Foods Causing Cancer



In Short ;

By heating whatever food, hundreds of different mutagenic substances originate. The more protein that food contains, the more mutagenics originate due to cooking etc. If we only live long enough, these substances eventually will cause cancer.

The activity of antioxidants is very limited ; not even large amounts of all the (semi-) antioxidants in the world combined can disarm a substantial part of these mutagenics.

The only way to effectively prevent cancer, is to prevent absorption of mutagenic substances from prepared food. Consume as little prepared food (proteinous prepared food in particular) and as much fruits and some fresh raw animal food regularly (like sashimi or fresh raw egg yolk, requiring an hour rest to digest by the way). See diet suggestions







In Detail ;


Mutagenics in Prepared Food

Consuming prepared meat increases the risk of contracting lung cancer (1), breast cancer (2), prostate cancer (3), and colon cancer (4).

This only means that prepared meat contains more mutagenic substances than prepared food. Of course vegetarians get cancer too, though in general a little less (5), because vegetarians do consume prepared food, but no prepared meat.

Prepared vegetables contain less mutagenic substances than prepared meat. Therefore, 2 out of 3 scientific investigations show that consuming prepared Soya beans instead of prepared meat, causes less cancer. (6) And therefore these scientists conclude that 'soy is protective against cancer'. This however only means that, on an average basis, soy (and other vegetables) causes less cancer than prepared food.

Generally, consuming vegetables ‘proves to be protective against cancer’, simply because consuming vegetables is less cancerous than consuming other prepared foods.


However ; all prepared foods (including vegetables) contain mutagenic substances. Foods increasing cancer risk the most, are prepared foods containing higher quantities of protein (like meat (7) and fish (8)), most fat (9), cholesterol (like eggs) (10) or iodide (like sea-fish, crustaceans and mollusks) (11).

Food that has been intensively heated, smoked (12), or salted (13), also highly increases cancer risk.


All prepared foods also contain non-HCA damaged protein, which is partly decomposed in the blood, originating free radicals. All prepared foods therefore will eventually cause cancer, ....if you live long enough.


Whenever again a scientific investigation proves that consuming vegetables is ‘protective’; remember that this only proves that a murderer is more criminal than a petty thief. And as releasing a petty thief does not prevent crime, consuming vegetables does not prevent cancer.

Vegetables are as healthy as 'healthy cigarettes containing 50% less mutagenic substances'.

Prepared vegetables are less cancerous than prepared meat, but to really lower cancer risk you should consume as little of all prepared foods. Consume as much fruits, some fresh raw animal food (like sashimi) and munch-foods to satisfy your cravings.






We don't like to change our diet. We rather believe that supplements or vegetables will provide us with substances that protect us against cancer. Unfortunately, such substances do not, and never will exist.


Many 'experts' say that anti-oxidants are 'good', preventing cancer, and oxidative radicals are 'bad'. But that is nonsense. The only reason why they do so, is because you can make lots of money by selling antioxidants to people who are afraid of getting cancer.

Stating that radicals are bad substances is criminal and misleading ; to obtain energy from sugars for example, these sugars first have to be oxidized, requiring oxidative radicals. Oxygen radicals also kill bacteria and clean up drug-residues, and are needed to compose hormones, to keep the veins flexible and to regulate blood pressure. Without oxygen radicals, you can't live !!!

However, if external radicals enter the body, these radicals can damage enzymes, organs or cell-DNA/RNA, and cause cancer.

By nature, our body uses antioxidants to prevent damage by natural radicals. But though antioxidants can actively bind to radicals, they can never ever disarm all dangerous exogenous radicals.




Where do those external radicals come from ?


From inhaling polluted air and from consuming prepared foods, containing damaged proteins or too much minerals.

Most damaged protein cannot easily be decomposed by enzymes in the digestive tract. Both decomposed- and partly-decomposed proteins are absorbed into the lymph and the blood. And in the blood radicals and enzymes decompose all substances that shouldn’t be there, step by step. Decomposing these substances, very often radicals originate. And sometimes these radicals damage cells before they are completely decomposed.




Can consuming more antioxidants prevent cancer ?


Only if your body has too little antioxidants at its disposal. Though toxic HCA originate oxidative radicals (14), and decrease antioxidant level (15), extra antioxidants cannot prevent the damaging effects of toxic HCA. (16)

To absorb sufficient antioxidants, you only need to consume lots of fruits, containing all the antioxidants you need. Consuming more antioxidants can impossibly prevent cancer. Don't force your body to absorb more antioxidants by taking supplements. Supplements are far too concentrated, not allowing the body to avert excessive antioxidants.




But how can too much antioxidants ever be bad ?


Antioxidants like vitamin C, E and beta-carotene actively bind to radicals. Antioxidant excess inhibits the useful functions of radicals, like decomposing tumor-cells, and can therefore enhance cancer !! (17) Radicals also kill mutagenic substances from cigarette smoke. Consuming supplementary ß-carotene therefore inhibits protective action of radicals, increasing lung cancer risk. (18)

Excessive vitamin C can cause cancer by activating mutagenic HCA from food (20) and can also enhance cancer because tumors need vitamin C to grow. (21) Vitamin C also increases transformation of harmless iron into pro-oxidative free iron. (22) 


To prevent antioxidants from causing damage, you should not take supplements. Simply eat as much fruit as you can, and some fresh raw animal food, to allow the body to absorb sufficient, but not too much antioxidants. Your body can much more effectively regulate absorption of antioxidants from food.


Note : Some people are allergic to specific substances in specific fruits, so increase fruit consumption gradually to make sure you can safely eat those fruits.






Some people refer to phenols, flavonoids, phyto-estrogens and phytate in vegetables and grains as antioxidants too. And again, people think that these semi-antioxidants are 'good', and radicals aren't. But again, these people are wrong;


These semi-antioxidants are not selective ; they are not 'smart bombs' knowing exactly what substances to kill. It is true that some of these substances can easily bind to radicals, to mutagenic substances, or to enzymes activating mutagenic substances. But substances that are most toxic, like cyanide, also most effectively bind to such pro-cancerous substances. And of course, that does not make them 'good'. It only makes them dangerous to mutagenic substances as well as to nutrients and healthy cells. Just like chemotherapy is effective because these drugs are toxic, enabling them to kill both cancer- and non-cancer cells. But should we therefore preventively use chemotherapy or antioxidants ?



Phyto-estrogens are 'weak' estrogens, and can replace common (powerful) estrogens. (23) And because excessive estrogen can cause breast cancer, these phyto-estrogens are regarded as 'good' substances. Soya contains most phyto-estrogen.



Absorbing phyto-estrogens and lignin’s stimulates SHBG production (Sex-Hormone Binding Globulin), intercepting common estrogens and phyto-estrogens. Decreasing too-high estrogen levels decreases prostate cancer- and breast cancer-risk. (23) In vegetarians SHBG level is increased. (24) Soya can contain very high levels of phyto-estrogens (like genisteine and daidzeine, also present in beer) (25). Genistein and daidzeine  also inhibit enzymes activating mutagenic substances. (26) (These enzymes however, are naturally designed to protect the body against natural mutagenics, absorbed through inhaling smoke from forest fires for example. Inhibiting those enzymes eliminates that protection.)



However, consuming high amounts of soy increases the level of some hormones (DHEA-sulphate) (27) Consuming soymilk for 3 months can already decrease estradiol level 27%, and lengthen menstruation cycle by 2 days. (28) Messing with your hormones is of course not a good thing. Estrogen for example is not a 'bad' substance, but essential. Therefore phyto-estrogens can cause infertility (29) and liver-diseases. (30) 

The main phyto-estrogen, genisteine, is even mutagenic !!! (31) Like coumestrol (also a phyto-estrogen), genisteine can damage DNA of common cells in our body (31), which can cause cancer. Like daidzeine (also a soy-phyto-estrogen), genisteine damages sperm cells. (32) And different phyto-estrogens, like genisteine, enhance prolactin-producing brain-tumors. (33)


Phyto-estrogens have to be regarded as drugs or chemotherapy ; both dangerous and useful. And being a healthy person, you don't take chemotherapy to prevent cancer, do you ?

For more scientific info about the down-sides of soy, click here.


To prevent cancer caused by estrogens, you should not use hormonal contraceptives (34), nor consume dairy products. (35) (see site6) Consuming alcohol also increases estradiol level. (36) (beer makes men grow 'breasts')



Genisteine inhibits tyrosine kinase and topoisomerase 2. These enzymes are essential to build up DNA, for constructing new cells. Without these enzymes you can't compose new cells, but tumors also can't multiply. (37)

Herbs containing phyto-estrogens have been used as medicines for ages ; phyto-estrogens from oregano, verbena, thyme, red clover and diamana can bind to progesterone-receptors, lowering progesterone level. Phyto-estrogens from liquorices, red clover, thyme, hop and verbena can bind to estrogen receptors. (38)



Also, Soya bean is unnatural food for humans ; it contains different substances inhibiting digestion and absorption of nutrients. Consuming lots of soy enhances vitamin A, -B12, -D and -E deficiencies. (39) These inhibiting substances are partly destroyed due to the preparation process, but the preparation process unfortunately also originates new mutagenic substances in soy. (40) (see this site)



Soya beans are high in insoluble fiber, enhancing bacterial decomposition of nutrients in the intestinal tract, originating gasses. Soya flour contains high amounts of polyurones, which can only partly be decomposed in the colon. Soy also contains phytate, which is only partly destroyed by heat, inhibiting absorption of minerals and probably vitamin B1. Soy also contains arabinoxylanes and tannins inhibiting digestion.



Phenols, from vegetables for example, are regarded as semi-antioxidants, preventing cancer. Polyphenols can bind to mutagenic substances (41), because they're so aggressive. That's why concentrated phenols are used to clean up bacteria and moulds.

Flavonoids for example, are polyphenols ; some flavonoids (like flavone, chrysine and apigenin) are anaesthetic. (42) Many flavonoďds become mutagenic by preparation. (43) Quercetine is the main flavonoid, and is also mutagenic. (44) Because quercetine (and caffeic acid in Lamb's lettuce) is that aggressive, it can inhibit enzymes activating other mutagenic substances, and is therefore regarded as an antioxidant. Those enzymes originally are designed to eliminate natural mutagenics. Some flavonoids inhibit those activating enzymes (45), other flavonoids act in an opposite manner. (46) Flavonoids / phyto-estrogens in soy, rye and linseed also easily bind to iodide, causing iodide deficiencies. (47)



Fiber, phytate, oxalate ; Even fiber, phytate and oxalate sometimes are regarded as antioxidants, because they can bind to lots of different substances, but especially to calcium, iron and zinc. And again, that does not at all make them 'good'. Especially grains (bran in particular), peas and beans contain too much insoluble fiber (6 times more than average fruit), causing bacterial decomposition of foods in the digestive tract (gasses).

Beans and cereals contain too much phytate, which isn't decomposed completely by preparation. (48) Vegetables like mangold, rhubarb, spinach, purslane, beetroot and bamboo shoots contain too much oxalate.



Lignins are indigestible, and regarded as antioxidants because they bind to cholesterol and mutagenic nitrosocompounds (49) But cholesterol is a very valuable, essential nutrient. (see this site) Why not regard diarrhea as anti-oxidative ; diarrhea also prevents absorption of cholesterol !!!

Lignins also easily mineralize, causing the loss of minerals. (50) Especially beans (and dried currants) contain about 4 to 140 times as much lignin as the average fruit has.



Isothiocyanates ; vegetables like broccoli, cabbage, cauliflower and Brussels sprouts contain isothiocyanates, which can both inhibit (51) or stimulate (52) enzymes activating mutagenic substances. Thiocyanates and nitrite (in vegetables) are also pro-oxidative. (53) Isothiocyanates can become mutagenic through reacting upon aromatic amines due to the influence of heat. (54)



Other mutagenics / toxins ; Many unnatural foods contain mutagenic substances by nature, or contain substances that originate toxins when partly decomposed in the body of the consumer, to prevent being consumed by animals like humans ;


Consuming beans containing pyrimidins (isouramile, divicine) and peas containing nitriles and toxins can highly stimulate the release of oxygen radicals.

Millet contains dhiurrin, originating toxic cyanide. Potato, cassava and sweet potato also contain cyanogenic substances. Cooking only partly destroys these substances. Rhubarb can contain mutagenic emodine. Parsley, celery, dill and fennel contain furocoumarins, which can become tumor-stimulating. Cacao, nutmeg, laurel, anis, mace, black pepper and ginger contain tiny amounts of carcinogenic saffron.

These 'foods' actually are not foods, but medicines, and therefore should not be commonly consumed.

Furthermore, grains, meat, milk and cheese (through feeding contaminated grains to cows) can contain very cancerous aflatoxins. If nuts are shelled and stored 'en masse', they can contain aflatoxins too. Buy un-shelled nuts. 

Grains also can contain cancerous polychloridebiphenyles, arsenium (cancerous to the skin), cadmium (decreases serotonine level) and lead (probably cancerous).

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(1) Sinha, R. et al, Fried, well-done meat and risk of lung cancer in women. (United States). Cancer Causes Control 1998 / 9 (6) / 621-630. , Swanson, C.A. et al, Dietary fats and lung cancer risk among women  the Missuri Wmen's Heath Study. Cancer Causes Control 1997 / 8 (6) / 883-893. , Koo, L.C. et al, An ecological study of trends in cancer incidence and dietary changes in Hong Kong. Nutr. Cancer 1997 / 28 (3) / 289-301. , De Stefani, E. et al, Fatty foods and the risk of lung cancer : a case control study from Uruguay. Int. J. Cancer 1997 / 71 (5) / 760-766. , Deneo-Pelligrini, H. et al, Meat consumption and risk of lung cancer : a case control study from Uruguay. Lung Cancer 1996 / 14 (2-3) / 195-205. , De Stefani, E. et al, Dietary nitrosodimethylamine and the risk of lung cancer : a case control study from Uruguay. Cancer Epidemiol. Biomarkers Prev. 1996 / 5 (9) / 679-682. , Alevanja, M.C. et al, Estimating the effect of dietary fat on the risk of lung cancer in nonsmoking women. Lung Cancer 1996 / 14 (suppl.1) / S63-S74. , Sankaranarayanan, R. et al, A case control study of diet and lung cancer in Kerala, south India. Int. J. Cancer 1994 / 58 (5) / 644-649. , Suzuki, I. et al, Risk factors for lung cancer in Rio de Janeiro, Brazil : a case control study. Lung Cancer 1994 / 11 (3-4) / 179-190. , Goodman, M.T. et al, High-fat foods and the rsik of lung cancer. Epidemiology 1992 / 3 (4) / 288-299. , Kodama, M. et al, Interrelation between Western type cancers and non-Western type cancers as regards their risk variations in time and space 2. Nutrition and cancer risk. Anticancer 1990 / 10 (4) / 1043-1049. , Hirayama, T. et al, A large scale cohort study on cancer risks by diet- with special reference to the risk reducing effects of green-yellow vegetable consumption. Princess Takamatsu Symp. 1985 / 6 / 41-53.
(2) Zheng, W. et al, N-acetyltransferase genetic polymorphism, cigarette smoking, well-done meat intake ,and breast cancer risk. Cancer Epidemiol. Biomarkers Prev. 1999 / 8 (3) / 233-239. , Morales Suarez-Varela, M. et al, Effect of the ingestion of food and gynaecologic risk factors on breast cancer risk in Valencia. (in spanish) Nutr. Hosp. 1998 / 13 (6) / 325-329. , Hebert, J.R. et al, The effect of dietary exposures on recurrence and mortality in early stage breast cancer. Breast Cancer Res. Treat. 1998 / 51 (1) / 17-28. , Zheng, W. et al, Well done meat intake and the risk of breast cancer. J. Natl. Cancer Inst. 1998 / 90 (22) / 1724-1729. , Hsing, A.W. et al, Risk factors for male breast cancer (United States) Cancer Causes Control 1998 / 9 (3) / 269-275. , Koo, L.C. et al, An ecological study of trends in cancer incidence and dietary changes in Hong Kong. Nutr. Cancer 1997 / 28 (3) / 289-301. , Jarvinen, R. et al, Diet and breast cancer risk in a cohort of Finnish women. Cancer Lett. 1997 / 114 (1-2) / 251-253. , Prieto-Ramos, F. et al, Mortality trends and past and current dietary factors of breast cancer in Spain. eur. J. Epidemiol. 1996 / 12 (2) / 141-148. , Ronco, A. et al, Meat, fish, and risk of breast cancer : a case control study from Uruguay. Int. J. Cancer 1996 / 65 (3) / 328-331. , Gaard, M. et al, dietary fat and the risk of breast cancer : a prospective study of 25,892 Norwegian women. Int. J. Cancer 1995 / 63 (1) / 13-17. , Landa, M.C. et al, diet and risk of breast cancer in Spain. Eur. J. Cancer Prev. 1994 / 3 (4) / 313-320. , Toniolo, P. et al, Consumption of meat ,animal products, protein, and fat and risk of breast cancer :a prospective cohort study in New York. Epidemiology 1994 / 5 (4) / 391-397. , Guo, W.D. et al, Diet, serum markers and breast cancer mortality in China. Jpn. J. Cancer Res. 1994 / 85 (6) / 572-577. , Levi, F. et al, Dietary factors and breast cancer risk in Vaud, Switserland. Nutr. Cancer 1993 / 19 (3) / 327-335. , Goodman, M.T. et al, The association of diet, obesity, and breast cancer in Hawaii. Cancer Epidemiol. Biomarkers Prev. 1992 / 1 (4) / 269-275. , Ingram, D.M. et al, The role of diet in the development of breast cancer : a case control study of patients with breast cancer, benign epithelial hyperplasia and fybrocystic disease of the breast. Br. J. Cancer 1991 / 64 (1) / 187-191. , Matos, E.L. et al, Breast cancer in argentina :case control study with special reference to meat eating habits. Neoplasma 1991 / 38 (3) / 357-366. , Hislop, T.G. et al, Diet and histologic types of benign breast disease defined by subsequent risk of breast cancer. Am. J. epidemiol. 1990 / 131 (2) / 263-270. , Hislop, T.G. et al, Influence of estrogen receptor status on dietary risk factors for breast cancer. CMAJ 1988 / 138 (5) / 424-430. , La Vecchia, C. et al, dietary factors and the role of breast cancer. Nutr. Cancer 1987 / 10 (4) / 205-214. , Shimada, A. et al, Ecological approach to the eating habits and the cancer mortality of Brazilian people. Gan No Rinsho 1986 / 32 (6) / 631-640. , La Vecchia, C. et al, Age at first birth, dietary practises and breast cancer mortality in various Italian regions. Oncology 1986 / 43 (1) / 1-6. , Hirayama, T. et al, A large scale cohort study on cancer risks by diet - with special reference to the risk reducing effects of green-yellow vegetable consumption. Pricess Takamatsu ymp. 1985 / 16 / 41-53. , Lubin, J.H. et al, Dietary factors and breast cancer. Int. J. Cancer 1981 / 28 (6) / 685-689.
(3) Ekman, P. ,Genetic and environmental factors in prostate cancer Genesis : Identifying high-risk cohorts. Eur. Urol. 1999 / 35 (5-6) / 362-369. , Giovanucci, E. ,Dietary influences of 1,25(OH)2 vitamin D in relation to prostate cancer : a hypothesis. Cancer Causes Control. 1998 / 9 (6) / 567-582. , Eichholzer, M. et al, The significance of nutrition in primary prevention of cancer. (in German) Ther. Umsch. 1997 / 54 (8) / 457-462. , Koo, L.C. et al, An ecological study of trends in cancer incidence and dietary changes in Hong Kong. Nutr. Cancer 1997 / 28 (3) / 289-301. , Willet, W.C. ,Nutrition and Cancer. Salud. Publica. Mex. 1997 / 39 (4) / 298-309. , Ewings, P. et al, A case control study of cancer of the prostate in Somerset and east Devon. Br. J. Cancer 1996 / 74 (4) / 661-666. , Key, T. ,Risk factors for prostate cancer. Cancer Surv. 1995 / 23 / 63-77. , De Stefani, E. et al, Tobacco, alcohol, diet and risk of prostate cancer. Tumori 1995 / 81 (5) / 315-320. , Gann, P.H. et al, Prospective study of plasma fatty acids and risk of prostate cancer. J. Natl. Cancer Inst. 1994 / 86 (4) / 281-286. , Le Marchand, L. et al, Animal fat consumption and prostate cancer : a prospective study in Hawaii. Epidemiology 1994 / 5 (3) / 276-282. , Giovanucci, E. et al, Aprospective study of dietary fat and risk of prostate cancer. J. Natl. Cancer Inst. 1993 / 85 (19) / 1571-1579. , Bravo, M.P. et al, Dietary factors and prostate cancer.Urol. Int. 1991 / 46 (2) / 163-166. , Talamini, R. et al, Nutrition, social factors, and prostate cancer in a northern Italian population. Br. J. Cancer 1986 / 53 (6) / 817-821. , Snowdon, D.A. et al, Diet, obesity, and risk of fatal prostate cancer. Am. J. Epidemiol. 1984 / 120 (2) / 244-250.
(4) Potter, J.D. ,Colorectal cancer : molecules and populations. J. Natl Cancer Inst. 1999 / 91 (11) / 916-932. , Willet, W.C. ,Dietary fat intake and cancer risk : a controversial and instructive story. Semin. Cancer Biol. 1998 / 8 (4) / 245-253. , Pence, B.C. et al, Feeding of a well-cooked beef diet containing a high heterocyclic content enhances colon and stomach carcinogenesis in 1,2-dimethylhydrazine-treated rats. Nutr. Cancer 1998 / 30 (3) / 220-226. , Eichholzer, M. The significance of nutrition in primary prevention of cancer (in German). Ther. Usch. 1997 / 54 (8) / 457-462. , Decarli, A. et al, Environmental factors and cancer mortality in Italy : correlational exercise. Oncology 1986 / 43 (2) / 116-26.
(5) Kuratsune, M. et al, Epidemiolgic studies on possible health effects of intakes of purolyzates of foods, with reference to mortality among Japanese Seventh Day Adventists . Environ. Health Persp. 1986 / 67 / 143-146. , Berkel, J. et al, Mortality and life expectancy of Seventh-day Adventists in the Netherlands. Int. J. Epidem. 1983 / 12 / 455-459. , Kinlen, L.J. et al, A proportionate study of cancer mortality among members of a vegetarian society. Br. J. Cancer 1983 / 48 (3) / 355-361. , Goldin, B.R. et al, effect of diet on excretion of estrogens. Cancer Res. 1981 / 41 (9 pt 2) / 3771-3773.
(6) Messina, M.J. et al, Soy intake and cancer risk : a revieuw of the in vitro and in vivo data. Nutr. Cancer 1994 / 21 (2) / 113-131.
(7) Zheng, W. et al, N-acetyltransferase 1 genetic polymorphism, cigarette smoking ,well-done meat intake, and breast cancer risk. Cancer Epidemiol. Biomarkers Prev. 1999 / 8 (3) / 233-239. , Zheng, W. et al, Well-done meat intake and the risk of breast cancer. J. Natl. Cancer Inst. 1998 / 90 (22) / 1724-1729. , Sinha, R. et al, Fried, well done red meat and risk of lung cancer in women. Cancer Causes Control 1998 / 9 (6) / 621-630. , Brown, L.M. et al, Dietary factors and the risk of squamous cell esophageal cancer among black and white men in the United States. Cancer Causes Control 1998 / 9 (5) / 467-474. , Kjarheim, K. et al, The role of alcohol, tobacco, and dietary factors in upper aerogastic tract cancers : a prospective study of 10,900 Norwegian men. Cancer Causes Control 1998 / 9 (1) / 99-108. , De Stefani, E. et al, Case-control study on the role of heterocyclic amines in the etiology of upper aerodigestive cancers in Uruguay. Nutr. Cancer 1998 / 32 (1) / 43-48. , Blowers, L. et al, Dietary and other lifestyle factors of women with brain gliomas in Los Angeles County. Cancer Causes Control 1997 / 8 (1) / 5-12. , De Stefani, E. et al, Meat intake, heterocyclic amines, and risk of breast cancer : a case-control study in Uruguay. Cancer Epidemiol. Biomarkers Prev. 1997 / 6 (8) / 573-581. , Le Marchand, L. et al, A case-control study of diet and colorectal cancer in a multiethnic population in Hawaii (United States) : Lipids and foods of animal origin. Cancer Causes Control 1997 / 8 (4) / 637-648. , Vineis, P. et al, Interplay between heterocyclic amines in cooked meat and metabolic phenotype in the etiology of colon cancer. Cancer Causes Control 1996 / 7 (4) / 479-486. , Howe, G.R. et al, Nutrition and pancreatic cancer, Cancer Causes Control 1996 / 7 (1) / 69-82. , Wolk, A. et al, Nutrition and renal cell cancer, Cancer Causes Control 1996 / 7 (1) / 5-18. , Kampman, E. et al, Vegetable and animal products as determinants of colon cancer risk in Dutch men and women. Cancer Causes Control 1995 / 6 (3) / 225-234. , Peters, J.M. et al, Processed meats and risk of childhood leukemia (California ,United States). Cancer Causes Control 1994 / 5 (2) / 195-202. , Chow, W.H. et al, Risk factors for small intestine cancer. Cancer Causes Control 993 / 4 (2) / 163-169. , Lee, H.P. et al, Risk factors for breast cancer by age and menopausal status : a case-control study in Singapore. Cancer Causes Control 1992 / 3 (4) / 313-327. , Rose, D.P. et al, International comparisons of mortality rates for cancer of the breast ,ovary, prostate, and colon, and per capita food consumption. Cancer 1986 / 58 (11) / 2363-2371.
(8) Mori, M. et al, Reproductive, genetic, and dietary risk factors for ovarian cancer. Am. J. Epidemiol. 1988 / 128 (4) / 771-777.
(9) Hill, H.A. et al, Nutrition and endometrial cancer, Cancer Causes Control 1996 / 7 (1) / 19-32. , Talamimi, R. et al, A case-control study of risk factor for renal cell cancer in northern Italy. Cancer Causes Control 1990 / 1 (2) / 125-131.
(10) Di Stefani, E. et al, Dietary fat and lung cancer : a case-control study in Uruguay. Cancer Causes Control 1997 / 8 (6) / 913-921.
(11) Glattre, E. et al, Norwegian case-control study testing the hypothesis that sea food increases the risk of thyroid cancer. Cancer Causes Control 1993 / 6 (1) / 11-16. , Kolonel, L.N. et al, An epidemiology study of thyroid cancer in Hawai. Cancer Causes Control 1990 / 1 (3) / 223-234.
(12) Knekt, P. et al, Risk of colorectal and other gastro-intestinal cancers after exposure to nitrate, nitrite and N-nitroso compounds : a follow-up study. Int. J. Cancer 1999 / 80 (6) / 852-856
(13) La Vecchia, C. et al, Case-control study on influence of methionine, nitrite, and salt on gastric carcinogenesis in northern Italy. Nutr. Cancer 1997 / 27 (1) / 65-68. , Chen, W. et al, Gastric carcinogenesis : 2-chloro-4-methyltiobutanoic acid, a novel mutagen in salted ,pickeld Sanma hiraki fish, or similarly treated methionine. Chem. Res. Toxicol. 1996 / 9 (1) / 58-66. Chow, W.H. et al, Risk factors for small intestine cancer. Cancer Causes Control 1993 / 4 (2 /163-169.
(14) Chiueh, C.C. et al, Enhanced hydroxyl radical generation by 2'-methyl analog of MPTP : suppression by clorgyline and deprenyl. Synapse 1992 / 11 (4) / 346-348.
(15) Desole, M.S. et al, Correlation between 1-methyl-4-phenylpyridinium (MPP+) levels, ascorbic acid oxidation and glutathione levels in the striatal synaptosomes of the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated rats. Neurosci. Lett. 1993 / 161 (2) / 121-123.
(16) Mihatsch, W. et al, Treatment with antioxidants does not prevent loss of dopamine in the striatum of MPTP-treated common marmosets : preliminary observations. J. Neural. Transm. Park. Dis. Dement. Sect. 1991 / 3 (1) / 73-78. , Sutphin, M.S. et al, Effects of low selenium diets on antioxidant status and MPTP toxicity in mice. Neurochem. Res. 1991 / 16 (12) / 1257-1263. , Gong, L. et al, Vitamine E supplements fail to protect mice from acute MPTP neurotoxicity. Neuroreport. 1991 / 2 (9) / 544-546. , Sanchez-Ramos, J.R. et al, Selective destruction of cultured dopaminergic neurons from fetal rat mesencephalon by 1-methyl-4-phenyl-pyridinium : cytochemical and morphological evidence. J. Neurochem. 1988 / 50 (6) / 1934-1944.
(17) Schwartz, J.L. ,The dual role of nutrients as antioxydants and prooxydants : Their effect on tumor cell growth. Journal of Nutrition 1996 / 126 (4suppl.) / 1221-1227.
(18) Rapola, J.M. et al, Randomised trial of alpha-tocopherol and beta-carotene supplements on incidence of major coronary events in men with previous myocardial infraction. Lancet 1997 / 349 (9067) / 1715-1720. , Goodman, G.E. et al, The association between participant characteristics and serum concentrations of beta-carotene, retinol, retinylpalmitate, and alpha-tocopherol among participants in The Carotene and Retinol Efficacy Trial (CARET) for prevention of lung cancer. Cancer Epidemiol. Biomarkers Prev. 1996 / 5 (10) / 815-821. , The Alpha-Tocoferol, Beta-carotene Cancer Prevention Group, The effect of vitamin E and beta carotene on the incidence of lung cancer and other cancers in male smokers. New England Journal of Medicine 1994 / 330 / 1029-1035. , Chow, W.H. et al, Risk factors for small intestine cancer. Cancer Causes Control 1993 / 4 (2 / 163-169. , Omenn, G.S. et al, Risk factors for lung cancer and for intervention effects in CARET, the Beta-Carotene and Retinol Efficacy Trial. J. Natl. Cancer Inst. 1996 / 88 (21) / 1550-1559.
(20) Hsieh, S.E. et al, The effect of vitamin C on N-acetyltransferase activity in Klebsiella pneumonia. Food and Chemical Toxicology 1997 / 35 (12) / 1151-1157.
(21) Agus, D.B. et al, Stromal cell oxidation : a mechanism by which tumors obtain vitamin C. Cancer Research 1999 / 59 (18) / 4555-4558.
(22) Simon, J.A. et al, Relation of serum ascorbic acid to serum vitamin B12, serum ferritin ,and kidney stones in the US adults. Arch.Intern. Med. 1999 / 159 (6) / 619-624. , Palmer, A.M. et al, Dietary antioxydant supplementation reduces lipid peroxidation but impairs vascular function in small mesenteric arteries of the sptreptozotocin-diabetic rat. Diabetologia 1998 / 42 (2) / 148-156. , Podmore, I.D. et al, Vitamin C exhibits pro-oxidant properties. Nature 1998 / 392 (6676) / 559. , Rehman, A. et al, The effects of iron and vitamin C co-supplementation on oxidative damage to DNA in healthy volunteers. Biochem. Biophys. Res. Commun. 1998 / 246 (1) / 293-298. , Horwitt, M.K., Do the metals in vitamin-mineral supplements produce undesirable oxidations ? Am. J. Clin. Nutr. 1997 / 65 (5) / 1571.
(23) Makela, S.I. et al, Dietary soybean may be antiestrogenic in male mice. Journal of Nutrition 1995 / 125 (3) / 437-445. , Fotsis, T. et al, Genistein, a dietary ingested isoflavonoid ,inhibits cell proliferation and in vitro angiogenesis. J. Nutr. 1995 / 125 (3-suppl.) / 790S-797S. , Karjalainen, J. et al, A bovine albumin peptide as a possible trigger of insulin-dependent diabetes mellitus. N. Engl. J. Med. 1992 / 327 (5) / pag.302-307.
(24) Armstrong, B.K. et al, Diet and reproductive hormones : a study of vegetarian and non-vegetarian post-menopausal women. J. Natl. Cancer Inst. 1981 / 67 (4) / 761-767.
(25) Rosenblum, E.R. ,Isolation and identification of phtyestrogens from beer. Alcohol. Clin. Exp. Res. 1992 / 16 (5) / 843-845.
(26) Weisburger, J.H. et al, Inhibition of PhIP mutagenicity by caffeďne ,lycopene, daďdzein, and genistein. Mutat. Res. 1998 / 416 (1-2) / 125-128.
(27) Persky, V. et al, Epidemiology of soy and cancer : perspectives and directions. J. Nutr. 1995 / 125 (3suppl.) / 709S-712S.
(28) Nagata, C. et al, Effect of soy milk consumption on serum estrogen concentrations in premenopausal Japanese women. J. Natl. Cancer Inst. 1998 / 90 (23) / 1830-1835..
(29) Zimmerli,B. en J.Schlatter, Sojamilch : Gefahr durch Phytohormone ?, Mitteilungen aus dem Gebiete der Lebensmittelhygiene, 1997 / 88 / pag.219-231. , Adams, N.R., Detection of the effects of phytoestrogens on sheep and cattle. J. Anim. Sci. 1995 / 73 (5) / 1509-1515.
(30) Setchell, K.D. et al, Dietary estrogens - - a probable cause of infertility and liver disease in captive cheetahs. Gastroendocrinology 1987 / 93 (2) / 225-233.
(31) Morris, S.M. et al, p53, mutations, and apoptosis in genistein-exposed human lymphoblastoid cells. Mutat. Res. 1998 / 405 (1) / 41-56. , Kulling, S.E. et al, Induction of micronuclei, DNA strand breaks and HPRT mutations in cultured Chinese hamster V79 cells by the phytoestrogen coumestrol. Food Chem. Toxicol. 1997 / 35 (6) / 605-613.
(32) Anderson, D. et al, Effect of various genotoxins and reproductive toxins in human lyphocytes and sperm in the Comet assay. Terat. Carcinog. Mutagen. 1997 / 17 (1) / 29-43.
(33) Stahl, S. et al, Phytoestrogens act as estrogen agonists in an estrogen-responsive pituitary cell line. Toxicol. Appl. Pharmacol. 1998 / 152 (1) / 41-48.
(34) Newcomb, P.A. et al, Recent oral contraceptive use and risk of breast cancer. Cancer Causes Control 1996 / 7 (5) / 525-532. , Palmer, J.R. et al, Oral contraceptive use and breast cancer risk among African-American women. Cancer Causes Control 1995 / 6 (4) / 321-331. , Paul, C. et al, Oral contraceptive use and risk of breast cancer in older women. (New Zealand) Cancer Causes Control 1995 / 6 (6) / 485-491. , Li, J.J. et al, Carcinogenic activities of various steroidal and non-steroidal estrogens in the hamster kidney : relation to hormonal activity and cell proliferation. Cancer Res. 1995 / 55 (19) / 4347-4351. , Schairer, C. et al, Menopausal estrogen and estrogen-progestin replacement therapy and risk of breast cancer (United States). Cancer Causes Control 1994 / 5 (6) / 491-500. , Yang, C.P. et al, Noncontraceptive hormone use and risk of breast cancer. Cancer Causes Control 1992 / 3 (5) / 475-479. , Colditz, G.A. et al, Type of post-menopausal hormone use and risk of breast cancer : a 12-year follow-up from the Nurses' Health Study. Cancer Causes Control 1992 / 3 (5) / 433-439. , Adami, H.O. ,Long term consequences of estrogen-progestin replacement. Cancer Causes Control 1992 / 3 (1) / 83-90. , Thomas, D.B. et al, Risk of breast cancer in relation to use of combined oral contraceptives near the age of menopause. WHO Collaborative Study of Neoplasia and steroid Contraceptives. Cancer Causes Control 1991 / 2 (6) / 389-390.
(35) Outwater, J.L. et al, Dairy products and breastcancer : the IGF-1 ,estrogen and bGH hypothesis. Med. Hypotheses 1997 / 48 (6) / 453-461.
(36) Hunter, D.J. et al, Nutrition and breast cancer ,Cancer Causes Control 1996 / 7 (1) / 56-68.
(37) Morisset, J. et al, Cell signalling pathway involved in PACAP-induced AR4-2J cell proliferation. Cell Signal 1995 / 195-205.
(38) Zava, D.T. et al, Estrogen and progestin bioactivity of foods, herbs, and spices. Proc. soc. Exp. Biol. Med. 1998 / 217 (3) / 369-378.
(39) Liener, I.E. ,Implications of antinutrial compounds in soybean foods. Crit. Rev. Food Sci. Nutr. 1994 / 34 (1) / 31-67. , Paladini, A.C. et al, Flavonoids and the central nervous system : from forgotten factors to potent anxiolytic compounds. J. Pharm. Pharmacol. 1999 / 51 (5) / 519-526.
(40) Beamand, J.A. et al, Effect of some cooked food mutagens on unscheduled DNA synthesis in cultured precision-cut rat, mouse and human liver slices. Food Chem. Toxicol. 1998 / 36 (6) / 455-466. , Pfau, W. et al, Pancreatic DNA adducts formed in vitro and in vivo by the food mutagens 2-amino-1-methyl-6-phenylimidazo(4,5-b)prydine (PhIP) and 2-amino-3-methyl-9H-pyrido(2,3-b)indole (MeAalphaC). Mutat. Res. 1997 / 378 (1-2) / 13-22. , Okogoni, H. et al, Induction of aberrent cryptfoci in C57BL/6N mice by 2-amino-9H-pyrido(2,3-b)indole (AalphaC) and 2-amino-3,8-dimethylimidazo- (4,5-f)quinoxaline (MeIQx) Cancer Lett. 1997 / 111 (1-2) / 105-109. , Zhang, X.B. et al, Intestinal mutagenicity of two carcinogenic food mutagens in transgenic mice : 2-amino-1-methyl-6-phenylimidazo(4,5-b)pyridine and amino(alpha)carboline. Carcinogenesis 1996 / 17 (10) / 2259-2265. , Pfau, W. et al, Characterization of the major DNA adduct formed by the food mutagen 2-amino-3-methyl-9H-pyrido(2,3-b)indole (MeAalphaC) in primary rat hepatocytes. Carcinogenesis 1996 / 17 (12) / 2727-2732. , Yoshida, D. et al, Formation of mutagens by heating foods and model systems. Environ. Health Perspect. 1986 / 67 / 55-58. , Yoo, M.A. et al, Mutagenic potency of heterocyclic amines in the Drosophila wing spot test and its correlation to carcinogenic potency. Jpn. J. Cancer Res. 1985 / 76 (6) / 468-473. , Ohgaki, H. et al, Carcinogenicity in mice of mutagenic compounds from glutamic acid and soybean globulin pyrolysates. Carcinogenesis. 1984 / 5 (6) / 815-819.
(41) Weisburger, J.H. et al, Tea polyphenols as inhibitors of mutagenicity of major classes of carcinogens. Mutat. Res. 1996 / 371 (1-2) / 57-63.
(42) Paladini, A.C. et al, Flavonoids and the central nervous system : from forgotten factors to potent anxiolytic compounds. J. Pharm. Pharmacol. 1999 / 51 (5) / 519-526.
(43) Sugimura, T. et al, Mutagenic factors in cooked foods. Crit. Rev. Toxicol. 1979 / 6 (3) / 189-209.
(44) National Research Council ,Washington 1996 ; Carcinogens and anticarcinogens in the human diet.
(45) Kanazawa, K. et al, Antimutagenicity of flavones and flavonols to heterocyclic amines by specific and strong inhibition of the cytochrome P450 1A family. Biosci. Biotechnol. Biochem. 1998 / 62 (5) / 970-977.
(46) Hirose, Y. et al, Induction of apoptosis in colonic epithelium treated with 2-amino-1-methyl-6-phenylimidazo(4,5-b)pyridine (PhIP) and its modulation by a P4501A2 inducer, beta-naphtoflavone, in male F344 rats. Cancer Lett. 1998 / 123 (2) / 167-172.
(47) Divi, R.L. et al, Anti-thyroid isoflavones from soyabean, isolation, characterization, and mechanisms of action. Biochemical Pharmacology 1997 / 54 (10) / 1087-1096.
(48) Robertson, I. et al, The role of cereals in the aetiology of nutritional rickets : The lesson of the Irish National Nutrition Survey 1943-8. British Journal of Nutrition 45 (1981) / 17-22. , Bhattacharyya, A.K. Nutritional Rickets in the Tropics. World Review of Nutrition and Dietetics 6 (1992) / 140-197.
(49) Slamenova, D. et al, Detection of lignin biopolymer- and vitamin E-stimulated reduction of DNA strand breaks in H2O2-and MNNG-treated mammalian cells by the omet assay. Nutr. Cancer 1999 / 33 (1) / 76-81.
(50) Hofrichter, M. et al, Production of manganese peroxidase and organic acids and mineralization of 14C'-labeled lignin (14C-DHP) during solid state fermentation of wheat straw with the white rot fungus nematoloma frowardii. Appl. Environ. Micriobiol. 1999 / 65 (5) / 1864-1870.
(51) Hamilton, S.M. et al, Effects of isothiocyanates on cytochrome P4501A1 and 1A2 activity and on the mutagenicity of heterocyclic amines. Anticancer Res. 1996 / 16 (16B) / 3597-3602.
(52) Probst Hensch, N.M. et al, Absence of the glutathione S-transferase M1 gene increases cytochrome P4501A2 activity among frequent consumers of cruciferous vegetables in a Caucasian population. Cancer Epidemiol. Biomarkers Prev. 1998 / 7 (7) / 635-638.
(53) Guiterrez-Correa, J. et al, Inactivation of myocardial dihydrolipoamide dehydrogenase by myeloperoxidase systems : effect of hallides, nitrite and thiol compounds. Free Radic. Res. 1999 / 30 (2) / 105-117. , Milligan, J.R. et al, Yield of DNA strand breaks after bus oxidation of plasmid DNA. Radiat. Res. 1999 / 151 (3) / 334-342.
(54) Ozawa, Y. et al, Occurence of stereoisomers of 1-(2'-pyrrolidinethione-3'-yl)-1,2,3,4-tetrahydro-beta-carboline- 3-carboxylic acid in fermented radish roots and their different mutagenic properties. Biosci. Biotechnol. Biochem. 1999 / 63 (1) / 216-219. , Lopez-Rodrigeuz, M. et al, Reaction of 6-hydroxy-tetrahydro-beta-carboline-3-carboxylic acids with isocyanates and isothiocyanates. Chem. Pharm. Bull. Tokyo 1994 / 42 (12) / 2108-2112.