A significant body of epidemiologic evidence associates certain dietary patterns with an increased risk of cancer. A diet rich in fat and meat, and low in cereals, fiber, fruits, and vegetables is associated with an increased risk of colorectal, mammary, and other common forms of cancer. Limited diets in some countries with evident micronutrient deficiencies are also associated with an increased risk for certain forms of cancer. A genetic polymorphism of the GSTM1 enzyme increases the risk for colon polyps, while the ingestion of cruciferous vegetables (broccoli, cauliflower, Brussels sprouts) cancels out the effects of the null genotype. While population studies such as these cannot establish a cause-effect relationship between nutrition and cancer, a number of studies in animals support the concept that cancer results from a gene-nutrient interaction. In animals with well-defined mutations affecting cell signaling, such as the p53 mutation, tumor development can be affected by diet.

The final common mechanism believed to mediate the effects of different diets on cancer and aging is the oxidation of the genome and other cellular and subcellular structures. Mutations induced by oxidative damage may then lead to increased cellular proliferation, reduced apoptosis or both. Therefore, genes confer susceptibility to oxidative damage through absence or malfunction of the extensive antioxidant defense and DNA repair mechanisms, while the diet can affect whether and to what extent that oxidative damage occurs.

In aging, oxidative damage is increased and aging is the predominant risk factor for cancer. The demonstration of the effects of nutrition on cancer requires using age-adjusted incidences. Furthermore, dietary restriction with vitamin and antioxidant supplementation can extend maximum lifespan significantly in rodents. In epidemiologic studies in humans, the intake of 400 to 600 grams per day of fruits and vegetables is associated with a reduced risk of gastric and other cancers. The most common cancers in developed societies are breast, prostate and colon cancer. Obesity, high fat diets, and reduced intake of fiber from cereals, grains, fruits and vegetables comprise a high risk dietary pattern. For each of the most common cancers, there is extensive evidence of a variation in incidence as individuals move from low risk to high risk countries. For prostate cancer, there is an equal incidence of latent prostate cancer in the U.S. and Japan, but clinical cancer is five times more frequent in the U.S. In animal experiments, nutrition affects the growth, progression and metastasis of established tumors as well as the incidence of new tumors.

There is limited information on nutrition intervention in humans, but a clear demonstration comes from a study of non-melanoma skin cancer, where incidence is clearly affected by dietary fat. This human intervention study confirms data in animals that carcinogen-induced skin cancer is enhanced by high fat diets. The antioxidant defenses are carried out by enzymes that are part of the drug-metabolizing enzyme family. These enzymes use dietary substances as co-factors and inactivate or activate carcinogens depending on their environment. Variations in nutritional intake can interact with these metabolic enzymes to provide a defense against carcinogenesis. Broccoli contains sulfurophane which induces a protective enzyme in the cell, that inactivates carcinogens.