Prostate Enlargement Protocol

The Optimal Extract from Saw Palmetto
Supercritical fluid extraction technology produces an extract of extraordinary purity while leaving behind no solvent residues on the product. The process uses carbon dioxide (CO2) in its supercritical fluid state, when it is neither liquid nor gas. The world's largest supercritical fluid extraction plant is probably operated by Maxwell House Coffee Company (Houston) for decaffeinating coffee beans.

The first medicinal herb to benefit from large-scale supercritical fluid extraction was saw palmetto. Clinical and experimental studies of supercritical fluid extracts of saw palmetto demonstrate some remarkable advantages over conventional hexane extracts found in most dietary supplements.

Because saw palmetto is thought to interfere with testosterone-induced growth of the prostate, researchers tested the effect of saw palmetto extracts on prostate weight in castrated rats given testosterone. The rats were divided into control and treatment groups and given placebo, testosterone, or testosterone plus saw palmetto extract for 10 days. Then, the rats were killed, and their prostate glands were weighed.

In the control groups, normal rats had an average prostate weight of 20.6 mg at the end of the experiment, while castrated rats given testosterone had nearly normal prostate weights averaging 17.4 mg. Castrated rats given placebo instead of testosterone had an average prostate weight of only 3.0 mg.

When a conventional hexane extract of saw palmetto was given to castrated rats along with testosterone, average prostate weight was reduced to 11.7 mg. However, when a supercritical fluid extract of saw palmetto was given (in the same dosage as the conventional extract) along with testosterone, average prostate weight dropped to 6.5 mg. Furthermore, the supercritical fluid extract given at half dosage reduced average prostate weight as effectively (to 11.9 mg) as the hexane extract at full dosage.

These data were presented in a review article on saw palmetto in the European journal Fitoterapia , one of the oldest and respected European botanical medicine journals, with an international roster of contributors in each issue (Cristoni et al. 1997).

One mechanism by which saw palmetto is thought to work is inhibiting the enzyme 5-alpha-reductase in the prostate gland. This enzyme converts testosterone to an active form called DHT that stimulates growth in prostatic tissue. A study in a German urology journal tested the ability of the supercritical fluid extract of saw palmetto to inhibit this enzyme. The researchers concluded that the extract is a strong inhibitor of 5-alpha-reductase.

We know that saw palmetto also exerts an anti-inflammatory effect on prostate tissue. Research in a German pharmaceutical journal demonstrates that the supercritical fluid extract of saw palmetto strongly inhibits the proinflammatory arachidonic acid cascade. They showed that the extract provides dual inhibition of the COX pathway and the 5-lipooxygenase pathway (Breu et al. 1992).

A well-designed clinical trial in Belgium with 132 patients compared two dose schedules for the supercritical fluid extract, the standard twice a day schedule and a new once a day schedule. Patients were randomly assigned to a group given the standard 160-mg capsule twice a day or to a group given one 320-mg capsule in the morning and a placebo capsule in the evening.

The study found the two dosing schedules to be equally safe and effective overall. In both groups, symptom scores on the IPSS scale dropped by about 60%, and maximum urinary flow rate increased by about 22%. The following chart provides the results in detail.

Eight patients in each group reported adverse effects; in three-quarters of these cases the physician judged the complaint to be a consequence of prostate enlargement itself rather than of the medication. Two patients in each group withdrew from the study due to side effects. The medication was well tolerated by the remaining patients. A supercritical fluid extract of saw palmetto in one-a-day capsules gives men an equally convenient alternative to the drug finasteride (Proscar). Finasteride, the standard drug for prostate enlargement, is normally taken once a day.

Finasteride causes diminished libido and sexual dysfunctions in some patients; in particular, about 3-4% of patients experience impotence. By contrast, saw palmetto is very well tolerated and inexpensive (Braeckman et al. 1997).

Another large observational study in Germany followed 2000 prostate enlargement patients given a standard dosage of the supercritical fluid extract (160-mg capsules twice a day) for 3-6 months. Three-fourths of the patients had Stage II prostate enlargement, while the remainder were in Stage III of the disease. The main variable studied, residual urine, declined on average from 80 to 45 mL. Patients without severe symptoms of dysuria (painful or difficult urination) increased from 24.9-62.5%. A significant 88% of patients subjectively evaluated the treatment as very good or good. Only 2-4% of patients reported side effects, which were mostly mild gastrointestinal disturbances.

Table 2:Comparison of saw palmetto supercritical fluid extract taken once or twice daily*
160 mg twice a day 320 mg once a day
Decrease in symptom score (IPSS) 59.5% 61.2%
Increase in maximum urinary flow 23.8% 21.4%
Increase in average urinary flow 21.3% 12.5%
Decrease in residual urine 6.2% 24.8%
Decrease in prostate volume 9.7% 14.7%
Rated successful by patient 75.0% 86.0%
Rated successful by physician 75.0% 88.0%
*C hart indicates that 320 mg of the supercritical extract of saw palmetto taken once a day produces similar benefits as 160 mg of the supercritical extract taken twice a day.

Nettle Root Extract Blocks DHT Binding to Prostate Cells
An extract from the nettle root called Urtica dioica has been used extensively in combination with saw palmetto or by itself as a drug to treat prostate enlargement. One study showed that after 8 weeks of treatment with 4 capsules of urtica extract, patients experienced an 82% improvement in disorders associated with prostate enlargement (Wolf 1980). Another study showed that those patients with prostate enlargement with Stage I-III hyperplasia (the abnormal multiplication of normal cells that can lead to prostate cancer) experienced an 86% improvement after 3 months of treatment with standardized urtica extract (Maar 1987).

After learning the results of these studies, researchers at St. Luke's Roosevelt Hospital in New York conducted a study to discover the mechanism by which standardized urtica extract relieves the symptoms of prostate enlargement. In their published study, the St. Luke's scientists showed that urtica extract inhibits the binding of a testosterone-estrogen-related protein to its receptor site on prostate cell membranes (Hryb et al. 1995).

It is known that when the testosterone metabolite DHT binds to prostate cell membranes, the result is the overproliferation of prostate cells. If cell membrane receptors are blocked, then DHT cannot latch on to the cell. Urtica extract appears to work by preventing the binding of testosterone metabolites to membrane receptor sites on prostate cells.

Saw palmetto and U. dioica are approved drugs in Germany for the treatment of benign prostate enlargement. While urtica is relatively new to Americans, it has been safely and successfully used in Germany for more than a decade.

Pygeum Reduces prostate enlargement Symptoms Via Additional Mechanisms
Pygeum originally was shown to reduce prostate swelling (edema) and block DHT binding to prostate cells. Later studies showed that pygeum also interferes with protein kinase C activity to inhibit the proliferation of prostate cells. Rapidly growing benign and malignant cells require the protein kinase C enzyme. The inhibition of protein kinase C by pygeum may help to prevent cancer, slow the growth of existing cancers, and reduce the proliferation of benign prostate cells.

Scientists analyzed 18 randomized, controlled trials using pygeum to treat prostate enlargement involving 1562 men. The mean study duration was 64 days. Compared to men receiving placebo, Pygeum africanum provided a moderately large improvement in the combined outcome of urologic symptoms and flow measures. Men using P. africanum were more than twice as likely to report an improvement in overall symptoms. Nocturia was reduced 19%, residual urine volume was reduced 24%, and peak urine flow was increased 23%. Adverse effects due to P. africanum were mild and comparable to placebo (Wilt et al. 2002).

Pygeum is sold as a drug in many countries for the specific indication of relieving urinary symptoms associated with prostate enlargement.

Saw palmetto, stinging nettle, and pygeum extracts standardized in the Natural Prostate Formula have been shown in independent studies to improve prostate function in aging men by these illustrated mechanisms.

How to Use European Phyto Extracts
Phyto is from the Greek phyton meaning plant. The term phytotherapeutics means using drugs that are derived from plants. The most effective phytotherapeutic agents for the treatment of prostate enlargement are saw palmetto, P. africanum, and nettle root (U. dioica) extracts.

For many men, one 320-mg capsule a day of the supercritical extract from saw palmetto will provide some relief from benign prostate disease.

Because we know that prostate enlargement is a progressive disease caused by several underlying mechanisms, the optimal approach is to take a combination of all three phytoextracts that have demonstrated efficacy against prostate enlargement. The objective is to achieve maximum relief from urinary discomfort, inhibit further gland enlargement, and possibly reduce prostate cancer risk. To duplicate the many successful prostate studies, the following phytoextracts should be taken twice a day:

Saw Palmetto (supercritical) Extract--160 mg
(85-95% sterols)
Stinging nettle root extract--120 mg
(U. dioica)
P. africanum--50 mg
(13% sterols)

Make Sure Prostate Herbal Extracts Are Standardized
Soon after standardized saw palmetto (and other European extracts) was introduced to the United States, many supplement companies began selling nonstandardized versions of these herbs. These nonstandardized herbs do not contain the active extracts needed to provide therapeutic benefits.

A study presented at the 2002 American Urological Association Convention found that a large number of health food products did not match the potency or quantity of ingredients listed on the label. Because of the lack of USP standards, be sure to purchase such products from a well-known, reliable, and trusted source.

We suggest that you carefully read the label of these products and buy them only from brand name companies. Make sure you are obtaining standardized extracts of saw palmetto, P. africanum, and U. dioica .

How Estrogen Estrogen to prostate enlargement

Using Aromatase Inhibiting Drugs
According to many conventional views, prostate enlargement develops when testosterone and its active metabolite DHT stimulate cell growth. Testosterone is converted to DHT systemically as well as within the prostate by an enzyme known as 5-alpha-reductase. DHT is up to 10 times more active than testosterone in binding to sites in prostate cells that regulate prostate growth. When DHT binds to these sites, it activates growth factors that stimulate cell proliferation.

Commonly used medications for prostate enlargement, such as the drug finasteride (Proscar), inhibit serum 5-alpha-reductase in order to reduce DHT-stimulated growth in the prostate. (Saw palmetto is thought to inhibit the 5-alpha-reductase enzyme in the prostate gland, but not in the blood.)

While it is hardly surprising that prostate growth is under hormonal control, the view that prostate enlargement is solely caused by excess levels of testosterone metabolites is difficult to explain when we consider the effects of aging. prostate enlargement is, after all, a disease of aging, and tes-tosterone production declines with age. Moreover, the levels of free, physiologically active testosterone decline more sharply due to increased testosterone binding by a protein called sex hormone-binding globulin (SHBG). It is estimated that levels of free testosterone decline by about 1% a year from age 40-70. So, if testosterone production declines with age, could there be another mechanism contributing to prostate enlargement?

The answer may be the growing imbalance in aging men between their levels of estrogen and tes-tosterone. While levels of estrogen appear to be relatively stable in the aging male, the level of free testosterone precipitously declines. Thus, with age, an imbalance develops between estrogens and androgens (male hormones).

Compared to younger men, the ratio of free estradiol (the most potent form of estrogen) to free tes-tosterone is up to 40% higher in older men. In the prostate itself, the contrast between rising estrogens and declining androgens is more sharply drawn. In the stroma of the prostate, the supporting tissue where prostate enlargement is thought to develop, estrogen levels increase significantly with age, while DHT levels remain stable. Estrogen levels in the stroma rise to even higher levels in prostate enlargement patients. In the epithelium of the prostate, DHT levels decline with age while estrogen levels remain stable (Shibata et al. 2000).

German researchers who have been studying this for more than 15 years describe a tremendous increase with age of the estrogen-androgen ratio in the human prostate. Their article in the Journal of Clinical Endocrinology and Metabolism concludes: "Our results indicate that the prostatic accumulation of DHT, estradiol, and estrone is in part intimately correlated with aging, leading with increasing age to a dramatic increase of the estrogen/androgen ratio particularly in stroma of prostate enlargement" (Krieg et al. 1993).

A study in the journal Prostate bears out the concept of an elevated serum estrogen-androgen ratio as a risk factor for prostate enlargement. Analyzing frozen blood samples collected in the course of a large-scale health study, the researchers found that prostate enlargement risk increased with higher estradiol levels, and that the risk was concentrated in men with relatively low androgen levels (Gann et al. 1995).

A Japanese study came to a similar conclusion, finding that prostate size correlates with estradiol level and with the ratio of estradiol to free testosterone. They suggest that the endocrine environment tended to be estrogen-dominant with age, in particular, after middle age and that patients with large prostates have more estrogen-dominant environments, concluding that estrogens are key hormones for the induction and the development of prostate enlargement (Suzuki et al. 1992).

Experimental attempts to induce prostate enlargement with hormones would answer many questions, but obviously cannot be carried out in humans. The only animals known to develop prostate enlargement with age are dogs and lions.

In experiments with dogs, it has been established that prostate enlargement cannot be induced without estrogen; however, it should be noted that endocrine regulation and prostate structure are quite different in dog and man (Habenicht et al. 1991).

In men, most estrogens are produced from androgens; specifically, most estradiol is produced from tes-tosterone. This conversion of androgens to estrogens is called aromatization. The specific enzyme causing this undesirable transformation of testosterone to estrogen is called aromatase. In addition to receiving estrogen circulating through the bloodstream, the stroma of the prostate produces its own estrogen through aromatization.

It has long been suspected that estrogen, especially the estrogen-androgen imbalance associated with aging, plays a role in prostate enlargement, but until recent years no direct effect of estrogen on the prostate could be demonstrated. A key piece of this puzzle has been supplied by a group of researchers at Columbia University in New York and the pharmaceutical company Merck.

Research has demonstrated the existence of a second hormonal pathway in the prostate whereby estrogens can mimic androgens. It may help to understand this breakthrough by thinking of hormones as chemical messengers. When a hormone attaches to its special binding site on a cell, it sends a signal to that cell. In the case of prostate enlargement, androgens signal cells to proliferate, causing prostate growth. These researchers have shown that messages sent to prostate cells by androgens can also be sent, along an alternative signaling pathway, by estrogens. Even more surprising, the estrogens send this signal, not by attaching to the usual cellular binding sites for estrogen, but instead to the sex hormone-binding globulin (SHBG) that is already bound to the cell membrane. As the authors put it, they have shown that in the prostate, estradiol is capable of activating pathways normally considered androgen responsive.

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