Prostate cancer has become a major public health problem worldwide. Yet, the etiology of prostate cancer remains largely unknown. Dietary factors, dietary supplements, and physical activity might be important in the prevention of the disease. In the majority of studies, it was observed that high consumption of meat and dairy products has been linked to a greater risk. In contrast, frequent consumption of fatty fish and tomato products has been associated with a reduced risk. It has been shown consistently that high levels of circulating insulin-like growth factor 1 (IGF-1) are associated with an increased risk of prostate cancer. Dietary factors are also recognized as determinants of circulating IGF-1, thus changes in diet may influence IGF-1 concentrations in serum. Furthermore, increased intake of vitamin E and selenium (from supplements) has been shown in intervention studies to decrease the risk. Possibly, high level of physical activity is also associated with decreased risk of prostate cancer. The accumulated scientific evidence concerning the associations between diet, lifestyle, and risk of prostate cancer development suggests that there are some identified modifiable risk factors that it might be recommended to change in order to decrease the risk for this common cancer site.

Wolk A.

Division of Nutritional Epidemiology, the National Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden. Alicja.Wolk@imm.ki.se

Acta Oncol. 2005;44(3):277-81.Links

Background: Reports from several studies have suggested that carotenoids, and in particular lycopene, could be prostate cancer–preventive agents. This has stimulated extensive laboratory and clinical research, as well as much commercial and public enthusiasm. However, the epidemiologic evidence remains inconclusive.

Materials and Methods: We investigated the association between prediagnostic serum carotenoids (lycopene, {alpha}-carotene, ß-carotene, ß-cryptoxanthin, lutein, and zeaxanthin) and risk of prostate cancer in the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial, a multicenter study designed to examine methods of early detection and risk factors for cancer. The study included 692 incident prostate cancer cases, diagnosed 1 to 8 years after study entry, including 270 aggressive cases, with regional or distant stage (n = 90) or Gleason score ≥7 (n = 235), and 844 randomly selected, matched controls. As study participants were selected from those who were assigned to annual standardized screening for prostate cancer, results are unlikely to be biased by differential screening, a circumstance that is difficult to attain under non–trial conditions.

Results: No association was observed between serum lycopene and total prostate cancer [odds ratios (OR), 1.14; 95% confidence intervals (95% CI), 0.82-1.58 for highest versus lowest quintile; P for trend, 0.28] or aggressive prostate cancer (OR, 0.99; 95% CI, 0.62-1.57 for highest versus lowest quintile; P for trend, 0.433). ß-Carotene was associated with an increased risk of aggressive prostate cancer (OR, 1.67; 95% CI, 1.03-2.72 for highest versus lowest quintile; P for trend, 0.13); in particular, regional or distant stage disease (OR, 3.16; 95% CI, 1.37-7.31 for highest versus lowest quintile; P for trend, 0.02); other carotenoids were not associated with risk.

Conclusion: In this large prospective study, high serum ß-carotene concentrations were associated with increased risk for aggressive, clinically relevant prostate cancer. Lycopene and other carotenoids were unrelated to prostate cancer. Consistent with other recent publications, these results suggest that lycopene or tomato-based regimens will not be effective for prostate cancer prevention.

(Cancer Epidemiol Biomarkers Prev 2007;16(5):962–8)

Full Text

Ulrike Peters1,2,3, Michael F. Leitzmann3, Nilanjan Chatterjee3, Yinghui Wang1, Demetrius Albanes3, Edward P. Gelmann4, Marlin D. Friesen5, Elio Riboli6 and Richard B. Hayes3

1 Fred Hutchinson Cancer Research Center; 2 University of Washington, Seattle, Washington; 3 Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Department of Health and Human Services, Rockville, Maryland; 4 Department of Oncology, Lombardi Comprehensive Cancer Center, Georgetown University, Washington, District of Columbia; 5 Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland; and 6 Nutrition and Cancer Unit, International Agency for Research on Cancer, Lyon, France

Requests for reprints: Ulrike Peters, Cancer Prevention Program, Fred Hutchinson Cancer Research Center, P.O. Box 19024, 1100 Fairview Avenue North M4-B402, Seattle, WA 98109-1024. Phone: 206-667-2450; Fax: 206-667-7850. E-mail: upeters@fhcrc.org