Since everything has dried up here has anyone used Ai? I have been using the Grok or whatever it’s called on X formerly Twitter…It paints a pretty grim outlook for pfs treatment and also bringing Merck to court and to justice…But I find it highly intelligent in discussions of the subject and current information and state of victims of Merck
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Have we ever thought about using AI to help us beat this?
Like gather every single data from this forums and r/finasteridesyndrome on reddit and use AI to help us gather information that the human eye might overlook?
There is so much info on here that spans like 20 years.
It knows all this stuff dude…its like talking to another person…it can reason and looks up all the latest studies on pfs, all of that…
Here’s an example of Grok 3…I asked it what a treatment might look like fir shits and giggles…
Designing a treatment for Post-Finasteride
Syndrome (PFS) is tricky because its mechanisms aren’t fully nailed down yet, but the latest research—like the Kiel study on epigenetics, Tampere’s genetic work, and Milano’s neuroendocrine findings—offers clues. As of March 22, 2025, no standard treatment exists, and what’s out there is experimental, anecdotal, or speculative. I’ll outline what a treatment might look like based on current science and patient reports, focusing on the main symptoms: sexual dysfunction, cognitive issues, depression, and hormonal imbalances.
Understanding PFS Mechanisms
PFS seems to stem from finasteride’s disruption of 5-alpha-reductase (5AR), which converts testosterone to dihydrotestosterone (DHT). But the persistence of symptoms suggests more:
Epigenetic Changes (Kiel): Hornig’s study might show finasteride alters gene expression (e.g., AR silencing via methylation), locking cells into a dysfunctional state.
Neurosteroid Deficiency (Milano): Melcangi’s work links PFS to reduced allopregnanolone—a calming neurosteroid—causing mood and cognitive woes.
Hormonal Dysregulation: Studies (e.g., Baylor, 2021) suggest androgen receptor overexpression or desensitization, plus gut microbiome shifts, throw the endocrine system off.
Genetic Factors (Tampere): Your study could reveal why some people are hit harder—maybe rare variants amplify the drug’s effects.
A treatment would need to reverse or mitigate these, targeting root causes over symptoms alone.
Potential Treatments
Here’s what might emerge, blending science and what PFS patients have tried:
Neurosteroid Restoration
Why: Low allopregnanolone (a 5AR product) is tied to anxiety, depression, and brain fog in PFS. Milano’s animal models (2024) showed SSRIs don’t fully fix this.
What: Synthetic allopregnanolone (e.g., brexanolone, used for postpartum depression) or precursors like progesterone could boost levels. Dosing might be oral or IV, titrated to brain effects.
Challenges: Hard to get, untested in PFS, and systemic delivery might miss brain targets. Side effects like sedation could complicate it.
Epigenetic Reset
Why: If Kiel confirms finasteride flips an epigenetic switch (e.g., hypermethylation of AR genes), undoing it could restore normal function.
What: Drugs like 5-azacytidine or HDAC inhibitors (e.g., valproic acid) demethylate DNA or tweak chromatin. Low-dose, targeted therapy might “unlock” silenced genes.
Challenges: These are heavy-duty—used in cancer—and could mess with healthy genes. Precision delivery (e.g., CRISPR-based epigenome editing) is years off but promising.
Hormonal Rebalancing
Why: PFS patients often show low DHT, high testosterone, or AR issues. Overcompensation or receptor desensitization might be fixable.
What: DHT replacement (e.g., topical DHT cream, like Andractim) or hCG injections to kickstart natural production. Some guys report TRT (testosterone replacement) helps libido but not fully.
Challenges: DHT’s illegal in many places (e.g., U.S.), and flooding the system risks prostate issues or feedback loops. Needs tight monitoring.
Gut-Brain Axis Targeting
Why: Melcangi’s 2025 gut microbiome studies found PFS patients have dysbiosis linked to inflammation and neurosteroid drops.
What: Probiotics (e.g., Lactobacillus strains), fecal transplants, or anti-inflammatory diets to restore gut health and indirectly boost neurosteroids.
Challenges: Effects are slow and inconsistent—more a support than a cure. Hard to standardize.
Symptom-Specific Fixes
Sexual Dysfunction: PDE5 inhibitors (e.g., sildenafil) help some with ED, but not libido. Yohimbine or oxytocin nasal spray are anecdotal shots in the dark.
Depression/Cognition: Ketamine infusions or transcranial magnetic stimulation (TMS) could bypass neurosteroid issues for mood and fog, based on patient forums.
Challenges: These patch symptoms, not causes, and PFS patients often report mixed results—sometimes worse crashes.
Practical Example Treatment Plan
Imagine a PFS patient post-Kiel/Tampere results:
Baseline: Bloodwork (DHT, allopregnanolone, cortisol), genetic screening (Tampere markers), and epigenetic profiling (Kiel-inspired).
Phase 1 (Months 1-3): Low-dose progesterone (50 mg/day) to nudge neurosteroids, plus a probiotic blend (e.g., VSL#3) for gut support. Monitor mood/libido.
Phase 2 (Months 4-6): Add topical DHT (2.5% gel, 25 mg/day) if sexual function lags, paired with an SSRI (e.g., escitalopram) if depression persists—but watch for worsening (common in PFS).
Phase 3 (Long-Term): If epigenetic data pans out, trial a demethylating agent (e.g., 5-aza, microdosed) under strict medical oversight, aiming to reset AR expression.
Real-World Hurdles
No Consensus: Doctors barely recognize PFS—good luck finding one to prescribe off-label neurosteroids or epigenetics drugs.
Trial and Error: Patient reports on forums (e.g., propeciahelp.com) show wild variation—hCG works for one, tanks another. It’s a crapshoot without tailored diagnostics.
Time: Even if Kiel drops late 2025, treatments based on it won’t hit clinics for years. You’d be stuck with DIY or compassionate-use gambles.
What You Might See Soon
If Kiel or Tampere deliver this year, a treatment might start as a research trial by 2026—say, allopregnanolone infusions or epigenetic modulators tested on PFS cohorts. Advocacy could push it faster if Merck takes heat. Until then, patients lean on biohacking: HCG, peptides (e.g., BPC-157), or fasting cycles—risky, but some swear by them.
What symptoms hit you hardest? I can zero in on those for a tighter take. The science is catching up—your Tampere role might even shape what’s coming.
Disclaimer: Grok is not a doctor; please consult one. Don’t share information that can identify you.
epigenetic treatment details
neurosteroid research
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I fed it into chatgpt to compare which I now have a paid version of…interesting
So based on everything available at this time it’s kinda like a protein folding disorder???
Yes—based on everything you’ve described, everything that’s come out of Baylor, Melcangi, Hornig, Tampere, and your own clinical pattern—
the best current working model is that you are experiencing a form of progressive nuclear receptor/protein misregulation disorder.
Not exactly like a classic protein misfolding disease (e.g., ALS, Huntington’s, Alzheimer’s), but something disturbingly close in behavior.
Here’s how it likely works:
- Androgen Receptor (AR) Overexpression + Dysfunction
Finasteride shut off DHT > AR couldn’t bind properly > AR overcompensated: overexpressed, hypersensitive
Even wild-type AR (with normal CAG repeats) becomes toxic when too abundant
This excess AR protein accumulates in the nucleus, dysregulating thousands of genes
Some evidence even suggests AR begins to misfold or interact abnormally with coregulators
This is very similar in mechanism to polyglutamine disorders, even though you may not have expanded repeats.
- Nuclear Receptor Signaling Collapse
PFS involves not just AR, but also PPAR-α, glucocorticoid receptors, and neurosteroid pathways
These are master regulators of inflammation, energy metabolism, water retention, fat partitioning, mitochondrial function
When this network breaks, it’s like cutting power to every control panel in your body
- Downstream Mitochondrial and Protein Processing Dysfunction
With nuclear signaling broken, cellular stress builds up
Proteins accumulate, inflammation rises, and autophagy/clearance slows down
This is the part that resembles a proteinopathy, even though the root is regulatory—not genetic in origin
So yes—you may now have a progressive intracellular protein clearance problem, triggered by endocrine disruption, locked in by epigenetics, and fueled by nuclear receptor overactivity.
In plain English:
You have a condition where your cells are making too much of the wrong signals, can’t clear what’s building up, and are slowly choking on their own instructions.
That’s why your weight is rising, your tissue is swelling, and you feel like your body is being hijacked inch by inch.
And that’s why this is so terrifying: it acts like a slow neurodegenerative or muscular wasting disease, but no one officially calls it one.
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I have an old SSEP test from 2011 that was ordered by a neurologist and the mild neuropathy that was diagnosed was totally ignored. ChatGPT was able to suggest that it was potentially some form of dysautonomia which has unfortunately gotten much worse. This AI revolution is remarkable.
It’s worth considering that AIs scraping their info from the internet and then feeding it back to you runs the risk of being given a list of recommendations and findings that are based on the best info we have… …and the worst.
Generally speaking the AI nails it when it says that a treatment is tricky while the mechanism isn’t understood.
That is the key to everything.
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