Overview Documents

Prostate Cancer and Hormonally Active Agents

Abstract

Prostate cancer is by far the most frequent cancer among Canadian and American men with a lifetime risk of about 11% for males in these countries and incidence rates about 14 times those in Hong Kong. Age-adjusted incidence rates have increased substantially in Canada, United States and several other countries since at least 1970 and most rapidly during the late 1980's, in parallel to the introduction of the prostate specific antigen (PSA) test for early detection. Both incidence and death rates appear to have decreased somewhat during the most recent few years for which data are available.

Despite much research, the main proven risk factors for prostate cancer risk are non-modifiable: age, family history, and ethnicity. Genes linked to prostate cancer risk include BRCA1, BRCA2 and several genes involved in sex steroid synthesis, transport, activation, inactivation and function. Polymorphisms of genes such as 5a-reductase or AR (androgen receptor) may partially explain the high incidence rates among African-American men (the highest rates in the world). Men with high serum testosterone (T) and low sex hormone binding globulin (SHBG) levels appear to have increased prostate cancer risks.

Energy imbalance resulting in abdominal adiposity or elevated body mass index and elevated serum insulin-like growth factor (IGF-1) levels appears to increase risk. There is inconsistent evidence of an inverse relation between exercise and prostate cancer. Dietary factors related to reduced risks include fruits and vegetables, soyfoods, and antioxidants (vitamin A, vitamin E, selenium, lycopene, ß-carotene); increased risks have been linked to animal fat, red meat and dairy products. Agricultural and other occupations involving pesticide exposure have been linked quite consistently to increased risks; there is also limited evidence of links to other occupations including metal fabricators, electrical power workers and teachers. There is inconsistent evidence of associations with smoking and alcohol consumption and limited evidence of weak associations with previous sexually transmitted infections and vasectomy. At present, the inconsistencies and inadequacies of the epidemiologic studies do not permit firm conclusions about environmental causes of prostate cancer including the potential role of hormonally active contaminants.

Get full text version