Finasteride
Propecia / Proscar
Finasteride (Propecia / Proscar) is a hormonal & sexual research compound. Inhibits 5-alpha-reductase type 2, cutting conversion of testosterone to DHT by roughly 65–70% at 1mg. Follicles miniaturise under DHT, so lowering it halts the process in most men.
Finasteride quick facts
| Reported research dose | 1mg daily (hair) or 5mg daily (BPH) |
| Route | Oral |
| Frequency | 1x |
| Half-life | ~6–8 hours, but the enzyme inhibition far outlasts the drug. |
| Forms | Oral |
| Evidence level | Large RCTs for androgenetic alopecia and BPH |
The most effective oral for male pattern hair loss and the most argued-about drug in this space. ⚠️ Sexual side effects occur in a minority in trials; **post-finasteride syndrome** — persistent symptoms after stopping — is reported, contested, and not well understood, and anyone considering this should know that going in rather than after. It lowers PSA by about half, which will mask a rising PSA unless your doctor doubles it. Contraindicated in women of childbearing potential.
How Finasteride works
Inhibits 5-alpha-reductase type 2, cutting conversion of testosterone to DHT by roughly 65–70% at 1mg. Follicles miniaturise under DHT, so lowering it halts the process in most men.
Proposed benefits
Researched for libido, hormonal signaling and reproductive / sexual function.
✅ Clinically validated
- Large randomised trials support it for androgenetic alopecia and benign prostatic hyperplasia. The PCPT trial in over 18,000 men found reduced overall prostate cancer incidence with an apparent increase in high-grade disease — later analyses attributed much of that to detection bias in smaller prostates.
- Post-finasteride syndrome is the live controversy. Persistent sexual and neurological symptoms after discontinuation are reported in the literature and acknowledged on the label in several countries; whether it is a distinct entity and how common it is remain genuinely unsettled.
📊 Correlative data
- Very heavy real-world use with a bimodal reported experience — the large majority report no issues, a minority report significant and sometimes persistent effects. Both of those are true at once and neither cancels the other.
- It halves PSA, so any PSA result must be doubled and the prescriber told.
🧪 Theoretical / extrapolated
- A 5-alpha-reductase type 2 inhibitor, blocking conversion of testosterone to DHT — the androgen driving both follicular miniaturisation and prostate growth.
- 5-alpha-reductase also produces neurosteroids such as allopregnanolone, which act on GABA-A receptors. That is the most plausible mechanistic account of the mood and cognitive symptoms a minority report, and it is why the topical route is of interest — less systemic enzyme inhibition.
These tiers tell you how much human evidence exists — not how well something works. This is the research space, and most of what’s in here is new rather than disproven. Something sitting at “theoretical” usually means nobody has funded the trial, not that the trial was run and failed.
The trap runs the other way too: something can be clinically validated and still do very little for you specifically. A statistically significant result in a study population is not a promise about your body.
- ✅ Clinically validated — human randomised trials or meta-analyses support it. The strongest footing available.
- 📊 Correlative — observational or epidemiological data. Suggestive, and genuinely useful for direction, but it cannot establish cause.
- 🧪 Theoretical / mechanistic — the mechanism is understood and often demonstrated in cells or animals, and the human trial doesn’t exist yet. Unproven is not the same as ineffective. Plenty of what’s standard practice today sat here five years ago.
✗ is a safety flag, not a grade. Where you see it, the concern is harm — not a disappointing trial. A compound tested for one purpose and found not to help there can still be worth studying somewhere else, so a negative result never gets rendered as a cross. It sits alongside the tier, because something can be both well-studied and genuinely risky.
My job is to tell you which one you’re looking at, and let you make the call. Grading something low isn’t me dismissing it — it’s me refusing to oversell it. This is the research space, and being able to reason forward from a mechanism matters as much as waiting for the trial.
Finasteride — safety, predicted from mechanism
Much of this compound class has never been through a human safety trial. Rather than say nothing — or print a generic warning — this is what its known mechanism predicts could go wrong, and what you can do about it. Predictions are labelled as predictions.
What the mechanism predicts
Derived from what this molecule does, not from a trial.
- These block 5-alpha-reductase, the enzyme converting testosterone to DHT. That is the point — DHT drives androgenetic hair loss and prostate growth — and it is also the mechanism behind every predicted problem, because DHT is not only a hair hormone.
- DHT contributes to libido, erectile function and mood. Suppressing it systemically predicts reduced libido, erectile difficulty and mood changes in a minority of users.
- Topical formulations (RU58841, topical finasteride) exist specifically to reduce systemic exposure. They are not exposure-free — measurable systemic absorption happens — but the argument for them is a real one rather than marketing.
What has actually been reported
- Sexual side effects are on the label and reported in trials at low single-digit percentages, typically resolving on discontinuation.
- Post-finasteride syndrome — persistent symptoms after stopping — is reported by a subset of users and remains genuinely contested. Its mechanism is not established, and dismissing it and asserting it are both overstating what is known.
- Finasteride and dutasteride roughly HALVE PSA. A 'normal' PSA of 2.0 on finasteride is effectively 4.0.
How to reduce the risk
Each of these follows from the same mechanism as the prediction.
- Get a baseline PSA before starting, or a later reading has nothing to be compared against and the halving effect hides a real rise.
- Start topical rather than oral if the concern is systemic exposure. Dutasteride inhibits both isoenzymes and has a much longer half-life than finasteride — it is the harder one to reverse quickly.
- Stop at the first sign of persistent sexual or mood change rather than waiting to see whether it settles.
What it does to your bloodwork
A fact about the assay, not a guess about the drug.
- PSA before starting and periodically after — and remember to double the reading for interpretation. Total testosterone, DHT if you want to confirm the drug is doing what you think.
Don't run this if
- You are or may become pregnant, or you are a woman of childbearing potential — these are teratogenic and the risk is to a male foetus. Do not handle crushed or broken tablets.
- You are actively trying to conceive; effects on semen parameters are documented.
The honest unknown
- Whether persistent post-treatment symptoms represent a distinct syndrome, and who is susceptible, is unresolved.
Not medical advice. If you take prescription medication or have a diagnosed condition, check this with a pharmacist or doctor.
Where to get Finasteride
Buy Finasteride at AlgoRx →Finasteride — interference & stacking
Predicted from mechanism, not from an interaction study. There are no trials of these combinations — what follows is what the biology implies, so treat it as a reason to watch something, not as a finding.
What Finasteride moves on your bloodwork
These are the markers this compound is expected to move, and which direction. Knowing that in advance is mostly about NOT panicking: some of these moving is the compound working.
- Complete Blood Count (CBC) with Differential — ↑ expected to rise
Haematocrit and haemoglobin rise — androgens stimulate erythropoiesis. This is the most reliably predictable movement of any compound in the Vault.
What to do: This is the number that decides whether you keep going. Baseline and every 3 months. Dehydration on the draw day inflates it, so hydrate normally or you will chase a false reading. - Total Testosterone — ↑ expected to rise
Expected. Trough vs peak matters enormously — the same protocol reads completely differently depending on when you drew.
What to do: Draw at the same point in the cycle every time or the trend is noise. - LH & FSH — ↓ expected to fall
Suppressed by negative feedback. This is the mechanism, not a side effect — and it is why exogenous androgen shuts down your own production.
What to do: Relevant if fertility matters to you. Worth knowing before, not after. - Estradiol, Sensitive (LC/MS-MS) — ↑ expected to rise
Aromatisation converts a fraction to estradiol, and it rises with the androgen. Use the sensitive (LC-MS/MS) assay — the standard immunoassay is unreliable in men and produces numbers people then medicate.
What to do: If you are reading estradiol in a man, the assay choice matters more than the result. - SHBG (Sex Hormone-Binding Globulin) — ↓ expected to fall
Falls with androgen exposure, which raises the free fraction — so free testosterone can climb faster than total.
What to do: Read total and SHBG together; total alone understates what changed. - Lipid Panel (Cholesterol, HDL, LDL, Triglycerides) — ↓ expected to worsen
HDL falls, sometimes markedly. Oral 17-alpha-alkylated compounds do this far more aggressively than injectable esters.
What to do: Baseline and 12 weeks. ApoB is the better long-term read than LDL-C. - PSA (Total + Free + % Free) — ↑ expected to rise
Androgens can raise PSA modestly. It does not create prostate cancer that wasn't there, but it can unmask it.
What to do: Baseline before starting matters — without it, a later number has nothing to be compared against.
- Which compounds push the same lever, and why the dose adds up faster than people count
- What blunts it — the stacks that waste your money
- What compounds the risk, so a side effect arrives sooner than any one of them suggests
- Coach Cam's read on running it alongside the rest of your protocol
Get the complete breakdown for Finasteride — inside the Academy alongside the full interactive Vault.
Unlock in the Academy — $10/mo →- How to work up to it, and when not to
- When to take it, and why that window
- Cycle length
- Time off between cycles
- Fasted or fed, and when in the day
- Coach Cam's personal notes
Get the complete breakdown for Finasteride — inside the Academy alongside the full interactive Vault.
Unlock in the Academy — $10/mo →Bloodwork to run alongside Finasteride
Run these before you start, and again after 8–12 weeks. A baseline you didn’t take is one you can never go back for.
| Marker | What it’s watching for |
|---|---|
| Total Testosterone | The baseline you can't reconstruct later |
| Free Testosterone | The fraction that does anything — total alone misleads |
| SHBG (Sex Hormone-Binding Globulin) | Explains a normal total sitting on top of a low free |
| Estradiol, Sensitive (LC/MS-MS) | The other half of the ratio, and the source of most symptoms |
| LH & FSH | Separates a testicular problem from a pituitary one |
The Low T? Rule Out the Reversible Causes First panel covers these in one order — 11 markers, $211.50 with the discount applied.
Check results you already have → · All 102 markers A–Z
Finasteride — frequently asked questions
What is Finasteride?
Finasteride (Propecia / Proscar) is a hormonal & sexual research compound. Inhibits 5-alpha-reductase type 2, cutting conversion of testosterone to DHT by roughly 65–70% at 1mg. Follicles miniaturise under DHT, so lowering it halts the process in most men.
Is the full Finasteride protocol on this page?
The reported research dose is on this page, along with how Finasteride works and the evidence behind it. The protocol — how to work up to it, frequency, cycle length, time off, what not to stack it with and Coach Cam's notes — is inside the Academy.
What is the half-life of Finasteride?
Finasteride has an approximate half-life of ~6–8 hours, but the enzyme inhibition far outlasts the drug., which is part of what determines how often it's dosed.
What's the evidence behind Finasteride?
Current evidence level: Large RCTs for androgenetic alopecia and BPH. Finasteride is offered for research purposes only and is not an approved medicine.
Want Coach Cam's exact Finasteride protocol?
Dosing schedules, stacking, cycle timing and my personal notes live inside the Academy — plus the full interactive Vault of 237 compounds & 350 supplements.
Join the Academy — $10/mo →What Finasteride is used for
Finasteride appears under 2 goals in the Vault’s goal router, grouped by the mechanism it works through rather than by how much trial evidence exists. Each link opens that pathway in full, with the alternatives beside it and the bloodwork that tests it.