[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--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.


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

-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


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.


Considering the potential to block DHT and increase aromatase adding fatty acids makes sense, only don't forget a fitness plan.

Anti-androgenic activity of fatty acids.

In this study, we show that 5alpha-reductase derived from rat fresh liver was inhibited by certain aliphatic free fatty acids. The influences of chain length, unsaturation, oxidation, and esterification on the potency to inhibit 5alpha-reductase activity were studied. Among the fatty acids we tested, inhibitory saturated fatty acids had C12-C16 chains, and the presence of a C==C bond enhanced the inhibitory activity. Esterification and hydroxy compounds were totally inactive. Finally, we tested the prostate cancer cell proliferation effect of free fatty acids. In keeping with the results of the 5alpha-reductase assay, saturated fatty acids with a C12 chain (lauric acid) and unsaturated fatty acids (oleic acid and alpha-linolenic acid) showed a proliferation inhibitory effect on lymph-node carcinoma of the prostate (LNCaP) cells. At the same time, the testosterone-induced prostate-specific antigen (PSA) mRNA expression was down-regulated. These results suggested that fatty acids with 5alpha-reductase inhibitory activity block the conversion of testosterone to 5alpha-dihydrotestosterone (DHT) and then inhibit the proliferation of prostate cancer cells.
http://www.ncbi.nlm.nih.gov/pubmed/19353546

Evening Primrose Oil- massage, Fibrocystic breast pain, treats hot flashes, relieves PMS symptoms, relieves Eczema, hormone balance, fights breast tumors and diabetes. Reports have GLA-Gamma-Linolenic Acid as helping with RA and arthritis, diabetic neuropathy, ADHD and CFS (chronic fatigue syndrome). And UPDATED to include it being an inhibitor of 5 alpha-reductase, the enzyme that converts testosterone to DHT, (DHT is bad for BOOB GROWTH).

Coconut Oil- Makes connective tissues stronger, superb antioxidant, neutralizes free radicals and slowing down aging, aids in breast feeding, nature's richest source of MCFAs. 5 ar inhibitor, pro-aromatase.

[myboobs]

Haven't seen jackp114 , post for a while here ! He seems to be doing a lot of herbal research [/i]

[spanky (aka Lola)]

Fantastic summary, Lotus! Thanks as always to our resident sage.

[Lotus]

Would anyone be willing to do a bit of a summary on the most noteworthy anti-androgens, their primary effects, important side effects and (roughly) recommended safe doses? A kind of pros vs cons for some of the more common AAs would be awesome.

I get that I could probably scrape this sort of information by reading through this thread, but seriously, it's 71 pages... I'd be grateful if someone who's been following this thread (or has knowledge on natural AAs from elsewhere) would write a kind of overview, or if such an overview already exists then direct me to it. Thanks in advance. <3

Trixy, great point, it's an updated version now, the FAQ section has most of the standard AA information. This long winded thread lol was to talk about the available anti-androgens, definitions, share ideas and maybe discover new ones (hopefully). You're right though, it needed a new summary update. Safe dosages would be to follow the mfg recommended daily amount, human metabolism is individually unique, meaning everybody reacts differently. Some see quick results and then plateau, others take longer then blossom, or are totally unaffected unfortunately. So long story short, start at the base dosages and then adjust, keep the liver in mind, it's a filter, hormone promoter, and the potential to back fire (the big casino, aka cancer), take care of it.

[Lotus]

Haven't seen jackp114 , post for a while here ! He seems to be doing a lot of herbal research [/i]

True, he's still active, just quiet I suppose.

Fantastic summary, Lotus! Thanks as always to our resident sage.

Thanks spanky, I think it's still missing some stuff lol. I'm adding Pharma AA's with some personal observations,


Both finasteride and dutasteride undergo extensive hepatic metabolism primarily via the cytochrome P450 3A4 (CYP 3A4) isoenzyme system

Finasteride modestly increases serum testosterone (T), estrone (E1), and estradiol (E2). Aka-it increases libido, acne, and oily skin, just FYI, or be on the look out, lol

finasteride blocks the conversion of testosterone to dihydrotestosterone (DHT) and of androstenedione to 5α-androstanedione-3,17-dione, which also leads to the reduction of DHT formation.

Androstenedione is the second most important circulating androgen in men (1st in women) besides testosterone and also a substrate for 5α-reductase enzyme. IMO genetic males go through a process of equilibrium known as upregulation. And upstream of testosterone sits androstenedione, which can go either way via 5 alpha reductase. Once this upregulation is achieved we maintain homeostasis (equilibrium), (not to be confused with hemostasis stops blood flow) I believe the andro to aromatase conversion is the dominate production, in other words, a cascade.

What hormones escape and continue downstream to T will also go through the same process, but with upregulation we're increasing the amount amount of E receptors. Receptors degrade rapidly, I don't know that exact timing of the degradation. But, in my signature below it stated the release and binding times.
Anyways, I'm drifting off topic lol, IMO Finasteride has a slight 22% chance of aromatase, (eventually) I determined that by a recent study (attached below). But, that just proves my point about the upregulation of androstenedione, (DHEA too).

Effect of Finasteride on Serum Androstenedione and Risk of Prostate Cancer Within the Prostate Cancer Prevention Trial: Differential Effect on High- and Low-grade Disease.
http://www.ncbi.nlm.nih.gov/pubmed/25733274#


glycyrrhetic acid on ovarian androgen production.

Abstract
We have shown that traditional herbal medicine, Shakuyaku-Kanzo-To consisted of Shakuyaku and Kanzo decreased serum testosterone levels in woman and rat. Therefore, paeoniflorin and glycyrrhizin, a main component of Shakuyaku and Kanzo, respectively, and glycyrrhetic acid, a metabolite of glycyrrhizin in vivo, were investigated for the steroid production in the rat ovary on the morning of proestrus. The homogenized tissues of one ovary were incubated in the Dulbecco's modified Eagle medium (pH 7.5) with 100 micrograms/ml of paeoniflorin, glycyrrhetic acid and glycyrrhizin and the medium only (the control) at 37 degrees C for 270 min. After the centrifugation, the concentrations of delta 4-androstenedione, testosterone and estradiol in the supernatants were determined by RIA. The production of the hormones expressed by [concentration x supernatant volume/weight of the ovary] was compared to the control. Paeoniflorin, glycyrrhetic acid and glycyrrhizin decreased significantly the testosterone production but did not change that of delta 4-androstenedione and estradiol. Testosterone/delta 4-androstenedione production ratio was lowered significantly by paeoniflorin, glycyrrhetic acid and glycyrrhizin. Estradiol/testosterone production ratio was increased significantly by glycyrrhetic acid and not changed by paeoniflorin and glycyrrhizin. These results suggest that paeoniflorin, glycyrrhetic acid and glycyrrhizin affect the conversion between delta 4-androstenedione and testosterone to inhibit testosterone synthesis and stimulate the aromatase activity to promote estradiol synthesis by the direct action on the rat proestrous ovary.

Here's another example of up-regulation from a recent study I found.

Overexpression of AIB1Δ3, especially combined with overexpressed ERα, led to an abnormal response to estrogen and progesterone with significant increases in stromal collagen content and development of a multilayered mammary epithelium. AIB1Δ3 overexpression was associated with a significant increase in PR expression and PR downstream signaling genes.


_______________________

I'll do spiro next, (and spiro is crazy) it's metabolized quite differently in men in women.

[Lotus]

I grew 2-3 cups using Reishi (w/no unfair advantages) 4+ cups overall with NBE. BO did not agree with me. Reishi coumarins ARE NOT the main bio actives that inhibitors 5 AR..........it's polysaccharides, triterpines, and other lipids are the main bioactives that does the inhibiting in the Prostate. Reishi has a 2,000 year track record, not sure how much more record keeping, accept HERE.........where it's used to grow breasts. Information (complete w/attached studies) continue to show the potential of reishi. I'll attach the related papers, (located in my project x thread). Btw Abi, none of your files are deleted, just moved here, so you and i dont hijack another thread, apologies for any inconvenience.

In many cases no lab research is related to NBE, or how it effects male breast growth. We are, in fact the lab test subjects to carry out the business of real world result (or not). FWIW.


Reishi has 5a-reductase inhibitory activity of more than 90% at 200 ug/ml.

5α-Reductase inhibitory activity-guided fractionation of the EtOH extract of the fruiting body of Ganoderma lucidum (LEYSS.:FR.) KARST. (Ganodermataceae), which is called Reishi, or Mannentake in Japan and Lingzhi in China, led to the isolation of two active compounds which were ganoderic acid DM and 5α-lanosta-7,9(11),24-triene-15α,26-dihydroxy-3-one with an IC50 of 10.6 μM and 41.9 μM respectively. A carboxyl group of side chain of ganoderic acid DM is essential to elicit the inhibitory activity because of much less activity of its methyl ester.
http://www.ncbi.nlm.nih.gov/pubmed/16462054
[/quote]


For those who need more science lol, here's a sampling:

i've been reading different things on this website, and i'd appreciate one more from this thread please =]]

is Green Tea (preferably green tea capsules - 500mg) an anti-androgen? or does it block DHT???

thanks in advance xoxoxo

Sorry 45 for the DHT frustration, green tea is not so cut and dry in terms of an effective DHT blocker, it depends on what research you find, meaning it's pretty confusing. If you want the short answer (which I assume is yes), I'd choose something else (e.g. reishi). According to this report its effective as a 5 ar inhibitor (blocks the conversion path to DHT). Human studies are lacking though.


Department of Biochemistry and Molecular Biology, The Ben May Institute for Cancer Research, and The Tang Center for Herbal Medicine Research MC6027, University of Chicago, 5841 S. Maryland, Chicago, IL 60637, USA.

The enzyme steroid 5 alpha-reductase (EC 1.3.99.5) catalyzes the NADPH-dependent reduction of the double bond of a variety of 3-oxo-Delta(4) steroids including the conversion of testosterone to 5 alpha-dihydrotestosterone. In humans, 5 alpha-reductase activity is critical for certain aspects of male sexual differentiation, and may be involved in the development of benign prostatic hyperplasia, alopecia, hirsutism, and prostate cancer. Certain natural products contain components that are inhibitors of 5 alpha-reductase, such as the green tea catechin (-)-epigallocatechin gallate (EGCG). EGCG shows potent inhibition in cell-free but not in whole-cell assays of 5 alpha-reductase. Replacement of the gallate ester in EGCG with long-chain fatty acids produced potent 5 alpha-reductase inhibitors that were active in both cell-free and whole-cell assay systems. Other flavonoids that were potent inhibitors of the type 1 5alpha-reductase include myricetin, quercitin, baicalein, and fisetin. Biochanin A, daidzein, genistein, and kaempferol were much better inhibitors of the type 2 than the type 1 isozyme. Several other natural and synthetic polyphenolic compounds were more effective inhibitors of the type 1 than the type 2 isozyme, including alizarin, anthrarobin, gossypol, nordihydroguaiaretic acid, caffeic acid phenethyl ester, and octyl and dodecyl gallates. The presence of a catechol group was characteristic of almost all inhibitors that showed selectivity for the type 1 isozyme of 5 alpha-reductase. Since some of these compounds are consumed as part of the normal diet or in supplements, they have the potential to inhibit 5 alpha-reductase activity, which may be useful for the prevention or treatment of androgen-dependent disorders. However, these compounds also may adversely affect male sexual differentiation.

Sorry people, I have to share this rather unique way to box out DHT, I stumbled across it when I was collecting some research, please follow along (my apologies for the technical crap explanation) I'll try to keep it in the ball park.

The problem with DHT is when it enters into receptors it locks it up, and thereby making Aromatase an after thought, Aromatase is enzyme that converts free T to estrogen. (Aka boob growth), here I suggest a novel (well, at least for BN) called "Androgen Decoy's".


http://www.ncbi.nlm.nih.gov/core/lw/2.0/html/tileshop_pmc/tileshop_pmc_inline.html?title=Click%20on%20image%20to%20zoom&p=PMC3&id=3132148_nihms255516f1.jpg





A transcriptional factor decoy strategy is the use of short double-stranded oligodeoxynucleotides containing a high-affinity binding site for specific transcription factors as a decoy DNA to be transfected into target cells [12–16]. Inside the cells, the decoy DNA competes with the endogenous high-affinity binding site of the target genes for binding to specific transcription factors, and consequently inhibits activated AR function [16]. Decoy DNA has potential for treatment of cardiovascular disease [12]. It also induces apoptosis in certain cell lines [13].

Androgen receptor decoy molecules block the growth of prostate cancer
http://www.pnas.org/content/104/4/1331.abstract


Androgen receptor: structure, role in prostate cancer and drug discovery
Androgens and androgen receptors (AR) play a pivotal role in expression of the male phenotype. Several diseases, such as androgen insensitivity syndrome (AIS) and prostate cancer, are associated with alterations in AR functions. Indeed, androgen blockade by drugs that prevent the production of androgens and/or block the action of the AR inhibits prostate cancer growth. However, resistance to these drugs often occurs after 2–3 years as the patients develop castration-resistant prostate cancer (CRPC). In CRPC, a functional AR remains a key regulator. Early studies focused on the functional domains of the AR and its crucial role in the pathology. The elucidation of the structures of the AR DNA binding domain (DBD) and ligand binding domain (LBD) provides a new framework for understanding the functions of this receptor and leads to the development of rational drug design for the treatment of prostate cancer. An overview of androgen receptor structure and activity, its actions in prostate cancer, and how structural information and high-throughput screening have been or can be used for drug discovery are provided herei
http://www.nature.com/aps/journal/vaop/n....html#fig1

The mechanism of action of testosterone.
Testosterone enters the cell by passive diffusion and is converted to DHT and estradiol. Testosterone and DHT bind to the androgen receptor located in the cytoplasm attached to heat-shock proteins (not shown). Upon binding of testosterone and DHT to androgen receptor, heat-shock protein is released and the receptor dimerizes. Estradiol binds to the estrogen receptors ERα, ERβ

Androgen and AR action. Genome organization of the human androgen receptor gene and the functional domain structure of the androgen receptor protein. (A) Androgen and AR signaling in prostate cells. After testicular synthesis, testosterone is transported to target tissues such as the prostate and becomes converted to dihydrotestosterone (DHT) by 5-α-reductase. DHT binds to the ligand-binding pocket and promotes the dissociation of heat-shock proteins (HSPs) from the AR. The AR then translocates into the nucleus, dimerizes and binds to the androgen response element (ARE) in the promoter region of target genes such as prostate-specific antigen (PSA) and TMPRSS2. At the promoter, the AR is able to recruit members of the basal transcription machinery [such as TATA-box-binding protein (TBP) and transcription factor IIF (TFIIF)] in addition to other coregulators such as members of the p160 family of coactivators and cAMP-response element-binding protein (CREB)-binding protein (CBP). SHBG: serum sex hormone-binding globulin. (B) The androgen receptor gene has been mapped to the long arm of the X-chromosome (locus: Xq11-q12). It contains eight exons interrupted by introns of varying lengths (0.7–2.6 kb) and codes for a protein of 919 amino acids consisting of several functional domains (N-terminal domain (NTD), DNA binding domain (DBD) and ligand binding domain (LBD); amino acid residue numbers are indicated above the AR protein domain map). Exon 1 codes for the NTD, exons 2 and 3 encode the DBD, and exons 4 to 8 encode both the hinge and LBD.






Comparison of crystal structures of human androgen receptor ligand-binding domain complexed with various agonists reveals molecular determinants responsible for binding affinity.

Abstract
Androgens exert their effects by binding to the highly specific androgen receptor (AR). In addition to natural potent androgens, AR binds a variety of synthetic agonist or antagonist molecules with different affinities. To identify molecular determinants responsible for this selectivity, we have determined the crystal structure of the human androgen receptor ligand-binding domain (hARLBD) in complex with two natural androgens, testosterone (Testo) and dihydrotestosterone (DHT), and with an androgenic steroid used in sport doping, tetrahydrogestrinone (THG), at 1.64, 1.90, and 1.75 A resolution, respectively. Comparison of these structures first highlights the flexibility of several residues buried in the ligand-binding pocket that can accommodate a variety of ligand structures. As expected, the ligand structure itself (dimension, presence, and position of unsaturated bonds that influence the geometry of the steroidal nucleus or the electronic properties of the neighboring atoms, etc.) determines the number of interactions it can make with the hARLBD. Indeed, THG--which possesses the highest affinity--establishes more van der Waals contacts with the receptor than the other steroids, whereas the geometry of the atoms forming electrostatic interactions at both extremities of the steroid nucleus seems mainly responsible for the higher affinity measured experimentally for DHT over Testo. Moreover, estimation of the ligand-receptor interaction energy through modeling confirms that even minor modifications in ligand structure have a great impact on the strength of these interactions. Our crystallographic data combined with those obtained by modeling will be helpful in the design of novel molecules with stronger affinity for the AR.

http://www.ncbi.nlm.nih.gov/pubmed/16641486?dopt=Abstract&holding=npg

[myboobs]

I grew 2-3 cups using Reishi (w/no unfair advantages) 4+ cups overall with NBE. BO did not agree with me. Reishi coumarins ARE NOT the main bio actives that inhibitors 5 AR..........it's polysaccharides, triterpines, and other lipids are the main bioactives that does the inhibiting in the Prostate. Reishi has a 2,000 year track record, not sure how much more record keeping, accept HERE.........where it's used to grow breasts. Information (complete w/attached studies) continue to show the potential of reishi. I'll attach the related papers, (located in my project x thread). Btw Abi, none of your files are deleted, just moved here, so you and i dont hijack another thread, apologies for any inconvenience.

In many cases no lab research is related to NBE, or how it effects male breast growth. We are, in fact the lab test subjects to carry out the business of real world result (or not). FWIW.


Reishi has 5a-reductase inhibitory activity of more than 90% at 200 ug/ml.

5α-Reductase inhibitory activity-guided fractionation of the EtOH extract of the fruiting body of Ganoderma lucidum (LEYSS.:FR.) KARST. (Ganodermataceae), which is called Reishi, or Mannentake in Japan and Lingzhi in China, led to the isolation of two active compounds which were ganoderic acid DM and 5α-lanosta-7,9(11),24-triene-15α,26-dihydroxy-3-one with an IC50 of 10.6 μM and 41.9 μM respectively. A carboxyl group of side chain of ganoderic acid DM is essential to elicit the inhibitory activity because of much less activity of its methyl ester.
http://www.ncbi.nlm.nih.gov/pubmed/16462054

For those who need more science lol, here's a sampling:

i've been reading different things on this website, and i'd appreciate one more from this thread please =]]

is Green Tea (preferably green tea capsules - 500mg) an anti-androgen? or does it block DHT???

thanks in advance xoxoxo

Sorry 45 for the DHT frustration, green tea is not so cut and dry in terms of an effective DHT blocker, it depends on what research you find, meaning it's pretty confusing. If you want the short answer (which I assume is yes), I'd choose something else (e.g. reishi). According to this report its effective as a 5 ar inhibitor (blocks the conversion path to DHT). Human studies are lacking though.


Department of Biochemistry and Molecular Biology, The Ben May Institute for Cancer Research, and The Tang Center for Herbal Medicine Research MC6027, University of Chicago, 5841 S. Maryland, Chicago, IL 60637, USA.

The enzyme steroid 5 alpha-reductase (EC 1.3.99.5) catalyzes the NADPH-dependent reduction of the double bond of a variety of 3-oxo-Delta(4) steroids including the conversion of testosterone to 5 alpha-dihydrotestosterone. In humans, 5 alpha-reductase activity is critical for certain aspects of male sexual differentiation, and may be involved in the development of benign prostatic hyperplasia, alopecia, hirsutism, and prostate cancer. Certain natural products contain components that are inhibitors of 5 alpha-reductase, such as the green tea catechin (-)-epigallocatechin gallate (EGCG). EGCG shows potent inhibition in cell-free but not in whole-cell assays of 5 alpha-reductase. Replacement of the gallate ester in EGCG with long-chain fatty acids produced potent 5 alpha-reductase inhibitors that were active in both cell-free and whole-cell assay systems. Other flavonoids that were potent inhibitors of the type 1 5alpha-reductase include myricetin, quercitin, baicalein, and fisetin. Biochanin A, daidzein, genistein, and kaempferol were much better inhibitors of the type 2 than the type 1 isozyme. Several other natural and synthetic polyphenolic compounds were more effective inhibitors of the type 1 than the type 2 isozyme, including alizarin, anthrarobin, gossypol, nordihydroguaiaretic acid, caffeic acid phenethyl ester, and octyl and dodecyl gallates. The presence of a catechol group was characteristic of almost all inhibitors that showed selectivity for the type 1 isozyme of 5 alpha-reductase. Since some of these compounds are consumed as part of the normal diet or in supplements, they have the potential to inhibit 5 alpha-reductase activity, which may be useful for the prevention or treatment of androgen-dependent disorders. However, these compounds also may adversely affect male sexual differentiation.

Sorry people, I have to share this rather unique way to box out DHT, I stumbled across it when I was collecting some research, please follow along (my apologies for the technical crap explanation) I'll try to keep it in the ball park.

The problem with DHT is when it enters into receptors it locks it up, and thereby making Aromatase an after thought, Aromatase is enzyme that converts free T to estrogen. (Aka boob growth), here I suggest a novel (well, at least for BN) called "Androgen Decoy's".


http://www.ncbi.nlm.nih.gov/core/lw/2.0/html/tileshop_pmc/tileshop_pmc_inline.html?title=Click%20on%20image%20to%20zoom&p=PMC3&id=3132148_nihms255516f1.jpg





A transcriptional factor decoy strategy is the use of short double-stranded oligodeoxynucleotides containing a high-affinity binding site for specific transcription factors as a decoy DNA to be transfected into target cells [12–16]. Inside the cells, the decoy DNA competes with the endogenous high-affinity binding site of the target genes for binding to specific transcription factors, and consequently inhibits activated AR function [16]. Decoy DNA has potential for treatment of cardiovascular disease [12]. It also induces apoptosis in certain cell lines [13].

Androgen receptor decoy molecules block the growth of prostate cancer
http://www.pnas.org/content/104/4/1331.abstract


Androgen receptor: structure, role in prostate cancer and drug discovery
Androgens and androgen receptors (AR) play a pivotal role in expression of the male phenotype. Several diseases, such as androgen insensitivity syndrome (AIS) and prostate cancer, are associated with alterations in AR functions. Indeed, androgen blockade by drugs that prevent the production of androgens and/or block the action of the AR inhibits prostate cancer growth. However, resistance to these drugs often occurs after 2–3 years as the patients develop castration-resistant prostate cancer (CRPC). In CRPC, a functional AR remains a key regulator. Early studies focused on the functional domains of the AR and its crucial role in the pathology. The elucidation of the structures of the AR DNA binding domain (DBD) and ligand binding domain (LBD) provides a new framework for understanding the functions of this receptor and leads to the development of rational drug design for the treatment of prostate cancer. An overview of androgen receptor structure and activity, its actions in prostate cancer, and how structural information and high-throughput screening have been or can be used for drug discovery are provided herei
http://www.nature.com/aps/journal/vaop/n....html#fig1

The mechanism of action of testosterone.
Testosterone enters the cell by passive diffusion and is converted to DHT and estradiol. Testosterone and DHT bind to the androgen receptor located in the cytoplasm attached to heat-shock proteins (not shown). Upon binding of testosterone and DHT to androgen receptor, heat-shock protein is released and the receptor dimerizes. Estradiol binds to the estrogen receptors ERα, ERβ

Androgen and AR action. Genome organization of the human androgen receptor gene and the functional domain structure of the androgen receptor protein. (A) Androgen and AR signaling in prostate cells. After testicular synthesis, testosterone is transported to target tissues such as the prostate and becomes converted to dihydrotestosterone (DHT) by 5-α-reductase. DHT binds to the ligand-binding pocket and promotes the dissociation of heat-shock proteins (HSPs) from the AR. The AR then translocates into the nucleus, dimerizes and binds to the androgen response element (ARE) in the promoter region of target genes such as prostate-specific antigen (PSA) and TMPRSS2. At the promoter, the AR is able to recruit members of the basal transcription machinery [such as TATA-box-binding protein (TBP) and transcription factor IIF (TFIIF)] in addition to other coregulators such as members of the p160 family of coactivators and cAMP-response element-binding protein (CREB)-binding protein (CBP). SHBG: serum sex hormone-binding globulin. (B) The androgen receptor gene has been mapped to the long arm of the X-chromosome (locus: Xq11-q12). It contains eight exons interrupted by introns of varying lengths (0.7–2.6 kb) and codes for a protein of 919 amino acids consisting of several functional domains (N-terminal domain (NTD), DNA binding domain (DBD) and ligand binding domain (LBD); amino acid residue numbers are indicated above the AR protein domain map). Exon 1 codes for the NTD, exons 2 and 3 encode the DBD, and exons 4 to 8 encode both the hinge and LBD.






Comparison of crystal structures of human androgen receptor ligand-binding domain complexed with various agonists reveals molecular determinants responsible for binding affinity.

Abstract
Androgens exert their effects by binding to the highly specific androgen receptor (AR). In addition to natural potent androgens, AR binds a variety of synthetic agonist or antagonist molecules with different affinities. To identify molecular determinants responsible for this selectivity, we have determined the crystal structure of the human androgen receptor ligand-binding domain (hARLBD) in complex with two natural androgens, testosterone (Testo) and dihydrotestosterone (DHT), and with an androgenic steroid used in sport doping, tetrahydrogestrinone (THG), at 1.64, 1.90, and 1.75 A resolution, respectively. Comparison of these structures first highlights the flexibility of several residues buried in the ligand-binding pocket that can accommodate a variety of ligand structures. As expected, the ligand structure itself (dimension, presence, and position of unsaturated bonds that influence the geometry of the steroidal nucleus or the electronic properties of the neighboring atoms, etc.) determines the number of interactions it can make with the hARLBD. Indeed, THG--which possesses the highest affinity--establishes more van der Waals contacts with the receptor than the other steroids, whereas the geometry of the atoms forming electrostatic interactions at both extremities of the steroid nucleus seems mainly responsible for the higher affinity measured experimentally for DHT over Testo. Moreover, estimation of the ligand-receptor interaction energy through modeling confirms that even minor modifications in ligand structure have a great impact on the strength of these interactions. Our crystallographic data combined with those obtained by modeling will be helpful in the design of novel molecules with stronger affinity for the AR.

http://www.ncbi.nlm.nih.gov/pubmed/16641486?dopt=Abstract&holding=npg

[/quote]

When I restart my nbe I am gona use Reishi instead of SP

[Lotus]

Myboobs, I hope you see some good results. One thing I think that could also help is raising serum estradiol levels. One way is from using green tea extract, which I believe GTE displaces it (estradiol) from SHBG (unbound state).

We know GTE increases SHBG (sex hormone binding globulin) levels. SHBG carries hormones in the blood to receptor target tissues, aka - breasts. An increase in SHBG also lowers Testosterone.

[myboobs]

Will add green tea extract to the regime

[Mickie]

A lot of great information there Lotus.. many thanks.. I will be altering my regimen for certain