Invited commentary: tomatoes, lycopene, and prostate cancer. How strong is the evidence?

Until only recently, there was little evidence that intakes of fruits and vegetables were related to prostate cancer risk. Findings from observational epidemiologic studies were weak and inconsistent, and the results from three large randomized clinical trials of supplemental p-carotene (an antioxidant carotenoid found primarily in yellow and orange vegetables) showed no effects on prostate cancer (1-3). In 1995, Giovannucci et al. reported a 35 percent reduced prostate cancer risk, comparing men who ate more than 10 weekly servings of tomato products with those who ate fewer than 1.5 servings weekly (4). They suggested that this effect might be attributable to lycopene, the antioxidant carotenoid found primarily in tomatoes. This result motivated heightened interest in lycopene and prostate cancer; subsequent scientific reports, including those by Freeman et al. (5) and Norrish et al. (6) in this issue of the Journal, provide additional insight into the associations of fruits and vegetables with prostate cancer risk. In this commentary, we give a very brief summary of this literature, make recommendations for further research, and present our perspective regarding the strength and coherence of the hypothesized protective effect of tomato products on prostate cancer risk. There is a large and quite variable literature on the associations of fruit and vegetable intakes with prostate cancer risk. Only eight studies examined total fruit and/or vegetable intakes (7-14), and only one found a significant protective association (11). We could find 17 studies that examined specific fruits and/or vegetables. Individual studies have found protective effects for beans, lentils, peas, carrots, greens, tomatoes, one or more cruciferous vegetables, tofu,