Crazy Nocturnal Hypererections at 52 Micrograms of Finasteride

Guys, just wanna give you a brief update on what can happen, when tappering off Finasteride at 0.5 Micrograms per day (that’s a 2000th of a single pill!):

A few of you already know that I am tappering off Finasteride at micro dosages since more than a year. Before tappering off I mainly had severe sleeping problems and a little bit of sexual dysfunction. All kinds of symptoms became worse and I got the full spectrum of symptoms while reducing the medication. I have to add that during that time my sexual functions got down to 15-30%, but I didn’t experience complete impotence at any time. The neurological symptoms though were a nightmare, with me not sleeping more than 1h per day for six weeks at the worst time and around only 2-3 good hours for another 10 months. Things seem to slightly improve.
Once I dropped under 180 Micrograms funny things started to happen: I didn’t had mornimg erections for years and suddenly they came back. But not normal morning erections but painful, prolonged, stone-hard erections that lasted for hours or the whole night, making me waking up in again and again. This wouldnt be associated with any kind of pleasure or sexual desire. It would happen completely automatically.
This would go for a week or two. Then they would suddenly stop completely and I wouldn’t have any nightly erections for 2 months.

I made DHT tests twice: once the day they suddenly stopped: DHT was normal. Once during a period when I didn’t had any erections at all: DHT was completely down.

I started tappering off because I saw that as a possible opportunity to avoid lasting PFS. I read that most guys start to get symptoms when they stopped taking Finasteride. Without knowing much about the pathomechanism I theorized that stopping finasteride or taking it irregulary, may cause disinhibition of the 5ar-enzyme with an overshoot of DHT as a consequence (some guys wrote they felt a lot better for a short period of time after stopping Fin before they finally crashed). I further theorized that the unnaturally high spike of DHT (just theory) would trigger a feedback loop that finally would cause the irreversible symptoms (epigenetic changes in the brain and /or other tissues - > depending on whether these changes would be rather in the brain or rather in peripheral tissue that would explain the differences in methylation and symptoms among patients).

I threw a look at the crazy inhibition curve of Finasteride:


Based on that and now also on the heaviness of symptoms, I reduce Finasteride.

Since a year I feel I am crashing every second week, but it seems to get slowly better.

I am writing this post mainly because I want to point out that even 52 Micrograms per day (2x26mcg) still have certain effects on the body and that even a reduction of 0.5 mcg per day results in symptoms (hypererections) that are most likely be cause by feedback loops that kick in although I reduce it that slowly.

I just want to say, we should have a closer look on what the process of disinhibition does to the hormone and neurosteroide feedback loops in the body and specific tissue.

I propose

  • testing various metabolites under the reduction of Finasteride at various points of time and dosage
  • doing the same experiments with rats (also looking at several tissues)
  • repeating these experiments under the use of body on a chip technology and brain on a chip technology, also using radio nucleotides to mark and trace finasteride during its binding and metabolism process.

Take care and cheers.
@axolotl @Dubya_B @Redivivus @Sibelio


Interesting do the changes in your nocturnal erections fluctuate with the quality or duration of your sleep? Or are they mostly independent?

Where did you find that inhibition curve? That’s amazing.

I’ve been seeing anecdotal reports on r/tressless that they are sometimes taking just 0.25 mg a few times a week to minimize side effects. According to this curve, maybe they should lower it down even further to 1/8mg or 1/16mg.

Your prolonged erections sound like Priapism:

Once when I was briefly on a drug around 2010, I experienced Priapism. It was a rare side effect of the drug. I wonder if finasteride predisposed me to that side effect.

I like your experimental proposals. Where is the body/brain on a chip technology now? I would be surprised if it could properly mimic androgen metabolism since I believe we don’t understand the whole cascade.

1 Like

At the suggestion of a primary care doctor I tried melatonin last night to help with sleep and got the first good night’s sleep in a long time. I took 5mg about 2 hours before bed and got so drowsy I could not stay awake.

For anyone trying melatonin: it has side effects which you should check before taking it.

1 Like

When not experiencing these Priapism-type symptoms: Do you have any nerve sensitivity in your penis, or is it numb?

I am already lower than 1/16mg. And the side effects of disinhibition like hypererections are strongly notable.

I wouldn’t call it priapism as there is no ischemic component. It is just super strong erection that lasts for hours and hours sometimes the whole night.

This is a typical side effect of DHT (which I think will raise under disinhibition of 5ar until my body regulates it down again). Look at the side effects of the DHT analogon Androstenidione:

Organ-on-chip technology lately had a breakthrough with a fully functional multi-organ chip. In this case it is not necessary to know all parts of the cascade as a body on a chip tries to fully replicate the human organism with all it’s tissues and metabolite cascades:

1 Like

A lot less sensitive at the tip (at least that’s my impression), but not numb. Especially in the shaft I do have feeling.

I think that inhibition curve is bullshit, .25 and 1mg a day were completely diff experiences for me in terms of hairloss and side effects


With regards to questions regarding the dose/response curve, it is highly unusual and nonlinear as indicated in the diagram. Finasteride is an unusually efficient pseudo-irreversible mechanism based inhibitor. The enzyme-bound inhibitor complex follows parallel reaction coordinates that proceed through closely related enolate intermediates as testosterone’s reduction to DHT, with the two reactions proving divergent in the final step, forming the reduced product dihydrofinasteride.

Finasteride is markedly suppressive of DHT at all daily doses between 0.04 and 100mg over two weeks. Steady-state DHT levels were reduced to between 0.1-0.15ng/ml at all doses tested by Stoner et al, with DHT levels returning to pre-treatment levels within 14 days of cessation (Gormley et al., 1990).

At the tissue level, 0.05 to 5mg finasteride produces a 60% reduction in DHT in scalp skin; “a 20 times smaller dose than recommended had the same effect on DHT”. Similarly, a dose of approximately 0.2 mg of finasteride is not appreciably different to 5mg in terms of serum DHT reduction, illustrating a profound efficiency of this drug at low doses (Frankel, 1999).

With regards to the OP, this is hard to follow and several inferences do not make clear sense or have a basis. Theoretical grounds for adaptation under the pressure of ADT would not indicate that tapering would be effective at avoiding the problem, although may relieve the symptomatic effects. Antiandrogenic substances often relieve PFS symptoms, but can be ultimately causative of a worsening. It would be interesting to share a clear write up of what you were taking and the progression of your symptoms, with hypothesis in a subsequent post or separated, as it is hard to read and parse. I am interested to read your story, and am puzzled as to why you embarked on this road in the first place as opposed to stopping Finasteride?

I would not recommend constant shopping lists of research. Having spent the past months in conversations with scientists operating NGS pipelines, credible researchers do not operate this way, and inferences from individual feelings are not grounds. It should be well appreciated this drug is well tolerated in millions of young men, to the point reasonably large placebo controlled trials would likely not even detect signal for PFS (Irwig 2020), so something is biologically differentiating PFS patients. Clearly there is a strong variability for predisposition within that.


Yes, it seems like that. In these times I seem to have m more energy and feel nearly good again. Sleep is not perfect then but better. Then full of energy I start planning activities and shorty after I crash with only 2-3 hours of decent sleep a night.

@simonsayss, with all due respect, what on Earth makes anyone think that rats given finasteride are an adequate model of PFS?

Melcagni already did this and there’s no way to tell if he mimicked PFS or the typical effects that might be observed in non-symptomatic patients after taking finasteride.

The idea of radiolabelling sounds interesting, but what would that achieve other than adding to the knowledge of tissue concentrations and metabolism of the drug?

This same line of reasoning led to rodent studies of Accutane, where a remarkable difference in certain brain regions was observed after the drug was administered. This was a dead end and it can’t be said these “after” observations reproduced the horrific state that rarely affects individuals who take the drug.

Just curious why there isn’t more intense interest in studying actual PFS patients?

1 Like

Of course we have to focus on the big questions first. Human trials and results are always prefered. For some kind of studies human trials are unethical and expensive though.

I do not propose a “shopping list of research”. This wasn’t meant as a elaborated study design, but just an idea.

If we want to get to a cure and not just a treatment then we also have to understand what is happening on a molecular level. Human trials probably won’t give the precise answer to that easily.

My suggestion: why don’t you guys post a transparent list - ordered by priority - of research projects that you have in mind? This would make it easier for others to see where you are heading.
… I think that is a subject that concerns all of us. These study proposals don’t need to be discussed. But more brains thinking about it could be helpful in many ways.

1 Like

Quick update: I reduced the speed of Fin reduction from 0.5 micrograms per day to 0.4 micrograms as erections were too strong and lasted the whole night.

Now I noticed that even with 0.4 micrograms of reduction nightly erections still last the whole night and sometimes are just too much. I reached a total dosage of 44 micrograms (22 in the morning, 22 in the evening). I have now these super strong erections since I am below 60 micrograms and they are lasting now since about 6 weeks.

Some people ask me why I just don’t stop the medication all at once?
I postulate that the cease of Finasteride or the fast reduction is causing a “hormone storm” that leads to the methylation and shutdown of the 5ar gene in some tissues. This hormone storm may also be just within the tissue, without high detectable DHT levels.

The fact that a very slow reduction of just 0.4 micrograms per day leads to these heavy all night lasting erections is pointing very heavily towards the truth of this theory.

In general I got more stemina. Sleep did improve only little so far. Skin still feels dry. Semen still seems to be very fluid. Sexual desire improved slightly. Sexual performance reaches 80% of normal levels.

One thing that is a bit weird, since the erections became so heavy my mouth feels constantly dry at night.


Update 03/19/20:

I am now at 42 micrograms - 21 in the morning, 21 in the evening.
Although I reduced the speed of tappering to 0.4 micrograms a day, ererctions still seem to increase and are painfully hard for the whole night. It feels like swallowing 3 pills of viagra and going to bed.
As I worry that my body may shut down 5ar and as it becomes more and more painful, I reduced the speed now to 0.3 micrograms until the erections get a bit more normal.

One thing I noticed lately is that I have more belly pain during the nights. These kinds of nightly belly pain come and go every few months. Another thing that I noticed is that I fall asleep faster and that I do not need to pee 2x per night. Sleep is slightly better.


Update 03/22/20:

Erections are getting unbearable. It really feels like swallowing 5 pills of viagra and trying to sleep. As I fear feedback loops could shut down the 5ar gene, I am reducing the speed of reduction to 0.2 micrograms a day until it normalises somewhat.