Vitamin D performs many critical functions, including helping to build strong bones by assisting in the absorption and use of calcium and phosphorus, and maintaining proper nerve function. Vitamin D also has a significant impact on prostate health through its anticancer properties and it’s demonstrated effect on managing the symptoms of BPH and prostatitis.
Most people have low levels or are deficient in vitamin D, mainly because they do not get sufficient sunlight (the best source of vitamin D) and/or they do not eat enough foods that contain the vitamin. Food, however, is not the best way to meet the body’s requirement for this vitamin, which is why sunlight and supplements are important. The US government’s recommendation for vitamin D is 600 IU daily. Many experts, however, believe this figure is too low including the Vitamin D Council which recommends 5000IU a day.
Vitamin D3 is indirectly derived from lanolin (a fat found in sheep wool). When the sheep are sheared, the wool is washed and lanolin is gathered. A molecule from lanolin can then be synthesized into vitamin D3. There is no lanolin in the end product. Vitamin D3 is not found in large quantities in milk; milk happens to be a good source of vitamin D3 only because milk manufacturers add it.
Vitamin D and Prostate Cancer
The relationship between vitamin D and prostate cancer is controversial. For example, results of the largest and most comprehensive study to date (February 2011) were reported by scientists at the University of Bristol. After reviewing more than 24,000 papers and evaluating the data regarding vitamin D and prostate cancer in 25 papers, they concluded “Published literature provides little evidence to support a major role of vitamin D in preventing prostate cancer or its progression.” (Gilbert 2011)
Numerous previous studies do not agree, however. One of those studies was published in November 2009 in BJU International, in which 26 men who had current prostate cancer were given a daily dose of vitamin D. The PSA levels in five men declined: two by more than 50 percent, two by 25 to 50 percent, and one by less than 25 percent. In the remaining patients, their PSA levels stabilized after treatment with vitamin D for up to 36 months. The investigators did not observe a significant correlation between response to vitamin D and stage of disease, Gleason grade, previous treatments or PSA level at diagnosis or initiation of vitamin D supplementation. However, the authors concluded that “Vitamin D therapy is an effective and well tolerated treatment for patients with asymptomatic progressive prostate cancer, and is a useful addition to the therapeutic options.” (Newsom-Davis 2009)
Stanford University School of Medicine was the site for a review that highlighted the anti-inflammatory capabilities of calcitriol, the hormonally active form of vitamin D. The authors pointed out that calcitriol inhibits both the synthesis and the pro-inflammatory actions of prostaglandins and suppresses the production of pro-inflammatory cytokines in prostate cancer cell studies. Calcitriol can also inhibit tumor angiogenesis, invasion, and metastasis (spread). Based on these findings, the authors hypothesized that the anti-inflammatory actions of calcitriol, “in addition to the other known anti-cancer effects of calcitriol, play an important role in its potential use as a therapeutic agent for PCa [prostate cancer],” and that it “should be evaluated in clinical trials in PCa patients with early or precancerous disease.” (Krishnan 2010)
Vitamin D and BPH
The relationship between vitamin D and BPH has been evaluated in a number of trials. One study evaluated 4,770 participants in the Prostate Cancer Prevention Trial who were free of BPH at baseline. Over seven years, 876 incident BPH cases were documented. When the investigators analyzed factors such as diet, alcohol, and supplement use via a food frequency questionnaire, they determined there were no associations between supplemental antioxidants and BPH risk, and there was “weak evidence for associations of lycopene, zinc, and supplemental vitamin D with reduced risk.” (Kristal 2008)
At least one study has reported that a low level of vitamin D circulating in the blood is linked to a greater risk of having an enlarged prostate or prostate cancer. An epidemiological study of 977 randomly chosen men investigated the prevalence of prostate disease based on blood samples, a questionnaire, and physical examination. Investigators found a 23.1 percent prevalence of BPH, 5.1 percent of prostatitis, and 3.7 percent of prostate cancer. Among other discoveries, the authors reported finding lower levels of vitamin D in men who had BPH and prostate cancer. Because vitamin D inhibits cellular proliferation, the authors noted that “lower levels are confirmatory with its loss of protective role against prostate cancer.” (Galic 2008)
Additional evidence can be found in a study conducted in Italy in which researchers identified how the vitamin D receptor agonist elocalcitol, a synthetic derivative of vitamin D3, is capable of stopping growth of the prostate in men who have BPH. The process by which elocalcitol both stops inflammation and the growth of BPH cells is complex, and involves elocalcitol’s ability to significantly inhibit production of IL-8, a substance involved in BPH pathogenesis, by BPH cells stimulated with inflammatory cytokines, and IL-8-induced proliferation of BPH cells. The authors concluded that their data “provide a mechanistic explanation for the anti-proliferative and anti-inflammatory properties of elocalcitol in BPH cells. (Penna 2009)
Vitamin D and Prostatitis
A review published in the International Journal of Andrology noted that scientists are beginning to appreciate chronic inflammation as a potentially important factor in men who have BPH, as well as the role of bacterial and nonbacterial chronic prostatitis. The authors also pointed out that “the mechanism of action of VDR [vitamin D receptor] agonists supports an important role of chronic inflammation in BPH pathogenesis and strengthens the concept of these agents as a therapeutic option for pharmacological treatmenet of BPH.” (Fibbi 2010)
The Journal of Autoimmunity recently published a study on prostatitis and vitamin D, in which investigators explored the effect of vitamin D receptor silencing on the development of experimental autoimmune prostatitis in mice. They concluded that “vitamin D receptor modulation holds the promise of interfering with autoimmune prostatitis.” (Motrich 2009)
The Vitamin D Council recommends that people take 5,000 IU daily for 2 to 3 months, then ask their healthcare provider for a 25-hydroxyvitamin D test to check their levels. Once individuals know their body’s level of vitamin D, they can adjust the dosage until their blood levels are between 50 and 80 ng/mL. That is the healthy range recommended by the Vitamin D Council and some other experts.
Fibbi B et al. Chronic inflammation in the pathogenesis of benign prostatic hyperplasia. Int J Androl 2010 Jun 1; 33(3): 475-88
Galic J, Simunovic D. Prostate disease prevalence with epidemiological and hormonal analysis in randomly selected male population in Crotia. Coll Anthropol 2008; 32(4):1195-1202.
Gilbert R et al. Associations of circulating and dietary vitamin D with prostate cancer risk: a systematic review and dose-response meta-analysis. Cancer Causes Control 2011 Mar; 22(3): 319-40
Krishnan AV, Feldman D. Molecular pathways mediating the anti-inflammatory effects of calcitriol: implications for prostate cancer chemoprevention and treatment. Endocr Relat Cancer 2010 Jan 29; 17(1): R19-38
Kristal AR et al. Dietary patterns, supplement use, and the risk of symptomatic benign prostatic hyperplasia: results from the prostate cancer prevention trial. Am J Epidemiol. 2008 Apr 15; 167(8):925-34.
Motrich RD et al. Impact of vitamin D receptor activity on experimental autoimmune prostatitis. J Autoimmun 2009 Mar; 32(2): 140-48
Newsom-Davis TE et al. The promiscuous receptor. BJU Int 2009 Nov; 104(9): 1204-7.
Penna G et al. The vitamin D receptor agonist elocalcitol inhibits IL-8-dependent benign prostatic hyperplasia stromal cell proliferation and inflammatory response by targeting the RhoA/Rho kinase and NF-kappaB pathways. Prostate 2009 Apr 1; 69(5): 480-93