Breast Growth For Genetic Males

5a-reductase, the enzyme responsible for converting testosterone to dihydrotestosterone, exists in 2 forms: Type 1 and Type 2. Finasteride selectively inhibits Type 2 (70%) whereas dutasteride inhibits both forms, (93%).

This is significant because dihydrotestosterone is thought to be important in the development of BPH; its suppression by these 2 agents may prove to be beneficial for patients with BPH.




Comparison of Clinical Trials With Finasteride and Dutasteride
http://www.ncbi.nlm.nih.gov/pmc/articles...9_0S31.pdf


Results of a phase II, double-blind, placebo-controlled, comparative dose-ranging trial of dutasteride and finasteride clearly demonstrated that serum DHT suppression was significantly greater with dutasteride (0.5 mg daily) than with finasteride (5 mg daily).3 The mean reduction in base-line DHT concentration in patients receiving 0.5 mg dutasteride daily was 94.7 ± 3.3% and for patients receiving finasteride 5 mg daily was 70.8 ± 18.3%, respectively (P < .001) (Figure 2). In non-comparative clinical trials, chronic therapy with dutasteride (0.5 mg daily) for up to 2 years in patients with BPH resulted in median reductions in serum DHT of 93%.4 In contrast, therapy with finasteride (5 mg daily) suppressed serum DHT concentrations by approximately 70% for up to 4 years in patients with BPH.5 These observations raise the question whether the pharmacologic differences in DHT suppression between a selective versus a dual inhibitor of 5AR results in clinically significant differences in the treatment of BPH.


Btw, rashes are reported in 5 AR therapy, the reason wasn't clear though.

Almost forgot,

The serum half-life of finasteride is 6 to 8 hours. Dutasteride has a serum half-life of approximately 4 weeks, and this long half-life was evident in the persistent suppression of DHT with the 0.5-mg and 2.5-mg doses after dutasteride treatment was stopped.

The Use of Dietary Supplements to Alleviate Androgen Deprivation Therapy Side Effects during Prostate Cancer Treatment
http://www.mdpi.com/2072-6643/6/10/4491/pdf


By George I think I've figured it out!, meaning a course for anti-androgen action.

Sorry (short on time), I'll fill in the details later, the study above will have some of the details, talk to you later.

(23-06-2015, 07:09 PM)Lotus Wrote: [ -> ]The Use of Dietary Supplements to Alleviate Androgen Deprivation Therapy Side Effects during Prostate Cancer Treatment
http://www.mdpi.com/2072-6643/6/10/4491/pdf


By George I think I've figured it out!, meaning a course for anti-androgen action.

Sorry (short on time), I'll fill in the details later, the study above will have some of the details, talk to you later.

Lotus ! Has a light turned on in ya brain ?

(23-06-2015, 09:41 PM)myboobs Wrote: [ -> ]

(23-06-2015, 07:09 PM)Lotus Wrote: [ -> ]The Use of Dietary Supplements to Alleviate Androgen Deprivation Therapy Side Effects during Prostate Cancer Treatment
http://www.mdpi.com/2072-6643/6/10/4491/pdf


By George I think I've figured it out!, meaning a course for anti-androgen action.

Sorry (short on time), I'll fill in the details later, the study above will have some of the details, talk to you later.

Lotus ! Has a light turned on in ya brain ?

Lol maybe,

How about this,

Inhibit LH (luteinizing hormone) using black cohosh (nbe) Goserelin (pharma)

Stimulate FSH (follicle stimulating hormone) E2 or red clover, *(essential fatty acids)

Inhibit DHT in the liver. (reishi inhibits serum DHT @ 80%) dutas @93%, finasteride @70% and saw palmetto inhibits DHT @ 32% (combo's possible).

Inhibit adrenal DHT (calmodulin -via the calcium/calmodulin/CaMK pathway) (spiro or licorice root)

Don't worry, I'm not suggesting an Orchiectomy.



[attachment=9789]

* I think future science will confirm that EFA's contribute to FSH synthesis (just my opinion, lol)

And quite possibly from Phospholipids

https://en.m.wikipedia.org/wiki/Phospholipid

This study found that more ER (estrogen receptors) subtypes are located in the butt as opposed to subcutaneous abdominal adipose tissue. (More research is needed to locate the missing ER subtypes for people wanting a bigger booty).




receptor subtypes alpha and beta in human adipose tissue: influences of adipose cell differentiation and fat depot localization.
Pedersen SB1, Bruun JM, Hube F, Kristensen K, Hauner H, Richelsen B.

Abstract
A novel ER-subtype, the ER-beta has recently been characterized in various tissues, furthermore five isoforms of the ER-beta are known (ER-beta1--ER-beta5). Using immunoblotting and real- time RT-PCR, ER-alpha and beta were studied in human adipose tissue. The expression of ER-alpha mRNA was equal in subcutaneous gluteal adipose tissue, subcutaneous abdominal and intra-abdominal adipose tissue, similar findings were obtained at the protein level. In contrast the amount of ER-beta1 (protein and mRNA) was significantly lower in intra-abdominal adipose tissue as compared with the subcutaneous adipose tissue (five-fold lower in women, P<0.005 and three-fold lower in men, P<0.005) whereas the expression of ER-beta4 and -beta5 mRNA isoforms were significantly higher in gluteal adipose tissue compared to subcutaneous abdominal adipose tissue. No significant gender differences in ER expression was detected in any of the fat depots investigated. During adipocyte differentiation the expression of ER-alpha, -beta4 and -beta5 mRNA declined, whereas, the expression of ER-beta1 mRNA was constant. In conclusion, the existence of ER-beta isoforms in human adipose tissue was demonstrated and the amount of these receptors was dependent upon fat depot localization, with much reduced expression of ER-beta1 in intra-abdominal adipose tissue compared to subcutaneous adipose tissue. These findings may indicate that estrogens could have differentiation and depot specific effects in human adipose tissue.

Here's a rather technical look at new a developing theory (estrogen secreted in male testes)
___________________________

Sertoli cells synthesize estradiol 17b from testosterone, and when testosterone is introduced with FSH (Follicle-stimulating hormone) it produced a 12 fold increase in E2 synthesis. And is markedly increase when cAMP (Cyclic adenosine monophosphate) is also added. Estrogen also triggers rapid activation of classical second messengers (cAMP, calcium, and inositol triphosphate). On another note, FSH and cAMP produce a 30 fold increase in aromatase, quite possibly making it the strongest aromatase.

Follicle-stimulating hormone stimulates estradiol-17f synthesis in cultured Sertoli cells. (testis/testosteronemetabolism/aromatizingenzyme/cyclicAMP/seminiferoustubules)
http://www.pnas.org/content/72/7/2677.full.pdf


Although aromatase level per adipose tissue fibroblast may be small, the sum of estrogen arising from billions of adipose tissue fibroblasts in the entire body makes a physiologic impact. The principal product of the ovary is the potent estrogen estradiol. In adipose tissue, estrogenically weak estrone is produced from androstenedione of adrenal origin in relatively large quantities. However, at least half of this peripherally produced estrone is eventually converted to estradiol in extraovarian tissues.

Molecular Bases and Phenotypic Determinants of Aromatase
http://downloads.hindawi.com/journals/ij...584807.pdf



Physiological regulation of aromatase expression. FSH induces aromatase expression via a cAMP-dependent pathway in ovarian granulosa cells via promoter II. SF-1 mediates this action of FSH. On the other hand, a combination of a glucocorticoid and a member of the class I cytokine family induces aromatase expression in skin and adipose tissue fibroblasts via promoter I.4 located 73 kb upstream of the coding region. Binding of STAT-3 and glucocorticoid receptor (GR) upstream of promoter I.4 mediates regulation of aromatase expression in these fibroblasts adipose tissue becomes the major aromatase-expressing body site after menopause

http://pharmrev.aspetjournals.org/conten....expansion

Lotus -

Your suggestions on anti-androgen combinations is very interesting. I am thinking of upping my game on this front.

I have looked unsuccessfully for recommendations for dosage levels for black cohosh and red clover.

For black cohosh, the labels often say something like "2.5% Triterpene Glycosides," but provide little additional information. Also, there has been a lot of commentary about potential liver damage from black cohosh, but I am not sure it is well documented.

Is 1,500 mg per day of red clover about right?

spanky

(28-06-2015, 12:06 PM)spanky Wrote: [ -> ]Lotus -

Your suggestions on anti-androgen combinations is very interesting. I am thinking of upping my game on this front.

I have looked unsuccessfully for recommendations for dosage levels for black cohosh and red clover.

For black cohosh, the labels often say something like "2.5% Triterpene Glycosides," but provide little additional information. Also, there has been a lot of commentary about potential liver damage from black cohosh, but I am not sure it is well documented.

Is 1,500 mg per day of red clover about right?

spanky

Hi spanky,

There's 2000 mg of red clover (2 ml/ 56 drops) in a extract form. And @ 400 mg in capsule form are taken (2) capsules 3x a day, or 2400 mg a day. Imo, 2000 mg is about right. It should be standardized for potency, same with black cohosh, I do remember the BC concerns and claims, the outcomes of those studies left more questions than answers. One (recent) study found that BC had no estrogenic properties. In fact they point out what makes BC effective with pre/post-menopause is that BC actually influences GABA A, and thru-opiate receptors. But, my own personal opinion is that 2 capsules of BC @ 45 mg each is what I would do. But I also believe BC has some link to GABA A and 5 alpha reductase, I'll have to post more on GABA, would you believe it has 11 subunits?, fascinating stuff.


Extracts of black cohosh are standardized to 26-deoxyactein content (erroneously reported in the scientific literature as 27-deoxyactein [2]), a member of a group of chemicals known as saponins. Commercially available preparations of black cohosh usually contain 1 mg of total triterpene saponins (expressed as 26-deoxyactein) in each 20-mg dose of extract. But black cohosh at 2.5% Triterpene Glycosides sounds pretty much standard.

http://ods.od.nih.gov/factsheets/BlackCo...fessional/

Black cohosh (Actaea racemosa, Cimicifuga racemosa) behaves as a mixed competitive ligand and partial agonist at the human mu opiate receptor

Abstract

Black cohosh is a commonly used botanical dietary supplement for the treatment of climacteric complaints. Since the opiate system in the brain is intimately associated with mood, temperature and sex hormonal levels, we investigated the activity of black cohosh extracts at the human μ opiate receptor (hMOR) expressed in Chinese hamster ovary cells. The 100% methanol-, 75% ethanol- and 40% 2-propanol- extracts of black cohosh effectively displaced the specific binding of [3H]DAMGO to hMOR. Further studies of the clinically used ethanol extract indicated that black cohosh acted as a mixed competitive ligand, displacing 77 ± 4% [3H]DAMGO to hMOR (Ki = 62.9 μg/ml). Using the [35S]GTPγS assay, the action of black cohosh was found to be consistent with an agonist, with an EC50 of 68.8 ± 7.7 μg/ml. These results demonstrate for the first time that black cohosh contains active principle(s) that activate hMOR, supporting its beneficial role in alleviating menopausal symptoms.

http://www.ncbi.nlm.nih.gov/pmc/articles...s61715.pdf

What interests me is androgen production rates, like how much DHT is produced, or where it's produced from (e.g. brain androgen, adrenal androgen, peripheral tissues, testes, ovaries, blood).

"When DHT formation is inhibited, the aromatization pathway of T to estradiol will prevail and induce a pronounced down-regulation of AR mRNA levels."

(11-03-2015, 02:21 AM)Lotus Wrote: [ -> ]

Steroid synthesis in intratumoral stromal and carcinoma cells and the potential sites at which flavones and isoflavones may inhibit the production of biologically active oestrogens. Androgens taken up by carcinoma cells include androstenedione and DHEA, the latter of which is converted to androstenedione by 3β-HSD1. Androstenedione is converted to oestrone by aromatase. Oestrone sulphate is converted to oestradiol by ETS and 17β-HSD.ETS, oestrogen sulfatase; EST, oestrogen sulfotransferase/SULT1E1; HSD, hydroxysteroid dehydrogenase.

Basically, it's stating flavones are anti-aromatase, while red clover is the on switch between 17 beta HSD and ER-a (estrogen receptor alpha, the growth receptor).

Black Cohosh-The weak estrogenlike effects of black cohosh suppressed increased luteinizing hormone secretion in menopausal women

In men, LH is also produced in the pituitary gland. LH binds to receptors in certain cells in the testes called Leydig cells. This leads to the release of testosterone, a hormone that is necessary for producing sperm cells. So I would think the BC is shutting the testes down by suppressing LH.

Thanks Lotus. Your sage advice is always appreciated.

I am thinking I will try black cohosh liquid extract, although I am not sure it is standardized, on the theory that liquid extract may carry less risk of causing liver damage than capsules. But then again, there may be no real difference in that regard.

I don't see a down-side for red clover, so will probably resume taking that as well.