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The exact mechanism of action, active ingredient, and clinical effectiveness of Saw Palmetto Extract are not completely known. However, recent research has shed some light on the many aspects of the extract and its use.

In a Cochrane Database  of Systematic Reviews in March of 2002, Wilt et al. performed a systematic review of literature to assess the effects of SPE in the treatment of LUTS consistent with BPH.  The main outcome measure was change in urologic symptom scale scores with secondary outcomes being changes in nocturia and urodynamic measures.  In this review, 3139 men from 21 randomized trials lasting from 4 to 48 weeks was assessed.  Treatment allocation was adequately concealed in 11 studies, with double blinding in 18 studies.  SPE improved urinary symptom scores, symptoms, and flow measures compared to placebo and had similar improvements in urinary symptom scores as finasteride.  The authors concluded that SPE has similar efficacy in improving urinary symptoms and flow as finasteride, with fewer adverse events.

Later in 2002,Veltri et al. examined the DNA structure and organization of epithelial cells looking for a saw palmetto mediated effect on a nuclear level.  In previous studies, it had already been shown that SPE suppresses DHT levels and causes contraction of epithelial cells in men with symptomatic BPH, but a mechanism had not been elucidated.  In a 6-month randomized trial comparing saw palmetto herbal blend (SPHB) to placebo, images were taken from 200 randomly selected epithelial cell nuclei and were examined based on nuclear morphometric descriptors (NMDs), such as size, shape, DNA content, and textural features.  It was found that no significant change from baseline was found in the NMDs in placebo groups, however 25 of 60 NMDs were significantly different compared with baseline in SPHB groups.  This study thus showed SPHB treatment appears to alter the DNA chromatin structure and organization in prostate epithelial cells, suggesting a possible molecular basis for the therapeutic effects. 

In August 2002, Talpur et al. demonstrated the ability of saw palmetto to inhibit prostatic hyperplasia via its effect on androgen metabolism.  Non-castrated rats and castrated rats were given testosterone.  The mass of the prostate in castrated rats increased nearly ten fold.  Castrated rats receiving both testosterone and SPE decreased the size to roughly the same as non-castrated rats, which was significantly smaller than rats treated with testosterone.  Non-castrated rats treated in the same manner showed similar results.  This data showed the ability of saw palmetto to decrease prostatic hyperplasia via its effects on androgen metabolism.

BPH tissues have documented changes in the IGF system, which is important for prostate growth and development.  The most important signaling pathway activated by IGF-I binding to its receptor are the ERK arm of the MAPK cascade and phosphoinositol-3-kinase (PI3K)/protein kinase B (PKB/Akt) cascade.  In a 2004 study by Wadsworth et al., it was hypothesized that SPE inhibition of IGF-I signaling suppresses growth and induces apoptosis in the P69 prostate epithelial cell line.  Via Western Blot analysis, they showed that SPE may work in part by inhibiting a specific component of the IGF-I signaling pathway and inducing JNK activation, thus resulting in antiproliferative and proapoptotic effects on prostate epithelia.  This blocks subsequent phosphorylation and activation of transcription factors responsible for gene expression patterns that trigger mitogenic or differentiative cellular responses.