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Healthy Living November Issue
HEART DISEASE:Conquering the Number One Killer


A Worldwide Problem

Sue never worried much about heart disease. Sure, her dad had died at 45 with a heart attack, but everyone knew that female hormones would protect her from heart problems at least until she went through menopause. Overnight, however, she was jolted back to reality. At the age of 40 her younger sister died with her first heart attack-before she went through the "change of life." Suddenly, Sue was confronted with what she feared deep inside all along: she was at risk of a heart attack.

Almost every American knows someone who has died of heart disease. Like Sue, you may have prematurely lost close relatives from this dreaded killer. Perhaps you have had neighbors, friends, or coworkers snatched away by heart disease. As a result of this killer’s predominance, most of us have at least occasionally wondered, "Will I be the next one with a heart attack?" Such concerns are warranted. Heart disease is the number one killer in the industrialized countries, as outlined in Figure 1: Heart Disease is Number One.1, 2

Contrary to popular misconceptions, heart disease is not only a disease of men. In America, heart disease is the leading killer of men and women alike. Despite all that medical science knows about how to prevent this disease, the latest statistics show that over 954,000 people died of diseases of the heart and blood vessels (cardiovascular disease) in the United States alone in 1994, up from 925,000 in 1992.3 Every 33 seconds an American dies of cardiovascular disease. Since 1900 the number one killer in the United States has been cardiovascular disease in every year but one (1918). When an airline crashes in the U.S. and hundreds of people die, the news is filled with this top story for days. In-depth analysis is performed and broadcast regarding the possible cause of the crash and how it might have been prevented. Consider that approximately 2600 deaths, many of them as sudden as in an airline crash, occur each day in the U.S. from cardiovascular disease alone. This is greater than 10 jumbo jet crashes per day. Yet, these deaths do not even make the news broadcasts except when a famous person dies from a heart attack, and then if the disease is mentioned at all, it is only as an afterthought, as if it was inevitable. The number one cause of death deserves more thorough attention in America.

Sadly, deaths only tell part of the story of this dreadful disease. Of the current U.S. population of about 258 million, more than 57 million people have some form of this disease.4 The annual cost to America for diseases of the heart and blood vessels is an astounding 259.1 billion dollars, which includes not only the medical and surgical treatment, but also lost productivity in the work force.5 If you personally happen to survive a stroke, the average lifetime cost in medical bills and lost earnings will be $103,576.6 How much better to prevent a stroke or a heart attack than to pay for one and still suffer the diminished quality of life that is almost certain to follow! No wonder Clyde Yancy, M.D., president of the American Heart Association’s Dallas division and researching cardiologist at the University of Texas Southwestern Medical Center in Dallas said recently, "No matter where somebody is in their maturity process, young, middle-aged, or old, incorporating a heart-healthy lifestyle is the most cost effective thing that can be done right now." Not only is it cost effective, but even more important will likely be life saving, and certainly will be life-enhancing!

How can the number of heart attacks be reduced? What can a person do to reduce the risk of a heart attack? Dr. Ivan Gyarfas, Chief of the World Health Organization’s Cardiovascular Disease Prevention Program, explains that prevention measures could save a significant number of people from premature death: "About twelve million people die [worldwide] every year of heart problems, but up to half of them could be saved if better prevention programs were in effect."7

Although better prevention programs could cut deaths due to heart disease (especially coronary heart disease) by about 50 percent, evidence suggests that optimal prevention programs could cut heart disease deaths by as much as 90 percent. In short, although heart disease is by far the number one cause of death in America, it does not need to be. Nine out of ten heart attacks may be preventable!



The Development of Heart and Blood Vessel Disease

Many people who have heart disease are not aware of it. This is because heart disease usually develops silently. Before any damage to the heart occurs, a process called atherosclerosis (or "hardening of the arteries") has been taking place in the arteries of the heart for many years. The early phase of atherosclerosis is called a "fatty streak."8 The process of atherosclerosis is not confined to the heart arteries (known as "coronary arteries"). The term "coronary artery disease" refers specifically to the gradual narrowing of atherosclerosis as it affects the heart arteries. Large and medium sized arteries throughout the body can become narrowed by this buildup of fatty material as a plaque is formed, illustrated in Figure 2: Atherosclerotic Fatty Streak Involvement of the Aorta.

Notice that there is more to the process of atherosclerosis than the buildup of fat. When fat accumulates on the inside of the coronary arteries (or any other artery), the body reacts to prevent a blood clot. It covers those fatty deposits with a tough, fibrous cap, as shown in the figure. This is an important response, because if fatty material is allowed to come into direct contact with the blood it can stimulate the blood to clot. The fibrous cap protects against this deadly clotting. In fact, this dual process gives atherosclerosis its name. "Athero" refers to the "mushy" or "gruel-like" fatty material that builds up inside the arteries. "Sclerosis" describes the hard fibrous material made by the body in response.

Unfortunately, an atherosclerotic plaque can ulcerate, causing a break in the protective cap as shown in the figure. When this happens, a combination of fibrous and fatty material is released into the blood stream. A now smaller, eroded fatty deposit, called an ulcerated plaque (sometimes called "lesion"), remains attached to the artery wall. Both the liberated fatty material and the ulcerated plaque itself can activate platelets, the body’s clotting cells. This often sets in motion a chain of events that can completely obstruct any artery that is already significantly narrowed by atherosclerosis.9 If this or another process results in complete obstruction of a coronary artery, the heart muscle that was dependent on the blood flow in that artery will die. This death of heart tissue is called a myocardial infarction (MI), or heart attack.

Atherosclerosis progresses at different rates in different people. The change over time in the arteries of a person who at the age of 60 or 70 will suffer from heart disease is shown in Figure 3: Progression of Coronary Artery Disease.10

Note that early atherosclerosis is present at age 20, as shown at the bottom of the figure. This is common in Western nations. In fact, it may be present at age 10 or 15. By the time a person reaches 20, fatty streaks can be so prominent that they are clearly visible when the coronary artery is cut open. If the unhealthy lifestyle continues, by age 30 the plaques progress to become even more pronounced. By age 40, it is not unusual to have significant coronary artery blockages that reduce the diameter of the artery by more than half. Even at this point, the effects of 30 years worth of atherosclerosis will likely still be "silent." Most individuals will have no symptoms at all, as noted on the figure by the area labeled "asymptomatic."

If symptoms do arise, they may be vague or "atypical," or they may be classic "angina pectoris," which is shown in the figure as the first symptom in the progression toward a heart attack (shown as MI in the figure). Angina pectoris refers to chest pain on exertion or severe emotional stress that is usually described as a heaviness, pressure, or tightness centered in the middle or left side of the chest. The pain can travel up to the neck or jaw or down either arm. Occasionally there is also back or stomach area pain. A large meal or cold weather may also precipitate this pain.11 The symptom of pain is caused by an insufficient blood supply to the heart muscle, referred to as "coronary insufficiency" in the figure.

Currently, approximately 6,750,000 people in the United States suffer from angina pectoris.12 Unfortunately, many have no such symptoms until they have their first heart attack. Even under situations of significant exertion, a heart artery must have at least 50 to 60 percent of its diameter blocked before the heart muscle suffers from lack of blood supply, which is the cause of the pain.13 Many individuals with narrowing even in the 70 percent range or greater have no recognizable symptoms.

As a result of the lack of symptoms, heart disease is often not detected in its earlier stages. A person may feel great, be working full time, and yet be on the verge of a major heart attack and perhaps even sudden death. Approximately 60 percent of heart attack deaths occur suddenly or outside of a hospital before treatment can be administered.14 Over half of all sudden deaths (almost two-thirds of sudden death cases in women) occur in individuals who were not previously diagnosed with coronary artery disease. It is a sobering reality for many that their first heart attack is their only heart attack. Sudden death offers no second chances.

Even when people survive a heart attack, over two-thirds do not make a complete recovery, leaving them with some form of disability and a permanently decreased quality of life.15 Following a heart attack, the heart is weaker because of lost muscle tissue.

This weakness can be significant, particularly if the heart attack was large. In such a case, the heart may be unable to adequately perform even routine pumping functions. This is an example of what is called ischemic cardiomyopathy referred to in Figure 3: Progression of Coronary Artery Disease. The term refers to a heart muscle ("cardio-myo") disease or pathology ("pathy") that was caused by lack of blood supply ("ischemia"). When such a diseased heart is not able to keep the body functions going, physicians use the term "congestive heart failure." In this situation, an affected individual may get short of breath easily, experience feet or ankle swelling, or be generally fatigued.

To prevent these progressive steps from leading to a fatal or crippling heart attack, it is unwise to put off heart evaluations until symptoms develop. A variety of tests is available to diagnose heart disease before a fatal event, such as an electrocardiogram (EKG) with or without a stress (treadmill) test. A resting EKG can reveal evidence of previous heart attacks, but it is a poor tool for detecting blockages that have not yet resulted in the loss of heart muscle. One significant exception is the occurrence of chest pain. In this situation, if a heart problem is causing the discomfort, the EKG, when performed while the pain is occurring, will often identify a potential coronary blockage.

In a person without symptoms, an EKG stress test is far superior for detecting coronary artery narrowing than the plain EKG. Even a 50 percent blockage of a single artery will sometimes show up on a good stress test. Unfortunately, however, even a stress test can miss a considerable number of diseased individuals. As many as 35 percent of those with significant heart vessel blockages will have a normal stress EKG.16 The number of falsely reassured individuals can be reduced significantly by the use of a radioactive tracer called Thallium or by doing the stress test in conjunction with echocardiography (an ultrasound test of the heart performed immediately before and after the stress test). Giving an injection of Thallium at the maximum level of exertion on the stress test will identify all but about eight percent of individuals with heart artery blockages and all but about four percent if the echocardiogram is utilized.17 Since coronary artery disease and chest pain are so common, as a practicing physician I perform one or more of these tests on a daily basis.

The most conclusive test that can be performed is a dye study of the heart and its blood vessels. It is very good for identifying blockages that are likely to cause problems. Such dye studies are sometimes referred to as "cardiac catheterizations" or "coronary angiograms." Unlike the previous tests mentioned, a cardiac catheterization is an invasive test (meaning we go inside the body with a catheter). Once a blockage narrows the diameter of the blood vessel by 40 to 50 percent or more, such a dye study usually identifies the problem.



Keys to Preventing Heart Disease

There are some factors that influence our risk of heart disease that we can do nothing about. For example, age and sex cannot be changed, yet they have a significant bearing on cardiovascular risk. The older we are, the greater our risk. Similarly, men are at higher risk than women of the same age-particularly in the years before menopause. Fortunately, however, medical research demonstrates that we can change a number of factors that influence our risk of heart disease. The three most important modifiable heart disease risk factors are cigarette smoking, high blood pressure, and high cholesterol.

Addressing all three can make a considerable impact, as was illustrated by a study of some 29,000 Finnish men and women over a 20-year period (1972 to 1992). When these individuals lowered the cholesterol in their diets, lowered their blood pressure, and stopped their tobacco use, they reduced their heart attack risk by more than half, as shown in Figure 5: Lifestyle Changes Reduced Heart Disease Deaths.18



Focusing on Cholesterol

Smoking and high blood pressure are each related to so many different health issues that they warrant individual chapters. We will examine them more closely later in the book. Cholesterol, on the other hand, is of primary interest because of its specific role in heart disease; consequently, we will focus on it here. However, before leaving the impression that cholesterol is only an issue as it relates to increasing heart disease risk, I must emphasize that cholesterol is an important and essential natural compound. This white, waxy fat is manufactured in our bodies and is used to build cell walls and make certain hormones. However, too much cholesterol in the blood stream (called "serum cholesterol") can contribute to atherosclerosis. For this reason, high blood cholesterol level as a single factor correlates well with coronary heart disease death rate. It is recommended that all Americans over the age of 20 know what their total blood cholesterol and HDL are.19 The higher the cholesterol level the greater the death rate, as demonstrated in Figure 6: Deaths for Coronary Heart Disease vs. Cholesterol Level in Men. This graph shows that the average serum cholesterol level in 19 countries is a predictor of the risk of heart disease among men in those nations.20 Note that Finland tops the scale, with a very high average cholesterol and a very high death rate. The United States is also relatively high on both scales. Ireland and England are higher than Poland, Yugoslavia, and Japan.



How to Achieve the Best Cholesterol Levels

How can we improve our cholesterol levels? Specifically, how can we decrease total cholesterol and LDL and at the same time raise HDL? The answer to this question is extremely important. To fully appreciate the answers, however, we must make sure we understand where cholesterol comes from.

It is of primary importance that we recognize that our livers manufacture more than enough cholesterol for all our body functions. For this reason, we do not need to eat any cholesterol whatsoever. In other words, cholesterol is totally unnecessary in the human diet. However, many of us get significant amounts of cholesterol from our foods. In fact, the average American eats about 300mg of cholesterol every day.35 Where does all this cholesterol come from? Figure 13: Sources of Dietary Cholesterol gives us the answer in simple terms.

Note that all the cholesterol we eat comes from animal products. It is critical that we understand that fruits, vegetables, grains, and even nuts contain no cholesterol. If the food comes exclusively from plant products, then it has no cholesterol in it. On the other hand, if the food product comes from an animal, it almost always has cholesterol in it. (A few exceptions exist where the cholesterol-containing portion of the animal product has been removed. Egg whites would be the main example of this.) Further information regarding dietary sources of cholesterol is tabulated in Figure 14: Cholesterol in Foods.36

All would be wise to pay careful attention to these examples in the figure. Although most people may be aware that organ meats such as liver and kidney are among the most intense sources of cholesterol as the figure shows, many still do not understand the basic prevalence of cholesterol in animal foods. They think that if they eat chicken, turkey, or fish they are not getting cholesterol. On the contrary, we see that every animal product contains cholesterol. Also, take note that chicken contains about the same amount as pork and beef. This bad news about "white meat" has not received much press. Furthermore, many kinds of fish have a high cholesterol content.

To what extent does our intake of cholesterol affect our blood cholesterol level? The more cholesterol we eat, the higher our blood cholesterol tends to be, as shown in Figure 15: Dietary Cholesterol Intake Raises Blood Cholesterol.37 Notice that as our intake of cholesterol increases, it is reflected as an increase in serum cholesterol. An increase of 75 points can occur if we consume 900 mg per day. If our intake is greater than 900 mg, not much further increase in serum cholesterol occurs. Fortunately, our bodies have protective mechanisms to keep blood cholesterol from going sky high after consuming extremely large amounts of cholesterol. The curve in the figure also shows that we can dramatically drop our cholesterol level by decreasing cholesterol intake substantially below that 900 mg daily level. For example, the figure shows that dropping the cholesterol in your diet from 900 mg to 200 mg daily may lower your cholesterol 50 or 60 points. Notice that you get even more benefit when you drop your cholesterol below 200. Going from an intake of 200 mg per day down to no cholesterol in your diet may drop your blood levels another 20 points. The important message is that you can dramatically lower your cholesterol by removing all cholesterol (all animal products) from your diet.



Typical Sources of Dietary Cholesterol

Americans get most of their cholesterol from meat and eggs, as shown in Figure 16: Food Sources of Cholesterol in the American Diet.38

Note that 35 percent of the cholesterol consumed in America each day comes from meat, fowl, and fish, and another 35 percent comes from eggs. The cooking fats and oils that contain cholesterol are animal in origin, such as butter, lard, and other fats. Commercial baked goods tend to use lard, which accounts for eight percent of the cholesterol consumed per day.

This figure shows that we can lower our cholesterol intake by 70 percent just by eliminating eggs, red meat, poultry, and fish. Of course we can lower it even further just by eliminating more of the animal products. If we really want to eliminate all the cholesterol in our diet, essentially all animal products must go.



Animal Fat’s Contribution to Cholesterol Levels

So far we have seen that elevated blood cholesterol levels are closely associated with fatal heart disease. We have also noted that cholesterol in the diet will raise blood cholesterol levels. There are a number of other factors, however, that contribute to elevated cholesterol levels. Some of these factors were clarified by one of the great cholesterol pioneers, Dr. Ancel Keys. In the 1960s, Dr. Keys demonstrated his ability to predict with astounding accuracy the average blood cholesterol levels of population groups. All he used was a knowledge of their habitual diets in order to make his startling predictions. Unfortunately, there was too much genetic variability from person to person to do this on an individual basis. However, when looking at large groups of people, the average genetic tendencies tended to be similar from one population to the next. Thus, Keys could make his cholesterol predictions based on habitual food choices alone-without dealing with genetics. He devised a mathematical formula that fit the data. This equation is often referred to as the "Keys Equation" and is illustrated in Figure 17: Keys Equation.39 Those with a math background will find the equation illuminating. Without going through the calculations, Dr. Keys proves with this equation that, apart from genetics, our blood cholesterol level is determined by our diet, and essentially only three variables in the diet: saturated fat (S), polyunsaturated fat (P), and cholesterol (C).

Many people do not understand the difference between the two fats. Imagine that you are sitting in front of two 10-gallon glass fish tanks. Each tank is filled with fat. One is filled entirely with saturated fat, and the other with polyunsaturated. It would be easy to tell the difference between the two. The saturated fat would be solid at room temperature and the polyunsaturated fat would be liquid. Generally, the more solid the fat, the more saturated it is. Most fats from animal products are predominately saturated, while most plant products are high in polyunsaturated fats. We will look at specific examples shortly.

With a basic understanding of the three terms used in the Keys equation, let me now explain what the equation tells us. First, it asserts that both saturated fat and cholesterol in the diet tend to raise blood cholesterol levels. Second, it makes the point that saturated fat is much more potent at raising your blood cholesterol than even dietary cholesterol itself. Third, polyunsaturated fat tends to lower cholesterol in the blood. However, saturated fat has twice the power to raise your cholesterol as polyunsaturated fat has to lower it. Expressed another way, to cancel out the cholesterol-raising effects of a given amount of saturated fat, you would have to eat twice as much polyunsaturated fat. This fact can be used to judge whether the fat content of a given food will raise or lower your blood cholesterol level. Since all naturally occurring foods have a combination of fats in them (both polyunsaturated and saturated), you can divide the amount of polyunsaturated fat in the food by the amount of saturated fat in it, and end up with what is called a "P to S ratio" (abbreviated "P/S ratio"). If this P/S ratio is greater than 2.0, the fat in the food will tend to lower one’s blood cholesterol level. Be aware that this ratio tells us nothing about other factors in the food (like cholesterol itself, for example) that may affect a person’s cholesterol level.

Since a high P/S ratio in our diet will tend to lower the blood cholesterol, we need to be aware of the P/S ratio of common foods. This ratio is listed in Figure 18: P/S Ratio of Foods for a variety of foods.40

Note that many of the animal products such as beef, venison (deer), lamb, and bacon have extremely low P/S ratios. These foods, based on their fat content, will tend to dramatically raise an individual’s serum cholesterol. Thus, red meats are undesirable not only because they contain cholesterol, but their harmfulness is compounded because they contain so much saturated fat, and so little polyunsaturated fat. The same is true of milk, butter, and cheese. Chicken and turkey have less saturated fat than red meats, but their P/S ratios are still lower than two to one, so they, too, will raise cholesterol levels. One of the greatest myths is that chicken, turkey, and fish lower a person’s cholesterol level. These foods actually raise a person’s cholesterol, but they raise it less than red meat does. As a result, a person’s cholesterol may go down when leaving off red meat and substituting fish and fowl. But the drop in cholesterol level occurs because chicken, turkey, and fish raise one’s cholesterol level less than red meat, not because they have a cholesterol-lowering effect. I have had people come into my office and tell me, "I just can’t understand what is happening. I have been eating mostly chicken and turkey but my cholesterol still has not come down that much!" When you understand the P/S ratio, it tells where part of the problem lies. Furthermore, as I mentioned earlier, chicken and turkey have as much cholesterol in them as do the red meats. We will see later that some of the cholesterol in fowl is undoubtedly oxidized. Switching from one kind of meat to another is simply not the ultimate solution for cholesterol control.

The story is similar with fish. Some fish have favorable P/S ratios (greater than 2.0), but many others do not. Furthermore, all fish contain cholesterol. In short, fish, like fowl, if substituted for red meat, will tend to lower cholesterol levels, possibly even more than fowl. However, your cholesterol levels would be lower yet if you left chicken, turkey, and fish completely out of your diet.



Vegetable Fat’s Effect on Cholesterol

In contrast to animal fats, vegetable fats have no cholesterol at all. There are different kinds of vegetable fats, and all but a few are highly polyunsaturated. In Figure 18: P/S Ratio of Foods, notice that coconut has a P/S ratio of 0.01. This is a highly saturated fat and will tend to raise cholesterol levels. Although coconut has no cholesterol, its saturated fat content dramatically increases blood cholesterol. On the other end of the spectrum, walnuts can have a rather dramatic effect in lowering an individual’s cholesterol.

Most nuts, in view of their fat content, are "heart healthy" foods, as shown in the figure. Nuts in general have been studied extensively and have been found not only to lower blood cholesterol levels, but also to provide a corresponding decrease in the risk of heart disease, as shown in Figure 19: Nuts Reduce Heart Disease Risk.41, 42

This study on nut consumption was conducted at Loma Linda University and has received international attention. The initial study focused on the amount of nuts eaten by the participants in the Adventist Health Study. They found that those consuming nuts less than once per week had the highest risk of heart attack. Those who consumed nuts one to four times per week lowered their risk about 25 percent as shown in the figure. Those who consumed nuts more than five times a week cut their risk in half. The study was controlled for other lifestyle variables so that the researchers could be more certain that the nuts were the only factor involved. Many health professionals were surprised by the findings of this study. Previously, health professionals commonly encouraged patients to avoid nuts because of their high fat content. Now we know that nuts in small to moderate amounts are part of a healthful diet because they supply some fat nutrients that are beneficial for preventing heart disease.

Regarding peanuts, the fat in peanuts has a specific chemistry and triglyceride structure (apart from the saturated and polyunsaturated content) that makes them surprisingly harder on your arteries than other vegetable fats.43 Thus, a person who wants to protect his arteries would be wise to choose other nuts such as almonds, walnuts, or pecans in place of peanuts. Almonds have another advantage. They are unique among the nut food group in that they contain far more vitamin E than other nuts; in fact, they exceed just about all other foods in this regard. We will see later that vitamin E reduces the risk of heart disease. The realization of some of peanut fat’s negative aspects leaves me impressed with a statement I read about nuts that was written nearly 100 years ago in the classic book on the principles of health, The Ministry of Healing, written by Ellen White and quoted in Figure 20: Almonds Preferable to Peanuts.44

Why did she warn against excessive nut consumption? One likely reason is that a high fat diet (even if from "good fats") tends to promote weight gain. For many people, a large a proportion of nuts in their diet may contribute to obesity. The overweight condition itself can raise cholesterol levels and increase the risk of heart disease and other health problems.



The Very Low Fat Theory

The research on nuts has helped to lay to rest a popular but fictitious approach to heart disease prevention sometimes called "the very low fat theory." For years, many have advocated that to maximally reduce the heart attack rate we must cut the fat in large amounts, to about 10 percent of calories. Some people have become famous by advocating such a very low fat diet. Unfortunately, very low fat diets are often not palatable and are not necessarily the answer to reducing heart disease risk. If the fat is coming from monounsaturated and polyunsaturated sources, a higher fat diet can actually be as good for the heart as the very low fat fare. The Committee on Diet and Health of the National Research Council said this in so many words when they posed the question, "Is the very low fat theory correct?" From a review of the current literature, they concluded, "No." They went on to state, "Intake of total fat per se, independent of the relative content of the different types of fatty acids, is not associated with high blood cholesterol and coronary heart disease."45 We now know that we can have a healthful diet that includes moderate levels of fat if we are using the best types of fat.

After the 1992 study of nuts and cholesterol, Dr. Sabate took the nut research a step further. Instead of using Seventh-day Adventists again, who are already on a better overall diet than most Americans, he now studied individuals on an average American diet. One half of the total group was placed on an average diet. The other half were fed an identical-looking diet with one major difference. Walnuts were blended up and added to various food items. Other sources of fat were decreased to keep the calorie and total fat levels the same in the two groups.

Eating walnuts daily had some amazing results. LDL cholesterol, the "bad cholesterol," dropped by 18 points. See Figure 21: Walnuts Reduce Cholesterol.46 This represents a remarkable lowering of heart attack risk. For each percentage point drop in the bad cholesterol, there is a two to three percent drop in the heart attack rate.47 An 18 point drop in LDL translates into a 36 to 54 percent drop in heart disease risk. The benefits of walnuts may not simply be due to their excellent P/S ratio. These nuts are also high in so-called omega-3 fatty acids, which have some special benefits. Chapter 5, "The Truth About Fish," has more information on this subject.



Fiber’s Cholesterol-Lowering Abilities

Fiber in our food will help lower cholesterol. Most Americans eat far less than the recommended 25 to 30 grams per day. Evidence now suggests that a low fat, high fiber, high carbohydrate diet offers a number of advantages. Eating at least 30 to 40 grams of fiber per day from a variety of plant foods can lower your risk of heart disease, cancer, intestinal disorders, and other diseases.53 A list of diseases associated with a typical American low-fiber diet appears in Figure 23: Diseases Associated with a Low-Fiber Diet.54

Many are surprised to learn that there are different types of fiber. Yet all fibers have one thing in common-they cannot be digested by the normal human intestinal system. One definition for fiber is "indigestible carbohydrate," meaning that fiber is not absorbed but is rather excreted. Different categories of fibers include celluloses, hemicelluloses, lignin, pectins, gums, mucilages, and algal polysaccharides.

A simpler classification of fiber divides fiber types simply into water soluble and insoluble fibers. It is the water-soluble fibers that are particularly valuable for lowering cholesterol. Fruits, vegetables, nuts, grains, and legumes, all in their natural, unrefined state, are the five main food groups that contain this cholesterol-lowering fiber. Examples of such water--soluble fibers are oat bran and fruit pectin. These compounds work by binding to cholesterol and bile acids (excreted by the liver) in the small intestine, thus preventing their absorption. Fortunately, neither bile nor cholesterol is absorbed high in the intestinal tract, but rather in the distal ileum (the last part of the small bowel). This allows the fiber plenty of time to bind up these compounds. If, however, adequate fiber is lacking, both bile and cholesterol are reabsorbed into the blood stream, raising blood cholesterol levels. Bile acids are actually made from cholesterol by the liver. As a result, the more bile you lose in the stool, the more cholesterol the body must utilize to make new bile acids that are necessary for fat digestion. The medical literature is replete with examples of fiber’s health-giving benefits. One study, published in 1992, found that adding 15 grams of fiber per day to the diet lowered serum cholesterol by 15 percent.55

The effect of fiber in lowering cholesterol correlates with the decrease in heart disease risk in people who consume high amounts of it. Those that consume a high fiber diet have a 65 percent less risk of heart disease, as shown in Figure 24: Dietary Fiber Reduces the Risk of Coronary Heart Disease.56 In another study, seven groups were fed differing amounts of either oatmeal, oat bran, or farina. At the end of six weeks there were significant improvements in total and LDL cholesterol for those daily consuming either one ounce of farina, two ounces of oat bran, (2/3 of a cup dry), or three ounces of oatmeal (one cup of dry rolled oats). 57 Because some skeptics were still not willing to believe that oats can lower cholesterol, a computer assessment (meta-analysis) of 20 carefully performed oat studies was completed in 1992. The results demonstrated that oat products in the diet significantly reduce cholesterol levels. 58 Another grain that has been found to have beneficial effects on blood cholesterol levels is buckwheat.59 A study from mainland China found buckwheat to lower both total cholesterol and LDL cholesterol; at the same time it lowered the ratio of total cholesterol to HDL.

Animal products (meat, milk, eggs, and cheese) have absolutely no fiber. Many wonder why, since animals often consume large quantities of fiber. For example, the cow, a total vegetarian, eats fiber all day long. You would think that eating the cow would furnish plenty of fiber, but it does not. The reason is that when a cow eats, it extracts and absorbs many nutrients, but the fiber in its food has a different fate. Some of this fiber can actually be digested by the cow (even though it is indigestible by humans). The rest of the fiber passes through the cow’s intestinal tract and is excreted onto the pasture. In either case, the cow’s meat or milk incorporates none of the beneficial fiber. In effect, when people eat cows or other animals, they are eating nutrients second hand. Unfortunately, they get no fiber, since the animal has "refined" the food through its process of digestion. If we want an abundant supply of fiber, we will choose to eat grains, fruits, vegetables, or nuts directly. Foods that are good sources of fiber are listed in Figure 25: Common Sources of Fiber.60

As we observed earlier, until very recently, most cholesterol education programs never went beyond the Keys equation. They told participants about the importance of cholesterol in the diet as well as the dangers of saturated fat with most of the emphasis being on saturated fat, but this is where discussions ended. More recently, the topic of fiber has found its way into lay educational efforts, but it often does not get the full attention that it deserves. Other information that is sadly lacking in most educational efforts is the topic of protein and oxidized cholesterol.



Animal Protein Raises Cholesterol

The relationships between cholesterol and protein have been published in the medical literature for some 20 years, but for the most part have been sadly neglected. An extensive body of research now has established that serum cholesterol is extremely dependent on the type of protein consumed.61, 62, 63 Animal protein alone (even skim milk protein) will increase blood cholesterol levels while plant proteins will decrease cholesterol. In fact, many people who are on otherwise heart-healthy diets will be unable to lower their cholesterol sufficiently unless they completely eliminate animal protein from their diets. Research has shown that switching from a low saturated fat, low cholesterol diet using skim milk protein to a low saturated fat, low cholesterol diet using soy protein as a milk substitute can drop cholesterol levels by as much as 60 to 80mg/dl in as little as three weeks. I have seen this happen in many of my patients who have tried a total vegetarian diet (no animal protein). If a dramatic reduction does not occur in such a diet, I thoroughly review what the patient is actually eating, and often find that animal protein has been unwittingly consumed in the form of casein in a milk substitute or a cholesterol-free egg product such as Egg Beaters. Once the animal protein is completely excluded, the expected dramatic result usually occurs. More complete information on the subject of protein sources and serum cholesterol is found in Chapter 7, "The Great Meat and Protein Myth."



The Problem with Oxidized Cholesterol

Cholesterol exposed to the atmosphere for a period of time tends to combine with oxygen in the air, producing what is called "oxidized cholesterol." Oxidized cholesterol is another important dietary factor that the Keys equation did not address. In fact, this compound may turn out to be the most important dietary factor that influences heart disease risk. As early as the 1940s it was discovered that not all cholesterol was the same in its likelihood of causing atherosclerosis. Dr. Chaikoff and associates found that chickens that were fed large amounts of cholesterol developed high blood cholesterol levels and a considerable amount of atherosclerosis. On the other hand, chickens that were given hormones to raise their cholesterol to similar levels had virtually no fatty buildup in their arteries.64 Drs. Peng and Taylor in Albany, New York carried on further experiments looking for something in dietary cholesterol that was particularly damaging to blood vessels. Their discoveries are stated in Figure 26: Stored Foods Containing Cholesterol can Become Lethal.65, 6

Some of the chemicals, called "oxidation products," were so toxic that they destroyed cells that line the arteries in less than 24 hours. Furthermore, it took only a small amount of these toxic chemicals to cause irreversible damage. In Peng and Taylor’s work, the deadly effects on blood vessels occurred when as little as one half of one percent of the blood cholesterol was oxidized.67 Their research is particularly important because destruction of artery-lining cells is one of the main factors that begins or accelerates the buildup of cholesterol in atherosclerosis. Peng and Taylor also made chemical measurements of specific foods to see how much oxidized cholesterol they contained. The researchers then tested the harmful compounds on blood vessel cells of monkeys to determine how dangerous they were. Foods that contained oxidized cholesterol products and produced damage to blood vessel cells are listed in Figure 27: Stored Foods Containing Harmful Cholesterol By-Products.68

The most harmful combination of cholesterol oxidation products was found in custard mix where sugar, milk, and eggs were combined. The dried mix was apparently exposed to air for a considerable period of time due to its long shelf life.

Over 100 years ago the dangers of custards and puddings was recognized by Ellen White. Her warning is quoted in Figure 28: %Especially Harmful%69

Some have observed that ice cream is the most common form of custard in America today. Pancake mixes containing eggs and dried powdered milk were equally as harmful as custard. The third most harmful item was Parmesan cheese; it turned out to be as damaging as lard.

Furthermore, eating oxidized cholesterol may raise blood cholesterol levels more than pure cholesterol alone.70 However, even if your blood cholesterol level remains normal, animal research demonstrates that eating oxidized cholesterol can have adverse consequences, as summarized in Figure 29: Vascular Damage from Oxidized Cholesterol.71

The rabbits were fed a moderate amount of pure, non-oxidized cholesterol for 45 days. Their blood cholesterols stayed in the normal range and they suffered no damage to their blood vessels. Those rabbits that were given the same amount of oxidized cholesterol also maintained normal blood cholesterol values.

However, they sustained significant damage to their blood vessels. Research on humans also supports the fact that oxidized cholesterol in the diet can increase your risk of heart disease even if your blood cholesterol levels stay normal. For example, we have known for years that-regardless of your blood cholesterol level-the more cholesterol you eat, the greater your risk of heart disease. Cholesterol in the diet is what is called an "independent risk factor" for the development of heart disease.72

Let me try to make this clearer with an example. Assume that twin sisters are identical in every factor that relates to heart disease. They have identical blood pressures, they both have never smoked, they have identical genes, etc. Let us also assume that they have identical blood cholesterol levels.

But suppose there is one difference: one of the sisters eats much more cholesterol than the other. What the research tells us is that the liberal cholesterol eater is much more likely to suffer a heart attack. Simply put, we know that cholesterol in your diet is harmful for more reasons than its tendency to raise blood cholesterol. I believe that a large amount of this added danger is explained by the presence of oxidized cholesterol.

Even though as of this date, detailed measurements of oxidized cholesterol have not been made on every food, it is logical to assume that every food that contains cholesterol has some oxidation products in it. The important message is that even individuals with normal blood cholesterols should be careful to limit cholesterol in their diets. If you are not on such a low cholesterol diet, then you are likely at increased risk of heart attack or stroke, regardless of what your cholesterol numbers are.

Atherosclerosis often begins early in life. The oxidized cholesterol studies may also help to explain why some individuals develop atherosclerosis earlier than others. One important early factor may be the type of milk that infants drink. When a baby consumes human breast milk directly from the human nipple, it does get cholesterol in that milk. However, the cholesterol that comes from mom is pure, not oxidized like that present in cow’s milk-based formulas that have been extensively processed in the presence of air. Peng and Taylor identified toxic oxidized cholesterol products in powdered infant milk formula.73 One theory is that babies that are fed on cow’s milk formula are predisposed to fatty streaks early in infancy. However, you should not conclude from this that the best way for adults to get their milk is to go down to the barn and get it straight from the cow to minimize exposure to air! That method might decrease your consumption of oxidized cholesterol, but it would also greatly increase your exposure to a host of infectious diseases as listed in Chapter 11, "Milk-Friend or Foe?"

Our growing understanding of oxidized cholesterol has lead me to conclude that any program that does not address this subject is neglecting one of the most important factors in decreasing heart disease risk. I think that the increased research attention on oxidation products of cholesterol will illuminate some other relationships. For instance, it is very possible that foods with high sugar content are more susceptible to oxidation.74 This would help further explain the abundant oxidation products that are found in things like custard and pancakes-foods with a source of cholesterol (milk and eggs) and sugar. It would also explain why dietary sugar has repeatedly been linked to atherosclerosis.



Vitamins Benefit Cholesterol Levels

We have seen that iron appears to increase the likelihood that normal cholesterol will become oxidized in our bodies. However, there are a number of substances in foods that appear to prevent oxidation from taking place inside of us. These substances are called antioxidants. Three of the most well-researched compounds in this regard are the antioxidant vitamins E, C, and beta-carotene.

Vitamin E intake has been found to reduce one’s risk of heart disease. A total of 40,000 men were categorized as to the amount of their daily vitamin E intake. Those who consumed 60 IU per day decreased their risk of heart disease by 34 to 50 percent, regardless of other food they consumed.77

How can we get enough vitamin E in our diet on a daily basis? Since animal products are low in vitamin E, this leaves us with a choice of taking supplements or making substantially more vegetarian food choices. Although there are no known toxic effects, there is also no medical justification for the use of large doses of vitamin E supplements to prevent heart disease, particularly since it is widely distributed in common foods.78 Good sources of Vitamin E are wheat germ, vegetable oils, legumes, nuts (particularly almonds), whole grains, and green, leafy vegetables. 79 As we have already noted, the protection against heart disease provided by vitamin E is thought to be due to the prevention of the oxidation of cholesterol within the body.



Beta-carotene Foods Benefit Cholesterol Levels

A Harvard University study found that the consumption of beta-carotene foods reduced cardiac deaths. Over a period of nearly five years, some 1300 individuals participated in this research. The results showed that an increased consumption of fruits and vegetables high in beta-carotene decreased subsequent cardiovascular disease deaths.80 Interestingly, taking supplements of beta-carotene does not lower the risk of heart disease.81 Thus, other antioxidant nutrients in the fruits and vegetables may be adding a protective effect to the blood vessels.

Beta-carotene is plentiful in carrots, tomatoes, broccoli, strawberries, and the leafy green vegetables such as kale, collards, and mustard greens. It is also found in watermelon, pineapples, and the yellow types of squash. In the study, when these foods were consumed, no matter what the cholesterol level was in the participants, there was an independent relationship in lowering the heart attack risk.



Exercise Benefits HDL Cholesterol Levels

When the HDL cholesterol is high, it extracts the bad cholesterol from the arteries and helps protect the arteries from damage. High levels of HDL may even help reverse coronary artery disease. How can we get our HDL levels up? Exercise has been shown to raise HDL.95 The exercise that raises HDL is not the weight-lifting type, but rather the more active or aerobic sort that gets the heart rate up and requires rhythmic body movements and deep breathing. The more aerobic exercise obtained the greater the rise in HDL.96 Because of the role of exercise in raising HDL and thus lowering the risk of atherosclerosis, low physical fitness should be thought of as an independent risk factor for the development of heart disease.97 A list of HDL-raising factors is shown in Figure 33: Factors that Raise HDL Levels. The best news is that if you are unfit now, and you get on a regular exercise program, research indicates that you can decrease your risk of heart disease by 50 percent.98



Other Factors That Raise HDL Cholesterol

Taking any of the drugs listed in Figure 33: Factors that Raise HDL Levels, that raise HDL is not the preferred method due to possible side effects.99, 100 High doses of the B vitamin, niacin, can boost HDL levels; however, in these doses the niacin is acting as a drug rather than a vitamin.101 Consequently, if you are taking high doses of niacin you should be under a doctor’s care. Careful medical monitoring for side effects is strongly recommended. Particular attention should be paid to the liver as high doses of niacin can be toxic to that organ on occasion.

Estrogen in women raises HDL. This may be one of the primary reasons why the average woman does not experience heart disease until 10 years later than the average man. After menopause, when estrogen production drops, women quickly catch up with men with regard to heart disease risk. Thus, 52 percent of all coronary heart disease deaths occur in women.102

Alcohol drinking has been associated with higher HDL levels. However, I strongly discourage alcohol use because of the significant hidden dangers that it carries. These dangers are covered more completely in Chapter 17, entitled "Want a Drink?" Furthermore, alcohol may not raise your HDL if you are already on an excellent program. Hartung and colleagues found that moderate alcohol consumption provided no HDL benefit for men that were running regularly.103 In addition to alcohol, there are other toxins that raise HDL levels, such as chlorinated pesticides. Again, I would obviously not recommend such agents as HDL enhancers. There are safer ways to raise HDL. When individuals stop smoking, their HDL usually rises significantly as a result. Weight loss can also help raise your HDL.104 Foods containing lecithin, ginseng, garlic, onions, brewer’s yeast, the trace mineral chromium, vitamin C, and vitamin E all can help raise HDL. An example of a food with HDL-boosting effects is garlic. One garlic study had individuals with coronary heart disease use up to four cloves of garlic each day for eight months. The results are impressive and are shown in Figure 34: Garlic's Effect on Cholesterol and Tiglycerides.105

At the start of the study, HDL levels were dismally low, at only 17 percent of the total cholesterol. They were solidly in the danger zone. However, at the end of eight months their absolute levels of HDLs were a full 65 percent higher, at 28 percent of the total. Moreover, garlic not only raised the desirable HDL, it also lowered total and LDL cholesterol as well as triglycerides. In other words, all cholesterol values moved in the right direction. The only significant variable in this study was the consumption of garlic. From many different perspectives, garlic is not only a food enhancer, but is part of a healthful diet.



Conclusion

The evidence is indeed clear. We can dramatically decrease our risk of heart disease by following an optimal lifestyle. We need to make these changes so that a known preventable disease no longer leads the list of America’s killers. I am aware that you probably will not change your lifestyle to merely alter general statistics about the lethal impact of heart disease in America. However, I am concerned about individuals, hundreds of thousands of who will unnecessarily go to their graves-this year alone-because they did not take the proper lifestyle steps in time. And I know that you are at least somewhat concerned about yourself.

At the risk of sounding trite or affected, I must honestly say I feel a deep sense of responsibility for each one of you who are reading this chapter. I want to do everything I can to help prevent the tragedy of heart disease from touching your life. I have seen too many that have been hurt, killed, and crippled by this murderer to be unimpassioned on the subject. From that perspective, let me make a closing request: if this chapter has convinced you of areas that you need to change in your life, do not delay. Now is the very best time to improve your diet and other lifestyle habits. Do not wait for warning signs or a first heart attack before getting serious about lifestyle changes. By then you may have already developed irreversible disease. Worse, yet, heart disease may claim your life before you are ever aware that you had a heart problem.

For your own sake and the sake of your loved ones, why not embark on at least some elements of a new lifestyle today? If you stick with such changes, I am convinced you will regard them as among your life’s wisest investments. After all, the investment will pay dividends in providing longer life, disability prevention, and an enhanced quality of life. Do not procrastinate-start to get more of the full benefits of a heart disease preventive lifestyle today.



References

  1. Gyarfas I. Chief of the World Health Organization Cardiovascular Disease Prevention Program: World Health Day, Apr. 1992.
  2. Murray CJ, Lopez AD. Mortality by cause for eight regions of the world: Global Burden of Disease Study. Lancet 1997 May 3;349(9061):1269-1276.
  3. American Heart Association. Heart and Stroke Fact: 1996 statistical supplement. 1996 p. 2.
  4. American Heart Association. 1997 Heart and Stroke Statistical Update. American Heart Association, 1997 p. 2.
  5. American Heart Association. 1997 Heart and Stroke Statistical Update. American Heart Association, 1997 p. 28.
  6. Presented by Thomas N. Taylor and others from the University of Iowa to the American Heart Association 1-25-96. Based upon total lifetime cost for a stroke occurring in 1990.
  7. Gyarfas I. Chief of the World Health Organization Cardiovascular Disease Prevention Program: World Health Day, Apr. 1992.
  8. Conner WE, Bristow JD, editors. Coronary Heart Disease: Prevention, Complications and Treatment. Philadelphia, PA: Lippincott, 1985 p. 194.
  9. Hutter AM JR. Ischemic Heart Disease: Angina Pectoris, 1991. In: Scientific American Medicine (CD ROM), 1995.
  10. Berenson GS. Author of the Bogalusa Heart Study, The First International-Conference on the Elimination of Coronary Artery Disease, Tucson, AZ, Oct. 1991.
  11. Hutter AM JR. Ischemic Heart Disease: Angina Pectoris, 1991. In: Scientific American Medicine (CD ROM), 1995.
  12. American Heart Association. Heart and Stroke Fact: 1996 statistical supplement. 1995 p. 10.
  13. Wilson RF, Marcus ML, White CW. Prediction of the physiologic significance of coronary arterial lesions by quantitative lesion geometry in patients with limited coronary artery disease. Circulation 1987 Apr;75(4):723-732.
  14. Kannel WB, Thom TJ. Declining cardiovascular mortality. Circulation 1984 Sep;70(3):331-336. See also Kannel WB, Schatzkin A. Sudden death: lessons from subsets in population studies. J Am Coll Cardiol 1985 Jun;5(6 Suppl):141B-149B.
  15. American Heart Association. Heart and Stroke Fact: 1996 statistical supplement. 1995 p. 1.
  16. Hutter AM JR. Ischemic Heart Disease: Angina Pectoris, 1991. In: Scientific American Medicine (CD ROM), 1995.
  17. Galanti G, Sciagra R, et al. Diagnostic accuracy of peak exercise echocardiography in coronary artery disease: comparison with thallium-201 myocardial scintigraphy. Am Heart J 1991 Dec;122(6):1609-1616.
  18. Vartiainen E, Puska P, et al. Changes in risk factors explain changes in mortality from ischaemic heart disease in Finland. BMJ 1994 Jul 2;309(6946):23-27.
  19. American Heart Assocation. Preventive Services, Basic Cardiovascular. In: Heart & Stroke A-Z Guide, 1997.
  20. From the World Health Organization data analyzed from 1970-1980.
  21. World Health Organization (WHO). Tobacco Alert April 1996. http://www.who.org/programmes/psa/toh/Alert/apr96/fulltext.html#2
  22. McGee D. The Framingham Study: An Epidemiological Investigation of Cardiovascular Disease, Section 28. U.S. Department Health Education and Welfare, DHEW Publication No. 79-618. 1973.
  23. Berenson GS, Wattigney WA, et al. Atherosclerosis of the aorta and coronary arteries and cardiovascular risk factors in persons aged 6 to 30 years and studied at necropsy (The Bogalusa Heart Study). Am J Cardiology 1992 Oct 1;70(9):851-858. Figure obtained from: The First International-Conference on the Elimination of Coronary Artery Disease, Tucson, AZ, Oct. 1991.
  24. American Heart Association. 1997 Heart and Stroke Statistical Update. American Heart Association, 1997 p. 10.
  25. Keys A. Serum Cholesterol and the Question of "Normal." In: Benson ES, editor. Multiple Laboratory Screening, Academic Press, New York, 1969 p. 169.
  26. Stamler J, Wentworth D, Neaton JD. Is relationship between serum cholesterol and risk of premature death from coronary heart disease continuous and graded? Findings in 356,222 primary screenees of the Multiple Risk Factor Intervention Trial (MRFIT). JAMA 1986 Nov 28;256(20):2823-2828.
  27. Stamler J, Wentworth D, Neaton JD. Is relationship between serum cholesterol and risk of premature death from coronary heart disease continuous and graded? Findings in 356,222 primary screenees of the Multiple Risk Factor Intervention Trial (MRFIT). JAMA 1986 Nov 28;256(20):2823-2828.
  28. Report of the National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. The Expert Panel. Arch Intern Med 1988 Jan;148(1):36-69.
  29. American Heart Association. 1997 Heart and Stroke Statistical Update. American Heart Association, 1997 p. 20.
  30. National Cholesterol Education Program Expert Panel. Second Report of the Expert Panel on detection, evaluation, and treatment of high blood cholesterol in adults. National Institutes of Health Publication No. 93-3095. September 1993.
  31. NIH Consensus conference. Triglyceride, high-density lipoprotein, and coronary heart disease. NIH Consensus Development Panel on Triglyceride, High-Density Lipoprotein, and Coronary Heart Disease. JAMA 1993 Jan 27;269(4):505-510. As found in Scientific American Medicine (CD-ROM) 1997.
  32. Wilson PW, Abbott RD, Castelli WP High density lipoprotein cholesterol and mortality. The Framingham Heart Study. Arteriosclerosis 1988 Nov-Dec;8(6):737-741.
  33. Bush TL, Riedel D. Screening for total cholesterol. Do the National Cholesterol Education Program’s recommendations detect individuals at high risk of coronary heart disease? Circulation 1991 Apr;83(4):1287-1293.
  34. Castelli WP, Anderson K. A population at risk. Prevalence of high cholesterol levels in hypertensive patients in the Framingham Study. Am J Med 1986 Feb 14;80(2A):23-32.
  35. Adapted from: McDowell MA, Briefel BB, et al. Energy and micronutrient intakes of persons ages 2 months and over in the United States: Third National Health and Nutrition Examination Survey, Phase 1, 1988-91. Advanced Data Number 255 Oct 24, 1994. DHHS Publication No. (PHS) 95-1250.
  36. The Food Processor for Windows: Nutrition Analysis & Fitness Software [computer program]. ESHA Research. Salem, Oregon.
  37. Stamler J, Shekelle R. Dietary cholesterol and human coronary heart disease. The epidemiologic evidence. Arch Pathol Lab Med 1988 Oct;112(10):1032-1040.
  38. Grundy SM. Cholesterol and coronary heart disease. A new era. JAMA 1986 Nov 28;256(20):2849-2858.
  39. Keys A, Parlin RW. Serum cholesterol response to changes in dietary lipids. Am J Clin Nutr 1966 Sep;19(3):175-181.
  40. The Food Processor for Windows: Nutrition Analysis & Fitness Software [computer program]. ESHA Research. Salem, Oregon.
  41. Sabate J, Fraser GE, et al. Effects of walnuts on serum lipid levels and blood pressure in normal men. N Engl J Med 1993 Mar 4;328(9):603-607.
  42. Fraser GE, Sabate J, et al. A possible protective effect of nut consumption on risk of coronary heart disease. The Adventist Health Study. Arch Intern Med 1992 Jul;152(7):1416-1424.
  43. Kritchevsky D. Dietary fat and experimental atherosclerosis. Int J Tissue React 1991;13(2):59-65.
  44. White EG. Diet and Health. In: The Ministry of Healing. Nampa, ID: Pacific Press Publishing Association, 1905 p. 298.
  45. Diet and Health: Implications for Reducing Chronic Disease Risk, National Research Council, National Academy Press, p 7.
  46. Sabate J, Fraser GE, et al. Effects of walnuts on serum lipid levels and blood pressure in normal men. N Engl J Med 1993 Mar 4;328(9):603-607.
  47. Report of the National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. The Expert Panel. Arch Intern Med 1988 Jan;148(1):36-69.
  48. Mensink RP, Katan MB. Effect of dietary trans fatty acids on high-density and low-density lipoprotein cholesterol levels in healthy subjects. N Engl J Med 1990 Aug 16;323(7):439-445.
  49. Willett WC, Stampfer MJ, et al. Intake of trans fatty acids and risk of coronary heart disease among women. Lancet 1993 Mar 6;341(8845):581-585.
  50. Awad AB, Herrmann T, et al. 18:1 n7 fatty acids inhibit growth and decrease inositol phosphate release in HT-29 cells compared to n9 fatty acids. Cancer Lett 1995 May 4;91(1):55-61.
  51. Seppanen-Laakso T, Vanhanen H, et al. Replacement of margarine on bread by rapeseed and olive oils: effects on plasma fatty acid composition and serum cholesterol. Ann Nutr Metab 1993;37(4):161-174.
  52. Vanderveen JE , Glinsmann WH. Fat substitutes: a regulatory perspective. Annu Rev Nutr 1992;12():473-487.
  53. Craig WJ. Nutrition for the Nineties. Eau Claire, MI: Golden Harvest Books 1992 p. 44.
  54. Burkitt D. Nutrition Today Jan/Feb 1976, p. 6-13.
  55. Haskell WL, Spiller GA, et al. Role of water-soluble dietary fiber in the management of elevated plasma cholesterol in healthy subjects. Am J Cardiol 1992 Feb 15;69(5):433-439.
  56. Khaw KT, Barrett-Connor E. Dietary fiber and reduced ischemic heart disease mortality rates in men and women: a 12-year prospective study. Am J Epidemiol 1987 Dec;126(6):1093-1102.
  57. Davidson MH, Dugan LD, et al. The hypocholesterolemic effects of beta-glucan in oatmeal and oat bran. A dose-controlled study. JAMA 1991 Apr 10;265(14):1833-1939.
  58. Ripsin CM, Keenan JM, et al. Oat products and lipid lowering. A meta-analysis. JAMA 1992 Jun 24;267(24):3317-3325.
  59. He J, Klag MJ, et al. Oats and buckwheat intakes and cardiovascular disease risk in an ethnic minority of China. Am J Clin Nutr 1995 Feb;61(2):366-372.
  60. The Food Processor for Windows: Nutrition Analysis & Fitness Software [computer program]. ESHA Research. Salem, Oregon.
  61. Anderson JW, Johnstone BM, Cook-Newell ME. Meta-Analysis of the Effects of Soy Protein Intake on Serum Lipids. N Engl J Med 1995 Aug 3;333(5) :276-282.
  62. Sirtori CR, Agradi E, et al. Soybean-Protein Diet in the Treatment of Type-II Hyperlipoproteinaemia. Lancet 1977 Feb 5;1(8006):275-277.
  63. Sirtori CR, Gatti E, et al. Clinical Experience with the Soybean Protein Diet in the Treatment of Hypercholesterolemia. Am J Clin Nutr 1979 Aug;32(8):1645-1658.
  64. Chaikoff IL, Lindsay S, et al. 1948 J Exp Med 88:373
  65. Peng SK, Morin RJ. Effects on membrane function by cholesterol oxidation derivatives in cultured aortic smooth muscle cells. Artery 1987;14(2):85-99.
  66. Hubbard RW, Ono Y, Sanchez A. Atherogenic effect of oxidized products of cholesterol. Prog Food Nutr Sci 1989;13(1):17-44.
  67. Peng SK, Taylor CB. Atherogenic Effect of Oxidized Cholesterol. In: Perkins EG, Visek WJ, editors. Dietary Fats and Health. Champaign, IL: American Oil Chemists’ Society, 1983 p. 919-933.
  68. Peng SK, Taylor CB. Atherogenic Effect of Oxidized Cholesterol. In: Perkins EG, Visek WJ, editors. Dietary Fats and Health. Champaign, IL: American Oil Chemists’ Society, 1983 p. 930.
  69. White EG. The Ministry of Healing. Nampa, ID: Pacific Press Publishing Association, 1905 p. 301.
  70. Kosykh VA, Lankin VZ, et al. Very low density lipoprotein secretion by cultured hepatocytes of rabbits fed purified or autoxidized cholesterol. Lipids 1989 Feb;24(2):109-115.
  71. Peng SK, Taylor CB. Atherogenic Effect of Oxidized Cholesterol. In: Perkins EG, Visek WJ, editors. Dietary Fats and Health. Champaign, IL: American Oil Chemists’ Society, 1983 p. 919-933.
  72. Stamler J, Shekelle R. Dietary cholesterol and human coronary heart disease. The epidemiologic evidence. Arch Pathol Lab Med 1988 Oct;112(10):1032-1040.
  73. Peng SK, Taylor CB. Atherogenic Effect of Oxidized Cholesterol. In: Perkins EG, Visek WJ, editors. Dietary Fats and Health. Champaign, IL: American Oil Chemists’ Society, 1983 p. 919-933.
  74. Colaco CA, Roser BJ. Atherosclerosis and glycation. Bioessays 1994 Feb;16(2):145-147.
  75. Salonen JT, Nyyssonen K, et al. High stored iron levels are associated with excess risk of myocardial infarction in eastern Finnish men. Circulation 1992 Sep;86(3):803-811.
  76. Ascherio A, Willett WC, et al. Dietary iron intake and risk of coronary disease among men. Circulation 1994 Mar;89(3):969-974.
  77. Rimm EB, Stampfer MJ, et al. Vitamin E consumption and the risk of coronary heart disease in men. N Engl J Med 1993 May 20;328(20):1450-1456.
  78. Nutrition Essentials and Diet Therapy-6th edition. Philadelphia, PA: W.B. Saunders Co., 1991 p. 106.
  79. Nutrition Essentials and Diet Therapy-6th edition. Philadelphia, PA: W.B. Saunders Co., 1991 p. 100.
  80. Gaziano JM, Hennekens CH. The role of beta-carotene in the prevention of cardiovascular disease. Ann N Y Acad Sci 1993 Dec 31;691():148-155. Presented at the American College of Cardiology. Dallas, TX, 1992.
  81. Greenberg ER , Baron JA, et al. Mortality associated with low plasma concentration of beta-carotene and the effect of oral supplementation. JAMA 1996 Mar 6;275(9):699-703.
  82. Selhub J, Jacques PF, et al. Association between plasma homocysteine concentrations and extracranial carotid artery stenosis. N Engl J Med 1995 Feb 2;332(5):286-291.
  83. Naurath HJ, Joosten E, et al. Effects of vitamin B12, folate, and vitamin B6 supplements in elderly people with normal serum vitamin concentrations. Lancet 1995 Jul 8;346(8967):85-89.
  84. Stampfer MJ, Malinow MR. Can lowering homocysteine levels reduce cardiovascular risk? N Engl J Med 1995 Feb 2;332(5):328-329.
  85. Stampfer MJ, Malinow MR. Can lowering homocysteine levels reduce cardiovascular risk? N Engl J Med 1995 Feb 2;332(5):328-329.
  86. Verhoef P, Kok FJ, et al. Plasma total homocysteine, B vitamins, and risk of coronary atherosclerosis. Arterioscler Thromb Vasc Biol 1997 May;17(5):989-995.
  87. Graham IM, Daly LE, et al. Plasma homocysteine as a risk factor for vascular disease. The European Concerted Action Project. JAMA 1997 Jun 11;277(22):1775-1781.
  88. Nyg~ard O, Refsum H, et al. Coffee consumption and plasma total homocysteine: The Hordaland Homocysteine Study. Am J Clin Nutr 1997 Jan;65(1):136-143.
  89. Hall J. University of British Columbia, Genetics Meeting at the Jackson Laboratory in Bar Harbor, Maine, July 24, 1995.
  90. Stampfer MJ, Rimm EB. Folate and cardiovascular disease. Why we need a trial now?. JAMA 1996 Jun 26;275(24):1929-1230.
  91. The Food Processor for Windows: Nutrition Analysis & Fitness Software [computer program]. ESHA Research. Salem, Oregon.
  92. The Food Processor for Windows: Nutrition Analysis & Fitness Software [computer program]. ESHA Research. Salem, Oregon.
  93. Elsas LJ 2nd, Acosta PB. Nutrition Support of Inherited Metabolic Diseases. In: Shils ME, Young VR, editors. Modern Nutrition in Health and Disease-7th edition. Philadelphia, PA: Lea and Febiger, 1988 p. 1363-1367.
  94. Bloch AS, Shils ME. Appendix: Table A-43a. In: Shils ME, Young VR, editors. Modern Nutrition in Health and Disease-7th edition. Philadelphia, PA: Lea and Febiger, 1988 p. 1629.
  95. Isselbacher KJ, Braunwald E, editors, et al. Atherosclerosis and Other Forms of Arteriosclerosis. In Harrison’s Principles of Internal Medicine-13th edition (CD-ROM). New York, NY: McGRAW-HILL, Inc. Health Professions Division, 1994 p. 1106-1116.
  96. Williams PT. High-density lipoprotein cholesterol and other risk factors for coronary heart disease in female runners. N Engl J Med 1996 May 16;334(20):1298-1303.
  97. Blair SN, Kohl HW 3rd, et al. Changes in physical fitness and all-cause mortality. A prospective study of healthy and unhealthy men. JAMA 1995 Apr 12;273(14):1093-1098.
  98. Blair SN, Kohl HW 3rd, et al. Changes in physical fitness and all-cause mortality. A prospective study of healthy and unhealthy men. JAMA 1995 Apr 12;273(14):1093-1098.
  99. Glueck CJ. Nonpharmacologic and pharmacologic alteration of high-density lipoprotein cholesterol: therapeutic approaches to prevention of atherosclerosis. Am Heart J 1985 Nov;110(5):1107-1115.
  100. Anzalone DA, Anzalone FL, Fos PJ. High-density lipoprotein-cholesterol: determining hygienic factors for intervention. J Occup Environ Med 1995 Jul;37(7):856-861.
  101. Glueck CJ. Nonpharmacologic and pharmacologic alteration of high-density lipoprotein cholesterol: therapeutic approaches to prevention of atherosclerosis. Am Heart J 1985 Nov;110(5):1107-1115.
  102. American Heart Association. 1997 Heart and Stroke Statistical Update. American Heart Association, 1997 p. 3.
  103. Hartung GH, Foreyt JP et al Effect of alcohol intake on high-density lipoprotein cholesterol levels in runners and inactive men. JAMA 1983 Feb 11;249(6):747-750.
  104. Gibbons LW, Mitchell TL. HDL Cholesterol and Exercise. Your Patient & Fitness 1995 July 16-August;9(4):6-13.
  105. Bordia A. Effect of garlic on blood lipids in patients with coronary heart disease. Am J Clin Nutr 1981 Oct;34(10):2100-2103.
  106. Willett WC, Manson JE, et al. Weight, weight change, and coronary heart disease in women. Risk within the ’normal’ weight range. JAMA 1995 Feb 8;273(6):461-465.
  107. Oster G, Epstein AM. Cost-effectiveness of antihyperlipemic therapy in the prevention of coronary heart disease. The case of cholestyramine. JAMA 1987 Nov 6;258(17):2381-2387.
  108. Jacobs S. American Heart Association Meeting, 1992.
  109. Mittleman M, Muller J. 1994 Harvard Medical School, Reported at the American Heart Association Meeting.
  110. Berkman LF, Leo-Summers L, Horwitz RI. Emotional support and survival after myocardial infarction. A prospective, population-based study of the elderly. Ann Intern Med 1992 Dec 15;117(12):1003-1009.
  111. Thorogood M, Cowen P, et al. Fatal myocardial infarction and use of psychotropic drugs in young women. Lancet 1992 Oct 31;340(8827):1067-1068.
  112. American Heart Association. 1997 Heart and Stroke Statistical Update. American Heart Association, 1997 p. 3.
  113. Johnson CL, Rifkind BM, et al. Declining serum total cholesterol levels among US adults. The National Health and Nutrition Examination Surveys. JAMA 1993 Jun 16;269(23):3002-3008.
  114. American Heart Association. 1997 Heart and Stroke Statistical Update. American Heart Association, 1997 p. 2.
  115. The Harvard Health Letter, 1992.
  116. Sacks FM, Pfeffer MA, et al. The Effect of Pravastatin on Coronary Events after Myocardial Infarction in Patients with Average Cholesterol Levels. N Engl J Med 1996 Oct 3;335(14):1001-1009.
  117. Bennett, H. Personal Communication. Adventist Health Study; Loma Linda University School of Public Health. August 1996.
  118. Phillips RL, Lemon FR, et al. Coronary heart disease mortality among Seventh-Day Adventists with differing dietary habits: a preliminary report. Am J Clin Nutr 1978 Oct;31(10 Suppl):S191-S198.
  119. American Heart Association. 1997 Heart and Stroke Statistical Update. American Heart Association, 1997 p. 2.
  120. Medical Tribune, Cardiology section, Mar 23, 1995, p. 5.
  121. American Heart Association. 1997 Heart and Stroke Statistical Update. American Heart Association, 1997 p. 2
  122. American Heart Association. 1997 Heart and Stroke Statistical Update. American Heart Association, 1997 p. 18.





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