1. ¹Department of Urology, David Geffen School of Medicine at UCLA, Los Angeles, California, USA
2. ²Department of Health Services, UCLA School of Public Health, Los Angeles, California, USA
3. ³UCLA Jonsson Comprehensive Cancer Center, Los Angeles, California, USA
4. ⁴Veterans Administration Greater Los Angeles Health Care System, Los Angeles, California, USA

Correspondence: MS Litwin, Department of Urology, University of California Los Angeles, Box 951738, Los Angeles, CA 90095-1738, USA. E-mail: mlitwin@mednet.ucla.edu

Received 1 July 2005; Accepted 18 July 2005; Published online 30 August 2005.

Abstract

Epidemiological studies suggest that environmental factors may mediate the transformation of latent prostate cancer into clinically apparent tumors and that diet appears to influence this progression. Close correlations between average per capita fat intake and prostate cancer mortality internationally generated interest in underlying mechanisms for this link, such as through serum levels of androgens, free radicals, proinflammatory fatty acid metabolites, or insulin-like growth factor. Much interest currently lies in the potential of HMG-CoA reductase inhibitors (statins) to play a chemopreventative role in prostate cancer. Lycopene, a potent antioxidant found in tomatoes, may exert a protective effect in the prostate. Selenium and vitamin E have also been shown to decrease the risk of prostate cancer in some men. Calcium may support vitamin D-related antiproliferative effects in prostate cancer. Certain soy proteins, common in the Asian diet, have been shown to inhibit prostate cancer cell growth. Finally, green tea may also have a chemopreventive effect by inducing apoptosis. Despite confounding factors present in clinical studies assessing the effect of diet on cancer risk, the data remain compelling that a variety of nutrients may prevent the development and progression of prostate cancer.