[Lotus]

Hey Lotus. One thing.. You talk about "estradiol degradation" in this method. For ME this isnt good is it now we know i might not metabolise estrogen right? Should i NOT try this methid?

Aloe lowers plasma glucose....though some people shouldn't take regular amounts (1-2 tablespoons) of Aloe for various reasons as discussed in the study. Meta analysis showed 1 report of increased hypothyroidism in a woman. Olive oil can alter estrogen metabolism (if needed) and improve thyroid function...soy lowers thyroid function....that's going in the wrong direction tbh. 


Extra virgin olive oil potentiates the effects of aromatase inhibitors via glutathione depletion in estrogen receptor-positive human breast cancer (MCF-7) cells.
Ismail AM1, In LL, Tasyriq M, Syamsir DR, Awang K, Mustafa AH, Idris OF, Fadl-Elmula I, Hasima N.
Author information

Abstract
There have been numerous evidences supporting the relationship between olive oil and cancer, with most of the attention being directed toward its fat and phenolic content. The aims of this study were to investigate whether EVOO and OA could enhance the effects of aromatase inhibitors (letrozole and anastrozole) in ER-positive MCF-7 cells, as well as to investigate its influence on cytochrome c release and GSH levels. It was observed that upon combination treatment, anti-proliferation effects and apoptosis induction were augmented. Apoptosis was triggered via the intrinsic pathway in accordance with cytochrome c release into the cytosol based on IF-IC and ELISA observations. Intracellular GSH levels were also reduced upon EVOO/OA treatment in combination with aromatase inhibitors, and were found to be inversely correlated to cytosolic cytochrome c levels. Additionally, the estrogenic suppressive effects of letrozole and anastrozole were amplified when used in combination with EVOO/OA. Therefore, the employment of aromatase inhibitors in combination with EVOO/OA could orchestrate a reduction in intracellular estrone biosynthesis which feeds ER-positive cells, while simultaneously depleting GSH levels and increasing ROS generation, thus releasing cytochrome c and subsequent induction of apoptosis in MCF-7 cells. 
Copyright © 2013 Elsevier Ltd. All rights reserved.

Can you say how much and how often you were applying the olive oil? 60% weight increase in a few weeks is amazing.  Did you rule out other effects that may have caused such a huge gain in such a short time, e.g., water weight gain? Or do you think the gain is in mammary tissue or fat or both? Is olive oil essential or is it just any oil with similar levels of oleic acid? From what I remember reading Almond oil goes deeper than olive oil at skin penetration with similar oleic acid percentage, and apricot oil may be even better than almond at penetration with high oleic acid as well. I don't have that info handy but I remember reading about it a few years ago when looking into moisturizing oils.

Thanks for the (excellent) questions Atom, 

I added olive oil (about 1 tsp. sublingually x2 daily) about 6-8 weeks ago with sublingual E2 (hrt), it's an adjustment at first (minor throat irritation). I also went more for a mediterranean diet and actually lost weight (about 8 pounds) in that time period....so water weight didn't factor (currently on spiro/magnesium). I did another weight test and haven't lost any of the increased breast weight, in fact  there was a 2-3% increase in breast weight since the last test (2 weeks ago?). The massage portion is 3x minimum a week in my case, (Jojoba oil I think could work too). 

When you analyze fat intake vs. fat expenditure therein lays the opportunity for breast growth in my opinion, of course supplementing with certain vitiamins & hormones are also critical for success too. I'll post the subsequent science for those interested. 

I will point out that the parathyroid plays a huge factor in bud development in embryonic delevolpment, but new science says it still can be revelant past puberty (protection of lost breast volume).........think vitamin D3. (study by Colorado state university). 

I choose Aloe Vera because of its lower molecular weight (ability to diffuse through the skin layers past the dermis) and its polymers. This dalton rule is helpful determining molecular weight for transdermal applications, the smaller the molecule the easier to diffuse......Almond oil looks interesting (thanks again atom). Now I also found out that the skin should be irritated prior for skin application for a higher success rate.....lol I know what your thinking   that Thailand breast slap...haha (no comment). Personally?, I'd say using a cayenne pepper extract (sauce?) would provide plenty of irritation. Btw, vitamin C produces collagen.

Btw, for those whose domes steam up during pumping I've determined it's a build up humidity, thus water (ambient air---inside the dome) being pulled into the breast. I also believe it's in part relevant to thermogenesis (or heat transfer) aiding synthesis of mitochondria......(I could be wrong though). 


The 500 Dalton rule for the skin penetration of chemical compounds and drugs
Authors
* Jan D. Bos, Marcus M. H. M. Meinardi
* First published: June 2000Full publication history
* DOI: 10.1034/j.1600-0625.2000.009003165.xView/save citation
* Cited by: 370 articles

Jan D. Bos, Department of Dermatology A0-235, Academic Medical Center, University of Amsterdam, P.O. Box 22700, 1100 DE Amsterdam, The Netherlands
Tel.: +31 20 566 2587. Fax: +31 20 696 0076
e-mail:  j.d.bos@amc.uva.nl
Abstract
Abstract: Human skin has unique properties of which functioning as a physicochemical barrier is one of the most apparent. The human integument is able to resist the penetration of many molecules. However, especially smaller molecules can surpass transcutaneously. They are able to go by the corneal layer, which is thought to form the main deterrent. We argue that the molecular weight (MW) of a compound must be under 500 Dalton to allow skin absorption. Larger molecules cannot pass the corneal layer. Arguments for this “500 Dalton rule” are; 1) virtually all common contact allergens are under 500 Dalton, larger molecules are not known as contact sensitizers. They cannot penetrate and thus cannot act as allergens in man; 2) the most commonly used pharmacological agents applied in topical dermatotherapy are all under 500 Dalton; 3) all known topical drugs used in transdermal drug-delivery systems are under 500 Dalton. In addition, clinical experience with topical agents such as cyclosporine, tacrolimus and ascomycins gives further arguments for the reality of the 500 Dalton rule. For pharmaceutical development purposes, it seems logical to restrict the development of new innovative compounds to a MW of under 500 Dalton, when topical dermatological therapy or percutaneous systemic therapy or vaccination is the objective.
http://onlinelibrary.wiley.com/doi/10.10...x/abstract



Molecular Weights: (g/mol)

Aloe Vera- 270.24

Palmitic- 270.46

Stearic - 298.52

Oleic -  282.46 

Linoleic - 298.48

Almond oil - 106.12

Estradiol - 272.4

Soybean oil -292.2

http://biodiesel.org/docs/ffs-performace...f?sfvrsn=4

[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 Spirolactone.


 If you'd like more information about " steroidal and natural lactones " see here:
http://www.breastnexum.com/showthread.ph...#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 anti-oxidant 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 nutriceutical 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 blood stream (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 hormone (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. Dutaseride inhibits type 1 & 2 @ about 93%, effective but carries risk. Red clover, genistien (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 increases 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 stimulates intracellular signaling pathways. In addition, EGCG is transported to intracellular compartments, cytosol, mitochondria, lysosome, and nucleus where it mediates additional biological actions.

What Are the Benefits of Green Tea Essential Oil?

Properties
Green tea essential oil has many useful properties that make it beneficial. It is an astringent; this means it has the property to constrict and shrink body tissue. It is an antioxidant; this means it neutralizes free radicals in the body. Free radicals occur naturally in the body, but are also produced by exposure to ultraviolet rays, radiation, cigarette smoke and air pollution. They are responsible for cell and DNA damage. Tea seed oil has anti-inflammatory properties. It also has anti-aging properties as it inhibits the breakdown of collagen that is responsible for keeping the skin firm and elastic.

Therapeutic Benefits
Green tea essential oil, and green tea leaves are widely used because of their beneficial properties. Green tea oil is used in the cosmetics industry to manufacture creams, soaps, shampoos, hair conditioners, lotions, perfumes and massage oils, because of its anti-aging, anti-inflammatory and astringent properties.

It is used as a therapeutic oil in aromatherapy. Five drops of tea seed oil mixed in 10 ml of carrier oil can be added to a warm bath to relax the muscles. Six drops can be added to water and used in a tea light oil burner or electric oil diffuser to create a soothing environment. Green tea essential oil is also used to make candles and potpourri.

Read more : http://www.ehow.com/about_6514882_benefi...-oil_.html

[Lotus]

Amino Acid Composition, Molecular Weight Distribution and Gel Electrophoresis of Walnut (Juglans regia L.)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3958834/

The results of size exclusion chromatogram indicated molecular weight of the major components of walnut proteins were between 3.54 and 81.76 kDa.

Meaning, the molecular weight of walnut oil is 3.54 g/mol, making it the lowest skin penetrating oil that i've seen.

As example " puerarin " is 343.5 g/mol and miroestrol @ 520.183 g/mol (bigger molecules vs. 3.53 g/mol of walnut oil). 

molecular weight (MW) of a compound must be under 500 Dalton to allow skin absorption. Larger molecules cannot pass the corneal layer....according to the  “500 Dalton rule”. 

A new miroestrol glycoside from the roots of Pueraria mirifica
https://www.researchgate.net/publication...a_mirifica

[AthenaDruid]

Thinking of a few herbs to put on the list and would like to know of any NBE experiences from our members:


Burdock root
Arctium Lappa
Anti-bacterial, anti-fungal, anti-inflammatory


Grape Seed
Vitis Vinifera
Rich in polyphenol proanthocyanidins, protects the skin from free radicals and premature aging, increases intracellular vitamin C levels, inhibits destruction of collagen

Witch Hazel
Hamamelis Virginia
Antioxidant, astringent, soothes and heals problem skin conditions


Yogurt
Rich in vitamins, calcium and minerals, growth factors stimulate fibroblast proliferation and extra cellular protein such as collagen, probiotic content increases immune function and has lactic acid component

Witch Hazel? Will this aid in breast growth? If so, I have Witch Hazel and A LOT of it!!

[Lotus]

Witch Hazel? Will this aid in breast growth? If so, I have Witch Hazel and A LOT of it!!

It could, meaning it has some properties used for breast growth, e.g. antioxidant, astringent (tightens collagen), anti-inflammatory, etc. 

In what form is the witch hazel (extract, cream, etc.).

L.

[Ashraf]

How about improving Lotus experiment with olive oil and aloe by adding 3rd step of alcoholic herbal infusion? I am using own herbal oil infusion it does wonders for me( recipe mentioned in my program), but maybe it could be improved by using same herbs in alcohol then top it with aloe and olive oil? Or even better olive infusion and alcohol infusion because I think not all compunds will get transferred in alcohol alone but these which does will penetrate deeper? I will test it from next month as first need to prepare infusions for 2-3 weeks.

Anybody curious about effects as much as me?

[Lotus]

How about improving Lotus experiment with olive oil and aloe by adding 3rd step of alcoholic herbal infusion? I am using own herbal oil infusion it does wonders for me( recipe mentioned in my program), but maybe it could be improved by using same herbs in alcohol then top it with aloe and olive oil? Or even better olive infusion and alcohol infusion because I think not all compunds will get transferred in alcohol alone but these which does will penetrate deeper? I will test it from next month as first need to prepare infusions for 2-3 weeks.

Anybody curious about effects as much as me?

I'm curious,   

What kind of alcohol?....ethanol (as in extracts) are pro-aromatase. I might have posted the alcohol rate of delivery in skin applications, I'll find it, (and the molecule size too)....though I tend to believe it's maybe a mini-cascade of circulating estrogen via ER-a (estrogen).

from the study:
alcohol intake has been associated to an increased level of circulating estrogens, we have postulated that aromatase expression could be increased following ethanol exposure. The results of our studies show a 1.3-fold increase in cell proliferation after 6 days of culture of MCF-7 cells in the presence of 0.1% ethanolJ
https://www.spandidos-publications.com/i...9/abstract

The polymers and compounds used in everyday products (e.g. antiseptics) have the right ingredients to be a carrier. I've also used progesterone cream with olive oil and aloe. Though walnut oil looks promising (walnut stinks a bit). 

But by all means experiment, (safely).  

[Lotus]

Lol..oops, forget to mention this:

Logically, alcohol stimulating fat cells in skin applications makes sense, my thought was adding (or aiding) to the stimulation of fat cells in breast cells that would unlock the stored estrogen in fat cells to release energy.....thus new synthesis. 

[Lotus]

Please check out the PDF:

Beneficial influences of Estrogen Metabolism-





Nutritional Influences on Estrogen Metabolism
http://www.afmcp-sa.com/ansr/MET451%20En...20ANSR.pdf

[Lotus]

Hi BN,

I'm attaching two recent posts made elsewhere at BreastNexus to here in the FAQ thread, (and in addition at BreastNexum). The complexity of the science needs further exposure for relevant discussion...(my apologies for any inconvenience it may cause, I will remove the posts if the op's wish, via pm ). My goal is a further elaboration of the many cleaved pathways of Human steroidogenesis..........I feel uncomfortable hijacking a thread with complex information, thus the move. Where I see this going (or the direction of NBE) is the ability to determine what each supplement does e.g metabolism, steroid synthesis, the optimal basal body temp (BBT) to metabolize supplements, timing of supplements, weight issues and many other related topics. It's time we put all this together.....we have the capability to get this done at BN.

(wiki has solid information on the topic of steroid metabolism)
Steroid
https://en.m.wikipedia.org/wiki/Steroid

Steroidogenic enzymes: structure, function, and role in regulation of steroid hormone biosynthesis.
https://www.ncbi.nlm.nih.gov/pubmed/22217824


The body temp is a critical factor in how well we metabolise drugs, and yet we don't take full advantage of the proper set point to benefit drug potency capabilities. For instance, the poor functioning thyroid is tied directly to lower body temp....I've talked about thermogenesis in previous posts, and my understanding (or analysis) of how to use this for NBE goes beyond a sluggish thyroid explanation. I've attached a few articles to better explain BBT, read dr. Mercola's link, see the connection of how soy destroys thyroids, more so if it's already compromised. 


The effects of drugs on thermoregulation.
Cuddy ML.
Abstract
Body temperature is a balance of the hypothalamic set point, neurotransmitter action, generation of body heat, and dissipation of heat. Drugs affect body temperature by different mechanisms. Antipyretics lower body temperature when the body's thermoregulatory set point has been raised by endogenous or exogenous pyrogens. The use of antipyretics may be unnecessary or may interfere with the body's resistance to infection, mask an important sign of illness, or cause adverse drug effects. Drugs may cause increased body temperature in five ways: altered thermoregulatory mechanisms, drug administration-related fever, fever from the pharmacologic action of the drug, idiosyncratic reactions, and hypersensitivity reactions. Certain drugs cause hypothermia by depression of the thermoregulatory set point or prevention of heat conservation. By affecting the balance of thermoregulatory neurotransmitters, drugs may prevent the signs and symptoms of hot flashes.
https://www.ncbi.nlm.nih.gov/pubmed/15461041


Body Temperature and Thyroid Problems
When your thyroid hormone is working properly inside cells you will make 65 percent energy and 35 percent heat as you burn calories for fuel. Thyroid hormone governs your basal metabolic rate, orchestrating the idling speed at which all cells make energy and thus heat. A classic symptom of poor thyroid function is being too cold. Conversely, a classic symptom of hyperthyroidism is being too hot (making too much heat). However, many people with low thyroid are too hot—a seeming paradox that I will explain shortly.
http://www.wellnessresources.com/weight_..._problems/

Many Symptoms Suggest Sluggish Thyroid -- Do You Have Any of These?
http://articles.mercola.com/sites/articl...yroid.aspx
[/quote]

So if I were to fill out that temperature form I then might come to understand how my body may or may not be metabolizing the herbs I take to their full potential? That makes a lot of sense. I am also having a spit hormone panel done this month when I go for my annual pap. So hopefully once I get that information in addition to recording my temperature I might be able to understand the science behind how my body is functioning and from there create an herbal routine to best support NBE? My understanding of this is very rudimentary so I appreciate your patience with me. I am also hoping to get my annual blood work done soon.  

I have a thought in regards to getting a hormone panel done, would the herbs I'm taking then skew the accuracy of hormone panel I'd like to do? Should I stop taking the herbs? And if so should I stop taking them immediately? I don't want to just drop off of a program because when I did that when I was freaked about my period within a handful of days I'd lost what seemed to be any growth I had gained.
[/quote]


Focus on how cholesterol starts the entire Steroidogenesis process, from there see how peptides, insulin, temperature, the hypothalamus/pituitary, lipids, leptin, energy produced in cells, and many others regulate our metabolism. Below is further information on how to better metabolize. 

Steroidogenesis is the biological process by which steroids are generated from cholesterol and changed into other steroids.[27] The pathways of steroidogenesis differ among species. 
https://en.m.wikipedia.org/wiki/Steroid#Steroidogenesis

The Molecular Biology, Biochemistry, and Physiology of Human Steroidogenesis and Its Disorders
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3365799/

Ribosomal (or mRNA) peptides are small (signaling) molecule in hormones and in an organism. 

A useful strategy for NBE could be to indenify what substrates will/won't work for us. We think hormone testing (yes useful) is the first line of progress, or problem areas (deficiencies). Instead, I think (finances permitting of course) a human genome test could map out (or eliminate) the drugs we can't use. Is cost analysis worth the investment compared to all the drama that comes from our lost time, money, sanity waiting for boobs to finally grow.

in the absence of such an endeavor (genome testing) this (below) is the next best thing, yes complicated, but didn't we just find out that MSM inhibits DHT and promotes aromatase by using this method below:

This is a post (smart fella, this MarDok42) from a PCOS board: 

In the last few days my pharmacist friend explained to me when you block testosterone with one herb it will only block its production from one or two gene pathways, and a lot of the pro-hormones (hormone precursors) will find another pathway to testosterone, but it does give it a little longer to possibly become an estrogen. So to have more effective herbs, block more pathways with different types of herbs. Here's what I got so far.

Below are the genes that are involved in testosterone syntheses, they are the ones that start with 'CYP'. I have begun to cross referenced them with known chemicals in herbs that are known to inhibit these genes. If you want to find a synergistic herbal combination you might want to find a few herbs with these chemicals or others in it to inhibit(block) the majority of this gene set.

This is by no means a comprehensive list because I only started this project a week ago in my free time. But I thought that there might be other science geeks out there that would like to poke around the gene websites too.  

Genes Involved in Testosterone Syntheses with corsponding inhibitors.

CYP1A2(also makes an Estrogen).....,cimetidine (inhibits)
CYP1B1(also makes an Estrogen)
CYP2B1– apigenin,Curcumin
CYP2B6– apigenin,Curcumin,Kaempferol
CYP2A3- lignans, genistein, Kaempferol
CYP2C11(Men Only)
CYP3A4 - lignans, Kaempferol, genistein, Curcumin (cimetidine, inhibits), sesame seeds and oil. Piperine
CYP3A5 - lignans, Kaempferol, genistein, Curcumin 
CYP3A9 -
CYP19A1 -


Some Herbs and the anti androgen chemicals in them. 

apigenin(chamomille)
Quercetin (chamomille)
genistein(Soy)
Curcumin(Vanalla, Turmeric)
Kaempferol(Peony, Dill)
lignans (Flax)

steroidogenic enzymes represent targets for complete suppression of systemic and intratumoral androgen levels, an objective that is supported by the clinical efficacy of the CYP17 inhibitor abiraterone.

I added a couple things to the op's notes, the following is a list I put together:

Remember, by identifying these enzymes it provides information of drug-drug interactions. What's also key is the fact that certain cancers can be identified by examining these ezymens with interactions. 


Here's a new one called CYP2C8, which metabolizes fatty acids. another CYP17's , which CYP17A modifies estrogen metabolism.


CYP2C8- lignans-Quercetin, linoleic acid
CYP17 -lignans-green tea (inhibits DHT)
CYP17A modifies estrogen metabolism

When used in quantities typical for flavoring food, black pepper is not likely to affect the disposition of most medications. However, excessive use of black pepper or intake of dietary supplements formulated with P. nigrum or P. longum extracts may produce clinically significant interactions with drugs. This may be of particular concern when CYP3A and/or ABCB1 substrates are ingested concomitantly with piperine or piperamides in excess of 10 mg.

http://www.ncbi.nlm.nih.gov/pubmed?filte...%5Bauth%5D

Estrogen pathway for mammary density
HSD3B1, (catalyses the biosynthesis of all classes of hormonal steroids)
HSD17B1 (estrogen activation and androgen inactivation)
CYP27B1, CYP24 metabolizes enzymes in mammary cells, Vit.D elongates breast
CYP1A1 (polypeptide protein)
CYP1A2 (estrogen link)
CYP17A1 (modifies estrogen / inhibits DHT)
CYP19A1 (aromatase) 
CYP1B1 (breaks down fats, aka-lipids) 
COMT-(catechol-O-methyltransferase)
UGT1A1-(uridine diphospho-glucuronosyltransferase -(catalyzes estrogen) 
SULT1A1, SULT1E1- (sulfotransferases)
ESR1, ESR2-(estrogen receptors alpha and beta)



CYP17 and CYP1A1-1 play a role in the pathogenesis of fibroadenoma. Meaning something like cigarette smoke can have direct role on the CYP1A1 enzyme metabolism, e.g. progression of fibroadenomas. In other words, as bad as smoking is, 2nd hand smoke can further exacerbate fibroadenomas.