T Nation

Finasteride while on TRT Questions


Currently I do 120mg testosterone weekly (divided into two 60mg doses) and 1mg arimidex weekly (divided into two 0.5mg doses).

However, apparently I am one of the few who get bad dark scarring acne while on TRT. I recently asked my doc about this and he prescribed finasteride (propecia) at 1.25mg/day, saying that it’s likely due to a high DHT conversion rate. For what its worth, for the first 8 months on TRT I had no such problem even though my dose of testosterone was higher.

My concern is about all the conflicting information I’ve read about propecia, primarily about ED and general poor libido. I’ve even read that it can be permanent after stopping propecia. What is the consensus about that here? Is it something I wouldn’t have to worry about since I’m on TRT? If not, what about the permanent effects I read about?

My current numbers as of this week:

Total testosterone: 1282ng/dl (250-1100)

Free testosterone: 234.7 pg/ml (35-155)

PSA total: 0.75ng/ml (0.3-3.8)

Hemoglobin: 17g/dl (13.7-17.5)

Hematocrit: 48.7% (40.1-51)

Estradiol: 21pg/ml (<61)

Vitamin D: 72ng/ml (>30)

Thank you!


I can only speak for myself but I tried finastiride for about 2 weeks last month. I am also on 120mg Testosterone and 1mg Anastrazole (both taken twice a week).

Anyway I took it for the usual reason, hair loss. I read about the sexual and mental side effects and post finastiride syndrome stuff and although it scared me I thought it was worth the risk and didn’t truly buy into the hype especially regarding post finastiride syndrome. Well after about a week I was starting to. My erections became really weak and my libido tanked. I also lost a bit of feeling in my penis, so sexual activities didn’t feel as good. I stopped taking it hoping the damage wasn’t permanent, it took another 2 weeks for things to go back to mostly normal (I still feel like I’m back to 90% not 100% of where I was sexually before taking it). This was all on just 1mg finastiride a day for 2 weeks. I never felt any mental sides but felt all the sexual ones. Now I just take Minoxidil daily instead. It’s not as good but for me losing my dick for some hair isn’t worth it.

Anyway if you are thinking of using it for acne I would suggest using a drug made for those issues instead of using a terrible one (IMO) like finastiride for off label use that it wasn’t really meant for to begin with. Accutane may be a bit overkill and has it’s own array of sides but I would still pick something like that over finastiride. There are weaker acne drugs too.


Very interesting, and very confirming of my worst fears. Accutane is a topical thing right? The problem is, The acne comes in all sorts of places. I cannot predict where. So my solution has to be systemic.

I’ve since lowered my testosterone dosage to 100mg/week like most people here, and the problem has not relented.

My doctor also let me have a prescription for nolvadex to mess with because of libido issues. Now if I take nolvadex, should I reduce my arimidex dose?


I’m no expert on hormones or skin issues, a beginner so can’t really advice you but it does seem weird to use Finastiride (a hair loss drug when used by men) for acne and a SERM like Nolvadex for sexual issues. What exactly is his reasoning here? High E2 can cause sexual problems (as can low E2) but for that you would increase your AI dosage not introduce a SERM. A SERM you would use if you were coming off testosterone and wanted to kickstart your own natural testosterone production again…or if you were developing gynecomastia since it blocks estrogen at the breast tissue.

Someone experienced can chime in but this doesn’t make any sense to me at all lol



Yeah, the nolvadex is a separate issue than the acne. I told the doc that I wanted to protect my testes from atrophy, and clomid doesn’t agree with me, and I cannot afford HCG at the moment. So he let me try nolvadex. However, since I know that nolvadex also blocks estrogen, I was wondering if I need to adjust my AI while on it.

Currently, in my last two labs, my E2 has been 21. So I don’t suspect E2 to be responsible for the acne or libido issues. But my doc did say that arimidex can cause libido issues on it’s own in other ways. So there’s a possibility of the libido issue coming from that.


Accutane is not a topical treatment. It is highly regulated and mostly prescribed by dermatologists. There is a battery of lab tests required, along with a requirement that you pledge not to become pregnant if a female, and not to impregnate if you are a male. Contraception (condoms for the guys) are absolutely essential while on therapy and for a period afterwards.

Accutane can cause severe birth defects, but can very effectively treat cystic acne. There is a push going on to move to accutane treatment earlier in cystic acne cases to prevent prolonged exoisure to antibiotics.


Holy crap, what’s in it? I thought accutane was just high dose vitamin A or something…

I have another thought…I know that 22 is the target E2 number in general, but would it be better to keep E2 within a certain ratio of your FT? For example, I know that my FT is higher than the average TRT user, so would it be better for me to have a higher E2 number? Maybe the drastic difference in ratio is causing my acne?

All I would have to do is back off of my AI a bit…


Why didn’t you test your DHT levels. How long after injecting was this test taken? Your T levels are very high, thought about lowering dose?


Doc is throwing BS. The objective with an AI is a favorable E2 level and Doc refers to taking E2 too low.

SERMs block effects of estrogens in Selected tissues, not all. If you use a SERM and E2 gets elevated, your liver will see the increased E2 and increase SHBG which will lower FT. The “S” in Serm is Selective. Other effects in brain probably too. And E2 tends to interfere with FT at T receptors, and SERM is not going to eliminate that.



The last set of numbers is only slightly over the norm, and I still felt really good there. Meaning I wasn’t all achy after training (bjj). That was at 120mg/week. Since then I’ve been at 100mg a week so my current numbers are surely lower, but I have returned to being achy all the time and I’ve lost some lean mass.

Why I didn’t test for DHT? Great question! And if this isn’t sorted out before my next set of labs roll around, I will add it to the form myself.


HCG also raises E2 in the same manner correct? As I understand it, both HCG and nolvadex raise LH and FSH?

Because if I stay at 100mg test a week and 1mg arimidex, that puts me pretty much where most everyone here currently sits…however, I don’t do HCG, so there is that difference to the mix. Meaning my overall testosterone numbers would be lower as would my E2 given the same amount of arimidex…


I took Finestride for 10 years. I developed gyno on it and I’m pretty sure it caused my low T issues. I now supplement with progesterone from the doc to combat high DHT.


[quote=“gtron, post:10, topic:225514”]
HCG also raises E2 in the same manner correct? As I understand it, both HCG and nolvadex raise LH and FSH?

If hCG increases T and FT, FT–>E2 increases just at a larger amount of injected T would.
If LH receptor stimulation is too high from high doses of hCG or SERM, then very high intratesticular testosterone can create a lot of FT–>E2 inside the testes and anastrozole cannot manage FT–>E2 there.

SERM’s [Nolvadex, Clomid and others] block estrogens at estrogen receptors, in selected tissues, including the hypothalamus. The hypothalamus is then partially blinded to the negative feedback signal of serum E2 and then stimulates the pituitary to release more LH+FSH.

hCG directly stimulates the testes, increasing T and more FT–>E2 occurs that increases the negative feedback signal on the hypothalamus and that reduces LH+FSH and in some situations would shut down LH+FSH completely. That could be from hCG dose being too high creating a lot of FT–>E2 inside the testes or hCG monotherapy in a younger guy with healthy testes where normal feedback actions would shutdown LH+FSH.

You should have a clear understanding of these SERM and hCG issues and should not have this confusion.


  • All T in the testes is FT/Bio-T because there is no SHBG there. Same for T in saliva for saliva blood testing. SHBG is in the blood stream. Intratesticular testosterone levels can be up near 100X higher than serum T levels and it is all available to feed FT–>E2 inside the testes.

  • There are aways odd variations in how things work and we do not know why some guys are exceptionally sensitive to hCG and have adverse amounts of FT–>E2. This may involve differences in aromatase structure [enzyme or amounts in the testes, possibly they do not metabolize hCG the same and serum levels are increased.

  • Same for anastrozole over-responders. In these situations there are differences in genetics or gene expression that alter anastrozole metabolic rates [enzymes], aromatase enzyme structure, LH receptors, LH gene expression etc. Several possibilities.

  • And some altered gene expression might be epigenetic change which is also known to span generations in some cases [records of starvation in Holland and health records showing problems affecting multiple generations].

  • Then we see hair loss drugs, 5-alpha reductase inhibitors reducing DHT that can in a few individuals, several in this forum, creating permanent damage to their HPTA’s, resistant to HPTA restart attempts. Also one guy damaged by a deca only cycle that his friend got him onto. These are epigenetic changes.

  • We need to understand the basics but also need to be watching out for situations where the game is subject to a different and unknown set of rules.



So progesterone combats high DHT? I had never heard of that. Do you think you’d have had any problems with finasteride if you had been on TRT and taking an AI at the time?


Understood…HCG acts as LH and FSH itself, and nolva tells the pituitary to increase LH and FSH…the other difference being that nolva also selectively blocks estrogen. The reason I asked for the nolva was to stimulate the testes (since I can’t afford HCG at the moment). The fact that it also blocks estrogen is an extra that I did not necessarily want. It’s an unwanted added consideration.

Here’s the thing guys and maybe there’s a clear answer to this…since I lowered my dosage (after the above labs), and in all likelihood my levels are sitting right at upper normal range right now, I have gotten very weak and sore. I have certain objective indicators I can measure myself with, and at the moment I’m significantly weaker than before I even started TRT…even though my testosterone levels are higher than when not on TRT. The question is, is this some kind of adjustment period where my strength will come back at this lowered dose?

I ask because at this lowered dose, the acne seems to be easing up. So if all else fails, this may be the answer…


You could get a blood test to see DHT levels. I didn’t do this before starting fin, the doc just gave it to me, but it seems that should be the first step to me in hindsight.

I looked at some charts/research about dose-response and was kinda crazy. Despite the half life it seemed to have effects on serum DHT 4 days later from a single dose, and testing various doses - at something like .1mg it still had 70% or so effect as a full dose. After seeing all that, I’ve changed to doing .5mg fin EOD. Which based on what I read would still be more than enough, but seems to be an easy to follow split.


No, hCG acts like LH and have very small FSH properties.


I’m going to call my doc and see if he can order me a solo DHT test for now so I don’t have to wait months for my regularly scheduled labs. In the meantime I’m gonna leave the nolva and finasteride alone. I’m reading too many horror stories regarding finasteride.

Also, just in case DHT is not the culprit and if it’s something to do with E2 instead, I have a question…

My last 2 labs showed my E2 at 21, yet libido and acne are still a problem yet prostate is not. I’m wondering what you guys thing about keeping your E2 range more in line within a perfered ratio to FT, as opposed to a static number like 22.

The reason I ask is, I was reading some stuff by Nelson Vergel, and he thinks people obsess too much on keeping a low E2 sweet spot. He mentioned something about only worrying about it if you start to get symptoms of high E2, but that E2 has many benefits so long as it’s kept under the negative symptom range.

That got me to thinking that possibly there is an advantage to having a higher E2 number if you have a high FT number…in other words there may be an optimum ratio as opposed to number. Thoughts?


If you have a therapeutic target of high range T, then a static E2 reference makes perfect sense.

“Nelson Vergel”: E2=22pg/ml seems to be optimal for energy, mood, initiative, fat loss/patterns and libido. You are free to find a number that works best for you. Vergel seems to be looking at this all wrong when he suggests to see if you have symptoms. Most guys would not know that aspects of their not feeling great would be E2 related. Often it would be a wife/GF asking why ‘he’ has become a moody bitch.


Interesting @KSman …in general, how small is the E2 window when finding your personal sweet spot? Let’s say someone feels great at 24…would I already start feeling less than optimal by 28?

As you know, my doc likes to have me on the higher T numbers side. My current lower doses are against his recommendation (100mg vs 150mg/week). At 100mg a week the acne seems to have mellowed (coincidence or causal I don’t know). However, I’ve softened out and am in very sharp pain after routine training…which was what I was hoping to overcome with TRT in the first place (and did with doses between 120 to 150mg).

So I’m kind of stuck. It’s weird, because for the first 6 months or so I was at the full 150mg and had zero problems with acne.

Also, can you point me to the specific sticky that describes how to turn adex pills into drops with vodka?

Thank you sir.



Thanks for the info…if that’s true, then it would only take a very tiny dose of finasteride twice a week to accomplish our needs…possibly many of the horror stories with finasteride are because of dosing being too large and too often, causing a significant over-accumulation in the body.


1 1mg tablet in 1ml vodka, dispense by the drop. Count drops per ml to get a conversion factor.

I do well around 22pg/ml, years ago I felt the change 28pg/m l–> 22pg/ml.
Others may not be as sensitive to that change.