Nutrition and prostate cancer: evidence or suspicion?

N factors have been hypothesized to be critical in the carcinogenesis of numerous cancers, and this holds true for prostate cancer. Studies of migrants moving from countries with a low prostate cancer incidence to North America, where their incidence increases to almost equal to that of white American populations within a generation, suggest that environmental factors have an influence on the development of the most frequent neoplasm in men.1 The large geographical differences observed are probably not due to genetic variations only, as individuals with the same genetic background raised in different environments have a risk of prostate cancer comparable to the incidence in the country they live in. Although several genetic predisposition factors for prostate cancer have been discovered during the previous years, an environmental trigger is probably necessary for the disease to become manifest, even for carriers of strong cancer susceptibility genes, because only a minority of these men will develop the disease. Indeed, a recent study of 44,788 pairs of twins listed in the Swedish, Danish, and Finnish twin registries found that inherited genetic factors make a minor contribution to susceptibility to most types of neoplasms, including prostate cancer, and indicated that environment played the principal role in causing sporadic cancers.2 Among these environmental factors, nutrition has been suspected to play a major role. Dietary habits and prostate cancer incidence are very different in several parts of the world. For instance, the incidence of prostate cancer is very low in most of Asia (incidence rate as low as 0.5 per 100,000 men in Qidong, China), where the dietary intake is low in animal fat but rich in fiber and soy protein.1 In contrast, excess weight and high amounts of dietary animal fat are very common in Western countries (with incidences peaking at 133.5 per 100,000 men in Sweden).1 There may be biases with cancer registries in some Far East countries, and it is likely that a low level of prostate cancer awareness, including access to prostate-specific antigen (PSA) testing, might also contribute to this situation. In breast cancer, the hypothesis that some investigators have suggested to best fit the epidemiologic data is that dietary fat is not itself the causal agent but produces a depletion of an essential factor that is normally protective against the development of breast cancer.3 Accumulating laboratory evidence shows that several agents found in the diet may prevent the effects of carcinogenic agents or suppress the promotional activity in already induced neoplastic prostatic cells. Preventive medicine is currently considered a key issue. Cardiovascular disease is a well-known example. The identification of atherosclerosis as one of the causative mechanisms of cardiovascular diseases has resulted in important lifestyle modifications, including in diet, tobacco use, and exercise. This has led to a 65% decrease in the incidence of heart disease in some series.4 Chemoprevention is the administration of drugs or other agents to prevent, inhibit, or delay cancer progression. Chemoprevention of colorectal cancer, for instance, has recently been evaluated, mainly because of existing preneoplastic polyps.5 Prostate cancer represents an ideal target, because of its long latency, its high incidence, tumor marker availability (PSA), and identifiable preneoplastic lesions and high-risk groups. Numerous case-control studies, but unfortunately very few prospective randomized trials, have analyzed the influence of diet on prostate cancer. To firmly establish the influence of a nutritional compound on cancer genesis or promotion, carefully designed, large-scale, prospective randomized trials (“interventional studies”) should further support the epidemiologic (“observational” studies) and experimental data. Are the current scientific data strong enough to From the Department of Urology, Erasme Hospital, University Clinics of Brussels, Brussels, Belgium Reprint requests: C. C. Schulman, M.D., Department of Urology, Erasme Hospital, University Clinics of Brussels, Route de Lennik 808, Brussels B-1070, Belgium Submitted: October 30, 2000, accepted (with revisions): May 8, 2001 REVIEW CME ARTICLE