Estrogen Receptor Puns

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Please discuss, and you can vote in the /r/truscum poll that I made here.

I myself plan on initially just using the usual antiandrogen plus normal dose (not microdose) estradiol when I am able to restart HRT, and switching to that strategy if I were to become dysphoric over breast development.

People who want to grow taller can usually take Aromatase inhibitor to delay the closure of the growth plates to allow for more time to grow. Can taking Turkesterone which affects the estrogen beta receptor do the opposite?

does tren modulate estrogen binding like DHT derivatives?

Could this be the mechanism as to why in men high and low estrogen seems to have similar side effects? As high estrogen + low estrogen receptor availability will cause the estrogen to compete with other molecules for binding. As seen with partial agonist causing antagonism of the estrogen receptor by decreasing estrogen's ability to bind to the receptor.

One paper I Found supporting this would be paper on the Androgen known as Ment or trestolone (in small amounts) showing that it was able to decrease the binding of estrogen to the receptor as well as estrogen itself despite having a very low affinity for the estrogen receptor. I'm not sure if the authors were trying to conclude with this as it seems like its left to partial interpretation, but they seem to reason that MENT is decreasing estrogen binding ability through the androgen receptor by decreasing the number of estrogen receptors as androgen are known to decrease the expression of the estrogen receptor.

Study- https://pubmed.ncbi.nlm.nih.gov/9879986/

Also any nutrition tips from bodybuilders / male fitness fanatics will be most welcome! Thanks :)

My question is does enclomiphene citrate cause the Estrogen receptors the become up regulated after using it in a pct.

Lots of different soy isoflavones out there with different affinities for each estrogen receptor, is there data on this

I just found out about SERMs, they're nicknamed "designer estrogen" because of their estrogen-like effects on bone density, and their anti-estrogen effects on chest tissue. However, similar to how hormone suppressants were designed as uterine and prostate chemo, SERMs are for breast cancer. I don't make enough hormones (afab he/him), just found out, but my endocrinologist doesn't want to give me SERMs because it's used to prevent osteoporosis in people with breast cancer who are over age 65. He said it's mostly concerning due to my age, mid 20s.

I'm prescribed half of an estrogen patch, but I don't realistically see myself being able to take estrogen or testosterone, regardless of consequences. The hope is having such a low dose of estrogen I don't really notice, we'll see. Any effects would be too distressing. Same goes for testosterone, so I'm out of options. Testosterone with finasteride to block some of it might be less terrible, but again not ideal or likely tolerable.

I'm hoping for more scientifically literate answers here, but everyone onboard the Turk bandwagon is convinced that there are no adverse effects from Turk supplementation, but if I am not mistaken, there are Estro-beta receptors within breast and prostate tissue, but I'm far too dumb to understand what these receptors actually do and if Turk agonizing these receptors could lead to cancer cells appearing for those of us who are genetically prone to these cancers.

Edit: Also, is beta agonization the only effect of Turk? Or does it have other effects?

https://www.frontiersin.org/articles/10.3389/fendo.2021.701364/full

> Here, we discuss the theoretical use of Selective Estrogen Receptor Modulators (SERMs) for non-binary people assigned male at birth (AMAB) who are seeking an androgynous appearance through partial feminization without breast growth. Given their unique range of pharmacodynamic effects, SERMs may represent a potential gender-affirming treatment for this population, but there is a lack of knowledge regarding their use and potentially adverse effects in this context.

Hi there,

In my research to determine the best HRT regime to follow (presently E mono therapy), I have come across information that suggests estrogen regulates its own receptor density.

I found this information via a paper by Richard Wassersug, a professor in the department of Medical Neuroscience at Dalhousie University who has published a number of papers of the use of Estradiol patches for high dose mono-therapy in the treatment of prostate cancer - including the treatment of his own prostate cancer in this way.

Does anyone else have further details on this phenomena? It seems to suggest that ‘steady‘ supply of estradiol is not necessarily desirable because of that function of receptor regulation and rather that fluctuating supplies of estradiol might be more effective and/or more ‘natural’.

My intuition has told me - prior to reading about this - that the menstrual cycle of cis women - one that produces a wide range of estradiol levels is perhaps a more natural state for the body and than constant levels (which is what my GP wants me on) and that this might not be very effective.

Further, perhaps the effectiveness of injectable estradiol might stem from the spikes and troughs of the administration route which meets this phenomenon of receptor density regulation.

Richard suggests that because estradiol is a naturally occurring hormone, it’s totally unlikely that the pharmaceutical industry would ever put research into developing a product that could deliver a variable menstrual cycle-like estradiol product but he feels such a thing would be fantastic research.

What are peoples thoughts on this? I feel like a pulsing or variable level of estradiol - at a level minium required to suppress testosterone via the HPG axis might produce excellent feminising effects for us trans women....

TL;DR if estradiol regulates its own receptor density, then a ‘steady supply’ of estradiol might not be advantageous and perhaps pulsing, or rising/falling levels or estradiol might explain why people have better results on injectable estradiol. Something that’s closer to the natural rhythms of a sis woman’s menstrual cycle.

Thoughts?

edit:spelling

I've seen this study come up a few times and think it might be an interesting read for folks here.

Of course, the sample size is small, and no single SNP will cause transexxualism on its own, but these are intriguing findings to say the least. IDK, what does everyone think about this study?

https://www.fertstert.org/article/S0015-0282(07)01228-9/pdf

https://beststartbirthcenter.com/male-circumcision/

The first result I saw - this is a good sign towards social progress :)

Thank you all for being such a supportive community

Mostly unsuccessful with trt as well as higher doses. I am somewhat better but in no way feels as if I am treating the route of the dysfunction - still cannot see any veins in my entire body/arms even with cialis and nitric boosters. I’ve used test before I tried SSRIS and it was extremely effective whereas now the results seem like they are unable to be tapped into due to the vascular/cardio dysfunction that comes with PSSD. I am thinking of trying nandrolone or trenbolone as an adjunct in order to upregulate both the androgen and estrogen receptor - these compounds do this through a sort of progestogenic mechanism that I’m going to delve into further. I’ve come across a few reports of low dose tren curing/reversing certain PSSD subtypes and given that I’ve been suffering for 3 years I’m willing to give it a go. Thoughts?

Also - estrogen is said to normalise SERT expression resulting in reduced systemic 5HT and desensitised 1A - progesterone is thought to be an antagonist to estrogen 🧐🤨

In a lot of anecdotal cases, we have heard how dihydrotestosterone (DHT) derivatives “mask” high estradiol (E2) side effects mainly pertaining to gynecomastia.

The most common DHT derivatives that are used by the community include, but are not limited to, 1-testosterone (DHB—dihydroboldenone), drostanolone (Masteron), mesterolone (Proviron), and metenolone (Primobolan).

I have mentioned multiple times throughout the AA threads that taking these DHT derivatives can prevent high E2 sides based on the ratio of DHT:E2 in the body being more in favor of DHT. While this is great broscience and has worked for many people throughout our community, it is crucial that we understand what the specific mechanism is that causes this suppression of E2 side effects.

Anecdotally, my total testosterone level measured at ~1600ng/dL with E2 at ~118pg/mL during my last blast (500mg test e weekly, 40mg Tbol ED for 50 days, 50mg Proviron ED) with no E2 side effects. Shortly after dropping all compounds and moving to my cruise dosage of 150mg test weekly, I experienced high E2 side effects (inadequate erections/libido and gyno lump) with bloodwork showing 657 test with 72 E2. Obviously, I’m a shitty responder to test and a heavy aromatizer, but on cycle with my test being barely above natural levels and E2 being 3x the upper natural limit, I had no problem whatsoever with gyno, blood pressure, mood, erections, or libido. I did have bloat, but I contribute that to a shitty diet.

While these compounds do not decrease circulating E2 levels, they do act as an indirect antagonist (a compound that acts against or blocks typical ligand-receptor action). What this means is that they do not block E2 receptors like SERMs do in the breast tissue, but somehow still prevent binding in a different way.

I did some poking around on the internet and found some studies that have looked at this phenomenon. See below:

Antiestrogenic Action of Dihydrotestosterone in Mouse Breast. Competition With Estradiol for Binding to the Estrogen Receptor

> Dihydrotestosterone does not compete for binding to the progesterone receptor, but it does inhibit estrogen-mediated increases of progesterone receptor content of breast tissue cytosol...

This suggests that DHT blocks elevated E2 from increasing progesterone receptors in breast tissue which can lead to milk production.

> Since [mice with X-linked testicular feminization] lack a functional androgen receptor, we conclude that this anties

Hello everyone! I was just wondering if it is possible to up-regulate estrogen receptors or to increase aromatase. I’ve been taking CPA for 6 months with sublingual estradiol. My testosterone is suppressed but my breasts have developed very poorly.

I was reading on a post that CPA can down-regulate estrogen receptors. I don’t know if this is true or not, but made me wonder if there is a way to up-regulate estrogen receptors or to increase aromatase. (I plan to switch AA on the future, however I am curious)

Thank you very much in advance 💜

I can't find my link and crosspost isn't an option on it but I just read something that says it's better to take oral HRT dose once a day because bodies naturally produces hormones on a 24 hour cycle and that they naturally drop at night to signal the brain to make more and also to not let our cells because immune to the signals from hormone levels constantly being high.

I have 0 medical knowledge but totally makes sense to me. I recently made a post on me having had more growth on oral low dose E at the start of my transition than I have no on sublingual. back then I took my E once a day. also maybe switching up estrone and estradiol once in a while helps ? I don't know, what do you all think about this?

I also recently saw a post that Dr.Powers posted some time back about some patients on injection (I think) being stalled and switching them back to oral E helped their progress. perhaps this could account for it in the sense that their cells became de-sensitized from the estradiol signals and then started responding the increased estrone better?

Nat Med

. 2021 Jan 18.

doi: 10.1038/s41591-020-01168-7.

Link: https://www.nature.com/articles/s41591-020-01168-7?utm_source=feedburner&utm_medium=feed&utm_campaign=Feed%3A+nm%2Frss%2Fcurrent+%28Nature+Medicine+-+Issue%29

Like many of us, I am struggling to squeeze out all the femininity that I can. Breasts are not my issue but facial feminization and hair improvement are.

It appears to me that younger people go immediately to prescriptions that hit the E and T targets right away. I believe this could be because issues with breast growth are much more rare for those under 25.

I have seen several papers that seem to indicate that if hair is your main issue and not breasts, then you do want to hit your targets as soon as possible since unlike other areas of the body, hair regrowth might be more like a binary light switch, either on or off but to turn it on, you have to have E and T in the target ranges. I think that this could be true for FF as well.

At the same time, however, we also know that breast growth can occur with trivial amounts of estrogen in the body in the presence of full testosterone. So with these receptors, maybe the effects are more analog.

For four years, I looked completely female below the neck and completely male above the neck so it does seem apparent to me anecdotally that some receptors are more easily triggered. I started growing very respectable breasts with menopausal creams and no T blockers or progesterone, just estriol and then estriol and estradiol for four years.

It was a very strange way to be non-binary because I considered myself feminized but no one else had a clue. I was also rubbing these creams directly into my breast tissue so maybe that distinguished things. I have found although it could be the placebo effect, that spot administration of estrogen does have strong localized effects at least below the neck. I would be interested in anecdotal accounts of others and what areas feminized first and last and at what approximate amounts of E and T in the blood and prescription amounts of E and anything else.

So my hrt is absolute mess, wish it wasn't but here we are.

It went like this:

First 3 weeks of August 2019 2mg estrofem sublingualy once daily

4th week of August and 1st of September 2mg estrofem sublingualy and one casodex pill(50mg bicalutamide) once daily

2nd and 3rd week of September 2mg estrofem sublingualy twice daily and one casodex pill once daily

And because one of roommates in the flat I moved in at the beginning of September that was supposed to be supportive LGBT friendly and what not turned out to be fucking TERF and I got kicked out after one week and didn't have money for any more hormones. All that changed was skin and tiny bit of boobs growth, nothing more than slightly more pronounced nips.

4th week of February 2020 and whole March 4mg estradiol buccaly 1at week of April 6mg estradiol buccaly

Then idk what happened, covid happened, I have lost my job, literally been rejected from entering my family home, rejected from from staying with my uncle, settled on staying at our garden cabin from which I also gotten kicked out after a week (yeah, cool family right) and even though I had pills for next couple months I gradually stopped taking them over next month. Sometimes 2 per day, sometimes only one, sometimes none for couple of days and stopped completely at the end of May. The only noticeable changes happened during that 6mg per day period and again, only skin changes.

16th September to 21th September 2 climara forte patches 21at September to 9th November 3 climara forte patches

And idk what happened. After few weeks of trial I wanted to order more since I found nice job and had money but they were out of stock. I have waited as long as I could and had to order estrofem and cypro supply for 2 months, just to wait till patches are available again because honestly I have had great results on them BUT this is me and my luck and they still haven't arrived. Idk if they have been seized by customs or what but here we are, detransitioning for over a week now. I can make new order but it kinda hit me really bad and I started panicking. This is the point where I'd repeat question in the title. Should I just wait patiently for new ones and everything will be as nothing happened or did I fuck up one too many times.

Really really thank you for reading it all, hope you can help me.

Hi all,

I am quite desperate right now - I discovered a small lump in my right breast - Fast forwarding everything, It was a cancer stage 1, and I did a lumpectomy, and it was confirmed HER2 + and estrogen and progesterone receptors by the biopsy.

The oncologist wanted me to start right away on KADCYLA (instead of the traditional Chemo) - My Insurance (AMBETTER in Florida) is denying the medication to me.

We had appealed 2 times - I'll still try one more time, but I am scared that they'll decline again.

Does someone is taking Kadcyla without traditional chemo? I need a bright light!! - TIA!!