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Breakthrough Treatment of Prostatic Disease


Many men today are living in fear. In fear that they may be the one – the one-in-six men that will be struck with prostate cancer. In fear that if struck, their doctor will seek ask to remove their prostate. In fear that if the prostate is removed, they will lose the ability to gain an erection. And perhaps the greatest fear of all, the spread of an existing tumor from the prostate to other vital tissues or organs. And if not in fear of prostate cancer, in fear of Benign Prostatic Hypertrophy (BPH).

Cancer of the prostate is responsible for 35,000 deaths every year in the United States, with an additional 184,000 men developing the disease in the same period. It is the most commonly found cancer in males over the age of 50, and the second most common cancer afflicting men. A recent study by the American Urological Association showed the incidence of precancerous prostate gland lesions to range from 22% to 41% in males between the ages of 30 and 49 years. About 20% of enlarged prostates are the result of cancer, the remaining 80% owing to BPH.

By the age of fifty, about 30% of all men will start to experience difficulties with urination related to enlargement of the prostate gland. Problems associated with this condition usually continue to worsen with age, increasing in incidence to about 50% of all males by the age of sixty and up to almost 80% past the age of seventy. Enlargement of the prostate is usually caused by an abnormal overgrowth and/or swelling of the tissue of the prostate, which then obstructs the urethra or opening from the bladder. Frequent need to urinate, especially at night, combined with reduction of force and caliber of urination are characteristic traits of BPH.

A Surprising Revelation

A widely held preconception is that excessive testosterone is the cause of prostate cancer and its close relative BPH. Recent research has revealed this widely held belief is little more than a misconception. In a surprising revelation researchers have found that testosterone is not the primary culprit, but instead its antitheses, the hormone estrogen! In fact a relative testosterone deficiency all but fuels the fire toward increased susceptibility of prostatic disease. Doesn’t this stand to reason? Biologically active “free-testosterone” begins to drop at about 1% a year from the age of 40 until the age of 70, whereas it peaks at the age of about sixteen. If testosterone were the true cause of prostate cancer and BPH, teenage men would be running around bald with enlarged prostates looking for the nearest restroom. We know this scenario to be the exact opposite of reality.

As testosterone levels decline with age, estrogen levels appear to remain relatively stable in the aging male. Compared to younger men, the ratio of estrogen to testosterone is up to 40% higher in older men. In the body, testosterone competes against estrogen for binding sites on special proteins that function to transport and hold sex-steroid hormones in reserve. These sex-hormone-binding proteins serve the valuable function of buffering sensitive prostate cells from excessive steroid exposure. In fact, at any one-given time 98% of combined testosterone and estrogen may be bound to circulating sex-hormone-binding protein. However, if these proteins are not carrying sex-hormones, they may directly bind to sensitive prostate tissue.

The Genesis of Prostatic Disease

The problem arises when sex-hormone-binding-protein is simultaneously bound to a prostate cell, and by sex steroids such as estrogen and/or testosterone. When aligned in this fashion, the sex-hormone-binding-protein acts like an electrical wire to transmit a strong hormonal message from the sex steroids to the prostate cell. In the case of testosterone, the message is no stronger than if testosterone were bound directly to the prostate cell. However, in the case of estrogen, the sex-hormone-binding-protein amplifies the hormonal stimulus to become 5-times more powerful than straight testosterone. The result is an increase in Prostate Specific Antigen (PSA) secretion and an increased susceptibility toward prostate cancer and BPH. Therefore, you can imagine the problem that is posed with a ratio of estrogen that is potentially 40% greater than testosterone.

In the aging male, estrogen molecules may significantly out number testosterone molecules in competing for available receptor sites on sex-hormone-binding-protein. The numerically dominant estrogen binds to a proportionately larger percentage of sex-hormone-binding-protein receptors as compared to testosterone. Due to the ill-proportioned testosterone vs. estrogen ratio, sensitive prostate cells become bombarded with excessive hormonal exposure. The effect is swollen, irritated prostatic tissue at least – and the beginnings of prostate cancer at most. According to Dr.s Griffiths and Adlercreutz writing in the medical text Nutrition and Cancer, “The change in the testosterone/ estrogen balance in the aging male could well be the factor that induces prostatic disease.”

Fueling the fire in aging men, an enzymatic process converts testosterone to estrogen. Only about 33% of estrogen in males is synthesized and secreted by the testes. The remaining 67% is formed by the enzymatic conversion of testosterone to estrogen.

A Breakthrough in Prevention and Treatment of Prostatic Disease

As you can see, as we age we are subjected to a vicious cycle. First, the reduction of testosterone leading to an imbalance in the ratio of testosterone to estrogen; then, the enzymatic conversion of testosterone to estrogen; lastly, estrogen crowding out testosterone for receptor sites on sex-hormone-binding protein.

While the problem may appear to be multi-factorial, a breakthrough discovery in plant-based medicines may offer a silver bullet by systematically defeating the above vicious cycle at every front. Laced within the cell-wall matrix of certain seeds, grains, legumes, fruits and vegetables are extremely powerful, yet gentle, natural plant compounds identified as lignans. Lignans have been highly researched for their ability to mimic natural human hormones. In fact, when first identified in human secretions, lignans were thought to be a newly discovered class of human hormone. Ultimately researchers discovered that mammalian lignans can only be produced in the body through the dietary ingestion and conversion of plant lignans. When high-in-lignan foods are ingested, bacterial action in the colon converts plant lignans to biologically active mammalian lignans.

While lignans structurally resemble natural hormones, they do not have the power to provoke cancer sensitive cells. The effect of lignans on hormonally sensitive cells is 1,000 times less than that of testosterone and estrogen. Due to their structural similarity, lignans can act as a surrogate to, and compete against, human hormones for hormonal receptor sites on the prostate and sex-hormone-binding-protein. Once docked, lignans effectively block the receptor from the more powerful hormones – where they are left to be eliminated from the body. Perhaps now the potential toward lignans to prevent and treat BPH as well as prostate cancer has begun to come into focus. Lignans not only hold the power to halt the vicious cycle, but to defeat it. With this in mind, let’s explore what researchers have discovered concerning lignans in the potential prevention and treatment of prostatic disease.

Lignans: Defeating the Vicious Cycle

An ideal approach toward the prevention and treatment of prostatic disease is to enhance the testosterone vs. estrogen ratio toward testosterone. The first tack is to preserve available testosterone in the aging male by thwarting the conversion of testosterone to more biologically volatile hormonal agents such dihydrotestosterone (DHT) and estrogen. The conversion of testosterone to these more powerful steroids is accomplished by two-different enzymatic processes in the body. Let’s tackle DHT first.

DHT, much like estrogen is much more irritating to prostatic tissue than testosterone alone. DHT has been implicated in provoking prostate cancer, BPH and male-pattern-baldness (MPB). Testosterone is converted to DHT in the body via a one-step enzymatic process. Block the enzyme and you spare testosterone, while limiting the production of DHT. Research indicates that lignans have the potential to inhibit the enzyme necessary for conversion of testosterone to DHT by as much as 45% to 75%. Compare this with the 60-75% inhibition achieved with the prescription drug Propecia and you understand the potential effectiveness of lignans. Propecia was developed to inhibit the identical enzyme for the treatment of prostatic disease as well as a secondary use as a treatment for baldness. Propecia is not without potential adverse-effects. Some men have suffered from impotence, lack of sexual desire and female-like enlargement of the male breast. There are no known adverse side effects related to human ingestion of lignans.

A similar enzymatic conversion is responsible for transforming testosterone to estrogen. As with DHT above, if the enzyme system for conversion is blocked, testosterone is spared, and estrogen production is hampered. The resultant rise in testosterone and decline in estrogen production can be visualized as occurring in a see-saw like fashion. Once again, lignan inhibits the conversion of testosterone to estrogen by blocking the enzyme responsible for conversion.

The next tack could be borrowed out of a book on basic military strategy. The primary indicator in predicting a victor in warfare is that of the largest military force. Through sheer-strength-of-numbers, the army with the most soldiers usually wins. You can consider lignans your recruits in the battle against prostate disease. By consumption of high lignan foods – or through lignan supplementation – you can create an army so powerful as to outnumber your enemies on a scale as great as 10,000 to one. The enemy in this case would be precarious estrogen, DHT and testosterone molecules. With a force of such magnitude lignans are more likely to win the competition for available receptor sites on sex-hormone-binding-protein and sensitive prostatic tissue. Excessive steroidal hormones, with no place to dock, are left to be eliminated thorough the bodies eliminative pathways. Through the amazing innate intelligence of the human body, lignans cannot fully saturate available receptor sites, but instead provide a near perfect hormonal balance. Perhaps this is the reason why researchers are referring to lignans as nature’s natural sex-hormone modulators.

New Technology Harnesses the Power of Lignans

Based on the above biological actions, lignans may effectively block a relevant percentage of receptor sites on both prostate cells and sex hormone-binding-protein. Simultaneously, lignan may improve the overall ratio of testosterone to estrogen, producing a more stable and less volatile situation in the first place. In so doing, lignans can normalize hormonal function in the aging male, preventing and treating prostatic disease.

While a wide variety of lignans exist in nature, those found to be beneficial toward prostatic disease are very specific. It has only been within the recent past that new technology has been developed to isolate, concentrate and purify these specific lignans from natural plant resources. The result of these efforts is a guaranteed-potency product formulated to provide a physiologic dose of lignans in a single capsule supplement. The product has been formulated to provide a dose that is correlated with the physiologic concentration of lignans found in men with the lowest incidence of prostate disease in the entire world.

Complimentary samples of PRxOVAIL are being provided free to the general public for a limited time by contacting Lignan Research LLC. at 888-503-8300 or email RxOVAILhealth.com">info@PRxOVAILhealth.com

References:
1. Lignans Interfering with 5a-Dihydrotestosterone Binding to Human Sex Hormone- Binding Globulin Matthias Schottner, Gerhard Spiteller; Journal of Natural Products, 1998, Vol. 61, No. 1
2. Inhibition of 5a-reductase in genital skin fibroblasts and prostate tissue by dietary lignans and Isofl avonoids; B.A. J. Evans, K Griffiths and M.S. Morton; Journal of Endocrinology (1995) 147, 295-302
3. Phytoestrogens and prostate cancer: Possible preventative role; F.O. Stephans MJA, Vol. 167 4, August 1997
4. Nutrition and Cancer: 1996 Isis Medical Media Ltd,; Saxxon Beck, 58 St. Aldates Oxford OX1 1st, UK
5. Dietary phytoestrogens. Kurzer MS Xu X; In: Annu Rev Nutr (1997) 17:353 81 6. Aldercreutz H Makela S Pylkkanen L SanttiR Kinzel J van Reijsen M, Markkanen H Kamarainen EL Watanabe S Fotsis T et al; Dietary phytoestrogens and prostate cancer (Meeting abstract).
7. Barrett J . Phytoestrogens. Friends or foes? [news]; In: Environ Health Perspect (1996 May) 104(5):478 82
8. Journal of the National Cancer Institute. Vol. 86 No.23. December 7, 1994 pg. 1748
9. Ren S Lien EJ. Natural products and their derivatives as cancer chemopreventive agents. In: Prog Drug Res (1997) 48:147 71
10. Adlercreutz H MousaviY Clark J Hockerstedt K Hamalainen E, Wahala K Makela T Hase T; Dietary phytoestrogens and cancer: in vitro and in vivo studies. In: J Steroid Biochem Mol Biol (1992 Mar) 41(3 8):331 7
11. Tham DM Gardner CD Haskell WL; Clinical review 97: Potential health benefits of dietary phytoestrogens: a review of the clinical, epidemiological, and mechanistic evidence. In: J Clin Endocrinol Metab (1998 Jul) 83(7):2223 35
12. Morton MS Wilcox G Wahlqvist ML Griffiths K. Determination of lignans and isoflavonoids in human female plasma following dietary supplementation.
13. Rickard SE Orcheson LJ Seidl MM LuyengiL Fong HH Thompson LU; Dose dependent production of mammalian lignans in rats and in vitro from the purified precursor secoisolariciresinol diglycoside in fl axseed. In: J Nutr (1996 Aug) 126(8):2012 9
14. Axelson M Sjovall J Gustafsson BE Setchell KD. Origin of lignans in mammals and identification of a precursor from plants.