Chris Sugg and Michael Wiggins
Thanks to the University of North Carolina School of Pharmacy
for the use of this article!
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.
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,
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
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.
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
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.
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
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.
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.
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.
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