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BO Help needed

#21

Hi Pandora.


Let the white peony due it's thing, see WP (Paeoniflorin) provides an excellent pathway (the PI3K/Akt/mTOR signaling pathway) for mediating DHT.
https://www.breastnexum.com/showthread.php?tid=17436&pid=190765&highlight=alpha#pid190765


When DHT formation is inhibited, the aromatization pathway of T to estradiol will prevail and induce a pronounced down-regulation of AR mRNA levels.  DHT has the slimmest chance to aromatize to E2, primarily as and end product (bodily excretion..in urine). Catching DHT before it has a chance to synthesize offers a more favorable option for breast growth.

Also confirmed by a scientist (clelia, from Italy). 

(31-03-2015, 09:41 PM)-Clelia- Wrote:  lotus, you reported:
"Concentrations of aromatase and estradiol in the prostate are low, indicating that estradiol may not be the only estrogenic molecule to play a role in the prostate. It is known that DHT can be metabolized to 5alpha-androstane-3beta,17beta-diol (3beta-diol), a hormone that binds to ERbeta but not to AR. The concentration of 3beta-diol in prostate is much higher than that of estradiol. Based on the high concentration of 3beta-diol and since this metabolite is a physiological ERbeta ligand, we hypothesized that 3beta-diol would be involved in the regulation of ERbeta expression."

and that's fine, but... you know that this is not the case in male breast tissue, otherwise you should have breast growth like bio-female...in men there is more androgenic expression than the estrogenic one. Maybe estradiol is not the only estrogen, but the DHT metabolite "3-b-diol" isn't enough to gain breast growth in biomale breast tissue.
I think that DHT is not converted to the "estrogen-like metabolite" in the breast, at least not in the same amount as it is in the prostate.

So that's why i think that is better low DHT for breast growth


Lemon water can do that, re: stops andorgen production before its cleaved into CYP17a ( via the "steroidogenic enzyme pathway from cholesterol to active steroid hormones")....or even Lauric Acid (in coconut oil) inhibits Type I @ II 5 AR.


(22-02-2015, 07:53 PM)Lotus Wrote:  From an earlier post,

DHT has an estrogenic action,

The existence of this estrogenic DHT metabolite has raised the possibility that estradiol may not be the major estrogen in males [29]. For instance, in the prostate there  is a growing body of evidence that 3β-diol, acting through ERβ, may regulate important physiological events.


Recent data have shown that DHT may be converted into 5α-androstane- 3β-17β-diol (3β-diol) in a virtually irreversible reaction. Once considered inactive, 3β-diol is present in high concentrations in the male and indeed has biological activity. However, 3β-diol does not bind to the androgen receptor (AR), but rather to ERα and ERβ, with higher affinity for ERβ. Based upon these findings, we hypothesized that the modulation of AQP9 by DHT could be indirectly mediated by 3β-diol.

---------------------------

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1615873/


Effects of 3-beta-diol, an androgen metabolite with intrinsic estrogen-like effects,

Abstract

Background: Fluid homeostasis is critical for normal function of the male reproductive tract and aquaporins (AQP) play an important role in maintenance of this water and ion balance. Several AQPs have been identified in the male, but their regulation is not fully comprehended. Hormonal regulation of AQPs appears to be dependent on the steroid in the reproductive tract region. AQP9 displays unique hormonal regulation in the efferent ductules and epididymis, as it is regulated by both estrogen and dihydrotestosterone (DHT) in the efferent ductules, but only by DHT in the initial segment epididymis. Recent data have shown that a metabolite of DHT, 5-alpha- androstane-3-beta-17-beta-diol (3-beta-diol), once considered inactive, is also present in high concentrations in the male and indeed has biological activity. 3-beta-diol does not bind to the androgen receptor, but rather to estrogen receptors ER-alpha and ER-beta, with higher affinity for ER-beta. The existence of this estrogenic DHT metabolite has raised the possibility that estradiol may not be the only estrogen to play a major role in the male reproductive system. Considering that both ER-alpha and ER-beta are highly expressed in efferent ductules, we hypothesized that the DHT regulation of AQP9 could be due to the 3-beta-diol metabolite.

Methods: To test this hypothesis, adult male rats were submitted to surgical castration followed by estradiol, DHT or 3-beta-diol replacement. Changes in AQP9 expression in the efferent ductules were investigated by using immunohistochemistry and Western blotting assay.

Results: Data show that, after castration, AQP9 expression was significantly reduced in the efferent ductules. 3- beta-diol injections restored AQP9 expression, similar to DHT and estradiol. The results were confirmed by Western blotting assay.

Conclusion: This is the first evidence that 3-beta-diol has biological activity in the male reproductive tract and that this androgen metabolite has estrogen-like activity in the efferent ductules, whose major function is the reabsorption of luminal fluids.


[Image: attachment.php?aid=8694]


a) It has been shown that 3β-diol may have hormonal activity, not acting through the AR, but rather as a ligand for both ERα and ERβ.

b) 3β-diol has higher affinity for ERβ [31], which is abundant in the efferent ductule epithelium [40].

c) In human testis, the 3β-diol concentration is higher than DHT and estradiol [44,45]. It is reasonable to postulate that high concentrations of this metabolite may enter the lumen of efferent ductules.

d) The existence of this estrogenic DHT metabolite has raised the possibility that estradiol may not be the major estrogen in males [29]. For instance, in the prostate there  is a growing body of evidence that 3β-diol, acting through ERβ, may regulate important physiological events [26,28,32,46].

Also noteworthy is the fact that 3β-diol stimulates ERβ induced transcriptional activity equal to the cognate ligand estradiol, and the transcriptional selectivity of 3β-diol for ERβ is much greater than its binding selectivity [30,46]

 -----------------------------


Concentrations of aromatase and estradiol in the prostate are low, indicating that estradiol may not be the only estrogenic molecule to play a role in the prostate. It is known that DHT can be metabolized to 5alpha-androstane-3beta,17beta-diol (3beta-diol), a hormone that binds to ERbeta but not to AR. The concentration of 3beta-diol in prostate is much higher than that of estradiol. Based on the high concentration of 3beta-diol and since this metabolite is a physiological ERbeta ligand, we hypothesized that 3beta-diol would be involved in the regulation of ERbeta expression.


[Image: attachment.php?aid=8696]


An endocrine pathway in the prostate, ERbeta, AR, 5alpha-androstane-3beta,17beta-diol, and CYP7B1, regulates prostate growth.
http://www.ncbi.nlm.nih.gov/pubmed/12370428

[/quote]
Reply
#22

So, White Peony & Lemon Water are better AA options now?
Reply
#23

Thank you lotus. I will put that knowledge to good use. 

Happy New Year!!!!!!
Reply
#24

(26-12-2018, 05:59 AM)Lotus Wrote:  Hi Pandora.


Let the white peony due it's thing, see WP (Paeoniflorin) provides an excellent pathway (the PI3K/Akt/mTOR signaling pathway) for mediating DHT.
https://www.breastnexum.com/showthread.php?tid=17436&pid=190765&highlight=alpha#pid190765


When DHT formation is inhibited, the aromatization pathway of T to estradiol will prevail and induce a pronounced down-regulation of AR mRNA levels.  DHT has the slimmest chance to aromatize to E2, primarily as and end product (bodily excretion..in urine). Catching DHT before it has a chance to synthesize offers a more favorable option for breast growth.

Also confirmed by a scientist (clelia, from Italy). 

(31-03-2015, 09:41 PM)-Clelia- Wrote:  lotus, you reported:
"Concentrations of aromatase and estradiol in the prostate are low, indicating that estradiol may not be the only estrogenic molecule to play a role in the prostate. It is known that DHT can be metabolized to 5alpha-androstane-3beta,17beta-diol (3beta-diol), a hormone that binds to ERbeta but not to AR. The concentration of 3beta-diol in prostate is much higher than that of estradiol. Based on the high concentration of 3beta-diol and since this metabolite is a physiological ERbeta ligand, we hypothesized that 3beta-diol would be involved in the regulation of ERbeta expression."

and that's fine, but... you know that this is not the case in male breast tissue, otherwise you should have breast growth like bio-female...in men there is more androgenic expression than the estrogenic one. Maybe estradiol is not the only estrogen, but the DHT metabolite "3-b-diol" isn't enough to gain breast growth in biomale breast tissue.
I think that DHT is not converted to the "estrogen-like metabolite" in the breast, at least not in the same amount as it is in the prostate.

So that's why i think that is better low DHT for breast growth


Lemon water can do that, re: stops andorgen production before its cleaved into CYP17a ( via the "steroidogenic enzyme pathway from cholesterol to active steroid hormones")....or even Lauric Acid (in coconut oil) inhibits Type I @ II 5 AR.


(22-02-2015, 07:53 PM)Lotus Wrote:  From an earlier post,

DHT has an estrogenic action,

The existence of this estrogenic DHT metabolite has raised the possibility that estradiol may not be the major estrogen in males [29]. For instance, in the prostate there  is a growing body of evidence that 3β-diol, acting through ERβ, may regulate important physiological events.


Recent data have shown that DHT may be converted into 5α-androstane- 3β-17β-diol (3β-diol) in a virtually irreversible reaction. Once considered inactive, 3β-diol is present in high concentrations in the male and indeed has biological activity. However, 3β-diol does not bind to the androgen receptor (AR), but rather to ERα and ERβ, with higher affinity for ERβ. Based upon these findings, we hypothesized that the modulation of AQP9 by DHT could be indirectly mediated by 3β-diol.

---------------------------

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1615873/


Effects of 3-beta-diol, an androgen metabolite with intrinsic estrogen-like effects,

Abstract

Background: Fluid homeostasis is critical for normal function of the male reproductive tract and aquaporins (AQP) play an important role in maintenance of this water and ion balance. Several AQPs have been identified in the male, but their regulation is not fully comprehended. Hormonal regulation of AQPs appears to be dependent on the steroid in the reproductive tract region. AQP9 displays unique hormonal regulation in the efferent ductules and epididymis, as it is regulated by both estrogen and dihydrotestosterone (DHT) in the efferent ductules, but only by DHT in the initial segment epididymis. Recent data have shown that a metabolite of DHT, 5-alpha- androstane-3-beta-17-beta-diol (3-beta-diol), once considered inactive, is also present in high concentrations in the male and indeed has biological activity. 3-beta-diol does not bind to the androgen receptor, but rather to estrogen receptors ER-alpha and ER-beta, with higher affinity for ER-beta. The existence of this estrogenic DHT metabolite has raised the possibility that estradiol may not be the only estrogen to play a major role in the male reproductive system. Considering that both ER-alpha and ER-beta are highly expressed in efferent ductules, we hypothesized that the DHT regulation of AQP9 could be due to the 3-beta-diol metabolite.

Methods: To test this hypothesis, adult male rats were submitted to surgical castration followed by estradiol, DHT or 3-beta-diol replacement. Changes in AQP9 expression in the efferent ductules were investigated by using immunohistochemistry and Western blotting assay.

Results: Data show that, after castration, AQP9 expression was significantly reduced in the efferent ductules. 3- beta-diol injections restored AQP9 expression, similar to DHT and estradiol. The results were confirmed by Western blotting assay.

Conclusion: This is the first evidence that 3-beta-diol has biological activity in the male reproductive tract and that this androgen metabolite has estrogen-like activity in the efferent ductules, whose major function is the reabsorption of luminal fluids.


[Image: attachment.php?aid=8694]


a) It has been shown that 3β-diol may have hormonal activity, not acting through the AR, but rather as a ligand for both ERα and ERβ.

b) 3β-diol has higher affinity for ERβ [31], which is abundant in the efferent ductule epithelium [40].

c) In human testis, the 3β-diol concentration is higher than DHT and estradiol [44,45]. It is reasonable to postulate that high concentrations of this metabolite may enter the lumen of efferent ductules.

d) The existence of this estrogenic DHT metabolite has raised the possibility that estradiol may not be the major estrogen in males [29]. For instance, in the prostate there  is a growing body of evidence that 3β-diol, acting through ERβ, may regulate important physiological events [26,28,32,46].

Also noteworthy is the fact that 3β-diol stimulates ERβ induced transcriptional activity equal to the cognate ligand estradiol, and the transcriptional selectivity of 3β-diol for ERβ is much greater than its binding selectivity [30,46]

 -----------------------------


Concentrations of aromatase and estradiol in the prostate are low, indicating that estradiol may not be the only estrogenic molecule to play a role in the prostate. It is known that DHT can be metabolized to 5alpha-androstane-3beta,17beta-diol (3beta-diol), a hormone that binds to ERbeta but not to AR. The concentration of 3beta-diol in prostate is much higher than that of estradiol. Based on the high concentration of 3beta-diol and since this metabolite is a physiological ERbeta ligand, we hypothesized that 3beta-diol would be involved in the regulation of ERbeta expression.


[Image: attachment.php?aid=8696]


An endocrine pathway in the prostate, ERbeta, AR, 5alpha-androstane-3beta,17beta-diol, and CYP7B1, regulates prostate growth.
http://www.ncbi.nlm.nih.gov/pubmed/12370428
[/quote]

Hey Lotus I need to know is having almost no libido good for aromatise? The reason for asking is Vitex can really do a number on the body and well I barely have much of a real sex drive now. Plus I only feel BO working more on my lower part of my body but not much up around the chest and all.
Reply
#25

Quote:BeautifulBambi

 Hey Lotus I need to know is having almost no libido good for aromatise? The reason for asking is Vitex can really do a number on the body and well I barely have much of a real sex drive now. Plus I only feel BO working more on my lower part of my body but not much up around the chest and all.
I remember you saying you bought bovine ovary on Ebay. What are the expiration dates on them?
Reply
#26

(26-12-2018, 04:12 PM)Stevenator Wrote:  So, White Peony & Lemon Water are better AA options now?


Hi Stevenator, remember these posts?...WP (it should be standardized above 10%) inhibits DHT and prostate cancer cells and is pro-aromatase, lemon water stems from research posted below, green tea plus lemons is a good strategy too. Reishi is also a good choice imo.

Gut health is supremely the first step towards solid nbe/hrt plan...stary with a Neutral PH balance and then add a good probiotic, though if you take Metformin you shouldn't need the probiotic.
(19-04-2017, 02:39 PM)Lotus Wrote:  
(19-04-2017, 06:20 AM)Stevenator Wrote:  So what is the best way to take advantage of the CYP's ?

Here's a couple examples of foods explaining the P450 Cytochromes enzymes, the goal is to map out as much as we can. Ultimately in the future we'd know ahead of time what medicines works best/worst by a simple lab test. Maybe the costs will be lower with more competitors joining the market?.


(19-04-2017, 01:10 AM)Lotus Wrote:  
(15-01-2016, 12:38 AM)Lotus Wrote:  Here's another example of how interactions can happen, multiplying its effects. Say you drink green tea (a CYP17 inhibitor of testosterone). Now because you add piperine (in certain supplements, or added by supplementing) it increases the EGCG (polyphenols) in green tea by 1.3 fold.


J Nutr. 2004 Aug;134(8):1948-52.
Piperine enhances the bioavailability of the tea polyphenol (-)-epigallocatechin-3-gallate in mice.
Lambert JD1, Hong J, Kim DH, Mishin VM, Yang CS.
Author information
Abstract
(-)-Epigallocatechin-3-gallate (EGCG), from green tea (Camellia sinensis), has demonstrated chemopreventive activity in animal models of carcinogenesis. Previously, we reported the bioavailability of EGCG in rats (1.6%) and mice (26.5%). Here, we report that cotreatment with a second dietary component, piperine (from black pepper), enhanced the bioavailability of EGCG in mice. Intragastric coadministration of 163.8 micromol/kg EGCG and 70.2 micromol/kg piperine to male CF-1 mice increased the plasma C(max) and area under the curve (AUC) by 1.3-fold compared to mice treated with EGCG only. Piperine appeared to increase EGCG bioavailability by inhibiting glucuronidation and gastrointestinal transit. Piperine (100 micromol/L) inhibited EGCG glucuronidation in mouse small intestine (by 40%) but not in hepatic microsomes. Piperine (20 micromol/L) also inhibited production of EGCG-3"-glucuronide in human HT-29 colon adenocarcinoma cells. Small intestinal EGCG levels in CF-1 mice following treatment with EGCG alone had a C(max) = 37.50 +/- 22.50 nmol/g at 60 min that then decreased to 5.14 +/- 1.65 nmol/g at 90 min; however, cotreatment with piperine resulted in a C(max) = 31.60 +/- 15.08 nmol/g at 90 min, and levels were maintained above 20 nmol/g until 180 min. This resulted in a significant increase in the small intestine EGCG AUC (4621.80 +/- 1958.72 vs. 1686.50 +/- 757.07 (nmol/g.min)). EGCG appearance in the colon and the feces of piperine-cotreated mice was slower than in mice treated with EGCG alone. The present study demonstrates the modulation of the EGCG bioavailablity by a second dietary component and illustrates a mechanism for interactions between dietary chemicals.

http://www.ncbi.nlm.nih.gov/pubmed?filters=&orig_db=PubMed&cmd=Search&term=134%2A%5Bvolume%5D%20AND%201948%5Bpage%5D%20AND%202004%5Bpdat%5D%20AND%20Lambert%20JD%5Bauth%5D

(09-01-2016, 04:52 AM)Lotus Wrote:  Hi BN,

Here's another idea to try..........." citrus for breast growth ". These enzymes C(17,20)-lyase  cyp 17, cyp 19, cyp 3A4 have direct pathways to breast/androgen synthesis. Cyp 3A4 controls more than 50% of how drugs are metabolized (I'd say that's a major regulator to piggy back off of), the only issue there is mapping out all these key regulators, (like mapping out the genome).


Example: star fruit inhibits CY3A, more potent than grapefruit,(as stated above inhibiting CY3A4 will help with breast growth).


Potent inhibition by star fruit of human cytochrome P450 3A (CYP3A) activity.
Hidaka M1, Fujita K, Ogikubo T, Yamasaki K, Iwakir

(05-01-2016, 08:36 AM)Lotus Wrote:  The C(17,20)-lyase...controls 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.
[Image: attachment.php?aid=11060]



Effect of paeoniflorin, glycyrrhizin and glycyrrhetic acid on ovarian androgen production. - 
https://www.ncbi.nlm.nih.gov/m/pubmed/1897494/z
Reply
#27

(27-12-2018, 12:09 AM)Pandora56 Wrote:  Thank you lotus. I will put that knowledge to good use. 

Happy New Year!!!!!!

You're welcome, Happy New Year too.
Reply
#28

(27-12-2018, 03:57 AM)BeautifulBambi Wrote:  Hey Lotus I need to know is having almost no libido good for aromatise? The reason for asking is Vitex can really do a number on the body and well I barely have much of a real sex drive now. Plus I only feel BO working more on my lower part of my body but not much up around the chest and all.

Hi BB, zero sex drive tells me T is low, a blood test would tell us how low. Are you taking vitex and BO together?...if so I'd drop the vitex asap and see if that starts a growth phase upstairs. The science behind aromatase is when DHT is inhibited the pathway for aromatase is much easier...T converts to E2 by way of aromatase, which makes T a regulator of aromatase, no libido (imo) is an indicator aromatase is working.

GL
Reply
#29

I do, Lotus. I just thought you liked RR better than WP. 
I’ll look into a probiotic. A guy at work is trying to get me 
to take one. Is there a brand you recommend? I switched 
to BO two months ago. The first few weeks were like a 
rocket ride, but things have settled down. I love the stuff, 
but have stalled with growth. I might add an AA, but within 
the next two months I hope to own a Schwinn Air Dyne 
exercise bike. I’m really looking forward to it. Thx
Reply
#30

(28-12-2018, 05:55 AM)Stevenator Wrote:  I do, Lotus. I just thought you liked RR better than WP. 
I’ll look into a probiotic. A guy at work is trying to get me 
to take one. Is there a brand you recommend? I switched 
to BO two months ago. The first few weeks were like a 
rocket ride, but things have settled down. I love the stuff, 
but have stalled with growth. I might add an AA, but within 
the next two months I hope to own a Schwinn Air Dyne 
exercise bike. I’m really looking forward to it. Thx

I love your avatar, btw. HaHa
Reply



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