Cancer will soon overtake heart disease as the leading cause of premature deaths in the United States, and there is a strong linkage between the kinds of food we eat and the incidence of specific types of the disease. It has been estimated that 50 percent of all cancers in women and 30 percent in men are associated with environmental factors. Food supply is one of the most important causes. Concern has been mounting that food additives of various kinds may be contributing to the rising incidence of certain types of malignancies. In addition, there is evidence that substances “contaminating” our food supply, such as pesticide residues or industrial wastes, are increasing our risks for certain cancers.
These data, important as they are, should not detract from linkage between the kinds of food we eat and the increasing incidence of specific types of cancer. This problem defies regulation and cannot be blamed on any product or any manufacturer. The evidence comes both from studies of large human populations and from experiments on animals. The best data relate to two very common types of cancer—those of the breast and colon.
Cancer of the breast is a leading cause of death in the United States. The incidence of breast cancer is much lower in other parts of the world. If we list countries in the order of incidence of breast cancer, we can make an important generalization. The more highly developed the country, the higher the incidence of breast cancer. More careful scrutiny of the data gives us certain clues about which aspects of “modern living” contribute to this problem. Certain westernized countries—for example, Japan—do not show this high incidence of breast cancer.
By contrast, when Japanese people migrate to California and adopt the Western eating pattern, their children have the same incidence of this cancer as other Californians. If, on the other hand, they continue to eat as their parents did in Japan, few have cancer of the breast. Therefore, some element in our Western diet contributes to the high incidence of the disease. The strongest correlation appears to be with the amount of fat in the diet. The more fat the population of a particular country consumes, the higher the incidence of breast cancer, regardless of how developed a country is. The United States, with its high-fat diet, ranks high; but certain countries that consume more fat, such as Finland, rank even higher.
How does this high consumption of fat contribute to breast cancer? We know that hormones play an important role. The disease appears predominately in women. Animal studies suggest that a diet high in fat will result in an imbalance of female hormones. It is postulated that this hormone imbalance in some way promotes the occurrence of cancer of the breast. Women may alter their hormonal balance by consuming a high-fat diet, becoming more susceptible to breast cancer.
Colon cancer (cancer of the large intestine) is very common in the United States, and its incidence is increasing. Like cancer of the breast, it occurs more often in developed countries. Certain migrating populations have an incidence of this cancer that more closely matches that of their adopted country. This increase is noticeable as soon as they change their eating patterns to resemble those of the native population. The best correlation of cancer of the colon is with dietary fat. The more fat consumed, the higher the incidence of the disease. People such as Seventh Day Adventists, who consume little fat, show a low incidence of colon cancer.
Sex hormones play little or no role in the development of colon cancer; it happens with equal frequency in men and women. How then does this disease originate? Animal experiments suggest that a high-fat diet changes the normal bacterial makeup in the large intestine to favor the survival of bacteria that can easily transform fat into other products. One or more products of this bacterial transformation may act as a carcinogen (cancer-producing agent) or may promote the activity of carcinogens already in the large intestine. For example, certain substances normally secreted in the bile are known to be carcinogens. A high-fat diet may indirectly increase the carcinogenic activity of these substances.
The low-fiber content of the American diet may intensify the problem. Fiber is the carbohydrate portion of our food that is not digested and absorbed by our bodies. It is derived from plant sources, such as the bran of certain grains and from the skin and fleshy portion of fruits and vegetables. Dietary fiber draws water into it. Hence, as the fiber passes through the gastrointestinal tract, it softens the stool. The softer the stool, the faster it moves through the colon and the less time it is in contact with the intestinal wall. Thus, if the diet is high in fiber, the length of time the wall of the colon is exposed to cancer-inducing components in the stool will decrease. This is the theoretical mechanism by which a high-fiber diet provides some protection against colon cancer.
Another of the most common forms of cancer in women affects the uterus. This form of cancer is slightly more frequent in obese than in lean women. This is particularly true in those who have been obese since childhood. In one study, uterine cancer was one and a half times as frequent in women who suffered from obesity since adolescence as in women who were not obese. (The adolescent form of obesity often leads to an intractable form of adult obesity.)
There is some evidence that cancer of the ovaries and of the prostate may also be directly related to dietary fat intake. Cancer of the stomach, while affected by diet, is probably not related to fat. This cancer is much more prevalent in Japan than in the United States, and its incidence decreases when Japanese people migrate to California or Hawaii. However, the incidence of stomach cancer in Japan is decreasing. This may be due to their increased use of refrigeration as opposed to salting to preserve foods. The use of food additives such as BHA and BHT (antioxidant preservatives) in processed foods is another explanation for decreases in the incidence of stomach cancer.
Certain other factors are implicated for cancer of the breast, which occurs almost exclusively in women. It is most common among Caucasian women, less common among African-American women, and least common among Oriental women. (The risk in men is so small that the male population can be excluded from our discussion.)
Any woman who wants to determine her risk for breast cancer should examine her family history as completely as possible. A strong family history increases a woman’s risk for the disease. The closer your relationship to the member of your family tree who has or had breast cancer, the higher your risk. If your mother had breast cancer, your chances of developing it are statistically greater than if your great-aunt or a cousin had the disease. If the disease appears regularly in your family, your risk is greater than if it appears sporadically.
Regardless of other risk factors, women of high socioeconomic status have a slightly higher incidence than women of lower social or economic status. The reason for this is not certain. We feel that it is due to higher amounts of fat consumed by the higher-status women.
Single women are at greater risk than married women. This may be because they are much less likely to have completed a pregnancy. The more times a woman has become pregnant and carried to term, the lower her risk for cancer of the breast. While some reduction in risk is associated with each subsequent pregnancy, the greatest difference is between women who have never carried a pregnancy to term and those who have completed at least one pregnancy. The younger a woman is when she completes her first pregnancy, the lower her risk for breast cancer. Most of the difference occurs in women who are over thirty-five at the time they complete their first pregnancy. Though significant, the increase in risk is very small.
Women who reached puberty (menarche) late are at lower risk than those who underwent an early puberty. The trend toward earlier puberty in girls in Western countries may be associated with the increasing incidence of breast cancer. This trend may relate to our “better” diet. Some epidemiological studies suggest that, to the extent that this “better” diet is higher in fat, it may be contributing to the increased incidence of breast cancer. Japanese girls attain puberty later than American girls. The average caloric intake of the Japanese diet is about 1,000 calories less than ours. The primary difference is in the amount of fat consumed. Some studies suggest that the heavier a girl is, the earlier her menstrual periods will occur. As Japanese girls in higher socioeconomic classes have adopted Western lifestyles and a Western diet, their average weight has increased, their dietary fat consumption has gone up, their menstrual periods have begun earlier, and their incidence of breast cancer has risen. Thus, the increased risk imparted by the early onset of menstruation may be indirect. The direct cause may be an increase in the fat content of the diet.
The later the occurrence of menopause and the longer a woman’s reproductive life, the higher her risk of developing cancer of the breast. Thus, women who have shorter reproductive lives because of late onset of menarche, early menopause, or both, are at lower risk than women who have long reproductive lives.
The risks for cancer of the uterus are not as well-defined as those for cancer of the breast. One risk seems to be obesity, especially a history of it during adolescence; but the increase is small and may be indirect. Obesity is associated with early menarche, and this combination of features may contribute to the incidence. Late menopause or the use of estrogens to prevent the discomforts associated with menopause also increases the risk somewhat. This is a major concern; but, as we shall see in the chapter on osteoporosis, the use of progesterone together with estrogen substantially reduces and may even eliminate the threat.
No general aspect of cancer of the colon separates people at high and low risk. However, one specific factor, the existence of polyps, under certain conditions, predisposes us to colon cancer. Polyps are non-cancerous growths that may occur within the intestine. If present, polyps should be treated by a physician.
Tests are now available to identify individuals in high-risk families who carry specific genes for cancer of the breast. However, while this form of cancer has the best-defined risk, it is not possible, at this stage of our knowledge, to separate all individuals who are at high risk from those at low or moderate risk. If you have several of the factors mentioned above, your risk is substantial. Cancer of the breast is serious enough that all women should consider dietary modification, especially if they are affected by one or more risk factor. Neither cancer of the colon nor uterine cancer can be quantitated. We can only recommend dietary changes based on the statistical chances of developing certain cancers. Someday we may identify everyone at risk for particular cancers and be able to recommend specific dietary changes for them.
Since the dietary modifications are similar to those needed to reduce the risk of breast cancer, a low-fat, high-fiber diet is the best protection from the diet-related cancers that occur in this country. There is already enough evidence to encourage prudence in the amount of fat we eat. We estimate that most Americans consume an average of 12 grams of fiber daily, compared with 20 to 30 grams recommended by the American Cancer Society. Fiber-rich foods are fruits, vegetables, peas, beans, nuts, and grains. These foods are also sources of complex carbohydrates (starches) and, except for nuts, are very low in fat.
On the other hand, whole milk and whole milk products are high in fat and virtually fiber-free. Ideally, fat, whether visible (as in meat) or invisible (as in cheese), should contribute no more than 25 percent of the day’s total calories. If you eat 2,000 calories a day, no more than 500 should come from fat, and that amount is equal to 55 grams of fat. To keep within that amount, fried foods and spreads are limited and low-fat protein foods are encouraged (see Table 19).
Table 19. Fat Content of Some Protein Foods
(in Servings Providing 10 Grams of Protein)
Food Amount Grams Fat
Skim milk 9 oz. 0.1
Uncreamed cottage cheese ½ oz. 0.17
Cooked shrimp 1½ oz. 0.5
Cooked rice and beans ½ cup 0.7
Chicken (no skin) 1½ oz. 1.5
Pink salmon (canned) 1¾ oz. 3.0
Haddock 1¾ oz. 3.3
Veal (trimmed) 1½ oz. 4.5
Low fat yogurt 10 oz. 5.0
Hamburger (lean) 1½ oz. 5.0
Hamburger (regular) 1½ oz. 8.5
Eggs (large) 1½ oz. 10.0
Ham 1½ oz. 10.0
American cheese 1½ oz. 13.5
The recommended changes require simple adjustments. Eat more vegetables—the more raw, the better—and whole-grain products. Eat the skin on your boiled or baked potato; consider raisins or almonds as alternatives to candy bars; and avoid fried foods in favor of fresh fruits and salads. Consider a slice or two of “fat free” cheese on whole wheat bread for breakfast or with an apple for your evening snack. It will contribute calcium to your diet without the hazards of the saturated fats in regular dairy products.
Table 20. High- and Low-Fiber Menus
8 oz. orange juice 1 orange
1 slice white bread 1 slice whole wheat bread
1 tsp. butter 1 tbs. apple butter
6 oz. whole milk 1 cup 40% bran flakes
½ cup canned peaches 6 oz. skim milk
1 cup corn flakes 1 tbs. almonds and
1 tbs. raisins
3 oz. roast beef 3 oz. turkey (white meat)
1½ tbs. mayonnaise on whole wheat bread
20 French fries mustard and lettuce
6 oz. instant onion soup tossed salad with lemon juice
Cola 1 cup vegetable soup
Gelatin dessert and topping 8 oz. apricot nectar
1 medium apple
Snack pie ½ cup dried fruit-and-nut mix
Coffee and cream 6 oz. vegetable juice
4 oz. fried chicken 4 oz. broiled fish
½ cup macaroni and cheese 1 cup gumbo (corn, tomatoes, okra)
¼ cup Cole slaw 1 cup brown rice
½ cup buttered peas 1 cup fresh relish (radishes, celery,
green pepper, carrot curls)
2 dinner rolls 1 slice Banana Bran Bread
2 tsp. margarine ¼ cantaloupe wedge
¾ cup frozen yogurt
10 potato chips 1½ cups popcorn
12 oz. carbonated beverage (plain, air popped)
12 oz. apple juice
Total 120 grams fat 45 grams fat
Tables 20 and 21 will help you select some of your favorite foods to increase the fiber content of your diet.
Table 21. Dietary Fiber Content of Some Foods
Food Measure Fiber(g)
Almonds ½ cup 3.2
Apple, unpeeled 1 small 2.8
Asparagus, cooked ½ cup 1.8
Bananas 1 small 2.2
Beans, green, cooked ½ cup 1.2
Beam, white, cooked ½ cup 5.0
Bran, wheat 2 tsp. 3.3
Bread, white or 2 slices 1.2
Bread, whole wheat 2 slices 3.0
Broccoli, cooked ½ cup 2.4
Bulgur wheat, dry 1 oz. 5.2
Cabbage, cooked ½ cup 1.8
Cabbage, shred, raw ½ cup 0.7
Carrots, cooked ½ cup 1.8
Lettuce, romaine 2 leaves 0.4
Macaroni, cooked ½ cup 1.1
Mushrooms 10 small 0.8
Noodles, cooked ½ cup 1.7
Oatmeal, cooked ½ cup 2.9
Orange 1 med. 0.9
Orange juice ½ cup 0.1
Peanuts, roasted ½ cup 5.8
Peas, green, cooked ½ cup 4.3
Popcorn 3 cups 3.0
Potatoes, baked 1 med. 1.8
Potatoes, mashed ½ cup 1.2
Prunes, dried 3 med. 1.7
Rice, brn, cooked ½ cup 2.4
A diet high in fiber and low in fat pleases people all over the world. People who live in the exotic islands of the Pacific eat a variety of fish, fruits, and vegetables. Herdsmen in parts of Europe and Russia drink low-fat cultured milk and eat whole-grain breads with fresh fruits and vegetables. Compare the total fat and fiber in the above menus (Table 20) and get hints from them.
There are numerous claims that large doses of certain vitamins or minerals will protect us against cancer. Some of these claims are based on theoretical considerations with little or no data to support them. Others do not even have a theoretical reason for being used. Yet, the practice of taking vitamin C or E or the mineral selenium to prevent cancer has become widespread. Vitamin E has been shown to offer some protection against certain cancers in animals. No studies in humans have confirmed this effect. The data we have in human populations do not show any protective effect for vitamin C. While high doses of vitamin C have not shown serious toxic effects, there has not been enough experience with these doses for long enough periods of time (over many years) to be sure.
While selenium may have some effect against cancer in humans, there has been no experience with long-term administration of high doses of the element. Such a practice could be dangerous. Like fluoride and other trace elements necessary for life in trace amounts but toxic in larger doses, the range between the amount that is optimum and the dosage at which this micro nutrient becomes toxic is very narrow.
Experimental data with vitamin A coupled with some human studies showing that populations with a high incidence of vitamin A deficiency also have a high incidence of certain cancers has led to recommendations that an abundant amount of vitamin A be included in our diet. Potent supplements of vitamin A have been shown to have a protective effect against some types of cancers; but the product is very toxic in high doses. The structure of vitamin A has been altered in the laboratory so that its toxicity is reduced while its cancer-preventing properties are preserved. Several such “analogs” of vitamin A are being tested in populations at very high risk for certain cancers—for example, people with bladder papillomas (a pre-cancerous condition) or asbestos workers, who are at very high risk for lung cancer. However, even in the animal experiments, these analogs, like vitamin A itself, are effective only as preventive measures. They are not a cure for cancer. Beta-carotene, the form of vitamin A in plants, is considered to be non-toxic. One study indicated that supplements of beta-carotene increased the incidence of lung cancer in heavy smokers (but not in non-smokers). We believe that was a valid finding and not a chance occurrence or a statistical fluke. One plausible explanation is that the beta-carotene provides more protection for cancer cells (or precancerous cells) than for normal tissue—in contrast to the selective lethal effects of toxic drugs on cancer cells.
Cruciferous vegetables (the cabbage family), such as Brussels sprouts and broccoli, are particularly noteworthy for their content of phytochemicals (substances of plant origin) which aid in prevention of some forms of cancer, and tomato-based products (rich in lycopene) seem to lower men’s risk for prostate cancer. In practice, this means eating carrots, squash, and other yellow/orange vegetables in addition to the green ones such as Brussels sprouts, spinach, collards, turnip greens and broccoli and the red ones such as tomatoes and red peppers. These vegetables also contribute fiber to our diets, and they are low in fat. Culinary artists displayed colorful vegetables on our dinner plates long before we knew about their protective values. Now, they even include edible flowers. While this is no sure way of preventing cancer, it is a reasonable step to take.
Lest we go overboard with any single food, it is important to reconsider the old adage, “You can get too much of a good thing.” Cabbage and other cruciferous foods, if eaten in large quantities, every day, can cause goiter. We can present a long list of beneficial phytochemicals in familiar foods, but we can also present a long list of toxins that, if consumed in large enough quantity, can make you sick. Don’t go overboard with any single food. Variety in our daily menus breaks monotony, and it also averts excesses of foods that are protective in reasonable amounts but toxic when carried to extreme.
A number of substances, some of them found in foods, have been promoted as cancer cures. Some of these claims have been made by sincere people; others, by out-and-out phonies. In either case, this is a serious problem. Cancer patients may forgo proven methods of treatment to try some unproved remedy. This practice is costing lives that may have been saved (while draining the victim’s family of its hard-earned savings). Many cancers can be cured if proper therapeutic measures are initiated during the early stages of the disease. Great progress has been made in identifying phytochemicals (taxol, for example) which are useful in treatment of cancer and other diseases; but the products are pharmaceuticals (not nutrients). A better known example is aspirin. It is a natural product, long known for its palliative properties as an extract from willow tree bark before it was synthesized in the laboratory. “Curative” products are often labeled as food supplements to avoid the rigid test standards of the Food and Drug Administration. These products are not on the market for their nutritive content and should not be classified as foods. There is no known nutrient that can cure cancer.