I have almost completely recovered, this is how I did it

General Discussion
#1

I quit Propecia 1mg a day cold turkey in march 2009, after using it for 11 months. I have been a long time lurker and now that I have been recovering and have been mostly recovered for the last 6th months, I have created an account to give back after spending hours and hours and hours lurking this forum over the last several years. I can’t post this in recoveries, because I just joined, filled out my symptom tracker, and have no credibility. I probably wont even make another post except to follow up on this post if anyone has questions.

So lets begin.

I am a very athletic individual, I have maintained a 6-12 percent body fat composition from the age of 16 and I have had a healthy diet by comparison to normalcy the whole time. I have been healthy before and and after taking Propecia.

I am relatively attractive, and very witty, and have had a continuous string of girlfriends since I was 18 along with many short term stints and a few one night stands all during these longterm relationships.

I had never had a problem even in the slightest before taking Propecia, and I would get horny one or two times a day. I would get an erection at the slightest intimacy with a woman.

When I began taking Propecia, my libido increased. after 9 month, I began noticing that I was not getting horny any more, and I would get difficult erections from time to time. at 11 month, I had no erection and I quit cold turkey the week after. My symptoms got worse for a few weeks and then started to improve for about a year until my improvements plateaued. I could get an erection, but difficult, and I still was not ever horny. Once I had an erection, I could usually keep it. After a year, I was unsatisfied at my diminished performance, I started trying new things. I would test each thing out for several month (±6) I started with eating foods that were supposedly good for libido, I tried supplements like yaohimbe and maca, which work very well, and allowed me to become honey again, but i grew dependent, and required higher dosages after just a few uses, and they became ineffective after couple weeks, so I stopped using them. I tried the 5Gs supliment regime, which made it easier to get an erection, but after a month or so, it diminished again.I tried strict paleo, strict vegitarian, etc. I tried going 5 month without masturbating, I tried weightlifting, yoga, and running.

The things I notice that led me to my cure. When I was getting off strict paleo, I would notice that my libido improved noticeably when I ate carbs, aerobic exercise improved my libido, but weight lifting, even though at the peak of weight lifting my T levels were around 800 didn’t work to improve it. The biggest thing I noticed was that 5 months of not masturbating, killed my libido, and made it very hard for me to get an erection.

With this in mind, this Is what I have beed doing since the beginning of the year. I can not say which one or combination of which things is responsible for my recovery, I can not even say that my recovery is a result of any of these things, it could just be completely coincidence. but I am going to give a list of things I have been doing since the beginning of the year, and in that time my libido has improved dramatically, I am able to get an erection every time without effort, and if I don’t masturbate for a day I am Horney, which is an amazing feeling. January 50%, Feb, 70%, march 80%, August 85, today, probably 90% Recovered.

So this is what I have been doing on order of how important I feel it has been towards my recovery:

  • I stopped drinking alcohol for a new years resolution (unrelated, but could affect it)

  • I Added starches back into my diet (It seemed to help a little)

  • I cut out all supplements except for calcium, antioxidant and zinc.

  • I Try an do more aerobic exercise (I now walk and bike long distances quite often)

  • I force myself to masturbate 3-5 times a day ( This is what I feel mostly led to my recovery)

While I cannot confirm anything, and my trials over the last few years have been very unscientific. I feel The primary reason for my recovery since the beginning of the year has been do to my masturbation. My libido declined dramatically after Propecia, and I did not masturbate very often, only a couple times a week. When I stopped masturbating for 5 months, it killed my libido and performance, so I decided to do the opposite, which was to force myself to masturbate 3-5 times a day. Since starting this regime, I have had a huge recovery. I am horny, my performance is great. This has been consistent for months, and my condition is improving every day.

This is not meant to make anybody stop their regimes, or avoid medical consultation. This is just what worked for me after 4 years of dealing with this problem, and if it works for you also, That’s Great.

TLDR: I am 85-90% recovered and I believe it is due to forcing myself to masturbate 3-5 times a day.

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Massive improvements with excessive masturbation
Success Stories Compilation
I believe masturbating four times a day has helped me
#2

I just dug this one up, not seen it before.

Oh well, it’s free - might as well (seriously) try it!

#3

I have noticed that after masturbation my libido increases noticeably and my errections are little better. A few days earlier I masturbate after a long no fap period, it was very difficult to get errect and thr errection it self was very bad.
So yeah it can help.

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#4

My word… in that case I definitely will. I used to (pre crash) masturbate at least once a day. I’ll try twice for a few months.

#5

Lots of Masturbation/sex/ejaculation has crashed some people here.

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#6

how is that possible ? i also done it multiple times while i stopped. but where is the relation?

#7

Most likely a rise / fall in hormones.

Some people here respond well to increasing testosterone, some poorly for example.

As a result, if you move a hormone in the wrong direction for your body, you could suffer a negative reaction.

I am not a scientist or a doctor. That would be my best guess without researching.

#8

thats quite interesting. i took maca a few days after stopping and a few days before my crash…

#9

Might be worth edging. That is to say, getting an erection and maintaing it for a while without ejaculating.

#10

Bad option I got blue balls doing that, extreme testicle and back/kidney pain with constant precum and reoccurring erections.

My viens in testicle swelled up alot.

#11

Oh, sorry to hear that.

#12

Ok. Cured by masturbation and maybe some exercise.

Exercise is a common theme in stories of cured people. Having sex is a good idea, I mean anything you practice gets better, any muscle or organ you don’t use atrophies. Makes sense.

Next story…

#13

Downregulation of AR via ejaculation

#14

WHAT!?

What do you mean?

#15

:thinking::roll_eyes: What is going on.

#16

I think there are two type of PFS, those that respond to DHT and testosterone and Those with PFS that get worse with the rise of the androgen.

I am planing to take an appointment to the following center, I believe that it is the perfect center to investigate what is really going on with PFS, This center it is probable the only of this type in the world.

https://www.utsouthwestern.edu/education/medical-school/departments/neurology/programs/rare-brain-disorders/clinic.html

https://www.utsouthwestern.edu/education/medical-school/departments/neurology/programs/rare-brain-disorders/

I will like to heard opinions

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#17

I bet they won’t even acknowledge any of this…Who knows but I would print or send all the published research thus far out such as the published Melcangi and the Triash paper on endocrine disruption…How are you gonna proceed when no one knows even what pfs is…No one knows you already talked to the world’s foremost expert on the condition or I would assume he is since he has lead the Baylor study Mohit Khera which appears to atleast have been dragging their feet on this now for 6 years and its not even complete yet…Many symptoms yet to be addressed or explained I always thought it was a brain dis order which Goldstein can show you on a functional MRI what is termed as brain damaged but my understanding its due to androgen receptors increasing in the brain in response to fin lowering dht and being flooded with a chemical type of brain trauma which would be endocrine disruption in of itself…Thus triggering some type of shut down which would be the actual culprit to continuing decline and symptoms such as these gene regulators and if Kheera is correct and androgen dependent genes have been silenced or turned off there is nothing anyone could do about it just as with lowering neurosteriods there is no reversal for this other than your own body’s ability to adapt to these changes over time…But I think your on a wild goose chase here till more is known and more studies are published…

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#18

Here is my opinion. Nothing going to happen, they will just suck money out of you. They cannot know more, than what the current studies are providing.

#19

Everything is an assumption, everything is an hypothesis, there is one thing here for sure, those recoveries and even temporary recovery is telling me that the system is working, irreversible conditions don’t switch like that, sometimes I do not believe that epigenetic will switch the gene on and you get recovered you and tomorrow will going to switch back off again.

2-I consulted a geneticist at Baylor and he told me that it is almost impossible that Finasteride could cause an epigenetic modification, he also told me that epigenetic changes are reversible and not permanents, he told me also that he dosen’t know how Khera will switch those genes.

In my pinion the Baylor study is not speeding the study in my opinion for the following reason:
Khera is a doctor and assistant professor at the university, what time left to dedicate to an study + he is not affected with Fin.

I think that taking the study to at monster center like this one it is different history.

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#20

Neuroactive steroids.

Neuroactive steroids are natural or synthetic steroids that rapidly alter the excitability of neurons by binding to membrane-bound receptors such as those for inhibitory and (or) excitatory neurotransmitters. The best-studied neuroactive steroids are a series of sedative-hypnotic 3 alpha-hydroxy ring A-reduced pregnane steroids that include the major metabolites of progesterone and deoxycorticosterone, 3 alpha-hydroxy-5 alpha-pregnan-20-one (allopregnanolone) and 3 alpha,21-dihydroxy-5 alpha-pregnan-20-one (allotetrahydroDOC), respectively. These 3 alpha-hydroxysteroids do not interact with classical intracellular steroid receptors but bind stereoselectively and with high affinity to receptors for the major inhibitory neurotransmitter in brain, gamma-amino-butyric acid (GABA). Biochemical and electrophysiological studies have shown that these steroids markedly augment GABA-activated chloride ion currents in a manner similar (but not identical) to that of anesthetic barbiturates. Several steroids have also been observed to have convulsant or proconvulsant properties, including the synthetic amidine 3 alpha-hydroxy-16-imino-5 beta-17-azaandrostan-11-one (RU5135) and the natural sulfate esters of pregnenolone and dehydroepiandrosterone. Several of these have been shown to be bicuculline or picrotoxin-like GABAA receptor antagonists. Examples of steroids that alter neuronal excitability rapidly by augmenting or inhibiting excitatory amino acid receptor-mediated responses have also been reported. Recently, allopregnanolone and allotetrahydroDOC have also been measured in brain and plasma where their levels have been shown to fluctuate in response to stress and during the estrous and menstrual cycles of rats and humans, respectively. Although the major fraction of allopregnanolone in tissue, including brain, is of adrenal and/or ovarian origin, appreciable levels of allopregnanolone can still be measured in the brains of adrenalectomized and/or oophorectomized animals. Receptor-active neurosteroids may represent an important class of neuromodulators that can rapidly alter central nervous system excitability via novel nongenomic mechanisms.

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