Or they can be environmental, such as pollution or cigarette smoke. Other vitamins and minerals. These include calcium, iodine, vitamins A, D, K, and the B vitamins. Dietary fiber. Fiber helps add bulk to stool. It moves food more quickly through the digestive system.

Fiber helps nourish a healthy community of microbes living in the digestive tract. This community is called a microbiome. A healthy microbiome has been linked with a lower cancer risk. Of these, red and processed meats raise the most concern in terms of cancer risk.

Red meat includes pork, beef, veal, and lamb. Processed meat includes bacon, ham, lunch meats, meat jerky, hot dogs, salami, and other cured meat products. Any amount of processed meat and more than around 18 ounces of fresh meat per week are most strongly linked with a higher risk of cancer.

Alcoholic beverages. Drinking alcohol increases the risk of developing certain types of cancer. Learn more about alcohol and cancer risk. These findings come from the Continuous Update Project and the Third Expert Report on Diet, Nutrition, Physical Activity and Cancer: a Global Perspective.

These reports are funded by the American Institute of Cancer Research AICR and World Cancer Research Fund WCRF.

Phytonutrients found in fruits and vegetables most likely work together to lower cancer risk, rather than a particular food component affecting risk. Some help regulate hormones, such as estrogen. Others slow cancer cell growth or block inflammation.

Many lower the risk of damage caused by oxidants. Cruciferous vegetables. These foods include broccoli, cauliflower, cabbage, Brussels sprouts, bok choy, and kale.

Frequently eating these foods is associated with a lower cancer risk. Several laboratory studies suggest cruciferous vegetables help regulate enzymes that defend against cancer. Studies also show that cruciferous vegetables may stop cancer cell growth in other ways. But these effects may differ between cells and animals used in the lab and people.

This carotenoid is found in tomato products. Other important sources of lycopene include pink grapefruit, watermelon, and apricots. But researchers have not yet demonstrated a direct link between lycopene and reduced cancer risk in controlled clinical trials. Soy contains unique phytonutrients.

Laboratory studies suggest that these substances help protect against some types of cancer. Clinical trials are more clearly defining the role of soy in cancer prevention. The relationship between soy and breast cancer risk is especially complex. Current studies suggest eating up to 3 servings of whole soy foods, such as edamame, tofu, soy milk, and miso, is safe and may reduce breast cancer risk.

But guidelines do not specifically recommend adding soy foods into the diet to reduce breast cancer risk. Doctors do recommend avoiding concentrated isoflavone pills and powders.

Some vitamins, minerals, and other nutrients are antioxidants. Research on their role in cancer prevention continues because studies show mixed results.

Beta carotene. High-dose beta carotene supplements do not seem to prevent cancer. Two large clinical trials have found that people at high risk for lung cancer, including smokers, former smokers, and people exposed to asbestos, have a higher risk of lung cancer if they take high-dose beta carotene supplements.

Calcium and vitamin D. Researchers studied the effects of supplemental calcium and vitamin D. They found that supplements did not affect colorectal cancer risk. One form, folic acid, is made in the laboratory and found in dietary supplements.

Enriched, white flour is fortified with it. This means that foods made with flour, including breads and cereals, contain folic acid. Studies show a link between folate and cancer risk. People with low folate levels have a higher risk of:. But clinical studies have not yet shown a relationship between taking extra folic acid and cancer prevention.

Currently, there is no strong enough evidence that multivitamins reduce cancer risk. But 1 study showed a potential benefit. People who took multivitamins for more than 10 years had reduced colon polyp formation. Some polyps can develop into colorectal cancer if not removed during colonoscopy cancer screening.

By reducing polyps, the study suggests multivitamins might also lower colorectal cancer risk. But this research can be difficult to interpret. Usually, the healthiest people get regular cancer screening.

And those people also commonly take multivitamins. One study evaluated whether selenium prevents cancer. Supplements did not prevent people with skin cancer from getting a second one. But it did reduce new cases of:. Some studies link selenium to a higher risk of diabetes.

The mean proliferation index of the experimental group was significantly lower and apoptotic indexes higher compared to historical matched controls.

Ground flax seed may be a very beneficial food for men battling prostate cancer. However, a meta-analysis of nine cohort and case-control studies revealed an association between flax seed oil intake or high blood levels of alpha-linolenic acid and prostate cancer risk [ 79 ].

It is quite likely that the lignans in flax seed are a major component of flax's anti-cancer effects so that flax oil without the lignans is not very beneficial.

Some brands of flax seed oil retain some of the seed particulate because of the beneficial properties of the lignans. One of the most important messages of modern nutrition research is that a diet rich in fruits and vegetables protects against cancer.

The greatest message is that this same diet protects against almost all other diseases, too, including cardiovascular disease and diabetes. There are many mechanisms by which fruits and vegetables are protective, and an enormous body of research supports the recommendation for people to eat more fruits and vegetables.

Block et al [ 80 ] reviewed about studies of cancer and fruit and vegetable intake. A statistically significant protective effect of fruits and vegetables was found in of studies that gave relative risks. Even in lung cancer, after accounting for smoking, increasing fruits and vegetables reduces lung cancer; an additional 20 to 33 percent reduction in lung cancers is estimated [ 1 ].

Steinmetz and Potter reviewed the relationship between fruits, vegetables, and cancer in human epidemiologic studies and 22 animal studies [ 81 ]. They found "the evidence for a protective effect of greater vegetable and fruit consumption is consistent for cancers of the stomach, esophagus, lung, oral cavity and pharynx, endometrium, pancreas, and colon.

Allium vegetables, carrots, green vegetables, cruciferous vegetables, and tomatoes also had a fairly consistent protective effect [ 81 ]. Allium vegetables garlic, onion, leeks, and scallions are particularly potent and have separately been found to be protective for stomach and colorectal cancers [ 82 , 83 ] and prostate cancer [ 84 ].

There are many substances that are protective in fruits and vegetables, so that the entire effect is not very likely to be due to any single nutrient or phytochemical. Steinmetz and Potter list possible protective elements: dithiolthiones, isothiocyanates, indolecarbinol, allium compounds, isoflavones, protease inhibitors, saponins, phytosterols, inositol hexaphosphate, vitamin C, D-limonene, lutein, folic acid, beta carotene and other carotenoids , lycopene, selenium, vitamin E, flavonoids, and dietary fiber [ 81 ].

A joint report by the World Cancer Research Fund and the American Institute for Cancer Research found convincing evidence that a high fruit and vegetable diet would reduce cancers of the mouth and pharynx, esophagus, lung, stomach, and colon and rectum; evidence of probable risk reduction was found for cancers of the larynx, pancreas, breast, and bladder [ 1 ].

Many of the recent reports from prospective population-based studies of diet and cancer have not found the same protective effects of fruits and vegetables that were reported earlier in the epidemiological and case-control studies [reviewed in [ 85 ]].

One explanation is that people's memory of what they ate in a case-cohort study may have been tainted by their disease state. Another problem might be that the food frequency questionnaires FFQ used to measure food intake might not be accurate enough to detect differences.

Such a problem was noted in the EPIC study at the Norfolk, UK site. Using a food diary the researchers found a significant correlation between saturated fat intake and breast cancer, but using a FFQ there was no significant correlation [ 86 ].

So, inaccurate measurement of fruit and vegetable intake might be part of the explanation as well. It must be noted that upper intakes of fruits and vegetables in these studies are usually within the range of what people on an American omnivorous diet normally eat.

In the Nurses Health Study the upper quintiles of fruit and vegetable intake were 4. Similarly, the upper quintiles of fruit and vegetable intake in the Health Professionals Follow-up Study were 4.

So, it is very possible that the range of intakes in the prospective population based studies do not have a wide enough intake on the upper end to detect the true possible impact of a very high intake of fruits and vegetables on cancer risk.

Cruciferous vegetables broccoli, cauliflower, cabbage, Brussels sprouts contain sulforophane, which has anti-cancer properties. Also, prostate cancer risk was found to be reduced by cruciferous vegetable consumption in a population-based case-control study carried out in western Washington state.

Similar protective effects of cruciferous vegetables were seen in a multi-ethnic case-control study [ 93 ]. Broccoli sprouts have a very high concentration of sulforophane since this compound originates in the seed and is not made in the plant as it grows [ 95 , 96 ].

One sprout contains all of the sulforophane that is present in a full-grown broccoli plant. So, if sulforophane is especially cancer-protective, it would seem reasonable to include some broccoli sprouts in an anti-cancer diet. Selenium is a mineral with anti-cancer properties. Many studies in the last several years have shown that selenium is a potent protective nutrient for some forms of cancer.

The Arizona Cancer Center posted a selenium fact sheet listing the major functions of selenium in the body [ 97 ]. These functions are as follows:. Selenium is present in the active site of many enzymes, including thioredoxin reductase, which catalyze oxidation-reduction reactions.

These reactions may encourage cancerous cells to under apoptosis. P enzymes in the liver may be induced by selenium, leading to detoxification of some carcinogenic molecules.

The selenium supplement was most effective in ex-smokers and for those who began the study with the lowest levels of serum selenium. Several prospective studies have also examined the role of selenium in cancer prevention, particularly for prostate cancer, summarized in Table 2.

Overall, it appears that poor selenium levels, especially for men, are a cancer risk. If a person has low selenium levels and other antioxidant defenses are also low the cancer risk is increased even further.

Women do not appear to be as sensitive to selenium, as breast cancer has not been found to be influenced by selenium status in several studies [ — ], although both men and women were found to be protected by higher levels of selenium from colon cancer [ ] and lung cancer [ , ].

Good vegetarian sources of selenium are whole grains and legumes grown in selenium-rich soil in the western United States, brazil nuts by far the most dense source of selenium , nutritional yeast, brewers yeast, and sunflower seeds. All green plants also contain chlorophyll, the light-collecting molecule.

Chlorophyll and its derivatives are very effective at binding polycyclic aromatic hydrocarbons carcinogens largely from incomplete combustion of fuels , heterocyclic amines generated when grilling foods , aflatoxin a toxin from molds in foods which causes liver cancer , and other hydrophobic molecules.

The chlorophyll-carcinogen complex is much harder for the body to absorb, so most of it is swept out with the feces. The chemoprotective effect of chlorophyll and its derivatives has been tested in laboratory cell cultures and animals [ , ]. There is so much compelling evidence for anti-carcinogenic effects of chlorophyll that a prospective randomized controlled trial is being conducted in Qidong, China to see if chlorophyllin can reduce the amount of liver cancer cases, which arise from aflatoxin exposure in their foods corn, peanuts, soy sauce, and fermented soy beans.

It was supposed that the chlorophyllin bound up aflatoxins, but there were chlorophyllin derivatives also detected in the sera which had a green tint to it of the volunteers who took the supplement, indicating a possible role in the body besides binding carcinogens in the gut [ ].

Vitamin B has not been proven to be an anti-cancer agent, but there is some evidence indicating that it could be beneficial. The form of administered vitamin B may be important. Some experimental cancer studies have been carried out with various forms of vitamin B Methylcobalamin inhibited tumor growth of SC-3 injected into mice [ ], and caused SC-3 mouse mammary tumor cells to undergo apoptosis, even when stimulated to grow by the presence of growth-inducing androgen [ ].

Methylcobalamin, but not cyanocobalamin, increased the survival time of mice bearing implanted leukemia tumor cells [ ]. Methylcobalamin also was able to increase survival time and reduce tumor growth in laboratory mice [ ]. Laboratory mechanistic evidence for the effects of vitamin B12 were seen in a laboratory study with vitamin B deficient rats.

In two prospective studies one in Washington Country, Maryland and the Nurses' Health Study a relation between lower vitamin B12 status but not deficiency and statistically significant higher risk of breast cancer was found [ , ].

So, there is evidence from laboratory studies, prospective cohort studies, and mechanistic studies showing that vitamin B is an important nutrient for genetic stability, DNA repair, carcinogenesis, and cancer therapy. Folic acid is the dark green leafy vegetable vitamin.

It has an integral role in DNA methylation and DNA synthesis. Folic acid works in conjunction with vitamin B-6 and vitamin B in the single carbon methyl cycle.

If insufficient folic acid is not available uracil is substituted for thymidine in DNA, which leads to DNA strand breakage. As shown in Tables 3 and 4 , many studies have found a significant reduction in colon, rectal, and breast cancer with higher intakes of folic acid and their related nutrients vitamin B-6 and B Alcohol is an antagonist of folate, so that drinking alcoholic beverages greatly magnifies the cancer risk of a low-folate diet.

Genetic polymorphisms common single DNA base mutations resulting in a different amino acid encoded into a protein in the methylenetetrahydrofolate reductase and the methionine synthase genes which increase the relative amount of folate available for DNA synthesis and repair also reduces the risk of colon cancer [ — ].

Cravo et al [ ] used 5 mg of folic acid a day a supraphysiological dose in a prospective, controlled, cross-over study of 20 patients with colonic adenoma polyps. They found that the folic acid could reverse DNA hypomethylation in 7 of 12 patients who had only one polyp.

Folate may be more important for rapidly dividing tissue, like the colonic mucosa. Therefore, the cancer risk associated with low folate intake is probably higher for colon cancer than for breast cancer. Most of the breast cancer studies only found a protective effect of folate among women who consumed alcohol see Table 4.

So, there may be a true protective effect that is masked in the western populations by so many other risk factors. Two studies showed that the risk of cancer due to family history can be modified by high folate intake, so a prudent anti-cancer diet would be high in dark green leafy vegetables.

Vitamin D is produced primarily from the exposure of the skin to sunshine. Even casual exposure of the face, hands, and arms in the summer generates a large amount of vitamin D.

In fact, simulated sunshine, equivalent to standing on a sunny beach until a slight pinkness of the skin was detected, was equivalent to a 20, IU oral dose of vitamin D 2 [ ]. Note that the RDA is IU for most adults. It has been estimated that 1, IU per day is the minimal amount needed to maintain adequate levels of vitamin D in the absence of sunshine [ ], and that up to 4, IU per day can be safely used with additional benefit [ ].

The concentration of the active hormonal form of vitamin D is tightly regulated in the blood by the kidneys. This active hormonal form of vitamin D has the potent anti-cancer properties. It has been discovered that various types of normal and cancerous tissues, including prostate cells [ ], colon tissue [ ], breast, ovarian and cervical tissue [ ], pancreatic tissue [ ] and a lung cancer cell line [ ] all have the ability to convert the major circulating form of vitamin D, 25 OH D, into the active hormonal form, 1,25 OH 2 D.

So, there is a local mechanism in many tissues of the body for converting the form of vitamin D in the body that is elevated by sunshine exposure into a hormone that has anticancer activity. Indeed, 25 OH D has been shown to inhibit growth of colonic epithelial cells [ ], primary prostatic epithelial cells [ ], and pancreatic cells [ ].

So, the laboratory work is confirming what had been seen some time ago in ecological studies of populations and sunshine exposure. The mortality rates for colon, breast, and ovary cancer in the USA show a marked north-south gradient [ ]. In ecological studies of populations and sunlight exposure no individual data sunlight has been found to have a protective effect for prostate cancer [ ], ovarian cancer [ ], and breast cancer [ ].

Recently Grant found that sunlight was also protective for bladder, endometrial, renal cancer, multiple myeloma, and Non-Hodgkins lymphoma in Europe [ ] and bladder, esophageal, kidney, lung, pancreatic, rectal, stomach, and corpus uteri cancer in the USA [ ].

Several prospective studies of vitamin D and cancer have also shown a protective effect of vitamin D see Table 5. It could be that sunshine and vitamin D are protective factors for cancers of many organs that can convert 25 OH D into 1,25 OH D 2. Carotenoids have been studied vigorously to see if these colorful compounds can decrease cancer risk.

In ecological studies and early case-control studies it appeared that β-carotene was a cancer-protective agent. Randomized controlled trials of β-carotene found that the isolated nutrient was either neutral [ ] or actually increased risk of lung cancer in smokers [ , ].

Beta-carotene may be a marker for intake of fruits and vegetables, but it does not have a powerful protective effect in isolated pharmacological doses.

However, there is a large body of literature that indicates that dietary carotenoids are cancer preventative See Table 6.

Alpha-carotene has been found to be a stronger protective agent than its well-known isomer β-carotene. Studies tend to agree that overall intake of carotenoids is more protective than a high intake of a single carotenoid. So, a variety of fruits and vegetables is still a better anti-cancer strategy than just using a single vegetable high in a specific carotenoid.

The richest source of α-carotene is carrots and carrot juice, with pumpkins and winter squash as a second most-dense source. There is approximately one μg of α-carotene for every two μg of β-carotene in carrots. The most common sources of β-cryptoxanthin are citrus fruits and red sweet peppers.

Of the various carotenoids lycopene has been found to be very protective, particularly for prostate cancer. The major dietary source of lycopene is tomatoes, with the lycopene in cooked tomatoes being more bioavailable than that in raw tomatoes.

Several prospective cohort studies have found associations between high intake of lycopene and reduced incidence of prostate cancer, though not all studies have produced consistent results [ , ].

Some studies suffer from a lack of good correlation between lycopene intake assessed by questionnaire and actual serum levels, and other studies measured intakes among a population that consumed very few tomato products. The studies with positive results will be reviewed here. In addition to the two reports above a nested case control study from the Health Professional Follow-up Study with cases and controls found an inverse relation between plasma lycopene and prostate cancer risk OR 0.

So, the results for lycopene have been found for dietary intakes as well as plasma levels. The β-carotene also had a protective effect, especially for those men with low lycopene levels [ ]. In addition to these observational studies, two clinical trials have been conducted to supplement lycopene for a short period before radical prostatectomy.

Results showed that the lycopene slowed the growth of prostate cancer. Subjects that took the lycopene for 3 weeks had smaller tumors, less involvement of the surgical margins, and less diffuse involvement of the prostate by pre-cancerous high-grade prostatic intraepithelial neoplasia [ ].

In another study before radical prostatectomy surgery 32 men were given a tomato sauce-based pasta dish every day, which supplied 30 mg of lycopene per day. After 3 weeks serum and prostate lycopene levels increaed 2-fold and 2. The apoptotic index was 3-fold higher in the resected prostate tissue, compared to biopsy tissue [ ].

These intervention studies raise the question of what could have been done in this intervention was longer and combined synergistically with other effective intervention methods, such as flax seed, increased selenium and possibly vitamin E, in the context of a diet high in fruits and vegetable?

Vitamin C, or ascorbic acid, has been studied in relation to health and is the most common supplement taken in the USA. Low blood levels of ascorbic acid are detrimental to health for a recent article see Fletcher et al [ ] and vitamin C is correlated with overall good health and cancer prevention [ ].

Use of vitamin C for cancer therapy was popularized by Linus Pauling. At high concentrations ascorbate is preferentially toxic to cancer cells. There is some evidence that large doses of vitamin C, either in multiple divided oral doses or intravenously, have beneficial effects in cancer therapy [ — ].

Oral doses, even in multiple divided doses, are not as effective as intravenous administration. Vitamin C at a dose of 1.

While vitamin C is quite possibly an effective substance, the amounts required for these therapeutic effects are obviously beyond dietary intakes. However, intravenous ascorbate may be a very beneficial adjuvant therapy for cancer with no negative side effects when administered properly.

There are many more substances that will have some benefit for cancer therapy. Most of these substances are found in foods, but their effective doses for therapy are much higher than the normal concentration in the food.

Also, green tea contains a flavanol, epigallocatechingallate EGCG , which can inhibit metalloproteinases, among several possible other mechanisms [ ]. And there are claims for various other herbal substances and extracts that might be of benefit, which are beyond the scope of this review.

The bacteria that reside in the intestinal tract generally have a symbiotic relationship with their host. Beneficial bacteria produce natural antibiotics to keep pathogenic bugs in check preventing diarrhea and infections and produce some B vitamins in the small intestine where they can be utilized.

Beneficial bacteria help with food digestion by providing extra enzymes, such as lactase, in the small intestine. Beneficial bacteria help strengthen the immune system right in the gut where much of the interaction between the outside world and the body goes on.

Beneficial bacteria can help prevent food allergies. They can help prevent cancer at various stages of development. These good bacteria can improve mineral absorption, maximizing food utilization. However, the balance of beneficial and potentially pathogenic bacteria in the gut is dependent on the diet.

Vegetable fiber encourages the growth of beneficial bacteria. A group of Adventist vegetarians was found to have a higher amount of beneficial bacteria and lower amount of potentially pathogenic bacteria compared to non-vegetarians on a conventional American diet [ ].

Differences in bacterial populations were seen between patients who recently had a colon polyp removed, Japanese-Hawaiians, North American Caucasians, native rural Japanese, and rural native Africans.

Lactobacillus species and Eubacterium aerofaciens , both producers of lactic acid, were associated with the populations with the lower risk of colon cancer, while Bacteroides and Bifidobacterium species were associated with higher risk of colon cancer [ ].

There is a solid theoretical basis for why probiotics should help prevent cancer, especially colon cancer, and even reverse cancer. Probiotics produce short chain fatty acids in the colon, which acidify the environment.

Lower colon pH is associated with lower incidence of colon cancer. Probiotic bacteria reduce the level of procarcinogenic enzymes such as beta-glucuronidase, nitroreductase, and azoreductase [ ]. casei was used in two trials of patients with superficial bladder cancer.

The second trial also showed that the probiotics worked better than the placebo, except for multiple recurring tumors [ ]. Except for the two studies noted above, most of the research of probiotics and cancer has been done in animals. Studies have looked at markers of tumor growth or at animals with chemically induced tumors.

Studies in rats have shown that probiotics can inhibit the formation of aberrant crypt foci, thought to be a pre-cancerous lesion in the colon. Some of the best results were obtained with a probiotic strain consumed with inulin, a type of fructooligosaccharide.

longum and inulin alone, respectively [ ]. There was a synergistic effect in using both products together. Similar synergy was seen in rats with azoxymethane-induced colon cancer in another study.

Rats fed Raftilose, a mixture of inulin and oligofructose, or Raftilose with Lactobacilli rhamnosus LGG and Bifidobacterium lactis Bb12 had a significantly lower number of tumors compared to the control group [ ]. In lab mice bred to be susceptible to colitis and colon cancer, a probiotic supplement, Lactobacillus salivarium ssp.

Salivarius UCC, reduced fecal coliform levels, the number of potentially pathogenic Clostridium perfringens , and reduced intestinal inflammation. In this small study two mice died of fulminant colitis and 5 mice developed adenocarcinoma in the control group of 10 mice, while there was no colitis and only 1 mouse with adenocarcinoma in the probiotic test group [ ].

The research on probiotics and disease is still an emerging field. There is a high degree of variation of health benefits between different strains of bacteria.

As new methods for selecting and screening probiotics become available, the field will be able to advance more rapidly. Many people diagnosed with cancer have digestion or intestinal tract disorders as well. Impaired digestion will greatly hinder a nutritional approach to treating cancer.

If the nutrients cannot be released from the food and taken up by the body, then the excellent food provided by the Hallelujah Diet will go to waste.

Digestive enzyme supplements are used to ensure proper and adequate digestion of food. Even raw foods, which contain many digestive enzymes to assist in their digestion, will be more thoroughly digested with less of the body's own resources with the use of digestive enzymes.

So, the enzymes taken with meals do not have a direct effect upon a tumor, but assist the body in getting all of the nutrition out of the food for healing and restoring the body to normal function.

Recently, an in vitro system was used to test the use of supplemental digestive enzymes. The digestive enzymes improved the digestibility and bioaccessibility of proteins and carbohydrates in the lumen of the small intestine, not only under impaired digestive conditions, but also in healthy human digestion [ ].

There is evidence that indicates the presence of an enteropancreatic circulation of digestive enzymes [ ]. Digestive enzymes appear to be preferentially absorbed into the bloodstream and then reaccumulated by the pancreas for use again.

There appears to be a mechanism by which digestive enzymes can reach systemic circulation. Enzymes, especially proteases, if they reach systemic circulation, can have direct anti-tumor activity. Wald et al [ ] reported on the anti-metastatic effect of enzyme supplements.

Mice inoculated with the Lewis lung carcinoma were treated with a proteolytic enzyme supplement, given rectally to avoid digestion. The primary tumor was cut out, so that the metastatic spread of the cancer could be measured. In the third group, which received the enzyme treatment since the initial inoculation of the Lewis lung carcinoma, no metastatic spread of the tumor was discernible.

In a similar experiment, an enzyme mixture of papain, trypsin, and chymotrypsin, as used in the preparation Wobe-Mugos E, was rectally given to mice that were inoculated with melanoma cells.

Survival time was prolonged in the test group 38 days in the enzyme group compared to 24 days in the control mice and 3 of the 10 enzyme-supplemented mice were cured. Again, a strong anti-metastatic effect of the proteolytic enzymes was seen [ ].

Further evidence of the efficacy of oral enzyme supplementation is available from clinical trials in Europe. Two different studies have demonstrated that two different oral proteolytic enzyme supplements were able to reduce high levels of transforming growth factor-β, which may be a factor in some cancers [ , ].

In the Slovak Republic an oral enzyme supplement was tested in a placebo-controlled trial of multiple myeloma. For stage III multiple myeloma, control group survival was 47 months, compared to 83 months a 3 year gain for patients who took the oral enzymes for more than 6 months [ ].

Enzyme supplements have also been shown to reduce side effects of cancer therapy. Enzyme supplementation resulted in fewer side effects for women undergoing radiation therapy for carcinomas of the uterine cervix [ ], for patients undergoing radiation therapy for head and neck cancers [ ], and for colorectal cancer patients undergoing conventional cancer treatments [ ].

In a large multi-site study in Germany women undergoing conventional cancer therapy were put into a control group or a group that received an oral enzyme supplement.

Disease and therapy related symptoms were all reduced, except tumor pain, by the enzyme supplement. Also, survival was longer with less recurrence and less metastases in the enzyme group [ ]. In all of these studies the oral enzyme supplements were well tolerated, with only a small amount of mild to moderate gastrointestinal symptoms.

Even though these few studies don't give a lot of evidence of the effectiveness of oral enzyme supplementation, it is clear that there are some circumstances that will be helped by enzyme supplementation, with very little danger of negative side effects.

At the least, enzymes will improve digestion and lessen the digestive burden on the body, leaving more reserves for disease eradication. However, as the research indicates, the effect may be much greater than that, with the potential for direct anti-tumor activity.

A diet-based cancer therapy, the Gerson Therapy, was used to treat melanoma cancer. The five-year survival rates from their therapy compared very favorably to conventional therapy reported in the medical literature, especially for more advanced stages of melanoma [ ] see Table 7. An Italian cohort of 8, women was followed for an average of 9.

Their diets were analyzed by patterns — salad vegetables raw vegetables and olive oil , western potatoes, red meat, eggs and butter , canteen pasta and tomato sauce , and prudent cooked vegetables, pulses, and fish.

The overall dietary pattern does make a very significant difference. In US-based studies the "prudent" diet has been shown to be protective for colon cancer, while the "western" diet has been shown to be detrimental.

The "salad vegetable" pattern is still more likely to be protective compared to the prudent dietary pattern, but this pattern did not exist in this study population.

A plant-based dietary pattern in being currently tested in the Women's healthy Eating and Living WHEL Study. About 3, women who were treated for an early stage of breast cancer have been randomized into two groups.

No guidelines were given for animal product intake, and initial results seem to confirm, since there were no changes in body weight, total cholesterol, or LDL cholesterol [ ], which would be affected by animal protein intake.

Also, plasma carotenoid concentrations increased significantly in the intervention group, but not in the control group. It will be very interesting to follow the results of this study. What is the result when all of these things are put together? What if all of these factors reviewed here were taken into account and put into practice?

This anticancer diet would have:. As reviewed above, reductions of 60 percent in breast cancer rates have already been seen in human diet studies, and a 71 percent reduction in colon cancer for men without the known modifiable risk factors. These reductions are without taking into account many of the other factors considered in this review, such as markedly increased fruit and vegetable intake, balanced omega 3 and 6 fats, vitamin D, reduced sugar intake, probiotics, and enzymes — factors which all are likely to have an impact on cancer.

Certainly cancer prevention would be possible, and cancer reversal in some cases is quite likely. Google Scholar. Vastag B: Obesity Is Now on Everyone's Plate. CAS PubMed Google Scholar. Sturm R: Increases in clinically severe obesity in the United States, — Arch Intern Med.

PubMed Google Scholar. Mokdad AH, Marks JS, Stroup DF, Gerberding JL: Actual causes of death in the United States, Calle EE, Rodriguez C, Walker-Thurmond K, Thun MJ: Overweight, obesity, and mortality from cancer in a prospectively studied cohort of U.

N Engl J Med. Hursting SD, Lavigne JA, Berrigan D, Perkins SN, Barrett JC: Calorie restriction, aging, and cancer prevention: mechanisms of action and applicability to humans.

Annu Rev Med. Epub Dec Dirx MJ, Zeegers MP, Dagnelie PC, van den Bogaard T, van den Brandt PA: Energy restriction and the risk of spontaneous mammary tumors in mice: a meta-analysis. Int J Cancer. Harvell DM, Strecker TE, Xie B, Pennington KL, McComb RD, Shull JD: Dietary energy restriction inhibits estrogen-induced mammary, but not pituitary, tumorigenesis in the ACI rat.

Matsuzaki J, Yamaji R, Kiyomiya K, Kurebe M, Inui H, Nakano Y: Implanted tumor growth is suppressed and survival is prolonged in sixty percent of food-restricted mice. J Nutr. Michels KB, Ekbom A: Caloric restriction and incidence of breast cancer. Foster-Powell K, Holt SH, Brand-Miller JC: International table of glycemic index and glycemic load values: Am J Clin Nutr.

Augustin LS, Gallus S, Negri E, La Vecchia C: Glycemic index, glycemic load and risk of gastric cancer. Ann Oncol. Augustin LS, Gallus S, Franceschi S, Negri E, Jenkins DJ, Kendall CW, Dal Maso L, Talamini R, La Vecchia C: Glycemic index and load and risk of upper aero-digestive tract neoplasms Italy.

Cancer Causes Control. Augustin LS, Gallus S, Bosetti C, Levi F, Negri E, Franceschi S, Dal Maso L, Jenkins DJ, Kendall CW, La Vecchia C: Glycemic index and glycemic load in endometrial cancer. Augustin LS, Polesel J, Bosetti C, Kendall CW, La Vecchia C, Parpinel M, Conti E, Montella M, Franceschi S, Jenkins DJ, Dal Maso L: Dietary glycemic index, glycemic load and ovarian cancer risk: a case-control study in Italy.

Franceschi S, Dal Maso L, Augustin L, Negri E, Parpinel M, Boyle P, Jenkins DJ, La Vecchia C: Dietary glycemic load and colorectal cancer risk. Slattery ML, Boucher KM, Caan BJ, Potter JD, Ma KN: Eating patterns and risk of colon cancer. Am J Epidemiol. Bostick RM, Potter JD, Kushi LH, Sellers TA, Steinmetz KA, McKenzie DR, Gapstur SM, Folsom AR: Sugar, meat, and fat intake, and non-dietary risk factors for colon cancer incidence in Iowa women United States.

Frazier AL, Li L, Cho E, Willett WC, Colditz GA: Adolescent diet and risk of breast cancer. Higginbotham S, Zhang ZF, Lee IM, Cook NR, Giovannucci E, Buring JE, Liu S: Dietary glycemic load and risk of colorectal cancer in the Women's Health Study.

J Natl Cancer Inst. CAS PubMed PubMed Central Google Scholar. Cho E, Spiegelman D, Hunter DJ, Chen WY, Colditz GA, Willett WC: Premenopausal dietary carbohydrate, glycemic index, glycemic load, and fiber in relation to risk of breast cancer. Cancer Epidemiol Biomarkers Prev. Folsom AR, Demissie Z, Harnack L: Glycemic index, glycemic load, and incidence of endometrial cancer: the Iowa women's health study.

Nutr Cancer. Higginbotham S, Zhang ZF, Lee IM, Cook NR, Buring JE, Liu S: Dietary glycemic load and breast cancer risk in the Women's Health Study.

Michaud DS, Liu S, Giovannucci E, Willett WC, Colditz GA, Fuchs CS: Dietary sugar, glycemic load, and pancreatic cancer risk in a prospective study. Holmes MD, Liu S, Hankinson SE, Colditz GA, Hunter DJ, Willett WC: Dietary carbohydrates, fiber, and breast cancer risk. Jonas CR, McCullough ML, Teras LR, Walker-Thurmond KA, Thun MJ, Calle EE: Dietary glycemic index, glycemic load, and risk of incident breast cancer in postmenopausal women.

Oh K, Willett WC, Fuchs CS, Giovannucci EL: Glycemic index, glycemic load, and carbohydrate intake in relation to risk of distal colorectal adenoma in women. Terry PD, Jain M, Miller AB, Howe GR, Rohan TE: Glycemic load, carbohydrate intake, and risk of colorectal cancer in women: a prospective cohort study.

Hu FB, Manson JE, Liu S, Hunter D, Colditz GA, Michels KB, Speizer FE, Giovannucci E: Prospective study of adult onset diabetes mellitus type 2 and risk of colorectal cancer in women.

Khaw KT, Wareham N, Bingham S, Luben R, Welch A, Day N: Preliminary communication: glycated hemoglobin, diabetes, and incident colorectal cancer in men and women: a prospective analysis from the European prospective investigation into cancer-Norfolk study.

Saydah SH, Platz EA, Rifai N, Pollak MN, Brancati FL, Helzlsouer KJ: Association of markers of insulin and glucose control with subsequent colorectal cancer risk.

Platz EA, Hankinson SE, Rifai N, Colditz GA, Speizer FE, Giovannucci E: Glycosylated hemoglobin and risk of colorectal cancer and adenoma United States.

Schoen RE, Tangen CM, Kuller LH, Burke GL, Cushman M, Tracy RP, Dobs A, Savage PJ: Increased blood glucose and insulin, body size, and incident colorectal cancer.

Colangelo LA, Gapstur SM, Gann PH, Dyer AR, Liu K: Colorectal cancer mortality and factors related to the insulin resistance syndrome. Coughlin SS, Calle EE, Teras LR, Petrelli J, Thun MJ: Diabetes mellitus as a predictor of cancer mortality in a large cohort of US adults.

La Vecchia C, Negri E, Decarli A, Franceschi S: Diabetes mellitus and colorectal cancer risk. Sandhu MS, Luben R, Khaw KT: Self reported non-insulin dependent diabetes, family history, and risk of prevalent colorectal cancer: population based, cross sectional study.

J Epidemiol Community Health. Anderson KE, Anderson E, Mink PJ, Hong CP, Kushi LH, Sellers TA, Lazovich D, Folsom AR: Diabetes and endometrial cancer in the Iowa women's health study. Calle EE, Murphy TK, Rodriguez C, Thun MJ, Heath CW: Diabetes mellitus and pancreatic cancer mortality in a prospective cohort of United States adults.

Slattery ML, Curtin KP, Edwards SL, Schaffer DM: Plant foods, fiber, and rectal cancer. Bingham SA, Hughes R, Cross AJ: Effect of white versus red meat on endogenous N-nitrosation in the human colon and further evidence of a dose response.

Chen J, Stampfer MJ, Hough HL, Garcia-Closas M, Willett WC, Hennekens CH, Kelsey KT, Hunter DJ: A prospective study of N-acetyltransferase genotype, red meat intake, and risk of colorectal cancer.

Cancer Res. Fernandez E, La Vecchia C, D'Avanzo B, Negri E, Franceschi S: Risk factors for colorectal cancer in subjects with family history of the disease. Br J Cancer. Franceschi S, Favero A, La Vecchia C, Negri E, Conti E, Montella M, Giacosa A, Nanni O, Decarli A: Food groups and risk of colorectal cancer in Italy.

Fung T, Hu FB, Fuchs C, Giovannucci E, Hunter DJ, Stampfer MJ, Colditz GA, Willett WC: Major dietary patterns and the risk of colorectal cancer in women. Giovannucci E, Stampfer MJ, Colditz G, Rimm EB, Willett WC: Relationship of diet to risk of colorectal adenoma in men.

Giovannucci E, Rimm EB, Stampfer MJ, Colditz GA, Ascherio A, Willett WC: Intake of fat, meat, and fiber in relation to risk of colon cancer in men.

Hsing AW, McLaughlin JK, Chow WH, Schuman LM, Co Chien HT, Gridley G, Bjelke E, Wacholder S, Blot WJ: Risk factors for colorectal cancer in a prospective study among U.

white men. Hughes R, Pollock JR, Bingham S: Effect of vegetables, tea, and soy on endogenous N-nitrosation, fecal ammonia, and fecal water genotoxicity during a high red meat diet in humans.

Kampman E, Verhoeven D, Sloots L, van 't Veer P: Vegetable and animal products as determinants of colon cancer risk in Dutch men and women. Kampman E, Slattery ML, Bigler J, Leppert M, Samowitz W, Caan BJ, Potter JD: Meat consumption, genetic susceptibility, and colon cancer risk: a United States multicenter case-control study.

Kato I, Akhmedkhanov A, Koenig K, Toniolo PG, Shore RE, Riboli E: Prospective study of diet and female colorectal cancer: the New York University Women's Health Study.

La Vecchia C, Chatenoud L, Altieri A, Tavani A: Nutrition and health: epidemiology of diet, cancer and cardiovascular disease in Italy. Nutr Metab Cardiovasc Dis. Le Marchand L, Donlon T, Seifried A, Wilkens LR: Red meat intake, CYP2E1 genetic polymorphisms, and colorectal cancer risk.

Levi F, Pasche C, La Vecchia C, Lucchini F, Franceschi S: Food groups and colorectal cancer risk. Platz EA, Willett WC, Colditz GA, Rimm EB, Spiegelman D, Giovannucci E: Proportion of colon cancer risk that might be preventable in a cohort of middle-aged US men. Seow A, Quah SR, Nyam D, Straughan PT, Chua T, Aw TC: Food groups and the risk of colorectal carcinoma in an Asian population.

Silvester KR, Bingham SA, Pollock JR, Cummings JH, O'Neill IK: Effect of meat and resistant starch on fecal excretion of apparent N-nitroso compounds and ammonia from the human large bowel. Singh PN, Fraser GE: Dietary risk factors for colon cancer in a low-risk population.

Sinha R, Chow WH, Kulldorff M, Denobile J, Butler J, Garcia-Closas M, Weil R, Hoover RN, Rothman N: Well-done, grilled red meat increases the risk of colorectal adenomas. Slattery ML, Curtin K, Ma K, Edwards S, Schaffer D, Anderson K, Samowitz W: Diet activity, and lifestyle associations with p53 mutations in colon tumors.

Thun MJ, Calle EE, Namboodiri MM, Flanders WD, Coates RJ, Byers T, Boffetta P, Garfinkel L, Heath CW: Risk factors for fatal colon cancer in a large prospective study.

Tiemersma EW, Kampman E, Bueno de Mesquita HB, Bunschoten A, van Schothorst EM, Kok FJ, Kromhout D: Meat consumption, cigarette smoking, and genetic susceptibility in the etiology of colorectal cancer: results from a Dutch prospective study.

Willett WC, Stampfer MJ, Colditz GA, Rosner BA, Speizer FE: Relation of meat, fat, and fiber intake to the risk of colon cancer in a prospective study among women. Norat T, Lukanova A, Ferrari P, Riboli E: Meat consumption and colorectal cancer risk: dose-response meta-analysis of epidemiological studies.

De Stefani E, Ronco A, Mendilaharsu M, Guidobono M, Deneo-Pellegrini H: Meat intake, heterocyclic amines, and risk of breast cancer: a case-control study in Uruguay.

London SJ, Sacks FM, Stampfer MJ, Henderson IC, Maclure M, Tomita A, Wood WC, Remine S, Robert NJ, Dmochowski JR: Fatty acid composition of the subcutaneous adipose tissue and risk of proliferative benign breast disease and breast cancer.

Bernard-Gallon DJ, Vissac-Sabatier C, Antoine-Vincent D, Rio PG, Maurizis JC, Fustier P, Bignon YJ: Differential effects of n-3 and n-6 polyunsaturated fatty acids on BRCA1 and BRCA2 gene expression in breast cell lines. Br J Nutr. Brooks JD, Ward WE, Lewis JE, Hilditch J, Nickell L, Wong E, Thompson LU: Supplementation with flaxseed alters estrogen metabolism in postmenopausal women to a greater extent than does supplementation with an equal amount of soy.

Thompson LU, Rickard SE, Orcheson LJ, Seidl MM: Flaxseed and its lignan and oil components reduce mammary tumor growth at a late stage of carcinogenesis.

Thompson LU, Seidl MM, Rickard SE, Orcheson LJ, Fong HH: Antitumorigenic effect of a mammalian lignan precursor from flaxseed. Yan L, Yee JA, Li D, McGuire MH, Thompson LU: Dietary flaxseed supplementation and experimental metastasis of melanoma cells in mice. Cancer Lett. Li D, Yee JA, Thompson LU, Yan L: Dietary supplementation with secoisolariciresinol diglycoside SDG reduces experimental metastasis of melanoma cells in mice.

Chen J, Stavro PM, Thompson LU: Dietary flaxseed inhibits human breast cancer growth and metastasis and downregulates expression of insulin-like growth factor and epidermal growth factor receptor.

Tan KP, Chen J, Ward WE, Thompson LU: Mammary gland morphogenesis is enhanced by exposure to flaxseed or its major lignan during suckling in rats. Exp Biol Med Maywood.

CAS Google Scholar. Chen J, Tan KP, Ward WE, Thompson LU: Exposure to flaxseed or its purified lignan during suckling inhibits chemically induced rat mammary tumorigenesis. Lin X, Gingrich JR, Bao W, Li J, Haroon ZA, Demark-Wahnefried W: Effect of flaxseed supplementation on prostatic carcinoma in transgenic mice.

Demark-Wahnefried W, Price DT, Polascik TJ, Robertson CN, Anderson EE, Paulson DF, Walther PJ, Gannon M, Vollmer RT: Pilot study of dietary fat restriction and flaxseed supplementation in men with prostate cancer before surgery: exploring the effects on hormonal levels, prostate-specific antigen, and histopathologic features.

Brouwer IA, Katan MB, Zock PL: Dietary alpha-linolenic acid is associated with reduced risk of fatal coronary heart disease, but increased prostate cancer risk: a meta-analysis. Block G, Patterson B, Subar A: Fruit, vegetables, and cancer prevention: a review of the epidemiological evidence.

Steinmetz KA, Potter JD: Vegetables, fruit, and cancer prevention: a review. J Am Diet Assoc. Fleischauer AT, Poole C, Arab L: Garlic consumption and cancer prevention: meta-analyses of colorectal and stomach cancers. Fleischauer AT, Arab L: Garlic and cancer: a critical review of the epidemiologic literature.

Hsing AW, Chokkalingam AP, Gao YT, Madigan MP, Deng J, Gridley G, Fraumeni JF: Allium vegetables and risk of prostate cancer: a population-based study. Riboli E, Norat T: Epidemiologic evidence of the protective effect of fruit and vegetables on cancer risk.

Bingham SA, Luben R, Welch A, Wareham N, Khaw KT, Day N: Are imprecise methods obscuring a relation between fat and breast cancer?. Joshipura KJ, Ascherio A, Manson JE, Stampfer MJ, Rimm EB, Speizer FE, Hennekens CH, Spiegelman D, Willett WC: Fruit and vegetable intake in relation to risk of ischemic stroke.

Donaldson MS: Food and nutrient intake of Hallelujah vegetarians. Fowke JH, Chung FL, Jin F, Qi D, Cai Q, Conaway C, Cheng JR, Shu XO, Gao YT, Zheng W: Urinary isothiocyanate levels, brassica, and human breast cancer. Zhang SM, Hunter DJ, Rosner BA, Giovannucci EL, Colditz GA, Speizer FE, Willett WC: Intakes of fruits, vegetables, and related nutrients and the risk of non-Hodgkin's lymphoma among women.

Michaud DS, Spiegelman D, Clinton SK, Rimm EB, Willett WC, Giovannucci EL: Fruit and vegetable intake and incidence of bladder cancer in a male prospective cohort. Cohen JH, Kristal AR, Stanford JL: Fruit and vegetable intakes and prostate cancer risk. Kolonel LN, Hankin JH, Whittemore AS, Wu AH, Gallagher RP, Wilkens LR, John EM, Howe GR, Dreon DM, West DW, Paffenbarger RS: Vegetables, fruits, legumes and prostate cancer: a multiethnic case-control study.

London SJ, Yuan JM, Chung FL, Gao YT, Coetzee GA, Ross RK, Yu MC: Isothiocyanates, glutathione S-transferase M1 and T1 polymorphisms, and lung-cancer risk: a prospective study of men in Shanghai, China.

Fahey JW, Zhang Y, Talalay P: Broccoli sprouts: an exceptionally rich source of inducers of enzymes that protect against chemical carcinogens.

Proc Natl Acad Sci U S A. Shapiro TA, Fahey JW, Wade KL, Stephenson KK, Talalay P: Chemoprotective glucosinolates and isothiocyanates of broccoli sprouts: metabolism and excretion in humans.

Selenium Information Sheet. htm ]. Duffield-Lillico AJ, Reid ME, Turnbull BW, Combs GF, Slate EH, Fischbach LA, Marshall JR, Clark LC: Baseline characteristics and the effect of selenium supplementation on cancer incidence in a randomized clinical trial: a summary report of the Nutritional Prevention of Cancer Trial.

Clark LC, Combs GF, Turnbull BW, Slate EH, Chalker DK, Chow J, Davis LS, Glover RA, Graham GF, Gross EG, Krongrad A, Lesher JL, Park HK, Sanders BB, Smith CL, Taylor JR: Effects of selenium supplementation for cancer prevention in patients with carcinoma of the skin.

A randomized controlled trial. Nutritional Prevention of Cancer Study Group. Ghadirian P, Maisonneuve P, Perret C, Kennedy G, Boyle P, Krewski D, Lacroix A: A case-control study of toenail selenium and cancer of the breast, colon, and prostate.

Cancer Detect Prev. van den Brandt PA, Goldbohm RA, van't Veer P, Bode P, Dorant E, Hermus RJ, Sturmans F: Toenail selenium levels and the risk of breast cancer.

Hunter DJ, Morris JS, Stampfer MJ, Colditz GA, Speizer FE, Willett WC: A prospective study of selenium status and breast cancer risk. van 't Veer P, van der Wielen RP, Kok FJ, Hermus RJ, Sturmans F: Selenium in diet, blood, and toenails in relation to breast cancer: a case-control study.

van Noord PA, Collette HJ, Maas MJ, de Waard F: Selenium levels in nails of premenopausal breast cancer patients assessed prediagnostically in a cohort-nested case-referent study among women screened in the DOM project. Int J Epidemiol.

Reid ME, Duffield-Lillico AJ, Garland L, Turnbull BW, Clark LC, Marshall JR: Selenium supplementation and lung cancer incidence: an update of the nutritional prevention of cancer trial.

van den Brandt PA, Goldbohm RA, van 't Veer P, Bode P, Dorant E, Hermus RJ, Sturmans F: A prospective cohort study on selenium status and the risk of lung cancer. Chernomorsky S, Segelman A, Poretz RD: Effect of dietary chlorophyll derivatives on mutagenesis and tumor cell growth.

Teratog Carcinog Mutagen. Sarkar D, Sharma A, Talukder G: Chlorophyll and chlorophyllin as modifiers of genotoxic effects. Mutat Res. Egner PA, Wang JB, Zhu YR, Zhang BC, Wu Y, Zhang QN, Qian GS, Kuang SY, Gange SJ, Jacobson LP, Helzlsouer KJ, Bailey GS, Groopman JD, Kensler TW: Chlorophyllin intervention reduces aflatoxin-DNA adducts in individuals at high risk for liver cancer.

Egner PA, Stansbury KH, Snyder EP, Rogers ME, Hintz PA, Kensler TW: Identification and characterization of chlorin e 4 ethyl ester in sera of individuals participating in the chlorophyllin chemoprevention trial.

Chem Res Toxicol. Nishizawa Y, Yamamoto T, Terada N, Fushiki S, Matsumoto K: Effects of methylcobalamin on the proliferation of androgen-sensitive or estrogen-sensitive malignant cells in culture and in vivo.

Int J Vitam Nutr Res. Nishizawa Y, Goto HG, Tanigaki Y, Fushiki S: Induction of apoptosis in an androgen-dependent mouse mammary carcinoma cell line by methylcobalamin.

Anticancer Res. Tsao CS, Myashita K: Influence of cobalamin on the survival of mice bearing ascites tumor. Tsao CS, Miyashita K, Young M: Cytotoxic activity of cobalamin in cultured malignant and nonmalignant cells.

Shimizu N, Hamazoe R, Kanayama H, Maeta M, Koga S: Experimental study of antitumor effect of methyl-B Choi SW, Friso S, Ghandour H, Bagley PJ, Selhub J, Mason JB: Vitamin B deficiency induces anomalies of base substitution and methylation in the DNA of rat colonic epithelium. Wu K, Helzlsouer KJ, Comstock GW, Hoffman SC, Nadeau MR, Selhub J: A prospective study on folate, B12, and pyridoxal 5'-phosphate B6 and breast cancer.

Zhang SM, Willett WC, Selhub J, Hunter DJ, Giovannucci EL, Holmes MD, Colditz GA, Hankinson SE: Plasma folate, vitamin B6, vitamin B12, homocysteine, and risk of breast cancer.

Blount BC, Mack MM, Wehr CM, MacGregor JT, Hiatt RA, Wang G, Wickramasinghe SN, Everson RB, Ames BN: Folate deficiency causes uracil misincorporation into human DNA and chromosome breakage: implications for cancer and neuronal damage.

Ma J, Stampfer MJ, Giovannucci E, Artigas C, Hunter DJ, Fuchs C, Willett WC, Selhub J, Hennekens CH, Rozen R: Methylenetetrahydrofolate reductase polymorphism, dietary interactions, and risk of colorectal cancer.

Ma J, Stampfer MJ, Christensen B, Giovannucci E, Hunter DJ, Chen J, Willett WC, Selhub J, Hennekens CH, Gravel R, Rozen R: A polymorphism of the methionine synthase gene: association with plasma folate, vitamin B12, homocyst e ine, and colorectal cancer risk. Giovannucci E, Chen J, Smith-Warner SA, Rimm EB, Fuchs CS, Palomeque C, Willett WC, Hunter DJ: Methylenetetrahydrofolate reductase, alcohol dehydrogenase, diet, and risk of colorectal adenomas.

Le Marchand L, Donlon T, Hankin JH, Kolonel LN, Wilkens LR, Seifried A: B-vitamin intake, metabolic genes, and colorectal cancer risk United States.