Dutasteride and finasteride: what suppressing DHT actually costs

Two drugs that do the same thing to different degrees, with a genuine benefit, a genuine and contested harm, and one practical consequence for bloodwork that gets missed more often than either.

Two isoenzymes, two drugs

5-alpha reductase converts testosterone to dihydrotestosterone, an androgen several times more potent at the receptor. It exists as two main isoenzymes: type II dominates in the prostate and hair follicles, type I in skin, liver and sebaceous glands. Established clinical use Finasteride inhibits type II and lowers serum DHT by roughly 70 per cent; dutasteride inhibits both and lowers it by roughly 90 per cent. That is the entire pharmacological difference, and it is a difference of degree.

The half-lives are not a difference of degree. Finasteride clears in hours. The app models dutasteride at about 35 days, which is among the longest in this whole reference, and the practical consequence is that stopping it is not an event but a process: serum DHT takes months to return, and anyone deciding whether an effect is drug-related is working against a very slow washout.

Both are established treatments — benign prostatic hyperplasia for both, male pattern hair loss for finasteride — and the hair-loss efficacy data is solid. This page is not arguing that they do not work. It is about what else they do.

The PSA correction almost nobody is told about

Established clinical use A 5-alpha reductase inhibitor roughly halves serum PSA after six to twelve months of use. That is a drug effect, not a change in the prostate, and it means a PSA drawn on one of these drugs has to be interpreted against that: the conventional adjustment is to double the measured value before comparing it to a reference range built on untreated men.

The failure mode is specific and serious. A man on finasteride with a PSA of 2.0 has an effective PSA nearer 4.0, and a clinician who does not know he is taking it reads a reassuring number. This is why the drug belongs on the medication list handed to whoever orders the test, and why a rising PSA on a 5-ARI — even one still inside the range — is the finding that matters rather than the absolute value.

The contested harm, described accurately

Off-label or community practice Sexual dysfunction — reduced libido, erectile difficulty, reduced ejaculate volume — is a recognised adverse effect and appears in the labelling. What is contested is whether a subset of men experience symptoms that persist after stopping, the cluster usually called post-finasteride syndrome. Reports are consistent enough that regulators in several countries have added warnings; controlled evidence establishing incidence, mechanism or predisposition does not exist, and the studies that have looked disagree.

Two things follow from that honestly. The risk is not zero and not quantified, which means a decision to take one of these is a decision made under genuine uncertainty rather than a settled calculation. And the long washout means a trial period is not really available with dutasteride the way it is with finasteride.

DHT is not a waste product. It contributes to libido, erectile function, and to the androgenic side of body composition, and the DHT page covers what a serum measurement can and cannot tell you about any of that. There is also a teratogenicity point that is not optional: these drugs are hazardous in pregnancy, and the tablets should not be handled by anyone who could be pregnant. Every part of this belongs in a conversation with the clinician who prescribes, before starting rather than after.

How long one dose lasts

Try other intervals on the half-life and steady-state calculator, which runs the same function against whatever cadence you type.

The dosing rows the app records

Established clinical use Reproduced from the app’s reference so you can see what it holds, not as a recommendation. Which row applies to a particular person, if any, is a clinical decision this page does not make — and rows describing supraphysiological or post-cycle use are filtered out before this table is built, so what you see here is a subset.

What the app monitors alongside it

The panel below is the app’s own monitoring note for Dutasteride / Finasteride, verbatim. The analytes in it that have a page here are linked; those pages cover what each one measures, which assay produced it and how to read a trend.

• Total testosterone
• Free versus total testosterone, and the three ways labs get the free number
• DHT (dihydrotestosterone)

Drawbacks and risks the app records

From the app’s own entry, and the first item is the one that deserves the most thought rather than the least.

• Post-Finasteride Syndrome — persistent sexual dysfunction, depression, cognitive impairment in susceptible men (rare but serious)
• Reduces DHT — important for libido, mood, erections
• Dutasteride: very long half-life makes discontinuation slow
• May reduce muscle fullness and body composition
• Teratogenic — women of childbearing age must not handle crushed tablets
• Debate continues on long-term CNS effects

Interaction rules that name Dutasteride / Finasteride

From the app’s interaction data, filtered so no rule naming a compound this site does not publish appears. Not exhaustive, and not a safety clearance: a combination that is not listed is one nobody has documented here, which is not the same as one that is fine. The combination checker has the rest.

Questions people actually ask

Is dutasteride simply stronger finasteride?

It inhibits both isoenzymes rather than one, so it suppresses more DHT, and it has a far longer half-life. "Stronger" is accurate for the suppression and misleading for the decision: more complete suppression is more of whatever you wanted and more of whatever you did not, and it is much harder to reverse.

Does it interact with testosterone therapy?

The app records a rule about the combination and it is in the interactions section on this page. The mechanism is straightforward — testosterone therapy raises the substrate, a 5-ARI blocks the conversion — and the reason people combine them is hair. What that costs is the subject of this page.

Can the dose be lowered instead of stopped?

Intermittent and reduced-dose schedules are described in practice, on the reasoning that suppression is dose-related. Whether that is a sensible course for a particular person is a prescribing decision, and with dutasteride the long half-life blurs what "intermittent" even means.

How long until DHT recovers after stopping?

With finasteride, days to weeks. With dutasteride, months — five half-lives at the modelled figure is roughly six months. Any assessment of whether an effect was drug-related has to be read against that timescale.

Where the load-bearing numbers come from

Named rather than linked. Publisher URLs move, and a citation that resolves to a 404 two years from now is worse than one you can search for by name — every entry below is findable from the title and year alone.