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The prostate is the gland below a man's bladder that produces fluid for semen. Prostate cancer is the third most common cause of death from cancer in men of all ages. It is rare in men younger than 40. Levels of a substance called prostate specific antigen (PSA) is often high in men with prostate cancer. However, PSA can also be high with other prostate conditions. Since the PSA test became common, most prostate cancers are found before they cause symptoms. Symptoms of prostate cancer may include Problems passing urine, such as pain, difficulty starting or stopping the stream, or dribbling Low back pain Pain with ejaculation Prostate cancer treatment often depends on the stage of the cancer. How fast the cancer grows and how different it is from surrounding tissue helps determine the stage. Treatment may include surgery, radiation therapy, chemotherapy or control of hormones that affect the cancer.

"Dec. 8 (Bloomberg) -- Drinking coffee may lower the risk of developing the deadliest form of prostate cancer, according to a Harvard Medical School study. In research involving 50,000 men over 20 years, scientists led by Kathryn Wilson at Harvard's Channing Laboratory found that the 5 percent of men who drank 6 or more cups a day had a 60 percent lower risk of developing the advanced form of the disease than those who didn't consume any. The risk was about 20 percent lower for the men who drank 1 to 3 cups a day, and 25 percent lower for those consuming 4 or 5 cups. The study is the first to associate coffee with prostate cancer, contradicting previous research that's found no link. The difference may be because Wilson and colleagues looked for the first time at the link between coffee and different stages of the disease, instead of grouping them all together. More research is needed to confirm the findings, she said. "

ScienceDaily (Mar. 10, 2009) - A study led by researchers at the University of Southern California (USC) found that men who took a daily folic acid supplement of 1 mg daily had more than twice the risk of prostate cancer compared with men who took a placebo.

Demark-Wahnefried W, Price DT, Polascik TJ, Robertson CN, Anderson EE, Paulson DF, Walther PJ, Gannon M, Vollmer RT. Pilot study of dietary fat restriction and flaxseed supplementation in men with prostate cancer before surgery: exploring the effects o

Dalais FS, Meliala A, Wattanapenpaiboon N, Frydenberg M, Suter DA, Thomson WK, Wahlqvist ML. Effects of a diet rich in phytoestrogens on prostate-specific antigen and sex hormones in men diagnosed with prostate cancer. Urology. 2004 Sep;64(3):510-5.

Rise in prostate-specific antigen in men with untreated low-grade prostate cancer is slower during spring-summer. Vieth R, Choo R, Deboer L, Danjoux C, Morton GC, Klotz L. Am J Ther. 2006 Sep-Oct;13(5):394-9. PMID: 16988533 doi: 10.1097/01.mjt.0000174346.36307.02

Phase II study of pomegranate juice for men with rising prostate-specific antigen following surgery or radiation for prostate cancer. Pantuck AJ, Leppert JT, Zomorodian N, Aronson W, Hong J, Barnard RJ, Seeram N, Liker H, Wang H, Elashoff R, Heber D, Aviram M, Ignarro L, Belldegrun A. Clin Cancer Res. 2006 Jul 1;12(13):4018-26. PMID: 16818701

Pilot study of dietary fat restriction and flaxseed supplementation in men with prostate cancer before surgery: exploring the effects on hormonal levels, prostate-specific antigen, and histopathologic features.\nDemark-Wahnefried W, Price DT, Polascik TJ, Robertson CN, Anderson EE, Paulson DF, Walther PJ, Gannon M, Vollmer RT.\nUrology. 2001 Jul;58(1):47-52.\nPMID: 11445478 \ndoi:10.1016/S0090-4295(01)01014-7  

Vieth R, Choo R, Deboer L, Danjoux C, Morton GC, Klotz L. \nRise in prostate-specific antigen in men with untreated low-grade prostate cancer is slower during spring-summer.\nAm J Ther. 2006 Sep-Oct;13(5):394-9.\nPMID: 16988533 [PubMed - indexed for MEDLI

ScienceDaily (July 2, 2006) - Drinking an eight ounce glass of pomegranate juice daily increased by nearly four times the period during which PSA levels in men treated for prostate cancer remained stable, a three-year UCLA study has found.

Lack of association between serum levels of 25-hydroxyvitamin D and the subsequent risk of prostate cancer in Finnish men. Faupel-Badger JM, Diaw L, Albanes D, Virtamo J, Woodson K, Tangrea JA. Cancer Epidemiol Biomarkers Prev. 2007 Dec;16(12):2784-6. PMID: 18086789 doi: 10.1158/1055-9965.EPI-07-0672

"MedWire News: High levels of selenium in the blood may worsen prostate cancer in some men who already have the disease, results of a US study suggest. In recent years, selenium supplements have been promoted as a means of preventing prostate cancer, largely based on observational studies that found higher prostate cancer incidence and mortality in geographical areas that are naturally low in selenium, compared with in those that are naturally high in the mineral. However, the current research findings suggest that "if you already have prostate cancer, it may be a bad thing to take selenium," said study researcher Dr Philip Kantoff, from the Dana-Farber Cancer Institute in Boston, Massachusetts, USA."

Serum vitamin D concentration and prostate cancer risk: a nested case-control study. Ahn J, Peters U, Albanes D, Purdue MP, Abnet CC, Chatterjee N, Horst RL, Hollis BW, Huang WY, Shikany JM, Hayes RB; Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial Project Team. J Natl Cancer Inst. 2008 Jun 4;100(11):796-804. Epub 2008 May 27. PMID: 18505967 doi:10.1093/jnci/djn152 CONCLUSION: The findings of this large prospective study do not support the hypothesis that vitamin D is associated with decreased risk of prostate cancer; indeed, higher circulating 25(OH)D concentrations may be associated with increased risk of aggressive disease. In summary, results from this large prospective study of men who underwent standardized prostate cancer screening in the context of a screening trial do not support the hypothesis that higher serum vitamin D status is associated with decreased risk of prostate cancer. The study showed no association of vitamin D level with nonaggressive disease; however, it raises the possibility that higher vitamin D level may be associated with increased risks for aggressive disease, although a clear monotonic dose-response relationship was lacking. Along with recent reports of adverse associations for higher vitamin D status and risk of pancreatic (32) and esophageal (33,34) cancer, caution should be taken in recommending high doses of vitamin D or sunlight exposure to the general public for prostate cancer prevention. Future analyses are warranted to confirm these results and to further clarify the effects of vitamin D on aggressive prostate cancer.

Vitamin D receptor (VDR) gene polymorphisms and haplotypes, interactions with plasma 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D, and prostate cancer risk. Mikhak B, Hunter DJ, Spiegelman D, Platz EA, Hollis BW, Giovannucci E. Prostate. 2007 Jun 15;67(9):911-23. PMID: 17440943 DOI: 10.1002/pros.20570 RESULTS No association was found between these SNPs or their associated haplotypes and all PC subtypes except that haplotype 2 (A-f-b) with Cdx2 A, Fok1 f, and Bsm1 b alleles and haplotype 3 (A-F-B) with Cdx2 A, Fok1 F and Bsm1 B alleles compared to the most common haplotype (A-F-b), were associated with reduced risk of aggressive PC (high stage or Gleason sum 7; P = 0.02), both with two alleles suspected of being low risk. Carriers of the variant Cdx2 A allele who were deficient in plasma 25-hydroxyvitamin D (15 ng/ml) compared to non-carriers with normal 25-hydroxyvitamin D, had a lower risk of total and poorly differentiated PCs (Gleason sum 7) (P for interaction = 0.02 and 0.04, respectively). Plasma 1,25-dihydroxyvitamin D deficiency (26 pg/ml) was associated with a threefold risk of poorly differentiated PC (P for interaction = 0.01) when comparing carriers of the Cdx2 A allele to non-carriers with normal 1,25-dihydroxyvitamin D. CONCLUSION In this population of men, none of the VDR polymorphisms studied was associated with susceptibility to PC. Carriers of the variant Cdx2 A allele with low plasma 25-hydroxyvitamin D may experience a reduction in risk of total and poorly differentiated prostate cancers compared to non-carriers with adequate 25-hydroxyvitamin D.

LYSAKER, Norway, April 11, 2008-An increased intake of vitamin K2 may reduce the risk of prostate cancer by 35 per cent, suggest results from the European Prospective Investigation into Cancer and Nutrition (EPIC). The findings, based on dietary intake from 11,319 men taking part in the EPIC Heidelberg cohort, are published in this month's issue of the American Journal of Clinical Nutrition.

Whether you're deciding on brachytherapy or are interested in nutraceuticals and diet, Prostate Forum tackles the latest on prostate cancer and beyond, responding with timely information for men of any age or at any stage of treatment.\n\nDr. Myers answer

Nov. 13, 2007 -- Forgoing carbohydrates may slow the growth of prostate cancer, according to preliminary lab tests in mice. The researchers aren't making dietary recommendations for men. But they say the topic deserves further study. "This study showed that cutting carbohydrates may slow tumor growth, at least in mice," Duke University urologist Stephen Freedland, MD, says in a news release.

Plasma selenium, manganese superoxide dismutase, and intermediate- or high-risk prostate cancer. Chan JM, Oh WK, Xie W, Regan MM, Stampfer MJ, King IB, Abe M, Kantoff PW. J Clin Oncol. 2009 Aug 1;27(22):3577-83. Epub 2009 Jun 15. PMID: 19528373 DOI: 10.1200/JCO.2008.18.8938 Conclusion: These data suggest that the relationship between circulating selenium levels at diagnosis and prognostic risk of prostate cancer is modified by SOD2 genotype and indicate caution against broad use of selenium supplementation for men with prostate cancer.

"(NaturalNews) Treatment with vitamin D supplements may slow the progress of , according to a study published in the journal BJU International. In the United States, prostate cancer is the second leading cause of cancer death among men, after lung cancer. Approximately 240,000 new cases are diagnosed every year, leading to 30,000 deaths. Researchers have suspected for nearly two decades that the so-called "sunshine vitamin" may play a role in the risk and progression of prostate cancer, but no studies have previously been conducted on its usefulness as a treatment."

Berberine, a natural product, induces G1-phase cell cycle arrest and caspase-3-dependent apoptosis in human prostate carcinoma cells. Mantena SK, Sharma SD, Katiyar SK. Mol Cancer Ther. 2006 Feb;5(2):296-308. PMID: 16505103 doi: 10.1158/1535-7163.MCT-05-0448 The effectiveness of berberine in checking the growth of androgen-insensitive, as well as androgen-sensitive, prostate cancer cells without affecting the growth of normal prostate epithelial cells indicates that it may be a promising candidate for prostate cancer therapy. The evaluation of ancient herbal medicines may indicate novel strategies for the treatment of prostate cancer, which remains the leading cause of cancer-related deaths in American men (1). In our present investigation, we show that a naturally occurring isoquinoline alkaloid, berberine, significantly inhibits the proliferation and reduces the viability of DU145 and PC-3 as well as LNCaP cells (Fig. 1), which suggests that berberine may be an effective chemotherapeutic agent against both androgen-sensitive and androgen-insensitive prostate cancer cells. Importantly, we found that berberine did not exhibit toxicity to nonneoplastic human prostate epithelial cells under the conditions used, except for a moderate reduction in cell viability at higher concentrations when cells were treated in vitro for an extended period of time. In conclusion, the results of the present study indicate that berberine inhibits proliferation and induces G1-phase arrest and apoptosis in human prostate cancer cells but not in normal human prostate epithelial cells. In addition, we provide mechanistic evidence that berberine-induced apoptosis in prostate carcinoma cells, particularly hormone-refractory prostate carcinoma cells, is mediated through enhanced expression of Bax, disruption of the mitochondrial membrane potential, and activation of caspase-3.