or no mortality and increased survival time as well as decreased incidence or severity of the renal lesions when 20% coconut oil was added to the deficient diet. A mixture of hydrogenated vegetable oil and corn oil did not show the same benefits.
The immune system is complex and has many feedback mechanism to protect it, but the wrong fat and oils can compromise these important mechanisms. The data from the several studies show the helpful effects of coconut fat. Additionally, there are anecdotal reports that consumption of coconut is beneficial for individuals with the chronic fatigue and immune dysfunction syndrome known as CFIDS.
U.S. Patents For Medical Uses Of Lauric Oils, Medium-Chain Fatty Acids, And Their Derivatives Such As Monolaurin
A number of patents have been granted in the United States for medical uses of lauric oils, lauric acid, and monolaurin. Although one earlier patent was granted to Professor Kabara more than three decades ago, the rest of these patents have been granted within the past decade.
In 1989 a patent was issued to the New England Deaconess Hospital (Bistrian et al 1989) for the invention titled "Kernel Oils and Disease Treatment." This treatment required lauric acid as the primary fatty acid source with lauric oils constituting up to 80% of the diet "using naturally occurring kernel oils."
In 1991 and 1995, two patents were issued to the group of researchers whose work has been reviewed above. The first invention (Isaacs et al 1991) was directed to antiviral and antibacterial activity of both fatty acids and monoglycerides, primarily against enveloped viruses.
The claims were for "a method of killing enveloped viruses in a host human...wherein the enveloped viruses are AIDS viruses...[or]...herpes viruses...[and the]...compounds selected from the group consisting of fatty acids having from 6 to 14 carbon atoms and monoglycerides of said fatty acids...[and]...wherein the fatty acids are saturated fatty acids."
The second patent (Isaacs et al 1995) was a further extension of the earlier one. This patent also included discussion of the inactivation of envelop viruses and specifically cited monoglycerides of caproic, caprylic, capric, lauric, and myristic acid. These fatty acids make up more than 80% of coconut oil. Also included in this patent was a listing of susceptible viruses and some bacteria and protozoa.
Although these latter patents may provide the owners of the patents with the ability to extract royalties from commercial manufacturers of monoglycerides and fatty acids, they cannot require royalties from the human gastrointestinal tract when it is the "factory" that is doing the manufacturing of the monoglycerides and fatty acids.
Clearly though, these patents serve to illustrate to us that the health-giving properties of monolaurin and lauric acid are well-recognized by some individuals in the research arena, and they lend credence to our appropriate choice of lauric oils for promoting health and as adjunct treatment of viral diseases.
How Can We Get Sufficient Coconut Fat Into The Food Supply In The U.S. And Other Countries That Need Its Benefits?
I would like to review for you my perception of the status regarding the coconut and coconut products market in the North American countries such as the United States and Canada at the end of the 20th century and the beginning of the 21st century.
Coconut products are trying to regain their former place in several small markets. The extraction of oil from fresh coconut has been reported in the past decade and my impression is that this is being considered as a desirable source of minimally processed oil, which produces an oil with desirable characteristics for the natural foods market.
There have been some niche markets for coconut products developing during the past half-decade. These are represented primarily by the natural foods and health foods producers. Some examples are the new coconut butters produced in the U.S. and Canada by Omega Nutrition and Carotec, Inc. And, this is no longer as small a market as it has been in past years.
Desiccated coconut products, coconut milk, and even coconut oil are appearing on the shelves of many of these markets. After years of packaging coconut oil for skin use only, one of the large suppliers of oils to the natural foods and health foods stores has introduced coconut oil for food use, and it has appeared within the last few months on shelves in the Washington, DC metropolitan area along with other oils. I believe I indirectly had something to do with this turn of events.
Conclusions And Recommendations
Coconut products for inedible and especially edible uses are of the greatest importance for the health of the entire world.
Some of what I have been telling you, most of you already know. But in saying these things for the record, it is my intention to tell those who did not know all the details until they heard or read this paper about the positive properties of coconut.
Coconut oil is a most important oil because it is a lauric oil. The lauric fats possess unique characteristics for both food industry uses and also for the uses of the soaps and cosmetic industries. Because of the unique properties of coconut oil, the fats and oils industry has spent untold millions to formulate replacements from those seed oils so widely grown in the world outside the tropics.
While it has been impossible to truly duplicate coconut oil for some of its applications, many food manufacturers have been willing to settle for lesser quality in their products. Consumers have also been willing to settle for a lesser quality, in part because they have been fed so much misinformation about fats and oils.
Desiccated coconut, on the other hand, has been impossible to duplicate, and the markets for desiccated coconut have continued. The powdered form of desiccated coconut now being sold in Europe and Asia has yet to find a market in the U.S., but I predict that it will become an indispensable product in the natural foods industry. Creamed coconut, which is desiccated coconut very finely ground, could be used as a nut butter.
APCC needs to promote the edible uses of coconut, and it needs to promote the reeducation of the consumer, the clinician, and the scientist. The researcher H. Thormar (Thormar et al 1999) concluded his abstract with the statement that monocaprin "...is a natural compound found in certain foodstuffs such as milk and is therefore unlikely to cause harmful side effects in the concentrations used."
It is not monocaprin that is found in milk, but capric acid. It is likely safe at most any level found in food. However, the levels in milk fat are at most 2 percent whereas the levels in coconut fat are 7 percent.
One last reference for the record. Sircar and Kansra (1998) have reviewed the increasing trend of atherosclerotic disease and type-2 diabetes mellitus in the Indians from both the subcontinent of India and abroad.
They note that over the time when there has been an alarming increase in the prevalence of these diseases, there has been a replacement of traditional cooking fats with refined vegetable oils that are promoted as heart-friendly, but which are being found to be detrimental to health. These astute researchers suggest that it is time to return to the traditional cooking fats like ghee, coconut oil, and mustard oil.
There are a number of areas of encouragement. The nutrition community in the United States is slowly starting to recognize the difference between medium chain saturated fatty acids and other saturated fatty acids. We predict now that the qualities of coconut, both for health and food function, will ultimately win out.
Mary G. Enig, Ph.D., F.A.C.N.
12501 Prosperity Drive
Silver Spring, MD, 20904-1689 USA
Tel: (301) 680-8600 Fax: (301) 680-8100