Showing posts with label enhancing sexual performance. Show all posts
Showing posts with label enhancing sexual performance. Show all posts

Monday, August 31, 2009

Saw Palmetto

Overview

Saw palmetto (Serenoa repens) is a dwarf (2-4 feet in height) palm tree found in the United States from the Carolinas to Texas. For centuries, the crude extracts of saw palmetto have been used to improve sperm production and to increase breast size and sexual vigor, but its most effective and only scientifically based use is to improve the symptoms of benign prostatic hyperplasia (BPH).


The premise for using saw palmetto is that it maintains normal prostate health by decreasing the metabolism and action of male steroids. Saw palmetto has been demonstrated to decrease the activity of 5-alpha reductase which stimulates the conversion of testosterone to dihydrotestosterone (DHT), its more active form. Since DHT is necessary for excessive growth (hyperplasia) of the prostate and is elevated in men with BPH, inhibition of 5-alpha reductase, and therefore DHT production, may alleviate BPH and the associated compression of the urethra (the tube that runs through the prostate gland to carry urine from the bladder). Additionally, studies have shown that saw palmetto helps to inhibit the production of various inflammatory factors, probably due to an effect of the fatty acids, thus serving to decrease overall prostate inflammation. The prescription medication for treating BPH, finasteride, is available as Proscar for BPH and a lower potency version called Propecia for treating hair loss in men (because the same conversion of testosterone to DHT is thought to result in thinning and loss of hair in men).


Comments

Considering that the possible health benefits are similar to the prescription drugs Proscar for BPH and Propecia for hair loss, and the fact that saw palmetto appears to be safe and effective and without side effects, in several scientific studies, saw palmetto should be considered an outstanding choice for natural therapy in diagnosed cases of BPH.


Scientific Support

Although studies of saw palmetto as a treatment for prostatitis has been disappointing (Kaplan et al. 2004), its effectiveness in treating BPH is supported by numerous well-controlled clinical trials. In one study of 155 men with BPH, International Prostate Symptom Scores (IPPS) and quality of life (QOL) were improved, as were measures of sexual function and prostate size following 6 months of supplementation with 320mg/d of saw palmetto extract (Pytel et al. 2002). In another study of 100 male outpatients, both 320mg/d and 480mg/d of saw palmetto extract for 3 months had similar significant effects in improving QOL scores, maximum and mean urinary flow rates, and residual urinary volume (Gainnakopoulos et al. 2002, Gerber et al. 2001). Several other smaller studies of saw palmetto extracts (160mg twice daily) have shown significant improvements in symptoms of BPH (Gerber et al. 1998) that are comparable to effects seen with drug treatment with the synthetic 5-alpha-reductase inhibitor finasteride (Sokeland 2000) such as improvements in maximum urinary flow rates, reduced trips to the bathroom, a greater ability to fully empty the bladder and an increased quality of life.


Safety/Dosage

Because saw palmetto has primarily been tested in adult males, it is not recommended for children, or for women who are pregnant or lactating. No drug interactions have been reported for saw palmetto (Markowitz et al. 2003). It is important to note that saw palmetto extract may only treat the symptoms of BPH, and therefore those with an enlarged prostate should consult with their physician on a regular basis to rule out prostate cancer or other causes of hypertrophy. Doses in clinical studies have typically used 160mg of the oil-based (“lipophilic”) berry extract taken twice a day (morning and evening) for at least 30 days (total daily dose of 320mg). Effective products are standardized for fatty acid and sterol content – approximately 80-90% total fatty acids and sterols is recommended.


References

1.Bauer HW, Casarosa C, Cosci M, Fratta M, Blessmann G. Saw palmetto fruit extract for treatment of benign prostatic hyperplasia. Results of a placebo-controlled double-blind study. MMW Fortschr Med. 1999 Jun 24;141(25):62.

2.Brown GA, Vukovich MD, Martini ER, Kohut ML, Franke WD, Jackson DA, King DS. Effects of androstenedione-herbal supplementation on serum sex hormone concentrations in 30- to 59-year-old men. Int J Vitam Nutr Res. 2001 Sep;71(5):293-301.

3.Brown GA, Vukovich MD, Martini ER, Kohut ML, Franke WD, Jackson DA, King DS. Endocrine and lipid responses to chronic androstenediol-herbal supplementation in 30 to 58 year old men. J Am Coll Nutr. 2001 Oct;20(5):520-8.

4.Brown GA, Vukovich MD, Reifenrath TA, Uhl NL, Parsons KA, Sharp RL, King DS. Effects of anabolic precursors on serum testosterone concentrations and adaptations to resistance training in young men. Int J Sport Nutr Exerc Metab. 2000 Sep;10(3):340-59.

5.Gerber GS, Kuznetsov D, Johnson BC, Burstein JD. Randomized, double-blind, placebo-controlled trial of saw palmetto in men with lower urinary tract symptoms. Urology. 2001 Dec;58(6):960-4; discussion 964-5.

6.Gerber GS, Zagaja GP, Bales GT, Chodak GW, Contreras BA. Saw palmetto (Serenoa repens) in men with lower urinary tract symptoms: effects on urodynamic parameters and voiding symptoms. Urology. 1998 Jun;51(6):1003-7.

7.Gerber GS. Saw palmetto for the treatment of men with lower urinary tract symptoms. J Urol. 2000 May;163(5):1408-12.

8.Giannakopoulos X, Baltogiannis D, Giannakis D, Tasos A, Sofikitis N, Charalabopoulos K, Evangelou A. The lipidosterolic extract of Serenoa repens in the treatment of benign prostatic hyperplasia: a comparison of two dosage regimens. Adv Ther. 2002 Nov-Dec;19(6):285-96.

9.Kaplan SA, Volpe MA, Te AE. A prospective, 1-year trial using saw palmetto versus finasteride in the treatment of category III prostatitis/chronic pelvic pain syndrome. J Urol. 2004 Jan;171(1):284-8.

10.Markowitz JS, Donovan JL, Devane CL, Taylor RM, Ruan Y, Wang JS, Chavin KD. Multiple doses of saw palmetto (Serenoa repens) did not alter cytochrome P450 2D6 and 3A4 activity in normal volunteers. Clin Pharmacol Ther. 2003 Dec;74(6):536-42.

11.Marks LS, Partin AW, Epstein JI, Tyler VE, Simon I, Macairan ML, Chan TL, Dorey FJ, Garris JB, Veltri RW, Santos PB, Stonebrook KA, deKernion JB. Effects of a saw palmetto herbal blend in men with symptomatic benign prostatic hyperplasia. J Urol. 2000 May;163(5):1451-6.

12.McPartland JM, Pruitt PL. Benign prostatic hyperplasia treated with saw palmetto: a literature search and an experimental case study. J Am Osteopath Assoc. 2000 Feb;100(2):89-96.

13.Preuss HG, Marcusen C, Regan J, Klimberg IW, Welebir TA, Jones WA. Randomized trial of a combination of natural products (cernitin, saw palmetto, B-sitosterol, vitamin E) on symptoms of benign prostatic hyperplasia (BPH). Int Urol Nephrol. 2001;33(2):217-25.

14.Pytel YA, Vinarov A, Lopatkin N, Sivkov A, Gorilovsky L, Raynaud JP. Long-term clinical and biologic effects of the lipidosterolic extract of Serenoa repens in patients with symptomatic benign prostatic hyperplasia. Adv Ther. 2002 Nov-Dec;19(6):297-306.

15.Segars LW. Saw palmetto extracts for benign prostatic hyperplasia. J Fam Pract. 1999 Feb;48(2):88-9.

16.Sokeland J. Combined sabal and urtica extract compared with finasteride in men with benign prostatic hyperplasia: analysis of prostate volume and therapeutic outcome. BJU Int. 2000 Sep;8 6(4):439-42.

17.Veltri RW, Marks LS, Miller MC, Bales WD, Fan J, Macairan ML, Epstein JI, Partin AW. Saw palmetto alters nuclear measurements reflecting DNA content in men with symptomatic BPH: evidence for a possible molecular mechanism. Urology. 2002 Oct;60(4):617-22.

18.Wilt TJ, Ishani A, Stark G, MacDonald R, Lau J, Mulrow C. Saw palmetto extracts for treatment of benign prostatic hyperplasia: a systematic review. JAMA. 1998 Nov 11;280(18):1604-9.


EDITOR'S NOTE: This monograph can be found in The Health Professional's Guide to Dietary Supplements (Lippincott, Williams & Wilkins) by Shawn M. Talbott, PhD and Kerry Hughes, MS.

Thursday, August 27, 2009

Yohimbe

Overview
Yohimbe is an African traditional medicinal herb that is almost legendary in the U.S. for its aphrodisiac and sexual performance enhancing reputation. Although it has been on the market in the U.S. for much longer than Viagra, there is a perception that little is known clinically about this herb drug. Quebracho is a South American herb known for aphrodisiac/sexual performance that contains small amounts of the same active component of yohimbe. The main active component in yohimbe is yohimbine, of which small amounts are also found in the South American aphrodisiac/performance enhancing herb quebracho. (Tam et al., 2001). Both herbs are commonly marketed in the U.S. as components of “herbal Viagra” supplements, and for body-building and athletic performance.
Yohimbe is an alkaloid stimulant that has central nervous system activity, and blocks the alpha-2-adrenergic receptors, which is the main theory on how it is able to increase energy levels and promote weight loss. Yohimbine also is a MAO (monoamine oxidase) inhibitor, thereby increasing norepinephrine, which is the main theory on how it may be helpful in depression. It is also a vasodilator, and has been shown to increase blood flow to the genitals in both men and women (Riley, 1994).
Comments
There is much concern about the safety and purity of yohimbe products on the market, and one study found that there was a large range of yohimbine in commercial products, therefore giving proof to the concern. Additionally, there has not been much clinical proof for yohimbe’s effectiveness in sexual performance, and certainly not for its several other claims. As yohimbe’s possible side effects are consistent with its pharmacological action, it may be a safe herb if used under the right conditions, and with the right quality, but it has currently has much potential for abuse and adulteration (Abebe, 2003; Tam, 2001).
Scientific Support
Yohimbine has been tested for erectile dysfunction in many uncontrolled clinical trials, but below is only a review of the key controlled studies, including one review.
Ernst and Pittler (1998) conducted a systematic review on the literature for yohimbine’s use in erectile dysfunction (ED). They found seven trials that fit the inclusion criteria of randomized, placebo-controlled trials for yohimbine monotherapy (ED). They found the trials to be of satisfactory quality, and that these trials demonstrated yohimbine to be better than placebo for treatment of ED. They found serious side effects to be infrequent and reversible in nature. Yohimbine was concluded to be a reasonable therapeutic option for early consideration of treatment for ED.
Mann et al. (1996) conducted a randomized, double-blind, placebo-controlled study on the use of yohimbine for erectile dysfunction. The 31 patients included in the trial were either given 15 mg daily of yohimbine or placebo for 7 weeks. The Clinical Global Impression (CGI) scale was used to assess erectile function as a primary outcome. Additional parameters included nocturnal penile tumescence and rigidity (NPTR). There was a significant greater improvement in the yohimbine group with nonorganic erectile dysfunction. There was no difference between placebo and the yohimbine group with organic erectile dysfunction, however. The NPTR was found unchanged between all groups.
In a double-blind, placebo-controlled, crossover trial, yohimbine was examined for its efficacy in ED. The 48 subjects were administered either 18 mg of yohimbine daily for 10 weeks or placebo. Overall, 46% of those on the yohimbine treatment reported beneficial results for yohimbine. The authors concluded yohimbine to be safe and effective treatment for ED that was either organic or nonorganic in cause (Reid et al., 1987).
Rowland et al (1997) investigated the effect of yohimbine on ED in a double-blind, placebo-controlled crossover study. Included in the trial was both a group of men with ED and a group of sexually functional men for comparison. Yohimbine was administered at the dosage of up to 30 mg daily, and assessment was recorded on a number of objective and subjective measures of ED through daily logs and psychophysiological laboratory procedures involving response to visual sexual stimulation (VSS). In the sexually functional men, there was no effect found for yohimbine on sexual response. In the mend with ED, there were mixed results on sexual function. Frequency of sexual activities increased, along with genital response to VSS, and masturbation. Sexual arousal did not change, however, during intercourse.
In a double-blind, placebo-controlled crossover study on the use of yohimbine for ED, mixed results were found. Of the 215 participants in the study with ED that took yohimbine, 38% reported subjective improvement, with only 5% being completely satisfied. The authors noted the effect appeared to occur in the central nervous system, and that the usual dose of yohimbine had little effect, whereas higher doses were needed to achieve better results (Sonda et al., 1990).
Susset et al. (1989) conduced a double-blind partial crossover study on the effect of yohimbine hydrochloride in ED patients. Assessment was multifactorial, and included cavernosography, penile brachial blood pressure index, sacral evoked response, testosterone and prolactin determination, and Derogatis sexual dysfunction inventory and daytime arousal test. Treatment of the 82 patients consisted of 42.0 mg of yohimbine hydrochloride daily (orally) for 1 month. 14% of the patients underwent full restoration of ED, 20% reported partial improvement, and 65% reported no improvement. There was a positive effect reported in only 3 of the placebo patients. The action of yohimbine seemed to take 2-3 weeks to reach full potential. The authors noted that the results of the study were encouraging, especially because the participants were of the Veterans Administration population, that had high incidence of diabetes and vascular pathological conditions not found in the regular population. Few side effects were found, and of a benign nature.
Vogt et al. (1997) conducted a double-blind, placebo-controlled clinical trial of yohimbine hydrochloride in patients with ED of both organic and nonorganic cause. The 85 patients were given either 30 mg yohimbine daily or placebo for 8 weeks. Subjective and objective criteria to assess ED were included in the outcome parameters. Yohimbine was found to be significantly more effective than placebo (71% vs 45%), and overall it was well tolerated. There were no serious side effects reported, and only 7% of the patients rated tolerability of yohimbine to be fair or poor.
Yohimbine was tested in a placebo-controlled study for its effectiveness on ED in men with organic ED. The 22 patients were given a high dose of yohimbine hydrochloride (100 mg orally) daily for 30 days or placebo. No significant difference was found between yohimbine treatment and placebo, even though 3% reported complete restoration of ED, and 12 % reported partial response (Teloken et al., 1998).
Safety / Dosage
Typical dosage recommendations are between 10-30 mg of alkloids in a yohimbe extract. There is no widely accepted standardization level for yohimbe, and dosage recommendations generally are based on yohimbine or total alkaloid content. However, there is a wide variety of products on the market, and caution should be exercised in finding a reputable product.
Adverse effects are a concern and have been reported with yohimbe use, including dizziness, headaches, loss of coordination, anxiety, high blood pressure, and hallucinations. Yohimbe is not recommended for diabetics, people with high blood pressure, kidney disease, or during pregnancy (or the chance of becoming pregnant). Caution is also advised for people taking nasal decongestants, diet aids, ephedrine, phenylpropanolamine, other antidepressants (as it may potentiate their effect), and in combination with tyramine containig foods (Abebe, 2003; Tam, 2001; Sandler and Aronson, 1993).
References
1.Abebe W. An overview of herbal supplement utilization with particular emphasis on possible interactions with dental drugs and oral manifestations. J Dent Hyg. 2003 Winter;77(1):37-46.
2.Ernst E, Pittler MH. Yohimbine for erectile dysfunction: a systematic review and meta-analysis of randomized clinical trials. The Journal of Urology 1998; 159:433-6.
3.Mann K, Klingler T, Noe S, Roschke J, Muller S, Benkert O. Effects of yohimbine on sexual experiences and nocturnal penile tumescence and rigidity in erectile dysfunction. Arch Sex Behav 1996; 25(1):1-16.
4.Reid K, Surridge DH, Morales A et al. Double-blind trial of yohimbine in treatment of psychogenic impotence. Lancet 1987; 2(8556):421-3.
5.Riley AJ. Yohimbine in the treatment of erectile disorder. Br J Clin Pract. 1994 May-Jun;48(3):133-6.
6.Rowland DL, Kallan K, Slob AK. Yohimbine, erectile capacity, and sexual response in men. Arch Sex Behav 1997; 26(1):49-62.
7.Sandler B, Aronson P. Yohimbine-induced cutaneous drug eruption, progressive renal failure, and lupus-like syndrome. Urology. 1993 Apr;41(4):343-5.
8.Sonda LP, Mazo R, Chancellor MB. The role of yohimbine for the treatment of erectile impotence. J Sex Marital Ther 1990; 16(1):15-21.
9.Susset JG, Tessier CD, Wincze J, Bansal S, Malhotra C, Schwacha MG. Effect of yohimbine hydrochloride on erectile impotence: a double-blind study. J Urol 1989; 141(6):1360-3.
10.Tam SW, Worcel M, Wyllie M. Yohimbine: a clinical review. Pharmacol Ther. 2001 Sep;91(3):215-43.
11.Teloken C, Rhoden EL, Sogari P, Dambros M, Souto CA. Therapeutic effects of high dose yohimbine hydrochloride on organic erectile dysfunction. J Urol 1998; 159(1):122-4.
12.Vogt HJ, Brandl P, Kockott G et al. Double-blind, placebo-controlled safety and efficacy trial with yohimbine hydrochloride in the treatment of nonorganic erectile dysfunction. Int J Impot Res 1997; 9(3):155-61.
EDITOR'S NOTE: This monograph can be found in The Health Professional's Guide to Dietary Supplements (Lippincott, Williams & Wilkins) by Shawn M. Talbott, PhD and Kerry Hughes, MS.