Breast Growth For Genetic Males

Hi BN,

I'm attaching some recent posts made at BreastNexus to here in this thread. My goal is a further elaboration of the many cleaved pathways of Human steroidogenesis.....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
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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. 

(14-01-2016, 07:27 PM)Lotus Wrote: [ -> ]

(14-01-2016, 01:18 AM)Lotus Wrote: [ -> ]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:

(05-01-2016, 12:10 AM)Lotus Wrote: [ -> ]This is a post (smart fella, this MarDok42) from a PCOS board: 

Quote: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?filters=&orig_db=PubMed&cmd=Search&term=134%2A%5Bvolume%5D%20AND%201948%5Bpage%5D%20AND%202004%5Bpdat%5D%20AND%20Lambert%20JD%5Bauth%5D

(14-01-2016, 07:57 PM)Lotus Wrote: [ -> ]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.

So what is the best way to take advantage of the CYP's ?

(19-04-2017, 06:20 AM)Stevenator Wrote: [ -> ]So what is the best way to take advantage of the CYP's ?

Here's a couple examples of foods explaining the P450 Cytochromes enzymes, the goal is to map out as much as we can. Ultimately in the future we'd know ahead of time what medicines works best/worst by a simple lab test. Maybe the costs will be lower with more competitors joining the market?. 

(19-04-2017, 01:10 AM)Lotus Wrote: [ -> ]

(15-01-2016, 12:38 AM)Lotus Wrote: [ -> ]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

(09-01-2016, 04:52 AM)Lotus Wrote: [ -> ]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.

(03-03-2016, 05:16 AM)Lotus Wrote: [ -> ]This is worth mentioning again, 

Lemons inhibit CYP3A4, and @ 60%?.......,,,,,,,,its pro breast growth.  

Application to drug-food interactions of living cells as in vitro model expressing cytochrome P450 activity: enzyme inhibition by lemon juice.
Baltes MR1, Dubois JG, Hanocq M.
Author information
Abstract
Classical inhibitors of human cytochrome P450 3A4 activity, such as ketoconazole and quercetin, are tested to prove the efficiency of a new metabolisation model using living entire cells. Grapefruit juice is a well-known potent inhibitor of cytochrome P450 3A4 activity. With regard to the clinical relevance of grapefruit juice-drug interactions, an investigation of other common juices is undertaken with this in vitro model. The CYP3A4 activity is measured by the formation of the 6beta-hydroxytestosterone, which is quantified by an isocratic high performance liquid chromatography. It is demonstrated for the first time that lemon juice significantly inhibits by 60+/-3% the CYP3A4-mediated oxidation. Grapefruit juice inhibits this activity by 82+/-4%. The mechanism of lemon juice inhibition is competitive, whereas it is mixed for grapefruit juice. These results suggest that our in vitro model combined with our analytical method is applicable for the investigation of the inhibition of CYP3A4 not only by chemical inhibitors but also by natural food products.


Whole Lemons are fairly inexpensive, in drinks or on food.....lemons boost the NBE/Hrt blood levels by the CYP3A4 enzyme pathway.......meaning most the drugs in your medicine cabinet.

Thank you for breaking that down.

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Great Scott!!!!!!

Your amazing mamms look incredible in the top!!!!

Happy continued growing Lotus!

Thanks for continually inspiring is all!

Hugs

~H

Looking good.  Are you still experiencing other effects from hrt?

SCIENCE !!

(28-04-2017, 04:54 PM)DDs_for_me Wrote: [ -> ]Great Scott!!!!!!

Your amazing mamms look incredible in the top!!!!

Happy continued growing Lotus!

Thanks for continually inspiring is all!

Hugs

~H

Awe thanks DDs (~H), 

I've been feeling awful dealing with a food poisoning infection and said screw it, I'm taking revenge with a couple of shots....even made gif  ( it won't load though?). 

And thanks again for cheering me up with your kind words, and thanks to all (come to think of it) for inspiring " me " over the past 3+ years, I try to help others when I can by giving back what I've gotten here at BN....it's been an immeasurable experience (and that's the truth).

 I feel bad however when i lose contact ( for whatever reason) with the people who've contacted me asking for help...never to hear from them again, I pray they found happiness. 

happy growing to you too. 

L.

(29-04-2017, 12:16 PM)froger Wrote: [ -> ]Looking good.  Are you still experiencing other effects from hrt?

Hey there froger, (thanks) ...good to hear from you again.

Good question, yes it's the typical stuff I see that most people experience on hrt...e.g. softer skin, looking younger, etc. However, odd is what E2 is doing in my blood, meaning it's steadily increased on the same amount (which is currently at 6 mg). Previously on 4 mg I had 1 test result come back at over 2200 pg/mL....crazy huh?. A retest the following week was 700 pg/mL.....that's about normal (though I went off E2 for three days to get it down prior to the test). However......  a most recent test was back to +2200 pg/mL. My thoughts are (in part) that a couple of things are driving the increase....certainly the pre-fasting (10-12 hours by the time I take the blood draw ) test requirement has a part, though other things I normally do (lemons to water.....other fresh fruit too), coffee (yup lol) and certain other foods all play a part I think. Also, I have a thyroid issue (hashimotos).....a disadvantage. My blood sugar, cholesterol are within normal limits....sodium is slightly elevated which is being addressed. My T however is tanked at 9 g/dL, but that was up slightly (from previous test).....I used reishi instead of spiro for 3 weeks......it worked great tbh. 

How about you froger?, are you still on hrt?.