Breast Growth For Genetic Males

(07-12-2016, 01:39 AM)Katana Wrote: [ -> ]

(08-09-2016, 08:25 PM)Lotus Wrote: [ -> ]

(07-09-2016, 03:25 PM)pom19 Wrote: [ -> ]Hi Lotus, does that mean fat people have less breast growth and smaller boobs?        Thanks, POM

It appears that the reduction (or absence) of ERalpha causes adipocyte hyperplasia, hypertrophy, insulin resistance, and glucose intolerance in both sexes (as stated).

In other words, exercise improved the sensitivity of ER-a, and obesity keeps breast growth to a minimum (if any) other than adding fat with increased obesity.

Hi Lotus! Long time since I have poked around here but just came across this in your thread and wanted to pick your brains about something.
Wen i was 17 i was rather overweight which quite large (mostly fat) breasts. I lost this weight over a few months and lost about 2 cup sizes then gained the weight back over 3 years along with the cup sizes but the shape of my breasts seemed somewhat underdeveloped despite their size (this is where my NBE began)
Sorry what I wanted to pick your brains about is could my weight have affected the development of my breasts and losing the weight I have lost since april helped them grow? They now have much fuller and rounder shape as well as being larger in size despite the weight loss.

Hi katana, 

Ok, I understand, let me please relate this statement above to your unique situation:

It appears that the reduction (or absence) of ERalpha during weight loss caused adipocyte hyperplasia, hypertrophy. Skip to the present, the combined fact you are losing weight and massaging breasts, eating right change any insulin resistance, and or glucose intolerance. 

In other words, exercise improved the sensitivity of ER-a, and obesity keeps breast growth to a minimum (if any) other than adding fat with increased obesity.

Here's a crazy idea that came to mind:

Take main NBE supplements 15. min prior to total energy expenditure composing of increasing total energy expenditure basal metabolic rate (BMR), plus the consumption of NBE to gain a thermic effect (or advantage if you will) of food (TEF) from combined physical activity. Now.....it's possible to add calories immediately following post work-out to effect insulin insensitivity?. I do think thermic effect of food initiates satiety (from personal experience). 

The influence of thermic effect of food on satiety.
https://www.ncbi.nlm.nih.gov/pubmed/9683329/

That is an interesting idea. Now that I am working nearly full time (2 part time jobs right now) I might look into supplements in the new year

Once your in you'll never get out! But as i talk with you do you have personal experience with tens devices? i ow one now..so ive been doing it and felt my legs all night long, constant tingles now they were hurt anyhosince they suddenly became longer. so maybe its good? i will continue anyhow but if you have any insiders information bout this i am all ears.:p

(08-12-2016, 12:13 AM)hannah Wrote: [ -> ]Once your in you'll never get out! But as i talk with you do you have personal experience with tens devices? i ow one now..so ive been doing it and felt my legs all night long, constant tingles now they were hurt anyhosince they suddenly became longer. so maybe its good? i will continue anyhow but if you have any insiders information bout this i am all ears.:p

Lol, so true. I've used a tens for a back issue some years ago, I can't say it was helpful in my case though. So your legs got longer?, or the pain lasted longer? (excuse my ignorance, lol). I do think there's specific locations where the leads go to achieve better pain relief (see attached chart). 

Transcutaneous electrical nerve stimulation (TENS) for chronic pain
https://www.ncbi.nlm.nih.gov/pubmed/18646088

Of the study participants above the use of tens unit help control pain (or in 60% who participated). 

How to use a tens unit to stimulate lactation
http://breastnotes.com/breastfeeding/BrF...c-TENS.htm

Thanks for the chart L, it is spot on...i have mild lower and mid back pain and looking at the chart I see allergies, acne....thats kinda me...itch followed by waxy/oily skin on my face/scalp.. kinda the same. But yes my legs got longer awhile back while I dont have the age for that anymore. The lactation thing is very interesting btw, I tried it on my nipples first day I got the device and ever since I have VERY painful breasts it deff helps with prolactin thus growth. Anyhow I'll keep on trying and let you know the outcome Thanks again

(10-12-2016, 12:55 PM)hannah Wrote: [ -> ]

(09-12-2016, 09:53 PM)Lotus Wrote: [ -> ]

(08-12-2016, 12:13 AM)hannah Wrote: [ -> ]Once your in you'll never get out! But as i talk with you do you have personal experience with tens devices? i ow one now..so ive been doing it and felt my legs all night long, constant tingles now they were hurt anyhosince they suddenly became longer. so maybe its good? i will continue anyhow but if you have any insiders information bout this i am all ears.:p

Lol, so true. I've used a tens for a back issue some years ago, I can't say it was helpful in my case though. So your legs got longer?, or the pain lasted longer? (excuse my ignorance, lol). I do think there's specific locations where the leads go to achieve better pain relief (see attached chart). 

Transcutaneous electrical nerve stimulation (TENS) for chronic pain
https://www.ncbi.nlm.nih.gov/pubmed/18646088

Of the study participants above the use of tens unit help control pain (or in 60% who participated). 

How to use a tens unit to stimulate lactation
http://breastnotes.com/breastfeeding/BrF...c-TENS.htm

Thanks for the chart L, it is spot on...i have mild lower and mid back pain and looking at the chart I see allergies, acne....thats kinda me...itch followed by waxy/oily skin on my face/scalp.. kinda the same. But yes my legs got longer awhile back while I dont have the age for that anymore. The lactation thing is very interesting btw, I tried it on my nipples first day I got the device and ever since I have VERY painful breasts it deff helps with prolactin thus growth. Anyhow I'll keep on trying and let you know the outcome Thanks again

Sorry to hear about the back pain, hopefully you get some relief. That chart is craZy huh?, seems like the spinal nerves can be connected to a ton of illness and or treatment. I have some new info I'll have to share on lactation and white peony.

I look fwd to your updates.

Hi Steve, (and thanks). 

Here's something interesting, the study and (follow up study below) track prolactin production in human breasts tissue indicating adipose (fat tissue) creates more prolactin than glandular tissue. Prolactin in adipose is described as a circulating hormone. Note the 10 fold increase by day 10. So, progesterone lowers PRL and estradiol had no effect in this study. 

In other words, having more fat in your breasts would indicate a higher presence of prolactin, conversely, more glandular would indicate higher progesterone.....in theory (lol, just an opinion). Higher prolactin in men turns off the pituitary signal to make more T, and although estradiol is unaffected (in this study) one should believe it's keeping estradiol low.....aka- no boob growth. So if indeed prolactin is cyclic in nature, (peaks on day 10) the other nine days are optimal growth cycles for breasts......feel free to chime in. 


Prolactin expression and secretion by human breast glandular and adipose tissue explants.
Zinger M1, McFarland M, Ben-Jonathan N.
Author information


Abstract
Prolactin (PRL) is a 23-kDa hormone produced by the pituitary and extrapituitary sites. The main target of PRL is the breast, where it affects cellular growth, differentiation, and milk production. Recent evidence suggests that locally produced PRL plays a role in breast tumorigenesis. Our objective was to examine PRL synthesis/release in different tissues of the human breast and determine the effect of ovarian steroids. Breast tissue, obtained from women undergoing mastectomy or breast reduction, was separated into glandular (nonmalignant) and adipose explants and incubated for 10 d. Conditioned media were analyzed for PRL by a bioassay. PRL release from glandular explants decreased by 60% from d 1-3, followed by a 4-fold increase on d 10. PRL release from adipose explants was unchanged from d 1-3 and increased more than 10-fold by d 10. PRL gene expression, determined by RT-PCR, was low on d 0 and markedly increased on d 10 in both types of explants. De novo synthesis of PRL was confirmed by metabolic labeling. Progesterone suppressed PRL release from glandular explants without affecting adipose explants. Estradiol did not alter PRL release from either tissue. In conclusion, the human breast produces and releases bioactive PRL, with a higher release rate by adipose than glandular tissue. The time-dependent rise in PRL release suggests removal from inhibitory control. Progesterone may be one of the factors that suppresses PRL production in the glandular compartment, whereas the factor(s) that regulate adipose PRL are unknown. These data suggest an autocrine/paracrine role for PRL in human glandular and adipose breast tissue.

Adv Exp Med Biol. 2015;846:1-35. doi: 10.1007/978-3-319-12114-7_1.
Prolactin (PRL) in adipose tissue: regulation and functions.
Ben-Jonathan N1, Hugo E.
Author information


Abstract
New information concerning the effects of prolactin (PRL) on metabolic processes warrants reevaluation of its overall metabolic actions. PRL affects metabolic homeostasis by regulating key enzymes and transporters associated with glucose and lipid metabolism in several target organs. In the lactating mammary gland, PRL increases the production of milk proteins, lactose, and lipids. In adipose tissue, PRL generally suppresses lipid storage and adipokine release and affect adipogenesis. A specific case is made for PRL in the human breast and adipose tissues, where it acts as a circulating hormone and an autocrine/paracrine factor. Although its overall effects on body composition are both modest and species-specific, PRL may be involved in the manifestation of insulin resistance. 
PMID: 25472532  DOI: 10.1007/978-3-319-12114-7_1

White peony was discovered to be a nontoxic chaperone- inducing compounds that promotes DNA binding. On top of what we now know about WP it seems to have this extra benefit that improves DNA binding. I don't believe we see any other NBE supplement in the arsenal that can do as many things (thus far documented). I'll make present the other scientific info posted here.


paeoniflorin (white peony) enhances phosphorylation and acquisition of the (DNA)deoxyribonucleic acid–binding ability of heat shock transcription factor 1 (HSF1), as well as the formation of characteristic HSF1 granules in the nucleus, suggesting that the induction of HSPs by paeoniflorin is mediated by the activation of HSF1. 

_______________________________________________


Paeoniflorin, a novel heat shock protein–inducing compound
[size=undefined]Dai Yan,[/size]1 Kiyoto Saito,1,2 Yuri Ohmi,1 Noriyo Fujie,1 and Kenzo Ohtsuka1
1Laboratory of Cell and Stress Biology, Department of Environmental Biology, Chubu University, 1200 Matsumoto-cho, Kasugai, Aichi 487-8501, Japan 2Department of Medical Imaging and Information, Graduate School, Suzuka University of Medical Science, 1001-1 Suzuka, Mie 510-0293, Japan

Abstract Heat shock proteins (HSPs) are induced by various physical, chemical, and biological stresses. HSPs are known to function as molecular chaperones, and they not only regulate various processes of protein biogenesis but also function as lifeguards against proteotoxic stresses. Because it is very useful to discover nontoxic chaperone- inducing compounds, we searched for them in herbal medicines. Some herbal medicines had positive effects on the induction of HSPs (Hsp70, Hsp40, and Hsp27) in cultured mammalian cells. We next examined 2 major constituents of these herbal medicines, glycyrrhizin and paeoniflorin, with previously defined chemical structures. Glycyrrhizin had an enhancing effect on the HSP induction by heat shock but could not induce HSPs by itself. In contrast, paeoniflorin had not only an enhancing effect but also an inducing effect by itself on HSP expression. Thus, paeoniflorin might be termed a chaperone inducer and glycyrrhizin a chaperone coinducer. Treatment of cells with paeoniflorin but not glycyrrhizin resulted in enhanced phosphorylation and acquisition of the deoxyribonucleic acid–binding ability of heat shock transcription factor 1 (HSF1), as well as the formation of characteristic HSF1 granules in the nucleus, suggesting that the induction of HSPs by paeoniflorin is mediated by the activation of HSF1. Also, thermotolerance was induced by treatment with paeoniflorin but not glycyrrhizin. Paeoniflorin had no toxic effect at concentrations as high as 80 g/ mL (166.4 . To our knowledge, this is the first report on the induction of HSPs by herbal medicines.

https://www.ncbi.nlm.nih.gov/pmc/article...-4-378.pdf

So I'm not very bright on all this stuff but from what I collect by this is that White Peony does just fine by it's self? Big words confuse me