[joanna_s]

Hi ladies!

I´ve been reading the endless threads about pros and cons of SP as an DHT blocker but instead of getting wiser I´m getting more end more confused.
Can you please explain me, what´s the benefit of using SP to reduce DHT if it works as an anti-estrogen at the same time. I´ve read a lot of other articles too, but the information is very controversial. Some say that when DHT gets lower, there´s more excess T to get converted to E which is a good thing for feminizing.

[Ethereal]

From my personal experience Reishi Mushroom and White Peony just work better. Sp from what I have read is anti-estrogenic so it kinda works against what you are trying to accomplish even though does limit conversion into dht. There is a big thread floating around here somewhere that goes into more detail about the information you are looking for.

[joanna_s]

What about spearmint? It´s said to have DHT lowering effect but does it have anti-estrogenic properties as well?

[Lotus]

What about spearmint? It´s said to have DHT lowering effect but does it have anti-estrogenic properties as well?

SP inhibits DHT @ 32% in the prostrate, while pharma AA's are 80 to 94%. Reishi is 80% inhibitor of DHT, that's significant.

Tissue effects of saw palmetto and finasteride: use of biopsy cores for in situ quantification of prostatic androgens.

Marks LS, Hess DL, Dorey FJ, Luz Macairan M, Cruz Santos PB, Tyler VE.
Urological Sciences Research Foundation, Culver City, California, USA.

OBJECTIVES:
To determine the effects of a saw palmetto herbal blend (SPHB) compared with finasteride on prostatic tissue androgen levels and to evaluate needle biopsies as a source of tissue for such determinations. METHODS: Prostate levels of testosterone and dihydrotestosterone (DHT) were measured on 5 to 10-mg biopsy specimens (18-gauge needle cores) in three groups of men with symptomatic benign prostatic hyperplasia: 15 men receiving chronic finasteride therapy versus 7 untreated controls; 4 men undergoing prostate adenomectomy to determine sampling variability (10 specimens each); and 40 men participating in a 6-month randomized trial of SPHB versus placebo, before and after treatment. RESULTS: Prostatic tissue DHT levels were found to be several times higher than the levels of testosterone (5.01 versus 1.51 ng/g), that ratio becoming reversed (1.05 versus 3.63 ng/g) with chronic finasteride therapy. The finasteride effect was statistically significant for both androgens (P <0.01), and little overlap of individual values between finasteride-treated and control patients was seen. In the randomized trial, tissue DHT levels were reduced by 32% from 6.49 to 4.40 ng/g in the SPHB group (P <0.005), with no significant change in the placebo group. CONCLUSIONS: For control versus finasteride-treated men, the tissue androgen values obtained with needle biopsy specimens were similar-both for absolute values and the percentage of change-to those previously reported using surgically excised volumes of prostatic tissue. The quantification of prostatic androgens by assay of needle biopsies is thus feasible and offers the possibility of serial studies in individual patients. The SPHB-induced suppression of prostatic DHT levels, modest but significant in a randomized trial, lends an element of support to the hypothesis that inhibition of the enzyme 5-alpha reductase is a mechanism of action of this substance.

Publication Types:
Clinical Trial
Randomized Controlled Trial

PMID: 11337315 [PubMed - indexed for MEDLINE]


(See a ton more info on AA's here)

Anti-Androgens
http://www.breastnexus.com/showthread.php?tid=17416

[Shae]

DHT is widely said to be an estrogen antagonist, so from that perspective blocking DHT can increase estrogen. I have read that SP is also an estrogen antagonist, but it is rarely mentioned and it appears (to me) that this is only a minor effect of SP compared to its effect of blocking DHT and thus increasing estrogen. In the end the net effect of SP seems to be to increase estrogen.

Also, estradiol is produced in part from testosterone. So when you use SP to block testosterone conversion to DHT, testosterone levels rise (because T is not being converted). So, from this perspective also, using SP to block DHT raises estrogen (only estradiol) levels.

See this chart :
http://www.keratin.com/az/androgenestrog...olism1.gif

The quote below is from
http://www.bodybuilding.com/fun/reform8.htm

"How does DHT protect against estrogen? There are at least three ways that this likely occurs. First of all, DHT directly inhibits estrogens activity on tissues. It either does this by acting as a competitive antagonist to the estrogen receptor or by decreasing estrogen-induced RNA transcription at a point subsequent to estrogen receptor binding.

"Second of all, DHT and its metabolites have been shown to directly block the production of estrogens from androgens by inhibiting the activity of the aromatase enzyme. The studies done in breast tissue showed that DHT, androsterone, and 5alpha-androstandione are potent inhibitors of the formation of estrone from androstenedione. 5alpha-androstandione was shown to be the most potent, while androsterone was the least.

"Lastly, DHT acts on the hypothalamus/pituitary to decrease the secretion of gonadotropins. By decreasing the secretion of gonadotropins you decrease the production of the raw materials for estrogen production testosterone and androstenedione (DHT itself cannot aromatize into estrogens). This property of DHT comes into particular utility when it is administered exogenously, and this is to be discussed in further detail in the next section."

[Lotus]

Research the BN forum, it provides answers. If you want slow growth stick with SP, if you note cellulite its from the fatty acids, the anti-estrogen in SP is also noted at inhibition of progesterone receptors, which makes it anti-estrogen......what in SP causes this?....answer provided in breast nexus. When I hear I can find it?, I laugh.......dig deeper.

[Lotus]

As I said, inside BN

The estrogenic DHT response, I wonder if we're seeing a possibility of any links to mammary DHT?. I mean, if we can explain it in normal function of the male reproductive tract and aquaporins what's the next logical step?, aromatase??, mammary DHT's???.

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.





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.





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

[Lotus]

.
Follow along please:

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.



Bottom line: there is solution to "this", (the potential breakthrough), I think somebody else can (should) provide the technology or key (besides myself). We shouldn't accept things at face value, never give up because someone suggests it's too difficult, or thst the answers don't exist.

[Shae]

Hey Lotus ... Would you be able to translate that in English, for those of us who don't speak biochemeese?

[Lotus]

Hey Lotus ... Would you be able to translate that in English, for those of us who don't speak biochemeese?

If we could reverse engineer DHT how would it look?, in other words, would you inhibit it up stream?........or influence its elimination?.