What I believe PFS is

General Discussion
#48

Precisely, when I meet Dr Khera I told him about this guy that recovered with Tribulus and he said that he can’t confirm it, but it is possible, due Tribulus work the libido side.

Supplementation of T. terrestris is regularly incapable of increasing levels of androgenic/estrogenic hormones in blood or urine samples, however, synergic actions over NO synthesis, GABAergic signaling inhibition (through DHEA), dopaminergic signaling and potential for bioconversion to androgens (1875mg doses), indicate a possible application in the treatment of erectile dysfunctions and HSDDA. Protodioscin (PTN), a common saponin from T. terrestris, may stimulate nitric oxide (NO) and other mediators tomodulate central dopaminergic activity and libido. PTN may also be converted to DHEA, which is capable of inhibiting GABA signaling, therefore promoting improvements in sexual function . B. The relationship between PTN and testosterone (TST), of stimulation or direct conversion, is still unknown, however, in vivo models indicates that T.terrestris may influence concentrations of TST and C. dihydrotestosterone (DHT). PubChem compound database
codes: CID=441891 (PTN); CID=6013 (TST) and CID=10635 (DHT). Adapt
https://www.researchgate.net/publication/320909030_Tribulus_terrestris_L_zygophyllaceae_safety_and_effectiveness_of_steroidal_metabolites

#49

I have a question for anybody that want to discus.

While on finasteride DHT levels are reduced to almos zero or very low,
allopregnanolone for example is made from DHT, It mean while in the drug allopregnanolone is going to be also very low probably undetected.
Many of us took the drug for many years and they where able to functioning sexually while in the drug with very low allopregnanolone and without proper levels of the rest of the active neuro-steroid that are derivative of DHT.
Now people still thinking that our sexual problem low libido is low level allopregnanolone.

Do this make sense?

#50

Alloregnanolone is not made from DHT, it’s made from DHP.
You are probably thinking of androstanediol, which is formed by further reduction of DHT by 3a-HSD enzymes.

To answer your question, it doesn’t make sense, but low allopregnanolone is exactly what has been found in PFS patients.

About the sexual symptoms, it’s almost as if something that detects testosterone and DHT, 2 important male sexual hormones that still serve a function in regulating sexuality in women, and sends some sort of signal as a response to detecting those homones, isn’t functioning correcly.

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#51

its strange, but when i was ON fin i had even higher libido. on fin men tend to have higher T, higher e2 because its sth left that didnt convert to dht. i also felt like having 0 cortisol on fin, superflat stomach,sleeping 11h soundly, always chilled mindset.no ambitions,yet no worries.
in few words: my version of PFS feels like going from no cortisol to skyhigh cortisol (high levels conirmed)

#52

I was taking clonzapaem off and on for 2 years before I took FIN… wondering if there is a connection. Oddly i don’t take it anymore though when I really think about our situation that makes me anxious so i try not to. I read somewhere that there might be a connectoin between those that had prior anxiety issues and pfs?

#53

Hey dude - I would keep hope. When I crashed for the first few months I literally felt like I was tripping on lsd or something. Total sensory disconnect with mind and body. One of the halmark things I noticed is that I couldn’t feel my muscles and they wouldn’t get sore - I was lifting like crazy to beat pfs. Benching 235 and I weigh 155. Stil couldn’t feel soreness. I even remember I would flex my biceps super hard (in the past this would cause pain cuz I squeezed too hard) and after the crash I felt nothing. Well… that’s all normal now. I workout and I get sore as shit and I can feel my body pretty well. So I think that will improve.

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#54

Did these scientists explain you why they believe that Di Loreto’s study is not reliable or why they believe that it is impossible for finasteride to cause an epigenetic change?

#55

If it is not epigenetic, which it has not been proven to be so and from the looks it may never be proven?? Only one other thing it could be…Autoimmune. Certainly because of testosterone nut functioning correctly but why? It appears that the body is just unable to readapt back to it for some reason…

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#56

No, man. You misunderstood. Melcangi and Santi consider both an epigenetic change and a reduction of neurosteroids, but that does not concern the AR receptor. This they said.

#57

I insist that the problem lies in penile tissue changes. The lack of libido comes in part because the body gets frustrated when blood is not flowing normally, nerves are not transmitting information as in the past, etc (whereas in the past, there were nice sensations instead).
We need to push for more detailed studies of penile tissues (not just corpora cavernosa, but also tunica albuginea). Eco-doppler can test some of those changes, but not all.
If many in the group have venous leak even after injection, it’s because the tissues have changed, it’s obvious.
Epigenetics, neurological changes, etc., can be a possibility, but I cannot understand why there is no serious research about penile tissue changes as the core of PFS.

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#58

PFS sufferers have been shown to have very low levels of neurosteroids in their brain. This will certainly have a strong effect on mood, libido, etc. Why fixate exclusively on the penis?

#59

It’s a problem of cause-effect.
Low levels of neurosteroids can be also found in depression and in post-traumatic stress disorders (PTSD).
How will you avoid depresion or PTSD if you see that your penis is unable to have a normal erection, you cannot masturbate as in the past, etc.?
I still don’t understand why the histological side (changes in the penile tissue) is still underestimated as the cause of the problem.

#60

Because it isn’t an issue for some PFS guys who still suffer from a host of other effects like brain fog. Therefore it can’t possibly be the root cause of the condition.

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#61

I also had brain fog for a couple of years (I was not even able to tell what I had for dinner the day before…). I am much better now. But the physical problem remains.
In any case, nobody knows exactly what is happening on the physical level either, and no matter how much I insist to urologist and even to people in this forum, nobody seems to care about this issue, and I think they are overlooking something important here.

#62

Totally agree, especially for me everything startet with ed then shrinkage and somehow later the anxiety/depressive issues. I can tolerate anything but the damage of my sexual organs. I don’t understand why there is only little research in that issue. I can’t think about injecting me stuff into my penis or take ed pills above 37,5mg of sildenafil otherwise I get heart palpitations but there is only little effect in that dosage. One time I had to go to the Emergency Room because I took 50mg of sildenafil I thought I had an heart attack. I don’t want to die at least not yet and especially not because of ED pills.

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#63

Did you try low dose Tadalafil? (5mg, at least 6 months).
Even if you don’t have erections, Tadalafil is working to improve blood flow.
Also, did you try vacuum device? After 3 months of daily (proper) use, it can help rehabilitation.

#64

Not yet but I will (tadalafil). But I doubt that I will get the results I’m expecting, I also have tinnitus because of Sildenafil. But it is tolerable.

#65

Why you want getting mechanical erections with drugs?

#66

…Because that is the only way some of us can get erections. It’s not something anyone prefers.

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#67

why would there be serious penile tissue research? I have PFS and almost no penile issues