Both hereditary and nutritional factors contribute to the development of colorectal cancer – a slow, stepwise process driven by the accumulation of genetic changes in the tumor cells and by progressive deregulation of growth. Dietary factors can both cause somatic mutations and stimulate tumor growth. This review explores the mechanisms of growth regulation in colonic tumors and the interaction between genetic changes and growth modulators derived from our diet. Most of the genetic defects observed in colon carcinogenesis have a potency of affecting growth control, creating a premalignant cell population that is highly susceptible to regulatory signals. Growth stimulators are bile acids, 1,2-diglycerides, and prostaglandins stemming from fat consumption, while fruits and vegetables contain various substances that might inhibit growth – like carotinoids, flavonoids and of course fiber. Similar protective effects may be caused by Ca2+ and the vitamins A and D. Diet is a complex mixture of all these tumor-enhancing and tumor-inhibiting constituents, whose effects and interactions have to be understood to develop cancer-protective dietary patte