[Lotus]

Hi Clelia,

It's nice to hear from you again, it's truly an honor and inspiration hearing your comments, it takes my breath away. Tbh, when I research the reward is finding anything that remotely benefits breast growth and overall health. Time after time science/research continually takes my breath away. It's like finding your first love , albeit in an abstract lol.....(does that sound craZy?) lol.......ok, that's probably over the top, buts it's something in that order. Im my case your never to old to rediscover my potential......

Finally, could you help me? I'm looking information for "bad estrogen" that make growth faster

Sure, my pleasure.....

Those E metabolites are 16α-OH estrone & 2-OH estrone, I list this study below from 2008, it's pretty interesting, the findings are different from what I've seen.

[These data do not support the hypothesized inverse associations with 2-OH estrone and the 2:16α-OH estrone ratio nor the hypothesized positive association with 16α-OH estrone].

Circulating 2-hydroxy and 16-α hydroxy estrone levels and risk of breast cancer among postmenopausal women
----------------------
Abstract

Circulating estrogens are associated with breast cancer risk in postmenopausal women. Given that estrogen metabolites are potentially both mitogenic and genotoxic, it is possible that plasma levels of estrogen metabolites are related to breast cancer risk. We conducted a prospective, nested case- control study within the Nurses' Health Study. Blood samples, collected in 1989-1990, were assayed for 2-OH estrone and 16α-OH estrone among 340 cases and 677 matched controls not taking postmenopausal hormones. Multivariate relative risks (RR) and 95% confidence intervals (CI) were calculated by conditional logistic regression, adjusting for breast cancer risk factors. Neither 2-OH estrone nor 16α-OH estrone concentrations were significantly associated with breast cancer risk overall (top vs. bottom quartile RR=1.19, 95% CI (0.80-1.79), p-trend=0.40 for 2-OH estrone and RR=1.04, 95% CI (0.71-1.53), p-trend=0.81 for 16α-OH estrone). The ratio between the two metabolites (2:16α-OH estrone) was similarly unrelated to risk overall (1.30, 95% CI (0.87-1.95), p- trend=0.35). While no associations were detected among women with ER+/PR+ tumors, significant positive associations were observed for 2-OH estrone and the 2:16α-OH estrone ratio among women with ER-/PR- tumors (2-OH estrone RR=3.65 95% CI (1.23-10.81), p-trend=0.01, p- heterogeneity=0.02; 2:16α-OH estrone RR=3.70, 95% CI (1.24-11.09), p-trend=0.004, p- heterogeneity=0.005). These data do not support the hypothesized inverse associations with 2-OH estrone and the 2:16α-OH estrone ratio nor the hypothesized positive association with 16α-OH estrone. The significant positive associations with 2-OH estrone and the 2:16 OH estrone ratio among women with ER-/PR- tumors needs to be replicated in future studies.

http://www.ncbi.nlm.nih.gov/pmc/articles...s52956.pdf
___________________________________

The following is model I'm trying to complete in my mind,

For instance--hormones diffuse across membranes, are ion channels the entry point??, ERE, ER, AR, PR exist in the same cell, can carrier proteins distinguish a preferential binding?, Dexamethasone is an aromatase, Palmitate is proteins in ER-a, assuming FA's can muscle their way into the cytoplasm, from there transcription?........ramblings of a lunatic lol, I get these screw ball ideas, sometimes they wake me from complete sleep...it's freaky.

Here's an example of that freakiness.

Lipoxygenases (EC 1.13.11.-) are a family of iron-containing enzymesthat catalyze the dioxygenation of polyunsaturated fatty acids in lipidscontaining a cis,cis-1,4- pentadiene structure. It catalyses the following reaction:

fatty acid + O2 = fatty acid hydroperoxide

Lipoxygenases are found in plants, animals and fungi. Products of lipoxygenases are involved in diverse cell functions.



-------------------------------

.[2] In mammals a number of lipoxygenases isozymes are involved in the metabolism of eicosanoids(such as prostaglandins, leukotrienes and nonclassic eicosanoids).[3] Sequence data is available for the following lipoxygenases:

compounds attack cell membranes and red blood cells, and they even cause damage to DNA and RNA strands, leading to cellular mutations in the body’s tissues. In skin, it causes wrinkles and premature aging. In blood vessels, the buildup of plaque. In tissues and organs, it can set the stage for tumors to form. I think you get the picture. Free radicals are bad, bad news, and they’re ever-present in industrial PUFA oils.
-----------------------

On a different note......

The TG (triglyceride) form of fish oil contains its own monoglyceride substrate; whereas EE fish oils, coupled to ethanol, do not. EE must therefore obtain a glycerol substrate from another source. Without a glycerol or monoglyceride substrate TG re-synthesis is delayed, suggesting that transport to the blood is more efficient in natural TG fish oils in comparison to EEs. Furthermore, this delay of TG re-synthesis in EE fish oils could cause an increase in free fatty acids and subsequent oxidation of those free fatty acids.

I'm gonna out on on limb here.....,I wonder if ethanol release stated below could be in part what converts to aromatase.

During the digestive process, EEs are converted back to TGs by intestinal enterocytes1 which, results in the release of ethanol. Although the amount of ethanol released in a typical dose of fish oil is small, those with sensitivities to alcohol or those who are alcoholics should refrain from the consumption of EEs.

Fish Oil Triglycerides vs. Ethyl Esters: A comparative review of absorption, stability and safety concerns
http://pi-bill-articles.blogspot.com/201...s.html?m=1

(Note-The above article is from a blog, I couldn't find any supported research, imo the perspective is eye opening (are all EFA supplements misidentified?, good grief.

. but i think that the king to fight here is DHT)
I didn't know about DHT metabolites, my thoughs are: if DHT (and metabolite) is more androgenic, then estrogenic in breast tissue, than it could be helpful low it.

I just so happens , I know what you mean, and there is a back door to DHT.......

From an earlier post,


DHT has an estrogenic action,

The existence of this estrogenic DHT metabolite has raised the possibility that estradiol may not be the major estrogen in males [29]. For instance, in the prostate there is a growing body of evidence that 3β-diol, acting through ERβ, may regulate important physiological events.


Recent data have shown that DHT may be converted into 5α-androstane- 3β-17β-diol (3β-diol) in a virtually irreversible reaction. Once considered inactive, 3β-diol is present in high concentrations in the male and indeed has biological activity. However, 3β-diol does not bind to the androgen receptor (AR), but rather to ERα and ERβ, with higher affinity for ERβ. Based upon these findings, we hypothesized that the modulation of AQP9 by DHT could be indirectly mediated by 3β-diol.

---------------------------

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1615873/


Effects of 3-beta-diol, an androgen metabolite with intrinsic estrogen-like effects,

Abstract

Background: Fluid homeostasis is critical for normal function of the male reproductive tract and aquaporins (AQP) play an important role in maintenance of this water and ion balance. Several AQPs have been identified in the male, but their regulation is not fully comprehended. Hormonal regulation of AQPs appears to be dependent on the steroid in the reproductive tract region. AQP9 displays unique hormonal regulation in the efferent ductules and epididymis, as it is regulated by both estrogen and dihydrotestosterone (DHT) in the efferent ductules, but only by DHT in the initial segment epididymis. Recent data have shown that a metabolite of DHT, 5-alpha- androstane-3-beta-17-beta-diol (3-beta-diol), once considered inactive, is also present in high concentrations in the male and indeed has biological activity. 3-beta-diol does not bind to the androgen receptor, but rather to estrogen receptors ER-alpha and ER-beta, with higher affinity for ER-beta. The existence of this estrogenic DHT metabolite has raised the possibility that estradiol may not be the only estrogen to play a major role in the male reproductive system. Considering that both ER-alpha and ER-beta are highly expressed in efferent ductules, we hypothesized that the DHT regulation of AQP9 could be due to the 3-beta-diol metabolite.

Methods: To test this hypothesis, adult male rats were submitted to surgical castration followed by estradiol, DHT or 3-beta-diol replacement. Changes in AQP9 expression in the efferent ductules were investigated by using immunohistochemistry and Western blotting assay.

Results: Data show that, after castration, AQP9 expression was significantly reduced in the efferent ductules. 3- beta-diol injections restored AQP9 expression, similar to DHT and estradiol. The results were confirmed by Western blotting assay.

Conclusion: This is the first evidence that 3-beta-diol has biological activity in the male reproductive tract and that this androgen metabolite has estrogen-like activity in the efferent ductules, whose major function is the reabsorption of luminal fluids.





a) It has been shown that 3β-diol may have hormonal activity, not acting through the AR, but rather as a ligand for both ERα and ERβ.

b) 3β-diol has higher affinity for ERβ [31], which is abundant in the efferent ductule epithelium [40].

c) In human testis, the 3β-diol concentration is higher than DHT and estradiol [44,45]. It is reasonable to postulate that high concentrations of this metabolite may enter the lumen of efferent ductules.

d) The existence of this estrogenic DHT metabolite has raised the possibility that estradiol may not be the major estrogen in males [29]. For instance, in the prostate there is a growing body of evidence that 3β-diol, acting through ERβ, may regulate important physiological events [26,28,32,46].

Also noteworthy is the fact that 3β-diol stimulates ERβ induced transcriptional activity equal to the cognate ligand estradiol, and the transcriptional selectivity of 3β-diol for ERβ is much greater than its binding selectivity [30,46]

-----------------------------


Concentrations of aromatase and estradiol in the prostate are low, indicating that estradiol may not be the only estrogenic molecule to play a role in the prostate. It is known that DHT can be metabolized to 5alpha-androstane-3beta,17beta-diol (3beta-diol), a hormone that binds to ERbeta but not to AR. The concentration of 3beta-diol in prostate is much higher than that of estradiol. Based on the high concentration of 3beta-diol and since this metabolite is a physiological ERbeta ligand, we hypothesized that 3beta-diol would be involved in the regulation of ERbeta expression.





An endocrine pathway in the prostate, ERbeta, AR, 5alpha-androstane-3beta,17beta-diol, and CYP7B1, regulates prostate growth.
http://www.ncbi.nlm.nih.gov/pubmed/12370428

I've spent more time researching on this backdoor estrogenic action of DHT, aka estrogen receptor beta. From what I see when DHT is metabolized in the liver we can force it to this ER-b back door, thereby lessening (or inactivating) it's potential. And imo cortisteriods inactivates DHT.

_____________________________________________

It's like deconstructing a model (call it a airplane model) that someone else built, only you're working in reverse to deconstruct right. Same applies here, you see a study that states 5 alpha reductase is reduced in the liver, now maybe this study was for cancer research or something similar. Let's take one of these studies,

Role of human type 3 3alpha-hydroxysteroid dehydrogenase (AKR1C2) in androgen metabolism of prostate cancer cells.

Aldo-keto reductases (AKRs) is another superfamily class of enzymes like the Cytochrome P450 enzyme super family, which are present in most tissues of the body, and play important roles in hormone synthesis and breakdown (including estrogen and testosterone synthesis and metabolism), cholesterol synthesis, and vitamin D metabolism. Cytochrome P450 enzymes also function to metabolize potentially toxic compounds, including drugs and products of endogenous metabolism such as bilirubin, principally in the liver.

AKRs are involved in the development and progression of many cancers, as well as chemotherapeutic drug resistance. AKR1B1 and AKR1B10 are overexpressed in tumors, such as liver, breast, and lung cancer. Several AKRs (AKR1A1, AKR1B10, and AKR1C1-3) are involved in tobacco-carcinogenesis, but they also catalyze the detoxication of nicotine derived nitrosamino ketones. In addition, AKR1C1-3 enzymes play a key role in the regulation of proliferative signaling in hormone dependent cancers.

So what they did in this study was to cut off the androgen synthesis to the receptors using another steroid , Four human aldo-keto reductases (AKRs) that belong to the AKR1C subfamily function in vitro as 3-keto-, 17-keto- and 20-ketosteroid reductases or as 3alpha-, 17beta- and 20alpha- hydroxysteroid oxidases to varying degrees. By acting as ketosteroid reductases or hydroxysteroid oxidases these AKRs can either convert potent sex hormones (androgens, estrogens and progestins) into their inactive metabolites or they can form potent hormones by catalyzing the reverse reaction. In this manner they may regulate occupancy and trans-activation of steroid hormone receptors.

In English, I want to find the link to activate AKR1c in the liver to shut off the androgen receptors therefore DHT never gets activated, simple right?.

Cha-Ching, found it.

Regulates access of 5alpha-DHT to the androgen receptor.

Abstract
Pairs of hydroxysteroid dehydrogenases (HSDs) govern ligand access to steroid receptors in target tissues and act as molecular switches. By acting as reductases or oxidases, HSDs convert potent ligands into their cognate inactive metabolites or vice versa. This pre-receptor regulation of steroid hormone action may have profound effects on hormonal response. We have identified the HSDs responsible for regulating ligand access to the androgen receptor (AR) in human prostate. Type 3 3alpha-hydroxysteroid dehydrogenase (aldo-keto reductase 1C2, aka-AKR acts solely as a reductase to convert 5alpha-dihydrotestosterone (DHT), a potent ligand for the AR (K(d)=10(-11)M for the AR), to the inactive androgen 3alpha-androstanediol (K(d)=10(-6)M for the AR); while RoDH like 3alpha-HSD (a short-chain dehydrogenase/reductase (SDR)) acts solely as an oxidase to convert 3alpha-androstanediol back to 5alpha-DHT. Our studies suggest that aldo-keto reductase (AKRs) and SDRs function as reductases and oxidases, respectively, to control ligand access to nuclear receptors.
http://www.ncbi.nlm.nih.gov/pubmed/17223255

Notice how Aldo-keto reductases (AKRs) position themselves between DHT and 3-diols, this is where the estrogenic action takes place. These actions of AKR1C's takes place in androgen metabolism of the prostate.

Aldo-keto reductases (AKRs) is another superfamily class of enzymes like the Cytochrome P450 enzyme super family.






Estrogen receptor β and 17β-hydroxysteroid dehydrogenase type 6, a growth regulatory pathway that is lost in prostate cancer

Estrogen receptor β (ERβ) is activated in the prostate by 5α-andros- tane-3β,17β-diol (3β-Adiol) where it exerts antiproliferative activity. The proliferative action of the androgen receptor is activated by 5α- dihydrotestosterone (DHT). Thus, prostate growth is governed by the balance between androgen receptor and ERβ activation. 3β- Adiol is a high-affinity ligand and agonist of ERβ and is derived from DHT by 3-keto reductase/3β-hydroxysteroid dehydrogenase en- zymes. Here, we demonstrate that, when it is expressed in living cells containing an estrogen response element-luciferase reporter, 17β-hydroxysteroid dehydrogenase type 6 (17βHSD6) converts the androgen DHT to the estrogen 3β-Adiol, and this leads to activation of the ERβ reporter. This conversion of DHT occurs at concentrations that are in the physiological range of this hormone in the prostate. Immunohistochemical analysis revealed that 17βHSD6 is expressed in ERβ-positive epithelial cells of the human prostate and that, in prostate cancers of Gleason grade higher than 3, both ERβ and 17βHSD6 are undetectable. Both proteins were present in benign prostatic hyperplasia samples. These observations reveal that for- mation of 3β-Adiol via 17βHSD6 from DHT is an important growth regulatory pathway that is lost in prostate cancer.

http://www.ncbi.nlm.nih.gov/pmc/articles...117772.pdf

[Lotus]

"On another note....I've seen that EPA and DHA reduces the risk of breast cancer by as much as a 32% reduction, I don't know the dosage."

Where did you see that? which paper? i quickly had a look on the one you linked before, but i didn't find that information

Here it's stated at 25%, I believe Dr. Mercola stated 32%mon his web series.


Marine Fatty Acid Intake Is Associated with Breast Cancer Prognosis1,2

Abstract

EPA and DHA, long-chain (n-3) PUFA largely obtained from fish, inhibit the proliferation of breast cancer cells in vitro and reduce the initiation and progression of breast tumors in laboratory animals. Our purpose in this analysis was to examine whether intake of these marine fatty acids (EPA and DHA) were associated with prognosis in a cohort of women who had been diagnosed and treated for early stage breast cancer (n = 3,081). Median follow-up was 7.3 y. Dietary intake was assessed using 24-h recalls (;4 recalls per dietary assessment obtained at 7 time points over 6 y). Survival models with time-dependent covariates were used to examine the association of repeated measures of dietary intake of EPA and DHA from food (i.e., marine sources) and supplements with disease-free survival and overall survival. Women with higher intakes of EPA and DHA from food had an approximate 25% reduced risk of additional breast cancer events [tertile 2: HR = 0.74 (95% CI = 0.58–0.94); tertile 3: HR = 0.72 (95% CI = 0.57–0.90)] compared with the lowest tertile of intake. Women with higher intakes of EPA and DHA from food had a dose-dependent reduced risk of all-cause mortality [tertile 2: HR = 0.75 (95% CI = 0.55–1.04); tertile 3: HR = 0.59 (95% CI = 0.43–0.82)]. EPA and DHA intake from fish oil supplements was not associated with breast cancer outcomes. The investigation indicates that marine fatty acids from food are associated with reduced risk of additional breast cancer events and all-cause mortality. J. Nutr. 141: 201–206, 2011.

http://www.ncbi.nlm.nih.gov/pmc/articles...410201.pdf

[Lotus]

have a look at this also:

http://joe.endocrinology-journals.org/co...0.full.pdf

That's a great find, genistien is a confusing herb, honestly the research gets on my nerves, lol, it does up-regulate cancer cells in some reports. It's also listed as one of the stronger pro-aromatase and up-regulated ER-b, which means it down-regulates breast growth, which is good in terms of breast proliferation, like I said......gets on my nerves, it can't make up its mind.

[Lotus]

Effects of n-3 PUFAs on breast cancer cells through their incorporation in plasma membrane

Nevertheless the mechanism by which n-3 PUFAs inhibit the growth of breast cancer cells is not well understood, but it has been suggested that these fatty acids might change the fluidity and structure of the cell membrane. In fact, changes in the structural characteris- tics of the plasma membrane in mammalian cells can modify the activity of proteins that function as ion chan- nels, transporters, receptors, signal transducers or enzymes [21-25].

In this study, we have investigated the impact of EPA, DHA and AA on breast cancer cell growth, on cell sig- nalling in apoptosis and on epidermal growth factor receptor (EGFR) activity. We hypothesize that the alteration of cellular cycle, of gene expression and the induction of apoptosis determined from n-3 PUFAs are also a consequence of membrane architecture modifica- tions. For these reasons we have analyzed PUFA incor- poration in breast cancer membrane and their PL- specific enrichment.


http://www.ncbi.nlm.nih.gov/pmc/articles...-10-73.pdf

___________________

Clelia-
From the linked study (btw, excellent)...I find this paragraph( which I referenced to your post),

Minireview: The Androgen Receptor in Breast Tissues: Growth Inhibitor, Tumor Suppressor, Oncogene?


Does sex hormone antagonism involve AR and ERα competing for the same DNA binding sites in a cell? 2) In the absence of ERα, can AR adopt an ERα-like oncogenic role? This review will describe the ability of AR action to inhibit normal breast tissue growth, examine the prevalence and prognostic value of AR in breast cancer, and critically appraise the evidence that AR has dichotomous roles in breast carcinogenesis that depend, at least in part, on whether it can duel with ERα or not.
http://www.ncbi.nlm.nih.gov/pmc/articles...rt=classic

the most potent natural ERα ligand, or DHT, the most potent natural AR ligand, via the activity of aromatase and 5α-reductase enzymes, respectively (12). Therefore, the influence of circulating testosterone on the proliferative capacity of breast epithelial cells is in part dependent upon the relative expression and activity of aromatase and 5α-reductase that occur within the breast tissues. In studies of transgenic mice that overexpress the aromatase gene (AROM+),

(This we know already).

when testosterone and E2 are administered conjointly, the stimulatory effects of E2 alone are abrogated, suggesting that testosterone is acting directly or being preferentially converted to DHT, to exert antiestrogenic, antiproliferative effects (20, 21).

Under normal physiological conditions, this adaptive intracrinology ensures that breast epithelial cells are stimulated to proliferate, enter cell cycle arrest, or die in a controlled manner via a balance of stimulatory and inhibitory sex hormone influences.

Therefore, AR signaling may exert antiproliferative effects that are not dependent on direct interaction with ERα in the same cell.


-----------------------

This is one of the best studies I've read, and I've read 100's. Curious.....what's your opinion?, sorry.... I've listed like 10 issues lol.

[Lotus]

Why we need progesterone,
-------------------------
It needs to be bio-identical.....

PC restores receptor sensitivity, meaning estrogen dominance caused the initial insensitivity. Or in other words......stalled growth.

PC in the presence of estrogen helps build breast tissue.

PC only has a half life of 5 minutes.

PC needs to be spread (thinly) over a large area for better absorption.

PC is a strong 5 ar inhibitor........aka anti DHT.

Progesterone may also lessen the risk of cancer associated with long-term estrogen treatment.

[Lotus]

The question we should be asking is how much......

As in how much Testosterone (DHT) do I need to overcome daily, or how much estradiol besides my .3 mg I produce daily is needed.

Here's what I mean--

According to the National Institutes of Health, the normal range of testosterone is 30 to 95 nanograms per deciliter (ng/dL) for women and 300 to 1,200 ng/dL for men, but individual laboratories might have a slightly different range that they consider normal. Also keep in mind that the levels vary with age. In women, the level of testosterone in the blood is lowest during puberty and adolescence, and is highest in pre- and post-menopausal women. For men, the levels increase during puberty and stay steady for much of their young adult life. They then slowly begin to decline during middle and older age.
http://www.livestrong.com/article/239396...r-a-woman/


Men and women produce exactly the same hormones, but in different amounts: as a rule, men produce 20 times more testosterone than women, while women produce more estrogen and progesterone. As with most things in nature, this "norm" can become imbalanced, and some women may have higher levels of testosterone, causing a unique set of symptoms.

Daily averages-

Endogenous avg. produced daily (males)

MEN
-Hormone ( FSH): 2 - 18 mIU/ml
-Testosterone 3mg to 10mg (daily)
-Prolactin 7 - 18 ng/ml
-FT-Free T is about 2% (this is the functional T)
-BT-Bound T or 98%
-Albumin 38% (bloodstream)
-SHBG is 60% (sex-hormone-binding-globulin)
-DHT approximately 7% of T is reduced by 5 ar
-Estradiol approximately 0.3% of testosterone is converted into E2 by aromatase (CYP19A1) of that 0.3%, 20% is directly produced by the testes. Roughly 60% of circulating estradiol is derived from direct testicular secretion or from conversion of testicular androgens. The remaining fraction is derived from peripheral conversion of adrenal androgens. The serum levels of estradiol in males (14 - 55 pg/mL) are roughly comparable to those of postmenopausal women (< 35 pg/mL).

Endogenous avg. produced daily (females)

WOMEN
-Testosterone 0.05 mg (produced daily)
-FT-Free T normal calculated free testosterone is 0.4 – 0.8 ng/dl (or 40 – 80 pg/dl).
-Albumin 34% bloodstream)
-SHBG is 66% (sex-hormone-binding-globulin)
-Estradiol 70 to 500 mg of estradiol daily, (depending on the phase of the menstrual cycle. This is converted primarily to estrone, which circulates in roughly equal proportion to estradiol, and to small amounts of estriol.)
-Estradiol in postmenopausal women (< 35 pg/mL).
-Progesterone levels tend to be < 2 ng/ml prior to ovulation, and > 5 ng/ml after ovulation. If pregnancy occurs, human chorionic gonadotropin is released maintaining the corpus leuteum allowing it to maintain levels of progesterone.

Avg tests

Hormone Follicular Day of LH Surge Mid-luteal
-Follicle Stimulating (FSH) < 10 mIU/ml > 15 mIU/ml -
-Luteinizing Hormone-(LH) < 7 mIU/ml > 15 mIU/ml -
-Prolactin < 25 ng/ml
-Thyroid Stimulating Hormone 0.4 - 3.8 uIU/ml (TSH)
-Estradiol ( E2) < 50 pg/ml ( Day 3) > 100 pg/ml
-Progesterone < 1.5 ng/ml > 15 ng/ml




Reference Values
Free Estradiol, Percent
Reference Ranges (%)

Adult Males 1.7 - 5.4
Adult Females 1.6 - 3.6

Free Estradiol, Serum
Reference Ranges (pg/mL)

Adult Males 0.2 - 1.5
Adult Females 0.6 - 7.1

Sex Hormone Binding Globulin (SHBG), Serum
Reference Ranges
Adult Males 20 - 60
Adult Female
Premenopausal 40 - 120
Postmenopausal 28 - 112

the most complete list here:
http://wikipedia.org/wiki/Reference_rang...lood_tests

This is very interesting:

Normal Hormone Proportions
http://georgiahormones.com/pdf/Brochure_...rtions.pdf

[Lotus]

The following information could explain breast development (or lack of) in AMAB, even if transitioning isn't in you're future.


Often during transition, the breast area values (numbers) do not show much change.  At first glance, one may feel that not much change is happening. Usually, more changes are occurring than you realize.  Keep in mind that your muscles are diminishing as fat is redistributing itself towards a normal female form. The change in breast size is seen by looking at the numeric differences between the chest, bust and rib cage measurements.  Additionally, the overall decrease in one's frame size (size decrease due to overall loss of muscle mass) is seen in these measurements.

The true degree of breast growth in the transgendered woman is often hidden by the fact that the chest wall diminishes as quickly as the breasts enlarge. Therefore, the overall breast measurement may stay the same even though it has enlarged by an inch or more because the chest wall has diminished by that amount.


So the changes happening, or not happening may in fact be giving you the idea there isn't any growth. This is why measurement would be a good indication in terms of your growth.

http://transgendercare.com/medical/resou...efault.asp

[-Clelia-]

Hi Lotus, i like reading your posts, now I have no much time to answer, but I can tell you something

Research is often controversial, because maybe in different studies there are differences that could affect results (for example, in vivo and in vitro can change final results).

Also, we should take account of the target of the subject: different tissues can respond in different ways, with same inizial conditions. This is due to the variability of the receptor expressed in every tissue, which often are not the same and in same amount (understandably).

So, your research about the "estrogen DHT metabolite", is based on prostate, not breast tissue or skin. That's why men become bald: there is androgen dominance in their skin, and fighting DHT is proved good to grow hair.
Also, the DHT metabolite, interacts with ERb, and we know that alfa is better for breast growth, isnt it?

Its good to try to convert DHT in estrogen metabolite, but i think its better to shut it down, at least for breast growth.
And if you do this, what about your prostate risk? Since the metabolite help prevent prostate cancer, what if you low it? I think you should read this also, maybe there are other mechanisms involved, in prostate cancer:

" Anti-androgenic activity of fatty acids." www.ncbi.nlm.nih.gov/pubmed/19353546 (2009)

[spanky]

That's a good find, Clelia. Thanks!

[Lotus]

Hi Lotus, i like reading your posts, now I have no much time to answer, but I can tell you something

Thanks Clelia, , I appreciate your time.

Research is often controversial, because maybe in different studies there are differences that could affect results (for example, in vivo and in vitro can change final results).

Great point, I noticed limitations in some studies (e.g. available test samples w/regards to country's ban or limitations) could affect results, but I understand what you mean.

Also, we should take account of the target of the subject: different tissues can respond in different ways, with same inizial conditions. This is due to the variability of the receptor expressed in every tissue, which often are not the same and in same amount (understandably).

Ok, Like multiple response, or unintended consequence.

So, your research about the "estrogen DHT metabolite", is based on prostate, not breast tissue or skin. That's why men become bald: there is androgen dominance in their skin, and fighting DHT is proved good to grow hair.
Also, the DHT metabolite, interacts with ERb, and we know that alfa is better for breast growth, isnt it?

BPH/prostate research does seemed skewed towards 5-ar inhibitors/ anti DHT. Since the prostate is pro ER-a it seems likely estrogen could be a mediator of cancers too.

Its good to try to convert DHT in estrogen metabolite, but i think its better to shut it down, at least for breast growth.

I've seen some promising research that includes androgen blockade therapy, 17beta -HSD, even using prolactin molecules to box out DHT because of their larger size, suggesting to me PRL is DHT inhibitor. But I think COX is also an aromatase at PGE.

And if you do this, what about your prostate risk? Since the metabolite help prevent prostate cancer, what if you low it? I think you should read this also, maybe there are other mechanisms involved, in prostate cancer:

Yes, elimaniting androgen/DHT ip even in Mtf has long term consequence. The biological affects of androgens are are still needed. The assumptation of testosterone being poison is often misinterpreted. Testosterone is the sex hormone that converts to all estrogens, without T Mtf wouldn't make the necessary conversion to transition. I think it's a mistake to reduce testosterone, the reduction is needed at DHT...... and the reason is quite obvious.

" Anti-androgenic activity of fatty acids." www.ncbi.nlm.nih.gov/pubmed/19353546 (2009)

Great link, thank you so much, I can only think of two supplements that cam meet that demand........coconut oil and EPO-evening primrose oil.