ABSTRACT
The etiology of cancer of the prostate remains unclear. Epidemiological studies have suggested that the cause of prostate cancer (PCa) is multifactorial, involving both genetic and environmental risk factors (age, race, geography, diet and hereditary factors) (Ruijter 1999). Some of these risk factors may be related to conditions that can alter vitamin D status. It has been estimated that approximately 10% of prostate cancer cases are hereditary, the majority of PCa (90%) being sporadic. A number of genes have been suggested to be associated with PCa risk, including androgen (AR) and vitamin D receptors (VDR), 5α-reductase, 1α-hydroxylase, 24-hydroxylase, cell cycle regulators and several growth factors (Cussenot et al. 1998, Ylikomi et al. 2001). Many of these genes are regulated by androgens and/or vitamin D. It has been estimated that approximately 6% of prostate cancer mortality is caused by vitamin D deficiency (Hanchette & Schwartz 1992, Schwartz & Hulka 1990). However, the estimate may be influenced by the geographic location. Our own estimation is significantly higher, with the possibility of 26% of PCa cases in Finland being related to vitamin D deficiency due to low UV radiation during the 7 months of the winter season (Ahonen et al. 2000a).
