37. Minoxidil & Hair Loss | The Side Effect That Became the Main Event

Minoxidil is one of the most recognised treatments for hair loss in the world. Millions of people use it. Few know how it was discovered.

In this episode of Mohivate, I explore the remarkable story of a medication that was never meant to grow hair. What began as a failed ulcer treatment became a powerful blood pressure drug, and an unexpected side effect went on to change dermatology forever.

Along the way, we explore the science of hair growth, why hair loss occurs, the difference between telogen effluvium and androgenetic alopecia, and what minoxidil is actually doing inside the hair follicle. We look at the science behind topical and oral minoxidil, why some people respond dramatically while others do not, the role of sulphotransferase enzymes, shedding, side effects, and what current evidence tells us about combination treatments including microneedling and low-dose oral minoxidil.

But this episode is about more than hair.

Hair loss, like so many things in health, sits at the intersection of biology and identity. It is rarely just about a hairline, a parting, or a reflection in the mirror. It is often about how we see ourselves, how we experience change, and the small things that carry more meaning than we realise.

With science, history, humour, and practical evidence, this episode explores one of medicine's most fascinating accidental discoveries, and why it continues to matter to millions of people around the world.

References:

1. Minoxidil and Its Use in Hair Disorders
   https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6691938/
2. Low-Dose Oral Minoxidil for Alopecia: A Comprehensive Review
   https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10806356/
3. Efficacy and Safety of Oral Minoxidil in Alopecia: A Systematic Review and Meta-analysis
   https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12188453/
4. Predicting Minoxidil Response Through Follicular Sulfotransferase Activity
   https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9326921/
5. Low-Dose Oral Minoxidil Initiation for Patients With Hair Loss: An International Delphi Consensus Statement
   https://jamanetwork.com/journals/jamadermatology/fullarticle/2826573

Just a gentle reminder: this episode is for information, education, and inspiration only. It’s not a substitute for your doctor’s advice. For any personal health concerns, always seek guidance from your doctor.

Transcript

SPEAKER_00 0:05

Hi everyone, welcome back to Mohivate. I'm Dr. Mohi Saraugi, a GP by profession, but here I'm swapping prescriptions for perspective. Last week, the mayor of New York City did something that almost no politician ever does. He came clean about his hairline. Zoran Mamdani, 34 years old, the youngest mayor New York has seen in generations, casually told the world he's using minoxidil to save his hair. The internet predictably lost its mind. One person said he's just like us. Another said New York has bigger problems. Someone commented he's either genuinely transparent or brilliantly strategic. In politics, sometimes those are the same thing. But love him or hate him, at least he's not pretending. Now I have a confession. My borderline obsession until very recently was his wife, artist, illustrator, Rama Duaji. Simply stunning. Have you seen their wedding pictures? White lace dress, knee-high black boots, city hall. This woman showed up to her own wedding looking like a fashion editorial, and nobody got the memo that you were not supposed to look that good at a courthouse. They met on Hinge, by the way. For those who do not know, Hinge is a dating app and Hinge got the free advertising it never went looking for. They are a remarkable couple, but I will say what everyone is thinking. She is carrying that relationship aesthetically, and honestly, we love that for her. Anyway, when a sitting male casually drops minoxidil into the conversation, we have to discuss it on Mohivate. Because minoxidil has one of the most accidentally brilliant origin stories in the history of medicine. It started as something else entirely, failed at that, and then stumbled into changing dermatology forever. Now hair loss is multifactorial. Genetics, hormones, nutrition, iron, protein, stress, thyroid, the overhyped biotin, the list is long. But today we are pulling one drug out of that list: minoxidil. What it actually is, how it works, why some people respond and others do not, how to use it, what has changed with oral minoxidil, and how one molecule ended up in bathroom cabinets of millions of people worldwide and whether it deserves to be there. So let's begin. In the early 1950s, researchers at a pharmaceutical company called Upjohn, based in Kalamazoo, Michigan, which is a real place and not something I invented for comic effect. Now, part of Pfizer were investigating a compound they had quite literally ordered from a chemical catalogue. The goal was to study its effects on stomach acid and develop a treatment for peptic ulcers. The compound failed completely at that, but in animal studies it dramatically lowered blood pressure. So they followed the thread. They synthesized hundreds of related compounds, and one of them was minoxidil. By every measure, it had failed its original job interview. But science rarely throws away a potent molecule just because it failed its first assignment. What minoxidil was was a powerful vasodilator. It relaxed the walls of blood vessels, causing them to widen and blood pressure to drop significantly. For patients struggling with severe treatment-resistant hypertension, the kind that did not respond to anything else, this was significant. The results were so dramatic that in 1971 the FDA approved an emergency use protocol for severely ill patients, but put a two-week limit on treatment duration because there were concerns about side effects they had not yet fully understood. What happened next? Nobody expected. Clinicians faced with patients who had no other options quietly kept their patients on minoxidil longer than the recommended two weeks. And that is when something very strange began to happen. Patients taking minoxidil started growing hair, not just on their scalps, on their foreheads, their backs, their cheeks, everywhere. A side effect called hypertrichosis, excessive hair growth all over the body. To a cardiologist, this was a nuisance. To a dermatologist, it was a miracle in the making. The executives at Upjohn were apparently less enthusiastic. They had spent years positioning themselves as a serious pharmaceutical company. They did not want to be associated with miracle baldness cures. But once minoxidil was on the market for blood pressure and word got out that it caused hair growth in 60 to 80% of patients who took it, Up John's headquarters in Kalamazoo was inundated with volunteers for hair loss trials. A letter published in the New England Journal of Medicine made the side effect impossible to ignore, and a doctor at the University of Colorado had the very sensible idea of asking, What if we applied this directly to the scalp? Not swallowed, just applied. Could we get the hair growth without the blood pressure effects? That question is how topical minoxidil was born. In 1988, the FDA approved 2% topical minoxidil for male pattern hair loss, also called androgenetic alopecia, under the brand name Rogaine. And for decades, that was the story, a foam or liquid applied to the scalp twice daily and hoped for the best. What started as a failed ulcer drug became a blood pressure medicine and then became one of the most widely used hair treatments in the world. The poison became the cure, which, if you think about it, is a very good description of most of pharmacology. Before we go any further, it helps to understand what your hair is actually doing on its own. Hair does not grow continuously, it grows in cycles. Every single follicle on your scalp is independently cycling through three phases. The first is the anogen phase, the growth phase. This is when the hair is actively being made. It lasts between 2 and 7 years, which is why some people can grow their hair to the waist and others struggle to get past their shoulders. That difference is largely genetic. Then the catogen phase, a brief transition. The hair follicle shrinks, the hair stops growing, and the whole structure prepares to rest. It lasts about two weeks. Brief, quiet, and easy to miss. Then the telogen phase, the resting phase. The hair sits in the follicle but is no longer growing. After two to four months, that hair sheds and a new anogen phase begins. On a healthy scalp, roughly 85 to 90% of your hair are in anogen at any given time. Losing 50 to 100 hair a day is entirely normal. It is not hair loss. It is a cycle completing itself. Now, two conditions worth understanding because they are different problems with different solutions. Tellogen effluvium is what happens when stress, illness, pregnancy, significant weight loss, a hormonal shift, or a nutritional deficiency pushes a large number of follicles out of anogen and into telogen simultaneously. A few months later, they all shed at once. It can be alarming, but in most cases, it is temporary. The follicles are still there. They just need time and the right conditions to cycle back. The most important step is finding and addressing the cause, whether that is iron, protein, thyroid, or something hormonal. There is good evidence that minoxidil, particularly low dose oral minoxidil, can help reduce shedding in chronic telogen effluvium while the underlying cause is being addressed. Think of it as scaffolding while the building repairs itself, not a replacement for treating the cause, a support alongside it. And I will add, I include myself among the people who have used topical monoxidil for exactly this reason. Then androgenetic allopesia, male and female pattern hair loss is a different problem entirely. Here, the issue is in the anogen phase itself. Under the influence of DHT, dihydrotestosterone, a hormone derived from testosterone, genetically susceptible follicles progressively miniaturize. Each energy phase gets shorter. Each hair produced gets thinner and finer until eventually, if nothing intervenes, the follicle stops producing visible hair altogether. This is the primary condition minoxidil was designed to address, and understanding the cycle is what makes everything about how it works and why it sometimes does not make complete sense. Now let's understand what minoxidil actually is and how it works. Minoxidal is a vasodilator, it widens blood vessels. Hair follicles are metabolically hungry. They need blood flow, oxygen, and nutrients to produce hair. Think of it as the full delivery service your follicles depend on. Minoxidal widens the tiny blood vessels around those follicles, improving that supply. But that is only part of the story. Once active, and I will explain that word in a minute, minoxidus sulfate works as a potassium channel opener. It works on the cells of the dermal papilla, the structure at the base of the hair follicle that controls hair growth. When these channels open, it stimulates the follicle to stay in its growth phase for longer. It can also rescue follicles that have miniaturized over time. Follicles that have slowly shrunk under the influence of hormones, particularly DHT, and nudge them back towards producing thicker, more visible hair. What it cannot do is restore follicles that have completely died. Long-standing untreated hair loss, significant scarring or decades of follicle miniaturization can reach a point of no return. If the follicle is gone, minoxidil cannot bring it back, which is why starting earlier when follicles are miniaturized but still present gives better results than waiting. Now let's understand why minoxidil works brilliantly for some people and does almost nothing for others. Minoxidal is a prodrug. It is not active in the form you apply it or swallow it. It has to be converted inside the body, specifically inside the hair follicle, into its active form called minoxidyl sulfate. And the enzyme that does this conversion is called sulfotransferase, specifically SULT1A1. The amount of this enzyme in your hair follicles is genetically determined and it varies enormously between people. If you have high sulfotransferase activity, minoxidyl gets converted efficiently. Minoxidyl sulfate does its job. You are a responder. If you have low sulfotransferase activity, minoxidil sits there largely unconverted. Your follicles never see the active ingredient, and you spend months applying it to your scalp, watching nothing happen, concluding that minoxidil does not work. It does work, it just does not work for you yet, and that distinction matters enormously. Research shows that only 30 to 40% of people achieve significant hair regrowth with topical minoxidil. The rest are partial responders or non-responders, and this enzyme is almost certainly a major reason why. There is now a diagnostic test called the minoxidal response test that can predict from plugged hair follicles whether someone is likely to respond to minoxidil before they even start treatment. It is currently available in the US through a company called Daniel Allain. Though not in all states, it is not yet clinically available in the UK or India, but it exists. And as personalized medicine develops, this kind of predictive testing is exactly where hair loss treatment is heading. Now let me share something I find particularly fascinating. Tretinoin, a topical retinoid most commonly known for acne treatment, can actually upregulate sulfotransferase activity in hair follicles. In one study, 43% of people predicted to be non-responders to minoxidil were converted to responders after just 5 days of topical tretinoin. 5 days, which means the combination of tritinoin and minoxidil may be a genuinely meaningful approach for people who have not responded to minoxidil alone. If you have been using minoxidil without results, this is a conversation worth having with your dermatologist. So that is how it works. Now let's talk about how you actually use it. For most of minoxidil's history, it came in one form for hair loss. Topical, a liquid or foam applied directly to the scalp. Two concentrations, 2% and 5%. The 2% was the original formulation approved for both men and women. The 5% came later, initially approved for men, though it is now widely used across genders. The foam formulation is generally better tolerated than the liquid. It does not contain propylene glycol, which is what causes most of the scalp irritation people experience with the liquid form. And then something shifted. Dermatologists began using low dose oral monoxidyl off label for hair loss, not the doses used for blood pressure, which were 10 to 40 milligrams, much, much lower, typically 0.25 to 5 mg per day, a fraction, and the results have been interesting. A 2026 review confirmed that low dose oral monoxidal produces measurable increases in hair density by 3 to 6 months with stabilization after that if treatment continues, which tells us something practically important. If oral minoxidil is going to work for you, you will likely know within the first six months that is your minimum trial period. The advantages of oral over topical are real. No sticky residue, no alcohol-based scalp irritation, better adherence because a tablet once a day is simply easier than applying a liquid twice a day without fail. And because oral monoxidal bypasses the skin absorption step, it may reach the follicle more consistently regardless of sulfotransferase activity in the scalp. But the disadvantages are real too, and I want to be honest about them. The most common side effect of oral monoxidal in approximately 15 to 24% of patients is hypertrichosis, unwanted hair growth in places you did not intend. Face, arms, legs, ears, the very thing that caused up john embarrassment in the 1970s is still happening just at much lower doses. Which does make you wonder whether anyone at upjohn is still slightly smug about it all. For women, hypertrichosis is a particular concern. The incidence is higher and it can affect the face. This is why women are typically started at much lower doses, 0.25 to 1 mg daily compared to men who are typically started at 2.5 to 5 mg. The principle is the same. The dose is not. Oral monoxidyl is used in women, but the conversation with your doctor about dose, monitoring, and what to watch for matters more. Fluid retention affects approximately 1 to 10% of patients, typically mild ankle swelling in the first 1 to 3 months. Not common but worth knowing. And one more thing worth being aware of aspirin. Low dose aspirin taken by millions of people daily for heart disease prevention inhibits the sulfotransferase enzyme. There is emerging evidence that it may reduce minoxidal response in people taking it regularly. The research is early, but if you're on daily aspirin and not responding to minoxidil, it is worth mentioning to your doctor. Then, anyone with pre-existing heart conditions, kidney disease, or significant fluid retention issues should have a proper assessment before starting oral minoxidil. It is a cardiovascular medication being used off label. Tropical minoxidil is far more forgiving, available over the counter and with an excellent safety record. A word on where you are in the world. Topical minoxidil is generally available over the counter. Oral minoxidil requires a prescription in the UK, US, Europe, and most countries. And wherever oral is available without one, please do not take it without medical guidance. Hair loss is multifactorial. Oral minoxidil is a cardiovascular medication. It deserves proper oversight. And two things worth watching in the near future: sublingual minoxidil dissolved under the tongue is currently in phase 3 trials. The potential advantage is bypassing liver metabolism, which could mean lower effective doses and fewer side effects. Results are expected in mid-2026. And separately, a company called Veradermix has just reported positive phase 3 results for an extended release oral menoxidal tablet, the first potential new oral approval in 30 years, with promising efficacy and a clean side effect profile. Neither is available yet, but the landscape is moving. Now, one of the things menoxidal does, among other mechanisms, is push follicles that have stalled intelligen back into anogen, back into the growth phase. And this brings us to one of the most important things you need to know about this drug. One of the most common reasons people stop using minoxidil in the first 6-8 weeks is because their hair starts falling out more in the shower, on the pillow, everywhere. Understandably, they panic. They assume the treatment is making things worse. Some have described it as watching their hair disappear in real time. It feels like a betrayal. It is not. When minoxidyl pushes a follicle from telogen into anogen, from resting into growing, the old resting hair has to shed first before the new hair can come through. It is the follicle clearing the way. So in the first 6-8 weeks of treatment, increased shedding is a sign that it is working. The mistake made by thousands of people every year is stopping at precisely the moment it is starting to work. The shed is the beginning. Minoxidal typically requires 3 to 6 months of consistent daily use before meaningful results appear. 6 months is the minimum fair assessment. And here is something equally important to understand before you begin. Minoxidal may have to be used indefinitely. If you stop, the progress is lost. Within 3 to 6 months of stopping, the follicles that minoxidal was supporting begin to regress. The hair that grew while you were on it begins to shed. This is one of the most common surprises people encounter. They stop minoxidal thinking the job is done, and a few months later experience a noticeable hairfall. That shedding is not a coincidence, it is directly related to stopping. Think of it like the gym. If you stop going, you lose the fitness. The hair follows exactly the same logic. Now, does that mean everyone who starts minoxidil is on it forever? Not necessarily. If your hair loss was driven by a specific and now resolved cause, nutritional deficiency that has been corrected, thyroid that is now treated, a period of dellagent effluvium that has settled, the conversation about whether to continue, reduce or stop is worth having with your doctor. Some people do not need it indefinitely, but that decision should be made with guidance based on the reason it was started in the first place. Not made alone in a moment of panic at six weeks. And if you're already using minoxidil, maybe you are three months in, maybe a year in, and it feels like it is working but not quite enough, or the hypertricosis is frustrating you, or you're simply not sure if what you're seeing is progress or visual thinking, that is a real and valid place to be. You're not doing it wrong. Hair responds slowly, and partial responses are common. The answer is rarely to stop. It is usually to look at what else might be contributing: the scalp, the nutrition, the combination approach, the dose. Bring that conversation to your doctor. Now, minoxidal does not exist in isolation anymore. The modern approach to hair loss, particularly androgenetic alopecia, increasingly combines multiple tools, and the evidence for combination approaches is genuinely compelling. Microneedling is probably the combination with the strongest current evidence. Fine needles create tiny controlled injuries in the scalp, triggering the body's healing response, increasing blood flow, and stimulating dormant follicles. They also create microchannels that dramatically increase the absorption of whatever you apply immediately after. Studies show micro needling combined with minoxidil produces roughly double the hair density improvement compared to minoxidil alone. For home use, a derma stamp is recommended over a derma roller. Unlike a roller which drags across the skin, a derma stamp delivers needles in a straight up and down motion, more precise, more consistent, and significantly less risk of hair tangling. Dermatologists also offer microneedling in clinic with deeper needle depths and more precision. Both work. The clinic version is stronger, the home version is consistent. Then copper peptides, particularly GHK copper, are found in scalp serums and increasingly studied for follicle support. They reduce scalp inflammation, support collagen around the follicle, and extend follicle longevity through different pathways to minoxidil, not a replacement, a complement. Then caffeine. Yes, the one in your morning cup has genuine follicle science behind it. Topical caffeine works through a different mechanism to minoxidil, and while the evidence is still building, a caffeine shampoo or serum alongside minoxidil is unlikely to hurt and may genuinely complement it. Then, low-level laser therapy, LED devices for the scalp stimulate mitochondrial activity in follicle cells. The evidence is modest but consistent. FDA clear devices exist for home use. They work best as part of a routine rather than a standalone treatment. And I will admit, I have a soft spot for LED therapy. Sitting under a light and calling it medical, I'm here for it. None of these tools replace minoxidil, but minoxidil alone, especially if you're a partial responder, may not give you everything you are hoping for. The current standard of care in hair restoration is increasingly combination-based. Minoxidal provides the foundation, everything else amplifies it, and it remains after all these decades a very good place to start. So here we are. A failed ulcer drug became a blood pressure medication. A blood pressure medication grew body hair as a side effect. And that side effect, inconvenient, embarrassing, and initially dismissed, became one of the most used hair treatments in the world. Minoxidal is not perfect. It does not work for everyone. It requires commitment and consistency, and stopping it means losing whatever ground you gained. But for the people it works for, and there are many, it is genuinely meaningful. Not vanity, identity, confidence, the daily decision to do something about something that matters to you. Which, now that I think about it, is exactly why a 34-year-old mayor of New York City told the world about his hairline. It takes a certain kind of ease with yourself to say this matters to me and I'm doing something about it. No apology, no pretending. Hair loss, like so many things in health, sits at the intersection of biology and identity. And if addressing it makes you feel more like yourself, use it, do it properly, do it with guidance, do it consistently, and do not let anyone tell you it should not matter to you. Beauty from within is real, and so is the confidence that comes from feeling at home in your own skin, your own hair, your own reflection. However, you like it, own it. I hope something today gave you clarity, gave you a smile, or simply made you pause. Thank you for listening. I'm Dr. Mohi. Until next time, remember this the things that matter to us are really just about the thing itself. And not everything that seems small is insignificant. Sometimes caring the parts of yourself that matter is its own way of coming home to yourself.