Data from ecologic and experimental studies clearly show a protective effect of dietary phytoestrogens against prostate cancer. Genetic factors are also of etiologic importance in prostate cancer and there is growing evidence for the importance of a gene-diet interaction in prostate cancer progression. The investigators have recently found a putative genetic interaction for this protective role of phytoestrogens. The overall decreased risk of prostate cancer in men with a high intake of phytoestrogens was strongly modified by a nucleotide sequence variant in the estrogen receptor-beta (ERß) gene. An American study found a similar interactive effect between intake of phytoestrogens, as well as body mass index (BMI), and another nucleotide sequence variant in ERß.The phytoestrogens isoflavonoids and coumestans bind tightly to the estrogen receptor-beta (ERß) and are mainly found in soy and other beans. ERß expression has been found to be involved in progression of prostate cancer, suggesting that phytoestrogens may interact with ERß in the development of prostate cancer. With regard to potential carcinogenic mechanisms, phytoestrogens may be involved in the endocrine control of prostate cell growth by influencing the balance between AR and ERß.Testosterone and its metabolite 5α-dihydrotestosterone (DHT) cause proliferation of prostate epithelial cells through binding to the AR. In contrast, by binding to ERß, 5α androstane-3ß,17ß-diol (3ßAdiol), a metabolite of DHT, represses the expression of AR and thereby inhibits androgen-driven proliferation while promoting cell differentiation. In terms of proliferation, current data suggests a combined stimulatory role of ERα and AR in the prostate whereas ERß inhibits proliferation and stimulates differentiation. Both estrogen ERα and ß have affinity for estradiol whereas phytoestrogens and 3ßAdiol selectively activate ERß. Phytoestrogens should, as a result, be able to restrict cancer growth by acting as a substitute for 3ßAdiol. This is confirmed by experimental studies.