[Lotus]

Thank you Gabrielle for links, the vitamin D3 looks okay. I've not heard of Neo-Nutrition PM so I can't comment on its effectiveness, though I'm always leary of flashy advertising lol (to gimmicky, like stand behind your product without some big bossomed gal smacking you in the face). What if someone stumbled upon your stash?...oops  but, if it's helping I'm happy for you 

Thanks Teddy, recently I found out that vitamin D3 and calcium lower SHBG, and this is exactly what the doctor ordered to free up the coveted free estradiol %...the magical boob gold dust that feminizes and grows breasts. For me? that means taking 5000iu of vitamin D3 and 600mg of calcium, but 3g of msm too.

[BigBoobieBen]

Hi Ben, if you follow the manufacturer's recommended dosage of 1800 mg 3x per day you are covered imho. 

If you need to see the research on GTE and EGCG it's located in Bobbie's DHT thread on page #3
https://www.breastnexum.com/showthread.php?tid=25123

Btw, EGCG inhibits DHT between 85-95%, it doesn't raise SHBG either. 

200 ug/ml of green tea, around 7 oz. 

 Btw, not only does EGCG inhibit DHT and cancer, it also activates AMPK similar to the way metformin does but it also inhibits SIRT1, and if you're familiar with SIRT1 (Sirtuins) you should be because it'll increase your longevity, more to follow.

Yes I had read that post, that's where I got thenidea. Now just need to add wp.

[Lotus]

While researching I came across something interesting on diosgenin which as you may know is in Fenugreek, Wild Yam and Shatavari and a few other herbs.

The present study shows that diosgenin exerts the antidepressant activity, which is associated with the enhancement of neurotrophic function and the inhibition of inflammatory and neuroendocrine activities via the regulation of gut microbiota.

In addition, diosgenin was found to reduce serum concentrations of proinflammatory cytokines and the activity of the hypothalamic-pituitary-adrenal (HPA) axis.

Gut microbiota mediated inflammation, neuroendocrine and neurotrophic functions involved in the antidepressant-like effects of diosgenin in chronic restraint stress
 hypothalamic-pituitary-adrenal (HPA) axis.
https://pubmed.ncbi.nlm.nih.gov/36349650/


Diosgenin (Fig. 11.5) is a steroid saponin found in fenugreek seeds and yam [136]. Diosgenin has been found to be effective in ameliorating diabetic condition in both type 1 [137,138] and type 2 diabetes [139].
https://www.sciencedirect.com/topics/chemistry/diosgenin

We also know Fenugreek lowers SHBG and blood sugar. And now, knowing the possibility of FG possessing an antidepressant activity (a dosage of 20mg was used in the study) helps our ability to make an informed decision on what herbs to choose from. 

Wild Yam has diosgenin, it blocks 16α-hydroxyestrone (16OH) which is the toxic form of estrogen and carcinogenic. Enhancing the production of 2-OH form is beneficial for breast health. Diosgenin stimulates growth of mammary epithelium, increase in DNA content and the number of ducts & terminal end buds

[tanysquirrel]

holy crapola Lotus, this thread has over 460 pages, thats a good winter's read! lol guess i better start from page 1 then... 

[Lotus]

 

Green Tea-(updated version 2017):

promotes aromatase, increases GABA, promotes estrogen and estrogen gene target receptor (pS2) and PR-progesterone, modifies signaling transduction pathways, antioxidant (relieves oxidative stress & reduces lipid oxidation), possess potent iron-chelating radical-scavenging and anti-inflammatory activities (polyphenols EGCG Epigallocatechin 3-gallate-inhibits DHT and are powerful free radical destroyers), protects against neurological diseases. Green tea catechins ameliorate adipose insulin resistance, anti-androgen (inhibits DHT), stimulates beta-receptors at fat cells to increase release of lipids into the bloodstream, Green Tea displaces estradiol in SHBG, making a higher bioavailability of E2 (in the blood) benefiting delivery to target tissues. I believe green tea acts like a generic herbal version of Spironolactone.


 If you'd like more information about " steroidal and natural lactones " see here:
http://www.breastnexum.com/showthread.php?tid=17436&pid=194280&highlight=Lactones#pid194280

http://www.sciencedirect.com/science/art...1714000056
New insights into the mechanisms of polyphenols beyond antioxidant properties; lessons from the green tea polyphenol, epigallocatechin 3-gallate ☆

Highlights
•
Many biological actions of EGCG are mediated by specific mechanisms other than its well-known antioxidant properties.
•
EGCG is a pro-oxidant per se in some biological contexts.
•
EGCG directly interacts with cell surface membrane proteins and specific known receptors.
•
Treatment of cells with EGCG regulates specific intracellular signaling pathways and transcription.
•
Specific biological actions of EGCG are regulated in a concentration-dependent manner.
Abstract
Green tea is rich in polyphenol flavonoids including catechins. Epigallocatechin 3-gallate (EGCG) is the most abundant and potent green tea catechin. EGCG has been extensively studied for its beneficial health effects as a nutraceutical agent. Based upon its chemical structure, EGCG is often classified as an antioxidant. However, treatment of cells with EGCG results in production of hydrogen peroxide and hydroxyl radicals in the presence of Fe (III). Thus, EGCG functions as a pro-oxidant in some cellular contexts. Recent investigations have revealed many other direct actions of EGCG that are independent from anti-oxidative mechanisms. In this review, we discuss these novel molecular mechanisms of action for EGCG. In particular, EGCG directly interacts with proteins and phospholipids in the plasma membrane and regulates signal transduction pathways, transcription factors, DNA methylation, mitochondrial function, and autophagy to exert many of its beneficial biological actions.

I guess you are saying that it is more important to squash the more potent DHT than whatever level of inhibition of aromatase is caused by Silybin? Also about the other thing you mentioned: how does its inactivation of P450 3A4 and inhibiting of Glucuronidation affect NBE? Thanx.

Exactly, squash DHT by multiple means (pathways) and we'd see better gains. 

Re: Glucuronidation- think of Glucuronidation as a process to eliminate toxins (too detoxify) from tissues, (via excretion). see this attached study below as an example of using glucuronidation. As we know, GTE inhibits DHT.......it's all relative lol. 

Free Radic Res. 2004 Sep;38(9):1025-31.
Glucuronidation of the green tea catechins, (-)-epigallocatechin-3-gallate and (-)-epicatechin-3-gallate, by rat hepatic and intestinal microsomes.
Crespy V1, Nancoz N, Oliveira M, Hau J, Courtet-Compondu MC, Williamson G.
Author information


Abstract
The flavonoids (-)-epigallocatechin-3-gallate (EGCg) and (-)-epicatechin-3-gallate (ECg) are major components of green tea and show numerous biological effects. We investigated the glucuronidation of these compounds and of quercetin by microsomes. Quercetin was almost fully glucuronidated by liver microsomes after 3 h, whereas ECg and ECGg were conjugated to a lesser extent (12.2 +/- 0.2 and 7.5 +/- 0.2%, respectively). The intestinal microsomes also glucuronidated quercetin much more efficiently than ECg and EGCg. Although the rates were lower than quercetin, intestinal microsomes exhibited higher activity on the galloyl group of ECg and EGCg compared to the flavonoid ring, whereas hepatic glucuronidation was higher on the flavonoid ring of EGCg and ECg compared to the galloyl groups. The low glucuronidation rates could partially explain why these flavanols are present in plasma as unconjugated forms.

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. 

Green Tea - stimulates beta-receptors at fat cells to increase release of lipids into the bloodstream. Why is this important? 95-98% fatty acids are bound in the bloodstream (just like hormones are), we needed something that displaces hormones and fatty acids, looks like green tea is up for the task. 

Green tea raises growth hormones (theanine in tea raises GABA), even at resting.
Determination of theanine, GABA, and other amino acids in green, oolong, black, and Pu-erh teas with dabsylation and high-performance liquid chromatography.
Syu KY, et al. J Agric Food Chem. 2008.
Show full citation
Abstract
Dabsyl chloride (dimethylaminoazobenzene sulfonyl chloride), a useful chromophoric labeling reagent for amino acids and amines, was developed in this laboratory in 1975. Although several methods have been developed to determine various types of amino acids, a quick and easy method of determining theanine, GABA, and other amino acids has not been developed in one HPLC system. In this paper are analyzed the free amino acid contents of theanine and GABA in different teas (green tea, black tea, oolong tea, Pu-erh tea, and GABA tea) with a dabsylation and reverse phase high-performance liquid chromatography (HPLC) system coupled with a detector at 425 nm absorbance. Two reverse phase columns, Hypersil GOLD and Zorbax ODS, were used and gave different resolutions of dabsyl amino acids in the gradient elution program. The data suggest that the tea source or the steps of tea-making may contribute to the theanine contents variations. High theanine contents of high-mountain tea were observed in both green tea and oolong tea. Furthermore, the raw (natural fermented) Pu-erh tea contained more theanine than ripe (wet fermented) Pu-erh tea, and the GABA contents in normal teas were generally lower than that in GABA tea.
PMID 18652476 [PubMed - indexed for MEDLINE]

Green Tea displaces estradiol in SHBG, making a higher bioavailability of E2 (in the blood) benefiting delivery to target tissues. As said before, green tea raises SHBG and free's E2 (blood serum), I really believe it acts like a generic herbal version of Spirolactone.

Green Tea Epigallocatechin-Green tea (camellia)-Reduce's the conversion of free testosterone into DHT and also raises SHBG (sex-hormone-binding-globulin). Also is for breast cancer prevention, reduces visceral fat.

In this study (animal) aromatase expression increased in the AT (318.5 +/- 60.6% of control in scAT, P n< 0.05, and 285.5 +/- 82.9% of control in vAT,

That's 60.6% in subcutaneous fat and 82.9% in visceral fat. 

Chronic green tea consumption decreases body mass, induces aromatase expression, and changes proliferation and apoptosis in adult male rat adipose tissue.

Abstract
Green tea (GT) and its components have been shown to possess antiobesity properties and the corresponding mechanisms of action are being investigated, given the epidemic proportions of obesity incidence. In the current work, we used 12-mo-old male Wistar rats to test the effect of 6 mo of treatment with GT as the sole drinking beverage (52.8 +/- 6.4 mL/d) on adipose tissue (AT). AT aromatase expression was determined by Western blotting, plasma concentrations of 17beta-estradiol and testosterone were determined by RIA, and adipocyte size determined by measuring diameter in tissue sections. Proliferation and apoptosis were also assessed by Ki67 immunostaining and terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end-labeling, respectively. Evaluations were made in subcutaneous (sc) AT and visceral (v) AT. Body weight increased over time in both groups (P < 0.001), but the increase was more pronounced in controls (P < 0.001) and food and fluid intake did not influence that effect. At the end of the experiment, aromatase expression increased in the AT (318.5 +/- 60.6% of control in scAT, P < 0.05, and 285.5 +/- 82.9% of control in vAT, P < 0.01). AT of GT-treated rats had a higher percentage of proliferating cells (204.1 +/- 19.5% of control in scAT, P < 0.01, and 246.6 +/- 50.2% of control in vAT, P < 0.01) and smaller adipocytes (78.3 +/- 1.7% of control in scAT, P < 0.001, and 87.9 +/- 3.2% of control in vAT, P < 0.05). GT also increased the number of apoptotic cells in vAT (320.4 +/- 21.9% of control; P < 0.001). These results suggest new mechanisms for GT on body weight and highlight its potential benefit to prevent or treat obesity and the metabolic syndrome.

http://www.ncbi.nlm.nih.gov/pubmed/18936213#

The polyphenols (EGCG) in green tea absolutely inhibit DHT, (and in pharma strength I might add). Polyphenols inhibit 5 alpha reductase type 1. Dutasteride inhibits type 1 & 2 @ about 93%, effective but carries risk. Red clover, genistein (others too) inhibit type 2 (5 ar). 

Green tea protects the prostate and also lowers PSA levels too, which is why I'd still take it.

Btw, 

Green tea can increase a steady state expression level of pS2 and PR mRNA, which mRNA conveys genetic information from DNA to the ribosome (in other words-synthesis).

pS2-is an estrogen target gene 
PR-is progesterone receptor

Epigallocatechin gallate induces the steady state mRNA levels of pS2 and PR genes in MCF-7 breast cancer cells.
C Mohan C Manjegowda, Gauri Deb, Anil M Limaye

Abstract
Investigations using in vitro and in vivo models of breast carcinogenesis have demonstrated anti-neoplastic activity of the green tea polyphenol, epigallocatechin gallate (EGCG). Although a number of molecular targets of EGCG have been identified, its impact on the expression of estrogen target genes is not completely understood. Here, we examined the mRNA expression levels of two estrogen target genes, namely Trefoil Factor 1 (pS2) and Progesterone Receptor (PR) in MCF-7 cells treated with EGCG. We observed that treatment with 40 microM EGCG, which caused only 20% decrease in cell viability, resulted in increased steady state expression levels of pS2 and PR mRNA. This suggests that EGCG may exert its biological activities, at least in part, by influencing the expression of estrogen target genes

Further benefits of Green Tea

EGCG plays an important role in lipid metabolism in whole body physiology as well as at the cellular level.

EGCG directly interacts with plasma membrane proteins and phospholipids which stimulate intracellular signaling pathways. In addition, EGCG is transported to intracellular compartments, cytosol, mitochondria, lysosome, and nucleus where it mediates additional biological actions.

Effect of green tea on metabolic and hormonal aspect of polycystic ovarian syndrome in overweight and obese women suffering from polycystic ovarian syndrome: A clinical trial
https://www.jehp.net//article.asp?issn=2...st=Tehrani

EGCG Inhibits Proliferation and Induces Apoptosis Through Downregulation of SIRT1 in Nasopharyngeal Carcinoma Cells

Shisheng Jiang et al. Front Nutr. 2022.
Abstract

Epigallocatechin-3-gallate (EGCG), a frequently studied catechin in green tea, has been shown to be involved in the anti-proliferation and apoptosis of human nasopharyngeal carcinoma (NPC) cells. However, the underlying molecular mechanism of the apoptotic effects of EGCG has not been fully investigated. Recent literature emphasized the importance of Sirtuin 1 (SIRT1), an NAD+-dependent protein deacetylase, in regulating cellular stress responses, survival, and organismal lifespan. Herein, the study showed that EGCG could significantly inhibit cell proliferation and promote apoptosis of 2 NPC (CNE-2 and 5-8F) cell lines. Moreover, it was also found that SIRT1 is down-regulated by EGCG, and the SIRT1-p53 signaling pathway participates in the effects of EGCG on CNE-2 and 5-8 F cells. Taken together, the findings of this study provided evidence that EGCG could inhibit the growth of NPC cell lines and is linked with the inhibition of the SIRT1-p53 signaling pathway, suggesting the therapeutic potential of EGCG in human NPC.

[Lotus]

Reposting the following information on why your penis gets smaller when starting NBE or HRT (lol, you have been warned) 

But...there is a hack to recover from this now. 

The fact that estrogen receptors and aromatase are localized in a diverse subpopulation of penile cells, including neurons, epithelia, stroma, glandular cells suggests that its function in the penis is likely to be cell-specific and complex (Jesmin et al., 2002, 2004; Crescioli et al., 2003; Dietrich et al., 2004; Goyal et al., 2004; Vignozzi et al., 2004). 

We've discussed estrogen being produced (synthesized) in the testes, and aromatase stored in germ cells, epididymis, and is present in spermatozoa. We've even talked about how DHT can be turned into estrogen via the DHT metabolite 3beta-diol. So, as testosterone is being inhibited the ratio of T to E2 is shifted favoring estradiol synthesis in the testes, thus a reduction in the size of your penis.

Oops, almost forget, the density of 5 alpha reductase is strongly present on the head of the penis. With that aside, please read this pdf:

The penis: a new target and source of estrogen in male reproduction http://www.hh.um.es/pdf/Vol_21/21_1/Mowa...7-2006.pdf

Summary. In the past decade, interest and knowledge in the role of estrogen in male reproduction and fertility has gained significant momentum. More recently, the cellular distribution and activity of estrogen receptors (α and ß)(ER) and aromatase (estrogen synthesis) has been reported in the penis, making the penis the latest “frontier” in the study of estrogen in male reproduction. ER and aromatase are broadly and abundantly expressed in various penile compartments and cell types (erectile tissues, urethral epithelia, vascular and neuronal cells), suggesting the complexity and significance of the estrogen-ER system in penile events. Unraveling this complexity is important and will require utilization of the various resources that are now at our disposal including, animal models and humans lacking or deficient in ER and aromatase and the use of advanced and sensitive techniques. Some of the obvious areas that require our attention include: 1) a comprehensive mapping of ER-α and -ß cellular expression in the different penile compartments and subpopulations of cells, 2) delineation of the specific roles of estrogen in the different subpopulations of cells, 3) establishing the relationship of the estrogen-ER system with the androgen-androgen receptor system, if any, and 4) characterizing the specific penile phenotypes in human and animals lacking or deficient in estrogen and ER. Some data generated thus far, although preliminary, appear to challenge the long held dogma that, overall, androgens have a regulatory monopoly of penile development and function.

Fig. 8. Schematic diagram shows an overview distribution of ER in the penile tissues (glans penis, penis spongiosus, penis cavernosus, penile urethra). Bottom right, cross section of penis.

Estrogens, 17ß-estradiol and estrone, are produced from C19 androgens, testosterone and androstenedione, respectively, by cytochrome P450 arom (P450arom), a product of CYP19 gene. P450arom is a mono-oxygenase microsomal enzyme complex present in endoplasmic reticulum that irreversibly converts the aromatizable C19 androgens to estrogens through 3 consecutive hydroxylation reactions at the A-ring (Lephart 1996; Pereyra-Martinez et al. 2001; Carreau et al. 2002; Wiszniewska 2002). Aromatase is expressed in a tissue- specific manner and is composed of two proteins, namely, 1) a ubiquitous NADPH-cytochrome P450 reductase and 2) a cytochrome P450 aromatase, which contain the heme and the steroid pocket (Lephart 1996; Carreau et al. 1999, 2002).

[Lotus]

New pic for 2023, braless 

Screenshot_20230210_190035_Gallery.jpg Size: 321.9 KB  Downloads: 427

   
w/bra

[Johanez]

Lotus:

Damn! Having some boob envy... lol. Looking great!

Jo

[Mashtenn]

New pic for 2023, braless 



w/bra

Very nice Lotus.  They are awesome and give you a nice cleavage.

[Eloise]

I’m loving the 2023 Lotus!  Looking great!  

And thank you for the science drop on Green Tea.  Since it is such an effective DHT blocker, would it make sense to max that and drop RR?  Or is there still value to doing both?