nettle root increases free testosterone?
March 20 2007 at 8:26 PM dunny (Login lil_dunny)
Nettle Root Extract
About 90% of testosterone is produced by the testes, the remainder by the adrenal glands. Testosterone functions as an aphrodisiac hormone in brains cells, and as an anabolic hormone in the development of bone and skeletal muscle. But testosterone that becomes bound to serum globulin is not available to cell receptor sites and fails to induce a libido effect. It is, therefore, desirable to increase levels of "free testosterone" in order to ignite sexual arousal in the brain.
A hormone that controls levels of free testosterone is called sex hormone-binding globulin (SHBG). When testosterone binds to SHBG, it loses its biological activity and becomes known as "bound testosterone," as opposed to the desirable "free testosterone." As men age past year 45, SHBG's binding capacity increases almost dramatically-by 40% on average-and coincides with the age-associated loss of libido.
Some studies show that the decline in sexual interest with advancing age is not always due to the amount of testosterone produced, but rather to the increased binding of testosterone to globulin by SHBG. This explains why some older men who are on testosterone replacement therapy do not report a long-term aphrodisiac effect. That is, the artificially administered testosterone becomes bound by SHBG, and is not bioavailable to cellular receptor sites where it would normally produce a libido-enhancing effect.
It should be noted that the liver also causes testosterone to bind to globulin. This liver-induced binding of testosterone is worsened by the use of sedatives, anti-hypertensives, tranquilizers and alcoholic beverages. The overuse of drugs and alcohol could explain why some men do not experience a libido-enhancing effect when consuming drugs and plant-based aphrodisiacs. An interesting review, "How Desire Dies" (Nature, 381/6584, 1996), discusses how frequently prescribed drugs, such as beta-blockers and antidepressants, cause sexual dysfunction. Prescription drugs of all sorts have been linked to inhibition of libido.
Logically, one way of increasing libido in older men would be to block the testosterone-binding effects of SHBG. This would leave more testosterone in its free, sexually activating form.
A highly concentrated extract from the nettle root provides a unique mechanism for increasing levels of free testosterone. Recent European research has identified constituents of nettle root that bind to SHBG in place of testosterone, thus reducing SHBG's binding of free testosterone. As the authors of one study state, these constituents of nettle root "may influence the blood level of free, i.e. active, steroid hormones by displacing them from the SHBG bindings site."
The prostate gland also benefits from nettle root. In Germany, nettle root has been used as a treatment for benign prostatic hyperplasia (enlargement of the prostate gland) for decades. A metabolite of testosterone called dihydrotestosterone (DHT) stimulates prostate growth, leading to enlargement. Nettle root inhibits the binding of DHT to attachment sites on the prostate membrane.
Nettle extracts also inhibit enzymes such as 5 alpha reductase that cause testosterone to convert to DHT. It is the DHT metabolite of testosterone that is known to cause benign prostate enlargement, excess facial hair and hair loss at the top of the head.
http://www.health-n-energy.com/ARTICLES/chrysin.htm
dunny
(Login lil_dunny)
Re: nettle root increases free testosterone?
March 21 2007, 5:04 AM
BPH
The Other Side of the Coin
BPH isn't just a matter of testosterone...new research reveals the role of estrogen and what you can do about it.
A surprising new discovery explains why so many men now contract prostate disease. Most doctors think testosterone is the culprit, but scientists have exposed serious flaws in this theory. Now you can be the first to learn the most advanced method of preventing and treating prostate enlargement.
According to the conventional view, benign prostatic hyperplasia (BPH) develops when an active form of testosterone called dihydrotestosterone (DHT) stimulates cell growth. Testosterone is converted to DHT systemically as well as within the prostate by an enzyme known as 5-alpha-reductase. DHT is far more active than testosterone in binding to sites in prostate cells that regulate prostate growth. When DHT binds to these sites, it activates growth factors that stimulate cell proliferation. Commonly used medications for BPH, such as saw palmetto and the drug finasteride, inhibit 5-alpha-reductase in order to reduce DHT-stimulated growth in the prostate.
While it is hardly surprising that prostate growth is under hormonal control, the above view of BPH is difficult to explain when we consider the effects of aging. BPH is after all a disease of aging, and testosterone production declines with age. Moreover, levels of free, physiologically active testosterone decline more sharply due to increased testosterone binding by a protein called sex hormone binding globulin (SHBG). It is estimated that levels of free testosterone decline by about 1% per year from age forty to age seventy.
So, if testosterone production declines with age, could there be another mechanism contributing to prostate enlargement? The surprising answer may be the growing imbalance in aging men between their levels of estrogen and testosterone.
While levels estrogen appear to be relatively stable in the aging male, the level of free testosterone precipitously declines. Thus with age, an imbalance develops between estrogens and androgens (female and male hormones). Compared to younger men, the ratio of free estradiol (the most potent form of estrogen) to free testosterone is up to 40% higher in older men.
In the prostate itself, the contrast between rising estrogens and declining androgens is more sharply drawn. In the stroma of the prostate, the supporting tissue where BPH is thought to develop, estrogen levels increase significantly with age, while DHT levels remain stable. Estrogen levels in the stroma rise to even higher levels in BPH patients. In the epithelium of the prostate, DHT levels decline with age, while estrogen levels remain stable. German researchers who have been studying this for more than fifteen years describe "a tremendous increase with age of the estrogen/ androgen ratio in the human prostate." Their article in the Journal of Clinical Endocrinology and Metabolism concludes:
"Our results indicate that the prostatic accumulation of DHT, estradiol, and estrone is in part intimately correlated with aging, leading with increasing age to a dramatic increase of the estrogen/androgen ratio particularly in stroma of BPH."
A study published in the journal Prostate bears out the concept of an elevated serum estrogen/androgen ratio as a risk factor for BPH. Analyzing frozen blood samples collected in the course of a large-scale health study, the researchers found that BPH risk increased with higher estradiol levels, and that the risk was concentrated in men with relatively low androgen levels.
A Japanese study came to a similar conclusion, finding that prostate size correlates with estradiol level and with the ratio of estradiol to free testosterone. They suggest that "the endocrine environment tended to be estrogen-dominant with age, in particular, after middle-age, and that patients with large prostates have more estrogen-dominant environments," concluding "estrogens are key hormones for the induction and the development of BPH."
Experimental attempts to induce BPH with hormones would answer many questions, but obviously cannot be carried out in humans. The only animals known to develop BPH with age are dogs and lions. In experiments with dogs it has been established than BPH cannot be induced without estrogen, however it should be noted that endocrine regulation and prostate structure are quite different in dog and man.
In men and postmenopausal women, most estrogens are produced from androgens; specifically, most estradiol is produced from testosterone. This conversion of androgens to estrogens is called aromatization, after the enzyme aromatase. In addition to receiving estrogen circulating through the bloodstream, the stroma of the prostate produces its own estrogen through aromatization.
It has long been suspected that estrogen - especially the estrogen/ androgen imbalance associated with aging - plays a role in BPH, but until recent years no direct effect of estrogen on the prostate could be demonstrated. A key piece of this puzzle has now been supplied by a group of researchers at Columbia University, St. Luke's/Roosevelt Hospital in New York, and the pharmaceutical company Merck. In a groundbreaking series of research papers culminating in articles published this past year in the journals Endocrinology and Steroids, they demonstrate the existence of a second hormonal pathway in the prostate whereby estrogens can mimic androgens.
It may help to understand this breakthrough by thinking of hormones as chemical messengers. When a hormone attaches to its special binding site in a cell, it sends a signal to that cell. In the case of BPH, androgens signal cells to proliferate, causing prostate growth. These researchers have shown that messages sent to prostate cells by androgens can also be sent, along an alternative signalling pathway, by estrogens. Even more surprisingly, the estrogens send this signal not by attaching to the usual cellular binding sites for estrogen, but instead to the sex hormone binding globulin (SHBG) that is already bound to the cell membrane. As the authors put it, they have shown that in the prostate, estradiol is "capable of activating pathways normally considered androgen responsive."
In a review article published in the journal Prostate in 1996, a pioneer of modern prostate research proposed a new model of prostate physiology and pathogenesis based in part upon this research. Wells Farnsworth, Professor of Urology at the Northwestern University Medical School, discovered the conversion of testosterone to DHT in the prostate in the early 60s. In his article in Prostate, Professor Farnsworth proposes that "estrogen, mediated by SHBG, participates with androgen in setting the pace of prostate growth and function."
Farnsworth notes that, as explained above, SHBG increases with age and "can act like an additional androgen receptor [binding site for androgen]" in the prostate cell. He suggests that, when estrogen binds to SHBG in the cell membrane, a growth factor called IGF-I (insulin-like growth factor I) is synthesized, causing proliferation of epithelial cells in the prostate. This sets the stage for further proliferation when androgens activate binding sites for growth factors. In Farnsworth's language, "estrogen not only directs stromal proliferation and secretion, but also, through IGF-I, conditions the response of epithelium to androgen." Subsequent research suggests that IGF-II, which is less well understood than IGF-I, may also be involved. In addition to its possible role in BPH, recent research indicates that elevated IGF-I levels may be a key predictor of prostate cancer risk. IGF-I may also contribute to the age-related increase in SHBG.
Farnsworth likens the protein SHBG to a hormone, concluding: [SHBG's] newfound capability to evoke BPH and its possible involvement in the transformation of normal to cancer cells by oncogenes calls for increased efforts to understand and manage SHBG and estrogen secretion.
The researchers who discovered the alternative signalling pathway concur: "...antagonism [inhibition] of the pathway by which SHBG leads to the induction of androgen-responsive genes may be a valuable therapeutic target for the treatment or prevention of BPH or prostate cancer."
Accordingly, these researchers studied an agent thought to inhibit the binding of SHBG to the prostate cell membrane, an extract of the root of the stinging nettle plant, Urtica dioica. In a paper published in 1995 in Planta Medica, they demonstrated that nettle root does indeed inhibit the binding of SHBG to the cell membrane.
In a subsequent series of articles, German researchers have identified a constituent of nettle root known as (-)-3,4-divanillyltetrahydrofuran whose very high binding affinity to SHBG they describe as "remarkable." These researchers suggest that the beneficial effects of plant lignans (such as found in flaxseed oil) on hormone-dependent cancers may be linked to their binding affinity to SHBG. The most potent known lignans in this respect are constituents of nettle root.
Studies show that the ethanolic extract of nettle root is not in inhibiting SHBG binding, while the aqueous and methanolic extracts are.
In addition to inhibiting SHBG binding, at least six constituents of nettle root inhibit aromatase, reducing conversion of androgens to estrogens. Combining nettle root with pygeum results in a stronger, synergistic inhibition. The studies on aromatase inhibition by nettle root used methanolic extracts.
A recent experimental study provides a dramatic demonstration of nettle root's effect on BPH tissue. This experiment was based upon the hypothesis that BPH is comparable to a reawakening of embryonic growth potential in the prostate. A fetal urogenital sinus was implanted into a lobe of the prostate gland in adult mice. After 28 days, the implanted lobes of mice fed a nettle root methanolic extract similar to an extract on the German pharmaceutical market showed 51.3% less growth than the lobes of mice in the control group.
Nettle root is widely used as a first-line therapy for BPH in Germany, where there are 15 pharmaceutical drugs consisting solely of nettle root. Nettle root has been extensively studied in European clinical trials over the past twenty years. Good study design is essential in evaluating BPH therapies, since sizable placebo effects are normal in BPH studies.
A well designed double-blind, placebo-controlled trial of nettle root was published in the German urological journal Urologe in 1996. This three month study involved 41 BPH patients with maximum urinary flow under 15 ml/sec. and an average score of 18.2 on the IPSS (International Prostate Symptom Score) scale. An IPSS score of 0-7 is considered as slightly symptomatic, 8-19 as moderately symptomatic, and 20-35 as highly symptomatic.
By the end of the trial, maximum urinary flow increased by an average of 66.1% (from 10.9 to 18.1 ml/sec.) in the group treated with nettle root, compared to 36.6% (from 12.3 to 16.8 ml/sec.) in the placebo group. Average IPSS scores dropped twice as much in the nettle root group (from 18.2 to 8.7) as in the placebo group (from 17.7 to 12.9). By comparison, trials of the standard BPH drug finasteride (Proscar) show more modest improvements relative to placebo. Again, this study used the methanolic nettle extract.
Eight previous trials of nettle root showed beneficial effects on a total of approximately 15,000 BPH patients. These trials used daily doses of nettle extract ranging from 600-1200 mg and lasted from 3 weeks to 180 days.
In Europe nettle root is also used in combination with saw palmetto. This combination is a logical one since nettle root acts through the alternative signalling pathway in the prostate cell, while saw palmetto acts on the primary signalling pathway by limiting DHT activity. In effect, nettle root addresses the estrogen side of BPH, while saw palmetto addresses the androgen side. Additionally, both herbs have anti-inflammatory actions.
Since 1995, three clinical studies of a standard saw palmetto/nettle combination have been published in German medical journals. The studies used two capsules per day of 160 mg saw palmetto extract plus 120 mg nettle root extract.
A randomized double-blind study compared the saw palmetto/nettle combination to the standard BPH drug finasteride in 543 patients suffering from BPH stages I to II. The herbal therapy and drug therapy proved similarly effective in all measures: urinary flow rate, urination time, IPSS scores, and patients' quality of life assessments. Both therapies increased in effectiveness over a period of months. For example, the average IPSS score in the herbal therapy group declined from 11.3 to 8.2 after 24 weeks and 6.5 after 48 weeks; in the finasteride group it declined from 11.8 to 8.0 after 24 weeks and 6.2 after 48 weeks. Patients tolerated herbal therapy better than finasteride which causes diminished libido and sexual dysfunctions including impotence in some patients.
Another placebo-controlled study used a crossover design. Forty patients with BPH stage I or II and urinary flow below 20 ml/sec. received either saw palmetto/nettle or placebo for 24 weeks. Patients receiving the herbal combination showed significant improvement in maximum urine flow rate (3.3 ml/sec.) compared to placebo, and there were similar improvements in average flow rate, total urination volume, urination time, and flow increase time. The was also a significant improvement on the American Urological Association symptom score compared to placebo. In the crossover phase of the trial, patients who had been on placebo for 24 weeks were switched to the herbal combination for another 24 weeks. These patients showed similar positive results.
A large observational study involving 419 urology practices followed 2,030 patients with mild to moderate BPH. All patients received saw palmetto/nettle for 12 weeks. This study found the following average improvements: maximum urinary flow increased 25.8%, average urinary flow increased 29.0%, residual urine decreased 44.7%, nocturia declined 50.4%, dysuria declined 62.5%, and post-urination dribbling declined 53.6%. 86% of patients reported symptom improvement. Fewer than 1% of the patients reported side effects, and these were mild.
Thus far, there have been no clinical trials of a saw palmetto/nettle/ pygeum combination. As mentioned above, nettle root and pygeum synergize in inhibiting aromatase. In addition, these three herbs affect growth factors in ways that appear to be beneficial in the prevention and treatment of BPH. According to a 1997 article in the Journal of Urology, pygeum inhibits cell proliferation induced by the growth factors EGF (epidermal growth factor), bFGF (basic fibroblast growth factor), and IGF-I (insulin-like growth factor I) in stromal cells from rat prostate. A 1998 study in European Urology found that saw palmetto inhibits bFGF-stimulated cell proliferation in human prostate cell cultures. Preliminary research suggests that a constituent of nettle root inhibits the binding of EGF to human prostate cells.
As is the case for many medicinal herbs, the clinical efficacy of nettle root was demonstrated at a time when medical science had not yet made the basic advances needed to understand its mechanism of action. This may be one reason that nettle root is relatively unknown in America whereas saw palmetto, with its relatively clearcut mechanism of action based upon testosterone, is in common use. As was the case for saw palmetto, it will probably take years for the pharmaceutical companies to develop a synthetic drug to effectively address the mechanism of action of nettle root. Both of these extraordinarily well tolerated herbal extracts are available now to BPH sufferers.
The Life Extension Foundation has expended significant resources to develop a better understanding of prostate cell proliferation and how to control it. The immediate benefit to members is that all of the prostate products offered by the Life Extension Buyers Club have been re-formulated to reflect these new findings.
http://www.lef.org/magazine/mag99/feb99-bph.html
dunny
(Login lil_dunny)
Re: nettle root increases free testosterone?
March 21 2007, 5:24 AM
(needless to say i've taken nettle root out of my routine)
faerycat
(Login faerycat)
SENIOR MEMBER
Re: nettle root increases free testosterone?
March 21 2007, 10:19 AM
It may be an idea to post this in the info section too.
x
MyJourney
(Login Myjourney)
Help??
March 21 2007, 3:01 PM
Ok, Little Dunny,
What does this all mean in plain English...I got lost...
dunny
(Login lil_dunny)
Re: nettle root increases free testosterone?
March 21 2007, 5:23 PM
basically, that prostate enlarges due to decreasing free testosterone... in the presence of same amount of estrogen in the aging males. nettle root, it says, inhibits aromatization, or the conversion of testosterone into estrogen (though i didn't quite get the binding bit).
Moon
(Login -Moon-)
SENIOR MEMBER
Re: nettle root increases free testosterone?
March 21 2007, 5:38 PM
Ok, here's my two cents: Over this past year or so that I've been into NBE, I have learnt one most important thing - don't try to apply theory in practice! You study the theory, it appears one thing, but the truth is that this stuff is just so d*amn complicated, that what's actually going on in the body is the exact opposite by some unestablished and ununderstood mechanism. I'm a student of medicine and still don't frickin get it. It appears that nettle and SP inhibit estrogen, but empyrical evidence shows us that this works. And I also think that nettle may work in men entirely differently than it woman. The thing is - we can't explain!
Now just think about this - the whole NBE principle is based on something that doesn't make sense - phytoestrogens are weaker than our own hormones and they compete with our hormones on the receptors and they cause growth. It doesn't make sense, but it works. I have come to think that empyrical evidence is in NBE a lot more useful than theoretical. So I won't try to explain anymore, I will do that which appears to be working. I have nettle prepared for my routine when I start and I will take it.
Lisa121
(no login)
I found this on SP and Nettle
March 22 2007, 8:42 PM
SAW PALMETTO
June 26 2006 at 4:39 PM HongKongGirl (Login HongKongGirl)
Hi
I am from Hong Kong and new to this forum. Today, I went to GNC and found that SAW PALMETTO is for men only. Would smart girls here mind telling me why SAW PALMETTO used for NBE? Can i take Wonderup accompany with SAW PALMETTO?
Thanks a lot!
Helen
(Login Helen_N)
EVE MEMBERS
Re: SAW PALMETTO
June 26 2006, 5:25 PM
Hi HongKongGirl
Yes you are right, herbs that can prevent testosterone from converting into DHT (a very potent version of testosterone) are MOST COMMONLY used by men to treat an enlarged prostate (a side effect of too much DHT).
Now for us women, excess amounts of DHT sabotage estrogen (they suppress estrogen activity and inhibit conversion of testosterone into estrogen). So for girls with elevated testosterone levels, DHT-blocking herbs like Saw Palmetto are an essential ingredient for breast enlargement. Other herbs with similar effect include Nettle, Licorice, Pumpkin Seeds, and Pygeum.
If you want to read more on Saw Palmetto and its properties, I suggest you go to "Other resources", then under "Related Information", click on "Information on Herbs", find a thread called: "ALL ABOUT SAW PALMETTO".
Hope this helps
Best boobie wishes,
Helen xx
Lisa121
(no login)
and this on Nettle vs SP
March 22 2007, 8:47 PM
sdm
(Login wsdm) Re: Nettle VS Saw Palmetto June 28 2006, 3:30 PM
From what I have learned so far:
Saw Palmetto inhibits an enzyme from converting testosterone to DHT, thus forcing testosterone to convert to estrogen.
Nettle root blocks the binding of hormones such as estrogen to SHBG (sex hormone binding globulin).
Estrogen and SBHG bind together to trigger activity in their target cells.
Nettle root blocks the action of an enzyme that converts testosterone to estrogen
Now as I mentioned before it is important for anyone starting NBE to have a hormone test. See where your levels are at.
If you have low estrogen levels it appears Saw Palmetto is good and nettle may not be so great.
If you have high estrogen levels Saw Palmetto is not so good and Nettle may be beneficial.
cool excerpt from http://www.lef.org/protocols/prtcl-095c.shtml
"Nettle Root Extract Blocks DHT Binding to Prostate Cells
An extract from the nettle root called Urtica dioica has been used extensively in combination with saw palmetto or by itself as a drug to treat BPH. One study showed that after 8 weeks of treatment with 4 capsules of urtica extract, patients experienced an 82% improvement in disorders associated with prostate enlargement (Wolf 1980). Another study showed that those patients with prostate enlargement with Stage I-III hyperplasia (the abnormal multiplication of normal cells that can lead to prostate cancer) experienced an 86% improvement after 3 months of treatment with standardized urtica extract (Maar 1987).
After learning the results of these studies, researchers at St. Luke's Roosevelt Hospital in New York conducted a study to discover the mechanism by which standardized urtica extract relieves the symptoms of BPH. In their published study, the St. Luke's scientists showed that urtica extract inhibits the binding of a testosterone-estrogen-related protein to its receptor site on prostate cell membranes (Hryb et al. 1995).
It is known that when the testosterone metabolite DHT binds to prostate cell membranes, the result is the overproliferation of prostate cells. If cell membrane receptors are blocked, then DHT cannot latch on to the cell. Urtica extract appears to work by preventing the binding of testosterone metabolites to membrane receptor sites on prostate cells.
Saw palmetto and U. dioica are approved drugs in Germany for the treatment of benign prostate enlargement. While urtica is relatively new to Americans, it has been safely and successfully used in Germany for more than a decade."
and http://www.lef.org/magazine/mag99/feb99-bph.html
"Farnsworth notes that, as explained above, SHBG increases with age and "can act like an additional androgen receptor [binding site for androgen]" in the prostate cell. He suggests that, when estrogen binds to SHBG in the cell membrane, a growth factor called IGF-I (insulin-like growth factor I) is synthesized, causing proliferation of epithelial cells in the prostate. This sets the stage for further proliferation when androgens activate binding sites for growth factors. In Farnsworth's language, "estrogen not only directs stromal proliferation and secretion, but also, through IGF-I, conditions the response of epithelium to androgen." Subsequent research suggests that IGF-II, which is less well understood than IGF-I, may also be involved. In addition to its possible role in BPH, recent research indicates that elevated IGF-I levels may be a key predictor of prostate cancer risk. IGF-I may also contribute to the age-related increase in SHBG.
Farnsworth likens the protein SHBG to a hormone, concluding: [SHBG's] newfound capability to evoke BPH and its possible involvement in the transformation of normal to cancer cells by oncogenes calls for increased efforts to understand and manage SHBG and estrogen secretion.
The researchers who discovered the alternative signalling pathway concur: "...antagonism [inhibition] of the pathway by which SHBG leads to the induction of androgen-responsive genes may be a valuable therapeutic target for the treatment or prevention of BPH or prostate cancer."
Accordingly, these researchers studied an agent thought to inhibit the binding of SHBG to the prostate cell membrane, an extract of the root of the stinging nettle plant, Urtica dioica. In a paper published in 1995 in Planta Medica, they demonstrated that nettle root does indeed inhibit the binding of SHBG to the cell membrane.
In a subsequent series of articles, German researchers have identified a constituent of nettle root known as (-)-3,4-divanillyltetrahydrofuran whose very high binding affinity to SHBG they describe as "remarkable." These researchers suggest that the beneficial effects of plant lignans (such as found in flaxseed oil) on hormone-dependent cancers may be linked to their binding affinity to SHBG. The most potent known lignans in this respect are constituents of nettle root.
Studies show that the ethanolic extract of nettle root is not in inhibiting SHBG binding, while the aqueous and methanolic extracts are.
In addition to inhibiting SHBG binding, at least six constituents of nettle root inhibit aromatase, reducing conversion of androgens to estrogens. Combining nettle root with pygeum results in a stronger, synergistic inhibition. The studies on aromatase inhibition by nettle root used methanolic extracts.
A recent experimental study provides a dramatic demonstration of nettle root's effect on BPH tissue. This experiment was based upon the hypothesis that BPH is comparable to a reawakening of embryonic growth potential in the prostate. A fetal urogenital sinus was implanted into a lobe of the prostate gland in adult mice. After 28 days, the implanted lobes of mice fed a nettle root methanolic extract similar to an extract on the German pharmaceutical market showed 51.3% less growth than the lobes of mice in the control group."
