Prostate cancer is common. In fact for men above the age of 50 it is the most common cancer in the U.S., where more than 200,000 new prostate cancer patients are diagnosed every year. It is twice as common in black American men than in white American men, but Japanese and Chinese men have 70-fold less cancer of the prostate than North American men (Ref. 2 and 3). This difference has been studied extensively and likely is due to two factors: a different diet and a lower concentration of the enzyme 5-alpha-reductase in the prostate gland. Let me explain: The Chinese and Japanese diet is rich in cancer protective agents, the North American diet is a high fat diet and is insufficient in unprocessed fruit and vegetables (which is where the cancer protective agents can be found).
Under the microscope prostatic tissue looks very similar with its glands as breast tissue and as the lining of uterine tissue (the endothelium). Developmentally (in the embryo) the uterus and the prostate are equivalents. All of these tissues have hormone receptors for estrogen, testosterone and progesterone. In this context it is important to know that men above the age of 35 to 40 are loosing testosterone from the testes and progesterone from the adrenal glands due to aging, but are often accumulating estrogen. Inside of the body there is a dysbalance of hormones as the enzyme aromatase in the fatty tissue makes estrogen out of testosterone. From outside the body xenoestrogens, which are insecticides, petrochemicals from work etc. contribute to the hormone dysbalance of the aging man. Dr. John Lee calls this “estrogen dominance” (Ref. 10). Rebalancing the male hormones will be discussed further under “prostate cancer prevention”, which can be a powerful tool maintaining in virility and improving life expectancy .
5-Alpha-Reductase is an enzyme within prostatic tissue and in the hair follicles. In the prostate it metabolizes testosterone into dihydrotestosterone (=DHT). DHT is the “culprit” that is responsible in stimulating the prostate to grow 2-3 times the normal size after the male menopause, which occurs at about the age of 50. This condition of prostate enlargement is called benign prostate hyperplasia or benign prostatic hypertrophy (see details under this link). After many years of having an enlarged prostate areas of abnormal cells develop within the enlarged prostate gland and eventually cancer occurs. This pathophysiology explains why the prostate cancer rate is higher in men that are older. Carcinogenesis (=the development of cancer) takes about 25 to 30 years.
The same enzyme (5-alpha-reductase) is present in androgen susceptible hair follicles on the scalp and it converts testosterone to DHT. Too much of this leads to premature hair loss, but fortunately this can now be remedied as described under hair loss. One of the means of reducing DHT is by taking finasteride, which is a 5-alpha-reductase inhibitor (known under the brand name “Proscar” for prostate hypertrophy and under the name of “Propecia” for baldness). It is less known that the hormone progesterone is a natural 5-alpha-reductase inhibitor, which is the reason that young men do not have hair loss or a large prostate (see Ref. 10). It is in older men when progesterone and testosterone levels are low that estrogen is not inhibited enough and the 5-alpha-reductase is no longer inhibited (missing progesterone), which allows the cancer producing estradiol and dihydrotestosterone to get the upper hand. Conventional medicine teaches (and I have believed this for many years) that testosterone would be the cause for prostate cancer. This was based on old observations by Dr. Huggins, a Canadian born surgeon who practiced in Chicago, that orchiectomy improved the survival of advanced prostate cancer patients a bit (Ref.12). Dr. Lee pointed out that Dr. Huggins neglected to realize that testicles make both testosterone and small amounts of estrogen. When an orchiectomy was done (because of the belief that testosterone production was the culprit) inadvertently the real cause of prostate cancer (an estrogen surplus) was also removed thus improving the survival of these patients somewhat. Nowadays we have more sophisticated testing methods. Dr. Abraham Morgentaler (Ref. 11) has compiled a lot of evidence about the importance of testosterone in men. He proved, based on a lot of more modern references that it is not testosterone that is the cause of prostate cancer. We know now that estrogen dominance is responsible for prostate cancer and that this develops as stated above because of the low testosterone and low progesterone during the male menopause (also called “andropause”; see also Ref.10). This fact will become very important below when it comes to treatment choices for prostate cancer.
About 3% of all deaths in men older than 55 years are due to prostate cancer. However, autopsy studies showed that 29% of North American men in their 50’s have histological proof of existing prostate cancer and men in their 80’s were 67% positive on autopsy. This led to an erroneous concept of distinguishing between “clinically important” versus “clinically unimportant” prostate cancer. This created confusion among the urologists for about 15 to 20 years and there are still urologists and health care providers who hold on to this useless distinction (Ref.1).
Fact is that these males who were proven positive for prostate cancer by autopsy would eventually have succumbed to their occult prostate cancer, had they not died of another disease first. But as the prostate gland is contained in a very tough capsule, the prostate cancer is also contained for a very long time (stage A and B) until the cancer eats its way through and turns into stage C. From here it is only a short step to stage D (distant metastases). Instead of ignoring stage A and B cancer of the prostate and calling it “clinically unimportant” it is better to do a selective radical prostatectomy and get rid of prostate cancer for good. This would give these men at least a chance to live much longer (see more under “prostate cancer treatment“).
The following references were used apart from my own clinical experience:
1. Cancer: Principles &Practice of Oncology, 4th edition, by V.T. De Vita,Jr.,et. al J.B. Lippincott Co.,Philadelphia, 1993.Vol.1: Chapter on Prostate cancer.
2. The Merck Manual, 7th edition, by M. H. Beers et al., Whitehouse Station, N.J., 1999.Chapter 233, p.1918-1919.
3. Cancer: Principles&Practice of Oncology. 5th edition, volume 1. Edited by Vincent T.DeVita, Jr. et al. Lippincott-Raven Publ., Philadelphia,PA, 1997. Chapter on prostate cancer.
4. A Waghray et al. Cancer Res 2001 May 15;61(10):4283-4286.
5. BM Fisch et al. Urology 2001 May;57(5):955-959.
6. CC Parker et al. BJU Int 2001 May;87(7):629-637.
7. B Aschhoff Drugs Exp Clin Res 2000;26(5-6):249-252.
8. Conn’s Current Therapy 2004, 56th ed., Copyright © 2004 Elsevier
9. Ferri: Ferri’s Clinical Advisor: Instant Diagnosis and Treatment, 2004 ed., Copyright © 2004 Mosby, Inc
10. John R. Lee: “Hormone Balance for Men – What your Doctor May Not Tell You About Prostate Health and Natural Hormone Supplementation”, © 2003 by Hormones Etc.
11. Abraham Morgentaler, MD “Testosterone for Life – Recharge your vitality, sex drive, muscle mass and overall health”, McGraw-Hill, 2008
12. Huggins, C., Stevens, R. E. Hodges, C. V. (1941). Studies on prostatic cancer, III. The effects of castration on advanced carcinoma of the prostate gland, Archives of Surgery, 43, 209–223.