From National Cancer Control Policy
Prostate cancer > Prevention

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The causes of prostate cancer are poorly understood and there are no proven prevention measures[1] although researchers continue to examine possible risk factors and preventive approaches.

Risk factors


Increasing age is by far the most important risk factor for prostate cancer, with more than 81% of cases diagnosed in 2010 occurring in men 60 years of age or older[2]. Younger men diagnosed with prostate cancer are more likely to die prematurely from the disease than older men, as there is, on average, more of their lifetime left in which the cancer can progress.


Family history of prostate cancer is also a risk factor for the disease. Between five and 10% of prostate cancers may be due to an inherited genetic predisposition. Men with first-degree relatives diagnosed with prostate cancer are two to three times more likely to develop prostate cancer as men with no affected relatives, and the risk may be higher if a first-degree relative was diagnosed before the age of 60 years[3][4][5].

The genetic basis for familial prostate cancer is not fully understood. Men carrying mutations of the breast cancer susceptibility genes BRCA1 or BRCA2 have an increased risk of several types of cancer, including prostate cancer[6]. Male carriers of BRCA2 mutations have a 3.5-fold increased risk of prostate cancer[7] and an earlier age of onset[8] and have been reported to have poorer survival rates than those without BRCA2 mutations[9][10][11].

A mutation of the gene HOXB13 has also been shown in recent research to substantially increase prostate cancer risk[12].

Sexually transmitted infection

The possibility that sexually transmitted infection (STIs) might increase the risk of prostate cancer has been extensively studied, without producing conclusive evidence that any specific STIs increase prostate cancer risk[13].


Evidence on the links between prostate cancer risk and modifiable lifestyle factors is limited. A comprehensive review of the impact of diet and physical activity on cancer by the World Cancer Research Fund concluded that foods containing lycopene (such as tomato) or selenium probably protect against prostate cancer, while diets high in calcium probably increase the risk[14]. However, a more recent review by the World Cancer Research Fund in 2014 concluded that links between prostate cancer risk and foods containing lycopene and selenium supplements have been downgraded from strong evidence of a decreased risk, to no conclusion possible. Additionally, the link between diets high in calcium and prostate cancer has been downgraded from strong evidence of an increased risk of prostate cancer, to limited evidence[15].

A randomised controlled trial, however, found no evidence that supplementary selenium reduced prostate cancer risk[16].

The World Cancer Research Fund review also concluded that there was limited suggestive evidence that processed meat and milk and dairy products increase the risk of prostate cancer, while fish and pulses, including soy foods, may decrease the risk[14][17].

There is some evidence that heavy alcohol consumption may be associated with a higher risk of prostate cancer[18][19].

Physical activity may be associated with a small reduction in prostate cancer risk[20], while being sedentary for long periods, irrespective of the overall amount of physical activity undertaken, is associated with an increased risk[21].

More research is required before any firm conclusions can be drawn regarding the link between lifestyle factors and prostate cancer risk.

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Chemoprevention, or the use of natural or synthetic agents to reduce the incidence of cancer in those at increased risk, is being investigated but is not in routine use for prostate cancer.

The anti-androgen drug finasteride is thought to prevent prostate cancer, but this apparent benefit was limited to less aggressive cancers and it appeared that risk of more aggressive cancers was increased by the drug[22][23][24]. The United States Food and Drug Administration accepted the December 2010 advice of its Oncologic Drugs Advisory Committee that finasteride and the closely related drug dutasteride “do not have a favourable risk-benefit profile for the proposed use of chemoprevention of prostate cancer in healthy men”[25].

A trial examining selenium and vitamin E supplementation in healthy men (The SELECT trial) found that these agents did not prevent prostate cancer[26] and that supplementation with vitamin E was associated with a significantly increased risk of prostate cancer of 17%[16].

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  1. Harris R, Lohr KN. Screening for prostate cancer: an update of the evidence for the U.S. Preventive Services Task Force. Ann Intern Med 2002 Dec 3;137(11):917-29 Abstract available at
  2. Australian Institute of Health and Welfare. ACIM (Australian Cancer Incidence and Mortality) books. Canberra: AIHW; 2014 Available from:
  3. Bratt O. What should a urologist know about hereditary predisposition to prostate cancer? BJU Int 2007 Apr;99(4):743-7; discussion 747-8 Abstract available at
  4. Johns LE, Houlston RS. A systematic review and meta-analysis of familial prostate cancer risk. BJU Int 2003 Jun;91(9):789-94 Abstract available at
  5. Melia J, Hewitson P, Austoker J. Introduction: Review of screening for prostate cancer. BJU Int 2005 Apr;95 Suppl 3:1-3 Abstract available at
  6. Liede A, Metcalfe K, Hanna D, Hoodfar E, Snyder C, Durham C, et al. Evaluation of the needs of male carriers of mutations in BRCA1 or BRCA2 who have undergone genetic counseling. Am J Hum Genet 2000 Dec;67(6):1494-504 Abstract available at
  7. kConFab Investigators, Willems AJ, Dawson SJ, Samaratunga H, De Luca A, Antill YC, et al. Loss of heterozygosity at the BRCA2 locus detected by multiplex ligation-dependent probe amplification is common in prostate cancers from men with a germline BRCA2 mutation. Clin Cancer Res 2008 May 15;14(10):2953-61 Abstract available at
  8. Agalliu I, Karlins E, Kwon EM, Iwasaki LM, Diamond A, Ostrander EA, et al. Rare germline mutations in the BRCA2 gene are associated with early-onset prostate cancer. Br J Cancer 2007 Sep 17;97(6):826-31 Abstract available at
  9. Dobson R. Prostate cancer patients with BRCA2 mutation face poor survival. BMJ 2008 Jul 10;337:a705 Abstract available at
  10. Hereditary Breast Cancer Study Group, Narod SA, Neuhausen S, Vichodez G, Armel S, Lynch HT, et al. Rapid progression of prostate cancer in men with a BRCA2 mutation. Br J Cancer 2008 Jul 22;99(2):371-4 Abstract available at
  11. Tryggvadóttir L, Vidarsdóttir L, Thorgeirsson T, Jonasson JG, Olafsdóttir EJ, Olafsdóttir GH, et al. Prostate cancer progression and survival in BRCA2 mutation carriers. J Natl Cancer Inst 2007 Jun 20;99(12):929-35 Abstract available at
  12. Ewing CM, Ray AM, Lange EM, Zuhlke KA, Robbins CM, Tembe WD, et al. Germline mutations in HOXB13 and prostate-cancer risk. N Engl J Med 2012 Jan 12;366(2):141-9 Abstract available at
  13. Sutcliffe S. Sexually transmitted infections and risk of prostate cancer: review of historical and emerging hypotheses. Future Oncol 2010 Aug;6(8):1289-311 Abstract available at
  14. 14.0 14.1 World Cancer Research Fund, American Institute for Cancer Research. Food, nutrition, physical activity, and the prevention of cancer: a global perspective. Washington DC: AICR; 2007.
  15. World Cancer Research Fund International. Continuous Update Project Report: Diet, Nutrition, Physical Activity, and Prostate Cancer. World Cancer Research Fund International; 2014 Available from:
  16. 16.0 16.1 Klein EA, Thompson IM Jr, Tangen CM, Crowley JJ, Lucia MS, Goodman PJ, et al. Vitamin E and the risk of prostate cancer: the Selenium and Vitamin E Cancer Prevention Trial (SELECT). JAMA 2011 Oct 12;306(14):1549-56 Abstract available at
  17. Ralph H, Chapman K, Yu X, O'Connel D. The association between omega-3 fatty acid and fish intake and the risk of breast, colon, rectum and prostate cancer: a systematic literature review. Sydney: Cancer Council NSW; 2005.
  18. Middleton Fillmore K, Chikritzhs T, Stockwell T, Bostrom A, Pascal R. Alcohol use and prostate cancer: a meta-analysis. Mol Nutr Food Res 2009 Feb;53(2):240-55 Abstract available at
  19. Gong Z, Kristal AR, Schenk JM, Tangen CM, Goodman PJ, Thompson IM. Alcohol consumption, finasteride, and prostate cancer risk: results from the Prostate Cancer Prevention Trial. Cancer 2009 Aug 15;115(16):3661-9 Abstract available at
  20. Liu Y, Hu F, Li D, Wang F, Zhu L, Chen W, et al. Does physical activity reduce the risk of prostate cancer? A systematic review and meta-analysis. Eur Urol 2011 Nov;60(5):1029-44 Abstract available at
  21. Lynch BM. Sedentary behavior and cancer: a systematic review of the literature and proposed biological mechanisms. Cancer Epidemiol Biomarkers Prev 2010 Nov;19(11):2691-709 Abstract available at
  22. REDUCE Study Group, Andriole GL, Bostwick DG, Brawley OW, Gomella LG, Marberger M, et al. Effect of dutasteride on the risk of prostate cancer. N Engl J Med 2010 Apr 1;362(13):1192-202 Abstract available at
  23. Lebdai S, Bigot P, Azzouzi AR. High-grade prostate cancer and finasteride. BJU Int 2010 Feb;105(4):456-9 Abstract available at
  24. Thompson IM, Goodman PJ, Tangen CM, Lucia MS, Miller GJ, Ford LG, et al. The influence of finasteride on the development of prostate cancer. N Engl J Med 2003 Jul 17;349(3):215-24 Abstract available at
  25. Theoret MR, Ning YM, Zhang JJ, Justice R, Keegan P, Pazdur R. The risks and benefits of 5α-reductase inhibitors for prostate-cancer prevention. N Engl J Med 2011;365(2):97-9 Abstract available at
  26. Lippman SM, Klein EA, Goodman PJ, Lucia MS, Thompson IM, Ford LG, et al. Effect of selenium and vitamin E on risk of prostate cancer and other cancers: the Selenium and Vitamin E Cancer Prevention Trial (SELECT). JAMA 2009 Jan 7;301(1):39-51 Abstract available at

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