Coconut Oil And Cancer

Lim-Sylianco (1987) has reviewed 50 years of literature showing
anticarcinogenic effects from dietary coconut oil. These animal studies
show quite clearly the nonpromotional effect of feeding coconut oil.

In a study by Reddy et al (1984) straight coconut oil was more inhibitory
than MCT oil to induction of colon tumors by azoxymethane. Chemically
induced adenocarcinomas differed 10-fold between corn oil (32%) and coconut
oil (3%) in the colon. Both olive oil and coconut oil developed the low
levels (3%) of the adenocarcinomas in the colon, but in the small intestine
animals fed coconut oil did not develop any tumors while 7% of animals fed
olive oil did.

Studies by Cohen et al (1986) showed that the nonpromotional effects of
coconut oil were also seen in chemically induced breast cancer. In this
model, the slight elevation of serum cholesterol in the animals fed coconut
oil was protective as the animals fed the more polyunsaturated oil had
reduced serum cholesterol and more tumors. The authors noted that “…an
overall inverse trend was observed between total serum lipids and tumor
incidence for the 4 [high fat] groups.”

This is an area that needs to be pursued.

I would now like to review for you some of the rationale for the use of
coconut oil as a food that will serve as the raw material to provide
potentially useful levels of antimicrobial activity in the individual.

The lauric acid in coconut oil is used by the body to make the same
disease-fighting fatty acid derivative monolaurin that babies make from the
lauric acid they get from their mothers= milk. The monoglyceride monolaurin
is the substance that keeps infants from getting viral or bacterial or
protozoal infections. Until just recently, this important benefit has been
largely overlooked by the medical and nutrition community.

Recognition of the antimicrobial activity of the monoglyceride of lauric
acid (monolaurin) has been reported since 1966. The seminal work can be
credited to Jon Kabara. This early research was directed at the virucidal
effects because of possible problems related to food preservation. Some of
the early work by Hierholzer and Kabara (1982) that showed virucidal
effects of monolaurin on enveloped RNA and DNA viruses was done in
conjunction with the Center for Disease Control of the US Public Health
Service with selected prototypes or recognized representative strains of
enveloped human viruses. The envelope of these viruses is a lipid membrane.

Kabara (1978) and others have reported that certain fatty acids (e.g.,
medium-chain saturates) and their derivatives (e.g., monoglycerides) can
have adverse effects on various microorganisms: those microorganisms that
are inactivated include bacteria, yeast, fungi, and enveloped viruses.

The medium-chain saturated fatty acids and their derivatives act by
disrupting the lipid membranes of the organisms (Isaacs and Thormar 1991)
(Isaacs et al 1992). In particular, enveloped viruses are inactivated in
both human and bovine milk by added fatty acids (FAs) and monoglycerides
(MGs) (Isaacs et al 1991) as well as by endogenous FAs and MGs (Isaacs et
al 1986, 1990, 1991, 1992; Thormar et al 1987).

All three monoesters of lauric acid are shown to be active antimicrobials,
i.e., alpha-, alpha’-, and beta-MG. Additionally, it is reported that the
antimicrobial effects of the FAs and MGs are additive and total
concentration is critical for inactivating viruses (Isaacs and Thormar 1990).

The properties that determine the anti-infective action of lipids are
related to their structure; e.g., monoglycerides, free fatty acids. The
monoglycerides are active, diglycerides and triglycerides are inactive. Of
the saturated fatty acids, lauric acid has greater antiviral activity than
either caprylic acid (C-10) or myristic acid (C-14).

The action attributed to monolaurin is that of solubilizing the lipids and
phospholipids in the envelope of the virus causing the disintegration of
the virus envelope. In effect, it is reported that the fatty acids and
monoglycerides produce their killing/inactivating effect by lysing the
(lipid bilayer) plasma membrane. However, there is evidence from recent
studies that one antimicrobial effect is related to its interference with
signal transduction (Projan et al 1994).

Some of the viruses inactivated by these lipids, in addition to HIV, are
the measles virus, herpes simplex virus-1 (HSV-1), vesicular stomatitis
virus (VSV), visna virus, and cytomegalovirus (CMV). Many of the pathogenic
organisms reported to be inactivated by these antimicrobial lipids are
those known to be responsible for opportunistic infections in HIV-positive
individuals. For example, concurrent infection with cytomegalovirus is
recognized as a serious complication for HIV+ individuals (Macallan et al
1993). Thus, it would appear to be important to investigate the practical
aspects and the potential benefit of an adjunct nutritional support regimen
for HIV-infected individuals, which will utilize those dietary fats that
are sources of known anti-viral, anti-microbial, and anti-protozoal
monoglycerides and fatty acids such as monolaurin and its precursor lauric

No one in the mainstream nutrition community seems to have recognized the
added potential of antimicrobial lipids in the treatment of HIV-infected or
AIDS patients. These antimicrobial fatty acids and their derivatives are
essentially non-toxic to man; they are produced in vivo by humans when they
ingest those commonly available foods that contain adequate levels of
medium-chain fatty acids such as lauric acid. According to the published
research, lauric acid is one of the best “inactivating” fatty acids, and
its monoglyceride is even more effective than the fatty acid alone (Kabara
1978, Sands et al 1978, Fletcher et al 1985, Kabara 1985).

The lipid coated (envelop) viruses are dependent on host lipids for their
lipid constituents. The variability of fatty acids in the foods of
individuals accounts for the variability of fatty acids in the virus
envelop and also explains the variability of glycoprotein expression.

Loss of lauric acid from the American diet

Increasingly, over the past 40 years, the American diet has undergone major
changes. Many of these changes involve changes of fats and oils. There has
been an increasing supply of the partially hydrogenated trans-containing
vegetable oils and a decreasing amount of the lauric acid-containing oils.
As a result, there has been an increased consumption of trans fatty acids
and linoleic acid and a decrease in the consumption of lauric acid. This
type of change in diet has an effect on the fatty acids the body has
available for metabolic activities.

The coconut producing countries

Whole coconut as well as extracted coconut oil has been a mainstay in the
food supply in many countries in parts of Asia and the Pacific Rim
throughout the centuries. Recently though, there has been some replacement
of coconut oil by other seed oils. This is unfortunate since the benefits
gained from consuming an adequate amount of coconut oil are being lost.

Based on the per capita intake of coconut oil in 1985 as reported by
Kaunitz (1992), the per capita daily intake of lauric acid can be
approximated. For those major producing countries such as the Philippines,
Indonesia, and Sri Lanka, and consuming countries such as Singapore, the
daily intakes of lauric acid were approximately 7.3 grams (Philippines),
4.9 grams (Sri Lanka), 4.7 grams (Indonesia), and 2.8 grams (Singapore). In
India, intake of lauric acid from coconut oil in the coconut growing areas
(e.g., Kerala) range from about 12 to 20 grams per day (Eraly 1995),
whereas the average for the rest of the country is less than half a gram.
An average high of approximately 68 grams of lauric acid is calculated from
the coconut oil intake previously reported by Prior et al (1981) for the
Tokelau Islands. Other coconut producing countries may also have intakes of
lauric acid in the same range.

The US experience
In the United States today, there is very little lauric acid in most of the
foods. During the early part of the 20th Century and up until the late
1950s many people consumed heavy cream and high fat milk. These foods could
have provided approximately 3 grams of lauric acid per day to many
individuals. In addition, desiccated coconut was a popular food in homemade
cakes, pies and cookies, as well as in commercial baked goods, and 1-2
tablespoons of desiccated coconut would have supplied 1-2 grams of lauric
acid. Those foods made with the coconut oil based shortenings would have
provided additional amounts.

Until two years ago, some of the commercially sold popcorn, at least in
movie theaters, had coconut oil as the oil. This means that for those
people lucky enough to consume this type of popcorn the possible lauric
acid intake was 6 grams or more in a three (3) cup order.

Some infant formulas (but not all) have been good sources of lauric acid
for infants. However, in the past 3-4 years there has been reformulation
with a loss of a portion of coconut oil in these formulas, and a subsequent
lowering of the lauric acid levels.

Only one US manufactured enteral formula contains lauric acid (e.g.,
Impact7); this is normally used in hospitals for tube feeding; it is
reported to be very effective in reversing severe weight loss in AIDS
patients, but it is discontinued when the patients leave the hospital
because it is not sufficiently palatable for oral use. The more widely
promoted enteral formulas (e.g., Ensure7, Nutren7) are not made with lauric
oils, and, in fact, many are made with partially hydrogenated oils.

There are currently some candies sold in the US that are made with palm
kernel oil, and a few specialty candies made with coconut oil and
desiccated coconut. These can supply small amounts of lauric acid.

Cookies such as macaroons, if made with desiccated coconut, are good
sources of lauric acid, supplying as much as 6 grams of lauric acid per
macaroon (Red Mill). However, these cookies make up a small portion of the
cookie market. Most cookies in the United States are no longer made with
coconut oil shortenings; however, there was a time when many US cookies
(e.g., Pepperidge Farm) were about 25% lauric acid.

Originally, one of the largest manufacturers of cream soups used coconut
oil in the formulations. Many popular cracker manufacturers also used
coconut oil as a spray coating. These products supplied a small amount of
lauric acid on a daily basis for some people.

How much lauric acid is needed?
It is not known exactly how much food made with lauric oils is needed in
order to have a protective level of lauric acid in the diet. Infants
probably consume between 0.3 and 1 gram per kilogram of body weight if they
are fed human milk or an enriched infant formula that contains coconut oil.
This amount appears to have always been protective. Adults could probably
benefit from the consumption of 10 to 20 grams of lauric acid per day.
Growing children probably need about the same amounts as adults.

The coconut oil industry needs to make the case for lauric acid now. It
should not wait for the rapeseed industry to promote the argument for
including lauric acid because of the increased demand for laurate. In fact
lauric acid may prove to be a conditionally essential saturated fatty acid,
and the research to establish this fact around the world needs to be
vigorously promoted.

Although private sectors need to fight for their commodity through the
offices of their trade associations, the various governments of coconut
producing countries need to put pressure on WHO, FAO, and UNDP to
recognizes the health importance of coconut oil and the other coconut
products. Moreover, those representatives who are going to do the
persuading need to believe that their message is scientifically correct —
because it is.

Among the critical foods and nutrition “buzz words” for the 21st Century is
the term “functional foods.” Clearly coconut oil fits the designation of a
very important functional food.


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