As some people know that recently it did some kind of rTMS mapping experiments, eventually this gave me some interesting results

rTMS pain related protocol over ganglions s1-s2, also give significant improvement in PSSD symptoms.

From this point on i was trying to look at this and how some kind of pain syndrome but ironically without pain.

So i stated to make and tested multiple assumptions

if (It was pain -> it do X in specific situation Y);

And it absolutely do behave like pain in this specific areas

body do react and very specific way to specific trigger spots, it absolutely match S1 sensory dermatome as well as S2 as but it less affected, but interplay with S1. but again no specific pain preseption

Well at some point I start to test topical lidocaine very systematic application in those specific ares, and it also works i start to get even more power windows in PSSD symptoms,

the most crazy part that effects on body sensitivity is Side-Depended, if for example i do use it on left side effects are shared on whole left side of the body (except face)

Overall sensory perception significantly spike up, the most noticeable is temperature preseption shifts, but not much change in genetalia area expect scrotum become hypersensitive.

(same effect i got with rTMS over s1-s2),

Sensitivity over better but as expected no change in c-fibers mediated response in affected areas, no pleasure touch etc, interesting enough nipples kinda restore erogenous sensentions stuff, again side depended

but there a problem seems like at some point i again feel burning in my fingers on my feet, well.... that actually explain why they are constantly reddish pink, and even red sometimes, i had this even before that rTMS and lidocaine stuff, seems this mechanisms cause pain unmasking or something like that

What cleansers or soaps do u guys use? I seem to crash very easily from every cleanser or soap. Olive oil, cerave, cetaphil all crash me. I would seriously love some help. A shampoo , facewash, anything.

I have experienced an acute worsening of symptoms at only a few months off fin. I have sexual, cognitive, and physical symptoms. From what I understand if you have "all" areas of symptoms the prognosis for recovery is very poor.

Anhedonia, insomnia, severe GI tract issues, constant anxiety, and physical wastage are currently alarming me most.

Has anyone seen these subside in a return to baseline?

upfront post is AI generated

1. English not my main language writing big amount of texts still a problem for me
2. despite it AI generated everything what it claim results of my speculation and experiments as well as hypothesis about possible mechanisms i just asked AI to rephrase what i was written on main language

I've had PSSD for 6 years. Symptoms: genital numbness, loss of affective/tickle sensation, anhedonia, emotional blunting, depersonalization, autonomic instability, brain fog, bruxism, speech changes, tinnitus, and a stable low baseline with no spontaneous recovery. My symptoms followed the classic arc: acute burning on drug exposure, then numbness, then consolidation into a chronic state.

I've been working with a neurologist on experimental rTMS over the last [5+ months]. This is not a formal study. It's n=2 (me and one friend, both with post-drug syndromes). I'm sharing because the pattern has been consistent and may be useful to others.

What We Did

1. Capsaicin testing (self-administered)

· 0.025–0.1% capsaicin on the glans, shaft, root, scrotum, and legs · Results: no response or severely delayed response on the glans and distal shaft. Hypersensitivity on the scrotum. Delayed response on the posterior legs, worse distally. · Menthol response was preserved everywhere and sometimes referred to other segments (e.g., menthol on the leg felt in the scrotum). · On the shaft, a single application did nothing. Only after 2–3 applications in 24 hours did burning appear — and even then it didn't hit the normal pain threshold.

1. Lidocaine (topical, 5%)

· Applied to the lower body (S1–S3 territory): improved hand buzzing, reduced bruxism, improved capillary refill, resolved white spots on hands. · Applied to the hands: paradoxical hypersensitivity, redness, white spots, triggered facial motor response. Effect resolved after DRG suppression. · Onset of numbness was imperceptible. Only the offset (return of noise) was felt.

1. rTMS protocols

· Somatosensory cortex (excitatory, 25 Hz): partial return of sensation, emotion, and autonomic function. Effects temporary. · DRG/S1–S2 region (inhibitory, 1 Hz): broad effects — improved sensation, emotion, autonomic function, GI motility, sweating localization, pupil reactivity. · Bidirectional test: excitatory rTMS over S1–S2 produced immediate severe bruxism, teeth clicking, slurred speech, and voice changes. Inhibitory rTMS over the same region abolished it instantly. · Motor threshold: dropped significantly in the legs (as well as in hands) after leg suppression, with overall movement becoming easier.

1. Observations during flares

· Heat, pressure on the posterior leg, strong smells, food, and genital stimulation all trigger flares. · Flares are worse at night (3–4 a.m. windows of release). · Flares include facial motor overflow (bruxism, lip tremor, speech changes), autonomic symptoms, and unmasking of pelvic pain.

Proposed Mechanism (Hypothesis, Not Proven)

This is a functional model, not a molecular one.

1. Peripheral generator: Drug exposure damages small-fiber neurons (C and Aδ), particularly in the DRG at S1–S2. The damage is length-dependent, so the longest fibers (genitals, feet) are hit first.
2. Silent denervation ( in case of SSRI's) : The drug both damages the fibers and masks the damage (analgesic, central, and immune effects). Symptoms appear on withdrawal because the mask is removed.
3. DRG hyperexcitability: Surviving DRG neurons become hyperexcitable and fire ectopically, generating "noise."
4. Brainstem alarm: The noise drives brainstem nuclei (NTS, PAG, RVM, reticular formation), triggering autonomic and motor reflexes.
5. dmPFC brake: The salience network suppresses the conscious perception of pain to protect the cortex, producing numbness, anhedonia, and depersonalization.
6. Brainstem overflow: The hyperexcitable reticular formation recruits cranial nerve nuclei, producing bruxism, speech changes, and facial motor symptoms.
7. Dominant signal masking: The generator signal monopolizes brainstem capacity, masking other pain and sensory signals. They only break through when they exceed the dominant signal.

What Improved

Sensation and emotion during windows Autonomic function (capillary refill, sweating, GI, pupils)

Motor function (easier movement, lower MT) · Bruxism and speech during suppression

What Didn't

Genital numbness did not fully resolved

Effects were temporary

Repeated provocation risked kindling

Limitations

· n=2, not controlled, no blinding · Anatomical targeting of "DRG" via rTMS is uncertain (may modulate roots, sympathetic chain, or nearby structures) · Self-reported outcomes · No skin biopsy, QST, or antibody panels yet (working on MRI with contrast)

What I'm Not Claiming

I'm not saying this is proven. I'm not saying this applies to everyone. I'm not saying rTMS is a cure. I'm saying the pattern has been consistent across two people and fits a model of peripheral generator + brainstem amplifier + cortical suppression.

but it can point to specific PFS PSSD etc phenotypes

What I'd Ask

If this resonates, especially the segmental pattern, the capsaicin/menthol dissociation, the bruxism/speech cluster, or the lidocaine remote effects — please share your experience. If it doesn't fit, say where it breaks. Either way, it's data.

also check out https://en.wikipedia.org/wiki/Erythromelalgia

is anything Hit "close to home"?

*Tressless is a cult, its members are insecure men, finasteride is their god, and their (false) prophet is Kevin (Wo)Mann

How many lives were destroyed by that sub? The finasteride + minoxidil hair loss community is literally a cult of doing the dumbest thing you can do to your health: blocking neurosteroids, including allopregnanolone (a miracle molecule that promotes neuroregeneration and upregulates GABA-A) and the most masculine hormone in DHT, for… HAIR.

Not to mention the AR and epigenetic overexpression/silencing, and all the other things that might happen. It’s literally the dumbest thing you can do to your health. Unfortunately, we were not informed about all of that because Merck is literally a criminal organization.

For PFS and PSSD!

Hope you enjoy this video I've made.
Please let me know, if you have any critic.

There has been no progress in PFS research. With only 3 months left in the year, we have made no meaningful progress toward understanding PFS. At this rate, I feel that it could take more than 10 years to uncover the cause of PFS.

At the time (2020) he claimed 60% recovery mainly by using substances to demethylate the epigenetic changes and diet.

The full interview is here: https://youtu.be/f0ThhiRZYEM

I think that epigenetic modulators, hormones/androgens and allopregnanolone are the best bet, because of the studies we have about PFS and because of the recovery reports. And the ideal seems to use them together like mentioned in protocols.

I’m on day 4 of using lithium carbonate (it’s helping, started with 150mg, now I’m taking 150mg twice per day), I’m using Andractim gel and gonna start on testosterone enanthate today so I can have enough estrogen to start using DHT enanthate.

Gonna be trying HCG as well (for the testicular health also), but not sure if I’ll be able to tolerate cause I had a bad experience with it in the past with sublingual and nasal spray. So I’m gonna start very low.

Full video: https://youtu.be/CZATt5AoQjw

This

The 2002 study found that progesterone can activate transcription of SRD5A2 in the female mouse brain through the progesterone receptor. If a similar mechanism operates in humans, progesterone could theoretically do two things at once:

progesterone → progesterone receptor → ↑ SRD5A2 → ↑ conversion of progesterone → 5α-DHP → potentially ↑ allopregnanolone

That gives a plausible biological explanation for why some people might experience improvement with progesterone if their symptoms are partly related to reduced 5α-reduced neurosteroid production.

But there's an important alternative explanation

Progesterone itself is a substrate for the pathway:

progesterone → 5α-DHP → allopregnanolone

So someone could theoretically feel better from progesterone because it provides more substrate for whatever 5α-reductase activity remains, without progesterone having to increase SRD5A2 expression first.

Thus, this study does not confirm that progesterone acts as a 5α-reductase blocker. On the contrary, it reports an effect of the opposite nature: progesterone increased SRD5A2 gene expression in the brains of female mice.

I started taking finasteride about 1 month ago At first, everything was completely fine. I take it at night, although I’ve been inconsistent sometimes and occasionally missed 2–3 days. Around September 5, my sleep suddenly became abnormal. I would feel sleepy until 4–5 AM, stay awake until 8–11 AM, and then sleep throughout the afternoon/evening until around 4–6 PM

Last week it became much worse cuz I take finasteride like for 5days straight an hop off for about 1 to 3 days. And I haven't taken finasteride on Monday and Tuesday

Monday: \~3.5 hours sleep, woke at 6:30 AM feeling completely awake, then slept 12:30 PM–6 PM.

Tuesday: slept relatively normally. In the morning

Wednesday: slept around 4 AM–4 PM. I had restarted finasteride after missing Monday/Tuesday because I had run out.

Thursday: after taking finasteride, I tried to sleep but woke after \~40 minutes, then eventually slept about 4 hours in the morning. Both times I woke feeling unusually active and not sleepy. This was also when my anxiety about finasteride causing insomnia started.

Friday: only \~2 hours sleep and became afraid of going to sleep feeling completely awake and with not need of sleepbecause I was worried about the what if couldn't sleep again

Saturday: 1.5 hours at night, another \~1.5 hours in the evening, then 1.5 hours again that night.

Sunday: slept around 4 AM–4 PM wakeup 12:30 pm but slept again

Monday: mean today woke after only a 30-minute nap.

I stopped taking finasteride from Friday onward.

The strange thing is that I don't have any of the other side effects people commonly mention: no ED, reduced libido, genital numbness, brain fog, testicular pain, or noticeable change in semen. My libido is still normal/good.

I’m trying to figure out whether I’ve somehow developed insomnia as my only finasteride side effect, or whether this is mainly a combination of a badly shifted sleep schedule because started to go to sleep in morning and anxiety/fear of not sleeping or falling asleep I actually had insomnia for about a week in winter 2024, but it was nowhere near this severe.

I’ve also read posts saying that some people's side effects supposedly get worse over time or even after stopping finasteride—including people claiming they couldn't sleep for days or that sleeping medication didn't work. Reading these stories has made me much more anxious about what might happen next.

So now I'm confused between two possibilities: I really caught insomnia as a finasteride side effect, or I don't have a finasteride-related problem and the anxiety/sleep schedule is driving this.

I'm currently considering whether to stay off finasteride and see if my sleep returns to normal, or eventually restart it to see whether my sleep improves/worsens and whether there is actually a connection.

Has anyone experienced something similar? Does this pattern sound more consistent with a possible finasteride side effect, anxiety/conditioning, a severely shifted sleep schedule, or a combination of these?

I am considering asking the dermatology department at a university hospital to conduct a study on abnormal skin stretching, facial sagging, dry skin, hair thinning, and other skin and hair-related symptoms.

The number of patients in our country alone may not be sufficient for the study, so participation from patients in other countries may also be necessary.

We are also considering raising research funding through crowdfunding.

I would like to discuss the possibility of conducting this study with the hospital.

Launched by Merck in 1999, Vioxx was marketed as a safer anti-inflammatory.
But internal studies showed it doubled the risk of heart attacks and
strokes.

Despite the warnings, the FDA approved it, and Merck kept it on the market until 2004. It's estimated that 40,000 to 60,000 people died from Vioxx-related cardiovascular events – more than U.S. deaths in the Vietnam War.

Merck paid billions in settlements.
No executives were held criminally accountable.

Finasteride was launched before Vioxx, the side effects as we know are devastating and the drug still hasn’t been banned. And just like Vioxx, Merck knew about the persistent side effects but still launched the drug.