Prostate Cancer Prevention (PDQ®): Prevention - Health Professional Information [NCI]

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Prostate Cancer Prevention (PDQ®): Prevention - Health Professional Information [NCI]

This information is produced and provided by the National Cancer Institute (NCI). The information in this topic may have changed since it was written. For the most current information, contact the National Cancer Institute via the Internet web site at or call 1-800-4-CANCER.

Prostate Cancer Prevention


Note: Separate PDQ summaries on Prostate Cancer Screening, Prostate Cancer Treatment, and Levels of Evidence for Cancer Screening and Prevention Studies are also available.

Benefits From Finasteride and Dutasteride Chemoprevention

Based on solid evidence, chemoprevention with finasteride and dutasteride reduces the incidence of prostate cancer, but the evidence is inadequate to determine whether chemoprevention with finasteride or dutasteride reduces mortality from prostate cancer.

Magnitude of Effect: Absolute reduction in incidence for more than 7 years with finasteride was 6% (24.4% with placebo and 18.4% with finasteride); relative risk reduction (RRR) for incidence was 24.8% (95% confidence interval [CI], 18.6%–30.6%). There was no difference in the number of men dying from prostate cancer in the two groups, though the number of deaths was small.

In the dutasteride trial, absolute risk reduction was 5.1% at 4 years, and RRR was 22.8% (95% CI, 15.2%–29.8%). There was no difference in prostate cancer or overall mortality. The reduction in prostate cancer incidence occurred primarily in Gleason 5 to 6 cancers. The reduction in incidence primarily in less aggressive cancers (i.e., Gleason 5–6) and not in more aggressive cancers (i.e., Gleason 7–10) raises the question of whether this reduction in incidence would lead to any reduction in mortality. This question is presently unanswered.

Study Design: Two randomized controlled trials; one for finasteride and one for dutasteride.
Internal Validity: Good for the outcome of incidence, poor for the outcome of mortality.
Consistency: Good.
External Validity: Fair for the finasteride trial, because of small numbers of African American and Hispanic men. In the dutasteride trial, all men were at higher risk, with a prostate-specific antigen (PSA) of 2.5 to 10.0. Thus, these results are generalizable primarily to high-risk men.

Harms From Finasteride and Dutasteride Chemoprevention


Men in the finasteride group had statistically significantly more erectile dysfunction, loss of libido, and gynecomastia than men in the placebo group. Men in the finasteride group had a statistically significant incidence of high-grade (Gleason sum 8–10) cancers during the study.[2] Whether this was a histological artifact or not is uncertain.

Magnitude of Effect: Statistically significant increases in the following outcomes were observed in the finasteride group (an additional 9% of men in the finasteride group discontinued therapy at least temporarily because of one of these side effects):

Percentage in finasteride group versus percentage in placebo group:
Reduced volume of ejaculate (60.4% vs. 47.3%).
Erectile dysfunction (67.4% vs. 61.5%).
Loss of libido (65.4% vs. 59.6%).
Gynecomastia (4.5% vs. 2.8%).


Men in the dutasteride group had a higher incidence of decreased libido and erectile dysfunction than men in the placebo group.[1]

Magnitude of Effect: Increases in the following outcomes were observed in the dutasteride group:

Percentage in dutasteride group versus percentage in placebo group:
Decreased libido (3.3% vs. 1.6%).
Erectile dysfunction (9.0% vs. 5.7%).
Study Design: Two randomized controlled trials; one for finasteride and one for dutasteride.
Internal Validity: Both randomized controlled trials (i.e., of finasteride and of dutasteride) used investigator interviews (rather than a patient-completed questionnaire) to examine erectile dysfunction and libido during treatment (rather than both before and during treatment).
Consistency: Good (evidence other than the randomized controlled trial supports these effects).
External Validity: Fair, because of small numbers of African American and Hispanic men. In the dutasteride trial, all men were at higher risk, with a PSA of 2.5 to 10.0. Thus, these results are generalizable primarily to high-risk men.

Other Prevention Interventions

The Selenium and Vitamin E Cancer Prevention Trial (SELECT [NCT00006392]) was a large randomized placebo-controlled trial of vitamin E and selenium. It showed no reduction in prostate cancer period prevalence.[3]

Magnitude of Effect: There was a statistically nonsignificant increase in prostate cancer in the vitamin E group (473 cases; 4.93%) but not in the selenium plus vitamin E group (437 cases; 4.56%) or in the selenium group (432 cases; 4.56%).

Study Design for Vitamin E and Selenium: Randomized, placebo-controlled trial of selenium (200 µg/d from L-selenomethionine), vitamin E (400 IU/d of all-rac-[alpha]-tocopheryl acetate), or both.
Internal Validity: Good.
Consistency: Good.
External Validity: Good.


1. Andriole GL, Bostwick DG, Brawley OW, et al.: Effect of dutasteride on the risk of prostate cancer. N Engl J Med 362 (13): 1192-202, 2010.
2. Thompson IM, Goodman PJ, Tangen CM, et al.: The influence of finasteride on the development of prostate cancer. N Engl J Med 349 (3): 215-24, 2003.
3. Lippman SM, Klein EA, Goodman PJ, 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 301 (1): 39-51, 2009.


Incidence and Mortality

Carcinoma of the prostate is the most common tumor in men in the United States, with an estimated 240,890 new cases and 33,720 deaths expected in 2011.[1] A wide range of estimates of the impact of the disease are notable. The disease is histologically evident in as many as 34% of men in their fifth decade and in up to 70% of men aged 80 years and older.[2,3] Prostate cancer will be diagnosed in almost one-fifth of U.S. men during their lifetime, yet only about 3% of men will be expected to die of the disease.[4] The estimated reduction in life expectancy of men who die of prostate cancer is approximately 9 years.[5]

The extraordinarily high rate of clinically occult prostate cancer in the general population compared with the 20-fold lower likelihood of death from the disease indicates that many of these cancers have low biologic risk. Concordant with this observation are the many series of patients with prostate cancer managed by surveillance alone with relatively good survival rates at 5 and 10 years of follow-up.[6] Data demonstrate, however, that with prolonged 10-year follow-up of moderately differentiated (which constitute the majority of tumors detected [7]) and poorly differentiated tumors, there is a substantial risk of disease progression and death from prostate cancer.[8]

Because of marked variability in tumor differentiation from one microscopic field to another, many pathologists will report the range of differentiation among the malignant cells that are present in a biopsy using the Gleason grading system. This grading system includes five histologic patterns distinguished by the glandular architecture of the cancer. The architectural patterns are identified and assigned a grade from 1 to 5 with 1 being the most differentiated and 5 being the least differentiated. The sum of the grades of the predominant and next most prevalent will range from 2 (well-differentiated tumors) to 10 (undifferentiated tumors).[9,10] Systematic changes to the histological interpretation of biopsy specimens by anatomical pathologists have occurred during the prostate-specific antigen (PSA) screening era (i.e., since about 1985) in the United States.[11] This phenomenon, sometimes called "grade inflation," is the apparent increase in the distribution of high-grade tumors in the population for a period of time but in the absence of a true biological or clinical change. It is possibly the result of an increasing tendency for pathologists to read tumor grade as more aggressive, resulting in a higher preponderance to treat these cancers aggressively.[12]

Treatment options available for prostate cancer include radical prostatectomy, external-beam radiation therapy, brachytherapy, cryotherapy, androgen deprivation with luteinizing hormone-releasing hormone analogs and/or antiandrogens, intermittent androgen deprivation, cytotoxic agents, and surveillance. Of all the means of management, only radical prostatectomy has been found to be superior to surveillance in men with localized prostate cancer in terms of reduced rates of metastases (relative hazard [RH] = 0.63; 95% confidence interval [CI], 0.41–0.96) and disease specific (RH = 0.5; 95% CI, 0.27–0.91) and overall mortalities.[13] However, the relative efficacy of radical prostatectomy to the other forms of treatment has not been adequately addressed.[14] Confounding issues in the treatment of prostate cancer include side effects with treatment, inability to predict the natural history of a given cancer, patient comorbidity that may affect an individual's likelihood of surviving long enough to be at risk for disease morbidity and mortality, and an increasing body of evidence suggesting that careful PSA monitoring following treatment may indicate a substantial fraction of treatment failures.[15]

Because of considerable uncertainty regarding the efficacy of treatment and the difficulty with selecting patients for whom there is a known risk of disease progression, opinion in the medical community is divided regarding screening for carcinoma of the prostate. While both digital rectal examination and PSA screening have demonstrated reasonable performance characteristics (sensitivity, specificity, and positive predictive value) for the early detection of prostate cancer, the lack of evidence that screening and treatment affects ultimate population morbidity or mortality has led many organizations to eschew screening.

The tremendous impact of prostate cancer on the U.S. population and the financial burden of the disease for both patients and society have led to an increased interest in primary disease prevention.


1. American Cancer Society.: Cancer Facts and Figures 2011. Atlanta, Ga: American Cancer Society, 2011. Also available online. Last accessed July 27, 2011.
2. Sakr WA, Haas GP, Cassin BF, et al.: The frequency of carcinoma and intraepithelial neoplasia of the prostate in young male patients. J Urol 150 (2 Pt 1): 379-85, 1993.
3. Hølund B: Latent prostatic cancer in a consecutive autopsy series. Scand J Urol Nephrol 14 (1): 29-35, 1980.
4. Altekruse SF, Kosary CL, Krapcho M, et al.: SEER Cancer Statistics Review, 1975-2007. Bethesda, Md: National Cancer Institute, 2010. Also available online. Last accessed May 20, 2011.
5. Horm JW, Sondik EJ: Person-years of life lost due to cancer in the United States, 1970 and 1984. Am J Public Health 79 (11): 1490-3, 1989.
6. Whitmore WF Jr, Warner JA, Thompson IM Jr: Expectant management of localized prostatic cancer. Cancer 67 (4): 1091-6, 1991.
7. Orozco R, O'Dowd G, Kunnel B, et al.: Observations on pathology trends in 62,537 prostate biopsies obtained from urology private practices in the United States. Urology 51 (2): 186-95, 1998.
8. D'Amico AV, Moul J, Carroll PR, et al.: Cancer-specific mortality after surgery or radiation for patients with clinically localized prostate cancer managed during the prostate-specific antigen era. J Clin Oncol 21 (11): 2163-72, 2003.
9. Gleason DF, Mellinger GT: Prediction of prognosis for prostatic adenocarcinoma by combined histological grading and clinical staging. J Urol 111 (1): 58-64, 1974.
10. Gleason DF: Histologic grading and clinical staging of prostatic carcinoma. In: Tannenbaum M: Urologic Pathology: The Prostate. Philadelphia, Pa: Lea and Febiger, 1977, pp 171-197.
11. Albertsen PC, Hanley JA, Barrows GH, et al.: Prostate cancer and the Will Rogers phenomenon. J Natl Cancer Inst 97 (17): 1248-53, 2005.
12. Thompson IM, Canby-Hagino E, Lucia MS: Stage migration and grade inflation in prostate cancer: Will Rogers meets Garrison Keillor. J Natl Cancer Inst 97 (17): 1236-7, 2005.
13. Holmberg L, Bill-Axelson A, Helgesen F, et al.: A randomized trial comparing radical prostatectomy with watchful waiting in early prostate cancer. N Engl J Med 347 (11): 781-9, 2002.
14. Middleton RG, Thompson IM, Austenfeld MS, et al.: Prostate Cancer Clinical Guidelines Panel Summary report on the management of clinically localized prostate cancer. The American Urological Association. J Urol 154 (6): 2144-8, 1995.
15. Moul JW: Prostate specific antigen only progression of prostate cancer. J Urol 163 (6): 1632-42, 2000.

Risk Factors for Prostate Cancer Development


Prostate cancer incidence escalates dramatically with increasing age. Although it is a very unusual disease in men younger than 50 years, rates increase exponentially thereafter. The registration rate by age cohort in England and Wales increased from eight per thousand population in men aged 50 to 56 years to 68 per thousand in men aged 60 to 64 years; 260 per thousand in men aged 70 to 74 years, and peaked at 406 per thousand in men aged 75 to 79 years.[1] In this same population, the death rate per thousand in 1992 in cohorts of men aged 50 to 54 years, 60 to 64 years, and 70 to 74 years was 4, 37, and 166, respectively.[1] At all ages, incidence of prostate cancer in blacks exceeds those of whites.[2]

Family History

Approximately 15% of men with a diagnosis of prostate cancer will be found to have a first-degree male relative (e.g., brother, father) with prostate cancer, compared with approximately 8% of the U.S. population.[3] Approximately 9% of all prostate cancers may result from heritable susceptibility genes.[4] Several authors have completed segregation analyses, and though a single, rare autosomal gene has been suggested to cause cancer in some of these families, the burden of evidence suggests that the inheritance is considerably more complex.[5,6,7]


The development of the prostate is dependent upon the secretion of dihydrotestosterone (DHT) by the fetal testis. Testosterone causes normal virilization of the Wolffian duct structures and internal genitalia and is acted upon by the enzyme 5 alpha-reductase (5AR) to form DHT. DHT has a 4-fold to 50-fold greater affinity for the androgen receptor than testosterone, and it is DHT that leads to normal prostatic development. Children born with abnormal 5AR (due to a change in a single base pair in exon 5 of the normal type II 5AR gene), are born with ambiguous genitalia (variously described as hypospadias with a blind-ending vagina to a small phallus) but masculinize at puberty because of the surge of testosterone production at that time. Clinical, imaging, and histologic studies of kindreds born with 5AR deficiency have demonstrated a small, pancake-appearing prostate with an undetectable prostate-specific antigen (PSA) level and no evidence of prostatic epithelium.[8] Long-term follow-up demonstrates that neither benign prostatic hyperplasia (BPH) nor prostate cancer develop.

Other evidence suggesting that the degree of cumulative exposure of the prostate to androgens is related to an increased risk of prostate cancer includes the following:

1.Neither BPH nor prostate cancer have been reported in men castrated prior to puberty.[9]
2.Androgen deprivation in almost all forms leads to involution of the prostate, a fall in PSA levels, apoptosis of prostate cancer and epithelial cells, and a clinical response in prostate cancer patients.[10,11]

Ecological studies have found a correlation between serum levels of testosterone, especially DHT, and overall risk of prostate cancer among African American, white, and Japanese males.[12,13,14] However, evidence from prospective studies of the association between serum concentrations of sex hormones, including androgens and estrogens, does not support a direct link.[15] A collaborative analysis of 18 prospective studies, pooling prediagnostic measures on 3,886 men with incident prostate cancer and 6,438 control subjects, found no association between the risk of prostate cancer and serum concentrations of testosterone, calculated-free testosterone, dihydrotestosterone sulfate, androstenedione, androstanediol glucuronide, estradiol, or calculated-free estradiol.[15] A caution for interpreting the data is the unknown degree of correlation between serum levels and prostate tissue level. Androstanediol glucuronide may most closely reflect intraprostatic androgen activity, and this measure was not associated with the risk of prostate cancer. This lack of association affirms that risk stratification cannot be made on serum hormone concentrations.


The risk of developing and dying from prostate cancer is dramatically higher among blacks, is of intermediate levels among whites, and is lowest among native Japanese.[16,17] Conflicting data have been published regarding the etiology of these outcomes, but some evidence is available that access to health care may play a role in disease outcomes.[18]

Dietary Fat

An interesting observation is that although the incidence of latent (occult, histologically evident) prostate cancer is similar throughout the world, clinical prostate cancer varies from country to country by as much as 20-fold.[19] Previous ecologic studies have demonstrated a direct relationship between a country's prostate cancer-specific mortality rate and average total calories from fat consumed by the country's population.[20,21] Studies of immigrants from Japan have demonstrated that native Japanese have the lowest risk of clinical prostate cancer, first generation Japanese-Americans have an intermediate risk, and subsequent generations have a risk comparable to the U.S. population.[22,23] Animal models of explanted human prostate cancer have demonstrated decreased tumor growth rates in animals who are fed a low-fat diet.[24,25] Evidence from many case-control studies has found an association between dietary fat and prostate cancer risk,[26,27,28] though studies have not uniformly reached this conclusion.[29,30,31] In a review of published studies of the relationship between dietary fat and prostate cancer risk, among descriptive studies, approximately half found an increased risk with increased dietary fat and half found no association.[32] Among case-control studies, about half of the studies found an increased risk with increasing dietary fat, animal fat, and saturated and monounsaturated fat intake while approximately half found no association. Only in studies of polyunsaturated fat intake were three studies reported of a significant negative association between prostate cancer and fat intake. Fat of animal origin seems to be associated with the highest risk.[18,33] In a series of 384 patients with prostate cancer, the risk of cancer progression to an advanced stage was greater in men with a high fat intake.[34] The announcement in 1996 that cancer mortality rates had fallen in the United States prompted the suggestion that this may be caused by decreases in dietary fat intake during the same time period.[35,36]

The explanation for this possible association between prostate cancer and dietary fat is unknown. Several hypotheses have been advanced, including:

1.Dietary fat may increase serum androgen levels, thereby increasing prostate cancer risk. This hypothesis is supported by observations from South Africa and the United States that changes in dietary fat intake change urinary and serum levels of androgens.[37,38]
2.Certain types of fatty acids or their metabolites may initiate or promote prostate carcinoma development. The evidence for this hypothesis is conflicting, but one study suggests that linoleic acid (omega-6 polyunsaturated fatty acid) may stimulate prostate cancer cells, while omega-3 fatty acids inhibit cell growth.[39]
3.An observation made in an animal model is that male offspring of pregnant rats who are fed a high-fat diet will develop prostate cancer at a higher rate than animals who are fed a low-fat diet.[40] This observation may explain some of the variations in prostate cancer incidence and mortality among ethnic groups; an observation has been made that first trimester androgen levels in pregnant blacks are higher than those in whites.[41]

Dairy and Calcium Intake

In a meta-analysis of ten cohort studies (eight from the United States and two from Europe), it was concluded that men with the highest intake of dairy products (relative risk [RR] = 1.11; 95% confidence interval [CI], 1.00–1.22; P = .04) and calcium (RR = 1.39; 95% CI, 1.09–1.77; P = .18) were more likely to develop prostate cancer than men with the lowest intake. The pooled RRs of advanced prostate cancer were 1.33 (95% CI, 1.00–1.78; P = .055) for the highest versus lowest intake categories of dairy products and 1.46 (95% CI, 0.65–3.25; P > .2) for the highest versus lowest intake categories of calcium. High intake of dairy products and calcium may be associated with an increased risk of prostate cancer although the increase may be small.[42]

Multivitamin Use

Regular multivitamin use has not been associated with the risk of early or localized prostate cancer.[43]


The Aspirin/Folate Polyp Prevention Study, a placebo-controlled randomized trial of aspirin and folic acid supplementation for the chemoprevention of colorectal adenomas, was conducted between July 6, 1994, and December 31, 2006. In a secondary analysis, the authors addressed the effect of folic acid supplementation on the risk of prostate cancer. Participants were followed for up to 10.8 (median = 7.0, interquartile range = 6.0–7.8) years and asked periodically to report all illnesses and hospitalizations.[44] Supplementation with 1 mg of folic acid was associated with an increased risk of prostate cancer. However, dietary and plasma levels among nonmultivitamin users were inversely associated with risk. These findings highlight the potentially complex role of folate in prostate carcinogenesis.[44,45]

Cadmium Exposure

Cadmium exposure is occupationally associated with nickel-cadmium batteries and cadmium recovery plant smelters and is associated with cigarette smoke.[46] The earliest studies of this agent documented an apparent association, but better-designed studies have failed to note an association.[47,48]

Dioxin Exposure

Dioxin (2,3,7,8 tetrachlorodibenzo-p-dioxin or TCDD) is a contaminant of an herbicide used in Vietnam. This agent is similar to many components of herbicides used in farming. A review of the linkage between dioxin and prostate cancer risk by the National Academy of Sciences Institute of Medicine Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides, found only two articles on prostate cancer with sufficient numbers of cases and follow-up to allow analysis.[49,50] The analysis of all available data suggests that the association between dioxin exposure and prostate cancer is not conclusive.[51]


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14. Wu AH, Whittemore AS, Kolonel LN, et al.: Serum androgens and sex hormone-binding globulins in relation to lifestyle factors in older African-American, white, and Asian men in the United States and Canada. Cancer Epidemiol Biomarkers Prev 4 (7): 735-41, 1995 Oct-Nov.
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17. Bunker CH, Patrick AL, Konety BR, et al.: High prevalence of screening-detected prostate cancer among Afro-Caribbeans: the Tobago Prostate Cancer Survey. Cancer Epidemiol Biomarkers Prev 11 (8): 726-9, 2002.
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24. Wang Y, Corr JG, Thaler HT, et al.: Decreased growth of established human prostate LNCaP tumors in nude mice fed a low-fat diet. J Natl Cancer Inst 87 (19): 1456-62, 1995.
25. Connolly JM, Coleman M, Rose DP: Effects of dietary fatty acids on DU145 human prostate cancer cell growth in athymic nude mice. Nutr Cancer 29 (2): 114-9, 1997.
26. Ross RK, Shimizu H, Paganini-Hill A, et al.: Case-control studies of prostate cancer in blacks and whites in southern California. J Natl Cancer Inst 78 (5): 869-74, 1987.
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29. Giovannucci E: Epidemiologic characteristics of prostate cancer. Cancer 75 (Suppl 7): 1766-1777, 1995.
30. Mettlin C, Selenskas S, Natarajan N, et al.: Beta-carotene and animal fats and their relationship to prostate cancer risk. A case-control study. Cancer 64 (3): 605-12, 1989.
31. Severson RK, Nomura AM, Grove JS, et al.: A prospective study of demographics, diet, and prostate cancer among men of Japanese ancestry in Hawaii. Cancer Res 49 (7): 1857-60, 1989.
32. Zhou JR, Blackburn GL: Bridging animal and human studies: what are the missing segments in dietary fat and prostate cancer? Am J Clin Nutr 66 (6 Suppl): 1572S-1580S, 1997.
33. Rose DP, Boyar AP, Wynder EL: International comparisons of mortality rates for cancer of the breast, ovary, prostate, and colon, and per capita food consumption. Cancer 58 (11): 2363-71, 1986.
34. Bairati I, Meyer F, Fradet Y, et al.: Dietary fat and advanced prostate cancer. J Urol 159 (4): 1271-5, 1998.
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36. Wynder EL, Cohen LA: Correlating nutrition to recent cancer mortality statistics. J Natl Cancer Inst 89 (4): 324, 1997.
37. Hill P, Wynder EL, Garbaczewski L, et al.: Diet and urinary steroids in black and white North American men and black South African men. Cancer Res 39 (12): 5101-5, 1979.
38. Hämäläinen E, Adlercreutz H, Puska P, et al.: Diet and serum sex hormones in healthy men. J Steroid Biochem 20 (1): 459-64, 1984.
39. Rose DP, Connolly JM: Effects of fatty acids and eicosanoid synthesis inhibitors on the growth of two human prostate cancer cell lines. Prostate 18 (3): 243-54, 1991.
40. Kondo Y, Homma Y, Aso Y, et al.: Promotional effect of two-generation exposure to a high-fat diet on prostate carcinogenesis in ACI/Seg rats. Cancer Res 54 (23): 6129-32, 1994.
41. Henderson BE, Bernstein L, Ross RK, et al.: The early in utero oestrogen and testosterone environment of blacks and whites: potential effects on male offspring. Br J Cancer 57 (2): 216-8, 1988.
42. Gao X, LaValley MP, Tucker KL: Prospective studies of dairy product and calcium intakes and prostate cancer risk: a meta-analysis. J Natl Cancer Inst 97 (23): 1768-77, 2005.
43. Lawson KA, Wright ME, Subar A, et al.: Multivitamin use and risk of prostate cancer in the National Institutes of Health-AARP Diet and Health Study. J Natl Cancer Inst 99 (10): 754-64, 2007.
44. Figueiredo JC, Grau MV, Haile RW, et al.: Folic acid and risk of prostate cancer: results from a randomized clinical trial. J Natl Cancer Inst 101 (6): 432-5, 2009.
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51. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides.: Veterans and Agent Orange: Update 1996. In: Washington DC, National Academy Press, 1996.

Opportunities for Prevention

Hormonal Prevention

The Prostate Cancer Prevention Trial (PCPT), a large randomized placebo-controlled trial of finasteride (an inhibitor of alpha-reductase), was performed in 18,882 men aged 55 years or older. At 7 years, the incidence of prostate cancer was 18.4% in the finasteride group versus 24.4% in the placebo group, a relative risk reduction (RRR) of 24.8% (95% confidence interval [CI], 18.6%–30.6%; P < .001). The finasteride group had more patients with Gleason grade 7 to 10, but the clinical significance of Gleason scoring is uncertain in conditions of androgen deprivation.[1] High-grade cancers were noted in 6.4% of finasteride patients, compared with 5.1% of men receiving a placebo. The increase in high-grade tumors was seen within 1 year of finasteride exposure and did not increase during this time period.[2]

Finasteride decreases the risk of prostate cancer but may also alter the detection of disease through effects on prostate-specific antigen (PSA) and decreased prostate volume (24%), creating a detection bias.[3] In men receiving finasteride, varying adjustment factors may be needed to determine whether PSA is in the normal range.[4] There may be an artifactual histological effect of finasteride on Gleason scoring.

It is possible that finasteride induced the development of high-grade epithelial neoplasia, but this has not been demonstrated.[3] With a finasteride-induced development of high-grade prostate cancer, a gradual and progressive increase in the number of high-grade tumors would have been expected for more than 7 years, compared with placebo; however, this was not the case. The increase in high-grade tumors was seen within 1 year of finasteride exposure and did not increase during this time period.[2] A statistical reanalysis of the PCPT data adjusted for the possible bias of decreased prostate volume in men on finasteride, perhaps making it easier to detect prostate cancer in smaller prostate volume. This reanalysis found that finasteride reduced the incidence of Gleason 5 to 7 and Gleason 3 to 4 prostate cancer, but not Gleason 2 to 3 or Gleason 8 to 10. The reduction in the incidence of Gleason 7 (22%) was less than the reduction in the incidence of Gleason 5 (58%) and Gleason 6 (52%).[5]

The Reduction by Dutasteride of Prostate Cancer Events trial randomly assigned 8,231 men aged 50 to 75 years at higher risk of prostate cancer (i.e., PSA 2.5–10.0) with one recent negative prostate biopsy to dutasteride at 0.5 mg daily or to placebo. The primary endpoint was prostate cancer diagnosed by prostate biopsy at 2 years and 4 years after randomization. After 4 years, among the 6,729 men (82% of initial population) who had at least one prostate biopsy, 25.1% of the placebo group and 19.9% of the dutasteride group had been diagnosed with prostate cancer, a statistically significant difference (absolute risk reduction = 5.1% and RRR = 22.8% [95% CI, 15.2%–29.8%]). The RRR in years 3 to 4 was similar to the RRR in years 1 to 2. The difference between the groups was entirely due to a reduction in prostate cancers with Gleason score 5 to 7. For years 3 to 4 there was a statistically significant increase in the dutasteride group compared with the placebo group in prostate cancers with Gleason score 8 to 10 (12 cancers in dutasteride group vs. 1 cancer in placebo group).[6]

Overall, there was no statistically significant difference of high-grade tumors for Gleason 8 to 10 cancers in years 1 to 4 (29 vs. 19, 0.9 vs. 0.6%; P = .15). However, in a retrospective analysis there was a statistically significant difference between years 3 to 4. Because this is a small retrospective subgroup, the finding of an increase in Gleason 8 to 10 cancers is of uncertain validity. However, the finding of no reduction in these cancers is more significant.[6]

There are several plausible explanations for the failure of finasteride or dutasteride to reduce the incidence of Gleason 8 to 10 cancers. Because of this uncertainty, the evidence is currently insufficient to determine the effect of prophylaxis with these drugs on prostate cancer mortality.

Agents that are used for hormonal therapy of existing prostate cancers would be unsuitable for prostate cancer chemoprevention because of the cost and wide variety of side effects including sexual dysfunction, osteoporosis, and vasomotor symptoms (hot flushes).[7] Newer antiandrogens may play a role as preventive agents in the future.[8]

Dietary Prevention With Fruit, Vegetables, and a Low-fat Diet

Results from studies of the association between dietary intake of fruits and vegetables and risk of prostate cancer are not consistent. A study evaluated 1,619 prostate cancer cases and 1,618 controls in a multicenter, multiethnic population. The study found that intake of legumes and yellow-orange and cruciferous vegetables was associated with a lower risk of prostate cancer.[9]

The European Prospective Investigation into Cancer and Nutrition examined the association between fruit and vegetable intake and subsequent prostate cancer. After an average follow-up of 4.8 years, 1,104 men developed prostate cancer among the 130,544 male participants. No statistically significant associations were observed for fruit intake, vegetable intake, cruciferous vegetable intake, or the intake of fruits and vegetables combined.[10]

One study of dietary intervention over a 4-year period with reduced fat and increased consumption of fruit, vegetables, and fiber had no impact on serum PSA levels.[11] It is unknown whether dietary modification through the use of a low-fat, plant-based diet will reduce prostate cancer risk. While this outcome is unknown, multiple additional benefits may be gleaned by such a diet, to include a lower risk of hyperlipidemia, better control of blood pressure, and a lower risk of cardiovascular disease—all of which may merit adoption of such a diet.


Several agents, including alpha-tocopherol, selenium, lycopene, difluoromethylornithine,[12,13,14,15,16] vitamin D,[17,18,19] and isoflavonoids,[20,21] have shown potential in either clinical or laboratory studies for chemoprevention of prostate cancer. Based mainly on clinical trial results, alpha-tocopherol, selenium, and lycopene are receiving the greatest public health interest and are highlighted in the chemoprevention discussions below.

Chemoprevention with selenium and vitamin E

The effects of selenium and vitamin E, alone or in combination, on the risk of prostate cancer were studied in the Selenium and Vitamin E Cancer Prevention Trial (SELECT [NCT00006392]).[22,23,24] SELECT was a randomized, placebo-controlled trial of selenium (200 µg/d from L-selenomethionine), vitamin E (400 IU/d of all rac-[alpha]-tocopheryl acetate), or both (planned follow-up for a minimum of 7 years and a maximum of 12 years) for prostate cancer prevention. The primary endpoint was prostate cancer incidence as determined by routine clinical management.

Neither 200 µg of selenomethionine or 400 IU of synthetic DL-(alpha)-tocopherol, given orally, alone or combined, for a median of 5.5 years had significant effects on the primary or secondary endpoints. A statistically nonsignificant increased incidence of prostate cancer (473 cases) was observed in the vitamin E group but not in the selenium plus vitamin E group (437 cases). Compared with placebo, there was a statistically nonsignificant increase in prostate cancer in the vitamin E group (P = .06) and not in the selenium plus vitamin E group (P = .52) or the selenium group (P = .62). There were no significant differences (all P > .15) in any prespecified secondary cancer endpoints. At 5 years, the cumulative death rate in the placebo group was 38 deaths per 1,000 participants (95% CI, 34 deaths per 1,000 participants to 42 deaths per 1,000 participants).

Chemoprevention with lycopene

Evidence exists that a diet with a high intake of fruits and vegetables is associated with a lower risk of cancer. Which, if any, micronutrients may account for this reduction is unknown. One group of nutrients often postulated as having chemoprevention properties is the carotenoids. Lycopene is the predominant circulating carotenoid in Americans and has a number of potential activities, including an antioxidant effect.[25] It is encountered in a number of vegetables, most notably tomatoes, and is best absorbed if these products are cooked and in the presence of dietary fats or oils.

The earliest studies of the association of lycopene and prostate cancer risk were generally negative before 1995 with only one study of 180 case-control patients showing a reduced risk.[26,27,28,29] In 1995, an analysis of the Physicians' Health Study found a one-third reduction in prostate cancer risk in the group of men with the highest consumption of tomato products when compared with the group with the lowest level of consumption, which was attributed to the lycopene content of these vegetables.[30] This large analysis prompted several subsequent studies, the results of which were mixed.[31,32] A review of the published data concluded that the evidence is weak that lycopene is associated with a reduced risk because previous studies were not controlled for total vegetable intake (i.e., separating the effect of tomatoes from vegetables), dietary intake instruments are poorly able to quantify lycopene intake, and other potential biases.[33] Specific dietary supplementation with lycopene remains to be demonstrated to reduce prostate cancer risk.


1. Thompson IM, Goodman PJ, Tangen CM, et al.: The influence of finasteride on the development of prostate cancer. N Engl J Med 349 (3): 215-24, 2003.
2. Thompson IM, Klein EA, Lippman SM, et al.: Prevention of prostate cancer with finasteride: US/European perspective. Eur Urol 44 (6): 650-5, 2003.
3. Andriole G, Bostwick D, Civantos F, et al.: The effects of 5alpha-reductase inhibitors on the natural history, detection and grading of prostate cancer: current state of knowledge. J Urol 174 (6): 2098-104, 2005.
4. Etzioni RD, Howlader N, Shaw PA, et al.: Long-term effects of finasteride on prostate specific antigen levels: results from the prostate cancer prevention trial. J Urol 174 (3): 877-81, 2005.
5. Kaplan SA, Roehrborn CG, Meehan AG, et al.: PCPT: Evidence that finasteride reduces risk of most frequently detected intermediate- and high-grade (Gleason score 6 and 7) cancer. Urology 73 (5): 935-9, 2009.
6. Andriole GL, Bostwick DG, Brawley OW, et al.: Effect of dutasteride on the risk of prostate cancer. N Engl J Med 362 (13): 1192-202, 2010.
7. Thompson I, Feigl P, Coltman C: Chemoprevention of prostate cancer with finasteride. Important Adv Oncol : 57-76, 1995.
8. Nelson PS, Gleason TP, Brawer MK: Chemoprevention for prostatic intraepithelial neoplasia. Eur Urol 30 (2): 269-78, 1996.
9. Kolonel LN, Hankin JH, Whittemore AS, et al.: Vegetables, fruits, legumes and prostate cancer: a multiethnic case-control study. Cancer Epidemiol Biomarkers Prev 9 (8): 795-804, 2000.
10. Key TJ, Allen N, Appleby P, et al.: Fruits and vegetables and prostate cancer: no association among 1104 cases in a prospective study of 130544 men in the European Prospective Investigation into Cancer and Nutrition (EPIC). Int J Cancer 109 (1): 119-24, 2004 Mar10.
11. Shike M, Latkany L, Riedel E, et al.: Lack of effect of a low-fat, high-fruit, -vegetable, and -fiber diet on serum prostate-specific antigen of men without prostate cancer: results from a randomized trial. J Clin Oncol 20 (17): 3592-8, 2002.
12. Heby O: Role of polyamines in the control of cell proliferation and differentiation. Differentiation 19 (1): 1-20, 1981.
13. Danzin C, Jung MJ, Grove J, et al.: Effect of alpha-difluoromethylornithine, an enzyme-activated irreversible inhibitor of ornithine decarboxylase, on polyamine levels in rat tissues. Life Sci 24 (6): 519-24, 1979.
14. Metcalf BW, Bey P, Danzin C, et al.: Catalytic irreversible inhibition of mammalian ornithine decarboxylase (E.C. by substrate and product analogues. J Am Chem Soc 100(8): 2551-2553, 1978.
15. Heston WD, Kadmon D, Lazan DW, et al.: Copenhagen rat prostatic tumor ornithine decarboxylase activity (ODC) and the effect of the ODC inhibitor alpha-difluoromethylornithine. Prostate 3 (4): 383-9, 1982.
16. Abeloff MD, Slavik M, Luk GD, et al.: Phase I trial and pharmacokinetic studies of alpha-difluoromethylornithine--an inhibitor of polyamine biosynthesis. J Clin Oncol 2 (2): 124-30, 1984.
17. Schwartz GG, Hulka BS: Is vitamin D deficiency a risk factor for prostate cancer? (Hypothesis). Anticancer Res 10 (5A): 1307-11, 1990 Sep-Oct.
18. Eisman JA, Barkla DH, Tutton PJ: Suppression of in vivo growth of human cancer solid tumor xenografts by 1,25-dihydroxyvitamin D3. Cancer Res 47 (1): 21-5, 1987.
19. Chida K, Hashiba H, Fukushima M, et al.: Inhibition of tumor promotion in mouse skin by 1 alpha,25-dihydroxyvitamin D3. Cancer Res 45 (11 Pt 1): 5426-30, 1985.
20. Adlercreutz H, Markkanen H, Watanabe S: Plasma concentrations of phyto-oestrogens in Japanese men. Lancet 342 (8881): 1209-10, 1993.
21. Peterson G, Barnes S: Genistein and biochanin A inhibit the growth of human prostate cancer cells but not epidermal growth factor receptor tyrosine autophosphorylation. Prostate 22 (4): 335-45, 1993.
22. Lippman SM, Klein EA, Goodman PJ, 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 301 (1): 39-51, 2009.
23. Gann PH: Randomized trials of antioxidant supplementation for cancer prevention: first bias, now chance--next, cause. JAMA 301 (1): 102-3, 2009.
24. Gaziano JM, Glynn RJ, Christen WG, et al.: Vitamins E and C in the prevention of prostate and total cancer in men: the Physicians' Health Study II randomized controlled trial. JAMA 301 (1): 52-62, 2009.
25. Gerster H: The potential role of lycopene for human health. J Am Coll Nutr 16 (2): 109-26, 1997.
26. Hsing AW, Comstock GW, Abbey H, et al.: Serologic precursors of cancer. Retinol, carotenoids, and tocopherol and risk of prostate cancer. J Natl Cancer Inst 82 (11): 941-6, 1990.
27. Mills PK, Beeson WL, Phillips RL, et al.: Cohort study of diet, lifestyle, and prostate cancer in Adventist men. Cancer 64 (3): 598-604, 1989.
28. Schuman LM, Mandel JS, Radke A, et al.: Some selected features of the epidemiology of prostatic cancer: Minneapolis-St. Paul, Minnesota case-control study, 1976-1979. [Abstract] Trends in Cancer Incidence: Causes and Practical Implications (Proceedings of a Symposium Held in Oslo, Norway, Aug. 6-7, 1980) pp 345-354.
29. Le Marchand L, Hankin JH, Kolonel LN, et al.: Vegetable and fruit consumption in relation to prostate cancer risk in Hawaii: a reevaluation of the effect of dietary beta-carotene. Am J Epidemiol 133 (3): 215-9, 1991.
30. Giovannucci E, Ascherio A, Rimm EB, et al.: Intake of carotenoids and retinol in relation to risk of prostate cancer. J Natl Cancer Inst 87 (23): 1767-76, 1995.
31. Jain MG, Hislop GT, Howe GR, et al.: Plant foods, antioxidants, and prostate cancer risk: findings from case-control studies in Canada. Nutr Cancer 34 (2): 173-84, 1999.
32. Key TJ, Silcocks PB, Davey GK, et al.: A case-control study of diet and prostate cancer. Br J Cancer 76 (5): 678-87, 1997.
33. Kristal AR, Cohen JH: Invited commentary: tomatoes, lycopene, and prostate cancer. How strong is the evidence? Am J Epidemiol 151 (2): 124-7; discussion 128-30, 2000.

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