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B.i.G.G (breast information growing guide Lv.2)
Testosterone released (24 hours)

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Targets of testosterone

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DHT (Dihydrotestosterone) , understanding how dht impacts breast growth helps to understand an effective course of action, which will be outlined in the upcoming posts.

Quote:The main androgen secreted by the testes is of course testosterone. However, in most of the body, the androgenic signal is not carried through by testosterone. In these tissues, which include the brain (CNS), skin, genitals – practically everything but muscle – the active androgen is actually DHT.

Testosterone in this case simply acts as a prohormone that is converted to the active androgen DHT by the action of the enzyme 5-AR. 5-AR is concentrated heavily in practically every androgen dependent area of the body except for skeletal muscle which results in very little testosterone actually getting through to these parts of the body to bind to androgen receptors. Instead, it is quickly transformed into DHT, which then interacts with receptors.This transformation serves a very important biological function in these tissues.

DHT is a much stronger androgen than testosterone – it binds about 3-5 times more strongly to the androgen receptor. If you took away 5-AR from these tissues and blocked the formation of DHT, then you would see some dramatic changes in physiology. DHT can also be used as an anti-estrogen. It works to do this through three different methods.

First, DHT directly inhibits estrogens activity on tissues. It either does this by acting as a competitive antagonist to the estrogen receptor or by decreasing estrogen-induced RNA transcription at a point subsequent to estrogen receptor binding. Second of all, DHT and its metabolites have been shown to directly block the production of estrogens from androgens by inhibiting the activity of the aromatase enzyme.

The studies done in breast tissue showed that DHT, androsterone, and 5alpha-androstandione are potent inhibitors of the formation of estrone from androstenedione. 5alpha-androstandione was shown to be the most potent, while androsterone was the least. Third, DHT acts on the hypothalamus / pituitary to decrease the secretion of gonadotropins.

Theory: Deny dht's ability to bind with androgen receptors and imagine the possibilities. *

Quote:If you took away 5-AR from these tissues and blocked the formation of DHT, then you would see some dramatic changes in physiology.

*Androgen receptor or estrogen receptor-beta blockade alters DHEA-, DHT-, and E(2)-induced proliferation and PSA production in human prostate cancer cells.

These findings support involvement of both AR and ERbeta in mediating DHEA-, DHT-, and E(2)-induced PSA expression in prostate cancer cells.


Ok, exactly how then?, the next steps are a new approach (new for NBE) and won't make sense at this point, but it will going forward.

Human type 3 3alpha-hydroxysteroid dehydrogenase (aldo-keto reductase 1C2) and androgen metabolism in prostate cells.
In prostate cells AKR1C2 acts as a 3-ketosteroid reductase to eliminate 5alpha-DHT and prevents activation of the androgen receptor. AKR1C2 does not act as an oxidase due to either potent product inhibition by NADPH or because it cannot surmount the oxidative 17beta-HSD present. Neither AKR1C2, retinol dehydrogenase/3alpha-HSD nor 11-cis-retinol dehydrogenase is a source of 5alpha-DHT in PC-3 cells.

Androgen inactivation and steroid-converting enzyme expression in abdominal adipose tissue in men.
In conclusion, androgen inactivation was detected in abdominal adipose tissue in men, with higher 3alpha/beta-HSD activity in the s.c. versus Om depot. Higher Om 5alpha-DHT inactivation rates were found in obese compared with lean men. Further studies are required to elucidate whether local androgen inactivation in abdominal adipose tissue is involved in the modulation of adipocyte metabolism and regional fat distribution in men.

Androgen metabolism in adipose tissue: recent advances.
We speculate that glucocorticoid-induced androgen inactivation could locally decrease the exposure of adipose cells to active androgens and partially remove their inhibitory effect on adipogenesis. We hypothesize that body fat distribution patterns likely emerge from the local adipose tissue balance between active androgens and glucocorticoids in each fat compartment.


Adipose tissue intracrinology: potential importance of local androgen/estrogen metabolism in the regulation of adiposity.

The present article summarizes some of the studies available on steroid hormone conversion through the specific expression of steroidogenic enzymes in adipose tissue (adipose tissue intracrinology) and discusses the potential impact of local adipose tissue steroid metabolism on the regulation of adipocyte function and other metabolic parameters. Several studies have demonstrated significant steroid hormone uptake and conversion by adipose tissues from various body sites and in various cell fractions. Activities and/or mRNAs of aromatase, 3beta-hydroxysteroid dehydrogenase (HSD), 3alpha-HSD, 11beta-HSD, 17beta-HSD, 7alpha-hydroxylase, 17alpha-hydroxylase, 5alpha-reductase and UDP-glucuronosyltransferase 2B15 have been detected in adipose tissue or adipose cells. These studies have demonstrated potentially important roles for these enzymes in obesity, central fat accumulation, and the metabolic syndrome. Future studies on adipose tissue intracrinology will contribute further to our understanding of steroid action in adipocytes.


Pre-receptor regulation of the androgen receptor.

The human androgen receptor (AR) is a ligand-activated nuclear transcription factor and mediates the induction of genes involved in the development of the male phenotype and male secondary sex characteristics, as well as the normal and abnormal growth of the prostate. We have identified the pair of hydroxysteroid dehydrogenases (HSDs) that regulate ligand access to the AR in human prostate. We find that type 3 3alpha-HSD (aldo-keto reductase (AKR)1C2) catalyzes the NADPH dependent reduction of the potent androgen 5alpha-dihydrotestosterone (5alpha-DHT) to yield the inactive androgen 3alpha-androstanediol (3alpha-diol). We also find that RoDH like 3alpha-HSD (RL-HSD) catalyzes the NAD(+) dependent oxidation of 3alpha-diol to yield 5alpha-DHT. Together these enzymes are involved in the pre-receptor regulation of androgen action. Inhibition of AKR1C2 would be desirable in cases of androgen insufficiency and inhibition of RL-HSD might be desirable in benign prostatic hyperplasia.


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Sources of testosterone and 3α-androstanediol in adult male. Adult male (A) and andropause (B) The solid box shows steroidogenesis in Leydig cells, and the dotted-box shows steroidogenesis in the adrenal gland. The pathway in gray shows a backdoor pathway to 5α-DHT via 3α-diol which does not involve the intermediates Δ4-androstene-3,17-dione or testosterone. Enzymes involved in the individual steps are italicized.

How do you recognize access DHT?, here's a few signs to look for,
  • Excess body hair growth
  • An increase in aggression/starting new projects
  • Hairs around the nipples, chin (ladies)
  • Hair loss (check the hairbrush for increased amounts of hair)
  • As crazy as it sounds, an increase in libido
  • Oily skin
Credit-Isabelle for the previous list

DHT it the KING of Androgens and seriously hampers breast growth, and once DHT is converted from Free Testosterone it can't be converted back to its free state making it unavailable (Stops boob growth)

The problem being that once it (DHT) enters into receptors it locks it up, and thereby making Aromatase an after thought, Aromatase is enzyme that converts free T to estrogen. (Aka boob growth)

Some DHT facts-
Dihydrotestosterone is a hormone that stimulates the development of male characteristics (an androgen). It is made through conversion of the more commonly known androgen, testosterone. Almost 10% of the testosterone produced by an adult each day is converted by the testes and prostate (in men), the ovaries (in women), the skin and other parts of the body to dihydrotestosterone.

How is dihydrotestosterone controlled?
The amount of dihydrotestosterone present in the body from day to day depends on the amount of testosterone present. When levels of testosterone increase, more of it is converted to dihydrotestosterone and so levels of dihydrotestosterone therefore also increase as a result. (A Thoery of mine Rolleyes is that an increase in Total T will see a correlating rise in FREE T which through Aromatase gets converted to Estrogen). This is where bio-males grows boobs, (you know, in the absence of ovaries).

Control of dihydrotestosterone levels in the body is therefore achieved through control of testosterone production, which is controlled by the hypothalamus and the pituitary gland. In response to decreasing levels of testosterone (and therefore reduced amounts of dihydrotestosterone), the hypothalamus releases gonadotrophin-releasing hormone which travels to the pituitary gland, stimulating it to produce and release luteinising hormone into the bloodstream. Luteinising hormone in the blood then travels to the Leydig cells in the testes in men (or ovaries in women) and stimulates them to produce more testosterone. As testosterone in the blood increases, more of it is also converted to dihydrotestosterone, resulting in higher levels of dihydrotestosterone as well.

As blood levels of testosterone and dihydrotestosterone increase, this feeds back to suppress the production of gonadotrophin-releasing hormone from the hypothalamus which, in turn, suppresses production of luteinising hormone by the pituitary gland. Levels of testosterone (and thus dihydrotestosterone) begin to fall as a result, so negative feedback decreases and the hypothalamus resumes secretion of gonadotrophin-releasing hormone.

What happens if I have too much dihydrotestosterone?
Too much dihydrotestosterone, often resulting from excess testosterone production, has variable effects on men and women. It is unlikely that levels of dihydrotestosterone will be raised before the start of puberty. It is also unlikely that adult men with too much dihydrotestosterone would undergo recognisable changes. Women with too much dihydrotestosterone may develop increased body, facial and pubic hair growth (called hirsutism), stopping of menstrual periods (amenorrhoea) and increased acne. Abnormal changes to the genitalia may also occur in women with too much dihydrotestosterone.

So as you age the prostrate grows, and as a result DHT will also grow causing a host of problems as we know. And of course we have meds for that.


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I will try to finish this guide asap, it's been sitting on the shelf for way too long. I'm sorry but I still want it closed for responses till completion.

Thanks Big Grin
It is now known that estrogens exert their end-organ effect by activating a complex intracellular mechanism. Tissues which respond to estrogen possess intracytoplasmic proteins (receptors) that preferentially bind specific steroids.

For instance, a cell from the uterus will possess 5000–15,000 estrogen receptors whereas a cell from the spleen will have none. These receptors recognize estrogens by their three dimensional and chemical characteristics and bind it with high affinity (KD =10-10), specificity, and saturability.

The estrogen molecules present in the circulation are relatively loosely bound to intravascular carrier proteins (sex-steroid-binding globulin [SBG]) (KD = 10-8) or to albumin. In excess of 95% of the estrogen in the circulation is found in the bound form. The estrogen readily diffuses across the cellmembrane in its active free form due to a concentration and a binding gradient. The estrogenmolecule is relatively small (molecular weight is 300) and lipophilic and probably passes through the cell membrane by simple diffusion.

Once in the cell, the estrogen is promptly bound to the intracellular (intracytoplasmic) receptor protein, which then undergoes a series of complex spatial changes prior to intranuclear transport. This nuclear transport occurs within 30–45 minutes after the target tissue is exposed to estrogen. The following system of nuclear interactions between receptor and DNA is a model that has been proposed by McCarty.3 The activated receptor–estrogen complex then nonspecifically binds to the DNA and protein of dispersed chromosomes (euchromatin) and stimulates acetylation of the histone protein.

This acetylation of the histones in nucleosomes causes the nucleosome to “open up” and expose specific DNA segments for transcription. The “estrogen message” is transcribed into new messenger RNA which then migrates back into the cytoplasm and activates various cellular processes including new protein synthesis. The now “freed” receptor protein is probably recycled back into the cytoplasm for further use.

The estrogen receptor recognizes a molecule as being “estrogen” if its size, three-dimensional configuration, and charge are similar to the parent molecule. Therefore, the nonsteroidal synthetic estrogens may not resemble the “prototype” estrogen (estradiol-17β) on paper diagrams but are very similar in shape and other properties as seen by the cellular receptor. Estrogen receptors are perhaps the determinants of potency for estrogenic substances.

The estrogen receptors preferentially bind estradiol over estriol (2x) and estrone (3x).5 This receptor also discriminates among the estrogens by binding estradiol within the cellular nucleus longer than the weaker estrogens estriol and estrone.

Therefore, estradiol is the most potent of the natural estrogens probably because of the greater affinity and duration of its receptor-binding compared with the other available estrogens. Receptors for estrogen and other steroid hormones can now be accurately quantified and studied. Estrogen in physiologic concentrations stimulates the synthesis of estrogen receptors and of progesterone and testosterone receptors.

Progesterone and testosterone, however, inhibit estrogen receptors. Progesterone inhibits its own receptor population in the secretory phase of human endometrium. Thus, it is apparent that for estrogen to bind and influence a tissue, the specific estrogen receptors must be present. The potency of a particular estrogen in a tissue roughly parallels and is probably dependent on the quantity of the estrogenreceptor in the cells of that tissue. Studies with estrogen receptors in breast cancers are being successfully utilized to predict the responsiveness of these tumors to hormonal manipulation.



The adrenal gland is the primary source of estrogen in postmenopausal women, and estrone is the dominant estrogen, the E2:E1 ratio being reversed after menopause. In comparison to those of cycling women, estrone levels are reduced to low follicular phase levels. There is an insignificant contribution to the estrone pool from estradiol conversion, ovarian estrone secretion, and conversion of ovarian androstenedione

However, virtually all the total estrone production can be accounted for by peripheral conversion of androstenedione in adipose tissue and liver. There is a strong correlation with age and obesity in the conversion efficiency of androstenedione to El. The nonobese postmenopausal woman has an average androstenedione to E1 conversion rate of 2.7%, compared with 5.1% for the obese postmenopausal patient with uterine bleeding secondary to increased endogenous estrogen.

Estrogen, 17-beta-estradiol binds to both the ER alpha and ER beta receptors but not to androgen, progestin, or thyroid receptors. Each receptor version may turn on and off different responses in different cells in different parts of the body. For instance, ER alpha, promotes tissue growth and is found in greater amounts in the uterus, pituitary gland, and epididymis (the male sperm storing structure). ER alpha stimulates certain breast cancer cells to grow in response to estrogen hormones. The other version, ER beta, inhibits growth (possibly suppressing cancer) and prevails in the ovary and prostate. It can act like a dimmer switch for ER alpha, turning down its growth-stimulating effect.

Binding produces two distinct signaling routines: either slower via gene expression (hours to days) or very rapidly via molecular exchanges, or cascades (seconds to minutes). In both cases, the cell responds to the signals by manipulating proteins or building new ones. The affected workhorse proteins carry out specialized functions, such as controlling cell processes, building cells and tissues, or carting messages elsewhere within the cell or around the body.
14-02-2015 04:14 PM

(10-03-2014, 04:13 AM)Lotus Wrote: Testosterone is responsible for sex drive, for Testosterone to promote youthful sexual interest it must be freely available to cell receptors. As we age T becomes bound to serum (blood) globulin. The component that renders free testosterone inactive is called sex hormone binding globulin (SHBG). This means your getting a double whammy of interference with sex drives in aging males,

1) Testosterone being bound to serum globulin (blood)
2) SHBG rendering it inactive

So that means estrogen takes it place!

Imagine if we knew more about Testosterone, we would find out that a reduction of free T also causes depression. High serum levels of estrogen also trick the brain into thinking that enough testosterone is being produced, further slowing the natural production of testosterone. This also stops the body's own natural estrogen from entering cells for binding.

High estrogen can shut down the normal testicular production of testosterone. Aging men sometimes convert testosterone to estrogen. For testosterone to produce long-lasting libido enhancing effects, it must be kept in the "free" form in the bloodstream. It does not matter how much serum free testosterone is available if excess estrogen is competing for the same cellular receptor sites.

Antagonism between estrogen and androgen hormone action is elegantly exemplified by the sexual dimorphism of breast development; full mammary gland growth and maturation occurs in females due to the dominance of estrogen action and does not occur in males due to the dominance of androgen action. Perturbations of sex-specific hormone levels can cause abnormal breast development in males and females. This also occurs at the receptor level, whereby the mammary gland fails to develop in females lacking a functional estrogen receptor α (ERα) and fully develops in males lacking a functional androgen receptor (AR).
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