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The Natural Prostate Cure
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Chapter 12: Estrogens
Men and women have exactly the same hormones, only in different amounts. There is no “estrogen” per se; estrogen is merely a convenient term to use when referring to the class of hormones collectively known as estrogens. Men have smaller amounts of estrogen than women until the age of fifty, when male levels begin to rise. Female levels fall after menopause, so middle-aged men commonly have more estrogen than women! This is a dangerous situation obviously, as men’s testosterone-to-estrogen ratio becomes reversed. The reversal of this ratio is the key to understanding not only prostate disease, but many other male illnesses, including cardiovascular health, immunity, gynecomastia (male breast growth), abdominal fat, cancer, baldness, and many of the other ills of aging males.
There are actually three basic estrogens: estradiol (the most powerful and most carcinogenic); estrone; and estriol (the least powerful, safest, and most beneficial). Estradiol and estrone comprise about 10-20 percent of human estrogen and estriol about 80-90 percent. Over the last thirty years there have been dozens of studies showing the harmful effect of excessive estrogen in aging males caused by the reversed androgen-to-estrogen ratio (including androstenedione and DHEA, in addition to testosterone) - the key to prostate disease. It is beyond the scope of this book, and would likely bore the reader to list and discuss these dozens of studies. We will pick twenty of them to quickly prove the point that testosterone is your friend and excess estrogen is your enemy, and that the reversal of the androgen-to-estrogen ratio is the most important insight we have into prostate disease. There are many, many other such studies.
At the University of Glasgow in Scotland,1 estradiol was added to human BPH and cancerous prostate tissue, completely changing the metabolism, clearance, and uptake rates of testosterone and androstenedione, and also increasing the uptake of DHT (dihydrotestosterone). DHT binding to the prostate is the main concern in prostate disease, and not simply DHT serum levels.
At the University of Vienna2 23 clinical trials spanning fifteen years were reviewed. They found that estrogen (not testosterone) suppression was the proper treatment for BPH. “The estrogen suppression … is considered as an efficient pharmacotherapeutic strategy in the medical treatment of uncomplicated BPH.” These good doctors should go a little further and realize that testosterone supplementation is the next step.
At Strangeways Research Laboratories in England3 estradiol stimulated the uptake of DHT in both human BPH and cancerous prostate tissue. Again, at the same lab4 estradiol was added to human BPH and prostate cancer cells. “Estradiol stimulated DHT, but not androstenedione or testosterone uptake by BPH cells. The effects of estradiol on carcinoma cells were similar to those of BPH cells.” The harmful DHT binds to the prostate instead of the healthful androstenedione and testosterone.
At the University of Oulu in Finland5 estradiol given to men raised both their SHBG (sex hormone binding globulin) and their bound free testosterone, thereby lowering available testosterone in men with prostate cancer. At the University of Bonn in Germany6 men with BPH were found to have high estrone levels, which excessively bound to their prostates. At Sabbatsberg Hospital in Sweden7 estrone was found to convert into the more dangerous and carcinogenic estradiol, in human BPH tissue.
In studies performed at the University of Hamburg in Germany8 men with BPH were found to have excessive estradiol in their prostates, high 5-alpha-reductase activity, and increased DHT accumulation. Again we see that DHT binding to the prostate gland is a central concern. At the American Health Foundation in New York9 high estradiol levels characterized the prostate fluid of men with cancer. At the Bielanski Hospital in Poland10 men with prostate cancer generally had high serum estradiol and low serum testosterone, showing the classic reversed testosterone-to-estrogen ratio. At the Sloan-Kettering Cancer Institute in New York11 human BPH tissue had more than twice the estradiol concentration as healthy tissue, showing that excessive estrogen production is a factor in both BPH and cancer. At Erasmus University in Holland12 researchers found that estrogen caused “striking” growth stimulation in LnCaP human prostate cancer cells, which are considered androgen-dependent, not estrogen-dependent. At the Schering AG Research Labs in Germany13 doctors finally started promoting the therapy of reducing estrogen in men with prostate disease, using aromatase inhibitors, which prevent estrogen formation. The idea of lowering estrogen, as therapy, is admirable here.
At Bergmannsheil University in Germany14 doctors found high levels of estradiol and estrone in human BPH tissue, and learned that the reversed androgen-to-estrogen ratio, as men age, basically accounts for BPH. At Harvard Medical School in Boston15 three-hundred twenty men with BPH were compared to 320 healthy men. High plasma estradiol levels were clearly related to BPH, as well as to the obviously reversed testosterone-to-estrogen ratio. Low androgen levels were clearly related to BPH. At the Genoa University Medical School in Italy16 researchers found that estradiol stimulated the growth of androgen-dependent LnCaP human cancer cell lines by up to 120 percent. This contradicts the “testosterone is bad for you” theory, as LnCaP cells are supposed to be stimulated by testosterone and androstenedione, and not by estrogens.
At Kiel University in Germany17 doctors, over 20 years ago, studied men with prostate enlargement for their plasma and urinary estrogen levels. They found a clear relation between BPH and estrogen levels, especially estradiol. “There was a highly significant increase of prostate stroma in association with higher individual estradiol concentrations and urinary estrogen excretion.” At the University of Hamburg18 doctors found exactly the same thing in men with prostate enlargement. “In conclusion, there is a distinct accumulation of estrogens in the nuclei of stroma, estradiol concentration being significantly higher — stimulating the growth of BPH.”
At Northwestern University in Chicago19 doctors found that it is estrogen and SHBG that promote prostate growth, and verified their results with forty-nine references. At the University of Palermo in Italy20 doctors learned that estradiol stimulates LnCaP lines, and that “the current model for hormone dependence of human prostate carcinoma should be revised.” In other words, the current medical dogma that testosterone is the cause of prostate disease is absolutely wrong; it is excess estrogen- and the reversed testosterone-to-estrogen ratio — that is the real cause of prostate disease. Unfortunately, it is difficult to lower estrogen levels. The current anti-aromatase drugs (which lower our levels of the enzyme aromatase) are generally dangerous and/or ineffective. Aromatase is the enzyme that converts testosterone to estradiol, and androstenedione to estrone. It is very difficult to lower aromatase or to prevent aromatase activity, except by the diet, exercise, and lifestyle changes described earlier, as well as taking DIM (di-indolyl methane) and flax oil.
Remember, you can only lower estrogen levels by losing weight, eating a low-fat diet, eating fewer calories, eating more fiber, avoiding alcohol, exercising regularly, taking DIM21 and flax oil, raising your testosterone, androstenedione, and DHEA levels, and by applying transdermal progesterone cream directly to your scrotum, to be absorbed by your testicles.
References: 1. Biochemical Journal 126 (1972), pp. 107-21 2. Wien.Klin.Woschenschr. 110 (1998), pp.817-23 3. J. Endocrinol 74 (1977), pp. 1-9 4. J. Endocrinol 71 (1976), pp. 97P 5. Investigative Urology 17 (1979), pp. 24-27 6. Hormone Metabolic Research 11(1979), pp. 635-40 7. Scandinavian Journal of Urology 14 (1980), pp. 135-37 8. Journal of Steroid Biochemistry 19 (1983), pp. 155-61 9. Prostate 5 (1984), pp. 47-53 10. Roczniki Akademii Medicina 42 (1984), pp. 175-76 11. Prostate 9 (1986), pp. 311-18 12. Journal of Steroid Biochemistry 44 (1993), pp. 573-76 13. Journal of Steroid Biochemistry 44 (1993), pp. 557-63 14. Journal of Clinical Endoc. Metabolism 77 (1993), pp. 375-81 15. Prostate 26 (1995), pp. 40-49 16. Endocrinology 136 (1995), pp. 2309-19 17. Journal of Clinical Endocrinology 47 (1978), pp. 1230-35 18. Prostate 3 (1982), pp. 433-38 19. Prostate 28 (1996), pp. 17-23 20. Ciba Foundation Symposium 191 (1995), pp. 269-89 21. Journal of the National Cancer Institute 89 (1997), pp. 718-23
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