Trichotin DHT Inhibitor

Technical info

Scheduling Status
S0

Proprietary Name and Dosage Form
Trichotin DHT Inhibitor (Caplet)

Composition
Each caplet provides:
Trichogenesis 772.5mg
Saw palmetto extract (45% fatty acids)
Nettle root extract
Beta-Sitosterol 95%
Co-Enzyme Q10
Panax Ginseng

Pharmacological Classification
Category D Medicine

Pharmacological  Action
Trichotin DHT Inhibitor has been formulated to provide beneficial nutrients and herbal extracts to assist with the inhibition of DHT and promote hair growth.

Indication
This product is indicated as a general supplement where a deficiency of any of the ingredients exists.

Contra-Indications
If you suffer from a chronic medical condition consult your healthcare practitioner before using this product. Women and individuals with hormone-dependent illnesses such as endometriosis, uterine fibroids, or cancers of the breast, ovaries, uterus or prostate, pregnant and breastfeeding should avoid using Trichotin DHT Inhibitor. If you are a diabetic or suffer from a heart condition, use this product only under the supervision of your healthcare practitioner.
 
Warnings
Keep out of reach of children.
Do not exceed the recommended dose.
Consult a medical practitioner prior to use

Interaction
Use this product under the supervision of your healthcare practitioner if you are using chronic prescription medication. Discontinue using this product at least 2 weeks prior to any surgical procedure.

Pregnancy and Lactation
Use should be avoided during pregnancy and breastfeeding.

Dosage and Directions for Use
Take one caplet every evening, 30 minutes before bedtime or as directed by your healthcare practitioner.

Side Effects and Special Precautions
Discontinue the use of this product where there is sensitivity to any of the ingredients. Gynecomastia is a possible side-effect of 5-alpha reductase inhibition.

Known Symptoms of Overdose and Treatment
No known symptoms.

Identification
Red coated, oval caplet

Presentation
Printed carton containing Printed glass bottle with 30 red caplets

Storage Instructions
Store below 25 degrees Celsius.
Protect from light and moisture.

Date of Publication of this Package Information
August 2014

Ingredients

Saw Palmetto 
Certified pure and imported from the USA, Saw Palmetto is a trusted herbal remedy known to impact hair loss positively and treat alopecia.

It neutralises the 5 alpha-reductase and therefore prevents the conversion of testosterone to dihydrotestosterone. Increased DHT in the body intensifies the sensitivity of hair follicles, reducing their growth phase and size.

Beta-Sitosterol
Reduction of cholesterol bioavailability by Beta-Siteosterol inhibits the action of 5AR and reduces biosynthesis of testosterone to DHT. Beta-Sitosteol, a plant sterol, further prevents hair loss by inhibiting the production of androgens including DHT.

Studies demonstrate the efficacy of beta sitosterol for treating androgenic alopecia especially when combined with Saw Palmetto.

In addition, Beta-Sitosterol benefits include the promotion of healthier regrowth.

Nettle Root
A herbal extract that contains polysaccharides with immunomodulating and anti-inflammatory properties to diminish the effects of androgenic hormones.

Co Enzyme Q10
Co Enzyme Q10, a potent anti-oxidant rejuvenates the scalp and stimulates follicle repair.

Studies indicate that individuals supplementing with Co Enzyme Q 10 daily, report thicker stronger hair growth.

Ginseng
Panax Ginseng increases circulation to the scalp specifically. This action ensures greater nutrient delivery, absorption and thereby enhances follicle health.

Research

Dihydrotestosterone (DHT)
Dihydrotestosterone (DHT) is a biologically active metabolite of the hormone testosterone, formed primarily in the prostate gland, testes, hair follicles, and adrenal glands by the enzyme 5α-reductase by means of reducing the 4,5 double-bond. Dihydrotestosterone belongs to the class of compounds called androgens, also commonly called androgenic hormones or testoids. Androgens are part of the biology of gender by stimulating and controlling the development and maintenance of masculine characteristics. DHT is 3 times more potent than testosterone; testosterone is 5-10 times more potent than adrenal androgens.

While DHT is best known for its roles in causing male pattern hair loss and prostate problems, it is crucial to virilization and is necessary to mitigate estrogen’s effects in men.

DHT is produced by males in vivo and is responsible for the formation of male sex-specific characteristics. DHT is an important contributor to other characteristics generally attributed to males, including facial and body hair growth, and deepening of the voice. DHT may also play a crucial role in both sex drive and the growth of muscle tissue. Unlike other androgens such as testosterone, DHT cannot be converted by the enzyme aromatase to estradiol.

DHT is the primary contributing factor in male-pattern baldness. Female-pattern baldness is more complex, and DHT is only one of many causes of women’s hair loss. Women with increased levels of DHT may develop certain androgynous male secondary sex characteristics, including a deepened voice and facial hair. DHT may play a role in the development or exacerbation of benign prostatic hyperplasia, or BPH, and prostate cancer, by enlarging the prostate gland. The role of DHT on the prostate is not completely understood. There are some theories that indicate that the combination of DHT with other changes in other hormones such as increasing estrogen may be a factor.

DHT is also known to participate in the development in some cases of acne.

The drugs belonging to the group known as 5α-reductase inhibitors are used for treatment of problems stemming from DHT. This group includes finasteride and dutasteride. Dutasteride is three times more potent than finasteride inhibiting the type II enzyme and 100 times more potent than finasteride inhibiting the type I form of the DHT-producing enzyme. Dutasteride is not approved by the FDA for the treatment of Male Pattern Hair Loss and is approved at a dose of 0.5 mg a day for the treatment of prostate enlargement. While both the type I and type II enzymes are found in the hair follicle, there is a recent study that shows that type I is present in the human brain. The function of this enzyme in the brain is still unclear.

5-alpha-reductase

Isoenzymes
There are two isoenzymes, steroid 5-alpha reductase 1 and 2 (SRD5A1 and SRD5A2).

Production and inhibition
The enzyme is produced only in specific tissues of the male human body, namely the skin, seminal vesicles, prostate and epididymis.

Inhibition of 5-alpha reductase results in decreased production of DHT, increased levels of testosterone, and, perhaps, increased levels of estradiol. Gynecomastia is a possible side-effect of 5-alpha reductase inhibition.

Pharmacology
5-Alpha-reductase inhibitor drugs are used in benign prostatic hyperplasia, prostate cancer, and baldness. Both isoforms are also produced in the brain, where they serve to create the neurosteroid Allopregnenolone (5AR type I) and convert testosterone to DHT(5AR type II). Finasteride inhibits the function of only one of the isoenzymes (type 2), whereas dutasteride inhibits both forms.

Trichotin DHT Inhibitor
Each capsule provides: 725.5mg
Saw Palmetto extract
Beta sitosterol
Nettle root extract
Co Enzyme Q10
Panax Ginseng

Saw Palmetto
Scientific Name:  Serenoa repens, synonyms Serenoa serrulata, Sabal serrulata.
Family: Arecaceae/Palmae.

Mechanism of Action
The applicable part of saw palmetto is the ripe fruit. The lipid fraction contains volatile oils and fatty oils, which are active in treating benign prostatic hyperplasia (BPH). Many saw palmetto products are standardized based on the fatty acid content. The most effective saw palmetto products seem to be whole berries or berry extracts prepared with lipophilic nonpolar solvents. Water extraction, including brewed tea, probably does not adequately extract fat-soluble active constituents.

Saw palmetto has antiandrogenic, antiproliferative, and anti-inflammatory properties that seem to be responsible for improving symptoms of benign prostatic hyperplasia (BPH). Saw palmetto appears to noncompetitively inhibit 5 alpha-reductase types 1 and 2 and to prevent the conversion of testosterone to dihydrotestosterone (DHT) in vitro, which might reduce prostate growth (6765,6769,6770,6773). However, 5 alpha-reductase levels in prostatic tissue and serum testosterone, DHT, and PSA are not significantly reduced by saw palmetto in vivo (2735,6771). Saw palmetto does not seem to affect overall prostate size, but shrinks the inner prostatic epithelium (2736,5093). Saw palmetto might slow prostate cell proliferation by inhibiting fibroblast growth factor and epidermal growth factor and stimulating apoptosis (6765,6769,6770).

Inhibition of 5 alpha-reductase and prevention of conversion of testosterone to DHT may contribute to activity of saw palmetto in androgenic alopecia. It is suggested that this condition involves increased sensitivity of hair follicles to DHT, reducing their growth phase and size (15550).

Inflammatory mediators appear to contribute to the etiology of BPH. In men with BPH, a liposterolic extract of saw palmetto berry seems to lower tumor necrosis factor (TNF)-alpha and interleukin (IL)-1beta, which are markers of inflammation in prostate tissue (11224). Laboratory evidence suggests that saw palmetto inhibits lipoxygenase and cyclooxygenase (COX), which are involved in inflammation (6769,6779).

Increased COX-2 expression is also associated with an increased incidence of prostate cancer. Preliminary research indicates that saw palmetto reduces the proliferation of experimental prostate cells, possibly by inhibiting COX-2 expression (8902).

Saw palmetto also seems to have antiestrogen, antispasmodic, and alpha-adrenergic inhibitory properties (5095,6766,6780). Laboratory fertility studies indicate that saw palmetto has no effect on oocytes or sperm motility, but it might induce metabolic changes in sperm (4239,4240).

There is conflicting evidence about the effects of saw palmetto on cytochrome P450 (CYP450) enzymes 2D6 (CYP2D6) and 3A4 (CYP3A4). In vitro evidence suggests that saw palmetto might inhibit CYP2D6 and CYP3A4 (11026). But when used in healthy volunteers, saw palmetto 320 mg/day does not seem to affect CYP2D6 or CYP3A4 (11225,13712). Saw palmetto also does not seem to affect CYP1A2 or CYP2E1 in healthy volunteers (13712).

Indications
Orally, saw palmetto is used for symptoms of benign prostatic hyperplasia (BPH). It is also used orally as a mild diuretic, a sedative, an anti-inflammatory, and as an antiseptic. Saw palmetto is used to increase breast size, to improve sexual vigor, and as an aphrodisiac. It is also used to treat chronic nonbacterial prostatitis/chronic pelvic pain syndrome, colds, coughs, irritated mucous membranes, sore throat, asthma, chronic bronchitis, migraines, cancer, and to stimulate hair growth. Saw palmetto is also used to prevent complications during transurethral resection of the prostate (TURP).

Benign prostatic hyperplasia (BPH). Multiple clinical studies lasting up to a year and data analyses have shown that saw palmetto provides mild to moderate improvement in urinary symptoms such as frequent urination, painful urination, hesitancy, urgency, and perineal heaviness. It also decreases nocturia, improves peak and mean urinary flow, and lowers residual urine volume in patients with BPH (2732,5094,6750,6751,6752,6762,6764,6772,6773,6777,6778) (8330,14275).

Saw palmetto seems to be comparable in efficacy to finasteride (Proscar), but saw palmetto might be better tolerated (6424,6763,14275). Alpha-adrenergic blockers such as prazosin (Minipress) seem to be superior to saw palmetto for relieving symptoms of BPH (6775,6776). However, other preliminary research suggests that saw palmetto is similar in efficacy to tamsulosin (Flomax) after 12 months (11243). The addition of saw palmetto to an alpha-blocker such as tamsulosin doesn’t seem to relieve symptoms any better than an alpha-blocker alone (8901). Treatment for one to two months with saw palmetto is usually necessary before significant symptomatic improvement occurs (2732,6750,6778).

A specific formulation containing saw palmetto and stinging nettle root (PRO 160/120) also seems to be comparable to finasteride (Proscar) for relieving symptoms of BPH (6763).

Although most research shows that saw palmetto is effective, some research has not been positive. In one high quality study, saw palmetto was ineffective for reducing symptoms in men with moderate to severe symptoms of BPH after a year of treatment (14274). The reason for this inconsistent finding might be due to different outcome measures, product selection, or other factors. In another study, saw palmetto was not effective for men with relatively mild BPH (11314). Another study using saw palmetto lipid extract 106 mg, nettle root extract 80 mg, pumpkin seed oil extract 160 mg, lemon bioflavonoid extract 33 mg, and beta-carotene 190 IU taken three times daily for 6 months found that this combination product was not effective for relieving symptoms (5093).

Saw palmetto does not seem to reduce prostate size or prostate-specific antigen (PSA) levels like finasteride (6424).

Most clinical studies have used a liposterolic extract of saw palmetto berry containing 80% and 90% fatty acids. This formulation is similar to Quanterra Prostate (Warner-Lambert), Super Saw Palmetto (Enzymatic Therapy), ProstaPro (Phytopharmica), Saw Palmetto (Centrum), Standardized Saw Palmetto Extract (Nature’s Way), and others.

Androgenic alopecia (alopecia areata). Preliminary clinical research suggests that a combination of saw palmetto extract 200 mg plus beta-sitosterol 50 mg taken twice daily improves subjective scores of hair quantity and quality in men with androgenic alopecia (15550).

Prostate cancer. Population research suggests that people who take saw palmetto supplements do not have a lower risk of developing prostate cancer (15217).

Prostatitis and chronic pelvic pain syndrome. Preliminary clinical research suggests that saw palmetto given orally for one year doesn’t help nonbacterial prostatitis and chronic pelvic pain syndrome (11354).

Transurethral resection of the prostate (TURP). Preliminary clinical research shows that taking saw palmetto 160 mg orally once daily, 5 weeks prior to transurethral resection of the prostate (TURP), does not lower the risk of perioperative hemorrhage or decrease the density of prostatic tissue (17202)

Adverse Reactions
Orally, the adverse effects of saw palmetto are generally mild and comparable to placebo. Dizziness, headache, and gastrointestinal complaints such as nausea, vomiting, constipation, and diarrhea are the most frequently reported adverse effects (6751,6752,6762,11354).

A combination of saw palmetto and beta-sitosterol has been associated with single reports of loss of appetite, flatulence, diarrhea, and worsening acne (15550).

There is one case report of cholestatic hepatitis associated with the use of the multi-ingredient product that contains saw palmetto (Prostata) (598). In another case, a patient who took saw palmetto developed acute hepatitis and pancreatitis. Symptoms resolved when saw palmetto was discontinued. Upon re-challenge with saw palmetto, symptoms reemerged. This strongly suggests that saw palmetto was the cause of these adverse events (14457). However, a product analysis was not conducted in order to rule out potential product contamination.

Some clinicians are concerned that saw palmetto might cause erectile dysfunction, ejaculatory disturbance, or altered libido because of its potential effects on 5-alpha-reductase. There is one case report of decreased ejaculatory volume associated with an herbal blend product containing saw palmetto extract, nettle root extract, pumpkin seed oil extract, lemon bioflavonoid extract, and beta-carotene (5093). However, clinical studies indicate that the occurrence of impotence in men taking saw palmetto is similar to placebo and significantly less than finasteride (2732,6424,6762).

There is also concern that saw palmetto might have antiplatelet effects and potentially increase the risk of bleeding in some patients. There is one report of excessive intraoperative bleeding in a patient who took saw palmetto prior to surgery. Bleeding time normalized when saw palmetto was discontinued (8659). To date, there are no documented cases of spontaneous bleeding in patients taking saw palmetto.

Dosage
ORAL: For benign prostatic hyperplasia (BPH), 160 mg twice daily or 320 mg once daily of a lipophilic extract containing 80% to 90% fatty acids has been used in clinical trials (2732,5094,6750,6751,6752,6762,6764,6772,6773,6777,6778) (8330,14274).

For androgenic alopecia (alopecia areata), 200 mg twice daily combined with beta-sitosterol 50 mg twice daily has been used (15550).

PREGNANCY AND LACTATION: Saw palmetto has hormonal activity (6766); avoid using.

Combined sabal and urtica extract compared with finasteride in men with benign prostatic hyperplasia: analysis of prostate volume and therapeutic outcome.

Sökeland J.

Urological Clinic of Dortmund, Training Hospital of the University of Münster, 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.

A randomized, double-blind, placebo-controlled trial to determine the effectiveness of botanically derived inhibitors of 5-alpha-reductase in the treatment of androgenetic alopecia.

Prager N, Bickett K, French N, Marcovici G.

Clinical Research and Development Network, Aurora, CO, USA.

Erratum in:

J Altern Complement Med. 2006 Mar;12(2):199.

BACKGROUND: Androgenetic alopecia (AGA) is characterized by the structural miniaturization of androgen-sensitive hair follicles in susceptible individuals and is anatomically defined within a given pattern of the scalp. Biochemically, one contributing factor of this disorder is the conversion of testosterone (T) to dihydrotestosterone (DHT) via the enzyme 5-alpha reductase (5AR). This metabolism is also key to the onset and progression of benign prostatic hyperplasia (BPH). Furthermore, AGA has also been shown to be responsive to drugs and agents used to treat BPH. Of note, certain botanical compounds have previously demonstrated efficacy against BPH. Here, we report the first example of a placebo-controlled, double-blind study undertaken in order to examine the benefit of these botanical substances in the treatment of AGA. OBJECTIVES: The goal of this study was to test botanically derived 5AR inhibitors, specifically the liposterolic extract of Serenoa repens (LSESr) and beta-sitosterol, in the treatment of AGA. Subjects: Included in this study were males between the ages of 23 and 64 years of age, in good health, with mild to moderate AGA. RESULTS: The results of this pilot study showed a highly positive response to treatment. The blinded investigative staff assessment report showed that 60% of (6/10) study subjects dosed with the active study formulation were rated as improved at the final visit. CONCLUSIONS: This study establishes the effectiveness of naturally occurring 5AR inhibitors against AGA for the first time, and justifies the expansion to larger trials.

Beta-sitosterol
Scientific Name:  22,23-dihydrostigmasterol; 24-beta-ethyl-delta-5-cholesten-3beta-ol; 24-ethyl-cholesterol; 3-beta-stigmast-5-en-3-ol.

Mechanism of Action
Beta-sitosterol is a plant sterol. It has a chemical structure similar to cholesterol with an ethyl group added at position 24. The average diet provides about 175-200 mg of beta-sitosterol, but less than 5% is actually absorbed when consumed orally. Therefore these plant sterols do not cause some of the atherogenic adverse effects associated with cholesterol from animal products. Beta-sitosterol is commonly added to margarines as a cholesterol reducing aid. Fats are needed to solubilize plant sterols so margarines are an ideal vehicle. Soybean phytosterols containing 48% beta-sitosterol, 26% campesterol, and 21% stigmasterol have been added to ground beef (8528). Capsules containing beta-sitosterol may not disperse properly in the gut, limiting their ability to reduce cholesterol absorption (5814). Beta-sitosterol actually inhibits intestinal absorption of cholesterol by competing for the limited space in mixed micelles, which decreases cholesterol absorption by about 50% (5814). Because there is less cholesterol available in the body, compensatory mechanisms kick in and increase cholesterol synthesis in the liver (5814).

For prostatic hyperplasia, animal research suggests that beta-sitosterol might inhibit 5-alpha-reductase activity, although finasteride (Proscar) appears to be more potent (11759). Laboratory research suggests beta-sitosterol might have antiproliferative effects on the prostate, possibly by inhibiting growth factors (11234). In animals, beta-sitosterol shrinks the prostate, but this has not been shown in humans (11759).

Inhibition of 5 alpha-reductase, which prevents conversion of testosterone to dihydrotestosterone (DHT), may contribute to activity of beta-sitosterol in androgenetic alopecia. Reduction of cholesterol bioavailability by beta-sitosterol may also reduce biosynthesis of testosterone and DHT (15550). It is suggested that androgenetic alopecia involves increased sensitivity of hair follicles to DHT, reducing their growth phase and size (15550).

There is some preliminary evidence that beta-sitosterol might also have anticancer and immunostimulant effects. Beta-sitosterol can inhibit the growth of human colon cancer cells in vitro (3667,3668). Mixtures of beta-sitosterol and its glycoside sitosterolin seem to also enhance proliferative responses of T-cells in vitro (3669,5342). Beta-sitosterol might also reduce the mild immune suppression and inflammation seen in marathon runners after a race (5335).

Indications
Orally, beta-sitosterol is used for coronary heart disease and hypercholesterolemia, benign prostatic hyperplasia (BPH) and prostatitis, and gallstones. It is also used orally for enhancing sexual activity and for preventing colon cancer. Beta-sitosterol is also used orally for boosting the immune system, preventing immune suppression and inflammation following participation in a marathon, common cold and flu (influenza), swine flu, HIV/AIDS, rheumatoid arthritis, tuberculosis, psoriasis, allergies, cervical cancer, fibromyalgia, systemic lupus erythematosus, asthma, alopecia, bronchitis, idiopathic thrombocytopenia purpura (ITP), migraine headache, chronic fatigue syndrome, and symptoms of menopause.

Benign prostatic hyperplasia (BPH). Taking beta-sitosterol orally significantly improves urinary symptoms, increases maximum urinary flow, and decreases postvoid residual urine volume; however, it does not affect prostate size (5327,5328,5329,7195,7198).

Hypercholesterolemia. Taking beta-sitosterol orally significantly reduces total and low-density lipoprotein (LDL) cholesterol levels, but has little or no effect on high-density lipoprotein (HDL) cholesterol levels (5330,5331,5332,5333,5334,5336,6668,7195,8528,10638).

Tuberculosis. There is some evidence that taking beta-sitosterol orally as an adjunct to conventional treatment for tuberculosis can increase lymphocyte counts; however, beta-sitosterol does not seem to decrease the time to cure based on negative sputum culture (5337).

Gallbladder disease. Taking beta-sitosterol orally isn’t effective for treating gallstones (5338,5339).

Androgenic alopecia (alopecia areata). Preliminary clinical research shows that a combination of beta-sitosterol 50 mg plus saw palmetto extract 200 mg taken twice daily improves subjective scores of hair quantity and quality in men with androgenetic alopecia (15550).

Burns. Preliminary clinical research suggests topical treatment of second degree burns with beta-sitosterol and berberine ointment is similar to conventional treatment with silver sulfadiazine (13526).

Adverse Reactions
Orally, beta-sitosterol is usually well tolerated. In some patients it can cause nausea, indigestion, gas, diarrhea, or constipation. It has also been associated with erectile dysfunction and loss of libido (5327,5328).

A combination of saw palmetto and beta-sitosterol has been associated with single reports of loss of appetite, flatulence, diarrhea, and worsening acne (15550).

PREGNANCY AND LACTATION: Insufficient reliable information available; avoid using.

Dosage: 

ORAL: For benign prostatic hyperplasia (BPH) and prostatitis, a typical dose is 60 to 130 mg of beta-sitosterol divided into 2-3 doses daily (5327,5328,5329).

For hypercholesterolemia, the usual dose is 800 mg to 6 grams per day divided and given before meals. Beta-sitosterol is typically given in conjunction with a low-fat diet (5327,5328,5329,5330,5331,5332,5333,5334,5336,5337,5338) (5339,10638). One supplier suggests that doses should be taken at least 30 minutes, but not more than 90 minutes, before meals for maximum effect on cholesterol absorption (3658).

For androgenic alopecia (alopecia areata), 50 mg twice daily combined with saw palmetto 200mg twice daily has been used (15550).

Nettle Root
Scientific Name:  Urtica dioica; Urtica urens.
Family: Urticaceae.

Mechanism of Action
The applicable parts of stinging nettle are the above ground parts and root. Stinging nettle root contains polysaccharides with immunomodulating and weak anti-inflammatory effects. The root seems to have an antiproliferative effect on prostatic epithelial and stromal cells (11227,11229); and may also lessen the effects of androgenic hormones by competitively blocking access to human sex hormone binding globulin (SHBG) (11228).

There is interest in using stinging nettle for prostate disease, including benign prostatic hyperplasia (BPH) and prostate cancer. Preliminary research shows that an aqueous extract of stinging nettle leaves can decrease adenosine deaminase activity in prostate tissue from men with localized prostate cancer (15196).

Stinging nettle contains beta-sitosterol (15196). Laboratory research suggests beta-sitosterol might have antiproliferative effects on the prostate, possibly by inhibiting growth factors (11234). In animals, beta-sitosterol shrinks the prostate, but this has not been shown in humans (11759). Some preliminary evidence also shows that extracts of stinging nettle can inhibit prostate tissue growth (15196).

Indications
Orally, stinging nettle root is used for urination disorders associated with benign prostatic hyperplasia (BPH), including nocturia, frequency, dysuria, urinary retention, and irritable bladder. Stinging nettle root is also used orally for joint ailments, as a diuretic, and an astringent.

Benign prostatic hyperplasia (BPH). There is contradictory evidence about the effectiveness of stinging nettle for symptoms of BPH. Taking a combination product (PRO 160/120, Willmar Schwabe GmbH, Germany) containing a specific extract of stinging nettle (WS 1031) 120 mg plus a specific extract of saw palmetto (WS 1473) 160 mg twice daily for 24-48 weeks seems to significantly improve urinary tract symptoms in men with BPH (15195,15551). This combination seems to be comparable to finasteride for relieving symptoms of BPH, and may be better tolerated (15551); however, it is not known if this benefit is due to stinging nettle, saw palmetto, or both ingredients. In another trial, an herbal product containing stinging nettle root extract 80 mg, saw palmetto lipoidal extract 106 mg, pumpkin seed oil extract 160 mg, lemon bioflavonoid extract 33 mg, and vitamin A (100% as beta-carotene) 190 IU taken three times daily for 6 months did not significantly improve symptoms of BPH (5093).

Adverse Reactions
Orally, stinging nettle root can cause gastrointestinal complaints, sweating, and allergic skin reactions (1,7).

PREGNANCY: when used orally due to possible abortifacient and uterine-stimulant effects (4,6,19).

Dosage
ORAL: For benign prostatic hyperplasia (BPH), a combination product (PRO 160/120, Willmar Schwabe GmbH, Germany) containing a specific extract of stinging nettle (WS 1031) 120 mg plus a specific extract of saw palmetto (WS 1473) 160 mg taken twice daily has been used (15195,15551). Another combination product containing stinging nettle root extract 80 mg, plus saw palmetto lipoidal extract 106 mg, pumpkin seed oil extract 160 mg, lemon bioflavonoid extract 33 mg, and vitamin A (100% as beta-carotene) 190 IU taken three times daily has also been used (5093).

Long-term efficacy and safety of a combination of sabal and urtica extract for lower urinary tract symptoms–a placebo-controlled, double-blind, multicenter trial.

Lopatkin N, Sivkov A, Walther C, Schläfke S, Medvedev A, Avdeichuk J, Golubev G, Melnik K, Elenberger N, Engelmann U.

Institute of Urology, 3rd Parkovaya Street 51, 105425 Moscow, Russia.

The efficacy and tolerability of a fixed combination of 160 mg sabal fruit extract WS 1473 and 120 mg urtica root extract WS 1031 per capsule (PRO 160/120) was investigated in elderly, male patients suffering from lower urinary tract symptoms (LUTS) caused by benign prostatic hyperplasia in a prospective multicenter trial. A total of 257 patients (129 and 128, respectively) were randomized to treatment with PRO 160/120 or placebo (127 and 126 were evaluable for efficacy). Following a single-blind placebo run-in phase of 2 weeks, the patients received 2 x 1 capsule/day of the study medication under double-blind conditions over a period of 24 weeks. Double-blind treatment was followed by an open control period of 24 weeks during which all patients were administered PRO 160/120. Outcome measures for treatment efficacy included the assessment of the patients’ LUTS by means of the I-PSS self-rating questionnaire and a quality of life index as well as uroflow and sonographic parameters. Using the International Prostate Symptom Score (I-PSS), patients treated with PRO 160/120 exhibited a substantially higher total score reduction after 24 weeks of double-blind treatment than patients of the placebo group (6 points vs 4 points; P=0.003, one tailed) with a tendency in the same direction after 16 weeks. This applied to obstructive as well as to irritative symptoms, and to patients with moderate or severe symptoms at baseline. Patients randomized to placebo showed a marked improvement in LUTS (as measured by the I-PSS) after being switched to PRO 160/120 during the control period (P=0.01, one tailed, in comparison to those who had been treated with PRO 160/120 in the double-blind phase). The tolerability of PRO 160/120 was comparable to the placebo. In conclusion, PRO 160/120 was clearly superior to the placebo for the amelioration of LUTS as measured by the I-PSS. PRO 160/120 is advantageous in obstructive and irritative urinary symptoms and in patients with moderate and severe symptoms. The tolerability of the herbal extract was excellent.

References

1   Monographs on the medicinal uses of plant drugs. Exeter, UK: European Scientific Co-op Phytother, 1997.

2   Blumenthal M, ed. The Complete German Commission E Monographs: Therapeutic Guide to Herbal Medicines. Trans. S. Klein. Boston, MA: American Botanical Council, 1998.

4   Newall CA, Anderson LA, Philpson JD. Herbal Medicine: A Guide for Healthcare Professionals. London, UK: The Pharmaceutical Press, 1996.

5   Foster S, Tyler VE. Tyler’s Honest Herbal: A Sensible Guide to the Use of Herbs and Related Remedies. 3rd ed., Binghamton, NY: Haworth Herbal Press, 1993.

6   The Review of Natural Products by Facts and Comparisons. St. Louis, MO: Wolters Kluwer Co., 1999.

7   Schulz V, Hansel R, Tyler VE. Rational Phytotherapy: A Physician’s Guide to Herbal Medicine. Terry C. Telger, transl. 3rd ed. Berlin, GER: Springer, 1998.

8   Wichtl MW. Herbal Drugs and Phytopharmaceuticals. Ed. N.M. Bisset. Stuttgart: Medpharm GmbH Scientific Publishers, 1994.

11   Leung AY, Foster S. Encyclopedia of Common Natural Ingredients Used in Food, Drugs and Cosmetics. 2nd ed. New York, NY: John Wiley & Sons, 1996.

19   Brinker F. Herb Contraindications and Drug Interactions. 2nd ed. Sandy, OR: Eclectic Medical Publications, 1998.

483   Anon. Quercetin. Alt Med Rev 1998;3:140-3.

598   Hamid S, Rojter S, Vierling J. Protracted cholestatic hepatitis after the use of Prostata. Ann Intern Med 1997;127:169-70.

764   Gerber GS, Zagaja GP, Bales GT, et al. Saw palmetto (Serenoa repens) in men with lower urinary tract symptoms: effects on urodynamic parameters and voiding symptoms. Urol 1998;51:1003-7.

2732   Wilt TJ, Ishani A, Stark G, et al. Saw palmetto extracts for treatment of benign prostatic hyperplasia: a systematic review. JAMA 1998;280:1604-9.

2735   Marks LS, Tyler VE. Saw palmetto extract: newest (and oldest) treatment alternative for men with symptomatic benign prostatic hyperplasia. Urology 1999;53:457-61.

2736   USRF Research. Clinical effects of saw palmetto extract in men with symptomatic BPH webpage: www.usrf.org/spepapers.html (Accessed 23 June 2004).

3658   Anon. W&B Associates Inc. website. URL http://www.wandb.com/cholesterol.6.htm (Accessed 30 March 2000).

3661   Patel SB, Honda A, Salen G. Sitosterolemia: exclusion of genes involved in reduced cholesterol biosynthesis. J Lipid Res 1998;39:1055-61.

3662   Salen G, Shore V, Tint GS, et al. Increased sitosterol absorption, decreased removal, and expanded body pools compensate for reduced cholesterol synthesis in sitosterolemia with xanthomatosis. J Lipid Res 1989;30:1319-30.

3663   Nguyen LB, Shefer S, Salen G, et al. Competitive inhibition of hepatic sterol 27-hydroxylase by sitosterol: decreased activity in sitosterolemia. Proc Assoc Am Physicians 1998;110:32-9.

3667   Awad AB, von Holtz RL, Cone JP, et al. Beta-sitosterol inhibits growth of HT-29 human colon cancer cells by activating the sphingomyelin cycle. Anticancer Res 1998;18:471-3.

3668   Awad AB, Chen YC, Fink CS, Hennessey T. Beta-sitosterol inhibits HT-29 human colon cancer cell growth and alters membrane lipids. Anticancer Res 1996;16:2797-804.

3669   Bouic PJ, Etsebeth S, Liebenberg RW, et al. Beta-sitosterol and beta-sitosterol glucoside stimulate human peripheral blood lymphocyte proliferation: implications for their use as an immunomodulatory vitamin combination. Int J Immunopharmacol 1996;18:693-700.

3672   Hidaka H, Kojima H, Kawabata T, et al. Effects of an HMG-CoA reductase inhibitor, pravastatin, and bile sequestering resin, cholestyramine, on plasma plant sterol levels in hypercholesterolemic subjects. J Atheroscler Thromb 1995;2:60-5.

3673   Ntanios FY, Jones PJ, Frohlich JJ. Effect of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor on sterol absorption in hypercholesterolemic subjects. Metabolism 1999;48:68-73.

3902   Barlet A, Albrecht J, Aubert A, et al. [Efficacy of Pygeum africanum extract in the medical therapy of urination disorders due to benign prostatic hyperplasia: evaluation of objective and subjective parameters. A placebo-controlled, double-blind, multicenter study]. [Article in German]. Wien Klin Wochenschr 1990;102:667-73.

3903   Breza J, Dzurny O, Borowka A, et al. 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;14:127-39.

3904   Dufour B, Choquenet C, Revol M, et al. Controlled study of the effects of Pygeum africanum extract on the functional symptoms of prostatic adenoma. Ann Urol (Paris) 1984;18:193-5.

4239   Ondrizek RR, Chan PJ, Patton WC, King A. Inhibition of human sperm motility by specific herbs used in alternative medicine. J Assist Reprod Genet 1999;16:87-91.

4240   Ondrizek RR, Chan PJ, Patton WC, King A. An alternative medicine study of herbal effects on the penetration of zona-free hamster oocytes and the integrity of sperm deoxyribonucleic acid. Fertil Steril 1999;71:517-22.

4301   Yablonsky F, Nicolas V, Riffaud JP, Bellamy F. Antiproliferative effect of Pygeum africanum extract on rat prostatic fibroblasts. J Urol 1997;157:2881-7.

4302   Andro MC, Riffaud JP. Pygeum africanum extract for the treatment of patients with benign prostatic hyperplasia. A review of 25 years of published experience. Curr Ther Res 1995;56:796-817.

5093   Marks L, Partin AW, Epstein JI, et al. Effects of a saw palmetto herbal blend in men with symptomatic benign prostatic hyperplasia. J Urol 2000;163:1451-6.

5094   Gerber GS. Saw palmetto for the treatment of men with lower urinary tract symptoms. J Urol 2000;163:1408-12.

5095   Goepel M, Hecker U, Krege S, et al. Saw palmetto extracts potently and noncompetitively inhibit human alpha1-adrenoceptors in vitro. Prostate 1999;38:208-15.

5326   Salen G, Shefer S, Nguyen L, et al. Sisterolemia. J Lipid Res 1992;33:945-55.

5327   Berges RR, Windeler J, Trampisch HJ, et al. Randomised, placebo-controlled, double-blind clinical trial of beta-sitosterol in patients with benign prostatic hyperplasia. Beta-sitosterol Study Group. Lancet 1995;345:1529-32.

5328   Klippel KF, Hiltl DM, Schipp B. A multicentric, placebo-controlled, double-blind clinical trial of beta-sitosterol (phytosterol) for the treatment of benign prostatic hyperplasia. Br J Urol 1997;80:427-32.

5329   Wilt TJ, MacDonald R, Ishani A. beta-sitosterol for the treatment of benign prostatic hyperplasia: a systematic review. BJU Int 1999;83:976-83.

5330   Becker M, Staab D, Von Bergmann K. Treatment of severe familial hypercholesterolemia in childhood with sitosterol and sitostanol. J Pediatr 1993;122:292-6.

5331   Oster P, Schlierf G, Heuck CC, et al. [Sitosterol in familial hyperlipoproteinemia type II. A randomized, double-blind, cross-over study]. [Article in German]. Dtsch Med Wochenschr 1976;101:1308-11.

5332   Schlierf G, Oster P, Heuck CC, et al. Sitosterol in juvenile type II hyperlipoproteinemia. Atherosclerosis 1978;30:245-8.

5333   Schwartzkopff W, Jantke HJ. [Dose-effect of beta-sitosterin in type IIa and IIb hypercholesterolemias]. [Article in German]. MMW Munch Med Wochenschr 1978;120:1575-8.

5334   Becker M, Staab D, Von Bergman K. Long-term treatment of severe familial hypercholesterolemia in children: effect of sitosterol and bezafibrate. Pediatrics 1992;89:138-42.

5335   Bouic PJ, Clark A, Lamprecht J, et al. The effects of B-sitosterol (BSS) and B-sitosterol glucoside (BSSG) mixture on selected immune parameters of marathon runners: inhibition of post marathon immune suppression and inflammation. Int J Sports Med 1999;20:258-62.

5336   Weststrate JA, Meijer GW. Plant sterol-enriched margarines and reduction of plasma total- and LDL-cholesterol concentrations in normocholesterolaemic and mildly hypercholesterolaemic subjects. Eur J Clin Nutr 1998;52:334-43.

5337   Donald PR, Lamprecht JH, Freestone M, et al. A randomised placebo-controlled trial of the efficacy of beta-sitosterol and its glucoside as adjuvants in the treatment of pulmonary tuberculosis. Int J Tubercul Lung Dis 1997;1:518-22.

5338   Gerolami A, Sarles H. Letter: Beta-sitosterol and chenodeoxycholic acid in the treatment of cholesterol gallstones. Lancet 1975;2:721.

5339   Tangedahl TN, Thistle JL, Hofmann AF, et al. Effect of beta-sitosterol alone or in combination with chenic acid on cholesterol saturation of bile and cholesterol absorption in gallstone patients. Gastroenterol 1979;76:1341-6.

5340   Anon. Cholesterol-lowering Margarines. Med Lett Drugs Ther 1999;41:56-8.

5342   Bouic PJ, Lamprecht JH, Plant sterols and sterolins: a review of their immune-modulating properties. Altern Med Rev 1999;4:170-7.

5814   Law M. Plant sterol and stanol margarines and health. BMJ 2000;320:861-4.

6368   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;54:473-8.

6424   Carraro JC, Raynaud JP, Koch G, et al. Comparison of phytotherapy (Permixon) with finasteride in the treatment of benign prostate hyperplasia: a randomized international study of 1,098 patients. Prostate 1996;29:231-40.

6500   Mills S, Bone K. Principles and Practice of Phytotherapy. London: Churchill Livingstone, 2000.

6668   Anon. FDA authorizes new coronary heart disease health claim for plant sterol and plant stanol esters. FDA. 2000. Available at: www.fda.gov/bbs/topics/ANSWERS/ANS01033.html

6750   Champault G, Patel JC, Bonnard AM. A double-blind trial of an extract of the plant Serenoa repens in benign prostatic hyperplasia. Br J Clin Pharmacol 1984;18:461-2.

6751   Braeckman J. The extract of serenoa repens in the treatment of benign prostatic hyperplasia: a multicenter open study. Curr Ther Res 1994;55:776-85.

6752   Reece-Smith H, Memon A, Smart CJ, Dewbury K. The value of permixon in benign prostatic hypertrophy. Br J Urol 1986;58:36-40.

6762   Wilt T, Ishani A, Stark G, et al. Serenoa repens for benign prostatic hyperplasia. Cochrane Database Syst Rev. 2000;(2):CD001423.

6763   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;86:439-42.

6764   Boyle P, Robertson C, Lowe F, Roehrborn C. Meta-analysis of clinical trials of permixon in the treatment of symptomatic benign prostatic hyperplasia. Urology 2000;55:533-9.

6765   Di Silverio F, Monti S, Sciarra A, et al. Effects of long-term treatment with Serenoa repens (Permixon) on the concentrations and regional distribution of androgens and epidermal growth factor in benign prostatic hyperplasia. Prostate 1998;37:77-83.

6766   Di Silverio F, D’Eramo G, Lubrano C, et al. Evidence that Serenoa repens extract displays an antiestrogenic activity in prostatic tissue of benign prostatic hypertrophy patients. Eur Urol 1992;21:309-14.

6769   Levin RM, Das AK. A scientific basis for the therapeutic effects of Pygeum africanum and Serenoa repens. Urol Res 2000;28:201-9.

6770   Bayne CW, Ross M, Donnelly F, Habib FK. The selectivity and specificity of the actions of the lipido-sterolic extract of serenoa repens (permixon®) on the prostate. J Urol 2000;164:876-81.

6771   Strauch G, Perles P, Vergult G, et al. Comparison of finasteride (Proscar) and Serenoa repens (Permixon) in the inhibition of 5-alpha reductase in healthy male volunteers. Eur Urol 1994;26:247-52.

6772   Stepanov VN, Siniakova LA, Sarrazin B, Raynaud JP. Efficacy and tolerability of the lipidosterolic extract of Serenoa repens (Permixon) in benign prostatic hyperplasia: a double-blind comparison of two dosage regimens. Adv Ther 1999;16:231-41.

6773   Bayne CW, Donnelly F, Ross M, Habib FK. Serenoa repens (Permixon): a 5 alpha-reductase types I and II inhibitor-new evidence in a coculture model of BPH. Prostate 1999;40:232-41.

6775   Grasso M, Montesano A, Buonaguidi A, et al. Comparative effects of alfuzosin versus Serenoa repens in the treatment of symptomatic benign prostatic hyperplasia. Arch Esp Urol 1995;48:97-103.

6776   Adriazola-Semino M, Lozano-Ortega JL, Garcia-Cobo E, et al. [Symptomatic treatment of benign hypertrophy of the prostate. Comparative study of prazosin and serenoa repens]. [Article in Spanish]. Arch Esp Urol 1992; 45:211-3.

6777   Carbin BE, Larsson B, Lindahl O. Treatment of benign prostatic hyperplasia with phytosterols. Br J Urol 1990;66:639-41.

6778   Descotes JL, Rambeaud JJ, Deschaseaux P, Faure G. Placebo-controlled evaluation of the efficacy and tolerability of Permixon in benign prostatic hyperplasia after exclusion of placebo responders Clin Drug Invest 1995; 9:291-7.

6779   Paubert-Braquet M, Mencia Huerta JM, Cousse H, Braquet P. Effect of the lipidic lipidosterolic extract of Serenoa repens (Permixon) on the ionophore A23187-stimulated production of leukotriene B4 (LTB4) from human polymorphonuclear neutrophils. Prostaglandins Leukot Essent Fatty Acids 1997;57:299-304.

6780   Gutierrez M, Garcia de Boto MJ, Cantabrana B, Hidalgo A. Mechanisms involved in the spasmolytic effect of extracts from Sabal serrulata fruit on smooth muscle. Gen Pharmacol 1996;27:171-6.

7035   Mittman P. Randomized, double-blind study of freeze-dried Urtica dioica in the treatment of allergic rhinitis. Planta Med 1990;56:44-7.

7195   Lichtenstein AH, Deckelbaum RJ. Stanol/sterol ester-containing foods and blood cholesterol levels: a statement for healthcare professionals from Nutrition Committee, Council on Nutrition, Physical Activity, Metabolism of American Heart Association. Circulation 2001;103:1177-9.

7196   Jones PJ, Raeini-Sarjaz M, Ntanios FY, et al. Modulation of plasma lipid levels and cholesterol kinetics by phytosterol versus phytostanol esters. J Lipid Res 2000;41:697-705.

7198   Berges RR, Kassen A, Senge T. Treatment of symptomatic benign prostatic hyperplasia with beta-sitosterol: an 18-month follow-up. BJU Int 2000;85:842-6.

8330   Romics I, Schmitz H, Frang D. Experience in treating benign prostatic hypertrophy with Sabal serrulata for one year. Int Urol Nephrol 1993;25:565-9.

8528   Matvienko OA, Lewis DS, Swanson M, et al. A single daily dose of soybean phytosterols in ground beef decreases serum total cholesterol and LDL cholesterol in young, mildly hypercholesterolemic men. Am J Clin Nutr 2002;76:57-64.

8659   Cheema P, El-Mefty O, Jazieh AR. Intraoperative haemorrhage associated with the use of extract of Saw Palmetto herb: a case report and review of literature. J Intern Med 2001;250:167-9.

8901   Glemain P, Coulange C, Grapin FN, Muszynski RC. No benefit in combining tamsulosin with Serenoa repens versus tamsulosin alone on storage/filling and voiding lower urinary tract symptoms. [Abstract]. J Urol 2001;167:374.

8902   Goldmann WH, Sharma AL, Currier SJ, et al. Saw palmetto berry extract inhibits cell growth and Cox-2 expression in prostatic cancer cells. Cell Biol Int 2001;25:1117-24.

10305   Stalenhoef AF. Images in clinical medicine. Phytosterolemia and xanthomatosis. N Engl J Med 2003;349:51.

10425   Ishani A, MacDonald R, Nelson D, et al. Pygeum africanum for the treatment of patients with benign prostatic hyperplasia: a systematic review and quantitative meta-analysis. Am J Med 2000;109:654-64.

10426   Wilt T, Ishani A, Mac Donald R, et al. Pygeum africanum for benign prostatic hyperplasia. Cochrane Database Syst Rev 2002;CD001044.

10457   Stalenhoef AF, Hectors M, Demacker PN. Effect of plant sterol-enriched margarine on plasma lipids and sterols in subjects heterozygous for phytosterolaemia. J Intern Med 2001;249:163-6.

10638   Neil HA, Meijer GW, Roe LS. Randomised controlled trial of use by hypercholesterolaemic patients of a vegetable oil sterol-enriched fat spread. Atherosclerosis 2001;156:329-37.

11026   Yale SH, Glurich I. Analysis of the inhibitory potential of Ginkgo biloba, Echinacea purpurea, and Serenoa repens on the metabolic activity of cytochrome P450 3A4, 2D6, and 2C9. J Altern Complement Med 2005;11:433-9.

11224   Vela Navarrete R, Garcia Cardoso JV, Barat A, et al. BPH and Inflammation: pharmacological effects of Permixon on histological and molecular inflammatory markers. Results of a double blind pilot clinical assay. Eur Urol 2003;44:549-55.

11225   Markowitz JS, Donovan JL, Devane CL, et al. Multiple doses of saw palmetto (Serenoa repens) did not alter cytochrome P450 2D6 and 3A4 activity in normal volunteers. Clin Pharmacol Ther 2003;74:536-42.

11226   Santa Maria Margalef A, Paciucci Barzanti R, Reventos Puigjaner J, et al. [Antimitogenic effect of Pygeum africanum extracts on human prostatic cancer cell lines and explants from benign prostatic hyperplasia]. [Article in Spanish]. Arch Esp Urol 2003;56:369-78.

11227   Konrad L, Muller HH, Lenz C, et al. Antiproliferative effect on human prostate cancer cells by a stinging nettle root (Urtica dioica) extract. Planta Med 2000;66:44-7.

11228   Schottner M, Gansser D, Spiteller G, et al. Lignans from the roots of Urtica dioica and their metabolites bind to human sex hormone binding globulin (SHBG). Planta Med 1997;63:529-32.

11229   Lichius JJ, Muth C. The inhibiting effects of Urtica dioica root extracts on experimentally induced prostatic hyperplasia in the mouse. Planta Med 1997;63:307-10.

11230   Vontobel HP, Herzog R, Rutishauser G, Kres H. [Results of a double-blind study on the effectiveness of ERU (extractum radicis Urticae) capsules in conservative treatment of benign prostatic hyperplasia]. [Article in German]. (Abstract). Urologe A 1985;24:49-51.

11234   Kassen A, Berges R, Senge T, et al. Effect of beta-sitosterol on transforming growth factor-beta-1 expression and translocation protein kinase C alpha in human prostate stromal cells in vitro. Eur Urol 2000;37:735-41.

11243   Debruyne F, Koch G, Boyle P, et al. [Comparison of a phytotherapeutic agent (Permixon) with an alpha-blocker (Tamsulosin) in the treatment of benign prostatic hyperplasia: a 1-year randomized international study]. [Article in French]. Eur Urol 2002;41:497-506.

11314   Willetts KE, Clements MS, Champion S, et al. Serenoa repens extract for benign prostate hyperplasia: a randomized controlled trial. BJU Int 2003;92:267-70.

11354   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;171:284-8.

11759   Cabeza M, Bratoeff E, Heuze I, et al. Effect of beta-sitosterol as inhibitor of 5 alpha-reductase in hamster prostate. Proc West Pharmacol Soc 2003;46:153-5.

11985   Salen G, von Bergmann K, Lutjohann D, et al. Ezetimibe effectively reduces plasma plant sterols in patients with sitosterolemia. Circulation 2004;109:966-71.

11989   Sudhop T, Lutjohann D, Kodal A, et al. Inhibition of intestinal cholesterol absorption by ezetimibe in humans. Circulation 2002;106:1943-8.

12490   Randall C, Randall H, Dobbs F, et al. Randomized controlled trial of nettle sting for treatment of base-of-thumb pain. J R Soc Med 2000;93:305-9.

13526   Ang ES, Lee ST, Gan CS, et al. Evaluating the role of alternative therapy in burn wound management: randomized trial comparing moist exposed burn ointment with conventional methods in the management of patients with second-degree burns. Med Gen Med 2001;3:3.

13712   Gurley BJ, Gardner SF, Hubbard MA, et al. In vivo assessment of botanical supplementation on human cytochrome P450 phenotypes: Citrus aurantium, Echinacea purpurea, milk thistle, and saw palmetto. Clin Pharmacol Ther 2004;76:428-40.

14274   Bent S, Kane C, Shinohara K, et al. Saw palmetto for benign prostatic hyperplasia. N Engl J Med 2006;354:557-66.

14275   Wilt T, Ishani A, Mac Donald R. Serenoa repens for benign prostatic hyperplasia. Cochrane Database Syst Rev 2002;(3):CD001423.

14457   Jibrin I, Erinle A, Saidi A, Aliyu ZY. Saw palmetto-induced pancreatitis. South Med J 2006;99:611-2.

15195   Lopatkin N, Sivkov A, Walther C, et al. Long-term efficacy and safety of a combination of sabal and urtica extract for lower urinary tract symptoms–a placebo-controlled, double-blind, multicenter trial. World J Urol 2005;23:139-46.

15196   Durak I, Biri H, Devrim E, et al. Aqueous extract of Urtica dioica makes significant inhibition on adenosine deaminase activity in prostate tissue from patients with prostate cancer. Cancer Biol Ther 2004;3:855-7.

15197   Caliskaner Z, Karaayvaz M, Ozturk S. Misuse of a herb: stinging nettle (Urtica urens) induced severe tongue oedema. Complement Ther Med 2004;12:57-8.

15217   Bonnar-Pizzorno RM, Littman AJ, Kestin M, White E. Saw palmetto supplement use and prostate cancer risk. Nutr Cancer 2006;55:21-7.

15550   Prager N, Bickett K, French N, Marcovici G. A randomized, double-blind, placebo-controlled trial to determine the effectiveness of botanically derived inhibitors of 5-alpha-reductase in the treatment of androgenetic alopecia. J Altern Complement Med 2002;8:143-52.

15551   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;86:439-42.

17202   Tuncel A, ener K, Han O, et al. Effects of short-term dutasteride and Serenoa repens on perioperative bleeding and microvessel density in patients undergoing transurethral resection of the prostate. Scand J Urol Nephrol Published online August 9, 2009. DOI: 10.1080/00365590903164498.

Frequently Asked Questions

Does Trichotin cure alopecia (baldness)?

Trichotin DHT Inhibitor has been designed to combat alopecia by lowering DHT levels, the enzyme responsible for degeneration of hair follicles.

Short circuiting this action prevents hair loss and stimulates regrowth.

Can Trichotin DHT Inhibitor be used by both men and women?

Women should generally not use Trichotin DHT Inhibitor unless it is prescribed by their physician.

Will it increase the growth of body hair?

Trichotin DHT Inhibitor promotes normal and regular scalp hair growth.

How long do I have to use Trichotin DHT Inhibitor before I notice results?

Fusion Labs recommends that Trichotin initially be used for at least three months. Within this period individuals should notice a substantial improvement in the condition of their hair.

For best results use in conjunction with Trichotin Hair Regenesis.

Results depend on other variables such as severity of condition, diet, metabolism and genetic make-up.

Can Trichotin Hair Regenesis and Trichotin DHT inhibitor be used concomitantly?

Yes, men can use both products simultaneously.

Why do I have to use Trichotin DHT Inhibitor at bedtime?
 
Trichotin DHT Inhibitor acts on testosterone levels. This action is best regulated during the REM phase of sleep.

Does Trichotin have clinical research backing to support its claims?

Clinical studies have been conducted using Saw Palmetto (liposterolic extract) with Beta-Sitosterol, as well as Saw Palmetto with Nettle in a randomized, double-blind, placebo-controlled trial to determine the effectiveness of botanically derived inhibitors of 5-alpha-reductase in the treatment of androgenic alopecia.

Prager N, Bickett K, French N, Marcovici G.

RESULTS: The results of this pilot study showed a positive response to treatment. The blinded investigative staff assessment report showed that 60% of (6/10) study subjects treated with the active study formulation, were rated as improved at the final visit.

CONCLUSIONS: This study establishes the effectiveness of naturally occurring 5AR inhibitors against AGA for the first time

Which clinical studies specifically prove Nettle Root assists in combating alopecia ?

Sökeland J.

COMBINING: Saw Palmetto and Nettle Root Extract
Combined sabal and urtica extract (PRO 160/120)

RESULTS:
Compares with Finasteride in men with benign prostatic hyperplasia: analysis of prostate volume and therapeutic outcome.

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.

120 mg of a specific Nettle root extract combined with Saw palmetto has therefore been shown to be effective for the treatment of the symptoms of BPH.

This combination is comparable to Finasteride but is better tolerated.

Nettle root extract also lessens the effects of androgenic hormones by competitively blocking access to human SHBG.

What is the difference between Trichotin Hair Regenesis and Trichotin DHT Inhibitor?

Trichotin Hair Regenesis is a unisex product specifically designed to prevent hair loss caused by hormonal imbalance, thyroid dysfunction, stress, nutrient deficiency, chemical damage, traction alopecia, poor circulation etc.

Trichotin Hair Regenesis also contains ingredients which improve follicle health and activity thereby stimulating regrowth.

Trichotin DHT Inhibitor is formulated to prevent hair loss by lowering levels of DHT, which is the enzyme primarily responsible for androgenic alopecia.

Only in exceptional cases of severe hair loss, with DHT excess being the confirmed cause, do we recommend the product for women.

Trichotin DHT Inhibitor also improves libido and prostate health.

Are there any adverse sexual side effects when using Trichotin DHT Inhibitor?

No. Trichotin DHT Inhibitor is a herbal DHT Inhibiting blend. Unlike scheduled DHT Inhibitors it does not cause this side effects.

At Fusion Labs we believe luxurious hair and a healthy sex drive should go hand in hand. You shouldn’t have to compromise either.

Plant-based ingredients including Beta Sitestreol, Ginseng and Saw Palmetto have proven DHT-inhibiting effects and also backed by research to, in fact, improve libido and sexual function.

What relationship does Trichotin DHT Inhibitor have on muscle building?

Trichotin DHT Inhibitor increases the muscle building process by preventing the breakdown of excess testosterone to DHT. This allows for improved free circulating testosterone levels to remain higher, for longer.

What other benefits does Trichotin DHT Inhibitor have?

Improves prostate health
Supports a health libido
Lowers body fat

Why is Trichotin DHT Inhibitor superior to other hair loss products?

• Trichotin DHT Inhibitor is based on and supported by credible research.
• Fusion Laboratories uses only the highest grade ingredients.
• The Saw Palmetto used in Trichotin DHT Inhibitor is a 45 % lipostrolic extract which is required by research and trials.
• The Saw Palmetto used in Trichotin DHT Inhibitor is specifically extracted using lipophilic non polar solvents. (Inferior grades of Saw Palmetto are derived from a water extraction process which does not adequately extract the fat-soluble actives required to effectively lower DHT levels).
• The Nettle used in Trichotin DHT Inhibitor is sourced from superior Nettle Root and not Nettle Leaf
• Each of the ingredients have proven benefits.
• All products of Fusion Laboratories conform to the stringent input, processing and quality control criteria of the relevant controlling authorities in the countries where they are marketed.
• Trichotin DHT Inhibitor is the only Luxury, Premier DHT Inhibitor.
• Fusion Laboratories uses the most advanced technology and research to develop its products.
• Trichotin has superior product formulation. Its smart and balanced formula is specially designed to allow for optimal absorption and efficacy.
• None of our ingredients have been tested on animals.
• Trichotin DHT Inhibitor does not contain artificial flavourants or preservatives.