What is St. Saw Palmetto?
 
   

What is St. Saw Palmetto?

This section is compiled by Frank M. Painter, D.C.
Send all comments or additions to:
   Frankp@chiro.org
 
   

Chris Sugg and Michael Wiggins

Thanks to the University of North Carolina School of Pharmacy
for the use of this article!


GENERAL DESCRIPTION

Saw palmetto is a small, scrubby palm tree native to the Atlantic coastal area (from South Carolina to Florida) and the West Indies. The plant typically grows to a height of 6 to 10 feet with large, 2 to 3 foot high, spiny-toothed leaves that form a circular, fan-shaped crown on the tree. The medicinal properties of the tree come from the berries. These 0.5 to 1 inch long berries are a deep red-brown to black color and are wrinkled, oblong and about a half-inch in diameter.

CHEMICAL COMPOSITION

The berries of the saw palmetto contain about 1.5 % of a fruity-smelling oil that contains saturated and unsaturated sterols and fatty acids. Free fatty acids (capric, caprylic, caproic, lauric, palmitic, and oleic acids) comprise about 63 % of this oil. The remaining oil is made up of ethyl esters of the above listed fatty acid and sterol, particularly beta-sitosterol and its glucoside. The berries are also comprised of carotenes, lipase, tannins, and sugars.

The lipid-soluble components of the berries are extracted and purified, yielding the pharmacologically active portion of the oil. This medicinally-used extract contains about 85 to 95 % fatty acids and sterols.

HISTORY AND FOLK USE

Saw palmetto berries were used by the American Indians to treat genitourinary tract conditions and also as a tonic for nutritional supplementation. It was given to males to increase testicle function and relieve irritation in the genitourinary tract and prostate. It has been given to females to cause the mammary glands to enlarge. It is considered by some herbalists to be an aphrodisiac.

PHARMACOLOGY

A standardized fat-soluble saw palmetto berry extract shows numerous effects relating to its main clinical application in treating benign prostatic hyperplasia. This condition is thought to be caused by an accumulation of testosterone in the prostate. Once within the prostate, testosterone is changed to a more potent hormone (dihyrotestosterone, DHT). This hormone is responsible for stimulating the cells in the prostate to multiply excessively, causing enlargement of the prostate.

Saw palmetto's primary therapeutic action is to inhibit the conversion of testosterone to DHT in the prostate, as well as inhibiting the binding and transport of DHT. In contrast, recent studies have shown that saw palmetto may in fact have antiestrogenic activity. Estrogen facilitates BPH because it interferes with the hydroxylation and elimination of DHT from the prostate.

CLINICAL APPLICATIONS

The primary clinical application of saw palmetto extract is in the treatment of benign prostatic hyperplasia, however, it may also be useful in women with androgen excess conditions, such as hirsutism and polycystic ovarian disease.

TOXICITY

According to most sources, saw palmetto extract is completely safe to use. There have been no significant reports of side effects in clinical trials and detailed toxicology studies performed in rats, mice and dogs indicate that the extract has no toxic effects.

DRUG AND DISEASE INTERACTIONS

There has been no published data on drug or disease interactions with the use of saw palmetto extract.

DOSAGE

As is the case with any complementary / alternative medicine product, a standardized extract is required to achieve the desired effect. Fat-soluble saw palmetto extracts containing 85 to 95 percent fatty acids and sterols should be used in dosages of 160 milligrams twice daily. It is not possible to obtain this dosage through the use of crude berries, fluid extracts, or tinctures. It is further recommended that saw palmetto be taken with a full glass of water and after meals

EVALUATION OF CLINICAL TRIALS

PAUBERT-BRAQUET et al STUDY (1996)

This study involved the use of rats treated with estradiol and testosterone in order to induce prostate enlargement and the degree of effect on reducing this enlargement by use of Sarenoa repens extract. The study involved 3-month-old Wistar rats kept in identical environments, given either S. repens extract plus carrier (2.5% ethanol) or just carrier alone. The rats were given hormones (17-D estradiol and testosterone) through silastic tubing implants. Twelve rats were treated for 30 days, five rats treated for 60 days, and 10 rats treated for 90 days. Treated rats received 50 mg / kg of body weight of S. repens extract daily (dose was based on the dosage used in humans). At the end of each time period, the prostatic tissues of the treated and untreated rats was dissected, weighed, and examined microscopically. The prostatic tissue was divided into three categories: dorsal lobe, lateral lobe, and ventral lobe. Following treatment for 30 days, there was a decrease in the weight of all lobes in the treated rats versus the untreated rats; however, only the decrease (16.6%) in the dorsal lobe was clinically significant. After 60 days of treatment, the decrease in prostatic total weight was highly significant for the dorsal and lateral lobes (51.4% and 42.1 %) but not significant for the ventral lobe. Finally, after 90 days of treatment the decrease in weight of the prostate was significant only for the dorsal lobe (45.5%). These results demonstrate that administering S. repens extract to hormone-treated castrated rats inhibits the increase in prostate weight gain. This may explain the beneficial effects of this extract in human subjects with BPH.

SULTAN, TERRAZA, et al STUDY (1984)

This study was intended to determine the effect of Serenoa repens extract on the binding and metabolism of androgens in human foreskin fibroblasts. All of these studies were carried out on the same strain of fibroblasts obtained from the foreskin of normal infants or adults. Serenoa repens extract(S.R.E.) of different dilutions (5.7 to28.6 U/mL*) was added to culture media containing testosterone or dihydrotestosterone (DHT) and incubated at 37° C with cultured fibroblasts. The 28.6 U/mL S.R.E. significantly altered the formation of DHT and strongly inhibited the 3-ketosteroid reductase-mediated conversion of DHT to 5aandrostane-3a,17D-diol. S.R.E. was also shown to be a good competitor for the whole cell androgen receptor as evidenced by the fact that 7.1 U/mL S.R.E. gave a 50% inhibition of the binding of 2 x 10-9 M DHT to its receptor. The results of this study showed that S.R.E. inhibits 5a-reductase, 3-ketosteroid reductase, and androgen receptor binding in cultured human fibroblasts.

*Strengths of S.R.E. are listed as U/mL, with one unit defined as the amount of S.R.E. required to inhibit 50% of the specific binding of [3H]1881 to rat prostate cytosol.

PROSCAR COMPARISON STUDY (1994)

This study involved a total of 32 healthy male volunteers age 20 to 30 years old in a 1-week open, randomized, placebo-controlled trial comparing finasteride (Proscar) and Permixon, the plant extract of Serenoa repens. This study's intention was to determine the effectiveness of single and multiple doses of the drugs on the inhibition of 5a-reductase as measured by serum dihydrotestosterone (DHT) levels. After taking baseline measurements on day 1, 10 volunteers randomly received finasteride 5 mg once daily,11 received Permixone 160 mg twice daily, and 11 received placebo once daily for 7 days. Serum testosterone and DHT levels were taken at 12, 24, 48, 72,120, and 168 hours following baseline measurements. Following a single dose of finasteride 5 mg, serum DHT levels were reduced by 65% from baseline at 12 hours. This extent of decrease remained constant throughout the seven days. Permixone and placebo caused no significant reductions in DHT over the seven days. Serum testosterone levels remained within the normal limits over the seven days of the study with all three groups. The effect seen with finasteride therapy supports its efficacy as an inhibitor of 5a-reductase. The lack of effect of Permixone on DHT levels does not support its hypothesis of a prostatic mechanism of action involving 5a-reductase inhibition.

CHAMPAULT, PATEL, BONNARD TRIAL (1984)

This was a double-blind, placebo-controlled trial involving 110 outpatients with established signs and symptoms of BPH, 55 receiving saw palmetto extract and 55 receiving placebo. Patients received 320 mg per day (2 x 80 x 2) of saw palmetto extract or placebo. Nocuria, intensity of dysuria, flow rate, post-micturition residue, self-rating by patients and global physician rating were assessed before treatment and after 30 days of therapy. Ninety-four (94) patients (44 placebo, 50 saw palmetto) completed the study and were evaluated at the end of 30 days. Patients receiving saw palmetto extract were significantly (compared to placebo) improved in each of the objective criteria as well as in the subjective patient and physician evaluations. The extract was very well-tolerated, with less patients reporting side effects (mild, eg. headaches) with saw palmetto than with placebo (5 vs.11). This data supports the use of saw palmetto extract in the treatment of BPH.

REFERENCES

Carilla E., Briley M., et al. "Binding of Permixon, a New Treatment for Prostatic Benign Hyperplasia, to the Cytostolic Androgen Receptor in the Rat Prostate." J. Steroid Biochem. Vol. 20, No.1, pp. 521 -523,1984.

Champault G., Patel J.C., and Bonnard A.M. "A double-blind trial of an extract of the plant Serenoa repens in benign prostatic hyperplasia." Br. J. Clin. Pharmac. Vol.18, pp. 461-462,1984.

Murray MT. The Healing Power of Herbs. Rocklin, CA: Prima Publishing, 1996, pp. 306-313.

Paubert-Braquet M., Richardson FO, et al. "Effect of Serenoa repens extract (Permixon) on estradiol/testosterone-induced experimental prostate enlargement in the rat." Pharmacological Research, Vol. 34, No. 3 / 4, pp. 171-179,1996.

Strauch G., et al. "Comparison of finasteride (Proscar) and Serenoa repens (Permixon) in the inhibition of 5-alpha reductase in healthy male volunteers." Eur. Urol. Vol. 26, pp. 247-252,1994.

Sultan C., Terraza A, et al. "Inhibition of androgen metabolism and binding by a liposterolic extract of Serenoa repens B in human foreskin fibroblasts." J. Steroid Biochem. Vol 20, No.1, pp. 515-519,1984.

The following internet sites:

http://botanical.com/botanical/mgmh/s/sawpal26.html

http://www.desertbloomherbs.com/monographs/sawpalmetto.html



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