[Lotus]

Sorry about this bump, here's some of the important things we need to keep in mind while grow boobs, and a few other things,

In other words, this confirms GID symptoms can be elevated by a suppression of T. So what are the things that inhibit the CYP17 enzyme, (plenty), the Pharma anti-fungal ketoconazole inhibits (strongly I might add) CYP17 enzyme. And guess what?, green tea, lemons inhibit CYP17.........amazing.

Thanks POM, sorry Ella.

Here's an example of what how interactions can happen, multiplying its effects. Say you drink green tea (a CYP17 inhibitor of testosterone). Now because you add piperine (in certain supplements, or added by supplementing) it increases the EGCG (polyphenols) in green tea by 1.3 fold.



J Nutr. 2004 Aug;134(8):1948-52.
Piperine enhances the bioavailability of the tea polyphenol (-)-epigallocatechin-3-gallate in mice.
Lambert JD1, Hong J, Kim DH, Mishin VM, Yang CS.
Author information
Abstract
(-)-Epigallocatechin-3-gallate (EGCG), from green tea (Camellia sinensis), has demonstrated chemopreventive activity in animal models of carcinogenesis. Previously, we reported the bioavailability of EGCG in rats (1.6%) and mice (26.5%). Here, we report that cotreatment with a second dietary component, piperine (from black pepper), enhanced the bioavailability of EGCG in mice. Intragastric coadministration of 163.8 micromol/kg EGCG and 70.2 micromol/kg piperine to male CF-1 mice increased the plasma C(max) and area under the curve (AUC) by 1.3-fold compared to mice treated with EGCG only. Piperine appeared to increase EGCG bioavailability by inhibiting glucuronidation and gastrointestinal transit. Piperine (100 micromol/L) inhibited EGCG glucuronidation in mouse small intestine (by 40%) but not in hepatic microsomes. Piperine (20 micromol/L) also inhibited production of EGCG-3"-glucuronide in human HT-29 colon adenocarcinoma cells. Small intestinal EGCG levels in CF-1 mice following treatment with EGCG alone had a C(max) = 37.50 +/- 22.50 nmol/g at 60 min that then decreased to 5.14 +/- 1.65 nmol/g at 90 min; however, cotreatment with piperine resulted in a C(max) = 31.60 +/- 15.08 nmol/g at 90 min, and levels were maintained above 20 nmol/g until 180 min. This resulted in a significant increase in the small intestine EGCG AUC (4621.80 +/- 1958.72 vs. 1686.50 +/- 757.07 (nmol/g.min)). EGCG appearance in the colon and the feces of piperine-cotreated mice was slower than in mice treated with EGCG alone. The present study demonstrates the modulation of the EGCG bioavailablity by a second dietary component and illustrates a mechanism for interactions between dietary chemicals.

http://www.ncbi.nlm.nih.gov/pubmed?filters=&orig_db=PubMed&cmd=Search&term=134%2A%5Bvolume%5D%20AND%201948%5Bpage%5D%20AND%202004%5Bpdat%5D%20AND%20Lambert%20JD%5Bauth%5D

Hi BN,

Here's a new idea to try...........citrus for breast growth (I'll explain). Three key enzymes (cyp 17, cyp 19, cyp 3A4) have direct pathways to breast/androgen synthesis. Cyp 3A4 controls more than 50% of how drugs are metabolized (I'd say that's a major regulator to piggy back off of), the only only issue there is mapping out all these key regulators, (it's like mapping out the genome).


Example: star fruit inhibits CY3A, more potent than grapefruit, ((which if you didn't notice, inhibiting CY3A4 will help with breast growth)).


Potent inhibition by star fruit of human cytochrome P450 3A (CYP3A) activity.
Hidaka M1, Fujita K, Ogikubo T, Yamasaki K, Iwakiri T, Okumura M, Kodama H, Arimori K.
Author information
Abstract
There has been very limited information on the capacities of tropical fruits to inhibit human cytochrome P450 3A (CYP3A) activity. Thus, the inhibitory effects of tropical fruits on midazolam 1'-hydroxylase activity of CYP3A in human liver microsomes were evaluated. Eight tropical fruits such as common papaw, dragon fruit, kiwi fruit, mango, passion fruit, pomegranate, rambutan, and star fruit were tested. We also examined the inhibition of CYP3A activity by grapefruit (white) and Valencia orange as controls. The juice of star fruit showed the most potent inhibition of CYP3A. The addition of a star fruit juice (5.0%, v/v) resulted in the almost complete inhibition of midazolam 1'-hydroxylase activity (residual activity of 0.1%). In the case of grape-fruit, the residual activity was 14.7%. The inhibition depended on the amount of fruit juice added to the incubation mixture (0.2-6.0%, v/v). The elongation of the preincubation period of a juice from star fruit (1.25 or 2.5%, v/v) with the microsomal fraction did not alter the CYP3A inhibition, suggesting that the star fruit did not contain a mechanism-based inhibitor. Thus, we discovered filtered extracts of star fruit juice to be inhibitors of human CYP3A activity in vitro.
PMID: 15155547 [PubMed - indexed for MEDLINE] Free full text

Here's what I'm thinking, tropicial fruits blocks the androgen pathway, like the enzyme CYP 17 does (inhibit androgen)........and, cyp 19 (is an aromatase promoter).

Inhibit CYP3A4
Inhibit CYP17
induce CYP19

In think incorporating a tropical fruit (call it a lotion?) massage, also adding a polyphenol (green tea extract, androgen inhibitor for max potential). Oral intake will still be the biggest bang though.

Anyways, with help from the one fella, I've got a head start on some of the enzymes (call them coregulators) mapped out. I'll post asap.

This is exciting stuff no? Who knew fruits would prove to be pro breast growth, and a healthy approach too.

This dumb fuffer's brain stopped working after reading one paragraph [/i]

Muther fluffin fuff myboobs ........j/k how about this?.

The DHT in ur nut sac can be made into estrogen without a big fuss. We can also reduce DHT in the prostate, reduce BPH and cancer by this second (newer estrogen) made from a side effect of DHT in the prostate and testes. Hopefully, this new process eliminates some of the supplements and lessens the strain on the liver, by all the NBE products. Not convinced?..........that crazy science mumbo jumbo I just listed says otherwise.

Could you summarize the supplements or procedure as to actually get your "DHT in ur nut sac [to be] made into estrogen" ? It looked like you first mentioned cortisol, so basically stress yourself out? Thanks!

If thats the case....no wonder transgender women are beautiful.....we stress over alot...thats alot of free flowing E in our veins.

Yes, stress makes you beautiful lol, wait what?. Isn't that typical though, one hormone gain means dealing with it's side effect and might impact the benefits of other hormones. However in this case cortisol has a direct effect on ER-b (estrogen receptor beta) in the prostrate and testes, HSD 11 beta type 1 reduces cortisone to the active hormone cortisol that activates glucocorticoid receptors, in that instance it (glucocorticoid receptors) helps with boob growth, which we have in boobs, about 20% (glucocorticoid receptors). Licorice and green tea reduce 11 beta HSD type 1. I believe Leptin does the same though. Soooo....following the science I colored highlighted the two key points of interest. As you read this process could go either way, imo if you suppress DHT it will upregulate estrogen to activate E1 to E2 the active form of estrogen (Estradiol), which is what feminizes. I do suggest (even with Hrt) you at least normalize the androgen production in the testes 1-2 times a month. The amino acids L-arginine, Tuarine, Tyrosine all helps in this new process, I will explain about those too.


Sex steroids and leptin regulate 11β-hydroxysteroid dehydrogenase I and P450 aromatase expressions in human preadipocytes: Sex specificities
Service de Biochimie et de Biologie Moléculaire, UPRES EA 2493, Faculté de Médecine Paris-Ile de France-Ouest, Université Versailles St Quentin, Centre Hospitalier de Poissy, 78303 Poissy Cedex, France.
The Journal of Steroid Biochemistry and Molecular Biology (Impact Factor: 3.63). 07/2006; 99(4-5):189-96. DOI: 10.1016/j.jsbmb.2006.01.007
Source: PubMed
ABSTRACT
Adipose tissue is an important site of steroid hormone biosynthesis, as type I 11beta-hydroxysteroid dehydrogenase (HSD1), the enzyme responsible for the conversion of cortisone into cortisol and the P450 aromatase, the enzyme catalysing androgens aromatization into estrogens, are both expressed in human adipose tissue. In the present report, we have investigated the possibility that sex steroids and leptin could regulate these two enzymes in cultured preadipocytes from men and women intra-abdominal fat depots. In women preadipocytes, human recombinant leptin down-regulates HSD1 mRNA expression (-58%) and P450 aromatase activity (-26%). Conversely, leptin up-regulates the HSD1 (2.4-fold) and the P450 aromatase (1.6-fold) mRNA expression in men preadipocytes. In women preadipocytes, 17beta-estradiol strongly stimulates HSD1 mRNA expression (10-fold) and, in contrast, decreases by half the P450 aromatase expression. In men, 17beta-estradiol has no influence on HSD1 expression but up-regulates P450 aromatase mRNA expression (2.4-fold). Finally, androgens increase by a factor of 2.5-5 the mRNA expression of both enzymes in men. These findings suggest that sex steroids and leptin either increase or decrease local cortisol and estrogens productions in men or in women preadipocytes, respectively. They also indicate that steroid metabolism in adipose tissue is controlled by a coordinated regulation of P450 aromatase and HSD1 expressions. Finally, the important sex-specific differences described herein may also contribute to explain the sexual dimorphism of body fat distribution in humans.

I'll post more info tomorrow (hopefully) have a good night.

Hi Lotuss, I was reading this:

Available research suggests that doses of more than 25 milligrams of lycopene daily may lower levels of low-density lipoprotein (LDL, or "bad") cholesterol and total cholesterol. Although this is promising, more high-quality research is needed in this area.

And I thought about the 'fat in fat out' sentence in the big post up here, could this be of help?.... Lowering ldl helps fat storage? Or is this totally off route..bc im already on green tea and coconutoil etc. Im searching for something new..

Hi Hannah,

This fat in/fat out is what I think that FAT Flux does for our fat cells, meaning that energy from new fat is used within that hour, in others words fuel for breasts cells to synthesize new growth. This is just a theory (lol, mine), but, I see the science, now extrapolating into NBE is the tough part. Emulsification in the intestines (or should I say, better Emulsification) is tied to progesterone and testosterone, (through a network of enzymes), I know, more complexity. however, insulin is the master control here, imo. Green tea helps in burning fat, (I think other fat supps can be helpful too), which can help fight LDL. Exercising can also benefit getting rid of storing the new fat. However, stored fats house estrogen, isn't that a huge potential to burn that stored estrogen?, I would think so considering we continue to add more and more phytoestrogens/estradiol. Studies show that the half life in E2 (Pharma) is present for days, so we may not think its (E2) there working (so I take more) but it's still working). TTYL


It is also possible for fat cells to take up glucose and amino acids, which have been absorbed into the bloodstream after a meal, and convert those into fat molecules. The conversion of carbohydrates or protein into fat is 10 times less efficient than simply storing fat in a fat cell, but the body can do it. If you have 100 extra calories in fat (about 11 grams) floating in your bloodstream, fat cells can store it using only 2.5 calories of energy. On the other hand, if you have 100 extra calories in glucose (about 25 grams) floating in your bloodstream, it takes 23 calories of energy to convert the glucose into fat and then store it. Given a choice, a fat cell will grab the fat and store it rather than the carbohydrates because fat is so much easier to store.

How Fat Cells Work
http://science.howstuffworks.com/life/ce...-cell2.htm

http://www.breastnexus.com/showthread.php?tid=17436&pid=163166&highlight=Green+tea#pid163166