[Lotus]

So if I read between the lines, pharma HRT effects ER-a, but PM effects ER-b. So, if I add some PM back into the mix it should assist growth rather than hinder it.

Yes E2 binds with ER-a, however!........bioidentical progesterone is still needed to complete ductal side branching (rounding). Too much prolactin produces tubular growth, while E2 produces elongation. Add in growth hormone and essential fatty acids and hopefully things start happening lol, (albeit a slow process).


I still wouldn't use PM with HrT:

miroestrol competes with estrogen and blocks the excessive stimulation of estrogen receptors often seen with breast or endometrial cancer.

How much prolactin is too much? as you may remember my levels have always been high, nearly double what the nhs would like at my last blood test

A few things stick out. Are the labs drawn at the times of the day (a few hours after waking up). I'd bet you have nil for T (or close to it, less than 25 ng/dL). Other things to look at are liver function, hypothyroidism, cirrhosis, stress, dopamine.

High prolactin could also mean you're having too much E2 in an HrT program.

[Lotus]

http://www.breastnexus.com/showthread.php?tid=1959

We use a lot of Acronyms on this site, hopefully this link will explain them all for you.

Thanks jannet

[Lotus]

If some of y'all on this site would get together and open a walk-in clinic, many of us would appreciate it. Thanks in advance... Many thanks!

That sounds cool char, I could see a spa, open bar, and for the non-alcohol types? maybe a juice bar, sushi, massage etc.

I do know what you meant though, I'm sure the others (as well I) appreciate the thought.

[Lotus]

Update on leucine:

L-Leucine Increases Skeletal Muscle IGF-1 Peptide But Has No Effect on Akt/mTOR Signaling in Response to Resistance Exercise in Trained Men
http://m.fasebj.org/content/29/1_Supplement/819.2.short

It appears IGF-1 is up-regulated in skeletal mass, and no changes to mTOR signaling respone.

Before I forget I wanted to share this tidbit, it's called Leucine. Leucine-rich proteins (amino-acids) are human co-regulators of estrogen receptor alpha (ER-a, the growth gene). (like I said, an onion).


Leucine works with the amino acids isoleucine and valine to repair muscles, regulate blood sugar, and provide the body with energy. It also increases production of growth hormones, and helps burn visceral fat, which is located in the deepest layers of the body and the least responsive to dieting and exercise.
http://www.vitaminstuff.com/amino-acid-leucine.html

Foods highest in Leucine
(based on levels per 200-Calorie serving)
http://nutritiondata.self.com/foods-0000...00000.html
Eggs whites, Soy, Tuna, etc.


J Biol Chem. 2001 Oct 12;276(41):38272-9. Epub 2001 Jul 31.
Molecular cloning and characterization of PELP1, a novel human coregulator of estrogen receptor alpha.
Vadlamudi RK1, Wang RA, Mazumdar A, Kim Y, Shin J, Sahin A, Kumar R.
Author information
Abstract
Nuclear hormone receptors (NRs) are transcription factors whose activity is regulated by ligands and by coactivators or corepressors. We report the characterization of a new NR coregulator: proline-, glutamic acid-, leucine-rich protein 1 (PELP1), a novel human protein that comprises 1,282 amino acids and is localized on chromosome 17. The primary structure of PELP1 consists of several motifs present in most transcriptional regulators including nine NR-interacting boxes (LXXLL motifs), a zinc finger, and glutamic acid- and proline-rich regions. We demonstrate that PELP1 is a coactivator of estrogen receptor alpha (ERalpha). PELP1 enhances 17beta-estradiol-dependent transcriptional activation from the estrogen response element in a dose-dependent manner. PELP1 interacts with ERalpha and also with general transcriptional coactivators p300 and cAMP response element-binding protein-binding protein. PELP1 was differentially expressed in various human and murine tissues with the highest expression levels in the testes, mammary glands, and brain. We also provide evidence supporting the developmental regulation of PELP1 expression in murine mammary glands, the detectable expression of PELP1 in human mammary cancer cell lines, and the enhanced expression of PELP1 in human breast tumors. These findings suggest that PELP1 is a novel coregulator of ERalpha and may have a role in breast cancer tumorigenesis.
http://www.endocrine-abstracts.org/ea/00...03p134.htm

[Lotus]

Epidermal growth factor (EGF) increases aromatase activity and expression in MCF-7 and adipose stromal cells and induces expression of cyclooxygenase 2 (COX-2) in adipose stromal cells (Richards et al. 2002). In breast tumors, prostaglandin (PG) E2 increases intracellular cAMP levels and stimulates estrogen biosynthesis (Zhao et al. 1996); furthermore, it up-regulates aromatase activity and expression in adipose stromal cells (Richards & Brueggemeier 2003). EGF affects the expression of 3B- hydroxysteroid dehydrogenase (3B-HSD) type II and CYP17 in NCI-H295R cells (Doi et al. 2001). Also in NCI-H295R cells, up-regulation of aromatase expression by PGE2 has been reported (Heneweer et al. 2004). However, the mechanisms of the effects of EGF and PGE2 on aromatase expression in NCI-H295R cells have not been examined in detail at the molecular biological level. Therefore, we conducted detailed studies on the effects.

Doses of GLA greater than 3,000 mg per day should be avoided because, at that point, production of AA-Arachidonic Acid(rather than DGLA) may increase.

believe it, after we gain a therapeutic edge lol over total T we could be producing more E2 in our testes than the typical post-menopausal women, who produce mainly E1 in their peripheral tissues. And if all you took was a minor AA and an aromatase herb you could still maintain the "therapeutic edge" over GID, of course that's just my opinion, but I think we see/hear more and more evidence to support that hypothesis. 

I've been testing that DHEA at 25 to 50 mg increases his estrogen level.  However, a woman taking this dose, will see her testosterone increase.

Epidermal growth factor (EGF) increases aromatase activity in adipose (fat) and up regulates cox 2 expression, also PGE2 (prostaglandin), which is done by GLA, gamma linolelic acid, like from evening primrose oil, above 3000mg which goes into AA  acid, that's when it's dicey. I might say forskolin does up regulate aromatase, but still risky spiking blood pressure,

Effect of epidermal growth factor and prostaglandin on the expression of aromatase (CYP19) in human adrenocortical carcinoma cell line NCI-H295R cells http://m.joe.endocrinology-journals.org/.../1/59.full
EGF significantly increased aromatase activity and CYP19 gene transcript in NCI-H295R cells.


Prostaglandins can be synthesized in an adrenocortical carcinoma, and they can work in an autocrine or paracrine fashion. In rabbit chondrocyte and human squamous carcinoma cell lines, EGF induced the secretion of PGE2 via up-regulation of the activities of phospholipase A2 (PLA2) and COX-2 (Sato et al. 1997, Huh et al. 2003). This may suggest that PGE2 acts as a secondary factor to EGF in the up-regulation of aromatase expression. Therefore, we checked whether PGE2 was secreted from NCI-H295R cells in response to EGF. In this study, NCI-H295R cells secreted PGE2 in response to EGF (Fig. 13), and PGE2 increased aromatase activity to a greater extent than other prostaglandins (Fig. 6). The inhibition of EGF-induced aromatase expression with PGE2 receptor antagonists confirmed that PGE2 is the secondary factor of aromatase expression with EGF (Fig. 14). PGE1 also increased aromatase activity to a degree similar to that of PGE2, but EGF could not stimulate NCI-H295R cells to secrete a sufficient concentration of PGE1 (data not shown) to increase aromatase activity. These results suggest that several prostaglandins are secreted in response to EGF, and that these prostaglandins evoke some intracellular signaling pathways. According to the experiments using several protein kinase inhibitors (Fig. 12), the intracellular signaling pathways that include MAP kinase, and calcium-calmodulin kinase are important for up-regulation of aromatase by EGF. In response to EGF, EGF receptors (receptor-type tyrosine kinase) activate the MAP kinase pathway through phosphorylation of Ras protein. It is also well known that EGF receptors increase the intracellular calcium concentration. Therefore, it would be reasonable to conclude that inhibition of MAP kinase kinase and calcium-calmodulin kinase II downregulate aromatase expression in NCI-H295R cells. Interestingly, a PKA inhibitor (H-89) down-regulated aromatase activity. This result suggests that the cAMP– PKA pathway is involved in the up-regulation of aromatase.

[bobie]

A few things stick out. Are the labs drawn at the times of the day (a few hours after waking up). I'd bet you have nil for T (or close to it, less than 25 ng/dL). Other things to look at are liver function, hypothyroidism, cirrhosis, stress, dopamine.

High prolactin could also mean you're having too much E2 in an HrT program.

I have always had my blood drawn around the same time, mid morning, i did consider how prolactin is highest during sleep so tend to get up a bit earlier on days of blood tests, yes my t is low, generally around 0.5 - 0.7 nmol/l which is to be expected on the gnrh analogues, liver function & thyroid have always come back fine, stress well plenty of that at times but i think i have it under control at the moment, you may remember me asking before whether finasteride can increase dopamine, well im still on the finasteride, my e2 levels have been pretty rubbish tbh at around 80pg/ml on 8mg oral e2 (4mg twice a day), i really want to try injections later in the year and see if that works for me

[Happyme]

You seem to know a lot Lotus and I envy what you have accomplished! When you first started NBE did you have a flat chest? if so, what did you do to get breast growth? Also, what is SP and PC?

Hi sabriel,

I did start with what we could call a typical male chest (ok, flat lol). When I started developing breast tissue (pre NBE) I was concerned and made an appt. to see my now former PCP of 12 years. Very nice Dr. [90 yrs. young lol], though very old school.

Anyways.......are you sure you want to hear about this? cause there will blood ((haha)), pain, self doubt & torture (true), and perhaps lack of proper guidance, but nothing more than a few visits (3-4 different shrinks actually) would cure huh?. Oh wait!, then there was the visit to the endo (jerk) who discouraged my path, which I think led to a dark period (1.5 yrs actually) ultimately that led me to my current doc (finally, a trans friendly Physician). Btw, the endo suggested I remove the breat tissue , that's after he said " yep, those are real female breasts. At the time my GID was heavy gender fluid, and when I mention it to him (the gender fluid) he became very annoyed at the mere mention of it, his quote " there's no such things, I don't believe in the gender variants, it's either your full transition or nothing ".........so I thought to myself ( " oh hell no, you mf'er " you just discriminated against me). And although some part of me told me to take his shitty advice it pushed me to a dark place that ended up going to DIY hormones, dangerous times indeed. As for the endo, I got a nice letter announcing his retirement shortly after. I wonder how many TG folks got his shitty care?. I was seeing (still am, no anti-depressants though) a shrink, number 4 (a great guy too), he found my current TG doc.

Getting back to pre-NBE (which wasn't even on the radar at the time) sent me for a mammogram, and was diagnosed with gyno (gynecomastia). So.......naturally seeking more info I jumped on the " World Wide Web " and found breast nexus, which I found inspiration from flamsabers, technical guidance from Abidrew and Isabelle. At that point I had what you would call puffy nipples, but the more important question is why did I want this path????, well, I still have my doubts about that, although I lean towards the thought my GID lay dormant (for years) and with the start of NBE, the walls (bells rang lol) came crashing down I guess.

I started with the typical NBE program of RC (red clover), FG (fenugreek) SP (saw palmetto), PC (progesterone cream), I stayed with that for about 6-8 months (if I remember correctly) which yielded about 1 cup increase. The next program i went with PM capsules (pueraria mirifica) add 1 cup more. I experimented with BO (w/disastrous infections) e.g. damaged my right eye permanently (a retinal hemorrhage, aka blood) requiring laser eye surgery to plug the leak. Add in a major ear/jaw infection, a trip to the ER for an acute bout of colitis, which was followed by a colonoscopy (btw, the prep was god awful) to rule out further problems. Which is the reason why I won't recommend BO (bovine ovary).

The 3-4th NBE program I went to extracts (for the most part), and then modified with different anti-androgens & pro aromatase supps........add 1-2 cups more growth from those mods. My idea (or thought process was to keep pushing with breast growth and some feminization), lol which obviously went further then expected ok. As I battled with GID, the two sides (male/female) clashed (still an epic throw down though) the female side demand(s) more control lmao, so call it what you will, meaning a two-spirit??, or non-binary gender/ gender fluid???, I'm still working on that part but I'm on path of transition, hey it works (or is working) for now. I will eventually add some essence to the female side (short term?? 3-6 months??? not sure), but I surely don't look like I did 2-3 years ago. Will I need cosmetics, maybe? maybe not, will see what HrT does in the near term first.

Sheesh, this has been therapeutic, thanks sabriel, I usually don't go this deep about myself lol (too boring imo lol) sorry for the long drawn out. whatever path you (we) take, finding the right care sometimes take a tortuous path (or journey) to find them (unfortunately). And sadly, good people are lost forever in this maddening process to find the right medical care, it needs to be fixed.

O, I did have a couple early puffy nipple pics up, but in a major dust up (here at BN) back in the day they were deleted (by me) (perhaps a discussion for another day).

Thanks for the great story Lotus! I love reading these real stories especially with the continuing gender bashing in the news. Its just so hard to explain to someone what its like.
Thanks for all that you have done and still do!
Bobbi

[Lotus]

So if I read between the lines, pharma HRT effects ER-a, but PM effects ER-b. So, if I add some PM back into the mix it should assist growth rather than hinder it.

Yes E2 binds with ER-a, however!........bioidentical progesterone is still needed to complete ductal side branching (rounding). Too much prolactin produces tubular growth, while E2 produces elongation. Add in growth hormone and essential fatty acids and hopefully things start happening lol, (albeit a slow process).


I still wouldn't use PM with HrT:

miroestrol competes with estrogen and blocks the excessive stimulation of estrogen receptors often seen with breast or endometrial cancer.

How much prolactin is too much? as you may remember my levels have always been high, nearly double what the nhs would like at my last blood test

A few things stick out. Are the labs drawn at the times of the day (a few hours after waking up). I'd bet you have nil for T (or close to it, less than 25 ng/dL). Other things to look at are liver function, hypothyroidism, cirrhosis, stress, dopamine.

High prolactin could also mean you're having too much E2 in an HrT program.

I have always had my blood drawn around the same time, mid morning, i did consider how prolactin is highest during sleep so tend to get up a bit earlier on days of blood tests, yes my t is low, generally around 0.5 - 0.7 nmol/l which is to be expected on the gnrh analogues, liver function & thyroid have always come back fine, stress well plenty of that at times but i think i have it under control at the moment, you may remember me asking before whether finasteride can increase dopamine, well im still on the finasteride, my e2 levels have been pretty rubbish tbh at around 80pg/ml on 8mg oral e2 (4mg twice a day), i really want to try injections later in the year and see if that works for me

80 pg/mL @ 8mg is rubbish tbh. This has to be a metabolism/bioavailability issue, 8 mg of E2 should yield 4-5 times your test results. I take half of what you do and get +800 pg/mL (last 3 blood tests). From my experience I've been splitting sublingual/oral delivery. But,,,, I tend to think a few things make my level higher, my T is in the cellar, (prolactin is normal), I either drink green tea or take GTE, take lemons in 6-8 cups of water, 2 oranges per day (all inhibit CYP17A1 and promote C19 aromatase).

600 pg/mL E2 is supposed to be optimal feminization range, although docs are overly cautious to even come close to that range and would rather it be 200-400 pg/mL. I'd also be inclined to say that you take steps to reduce stress in your daily life. Cut sugars, alcohol, meds that interfere with metabolism (aka P450 enzyme inducers) that reduce bioavailability of HrT.

If you went IM ? I'd also check on pellets (or implants). Long term? if T is in the CC range I'd rule out an orchi and save for SRS, just my opinion though.

[Lotus]

Thanks for the great story Lotus! I love reading these real stories especially with the continuing gender bashing in the news. Its just so hard to explain to someone what its like.
Thanks for all that you have done and still do!
Bobbi

Aw thanks bobbie, I appreciate that. Yep, bashing is full on hate and hostility, very sad indeed.

[bobie]

Agreed its rubbish but i know of a number of people getting similar results on that dosage so i know im not alone, not that it makes it any better, i have often wondered whether if they gave me something to lower prolactin levels whether i would then see things happening, here the nhs really are conservative wanting you in the 54-163 pg/ml range, tbh i have little faith in the gic and will be glad when i can do my own thing, im going to send you a pm shortly