Hair Loss

Hair loss is one of those things men don’t bring up first. They come in for testosterone questions or sleep or low mood, and somewhere in the second half of the visit, usually after a pause, they’ll mention the hairline. Or they won’t mention it and I’ll notice the haircut they’ve been getting for three years to camouflage it. Either way, it’s on the list of things they’re thinking about more than they let on.

The frustrating part of androgenetic alopecia is that we actually know what’s happening. Hair follicles on the top of the scalp are genetically sensitive to dihydrotestosterone (DHT), which is what 5-alpha reductase makes out of regular testosterone. DHT miniaturizes those follicles over years. Each growth cycle produces a slightly thinner, slightly shorter hair, until the follicle gives up and produces nothing. The follicles on the back and sides are mostly DHT-insensitive, which is why bald guys still grow a horseshoe.

Most of the treatments we have work by interrupting that DHT pathway or by keeping the follicle in its growth phase longer. None rebuild a follicle that’s already dead. That’s the timing pressure nobody likes to hear about.

The finasteride conversation, in honest terms

Finasteride 1mg daily is the workhorse. It blocks the type 2 isoform of 5-alpha reductase and drops scalp DHT by something like 60 to 70 percent. About 90 percent of men who take it stop losing hair. Somewhere around 30 to 40 percent get visible regrowth, mostly at the crown, less so at the hairline. The data on this has been steady since the late nineties. It’s not flashy and it’s not a cure, but as far as drugs go for a chronic genetic process, it’s one of the better ones we have.

The conversation that takes up most of the visit is the side effect one. The studies put sexual side effects (lower libido, erectile issues, ejaculatory volume changes) somewhere in the 2 to 4 percent range, with a placebo arm that’s annoyingly close to that number. In clinic the rate I see is in roughly the same neighborhood, maybe a touch higher because people who notice something are the ones who call. Most of the time those side effects resolve when the drug is stopped, and a meaningful chunk of them resolve while still on the drug after a few months.

Then there’s post-finasteride syndrome. A small subset of men report persistent sexual, cognitive, or mood symptoms that don’t resolve after stopping the drug, sometimes for years. The reports are real in the sense that the people reporting them are clearly suffering. The mechanism is unclear. Studies trying to establish causality have been mixed, and the population of men who’ve taken finasteride is large enough that some baseline rate of these symptoms would happen anyway. So you’ve got a real signal that might be a drug effect, might be a nocebo effect amplified by online communities, and is probably some combination of both.

The way I handle it in clinic is to actually tell people this. I don’t minimize PFS and I don’t pretend the data is settled. The absolute risk of a persistent problem appears small, the risk of a transient problem is in the single digits, and the only honest way to know how your body responds is to try it for three to six months and pay attention. If something feels off, we stop. The drug clears in days.

Most of the treatments work by interrupting DHT or by keeping the follicle in its growth phase longer. None of them rebuild a follicle that’s already dead.

Minoxidil, topical versus oral

Minoxidil is the second pillar. It was originally a blood pressure drug, and the hair growth was an accidental discovery in the seventies. The mechanism is still not totally pinned down. It opens potassium channels, increases blood flow at the follicle level, and extends the anagen (growth) phase of the hair cycle. It works regardless of DHT sensitivity, which is why it pairs well with finasteride. Finasteride attacks the cause, minoxidil pushes the follicle to grow harder.

The topical 5% solution or foam, twice daily, is the version most people start with. It works. It also requires daily application for life, can cause scalp irritation, and a lot of guys find the foam annoying to use on dry hair in the morning. Compliance is the actual ceiling on how well topical minoxidil works.

The oral version, 1.25 to 5mg daily, has become a much bigger part of the conversation in the last five or six years. Technically off-label but the data is increasingly solid. It seems to work at least as well as topical, often better, with the benefit that taking a pill is something people actually do. Side effects are mostly cardiovascular at higher doses (mild ankle swelling, occasionally palpitations, more body hair than you wanted) and at hair-loss doses those are uncommon but not zero. I check a blood pressure before starting and I don’t start it casually in someone with heart issues.

Timing, expectations, and what regrowth actually looks like

The single most useful piece of information about treating male pattern hair loss is that earlier is better. A lot better. If you’re in your mid-twenties and you’ve started thinning at the crown, the version of you who starts treatment in the next year ends up with significantly more hair at 45 than the version who waits five years to see how it plays out. The reason is mechanical. Once a follicle has been miniaturized into nonexistence, no medication brings it back. You can only protect what you still have and modestly improve what’s still alive.

I had a patient last year, 31, software guy, came in because he’d noticed his hairline retreating over the previous two years. He started finasteride and topical minoxidil. At three months he was convinced it wasn’t working. At six months his wife noticed the temples filling in. At a year his hair was visibly thicker than the photos he’d taken when we started. That trajectory is the rule, not the exception, and the three-month checkpoint where people get discouraged is the part I spend the most time warning new patients about. Hair grows roughly half an inch a month. You will not see anything meaningful before month four or five. The before-and-after photos that finally convince people are usually somewhere in the nine-to-twelve-month range.

When transplant enters the conversation

Hair transplant is for the back end of the problem, not the front end. The standard surgical approach, FUE in most clinics now, moves DHT-insensitive follicles from the back of the head to the bald areas. It works because those follicles keep their genetic resistance even after moving. What it can’t do is replace follicles in someone whose loss is still actively progressing, because the surrounding native hairs will keep thinning around the transplanted ones and the result looks weird inside of three years.

The honest sequencing is: stabilize medically first, ideally for 12 to 24 months, then consider transplant for the regions that didn’t respond. Surgeons who’ll transplant a 24-year-old without putting him on finasteride first are doing him a financial and cosmetic disservice. I’ve seen the results of that approach show up in clinic looking for a fix, and there isn’t a great one.

For women with female-pattern thinning the algorithm shifts. Oral spironolactone at 50 to 200mg gets used as an anti-androgen, topical minoxidil is first-line, finasteride is off-label. The endocrine workup matters more in women because thyroid disease, iron deficiency, and PCOS show up disguised as hair loss often enough to warrant bloodwork.

The thing about treating hair loss is that nobody finishes treatment. You’re not curing something, you’re maintaining a holding pattern against a genetic process that wants to keep going. The guys who do best are the ones who started early, understood that, and stopped expecting a finish line.