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Section Two: Cancer Prevention

Cancer starts when the DNA in a cell is damaged by a toxic chemical, radiation, or other factors, causing it to multiply. Eventually, the growing tumor invades healthy tissues and may also release some of its cells to travel to other parts of the body where new tumors form, a process called metastasis.

While detection and treatment remain vitally important in our battle against cancer, research has given us powerful tools that help prevent it. According to the National Cancer Institute, as many as 80 percent of cancers can be attributed to environmental factors, the most important of which are diet and smoking. Tobacco is responsible for approximately 30 percent of cancers, including those arising in the lung, mouth, esophagus, kidney, and bladder. Food accounts for roughly 35 percent to 60 percent of cancers, including cancers of the stomach, colon, liver, prostate, breast, uterus, and ovary, among other sites. By helping our patients change their smoking and diet habits, we help them reduce their cancer risk.

Most people are aware that some foods contain chemical carcinogens. However, there are other very important ways that foods influence cancer risk. First, foods affect the concentration of sex hormones in the blood, which influences the risk of cancer of the prostate, breast, uterus, and ovary. Second, some foods increase the formation of carcinogens in the digestive tract, while others have the opposite effect. This is of particular importance in cancers of the colon and rectum. Third, foods can alter the ability of the immune system to recognize and eliminate cancer cells.

The link between diet and cancer is not new. An article in Scientific American in January 1982, observed that “cancer is most frequent among those branches of the human race where carnivorous habits prevail.” Our knowledge has grown enormously since then, and we can now use this knowledge for our patients’ benefit.

To the extent we succeed at preventing cancer, we help our patients avoid the rigors, frustrations, and expense of cancer treatment, and the toll that this disease would otherwise continue to take.

Estimated Percentages of Cancer Due to Selected Factors1,2

Diet 35-60%
Tobacco 30%
Air and Water Pollution 1-5%
Alcohol 3%
Radiation 3%
Medications 2%

Breast Cancer

When your patients consider what they can do to prevent breast cancer, they think of mammography and breast examinations, techniques that are useful and often life-saving. However, they do not prevent cancer. They are designed to find cancer so that treatment can begin at the earliest possible point. Preventing cancer is much more desirable than detecting or treating it, particularly since a tumor that is big enough to be detected through mammography or examination has already been present for several years and may already have spread to other organs.

In 1982, the National Research Council published a report called Diet, Nutrition, and Cancer,3 detailing the existing evidence linking specific dietary factors to cancer of the breast and other organs. Asian countries, such as Japan, have low breast cancer rates, while rates in Western countries are many times higher. When Japanese women westernize their diets, as has been happening since the 1950s, their breast cancer rates climb. Among affluent Japanese women, those who eat meat daily have approximately six times higher risk of breast cancer compared with those who rarely or never eat meat.4 When Japanese families move to the United States, their daughters acquire the same risk of cancer as the other American women.4,5

Fat Increases Estrogens

Part of the explanation relates to fat. In the 1940s and 1950s, when breast cancer was particularly rare in Japan, only 7 percent to 10 percent of the calories in the Japanese diet came from fat, because of the generous quantities of rice and vegetables that were dietary staples.6 In the American diet, however, approximately 35 percent of calories come from fat, due to the routine use of animal products, fried foods, and added oils.

Countries with a higher intake of fat, especially animal fat, have a higher incidence of breast cancer.5,7,8 The 1988 Surgeon General’s Report on Nutrition and Health stated: “Indeed, a comparison of populations indicates that death rates for cancers of the breast, colon, and prostate are directly proportional to estimated dietary fat intakes.”9

While it is easy for patients to picture how fatty foods could increase colon cancer risk, the effect of fatty foods on breast cancer risk requires more explanation.

Fat stimulates the production of estrogens, which encourage the growth of breast cancer cells. High-fat diets increase estrogen levels. On the other hand, reducing the amount of fat in the diet reduces estrogen levels within a matter of weeks.10-12

Vegetarians have significantly lower estrogen levels than non-vegetarians, in part because of the lower fat content of their diet. They also have more of the carrier molecule, sex hormone binding globulin (SHBG), that has the job of holding onto estrogen until it is needed.

Animal fats may be a bigger problem than vegetable oils. Researchers from the New York University Center compared the diets of 250 women with breast cancer to 499 women without cancer from the same province in northwestern Italy. The two groups ate about the same amount of olive oil and carbohydrates. However, the cancer patients had habitually eaten more meat, cheese, butter, and milk. Women who consumed more animal products had as much as three times the cancer risk of other women.13

An additional benefit of traditional Asian diets may be their use of soy products, such as tofu, miso, and tempeh. Soybeans contain natural phytoestrogens (the prefix “phyto” simply means “plant”). These very weak plant estrogens can occupy the estrogen receptors on breast cells, displacing normal estrogens. The result is less estrogen stimulation of each cell.

How Much Fat Is Too Much?

While some cancer organizations recommend diets encouraging a shift from “red meat” to “white meat” and a reduction in fat to no more than 30 percent of calories, such changes are probably too minor to be of benefit. Indeed, the Harvard Nurses’ Study studied a large group of women over an eight-year period and found no reduction in cancer rates among those whose diets contained 30 percent of calories from fat, compared to those eating more fat.14 While some have interpreted this to mean that diet has nothing to do with breast cancer, a more reasonable conclusion is that the diets these women followed were still high-risk diets.

Fiber Reduces Estrogens

While many people are now conscious of the amount of fat in the foods they eat, other parts of foods also play important roles in breast cancer risk. Almost certainly, the total diet composition, not simply fat, is important. For example, vegetables, fruits, grains, and beans provide fiber, which helps the body eliminate waste estrogens.

Normally, as the liver filters the blood, it removes excess estrogens and sends them through the bile duct into the intestinal tract. There, fiber soaks them up like a sponge, carrying them out with the wastes. Animal products and refined sugars have no fiber, and, to the extent that such foods displace fiber-rich foods in the digestive tract, waste estrogens can pass back into the bloodstream. Whole grains, legumes, vegetables, and fruits supply fiber to help insure that waste estrogens are eliminated properly.

Many vegetables and fruits are also rich in vitamin C and beta-carotene, and grains supply selenium, both of which are linked to lower cancer risk. Several studies have shown that the more high-fiber, vitamin- and mineral-packed foods women consume, the lower their cancer risk.15,16

Alcohol increases breast cancer risk, apparently through estrogenic effects. Even one drink a day can increase breast cancer risk by more than 50 percent, compared to non-drinkers.17 This is largely unknown to patients, many of whom have heard that a glass of red wine every day is supposed to be good for the heart, not realizing its contribution to cancer risk.

Other Risk Factors

Other factors that increase breast cancer risk have been identified:

Hormones: Although newer birth control pills contain less estrogen and progesterone than older versions, evidence suggests some increase in risk from oral contraceptives.18 The same is true of supplemental estrogens given to women after menopause.19 While manufacturers aggressively market estrogen “replacement” products to reduce the risk of heart disease and osteoporosis, their effect on breast cancer risk suggests that other approaches to these conditions should be strongly considered. See Section 1 and Section 7 for more information.

Overweight: Higher body weight is associated with higher postmenopausal breast cancer risk.20 The same low-fat, plant-based diet that reduces estrogens is also the most effective means for permanent weight control.

Radiation: Breast cells are very sensitive to the damage of radiation, and there is little doubt that x-ray irradiation to the breast can cause cancer.21 This raises an obvious question about mammography, which, of course, are x-ray examinations. However, compelling evidence shows that mammograms can be life-saving for women over the age of 50, and the use of modern, well-maintained equipment minimizes radiation dosage.

Genetics: About 5 percent of breast cancer cases are purely attributable to genetics.22 In such cases, cancer is passed from parent to child as a dominant trait, and the family tree is riddled with the disease. For a larger group of individuals, genetics probably make a contribution in more subtle ways, influencing susceptibility to carcinogens, immune strength, the reproductive cycle, or other factors that are relevant to cancer risk.

Toxic Chemicals: Breast cancer is not evenly distributed geographically. Areas near toxic waste sites tend to have higher than average rates of cancer of the breast and other organs, suggesting that chemical carcinogens play an important role in cancer risk.23 While little evidence has been gathered to support this hypothesis, most attention is directed at organochlorines, used in pesticides and industrial chemicals, which appear to act as estrogen mimics. Traces of fat-soluble pesticides from livestock feed grains tend to concentrate in animal tissues and milk.

A major route of human exposure to organochlorines is through animal fats, particularly from fish, meats, and dairy products.24 Smaller organochlorine residues are found on non-organic fruits or vegetables. Organochlorines are also used in household pesticides.

To measure the concentration of organochlorines in a woman’s body, researchers sometimes check samples of breast milk. In such studies, vegetarians have been found to have much lower levels of pollutants in their breast milk, compared to other women.25

Some evidence suggests that high-fat diets may also encourage the absorption of inhaled carcinogens into the body. Researchers have observed that tobacco carcinogens are absorbed through the lung tissue onto lipoproteins and travel with them in the bloodstream.26 It may be that low-fat diets that reduce lipoprotein levels also help reduce the absorption and transport of carcinogens.

Time between Menarche and First Pregnancy: Early menarche is associated with higher breast cancer risk. Also, the later the age of first pregnancy, the higher the risk. These factors may simply reflect a greater exposure to estrogen early in life.

According to World Health Organization records, the mean age of menarche in Europe dropped from about 17 in 1840 to 12.5 today. This change parallels the gradual spread of high-fat, low-fiber diets, which had been limited mainly to wealthy people, to essentially the entire population of Western countries.

In addition, early pregnancy also interrupts the continuous cycling of estrogens that stimulate the breast tissue.

Cancer of the Uterus and Ovary

The uterus and ovary, like the breast, are hormone-sensitive organs. Not surprisingly, uterine and ovarian cancers are both linked to fatty diets in epidemiologic studies.5,27-29 Obesity also increases risk of uterine cancer. In addition, supplemental estrogen that is given without added progestins also increases uterine cancer risk.

Another possible contributor to ovarian cancer is galactose, a monosaccharide that comes from the breakdown of lactose in dairy products. Galactose appears to be toxic to the ovaries and is linked both to ovarian cancer and infertility. Some women have particularly low levels of the enzymes that eliminate galactose, and, when they consume dairy products on a regular basis, their risk of ovarian cancer can be triple that of other women. The problem is the milk sugar, not the milk fat, so it is not solved by using non-fat products.30

Prostate Cancer: The Leading Cancer in Men

The prostate gland is just below the bladder in men, where it produces semen to be mixed with sperm cells. Cancer of the prostate is an increasingly common form of cancer in American men.

Cancer of the prostate is strongly linked to dietary factors in epidemiologic studies, particularly animal products: milk, meat, eggs, cheese, cream, butter, and fats.31-40 Countries with a higher consumption of rice, soybean products, or green or yellow vegetables in the diet have far fewer prostate cancer deaths.31,38,41,42 As is common with hormone-related cancers, vegetarians have lower prostate cancer rates.3

The link between fatty, fiber-deficient foods and prostate cancer may be explained by their tendency to increase testosterone activity. Vegetables and fruits are low in fat and high in fiber, resulting in reduced testosterone levels.

Consumption of fruits rich in lycopene is also associated with reduced prostate cancer risk. Lycopene is a strong antioxidant related to beta-carotene, and is the red pigment that gives watermelons and tomatoes their rich red color. A Harvard study of 47,000 health professionals found that men who had ten or more servings a week of lycopene-rich foods had a 45 percent reduced risk of prostate cancer.43

Colon Cancer

International comparisons and analyses of the past diets of cancer patients show clear links between meat-based Western diets and colon cancer.3,44,45 Meat-eaters have approximately three times the risk of colon cancer compared to those who rarely or never eat meat.

The association may be explained by the actions of bile acids. After a fatty meal, the gallbladder releases bile acids into the intestine, where they chemically modify fats so they can be absorbed. Colonic bacteria turn bile acids into cancer-promoting secondary bile acids. Meat consumption fosters the growth of bacteria that encourage the production of secondary bile acids. Fiber has the opposite effect, reducing production of carcinogenic secondary bile acids. Fiber also absorbs and dilutes bile acids.

In addition, as animal proteins are heated, they produce cancer-causing chemicals called heterocyclic amines. While this has long been known to be true for beef, it has also been shown to occur even more aggressively in chicken. According to a report from the National Cancer Institute, a well-done hamburger or steak contains about 30 nanograms per gram of the carcinogen PhIP. Grilled chicken actually contains 480 nanograms per gram, 15 times higher than beef.46

High-fiber diets have been shown to help people who are at high risk for colon cancer. Jerome J. DeCosse, M.D., a surgeon at Cornell Medical Center, gave bran to patients with recurrent colonic polyps, small growths that have a tendency to become cancerous. Within six months, the polyps became smaller and fewer in number. The key, Dr. DeCosse believes, is pentose fiber, which is plentiful in wheat.47

Vegetables, particularly cruciferous vegetables, such as broccoli, cauliflower, Brussels sprouts, and cabbage, also lower the risk of colon cancer.3

Other digestive tract cancers are also linked to diet. Alcohol and tobacco act synergistically to increase the risk of esophageal cancer. Pickled foods and very hot beverages also increase risk, while fruits and vegetables reduce it. Stomach cancer is linked to smoked and salt-pickled foods, and, again, vegetables seem to have a protective effect. Liver cancer is linked to a carcinogenic chemical, called aflatoxin, which is produced by a mold which can grow on peanuts and corn. This disease is uncommon in most Western countries, but is very common in sub-Saharan Africa and Southeast Asia, where this mold is common. Pancreatic cancer has been linked to consumption of alcohol, coffee, and meat.3

The Antioxidant Defenses

While fatty foods, particularly animal products, are consistently associated with higher cancer risk, vegetables and fruits are protective. Aside from being low in fat and high in fiber, these plant foods are also rich in antioxidants that neutralize free radicals.

Free radicals are unstable oxygen species produced in the course of cellular metabolism. The damage they do to DNA is believed to be the initiating step in cancer. Antioxidants neutralize free radicals. Common ones include the following:

  • Vitamin C is plentiful in many fruits and vegetables, particularly citrus fruits.
  • Beta-carotene is found in orange, yellow, and green vegetables.
  • Vitamin E is found in many grains and beans.
  • Selenium is a mineral which is found in many grains, vegetables, fruits, and legumes.

People who include generous amounts of fruits and vegetables in their daily diets have lower rates of a surprising range of cancer types, including lung, breast, colon, bladder, stomach, mouth, larynx, esophagus, pancreas, and cervix, compared to people who avoid such foods.48

The human body’s mechanisms for DNA repair depend on folic acid, which is found in dark-green leafy vegetables, fruits, peas, and beans. The U.S. Recommended Daily Allowance of folic acid for adults is 400 micrograms per day. As the table below shows, beans and vegetables supply plenty of folic acid.

Folic Acid in Foods

(micrograms per 1-cup cooked serving)

Asparagus 176
Vegetarian baked beans 61
Black beans 256
Blackeyed peas 356
Broccoli 108
Brussels sprouts 94
Chick peas 282
Great northern beans 181
Kidney beans 229
Lentils 358
Lima beans 156
Navy beans 255
Pinto beans 294
Soybeans 93
Spinach 262

Source: Pennington JAT. Bowes and Church’s Food Values of Portions Commonly Used. 16th Edition, Philadelphia, J.B. Lippincott, 1994.

Smokers provide a dramatic demonstration of the power of vegetables and fruits. A 55-year-old male smoker whose diet is low in vitamin C has a 25 percent risk of dying of lung cancer in the next 25 years. But with a high intake of vitamin C, either through diet or supplements, a smoker’s risk drops to only 7 percent.49 Similarly, researchers at the University of Texas found that former smokers who do not eat many vegetables and fruits are five and one-half times more likely to develop throat cancer compared to ex-smokers who eat more fruits and vegetables.

Steps to Cancer Prevention

Avoid tobacco.
Enjoy a varied menu of whole grains, vegetables, fruits, and beans, which supplies generous amounts of fiber, vitamins, and minerals, and less than 10 percent of its calories will be from fat.
Have more than one vegetable at a meal. Choose organic produce whenever possible.
Avoid animal products and minimize added vegetable oils
Minimize alcohol intake.
Maintain weight at or near your ideal weight.
Avoid excessive sunlight and unnecessary X-rays.

Foods and Immunity

White blood cells, particularly natural killer cells, are able to engulf and destroy aberrant cells. Certain foods improve these immune defenses, while others weaken them.

In both human and in-vitro tests, beta-carotene increases the percentage of cells in the body acting as natural killer cells and as T-helper cells.50,51 This benefit is apparent with only 30 milligrams of beta-carotene per day, the amount in two large carrots. Beta-carotene can also counteract some of the age-related immune loss.50 Beta-carotene is best obtained from diet, rather than from supplements. In fact, tests of beta-carotene supplements in smokers have shown them to actually increase the risk of cancer.

Zinc is also important in immune strength, and vitamins C and E and selenium bolster immune function in addition to their antioxidant effects, but the importance of these effects against cancer is not yet clear.52-54

Fats impair immune function. In both in-vitro tests and experiments using intravenous soybean oil infusions in volunteers, fats reduce the vigilance of white blood cells.55,56 Researchers in New York put healthy volunteers on diets that reduced fat content to 20 percent of calories. Three months later, blood samples showed that natural killer cell activity was greatly improved.57 Not surprisingly, vegetarians have been shown to have more than double the natural kill cell ability, compared to non-vegetarians.58

Cancer Prevention Study Questions

  1. What influence does a traditional Asian diet have on estrogen levels?
  2. What dietary factors reduce estrogen levels? Why is this important?
  3. What factors increase the risk for developing breast cancer?
  4. How does consumption of animal products affect cancer risk?
  5. What are the benefits of fiber in the diet?
  6. What are some common antioxidants and what role do they play in reducing cancer risk? What foods contain these antioxidants?
  7. How will you address dietary changes with patients? With colleagues or other staff members?

1. National Cancer Institute. Cancer rates and risks. Washington, DC, 1985.
2. Doll R, Peto R. The causes of cancer: quantitative estimates of avoidable risks of cancer in the United States today. J Natl Canc Inst 1981;66:1191-308.
3. National Research Council. Diet, nutrition, and cancer. Washington, National Academy Press, 1982.
4. Hirayama T. Epidemiology of breast cancer with special reference to the role of diet. Prev Med 1978;7:173-95.
5. Armstrong B, Doll R. Environmental factors and cancer incidence and mortality in different countries, with special reference to dietary practices. Int J Cancer 1975;15:617-31.
6. Lands WEM, Hamazaki T, Yamazaki K, et al. Changing dietary patterns. Am J Clin Nutr 1990;51:991-3.
7. Carroll KK, Braden LM. Dietary fat and mammary carcinogenesis. Nutrition and Cancer 1985;6:254-9.
8. Rose DP, Boyar AP, Wynder EL. International comparisons of mortality rates for cancer of the breast, ovary, prostate, and colon, and per capita food consumption. Cancer 1986;58:2363-71.
9. U.S. Department of Health and Human Services. Surgeon General’s report on nutrition and health. DHHS Publ No. 88-50210, 1988.
10. Rose DP, Boyar AP, Cohen C, Strong LE. Effect of a low-fat diet on hormone levels in women with cystic breast disease. 1. Serum steroids and gonadotropins. J Natl Cancer Inst 1987;78:6233-326.
11. Ingram DM, Bennett FC, Willcox D, de Klerk N. Effect of low-fat diet on female sex hormone levels. J Natl Cancer Inst 1987;79:1225-9.
12. Goldin BR, Gorbach SL. Effect of diet on the plasma levels, metabolism and excretion of estrogens. Am J Clin Nutr 1988;48:787-90.
13. Toniolo P, Riboli E, Protta F, Charrel M, Cappa AP. Calorie-providing nutrients and risk of breast cancer. J Natl Cancer Inst 1989;81:278.
14. Willett WC, Hunter DJ, Stampfer MJ, et al. Dietary fat and fiber in relation to risk of breast cancer: an 8-year follow-up. JAMA 1992;268:2037-44.
15. Howe GR, Hirohata T, Hislop T, et al. Dietary factors and risk of breast cancer: combined analysis of 12 case-control studies. J Natl Cancer Inst 1990;82:561-9.
16. Willett WC, Polk BF, Morris MJ, et al. Prediagnostic serum selenium levels and risk of cancer. Lancet 1983;2:130-4.
17. Willett WC, Stampfer MJ, Colditz FA, et al. Moderate alcohol consumption and the risk of breast cancer. N Engl J Med 1987;316:1174-80.
18. Miller DR, Rosenberg L, Kaufman DW, et al. Breast cancer before age 45 and oral contraceptive use: new findings. Am J Epidemiol 1989;129:269.
19. Bergkvist L, Adami AO, Persson I, et al. The risk of breast cancer after estrogen and estrogen-progestin replacement. N Engl J Med 1989;321:293.
20. Lubin F, Ruder AM, Wax Y, Modan B. Overweight and changes in weight throughout adult life in breast cancer etiology. Am J Epidemiol 1985;122:579-88.
21. Miller FA, Hempelmann LH, Dutton AM, Pifer JW, Toyooka ET, Ames WR. Breast neoplasms in women treated with X rays for acute postpartum mastitis: a pilot study. J Natl Cancer Inst 1969;43:803-11.
22. Lynch HT, Albano WA, Heieck JJ, et al. Genetics, biomarkers, and control of breast cancer: a review. Cancer, Genetics, and Cytogenetics 1984;13:43-92.
23. Goldman BA. The Truth about Where You Live. New York, Random House, 1991.
24. Ahlborg UG, Lipworth L, Titus-Ernstoff L, et al. Organochlorine compounds in relation to breast cancer, endometrial cancer, and endometriosis: an assessment of the biological and epidemiological evidence. Crit Rev Toxicol 1995;25:463-531.
25. Hergenrather J, Hlady G, Wallace B, Savage E. Pollutants in breast milk of vegetarians. Lancet 1981;304:792.
26. Benditt EP. The origin of atherosclerosis. Scientific American 1977;236:74-85.
27. Wynder EL, Escher GC, Mantel N. An epidemiological investigation of cancer of the endometrium. Cancer 1966;19:489-520.
28. Elwood JM, Cole P, Rothman KJ, Kaplan SD. Epidemiology of endometrial cancer. J Natl Cancer Inst 1977;59:1055-60.
29. Lingeman CH. Etiology of cancer of the human ovary: a review. J Natl Cancer Inst 1974;53:1603-18.
30. Cramer DW, Willett WC, Bell DA, et al. Galactose consumption and metabolism in relation to the risk of ovarian cancer. Lancet 1989;2:66-71.
31. Howell MA. Factor analysis of international cancer mortality data and per capita food consumption. Br J Cancer 1974;29:328-36.
32. Blair A, Fraumeni JF, Jr. Geographic patterns of prostate cancer in the United States. J Natl Cancer Inst 1978;61:1379-84.
33. Kolonel LN, Hankin JH, Lee J, Chu SY, Nomura AMY, Hinds MW. Nutrient intakes in relation to cancer incidence in Hawaii. Br J Cancer 1981;44:332-9.
34. Rotkin ID. Studies in the epidemiology of prostatic cancer: expanded sampling. Cancer Treat Rep 1977;61:173-80.
35. Schuman LM, Mandel JS, Radke A, Seal U, Halberg F. Some selected features of the epidemiology of prostatic cancer: Minneapolis-St. Paul, Minnesota case control study, 1976-1979. In: Magnus K, ed. Trends in Cancer Incidence: Causes and Practical Implications. Washington, Hemisphere Publishing Corp., 1982.
36. Graham S, Haughey B, Marshall J, et al. Diet in the epidemiology of carcinoma of the prostate gland. J Natl Cancer Inst 1983;70:687-92.
37. Ross RK, Shimizu H, Paganini-Hill A, Honda G, Henderson BE. Case-control studies of prostate cancer in blacks and whites in Southern California. J Natl Cancer Inst 1987;78:869-74.
38. Severson RK, Nomura AM, Grove JS, Stemmermann GN. A prospective study of demographics, diet, and prostate cancer among men of Japanese ancestry in Hawaii. Cancer Research 1989;49:1857-60.
39. Oishi K, Okada K, Yoshida O, et al. A case-control study of prostatic cancer with reference to dietary habits. Prostate 1988;12:179-90.
40. Mettlin C, Selenskas S, Natarajan N, Huben R. Beta-carotene and animal fats and their relationship to prostate cancer risk: a case-control study. Cancer 1989;64:605-12.
41. Hirayama T. Changing patterns of cancer in Japan with special reference to the decrease in stomach cancer mortality. Pp. 55-75 in Hiatt HH, Watson JD, Winsten JA, eds. Origins of Human Cancer. Book A, Incidence of Cancer in Humans. Cold Spring Harbor Laboratory, Cold Spring Harbor, NY, 1977.
42. Hirayama T. Epidemiology of prostate cancer with special reference to the role of diet. Natl Cancer Inst Monogr 1979;53:149-54.
43. Giovannucci E, Ascherio A, Rimm EB, Stampfer MJ, Colditz GA, Willett WA. J Natl Cancer Inst 1995;87:1767-76.
44. Willett WC, Stampfer MJ, Colditz GA, Rosner BA, Speizer FE. Relation of meat, fat, and fiber intake to the risk of colon cancer in a prospective study among women. N Engl J Med 1990;323:1664-72.
45. Gerhardsson de Verdier M, Hagman U, Peters RK, Steineck G, Overvik E. Meat, cooking methods and colorectal cancer: a case-referrent study in Stockholm. Int J Cancer 1991;49:520-5.
46. Sinha R, Rothman N, Brown ED, et al. High concentrations of the carcinogen 2-amino-1-methyl-6-phenylimidazo-[4,5]pyridine (PhlP) occur in chicken but are dependent on the cooking method. Cancer Research 1995;55:4516-9.
47. DeCosse JJ, Miller HH, Lesser ML. Effect of wheat fiber and vitamins C and E on rectal polyps in patients with familial adenomatous polyposis. J Natl Cancer Inst 1989;81:1290-7.
48. Block F. Epidemiologic evidence regarding vitamin C and cancer. Am J Clin Nutr 1991;54:1310S-4S.
49. Kromhout D. Essential micronutrients in relation to carcinogenesis. Am J Clin Nutr 1987;45:1361-7.
50. Watson RR, Prabhala RH, Plezia PM, Alberts DS. Effect of beta-carotene on lymphocyte subpopulations in elderly humans: evidence for a dose-response relationship. Am J Clin Nutr 1991;53:90-4.
51. Makinodan T, Lubinski J, Fong TC. Cellular, biochemical, and molecular basis of T-cell senescence. Arch Pathol Lab Med 1987;111:910-4.
52. Beisel WR. Single nutrients and immunity. Am J Clin Nutr 1982;35:Feb(suppl):417-68.
53. Watson RR. Immunological enhancement by fat-soluble vitamins, minerals, and trace metals: a factor in cancer prevention. Cancer Detection and Prevention 1986;9:67-77.
54. Chandra S, Chandra RK. Nutrition, immune response, and outcome. Progress in Food and Nutr Science 1986;10:1-65.
55. Nordenstrom J, Jarstrand C, Wiernik A. Decreased chemotactic and random migration of leukocytes during Intralipid infusion. Am J Clin Nutr 1979;32:2416-22.
56. Hawley HP, Gordon GB. The effects of long chain free fatty acids on human neutrophil function and structure. Lab Invest 1976;34:216-22.
57. Barone J, Hebert JR, Reddy MM. Dietary fat and natural-killer-cell activity. Am J Clin Nutr 1989;50:861-7.
58. Malter M, Schriever G, Eilber U. Natural killer cells, vitamins, and other blood components of vegetarian and omnivorous men. Nutr Cancer 1989;12:271-8.


Table of Contents

Study questions included at the end of each section


Section One:
Preventing and Reversing Heart Disease

Section Two:
Cancer Prevention

Section Three:
Cancer Survival

Section Four:

Section Five:
Foods and Blood Pressure

Section Six:
Nutrition and Renal Disease

Section Seven:
Preventing and Reversing Osteoporosis

Section Eight:
Nutrition and Arthritis

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