[The First Aria]

Looking great d thanks

Ella your mouth is wide open :p

And saliva running down my chin..

It was meant sincerely..*with saliva still in my throat* How Lotus as a guy can grow such big breasts really got me surprised!

Hannah, you don't get it do ya..... He is really a she, who had plastic surgery and took tons of androgens but was saved by the boob fairy to come back to the light. But unfortunately, he is a converted Catholic, that was once Hasidic, then went to Baptism and figured out he was just a Pregnant Indian Priestess who was into women only. But due to pressures from his / her tribe joined the navy.

How close am I Lotus. LOL.... Whew, that took a lot of research on my part to uncover the true you. ROFLMAO That is the reason I consider him my "Blood Brother" Ha ha.

[ellacraig]

Looking great d thanks

Ella your mouth is wide open :p

And saliva running down my chin..

It was meant sincerely..*with saliva still in my throat* How Lotus as a guy can grow such big breasts really got me surprised!

Hannah, you don't get it do ya..... He is really a she, who had plastic surgery and took tons of androgens but was saved by the boob fairy to come back to the light. But unfortunately, he is a converted Catholic, that was once Hasidic, then went to Baptism and figured out he was just a Pregnant Indian Priestess who was into women only. But due to pressures from his / her tribe joined the navy.

How close am I Lotus. LOL.... Whew, that took a lot of research on my part to uncover the true you. ROFLMAO That is the reason I consider him my "Blood Brother" Ha ha.

What the .......k....
Lotus you fucken lied to me!

[Lotus]

Ella your mouth is wide open :p

And saliva running down my chin..

It was meant sincerely..*with saliva still in my throat* How Lotus as a guy can grow such big breasts really got me surprised!

Hannah, you don't get it do ya..... He is really a she, who had plastic surgery and took tons of androgens but was saved by the boob fairy to come back to the light. But unfortunately, he is a converted Catholic, that was once Hasidic, then went to Baptism and figured out he was just a Pregnant Indian Priestess who was into women only. But due to pressures from his / her tribe joined the navy.

How close am I Lotus. LOL.... Whew, that took a lot of research on my part to uncover the true you. ROFLMAO That is the reason I consider him my "Blood Brother" Ha ha.

What the .......k....
Lotus you fucken lied to me!

Lol,

Plastic surgery?, that's not me, I'm to chicken for that. Androgens and boob fairy? (yes, I'll go with that), still a dude though. Converted?, no I was born that way which also means being a non-hasidic or mystic pregnant lady. Hell yeah, into women only. Sailed the seven seas?, oh yeah, I still got salt water in my veins.

That's pretty good though,

[ellacraig]

And saliva running down my chin..

It was meant sincerely..*with saliva still in my throat* How Lotus as a guy can grow such big breasts really got me surprised!

Hannah, you don't get it do ya..... He is really a she, who had plastic surgery and took tons of androgens but was saved by the boob fairy to come back to the light. But unfortunately, he is a converted Catholic, that was once Hasidic, then went to Baptism and figured out he was just a Pregnant Indian Priestess who was into women only. But due to pressures from his / her tribe joined the navy.

How close am I Lotus. LOL.... Whew, that took a lot of research on my part to uncover the true you. ROFLMAO That is the reason I consider him my "Blood Brother" Ha ha.

What the .......k....
Lotus you fucken lied to me!

Lol,

Plastic surgery?, that's not me, I'm to chicken for that. Androgens and boob fairy? (yes, I'll go with that), still a dude though. Converted?, no I was born that way which also means being a non-hasidic or mystic pregnant lady. Hell yeah, into women only. Sailed the seven seas?, oh yeah, I still got salt water in my veins.

That's pretty good though,

Us sailors have to stick together right! Won't tell you Im on holiday at a seaside resort looking out at the sea , went on a charter yesterday out in he ocean with amazing views and drinking beer at local seaside taverns each night then eh...

[The First Aria]

Hey sailors, got change for a $20??? LOL. I am NOT that kind either. Looking to break a $20 for my wife. I KNOW what you two were thinking. ROFL

[Lotus]

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.

Hi spanky,

I agree, I have RC as a slight aromatase/progesterone and ERa promoter, as with all NBE use it in moderation.

As mentioned, FSH follicle stimulating hormone stimulates estradiol synthesis, the science is there, so it's possible. Same with vitamin D3, the science is there too, meaning it upreglates T and E2. And as we know, when we try to eliminate most of DHT, what remains?, exactly, T and E2, other hormones too , but for this purpose we'll limit it to the 2 . But let's say we use an anti-androgen in the presence of an aromatase promoter (pick one, WP, forskolin, inositol triphosphate, FSH, etc) which will upregluate both (T and E2) then synthesize thru aromatase. More research (by BN members) should be done on second messengers, (e.g-cAMP,) which imo is key in aroamtase expression and will result in improved breast growth.

Interactions between FSH, estradiol-17 beta and transforming growth factor-beta regulate growth and differentiation in the rat gonad.

Estradiol-17 beta (E2) is a mitogen in vivo for the proliferation of granulosa cells in the rat ovary. E2 is synthesized by the preovulatory follicle through a series of gonadotrophin-dependent events: LH stimulates thecal cells to synthesize androgens (androstenedione and testosterone) which are substrates for FSH-induced aromatization to estrogens in granulosa cells. More recently, we have found that transforming growth factor-beta (TGF-beta) stimulates DNA synthesis in rat granulosa cells in vitro and this effect is augmented by FSH. Since E2 is a mitogen in vivo and TGF-beta is the only known growth factor to stimulate proliferation in vitro, the possible link between the actions of E2 and TGF-beta were examined. E2 stimulated the secretion of a TGF-beta-like factor by rat granulosa cells in culture, and with time DNA synthesis was stimulated. The mitogenic action of E2 was enhanced in the presence of FSH, and attenuated by a neutralizing antibody to TGF-beta. The latter observations have identified TGF-beta as the "missing-link" in the mitogenic actions of E2 on rat granulosa cells. In addition to the growth-promoting actions of TGF-beta plus FSH, TGF-beta enhanced FSH-induced aromatase activity. Consequently, FSH plus TGF-beta stimulates both the proliferation and aromatization capacity of rat granulosa cells. We propose that interactions between FSH, E2 and TGF-beta lead to the exponential increase in serum E2 levels that occurs during the follicular phase of the cycle. Similarly, FSH stimulates the aromatization of exogenous androgens to estrogen by Sertoli cells isolated from immature rat testes, and there is a correlation between FSH-induced aromatization and mitotic activity. We have shown that FSH plus TGF-beta stimulates DNA synthesis in Sertoli cells. Since E2 increases the secretion of TGF-beta by Sertoli cells, interactions between FSH, E2 and TGF-beta may provide the mitogenic stimulus for Sertoli cells during the prepubertal period. In summary, our findings suggest that the estrogen-induced growth of rat granulosa cells is mediated through the production of TGF-beta, which acts as an autocrine regulator of proliferation. We also propose that the growth-promoting actions of FSH on Sertoli cells may depend upon a cascade series of events involving estrogens and TGF-beta.



From post #2618
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.

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)





* 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

Some fringe science theory for NBE, (which I'm crazy enough to believe) if you deny testis and adrenals the ability to make DHT that leaves just testosterone to make E2. In many ways we (genetic males) model post-menopausal women, which means we produce E1 in our peripheral tissues. The E2 we do get endogenously is from the conversion of aromatase of E2 from free testosterone . Using Sertoli cells (inside the testes) we turn them (utilize) into a endogenous power plant for E2 and aromatase synthesis. In other words "use them" don't "lose them". Or to take it further for my geek friends "reverse engineer them.". (engineereder)

Using cAMP (second messenger) and NO (nitric oxide) and increasing GH through "high intense interval training" and added with "intermittent fasting" (which helps to starve fat cells) explodes Growth Hormones and fat cell synthesis.

Essential fatty acids can be used as carriers to get hormones to interact with receptors. Presently, I believe we have plenty of vehicle transports to get the job done, newest one I believe is COQ-10. Old ones, Vitamin C and D, which are very underestimated for NBE/Hrt imo.

[Lotus]

This study explains about starving fat cells for (massive) synthesis. It all ties together.

Free fatty acids: continuously released from adipose tissue, with a peak in secretion during fastting and a decrease during postprandial periods. During obesity, when resistance of adipose tissue to insulin develops (partly because of hypoxia generated following adipocyte hypertrophia/hyperplasia), enhanced lipolysis leads to a massive increase in plasma free fatty acids. Free fatty acids will then perturb liver and muscle insulin action.


Lipophilic Micronutrients and Adipose Tissue Biology
http://www.ncbi.nlm.nih.gov/pmc/articles...-01622.pdf

[Lotus]

Like I said, vitamin D (D3) is underestimated for NBE. Not only is it an aromatase, it will increase E2 synthesis, and get rid of visceral fat.

This (D3) clears off the shelf of about 3-4 NBE products and keeps money in your pocket, how cool is that?.

____________________


We conclude that 1,25-dihydroxyvitamin D3 directly regulates adipocyte 11beta-HSD 1 expression and, consequently, local cortisol levels and that this may contribute to the preferential loss of visceral adiposity by high- calcium diets.

1,25-Dihydroxyvitamin D3 Modulation of Adipocyte Glucocorticoid Function
http://onlinelibrary.wiley.com/store/10.1038/oby.2005.75/asset/oby.2005.75.pdf?v=1&t=icfkstuw&s=b5a9d9b5caa4998c3c65827467cc842bb9dda82a

vitamin D analogs significantly upregulated E2- and DHT-induced CK response. These analogs upregulated the CK response to selective estrogen receptor modulators (SERMs). An estrogenic response (from vitamin D) is seen in the intestinal tract. Vitamin D also helps with hair growth.
http://www.howtomakeyourhairgrowfast.net...rowth.html


Interaction Between Estrogen and Vitamin D–Endocrine System: A Potential Addition to the Unitary Model of Osteoporosis
http://onlinelibrary.wiley.com/doi/10.13....1954/full

Vitamin D modulation of the activity of estrogenic compounds in bone cells in vitro and in vivo.
Somjen D1.
Author information
Abstract
Vitamin D analogs modulate different organs, including modulation of energy metabolism, through the induction of creatine kinase (CK) activity. Skeletal organs from vitamin D-depleted rats showed lower constituent CK than those from vitamin D-replete rats. Moreover, estradiol-17beta (E2) or dihydrotestosterone (DHT), which increased CK in organs from intact female or male rats, respectively, stimulated much less CK in vitamin D-depleted rats. Treatment of intact female rats with noncalcemic vitamin D analogs significantly upregulated E2- and DHT-induced CKresponse. These analogs upregulated the CK response to selective estrogen receptor modulators (SERMs) in organs from intact or ovariectomized (Ovx) female rats but abolished SERMs' inhibitory effect on E2-induced CK. These analogs significantly increased estradiol receptor alpha (ERalpha) protein in skeletal organs as well as histomorphological and biochemical changes due to this treatment followed by E2 or DHT. The analogs alone markedly altered the growth plate and the trabeculae and increased trabecular bone volume (%TB V) and trabecular width. The addition of E2 or DHT to this treatment restored all parameters as well as increased %TBV and cell proliferation. Treatment of Ovx female rats with JK 1624 F2-2 (JKF) decreased growth-plate width and increased %TB V, whereas QW1624 F2-2 (QW) restored growth-plate width and %TB V. Treatment of E2 with JKF restored %TBV and growth-plate width, whereas E2 with QW restored all parameters, including cortical width. There was also upregulation of the response of CK to E2 in both combined treatments. Our human-derived osteoblast (hObs)-like cell cultures respond to estrogenic compounds, and pretreating them with JKF upregulated the CK response to E2, raloxifene (Ral), and some phytoestrogens. ERalpha and ERbeta proteins, as well as mRNA, were modulated by CB 1093 (CB) and JKF. JKF increased specific nuclear E2 binding in female hObs but inhibited specific membranal E2 binding. hObs express 25 hydroxyvitamin D3-1alpha hydroxylase (1-OHase)-mRNA and its biological activity, which are both modulated by parathyroid hormone (PTH) and estrogenic compounds. Our results demonstrate mutual interaction between vitamin D and estrogenic compounds. We therefore conclude that combined treatment with less-calcemic analogs of vitamin D and estrogenic compounds might be superior for treatment of bone damage caused by ovariectomy in female rats, with possible application for postmenopausal osteoporosis.
PMID: 17725484 [PubMed - indexed for MEDLINE]


http://www.ncbi.nlm.nih.gov/pubmed/17725484

[EvaMarie]

Best thing about vitamin D is you get all you need in the summer out in the sun

[Lotus]

Hi BN,


So I was looking into some research on cold water therapy and how it aids in recovery times in post HIIT workouts. Turns out that it also builds new brown fat cells, hmm, interesting huh?. Well.....it got me thinking on different ways to promote new cell growth for breast tissue. As we know fat cells produce aromatase enzyme, which converts testosterone into estrogen. We also know HIIT produces natural growth hormone and lactate, (initiates new muscle synthesis). It's quite possible (imo) using that cold water therapy and HIIT can trigger breast growth, the science says it's possible.

Another example: From a clinical study I found that it stated that cAMP (2nd messengers) levels significantly increased lipolysis in adipose tissue, at 4°C, (39 degrees). Adipocytes increased the release of glycerol, indicating that the high rate of lipolysis occurred in these cells.


So how do this apply to NBE?, my opinion?..........hmm....... use ice packs on the boobs after massage/boobie exercises (you still do those grab n pull method boob exercises right?) I hope so cause that in-itself triggers breast growth. This method along with HIIT, cold water therapy is free, cept the cost of water.

Initiation of myoblast/brown fat switch through a PRDM16-C/ EBP-β transcriptional complex:

These data indicate that the PRDM16-C/EBP-β complex initiates brown fat development from myoblastic precursors, and may provide opportunities for the development of novel therapeutics for obesity and type-2 diabetes.
http://www.ncbi.nlm.nih.gov/pmc/articles...132247.pdf

EFFECT OF IMMEDIATE AND DELAYED COLD WATER IMMERSION AFTER A HIGH INTENSITY EXERCISE SESSION ON SUBSEQUENT RUN PERFORMANCE
http://www.jssm.org/vol10/n4/10/v10n4-10text.php

In summary, quantitative and qualitative analyses demonstrated that immediate CWI performed after a HIIS resulted in better next day running performance (YRT), while delayed (3 h) CWI was also likely to result in improved YRT performance, compared to no CWI. Importantly, greater benefit was associated with immediate CWI. This information is pertinent to athletes, particularly if they do not have immediate access to recovery facilities following exercise performance.

______________________________________________

The 16 Secret Benefits of Taking a COLD SHOWER
http://www.naturalmuscle.net/#!The-16-Se...1a764c7ad6