Diet and Nutrition

Associations between dietary factors and prostate cancer risk have been summarized elsewhere [10,13,17,55-57]. Most studies indicate that a high intake of fat, particularly total fat and saturated fat, is a risk factor for prostate cancer, but the strength of the associations is modest [57] and may be greater in African Americans than European Americans [58]. As much as 25% of prostate cancer in the US may be attributable to a high saturated fat intake [59]. However, Whittemore et al. [22] estimated that dietary fat intake may account for only 10-15% of the difference in prostate cancer occurrence between European Americans and African Americans or Asians. A mechanism of an enhancing effect of fat on prostate carcinogenesis is not understood, but several hypotheses, including hormonal mediation, have been discussed elsewhere [13, 17,57,60]. In addition, a high intake of protein and energy and a low intake of dietary fiber and complex carbohydrates have been found associated with increased risk for prostate cancer in some studies [10,13,17,56]. The associations with prostate cancer risk reported for individual nutrients or foods are not very strong, but migration from low-risk areas such as Japan to high risk countries, such as the US, increases risk considerably (see [10,13]). These changes in risk are thought to be due to differences in environment including life-style, particularly dietary habits (see [10,13]). It is conceivable that the combined effects on prostate carcinogenesis of several dietary factors are more important than the separate effects of any individual dietary factor [61]. This notion is consistent with the observed lack of any effect of dietary fat as a single factor on the induction of prostate cancer in animal models whereas epidemiological studies consistently show a positive association between prostate cancer risk and dietary fat intake (see [13,17,61]).

Most studies of effects of dietary changes and the consumption of vegetarian or health food diets on hormonal status ([62-66],summarized in [13]) have not separately addressed effects of dietary fat. However, they clearly indicate that diet can influence circulating hormone levels by changing androgen production rates or the metabolism and clearance of androgens and estrogens. Recently, Dorgan et al. [67] reported that the combination of a high fat-low fiber diet given to healthy men increased total testosterone and testosterone bound to SHBG (sex hormone binding globulin) in the plasma and urinary testosterone excretion as compared to a low fat-high fiber diet, but lowered urinary excretion of estrone, 17^-estradiol, and the 2-hydroxy metabolites of these estrogens. Although these studies did not address the separate effects of single dietary factors such as total fat intake, they indicate that diet can affect sex steroid hormonal status.

There is no consistency among epidemiologic studies of prostate cancer risk and intake of dietary vitamin A and ^-carotene (see [10,13,17]), and it is possible that retinoids or carotenes enhance rather than inhibit prostatic carcinogenesis under certain circumstances or in certain populations [68]. A major retinol metabolite in mammalian species, 9-cis-retinoic acid, strongly inhibited the induction of prostate cancer in a rat model [69], but N-(4-hydroxyphenyl)-retinamide (4-HPR), a synthetic retinoid, did not have any effect [70]. In vitro, however, both 9-cis-retinoic acid and 4-HPR inhibit the growth and induce apoptosis of the androgen-sensitive human prostate cancer LNCaP cell line, and so does all-trans-retinoic acid which only binds to RAR receptors [71-73]. 9-czs-Retinoic acid is a pan-agonist for retinoic acid receptors binding both RAR and RXR receptors, but 4-HPR may act via a non-receptor mechanism [73]. Retinoic acid receptors and androgen receptors both belong to the steroid receptor superfamily [74], which raises the possibility that retinoids may be able to bind to and activate mutated androgen receptors, or that the retinoic acid RAR and/or RXR receptors may activate transcription of androgen-regulated genes, as suggested by studies on regulation by sex steroids and retinoic acid of glutathione-S-transferase in hamster smooth muscle tumor cells [75] and on androgen receptor gene expression in human breast cancer cells [76].

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