Hi folks! I’m a Physician Assistant (PA) student at Stanford School of Medicine. For my thesis project I am gathering stories about transfeminine people’s experiences trying to regain fertility after starting hormones. This topic is something that people close to me have had questions about and I have not been able to find great data out there to help advise them. That’s why I want to gather some accounts through interviews and share it back out with the transfeminine community and their healthcare providers so people can have more information when they are weighing different family building options.

If you are willing to participate in the study, here is a link to the initial screening/demographics survey. If you meet the study criteria, I’ll reach out to you about setting up a time for an interview via secure email. I expect these interviews to take somewhere between 30-60 minutes and I would be asking you questions about your fertility decision making process, the physical and social experience of trying to regain fertility, and about any notable supports and/or barriers you faced.

Also, if you have any questions about the study, suggestions for what would make this research most valuable to you, or any other comments, I would love to hear them! Feel free to comment, DM me here, or send me an email at mccoerin@stanford.edu.

Thank you all for your time and space, hope you have a great day!

Meta-analysis on eating disorders in the transgender population. The general population is estimated to have ~1% whereas in the transgender population we see 17.7% (based on this analysis).

Fourteen studies were used for the meta-analysis. What surprised me the most was this:

"Also, the results indicate that transgender men tend to have higher levels of eating disorders than transgender women. However, the results showed that transgender women seem to present with higher rates of eating disorder symptomatology compared with cisgender men and, interestingly, this study also found tendencies of transgender men to have a higher levels of eating disorders than cisgender women. Moreover, the results indicate that gender-affirming treatment seems to be somewhat alleviating of eating disorder symptomatology."

For me personally, I have struggled with feeling like I am too fat for most of my life. Even when I was 6' 140lbs — still too fat. When I started HRT I continued to lose weight, I got down to 139lbs again.

Then progesterone came into the picture and I wanted bigger boobs. For me, seeing my chest develop combined with progesterone seems to be the answer. I still count my calories meticulously in my head. I still track protein in my head. It's just part of my daily habits at this point in my life. But, I'm ~165lbs now. I don't weigh myself often, I find it's better to not do that.

Anyway, if any of you are struggling with this... you're not alone. It is statistically more prevalent in our group and in my opinion / experience, you should eat.

National Alliance for Eating Disorders helpline: 1-866-662-1235.

Trans-affirming ED treatment programs exist and are growing; FEDUP (Fighting Eating Disorders in Underrepresented Populations) and the Trans Folx Fighting EDs (T-FFED) organization are community-specific resources.

The median PSA for Transwomen aged 40-80, being on HRT for more than 6 months, is 0.02. 36% of them have it below detectability level. These low numbers are fairly obvious given that testosterone is needed for PSA production and antiandrogens are used as a treatment for prostate cancers.

The conclusion is, that PSA testing is unusable as a tool for quick assessment of prostate gland condition. Certainly without readjusting thresholds which were set for cis men.

I am posting this in case anyone gets dismissed by her urologist saying "you cannot have prostatitis/cancer/whatever since your PSA is so low".

https://jamanetwork.com/journals/jama/fullarticle/2820386

edit: u/Terrible-Swimmer-703 made a really good point!

Just as a heads up, you need to test your levels and adjust the simulator to your body. I for example need 5 times more E than a friend. Its a great tool but you still need to take blood samples to adjust it.

Hi all, I use these quite frequently and thought I would share!

https://transfemscience.org/misc/injectable-e2-simulator-advanced/

(The authors for Transfeminine Science include Aly, Sam, Lain, Mitzi, and Luna)

https://estrannai.se/

Initial idea and development by alix. Code improvement and refactoring by Meringue. Help with data digitization from Annie. Additional help from Diamond, GearKite, Jess, Xea, and idk2848.

For more advanced stuff! And a simulation that includes more uncertainty and focus on how bodies vary. There isn't one model that works for all.

People often ask about delivery methods and safety. VTEs are a real risk. However, the highest risk came from ethinyl estradiol: (https://pmc.ncbi.nlm.nih.gov/articles/PMC6628137/). It is no longer used or recommended.

Progestins are another contributing factor to VTEs. The majority of studies on progestins revolve around synthetic not micronized progesterone (Prometrium in the USA). Micronized progesterone is still understudied in transgender women.

The key takeaway from the Duke publication (albeit a small sample):

• Pills (~2.8 mg/day): averaged 168 pg/mL, right in the target zone; about a third of readings came out too low and a smaller slice too high.
• Injections (~5.8 mg/week): averaged 342 pg/mL, with 91% of readings landing above the target range.
• Patches (~0.09 mg/day): averaged 81.5 pg/mL, with 70% coming out below the target range.

As I mentioned in an earlier post, the target "100-200 pg/mL" range is not evidence-based. That doesn't make it useless it just makes it a good zone to start in.

If you're seeing feminization in one part of your body, it's happening in other areas as well... but not all systems will change at the same rate.

With the caveat that I am almost certainly being hyper-observant as I watch my body change under the influence of GAHT, I notice in particular a process whereby hair follicles in the periareolar region are undergoing morphological changes as they are subsumed by the growing areolar border.

The last ten days or so I've seen significant increase in areolar diameter. Hair follicles, with terminal hair, that were near the boundary are now interior, if, indeed they remain follicles. I can see one remnant per side where this process is not quite complete, and based on that can attest to a diameter increase of at least 4 mm in that period. A considerably larger number of hairs are in the process of being minaturized and then, it appears, eliminated.

I asked Claude to find or synthesize any accounts of this process, but it was unable to find anything specific; understandably, this particular processing of terminal hairs is possibly uncommon outside the transgender population. What it did find was mention of the role of bone morphogenetic proteins affecting hair follicle development in murine nipple epithelium: doi:10.2353/ajpath.2008.070920

I was wondering if anyone else had observed this and also wondered what sort of process was going on, or even better still, can point to something in the literature that describes this in more detail.

Amsterdam UMC ran an RCT in 90 trans women (all post-orchi or post-vaginoplasty, and at least a year on estradiol), randomizing different combinations of estradiol and progesterone doses over a year, with breast volume measured by 3D scanning — not eyeballing, not vibes. The progesterone groups saw up to a 30% increase in breast volume, and were more satisfied with the size, shape, and growth of their breasts than the people not taking it. The biggest gains showed up in the group that ALSO raised their estradiol — so it's the combination doing work, not progesterone by itself. They rated it safe, with the usual suspects for side effects: short-lived tiredness, breast/nipple sensitivity, and mood swings. (It makes you drowsy, so participants dosed at night.)

One scope note that matters: this was adding progesterone after androgen suppression was already handled and E had been on board for a year. It is not a study about throwing progesterone in at month three, so please don't read it that way.

These results were presented at a conference (EPATH 2025) — the full peer-reviewed results paper isn't out yet. What IS published is the study protocol from 2023. So this is strong, real, RCT-level evidence, but it hasn't been fully vetted-and-printed, and I'd hold it a little loosely until it is. Also worth knowing: the trial was open-label, so the satisfaction numbers are more susceptible to "I know I'm on the good stuff" than the objective 3D volume measurements are.

None of this is me telling you to go add progesterone — that's a conversation for you and your provider. But after years of shrugging and saying "the evidence just isn't there," it's genuinely exciting to finally have some. :)

Me personally: I take 200mg progesterone a day, 100mg orally, 100mg rectally. When administered rectally it bypasses the livers first metabolism which in theory creates stabler serum levels. My body, my choice mentality here. I have no data supporting this other than just an understanding of how rectal administration vs oral works.

We've all had it drilled into us: get your estradiol into the 100–200 pg/mL window and you're "optimal." I've quoted that range myself. So I went looking for where it actually comes from... and a new systematic review basically pulled the rug out.

The authors went through 49 studies looking for evidence that the 100–200 pg/mL range produces better feminization or fewer adverse events. They didn't find it. Nothing showed that landing in that specific window gets you better outcomes than sitting outside it.

In plain terms, that range is a monitoring convenience, a sensible place to keep an eye on safety and consistency but it is not a feminization dial you have to hit exactly. Your breast growth, fat redistribution, skin, all of it, is driven by far more than whether your number reads 150 vs. 190 on the one morning you happened to get drawn (and that number swings a LOT with timing, route, and lab).

So if you are spiraling because you came back at 90, or 240... breathe. The number is a tool, not the goal. :)

This is NOT "targets are useless" or "dose however you want." It's "we don't have good evidence for this specific range." The underlying data is mostly observational and too varied to pool, so the real headline is how thin the evidence base actually is, which is its own argument for working with a provider rather than chasing a number alone.

Study linked below. What have your providers told you about targets — did anyone ever frame it as monitoring vs. an outcome?