This is the first time I’ve seen that, and it breaks my heart.
I don’t believe in fairytales, in God, in acupuncture, in astrology or in any other sort of bullshit quackery. I may have a history of depression but I’m not delusional. I mean sure, depression is awful but it’s absolutely horrid to live with erectile dysfunction as a 29 year old guy… And to be dismissed as a hypochondriac for it on top of that is just evil. Not being able to have morning or nocturnal erections should at least indicate it’s a physical thing and not between my ears? I hope supporting the researchers who are conducting real research on all this will prove fruitful soon. I am truly heartbroken.
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I can understand feeling that way. It’s an obnoxious title and seems like an effort to undermine credibility of people with PFS. The good news is that this one crackpot is far outnumbered by many other researchers around the world who are giving serious attention to PFS. A bibliography is here:
https://finasteride.network
The scientists who have done valuable work include: Abdulmaged Traish at BU, George Zakhem and colleagues at NYU Dermatology, Steven Belknap at Northwestern, Michael Irwig at GW, and Roberto Melcangi and his group at U. Milan. Read those papers and forget about this one-off which adds nothing to the effort to understand and treat PFS.
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You probably know that the journal where an article is published is part of how scientists judge its credibility. Journals have an “impact factor” to evaluate how influential they are.
Skin Appendage Disorders, where Trüeb published the article, doesn’t appear to even have an impact factor. In the greater world of dermatology and urology, it is totally ignorable and unimportant.
On the other hand, the other authors I mentioned have published in journals such as JAMA Dermatology, whose impact factor of 7.99 makes it “the highest ranking dermatology journal in the world.” (See ‘For authors’ page)
The Journal of the American Academy of Dermatology, where another PFS paper appeared, has an impact factor of 7.1 making it the #2 dermatology journal. (See JAAD home page)
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That one article can be completely ignored from a scientific standpoint. If anything, to a scientist it reduces the credibility of that viewpoint. However, we can see that a lot of people want to see us get dismissed as lunes. So we need to get serious and start acting like credible people rather than just people who sit and complain about conspiracies. It’s been something like 15 years. At a certain point a group of people who don’t do anything except sit, complain, and talk herbs and broscience get ignored and dismissed.
It could also be how fast/ often the new 5-AR enzymes are created, and that may change from Fin.
Any dosages are not enough to completely shut down 5-AR. Meaning that there are always new enzymes being created, but once your using Fin to constantly inhibit them, the body must produce them very quickly, and could get stuck in that mode.
That could be why guys feel great before crashing. New 5-AR is restored quickly, but in a short time, it becomes too much 5-AR.
If I had a batch of mice with PFS, the first treatment I would try on them would be a very high dose of DHT. No doubt this would be risky in people due to the cardiac and mental side effects of high serum DHT.
I believe the protocol described by this user indeed has a theoretical chance of working, in addition to the apparent practical success. The theory I have proposed before may explain why that would be the case.
The evidence indicates that in PFS (type 2) the gene for 5ar2 is epigenetically silenced. As a result, little DHT is produced in key tissues responsible for sexual and other functions. Consequently, the AR is overexpressed but this is a consequence, not a cause of the problem. Here is a schematic mechanism of how this could work.
5ar expression and the AR together control androgen signaling in the cell. DHT, working through the AR (there is literature that indeed it does), positively upregulates 5ar expression: more DHT means more 5ar expression, and thus even more DHT (there is literature about this too).
Conversely, more DHT negatively controls AR expression: more DHT means downregulation of the AR, which would in turn downregulate 5ar expression. Two two regulatory processes oppose each other and thus bring the system into equilibrium.
The evidence indicates that PFS (type 2) occurs when DHT drops too much or too rapidly for the AR to be able to upregulate itself in time to stop the rapid downregulation of 5ar. Once 5ar is completely silenced, there is not enough DHT to jump-start the system even with an AR upregulated to the maximum. The cell is stuck in a bad equilibrium.
Let me rephrase that: a precipitous drop in DHT most likely crashes the DHT regulatory system and DHT cannot recover on its own.
In theory it should be possible to upregulate 5ar if enough DHT is delivered to the cell. This is a challenge because tissue concentrations of DHT in key tissues is 10 times higher than serum concentration. Therefore, high levels of serum concentrations need to be achieved or local application needs to be used where possible (as I did with some success).
The key part of such a strategy would be to avoid sudden removal of exogenous DHT, as that will lead to a PFS-like crash. I believe this is what happened in my latest experiment. I don’t know if gradual removal of DHT could lead to the gradual upregualtion of the AR so that 5ar expression does not collapse. It is possible in theory. Gradual removal of exogenous DHT would also help restore endogenous T production, which might be reduced with high serum DHT.
I have written another post describing this putative mechanism in some detail here:
@anon5006275 @anon22245532 @AaronF @orthogs @slavoushka @airforlife @PFSnb @Scott.H @Chapman @Dubya_B
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Very difficult to say, but maybe the sudden removal of DHT (like the sudden removal of fin) is what the body force to demethylise the silenced 5ar gene. But it is difficult to prove. Maybe a slow removal after a long time of very high DHT could have the same effect. I am coming very slowly down from Fin and although I had symtomes since 2.5 years they seem gradually to improve (practically the opposite of gradually reducing ultra high DHT).
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If we assume, as a thought experiment, that the reasoning behind this particular case is correct, wouldn’t that mean that people who gradually / controlled quit finasteride simply wouldn’t get PFS, because they would have allowed their receptors to re-adjust? In most surveys I’ve seen people have quit the drug cold turkey. Are there any cases where people have quit gradually?
Here are some past posts matching “taper finasteride”:
https://forum.propeciahelp.com/search?q=taper%20finasteride
sure i will
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I’ve tested things for 11 years, sadly I’ve not written everything down but this is what I remember testing, I’m sure I’ve forgotten some. Usually I just test one thing for at least a month or two to see if it has a positive effect or not. I still have most of these bottles or medicines so I could prove it if really required. Obviously I ran some for far longer, like undecanoate.
Testosterone therapy:
- HCG monotherapy
- HCG + injections.
- Just injections both subq and IM with and without aromatase inhibitor.
- The esters cypionate, propionate and undecanoate.
- Testosterone gel, applied to either scrotum or shoulders.
- Clomid monotherapy
- AI monotherapy.
- SERMs (tamoxifene and toremifene)
- I’ve gone through PowerPCT.
- I also tried Proviron (obviously).
Hormones:
- Both oral and dermatological application of progesterone.
- DHEA (orally).
- Pregnenolone (sadly just orally).
Methylation:
- 5-MTHF
- B-methyl complex.
Boosters:
- Tribulus
- Ginko Bilboa
- Maca
- Korean ginseng
- Fenugreek
- Boron
- D-Aspartic Acid
- ZMA
- Anacyclus pyrethrum
- Ginger
- Olive oil (2 tbsp)
- Tongkat ali
- Shivlingi beej extract.
Supplements/medicine:
- Taurine
- Naringin (for highish HB)
- Various vitamins
- Ashwagandha
- Aged garlic extract
- Resveratrol
- Pycnogenol + l-Aringine + l-citrulline
- Daily cialis
- Rhodiola rosea
- Alpha-GPC
- Various probiotics
- Pomegranate extract
- Curcumin
- Glycin.
Monoamine oxidase A inhibitor (tried after genetic test showed an indicator):
- Moclobemide.
Antibiotics/antifungal:
- Doxycycline
- Minocycline
- Tetracycline
- Fluconazol
I’ve also tried various mechanical things, resistance training, endurance training, pumping, and yoga stretching.
Some of these helped a bit with a specific symptom (like cialis) but the only ones that I had some broader overall success with for a shorter while was testosterone gel applied to shoulders, anacyclus pyrethrum very mildly about two weeks after I stopped taking it and doxycycline for about a week after I stopped taking it. I just took the doxycycline for one week for an illness however. Interestingly enough the testosterone gel was the only testosterone therapy that worked for a while. Possibly because less DHT conversion and more estrogen conversion through the skin.
I tried progesterone cream after reading through the entire 1000 post thread on this site and tested my levels (which were low). Oddly enough, pretty much no one in the thread actually tested their levels. It did clear my head slightly after a few weeks and seemed to give me slight gyno but that was it. I also tried the oral route with Utrogestan but it gave me major breast tenderness after just a few days so I stopped. I couldn’t really decrease the dose easily as Utrogestan is some kind of capsule filled with liquid. I contemplated just diluting parts of it with water or ethanol but I figured it would end up the same as the cream then anyway and I wasn’t sure the liquid alone without the outer shell would be able to survive the stomach acids.
As I mentioned earlier, Proviron increased my symptoms by a lot, I felt horrible on it. I’ve tested my DHT levels some two years back and they came back normal. Since DHT increased my symptoms and I didn’t want to try the finasteride route in decreasing the DHT, the only conclusion I could come to after testing so many things and the levels themselves being normal was that there was an issue with DHT sensitivity at the receptor level. Which is why I wanted to try overloading the receptor with DHT, to decrease sensitivity. Which is what worked in the end.
If anyone considers testing a similar route, I’d try at first just taking a normal amount of Proviron (50mg) for 3 days or so as that is quite mild. If you feel noticeably worse on it, you may have a similar receptor issue as me. If you don’t, that route is likely not worth considering.
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You could describe in more detail what your symptoms were (specially sexuals, like penile shape changes, “hanging”, size and girth loss, pain etc.) and how you took 200mg Proviron (once or twice a day, for example) and how long.
Don’t you think that over the years you “changed” your receptors with injections of HCG and testosterone, and Proviron was just another detail in your recovery?
Did you cycle the 200mg of proviron or have it been continuous?
Did you notice that recovery came slowly or did it come at once (from the point of view of your perception)?
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You mention you did a lot of tests to know your hormonal levels. What kind of tests did you do? Did you have an endocrinologist or a doctor by your side whom arranged these tests for you? I know Sweden has a good social healthcare system and my situation may be similar. I find it a daunting thing that you may have experimented and tested with these hormone-influencing substances on your own. Could you post the results of your latest hormonal tests and share it with us? Maybe before the 7 week experiment?
I will be having my first hormonal tests soon after the corona crisis subsides. I would like to compare if our situations are similar because if so, I might try this.
Also, about your final 7 weeks of Proviron. Were you using any supplements or any particular diet during this time? What were the supplements and diet you used before that time?
Here’s a post on a different forum with test results posted.
The website might be slow to load.
He did a different protocol and thought it was DHT cream that worked.
Hi @pal,
I am very happy about your recovery and I am very grateful that you have come to PH to tell us about your experience! I would like to ask you a couple of questions.
You say that you felt worse while on Proviron:
Can I ask you which exact symptoms of PFS got worse while you were on Proviron? Please try to differentiate if you can the effect of Proviron on symptoms of PFS you had before taking Proviron and on any new symptoms you got while on Proviron. In particular, I am curious to know what was the effect on sexual function.
Secondly, why did you feel miserable? What was the worst effect of Proviron?
Third, you say that despite feeling worse on Proviron, it made you realize you were on to something. Can you elaborate on this if you can? What made you think you were on to something? Did any symptom improve while you were on Proviron?
Finally, you said that after you stopped Proviron, things felt off for a few weeks.
Can you try to describe what exactly you mean by that - in general but also as regards PFS symptoms and especially in comparison to how you felt while you were on Proviron?
Your answers would be most appreciated. Thanks in advance!
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The main symptom that got worse was extreme fatigue and a sense of derealization. I was so tired that I couldn’t do anything, I could not function. I had no desire to do anything, sex was the last thing on my mind. It was bad before but got a lot worse with proviron. It is the worst I’ve felt mentally in my life.
Since I felt so much worse on proviron, I figured I’d try to achieve the opposite in order to feel better. The opposite would be to either lower DHT but that would be similar to the finasteride route which caused the problem to begin with. I also knew from testing that my DHT was fairly normal. I know low DHT caused the problem to begin with while on fin, so the logical thing to do was to increase DHT for a prolonged time in order reduce the super sensitivity the receptors had.
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Good that your better now that’s all that matters, thank you for posting and giving some hope to us.
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Regarding the HairLossTalk thread, post #14 mentions histamine intolerance. There was another cure on here where the guy mentioned the amino acid L-Histidine was “the final piece to the puzzle.”
Similar names, but I’ve seen L-Histidine claims for allergies aka Histamine.
Thanks a lot @pal. As others also asked, i want to ask that did your sexual sides also came back to 100% normal? What was your sexual sides?
- Did you suffer from pleasureless orgasms/ weak pelvic floor muscles? And no climax feeling? If so, did they completely resolved?
- You had any erect penis size loss? If so, did it come back to normal size now, after 11 years of sleep?
- How about your semen volume and morning woods now?
Thanks. I hope you answer these questions in detail, that would be really awesome and could give us some hope. It must be hard for you to remember how it should really feel to have a healthy orgasm after 11 years…
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I had zero libido. I didn’t feel much of anything if touching the penis, it was like touching a finger. It reduced in size, at times it looked almost child-like when flaccid. I took 200mg Proviron once per day after breakfast.
I do not think HCG changed anything for me in terms of cure. I’ve been on and off HCG for years earlier when on TRT without any progress at all. Recovery wasn’t instant. When I stopped Proviron I didn’t immediately feel good but I did feel different. It took some two months after stopping to gradually feel better. Quite possible due to HPA axis restoring, which I’ve experienced before but then the receptor issue with DHT was still there so it didn’t really help. After taking a large dose of proviron for a longer period of time however, the receptors seemed to have gone back to no longer be super sensitive to DHT, or perhaps they simply reduced in number. Either way, it worked out.
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