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NBE-Research
#41
(30-06-2016, 09:42 PM)Huggy Wrote: Hiya bud :-)

(Just noticed.... Lotus... Bud.... :-)

Anyway, just done a check and Cimetidine is prescription only in the UK. It seems to have a bad rep for side effects (at least over here).

It might be possible to find it as a minor ingredient in an over the counter med? But as far as I have found so far, that's about it.

Huggs


Walmart carries Cimitidine..OTC (over the counter..) as well as it is an ingredient in Pepcid ....another over the counter stomach acid preventer. not sure if the amazon in UK carries it. or your Walmart if you have any there. check the stomach acid aisle... Tagamet has rantadine ( if I am correct) which has similar, yet weaker effects.
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#42
This may be hard but can you do a case study on my NBE plan?

My new idea: Make bra fitting high tech. Combine my breast photos and bra photos overlayed to see if color, cup, band size and preference can be determined. I call it new bra sizing technique. Any impressions?
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#43
(01-07-2016, 01:01 AM)BillyBoy_Delano Wrote: This may be hard but can you do a case study on my NBE plan?

My new idea: Make bra fitting high tech. Combine my breast photos and bra photos overlayed to see if color, cup, band size and preference can be determined. I call it new bra sizing technique. Any impressions?


There's a low tech solution to finding out cup size, all that's needed is sewing tape.

1). Measure from the middle of the arm pit to the center of the chest. This measurement is the cup size, from that analysis weekly tracking is highly recommended. Band size is the difference between chest circumference and under breast difference, don't be surprised if the difference between cup size and breast (bra) size aren't the same.

As for the color...........personal preference I guess.
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#44
Awesome, " co-activators " such SRC-2 (steroid receptor coactivator ) enhances transcriptional activity of a variety of nuclear receptors, including ER, PR and AR (Voegel et al., 1996). Translation?....we can improve the bioavailability of hormone receptors (loosely translated)  Shy that essentially tells the steroid receptor to behave the way WE want them too. Btw, transcription (basically) means growth.     https://en.m.wikipedia.org/wiki/Transcription_(biology)

In others words......a co-administration of E2, an antihistamine or H2 receptor antagonist supplement, vitamin D, and spirolactone (or similar) should elicit SRC-2 covactivator to upregulate Estrogen Receptor Alpha, and there on to sexual differentiation (aka feminization). The following study explains my meaning. For NBE/hrt I think this opens the door of neuro-endocrinology to new findings to stimulate sex steroids in a disease free state. 

more info see here:
Neuroactive steroids: An update of their roles in central and peripheral nervous system 
https://www.researchgate.net/profile/Rob...system.pdf


Nuclear Receptor Coactivators
Abstract
The effects that steroid hormones exert on gene expression via their nuclear receptors (NRs) must be tightly regulated, in particular because of their pleiotropic effects in many tissues. To that end, regulation of receptor activity takes place at multiple levels, which include ligand availability, epigenetic modifications of chromatin around tissue-specific target genes, expression levels of the receptor, and the presence or absence of other NRs in the same cell. One of the levels of transcriptional control is that of the NR coregulators, proteins that can interact with NRs and modulate their function. Coregulators can interact with multiple NRs and NRs can interact with multiple coregulators. As a consequence, coregulator expression in certain cell types may play the roles of hubs and bottleneck that offers gene target, cell type, or context specificity. Below we offer an overview of NR coregulator function, highlighting the best-described coregulators in the brain, as well as possibilities for the manipulation of NR–coregulator interactions for therapeutic or experimental purposes.



TIF2, a 160 kDa transcriptional mediator for the ligand-dependent activation function AF-2 of nuclear receptors.
Nuclear receptors (NRs) act as ligand-inducible transcription factors which regulate the expression of target genes upon binding to cognate response elements. 
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC452006/


Modulation of steroid action in the central and peripheral nervous systems by nuclear receptor coactivators 

Summary Steroid hormones act in the central and peripheral nervous systems to regulate a variety of functions, including development, cell proliferation, cognition and behavior. Many of these effects of steroid hormones are mediated by their respective receptors, which are members of the nuclear receptor superfamily of transcriptional activators. A variety of cell culture studies reveal that nuclear receptor coactivators are recruited to the steroid receptor complex and are critical in modulating steroid-dependent transcription. Thus, in addition to the availability of the hormone and its receptor, the expression of nuclear receptor coactivators is essential for modulating steroid receptor-mediated transcription. This review will discuss the significance of nuclear receptor coactivators in modulating steroid-dependent gene expression in the central and peripheral nervous systems and the regulation of behavior. # 2009 Elsevier Ltd. All rights reserved.




Coactivators enable glucocorticoid receptor recruitment to fine-tune estrogen receptor transcriptional responses 

Nuclear receptors (NRs) are central regulators of pathophysiological processes; however, how their responses intertwine is still not fully understood. The aim of this study was to determine whether and how steroid NRs can influence each other’s activity under co-agonist treatment. We used a unique system consisting of a multicopy integration of an estrogen receptor responsive unit that allows direct visualization and quantification of estrogen receptor alpha (ER) DNA binding, co-regulator re- cruitment and transcriptional readout. We find that ER loading is required for other type I nuclear receptors to be co-recruited after dual agonist treat- ment. We focused on ER glucocorticoid receptor interplay and demonstrated that it requires steroid receptor coactivators (SRC-2, SRC-3) and the mediator component MED14. We then validated this cooperative interplay on endogenous target genes in breast cancer cells. Taken together, this work highlights another layer of mechanistic com- plexity through which NRs cross-talk with each other on chromatin under multiple hormonal stimuli. 

https://oup.silverchair-cdn.com/oup/back...A4LVPAVW3Q

Chromatin regulation

Histones undergo posttranslational modifications that alter their interaction with DNA and nuclear proteins. The H3 and H4 histones have long tails protruding from the nucleosome, which can be covalently modified at several places. Modifications of the tail include methylationacetylationphosphorylationubiquitinationSUMOylationcitrullination, and ADP-ribosylation. The core of the histones H2A and H2B can also be modified. Combinations of modifications are thought to constitute a code, the so-called "histone code".[27][28] Histone modifications act in diverse biological processes such as gene regulationDNA repair, chromosome condensation (mitosis) and spermatogenesis (meiosis).[29]

https://en.m.wikipedia.org/wiki/Histone
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#45
(17-06-2017, 08:11 AM)Lotus Wrote: I now understand how highly organized molecules function inside the mitochondrial matrix, for instance: ATP (which stands for Adenosine Triphosphate) is the Energy Currency for Cells, but before I get into the science (which blows my mind) I must admit ignorance in my early NBE programs.....yup!, I didn't know any better back then  Rolleyes  but here I am now better prepared/informed and ready take on the science of NBE/hrt.

Btw, only using 600 mg of fenugreek (with 50% saponins) works just fine:
Fenugreek increases estradiol
http://www.breastnexus.com/showthread.php?tid=26172

Part of the reason (which I know believe) what makes fenugreek useful for NBE is how it works in stomach acid...the saponins (emulsifiers) in FG is mechanism for boosting estradiol in stomach acid, I'll follow up on that later though.
 

How ATP Transfers Energy
Energy is usually liberated from the ATP molecule to do work in the cell by a reaction that removes one of the phosphate-oxygen groups, leaving adenosine diphosphate (ADP). When the ATP converts to ADP, the ATP is said to be spent. Then the ADP is usually immediately recycled in the mitochondria where it is recharged and comes out again as ATP. In the words of Trefil (1992, p. 93) “hooking and unhooking that last phosphate [on ATP] is what keeps the whole world operating.”

The enormous amount of activity that occurs inside each of the approximately one hundred trillion human cells is shown by the fact that at any instant each cell contains about one billion ATP molecules. This amount is sufficient for that cell’s needs for only a few minutes and must be rapidly recycled. Given a hundred trillion cells in the average male, about 10 to the 23rd power * or one sextillion ATP molecules normally exist in the body. For each ATP “the terminal phosphate is added and removed 3 times each minute” (Kornberg, 1989, p. 65).




The total human body content of ATP is only about 50 grams, which must be constantly recycled every day. The ultimate source of energy for constructing ATP is food; ATP is simply the carrier and regulation-storage unit of energy. The average daily intake of 2,500 food calories translates into a turnover of a whopping 180 kg (400 lbs) of ATP (Kornberg, 1989, p. 65).

The Structure of ATP
ATP contains the purine base adenine and the sugar ribose which together form the nucleoside adenosine. The basic building blocks used to construct ATP are carbon, hydrogen, nitrogen, oxygen, and phosphorus which are assembled in a complex that contains the number of subatomic parts equivalent to over 500 hydrogen atoms. One phosphate ester bond and two phosphate anhydride bonds hold the three phosphates (PO4) and the ribose together. The construction also contains a b-N glycoside bond holding the ribose and the adenine together.
https://www.trueorigin.org/atp.php

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I  believe I can now offer an explanation why bellies get bigger (for some) when using NBE/hrt.


Mitochondrial respiration in subcutaneous and visceral adipose tissue from patients with morbid obesity
Kraunsøe R1, Boushel R, Hansen CN, Schjerling P, Qvortrup K, Støckel M, Mikines KJ, Dela F.
Author information

Erratum in
* J Physiol. 2010 Oct 15; 588(Pt 20):4055.
Abstract
Adipose tissue exerts important endocrine and metabolic functions in health and disease. Yet the bioenergetics of this tissue is not characterized in humans and possible regional differences are not elucidated. Using high resolution respirometry, mitochondrial respiration was quantified in human abdominal subcutaneous and intra-abdominal visceral (omentum majus) adipose tissue from biopsies obtained in 20 obese patients undergoing bariatric surgery. Mitochondrial DNA (mtDNA) and genomic DNA (gDNA) were determined by the PCR technique for estimation of mitochondrial density. Adipose tissue samples were permeabilized and respirometric measurements were performed in duplicate at 37 degrees C. Substrates (glutamate (G) + malate (M) + octanoyl carnitine (O) + succinate (S)) were added sequentially to provide electrons to complex I + II. ADP ((D)) for state 3 respiration was added after GM. Uncoupled respiration was measured after addition of FCCP. Visceral fat contained more mitochondria per milligram of tissue than subcutaneous fat, but the cells were smaller. Robust, stable oxygen fluxes were found in both tissues, and coupled state 3 (GMOS(D)) and uncoupled respiration were significantly (P < 0.05) higher in visceral (0.95 +/- 0.05 and 1.15 +/- 0.06 pmol O(2) s(1) mg(1), respectively) compared with subcutaneous (0.76 +/- 0.04 and 0.98 +/- 0.05 pmol O(2) s(1) mg(1), respectively) adipose tissue. Expressed per mtDNA, visceral adipose tissue had significantly (P < 0.05) lower mitochondrial respiration. Substrate control ratios were higher and uncoupling control ratio lower (P < 0.05) in visceral compared with subcutaneous adipose tissue. We conclude that visceral fat is bioenergetically more active and more sensitive to mitochondrial substrate supply than subcutaneous fat. Oxidative phosphorylation has a higher relative activity in visceral compared with subcutaneous adipose tissue.

So you see----visceral fat contains more mitochondrial matrix to make more fat from, and this can be completed as seen in billions of signals within minutes inside the mitochondrial matrix. So either burn the excess (energy) so it doesn't go to fat storage. Or....add a supplement that break down fats.

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Why does breast growth fail/falter or disappear?....the reason (imo) is that it's lacking a vascular network, and without a current blood supply to new tissue (breast) disappears, and while this is a new explanation, it's not new in terms of science. Recently scientists have created a vascular network using a spinach leaf.....(simple amazing) see here:
https://www.sciencedaily.com/releases/20...152753.htm

And what this tells me is that new breast tissue needs to be of muscle....then a vascular network can be added (to muscle), the technology gets a little complicated but think in terms of when using breast pumps, like when breast tissue is expanded using static pressure it's pumping/pulling fats to expand fat cells, where pumping falters is not having a blood supply to keep the oxygen a float (so to speak), my answer would be to build a muscular structure for breast tissue, I know this works because I've been building muscle from my beginning days of NBE, it's a combination of a grab n' pull method to build strength in all the quadrants of the breast. And this is where ATP will help us build a cellular network (for example) for the energy needed to build new muscle, so go back and re-read up on ATP, pay note to this paragraph:

" Adenylate kinase " requires an atom of magnesium—and this is one of the reasons why sufficient dietary magnesium is important.


Here's the home run (scratch that, it's the grand slam) to all this:

Localized expression of aromatase in human vascular tissues.
Harada N1, Sasano H, Murakami H, Ohkuma T, Nagura H, Takagi Y.
Author information


Abstract
The atheroprotective effects of estrogen are well established and the presence of an estrogen receptor in vascular tissues has recently been reported. Therefore, we investigated the localization of the estrogen-producing enzyme aromatase in vascular tissues to assess the possible contribution of endocrine, paracrine, and autocrine modes of action. Aromatase was found in human vascular smooth muscle cells (SMCs) but not in endothelial cells on in situ hybridization. These observations were further supported by quantitative analysis of aromatase mRNA and the activity in 15 human vascular specimens. Only trace levels of expression were detected in the 3 infants examined, whereas 0.0088 to 0.0806 amol/ microg RNA of aromatase mRNA and 12.9 to 122.3 fmol. h-1. mg-1 protein of the activity were detected in 12 of the adult individuals. The switching of tissue-specific exon 1 of the human aromatase gene was also observed in some cases. Aromatase was found to be expressed only in cultured SMCs and not in cultured endothelial cells of human aorta and pulmonary artery and to be regulated through dexamethasone and the signaling pathways of protein kinase A and C. Study results revealed the localized expression of aromatase in vascular SMCs, which indicated a possible direct action of locally produced estrogen in an autocrine or paracrine manner, with possible cross talk between smooth muscle and endothelial cells.
PMID: 10364566

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#46
Ok so please break this down in laymans terms?
Fenugreek 600mg but no more?
Building vascular in breasts by grab and pull PLEASE SHOW METHOD?
Noogleberry? Once vascular built up?

Thanks x
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#47
(20-09-2017, 07:52 PM)EllaC Wrote: Ok so please break this down in laymans terms?
Fenugreek 600mg but no more?
Building vascular in breasts by grab and pull PLEASE SHOW METHOD?
Noogleberry? Once vascular built up?

Thanks x



Hi Ella,

Here's massages i do that i think helps build musculature in breasts (which they did for me).....btw, i'll post info on FG (hopefully later tonight).
(13-03-2017, 03:37 AM)Lotus Wrote: On breast massages I've used the following techniques from the beginning. This thread (in parts) is  highly technical.....I didn't intend it that way, it just kinda (lol) developed that way. Attached is another tip about fat energy.....useful for breast growth (imo).

(21-11-2014, 09:02 AM)Lotus Wrote: The massages I do,

Massage
1) While in a seated position, arms rested at your side and hands on your thighs.
2) Now raise your arms (elbows) as high as you can while keeping your hands on your thighs.
3) Then slowly squeeze your arms back down to your sides while adding pressure.(As if you had a ball under your arms and your simulating squeezing that ball as hard as you can on the way back down)
4) Do 3 sets of 10 ea. (or more if you can)
(Use a ball if it works better) Wink

______________________________

Another massage
Also been working this Breast massage/exercise:
* With your hand grab your breast from your side, pull it towards the center of your chest, now hold and flex for 2-3 seconds or longer if you can, repeat up to 10 times!
* Try it with your palms pushing your breasts towards the center, as if your trying to touch your nipples together, now interlock your fingers together, using your hands squeeze like a cupping motion, also flex your pec's (tighten) at the same or alternate hand/pecs....up to 10 times.

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Training the pectorals, the pectoralis major and minor (the chest "pecs") are the muscles that lie directly underneath the the breasts. As these muscles get bigger, they can push breast tissue upwards and outwards, providing visual volume, and resulting in a "perkier" appearance.

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I've been doing my own version of an Isometric chest contraction, but for the purpose of demonstration, follow the first part of the video. This can be done anytime, standing or sitting, that's what is so perfect about it, no weights or mats.

No equipment needed chest exercise
http://youtube.com/watch?v=geOC7hCs930&d...eOC7hCs930
 



(22-12-2015, 10:29 PM)Lotus Wrote:
(22-12-2015, 10:09 PM)hannah Wrote: Hi Lotus, 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. Rolleyes 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 E2 is working (so I take more) but it's still working despite not feeling any therapeutic edge. TTYL Smile


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 attach itself to existing fat and store it rather than the carbohydrates because fat is so much easier to store, plus it likes it that way.....stubborn aren't they?.

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

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