Monday, August 31, 2009

Slippery Elm

Overview

Slippery elm contains mucilaginous compounds that gives it the description of being “slippery” and also are the reasoning for its herbal therapeutic uses. The mucilaginous effect of slippery elm has been used traditionally and safely for soothing the throat and other mucous membranes during colds and sore throat, and for the irritated mucous membranes of the digestive system during digestive complaints (diarrhea, constipation, Crohn’s disease), and topically on skin during minor irritations (such as poison oak and wound healing).


Comments

Although slippery elm lacks clinical support, the soothing effect of the mucilaginous components is well known. Additionally, related elm species have showed evidence of antimicrobial activity and promise for inflammation and diseases of the mucous membranes (Youn et al., 2003; Song et al., 2003; Jun et al, 1998; Ye et al., 1990).


Scientific Support

No direct clinical support could be found on slippery elm as a single phytotherapeutic agent.


Safety / Dosage

Slippery elm lacks clinical and toxicity testing, but it has been used as a traditional remedy without any adverse reports. It is generally thought to be completely safe and non-toxic, with no drug-interactions.


Slippery elm is available in different preparations, such as lozenges, capsules, tablets and teas. Generally, 800 mg is taken 3-4 times daily for the soothing of mucous membranes.


References

1.Jun CD, Pae HO, Kim YC, Jeong SJ, Yoo JC, Lee EJ, Choi BM, Chae SW, Park RK, Chung HT. Inhibition of nitric oxide synthesis by butanol fraction of the methanol extract of Ulmus davidiana in murine macrophages. J Ethnopharmacol. 1998 Sep;62(2):129-35.

2.Oiseth D. Study on carbohydrate constituents of mucilage of Ulmus glabra Huds. Pharm Acta Helv. 1954 Aug;29(8):251-6.

3.Song SE, Choi BK, Kim SN, Yoo YJ, Kim MM, Park SK, Roh SS, Kim CK. Inhibitory effect of procyanidin oligomer from elm cortex on the matrix metalloproteinases and proteases of periodontopathogens. J Periodontal Res. 2003 Jun;38(3):282-9.

4.Ye G, Cao Q, Chen X, Li S, Jia B. Ulmus macrocarpa hance for the treatment of ulcerative colitis--a report of 36 cases. J Tradit Chin Med. 1990 Jun;10(2):97-8.

5.Youn HJ, Lakritz J, Kim DY, Rottinghaus GE, Marsh AE. Anti-protozoal efficacy of medicinal herb extracts against Toxoplasma gondii and Neospora caninum. Vet Parasitol. 2003 Aug 29;116(1):7-14.


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.

Yellow Dock

Overview

Yellow dock—also called curly dock and sour dock—is a member of the buckwheat family that can be found naturalized in many parts of the world. Originally from northern Europe and Asia, it has a long history of use in traditional medicines as a digestive aid, for skin conditions, and for liver health. Yellow dock is known as an astringent due to its content of tannins, which may be the reason for its use in skin conditions. Yellow dock extracts have been confirmed to have antioxidant and antimicrobial activity. Additionally, yellow dock contains the anthraquinone glycosides, a group of compounds that are known for their laxative activity. The antraquinone glycosides are also the primary active components in other popular herbal laxatives, such as senna, cascara and aloe. The bitter principles of yellow dock leaves make them useful as digestive aids. Yellow dock is also rich in iron (Bruneton, 1995).


Comments

Yellow dock lacks clinical backing as a single phytotherapeutic agent, however, the anthraquinone glycosides are well known and have clinically confirmed activity.


Scientific Support

No clinical studies could be found that used yellow dock alone as a therapeutic agent, however, several clinical studies confirm the activity of the anthraquinone glycosides from other herbal laxatives.


Safety / Dosage

The laxative effect of yellow dock appears to be mild and safe. The fresh leaves are high in oxalates, and there have been a few reports of yellow dock toxicity in grazing sheep and at least one report of a human toxicity. If the oxalates are taken in high amounts they may inhibit nutrient absorption. Root preparations are typical, and the dosage is generally 1 gram of the dried root daily or 3-4 ml of the root extract, 3 times daily.


As with any laxative product, caution should be used by anyone who is pregnant or nursing.


References

1.Bruneton, J. Pharmacognosy, Phytochemistry, Medicinal Plants. 1995. Lavoisier Publishing, New York.

2.Gunaydin K, Topcu G, Ion RM. 1,5-dihydroxyanthraquinones and an anthrone from roots of Rumex crispus. Nat Prod Lett. 2002 Feb;16(1):65-70

3.Panciera RJ, Martin T, Burrows GE, Taylor DS, Rice LE. Acute oxalate poisoning attributable to ingestion of curly dock (Rumex crispus) in sheep. J Am Vet Med Assoc. 1990 Jun 15;196(12):1981-4.

4.Reig R, Sanz P, Blanche C, Fontarnau R, Dominguez A, Corbella J. Fatal poisoning by Rumex crispus (curled dock): pathological findings and application of scanning electron microscopy. Vet Hum Toxicol. 1990 Oct;32(5):468-70.

5.Yildirim A, Mavi A, Kara AA. Determination of antioxidant and antimicrobial activities of Rumex crispus L. extracts. J Agric Food Chem. 2001 Aug;49(8):4083-9


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.

Maca

Overview

Maca is a South American tuber that has been used since ancient times as a staple food crop in the Andes. Although maca has been long known as a folkloric medicine and food for increasing energy, physical and mental endurance and stamina, it has recently been in the spotlight for its use in altering sexual function (Balick and Lee, 2002). Maca is thought to be able to increase libido in both men and women, although this effect has only clinically been tested in men. Recent preliminary clinical studies have shown that maca has effects on increasing libido and fertility that are independent of sexual hormone functioning and parameters of mood (depression and anxiety). Several positive studies have been performed in animals (mice) and found increased sexual performance, libido and fertility parameters (Cicero et al., 2002; Cicero et al., 2001; Gonzales et al., 2001; Zheng et al., 2000).


It is interesting to note that the tall physical height and strength of the people of the Andes who live at such high elevations (where maca was popular as a food staple) has been theorized to be linked to the use of maca in their diet (Canales et al., 2000). Maca is rich in nutrients, such as amino acids and glucosinolates, which have been linked to its activity (Piacente et al., 2002).


Comments

The jury is still out as to the best dosage form and health conditions for which maca benefits, however, the clinical evidence of its effect in altering libido and fertility is promising. In either case, maca enjoys a long history of use as a food that makes people feel good and strong and it continues to do so in Peru and in the Andes of South America.


Scientific Support

Hormonal Regulation, Mood and Libido

In a randomized, double-blind, placebo-controlled, parallel study, maca was tested for its effect on hormone levels when administered for libido and fertility-enhancement. Maca was given in either 1500 mg or 3000 mg daily doses for 12 weeks and hormone levels were tested (serum lutenizing (LH), follicle stimulating hormone (FSH), prolactin (PRL), testosterone (T) and estradiol (E2), and 17-alpha hydroxyprogesterone). Maca was found not have any effect on reproductive hormone levels (Gonzales et al., 2003).


The reported effect of maca on libido was examined to see if it was related to serum testosterone or mood levels in a randomized, double-blind, placebo-controlled study. Either 1500 or 3000 mg of maca was given for 12 weeks and the self perception of sexual desire, Hamilton test for depression, and Hamilton test for anxiety was measured at 4, 8 and 12 weeks of treatment. At 8 weeks of treatment, maca produced an improvement in sexual desire, however, serum testosterone and oestradiol levels were not found to be changed. There was also no correlation found in Hamilton scores for depression or anxiety. The effect of maca on libido was found to be separate from testosterone or mood regulation (Gonzales et al., 2002).


Semen Production

The effect of Maca supplementation on semen function and health parameters was studied in a preliminary clinical study. Nine men were administered Maca (L. meyenii; 1500 or 3000 mg daily) for four months and seminal analysis was performed along with hormonal analysis on LH, FSH, PRL, T and E2. Seminal analysis followed guidelines of the World Health Organization (WHO). Maca was found to improve sperm production in a non-dose dependent manner by mechanisms not related to hormonal production (Gonzales et al., 2001).


Safety / Dosage

As it has a long historical use as a staple food, maca is thought to be very safe and free of side effects or drug interactions. Maca is generally recommended in dosages of 1.5-5 grams per day (of dried tuber), or approximately 900 mg of the extract daily. Different manufacturers have varying preparations, so it is best to read the label recommendations.


References

1.Balick MJ, Lee R. Maca: from traditional food crop to energy and libido stimulant. Altern Ther Health Med. 2002 Mar-Apr;8(2):96-8.

2.Canales M, Aguilar J, Prada A, Marcelo A, Huaman C, Carbajal L. Nutritional evaluation of Lepidium meyenii (MACA) in albino mice and their descendants. Arch Latinoam Nutr. 2000 Jun;50(2):126-33.

3.Cicero AF, Bandieri E, Arletti R. Lepidium meyenii Walp. improves sexual behaviour in male rats independently from its action on spontaneous locomotor activity. J Ethnopharmacol. 2001 May;75(2-3):225-9.

4.Cicero AF, Piacente S, Plaza A, Sala E, Arletti R, Pizza C. Hexanic Maca extract improves rat sexual performance more effectively than methanolic and chloroformic Maca extracts. Andrologia. 2002 Jun;34(3):177-9.

5.Gonzales GF, Cordova A, Vega K, Chung A, Villena A, Gonez C. Effect of Lepidium meyenii (Maca), a root with aphrodisiac and fertility-enhancing properties, on serum reproductive hormone levels in adult healthy men. J Endocrinol. 2003 Jan;176(1):163-8.

6.Gonzales GF, Cordova A, Vega K, Chung A, Villena A, Gonez C, Castillo S. Effect of Lepidium meyenii (MACA) on sexual desire and its absent relationship with serum testosterone levels in adult healthy men. Andrologia. 2002 Dec;34(6):367-72.

7.Gonzales GF, Cordova A, Gonzales C, Chung A, Vega K, Villena A. Lepidium meyenii (Maca) improved semen parameters in adult men. Asian J Androl. 2001 Dec;3(4):301-3.

8.Gonzales GF, Ruiz A, Gonzales C, Villegas L, Cordova A. Effect of Lepidium meyenii (maca) roots on spermatogenesis of male rats. Asian J Androl. 2001 Sep;3(3):231-3.

9.Piacente S, Carbone V, Plaza A, Zampelli A, Pizza C. Investigation of the tuber constituents of maca (Lepidium meyenii Walp.). J Agric Food Chem. 2002 Sep 25;50(20):5621-5.

10.Zheng BL, He K, Kim CH, Rogers L, Shao Y, Huang ZY, Lu Y, Yan SJ, Qien LC, Zheng QY. Effect of a lipidic extract from lepidium meyenii on sexual behavior in mice and rats. Urology. 2000 Apr;55(4):598-602.


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.

Pygeum

Overview

Pygeum (Pygeum africanum), also known as African plum (a related plant, African Cherry or Prunus africana is also used as pygeum to treat BPH), is a large evergreen tree that grows in the high plateaus of Southern Africa. The pygeum bark is traditionally powdered and drunk as a tea for genito-urinary complaints such as bladder pain and urinary difficulty. As with saw palmetto, pygeum has predominantly been used and tested throughout Europe for the treatment of Benign Prostatic Hyperplasia (BPH) and its most common symptoms including effectiveness in decreasing frequency of nocturnal urination, increasing urine volume, decreasing incidence of incomplete bladder emptying, and reducing prostate enlargement. In France and Italy, pygeum is the main course of natural treatment for BPH and is usually used in combination products that contain other herbal BPH treatments such as saw palmetto (the most popular in Germany) and nettle root. Increased demand for pygeum has led to over-harvesting and is threatening the survival of the species, with international trade currently being monitored.


Comments

Although the mechanism of action of pygeum is largely unknown, it is theorized to inhibit fibroblast hyperproliferation and prevent bladder contractile dysfunction through effects on 5-alpha-reductase, a major enzyme shown to play a role in prostate growth (Cristoni et al. 2000, Levin and Das 2000). As such, pygeum may decrease excessive prostate growth (hyperplasia) and could allow for better contraction of the bladder for more productive urination. Both of these actions could improve the quality of life of men with BPH. The chemical composition of pygeum bark extracts are known to be rich in phytosterols such as beta-sitosterol, beta sitosterone, and campesterol, as well as ferulic acid esters including n-docosanol, and triterpenes including oleanolic acid, crataegolic acid and ursolic acid.


Scientific Support

Animal studies indicate that partial bladder obstruction may lead to bladder contractile problems – with BPH-like symptoms prevented by pre-treatment with pygeum extract. In humans, several clinical trials have demonstrated the benefits of pygeum extract in alleviating symptoms of BPH (Breza et al. 1998, Chatelain et al. 1999, Ishani et al. 2000, Krzeski et al. 1993, Wilt et al. 2000, Wilt et al. 2002). In general, daily doses of pygeum bark extract at 25-100mg have demonstrated significant reductions in measures of the International Prostate Symptom Score (IPSS) of about 40% and increased quality of life (QOL) of about 30% (Breza et al. 1998). In one study, 209 patients with symptomatic BPH consumed 50mg or 100mg of pygeum extract for 2 months – with result showing similar effects in both dosage groups including 35% improvement in IPSS and 28% improvement in QOL (Chatelain et al. 1999). Other studies 18 controlled trials involving 1,562 men) have shown pygeum supplementation to decrease the frequency of nocturnal urination by 19%-32%, reduce residual urine volume by 24%, increase peak urine flow by 23%, and reduce nocturnal frequency by 32% (Breza et al. 1998, Ishani et al. 2000, Krzeski et al. 1993, Wilt et al. 2000).


The ferulic acid component of pygeum bark extracts has been noted to possess some modest anti-androgenic activity – leading bodybuilding enthusiasts to supplement with pygeum as a way to reduce conversion of testosterone to dihydrotestosterone (DHT) and thus enhance muscle cell exposure to free tesosterone. Such an effect has not been demonstrated in human trials. Likewise, the phytosterol component of pygeum bark extracts appear to compete with androgen precursors and in turn may be able to inhibit prostaglandin synthesis and provide a modest anti-inflammatory action (along with the triterpene components).


Safety/Dosage

Side effects for those taking pygeum are relatively rare and mild, and are generally gastrointestinal in nature. No drug interactions have been reported. It is important for any man with an enlarged prostate to consult with his personal physician to determine the cause of prostate enlargement and to rule out prostate cancer.


Pygeum africanum bark extract is generally taken twice per day in 50mg capsules, although taking 100mg in a single dose has been shown to be just as effective and safe. The extract consists of three groups of active constituents: phytosterols, pentacyclic triterpenoids, and ferulic esters of long-chained fatty alcohols. Thus, this oily extract is typically sold in softgel capsule form that are standardized 14% triterpenes and 0.5% n-docosanol.


References

1.Barry M. Review: Pygeum africanum extracts improve symptoms and urodynamics in symptomatic benign prostatic hyperplasia. ACP J Club. 2002 Sep-Oct;137(2):61.

2.Breza J, Dzurny O, Borowka A, Hanus T, Petrik R, Blane G, Chadha-Boreham H. Efficacy and acceptability of tadenan (Pygeum africanum extract) in the treatment of benign prostatic hyperplasia (BPH): a multicentre trial in central Europe. Curr Med Res Opin. 1998;14(3):127-39.

3.Buck AC. Is there a scientific basis for the therapeutic effects of serenoa repens in benign prostatic hyperplasia? Mechanisms of action. J Urol. 2004 Nov;172(5 Pt 1):1792-9.

4.Chatelain C, Autet W, Brackman F. Comparison of once and twice daily dosage forms of Pygeum africanum extract in patients with benign prostatic hyperplasia: a randomized, double-blind study, with long-term open label extension. Urology. 1999 Sep;54(3):473-8.

5.Cristoni A, Di Pierro F, Bombardelli E. Botanical derivatives for the prostate. Fitoterapia. 2000 Aug;71 Suppl 1:S21-8.

6.Ishani A, MacDonald R, Nelson D, Rutks I, Wilt TJ. Pygeum africanum for the treatment of patients with benign prostatic hyperplasia: a systematic review and quantitative meta-analysis. Am J Med. 2000 Dec 1;109(8):654-64.

7.Krzeski T, Kazon M, Borkowski A, Witeska A, Kuczera J. Combined extracts of Urtica dioica and Pygeum africanum in the treatment of benign prostatic hyperplasia: double-blind comparison of two doses. Clin Ther. 1993 Nov-Dec;15(6):1011-20.

8.Levin RM, Das AK. A scientific basis for the therapeutic effects of Pygeum africanum and Serenoa repens. Urol Res. 2000 Jun;28(3):201-9.

9.Mathe G, Hallard M, Bourut CH, Chenu E. A Pygeum africanum extract with so-called phyto-estrogenic action markedly reduces the volume of true and large prostatic hypertrophy. Biomed Pharmacother. 1995;49(7-8):341-3.

10.McQueen CE, Bryant PJ. Pygeum. Am J Health Syst Pharm. 2001 Jan 15;58(2):120-3.

11.Strong KM. African plum and benign prostatic hypertrophy. J Herb Pharmcother. 2004;4(1):41-6.

12.Wilt T, Ishani A, Mac Donald R, Rutks I, Stark G. Pygeum africanum for benign prostatic hyperplasia. Cochrane Database Syst Rev. 2002;(1):CD001044.

13.Wilt TJ, Ishani A, Rutks I, MacDonald R. Phytotherapy for benign prostatic hyperplasia. Public Health Nutr. 2000 Dec;3(4A):459-72.


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

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.