There are only few clearly established and strong risk factors for prostate cancer which are consistently observed in epidemiologic studies: (1) African-American descent, (2) a Western life style, in particular Western dietary habits, and (3) a family history of prostate cancer. Less consistently found and weaker risk factors are a history of venereal disease, and employment in farming, the armed services, and the nuclear industry.
Elevation of bioavailable and bioactive androgens in the circulation and in the prostatic target tissue may be an important and biologically very plausible risk factor. As will be detailed later, the results of several animal model studies strongly support this contention, but more research is needed to confirm and further define this association in humans, and to establish its underlying biological mechanisms (increased androgen production or 5a-reductase activity and decreased DHT catabolism) (see also ). Since circulating testosterone levels may be lower in men with a family history of prostate cancer than in other men, hormonal involvement in familial aggregation of prostate cancer risk seems paradoxical and the data suggest that the involvement of androgens in hereditary prostate cancer is different from sporadic prostate cancer. Similarly paradoxical is the well-established inverse relationship between decreasing circulating androgen levels and increasing prostate cancer risk with aging. Although body mass index or obesity does not appear to be a risk factor, there are some indications that muscle mass is positively correlated with risk, perhaps reflecting exposure to endogenous androgens or anabolic steroids. Another risk factor may be increased androgen receptor activity related to genetic polymorphisms in the androgen receptor gene. Heavy alcohol use accompanied with liver disease may increase risk and be related with decreased clearance of estrogens and elevated circulating estrogen levels. Estrogen levels were also elevated in healthy black men living in the US or Africa as compared with European American men, and this is perhaps associated with the very high risk for prostate cancer of black men living in the US. However, no association between risk and circulating estrogen levels was found in nested case-control studies in predominantly European American cohorts. Thus, the epidemiologic evidence for involvement of androgenic and estrogenic steroid hormones in human prostate carcinogenesis remains inconclusive (see also ).
The strongest single risk factor appears to be a Western life style, particularly Western dietary habits, including a high fat intake. It is conceivable that dietary risk factors exert their enhancing effects mediated by a hormonal mechanism that involves androgens. However, it is unlikely that life style is the sole factor that explains the differences in prostate cancer risk between Asian and American populations [10,135]. The single most important combination of risk factors is to be of sub-Saharan African descent and to reside in the US - African Americans have, as a group, twice the risk of white Americans. The reasons for the black-white disparity in prostate cancer rates in the US are not understood. While genetic factors, such as genetically determined elevated 5a-reductase activity, are possibly involved, environmental exposures (in the broadest sense of the term) are probably responsible for a large fraction of this disparity [10,13, 17,189]. A relation with similar racial disparities in exposure to potential carcinogens and high-risk dietary habits has been proposed [13, 22, 58]. A hormonal mechanism may be involved as well, possibly acting in utero, because young African-American men and pregnant African-American women have been reported to have higher circulating levels of androgens and estrogens than European Americans .
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