Another article about Finasteride induced depression, sexual issues, and suicide.
VERY IMPORTANT to note that there is an email address for a journalist looking for stories about Finasteride adverse reactions.
Zoe Hardy: zoe.hardy@dailymail.co.uk
Also, there is the daily mail comment section, get stuck in there if you can lads.
Just wondering if there's any cases where anyone's heart reverts back to normal. I've been dealing with this symptom without medication for over a year now without any progress.
As mentioned on SIDEfxHUB, anyone aware of current progress?
The Milano Project aims to:
- Complete 7 human investigations on PFS and PSSD by the end of 2026
- Identify biomarkers proving the biological basis of these conditions
- Map how finasteride and SSRIs disrupt neurosteroid synthesis, including allopregnanolone
- Build the foundation for human clinical trials in Italy
- Share all data with qualified researchers worldwide
So I’ve been reading on this sub that there’s a lot of reason for hope. In the comments, I asked what new developments there actually are, but I haven’t gotten a clear answer. Are there any new initiatives that genuinely justify this optimism?
Concretely, we have the PFSN studies on the background, but it’s unclear what they will yield. There’s also Dr. Powers’ theory, which still needs proper research to even get off the ground. The proposed castration-based therapy sounds very risky. Status of Melcangi’s research is unclear to me, and his suggested treatment with zuranolone has unfortunately already been tried without success. My humble opinion, these 3 ‘projects’ each, do not seem te be anywhere near safe and reproducible treatment for pfs.
Given all the optimism I’m reading here, I’m wondering if I’m missing any other initiatives beyond these three?
I want to echo this. Regardless of differing opinions about the PFS Network, I believe they’re genuinely focused on patient wellbeing.
There is clearly a lot to look forward to as more researchers take an interest in exploring potential genetic predispositions and biomarkers of PFS. At the same time, many of them have responsibly stated that much of this is still experimental and in the theory phase.
People need to understand there is always risk when experimenting, especially with compounds or interventions that may impact androgen signaling, even if they seem benign. I don’t personally encourage experimentation given what we’ve seen. At the same time, I understand the deep level of desperation many of us feel to regain our health, and why some people choose to go down that path. I can tell you from experience that just when you think it can’t get worse, it can. If you do choose to experiment, it’s critical to approach it with extreme caution and a clear understanding of the risk. Too many people have gotten worse.
Despite what some may think, we’re in a pivotal moment. Awareness is growing, people are starting to take this seriously, and we have incredible scientists and researchers investigating this.
Please know there is real hope right now. But it’s also really important that we maintain the discipline to keep speaking out, supporting one another, and contributing to the research that’s moving this forward.
Stay strong, and above all, please stay safe.
Unfortunately I have discovered a small lump on my right testicle. I very conveniently have a urologist appt scheduled for this Tuesday and that will obviously be the focus of my appt.
My question is do any of you have experience with this and PFS? It certainly could be a tumor (cancerous or benign), but I’m also seeing online that other common causes are varicocele or fluid buildup. I’ve had testicular fullness/vein issues since I got PFS off one pill 6+ months ago so the buildup of that would maybe make sense (hopefully).
It’s kinda hard to describe but sometimes it feels like it’s just a small pea sized lump and then other times it feels less like a small lump and more that the surrounding area is inflamed or just messed up a bit.
Probably not a large group of ppl that can comment on this but just curious since I just noticed it today.
Hi,
If you’re a woman with PFS let’s get in touch.
I’m researching how this medication affects cis women’s fertility but there are so few that there is almost no data to work with.
Whether you took finasteride, saw palmetto, spiro or something else it doesn’t matter as long as you got the syndrome.
If you see this, please comment or DM me!
I should say upfront: none of this is a cure. It's just a collection of things that have helped me survive and, in some cases, regain a bit of function.
I've been dealing with severe PSSD for about 6 years now, triggered by escitalopram. Over time I've had to figure out my own approach because the medical system in my country has been hostile (they tried to label me schizophrenic at one point). I finally found a neurologist who is open-minded and willing to look at my documented evidence, but most of what I do is still self-directed out of necessity. I wanted to share the rough protocol that I've slowly put together, in case any of it is useful for others to discuss with their own doctors.
As symptoms goes i have ("Full Blown PSSD") - this means all of it.
The model I've been working from is based on the idea that SSRIs like escitalopram are possibly mitochondrial toxins. There's some published research showing they can inhibit Complex I of the electron transport chain, at least in vitro. In a susceptible person, that might cause an energy deficit in the longest, thinnest nerve fibers—the C-fibers—leading to a kind of length-dependent small-fiber neuropathy. This would likely affect axonal transport, so the delivery of ion channels like TRPV1 (the capsaicin receptor) to the nerve endings slows down or stops. That might explain the selective sensory loss pattern a lot of us see, like a delayed or absent capsaicin response but a preserved menthol response, because TRPM8 seems less dependent on that transport pathway. The autonomic problems like orthostatic hypotension could be from damaged C-fibers failing to help constrict blood vessels properly. That's my best guess, anyway; it's hard to prove.
Given that framework, my stack has a couple layers.
First was, tranylcypromine (Parnate). It's an older MAOI antidepressant. Without it, I can't even get out of bed. It doesn't fix the PSSD symptoms, but it keeps the baseline depression at a level where I can function. It seems to be a lifeline for me. Yes Serotonin but in my case don't cause worsening of PSSD symptoms but helps depression and cognition
For the orthostatic hypotension and blood pressure crashes, I stumbled onto fludrocortisone. It's a mineralocorticoid that expands blood volume. My labs showed high renin with inappropriately normal aldosterone and high hematocrit, so it looked like I was chronically hypovolemic. Fludrocortisone brought my resting heart rate down from the 90s–100s to the 70s–80s, which was a clear sign it was doing something. Combined with iron supplements (my ferritin was suboptimal), it made the orthostatic stuff more manageable.
Then there's the rTMS Not just classical rTMS for depression - I've been mapping my own cortex, essentially. The most dramatic response is from the motor cortex; stimulating the hand area makes my tremor and weakness disappear on the contralateral side almost instantly, which my neurologist saw. That was huge because it showed the problem isn't just psychiatric. The frontal pole stimulation, targeting orbitofrontal and rostromedial prefrontal areas, seems to bring back smells, tastes, hearing clarity, and even a bit of libido for a while. The somatosensory association area stimulation is intense - it improves bodily awareness and multisensory integration for up to two days, but the session itself causes overstimulation and a crash. It seems like those higher-order sensory integration hubs are intact but in some kind of hibernation, probably from lack of input.
I also use mitochondrial support. A mix of peptides - SS-31 for cardiolipin stabilization, MOTS-c for biogenesis, Humanin for anti-apoptotic protection, and BPC-157 for nerve repair and angiogenesis. And BAM15 as a pulsed, very low-dose mitochondrial uncoupler, which seems to create a hormetic rebound. I've noticed that after a meal, I no longer get the crushing postprandial fatigue; instead I have a little more energy, which is a big change.
It's a long story i also use PEA+TCP , but PEA itself made me worse - caused paradoxical hypotension and weakness, likely because my peripheral norepinephrine stores are depleted. But its N,N-dimethyl derivative (N,N-DMPEA) had a positive effect, possibly because it bypasses the broken nerve terminals and acts more directly.
All of this is documented with detailed notes, lab tests, and videos. My neurologist is now on board and we're pursuing skin biopsy, QST, and autoantibody panels to try to get objective evidence of SFN. The capsaicin test with its delayed length-dependent response was the key that got him to take me seriously.
I don't know if any of this will help others, It's possible some of these ideas are off base, and I'm just one person self-experimenting under absurd circumstances. But maybe some of it might spark a useful conversation with a doctor or a researcher.
I as me for evryoine else think rTMS a very first priority thing to try for this all
As effect for me goes:
(TCP>rTMS>PEA>PEP)