How long does Feminization actually take? Are you stunted?

When reading about how long fat changes take once HRT (Hormone Replacement Therapy) begins (Estradiol, or E2), you’ll find the scale of months or years; both anecdotally and on Wikipedia:

1. Transgender hormone therapy (male-to-female)

https://en.wikipedia.org/wiki/Transgender_hormone_therapy_(male-to-female)

Effect	Time to expected onset of effect[a]	Time to expected maximum effect[a][b]	Permanency if hormone therapy is stopped
Breast development and nipple/areolar enlargement	2–6 months	1–3 years	Permanent
Thinning/slowed growth of facial/body hair	4–12 months	>3 years[c]	Reversible
Cessation/reversal of male-pattern scalp hair loss	1–3 months	1–2 years[d]	Reversible
Softening of skin/decreased oiliness and acne	3–6 months	Unknown	Reversible
Redistribution of body fat in a feminine pattern	3–6 months	2–5 years	Reversible
Decreased muscle mass/strength	3–6 months	1–2 years[e]	Reversible
Widening and rounding of the pelvis[f]	Unspecified	Unspecified	Permanent
Changes in mood, emotionality, and behavior	Unspecified	Unspecified	Reversible
Decreased sex drive	1–3 months	3–6 months	Reversible
Decreased spontaneous/morning erections	1–3 months	3–6 months	Reversible
Erectile dysfunction and decreased ejaculate volume	1–3 months	Variable	Reversible
Decreased sperm production/fertility	Unknown	>3 years	Reversible or permanent[g]
Decreased testicle size	3–6 months	2–3 years	Unknown
Decreased penis size	None[h]	Not applicable	Not applicable
Decreased prostate gland size	Unspecified	Unspecified	Unspecified
Voice changes	None[i]	Not applicable	Not applicable

Anecdotal

So when I started Estradiol at age 37, I didn’t have much expectation of changes… but within 3 weeks I had noticeable fat distribution changes. “But that takes years!” I thought… I went from a 36″ waist x 40″ hip to 35″ waist x 44″ hip.

I started on 2mg Estradiol Oral Sublingual to 3mg after a month, then to 7mg Estradiol Valerate IM (Intramuscular Injection) every 5 days. When my labs came in (measured at peak absorption curve), my doctor said my Estradiol was too high and I wanted a smoother absorption curve, so I switched to Estradiol Patches. I was given a single 0.1mg patch, changed 2x per week. I was miserable on this dose and within a couple of weeks my waist was back up to 36″ and my hips were slightly under 44″. This was while I was actively LOSING weight, yet my waist actually went UP.

I switched doctors and doubled up my patches so I used 2x 0.1mg patches concurrently. Immediately I felt much better and within 1 week my waist went down to 35″ and my hips up to 45″. ONE WEEK.

Also interestingly, during my one month of hell of being under dosed, I went a little stir crazy as my body was losing feminine qualities, realizing I was actually recognizing body dysphoria (or maybe gender dysphoria?) for the first time. I asked my doctor for Finasteride and he prescribed 5mg as a starting point… which I thought was really high. Regardless I started at 5mg and looked out for side effects. Interestingly my breast development restarted and for the first time my face started to plump up with fat. No matter what my serum Testosterone and Estradiol indicated in level, fat did NOT move to my face. Yet when my Testosterone was going up and my Estradiol going down, after adding Finasteride my face started to plump, and my breasts started to grow again. Cool… but no fat moved at around my waist or hips.

To me this indicates that DHT (Dihydrotestosterone; what Finasteride/Dutasteride block really well), seems to affect a different fat distribution in signaling than Estradiol alone does. Note: I had to stop Finasteride due to side effects and within a few days my facial fat gains were again lost.

My Estradiol on a single 0.1mg patch was only 81 pg/mL at peak, Testosterone was 18 ng/dL at peak (morning), and my DHT was 3.3 ng/dL; yet I lost my feminine fat distribution quickly. Finasteride did not help with hips/waist at all, and Estradiol did not help with face/breasts particularly. Isn’t the only metric we care about the Estradiol/Testosterone balance? Certainly it’s all my doctor cared about at the time.

2. Breast Development

In contrast to the female-associated sex hormones, estrogen and progesterone, the male-associated sex hormones, the androgens, such as testosterone and dihydrotestosterone (DHT), powerfully suppress the action of estrogen in the breasts.

https://en.wikipedia.org/wiki/Breast_development

3. Dihydrotestosterone

Circulating levels of DHT are 1/10th and 1/20th those of testosterone in terms of total and free concentrations, respectively,[6] whereas local DHT levels may be up to 10 times those of testosterone in tissues with high 5α-reductase expression such as the prostate gland.

DHT is a potent agonist of the AR, and is in fact the most potent known endogenous ligand of the receptor. It has an affinity (Kd) of 0.25 to 0.5 nM for the human AR, which is about 2- to 3-fold higher than that of testosterone (Kd = 0.4 to 1.0 nM)[46] and 15–30 times higher than that of adrenal androgens.[47] In addition, the dissociation rate of DHT from the AR is 5-fold slower than that of testosterone.[48] The EC50 of DHT for activation of the AR is 0.13 nM, which is about 5-fold stronger than that of testosterone (EC50 = 0.66 nM).[49] In bioassays, DHT has been found to be 2.5- to 10-fold more potent than testosterone.[46]

https://en.wikipedia.org/wiki/Dihydrotestosterone

If you follow Dr. William Powers; he often speaks about “DHT Mutants” which are transgender patients who instead of having 10-20% DHT levels relative to Testosterone, have more like 200%+ DHT compared to Testosterone. Since DHT is also localized[4] in production, serum levels in blood aren’t necessarily the full picture; though may inform antiandrogen therapy focus.

4. Testosterone and DHEA activate the glucose metabolism-related signaling pathway in skeletal muscle

These findings suggest that skeletal muscle is capable of synthesizing DHT from testosterone, and that DHT activates the glucose metabolism-related signaling pathway in skeletal muscle cells.

https://pubmed.ncbi.nlm.nih.gov/18349113/

One observation I’ve had since starting Estradiol therapy is that regardless of my serum Testosterone level and serum Estradiol level, my muscle gains and performance are still very high. Finasteride/Dutasteride are designed for anti-cancer effects in the prostate by reducing DHT conversion in the prostate and shrinking the prostate tissues. Some other antiandrogens such as Bicalutamide, only prevent 60% of this DHT conversion; though also blockage the androgen receptors in high clinical quantities.

5. Bicalutamide

The affinity of bicalutamide for the AR is relatively low as it is approximately 30 to 100 times lower than that of DHT, which is 2.5- to 10-fold as potent as an AR agonist as testosterone in bioassays and is the main endogenous ligand of the receptor in the prostate gland.[160][151][2][161] However, typical clinical dosages of bicalutamide result in circulating levels of the drug that are thousands of times higher than those of testosterone and DHT, allowing it to powerfully prevent them from binding to and activating the receptor.[162][163][154][164][19][79][165][20][166] This is especially true in the case of surgical or medical castration, in which testosterone levels in the circulation are approximately 95% reduced and DHT levels in the prostate gland are about 50 to 60% reduced.[151][167]

https://en.wikipedia.org/wiki/Bicalutamide

I stopped Finasteride because it was stimulating to my brain – it had effects very similar to Adderall for me personally (someone with ADHD – Attention Deficit Hyperactivity Disorder); however, the DHT affinity made a huge difference. I switched to Bicalutamide 50mg and although it has helped somewhat, my facial fat distribution was much better with Finasteride (1mg – 5mg; titrated experimentally). Bicalutamide can take 30 days to fully stabilize in levels, and it has only been a little over 1 week at the time of this writing; so, it’s possible it will do more eventually.

Speculations

I often read posts on Reddit about feminization being stunted and the folks who post are often on no antiandrogens, Spironolactone or Cyproterone acetate (CPA); however, I haven’t seen these same people focus in on DHT antiandrogens specifically.

Since serum levels of DHT and Testosterone are not the full picture of DHT production, there isn’t necessarily an easy way to know if DHT blocking will further feminization.

Finasteride/Dutasteride also have some bad press due to the high possibility of causing mental depression and other side effects; however, this may be mitigated or controlled with titration or periodic usage; perhaps only to restart feminization by putting a dent in DHT activity. If nothing else it seems worth a shot in the dark if everything else has failed to induce good feminization.

6. Finasteride

Post-finasteride syndrome may also have reduced levels of neurosteroids such as allopregnanolone in their cerebrospinal fluid. One study found that 1.4% developed persistent sexual dysfunction.[13]

https://en.wikipedia.org/wiki/Finasteride

A word of caution, Finasteride may have long term or permanent side effects. Although Dutasteride doesn’t have the same long term effects formally documented; having a similar action indicates it may simply not be as well documented as Finasteride.

Speculations on Nuance

Between the selective efficacy of Finasteride/Dutasteride with high affinity for DHT and my selective fat distribution changes; I would conclude in my case greater feminization would occur through high DHT affinity antiandrogens vs. more general purpose antiandrogen therapy; coupled with Estradiol levels approaching 200 pg/mL.

I also wanted to mention Dr. William Powers as of late 2020/early 2021 has summarized his serum level goals like so:

7. Early leak of some V 7.0 powerpoint changes: The Magic E2 Number

I will no longer be recommending a “range” for estradiol. I have come to realize this is foolish, as there appears to be what I will now call “The magic number” for everyone. That magic Estradiol total value is the value at which SHBG remains under 115, LH and FSH are zero, and the patient has a free estradiol greater than 1% without boron. Optimized further, its the Estradiol value with those before things and whatever produces the greatest fraction of free E2.

After collecting about 200 labs with my new order set, I can now confidently say that the amount of SHBG produced at different levels varies wildly by humans. Almost never does an estradiol over 700pg/ml seem to benefit the patient. Above that threshold, SHBG goes crazy and the free estradiol level drops. Pushing E2 above that level almost NEVER seems to increase the % free, thereby I have to admit, the old adage from conservative docs of “If you use too much Estradiol it will slow down your transition” is probably true. No, it wont convert into testosterone, and no, thats definitely not happening at an E2 around 150pg/ml, but it does happen to most people over 700 (but not all).

In short, I will now be setting my goal estradiol level for each individual patient at the level at which they have the greatest fraction of E2 free pre-boron and simultaneously have an LH and FSH of zero with a SHBG goal of 115.

That number seems to range from 200pg/ml to 700pg/ml in 95% of my patients, and so I think that in doing so, I can use less estrogen to get more effect if I figure out exactly what that happy number is.

In addition, ALL MTF patients now get a DHT ordered along side their T. While most of my zeroed LH/FSH patients have a Total T of 10-20ng/dl and a DHT below the detectable limit, there appears to be a subset who when testicular T production tanks, the adrenal glands and their swift 5AR gets to work on producing DHT. I had a patient yesterday with a T of 10ng/dl and a DHT of 25ng/dl which literally makes no sense when in cis males the DHT should be 10%. Clearly this falls under the category of “trans people are weird” and have weird enzyme mutations. For these patients I’m using microdosing of 5AR drugs or Bicalutamide, whichever the patient prefers. I prefer bica, and for them I’m doing twice a week dosing due to its long half life.

https://www.reddit.com/r/DrWillPowers/comments/h8yn21/early_leak_of_some_v_70_powerpoint_changes_the/

I appreciate the pivot to SHBG focus instead of serum Estradiol/Testosterone/DHT range; however, in my own experience so far since starting HRT, serum levels are only a partial picture of feminization. Based upon my own levels jumping around dramatically and selective fat distribution since adding antiandrogens, it seems like serum levels are like steering the ship in a direction, but precisely tuning feminization is more unique to each individual.

For the people who experience extremely limited or selective feminization, coming at the problem from different angles regardless of serum levels may be more productive than screaming into the void “serum levels are fine, why am I not feminizing?!” Perhaps the issue is genetic regarding androgen receptor sensitivity, or certain levels of interplay between LH / FSH / DHEA / DHT / T / E2 / E1, or even more localized disparity in different tissues.

One thing I noted regarding LH / FSH, cis women are not at a level of zero, so I’m not sure why that should be a goal? When my Estradiol level was peaked at 650 pg/mL during a previous blood draw, my LH / FSH were indeed at zero, but that doesn’t seem to fit an average biological normal in humans. Dr. Powers has gotten a lot of criticism for “hyper feminization” being a goal with patients; but, let’s be honest – that is the goal for these patients.