Effects of a Saw Palmetto Herbal Blend in Men With Symptomatic Benign Prostatic Hyperplasia

Abstract

Purpose: We tested the effects of a saw palmetto herbal blend in men with symptomatic benign prostatic hyperplasia (BPH) via a randomized, placebo controlled trial.Materials and Methods: We randomized 44 men 45 to 80 years old with symptomatic BPH into a trial of a saw palmetto herbal blend versus placebo. End points included routine clinical measures (symptom score, uroflowmetry and post-void residual urine volume), blood chemistry studies (prostate specific antigen, sex hormones and multiphasic analysis), prostate volumetrics by magnetic resonance imaging, and prostate biopsy for zonal tissue morphometry and semiquantitative histology studies.Results: Saw palmetto herbal blend and placebo groups had improved clinical parameters with a slight advantage in the saw palmetto group (not statistically significant). Neither prostate specific antigen nor prostate volume changed from baseline. Prostate epithelial contraction was noted, especially in the transition zone, where percent epithelium decreased from 17.8% at baseline to 10.7% after 6 months of saw palmetto herbal blend (p Ͻ0.01). Histological studies showed that the percent of atrophic glands increased from 25.2% to 40.9% after treatment with saw palmetto herbal blend (p Ͻ0.01). The mechanism of action appeared to be nonhormonal but it was not identified by tissue studies of apoptosis, cellular proliferation, angiogenesis, growth factors or androgen receptor expression. We noted no adverse effects of saw palmetto herbal blend. When the study was no longer blinded, 41 men elected to continue therapy in an open label extension.Conclusions: Saw palmetto herbal blend appears to be a safe, highly desirable option for men with moderately symptomatic BPH. The secondary outcome measures of clinical effect in our study were only slightly better for saw palmetto herbal blend than placebo (not statistically significant). However, saw palmetto herbal blend therapy was associated with epithelial contraction, especially in the transition zone (p Ͻ0.01), indicating a possible mechanism of action underlying the clinical significance detected in other studies.

Effects of pumpkin seed oil and saw palmetto oil in Korean men with symptomatic benign prostatic hyperplasia

“…But several of reports demonstrated only a minimal change of prostate volume within 1 year (Marks et al, 2000; Wilt et al, 1998). We also could not detect any significant decrease of the prostate volume even within 12 months.…”

“…A phytochemical based therapy is widely given to men with symptomatic BPH in Western Europe, where physicians prescribe phytochemical products in the same manner as they prescribe drugs (Marks et al, 2000). …”

Role of Oxidative Stress Response Elements and Antioxidants in Prostate Cancer Pathobiology and Chemoprevention -- A Mechanistic Approach

“…Antioxidants, both natural and synthetic, have recently gained significant attention by the health, cosmetic, nutritional, educational, and pharmaceutical industries. Such dietary supplements and chemopreventive agents (e.g., green tea, Saw-Palmetto, St. John Wart, retinoids, organoselenium, lycopene, vitamins E, C, and D and soy extracts) have been claimed to prevent or delay the progression of BPH and/or PC [68][69][70][71]. Currently these are under many scientific investigations as potential chemoprotectors to establish their usefulness in preventing PC.…”

Kaposi’s Sarcoma-Associated Herpesvirus Subversion of the Anti-Inflammatory Response in Human Skin Cells Reveals Correlates of Latency and Disease Pathogenesis

“…Alternatively (or in addition), it is possible that mechanisms for virus reactivation such as virus-induced apoptosis [79, 80] may be expressed in Mel1700 cells and not MeWo cells, an interesting concept that should be the focus of follow-on studies beyond the scope of the current study. In addition, isolation and characterization of correlates that control the timing and aggressiveness of KS at a population level may provide predictive power with respect to stratification of individuals at high risk for development of the lesion based on differential exposure to pro-inflammatory cofactors that foment inflammation, including toxins, UV radiation, allergens, trauma, or persistent infections [81]. We note, for example, that in KSHV/HIV coinfected individuals who are generally at a greater risk of developing the most aggressive form of KS, HIV serves as a cofactor for KS not only through establishment of an immunosuppressed environment but also through upregulation of the KSHV receptor, xCT [82], to facilitate KSHV dissemination.…”