Prostate, a Greek word meaning “protector” or “guardian” is the gland of male reproductive system in most mammals. The function of the prostate is to secrete a slightly alkaline fluid, milky or white in appearance, that usually constitutes roughly 30% of the volume of the semen along with spermatozoa and seminal vesicle fluid. The prostatic fluid is expelled in the first ejaculate fractions, together with most of the spermatozoa. In comparison with the few spermatozoa expelled together with mainly seminal vesicular fluid, those expelled in prostatic fluid have better motility, longer survival and better protection of the genetic material.

Prostate cancer is the second most frequently diagnosed cancer (at 15% of all male cancers) and the sixth leading cause of cancer death in males worldwide. In 2010 it resulted in 256,000 deaths up from 156,000 deaths in 1990. Rates of prostate cancer is the least common in South and East Asia, and more common in Europe, North America, Australia and New Zealand. Prostate cancer has a higher inheridetary factor than breast, ovarian and endometrial cancers, all of reproductive system and develop in the old age (40% for prostate vs. 5-10% for breast, 5% for ovarian and 2-10% for endometrial or uterine cancer)! As discussed in “Breast cancer: Revisited”, all these reproductive systems cancers surprisingly, no matter in males or females, share the genetic link with abnormalities in BRCA1 & 2 that are “tumor suppressor genes”! Prostate cancer has also more of infection risk factors than his female reproductive organ counterparts, specially through STD (Sexually Transmitted Diseases). This makes sense as discussed in “ A new look at Cancer”, “A new look at Infections” and “Trauma and insults” that a common offending cause of human’s cancers are through microbiological offences! This may explain the higher genetic risk in prostate cancer as microbiological insults will leave their long term impacts on the genetic machinery for generations to come! Interestingly among cancers of male and female reproductive organs, only there is a common link between prostate and uterine cervix in causation by HPV (Human Papiloma Virus) infection.

Other than microorganisms that could be blamed for about 30% genetic risk difference between the prostate cancer and female reproductive system cancers, they all seem to share similar risk factors. As discussed in “Breast cancer: Revisited”, “Ovarian and Endometrial Cancers: Revisited”, the common risk factor is in the use of reproductive system itself! Lack or low use of these reproductive organs, e.g. no breastfeeding leading to breast cancer, no reproduction leading to ovarian and endometrial cancers, low use of prostate, the male reproductive organ by lower ejaculation and reproduction by vasectomy, will lead to prostate cancer. Of course the nature gives sufficient time for the use of these reproductive organs, so that is why all these cancers do not develop in young reproductive age but in old age. But if vasectomy is done early on, the prostate cancer may appear earlier than usual late age of >70!

Therefore as discussed in other related posts here, we need to redirect our medicinal efforts from treatment to prevention and educate the public of the high risk of not using their reproductive systems and infections and traumas in the development of such cancers.

Dr.Mostafa Showraki, MD, FRCPC                                                               Lecturer, University of Toronto,School of Medicine,Author: “ADHD:Revisited” Book “adhdrevisited.com”/”medicinerevisited.com”

References:

1. Hsing AW, Chokkalingam AP (2006). “Prostate cancer epidemiology”. Frontiers in Bioscience 11: 1388–413.
2. Struewing JP, Hartge P, Wacholder S, Baker SM, Berlin M, McAdams M, Timmerman MM, Brody LC, Tucker MA (May 1997). “The risk of cancer associated with specific mutations of BRCA1 and BRCA2 among Ashkenazi Jews”. N. Engl. J. Med. 336 (20): 1401–8.
3. Dennis LK, Lynch CF, Torner JC (July 2002). “Epidemiologic association between prostatitis and prostate cancer”. Urology 60 (1): 78–83.
4. Dennis LK, Dawson DV (January 2002). “Meta-analysis of measures of sexual activity and prostate cancer”. Epidemiology (Cambridge, Mass.) 13 (1): 72–9.
5. Sarma AV, McLaughlin JC, Wallner LP, Dunn RL, Cooney KA, Schottenfeld D, Montie JE, Wei JT (September 2006). “Sexual behavior, sexually transmitted diseases and prostatitis: the risk of prostate cancer in black men”. The Journal of Urology 176 (3): 1108–13.
6. Sutcliffe S, Platz EA (May 2008). “Inflammation and prostate cancer: a focus on infections”. Current urology reports 9 (3): 243–9.
7. Hisada M, Rabkin CS, Strickler HD, Wright WE, Christianson RE, van den Berg BJ (Jan 19, 2000). “Human papillomavirus antibody and risk of prostate cancer”. JAMA: the Journal of the American Medical Association 283 (3): 340–1.
8. Siddiqui MM, Wilson KM, Epstein MM, Rider JR, Martin NE, Stampfer MJ, Giovannucci EL, Mucci LA. Vasectomy and Risk of Aggressive Prostate Cancer: A 24-Year Follow-Up Study. J Clin Oncol. 2014 Jul 7; . Epub 2014 Jul 7.
9. Stanford JL, Wicklund KG, McKnight B, Daling JR, Brawer MK. Vasectomy and risk of prostate cancer. Cancer Epidemiol Biomarkers Prev. 1999 Oct; 8(10):881-6.
10. Leitzmann MF, Platz EA, Stampfer MJ, Willett WC, Giovannucci E. Ejaculation frequency and subsequent risk of prostate cancer. JAMA. 2004 Apr 7; 291(13):1578-86.
11. Showraki, Mostafa.  “Breast Cancer:Revisited”. medicinerevisited.com.
12. Showraki, Mostafa.  “A new look at Cancer”. medicinerevisited.com.
13. Showraki, Mostafa.  “A new look at infections”. medicinerevisited.com.
14. Showraki, Mostafa.  “Trauma and insults”. medicinerevisited.com.
15. Showraki, Mostafa.  “Ovarian and endometrial Cancers:Revisited”. medicinerevisited.com.