Breast Growth For Genetic Males

very very interesting:
Effects of soybean isoflavones on reproductive parameters in Chinese mini-pig boars
http://jasbsci.biomedcentral.com/article...-1891-3-31

http://www.ncbi.nlm.nih.gov/pubmed/9800352
http://rstb.royalsocietypublishing.org/c...1546/1501/

https://www.researchgate.net/publication...ular_cells

lecithin and milk duct growth :
http://www.livestrong.com/article/524606...ingestion/
Cancer

A compound of soy lecithin, phytoestrogen, can produce effects on the body similar to the hormone estrogen. Soy phytoestrogens may promote an increased risk of breast cancer in adult women by altering or decreasing natural estrogen, although the direct link to cancer is inconclusive. One study reported by Cornell University examined 28 women receiving soy supplements for six months. The women were found to have an increased growth of milk ducts in their breasts, which is a leading forerunner of cancer, according to the Program on Breast Cancer and Environmental Risk Factors in New York State. Conclusions suggest that premenopausal women may be at greatest risk, but further research is needed

possible that one can increase the milk ducts without creating cancer>?

i just had to laugh when I saw this one:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3473255/

"The aim of this study was to elucidate the regulatory role of androgen in the follicular development of wild female ground squirrels. Immunohistochemical staining of FSHR, LHR, P450c17, P450arom, androgen receptor (AR), estrogen receptors (ERa and ERb) were executed in ovaries of female ground squirrels from both breeding and nonbreeding seasons. In addition, total ovarian proteins were extracted from the ovaries of squirrels from breeding and nonbreeding seasons, and Western blot analysis were performed in order to probe for FSHR, LHR, P450c17, P450arom, AR, ERa and ERb. The results of immunohistochemical staining and Western blotting of P450c17 showed that there was no significant difference between the breeding and nonbreeding seasons....."

Gper, creeper, where did ya get those peepers....
interesting ,not only ERa and ERb, but also. GPER.

G protein-coupled estrogen receptor 1/G protein-coupled receptor 30 (GPR30),

https://en.wikipedia.org/wiki/GPER

"GPER is expressed in the breasts, and activation by estradiol produces cell proliferation in both normal and malignant breast epithelial tissue.[13][14] However, GPER knockout mice show no overt mammary phenotype, unlike ERα knockout mice, but similarly to ERβ knockout mice.[13] This indicates that although GPER and ERβ play a modulatory role in breast development, ERα is the main receptor responsible for estrogen-mediated breast tissue growth.[13] GPER is expressed in germ cells and has been found to be essential for male fertility, specifically, in spermatogenesis.[15][16][17][18] GPER has been found to modulate gonadotropin-releasing hormone (GnRH) secretion in the hypothalamic-pituitary-gonadal (HPG) axis.["
symbiotic to ERa?

more research needed.

(14-05-2016, 01:30 AM)Tanya Marie Squirrel Wrote: [ -> ]

(14-05-2016, 12:04 AM)blessedbreasts Wrote: [ -> ]

(13-05-2016, 09:52 PM)Tanya Marie Squirrel Wrote: [ -> ]Vanilla its not so "vanilla" after all.

even though it IS vanilla, it is also a hormone regulator (not imitation vanilla).

http://www.rethinkingcancer.org/blog/spi...h-vanilla/
"Cancer: Numerous studies have demonstrated that vanillin, the major component of vanilla, has anti-carcinogenic properties, killing human cancer cells, limiting metastasis (movement of cancer cells from the original site to the rest of the body), inhibiting angiogenesis (creation of new blood supply for tumor). Bromovanin, a vanillin derivative, has been found to stop the advance of a broad spectrum of human cancers. Research at New York University School of Medicine concluded that vanillin is antimutagenic – in human cells it reduced by up to 73% the ability of toxins to mutate DNA in 64 genes that may play a role in cancer."
and:
' This oil stimulates secretion of certain hormones like testosterone, estrogen, etc., which can help bring about normal sexual behavior, as well as promote arousal. The oil has also been shown to regularize menstruation by activating certain hormones like estrogen and progesterone.'

it also contains: Hexanoic acid which is caproic acid aka : Hydroxyprogestrone Caproate which is : Proluton Depot - 250 mg
Hydroxyprogestrone Caproate
resources: https://en.wikipedia.org/wiki/Hydroxypro...e_caproate
https://en.wikipedia.org/wiki/Hexanoic_acid
http://www.alldaychemist.com/proluton-depot.html

imitation vanilla extract contains( both similar to vanillin (main chemical of vanilla) :
Guaiacol :https://en.wikipedia.org/wiki/Guaiacol
https://en.wikipedia.org/wiki/Lignin
resource: https://en.wikipedia.org/wiki/Vanilla_extract
Natural vanilla flavoring is derived from real vanilla beans with little to no alcohol. The maximum amount of alcohol that is usually present is only 2–3%. Imitation vanilla extract contains vanillin, made either from guaiacol or from lignin, a byproduct of the wood pulp industry

Lignin and breast cancer: http://www.ncbi.nlm.nih.gov/pubmed/17374837
'CONCLUSIONS:

High dietary intakes of plant lignans and high exposure to enterolignans were associated with reduced risks of ER- and PR-positive postmenopausal breast cancer in a Western population that does not consume a diet rich in soy.'

Hold up, stop the presses. I've been wanting to add vanilla oil to my next batch of boobie butter (shea butter whipped together with coconut oil and cocoa butter). I wonder if the vanilla oil can affect hormones even when absorbed through the skin.

Fantastic info! Keep it up, Squirrel.

I have seen several sites (which I did not include) that vanillin (pure vanilla) was used as a transdermal application for medicinal application, mostly are patented . but yes, it seems so.
this is one site :
http://www.google.com/patents/US20130084257
"vanillin propylene glycol acetal, ethyl vanillin propylene glycol acetal"

also of particular note, as described in one of the previous linked sites, vanilla is also and aphrodisiac , so it seems to attract amorous attention from your significant other, as it is very aromatic, as well as relaxing .. the olefactory (scent) implications alone are interesting...never mind the medicinal ones

to note: propylene glycol is safe for transdermal use. it is a humectant, which will draw moisture to skin, it is highly hydrophilic (absorbs water). so I would, if I were you, leave out the propylene glycol, if you can.

Well I certainly haven't got a significant other (and never have, and it's starting to seem like I never will... sigh), but I sure like the way it smells.

I wonder if just buying the extract from the grocery store and adding it to my mixture would work.

Thanks for the information. I really want to add vanilla to my routine.

red clover - contains : Coumestrol- phytoestrogen.
https://en.wikipedia.org/wiki/Coumestrol
"Coumestrol is a phytoestrogen, mimicking the biological activity of estrogens. Phytoestrogens are able to pass through cell membranes due to their low molecular weight and stable structure, and they are able to interact with the enzymes and receptors of cells.[4] Coumestrol interacts with the ER-β estrogen receptor and has approximately the same binding affinity for the receptor as 17β-estradiol, but much less affinity than 17α-estradiol, although the estrogenic potency of coumestrol at both receptors is much less than that of 17β-estradiol.[5]

....When bulls graze on pastures containing coumestrol, metaplasia occurs in the prostate and bulbourethral glands, and sperm maturation is suppressed"

Coumestrol and other phytoestrogens have been shown to have an effect on sexual behavior in rats by antagonizing the action of estrogen within the brain; male rats that nursed from females with coumestrol in their diets were both less likely to mount a female rat and less likely to ejaculate, despite producing normal levels of testosterone. Exposure produced similar decreases of sexual behavior in female rats, as a result of the disruption of estrogen dependent gene expression in the brain. Effects were seen in three areas of the hypothalamus, the ventromedial nucleus, the paraventricular nucleus, and the medial preoptic area, all of which play a role in sexual behavior and sexual activity. Female rats that were exposed to coumestrol neonatally did not adopt the lordosis position as much as those that were not exposed to coumestrol.[12]


affects: Estrogen Receptor Alpha (ERa), Red CLover is highest amount of coumestrol at 1322.00 mg/100g.

"Coumestrol and other phytoestrogens have also been investigated as a possible substitute for hormone therapy and chemotherapy in breast cancer patients. The results of various studies regarding the use of phytoestrogens in treating breast cancer have been somewhat contradictory and ambiguous, and as a result, researchers cannot clearly define phytoestrogens like coumestrol as being chemoprotective agents or potentially having negative effects, such as inducing further growth of existing breast cancer tumors by
activating ERα receptors"
this may explain why some people have success with red clover extract.

Amphiregulin
https://en.wikipedia.org/wiki/Amphiregulin
The protein encoded by this gene is a member of the epidermal growth factor (EGF) family.[1]

It is an autocrine growth factor as well as a mitogen for astrocytes, Schwann cells, fibroblasts. It is related to epidermal growth factor (EGF) and transforming growth factor alpha (TGF-alpha). This protein interacts with the Epidermal growth factor receptor (EGFR) to promote the growth of normal epithelial cells
Biological role[edit]

Estradiol and progesterone mostly induce amphiregulin expression to mediate ductal development of the mammary glands.[4][5][6][7][8] Amphiregulin has been found to be essential for mammary ductal development, as evidenced by absence of ductal growth in amphiregulin knockout mice.[7] This is similar to the phenotypes of EGFR and ERα knockout mice, which also show absence of ductal growth

https://en.wikipedia.org/wiki/Progesterone
Progesterone binds extensively to plasma proteins, including albumin (50–54%) and transcortin (43–48%).[28] It has similar affinity for albumin relative to the PR.

Albumin
https://en.wikipedia.org/wiki/Albumin
Serum albumin is the most abundant blood plasma protein and is produced in the liver and forms a large proportion of all plasma protein. The human version is human serum albumin, and it normally constitutes about 50% of human plasma protein.[7]

Serum albumins are important in regulating blood volume by maintaining the oncotic pressure (also known as colloid osmotic pressure) of the blood compartment.[7] They also serve as carriers for molecules of low water solubility this way isolating their hydrophobic nature, including lipid-soluble hormones, bile salts, unconjugated bilirubin, free fatty acids (apoprotein), calcium, ions (transferrin), and some drugs like warfarin, phenobutazone, clofibrate & phenytoin. For this reason, it's sometimes referred as a molecular "taxi". Competition between drugs for albumin binding sites may cause drug interaction by increasing the free fraction of one of the drugs, thereby affecting potency

Insulin-like growth factor 1

https://en.wikipedia.org/wiki/Insulin-li...h_factor_1
Insulin-like growth factor 1 (IGF-1), also called somatomedin C, is a protein that in humans is encoded by the IGF1 gene. IGF-1 has also been referred to as a "sulfation factor" and its effects were termed "nonsuppressible insulin-like activity" (NSILA) in the 1970s.

IGF-1 is a hormone similar in molecular structure to insulin. It plays an important role in childhood growth and continues to have anabolic effects in adults. A synthetic analog of IGF-1, mecasermin, is used for the treatment of growth failure.

Protein intake increases IGF-1 levels in humans, independent of total calorie consumption.

IGF-1 is a primary mediator of the effects of growth hormone (GH). Growth hormone is made in the anterior pituitary gland, is released into the blood stream, and then stimulates the liver to produce IGF-1. IGF-1 then stimulates systemic body growth, and has growth-promoting effects on almost every cell in the body, especially skeletal muscle, cartilage, bone, liver, kidney, nerves, skin, hematopoietic cell, and lungs. In addition to the insulin-like effects, IGF-1 can also regulate cell growth and development, especially in nerve cells, as well as cellular DNA synthesis.

https://en.wikipedia.org/wiki/Mammary_gland#Structure
Estrogen and growth hormone (GH) are essential for the ductal component of mammary gland development, and act synergistically to mediate it.[12][13][14][15][16] Neither estrogen nor GH are capable of inducing ductal development without the other. The role of GH in ductal development has been found to be mostly mediated by its induction of the secretion of insulin-like growth factor 1 (IGF-1), which occurs both systemically (mainly originating from the liver) andlocally in the mammary fat pad through activation of the growth hormone receptor (GHR). However, GH itself also acts independently of IGF-1 to stimulate ductal development by upregulating estrogen receptor (ER) expression in mammary gland tissue, which is a downstream effect of mammary gland GHR activation.[16] In any case, unlike IGF-1, GH itself is not essential for mammary gland development, and IGF-1 in conjunction with estrogen can induce normal mammary gland development without the presence of GH.[16] In addition to IGF-1, other paracrine growth factors such as epidermal growth factor (EGF), transforming growth factor beta (TGF-β),[18] amphiregulin,[19] fibroblast growth factor (FGF), and hepatocyte growth factor (HGF)[20] are involved in breast development as mediators downstream to sex hormones and GH/IGF-1



soooo...as I see it.. since GH is not necessarily needed according to this info, the idea is to increase the IGF-1 in the breast fat pad area..how do we do that? more research to come.

Hormonal breast enhancement

https://en.wikipedia.org/wiki/Hormonal_b...nhancement

some herbal breast enlargement supplements contain phytoestrogens such as 8-prenylnaringenin (found in hops) and miroestrol (a constituent of Pueraria mirifica) and thus may be regarded as a form of hormonal breast enhancement.[3] However, evidence of their effectiveness, as well as safety data, are lacking.
Hormonal manipulation and breast growth

research has found that girls with growth hormone deficiency (GHD) who are treated with GH experience accelerated breast growth[25] and that boys with GHD treated with GH sometimes experience gynecomastia.[26] Moreover, IGF-1 levels and activity have been found to be correlated with breast volume in the female general population.

Certain long-acting growth hormone secretagogues, such as CJC-1295[30] and ibutamoren (MK-677),[31] are capable of reliably and effectively increasing serum GH and IGF-1 concentrations in humans.[32][33][34] Alternatively, exogenous, pharmaceutical GH and IGF-1 (as mecasermin or mecasermin rinfabate) themselves, or analogues of IGF-1 such as des(1-3)IGF-1 and IGF-1 LR3, may be employed to increase GH/IGF-1 axis function. .[35][36][37][38][39] Vitamin D has been found to increase IGF-1 levels in both healthy subjects and individuals with GHD, and vitamin D deficiency is associated with low IGF-1 levels.[40][41][42] However, there is evidence that vitamin D may also potently inhibit breast growth via activation of the vitamin D receptorA number of dietary supplements, including L-arginine, L-ornithine, L-lysine, acetyl-L-carnitine, and creatine, may be able to significantly increase GH levels, although evidence is mixed

to a lesser extent, medroxyprogesterone acetate (MPA), when taken orally, induce IGF-1 production via activation of the androgen receptor (AR) in the liver.

Cyclooxygenase-2 (COX-2) overexpression in mammary gland tissue produces mammary gland hyperplasia as well as precocious mammary gland development in female mice, indicating a strong stimulatory effect of this enzyme on the growth of the mammary glands.[65][66] These effects appear to be downstream actions of increased activation of the prostaglandin EP2, EP3, and EP4 receptors, but not the EP1 receptor, in mammary gland tissue, which in turn results in the potent induction of amphiregulin expression, a critical growth factor involved in normal mammary gland development.[65][66] In addition, agonists of the epidermal growth factor receptor (EGFR), the molecular target of amphiregulin, induce COX-2 expression in mammary gland tissue, potentially resulting in a self-perpetuating cycle of growth amplification by COX-2.[65][66] This mechanism is closely related to formation, growth, and spreading of cancers with poor prognosis, and is in accordance with the fact that long-term administration of aspirin, a COX inhibitor, as well as of other COX-inhibiting non-steroidal anti-inflammatory drugs (NSAIDs), have been found to slightly reduce the risk of breast cancer in women (it is notable here that breast growth/size and breast cancer risk are positively associated).[67] Taken together, these findings indicate that COX-2 inhibitors, such as aspirin, ibuprofen, naproxen, paracetamol (acetaminophen), and celecoxib, may suppress growth of breast tissue.[65][66]


so..if you want breast growth, increase the igf-1, and try not to take any pain pills , asprin etc.

hops

contains: 8-prenylnaringenin
https://en.wikipedia.org/wiki/8-Prenylnaringenin

is a prenylflavonoid phytoestrogen. It is reported to be the most estrogenic phytoestrogen known.[1] The compound is equipotent at ERα and ERβ,[2] and acts as a full agonist of ERα.[3] Its effects are similar to those of estradiol, but it is considerably less potent in comparison.

8-PN is found in hops (Humulus lupulus) and in beer, and is responsible for the estrogenic effects of the former.[2][4] It can be produced from isoxanthohumol in fungal cells cultures,[5] and by flora in the human intestine.

Estrogenic[edit]

8-PN was shown to preserve bone density[1] and has been demonstrated to reduce hot flashes.[1][8] 8-PN also induces the secretion of prolactin, and increases other estrogenic responses.[9] The compound binds to and activates ERα more times than it does to ERβ.[1][2][10]

This prenylflavanoid has drawn interest in the study of hormone replacement therapy, and it is comparable to selective estrogen-receptor modulators.[11][12]

In an in vivo study, 8-PN has activated proliferation of mammary cells.[9] At the concentration found in beer, it is unlikely to have an estrogenic effect in breast tissue.[13] Prenylflavonoids from hops, namely 8-PN, are common in herbal breast enlargement preparations.[14]

Similarly to other estrogens, 8-PN induces the expression of the progesterone receptor in various tissues

very interesting.. more research needed.

(15-05-2016, 08:45 PM)Lotus Wrote: [ -> ]

(19-01-2015, 08:01 AM)Lotus Wrote: [ -> ]PUFA have been known for nearly 40 years to uniquely suppress lipid synthesis. PUFA, particularly n-3, accomplish this by coordinating an upregulation of lipid oxidation and a downregulation of lipid synthesis. In other words, PUFA function as metabolic fuel “repartitioners.” Such fuel repartitioning may protect cells against the accelerated rates of apoptosis reportedly observed with excessive triglyceride accumulation (12, 25). PUFA exert their effects on metabolic pathways by governing the DNA binding activity and nuclear abundance of select transcription factors responsible for regulating the expression of genes encoding key regulatory proteins of lipid and glucose metabolism. With respect to their role in fatty acid oxidation, PUFA increase the fatty acid oxidative capacity of tissues through their ability to function as ligand activators of PPAR-α and thereby induce the transcription of several genes encoding proteins affiliated with fatty acid oxidation. On the other hand, PUFA suppress lipid synthesis by inhibiting transcription factors that mediate the insulin and carbohydrate control of lipogenic and glycolytic genes. In this regard, PUFA rapidly generate an intracellular signal that immediately suppresses the proteolytic release-

Molecular mechanism for polyunsaturated fatty acid regulation of gene transcription
http://ajpgi.physiology.org/content/281/4/G865

lotus your a peach , I almost missed these replies as I tend to go all gung-ho and don't look back , in this instance I did. thanks for clearing that up