The Coconut Oil Miracle (8 page)

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. If you could reach inside the body and touch healthy blood cells while they were surging around your arteries, they would feel slippery. But in recent heart attack victims, the blood in their bodies has been found to be about 4.5 times stickier than that in people who have not experienced a heart attack. Under a microscope you would be able to see platelets sticking to each other and to arterial walls. This can result in the formation of clots, which can block the flow of blood and lead to a heart attack or stroke.

A common criticism of saturated fat is that it increases platelet adhesiveness (blood stickiness), thus promoting the development of blood clots. Some of the long-chain saturated fats do increase
platelet stickiness, but so do most polyunsaturated fats found in vegetable oils.

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 reduces that risk.

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. This idea is called the cholesterol or lipid hypothesis of heart disease. While still loudly proclaimed in the popular press (and by the soybean industry), this theory never really fit clinical observation or scientific studies and has since been replaced with the response-to-injury hypothesis.

What causes plaque to build up in the arteries and atherosclerosis to develop? When we think of hardened arteries we generally associate the condition with cholesterol. Cholesterol, however, doesn’t simply come dancing freely down the artery and suddenly decide to stick
somewhere. The body uses cholesterol to patch up and repair injuries to arterial walls. In fact, cholesterol isn’t even necessary for atherosclerosis or the formation of plaque. Contrary to popular belief, the principle component of arterial plaque is not cholesterol but protein (mainly scar tissue). Some atherosclerotic arteries 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 arterial canal like mud in a garden hose. It grows inside the artery wall, becoming part of the artery wall itself. (see illustrations
here
). 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.

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.

Figure 3.1. Injury occurs on the inside surface of the artery.

Figure 3.2. Plaque begins to develop inside artery wall.

Figure 3.3. Plaque buildup causes the wall of the artery to bulge inward, restricting blood flow.

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.

One area of investigation that is gaining a great deal of interest is the relationship between chronic infection and atherosclerosis. It appears that there is a cause-and-effect relationship associated with persistent low-grade infections and heart disease. Recent research has shown that certain microorganisms can cause or are at least involved in the development of arterial plaque, which leads to heart disease.

A large number of studies have reported associations between heart disease and chronic bacterial and viral infections. As far back as the 1970s researchers identified the development of atherosclerosis in the arteries of chickens when they were experimentally infected with a herpes virus. In the 1980s similar associations were reported in humans infected with a number of bacteria (e.g.,
Helicobacter pylori
and
Chlamydia pneumoniae
) and certain herpes viruses (particularly cytomegalovirus). In one study, for example, Petra Saikku and her colleagues at the University of Helsinki in Finland found that 27 out of 40 heart attack patients and 15 out of 30 men with heart disease carried antibodies related to chlamydia, which is more commonly known to cause gum disease and lung infections. In subjects who were free of heart disease, only 7 out of 41 had such antibodies. In another study at Baylor College of Medicine in Houston, Texas, researchers found that 70 percent of patients undergoing surgery for atherosclerosis carried antibodies to cytomegalovirus (CMV), a common respiratory infection, while only 43 percent of controls did.

More evidence supporting the link between infection and cardiovascular disease showed up in the early 1990s, when researchers found fragments of bacteria in arterial plaque. One of the first to discover microorganisms in atherosclerotic plaque was Brent Muhlestein, a cardiologist at the LDS Hospital in Salt Lake City and the University of Utah. Muhlestein and colleagues found evidence of chlamydia in 79 percent of plaque specimens taken from the coronary arteries of 90 heart disease patients. In comparison, fewer than 4 percent of normal individuals had evidence of chlamydia in artery walls. Animal studies provided more direct evidence that bacteria might contribute to chronic inflammation and plaque formation. Muhlestein showed that infecting rabbits with chlamydia measurably thickens the animals’ arterial walls. When the animals were given an antibiotic to kill the chlamydia, the arteries became more normal in size.

Some of the bacteria associated with atherosclerosis are also involved in the development of dental cavities and gum disease. Studies by James Beck of the University of North Carolina and others looked at dental data and found that those people with dental infections tended to have a higher rate of heart disease and strokes. These studies helped establish the link between dental health and heart disease. The connection between dental health and general health has been observed for decades. Weston A. Prince, D.D.S., observed this during his studies of the Pacific Islanders in the 1930s. Those who had the best overall health (who, by the way, were those who regularly ate coconuts and coconut oil) also had the best dental health.

At least one out of every two adults in developed countries has antibodies to
Helicobacter pylori, Chlamydia pneumoniae,
or cytomegalovirus (CMV). The presence of antibodies does not necessarily
indicate an active infection or the presence of atherosclerosis, but it is a sign that infection has occurred at some time. It’s common for infections from these organisms to persist indefinitely. Once one is infected with herpes, for example, the virus remains for life. The effectiveness of the immune system determines the degree of trouble the virus may cause. The weaker the immune system, the more likely an infection is to hang on and cause problems. When these microorganisms enter the bloodstream they can attack the artery wall, causing chronic low-grade infections that lack any noticeable symptoms. As microorganisms colonize an artery wall, they cause damage to arterial cells. In an effort to heal the injury, blood platelets, cholesterol, and protein combine in the artery wall, setting the stage for plaque formation and atherosclerosis. As long as the infection and inflammation persist, plaque continues to develop. Infection can both initiate and promote growth of atherosclerosis in arteries, which in turn leads to heart disease.

At this point, researchers are not ready to say that infection is responsible for every case of heart disease. Other factors (e.g., free radicals, high blood pressure, diabetes, etc.) can also cause injuries to the arterial wall and initiate plaque formation. And not all infections promote atherosclerosis. Only when the immune system is incapable of controlling the infection is there cause for alarm. Anything that may lower immune efficiency such as serious illness, poor diet, exposure to cigarette smoke, stress, and lack of exercise (i.e., many of the typical risk factors associated with heart disease) will also open up the body to chronic low-grade infections that can promote atherosclerosis.

We now know that, at least in some cases, heart disease may be treated with antibiotics. But antibiotics are limited because they
work only against bacteria, and infections caused by viruses remain unaffected. However, there is something that will destroy both the bacteria (
Helicobacter pylori
and
Chlamydia pneumoniae
) and viruses (CMV) that are most commonly associated with atherosclerosis, and that is MCFAs, or coconut oil. Yes, believe it or not, the MCFAs in coconut oil are known to kill all three of the major types of atherogenic organisms. These special fatty acids are harmless to us and even provide us nourishment and energy but are deadly to microorganisms that cause infection and illness. Research has shown that MCFAs from coconut oil can kill bacteria and viruses that cause influenza, herpes, bladder infections, gum disease, and numerous other conditions. Coconut oil provides a safe and effective way to prevent and even overcome many common illnesses. This topic is discussed in more detail in the following chapter.