I’m with you there @Barnabas I’ve experienced the same side effects on Dutasteride 0.5 mg.
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Maybe take with tadalafil?
Again, I never had ED issues as a 33 years plus user nor my son a user of 3 years - he is 34 years old. For the majority - reseach says no issue. Not impossible. Worth trying.
Prevalence and Persistence
- Low risk for most: The risk of developing ED with finasteride is generally low.
- Possible persistence: While most instances of sexual dysfunction resolve after stopping finasteride, a small group of men report persistent symptoms that are difficult to treat.
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I don’t think it’s a matter of the drug being good or bad. Side effects happen to some people and not others, and if it works well for somebody without side effects that outweigh the benefits that’s great. I don’t think I need tadalafil. Maybe when I am older. For me getting my libido crushed was kind of a blessing more than a curse. I basically just stopped being an eternal eighth grader having a cartoon wolf moment once or twice a day.
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I’m still waiting for causal case reports where the patient isn’t suspected of being mentally ill 
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Dutasteride has given me endurance. Intimacy with my wife has gone from a sprint to a marathon.
I prefer it this way. 
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Reduced Screening May Have Led to Rise in Advanced Prostate Cancer Diagnoses
Changes in screening recommendations over a decade ago may have inadvertently resulted in later diagnosis of the most common cancer in men, a new study has found.
Prostate cancer diagnoses have been rising in recent years, with a sharp increase in cases diagnosed at advanced stages, when it is harder to treat, according to a new report by the American Cancer Society. Many experts attributed the increase to a guideline change made over a decade ago that discouraged routine screening for the common cancer.
The new analysis also highlighted racial disparities that have persisted, despite overall declines in mortality. Black men develop prostate cancer at significantly higher rates than white men and die at twice the rate of white men. Native Americans die at higher rates although they have a lower incidence of the disease.
The report, published on Tuesday in the medical journal CA: A Cancer Journal for Clinicians, underscores the challenge of finding the right balance in cancer screening: Screen too much and you may end up causing harm by aggressively treating indolent disease that will never be life-threatening; screen too little and you may miss deadly disease.
In 2018, the task force said screening should be an individual decision for men 55 to 69 and should stop altogether at 70. The latter recommendation has given many doctors pause, now that men are living longer and could benefit from treatment even if they are in their 70s.
Many experts in the field say that reducing routine screening may have inadvertently led to a bump in severe disease.
Prostate cancer is the most common cancer affecting men, making up almost one-third of the cancers diagnosed. It is the second leading cause of cancer death for men after lung cancer. Some 313,780 cases of prostate cancer are expected to be diagnosed in the United States this year, and about 35,770 men will die of it.
Full story:
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I had a TURP 5 years ago for BPH and now my prostate has regrown to 52cc in size. My GP has prescribed Flomax 0.4mg and Finasteride 5mg. I have some concerns regarding side effects but I’m running out of non-invasive options.
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Have him prescribe tadalafil too. If you’re concern about ED. It a solid life extension medication and should put to bed (literally) any performance concerns.
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And maybe consider at least low-dose testosterone replacement/optimization which could help to offset potential finasteride side effects on mood, as long as the extra testosterone wouldn’t prevent your prostate from shrinking (if it did, it would be the T itself not DHT since you have that conversion blocked).
If you’re being managed by someone who knows what they’re doing, hopefully you could get it all dialed in and get the positives without the negatives.
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Find a good HOLEP surgeon in your area and fix the problem. You won’t regret it.
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This is quite interesting… for prostate health. Has anyone every tried this or heard of it?
For the management of Benign Prostatic Hyperplasia (BPH) and associated Lower Urinary Tract Symptoms (LUTS)
Based on clinical trial data and pharmacognostical reviews, the following dosage protocols for Urtica dioica root (rhizome) have been established for the management of Benign Prostatic Hyperplasia (BPH) and associated Lower Urinary Tract Symptoms (LUTS).
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Yes. I am on it. It is part of my polypharmacy to counter BPH and small lesions (benign?). Dutasteride 0.25 mgs is lead actor. Supporting cast - Pygeum extract, Stinging nettle extract, Saw Palmetto berry extract, lycopene, sulphoraphane and black cumin seed extract. Results (most likely due to dutasteride) shrunk my prostate from 39 to 24! Decimated my DHT from 520 to 3.6!! Going to revise my strategy in 2026.
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I’m asking myself: what are the countermeasures for known DHT-lowering side effects when taking 5α-reductase inhibitors like finasteride?
Erectile Dysfunction: DHT is more potent than testosterone at activating nitric oxide synthase in penile tissue. Less DHT = less NO = weaker erections. → Tadalafil + L-Citrulline: Tadalafil is FDA-approved in combination with finasteride for BPH; L-Citrulline converts to L-arginine and increases NO production.
Low Libido: DHT activates androgen receptors in the brain controlling sexual desire. Reducing it weakens central arousal signaling. → Zinc: Zinc inhibits aromatase enzyme, preventing testosterone-to-estrogen conversion and maintaining favorable androgen balance.
Depression: DHT reduction depletes allopregnanolone - a neurosteroid that calms the brain via GABA-A receptors. Low levels = mood instability. → Pregnenolone + Magnesium Glycinate: Pregnenolone is the upstream precursor to allopregnanolone; magnesium is a positive allosteric modulator of GABA-A receptors, enhancing their sensitivity.
Gynecomastia: Blocked DHT pathway pushes more testosterone toward estrogen conversion. Elevated estrogen = breast tissue growth. → DIM: DIM shifts estrogen metabolism toward 2-hydroxyestrone (protective) over 16-hydroxyestrone (proliferative), reducing estrogenic tissue stimulation.
Anything else on top?
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While this is true, guess which enzyme is responsible for converting pregnenolone to allopregnanolone?
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Thank you, @Davin8r, was not obvious for me.
So if you’re on finasteride, adding pregnenolone won’t restore ALLO because the 5α-reductase step is blocked.
A more mechanistic alternative for „depression side effects from finasteride“ could be PEA (palmitoylethanolamide): via PPAR-α it can upregulate steroidogenic machinery (e.g., StAR/P450scc) and has evidence of boosting neurosteroidogenesis/ALLO signaling in glia when 5α-reductase activity is still present (even on finasteride it is not completely inhibited) plus it buffers symptoms through anti-neuroinflammatory “entourage” effects even if ALLO remains partly suppressed ( anti-inflammatory, mast cell calming, endocannabinoid/TRPV1 modulation). Just hypothesis - will try it in my n=1.
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That’s an interesting hypothesis! I happened to have just started PEA a couple of days ago for some chronic low back pain.
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Always important to remember that finasteride, in humans, does not affect 5ar type 1 enzyme to any significant degree so neurosteroid production in the brain will not be affected. Serum allopregnanolone is only affected because apparently the spine also produces allopregnanolone via the 5ar type 2 enzyme.
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Link to query with full clickable reference list: