Finasteride stops baldness; user claims EMA admits suicide risk
Is it worth risking libido, mood, and brain chemistry to keep your hair? This question has circulated quietly among those treating alopecia for years. Now, one participant provides uncomfortable backing by citing the European Medicines Agency (EMA): according to their version, the agency confirmed in 2025 that finasteride can cause suicidal ideation as a recognized adverse effect. The same participant adds that for dutasteride, which acts on the same hormonal pathway, evidence is less conclusive with no direct link established, though close monitoring was recommended. For some thread participants, the verdict is blunt: the drug is trash.
The treatment slows hair loss by inhibiting the enzyme that converts testosterone into DHT, the hormone that miniaturizes trinc in those with genetic predisposition. It works. And precisely because it works, it is hard to stop.
Why do some patients consider finasteride poison?
The mechanism is known. The drug blocks the conversion of testosterone into dihydrotestosterone and reduces its production. According to a calculation circulating among critics, this reduction is systemic and around 70%, dragging down neurosteroids like allopregnanolone. The central argument is that this is not just a hair problem but a brain chemistry issue: DHT receptors are also in the brain, and they are there for a reason.
Against this stands the experience of those who have taken it for decades without noticing anything. A specific case cited is a participant who claims to have used Propecia and liquid minoxidil since 1999—switched to 2.5 mg capsules about five years ago—without any side effects: semi-annual blood and urine tests, ultrasounds, and almost daily exercise. Their conclusion is that it affects some people and not others. The rebuttal arrives immediately: without a control group, comparing oneself to oneself is a useless exercise. Hence another participant's proposal: compare 1,000 men who have never taken it with 1,000 others who have been taking it for more than a decade.
What is attributed to the EMA and what is post-finasteride syndrome?
According to the participant citing the EMA, the agency confirmed suicidal ideation as an adverse effect of finasteride in 2025. Dutasteride remained under close surveillance due to operating on the same pathway, although no direct proven link exists. Added to this is so-called post-finasteride syndrome, described by those experiencing it as a disconnection from the hormonal axis: loss of libido, less pleasurable orgasms, mental fog, mood changes, or apathy. Hardest testimonies speak of being anesthetized, antiestéticarful, and sensual unresponsive, losing diffuse sensations that previously gave pleasure.
It is useful to separate this noise from data: serious adverse effects, though rare, are reported by those who suffered them. The repeated explanation is individual sensitivity: some argue that a single pill can leave sequelae in genetically predisposed individuals, and this greater vulnerability has been given a specific name.
The Istanbul mirage: transplants don't free you from pills
Here is one of the most useful points in the discussion. Popular belief says transplanted hair, extracted from the nape, is immune to DHT. This is a misunderstanding. Hair from the donor zone resists DHT there, but when reimplanted in a predisposed area, it is exposed to local DHT. Without supportive medication, the result can be a bald spot crowned by a ring of hair, forcing another surgery.
The defended protocol is different: stabilize the area with treatment at least a year before surgery, operate afterwards, and maintain medication—presumably for life—to preserve gains. The ticket to Istanbul appears in the thread as an alternative; however, the bill for the pill prolongs.
Is minoxidil the only option without hormonal damage?
Minoxidil is a vasodilator, not an antiandrogen. Its mechanism is different: it improves irrigation and nutrient supply to the trinc, making it more resistant to DHT. It does not stop androgenetic alopecia, it delays it, like other approved drugs. Defenders emphasize this milder profile compared to hormonal inhibitors, using both topical and oral versions; the latter, according to some users, in 2.5 mg capsules prepared as compounding formulas in pharmacies due to lack of commercial presentation.
Its effects are not neutral either, according to those taking it: it thickens body hair, including nails. And it leaves an uncomfortable doubt running through the conversation: if minoxidil is not as potent as finasteride or dutasteride, how effective is it alone?
Why new drugs aren't arriving
The repeated answer in the thread is economic. Minoxidil had negligible development costs, born from an almost accidental discovery, and is no longer patented, so according to these users, nobody is interested in pushing it as a main solution. The industry bet is different: finding new molecules that do not touch the hormonal system. Lines are reportedly in development, though with no confirmed results visible.
Meanwhile, the market lives off a comfortable paradox: the treatment that works generates doubts, and the one that barely bothers barely convinces. Everyone waits for the perfect pill. Nobody has seen it yet.
With available evidence, each person decides what they pay for hair with: money, patience, or chemistry. Meanwhile, according to these accounts, the industry is in no hurry.
Summary of a discussion on Burbuja.info - Foro de economía, actualidad y política., translated from Spanish and reviewed before publication.
Read the full discussion (175 replies).
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