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When it comes to hair loss treatments, oral dutasteride often emerges as the most powerful option, consistently outperforming FDA-approved alternatives like finasteride in clinical studies. Across the internet, personal stories echo this sentiment: discussion boards and Reddit threads feature dramatic recoveries, with some users claiming transformations from advanced thinning to a full, healthy head of hair.

(You can read more about this one below.)

However, online spaces tend to spotlight the extremes, either remarkable success stories or reports of failure, creating a distorted picture of what typical results look like. 

So, where does dutasteride truly stand? How do we distinguish between what’s possible and what’s probable? How can you weigh anecdotal experiences against the outcomes you’re most likely to see? And importantly, what might your pattern of regrowth look like after 1, 2, 3, or even 10 years of therapy?

This article addresses these questions directly. We’ll set clear expectations for oral dutasteride, explore how to interpret results shared online, highlight some of the most dramatic dutasteride before and after photos, and offer guidance on what an average treatment journey may look like. 

Finally, we’ll introduce a framework you can use to evaluate and compare all hair loss therapies, helping you see dutasteride ranks in terms of regrowth potential, evidence quality, and long-term safety.

Quick Refresher on Androgenic Alopecia (AGA)

Androgenic alopecia (AGA) is the most common form of hair loss affecting both men and women, marked by progressive thinning and miniaturization of hair follicles. This is primarily thought to be a result of genetic predisposition and the influence of androgens, especially dihydrotestosterone (DHT).^[1]Chen, S., Xie, X., Zhang, G., Zhang, Y. (2022). Comorbidities in Androgenetic Alopecia: A Comprehensive Review. Dermatology and Therapy. 12(10). 2233-2247. Available at: … Continue reading 

There is a huge choice of treatment options for AGA, with FDA-approved therapies such as topical minoxidil and oral finasteride. Many other options are either used off-label or under investigation, including low-level laser therapy, platelet-rich plasma injections, hair transplant surgery, herbal compounds, and emerging agents like prostaglandin analogs and caffeine-based solutions.^[2]Bajoria, P.S., Dave, P.A., Rohit, R.K., Tibrewal, C., Modi, N.S., Gandhi, S.K., Patel, P. (2023). Comparing Current Therapeutic Modalities of Androgenic Alopecia: A Literature Review of Clinical … Continue reading This diversity reflects both the complexity of the disease and a significant unmet need in achieving consistent, satisfactory results for patients.

Despite existing for decades, oral dutasteride has recently surged in popularity as an off-label AGA treatment. Like finasteride, it inhibits the conversion of testosterone to DHT. But it blocks both type I and II 5-alpha-reductase enzymes more effectively, potentially offering a more potent effect. 

Dutasteride 101

Dutasteride blocks both type I and type II isoforms of the 5ɑ-reductase enzyme. This enzyme converts testosterone to DHT, a key hormone driving male pattern hair loss and prostate growth. By inhibiting both isoforms, dutasteride causes a near-complete suppression of DHT, reducing its levels in blood by up to 98%, which is higher than finasteride’s reduction of around 65-70%.^[3]Clark, R.V., Hermann, D.J., Cunningham, G.R., Wilson, T.H., Morrill, B.B., Hobbs, S. (2004). Marked Suppression of Dihydrotestosterone in Men with Benign Prostatic Hyperplasia by Dutasteride, a Dual … Continue reading,^[4]Nickel, J.C. (2004). Comparison of Clinical Trials with Finasteride and Dutasteride. Reviews in Urology. 6(Suppl 9). S31-S39. Available at: PMID: 16985923

The standard and most studied dose is 0.5 mg daily. This is the FDA-approved dose for benign prostatic hyperplasia and the most common dose used off-label for hair loss. Lower doses like 0.2 mg daily have been used in one clinical trial, though 0.5 mg remains the norm.^[5]Escamilla-Cruz, M., Magana, M., Escandon-Perez, Bello-Chavolla, O.Y. (2023). Use of 5-Alpha Reductase Inhibitors in Dermatology: A Narrative Review. Dermatology and Therapy. 13(8). 1721-1731. … Continue reading,^[6]Lee, S., Kim, J.E., Lew, B-L., Huh, C.H., Kim, J., Kwon, O., Kim, B.M., Lee, Y.W., Lee, Y., Park, J., Kim, S., Kim, D.Y., Choi, G.S., Kang, S. (2025). Efficacy and Safety of Low-Dose 0.2 mg … Continue reading 

Why “Expectation Setting” Matters

Realistic expectation setting is fundamentally important for anyone starting their AGA treatment journey, particularly with treatments that do not have a large amount of evidence.

Some people may expect dramatic hair regrowth, often influenced by online testimonials or dutasteride before and after photos showing “hyper responders”.

Others may experience disappointment, frustration, and a decline in self-esteem when their own results are modest or average.

On the other hand, those with overly low expectations may forgo potentially beneficial treatments altogether, missing out on improvements that could positively impact their quality of life.

Online before-and after photos and personal anecdotes present another challenge. They are not standardized, can be misleading, and often feature individuals who have responded exceptionally well to a product, rather than the majority who see more moderate effects. These images rarely account for factors like lighting, hair styling, photo angles, or even digital enhancement, all of which can distort perceived efficacy.

To help guide your treatment selections & expectations, here are two key principles that, once understood, will make all the difference in how you approach your hair growth journey.

Principle #1: What’s Possible ≠ What’s Probable

Consider the following chart.

Note the individual datapoints and how scattered they appear. Also note the trendline, which represents the average of all individual datapoints shown in the chart.

The individual datapoints represent what’s possible for any one individual. The trendline represents what’s probable.

 

Resultantly, people see these dutasteride before and after success stories, and think, “This is all I see. And so I’ll probably get the same regrowth, too.” This shifts their expectations for the drug far above the trendline:

Then they try dutasteride and either quit too early to see regrowth (more on that soon)… or they don’t get the same results, and determine (often erroneously) that the drug just isn’t working for them.

The solution: don’t set expectations by what’s possible. Set expectations by what’s probable. Understand the trendlines for oral dutasteride: when results will typically first start to show, when results will peak and/or plateau, and what results will look like 5+ years into the future.

You can do this by using a standardized rubric we created called Regrowth Potential.

Regrowth Potential

As mentioned above, Principle 1 shows us that results tend to scatter across a spectrum: some datapoints high, some low, with a trendline running through the middle. The problem is that online anecdotes usually highlight only the high datapoints, while clinical trial data can feel abstract and hard to translate into lived experience. 

Regrowth Potential is our way of standardizing this landscape. It’s designed to cut through anecdotal extremes and align patients with the trendline, what most people can realistically expect.

So what does the average look like?

Most people see stabilization first, regrowth second, and a slowing of hair loss, with partial reversal layered on top. 

Gains usually peak within 6-12 months, then plateau.^[8]Nestor, S, M., Ablon, G., Gade, A., Han, H., Fischer, D.L. (2021). Treatment options for androgenetic alopecia: Efficacy, side effects, compliance, financial considerations, and ethics. Journal of … Continue reading

Typical regrowth brings hair back to where it was 1-3 years earlier, not to pre-hair-loss density. 

And what influences where you fall on that spectrum?

1. How long you’ve been losing hair: Earlier intervention = higher trendline. Long-standing bald spots rarely respond.^[9]Feldman, P.R., Gentile, P., Piwko, C., Motswaledi, H.M., Gorun, S., Pesachov, J., Markel, M., Silver, M., Brenkel, M., Feldman, O.J., Kamen, C.L., Uleryk, E., Guevara-Aguirre, J., Fiebig, K.M. … Continue reading 
2. Which therapy you use: Some are more effective at certain stages or patterns.
3. How consistent you are: Skipped doses or stopping early push results below the trendline.

Most patients should expect stabilization and modest regrowth. A small minority will experience “hyper-responsiveness,” but these rare outcomes should not set the benchmark. 

Principle #2: Poorly-Studied Treatments = More Variability In Results

When fewer studies exist on a treatment, expectations for hair regrowth become harder to pin down. With limited data, some patients may get spectacular results, while others see very little. But, without enough trials, it’s nearly impossible to know how common each outcome really is.

Take finasteride and oral dutasteride as examples. Finasteride has been tested in dozens of randomized controlled trials, which means we can say with high confidence what the average regrowth looks like and where most patients will land. Oral dutasteride, by contrast, has fewer high-quality studies. 

That doesn’t mean dutasteride is ineffective. In fact, the regrowth gains by dutasteride have often outperformed finasteride users. But it does mean the range of possible outcomes is wider, with more unpredictability between “great responders” and “minimal responders”. 

When it comes to understanding expectations for androgenic alopecia treatments, the normal distribution model helps clarify why individual results can be so different, even when clinical averages sound reassuring. Treatment outcomes typically form a bell-shaped curve rather than a single value, meaning people experience a range of responses. 

• Clinical averages, which are often cited in studies, represent the peak of this curve, not the experience of every patient. Most individuals see results somewhere near this average, but plenty fall above or below it.

• Wide curve (high variability, low evidence): When evidence for a treatment is limited or inconsistent, like with newer therapies, the curve is broad. Some may see fantastic regrowth, others very little, and outcomes are harder to predict. 
• Narrow curve (predictable outcomes, high evidence): For well-researched medications, the curve is tight. Most people’s results cluster close to the average, giving new patients more confidence in knowing what to expect.

Importantly, average never means “everyone”. Treatment outcomes often show a spread, so while clinical trials help set realistic expectations, individual journeys may differ depending on genetics, age, stage of hair loss, and treatment adherence. 

This variability also explains why anecdotes online can feel so misleading. When people share their results in forums, they’re often the outliers, the best or worst cases. On a scatterplot of individual datapoints, these stories sit at the edges. With dutasteride, the scatter is typically above the trendline, meaning a Reddit “success story” may be far removed from what most users should expect.

The rubric we can use to get a sense of whether our results will be predictable or variable is Evidence Quality.

Evidence Quality

Evidence quality answers the question “How reliable is the evidence that this intervention will actually help regrow my hair?” The strength of this evidence is determined not only by the number of studies available but also by their design, especially RCTs, which typically provide the most trustworthy evidence.

The concept of confidence in treatment outcomes can be likened to a game show in which money is hidden behind two doors. Behind door number 1, the amount of money behind it could be anywhere between $0 and $100. You might walk away with nothing, a little, or a lot, and there’s no way to know for sure, because there just isn’t enough evidence to narrow down the possibilities. 

With door number 2, the money behind it ranges tightly between $49 and $51. Because so many high-quality studies exist, you can be confident that your outcome will almost certainly fall within this narrow window, making it much easier to know what to expect.

More evidence means a smaller range and greater predictability; less evidence means more uncertainty and a wider range of possible outcomes.

Relating this back to oral dutasteride, the treatment has fewer published randomized controlled trials compared to finasteride. This means less outcome certainty, so patients considering dutasteride face a wider bell curve of potential results (as shown above), from exceptional regrowth to only minor improvement.

To summarize: 

• More and better studies = tighter confidence around the true average results
• Fewer studies = more uncertainty, a wider range of possible outcomes, and less ability to predict what will happen for any individual. 

Understanding the evidence quality of a treatment empowers patients to interpret clinical claims and anecdotal stories with a critical eye, helping them choose interventions with the best established track record and manage expectations where data is still emerging.  

Anecdotal Successes

In the world of hair loss drugs, Redditors and hair loss forums tend to overshare the best of what’s “possible”. 

Let’s have a look at 10 real-life anecdotal reports shared by Reddit users. 

It goes without saying that the experiences related below, including any before-and-after photos, are anonymously submitted by users and strictly represent their personal experiences. They are not considered medical evidence, nor should they be relied upon as medical advice. 

It should also be noted that some of these individuals used other treatments alongside dutasteride to assist in their hair regrowth journey. With combination treatments, it is not easy to see what’s causing the hair growth, so we need to be even more cautious about the success seen.

Case 1: 14-month course of oral dutasteride 0.5 mg daily

This 25-year-old male reported aggressive hair thinning between ages 19–21, which he reportedly stabilized with dutasteride monotherapy at 0.5mg/day. He had previously tried finasteride for about a year but did not report any visible regrowth. The patient described significant regrowth of previously thin hairs, with increased hair density compared to treatment start. He noted that there were no side effects throughout treatment. Notably, he mentioned that finasteride provided stabilization only, while dutasteride produced visible regrowth after one year of use. Other users also highlighted the greater potency and longer half-life of dutasteride compared to finasteride.

Case 2: 10-month course on dutasteride 0.5 mg and oral minoxidil 0.625 mg daily

A female individual (age unspecified) with diffuse thinning, especially around the parting, reported on her experience using dutasteride 0.5mg/day, along with oral minoxidil 0.625mg/day (which was scaled back from an initial dose of 1.25mg). Further into the treatment, she added topical minoxidil to her treatment stack. At the 10-month mark, she reported a significant increase in hair density compared to baseline, with notable thickening at the part line, as confirmed by the user-submitted photos. The user was delighted with her results and intends to decrease her dutasteride use to a maintenance dose eventually. 

Case 3: 10-month course on dutasteride 0.5 mg and oral minoxidil 5 mg daily

This report was from a 26-year-old male with clearly noticeable balding by age 20 and a family history of male pattern baldness, including his father and both grandfathers. The user’s protocol included oral dutasteride 0.5mg and oral minoxidil 5mg daily. The user noted heavy shedding in the first two months of treatment, with the first noticeable signs of improvement appearing at months 2-3, before achieving a successful outcome by month 10, when they reported marked hair thickening and a renewed sense of confidence and self-esteem. The user did not report any side effects from dutasteride, but linked minoxidil use to a mild increase in arm hair. It’s worth noting that the user’s physician had recommended he switch from his initial finasteride therapy to dutasteride due to their “aggressive” alopecia.

Case 4: 3.5 months on oral dutasteride 0.5 mg and minoxidil 5 mg daily

A 22-year-old male shared his experience using oral dutasteride (0.5mg/daily), oral minoxidil (5mg/daily), plus dermarolling (1.5mm/weekly) for 3.5 months. The user achieved significant increases in hair density and regrowth, a self-reported improvement in self-esteem, and no reported side effects, namely as to his libido and sexual function. He noted his consistent use and starting relatively early in the hair loss process as reasons for his favorable outcome. Additionally, he highlighted that he did not titrate up to his final doses but started the full protocol from day one.

Case 5: 6 months on dutasteride 0.5 mg (ed 1st month – 3x/wk) + microneedling 1.0 mm weekly

This male (23 y/o) used dutasteride at the dose of 0.5mg daily for the first month, then reduced to 0.5mg thrice weekly, along with microneedling 1.0mm once weekly, over the course of six months. The apparent results include hairline and temple regrowth, with the hair improving in thickness and health overall. The user did not report any side effects beyond bleeding associated with microneedling, noting that he began to notice changes within a month. In explaining his results, he also believed himself to be highly responsive to the treatment. 

Case 6: 2+ years on dutasteride 0.5 mg daily and sublingual minoxidil 0.9 mg – 2.7 mg daily

In this report, a 31-year-old male shared his results on a protocol of oral dutasteride (0.5mg daily) and sublingual minoxidil (gradually increased from 0.9mg to 2.7mg daily). While he started treatment with oral finasteride, he switched to dutasteride and sublingual minoxidil at the advice of his dermatologist. The users reported significant improvement after 3–4 months, with darker hair color and thickening of hair at the crown and mid-scalp. He added that most improvements came within 12 months, noting that he did experience any shedding with minimal side effects.

Case 7: 2 months on dutasteride 0.5 mg daily and oral minoxidil 2.5 mg daily

A 31-year-old male detailed his experience taking dutasteride 0.5mg daily alongside oral minoxidil following a series of unsuccessful treatments. He initially began with finasteride 1mg, which slowed hair loss but did not affect major regrowth. He then tried minoxidil and microneedling, before restarting finasteride and topical minoxidil alongside dermarolling. Upon switching to dutasteride, he noted major improvement in just two months, including achieving thicker hair and the disappearance of bald spots. The user reported no major side effects and noted supplementing his protocol with a daily multivitamin (Becadexamin) and a collagen supplement to support skin and hair.

Case 8: 3.5 months on dutasteride 0.5 mg daily and topical minoxidil 2x daily

A 24-year-old male reported significant improvement in hair density and coverage following 3.5 months of oral dutasteride 0.5mg/day and topical minoxidil (Rogaine) applied twice daily. The Redditor reported hair shedding, especially around the hairline, at month one. In the second half of the treatment period (months 2-3.5), however, he experienced accelerated hair regrowth with the appearance of a full head of hair. He was prescribed dutasteride directly (no prior finasteride use) and reported no major side effects as of the 3.5-month mark. 

Case 9: 1 year on dutasteride 0.5 mg daily and 10 years on topical minoxidil

This user (age 31) used daily dutasteride (Avodart 0.5mg) for one year in addition to ten years of consistent topical minoxidil use. He had previously used finasteride for two years with satisfactory results, stating that he could have achieved more regrowth by combining minoxidil with a DHT blocker. Following his switch from finasteride to dutasteride, he noted improvements in hair strength, libido increase, and clearer thinking. Months 3-8 were marked by shedding and brittle, weaker hair, with the patient considering switching back to finasteride. But after month 8, he saw thicker strands and mild regrowth. He also noted longer hair cycles, which now allow him to better maintain hair length. The user planned to continue with treatment and reevaluate at the two-year mark.

Case 10: 8 months on dutasteride 0.5 mg and 10 months on oral minoxidil 2.5 mg

This male user (29 y/o) undertook a protocol of oral dutasteride 0.5mg/day and oral minoxidil 0.5mg/day concurrently for eight months, with strong improvements in hair regrowth and thickness. He reported shedding at months 1-3 followed by regrowth starting at the 3-month mark. He observed increased hair density in the crown and temples from months 3 to 8, and noted major progress by month 10, with the crown nearly full, despite a persistent “M-shaped” hairline. The user reported no major side effects and plans to undergo a hair transplant, notwithstanding the favorable outcome. 

But these anecdotes are often far above the trendline, over “average” expectations.

Probable Regrowth Timeline for Oral Dutasteride

We have laid out a likely timeline for oral dutasteride treatment. However, this is based on four studies that we could find using oral dutasteride for hair loss, including one where it was used for frontal fibrosing alopecia.^[10]Tsunemi, Y., Irisawa, R., Yoshiie, H., Brotherton, B., Ito, H., Tsuboi, R., Kawashima, M., Manyak, M. (2016). Long-term safety and efficacy of dutasteride in the treatment of male patients with … Continue reading,^[11]Pindado-Ortega, C., Saceda-Corralo, D., Moreno-Arrones, O., Rodrigues-Barata, A.R., Hermosa-Gelbard, A., Jaen-Olasolo, P., Vano-Galvan, S. (2020). Effectiveness of Dutasteride in a Large Series of … Continue reading,^[12]Vano Galvan, S., Saceda-Corralo, D., Morena-Arrones, O.M., Rodrigues-Barata, R., Morales, C., Gil-Redondo, R., Bernardez-Guerra. C., Hermosa-Gelbard, A., Jaen-Olasolo, P. (2019). Effectiveness and … Continue reading,^[13]Harcha, W.G., Martinez, J.B., Tsai, T-F., Katsuoka, K., Kawashima, M., Tsuboi, R., Barnes, A., Ferron-Brady, G., Chetty, D. (2014). A randomized, active and placebo-controlled study of the efficacy … Continue reading

Month 0-3: No visible changes:

• Most studies note minimal to no observable regrowth in the first 3 months as dutasteride begins to reduce DHT levels, but hair follicles have not yet responded morphologically. 

Month 3-6: Early results seen:

• Clinical improvements in hair thickness and reduced shedding are often first noted from around month 3 onward.
• Quantitative hair count changes become statistically significant compared with placebo after 12 weeks; global photographic assessments begin to reflect mild positive change (~22-31% of subjects with slight/moderate increase at week 12).

Month 6-9: First cosmetic improvements:

• By 6-9 months, most patients exhibit visible improvement in hair density and coverage, with the peak initial response typically building upon earlier thickening. 
  • In a Japanese study, mean hair count increased significantly at 26 weeks and continued to improve at 52 weeks (68-87 hairs in a 2.54cm area).
  • Panel assessments at month 6 indicated ~75-85% of patients had some improvement in global photographs.

Months 9-15: Peak response period:

• Maximum regrowth and cosmetic benefits are typically observed within the first 12-15 months, based on clinical results.
  • “Marked improvement” rates ranged from 23-25% at 12 months with daily dosing in large cohorts. Median improvement in photographic rating scores and increases in terminal hair count continue through this period.
  • Sustained effects shown to persist up to 1 year in an open-label extension study.

Months 15-24: Maintenance phase: 

• Most patients maintain results with continued therapy, improvements plateau or slightly decline, but remain superior to baseline and other treatments.
  • Longer-term users (mean follow-up up to 17 months) show stabilization and ongoing maintenance with only rare further large gains.
  • Clinical improvement was seen in studies where doses ranged 3-7 capsules/week, with higher doses correlating to better maintenance and slightly higher efficacy.

Months 24-26: Possible plateau, limited data:

• Efficacy plateaus; possible mild regression or fluctuation, but proper adherence maintains gains for most patients. 
  • Real-world data of up to at least 24 months confirm sustainability in appropriately selected patients, especially at higher doses.
  • No long-term studies exceed 36 months, so late-stage trends remain speculative.

But what about all the success stories we see online, users on Reddit or other forums who have experienced dramatic hair regrowth?

Well, this difference usually stems from a phenomenon called survivorship bias. 

What is Survivorship Bias?

• Survivorship bias happens when the accounts you see are not representative of all experiences but are disproportionately skewed toward the most remarkable, positive cases.^[14]Rao, T. (2024). Understanding Survivorship Bias: Implications for Research and Decision-Making. Journal of Emerging Technologies and Innovative Research, 11(6). JETIR2406276
• People with extreme positive results are much more likely to post about their experiences, eager to share their success.
• In contrast, those who experience average or mediocre outcomes (which is the majority) rarely feel motivated to post.
• As a result, the outcomes you typically see online are samples from the tails of the bell curve: exceptional or very poor cases, not the “center” or average results.

Clinical Trial vs. Online Reports

• Clinical trials measure average results across a large, diverse population, using objective metrics.
• Online reports are anecdotal and self-selected. Because impressive transformations are inspiring, these are far more likely to be posted and shared.
• This dynamic can mislead readers into believing that dramatic regrowth is almost guaranteed, when in reality it is just one possibility among many, and not the most probable outcome.

Combining Treatments: Narrowing the Curve

While oral dutasteride is one of the most effective monotherapies for AGA, if you want to increase your odds of good results, combining it with additional therapies can have a dramatic impact. 

Studies have shown that adding minoxidil to dutasteride can further improve regrowth outcomes, leveraging the vasodilatory and follicle-activating effects of minoxidil, alongside DHT suppression from dutasteride.^[15]Obeid, M.N.A., Fattah, N.S. A., Elfangary, M.M., Al Husseni, R.M. (2024). Comparison between topical minoxidil 5% alone versus combined with dutasteride (topical 0.02% through microneedling or oral … Continue reading

Furthermore, adding low-dose dutasteride to ongoing finasteride therapy in patients with suboptimal response resulted in a dramatic increase in hair density, suggesting that combined therapy can be beneficial for those not fully responding to finasteride alone.^[16]Boyapati, A., Sinclair, R. (2013). Combination therapy with finasteride and low-dose dutasteride in the treatment of androgenetic alopecia. Australasian Journal of Dermatology. 54(1). 49-51. … Continue reading 

Going back to the bell curves, more modalities = less variability. By targeting different mechanisms (like minoxidil) or by targeting more types of 5-alpha-reductase (like in the finasteride study), outcomes become less dependent on any single pathway. This leads to more predictable, less variable results across a wider patient group.^[17]Mysore, V., Kumaresan, M., Dashore, S., Venkatram, A. (2023). Combination and rotational therapy in androgenetic alopecia. Journal of Cutaneous and Aesthetic Surgery. 16(2). 71-80. Available at: … Continue reading 

How Can I Maintain “Realistic Expectations”?

To keep realistic expectations on oral dutasteride for hair regrowth, it’s critical to understand both the typical timelines and the nature of outcome variability:

What does “realistic” mean?

• Realistic does not mean pessimistic: Most users will benefit, but responses vary between individuals. A realistic expectation is based on clinical averages, not the best or worst case.
• Don’t expect to be “cured” of your hair regrowth. Most treatments “rewind the clock” a certain amount. Oral dutasteride may reverse hair loss by 6-24 months on average. However, dramatic multi-year regrowth is much less common, possible but not probable for most users.
• Your most probable result is noticeable improvement and stabilization, rather than full reversal of all past hair loss. 

Practical Takeaways

• Be patient: Oral dutasteride takes time – most users don’t see meaningful change until at least 6 months in, with optimal results often peaking around 12-15 months. 

• Track your own progress: Use consistent photos or, ideally, hair counts in a fixed area to monitor changes. Comparing to internet success stories often skews expectations and reflects outliers rather than the norm.

• Define success on your own terms: For some, success means stopping hair loss. For others, it’s regaining density. Know what you’re aiming for and adjust expectations accordingly. 

• Consider combination treatments: Pairing dutasteride with therapies like minoxidil or microneedling may improve outcomes and reduce variability, especially if you’re not seeing early improvements. 

• Use clinical data to ground your expectations: Clinical trials give you an average expectation, not a guarantee. Use online anecdotes as inspiration, not prediction.

Final Thoughts

Your expectations for any hair loss treatment, even oral dutasteride, should rest on two key pillars:  regrowth potential x evidence quality.

Together, they shape your position on the “bell curve” of likely outcomes.

• If you’re early in your hair loss journey, consistently take the medication, and possibly combine it with other therapies, you’re more likely to end up closer to the favorable side of the curve.
• If your hair loss is advanced or you’ve tried many options before, you might fall closer to the average or lower end.

Either way, understanding that most people land somewhere near the middle of the curve, not at the extremes, helps you avoid frustration and stay committed.

Setting expectations isn’t about limiting hope or being overly pessimistic; it’s about anchoring your treatment outcomes to reality, so you can make better, more sustainable decisions about your treatment journey.

Oral finasteride has established itself as a highly effective treatment for androgenic alopecia (AGA) and is widely prescribed around the globe. Its success can be largely attributed to its proven ability to slow hair loss and stimulate regrowth by inhibiting the conversion of testosterone to DHT, the hormone chiefly responsible for follicular miniaturization. 

However, despite its well-documented efficacy, oral finasteride has become equally notorious for its potentially systemic side effects. Some men experience adverse effects such as decreased libido, erectile dysfunction, mood changes, and even persistent symptoms after discontinuation, a phenomenon called post-finasteride syndrome.^[1]Diviccaro, S., Melcangi, R.C., Giatti, S. (2019). Post-finasteride syndrome: an emerging clinical problem. Neurobiology of Stress. 12. 100209. Available at: https://doi.org/10.1016/j.ynstr.2019.100209 This reputation has prompted many to seek alternatives that are both effective and safer for long-term use.

Recently, topical finasteride formulations have garnered attention as a promising alternative. By delivering the medication directly to the scalp, topical finasteride aims to minimize systemic absorption and thereby reduce the likelihood of side effects while still providing the benefits of DHT inhibition where it matters most. This alternative approach has piqued the interest of both patients wary of systemic issues and clinicians seeking tailored treatments.

In this article, we will examine whether topical finasteride can serve as a viable alternative to its oral counterpart. The main focus will be on answering three questions:

1. Can topical finasteride effectively regrow hair in those affected by AGA?
2. Does it match the efficacy results seen with oral finasteride?
3. Can it reduce hair loss while offering a more favorable side effect profile?

Ulo offers finasteride options that range from low to high dose finasteride – allowing you to be flexible in your treatment choices.

Oral vs. Topical Finasteride

Some research directly compares oral finasteride (1 mg daily) with various concentrations of topical finasteride, aiming to match hair regrowth efficacy while minimizing systemic side effects. Let’s take a look at a couple of examples:

Study 1 – Piraccini et al., 2022 (Phase III RCT, 24 weeks)

• Compared topical finasteride (0.25% spray) to oral finasteride (1 mg/day) and placebo in men with AGA.^[2]Piraccini, B.M., Blume-Peytavi, U., Scarci, F., Jansat, J.M., Falques, M., Otero, R., Tamarit, M.L., Galvan, J., Tebbs, V., Massana, E., Topical Finasteride Study Group. Efficacy and safety of … Continue reading
• The increase in hair count on a defined scalp area was similar for topical and oral finasteride, both outperforming the placebo, suggesting comparable clinical benefit.
• Systemic finasteride (oral) reduced mean serum DHT by 55.6%,  whereas topical finasteride reduced it by 34.5%. Plasma finasteride exposure from topical application was over 100 times lower than from oral administration. 
• Both had similar low rates of mild side effects, but sexual side effects, but sexual side effects were more associated with oral treatment. 
• Caveats: The “target area” measured may not represent the full scalp effects; although systemic absorption, albeit at a much lower level with topical application, still occurred and varied by formulation. 

Study 2 – Bhura, 2013 (RCT, 8 months)

• Parallel-group comparison in male AGA, tracking hair density and systemic DHT.^[3]Bhura, M. (2013). Comparative Analysis of Topical and Oral Finasteride in Androgenetic Alopecia: Impact on Hair Growth, Systemic Absorption, and Adverse Effects. Indian Journal of Basic and Applied … Continue reading 
• Oral finasteride resulted in slightly superior increases in hair number and thickness, although the difference was not statistically significant.
• Oral finasteride significantly reduced systemic DHT and caused more sexual side effects; topical finasteride led to minimal serum DHT changes and almost no systemic side effects, with most reactions being local (e.g., irritation).
• Those worried about long-term systemic effects preferred topical use, despite slightly less pronounced gains.

Study 3 – Hajheydari, 2009 (RCT, 6 months)

• Compared a 1% topical gel + placebo tablet with oral finasteride 1 mg/day + placebo gel.^[4]Hajheydari, Z., Akbari, J., Saeedi, M., Shokoohi, L. (2009). Comparing the therapeutic effects of finasteride gel and tablet in treatment of the androgenetic alopecia. Indian Journal of Dermatology, … Continue reading 
• Both the gel and tablet produced statistically significant increases in total hair count and terminal hair count.
• There were no significant differences in hair thickness, hair count, or size of the bald area between the two groups. 

Mechanism of Action

Finasteride Pharmacodynamics

Finasteride is a competitive inhibitor of 5α-reductase, primarily targeting the type II isoenzyme at therapeutic doses, which predominates in the hair follicles and prostate. As mentioned above, this enzyme catalyzes the conversion of testosterone to DHT. 

At higher tissue concentrations, finasteride can also inhibit type I 5α-reductase, which is primarily found in the skin and sebaceous glands; however, its clinical significance for hair loss at standard doses is limited. By selectively inhibiting the type II enzyme, finasteride effectively lowers local and systemic DHT levels.^[5]Finn, D.A., Beadles-Bohling, A., Beckley, E.H., Ford, M.M., Gililland, K.R., Gorin-Meyer, R.E., Wiren, K.M. (2006). 12(1). 53-76. A New Look at the 5α-reductase Inhibitor Finasteride. CNS Drug … Continue reading 

What is Finasteride’s Effect on DHT Suppression?

Finasteride’s effect on DHT suppression is characterized by a logarithmic dose-response curve, meaning that even very low systemic levels can produce a marked reduction in both serum and scalp DHT. Most of the drug’s inhibitory action is achieved at low doses, with additional dosing yielding only marginal further effect.

As a result, even minimal “leakage” of topically applied finasteride into the bloodstream can decrease DHT levels elsewhere in the body.

Pharmacokinetic studies show that inhibition of type-II 5ɑ-reductase reaches saturation at typical clinical dosage, while type-1 enzyme inhibition requires much higher concentrations. This nonlinear pharmacodynamic profile explains both the strong efficacy and the wide safety margin of topical finasteride: a small amount achieves most of the desired effect, so careful formulation is crucial to maximize scalp delivery while minimizing unwanted systemic exposure.^[6]Suzuki, R., Satoh, H., Ohtani, H., Hori, S., Sawada, Y. (2010). Saturable Binding of Finasteride to Steroid 5ɑ-reductase as Determinant of Nonlinear Pharmacokinetics. Drug Metabolism and … Continue reading 

What the Science Says

Topical finasteride has been studied across a 200-fold concentration range, from 0.005% solutions to 1% gels. Collectively, these trials demonstrate meaningful reductions in shedding and measurable regrowth; however, systemic exposure increases with dose and vehicle potency.

Study	Concentration & Vehicle	Hair Growth-Outcomes	Systemic/Serum Findings
Mazzarella 1997, single-blind, 52 men/women, 16 months.	0.005% hydro-alcoholic solution	73% reported “high effectiveness”; wash-test hair counts improved; slowed shedding by month 6	No significant change in plasma DHT or testosterone; absorption was negligible.
Tanglertsampan 2012 RCT, 33 men, 24 weeks.	0.1% lotion + 3% minoxidil	The combination arm gained more hairs/cm2 and thicker shafts than minoxidil alone.	Local irritation mild; systemic parameters not monitored.
Datta 2021 double-blind trial, 35 participants completed, 6 months.	0.1% lotion +5% minoxidil vs oral 1 mg.	The topical combination was non-inferior to oral minoxidil for reducing the Hamilton-Norwood stage.	Sexual adverse events only occurred in the oral group; topical was well-tolerated.
Caserini 2016 OK study, 50 men, 1 week; Piraccini 2022 phase III, 323 completers, 24 weeks.	0.25% solution.	-70% scalp DHT after once-daily 1 mL; +20.2 hairs in 1 cm2 target area at 24 weeks – numerically equal to oral 1 mg.	100-200 μL doses reduced serum DHT by only 24-26%; 400 μL treatment reduced levels by 44-48%; Cmax was more than 100 times lower than oral.
Rossi 2020 retrospective, 69 women, 12-18 months.	0.5% lotion (postmenopausal women)	The Finasteride + minoxidil group scored higher on a 7-point global scale compared to the 17ɑ-estradiol + minoxidil group.	No androgenic side effects reported.
Hajheydari 2009 DB-RCT, 45 men, 6 months.	1% gel	Increases in total and terminal hair counts matched those of oral 1 mg; the bald area remained unchanged.	Serum DHT not assayed; clinical side-effects minimal.

Low-Dose Takeaways

Even a micro-dose of 0.005% twice daily (~0.1 mg/day) curbed shedding and improved density without measurable systemic suppression, making it an attractive option for highly risk-averse users.^[7]Mazzarella, F., Loconsole, F., Cammisa, A., Mastrolonardo, M., Vena, G.A. (1997). Topical finasteride in the treatment of androgenic alopecia. Preliminary evaluations after a 16-month therapy course. … Continue reading

Mid-Range (0.1-0.25%)

Adding 0.1% finasteride to minoxidil amplifies regrowth compared to minoxidil alone, while standalone 0.25% sprays deliver oral-level scalp DHT blockade, maintaining serum exposure roughly one-tenth that of tablets. Dose and volume are critical.^[8]Caserini, M., Radicioni, M., Leuratti, C., Terragni, E., Iorizzo, M., Palmieri, R. (2016). Effects of a novel finasteride 0.25% topical solution on scalp and serum dihydrotestosterone in healthy men … Continue reading

High-Dose (0.5-1%)

Topical finasteride options at 0.5% have been shown to extend benefits to female pattern hair loss with good tolerability.^[9]Rossi, A., Magri, F., D’Arino, A., Pigliacelli, F., Muscianese, M., Leoncini, P., Caro, G., Federico, A., Fortuna, M.C., Carlesimo, M. (2020). Efficacy of Topical Finasteride 0.5% vs 17ɑ-Estradiol … Continue reading

Why Formulation and Dose Matter

1. The vehicle drives absorption: according to the studies, hydro-alcoholic sprays penetrate faster than gels or liposomes, explaining divergent serum DHT curves at equal nominal strengths. 
2. Daily drug load, not percentage alone, predicts systemic spill over; 0.025% at 400 μL approaches the systemic impact of oral dosing, whereas 100 μL does not.
3. Combination therapy often allows for a lower finasteride concentration to achieve equal cosmetic benefits, thereby minimizing exposure.

Minimizing Systemic Absorption

While topical finasteride offers an option for minimizing systemic exposure, several key variables influence the amount that enters the bloodstream, and this can occur surprisingly quickly.

Key Factors Affecting Systemic Absorption

• Carrier Agent: The vehicle used to deliver finasteride dramatically alters absorption. Alcohol-based (ethosomal) carriers enhance drug penetration through the skin and into deeper layers like the dermis much more than conventional liposomes, which tend to remain more superficial. One study found that ethosomes resulted in approximately six times greater dermal accumulation than liposomes, highlighting the direct impact of carrier choice on systemic exposure.^[10]Rao, Y., Zheng, F., Zhang, X., Gao, J., Liang, W. (2008). In Vitro Percutaneous Permeation and Skin Accumulation of Finasteride Using Vesicular Ethosomal Carriers. AAPS PharmSciTech. 9(3). 860-865. … Continue reading
• Time on Scalp Before Washing: The longer finasteride remains on the scalp before washing, the greater the chance for absorption through the skin. Washing off too soon reduces drug uptake, but leaving it for extended periods increases both local efficacy and systemic exposure. Guidelines often recommend allowing at least 4-6 hours on the scalp, though this can vary by formulation. 
• Frequency of Use: If you can keep topical finasteride on your scalp for at least 10-12 hours, once-daily applications of low-dose topical finasteride might be beneficial. For those who can only tolerate finasteride for 4-6 hours, twice-daily applications may be better. You can read more about how often topical finasteride should be applied here.
• Individual Skin Permeability: Personal factors, including skin thickness, barrier integrity, genetics, and even scalp conditions, can strongly influence how much finasteride penetrates the scalp. Individuals with more permeable skin may absorb a greater amount of the drug systemically, increasing the risk of side effects.^[11]Brito, S., Baek, M., Bin, B-H. (2024). Skin Structure, Physiology, and Pathology in Topical and Transdermal Drug Delivery. Pharmaceutics. 16(11). 1403. Available at: … Continue reading 

How To Maximize Gains and Minimize Risk

To achieve the best results and reduce the likelihood of side effects, there are several strategies you can employ:

• Establish a Baseline with Serum DHT Testing

Before starting topical finasteride, get a baseline measurement of your serum DHT levels through a blood test. This serves as a reference to assess the extent to which systemic DHT is affected by your treatment. 

• Retest After 30 Days

After one month of consistent topical use, repeat the serum DHT test under the same conditions (preferably in the morning, fasted, and at a similar time of day). This helps you gauge systemic absorption and adjust your regimen if your serum DHT levels drop excessively. Hormone levels fluctuate based on daily rhythms, food intake, and stress, so always test under similar circumstances: morning, fasted, and ideally before applying the day’s finasteride.

• Avoid Confounding Supplements

Avoid supplements that may directly affect DHT, such as those that increase DHT (e.g., creatine) or quercetin (which may lower it). This ensures your test results and progress are a direct reflection of the topical finasteride.^[12]van der Merwe, J., Brooke, N.E., Myburgh, K.H. (2009). Three weeks of creatine monohydrate supplementation affects dihydrotestosterone to testosterone ratio in college-aged rugby players. Clinical … Continue reading,^[13]Ma, Z., Nguyen, T.H., Huynh, T.H., Do, P.T., Huynh, H. (2004). Reduction of rat prostate weight by combined quercetin-finasteride treatment is associated with cell cycle deregulation. Journal of … Continue reading 

• Be Patient – It Takes Time

Visible improvements often require 12-24 months. Don’t make hasty adjustments if you don’t see immediate changes; hair cycles are slow. 

• Track Your Progress Objectively

Use standardized, high-quality photo documentation, same angle, lighting, and distance each time, to objectively monitor changes in hair density and coverage.

Combination Therapies

Robust evidence supports the use of combination therapies for AGA, with multi-modal approaches consistently outperforming monotherapy in terms of efficacy and speed of regrowth.

Finasteride + Minoxidil: Studies show that pairing topical finasteride with 5% minoxidil yields superior hair density and patient satisfaction compared to either agent alone, particularly after 24 weeks of treatment.^[14]Apoorva, V.B., Vibhu, M., Singh, R.H., Smita, T. (2023). Comparative Efficacy of Topical Finasteride (0.25%) in Combination with Minoxidil (5%) Against 5% Minoxidil or 0.25% Finasteride Alone in Male … Continue reading,^[15]Rossi, A., Caro, G. (2023). Efficacy of the association of topical minoxidil and topical finasteride compared to their use in monotherapy in men with androgenetic alopecia: A prospective, randomized, … Continue reading,^[16]Abeck, F., Hansen, I., Kott, J., Schroder, F., Garrahy, E., Veneroso, J., Runger, A., Torster, L., Schneider, S.W., von Buren, J. (2024). Patient-reported outcomes of topical finasteride/minoxidil … Continue reading This combination is effective for both new users and those who have experienced shedding after discontinuing oral finasteride.

Finasteride + Microneedling: Adding microneedling to topical therapy can significantly enhance outcomes. Clinical trials demonstrated that combining microneedling with minoxidil and/or finasteride increased hair density and shaft diameter more than minoxidil alone, with effects noticeable within just 12 weeks.^[18]Chang, Y., Zhang, W., Zhou, J., Lv, L., He, Q., Chen, Y., Wang, P., Zhai, Q. (2025). Clinical efficacy of microneedle combined with 5% Minoxidil solution and finasteride in the treatment of … Continue reading,^[19]Adistri, K., Sirait, S.P., Rihatmadja, R., Legiawati, L., Indriatmi, W., Saldi, S.R.F. (2024). Effectiveness and safety of the combination therapy of micro-needling and minoxidil in androgenetic … Continue reading 

Triple Topical Therapy: Preliminary studies on formulations that combine finasteride, dutasteride, and minoxidil show promising results, with visible regrowth as early as three months in some cases.^[20]Rafi, A.W., Katz, R.M. (2011). Pilot Study of 15 Patients Receiving a New Treatment Regimen for Androgenic Alopecia: The Effects of Atopy on AGA. ISRN Dermatology. 241953. Available at: … Continue reading

So, combination therapy appears to be more effective than monotherapy. Therefore, leveraging two or more topical therapies or adding microneedling can support hair regrowth outcomes.

Who Should (or Shouldn’t) Use Topical Finasteride?

Good Candidates:

• Men diagnosed with AGA.
• Those who tolerate oral finasteride but seek to minimize systemic risks.

Not Ideal For: 

• People with hair loss from causes other than AGA (e.g., alopecia areata, telogen effluvium). 
• Those who have previously shown a poor response to finasteride.
• Anyone trying to conceive, or with infants, toddlers, or pregnant individuals in close contact.
• Users who are unable or unwilling to follow consistent application routines or medical monitoring. 

Final Verdict

Topical finasteride is a legitimate option for hair regrowth. When formulated and used properly, it can rival oral finasteride’s effectiveness with a lower risk of systemic side effects. Success hinges on the right delivery method, correct dilution, and consistent application. While not flawless, it excels as part of a comprehensive regimen, especially when paired with therapies like minoxidil or microneedling. 

For those hesitant about oral medication, topical finasteride offers a practical, lower-risk compromise, provided users carefully follow evidence-based protocols to optimize both safety and results. Used strategically, it is a potent addition to hair loss treatment plans.

Topical minoxidil is one of the most widely used treatments for hair loss, known for its accessibility, relatively low risk profile, and ability to slow or partially reverse androgenetic alopecia in both men and women. First developed as a blood pressure medication, it gained FDA approval in the 1980s after researchers observed its unexpected side effect, stimulating hair growth when applied to the scalp.

In this article, we examine the mechanisms of action, formulation differences, dosing strategies, long-term efficacy, side effects, and methods to enhance results through combination therapies, such as microneedling or retinoids. Whether you’re just starting your hair restoration journey or reassessing your regimen, this guide provides an evidence-based foundation to help you make informed decisions.

Key Takeaways

• What is it? Topical minoxidil is an over-the-counter, FDA-approved liquid or foam. It is usually supplied as 2% or 5% as standard (although it can be offered at higher concentrations). It acts locally and is converted to minoxidil sulfate by scalp SULT1A1.
• Clinical Data. Topical minoxidil has been demonstrated in multiple randomized controlled trials to increase hair count, prolong the anagen phase, and enhance patient satisfaction in the short term, particularly at a 5% concentration. However, long-term data reveal diminishing efficacy over time, with many users reporting waning results or plateauing benefits after 12–18 months, particularly when used without adjunctive therapies like microneedling or anti-androgens.
• Safety. Topical minoxidil is generally safe, with a low incidence of systemic side effects due to minimal absorption. The most common adverse reactions are local, including scalp irritation, itching, and flaking, which are primarily attributed to the presence of propylene glycol in liquid formulations. More severe side effects like hypertrichosis or cardiovascular symptoms are rare and typically linked to misuse or high-sensitivity individuals. It is highly toxic to cats and should be handled with care by pet owners.
• Evidence Quality. Topical minoxidil scored 97/100 for evidence quality by our metrics.
• Best Practices. Apply topical minoxidil to a dry scalp once or twice daily, using 1 mL of solution or half a capful of foam per session. Gently massage to enhance penetration and avoid washing the scalp for at least two hours after application. Foam formulations are often better tolerated due to their lack of propylene glycol. For enhanced results, consider combining this treatment with microneedling, topical retinoids to boost SULT1A1 activity, or anti-androgenic therapies to counteract ongoing miniaturization.

What is Topical Minoxidil?

Topical minoxidil formulations were originally developed in the early 1980s after an interesting side effect was discovered when it was used as an oral hypertensive agent. This side effect was hypertrichosis, or increased hair growth. The U.S. FDA approved topical minoxidil for male pattern hair loss in 1988 and for female pattern hair loss in 1991.^[1]Suchonwanit, P., Thammarucha, S., Leerunyakul, K. (2019). Minoxidil and its use in hair disorders: a review. Drug Design, Development and Therapy. 13. 2777-2786. Available at: … Continue reading

Minoxidil is a pro-drug: it requires enzymatic activation to exert its pharmacological effect on hair follicles. The key enzyme involved in this is sulfotransferase SULT1A1, which is highly expressed in the outer root sheath (ORS) of hair follicles.^[2]Bacqueville, D., Jacques, C., Duprat, L., Jamin, E.L., Guiraud, B., Perdu, E., Bessou-Touya, S., Zalko, D., Duplan, H. (2017). Characterization of xenobiotic metabolizing enzymes of a reconstructed … Continue reading The level of SULT1A1 activity in the hair follicle correlates strongly with clinical response to topical minoxidil; individuals with low SULT1A1 activity are less likely to benefit from treatment.^[3]Pietrauszka, K., Bergler-Czop, B. (2020). Sulfotransferase SULT1A1 activity in hair follicle, a prognostic marker of response to the minoxidil treatment in patients with androgenetic alopecia: a … Continue reading

Topical minoxidil typically comes in two main formulations:

• Solution: The original and most widely used form. Some use carrier agents like propylene glycol to improve solubility and scalp penetration, but it is a common cause of local irritation (itching, redness, flaking).^[4]Epstein, G.K., Epstein, J., Cohen, J. (2019). Hair Loss in Men and Women: Medical and Surgical Therapies. 2(1). 161-176. Available at: https://doi.org/10.1016/j.yacs.2019.02.006 
• Foam: Developed to address PG sensitivity. The foam formulation is propylene glycol-free, reducing the risk of irritation and allergic reactions. It is easier to apply, dries quickly, and is FDA-approved at 5% strength.^[5]Lupatini, R., Sidhu, R., Patel, H., Bichar, K. (2021). Stability Evaluation of Minoxidil in FOAMIL Foam Base with Bracketing Study Design. International Journal of Pharmaceutical Compounding. 25(3) … Continue reading

Some options also offer propylene glycol-free solutions and gels. Some newer products use water-based or liposomal vehicles to cater to users with sensitive skin or allergies.

Why Might I Consider Topical Minoxidil Over Oral?

Many people opt for topical minoxidil over oral formulations due to key differences in safety, accessibility, and side effect profiles. 

Over-the-Counter Access & fewer Barriers

Topical minoxidil is available over the counter, making it easy to obtain and start treatment promptly. Oral minoxidil, however, requires a prescription and is typically used off-label for hair loss, which can delay access and introduce hurdles within the healthcare system.

Minimal Systemic Exposure

Applying minoxidil directly to the scalp results in minimal absorption into the bloodstream. This localized delivery reduces the risk of systemic side effects that are more common with oral minoxidil, which circulates throughout the body.^[6]Ashique, S., Sandhu, N.K., Haque, S.N., Koley, K. (2020). A Systemic Review on Topical Marketed Formulations, Natural Products, and Oral Supplements to Prevent Androgenic Alopecia: A Review. Natural … Continue reading

Lower Risk of Hypertrichosis, Edema, and Cardiac Events

Oral minoxidil demonstrates a high incidence of hypertrichosis, whereas in topical minoxidil, it is usually localized and linked to misuse.^[7]Jiminez-Cauhe, J., Sicco, K.I.L., Shapiro, J., Hermosa-Gelbard, A., Burgos-Blasco, P., Melian-Olivera, A., Ortega-Quijano, D., Pindado-Ortega, C., Buendia-Castano, D., Asz-Sigall, D., Vano-Galvan, S. … Continue reading

Similarly, edema (fluid retention/swelling) and cardiac side effects (such as tachycardia, pericardial effusion, and exacerbation of angina) are rare with topical use but do have the potential to cause issues for those with preexisting cardiovascular, renal, or hepatic conditions.^[8]do Nascimento, I.J.B., Harries, M., Rocha, V.B., Thompson, J.Y., Wong, C.H., Varkaneh, H.K., Guimaraes, N.S., Arantes, A. J. R., Marcolini, M.S. (2020). Effect of Oral Minoxidil for Alopecia: … Continue reading

How Does Topical Minoxidil Work?

Topical minoxidil stimulates hair growth through a variety of interconnected biological mechanisms, many of which have been elucidated in peer-reviewed research.

Local Vasodilation and VEGF Up-Regulation

Minoxidil acts as a potent vasodilator by opening potassium channels in vascular smooth muscle, leading to increased blood flow around hair follicles. This enhanced microcirculation delivers more oxygen and nutrients to the follicular environment, creating conditions favorable for hair growth.

Additionally, minoxidil upregulates the expression of vascular endothelial growth factor (VEGF) in dermal papilla cells. VEGF is a key mediator of angiogenesis, supporting the development and maintenance of the follicular blood supply necessary for robust hair growth.^[9]Zeltzer, A.A., Keren, A., Paus, R., Gilhar, A. (2024). Topical minoxidil rejuvenates hair follicles from men with androgenetic alopecia in vivo. Acta Dermato Venereologica. 104(24213). Available at: … Continue reading

Anagen Induction and Telogen Shortening

One of the hallmark effects of topical minoxidil is its ability to induce the anagen (growth) phase of the hair cycle and shorten the telogen (resting) phase.^[10]Van Neste, D. (2020). Placebo-controlled dose-effect studies with topical minoxidil 2% or 5% in male-patterned hair loss treated with oral finasteride employing an analytical and exhaustive study … Continue reading By prompting resting hair follicles to re-enter the growth phase more rapidly, minoxidil effectively “resets” the hair cycle, leading to increased hair density and thickness over time. This is a central reason for its clinical efficacy in treating AGA and other hair loss disorders.

Wnt/ꞵ-Catenin Activation in Dermal Papilla

Recent studies have shown that minoxidil activates the Wnt/ꞵ-catenin signaling pathway within dermal papilla cells. This pathway is essential for hair follicle development, regeneration, and maintenance. Activation of ꞵ-catenin dermal papilla cells prolongs the anagen phase and supports the proliferation and differentiation of follicular cells, further enhancing hair growth.^[11]Kwack, M.H., Kang, B.M., Kim, M.K., Kim, J.C., Sung, Y.K. (2011). Minoxidil activates ꞵ-catenin pathway in human dermal papilla cells: a possible explanation for its anagen prolongation effect. … Continue reading

Prostaglandin Modulation (PGE2)

Minoxidil has been found to increase the production of prostaglandin E2 (PGE2) by activating prostaglandin synthase-1 (PGHS-1) in dermal papilla fibroblasts. Elevated PGE2 levels are associated with hair growth promotion, possibly by providing cytoprotective effects and modulating local inflammation within the follicle environment.^[12]Michelet, J.F., Commo, S., Billoni, N., Mahe, Y.F., Bernard, B.A. (1997). Activation of cytoprotective prostaglandin synthase-1 by minoxidil as a possible explanation for its hair growth-stimulating … Continue reading This prostaglandin modulation may also counteract the inhibitory effects of certain nonsteroidal anti-inflammatory drugs (NSAIDs).

Penetration Factors: Vehicle, Skin Barrier, and Enzymes

The effectiveness of topical minoxidil depends significantly on its ability to penetrate the scalp and reach the hair follicle. Only about 1.4% of applied minoxidil is typically absorbed through intact skin.^[13]Gupta, A.K., Talukder, M., Venkataraman, M., Bamimore, M.A. (2022). Minoxidil: a comprehensive review. Journal of Dermatological Treatment. 33(4). 1896-1906. Available at: … Continue reading

The formulation’s vehicle (e.g., alcohol-based solution, foam, or novel delivery systems like cetosomes), the integrity of the skin barrier (stratum corneum), and the presence of activating enzymes (notably sulfotransferase SULT1A1 in the outer root sheath) all influence absorption and efficacy.^[14]Sattur, S. Talathi, A., Shetty, G., Arsiwala, S., Pereira, R., Dhoot, D. (2023). Comparative Clinical Study Evaluating the Efficacy and Safety of Topical 5% Cetosomal Minoxidil and Topical 5% … Continue reading

Dosing and Application Logistics

Once vs Twice Daily – What the Evidence Shows

Clinical studies have demonstrated that once-daily application of 5% topical minoxidil achieves hair count improvements comparable to twice-daily use of the 2% solution in men with AGA.^[15]Olsen, E.A., Dunlap, F.E., Funicella, T., Koperski, J.A., Swinehart, J.M., Tschen, E.H., Trancik, R.J. (2002). A randomized clinical trial of 5% topical minoxidil versus 2% topical minoxidil and … Continue reading In long-term studies, men who switched from twice daily to once-daily minoxidil maintained most of their hair gains, though there was a slightly greater mean loss in those on the once-daily regimen compared to those who remained on twice-daily dosing.^[16]Olsen, E.A., DeLong, E.R., Weiner, M.S. (1987). Long-term follow-up of men with male pattern baldness treated with topical minoxidil. Journal of the American Academy of Dermatology. 16(3 Pt 2). … Continue reading

Importantly, using 5% minoxidil twice daily can provide an incremental benefit, approximately 10-15% greater hair regrowth, over once-daily 5% application or twice-daily 2% solution, though this comes with a higher risk of local irritation.^[17]Olsen, E.A., Dunlap, F.E., Funicella, T., Koperski, J.A., Swinehart, J.M., Tschen, E.H., Trancik, R.J. (2002). A randomized clinical trial of 5% topical minoxidil versus 2% topical minoxidil and … Continue reading

For women with FPHL, randomized clinical trials have shown that once-daily application of 5% minoxidil foam is non-inferior to twice-daily use of the 2% minoxidil solution in terms of hair regrowth and target area hair counts.^[18]Blume-Peytavi, U., Hillmann, K., Dietz, E., Canfield, D., Bartels, N.G. (2011). A randomized, single-blind trial of 5% minoxidil foam once daily versus 2% minoxidil solution twice daily in the … Continue reading Both regimens lead to similar improvements, but the once-daily 5% foam offers a significant compliance advantage, as it is easier to incorporate into daily routines and is associated with fewer reports of scalp irritation.^[19]Ramos, P.M., Melo, D.F., Radwanski, H., de Almeida, R.F.C., Miot, H.A. (2023). Female-pattern hair loss: therapeutic update. Anais Brasileiros de Dermatologica. 98(4). 506-519. Available at: … Continue reading This practical benefit makes once-daily 5% foam a preferred initial therapy for many women.

Choosing a Topical Minoxidil Concentration

Selecting the right minoxidil concentration depends on your goals, tolerance, and clinical context. 

2% Minoxidil

• Profile: Traditionally labeled for women, especially those with sensitive scalps or mild hair loss.
• Efficacy: Offers modest improvement in hair counts and density; superior to the placebo but less effective than higher strengths.^[20]Olsen, E.A., Dunlap, F.E., Funicella, T., Koperski, J.A., Swinehart, J.M., Tschen, E.H., Trancik, R.J. (2002). A randomized clinical trial of 5% topical minoxidil versus 2% topical minoxidil and … Continue reading
• Tolerability: Minimal irritation and side effects; preferred for those prone to dermatitis or with a low threshold for adverse reactions.
• Best for: Mild AGA, sensitive skin, or those who prioritize safety over maximal regrowth.

5% Minoxidil

• Profile: The most widely studied and FDA-approved concentration for both men and women.
• Efficacy: Consistently outperforms 2% for both hair counts and patient satisfaction; considered the best balance between response rate and tolerability.^[21]Olsen, E.A., Dunlap, F.E., Funicella, T., Koperski, J.A., Swinehart, J.M., Tschen, E.H., Trancik, R.J. (2002). A randomized clinical trial of 5% topical minoxidil versus 2% topical minoxidil and … Continue reading
• Tolerability: Slightly higher risk of local irritation (itching, redness, flaking) than 2%, but generally well-tolerated, especially in foam (propylene glycol-free) formulations.
• Best for: Most patients with AGA seeking robust, evidence-based results.

7% Minoxidil

• Profile: Custom-compounded, not commercially available or FDA-approved; sometimes used for those with low follicular sulfotransferase activity (“enzyme low-responders”). 
• Efficacy: May offer incremental benefit for select non-responders to 5%, though supporting data are limited and mixed.^[22]Singh, S., Patil, A., Kianfar, N., Waskiel-Burnat, A., Rudnicka, L., Sinclair, R., Goldust, M. (2022). Does topical minoxidil at concentrations higher than 5% provide additional clinical benefit? … Continue reading 
• Tolerability: Higher risk of contact dermatitis due to increased propylene glycol and alcohol content; requires careful monitoring for irritation.
• Best for: Patients who do not respond to 5% and have confirmed low enzyme activity, under clinical supervision.

10-15% Minoxidil

• Profile: Compounded, not FDA-approved; considered a last-line topical option before transitioning to oral minoxidil.
• Efficacy: Evidence is conflicting; some studies suggest no added benefit over 5%, while others report modest gains in select cases. Side effects increase substantially with higher concentrations.^[23]Vasantha, K.L. (2025). Efficiency and Safety of 10% Minoxidil in the Treatment of Alopecia Areata: A Randomised Controlled Trial. Journal of Population Therapeutics and Clinical Pharmacology. 32(4). … Continue reading,^[24]Ghonemy, S., Alarawi, A., Bessar, H. (2021). Efficacy and safety of a new 10% topical minoxidil versus 5% topical minoxidil and placebo in the treatment of male androgenetic alopecia: a trichoscopic … Continue reading
• Risks: Marked increase in scalp irritation, dermatitis, and cost. Formulations typically require more propylene glycol and alcohol for solubility, compounding the risk of adverse reactions.
• Best for: Refractory cases under specialist care, when all lower strengths have failed, and before considering oral therapy.

Vehicle and Formulation Tweaks

There are a number of options you can take in terms of formulation or additional treatments to improve the efficacy of topical minoxidil. 

Foam vs. Liquid: Propylene Glycol, Irritation, and Drying Time

Liquid minoxidil formulations can contain propylene glycol, which improves drug solubility and skin penetration.^[25]Grice, J.E., Ciotti, S., Weiner, N., Lockwood, P., Cross, S.E., Roberts, M.S. (2010). Relative uptake of minoxidil into appendages and stratum corneum and permeation through human skin in vitro. … Continue reading However, propylene glycol is a frequent cause of scalp irritation; itching, redness, and flaking are common complaints, especially among users with sensitive skin.^[26]Patel, K., Palmer, A., Nixon, R. (2023). Allergic contact dermatitis from propylene glycol: A case series from Australia. Contact Dermatitis. 89(2). 79-84. Available at: … Continue reading

Foam minoxidil was specifically developed to avoid propylene glycol usage and minimize irritation. As a result, foam is generally much better tolerated, especially for individuals prone to dermatitis or scalp discomfort.^[27]Nestor, M.S., Ablon, G., Gade, A., Han, H., Fischer, D.L. (2021). Treatment options for androgenetic alopecia: Efficacy, side effects, compliance, financial considerations, and ethics. Journal of … Continue reading  Additionally, the foam dries faster than the traditional liquid, making it more convenient for daily use.

Efficacy: Most comparative studies and clinical experience suggest the 5% foam and 2% liquid are equivalent in hair regrowth when used appropriately; the choice often comes down to scalp tolerance and application preference.^[28]Blume-Peytavi, U., Hillmann, K., Dietz, E., Canfield, D., Bartels, N.G. (2011). A randomized, single-blind trial of 5% minoxidil foam once-daily versus 2% minoxidil solution twice daily in the … Continue reading

Propylene Glycol Free, Fast-Drying, Glycerin-Based Recipes.

For patients unable to tolerate propylene glycol or those seeking even less greasy, faster-drying options, newer propylene glycol-free formulations have been developed. These often use other solvents or humectants, with in vitro and clinical studies showing similar efficacy to products containing propylene glycol.^[29]Barbareschi, M., Vescovi, V., Starace, M., Piraccini, B.M., Milani, M. (2020). Propylene glycol free 5% minoxidil lotion formulation: cosmetic acceptability, local tolerability, clinical efficacy and … Continue reading

Addition of Retinol/Tretinoin (0.01%-0.025%) to Up-Regulate SULT1A1

As mentioned above, SULT1A1 is the key enzyme in the hair follicle that activates minoxidil by converting it to minoxidil sulfate, its effective form. Retinoids, notably tretinoin (0.01-0.025%), can be added to topical regimens to upregulate SULT1A1 in the outer root sheath, enhancing the local activation of minoxidil.^[30]Sharma, A., Goren, A., Dhurat, R., Agrawal, S., Sinclair, R., Trueb, R.M., Vano-Galvin, S., Chen, G., Tan, Y., Kovacevic, M., Situm, M., McCoy, J. (2019). Tretinoin enhances minoxidil response in … Continue reading

The mechanism appears to involve both increased skin permeability and direct modulation of SULT1A1 gene expression, making this combination particularly useful for patients with known or suspected low enzyme activity.

Topical Minoxidil Efficacy

When assessing the benefits of topical minoxidil, it’s critical to consider how response rates, regrowth rates, and especially months of use influence real-world outcomes for individuals with AGA. While many early studies highlight minoxidil’s promise, longer-term data reveal a more nuanced reality.

Short-Term Response

Within 3-6 months, minoxidil demonstrates high response rates. Surveys and clinical studies consistently show that roughly 60% of men perceive a meaningful response (slowing, stopping, or reversal of hair loss) in this window (as per self-assessment and investigator evaluations).^[31]Asilian, A., Farmani, A., Saber, M. (2023). Clinical efficacy and safety of low-dose oral minoxidil versus topical solution in the improvement of androgenetic alopecia: A randomized controlled trial. … Continue reading

Long-Term Response

After one year or longer, response rates drop dramatically. Multiple studies report rates below 30%, and even lower in five-year follow-up populations, with only about 20-30% of users satisfied with the results.^[32]Olsen, E.A., Weiner, M.S., Amara, I.A., DeLong, E.R. (1990). Five-year follow-up of men with androgenetic alopecia treated with topical minoxidil. Journal of American Academy of Dermatology. 22(4). … Continue reading

Real-world data indicate discontinuation rates of 86–95% by the one-year mark. The leading reason cited by users for stopping? “Low effect,” or disappointment with the cosmetic improvement offered by the drug.^[33]Shadi, Z. (2023) Compliance to Topical Minoxidil and Reasons for Discontinuation among Patients with Androgenetic Alopecia. Dermatology and Therapy. 13(5). 1157-1169. Available at: … Continue reading

Regrowth Rate: Short-Lived Gains

In one pivotal trial, men using 5% minoxidil twice daily saw a nearly 60% increase in hair “weight” (total mass of regrown/thickened hair) at 6 months. By 96 weeks, gains had diminished to just 25% above the baseline, a significant drop from the initial response.^[34]Van Neste, D. (2020). Placebo-controlled dose-effect studies with topical minoxidil 2% or 5% in male-patterned hair loss treated with oral finasteride employing an analytical and exhaustive study … Continue reading

Over 48 weeks, users displayed a 12% rise in hair count compared with 3% for placebo (statistically significant). Still, these increases in hair number did not always correspond to better visible scalp coverage when judged by experts, indicating that raw hair counts may overstate clinical benefit.

Why Does Efficacy Diminish With Time?

Lack of DHT Targeting and Ongoing Miniaturization

Minoxidil’s primary action is to stimulate hair follicles into a growth (anagen) phase; however, it does not block the effects of DHT, the androgen responsible for follicle miniaturization in genetic hair loss.^[35][Updated 2023 Feb 24]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK482378/ Accessed: July 2025 Therefore, hair shafts may still become thinner despite greater numbers, diminishing real-world cosmetic impact.

Fibrosis: The Hidden Limitation

Emerging evidence points to fibrosis, the gradual formation of restrictive, scar-like tissue around miniaturizing follicles, as a rate-limiting factor in AGA.^[36]Trueb, R.M., Dias, M.F.R.G., Rezende, H.D. (2021). Comment on Follicular Inflammation and Fibrosis in Pattern Hair Loss. Skin Appendage Disorders. 7(2). 159-160. Available at: … Continue reading Minoxidil does not directly address this fibrotic process, so even if follicles are nudged back into growth, their ability to produce robust hair continues to decline as surrounding tissue stiffens and shrinks.

The Limits of Hair Count as a Metric

Statistical increases in hair count do not guarantee clinical satisfaction. Studies repeatedly show that even impressive numeric gains in hair counts (or surrogate measures, such as hair mass index) are not always matched by noticeable differences in scalp coverage or user satisfaction.^[37]Van Neste, D. (2020). Placebo-controlled dose-effect studies with topical minoxidil 2% or 5% in male-patterned hair loss treated with oral finasteride employing an analytical and exhaustive study … Continue reading Patient dissatisfaction and discontinuation remain high in the absence of true visual improvement, underscoring the practical limits of relying on surrogate endpoints.

Combining Minoxidil with Microneedling

Recent clinical trials have shown that adding microneedling to minoxidil treatment can significantly enhance both response and regrowth rates. One landmark study reported a nearly fourfold greater increase in hair count (approximately a 40% gain) compared to minoxidil alone at 12 weeks, with participants experiencing actual visible improvements in density.^[38]Ahmed, K.M.A., Kozaa, Y.A., Abuawwad, M.T., Al-Najdawi, A.I.A., Mahmoud, Y.W., Ahmed, A.M., Taha, M.J.J., Fadhli, T., Giannopoulou, A. (2025). Evaluating the efficacy and safety of combined … Continue reading

A six-month trial showed an 85% effective rate and a significant increase in hair count for the combination approach.^[39]Zhang, Y., Sheng, Y., Zeng, Y., Hu, R., Zhao, J., Wang, W., Yang, Q. (2022). Randomized trial of microneedling combined with 2% minoxidil topical solution for the treatment of female pattern hair … Continue reading

Why Does Microneedling Work So Well?

• Improved drug absorption: Microneedling transiently disrupts the scalp’s barrier, allowing minoxidil to penetrate more effectively.
• Enzyme upregulation: The procedure may increase the local activity of sulfotransferase enzymes needed for minoxidil activation, potentially overcoming a key bottleneck for some non-responders.^[41]Sharma, A., Surve, R., Dhurat, R., Sinclair, R., Tan, T., Zou, Y., Ramos, M.P., Wambier, C., Vernier, I., Kovacevic, M., Goren, A. (2020). Microneedling improves minoxidil response in androgenetic … Continue reading
• Counteracting fibrosis: Early research suggests that microneedling may help remodel fibrotic tissue, making the scalp environment more conducive to robust hair regrowth.

Non-Responder Pathway (SULT1A1-Guided)

For people who don’t respond adequately to topical minoxidil, several strategies can help overcome this resistance and optimize hair growth.

Increase Topical Minoxidil Concentration (7-10%)

Raising the concentration of topical minoxidil beyond 5%, to compounded strengths such as 7% or 10%, is a common clinical approach for patients identified as poor responders. The rationale is that higher drug levels may compensate, at least partially, for suboptimal enzymatic conversion of minoxidil to its active sulfate form in the outer root sheath.

Add Topical Retinoic Acid (0.01-0.05%)

Topical retinoic acid (such as tretinoin) can be combined with minoxidil to upregulate SULT1A1 activity, thereby enhancing the local activation of minoxidil in the hair follicle. Peer-reviewed research indicates that applying topical tretinoin upregulates follicle sulfotransferase enzymes, thereby enhancing the response to minoxidil.^[42]Sharma, A., Goren, A., Dhurat, R., Agrawal, S., Sinclair, R., Trueb, R.M., Vano-Galvan, S., Chen, G., Tan, Y., Kovacevic, M., Situm, M., McCoy, J. (2019). Tretinoin enhances minoxidil response in … Continue reading

Incorporate Weekly Microneedling (0.5-1.5 mm)

Microneedling is an increasingly popular adjunctive treatment for hair loss, particularly in individuals who do not respond to minoxidil. Weekly sessions using devices with needles 0.5–1.5 mm in length create controlled micro-injuries in the scalp, stimulating growth factors, activating dermal papilla cell signaling (such as Wnt/β-catenin), and boosting SULT1A1 enzyme expression.^[43]Dhurat, R., Sukesh, M.S., Avhad, G., Dandale, A., Pal, A., Pund, P. (2013). A Randomized Evaluator Blinded Study of Effect of Microneedling in Androgenetic Alopecia: A Pilot Study. International … Continue reading,^[44]Kumar, K.M., Inamadar, A.C., Palit, A. (2018). A Randomized Controlled, Single-Observer Blinded Study to Determine the Efficacy of Topical Minoxidil plus Microneedling versus Topical Minoxidil Alone … Continue reading,^[45]Zhang, Y., Sheng, Y., Zeng, Y., Hu, R., Zhao, J., Wang, W., Yang, Q. (2022). Randomized trial of microneedling combined with 2% minoxidil topical solution for the treatment of female pattern hair … Continue reading

Switch to or Add Low-Dose Oral Minoxidil

Low-dose oral minoxidil, typically 0.25–5 mg daily, offers systemic activation, as minoxidil is converted to its active sulfate in the liver (where SULT1A1 levels are abundant).^[46]Ramirez-Marin, H.A., Tosti, A. (2022). Role of Oral Minoxidil in Patterned Hair Loss. Indian Dermatology Online Journal. 13(6). 729-733. Available at: https://doi.org/10.4103/idoj.idoj_246_22 For individuals whose follicular SULT1A1 is insufficient for topical efficacy, oral minoxidil can bypass the need for high local enzyme activity. Recent comprehensive reviews and clinical experience suggest that low-dose oral minoxidil is effective for hair regrowth in male and female pattern hair loss, with a favorable safety profile when started at low dosages.^[47]Gupta, A.K., Talukder, M., Shemer, A., Piraccini, B.M., Tosti, A. (2023). Low-Dose Oral Minoxidil for Alopecia: A Comprehensive Review. Skin Appendage Disorders. 9(6). 423-437. Available at: … Continue reading

Explore Compounded Minoxidil Sulfate (Direct Active Form)

Compounding pharmacies can prepare topical formulations containing minoxidil sulfate, the direct, active metabolite, bypassing the need for SULT1A1 conversion. Though theoretically attractive for SULT1A1 nonresponders, minoxidil sulfate is chemically less stable than parent minoxidil and is also more expensive.^[48]Chemical Book. (no date). Minoxidil Sulphate. ChemBook. Available at: https://www.chemicalbook.com/Price/Minoxidil-sulphate.htm Accessed: July 2025,^[49]Shan, Y., Xu, C., Guo, Y., Wen, L., Zhou, S., Fang, L., Xu, J., Zhen, H. (2025). Liposomes enhance the hair follicle delivery of minoxidil sulfate with improved treatment of androgenetic alopecia. … Continue reading Its shelf-life, risk of degradation, and limited availability currently constrain its widespread clinical use. Efficacy and safety data are lacking beyond case reports and experimental settings, and this approach remains investigational.

What To Expect Time-Line Wise

Understanding the typical milestones and changes during minoxidil treatment helps set realistic expectations, avoids premature discontinuation, and guides regimen adjustments for optimal hair regrowth. Here’s a week-by-week and month-by-month breakdown based on clinical evidence and peer-reviewed research.

Weeks 4-6: The Shedding Spike (“Telogen Synch”)

What happens: Many users notice an initial increase in hair shedding after starting minoxidil, usually peaking around weeks 4–6.

Why: This effect, known as telogen effluvium, occurs as minoxidil accelerates the transition of hair follicles from the resting (telogen) to the active (anagen) growth phase. Older, miniaturized hairs are shed to make way for new ones.

What to do: This shedding is temporary and generally indicates that the treatment is starting to take effect. Stopping minoxidil because of early shedding is unnecessary and may forfeit later gains.

Month 3: Early Vellus Thickening and the First Cosmetic Hints

What happens: Fine, soft “vellus” hairs begin to thicken. With combination treatments (such as minoxidil plus microneedling), these changes may be more pronounced and start to become cosmetically noticeable.

Why: Follicles kickstart new anagen cycles, and some can already be seen transitioning to more pigmented, visible hairs.^[50]Rafi, A.W., Katz, R.M. (2011). Pilot study of 15 patients receiving a new treatment regimen for androgenic alopecia: the effects of atopy on AGA. ISRN Dermatology. 11. 241953. Available at: … Continue reading

Expectations: While cosmetic gains are modest at this stage using monotherapy, up to 60–74% of users report improvement in density and coverage when asked at 3–4 months.^[51]Rundegren, J. (2004). Rapid onset of action of minoxidil 5% topical solution in a 4-month German observational study on both patients and physicians. Journal of the American Academy of Dermatology. … Continue reading

Months 6 – 8: Peak Visible Gains (Most Noticeable Results) and Plateau

What happens: The majority of the visible thickening and coverage improvements emerge by 6-8 months. Around this time, many people also see gains plateau and further visible regrowth slows considerably

Clinical evidence: At this point, studies show peak increases in terminal hair count and density (e.g., a 12–15% rise for standard 5% twice-daily solutions in men).^[52]Olsen, E.A., Dunlap, F.E., Funicella, T., Koperski, J.A., Swinehart, J.M., Tschen, E.H., Trancik, R.J. (2002). A randomized clinical trial of 5% topical minoxidil versus 2% topical minoxidil and … Continue reading

What to do: Regimen reevaluation is appropriate here; ensure ongoing compliance, assess satisfaction, and consider any adjuncts or boosters if progress is suboptimal.  If additional improvement is desired, this is the window to explore adjunctive approaches, such as adding microneedling, retinoids, or anti-androgen therapies, to enhance or sustain growth.

Month 9 +: Gradual Waning Without Additional Support

What happens: Many users see diminishing improvements after 9 months; some may even experience slow retreating benefits despite continued use.

Why: Minoxidil alone does not address the underlying drivers of androgenetic alopecia, namely, DHT-mediated follicle miniaturization and progressive perifollicular fibrosis. Without combining minoxidil with anti-DHT agents or regenerative wounding therapies, natural progression often limits sustained gains.

Long-term evidence: Only ~30% of users report being satisfied after several years; discontinuation is common, with the lack of a visible effect being the primary reason.^[53]Shadi, Z. (2023) Compliance to Topical Minoxidil and Reasons for Discontinuation among Patients with Androgenetic Alopecia. Dermatology and Therapy. 13(5). 1157-1169. Available at: … Continue reading 

Safety and Side Effects

Dermatitis (2-6%): Mainly Propylene Glycol

• Incidence: Irritant or allergic contact dermatitis occurs in ~2-6% of users.
• Primary Cause: Most cases are induced by propylene glycol, a key solvent in liquid minoxidil solutions, rather than by minoxidil itself.^[54]Jadeed, H.B., Almudimeegh, A.M., Alomran, S.A., Alshathry, A.H. (2021). A Case of Contact Allergic Dermatitis to Topical Minoxidil. Cureus. 13(1). E12510. Available at: … Continue reading
• Symptoms: Itching, redness, scaling, and sometimes localized swelling.
• Management: Switching to propylene glycol-free foam formulations or compounded solutions using alternative solvents (like glycerol or butylene glycol) can resolve symptoms for sensitive users. Those with confirmed allergy to minoxidil itself should avoid all forms.

Scalp Dryness and Flaking

• Presentation: Dryness and flaking of the scalp are common, primarily due to the alcohol and propylene glycol content in the formulation.
• Management: 
  • Use gentle, sulfate-free shampoos.
  • Prefer shorter contact times and allow the product to dry completely.
  • Consider propylene glycol or alcohol-free versions when persistent dryness occurs.

Facial Hypertrichosis

• Incidence: Mild, reversible facial hair growth (hypertrichosis) may develop, especially with high doses or accidental application beyond the intended area, such as the scalp.
• Course: Usually appears within 2-5 months of starting minoxidil and typically resolves within one to five months after stopping or reducing use.
• Mechanism: Thought to result from inadvertent transfer or high follicular sensitivity, not systemic toxicity.^[55]Chellini, P.R., Pirmez, R., Raso, P., Sodre, C.T. (2015). Generalized hypertrichosis induced by topical minoxidil in an adult woman. International Journal of Trichology. 7(4). 182-183. Available at: … Continue reading

Toxicity to cats (prevalence: low if you’re careful; high if you’re reckless)

• Cats lack the enzyme required to metabolize minoxidil, much like dogs lack the enzymes required to quickly metabolize substances within chocolate. Resultantly, minoxidil is highly toxic to cats.^[56]DeClementi, C., Bailey, K.L., Goldstein, S.C., Orser, M.S. (2004). Suspected toxicosis after topical administration of minoxidil in 2 cats. Veterinary Emergency & Critical Care. 14(4). 287-292. … Continue reading From 2001 to 2014, there were four reported feline deaths from minoxidil exposure.
• This doesn’t mean that if you have cats, you can’t use minoxidil. It simply means that you need to take extra precautions during storage, application, and drying, and ensure your cats don’t come into contact with the drug (even through their fur).

Heart palpitations (prevalence: very low)

• There is some systemic absorption from the use of topical minoxidil. As such, a small percentage of users have reported blood pressure-related effects ranging from dizziness to heart palpitations.^[57]Leenen, F.H., Smith, D.L., Unger, W.P. (1988). Topical minoxidil: cardiac effects in bald man. British Journal of Clinical Pharmacology. 26(4). 481-485. Available at: … Continue reading

Stopping Topical Minoxidil

Discontinuing topical minoxidil is a significant decision, as virtually all clinical evidence and real-world experience indicate that hair gains made during treatment will be lost, usually within 3 to 12 months. This process is driven by the underlying physiology of follicles and the progressive nature of AGA.

The Physiology Behind Minoxidil Withdrawal

• Follicular Cycling: When minoxidil is stopped, hair follicles revert to their pre-treatment anagen (growth phase) timing within approximately three months. This leads to a synchronized shedding phase and a temporary drop in hair density, often falling below pre-treatment baseline before returning to the genetic trajectory over the subsequent months.
• Rebound Shedding: After ceasing minoxidil, the majority of users experience significant shedding, which can sometimes be more aggressive than before they began treatment. Typically, this shedding lasts for 3–6 months, but can persist for up to a year in some cases. The extent of the shed varies from person to person, but those who respond best to the drug are usually most affected, simply because they maintain or regrow more hair than they lose.

Evidence in Clinical Studies

One 96-week study on both 2% and 5% topical minoxidil found that after treatment was halted, hair counts and weight fell below both baseline and placebo levels within 3 months.^[58]Price, V.H., Menefee, E., Strauss, P.C. (1999). Changes in hair weight and hair count in men with androgenetic alopecia, after application of 5% and 2% topical minoxidil, placebo, or no treatment. … Continue reading By six months post-withdrawal, most subjects’ hair counts rebounded to baseline, indicating the temporary and reversible effects of minoxidil therapy in AGA.

Tapering Off: Protocol to Blunt Rebound Shedding

Abruptly ceasing minoxidil use (“cold turkey”) tends to induce more severe and acute shedding. To mitigate this shock to the hair cycle and scalp, expert opinion and clinical guidelines recommend a gradual taper, similar to protocols used for oral minoxidil or other hair loss medications.

A 6-month Tapering Schedule could look like this.

Weeks	Protocol Description
1-2	Alternate once-daily and twice-daily applications
3-4	Three days once-daily, one day twice-daily
5-6	Once daily, Monday-Friday, twice on weekends
7-9	Once daily
10-12	Once daily on weekdays, off weekends
13-15	Once daily, Monday-Thursday, off Friday-Sunday
16-18	Apply every other day
19	Every third day
20	Every fourth day
21	Every fifth day
22	Every sixth day
23	Once weekly, then discontinue

Bridging Strategies During the Transition

No protocol can eliminate post-minoxidil shedding, but supporting the scalp with additional therapies may enhance retention and cushion the transition.

• Microneedling: Weekly sessions (with or without ongoing minoxidil) can upregulate growth factors and SULT1A1, thereby enhancing follicle health, and have been shown to help some users retain density for several months after discontinuing minoxidil.
• Anti-Androgens: Initiating topical or oral anti-androgens (e.g., finasteride, spironolactone) before and during withdrawal can help offset DHT-driven miniaturization—a process that is not alleviated by minoxidil alone.
• Low-Level Laser Therapy (LLLT): LLLT devices supply scalp stimulation and may decrease shedding when minoxidil is reduced or stopped.
• Alternative Topicals: Some transitioners try diluted rosemary oil (2–5%) or similar topicals for additional support, though strong clinical evidence for these alternatives is limited.

You can read our article on what happens when you quit taking minoxidil here.

Best Practices

• Apply only to a dry scalp: Before treatment, ensure both hair and scalp are completely dry. This maximizes absorption and efficacy.
• Dosage: For solution, use exactly 1 mL (measure with the supplied dropper); for foam, use half a capful per application.
• Massage in: Gently massage the product into thinning areas for approximately 30 seconds to improve penetration.
• Wait before washing: Allow at least 2 hours after application before shampooing or rinsing your scalp. This ensures adequate drug absorption.

Who Is an Ideal Candidate for Topical Minoxidil?

You’re a good candidate if you are:

• An adult man or woman with AGA: This is the main, FDA-approved indication for topical minoxidil. It has the strongest evidence in these groups.
• Able to commit to at least 6 months of consistent use: Appreciable improvements are most common with twice-daily application and become noticeable after 3–6 months. Stopping before this period makes it hard to judge the benefit.
• Ready for ongoing, indefinite use: All gains from minoxidil are lost within 3–6 months of discontinuation, so lifelong adherence is necessary for persistent effects.
• Prepared for manageable, mostly mild side effects: Most users tolerate minoxidil well, but 2–6% experience skin irritation, mainly from propylene glycol in liquid formulas. Switching to propylene glycol-free foams or other vehicle-adjusted products usually solves these issues.
• Willing to pair with additional therapies (optional, but recommended): Combining minoxidil with weekly microneedling or oral/topical finasteride increases efficacy by two- to four-fold, with up to 70%+ response rates and greater visual gains. Microneedling notably enhances regrowth and can prolong the effectiveness of minoxidil.
• Financially able to sustain $15–$30/month long-term: Over the years of use, the accumulated cost is a practical consideration.
• Comfortable following a simple scalp-care routine: Best practices include applying the product to a dry scalp, massaging for at least 30 seconds, allowing it to absorb for 2 hours, and treating any scalp inflammation first with anti-inflammatory shampoos (like ketoconazole or zinc pyrithione).

Who May Want to Reconsider?

• Catowners unable to limit pet exposure: Cats are highly sensitive to minoxidil and can suffer fatal toxicity from even minute exposure. Strict precautions are required to keep pets safe.
• People with severe or persistent skin sensitivity/allergy: If unable to tolerate any formulation or if allergic to both minoxidil and carrier ingredients, other options may be preferable.
• Individuals seeking a permanent or “cure-all” solution: Minoxidil does not address androgenic miniaturization (DHT effect) or scalp fibrosis. On its own, efficacy usually plateaus or wanes, making it mostly a maintenance or adjunct therapy.
• Those seeking visible, dramatic regrowth from monotherapy alone: Statistical hair count increases may not always correspond to better scalp coverage or visually satisfying restoration.

FAQs

Will minoxidil lower my libido? No, minoxidil is not known to lower libido, as it does not affect hormones and has shown no significant link to sexual side effects in clinical studies or post-marketing data. For more information, refer to the following resources: Minoxidil: Getting Started (Interactive Guide).

Can I dilute topical minoxidil without losing its efficacy? You can dilute topical minoxidil or mix it with other topicals, but doing so may reduce its efficacy if it alters absorption, concentration, or stability, so it’s best to either separate applications (morning vs. evening) or use professionally compounded combinations to ensure reliable results. For more information, watch this video.

Can I use topical minoxidil alongside other topicals? Yes, you can use topical minoxidil alongside other topicals, but to avoid interference with absorption, it’s best to either apply them at different times of day (e.g., morning vs. evening) or combine them into a single formulation, ideally through a compounding pharmacy or by carefully preparing them at home following best practices.

How long should I leave minoxidil on my scalp? You should leave minoxidil on your scalp for at least one hour, but ideally for four hours or more, to ensure optimal absorption, especially if you’re applying it only once a day. Most of the drug is absorbed within the first few hours, so extending contact time helps maximize its effectiveness.

Does minoxidil accelerate skin aging? Minoxidil is unlikely to accelerate skin aging; reported changes in facial skin quality are more likely due to mild allergic reactions to propylene glycol or temporary water retention, both of which are typically reversible and manageable with formulation changes or improved application practices.

Final Thoughts

Topical minoxidil remains the cornerstone over‑the‑counter therapy for androgenetic alopecia, valued for its solid safety record, ease of access, and decades of clinical data supporting meaningful, if often modest, improvements in hair density and retention. For many men and women, especially those early in their hair-loss journey or those averse to systemic medications, it offers a practical first line of defense that can be further amplified with adjuncts such as microneedling, retinoids, or anti-androgens. 

Yet its benefits are not limitless: results plateau without complementary treatments, lifelong use is required to maintain gains, and irritation or simple user fatigue remain common reasons for discontinuation. Approached realistically, committing to at least six months of consistent, correctly dosed application, monitoring scalp health, and integrating synergistic therapies where appropriate, topical minoxidil can serve as a reliable, evidence‑based pillar in a comprehensive hair‑restoration plan.

Oral minoxidil is an increasingly popular off-label treatment for hair loss, offering a convenient alternative to topical solutions for both men and women. Originally developed as a blood pressure medication, it was discovered to promote hair growth, sometimes dramatically, by enhancing blood flow and stimulating key pathways involved in hair growth.

In this article, we break down what oral minoxidil is, how it works, what the research reveals across different types of hair loss, potential side effects, and best practices for safe and effective use.

Key Takeaways:

• What is it? Oral minoxidil is a prescription vasodilator originally used to treat high blood pressure. At lower doses (0.25–5 mg daily), it’s increasingly prescribed off-label to treat hair loss, especially in people who don’t respond well to topical minoxidil. It promotes regrowth by enhancing blood flow, shortening the hair’s resting phase, and activating key follicular growth pathways.
• Clinical Data. Studies have shown that oral minoxidil is effective for multiple types of hair loss, including androgenic alopecia (AGA), chronic telogen effluvium, and even permanent chemotherapy-induced alopecia. For AGA, it offers comparable or better results than 5% topical minoxidil, particularly at doses of 2.5–5 mg in men. In women, low-dose therapy (0.25–1.25 mg) is also effective, often combined with spironolactone for added benefit.
• Safety. At low doses, oral minoxidil is generally well-tolerated. The most common side effects include excess body hair, mild fluid retention, and lightheadedness. Rarely, serious cardiac issues like pericardial effusion may occur, especially in individuals with underlying health conditions. Most side effects are dose-dependent and reversible with adjustment or discontinuation.
• Evidence Quality. Oral minoxidil scored 63/100 for evidence quality by our metrics.
• Best Practices. Start with a low dose (2.5 mg for men, 0.25–1.25 mg for women) and titrate upward only if needed. Splitting doses between morning and night may improve tolerability. Sublingual minoxidil is a promising alternative to reduce systemic exposure. Combine with microneedling or topical agents if the results plateau. Always consult a healthcare provider, especially if you have concerns related to cardiovascular, renal, or hepatic health.

What is Oral Minoxidil?

Oral minoxidil is a medication originally developed in the 1970s as an oral hypertensive agent, designed to lower high blood pressure by acting as a potent vasodilator. During its use for hypertension, clinicians observed a notable side effect: increased hair growth, or hypertrichosis.^[1]Patel, P., Nessel, T.A., Kumar, D. (2023). Minoxidil. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing. Available from: https://www.ncbi.nlm.nih.gov/book/NBK482378/ Accessed: … Continue reading

This unexpected effect led to the development of topical minoxidil for hair loss, which was approved by the FDA in 1988 for male patients and in 1992 for female patients.^[2]Nestor, M.S., Ablon, G., Gade, A., Han, H., Fischer, D.L. (2021). Treatment options for androgenetic alopecia: Efficacy, side effects, compliance, financial considerations, and ethics. Journal of … Continue reading Oral minoxidil is also used as an off-label treatment for both men and women.

Why Might I Consider Oral Over Topical Minoxidil?

Many people consider oral minoxidil over topical due to fundamental differences in how each form is activated and delivered to hair follicles. Topical minoxidil is a pro-drug that requires conversion to its active form, minoxidil sulfate, by the sulfotransferase enzyme (specifically SULT1A1) located in the outer root sheath of scalp hair follicles.^[3]Pietrauszka, K., Bergler-Czop, B. (2020). Sulfotransferase SULT1A1 activity in hair follicle, a prognostic marker of response to the minoxidil treatment in patients with androgenetic alopecia: a … Continue reading

However, the activity of this enzyme varies significantly between individuals. For example, in one study on 120 patients, 40.8% exhibited low levels of sulfotransferase activity in the scalp.^[4]Chitalia, J., Dhurat, R., Goren, A., McCoy, J., Kovacevic, M., Situm, M., Naccarato, T., Lotti, T. (2018). Characterization of follicular minoxidil sulfotransferase activity in a cohort of pattern … Continue reading

Additionally, topical minoxidil faces a “penetration problem” where only about 1.4% of the drug applied is actually absorbed into the scalp skin under normal conditions.^[5]Suchonwanit, P., Thammarucha, S., Leerunyakul, K. (2019). Minoxidil and its use in hair disorders: a review. Drug Design, Development and Therapy. 13. 2777-2786. Available at: … Continue reading

Oral minoxidil largely bypasses these limitations. When taken by mouth, minoxidil is absorbed through the gastrointestinal tract and converted to its active form in the liver, where sulfotransferase activity is abundant. This ensures that nearly all ingested minoxidil is activated and delivered systemically, reaching hair follicles throughout the scalp and body, regardless of individual differences in scalp enzyme activity. As a result, oral minoxidil can be effective even for those who are non-responders to topical therapy due to low scalp sulfotransferase activity or poor drug penetration.^[6]Beach, R.A. (2018). Case series of oral minoxidil for androgenetic and traction alopecia: Tolerability & the five C’s of oral therapy. Dermatologic Therapy. 31(6). E12707. Available at: … Continue reading

How Does Oral Minoxidil Work?

Oral minoxidil promotes hair growth through several interrelated mechanisms at the cellular and molecular levels.

Potassium Channel Activation and Vasodilation

Minoxidil is converted in the liver to its active form, minoxidil sulfate (first phase metabolism), which opens adenosine triphosphate (ATP)-sensitive potassium channels in vascular smooth muscle and hair follicle cells.^[7]Gupta, A.K., Talukder, M., Shemar, A., Priaccini, B.A., Tosti, A. (2023). Low-Dose Oral Minoxidil for Alopecia: A Comprehensive Review. Skin Appendage Disorders. 9(6). 423-437. Available at: … Continue reading

This action triggers a process known as membrane hyperpolarization, resulting in vasodilation and increased blood flow to the scalp. This increased microcirculation delivers more oxygen, nutrients, and growth factors to hair follicles, creating a favorable environment for hair growth.

Stimulation of the Hair Growth Cycle

Minoxidil shortens the telogen (resting) phase and induces early entry of hair follicles into the anagen (growth) phase.^[8]Suchonwanit, P., Thammarucha, S., Leerunyakul, K. (2019). Minoxidil and its use in hair loss disorders. Drug Design, Development and Therapy. 13. 2777-2786. Available at: … Continue reading It also prolongs the duration of anagen, leading to longer and potentially thicker hair.

Activation of Wnt/ꞵ-Catenin Signaling

Minoxidil has been shown to activate the Wnt/ꞵ-Catenin pathway in dermal papilla cells. This pathway is a critical signaling route for hair follicle regeneration and maintenance of the anagen phase.^[9]Kwack, M.H., Kang, B.M., Kim, M.K., Kim, J.C., Sung, Y.K. (2011). Minoxidil activates ꞵ-catenin pathway in human dermal papilla cells: a possible explanation for its anagen prolongation effect. … Continue reading It also promotes the growth and specialization of hair follicle stem cells, supporting follicle growth.^[10]Wang, X., Liu, Y., He, J., Wang, J., Chen, X., Yang, R. (2022). Regulation of signaling pathways in hair follicle stem cells. Burns Trauma. 10. 1-19. Available at: … Continue reading

Direct Effects on Dermal Papilla Cells

Minoxidil stimulates the proliferation and survival of dermal papilla cells (DPCs), which are essential for hair follicle health.^[11]Kang, J-I., Choi, K.Y., Han, S-C., Nam, H., Lee, G., Kang, J-H., Koh, Y.S., Hyun, J.W., Yoo, E.S., Kang, H.K. (2022). 5-Bromo-3,4-dihydroxybenzaldehyde Promotes Hair Growth through Activation of … Continue reading

It also activates the extracellular signal-regulated kinase (ERK) and protein kinase B signaling pathways, increases the ratio of anti-apoptotic to pro-apoptotic proteins (Bcl-2/Bax), and prevents cell death, thereby prolonging the anagen phase.^[12]Jan, J.H., Kwon, O.S., Chung, J.H., Cho, K.H., Eun, H.C., Kim, K.H. (2004). Effect of minoxidil on proliferation and apoptosis in dermal papilla cells of human hair follicle. Journal of … Continue reading

Minoxidil also increases the expression of key growth factors, such as vascular endothelial growth factor (VEGF) and insulin-like growth factor 1 (IGF-1), which further support follicle nourishment and angiogenesis.^[13]Nagai, N., Iwai, Y., Sakamoto, A., Otake, H., Oaku, Y., Abe, A., Nagahama, T. (2019). Drug Delivery System Based on Minoxidil Nanoparticles Promotes Hair Growth in C57BL/6 Mice. International Journal … Continue reading

Anti-Inflammatory and Anti-Fibrotic Properties

Minoxidil exhibits anti-inflammatory effects by modulating the production of prostaglandins and other inflammatory mediators.^[14]Shin, D.W. (2022). The physiological and pharmacological roles of prostaglandins in hair growth. The Korean Journal of Physiology and Pharmacology. 26(6). 405-415. Available at: … Continue reading ^[15]Majewski, M., Gardas, K., Waskiel-Burnat, A., Ordak, M., Rudnicka, L. (2024). The Role of Minoxidil in Treatment of Alopecia Areata: A Systematic Review and Meta-Analysis. Journal of Clinical … Continue reading It also inhibits collagen synthesis, which could reduce fibrosis around hair follicles, maintaining a healthy microenvironment for hair growth.^[16]Fechine, C.O.C., Valente, N.Y.S., Romiti, R. (2022). Lichen planopilaris and frontal fibrosing alopecia: review and update of diagnostic and therapeutic features. Anais Brasileiros de Dermatologia. … Continue reading

How Effective Is Oral Minoxidil?

Let’s break this down into the types of hair loss that minoxidil can assist with.

Pattern Hair Loss/Androgenic Alopecia (Females)

Oral minoxidil has been found to be as effective as 5% topical minoxidil at treating female pattern hair loss. The study found no significant difference between topical and oral minoxidil 1 mg daily in terms of efficacy for female pattern hair loss (FPHL).^[17]Ramos, M.P., Sinclair, R.D., Kasprzak, M., Miot, H.A. (2020). Minoxidil 1 mg oral versus minoxidil 5% topical solution for the treatment of female-pattern hair loss. Journal of the American Academy … Continue reading There were, however, differences in the occurrence of adverse events. While scalp itching occurred only in the topical group, only users of oral minoxidil experienced excess hair growth outside of the scalp.

Another study combined low-dose minoxidil (0.25 mg) and 25 mg spironolactone to treat FPHL.^[18]Sinclair, R.D. (2018). Female pattern hair loss: a pilot study investigating combination therapy with low-dose oral minoxidil and spironolactone. International Journal of Dermatology. 57(1). 104-109. … Continue reading The results of the study demonstrated that the combined therapy:

• Decreased hair shedding as early as 3 months into the treatment.
• Increased hair density after 6 months.

However, the authors didn’t report any objective measurements of hair density, either at baseline or at the end of the study period. This makes it impossible to effectively compare the results of the previously mentioned study with those of this study.

So, we can’t effectively assess the difference in efficacy of spironolactone and low-dose oral minoxidil combination therapy or oral minoxidil monotherapy. However, the authors of this study do note that they believe the combination has an added benefit for FPHL.

Pattern Hair Loss/Androgenic Alopecia (Males)

Of all forms of hair loss, AGA may derive the most benefit from minoxidil (whether oral or topical). This is because one of the main mechanisms of action directly addresses one of the pathological facets of AGA: reduced blood flow.

This is evidence in one study on men with AGA.^[19]Lueangarun, S., Panchaprateep, R., Tempark, T., Noppakun, N. (2015). Efficacy and safety of oral minoxidil 5 mg daily during 24-week treatment in male androgenetic alopecia. Journal of the American … Continue reading In particular, it demonstrates a 100% response rate to a daily dose of 5 mg oral minoxidil. Even more impressively, subjects achieved an average 19% increase in hair count after 24 weeks.

The risk profile also appears to be favorable, with only 10% of participants reporting leg swelling. Ten percent of participants also reported a more significant side effect: an alteration in electrocardiogram (EKG) results.

These risks could theoretically be mitigated by lowering the dosage; however, one would need to consider the potential for reduced benefit. To better understand this, we’ll have to look at another study.

In line with the above results, this retrospective study showed a 90% response rate at 6-12 months for men taking 2.5-5.0 mg of oral minoxidil daily.^[20]Jiminiez-Couche, J., Saceda-Corralo, D., Rodrigues-Barata, R., Hermosa-Gelbard, A., Moreno-Arrones, O.M., Fernandez-Nieto, D., Vano-Galvan, S. (2019). Effectiveness and safety of low-dose oral … Continue reading Perhaps even more impressive is the fact that 60% of these men had tried other treatments for AGA, but had previously quit due to side effects or lack of efficacy.

In line with the trend of “decreasing dosage, decreasing efficacy”, one study using 0.25 mg of oral minoxidil found a 60% response rate in male AGA patients.^[22]Pirmez, R., Salas-Callo, C-I. (2020). Very-low-dose oral minoxidil in male androgenetic alopecia: A study with quantitative trichoscopic documentation. Journal of the American Academy of Dermatology. … Continue reading That’s on the low side for oral minoxidil overall, but on the high side when compared to topical minoxidil.

It’s also worth noting that there’s a key difference between this study and the one showing a 100% response rate at a 5mg daily dose. The 5mg study only included men with mild to moderate AGA; this study included both mild to moderate and severe AGA patients.

The mild to moderate group comprised 40% of study subjects, with the remaining 60% in the severe category. This suggests that low doses, such as 0.25mg, may be effective in severe AGA cases, at least in slowing and/or stopping their progression.

Notably, this study recorded leg swelling in only 4% of the group and found no difference in arterial pressure, suggesting that the risk of side effects reduces with decreasing dose. If these results were indeed confounded by the addition of severe AGA patients, these findings may indicate that 0.25 mg has a similar efficacy to 5 mg with a better risk profile.

All in all, it’s challenging to draw conclusions because the study designs differ significantly. In the future, it would be interesting to see how different groups with the same grade of AGA respond to 0.25 mg of minoxidil versus 5 mg of minoxidil. This could help us construct realistic treatment regimens that are both effective and minimize the risk of side effects.

Telogen Effluvium

Chronic telogen effluvium (CTE) is a common condition characterized by excessive hair shedding. Because one of minoxidil’s proposed mechanisms of action is its ability to shorten the “resting” telogen phase (where a lot of follicles stay in CTE, as opposed to the anagen growing phase), researchers have hypothesized that oral minoxidil may be a helpful treatment for the condition.

These hypothetical notions were explored in a recent 2017 study.^[24]Perera, E., Sinclair, R. (2017). Treatment of chronic telogen effluvium with oral minoxidil: A retrospective study. F1000 Research. 6. 1650. Available at: … Continue reading This particular study was retrospective and looked at individuals with CTE who had been prescribed oral minoxidil (dosages ranging from 0.25 mg to 2.5 mg, with the most common being 1 mg) in-clinic.

They found that most patients experienced a decrease in hair loss after 6 months, with all patients showing an improvement either at the 6 or 12-month mark. This does not make minoxidil the be-all and end-all for CTE. The oral minoxidil treatment wasn’t compared against a placebo or any other potential treatments (including combination therapies) for the condition, so we can only conclude that topical minoxidil is one potential treatment for CTE.

We also need to acknowledge that most CTE cases may have an underlying cause that, when resolved, could improve hair shedding. In these cases, addressing the root cause of CTE, whenever possible, is far more effective.

Alopecia Areata

Upon investigation of topical minoxidil’s benefits for alopecia areata (AA), an autoimmune form of hair loss, researchers found that topical minoxidil, on its own, really doesn’t do much for alopecia areata (AA) patients.^[25]Suchonwanit, P., Thammarucha, S., Leerunyakul, K. (2019). Minoxidil and its use in hair disorders: a review. Drug Design, Development and Therapy. 13. 2777-2786. Available at: … Continue reading However, interestingly, oral minoxidil at a dose of 5 mg daily appears to be effective.

Although oral minoxidil for AA hasn’t been well-studied, one study reported that 18% of AA subjects taking oral minoxidil showed an improved cosmetic response after ~35 weeks of use.

Considering the side effects of oral minoxidil are increased at a dose of 5 mg, the 18% response rate doesn’t seem too promising. But there may be one combination therapy that proves to be more effective.

Another study found that adding oral minoxidil to a current alopecia areata treatment may enhance outcomes without increasing the current dosage.

Tofacitinib is an immunomodulator drug currently used to treat alopecia areata. Although the drug is usually effective for most individuals at a 10 mg daily dosage, some users may need to double the dose to see hair growth.^[26]Wambier, C.G., Craiglow, B.G., King, B.A. (2021). Combination tofacitinib and oral minoxidil treatment for severe alopecia areata.  Journal of the American Academy of Dermatology. 85(3). 743-745. … Continue reading

While this usually resolves treatment resistance, increasing the dose may also increase the risk associated with strong immunomodulatory effects, as well as the cost. So, there’s a real need for safe combination therapies to improve treatment outcomes without increasing the tofacitinib dose.

Oral minoxidil may be able to do just this. One study demonstrated that daily addition of oral minoxidil (2.5 mg for women and 5 mg, split into 2.5 mg doses, for men) to doses of tofacitinib ranging from 10 mg to 20 mg daily resulted in: 

• 67% of patients achieved 75% or greater hair regrowth, compared to another study’s results, which demonstrated that 20% of patients achieved cosmetically acceptable regrowth on oral minoxidil alone.
• The remaining 33% of patients experienced hair regrowth, with a range of 11% to 74%.

Chemotherapy-Induced Hair Loss

Permanent chemotherapy-induced alopecia (PCIA), a hair-shedding disorder in which hair lost to chemotherapy does not grow back 6 months after the end of chemotherapy, is considered to be generally irreversible.

One case study challenges this.^[27]Yang, X., Thai, K-E. (2016). Treatment of permanent chemotherapy-induced alopecia with low-dose oral minoxidil. The Australasian Journal of Dermatology. 57(4). E120-e132. Available at: … Continue reading After one year of 1 mg daily oral minoxidil treatment, a woman with PCIA achieved considerable growth. This is pretty amazing, considering no consistently effective treatment has been found for PCIA patients, yet. While future studies are still needed to confirm these findings, these results are certainly promising.

Is Oral Minoxidil Safe?

Oral minoxidil has gained attention as an effective treatment for hair loss, but questions about its safety persist, particularly in comparison to the topical form. Here’s what the evidence shows.

Cardiovascular Risks: Myocardial and Pericardial Effusion

There are documented cases where people taking oral minoxidil developed pericardial effusion (fluid around the heart) and even pericarditis, sometimes at low doses used for hair loss.^[28]Dlova, N.C., Jacobs, T., Singh, S. (2022). Pericardial, pleural effusion and anasarca: A rare complication of low-dose oral minoxidil for hair loss. JAAD Case Reports. 11(28). 94-96. Available at: … Continue reading These events are rare but have prompted caution within the medical community.

Severe cardiovascular complications like pericardial effusion have been recorded the high doses (10-40 mg) used for hypertension, with rates around 3% in these populations.^[29]Bentivegna, K., Zhou, A.E., Adalsteinsson, J.A., Sloan, B. (2022). Letter in reply: Pericarditis and peripheral edema in a healthy man on low-dose oral minoxidil therapy. JAAD Case Reports. 20(29). … Continue reading However, it should be noted that this was reported in the 1980s in patients with severe hypertension, with no recent data available.

However, at the lower doses used for hair loss (0.25-5 mg), these complications are much less common and appear to be idiosyncratic (based on the individual response) rather than dose-dependent.^[30]Gupta, A.K., Bamimore, M.A., Abdel-Qadir, H., Williams, G., Tosti, A., Piguet, V., Talukder, M. (2024). Low-Dose Oral Minoxidil and Associated Adverse Events: Analyses of the FDA Adverse Event … Continue reading

Large observational studies and clinical experience with thousands of patients using low-dose oral minoxidil have not shown a significant increase in life-threatening cardiac events.^[31]Vano-Galvan, S., Pirmez, R., Hermosa-Gelbard, A., Moreno-Arrones, O.M., Saceda-Corralo, D., Rodrigues-Barata, R., Jiminez-Cauhe, J., Koh, W.L., Poa, J.E., Jerjen, R., de Carvalho, L.T., John, J.M., … Continue reading Most side effects are mild and reversible with dose adjustments or discontinuation of the medication.^[32]Bloch, D.L., Carlos, R.M.D. (2025). Side Effects’ Frequency Assessment of Low Dose Oral Minoxidil in Male Androgenetic Alopecia Patients. Skin Appendage Disorders. 11(1). 14-18. Available at: … Continue reading

Autopsy reports from patients who took extremely high doses (e.g., 60 mg) have not consistently shown pericardial or myocardial effusion, suggesting the risk is not universal or inevitable, even at high exposures.^[33]Sobota, J.T. (1989). Review of cardiovascular findings in humans treated with minoxidil. Toxicologic pathology. 17(1 Pt 2). 193-202. Available at: https://doi.org/10.1177/019262338901700115

Subclinical and EKG Changes

At high doses, minoxidil can cause changes in the heart’s electrical activity, and this has been observed in up to 60-90% of patients.^[34]Hall, D., Charocopos, F., Froer, K.L., Rudolph, W. (1979). ECG changes during long-term minoxidil therapy for severe hypertension. Archives of Internal Medicine. 139(70. 790-794. Available at: PMID: … Continue reading These changes are typically subclinical, meaning they do not cause symptoms or progress to life-threatening arrhythmias, and often resolve with continued use or a reduction in the dose.

In studies of low-dose minoxidil for hair loss, only minor, asymptomatic EKG changes have been observed, with no evidence of clinically significant heart rhythm disturbances in otherwise healthy individuals.^[35]Jiminiez-Cauhe, J., Pirmez, R., Muller-Ramos, P., Melo, D.F., Ortega-Quijano, D., Moreno-Arrones, O.M., Saceda-Corralo, D., Gil-Redondo, R., Hermosa-Gelbard, A., Dias-Sanabria, B., Restom, D., … Continue reading

Real-World Safety: Observational and Clinical Data

The most common side effects at hair loss doses are hypertrichosis, mild ankle swelling, lightheadedness, and occasional palpitations.^[36]Bloch, D.L., Carlos, R.M.D. (2025). Side Effects’ Frequency Assessment of Low Dose Oral Minoxidil in Male Androgenetic Alopecia Patients. Skin Appendage Disorders. 11(1). 14-18. Available at: … Continue reading Serious cardiac events are exceedingly rare. Most patients who experience side effects can continue treatment with dose adjustments. Only a small fraction discontinue due to adverse effects.

This favorable safety profile is not only a function of the lower dose but may also reflect the generally healthier status of this population compared to those prescribed high-dose minoxidil for hypertension. Most studies examining minoxidil for hair growth routinely exclude individuals with significant underlying disease.

Experts recommend that patients, especially those with pre-existing heart, kidney, or liver conditions, be monitored by a healthcare provider when starting oral minoxidil.^[38]Gupta, A.K., Bamimore, M.A., Haber, R., Williams, G., Piguet, V., Talukder, M. (2024). The Role of Patient- and Drug-Related Factors in Oral Minoxidil and Pericardial Effusion: Analyses of Data from … Continue reading

How Can I Make Oral Minoxidil Safer?

Here are a number of strategies you can use to help minimize side effects while maintaining results:

• Titrate Your Dose

Begin with the lowest effective dose and increase gradually if needed. This approach helps your body adjust and can reduce the risk of side effects, such as swelling, dizziness, or heart palpitations. 

Based on the published evidence, we believe that the best balance between efficacy and safety is 2.5 mg daily for men and 0.25-1.25 mg daily for women.

• Split the Dose: Morning & Evening

Oral minoxidil has a short half-life (about 3 hours). Taking your daily dose all at once can cause higher peak blood levels, increasing the risk of side effects. Taking half in the morning and half in the evening can help keep blood levels steadier and may reduce side effects.

• Consider Sublingual Administration

Taking minoxidil sublingually (letting it dissolve under your tongue) allows the drug to enter your bloodstream directly, bypassing the liver’s first-pass metabolism. Sublingual minoxidil becomes active when it reaches tissues with the right enzymes, such as those in the scalp, potentially enhancing its effectiveness. Studies suggest that sublingual minoxidil can lead to lower peak blood concentrations and fewer systemic side effects, while still promoting hair growth.^[39]Guo, R-X., Zhao, Y-K., Hu, K-J., Hia, K.M., Shi, W., Yi, Y-X., Gong, H-Y., Wang, J-B., Gao, Y. (2025). Research progress in the treatment of non-scarring alopecia: mechanism and treatment. Frontiers … Continue reading

• Switch To Topical Minoxidil

If oral minoxidil isn’t working for you because of the side effects, consider switching to the topical formulation. And, if you’re able to tolerate a 2% or 5% formulation well, you could consider adding microneedling or retinoic acid to boost your gains. 

To find out more information about the potential side effects and how to avoid them, watch our video: Oral Minoxidil: How to Eliminate Side Effects.

Is Oral Minoxidil Better Than Topical Minoxidil?

Deciding between oral and topical minoxidil involves weighing efficacy, convenience, safety, and individual response. 

Efficacy: Which Works Better?

At standard strengths, both 5% topical minoxidil and low-dose oral minoxidil (1-5 mg) show similar efficacy in clinical trials for total area hair count (TAHC).^[40]Fazal, F., Malik, B.H., Malik, H.M., Sabir, B., Mustafa, H., Ahmed, M., Abid, A., Adil, M.L., Shafi, U., Saad, M. (2025). Can oral minoxidil be the game changer in androgenetic alopecia? A … Continue reading However, oral minoxidil often leads to slightly thicker, more robust regrowth for some users, especially those with diffuse thinning.

When topical minoxidil is combined with enhancers, such as retinoic acid, at concentrations of 7-8% (or higher), the results can surpass those seen with oral minoxidil. Our members consistently report better outcomes with these combinations, even compared to 5 mg oral minoxidil.

Advantages of Oral Minoxidil

• More convenient: Oral minoxidil is taken as a pill once or twice daily, while topical minoxidil requires 1-2 daily applications, which can be inconvenient and affect adherence.
• No product residue: Oral minoxidil eliminates the sticky residue and styling issues associated with topical solutions.
• Cost-effective: Oral minoxidil is generally about half the price of topical formulations.
• Bypasses scalp enzyme variance: Oral minoxidil is activated in the liver, sidestepping the variability in scalp sulfotransferase enzyme activity that limits topical efficacy for some users.^[41]Goren, A., Shapiro, J., Roberts, J., McCoy, J., Desai, N., Zarrab, X., Pietrzak, A., Lotti, T. (2014). Clinical utility and validity of minoxidil response testing in androgenetic alopecia. … Continue reading
• Less scalp irritation: Oral minoxidil avoids the dryness, irritation, and brittleness sometimes caused by topical applications.
• May improve beard density: Some users report increased facial hair growth, which can be a benefit or drawback, depending on personal preference.^[42]Pirmez, R., Salas-Callo, C-I. (2020). Very-low-dose oral minoxidil in male androgenetic alopecia: a study with quantitative trichoscopic documentation. Journal of the American Academy of Dermatology. … Continue reading
• Better for brittle hair: Those with fragile or chemically treated hair may prefer oral minoxidil to avoid further brittleness.

Drawbacks of Oral Minoxidil

• Unwanted body hair: Oral minoxidil can cause hair growth on other parts of the body, which is especially concerning for women.
• Systemic side effects: Risks include fluid retention, rare cardiovascular effects, headaches, and skin rashes. These are uncommon at hair loss doses (0.25-5 mg), but still possible. 
• Prescription required: Unlike topical minoxidil, oral formulations require a prescription from a doctor.

Advantages of Topical Minoxidil

• Fewer systemic effects: Topical minoxidil acts locally, so there’s less risk of systemic side effects.
• Easier access: Available over-the-counter without a prescription.
• Customizable formulations: Various strengths and enhancers (like retinoic acid) can be tailored to individual needs.

Drawbacks of Topical Minoxidil

• Variable response:  Efficacy depends on scalp enzyme activity, which varies between individuals. 
• Scalp irritation: Some may experience irritation, dryness, or increased hair brittleness.^[43]Shadi, Z. (2023). Compliance to Topical Minoxidil and Reasons for Discontinuation among Patients with Androgenetic Alopecia. Dermatological Therapy (Heidelb). 13(5). 1157-1169. Available at: … Continue reading
• Residue and Compliance: Daily application can be messy and inconvenient, which can impact adherence.

Special Considerations: Scalp Inflammation

Underlying scalp inflammation (like seborrheic dermatitis) can reduce the effectiveness of topical minoxidil.^[44]Mahe, Y.F., Cheniti, A., Tacheau, C., Antonelli, R., Planard-Luong, L., de Bernard, S., Buffat, L., Barbarat, P., Kanoun-Copy, L. (2021). Low-Level Light Therapy Downregulates Scalp Inflammatory … Continue reading Addressing inflammation is crucial before starting or modifying any hair loss treatment.

The bottom line: 

Oral minoxidil is more convenient, cost-effective, and bypasses scalp enzyme limitations, making it a strong option, especially for those who don’t respond to topical or want to avoid scalp irritation. 

High-strength topical minoxidil, when combined with treatments such as retinoic acid and microneedling, often delivers the best results but comes with more hassle, a higher cost, and a greater risk of scalp irritation.

Standard topical minoxidil remains a solid, accessible first-line option, especially for those who prefer to avoid systemic medications. 

Ultimately, the best choice depends on your hair loss pattern, your response to treatment, your tolerance for side effects, and your lifestyle. 

Can You Take Them Together?

Yes, it is possible to use oral and topical minoxidil together; however, this approach should only be considered under the supervision of a healthcare provider. Combining both forms may provide a more robust treatment for hair loss.

Some dermatologists suggest that using both can enhance efficacy, especially for individuals who have not achieved optimal results with one form alone. However, using both simultaneously increases the risk of side effects. Therefore, the decision to combine oral and topical minoxidil should be made with professional guidance to ensure proper dosing and monitoring for adverse effects.

Who are the Best Candidates for Oral Minoxidil?

According to the research we just outlined, you’re a good candidate for oral minoxidil if:

• You’re a male with AGA, TE, or permanent chemotherapy-induced alopecia who doesn’t respond to topical minoxidil and/or finds it difficult to comply with the treatment protocol.
• You’re a female with FPHL, TE, or permanent chemotherapy-induced alopecia who doesn’t respond to topical minoxidil and/or finds it difficult to comply with the treatment protocol, and you’re okay with a chance of increased hair growth in other places of the body.
• You have a healthy liver and normal to high blood pressure. If you are somewhat hypertensive, oral minoxidil may have the joint benefit of hair growth and antihypertensive effects.
• You’re a female who’s already taking spironolactone for FPHL and wants to see better results, or has seen a plateau with spironolactone alone.
• You’re an AA patient resistant to traditional immunomodulatory treatment.
• You suffer from a brittle hair disorder or hair loss and brittle hair and want to avoid exacerbating brittleness with topical minoxidil.
• You can obtain a prescription.

On the other hand, you’re not a good candidate for oral minoxidil if…

• You’re a female who’s not comfortable with the idea of increased hair growth outside of the scalp.
• You regularly drink alcohol, which can exacerbate the antihypertensive effects of minoxidil.
• You have or have had kidney, cardiovascular, or liver issues.
• You’re pregnant or planning on becoming pregnant.
• You’re currently taking another vasodilating/antihypertensive drug or a muscle relaxer like tizanidine. Taking two vasodilating drugs at once can increase the risk of side effects associated with low blood pressure.

What Are The Best Practices for Taking Oral Minoxidil?

When taking oral minoxidil for hair loss, it’s best to start with the lowest effective dose, typically 2.5 mg daily for men and 0.25–1.25 mg daily for women. The dose should be increased gradually only if needed, under the supervision of a healthcare provider. Splitting the total daily dose into morning and evening halves can help maintain steady blood levels and reduce the risk of side effects, such as palpitations, swelling, or dizziness. 

Sublingual administration (allowing the tablet to dissolve under your tongue) is an alternative that may further minimize systemic side effects by bypassing the liver’s first-pass metabolism, potentially making the medication more tolerable for individuals who are sensitive to it. Throughout treatment, monitor for common side effects, such as unwanted hair growth (hypertrichosis), ankle swelling, or lightheadedness, and promptly report any serious symptoms, including chest pain or significant changes in heart rate. 

Regular check-ins with your healthcare provider are essential, especially if you have underlying heart, kidney, or liver issues or take other medications that affect blood pressure. If side effects occur, consider reducing the dose, splitting it further, switching to a sublingual or topical minoxidil formulation, or discontinuing use as advised by your healthcare provider. 

Avoid combining oral minoxidil with other vasodilators or muscle relaxants without consulting a healthcare professional. Address any scalp inflammation before starting or adjusting therapy to maximize results and safety.

Final Thoughts

Oral minoxidil has emerged as a compelling option for individuals seeking effective hair loss treatment, offering robust regrowth potential and convenience for both men and women who may not respond to or tolerate topical formulations. While research supports its efficacy across a range of hair loss conditions, including androgenic alopecia and chronic telogen effluvium, it is not without risks, most notably rare but serious cardiovascular side effects, as well as more common issues such as unwanted hair growth and mild edema. For many, oral minoxidil represents a powerful, evidence-based tool in the fight against hair loss, but its use should always be informed, individualized, and guided by medical expertise to ensure both safety and satisfaction. If you are a good candidate and proceed thoughtfully, oral minoxidil can play a pivotal role in your hair restoration journey.

We’re thrilled to announce the arrival of Ulo: a haircare brand that offers best-in-class hair growth products and focuses on solving the biggest problems plaguing the hair loss industry.

Ulo’s core commitment to hair loss sufferers is its prioritization of evidence, personalization, and consumer safety. And there’s a reason we’re so confident in Ulo’s ability to deliver: we co founded the brand.

In fact, the Perfect Hair Health team was involved in every aspect of Ulo’s product development: its selection of manufacturers, ingredients, formulations, concentrations, & more. Now the product formulations for which we’ve been advocating for 10+ years are finally offered, all through a single provider.

Whether it’s over-the-counter serums or prescription products, Ulo represents the next evolution in telehealth haircare: one that puts the consumer first, sets realistic expectations, and supports customers at every step on their journey to better hair.

Below, we’ll detail our journey to launching Ulo, the problems Ulo solves, its core offerings, and why we currently consider Ulo to be a revolutionary step forward for consumers.

For those interested in this level of product personalization and support, Ulo is also offering 15% off all their products, forever. Any purchase made through the links in this article will result in a 15% discount applied to all product purchases, including all renewals. This is our thank you to you, and your opportunity to lock in a permanently discounted price on all products.

Why Ulo?

For 11 years, Perfect Hair Health has acted solely as a consumer advocacy resource for men and women fighting hair loss.

During this time, we never once endorsed a single hair growth product: no pill, supplement, topical, shampoo, or device. Instead, we focused entirely on educating hair loss sufferers on how to properly read studies, select treatments, and maximize their chances for hair regrowth.

For just a few examples of this commitment, see the following content pieces:

• What Causes Hair Loss? (Interactive Guide)
• Understanding Hair Loss Disorders (Interactive Guide)
• The Hair Loss Industry Is Broken: Evidence Quality Masterclass (Video)
• Nutrafol: The Problem With Their Clinical Studies (Company Investigation)
• Our Peer-Reviewed Studies (Publications)
• Independent Third-Party Lab Testing Results (Product Investigations)

But, as the hair loss industry continued to evolve, so too did its bad practices – particularly the sale of dangerous, improperly formulated products with ingredients that were “trending” on social media, but that lacked adequate efficacy and safety data.

For years, our organization called attention to these concerns – creating free evidence-based articles, videos, & interactive guides detailing these exact problems & how to protect yourself. And yet this entire time, as the hair loss industry expanded, we watched these problems only grow worse. We’ll detail several of them later in this article.

Two years ago, Perfect Hair Health was offered a once-in-a-lifetime opportunity to become more than just a voice of advocacy. We were approached with an offer to go beyond education and to start solving the very problems that have plagued this industry for years.

This meant an opportunity to create products that could finally serve as the antidote to every bad practice currently employed by other haircare brands at scale.

Initially, we were skeptical. We’ve seen firsthand how other brands deprioritize consumer safety in the name of “business decisions,” like with brands that include corticosteroids in their Rx topicals to offset irritation and increase recurring purchases… but at the expense of the risk of long-term, permanent skin thinning for their patients.

If we were going to become involved in a brand, we would need full control over the entire production process for hair loss. We wanted the sole ability to fire compounding pharmacies that failed to meet purity standards. We wanted final say in every aspect of product development: the ingredients, concentrations, formulations, & more. Without this level of control, we would never be able to prioritize what’s right for the consumer over what’s right for business.

We were pleasantly surprised to find 100% alignment with those offering a partnership. With just how easy it is to “cut corners” in the hair loss industry, we can’t describe how refreshing it was to connect with others who actually wanted to do right by the consumer.

After much reflection, we decided to step off the sidelines as critics and instead, start building a brand that walked the walk and started solving the hair loss industry’s biggest problems.

That brand is Ulo: a telehealth company dedicated exclusively to hair growth, and founded on three key pillars: evidence, personalization, and consumer safety.

What Problems Need Solving In The Hair Loss Industry?

Over the years, we’ve watched haircare brands adopt a set of bad practices that seemed uniquely targeted toward their bottom line, rather than consumer interests.

We’ll detail just a few of these below, along with how Ulo solves these problems and sets the bar higher.

Problem #1: Mega-Dosed Topicals

Other telehealth brands are selling mega-dose versions of topical finasteride & topical dutasteride – letting people think it’s staying on the scalp, when in reality, the dose is 60x too high, so it leaks into the blood & causes hormonal changes to the same extent as oral finasteride.

Videos here and here. FDA warning here.

Ulo’s Solution: Low-Dose Topical Finasteride & Low-Dose Topical Dutasteride

Ulo offers two kinds of topical finasteride & topical dutasteride: low-dose and full-strength.

For those truly interested in localization, the lower-dose topicals are far more appropriate than the mega-dosed topicals sold by other telehealth brands. And even more encouragingly, Ulo offers full customization of either topical – with the ability to add in ingredients like 7% minoxidil, 0.01% retinoic acid (tretinoin), 0.2% caffeine, 0.01% melatonin, and 1% cetirizine – so prospective users can ensure better control over every ingredient, pending a prescription:

Ulo’s Topical Finasteride

• Low-Dose Topical Finasteride (Optional: Add Enhancers)

• Full-Strength Topical Finasteride (Optional: Add Enhancers)

Ulo’s Topical Dutasteride

• Low-Dose Topical Dutasteride (Optional: Add Enhancers)

• Full-Strength Topical Dutasteride (Optional: Add Enhancers)

Problem #2: Corticosteroids In Rx Topicals (Permanent Skin Thinning)

Brands are adding dangerous ingredients to their Rx topicals –– like corticosteroids. They do this because their serums often contain propylene glycol, which helps with ingredient penetration but also causes skin irritation. Yet rather than fix their formulations, brands offset the irritation with corticosteroids (hydrocortisone, fluocinolone, etc.). This works in the short-term, and very likely, causes permanent, irreversible skin thinning after years of uninterrupted use. 

Article here. Video here. Study here.

Ulo’s Solution: No Corticosteroids, No Propylene Glycol, & Less-Irritating Formulations

Ulo doesn’t use propylene glycol in any of its topicals. Instead, its partner pharmacies have spent significant time developing & iterating base formulations containing water, alcohol, and glycol-like compounds – formulations that apply easily, dry quickly, allow for ample ingredient penetration into the hair follicles, and above all, are less irritating.

The end-result: Ulo’s topicals don’t need to add corticosteroids to mask irritation – because they were formulated properly from the start.

Note: some of Ulo’s optional ingredients – like retinoic acid (tretinoin) – can enhance the activation and penetration of minoxidil, but may also cause mild irritation in a subset of individuals. For those who discover they cannot tolerate retinoic acid (tretinoin), Ulo’s physician partners can easily remove this ingredient for them. This is a much better, much more sustainable alternative than simply masking irritation with a corticosteroid, especially given the long-term risks of skin irritation.

Ulo’s topicals can be found here, with a guide to help you select your offering here.

Problem #3: Selling Dangerous, “Trending” Ingredients

Other telehealth brands are offering “trending” drugs with long-term safety risks, like latanoprost. Originally developed to treat glaucoma, latanoprost is now widely added to Rx topicals for hair growth. The basis? Two small clinical studies, the longest of which ran for 9 months. The problem? The doses sold by telehealth brands are, at times, thousands of times higher than what was used to treat glaucoma. They absolutely go systemic. And there’s a permanent side effect that occurs in up to 20% of glaucoma patients using latanoprost – one that typically isn’t noticeable until after 12 months of use: the blackening of your irises, an effect that often persists even after quitting the medication. No studies exist evaluating this risk for topical latanoprost, and also, no telehealth brand seems to care.

Article here. Video here.

Ulo’s Solution: No “Trending” Ingredients That Risk Your Safety. Ever.

Unless an off-label ingredient offers notable hair gains through mechanisms distinct from other Ulo ingredients – and unless that ingredient has a respectable safety profile – Ulo will not include it as an offering to its product line.

That means no Carbon 60. No copper peptides. No latanoprost. No bimatoprost.

Ulo focuses on getting you results without compromising your safety. While the telehealth brand does offer off-label ingredients to certain users pending a prescription, such as dutasteride, spironolactone, melatonin, caffeine, and cetirizine, it only does so if safety & efficacy thresholds are met to justify their inclusion for added hair gains.

This is distinct from many other companies out there who simply attempt to capture your interest in ingredients “trending” on social media, but without enough data to determine whether these ingredients are safe, effective, and right for you.

You can see a sample of Ulo’s ingredient selections & concentrations here.

Problem #4: Compounding Dutasteride Without Emulsifiers

Other telehealth brands are compounding drugs that can’t be compounded, like dutasteride. To differentiate from the competition, telehealth brands often compound drugs like dutasteride & minoxidil into a single capsule, claiming bigger hair gains than finasteride and the convenience of a single daily pill.

The truth? When these companies “compound” dutasteride, they turn it from a soft gel into a powder, and inadvertently, they destroy its bioavailability, rendering dutasteride less effective than finasteride & causing major hair loss for customers who unknowingly switch to the 2-in-1 pills.

We have the lab tests to prove it. Post here. Video here.

Ulo’s Solution: No Compounded Dutasteride. Just The Real Thing.

Rather than offer compounded dutasteride, Ulo offers dutasteride as a soft gel – and in a formulation that has undergone bioequivalence testing, such that the efficacy should match that of the studies showing oral dutasteride outperformed oral finasteride for hair gains.

This is a distinction unrivaled by many other brands. Rather than sell you convenience in a 2-in-1 pill, Ulo sells you what works.

Better yet, Ulo still offers both oral dutasteride and oral minoxidil to those who want to multi-target their hair loss. They are just delivered as separate pills, in separate formulations, to maximize your potential for hair growth.

You can see Ulo’s oral Rx offerings here.

Beyond Ulo’s Products: Personal Support, Every Step Of The Way, Through Ulo’s Partner Physicians

As part of Ulo’s commitment to consumers, all subscriptions to their Rx product lines come with unlimited access to partner physicians – one of whom you’ll personally partner with to support your hair growth journey.

What does this look like? A completely different experience compared to other brands:

• • Real customization: dosing & ingredient adjustments made by our partner physicians depending on your goals & real-time experiences with the products.
  • Realistic expectations: separate “possibility” from “probability”. Our network physicians rely on clinical data to set realistic responses to your hair loss medications, including guides for when regrowth starts, when it might plateau, and what to do next to escalate your current protocol.
  • Unrivaled personal support: the ability to contact a doctor, any time, through Ulo’s portal. Someone in your corner who not only assumes care for you, but also wants to help you achieve the best possible outcomes.

We hope you feel the difference. This piece is something we see other brands “promise”, but rarely deliver. It’s time to change that.

15% Off All Ulo Orders, Forever

Ulo is a part of the Perfect Hair Health ecosystem, and as a thank you for being a part of our community, all orders made through this article will automatically receive 15% off the purchase price, forever. That includes all future renewals, so long as the orders are made through these links.

We hope you enjoy everything Ulo has to offer. We certainly love the product line and are thrilled that we finally have the chance to offer products in the exact formulations for which we’ve advocated over the past 10+ years.

We wish you the best with your hair health journey, and we look forward to supporting you every step of the way.

OS-01 is a topical scalp serum developed by OneSkin, a biotech company based in San Francisco. Marketed as both an anti-aging skin treatment and a hair regrowth product, OS-01 aims to address hair thinning by targeting cellular senescence in the scalp. The serum has gained attention through social media and interviews with the company’s CEO, Carolina Reis Oliveira. In this article, we will examine what OS-01 is, explore the science of cellular senescence and its role in hair loss, and assess the evidence behind OS-01’s claims as a potential treatment for androgenetic alopecia.

Key Takeaways:

• Branding. OS-01 has positioned itself as a biotech-backed anti-aging and hair regrowth serum from OneSkin, a company known for its focus on longevity science. The branding strongly emphasizes scientific credibility and a “rooted in science” approach.
• Unique Selling Point. OS-01 is a peptide that specifically targets cellular senescence in the scalp, aiming to rejuvenate the hair follicle microenvironment by modulating the senescence-associated secretory phenotype (SASP).
• Clinical Support. OneSkin reports a 6-month third-party clinical study showing improvements in hair density, thickness, and hair cycling when used with daily dermarolling. However, these results have not been published in peer-reviewed journals and rely on company-provided summaries.
• Concerns. Key concerns include the lack of independently published human data, reliance on dermarolling for efficacy, marketing claims that oversimplify complex skin and hair biology, and typical limitations seen in brand-led before-and-after photos.
• Evidence Quality. The OS-01 serum scored 31/100 for evidence quality by our metrics.
• Recommendations. We recommend that OS-01 consider publishing the results of their 6-month pilot study and, ideally, conduct a larger, registered, placebo-controlled clinical trial.

What Is OS-01?

OS-01 for hair is a topical scalp serum developed by OneSkin, a biotech company based in San Francisco, as both an anti-aging skin product and a hair regrowth product. The product is claimed to address hair thinning and loss by targeting the biological process of cellular senescence in the scalp.^[1]OneSkin. (no date). Rooted in Science: The Clinical Evidence Supporting OS-01 Hair. Available at:  … Continue reading

The product is sold in 1.7 fl oz bottles, available in 1-, 3-, or 6-month supplies, and comes with a dermaroller for $69, $207, or $424.

The product contains a number of ingredients, of which you can see the whole list here: 

“Water, Glycerin, 1,2-Hexanediol, Butylene Glycol, Hydroxyacetophenone, Panthenol, Inulin, Helianthus Annuus (Sunflower) Sprout Extract, Cellulose Gum, Alpha-Glucan Oligosaccharide, Tetrasodium Glutamate Diacetate, Propanediol, Morus Nigra Leaf Extract, Arginine, Acetyl Tyrosine, Rehmannia Chinensis Root Extract, Pentylene Glycol, Sodium PCA, Erythritol, Chondrus Crispus, PEG-12 Dimethicone, Oryza Sativa (Rice) Bran Water, Decapeptide-52*, Calcium Pantothenate, Zinc Gluconate, Sodium Benzoate, Niacinamide, Ornithine HCL, Caprylyl Glycol, Polyquaternium-11, Citrulline, Hydrolyzed Soy Protein, Xanthan Gum, Glucosamine HCL, Disodium Succinate, Fisetin, Raspberry Ketone, Sodium Benzoate, Citric Acid, Potassium Sorbate, Arctium Majus Root Extract, Panax Ginseng Root Extract, Biotin. *OS-01 Peptide.”

Several familiar ingredients are present here, including niacinamide, calcium pantothenate, zinc gluconate, raspberry ketone, ginseng, fisetin, and biotin.

• Niacinamide: Research shows that it may help protect hair follicle cells from oxidative stres, reduce the expression of DKK-1 (a protein that promotes hair follicle regression), and prolong the anagen (growth) phase of hair follicles.^[2]Choi, Y-H., Shin, J.Y., Kim, J., Kang, N-G., Lee, S. (2021). Niacinamide down-regulates the expression of DKK-1 and protects cells from oxidative stress in cultured human dermal papilla cells. … Continue reading Clinical studies have demonstrated increased hair fullness and thickness in some participants using niacinamide derivatives, though it is thought that it doesn’t actually increase hair density.^[3]Draelos, Z.D., Jacobson, E.L., Kim, H., Kim, M., Jacobson, M.K. (2005). A pilot study evaluating the efficacy of topically applied niacin derivatives for treatment of female pattern alopecia. Journal … Continue reading
• Calcium Pantothenate: This ingredient is commonly found in hair care products and supplements. Some studies suggest it may help improve hair thickness and reduce hair loss, especially when combined with zinc. For example, a clinical trial in women found that co-administration of zinc sulfate and calcium pantothenate alone was less pronounced, and more research is needed.^[4]Siavash, M., Tavakoli, F., Mokhtari, F. (2017). Comparing the effects of zinc sulfate, calcium pantothenate, their combination and minoxidil solution regimens on controlling hair loss in women: a … Continue reading
• Raspberry Ketone: This has been studied in small human trials and animal models. Topical application promoted hair growth in about 50% of humans with alopecia, possibly by increasing dermal IGF-1 production through sensory neuron activation.^[5]Harada, N., Okajima, K., Narimatsu, N., Kurihara, H., Nakagata, N. (2008). Effect of topical application of raspberry ketone on dermal production of insulin-like growth factor-I in mice and on hair … Continue reading However, the evidence base remains limited, and larger studies are necessary to confirm these effects.
• Fisetin: Fisetin is a polyphenol that has shown promise in preclinical studies. It may promote hair growth by increasing telomerase reverse transcriptase (TERT) expression, activating hair follicle stem cells, and facilitating the transition from a resting to a growth phase.^[6]Kubo, C., Ogawa, M., Uehara, N., Katakura, Y. (2020). Fisetin promotes hair growth by augmenting TERT expression. Frontiers in Cell and Developmental Biology. 8(566617). Available at … Continue reading Animal studies suggest that fisetin may induce hair growth; however, human data are currently lacking.
• Biotin: This ingredient is widely marketed for hair health, but strong evidence for its effectiveness in preventing hair loss or promoting hair growth in people without a deficiency is lacking. Biotin supplementation can help restore hair growth in cases of true biotin deficiency, but such deficiencies are rare. Most studies do not support its use for hair loss in otherwise healthy individuals, though it remains a popular ingredient.^[7]Yelich, A., Jenkins, H., Holt, S., Miller, R. (2024). Biotin for Hair Loss: Teasing Out the Evidence. Journal of Clinical and Aesthetic Dermatology. 17(8). 56-61. Available at: … Continue reading

However, the one we will be focusing on in this article is Decapeptide-52, also known as the OS-01 Peptide.

There has been a lot of hype on social media about this product, including a particularly interesting YouTube video featuring Dave Asprey, who talks with Carolina Reis Oliveira, the CEO and Co-founder of OneSkin.^[8]Asprey. D. (2025). Hair Growth Expert: Scientists Discover a Secret Peptide that Reverses Balding | Caroline Oliveria. YouTube. Available at: https://www.youtube.com/watch?v=FSY1x40N2ys Accessed: … Continue reading Carolina holds degrees in stem cell biology and tissue engineering, as well as a doctorate in immunology, which bodes well for the scientific integrity of the product.

However, in the first ~15 seconds of the above video, Carolina makes some interesting statements:

1. “The scalp of the skin basically has a similar structure of the skin in your face…”
2. “Your hair follicles are basically embedded in the epidermal layer…”
3. “…a lot of the things that we see happening in the skin of our face also happen in our scalp”

Now let’s break down what is wrong with these statements:

• “The scalp of the skin basically has a similar structure of the skin in your face…”

This statement is partially accurate. While the scalp and facial skin share the same basic layers (epidermis, dermis, etc.), there are significant structural and functional differences:

• When measuring total skin thickness in both men and women, scalp skin was found to be among the thickest.^[9]Oitulu, P., Tekecik, M., Taflioglu, T., Kilinc, F., Ince, B. (2022). Measurement of Epidermis, Dermis, and Total Skin Thicknesses from Six Different Face Regions. Selcuk Medical Journal. 38(4). … Continue reading
• The scalp contains a much higher density of hair follicles and sebaceous glands than facial skin.^[10]Gao, J., Liu, C., Zhang, S., Teacher, M.P., Bouabbache, S., Pouradier, F., Pangard. (2018). Revisiting, in vivo, the hair greasing process by the Sebuprint method. Skin Research and Technology. … Continue reading 
• The scalp is more prone to certain inflammatory and microbiome-related disorders due to its unique structure and physiology.^[11]Xu, Z., Wang, Z., Yuan, C., Liu, X., Yang, F., Wang, T., Wang, J., Manabe, K., Qin, O., Wang, X., Zhang, Y., Zhang, M. (2016). Dandruff is associated with the conjoined interactions between host and … Continue reading 

So, while the basic structure is similar, the differences are clinically and biologically significant.

• “Your hair follicles are basically embedded in the epidermal layer…”

This is factually incorrect. Hair follicles are not embedded in the epidermal layer; they are skin appendages that extend deep into the dermis, with the bulb even reaching the hypodermis (subcutaneous tissue).^[12]Oh, J.W., Kloepper, J., Langan, E.A., Kim, Y., Yeo, J., Kim, M.J., Hsi, T.C., Rose, C., Yoon, G.S., Lee, S.J., Seykora, J., Kim, J.C., Sung, Y.K., Kim, M., Paus, R., Plikus, M.V. (2016). A guide to … Continue reading 

• “…a lot of the things that we see happening in the skin of our face also happen in our scalp”

This is generally true, but it oversimplifies the differences. Many skin conditions (like psoriasis, eczema, and seborrheic dermatitis) can occur on both the scalp and face. However, the scalp’s unique anatomy, thicker skin, increased hair follicles, more sebaceous glands, and its coverage by hair, means it is prone to specific issues (like dandruff and increased oiliness) that are less common or present differently on facial skin. So, while there is overlap, the statement ignores important distinctions in disease prevalence and presentation.

These statements reinforce what we have been discussing in other articles – that you cannot blindly trust what people say. We should always adopt a scientific approach to the information we read online and attempt to find the scientific basis for their claims. 

With this in mind, we will explore the science of the product, examine what senescence is, and explore the data that suggests OS-01 can enhance hair growth.

What is Senescence and How is It Involved in Hair Cycling and Loss?

Before we get into how OS-01 works, it is essential to understand what senescence is, when it can be beneficial for hair growth, and when it can be detrimental.

Cellular senescence can be thought of as a “pause button for cells”. When cells are stressed or damaged due to factors such as DNA damage, aging, or excessive environmental stress, they cease to divide permanently. But instead of dying like in programmed cell death (apoptosis) they stay active, sending out signals to their neighboring cells, and beyond. 

Key features of these cells include:^[14]Nakanishi, M. (2025). Cellular senescence as a source of chronic microinflammation that promotes the aging process. Proceedings of the Japan Academy, Ser.B, Physical and Biological Sciences. 101(4). … Continue reading 

• A permanent stop in cell division: They’re kept in check by guardian pathways (p54/p2 and p16/Rb) that make sure they never divide again.
• Shape changes: They get bigger, flatter, and may look like “fried eggs” under the microscope.
• Special markers: Scientists detect them using a blue stain (called senescence-associated β-galactosidase (SA-β-gal)) that shows they have more lysosomes – cell “recycling bins”. 
• Secretory profile: They secrete a cocktail of chemicals, cytokines, growth factors, and enzymes, known as the senescence-associated secretory phenotype (SASP). This cocktail affects the surrounding tissue, sometimes beneficially, sometimes harmfully.

In recent years, senescence has become a trendy buzzword in the beauty and longevity industries, often used to market products as anti-aging breakthroughs. While genuine scientific research shows that senescent cells play a real role in aging and tissue decline, many companies oversimplify or exaggerate this science to promote creams, serums, or supplements with vague claims of “targeting senescence”. In reality, effectively targeting senescent cells is complex and context-dependent, and not every product touted as a senescence solution is supported by robust clinical evidence. As a result, the term is sometimes misappropriated more as a marketing hook than a rigorously validated mechanism.

Furthermore, while senescence was once thought of as a detrimental mechanism, it can actually be beneficial for both overall health and hair health.

Helpful Senescence: Encouraging Hair Growth

As mentioned above, some senescent cells can actually benefit hair growth:^[15]Wang, X., Ramos, R., Phan, A.Q., Yamaga, K., Flesher, J.L., Jiang, S., et al. (2023). Signalling by senescent melanocytes hyperactivates hair growth. Nature. 618(7966). 808-817. Available at: … Continue reading 

• Osteopontin signal: Senescent pigment cells (melanocytes) in skin moles produce a molecule called osteopontin. This acts like a motivational speaker for nearby hair cells by binding to CD44 receptors, waking them up.
• Stem cell activation: This process prompts hair follicles to exit their resting phase and re-enter growth mode, much like flipping the switch from winter to spring. 
• Proven boost: Injecting osteopontin or turning up its production in lab animals triggered hair growth; blocking it canceled the effect.

Harmful Senescence: Fueling Hair Loss

Recent studies show that accumulation of senescent cells can play a role in both androgenic alopecia (AGA) and age-related hair thinning.

As we age, more cells in the hair follicle’s support structures, like dermal papilla cells (DPCs) and hair follicle stem cells (HFSCs), become senescent.^[16]Shin, W., Rosin, N.L., Sparks, H., Sinha, S., Rahmani, W., Sharma, N., Workentine, M., Abbasi, S., Labit, E., Stratton, J.A., Biernaskie, J. (2020). Dysfunction of Hair Follicle Mesenchymal … Continue reading These cells lose their ability to renew themselves and support healthy hair growth, resulting in weaker follicles that gradually shrink over time. This process, known as hair follicle miniaturization, is why aging hair tends to become thinner and sparser.

Age-related hair thinning features a gradual loss of follicle stem/progenitor cell function, increased senescent cell burden, and mitochondrial dysfunction.^[17]Shin, W., Rosin, N.L., Sparks, H., Sinha, S., Rahmani, W., Sharma, N., Workentine, M., Abbasi, S., Labit, E., Stratton, J.A., Biernaskie, J. (2020). Dysfunction of Hair Follicle Mesenchymal … Continue reading This leads to both HFSC and DPC dysfunction.

Preclinical studies (studies done in cells or animals) have shown that antioxidants, senolytics, and interventions that reduce DPC/HFSC senescence or SASP can delay or ameliorate hair loss.^[18]Deng, Y., Wang, M., He, Y., Liu, F., Chen, L., Xiong, X. (2023). Cellular senescence: Ageing and Androgenetic Alopecia. Dermatology. 239(4). 533-541. Available at: https://doi.org/10.1159/000530681 However, clinical translation remains limited. Furthermore, some evidence suggests that senescence may be a consequence, rather than a sole cause, of follicle dysfunction, meaning that treating just the senescence aspect alone may not be beneficial for hair regrowth.^[19]Mirmirani, P., Karnik, P. (2010). Comparative Gene Expression Profiling of Senescent and Androgenetic Alopecia Using Microarray Analysis. Aging Hair. 67-76. Available at: … Continue reading

How Does the OS-01 Peptide Work?

According to OneSkin, OS-01 for hair targets senescent cells in the hair follicle to improve hair regrowth. One study frequently referenced on their website was conducted using human skin models.^[20]Zonari, A., Brace, L.E., Al-Katib, K., Porto, W.F., Foyt, D., Guiang, M., Cruz, E.A.O., Marshall, B., Gentz, M., Guimaraes, G.R., Franco, O.L., Oliveira, C.R., Boroni, M., Carvalho, J.L. (2023). … Continue reading In this study, OS-01 (referred to as pep14) was identified and characterized for its senomorphic activity. As a senomorphic, the OS-01 peptide reduces the burden of cellular senescence by suppressing the harmful secretions associated with the senescence-associated secretory phenotype (SASP) and by preventing pre-senescent cells from progressing to full senescence. Importantly, it does not kill or eliminate existing senescent cells.

OneSkin also seems to have conducted a laboratory study using outer root sheath keratinocytes (ORSKs).^[21]OneSkin. (no date). Discover the science behind every claim. Available at: https://www.oneskin.co/pages/claims?_ab=0&_fd=0&_sc=1 Accessed: June 2025

Interestingly, we had some difficulty determining the source of this information. It’s present on their shop page for OS-01 HAIR, but they cite 6 studies that don’t contain any information about this study. We then went to their Claims section and found the information below – again, however, there was no reference. 

We went to read some of the blogs where this information was also stated; the citation, however, led us back to the Claims section. The only conclusion we can draw is that OneSkin conducted an internal study that has not yet been published. Therefore, we should take all results with a pinch of salt.

OneSkin treated the cells with corticotropin-releasing hormone (CRH) (to induce senescence) alone or in combination with OS-01. According to the website, after 72 hours, cells treated with OS-01 + CRH showed significantly lower CDKN1A (p21) levels compared to those treated with CRH alone. 

Unfortunately, they don’t have any further data or information about this, so we can only go with what is written here.

Can OS-01 Benefit Patients with Androgenetic Alopecia?

OneSkin has also conducted a 6-month independent third-party clinical study in which 30 participants (23 women and 7 men) applied OS-01 HAIR twice daily and dermarolled their scalps once daily.^[22]OneSkin. (no date). Discover the science behind every claim. Available at: https://www.oneskin.co/pages/claims?_ab=0&_fd=0&_sc=1 Accessed: June 2025 Again, this data is unpublished in any peer-reviewed journal and so we are just having to go from what is on the site.

The overall results showed:

Category	Details
Hair Density	86.67% showed 39.62% avg increase after 6 months
Hair Density	70% showed 9.97% avg increase after 3 months
Hair Density	Double-blind, 30 participants, twice daily + dermarolling
Hair Density (Men)	85.71% men showed 34.86% avg increase after 6 months (7 men)
Hair Thickness	83.33% showed 42.58% avg increase after 6 months
Hair Thickness	Significant increase between 3 and 6 months
Hair Thickness (Men)	100% men showed 36.68% avg increase after 6 months; 85.71% men 28.42% after 3 months
Hair Cycle	73.33% showed 42.39% avg increase in anagen hairs after 6 months
Hair Cycle	Significant increase between 3 and 6 months
Hair Cycle (Men)	85.71% men showed 20.19% avg increase at 3 months, 35.42% at 6 months
Scalp Microbiome	Supported scalp microbiome: increased M. globosa, improved ratio, better bacterial diversity
Consumer Perception (Clinical) – 3 Months	80% saw hair improvement, 76.67% healthier hair, 70% faster growth, 73.33% fuller hair, 70% nourished scalp
Consumer Perception (Clinical) – 6 Months	70% faster growth, 76.67% healthier hair, 73.33% less shedding, 83.33% nourished hair, 70% thicker, 73.33% stronger, 70% better texture
Consumer Perception (Brand-led) – Immediate	89.47% could style hair, 85% lightweight
Consumer Perception (Brand-led) – 2 Months	80.95% more hydrated scalp
Consumer Perception (Brand-led) – 3 Months	81.82% new hair growth, 72.73% denser hair
Sensitive Skin	Dermatologically tested on 55 volunteers; no reactions
Lab Data – Senescence	OS-01 peptide reduces cellular senescence (lab data)
Lab Data – Senescence (Stress-induced)	Significant reduction in CRH-induced senescence (*p<0.05)
Lab Data – Inflammation	Significant reduction in IL-6 inflammation marker (*p<0.05)

We see some issues immediately jumping out about the clinical trial OneSkin has conducted:

• OneSkin do not explicitly mention whether the participants have any type of hair loss.
• The study included no placebo or treatment group – this means we can’t find out if hair cycle seasonality played any part in the participants’ hair growth.
• The treatment was combined with microneedling. Microneedling has been shown to potentially improve terminal hair counts by itself (we covered one here) so how can we separate out the effects of the peptide vs. the microneedling?
• In a similar vein, the product itself contains a number of other ingredients (with varying evidence showing improvement on hair regrowth) – so how can we separate out the effects of these compared to the peptide?
• While OneSkin do tell us how the hair counts were done, there was no disclosure of how terminal hairs were defined and starting hair zone parameters for the participants. For example in the niostem study, the researchers clearly outlined how they categorized terminal/vellus hair density (vellus (< 40 μm) and terminal (> 40 μm) hairs). A number of other studies however also don’t define terminal hairs (one that comes to mind is the CBD oil study) – so while it does happen, it is not good practice.
• Certain phrasings appear to be potentially misleading:
  • From the Claims section: “After 6 months, 83.33% of participants experienced a 42.58% average increase in hair thickness (sum of hair widths). (****p < 0.0001)”. The statistic refers only to the subset (83.33%) of participants who experienced an increase, not the entire study population. This means that 16.67% of participants did not experience an increase, but their results are not included in the average, potentially inflating the reported effect. The phrasing also raises the question of whether participants with no improvement or negative outcomes were excluded from the calculation. If so, and if those excluded participants had poor or negative results, the true average increase would be lower than reported.
    • This is not the only claim that does this and so we have to wonder what is happening with the other participants?
  • From the Claims section: “Participants saw a significant increase in hair thickness (sum of hair widths) between 3 and 6 months (**p < 0.01)”. Because we don’t have any graphs or data for this, we have to wonder…do we have a Niostem problem all over again? Niostem published their clinical data in February 2025 and claimed that “Terminal hair density improved significantly over time…” but this is not compared to the baseline – it’s compared to the three month time point, where there was actually a decrease in terminal hair density from the baseline. You can read our article about this here. Unfortunately we do not have any further information from OneSkin so we can’t know exactly what is happening.

You can read or watch some of our content that talk about these subjects here:

Deceptive But Legal: 3 Ways Marketers Cheat Hair Loss Studies

The Hair Loss Industry Is Broken | Evidence Quality Masterclass

Understanding Evidence Quality | How Hair Loss Companies Cheat Clinical Trials

Oneskin also has some before-and-after photos on their website, allowing us to see the progress people have experienced. However, they do fall for the usual pitfalls that we have mentioned in other articles, including different lighting, angles, and manipulating the hair so that it appears different in the before-and-after images (see below).

According to OneSkin, several positive results have been observed in their clinical trial; however, like many of these companies, the information has only been published on their website, and we have no way of verifying the data.

Let’s break down the biological plausibility of OS-01 HAIR, based on the mechanism OneSkin claims it has and current scientific understanding:

• Targeting Cellular Senescence

There is solid evidence that senescent cells accumulate in the hair follicle microenvironment with age and stress, disrupting the stem cell niche and impairing normal cycling. Studies show that hair follicle cells lose inductive capacity partly due to senescence and SASP-driven inflammation.^[23]Pappalardo, A., Kim, J.Y., Abaci, H.E., Christiano, A.M. (2024). Restoration of hair follicle inductive properties by depletion of senescent cells. Aging Cell. 24(1). E14353. Available at: … Continue reading So, reducing senescence or its effects could, in theory, rejuvenate follicle activity.

• OS-01 Peptide Mechanism

As mentioned above, OS-01 has been shown to reduce markers of cellular senescence in skin cells in vitro (and has been claimed to do the same in ORSKs). While these are promising cell culture results, translating that to sustained, clinically meaningful effects in human follicles in vivo is the critical step. 

• Delivery and Context

Topical peptides face challenges: skin penetration, stability, and reaching target cells in viable concentrations.^[24]Pintea, A., Manea, A., Pintea, C., Vlad, R.A., Birsan, M., Antonoaea, P., Redai, E.M., Ciurba, A. (2025). Peptides: Emerging Candidates for the Prevention and Treatment of Skin Senescence: A Review. … Continue reading Dermarolling (used in the clinical study) does enhance delivery through microchannels, aligning with other evidence that microneedling can improve topical drug uptake for hair growth.^[25]Zhang, S., Qiu, Y., Gao, Y. (2014). Enhanced delivery of hydrophilic peptides in vitro by transdermal microneedle pretreatment. Acta Pharmaceutica Sinica B. 4(1). 100-104. Available at: … Continue reading 

• Supporting Evidence

The company’s small clinical trial shows statistically significant improvements in hair density, thickness, and anagen hairs, aligning with the proposed mechanism. However, the studies are short-term, small, and unpublished in peer-reviewed journals. Larger, independent trials would strengthen credibility.

How Does OS-01 Compare to Rapamycin?

Rapamycin is a well-studied compound that has garnered significant attention in aging research due to its ability to slow cellular senescence, promote autophagy, and extend lifespan in multiple animal models. Rapamycin’s unique mechanism, which targets the mechanistic target of rapamycin (mTOR pathway), a central regulator of cell growth and aging, makes it a gold standard for interventions aimed at reducing age-related cellular dysfunction and tissue decline. So, let’s see how OS-01 stands up to it.

Both OS-01 and rapamycin aim to mitigate cellular senescence but use distinct mechanisms and applications.

Aspect	OS-01	Rapamycin
Primary target	Senescence-associated secretory phenotype (SASP).	mTOR pathway.
Senotherapeutic Class	Senomorphic (modulates SASP, prevents progression of pre-senescent cells).	Dual senomorphic/senolytic- inhibits mTOR and promotes autophagy (a process where a cell breaks down and recycles its own components).
Key Action	Reduces SASP markers, including IL-6, CXCL1, and CXCL8, in skin cells.	Inhibits mTORC1, enhances autophagy, and clears senescent cells.[26]Selvarani, R., Mohammed, S., Richardson, A. (2020). Effect of rapamycin on aging and age-related diseases – past and future. GeroScience. 43(3). 1135-1158. Available at: … Continue reading
Delivery	Topical serum applied with dermarolling for enhanced penetration.	Systemic (oral/injected) or localized formulations.

Efficacy in Hair and Senescence

OS-01

• Lab Studies: Reduced CRH-induced senescence in outer root sheath keratinocytes (ORSKs) by lowering p21 levels.
• Clinical Claims: In a 6-month trial (30 participants), reported 39.6% average hair density and 42.6% thickness improvement with dermarolling.
• Limitations: Small sample size, unpublished peer-reviewed data, and reliance on self-reported metrics.

Rapamycin

• Preclinical Evidence: Reduces senescence in cardiac progenitor cells and hair follicles by suppressing mTOR and promoting autophagy.
• Hair Growth: Extends the anagen phase and increases follicle size and density in animal models.^[27]Suzuki, T., Cheret, J., Scala, F.D., Akhundlu, A., Gherardini, J., Demetrius, D.L., O’Sullivan, J.D.B., Epstein, G.K., Bauman, A.J., Demetriades, C., Paus, R. (2023). mTORC1 activity negatively … Continue reading 
• Human Data: Limited direct hair studies, but show systemic anti-aging benefits (e.g., improved vascular function, cognitive decline reversal).

Safety and Practical Considerations

Factor	OS-01	Rapamycin
Side Effects	Minimal (skin dryness and irritation).[28]Zonari, A., Brace, L.E., Harder, N.H.O., Harker, C., Oliveira, C.R., Boroni, M., Carvalho, J.L. (2024). Double-blind, vehicle-controlled clinical investigation of peptide OS-01 for skin rejuvenation. … Continue reading	Immunosuppression and metabolic disruptions.
Application	Twice daily topical use and dermarolling.	Requires systemic dosing or specialized delivery.
Evidence Strength	Early-stage, company-led studies.	Robust preclinical and some clinical data.

Key Differences

• Approach: OS-01 focuses on localized SASP modulation, while rapamycin systemically targets mTOR to influence multiple aging pathways.
• Accessibility: OS-01 is available as a consumer product, whereas rapamycin is primarily used off-label or in research settings.
• Scope: Rapamycin has broader anti-aging applications beyond hair (e.g., cardiovascular, cognitive), while OS-01 targets scalp senescence and hair metrics.

In summary, OS-01 may offer a targeted, low-risk option for hair senescence; however, the data is preliminary and unpublished. Rapamycin, however, offers systemic or targeted action to provide broader anti-aging benefits but may have higher complexity and a more severe risk profile.

Is OS-01 Safe?

As mentioned above, in the clinical trial in which OS-01 was used for skin aging, skin dryness and irritation was observed in two participants. 

Beyond this, OneSkin mentioned that the peptide has been tested in in vitro toxicity and irritation tests, genotoxicity testing, and a repeated insult patch test (RIPT), and its effect on cancer cells has also been evaluated, with no negative effects observed.^[29]OneSkin. (no date). How Do We Know the OS-01 Peptide is Safe? Available at: https://www.oneskin.co/blogs/reference-lab/how-os-01-peptide-safety Accessed: June 2025,^[30]Zonari, A., Brace, L.E., Alencar-Silva, T., Porto, W.F., Foyt, D., Guiang, M., Cruz, E.A.O., Franco, O.L., Oliveira, C.R., Boroni, M., Carvalho, J.L. (2022). In vitro and in vivo toxicity assessment … Continue reading

However, it is worth noting that there have been no long-term human studies to evaluate any other potential effects.

Is OS-01 for Me?

OS-01 for hair may be worth a try for you:

• You want to add another product to your routine (it can be used alongside topical minoxidil, etc.)
• You do not suffer from inflammatory scalp conditions, which might mean you can’t use a dermaroller.
• Are happy using a dermaroller every day to facilitate penetration of the peptide into the scalp.

Final Thoughts

While OS-01 shows promise as an innovative approach to addressing hair thinning through targeting cellular senescence, the current evidence is still early and largely company-reported. Laboratory and small-scale clinical data suggest that it may help improve hair density and thickness, particularly when combined with dermarolling; however, these results need to be confirmed by larger, independent studies. There is no definitive proof yet that OS-01 can effectively reverse androgenic alopecia in the long term. If you are interested in trying OS-01, it may be reasonable to use it in conjunction with established treatments like minoxidil; however, it’s best to manage expectations and continue to follow emerging research as more data becomes available.

In dermatology, clear and accurate reporting of research findings isn’t just important; it’s essential. Yet, data misinterpretation and misrepresentation remain a persistent issue, often slipping through in abstracts, press releases, and articles from otherwise trusted sources. These distortions can have real consequences, affecting how products are marketed, how clinicians make decisions, and the public’s understanding of the science.

In this article, we break down recent examples from hair growth research to illustrate exactly how scientific data can be misinterpreted, why it matters more than ever in our 24-hour news cycle culture, and what that means for companies that prefer to share their data rather than relying on press releases.

Thermos Thermophilus Extract (TTFE) and Hair Density

A striking example of data misinterpretation appeared in a recent Dermatology Times article, which claimed that Thermus Thermophilus Ferment Extract (TTFE) increased hair density by 96.88%.^[1]Bosslett, M. (2025). Thermos Thermophilus Fermentation Extract Can Treat Androgenic Alopecia. Dermatology Times. Available at: … Continue reading  At first glance, this figure suggests a near doubling of hair density, an extraordinary claim that would be making waves in cosmetic dermatology.

However, a closer examination of the original peer-reviewed study reveals a critical nuance: the figure refers not to the magnitude of increase in hair density, but to the proportion of participants who experienced any increase in hair density. In other words, nearly all subjects showed some improvement, but the actual percentage increase in hair density was much smaller.

This distinction is vital. Reporting the statistic as a 96.88% increase in hair density grossly inflates the effect size and misleads readers about the product’s efficacy. Read more about what we thought about this here.

Niostem Device Pilot Study

Another recent example involves the Niostem device. The device’s pilot study, published in the Journal of Cosmetic Dermatology, reported increases in total hair density (12% at 3 months, 19.3% at 6 months) and hair shaft thickness (8.8% over 6 months).^[2]Jellard, S., Moore, S., Chacon-Martinez, C.A. (2025). Novel Electrotrichogenic Device Promotes Hair Growth in Men with Androgenetic Alopecia: A Pilot Study. Journal of Cosmetic Dermatology. 24. … Continue reading

While these results are promising, the study’s abstract contains a potentially misleading statement, claiming: “terminal hair density improved significantly over time”.

However, the data showed that terminal hair density initially decreased at 3 months compared to baseline before increasing at 6 months. The significant increase is relative to the 3-month point, not the baseline, which would be the more relevant comparison for assessing treatment efficacy (and for which there was no statistically significant change).

This subtle but important spin in the abstract can create an overly optimistic impression of the device’s performance. You can read more in our article here.

CB-03-01 Phase II Study and Press Release Limitations

The second Phase II study of CB-03-01, a topical antiandrogen for female pattern hair loss, illustrates the pitfalls of relying on press releases rather than peer-reviewed publications. The press release summarized the main findings from a 293-participant study, but omitted critical details such as how CB-03-01 compared to the 2% minoxidil group.^[4]Cassiopea Spa, (2021). Cassiopea SpA Announces Topline Results of Phase II Proof of Concept Trial of Clascoterone Solution for the Treatment of Androgenetic Alopecia in Females. Available at: … Continue reading

Without all the data, readers can’t fully assess the study’s methodology, statistical analysis, or properly contextualize the results.

Should we trust the Kintor Pharma Press Releases?

When you see mistakes, misrepresentations, or only partial displays of results like these, it casts a shadow across companies like Kintor Pharmaceuticals, which have disseminated their efficacy and safety data primarily through press releases, investor announcements, and conference abstracts, rather than peer-reviewed journal articles. This lack of transparency makes it difficult for independent experts to critically appraise the robustness and clinical relevance of the findings.

For instance, Kintor’s Phase II trials report increases in target area hair count of approximately 10 to 22 hairs per cm2 compared to baseline or placebo after 24 weeks.^[6]Kintor Pharma. (2023). Kintor Pharma Announces Successful Completion of Phase II Clinical Trial of KX-826 for Treatment of Androgenetic Alopecia in the US. Available at: … Continue reading While these numbers appear promising, without full access to raw data, confidence intervals, or responder analyses, it is impossible to determine how consistent or meaningful these improvements are across the treated population. Moreover, the clinical significance of such hair count increases, whether they translate into visibly noticeable hair regrowth or improved patient satisfaction, is unclear without detailed patient-reported outcomes or photographic evidence.

Kintor’s decision to market KX-826-containing products as cosmetics rather than drugs in some regions further complicates trust in their claims. Cosmetics do not require FDA approval or demonstration of efficacy, and safety requirements are less stringent. This positioning allows products to be sold despite incomplete evidence of clinical benefit, potentially exposing consumers to unproven treatments.

Why Misrepresentation Happens and Its Consequences

Misrepresentation or “spin” in scientific communication can be intentional or unintentional. Authors and publishers may emphasize positive findings to attract attention, secure funding, or support marketing goals. Press releases often simplify complex results to appeal to broader audiences, sometimes glossing over limitations or nuances.^[7]PR Newswire. (no date). How Healthcare Companies are Using Press Releases. Available at: https://www.prnewswire.com/resources/articles/healthcare-company-press-releases/ (Accessed: June 2025) 

Done wrong, data can be misrepresented or misinterpreted, leading to:

• Mislead clinicians and potential consumers
• Dissemination of misinformation through social media and other internet sources
• Confusion and skepticism in scientific and medical fields
• Loss of trust from the consumer

The Role of Peer Review and Scientific Literacy

Peer review serves as a critical quality control mechanism, ensuring that research is rigorously evaluated by experts before it is published.^[8]Taylor & Francis. (no date). Understanding the peer review process. Available at: https://authorservices.taylorandfrancis.com/publishing-your-research/peer-review/ (Accessed: June 2025) It helps prevent unwarranted claims and promotes transparent reporting of methods and results. However, peer review is not foolproof, and errors or spin can still appear in abstracts or articles.

Peer review is only one part of the equation, however. Scientific literacy, especially source literacy, remains essential for anyone navigating research claims, whoever you are. This means not just reading headlines or abstracts, but digging into the methods, understanding what is being measured, and questioning whether the reported outcomes are truly meaningful in a real-world context. 

In today’s environment, where information can be amplified and distorted through social media and marketing, the responsibility for critical evaluation doesn’t just fall on scientists or peer reviewers; it’s shared by all of us who read, share, and act on scientific news.

Final Thoughts

The examples from TTFE, Niostem, and CB-03-01 illustrate how easily data can be misrepresented, whether intentionally or not. While press releases can be useful for quick updates, they are no substitute for full, peer-reviewed publications that allow for independent scrutiny. As the boundaries between scientific communication, marketing, and media continue to blur, the risk of misinterpretation and the consequences for patient care, consumer trust, and scientific progress only increase. 

Therefore, when it comes to companies that only publish their data through press releases, we would advise approaching with caution. It is good to have an open mind, but try not to blindly trust everything you see.

If you’d like a deeper dive into these topics, visit these videos here and here.

Minoxidil is a medication that began as a treatment for hypertension (high blood pressure). However, after observing excess hair growth during the testing stages of the drug, minoxidil was repurposed as a treatment for hair loss. Topical minoxidil soon received FDA approval for the treatment of both male and female pattern hair loss, while oral minoxidil is also used as an off-label treatment for hair loss.^[1]Suchonwanit, P., Thammarucha, S., & Leerunyakul, K. (2019). Minoxidil and its use in hair disorders: a review. Drug design, development and therapy. 2777-2786. Available at: … Continue reading

So, if minoxidil is a treatment for hair loss, why does it cause an increase in hair loss when you start using it? Yes, you did read that right – minoxidil can actually cause an increase in hair loss as part of what is often called the ‘dread shed.’ This phenomenon was demonstrated in a retrospective study of 435 patients with androgenic alopecia (AGA) who were prescribed low-dose oral minoxidil [≤5 mg per day] by the same clinic. Self-reported adverse events were recorded for each of the users and, of the 435 patients, 32% experienced increased hair shedding.^[2]Sanabria, B., de Nardo Vanzela, T., Miot, H. A., & Ramos, P. M. (2021). Adverse effects of low-dose oral minoxidil for androgenetic alopecia in 435 patients. Journal of the American Academy of … Continue reading

This is evidently cause for concern – if you have just started minoxidil treatment to prevent hair loss, a sudden increase in hair loss is possibly the last thing you would hope and expect to experience. So what is it about minoxidil that causes this to happen, how long does it usually last, and is it actually a good thing? In this article, we will explore the hair cycle and minoxidil in detail to provide answers to each of these questions.

The Hair Cycle

To understand why minoxidil can increase hair shedding, let’s first take a refresher on the hair cycle. Our hair is constantly going through a cycle of growing (anagen), regression and transition (catagen), resting (telogen), and shedding (exogen), which it repeats continuously. 

Healthy hairs grow for anywhere between 2 and 8 years, and there is a correlation between the length and strength of a hair and the time spent in anagen. Catagen is the transition from anagen to telogen, a period of approximately 2 weeks during which the follicle regresses from the hair shaft and disconnects it from the blood supply, preventing any further growth. Telogen follows and lasts for 2-3 months, with a new hair shaft beginning to develop at the base of the follicle underneath the now resting hair shaft. Exogen then represents the transition from telogen to anagen, with the growing hair shaft pushing out the old hair shaft.^[3]Natarelli, N., Gahoonia, N., & Sivamani, R. K. (2023). Integrative and mechanistic approach to the hair growth cycle and hair loss. Journal of clinical medicine. 12(3). 893. Available at: … Continue reading 

In the healthy scalp, the percentage of hairs in each of the hair cycle stages is thought to remain fairly consistent. At any one time, evidence suggests that approximately 9% of the hairs on a healthy scalp are in the telogen phase (although there are some suggestions that this figure may actually be too high).^[4]Natarelli, N., Gahoonia, N., & Sivamani, R. K. (2023). Integrative and mechanistic approach to the hair growth cycle and hair loss. Journal of clinical medicine. 12(3). 893. Available at: … Continue reading These hairs exist in a largely asynchronous fashion, with hair follicles progressing through the hair cycle according to their own unique pattern. Hair follicles undergo between 10 and 30 full cycles, and it is normal for up to 150 hairs to fall out per day without there being an underlying hair loss problem, as the hairs are constantly being replaced.^[5]Bergfeld, W. (2009). Diffuse hair loss: its triggers and management. Cleve Clin J Med. 76(6). 361-370. Available at: https://doi.org/10.3949/ccjm.76a.08080 This keeps hair fall relatively consistent, preventing periods of significant hair shedding.

What Happens to the Hair Cycle during AGA?

AGA, the hair loss condition for which topical minoxidil is an approved treatment, is caused by damage to the hair follicle that contributes to its miniaturization. This is when individual strands of hair become smaller and smaller over time, eventually becoming vellus hairs that are shorter, thinner, and more white, which makes them difficult to see. We have a previous article that explores AGA-induced hair loss in great detail, but let’s summarize the key characteristics below:

• Perifollicular fibrosis – collagen deposition in the spaces around the hair follicles restricts the room within which hair shafts are able to grow, acting as a physical barrier to hair growth.
• Increased telogen:anagen ratio – healthy scalps typically have 1 telogen hair for every 12 anagen hairs (1:12 telogen:anagen), but people with AGA may exhibit ratios that are as high as 1:4 or even 2:5. The telogen phase also lengthens, with hairs spending longer in a state of non-growth.
• Shortened anagen phase – as previously mentioned, the length of an anagen phase directly corresponds to the length of the eventual hair shaft, and people with AGA typically exhibit anagen phases that become shorter with every hair cycle.

Although the exact mechanisms underlying AGA are yet to be fully understood, it is evident that AGA is a progressive and cumulative process that occurs due to harmful factors damaging the hair follicle and shortening the anagen phase.

How Minoxidil Works

Minoxidil is also yet to be fully understood, but several mechanisms have been suggested that could explain how it reduces hair loss:

• Vasodilation – Minoxidil started out as a treatment for hypertension, so its function as a vasodilator is well documented. Studies have shown that minoxidil increases blood flow by opening potassium channels, reducing high blood pressure. However, an unintended benefit of this function is increased blood flow to the hair follicles, providing them with nutrients and oxygen that help to prolong the anagen phase.^[7]Messenger, A. G., & Rundegren, J. (2004). Minoxidil: mechanisms of action on hair growth. British journal of dermatology. 150(2). 186-194. Available at: … Continue reading
• Prostaglandin mediation – Minoxidil has been shown to increase the production of prostaglandin E2 (PGE2) in cultured human dermal papilla fibroblasts, the specialized cells that sit at the base of the hair follicle. It is thought that PGE2 may protect hair follicles from damage.^[8]Michelet, J. F., Commo, S., Billoni, N., Mahé, Y. F., & Bernard, B. A. (1997). Activation of cytoprotective prostaglandin synthase-1 by minoxidil as a possible explanation for its hair … Continue reading
• Growth factor mediation – Studies have shown that minoxidil has the potential to upregulate the expression of several growth factors that support hair growth, including vascular endothelial growth factor in human dermal papilla cells.^[9]Lachgar, Charveron, Gall, & Bonafe. (1998). Minoxidil upregulates the expression of vascular endothelial growth factor in human hair dermal papilla cells. British Journal of Dermatology. 138(3). … Continue reading

It is likely that minoxidil reduces hair loss through a combination of several mechanisms, including those noted above and perhaps others that are yet to be discovered.

How Might Minoxidil Cause the Dread Shed?

So, we know the basics of the hair cycle, some of the mechanisms that contribute to pattern hair loss, and some of the mechanisms by which minoxidil may reduce hair loss. But what does all this have to do with the ‘dread shed ’? Fortunately, observing the effects of minoxidil is more straightforward than trying to understand how it works, and there is one key effect which is believed to contribute to the increase in shedding: shortening of the telogen phase.

As we previously discussed, a key characteristic of AGA is lengthening of the telogen phase, which causes an abnormal amount of scalp hair to be in a state of arrested growth at the same time. It is widely believed that minoxidil directly addresses this issue by both shortening the telogen phase and accelerating the telogen to anagen transition. In one study,  application of topical minoxidil to rats caused a dramatic shortening of the telogen phase, falling from 20 days to just 1-2 days.^[10]Mori, O., & Uno, H. (1990). The effect of topical minoxidil on hair follicular cycles of rats. The Journal of dermatology. 17(5). 276-281. Available at: … Continue reading In a separate study that was also conducted in rats, topical minoxidil caused a significant switch from the telogen to anagen phase as quickly as 10 days after beginning treatment (Figure 2).^[11]Shatalebi, M. A., & Rafiei, Y. (2014). Preparation and evaluation of minoxidil foamable emu oil emulsion. Research in pharmaceutical sciences. 9(2). 123-133. Available at: … Continue reading

We could only find one clinical study that has investigated the telogen-anagen shift in humans at an early stage after beginning minoxidil use. They conducted a 24-week trial in which men with AGA either applied topical minoxidil [5%] or topical cetirizine for the first 16 weeks, then stopped use for 8 weeks. Although the results were not statistically significant, they showed that minoxidil caused an increase in the percentage of anagen hair and a decrease in the percentage of telogen hair, supporting the idea that minoxidil rapidly induces shortening of the telogen phase.^[13]Mostafa, D. H., Samadi, A., Niknam, S., Nasrollahi, S. A., Guishard, A., & Firooz, A. (2021). Efficacy of cetirizine 1% versus minoxidil 5% topical solution in the treatment of male alopecia: a … Continue reading

In accelerating the telogen to anagen transition, minoxidil also causes “hair follicle synchronization” or synchronization of the hair cycle. As we highlighted earlier, healthy scalps are somewhat ‘protected’ from significant hair shedding events due to the asynchronous nature of the hairs and their individual hair cycles. However, due to the increased density of telogen follicles in the AGA-affected scalp, minoxidil causes a greater-than-normal percentage of hairs to enter anagen at the same time. This syncing of the hair cycles then results in more hairs being pushed out at the same time.

So, to summarize the process that is believed to be the key factor behind the dread shed:

• In AGA, a greater number of hair follicles are in telogen
• Minoxidil treatment accelerates the transition of these hair follicles from telogen to anagen and causes many follicular units to become synchronized
• The transition leads to initiation of the shedding phase (exogen)
• Increased hair shedding occurs

Is The ‘Dread Shed’ Real?

Until very recently, evidence of minoxidil-induced hair shedding was either anecdotal or provided by studies of minoxidil in which increased hair shedding was noted as an adverse event. However, a newly published study sought to investigate the shedding phase in detail.

In this 2025 study, 49 patients with AGA used topical minoxidil [2% or 5%] for 24 weeks. Total hair shedding was quantified daily by the participants, who self-assessed their hair fall after combing, after washing, and on the pillow after sleeping. This was then averaged every 4 weeks and compared to the level of hair shedding prior to starting treatment. They found that the participants who used 5% minoxidil exhibited increased hair shedding (relative to pre-treatment) for 4-8 weeks, while the participants who used 2% minoxidil exhibited increased shedding for 8-12 weeks (Figure 2).^[14]Bi, L., Kan, H., Wang, J., Ding, Y., Huang, Y., Wang, C., Du, Y., Lu, C., Zhao, M., Sun, W. & Su, T. (2025). Whether the transient hair shedding phase exist after minoxidil treatment and does it … Continue reading 

This study provides definitive evidence that minoxidil does cause an initial shedding phase. However, importantly, hair shedding eventually fell below baseline levels in both groups, indicating that the initial shedding phase is temporary and that minoxidil did begin to reduce hair loss.

Is Initial Hair Loss Actually a Good Sign?

The same authors investigating the minoxidil shedding phase also sought to determine whether the amount of shedding had any association with treatment efficacy. They compared peak relative hair shedding (within the first 12 weeks) to changes in AGA severity using the Basic and Specific classification (BASP), which is a universal hair loss classification system that is used to assess the distribution and severity of hair loss in men and women of all races. They also compared peak relative hair shedding to several trichoscopy measurements, including hair density, hair diameter, and terminal hair proportion.^[16]Bi, L., Kan, H., Wang, J., Ding, Y., Huang, Y., Wang, C., Du, Y., Lu, C., Zhao, M., Sun, W. & Su, T. (2025). Whether the transient hair shedding phase exist after minoxidil treatment and does it … Continue reading

Interestingly, in the 5% minoxidil group, a significant association was found between the amount of initial hair shedding and hair density, hair diameter, and the proportion of terminal hairs. In other words, people who lost more hair in the ‘dread shed’ actually experienced greater outcomes from minoxidil treatment. Furthermore, participants who initially shed the most hair in both the 2% and 5% minoxidil groups demonstrated the greatest improvements in AGA severity by week 24.^[17]Bi, L., Kan, H., Wang, J., Ding, Y., Huang, Y., Wang, C., Du, Y., Lu, C., Zhao, M., Sun, W. & Su, T. (2025). Whether the transient hair shedding phase exist after minoxidil treatment and does it … Continue reading 

These results are very interesting – not only does the initial shedding phase indicate that the minoxidil is working, but more shedding may even predict better treatment outcomes! So, if you’ve just started treatment, don’t fear the shed!

Final Thoughts

Minoxidil is an FDA-approved treatment for AGA but, in some cases, it can cause increased hair shedding in the early stages of use. Known as the ‘dread shed,’ this phase is believed to be caused by minoxidil shortening the telogen phase of the hair cycle, causing old hairs to fall out. This shedding is even more pronounced due to the increased density of telogen hairs present in the scalps of people with AGA. However, this shedding is only temporary, typically lasting between 4 and 8 weeks. Moreover, people who experience more shedding in this initial phase may actually experience greater overall outcomes from their minoxidil treatment. So, if you have just started minoxidil and are noticing increased shedding, don’t panic – it is most likely a sign that the minoxidil is working.

What is Minoxidil?

Minoxidil was originally developed in the 1970s as an oral medication for the treatment of hypertension (high blood pressure). This was due to its key function as a vasodilator, widening the blood vessels and, in turn, increasing blood flow and reducing blood pressure. However, an unintended side effect quickly became apparent in nearly all use cases: excessive hair growth. 

Seeking to take advantage of this, minoxidil was re-formulated as a topical solution for the treatment of hair loss. After showing great efficacy in clinical trials of patients with androgenetic alopecia (AGA), topical minoxidil [5%] received FDA approval for the treatment of male pattern hair loss in 1988, with a lower dose of topical minoxidil [2%] later being approved for the treatment of female pattern hair loss. And, while it is not technically an FDA-approved treatment, oral minoxidil is also used off-label to treat hair loss.^[1]Suchonwanit, P., Thammarucha, S., & Leerunyakul, K. (2019). Minoxidil and its use in hair disorders: a review. Drug design, development and therapy. 2777-2786. Available at: … Continue reading

Given that this application of minoxidil was first identified as an unintended side effect, it is unsurprising that the use of both topical and oral minoxidil can lead to other unwanted effects. In a previous article, we discussed the most common and widely recognized side effects of minoxidil use. Here, however, we will explore a potential side effect that has been reported by some minoxidil users: accelerated skin aging.

Is it possible that minoxidil can accelerate skin aging? In this article, we’ll review the current landscape of research and dive into the anecdotes, the biological mechanisms, alternative explanations, and where we currently stand on this topic.

What is Skin Aging?

Skin aging is a multifactorial biological process that is mediated by intrinsic (genetically determined) and extrinsic (environmental) factors. Natural, intrinsic aging occurs over a long time, with a gradual decrease in skin structure and function leading to the formation of fine lines, wrinkles, thinning, dryness, and reduced elasticity. This is compounded by the extrinsic factors, such as ultraviolet radiation and pollution, which can cause wrinkles that are more coarse, more severe loss of elasticity, and pigmentation disorders.^[2]Shin, S. H., Lee, Y. H., Rho, N. K., & Park, K. Y. (2023). Skin aging from mechanisms to interventions: focusing on dermal aging. Frontiers in physiology. 14. 1195272. Available at: … Continue reading

There are several key mechanisms that underlie these factors, including:

• Oxidative stress: the accumulation of reactive oxygen species leads to oxidative stress, which subsequently causes damage to the DNA, proteins, and lipids that are found in the skin.^[3]Rinnerthaler, M., Bischof, J., Streubel, M. K., Trost, A., & Richter, K. (2015). Oxidative stress in aging human skin. Biomolecules. 5(2). 545-589. Available at: … Continue reading
• Cellular senescence: aged cells of the skin enter a permanent state of arrest whereby they no longer divide, impairing the ability of the skin to repair and regenerate. Moreover, senescent cells release harmful factors (senescence-associated secretory phenotype) that can disrupt the homeostasis of the skin and promote inflammation.^[4]Chin, T., Lee, X. E., Ng, P. Y., Lee, Y., & Dreesen, O. (2023). The role of cellular senescence in skin aging and age-related skin pathologies. Frontiers in physiology. 14. 1297637. Available at: … Continue reading
• Altered collagen homeostasis: with age, collagen production (primarily type I collagen) decreases in the skin. This compromises the structural integrity of the skin, reducing its elasticity and firmness and leading to the appearance of wrinkles.^[5]He, X., Gao, X., & Xie, W. (2023). Research progress in skin aging, metabolism, and related products. International journal of molecular sciences. 24(21). 15930. Available at: … Continue reading

As stated, intrinsic factors and genetics means that these mechanisms will naturally cause skin health to deteriorate as we get older. However, we also know that certain environmental factors can accelerate the aging process by promoting the activity of the described mechanisms. It is therefore possible that a therapy that acts upon these mechanisms could influence the aging process.

Is There a Link Between Minoxidil and Skin Aging?

On reddit, some people using topical minoxidil have reported what sounds like accelerated aging: that their under-eye bags worsened and that their facial skin seemed drier and less smooth than before. Others have documented these changes with before-and-after photos taken just 1-2 months after starting the topical medication. Similar anecdotes have been reported by some users of oral minoxidil. This has led to claims that minoxidil use may accelerate skin aging.

But do these anecdotes make sense biologically? And are these reports truly suggestive of faster skin aging, or is something else going on?

Let’s take a look at what the scientific evidence says.

Could Minoxidil Accelerate Skin Aging?

There is a lack of understanding regarding the specific underlying mechanism by which minoxidil promotes hair growth. Indeed, several different mechanisms have been suggested, and it is believed that more than one may be responsible for mediating the effects of minoxidil. In the context of aging skin, one of these mechanisms is particularly interesting: the minoxidil-induced increase in prostaglandin E2 (PGE2) production.

Back in 1997, researchers discovered that minoxidil significantly increased the production of PGE2 in murine fibroblast cells in vitro. Moreover, they showed that minoxidil also increased the production of PGE2 in human dermal papilla fibroblasts, cells that sit within the base of the hair follicle and play an important role in maintaining hair health.^[6]Michelet, J. F., Commo, S., Billoni, N., Mahé, Y. F., & Bernard, B. A. (1997). Activation of cytoprotective prostaglandin synthase-1 by minoxidil as a possible explanation for its hair … Continue reading Later, in mice, it was also demonstrated that the topical application of PGE2 exhibited some, albeit limited, ability to promote hair growth. ^[7]Sasaki, S., Hozumi, Y., & Kondo, S. (2005). Influence of prostaglandin F2α and its analogues on hair regrowth and follicular melanogenesis in a murine model. Experimental dermatology. 14(5). … Continue reading

So PGE2 may be part of a mechanism that minoxidil uses to promote hair growth, but what does that have to do with skin aging?

One study found that PGE2 levels in the skin increase with age, with fibroblasts being the main source of increased production. When the same researchers cultured fibroblasts with PGE2 in vitro, they also demonstrated that PGE2 treatment causes a reduction in the expression of type I procollagen.^[9]Li, Y., Lei, D., Swindell, W.R., Xia, W., Weng, S., Fu, J., Worthen, C.A., Okubo, T., Johnston, A., Gudjonsson, J.E. and Voorhees, J.J. 2015. Age-associated increase in skin fibroblast–derived … Continue reading 

Additional studies have provided further evidence that PGE2 impairs collagen homeostasis within the skin. In cultured human dermal fibroblasts, it was shown that treatment with PGE2 significantly decreased collagen type I levels, which may have been driven by the significant increase in matrix metallopeptidase 1 (MMP1) levels.^[11]Shim, J. H. (2019). Prostaglandin E2 induces skin aging via E-prostanoid 1 in normal human dermal fibroblasts. International Journal of Molecular Sciences, 20(22), 5555. Available at: … Continue reading Thus, there exists a wealth of evidence which suggests that PGE2 plays a role in the aging of skin by impairing collagen homeostasis.

Does Minoxidil Really Accelerate Skin Aging?

Given that minoxidil has been shown to increase PGE2, and that PGE2 is associated with aging skin, does this mean that minoxidil use leads to accelerated aging of the skin?

Not necessarily.

Firstly, and most crucially, there are currently no studies that have shown a direct link between the use of minoxidil and accelerated skin aging. Until such research is conducted, it is not possible to draw an accurate conclusion.

Now, in general, with safety concerns — it’s usually important to emphasize that the absence of evidence does not mean evidence against a concept. For instance, just because we don’t have a randomized, controlled clinical study determining the likelihood of death from jumping out of an airplane without a parachute, the risk here is inherently obvious: we don’t need a study to prove death is likely. We can just look at surrogate data on max velocity, the heights of falls, and the human capacity to endure such a violent impact. And then we can presume death is the most likely outcome.

So, can we use surrogate data on minoxidil — such as these in vitro studies — and then can we associate these to skin thinning, pair those with the anecdotal reports from Reddit, and presume that topical minoxidil is accelerating skin aging in some people, regardless of what the clinical studies say?

You could. But given that this side effect wasn’t picked up in any of the large, randomized, controlled clinical trials on minoxidil prior to these internet posts, our opinion is that we should exercise extreme caution in coming to this conclusion. Why? Because beyond the absence of clinical data on minoxidil doing this in well-designed studies, there are also two side effects of minoxidil application that might be fully-to-blame for why some think minoxidil use accelerates skin aging. And encouragingly, these side effects aren’t permanent:

• Water retention
• Allergic dermatitis (skin dryness)

We’ll take these one-by-one.

Minoxidil & water retention

Minoxidil is able to function as a vasodilator by opening potassium channels, thus relaxing the vascular smooth muscle and lowering blood pressure. However, this modification of potassium channels also increases sodium reabsorption by the kidneys which, in turn, leads to greater retention of water by the body.^[12]Sica, D. A. (2004). Minoxidil: an underused vasodilator for resistant or severe hypertension. The Journal of Clinical Hypertension. 6(5). 283-287. Available at: … Continue reading 

Water retention can lead to edema (swelling) and, although this is typically seen in peripheral regions such as the feet, use of oral minoxidil (even at low doses) has been found to cause facial edema in up to 1% of use cases.^[13]Sanabria, B., de Nardo Vanzela, T., Miot, H. A., & Ramos, P. M. (2021). Adverse effects of low-dose oral minoxidil for androgenetic alopecia in 435 patients. Journal of the American Academy of … Continue reading Indeed, a recent study demonstrated a dose-dependent relationship between oral minoxidil and the incidence of edema.^[14]Salas, J., Esse, I., Kincaid, C. M., Birda, A., Choe, S., & Mesinkovska, N. A. (2025). Characterizing low-dose oral minoxidil-induced peripheral edema in alopecia patients. Journal of the … Continue reading Some users of topical minoxidil have also reported swelling around the face after use, particularly in the region surrounding their eyes.

A consequence of facial edema is a more plump appearance of the face and potentially sagging of the skin, which can also accentuate under-eye bags and make it appear as though someone is less rested than they actually are. These symptoms mimic those of aging skin and they can make it seem like minoxidil is accelerating the aging process. However, the same studies that observed the cases of facial edema also noted that the swelling typically resolved within two weeks of stopping treatment, so it is unlikely that these effects are truly reflective of accelerated skin aging.

Minoxidil & skin dryness (allergic dermatitis)

Another side effect of minoxidil use, particularly when it is applied topically, is allergic dermatitis. At the site of application, symptoms of allergic dermatitis such as itching, redness, and scaling, were observed in 5.7% of topical minoxidil [5%] users.^[15]Friedman, E. S., Friedman, P. M., Cohen, D. E., & Washenik, K. (2002). Allergic contact dermatitis to topical minoxidil solution: etiology and treatment. Journal of the American Academy of … Continue reading 

It was initially believed that the majority of allergic dermatitis incidences were caused by the carrier, not by the minoxidil. A 2002 study used patch testing to demonstrate that 81.8% of patients reacted to propylene glycol, which is a solvent that is used to improve the delivery of minoxidil. This was compared to just 36.4% of patients being allergic to minoxidil itself, and an even lower 9.1% showing a reaction to the alternative carrier butylene glycol.^[17]Friedman, E. S., Friedman, P. M., Cohen, D. E., & Washenik, K. (2002). Allergic contact dermatitis to topical minoxidil solution: etiology and treatment. Journal of the American Academy of … Continue reading However, more recent studies have started to challenge this theory. By reviewing 21 studies that investigated allergic dermatitis from minoxidil use, a 2025 study found that minoxidil is the predominant allergen, followed by propylene glycol.^[18]Junge, A., Radonjic-Hoesli, S., Bossart, S., Simon, D., De Viragh, P., Hunger, R.E., Heidemeyer, K. and Jafari, S.M.S., 2025. Contact Dermatitis Caused by Topical Minoxidil: Allergy or Just … Continue reading

Whether the allergen is minoxidil, propylene glycol, or another ingredient, it is clear that topical minoxidil has the potential to cause allergic dermatitis. Of course, the relevance of this is that the symptoms associated with allergic dermatitis may mimic signs of aging skin, once again leading users to believe that minoxidil is causing accelerated skin aging. However, as observed with water retention, it has been shown that the symptoms of contact dermatitis stop after ceasing minoxidil use.^[19]Pasricha, J. S., Nanda, A., & Bajaj, N. (1991). Contact dermatitis due to minoxidil. Indian Journal of Dermatology, Venereology and Leprology. 57. 235. Available at: … Continue reading 

Together, these effects are probably more likely to explain the skin quality-topical minoxidil connection than true accelerated skin aging. Otherwise, the results would sustain even after quitting the medication, but there is no scientific or anecdotal evidence of this.

What Can Be Done To Prevent These Effects?

How can one avoid potential skin-related minoxidil side effects? There are several options at your disposal:

1. If you are getting allergic dermatitis, it may be useful to determine which ingredient(s) in the minoxidil are driving that reaction. There are many alternative carrier ingredients available for topical minoxidil, and switching to a different brand of minoxidil (which uses different ingredients) may prevent these symptoms from emerging.
2. Switching to oral minoxidil may be another option for anyone struggling with allergic dermatitis from topical minoxidil. To date, there is no scientific evidence that the systemic effects of oral minoxidil can cause allergic dermatitis. However, if you do make the switch, be aware that oral minoxidil is linked to increased water retention in a small number of people.
3. Allow topical minoxidil to dry fully before going to bed. Some people apply topical minoxidil and then immediately go to bed – thereby pressing their heads against their pillow before letting the topical minoxidil fully dry. If this is you, you might be creating a situation whereby any undried topical minoxidil can spread to the pillow and, therefore, the face (when you move around throughout the night). This increased spread may lead to increased risk of allergic dermatitis and water retention in areas of the face where topical minoxidil is not applied, nor is supposed to reach. So, let the topical minoxidil fully dry and wait at least 20-30 minutes after an application before putting your head down at night.

Final Thoughts

There is some anecdotal evidence which suggests that the use of minoxidil causes accelerated aging of the skin. Although minoxidil does drive increased production of PGE2, which is associated with reduced collagen production in the skin, there is no direct scientific evidence that has proven a link between the use of minoxidil and skin aging. Furthermore, two side effects of minoxidil use – increased water retention and allergic dermatitis – produce symptoms that mimic those of aging skin. Therefore, it is possible that temporary side effects of minoxidil use, the effects of which reverse after stopping treatment, are simply being mistaken for accelerated skin aging. Based on this, it is unlikely (though not impossible) that there is a link between minoxidil and skin aging.

Retinoic acid (RA) is the biologically active form of Vitamin A, playing an important role in regulating cell growth, differentiation, and tissue maintenance in the body.^[1]Peehl, D.M., Wong, S.T., Stamey, T.A. (1993). Vitamin A regulates proliferation and differentiation of human prostatic epithelial cells. Prostate. 23(1). 69-78. Available at: … Continue reading Its signaling pathway is essential not only for embryonic development but also for the maintenance of healthy skin and hair.^[2]VanBuren, C.A., Everts, H.B. (2022). Vitamin A in Skin and Hair: An Update. Nutrients. 14(14). 2952. Available at: https://doi.org/10.3390/nu14142952 

Interest in using retinoids (RA and its derivatives, such as tretinoin and retinol) as hair loss treatments stems from their potential to regulate the hair growth cycle and potentially prolong the anagen (growth) phase of hair follicles. In this article, we will explore what RA is and its derivatives, as well as how they can impact the hair follicle. We will also evaluate the available efficacy and safety data.

Key Takeaways

• Drug. Retinoic acid (RA), especially in the form of tretinoin, is a vitamin A derivative that regulates hair follicle stem cell activation through Wnt/β-catenin signaling. It is available in various topical formulations and is often used in combination with minoxidil to enhance hair regrowth in androgenetic alopecia (AGA).

• Clinical Data.  RA/tretinoin shows moderate standalone efficacy in promoting hair regrowth, particularly in early-stage AGA, but results improve significantly when used with minoxidil. Clinical trials from 1986 to 2024 have demonstrated enhanced hair density, thickness, and stem cell activity with combination therapy. RA also improves sulfotransferase enzyme activity, boosting minoxidil’s effectiveness, and has shown positive results in alopecia areata when combined with pimecrolimus.

• Safety. Generally well-tolerated at concentrations ≤0.025%, but may cause local irritation (redness, itching, dryness). Adverse effects are dose-dependent and typically self-limiting. Systemic side effects are rare with topical use but retinoids should be avoided during pregnancy and in individuals with photosensitivity or scalp inflammation.

• Evidence Quality.  Retinoic Acid scored 34/100 for evidence quality by our metrics.

• Best Practices. 
  • Use in combination with topical minoxidil for optimal results, especially in early AGA.
  • Apply tretinoin in low concentrations (≤0.025%) once daily to minimize irritation.
  • Consider tretinoin if you’re a minoxidil non-responder or wish to reduce application frequency.
  • Avoid if pregnant, photosensitive, or prone to dermatitis.
  • Always consult a dermatologist before starting treatment.

What is Retinoic Acid?

RA is a biologically active metabolite of vitamin A (all-trans-retinol) and serves as a potent regulator of cell differentiation and proliferation. It plays essential roles in embryonic development, immune function, male fertility, and the regulation of bone growth and development.^[3]de Mendoca Oliveira, L., Teixera, F.M.E., Sato, M.N. (2018). Impact of Retinoic Acid on Immune Cells and Inflammatory Diseases. Mediators of Inflammation. 9(3067126). Available at: … Continue reading 

RA is produced in the body through a two-step oxidation process: retinol (vitamin A) is first reversibly oxidized to retinaldehyde, and then retinaldehyde is irreversibly oxidized to retinoic acid.^[5]Kedishvili, N.Y. (2017). Retinoic Acid Synthesis and Degradation. Subcellular Biochemistry. 81. 127-161. Available at: https://doi.org/10.1007/978-94-024-0945-1_5 This process is catalyzed by retinol dehydrogenases and retinaldehyde dehydrogenases (RALDH1, RALDH2, RALDH3). RA cannot be converted back to retinol, making its synthesis a tightly regulated process.

Structurally, RA is a polyunsaturated carboxylic acid with a long conjugated hydrocarbon chain and a terminal carboxyl group.^[6]Sani, B.P., Hill, D.L. (1990). [3] Structural characteristics of synthetic retinoids, Methods in Enzymology, Academic Press, 189. 43-50. Available at: https://doi.org/10.1016/0076-6879(90)89274-L The most prevalent naturally occurring form is all-trans-retinoic acid (ATRA), but other isomers such as 13-cis-retinoic acid (isotretinoin) and 9-cis-retinoic acid (alitretinoin) also exist in lower concentrations.^[7]Bayeva, N., Coll, E., Piskareva, O. (2021). Differentiating Neuroblastoma: A Systematic Review of the Retinoic Acid, Its Derivatives, and Synergistic Interactions. Journal of Personalized Medicine. … Continue reading 

RA is part of a broader class of compounds called retinoids, which includes both natural and synthetic derivatives of vitamin A.^[8]Bushue, N., Wan, Y-J, Y. (2010). Retinoid pathway and cancer therapeutics. Advanced Drug Delivery Reviews. 62(13). 1285-1298. Available at: https://doi.org/10.1016/’j.addr.2010.07.003 

Retinoids are categorized into generations based on their structure:^[9]Baldwin, H., Webster, G., Gold, L.S., Callender, V., Cook-Bolden, F.E., Guenin, E. (2021). 50 Years of Topical Retinoids for Acne: Evolution of Treatment. American Journal of Clinical Dermatology. … Continue reading 

• First Generation: Naturally occurring compounds and their isomers, including retinol, retinal, tretinoin (ATRA), isotretinoin, and alitretinoin.

• Second Generation: Synthetic analogs such as etretinate and acitretin, primarily used for severe psoriasis.

• Third Generation: Polyaromatic retinoids, such as adapalene, bexarotene, and tazarotene, are designed to achieve greater receptor sensitivity and reduced side effects.

• Fourth Generation: Newer compounds with enhanced selectivity, such as trifarotene.

Other commonly used derivatives include retinyl esters (e.g., retinyl palmitate), retinol, retinaldehyde, and synthetic esters like hydroxypinacolone retinate.

How Does Retinoic Acid Work?

RA acts primarily by binding to nuclear receptors in cells, specifically retinoic acid receptors (RARs) and retinoid X receptors (RXRs).^[10]Jin, Q., Huo, C., Yang, W., Jin, K., Cai, S., Zheng, Y., Huang, B., Wei, L., Zhang, M., Han, Y., Zhang, X., Liu, Y., Wang, X. (2022). Regulation of Tyrosinase Gene Expression by Retinoic Acid Pathway … Continue reading Once activated, these receptors function as transcription factors, directly regulating the expression of genes involved in cell proliferation, differentiation, and programmed cell death, also known as apoptosis. This ability to modulate gene expression is what gives RA its wide range of biological effects, from skin remodeling to influence over hair follicle dynamics.

What is the Impact of Retinoic Acid on Hair Follicle Biology?

Retinoic acid (RA) plays a powerful but finely tuned role in hair follicle biology. It affects how hair grows by turning certain genes on or off, acting through specialized receptors found in hair follicle cells, oil glands, and nearby skin tissue.

Too little or too much RA can disrupt the hair cycle. That’s why the body tightly regulates how much RA is made and broken down inside the follicle.

How Is Retinoic Acid Synthesized in the Hair Follicle?

RA is produced in two steps:

The enzyme SDR16C5 converts vitamin A (retinol) into an intermediate form called retinaldehyde.^[11]Wu, L., Belyaeva, O.V., Adams, M.K., Klyuyeva, A.V., Lee, S-A., Goggans, K.R., Kesterson, R.A., Popov, K.M., Kedishbili, N.Y. (2019). Mice lacking the epidermal retinol dehydrogenases SDR16C5 and … Continue reading This mostly occurs in the hair follicle bulge, a crucial area where stem cells reside, and in the dermal papilla, which plays a key role in controlling hair growth. SDR16C5 activity peaks during the growth phase (anagen) and helps stimulate both stem cell activity and hair matrix cell development.

In mice, the absence of SDR16C5 and its related enzyme, SDR16C6, results in an 80% decrease in RA levels.^[12]Foitzik, K., Spexard, T., Nakamura, M., Halsner, U., Paus, R. (2005). Towards Dissecting the Pathogenesis of Retinoid-Induced Hair Loss: All-Trans Retinoic Acid Induces Premature Hair Follicle … Continue reading 

This causes hair follicles to exit their resting phase (telogen) prematurely, leading to abnormal cycling and lower levels of key stem cell markers, such as Lgr5 and Sox9.^[13]Goggans, K.R., Belyaeva, O.V., Klyuyeva, A.V., Studdard, J., Slay, A., Newman, R.B., Christine, VanBuren, A., Everts, H.B., Kedishvili, N.Y. (2024). Epidermal retinol dehydrogenases cyclically … Continue reading  

Another enzyme, ALDH1A2, completes the process by converting retinaldehyde into the active form of retinoic acid. ALDH1A2 is most active in the outer root sheath of the follicle and especially in the bulge during the early growth and regression phases.^[14]Everts, H.B., King Jr, L.E., Sundberg, J.P., Ong, D.E. (2004). Hair cycle-specific immunolocalization of retinoic acid synthesizing enzymes ALDH1A2 and ALDH1A3 indicates complex regulation. Journal … Continue reading One of its key roles is to lower levels of BMP4, a protein that keeps stem cells in a resting state. By reducing BMP4, ALDH1A2 helps “awaken” stem cells and initiate new hair growth.^[15]Suo, L., VanBuren, C., Hovland, E.D., Kedishvili, N.Y., Sundberg, J.P., Everts, H.B. (2021). Dietary Vitamin A Impacts Refractory Telogen. Frontiers in Cell and Developmental Biology. 9. Available … Continue reading When this enzyme is missing, hair follicles take longer to enter the growth phase, and their circadian rhythm becomes disrupted.

How is Retinoic Acid Broken Down?

While synthesizing RA is important, too much can be harmful. That’s where CYP26B1 comes in. CYP26B1 is an enzyme that breaks down RA into inactive forms. During the growth phase, it is found in the dermal papilla and pre-cortex; during rest, it shifts to the bulge to prevent RA levels from building up excessively.^[16]Okano, J., Levy, C., Lichti, U., Sun, H-W., Yuspa, S.H., Sakai, Y., Morasso, M.I. (2012). Cutaneous retinoic acid levels determine hair follicle development and downgrowth. Journal of Biological … Continue reading 

This careful back-and-forth between making and breaking down RA shows how tightly the hair follicle controls its environment. Low, well-regulated levels of RA can support stem cell activity and help promote healthy hair growth. However, high or unbalanced levels can actually prompt follicles to regress or block growth altogether.

To put it plainly: Your hair follicles need just the right amount of retinoic acid. When the balance is right, it may help stimulate hair growth, but when it’s off, it can slow or even reverse it.

Importantly, these regulatory mechanisms are not just theoretical; they appear to be directly involved in common hair disorders, such as androgenic alopecia (AGA).

In vivo/In vivo Evidence

Recent research has demonstrated that retinoic acid signaling is suppressed in miniaturized hair follicles from AGA patients which coincides with impaired hair follicle stem cell (HFSC) activation.^[17]Wen, L., Fan, Z., Huang, W., Miao, Y., Zhang, J., Liu, B., Zhu, D., Dai, D., Zhang, J., Le, D., Zhang, Y., Qu, Q., Hu, Z., Chen, R. (2024). Retinoic acid drives hair follicle stem cell activation via … Continue reading  

Using transcriptomic, in vivo (mouse), ex vivo (human hair follicle organ culture), in vitro (HFSC culture), and clinical approaches, the authors showed that retinoic acid supplementation restored HFSC function by activating Wnt7a/7b and downstream ꞵ-catenin signaling. This promotes HFSC proliferation, differentiation into progenitor cells, and entry into the anagen phase, resulting in improved hair follicle growth (Figure 2), accelerated hair regrowth in mice (Figure 3), and improved hair density and diameter in AGA patients, particularly in early treatment (more on that below). 

Mechanistically, blocking either retinoic acid receptors or Wnt signaling reduced these effects, confirming that retinoic acid acts via Wnt/ꞵ-catenin to drive HFSC activation and hair regeneration. 

Is Retinoic Acid Clinically Effective at Treating Hair Loss?

Retinoic acid and its derivative, tretinoin, have been investigated in clinical trials for treating both androgenetic alopecia (AGA) and alopecia areata (AA). Studies have shown potential synergistic effects with minoxidil, including improved enzyme activity and increased hair regrowth rates, although efficacy typically varies by condition and formulation. 

Study One -1986 (AGA)

This study was an open-label trial of 56 participants with AGA treated with tretinoin alone or in combination with 0.5% minoxidil for 1 year.^[20]Bazzano, G.S., Terezakis, N., Galen, W. (1986). Topical tretinoin for hair growth promotion. Journal of the American Academy of Dermatology. 15.880-883. Available at: … Continue reading Twelve participants received 0.025% topical tretinoin, 36 participants received a combination of 0.025% tretinoin and 0.5% minoxidil, 3 participants received 0.5% minoxidil alone, and 5 participants received a topical placebo.

Hair growth was evaluated through photographs and hair counts in a defined 1-inch diameter target area on the scalp. The duration of participation averaged 8-10 months, with some subjects following the protocol up to 18 months. Participants were categorized as:

• Good responders (Group A): ≥46% increase in terminal hairs.
• Moderate responders (Group B): 21–45% increase.
• Non-responders (Group C): <20% increase.

Placebo and Minoxidil Alone:

Placebo goup: No participants showed hair growth

Minoxidil alone: No participants showed terminal hair regrowth; one participant showed vellus hair growth.

Tretinoin Alone:

12 participants: 58% (7 participants) responded positively, 16% (2 participants) shows a “good response”, 42% (5 participants) had a “moderate” response, and 42% had no response.

However, one woman appeared to be highly responsive to treatment with a 1100% increase in hair counts after 18 months of tretinoin-only treatment.

Combination of Tretinoin and Minoxidil:

36 participants: 66% (24 participants) responded positively, 44% (16 participants) had a “good” response, 22% (8 participants) had a “moderate” response, and 33% (12 participants) had no response.

Responses were observed within 4 to 18 months, with photographic documentation showing visible regrowth in both men and women.

Ultimately, this study showed that tretinoin alone moderately improved hair regrowth, but combining the treatment with minoxidil was more effective, with two-thirds of participants showing terminal hair regrowth.

Study Two – 2007 (AGA)

31 male participants aged 28-45 were recruited for this 18-week study, which compared the efficacy and safety of a combined solution of 5% minoxidil and 0.01% tretinoin applied once daily versus conventional 5% minoxidil applied twice daily for male AGA.^[21]Shin, H.S., Won, C.H., Lee, S.H., Kwon, O.S., Kim, K.H., Eun, H.C. (2007). Efficacy of 5% minoxidil versus combined 5% minoxidil and 0.01% tretinoin for male pattern hair loss. American Journal of … Continue reading 

Five parameters were evaluated: total hair count, non-vellus hair count, anagen hair ratio, linear hair growth rate, and mean hair diameter. Subjective global assessments were also conducted by patients and investigators at 9 and 18 weeks. 

Both groups showed significant increases in total hair count and non-vellus hair count after 18 weeks. Mean hair diameter increased significantly in the minoxidil-only group. However, there were no significant changes in anagen hair ratio or linear hair growth rate in either group. Furthermore, there were no statistically significant differences between groups in any hair growth parameter after 18 weeks.

No significant differences were observed between the two groups in patient-reported improvement or satisfaction scores at any time point. Furthermore, the investigator’s global assessment also showed no significant differences between groups.

Safety outcomes showed that mild adverse effects (itching, irritation) were observed in 5/15 patients in the combined group and 4/14 in the minoxidil-only group, but these were all self-limiting.

The conclusion? The once-daily application of combined 5% minoxidil and 0.01% tretinoin was as effective and safe as twice-daily 5% minoxidil for treating AGA in men. This means it could potentially be a more convenient alternative to twice-daily minoxidil.

Study Three – 2019 (AGA)

Another study found that combining tretinoin with minoxidil could increase follicular sulfotransferase activity and therefore responsiveness to minoxidil.^[23]Sharma, A., Goren, A., Dhurat, R., Agrawal, S., Sinclair, R., Trueb, R.M., Vano-Galvan S., Chen, G., Tan, Y., Kovacevic, M., Situm, M., McCoy, J. (2019). Tretinoin enhances minoxidil response in … Continue reading  

Sulfotransferase (SULT1A1) is the enzyme responsible for converting minoxidil, a prodrug, into its active metabolite minoxidil sulfate within hair follicles.^[24]Dhurat, R., Daruwalla, S., Paj, S., Kovacevic, M., McCoy, J., Shapiro, J., Sinclair, R., Vano-Galvan, S., Goren, A. (2022). SULT1A1 (Minoxidil Sulfotransferase) enzyme booster significantly improves … Continue reading This sulfation reaction is critical because minoxidil sulfate directly stimulates hair growth.

Twenty participants (10 male and 10 female) with AGA were recruited for this study, which determined the effect of topical tretinoin on follicular sulfotransferase. Non-responders to minoxidil often exhibit follicular SULT1A1 activity <0.4 OD 405 nm. In this trial, pretreatment SULT1A1 levels in participants who were minoxidil non-responders averaged 0.28 OD 405 nm. 

Treatment with topical tretinoin (0.1%) increased SULT1A1 activity by 1.8-fold in 75% of subjects after 5 days, raising levels to around 0.51 OD 405 nm. This shift moved 43% of non-responders above the 0.4 OD cutoff, enabling sufficient minoxidil activation.

Study Four – 2024 (AGA)

The most recent trial was conducted in 2024, with 60 total participants with AGA.^[25]Wen, L., Fan, Z., Huang, W., Miao, Y., Zhang, J., Liu, B., Zhu, D., Dai, D., Zhang, J., Le, D., Zhang, Y., Qu, Q., Hu, Z., Chen, R. (2024). Retinoic acid drives hair follicle stem cell activation via … Continue reading 30 participants received a 0.025% topical tretinoin cream, while 30 received 5% minoxidil solution alone. Each treatment was applied twice daily to the bald scalp. 

Hair growth was measured using photography and dermoscopy assessments at 1, 3, and 6-month follow-ups.

The participants treated with the topical tretinoin cream showed a significant improvement in mean hair count, density, and diameter after the first month compared to the Baseline. A significant increase was also observed in hair count, density, and terminal hair ratio in the tretinoin group compared to the minoxidil-treated group.

Study 5 – 2014 (AA)

A randomized controlled trial was conducted with 80 participants with alopecia areata aged 18-25 years, with one to four lesions on the scalp, and lesion diameter of 1.5 to 6 cm.^[27]Jalai, M.H.A., Mobasher, P., Rabbani, R., Jazi, G.A. (2014). Comparing the Efficiency of Elidel Cream and Elidel Accompanied with Tretinoin Cream in Treatment of Alopecia Areata. Journal of Skin Stem … Continue reading 

Participants were treated with either 1% Elidel (pimecrolimus cream) (40 participants) or Elidel + 0.05% tretinoin (40 participants) twice daily for three days. Treatment response was categorized as complete cure, relative cure, no change, or aggravation of lesions. 

Elidel Group:

• Complete cure: 8 patients (20%)
• Relative cure: 14 (35%)
• No change: 10 (25%)
• Aggravation: 8 (20%)

Eliden and Tretinoin Group:

• Complete cure: 18 patients (45%)
• Relative cure: 12 (30%)
• No change: 8 (20%)
• Aggravation: 2 (5%)

The combination therapy group had significantly higher rates of complete cure and lower rates of disease aggravation. However, adverse effects (mainly redness and burning) were more common in the combination group (45%), leading to dose reduction or discontinuation in some cases, but no serious complications were reported.

Unfortunately, the study included no images to show what the initial hair loss severity was and whether the improvements were actually noticeable/

Overall, the clinical evidence suggests that retinoic acid/tretinoin may be most effective as part of a combination therapy, and that patient selection, dosing, and timing play crucial roles in treatment success.

Another point that we can learn from these studies is that tretinoin appears to enhance the effectiveness of minoxidil (and potentially Eliden). This could be due to several mechanisms:

• Enhanced Penetration: Tretinoin may increase skin permeability, allowing better minoxidil absorption.
• Boosts Sulfotransferase Enzymes: Tretinoin upregulates SULT1A1, the enzyme responsible for converting minoxidil into its active form (minoxidil sulfate).
• Stimulates Stem Cell Activity: Both agents independently promote anagen phase entry and follicle regeneration via different pathways (minoxidil via potassium channels, RA via Wnt signaling).

Together, they work on complementary pathways, which helps explain why multiple trials (1986, 2007, 2019, 2024) found better hair growth outcomes with combined use.

How Safe is Retinoic Acid/Tretinoin?

While generally safe, retinoic acid and tretinoin can cause local irritation, especially when used topically on the scalp:

• Common Side Effects: Redness, itching, dryness, and burning sensations.^[28]Yoham AL, Casadesus D. Tretinoin. [Updated 2023 Mar 27]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Available from: … Continue reading
• Dose-Dependent: Higher concentrations (e.g., 0.1%) are more likely to cause irritation.^[29]Griffiths, C.E., Kang, S., Ellis, C.N., Kim, K.J., Finkel, L.J., Ortiz-Ferrer, L.C., White, G.M., Hamilton, T.A., Voorhees, J.J. (1995). Two concentrations of topical tretinoin (retinoic acid) cause … Continue reading
• Mitigation: Reducing application frequency or using lower strengths can improve tolerability. Some studies reported treatment discontinuation due to discomfort.
• Systemic Risks: Rare with topical use, but oral retinoids like isotretinoin carry higher risks and should not be used for hair loss without medical supervision.

In clinical trials, adverse events were mild and reversible, making tretinoin a relatively low-risk addition to hair loss regimens, especially in concentrations ≤0.025%.

Is Retinoic Acid/Tretinoin for Me?

Retinoic acid or tretinoin may be right for you if:

• You’ve had limited success with minoxidil alone, especially if you’re a non-responder.
• You’re seeking enhanced regrowth or wish to reduce the frequency of minoxidil application (e.g., once-daily combo vs. twice-daily minoxidil).
• You’re in the early stages of hair loss, where interventions tend to be more effective.

Caution is warranted if:

• You are hypersensitive to the drug, drug class, or drug formulation. 
• If you are prone to sunburn.
• You have photosensitivity issues.
• You have eczema, seborrheic dermatitis, or other scalp inflammation problems.
• You are pregnant and in the first trimester (retinoids are dangerous for the fetus if they become systemic).

Always consult a dermatologist before starting any retinoid-based hair regimen.

Final Thoughts

Retinoic acid and tretinoin offer a scientifically grounded, mechanistically rich approach to hair loss treatment, particularly for androgenetic alopecia. Although not a magic bullet, they can:

• Enhance minoxidil efficacy
• Support hair follicle stem cell activation
• Offer a new avenue for patients who have plateaued on existing treatments.

That said, results are highly individual, and the treatment must be carefully tailored, balancing dose, frequency, and formulation to optimize results while minimizing irritation. Therefore, we don’t recommend using it by itself.

For now, tretinoin appears best used in combination, especially for those seeking to maximize outcomes from minoxidil therapy.

Cetirizine is a second-generation antihistamine that is approved by the FDA for the treatment of allergies. It works by blocking the H1 receptor and preventing the function of histamine, the biological compound that is responsible for causing allergic symptoms.^[1]Curran, M. P., Scott, L. J., & Perry, C. M. (2004). Cetirizine: a review of its use in allergic disorders. Drugs. 64. 523-561. Available at: https://doi.org/10.2165/00003495-200464050-00008

In this article, we will explore the way in which cetirizine has been proven to work and look at some additional functions that may influence hair health. We will also look to see if there are any clinical studies that show cetirizine can promote hair growth, as well as any safety data that indicates whether it is safe to use.

Key Takeaways

• What is it? Cetirizine is a second-generation antihistamine that is approved for use as an oral medication to treat allergies. It primarily works by binding the H1 receptor, preventing histamine from binding and causing allergic symptoms. Studies have also shown that cetirizine has anti-inflammatory effects, inhibiting the migration of inflammatory mediators. Moreover, it has been shown to reduce PGD2 production, a molecule with strong links to hair loss.
• Clinical Data. In clinical studies, the topical application of cetirizine has been shown to increase hair density, hair thickness, hair regrowth, and the proportion of hairs in the anagen (growing) phase. This indicates that topical cetirizine may promote hair growth, but there are also several limitations that are discussed in detail below.
• Safety. Oral cetirizine is FDA-approved and has been shown to cause limited side effects, none of which are considered serious. No conclusive safety data for topical cetirizine exists, but it is likely to be safe based on the safety profile of oral cetirizine. That said, people who are breastfeeding or have kidney failure may not be able to use cetirizine. 
• Evidence Quality.  Cetirizine scored 57/100 for evidence quality by our metrics.
• Best Practices. Cetirizine is approved for use at the following dosages: 10mg within a 24-hour period in adults, 5mg twice daily in children aged 6-11 years, 2.5mg twice daily in children aged 2-5 years. No recommended dosages exist for the use of topical cetirizine, but 1% cetirizine formulations applied at 1-2 mL daily have shown benefit in several clinical studies.

What is Cetirizine?

Cetirizine is a second-generation antihistamine that is widely used for its anti-allergic properties, which makes it particularly effective for treating the symptoms of seasonal allergic rhinitis (otherwise known as hayfever) and chronic idiopathic urticaria (hives).^[2]Curran, M. P., Scott, L. J., & Perry, C. M. (2004). Cetirizine: a review of its use in allergic disorders. Drugs. 64. 523-561. Available at: https://doi.org/10.2165/00003495-200464050-00008 Such is the importance of cetirizine that it is included in the World Health Organizations List of Essential Medicines.^[3]World Health Organization. (2023). WHO Model List of Essential Medicines – 23rd list, 2023. WHO/MHP/HPS/EML/2023.02. Available at: … Continue reading

Origin and Structure

Cetirizine, a second-generation antihistamine, is derived from the metabolism of hydroxyzine, a first-generation antihistamine. A common feature of second-generation antihistamines, including cetirizine, is limited crossing of the blood-brain barrier and the rapid efflux of any molecules that do enter the brain.^[4]Pagliara, A., Testa, B., Carrupt, P.A., Jolliet, P., Morin, C., Morin, D., Urien, S., Tillement, J.P. and Rihoux, J.P. (1998). Molecular properties and pharmacokinetic behavior of cetirizine, a … Continue reading This reduced uptake limits the effects on the central nervous system, thus lowering the potential for side effects such as drowsiness which were common in the first-generation.^[5]Curran, M. P., Scott, L. J., & Perry, C. M. (2004). Cetirizine: a review of its use in allergic disorders. Drugs. 64. 523-561. Available at: https://doi.org/10.2165/00003495-200464050-00008

How Does Cetirizine Work?

When used for treating the symptoms of allergies, cetirizine is delivered orally as a liquid or tablet. Cetirizine has been used to treat allergies since the 1980s and its mechanism of action, as well as its therapeutic effects, are very well documented. We’ll start by summarizing these effects, before taking a closer look at more recent research that has explored the potential benefits of topical cetirizine in the treatment AGA.

H1-Receptor Antagonism

Cetirizine primarily functions as a potent and selective antagonist of the histamine H1 receptors. Hypersensitive reactions, which manifest as allergies, are initiated when allergens trigger the release of histamine from cells of the immune system. The released histamine binds to H1 receptors, which is the mechanism that is responsible for producing the classic symptoms of allergies.^[6]Ghosh, S., Debnath, I., Bhunia, S., Hazra, S., Nandi, S., & Mandal, S. K. (2025). A Review on Mechanism of Histamine Mediated Allergic Reactions: Therapeutic Role, Safety, and Clinical Efficacy … Continue reading Cetirizine blocks this mechanism by binding to the H1 receptors and blocking the histamine, preventing it from activating the allergic response.^[7]Curran, M. P., Scott, L. J., & Perry, C. M. (2004). Cetirizine: a review of its use in allergic disorders. Drugs. 64. 523-561. Available at: https://doi.org/10.2165/00003495-200464050-00008

Anti-inflammatory Properties

Beyond its role as an antihistamine, cetirizine exhibits significant anti-inflammatory effects that contribute to its therapeutic value. This is particularly beneficial because allergic reactions are characterized by inflammation and the infiltration of immune cells into the different tissues of the body.^[8]Curran, M. P., Scott, L. J., & Perry, C. M. (2004). Cetirizine: a review of its use in allergic disorders. Drugs. 64. 523-561. Available at: https://doi.org/10.2165/00003495-200464050-00008

In an animal study, rats were orally administered cetirizine (900µg/kg; equivalent to the standard human dose of 10mg/kg) or a control substance. Acute inflammation was then induced by injecting the pro-inflammatory substance carrageenin into the paw. After 3 hours, the volume of edema (swelling) in the paw was quantified and compared between the treated and untreated rats. This revealed that there was significantly less swelling (-41.93%) in the cetirizine-treated rats compared to the untreated rats.^[9]Vardhamane, S. H., Santoshkumar, J., & Vardhamane, S. H. (2013). Anti-inflammatory activity of H1 receptor antagonist Cetirizine in animal models. Journal of Evolution of Medical and Dental … Continue reading

The same authors also tested cetirizine in rats with chronic inflammation. Once again, rats were provided with orally administered cetirizine (900µg/kg; equivalent to the standard human dose of 10mg/kg) or a control substance. Inflammation was induced by inserting rexin pellets underneath skin and the rats monitored for 7 days, receiving a daily dose of cetirizine. After 7 days, the granuloma (area of tissue indicative of inflammation) was excised from the rats and weighed. They showed that treatment with cetirizine reduced the granuloma weight (-50.05%), indicating that cetirizine inhibited inflammation.^[10]Vardhamane, S. H., Santoshkumar, J., & Vardhamane, S. H. (2013). Anti-inflammatory activity of H1 receptor antagonist Cetirizine in animal models. Journal of Evolution of Medical and Dental … Continue reading

There are also several clinical trials that have shown its anti-inflammatory properties. In one such study, a total of 12 patients faced an allergen-specific conjunctival challenge, where a known allergen was dropped into the eye. These patients were randomly assigned into one of two groups – 10 mg cetirizine or placebo, both twice daily. Although the number of inflammatory cells increased following the allergen challenge, their levels were still significantly lower in the cetirizine group than the untreated controls.^[11]Ciprandi, G., Buscaglia, S., Pesce, G., Passalacqua, G., Rihoux, J. P., Bagnasco, M., & Canonica, G. W. (1995). Cetirizine reduces inflammatory cell recruitment and ICAM-1 (or CD54) expression on … Continue reading

A double-blinded, placebo-controlled study was also conducted in 14 patients with atopic dermatitis (eczema) and 16 healthy subjects. Participants either received cetirizine (10mg in the morning, 20mg in the evening) or the placebo, and they consumed their respective product every day for 3 days. They took blood samples after Day 2 and then tested the ability of monocytes, key cells of the immune system, to migrate towards a chemical stimulus. The migration of these cells forms a key part of their ability to induce inflammation, so a reduction in the ability to migrate would suggest a reduced inflammatory response. Their results showed that treatment with cetirizine reduced or even abolished ex vivo monocyte migration in both the healthy subjects and the patients with atopic dermatitis.^[12]Jinquan, T., Reimert, C. M., Deleuran, B., Zachariae, C., Simonsen, C., Thestrup-Pedersen, K., & May, R. (1995). Cetirizine inhibits the in vitro and ex vivo chemotactic response of T lymphocytes … Continue reading

Therefore, the literature strongly suggests that cetirizine exhibits anti-inflammatory properties.

Mast Cell Stabilization

Studies also suggest that some of the effects of cetirizine may be mediated by its regulation of mast cells. These white blood cells are found throughout the body and they form part of the immune response, particularly the allergic response. This is because they contain inflammatory mediators (including histamine). When mast cells are stimulated by an allergen, they degranulate and release their inflammatory compounds, driving inflammation and the classic signs of allergy.^[13]Amin, K. (2012). The role of mast cells in allergic inflammation. Respiratory medicine. 106(1). 9-14. Available at: https://doi.org/10.1016/j.rmed.2011.09.007

The effect of cetirizine on mast cells has been demonstrated in vitro. Mast cells were isolated from rats and then treated with increasing concentrations of cetirizine, before exocytosis (degranulation) was induced using a chemical compound. The authors observed a significant decrease in degranulation at a cetirizine concentration of 100µM, while the highest concentration of 1mM induced near-total suppression of degranulation (Figure 1). Furthermore, cetirizine was also shown to significantly outperform a first-generation antihistamine (diphenhydramine) when comparing the relative reduction of degranulation.^[14]Fujimura, R., Asada, A., Aizawa, M., & Kazama, I. (2022). Cetirizine more potently exerts mast cell-stabilizing property than diphenhydramine. Drug Discoveries & Therapeutics. 16(5). 245-250. … Continue reading Thus, this study provides evidence that cetirizine may exert its anti-allergic and anti-inflammatory effects via the mediation of mast cell activity.

Histamine and Hair Loss: Why It Matters

What is Histamine?

Histamine is a biologically active compound that is derived from the amino acid histidine. As previously noted, histamine is stored in the mast cells that are found throughout the body, but it can also be found in basophils (another type of white blood cell). Histamine may also be found in the neurons of the brain, but the white blood cells are its primary store.^[16]Carthy, E., & Ellender, T. (2021). Histamine, neuroinflammation and neurodevelopment: a review. Frontiers in neuroscience. 15. 680214. Available at: https://doi.org/10.3389/fnins.2021.680214

Histamine primarily functions by binding to the H1, H2, H3, and H4 receptors that are found in the brain, blood vessels, heart, neurons, and many other tissues throughout the body. Depending on the receptor it binds to, histamine can exert effects that include initiating inflammation, changing the blood flow, or making the blood vessels more permeable which facilitates the leakage of fluid into surrounding tissues (causing swelling).^[17]Branco, A. C. C. C., Yoshikawa, F. S. Y., Pietrobon, A. J., & Sato, M. N. (2018). Role of histamine in modulating the immune response and inflammation. Mediators of inflammation. 2018(1). … Continue reading

This wide range of functions means that histamine can exert influence over many bodily processes, so it is not surprising that histamine has been linked to hair loss.

Histamine’s Role in Hair Biology

Although the evidence is rather limited, there are a number of studies that have suggested histamine could be contributing to hair loss.

Scalp biopsies from patients with telogen effluvium (TE; 10 patients), alopecia areata (AA; 7 patients), androgenetic alopecia (AGA or ANDRO; 9 patients) were compared to those of healthy volunteers (8 patients). They stained each of these biopsies to count the number of mast cells and determine if there was a difference between conditions. Sure enough, they found that the TE biopsies contained a significantly greater number of mast cell granules (indicated by Giemsa staining) and a greater abundance of the enzyme tryptase (Figure 2).^[18]Grace, S. A., Sutton, A. M., Abraham, N., Armbrecht, E. S., & Vidal, C. I. (2017). Presence of mast cells and mast cell degranulation in scalp biopsies of telogen effluvium. International journal … Continue reading

These results are indicative of an increased number of mast cells and greater mast cell activation in the scalp of people with TE. It has been suggested by this and a number of other studies that mast cells play an important role in hair loss, involved in a system that is triggered by stress and characterized by a switch to a pro-inflammatory phenotype.^[19]Arck, P. C., Handjiski, B., Hagen, E., Joachim, R., Klapp, B. F., & Paus, R. (2001). Indications for a brain‐hair follicle axis: inhibition of keratinocyte proliferation and up‐regulation of … Continue reading

A separate study investigated scalp biopsies from 55 patients with AA and quantified the levels of immune cells and inflammatory mediators, comparing the results to healthy controls. They showed increased CD4+ T cells, CD8+ T cells, and mast cells in the deep perifollicular and deep perivascular areas of the scalp (Figure 3). They also observed increased expression of nerve growth factor, which is potentially indicative of inflammation within the scalp.^[21]Zhang, X., Zhao, Y., Ye, Y., Li, S., Qi, S., Yang, Y., Cao, H., Yang, J. and Zhang, X. (2015). Lesional infiltration of mast cells, Langerhans cells, T cells and local cytokine profiles in alopecia … Continue reading

This provides further evidence that suggests mast cells, and therefore histamine, may play a role in hair loss. Indeed, histamine release from mast cells can trigger the release of T cells, so it is possible that the increase in T cells was driven by increased histamine.^[22]Jutel, M., Watanabe, T., Klunker, S., Akdis, M., Thomet, O.A., Malolepszy, J., Zak-Nejmark, T., Koga, R., Kobayashi, T., Blaser, K. and Akdis, C.A. (2001). Histamine regulates T-cell and antibody … Continue reading

There is also evidence that mast cells may contribute to the extracellular matrix remodelling that is seen in patients with AGA. Biopsies were taken from the balding (vertex) and non-balding (occipital) areas of 10 males with AGA, as well as biopsies from the same regions of 5 healthy control subjects. Using tryptase quantification, they showed that active mast cell counts were almost 2-fold greater in the scalps of AGA patients relative to the healthy controls (Figure 4). Furthermore, they showed an increase in the number of collagen bundles and elastic fibres within the balding regions of the scalp, and a positive correlation between the number of active mast cells and the number of elastic fibres.^[24]Won, C.H., Kwon, O.S., Kim, Y.K., Kang, Y.J., Kim, B.J., Choi, C.W., Eun, H.C. and Cho, K.H. (2008). Dermal fibrosis in male pattern hair loss: a suggestive implication of mast cells. Archives of … Continue reading

It should be noted that the small study size is a limiting factor. However, the results suggest that mast cells may contribute to the remodelling that is observed in AGA. This is supported by studies that have linked tryptase to fibroblast proliferation, collagen production, and elastin production.

It is possible that this recruitment and activation of mast cells (and, potentially, histamine) is caused by changes to the skin microbiome. A study was conducted on hairless mice to compare mast cell activation against control mice with hair. They found that the number of activated mast cells was significantly greater in the hairless mice. Additionally, the patchy sections of hair had fewer mast cells than the hairless sections, but more than the control mice (with a full coat of hair). This difference was associated with a greater amount of gram-positive bacteria on the skin of the hairless mice. Interestingly, when the TLR2 receptor (that recognizes the bacteria) was deleted in hairless mice, the number of mast cells reduced.^[26]Wu, C. C., Kim, J. N., Wang, Z., Chang, Y. L., Zengler, K., & Di Nardo, A. (2019). Mast cell recruitment is modulated by the hairless skin microbiome. Journal of Allergy and Clinical Immunology. … Continue reading

Collectively, these studies suggest that mast cell activation may contribute to hair loss. As an effector of mast cell activity, this might suggest that histamine is also contributing to hair loss. Therefore, this raises the question of whether antihistamines could be used to prevent hair loss.

How Does Cetirizine Have an Impact on Hair Follicles?

To answer the following question, we checked the literature for studies that have investigated the use of antihistamines in hair loss treatment. Despite the limited research, cetirizine has been tested in a number of different studies and generated some interesting results. Let’s start by looking at the mechanistic effects of cetirizine that suggest it could influence hair health.

A double-blind, placebo-controlled crossover study was conducted in 10 people with ragweed allergies. The patients were given oral cetirizine (20mg) or placebo once a day, for two days, before their skin was exposed to the allergen. The exposed portion of the skin was then biopsied for testing. Surprisingly, although erythema (reddening) was reduced, cetirizine did not inhibit the release of histamine. However, the authors found that cetirizine treatment did significantly reduce the production of prostaglandin D2 (PGD2), and there was also a significant reduction in the migration of inflammatory cells white blood cells (eosinophils and neutrophils) to the exposed site.^[27]Charlesworth, E. N., Kagey-Sobotka, A., Norman, P. S., & Lichtenstein, L. M. (1989). Effect of cetirizine on mast cell-mediator release and cellular traffic during the cutaneous late-phase … Continue reading

These results are interesting when it comes to hair health. PGD2 has a previously documented role in promoting hair loss, particularly in those with AGA. PGD2 is thought to block key receptors within hair follicles and prevent hairs from entering the anagen (growth phase). This consequently prevents hair growth and contributes to hair follicle miniaturization. Furthermore, suppression of PGD2 has been shown to have beneficial effects, suggesting that it may be a therapeutic target.^[28]Shin, D. W. (2022). The physiological and pharmacological roles of prostaglandins in hair growth. The Korean Journal of Physiology & Pharmacology: Official Journal of the Korean Physiological … Continue reading

However, it should be noted that recent studies using PGD2 inhibitors are yet to show improvement in hair loss outcomes. You can read more about this in our GPR44 article.

Studies have also shown that inflammation plays a role in driving hair loss. Numerous studies have shown a significant inflammatory response in the scalp of people suffering with hair loss, driven by infiltration of inflammatory mediators (including mast cells) into the hair follicles. This then disrupts the hair cycle and impairs hair growth.^[29]Peyravian, N., Deo, S., Daunert, S., & Jimenez, J. J. (2020). The inflammatory aspect of male and female pattern hair loss. Journal of inflammation research. 879-881. Available at: … Continue reading

Therefore, it is plausible that cetirizine could be beneficial for hair loss.

Clinical Evidence

Thankfully, a number of clinical studies have been conducted to test the efficacy of cetirizine as a hair loss treatment.

One study was conducted on 60 males with AGA between the ages of 22 and 55. The study was double-blinded and the participants were randomized into the placebo or cetirizine group. Those in the cetirizine group were required to apply 1mL of a topical lotion (1% cetirizine) to their scalp every day, while the placebo group followed the same procedure with their respective product. At the beginning and end of the study, assessments of hair regrowth were performed by a dermatologist, photographs were assessed by dermatologists to provide a Hamilton-Norwood classification, and subjective assessments were provided by the participants in the form of questionnaires. The change in each parameter relative to the start of the study was then compared between groups.^[30]Zaky, M. S., Abo Khodeir, H., Ahmed, H. A., & Elsaie, M. L. (2021). Therapeutic implications of topical cetirizine 1% in treatment of male androgenetic alopecia: a case‐controlled study. … Continue reading

Dermatological assessment determined hair regrowth to be significantly greater in the cetirizine group, with 43.3% of participants exhibiting hair regrowth compared to 0% of the placebo group. Similarly, photographic assessment determined that 43.3% of the cetirizine group exhibited improvements in Hamilton-Norwood classification, compared to 0% of the placebo group, which was also a significant difference. Finally, self-assessment by questionnaire revealed significantly greater satisfaction in the cetirizine group, with 43.3% stating that their hair growth had shown an improvement compared to 0% of the placebo group.^[31]Zaky, M. S., Abo Khodeir, H., Ahmed, H. A., & Elsaie, M. L. (2021). Therapeutic implications of topical cetirizine 1% in treatment of male androgenetic alopecia: a case‐controlled study. … Continue reading

In another study, 40 males between the ages of 18 and 49 were recruited to compare topical cetirizine (1%) and minoxidil (5%), and FDA approved therapy for hair loss. Participants in this single-blind study were randomized into one of the two groups and then applied 1mL of solution per day to the balding area of their head. After 16 weeks, every participant was switched to a placebo product for a further 8 weeks.^[33]Mostafa, D. H., Samadi, A., Niknam, S., Nasrollahi, S. A., Guishard, A., & Firooz, A. (2021). Efficacy of cetirizine 1% versus minoxidil 5% topical solution in the treatment of male alopecia: a … Continue reading

Using Trichoscan to conduct objective assessments of the hair, they found that both cetirizine and minoxidil caused a significant increase in total hair density and vellus hair density after 16 weeks, with minoxidil outperforming cetirizine. The percentage of hair in anagen phase increased in both groups after 16 weeks, then subsequently diminished after placebo use. Assessments completed by physicians suggested that a comparable percentage of participants in each group showed improvement in hair density, although 17% of the cetirizine group were determined to have exhibited a reduction compared to 0% of the minoxidil group. Furthermore, the participants in the minoxidil group reported greater satisfaction with their treatment.^[34]Mostafa, D. H., Samadi, A., Niknam, S., Nasrollahi, S. A., Guishard, A., & Firooz, A. (2021). Efficacy of cetirizine 1% versus minoxidil 5% topical solution in the treatment of male alopecia: a … Continue reading

A third study recruited 85 males and females between the ages of 20 and 65 with AGA. 67 participants were placed in the treatment group and used 1mL of topical cetirizine (1%) daily for 6 months, with 18 participants using a placebo product for the same length of time. Using macrophotographs and Trichoscan, they found that total hair density and terminal hair density were both significantly increased in the cetirizine treatment group.^[36]Rossi, A., Campo, D., Fortuna, M.C., Garelli, V., Pranteda, G., De Vita, G., Sorriso-Valvo, L., Di Nunno, D. and Carlesimo, M., 2018. A preliminary study on topical cetirizine in the therapeutic … Continue reading

One last study recruited 60 female patients, with AGA, between the ages of 20 and 50. The study was double-blinded and randomized. Both groups applied 1mL topical minoxidil (5%) every morning for 6 months; one of these groups also applied 1mL topical cetirizine (1%) in the evening, while the other group applied a placebo. Phototrichscopy was used to show that both groups exhibited a significant increase in frontal and vertex terminal and vellus hair density. Interestingly, the minoxidil+cetirizine group also showed a significant increase in hair thickness and number of hairs per follicular unit, which was not present in the minoxidil only group. However, it should be noted that change relative to baseline in both groups was comparable across all parameters. Participants in the minoxidil+cetirizine group also scored better in the self-assessment of new hairs, hair growth, bald areas, and satisfaction with the treatment.^[38]Bassiouny, E. A., El-Samanoudy, S. I., Abbassi, M. M., Nada, H. R., & Farid, S. F. (2023). Comparison between topical cetirizine with minoxidil versus topical placebo with minoxidil in female … Continue reading

Collectively, these studies provide evidence that suggests topical cetirizine may be beneficial in the treatment of hair loss. However, there are limitations with the studies that have been described. For one, it would be good to assess the efficacy of cetirizine over a longer period of time (more than 6 months), to determine whether its beneficial effects improve further, plateau, or even reverse. Larger studies would be highly beneficial, particularly with the inclusion of more females. All of these studies were also limited to the inclusion of AGA patients which, while useful, means that the efficacy of cetirizine in treating other hair loss conditions remains unknown. Some of the studies also lack placebo controls, which means definitive conclusions on the effectiveness of cetirizine cannot be drawn from their results. That said, the results are promising, and seemingly suggest that cetirizine may provide some beneficial effects.

Safety and Side Effects

Oral cetirizine has received FDA approval for treating allergies and is considered safe at the recommended dose (10mg within a 24-hour period in adults, 5mg twice daily in children aged 6-11 years, 2.5mg twice daily in children aged 2-5 years).^[40]NICE. (No date). Cetirizine hydrochloride. National Institute for Health and Care Excellence. Available at: https://bnf.nice.org.uk/drugs/cetirizine-hydrochloride/ (Accessed: 29 April 2025)

Common side effects include feeling of sleepiness and tiredness, as well as headaches, dizziness, dry mouth, diarrhea, sore throat, and sneezing. However, it has been reported that small amounts of cetirizine can get into breast milk, so those who are breastfeeding should use cetirizine with caution. Additionally, people with kidney failure may be unable to use cetirizine.^[41]NHS. (2025). Side effects of cetirizine. National Health Service. Available at: https://www.nhs.uk/medicines/cetirizine/side-effects-of-cetirizine/ (Accessed: 29 April 2025)

In the three clinical studies that used topical cetirizine (1%) alone, no notable adverse events or side effects were reported. In the study that used minoxidil (5%) together with cetirizine (1%), itching, dry hair, initial hair loss, and dandruff were reported. However, these are known side effects of minoxidil, and there were no differences in the number of adverse events between the two groups. Although there is no conclusive safety data related to topical cetirizine, it is safe to use (up to the recommended dosage) as an oral therapeutic. Given that oral therapeutics are more likely to trigger systemic effects, this suggests that topical cetirizine may be safe for use, though some side effects may occur in relation to its application on the skin. However, please note that there is no recommended dosage for topical cetirizine.

 Is Cetirizine For Me?

You may want to experiment with topical cetirizine if:

• You are happy to use a product with limited evidence of efficacy.
• You are happy to use a product with no evidence of efficacy beyond 6 months of use.
• You have not seen beneficial effects from treatment with minoxidil and would like to try something else.
• You want to try a combined treatment with other products like minoxidil.

Final Thoughts

Cetirizine is a second-generation antihistamine that has been FDA approved (as an oral medication) for the treatment of allergies since the 1990s. It primarily works by binding the H1 receptor and preventing histamine from binding there, the molecule that is responsible for allergic symptoms. Alongside its well documented function, oral cetirizine has been shown to both reduce inflammation and inhibit the production of PGD2, the activity of which is strongly linked to hair loss. Several clinical studies have been conducted in AGA patients who used topical cetirizine as a treatment, with the results showing improvements in hair growth, hair density, and hair thickness. Furthermore, no side effects were associated with the topical use of cetirizine, and the oral version of the therapeutic is considered safe for use. Although there is a lack of large, long-term studies that have investigated topical cetirizine, the results suggest that it may provide help to improve hair loss.

From thick, scaly patches to itching and irritation, scalp psoriasis is an autoimmune condition that can be both uncomfortable and persistent. But what triggers it, and how can you manage flare-ups effectively? In this article, we’ll explore what scalp psoriasis is, its symptoms and causes, treatment options, how it affects hair health, and simple ways to support your scalp long-term.

Key Takeaways

• What is it? Scalp psoriasis is a chronic autoimmune skin condition that causes the skin on the scalp to produce cells too quickly, resulting in thick, scaly patches. These plaques can be itchy and painful and extend beyond the scalp to the forehead, neck, and ears. It’s a form of plaque psoriasis and is driven by an overactive immune response influenced by genetic and environmental factors.

• What are the symptoms?  Common symptoms include raised red, salmon-colored, or purple patches, depending on skin tone, covered with silvery or gray scales. Other signs are flaking (often mistaken for dandruff), intense itching, soreness, burning, and sometimes temporary hair loss due to inflammation or scratching. In more severe cases, plaques can cover the entire scalp and cause sleep disturbances or discomfort.

• What is the prevalence? Scalp psoriasis affects an estimated 50–80% of people with psoriasis. While one study reported a 7.6% prevalence among psoriasis patients in Malaysia, this likely underrepresents the global burden. It can develop at any age, though most cases are diagnosed in adulthood, with women being slightly more affected than men.

• What are the most common treatments? Treatment often starts with topical corticosteroids and vitamin D analogs to reduce inflammation and slow cell turnover. Medicated shampoos with salicylic acid, coal tar, or ketoconazole are widely used. In more persistent or severe cases, systemic medications like methotrexate or biologics may be prescribed. Combination therapies such as Enstilar foam are also effective.

• How else can I improve it? Using gentle hair care products, avoiding scratching or picking, and alternating medication with moisturizing shampoos can help. Natural remedies like aloe vera or apple cider vinegar may provide soothing relief. Managing stress, avoiding known triggers (like smoking, certain medications, or cold weather), and making dietary adjustments may also reduce flare-ups.

• Final thoughts. Scalp psoriasis is a complex and often frustrating condition, but with the right treatment plan and supportive care, it can be effectively managed. Taking a proactive approach by addressing both medical treatment and lifestyle adjustments can significantly reduce symptoms and improve overall scalp health and quality of life.

What is Scalp Psoriasis?

Scalp psoriasis is a chronic autoimmune skin condition affecting the scalp but often spreading below the hairline to the forehead, ears, and neck.^[1]Leong, W.C., Tang, J.J. (2022). Scalp psoriasis and Dermatology Life Quality Index: A retrospective study based on 12-year data from the Malaysian Psoriasis Registry. Malaysian Family Physician. … Continue reading It causes an overproduction of skin cells, leading to the formation of thick, scaly patches on the skin. 

Scalp psoriasis is a form of plaque psoriasis that specifically targets the scalp region. It results from an overactive immune system, genetics, and environmental factors (which we will cover below). The condition causes skin cells to reproduce too quickly, creating raised, discolored plaques that can be dry, itchy, and irritating.^[2]National Institute of Arthritis and Musculoskeletal and Skin Diseases. (no date). Psoriasis. NIH. Available at: https://www.niams.nih.gov/health-topics/psoriasis (Accessed: March 2025)

How Does Scalp Psoriasis Present?

Macroscopic Presentation

Scalp psoriasis typically presents as raised reddish or salmon-colored patches with white scales on light to medium skin tones.^[3]NHS. (no date). Psoriasis). National Health Service. Available at: https://www.nhs.uk/conditions/psoriasis/ (Accessed: March) On darker skin, the patches may appear purple with gray scales. These lesions can be a single patch or multiple patches, or they may affect the entire scalp and extend to the forehead, back of the neck, and behind and inside the ears.^[4]Blakely, K., Gooderham, M. (2016). Management of scalp psoriasis: current perspectives. Psoriasis. 29(6). 33-40. Available at: https://doi.org/10.2147/PTT.S85330 

This condition can range from mild and almost unnoticeable to severe, with thick, crusted sores. Intense itching is common and can significantly impact sleep and daily life.^[5]AAD. (no date). Scalp Psoriasis: Symptoms. American Academy of Dermatology Association. Available at: https://www.aad.org/public/diseases/psoriasis/treatment/genitals/scalp-symptoms (Accessed: March) Scalp psoriasis often results in skin flaking, which may be mistaken for dandruff, but it also includes additional symptoms such as red or purple bumpy patches, soreness, and burning.

Scalp psoriasis is typically diagnosed clinically by a dermatologist through a physical examination of the skin, scalp, and nails.^[6]National Psoriasis Foundation. (2025). Scalp Psoriasis. National Psoriasis Foundation. Available at: https://www.psoriasis.org/scalp (Accessed: March 2025)  Your healthcare provider may also refer you for a biopsy to confirm the diagnosis and rule out other conditions.

Microscopic Presentation

Scalp psoriasis shows distinct microscopic features that reveal its underlying inflammatory nature and accelerated skin turnover. 

The epidermal changes are most noticeable with a thickened skin layer, known as regular acanthosis, with elongated “finer-like” extensions into the deeper tissue, referred to as rete ridges.^[8]Raychaudri, S.K., Maverakis, E., Raychaudhri, S.P. (2014). Diagnosis and classification of psoriasis. Autoimmune Review. 13(4-5). 490-495. Available at: https://doi.org/10.101016/j.autrev.2014.01.008 

Other common features are patchy areas with reduced or excess skin cell maturation (hypo- or hypergranulosis) and thinning of the upper skin layers, or supra papillary plates, making blood vessels more visible.^[9]Basir, H.R.G., Alirezaei, P., Hamian, Z., Khanlarzadeh, E. (2018). Are quantitative histopathologic criteria capable of differentiating psoriasis from chronic dermatitis? Clinical, Cosmetic, and … Continue reading 

Furthermore, people with scalp psoriasis typically experience abnormal skin shedding with an accumulation of immature skin cells (parakeratosis) mixed with neutrophil immune cells, forming tiny abscesses called Munro microabscesses.^[11]Butacu, A.I., Toma, C., Negulet, I-E., Manole, I., Banica, A.N., Plesea, A., Badircea, I.A., Iancu, I., Tiplica, G-S. (2024). Updates on Psoriasis in Special Areas. Journal of Clinical Medicine. … Continue reading 

In the dermal layer, there are also significant changes. Immune cells accumulate around blood vessels in the middle skin layers, forming a perivascular lymphocytic infiltrate. The blood vessels themselves are dilated and twisted, contributing to the typical redness seen in psoriasis. 

Other unique diagnostic clues help differentiate scalp psoriasis from other conditions. For instance, there are “spongy” pustules in the spinous later, known as Kogoj pustules, which are collections of neutrophils.^[12]Mirza, H.A., Badri, T., Kwan, E. (2025). Generalized Pustular Psoriasis. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing. Available at:  … Continue reading Another unique feature is the atrophy (shrinking) of sebaceous glands, which contrasts with the normal scalp, where these glands are active.^[13]Werner, B., Brenner, F.M., Boer, A. (2008). Histopathologic Study of Scalp Psoriasis: Peculiar Features Including Sebaceous Gland Atrophy. The American Journal of Dermatopathology. 30(2). 93-100. … Continue reading 

The epidermal surface also becomes irregular with scalp psoriasis, leading to wart-like bumps (papillomatosis) scaling around hair follicles and pinpoint bleeding (Auspitz’s sign).^[15]Dias, M.F.R.G., Loures, A., El Kadi, N., Aranha, N.S., Machado, A., Fontinha, P.R.B., Dutra, H., Trueb, R.M. (2024). Trichoscopic pearl: dynamic trichoscopy sequence of scalp psoriasis before and … Continue reading

Affected areas of the scalp may also show reduced hair density, and the hair strand itself may have a fragile, damaged cuticle. Moreover, biofilms form on the scalp surface, consisting of clusters of bacteria and yeast linked by sticky strands.^[17]Stepanova, A.A., Kornisheva, V.G., Raznatovskiy, K.I., Semolina, O.A. (2020). Scalp Psoriasis and Biofilms: Electron Microscopy. Journal of Microbiology & Experimentation. 8(5). 179-182. … Continue reading These biofilms can contribute to the disease’s persistence and severity. 

What is the Difference Between Scalp Eczema and Scalp Psoriasis?

We cover some distinctions between scalp eczema and scalp psoriasis in our Scalp Eczema Ultimate Guide – here’s a summary:

Visual Distinctions

Scalp eczema and psoriasis have subtle visual differences.

Scalp eczema causes patches of dry skin that may be itchy and inflamed. The size and shape of these patches can change over time. The rash tends to blend into the surrounding skin and may be less well-defined.

Scalp psoriasis typically presents as thicker white scales with more well-defined areas of involvement. It often causes red patches with silvery scales that appear thick and raised. Psoriasis plaques usually extend beyond the hairline.

Differences in Causes and Triggers

The underlying causes and triggers for both conditions differ significantly. 

Scalp eczema conditions can be caused by a combination of genetic and environmental factors, triggered by skin irritants like soaps, detergents, and disinfectants, exacerbated by allergens like dust, pollen, and certain foods, and heat exposure and increased sweating can lead to flare-ups.

Scalp psoriasis, however, results from an overactive immune system and is classified as an autoimmune disease.^[18]Medical News Today (2025). How to tell the difference between scalp eczema and psoriasis. Available at: https://www.medicalnewstoday.com/articles/scalp-eczema-vs-psoriasis (Accessed: March 2025) It can be triggered by factors like stress, infections, skin injuries, and certain medications. 

Treatment Approaches

Common treatments used to treat both scalp eczema and scalp psoriasis include:

• Topical corticosteroids to reduce inflammation and itching.
• Medicated shampoos.
• Moisturizers.
• Light therapy (phototherapy).
• Lifestyle changes to avoid triggers and reduce stress.

Several treatments for the two conditions differ, however.

Treatments typically used to treat scalp eczema include:

• Antihistamines to relieve itching.
• Topical calcineurin inhibitors (e.g., tacrolimus, pimecrolimus) for non-steroidal treatment.
• Wet wrap therapy for severe cases.
• Prescription anti-inflammatory creams.

Treatments typically used to treat scalp psoriasis include:^[19]American Academy of Dermatology Association. (no date). Scalp Psoriasis: Shampoos, Scale Softeners, and Other Treatments. AAD. Available at: … Continue reading

• Salicylic acid-based products to help remove scales.
• Vitamin D analogs (e.g., calcipotriene) to slow skin cell growth.
• Tazarotene (a topical retinoid) slows cell growth and reduces inflammation.
• Systemic medications for severe cases, including methotrexate, cyclosporine, and biologics (e.g., adalimumab, etanercept, and ustekinumab).
• Excimer laser treatment for targeted therapy of psoriasis plaques.

What Are the Causes of Scalp Psoriasis?

Scalp psoriasis is a complex condition influenced by multiple factors. 

Genetic predisposition plays a significant role, as the condition tends to run in families. Over two dozen genes have been identified that may contribute to psoriasis development, with the HLA-C*6:02 gene being the strongest genetic risk factor.^[20]Patel, H.A., Revankar, R.R., Pedroza, S.T., Graham, S., Feldman, S.R. (2023). The Genetic Susceptibility to Psoriasis and the Relationship of Linked Genes to Our Treatment Options. International … Continue reading Other genetic variants, such as those in interleukins 17A, 12B, and 10 genes, are also associated with an increased risk of developing psoriasis.

Scalp psoriasis is mainly caused by a dysfunction in the immune system. In this condition, the immune system mistakenly attacks healthy skin cells, resulting in rapid cell turnover. T-cells, which are normally responsible for fighting infections, begin to target healthy skin cells instead.^[21]Schadler, E.D., Ortel, B., Mehlis, S.L. (2019). Biologics for the primary care physician: Review and treatment of psoriasis. Disease-a-month:DM. 65(3). 51-90. Available at: … Continue reading This immune dysfunction leads to the overproduction of skin cells, which causes the characteristic plaques and scaling associated with psoriasis.

Several environmental triggers can also initiate or exacerbate scalp psoriasis. These include infections, particularly strep throat and skin infections, as well as skin trauma like cuts, scrapes, bug bits, or severe sunburns.^[22]Zhou, S., Yao, Z. (2022). Roles of Infection in Psoriasis. International Journal of Molecular Sciences. 23(13). 6955. Available at: https://doi.org/10.3390/ijms23136955 Stress is another significant trigger, as it can initiate or worsen psoriasis symptoms.^[23]Yang, H., Zheng, J. (2020). Influence of stress on the development of psoriasis. Clinical and Experimental Dermatology. 45(3). 284-288. Available at: https://doi.org/10.1111/ced.14105

Additionally, cold, dry weather conditions, smoking, exposure to secondhand smoke, and heavy alcohol consumption can also contribute to flare-ups.^[24]Zheng, X., Wang, Q., Luo, Y., Lu, W., Jin, L., Chen, M., Zhu, W., Kuang, Y. (2021). Seasonal Variation of Psoriasis and Its Impact in the Therapeutic Management: A Retrospective Study on Chinese … Continue reading,^[25]Miao, M., Yan, J., Sun, Y., Liu, J., Guo, S. (2025). Psoriasis: Unraveling Disease Mechanisms and Advancing Pharmacological and Nontechnological Treatments. Journal of Inflammation Research. 10(18). … Continue reading 

In some cases, medications can trigger or worsen scalp psoriasis:

• Lithium.^[26]Mayo Clinic. (no date). Psoriasis. Available at: https://www.mayoclinic.org/diseases-conditions/psoriasis/symptoms-causes/syc-20355840 (Accessed: March 2025)
• High blood pressure medications like ACE inhibitors.
• Antimalarials.
• Rapid withdrawal of oral or injected corticosteroids.
• Some anti-inflammatory medicines, including ibuprofen.^[27]NHS. (2022). Psoriasis. Available at: https://www.nhs.uk/conditions/psoriasis/causes/ (Accessed: March 2025)

It should be noted that while these factors may contribute to the pathogenesis of scalp psoriasis, the condition usually results from a combination of multiple factors. Not everyone with genetic risk factors will develop scalp psoriasis, and the severity and frequency of flare-ups can vary widely among individuals.

What is the Prevalence of Scalp Psoriasis?

According to a study in Malaysia, scalp psoriasis is estimated to affect about 7.6% of patients with psoriasis in places other than the scalp.^[28]Leong, W.C., Tang, J.J. (2022). Scalp psoriasis and Dermatology Life Quality Index: A retrospective study based on 12-year data from the Malaysian Psoriasis Registry. Malaysian Family Physician. … Continue reading However, this figure may be underestimated, as other sources suggest that scalp involvement occurs in 50-80% of psoriasis patients.^[29]Blakely, K., Gooderham, M. (2016). Management of scalp psoriasis: current perspectives. Psoriasis. 29(6). 33-40. Available at: https://doi.org/10.2147/PTT.S85330 

Scalp psoriasis can occur at any age, but it typically follows patterns similar to general psoriasis: 

• The mean age of onset is ~29 years of age for women and ~36 years for men.
• More common in adults, but about one-third of cases are diagnosed before age 20.
• Slightly more prevalent in women, with a male-to-female ratio of 1:1.56.

What is the Impact of Scalp Psoriasis on Hair Loss?

While scalp psoriasis doesn’t directly cause permanent hair loss, there is a relationship between the condition and increased hair shedding.

Correlation with Hair Loss Conditions

Scalp psoriasis is associated with increased hair shedding and decreased hair density, particularly in areas affected by psoriatic plaques. These lesions can lead to diffuse hair loss, which may be exacerbated by inflammation and itching.^[30]Almeida, M.C., Romiti, R., Doche, I., Valente, N.Y.S., Donati, A. (2013). Psoriatic scarring alopecia. Anais Brasileiros de Dermatologia. 88(6 Suppl 1). 29-31. Available at: … Continue reading It can also result in localized alopecia where the psoriatic plaques are located and generalized telogen effluvium.^[31]Song, B., Liu, X., Jin, H. (2024). Ixekizumab Improved Refractory Erythrodermic Psoriasis with Comorbid Diffuse Alopecia: A Case Report with 52-Week Follow-Up. Clinical, Cosmetic and Investigational … Continue reading 

The mechanism of hair loss in scalp psoriasis includes inflammatory destruction of the hair follicle, as seen in scarring alopecias. Histological studies have shown inflammatory destruction of the infundibular (upper) region of the hair follicle, leading to the loss of the hair follicle (follicular drop-out) and fibrosis.^[32]Wright, A.L., Messenger, A.G. (1990). Scarring alopecia in psoriasis. Acta Dermato-Venereologica. 70(2). 156-159. Available at: PMID:1969203

Factors That May Worsen Hair Loss

• Scratching: Persistent itching and scratching damage hair shafts and follicles, potentially leading to scarring or infections that worsen hair loss.

• Harsh Treatments: Overuse of strong medicated shampoos or aggressive removal of scales can weaken hair and increase shedding.

• Plaque Build-Up: Thick plaques block follicles, preventing new hair growth and increasing breakage.

Preventive Measures

To minimize hair loss:

• Use gentle medicated shampoos and topical treatments.
• Avoid scratching or picking at plaques, and keep nails trimmed and smooth.
• Alternate between medicated and non-medicated shampoos to prevent dryness
• Avoid aggressive hair regrowth treatments that might increase local inflammation, like microneedling, topicals containing retinoic acid, scalp massages, PRP, and mesotherapy.

How Can I Treat Scalp Psoriasis?

Medical Treatments

There are a diverse array of medical treatments for scalp psoriasis. Topical corticosteroids and vitamin D analogs are commonly prescribed.^[33]Kim, G.K. (2010). The Rationale Behind Topical Vitamin D Analogs in the Treatment of Psoriasis. Journal of Clinical and Aesthetic Dermatology. 3(8). 46-53. Available at: PMID: 2087752 Corticosteroids help reduce inflammation, while vitamin D analogs like calcipotriene (Dovonex) can be applied at night to promote healthy skin cell growth. Combination products such as Talconex Scalp or Enstilar Foam, which contain both a vitamin D analog and a strong steroid, are also effective. 

Medicated shampoos play an important role in managing scalp psoriasis. Shampoos containing salicylic acid help soften and remove scales, while coal tar shampoos can reduce itching and inflammation.^[34]National Psoriasis Foundation. (no date). Best Psoriasis Shampoos Your Scalp Will Love. Available at: https://www.psoriasis.org/advance/best-psoriasis-shampoos (Accessed: March 2025) Ketoconazole shampoos may be recommended for their anti-inflammatory properties.

For moderate to severe cases, systemic medications like biologics or small molecules may be prescribed. These include methotrexate, ciclosporin, and oral retinoids, which are used by about 10-20% of people with moderate or severe psoriasis.^[35]Sbidian, E., Chaimani, A., Garcia-Doval, I., Doney, L., Dressler, C., Hua, C., Hughes, C., Naldi, L., Afach, S., Le Cleach, L. (2021). Systemic pharmacological treatments for chronic plaque … Continue reading 

Natural and Home Remedies

Natural remedies can complement medical treatments by providing relief and soothing the scalp. Aloe vera gel and apple cider vinegar can help to relieve some of the irritation and assist in maintaining moisture levels.^[36]Medical News Today. (2019). Can aloe vera treat psoriasis? Available at: https://www.medicalnewstoday.com/articles/320081 (Accessed: March 2025)

Stress management techniques like meditation or yoga may help prevent flare-ups. Some people report symptom improvement after removing dairy or gluten from the diet, although this varies from person to person.^[37]National Psoriasis Foundation. (no date). Dietary Modifications. Available at: https://www.psoriasis.org/dietary-modifications (Accessed: March 2025)

Final Thoughts

Scalp psoriasis is a chronic, immune-mediated condition that can significantly impact the quality of life due to the inflammation and discomfort it causes. Rooted in genetic susceptibility and driven by immune dysfunction, scalp psoriasis is often worsened by environmental and lifestyle triggers. While it doesn’t directly cause permanent hair loss, inflammation, itching, and harsh treatments can lead to increased hair thinning. Managing scalp psoriasis effectively often requires a combination of medical therapies and supportive care, including gentle scalp practices and trigger avoidance.