[Lotus]

An androgen antagonist (anti-androgen) can broadly be defined as any compound that has the biological effect of blocking or suppressing the action of male sex hormones such as testosterone within the human body. DHT blocks the conversion of aromatase (bad for breast growth).
____________________________________________________________________

Reishi-reishi mushrooms significantly reduced levels of 5-alpha reductase, preventing conversion of testosterone into the more potent DHT. High levels of DHT are a risk factor for conditions such as benign prostatatic hypertrophy (BPH), acne, and baldness.

White Peony--Estrogenic, blocks 5ar and pro-aromatase - Strong.
A compound found in white peony inhibits the production of testosterone and promotes the activity of aromatase, which converts testosterone into estrogen.

Spearmint-anti-androgenic properties reduce the level of free testosterone in the blood, while leaving total testosterone and DHEAS unaffected.


Green Tea Epigallocatechin-Green tea (camellia)-Reduce's the conversion of free testosterone into DHT and also raises SHBG (sex-hormone-binding-globulin).


Pygeum-include phytosterols that inhibit the production of dht. Pygeum also reduce's prolacting levels and block the accumulation of cholesterol in the prostate. Prolactin increase's the uptake of testosterone by the prostate. Pygeum reduces the levels of DHT in the blood and reduces the number of sites where the dht can attach.


Saw palmetto-Saw palmetto-Beta-sitosterol is a natural alpha-adrenergic receptor blocker. Prevents DHT from accumulating in prostate tissue that would otherwise cause excessive cell growth and inflammation. The plant steroids in saw palmetto also act on progesterone receptors, an action that causes a reduction in estrogen levels.

DIM is Diindolylmethane-It is an anti carcinogen and also improves estrogen metabolism. Plant-derived 3,3′-Diindolylmethane Is a Strong Androgen Antagonist in Human Prostate Cancer Cells* DIM is remarkably similar in conformational geometry and surface charge distribution to an established synthetic AR antagonist, Taken with estrogen agonist, activities of DIM are seen as an hormone disrupter. DIM is the first example of a pure androgen receptor antagonist from plants.

Nettle Root- should be in the conversation

Nettle Root--Binds to SHBG (hormone that binds to excess hormones by decreasing hormone levels), and decreases 5ar and aromatase. Taking this tends to increase estrogen and testosterone. Would need to be taken with a pro-aromatase, and maybe estrogen.


Nettle root can interfere with or block a number these hormone-related chemical processes in the body that are implicated in the development of BPH. In clinical research, nettle has demonstrated the ability to stop the conversion of testosterone to dihydrotestosterone (by inhibiting aromatase, an enzyme required for the conversion), as well as to directly bind to SHBG itself - thereby preventing SHBG from binding to other hormones. Other research also reveals that nettles can prevent SHBG that has already bound to a hormone from attaching to the receptor sites on the prostate, as well as to decrease the production of estrogens (estradiol and estrone) by inhibiting an enzyme required for their production. The effect of nettle root on dihydrotestosterone (DHT) levels has also made it a treatment for hair loss, as male pattern balding has often been linked to an excess of DHT, as has hair loss in women too.

Chinese Skullcap should be in the conversation too-

Chinese Skullcap Inhibits the 5alpha-reductase enzyme-
Baicalein has been shown to inhibit the 5alpha-reductase enzyme, which converts testosterone to dihydrotestosterone (DHT). DHT is strongly associated with the development of prostate enlargement (benign prostatic hyperplasia) and prostate cancer. As such, baicalein is reported to be potentially useful for the prevention and/or treatment of androgen-dependent (testosterone-driven) disorders, including prostate enlargement and prostate cancer.

Licorice needs to be in the list
Use with extreme caution

Licorice (Glycyrrhiza glabra)-Anti-androgenic and activates alpha and beta estrogen receptors and blocks 5-ar - Strong, but take in moderation!

Licorice is a flavorful substance that has been used in food and medicinal remedies for thousands of years. It is also known as “sweet root,” licorice root contains a compound that is about 50 times sweeter than sugar. It has been used in both Eastern and Western medicine to treat a variety of illnesses ranging from the common cold to liver disease. Licorice affects the endocrine system because it contains isoflavones (phytoestrogens), which are chemicals found in plants that may mimic the effects of estrogen and relieve menopausal symptoms and menstrual disorders. Licorice may also reduce testosterone levels, which can contribute to hirsutism in women.

A small clinical trial published in 2004 by Armanini and colleagues found that licorice root significantly decreases testosterone levels in healthy female volunteers. Women taking daily licorice root experienced a drop in total testosterone levels after 1 month and testosterone levels returned to normal after discontinuation. It is unclear as to whether licorice root affects free testosterone levels. The endocrine effect is thought to be due to phytoestrogens and other chemicals found in licorice root, including the steroid glycyrrhizin and glycyrrhetic acid, which also have a weak anti-androgen effect
http://www.breastnexus.com/showthread.php?tid=5250

More about licorice-FOR REFERENCE (please add on as necessary)
I'm not sure how you would take LR at night before sleeping as it was suggested. 



-Licorice root is the only herb that balances estrogen, stimulates prolactin, and blocks testosterone all at the same time. Licorice contains numerous phytoestrogenic compounds such as glabridin, glaberine, and 3-hydroxyglabrol. 


-Beneficial for hypoglycemia, bronchitis, colitis, diverticulosis, gastritis, stress, colds, nausea, and inflammation. Cleanses the colon, promotes adrenal gland function, decreases muscle or skeletal spasms, and increases the fluidity of mucus from the lungs and bronchial tubes. Has estrogen-like hormone effects; changes the voice. Studies show licorice root stimulates the production of interferon. Warning: Do not use if you have high blood pressure."


-Researchers are currently excited about the diverse healing properties of licorice, from its anti-inflammatory abilities to its capacity to soothe stomach upset and control coughs. Even the National Cancer Institute has investigated the medicinal benefits of licorice.


-Lessen symptoms of chronic fatigue syndrome and fibromyalgia. By enhancing cortisol activity, glycyrrhizin helps to increase energy, ease stress, and reduce the symptoms of ailments sensitive to cortisol levels, such as chronic fatigue syndrome and fibromylagia. In the 1800s, licorice extract was a common remedy for a type of persistent fatigue known as neurasthenia, the condition now known as chronic fatigue syndrome.


-Soothe skin irritations such as eczema and shingles. Licorice cream applied directly to irritated skin can help to reduce inflammation and relieve such symptoms as itching and burning. It also boosts the effectiveness of cortisone creams.


-For most disorders: Take 200 mg standardized extract in pill form three times a day, or 20 to 45 drops, three times a day, of a 1:5 tincture. (The 1:5 tincture represents one part herb is soaked in five parts liquid


-Don't use licorice candy in place of supplements. Most red or black licorice candy sold in the United States contains anise oil as a flavoring rather than licorice. Candy made in Europe may contain licorice, but the quantities are not standardized.


-Licorice can raise blood pressure--a function of glycyrrhizin's action on the adrenal glands--so avoid taking more than the recommended dosage. If you take licorice for more than four weeks, have your blood pressure checked. (Stop taking the herb at the first sign of high blood pressure; this side effect is reversible.)


-At high doses taken over long periods of time, licorice can result in excessive salt loss from the blood, heart irregularities, and other serious health problems. Symptoms of this type of overdose may include headache, swelling, stiffness, shortness of breath, upper abdominal pain, and lethargy, among others.


-Side effects should disappear very shortly after stopping licorice. If not, see a doctor at once.

Sources:
http://www.breastnexus.com/showthread.php?tid=5250
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3693613/
http://endometabol.com/?page=article&article_id=3644
http://www.meschinohealth.com/ArticleDir..._Treatment



Abstracts-See frequently used supplements

[Lotus]

Here's a few more anti-androgens to consider:


Pumpkin Seed Oil: Has been demonstrated to inhibit DHT formation through the inhibitory effect on 5-alpha-reductase activity. Pumpkin seed oil breaks down DHT via the liver.


Emu Oil: Research has shown that emu oil contains a high level of linolenic acid which further research has shown to be an efficient antiandrogen. Linolenic acid is a potent 5 alpha reductase inhibitor and may be usefull in the treatment of disorders related to the hormone Dihydrotestosterone. Linolenic Acid has been suggested to be of use in the disorders such as benign prostratic hyperplasma, acne androgenetic alopecia and hirsuitism.


Even though it's not an AA it's worth mentioning because of its interaction.


L-Lysine: While L-Lysine is NOT a DHT blocker, it may make DHT blockers more effective. Researchers have found that adding a supplementation of L-Lysine can make drugs like Propecia more effective. Since propecia is a DHT inhibitor, as all the natural products mentioned here, the addition of a L-Lysine supplement can make these products also more effective. Studies has shown that L-Lysine combined with a DHT inhibitor can for example promote hair growth in people suffering from androgenetic alopecia.

[Lotus]

Hi NBE friends:

I think we need to remove DIM from being on the list of anti-androgens for the following reason:

From an anabolic point of view, the level of free testosterone rises in the blood with use of diindolylmethane. The mechanism behind this is that 2-hydroxy estrogens have a greater binding affinity for the blood proteins that "lock up" testosterone in the blood. Thus, these plasma binding proteins instead latch on to 2-hydroxy, leaving greater levels of free testosterone, including that produced through the use of supplemental prohormones.

The 2-hydroxy estrogens promoted by usage also increase testosterone synthesis through another mechanism. Estrogen, even more than testosterone itself, incurs a negative hormonal feedback loop to the pituitary gland, where the rate-limiting gonadotropin for testosterone synthesis, luteinizing hormone (LH) is synthesized and released. What this means is that high blood levels of estrogen, as may occur through aromatization of free testosterone, turn off the release of LH from the pituitary gland. This leads to a vicious biochemical cycle characterized by an imbalance between testosterone and estrogen in favor of the latter. These events, however, are nullified by 2-hydroxy, which doesn't provide the negative feedback message to the pituitary induced by estrogen. The net effect is greater testosterone synthesis in the Leydig cells of the testes, as well as lower levels of bad estrogen and all the effects that go with it.



DIM is Diindolylmethane-It is an anti carcinogen and also improves estrogen metabolism. Plant-derived 3,3′-Diindolylmethane Is a Strong Androgen Antagonist in Human Prostate Cancer Cells* DIM is remarkably similar in conformational geometry and surface charge distribution to an established synthetic AR antagonist, Taken with estrogen agonist, activities of DIM are seen as an hormone disrupter. DIM is the first example of a pure androgen receptor antagonist from plants.


Of course any thoughts are welcomed, and will wait for any feedback before removing!

[Miranda-nata-est]

Hi Lotus,

Hi everyone - nice to be back - all sorts of things have been occurring culminating in 'The Chat' with the GP two days ago and I have been taking my own advice to think through all this without too much outside influence . Will spill all soon when I have more time.

Meanwhile - does anyone know if there is any difference in the NBE effects of White Paeony with bark (often termed Red Paeony) and without bark (white)?

When Googled, there is a distinction made in Chinese medicine between the two :-

................INSERT ..........................


In Chinese medicine, Bai Shao, or "white peony" is actually the root, with root bark removed, of the cultivated Paeonia lactiflora plant having any colored flower. Chi Shao, or "red peony", is the root with root bark intact, of the wild-harvested Paeonia lactiflora or Paeonia veitchii, also of any colored flower.


................. END OF INSERT ......

Source

http://www.jadeinstitute.com/jade/herbal-detail-page.php?show=39&order=chinese_name


Thanks Lotus


M x

[undecided]

Hi NBE friends:

I think we need to remove DIM from being on the list of anti-androgens for the following reason:

From an anabolic point of view, the level of free testosterone rises in the blood with use of diindolylmethane. The mechanism behind this is that 2-hydroxy estrogens have a greater binding affinity for the blood proteins that "lock up" testosterone in the blood. Thus, these plasma binding proteins instead latch on to 2-hydroxy, leaving greater levels of free testosterone, including that produced through the use of supplemental prohormones.

The 2-hydroxy estrogens promoted by usage also increase testosterone synthesis through another mechanism. Estrogen, even more than testosterone itself, incurs a negative hormonal feedback loop to the pituitary gland, where the rate-limiting gonadotropin for testosterone synthesis, luteinizing hormone (LH) is synthesized and released. What this means is that high blood levels of estrogen, as may occur through aromatization of free testosterone, turn off the release of LH from the pituitary gland. This leads to a vicious biochemical cycle characterized by an imbalance between testosterone and estrogen in favor of the latter. These events, however, are nullified by 2-hydroxy, which doesn't provide the negative feedback message to the pituitary induced by estrogen. The net effect is greater testosterone synthesis in the Leydig cells of the testes, as well as lower levels of bad estrogen and all the effects that go with it.



DIM is Diindolylmethane-It is an anti carcinogen and also improves estrogen metabolism. Plant-derived 3,3′-Diindolylmethane Is a Strong Androgen Antagonist in Human Prostate Cancer Cells* DIM is remarkably similar in conformational geometry and surface charge distribution to an established synthetic AR antagonist, Taken with estrogen agonist, activities of DIM are seen as an hormone disrupter. DIM is the first example of a pure androgen receptor antagonist from plants.


Of course any thoughts are welcomed, and will wait for any feedback before removing!

Ok .... I read, re-read and read again. Part of the he quote confusing me the most was the what 2-hydroxy does " [color=#FF0000]as well as lower levels of bad estrogen and all the effects that go with it[/ color] " ( What is bad estrogen ?) So I did a search and found this ...

http://www.chiro.org/nutrition/FULL/Estr...reet.shtml

New research pinpoints how nutrition may prevent estrogen's carcinogenic activity by directing metabolites down favorable pathways

By Dan Lukaczer, N.D.


The continuing controversy over the health benefits and risks of estrogen is a complex and evolving story. Part of the reason is because estrogen is a much more complicated substance than originally believed. Although most people think of estrogen as a single entity, these hormones are actually three biochemically distinct molecules the body produces naturally—estrone (E1), estradiol (E2), and estriol (E3). These three estrogen molecules have different activities that make them more or less "estrogenic." The estrogenic activity often determines the mutagenic or carcinogenic potential of an estrogen.

It is widely believed that cumulative estrogen exposure is the most critical breast cancer risk factor. Breast cancer risk increases with early menarche, late menopause, long-term use of birth control pills, and estrogen replacement therapy. [1] When women gain weight, grow taller, have fewer children (and have them later in life), they increase their lifetime exposure to estrogen, and its associated risks.

Researchers are gaining new insights into the processes through which E1, E2, and E3 are metabolized, detoxified, and excreted. These estrogens break down or are detoxified into estrogen metabolites—daughter compounds—called 2-hydroxyestrone, 4-hydroxyestrone, and 16-hydroxyestrone. These metabolites can have stronger or weaker estrogenic activity—and thus increase a woman's risk of breast, uterine, and other cancers—depending on how they are metabolized.

We know estrogen metabolism depends on three factors: a woman's genetic makeup, lifestyle and diet, and environment. Therefore, understanding estrogen metabolism, and the things we can do to affect it, offers significant opportunities to reduce cancer risks, particularly of breast and uterine cancers.


Estrogen Metabolism

In premenopausal women, the ovaries produce the estrogen estradiol (E2), which converts into estrone (E1), both of which must eventually be broken down and excreted from the body. This breakdown occurs primarily in the liver, and the excreted metabolites flow out in the bile or urine. Estradiol and estrone undergo this breakdown through a process called hydroxylation, an enzymatic activity in which the parent estrogen is transformed by the addition of a hydroxyl (OH) group at specific positions on estrogen's molecular ring.

Estrogen molecules are composed of carbon ring structures that are named numerically. Estradiol has 17 carbon atoms and can be hydroxylated at particular points on that ring. Considerable research has shown that major metabolites of estradiol and estrone are those hydroxylated at either the C-2 or the C-16 positions. Hydroxylated metabolites at the C-4 position also are present, but in lesser amounts. We might think of this process as parent estrogens (estradiol and estrone) begetting daughter estrogens (C-2, C-4, and C-16 hydroxyestrones and hydroxyestradiols). The problem is, some of these are the proverbial good daughters and some are bad daughters. I'll describe how the "bad" daughters can cause significant trouble.

What makes an estrogen good or bad? That has to do with the biological activity, or potency, of that estrogen. Estrogens are important in a host of cellular activities that affect growth and differentiation in various target cells. This is normal and beneficial, but too much estrogenic stimulation can have a negative effect. Therefore, properly metabolizing and excreting estrogens is crucial. This is how the daughter compounds differ substantially. If these estrogens are metabolized into the 2-hydroxylated estrone and estradiol, they lose much of their cell proliferative and estrogenic activity and are termed "good" estrogen metabolites. Studies show that when 2-hydroxylation increases, the body resists cancer, and that when 2-hydroxylation decreases, cancer risk increases.

However, the C-4 and C-16 hydroxylated estrone and estradiol metabolites are different from C-2 because these metabolites have more estrogenic activity than their mother compound. [3] Research strongly suggests that women who metabolize a larger proportion of their estrogens down the C-16 pathway, as opposed to the C-2 pathway, have elevated breast cancer risk, [4] and that the daughter estrogens metabolized down the C-16 route may be associated with direct genotoxic effects and carcinogenicity. [5]


Predicting Cancer Risks

In one recent large trial of 10,786 premenopausal women at the State University of New York at Buffalo, researchers found that those who went on to develop breast cancer had significantly less 2-hydroxyestrone and more 16-alphahydroxyestrone metabolites than women who did not. Following women for 5.5 years, they found that participants with increased levels of 2-hydroxyestrone had a 40 percent decrease in the occurrence of breast cancer. [6]

In a longer-term study on postmenopausal women, women with the highest C-2:C-16 ratio (a higher ratio means more C-2 and less C-16, proportionally) had 30 percent less risk of developing breast cancer than women with lower ratios. [7] With this information, it would seem useful to discover what, if any, dietary or lifestyle modifications could guide estrogens down the C-2 pathway.

Estrogens are metabolized by a series of oxidizing enzymes in the cytochrome P450 family. These are the detoxification enzymes that break down all manner of drugs, hormones, and environmental toxins into generally less harmful metabolites. By closely studying this family of 30 or so enzymes, scientists have discovered how the parent estrogen compounds are modified in the C-2, C-4, or C-16 pathways. Researchers found that if particular enzymes within this family, namely cytochrome P450 1A1 and 1A2, are activated or stimulated, then more parent estrogens are metabolized into C-2-hydroxylated compounds. [8] However, if cytochrome P450 3A4 and 1B1 are activated, then more C-4 and C-16 are produced [9]. The C-16-alpha version tends to damage DNA and cause abnormal cellular proliferation, while the C-2 metabolite has less estrogenic activity. [2-4] If the proportion of C-16-alpha-hydroxyestrone can be decreased while the C-2-hydroxyestrone is increased—changing the ratio between the two—cancer risk could be reduced.


Nutrition And Estrogen

Epidemiological studies suggest the protective effects of soy protein on breast cancer rates in Asian countries where soy is a dietary mainstay. [10] While soy protein is a complex mixture of nutrients and phytochemicals, it appears that part of its benefit is related to the isoflavones genistein and daidzein. Studies suggest that they change the way estrogens are metabolized, therefore changing the C-2:C-16 ratio. In studies on both pre- and postmenopausal women, it has been shown that isoflavones increase the beneficial C-2-hydroxyestrone at the expense of the C-16-hydroxyestrone, therefore increasing the C-2:C-16 ratio. [11,12]

It appears that isoflavones found in other plants might also have beneficial effects. Kudzu (Pueraria lobata), a vine found in the southern United States, contains unique isoflavones. It was found that one of kudzu's isoflavones—puerarin—induced cytochrome P450 enzymes 1A1 and 1A2, among others, which pushed estrogen through the beneficial C-2-hydroxylation metabolic pathway. [13 ]

Lignans found in fiber-rich foods such as seeds and grains, and in particularly high concentrations in flaxseeds, contain phytochemicals that, when acted upon by bacteria in the gut, are converted to the metabolites called enterolactone and enterodiol, which appear to have similar effects as isoflavones. Researchers have demonstrated in animal and cell studies that lignans have chemoprotective effects, and they may influence estrogen production and metabolism. [14,15] Studies also have shown that women with breast cancer, or at risk for breast cancer, have low excretion levels of urinary lignans. In cell-culture studies, lignans have been shown to inhibit estrogen-sensitive breast cancer cell proliferation. [14] When flax was supplemented at five and 10 grams per day for three seven-week periods in a group of 28 postmenopausal women, the levels of C-2 hydroxyestrone increased in the urine, which increased the ratio of C-2:C-16. [15 ] This suggests that flax may have a beneficial effect on estrogen metabolism.


The Phytonutrient I3C

The results of epidemiological studies on cruciferous and mustard family vegetables (Brassica genus)—including bok choy, broccoli, brussels sprouts, cabbage, cauliflower, kale, kohlrabi, mustard, rutabaga, and turnip—suggest that diets high in these vegetables lower the breast cancer rate. Increasing the amount of cruciferous vegetables in the diet can increase the C-2: C-16-estrogen ratio. [16] The vegetables' phytochemicals seem to have a specific estrogen-modulating effect, and indole-3-carbinol (I3C) may be the most important phytonutrient in this regard.

Eating broccoli, kale, or other crucifers releases I3C, which is transported to the stomach. I3C is not the only indole formed [17] but is probably the most important and well studied.

In the stomach, I3C is converted into many active compounds, one of which is diindolylmethane (DIM). Although DIM appears to be one important metabolite of I3C, most of the past and ongoing studies are performed on I3C itself. This is because I3C breaks down into a number of indole products, aside from DIM, which also may have estrogen-modulating activity. [18,19] Cell-culture studies and human clinical trials have shown that I3C at doses of 200400 mg/day can influence estrogen metabolism and promote formation of 2-OH-estrone, and therefore may be useful in breast cancer prevention. [20,21 ] Current U.S. research studies are under way on I3C and women at increased risk for breast cancer. [22]

There is some controversy with I3C and when it should be administered. Most studies with I3C suggest it is best used as a preventive agent for women at high risk. Supplementing with I3C after cancer is present is less clear as far as benefit, as animal studies have been conflicting on this issue. [23,24]


Environmental Effects

Researchers who completed a large study last year concluded that the environment plays a much larger role in cancer development than most people realize. For example, more than 44,000 pairs of twins were assessed for a possible cancer connection in each pair. If inheritance played a major role, there would have been a strong health and disease correlation in both twins, but inherited factors for breast cancer were estimated at 30 percent, at most. Researchers concluded that inherited genetic factors make a minor contribution to cancer susceptibility, and that environmental factors play the principal role. [25]

Genes and the environment work together, and if a person has high genetic risk factors, greater attention should be focused on environment.

The World Health Organization recently reported that breast cancer has become the most common cancer in women throughout the world. [26] D. Lindsay Berkson, in Hormone Deception (Contemporary Books, 2000), reports on the accumulation of synthetic molecules in the environment from pesticides, plastics, and a variety of other sources that mimic the effects of the "bad" estrogens and add to cancer risk. Even if a woman doesn't have cancer in her family, with this ever-increasing environmental burden of estrogen-mimicking molecules, she needs to think about cutting her risk: what to do about internal and external environments. There is credible scientific evidence to suggest that consuming certain foods and phytonutrients may have a favorable effect on the risk of estrogen-related cancers.

Sidebars:

The Estrogen Dilemma

Dan Lukaczer, N.D., is director of clinical research at the Functional Medicine Research Center, a division of Metagenics International Inc., in Gig Harbor, Wash. Metagenics supplies medical foods and supplements, including those containing lignans, isoflavones, and I3C, to health care practitioners.

References:

1. Yager JD. Endogenous estrogens as carcinogens through metabolic activation. J Natl Cancer Inst Monogr 2000;27: 67-73.

2. Bradlow HL, et al. 2-hydroxyestrone: the 'good' estrogen. J Endocrinol 1996;150 Suppl:S259-65.

3. Gupta M, et al. Estrogenic and antiestrogenic activities of 16 alpha- and 2-hydroxy metabolites of 17 beta-estradiol in MCF-7 and T47D human breast cancer cells. J Steroid Biochem Mol Biol 1998;67(5-6):413-9.

4. Kabat GC, et al. Urinary estrogen metabolites and breast cancer: a case-control study. Cancer Epidemiol Biomarkers Prev 1997;6(7):505-9.

5. Bolton JL, et al. Role of quinoids in estrogen carcinogenesis. Chem Res Toxicol 1998;11(10):1113-27.

6. Muti P, et al. Estrogen metabolism and risk of breast cancer: a prospective study of the 2:16 alpha-hydroxyestrone ratio in premenopausal and postmenopausal women. Epidemiology 2000;11(6):635-40.

7. Meilahn EN, et al. Do urinary oestrogen metabolites predict breast cancer? Guernsey III cohort follow-up. Br J Cancer 1998;78(9):1250-5.

8. Bradlow HL, et al. Multifunctional aspects of the action of indole-3-carbinol as an antitumor agent. Ann NY Acad Sci 1999;889:204-13.

9. Huang Z, et al. 16-alpha-hydroxylation of estrone by human cytochrome P4503A4/5. Carcinogenesis 1998;19(5):867-72.

10. Vincent A, Fitzpatrick LA. Soy isoflavones: are they useful in menopause? Mayo Clin Proc 2000;75(11):1174-84.

11. Xu X, et al. Effects of soy isoflavones on estrogen and phytoestrogen metabolism in premenopausal women. Cancer Epidemiol Biomarkers Prev 1998;7(12):1101-8.

12. Xu X, et al. Soy consumption alters endogenous estrogen metabolism in postmenopausal women. Cancer Epidemiol Biomarkers Prev 2000;9(8):781-6.

13. Guerra MC, et al. Comparison between Chinese medical herb Pueraria lobata crude extract and its main isoflavone puerarin antioxidant properties and effects on rat liver CYP-cataly-sed drug metabolism. Life Sci 2000;67(24):2997-3006.

14. Mousavi Y, Adlercreutz H. Enterolactone and estradiol inhibit each other's proliferative effect on MCF-7 breast cancer cells in culture. J Steroid Biochem Mol Biol 1992;41(3-8):615-9.

15. Haggans CJ, et al. Effect of flaxseed consumption on urinary estrogen metabolites in postmenopausal women. Nutr Cancer 1999;33(2):188-95.

16. Fowke JH, et al. Brassica vegetable consumption shifts estrogen metabolism in healthy postmenopausal women. Cancer Epidemiol Biomarkers Prev 2000;9(8):773-9.

17. Stephenson PU, et al. Modulation of cytochrome P4501A1 activity by ascorbigen in murine hepatoma cells. Biochem Pharmacol 1999;58(7):1145-53.

18. Liu H, et al. Indolo[3,2-b]carbazole: a dietary-derived factor that exhibits both antiestrogenic and estrogenic activity. J Natl Cancer Inst 1994;1758-65.

19. Wong GY, et al. Dose-ranging study of indole-3-carbinol for breast cancer prevention. J Cell Biochem Suppl 1997;29:111-6.

20. Telang NT, et al. Inhibition of proliferation and modulation of estradiol metabolism: novel mechanisms for breast cancer prevention by the phytochemical indole-3-carbinol. Proc Soc Exp Biol Med 1997;216(2):246-52.

21. Michnovicz JJ, et al. Changes in levels of urinary estrogen metabolites after oral indole-3- carbinol treatment in humans. J Natl Cancer Inst 1997;89(10):718-23.

22. Osborne MP. Chemoprevention of breast cancer. Surg Clin North Am 1999;79(5):1207-21. 23. Bailey GS, et al. Enhancement of carcinogenesis by the natural anticarcinogen indole-3-carbinol. J Natl Canc Inst 1987 May;78(5):931-4.

24. Xu M, et al. Post-initiation effects of chlorophyllin and indole-3-carbinol in rats given 1,2-dimethylhydrazine or 2-amino-3-methyl-imidazo[4,5-f]quinoline. Carcinogenesis 2001;22:309-14.

25. Lichtenstein P, et al. Environmental and heritable factors in the causation of cancer—analyses of cohorts of twins from Sweden, Denmark, and Finland. N Engl J Med 2000;343(2):78-85.

26. Davis DL, et al. Rethinking breast cancer risk and the environment: the case for the precautionary principle. Environ Health Perspect 1998;106(9):523-9

[BestBreasts]

Hi Lotus.

I really want to decrease my DHT, but i am on birth control shot (progesterone depo provera).

i read that spearmint & saw palmetto might interfere w/ the birth control.

do you know of any DHT inhibitors that are okay to use while on birth control???? i don't want to get pregnant, but i really want to inhibit my DHT. I'm sick of my facial hair ughhhhh

thanks in advance!!!!!! xoxoxo

[Lotus]

Hi Lotus,

Hi everyone - nice to be back - all sorts of things have been occurring culminating in 'The Chat' with the GP two days ago and I have been taking my own advice to think through all this without too much outside influence . Will spill all soon when I have more time.

Meanwhile - does anyone know if there is any difference in the NBE effects of White Paeony with bark (often termed Red Paeony) and without bark (white)?

When Googled, there is a distinction made in Chinese medicine between the two :-

................INSERT ..........................


In Chinese medicine, Bai Shao, or "white peony" is actually the root, with root bark removed, of the cultivated Paeonia lactiflora plant having any colored flower. Chi Shao, or "red peony", is the root with root bark intact, of the wild-harvested Paeonia lactiflora or Paeonia veitchii, also of any colored flower.


................. END OF INSERT ......

Source

http://www.jadeinstitute.com/jade/herbal-detail-page.php?show=39&order=chinese_name


Thanks Lotus


M x

Hey there Miranda, long time no hear gurl, welcome back!. Great question! (Thanks for the link).


There's three main peonies, medicinally they appear to be very similar, I can't say for sure what all the main differences are yet, (short on time) so I'll share the info I do have. I'll post more later.

WHITE PEONY, RED PEONY, AND MOUTAN:
Three Chinese Herbs Derived from Paeonia


Red peony and white peony come from similar plants. Both are cold in nature and enter the blood and the liver meridian. Because red peony is cold and bitter, it is able to reduce liver heat as well as heat in the blood. It has a dispersing property, can invigorate the blood, and remove congealed blood, and is therefore often used in treating pain due to blood stagnation.
White peony is less cold but bitter, so it can clear liver heat or heat in the blood, but its function is weaker than that of red peony. One difference is its sour taste, which results in an astringent property. Cold and sourness may generate and stabilize the yin. As it enters the liver meridian, it particularly nourishes the liver yin and blood. It is an appropriate herb when there is yin deficiency with slight empty heat in the blood. In this situation, the main symptoms are dizziness, dry and burning eyes, irritability, and hypochondriac pain and distention.
Like red peony, white peony can also alleviate pain, but pain caused by liver yin and blood deficiency, in which the muscles and tendons lose their nourishment. This pain is cramping in nature, such as in abdominal pain and cramp after diarrhea, menstruation, labor, or cramp of the muscles of the limbs. Moreover, as white peony has a sour taste, it may stabilize the yin and body fluids and inhibit sweating, so is used for spontaneous sweating and night sweating.


CONSTITUENTS AND CHARACTERISTICS
All three of the peony materials used in Chinese herbal medicine contain paeoniflorin, a monoterpene glycoside that contributes the bitter taste. In a test of 19 species and 6 varieties of Peonia, paeoniflorin was the major and characteristic component of all of them, while Paeonia lactiflora was one of three (along with P. tenuifolia and P. veitchii) that had the largest amount, with up to 5.8% paeoniflorin (12, 13), though average amounts are about half that, about 3%. The root epidermis appears to contain a similar amount of paeoniflorin as found in the central root, with one study indicating about 2.3%; it has been suggested that removing the root epidermis to make white peony may simply be wasteful (14). There do not seem to be any studies indicating a notable difference in chemical constituents between red and white peony, though this does not rule out the possibility of a significant difference. Laboratory research shows that paeoniflorin has sedative, antispasmodic, and anti-inflammatory effects. The peony roots also contain slightly modified versions of this basic compound, such as oxypaeoniflorin and benzoylpaeoniflorin.

A simple ketone-paeonol-is an additional main component of moutan (about 1.5% of the root bark); there are also lesser amounts of glycoside compounds derived from it, such as paenoside (paeonol glucoside) and paeonolide (paeonol glucose-arabinose); these are found only in Paeonia suffruticosa and other woody species of Paeonia. These compounds have been shown to be antibacterial, antifungal, analgesic, sedative, and anti-spasmodic (16). In addition, it is reported to reduce lipid peroxidation (15). Paeonol is also a key component of cyanchum (xuchangqing), used as an analgesic for arthritis and anti-inflammatory for skin rashes, listed with herbs that dispel wind-damp (17). Paeonol is the aromatic component that gives moutan its characteristic fragrance and acrid taste. It is easily lost during drying and storage; [paeonol content is used as a quality measure for patent preparations for Liuwei Dihuang Wan (Rehmannia Six Formula) and Jiawei Xiaoyao Wan (Bupleurum and Peony Formula) since it is the main volatile component of those widely used formulas. The pharmacological actions of paeoniflorin and paeonol appear to be similar.

http://www.itmonline.org/arts/peony.htm

[Lotus]

Janet, nice post and thanks for sharing, the importance of E metabolism is often understated and under appreciated. A good NBE program can contribute to healthy E metabolism, meaning healthy breast growth.

[Lotus]

Hi Lotus.

I really want to decrease my DHT, but i am on birth control shot (progesterone depo provera).

i read that spearmint & saw palmetto might interfere w/ the birth control.

do you know of any DHT inhibitors that are okay to use while on birth control???? i don't want to get pregnant, but i really want to inhibit my DHT. I'm sick of my facial hair ughhhhh

thanks in advance!!!!!! xoxoxo

45,

Yes, that's correct SP interferes w/bc, I'd say check into pumpkin seed oil or Emu oil, (needs to be verified against bc though) spearmint doesn't block DHT.


Pumpkin Seed Oil: Has been demonstrated to inhibit DHT formation through the inhibitory effect on 5-alpha-reductase activity. Pumpkin seed oil breaks down DHT via the liver.


Emu Oil: Research has shown that emu oil contains a high level of linolenic acid which further research has shown to be an efficient antiandrogen. Linolenic acid is a potent 5 alpha reductase inhibitor and may be usefull in the treatment of disorders related to the hormone Dihydrotestosterone. Linolenic Acid has been suggested to be of use in the disorders such as benign prostratic hyperplasma, acne androgenetic alopecia and hirsuitism.

I know I have more info on both, so I'll post it later, (short on time at the moment) other herbs to consider too.



Evidence that Serenoa repens extract displays an antiestrogenic activity in prostatic tissue of benign prostatic hypertrophy patients.
http://www.ncbi.nlm.nih.gov/pubmed/?term...%3A309-314

[groentje]

what about Nymphaea alba (white lily) apparently it has an anaphrodisiac effect in men-monks and nuns used to take it. Would it have an anti-androgen effect ? I find very little about it. Maybe anyone else knows ?
It is also supposed to be very relaxing.