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Institute of Medicine (US) Committee on Diet and Health; Woteki CE, Thomas PR, editors. Eat for Life: The Food and Nutrition Board's Guide to Reducing Your Risk of Chronic Disease. Washington (DC): National Academies Press (US); 1992.

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Eat for Life: The Food and Nutrition Board's Guide to Reducing Your Risk of Chronic Disease.

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Chapter 6Fats, Cholesterol, And Chronic Diseases

Without a doubt, fats and cholesterol are the single most important group of nutrients to limit in your diet if you want to help to reduce your risk of chronic disease. Heart disease and cancer, this nation's two leading killers, are linked to diets high in fat, and other chronic health problems may be exacerbated by high-fat diets. And yet our national diet contains as much as one-third more fat than it should.

If your diet is too high in fat—and the chances are good that it is—then read this chapter carefully. It will give you the reasons—and the motivation—to change your diet for the better.

Heart Disease

Cornelius de Langen, a Dutch physician working in Java, reported in 1916 that native Indonesians had much less heart disease than did the Dutch colonists living on the island. He associated the natives' healthy hearts with their lower serum cholesterol levels. De Langen also observed that when Indonesians worked as stewards on Dutch passenger ships and ate typical Dutch food, their cholesterol levels soared, and so did their incidence of heart disease.

Although this report lay unnoticed for more than 40 years—it was published in an obscure research journal—it was the first recorded suggestion that diet and serum cholesterol levels in humans were somehow related to heart disease. In the years between then and now, scientists have accumulated an impressive amount of evidence firmly linking the amount and kind of fat and the amount of cholesterol people eat to the risk they stand of having a heart attack. In fact, nowhere is the connection between diet and chronic illness more scientifically firm and convincing than it is with fats and heart disease.

This story of fats and heart disease has three parts. The first reveals the association of high serum cholesterol levels with increased risk of having a heart attack. The second links high saturated fatty acid and cholesterol consumption to high serum cholesterol levels. And the third ties high saturated fatty acid and cholesterol consumption to an increased risk of having a heart attack.

The Case for Lower Serum Cholesterol

Serum cholesterol levels vary widely both among groups of people in various parts of the world and among individuals of those groups. For example, scientists in seven countries worked together to measure serum cholesterol levels in different groups of middle-aged men. The results showed that the average serum cholesterol level of Japanese men was 157 milligrams per deciliter (mg/dl), whereas men living in eastern Finland averaged 262 mg/dl.

There are also large differences among the different peoples of the world in the incidence of heart disease. For example, heart attacks are rare in Mediterranean countries, whereas they are fairly common in Scandinavia.

Because both cholesterol levels and the incidence of heart disease vary greatly among different groups of people, might the two be connected? In other words, do groups of people with high serum cholesterol levels have more heart attacks than populations with low levels? By comparing the rates of heart disease—how many individuals have a heart attack for every 1000 people, for example—with the average serum cholesterol levels among groups of people, scientists have determined that the answer is definitely yes. Populations in which the average serum cholesterol level is less than 180 mg/dl are virtually free of both atherosclerosis and heart disease. In contrast, those groups of people in which the average serum cholesterol level is above 220 mg/dl have high rates of heart attacks.

Further evidence for linking high blood cholesterol levels with the incidence of heart disease comes from many studies of people within a particular population group. Since 1948, for example, thousands of volunteers from the city of Framingham, Massachusetts, have been examined every 2 years as part of a comprehensive scientific effort to identify and understand the factors that affect heart health. Results from this study show that, among both men and women, the higher the blood cholesterol level, the greater the risk of developing heart disease. The same relationship was shown in a group of more than 300,000 men across the country aged 35 to 57 years who were medically evaluated as part of a study that came to be known as MR. FIT.

Another way to examine the link between cholesterol level and risk of heart disease is to lower blood cholesterol levels in a large group of volunteers by diet, drugs, or both, and to monitor the number of heart attacks and deaths from heart disease in the group over time. These experiments, known as clinical trials, have enabled scientists to develop the following rule of thumb: each 1 percent reduction in blood cholesterol can be expected to lead to a 2 percent reduction in the risk of heart disease.

As is shown in Chapter 3, not all serum cholesterol is alike. Cholesterol travels through the blood not by itself, but as part of lipoproteins, which are aggregates of lipids and proteins. There are three types of lipoproteins that ferry cholesterol through the blood stream to and from the billions of cells in the body. Low-density lipoproteins (LDLs) carry between 60 and 70 percent of the cholesterol in the blood stream, and high-density lipoproteins (HDLs) carry another 20 to 30 percent. A third lipoprotein, very-low-density lipoproteins (VLDLs), carries the rest, though its main role in the body is to carry triglycerides through the blood stream. In industrial societies, typical LDL-cholesterol values range from 110 to as high as 200 mg/dl or more, and HDL-cholesterol values run from around 30 to near 60 mg/dl.

Once the connection between total serum cholesterol levels and heart disease was firmly established, scientists began wondering if one particular lipoprotein was involved in the relationship. To find the answer, they conducted the same type of studies they did before—they measured lipoprotein levels in different groups of people and determined the rate of heart attacks in those groups.

What these studies showed was that within populations elevated LDL-cholesterol levels were important contributors to high rates of heart disease. Moreover, LDL levels were almost totally responsible for differences among populations in blood cholesterol levels and heart disease risk. What is more, any change in LDL-cholesterol levels was associated with a corresponding change in the incidence of heart attacks. When LDL-cholesterol levels rose, more people had heart attacks.

Another piece of evidence in the case against LDL-cholesterol comes from studies of a disease called familial hypercholesterolemia, FH for short. This is an inherited disease in which there is a defect in the mechanism by which cells take up LDL from the blood stream. Because of that defect, LDL-cholesterol levels are very high in people with FH.

With the less severe (heterozygous) form of FH, in which the mechanism works at about half its normal rate, LDL-cholesterol levels rise to more than 300 mg/dl. About 1 person in 500 in the United States has heterozygous FH. People affected with heterozygous FH often develop premature heart disease, men in their 40s or earlier, women in their 60s. About 5 percent of men who have heart attacks before they turn 60 have heterozygous FH.

About one in a million people suffer from the very severe (homozygous) form of FH, in which the LDL-removal system is missing entirely. LDL-cholesterol levels soar and can reach 600 to 1000 mg/dl. With very severe FH, heart attacks during the teenage years are common. People with very severe FH rarely survive past age 30.

The story with HDLs is not as clear. Within the United States and most industrialized countries, people with high HDL-cholesterol levels have lower rates of heart disease, and those with low HDL-cholesterol levels are at increased risk of heart disease. Thus, in the popular press and other media, HDL-cholesterol is often referred to as the "good" cholesterol and LDL-cholesterol as the "bad" cholesterol.

The wisdom of lowering total serum cholesterol and LDL-cholesterol levels to prevent heart disease is unquestioned by almost all researchers in cardiovascular diseases. The problem, then, is to determine what, if any, factors in the diet cause total serum cholesterol and LDL-cholesterol to be high in the first place. That brings us to the second part of the story.

The Effects of Fatty Acids (Saturated, Monounsaturated, and Polyunsaturated) and Cholesterol in the Diet

To establish a correlation between diet and serum cholesterol levels, researchers once again studied groups of people. In the early 1950s, scientists examined the eating habits of working-class residents of Naples, in southern Italy. The great bulk of these people's diets consisted of bread and pasta, with only 20 percent of their calories coming from fat. They ate cheese and meat in small amounts, used olive oil sparingly, and ate no butter at all. Their serum cholesterol levels averaged a healthy 172 mg/dl.

At about the same time, other investigators examined a group of apparently healthy male factory workers who had lived their adult lives in the United States but whose parents had been born near Naples. These men got about 43 percent of their calories from fat—most of it from animal fats—and their average serum cholesterol level was 239 mg/dl.

Similar studies have shown consistently the same results: People who get a big share of their calories from fats, particularly animal fats with a high proportion of saturated fatty acids, have higher total cholesterol and LDL-cholesterol levels than people who eat diets that are relatively low in fat, particularly saturated fatty acids.

The story is a little more complicated than this, however, for not all saturated fatty acids have the same cholesterol-raising effect. In experiments that began in the late 1950s, scientists fed volunteers foods that were rich in saturated fatty acids. All the foods but one—cocoa butter—had the predicted effect of raising serum cholesterol levels. The major saturated fatty acid in cocoa butter is stearic acid, which contains 18 carbon atoms.

Other studies confirmed this observation and, in addition, showed that saturated fatty acids with 10 or fewer carbon atoms have no effect on serum cholesterol levels either. These studies have shown that palmitic acid (16 carbon atoms) and myristic acid (14 carbon atoms) are the major cholesterol-raising saturated fatty acids. Lauric acid (12 carbon atoms) probably also raises serum cholesterol levels.

Scientists suspect that these saturated fatty acids interfere somehow with the LDL-removal system of the body's cells. As a result, LDL-cholesterol accumulates in the blood stream and eventually deposits its cholesterol onto atherosclerotic plaques in arteries. In a way, these saturated fatty acids mimic the effects of FH, the inherited disorder that causes LDL-cholesterol to rise.

Now what about cholesterol itself: Does eating a lot of cholesterol raise the levels of LDL-cholesterol? The answer is yes, although the LDL-raising effect of dietary cholesterol is not as large as that of the cholesterol-raising saturated fatty acids. On average, eating 200 mg of cholesterol per 2000 calories raises LDL-cholesterol levels by about 8 to 10 mg/dl above what they would be without eating any cholesterol; eating larger amounts of cholesterol produces a further rise. So if you now eat 750 mg of cholesterol a day, you should be able to cut your LDL-cholesterol levels simply by lowering the amount of cholesterol you eat to 250 mg a day. As a result, you might also reduce significantly your risk of having a heart attack.

The foregoing discussion is based on how groups of people respond to different levels of dietary cholesterol. Within the group, however, individuals vary in how responsive they are. Some people are resistant to the LDL-raising effect of dietary cholesterol, whereas others—at least one-third of the U.S. population—are quite sensitive. Unfortunately, it is not feasible on a national scale to find out who is sensitive to dietary cholesterol and who is not; testing cholesterol responsiveness involves eating a controlled diet for weeks and analyzing several blood samples. So until the day comes that we can take a cholesterol response test as easily as we can a serum cholesterol test, we should all try to reduce our cholesterol levels by not eating a large amount of foods that are high in cholesterol.

Whereas cholesterol and saturated fatty acids in the diet have been shown to have detrimental effects, monounsaturated and polyunsaturated fatty acids in the diet are a different story.

In the 1950s, researchers observed that diets containing various vegetable oils reduced serum cholesterol levels when compared with animal fats, regardless of dietary cholesterol intake. These findings have been widely confirmed. It has also been shown that replacing saturated fatty acids with monounsaturated or polyunsaturated fatty acids causes LDL-cholesterol levels to drop substantially. With monounsaturated fatty acids, there is no effect on HDL-cholesterol levels, whereas with polyunsaturated fatty acids there is a tendency for HDL-cholesterol levels to fall as well.

These findings have important practical implications. You do not need to lower your fat intake drastically to reduce your serum cholesterol and LDL-cholesterol levels. Rather, reduce your intake of saturated fatty acids by replacing them in part with carbohydrates and in part with vegetable oils rich in monounsaturated fatty acids (such as olive and canola oil). These measures will help to keep your diet palatable and interesting.

Studies in animals and the study in two groups of veterans mentioned in the next section suggest that diets high in polyunsaturated fatty acids may be linked to other chronic diseases. Because there are no human diets that are naturally high in polyunsaturated fatty acids and because information is lacking about the long-term health consequences of such a diet, you should not increase your intake of polyunsaturated fatty acids over what is now in the U.S. diet (an average of 7 percent of daily calories).

Saturated Fatty Acids and Heart Disease

There is a famous truth in mathematics that states: If A equals B, and B equals C, then A must equal C.

Applying the same logic to nutrition, we would arrive at the conclusion that eating a lot of saturated fatty acids raises the risk of developing heart disease. For if diets high in saturated fatty acids ''equal" high total serum cholesterol and high LDL-cholesterol, and if high serum and LDL-cholesterol "equal" high incidence of heart disease, then it must be true that diets high in saturated fatty acids "equal" high incidence of heart disease.

Scientists, however, are rarely content to prove such important connections using mathematical logic, and so they turned once again to examining the rates of heart disease in various populations around the world. They found that there is indeed a strong association between diets high in saturated fatty acids and a high incidence of heart attacks.

These studies also showed clearly that saturated fatty acids could explain the association. On the island of Crete, for example, many of the residents consumed a diet that contained as much as 40 percent of their daily calories as fat, and yet they suffered very little from heart disease. The investigators concluded that the relationship was probably due to the low level of saturated fatty acids, which accounted for only 8 percent of the daily calories in Crete, while monounsaturated fatty acids made up 29 percent of the calories.

In another study, designed as a controlled dietary trial, researchers compared the incidence of heart attacks in two groups of veterans who were randomly assigned to two diets. The men in both groups ate diets in which fat provided 40 percent of the calories. But while one group ate a typical U.S. diet high in saturated fatty acids, the other group ate a diet in which monounsaturated fatty acids and polyunsaturated fatty acids each accounted for about 15 percent of the total calories and saturated fatty acids were reduced to approximately 10 percent of total calories. Almost immediately, the serum cholesterol levels in the group with the diet low in saturated fatty acids dropped nearly 13 percent. The number of deaths from heart disease in this group fell 31 percent.

High Blood Pressure

People who follow a strict vegetarian diet—no meat, poultry, fish, eggs, or dairy products—tend to have lower blood pressure than those who eat a typical U.S. diet. Since strict vegetarians eat more monounsaturated fatty acids and polyunsaturated fatty acids, and less total fat, saturated fatty acids, and cholesterol, it is reasonable to suspect that dietary fat may have something to do with developing hypertension. Other factors that help keep the blood pressures of strict vegetarians low are their tendencies to refrain from smoking, to be within their ideal weights, and to get regular exercise.

What a number of studies show is that the total amount of fat in the diet does not seem to affect blood pressure. In some studies, however, the levels of saturated fatty acids and of linoleic acid seem to have a modest effect. People living in rural Finland, for example, eat more saturated fatty acids and on average have higher blood pressures than rural residents of the United States and Italy. When volunteers eat special diets containing various amounts of saturated fatty acids and polyunsaturated fatty acids, those people eating a diet in which the amounts of saturated fatty acids and polyunsaturated fatty acids were equal have lower blood pressures, on average, than those eating food high in saturated fatty acids and low in polyunsaturated fatty acids.

Again, these results do not mean you should eat more polyunsaturated fatty acids and less saturated fatty acids to lower your blood pressure. Rather, you should eat less saturated fatty acids while keeping the amount of polyunsaturated fatty acids in your diet about constant at about 7 percent of your daily calories. Polyunsaturated fatty acid intake should not exceed 10 percent of caloric intake.


Eating a diet high in fat can increase the risk of developing cancer, particularly cancers of the colon and breast. Studies of cancer rates and eating habits among the different people of the world show a consistent relationship between high-fat diets and high overall cancer rates. None of these studies, though, are as conclusive as those linking high-fat diets to heart disease.

Studies of the relationship of dietary fat to the development of cancer are confounded by several factors. High-fat diets tend to be low in complex carbohydrates, fiber, and fruits and vegetables—all thought to help prevent cancer. High-fat diets are also associated with higher caloric intakes and obesity, factors that are suspected to encourage the development of some cancers.

It has been difficult, too, to pinpoint any connections between dietary fat and specific cancers, or between specific types of fat and cancer. Studies of breast cancer, for example, tend to support a weak link between dietary fat and the risk of developing breast cancer. Some of these studies also single out saturated fatty acids, while others do not.

Why the inconsistencies? One reason might be that the amount of fat eaten early in life may have a greater influence on breast cancer risk than fat eaten as adults. Therefore, when adults lower their fat intake, it might take years to show a beneficial effect on cancer rates.

Another plausible explanation for the less-than-conclusive results of population studies is that it is difficult to reconstruct a person's diet over the many years before cancer develops. In addition, population studies are often not sensitive enough to detect links between diet and disease. Such confusion would help to obscure any diet-cancer link. These last two problems are not specific to studies of breast cancer.

Diets high in fat, particularly saturated fatty acids, appear to increase the risk of developing colon and rectal cancers. There is also evidence of a link between diets high in animal fat and prostate cancer. One study has shown that endometrial cancer occurs more often in parts of the world where the residents eat a high-fat diet, but other studies have been inconclusive. Overall, the evidence is strong enough to support a recommendation to eat less fat in order to reduce the risk of cancer.

Other Chronic Degenerative Diseases

There is little conclusive evidence that dietary fat plays a role in causing any chronic diseases other than heart disease and cancer. Some studies suggest that lowering fat intake, as well as reducing alcohol intake, may allow obese and overweight people to lose weight, but this may be mainly an effect of lowering the total number of calories in the diet.

Gallstones are more common in people who eat diets high in fat and who are overweight or obese, but weight seems to be the major contributing factor. Thus if a low-fat diet can enable overweight and obese people to lose weight, such a diet will indirectly reduce the risk for gallbladder disease.

Children: A Special Case?

The evidence is clear that U.S. adults need to reduce the amount of fat, particularly saturated fatty acids, that they eat. It appears that children eat too much fat as well. Because diet and exercise patterns are established in youth, it is particularly important for parents to move their children away from a high-fat diet and sedentary life and into a low-fat diet and an active life.

Infants and toddlers, that is, children who are less than two years old, are a special case, however. An infant's diet is high in cholesterol and fat—about half the calories in mother's milk come from fat, and saturated fatty acids make up almost half of those calories. Cow's milk and infant formula are also high in fat, but they contain a different mix of fatty acids than mother's milk. Cow's milk, for example, has more saturated fatty acids, less monounsaturated fatty acids, and much less polyunsaturated fatty acids. In contrast, infant formulas are higher in polyunsaturated fatty acids, but contain virtually no cholesterol.

Infants respond to high-fat, high-cholesterol milk in the same way that adults would—their serum cholesterol levels are raised. But most health experts believe this should be no cause for concern. For one thing, children breastfeed or take formula for only a short period of time, so the high cholesterol level probably has no lasting effects. Perhaps even more important, however, breast milk, in particular, meets other nutritional needs of infants. Thus, parents should not try to reduce the amount of fat their infants and toddlers eat.

But that is not the case with children once they start eating the same foods as adults. Several studies of children's eating habits show that U.S. school-age children's diets contain an average of 38 percent fat—much of it saturated fatty acids—and 300 mg of cholesterol. As a result, children in the United States have relatively high serum cholesterol levels.

The consequences of having high serum cholesterol as a child are not yet clear, but two pieces of evidence suggest that the outcome may not be good. For one thing, children with high cholesterol levels tend to become teenagers and young adults with high cholesterol. In addition, doctors have found that significant numbers of young adults already have detectable atherosclerosis. Therefore it seems that children have as much to gain from reducing their fat intake as do adults.

Some people have questioned the safety of tampering with our children's diets. After all, our children are far healthier today than they were at the beginning of this century, thanks in part to improved nutrition. But many studies show that a low-fat diet is safe for children. These studies show, too, that there is no need for anyone over the age of two to get more than 30 percent of their calories from fat.

Copyright © 1992 by the National Academy of Sciences.
Bookshelf ID: NBK235018


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