coconut oil cancer prevention. Historical studies everyone should know about.

Cancer is a word that brings with it sorrow, fear, uncertainty and a lot of times, most sadly, a sense of defeatism. While there is no known cure for the disease, over the last couple of decades, we have learned that things like diet and lifestyle are deeply linked to the habitat which allows cancer to form and to spread. And that’s where extra virgin coconut oil comes into play. Coconut oil cancer prevention is something everyone in the western world should know more about.

First off, coconut oil in its raw state is anti-carcinogenic, which means its own properties fight the agents responsible for causing and spreading cancer. Carcinogens potentially increase a person’s cancer risk by altering the way in which cells metabolize or by damaging the DNA of cells. The Medium Chain Fatty Acids (MCFA) found in coconut oil is also anti-microbrial, which prevents cancer cells from spreading and boost the immune system. Cancer, in itself, needs to spread and it needs a weakened immune system to do so. In a study with rats, a group of rats were injected with breast cancer. Safflower oil, olive oil, corn oil, and coconut oil were given to the rats. The rats that took the coconut oil did not develop a tumor. Same rats, this time colon cancer injected: Rats that were given coconut oil and olive oil had the lowest incidence of occurrence.

In studies done by the late Weston Price, it was discovered that societies that consumed virgin coconut oil didn’t even know what arthritis, diabetes, heart disease and cancer was.

Here is a more detailed look via excerpts pulled from

IV. 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.

V. Coconut Oil Antimicrobial Benefits

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 acid.

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.



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