[stefanie_s]

Hey Lotus, if you would be so kind, I thought I would go to the expert.  Progesterone yes or no?  What does it do for someone on PM? Over the counter or prescription?  Your choice of brand?  Is it safe?  I keep hearing stories of strokes.  Please help, thank you!

[Lotus]

Hey Lotus, if you would be so kind, I thought I would go to the expert.  Progesterone yes or no?  What does it do for someone on PM? Over the counter or prescription?  Your choice of brand?  Is it safe?  I keep hearing stories of strokes.  Please help, thank you!

Agreed, some information about progesterone is contradictory, and even biased towards the use of progesterone in TG's. Nonetheless, if one pushes past the disinformation then things become a bit clearer....that's how I make sense of it fwiw. 

From my experience PC (progesterone cream) worked...or continues to work, though I've used different combinations of PC too. Some new research I came across shows progesterone plus prolactin increases breast growth some 400% over using just straight E2, though PM will be at a much lower percentage over E2.

Other studies point out the combination of E2 plus progesterone increases breast growth over single use therapy.....such as estradiol or progesterone used separately. 

In some new experiments I'm using MSM cream plus PC...plus vitamin D3...plus an oral H2 antagonist (aka cimetidine) which promotes prolactin (PRL) in gastrin (stomach acid) with promising results. And in even more promising news I've have broken down most enzymes that promote certain pathways for breast growth....and when to use them as it relates to the daily dinural cylces, time permitting lol I'd like to finish asap,,,,though IRL things don't always work they way we'd like.  


My own PC brand preference is called smoky mountain parabren-free progesterone cream .....about $17.00 (amazon), its mild imo. I'll apply to breasts where I think it does the most benefit (including fighting breast cancer)....w/PM and possibly WP and or Reishi pairs well. Though PC fights DHT very well by itself, of course individual results will vary as a rule of thumb.

[stefanie_s]

Lotus:
I saw this review on Amazon's site.  Says in men, lowers E and increases T??  Is that right?  How much should I take?

Verified Purchase

My wife was showing symptoms of low progesterone so I thought for 15 dollars it's worth a shot. Being very scientifically minded and protective I had to use it first to look for adverse effects. I had to end up doing research on males and progesterone and I came to find that it lowers estrogen in both men and women to proper levels and in males tends to act more like testosterone. It even has success in treating gynocomastia (man boobs). I would suggest a man only use half of the recomended dose 2 weeks on 2 weeks off.

[Lotus]

Lotus:
I saw this review on Amazon's site.  Says in men, lowers E and increases T??  Is that right?  How much should I take?

Verified Purchase

My wife was showing symptoms of low progesterone so I thought for 15 dollars it's worth a shot. Being very scientifically minded and protective I had to use it first to look for adverse effects. I had to end up doing research on males and progesterone and I came to find that it lowers estrogen in both men and women to proper levels and in males tends to act more like testosterone. It even has success in treating gynocomastia (man boobs). I would suggest a man only use half of the recomended dose 2 weeks on 2 weeks off.

In my opinion this isn't the case (the above product reviews) , progesterone is a precursor for androgens and estrogens, so they (hormone precursors) can be manipulated to perform the way we'd like them to behave (or synthesize). When genetic males alter their horomones to grow breasts we fundamentally change our DNA to reflect (or resemble) menopausal women....after a certain period of time. Progesterone resets estrogen receptors to almost original order, which is part of the reason females take PC....to re-establish order of estrogen sensitivity. Progesterone also inhibits DHT....in men and women....which can change the ratio to make more estrogen via inhibiting 5 alpha reductase. I'll read product reviews too before buying, but I don't base my sole decision on what is being said, and without listing science to what a person stated it holds little weight in my book. On a personal note about PC plus PM...I've used PC for close to 5 years and believe what it does (promotes breast growth), and during that time I've never lost breast tissue. In fact I list a MTF study that found when progesterone was used with HRT it grew more breast tissue than HRT only (verified from biopsied breast tissue). The following information explains more about using progesterone, I have much more on PC and progesterone (scientific posts) listed in my program thread, just use the search function using progesterone. How much to use (or needed) is however much PC is needed to cover all the breast.

I posted a few studies that introduced prolactin and E2 simultaneously, which they worked synergistically (what a mouthful lol). The same is held true about introducing progesterone and E2. 

And for that reason it (imo) explains the essence of how the combo birth control works, (2 hormone release). 

In terms of a cycle its best to gain back stability, the fatigue is (can be) from an increase in prolactin. 

There's other ways (things) to make add-ons but I wouldn't until you get PRL in order, first. 

Progesterone and estrogen E2 (together) in-quote-"induced proliferation that resulted in sidebranching and alveologenesis," but E+P treatment produced more proliferation sooner and extensive sidebranching and alveologenesis. The exact amounts of E2 (estradiol) and progesterone weren't given. In other words having progesterone combined with E2 produces side-branching of the breasts (outward growth), 

function of progesterone receptor isoforms in normal adult mouse mammary gland.
Aupperlee MD1, Haslam SZ.
Author information
Abstract
In normal mouse mammary gland, the mitogenic action of progesterone (P) is mediated by two P receptor (PR) isoforms, PRA and PRB. PRA is predominantly expressed in the adult virgin, and PRB is predominantly expressed during pregnancy. To investigate hormonal regulation of PR isoform expression and isoform-specific functions in vivo, adult ovariectomized BALB/c mice were treated for 3, 5, or 10 d with estrogen (E), P, or estrogen plus progesterone (E+P). Using an immunohistochemical approach with isoform-specific antibodies, we investigated hormonal regulation of PRA and PRB and their functional roles in proliferation and morphogenesis. Significant E-induced proliferation was only observed after 5 d at the distal tips of ducts; there was no sidebranching or alveologenesis. P induced proliferation that resulted in sidebranching and alveologenesis, but E+P treatment produced more proliferation sooner and more extensive sidebranching and alveologenesis. PRA levels were increased by E and decreased by P. Increased PRB levels were induced by treatment with P or E+P and coincided with the formation of alveoli. PRA was the predominant PR isoform expressed during sidebranching, and colocalization of PRA with 5-bromo-2'-deoxyuridine revealed that proliferation of PRA-positive and -negative cells was responsible for P-induced sidebranching. PRB was the predominant PR isoform expressed during alveologenesis, and colocalization of PRB with 5-bromo-2'-deoxyuridine showed that both PRB-positive and -negative cells proliferated during alveolar expansion. These results demonstrate different hormonal regulation of PRA and PRB levels in vivo and suggest that P can induce proliferation through either PRA or PRB via direct and paracrine mechanisms.
http://www.ncbi.nlm.nih.gov/pubmed?filters=&orig_db=PubMed&cmd=Search&term=148%2A%5Bvolume%5D%20AND%202290%5Bpage%5D%20AND%202007%5Bpdat%5D%20AND%20Aupperlee%20MD%5Bauth%5D

Prolactin stimulates breast growth in the presence of high estrogens, progesterone and estrogen stimulate growth too, and from what I've seen (still needs to be verified)  pharma progestins up-regulate IGF-1. However, imo peptides look very promising. 


Hormone-Dependent Mammary Gland Development

Hormone-dependent mammary gland development occurs after puberty and results in ductal elongation; recurrent estrous cycles in adulthood trigger side branching; pregnancy enhances side branching and induces alveolo-genesis with lactational differentiation followed by involution at weaning (Brisken 2002). In the late fifties, a series of experiments defined the minimal hormonal requirements for mammary gland development in mice (Nandi 1958) and rats (Lyons 1958). Endocrine ablation was achieved by surgically removing the major sources of reproductive hormones from mature females, the ovaries, which secrete estrogens and progesterone, the pituitary gland, a major source of growth hormone (GH) and prolactin (Prl), and for some experiments the adrenal glands, which release cortisol and precursors of sex steroids (see Fig. 1). Hormone replacement in hormone-deprived animals established that additive and sequential treatment with 17-b-estradiol, progesterone, and prolactin in conjunction with cortisol and GH can recapitulate mammary gland development.

 http://www.ncbi.nlm.nih.gov/pmc/articles...003178.pdf

I almost forgot, I have this one of kind study (2006?) on mtf's that proved progesterone and E2 promoted tissue growth, I'll put it up asap, (when I find it lol). 

The study was from 2000, not '06.

Short-term and long-term histologic effects of castration and estrogen treatment on breast tissue of 14 male-to-female transsexuals in comparison with two chemically castrated men.
Kanhai RC1, Hage JJ, van Diest PJ, Bloemena E, Mulder JW.
Author information
Abstract
The histologic changes induced in the mammary gland of male-to-female transsexuals have not yet been reported in the literature. We studied the histologic changes induced by chemical and surgical castration and estrogen therapy in the breasts of 14 such patients, with particular reference to acinar and lobular formation. To objectify the influence of cross-sex treatment, the histologic findings were compared with those in two men treated hormonally for prostate cancer. The slight increase in the plasma estrogen-to-androgen ratio seen in idiopathic gynecomastia usually does not induce acinar and lobular formation in the male breast. In men treated with nonprogestative antiandrogens for prostate cancer, only moderate acinar and lobular formation occurs. Only in male-to-female transsexuals in whom progestative chemical castration is combined with feminizing estrogen therapy will full acinar and lobular formation occur with hormonally stimulated nuclei and pseudolactational changes. Hence, combined progestative antiandrogens and estrogens are necessary for genetically male breast tissue to mimic the natural histology of the female breast. Orchidectomy does not contribute to this. Apocrine metaplasia may occur in breasts of male-to-female transsexuals, but so far, only four cases of breast cancer in male-to-female transsexuals have been documented.

Here's the full paper, or view the PDF as listed on the site. 
http://journals.lww.com/ajsp/Fulltext/20..._of.9.aspx

Interesting this..about P.

''Your breasts needs progesterone as well as estrogen to grow. It is progesterone that activates estrogen receptors so that estrogen can bind to them. Progesterone is also the hormone responsible for building up fat stores in the breast.''

Absolutely true, the combined therapy is like a bio-directional response, for instance free T (the bio-active T) decreases by two-fold by the combined E and progesterone. 

The effect of combined oral contraception on testosterone levels in healthy women: a systematic review and meta-analysis.
http://www.ncbi.nlm.nih.gov/pubmed/24082040

The current literature review and meta-analysis demonstrates that COCs decrease circulating levels of total T and free T and increase SBHG concentrations. Due to the SHBG increase, free T levels decrease twice as much as total T. The estrogen dose and progestin type of the COC do not influence the decline of total and free T, but both affect SHBG. The clinical implications of suppressed androgen levels during COC use remain to be elucidated.

Another similar study states a higher result from staggering dosages (orally). Imo this suggests a cyclic approach to lower androgens. Which btw androstenedione is the androgen culprit in GG's........not DHT. 

contraceptives containing ethinylestradiol and gestodene or norgestimate upon androgen parameters and serum binding proteins.

Abstract
The effect of a triphasic oral contraceptive containing ethinylestradiol and gestodene (EE/GSD) on various serum hormonal parameters was compared with that of a monophasic formulation containing 35 micrograms ethinylestradiol and 250 micrograms norgestimate (EE/NGM). Blood samples were collected from 46 women on days 2, 11, and 21 of the preceding control cycle and of the third, sixth and twelfth treatment cycle. There was no significant difference in the influence on any hormonal parameter between both formulations. Both EE/GSD and EE/NGM caused a time-dependent suppression of serum dehydroepiandrosterone sulphate (DHEA-S) by 20-30% (p < 0.01) and a reduction of 5 alpha-androstane-3 alpha, 17 beta-diol glucuronide by 50-60% (p < 0.01) during each treatment cycle, while androstenedione levels were reduced by 25% (p < 0.01). There was also a significant decrease in the levels of total testosterone by 30-35% (p < 0.01) and free testosterone by 60% (p < 0.01), while sex hormone-binding globulin (SHBG) was increased by 200-240% on days 11 and 21 (p < 0.01). During the pill-free interval the SHBG levels were reduced to a certain degree but remained elevated by 100% as compared to the pretreatment values. The serum levels of corticosteroid-binding globulin (CBG) which is known to be influenced only by the estrogenic component of combination pills, increased significantly by 170% (p < 0.01) during each treatment cycle. During the pill-free interval of 7 days, the CBG levels decreased but were still elevated by 90-100% as compared to the control cycle. Similarly, the serum levels of cortisol were significantly elevated by 110-140% (p < 0.01) during treatment with both preparations. The results demonstrate a profound suppression of androgen levels and peripheral androgen metabolism.

[stefanie_s]

Lotus:
I saw this review on Amazon's site.  Says in men, lowers E and increases T??  Is that right?  How much should I take?

Verified Purchase

My wife was showing symptoms of low progesterone so I thought for 15 dollars it's worth a shot. Being very scientifically minded and protective I had to use it first to look for adverse effects. I had to end up doing research on males and progesterone and I came to find that it lowers estrogen in both men and women to proper levels and in males tends to act more like testosterone. It even has success in treating gynocomastia (man boobs). I would suggest a man only use half of the recomended dose 2 weeks on 2 weeks off.

In my opinion this isn't the case (the above product reviews) , progesterone is a precursor for androgens and estrogens, so they (hormone precursors) can be manipulated to perform the way we'd like them to behave (or synthesize). When genetic males alter their horomones to grow breasts we fundamentally change our DNA to reflect (or resemble) menopausal women....after a certain period of time. Progesterone resets estrogen receptors to almost original order, which is part of the reason females take PC....to re-establish order of estrogen sensitivity. Progesterone also inhibits DHT....in men and women....which can change the ratio to make more estrogen via inhibiting 5 alpha reductase. I'll read product reviews too before buying, but I don't base my sole decision on what is being said, and without listing science to what a person stated it holds little weight in my book. On a personal note about PC plus PM...I've used PC for close to 5 years and believe what it does (promotes breast growth), and during that time I've never lost breast tissue. In fact I list a MTF study that found when progesterone was used with HRT it grew more breast tissue than HRT only (verified from biopsied breast tissue). The following information explains more about using progesterone, I have much more on PC and progesterone (scientific posts) listed in my program thread, just use the search function using progesterone. How much to use (or needed) is however much PC is needed to cover all the breast.

I posted a few studies that introduced prolactin and E2 simultaneously, which they worked synergistically (what a mouthful lol). The same is held true about introducing progesterone and E2. 

And for that reason it (imo) explains the essence of how the combo birth control works, (2 hormone release). 

In terms of a cycle its best to gain back stability, the fatigue is (can be) from an increase in prolactin. 

There's other ways (things) to make add-ons but I wouldn't until you get PRL in order, first. 

Progesterone and estrogen E2 (together) in-quote-"induced proliferation that resulted in sidebranching and alveologenesis," but E+P treatment produced more proliferation sooner and extensive sidebranching and alveologenesis. The exact amounts of E2 (estradiol) and progesterone weren't given. In other words having progesterone combined with E2 produces side-branching of the breasts (outward growth), 

function of progesterone receptor isoforms in normal adult mouse mammary gland.
Aupperlee MD1, Haslam SZ.
Author information
Abstract
In normal mouse mammary gland, the mitogenic action of progesterone (P) is mediated by two P receptor (PR) isoforms, PRA and PRB. PRA is predominantly expressed in the adult virgin, and PRB is predominantly expressed during pregnancy. To investigate hormonal regulation of PR isoform expression and isoform-specific functions in vivo, adult ovariectomized BALB/c mice were treated for 3, 5, or 10 d with estrogen (E), P, or estrogen plus progesterone (E+P). Using an immunohistochemical approach with isoform-specific antibodies, we investigated hormonal regulation of PRA and PRB and their functional roles in proliferation and morphogenesis. Significant E-induced proliferation was only observed after 5 d at the distal tips of ducts; there was no sidebranching or alveologenesis. P induced proliferation that resulted in sidebranching and alveologenesis, but E+P treatment produced more proliferation sooner and more extensive sidebranching and alveologenesis. PRA levels were increased by E and decreased by P. Increased PRB levels were induced by treatment with P or E+P and coincided with the formation of alveoli. PRA was the predominant PR isoform expressed during sidebranching, and colocalization of PRA with 5-bromo-2'-deoxyuridine revealed that proliferation of PRA-positive and -negative cells was responsible for P-induced sidebranching. PRB was the predominant PR isoform expressed during alveologenesis, and colocalization of PRB with 5-bromo-2'-deoxyuridine showed that both PRB-positive and -negative cells proliferated during alveolar expansion. These results demonstrate different hormonal regulation of PRA and PRB levels in vivo and suggest that P can induce proliferation through either PRA or PRB via direct and paracrine mechanisms.
http://www.ncbi.nlm.nih.gov/pubmed?filters=&orig_db=PubMed&cmd=Search&term=148%2A%5Bvolume%5D%20AND%202290%5Bpage%5D%20AND%202007%5Bpdat%5D%20AND%20Aupperlee%20MD%5Bauth%5D

Prolactin stimulates breast growth in the presence of high estrogens, progesterone and estrogen stimulate growth too, and from what I've seen (still needs to be verified)  pharma progestins up-regulate IGF-1. However, imo peptides look very promising. 


Hormone-Dependent Mammary Gland Development

Hormone-dependent mammary gland development occurs after puberty and results in ductal elongation; recurrent estrous cycles in adulthood trigger side branching; pregnancy enhances side branching and induces alveolo-genesis with lactational differentiation followed by involution at weaning (Brisken 2002). In the late fifties, a series of experiments defined the minimal hormonal requirements for mammary gland development in mice (Nandi 1958) and rats (Lyons 1958). Endocrine ablation was achieved by surgically removing the major sources of reproductive hormones from mature females, the ovaries, which secrete estrogens and progesterone, the pituitary gland, a major source of growth hormone (GH) and prolactin (Prl), and for some experiments the adrenal glands, which release cortisol and precursors of sex steroids (see Fig. 1). Hormone replacement in hormone-deprived animals established that additive and sequential treatment with 17-b-estradiol, progesterone, and prolactin in conjunction with cortisol and GH can recapitulate mammary gland development.

 http://www.ncbi.nlm.nih.gov/pmc/articles...003178.pdf

I almost forgot, I have this one of kind study (2006?) on mtf's that proved progesterone and E2 promoted tissue growth, I'll put it up asap, (when I find it lol). 

The study was from 2000, not '06.

Short-term and long-term histologic effects of castration and estrogen treatment on breast tissue of 14 male-to-female transsexuals in comparison with two chemically castrated men.
Kanhai RC1, Hage JJ, van Diest PJ, Bloemena E, Mulder JW.
Author information
Abstract
The histologic changes induced in the mammary gland of male-to-female transsexuals have not yet been reported in the literature. We studied the histologic changes induced by chemical and surgical castration and estrogen therapy in the breasts of 14 such patients, with particular reference to acinar and lobular formation. To objectify the influence of cross-sex treatment, the histologic findings were compared with those in two men treated hormonally for prostate cancer. The slight increase in the plasma estrogen-to-androgen ratio seen in idiopathic gynecomastia usually does not induce acinar and lobular formation in the male breast. In men treated with nonprogestative antiandrogens for prostate cancer, only moderate acinar and lobular formation occurs. Only in male-to-female transsexuals in whom progestative chemical castration is combined with feminizing estrogen therapy will full acinar and lobular formation occur with hormonally stimulated nuclei and pseudolactational changes. Hence, combined progestative antiandrogens and estrogens are necessary for genetically male breast tissue to mimic the natural histology of the female breast. Orchidectomy does not contribute to this. Apocrine metaplasia may occur in breasts of male-to-female transsexuals, but so far, only four cases of breast cancer in male-to-female transsexuals have been documented.

Here's the full paper, or view the PDF as listed on the site. 
http://journals.lww.com/ajsp/Fulltext/20..._of.9.aspx

Interesting this..about P.

''Your breasts needs progesterone as well as estrogen to grow. It is progesterone that activates estrogen receptors so that estrogen can bind to them. Progesterone is also the hormone responsible for building up fat stores in the breast.''

Absolutely true, the combined therapy is like a bio-directional response, for instance free T (the bio-active T) decreases by two-fold by the combined E and progesterone. 

The effect of combined oral contraception on testosterone levels in healthy women: a systematic review and meta-analysis.
http://www.ncbi.nlm.nih.gov/pubmed/24082040

The current literature review and meta-analysis demonstrates that COCs decrease circulating levels of total T and free T and increase SBHG concentrations. Due to the SHBG increase, free T levels decrease twice as much as total T. The estrogen dose and progestin type of the COC do not influence the decline of total and free T, but both affect SHBG. The clinical implications of suppressed androgen levels during COC use remain to be elucidated.

Another similar study states a higher result from staggering dosages (orally). Imo this suggests a cyclic approach to lower androgens. Which btw androstenedione is the androgen culprit in GG's........not DHT. 

contraceptives containing ethinylestradiol and gestodene or norgestimate upon androgen parameters and serum binding proteins.

Abstract
The effect of a triphasic oral contraceptive containing ethinylestradiol and gestodene (EE/GSD) on various serum hormonal parameters was compared with that of a monophasic formulation containing 35 micrograms ethinylestradiol and 250 micrograms norgestimate (EE/NGM). Blood samples were collected from 46 women on days 2, 11, and 21 of the preceding control cycle and of the third, sixth and twelfth treatment cycle. There was no significant difference in the influence on any hormonal parameter between both formulations. Both EE/GSD and EE/NGM caused a time-dependent suppression of serum dehydroepiandrosterone sulphate (DHEA-S) by 20-30% (p < 0.01) and a reduction of 5 alpha-androstane-3 alpha, 17 beta-diol glucuronide by 50-60% (p < 0.01) during each treatment cycle, while androstenedione levels were reduced by 25% (p < 0.01). There was also a significant decrease in the levels of total testosterone by 30-35% (p < 0.01) and free testosterone by 60% (p < 0.01), while sex hormone-binding globulin (SHBG) was increased by 200-240% on days 11 and 21 (p < 0.01). During the pill-free interval the SHBG levels were reduced to a certain degree but remained elevated by 100% as compared to the pretreatment values. The serum levels of corticosteroid-binding globulin (CBG) which is known to be influenced only by the estrogenic component of combination pills, increased significantly by 170% (p < 0.01) during each treatment cycle. During the pill-free interval of 7 days, the CBG levels decreased but were still elevated by 90-100% as compared to the control cycle. Similarly, the serum levels of cortisol were significantly elevated by 110-140% (p < 0.01) during treatment with both preparations. The results demonstrate a profound suppression of androgen levels and peripheral androgen metabolism.

Damn! I need a biology degree.  lol

[tanysquirrel]

Lotus:
I saw this review on Amazon's site.  Says in men, lowers E and increases T??  Is that right?  How much should I take?

Verified Purchase

My wife was showing symptoms of low progesterone so I thought for 15 dollars it's worth a shot. Being very scientifically minded and protective I had to use it first to look for adverse effects. I had to end up doing research on males and progesterone and I came to find that it lowers estrogen in both men and women to proper levels and in males tends to act more like testosterone. It even has success in treating gynocomastia (man boobs). I would suggest a man only use half of the recomended dose 2 weeks on 2 weeks off.

In my opinion this isn't the case (the above product reviews) , progesterone is a precursor for androgens and estrogens, so they (hormone precursors) can be manipulated to perform the way we'd like them to behave (or synthesize). When genetic males alter their horomones to grow breasts we fundamentally change our DNA to reflect (or resemble) menopausal women....after a certain period of time. Progesterone resets estrogen receptors to almost original order, which is part of the reason females take PC....to re-establish order of estrogen sensitivity. Progesterone also inhibits DHT....in men and women....which can change the ratio to make more estrogen via inhibiting 5 alpha reductase. I'll read product reviews too before buying, but I don't base my sole decision on what is being said, and without listing science to what a person stated it holds little weight in my book. On a personal note about PC plus PM...I've used PC for close to 5 years and believe what it does (promotes breast growth), and during that time I've never lost breast tissue. In fact I list a MTF study that found when progesterone was used with HRT it grew more breast tissue than HRT only (verified from biopsied breast tissue). The following information explains more about using progesterone, I have much more on PC and progesterone (scientific posts) listed in my program thread, just use the search function using progesterone. How much to use (or needed) is however much PC is needed to cover all the breast.

I posted a few studies that introduced prolactin and E2 simultaneously, which they worked synergistically (what a mouthful lol). The same is held true about introducing progesterone and E2. 

And for that reason it (imo) explains the essence of how the combo birth control works, (2 hormone release). 

In terms of a cycle its best to gain back stability, the fatigue is (can be) from an increase in prolactin. 

There's other ways (things) to make add-ons but I wouldn't until you get PRL in order, first. 

Progesterone and estrogen E2 (together) in-quote-"induced proliferation that resulted in sidebranching and alveologenesis," but E+P treatment produced more proliferation sooner and extensive sidebranching and alveologenesis. The exact amounts of E2 (estradiol) and progesterone weren't given. In other words having progesterone combined with E2 produces side-branching of the breasts (outward growth), 

function of progesterone receptor isoforms in normal adult mouse mammary gland.
Aupperlee MD1, Haslam SZ.
Author information
Abstract
In normal mouse mammary gland, the mitogenic action of progesterone (P) is mediated by two P receptor (PR) isoforms, PRA and PRB. PRA is predominantly expressed in the adult virgin, and PRB is predominantly expressed during pregnancy. To investigate hormonal regulation of PR isoform expression and isoform-specific functions in vivo, adult ovariectomized BALB/c mice were treated for 3, 5, or 10 d with estrogen (E), P, or estrogen plus progesterone (E+P). Using an immunohistochemical approach with isoform-specific antibodies, we investigated hormonal regulation of PRA and PRB and their functional roles in proliferation and morphogenesis. Significant E-induced proliferation was only observed after 5 d at the distal tips of ducts; there was no sidebranching or alveologenesis. P induced proliferation that resulted in sidebranching and alveologenesis, but E+P treatment produced more proliferation sooner and more extensive sidebranching and alveologenesis. PRA levels were increased by E and decreased by P. Increased PRB levels were induced by treatment with P or E+P and coincided with the formation of alveoli. PRA was the predominant PR isoform expressed during sidebranching, and colocalization of PRA with 5-bromo-2'-deoxyuridine revealed that proliferation of PRA-positive and -negative cells was responsible for P-induced sidebranching. PRB was the predominant PR isoform expressed during alveologenesis, and colocalization of PRB with 5-bromo-2'-deoxyuridine showed that both PRB-positive and -negative cells proliferated during alveolar expansion. These results demonstrate different hormonal regulation of PRA and PRB levels in vivo and suggest that P can induce proliferation through either PRA or PRB via direct and paracrine mechanisms.
http://www.ncbi.nlm.nih.gov/pubmed?filters=&orig_db=PubMed&cmd=Search&term=148%2A%5Bvolume%5D%20AND%202290%5Bpage%5D%20AND%202007%5Bpdat%5D%20AND%20Aupperlee%20MD%5Bauth%5D

Prolactin stimulates breast growth in the presence of high estrogens, progesterone and estrogen stimulate growth too, and from what I've seen (still needs to be verified)  pharma progestins up-regulate IGF-1. However, imo peptides look very promising. 


Hormone-Dependent Mammary Gland Development

Hormone-dependent mammary gland development occurs after puberty and results in ductal elongation; recurrent estrous cycles in adulthood trigger side branching; pregnancy enhances side branching and induces alveolo-genesis with lactational differentiation followed by involution at weaning (Brisken 2002). In the late fifties, a series of experiments defined the minimal hormonal requirements for mammary gland development in mice (Nandi 1958) and rats (Lyons 1958). Endocrine ablation was achieved by surgically removing the major sources of reproductive hormones from mature females, the ovaries, which secrete estrogens and progesterone, the pituitary gland, a major source of growth hormone (GH) and prolactin (Prl), and for some experiments the adrenal glands, which release cortisol and precursors of sex steroids (see Fig. 1). Hormone replacement in hormone-deprived animals established that additive and sequential treatment with 17-b-estradiol, progesterone, and prolactin in conjunction with cortisol and GH can recapitulate mammary gland development.

 http://www.ncbi.nlm.nih.gov/pmc/articles...003178.pdf

I almost forgot, I have this one of kind study (2006?) on mtf's that proved progesterone and E2 promoted tissue growth, I'll put it up asap, (when I find it lol). 

The study was from 2000, not '06.

Short-term and long-term histologic effects of castration and estrogen treatment on breast tissue of 14 male-to-female transsexuals in comparison with two chemically castrated men.
Kanhai RC1, Hage JJ, van Diest PJ, Bloemena E, Mulder JW.
Author information
Abstract
The histologic changes induced in the mammary gland of male-to-female transsexuals have not yet been reported in the literature. We studied the histologic changes induced by chemical and surgical castration and estrogen therapy in the breasts of 14 such patients, with particular reference to acinar and lobular formation. To objectify the influence of cross-sex treatment, the histologic findings were compared with those in two men treated hormonally for prostate cancer. The slight increase in the plasma estrogen-to-androgen ratio seen in idiopathic gynecomastia usually does not induce acinar and lobular formation in the male breast. In men treated with nonprogestative antiandrogens for prostate cancer, only moderate acinar and lobular formation occurs. Only in male-to-female transsexuals in whom progestative chemical castration is combined with feminizing estrogen therapy will full acinar and lobular formation occur with hormonally stimulated nuclei and pseudolactational changes. Hence, combined progestative antiandrogens and estrogens are necessary for genetically male breast tissue to mimic the natural histology of the female breast. Orchidectomy does not contribute to this. Apocrine metaplasia may occur in breasts of male-to-female transsexuals, but so far, only four cases of breast cancer in male-to-female transsexuals have been documented.

Here's the full paper, or view the PDF as listed on the site. 
http://journals.lww.com/ajsp/Fulltext/20..._of.9.aspx

Interesting this..about P.

''Your breasts needs progesterone as well as estrogen to grow. It is progesterone that activates estrogen receptors so that estrogen can bind to them. Progesterone is also the hormone responsible for building up fat stores in the breast.''

Absolutely true, the combined therapy is like a bio-directional response, for instance free T (the bio-active T) decreases by two-fold by the combined E and progesterone. 

The effect of combined oral contraception on testosterone levels in healthy women: a systematic review and meta-analysis.
http://www.ncbi.nlm.nih.gov/pubmed/24082040

The current literature review and meta-analysis demonstrates that COCs decrease circulating levels of total T and free T and increase SBHG concentrations. Due to the SHBG increase, free T levels decrease twice as much as total T. The estrogen dose and progestin type of the COC do not influence the decline of total and free T, but both affect SHBG. The clinical implications of suppressed androgen levels during COC use remain to be elucidated.

Another similar study states a higher result from staggering dosages (orally). Imo this suggests a cyclic approach to lower androgens. Which btw androstenedione is the androgen culprit in GG's........not DHT. 

contraceptives containing ethinylestradiol and gestodene or norgestimate upon androgen parameters and serum binding proteins.

Abstract
The effect of a triphasic oral contraceptive containing ethinylestradiol and gestodene (EE/GSD) on various serum hormonal parameters was compared with that of a monophasic formulation containing 35 micrograms ethinylestradiol and 250 micrograms norgestimate (EE/NGM). Blood samples were collected from 46 women on days 2, 11, and 21 of the preceding control cycle and of the third, sixth and twelfth treatment cycle. There was no significant difference in the influence on any hormonal parameter between both formulations. Both EE/GSD and EE/NGM caused a time-dependent suppression of serum dehydroepiandrosterone sulphate (DHEA-S) by 20-30% (p < 0.01) and a reduction of 5 alpha-androstane-3 alpha, 17 beta-diol glucuronide by 50-60% (p < 0.01) during each treatment cycle, while androstenedione levels were reduced by 25% (p < 0.01). There was also a significant decrease in the levels of total testosterone by 30-35% (p < 0.01) and free testosterone by 60% (p < 0.01), while sex hormone-binding globulin (SHBG) was increased by 200-240% on days 11 and 21 (p < 0.01). During the pill-free interval the SHBG levels were reduced to a certain degree but remained elevated by 100% as compared to the pretreatment values. The serum levels of corticosteroid-binding globulin (CBG) which is known to be influenced only by the estrogenic component of combination pills, increased significantly by 170% (p < 0.01) during each treatment cycle. During the pill-free interval of 7 days, the CBG levels decreased but were still elevated by 90-100% as compared to the control cycle. Similarly, the serum levels of cortisol were significantly elevated by 110-140% (p < 0.01) during treatment with both preparations. The results demonstrate a profound suppression of androgen levels and peripheral androgen metabolism.

Damn! I need a biology degree.  lol

That is why we have our resident Biologist/scholar- Lotus

[Lotus]

Lol thanks squirrel... I was going to say " nah, you don't need a degree...I got u covered on this one." Or think of it this way, progesterone matures breasts (gives roundness, aka side branching) where estrogen leaves some stranded wanting more, meaning only growing breasts outward (forward). 

So if you feel stalled in growth consider adding PC to help build breast structure.

[The First Aria]

My GD prescribed it mainly as a AA blocker since my body goes wacky with more than 100mg of Spiro.  He also said that some have said it does help boost the breast growth.

[jannet.duff]

I started progesterone last week, the sensitivity and feelings we get as our breasts are growing increased significantly.

[The First Aria]

My GD prescribed it mainly as a AA blocker since my body goes wacky with more than 100mg of Spiro.  He also said that some have said it does help boost the breast growth.

I am not sure if it has helped with breast growth, but it did bring back "budding" discomfort.