Breast Growth For Genetic Males

** fatty acid synthase (FASN) in (humans)

Gene ID: 2194, updated on 21-Mar-2015

The enzyme encoded by this gene is a multifunctional protein. Its main function is to catalyze the synthesis of palmitate from acetyl-CoA and malonyl-CoA, in the presence of NADPH, into long-chain saturated fatty acids. In some cancer cell lines, this protein has been found to be fused with estrogen receptor-alpha (ER-alpha), in which the N-terminus of FAS is fused in-frame with the C-terminus of ER-alpha. [provided by RefSeq, Jul 2008]
http://www.ncbi.nlm.nih.gov/gene/2194

More scientific proof that fatty acids helps with the binding process of estrogen receptor alpha (ER-a, the growth receptor). Specifically---palmitate (a solid unsaturated fat). I hope this is making sense for everybody. In other words- omega 3's and 6's needs to be in an NBE plan, the health benefits alone are worth looking into, another benefit is its ability to block DHT (e.g. Evening primrose oil, EPO).

Coconut oil
Evening primrose oil
Macadamia nut oil
Krill oil

And organic when possible.

Thanks Lotus for this info. I really can use it. POM

(23-03-2015, 04:38 AM)Lotus Wrote: [ -> ]** fatty acid synthase (FASN) in (humans)

Gene ID: 2194, updated on 21-Mar-2015

The enzyme encoded by this gene is a multifunctional protein. Its main function is to catalyze the synthesis of palmitate from acetyl-CoA and malonyl-CoA, in the presence of NADPH, into long-chain saturated fatty acids. In some cancer cell lines, this protein has been found to be fused with estrogen receptor-alpha (ER-alpha), in which the N-terminus of FAS is fused in-frame with the C-terminus of ER-alpha. [provided by RefSeq, Jul 2008]
http://www.ncbi.nlm.nih.gov/gene/2194

More scientific proof that fatty acids helps with the binding process of estrogen receptor alpha (ER-a, the growth receptor). Specifically---palmitate (a solid unsaturated fat). I hope this is making sense for everybody. In other words- omega 3's and 6's needs to be in an NBE plan, the health benefits alone are worth looking into, another benefit is its ability to block DHT (e.g. Evening primrose oil, EPO).

Coconut oil
Evening primrose oil
Macadamia nut oil
Krill oil

And organic when possible.

(23-03-2015, 04:41 AM)pom19 Wrote: [ -> ]Thanks Lotus for this info. I really can use it. POM

Thanks Pom, I hope it helps.

(30-01-2015, 07:27 PM)Lotus Wrote: [ -> ]PUFA's- polyunsaturated -fats increase estrogen.

Monounsaturated-fats increase testosterone

Polyphenols (specifically Green Tea) promotes aromatase, anti-oxidation, estrogen, modifies signaling transduction pathways, relieves oxidative stress (reduces lipid oxidation), possess potent iron-chelating radical-scavenging and anti-inflammatory activities (polyphenols are powerful free radical destroyers), protects against neurological diseases. Green tea catechins ameliorate adipose insulin resistance.

(09-01-2015, 09:55 PM)Lotus Wrote: [ -> ]Sorry for the redundancy, but in case you missed it, this is extremely important:

(08-01-2015, 06:01 AM)Lotus Wrote: [ -> ]Considering the potential to block DHT and increase aromatase adding fatty acids makes sense, only don't forget a fitness plan.

Anti-androgenic activity of fatty acids.

In this study, we show that 5alpha-reductase derived from rat fresh liver was inhibited by certain aliphatic free fatty acids. The influences of chain length, unsaturation, oxidation, and esterification on the potency to inhibit 5alpha-reductase activity were studied. Among the fatty acids we tested, inhibitory saturated fatty acids had C12-C16 chains, and the presence of a C==C bond enhanced the inhibitory activity. Esterification and hydroxy compounds were totally inactive. Finally, we tested the prostate cancer cell proliferation effect of free fatty acids. In keeping with the results of the 5alpha-reductase assay, saturated fatty acids with a C12 chain (lauric acid) and unsaturated fatty acids (oleic acid and alpha-linolenic acid) showed a proliferation inhibitory effect on lymph-node carcinoma of the prostate (LNCaP) cells. At the same time, the testosterone-induced prostate-specific antigen (PSA) mRNA expression was down-regulated. These results suggested that fatty acids with 5alpha-reductase inhibitory activity block the conversion of testosterone to 5alpha-dihydrotestosterone (DHT) and then inhibit the proliferation of prostate cancer cells.
http://www.ncbi.nlm.nih.gov/pubmed/19353546

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(18-12-2014, 05:48 AM)Lotus Wrote: [ -> ]I'd say to consider the many different options out there, currently I take coconut oil, (although not a GLA) I'd consider EPO, and from what I understand you can vary (trade off) between say (borage oil, EPO, flaxseed oil or others), which FSO isn't said to contain anti-aromatase properties. But I don't mind giving T a pass through anti-aromatase while on CO, I like it, but that's just my opinion, if you don't mind smelling like a nut, it's absolutely wonderful for soft soft hair.

http://www.livestrong.com/article/441704...-primrose/
http://www.drugs.com/drug-interactions/e...10681.html
https://www.consumerlab.com/reviews/Blac.../flaxseed/
http://www.livestrong.com/article/525321...mrose-oil/

Fats and oils are essential to your health and many of your body's functions. The oils most important for brain, nerves and skin include the essential fatty acids, which are available in a variety of foods that include olive oil and avocados. Flaxseeds also provide an important essential fatty acid called omega-3, which is strongest in its oil. Evening primrose, which contains omega-6s, is not usually consumed as a food, but rather its oil is taken in supplement form.


Flaxseed oil comes from the seeds of the flax plant. This oil provides the important essential fatty acids linolenic acid and linoleic acid, according to Shawn M. Talbott in his book "The Health Professional's Guide to Dietary Supplements." Flaxseed oil contains about 57 percent linolenic acid, which is an omega-3 fatty acid, and about 17 percent linoleic acid, an omega-6 fatty acid. It is important to get a balance of omega-3 fatty acids to omega-6 fatty acids. However, the standard American diet contains too many omega-6 fatty acids and few omega-3 fatty acids. Omega-3 fatty acids help counter inflammation and increase brain function. Flaxseed oil also contains lignan, which is a phytochemical that may help cancer prevention.

Evening primrose oil comes from the herb Oenothera biennis, which has bright yellow flowers that bloom in the evening, writes Talbott. The plant grows wild in dry, arid environments, and was first documented in Britain as being used for medicinal purposes. The main oil found in evening primrose oil is gamma-linolenic acid, another essential fatty acid, though it also contains linoleic acid. People have taken evening primrose oil include to relieve PMS, hot flashes and fibrocystic breasts.

How They Differ
The main difference between flaxseed oil and evening primrose oil is that the former contains the omega-3 linolenic acid, while the latter contains the omega-6 gamma-linolenic acid, or GLA for short. Omega-3s are linked to a lower risk of heart disease, cancer and arthritis, often through their anti-inflammatory properties, notes the University of Maryland Medical Center. Though GLA is an omega-6 fatty acid, which is sometimes connected to inflammation, it is one form of omega-6 that also can reduce inflammation, but is geared more toward skin, hair, reproductive and bone health. But the University of Maryland reports that more research favors the anti-inflammatory properties of the omega-3 fatty acids found in flaxseed oil more than that of GLA found in evening primrose oil.

What to Consider
Both flaxseed oil and evening primrose oil can be healthy parts of your diet, and you can consume both at the same time. Ingesting more flaxseed oil or flaxseeds than evening primrose oil can help balance your intake of omega-3 fatty acids and omega-6 fatty acids. Possible side effects related to flaxseed oil are diarrhea if you consume large amounts and the increased risk of bleeding if you suffer from a bleeding disorder. Nausea, upset stomach or diarrhea may occur if you take too much evening primrose oil.

Lotus,

I was wondering if Vitex and PM may be used in the same program? I was thinking of low dose PM during folli and vitex all throughout...?

(23-03-2015, 09:54 AM)Koko Wrote: [ -> ]Lotus,

I was wondering if Vitex and PM may be used in the same program? I was thinking of low dose PM during folli and vitex all throughout...?

Hi Koko,

I think it could work, I don't see any conflicts.

(22-02-2015, 07:53 PM)Lotus Wrote: [ -> ]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

I've spent more time researching on this backdoor estrogenic action of DHT, aka estrogen receptor beta. From what I see when DHT is metabolized in the liver we can force it to this ER-b back door, thereby lessening (or inactivating) it's potential. And imo cortisteriods inactivates DHT.

_____________________________________________

(07-02-2015, 08:33 AM)Lotus Wrote: [ -> ]

(13-01-2015, 07:44 PM)Lotus Wrote: [ -> ]It's like deconstructing a model (call it a airplane model) that someone else built, only you're working in reverse to deconstruct right. Same applies here, you see a study that states 5 alpha reductase is reduced in the liver, now maybe this study was for cancer research or something similar. Let's take one of these studies,

Role of human type 3 3alpha-hydroxysteroid dehydrogenase (AKR1C2) in androgen metabolism of prostate cancer cells.

Aldo-keto reductases (AKRs) is another superfamily class of enzymes like the Cytochrome P450 enzyme super family, which are present in most tissues of the body, and play important roles in hormone synthesis and breakdown (including estrogen and testosterone synthesis and metabolism), cholesterol synthesis, and vitamin D metabolism. Cytochrome P450 enzymes also function to metabolize potentially toxic compounds, including drugs and products of endogenous metabolism such as bilirubin, principally in the liver.

AKRs are involved in the development and progression of many cancers, as well as chemotherapeutic drug resistance. AKR1B1 and AKR1B10 are overexpressed in tumors, such as liver, breast, and lung cancer. Several AKRs (AKR1A1, AKR1B10, and AKR1C1-3) are involved in tobacco-carcinogenesis, but they also catalyze the detoxication of nicotine derived nitrosamino ketones. In addition, AKR1C1-3 enzymes play a key role in the regulation of proliferative signaling in hormone dependent cancers.

So what they did in this study was to cut off the androgen synthesis to the receptors using another steroid , Four human aldo-keto reductases (AKRs) that belong to the AKR1C subfamily function in vitro as 3-keto-, 17-keto- and 20-ketosteroid reductases or as 3alpha-, 17beta- and 20alpha- hydroxysteroid oxidases to varying degrees. By acting as ketosteroid reductases or hydroxysteroid oxidases these AKRs can either convert potent sex hormones (androgens, estrogens and progestins) into their inactive metabolites or they can form potent hormones by catalyzing the reverse reaction. In this manner they may regulate occupancy and trans-activation of steroid hormone receptors.

In English, I want to find the link to activate AKR1c in the liver to shut off the androgen receptors therefore DHT never gets activated, simple right?.

Cha-Ching, found it.

Regulates access of 5alpha-DHT to the androgen receptor.

Abstract
Pairs of hydroxysteroid dehydrogenases (HSDs) govern ligand access to steroid receptors in target tissues and act as molecular switches. By acting as reductases or oxidases, HSDs convert potent ligands into their cognate inactive metabolites or vice versa. This pre-receptor regulation of steroid hormone action may have profound effects on hormonal response. We have identified the HSDs responsible for regulating ligand access to the androgen receptor (AR) in human prostate. Type 3 3alpha-hydroxysteroid dehydrogenase (aldo-keto reductase 1C2, aka-AKR acts solely as a reductase to convert 5alpha-dihydrotestosterone (DHT), a potent ligand for the AR (K(d)=10(-11)M for the AR), to the inactive androgen 3alpha-androstanediol (K(d)=10(-6)M for the AR); while RoDH like 3alpha-HSD (a short-chain dehydrogenase/reductase (SDR)) acts solely as an oxidase to convert 3alpha-androstanediol back to 5alpha-DHT. Our studies suggest that aldo-keto reductase (AKRs) and SDRs function as reductases and oxidases, respectively, to control ligand access to nuclear receptors.
http://www.ncbi.nlm.nih.gov/pubmed/17223255

Notice how Aldo-keto reductases (AKRs) position themselves between DHT and 3-diols, this is where the estrogenic action takes place. These actions of AKR1C's takes place in androgen metabolism of the prostate.

Aldo-keto reductases (AKRs) is another superfamily class of enzymes like the Cytochrome P450 enzyme super family.



[attachment=9517]


Estrogen receptor β and 17β-hydroxysteroid dehydrogenase type 6, a growth regulatory pathway that is lost in prostate cancer

Estrogen receptor β (ERβ) is activated in the prostate by 5α-andros- tane-3β,17β-diol (3β-Adiol) where it exerts antiproliferative activity. The proliferative action of the androgen receptor is activated by 5α- dihydrotestosterone (DHT). Thus, prostate growth is governed by the balance between androgen receptor and ERβ activation. 3β- Adiol is a high-affinity ligand and agonist of ERβ and is derived from DHT by 3-keto reductase/3β-hydroxysteroid dehydrogenase en- zymes. Here, we demonstrate that, when it is expressed in living cells containing an estrogen response element-luciferase reporter, 17β-hydroxysteroid dehydrogenase type 6 (17βHSD6) converts the androgen DHT to the estrogen 3β-Adiol, and this leads to activation of the ERβ reporter. This conversion of DHT occurs at concentrations that are in the physiological range of this hormone in the prostate. Immunohistochemical analysis revealed that 17βHSD6 is expressed in ERβ-positive epithelial cells of the human prostate and that, in prostate cancers of Gleason grade higher than 3, both ERβ and 17βHSD6 are undetectable. Both proteins were present in benign prostatic hyperplasia samples. These observations reveal that for- mation of 3β-Adiol via 17βHSD6 from DHT is an important growth regulatory pathway that is lost in prostate cancer.

http://www.ncbi.nlm.nih.gov/pmc/articles...117772.pdf

Here's an excellent study on adipose (fat), adipose tissue acts as its own steroid hormone organ, that's pretty cool, And the predominant activity of adipose tissue, comes from the reduction of inactive cortisone to active cortisol.

Pathways of adipose tissue androgen metabolism in women: depot differences and modulation by adipogenesis

A SURVEY OF THE LITERATURE on adipose tissue steroid conversions indicated that several isoforms of steroidogenic and steroid-inactivating enzymes can be detected in adipose tissue (3). Specifically, as many as 15 steroidogenic and steroid-inactivating enzyme mRNAs/activities have been detected to date in human adipose tissue, including aromatase, 3β-hydroxysteroid dehydrogenase (HSD) type 1, 3α-HSD type 3 [aldo-keto reductase 1C2 (AKR1C2)], 11β-HSD type 1 and type 2, 17β-HSD types 2, 3, and 5 (AKR1C3), 20α-HSD (AKR1C1), 7α-hydroxylase, 17α-hydroxylase, 5α-reductase, steroid sulfatase, and UDP-glucuronosyltransferase 2B15 (3–7, 11, 38). The capacity of peripheral tissues to synthesize and inactivate androgens/estrogens has been termed intracrinology (21, 22). Thus, in addition to its widely recognized endocrine chracteristics (20), adipose tissue also functions as an intracrine organ with respect to steroid hormones.

One of the steroidogenic enzymes expressed in adipose tissue, 11β-HSD-1, has attracted much scientific attention in recent years. Expression and activity of 11β-HSD-1 was demonstrated in fat cells from breast, omental, and subcutaneous adipose tissue (8, 42). Studies have found that the predominant activity in adipose tissue was the reduction of inactive cortisone to active cortisol (8, 19). Using cell cultures and transgenic mouse model studies by Bujalska et al. (9) and Masuzaki et al. (24) led to the demonstration that increased local cortisol production by 11β-HSD-1 may be one of the causal factors in the etiology of visceral obesity. These studies on local cortisol metabolism in fat have dramatically emphasized the importance of steroidogenic enzyme expression in the etiology of visceral obesity and related metabolic complications (9, 24). The impact of other steroidogenic enzymes that could modulate in a similar manner the exposure of abdominal adipocytes to active steroids, namely androgens and estrogens, remains to be established. In addition, regional adipose tissue depot differences in steroid-converting enzymes have not been examined for most of the enzymes identified in adipose tissue.
http://ajpendo.physiology.org/content/296/2/E244

11β-HSD-1 is influenced by Licorice Root

Great news, I think.. But how does that help us boob lover's?

(24-03-2015, 02:24 AM)iaboy Wrote: [ -> ]Great news, I think.. But how does that help us boob lover's?

Inactivating DHT.......