The Vegan Post

Cancer and the Vegetarian Diet

by William Harris, M.D. Cancer is not caused by bacteria, faulty diet, inadequate exercise, environmental contaminants, ionizing radiation, tobacco, viruses, nor heredity. Cancer is caused by a series of genetic mutations in DNA which may be either germline (inherited) or somatic (acquired during life). However, the chances of these mutations occurring in sufficient number to result in cancer is affected by all of the preceding factors. DNA is the critical target molecule in carcinogenesis (1). Although DNA has various repair mechanisms, some types of damage persist and become the basis of the defective molecular biology that is cancer. Oncogenes (tumor genes), tumor suppressing genes, and aptotic genes (causing programmed cell death) normally interact to build normal cells, to prevent excessive growth, and finally to kill the cell before genetic mutations cause it to malfunction. Table 1. U.S. cancer rates. Cancer is the second most common cause of death in the United States, where over 1.3 million new cases of cancer are diagnosed annually, with 550,000 deaths. Current United States incidence figures for the ten leading types of cancer are shown (2). Women have an approximately 1:8 lifetime chance of developing breast cancer, and men have an approximately 1:5 chance of developing prostate cancer. Rates above are per 100,000 in 1992. Both Hodgkin’s disease and non-Hodgkin’s lymphoma are included under lymphoma. There are three categories of evidence suggesting that a veg*n (vegetarian or vegan) diet reduces risk for various types of cancer. Epidemiologically, the intake of animal source food correlates with the country-by-country incidence of six types of cancer. Although none of the reporting countries can be assumed to have large vegan or even vegetarian populations, it appears that the less animal source food per capita, the lower the cancer rate. In the graphs below, the Y axis contains the disease, the X axis contains the animal source dietary risk factor. R is the correlation coefficient which reflects the “goodness of fit” of the data points to the sloping regression line. The p-value is the probability the apparent relationship is merely a mathematical coincidence. An R of 1 would indicate a direct linear relationship, while an R of zero would indicate no relationship. A p-value of .05 indicates a 5% chance of mathematical coincidence but numbers less than .05 are traditionally taken to suggest a non-coincidental relationship. A. Breast Cancer The etiology of breast cancer, as with most cancer, is multi-factorial, with a strong hereditary component. Using BMDP (3) statistical software, I performed multiple regression analysis on breast cancer incidence(4) country by country using Food and Agriculture Organization food consumption data (5) for animal source calcium, animal Calories, animal fat, animal protein, butter and ghee, cheese, eggs, milk production (metric tons/yr), plant source calcium, plant fat, plant protein, plant Calories, total calcium, total fat, total Calories, and total protein. I included additional vital statistics from The Book of World Rankings (6,7) for birth rate, female life expectancy, GNP/caput($), infant mortality, male life expectancy, male/female cancer ratios, meat consumption (kg/caput/yr early 70’s), sugar consumption (kg/caput/yr -1976), and total population. Of these (sometimes not independent) variables, the highest correlation ( R=.76, p<.001) with breast cancer incidence was from animal source Calories, (with animal fat and the other animal constituents close behind). Plant protein consumption had a moderate negative (protective) correlation (R= -.36, p=.046). Of the other positive correlations, animal source calcium had an R value of .62 and p=.0026. This would support the contention that dairy hormones are a risk for human breast cancer (8). Insulin-like growth factor (ISGF-1), present in both cow milk and human milk is known to stimulate the growth of human breast cancer cells (9, 10). The vegetarian diet has been shown to lower the level of estradiol (11) (an estrogen) and raise sex hormone binding globulin (SHBG) levels (12). Some forms of breast cancer are estrogen-receptor (ER) sensitive and the phytoestrogens from plant foods (13, 14), particularly soy products, are thought to block ERs in a manner similar to tamoxifen. Lower post-treatment ER-rich breast cancer survival rates in women who reported higher dietary fat intake have been found.(15) Although the most recent pooled-analysis of fat intake as a risk factor for breast cancer produced negative results (16), a case-control study (17) conducted in Italy on 2,569 incident cases of breast cancer and 2,588 controls found an odds ratio (OR) of 1.22 for saturated fat, and 0.89 for unsaturated fat. B. Intestinal cancer Intestinal cancer also correlates with animal food consumption (R=.83, p<.001) (18). Suggested explanations here are that meat increases the rate of carcinogenic bile acid formation (19), lack of fiber has an adverse effect on colonic bacteria (20), and additionally lengthens the intestinal transit time so that both dietary carcinogens in meat (21), and endogenous ones (the bile acids), are in contact with the intestinal mucosa for a longer period. C. Lung Cancer. Lung cancer mortality correlates with animal fat consumption (R=.71, p<.01) (22) and with the consumption of animal source protein and calcium. Plant nutrients had negative (protective) R values but p values were above .05, so they were not deemed statistically significant. However, the World Cancer Research Fund (WCRF) (23) judges that “diets high in a variety of vegetables and fruit, and the microconstituents they contain, may prevent 20-33% of cases of lung cancer in both smokers and non-smokers.” Data on tobacco use was not available, but there is little doubt that it would prove to be the most important predictor of lung cancer mortality, exceeding dietary factors by a wide margin. D. Lymphatic Cancer In 1977 Cunningham (24) examined the correlation between age-adjusted lymphoma mortality as reported by the WHO (25), and food intake as reported by the O.E.C.D. (26). Using multiple regression analysis for the intake of cereal grain, eggs, fish, nuts, pork, potatoes, poultry, pulses, seeds, starches, animal protein, crop protein, and total protein, he found the highest positive correlation with beef and dairy protein intake (R=.78, p<.001). Fish and all of the plant foods had a slight negative correlation. A 1997 case-control study conducted in Northern Italy between 1983 and 1992 involving 829 cases and 1,157 controls (27) found that “Compared with the lowest tertile, the odds ratio (OR) for the highest tertile of milk intake was 1.8 for Non-Hodgkins Lymphoma (NHL) and 1.9 for sarcomas. Liver intake was an indicator of the risk of Hodgkins Disease (HD) (OR = 1.8), NHL (OR = 1.6), and myelomas (OR = 2.0), ham another indicator of HD (OR = 1.7), and butter an indicator of myelomas (OR = 2.8). A high consumption of green vegetables was inversely related to myelomas (OR = 0.4), and frequent use of whole-grain foods was inversely related to NHL (OR = 0.4) and soft tissue sarcomas (OR = 0.2). The OR for the highest tertile of intake of beta-carotene ranged between 0.5 and 0.7, whereas the OR for retinol ranged between 1.5 and 2.3.” E. Ovarian Cancer Ovarian cancer also appears related to animal food consumption (28). Animal source Calorie intake showed the highest positive correlation (R=.81, p<.007). Plant source Calories were protective, with an R value of -.62 and p<.005. Animal source calcium intake was also a risk, with an R value of .72, p=.0005. This latter finding is consistent with the hypothesis that consumption of milk lactose may be a dietary risk factor for ovarian cancer in women with a an inherited deficiency of the enzyme galactose-1-phosphate uridyl transferase. (29). Additionally, insulin-like growth factor-I (IGF-I) present in both cow and human milk, is elevated in the cystic fluid of ovarian cancer (30). A study from Canada (31) implicated saturated fat and egg cholesterol consumption as risk factors for ovarian cancer, with reduced risk from vegetable fiber consumption. F. Prostate Cancer. Surprisingly, multiple regression analysis of prostate cancer incidence (32) versus the same dietary and social variables showed the highest correlation with animal source calcium intake (R=.74, p<.01) (33), which in general means dairy products. Animal source Calories came in second and plant protein had the highest negative correlation coefficient (R= -.49, p=.0052). This finding is consistent with a cohort study of 20,316 men of various ethnicities interviewed between 1975 and 1980 in Hawaii (34) that found beef and milk consumption to increase risk for prostate cancer. Prostate cancer, once again, is a sex hormone dependent cancer (35). A more recent study again identified animal source fat as a risk factor for prostate cancer, particularly in blacks (36). The World Cancer Research Fund (37) recommends a “predominantly plant-based diet” and lists fruits and vegetables as [convincing, probable, or possible] risk reducers for cancer of the bladder, breast, cervix, colon, endometrium, esophagus, kidney, larynx, liver, lung, mouth and pharynx, ovary, pancreas, prostate, rectum, stomach, and thyroid. This organization recommends five or more portions of vegetables and fruit daily, and “if eaten at all, red meat to provide no more than 10% of total energy” (Calories). There are biochemical studies that suggest how plant foods protect against cancer. Since DNA damage is crucial to cancer, its cause and prevention should be reviewed. Important in current thinking is the effect of lipid peroxidation in the generation of free radicals, small molecular fragments of fat with incorporated oxygen. Lipid peroxidation is a branching chain reaction with devastating side effects due to the ability of the oxidized fat fragments to covalently bond with DNA, damaging its structure and function. There is a large category of antioxidants, many of them man-made such as the food preservatives BHA and BHT. Naturally occurring antioxidants include vitamins C, E, the carotenoids (lycopene-[tomatoes], luteins and beta-carotene [leafy greens]) ellagic acid (4-carbon ring metabolic artifacts found in berries) (38), and saponins ( plant sterols attached to a short chain of sugars) (39). All of these substances help to quench the free radical chain reaction. Not all of these antioxidants are listed in the USDA database, but of the ones that are, I sorted by nutrient/Calorie ratio to find the highest plant source and the highest animal source for -carotene, vitamin C, and vitamin E. Included were 232 foods including beans, dairy, eggs, fish, fruit, grains, meat, nuts, poultry, and vegetables. Sorting by nutrient/weight ratio produces roughly similar results. Clearly animal source food is no anti-oxidant match for plant foods. It’s likely that by the time animal source food reaches the table the animal’s tissues have already utilized most of the anti-oxidants that were synthesized by the plants the animal ate. A diet high in plant food, particularly fruits and vegetables, will be high in these anti-oxidants, thus protective against cancer. A diet high in animal food will be low in these anti-oxidants, since the food itself is low and its presence in the diet displaces the fruits and vegetables that might otherwise be present. It should be noted that of 20 flours, breads, grains, and grain products included in the 232 foods, all were well below 100% of the RDA/Calorie for these three antioxidants with the exception of wheat germ oil (vitamin E). This may bear slightly on a recent study showing no reduction in colon cancer by high fiber intake (40). Admittedly grains are high in fiber, but they are not high in cancer-protective anti-oxidants. The respondents with high fiber intake may have been consuming large amounts of cereals and grains as they had been advised to, but the cancer-preventive agents are mostly in fruits and vegetables. The same grain products added in 100 gram increments and averaged, also proved to have less than 100% of the RDA/Calorie for calcium, folate, and riboflavin. Ninety three vegetables treated in the same manner were well over 100% RDA/Cal for 18 common nutrients except for vitamin B12 and had 800% of the RDA/Cal for -carotene, 1250% for vitamin C, and 300% for Vitamin E. Fiber, plentiful in grains, is not a nutrient since it is not absorbed. It acts, in the words of one medical editor, as “a sort of colonic broom” and while this may be advantageous, a repeat of the study, this time using fruits and vegetables, rather than fiber, as dietary intake markers might produce more favorable results. Steinmetz and Potter (41) report that the cancer protective substances in fruits and vegetables include, in addition to antioxidants, the following: allium compounds (diallyl sulfide, allyl methyl trisulfide), coumarins, dietary fiber, dithiolthiones, flavonoids (quercetin, kaempferol), folic acid, indole-3-carbinol, inositol hexaphosphate, genistein, biochanin A, isothiocyanates, sulphorophane, d-limonene, phytosterols, protease inhibitors, and selenium. The means by which these substances protect against cancer cell initiation include effects on cell differentiation, increased activity of enzymes that detoxify carcinogens, blocked formation of nitrosamines, altered estrogen metabolism, altered colonic milieu (including bacterial flora, bile acid composition, pH, fecal bulk), preserved integrity of intracellular matrixes, effects on DNA methylation, maintenance of normal DNA repair, increased apoptosis (programmed cell death) of cancer cells, and decreased cell proliferation. Cancer cell metastasis may be blocked by a plant-based diet. German investigators have shown that vegetarian men have roughly twice the natural killer cell activity as age-matched omnivorous controls (42). A recent study from Britain (43) concluded that: “Vegetables and fruit are almost invariably protective for the major cancers. The evidence is best for a protective effect of vegetables in the large bowel and for fruits and vegetables in stomach cancer…. High consumption of meat, especially red meat and processed meat, is linked with higher risk of bowel, breast, prostate, and pancreatic cancer. There is some evidence of an association with lung cancer, and of an association of barbecued meat and oesophageal cancer.” This study also concluded that “up to 80% of bowel and breast cancer may be preventable by dietary change.” Practical aspects of the veg*n (vegetarian or vegan) diet. A straightforward and simple dictum is: “Eat as wide a variety of plant foods in as unprocessed a form as possible.” -Susan Havala, R.D. All the essential amino acids, essential fatty acids, and vitamins required in the human diet are synthesized either by plants or micro-organisms (44), not by animals. The essential inorganic nutrients (iron, calcium, zinc, etc.) were synthesized in nuclear fusion reactions that occurred in stars that blew up more than 5 billion years ago (45). The notion that veg*n diets are more likely than omnivorous ones to be nutrient deficient is the result of sorting foods by nutrient/weight ratio. Since there is no RDA for weight in the diet, while there is an RDA for Calories, a more rational approach to food analysis is by nutrient/Calorie ratio, in which case it is seen that animal source foods, because of their high fat content, have little advantage over plant foods (46). Although poorly designed veg*n diets have produced reports of nutritional deficiency, particularly in children (47), the notion that vegans are more likely than omnivores to suffer nutrient deficiencies is not supported by the literature (48). In general, a diet centered on vegetables and fruit, preferably raw, with grains, nuts, seeds, and starches used to fill in Calorie requirements will satisfy nutrient requirements, with the exception of Vitamin B12, which must be supplemented, at least until the scientific dust settles. Numerous vegetarian and vegan cookbooks and handbooks are available and should be consulted by new veg*ns. Conclusion Evidence from a broad scientific literature suggests: A. Rates for at least six common types of cancer, country by country, correlate with the consumption of animal source food. B. There is a modest negative correlation with these cancers and plant source food consumption. C. A variety of phytochemicals present in plant foods have been demonstrated to be protective against the DNA damage that leads to cancer. D. The veg*n diet, extolled by its advocates for at least 150 years as a cancer preventive strategy, is the logical end point of the dietary recommendations, now made by scientific organizations, to reduce animal food consumption. E. A recent clinical review (49) concluded: “Up to 80% of bowel and breast cancer may be preventable by dietary change… Diet contributes to varying extent to the risk of many other cancers, including cancers of the lung, prostate, stomach, oesophagus, and pancreas… Generally, fruit, vegetables, and fibre have a protective effect, whereas red and processed meat increase the risk of developing cancer.” There are no logical arguments for the continued use of animal source food in the human diet. However, logic is not the key factor here. The United States Department of Agriculture (USDA) has shielded the meat and dairy industries from normal market forces since at least the beginning of the Commodities Credit Corporation (CCC) in 1933 (50), by giving direct price supports to dairy production, and de facto supports to the meat industry in the form of feed grain price supports (51, 52).. In 1998 USDA Secretary Dan Glickman bought up at least $250 million worth of beef, chicken, dairy, eggs, fish, lamb, and pork that could not be sold on an already flooded market. These goods will be dumped into public feeding troughs such as the National School Lunch Program (53). This is contrary to advice given by the National Cancer Institute, the U.S. Department of Health and Human Services (DHHS), and the USDA itself, to consume daily at least five servings of fruit and vegetables. Only a third of the U.S. public is aware of the “5-A-Day” recommendation (54). Vegetable and fruit growers have for the most part been excluded from support programs…”All crops may be harvested on flex acreage except…fruits and vegetables…” (55), and apparently don’t want government assistance or large ad campaigns(56) to market their products. Evidence indicates that animal industries have exerted enormous pressure on the government for continuation of their supports (57). These industries then plow their profit margins into massive ad campaigns, nutritional “education”, and political action to insure that their benefits will continue. A glance at IRS Corporate Income Tax Form 1120 and most state corporate tax forms shows also that advertising is a tax deductible business expense. There is little doubt that the animal food interests are taking full advantage of this as they suborn the media, the nutritional establishment, and the government to push their wares on a naive public. Until the government stops using public tax moneys to bail out the animal food interests and stops giving tax breaks for their massive advertising programs that virtually freeze vegetarian information out of the public consciousness, there is not much chance that we will see a reduction in cancer rates. William Harris, M.D. Medical Director Kaiser-Permanente Vegan Lifestyle Clinic (VLC) 1765 Ala Moana Blvd. #1880 Honolulu, HI 96815 INTERNET:vegidoc@compuserve.com ENDNOTES 1 Murray RK, Granner DK, Mayes PA, and Rodwell VW.Harper’s Biochemistry. Appleton and Lange Norwalk, CT 1990. ISBN 0-8385-3640-9 p 653. 2 McPhee SJ, Papadakis, Gonzales, Tierney. Current Medical Diagnosis & Treatment (CMDT) on CD-ROM 1998. Appleton Lange 1998. Norwalk, 1990. ISBN 0-8385-1480-4. 3 BMDP Statistical Software. BMDP New System for Windows v1.0 Los Angeles,1994. ISBN 0-935386-30-0. 4 Tominaga S., Aoki K, Fujimoto I, Kurihara M. Cancer Mortality and Morbidity Statistics Japan and the World -1994. Age adjusted breast cancer incidence/100,000/year 1983-87. Japan Scientific Societies Press CRC Press 2000 Corporate Blvd., N.W. Boca Raton Fl 33431ISBN 0-8493-7748-X . Table I-13. p194. 5 Food and Agriculture Organization of the United Nations. FAO Production Yearbook.Rome,1987 6 Kurian, George Thomas. The Book of World Rankings. Facts on File Inc. 119 West 57th St. New York,N.Y.10019. 1979.ISBN 0-87196-394-9. 7 Kurian, George Thomas. The New Book of World Rankings. Facts on File Inc. 460 Park Ave. So. New York, N.Y. 10016. 1991 ISBN 0-8160-1931-2. 8 Outwater JL; Nicholson A; Barnard N. Dairy products and breast cancer: the IGF-I, estrogen, and bGH hypothesis. Med Hypotheses (ENGLAND) Jun 1997, 48 (6) p453-61, ISSN 0306-9877. 9 Musgrove EA, Sutherland RL. Acute effects of growth factors on T-47D breast cancer cell cycle progression. Eur J Cancer 1993;29A(16):2273-9. 10 Figueroa JA, Sharma J, Jackson JG, McDermott MJ, Hilsenbeck SG, Yee D. Recombinant insulin-like growth factor binding protein-1 inhibits IGF-I, serum, and estrogen-dependent growth of MCF-7 human breast cancer cells. J Cell Physiol 1993 Nov;157(2):229-36. 11 Prentice R, Thompson D, Clifford C, Gorbach S, Goldin B, Byar D. Dietary fat reduction and plasma estradiol concentration in healthy postmenopausal women. The Women’s Health Trial Study Group. J Natl Cancer Inst 1990 Jan 17;82(2):129-34. 12 Bennett FC; Ingram DM. Diet and female sex hormone concentrations: an intervention study for the type of fat consumed. Am J Clin Nutr Nov 1990, 52 (5) p 808-12, ISSN 0002-9165. 13 Reinli K, Block G. Phytoestrogen content of foods–a compendium of literature values. Nutr Cancer 1996;26(2):123-48. 14 Adlercreutz H; Mousavi Y; Clark J; Hockerstedt K; Hamalainen E; Wahala K; Makela T; Hase T. Dietary phytoestrogens and cancer: in vitro and in vivo studies. J Steroid Biochem Mol Biol Mar 1992, 41 (3-8) p331-7, ISSN 0960-0760. 15 Holm LE, Nordevang E, Hjalmar ML, Lidbrink E, Callmer E, Nilsson B. Treatment failure and dietary habits in women with breast cancer. J Natl Cancer Inst 1993 Jan 6;85(1):32-6. 16 Hunter DJ, Spiegelman D, Adami HO, Beeson L, van den Brandt PA, Folsom AR, Fraser GE, Goldbohm RA, Graham S, Howe GR, et al. Cohort studies of fat intake and the risk of breast cancer–a pooled analysis. N Engl J Med 1996 Feb 8;334(6):356-61. 17 Decarli A, Favero A, La Vecchia C, Russo A, Ferraroni M, Negri E, Franceschi S Macronutrients, energy intake, and breast cancer risk: implications from different models. Epidemiology 1997 Jul;8(4):425-8 18 Wynder EL. The Dietary Environment and Cancer. J Amer Dietetic Assoc. 1977;71:385-92. 19 Shils ME, Olson JA., Shike M. Modern nutrition in health and disease-8th ed. Lea & Febiger Malvern, PA. 1994. ISBN 0-8121-1485-X. p 580. 20 van Faassen A; Bol J; van Dokkum W; Pikaar NA; Ockhuizen T; Hermus RJ. Bile acids, neutral steroids, and bacteria in feces as affected by a mixed, a lacto-ovovegetarian, and a vegan diet. Am J Clin Nutr Dec 1987, 46 (6) p 962-7, ISSN 0002-9165. 21 Bingham SA, Pignatelli B, Pollock JRA, Ellul A, Mallaveille C, Gross G, et al. Does increased endogenous formation of N-nitroso compounds in the human colon explain the association between red meat and colon cancer? Carcinogenesis 1996;17:515-23. 22 National Institutes of Health. National Cancer Institute. Cancer Rates and Risks: Cancer Death Rates Among 50 Countries (Age adjusted to the world standard) 4th Edition. Source: World Health Organization data as adapted by the American Cancer Society 1996. U.S. Department of Health and Human Services. Lung cancer p 39. 23 World Cancer Research Fund / American Institute for Cancer Research. Food, Nutrition and the Prevention of Cancer: a global perspective. 1997 1759 R St. NW Washington, DC 20009. 178-FNS/F27 p 12. 24 Cunningham AS. Lymphomas and Animal-Protein Consumption. Lancet.1976;Nov.27:1184-86.ISSN 0023-7507. 25 World Health Organization. Mortality from Malignant Neoplasms 1955-1965. Geneva, 1970. 26 Organization for Economic Cooperation and Development (O.E.C.D.) Food Consumption Statistics 1955-1971. Paris, 1973. 27 Tavani A; Pregnolato A; Negri E; Franceschi S; Serraino D; Carbone A; La Vecchia C. Diet and risk of lymphoid neoplasms and soft tissue sarcomas. Nutr Cancer (UNITED STATES) 1997, 27 (3) p256-60, ISSN 0163-5581. 28 Tominaga S, Aoki K, Fujimoto I, Kurihara M. Cancer Mortality and Morbidity Statistics. Japan and the World-1994. Japan Scientific Societies Press CRC Press 2000 Corporate Blvd., N.W. Boca Raton Fl 33431. ISBN 0-8493-7748-X. Table I-15 p 196. 1983-87. 29 Cramer DW; Harlow BL; Willett WC; Welch WR; Bell DA; Scully RE; Ng WG; Knapp RC. Galactose consumption and metabolism in relation to the risk of ovarian cancer . Lancet Jul 8 1989, 2 (8654) p 66-71, ISSN 0023-7507. 30 Karasik A, Menczer J, Pariente C, Kanety H. Insulin-like growth factor-I (IGF-I) and IGF-binding protein-2 are increased in cyst fluids of epithelial ovarian cancer. J Clin Endocrinol Metab 1994 Feb;78(2):271-6. 31 Risch HA; Jain M; Marrett LD; Howe GR Dietary fat intake and risk of epithelial ovarian cancer. J Natl Cancer Inst Sep 21 1994, 86 (18) p 1409-15, ISSN 0027-8874. 32 Tominaga S., Aoki K, Fujimoto I, Kurihara M. Cancer Mortality and Morbidity Statistics. Japan and the World-1994. Japan Scientific Societies Press CRC Press 2000 Corporate Blvd., N.W. Boca Raton Fl 33431ISBN 0-8493-7748-X . Table I-16. p 197. 1983-87. “Cancer mortality statistics in 33 countries of the world were compiled and calculated from data edited from a magnetic tape copy of the WHO data base of cancer mortality.” All figures are age-adjusted and represent death rate per 100,000 population. 33 Food and Agriculture Organization of the United Nations. FAO Production Yearbook. Rome, 1987. Calcium/caput/day-milligrams 1983-85. Table 109. p 252. 34 Le Marchand L; Kolonel LN; Wilkens LR; Myers BC; Hirohata T. Animal fat consumption and prostate cancer: a prospective study in Hawaii. Epidemiology May 1994, 5 (3) p 276-82, ISSN 1044-3983. 35 Mousavi Y, Adlercreutz H. Genistein is an effective stimulator of sex hormone-binding globulin production in hepatocarcinoma human liver cancer cells and suppresses proliferation of these cells in culture. Steroids. Jul 1993, 58 (7) p 301-4, ISSN 0039-128X. 36 Mousavi Y, Adlercreutz H. Genistein is an effective stimulator of sex hormone-binding globulin production in hepatocarcinoma human liver cancer cells and suppresses proliferation of these cells in culture. Steroids. Jul 1993, 58 (7) p 301-4, ISSN 0039-128X. 37 World Cancer Research Fund / American Institute for Cancer Research. Food, Nutrition and the Prevention of Cancer: a global perspective. 1997 1759 R St. NW Washington, DC 20009. 178-FNS/F27 pgs 10, 14. 38 Goodwin and Mercer. Introduction to Plant Biochemistry. Pergamon Press.Oxford, 1983. p 562. 39 Salisbury FB, and Ross CW. Plant Physiology. Wadsworth Publishing Co. Belmont 1985. ISBN 0-534-04482-4 p 276. 40 Fuchs CS, Giovannucci E., Colditz GA, Hunter DJ, Stampfer MJ, Rosner BR, Speizer FE, Willett WC. Dietary Fiber and the Risk of Colorectal Cancer and Adenoma in Women. N Engl J Med 1999;340:169-76. 41 Steinmetz (1)KA, Potter JD. Vegetables, fruit, and cancer prevention: a review. Journal of the American Dietetic Association, Oct 1996;(10): 1027(13). 42 Malter M; Schriever G; Eilber U. Natural killer cells, vitamins, and other blood components of vegetarian and omnivorous men. Nutr Cancer (UNITED STATES) 1989, 12 (3) pp 271-8, ISSN 0163-5581. 43 Cummings, JH, Bingham,SA. Diet and the prevention of cancer. BMJ 1998;317:1636-1640. 44 Lindner M. Nutritional Biochemistry and Metabolism. Elsevier Science Publishing Co. New York, 1985. ISBN 0-444-01241-9 pp 70-71. 45 Random House. Random House Encyclopedia. New York, 1977. ISBN 0-394-40730-X. p 48. 46 Harris W. The Scientific Basis of Vegetarianism. Hawaii Health Publishers. 1415 Victoria St. Suite 1106. Honolulu, HI 96822-3663. ISBN 0-9646538-0-X. p 91. 47 Jacobs C, and Dwyer T. Vegetarian children: appropriate and inappropriate diets. Am J Clin Nutr. 1988;48(3):811. 48 Langley G. Vegan Nutrition, a Survey of Research. The Vegan Society. Oxford, 1988. ISBN 0-907337-15-5. 49 Cummings JH, Bingham SA. Diet and the prevention of cancer. BMJ 1998;317:1636-1640. 50 Luttrell, Clifton B. The High Cost of Farm Welfare. Cato Institute. Washington, 1989. ISBN 0-932790-70-4. p 15. 51 United States Department of Agriculture. Agricultural Statistics, 1989. United States Government Printing Office. Washington, 1989. Table 623. 52 United States Department of Agriculture. History of Budgetary Expenditures of the Commodity Credit Corporation: Fiscal Year 1990-1991 Actual. ASCS/BUD/CPB Book 3.p 2. 53 http://www.ams.usda.gov/cp/index.htm 54 http://dcp.nci.nih.gov/5aday/week98/CommunityKit98.html 55 ASCS Commodity Fact Sheet. Feed Grains: Summary of Support Program and Related Information. United States Department of Agriculture. June 1991. 56 GAO/RCED-92-15. Generic Promotion of Produce. Resources,Community, and Economic Division. United States General Accounting Office. Washington, 1991. 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