Gyno & testoterone level

Hey everyone,

I’ll get straight to the point. I’ve been undergoing treatment since February and have been using both finasteride and dutasteride (finasteride for 1.5 months, then switched to dutasteride, and last month I went back to finasteride).

During the early stages of using finasteride and dutasteride, I didn’t experience any gyno, and I remember feeling pretty energetic and enthusiastic… basically, it seemed like my testosterone levels were normal.

But when I switched back to finasteride last month, I suddenly developed gyno. Last month, I was going out late a lot and felt really tired, fatigued, and unmotivated. At first, I thought it was due to my diet and lifestyle changes, but after thinking it over, I’m pretty sure my testosterone levels dropped last month.

So, what I want to ask or discuss is that, based on my gut feeling (I can’t back up my claim with journal articles or anything), I believe that the gyno appearing during treatment with either finasteride or dutasteride is due to a lack of testosterone or at least had some connection with testoterone… The more sluggish and unenergetic I feel, the more sensitive the breast lump feels.

What do you all think?



TLDR: get yourself tested for Testosterone and Estradiol levels. It’s probably not that expensive. Breast bud development is permanent, so if this bothers you, you should probably stop.

HUGE DISCLAIMER: I am not a doctor. My speculations and my advice should not be considered actual medical advice. Take everything I say with a grain of salt.

Trans woman here from a STEM background, and I have read some literature on HRT, so I know a bit about breast growth and hormones. I’ll first talk about breast growth and hormones, then I’ll talk about what could be happening to you, and what you can do.

Breasts and Hormones

In general, breast growth can be attributed to both a lack of testosterone (I’ll call this T from now on) and the presence of estradiol (I’ll call this E from now on) beyond a certain threshold. Both factors are semi-independent.

Why independent?

You can have both too much T and too much E, too few of both, too much of one and too few of the other, etc…

Why semi independent?

Your body has some built-in control mechanisms to balance your hormones.

  • It can (and probably will) convert T to E if you have too much T.
  • If you have too much E, your body will produce something called SHBG, which will bind to both E and T, reducing their impact on your body.
  • Probably a bunch of other checks and balances.

How do both hormones relate to breast growth?

  • In very simplified terms, the default state of the human body is “female”. T suppresses breast growth, and if you have too few, you can start developing breasts. We know this happens because castrati and eunuchs of bygone eras are recorded to have experienced some breast growth after the removal of testicles, despite not taking any E.
  • E encourages some breast growth (but YMMV) so an excess of E even if you have enough T, will also cause you start developing breasts. We know this happens because some steroid users develop breasts despite having an excess in T (and some of that T is converted to E)
  • Again, in very simplified terms, there is a delicate balance of high-enough T, and low-enough E, where you do not develop breasts. Any other combination (Both high, both low, high E low T) will cause some breast development.

What could be happening to you

Each person’s body is different. The fact that many of us in this forum have hair follicles that are sensitive to DHT, while the rest of the population does not, is a testament to this. Likewise, there are a number of known reactions to the reduction of DHT.

Generally speaking, our body is used to a certain balance of things. Outside that balance, it will try to bring itself back into balance. For example, your body expects some concentration of blood sugar. If there’s too much, the pancreas will produce more insulin to either store or use the glucose, and consequently your blood sugar will decline. If there’s too little, there’s a different mechanism involving a molecule called glucagon.

Likewise, your body expects some amount of DHT. For many people, if your DHT drops below an expected range, your body will try to produce more T (because the 5ar enzyme converts T to DHT) Over time, your body will get used to the new level of DHT, and bring T back down, but when this happens, and to what degree, varies from person to person.

Case A

  1. You’re taking 5ar inhibitors, DHT goes down
  2. Body is like, “whoa, where did the DHT go?”, and makes more T.
  3. Your T levels rise, but not to the point that your body converts some to E. You have more energy, and have pretty good mood.
  4. Your body does not stop elevated T production, and T goes into excess, triggering the aromatase pathway. You now have too much T and E. Gynecomastia, and mood imbalance happens.

Case B

(1-3 copied from Case A)
4. Your body realizes that the decreased DHT is the new normal and your body decides to wind down T production.
5. Your body winds down too much for some reason, and now you have a lack of both T and E. Gynecomastia, and mood imbalance happens.

Case C

(1-4 copied from Case B)
5. Your body winds down T production back to normal, but it just so happens that your body has some mutation wherein the DHT in your body was doing more of the heavy lifting for both mood and the suppression of breast development. Now that you don’t have enough DHT, you’re experiencing these symptoms, despite having normal T and E.

This is all speculation. I could be right on the money, off by a bit, or completely off. But the point I’m trying to make, I guess, is that you are probably right that it’s hormonal.

What you can do about this

The ideal would have been, as would be the case for anyone taking HRT to transition, is to take baseline hormone readings before taking medication. At the very least, T and E. (DHT too, if you can afford it) But chances are you haven’t taken any hormone baseline.

It’s still useful to take hormone readings now because while we will likely never know the exact change in your hormone levels, we are aware of general normal ranges for the population in general, and can thus see if your levels are out of expected ranges.

In my country, testing T and E together costs about 50-60 USD. It’s not cheap, but it’s not terribly expensive. I don’t know how it is in your country. If you can afford it, it can help you know for sure if there’s something off about your hormones. This test can also help you identify your next steps.

For example, if you have an excess of both T and E, then it’s possible that you simply need to wait until your body gets used to your new DHT levels, and then maybe your T goes down on its own back to normal, and likewise for your E.

If it turns out your T and E are too low, then you’d have to take a different path.

As I said in the TLDR, breast bud development is permanent, so if this bothers you, you should probably stop taking fin/dut. If you’re okay with a bit of puffiness, then proceed at your own risk.


I also had gynecomastia induced by finasteride and then dutasteride.

Basically, by blocking 5AR, more testosterone is “left over” and, consequently, this will be aromatized to estradiol (E2). E2 levels don’t usually skyrocket, but now there’s another issue: your DHT levels are too low.

DHT is a hormone that acts to counteract estrogen. In breast tissue, it is as if the two have opposing functions. Without DHT, estrogen becomes stronger and tissues more sensitive to it.

Mood changes and tiredness are also symptoms of high E2.

I don’t believe the problem is about your testosterone directly. As I said, these medications INCREASE, not decrease, your testosterone. The rule this increase on datas is between 10-25%, but some (like me) increase by 50-100% or even more, which generates a very high e2 response as well.


  1. Use of Tamoxifen or Raloxifene. These medications are SERMs and bind to the breast tissue selectively, preventing stimulation, reducing the size of the breast tissue and even completely reversing gynecomastia in some cases. Cons: May have significant side effects for some people (such as depressive symptoms, loss of libido, and erectile dysfunction). If you can stand them for 3-6 months, they are your best bet.

  2. Low dose of Anastrozole. Anastrozole inhibits aromatase, the enzyme that converts T into E2. Similar to what Finasteride and Dutasteride do with 5AR (which converts T into DHT). With a low dose of Anastrozole you will be able to adjust your E2 levels until your body readapts (which can take months or years, something extremely individual). You will need to know your T and Estradiol (E2) levels before you begin, as you will not want to drop your estradiol. Start with a low dose and monitor your E2 levels. Levels between 20-25pg/ml are healthy. Below 20 can bring bad symptoms; above 25-30 can cause the symptoms you are experiencing.

In my experience, I tried Tamoxifen and Raloxifene, but I had really bad side effects with them (ED, low libido, depressive mood, etc) and I just stopped.

So now I use a low dose of Anastrozole (0.25mg or 1/4 of a tablet every 5 days) and monitor my E2 tests periodically to make sure the Anastrozole is not lowering it too much (as I said, 20-25pg/ml is the point ideal for most of us, but you need to find yours).

I’m not a doctor, but this is what worked for me.

Long-term use of low dose Anastrozole should not be concerning for your health if you keep your E2 at healthy levels.

Tamoxifen and Raloxifene can have serious health side effects in the long term, as they increase the risk of deep vein thrombosis in more isolated cases, so do not use them for more than 3-6 months (during this time they are usually well tolerated and prescribed for gynecomastia, with sexual side effects only, if present) and, preferably, under medical supervision.

Talk to your doctor about these alternatives, get tested and, most importantly, educate yourself about this process.