Need to Know
Eat risk-reducing foods
Load up on healthy portions of fiber, tomato products, cruciferous vegetables (broccoli, kale, cabbage, Brussels sprouts), garlic, and onions, and eat less meat
Try selenium supplementation
Taking 200 mcg a day of this essential trace mineral may offer protection against a variety of cancers
Go for green tea
Drink several cups of green tea a day to benefit from the protective polyphenols found in tea leaves
Try vitamin C
Vitamin C has been shown to improve precancerous conditions in at-risk people
About This Condition
Colon cancer is a malignancy in the colon. It is characterized by unregulated replication of cells creating tumors, with the possibility of some of the cells spreading to other sites (metastasis).
This article includes a discussion of studies that have assessed whether certain vitamins, minerals, herbs, or other dietary ingredients offered in dietary or herbal supplements may be beneficial in connection with the reduction of risk of developing colon cancer, or of signs and symptoms in people who have this condition.
This information is provided solely to aid consumers in discussing supplements with their healthcare providers. It is not advised, nor is this information intended to advocate, promote, or encourage self prescription of these supplements for cancer risk reduction or treatment. Furthermore, none of this information should be misconstrued to suggest that dietary or herbal supplements can or should be used in place of conventional anticancer approaches or treatments.
It should be noted that certain studies referenced below, indicating the potential usefulness of a particular dietary ingredient or dietary or herbal supplement in connection with the reduction of risk of colon cancer, are preliminary evidence only. Some studies suggest an association between high blood or dietary levels of a particular dietary ingredient with a reduced risk of developing colon cancer. Even if such an association were established, this does not mean that dietary supplements containing large amounts of the dietary ingredient will necessarily have a cancer risk reduction effect.
In Western countries, cancers of the colon and rectum account for more new cancer cases each year than any other site except the lung. Although the genetic susceptibility is low, some families have a predisposition for colon cancer that usually occurs before age 40. Ulcerative colitis and Crohn’s disease as well as familial polyposis, are disorders that, to varying degrees, increase the risk of colon cancer.
The initial symptoms of colon cancer depend on the location of the tumor. Cancer in the portion of the colon nearest the left side of the body and areas close to the rectum are the most common cause for a change in bowel habits and consistency of the stool. Cancer in this part of the colon may also cause a colicky pain that is made worse by eating. Blood mixed with the stool and bowel obstruction are other symptoms that characterize cancer at this site. Ineffectual and painful straining at stool may be a sign that the cancer is more advanced. Cancer localized to the part of the colon nearest the right side of the body may cause a generalized abdominal pain and brick red blood. It is commonly associated with iron-deficiency anemia, especially when no other cause can be identified. Cancers closer to the rectum often cause a steady gnawing pain and bright red blood coating the stool.
The right diet is the key to managing many diseases and to improving general quality of life. For this condition, scientific research has found benefit in the following healthy eating tips.
|Eat your veggies||Cruciferous vegetables, such as cabbage, Brussels sprouts, broccoli, and cauliflower, are associated with a reduced colon cancer risk.|
Eat your veggies
Cabbage, Brussels sprouts, broccoli, and cauliflower belong to the Brassica family of vegetables, also known as “cruciferous” vegetables. In test-tube and animal studies, these foods have been associated with anticancer activity,1 possibly due to several substances found in these foods, such as indole-3-carbinol,2 glucaric acid (calcium D-glucarate),3 and sulforaphane.4 In a preliminary human study, people who eat cruciferous vegetables were reported to have lower-than-average risks for colon cancer.5
|Enjoy coffee||Preliminary studies suggest that coffee drinkers may have a lower colon cancer risk than those who do not drink coffee, but more research is needed to confirm this link.|
“Secondary bile acids” are substances in the gut that may increase the risk of colon and rectal cancers. Some researchers have hypothesized that coffee drinking might reduce the risks of colon and rectal cancers by decreasing the intestinal level of these substances.6 , 7 An analysis of preliminary studies suggests coffee drinkers have a significantly lower risk of these cancers compared to the risk in people who do not drink coffee.8 However, only studies using the weakest methods of inquiry have found this protective effect. Due to the lack of support from studies using stronger methodology, the association between coffee drinking and protection against colon or rectal cancers remains unproven.9
|Feast on fiber||Some, though not all, studies have shown that people who eat high amounts of fiber have a lower risk for colon cancer.|
Feast on fiber
Until recently, most studies reported that people who ate a high-fiber diet were found to be at low risk for colon cancer.10 Some researchers believed protection against colon cancer comes specifically from eating wheat bran11 , 12 , 13 as opposed to other fibers. A clear understanding of how fiber might protect against colon cancer risk remains somewhat elusive.14
Recent research has begun to cast doubt on whether fiber provides significant protection against colon cancer,15 , 16 suggesting instead that consumption of meat and other animal products may be the primary culprit. Despite these recent reports, however, some doctors continue to believe that, until more definitive information is available, people wishing to reduce their risk of colon cancer should consume more fiber in their diets.
Consuming a diet high in insoluble fiber is best achieved by switching from white rice to brown rice and from bakery goods made with white flour or mixed flours to 100%-whole-wheat bread, whole-rye crackers, and whole-grain pancake mixes. Refined white flour is generally listed on food packaging labels as “flour,”“enriched flour,”“unbleached flour,”“durum wheat,”“semolina,” or “white flour.” Breads containing only whole wheat are often labeled “100% whole wheat.”
|Spice it up with garlic and onions||Components in garlic and onions prevent nitrates from being converted into cancer-causing substances, and people who eat them often appear to have reduced colon cancer risk.|
Spice it up with garlic and onions
Garlic (Allium sativum) and onion (Allium cepa) belong to the group of plants known as Allium. Many other edible plants are found in this group, including leeks and chives. Preliminary studies have investigated the association between eating Allium herbs and the incidence of cancer. The most consistent data come from research focusing on the protective effects of Allium consumption against cancers of the gastrointestinal tract.17 , 18 , 19 , 20 , 21 , 22 Several preliminary studies have found that people who consume more Allium vegetables appear to have a reduced risk of colon cancer23 , 24 and precancerous colon polyps.25
Constituents in garlic and onions prevent the conversion of nitrates (compounds found in vegetables and, to a lesser extent, in water) to cancer-causing nitrites and nitrosamines.26
|Steer clear of sugar||Try satisfying your sweet tooth with fruit and unsweetened treats, as people who eat high amounts of sugar-containing foods have had an increased colon cancer risk. Whether this is due to other dietary or lifestyle factors remains unknown.|
Steer clear of sugar
Preliminary studies have reported associations between an increasing intake of sugar or sugar-containing foods and an increased risk colon cancer.27 , 28 Whether this association exists because sugar directly promotes cancer, or because sugar consumption is only a marker for some other dietary or lifestyle factor, remains unknown.
|Team up with tomatoes||High in the antioxidant lycopene, tomatoes may protect against a variety of cancers including colon cancer.|
Team up with tomatoes
Tomatoes contain lycopene—an antioxidant similar in structure to beta-carotene. Most lycopene in our diet comes from tomatoes, though traces of lycopene exist in other foods. Lycopene inhibits the proliferation of cancer cells in test-tube research.29
A review of published research found that higher intake of tomatoes or higher blood levels of lycopene correlated with protection from cancer in 57 of 72 studies. Findings in 35 of these studies were statistically significant.30 Evidence of a protective effect for tomato consumption was strongest for a variety of other cancers, but some evidence of a protective effect also appeared for colon cancer. Many doctors recommend that people who are not allergic to tomatoes increase their intake to reduce their risk of cancer.
|Cut back on salt||Associations between salt intake and colon cancer are reported in some preliminary studies. Although this connection has not been proven, it would be prudent to avoid excess salt.|
Cut back on salt
Associations between salt intake and colon and rectal cancers are reported in some,31 but not all, preliminary studies.32 Doctors often do not mention salt restriction as part of a cancer-prevention diet because the only malignancy strongly associated with salt—stomach cancer—is no longer common in the United States despite our high intake of salt.
|Limit meat||Eat less meat or opt for meat that isn’t well-done, fried, or heavily browned to reduce your colon cancer risk.|
Most, but not all, studies33 show meat eaters have a high risk of colon cancer.34 , 35 , 36 In some colon cancer studies, the association has been limited to consumption of sausage or other processed meats.37 , 38
The association between cancer and consumption of meat depends in part on how well the meat is cooked. Well-done meat contains more carcinogenic material than does lightly cooked meat.39 Recent evidence from preliminary studies shows that people who eat well-done,40 fried or heavily-browned meat41 have a high risk of colon cancer.
However, not every report has found that exposure to carcinogens found in well-done meat leads to an increased risk of colon cancer.42 Some studies may have failed to find this link because they did not consider the effect of genetics. Susceptibility to the colon cancer-causing effects of well-cooked meat appears to be genetically determined.43 Therefore, only some people appear to increase their risk of colon cancer by consuming well-cooked meat. However, people are rarely tested to see if they are “rapid acetylators”—meat-eaters considered to be at high risk of colon cancer44—except as subjects in a research experiment.
Most nutritionally oriented doctors tell people wishing to reduce their risk of colon cancers to stop eating meat, or at least significantly reduce consumption, and to limit intake to meat that is rare or medium-cooked. Removing all meat from the diet may be safest because consumption of even rare or medium-cooked meat has been associated with at least some increase in risk.45
|Watch the fat||Dietary fat has long been regarded as an important influence on colon cancer development, but the association between the two remains inconsistent.|
Watch the fat
Dietary fat intake has long been regarded as an important nutritional influence on colon cancer development. Nevertheless, the association between colon cancer and total dietary fat remains inconsistent. Although there are known mechanisms by which a high dietary fat intake could promote tumor growth in the colon,46 a review of the research shows the strongest dietary association with colon cancer to be the intake of meat, not necessarily the fat content of the meat.47 See the discussion about Meat (how it is cooked), above.
|Cut down on alcohol||Doctors recommend that people wishing to reduce their colon cancer risk abstain from drinking alcohol. Those who continue to drink should take folic acid supplements.|
Cut down on alcohol
Most,48 , 49 , 50 but not all,51 preliminary reports have found an association between beer drinking (though not consumption of other forms of alcohol) and rectal cancer. Beer drinking has also been associated with an increased risk of precancerous changes in the colon.52 Nitrosamines––cancer-causing chemicals found in beer––may be partially responsible for these associations.53 Several studies have found consumption of any form of alcohol to be associated with an increased risk of rectal and colon cancers, the link between rectal cancer and beer being only slightly stronger than the association between rectal cancer and consumption of other forms of alcohol.54 , 55
Alcohol can indirectly damage DNA—the material that allows cells to replicate normally. Abnormal replication of cells can lead to cancer. Folic acid, a B vitamin, appears to protect against alcohol-induced DNA damage. Increasingly, researchers believe that folic acid may be able to protect against some of the colon cancer-causing effects of alcohol.56 , 57 Doctors recommend that people wishing to reduce their risks of colon and rectal cancers abstain from drinking alcohol.
Those who continue to drink should take folic acid supplements. In one report, women taking multivitamins (often containing 400 mcg of folic acid per day) for at least 15 years had a 75% lower risk of colon cancer compared with women not taking such supplements.58
What Are "Star" Ratings?
Reliable and relatively consistent scientific data showing a substantial health benefit.
Contradictory, insufficient, or preliminary studies suggesting a health benefit or minimal health benefit.
For an herb, supported by traditional use but minimal or no scientific evidence. For a supplement, little scientific support.
Our proprietary “Star-Rating” system was developed to help you easily understand the amount of scientific support behind each supplement in relation to a specific health condition. While there is no way to predict whether a vitamin, mineral, or herb will successfully treat or prevent associated health conditions, our unique ratings tell you how well these supplements are understood by the medical community, and whether studies have found them to be effective for other people.
For over a decade, our team has combed through thousands of research articles published in reputable journals. To help you make educated decisions, and to better understand controversial or confusing supplements, our medical experts have digested the science into these three easy-to-follow ratings. We hope this provides you with a helpful resource to make informed decisions towards your health and well-being.
|400 mcg daily||
Folic acid appears to be effective against colon cancer, especially in people with ulcerative colitis, people who drink alcohol, and people in remission from colon cancer.
400 mcg daily
People with ulcerative colitis (UC) are at increased risk for colon cancer. Many patients with this disease take the drug sulfasalazine, which depletes folic acid.59 In a preliminary report, patients with long-standing UC who took folic acid supplements (at least 400 mcg per day) had a 62% lower incidence of colon cancer or precancerous changes in the colon, compared with those who did not supplement with folic acid.60 Although this difference was not statistically significant, the researchers recommended that people who take sulfasalazine should supplement with folic acid to potentially reduce the risk of colon cancer.61
As dietary folate increases, the risks of precancerous polyps in the colon62 and colon cancer itself decrease, according to some,63 but not all, reports.64 In one study, women who had taken folic acid supplements had a statistically significant 75% reduction in the risk of colon cancer, compared with women not taking folic acid supplements, but only when they had been supplementing with folic acid for more than 15 years.65 In another report, the association between dietary folate and protection from precancerous polyps grew much stronger when use of folic acid supplements was considered (as opposed to studying only folate intake from food).66 However, one double-blind study found that supplementing with 1 mg of folic acid per day for three to eight years did not prevent recurrences of precancerous polyps in people who had already had at least one polyp.67
The protection from colon cancer associated with high intake of folate has been reported to occur more in consumers of alcohol than in nondrinkers.68 This finding fits well with evidence that folate reverses damage to DNA caused by alcohol consumption.69 Damaged DNA can lead to abnormal cellular replication—a step toward cancer.
Some nutritionally oriented doctors recommend folic acid supplementation for prevention of recurrences in patients who formerly had colon cancer but are now in complete remission. However, no research has yet explored the effect of folic acid supplementation in people who have already been diagnosed with cancer. Cancer patients taking the chemotherapy drug methotrexate must not take folic acid supplements without the direction of their oncologist.
|Drink a few cups per day||
The polyphenols in green tea leaves may help protect against colon cancer.
Drink a few cups per day
Green tea and black tea (Camellia sinensis) have both been studied to determine whether they cause or prevent cancer. The evidence on the protective effect of either type of tea is inconsistent.70 , 71 , 72 , 73 , 74 , 75 , 76 , 77
A number of preliminary studies have shown an association between drinking green tea and a reduced risk of some types of cancer,78 , 79 , 80 , 81 including colon cancer.82 , 83 In contrast, preliminary studies found that consumers of black tea do not appear to have a reduced risk of any type of cancer.84 , 85 , 86 , 87
|20 mg at bedtime||
If you have colon cancer, taking melatonin under medical supervision may help improve prognosis and quality of life.
20 mg at bedtime
The hormone melatonin is available as a supplement and is believed by some researchers to have anticancer activity because of its effects on the immune system.88 In research trials, melatonin has been evaluated as a potential agent for use in connection with treatment for cancer patients—not to protect healthy people from getting cancer.
Patients with advanced colon cancer who had either not responded to chemotherapy, or who had relapsed after a response to chemotherapy, were given either no additional treatment (control group) or a combination of interleukin-2 and 40 mg of melatonin per day.89 Nine of 25 patients given melatonin plus interleukin-2 survived for a year compared with only three of 25 patients in the control group, a difference that was statistically significant.
Many other controlled trials suggest that melatonin may extend survival, disease-free survival, and/or quality of life in cancer patients.90 , 91 , 92 , 93 , 94 , 95 , 96 , 97 , 98 , 99 , 100 , 101 , 102Most of these trials used 20 mg of melatonin taken at bedtime. Taking such a high amount of melatonin should be done only under the supervision of a doctor familiar with its use. Animal research suggests that the anticancer effects of this hormone may be reversed if melatonin is taken during the day. Therefore, melatonin should be taken only at night.
|200 mcg daily||
Selenium appears to protect against a variety of cancers, including colon cancer.
200 mcg daily
Selenium has been reported to have diverse anticancer actions.103 , 104 Selenium inhibits cancer in animals.105 Low soil levels of selenium, probably associated with low dietary intake, have been associated with increased cancer incidence in humans.106 Blood levels of selenium have been reported to be low in patients with a variety of cancers,107 , 108 , 109 , 110 , 111 , 112 , 113 , 114 including colon cancer.115 In preliminary reports, people with the lowest blood levels of selenium had between 3.8 and 5.8 times the risk of dying from cancer compared with those who had the highest selenium levels.116 , 117
The strongest evidence supporting the anticancer effects of selenium supplementation comes from a double-blind trial of 1,312 Americans with a history of skin cancer who were treated with 200 mcg of yeast-based selenium per day or placebo for 4.5 years, then followed for an additional two years.118 Although no decrease in skin cancers occurred, a dramatic 50% reduction in overall cancer deaths and a 37% reduction in total cancer incidence were observed. A statistically significant 58% decrease in cancers of the colon and rectum was reported.
Little is known about the effects of selenium in the treatment of people with existing cancer. Selenium supplementation was reported to improve immune function in colon cancer patients,119 but no long-term follow-up was done to evaluate whether these patients ultimately lived longer or fared better.
In the double-blind study cited above,120 the large reduction in cancer deaths found in such a short period of time (6.5 years) suggests that these researchers may have been successfully, though unknowingly, treating some people with undiagnosed cancer. However, this speculation has yet to be proven.
|Refer to label instructions||
Through a variety of mechanisms, calcium appears to reduce precancerous conditions in the colon and the risk of colon cancer.
Caution: Calcium supplements should be avoided by prostate cancer patients.
Through a variety of mechanisms, calcium may have anticancer actions within the colon. Most,121 , 122 , 123 but not all,124 preliminary studies have found associations between taking calcium supplements and a reduced risk of colon cancer or precancerous conditions in the colon. In double-blind trials, calcium supplementation has significantly protected against precancerous changes in the colon in some,125 , 126 but not all, reports.127 , 128 While most evidence examining the ability of calcium supplementation to help prevent colon cancer appears hopeful, no research findings yet support the use of calcium supplements in people already diagnosed with colon cancer.
Conjugated Linoleic Acid
|Refer to label instructions||
Preliminary and test tube studies indicate that CLA may reduce the risk of colon cancer.
Conjugated Linoleic Acid
Preliminary animal and test tube research suggests that CLA might reduce the risk of cancers at several sites, including breast, prostate, colorectal, lung, skin, and stomach.129 , 130 , 131 , 132 One preliminary study in humans suggests that increasing CLA intake may reduce the risk of colorectal cancer.133
|Refer to label instructions||
Several studies have found that supplementing with fish oil reduces markers for colon cancer risk.
Several human studies have found that supplementation with omega-3 fatty acids from fish oil leads to a reduction in markers for the risk of colon cancer.134 , 135 , 136 In each case, enough fish oil was supplemented to supply several grams of omega-3 fatty acids per day, though the optimal amount remains unknown. Despite these promising reports, no trial has yet investigated whether supplementation with fish oil would actually help in the prevention of colon cancer, or be useful in connection with the treatment of people who already have been diagnosed with colon cancer.
|Refer to label instructions||
Preliminary research suggests that glutathione might have anticancer activity by binding with cancer-causing agents or by acting as an antioxidant.
Glutathione is an antioxidant made in the body, found in some foods, and available as a supplement. Preliminary research suggests that glutathione might have anticancer activity by binding with cancer causing agents or by acting as an antioxidant.
In a preliminary report, 11 patients with late-stage or terminal colon cancer were given 800 mg of glutathione twice per day for at least three months.137 After an average of 21 weeks, three had died, four others did not improve, and four “recovered with normal diet [and] increased weight. . . . Three of the four were able to return home.” In that report, glutathione was combined with the amino acid cysteine and with anthocyans—a type of flavonoid. More research is needed to evaluate whether glutathione is an effective agent for use in connection with treatment of people with late-stage colon cancer.
|Refer to label instructions||
Vitamin C has been shown to improve precancerous conditions in at-risk people.
Women, but not men, who took vitamin C supplements were reported to have a reduced risk of colon cancer, according to a preliminary report.138
Familial polyposis is a disease that usually leads to colon cancer. In a double-blind study, supplementation with 3 grams per day of vitamin C for nine months led to a reduction in the number of precancerous polyps in people with familial polyposis.139 In another controlled trial, combining vitamin C with vitamin A and vitamin E led to a dramatic reduction in the recurrence of adenomatous polyps—another precancerous condition of the colon.140 However, other trials attempting to prevent recurrence of adenomatous polyps using vitamin C alone or in combination with other vitamins have reported no therapeutic effect141 or only weak trends favoring the group given supplements.142 , 143
Therefore, the ability of vitamin C supplementation to reduce recurrences of precancerous polyps remains unproven. Whether long-term supplementation with vitamin C would directly help in the prevention of colon cancer has not yet been studied.
Cancer patients’ white blood cells (WBCs) have been reported to contain low levels of vitamin C when compared with WBCs of healthy people.144 In the 1970s, Linus Pauling and Ewan Cameron, a Scottish surgeon, gave 100 terminal cancer patients 10 grams of vitamin C per day (2.5 grams four times per day) and followed them until death.145 These patients lived an average of 210 days, compared with an average of 50 days for similar cancer patients who did not receive vitamin C. A follow-up report on the same patients revealed an even greater gap in survival time between the two groups.146
Mayo Clinic researchers studied the effect of vitamin C in terminal cancer patients, but unlike Pauling and Cameron, they gave about half of the patients a placebo. The Mayo Clinic findings showed that vitamin C had no therapeutic effect.147 Pauling claimed that his trial differed from the Mayo Clinic study because his patients had received much less chemotherapy. In theory, chemotherapy might inactivate vitamin C’s anticancer effects.
The Mayo Clinic therefore conducted a second controlled study, this time in colon cancer patients who had not received chemotherapy.148 Again, the Mayo Clinic reported that vitamin C was ineffective. In response, Pauling said that his patients had been given vitamin C supplements until they died. The Mayo Clinic’s colon cancer patients, in contrast, were no longer given vitamin C once their cancers progressed. Thus Pauling’s premise—that vitamin C would increase survival in terminal cancer patients if they continued to take vitamin C until they died—had not been adequately tested by the Mayo Clinic.
Pauling was also concerned that some of the colon cancer patients assigned to the placebo group may have been taking vitamin C supplements even though they had been instructed not to. The Mayo Clinic had made only limited attempts to monitor whether people in the control group were surreptitiously taking vitamin C.
In an attempt to duplicate Pauling’s findings, Japanese researchers conducted a trial with terminal cancer patients.149 As with the Pauling trial, a control group existed but was not given placebo. Patients assigned to vitamin C lived an average of 246 days compared with 43 days in those not receiving vitamin C. Thus, the Japanese research results independently confirmed the outcome of the Pauling and Cameron trial. Nonetheless, the negative reports from the controlled Mayo Clinic trials—despite criticisms of those trials—leave the issue unresolved. None of these studies investigated what effect, if any, vitamin C might have in patients with early stage colon cancer.
|Refer to label instructions||
People who take vitamin D supplements have been shown to be at low risk for colon cancer.
Ultraviolet light from sun exposure increases the risk of skin cancers and melanoma. Nonetheless, where sun exposure is low, rates of several cancers have been reported to be high.150 , 151 , 152 An association between greater sun exposure and a reduced risk of colon cancer has appeared in some,153 but not all, studies.154
In preliminary reports, people who take vitamin D supplements have been reported to be at low risk for colon cancer, though the differences between supplement takers and others might have been due to chance.155 , 156 More research is needed to determine whether vitamin D supplements may be useful in connection with the prevention of colon cancer.
|Refer to label instructions||
In most preliminary reports, vitamin E appears to protect against cancer.
In most,157 , 158 but not all, preliminary reports, people who take vitamin E supplements were found to have decreased risks of precancerous colon polyps and colon cancer, compared with those who do not take vitamin E.159 Although a double-blind study of male smokers reported that those receiving low amounts of vitamin E (equivalent to approximately 50 IU per day) had a higher incidence of precancerous colon polyps than those assigned to placebo,160 the same trial found a trend toward lower risk of colon cancer in the vitamin E group.161 Insufficient information exists for making recommendations regarding the use of vitamin E in connection with the prevention of colon cancer.
1. Beecher CWW. Cancer preventive properties of varieties of Brassica oleracea: a review. Am J Clin Nutr 1994;59(suppl):1166S–70S.
2. Cover CM, Hsieh SJ, Cram EJ, et al. Indole-3-carbinol and tamoxifen cooperate to arrest the cell cycle of MCF-7 human breast cancer cells. Cancer Res 1999;59:1244–51.
3. Walaszek Z, Hanausek-Walaszek M, Minton JP, Webb TE. Dietary glucarate as anti-promoter of 7,12-demethylbenz [a]anthracene-induced mammary tumorigenesis. Carcinogenesis 1986;7:1463–6.
4. Zhang Y, Kensler TW, Cho C-G, et al. Anticarcinogenic activities of sulforaphane and structurally related synthetic norbornyl isothiocyanates. Proc Natl Acad Sci USA 1994;91:3147–50.
5. Kohlmeier L, Su LJ. Cruciferous vegetable consumption and colorectal cancer risk: meta-analysis of the epidemiological evidence. Am J Epidemiol 1996;143(11Suppl):S61 [abstr #242].
6. Rosenberg L. Coffee and tea consumption in relation to the risk of large bowel cancer: a review of epidemiologic studies. Cancer Lett 1990;52:163–71.
7. Jacobsen BK, Thelle DS. Coffee, cholesterol, and colon cancer: is there a link? BMJ 1987;294:4–5 [editorial].
8. Giovannucci E. Meta-analysis of coffee consumption and risk of colorectal cancer. Am J Epidemiol 1998;147:1043–52.
9. Giovannucci E. Meta-analysis of coffee consumption and risk of colorectal cancer. Am J Epidemiol 1998;147:1043–52.
10. Hill MJ. Cereals, cereal fibre and colorectal cancer risk: a review of the epidemiological literature. Eur J Cancer Prev 1997;6:219–25.
11. Reddy BS. Role of dietary fiber in colon cancer: an overview. Am J Med 1999;106:16S–9S.
12. Kritchevsky D. Protective role of wheat bran fiber: preclinical data. Am J Med 1999;106:28S–31S.
13. Earnest DL, Einspahr JG, Alberts DS. Protective role of wheat bran fiber: data from marker trials. Am J Med 1999;106:32S–7S.
14. Klurfeld DM. Fiber and cancer protection—mechanisms. Adv Exp Med Biol 1997;427:249–57.
15. O’Keefe SJD, Kidd M, Espitalier-Noel G, Owira P. Rarity of colon cancer in Africans is associated with low animal product consumption, not fiber. Am J Gastroenterol 1999;94:1373–80.
16. Fuchs CS, Giovannucci EL, Colditz GA, et al. Dietary fiber and the risk of colorectal cancer and adenoma in women. N Engl J Med 1999;340:169:169–76.
17. Gao CM, Takezaki T, Ding JH, et al. Protective effect of allium vegetables against both esophageal and stomach cancer: A simultaneous case-referent study of a high-epidemic area in Jiangsu province, China. Jpn J Cancer Res 1999;90:614–21.
18. You W, Blot WJ, Chang Y, et al. Diet and high risk of stomach cancer in Shadong, China. Cancer Res 1988;48:3518–23.
19. You W-C, Blot WJ, et al. Allium vegetables and reduced risk of stomach cancer. J Natl Cancer Inst 1989;81:162–4.
20. Buiatti E, Palli D, Decarli A, et al. A case-control study of gastric cancer and diet in Italy. Int J Cancer 1989;44:611–6.
21. Cipriani F, Buiatti E, Palli D. Gastric cancer in Italy. Ital J Gastroenterol 1991;23:429–35.
22. Mei X, Wang ML, Xu HX, et al. Garlic and gastric cancer: The influence of garlic on the level of nitrate and nitrite in gastric juice. Acta Nutr Sin 1982;4:53–6.
23. Steinmetz KA, Kushi LH, et al. Vegetables, fruit and colon cancer in the Iowa women’s health study. Am J Epidemiol 1994;139:1–5.
24. Levi F, Pasche C, La Vecchia C, et al. Food groups and colorectal cancer risk. Br J Cancer 1999;79:1283–7.
25. Witte JS, Longnecker MP, Bird CL, et al. Relation of vegetable, fruit and grain consumption to colorectal adenomatous polyps. Am J Epidemiol 1996;144:1015–25.
26. Dorant E, van der Brandt PA, et al. Garlic and its significance for the prevention of cancer in humans: A critical view. Br J Cancer 1993;67:424–9 [review].
27. Franceschi S, Favero A, La Vecchia C, et al. Food groups and risk of colorectal cancer in Italy. Int J Cancer 1997;72:56–61.
28. Bostick RM, Potter JD, Kushi LH, et al. Sugar, meat, and fat intake, and non-dietary risk factors for colon cancer incidence in Iowa women (United States). Cancer Causes Control 1994;5:38–52.
29. Levy J, Bosin E, Feldman B, et al. Lycopene is a more potent inhibitor of human cancer cell proliferation than either a-carotene or ß-carotene. Nutr Cancer 1995;24:257–66.
30. Giovannucci E. Tomatoes, tomato-based products, lycopene, and cancer: review of the epidemiologic literature. J Natl Cancer Inst 1999;91:317–31.
31. Tuyns AJ. Salt and gastrointestinal cancer. Nutr Cancer 1988;11:229–32.
32. Negri E, La Vecchia C, D’Avanzo B, et al. Salt preference and the risk of gastrointestinal cancers. Nutr Cancer 1990;14:227–32.
33. Ambrosone CB, Freudenheim JL, Sinha R, et al. Breast cancer risk, meat consumption and N-acetyltransferase (NAT2) genetic polymorphisms. Int J Cancer 1998;75:825–30.
34. Giovannucci E, Rimm EB, Stampfer MJ, et al. Intake of fat, meat, and fiber in relation to risk of colon cancer in men. Cancer Res 1994;54:2390–7.
35. Willett WC, Stampfer MJ, Colditz GA, et al. Relation of meat, fat, and fiber intake to the risk of colon cancer in a prospective study among women. N Engl J Med1990;323:1664–72.
36. O’Keefe SJD, Kidd M, Espitalier-Noel G, Owira P. Rarity of colon cancer in Africans is associated with low animal product consumption, not fiber. Am J Gastroenterol 1999;94:1373–80.
37. Goldbohm RA, van den Brandt, van ‘t Veer P, et al. A prospective cohort study on the relation between meat consumption and the risk of colon cancer. Cancer Res 1994;54:718–23.
38. Gaard M, Tretli S, Loken EB. Dietary factors and risk of colon cancer: a prospective study of 50,535 young Norwegian men and women. Eur J Cancer Prev 1996;5:445–54.
39. Bjeldanes LF, Morris MM, Felton JS, et al. Effect of meat composition and cooking conditions on mutagen formation in fried ground beef. J Agriculture Food Chem 1983;31:18–21.
40. Sinha R, Chow WH, Kulldorff M, et al. Well-done grilled red meat increases the risk of colorectal adenomas. Cancer Res 1999;59:4320–4.
41. De Verdier MG, Hagman U, Peters RK, et al. Meat, cooking methods and colorectal cancer: a case-referent study in Stockholm. Int J Cancer 1991;49:520–5.
42. Augustsson K, Skog K, Jägerstad M, et al. Dietary heterocyclic amines and cancer of the colon, rectum, bladder, and kidney: a population-based study. Lancet 1999;353:703–7.
43. Vieneis P, McMichael A. Interplay between heterocyclic amines in cooked meat and metabolic phenotype in the etiology of colon cancer. Cancer Causes Control 1996;7:479–86.
44. Roberts-Thompson IC, Ryan P, Khoo KK, et al. Diet, acetylator phenotype, and risk of colorectal neoplasia. Lancet 1996;347:1372–4.
45. Sinha R, Chow WH, Kulldorff M, et al. Well-done grilled red meat increases the risk of colorectal adenomas. Cancer Res 1999;59:4320–4.
46. Reddy BS. The Fourth DeWitt S. Goodman lecture. Novel approaches to the prevention of colon cancer by nutritional manipulation and chemoprevention. Cancer Epidemiol Biomarkers Prev 2000;9:239–47 [review].
47. Giovannucci E, Goldin B. The role of fat, fatty acids, and total energy intake in the etiology of human colon cancer. Am J Clin Nutr 1997;66(suppl):1564S–71S [review].
48. Kabat GC, Howson CP, Wynder EL. Beer Consumption and rectal cancer. Int J Epidemiol 1986;15:494–501.
49. Kune S, Kune GA, Watson LF. Case-control study of alcoholic beverages as etiological factors: the Melbourne Colorectal Cancer Study. Nutr Cancer 1987;9:43–56.
50. Riboli E, Cornée, Macquart-Moulin G, et al. Cancer and polyps of the colorectum and lifetime consumption of beer and other alcoholic beverages. Am J Epidemiol 1991;134:157–66.
51. La Vecchia C, Negri E, Franceschi S, D’Avanzo B. Moderate beer consumption and the risk of colorectal cancer. Nutr Cancer 1993;19:303–6.
52. Sandler RS, Lyles CM, McAuliffe C, et al. Cigarette smoking, alcohol, and the risk of colorectal adenomas. Gastroenterology 1993;104:1445–51.
53. Riboli E, Cornée, Macquart-Moulin G, et al. Cancer and polyps of the colorectum and lifetime consumption of beer and other alcoholic beverages. Am J Epidemiol 1991;134:157–66.
54. Klatsky AL, Armstrong A, Friedman GD, Hiatt RA. The relations of alcoholic beverage use to colon and rectal cancer. Am J Epidemiol 1988;128:1007–15.
55. Freudenheim JL, Graham S, Marshall JR, et al. Lifetime alcohol intake and risk of rectal cancer in Western New York. Nutr Cancer 1990;13:101–0.
56. Boutron-Ruault M-C, Senesse P, Faivre J, et al. Folate and alcohol intakes: related or independent roles in the adenoma-carcinoma sequence? Nutr Cancer 1996;26:337–46.
57. Giovannucci E, Stampfer MJ, Colditz GA, et al. Folate, methionine, and alcohol intake and risk of colorectal adenoma. J Natl Cancer Inst 1993;85:875–84.
58. Giovannucci E, Stampfer MJ, Colditz GA, et al. Multivitamin use, folate, and colon cancer in women in the Nurses’ Health Study. Ann Intern Med 1998;129:517–24.
59. Longstretch GF, Green R. Folate status in patients receiving maintenance doses of sulfasalazine. Arch Intern Med 1983;143:902–4.
60. Lashner BA, Heidenreich PA, Su GL, et al. Effect of folate supplementation on the incidence of dysplasia and cancer in chronic ulcerative colitis. Gastroenterology 1989;97:255–9.
61. Lashner BA, Heidenreich PA, Su GL, et al. Effect of folate supplementation on the incidence of dysplasia and cancer in chronic ulcerative colitis. Gastroenterology 1989;97:255–9.
62. Giovannucci E, Stampfer MJ, Colditz GA, et al. Folate, methionine, and alcohol intake and risk of colorectal adenoma. J Natl Cancer Inst 1993;85:875–84.
63. Benito E, Stiggelbout A, Bosch FX, et al. Nutritional factors in colorectal cancer risk: a case-control study in Majorca. Int J Cancer 1991;49:161–7.
64. Baron JA, Sandler RS, Haile RW, et al. Folate intake, alcohol consumption, cigarette smoking, and risk of colorectal adenomas. J Natl Cancer Inst 1998;90:57–62.
65. Giovannucci E, Stampfer MJ, Colditz GA, et al. Multivitamin use, folate, and colon cancer in women in the Nurses’ Health Study. Ann Intern Med 1998;129:517–24.
66. Giovannucci E, Stampfer MJ, Colditz GA, et al. Folate, methionine, and alcohol intake and risk of colorectal adenoma. J Natl Cancer Inst 1993;85:875–84.
67. Cole BF, Baron JA, Sandler RS, et al. Folic acid for the prevention of colorectal adenomas: a randomized clinical trial. JAMA 2007;297:2351–9.
68. Boutron-Ruault M-C, Senesse P, Faivre J, et al. Folate and alcohol intakes: related or independent roles in the adenoma-carcinoma sequence? Nutr Cancer 1996;26:337–46.
69. Cravo ML, Pinto AG, Chaves P, et al. Effect of folate supplementation on DNA methylation of rectal mucosa in patients with colonic adenomas: correlation with nutrient intake. Clin Nutr 1998;17:45–9.
70. Kono S, Ikeda M, Tokudome S, Kuratsune M. A case-control study of gastric cancer and diet in northern Kyushu, Japan. Jpn J Cancer Res 1988;79:1067–74.
71. Gao YT, McLaughlin JK, Blot WJ, et al. Reduced risk of esophageal cancer associated with green tea consumption. J Natl Cancer Inst 1994;86:855–8.
72. Ji BT, Chow WH, Hsing AW, et al. Green tea consumption and the risk of pancreatic and colorectal cancers. Int J Cancer 1997;70:255–8.
73. Ohno Y, Wakai K, Genka K, et al. Tea consumption and lung cancer risk: A case-control study in Okinawa, Japan. Jpn J Cancer Res 1995;86:1027–34.
74. Fujiki H. Two stages of cancer prevention with green tea. J Cancer Res Clin Oncol 1999;125:589–97 [review].
75. Goldbohm RA, Hertog MGL, Brants HAM, et al. Consumption of black tea and cancer risk: A prospective cohort study. J Natl Cancer Inst 1996;88:93–100.
76. Heilbrun L, Nomura A, Stemmermann G. Black tea consumption and cancer risk: A prospective study. Br J Cancer 1986;54:677–83.
77. Phillips RL, Snowdon DA. Dietary relationship with fatal colorectal cancer among Seven-Day Adventists. J Natl Cancer Inst 1985;74:307–17.
78. Kono S, Ikeda M, Tokudome S, Kuratsune M. A case-control study of gastric cancer and diet in northern Kyushu, Japan. Jpn J Cancer Res 1988;79:1067–74.
79. Gao YT, McLaughlin JK, Blot WJ, et al. Reduced risk of esophageal cancer associated with green tea consumption. J Natl Cancer Inst 1994;86:855–8.
80. Ji BT, Chow WH, Hsing AW, et al. Green tea consumption and the risk of pancreatic and colorectal cancers. Int J Cancer 1997;70:255–8.
81. Ohno Y, Wakai K, Genka K, et al. Tea consumption and lung cancer risk: A case-control study in Okinawa, Japan. Jpn J Cancer Res 1995;86:1027–34.
82. Fujiki H. Two stages of cancer prevention with green tea. J Cancer Res Clin Oncol 1999;125:589–97 [review].
83. Yang G, Shu XO, Li H, et al. Prospective cohort study of green tea consumption and colorectal cancer risk in women. Cancer Epidemiol Biomarkers Prev 2007;16:1219–23.
84. Goldbohm RA, Hertog MGL, Brants HAM, et al. Consumption of black tea and cancer risk: A prospective cohort study. J Natl Cancer Inst 1996;88:93–100.
85. Heilbrun L, Nomura A, Stemmermann G. Black tea consumption and cancer risk: A prospective study. Br J Cancer 1986;54:677–83.
86. Phillips RL, Snowdon DA. Dietary relationship with fatal colorectal cancer among Seven-Day Adventists. J Natl Cancer Inst 1985;74:307–17.
87. Shimizu M, Fukutomi Y, Ninomiya M, et al. Green tea extracts for the prevention of metachronous colorectal adenomas: a pilot study. Cancer Epidemiol Biomarkers Prev 2008;17:3020–5.
88. Neri B, De Leonardis V, Gemelli MT, et al. Melatonin as biological response modifier in cancer patients. Anticancer Res 1998;18:1329–32.
89. Barni S, Lissoni P, Cazzaniga M, et al. A randomized study of low-dose subcutaneous interlekin-2 plus melatonin versus supportive care alone in metastatic colorectal cancer patients progressing under 5-fluorouracil and folates. Oncology 1995;52:243–5.
90. Lissoni P, Barni S, Crispino S, et al. Endocrine and immune effects of melatonin therapy in metastatic cancer patients. Eur J Cancer Clin Oncol 1989;25:789–95.
91. Lissoni P, Barni S, Ardizzoia A, et al. A randomized study with the pineal hormone melatonin versus supportive care alone in patients with brain metastases due to solid neoplasms. Cancer 1994;73:699–701.
92. Lissoni P, Barni S, Ardizzoia A, et al. Randomized study with the pineal hormone melatonin versus supportive care alone in advanced nonsmall cell lung cancer resistant to a first-line chemotherapy containing cisplatin. Oncology 1992;49:336–9.
93. Lissoni P, Cazzanga M, Tancini G, et al. Reversal of clinical resistance to LHRH analogue in metastatic prostate cancer by the pineal hormone melatonin: efficacy of LHRH analogue plus melatonin in patients progressing on LHRH analogue alone. Eur Urol 1997;31:178–81.
94. Lissoni P, Paolorossi F, Tancini G, et al. Is there a role for melatonin in the treatment of neoplastic cachexia? Eur J Cancer 1996;32A:1340–3.
95. Lissoni P, Barni S, Tancini G, et al. A randomised study with subcutaneous low-dose interleukin 2 alone vs interleukin 2 plus the pineal neurohormone melatonin in advanced solid neoplasms other than renal cancer and melanoma. Br J Cancer 1994;69:196–9.
96. Lissoni P, Brivio F, Ardizzoia A, et al. Subcutaneous therapy with low-dose interlekin-2 plus the neurohormone melatonin in metastatic gastric cancer patients with low performance status. Tumori 1993;79:401–4.
97. Aldeghi R, Lissoni P, Barni S, et al. Low-dose interlekin-2 subcutaneous immunotherapy in association with the pineal hormone melatonin as a first-line therapy in locally advanced or metastatic hepatocellular carcinoma. Eur J Cancer 1994;30A:167–70.
98. Lissoni P, Paolorossi F, Tancini G, et al. A phase II study of tamoxifen plus melatonin in metastatic solid tumour patients. Br J Cancer 1996;74:1466–8.
99. Lissoni P, Barni S, Mandalà, et al. Decreased toxicity and increased efficacy of cancer chemotherapy using the pineal hormone melatonin in metastatic solid tumour patients with poor clinical status. Eur J Cancer 1999;35:1688–92.
100. Lissoni P, Brivio O, Brivio F, et al. Adjuvant therapy with the pineal hormone melatonin in patients with lymph node relapse due to malignant melanoma. J Pineal Res 1996;21:239–42.
101. Lissoni P, Barmo S. Meregalli S, et al. Modulation of cancer endocrine therapy by melatonin: a phase II study of tamoxifen plus melatonin in metastatic breast cancer patients progressing under tamoxifen alone. Br J Cancer 1995;71:854–6.
102. Neri B, Fiorelli C, Moroni F, et al. Modulation of human lymphoblastoid interferon activity by melatonin in metastatic renal cell carcinoma. Cancer 1994;73:315–9.
103. Medina D. Mechanisms of selenium inhibition of tumorigenesis. Adv Exp Med Biol 1986;206:465–72.
104. Beisel WR. Single nutrients and immunity. Am J Clin Nutr 1982;35:417–68.
105. Medina D, Morrison DG. Current ideas on selenium as a chemopreventative agent. Pathol Immunopathol Res 1988;7:187–99.
106. Shamberger RJ, Rukoven E, Lonfield AK, et al. Antioxidants and cancer. I. Selenium in the blood of normals and cancer patients. J Natl Cancer Inst 1973;4:863–70.
107. Burney PGJ, Comstock GW, Morris JS. Serologic precursors of cancer: serum micronutrients and the subsequent risk of pancreatic cancer. Am J Clin Nutr 1989;49:895–900.
108. Toma S, Micheletti A, Giacchero A, et al. Selenium therapy in patients with precancerous and malignant oral cavity lesions: preliminary results. Cancer Detection Prev 1991;15:491–3.
109. Willett WC, Polk BF, Morris JS, et al. Prediagnostic serum Selenium and risk of cancer. Lancet 1983;42:130–4.
110. Helzlsouer KJ, Comstock GW, Morris JS. Selenium, lycopene, alpha-tocopherol, ß-carotene, retinol, and subsequent bladder cancer. Cancer Res 1989;49:6144–8.
111. Jaskiewicz K, Marasas WF, Rossouw JE, et al. Selenium and other mineral elements in populations at risk for esophageal cancer. Cancer 1988;62:2635–9.
112. Knekt P, Aromaa A, Maatela J, et al. Serum selenium and subsequent risk of cancer among Finnish men and women. J Natl Cancer Inst 1990;82:864–8.
113. Yu M-W, Horng I-S, Hsu K-H, et al. Plasma selenium levels and risk of hepatocellular carcinoma among men with chronic hepatitis virus infection. Am J Epidemiol 1999;150:367–74.
114. Knekt P, Marniemi J, Teppo L, et al. Is low selenium status a risk factor for lung cancer? Am J Epidemiol 148:975–82.
115. Scieszka M, Danch A, Machalski M, Drozdz M. Plasma selenium concentration in patients with stomach and colon cancer in the Upper Silesia. Neoplasma 1997;44:395–7.
116. Fex G, Pettersson B, Akesson B. Low plasma selenium as a risk factor for cancer death in middle-aged men. Nutr Cancer 1987;10:221–9.
117. Salonen J, Salonen R, Lappetelainen R, et al. Risk of cancer in relation to serum concentrations of selenium and vitamins A and E; matched case-control analysis of prospective data. BMJ 1985;290:417–20.
118. Clark LC, Combs GF Jr, Turnbull BW, et al. Effects of selenium supplementation for cancer prevention in patients with carcinoma of the skin. JAMA 1996;276:1957–63.
119. Yu B, Wang M, Li D. Chung Hua Wai Ko Tsa Chih 1996;34:50–3.
120. Clark LC, Combs GF Jr, Turnbull BW, et al. Effects of selenium supplementation for cancer prevention in patients with carcinoma of the skin. JAMA 1996;276:1957–63.
121. Whelan RL, Horvath KD, Gleason NR, et al. Vitamin and calcium supplement use is associated with decreased adenoma recurrence in patients with a previous history of neoplasia. Dis Colon Rectum 1999;42:212–7.
122. White E, Shannon JS, Patterson RE. Relationship between vitamin and calcium supplement use and colon cancer. Cancer Epidemiol Biomarkers Prev 1997;6:769–74.
123. Kampman E, Slattery ML, Caan B, Potter JD. Calcium, vitamin D, sunshine exposure, dairy products and colon cancer risk (United States). Cancer Causes Control 2000;11:459–466.
124. Neugut AI, Horvath K, Whelan RL, et al. The effect of calcium and vitamin supplements on the incidence and recurrence of colorectal adenomatous polyps. Cancer 1996;78:723–8.
125. Baron JA, Beach M, Mandel JS, et al. Calcium supplements for the prevention of colorectal adenomas. N Engl J Med 1999;340:101–7.
126. Bostick RM, Fosdick L, Wood JR, et al. Calcium and colorectal epithelial cell proliferation in sporadic adenoma patients: a randomized, double-blinded, placebo-controlled clinical trial. J Natl Cancer Inst 1995;87:1307–15.
127. Cats A, Kleibeuker JH, van der Meer R, et al. Randomized, double-blinded, placebo-controlled intervention study with supplemental calcium in families with hereditary nonpolyposis colorectal cancer. J Natl Cancer Inst 1995;87:598–603.
128. Baron JA, Tosteson TD, Wargovich MJ, et al. Calcium supplementation and rectal mucosal proliferation: a randomized controlled trial. J Natl Cancer Inst 1995;87:1303–7.
129. Cesano A, Visonneau S, Scimeca JA, et al. Opposite effects of linoleic acid and conjugated linoleic acid on human prostatic cancer in SCID mice. Anticancer Res 1998;18:1429-34.
130. Thompson H, Zhu Z, Banni S, et al. Morphological and biochemical status of the mammary gland as influenced by conjugated linoleic acid: implication for a reduction in mammary cancer risk. Cancer Res 1997;57:5067-72.
131. Ip C. Review of the effects of trans fatty acids, oleic acid, n-3 polyunsaturated fatty acids, and conjugated linoleic acid on mammary carcinogenesis in animals. Am J Clin Nutr 1997;66(suppl):1523S-29S [review].
132. Parodi PW. Cows’ milk fat components as potential anticarcinogenic agents. J Nutr 1997;127:1055-60 [review].
133. Larsson SC, Bergkvist L, Wolk A. High-fat dairy food and conjugated linoleic acid intakes in relation to colorectal cancer incidence in the Swedish Mammography Cohort. Am J Clin Nutr 2005;82:894–900.
134. Bartram H-P, Gostner A, Kelber E, et al. Effects of fish oil on fecal bacterial enzymes and steroid excretion in healthy volunteers: implications for colon cancer prevention. Nutr Cancer 12996;25:71–8.
135. Huang Y-C, Jessup JM, Forse RA, et al. n-3 fatty acids decrease colonic epithelial cell proliferation in high-risk bowel mucosa. Lipids 1996;31:S313–7.
136. Anti M, Armelaoe F, Marra G, et al. Effects of different doses of fish oil on rectal cell proliferation in patients with sporadic colonic adenomas. Gastroenterology 1994;107:1709–18.
137. Garcia-Girlat E, Perdereau B, Brixy F, et al. Preliminary study of glutathione, L-cysteine and anthocyans (Recancostat Compositum™) in metastatic colorectal carcinoma with malnutrition. Seventh International Congress on Anti-cancer Treatment, February 3–6, 1997, Palai des Congrès, Paris, France.
138. Shibata A, Paganini-Hill A, Ross RK, Henderson BE. Intake of vegetables, fruits, beta-carotene, vitamin C and vitamin supplements and cancer incidence among the elderly: a prospective study. Br J Cancer 1992;66:673–9.
139. Bussey HJR, DeCosse JJ, Deschner EE, et al. A randomized trial of ascorbic acid in polyposis coli. Cancer 1982;50:1434–9.
140. Ponz de Leon M, Roncucci L. Chemoprevention of colorectal tumors: role of lactulose and of other agents. Scand J Gastroenterol Suppl 1997;222:72–5.
141. Greenburg ER, Baron JA, Tosteson TD, et al. A clinical trial of antioxidant vitamins to prevent colorectal adenoma. N Engl J Med 1994;331:141–7.
142. McKeown-Eyssen G, Holloway C, Jazmaji V, et al. A randomized trial of vitamins C and E in the prevention of recurrence of colorectal polyps. Cancer Res 1988;48:4701–5.
143. 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.
144. Hanck A. Vitamin C and cancer. Int J Vit Nutr Res 1983;(Suppl #24):87–104 [review].
145. Cameron E, Pauling L. Supplemental ascorbate in the supportive treatment of cancer: prolongation of survival times in terminal human cancer. Proc Natl Acad Sci USA 1976;73:3685–9.
146. Cameron E, Pauling L. Supplemental ascorbate in the supportive treatment of cancer: reevaluation of prolongation of survival times in terminal human cancer. Proc Natl Acad Sci USA 1978;75:4538–42.
147. Creagan ET, Moertel CG, O’Fallon JR, et al. Failure of high dose vitamin C (ascorbic acid) therapy to benefit patients with advanced cancer. A controlled trial. N Engl J Med 1979;301:687–90.
148. Moertel CG, Fleming TR, Creagan ET, et al. High-dose vitamin C versus placebo in the treatment of patients with advanced cancer who have had no prior chemotherapy. A randomized double-blind comparison. New Engl J Med 1985;312(3):137–41.
149. Murata A, Morishige F, Yamaguchi H. Prolongation of survival times of terminal cancer patients by administration of large doses of ascorbate. Int J Vit Nutr Res 1982;(Suppl #23):103–14.
150. Gorham ED, Garland FC, Garland CF. Sunlight and breast cancer incidence in the USSR. Int J Epidemiol 1990;19:820–4.
151. Lefkowitz ES, Garland CF. Sunlight, vitamin D, and ovarian cancer mortality rates in US women. Int J Epidemiol 1994;23:113–6.
152. Studzinski GP, Moore DC. Sunlight––can it prevent as well as cause cancer? Cancer Res 1995;55:4014–22 [review].
153. Garland CF, Garland FC, Gorham ED. Calcium and vitamin D. Their potential roles in colon and breast cancer prevention. Ann N Y Acad Sci 1999;889:107–19.
154. Kampman E, Slattery ML, Caan B, Potter JD. Calcium, vitamin D, sunshine exposure, dairy products and colon cancer risk (United States). Cancer Causes Control 2000;11:459–66.
155. Kampman E, Slattery ML, Caan B, Potter JD. Calcium, vitamin D, sunshine exposure, dairy products and colon cancer risk (United States). Cancer Causes Control 2000;11:459–66.
156. Kearney J, Giovannucci E, Rimm EB, et al. Calcium, vitamin D, and dairy foods and the occurrence of colon cancer in men. Am J Epidemiol 1996;143:907–17.
157. Whelan RL, Horvath KD, Gleason NR, et al. Vitamin and calcium supplement use is associated with decreased adenoma recurrence in patients with a previous history of neoplasia. Dis Colon Rectum 1999;42:212–7.
158. White E, Shannon JS, Patterson RE. Relationship between vitamin and calcium supplement use and colon cancer. Cancer Epidemiol Biomarkers Prev 1997;6:769–74.
159. Neugut AI, Horvath K, Whelan RL, et al. The effect of calcium and vitamin supplements on the incidence and recurrence of colorectal adenomatous polyps. Cancer 1996;78:723–8.
160. Malilila N, Virtamo J, Virtanen M, et al. The effect of alpha-tocopherol and beta-carotene supplementation on colorectal adenomas in middle-aged male smokers. Cancer Epidemiol Biomarkers Prev 1999;8:489–93.
161. Albanes D, Malila N, Taylor PR, et al. Effects of supplemental a-tocopherol and ß-carotene on colorectal cancer: results from a controlled trial (Finland). Cancer Causes Control 2000;11:197–205.
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