Ok, I assume we want the uncomplicated version?, ok, hang with me on this one, it may take a few posts to lay it all out.

1. Where does the androgen pathway begin?, from cholesterol. We start with the cholesterol to testosterone pathways where DHT can do its damage.

17α-hydroxylase and 17,20-lyase see the diagram (and the position in green) which these enzymes start.

A complete inhibition of 17α-hydroxylase/17,20-lyase (a key enzyme in the biosynthesis of androgens) can suppress androgens. A new class steroidal of CYP17 inhibitors are being presently used. They inhibit DHT @ nearly 90%, from what I've been able to see is also lowers estrogen by 13%......not worry though, I have an solution.

the evaluation of potent inhibitors of male rat 17alpha-hydroxylase/C17,20-lyase.
Duc I1, Bonnet P, Duranti V, Cardinali S, Rivière A, De Giovanni A, Shields-Botella J, Barcelo G, Adje N, Carniato D, Lafay J, Pascal JC, Delansorne R.
Author information

Abstract
The C(17,20)-lyase is a key enzyme in the biosynthesis of androgens by both the testes and adrenals. A complete inhibition of this enzyme would provide an alternative means of androgen suppression for the treatment of prostatic cancers. In the present study, the inhibitory effects of new non-steroidal compounds were tested in vitro on rat C(17,20)-lyase versus abiraterone, a reference steroidal inhibitor. Their activities were also evaluated in vivo on plasma testosterone (T) and luteinizing hormone (LH) levels and on testes, adrenals, seminal vesicles (SV) and ventral prostate (VP) weights after 3 days of oral treatment to adult male rats (50mg/kg per day p.o.). Inhibition in the nanomolar range was obtained with TX 977, the lead racemate product in this series, and optimization is ongoing based on a slight dissociation observed between its two diastereoisomers, TX 1196-11 (S) and TX 1197-11 ®. These non-steroidal compounds (including YM 55208, a reference competitor) proved to be more active in vivo than abiraterone acetate in this model, but the observed impact on adrenal weight suggests that the specificity of lyase inhibition versus corticosteroid biosynthesis deserves further investigations with this new class of potentially useful agents for the treatment of androgen-dependent prostate cancer.p

The abiraterone is a steroid compound CYP17 inhibitor, we want non-steroid inhibitors

Which I see we have some on the NBE list, oddly PM has a slight suppression of CYP17, how much I'm not sure. Though I'm pretty sure it's from Miroestrol, but because dexymirestrol is 10x stronger it hard to say.

Spiro is another example of a steroidal CYP 17 inhibitor.

Spirolactone increases the metabolic clearance of testosterone and inhibits androgen production


1. Prisant LM, Chin E. Gynecomastia and hyperten- sion. J Clin Hypertens (Greenwich) 2005;7:245-8. 

2. Rose LI, Underwood RH, Newmark SR, et al. Pathophysiology of spironolactone-induced gy- necomastia. Ann Intern Med 1977;87:398-403. 

DOI:10.1503/cmaj.061286


Many medications have been associated with gynecomastia, including phytoestrogens, estrogens and drugs with estrogen-like properties (e.g., digitalis), inhibitors of testosterone synthesis or action (e.g., ketoconazole, metronidazole, cimetidine, alkylating agents, finasteride) and other agents with unknown mechanisms (isoniazid, methyldopa, tricyclic antidepressants, penicillamine, diazepam, omeprazole, calcium-channel blockers, angiotensin-converting-enzyme inhibitors, marijuana and heroin).
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1800323/pdf/20070227s00013p620.pdf

I can only relate what my doctor said after prescribing Spiro for my blood pressure . She suggested taking it morning or no later than noon.

She explained that spiro aggravates my gyne by nearly stopping DHT. And that by keeping on a regular regimen, my body would adjust and slowly slow DHT to almost negligible amounts. And boosting what ever Estrogen my body already made on it's own.

Now granted, she is no Endo, but I think it's the easiest explanation for a novice to understand...

I would think that since herbs are far weaker, that what Lotus said is very true. It's just not strong enough, nor does it last long enough to put a stop to a fully functioning Endo system. Spiro, I suspect, has a far greater chance.

DHT is like playing "whack a mole"..........it finds a pathways for docking (binding). I say we go further upstream before DHT can find certain pathways.

I've found the answer if anyone is interested in (near) complete androgen suppression.

As I said, that is how she describe the process. Maybe she is just used to dealing with some with less than 100 I.Q.??? Some days, I feel I fit that description.

Here's my attempt to tie this into a nice little bow.

Think about it, if we start attacking androgens pathway in the beginning we nearly euthanize DHT's chance to synthesize down stream. in essence we create a larger pool of free estrogen...... Sooo.....our goal is to find more non steroidal CYP inhibitors:

For those of us on Hrt we'd start this dissuasion with our Physicians about androgen deprecation therapy aka ADT. Although, I'd expect some rejection because it's less understood. Look, it's a novel (newer) way of chemical castration. And, if there's a way to eliminate or reduce (drugs we use) the potential harmful side effects (e.g. DVT, cancers) i think it's a smart move.

Sorry Happyme, I hope you don't mind the info dump:


This is a post (smart fella, this MarDok42) from a PCOS board:

In the last few days my pharmacist friend explained to me when you block testosterone with one herb it will only block its production from one or two gene pathways, and a lot of the pro-hormones (hormone precursors) will find another pathway to testosterone, but it does give it a little longer to possibly become an estrogen. So to have more effective herbs, block more pathways with different types of herbs. Here's what I got so far.

Below are the genes that are involved in testosterone syntheses, they are the ones that start with 'CYP'. I have begun to cross referenced them with known chemicals in herbs that are known to inhibit these genes. If you want to find a synergistic herbal combination you might want to find a few herbs with these chemicals or others in it to inhibit(block) the majority of this gene set.

This is by no means a comprehensive list because I only started this project a week ago in my free time. But I thought that there might be other science geeks out there that would like to poke around the gene websites too.

Genes Involved in Testosterone Syntheses with corsponding inhibitors.

CYP1A2(also makes an Estrogen).....,cimetidine (inhibits)
CYP1B1(also makes an Estrogen)
CYP2B1– apigenin,Curcumin
CYP2B6– apigenin,Curcumin,Kaempferol
CYP2A3- lignans, genistein, Kaempferol
CYP2C11(Men Only)
CYP3A4 - lignans, Kaempferol, genistein, Curcumin (cimetidine, inhibits)
CYP3A5 - lignans, Kaempferol, genistein, Curcumin
CYP3A9 -
CYP19A1 -


Some Herbs and the anti androgen chemicals in them.

apigenin(chamomille)
Quercetin (chamomille)
genistein(Soy)
Curcumin(Vanalla, Turmeric)
Kaempferol(Peony, Dill)
lignans (Flax)

steroidogenic enzymes represent targets for complete suppression of systemic and intratumoral androgen levels, an objective that is supported by the clinical efficacy of the CYP17 inhibitor abiraterone.

Thank you Lotus for all the smart analysis. I didn't follow three
quarters of it and kind of kept an eye out for key words. Chemical
castration comes to mind. I have no interest in that at all. That might
be something you want to lead with. I for one, would like to keep my
male bits active.

Thank you Lotus for all the smart analysis. I didn't follow three
quarters of it and kind of kept an eye out for key words. Chemical
castration comes to mind. I have no interest in that at all. That might
be something you want to lead with. I for one, would like to keep my
male bits active.

Um hello, if your growing breasts by way of nbe/hrt what do think you're already doing?. There are those who could care less about function, a testosterone level of 50 ng/dL is a chemical castrastion. In other words when you lose function.

If moobs satisfy you, terrific......stay the course of little to no growth. If you want function and real female breast?, it's nearly impossible, but it can be done with the right know how.

Some lose function within 6 months.....some take longer, everybody is different. Key words or not, don't let some wording send you heading towards the exit ramp before you grasp the science.

As stated in the posted research paper:

The C(17,20)-lyase is a key enzyme in the biosynthesis of androgens by both the testes and adrenals. A complete inhibition of this enzyme would provide an alternative means of androgen suppression for the treatment of prostatic cancers. ........and the first means?, castration. And for the record, I'm not turning in mine yet. As you can see, CYP 17 inhibitors are used as alternative means (in red).

YIKES
function loss ????????????????????????

Many on here still have full functon and have had growth ?

also

Many married ts on hrt run low doses for pretty well full function and have good racks although takes twice as long

Am I missing something here ?

Julie