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Clinical use of saw palmetto

Robert B Saper, MD, MPH
Section Editor
Joann G Elmore, MD, MPH
Deputy Editor
Howard Libman, MD, FACP


Extracts of the fruit from saw palmetto (Serenoa repens), the American dwarf palm tree (picture 1), are commonly used to treat benign prostatic hypertrophy (BPH). The first evidence of saw palmetto use for urinary symptoms in men is from Egypt in the 15th century BC [1]. Native Americans in Florida in the early 1700s utilized saw palmetto to treat prostate gland swelling and inflammation, testicular atrophy, and erectile dysfunction [2,3].

In the 1870s, eclectic medical practitioners used the plant for urologic conditions. Saw palmetto berries were officially listed in the United States Pharmacopoeia in the first half of the 20th century [4]. Saw palmetto use is common in Europe and somewhat less popular in the United States [5].

A number of studies and meta-analyses have evaluated extracts of the saw palmetto berry for its safety and efficacy in the treatment of BPH; these are reviewed here. Detailed discussions of the treatment of BPH and the use of saw palmetto in the combination herbal product PC-SPES for the treatment of prostate cancer are discussed separately. (See "Alternative endocrine therapies for castration-resistant prostate cancer" and "Medical treatment of benign prostatic hyperplasia", section on 'Herbal therapies'.)


The saw palmetto berry contains over 100 known compounds. The active ingredients in saw palmetto appear to be contained in the purified lipid soluble extract of the saw palmetto berry. This has been found to contain 85 to 95 percent fatty acids (predominantly lauric, caprylic, and caproic), long-chain alcohols, and sterols (including beta-sitosterol, stigmasterol, cycloartenol, lupeol, lupenone, and methylcycloartenol) [6].

The exact mechanisms of action of saw palmetto are unknown [6]. Proposed mechanisms include antiandrogenic effects [6,7]; inhibition of type 1 and type 2 isoenzymes of 5-alpha-reductase [8-10]; inhibition of growth factors such as the insulin-like growth factor-I [11]; relaxation of lower urinary tract smooth muscle through antagonism of muscarinic receptors [12]; antiinflammatory effects through inhibition of lipoxygenase, cyclooxygenase [13], and leukotrienes [14]; alteration of cholesterol metabolism; antiestrogenic effects; and a decrease in available sex hormone-binding globulin [6,15-18].

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Literature review current through: Nov 2017. | This topic last updated: Aug 16, 2016.
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