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
![[Image: attachment.php?aid=8137]](http://www.breastnexus.com/attachment.php?aid=8137)
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 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