Dietary Prostate Cancer Risk Factors

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There are at least seven major dietary macro- or micronutrients that are under intense scrutiny currently as dietary risk or protective factors (Table 15.1). Prominent among these is dietary fat or some component of fat (e.g., saturated fat), which first received attention as a mechanism to possibly explain the low risk in native Asian populations and the apparent rapid shift in risk upon migration of Asian populations to the United States. There are suggestive data that increased fat consumption is associated with higher circulating testosterone levels, providing a possible mechanism for a fat-prostate cancer relation ship.9 Both case-control and cohort data tend to support a relationship between fat consumption overall and prostate cancer risk;10,11 however, there are sufficient inconsistencies in the data, and the magnitude of risk even between extreme categories of estimated fat intake is sufficiently modest that fat is still not considered a proven prostate cancer risk factor.

Antioxidant vitamins and minerals are of great current interest, not only as antiprostate cancer agents but also as anticarcinogenic agents in a broad sense. Antioxidants are potential anticancer agents because they bind free radicals, chemical entities that can damage DNA, create mutations, and lead to malignant transforma-tion.12 Two antioxidants are of special interest in the context of prostate cancer. Lycopene is a member of the carotenoid family of vitamins and is the major antioxidant in tomatoes and tomato products. It is concentrated in the prostate and may suppress prostate cancer growth.13 Observational studies have demonstrated inverse relationships between lycopene and/or frequency of consumption of tomato products and prostate cancer risk.14 Moreover, prospective serological studies have shown that high circulating levels of lycopene predict low prostate cancer risk.15 Additional prospective dietary and serological studies are ongoing to confirm this relationship and evaluate lycopene as a potential protective agent in greater detail. Vitamin E is an antioxi-dant vitamin that has been tested in a clinical trial setting as a chemopreventive agent for lung cancer in heavy smokers. Although vitamin E was ineffective against lung cancer in that setting, prostate cancer risk was substantially reduced in the trial arm that received vitamin E.16 While this observation is highly encouraging, it is unclear why there would be specificity to the prostate in terms of cancer reduction. This fac

Table 15.1 Suggested Dietary Risk or Protective Factors for Prostate Cancer and Their Possible Mechanisms of Action

Dietary Factor

Direction of Risk

Possible Mechanism

Fat

Increased

Androgen activity/cell proliferation

Fiber

Decreased

Androgen activity/reduced cell proliferation

Lycopene

Decreased

Antioxidant

Phytoestrogens

Decreased

Androgen activity/reduced cell proliferation

Selenium

Decreased

Antioxidant, proapoptosis

Vitamin D

Decreased

Vitamin D activity/reduced cell proliferation/pro-differentiation

Vitamin E

Decreased

Antioxidant

tor plus the incidental nature of the finding require that additional confirmatory studies be conducted.

Selenium is a trace mineral that has generated considerable interest as an anticancer agent. Like the carotenoids and vitamin E, selenium is a potent antioxidant, but it also has additional anticancer properties experimentally, including especially proapoptotic activity, although other mechanisms may also be involved.17 As with vitamin E, selenium was observed to reduce prostate cancer risk as an incidental finding in a clinical trial of secondary skin cancer preven-tion.18 In part because of its proven efficacy as an anticancer agent experimentally and because there are epidemiological biomarker data supporting selenium as a prostate cancer chemo-preventive agent, there are ongoing short- and long-term clinical trials to directly test the efficacy of selenium to prevent prostate cancer. Results of the short-term trials, which will evaluate the impact of selenium supplementation on the prostate cancer precursor lesion prostate in-traepithelial neoplasia (PIN) and on possible biomarkers of prostate cancer risk (e.g., rate of epithelial cell proliferation) should be available within 2 years. However, results of full-scale trials to determine the impact of selenium supplementation on clinical prostate cancer risk per se in healthy men will not be available for at least 7-10 years.

Phytoestrogens, i.e., plant-derived estrogens such as from soy products, have been hypothesized to protect against prostate cancer, possibly by antagonist actions of estrogens on androgen-mediated growth.19 There are some experimental animal data supporting an inhibitory effect of phytoestrogen intake on prostate tumor growth.19,20 Phytoestrogen intake has been hypothesized to play a role in the reduced prostate cancer rates observed in Asian populations. Cross-sectional population studies have shown urinary phytoestrogen biomarkers to be substantially higher in native Japanese than other racial/ethnic groups, but there is little direct evidence linking high phytoestrogen consumption to low prostate cancer risk.21 One study found tofu consumption, a soy source of phytoestro-gens, to be associated with reduced risk; but there is great need for further epidemiological investigations.22

Fiber can bind steroid hormones that are being recirculated through the enterohepatic circulation. Fiber binds these hormones, causing them to be excreted rather than reabsorbed, which, in theory, will reduce circulating levels of steroid hormones. Thus, fiber intake might be expected to result in some reduction in prostate cancer risk by reducing androgen stimulation of the prostate, but this hypothesis is also largely untested.

Vitamin D is a promising potential chemo-preventive agent for prostate cancer. 1,25-Dihy-droxyvtamin D, the active form of vitamin D, can reduce cell proliferation and induce differentiation of prostate cancer cells in vitro.23,24 Both of these actions would be anticipated to reduce prostate cancer risk or at least reduce progression from occult to clinically relevant disease. Epidemiological studies are generally supportive. Low circulating levels of 1,25-dihy-droxyvitamin D have been associated with high prostate cancer risk, either overall or in the subgroup of men with low 25-hydroxyvitamin D lev-els.25,26 No chemoprevention trials are under way as hypercalcemia is an unacceptable side effect of supplementation with the natural form of active vitamin D. A large number of vitamin D analogues have been developed, but as yet none exists with absolutely no hypercalcemic potential. The molecular genetic epidemiology of vitamin D and prostate cancer risk is described below.

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