TRT and Finasteride?

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SixHouse

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I inject 150mg per week Testosterone Cypionate. I'm about to start 1mg per day oral Finasteride for hair loss.

The internet says this is totally fine.
The internet says this is a terrible idea.
The internet says Finasteride is poison that will ruin your life.

What do we KNOW about this combination? Are there guys here on TRT and Finasteride who can comment?
 
Defy Medical TRT clinic doctor
I inject 150mg per week Testosterone Cypionate. I'm about to start 1mg per day oral Finasteride for hair loss.

The internet says this is totally fine.
The internet says this is a terrible idea.
The internet says Finasteride is poison that will ruin your life.

What do we KNOW about this combination? Are there guys here on TRT and Finasteride who can comment?
Finasteride completely fucked me up and lead me to HRT in ways I’m still dealing with. I took it without and later on HRT and I was fucked both times. It seemingly has nothing to do with DHT but all the other things 5AR regulates, like cortisol, and the damage done thereafter from it.
 

That's one common theme, but there are thousands of guys who have zero side effects and have been on Finasteride for many years. It's important to present both sides and not fall victim to confirmation bias.

I read a study that concluded that Finasteride should not "get in the way" of the beneficial effects of TRT. Can anyone confirm this?
 
Last edited:
There are people who claim to use it in small doses no more than twice a week. That seems to lower DHT and give some hair loss and prostate benefits without totally crushing your dht levels. However, it just may be anecdotal.
 
Finasteride completely fucked me up and lead me to HRT in ways I’m still dealing with. I took it without and later on HRT and I was fucked both times. It seemingly has nothing to do with DHT but all the other things 5AR regulates, like cortisol, and the damage done thereafter from it.
Can you elaborate? How old were you? What dosage were you using? How long were you using it? From what I read, the guys that get side effects are commonly already suffering from low testosterone and/or are on a higher dosage of Finasteride that the usual 1mg per day.
 
Can you elaborate? How old were you? What dosage were you using? How long were you using it? From what I read, the guys that get side effects are commonly already suffering from low testosterone and/or are on a higher dosage of Finasteride that the usual 1mg per day.
I was in my early 30s. I used a very small dose, something along the lines of .25mg every 3rd day or something. Been a while but it was ultra conservative. I looked at the charts online and saw what the minimum I’d need to take would be to still make a good dent in DHT. I was on it for about 4-6 months. I actually felt better at first, which I now know is from the cortisol bump it gave me. I stopped because I became suicidal and emotional and depressed and had rapid visceral weight gain and stopped retaining muscle glycogen and just fell apart. Pretty much any stress during that time would be amplified by 100x. I also lost the ability to sweat, which is one of the tell tale signs in my opinion that other things don’t overlap with. I quite literally mean my body stopped perspiring. I sat in a sauna at the height of it and nothing happened, though I felt bad. No BO. No sweat during sex, which thankfully I didn’t have an issue with. Not during workouts or running. Nothing. Upside was I didn’t have to wash my clothes much.

Based on my blood tests after taking it, it probably had nothing to do with testosterone, and honestly my testosterone even while having symptoms at the time was a little low (480) but really wasn’t all that low for someone doing too much and training too hard and stressed out from fin and hadn’t slept much in weeks from it all. I’d be a good candidate for having been naturally high T given that I was doing better than most people on roids when it came to results without having touched anything, but I never tested before, only after.

Having since experimented with many things and protocols across the full HRT spectrum that few people venture into, and the holistic realm, I can definitively say that at least in my case, cortisol being unregulated was the issue. I was already someone that was pushing things too hard, and finasteride pushed me over the edge, causing me thereafter to down regulate. If cortisol is out of whack, thyroid and all else up the chain goes to shit. I’ve had my test everywhere from 800 to 1500 and my free T all over the range and double it and it means jack shit if I can’t get it into the cells or have it work. When I do, it feels like I’m suddenly on HRT and I look like I transform into another human being.

From the initial finasteride issues people have, I think one of the main things that makes guys go down different paths with it is that if you’re in a fucked up state like that, you develop other issues that exacerbate it, and potentially get damaged in some ways. In my case, I developed massive gut issues, and some nerve damage in my right foot. That may be partly because while on it I had to eat massive amounts of salt to avoid passing out and going to the ER, which is what happened and the moment I decided to try HRT since I was not managing whatever happened to me on my own.

I’ve talked to and worked with many, many doctors in the field about this. If you’re already on TRT, most guys seem to be fine on finasteride, or report that they are. It will by definition affect your body’s ability to regulate itself in regards to stress, however. If you’re already okay on that front, it might mean nothing. If you’re not, or had some issues down the line, it could mean everything. It seemingly has nothing to do with DHT because it’s not like you couldn’t just inject a DHT analog, which doesn’t work for almost anyone having post finasteride syndrome. Test doesn’t help most guys, either, and if it does it’s not usually for very long.

I read all the shit online about fin too and talked to folks before I tried it and would laugh at the PropeciaHelp folks. I thought maybe they were just on it for 10 years and got mad that in 10 years they aged 10 years. The things they said were too wide ranging to seem real. At worst I figured I’d just get on HRT. I get it now though, and wish I didn’t have first hand knowledge of it. I’ve been there, and at times if I’m not careful I end up back where I was with it and ‘crash’. I have a deep and unending sympathy for them.

I would tread very lightly around finasteride. I really wish someone back then had written this to me before I tried it. It irrevocably upended my entire life. It is my biggest regret. It doesn’t do that to everybody. When it does though? You end up like those guys on PropeciaHelp. It’s a very real thing. I really wish it wasn’t.
 
I was in my early 30s. I used a very small dose, something along the lines of .25mg every 3rd day or something. Been a while but it was ultra conservative. I looked at the charts online and saw what the minimum I’d need to take would be to still make a good dent in DHT. I was on it for about 4-6 months. I actually felt better at first, which I now know is from the cortisol bump it gave me. I stopped because I became suicidal and emotional and depressed and had rapid visceral weight gain and stopped retaining muscle glycogen and just fell apart. Pretty much any stress during that time would be amplified by 100x. I also lost the ability to sweat, which is one of the tell tale signs in my opinion that other things don’t overlap with. I quite literally mean my body stopped perspiring. I sat in a sauna at the height of it and nothing happened, though I felt bad. No BO. No sweat during sex, which thankfully I didn’t have an issue with. Not during workouts or running. Nothing. Upside was I didn’t have to wash my clothes much.

Based on my blood tests after taking it, it probably had nothing to do with testosterone, and honestly my testosterone even while having symptoms at the time was a little low (480) but really wasn’t all that low for someone doing too much and training too hard and stressed out from fin and hadn’t slept much in weeks from it all. I’d be a good candidate for having been naturally high T given that I was doing better than most people on roids when it came to results without having touched anything, but I never tested before, only after.

Having since experimented with many things and protocols across the full HRT spectrum that few people venture into, and the holistic realm, I can definitively say that at least in my case, cortisol being unregulated was the issue. I was already someone that was pushing things too hard, and finasteride pushed me over the edge, causing me thereafter to down regulate. If cortisol is out of whack, thyroid and all else up the chain goes to shit. I’ve had my test everywhere from 800 to 1500 and my free T all over the range and double it and it means jack shit if I can’t get it into the cells or have it work. When I do, it feels like I’m suddenly on HRT and I look like I transform into another human being.

From the initial finasteride issues people have, I think one of the main things that makes guys go down different paths with it is that if you’re in a fucked up state like that, you develop other issues that exacerbate it, and potentially get damaged in some ways. In my case, I developed massive gut issues, and some nerve damage in my right foot. That may be partly because while on it I had to eat massive amounts of salt to avoid passing out and going to the ER, which is what happened and the moment I decided to try HRT since I was not managing whatever happened to me on my own.

I’ve talked to and worked with many, many doctors in the field about this. If you’re already on TRT, most guys seem to be fine on finasteride, or report that they are. It will by definition affect your body’s ability to regulate itself in regards to stress, however. If you’re already okay on that front, it might mean nothing. If you’re not, or had some issues down the line, it could mean everything. It seemingly has nothing to do with DHT because it’s not like you couldn’t just inject a DHT analog, which doesn’t work for almost anyone having post finasteride syndrome. Test doesn’t help most guys, either, and if it does it’s not usually for very long.

I read all the shit online about fin too and talked to folks before I tried it and would laugh at the PropeciaHelp folks. I thought maybe they were just on it for 10 years and got mad that in 10 years they aged 10 years. The things they said were too wide ranging to seem real. At worst I figured I’d just get on HRT. I get it now though, and wish I didn’t have first hand knowledge of it. I’ve been there, and at times if I’m not careful I end up back where I was with it and ‘crash’. I have a deep and unending sympathy for them.

I would tread very lightly around finasteride. I really wish someone back then had written this to me before I tried it. It irrevocably upended my entire life. It is my biggest regret. It doesn’t do that to everybody. When it does though? You end up like those guys on PropeciaHelp. It’s a very real thing. I really wish it wasn’t.
wow. Thank you. I don't know what the fuck to do. I'm 48, losing hair rapidly. Been on trt for 5 years. My health is great, blood work perfect, physique better than 99 out of 100 guys my age, or any age for that matter (knock on wood for all that). Does any of that matter? I want to TRY Finasteride, and if I experience side effects just stop. But it just doesn't sound like that always works. Statistically the number of guys getting these side effects is very low when you consider how many millions of people are using the drug. But still. What should I do??!?
 
I inject 150mg per week Testosterone Cypionate. I'm about to start 1mg per day oral Finasteride for hair loss.

The internet says this is totally fine.
The internet says this is a terrible idea.
The internet says Finasteride is poison that will ruin your life.

What do we KNOW about this combination? Are there guys here on TRT and Finasteride who can comment?

Come to your own conclusion!


post #6


 
Come to your own conclusion!


post #6


Someone wanna explain to this tool why forums exist?
 
U need people to decide for ya!
Hmm. Well no, but if all we did was Google search and read things to make a decision, we wouldn't need forums like this, where you can hear about other people's experiences and and share opinions. See how that works, moron?
 
Hmm. Well no, but if all we did was Google search and read things to make a decision, we wouldn't need forums like this, where you can hear about other people's experiences and and share opinions. See how that works, moron?

Everyone and their brothers gonna give you an opinion (one extreme or the other) when it comes to such!

The internet says this is totally fine.
The internet says this is a terrible idea.

The internet says Finasteride is poison that will ruin your life.


Read the literature!

Man up and do what you feel is best for you.

I want to TRY Finasteride, and if I experience side effects just stop. But it just doesn't sound like that always works. Statistically the number of guys getting these side effects is very low when you consider how many millions of people are using the drug. But still. What should I do??!?


* Statistically the number of guys getting these side effects is very low when you consider how many millions of people are using the drug.



Not to f**king hard is it?



 
wow. Thank you. I don't know what the fuck to do. I'm 48, losing hair rapidly. Been on trt for 5 years. My health is great, blood work perfect, physique better than 99 out of 100 guys my age, or any age for that matter (knock on wood for all that). Does any of that matter? I want to TRY Finasteride, and if I experience side effects just stop. But it just doesn't sound like that always works. Statistically the number of guys getting these side effects is very low when you consider how many millions of people are using the drug. But still. What should I do??!?
Personally I use RU58 whatever and haven’t had any issues with that. My current hair issues are from thyroid and cortisol problems though. The hair just doesn’t grow and gets dry and shriveled. If I’m not doing well I can go 2 months and my hair doesn’t grow more than an inch if I’m lucky. It can change rapidly if I’m doing well and the hairs seemingly double in thickness, but that can be hard to maintain happening. If I get on T3 it’ll turn around quickly but I deplete myself of something and it starts falling out indefinitely.

I actually wasn’t losing my hair from DHT back in the day, making my initial use of it pointless on top of all that. My hair just wasn’t growing.

RU at least has a completely different pathway of action. I would be very, very cautious of messing around with 5AR though. Most guys are fine according to them, and I completely believe them. Then there are guys like me who aren’t, and I also believe them. I wasn’t on it for long and it still fucked me up.

There’s a reason a lot of guys that are rich and have access to all this and more from experts decide not to fuck with finasteride. It’s your decision, but I wish I’d followed their lead and not the lead of people telling me to take the risk. I know plenty of people that say they’re fine on fin. And I know plenty of people, like me, who really, really are not, and struggle dealing with it for years after, if not indefinitely. One time I went to the ER with hyperkalemia, and still have marks on my face from that night.
 
You must be one of the clowns from the bro forums that hold a grudge.....almost as bad as the manchild who lurks on here!

Let me put it plain and simple numbskull...the metabolites estradiol and DHT are needed in healthy amounts to experience the full spectrum of testosterones beneficial effects.

Mood, energy, libido, erectile function, cardiovascular/brain/bone/immune system health, body composition.

*Considerable evidence exists in the contemporary literature regarding the physiological role of 5a-reductases in the peripheral tissues and CNS and the pathophysiological implication of inhibiting this family of enzymes and blunting biosynthesis of neurosteroids, which are critical biological mediators in the CNS, and contribute to altered mood, cognition, and libido (23–50). Also, significant pre-clinical evidence exists demonstrating that inhibition of 5a-RIs contributes to erectile dysfunction (16–22) and may also contribute to neurological symptoms (Fig. 4 (36).




Let's dig a Lil deeper champ!


DISCUSSION

Until recently, the adverse effects of finasteride and dutasteride therapy on sexual function were not recognized or well understood. However, a body of emerging evidence suggests that the assessment of sexual side effects of finasteride in many clinical studies was not accurately captured or reported (83). In addition, considerable bias and inaccuracies in reporting adverse effects of finasteride or dutasteride in most clinical trials of men AGA (83). An editorial following the report by Belknap (83) highlighted the need to re-think the safety of these drugs (188).

It is not surprising that almost all studies published to date do report increased sexual adverse effects. However, even when such sexual adverse events were reported, many argued that the numbers of subjects afflicted are small and propagated the falsehood that the adverse effects do resolve with continued treatment. This is unfortunately willful blindness and a deceptive method to continue to prescribe these drugs to unsuspecting young men. The number of subjects experiencing adverse events is neither small nor irrelevant, given the persistent nature of adverse events in susceptible individuals. For those individuals afflicted, this constitutes a life sentence of sexual dysfunction, depression, and/or anxiety. To put this in perspective, approximately 30 million young men, worldwide, would be prescribed finasteride or dutasteride treat male pattern hair loss. Even if the incidence of persistent sexual adverse events is 3% to 5%, which may be viewed as a small number, approximately 900,000 to 1.5 million men would suffer persistent sexual and psychiatric adverse events. By no means this would be considered a small number and should not be dismissed or ignored.

The key argument raised by many clinicians remains:
What is the level of evidence supporting the persistent nature of the sexual adverse effects and psychological symptoms caused by finasteride?

Considerable evidence exists in the contemporary literature regarding the physiological role of 5a-reductases in the peripheral tissues and CNS and the pathophysiological implication of inhibiting this family of enzymes and blunting biosynthesis of neurosteroids, which are critical biological mediators in the CNS, and contribute to altered mood, cognition, and libido (23–50). Also, significant pre-clinical evidence exists demonstrating that inhibition of 5a-RIs contributes to erectile dysfunction (16–22) and may also contribute to neurological symptoms (Fig. 4 (36).


*Data from several studies as well as from the manufacturer own reporting that some adverse events do not resolve and may persist. A number of studies discussed in this review demonstrated that not all adverse events resolve with drug discontinuation and in some cases, they persist or become irreversible (8,12, 13, 52–54, 83, 84, 88, 67, 68, 115, 127, 129, 130, 170, 186–189). For these reasons, we find the argument that sexual adverse events resolve with continued treatment is outright inaccurate and, at best, deceptive.


The increased reporting of and documentation of persistent side effects in the clinical literature resulted in warnings by the Medicine Health Care Products Regulatory Agency (MHRA) public assessment report on the risk of finasteride published in December of 2009 in Section 4.8 Undesirable Effects, it was stated, ‘‘In addition, the following have been reported in post-marketing use: persistence of ED after discontinuation of treatment with PROPECIA.’’ Clearly, the sexual adverse events do not necessarily resolve completely in all patients, who discontinue use of finasteride, again supporting the premise that in some patients these sexual side effects remain ‘‘persistent.’’ Furthermore, in December 2008, the Swedish Medical Products Agency concluded its safety investigation of Propecia. The Agency's updated safety information now lists as a possible side-effect difficulty in obtaining an erection that persists even after discontinuing Propecia. In addition, in 2011, the USA FDA mandated that labeling of finasteride includes information about potential risks of depression as well as sexual dysfunction and problems and high-grade prostate cancer. In 2017, the European Medical Agency recommended adding depression and suicidal ideation to the finasteride label.

One other argument consistently made in the literature is that the low-quality evidence available does not support a causal link between finasteride and persistent symptoms. Examining the contemporary clinical literature, it appears that almost all studies published to date (Tables 1–3) demonstrated the increased onset of sexual dysfunction and psychiatric dysfunction, irrespective of the assessment method, age, or drug dose. How could such evidence be totally ignored and dismissed as low-quality evidence? Given that considerable level of bias is introduced in many of these studies since a large number of these clinical trials were funded and administered by the drug manufacturers, it is paramount that clinicians do their due diligence and not fall for the slogan, ‘‘these drugs are well-tolerated and safe.’’

It is imperative that we consider how safety reporting of adverse events due to finasteride and dutasteride have been inadequate in most clinical trials (83, 84). Indeed, this inaccurate reporting of harm makes the evidence regarding the adverse events to be limited and may appear of poor quality. Given the level of bias due to conflict of interest, it is not surprising that the level of harm is tampered down significantly. Well-trained and experienced clinicians may see the coexistence of adverse events as a distinct syndrome with its own pathogenesis rather than a simple random or haphazard co-occurrence. Despite the lack of final proofs, the presence of severe and persistent side effects induced by these drugs raises serious concerns for clinicians. Simply, a low estimated prevalence of PFS should not be used as an excuse for non-vigilance, given that these drugs are prescribed for millions of relatively young healthy men.
 
You must be one of the clowns from the bro forums that hold a grudge.....almost as bad as the manchild who lurks on here!

Let me put it plain and simple numbskull...the metabolites estradiol and DHT are needed in healthy amounts to experience the full spectrum of testosterones beneficial effects.

Mood, energy, libido, erectile function, cardiovascular/brain/bone/immune system health, body composition.

*Considerable evidence exists in the contemporary literature regarding the physiological role of 5a-reductases in the peripheral tissues and CNS and the pathophysiological implication of inhibiting this family of enzymes and blunting biosynthesis of neurosteroids, which are critical biological mediators in the CNS, and contribute to altered mood, cognition, and libido (23–50). Also, significant pre-clinical evidence exists demonstrating that inhibition of 5a-RIs contributes to erectile dysfunction (16–22) and may also contribute to neurological symptoms (Fig. 4 (36).




Let's dig a Lil deeper champ!


DISCUSSION

Until recently, the adverse effects of finasteride and dutasteride therapy on sexual function were not recognized or well understood. However, a body of emerging evidence suggests that the assessment of sexual side effects of finasteride in many clinical studies was not accurately captured or reported (83). In addition, considerable bias and inaccuracies in reporting adverse effects of finasteride or dutasteride in most clinical trials of men AGA (83). An editorial following the report by Belknap (83) highlighted the need to re-think the safety of these drugs (188).

It is not surprising that almost all studies published to date do report increased sexual adverse effects. However, even when such sexual adverse events were reported, many argued that the numbers of subjects afflicted are small and propagated the falsehood that the adverse effects do resolve with continued treatment. This is unfortunately willful blindness and a deceptive method to continue to prescribe these drugs to unsuspecting young men. The number of subjects experiencing adverse events is neither small nor irrelevant, given the persistent nature of adverse events in susceptible individuals. For those individuals afflicted, this constitutes a life sentence of sexual dysfunction, depression, and/or anxiety. To put this in perspective, approximately 30 million young men, worldwide, would be prescribed finasteride or dutasteride treat male pattern hair loss. Even if the incidence of persistent sexual adverse events is 3% to 5%, which may be viewed as a small number, approximately 900,000 to 1.5 million men would suffer persistent sexual and psychiatric adverse events. By no means this would be considered a small number and should not be dismissed or ignored.

The key argument raised by many clinicians remains:
What is the level of evidence supporting the persistent nature of the sexual adverse effects and psychological symptoms caused by finasteride?

Considerable evidence exists in the contemporary literature regarding the physiological role of 5a-reductases in the peripheral tissues and CNS and the pathophysiological implication of inhibiting this family of enzymes and blunting biosynthesis of neurosteroids, which are critical biological mediators in the CNS, and contribute to altered mood, cognition, and libido (23–50). Also, significant pre-clinical evidence exists demonstrating that inhibition of 5a-RIs contributes to erectile dysfunction (16–22) and may also contribute to neurological symptoms (Fig. 4 (36).


*Data from several studies as well as from the manufacturer own reporting that some adverse events do not resolve and may persist. A number of studies discussed in this review demonstrated that not all adverse events resolve with drug discontinuation and in some cases, they persist or become irreversible (8,12, 13, 52–54, 83, 84, 88, 67, 68, 115, 127, 129, 130, 170, 186–189). For these reasons, we find the argument that sexual adverse events resolve with continued treatment is outright inaccurate and, at best, deceptive.


The increased reporting of and documentation of persistent side effects in the clinical literature resulted in warnings by the Medicine Health Care Products Regulatory Agency (MHRA) public assessment report on the risk of finasteride published in December of 2009 in Section 4.8 Undesirable Effects, it was stated, ‘‘In addition, the following have been reported in post-marketing use: persistence of ED after discontinuation of treatment with PROPECIA.’’ Clearly, the sexual adverse events do not necessarily resolve completely in all patients, who discontinue use of finasteride, again supporting the premise that in some patients these sexual side effects remain ‘‘persistent.’’ Furthermore, in December 2008, the Swedish Medical Products Agency concluded its safety investigation of Propecia. The Agency's updated safety information now lists as a possible side-effect difficulty in obtaining an erection that persists even after discontinuing Propecia. In addition, in 2011, the USA FDA mandated that labeling of finasteride includes information about potential risks of depression as well as sexual dysfunction and problems and high-grade prostate cancer. In 2017, the European Medical Agency recommended adding depression and suicidal ideation to the finasteride label.

One other argument consistently made in the literature is that the low-quality evidence available does not support a causal link between finasteride and persistent symptoms. Examining the contemporary clinical literature, it appears that almost all studies published to date (Tables 1–3) demonstrated the increased onset of sexual dysfunction and psychiatric dysfunction, irrespective of the assessment method, age, or drug dose. How could such evidence be totally ignored and dismissed as low-quality evidence? Given that considerable level of bias is introduced in many of these studies since a large number of these clinical trials were funded and administered by the drug manufacturers, it is paramount that clinicians do their due diligence and not fall for the slogan, ‘‘these drugs are well-tolerated and safe.’’

It is imperative that we consider how safety reporting of adverse events due to finasteride and dutasteride have been inadequate in most clinical trials (83, 84). Indeed, this inaccurate reporting of harm makes the evidence regarding the adverse events to be limited and may appear of poor quality. Given the level of bias due to conflict of interest, it is not surprising that the level of harm is tampered down significantly. Well-trained and experienced clinicians may see the coexistence of adverse events as a distinct syndrome with its own pathogenesis rather than a simple random or haphazard co-occurrence. Despite the lack of final proofs, the presence of severe and persistent side effects induced by these drugs raises serious concerns for clinicians. Simply, a low estimated prevalence of PFS should not be used as an excuse for non-vigilance, given that these drugs are prescribed for millions of relatively young healthy men.
Alongside that, you’ll have guys like me who were royally fucked by it and I doubt most of us report it to anybody. I’ve never been in any kind of report or anything. You get it from your doctor and then say something’s wrong and they say “well, I dunno, stop taking it” and then you bounce around dealing with it indefinitely.
 
I know 3 guys on finasteride and they all have been on for 15-20 years. None of them has any side effects. They did keep their hair.
 
Beyond Testosterone Book by Nelson Vergel
4. Impact of 5α-reductase inhibitors on sexual function


5-ARIs, mainly including finasteride and dutasteride, represent a class of drugs that competitively inhibit 5-alpha reductase isoenzymes (5-ARs). In humans, three types of 5-ARs have been described so far: type-1 is temporarily expressed in newborn skin and scalp and is permanently detectable in the skin after puberty onset; type-2 localizes predominately in fetal genital skin and male accessory glands including prostate [40]; type-3 is expressed both into androgen-dependent tissues (e.g. smooth muscle and prostate) and in the brain, heart, and other peripheral tissues [41].

In vitro experiments have shown a higher inhibitory activity of dutasteride on type 3 than type 2( 5-ARs). By contrast, these isoenzymes are similarly sensitive to finasteride [41]. Several mechanisms have to be considered when the impact of 5-ARIs on sexual function is considered.

*First of all, dihydrotestosterone (DHT) more effectively than T enhances nitric oxide (NO) availability in the endothelium [42]. Thus, 5-ARIs can indirectly reduce the peripheral amount of NO concentration and, consequently, have a negative impact on erection.

*The reduction in DHT explains the reduced volume of ejaculate experienced by treated patients and, in addition, these drugs are able to prevent the conversion of progesterone and deoxycorticosterone into neurosteroids, the latter playing a role in regulating mood, anxiety, sleep, and sexual function [43,44].

*Finally, finasteride can exert a central effect by crossing the blood-brain barrier and reducing the hormonal impregnation of the central nervous system [45,46].
 
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