Qualcuno ha oltrepassato il limite, ADESSO BASTA - x Lawrence, Parsifal e Joblack
Rispondo a Lawrence che mi scrive:
e a Persifal e JOBLACK che gli hanno dato ragione:
Come al solito qui si offende, ci si fa un culo così per poi essere chiamato ciarlatano, a me non piace offendere ma CERCHIAMO DI ESSERE MENO IGNORANTI:
nessuno ha mai usato con successo la clorofilla per curare deficienze di testosterone (infatti non serve a niente, forse le piante le aiuta...) MA ADDIRITTURA IL SAW PALMETTO VIENE USATO IN AMBITO MEDICO PER CURARE ALCUNE FORME DI IPERTROFIA PROSTATICA O LIEVI FORME DI CALVIZIE CAUSATE PROPRIO DAL DHT!
Cercate di offendere di meno, ricordate che la persona che giudica è la persona che non ha forza di farsi valere facendo perno sulle proprie capacità e si propone dicendo "x è stronzo" oppure "y è ciarlatano" oppure "z è cattivo" invece di COSTRUIRE.
Cercate di non superare il limite.
Lawrence ti do un consiglio: la prossima volta che ti va di insultare una persona ti consiglio di fare questo, ti farà bene allo spirito e al rapporto che hai con gli altri: conta fino a 10 o mangiati un pezzo di cioccolata o leggiti una pagina di un qualsiasi libro (non necessariamente un testo di endocrinologia!) o fai qualsiasi cosa che ti impegni la mente in modo da non insultare.
Lawrence io ti rispondo con studi clinici, tu mi rispondi con insulti dato che non hai argomenti; non credi nell'efficacia del saw palmetto (o serenoa repens) beccati questi (PS: dopo ci sono anche le prove dell'efficacia dell'Acetyl L-Carnitina sull'aumento di testosterone):
In a randomized placebo-controlled clinical study conducted on 25 men with BPH given the standard dose of 320 mg per day of a proprietary SP extract (Permixon®), those with SP experienced statistically significant reductions in levels of prostatic dihydrotestosterone (DHT) and epidermal growth factor (EGF) and increased levels of testosterone (Di Silverio et al., 1998). Additionally, these levels were distinct to the periurethral regions: those with the herb had lower DHT and EGF levels in the periurethral zone. This appears to be evidence of the 5-a-reductase-lowering effects of SP and its more specific regionalized effects compared to the conventional drug finasteride (Proscar®) (Strauch et al., 1994).
-------------------------
Saw palmetto for the treatment of men with lower urinary tract symptoms.
Gerber GS
Section of Urology, Department of Surgery, University of Chicago Pritzker School of Medicine, Chicago, Illinois, USA.
PURPOSE: A comprehensive review of the literature on the use of saw palmetto in men with lower urinary tract symptoms is provided. MATERIALS AND METHODS: A literature search of studies that have assessed the mechanism of action and clinical results of saw palmetto in men with benign prostatic hyperplasia was performed. RESULTS: A variety of potential mechanisms of action of saw palmetto have been demonstrated through in vitro studies, including 5-alpha reductase inhibition, adrenergic receptor antagonism and intraprostatic androgen receptor blockade. Clinical evidence of the relevance of these effects is largely unavailable. The use of saw palmetto in men with benign prostatic hyperplasia is safe with no recognized adverse effects. No effect on serum prostate specific antigen has been noted. Placebo controlled trials and meta-analyses have suggested that saw palmetto leads to subjective and objective improvement in men with lower urinary tract symptoms. However, most studies are significantly limited by methodological flaws, small patient numbers and brief treatment intervals. CONCLUSIONS: Evidence suggests that saw palmetto may have a significant effect on urinary flow rates and symptom scores compared to placebo in men with lower urinary tract symptoms. However, large scale, placebo controlled trials are needed to assess the efficacy of saw palmetto.
------------------------
Combined sabal and urtica extract compared with finasteride in men with benign prostatic hyperplasia: analysis of prostate volume and therapeutic outcome.
Sokeland J
Urological Clinic of Dortmund, Training Hospital of the University of Munster, Germany.
OBJECTIVE: To test the hypothesis that in patients with benign prostatic hyperplasia (BPH), the outcome of drug therapy with finasteride may be predictable from the baseline prostate volume and that positive clinical effects might be expected only in patients with prostate volumes of > 40 mL, using a subgroup analysis of results from a previously reported clinical trial of finasteride and phytotherapy. PATIENTS AND METHODS: A subgroup of 431 patients was analysed from a randomized, multicentre, double-blind clinical trial involving 543 patients with the early stages of BPH. Patients received a fixed combination of extracts of saw palmetto fruit (Serenoa repens) and nettle root (Urtica dioica) (PRO 160/120) or the synthetic 5alpha-reductase inhibitor finasteride. The patients assessed had valid ultrasonographic measurements and baseline prostate volumes of either </= 40 mL or > 40 mL. All 516 patients were included in the safety analysis. The results of the original trial showed equivalent efficacy for both treatments. RESULTS: The mean (SD) maximum urinary flow (the main outcome variable) increased (from baseline values) after 24 weeks by 1.9 (5.6) mL/s with PRO 160/120 and by 2.4 (6.3) mL/s with finasteride. There were no statistically significant group differences (P = 0.52). The subgroups with small prostates (</= 40 mL) showed similar improvements, with mean values of 1.8 (5.2) mL/s with PRO 160/120 and 2.7 (7.4) mL/s with finasteride. The mean values for the subgroups with prostates of > 40 mL were similar, at 2.3 (6.1) and 2. 2 (5.3) mL/s, respectively. There were improvements in the International Prostate Symptom Score in both treatment groups, with no statistically significant differences. The subgroup analysis showed slightly better results for voiding symptoms in the patients with prostates of > 40 mL, but there were also improvements in the subgroup with smaller prostates. The safety analysis showed that more patients in the finasteride group reported adverse events and also there were more adverse events in this group than in patients treated with PRO 160/120. CONCLUSION: The present analysis showed that the efficacy of both PRO 160/120 and finasteride was equivalent and unrelated to prostate volume. However, PRO 160/120 had better tolerability than finasteride.
----------------------
Saw palmetto extracts for treatment of benign prostatic hyperplasia: a systematic review.
Wilt TJ, Ishani A, Stark G, MacDonald R, Lau J, Mulrow C
Department of Veterans Affairs Coordinating Center of the Cochrane Collaborative Review Group in Prostatic Diseases and Urologic Malignancies, Minneapolis Veterans Affairs Medical Center, Minn 55417, USA. wilt.timothy@minneapolis.va.gov
OBJECTIVE: To conduct a systematic review and, where possible, quantitative meta-analysis of the existing evidence regarding the therapeutic efficacy and safety of the saw palmetto plant extract, Serenoa repens, in men with symptomatic benign prostatic hyperplasia (BPH). DATA SOURCES: Studies were identified through the search of MEDLINE (1966-1997), EMBASE, Phytodok, the Cochrane Library, bibliographies of identified trials and review articles, and contact with relevant authors and drug companies. STUDY SELECTION: Randomized trials were included if participants had symptomatic BPH, the intervention was a preparation of S repens alone or in combination with other phytotherapeutic agents, a control group received placebo or other pharmacological therapies for BPH, and the treatment duration was at least 30 days. DATA EXTRACTION: Two investigators for each article (T.J.W., A.I., G.S., and R.M.) independently extracted key data on design features, subject characteristics, therapy allocation, and outcomes of the studies. DATA SYNTHESIS: A total of 18 randomized controlled trials involving 2939 men met inclusion criteria and were analyzed. Many studies did not report results in a method that permitted meta-analysis. Treatment allocation concealment was adequate in 9 studies; 16 were double-blinded. The mean study duration was 9 weeks (range, 4-48 weeks). As compared with men receiving placebo, men treated with S repens had decreased urinary tract symptom scores (weighted mean difference [WMD], -1.41 points [scale range, 0-19] [95% confidence interval (CI), -2.52 to -0.30] [n = 1 study]), nocturia (WMD, -0.76 times per evening [95% CI, -1.22 to -0.32] [n = 10 studies]), and improvement in self-rating of urinary tract symptoms; risk ratio for improvement (1.72 [95% CI, 1.21-2.44] [n = 6 studies]), and peak urine flow (WMD, 1.93 mL/s [95% CI, 0.72-3.14] [n = 8 studies]). Compared with men receiving finasteride, men treated with S repens had similar improvements in urinary tract symptom scores (WMD, 0.37 International Prostate Symptom Score points [scale range, 0-35] [95% CI, -0.45 to 1.19] [n = 2 studies]) and peak urine flow (WMD, -0.74 mL/s [95% CI, -1.66 to 0.18] [n = 2 studies]). Adverse effects due to S repens were mild and infrequent; erectile dysfunction was more frequent with finasteride (4.9%) than with S repens (1.1%; P<.001). Withdrawal rates in men assigned to placebo, S repens, or finasteride were 7%, 9%, and 11%, respectively. CONCLUSIONS: The existing literature on S repens for treatment of BPH is limited in terms of the short duration of studies and variability in study design, use of phytotherapeutic preparations, and reports of outcomes. However, the evidence suggests that S repens improves urologic symptoms and flow measures. Compared with finasteride, S repens produces similar improvement in urinary tract symptoms and urinary flow and was associated with fewer adverse treatment events. Further research is needed using standardized preparations of S repens to determine its long-term effectiveness and ability to prevent BPH complications.
-------------------------
Biologically active acylglycerides from the berries of saw-palmetto (Serenoa repens).
Shimada H, Tyler VE, McLaughlin JL
Department of Medicinal Chemistry and Molecular Pharmacology, School of Pharmacy and Pharmacal Sciences, Purdue University, West Lafayette, Indiana 47907, USA.
Brine shrimp lethality-directed fractionation of the 95% EtOH extract of the powdered, dried berries of Serenoa repens (Bart.) Small (saw-palmetto) (Palmae) led to the isolation of two monoacylglycerides, 1-monolaurin (1) and 1-monomyristin (2). Compounds 1 and 2 showed moderate biological activities in the brine shrimp lethality test and against renal (A-498) and pancreatic (PACA-2) human tumor cells; borderline cytotoxicity was exhibited against human prostatic (PC-3) cells. The fruits and extracts of saw-palmetto are taken orally as an herbal medicine to prevent prostatic hyperplasias.
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VOLETE PROVE SULL'EFFICACIA DELL'ACETYL L-Carnitina per ACCRESCERE LA PRODUZIONE DI TESTOSTERONE?
Beccateve questo:
Neuroendocrinology 1993 Jun;57(6):985-90
Effect of different chronic intermittent stressors and acetyl-l-carnitine on hypothalamic beta-endorphin and GnRH and on plasma testosterone levels in male rats.
Bidzinska B, Petraglia F, Angioni S, Genazzani AD, Criscuolo M, Ficarra G, Gallinelli A, Trentini GP, Genazzani AR
Department of Endocrinology, Medical School of Wroclaw, Poland.
Chronic stress affects the reproductive function by modifying the neuroendocrine homeostasis. The aim of the present study was to clarify the neuroendocrine and the gonadal changes following chronic intermittent stress in male rats and the action of a neuroactive drug, acetyl-l-carnitine (ALC). The effect of two different stressors, cold water swimming or ether, on central beta-endorphin (beta-EP) and GnRH contents, and on plasma testosterone levels was investigated. In addition, the response to an acute stress in chronically stressed rats, treated or untreated with ALC (10 mg/day/rat p.o.), was evaluated. The stressors were applied twice a day for 10 days, and rats were killed before, during and after the last stress session. Mediobasal hypothalamus (MBH) beta-EP and GnRH contents, and plasma testosterone levels were evaluated by radioimmunoassay. The following results were obtained: (1) both chronic swimming and ether stress caused a decrease in hypothalamic beta-EP contents; (2) MBH GnRH contents increased after chronic swimming stress but not after ether stress; (3) chronic swimming stress induced a twofold decrease in plasma testosterone levels, while no changes were observed after ether stress; (4) the treatment with ALC prevented the decrease in plasma testosterone levels after chronic swimming stress, and (5) acute stress in chronically stressed animals caused an increase in MBH-beta-EP. The present data showed that chronic swimming stress reduces the reproductive capacity and impairs the capacity to respond to the acute stress and that ALC modulates the hormonal changes to physical stress and prevents the antireproductive effect of chronic cold swimming.
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Acetyl L-Carnitine retards some aspects of the Aging Process in the Skin:
ALC improves the reaction times of persons afflicted with Cerebral Insufficiency.
ALC (2-4 grams per day) improves walking distance without Pain in persons afflicted with Intermittent Claudication.
ALC prevents the age-related impairment of Eyesight (by protecting the Neurons of the Optic Nerve and the Occipital Cortex of the Brain.
ALC enhances the ability of Macrophages to function as Phagocytes.
ALC improves Athletic Performance [ALC given prior to Exercise increased the maximum running speed of animals].
ALC enhances the function of Cytochrome Oxidase (an essential enzyme of the Electron Transport System (ETS).
ALC improves the Energy metabolism of Neurons (by enhancing the transport of Medium-Chain Saturated Fatty Acids and Short-Chain Saturated Fatty Acids across the Cell Membranes of Neurons into the Mitochondria).
ALC inhibits the damage caused by Hypoxia.
ALC transports Lipids into the Mitochondria of Cells.
ALC alleviates Age Associated Memory Impairment (AAMI):
ALC improves Creativity in persons afflicted with AAMI.
ALC improves Memory in persons afflicted with AAMI.
ALC improves Mood in persons afflicted with AAMI.
ALC improves Mental Function where Alcohol (Ethanol) induced cognitive Impairment exists.
ALC increases Alertness.
Acetyl-L-Carnitine inhibits the deterioration in Mental Function associated with Alzheimer’s Disease and slows the progression of Alzheimer’s Disease [persons afflicted with Alzheimer’s Disease exhibited significantly less deterioration in Mental Function following the administration of supplemental ALC for 12 months. This finding was verified by using nuclear magnetic resonance on the subjects].
ALC increases Alertness in persons afflicted with Alzheimer's Disease - 2,500-3,000 mg per day for 3 months].
ALC inhibits the toxicity of Amyloid-Beta Protein (ABP) to Neurons.
ALC improves Attention Span in persons afflicted with Alzheimer's Disease.
ALC improves Short Term Memory in persons afflicted with Alzheimer's Disease.
High concentrations of ALC are naturally present in various regions of the Brain.
ALC reverses the age-related decline that occurs in Cholinergic Receptors (i.e. the Receptors that receive Acetylcholine).
ALC improves (eye to hand) Coordination [supplemental ALC @ 1.5 grams per day for 30 days improved eye to hand coordination in healthy, sedentary subjects by a factor of 300-400%].
ALC improves the Interhemispheric Flow of Information across the Corpus Callosum of the Brain.
ALC retards the decline in the number of Dopamine Receptors that occurs in tandem with the Aging Process and (more rapidly) with the onset of Parkinson's Disease.
ALC enhances the release of Dopamine from Dopaminergic Neurons and improves the binding of Dopamine to Dopamine Receptors.
ALC can prevent the destruction of Dopamine Receptors by MPTP (a neurotoxin capable of causing Parkinson's Disease via Dopaminergic Receptor death.
ALC improves Attention Span and Memory in persons afflicted with Down’s Syndrome.
ALC retards the inevitable decline in the number of Glucocorticoid Receptors that occurs in tandem with the Aging Process.
ALC enhances the recovery of persons afflicted with Hemiplegia (Paralysis of one side of the body) and improves their Mood and Attention Span.
ALC retards the age-related deterioration of the Hippocampus [research - rats].
Acetyl-L-Carnitine (ALC) improves Learning ability [women aged 22 - 27 were supplemented with ALC for 30 days. Complex video game tests before and after supplementation concluded that supplemental ALC caused large increases in speed of Learning, speed of reaction and reduction in errors].
ALC improves both Short-Term Memory and Long-Term Memory.
ALC improves Mood [ALC improves Mood in 53% of healthy subjects].
ALC inhibits (and possibly reverses) the degeneration of Myelin Sheaths that occurs in tandem with the progression of the Aging Process [scientific research - hyperglycemic mice treated with ALC for 16 weeks exhibited improved nerve conduction velocity and exhibited thicker Myelin Sheaths and larger myelinated Nerve Fibers].
ALC retards the inevitable decline in the number of Nerve Growth Factor (NGF) Receptors that occurs in tandem with the Aging Process.
ALC stimulates and maintains the growth of new Neurons within the Brain (both independently of Nerve Growth Factor (NGF) and as a result of preserving NGF) and helps to prevent the death of existing Neurons [ALC inhibits Neuron death in the Striatal Cortex, Prefrontal Cortex and the Occipital Cortex of the Brain].
ALC inhibits the degeneration of Neurons that is implicit in Neuropathy.
ALC rejuvenates and increases the number of N-Methyl-D-Aspartate Receptors (NMDA Receptors) in the Brain [even a single dose of ALC increases the number of functional NMDA Receptors]:
ALC protects the NMDA Receptors in the Brain from the natural decline that occurs in tandem with the Aging Process [research - animals].
ALC is presently being researched as a treatment for Parkinson's Disease.
ALC inhibits the loss of Vision, degeneration of Neurons and damage to the Retina associated with Retinopathy (including Diabetic Retinopathy).
ALC improves the quality of Sleep and reduces the quantity of Sleep required.
ALC improves the function of (reduces the over-excitability of) Motor Nerves in persons afflicted with Spasticity.
ALC improves Spatial Memory (an aspect of Short Term Memory that involves remembering one’s position in space).
ALC inhibits the excessive release of Cortisol in response to Stress and inhibits the depletion of Luteinising Hormone Releasing Hormone (LHRH) and Testosterone that occurs as a result of excessive Stress.
ALC improves Verbal Fluency.
ALC enhances the function of Cytochrome Oxidase (also called Complex IV) - an essential enzyme of the Electron Transport System.
ALC normalizes Beta-Endorphin levels.
ALC reduces Stress-induced Cortisol release [research - animals].
ALC prevents the depletion of Luteinising Hormone Releasing Hormone (LHRH) caused by exposure to excessive Stress.
ALC retards the decline in the production of Nerve Growth Factor (NGF) that occurs in tandem with the Aging Process.
ALC increases plasma Testosterone levels (via its influence on Acetylcholine neurotransmission in the Striatal Cortex of the Brain) and prevents the depletion of Testosterone caused by exposure to excessive Stress [research - rats].
ALC increases the body's levels of circulating Thyrotrophin.
ALC facilitates the production of Adenosine Triphosphate (ATP) [research - animals].
ALC "shuttles" Long Chain Fatty Acids between the Cytosol and the Mitochondria of Cells.
ALC facilitates both the release and synthesis of Acetylcholine.
ALC's ability to increase the synthesis of Acetylcholine occurs as a result of it donating its Acetyl group towards the production of Acetylcholine.
ALC increases the Brain's levels of Choline Acetylase (which in turn facilities the production of Acetylcholine).
ALC enhances the release of Dopamine from Dopaminergic Neurons and improves the binding of Dopamine to Dopamine Receptors.
References
De Falco, F. A., et al. Effect of the chronic treatment with L-acetylcarnitine in Down’s syndrome. Clin Ther. 144:123-127, 1994.
Bowman, B. Acetyl-carnitine and Alzheimer’s disease. Nutr Rev. 50:142-144, 1992.
Bruno, G., et al. Acetyl-L-carnitine in Alzheimer disease: a short-term study on CSF neurotransmitters and neuropeptides. Alzheimer Dis Assoc Disord (USA). 9(3):128-131, 1995.
Calvani, M., et al. Action of acetyl-L-carnitine in neurodegeneration and Alzheimer’s disease. Annals of the New York Academy of Sciences (USA). 663:483-486, 1993.
Carta, A., et al. Acetyl-L-carnitine: a drug able to slow the progress of Alzheimer’s Disease? Annals of the New York Academy of Sciences (USA. 640:228-232, 1991.
Guarnaschelli, C., et al. Pathological brain ageing: evaluation of the efficacy of a pharmacological aid. Drugs under Experimental and Clinical Research. 14(11):715-718, 1988.
Passeri, M., et al. Acetyl-L-carnitine in the treatment of mildly demented elderly patients. International Journal of Clinical Pharmacology Research. 10(1-2):75-79, 1990.
Pettegrew, J. W., et al. Clinical and neurochemical effects of acetyl-L-carnitine in Alzheimer’s disease. Neurobiol Aging. 16:1-4, 1995.
Rai, G., et al. Double-blind, placebo controlled study of acetyl-L-carnitine in patients with Alzheimer’s dementia. Current Medical Research and Opinion. 11(10):638-647, 1989.
Sano, M., et al. Double-blind parallel design pilot study of acetyl levocarnitine in patients with Alzheimer’s disease. Arch Neurol. 49:1137-1141, 1992.
Sinforiani, E., et al. Neuropsychological changes in demented patients treated with acetyl-L-carnitine. International Journal of Clinical Pharmacology Research. 10(1-2):69-74, 1990.
Spagnoli, A. U., et al. Long-term acetyl-l-carnitine treatment in Alzheimer’s disease. Neurology. 41(11):1726-1732, 1991.
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CIARLATANO AAAAAAAACCCCHIIIIII?
La prossima volta che volete insultare RIFLETTETE, potreste rischiare di fare FIGURE DI MERDA!
Originally posted by Lawrence:
...ci ho ripensato!
Nico, mi fai fare tanti discorsi e poi mi riproponi le tue cazzate su ALC + saw palmetto...a questo punto ti dico che sei davvero un CIARLATANO e che non stai a sentire i discorsi degli altri!
...ci ho ripensato!
Nico, mi fai fare tanti discorsi e poi mi riproponi le tue cazzate su ALC + saw palmetto...a questo punto ti dico che sei davvero un CIARLATANO e che non stai a sentire i discorsi degli altri!
Come al solito qui si offende, ci si fa un culo così per poi essere chiamato ciarlatano, a me non piace offendere ma CERCHIAMO DI ESSERE MENO IGNORANTI:
nessuno ha mai usato con successo la clorofilla per curare deficienze di testosterone (infatti non serve a niente, forse le piante le aiuta...) MA ADDIRITTURA IL SAW PALMETTO VIENE USATO IN AMBITO MEDICO PER CURARE ALCUNE FORME DI IPERTROFIA PROSTATICA O LIEVI FORME DI CALVIZIE CAUSATE PROPRIO DAL DHT!
Cercate di offendere di meno, ricordate che la persona che giudica è la persona che non ha forza di farsi valere facendo perno sulle proprie capacità e si propone dicendo "x è stronzo" oppure "y è ciarlatano" oppure "z è cattivo" invece di COSTRUIRE.
Cercate di non superare il limite.
Lawrence ti do un consiglio: la prossima volta che ti va di insultare una persona ti consiglio di fare questo, ti farà bene allo spirito e al rapporto che hai con gli altri: conta fino a 10 o mangiati un pezzo di cioccolata o leggiti una pagina di un qualsiasi libro (non necessariamente un testo di endocrinologia!) o fai qualsiasi cosa che ti impegni la mente in modo da non insultare.
Lawrence io ti rispondo con studi clinici, tu mi rispondi con insulti dato che non hai argomenti; non credi nell'efficacia del saw palmetto (o serenoa repens) beccati questi (PS: dopo ci sono anche le prove dell'efficacia dell'Acetyl L-Carnitina sull'aumento di testosterone):
In a randomized placebo-controlled clinical study conducted on 25 men with BPH given the standard dose of 320 mg per day of a proprietary SP extract (Permixon®), those with SP experienced statistically significant reductions in levels of prostatic dihydrotestosterone (DHT) and epidermal growth factor (EGF) and increased levels of testosterone (Di Silverio et al., 1998). Additionally, these levels were distinct to the periurethral regions: those with the herb had lower DHT and EGF levels in the periurethral zone. This appears to be evidence of the 5-a-reductase-lowering effects of SP and its more specific regionalized effects compared to the conventional drug finasteride (Proscar®) (Strauch et al., 1994).
-------------------------
Saw palmetto for the treatment of men with lower urinary tract symptoms.
Gerber GS
Section of Urology, Department of Surgery, University of Chicago Pritzker School of Medicine, Chicago, Illinois, USA.
PURPOSE: A comprehensive review of the literature on the use of saw palmetto in men with lower urinary tract symptoms is provided. MATERIALS AND METHODS: A literature search of studies that have assessed the mechanism of action and clinical results of saw palmetto in men with benign prostatic hyperplasia was performed. RESULTS: A variety of potential mechanisms of action of saw palmetto have been demonstrated through in vitro studies, including 5-alpha reductase inhibition, adrenergic receptor antagonism and intraprostatic androgen receptor blockade. Clinical evidence of the relevance of these effects is largely unavailable. The use of saw palmetto in men with benign prostatic hyperplasia is safe with no recognized adverse effects. No effect on serum prostate specific antigen has been noted. Placebo controlled trials and meta-analyses have suggested that saw palmetto leads to subjective and objective improvement in men with lower urinary tract symptoms. However, most studies are significantly limited by methodological flaws, small patient numbers and brief treatment intervals. CONCLUSIONS: Evidence suggests that saw palmetto may have a significant effect on urinary flow rates and symptom scores compared to placebo in men with lower urinary tract symptoms. However, large scale, placebo controlled trials are needed to assess the efficacy of saw palmetto.
------------------------
Combined sabal and urtica extract compared with finasteride in men with benign prostatic hyperplasia: analysis of prostate volume and therapeutic outcome.
Sokeland J
Urological Clinic of Dortmund, Training Hospital of the University of Munster, Germany.
OBJECTIVE: To test the hypothesis that in patients with benign prostatic hyperplasia (BPH), the outcome of drug therapy with finasteride may be predictable from the baseline prostate volume and that positive clinical effects might be expected only in patients with prostate volumes of > 40 mL, using a subgroup analysis of results from a previously reported clinical trial of finasteride and phytotherapy. PATIENTS AND METHODS: A subgroup of 431 patients was analysed from a randomized, multicentre, double-blind clinical trial involving 543 patients with the early stages of BPH. Patients received a fixed combination of extracts of saw palmetto fruit (Serenoa repens) and nettle root (Urtica dioica) (PRO 160/120) or the synthetic 5alpha-reductase inhibitor finasteride. The patients assessed had valid ultrasonographic measurements and baseline prostate volumes of either </= 40 mL or > 40 mL. All 516 patients were included in the safety analysis. The results of the original trial showed equivalent efficacy for both treatments. RESULTS: The mean (SD) maximum urinary flow (the main outcome variable) increased (from baseline values) after 24 weeks by 1.9 (5.6) mL/s with PRO 160/120 and by 2.4 (6.3) mL/s with finasteride. There were no statistically significant group differences (P = 0.52). The subgroups with small prostates (</= 40 mL) showed similar improvements, with mean values of 1.8 (5.2) mL/s with PRO 160/120 and 2.7 (7.4) mL/s with finasteride. The mean values for the subgroups with prostates of > 40 mL were similar, at 2.3 (6.1) and 2. 2 (5.3) mL/s, respectively. There were improvements in the International Prostate Symptom Score in both treatment groups, with no statistically significant differences. The subgroup analysis showed slightly better results for voiding symptoms in the patients with prostates of > 40 mL, but there were also improvements in the subgroup with smaller prostates. The safety analysis showed that more patients in the finasteride group reported adverse events and also there were more adverse events in this group than in patients treated with PRO 160/120. CONCLUSION: The present analysis showed that the efficacy of both PRO 160/120 and finasteride was equivalent and unrelated to prostate volume. However, PRO 160/120 had better tolerability than finasteride.
----------------------
Saw palmetto extracts for treatment of benign prostatic hyperplasia: a systematic review.
Wilt TJ, Ishani A, Stark G, MacDonald R, Lau J, Mulrow C
Department of Veterans Affairs Coordinating Center of the Cochrane Collaborative Review Group in Prostatic Diseases and Urologic Malignancies, Minneapolis Veterans Affairs Medical Center, Minn 55417, USA. wilt.timothy@minneapolis.va.gov
OBJECTIVE: To conduct a systematic review and, where possible, quantitative meta-analysis of the existing evidence regarding the therapeutic efficacy and safety of the saw palmetto plant extract, Serenoa repens, in men with symptomatic benign prostatic hyperplasia (BPH). DATA SOURCES: Studies were identified through the search of MEDLINE (1966-1997), EMBASE, Phytodok, the Cochrane Library, bibliographies of identified trials and review articles, and contact with relevant authors and drug companies. STUDY SELECTION: Randomized trials were included if participants had symptomatic BPH, the intervention was a preparation of S repens alone or in combination with other phytotherapeutic agents, a control group received placebo or other pharmacological therapies for BPH, and the treatment duration was at least 30 days. DATA EXTRACTION: Two investigators for each article (T.J.W., A.I., G.S., and R.M.) independently extracted key data on design features, subject characteristics, therapy allocation, and outcomes of the studies. DATA SYNTHESIS: A total of 18 randomized controlled trials involving 2939 men met inclusion criteria and were analyzed. Many studies did not report results in a method that permitted meta-analysis. Treatment allocation concealment was adequate in 9 studies; 16 were double-blinded. The mean study duration was 9 weeks (range, 4-48 weeks). As compared with men receiving placebo, men treated with S repens had decreased urinary tract symptom scores (weighted mean difference [WMD], -1.41 points [scale range, 0-19] [95% confidence interval (CI), -2.52 to -0.30] [n = 1 study]), nocturia (WMD, -0.76 times per evening [95% CI, -1.22 to -0.32] [n = 10 studies]), and improvement in self-rating of urinary tract symptoms; risk ratio for improvement (1.72 [95% CI, 1.21-2.44] [n = 6 studies]), and peak urine flow (WMD, 1.93 mL/s [95% CI, 0.72-3.14] [n = 8 studies]). Compared with men receiving finasteride, men treated with S repens had similar improvements in urinary tract symptom scores (WMD, 0.37 International Prostate Symptom Score points [scale range, 0-35] [95% CI, -0.45 to 1.19] [n = 2 studies]) and peak urine flow (WMD, -0.74 mL/s [95% CI, -1.66 to 0.18] [n = 2 studies]). Adverse effects due to S repens were mild and infrequent; erectile dysfunction was more frequent with finasteride (4.9%) than with S repens (1.1%; P<.001). Withdrawal rates in men assigned to placebo, S repens, or finasteride were 7%, 9%, and 11%, respectively. CONCLUSIONS: The existing literature on S repens for treatment of BPH is limited in terms of the short duration of studies and variability in study design, use of phytotherapeutic preparations, and reports of outcomes. However, the evidence suggests that S repens improves urologic symptoms and flow measures. Compared with finasteride, S repens produces similar improvement in urinary tract symptoms and urinary flow and was associated with fewer adverse treatment events. Further research is needed using standardized preparations of S repens to determine its long-term effectiveness and ability to prevent BPH complications.
-------------------------
Biologically active acylglycerides from the berries of saw-palmetto (Serenoa repens).
Shimada H, Tyler VE, McLaughlin JL
Department of Medicinal Chemistry and Molecular Pharmacology, School of Pharmacy and Pharmacal Sciences, Purdue University, West Lafayette, Indiana 47907, USA.
Brine shrimp lethality-directed fractionation of the 95% EtOH extract of the powdered, dried berries of Serenoa repens (Bart.) Small (saw-palmetto) (Palmae) led to the isolation of two monoacylglycerides, 1-monolaurin (1) and 1-monomyristin (2). Compounds 1 and 2 showed moderate biological activities in the brine shrimp lethality test and against renal (A-498) and pancreatic (PACA-2) human tumor cells; borderline cytotoxicity was exhibited against human prostatic (PC-3) cells. The fruits and extracts of saw-palmetto are taken orally as an herbal medicine to prevent prostatic hyperplasias.
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VOLETE PROVE SULL'EFFICACIA DELL'ACETYL L-Carnitina per ACCRESCERE LA PRODUZIONE DI TESTOSTERONE?
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Neuroendocrinology 1993 Jun;57(6):985-90
Effect of different chronic intermittent stressors and acetyl-l-carnitine on hypothalamic beta-endorphin and GnRH and on plasma testosterone levels in male rats.
Bidzinska B, Petraglia F, Angioni S, Genazzani AD, Criscuolo M, Ficarra G, Gallinelli A, Trentini GP, Genazzani AR
Department of Endocrinology, Medical School of Wroclaw, Poland.
Chronic stress affects the reproductive function by modifying the neuroendocrine homeostasis. The aim of the present study was to clarify the neuroendocrine and the gonadal changes following chronic intermittent stress in male rats and the action of a neuroactive drug, acetyl-l-carnitine (ALC). The effect of two different stressors, cold water swimming or ether, on central beta-endorphin (beta-EP) and GnRH contents, and on plasma testosterone levels was investigated. In addition, the response to an acute stress in chronically stressed rats, treated or untreated with ALC (10 mg/day/rat p.o.), was evaluated. The stressors were applied twice a day for 10 days, and rats were killed before, during and after the last stress session. Mediobasal hypothalamus (MBH) beta-EP and GnRH contents, and plasma testosterone levels were evaluated by radioimmunoassay. The following results were obtained: (1) both chronic swimming and ether stress caused a decrease in hypothalamic beta-EP contents; (2) MBH GnRH contents increased after chronic swimming stress but not after ether stress; (3) chronic swimming stress induced a twofold decrease in plasma testosterone levels, while no changes were observed after ether stress; (4) the treatment with ALC prevented the decrease in plasma testosterone levels after chronic swimming stress, and (5) acute stress in chronically stressed animals caused an increase in MBH-beta-EP. The present data showed that chronic swimming stress reduces the reproductive capacity and impairs the capacity to respond to the acute stress and that ALC modulates the hormonal changes to physical stress and prevents the antireproductive effect of chronic cold swimming.
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Acetyl L-Carnitine retards some aspects of the Aging Process in the Skin:
ALC improves the reaction times of persons afflicted with Cerebral Insufficiency.
ALC (2-4 grams per day) improves walking distance without Pain in persons afflicted with Intermittent Claudication.
ALC prevents the age-related impairment of Eyesight (by protecting the Neurons of the Optic Nerve and the Occipital Cortex of the Brain.
ALC enhances the ability of Macrophages to function as Phagocytes.
ALC improves Athletic Performance [ALC given prior to Exercise increased the maximum running speed of animals].
ALC enhances the function of Cytochrome Oxidase (an essential enzyme of the Electron Transport System (ETS).
ALC improves the Energy metabolism of Neurons (by enhancing the transport of Medium-Chain Saturated Fatty Acids and Short-Chain Saturated Fatty Acids across the Cell Membranes of Neurons into the Mitochondria).
ALC inhibits the damage caused by Hypoxia.
ALC transports Lipids into the Mitochondria of Cells.
ALC alleviates Age Associated Memory Impairment (AAMI):
ALC improves Creativity in persons afflicted with AAMI.
ALC improves Memory in persons afflicted with AAMI.
ALC improves Mood in persons afflicted with AAMI.
ALC improves Mental Function where Alcohol (Ethanol) induced cognitive Impairment exists.
ALC increases Alertness.
Acetyl-L-Carnitine inhibits the deterioration in Mental Function associated with Alzheimer’s Disease and slows the progression of Alzheimer’s Disease [persons afflicted with Alzheimer’s Disease exhibited significantly less deterioration in Mental Function following the administration of supplemental ALC for 12 months. This finding was verified by using nuclear magnetic resonance on the subjects].
ALC increases Alertness in persons afflicted with Alzheimer's Disease - 2,500-3,000 mg per day for 3 months].
ALC inhibits the toxicity of Amyloid-Beta Protein (ABP) to Neurons.
ALC improves Attention Span in persons afflicted with Alzheimer's Disease.
ALC improves Short Term Memory in persons afflicted with Alzheimer's Disease.
High concentrations of ALC are naturally present in various regions of the Brain.
ALC reverses the age-related decline that occurs in Cholinergic Receptors (i.e. the Receptors that receive Acetylcholine).
ALC improves (eye to hand) Coordination [supplemental ALC @ 1.5 grams per day for 30 days improved eye to hand coordination in healthy, sedentary subjects by a factor of 300-400%].
ALC improves the Interhemispheric Flow of Information across the Corpus Callosum of the Brain.
ALC retards the decline in the number of Dopamine Receptors that occurs in tandem with the Aging Process and (more rapidly) with the onset of Parkinson's Disease.
ALC enhances the release of Dopamine from Dopaminergic Neurons and improves the binding of Dopamine to Dopamine Receptors.
ALC can prevent the destruction of Dopamine Receptors by MPTP (a neurotoxin capable of causing Parkinson's Disease via Dopaminergic Receptor death.
ALC improves Attention Span and Memory in persons afflicted with Down’s Syndrome.
ALC retards the inevitable decline in the number of Glucocorticoid Receptors that occurs in tandem with the Aging Process.
ALC enhances the recovery of persons afflicted with Hemiplegia (Paralysis of one side of the body) and improves their Mood and Attention Span.
ALC retards the age-related deterioration of the Hippocampus [research - rats].
Acetyl-L-Carnitine (ALC) improves Learning ability [women aged 22 - 27 were supplemented with ALC for 30 days. Complex video game tests before and after supplementation concluded that supplemental ALC caused large increases in speed of Learning, speed of reaction and reduction in errors].
ALC improves both Short-Term Memory and Long-Term Memory.
ALC improves Mood [ALC improves Mood in 53% of healthy subjects].
ALC inhibits (and possibly reverses) the degeneration of Myelin Sheaths that occurs in tandem with the progression of the Aging Process [scientific research - hyperglycemic mice treated with ALC for 16 weeks exhibited improved nerve conduction velocity and exhibited thicker Myelin Sheaths and larger myelinated Nerve Fibers].
ALC retards the inevitable decline in the number of Nerve Growth Factor (NGF) Receptors that occurs in tandem with the Aging Process.
ALC stimulates and maintains the growth of new Neurons within the Brain (both independently of Nerve Growth Factor (NGF) and as a result of preserving NGF) and helps to prevent the death of existing Neurons [ALC inhibits Neuron death in the Striatal Cortex, Prefrontal Cortex and the Occipital Cortex of the Brain].
ALC inhibits the degeneration of Neurons that is implicit in Neuropathy.
ALC rejuvenates and increases the number of N-Methyl-D-Aspartate Receptors (NMDA Receptors) in the Brain [even a single dose of ALC increases the number of functional NMDA Receptors]:
ALC protects the NMDA Receptors in the Brain from the natural decline that occurs in tandem with the Aging Process [research - animals].
ALC is presently being researched as a treatment for Parkinson's Disease.
ALC inhibits the loss of Vision, degeneration of Neurons and damage to the Retina associated with Retinopathy (including Diabetic Retinopathy).
ALC improves the quality of Sleep and reduces the quantity of Sleep required.
ALC improves the function of (reduces the over-excitability of) Motor Nerves in persons afflicted with Spasticity.
ALC improves Spatial Memory (an aspect of Short Term Memory that involves remembering one’s position in space).
ALC inhibits the excessive release of Cortisol in response to Stress and inhibits the depletion of Luteinising Hormone Releasing Hormone (LHRH) and Testosterone that occurs as a result of excessive Stress.
ALC improves Verbal Fluency.
ALC enhances the function of Cytochrome Oxidase (also called Complex IV) - an essential enzyme of the Electron Transport System.
ALC normalizes Beta-Endorphin levels.
ALC reduces Stress-induced Cortisol release [research - animals].
ALC prevents the depletion of Luteinising Hormone Releasing Hormone (LHRH) caused by exposure to excessive Stress.
ALC retards the decline in the production of Nerve Growth Factor (NGF) that occurs in tandem with the Aging Process.
ALC increases plasma Testosterone levels (via its influence on Acetylcholine neurotransmission in the Striatal Cortex of the Brain) and prevents the depletion of Testosterone caused by exposure to excessive Stress [research - rats].
ALC increases the body's levels of circulating Thyrotrophin.
ALC facilitates the production of Adenosine Triphosphate (ATP) [research - animals].
ALC "shuttles" Long Chain Fatty Acids between the Cytosol and the Mitochondria of Cells.
ALC facilitates both the release and synthesis of Acetylcholine.
ALC's ability to increase the synthesis of Acetylcholine occurs as a result of it donating its Acetyl group towards the production of Acetylcholine.
ALC increases the Brain's levels of Choline Acetylase (which in turn facilities the production of Acetylcholine).
ALC enhances the release of Dopamine from Dopaminergic Neurons and improves the binding of Dopamine to Dopamine Receptors.
References
De Falco, F. A., et al. Effect of the chronic treatment with L-acetylcarnitine in Down’s syndrome. Clin Ther. 144:123-127, 1994.
Bowman, B. Acetyl-carnitine and Alzheimer’s disease. Nutr Rev. 50:142-144, 1992.
Bruno, G., et al. Acetyl-L-carnitine in Alzheimer disease: a short-term study on CSF neurotransmitters and neuropeptides. Alzheimer Dis Assoc Disord (USA). 9(3):128-131, 1995.
Calvani, M., et al. Action of acetyl-L-carnitine in neurodegeneration and Alzheimer’s disease. Annals of the New York Academy of Sciences (USA). 663:483-486, 1993.
Carta, A., et al. Acetyl-L-carnitine: a drug able to slow the progress of Alzheimer’s Disease? Annals of the New York Academy of Sciences (USA. 640:228-232, 1991.
Guarnaschelli, C., et al. Pathological brain ageing: evaluation of the efficacy of a pharmacological aid. Drugs under Experimental and Clinical Research. 14(11):715-718, 1988.
Passeri, M., et al. Acetyl-L-carnitine in the treatment of mildly demented elderly patients. International Journal of Clinical Pharmacology Research. 10(1-2):75-79, 1990.
Pettegrew, J. W., et al. Clinical and neurochemical effects of acetyl-L-carnitine in Alzheimer’s disease. Neurobiol Aging. 16:1-4, 1995.
Rai, G., et al. Double-blind, placebo controlled study of acetyl-L-carnitine in patients with Alzheimer’s dementia. Current Medical Research and Opinion. 11(10):638-647, 1989.
Sano, M., et al. Double-blind parallel design pilot study of acetyl levocarnitine in patients with Alzheimer’s disease. Arch Neurol. 49:1137-1141, 1992.
Sinforiani, E., et al. Neuropsychological changes in demented patients treated with acetyl-L-carnitine. International Journal of Clinical Pharmacology Research. 10(1-2):69-74, 1990.
Spagnoli, A. U., et al. Long-term acetyl-l-carnitine treatment in Alzheimer’s disease. Neurology. 41(11):1726-1732, 1991.
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