The Coconut Oil Miracle

Home > Other > The Coconut Oil Miracle > Page 5
The Coconut Oil Miracle Page 5

by Bruce Fife


  The early explorers who visited the South Sea islands in the sixteenth and seventeenth centuries described the islanders as being exceedingly strong, vigorously built, beautiful in body, and kindly disposed. The islanders gained a reputation for their beauty, excellent physical development, and good health. Some of the islands were viewed as the equivalent to the Garden of Eden where the inhabitants were near perfect in stature and appearance. Such observations may have even fueled interest in the folklore of a fountain of youth. Tales of a mystical island containing such a fountain had been popular for centuries in Europe and led explorers, such as Juan Ponce de Leon, to search in vain for the mythical waters. While a fountain whose waters brought eternal youth was not to be found, the islanders did have a fountain of youth of sorts. That fountain was in the fruit of the coconut tree, the Tree of Life, as they call it. The coconut, with its life-giving water (the oil and milk), bestowed a level of youthful health on these people that far surpassed that of their European visitors.

  It wasn’t until relatively recently that science began to unlock the secrets to the islanders’ good health and discover the many healing miracles of coconut oil. Through the pioneering research of people like Weston A. Price, Ian A. Prior, Jon J. Kabara, and others, we now know that it was the coconut-based diet that was largely responsible for the Islanders’ good health and youthful appearance. It was and still is the reason Pacific Islanders don’t get heart disease.

  THE PUKAPUKA AND TOKELAU STUDIES

  It has long been observed that people of the Pacific Islands and Asia, whose diets are high in coconut, are surprisingly free from cardiovascular disease, cancer, and other degenerative diseases. Some of the most thorough research conducted on people who have a high-fat diet derived primarily from coconuts is the Pukapuka and Tokelau Island study. This was a long-term multidisciplinary study set up to evaluate the health of those living on island atolls and the consequences of migrating to New Zealand, where they are exposed to Western foods and influences. The Tokelau and Pukapuka studies were begun in the early 1960s and included the entire populations of both islands, which was about 2,500 people.

  The islands of Pukapuka and Tokelau lie near the equator in the South Pacific. Pukapuka is an atoll in the Northern Cooks Islands, and Tokelau, another atoll, lies about 400 miles southeast. Both are under the jurisdiction of New Zealand. The populations of both islands have been relatively isolated from Western influences. Their native diet and culture remain much as they have for centuries. Pukapuka and Tokelau are among the more isolated Polynesian islands and have had relatively little interaction with non-Polynesians.

  The coral sands of these atolls are porous, lack humus, and will not support the food plants that flourish on other tropical islands. Coconut palms and a few starchy tropical fruits and root vegetables supply the vast majority of the diet for the population. Fish from the ocean, pigs, and chickens make up what little meat they eat. Some flour, rice, sugar, and canned meat are obtained from small cargo ships that occasionally visit the islands. Their diet is high in fiber but low in sugar.

  The standard diet on both islands is high in fat derived from coconuts but remains low in cholesterol. Every meal contains coconut in some form: the green nut provides the main beverage; the mature nut, grated or as coconut cream, is cooked with taro root, breadfruit, or rice; and small pieces of coconut meat make an important snack food. Plants and fruitfish are cooked with coconut oil. In Tokelau, coconut sap or toddy is used as a sweetener and as leavening for bread.

  The researchers reported that 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, and 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 were rare, constipation uncommon. The people averaged two or more bowel movements a day. Atherosclerosis, heart disease, colitis, colon cancer, hemorrhoids, ulcers, diverticulosis, and appendicitis are conditions with which they were generally unfamiliar.

  SATURATED-FAT CONSUMPTION

  The American Heart Association recommends that we get no more than 30 percent of our total calories from fat and that saturated fat should be limited to no more than 10 percent, but the Tokelauans apparently aren’t aware of these guidelines—nearly 60 percent of their energy is derived from fat, and almost all of that is saturated fat derived largely from coconuts. The fat in the Pukapukan diet is also primarily from saturated fatty acids from coconut, with total energy from fat at 35 percent.

  Most Americans and others who eat typical Western diets get 32–38 percent of their calories from fat, most of which is in the form of unsaturated vegetable oils. Yet they still suffer from numerous degenerative conditions and weight problems. In contrast, the islanders in this study consumed as much or more total fat and a far greater amount of saturated fat than typical Americans yet were relatively free from degenerative disease and generally lean and healthy.

  Dr. Ian A. Prior and his colleagues calculated the cholesterol levels of the islanders based on rates observed in Western countries. The islanders’ actual blood cholesterol levels were 70 to 80 milligrams lower than predicted, ranging from about 170 to 208 milligrams per deciliter. Cholesterol levels of the Tokelauans were the higher of the two because they derived 57 percent of total calories from fat, about 50 percent from saturated fat. Their total food consumption, including imported flour, rice, sugar, and meat, was also higher. Dietary cholesterol and polyunsaturated fatty acids of both groups were low. Dr. Prior noted that vascular disease is uncommon in both populations, and there is no evidence that the high-saturated-fat intake from coconut has a harmful effect.

  DIETARY CHANGES AFFECT HEALTH STATUS

  The migration of Tokelau Islanders from their island atolls to the very different environment of New Zealand was associated with changes in fat intake that indicate increased risk of atherosclerosis. The migration was also associated with an actual decrease in saturated fat intake from about 50 percent to 41 percent of energy, an increase in dietary cholesterol intake to 340 milligrams, and an increase in polyunsaturated fat and sugar. Fat changes included increased total cholesterol, higher LDL (bad cholesterol) and triglycerides, and lower HDL (good cholesterol) levels.

  The blood cholesterol of Tokelau Islanders increased when they migrated to New Zealand, despite the fact that the total fat content of their diet dropped, declining from 57 percent in Tokelau, with 80 percent of that from coconut oil, to around 43 percent in New Zealand. They ate more white bread, rice, meat, and other Western foods and less of their high-fiber, coconut-rich foods.

  The conclusion we can make from these island studies is that a high-saturated-fat diet consisting of coconut oil is not detrimental to health and does not contribute to arteriosclerosis. Indeed, those people who eat coconut oil in place of other vegetable oils are amazingly free from the degenerative diseases that are so common in the West. They also have nearly ideal body weight and appear to be examples of perfect health. But when these people replace coconut oil in their diets with other oils and processed foods (which are typically loaded with polyunsaturated and hydrogenated oils) their health declines.

  SATURATED FAT AND CHOLESTEROL

  Saturated fat has been labeled a dietary villain that should be avoided at all costs. We buy lean cuts of meat, nonfat milk, and low-fat foods of all types in order to limit our intake of this dreaded substance. But why is saturated fat so bad? There is really only one suggested reason: saturated fat is easily converted by the liver into cholesterol, which can raise blood cholesterol levels, increasing the risk of heart disease.

  But, contrary to popular belief, neither saturated fat nor cholesterol cause heart disease. This is a fact that all fat researchers and medical professionals know but many of the rest of us do not. High blood
cholesterol is only one of many so-called risk factors associated with heart disease. What this means is that those people who have heart disease sometimes also have elevated blood cholesterol levels. Not all people with high blood cholesterol develop heart disease, and not everyone with heart disease has high blood cholesterol. If high blood cholesterol were the cause of heart disease, everybody who dies from this disease would have elevated cholesterol levels, but they don’t. In fact, most people who have heart disease do not have high blood cholesterol.

  Other risk factors associated with heart disease include high blood pressure, age, gender (being male), tobacco use, diabetes, obesity, stress, lack of exercise, insulin levels, and homocysteine levels. High blood cholesterol is no more the cause of heart disease than age or male gender is. It’s guilty only by association.

  Blood level of homocysteine is one of the most accurate of the risk factors. Recent research has shown that elevated homocysteine levels in the blood are much more strongly associated with heart disease than cholesterol. Homocysteine is an amino acid derived from protein found in meat, milk, and other foods. Homocysteine may help raise blood cholesterol, and the association of high blood cholesterol with heart disease may result more from homocysteine (derived primarily from protein found in meat and dairy products) than from cholesterol (or saturated fat).

  The term “artery-clogging saturated fat” is a misnomer. The fat that collects in arterial plaque is primarily unsaturated fats (74 percent) and cholesterol. Saturated fat does not collect in the arteries like poly-and monounsaturated fats because it is not easily oxidized, and only oxidized fat ends up as arterial plaque. Vegetables oils are easily oxidized by overprocessing and heating. Furthermore, saturated fat is not the only substance that your liver converts into cholesterol. Other fats, and even carbohydrate, the main nutritional component of all fruits, vegetables, and grains, also end up as cholesterol in our bodies. To infer that only saturated fat raises blood cholesterol is grossly inaccurate and misleading.

  COCONUT OIL AND CHOLESTEROL

  All of the criticism that has been aimed at coconut oil is based primarily on the fact that it is a saturated fat and saturated fat is known to increase blood cholesterol. No legitimate research, however, has ever demonstrated any proof that natural, nonhydrogenated coconut oil adversely affects blood cholesterol levels. In fact, numerous studies have clearly demonstrated that coconut oil has a neutral effect on cholesterol levels.

  The reason coconut oil does not adversely affect cholesterol is because it is composed primarily of medium-chain fatty acids. These fatty acids are different from those commonly found in other food sources and are burned almost immediately for energy production, and so they are not converted into body fat or cholesterol to the degree other fats are and do not affect blood cholesterol levels.

  While coconut oil’s direct effect on blood cholesterol has generally been shown to be neutral, it may indirectly lower LDL (bad) cholesterol and increase HDL (good) cholesterol by stimulating metabolism (see chapter 5 for a more complete discussion on metabolic effects). In one study performed in the Philippines, for example, 10 medical students tested diets consisting of different levels of animal fat and coconut oil. Animal fat is known to raise blood cholesterol. Total calories from dietary fat consisted of 20 percent, 30 percent, and 40 percent, using different combinations of coconut oil and animal fat. At all three levels with a ratio of 1 to 1, 1 to 2, and 1 to 3, animal fat to coconut oil, no significant change in cholesterol levels was observed. Only when the ratio was reversed so that animal fat consumption was greater than coconut oil and when total fat calories reached 40 percent was a significant increase in blood cholesterol reported. This study demonstrated that not only did coconut oil not have a bad effect on cholesterol levels, it even reduced the cholesterol-elevating effects of animal fat.

  CLOTTING AND HEART DISEASE

  One of the important factors that influences cardiovascular health is the blood’s tendency to form clots. When you cut yourself, proteins in your blood called platelets stick together and form a clot, which prevents your bleeding to death. In healthy people, the blood becomes sticky only when it comes in contact with a wound or injury. But when platelets stick to arterial walls, they can form dangerous clots that can block the flow of blood and cause a heart attack or stroke. In recent heart attack victims, the blood in their bodies has been found to be about 4.5 times stickier than that in normal people.

  As a result, many doctors warn against saturated fat, as it has been blamed for increasing platelet adhesiveness (blood stickiness), thus promoting the development of blood clots. Some of the long-chain saturated fats, like those found in beef fat, lard, and butter, do increase platelet stickiness. But what is often left unsaid is that most polyunsaturated fats found in vegetable oils also promote clotting. In fact, all dietary oils, both saturated and unsaturated, with the exception of the omega-3 fatty acids (e.g., flaxseed oil, fish oil) and the medium-chain fatty acids(e.g., tropical oils), increase platelet stickiness. Even the so-called heart-healthy olive oil increases blood clot risk. So when you eat corn, safflower, soybean, cottonseed, canola, and peanut oils you are increasing your risk of suffering a heart attack or stroke. Eating omega-3 fatty acids and MCFAs, like coconut oil, has the opposite effect on blood platelets. Medium-chain fatty acids are burned up immediately after consumption and therefore do not affect platelet stickiness either one way or the other. Studies have revealed that populations who traditionally consume large quantities of coconut as a part of their diet have a low incidence of health problems associated with blood clotting, including heart disease and stroke.

  ATHEROSCLEROSIS AND HEART DISEASE

  To understand how coconut oil can help prevent heart disease, you need to have a basic understanding of how the disease develops. Heart disease is caused by atherosclerosis, or hardening of the arteries, which is manifested by the formation of plaque in the arteries. If you asked most people what causes atherosclerosis, they would probably tell you it was from too much cholesterol in the blood. But cholesterol doesn’t simply come dancing freely down the artery and suddenly decide to stick somewhere. In fact, cholesterol isn’t even necessary for atherosclerosis or the formation of plaque. The body uses cholesterol to patch up and repair injuries to the arterial wall. Contrary to popular belief, the principle component of arterial plaque is not cholesterol but protein, mainly in the form of scar tissue. Some atherosclerotic arteries actually contain little or no cholesterol.

  According to the response-to-injury hypothesis, atherosclerosis initially develops as a result of injury to the inner lining of the arterial wall. The injury can be the result of a number of factors such as toxins, free radicals, viruses, or bacteria. If the cause of the injury is not removed, further damage may result, and as long as irritation and inflammation persist, scar tissue continues to develop.

  When blood-clotting proteins (platelets) encounter an injury, they become sticky and adhere to each other and to the damaged tissue, acting somewhat like a bandage to facilitate healing. This is how blood clots are formed. Injury from any source triggers platelets to clump together, or clot, and arterial cells to release protein growth factors that stimulate growth of the muscle cells within the artery walls. A complex mixture of scar tissue, platelets, calcium, cholesterol, and triglycerides is incorporated into the site to heal the injury. This mass of fibrous tissue, not cholesterol, forms the principle material in plaque. The calcium deposits in the plaque cause the hardening, which is characteristic of atherosclerosis.

  Contrary to popular belief, plaque isn’t simply plastered along the inside of the artery canal like mud in a garden hose. It grows inside the artery wall, becoming part of the artery wall itself. Arterial walls are surrounded by a layer of strong circular muscles that prevent the plaque from expanding outward. As the plaque grows, because it can’t expand outward, it begins to push inward and close the artery opening, narrowing the artery and choking off blood flow.

  Injury occurs on
the inside surface of the artery.

  Plaque begins to develop inside artery wall.

  Plaque buildup causes the wall of the artery to bulge inward, restricting blood flow.

  Platelets gather at the site of injury to form blood clots, plugging the holes in the damaged vessel. But if the injury persists or if the blood is prone to clotting, clots may continue to grow to the point that they completely block the artery. An artery already narrowed by plaque can easily be blocked by blood clots. When this process occurs in the coronary artery, which feeds the heart, it is referred to as a heart attack. If it happens in the carotid artery, which goes to the brain, the result is a stroke.

  CHRONIC INFECTION AND ATHEROSCLEROSIS

  Although many risk factors are associated with heart disease, none has actually been proven to cause the illness. Lack of exercise is a risk factor just as high blood cholesterol is, but neither one actually causes heart disease. If lack of physical activity caused heart disease, then everyone who doesn’t exercise would die of a heart attack, but they don’t. Likewise, everyone with high cholesterol doesn’t get heart disease, and everyone who has heart disease doesn’t have high cholesterol. Risk is only an observed association and not necessarily a cause. A substantial proportion of people with heart disease, however, do not have any of the standard risk factors. The actual cause of heart disease is elusive and appears to be multifactorial.

 

‹ Prev