[sioctober]

I have been reading that bicalutimide 50mg will block T receptors, thus more free T is available for aromatase. The T levels increase, but no receptors. Whereas spiro simply blocks T. Dr Will Powers in MI is using this. Have you heard of this or have a comment? I do not think there is a lot of history or records on this.

[Lotus]

I have been reading that bicalutimide 50mg will block T receptors, thus more free T is available for aromatase. The T levels increase, but no receptors. Whereas spiro simply blocks T. Dr Will Powers in MI is using this. Have you heard of this or have a comment? I do not think there is a lot of history or records on this.

Hi Sioctober,

Apologies for the late response. I've posted many times in the past about having more free T available potentially creates a cascade of estrogen. The only problem is finding what works for the conversion, meaning everyone is different because of the varying degrees of individual metabolism. Now, I believe there's things in the NBE medicine cabinet to achieve the conversion of aromatase. The top in my mind is using second messengers, check the FAQ aromatase section for examples, personally?...I prefer glycosides. I'll add the following info below as an example though.

_________________________________________________

Remember-only hormones that detach from SHBG and Albumin are considered in the FREE state, about 2-5%, that's FREE testosterone and FREE estradiol, which will be available the bind with receptors and induce growth.

* Certain metabolic pathway that has direct impact on breast growth.

* For instance, there's a specific agonist for a nongenomic pathway of sex steroid receptors that stimulates breast growth.

* Ginsenosides (like panax ginseng) are a class of steroid glycosides, and triterpene saponins. Brilliant huh?...

cAMP-dependent signaling pathways (cyclic adenosine monophosphat).
COX2 inhibitors (PGE2), problematic
protein kinase A (PKA)
Free fatty acids

* Aromatase expression is switched to promoters I.3 and II which are transactivated by protein kinase A (PKA) and cAMP-dependent signaling pathways.

These are promoters genes for aromatase.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3142499/

* History of high blood pressure, PCOS, HIGH cortisol, diabetes...latest blood work, any other complications, current meds and herbals.

* Please read this study.
Pharmacology of ginsenosides: a literature review
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2893180/

(Especially this section in the study)
Ginsenosides are agonists to steroidal receptors

* Cortisol + glucocorticoids + cAMP = aromatase.

Now that's just the starting point, you'll also need a balanced gut PH, proper diet/exercise, and balanced hormones. 

These studies listed below sets forth the ground work that taking the aromatase we have in our system and combining it with a cAMP (second messenger....which is panax ginseng) and a glucocorticoid (vitamin D3) reaches the breast growth pathway in no uncertain terms. I'm not concerned all the low bioavailability of the Ginsenoside's in ginseng, you don't need alot...maybe 4-6% of standardized ginsenoside.

* A balanced gut PH (which is about 7 to 7.5 ph) helps to metabolize drugs and herbs...prevents leaky gut syndrome.

* Now a person with high stress might see a bigger impact using this formula. It's also possible that 30-35% users might not see results, ruling out certain metabolic conditions of course too.

* Beta blockers and PDE 5 inhibitors (E.D. aka erectile dysfunction drugs) works also in combination with ginseng by relaxing blood vessels and slowing heart rate...which  improve blood flow and decrease blood pressure.


https://www.ncbi.nlm.nih.gov/pmc/article...o=0.471698

https://www.ncbi.nlm.nih.gov/m/pubmed/22315456/

Actions and interactions of estradiol and glucocorticoids in cognition and the brain: Implications for aging women.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4501869/

https://www.researchgate.net/publication...rain_cells

https://en.m.wikipedia.org/wiki/Ginsenoside
Phosphodiesterase (PDE) inhibitors in the treatment of lower urinary tract dysfunction
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3162649/

[Stevenator.]

[Lotus]

I've written about that by reducing DHT it up-regulates estrogen receptors in the past. E1 plays a role in peripheral aromatization of androstenedione (that's through the A4 pathway), but...E2 is the strongest form of estrogen. I read Dr. Powers stated he thinks more E1 is needed in the intial phase of breast growth, and as we know PM acts more E1, perhaps why some see results on just using PM to begin with. Now to further breast growth through tanner 3 to 5 you need a combination of progesterone, prolactin, IGF-1, glucocorticoid, free fatty acids, collagen, thermogenic repsone  of hormone receptors, and a few other things.

From experience I've found that hyperinsulinaemia (too much glucose) has negative impact on breast growth. Evidence suggests this is the case in women with PCOS, which PCOS is hyperandrogenism....(a negative impact for breast growth) amongst stress and inflammation too a driving of PCOS, and stress decreases aromatase in ovarian cells, so...what does that tell yah.

E2 and E1 can be converted into each other, and both can be inactivated via hydroxylation and conjugation. E2 demonstrates 1.25 to 5 times the biological potency of E1. E2 circulates at 1.5 to 4 times the concentration of E1 in premenopausal, nonpregnant women.
(Mayo clinic).

Glucocorticoids increase androgen inactivation, I see resihi increases glucocorticoids to a degree thereby inactivatating androgens. Also, androgens, but not estrogens, increase beta adrenergic receptors while decreasing alpha adrenergic receptors- which results in increased levels of epinephrine/ norepinephrine due to lack of alpha-2 receptor negative feedback and decreased fat accumulation. In other words, epinephrine/ norepinephrine then act on lipolysis-inducing beta receptors.

So, one can say that by using beta blockers it can help with breast growth (by the above pathway) to liberate lipolysis for a thermogenic response. And from my experience this creates fullness in breast tissue (lol, mine).

And here's how:.
Beta 2 adrenergic receptor (β2-AR)-agonists activation increases the intracellular cyclic AMP levels that activate protein kinase A, which in turn promotes activation of hormone-sensitive lipase that catalyses the ratelimiting step in lipolysis.

Metformin, blood pressure meds, ACE inhibitors come to mind.

Hi Stevenator...

[sioctober]

Thank you very much - still reading - you are a very wonderful person to share with us. Si.

[Lotus]

Greetings,

I wanted to introduce (and explain) the first of it's kind model for increasing breast growth using cell energy. Cell's (in the human body) have a lipid bilayer which can either let certain (messages/signals) molecules and ions pass through its receptor sites (on the outside of the cell membrane) or block them.

Fat burning hormones want in...to the nucleus that is. But....when cellular inflammation is occuring outside of this lipid bilayer the signals (messages) won't be able to pass.

What this means is those fat burning hormones unable to synthesize in this scenario is highly inefficient....meaning lost potential for cells to complete its goal of synthesizing DNA into new tissue growth...so to speak.

What causes inflammation of cells?, a number of things quite honestly (e.g. stress, diabetes, poor sleep, poor diet, environmental toxins, cancers, thyroid issues, leaky gut, etc etc...you get the picture)

Fat burning hormones I spoke of are/is Leptin. And let's say Leptin makes it way in to the mitochondria (barring mitochondrial dysfunction...which is topic for another discussion) Leptin stimulate aromatase, I'll repeat...stimulating Leptin releases the enzyme aromatase...and as we know aromatase stimulates the conversion of androgens into estrogen.

Leptin explained, a Hormone That Regulates Body Weight. Leptin is a hormone that is produced by your body's fat cells ( 3 ). It is often referred to as the "satiety hormone" or the "starvation hormone." Leptin's primary target is in the brain — particularly ...
https://www.healthline.com/nutrition/leptin-101

Leptin directly stimulates aromatase activity in human luteinized granulosa cells.
https://www.ncbi.nlm.nih.gov/m/pubmed/10421796/

So how do we get this done?, by using exogenous ketones. Exogenous ketones double the electron transport chain and uncoupling protiens thereby improving the mitochondrial proteins in brown fat....think thermogenesis and stimulation of ATP. ATP adenosine triphosphate, is known as cellular currency....ENERGY, and all cells use ATP. I use a HMB (short for β-Hydroxy β-methylbutyric acid) which the one use is a free form-beta-acid-hydroxy-methylbutyrate for my exogenous ketone, it induces protein synthesis through the mTOR pathway and appears to be more active than the using calcium bound butyrate brand.


What Are Exogenous Ketone Supplements?
https://www.healthline.com/nutrition/exo...upplements

Excitatory amino acids activate the enzyme aromatase. Now, estrogen can trigger excitatory neurotransmitters like glutamate, which it appears it will calm the dopamine response. And perhaps one benefit of that calming would reduce food craving. This would help let the Ketones do their thing imo, I think taking 1000 to 1500 mg of glutamine could work though.

Not getting too far ahead here, but the branching of breast tissue (aka TEBs- terminal end buds) is a combination of integrins, amphiregulin, metalloproteinase and epidermal growth factor receptors (EGFR). The pituitary stimulates IGF-1 (insulin growth favtor) which then stimulates TEB formation and mammary epithelial branching, but you'll need estrogen for this magic to work. And this activation is using the PrlR/Jak2 pathway by utilizing prolactin leads to the induction of other signaling pathways, such as the mitogen-activated protein kinase (MAPK) and PI 3-kinase (PI3K) pathways. And whoever said prolactin has nothing to do with breast growth is (sorry to say) just plain nuts lol.

Sheesh...look at the time, gotta run. But let the revolution begin.

[Happyme]

Thanks Lotus!
Its been a long time since I've read your scientific works, but I surprised my self and actually understood it... well kinda
Welcome back, I hope you are doing well and all your dreams are coming true.
Looking forward to part two.
love ya
Bobbi

[Lotus]

Thanks Lotus!
Its been a long time since I've read your scientific works, but I surprised my self and actually understood it... well kinda
Welcome back, I hope you are doing well and all your dreams are coming true.
Looking forward to part two.
love ya
Bobbi

Hi Bobbi,

thanks, I'm doing good, I hope you are doing the same, have you added new muscle to the auto collection?. I'm glad the info makes some sense. I think it's high time we find something that works for NBE for the least amount of cash, don't you?, and what better way to do that than looking inward...under the hood so to speak (meaning the human body).

So basically insulin is a hormone that stores fat...while Leptin burns fat. And by using these two hormones to make aromatase seems quite simple...eh?, well that's the plan anyways.

Part of that trick is to use up ATP...adenosine triphosphate (aka that cellular energy discussed in the previous post), meaning when a cell uses up all its energy it flips to using ketones for energy rather than glucose.

Biochemistry, Ketogenesis
https://www.ncbi.nlm.nih.gov/books/NBK493179/

So once the body burns up all stored fat as energy then the magic begins to utilize leptin, and this happens not just in fat cells but in the brain too, yup, the brain uses leptin stored in ye old noggin. Which also means the brain releases aromatase.

But the physiological mechanisms of how the brain populates leptin-sensitive neurons is truly astonishing. I won't go down that rabbit just yet, trust me when I say that leptin stimulates the hypothalamus through the Jak-Stat signaling pathway, which i've clearly shown the linkage of this pathway for breast growth in dozens of posts.

Leptin signaling in brain: A link between nutrition and cognition?
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2670357/

So I'll close with this for tonight, if i told you one can take a PM supplement or E2 tablet (or injection) with an anti-androgen (reishi or finasteride...or you choose) with an exogenous-ketone supplement, and with MSM (because it stimulates the Stat5 pathway) and possibly taking L-carnitine (Acetyl-CoA [acetyl coenzyme A] is a precursor to beta hydroxy butyrate and stimulates ATP) would you believe me it will stimulate breast growth?

Lol...stayed tuned then.

Acetyl-CoA
https://en.m.wikipedia.org/wiki/Acetyl-CoA

[PleasantlyFascinated]

I haven’t yet taken the time yet to explore and digest the provided links, but am confused by the connection you are making.

My dietary practice has been ketogenic for at least three years. I use MSM by the kilo (8000 mg./day).  I use 1000 mg. Acetyl L-Carnitine daily.  I use reishi, saw palmetto, progesterone daily, stinging nettle, and likely several other things that curtail DHT conversion.  I even have a mild addiction to a small amount of topical estriol daily.

I have noticed effects, but not any boob growth.  Should I have? Not that I am trying for breasts.  Rather, this now has me mildly concerned.

[Lotus]

I haven’t yet taken the time yet to explore and digest the provided links, but am confused by the connection you are making.

My dietary practice has been ketogenic for at least three years. I use MSM by the kilo (8000 mg./day).  I use 1000 mg. Acetyl L-Carnitine daily.  I use reishi, saw palmetto, progesterone daily, stinging nettle, and likely several other things that curtail DHT conversion.  I even have a mild addiction to a small amount of topical estriol daily.

I have noticed effects, but not any boob growth.  Should I have? Not that I am trying for breasts.  Rather, this now has me mildly concerned.

I like the fact that you're using MSM, reishi, L-carnitine, progesterone (though I would suggest using only 3 days per week), stinging nettle and maybe even the estriol cream. Personally I think saw using palmetto and the other DHT stuff you mention is redundant. You see stinging nettle (from my research is a pro-aromatase, and I'll explain why). Stinging nettle is a PDE inhibitor, PDE stands for phosphodiesterase, which PDE is present in every cell, however PDE wants to shut the the second messenger signal of cAMP
(cyclic adenosine monophosphate), which is pro-aromatase, so using a PDE inhibitor like stinging nettle it potentiates the action of aromatase.

Quote:
membrane estrogen receptors initiate signal cascades directly via conventional second messengers, which include adenylate cyclase, cyclic adenosine monophosphate (cAMP), phospholipase C, protein kinase C, and mitogen‐activated protein kinase (MAPK), producing rapid responses to phytoestrogens (Sirotkin, 2016; Yanagihara et al., 2014).

cyclic AMP (cAMP) is a common second messenger involved in signal transduction cascades.

cAMP is synthesized from ATP by the enzyme adenylyl cyclase, which resides in the cell membrane.

activation of adenylyl cyclase can result in the manufacture of hundreds or even thousands of cAMP molecules

Activation of receptors can trigger the synthesis of small molecules called second messengers, which initiate and coordinate intracellular signaling pathways. For example, cyclic AMP (cAMP) is a common second messenger involved in signal transduction cascades. (In fact, it was the first second messenger ever discovered.) cAMP is synthesized from ATP by the enzyme adenylyl cyclase, which resides in the cell membrane. The activation of adenylyl cyclase can result in the manufacture of hundreds or even thousands of cAMP molecules. These cAMP molecules activate the enzyme protein kinase A (PKA), which then phosphorylates multiple protein substrates by attaching phosphate groups to them. Each step in the cascade further amplifies the initial signal, and the phosphorylation reactions mediate both short- and long-term responses in the cell (Figure 2). How does cAMP stop signaling? It is degraded by the enzyme phosphodiesterase.
https://www.nature.com/scitable/topicpag...-14047077/

Good to see you've adopted keto, I've been on it for a few years. Do you incorporate IM (intermittent fasting) and exercise?. If you're in ketosis you shouldn't need exogenous-ketones supplements. I would encourage you to test your testosterone and estradiol, just to see what the current results look like from your regime, knowing those results can identify specific goals you want to achieve.

I would also suggest using a organic bone broth, glucosamine (which I can explain later), vitamin D with organic olive oil (not soybeans oil), Calcium citrate, (not Calcium carbonate which neutralizes stomach acid), monitor mineral intake. Pharma meds can inhibit/and or help NBE, just depends what's prescribed to you.