Breast Growth For Genetic Males

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(25-03-2015, 01:33 AM)Lotus Wrote: [ -> ]"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."

(24-03-2015, 11:15 PM)-Clelia- Wrote: [ -> ]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

(24-03-2015, 11:35 PM)-Clelia- Wrote: [ -> ]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. Rolleyes

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.

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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.

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.

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--

(17-07-2014, 05:36 PM)Lotus Wrote: [ -> ]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

(23-02-2014, 05:55 AM)Lotus Wrote: [ -> ]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

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)

That's a good find, Clelia. Thanks!

(25-03-2015, 11:03 AM)-Clelia- Wrote: [ -> ]Hi Lotus, i like reading your posts, now I have no much time to answer, but I can tell you something

Thanks Clelia, Big Grin

, I appreciate your time.

(25-03-2015, 11:03 AM)-Clelia- Wrote: [ -> ]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.

(25-03-2015, 11:03 AM)-Clelia- Wrote: [ -> ]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.

(25-03-2015, 11:03 AM)-Clelia- Wrote: [ -> ]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.

(25-03-2015, 11:03 AM)-Clelia- Wrote: [ -> ]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.

(25-03-2015, 11:03 AM)-Clelia- Wrote: [ -> ]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.

(25-03-2015, 11:03 AM)-Clelia- Wrote: [ -> ]" 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.

[Image: attachment.php?aid=8784]

Lotus, could there be side effects from 'blocking' androgens over time? Or can you do this for longer periods? And thank you for the information Smile

Breast Growth For Genetic Males

Lotus

Lotus

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Lotus

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-Clelia-

spanky

Lotus

hannah