Hair Loss Questions, Answered

The question

I would love your input on the recent study on RU58841, “Investigation Into the Metabolism and Elimination Behavior of RU 58841, and Its Influence on the Steroid Profile in Humans” (Okutan et al., 2026). The researchers found that topically applied RU enters systemic circulation, and found several metabolites, some detectable in urine for several days. I have personally used RU for several years and it has yielded good results, but this, although quite a small study, made me think I might consider a different anti-androgen, or even topically applied finasteride. So basically I am wondering if the results change our perspective on long-term safety. I know most medications metabolize and that alone does not need to be alarming. Systemic absorption does not equal toxicity, and from what I understand most of the metabolites identified are known and not known to cause cancer, autoimmune disorders or heart complications.

Asked by Toyn

The answer

You have read this closer than almost anyone who has sent it to me, and I want to start by saying where I think your reasoning is right, because most of it is. Then I want to correct one piece of it, and then tell you why the paper does not answer the question you actually asked. It is a good paper. It is just not a safety study, and the authors never claimed it was.

Since a reader sent me this paper two weeks ago the full text has come out from behind the paywall, so I have now read the results rather than just the title, and I can put numbers on it.

What the study actually was. Six healthy men. One single application of 1 ml of an RU58841 hair serum to the scalp, 30 mg of drug, and then blood and urine collected for seven to ten days. It came out of the Institute of Biochemistry at the German Sport University in Cologne, and the question they were asking was an anti-doping question: if an athlete uses this, what shows up in a sample, for how long, and does it disturb the steroid profile that doping control reads. Hair was not the point. That is worth holding onto, because it explains what the study measures well and what it does not measure at all.

On absorption you are completely right, and this is the real result. The intact parent compound was found in dried blood spots in all six men. It climbed fast, peaked inside the first twelve hours, and the highest concentration they measured was around 5 micrograms per millilitre. Five metabolites turned up in urine, and the glucuronide ones were still detectable at roughly 213 hours, which is about nine days. The authors’ own phrase is “considerable systemic exposure.” The earlier preclinical work, Pan 1998 in macaques, had suggested systemic exposure was limited. In humans, that is now wrong. So the line you have heard a thousand times on forums, that it is topical so it stays on your head, is finished. It was never a finding. It was a hope, and somebody finally checked.

Now the part where I have to push back, and it is the metabolites. You wrote that most of the metabolites identified are known and not known to cause cancer, autoimmune disorders or heart complications. The second half of that sentence is doing much more work than it looks like. These are the first human metabolites of RU58841 ever characterised. That is what the paper is for. Two of the six had been seen before, in an animal study from 1994. The other four are new. So “not known to cause” those things is not a safety result, it is the absence of anyone having ever looked. In a licensed drug those two statements are close enough to each other to treat as the same. In a compound with no human trial and thirty years of nobody funding one, they are completely different statements, and the gap between them is the entire risk.

One detail in there is worth your attention rather than your alarm. One of the new metabolites is an acyl glucuronide, and the authors flag that class themselves as chemically reactive and suspected of contributing to drug toxicity, while saying in the same breath that direct in vivo evidence for that is scarce. I am repeating that with both halves attached, because the first half on its own would be scaremongering and the second half on its own would be a dismissal. It is a thing to watch, not a finding.

The genuinely reassuring result, properly fenced. The steroid profile did not move. Not in any of the six men, not on any of the markers, including the ratios that are most sensitive to testosterone use. That is better news than you might expect, because blocking the androgen receptor normally lifts luteinising hormone and testosterone through the feedback loop, and that is exactly the kind of disturbance they were looking for. It did not happen. But read the fence: one dose, six men, three baseline samples, and the authors describe their own finding as preliminary and call for confirmation in larger groups.

And here is why none of it answers your question. You asked about long term. The study dosed once. Blood levels were back near baseline by 36 hours. The authors say the thing you are asking about in plain words: RU58841 is intended for long-term use, repeated daily use may produce cumulative or steady-state endocrine adaptations through feedback, and longitudinal studies are needed to determine the endocrine effects of chronic daily use. Your question is the open question the paper names on its way out. Nobody has run it. That is the honest answer, and anybody who tells you this paper cleared RU58841 for long-term use, or that it condemned it, has not read past the abstract.

I will put my own position in the same frame rather than leaving it implied. I run considerably more than this study gave, and I run it every night rather than once. So the arithmetic in that paragraph is about my head too, and I have no more data on it than you do. I also earn a commission when somebody buys RU58841 through my links, which is exactly why I would rather tell you what the paper does not show than let you read reassurance into it.

The detail nobody is talking about, and the one I would act on this week. They tested the product before they used it. The serum they bought online was labelled 50 mg per millilitre. It measured 30 mg per millilitre. Sixty percent of label, in the one bottle anybody has bothered to assay in a published paper. Nothing else was contaminating it, which is something, but if you have used RU for several years and tracked your dose carefully, that single line should unsettle you more than the metabolite list does. You do not know your dose. You know what the label says.

On switching. If you move to topical finasteride because this paper showed systemic absorption, you have not solved the problem you think you have solved. Topical finasteride is systemically absorbed too, that is well documented, and it measurably lowers serum DHT. Absorption is not the thing that separates them. What separates them is that finasteride is a licensed medicine with decades of post-marketing data and a side-effect profile you can actually look up and argue with, and RU58841 has one human pharmacokinetic paper and nothing else. That argument for finasteride was true before this study and it is true now, at the same strength. What the paper changed is not the risk, it is how concrete the unknown feels. If that moves you, it is a reasonable thing to be moved by. Just be clear that you are acting on an absence of data rather than on a finding of harm, because those call for different amounts of panic.

Credit where it is due: you found the paper, read the results and worked out most of this yourself before you wrote to me. That is the standard, and if I have got something wrong here, that is how it gets fixed.

RU58841 is not a licensed medicine anywhere, there is still no human efficacy trial behind it, and nothing on this page is medical advice.

Where this paper first came up: have you seen the 2026 RU58841 study? What I run and why, with the commissions disclosed: my protocol.

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The question

I am about to place my second order. My original order was two bottles each of RU58841 and JXL069. Since you have a lot of experience with these products, do you consider one more important than the other? Should I buy an equal supply of each, or do you see RU58841 as more important, and buy say 75% RU58841 and 25% JXL069? Also, how important is pyrilutamide? Should that be included as well? I am about to be 64. I have hair all over the top of my head, it is just quite sparse.

Asked by a reader

The answer

There is an answer to the ratio question, but it sits underneath a more useful one, so let me take that first. A percentage split assumes the two things are interchangeable and that you are trading some of one for more of the other. They are not interchangeable. They do different jobs by different mechanisms, and more to the point they do not want the same schedule, and once you see that, the split more or less decides itself.

What each one is doing. RU58841 is an androgen receptor antagonist. It sits on the receptor in the follicle and stops androgens from signalling there. It is defensive, and it is aimed squarely at the thing causing your hair loss. JXL069, which carries the proposed name suvomipic, has nothing to do with androgens at all. It inhibits the mitochondrial pyruvate carrier, which is a metabolic switch inside the follicle, and the idea is to push follicles into a growth phase. So one is holding the line and the other is trying to start something. They are not competing for the same slot in your stack, and that is the whole reason the ratio framing misleads.

Now the schedule, which is the part that answers you. RU58841 is a competitive, reversible blocker. It works while it is sitting on the receptor and it stops working when it is not. Skip a night and the androgen has that receptor back for the night, and your hair loss is a process that runs every hour of every day whether you treated it or not. The MPC inhibitor evidence points the other way entirely. In the one human trial of that molecule, dosing ran for four weeks, and the density response showed up at week eight, four weeks after dosing stopped. Whatever that is, it behaves like a trigger rather than a blockade, and a trigger tolerates gaps in a way a blockade does not.

So the version that fits the mechanisms is RU58841 every night, JXL069 every other day on top. Which turns your question into something easier to shop for: buy enough RU58841 that you never have to skip a night, and buy JXL069 at whatever cadence the money allows. If the budget forces a lean, lean toward RU58841, and not because it is the better compound. Because intermittent androgen blockade is the one where skipping actually gives something back to the condition. Intermittent JXL069 is just a slower schedule.

Two honest fences around the JXL069 part, because I would rather you heard them from me. What is solid is that JXL069 and suvomipic are one molecule with one registry number. Whether the compound in the Pelage trials is also that molecule is not something anybody has confirmed, because the structure was never disclosed, so I am describing the trial of a molecule and not making a promise about a product. And molecule identity is not product identity either way: that trial used an engineered 0.05% gel built for follicular penetration, which is not the same drug as a solution in a bottle even when the molecule matches. A registry number also tells you nothing about what is actually in your vial without a batch certificate of analysis.

On pyrilutamide, the answer is cleaner than you would expect. Pyrilutamide, KX-826, is a topical androgen receptor antagonist. That is the same mechanism as RU58841. So of everything on your list, adding it to RU58841 is the one combination that makes the least sense, because you would be buying two drugs to compete for the same receptor and paying twice to occupy a site that is already occupied. It is an alternative to RU58841, not an addition to it.

It is a serious alternative, and in one respect a better-evidenced one. It is the only compound in this class with real company-run human trials behind it, and Kintor reported a positive Chinese phase 3 in 2026, in the region of ten hairs per square centimetre over placebo at 24 weeks. Keep the caveats attached: that is company-reported rather than published in full, and it is not approved anywhere yet. My own experience is one head and not evidence, but since you asked: I ran pyrilutamide in 2023 and stopped it after a shed. I would not read anything into that beyond what one head is worth.

The gap I would actually point at in your stack. You have two topicals, you are asking me about a third, and nothing you have described works from the inside. The foundation of my own protocol is not a topical, it is a 5-alpha-reductase inhibitor, and that is a prescription conversation with a doctor rather than an order you place. Worth knowing the real number before you have it: Olsen 2006, 416 men, 24 weeks, dutasteride 0.5 mg a day dropped serum DHT by 92% but scalp DHT by only 51%. That is the figure that matters for your hair and it is almost never the one quoted. Even at 51% it is working across your whole scalp every hour, which is something no solution you spread by hand at night does evenly. Finasteride is the usual and gentler starting point of that conversation. Both are a doctor’s call, not mine.

And on being 64 with sparse hair all over the top. That is the better version of this situation, not the worse one, and there is a specific reason. The best RU58841 evidence is still Brouwer 1997, human balding scalp grafted onto mice. After six months the number of actively growing follicles was the same in both groups, 28 against 29. What changed was how many follicles went on to enter a second growth cycle, 7% on vehicle against 28% on the drug. It did not wake anything up. It changed what happened when a follicle finished a cycle and began the next one. Which means it needs follicles that are still cycling to work with, and hair all over the top that is merely sparse is exactly that. A scalp that has gone smooth has nothing left for it to act on.

The other half of that, said plainly because you are 64 and deserve it straight: some of those follicles have been miniaturising for decades, and nothing in this conversation reliably brings back a follicle that is already gone. Holding what you have, and thickening what is thinning, is the realistic win. Judge it on photographs in the same spot and the same light once a month, never in the mirror, and give it six months before you form a view and twelve before you call anything a failure.

Disclosure, since it is your money: I earn a commission when somebody buys RU58841 or JXL069 through my links. Neither is a licensed medicine anywhere, RU58841 has no human efficacy trial behind it at all, and nothing on this page is medical advice.

On how the two layer together: applying RU58841 and PP405 on the same night. On the identity question: are JXL069 and PP405 the same molecule? What I run and why: my protocol.

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The question

I have seen a lot of your videos, even an old one about the RU timeline. With more years passed and more experience, when would you say that RU58841 results reach a plateau? I see online from 6 months to 14 months. What is your take?

Asked by Vincenzo

The answer

The first thing I owe you is the reason that range is so wide, and it is not that some men respond faster. It is that RU58841 has no published human efficacy trial, so there is no density curve for anyone to read a plateau off. Every month number you have seen online, including every one I have given on camera, is somebody describing their own head. That is not nothing, but it is not a timeline either, and you should hear it that way before you hear my number.

What does set the pace is the hair cycle, and there we do have something to go on. The best piece of RU58841 evidence is still Brouwer 1997, where human balding scalp was grafted onto mice and treated with 1% RU58841 five days a week for six months. At the end, the number of actively growing follicles was the same in both groups, 28 against 29. What differed was how many follicles went on to enter a second growth cycle, 7% on the vehicle against 28% on the drug, and how fast the hair grew in length.

Read that again, because it is the whole answer. It did not wake up follicles that were already awake. It changed what happened when a follicle finished a cycle and started the next one. A scalp hair grows for years, rests for months, then begins again, and a scalp does not do this in unison, every follicle is on its own schedule. So you do not get a smooth line climbing upward, you get steps, and each step is one more follicle taking its turn. The men who tell you six months and the men who tell you fourteen are describing the same process at different points in it.

My own take, on the head I have tracked longest: most of what I was visibly going to get had shown up inside the first twelve months, and the second year looked like holding rather than climbing. Month six is the earliest point worth judging anything at all, and I would not call a result finished before a year.

But the word plateau is doing you a disservice, so let me take it apart. It makes this sound like a ceiling you climb to and then sit on, with the drug slowly running out of effect. That is not what a flat line means here. Androgenetic alopecia is still running underneath the whole time, every month, whether you are treating it or not. So a flat line at eighteen months is not the compound fading, it is regrowth and ongoing loss cancelling each other out, and that cancellation is the result. Holding the line is what success looks like on a progressive condition.

Which matters practically, because the most common mistake I see is a man reading flat as failure at month fourteen and adding a fifth bottle to a stack that was working. If your photographs are flat two years in, you are winning and you should leave it alone. Same spot, same light, same phone, once a month, because the mirror will tell you whatever mood you are in.

And the usual caveat, which is real here rather than decorative: RU58841 is not a licensed medicine anywhere, there is no human trial behind it, and nothing on this page is medical advice.

On judging any treatment honestly: how long hair loss treatments actually take. What I run and why: my protocol.

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The question

Have you seen the 2026 studies on RU58841? There was a lot of it in the blood. What if we found a way of raising funds to get bloodwork done on you, or on one of your followers, looking for RU58841?

Asked by Vincenzo

The answer

I had not seen it, and you were right to push on it, because it changes a line I have been saying for a long time.

In the newsletter you were replying to I wrote that RU58841 has no published human trial. As a statement about efficacy, does this grow hair on an actual person, that is still true and I will keep saying it. As a statement about human data of any kind, it is no longer true. There is a 2026 paper: Okutan, Krug, Fusshoeller, Piper and Thevis, “Investigation Into the Metabolism and Elimination Behavior of RU 58841, and Its Influence on the Steroid Profile in Humans”, Biomedical Chromatography, October 2026. It comes out of the Institute of Biochemistry at the German Sport University in Cologne, which is one of the world’s anti-doping laboratories.

It is worth knowing why a doping lab is the group that got there first. They are not studying hair. An androgen receptor blocker is a banned substance in sport, so they need to know what it breaks down into, how long it takes to leave, and what it does to the pattern of steroid hormones they measure in an athlete’s sample. Hair loss research never funded a human RU58841 study in thirty years. Anti-doping needed one, so anti-doping ran one.

Now the part where I stop short, deliberately. The full text is paywalled and I have not read the results, so I am not going to put numbers on it, and you should be wary of anyone who does. What I can tell you is what the study is, and that alone is useful: it measures metabolism and elimination in humans, and it looks at the steroid profile. Which means the question people have waved away for years, whether a topical anti-androgen stays where you put it, finally has somewhere real to look. “It is topical, so it does not go systemic” was never a finding. It was an assumption that sounded reasonable, and it is now checkable.

On the crowdfunded bloodwork, my answer is no, and there are two reasons.

The first is that it would not be a study. One man’s blood, drawn once, with no control, no second laboratory and no standardised dose, tells you what was in one person on one day. It would get screenshotted and quoted for years as though it were evidence, and it would be worse than nothing because it would feel like something. The Cologne paper is what the real version of that question looks like, and it already exists.

The second reason is the one I would rather say out loud. I earn a commission when somebody buys RU58841 through my links. That is exactly why I am not going to ask my readers to put money into research on it. There is no version of me collecting funds from this audience to investigate a compound I profit from that I would be comfortable defending, and the fact that the idea came from you rather than me does not change that.

Credit where it is due: Vincenzo found the paper and sent it over. If you spot something I have got wrong, that is how it gets fixed.

What I run and why, with the commissions disclosed: my protocol.

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The question

I have just got hold of some dutasteride. I have been on finasteride for three months and I think I am still thinning. I am terrified of post-finasteride syndrome and I can nocebo myself into side effects. What about a finasteride and dutasteride protocol, like finasteride Saturday, Sunday, Tuesday and Thursday, and dutasteride Monday, Wednesday and Friday? Your thoughts?

Asked by a reader

The answer

I would not do it, and the reason is not caution. It is that the schedule does not do what you think it does. Once you understand how long each drug stays in you, the calendar stops making sense.

Finasteride has a half-life of about 6 to 8 hours. Take it, and it is largely gone the next day. Dutasteride has a terminal half-life of around five weeks, and takes months to fully clear.

So taking dutasteride on Monday, Wednesday and Friday does not give you three days of dutasteride. It gives you dutasteride. It accumulates. After about a month on that pattern you have dutasteride working in your body every hour of every day, Saturday and Sunday included, and the finasteride you swallow on those days is landing on an enzyme that is already mostly blocked. You have not built a gentler version of dutasteride. You have built dutasteride, plus four tablets a week that are close to doing nothing.

Which matters most for the exact thing you are afraid of. The one real advantage finasteride holds over dutasteride is the exit. Get a side effect on finasteride and you stop, and you are near baseline within a week or two. On dutasteride the exit takes months whether you want it to or not. That asymmetry, more than the potency, is why doctors start men on finasteride and keep dutasteride for the men who need more. Your schedule gives that exit away in the first week, while feeling like a hedge. And if something does go wrong on a mixed calendar, you will not know which of the two drugs did it, and the one you cannot clear quickly is still in you.

On the nocebo point, which I am taking seriously because you raised it yourself: a rotating two-drug calendar is the worst possible protocol for a man who knows he can talk himself into symptoms. It gives you days that are different from other days, two things to monitor instead of one, and a second candidate to pin every sensation on. If you are prone to that, simpler is not just easier, it is more accurate.

There is a real middle road, and it is worth taking to a doctor. It is lower-frequency dutasteride on its own. That five-week half-life is exactly why such a thing is even possible, and it has been tested: Sereepanpanich and colleagues ran a randomised pilot of dutasteride twice a week and three times a week against daily finasteride. So dutasteride two or three times a week, and nothing else on the other days. That is a genuinely lighter dose of the stronger drug. Alternating two drugs is not.

The last thing, and maybe the most useful. Three months on finasteride and thinking you are still thinning is not a finished experiment. Finasteride’s own label says three months or more of daily use before benefit is seen, and my rule is six months before you judge a DHT blocker and twelve before you call it a failure, judged on monthly photographs in the same spot and the same light, not in the mirror. Switching at month three is how men take the shed and then quit before collecting the regrowth.

None of this is medical advice, and dutasteride is a prescription drug for a reason. If you want to move onto it, that is a conversation with a doctor, not a calendar you build yourself.

The full comparison: when the switch to dutasteride actually makes sense. On the fear itself: what the evidence on post-finasteride syndrome shows.

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The question

I am running topical and oral finasteride at 1 mg, topical minoxidil at 5%, 2 ml, and for the last three months 1 ml of RU58841 at 5%. Hairs going down so fast I really don’t know what to do next. I see you are getting some improvement with JXL069. Out of curiosity, why don’t you use minoxidil? And do you think that using dutasteride instead of finasteride I could keep my hair if I start testosterone?

Asked by Vincenzo

The answer

Three questions, so three answers.

Why minoxidil is not in my stack. Not because it does nothing. Because it does nothing to the cause, and because most men cannot even use it.

Your hair loss is driven by DHT, a hormone that shrinks your follicles a little more every cycle until they quit. Finasteride and dutasteride lower it. A topical anti-androgen like RU58841 blocks the spot it plugs into. Minoxidil does neither. It walks past the cause and tries to force a bit of extra growth anyway. Picture a boat with a hole in it: DHT is the hole, minoxidil is you bailing water. Keep bailing twice a day and you stay afloat. Stop, and within a few months your hair sits back where it would have been. You are not fixing the boat, you are renting a bucket.

And the bucket only helps if your body can use the stuff. Minoxidil does not arrive ready to work. Think of a blank key: your scalp has to cut it into the shape that opens the follicle, and the tool that does the cutting is an enzyme called sulfotransferase. Some men are loaded with it. Plenty are not. In the clinical trials, only about 30 to 40 percent of men get real regrowth from 5% minoxidil. There is a study on exactly this, where researchers plucked hair follicles, measured that one enzyme, and used it to predict who would respond: it ruled out the non-responders with about 96 percent accuracy. Most of the time, whether minoxidil works on you was decided before you ever opened the bottle.

Which has a direct consequence for your routine. The 2 ml you are applying every day may be doing nothing whatsoever, and there is no way to tell by looking at it. That is worth knowing in both directions: it means minoxidil is probably not the part of your stack that is failing you, and it also means it is not going to be the thing that rescues you.

For what it is worth, my own stack is dutasteride to lower DHT, a topical on the scalp to block it at the follicle, and microneedling once a week. The hormone side does the heavy lifting. I have never needed the bucket.

On what to do next. Two things, and the first one is the boring one that matters. Your RU58841 has been on for three months. Three months is not a verdict on anything. Six months before you judge it, twelve before you have seen its ceiling, and judged on photographs taken monthly in the same spot, the same light, hair damp and combed flat. The mirror is the worst measuring instrument you own, purely because you look in it every day, which is exactly how it hides slow change and then delivers a bad day as if it were news. “Going down fast” read off the mirror and the drain is the reading most likely to be wrong.

The second thing I will say plainly. If you are on oral finasteride and topical finasteride and minoxidil and RU58841, and a fair six-month window on photographs still shows real ground lost, then a fifth bottle is not the answer and you have reached the point where this needs a doctor rather than a forum. Two reasons. One, that much treatment failing at once raises the question of whether pattern loss is the only thing going on, and loss that is diffuse across your whole head rather than concentrated at the crown and hairline points somewhere else entirely: thyroid, iron, stress, a recent illness. Two, running oral and topical finasteride together is more systemic finasteride than most men assume, because topical still absorbs, and that is worth someone looking at properly.

On dutasteride and testosterone. The honest answer is that it is a stronger defence, not a promise, and nobody can tell you in advance that you would keep your hair.

Here is the mechanism you are up against. Exogenous testosterone raises the raw material your body converts into DHT, so in a man who is genetically susceptible, it commonly speeds pattern loss up rather than leaving it where it was. Dutasteride does block more of that conversion: around 90 percent of the DHT in your blood against finasteride’s roughly 70 percent, and it grew more hair than finasteride in the randomised head-to-head trials. So yes, it is the stronger wall to have up in that situation. What it is not is a guarantee, because you would be raising the pressure and strengthening the wall at the same time, and which of the two wins on your particular head is not predictable.

Three things I would put in front of a doctor rather than settle here. The exit: finasteride clears in days, dutasteride keeps suppressing your DHT for months, so committing to dutasteride and testosterone together means accepting a slow exit on one of them. The metabolic side: Upreti and colleagues randomised men to the two drugs and measured how their bodies handled sugar, and dutasteride reduced insulin sensitivity and increased body fat where finasteride did not, which belongs in the conversation if you are about to change your hormones anyway. And the obvious one: starting testosterone is a far bigger decision than your hairline, and it should not be decided on hair. If you already have a doctor for the testosterone, the hair plan belongs in that same appointment.

The long version on minoxidil: why I don’t take minoxidil. On hair and testosterone: how to keep your hair on TRT. And if a full stack is still losing ground: what to do when finasteride is not working.

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The question

Do I have to take finasteride for the rest of my life? And if I come off it, do I lose everything I gained, or does some of it stay?

The question I get more than any other

The answer

Yes, for as long as you want to keep the hair. Finasteride does not cure pattern baldness. It pauses it. The gains last exactly as long as you keep taking it, and stopping does not reset you to neutral, it puts you back on the road you were already on.

Here is the mechanism, because the rest only makes sense with it. Pattern loss is driven largely by DHT, which your body makes from testosterone using type II 5-alpha-reductase. Finasteride blocks that enzyme and cuts scalp and serum DHT substantially, which lifts the pressure that was miniaturising your follicles. What it does not do is touch the genetic susceptibility. Your follicles are still primed to respond to DHT. You have just lowered the DHT.

Picture a finger holding down a spring. Press, and it stays compressed. The spring is not gone, it is loaded. Lift your finger and DHT climbs back to baseline within days to weeks, and the spring starts pushing again.

That is why stopping fools people. A reader once came off it for two weeks before a holiday, looked in the mirror, saw nothing different, and decided the drug had never been doing anything. Six months later he sent me a worried photo. Follicles respond over hair cycles, not overnight, so the drift back happens over roughly six to twelve months. Slowly enough that you do not feel the first steps.

The number that settles it for me is the placebo line. In the pivotal trials, men on 1 mg gained about 107 more hairs in a one-inch circle of vertex scalp at one year and 138 at two years, while the placebo group lost hair steadily the entire time, out to five years. That placebo line is your untreated trajectory. Stopping does not snap you onto it, but it starts you drifting toward it.

So the real choice is not drug or no drug. It is which of those two lines you want to be on. If the drug itself does not agree with you, that is a completely different question and there are other mechanisms worth looking at.

The long version, with the five-year data: when should you stop taking finasteride. If it is side effects pushing you off it, read the answer below on switching mechanism.

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The question

Three weeks in and there is noticeably more hair in the shower drain than before I started. Am I making it worse? Everyone online says to push through but I am losing my nerve.

A message I get every single week

The answer

Do not stop. Quitting during this window is probably the most expensive mistake in all of hair loss, because it happens at the exact moment the treatment starts working.

Minoxidil’s main trick is that it shortens telogen, the resting phase, and kicks resting follicles back into growth early. That is the whole point of the drug. The consequence nobody warns you about clearly enough is what happens to the old hair. A resting follicle is holding a placeholder hair. Force it to restart and that old hair gets ejected to make room for the new one growing underneath. Do that to a lot of follicles at once and you get a wave of shedding, all synchronised.

The shed is not the drug destroying hair. It is the drug evicting old tenants so new ones can move in.

The timeline that should calm you down: for most men it starts somewhere around weeks two to eight, peaks, and settles. By months three to six the new growth has caught up and gone past what you lost. That is why nearly every minoxidil trial measures its real result at six and twelve months, not at week four. Judge it at week four and you are reading the chapter where it looks worst and closing the book right before the turn.

I am not going to tell you all shedding is fine, because that is how people miss real problems. Here is when I would actually be concerned:

Heavy shedding still going strong past four to six months is not the normal pattern. Get it looked at. Shedding with scalp irritation, flaking or burning is more likely a reaction to the vehicle, often propylene glycol, and is worth switching formula for rather than quitting. And shedding that is diffuse across your whole head rather than concentrated in the area you are treating points somewhere else entirely: thyroid, iron, stress, a recent illness.

The practical move for the next four months is to stop reading the drain and start taking photos. Same spot, same light, same angle, dry hair, once a month. The drain is noise, the photo is signal.

The full timeline, anchored to what the trials measured: how long hair loss treatments actually take.

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The question

I finally started taking creatine properly and now I keep reading it will make me go bald. I am already thinning a bit at the temples. Do I need to drop it?

The question my audience asks me most

The answer

Almost the entire scare traces back to one study, so let us look at it properly.

Van der Merwe and colleagues, 2009. Twenty college-aged rugby players, creatine on a loading week then maintenance, crossover design, hormones measured. Testosterone barely moved. DHT jumped 56% after the loading phase and stayed about 40% above baseline during maintenance. The DHT to testosterone ratio rose 36%, then settled around 22% up. That single result is the whole foundation of “creatine causes hair loss”.

Here is the catch, and it is a big one. They measured hormones in blood. They never measured a single hair. Nobody counted follicles, nobody graded scalps, nobody tracked shedding. The study found a hormonal change and everyone else filled in the rest of the story themselves. That is a leap, not a finding.

And a finding from one small study is not knowledge yet, it is a lead. You turn a lead into knowledge by repeating it. In the seventeen years since, no study has cleanly reproduced that DHT spike, and none has shown creatine causing hair loss in a controlled trial. Broader reviews of creatine and hormones generally find no consistent, meaningful effect on testosterone or DHT.

So is the answer just no? Not quite, and I am not going to pretend it is a clean zero. If creatine does nudge DHT up a little in some men, the people who would care are exactly the people genetically sensitive to DHT, which is to say the ones already prone to pattern loss. For follicles that do not carry that sensitivity, a small DHT bump means basically nothing.

Which means the useful question is not yes or no, it is who are you. No family history and a full head of hair: this is noise, keep taking it. Already watching your hairline, like you are: worth being aware of, while knowing the evidence that it matters in practice is thin. And if you are already on something that lowers or blocks DHT, a theoretical nudge upward is the exact thing that drug is there to absorb.

What I would not do is quit the most evidence-backed supplement on the shelf over one unreplicated hormone panel from 2009.

The full read of the study: does creatine cause hair loss.

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The question

It has been six weeks and I honestly cannot tell if anything is different. At what point should I accept it is not working for me and try something else?

The most common message in my inbox

The answer

Six weeks is far too early to know anything, and the reason is biological rather than a flaw in whatever you are taking.

You cannot see a follicle’s decision. You can only see the hair it already pushed out. When a treatment tells a resting follicle to wake up, that new hair still has to physically grow out from under your scalp before your eyes register it. Judging a hair treatment at week four is like judging a vegetable garden the morning after you plant the seeds. The work is happening underground. Looking harder will not speed it up, and an empty bed on day three tells you nothing about the harvest.

Minoxidil moves fastest, and that speed is exactly what scares people off it. Shedding at weeks two to eight, visible change typically around months three to six, peak benefit closer to twelve. In Olsen’s 48-week randomised trial of 393 men, 5% minoxidil beat both 2% and placebo on hair count and produced 45% more regrowth than the 2% solution by week 48, and the response showed up earlier at the stronger concentration. The honest limitation in that same trial: results varied a lot man to man, which is why nobody can promise you a personal timeline.

Finasteride plays the longer game. It removes the thing shrinking your follicles rather than whipping them awake, so it starts slower and compounds. About 107 extra hairs in a one-inch vertex circle at one year, 138 at two.

So the rule I would give you is: six months before you judge it, twelve before you decide you have seen its ceiling. And judge it with photographs, not with the mirror. Same spot, same light, same angle, dry hair, once a month. Then compare month zero to month six, not Tuesday to Wednesday. The mirror is the worst measuring instrument you own, purely because you use it every single day and it hides slow change from you.

The one thing that genuinely resets this clock is bouncing between products. Every change starts its own shed and its own waiting period. Pick a lane you can tolerate and run it, boring and unchanged, for the full six months.

The full timeline with the trial numbers: how long hair loss treatments actually take.

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The question

I keep seeing that a study found rosemary oil works as well as minoxidil. I would much rather use that than a pharmaceutical every day for the rest of my life. Is it true?

Asked every time I mention minoxidil

The answer

That line is technically true and badly misleading at the same time, which is the most dangerous kind of true.

The study is Panahi 2015, in Skinmed. A hundred men with pattern baldness randomised to either rosemary essential oil or 2% minoxidil for six months. At the end both groups had a meaningful increase in hair count and the difference between them was not statistically significant. The rosemary group also had less scalp itching. On paper, a tie.

Three details turn that tie into something much softer.

First, it was 2% minoxidil, the weaker concentration. Almost nobody serious uses 2% any more, because 5% outperforms it in head-to-head data. Rosemary tied the junior version of the drug, not the one people actually reach for.

Second, both groups only separated clearly from baseline late, around the six-month mark, and the early months showed some shedding. Normal, but it tells you patience is mandatory either way, so you are not buying a faster route.

Third, it is one trial, of modest size, that as far as I can tell has not been cleanly replicated at scale. Minoxidil has more than thirty years of randomised data and regulatory approval behind it. One encouraging study against three decades is not a fair fight.

Credit where it is due: rosemary is not pure snake oil. It contains carnosic acid and rosmarinic acid, which have anti-inflammatory and antioxidant activity, and there is some lab signal for mild anti-androgen and circulation effects. A lot of scalp trouble has an inflammatory component, so a soothing topical helping a little is biologically plausible. The mechanism is not magic. It is just mild.

The analogy I keep coming back to: a man dying of thirst in the desert is genuinely helped by a few drops of water. The drops are real and the help is real. It is still nowhere near enough to save him. If your follicles are miniaturising under DHT pressure, a herb that gently soothes your scalp is not going to hold the line.

So the honest question is not whether rosemary oil does anything. It is whether it does enough. For a hairline that is actively receding, almost certainly not. Use it alongside something that works if you like it. Do not use it instead.

The full read of the 2015 trial: rosemary oil vs minoxidil.

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The question

Just wondering how you use PP405 and RU58841 together. Do you apply the RU and then the PP405 straight after, or something else?

Asked by a reader

The answer

RU58841 goes on first, and then I wait a minute or two before the second one goes anywhere near my scalp. So the order you guessed is right, but the gap between them is the part that actually matters.

Here is why. If you put the second liquid on while the first is still sitting wet on your scalp, you are not applying two treatments, you are diluting the first one and dragging it around into places you did not part for. Both end up thinner and more scattered than you intended. Giving the first one a minute or two to dry means each one stays where you put it.

A minute or two is usually enough. You are waiting for it to stop looking wet, not for your whole scalp to feel bone dry.

The other half of the answer is the nights when neither one goes on at all. On microneedling days I apply nothing afterwards. The channels are still open, absorption becomes unpredictable, and that is how a normal dose turns into an irritated scalp.

On the naming, since you used both terms in one sentence: PP405 and JXL069 are the same molecule. The World Health Organization assigned it the name suvomipic, CAS registry number 2260696-63-5, and the monograph lists PP-405 and JXL069 as its other names. Same compound, different labels depending on who is talking.

That matters for a reason worth being clear about. What Pelage runs in its trials is a specific 0.05% gel with its own vehicle, built to carry the molecule into the follicle and break down before it reaches your bloodstream. Raw powder mixed into a solvent at home is not that product, even when the molecule on the label matches. And an official chemical name tells you what the reference compound is, not what is actually in a vial you bought. Purity and dosing accuracy are still entirely on whoever sold it to you.

For what it is worth, I run RU58841 at 5%. I have seen people go to 8%, but I would not go past that, and I would not read a higher number as a faster result.

Full stack, sourcing and dosing: the free protocol.

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The question

I just found out that the WHO INN registry appears to link PP405 to the active compound suvomipic. Even the CAS number is the same for suvomipic and JXL069. Does this basically mean that JXL069 is most likely the same exact chemical as PP405 (2260696-63-5)?

Asked by Toyn

The answer

Yes. And I want to be straight with you about this, because I have said the opposite on this site and on camera, more than once and quite forcefully.

Here is what the record now shows. On 19 July 2026 the World Health Organization published Proposed INN List 135, which assigns the international nonproprietary name suvomipic. The entry gives the chemical name as (2E)-3-(1-{[3,5-bis(trifluoromethyl)phenyl]methyl}-1H-pyrrolo[2,3-b]pyridin-3-yl)-2-cyanoprop-2-enoic acid, molecular formula C20H11F6N3O2, CAS registry number 2260696-63-5. That is JXL069, exactly. Same name, same formula, same CAS. The suvomipic monograph now lists its other names as PP-405, JXL069 and JXL-069, and describes it as a topical 0.05% scalp gel, which is the PP405 clinical product.

An INN is assigned to the molecule a company files for. So the compound Pelage has been running through its trials as PP405 is, chemically, JXL069. That directly contradicts Pelage’s earlier public statement that PP405 is not JXL069, and it contradicts what I told you.

Three caveats I am not going to skip over, because they change what you should actually do with this.

First, List 135 is a proposed list. There is a four-month window in which objections can be filed. It is a regulatory filing rather than a peer-reviewed structure paper, and proposed names are rarely overturned, but it is not yet final.

Second, knowing the molecule is not the same as having the drug. What Pelage is testing is a specific 0.05% gel formulation with its own vehicle and penetration profile, developed to deliver that molecule to the follicle and to break down before it reaches your bloodstream. Raw powder in a solvent you mixed yourself is not that, even if the molecule on the label matches.

Third, and this is the one that catches people, an INN tells you what the reference compound is. It tells you nothing about what is actually in a vial you bought online. Purity, identity and dosing accuracy are still entirely on the seller, and most of them have never been independently tested.

So: you are right about the chemistry, and thank you for bringing it, because you spotted it before I did. I am working through what this means for my own six-month run on JXL069, and I will correct the record properly, on camera, rather than quietly editing the old pages and hoping nobody notices.

The full correction and the background: the PP405 article.

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The question

I was curious about the protocol you use with microneedling and salmon DNA. I actually have some salmon DNA, so I was thinking about giving it a try. It does not seem like the protocol would be that complicated. Is it basically just microneedle first, apply the salmon DNA afterward, and repeat once a week? Or is there anything else you do?

Asked by Eric

The answer

Almost, but you have the order slightly wrong, and it is the part that matters most.

Salmon DNA (polynucleotides, or PDRN) is a big molecule. Sitting on top of your scalp it does close to nothing. In every study that showed a result, it was driven into the skin: needled in, injected, or pushed with a laser. The needling is not a step that happens before the good part, the needling is the delivery. So you do not want to microneedle and then apply it on top of skin that is already closing.

Here is what I actually do, session by session.

Depth 1.0 mm, and no deeper. The dial goes up to 2.5 mm but that range is for the face. On the scalp, deeper does not grow more hair, it just puts the follicle you are trying to save at risk. I run the speed near the top of its range, which gives cleaner channels and less dragging.

Fresh cartridge every single session. One use, then binned. A blunt or dirty tip is how you turn this into a problem instead of a result.

Ampoule on the section first. I part the hair, put a few drops of the salmon DNA straight onto that section, and then run the pen over it. The tip carries it down into the channels as it goes. That is the whole reason for doing it this way.

Work in small squares, light cross pattern. A couple of passes each way, light pressure, let the motor do the work. You are aiming for faint pinpoint redness, not blood. The thin spots sting and the hairline always makes me wince. That is normal. Whole scalp takes me about ten minutes.

Finish with more on top while the channels are still open, and that is it for the night.

About 2 ml a session, which is roughly a quarter of the ampoule. Once a week. Not more. The scalp needs the week to recover, and doing it more often is how you end up with irritation instead of regrowth.

One thing to check before you start: make sure what you have is a topical formulated for microneedling delivery, not an injectable or medical-grade product meant for a clinician. Those are not interchangeable and you do not want to be needling the wrong one into your own head.

And a note on expectations, since you are about to spend time on this. The microneedling is doing the heavy lifting here. It grows hair on its own, and that is well established. The salmon DNA is the bonus you drive in with it, on top of what you are already doing, not instead of anything. I am running it as a clean twelve-week test with the salmon DNA as the only thing I have changed, so if my crown moves there is only one new variable it can be. Monthly crown photos, same spot, same light, same angle, dry hair.

I am filming my full first session, start to finish, including the setup and every step above. It goes live this weekend, so if you want to watch me do it before you do it yourself, it is worth the wait.

Where microneedling sits in the rest of the stack: the free protocol.

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The question

I have been losing hair for 18 months, starting around age 32. I tried oral finasteride twice and got stomach and digestion side effects both times (bloodwork and stomach scans came back clear). I moved to topical finasteride, a homemade version first and then pharmacy 0.1% trichosol, which stabilised things but gave me the same stomach sides. I dropped to 0.025%, which I tolerated, but I started shedding and losing density, so I went up to 0.05% and the sides crept back along with continued progression, plus some minor scalp irritation. I am either looking to manage the side effects or move to something with a different mechanism. I am hesitant about dutasteride because of the extra DHT reduction.

Asked by Kye

The answer

Here is the pattern: finasteride gives you stomach side effects on every route you have tried, oral and topical, and the only dose that did not bother you, 0.025%, was too low to hold your hair. That is the worst kind of bind, because the dose that works gives you sides and the dose you tolerate does not work. To me that says finasteride as a molecule simply does not agree with you, and dose-tweaking will not fix it, since topical finasteride still absorbs systemically (especially homemade and at 0.1%).

On managing the side effects: I do not think you can. The stomach symptoms are systemic absorption of the drug itself, not the carrier, so the only lever is lowering the dose, and you have already found the tolerable dose does not hold the line. The scalp irritation is a separate issue and is probably the carrier (the crushed-tablet base, or propylene glycol if present); a cleaner non-PG base and a patch test would help that, but it will not touch the stomach side.

On a different mechanism, your instinct is right. I would not move to dutasteride. It is a stronger version of the same mechanism (it blocks more of the enzyme and lowers DHT harder) and its half-life is measured in weeks, so if finasteride upsets your stomach, dutasteride is likely to do it more and linger far longer.

The move that actually fits you is to stop trying to lower your DHT and instead block it at the scalp. Finasteride and dutasteride both work by reducing DHT through your whole body, which is the mechanism causing your sides. Topical anti-androgens work differently: they sit on the androgen receptor at the follicle and block DHT locally, without dropping your systemic DHT, so they sidestep the exact effect hitting your gut. The cleanest option is clascoterone (sold as Winlevi for acne), which is broken down very fast so almost nothing reaches your bloodstream. RU58841 and pyrilutamide are the research-compound versions of the same receptor-blocking idea, but they are not FDA-approved for hair, so they need your own research and ideally a doctor in the loop.

Around whichever you choose, you can add things that do not touch systemic DHT at all: weekly microneedling at 1 mm, a 2% ketoconazole shampoo a couple of times a week, and keeping the scalp clean. And stop bouncing the dose, because each change sets off its own shed. Pick one tolerable lane, give it 4 to 6 months, and track with monthly photos in the same lighting.

None of this is medical advice, and since you have had real stomach symptoms it is worth running the switch past a doctor. But you are early, and you have good options that do not have to wreck your stomach. My full stack with sourcing and dosing is in the free protocol.

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