Abstract
Part I of this 3-part series provided the groundwork for understanding the role of a standardized lipidosterolic extract of Serenoa repens (LSESr) in the treatment of LUTS. It documented that a treatment having a high therapeutic index (i.e., a ratio of benefit to adverse reactions) is a critical need in the demographic context of a rapidly growing elder population. Part I described the clinical symptomatology of LUTS and how it is quantified. A critique of the reports from four authoritative bodies: the European Scientific Cooperative on Phytotherapy (ESCOP), Cochrane 2012, the European Medicines Agency (EMA), and the AUA (American Urological Association) was presented. The foundation above then fine-tuned our search to require (a) consistent evaluability criteria, (b) the quantification of clinical findings, (c) the need to focus on studies employing a standardized LSESr product meeting the fatty acid profile set forth by the European Medicines Agency (EMA) and the US Pharmacopeia and (d) a global assessment of scientific investigations published in all languages and not limited to only English. With the above four constraints, “new” findings about LSESr vs. LUTS are presented. How did the search strategy and selection criteria lead to new understandings about the role of LSESr vs. LUTS? How safe is LSESr in contrast to its counterpart prescription drugs? Of the proposed major mechanisms of action of LSESr (e.g., 5-alpha reductase inhibition and anti-inflammatory activity), what are the key points? After initiating treatment with LSESr, when is clinical improvement seen? How durable is LSESr in ameliorating LUTS? Can LSESr prevent the progression of BPH?
Highlights
Part I of this 3-part series provided the groundwork for understanding the role of a standardized lipidosterolic extract of Serenoa repens (LSESr) in the treatment of LUTS
How did the search strategy and selection criteria lead to new understandings about the role of LSESr vs. LUTS? How safe is LSESr in contrast to its counterpart prescription drugs? Of the proposed major mechanisms of action of LSESr (e.g., 5-alpha reductase inhibition and anti-inflammatory activity), what are the key points? After initiating treatment with LSESr, when is clinical improvement seen? How durable is LSESr in ameliorating LUTS? Can LSESr prevent the progression of benign prostatic hyperplasia (BPH)?
The authors concluded that “this type of therapy can stop the progression of BPH growth and improve bladder function . . . ” The PSA values remained stable in all patients, no patients were diagnosed with acute urinary retention, and there were no adverse effects due to LSESr [38]
Summary
Ν Redecker data evaluated nocturia reported symptoms based on % improvement involving weak stream, hesitancy, incomplete emptying, frequency, and nocturia. +, positive change; CO 2, al Prostate Symptom Score; mos, months; QoL, quality of life; Qmax, peak urinary flow (mL/s); Ref., The mean number of patients in the evaluable non-English-language studies for LSESr for efficacy in LUTS was 460, influenced by the Vahlensieck 1993 study with 1334. The mean number of patients in the evaluable non-English-language studies for LSESr for efficacy in LUTS was 460, influenced by the Vahlensieck 1993 study with 1334 patients [16], the Derakhshani 1997 study with 1047 patients at the study end [19] and the Eickenberg 1997 study with 6967 patients [20]. The noted American news broadcaster Paul Harvey would conclude each episode with “The rest of the story.” Our scientific research should do just that (i.e., review the full scope of the literature and tell the full story)
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