Hair Loss: What the Evidence Supports
8 min readReviewed 2026-08-23
Hair loss has a large market and a small evidence base, and the two are not proportionate. A useful starting point is that only a handful of interventions have solid support, and none of them work well on follicles that are already gone.
What androgenetic hair loss is
The common pattern in both men and women is androgenetic alopecia. Susceptible follicles progressively miniaturise under the influence of dihydrotestosterone, a more potent androgen converted from testosterone by the enzyme 5-alpha reductase. Each growth cycle produces a finer, shorter hair, until the follicle produces nothing visible. Two things follow. The susceptibility is largely genetic, and it is regional — which is why the pattern is a pattern, and why hair from the back of the scalp retains its character when transplanted. And the process is progressive, so treatment that halts further miniaturisation is doing the most important part of the job even when nothing appears to change.
Not everything is androgenetic
Before treating, it is worth being confident about what is happening. Telogen effluvium is diffuse shedding triggered a few months after a stressor — illness, surgery, childbirth, significant weight loss, a new medication — and it generally resolves once the trigger passes. Alopecia areata is autoimmune and produces discrete patches. Thyroid disease and iron deficiency both contribute to diffuse loss, and both are readily tested for. This matters because the treatments differ, and because treating androgenetic loss will not help someone whose ferritin is on the floor.
Finasteride
Finasteride inhibits 5-alpha reductase, reducing DHT. It is FDA-approved at 1 mg daily for male pattern hair loss and has the strongest evidence base of the oral options. The trial data describe maintenance and some regrowth in a majority of men over twelve months. As with everything in this area, the effect is on follicles still capable of producing hair. Sexual side effects — reduced libido, erectile difficulty, reduced ejaculate volume — are described in the prescribing information at low single-digit rates in trials, with discontinuation typically resolving them. Reports of symptoms persisting after stopping exist in the literature and are the subject of continuing discussion and disagreement. Mood changes have also been reported. This is a conversation to have with a provider before starting rather than something to discover afterwards. Finasteride is not prescribed to women who are or may become pregnant, because of the risk to a male foetus. Topical finasteride is prescribed in compounded form on the reasoning that systemic exposure is lower; the evidence base is smaller than for the oral product and systemic absorption is not zero.
Minoxidil
Minoxidil was developed as an antihypertensive; the hair effect was an observed side effect. The mechanism is not fully established but involves vasodilation and prolongation of the growth phase. It does not act on DHT, which is why it is often used alongside finasteride rather than instead of it. Topical minoxidil is available over the counter and is FDA-approved for pattern hair loss in both men and women. It requires consistent daily application, and the effect reverses if it stops. Low-dose oral minoxidil is prescribed off-label and has grown substantially in use. Because it acts systemically, it requires screening for cardiovascular considerations, and it can cause hair growth in places you did not want it — the face is the common complaint — as well as fluid retention. It is a provider decision, not an obvious upgrade. An important practical point: both produce a shedding phase in the first weeks to months as follicles are pushed into a new cycle. It is expected and it is the most common reason people stop before the treatment has had a chance to work.
Timing dominates product choice
The single largest determinant of outcome is when you start. Miniaturised follicles can respond; follicles that have been dormant for years generally cannot. Someone starting at the first sign of recession has a materially different prospect from someone starting after a decade, and no choice between products closes that gap.
Assessing change honestly
Hair grows about a centimetre a month and the follicular cycle is measured in months, so meaningful assessment happens over six to twelve months, not weeks. Day-to-day appearance is dominated by lighting, wetness and styling. The reliable method is standardised photography: same location, same lighting, same angle, same dry styling, at fixed intervals. Compare the photographs, not your memory.
What has weaker support
Low-level laser devices have FDA clearance — a different and lower bar than approval — with a mixed evidence base. Platelet-rich plasma injections have small studies with heterogeneous protocols. Ketoconazole shampoo has limited supporting data as an adjunct. Most supplements marketed for hair have no controlled evidence in people who are not deficient; correcting a genuine iron or vitamin D deficiency is a different matter and is worth testing for.
The realistic frame
For androgenetic loss, the honest framing is that treatment is a maintenance programme, not a course. Stopping returns the process to where it would have been. That is a genuine commitment, and it is better understood at the start than discovered at month eighteen.