Most tools assume pattern baldness and hand you the same two drugs. Six different things cause hair loss in men and they need completely different treatment. This works out which one you have first, then builds the protocol around it, including how your compounds change what will and will not work.
The pattern is the strongest single clue. Select everything that applies.
Pattern loss, sudden diffuse shedding, seborrheic dermatitis, a nutritional or thyroid driver, alopecia areata and scarring alopecia all present differently and none of them share a treatment. The differential comes first because it decides everything downstream, including whether finasteride is even the right conversation to be having. Reversible causes are checked against the same markers used in the Bloodwork Analyzer, since low ferritin in particular is common and routinely reported as normal when it is not optimal for hair.
Finasteride has exactly one mechanism, blocking testosterone's conversion to DHT, and that mechanism simply does not apply to compounds that are already DHT-derived or that do not rely on 5-alpha reductase to be androgenic. The tool reads your compound history and tells you plainly where a 5ARi has nothing to act on, and flags the nandrolone case specifically, where blocking 5-alpha reductase can remove a deactivation step rather than provide one. Cross-check compound classes against the Gynecomastia Assessment Engine if you are trying to separate androgen-driven effects more broadly.
Reversible causes get corrected first, the core evidence-backed protocol comes second, and adjuncts with thinner evidence are kept separate and honestly labelled rather than blended in as equally proven. The timeline is explicit about the weeks-two-to-eight shedding phase on minoxidil, which is the single most common reason people quit a protocol that was working.
Because six different things cause hair loss in men and they need opposite treatments. Androgenetic alopecia is patterned and gradual, telogen effluvium is diffuse and sudden, and finasteride does nothing for the second. Assuming pattern baldness by default, which is what most tools do, is the single most expensive mistake in this area because it leads to years of the wrong medication.
No, and this is the part almost nothing else accounts for. Finasteride only blocks testosterone converting to DHT. DHT-derived compounds like drostanolone, stanozolol, methenolone and oxandrolone don't need that conversion step to be androgenic, so finasteride offers essentially no protection against them at the scalp.
Potentially, yes, on nandrolone specifically. Nandrolone is 5-alpha reduced into dihydronandrolone, which is less androgenic than nandrolone itself, so that conversion is actually deactivating it. Blocking 5-alpha reductase with finasteride removes that deactivation step, which means it can increase androgenic activity at the follicle rather than reduce it. This is the opposite of what most people assume a 5ARi does.
Because scalp DHT, not serum DHT, is what predicts regrowth, and the two don't move together at the same rate. Dutasteride 0.5 mg reduces serum DHT by around 92% but scalp DHT by only around 51%. Finasteride 1 mg reduces scalp DHT by around 64%. The published efficacy ranking still places dutasteride above finasteride overall, but the serum figure alone is misleading if read as the whole story.
Usually the opposite. Increased shedding in weeks two to eight is old hairs in the resting phase being displaced by new growth underneath, and stopping at this point is the most common reason people conclude minoxidil failed. The tool places this on an explicit timeline so it can be recognised for what it is rather than mistaken for a bad reaction.
