There is good evidence that vitamin D increases survival rates once PCa develops.
A study in Norway with a median time of follow-up was 44.0 months (range, 1.2-154.6) found serum 25(OH)D at medium or high levels were significantly related to better prognosis [RR = 0.33; 95% CI 0.14-0.77; RR = 0.16; 95% CI 0.05-0.43] compared with the low level1.
One way vitamin D reduces the risk of death from PCa is by inhibiting metastasis by blocking signal transducer and activator of transcription 3 (stat3)2.
In PCa cells:
“calcitriol inhibits the synthesis and biological actions of prostaglandins (PGs) by three actions: (i) the inhibition of the expression of cyclooxygenase-2 (COX-2), the enzyme that synthesizes PGs, (ii) the upregulation of the expression of 15-prostaglandin dehydrogenase (15-PGDH), the enzyme that inactivates PGs and (iii) decreasing the expression of EP and FP PG receptors that are essential for PG signaling. Since PGs have been shown to promote carcinogenesis and progression of multiple cancers, it is hypothesize that the inhibition of the PG pathway contributes to the ability of 1,25(OH)2D3 to prevent or inhibit PCa development and growth. It was shown that the combination of 1,25(OH)2D3 and non-steroidal anti-inflammatory drugs (NSAIDs) result in a synergistic inhibition of the growth of PCa cell cultures and this combination therapy offers a potential therapeutic strategy. In a clinical trial combining the non-selective NSAID naproxen with 1,25(OH)2D3 in men with early recurrent PCa. The results indicate that the combination of high dose weekly 1,25(OH)2D3 with naproxen slows the rate of rise (doubling time) of PSA in most patients indicating the slowing of disease progression. Further studies are warranted to determine the role of this combination therapy in the management of recurrent PCa”3.
“1,25(OH)2D3 increases the expression of mitogen-activated protein kinase phosphatase 5 in prostate cells resulting in the subsequent inhibition of p38 stress kinase signaling and the attenuation of the production of pro-inflammatory cytokines. Third, 1,25(OH)2D3 also exerts anti-inflammatory activity in PCa through the inhibition of nuclear factor-kappaB signaling that results in potent anti-inflammatory and anti-angiogenic effects. Other important direct effects of 1,25(OH)2D3 as well as the consequences of its anti-inflammatory effects include the inhibition of tumor angiogenesis, invasion, and metastasis”4.
A study in Sweden with PCa cells found that 1,25(OH)2D3 regulates prostate cell biology via multiple pathways and targeting specific pathways for 1,25(OH)2D3 might provide more effective therapies compared to the vitamin D therapies currently clinically tested5.
Page last edited: 24 August 2011
- Tretli, S. Hernes, E. Berg, J. P. Hestvik, U. E. Robsahm, T. E. Association between serum 25(OH)D and death from prostate cancer. Br J Cancer. 2009 Feb 10; 100 (3): 450-4.
- Grant, W. B. Vitamin D may reduce prostate cancer metastasis by several mechanisms including blocking Stat3. Am J Pathol. 2008 Nov; 173 (5): 1589-90.
- Krishnan, A. V. Srinivas, S. Feldman, D. Inhibition of prostaglandin synthesis and actions contributes to the beneficial effects of calcitriol in prostate cancer. Dermatoendocrinol. 2009 Jan; 1 (1): 7-11.
- Krishnan, A. V. Feldman, D. Molecular pathways mediating the anti-inflammatory effects of calcitriol: implications for prostate cancer chemoprevention and treatment. Endocr Relat Cancer. 2010 Mar; 17 (1): R19-38.
- Karlsson, S. Olausson, J. Lundh, D. Sogard, P. Mandal, A. Holmstrom, K. O. Stahel, A. Bengtsson, J. Larsson, D. Vitamin D and prostate cancer: the role of membrane initiated signaling pathways in prostate cancer progression. J Steroid Biochem Mol Biol. 2010 Jul; 121 (1-2): 413-6.