Whenever prostate cancer is mentioned, there are many questions about it: How to prevent it? How can it be detected early? Is there the most effective way to cure it? And is treatment necessary? Here are six common misconceptions about prostate cancer provided by scientists from the Fred Hutchinson Cancer Research Center with research to help people separate fact from rumor. The vast majority of studies show no link between the two,” says Alan Kristal, PhD, deputy director of the Hutchinson Center’s Cancer Prevention Program and a national prostate cancer prevention panel. ” Kristal and colleagues last year published the results of one of the largest studies to date on whether foods containing lycopene, a nutrient that makes tomatoes red, actually prevent prostate cancer. By testing lycopene levels in the blood of 3,500 men nationwide they found no link. In the journal Cancer Epidemiology, Biomarkers & Prevention, the authors state that “scientists and the public should understand that the earlier findings of a link between dietary lycopene and a reduced risk of prostate cancer cannot be replicated.” The professional society’s recommendation to the public should be modified to state that increased lycopene intake may not be associated with prostate cancer risk. Misconception No. 2: High levels of testosterone increase the risk of prostate cancer. says Kristal: “That’s a very cute assumption – based on a very simple understanding of the metabolism of testosterone and the effects on prostate cancer, which is unfortunately wrong.” Unlike the strong link between estrogen and breast cancer, there is no link between testosterone levels and prostate cancer risk, he said. A 2008 study published in the Journal of the National Cancer Institute, a top international journal, combined data from 18 large studies and found no link between serum testosterone concentrations and prostate cancer risk, and more recent studies have further confirmed this conclusion. Myth No. 3: Cod liver oil (omega-3 fatty acids) can reduce prostate cancer risk, Kristal says. “Based on the link between prostate cancer and inflammation and the anti-inflammatory effects of omega-3 fatty acids, this sounds reasonable.” Yet two well-designed bulk studies (one of which was led by Kristal and published last year in the American Journal of Epidemiology) have shown that high omega-3 fatty acids in the blood instead increase the risk of prostate cancer. Analyzing data related to nearly 3,500 men from around the world, they found that those with the highest percentage of fatty acids in their blood docosahexaenoic acid, or DHA, an Omega-3 fatty acid that reduces the inflammatory response and is found primarily in fish, had a risk of aggressive, high-grade prostate cancer that was 2.5 times greater than those with the lowest percentage of DHA. “This surprising finding suggests that we do not yet fully understand the role of Omega-3 fatty acids” Myth #4: Dietary supplements can prevent prostate cancer. Several large, randomized clinical trials have studied the effects of dietary supplements on a variety of cancers, including prostate cancer; the results show either no effect, a significant effect – or, worryingly, a significant increase in risk. says Kristal: “The more we think certain dietary supplements can do the job, the more likely it seems they are to increase the risk of cancer. ” For example, the largest prostate cancer prevention study to date: the Selenium and Vitamin E Cancer Prevention Clinical Trial (SELECT) was earlier called off because neither selenium or vitamin E supplementation alone or in combination had any effect on reducing the risk of prostate cancer. A selective follow-up study published in JAMA last year found that vitamin E actually increased the risk of prostate cancer in healthy men, and the Hutchinson Center reviewed the analysis of data from the study, which included nearly 35,000 men from the United States, Canada, and Puerto Rico. Myth #5: We don’t know which prostate cancers screened for by PSA (prostate-specific antigen) need to be treated and which don’t. Dr. Ruth Etzioni, a biostatistician and member of the Hutchinson Center’s Department of Public Health Sciences, says, “The truth is, we know very well which cancers are less likely to progress malignantly and which are likely to metastasize if left untreated.” In addition to serum PSA levels, criteria for determining tumor aggressiveness include tumor volume (the number of biopsy samples containing cancerous tissue) and the Gleason score (which predicts tumor aggressiveness by looking at a sample of cancerous tissue under a microscope). 2-5 on the Gleason scale is low risk, 6-7 is intermediate risk and 8-10 is high risk, Etzioni said. “If a person has a low PSA level, a biopsy sample with a Gleason score of 6 or less, and very few biopsies containing cancerous tissue, then they are considered low-risk.” Such men with newly diagnosed prostate cancer should more than likely be given primary wait-list treatment (a form of watchful waiting) in lieu of previous treatment unless they are older or have a short life expectancy. “If these patients are not treated, the chances of dying from this disease are small, about 3 percent,” she said. Similarly, if these patients choose to be treated, the mortality rate is roughly 2 percent. “For most of those patients who are newly diagnosed with prostate cancer, as long as we have access to their original clinical data and tissue biopsy information, we can determine which ones need to be treated immediately and which ones would benefit more from delayed therapy.” Myth No. 6: Only one in 50 patients with prostate cancer diagnosed through PSA screening benefit from treatment. “This data from the preliminary publication of the ‘European Randomized Trial of Prostate Cancer Screening’ is clearly wrong,” Etzioni said, “and produces a very unfavorable harm-to-benefit ratio for PSA screening. It implies that if there is one person whose life is saved by PSA screening, there are 50 people who are simultaneously overdiagnosed and overtreated.” “Overdiagnosis” is a diagnosis of a disease that does not cause any adverse symptoms, much less death, during a person’s lifetime. “The 50-to-1 ratio is based on short-term follow-up and “grossly underestimates” the number of patients who benefit from prolonged screening and overestimates the number of “overdiagnoses. The 50-to-1 ratio is based on short-term follow-up and a “gross underestimation” of patients who benefit from prolonged screening and an overestimation of the number of “overdiagnoses. The ratio of “overdiagnosed” and “overtreated” men diagnosed by PSA testing to those who benefit from long-term treatment should be correctly 10 to 1, she said.