It’s been a bit over a year since I last shared my transition progress on here so I thought I want to update you all.

Here is my last post: https://phtn.app/post/lemmy.dbzer0.com/7781431

Forgot to add:

  • first pic is 0 laser sessions
  • second pic is 6 laser sessions
  • third pic is 9 laser sessions
  • dandelionEnglish
    5·
    2 days ago

    Yes, there are many factors and reasons for that.

    Certainly dose and route of administration do determine things like E2 blood levels and does impact T, but if you are taking oral, for example, your blood E2 levels are fluctuating throughout the day much more than with, for example, injections. Your blood labs are a single snapshot, not representative of your blood levels all the rest of the time. I always try to get my blood labs done at trough, just before my next injection, when my levels are likely to be the lowest.

    Even what ester you use matters, e.g. injecting estradiol valerate (which has a shorter half-life) causes your blood levels to fluctuate (higher and then lower) than an ester like estradiol enanthate, which is slower and more gradual.

    All of this can influence the feminizing effects, and of course genetics, diet, hydration, exercise, age, and so many other things can play a role as well.

    Most of the estrogen taken orally is absorbed by the liver, so it’s an inefficient method of raising blood estrogen levels, and anecdotally I notice a slower / reduced feminizing effect from trans women I know taking oral routes rather than injections.

    Whether you’ve had surgery also plays a role, again anecdotes, but I’ve read reports that feminizing effects were slower before gonad removal and increased after surgery.

    Anyway - when I see progress pics I want to know what dose, route of administration, and other relevant notes to contextualize the progress.

    I know trans women IRL who have been on oral estrogen for over a year and seen very little effect despite “good” blood labs (she didn’t have the numbers so I don’t know what she thought “good” was, and she was just repeating what her doctors told her).

    I know another trans woman IRL who has been on oral estrogen for months and still has male levels of testosterone and very mild feminization.

    I also have a trans woman friend and colleague who has been on oral estrogen for nearly a year and she likes her results, but I’ve been on estrogen about the same amount of time with injections and I would subjectively say she hasn’t feminized as much in the same amount of time.

    Still, ultimately it’s about what your goals and desires are, my friend has no motivation to change her setup and is happy with her changes. That’s ultimately what’s important.

      • dandelionEnglish
        2·
        18 hours ago

        Nice, I don’t know doses well for patches but I’ve heard it’s not a bad method. The main problems I hear are that they can come off and be expensive to replace, they can cause rashes and irritated skin, and sometimes there can be poor absorption / lower-than-ideal blood levels from patches (better than oral, though!).

        I never considered patches because my skin is very sensitive and I am often rough on my body and I think I would lose patches due to daily activities (exercising, soaking in hot baths, brushing up against things when doing manual labor, etc.).

        Cypro sounds better than spiro, but reading about it I don’t like the idea of taking a synthetic progestogen, since it causes increased risk of blood clots and breast cancer:

        https://transfemscience.org/articles/transfem-intro/#cyproterone-acetate

        As CPA is a progestogen, it is associated with increased risks of breast cancer (Fournier, Berrino, & Clavel-Chapelon, 2008; CGHFBC, 2019; de Blok et al., 2019; Aly, 2020; Wiki) and blood clots (Seaman et al., 2007; Connors & Middeldorp, 2019; Aly, 2020; Wiki) even at very low doses (e.g., 2 mg/day). Higher doses of CPA, likewise presumed to be due to its progestogenic activity, are additionally associated with elevated prolactin levels (Sofer et al., 2020; Wilson et al., 2020; Wiki) as well as with certain generally non-cancerous brain tumors including prolactinomas (McFarlane, Zajac, & Cheung, 2018; Nota et al., 2018; Wiki) and meningiomas (McFarlane, Zajac, & Cheung, 2018; Nota et al., 2018; Millward et al., 2021; Weill et al., 2021; Aly, 2020; Wiki). These risks appear to be dose-dependent, and thus are likely to be minimized with lower doses of CPA. Besides risks related to its progestogenic activity, CPA at high doses has shown weak but significant androgenic effects in the liver and has been associated with an unfavorable influence on lipid profile, for instance decreased HDL (“good”) cholesterol levels (Coleman et al., 2022; Wiki). Long-term, this could result in an increase in the risk of coronary heart disease. Other potential adverse effects of CPA at high doses with unclear mechanisms may include increased blood pressure and heightened insulin resistance (Martinez-Martin et al., 2022). Additionally, CPA has been associated with abnormal liver function tests and rare cases of liver toxicity, including at doses used in transfeminine people of 25 to 50 mg/day (Heinemann et al., 1997; Bessone et al., 2016; Kumar et al., 2021; Wiki; Table). The likelihood of abnormal liver function tests with CPA, and probably of liver toxicity, appears to be much lower at doses of less than 20 mg/day (Wiki). More than 100 cases of clinically significant liver toxicity have been reported with CPA, but only two cases have been reported with CPA at doses of 50 mg/day or less (Wiki; Table). Monitoring of prolactin levels to detect prolactinomas, and monitoring of liver function to detect liver toxicity, may both be advisable in people taking CPA. Regular magnetic resonance imaging (MRI) scans have also been recommended to monitor for meningiomas in people taking CPA (at ≥10 mg/day) (Aly, 2020).

        I wouldn’t be too worried about it, but I’m just glad I can avoid that risk entirely with estrogen monotherapy (and in the long term with surgery).

        • Tywèle [she|her]@lemmy.dbzer0.comOP
          2·
          17 hours ago

          For me patches work really good. I apply them to my butt and put a tegaderm patch over it to make it more resistant to water and movement, I don’t ever have to worry about it coming off. Cost is also not really a problem since most of the cost is covered by insurance anyway. My last blood levels were 123 pg/ml for E and 39 ng/dl for T (these are my levels with my starting dose (75μg/24hours estradiol (with 2 patches per week) and 10mg cypro), since then I could decrease my cypro intake by a little bit). Regarding the anti androgen I don’t really have a choice since that is whats used here in Germany and also my endo only prescribes dermal application estradiol, so spray, gel or patches and she doesn’t do monotherapy as far as I know. But since I’m planning on doing bottom surgery in the near future anyway I don’t worry about that too much.

          Edit: And injections are unfortunately almost impossible to get here.

    • 🦄🦄🦄@feddit.org
      5·
      2 days ago

      Thank you so much for the write-up!

      I am on injections myself. Wish I could get EE but currently stuck with EV, since that is the only available form here.

      • dandelionEnglish
        1·
        18 hours ago

        I’m on EV as well because it’s the main ester that doctors can prescribe here. I was able to get a Rx for estradiol cypionate, but the concentration was so low that I had to fill my syringe and inject three times to get a single dose and that just wasn’t worth it. Maybe post-orchi when I’m no longer on high-dose monotherapy I could revisit that.

        EEn is more common for DIY, and if you’re in the U.S. for the next 4 years, it’s probably worth figuring out how to source that (probably better sooner vs later, having a stockpile is a good idea).