Prostate cancer risk factors

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Overview

Common risk factors in the development of prostate cancer are family history, African American men, dietary factors, obesity, elevated blood levels of testosterone, inherited gene mutation, inflammation of the prostate, tall adult height, exposure to pesticides, and occupational exposures.

Risk Factors

Common risk factors in the development of prostate cancer include:

  • Age
  • Ethnicity
  • Diet
  • Animal fat
  • vegetables
  • Lycopene and tomato based products
  • Soy intake
  • omega 3-fatty acids
  • caffeine
  • Vitamins and minerals
  • Multivitamins
  • Folic acid and Vitamin B12
  • selenium
  • zinc
  • Calcium and Vitamin D
  • Cigarette Smoking
  • Hormones levels and Obesity
  • Sex hormones
  • Insulin and Insulin like growth factor
  • Obesity
  • Physical activity
  • Other factors
  • 5 Alpha reductase inhibitor
  • Prostatitis
  • Trichomonas Vaginalis infection
  • Environmental Carcinogen
  • Agent Orange
  • Choldecone
  • Bisphenol A
  • NSAIDS
  • Vasectomy
  • Ultraviolet light exposure

EBRT for rectal cancer

AGE

  • Prostate cancer has strongest relationships between age and any human malignancy.
  • Prostate cancer rarely occurs before the age of 40.
  • The incidence rises rapidly and the annual incidence of new cases of prostate cancer in white men in 1995 was approximately 0.1, 0.6, and 1 percent in men in their 50s, 60s, and 70s, respectively[1].

ETHNICITY

  • Prostate cancer is more common in black than white or Hispanic men.[2]
  • African American men have higher serum PSA levels, worse Gleason scores, and more advanced stage of disease at the time of diagnosis[3].

DIET

  • The association between intake of nutrients and the risk of prostate cancer are available[4].
  • Animal fat —
    • A diet high in animal fat may be an important factor in the development of prostate cancer[5].
    • Intake of large amounts of alpha-linolenic acid and low amounts of linoleic acid appear to be associated with increased risk[6].
  • Vegetables —
    • A diet low in vegetables may be another risk factor for prostate cancer[7].
    • There is higher prostate cancer risk in men who consume fewer than 14 servings of vegetables weekly.[7].
    • There was no association between fruit and/or vegetable consumption and the risk of prostate cancer[8]
  • Lycopene and tomato based products —
    • Tomato-based products are rich in lycopene has potent anti-oxidant properties.
    • There is only limited evidence to support an association between tomato consumption and reduced prostate cancer risk[9].
    • Dietary intake of lycopene is associated with a lower incidence of prostate cancer and a decreased risk of lethal prostate cancer[10].
  • Soy intake —
    • Phytoestrogens (flavones, isoflavones, lignans) are naturally occurring plant compounds that have estrogen-like activity.
    • Phytoestrogens found in soy foods may reduce prostate cancer risk either via their inherent estrogenic properties, or by inhibition of the enzyme 5-AR.
  • Omega-3 fatty acids —
    • High levels of omega-3 fatty acids, such as fish oil, were associated with an increased risk of high grade prostate cancer[11].
  • Coffee —
    • Increasing consumption of coffee appears to be associated with a decreased risk of lethal prostate cancer.[12]

Vitamin and mineral supplements

  • Multivitamins-
    • The regular use of multivitamins does not appear to affect the risk of early or localized prostate cancer[13].
    • There is increased risk of advanced or fatal prostate cancer in men using relatively large amounts of multivitamins[14].
  • Folic acid and B12 — High serum folic acid and B12 levels may be associated with a small increase in the risk of prostate cancer. Data supporting a possible causal relationship come from cohort studies and from a secondary analysis of a randomized trial.
  • Selenium — The relationship between prostate cancer, and selenium intake and level is complex.In the subset of cases where selenium levels were measured in the blood, the selenium level was not associated with a difference in the risk of prostate cancer (odds ratio 1.01, 95% CI 0.83-1.23). However, high blood levels were associated with lower risk of aggressive disease (advanced-stage disease and/or prostate cancer death).
  • Zinc — At least two studies have suggested an association between zinc supplement use and an increased risk of prostate cancer[15]. In the Health Professionals Follow-Up Study, which included 46,974 American men, 2901 cases of prostate cancer were diagnosed over a 14 year period. Compared with nonusers, men who consumed over 100 mg of supplemental zinc daily had a 2.29-fold increased risk of prostate cancer; the RR was 2.37 in those who took zinc for 10 or more years.
  • Calcium and vitamin D — A link between intake of dairy products and calcium and a higher risk of prostate cancer risk has been suggested in many[16].There was no statistically significant trend in overall prostate cancer risk associated with the serum vitamin D levels, although higher levels of vitamin D were associated with increased aggressiveness in those men diagnosed with prostate cancer, as manifested by Gleason score ≥7 or stage III or IV disease at diagnosis[17].

CIGARETTE SMOKING

  • Cigarette smoking may have an effect on both the risk of developing prostate cancer and its prognosis once a diagnosis is established.While most case-control studies have found either an increased risk for prostate cancer or more frequent high-grade prostate cancer and advanced stages in smokers[18].There are consistent data on the association of smoking at the time of diagnosis with risk of a cancer recurrence and cancer-related mortality[19].Men with prostate cancer should be strongly encouraged to stop smoking.

HORMONE LEVELS AND OBESITY

  • Sex hormones and Insulin like growth factor-The most definitive data regarding the relationship between serum sex hormone levels and prostate cancer come from a pooled analysis of 18 prospective trials, which included 3886 men with prostate cancer and 6438 controls[20]. Serum concentrations of testosterone, dihydrotestosterone (DHT), and other active androgen derivatives obtained prior to diagnosis were NOT associated with an increased risk of subsequent prostate cancer. In addition, no association was seen with pre-diagnosis serum levels of estrogens (estradiol, free estradiol).In addition, testosterone supplementation as a treatment for hypogonadism does not appear to be associated with an increased risk of prostate cancer, although monitoring for prostate abnormalities is recommended.A meta-analysis based upon individual patient data from 3700 men with prostate cancer and 5200 controls found a modest increased risk of prostate cancer in those men with the highest circulating levels of IGF[21]. The association appeared strongest for low-grade, rather than high-grade, prostate cancers.
  • Obesity-meta-analyses have consistently demonstrated a small but statistically significant association between obesity and prostate cancer incidence[22].There is a clear relationship between obesity and disease aggressiveness, with an increase in both biochemical recurrence rate following treatment and prostate cancer-specific mortality[23].
  • Physical activity-There was no association overall between prostate cancer incidence and total, vigorous or non-vigorous physical activity in the entire population. However, men over the age of 65 who were in the highest category of vigorous activity (more than three hours per week of vigorous activity) had a significantly lower risk of advanced (relative risk [RR] 0.33, 95% CI 0.17-0.62) or fatal (RR 0.26, 95% CI 0.11-0.66) prostate cancer. Younger men derived no benefit. However, in all age groups, men with high levels of physical activity (more than 29 metabolic equivalent hours versus none) were less likely to be diagnosed with high-grade (Gleason score ≥7) prostate cancers.In contrast to these data, another report from the same investigators suggests that young lean men who are more physically active have an increased risk of developing metastatic disease and fatal prostate cancer if they had a high energy intake[24].

5-alpha reductase inhibitors

  • 5-alpha reductase inhibitors lower the prostate-specific antigen (PSA), they potentially increase the risk of high-grade prostate cancer.

Prostatitis

  • The available data from case-control studies, cohort studies, and meta-analyses suggest a significant but modest increase (approximately 1.5- to 2-fold) in the risk of prostate cancer in men with prostatitis, but the data are generally of low quality and the relationship between prostatitis and prostate cancer remains unclear in African Americans[25]. Despite a significant body of work relating inflammation to cancer, a cause and effect relationship has not been established between prostate cancer and prostatitis

Trichomonas vaginalis infection

  • Case-control series from the Health Professionals Follow-up Study and the Physician's Health Study both have shown an increased incidence of seropositivity for antibodies against trichomonas vaginalis in men who subsequently are diagnosed with prostate cancer[26].
  • This association was more pronounced in those with more advanced or higher Gleason grade tumors.

Environmental carcinogens

  • Agent Orange — Exposure to Agent Orange, an herbicide defoliant sprayed extensively in Vietnam between 1965 and 1971 that contained dioxins, appears to be associated with an increased incidence of prostate cancer. The cases of prostate cancer arising in those exposed to Agent Orange appear to be more aggressive[27]
  • Chlordecone — Chlordecone is an organochlorine insecticide with estrogenic properties, which was widely used in the West Indies from 1973 to 1993. Chlordecone has been shown to be carcinogenic in laboratory animal models. A case-control series compared plasma levels of chlordecone and exposure history in 623 men with prostate cancer with 671 controls[28]. There was a statistically significant increase in the incidence of prostate cancer, which was related to the measured level of this agent as well as exposure history.
  • Bisphenol A — Exposure to abnormal concentrations of estrogen early in life may initiate changes in prostate stem cells. These changes have been postulated to persist into later life and potentially contribute to the development of prostate cancer[29].

NSAIDs

  • Intake of aspirin and other nonsteroidal antiinflammatory drugs (NSAIDs) has been associated with a decreased risk of some cancers, particularly colorectal cancer. An inverse association between long-term NSAID use and prostate cancer risk has also been suggested,
  • A meta-analysis that looked specifically at the potential effects of aspirin analyzed data from 24 observational studies[30]. There was a decreased risk for the overall incidence of prostate cancer and for advanced prostate cancer (RRs 0.86, 95% CI 0.81-0.92, and 0.83, 95% CI 0.75-0.91, respectively).

Vasectomy

  • Whether a prior vasectomy also increases a man's risk of getting prostate cancer is controversial, with some, but not all, studies showing a weak association.
  • In a European Prospective Investigation into Cancer and Nutrition (EPIC) study, 84,753 men were followed for an average of 15 years. In this series, 4377 men were diagnosed with prostate cancer, including 641 who had a prior vasectomy[31]. There was no statistically significant association between prior vasectomy and prostate cancer incidence or death.
  • In a cohort study of almost 50,000 men in the Health Professionals Follow-up Study, 6023 men developed prostate cancer[32]. On multivariable analysis incorporating a range of potentially confounding factors, vasectomy was associated with a statistically significant increase in the risk of high-grade (Gleason 8 to 10), lethal (death or the development of metastatic disease), or advanced (T3b or higher, or lethal) prostate cancer (RRs 1.22, 1.19, and 1.20, respectively).
  • A meta-analysis that incorporated data from 16 cohort studies, 33 case-control series, and 4 cross-sectional studies concluded that there was at most a weak association between vasectomy and prostate cancer, and that there was no association with high-grade, advanced, or fatal disease[33].

Ultraviolet light exposure

  • In one case-control study exposure to ultraviolet (UV) light had a protective effect on the development of prostate cancer[34].

Although the mechanism underlying this association is unclear, involvement of vitamin D and/or its receptor has been hypothesized[35].

EBRT for rectal cancer

  • Although external beam radiation therapy (EBRT) for prostate cancer is associated with an increased risk of rectal cancer, RT for rectal cancer has not been associated with an increased risk of subsequent prostate cancer.

In a study based upon the Surveillance, Epidemiology, and End Results (SEER) database, the risk of prostate cancer was decreased by 72 percent in 1572 men who had previously received EBRT as a component of their treatment for rectal cancer[36].

References

  1. ↑ Hankey BF, Feuer EJ, Clegg LX, Hayes RB, Legler JM, Prorok PC, Ries LA, Merrill RM, Kaplan RS (June 1999). "Cancer surveillance series: interpreting trends in prostate cancer--part I: Evidence of the effects of screening in recent prostate cancer incidence, mortality, and survival rates". J. Natl. Cancer Inst. 91 (12): 1017–24. PMID 10379964.
  2. ↑ Baquet CR, Horm JW, Gibbs T, Greenwald P (April 1991). "Socioeconomic factors and cancer incidence among blacks and whites". J. Natl. Cancer Inst. 83 (8): 551–7. PMID 2005640.
  3. ↑ Powell IJ, Banerjee M, Sakr W, Grignon D, Wood DP, Novallo M, Pontes E (January 1999). "Should African-American men be tested for prostate carcinoma at an earlier age than white men?". Cancer. 85 (2): 472–7. PMID 10023717.
  4. ↑ Chan JM, Gann PH, Giovannucci EL (November 2005). "Role of diet in prostate cancer development and progression". J. Clin. Oncol. 23 (32): 8152–60. doi:10.1200/JCO.2005.03.1492. PMID 16278466.
  5. ↑ Giovannucci E, Rimm EB, Colditz GA, Stampfer MJ, Ascherio A, Chute CG, Chute CC, Willett WC (October 1993). "A prospective study of dietary fat and risk of prostate cancer". J. Natl. Cancer Inst. 85 (19): 1571–9. PMID 8105097.
  6. ↑ Sinha R, Park Y, Graubard BI, Leitzmann MF, Hollenbeck A, Schatzkin A, Cross AJ (November 2009). "Meat and meat-related compounds and risk of prostate cancer in a large prospective cohort study in the United States". Am. J. Epidemiol. 170 (9): 1165–77. doi:10.1093/aje/kwp280. PMC 2781742. PMID 19808637.
  7. ↑ 7.0 7.1 Cohen JH, Kristal AR, Stanford JL (January 2000). "Fruit and vegetable intakes and prostate cancer risk". J. Natl. Cancer Inst. 92 (1): 61–8. PMID 10620635.
  8. ↑ Kirsh VA, Peters U, Mayne ST, Subar AF, Chatterjee N, Johnson CC, Hayes RB (August 2007). "Prospective study of fruit and vegetable intake and risk of prostate cancer". J. Natl. Cancer Inst. 99 (15): 1200–9. doi:10.1093/jnci/djm065. PMID 17652276.
  9. ↑ Kavanaugh CJ, Trumbo PR, Ellwood KC (July 2007). "The U.S. Food and Drug Administration's evidence-based review for qualified health claims: tomatoes, lycopene, and cancer". J. Natl. Cancer Inst. 99 (14): 1074–85. doi:10.1093/jnci/djm037. PMID 17623802.
  10. ↑ Zu K, Mucci L, Rosner BA, Clinton SK, Loda M, Stampfer MJ, Giovannucci E (February 2014). "Dietary lycopene, angiogenesis, and prostate cancer: a prospective study in the prostate-specific antigen era". J. Natl. Cancer Inst. 106 (2): djt430. doi:10.1093/jnci/djt430. PMC 3952200. PMID 24463248.
  11. ↑ Brasky TM, Till C, White E, Neuhouser ML, Song X, Goodman P, Thompson IM, King IB, Albanes D, Kristal AR (June 2011). "Serum phospholipid fatty acids and prostate cancer risk: results from the prostate cancer prevention trial". Am. J. Epidemiol. 173 (12): 1429–39. doi:10.1093/aje/kwr027. PMC 3145396. PMID 21518693.
  12. ↑ Wilson KM, Kasperzyk JL, Rider JR, Kenfield S, van Dam RM, Stampfer MJ, Giovannucci E, Mucci LA (June 2011). "Coffee consumption and prostate cancer risk and progression in the Health Professionals Follow-up Study". J. Natl. Cancer Inst. 103 (11): 876–84. doi:10.1093/jnci/djr151. PMC 3110172. PMID 21586702.
  13. ↑ Lawson KA, Wright ME, Subar A, Mouw T, Hollenbeck A, Schatzkin A, Leitzmann MF (May 2007). "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. doi:10.1093/jnci/djk177. PMID 17505071.
  14. ↑ Stevens VL, McCullough ML, Diver WR, Rodriguez C, Jacobs EJ, Thun MJ, Calle EE (August 2005). "Use of multivitamins and prostate cancer mortality in a large cohort of US men". Cancer Causes Control. 16 (6): 643–50. doi:10.1007/s10552-005-0384-5. PMID 16049802.
  15. ↑ Leitzmann MF, Stampfer MJ, Wu K, Colditz GA, Willett WC, Giovannucci EL (July 2003). "Zinc supplement use and risk of prostate cancer". J. Natl. Cancer Inst. 95 (13): 1004–7. PMID 12837837.
  16. ↑ Giovannucci E, Liu Y, Stampfer MJ, Willett WC (February 2006). "A prospective study of calcium intake and incident and fatal prostate cancer". Cancer Epidemiol. Biomarkers Prev. 15 (2): 203–10. doi:10.1158/1055-9965.EPI-05-0586. PMID 16492906.
  17. ↑ Ahn J, Peters U, Albanes D, Purdue MP, Abnet CC, Chatterjee N, Horst RL, Hollis BW, Huang WY, Shikany JM, Hayes RB (June 2008). "Serum vitamin D concentration and prostate cancer risk: a nested case-control study". J. Natl. Cancer Inst. 100 (11): 796–804. doi:10.1093/jnci/djn152. PMC 3703748. PMID 18505967.
  18. ↑ Ho T, Howard LE, Vidal AC, Gerber L, Moreira D, McKeever M, Andriole G, Castro-Santamaria R, Freedland SJ (October 2014). "Smoking and risk of low- and high-grade prostate cancer: results from the REDUCE study". Clin. Cancer Res. 20 (20): 5331–8. doi:10.1158/1078-0432.CCR-13-2394. PMC 4199866. PMID 25139338.
  19. ↑ Kenfield SA, Stampfer MJ, Chan JM, Giovannucci E (June 2011). "Smoking and prostate cancer survival and recurrence". JAMA. 305 (24): 2548–55. doi:10.1001/jama.2011.879. PMC 3562349. PMID 21693743.
  20. ↑ Roddam AW, Allen NE, Appleby P, Key TJ (February 2008). "Endogenous sex hormones and prostate cancer: a collaborative analysis of 18 prospective studies". J. Natl. Cancer Inst. 100 (3): 170–83. doi:10.1093/jnci/djm323. PMC 6126902. PMID 18230794.
  21. ↑ Roddam AW, Allen NE, Appleby P, Key TJ, Ferrucci L, Carter HB, Metter EJ, Chen C, Weiss NS, Fitzpatrick A, Hsing AW, Lacey JV, Helzlsouer K, Rinaldi S, Riboli E, Kaaks R, Janssen JA, Wildhagen MF, Schröder FH, Platz EA, Pollak M, Giovannucci E, Schaefer C, Quesenberry CP, Vogelman JH, Severi G, English DR, Giles GG, Stattin P, Hallmans G, Johansson M, Chan JM, Gann P, Oliver SE, Holly JM, Donovan J, Meyer F, Bairati I, Galan P (October 2008). "Insulin-like growth factors, their binding proteins, and prostate cancer risk: analysis of individual patient data from 12 prospective studies". Ann. Intern. Med. 149 (7): 461–71, W83–8. PMC 2584869. PMID 18838726.
  22. ↑ MacInnis RJ, English DR (October 2006). "Body size and composition and prostate cancer risk: systematic review and meta-regression analysis". Cancer Causes Control. 17 (8): 989–1003. doi:10.1007/s10552-006-0049-z. PMID 16933050.
  23. ↑ Allott EH, Masko EM, Freedland SJ (May 2013). "Obesity and prostate cancer: weighing the evidence". Eur. Urol. 63 (5): 800–9. doi:10.1016/j.eururo.2012.11.013. PMC 3597763. PMID 23219374.
  24. ↑ Platz EA, Leitzmann MF, Michaud DS, Willett WC, Giovannucci E (December 2003). "Interrelation of energy intake, body size, and physical activity with prostate cancer in a large prospective cohort study". Cancer Res. 63 (23): 8542–8. PMID 14679023.
  25. ↑ Perletti G, Monti E, Magri V, Cai T, Cleves A, Trinchieri A, Montanari E (December 2017). "The association between prostatitis and prostate cancer. Systematic review and meta-analysis". Arch Ital Urol Androl. 89 (4): 259–265. doi:10.4081/aiua.2017.4.259. PMID 29473374.
  26. ↑ Sutcliffe S, Giovannucci E, Alderete JF, Chang TH, Gaydos CA, Zenilman JM, De Marzo AM, Willett WC, Platz EA (May 2006). "Plasma antibodies against Trichomonas vaginalis and subsequent risk of prostate cancer". Cancer Epidemiol. Biomarkers Prev. 15 (5): 939–45. doi:10.1158/1055-9965.EPI-05-0781. PMID 16702374.
  27. ↑ Zafar MB, Terris MK (July 2001). "Prostate cancer detection in veterans with a history of Agent Orange exposure". J. Urol. 166 (1): 100–3. PMID 11435832.
  28. ↑ Multigner L, Ndong JR, Giusti A, Romana M, Delacroix-Maillard H, Cordier S, Jégou B, Thome JP, Blanchet P (July 2010). "Chlordecone exposure and risk of prostate cancer". J. Clin. Oncol. 28 (21): 3457–62. doi:10.1200/JCO.2009.27.2153. PMID 20566993.
  29. ↑ Lobaccaro JM, Trousson A (March 2014). "Environmental estrogen exposure during fetal life: a time bomb for prostate cancer". Endocrinology. 155 (3): 656–8. doi:10.1210/en.2014-1057. PMID 24564415.
  30. ↑ Huang TB, Yan Y, Guo ZF, Zhang XL, Liu H, Geng J, Yao XD, Zheng JH (September 2014). "Aspirin use and the risk of prostate cancer: a meta-analysis of 24 epidemiologic studies". Int Urol Nephrol. 46 (9): 1715–28. doi:10.1007/s11255-014-0703-4. PMID 24687637.
  31. ↑ Smith K, Byrne, Castaño JM, Chirlaque MD, Lilja H, Agudo A, Ardanaz E, Rodríguez-Barranco M, Boeing H, Kaaks R, Khaw KT, Larrañaga N, Navarro C, Olsen A, Overvad K, Perez-Cornago A, Rohrmann S, Sánchez MJ, Tjønneland A, Tsilidis KK, Johansson M, Riboli E, Key TJ, Travis RC (April 2017). "Vasectomy and Prostate Cancer Risk in the European Prospective Investigation Into Cancer and Nutrition (EPIC)". J. Clin. Oncol. 35 (12): 1297–1303. doi:10.1200/JCO.2016.70.0062. PMC 5455458. PMID 28375714.
  32. ↑ Siddiqui MM, Wilson KM, Epstein MM, Rider JR, Martin NE, Stampfer MJ, Giovannucci EL, Mucci LA (September 2014). "Vasectomy and risk of aggressive prostate cancer: a 24-year follow-up study". J. Clin. Oncol. 32 (27): 3033–8. doi:10.1200/JCO.2013.54.8446. PMC 4162499. PMID 25002716.
  33. ↑ Bhindi B, Wallis C, Nayan M, Farrell AM, Trost LW, Hamilton RJ, Kulkarni GS, Finelli A, Fleshner NE, Boorjian SA, Karnes RJ (September 2017). "The Association Between Vasectomy and Prostate Cancer: A Systematic Review and Meta-analysis". JAMA Intern Med. 177 (9): 1273–1286. doi:10.1001/jamainternmed.2017.2791. PMC 5710573. PMID 28715534. Vancouver style error: initials (help)
  34. ↑ Luscombe CJ, Fryer AA, French ME, Liu S, Saxby MF, Jones PW, Strange RC (August 2001). "Exposure to ultraviolet radiation: association with susceptibility and age at presentation with prostate cancer". Lancet. 358 (9282): 641–2. doi:10.1016/S0140-6736(01)05788-9. PMID 11530156.
  35. ↑ Tuohimaa P, Pukkala E, Scélo G, Olsen JH, Brewster DH, Hemminki K, Tracey E, Weiderpass E, Kliewer EV, Pompe-Kirn V, McBride ML, Martos C, Chia KS, Tonita JM, Jonasson JG, Boffetta P, Brennan P (July 2007). "Does solar exposure, as indicated by the non-melanoma skin cancers, protect from solid cancers: vitamin D as a possible explanation". Eur. J. Cancer. 43 (11): 1701–12. doi:10.1016/j.ejca.2007.04.018. PMID 17540555.
  36. ↑ Hoffman KE, Hong TS, Zietman AL, Russell AH (February 2008). "External beam radiation treatment for rectal cancer is associated with a decrease in subsequent prostate cancer diagnosis". Cancer. 112 (4): 943–9. doi:10.1002/cncr.23241. PMID 18098220.

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