[-Clelia-]

hi, i think the main difference between male and female is in the AR receptor number in breast tissue. Also, hormones play another important role. What is fondamental to development are the ratios: AR/ER, androgen/estrogen. The higher are those numbers, the smaller is your breast

[-Clelia-]

sorry lotus, i know you had more questions, but i have to go now. Moreover my laptop stuck, after opening about 20windows... I shut down and i will go on tomorrow. Bye

[The First Aria]

hi, i think the main difference between male and female is in the AR receptor number in breast tissue. Also, hormones play another important role. What is fondamental to development are the ratios: AR/ER, androgen/estrogen. The higher are those numbers, the smaller is your breast

Then why are some of us males, able to get DD size breast's then, while men on mtf are sometimes lucky to get B's? I think it has more to do with your basic genetic makeup. Like, were you developing as a female or male in the womb.

[Lotus]

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

Hi Clelia,

Thanks for the excellent info, now this is telling........I do have a hypothesis of my own too.

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.

a hypothetical about DHT, (but first), for the longest time I thought DHT had no usable purpose in terms of breast growth. Now, we discover it has a back door useable metabolite in the prostate and Sertoli cells. So....then, is it yet to be discovered that DHT in breast tissue "can" in fact....have the usable ER-beta metabolite??.....that is my hypothetical, I see you think perhaps the same is true.

We've just opened a whole can of worms.......imo it's the gummi type (yum yum).

sorry about that :-/ i'm not mothertongue

No problem, Io capisco perfettamente,

Sorry, but I've have 4-5 research papers just related to our discussion that I'll share next.

[Lotus]

Moreover, there is 35% of population that has not the enzimatic process which converts and activate genisteine and daidzeine (they both need to cut off the glycone, to be active), this occurs in the gut.

Ok thanks, (please see related source below).

sorry, i was wrong, the correct pathway is: 35% of population can convert daidzein and genistein to the active compound "equol".
(glycone is cut off by everyone, i think)
i'm sorry but the source is in italian, i didnt find it yet in english:
http://www.iss.it/binary/cnra/cont/ALIME...270810.pdf
(page 18)

The source looks very interesting, sorry....I suck at translations

"What's also interesting is how upon excertion steroids are water soluble"-->
mmh... why do you want to know that? for transport?

Yes exactly, (for transport), ion channels are the access of cell diffusion correct?, assuming carrier proteins are the vehicles to mitochondria, what keeps the channels open long enough expression?, I see its from 1/100 hundredth to 1/1000 thousands of seconds, could this explain partial binding?.


Comparative effects of R- and S-equol and implication of transactivation functions (AF-1 and AF-2) in estrogen receptor-induced transcriptional activity.

Abstract
Equol, one of the main metabolites of daidzein, is a chiral compound with pleiotropic effects on cellular signaling. This property may induce activation/inhibition of the estrogen receptors (ER) a or b, and therefore, explain the beneficial/deleterious effects of equol on estrogen-dependent diseases. With its asymmetric centre at position C-3, equol can exist in two enantiomeric forms (R- and S-equol). To elucidate the yet unclear mechanisms of ER activation/inhibition by equol, we performed a comprehensive analysis of ERa and ERb transactivation by racemic equol, as well as by enantiomerically pure forms. Racemic equol was prepared by catalytic hydrogenation from daidzein and separated into enantiomers by chiral HPLC. The configuration assignment was performed by optical rotatory power measurements. The ER-induced transactivation by R- and S-equol (0.1-10 µM) and 17b-estradiol (E2, 10 nM) was studied using transient transfections of ERα and ERβ in CHO, HepG2 and HeLa cell lines. R- and S-equol induce ER transactivation in an opposite fashion according to the cellular context. R-equol and S-equol are more potent in inducing ERα in an AF-2 and AF-1 permissive cell line, respectively. Involvement of ERα transactivation functions (AF-1 and AF-2) in these effects has been examined. Both AF-1 and AF-2 are involved in racemic equol, R-equol and S-equol induced ERα transcriptional activity. These results could be of interest to find a specific ligand modulating ER transactivation and could contribute to explaining the diversity of equol actions in vivo.

[Lotus]

O.k., I am no scientist, but here is a wild thought. Could the membranes in female breast's be somewhat different than their brother's?? Maybe the xy combo chromosome double locks the male breast somehow?? Or at the least makes it less permeable to Estradol expression or straight out E in all forms?????

iaboy, I like Clelia's explaination, what's weird is that I tried to address/explain the exact cause (or, lack of cause) for why the breast growth response is individually diverse. And.....well.....you know me to go over board with info. but...here's my .02 cents worth.

hi, i think the main difference between male and female is in the AR receptor number in breast tissue. Also, hormones play another important role. What is fondamental to development are the ratios: AR/ER, androgen/estrogen. The higher are those numbers, the smaller is your breast

Out of interest, would they have been markedly different on an HRT regimen, do you think? (Not that I propose to follow one).

It's hard to say. What is interesting is when PM gets carried over to hrt from nbe. The two receptor proteins (alpha and beta) are well documented, the relationship between NBE, HRT, Breast Cancer is somewhat tied together, and explains how/why growth is mediated.

Role of receptor complexes in the extranuclear actions of estrogen receptor a in breast cancer
http://erc.endocrinology-journals.org/co...3.full.pdf


We've seen folks on hrt return to nbe, and then go back on hrt. Receptor mediated growth (or lack thereof) explains quite a bit. For instance (and this will sound crazy) you've heard the term "they have good genes, or the good genes passed on, etc etc, its quite possible and directly related to the amount of breast growth genes (per this example), imo it best describes the relationship between small breasted to large breasted women ( put men in this group too, since we have the same receptors).

I tend to look at how these proteins (enzymes) are structured, meaning what influences the binding process, e.g. protein kinase or the phosphorylation of proteins, PPK, TNF receptor family, cAMP, caveolin, with signaling proteins, G-proteins, Src-like kinases, I mean the list goes on and on.

Tap into signaling pathways (intracellular) or.... what inhibits cells migration ..... LBD (ligand binding domain) which is mediated somewhere @ 66% of ER-a domain and the doors start opening for breast growth......well....that's certainly my opinion. All the research is there, it's just interpreting into language humans can understand, easy right?.

Now Clelia is here to help interpret (lol, translate) right Clelia.

[Lotus]

Oh yeah ......you know I'll want to talk about this research studies , their just screaming "hey I'm here, read me" ......solve me......

Structure, function and tissue-specific gene expression of 3β-hydroxysteroid dehydrogenase/5-ene-4-ene isomerase enzymes in classical and peripheral intracrine steroidogenic tissues.
________________________________________
data indicate that the presence of multiple 3β-HSD isoenzymes offers the possibility of tissue-specific expression and regulation of this enzymatic activity that plays an essential role in the biosynthesis of all hormonal steroids in classical as well as peripheral intracrine steroidogenic tissues.

http://www.ncbi.nlm.nih.gov/pubmed/22217825

Bovine adrenal 3beta-hydroxysteroid dehydrogenase (E.C. 1.1.1. 145)/5-ene-4-ene isomerase (E.C. 5.3.3.1): characterization and its inhibition by isoflavones.
____________________________________________
The isoflavones daidzein, genistein, biochanin A and formononetin inhibit potently and preferentially the gamma-isozymes of mammalian alcohol dehydrogenase (gammagamma-ADH), the only ADH isozyme that catalyzes the oxidation of 3beta-hydroxysteroids. Based on these results, we proposed that these isoflavones might also act on other enzymes involved in 3beta-hydroxysteroid metabolism. Recently, we showed that they indeed are potent inhibitors of a bacterial beta-hydroxysteroid dehydrogenase (beta-HSD). To extend this finding to the mammalian systems, we hereby purified, characterized and studied the effects of isoflavones and structurally related compounds on, a bovine adrenal 3beta-hydroxysteroid dehydrogenase (3beta-HSD). This enzyme catalyzes the oxidation of 3beta-hydroxysteroids but not 3alpha-, 11beta- or 17beta-hydroxysteroids. The same enzyme also catalyzes 5-ene-4-ene isomerization, converting 5-pregnen 3, 20-dione to progesterone. The K(m) values of its dehydrogenase activity determined for a list of 3beta-hydroxysteroid substrates are similar (1 to 2 microM) and that of its isomerase activity, determined with 5-pregnen 3, 20-dione as a substrate, is 10 microM. The k(cat) value determined for its isomerase activity (18.2 min(-1)) is also higher than that for its dehydrogenase activity (1.4-2.4 min(-1)). A survey of more than 30 isoflavones and structurally related compounds revealed that daidzein, genistein, biochanin A and formononetin inhibit both the dehydrogenase and isomerase activity of this enzyme. Inhibition is potent and concentration dependent. IC(50) values determined for these compounds range from 0.4 to 11 microM, within the plasma and urine concentration ranges of daidzein and genistein of individuals on vegetarian diet or semi-vegetarian diet. These results suggest that dietary isoflavones may exert their biological effects by inhibiting the action of 3beta-HSD, a key enzyme of neurosteroid and/or steroid hormone biosynthesis.
http://www.ncbi.nlm.nih.gov/pubmed/10704908

estrogenic isoflavones are potent inhibitors of beta-hydroxysteroid dehydrogenase of P. testosteronii.
___________________________________________
The isoflavones daidzein, genistein, biochanin A and formononetin selectively inhibit the gamma-isozymes of mammalian alcohol dehydrogenase (ADH). Since gamma-ADH is the only ADH isoform that catalyzes 3 beta-hydroxysteroid oxidation, it was conjectured that these isoflavones might also inhibit other enzymes involved in 3 beta-hydroxysteroid metabolism. P. testosteronii beta-hydroxysteroid dehydrogenase (beta-HSD) was used to evaluate this hypothesis. Indeed, all isoflavones that inhibit gamma-ADH were found to be potent inhibitors of beta-HSD. Both the 3 beta- and 17 beta-HSD activities of the enzyme are inhibited. Kinetic analyses with pregnenolone (3-beta-OH) and testosterone (17-beta-OH) as substrates reveal that daidzein and genistein inhibit beta-HSD competitively with respect to the sterol substrates. Their Ki values are very similar and range from 0.013 to 0.02 microM. These results suggest that isoflavones may exert some of their biological effects by modulating activities of enzymes that metabolize steroids critical to hormonal and/or neuronal functions.
http://www.ncbi.nlm.nih.gov/pubmed/7488041#

[-Clelia-]

mmh... i never liked soy, imo is not a healthy food. Maybe there is some advantage for some people (after menopause, or before to low breast cancer risk), but I dont like the way it interferes in the brain.
That's just my opinion.
I will attach a study about food and phytoestrogen content. Soy is the highest source of genistein and daidzein.
With your findings, you should be carefull for prostate risk. Because those compounds exert antiestrogenic effect in 2 ways: occupying er receptor, giving weak or no response, and also 3b-diol is inhibited. Now i see how asian women (high soy consumer) have the smallest breast average in the world, and lower cancer risk in young women

[-Clelia-]

google: Phytoestrogen Content of Foods Consumed in Canada, Including
Isoflavones, Lignans, and Coumestan

Lilian U. Thompson, Beatrice A. Boucher, Zhen Liu, Michelle Cotterchio, and Nancy Kreiger

[-Clelia-]

O.k., I am no scientist, but here is a wild thought. Could the membranes in female breast's be somewhat different than their brother's?? Maybe the xy combo chromosome double locks the male breast somehow?? Or at the least makes it less permeable to Estradol expression or straight out E in all forms?????

iaboy, I like Clelia's explaination, what's weird is that I tried to address/explain the exact cause (or, lack of cause) for why the breast growth response is individually diverse. And.....well.....you know me to go over board with info. but...here's my .02 cents worth.

hi, i think the main difference between male and female is in the AR receptor number in breast tissue. Also, hormones play another important role. What is fondamental to development are the ratios: AR/ER, androgen/estrogen. The higher are those numbers, the smaller is your breast

Out of interest, would they have been markedly different on an HRT regimen, do you think? (Not that I propose to follow one).

It's hard to say. What is interesting is when PM gets carried over to hrt from nbe. The two receptor proteins (alpha and beta) are well documented, the relationship between NBE, HRT, Breast Cancer is somewhat tied together, and explains how/why growth is mediated.

Role of receptor complexes in the extranuclear actions of estrogen receptor a in breast cancer
http://erc.endocrinology-journals.org/co...3.full.pdf


We've seen folks on hrt return to nbe, and then go back on hrt. Receptor mediated growth (or lack thereof) explains quite a bit. For instance (and this will sound crazy) you've heard the term "they have good genes, or the good genes passed on, etc etc, its quite possible and directly related to the amount of breast growth genes (per this example), imo it best describes the relationship between small breasted to large breasted women ( put men in this group too, since we have the same receptors).

I tend to look at how these proteins (enzymes) are structured, meaning what influences the binding process, e.g. protein kinase or the phosphorylation of proteins, PPK, TNF receptor family, cAMP, caveolin, with signaling proteins, G-proteins, Src-like kinases, I mean the list goes on and on.

Tap into signaling pathways (intracellular) or.... what inhibits cells migration ..... LBD (ligand binding domain) which is mediated somewhere @ 66% of ER-a domain and the doors start opening for breast growth......well....that's certainly my opinion. All the research is there, it's just interpreting into language humans can understand, easy right?.

Now Clelia is here to help interpret (lol, translate) right Clelia.

ouch..!
yes, I think, different sizes obtained with NBE can be explained:
the same followed program is good for some, and not the best for others, for physiological differences (different receptor response, different signallin pathways, different number of total hormone receptor, and different amount of circulating hormones)