In a review article in the journal Prostate in 1996, a pioneer of modern prostate research proposed a model of prostate physiology and pathogenesis based in part upon this research. Wells Farnsworth (professor of urology at Northwestern University Medical School) discovered the conversion of testosterone to DHT in the prostate in the early 1960s. In his article in Prostate, Farnsworth proposes that estrogen, mediated by SHBG, participates with androgen in setting the pace of prostate growth and function. Farnsworth notes that, as explained, SHBG increases with age and can act like an additional androgen receptor (binding site for androgen) in the prostate cell. He suggests that when estrogen binds to SHBG in the cell membrane, a growth factor called insulin-like growth factor I (IGF-I) is synthesized, causing proliferation of epithelial cells in the prostate. This sets the stage for further proliferation when androgens activate binding sites for growth factors. In Farnsworth's language, estrogen not only directs stromal proliferation and secretion, but also through IGF-I conditions the response of epithelium to androgen (Farnsworth 1996).

The researchers who discovered the alternative signaling pathway concur: antagonism (inhibition) of the pathway by which SHBG leads to the induction of androgen-responsive genes may be a valuable therapeutic target for the treatment or prevention of prostate enlargement or prostate cancer. Accordingly, these researchers studied an agent thought to inhibit the binding of SHBG to the prostate cell membrane, an extract of the root of the stinging nettle plant, U. dioica. In a paper in 1995 in Planta Medica, they demonstrated that nettle root does indeed inhibit the binding of SHBG to the cell membrane (Hryb et al. 1995).

In a subsequent series of articles, German researchers have identified a constituent of nettle root known as (-)-3,4-divanillyltetrahydrofuran, whose very high-binding affinity to SHBG they describe as remarkable. These researchers suggest that the beneficial effects of plant lignans (such as found in flaxseed oil) on hormone-dependent cancers may be linked to their binding affinity to SHBG. The most potent known lignans in this respect are constituents of nettle root. In addition to inhibiting SHBG binding, at least six constituents of nettle root inhibit aromatase, reducing conversion of androgens to estrogens (Schottner et al. 1997a, 1997b, 1998).

Combining nettle root with pygeum results in a stronger synergistic inhibition. The studies on aromatase inhibition by nettle root used methanolic extracts.

An experimental study provides a dramatic demonstration of nettle root's effect on prostate enlargement tissue. This experiment was based upon the hypothesis that prostate enlargement is comparable to a reawakening of embryonic growth potential in the prostate. A fetal urogenital sinus was implanted into a lobe of the prostate gland in adult mice. The implanted lobes of mice fed a nettle root methanolic extract similar to an extract on the German pharmaceutical market showed 33.8% less growth than the lobes of mice in the control group (Lichius et al. 1999). Nettle root is widely used as a first-line therapy for prostate enlargement in Germany, where there are 15 pharmaceutical drugs consisting solely of nettle root. Nettle root has been extensively studied in European clinical trials over the past 20 years.

In Europe, nettle root is also used in combination with saw palmetto. This combination is a logical one because nettle root acts through the alternative signaling pathway in the prostate cell, while saw palmetto acts on the primary signaling pathway by limiting DHT activity. In effect, nettle root addresses the estrogen side of prostate enlargement, while saw palmetto addresses the androgen side. Additionally, both herbs have anti-inflammatory actions.

A randomized double-blind study compared the saw palmetto/nettle combination to the standard prostate enlargement drug finasteride in 543 patients with prostate enlargement Stages I-II. The herbal therapy and drug therapy proved similarly effective in all measures: urinary flow rate, urination time, IPSS scores, and patients' quality of life assessments. Both therapies increased in effectiveness over a period of months. For example, the average IPSS score in the herbal therapy group declined from 11.3 to 8.2 after 24 weeks and to 6.5 after 48 weeks; in the finasteride group it declined from 11.8 to 8.0 after 24 weeks and to 6.2 after 48 weeks. Patients tolerated herbal therapy better than finasteride, which causes diminished libido and sexual dysfunction, including impotence in a small minority of patients (Sokeland 2000).

The combined use of nettle root and pygeum has been shown to synergize in inhibiting aromatase. In addition, these three herbs affect growth factors in ways that appear to be beneficial in the prevention and treatment of prostate enlargement. According to a 1997 article in the Journal of Urology, pygeum inhibits cell proliferation induced by the growth factors epidermal growth factor (EGF), basic fibroblast growth factor (bFGF), and IGF-I in stromal cells from rat prostate (Yablonsky et al. 1997).

A 1998 study in European Urology found that saw palmetto inhibits bFGF-stimulated cell proliferation in human prostate cell cultures (Paubert-Braquet et al. 1998). Preliminary research suggests that a constituent of nettle root inhibits the binding of EGF to human prostate cells. As is the case for many medicinal herbs, the clinical efficacy of nettle root was demonstrated at a time when medical science had not yet made the basic advances needed to understand its mechanism of action. This may be one reason that nettle root is relatively unknown in America whereas saw palmetto, with its relatively clear-cut mechanism of action based upon testosterone, is in common use. As was the case for saw palmetto, it will probably take years for the pharmaceutical companies to develop a synthetic drug to effectively address the mechanism of action of nettle root. Both of these extraordinarily well-tolerated herbal extracts are available now to men with prostate enlargement.

These new discoveries of how estrogen, SHBG, and DHT induce prostate enlargement provide a rationale basis for the prostate enlargement sufferer to supplement with pharmaceutical-potencies of nettle root, pygeum, and saw palmetto (supercritical extract).

Using Aromatase Inhibiting Drugs
Some men with severe prostate enlargement do not obtain adequate symptomatic relief from European phyto extracts and/or finasteride (Proscar).

A novel approach to treating these intractable cases of prostate enlargement is to inhibit the amount of estrogen in a man's body by using an aromatase inhibiting drug. As men age, they often produce too much aromatase enzyme that causes testosterone and other steroid hormones to be aromatized (converted) into estrogen. Estrogen can be a prime culprit leading to prostate cell proliferation in men, and preliminary studies show that suppressing estrogen levels by inhibiting the aromatase enzyme may be an effective therapy.

A description of a study reported in the Austrian journal Wien Klinische Wochenschrift follows:

Estrogen suppression has been introduced as a therapeutic strategy in the medical treatment of benign prostatic hyperplasia. Recent negative results obtained in
placebo-controlled trials with the aromatase inhibitor atamestane raised doubts about the efficacy of estrogen reduction. However, inhibition of aromatase not only reduces estrogens, but also increases androgens (DHT) which may promote prostatic growth. In order to reevaluate the therapeutic efficacy of estrogen suppression, we summarize clinical trials investigating the therapeutic effects of mepartricin in the treatment of uncomplicated benign prostatic hyperplasia. Mepartricin has been reported to lower the levels of circulating estrogens without causing changes in other hormones such as androgens. By applying stringent inclusion criteria, 23 studies (including 7 placebo-controlled trials, 3 post-marketing surveillance studies, and 13 open trials) published between 1982 and 1996 were selected to be included in this report. In 79.9% of 4635 patients treated with mepartricin, its therapeutic effect was rated "good" or "excellent." In six out of seven placebo-controlled trials, the therapeutic efficacy of mepartricin was significantly superior to that of placebo. Comparison of these data with results obtained with alpha
1-adrenoceptor antagonists or with the 5 alpha-reductase inhibitor finasteride indicates that mepartricin is as efficient as these widely accepted medical treatments for benign prostatic hyperplasia. Since mepartricin acts selectively upon estrogens, the present results show that estrogen suppression may be considered an efficient pharmacotherapeutic strategy in the medical treatment of uncomplicated benign prostatic hyperplasia. (Boehm et al. 1998)
The drug mepartricin is not yet approved in the United States, but a strategy might be to use an approved aromatase inhibitor such as Arimidex in the low dose of 0.5 mg twice a week. In order to block the increase in DHT production that would most likely occur, 5 mg of Proscar taken every day or every other day should suppress excess formation of DHT, while enabling the Arimidex to eradicate overproduction of estrogen. This dual effect of suppressing excess DHT and estrogen may result in significant clinical improvement and address the underlying cause of most cases of severe prostate enlargement. Side effects of Arimidex and Proscar are minimal if therapeutic results are obtained. The Male Hormone Modulation protocol provides a scientific rationale for a multitude of health benefits aging men can expect if they suppress excess estrogen and DHT levels. For assistance, call (800) 544-4440 for additional information.

Another study in the International Journal of Andrology evaluated five beagles with prostate enlargement treated by drugs that suppressed both estrogen and testosterone. The results showed that mean prostatic volume decreased to 56% of the pretreatment value. Histological examination of the prostate 4 weeks after treatment revealed reduction in diameter of the alveoli and in height of the glandular epithelium. Degeneration and atrophy of the glands were marked 4-12 weeks after treatment. After treatment, levels of testosterone and estrogen were lower than before treatment. The results of this study indicate that suppression of estrogen and testosterone brings about resolution of the clinical signs and marked reduction in prostatic volume within 1 week of treatment. Since maintaining free testosterone is so important in maintaining the health and well-being in aging men, the rationale for using a drug to suppress estrogen and DHT (instead of testosterone) might be a more tolerable long-term treatment strategy. Remember, testosterone produces its most profound effect on prostate enlargement by converting to the far more potent prostate cell-proliferating metabolite DHT (Kawakami et al. 1995).

Clearly, more research is needed, but this relatively safe approach using an aromatase inhibiting drug along with a potent DHT-blocking drug, such as Proscar and the European phytoextracts, may be considered in prostate enlargement patients who want to avoid potentially damaging surgery (refer to the Male Hormone Modulation protocol for comprehensive information about correcting estrogen and testosterone imbalance conditions).

For those for whom all nutrient and drug therapies fail, testosterone blockade of prostate cell receptor sites with the drug Casodex for 3 months may provide prostate-gland shrinkage.

Recommended Blood Testing

Because men with prostate enlargement are at an increased risk of developing prostate cancer, PSA and free-PSA blood tests should be considered every 3-6 months. A free-PSA test helps to determine if a moderately elevated PSA (with levels of 2.6-10) is indicative of early-stage prostate cancer. Testing for excess estrogen is also important in identifying the underlying cause of prostate enlargement. Again, please refer to the Male Hormone Modulation protocol for complete information on testing the blood for estrogen.

Prevention of prostate enlargement

The incidence of prostate cancer and prostate enlargement in Japanese men is only a fraction of that found in the United States. Yet autopsies performed on Japanese men show that they may have the same amount of small cancers in their prostate as found in men in the United States. These small indolent cancers may not cause any problems. One can live very well with cancers that do not grow or spread to vital organs. Yet if a Japanese man moves to the United States, by the second generation, his sons will have the same significant prostate cancer and prostate enlargement incidence as other Americans. It seems clear that diet has an enormous impact on these diseases.

The Japanese eat very little red meat. Over 120 million people live in a very small area. There simply is no room to raise cattle. What little red meat that is available is very expensive (as much as $15 or more a pound). Instead of red meat, the Japanese eat fish and soy products. Soy is a very versatile vegetable that can be served in dozens of different ways. It has about the same amount of protein that is found in meat but does not have the fat that is blamed for a lot of our health problems.

There are many soy products that can be used such as soy milk, tofu, miso, and even meatless veggieburgers.

The two most studied anticancer constituents in soy are genistein and daidzein. Some people do not want to eat whole soy but want to obtain an effective amount of genistein and daidzein, which are also known as the isoflavones. There are standardized soy extracts that provide more than 40% isoflavones, thus enabling men to obtain the active constituents of soy in 1-2 tiny capsules.

As noted earlier, fish is also very important and should be a part of your diet. Omega-3 fish oils help the body in many ways. Omega-3 fish oil is an essential fatty acid. Some claim that it helps protect against a large number of diseases such as cancer, arthritis, heart disease, and many others.

Of course, watch your diet and your weight. By all means, take a good multivitamin and mineral supplement every day. Be sure that you get vitamins and supplements from a trusted resource.

There is no guarantee that following a healthy diet can prevent prostate enlargement or prostate cancer, but it will reduce the odds based on a plethora of published research data.

Prostatitis

Acute Bacterial Prostatitis
Chronic Bacterial Prostatitis
Asymptomatic Inflammatory Prostatitis
Prostatic Massage to Relieve Prostatitis
Besides prostate enlargement, there are other significant diseases that occur in the prostate. Prostatitis is one of the most neglected male diseases in the United States, affecting more men than either prostate cancer or prostate enlargement. In addition, protastitis can cause more pain and suffering than prostate enlargement. A chronic case may be very difficult to cure. Some men may suffer for years and incur costs of several thousands of dollars trying to find relief. Some men have even resorted to having the prostate removed just to be free of prostatitis.

Urologists have estimated that one in every four men who see a doctor about a problem involving the penis, urethra, testicles, prostate, bladder, or kidneys is suffering from prostatitis. There are at least three types of this disease.

Acute Bacterial Prostatitis
Acute bacterial prostatitis is the least common of the four types, but it is also the easiest to diagnose and treat effectively. Men with this disease often have chills, fever, pain in the lower back and genital area, urinary frequency and urgency (often at night), burning or painful urination, body aches, and a demonstrable infection of the urinary tract as evidenced by white blood cells and bacteria in the urine. Acute bacterial prostatitis is treated with an appropriate antibiotic.

Often a case of prostatitis will cause an elevated PSA. Many doctors will institute a series of antibiotics to see if that will bring the PSA down. If it does, then a physician can be fairly certain that the elevated PSA was due to a bacterial prostatitis. One major difference is that prostatitis can be accompanied by pain; prostate enlargement and early prostate cancer usually do not cause pain.

Prostate Enlargement Protocol Pg (1) (2) (3) (4) (5) (6)

These statements have not been evaluated by the FDA. These products are not intended to diagnose, treat, cure, or prevent any disease