HEALING POWERS OF COCONUT OIL
If there was an oil you could use for your daily cooking needs that helped protect you from heart disease, cancer, and other degenerative conditions, improved your digestion, strengthened your immune system, and helped you lose excess weight, would you be interested?
No such oils exists you say? Not so! There is an oil that can do all this and more. No, it’s not olive oil, it’s not canola oil, or safflower oil or any of the oils commonly used for culinary purposes. It’s not flaxseed oil, evening primrose oil, or any of the oils sold as dietary supplements. It’s not rare or exotic. IT IS WONDERFUL AND HEALTHFUL COCONUT OIL.
Plain and simple… COCONUT OIL is the healthiest oil we can use. Some 50 years ago coconut oil was used in pies, cakes, cookies. crackers, candy and other confections. Then in the late 1950’s most of this healthy oil was replaced with polyunsaturated oils and partially hydrogenated oils and our health since has been on a downward spiral with increased cancer, heart disease, asthma, diabetes, allergies and on and on.
But wait, isn’t coconut oil a saturated fat? And isn’t saturated fat bad? because coconut oil is primarily a saturated oil, it has been blindly labeled as bad. It is lumped right along with beef fat and lard with the assumption that they all carry the same health risks. However, researchers have clearly shown that the oil from coconuts, a plant source, acts differently than the saturated fat from animal sources. The oil from coconuts is unique in nature and provides many health benefits obtainable from no other source.
What Coconut Oil DOES NOT Do: * Does not contain cholesterol. * Does not increase blood cholesterol level. * Does not promote platelet stickiness which leads to blood clot formation. * Does not contribute to atherosclerosis or heart disease. * Does not promote cancer or any other degenerative disease. * Does not contribute to weight problems.
What Coconut Oil DOES Do: * Reduces risk of atherosclerosis and related illnesses. * reduces risk of cancer and other degenerative conditions. * Helps prevent bacterial, viral, and fungal (including yeast) infections. * Supports immune system function. * Helps prevent osteoporosis. * Helps control diabetes. * Promotes weight loss. * Supports healthy metabolic function. * Provides an immediate source of energy. * Supplies fewer calories than other fats. * Supplies important nutrients necessary for good health. * Improves digestion and nutrient absorption. * Has a mild delicate flavor. * Is highly resistant to spoilage (long shelf life). * Is heat resistant (the healthiest oil for cooking). * Helps keep skin soft and smooth. * Helps prevent premature aging and wrinkling of the skin. * Helps protect against skin cancer and other blemishes.
ALSO FROM DR. BRUCE FIFE’S BOOK — “”THE HEALING MIRACLES OF COCONUT OIL””:
HEALTH BENEFITS OF COCONUT OIL
- Research and clinical observation have shown that medium-chain fatty acids (MCFA’s), like those found in coconut oil, may provide a wide range of health benefits. Some of these are summarized below:
- Kills viruses that cause mononucleosis, influenza, hepatitis C. measles, herpes, AIDS and other illnesses
- Kills bacteria that cause pneumonia, earache, throat infections, dental cavities, food poisoning, urinary tract infections, meningitis, gonorrhea, and dozens of other diseases
- Kills fungi and yeast that cause candida, jock itch, ringworm, athlete’s foot, thrush, diaper rash and other infections
- Expels or kills tapeworms, lice, giardia, and other parasites
- Provides a nutritional source of quick energy
- Boosts energy and endurance enhancing physical and athletic performance
- Improves digestion and absorption of fat-soluble vitamins and amino acids
- Improves insulin secretion and utilization of blood glucose
- Relieves stress on pancreas and enzyme systems of the body
- Reduces symptoms associated with pancreatitis
- Helps relieve symptoms and reduce health risks associated with diabetes
- Reduces problems associated with malabsorption syndrome and cystic fibrosis
- Improves calcium and magnesium absorption and supports the development of strong bones and teeth.
- Helps protect against osteoporosis
- Helps relieve symptoms of gallbladder disease
- Relieves symptoms associated with Crohn’s disease, ulcerative colitis, and stomach ulcers
- Relieves pain and irritation caused by hemorrhoids
- Reduces chronic inflammation
- Supports tissue healing and repair
- Supports and aids immune system function
- Helps protect the body from breast, colon, and other cancers
- Is heart healthy; does not increase blood cholesterol or platelet stickiness
- Helps prevent heart disease, atherosclerosis, and stroke
- Helps prevent high blood pressure
- Helps prevent periodontal disease and tooth decay
- Functions as a protective antioxidant
- Helps to protect the body from harmful free-radicals that promote premature aging and degenerative disease
- Does not deplete the body’s antioxidant reserves like other oils do
- Improves utilization of essential fatty acids and protects them from oxidation
- Helps relieve symptoms associated with chronic fatigue syndrome
- Relieves symptoms associated with benign prostatic hyperplasia (prostate enlargement)
- Reduces epileptic seizures
- Helps protect against kidney disease and bladder infections
- Helps prevent liver disease
- Is lower in calories than all other fats
- Supports thyroid function
- Promotes loss of excess weight by increasing metabolic rate
- Is utilized by the body to produce energy in preference to being stored as body fat like other dietary fats.
- Helps preven OILesity and overweight problems
- Applied topically helps to form a chemical barrier on the skin to ward off infection
- Reduces symptoms associated with psoriasis, eczema, and dermatitis
- Supports the natural chemical balance of the skin
- Softens skin and helps relieve dryness and flaking
- Prevents wrinkles, sagging skin, and age spots
- Promotes healthy-looking hair and complexion
- Provides protection from the damaging effects of ultraviolet radiation from the sun
- Controls dandruff
- Helps you look and feel younger
- Is resistant to oxidation, so has a long shelf life
- Does not form harmful by-products when heated to normal cooking temperatures like other vegetable oils do
- Has no harmful or discomforting side effects
- Is completely non-toxic to humans
DAILY DOSE COMPARISON
The amount of medium-chain fatty acids that is believed to be necessary for optional health can be obtained from a variety of coconut products. The following all contain about the same amount of MCFA’s and is the recommended daily amount one should try to take. The amount of MCFA’s in…
2 – TABLESPOONSFUL OF COCONUT OIL DAILY:
= 5 ounces fresh coconut meat (about half a coconut)
= 1 3/4 cups dried, shredded coconut
= 7 ounces of coconut milk (see below)
As unbelievable as it sounds, the oil in coconuts has been found to aid the body in destroying dozens of harmful viruses including hepatitis C, herpes, and HIV. Coconut oil has been called the healthiest dietary oil on earth. If you’re not using coconut oil for your daily cooking and body care needs you’re missing out on one of nature’s most amazing health products.
The Healing Miracles of Coconut Oil
by Bruce Fife, N.D.
WHERE TO ORDER COCONUT OIL PRODUCTS:
1. TROPICAL TRADITIONS
This company distributes virgin coconut oil produced using traditional methods by local farmers. They can ship anywhere in the world. This is the BEST Coconut Oil in the World. Orders can be placed at: Tropical Traditions or call 1-866-311-2626 X704.
2. Quality First International Inc.
6852 Wellington Road #34, R.R. #22, Cambridge, ON, N3C 2V4, Canada, (877) 441-9479, www.qualityfirst.on.ca They call their oil “”Virgin Oil Dc Coco-Creme.”” It is extracted from coconut milk and has a delightfully delicate flavor and aroma. Very high quality. So good you can eat it by the spoon.
3. Coconut Oil Supreme
Coconut Oil Supreme? is now available in consumer-friendly (and reasonably priced)1lb (454g) pouches. This coconut oil is biologically pure and is extracted from fresh coconut milk without heat, solvents, fermentation, etc. Once you experience this unique oil we doubt that you will be satisfied with any other. Orders may beplaced at www.coconutoil-online.com
NOTE: MORE SOURCES OF COCONUT PRODUCTS WILL BE ADDED AS SOON AS I FIND THEM.
W. Greene, D.C.
How to make your own
Coconut meat and the milk made from it are key components in Brazilian cookery. It is easy to make coconut milk from freshly grated coconut and capture the authentic taste of Brazilian dishes using it. Thick, rich milk is produced from the first squeezing of the gratings and is often called “”coconut cream””; a thinner milk is derived from a second round of squeezing.
1/2 cup warm water (for thick milk)
2 to 3 cups warm water (for thin milk)
Heat the coconut in a preheated oven (350 degrees F) for 10 minutes to crack the coconut. Remove the coconut from the oven (with pot holders!) and place it in a large metal bowl on the floor. Cover the bowl with a towel and hit the coconut with a hammer to break it completely open. More than one strike may be necessary. Remove the pieces of broken coconut from the bowl. Strain the coconut water (agua de cuco) that is released through a coffee filter to remove any fibers, and set aside. Separate the coconut meat from the shell, using a dull knife to pry them apart if necessary.
Remove the brown skin (optional) from the coconut meat with a vegetable peeler and grate the meat in a food processor.
To make the thick milk, put the gratings into cheesecloth or a clean white dish towel and hold the ends together. Soak the wrapped gratings in 1/2 cup warm water in a small bowl for a few minutes. Firmly squeeze the gratings over the bowl. About 3/4 cup of thick milk will be obtained. A less efficient method of making thick coconut milk is to put the grated coconut in a sieve, wet it with warm water, and press out the milk with a spoon.
Thin milk is made by soaking the same wrapped gratings in 2 to 3 cups of warm water and repeating the squeezing procedure. (Use the reserved coconut water and bring the volume to 2 to 3 cups with warm water.)
Making Your Own Coconut Milk
You can use either fresh grated flesh of coconut or desiccated (dried) coconut. The ready-made dried coconut is easy to use and can save you time in preparation.
— Put 4 ounces desiccated coconut andnd tBD her (4 ounces) hot water in blender, cover and blend for 1-2 minutes.
— Strain through a fine sieve or a piece of muslin. This will yield around 1 cup (8 ounces) of ‘thick coconut milk or cream?). This may be further diluted with equal parts of water.
— Repeat process, using the used coconut and a little less water. A second extract is ‘thin coconut milk?)
— Use mixture of the above when the recipe calls for coconut milk.
An easy way to obtain coconut milk is to buy ready-made coconut milk in Asian stores or health food stores. The coconut milk (or cream, if undiluted) can be used full strength right from the container. The coconut milk can be diluted by mixing one part of the ready-made product with one part of water. The canned coconut milk requires a ‘shake well? before opening because it may separate.
INTRODUCTION TO COCONUT OIL
by STEPHEN BYRNES, N.D.
The Politics of Tropical Oils
“”Coconut oil is the healthiest oil we can eat.””
So why has coconut oil gotten such a bad rap in the recent past? After all, much of the research supporting coconut oil as a healthy fat has been around for some time. The answer is politics and economics. Coconut oil was heavily used in the US at one time, being used for baking, pastries, frying, and theater popcorn. But starting in the 1980s some very powerful groups in the US, including the American Soybean Association (ASA), the Corn Products Company (CPC International) and the Center for Science in the Public Interest (CSPI), began to categorically condemn all saturated oils. Faulty science was used to convince the public that ALL saturated fats were unhealthy, when in fact saturated fats rich in the medium chain faveryacids, like lauric acid, are very healthy. These organizations were aided by the United States Food and Drug Administration (FDA), many of whose key personnel reportedly are recruited from and return to the vegetable oil industry. The result was that most people switched to vegetable oils, and the main source of lauric acid from tropical oils in the American diet was lost. The countries that these tropical oils came from, mainly the Philippines and Malaysia, were too poor to counter these untrue claims with advertising investments for the truth.
While some clinical studies have been conducted recently, like the study on AIDS patients in the Philippines (1999 – 2000), much of the studies have been done on tropical populations where coconut products are a main part of the diet. One such study was done in the South Pacific islands of Pukapuka and Tokelau near New Zealand. The studies were started in the 1960s before either island was exposed to Western refined food. These populations ate only natural foods, and coconut foods were the most prevalent, being consumed at each meal in one form or another. While most people in western countries get 30-40 percent of their calories from fats, the people in these islands averaged between 50 and 60 percent of their calories from fat, most of that being saturated fat from coconuts. So what kind of health did these studies find among the populations in these two islands? Bruce Fife reports in his book: “”The overall health of both groups was extremely good compared to Western standards.
There were no signs of kidney disease or hypothyroidism that might influence fat levels. There was no hypercholesterolemia (high blood cholesterol). All inhabitants were lean and healthy despite a very high saturated-fat diet. In fact, the populations as a whole had ideal weight-to-height ratios as compared to the Body Mass Index figures used by nutritionists. Digestive problems a I nare. Constipation is uncommon. They average two or more bowel movements a day. Atherosclerosis, heart disease, colitis, colon cancer, hemorrhoids ulcers, diverticulosis, and appendicitis are conditions with which they are generally unfamiliar.”” (The Healing Miracles of Coconut Oil)
A fat that causes weight loss??
Another incredible fact about coconut oil is that even though it is a fat, it actually promotes weight loss!! The reason is again because of the healthy medium chain fatty acids. These fatty acids do not circulate in the bloodstream like other fats, but are sent directly to the liver where they are immediately converted into energy, just like carbohydrates. So the body uses the fat in coconut oil to produce energy, rather than be stored as body fat. Medium chain fatty acids found in coconut oil also speed up the body’s metabolism burning more calories and promoting weight loss. The weight-loss effects of coconut oil have clearly been demonstrated by many researchers. (There are a list of references in Bruce Fife’s book The Healing Miracles of Coconut Oil.)
So how much coconut oil should one consume? A good therapeutic dosage is 3 to 4 tablespoons a day. This provides enough lauric acid to build the immune system. Also, look for unrefined coconut oil. Stay away from all hydrogenated oils, whether it is coconut oil or vegetable oils. Hydrogenated oils are oils with trans fatty acids, which have been altered from their original chemical composition, and have been shown to raise serum cholesterol levels that can lead to heart disease.
Also look for unrefined coconut oils, like Virgin Coconut Oil. Most commercial coconut oils are RBD (refined, bleached, and deodorized). While these RBD oils do maintain the beneficial chemical structures of the medium chain fatty acids, they also contain chemicals used in processing.
If one is interested in learning about all the other health benefits of coconut oil, go to the coconut-info website and read the research. There is also a discussion list one can join and interact with some of the world’s best authorities on coconut oil, including Dr. Mary Enig, Dr. Bruce Fife, and many others who have done research or experienced first hand the healing properties of coconut oil, and can back up the claim: “”Coconut oil is the healthiest oil on earth!””
THE FOLLOWING IS A 1996 ARTICLE WRITTEN BY RAYMOND PEAT, Ph.D.
I have already discussed the many toxic effects of the unsaturated oils, and I have frequently mentioned that coconut oil doesn’t have those toxic effects, though it does contain a small amount of the unsaturated oils. Many people have asked me to write something on coconut oil. I thought I might write a small book on it, but I realize that there are no suitable channels for distributing such a book–if the seed-oil industry can eliminate major corporate food products that have used coconut oil for a hundred years, they certainly have the power to prevent dealers from selling a book that would affect their market more seriously. For the present, I will just outline some of the virtues of coconut oil.
The unsaturated oils in some cooked foods become rancid in just a few hours, even at refrigerator temperatures, and are responsible for the stale taste of left-over foods. (Eating slightly stale food isn’t particularly harmful, since the same oils, even when eaten absolutely fresh, will oxidize at a much higher rate once they are in the body, where they are heated and thoroughly mixed with an abundance of oxygen.) Coconut oil that has been kept at room temperature for a year has been tested for rancidity, and showed no evidence of it. Since we would expect the small percentage of unsaturated oils naturally contained in coconut oil to become rancid, it seems that the other oils (saturated) have an anti-oxidative effect: I suspect that the dilution keeps the unstable unsaturated fat molecules spatially separated from each other, so they can’t interact in the destructive chain reactions that occur in other oils. To interrupt chain-reactions of oxidation is one of the functions of antioxidants, and it is possible that a sufficent quantity of coconut oil in the body has this function. It is well established that dietary coconut oil reduces our need for vitamin E, but I think its antioxidant role is more general than that, and that it has both direct and indirect antioxidant activities.
Coconut oil is unusually rich in short and medium chain fatty acids. Shorter chain length allows fatty acids to be metabolized without use of the carnitine transport system. Mildronate, which I discussed in an article on adaptogens, protects cells against stress partly by opposing the action of carnitine, and comparative studies showed that added carnitine had the opposite effect, promoting the oxidation of unsaturated fats during stress, and increasing oxidative damage to cells. I suspect that a degree of saturation of the oxidative apparatus by short-chain fatty acids has a similar effect–that is, that these very soluble and mobile short-chain saturated fats have priority for oxidation, because they don’t require carnitine transport into the mitochondrion, and that this will tend to inhibit oxidation of the unstable, peroxidizable unsaturated fatty acids.
When Albert Schweitzer operated his clinic in tropical Africa, he said it was many years before he saw any cases of cancer, evehe believed that the appearance of cancer was caused by the change to the European type of diet. In the l920s, German researchers showed that mice on a fat-free diet were practically free of cancer. Since then, many studies have demonstrated a very close association between consumption of unsaturated oils and the incidence of cancer.
Heart damage is easily produced in animals by feeding them linoleic acid; this “”essential”” fatty acid turned out to be the heart toxin in rape-seed oil. The addition of saturated fat to the experimental heart-toxic oil-rich diet protects against the damage to heart cells.
Immuno-suppression was observed in patients who were being “”nourished”” by intravenous infusions of “”essential fatty acids,”” and as a result coconut oil is used as the basis for intravenous fat feeding, except in organ-transplant patients. For those patients, emulsions of unsaturated oils are used specifically for their immunosuppressive effects.
General aging, and especially aging of the brain, is increasingly seen as being closely associated with lipid peroxidation.
Several years ago I met an old couple, who were only a few years apart in age, but the wife looked many years younger than her doddering old husband. She was from the Philippines, and she remarked that she always had to cook two meals at the same time, because her husband couldn’t adapt to her traditional food. Three times every day, she still prepared her food in coconut oil. Her apparent youth increased my interest in the effects of coconut oil.
In the 1960s, Hartroft and Porta gave an elegant argument for decreasing the ratio of unsaturated oil to saturated oil in the diet (and thus in the tissues). They showed that the “”age pigment”” is produced in proportion to the ratio of oxidants to antioxidants, multiplied by the ratio of unsaturated oils to saturated oils. More recently, a variety of studies have demonstrated that ultraviolet light induces peroxidation in unsaturated fats, but not saturated fats, and that this occurs in the skin as well as in vitro. Rabbit experiments, and studies of humans, showed that the amount of unsaturated oil in the diet strongly affects the rate at which aged, wrinkled skin develops. The unsaturated fat in the skin is a major target for the aging and carcinogenic effects of ultraviolet light, though not necessarily the only one.
In the 1940s, farmers attempted to use cheap coconut oil for fattening their animals, but they found that it made them lean, active and hungry. For a few years, an anti-thyroid drug was found to make the livestock get fat while eating less food and it also probably proteced hypothyroidism in the people who ate the meat. By the late 1940s, it was found that the same anti-thyroid effect, caus no animals to get fat without eating much food, could be achieved by using soybeans and corn as feed.
Later, an animal experiment fed diets that were low or high in total fat, and in different groups the fat was provided by pure coconut oil, or a pure unsaturated oil, or by various mixtures of the two oils. At the end of their lives, the animals’ obesity increased directly in proportion to the ratio of unsaturated oil to coconut oil in their diet, and was not related to the total amount of fat they had consumed. That is, animals that ate just a little pure unsaturated oil were fat, and animals that ate a lot of coconut oil were lean.
In the 1930s, animals on a diet lacking the unsaturated fatty acids were found to be “”hypermetabolic.”” Eating a “”normal”” diet, these animals were malnourished, and their skin condition was said to be caused by a “”deficiency of essential fatty acids.”” But other researchers who were studying vitamin B6 recognized the condition as a deficiency of that vitamin. They were able to cause the condition by feeding a fat-free diet, and to cure the condition by feeding a single B vitamin. The hypermetabolic animals simply needed a better diet than the “”normal,”” fat-fed, cancer-prone animals did.
G. W. Crile and his wife found that the metabolic rate of people in Yucatan, where coconut is a staple food, averaged 25% higher than that of people in the United States. In a ht oilimate, the adaptive tendency is to have a lower metabolic rate, so it is clear that some factor is more than offsetting this expected effect of high environmental temperatures. The people there are lean, and recently it has been observed that the women there have none of the symptoms we commonly associate with the menopause.
By 1950, then, it was established that unsaturated fats suppress the metabolic rate, apparently creating hypothyroidism. Over the next few decades, the exact mechanisms of that metabolic damage were studied. Unsaturated fats damage the mitochondria, partly by suppressing the respiratory enzyme, and partly by causing generalized oxidative damage. The more unsaturated the oils are, the more specifically they suppress tissue response to thyroid hormone, and transport of the hormone on the thyroid transport protein.
Plants evolved a variety of toxins designed to protect themselves from “”predators,”” such as grazing animals. Seeds contain a variety of toxins, that seem to be specific for mammalian enzymes, and the seed oils themselves function to block proteolytic digestive enzymes in the stomach. The thyroid hormone is formed in the gland by the action of a proteolytic enzyme, and the unsaturated oils also inhibit that enzyme. Similar proteolytic enzymes involved in clot removal and phagocytosis appear to be similarly inhibited by these oils.
Just as metabolism is “”activated”” by consumption of coconut oil, which prevents the inhibiting effect of unsaturated oils, other inhibited processes, such as clot removal and phagocytosis, will probably tend to be restored by continuing use of coconut oil.
Brain tissue is very rich in complex forms of fats. The experiment (around 1978) in which pregnant mice were given diets containing either coconut oil or unsaturated oil showed that brain development was superior in the young mice whose mothers ate coconut oil. Because coconut oil supports thyroid function, and thyroid governs brain development, including myelination (the insulation around the nerves), the result might simply reflect the difference between normal and hypothyroid individuals. However, in 1980, experimenters demonstrated that young rats fed milk containing soy oil incorporated the oil directly into their brain cells, and had structurally abnormal cells as a result.
Lipid peroxidation occurs during seizures, and antioxidants such as vitamin E have some anti-seizure activity. Currently, lipid peroxidation is being found to be involved in the nerve cell degeneration of Alzheimer’s disease.
Various fractions of coconut oil are coming into use as “”drugs,”” meaning that they are advertised as treatments for diseases. Butyric acid is used to treat cancer, lauric and myristic acids to treat virus infections, and mixtures of medium-chain fats are sold for weight loss. Purification undoubtedly increases certain effects, and results in profitable products, but in the absence of more precise knowledge, I think the whole natural product, used as a regular food, is the best way to protect health. The shorter-chain fatty acids have strong, unpleasant odors; for a couple of days after I ate a small amount of a medium-chain triglyceride mixture, my skin oil emitted a rank, goaty smell. Some people don’t seem to have that reaction, and the benefits might outweigh the stink, but these things just haven’t been in use long enough to know whether they are safe.
We have to remember that the arguments made for aspartame, monosodium glutamate, aspartic acid, and tryptophan–that they are like the amino acids that make up natural proteins–are dangerously false. In the case of amino acids, balance is everything. Aspartic and glutamic acids promote seizures and cause brain damage, and are intimately involved in the process of stress-induced brain aging, and tryptophan by itself is carcinogenic. Treating any complex natural product as the drug industry does, as a raatesterial to be fractionated in the search for “”drug”” products, is risky, because the relevant knowledge isn’t sought in the search for an association between a single chemical and a single disease.
While the toxic unsaturated paint-stock oils, especially safflower, soy, corn and linseed-flaxseed) oils, have been sold to the public precisely for tre r drug effects, all of their claimed benefits were false. When people become interested in coconut oil as a “”health food,”” the huge seed-oil industry–operating through their shills–are going to attack it as an “”unproved drug.””
While components of coconut oil have been found to have remarkable physiological effects (as antihistamines, anti-infectives/antiseptics, promoters of immunity, glucocorticoid antagonist, nontoxic anticancer agents, for example), I think it is important to avoid making any such claims for the natural coconut oil, because it very easily could be banned from the import market as a “”new drug”” which isn’t “”approved by the FDA.”” We have already seen how money and propaganda from the soy oil industry eliminated long-established products from the U.S. market. I saw people lose weight stably when they had the habit of eating large amounts of tortilla chips fried in coconut oil, but those chips disappeared when their producers were pressured into switching to other oils, in spite of the short shelf life that resulted in the need to add large amounts of preservatives. Oreo cookies, Ritz crackers, potato chip producers, and movie theater popcorn makers have experienced similar pressures.
The cholesterol-lowering fiasco for a long time centered on the ability of unsaturated oils tobeleghtly lower serum cholesterol. For years, the mechanism of that action wasn’t known, which should have suggested caution. Now, it seems that the effect is just one more toxic action, in which the liver defensively retains its cholesterol, rather than releasing it into the blood. Large-scale human studies have provided overwhelming evidence that whenever drugs, including the unsaturated oils, were used to lower serum cholesterol, mortality increased, from a variety of causes including accidents, but mainly from cancer.
Since the 1930s, it has been clearly established that suppression of the thyroid raises serum cholesterol (while increasing mortality from infections, cancer, and heart disease), while restoring normal thyroid function brings cholesterol down to normal. In this situation, however, thyroid isn’t suppressing the synthesis of cholesterol, but rather is promoting its use to form hormones and bile salts. When the thyroid is functioning properly, the amount of cholesterol in the blood entering the ovary governs the amount of progesterone being produced by the ovary, and the same situation exists in all steroid-forming tissues, such as the adrenal glands and the brain. Progesterone and its precursor, pregnenolone, have a generalized protective function: antioxidant, anti-seizure, antitoxin, anti-spasm, anti-clot, anti-cancer, pro-memory, pro-myelination, pro-attention, etc. Any interference with the formation of cholesterol will interfere with many of these exceedingly important protective functions.
As far as the evidence goes, it suggests that coconut oil, added regularly to a balanced diet, lowers cholesterol to normal by promoting its conversion into pregnenolone. (The coconut family contains steroids that resemble pregnenolone, but these are probably mostly removed when the fresh oil is washed with water to remove the enzymes, which would digest the oil.) Coconut-eating cultures in the tropics have consistently lower cholesterol than people in the U.S. Everyone that I know who uses coconut oil regularly happens to have cholesterol levels of about 160, while eating mainly cholesterol rich foods (eggs, milk, meat, shellfish). I encourage people to eat sweet fruits, rather than starches, if they want to increase their production of cholesterol, since fructose has that effect.
Many people see coconut oil in its hard, white state, and–as a result of their training watching television or going to medical school?implicate these in cholesterol-rich plaques in blood vessels. Those lesions in blood vessels are caused mostly by lipid peroxidation of unsaturated fats, and relate to stress, because adrenaline liberates fats from storage, and the lining of blood vessels is exposed to high concentrations of the blood-borne material. In the body, incidentally, the oil can’t exist as a solid, since it liquefies at 76 degrees. (Incidentally, the viscosity of complex materials isn’t a simple matter of averaging the viscosity of its component materials; cholesterol and saturated fats sometimes lower the viscosity of cell components.)
Most of the images and metaphors relating to coconut oil and cholesterol that circulate in our culture are false and misleading. I offer a counter-image, which is metaphorical, but it is true in that it relates to lipid peroxidation, which is profoundly important in our bodies. After a bottle of safflower oil has been opened a few times, a few drops that get smeared onto the outside of the bottle begin to get very sticky, and hard to wash off. This property is why it is a valued base for paints and varnishes, but this varnish is chemically closely related to the age pigment that forms “”liver spots”” on the skin, and similar lesions in the brain, heart, bloohen ssels, lenses of the eyes, etc. The image of “”hard, white saturated coconut oil”” isn’t relevant to the oil’s biological action, but the image of “”sticky varnish-like easily oxidized unsaturated seed oils”” is highly relevant to their toxicity.
The ability of some of the medium chain saturated fatty acids to inhibit the formation of fat very likely synergizes the pro-thyroid effect, in creating energy to be used, rather than stored. When fat isn’t formed from carbohydrate, the sugar is available for use, or for storage as glycogen. Therefore, shifting from unsaturated fats in foods to coconut oil involves several anti-stress processes, reducing our need for the adrenal hormones. Decreased blood sugar is a basic signal for the release of adrenal hormones. Unsaturated oil tends to lower the blood sugar in at least three basic ways. It damages mitochondria, causing respiration to be uncoupled from energy production, meaning that fuel is burned without useful effect. It suppresses the activity of the respiratory enzyme (directly, and through its anti-thyroid actions), decreasing the respiratory production of energy. And it tends to direct carbohydrate into fat production, making both stress and obesity more probable. For those of us who use coconut oil consistently, one of the most noticeable changes is the ability to go for several hours without eating, and to feel hungry without having symptoms of hypoglycemia.
One of the stylish ways to promote the use of unsaturated oils is to refer to their presence in “”cell membranes,”” and to claim that they are essential for maintaining “”membrane fluidity.”” As I have mentioned above, it is the ability of the unsaturated fats, and their breakdown products, to interfere with enzymes and transport proteins, which accounts for many of their toxic effects, so they definitely don’t just harmlessly form “”membranes.”” They probably bind to all proteins, and disrupt some of them, but for some reason their affinity for proteolytic and respiration-related enzymes is particularly obvious. (I think havchemistry of this association is going to give us some important insights into the nature of organisms.
Unsaturated fats are slightly more water-soluble than fully saturated fats, as they do have a greater tendency to concentrate at interfaces between water and fats or proteins, but there me rrelatively few places where these interfaces can be usefully and harmlessly occupied by unsaturated fats, and at a certain point, an excess becomes harmful. We don’t want “”membranes”” forming where there shouldn’t be membranes. The fluidity or viscosity of cell surfaces is an extremely complex subject, and the degree of viscosity has to be appropriate for the function of the cell. Interestingly, in some cells, such as the cells that line the air sacs of the lungs, cholesterol and one of the saturated fatty acids found in coconut oil can increase the fluidity of the cell surface.
In many cases, stressful conditions create structural disorder in cells. These influences have been called “”chaotropic,”” or chaos-producing. In red blood cells, which have sometimes been wrongly described as “”hemoglobin enclosed in a cell membrane,”” it has been known for a long time that lipid peroxidation of unsaturated fats weakens the cellular structure, causing the cells to be destroyed prematurely. Lipid peroxidation products are known to be “”chaotropic,”” lowering the rigidity of regions of cells considered to be membranes. But the red blood cell is actually more like a sponge in structure, consisting of a “”skeleton”” of proteins, which (if not damaged by oxidation) can hold its shape, even when the hemoglobin has been removed. Oxidants damage the protein structure, and it is this structural damage which in turn increases the “”fluidity”” of the associated fats.
So, it is probably true that in many cases the liquid unsaturated oils do increase “”membrane fluidity,”” but it is now clear that in at least some of those cases the “”fluidity”” corresponds to the chaos of a damaged cell protein structure. (N. V. Gorbunov, “”Effect of structural modification of membrane proteins on lipid-protein interactions in the human erythrocyte membrane,”” Bull. Exp. Bioles& Med. 116(11), 1364-67. 1993.
Although I had stopped using the uf gaurated seed oils years ago, and supposed that I wasn’t heavily saturated with toxins. saturated fat, when I first used coconut oil I saw an immediate response, that convinced me my metabolism was chronically inhibited by something that was easily alleviated by “”dilution”” or molecular competition. I had put a tablespoonful of coconut oil on some rice I had for supper, and half an hour later while I was reading, I noticed I was breathing more deeply than normal. I saw that my skin was pink, and I found that my pulse was faster than normal–about 98, I think. After an hour or two, my pulse and breathing returned to normal. Every day for a couple of weeks I noticed the same response while I was digesting a small amount of coconut oil, but gradually it didn’t happen any more, and I increased my daily consumption of the oil to about an ounce. I kept eating the same foods as before (including a quart of ice cream every day), except that I added about 200 or 250 calories per day as coconut oil. Apparently the metabolic surges that happened at first were an indication that my body was compensating for an anti-thyroid substance by producing more thyroid hormone; when the coconut oil relieved the inhibition, I experienced a moment of slight hyperthyroidism, but after a time the inhibitor became less effective, and my body adjusted by producing slightly less thyroid hormone. But over the next few months, I saw that my weight was slowly and consistently decreasing. It had been steady at 185 pounds for 25 years, but over a period of six months it dropped to about 175 pounds. I found that eating more coconut oil lowered my weight another few pounds, and eating less caused it to increase.
NOTE: You can buy coconut oil in most health food stores. It is available in the “”unrefined”” form in the oil section under the name of Spectrum. It may also be found in the cosmetics section of the store in jars in the “”refined”” form, or you can buy it online from the above-noted link. I prefer using the refined oil when cooking and the unrefined oil if I eat it straight from the jar. W. Greene, D.C.
Re: Coconut oil and raging controversy
Date: 01 Jun 1999
Yes, EM, I read Ray Peat’s articles and I remember the post on ZoneTalk that you are referring to. I probably would have discounted Peat’s article had it not been for the articles written by Enig. And, you are so right about “”partially hydrogenated”” oils – truly bad stuff.
I only saute with olive oil and I never fry anything, so I don’t really have any reason to use coconutromi and I doubt that I’ll be including it in my diet anytime soon. However, I do use a little butter practically every day.
Here’s some background on Mary Enig: She is a nutritionist widely known for her research on the nutritional aspects of fats and oils, is a consultant, clinical researcher and the Director of the Nutritional Sciences Division of Enig Associates, Inc., Silver Spring, Maryland. She received her PhD in Nutritional Sciences from the University of Maryland, College Park in 1984, taught a graduate course in nutrient- drug interactions for the University’s Graduate Program in Nutritional Sciences, and held a Faculty Research Associateship from 1984 through y sa with the Lipids Research Group in the Department of Chemistry and Biochemistry. Dr. Enig is a Fellow of the American College of Nutrition, and a member of the American Institute of Nutrition. Her many years of experience as a “”bench chemist”” in the analysis of food fats and oils, provides a foundation for her active roles in food labeling and composition issues at the federal and state levels.
Dr. Enig is a Consulting Editor to the “”Journal of the American College of Nutrition”” and formerly served as a Contributing Editor to “”Clinical Nutrition.”” She has published 14 scientific papers on the subject of food fats and oils, several chapters on nutrition for books, and presented over 35 scientific papers on food and nutrition topics. She is the President of the Maryland Nutritionists Association, past President of the Coalition of Nutritionists of Maryland and was appointed by the Governor in 1986 to the Maryland State Advisory Council on Nutrition and served as the Chairman of the Health Subcommittee until the Council was disbanded in 1988.
Pretty impressive and she is also involved in researching the effects of coconut oil on the HIV virus. Here’s more on what she has to say:
MARY ENIG Ph.D. ON THE EFFECTS OF COCONUT OIL ON SERUM CHOLESTEROL LEVELS AND HDLs
Dr. Mary Enig MS (Nutritional Sciences), Ph.D. did original research that showed a positivewas k between vegetable oil and cancer and a negative correlation for animal fat. She originated comprehensive analysis of trans fatty acid components of over 200 foods. Trans fatty acids are formed when vegetable oils are hydrogenated or heated to high temperatures. With high temperatures, trans fatty acids are fats that are twisted, which alter their natural “”cis”” shape. She studied how the trans fatty acids from foods affected the liver’s mixed function oxidase enzyme system that metabolizes drugs and environmental pollutants in the body. An important finding of thi neutter stubateas that laboratory animals fed experimental diets containing trans fatty acids have altered activity of this enzyme system. These results were partly responsible for the review of the “”Health Aspects of Dietary Trans Fatty Acids”” held by the Federation of American Societies for Experimental Biology, Life Sciences Research Office, at the request of the Food and Drug Administration. Mary Enig has had 17 articles published in scientific journals since 1976. In 1986, she was appointed by the Governor of Maryland to the “”State Advisory Council on Nutrition.”” She was contributing editor to “”Clinical Nutrition”” magazine and consulting editor for the “”Journal of the American College of Nutrition.”” She has given over 50 seminars and lectures on since 1979 on foods and nutrition topics.
In an article published in the Indian Coconut Journal, Sept., 1995, Dr. Enig stated that “”Ancel Keys is largely responsible for starting the anti-saturated fat agenda in the United States.”” She quoted Keys as saying that “”All fats raise serum cholesterol; saturated fats raise and polyunsaturated fats lower serum cholesterol; Hydrogenated fats are the problem; Animal fats are the problem.”” Enig stated: “”As can be seen, his findings were inconsistent.””
Enig also stated: “”The problems for coconut oil started four decades ago when researchers fed animals hydrogenated coconut oillatet was purposely altered to make it completely devoid of any essential fatty acids…The animals fed the hydrogenated coconut oil (as the only fat source) naturally became essential fatty acid deficient; their serum cholesterol increased. Diets that cause an essential fatty acid deficiency always produce an increase in serum cholesterol levels as well as in increase in the atherosclerotic indices. The same effect has also been seen when other …highly hydrogenated oils such as cottonseed, soybean or corn oils have been fed; so it is clearly a function of the hydrogenated products, eirlen because the oil is esselsWhat about studies where animals were fed unprocessed coconut oil? Enig wrote: “”Hostmark et al (1980) compared the effects of diets containing 10% coconut oil and 10% sunflower oil on lipoprotein distribution in male Wistar rats. Coconut oil feeding produced significantly lower levels (p=0.05) of pre-beta lipoproteins (VLDL) and significantly higher (p=<0.01) alpha-lipoproteins (HDL) relative to sunflower feeding.”” (Editor’s note: HDLs are considered the good cholesterol as they prevent deposits of LDL cholesterol on artery walls.) She also cited a study by Awad (1981) on Wistar rats fed a diet of either 14% (natural) coconut oil or 14% safflower oil. She stated:””Total tissue cholesterol accumulation for animals on the safflower diet was six times greater than for animals fed the [unhydrogenated] coconut oil. A conclusion that can be drawn from some of the animal research is that feeding hydrogenated coconut oil devoid of essential fatty acids (EFA)…potentiates the formation of atherosclerosis markers. It is of note that animals fed regular coconut oil have less cholesterol deposited in their livers and other parts of their bodies.”” Enig also referred to epidemiological studies done by Kaunitz and Dayrit (1992) on ctly ut eating societies who found that “”available population studies show that dietary coconut oil does lead to high serum cholesterol nor to high coronary heart disease..”” It is noteworthy that hydrogenated coconut oil was not consumed by these coconut-eating societies; they only consumed natuy hecoconut oil.
Kaunitz and Dayrit noted in 1989 that Mendis et al reported when Sri Lankan males were changed from their normal diet of natural coconut oil to corn oil, their LDL cholesterol declined 23.8% which is good news, but their HDL cholesterol declined 41.4% which is bad news. This created a more unfavorable LDL/HDL ratio meaning that on the corn oil diet there would be more cholesterol depositing on the artery walls than on the coconut oil diet. In plain English, a diet using liquid corn oil will lead to cholesterol deposits faster than a diet using natural coconut oil. Natural coconut oil, by increasing the good HDL cholesterol, may help prevent atherosclerosis and heart disease. Enig cited several other studies in her article that showed that natural coconut oil (not hydrogenated coconut oil) had health benefits markers indicating that coconut oil was more beneficial in preventing heart disease than most vegetable oils. Enig also cited the research of Tholstrup et al (1994) on natural (NOT hydrogenated) palm kernel oil, which is high in lauric acid and also contains myristic acid. Tholstrup found that with palm kernel oil, “”HDL cholesterol levels increased significantly from baseline values.””
Enig reported in her article that the effects of coconut oil on persons with low cholesterol levels was the opposite of persons with high cholesterol levels. Of persons with low total cholesterol levels, she wrote that “”there may be a rising of serum cholesterol, LDL cholesterol and especially HDL cholesterol.”” In persons with high cholesterol levels, “”there is lowering of total cholesterol and LDL cholesterol.”” The studies she cited showed that in both groups the LDL/HDL ratio moved in a favorable direction. In persons with AIDS or immune-compromised from other causes, the conclusions of this research are profound. It means everything the public has been told about vegetable oils on television for the past 15 years has been half truths and leading the public to the wrong conclusions. The public has been led to believe that tropicals will clog your arteries and cause heart disease. In fact, the opposite is true; natural tropical oils will help prevent hardening of the arteries while most liquid vegetable oils will increase hardis. is * Hhe arteries! In a phone call to Mary Enig in April, 1997, she told me that the worst oil to use for any purpose is Canola oil. When used in cooking, it produces the very high levels of trans fatty acids.
MARY ENIG Ph.D. ON NATURAL COCONUT OIL FOR AIDS and OTHER VIRAL INFECTIONS
On July 19, 1995, Enig was quoted in an article published in The HINDU, India’s National Newspaper as stating that coconut oil is converted by the body into “”Monolaurin”” a fatty acid with anti-viral properties that might be useful in the treatment of AIDS. The staff reporter for The HINDU wrote about Enig’s presentation at a press conference in Kochi and wrote the following:
“”There was an instance in the US in which an infant tested HIV positive had become HIV negative. That it was fed with an infant formula with a high coconut oil content gains significance in this context and at present an effort was on to find out how the “”viral load”” of an HIV infected baby came down when fed a diet that helped in the generation of Monolaurin in the body.””
The reporter commented on Enig hre observations that “”Monolaurin helped in inactivating other viruses such as measles, herpes, vesicular stomatitis and Cytomegalovirus (CMV) and that research undertaken on coconut oil so far also indicated that it offered a certain measure of protecton against cancer-inducing substances.
In another article published in the Indian Coconut Journal, Sept., 1995, Dr. Enig stated:
“”Recognition of the antimicrobial activity of the monoglyceride of lauric acid (Monolaurin) has been reported since 1966. The seminal work can be credited to 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 strains of enveloped viruses. The envelope of these viruses is a lipid membrane.””
Enig stated in her article that Monolaurin, of which the precursor is lauric acid, disrupted the lipid membranes of envelope viruses and also inactivated bacteria, yeast and fungi. She wrote:””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 ..in the envelope of the virus causing the disintegration of the virus envelope.”” In India, coconut oil is fed to calves to treat Cryptosporidium as reported by Lark Lands Ph.D. in her upcoming book “”Positively Well”” (1).
While HHV-6A was not mentioned by Enig, HHV-6A is an enveloped virus and would be expected to disintegrate in the presence of lauric acid and/or Monolaurin. Some of the pathogens reported by Enig to be inactivated by Monolaurin include HIV, measles, vercular stomatitis virus (VSV), herpes simplex virus (HSV-1), visna, cytomegalovirus (CMV? aC Influenza virus, Pneumonovirus, Syncytial virus and Rubof c. Some bacteria inactivated by Monolaurin include listeria, Staphylococcus aureus, Streptococcusmulalactiae, Groups A, B, F and G streptococciill Gram-positive organisms; and gram-negative organisms, if treated with chelator.
Enig reported that only one infant formula “”Impact”” contains lauric acid while the more widely promoted formulas like “”Ensure”” do not contain lauric acid and often contain some hydrogenated fats (trans fatty acids). A modified ester of lauric acid, Monolaurin (available in capsules), is sold in health food stores and is manufactured by Ecological Formulas, Concord, CA.
ENIG ON A THERAPEUTIC DOSE
Based on her calculations on the amd re of lauric acid found in human Mother’s milk, Dr. Enig suggests a rich lauric acid diet would contain about 24 grams of lauric acid daily for the average adult. This amount could be found in about 3.5 tablespoons of coconut oil or 10 ounces of “”Pure Coconut Milk.”” Coconut Milk is made in Sri Lanka and imported into the United States. It can be found in health food stores and in local grocery stores in the International Foods section or in specialty grocery stores that sell products imported from Thailand, the Philippines or East India. About 7 ounces of raw coconut daily would contain 24 grams of lauric acid. 24 grams of lauric acid is the therapeutic daily dose for adults suggested by Mary Enig based on her research of the lauric acid content of mother’s milk.
Health and Nutritional Benefits from Coconut Oil: An Important Functional Food for the 21st Century
by Mary G. Enig, Ph.D.
Presented at the AVOC Lauric Oils Symposium, Ho Chi Min City, Vietnam, 25 April 1996
Coconut oil has a unique role in the diet as an important physiologically functional food. The health and nutritional benefits that can be derived from consuming coconut oil have been recognized in many parts of the world for centuries. Although the advantage of regular consumption of coconut oil has been under appreciated by the consumer and producer alike for the recent two or three decades, its unique benefits should be compelling for the health minded consumer of today. A review of the diet/heart disease literature relevant to coconut oil clearly indicates that coconut oil is at worst neutral with respect to atherogenicity of fats and oils and, in fact, is likely to be a beneficial oil for prevention and treatment of some heart disease. Additionally, coconut oil provides a source of antimicrobial lipid for individuals with compromised immune systems and is a non-promoting fat with respect to chemical carcinogenesis.
Mr. Chairman and members of the ASEAN Vegetable Oils Club, I would like to thank you for inviting me to participate in this Lauric Oils Symposium. I am pleased to have the opportunity to review with you some information that I hope will help redress some of the anti-tropical oils rhetoric that has been so troublesome to your industry.
I will be covering two important areas in my presentation. In the first part, I would like to review the history of the major health challenge facing coconut oil today. This challenge is based on a supposed negative role played by saturatedeven in heart disease. I hope to dispel any acceptance of this notion with the information I will present to you today. I will show you how both animal studies and human studies have exonerated coconut oil of causing the problem.
In the second part of my talk I will suggest some new directions where important positive health benefits are seen for coconut oil. These benefits stem from coconut oil’s use as a food with major anti-microbial and anticancer benefits. I will present to you some of the rationale for this effect and some of the supporting literature.
The health and nutritional benefits derived from coconut oil are unique and compelling. Although the baker and food processor have recognized the functional advantages of coconut oil in their industry, over most competing oils, for many years, I believe these benefits are under-apiddeiated today by both the producer and the consumer. It is time to educate and reeducate all those who harbor this misinformation.
Historically, coconuts and their extracted oil have served man as important foods for thousands of years. The use of coconut oil as a shortening was advertised in the United States in popular cookbooks at the end of the 19th century. Both the health-promoting attributes of coconut oil and those functional properties useful to the homaker recognized 100 years ago. These same attributes in addition to some newly discovered ones, should be of great interest to both the producing countries as well as the consuming countries.
II. ORIGINS OF THE DIET/HEART HYPOTHESIS
Although popular literature of epidemiological studies usually attribute an increased risk of coronary heart disease (CHD) to elevated levels of serum cholesterol, which in turn are thought to derive from a dietary intake of saturated fats and cholesterol. But, saturated fats may be considered a major culprit for CHD only if the links between serum cholesterol and CHD, and between saturated fat and serum cholesterol are each firmly established. Decades of large-scale tests and conclusions there from have purported to establish the first link. In fact, this relationship has reached the level of dogma. Through the years metabolic ward and animal studies have claimed that dietary saturated fats increase serum cholesterol levels, thereby supposedly establishing the second link. But the scientific basis for these relationships has now been challenged as resulting from large-scale misinterpretation and misrepresentation of the data. (Enig 1991, Mann 1991, Smith 1991, Ravnskov 1995).
Ancel Keys is largely responsible for starting the anti-saturated fat agenda in the United States. From 1953 to 1957 Keys made a series of statements regarding the atherogenicity of fats. These pronouncements were: “”All fats raise serum cholesterol; Nearly half of total fat comes from vegetable fats and oils; No difference between animal and vegetable fats in effect on CHD (1953); Type of fat makes no difference; Need to reduce margarine and shortening (1956); All fats are comparable; Saturated fats raise and polyunsaturated fats lower serum cholesterol; Hydrogenated vegetable fats are the problem; Animal fats are the problem (1957-1959).
As can be seen, his findings were inconsistent.
What was the role of the edible oil industry in promoting the diet/heart hypothesis?
It is important to realize that at that time (1960s) the edible oil industry in the United States seized the opportunity to promote its polyunsaturates. The industry did this by developing a health issue focusing on Key’s anti-saturated fat bias. With the help of the edible oil industry lobbying in the United States, federal government dietary goals and guidelines were adopted incorporating this mistaken idea that consumption of saturated fat was causing heart disease. This anti-saturated fat issue became the agenda of government and private agencies in the US and to an extent in other parts of the world. This is the agenda that has had such a devastating effect on the coconut industry for the past decade. Throughout the 1960s, the 1970s, the 1980s, and the 1990s, the anti-saturated fat rhetoric increased in intensity.
What are some of the contradictions to the hypothesis blaming saturated fat?
Recently, an editorial by Harvard’s Walter Willett, M.D. in the American Journal of Public Health (1990) acknowledged that even though “”the focus of dietary recommendations is usually a reduction of saturated fat intake, no relation between saturated fat intake and risk of CHD was observed and was the most informative prospective study to date.”” In yet another editorial, this time by Framingham’s William P. Castelli in the Archives of Internal Medicine (1992), declared for the record that “”…in Framingham, Mass, the more saturated fat one ate, the more cholesterol one ate, the more calories one ate, the lower the person’s serum cholesterol… the opposite of what the equations provided by Hegsted at al (1965) and Keys et al (1957) would predict…””
Castelli further admitted that “”…In Framingham, for example, we found that the people who ate the most cholesterol, ate the most saturated fat, ate the most calories, weighed the least, and were the most physically active.””
III. COCONUT OIL AND THE DIET/HEART HYPOTHESIS
For the past several decades you have heard about animal and human studies feeding coconut oil that purportedly showed increased indices for cardiovascular risk. 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 A…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.
How did coconut oil get such a negative reputation?
The question then is, how did coconut oil get such a negative reputation? The answer quite simply is, initially, the significance of some changes that occurred during some feeding studies were misunderstood. The wrong protocol was then repeated until ultimately the misinformation and disinformation took on a life of its own.
The problems for coconut oil started four decades ago when researchers fed animals hydrogenated coconut oil that was purposefully altered to make it completely devoid of any essential fatty acids. The hydrogenated coconut oil was selected instead of hydrogenated cotton seed, corn or soybean oil because it was a soft enough fat for blending into diets due to the presence of the lower melting medium chain saturated fatty acids. The same functionality could not be obtained from the cottonseed, corn or soybean oils if they were made totally hydrogenated, since all their fatty acids were long chain and high melting and could not be easily blended nor were they as readily digestible.
The animals fed the hydrogenated coconut oil (as the only fat source) naturally became essential fatty acid deficient; their serum cholesterol levels increased. Diets that cause an essential fatty acid deficiency always produce an increase in serum cholesterol levels as well as an increase in the atherosclerotic indices. The same effect has also been seen when other essential fatty acid deficient, highly hydrogenated oils such as cottonseed, soybean, or corn oils have been fed; so it is clearly a function of the hydrogenated product, either because the oil is essential fatty acid (EFA) deficient or because of trans fatty acids (TFA).
What about the studies where animals were fed with unprocessed coconut oil?
Awad (1981) compared the effects of diets containatur%25 coconut oil, 14% safflower oil or a 5% “”control”” (mostly soybean) oil on accumulation of cholesterol in tissues in male Wistar rats. The synthetic diets had 2% added corn oil with a total fat of 16% Total tissue cholesterol accumulation for animals on the safflower diet was six times greater than for animals fed the coconut oil, and twice that of the animals fed the control oil.
A conclusion that can be drawn from some of this animal research is that feeding hydrogenated coconut oil devoid of essential fatty acids (EFA) in a diet otherwise devoid of EFA leads to EFA deficiency and potentiates the formation of atherosclerosis markers. It is of note that animals fed regular coconut oil have less cholesterol deposited in their livers and other parts of their bodies.
What about the studies where coconut oil is part of the normal diet of human beings?
Kaunitz and Dayrit (1992) have reviewed some of the epidemiological and experimental data regarding coconut-consuming 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 them below the acceptable lower limit) and the LDL/HDL ratio increased 30% from 3.0 to 3.9. These latter two changes would be considered quite undesirable. As noted above, Kurup and Rajmohan (1995) studied the addition of coconut oil alone to previously mixed fat diets and report no significant difference
Previously, Prior et al (1981) had noted that islanders with high intake 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.
What about the studies where coconut oil was deliberately fed to human beings?
Some of the studies reported trobly and more years ago should have cleared coconut oil of any implication in the development of coronary heart disease (CHD).
For example, when Frantz and Carey (1961) fed an additional 810 kcal/day fat supplement for a whole month to males with high normal serum cholesterol levels, there was no significant difference from the original levels even though the fat supplement was hydrogenated coconut oil.
Halden and Lieb (1961) also showed similar results in a group of hypercholesterolemics when coconut oilate included in their diets. Original serum cholesterol levels were reported as 170 to 370 mg/dl. Straight coconut oil produced a range from 170 to 270 mg/dl. Coconut oil combined with 5% sunflower oil and 5% olive oil produced a range of 140 to 240 mg/dl.
Earlier, Hashim and colleagues (1959) had shown quite clearly that feeding a fat supplement to hypercholesterolemics, where half of the supplement (21% of energy) was coconut oil (and the other half was safflower oil), resulted in significant reductions in total serum cholesterol. The reductions averaged -29% and ranged from -6.8 to -41.2%.
And even earlier, Ahrens and colleagues (1957) had shown that adding coconut oil to the diet of hypercholesterolemics lowers serum cholesterol from, e.g., 450 mg/dl to 367 mg/dl. This is hardly a cholesterol-raising effect.
Bierenbaum et al (1967) followed 100 young men with documented myocardial infarction for 5 years on diets with fat restricted to 28% of energy. There was no significant difference between the two different fat mixtures (50/50 corn and safflower oils or 50/50 coconut and peanut oils), which were fed as half of the total fat allowance; both diets reduced serum cholesterol. This study clearly showed that 7% of energy as coconut oil was as beneficial to the 50 men who consumed it as for the 50 men who consumed 7% of energy as other oils such as corn oil or safflowAMore recently, Sundram et al (1994) fed whole foods diets to healthy normo-cholesterolemic males, where approximately 30% of energy was fat. Lauric acid (C12:0) and myristic acid (C14:0) from cococonuoil supplied approximately 5% of energy. Relative to the baseline measurements of the subjects prior to the experimental diet, this lauric and myristic acid-rich diet showed an increase in total seruismsolesterol from 166.7 to 170.0 mg/dl (+1.9%), a decrease in low density lipoprotein cholesterol (LDL-C) from 105.2 to 104.4 mg/dl (-0.1%), an increase in high density lipoprotein cholesterol (HDL-C) from 42.9 to 45.6 mg/dl (+6.3%). There was a 2.4% decrease in the LDL-C/HDL-C ratio from 2.45 to 2.39. These findings indicate a favorable alteration in serum lipoprotein balance was achieved when coconut oil was included in a whole food diet at 5% of energy.
Tholstrup et al (1994) report similar results with whole foods diets high in lauric and myristic acids from palm kernel oil. The HDL cholesterol levels increased significantly from baseline values (37.5 to 46.0 mg/dl, P<0.01) and the LDL-C/HDL-C ratios decreased from 3.08 to 2.69. The increase in total cholesterol was from 154.7 (baseline) the c0.9 mg/dl on the experimental diet.
Ng et al (1991) fed 75% of the fat ration as coconut oil (24% of energy) to 83 adult normo-chlosterolemics (61 males and 22 females). Relative to baseline values, the highest values on the experimental diet for total cholesterol was increased 17% (169.6 to 198.4 mg/dl), HDL cholesterol was increased 21.4% (44.3 to 53.8 mg/dl), and the LDL-C/HDL-C ratio was decreased 3.6% (2.51 to 2.42).
When unprocessed coconut oil is added to an otherwise normal diet, there is frequently no change in the serum cholesterol although some studies have shown a decrease in total cholesterol.
It appears from many of the research reports that the effect coconut oil has on serum cholesterol is the opposite in individuals with low serum cholesterol values and those with high serum values. We see that there may be a raising of serum total cholesterol, LDL cholesterol and especially HDL cholesterol in individuals with low serum cholesterol. On the other hand there is lowering of total cholesterol and LDL cholesterol in hypercholesterolemics as noted above.
Studies that supposedly showed a hypercholesterolemic effect of coconut oil feeding, in fact, usually only showed the oil was not as effective at lowering the serum cholesterol as was the more unsaturated fat 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 and 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).
Should coconut oil be used to prevent coronary heart disease?
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 is suggestive that there is a causative role for the herpes virus and cytomeglvirus in the initial formation of atherosclerotic plaques and the re-clogging of arteries after angioplasty (New York Times 1991) What is so interesting is that the herpes virus and cytomegalovirus are both iof sited by the anti-microbial 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.
Perhaps more important than any effect of coconut oil on serum cholesterol is the additional effect of coconut oil on the disease fighting capability of the animal or person consuming the coconut oil.
IV. COCONUT OIL AND CANCER
Lim-Sylianco (1987) has reviewed 50 years of literature showing anti-carcinogenic effects from dietary coconut oil. These animal studies show quite clearly the non-promotional 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 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 non-promotional 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 anti-microbial 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. Ttelyonoglyceride 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.
¥e AKabara (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 n a FAs and MGs are additive and total concentration is critical for inactivating viruses (Isaacs and Thormar 1990).
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 of the plasma membrane.
Some of the viruses inactivated by these lipids, theddition to e dr2C are the measles virus, herpes simplex virus-1 (HSV-1), vesicular stomatitis faxus (VSV), visna virus, and cytomegalovirus (CMV). Many of the pathogenic organisms ren ised 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).
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 consumptugh of lauric acid. This type of change in diet has an effect on the fatty acids the body has available for metabolic activities.
VI. LAURIC ACID IN FOODS
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 produciswitountries 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 our 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.
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 brand). However, tmort cookies make up a small portion of the cookie market. Most cookies made 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 thwhy her 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 and coconut oil fits the designation of very important functional foods.