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Finasteride is one of the most effective treatments available for pattern hair loss. At 1 mg, oral finasteride is one of the only FDA-approved drugs for treating thinning hair and has decades of clinical research to back its use.

But despite the robust clinical evidence, many men are hesitant to use finasteride. Online forums are full of users questioning whether finasteride’s benefits for hair loss are worth the risk of side effects.

Finasteride reduces dihydrotestosterone (DHT), the male hormone implicated in male pattern baldness. Men who experience patterned hair thinning have hair follicles that are genetically more sensitive to this hormone and, as a result, experience hair loss caused by DHT.

Because DHT is involved in overall male biology, lowering DHT levels with drugs like finasteride is believed to have an impact, especially on sexual function. But in reality, the risk of side effects with oral finasteride is rare.^[1]Propecia (Finasteride) Tablets 1 mg: Prescribing Information, Clinical Studies in Men With Male Pattern Hair Loss. U.S. Food and Drug Administration Label. … Continue reading

In men who do experience side effects, lowered levels of DHT throughout the body are suspected to be the culprit, along with reduced levels of related hormones in the brain called neurosteroids. The exact mechanisms are still being studied. ^[2]Traish, A.M., Melcangi, R.C., Bortolato, M., Garcia-Segura, L.M., Zitzmann, M., et al. (2015). Adverse Effects Of 5α-Reductase Inhibitors: What Do We Know, Don’t Know, And Need To Know? … Continue reading

So in an effort to minimize the negative side effects of finasteride, researchers have endeavored to formulate topical finasteride products that:

1. result in less finasteride absorption,
2. reduce DHT at the follicle level (where it really matters), and
3. minimize systemic (blood) reductions of DHT.

And many have been successful. In one 2022 study, a once-daily 0.25% finasteride spray grew nearly as much hair as the finasteride pill, but with more than 100x lower blood levels of finasteride. ^[3]Piraccini, B.M., Blume-Peytavi, U., Scarci, F., Jansat, J.M., Falqués, M., Otero, R., Tamarit, M.L., Galván, J., Tebbs, V., Massana, E. (2022). Efficacy And Safety Of Topical Finasteride Spray … Continue reading

The question is not necessarily if topical finasteride works (studies show it does), but what the ideal formulation of topical finasteride is to both 1) minimize systemic absorption and 2) maximize the availability of finasteride to hair follicles.

While there are plenty of formulations for topical finasteride, there’s one formula that stands out for achieving these objectives: liposomal finasteride.

Liposomal finasteride is finasteride delivered in a liposomal gel or cream, a unique delivery vehicle that minimizes systemic absorption and maximizes delivery to hair follicles.

But is there research showing liposomal finasteride works, or that it’s better than the alternatives?

In this article, we’ll unpack the evidence about liposomal finasteride, whether it works, why it might be an ideal delivery system, and who it might not be well suited to.

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What Is Liposomal Finasteride?

Liposomal finasteride is a topical form of finasteride that uses microscopic structures called liposomes to help deliver the medication into the scalp.

Liposomes are made from phospholipids, the same type of fat molecules that make up the membranes surrounding our cells.

Each phospholipid has two distinct parts: a water-loving head and a fat-loving tail. When placed in water, these molecules naturally arrange themselves into a double layer, forming tiny spherical structures that can carry active ingredients either within their membranes or inside their hollow centers.

These physical characteristics make liposomes an ideal candidate for topical drug delivery.

The skin’s outermost layer, called the stratum corneum, is held together by a protective network of lipids (fats). This barrier makes it difficult for many medications to penetrate.

Because liposomes are also made from lipids, they are compatible with the skin barrier, allowing their contents to be transferred into the skin more effectively. Depending on their composition, liposomes may also accumulate within hair follicle openings, where they can release medication close to the structures we’re trying to target.

This means liposomes can potentially do more than simply increase how much medication penetrates the skin. They can also influence where the medication accumulates, how much remains within the skin, and how quickly it’s released.

And for finasteride, these characteristics could offer an important advantage: concentrating more of the medication around hair follicles while limiting how much passes through the skin and enters the bloodstream.

And for finasteride, this could offer an important advantage.

How Does Liposomal Finasteride Work?

To understand why liposomal delivery might be beneficial, we first need to understand how finasteride works.

Finasteride inhibits 5-alpha-reductase, the enzyme responsible for converting testosterone into dihydrotestosterone (DHT).

DHT is the hormone primarily responsible for pattern hair loss. In genetically susceptible individuals, it binds to receptors in hair follicles and triggers a gradual process called follicle miniaturization, where the follicles shrink and produce progressively thinner hairs.

By inhibiting 5-alpha-reductase, finasteride reduces DHT levels and, as a result, dramatically reduces the amount of DHT hair follicles and the surrounding scalp skin are exposed to. In turn, finasteride is believed to help slow, stop, prevent, and possibly even reverse this process of miniaturization.

And it’s proven effective very effective at doing so.

In a 1999 study, researchers found that taking 1 mg of oral finasteride daily reduced DHT levels in the scalp by approximately 64% after 42 days. However, the medication also reduced circulating DHT levels by approximately 71%. ^[4]Drake, L., Hordinsky, M., Fiedler, V., Swinehart, J., Unger, W.P., Cotterill, P.C., Thiboutot, D.M., Lowe, N., Jacobson, C., Whiting, D., Stieglitz, S., Kraus, S.J., Griffin, E.I., Weiss, D., … Continue reading

When finasteride is taken orally, it enters the bloodstream and inhibits 5-alpha-reductase throughout the body, not just in the scalp. But for treating pattern hair loss, our primary goal is to reduce DHT activity around the hair follicles. Systemic DHT inhibition still achieves this objective, but isn’t required so long as scalp DHT is effectively reduced.

By applying the medication directly to the scalp, we can deliver finasteride closer to where it’s needed while reducing how much circulates throughout the body. And clinical research suggests that this approach works.

In a large Phase III trial published in 2022, topical finasteride reduced circulating DHT by approximately 35%, compared with 56% for oral finasteride. ^[5]Piraccini, B.M., Blume-Peytavi, U., Scarci, F., Jansat, J.M., Falqués, M., Otero, R., Tamarit, M.L., Galván, J., Tebbs, V., Massana, E. (2022). Efficacy And Safety Of Topical Finasteride Spray … Continue reading

In other words, topical finasteride still affected DHT levels throughout the body, but to a substantially lesser extent than the oral medication.

So, could we reduce systemic absorption even further?

One factor that may influence this is the vehicle, or the formulation used to deliver finasteride into the skin.

Most conventional topical finasteride solutions rely on alcohol, propylene glycol, or a combination of the two. These ingredients help dissolve finasteride and facilitate its penetration into the skin. However, they aren’t specifically designed to concentrate the medication within hair follicles.

This is where liposomes come in.

Rather than simply helping finasteride penetrate the skin, liposomes may allow more of the medication to accumulate around hair follicles while limiting how much passes through the skin into circulation. This means more finasteride concentrated to the follicle and even less finasteride being absorbed into the blodstream.

In other words, greater local delivery of finasteride with less systemic exposure.

And while this hasn’t yet been demonstrated conclusively in humans, several decades of research into liposomal drug delivery provide good reasons to investigate the approach.

Let’s look at what the studies have found.

Does Liposomal Finasteride Work?

Researchers have been investigating liposomes as a way to deliver ingredients directly to hair follicles for more than 30 years. And the findings suggest that liposomes may offer a significant advantage over conventional topical formulations.

One of the earliest studies was published in 1992. Researchers compared how effectively liposomes delivered a fluorescent marker into the hair follicle. The fluorescent marker allows researchers to easily detect how much of the applied substance is localized to the hair follicles.

Using hamster ear skin, they found that liposomes deposited more of the marker into these structures than conventional vehicles, including water, alcohol, and propylene glycol solutions. ^[6]Lieb, L.M., Ramachandran, C., Egbaria, K., Weiner, N. (1992). Topical Delivery Enhancement With Multilamellar Liposomes Into Pilosebaceous Units: I. In Vitro Evaluation Using Fluorescent Techniques … Continue reading

In other words, liposomes were better at delivering their encapsulated materials than other solutions made with water, alcohol, or propylene glycol.

And this wasn’t an isolated finding. Subsequent studies successfully demonstrated the delivery of very different substances into hair follicles using liposomes, including melanin (the pigment responsible for hair and skin color) in cultured skin and even genetic material in mice. ^[7]Li, L., Lishko, V., Hoffman, R.M. (1993). Liposomes Can Specifically Target Entrapped Melanin To Hair Follicles In Histocultured Skin. In Vitro Cellular & Developmental Biology. 29A. 192-194. ^[8]Li, L., Hoffman, R.M. (1995). The Feasibility Of Targeted Selective Gene Therapy Of The Hair Follicle. Nature Medicine. 1. 705-706. https://doi.org/10.1038/nm0795-705

Together, these experiments demonstrated that liposomes could successfully target hair follicles with a range of substances, supporting their potential as a delivery system for topical treatments.

More importantly for hair loss treatment, researchers have also investigated whether liposomes can improve the delivery of finasteride. In their research, they found that liposomal finasteride was better at delivering finasteride to hair follicles and decreasing systemic absorption.

In an investigative study, researchers compared liposomal formulations with a conventional water-alcohol solution using hamster skin. Over 24 hours, approximately 24% of the finasteride in the conventional solution passed through the skin, compared with just 5.5–13% from the vesicle formulations. Liposomes also produced the greatest retention of finasteride within the deeper layers of the skin. ^[9]Daneshamouz, S., Tabbakhian, M., Tavakoli, N., Jaafari, M.R. (2005). Influence Of Liposomes And Niosomes On The In Vitro Permeation And Skin Retention Of Finasteride. Iranian Journal of … Continue reading

Together, the findings of these studies suggest that appropriately formulated liposomes can deliver more finasteride into hair follicles while reducing how much passes through the skin into the bloodstream. Although these findings come from animal models, they provide a compelling rationale for liposomal finasteride as a way to improve targeted delivery and potentially limit systemic exposure.

And if we can maintain sufficient finasteride activity in the scalp while reducing its effects elsewhere in the body, we may be able to preserve its hair growth benefits while lowering the risk of systemic side effects.

But how much evidence do we actually have that this approach works? Let’s look at the research.

Liposomal Finasteride: The Human Studies

Unfortunately, there haven’t been any peer-reviewed studies on liposomal finasteride formally published in scientific journals. However, there have been some informal studies published as part of patents.

In a study described in a European patent, seven men applied a 2.5% liposomal finasteride gel to their scalps daily for three weeks.

Researchers measured finasteride and DHT levels in their blood and found that circulating DHT decreased by an average of 31%. That’s about half of the 60–70% reduction typically associated with oral finasteride, despite a far higher daily dose (1 ml of 2.5% finasteride provides about 25 mg of finasteride, or 25 times the standard 1 mg oral dose). ^[10]Hasson, V., Castiglione, M. (2021). Topical Formulations For Treating Dermatological Disorders Including Male Pattern Baldness. European Patent EP3700506B1. Example 4. … Continue reading

For reference, a 0.25% topical finasteride spray reduced systemic DHT levels by about the same (35%) despite a 10x higher concentration.

The same patent also investigated whether the liposomal finasteride could regrow hair in men.

Of the nine men included in the small study, all nine reportedly experienced improvements in hair density and new growth after using the 2.5% liposomal gel. No side effects were reported.

These findings are encouraging, particularly because they suggest that a liposomal formulation may be capable of delivering enough finasteride to produce visible improvements in hair growth.

However, there are some important limitations. The study was small, lacked a described randomized placebo comparison, and was reported in a patent rather than a peer-reviewed scientific journal. ^[11]Hasson, V., Castiglione, M. (2021). Topical Formulations For Treating Dermatological Disorders Including Male Pattern Baldness. European Patent EP3700506B1. Example 8. … Continue reading

So, what can we take away from all of this?

There is substantial experimental evidence supporting liposomes and related vesicles as delivery systems for finasteride, along with preliminary human findings suggesting that liposomal formulations can support hair growth.

Does Liposomal Finasteride Reduce Side Effects?

One of the main reasons people choose topical finasteride over oral finasteride is to reduce the risk of side effects, particularly sexual side effects like erectile dysfunction and reduced libido.

But how common are these side effects in the first place?

In a systematic review of 12 randomized trials involving 3,927 men, researchers found that oral finasteride approximately doubled the relative risk of erectile dysfunction compared with placebo.

While that might sound concerning, the absolute increase was relatively small: approximately one additional case of erectile dysfunction for every 82 men treated. The researchers also found that men taking finasteride were no more likely than those taking placebo to discontinue treatment because of sexual side effects. ^[12]Mella, J.M., Perret, M.C., Manzotti, M., Catalano, H.N., Guyatt, G. (2010). Efficacy And Safety Of Finasteride Therapy For Androgenetic Alopecia: A Systematic Review. Archives of Dermatology. … Continue reading

That said, side effects remain a legitimate concern. Some men have also reported sexual dysfunction that persisted after stopping finasteride, prompting the FDA to update the drug’s labeling in 2012, and the continued interest in topical finasteride.

As we’ve discussed, clinical trials have shown that topical finasteride can produce similar improvements in hair growth to oral finasteride while resulting in substantially lower concentrations of the medication in the bloodstream. Some trials have also reported fewer sexual side effects with topical treatment.^[13]Piraccini, B.M., Blume-Peytavi, U., Scarci, F., Jansat, J.M., Falqués, M., Otero, R., Tamarit, M.L., Galván, J., Tebbs, V., Massana, E. (2022). Efficacy And Safety Of Topical Finasteride Spray … Continue reading

The goal of liposomal finasteride is to achieve this, but to an even greater degree than standard topical finasteride. If liposomal finasteride achieves this, we might also be able to further reduce the risk of systemic side effects.

But does the research support this possibility?

We don’t yet have controlled human trials comparing the side effects of liposomal finasteride with conventional topical formulations. However, we do know that 1) the physical characteristics of liposomes very likely lead to accumulation within the skin, reducing the amount absorbed into the blood and 2) animal research studies suggest liposomal medications, including liposomal finasteride, likely behave in this way.

Moreover, some studies have investigated whether liposomal application of drugs results in less systemic side effects.

In one study, researchers investigated whether liposomes could improve the delivery of topical cyclosporine, an immunosuppressant used to treat conditions like psoriasis.

Cyclosporine is effective when taken orally, but its use can be limited by systemic side effects, including high blood pressure and kidney problems. Researchers have also struggled to develop effective topical formulations because the medication doesn’t penetrate the skin easily.

After 14 weeks of treatment with the liposomal cyclosporine, 41% of psoriasis lesions treated had completely cleared, compared with none treated with conventional cyclosporine cream or placebo.

Importantly, researchers also monitored systemic absorption and safety. They found no evidence of cyclosporine accumulating in the bloodstream following repeated application, while blood pressure, kidney function, and liver function remained within normal limits. ^[14]Kumar, R., Dogra, S., Amarji, B., Singh, B., Sharma, S.K., Vinay, K., Mahajan, R., Katare, O.P. (2016). Efficacy Of Novel Topical Liposomal Formulation Of Cyclosporine In Mild To Moderate Stable … Continue reading

These findings tell us that liposomal delivery can improve the effectiveness of a topical medication in humans while maintaining low systemic exposure.

Of course, cyclosporine and finasteride are different medications, and this study doesn’t establish that liposomal finasteride causes fewer side effects than conventional formulations.

However, it provides encouraging clinical evidence for the principle behind liposomal finasteride: delivering enough medication into the skin to produce a therapeutic effect and minimizing related side effects.

For finasteride, this could mean maintaining its effects around hair follicles while reducing exposure elsewhere in the body. But more research is needed to determine the true impact of a liposomal formulation on side effects.

Is Liposomal Finasteride Better Than Other Topical Finasteride?

At this point, we have good evidence that topical finasteride works. What we don’t yet know is whether delivering it as liposomal finasteride makes it more effective, or reduces its risk of side effects even further.

That being said, liposomes have been used in medicine for decades, including in FDA-approved treatments. Their ability to carry medications and influence how those medications are distributed throughout the body is well established.

And when we look specifically at topical drug delivery, the findings are encouraging.

As we covered earlier, researchers have repeatedly demonstrated that liposomes can deliver different substances into hair follicles. In finasteride studies, certain liposomal formulations retained more medication within the skin, slowed its passage through the skin, and delivered approximately three times more finasteride into hair follicles than a conventional solution.

This is significant because the goal of topical finasteride is to inhibit DHT activity around hair follicles while limiting how much of the medication enters the bloodstream.

In theory, a delivery system that concentrates more finasteride around the follicle, while simultaneously decreasing systemic absorption would have a significant advantage over regular topical finasteride.

Put simply: liposomal finasteride is theoretically better than regular finasteride. But, it hasn’t yet been proven.

With the current state of the evidence, it’s reasonable to say that liposomal finasteride is a potentially better option worth exploring. But whether it’s better for you is entirely dependent on your treatment preferences.

If your primary concern is maximizing the benefits of finasteride while also minimizing the side effects of finasteride, a liposomal finasteride is an option to seriously consider. It offers the best technical advantage, even if it hasn’t been proven. However, if your primary goal is to use a clinically-studied topical finasteride, you might be better suited to a standard topical finasteride solution.

There are also some practical considerations.

Conventional topical finasteride is often formulated with alcohol, propylene glycol, or both, producing relatively lightweight solutions that dry quickly on the scalp. You can apply your medication any time of day, let it dry, and style your hair as usual.

Some liposomal formulations, particularly gels and creams, can feel heavier or leave more residue in the hair. Depending on the formula, this may mean washing your hair more frequently or finding it harder to style after application.

If that’s a concern, applying the product in the evening may be preferable.

Similarly, if you prefer a formulation without alcohol or propylene glycol or have an extremely sensitive scalp, a liposomal formula, often formulated without these ingredients, may be preferred. Additionally, liposomal finasteride is typically made with lipids that soothe and repair the skin, making it a suitable fit for senstive skin types.

Ultimately, the best formulation is one that delivers an effective amount of finasteride to the scalp, minimizes unwanted systemic exposure, and fits your preferences enough to use consistently.

What to Look for in a Liposomal Finasteride

Because there’s no clinical trial to point to, choosing a liposomal finasteride comes down to how well it fits your routine. A few factors matter most:

• Pricing built for long-term use. Finasteride takes several months to produce visible results, and maintaining those results requires continued treatment. Ulo offers multi-month plans that reduce the monthly cost, making long-term treatment more affordable.
• More treatment options if you need them. While finasteride is effective for most men, some may benefit from a different approach. Ulo also offers topical dutasteride and oral hair loss medications, allowing you to explore alternative treatments without switching providers.
• Treatment that adapts to your progress. Finasteride is often combined with minoxidil to target hair loss through different mechanisms. Ulo offers combination formulas and ongoing clinician support, so your treatment can be adjusted based on your response and individual needs.

Our Pick: Ulo’s Liposomal Topical Finasteride

Ulo’s liposomal topical finasteride checks each of these boxes.

More affordable long-term treatment. Hair loss treatment requires consistency, often for years. Ulo offers 3-, 6-, and 12-month plans that reduce the monthly cost, making it easier to maintain treatment over the long term.

More treatment options if you need them. Not everyone responds to finasteride equally. For those who need a different approach, Ulo also offers topical dutasteride and oral hair loss medications, allowing patients to explore other options without switching providers.

Treatment that can evolve with your progress. Ulo offers combination formulas that pair DHT blockers with other hair growth ingredients like minoxidil. A licensed clinician reviews your medical history and can adjust your regimen based on your response to treatment.

For men who are interested in finasteride but concerned about systemic side effects, or those who have used oral finasteride and want to explore a topical alternative, Ulo’s liposomal formulation is a reasonable option to explore for hair loss treatment.

Liposomal Finasteride From our partners at Ulo

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Finasteride encapsulated in liposomes for targeted delivery to the follicle. Prescribed 100% online. Choose a multi-month plan and get up to 30% plus a free gift bundle.

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Liposomal deliveryTargeted to the follicle

*Only available in the U.S. Prescription requires an online medical consultation at no extra cost. Off-label products are not endorsed by the FDA. Free gifts included with select multi-month plans while supplies last. Ulo is a partner of Perfect Hair Health; we may earn a commission on purchases.

Frequently Asked Questions

Is liposomal finasteride better than oral finasteride?

It depends on what you’re looking to achieve. Oral finasteride has decades of clinical evidence supporting its effectiveness for hair loss. Liposomal finasteride, on the other hand, hasn’t been studied nearly as extensively.

However, clinical trials of conventional topical finasteride have shown improvements in hair growth comparable to oral finasteride, with far less systemic exposure.

Liposomal formulations may improve on this by delivering more finasteride directly to hair follicles while limiting systemic absorption. Whether this translates into better results or fewer side effects than oral finasteride still needs to be established.

Is liposomal finasteride better than regular topical finasteride?

Potentially. Laboratory and animal studies suggest that liposomes can improve the accumulation of finasteride in hair follicles while reducing how much passes through the skin.

These findings are encouraging, particularly for people concerned about systemic exposure. However, we don’t yet have controlled human trials comparing liposomal finasteride with conventional topical formulations, so any clinical advantage is still theoretical.

Does topical finasteride still lower DHT in the blood?

Yes. Although topical finasteride generally produces lower systemic exposure than oral finasteride, some of the medication can still enter the bloodstream and reduce circulating DHT.

In a Phase III clinical trial, a 0.25% topical finasteride spray reduced circulating DHT by approximately 35%, compared with 56% for oral finasteride. In a patent study, 2.5% liposomal finasteride reduced circulating DHT by about the same, despite a 10x a higher dose of finasteride. However, this study wasn’t peer-reviewed or published in a scientific journal.

This suggest liposomal delivery may help limit systemic absorption further, but we don’t yet have enough human evidence to determine how much of a difference it makes.

Can I use liposomal finasteride with minoxidil?

Yes. Finasteride and minoxidil work through different mechanisms, which is why they’re frequently prescribed together.

Finasteride reduces DHT, the hormone responsible for gradually shrinking susceptible hair follicles. Minoxidil works through different pathways to support hair growth and help follicles remain in their growth phase longer.

Because they target different aspects of hair loss, combining them can be more effective than using either treatment alone. Your clinician can help determine the appropriate formulation and treatment schedule.

How long does liposomal finasteride take to work?

Like other hair loss treatments, liposomal finasteride requires consistent use before visible improvements can be expected.

In clinical trials of conventional topical finasteride, researchers observed measurable improvements in hair count after 24 weeks, or approximately six months.

However, hair growth varies from person to person, and it can take 6–12 months to properly evaluate a treatment’s effectiveness. In particular, DHT reducers like finasteride can continue to produce results after the 12 month mark.

We recommend taking baseline photographs before starting treatment and repeating them under consistent lighting every few months. This makes it much easier to evaluate changes in hair density over time.

Can women use liposomal finasteride?

Finasteride is sometimes prescribed off-label to women with pattern hair loss after menopause.

However, any form finasteride, including liposomal finasteride, must not be used during pregnancy or by women who may become pregnant because of the risk of harm to a developing male fetus.

Bottom Line

Liposomal finasteride represents a promising advancement in how we approach hair loss treatment: delivering more finasteride to the hair follicles while minimizing how much of the medication reaches the rest of the body.

And the research gives us good reason to be optimistic.

Large clinical trials have already demonstrated that conventional topical finasteride can produce hair growth comparable to oral finasteride, but with substantially lower concentrations of the medication in the bloodstream. Meanwhile, laboratory and animal studies suggest that liposomal delivery can improve how much finasteride accumulates around hair follicles while further reducing its absorption into the bloodstream.

Taken together, these findings suggest that liposomal finasteride could offer the benefits of conventional finasteride with even less systemic exposure.

Of course, we still need controlled human trials to determine whether these improvements in drug delivery translate into better hair growth or fewer side effects. But the underlying science is encouraging, and liposomal finasteride offers a compelling approach to improving an already effective treatment.

For men who are concerned about the potential side effects of oral finasteride, or who simply prefer a more targeted approach to treatment, liposomal finasteride is certainly worth discussing with a clinician.

As with any hair loss treatment, consistency is important. Give your treatment at least 6–12 months, document your progress with photographs, and remember that improvements can continue well beyond the first year.

Topical minoxidil has been a cornerstone of androgenic alopecia (AGA) treatment since its FDA approval in the 1980s. With millions of users worldwide, it stands as one of the most widely adopted therapies for hair loss, supported by decades of clinical evidence, and an enormous body of real-world anecdotes, reviews, and before-and-after photos. 

However, results with minoxidil can be highly variable, and this variability can be traced in part to biological differences, particularly in the activity of the sulfotransferase enzyme (SULT1A1), which is responsible for converting minoxidil into its active form. Not everyone sulfates minoxidil effectively, meaning that while some achieve meaningful regrowth, others see little to no improvement. 

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Adding to this challenge is the influence of online topical minoxidil before and after photos (like you can see below), which can create inflated expectations compared to the more modest, probable outcomes seen in practice. 

This article will break through that noise to answer a critical question: when it comes to minoxidil, what is actually the most probable result, not just possible? 

First, let’s take a look at what topical minoxidil is.

Refresher: What is Topical Minoxidil?

Topical minoxidil was the first therapy ever approved by the FDA for the treatment of AGA, making it a landmark in the medical management of pattern hair loss.^[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 Introduced in the 1980s, it has since become one of the most widely available and researched treatments across the globe. Its primary action is as a potassium channel opener, which helps to stimulate blood flow, prolong the hair’s growth phase (anagen), and increase follicle size, mechanisms that together can support thicker, denser hair regrowth over time.^[2]Messenger, A.G., Rundegren, J. (2004). Minoxidil: mechanisms of action on hair growth. British Journal of Dermatology. 150(2). 186-194. Available at: https://doi.org/10.1111/j.1365-2133.2004.05785.x

Minoxidil is known as a “pro-drug”, meaning that it needs to be activated within the body to exert its effect. The enzyme responsible for this is called sulfotransferase or, more specifically, SULT1A1. The level of sulfotransferase activity differs depending on the individual, which means that the effectiveness of treatment also differs depending on who you are.^[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 

Formulations typically come in 2% and 5% strengths. The 2% solution was originally FDA-approved for women, while the 5% concentration was approved for men; however, both are now commonly used off-label across genders. Beyond these standard strengths, compounding pharmacies have made higher concentrations available for patients seeking more individualized treatment approaches, with some online telehealth providers (such as Ulo) offering customized formulations. Standard dose topical minoxidil is available over-the-counter in most countries, ensuring accessibility without the need for a prescription.

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Sublingual deliveryDissolves under the tongue

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The Evidence

Topical minoxidil’s robust efficacy for hair regrowth is supported by dozens of high-quality randomized controlled trials (RCTs) and meta-analyses across men and women, consistently demonstrating average increases in hair count of around 10-20% over 6-12 months. 

We have collated many of these studies into a table, which you can look at here. However, we have summarised some of the most recent topical minoxidil studies.

Liang et al. (2022)

• Prospective, evaluator-blinded RCT with 120 women with female pattern hair loss (FPHL) assigned to three groups: 5% topical minoxidil alone; 5% minoxidil + oral spironolactone (80-100 mg); and 5% minoxidil and microneedling every 2 weeks.^[4]Liang, X., Chang, Y., Wu, H., Liu, Y., Zhao, J., Wang, L., Zhuo, F. (2022). Efficacy and Safety of 5% Minoxidil Alone, Minoxidil Plus Oral Spironolactone, and Minoxidil Plus Microneedling on Female … Continue reading
• Duration: 24 weeks; outcomes measured included dermascope, ultrasound biomicroscopy, physician, and patient assessments.
• Effective rate at week 2:
  • 55.27% (topical minoxidil)
  • 86.49% (topical minoxidil and oral spironolactone)
  • 95% (topical minoxidil and microneedling)
• Combo therapies (Groups 2&3) outperformed topical minoxidil alone for hair density, shaft diameter, scalp/thickness, shedding, and quality of life; Group 3 showed the greatest benefit.
• Adverse effects were reported across all groups; more menstrual disorders were reported in the spironolactone group. Main limitations: small sample, exclusion of severe cases, possible bias from unblinded treatments.

Hassan et al. (2022)

• Comparative study in 60 women with FPHL: 5% minoxidil topical foam and oral vitamin D3, minoxidil foam only, or vitamin D3 for 12 weeks (plus 15 controls for vitamin D comparison).^[5]Hassan, G.F.R., Sadoma, M.E.T., Elbatsh, M.M., Ibrahim, Z.A. (2022). Treatment with oral vitamin D alone, topical minoxidil, or combination of both in patients with female pattern hair loss: A … Continue reading 
• Primary outcomes: reduction in thin hair count and Ludwig stage improvement via clinical and dermoscopic evaluation. 
• Best results from combination therapy (minoxidil foam and vitamin D3), followed by minoxidil foam alone; vitamin D3 monotherapy had minimal effect.
• Vitamin D3 appeared to enhance minoxidil efficacy, though the sample size was small, and adverse events were not reported. 

Bao et al. (2022)

• RCT with 71 men, split into: 5% topical minoxidil twice daily, electrodynamic microneedling every 3 weeks, or topical minoxidil and microneedling combined.^[6]Bao, L., Zong, H., Fang, S., Zheng, L., Li, Y. (2019). Randomized trial of electrodynamic microneedling combined with 5% minoxidil topical solution for treating androgenetic alopecia in Chinese males … Continue reading
• Follow-up: 24 weeks, with an additional 6-month observation period.
• All treatments increased non-vellus hair density; the combined group had the greatest improvements in hair density and diameter. 
• The combination group received additional scalp massages (potential confounder); 12 participants experienced adverse reactions (dermatitis, dandruff, lymph node enlargement), none severe.

Singh et al. (2020)

• Double-blind, placebo-controlled RCT in 80 men: Groups received either 5% topical minoxidil, 5% topical minoxidil and PRP injections, placebo, or PRP alone.^[7]Singh, S.K., Kumar, V., Rai, T. (2020). Comparison of efficacy of platelet-rich plasma therapy with or without topical 5% minoxidil in male-type baldness: A randomized, double-blind placebo control … Continue reading
• 12 weeks’ treatment with 2-month follow-up; outcome: changes in total, terminal, vellus, and non-vellus hair density, pigmentation, and global assessments.
• Highest hair density and satisfaction with topical minoxidil and PRP; both monotherapies are better than placebo, but the combo was most effective.
• Limitations: short-term follow-up, some subjective outcomes; low adverse event rate (mostly mild, e.g., scalp pruritus, facial hair growth).

Overall, when you look across all of the data, consistent benefits are seen with topical minoxidil usage. However, these results are variable. The key reason for this is differences in sulfotransferase activity. As we mentioned before, minoxidil is a pro-drug, and it needs to be enzymatically activated to exert its effect. We will go into more detail about this below.

What’s Possible ≠ What’s Probable

When evaluating treatment outcomes, especially online minoxidil before and after photos, it’s important to separate possibility from probability. The scattered data points below show the full range of what might occur for individuals, while the central trendline reflects the average outcome (i.e., what typically happens).

Online anecdotes often showcase what we would call “hyper-responders” – people who experience dramatic results. These people may also have higher levels of sulfotransferase activity.

These stories, while real, represent outcomes that are well above average. The issue arises when patients focus only on these peak results and expect the same for themselves. If their own progress seems slower or less dramatic, they may stop prematurely or mistakenly believe the treatment is ineffective.

Dramatic results are often showcased more than modest outcomes because of survivorship bias. This bias occurs when only the most striking successes are noticed or shared, while the many average or less impressive results go unreported.

Why Results Are Variable: The SULT1A1 Enzyme

Minoxidil must be converted into minoxidil sulfate by the sulfotransferase enzyme SULT1A1, which is present in the outer root sheath of hair follicles, to become pharmacologically active and stimulate hair growth. 

Several peer-reviewed studies confirm that the level of SULT1A1 activity in scalp follicles is a key determinant of how well a patient responds to minoxidil therapy.^[9]Goren, A., Castano, J.A., McCoy, J., Bermudez, F., Lotti, T. (2014). Novem enzymatic assay predicts minoxidil response in the treatment of androgenetic alopecia. Dermatologic Therapy. 27(3). 171-173. … Continue reading Enhancing SULT1A1 activity, such as by using enzyme-boosting adjuvants, has been shown in recent trials to convert a majority of prior non-responders into responders, further confirming the mechanistic role of this enzyme.^[10]Chandrashekar, B.S., Chandu, M., Shenoy, C., Chander, A., Roopa, M.S. (2024). SULT1A1 enzyme booster to amplify topical minoxidil response in androgenic alopecia: a single-center prospective study. … Continue reading 

This enzyme-based variability explains why two people can apply minoxidil in the same way but see very different outcomes, and why more than half of users may see only limited or no benefit despite consistent application.

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Fixing the Enzymatic Problem

A number of evidence-based strategies exist to improve minoxidil response. These include microneeding, retinoic acid co-application, formulation changes, consistency, and combination therapy.

Microneedling

Multiple systematic reviews and clinical trials confirm microneedling significantly improves minoxidil efficacy. A 2023 meta-analysis showed that combining the two led to a significantly greater increase in hair count compared to minoxidil alone, regardless of needle depth or device used. Hair count improvements are notable after 12 to 24 weeks of combined treatment.^[11]Ahmed, K.M.A., Kozaa, Y.A., Abuawwad, M.T., Al-Najdawi, A.I., Mahmoud, Y.W., Ahmed, A.M., Taha, M.J.J., Fadhli, T., Giannopoulou, A. (2025). Evaluating the efficacy and safety of combined … Continue reading 

You can read more about how microneedling improves minoxidil efficacy here.

Retinoic Acid (Tretinoin)

Topical tretinoin has been shown in peer-reviewed studies to upregulate follicular SULT1A1, thereby enhancing the conversion of minoxidil to its active form. In a 2019 study, tretinoin not only improved clinical response in difficult cases but also increased scalp SULT1A1 activity, supporting its role as a mechanistic booster.^[12]Sharma, A., Goren, A., Dhurat, R., Agrawal, S., Sinclair, R., Trueb, R.M., Vano-Galvan, S., Chen, G., Tan, Y., Kovacevic, M. (2019). Tretinoin enhances minoxidil response in androgenetic alopecia … Continue reading

You can see the benefits of adding retinoic acid in our Compare Treatments graph below.

Learn more about retinoic acid and its effects on sulfotransferase here.

Formulation Adjustments (Foam vs. Solution 2% vs. 5%)

Clinical research shows that 5% minoxidil is more effective than 2% for both men and women. Foam is as effective as a solution but better tolerated, with reduced risk of contact dermatitis due to the absence of propylene glycol. Some evidence suggests liquid formulations might yield slightly higher absorption, but both forms are clinically comparable.^[13]Purnak, T., Senel, E., Sahin, C. (2011). Liquid formulation of minoxidil versus its foam formulation. Indian Journal of Dermatology. 56(4). 462. Available at: https://doi.org/10.4103/0019-5154.84714 

Consistency and Adherence

Missed doses can reduce topical minoxidil efficacy. Some clinical guidance suggests that missing minoxidil applications even once per week can diminish results, and consistent, daily use is necessary to achieve and maintain hair regrowth.^[14]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 

Combination Therapy

Combining minoxidil with finasteride/dutasteride, PRP, low-level laser therapy (LLLT), or, in resistant cases, oral minoxidil, provides superior results versus monotherapy. Meta-analyses and randomized trials consistently find greater improvement in hair density, count, and patient satisfaction when using combination regimens.^[15]Xia, Y., Chen, H., Chen, Y., Chen, Z. (2025). Relative efficacy of minoxidil in combination with other treatments for androgenic alopecia: a network meta-analysis based on randomized controlled … Continue reading 

So, what do online topical minoxidil before and after photos look like?

Online Topical Minoxidil Successes

Now that we have discussed how topical minoxidil works, potential regimens, and likely timelines, here are 10 reports published by Reddit users with before and after photos.

Disclaimer: The stories below are unverified anecdotes. Consequently, they illustrate individual outcomes and should not be construed as clinical proof or medical advice.

Case 1: Male (age unknown), 6 months on topical minoxidil monotherapy (5% once daily)

This individual applied 5% topical minoxidil once daily for six months. They chose topical minoxidil out of a general preference for avoiding oral medications. From the before-and-after photos, diffuse thinning can be observed from the center of the crown, and the protocol yielded a noticeable increase in crown density by month six. No side effects or early shedding have been reported.

Case 2: Female (age unknown), about 5 months on topical minoxidil monotherapy (5% once nightly)

This user applied 5% topical minoxidil once nightly for about 5 months, using a liquid solution that she purchased over the counter after a telemedicine consult. She stated that she had AGA and did not note any other treatment. Based on both her comments and photos, she experienced marked improvement in hair density and coverage, stating that minoxidil “saved her hair” and that she wishes she had started earlier. She did not describe any notable early shedding, but noted dry scalp and some dandruff as potential side effects.

Case 3: Male (age unknown), 60 days on topical minoxidil monotherapy (5% foam nightly)

This Redditor applied 5% minoxidil foam once nightly before bed for two months without any concurrent treatment. He reports the typical amount applied daily as “one cap-full”, rinsed out the next morning. The user has Crohn’s disease with prior nutrient absorption issues, and chose to avoid ifnasteride due to side-effect concerns. He had about one year of noticeable thinning before starting. Upon starting minoxidil, shedding increased for the first two weeks, then eased. The first measurable improvement was visible by day 30, with clear density gains at day 60. The crown region improved the fastest, while hairline changes were slower.

Case 4: Female (age unknown), 1 year 5 months on topical minoxidil foam (5% once daily)

This user had AGA with prior telogen effluvium, reporting diffuse thinning along the part and temples and a reportedly high daily shedding. She began therapy with Rogaine Men’s Foam 5% once nightly, supported by Ketoconazole 2% shampoo once weekly. At 2 months of treatment, “peach fuzz”/baby hairs were visible at the hairline and temples. At 6 months, there was a noticeable density across the top with new hairs evident but still short. After 1 year and 5 months of therapy, she notes ongoing thickening and widespread new hair growth. She also reported that her shower shed decreased from ~70 hairs to ~10-15, with visual density improving at the part and temples. She reported a mild scalp itch at the start and subtle peach-fuzz on the upper lip and chin as side effects. 

Case 5: Male (age unknown), 2.5 months on topical minoxidil (5% liquid 1 mL twice daily)

This male user, likely with AGA, reported recession at the hairline and thinning at the crown after 2.5 months of using a Rogaine-style 5% liquid at 2 mL/day, without any concurrent DHT blocker. He experienced an early shedding phase ~1 month into treatment, which stabilized with continued use. He exhibited visible thickening at the hairline and crown by 2.5 months of therapy. He did not report any systemic or local side effects and plans to continue minoxidil while considering adding weekly microneedling and/or topical finasteride if progression resumes. 

Other Redditors have used combination treatments to further improve their hair regrowth. As you can see below, some of the results look dramatic.

Case 6: Male (age unknown), 3 months on topical combo (minoxidil 5% and finasteride 0.1% once nightly)

This user had thinning at the hairline and vertex areas of the scalp and began treatment to improve hair density and maintenance. He applied a single compounded solution (Novegrow) containing minoxidil 5% and finasteride 0.1%, once nightly, for three months before reporting on progress. Additionally, he dermarolled his scalp with a 0.5 mm needle twice weekly and supplemented with daily biotin and a multivitamin. He reported mild shedding in the first two weeks of therapy, and by month 3, he noted visible thickening and improved coverage. He did not report any side effects and added that the once-daily schedule was practical and helped with adherence.

Case 7: Male (25), 11 months on combination therapy (finasteride 1 mg daily and topical minoxidil foam 5% once daily)

This Redditor exhibited typical AGA with frontal recession and diffuse vertex thinning. His core regimen is oral finasteride 1 mg daily and minoxidil 5% foam (Kirkland) once daily. He noted he took regular ice/cold baths, ensured an increased water intake, engaged in exercise, avoided junk food, and did not smoke. He saw noticeable thickening from around 6 months after several shedding cycles. By month 11, he experienced substantial cosmetic improvement, with some commenters even comparing the results to transplant-level density. He did not report any adverse effects from finasteride or minoxidil, and subjectively felt less “brain fog” after starting finasteride.

Case 8: Male (37), 4 months on topical minoxidil 5% and topical finasteride 0.1% (1 mL nightly)

This male had crown-predominant thinning with a stable hairline at baseline. His core regimen is a single combined solution containing minoxidil 5% and finasteride 0.1%, applied to the crown only. He did not report any microneedling or supplementation. He reported that shedding began around week 3 and was “heavy” for approximately 4 weeks. The shedding tapered and largely stopped at the 2.5-month mark. By month 4, he achieved visible crown regrowth and thickening compared to the baseline, despite the application being limited to the crown. He perceived an increase in overall density and did not report any side effects.

Case 9: Male (34), about 12 months on topical finasteride 0.3% and minoxidil 6% (twice daily)

This male reported on his progress after using a combination of topical finasteride 0.3% and minoxidil 6% treatment twice daily for nearly one year. He first experienced hair thinning and hairline recession beginning in his late 20s. Alongside the topical treatments, he also applied a dermastamp at approximately 1.5 mm every 10 days. He reported significant shedding during the first two months of treatment along with mild chest tenderness in the first month, which resolved after temporarily halving the topical dose. He reported month-on-month thickening, with clear improvement by months 7-8 and robust density by the one-year mark.

Case 10: Male (22), 90 days on finasteride 1 mg and minoxidil 5% twice daily plus dermarolling

This user with early temple recession began a combination therapy of finasteride 1 mg oral daily, minoxidil 5% foam twice daily, and dermaoll 1.5 mm weekly. He experienced noticeable shedding at weeks 3-6 of therapy, and at the 90-day progress mark, he reported visible filling in of the temple and general thickening of the hair. He did not report any side effects and noted that pushing through the initial shedding phase was crucial to his progress thus far.

Probable Regrowth Timeline

Based on the available evidence, we have mapped out a likely regrowth timeline (although some may experience results faster or later).

Months 0-3: Initial shedding

• Temporary shedding may occur as follicles shift into a new growth phase.
• This usually resolves within the first 4-8 weeks.

Months 3-6: Early cosmetic improvements

• Early visible improvements, such as reduced shedding and appearance of fine new hairs, can be expected.
• Thicker, darker regrowth starts to become apparent for most users during this period.

Months 6-12: Peak cosmetic changes

• Cosmetic changes peak, with stronger hair, increased density, and the greatest coverage observed.
• This is the period of maximum regrowth for most individuals.

Months 12+: Plateau, maintenance, & slight regression

• Further gains plateau, with 5-year studies showing hair counts remaining above baseline –– but with some loss in “peak” results from year one. Continued daily use is needed to maintain improvements, as stopping treatment leads to a gradual reversal within a few months.

Safety and Side Effects

Local side effects are relatively common with topical minoxidil, especially with the liquid formulations. The principal culprits are propylene glycol and ethanol, which frequently cause redness, itching, dryness, and a dandruff-like scaling of the scalp.^[16]Makhlouf, A., Elnawawy, T. (2023). Hair regrowth boosting via minoxidil cubosomes: Formulation development, in vivo hair regrowth evaluation, histopathological examination and confocal laser … Continue reading Patients with sensitive skin are particularly prone to these adverse reactions and may experience contact dermatitis, which can make long-term use uncomfortable.

The foam formulation is generally better tolerated because it lacks propylene glycol. Most clinical trials and user surveys report fewer cases of scalp irritation, itching, or flaking with foam compared to the liquid version.^[17]Purnak, T., Senel, E., Sahin, C. (2011). Liquid formulation of minoxidil versus its foam formulation. Indian Journal of Dermatology. 56(4). 462. Available at: https://doi.org/10.4103/0019-5154.84714 

While systemic absorption of topical minoxidil is rare, some users may experience unwanted side effects such as dizziness and the growth of facial or body hair away from the application site. These effects are more likely if the medication is used excessively or applied to broken or abraded skin, which can increase absorption. We do not recommend using topical products if you have an inflammatory scalp condition – deal with that problem first, and then take a look at topical hair regrowth products.

Overall, when used as directed, topical minoxidil has a strong safety profile, with most side effects limited to mild local irritation.

Practical Takeaways

• Topical minoxidil is effective and well-established, but clinical results vary between individuals.
• Most patients achieve stabilization of hair loss with modest regrowth, though complete restoration is uncommon.
• Response depends partly on scalp sulfotransferase enzyme activity, which explains why some non-responders see little or no improvement.
• Best results come with consistent, long-term use and may be enhanced by adjuncts such as microneedling or topical retinoids to improve absorption and efficacy.

Final Thoughts

When evaluating minoxidil, it is important to recognize it as the most widely accessible and evidence-backed treatment for androgenetic alopecia. While outcomes can vary, most users see stabilization and modest regrowth rather than dramatic reversal. Success depends on realistic expectations, consistent use, and optimized regimens that may include adjunctive therapies. Applying a framework that emphasizes the likely trendline over anecdotal extremes can help you stay committed, avoid discouragement, and make informed decisions grounded in evidence and personal treatment goals.

Oral finasteride remains the most clinically validated medication for androgenic alopecia (AGA). Over 20 years of trials and follow-up data show consistent, predictable outcomes in slowing miniaturization and restoring density, particularly in the vertex and mid-scalp.

Yet, despite this wealth of data, online forums and “miracle” before-and-after photos often distort expectations. These transformations represent the upper end of the response curve, while most users experience more moderate, steady results that unfold over months to years.

This article explores what realistic regrowth looks like with oral finasteride, how to interpret finasteride before and after photos critically, and what to expect when used correctly and consistently. 

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What is Oral Finasteride?

Oral finasteride is a type II 5ɑ-reductase inhibitor that reduces the conversion of testosterone to dihydrotestosterone (DHT), the key androgen responsible for hair follicle miniaturization in AGA. 

Originally approved by the FDA at a dose of 1 mg for male pattern hair loss, oral finasteride has since become widely known as the gold-standard treatment for hair loss. Its primary mechanism is systemic DHT suppression, lowering circulating levels by roughly 60-70% and scalp DHT by up to 65%.^[1]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

Mechanism of Action

As mentioned above, finasteride is a competitive inhibitor of the 5ɑ-reductase enzyme, specifically targeting the type II (and to a lesser extent, type III) isoenzymes.^[2]Zito, P.M., Bistas, K.G., Patel, P., Syed, K. (2024). Finasteride. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing. Available from: https://www.ncbi.nlm.nih.gov/books/NBK513329/

Treatment with finasteride leads to a significant decrease in both scalp and serum DHT concentrations. This effect is dose-dependent and has been observed as early as 28 days after starting treatment.^[3]Dallob, A.L., Sadick, N.S., Unger, W., Lipert, S., Geissler, L.A., Gregoire, S.L., Nguyen, H.H., Moore, E.C., Tanaka, W.K. (1994). The effect of finasteride, a 5 alpha-reductase inhibitor, on scalp … Continue reading Lower DHT levels in the scalp prevent androgen-dependent miniaturization of hair follicles, promoting the maintenance and improvement of hair follicle size and number in the anagen (growth) phase.

Unlike topical formulations, oral finasteride exerts a systemic effect. More comprehensive, but also more likely to cause side effects in sensitive individuals.

Adverse Effects

The most commonly reported adverse effects of oral finasteride are sexual in nature, including decreased libido, erectile dysfunction, and reduced ejaculatory volume. These occur in a range of users depending on the study and determination of what a side effect is (<1% to 25%).^[4]Traish, A.M., Hassani, J., Guay, A.T., Zitzmann, M., Hansen, M.L. (2011). Adverse side effects of 5ɑ-reductase inhibitors therapy: persistent diminished libido and erectile dysfunction and … Continue reading 

Other potential side effects include psychological and neuropsychiatric effects and post-finasteride syndrome (PFS). PFS refers to persistent sexual, neurological, and physical symptoms that continue after stopping finasteride. However, the existence and prevalence of PFS are debated, with some studies suggesting a possible genetic predisposition.^[5]Gupta, A.K., Talukder, M., Keene, S.A., Bamimore, M.A. (2025). Is the safety of finasteride correlated with its route of administration: topical versus oral? A pharmacovigilance study with data from … Continue reading 

You can read in more depth about the potential side effects in our oral finasteride ultimate guide.

Why Expectation Setting Matters

Finasteride is powerful and predictable, but even the best data can get lost when you see incredible results online. Online before-and-after posts tend to showcase outliers, individuals who happen to respond at the extreme high end of the efficacy curve. 

Meanwhile, clinical averages show that:

• Most men stop or reverse their hair loss progression.
• Around 65-80% experience visible thickening after 12-24 months.
• Only a small subset achieves “complete restoration”.

Unrealistic expectations can lead to disappointment, early discontinuation, or cycling through treatments unnecessarily. Grounding expectations in clinical probabilities rather than forum anecdotes helps users stay consistent long enough to see results. 

What’s Possible ≠ What’s Probable

While oral finasteride can produce impressive regrowth, most users experience gradual thickening and stabilization rather than dramatic restoration. 

Treatment outcomes typically follow a distribution pattern:

• A minority are “hyper responders”, achieving rapid and substantial visible improvement.
• The majority notice moderate, progressive gains, such as fuller density or slowed shedding.
• A smaller subset experience arrest of hair loss but remain unsatisfied with new hair growth.^[6]Dhurat, R., Mathapati, S. (2015). Response to Microneedling Treatment in Men with Androgenetic Alopecia Who Failed to Respond to Conventional Therapy. Indian Journal of Dermatology. 60(3). 260-263. … Continue reading 

Factors influencing response:

• Age and duration of hair loss: Finasteride efficacy is higher in younger patients and those with less advanced disease at treatment initiation.^[7]Camacho, F.M., Garcia-Hernandez, M.J., Fernandez-Crehuet, J.L. (2008). Value of hormonal levels in patients with male androgenetic alopecia treated with finasteride: better response in patients under … Continue reading Starting treatment at age 40 or higher is an independent risk factor for insufficient efficacy.^[8]Yoshitake, T., Takeda, A., Ohki, K., Inoue, Y., Yamawaki, T., Otsuka, S., Akimoto, M., Nemoto, M., Shimakura, Y., Sato, A. (2015). Five-year efficacy of finasteride in 801 Japanese men with … Continue reading 

• Consistency: Missing doses or cycling off can interrupt the stabilization of hair loss.

• Adjunct therapies: Combining finasteride with other therapies like topical minoxidil can improve results.^[9]Hu, R., Xu, F., Sheng, Y., Qi, S., Han, Y., Miao, Y., Rui, W., Yang, Q. (2015). Combined treatment with oral finasteride and topical minoxidil in male androgenetic alopecia: a randomized and … Continue reading 
• Genetics: Variations in the androgen receptor (AR) gene sensitivity affect responsiveness.^[10]Keene, S., Goren A. (2011). Therapeutic hotline. Genetic variations in the androgen receptor gene and finasteride response in women with androgenetic alopecia mediated by epigenetics. Dermatologic … Continue reading 

Strong Evidence = Predictable Results

Unlike many newer (and even potentially stronger acting treatments), oral finasteride benefits from decades of standardized data, making outcomes highly predictable. A good example of this is comparing finasteride to dutasteride. Finasteride is extremely well-studied; therefore, we can usually predict the type of results we will see. Dutasteride, on the other hand, has studies showing it can outperform even the likes of finasteride in terms of hair regrowth. But the number of clinical studies is lacking, meaning that it is more difficult to predict a consistent outcome.

This predictability helps clinicians set clear, realistic expectations and provides users with confidence that consistency will lead to steady results.

Real Case Studies: Oral Finasteride Before and After

The examples below help see what’s possible and do not represent what every user should expect. They are purely anecdotal and not independently verified by us or any qualified third party.

Case Summary #1: Male (23), 3 Months on Oral Finasteride 1 mg (then every other day) + Topical Minoxidil Foam (twice daily)

This 23-year-old male took oral finasteride 1 mg daily for 2 months before titrating down to 1 mg every other day due to side effects. He also applied topical minoxidil foam twice daily, initially to the whole scalp but later exclusively to the hairline. He noted an initial shedding phase and early side effects on finasteride in the first month of treatment. In the second month, he described visible thickening while still on 1 mg daily. By month 3, he reduced finasteride to every other day and continued with minoxidil to maintain the progress. He reported marked improvement in hairline and density over the 3 months. 

The user also described early transient effects, including testicular ache (first week), watery semen, heightened libido, and less intense orgasm, which resolved after dialing the finasteride down to every other day. 

Case Summary #2: Male (25), 1-Year Course of Finasteride (1 mg) + Topical Minoxidil (1–2x Daily) + Monthly Dermarolling

This male Redditor started treatment at age 24 after severe crown thinning since he was about 18. His one-year course consisted of finasteride 1 mg daily (generic), topical liquid minoxidil 1–2/day, and dermarolling roughly monthly (post-shower, before nightly minoxidil). He supplemented with vitamin D and occasional biotin, and he regularly used argan oil after showers to limit flaking.

The patient noted a strong early response, but felt his results peaked roughly halfway into treatment. He stopped minoxidil for 1 month and missed some doses in the months leading up to the post. His photos indicated a significant improvement in density compared to baseline, particularly at the hairline and the top. He noted more coverage at the crown but felt it was still noticeably weaker than desired. The patient reported no sexual side effects or skin issues.

Case Summary #3: Male (24), 6 Months on Oral Finasteride 1 mg Daily + Oral Minoxidil 2.5 mg Daily

This 24-year-old male’s intervention consisted of oral finasteride 1 mg once daily and oral minoxidil 2.5 mg once daily. The user noted the emergence of small baby hairs at the hairline and temples at month 2 of treatment. By months 4-5, he reported noticeable thickening, with longer eyelashes and denser eyebrows. By month 6, the user showed clear improvement, as evidenced by his wet-hair photos and day-to-day density. He reported visible density gains at the hairline with better coverage under bright light, with his crown improved from baseline, though not fully closed. He reported no side effects, apart from brief mild erectile difficulty early on that resolved. 

Case Summary #4: Male (25), 3 Months on Oral Finasteride 1 mg Daily + Oral Minoxidil 2.5 mg Daily (added at month 2) + Ketoconazole Shampoo 3x/week + Microneedling 1.5 mm Weekly 

This 24-year-old male’s intervention was oral finasteride 1 mg daily for 3 months, oral minoxidil 2.5 mg daily (added 2 weeks before the 3-month update), ketoconazole shampoo (Nizoral) about three times weekly, and dermaroller 1.5 mm once weekly over the whole scalp.

The user described gradual thickening over the 3-month finasteride course, with minoxidil introduced at month 2.5. He reported a noticeable improvement in density at the hairline and mid-scalp compared with baseline. He described a possible mild libido reduction on finasteride and thinning of the eyebrows thinned on finasteride, which appeared fuller after starting minoxidil. He reported no other significant effects. 

Case Summary #5: Male (38), 7 Months on Oral Finasteride + Topical Finasteride + Topical Minoxidil + Weekly Microneedling

This 38-year-old male started the current treatment with oral finasteride 1 mg daily and topical minoxidil (strength/frequency not specified). He added topical finasteride (concentration not specified) and weekly microneedling at 0.25 mm in month 5. The patient reported a slight but noticeable improvement vs. baseline at month 5 and, at month 7, likewise described his progress as modest. In the 7 months, he achieved stabilization with modest density improvement, most visible anteriorly, with the crown remaining limited. He reported no side effects from finasteride and minoxidil. 

Case Summary #6: Male (28), 10 Years on Oral Finasteride + 4–5 Months on Oral Minoxidil 

This 28-year-old male reported on his 10-year treatment progress on oral finasteride 1 mg daily, before adding oral minoxidil 2.5 mg twice daily 4-5 months before the progress report. He confirmed no dermarolling or topical agent application. The patient reported that, between the ages of 18 and 27, he was on finasteride monotherapy, achieving significant regrowth and strong maintenance. Towards the end of that period, he reported subtle renewed thinning, prompting him to add oral minoxidil. Within 4 months thereafter, his hair density and thickness nearly doubled. 

He reported good tolerance to finasteride with no noticeable side effects. He added that oral minoxidil caused mild generalized hypertrichosis (slightly darker chest/back hair, fuller beard, higher cheek/temple hairs), but was otherwise tolerated. 

Case Summary #7: Male (28), 2–3 Months on Oral Finasteride 1 mg Monotherapy

This 28-year-old male’s intervention included oral finasteride 1 mg daily, weekly microneedling with dermastamp 1.0–1.5 mm, and supplementation with vitamin D3 + K2, zinc, folate, magnesium glycinate, and ketoconazole 2% shampoo. Additionally, he made lifestyle adjustments, including going to the gym 2x/week and starting a higher-protein diet.

He noted a mild shedding phase in the first month of treatment. By month 2, he described the first visible tiny regrowth after a buzz cut, by which point the shedding had reduced. Overall, the patient described early regrowth at the hairline and thinning zones. He reported no side effects on finasteride 1 mg daily, stating that libido and energy have remained unchanged or improved.

Case Summary #8: Male (unspecified age), 3 Years on Oral Finasteride 1 mg Daily + Topical Minoxidil

This male Redditor’s intervention over 3 years was oral finasteride 1 mg daily and topical minoxidil (strength not specified).

In the first year, he noted steady cosmetic improvement, followed by continued thickening and maintenance of gains over years 2-3. Overall, the user reported substantial density gain, with perceived improvement in the hairline and temples over time. He mentioned no significant side effects and confirmed his sex drive had remained unchanged throughout treatment. He noted that the minoxidil sometimes caused dandruff and that on finasteride, he required greater mental focus to push weight-lifting sets to failure. 

Case Summary #9: Male (early 30s), 3.5 Months on Oral Finasteride 1.25 mg Daily

This male, in his early 30s, opted for a treatment consisting of oral finasteride monotherapy at 1.25 mg daily (5 mg tablets quartered). He described a mild daily shedding phase within the first month of treatment. By month 2.5, he reported his first visible thickening. At the 3.5-month progress report, the user achieved a fuller crown with reduced scalp show-through. He reported no side effects. 

Case Summary #10: Male (25), 5.5 Months on Oral Finasteride 1.25 mg Daily + Oral Minoxidil 5 mg Daily

This 25-year-old South Asian male’s intervention was oral finasteride 1.25 mg daily (5 mg tablets quartered) and oral minoxidil, starting at 2.5 mg daily, titrated to 5 mg after 3 months. He described a substantial shedding phase, particularly in the first 3 weeks of month 3. The following month, he reported progressive thickening and density gains with improved coverage. As of month 5.5, he is still improving and continuing both agents unchanged. Overall, he reported a marked increase in density, with a thicker texture, and the crown and hairline both looked fuller than baseline. He reported no side effects on either dose level for finasteride or oral minoxidil. 

Probable Regrowth Timeline

Based on the available research (which you can take a look at with our research tables here), we have created a probable hair regrowth timeline.

Months 0-3: Adjustment Phase

In the first three months, most users experience minimal visible change. Finasteride actively lowers scalp and serum DHT levels, initiating follicle recovery. Some users notice a temporary increase in shedding as older hairs are shed to make way for new growth, while others observe subtle stabilization of hair loss.

Months 3-6: Reduction in Shedding

By this stage, a clear reduction in hair shedding often becomes noticeable. Although visible thickening remains limited for many, the treatment is beginning to normalize hair cycling. Early responders may report small areas of improved density, particularly in the crown or vertex.

Months 6-12: Early Cosmetic Improvements

Between 6 and 12 months, most responders start to see visible regrowth. Hair density gradually improves, strands appear thicker, and areas of thinning begin to fill in. The crown region typically shows improvement sooner than the frontal hairline, which tends to respond more slowly. Continued adherence is essential during this phase to sustain progress.

Months 12-24: Peak Response Period

During the second year, responders generally achieve their maximum results. Hair density, coverage, and stabilization reach their highest levels, with further visible gains possible in some individuals. Those starting with more advanced thinning usually experience consolidation rather than full growth.

Months 24+: Maintenance and Long-Term Stability

After two years, most users reach a plateau in visible improvement. Continued daily use of finasteride is needed to preserve these gains, as stopping the medication often results in gradual hair loss returning to baseline within 6-12 months. Some people combine treatments at this point to achieve further outcomes.

For most users, oral finasteride provides progressive, steady improvements over time, with long-term commitment being the key to maintaining results.

Setting Realistic Expectations

It’s important to set realistic expectations when starting any treatment. Finasteride primarily stabilizes hair loss during the early months, with noticeable growth typically developing later in the treatment course. True cosmetic improvement usually unfolds gradually over 12 to 24 months rather than weeks, reflecting the natural pace of the hair growth cycle. 

Clinical trials suggest that most men experience visible thickening and halting of progression rather than full restoration, effectively “turning back the clock” by two to five years in terms of density and coverage.^[11]Kaufman, K.D., Olson, E.A., Whiting, D., Savin, R., DeVillez, R., Bergfeld, W., Price, V.H., Van Neste, D., Roberts, J.L., Hordinsky, M., Shapiro, J., Binkowitz, B., Gormley, G.J. (1998). Finasteride … Continue reading,^[12]Price, V.H., Roberts, J.L., Hordinsky, M., Olsen, E.A., Savin, R., Bergfeld, W., Fiedler, V., Lucky, A., Whiting, D.A., Pappas, F., Culbertson, J., Kotey, P., Meehan, A., Waldstreicher, J. (2000). … Continue reading,^[13]Rossi, A., Mari, E., Scarno, M., Garelli, V., Maxia, C., Scali, E., Iorio, A., Carlesimo, M. (2012). Comparative effectiveness of finasteride vs Serenoa repens in male androgenetic alopecia: a … Continue reading 

Consistent photographic tracking using identical lighting and angles can help visualize these incremental gains. Long-term adherence is crucial, as discontinuation typically leads to renewed miniaturization and hair loss within several months of stopping treatment.

Practical Takeaways

• Oral finasteride remains the most effective DHT blocker for male AGA
• Decades of clinical data make results highly predictable and durable
• The safety profile is well-established, with sexual side effects uncommon and often reversible
• Combining treatments can improve outcomes, especially for advanced loss.

Final Thoughts

Oral finasteride remains the most extensively studied and clinically validated treatment for androgenic alopecia, offering predictable outcomes for most users through gradual thickening, stabilization of shedding, and preservation of existing hair rather than dramatic restoration. While newer options like oral minoxidil are gaining popularity, they remain off-label despite growing supportive evidence and should be used under medical supervision. 

The key to achieving and maintaining meaningful results lies in consistency, patience, and realistic expectations, recognizing that hair regrowth is a slow, cumulative process measured over months and years. By grounding expectations in clinical evidence rather than anecdotal extremes, patients can make informed, balanced decisions and stay committed to a long-term plan that maximizes both safety and effectiveness.

Can Scalp Tension Cause Hair Loss? It’s Possible.

Is there a connection between scalp tension and pattern hair loss (androgenic alopecia)? Sixty years ago, researchers thought no. Today, many are changing their tune.

The scalp tightness theory recently regained popularity in hair loss forums, but it isn’t new. Over 100 years ago, Bernarr Macfadden noted an association between scalp tightness and androgenic alopecia (AGA) in his book Hair Culture. And in 1950, the scalp tension theory of hair loss even advanced into the academia. For the next decade, androgenic alopecia researchers supported its plausibility.

Then in 1959, everything changed. Most of the scalp tightness theory’s advocates turned from supportive to dismissive… and almost overnight.

What happened? Why did researchers change their minds?

Well, a series of hair transplantation studies were published that contradicted the scalp tightness theory of androgenic alopecia. This led researchers to assess the evidence, reevaluate their opinions, and abandon the scalp tightness theory altogether. For the next forty years, the idea that scalp tension could cause hair loss remained “unrealistic.”

That is, until recently.

In the last five years, new studies have emerged that are forcing researchers to reevaluate the scalp tension-androgenic alopecia hypothesis yet again. These studies not only help build a biological rationale for the scalp tightness hypothesis, but they also present evidence opposing the counterarguments of theory.

So what are these studies? And what’s making researchers waver yet again? This article series explains it all.

This is a three-part series on the scalp tightness theory of hair loss. In this article, we’ll uncover the science behind scalp tension and its potential relationship to pattern hair loss.

In the next article, we’ll dive into the debate over this theory. After all, a few studies from the 50’s and 70’s seemingly contradicted the theory entirely. But now – over forty years later, new evidence is challenging these counterarguments… and bringing the debate back to life again.

In the last article, we’ll try to settle this debate and uncover where scalp tension might come from. Does scalp tightness cause androgenic alopecia? Is scalp tension merely associative with hair loss? And if does cause pattern hair loss… what can we do about it? As always, when it comes to hair loss research, the answers aren’t so cut-and-dry.

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Scalp Tension Theory: The Basics

We’ll soon get into the details of the scalp tension-androgenic alopecia hypothesis. For now, here are the basic principles.

Skin tension tends to restrict blood flow to tissues – much like a bent finger tightens our knuckle and turns it white. Interestingly, research suggests that balding men and women tend to have chronically tighter scalps than those without hair loss.

Across the body, excessive tissue tension can evoke an inflammatory response which, if left unresolved, leads to scar tissue formation. We’ve seen this in stressed periodontal ligaments, the eyelids of patients with Graves’ disease, enlarged prostates, and in the hand tissues of people with Dupuytren’s contracture. The bottom line: more tissue tension, more inflammation, more scar tissue.

As scar tissue settles in, it simultaneously restricts blood, oxygen, and nutrients to tissues. Fascinatingly, the same phenomena and observations – tissue tension, inflammation, reduced blood flow, lower oxygen, and increased scar tissue – are also seen in balding scalps. In fact, we see the onset of these observations in the same pattern and progression as hair loss.

Interestingly, studies on scarring-related diseases – like scleroderma – reveal that once enough scarring settles, hair cannot grow. Putting it all together, this suggests that scalp tension might be involved in the inflammatory cascade which leads to pattern hair loss.

Tension evokes inflammation, inflammation evokes scar tissue, scar tissue restricts oxygen and nutrients to the hair follicles, and this slowly miniaturizes the hair follicles until eventually… we’re left with pattern baldness. Thus, in its most basic form, the scalp tightness-androgenic alopecia theory looks something like this:

Scalp tissue tension >> inflammation >> scar tissue >> pattern hair loss

Does the scalp tension theory differ from our current understanding of androgenic alopecia?

Yes and no. The scalp tightness-hair loss theory fits well in the literature, and of what we already know about androgenic alopecia (or AGA). In fact, it might even enhance our understanding of AGA.

To get a full picture of why, we need to understand…

1. The current model of AGA pathology (what researchers currently believe is the cause of AGA).
2. Questions this AGA model cannot answer
3. How the scalp tension theory answers these questions while still making sense of previous findings in AGA research.

Let’s take these one-by-one.

What Causes AGA? Our Current Understandings

AGA is the world’s most common hair loss disorder – affecting 50% of women and 80% of men throughout a lifetime. And it’s unique because it only affects a certain region: the top part of our scalps.

In men, the hair loss often begins at the temples and vertex. In women, it begins as more globalized (diffuse) thinning. In both genders, the condition is chronic and progressive – meaning that with time and without treatment, it will continue to worsen.

If you’ve ever looked into the causes of AGA, you’ve probably come across the term dihydrotestosterone, or DHT. DHT is a hormone that’s made from testosterone. In fact, most dermatologists will tell you that an interaction of our genetics and DHT is what causes pattern hair loss. Hence the medical name, androgenic alopecia. Andro = androgens; genic = genes; alopecia = hair loss.

So is there any truth to this claim? Yes. There’s an overwhelming amount of evidence that DHT is causally linked to pattern hair loss.

Firstly, studies show that DHT is higher in the scalps of men with thinning hair. Secondly, if a man is castrated, his testosterone (and DHT) levels plummet permanently. Men castrated before puberty (i.e., before their DHT levels spike) don’t go bald later in life. And thirdly, men with a genetic deficiency in an enzyme that converts testosterone into DHT in scalp tissues never develop pattern hair loss.

These are pretty indicting findings. Just look at the endpoints: men who never produce DHT never develop pattern hair loss. Men with higher amounts of DHT in their scalps have AGA. Based on these findings, DHT must play some causal role in AGA.

But beyond that, things start to get complicated…

DHT is causally linked to AGA. But eliminating DHT doesn’t lead to a complete hair recovery

Finasteride is an FDA-approved drug that men use to help fight AGA. It works by reducing DHT levels. In fact, when taken as prescribed, finasteride can reduce scalp DHT levels by over 60%.

But just how effective is it at treating AGA?

Well, clinical studies suggest finasteride improves hair loss outcomes for 80-90% of users. That means it helps slow, stop, or partially reverse hair loss for 80-90% of the people taking it. But just how much hair can we expect to recover?

Over a two-year period, those same studies suggest that finasteride, on average, leads to just a 10% increase in hair count – with hair count plateauing thereafter.

This suggests that finasteride is mostly limited to stopping hair loss progression, rather than reversing the condition entirely. Similar observations were made in castrates. Castration (and thereby near-full DHT reduction) only seems to stop pattern baldness. It doesn’t fully reverse it.

And therein lies the first big “question” of the DHT-hair loss hypothesis.

Question: If DHT causes pattern hair loss, how come eliminating DHT only stops AGA? How come it doesn’t lead to a full hair recovery?

This actually isn’t impossible to answer.

Many researchers have hypothesized that this may be due to DHT’s relationship with scar tissue. In scalp tissues, the arrival of DHT seems to also remodel our scalps – causing increased disorganized collagen crosshatchings. In other words, scalp DHT causes fibrosis (or scarring).

In fact, balding scalp regions have four times the amount of excess collagen deposition (scar tissue) than non-balding regions. And as we’ve learned in scleroderma studies, where there’s scar tissue, hair cannot grow.

DHT >> scar tissue >> hair loss

So maybe the reason why eliminating DHT doesn’t fully reverse hair loss… is simply because stopping DHT only stops the progression of scar tissue. It doesn’t necessarily reverse the scar tissue already present.

This makes sense. In fact, this is the explanation many AGA researchers use to describe why our recovery from AGA is “limited”. But interestingly, this explanation brings up another question that the DHT-hair loss theory has a much harder time answering.

Question: If DHT causes scarring and hair loss in the scalp… why does DHT encourage hair growth in other parts of the body?

Why does DHT encourage hair loss in the scalp… but hair growth in the chest and face?

You may have noticed that a lot of bald men also have incredibly hairy bodies. Well, this is because DHT can have two totally opposite effects on hair. It all depends on its location in the body.

For instance, studies show that while DHT in our scalps appears to encourage hair loss, DHT in body tissues (i.e., facial and chest skin) appears to encourage hair growth.

How can that be? How can DHT encourage hair growth in secondary body and facial hair… while simultaneously encouraging hair loss in our scalps?

Unfortunately, this is something the current DHT-androgenic alopecia pathology model cannot explain. So its supporters chalk it up to genetics – explaining it must be due to gene variants that are associated with more androgen receptors and their co-activators.

There’s some truth to this, but the reality is that nearly every single cell in our body carries the exact same genes. What differentiates a cornea cell from a skin cell is the combined influence of gene programming + a cell’s environment.

This means that “genetics” is sort of a blanket explanation for things we don’t understand. Not only is it the go-to answer for questions that exceed our knowledge base… it also completely undermines the influence of environment – which is often half (or more) of the equation.

In fact, there are several more questions that the DHT-AGA pathology model answers with the idea of “genetics” – but in reality, isn’t as supported by the literature as most tend to believe. Here they are:

Question #1: what causes DHT to increase in balding scalp tissues in the first place?

Question #2: why does DHT encourage hair loss in the scalp… but secondary hair growth in the body and face?

Question #3: why is there a pattern to AGA? Why does it begin at the temples and vertex for most men and generalized thinning for most women?

Question #4: why does AGA only affect the top part of our scalps – in areas that overlie the dense fibrous membrane known as the galea aponeurotica?

So, is it possible to answer these unanswered questions of AGA pathology, and in doing so, create a better model to explain the causes of pattern hair loss… all while not undermining any research demonstrating that DHT is causally linked to AGA?

Potentially. This is where the scalp tension theory of hair loss comes into play.

Scalp Tightness-Pattern Hair Loss Theory: A Deep-Dive

In 2017, I reintroduced the scalp tightness theory in a scholarly paper – particularly in light of new studies that reinforce its role in AGA. The rest of this article will explain the basics of that paper.

The best place to start is to attempt to provide answer those unanswered questions – and beyond “genetics”. Our first question: why does DHT increase in balding scalps?

Question #1: Why does DHT increase in balding scalps?

To get an idea of what might cause DHT to increase in balding scalp tissues, we need to have a bigger picture of what’s going on balding scalp tissues. That means it’s worth cataloguing most of the observations researchers have seen in balding scalps.

We’ve already discussed a few of these – like DHT and scar tissue. But there are many other things happening, too. And if we know what they are, maybe we can begin to parcel out a cause-and-effect relationship between balding scalps and increased DHT.

Here are the big ones from the paper.

Biological. Balding scalps have higher levels of androgen activity – specifically, DHT. And interestingly, balding scalps also express higher amounts of inflammation. We see this in the form of specific signaling proteins and reactive oxygen species (more on this later). These are things that commonly arrive in sites of “stress” – i.e., where the body senses an injury or an infection.

Physiological. Balding scalps have four-fold more disorganized collagen fibers (i.e., scar tissue) than non-balding scalps. And interestingly, the patterning and progression of this scar tissue appears to match the patterning and progression of AGA. In other words, where we see an increase in disorganized collagen cross-hatchings, we also see hair loss. Moreover, we also see that balding scalps have lower blood flow and lower oxygen levels than non-balding tissues – and that in all likelihood, the reduced blood flow occurs outside of our natural hair cycling.

Structural. Several dermatologists and AGA researchers have noted, anecdotally, that balding scalps appear to just “feel” tighter than non-balding scalps. This was also discussed by Dr. Brian Freund – a former university lecturer and hair loss researcher. He mentioned that his male and female patients with AGA almost always had incredibly tight scalps. There’s some evidence that this tension may come from involuntary contractions from our scalp’s perimeter muscles – which would pull the top of the scalp tightly – much like bending a finger pulls the knuckles tight.

Now that we have a better understanding of what’s going on in a balding scalp, we can revisit that initial question:

What causes DHT to increase in balding scalp tissues?

After all, maybe the answer is in one of these observations…

Clue #1: DHT is anti-inflammatory

Beyond its role in sexual maturation, studies also show that DHT can over-express in tissues as a response to inflammation – and that specifically, DHT is anti-inflammatory.

This is incredibly telling, especially in regard to androgenic alopecia research. After all, balding scalps show both increased inflammation and increased DHT. Maybe the inflammation observed in balding scalp tissues is what causes DHT to increase.

However, this opens a new question. If inflammation is what causes DHT to increase in balding scalps… what causes inflammation in the first place?

Reflecting back on our catalogue, there’s at least one possible culprit: chronic tissue tension.

Clue #2: tissue tension can “activate” inflammation and DHT

The relationship between tension, inflammation, and androgen activity isn’t very shocking. In fact, it’s been observed in several other regions. For instance…

1. Inflamed periodontal tissues can signal to increase androgen activity.
2. Men with a tendon-contracting condition known as Dupuytren’s contracture also express more inflammation and male hormones in the affected tissues.
3. Graves’ disease sufferers often have chronic eyelid retraction due to the involuntary contraction of the Mueller muscle). In biopsies, this muscle shows higher markers of inflammation and often androgen activity.
4. Prostate tissues, when exposed to cyclical stretching, induce inflammation and DHT-induced transforming growth factor beta-1 (more on that later).

All of this suggests that in balding scalps, chronic tension may induce the arrival of inflammation and DHT. To put it simply:

Chronic tension >> inflammation >> DHT

Now that we’ve have a potential reason for the “arrival” of DHT, we can ask a harder question:

Why is DHT linked to hair loss in the scalp… but hair growth in other body regions?

Fascinatingly, tension might also help explain this DHT paradox. Here’s how.

Chronic tension and androgens can induce scar tissue

Research shows that DHT behaves differently depending on its location. Specifically, DHT can increase hair loss in the scalp but also increase hair growth in the best and face. This suggests, at a minimum, that a tissue’s location has some sort of influence on the effects of DHT.

So, can tissue tension help us answer this DHT paradox?

Yes.

When DHT in chest and facial tissues, it induces more hair growth. But when DHT is expressed in the scalp – i.e., in tissues under chronic tension – DHT induces the arrival of a signaling protein called transforming growth factor beta 1 (or TGFβ-1).

This is interesting, because DHT doesn’t always appear to induce this signaling protein in tissues that aren’t under added contraction.

However, we do see DHT-induced TGFβ-1 in periodontal tissues, Dupreyene’s contracture, and in benign prostate hyperplasia. And fascinatingly, we also see DHT induce TGFB-1 in balding scalp dermal papilla cells (i.e., the cell clusters that influence the size of our hair follicle).

This signaling protein – TGFβ-1 – is universally condemned across biology as a biomarker for aging, and more specifically, as a prerequisite for the onset of fibrosis (scar tissue).

Studies have shown that wherever TGFβ-1 over-expresses, fibrosis soon follows. And as a reminder, balding scalps have four-fold more disorganized collagen crosshatchings (i.e., fibrosis) than non-balding scalps.

In fact, this scar tissue seems to develop alongside the pattern and progression of AGA. For men, it begins at the temples and vertex… and spreads to the rest of the scalp in accordance with hair follicle miniaturization.

The DHT-hair loss hypothesis suggests that fibrosis might be what limits our ability to regrow hair. But if fibrosis actually causes hair follicle miniaturization, then this would explain why DHT grows hair in the chest and face… but leads to hair loss in the scalp.

So, is there evidence that fibrosis or excess collagen deposition leads to baldness?

Yes.

Excess collagen (or scar tissue) can prevent hair growth

In the medical literature, one defining characteristic of scar tissue (i.e., fibrosis) is the absence of hair. In fibrosis-related disorders (like scleroderma), researchers have consistently observed that as fibrosis sets in, hair loss soon follows – even in the scalp.

And in this article, I lay out a few step-processes behind how fibrosis might contribute to hair follicle miniaturization. The gist is that excess collagen appears to onset outside of normal hair cycling and it seems to progress throughout hair follicle miniaturization – implying that its presence may possibly explain the production of smaller hairs in AGA.

This suggests that in AGA, fibrosis may cause hair loss, and through a few mechanisms: firstly, through the constriction of space for a hair follicle to grow. And secondly, through tissue degradation. Specifically, the restriction of blood, oxygen, and nutrients to the hair follicles.

DHT >> TGFβ-1 >> fibrosis >> reduced blood and oxygen >> hair loss

Taking a step back, DHT’s opposing “behavior” in the scalp versus the body might be explainable through the evidence that…

1. In the presence of chronic tension, DHT induces signaling proteins which lead to scar tissue (and thereby hair follicle miniaturization)
2. In the absence of chronic tension, DHT doesn’t induce these signaling proteins… so it simply encourages hair growth.

This is a subtle difference, but with potentially huge implications in the world of AGA. And we can now add these findings to our revised AGA model.

Chronic tension >> inflammatory response >> DHT >> TGFβ-1 >> fibrosis >> restricted blood flow >> hair follicle miniaturization >> pattern hair loss

However, there’s still one outstanding question… can tension also explain the pattern and progression of AGA? And if so, can it explain the differences in thinning patterns for both men and women?

The evidence points to yes.

Scalp tension may also explain the pattern and progression of AGA

In men with AGA, hair loss often starts at the temples and vertex. And fascinatingly, we also see this same patterning with scalp tension.

There are certain modeling softwares that allow us to estimate the tensile force of any surface – so long as we know the surface area and the direction and magnitude of forces applied to that surface.

In 2015, researchers decided to use a modeling software to map the tensile projections of the tops of male scalps. The forces applied to that surface? The contractions of the scalp perimeter muscles – the same chronic contractions noted by Dr. Brian Freund and other AGA researchers.

The findings? A near-perfect correlation between scalp tension peaks, the patterning of AGA, and the progression of male pattern hair loss. For a graphic reference…

(source)

Since scar tissue also onsets in the pattern and progression of male AGA – this perfectly aligns with the idea that scalp tension might be the beginning of the hair loss cascade.

But what about women?

Unlike most men, most women don’t start thinning at the temples or vertex. Rather, they tend to lose hair in a diffuse pattern.

And what about hair loss that occurs in advanced stages of AGA – like hair loss we see at the nape of the neck, or behind the ears? Could tension also explain this?

Preliminary research points to yes.

In fact, other investigators have used the same modeling software to “play” with these tension projections. What they’ve found is that by making small tweaks head shape, size, and contraction force, it’s possible to create tensile patterns that match the pattern of hair loss we see in women.

In fact, it’s also possible to do the same for more advanced stages of AGA – like hair loss above the ears and at the nape of the neck. One researcher even shared his findings for free – which you can access here.

Where might this scalp tension come from?

This is going to be saved for another article. The short answer is that there are likely three major sources of scalp tension, and each creates a feedback loop with the others:

1. The chronic involuntary contraction of muscles surrounding the perimeter of our scalps. Specifically, the muscles connected to the galea aponeurotica.
2. Skull bone growth and skull suture settlement during and after puberty.
3. Fascia remodeling surrounding the galea and its connected tissue networks.

Tying it all together – genetics, scalp tension, and AGA

This is a lot of information, and as such, it might help to see a visualization of everything above. As such, here’s the flowchart that I presented in my paper:

I know we didn’t cover every aspect on this flowchart. Doing so would’ve made this post twice as long. But I hope you can see the logic progression, and how everything ties together:

Scalp tension >> inflammation >> DHT >> TGFβ-1 >> fibrosis >> restricted blood flow >> hair follicle miniaturization >> pattern hair loss

So if scalp tension is a contributor to AGA… does relieving scalp tension improve AGA outcomes?

Yes.

Dr. Brian Freund demonstrated that in AGA sufferers, botox injections to relieve tension in chronically contracted scalp muscles increased hair counts by 18%. And this year, a new study confirmed Dr. Freund’s original findings. Finally, tension offloading devices also appear to improve hair growth in AGA subjects over 3-12 months periods. So at a minimum, it seems like targeting scalp tension improves hair growth in men and women with AGA.

Does the scalp tightness-hair loss hypothesis fit into all of the literature on AGA?

At face-value, the AGA theory of scalp tension satisfies the questions left unanswered in the current DHT-hair loss pathology model.

1. Why does DHT increase in balding scalp tissues? It increased as part of an inflammatory response, and this inflammation is mediated by skin tension.
2. Why is DHT associated with scalp hair loss and body hair growth? If expressed while under tension, DHT induces the expression of transforming growth factor beta 1, which leads to scarring and thereby hair loss. This tension is present in the scalp, but not in body tissues.
3. Why is there a specific pattern and progression to AGA? This patterning matches the tensile patterning and progression of scalp tissues – with the highest tension points as the first to suffer from hair loss.

But does the scalp tightness-AGA theory make sense of all aspects of AGA research?

Not necessarily.

The reality is that I just presented the entire scalp tension argument to you in a bubble. I didn’t yet  introduce a layer of complexity that, at first glance, could dismantle the theory entirely.

There is a complication to the scalp tightness hypothesis: a compelling counterargument. And it’s a big one. It’s the early findings from hair transplantation studies.

The scalp tension counterargument: hair transplantations

Remember in 1950 – when the scalp tension hypothesis made its way into academia? And in 1959 – how the scalp tightness theory was swiftly abandoned?

This is because that year (and the years following), researchers published several studies on hair transplants which completely changed the trajectory of hair loss research.

These studies sought to confirm if going bald had anything to do with the environment of our scalp tissues. Specifically, things like scalp tension.

To test this question, researchers decided to transplant skin grafts containing healthy hair into balding regions… and take skin grafts containing balding hair and transplant them into other parts of the body.

The findings? If we transplant hair follicles to or from a balding region…

1. Non-thinning hairs moved to balding scalps keep growing normally.
2. Thinning hairs moved to non-thinning regions keep thinning… at the same rate as thinning scalp hairs.

What did this suggest? That our scalp environment has nothing to do with balding.

Otherwise, why would thinning hairs transplanted out of a tense scalp environment keep thinning – even when placed in non-thinning regions? And why would healthy hairs transplanted into a tense environment keep growing – even as the hairs around them continue to thin?

This led researchers to abandon the scalp tension hypothesis, and instead conclude that baldness must be due to genetic programming within the hair follicle itself.

This idea of genetic determinism has been the prevailing theory for the last sixty years… until recently. Now new studies are making us question whether we drew the right conclusions about hair follicle miniaturization all those years ago.

And what are those studies? That’s for the next article.

Scalp Tension Summary

Research shows that balding men and women tend to have tighter scalp tissues than their non-balding counterparts. And interestingly, this scalp tension tends to align with the pattern and progression of AGA.

In men, tension is the highest where hair loss first begins (i.e., the vertex and temples), with skin tension dissipating alongside the “spread” of pattern hair loss. In women, equal tension can be modeled throughout the scalp skin – similar to a diffuse thinning pattern.

When our bodies sense a stressor (i.e., a cut, an impact, or an infection), they evoke an inflammatory response. Interestingly, this is also true for tissues under chronic tension. DHT has been shown to be anti-inflammatory, and when a tissue is under chronic tension, DHT tends to over-express. We’ve seen this in several disease states related to involuntary contractions. Resultantly, chronic scalp tension might not only explain the inflammatory biomarkers we see in balding scalps, but also the arrival of DHT (something the DHT-gene theory of AGA does not satisfactorily answer).

In cases where DHT is activated through tension, we also see DHT induce a signaling protein that causes scarring; specifically, TGFβ-1. This creates excess collagen deposition and scarring (or fibrosis), which then restricts blood, nutrient, and oxygen supplies to the affected tissues.

Interestingly, we see all of the above in balding tissues: increased DHT, increased TGFβ-1, increased fibrosis, lower blood flow, and lower oxygen levels… and in the exact same patterning as AGA.

Studies on scarring-related diseases demonstrate that where scar tissue accumulates, hair does not grow. And evidence suggests that fibrosis in our scalps may precede hair thinning. As fibrosis accumulates, this would cause hair follicle miniaturization through space restrictions alongside tissue degradation (i.e., reduced blood supply). The end-result: hair thinning in the pattern of AGA.

The scalp tension-AGA hypothesis, in my opinion, is the only hypothesis that satisfactorily makes sense of these unanswered questions in AGA research: 1) why does DHT increase in balding scalps, 2) why does DHT encourage hair loss and hair growth depending on its tissue location, and 3) why is there a “pattern” to pattern hair loss?

Unfortunately, hair transplantation studies from fifty years ago led researchers to conclude that our scalp environment – and specifically, scalp tension – have nothing to do with the onset of pattern hair loss. This led to the abandonment of the theory…

Until recently. In the next article, we’ll uncover why.

Note: Regardless of the evidence for or against scalp tension, there are potentially dozens of other factors kickstarting the inflammatory cascade that leads to hair loss. Therefore, scalp tension – if it truly does cause hair thinning – is just a contributor (and not a root cause). Future articles will explain why.

Ketoconazole is a versatile antifungal drug with widespread applications. It is commonly employed to address dandruff issues. It is also utilized off-label as a remedy for hair loss in both men and women, specifically targeting conditions like androgenic alopecia and telogen effluvium that result from an overgrowth of microorganisms on the scalp.

In this guide, we’ll delve into why you might be shedding after using ketoconazole, the difference between normal and abnormal shedding, solutions, and recommendations for those experiencing hair shedding.

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What is Ketoconazole?

If you have been using ketoconazole for 1-3 months and are experiencing shedding, it may be because the scalp is still adjusting (and responding) to new treatments. Therefore, it’s possible that some of your shedding is due to a positive treatment response.

Ketoconazole Side Effect

In less than a decade since its founding, Hims has grown into an internationally recognized brand. With a range of products available in the USA that can boost testosterone, help with weight loss, and tackle issues in the bedroom, Hims is, unsurprisingly, targeted directly at men. In keeping with this approach, they also have a strong selection of products to tackle hair loss and androgenic alopecia (AGA). As a telehealth provider, Hims offers prescription medications alongside shampoos and supplements. 

The brand positions itself as providing highly individualized care: “It’s more than a plan, it’s personal.” Given the diversity of ways in which hair loss can present, and the sometimes unpredictable nature of men’s response to treatment, this approach is often a strong route to a successful regrowth. But how does Hims’ offering stack up? We’ll examine the range of products available through Hims’ telehealth service in the USA, assess the clinical evidence supporting each option, and explore whether the brand can support effective hair loss management.

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Key Takeaways

• Hims offers proven medications like finasteride and minoxidil in convenient formats, which can be effective for many users.
• Hims promises personalization and individualized plans. However, this personalization is mostly limited to a smaller assortment of Rx options than the involvement of their assessment surveys might lead users to believe, with fewer than 5 Rx products for each gender (male and female) from which to choose. 
• The absence of treatment options, escalation routes, and dosing changes makes sustained management more difficult – especially under circumstances where side effect troubleshooting is warranted. While Hims’ Rxproducts surely help boost hair growth, the limits of customization might still mean many of its customers may lack the options needed to resolve side effects, address scalp inflammation, or even further boost hair growth.

What Does Hims Offer?

Hims offers a range of prescription hair loss drugs, as well as over-the-counter products, including 5% minoxidil and anti-dandruff shampoos. The Rx offering features reliable, clinically proven pharmaceuticals delivered in an impressive range of vehicles: oral supplements are available in pills and “chews”, while topical formulations are available as sprays, serum, and foams. 

We’ll take a tour of the product range and see what the Rx catalog offers. Does the science back up the use of the selection to tackle hair loss? And to what extent is it “personal”?

Finasteride (from $22 a month)

Starting off simple, 1 mg a day of finasteride is FDA-approved for the treatment of androgenic AGA in men. There’s a reason finasteride is one of the most popular treatments for hair loss globally. It has been widely studied both for its efficacy in reversing the impact of AGA and for its potential long-term side effects. It’s reliable, widely available, and relatively cheap. 

Finasteride lowers levels of a hormone called dihydrotestosterone (DHT), which is known to be involved in AGA. An enzyme called 5-alpha reductase converts testosterone into DHT, which then binds to androgen receptors in susceptible hair follicles in the scalp. This leads to shortening of the growth phase in hair follicles, resulting in miniaturizing the follicles until they produce thin vellus‑like hairs or none at all.^[1]Makridakis, N., & Reichardt, J. K. V. (2005). Pharmacogenetic analysis of human steroid 5α-reductase type II: comparison of finasteride and dutasteride. *Journal of Molecular Endocrinology.* … Continue reading

Finasteride blocks 5AR, thereby reducing levels of DHT and inhibiting its effect on hair follicles. Clinical studies suggest that dutasteride can reduce serum levels of DHT (levels circulating in the blood) by around 50%.^[2]Olsen, E. A., Hordinsky, M., Whiting, D., Stough, D., Hobbs, S., Ellis, M. L., Wilson, T., Rittmaster, R. S., & Dutasteride Alopecia Research Team. (2006). The importance of dual 5α-reductase … Continue reading Long-term clinical trials have shown that 1 mg finasteride daily stops AGA progression in 80-90% of men and can lead to a 10% increase in hair count on average after two years.^[3]Shapiro, J., & Kaufman, K. D. (2003). Use of finasteride in the treatment of men with androgenetic alopecia (male pattern hair loss). *Journal of Investigative Dermatology Symposium Proceedings.* … Continue reading

Because finasteride is a hormonally active drug, it can cause side effects throughout the body. This can include decreased libido, sexual dysfunction, breast enlargement or tenderness, and issues with mood in some rare cases. Long-term studies suggest that some level of side effects are experienced by between 2.6% and 13.4% of individuals, although these normally stop after treatment is halted.^[4]Olsen, E. A., Hordinsky, M., Whiting, D., Stough, D., Hobbs, S., Ellis, M. L., Wilson, T., Rittmaster, R. S., & Dutasteride Alopecia Research Team. (2006). The importance of dual 5α-reductase … Continue reading, ^[5]Shanshanwal, S. J., & Dhurat, R. S. (2017). Superiority of dutasteride over finasteride in hair regrowth and reversal of miniaturization in men with androgenetic alopecia: a randomized controlled … Continue reading,^[6]Choi, G.-S., Sim, W.-Y., Kang, H., Huh, C. H., Lee, Y. W., Shantakumar, S., Ho, Y.-F., et al. (2022). Long-term effectiveness and safety of dutasteride versus finasteride in patients with male … Continue reading

It’s because of these potentially serious side effects that finasteride is prescription-only and should be taken with medical supervision. 

Outside of their sleek branding, there is nothing unique about Hims’ offering here, and the generic finasteride pill is the same you would receive from any vendor. 

Finasteride & Minoxidil + Supplement Blend (from $35 a month)

Things start getting more interesting when we look at combination therapies. Clinical data and anecdotal evidence from our members’ point to combinations of therapies as potentially powerful routes to address AGA. The impact of multiple drugs targeting different causes of hair loss can be additive and may lead to improved results.^[7]Hu, R., Xu, F., Sheng, Y., Qi, S., Han, Y., Miao, Y., Rui, W., & Yang, Q. (2015). Combined treatment with oral finasteride and topical minoxidil in male androgenetic alopecia: a randomized and … Continue reading

Finasteride with minoxidil is a popular combination. While finasteride works by regulating hormonal causes of AGA, the mechanism of action of minoxidil is less clear-cut. The drug appears to shorten the resting phase in hair follicles, promoting earlier entry into the growth phase.^[8]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

Evidence suggests that minoxidil also increases local blood flow to the follicles, activates the Wnt/β-catenin signaling pathway involved in follicular cell proliferation and differentiation, and may have cytoprotective and anti-inflammatory effects. 

Minoxidil is most commonly applied in topical formulations, while finasteride is typically taken orally. That rule isn’t universal, however, and there is plenty of clinical evidence supporting oral minoxidil and topical finasteride. You can read more about oral minoxidil and topical finasteride in our in-depth articles.

Hims’ combination approaches offer either oral blends or topical blends. This will simplify the production of the drugs, and also help adherence: it’s much easier to take a single pill every day or apply a single lotion than remember to use a combination of both. 

Does Combination Oral Finasteride and Minoxidil Work?

Their finasteride-minoxidil combination includes 1.2 mg finasteride and 3 mg minoxidil, with the option to add a supplemental blend. 

There hasn’t been much research into the impact of the combination of oral finasteride and minoxidil on hair loss. One retrospective study, involving 502 men, found that, after one year of 1 mg finasteride and 2.5 mg minoxidil daily, 92.4% of men were stable or improved, while 57.4% showed overt regrowth. This is a retrospective study with no control group, so we can’t make any comparisons to individual therapies.^[9]Johnson, H., Huang, D., Clift, A. K., Ângela, B. F., & Guimarães, G. A. (2025). Effectiveness of combined oral minoxidil and finasteride in male androgenetic alopecia: a retrospective service … Continue reading

The lack of direct evidence doesn’t mean that this combination won’t be effective, and we know that both therapies are effective independently. What we still lack, however, is long-term safety data on low-dose oral minoxidil.

We’ve discussed the potential side effects of finasteride, and oral minoxidil also raises safety concerns. Unlike topical minoxidil, which is FDA-approved for hair loss, oral formulations can act systemically throughout the body. The most common side effect is hypertrichosis, or unwanted hair growth outside the scalp, including on the face. Other commonly reported side effects include lightheadedness, fluid retention, an elevated heart rate, and headache.^[11]Vañó-Galván, S., Pirmez, R., Hermosa-Gelbard, A., Moreno-Arrones, Ó. M., Saceda-Corralo, D., Rodrigues-Barata, R., Jimenez-Cauhe, J., et al. (2021). Safety of low-dose oral minoxidil for hair … Continue reading

This leads us to a major issue with Hims’ offerings for hair loss. The brand is marketed as highly personalizable, and there is a range of options available to suit your practical needs: do you prefer a pill or a chew, would you rather spray on or apply a topical solution? However, this customization doesn’t stretch to the actual treatment itself. If you find that the oral minoxidil and finasteride combination is causing side effects, there is no route to decrease your concentration or find a safer option. 

Similarly, if you find the plan tolerable or your regrowth plateaus and you want to escalate your treatment, there is no path to do so with Hims. Dutasteride is a very common escalation route from finasteride: it has been shown to better reduce DHT and can lead to better regrowth, but is not available here.^[12]Harcha, W. G., Barboza Martínez, J., Tsai, T.-F., Katsuoka, K., Kawashima, M., Tsuboi, R., Barnes, A., Ferron-Brady, G., & Chetty, D. (2014). A randomized, active- and placebo-controlled study … Continue reading

A one-size-fits-all treatment plan goes against Hims’ stated aim of providing a personalized approach. In the absence of alternatives or proper guidance, many men will simply persevere with their (potentially harmful) treatment or stop treating their hair loss altogether. 

Does the Supplement Blend Help?

Hims’ oral finasteride and minoxidil are available with a supplement including biotin, vitamin B12, vitamin C, resveratrol, and zinc to “support healthy hair”. It’s unlikely that any supplement will have any substantial impact on hair growth compared to the highly active pharmaceutical ingredients. Instead, these ingredients are typically included to improve the condition and appearance of existing hair. 

Biotin is commonly found in supplements and shampoos, but there is limited data to support its use for supporting hair growth. In fact, data supporting the use of biotin for hair loss comes almost exclusively from studies done on children with a biotin deficiency. Because biotin is a component of keratin, it is essential for hair growth. For people who can’t absorb dietary biotin, supplementation can make a real difference. Unfortunately, this only accounts for around 1 in 110,000 people.^[13]Patel, D. P., Swink, S. M., & Castelo-Soccio, L. (2017). A review of the use of biotin for hair loss. *Skin Appendage Disorders.* 3(3). 166–169. Available at: https://doi.org/10.1159/000462981 

Other inclusions, like vitamin B12, vitamin C, and zinc, are also unlikely to provide boosts in growth to anyone without a vitamin deficiency. For Hims customers in the US, the likelihood of deficiencies in these nutrients is highly unlikely. Instead, these ingredients are typically added to increase the value of the average purchase, rather than because of any proven gains.

Rx Hair Loss Spray (from $35 a month)

Hims’ Hair Loss Spray pairs 6% minoxidil with 0.3% finasteride. Topical formulations are often used to avoid some of the more severe, systemic side effects associated with oral pharmaceuticals. Because treatment is localized to the scalp, off-target effects on other organs are minimized.

Topical minoxidil at 6% is higher than the over-the-counter dose of 5%. There is some clinical data suggesting that increased dosing can improve results for some people, though there is diminishing returns at concentrations of 10% and higher, while the risk of side effects such as irritation and unwanted hair growth increases.^[14]Singh, S., Patil, A., Kianfar, N., Waśkiel-Burnat, A., Rudnicka, L., Sinclair, R., & Goldust, M. (2022). Does topical minoxidil at concentrations higher than 5% provide additional clinical … Continue reading, ^[15]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 … Continue reading

Topical finasteride is a relatively recent development and has shown promising results in clinical trials. One study suggested that improvements from 1% topical solution were comparable to 1 mg oral finasteride.^[16]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 … Continue reading 

Given the power of topical minoxidil and finasteride to combat hair loss independently, there has been clinical research into the potential of combined therapies. A meta-analysis, which pools the results from multiple studies to find if results are repeatable, found that the combination was superior to minoxidil alone.^[17]Li, Y., Huang, Q., Zhou, Z., & Zhang, Y. (2025). Comparing minoxidil-finasteride mixed solution with minoxidil solution alone for male androgenetic alopecia: a systematic review and meta-analysis … Continue reading As such, there’s reason to believe that Hims’ Hair Loss Spray can provide meaningful improvements for many users.

Where Does Hims’ Rx Hair Loss Spray Come Up Short?

Unfortunately, we find the same problems with the Hair Loss Spray offering as we did with the tablet and chew. A one-size-fits-all approach doesn’t provide the nuance that is essential to provide effective care. There is no standard, safe dosing regimen for topical finasteride, and one study has shown that aa 0.25% solution can reduce serum DHT by 35%. While this is lower than oral (55%), it does suggest that there is still a risk of side effects.^[18]Piraccini, B. M., Blume-Peytavi, U., Scarci, F., Jansat, J. M., Falqués, M., Otero, R., Tamarit, M. L., et al. (2022). Efficacy and safety of topical finasteride spray solution for male androgenetic … Continue reading

Some users may find that the high concentration used here is not sustainable, but will have no route to try alternatives. Furthermore, Hims’ Hair Loss spray includes propylene glycol, which is unfortunately common in hair growth treatments. Propylene glycol causes irritation in around 7% of users and can add to inflammation in the scalp. This acts to worsen, rather than improve, hair growth outcomes.^[19]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 

Sprays also cause issues for users. Particularly for men who wear their hair longer, sprays are often absorbed by the hair and cannot reach the follicles, where drugs are active. This is also likely to increase the proportion of the drug that does not reach the target areas, thereby increasing systemic absorption and the likelihood of further reductions in serum DHT.

What Else is Missing?

As we’ve noted above, dutasteride is a common route to escalate therapy when finasteride isn’t having the expected impact. Dutasteride can provide stronger DHT reduction, with a similar incidence of side effects.^[20]Shanshanwal, S. J., & Dhurat, R. S. (2017). Superiority of dutasteride over finasteride in hair regrowth and reversal of miniaturization in men with androgenetic alopecia: a randomized controlled … Continue reading,^[21]Choi, G.-S., Sim, W.-Y., Kang, H., Huh, C. H., Lee, Y. W., Shantakumar, S., Ho, Y.-F., et al. (2022). Long-term effectiveness and safety of dutasteride versus finasteride in patients with male … Continue reading. 

In fact, the FDA recently issued a warning for topical finasteride, noting that “Absorption of finasteride through the skin into the bloodstream is expected, and the reports describe adverse events that are consistent with those reported in association with the approved oral finasteride products”.^[22]U.S. Food and Drug Administration. (n.d.). FDA alerts health care providers, compounders, and consumers about potential risks associated with compounded drugs. *FDA.* Available at: … Continue reading This further highlights the need for ongoing physician involvement and expert input.

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There is also no option to include add-ons to help promote the activity of the pharmaceutical components. Tretinoin, for example, can help minoxidil penetrate into the skin and hair follicles, enhancing its activity

Rx Hair Loss Serum (from $35 a month)

Hims’ Hair Loss Serum contains the same ingredients as the Hair Loss Spray, except for the absence of propylene glycol. This would reduce the chances of scalp irritation. It is also applied directly to the scalp, avoiding the issues associated with spray-on topicals. The serum should, therefore, help with adherence and increase the proportion of active ingredients reaching the scalp when compared to the spray.

Where to Find Real Personalization

Unfortunately, the issues found in Hims’ products are systemic in the hair loss industry. Over-standardized dosing, limited escalation paths, and a lack of meaningful medical oversight are widespread and pose a major hurdle for men looking to combat hair loss.

Ulo was launched in response to these issues. Rather than offering fixed, one-size-fits-all protocols, Ulo was designed to give patients and physicians the flexibility needed to manage hair loss as it presents and was built around three core pillars: evidence, personalization, and consumer safety.

At a practical level, this personalization is built-in in several important ways:

• True dosing flexibility
• Ingredient-level customization
• Access to escalation pathways
• Formulations designed for long-term use
• Ongoing physician involvement

Where many brands promise personalization but deliver rigid protocols, Ulo was built to support informed medical decision-making over time.

Final Remarks

Hims offers a broad, accessible entry point into hair loss treatment, with clinically proven medications and tested delivery methods. For many men, these products may slow or stabilize androgenic alopecia, particularly when well tolerated. 

However, beneath the convenience and branding, we find consistent limitations: rigid dosing, limited escalation pathways, high-concentration formulations with unclear long-term safety margins, and a lack of meaningful personalization once side effects or plateaus emerge. These issues are not unique to Hims, but they underscore broader problems in telehealth hair loss care.

Men are becoming increasingly skeptical about hair loss solutions due to the flooding of the market with pseudoscience-backed products that aren’t effective. Keeps is a telehealth brand offering hair loss and sexual health products. According to their website, their main focus is providing customers with access to proven, science-backed hair loss treatments produced using FDA-approved ingredients. They have strong claims about the effectiveness of their products, but what does the research actually say?

In this article, we’ll explore the products offered by Keeps, the science behind their hair loss treatments, whether their claims and recommendations align with current research, and any safety considerations associated with their products. 

Finally, we’ll also discuss certain limitations in treatment options related to personalization. This is a problem less reflective of Keeps in particular, and more reflective of the current state of the telehealth hair care industry. It’s also why, after 10+ years of consumer advocacy, Perfect Hair Health decided to cofound the brand Ulo – a U.S.-based telehealth brand that focuses on hair loss, and also attempts to address core issues that have remained relatively neglected by other brands.

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Key Takeaways

• Convenient and affordable. Keeps’ platform offers access to Rx hair loss medications throughout the U.S., along with online medical appointments to facilitate the prescription process. They also offer these products at mostly-affordable prices.
• Supported by science. The science supports the core treatments offered by Keeps – both finasteride and minoxidil reliably slow hair loss and promote regrowth for many men. Keeps also offers both medications orally and topically, which adds to the convenience and flexibility of their platform.
• Dosing concerns. While Keeps offers a range of product formulations, some active ingredients offered in their Rx topicals – such as finasteride – come at doses so high that they leak into the bloodstream and impact systemic hormones not dissimilarly to oral finasteride. As many users often turn to Rx topicals under the assumption that they’re more localized and cause fewer side effects, these larger doses may warrant revisiting by Keeps – or perhaps a change in messaging around these doses.

What Causes Male Pattern Hair Loss?

Androgenic alopecia (AGA) is the medical name of male pattern hair loss. It involves the progressive miniaturization of hair follicles, a process that is induced by androgen sensitivity and driven predominantly by interactions between genes and the hormone dihydrotestosterone (DHT).^[1]Ho, C.H., Sood, T., Zito, P.M., (2024), Androgenetic Alopecia. Available at: https://www.ncbi.nlm.nih.gov/books/NBK430924/ (Accessed: 07 January 2026) 

DHT is the key androgen driving follicular miniaturization and AGA. The 5-alpha reductase (5AR) enzyme binds to free testosterone and converts it into DHT. DHT then binds to cells via androgen receptors and influences the behavior of those cells. In AGA-sensitive hair follicles, this interaction ultimately results in increased rates of hair shedding, followed by progressive hair follicle miniaturization – both of which tend to worsen without treatment.

What Does Keeps Offer?

Keeps offers a range of treatments for hair loss, with a focus on minoxidil and finasteride. In addition, they offer various other products, including shampoos, a styling product, and supplements. Their Rx offerings include reliable, clinically-proven products delivered in multiple formats, such as sprays, gels, and pills.

We will investigate their product range, exploring what their catalog offers, and examine if the science backs their claims.

Keeps Finasteride (1mg Oral)

Formulations

Keeps offers Finasteride as an oral drug; they do not offer topical finasteride without it being in combination with minoxidil. The oral drug offered contains 1 mg finasteride.

What is Finasteride?

Finasteride is a drug originally created to treat benign prostatitic hyperplasia and now commonly used to treat AGA. It is a prescription drug that has been approved by the FDA for oral use, and is commonly also prescribed off-label for topical use.

How Does Finasteride Work?

Finasteride selectively inhibits type II 5AR, the enzyme that converts testosterone to DHT. As DHT is the primary driver of AGA, blocking its production interrupts the hormonal processes causing pattern hair loss. As such, finasteride helps to maintain existing hair and induce hair regrowth.

Clinical trials have demonstrated that finasteride treatment decreased levels of DHT in the scalp by 64-60%.^[2]Drake, L., Hordinsky, M., Fiedler, V., Swinehart, J., Unger, W.P., Cotterill, P.C., Thiboutot, D.M., Lowe, N., Jacobson, C., Whiting, D., Stieglitz, S., Kraus, S.J., Griffin, E.I., Weiss, D., … Continue reading Finasteride also contributes to anti-cell death effects, in addition to promoting pathways that are important in hair follicle maintenance.

Clinical Effectiveness

Multiple clinical trials have demonstrated the effectiveness of finasteride in improving hair growth. Long-term trials have shown its ability to enhance hair growth and reduce further hair loss across 1-year, 2-year, and 5-year clinical trials. These trials have demonstrated that approximately 65% of men show increased hair counts after 5 years of use.^[3]Finasteride Male Pattern Hair Loss Study Group. (2002). Long-Term (5-Year) Multinational Experience With Finasteride 1 mg in the Treatment of Men With Androgenetic Alopecia. Eur J Dermatol. 12:38-49. … Continue reading,^[4]Shapiro, J., Kaufman, K.D. (2003). Use of Finasteride in the Treatment of Men With Androgenetic Alopecia (Male Pattern Hair Loss). J Investig Dermatol Symp Proc. 8(1):20-23. Available at: … Continue reading

Are There Any Side Effects?

Finasteride works by altering certain hormones; as such, it can cause side effects throughout the body. These include altered libido, erectile dysfunction, breast enlargement, or mood alterations. 

In controlled clinical trials, side effects are uncommon. A meta-analysis (a study where data from multiple independent studies are analyzed) of 15 clinical trials found that only 5.31% of users experienced sexual side effects when taking 1 mg finasteride, whereas these were seen in 3.05% of those taking a sugar pill.^[5]Lee, S., Lee, Y.B., Choe, S.J., Lee, W.S. (2019). Adverse Sexual Effects of Treatment with Finasteride or Dutasteride for Male Androgenetic Alopecia: A Systematic Review and Meta-Analysis. Acta … Continue reading

Although rare, these side effects can seriously impact the lives of those experiencing them, and it is for this reason that finasteride is a prescription-only product that requires medical supervision.

Does the Science Support Keeps’ Claims?

Claim 1: Blocks the production of DHT

Conclusion: True

Finasteride has demonstrated its ability to reduce DHT in multiple clinical trials, in one study showing a 69.4% decrease in DHT in the scalp (although at a higher dose of 5 mg/day).^[6]Drake, L., Hordinsky, M., Fiedler, V., et al., (1999). The Effects of Finasteride on Scalp Skin and Serum Androgen Levels in Men with Androgenetic Alopecia. Journal of the American Academy of … Continue reading

Claim 2: Works on a receding hairline and for overall hair thinning

Conclusion: True, but slightly misleading

While finasteride does “work” on a receding hairline, it often does not move a users’ hairline several inches forward – nor does it regrow hair lost 5-10 years ago. In general, drugs like finasteride typically produce a slowing, stopping, or partial reversal of hair loss in 80-90% of men affected by AGA – along with a 10% increase in terminal hair counts over 2 years. Thereafter, hair gains tend to (mostly) plateau. Without treatment, men with androgenic alopecia tend to lose ~5% hair density per year. So, with this in mind, a good rule-of-thumb is that after starting finasteride, a good responder will typically “rewind the clock” on how their hair looked 6-36 months prior. If significant hairline recession happened before then, it’s unlikely to see significant hairline recovery. For more information, see this video.

Encouragingly, finasteride tends to work in most AGA-affected scalp regions.^[7]Leyden, J., Dunlap, F., Miller, B. (1999). Finasteride in the Treatment of Men with Frontal Male Pattern Hair Loss. Journal of the American Academy of Dermatology. 40(6). 930–937. Available at: … Continue reading Finasteride acts on all androgen-sensitive scalp areas – the frontal, mid-scalp, and vertex – with some evidence that the vertex (crown) may respond more robustly in some men.^[8]Olsen, E.A., Whiting, D.A., Savin, R. (2012). Global Photographic Assessment of Men Aged 18 to 60 Years with Male Pattern Hair Loss Receiving Finasteride 1 mg or Placebo. Journal of the American … Continue reading

Finasteride is effective at improving overall scalp hair thinning.

Claim 3: 90% effective at treating hair loss

Conclusion: True, but requires more context

High-quality, randomized controlled trials (the optimal method of testing claims) have shown that finasteride can slow, stop, or partially reverse hair loss in 80-90% of men with AGA. This has been loosely corroborated by in-clinic, population-level data that acts as a proxy for outcomes of real-world finasteride prescriptions.^[9]Sato, A., Takeda, A. (2011). Evaluation of Efficacy and Safety of Finasteride 1 mg in 3177 Japanese Men with Androgenetic Alopecia. Journal of Dermatology. 39(1). 27–32. Available at: … Continue reading,^[10]Shin, J., Chung, E., Kim, M., Kim, T., Kim, W., Huh, C. (2018). Evaluation of Long-Term Efficacy of Finasteride in Korean Men with Androgenetic Alopecia Using the Basic and Specific Classification … Continue reading

Having said that, the word “effective” needs further unpacking.

Yes, finasteride is “effective” for 80-90% of men with AGA. However, in this case, the term “effective” is in reference to any slowing, stopping, or partial reversal of hair loss over placebo. That means that being effective might mean you see hair regrowth… but it also might mean you just see hair loss stabilization or, in some cases, a slowing down of your prior speed of hair loss.

For everyday consumers looking to get hair loss support, the term “effective” is more likely to be interpreted as “regrows hair”. But in the world of hair loss research – and in the way Keeps refers to “effective” – the term is actually much broader, and includes those who experience both hair loss stabilization and a slowing down of hair loss, even without reversal. This isn’t necessarily a deliberate misapplication of the term! But it is context that we want readers of this article to have when making treatment decisions.

Claim 4: Results within 4-6 months of consistent use

Conclusion: True, but that’s not the whole story. 

Improved hair growth is consistently seen in controlled clinical trials within 6 months of taking finasteride.^[11]Van Neste, D., Fuh, V., Sanchez-Pedreno, P. (2000). Finasteride Increases Anagen Hair in Men with Androgenetic Alopecia. British Journal of Dermatology. 143(4). 804–810. Available at: … Continue reading

However, just as with the term “effective”, we also must look at the term “results” and unpack what this means.

Two-year studies on finasteride show that microscopic hair gains typically present in the first 3 months, with those results first beginning to show cosmetically around month 6 (as the hair grows out). However, results don’t stop at month 6. Instead, they keep improving through months 18-24, at which point, hair improvement plateaus. For more information, see this video.

So, if you don’t see results within the first 6 months, please understand that you have 12-18 remaining months before results officially “peak”. There is still a lot of time!

Keeps Minoxidil Solution (5%)

Formulations

Minoxidil exists in oral and topical forms. The oral form requires a prescription, whereas the topical form can be purchased over the counter.

What is Minoxidil?

Minoxidil was originally developed as an oral drug to treat high blood pressure. However, a side effect of this product was noted to be increased hair growth. This was corroborated in follow-up clinical studies on topical minoxidil, and in 1988, the FDA approved topical minoxidil for male pattern hair loss (AGA).^[12]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

How Does Minoxidil Work?

Minoxidil is thought to stimulate hair growth through a combination of biological mechanisms:

• Local Vasodilation: Minoxidil causes vasodilation, enhancing blood circulation around the hair follicles and delivering more oxygen and nutrients to the follicular environment, creating enhanced conditions for hair growth.^[13]Patel, P., Nessel, T.A., Kumar, D.D. (2023). Minoxidil. StatPearls. Available at: http://www.ncbi.nlm.nih.gov/books/NBK482378/ (Accessed: 04 February 2026)
• Anagen Induction and Telogen Shortening: Minoxidil can induce the anagen phase (growth) and shorten the telogen phase (resting).^[14]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 influencing resting hair follicles to re-enter the growth phase, minoxidil treatment causes increased hair density and thickness.
• Prostaglandin Modulation: Minoxidil is thought to increase the production of prostaglandin E2 (PGE2), promoting hair growth, potentially through providing cytoprotective effects and modulating inflammation within the surrounding follicle environment.^[15]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 Growth-Stimulating … Continue reading

However, it’s still unclear how, exactly, minoxidil regrows hair. If you’re interested in learning more, see this article on 3 hypotheses for how minoxidil works.

Clinical Effectiveness

The effectiveness of minoxidil can be split into response rates (proportion of men for whom minoxidil works) and regrowth rates.

Response rates

Surveys and clinical studies demonstrate that approximately 60% of men show a response to minoxidil (the slowing, stopping, or reversal of hair loss) within 3-6 months of beginning treatment.^[16]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 However, increasing the treatment time up to over 12 months does not show continued improvements. Instead, response rates drop to approximately 30%.^[17]Rietschel, R.L., Duncan, S.H. (1987). Safety and Efficacy of Topical Minoxidil in the Management of Androgenetic Alopecia. Journal of the American Academy of Dermatology. 16(3). 677–685. Available … Continue reading

After the 12-month mark, the rate of discontinuation is approximately 90%, with “low effect” as the leading reason given for stopping.^[18]Shadi, Z. (2023). Compliance to Topical Minoxidil and Reasons for Discontinuation among Patients with Androgenetic Alopecia. Dermatology and Therapy (Heidelberg). 13(5). 1157–1169. Available at: … Continue reading

Regrowth rate

Multiple clinical trials have been carried out to assess the effects of minoxidil on hair growth, with the majority demonstrating measurable regrowth after 4-12 months of use.^[19]Olsen, E.A., Whiting, D., Bergfeld, W. (2007). A Multicenter, Randomized, Placebo-Controlled, Double-Blind Clinical Trial of a Novel Formulation of 5% Minoxidil Topical Foam Versus Placebo in the … Continue reading,^[20]Hasanzadeh, H., Nasrollahi, S.A., Halavati, N., Saberi, M., Firooz, A. (2016). Efficacy and Safety of 5% Minoxidil Topical Foam in Male Pattern Hair Loss Treatment and Patient Satisfaction. Acta … Continue reading^[21]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 The exact level of regrowth varies; however, estimates of regrowth are approximately 50-70% over 12 months. Few trials carry out assessments beyond 12 months. Those assessing longer-term effects see reduced regrowth after 12 months.^[22]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). 688–695. … Continue reading

Does the Science Support Keeps’ Claims?

Claim 1: Increases new hair growth in men with AGA

Conclusion: True

Minoxidil has been shown in multiple clinical trials to have a positive effect on hair growth.

Claim 2: Works at the crown and middle of the head

Conclusion: True, but it can also work at the temples

Evidence from clinical trials has not shown that minoxidil only or primarily works at the crown or middle of the head. This misconception arose due to early important trials specifically focusing on these areas, such as a 2002 trial that recruited men with a blading spot on their crown.^[23]Olsen, E.A., Dunlap, F.E., Funicella, T. (2002). A Randomized Clinical Trial of 5% Topical Minoxidil Versus 2% Topical Minoxidil and Placebo in the Treatment of Androgenetic Alopecia in Men. Journal … Continue reading

More recent trials have demonstrated the effectiveness of minoxidil across the scalp, with no significant differences in effects seen between the frontotemporal and vertex areas.^[24]Kanti, V., Hillmann, K., Kottner, J., Stroux, A., Canfield, D., Blume-Peytavi, U. (2016). Effect of Minoxidil Topical Foam on Frontotemporal and Vertex Androgenetic Alopecia in Men: A 104-Week … Continue reading

Claim 3: Increases hair growth by up to 35%

Conclusion: True, but also unspecific

What does it mean to increase hair growth by up to 35?% This might mean increasing hair length, or hair growth speed, or total hair counts, or vellus hair counts, or terminal hair counts, or hair density including or excluding vellus hairs, or hair diameters.

All in, the term is consumer-friendly, but also unspecific. It implies that users of minoxidil might expect a 35% visual increase in hair on their heads, when this just often isn’t the case. The improvements are often much smaller, much subtler, and shorter-lived relative to finasteride – which tends to sustain results much longer.

Keeps Minoxidil Foam (5%)

The Keeps Minoxidil Foam claims to offer the same benefits as the Minoxidil Solution. It could be assumed that the exact ingredients forming the products are not the same; however, no readily accessible list of ingredients is provided on the website.

Keeps Minoxidil+ Spray

The Minoxidil+ Spray contains additional ingredients aimed at improving minoxidil’s efficacy and supporting hair growth.

Formulation

The Minoxidil+ Spray consists of 5% minoxidil, 0.01% tretinoin, 0.2% caffeine, and 0.1% melatonin.

Clinical Effectiveness

0.01% Tretinoin

Tretinoin (also known as retinoic acid) helps to increase cell turnover in application sites and, resultantly, also helps to improve the penetration and activation of certain hair loss drugs. It has been studied in combination with other hair loss drugs, such as minoxidil.

Tretinoin is thought to increase responsiveness to minoxidil by increasing the activity of the enzyme that converts minoxidil in the body into its active form.^[25]Sharma, A., Goren, A., Dhurat, R. (2019). Tretinoin Enhances Minoxidil Response in Androgenetic Alopecia Patients by Upregulating Follicular Sulfotransferase Enzymes. Dermatologic Therapy. 32(3). … Continue reading Clinical trials have shown that the once-daily application of a combination of 5% minoxidil and 0.01% tretinoin is as effective (and safe) as twice-daily application of 5% minoxidil alone.^[26]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

See our article for a more in-depth look at tretinoin.

0.2% Caffeine

Caffeine is a popular (but less-supported) intervention for hair growth. It acts as a phosphodiesterase inhibitor, which may boost IGF-1 levels near hair follicles (amongst other benefits). As a result, limited research suggests that caffeine may prolong the growth stage of the hair cycle, encourage new hair growth, and reduce hair shedding. For more information, see our article assessing the effectiveness of topical caffeine.

The clinical studies supporting the use of topical caffeine (including in conjunction with minoxidil) are generally positive. However, these studies are not without their methodological flaws. For this reason, caffeine ranks lower in terms of regrowth potential and evidence quality relative to FDA-approved hair loss medications, like minoxidil and finasteride.^[27]Dressler, C., Blumeyer, A., Rosumeck, S., Arayesh, A., Nast, A. (2017). Efficacy of Topical Caffeine in Male Androgenetic Alopecia. Journal der Deutschen Dermatologischen Gesellschaft. 15(7). … Continue reading For more information, see our Treatment Metrics.

For those using caffeine, please consider it an adjuvant to better-supported interventions – and not a replacement. 

0.1% Melatonin

Melatonin is an endogenously-produced hormone that has long been associated with sleep quality. More recently, research suggests this hormone may also have anti-inflammatory effects that may benefit AGA-affected hair follicles.

While the mechanisms for melatonin’s impact on hair loss are not yet fully elucidated, a few clinical studies have shown that it appears to have a positive effect on hair growth and reducing hair loss.^[28]Fischer, T.W., Burmeister, G., Schmidt, H.W., Elsner, P. (2004). Melatonin Increases Anagen Hair Rate in Women with Androgenetic Alopecia or Diffuse Alopecia: Results of a Pilot Randomized Controlled … Continue reading^[29]Fischer, T.W., Trüeb, R.M., Hänggi, G., Innocenti, M., Elsner, P. (2012). Topical Melatonin for Treatment of Androgenetic Alopecia. International Journal of Trichology. 4(4). 236–245. Available … Continue reading

Like caffeine, the research on topical melatonin for hair regrowth is limited. Our summary of the clinical data can be found here.

However, like with all topical ingredients, there must be dosing considerations.

Currently, the only concentration of topical melatonin shown to (1) improve hair parameters and (2) not impact serum melatonin levels is a daily dose equating to 0.1 mg of topical melatonin exposure per day. This can be achieved through a variety of means: 0.0033% x 3  mL daily, 0.005% x 2 mL daily, or even 0.01% x 1 mL daily.

Keeps’ melatonin content is 10x higher than this – and likely exposes users to 1-2 mg per day topically, which likely increases circulating melatonin levels and may come with an increased risk of melatonin-produced side effects. As such, users  may want to keep this in mind and apply the topical only at night – during windows close to bed. Or, they may want to opt for a minoxidil + melatonin combination product that uses lower doses of melatonin that better localize to just the scalp skin. One example would be the combination Rx topicals from Ulo, a telehealth brand we helped to cofound, in part based on these dosing considerations that seemed neglected by other brands:

Interested in Topical Minoxidil?

High-strength topical minoxidil available, if prescribed*

Take the next step in your hair regrowth journey. Get started today with a provider who can prescribe a topical solution tailored for you.

Click Here For 15% Off

*Only available in the U.S. Prescriptions not guaranteed. Restrictions apply. Off-label products are not endorsed by the FDA.

Does the Science Support Keeps’ Claims?

Claim 1: Topical minoxidil improves blood flow to hair follicles to boost hair regrowth by up to 35%

Conclusion: True, but requires a little more context

As discussed above, minoxidil might boost hair counts microscopically by 35% within 4-6 months. However, this rarely results in a 35% visual improvement to hair density – as microscopic hair count changes do not linearly track with cosmetic changes to hair volume. Consumers may want to understand this, especially those who don’t closely follow hair loss research.

Claim 2: Tretinoin gently exfoliates to enhance minoxidil’s efficacy, making for easy once-daily application

Conclusion: Mostly true

Tretinoin has been shown to enhance minoxidil’s efficacy to enable once-daily instead of twice-daily application. This comes through two factors: enhancing (1) skin penetration, and (2) drug activation. The former is a close proxy for exfoliation, and even though that’s not exactly how tretinoin works, the language is more consumer-friendly and mostly within agreement of the science.

Claim 3: Caffeine supports thicker, healthier hair growth and makes thinning hair look thicker

Conclusion: Requires larger, better-designed studies

Preliminary evidence suggests caffeine might improve hair parameters. However, the quality of evidence supporting caffeine remains incredibly low relative to the proven results of minoxidil and finasteride. For this reason, caffeine may be worth exploring as an adjuvant (i.e., addition) to be used alongside better-supported ingredients. Fortunately, Keeps’ topical formulation does this with the inclusion of minoxidil.

Claim 4: Melatonin helps increase hair growth on the scalp

Conclusion: Requires larger, better-designed studies

Studies have demonstrated that melatonin increases hair growth and reduces hair loss. But, like with caffeine, the evidence quality remains low.

Topical Finasteride and Minoxidil Gel

Formulation

Keeps offers this two-in-one prescription topical treatment consisting of 0.25% finasteride and 5% minoxidil.

Clinical Effectiveness

Finasteride and minoxidil function through two separate mechanisms. As such, their combination offers users the opportunity to attack hair loss from two different angles.

Multiple clinical trials have demonstrated the efficacy of combining finasteride with minoxidil, showing that the combined therapy is more effective than minoxidil or finasteride alone.^[30]Suchonwanit, P., Srisuwanwattana, P., Chalermroj, N., Khunkhet, S. (2018). A Randomized, Double-Blind Controlled Study of the Efficacy and Safety of Topical Solution of 0.25% Finasteride Admixed with … Continue reading,^[31]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^[32]Bharadwaj, A.V., Mendiratta, V., Rehan, H.S., Tripathi, S. (2023). Comparative Efficacy of Topical Finasteride (0.25%) in Combination with Minoxidil (5%) Against 5% Minoxidil or 0.25% Finasteride … Continue reading, with a meta-analysis also backing up these findings.^[33]Li, Y., Huang, Q., Zhou, Z., Zhang, Y. (2025). Comparing Minoxidil-Finasteride Mixed Solution with Minoxidil Solution Alone for Male Androgenetic Alopecia: A Systematic Review and Meta-Analysis of … Continue reading

Does the Science Support Keeps’ Claims?

Claim 1: Finasteride stops hair loss by blocking the production of DHT, the hormone responsible for male pattern baldness

Conclusion: True

Studies have shown that the topical application of finasteride also successfully lowers DHT levels in the scalp.^[35]Lee, S.W., Juhasz, M., Mobasher, P., Ekelem, C., Mesinkovska, N.A. (2018). A Systematic Review of Topical Finasteride in the Treatment of Androgenetic Alopecia in Men and Women. Journal of Drugs in … Continue reading

Claim 2: Minoxidil increases blood flow to hair follicles to stimulate hair regrowth

Conclusion: True

Minoxidil has been shown in multiple clinical trials to have a positive effect on hair growth.

Keeps Daily Hair Defense Supplement

Formulation

The Daily Hair Defense Supplement contains saw palmetto, vitamins A, B6, B12, C, D, calcium, selenium, zinc, and biotin.

Clinical Effectiveness

Saw Palmetto

Saw palmetto is a popular hair growth supplement as it does not require a prescription to obtain. But is it actually effective? 

Early studies demonstrated positive results, showing that 60% of men taking 200 mg of saw palmetto experienced some degree of hair regrowth compared to 11% in the control group, although the researchers agreed that more work needed to be done given the small size of the trial.^[36]Prager, N., Bickett, K., French, N., Marcovici, G. (2002). A Randomized, Double-Blind, Placebo-Controlled Trial to Determine the Effectiveness of Botanically Derived Inhibitors of 5-Alpha-Reductase … Continue reading

Saw palmetto is able to reduce DHT, although not to the same degree as finasteride, resulting in reduced effectiveness at inducing hair growth compared to finasteride.^[37]Rossi, A., Mari, E., Scarnò, M. (2012). Comparative Effectiveness of Finasteride vs Serenoa Repens in Male Androgenetic Alopecia: A Two-Year Study. International Journal of Immunopathology and … Continue reading However, hair growth was still seen on saw palmetto supplementation, indicating its potential for use in a supplement.

For more information, see our article on saw palmetto. Or review saw palmetto inside our Ingredient Database.

Vitamins A, B6, B12, C, and D

There is little-to-no convincing clinical evidence that supplementation with Vitamins A, B6, B12, C, and D has any effect on hair growth, although they may have positive effects in cases where people have a severe deficiency.^[38]Cheung, E.J., Sink, J.R., English, J.C. (2016). Vitamin and Mineral Deficiencies in Patients With Telogen Effluvium: A Retrospective Cross-Sectional Study. Journal of Drugs in Dermatology. 15(10). … Continue reading

Calcium

No strong clinical trials have shown any role of calcium in hair growth.^[39]Almohanna, H.M., Ahmed, A.A., Tsatalis, J.P., Tosti, A. (2018). The Role of Vitamins and Minerals in Hair Loss: A Review. Dermatology and Therapy (Heidelberg). 9(1). 51–70. Available at: … Continue reading

Selenium

Both severe selenium deficiency and too much selenium can cause hair loss. A clinical trial in chemotherapy patients receiving a selenium supplement showed reduced hair loss, but no successful clinical trials have been carried out in people representative of the general population (i.e., individuals most likely to buy the Keeps supplements).^[40]Almohanna, H.M., Ahmed, A.A., Tsatalis, J.P., Tosti, A. (2018). The Role of Vitamins and Minerals in Hair Loss: A Review. Dermatology and Therapy (Heidelberg). 9(1). 51–70. Available at: … Continue reading

Biotin

Biotin deficiencies also cause hair loss. However, they have to be extreme – often caused by rare genetic mutations (i.e., biotinidase deficiencies), long-term abuse of alcohol, and/or irritable bowel disease. To date, no high-quality clinical trials have demonstrated any effectiveness for otherwise-healthy people supplementing with biotin to improve androgenic alopecia.^[41]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

Does the Science Support Keeps’ Claims?

Claim 1: The key ingredient, saw palmetto, stabilizes hair loss and promotes healthy hair growth

Conclusion: Potentially misleading

Saw palmetto is thought to support hair growth and reduce hair loss, although not as successfully as finasteride. While short-term (i.e., 6-month) clinical studies have shown that saw palmetto can improve hair loss in those with AGA, and long-term (i.e., 2-year) studies show hair stabilization – the long-term studies did not rely on objective hair counting metrics, such as a phototrichogram. Instead, they relied on visual observations made by the investigators. For these reasons, the evidence supporting long-term stabilization of saw palmetto remains limited. Our personal opinion is that it likely helps, but not nearly as much as more powerful DHT reducers, and its durability long-term remains a subject of debate. For more information, see this article.  

Claim 2: Vitamins A, B6, B12, C, D, Calcium, Selenium, Zinc, and Biotin support overall health, immune function, and vitality

Conclusion: True

These vitamins and minerals do not have any significant effects on hair growth on otherwise-healthy people. But they may contribute to improved overall health by reducing the risk of deficiency.

Problems with Keeps’ Approach: Our Recommendations

Overall, Keeps provides a range of comprehensive and affordable offerings for those with androgenic alopecia – including OTC products and Rx medications. Their range of topical formulations (gels, sprays, serums) also offer several alternatives for those still looking to use topicals, but may need to make adjustments due to having a sensitive scalp and/or longer hair. In our eyes, these are all steps in the right direction. The brand is a positive force in the telehealth haircare space.

Having said that, we also see areas of opportunity for Keeps to improve both personalization and outcomes for consumers. Here are a few:

1. Better Guidance On How To Improve Results

In the world of hair loss treatments, many consumers often quit therapies due to the perception of “no effect”. This often happens because of an educational gap:

1. Consumers don’t often have clear guidance on how long to use products before expecting results. In Keeps’ marketing language on finasteride, there is an emphasis on results occurring within 6 months. While this is often true microscopically and, in some cases, cosmetically – the totality of clinical data on finasteride show that results continue to improve through 18-24 months before plateauing. For this reason, we see an opportunity for Keeps to update their marketing language to specify that, if someone isn’t seeing results in 6 months, that doesn’t mean they’re not getting results. They still have 12-18 more months of progress before being in a fully-informed position to judge. Results will happen sooner for some, and later for others.
2. Consumers don’t often have clear guidance on “escalation” protocols. Non-responders of Keeps’ 5% minoxidil might want to learn that the addition of topical tretinoin might amplify their results and put them in a better position for success. But for those purchasing Keeps’ 5% minoxidil, this escalation protocol isn’t always clearly stated. Similarly, for true non-responders to finasteride – or for those whose goals are to maximize hair gains – oral dutasteride can help achieve this.^[42]Harcha, W. G., Barboza Martínez, J., Tsai, T.-F., Katsuoka, K., Kawashima, M., Tsuboi, R., Barnes, A., Ferron-Brady, G., & Chetty, D. (2014). A randomized, active- and placebo-controlled study … Continue reading This option is also not available with Keeps, limiting the opportunity for effective hair growth. However, at the time of this writing, Keeps does not yet offer oral dutasteride to its customers.

2. More Flexibility With Mega-Dosed Topicals

One of Keeps’ strengths is its flexibility of its topical base formulas – including gel, spray, and serum options. But there remains an area of opportunity to expand this flexibility not just to its base formulas, but also its ingredient doses.

This is especially true with two ingredients that have a high capacity to travel from the scalp into the body and potentiate side effects: namely, finasteride and melatonin.

Finasteride Dosing Concerns

Keeps offers combination topicals (if prescribed) of 5% minoxidil and 0.25% finasteride. Many consumers turn to hair loss topicals because they’re hoping to avoid the systemic effects of drugs. However, what isn’t always communicated to consumers seeking Rx topicals is that high-strength concentrations of finasteride (i.e., 0.25%) are virtually guaranteed to go systemic, and lower blood levels of DHT (our best proxy for systemic absorption) by nearly the same amount as oral finasteride.{{Piraccini, B. M., Blume-Peytavi, U., Scarci, F., Jansat, J. M., Falqués, M., Otero, R., Tamarit, M. L., et al. (2022). Efficacy and safety of topical finasteride spray solution for male androgenetic alopecia: a phase III, randomized, controlled clinical trial. *Journal of the European Academy of Dermatology and Venereology.* 36(2). 286–294. Available at: https://doi.org/10.1111/jdv.17738}}

This issue has been recognized by the FDA, who have recently issued a warning for topical finasteride, stating that “Absorption of finasteride through the skin into the bloodstream is expected, and the reports describe adverse events that are consistent with those reported in association with the approved oral finasteride products”.^[43]U.S. Food and Drug Administration. (n.d.). FDA alerts health care providers, compounders, and consumers about potential risks associated with compounded drugs. *FDA.* Available at: … Continue reading 

Encouragingly, there is a clinical study showing that an ultra low-dose of topical finasteride (0.005% x 2 mL daily) improved hair parameters without affecting serum DHT levels. We discuss the study in this article.

At the time of this writing, Keeps does not offer this ultra-low dose of topical finasteride. They only offer the high-strength topical finasteride. And while an ultra-low dose of topical finasteride does not guarantee zero systemic absorption or complete protection of any side effect, we think the lower-dose is better-aligned with the ethos of why hair loss sufferers pursue topicals in the first place: an attempt to localize a medication’s impact mainly to the scalp.

Melatonin Dosing Concerns

Similarly, Keeps offers an Rx topical containing 0.1% melatonin – which is supported by the clinical literature and may improve hair parameters in those with androgenic alopecia.

However, this dose of melatonin (i.e., 1 mg per mL) has also been shown to raise circulating levels of melatonin throughout the body – with no large, randomized clinical trials to tease out whether these elevated melatonin levels interfere were sleep quality or cause drowsiness.

At the same time, there are studies showing that low-dose topical melatonin (i.e., 0.1 mg per day, or 1/10th the concentration offered by Keeps if applying 1 mL daily) can improve also hair parameters, but without significantly impacting serum melatonin levels. At least for us, the lower concentration of melatonin appears to better-align with the goals of most topical users: to localize a medication’s effects and reduce the potential for side effects. And so we see another area of opportunity for Keeps to revisit the concentration of this ingredient, as well.

For those interested in more customization, more flexible doses of topical finasteride, and lower concentrations of melatonin that better localize to the scalp – we created the telehealth brand, Ulo, to finally offer consumers this level of personalization.

Keeps does a lot of things right, and we’re thrilled that they exist to serve hair loss sufferers. But for those particularly interested in topical localization, side effect mitigation, and an added level of personalization – Ulo was built to fill this large gap in the marketplace. Not only do we offer clear escalation protocols for non-responders to treatments (i.e., topical minoxidil + tretinoin, oral dutasteride, etc.), but we also offer lower-dose topicals that may finally enable those with higher drug sensitivities to finally begin to tolerate (and benefit from) hair growth medications. For these reasons, we’re thrilled to be cofounders of the brand. You can learn more here:

Interested in Topical Finasteride?

Low-dose & full-strength finasteride available, if prescribed*

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*Only available in the U.S. Prescriptions not guaranteed. Restrictions apply. Off-label products are not endorsed by the FDA.

Final Remarks

Keeps offers multiple clinically-backed medications via a range of delivery methods, providing a broad and accessible entry point for hair loss treatments that are proven to work. These treatments have the potential to successfully slow hair loss and increase hair growth in many users.

Even still, there are areas of opportunity where Keeps may want to expand their core offerings for hair loss sufferers. This may include lower-dose finasteride and melatonin topical options that better localize to the scalp. It may also include the addition of oral dutasteride for those looking to unlock bigger hair gains than finasteride.

All in, Keeps enables easier access to clinically-proven hair loss medications via their telehealth model. We hope they consider our above recommendations, and in the interim, we wish them continued success.

Dihydrotestosterone (DHT) is a male hormone, and one of the factors that can cause androgenic alopecia (AGA). Naturally, there are many products on the market that use “DHT-blocking” ingredients and offer a “science-backed” way to improve hair loss through use of their formulation.

DHT-blocking has proven effective in treating hair loss. After all, oral finasteride is an FDA-approved medication for androgenic alopecia, and it blocks DHT by inhibiting the DHT-forming enzyme, 5-α-reductase. 

We are now seeing more haircare products incorporating “DHT-blocking” ingredients into their formulations, including shampoos. These products offer a milder option to FDA-approved medications that can be incorporated into an everyday routine. But do they really work?

With so many options on the market, sorting the science from the marketing can feel daunting. That’s why we’ve researched the evidence behind key shampoo ingredients, from speculative herbal formulas to clinically proven ingredients. In this article, we break down the 10 best DHT-blocking shampoos and assess whether they are worthy hair loss products to incorporate into your routine. 

Ketoconazole Shampoo From our partners at Ulo

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Free gifts included with select multi-month plans while supplies last. Ulo is a partner of Perfect Hair Health; we may earn a commission on purchases. This product is a cosmetic and is not intended to diagnose, treat, cure, or prevent any disease.

What is DHT and DHT-Blocking? 

DHT is an androgen, a hormone that is formed from testosterone by the enzyme 5-ɑ-reductase. It is involved in the growth of facial, underarm, pubic, and body hair. While this might sound great, DHT is also implicated in the development of pattern hair loss. 

The binding of DHT to androgen receptors causes hair follicles to shrink. It shortens their growth phase while also prolonging their non-growing phase. This leads to hair thinning and shorter hair that may fall out or stop growing. 

Those with AGA often have elevated levels of 5-ɑ-reductase, DHT androgen receptors, and DHT itself.^[1]Ustuner, E. T. (2013). Cause of Androgenic Alopecia: Crux of the Matter. Plast Reconstr Surg Glob Open. 1(7). e64. Available at: https://doi.org/10.1097/GOX.0000000000000005,^[2]Sekhavat, H., Bar Yehuda, S., Asotra, S. (2025). Using the Mechanisms of Action Involved in the Pathogenesis of Androgenetic Alopecia to Treat Hair Loss. Int J Mol Sci. 26(21). 10712. Available at: … Continue reading

DHT blockers do what their name suggests – they block DHT. To do this, they often operate in one of two ways, or sometimes a combination of both:

• They inhibit 5-ɑ-reductase, reducing the formation of DHT
• They bind to androgen receptors and block DHT binding

These are not the only ways an ingredient may act to block DHT, but they are the most common.

What Are DHT-Blocking Shampoos?

Elevated DHT is often the primary cause of a balding scalp. So, naturally, there are a plethora of products available that act to block DHT, including DHT-blocking shampoos. These shampoos are formulated with ingredients that have been shown in laboratory research or in human clinical trials to reduce DHT levels.

 

The Problem With DHT-Blocking Shampoos

A DHT-blocking shampoo may appear like a great addition to your daily routine if you are concerned about hair loss. However, shampoos may not be the best option if you have AGA, and there are several factors to consider before purchasing a shampoo that claims to support hair growth. 

Regulation

You’ve probably seen shampoos advertised as “DHT-blocking” or “clinically proven to stop hair loss.” But here’s the truth: there are currently no over-the-counter shampoos that have been clinically proven to lower DHT in humans.

That doesn’t mean the ingredients are useless; it just means the science doesn’t support the marketing claims being made.

Marketing vs. Science

Many hair loss shampoos include ingredients like:

• Saw palmetto
• Green tea extract
• Rosemary oil
• Pumpkin seed extract

Marketers label these as “DHT blockers” because some research suggests these compounds might reduce DHT, but this is where the story gets complicated.

Firstly, laboratory studies are not human studies. Much of the evidence behind these claims comes from petri dish experiments (cells in a lab) or animal models (usually mice).

For example, green tea extract might reduce androgen activity in a dish of cultured cells. But real human scalps are a completely different environment. So if something works in a lab, the safest assumption is actually that it won’t work the same way in people until proven otherwise.

This is why evidence quality is so important, and why we include evidence quality rubrics with every ingredient in our ingredient database.

Delivery Mechanism 

Even when ingredients have been studied in humans, most studies use oral supplements or leave-on topical products.

That matters because oral products circulate throughout your entire body, and leave-on topicals sit on your scalp for 12+ hours. But shampoo remains on the scalp for only 1 to 2 minutes, typically 3 to 4 times per week.

That is usually not enough time for meaningful absorption, and even if some does get in, the dose is likely small. So it’s a big leap to take results from pills or leave-on products and assume the same ingredient will work in a rinse-off shampoo.

For this very reason, we organise our product metrics by formulation at Perfect Hair Health.

Hypothesis vs. Reality

Ketoconazole shampoo is often called the “best DHT-blocking shampoo”. 

Oral ketoconazole can lower male androgens (like DHT), and ketoconazole shampoo has been shown to improve hair outcomes in patients with androgenic alopecia.^[3]Perez, H.B.S. (2004). Ketoconazole as an Adjunct to Finasteride in the Treatment of Androgenetic Alopecia in Men. Medical Hypotheses. 62(1). 112-115. Available at: … Continue reading,^[4]Khandpur, S., Suman, M., Reddy, B.S. (2002). Comparative Efficacy of Various Treatment Regimens for Androgenetic Alopecia in Men. Journal of Dermatology. 29(8). 489-498. Available at: … Continue reading,^[5]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. 2011. 241953. Available at: … Continue reading But we don’t actually know whether ketoconazole shampoo helps hair by lowering scalp DHT. 

It might help hair for completely different reasons, such as reducing scalp inflammation, killing Malassezia yeast, or improving overall scalp health.^[6]Prohic, A., Simic, D., Sadikovic, T.J., Krupalija-Fazlic, M. (2014). Distribution of Malassezia Species on Healthy Human Skin in Bosnia and Herzegovina: Correlation With Body Part, Age and Gender. … Continue reading,^[7]Piérard-Franchimont, C., De Doncker, P., Cauwenbergh, G., Piérard, G.E. (1998). Ketoconazole Shampoo: Effect of Long-Term Use in Androgenic Alopecia. Dermatology. 196(4). 474-477. Available at: … Continue reading

While ketoconazole shampoo appears helpful, its benefit may have little or no relationship to DHT.

The 10 Best DHT-Blocking Shampoos 

When it comes to DHT-blocking shampoos, the claims go far beyond the science. Laboratory studies do not translate to human results; supplements and leave-on products are not the same as rinse-off shampoos; and even the most promising examples are based on hypotheses, not proven evidence.

Considering this, to say that there was a particular brand of DHT-blocking shampoo that is the “best” would be incorrect. Instead, we can consider ingredients that are common to many of these shampoo products. So here, we rank the 10 most common DHT-blocking ingredients in shampoos. We dissect the science, evidence quality, and growth potential behind each of them as hair loss products, so you can decide whether these ingredients in DHT-blocking shampoos really stack up to their marketing claims. 

1. Ulo Ketoconazole Shampoo

Ketoconazole was a medication formulated to treat fungal infections, but it has also been shown to treat hair loss. Ketoconazole can inhibit 5‑α‑reductase activity and could disrupt DHT binding to androgen receptors.^[8]Hugo Perez, B. S. (2004). Ketocazole as an adjunct to finasteride in the treatment of androgenetic alopecia in men. Med Hypotheses. 62(1). 112-115. Available at: … Continue reading

Unlike many of the ingredients on this list, there is clinical evidence of ketoconazole shampoo as a product for hair loss. 

A 1998 trial of 39 participants with androgenic alopecia directed participants to apply 2% kentoconazole for six months. After six months, participants using the ketoconazole shampoo showed an increase in hair diameter, while those using a placebo shampoo showed a decrease. Hair density improvements were similar between those using the ketoconazole shampoo and a 2% minoxidil therapy.^[9]Piérard-Franchimont, C., De Doncker, P., Cauwenbergh, G., Piérard, G. E. (1998). Ketoconazole Shampoo: Effect of Long-Term Use in Androgenic Alopecia. Dermatology. 196(4). 474-477. Available at: … Continue reading

In support of this, a review summarising seven studies using topical ketoconazole concluded that ketoconazole appears to increase hair diameter and result in clinical improvement in those with androgenic alopecia.^[10]Fields, J. R., Vonu, P. M., Monir, R. L., Schoch, J. J. (2020). Topical ketoconazole for the treatment of androgenetic alopecia: A systematic review. Dermatol Ther. 33(1). e13202. Available at: … Continue reading 

Although more trials are needed, and only prescription-grade 2% ketoconazole has shown to improve hair loss, this promising clinical evidence places ketoconazole at the top of the list for DHT-blocking shampoos. 

Our evidence score – 54/100 (shampoo)

Interested in learning more about ketoconazole? Read our article.

Example ketoconazole shampoos:

• Ulo Ketoconazole Shampoo – from $29
• Nizoral Anti‑Dandruff Shampoo 1% Ketoconazole – $15.89
• Minoxidil Max Hair Covet Hair Restoration Shampoo – $40
• Ketoconazole 2% Medicated Shampoo – $12.50 to $47.00 (Prescription)

Ketoconazole Shampoo From our partners at Ulo

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Free full-size gifts with 3-month+ plans No prescription needed

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KetoconazoleSupports a healthy scalp

Free gifts included with select multi-month plans while supplies last. Ulo is a partner of Perfect Hair Health; we may earn a commission on purchases. This product is a cosmetic and is not intended to diagnose, treat, cure, or prevent any disease.

2. Ginseng Root Shampoo

Ginseng root is often derived from the Panax species of plant. Two different extracts of Panax ginseng root have shown to inhibit 5-α-reductase activity by 50% at certain concentrations.^[11]Murata, K., Takeshita, F., Samukawa, K., Tani, T. and Matsuda, H. (2012). Effects of ginseng rhizome and ginsenoside Ro on testosterone 5α-reductase and hair re-growth in testosterone-treated mice. … Continue reading In rats, oral administration of ginseng root has been found to reduce DHT levels, suggesting ginseng maintains its inhibitory activity against 5-α-reductase in vivo (in living organisms).^[12]Park, J. Y., Park, W. Y., Song, G., et al. (2023). Panax ginseng C.A. meyer alleviates benign prostatic hyperplasia while preventing finasteride-induced side effects. Front Pharmacol. 14. Available … Continue reading,^[13]Park, H. K., Kim, S. K., Lee, S. W., et al. (2017). A herbal formula, comprising Panax ginseng and bee-pollen, inhibits development of testosterone-induced benign prostatic hyperplasia in male Wistar … Continue reading

Clinical trials have also shown that oral ingestion of Panax ginseng was found to increase hair density and thickness over 24 weeks in those with androgenic alopecia.^[14]Kim, J.H., Yi, S.M., Choi, J.E. and Son, S.W. (2009). Study of the efficacy of Korean red ginseng in the treatment of androgenic alopecia. Journal of Ginseng Research. 33(3). 223–228. Available at: … Continue reading Notably this has limited applicability to topical application, and the study does not specify whether total hair or just terminal hairs (i.e. those that actually contribute to hair looking cosmetically dense) were included, so results should be taken with a pinch of salt. 

In another trial, Panax ginseng extracts were found to improve hair density and thickness in those with female pattern alopecia when used in combination with 3% minoxidil compared to 3% minoxidil alone.^[15]Ryu, H.J., Yoo, M.G. and Son, S.W. (2014). The efficacy of 3% minoxidil vs. combined 3% minoxidil and Korean red ginseng in treating female pattern alopecia. International Journal of Dermatology. … Continue reading. However, this was again with oral intake, not topical application, and the study appeared to lack a control group to fully validate changes.  

In the laboratory, ginseng extracts have been shown to promote hair growth in human hair follicles.^[16]Park, G. H., Park, K. Y., Cho, H. I., et al. (2015). Red Ginseng Extract Promotes the Hair Growth in Cultured Human Hair Follicles. J Med Food. 18(3). 354-362. Available at: … Continue reading However, for use topically, there is not yet any clinical evidence to indicate whether Panax ginseng is effective at stopping hair loss or supporting hair growth. 

Our evidence score – 8/100 (shampoo)

Example ginseng root shampoos:

• Neofollics Scalp Therapy Exfoliating Shampoo – $32.84
• DS Laboratories REVITA Antioxidant Hair Density CBD Shampoo – $38
• Xyon Health Performance DHT-Blocking Shampoo – $45

3. Ecklonia Cava Shampoo

Also called paddle weed, this is a marine algae found off Japan and Korea. A component of this species, dieckol, has been shown to significantly inhibit 5-ɑ-reductase activity in laboratory tests and reduce DHT levels.^[17]Kang, J. I., Kim, S. C., Kim, M. K., et al. (2012). Effect of Dieckol, a Component of Ecklonia cava, on the Promotion of Hair Growth. Int J Mol Sci. 13(5). 6407-6423. Available at: … Continue reading

In the same study, daily topical application of 0.4% Ecklonia cava for 33 days stimulated active hair growth in the hair follicles of mice.^[19]Kang, J. I., Kim, S. C., Kim, M. K., et al. (2012). Effect of Dieckol, a Component of Ecklonia cava, on the Promotion of Hair Growth. Int J Mol Sci. 13(5). 6407-6423. Available at: … Continue reading Although hair growth was not as substantial as in mice receiving 5% minoxidil, the study shows the potential of topical Ecklonia cava as a natural hair loss ingredient.

However, clinical trials in humans showing the effectiveness of Ecklonia cava as a DHT blocker and hair loss product are unfortunately absent. Until then, Ecklonia cava can only be stated as an effective DHT blocker in vitro (in the test tube).

Our evidence score – 8/100 (shampoo)

Example Ecklonia cava shampoos:

• Zenluca Hair Growth Stimulating Shampoo – €19,95 ($23.38)
• Neofollics Hair Growth Stimulating Shampoo – $32.84

4. Oleanolic Acid Shampoo

Oleanolic acid is a natural compound found in many plants, fruits, and herbs. It is a natural inhibitor of 5-ɑ-reductase. At a 2014 conference, researchers reported that formulations of 3% oleanolic acid were found to inhibit 5-ɑ-reductase by 68% and inactivated 54% of testosterone conversion to DHT.^[20]Ashtiani, H. A., Ehsani, A. H., Brikbin, B., Krimlou, Z., Pouya, F. B. (no date). Effectiveness of the formulation that containing oleanolic acid 3% on inhibition of 5-and#945; reductase activity on … Continue reading

While this report might sound positive, the research has not been submitted for peer review and publication. Thus, the robustness of these findings is questionable. 

There is, however, in vivo evidence to support the DHT-blocking activity of oleanolic acid. In a study using mice, topical oleanolic acid was found to not only promote hair growth but to also reduce the levels of 5-ɑ-reductase and DHT in blood.^[21]Zhang, B., Zhang, W., Luo, J., et al. (2023). Effects of oleanolic acid on hair growth in mouse dorsal skin mediated via regulation of inflammatory cytokines. J Appl Biomed. 21(1). 48-57. Available … Continue reading

Clinical evidence with humans is also available. In a trial examining the effectiveness of a topical hair loss lotion that included oleanolic acid, participants were found to have reduced hair shedding.^[22]Garre Contreras, A., Piquero-Casals, J., Trullas, C., Martinez, G. (2018). Efficacy and Safety of a New Topical Hair Loss-Lotion Containing Oleanolic Acid, Apigenin, Biotinyl Tripeptide-1, … Continue reading Of course, this was a multi-ingredient lotion, so it is hard to attribute this to the effect of oleanolic acid alone. However, this does suggest topical application of oleanolic acid could be promising as a hair loss ingredient, and clinical trials with an oleanolic acid shampoo are warranted.

Our evidence score – 7/100 (shampoo)

Example oleanolic acid shampoos:

• Nourkrin Shampoo – $16.53
• Keeps Thickening Shampoo – $24
• DS Laboratories RADIA Purifying Shampoo for Dry, Sensitive or Irritated Scalp – $32

5. Green Tea Extract Shampoo

Green tea is a very common herbal remedy and has a multifaceted role as a DHT blocker. 

Laboratory studies show that green tea extract can bind androgen receptors, preventing the binding of DHT.^[23]Siddiqui, I. A., Asim, M., Hafeez, B. B., Adhami, V. M., Tarapore, R. S., Mukhtar, H. (2011). Green tea polyphenol EGCG blunts androgen receptor function in prostate cancer. FASEB J. 25(4). … Continue reading This would reduce the downstream impact of DHT-mediated hair loss.

Green tea extract has also been shown to be a 5-ɑ-reductase inhibitor in test tubes. However, when testing whether green tea extract could also inhibit 5-ɑ-reductase within cells, this was found not to be the case.^[24]Hiipakka, R. A., Zhang, H. Z., Dai, W., Dai, Q., Liao, S. (2002). Structure-activity relationships for inhibition of human 5alpha-reductases by polyphenols. Biochem Pharmacol. 63(6). 1165-1176. … Continue reading,^[25]Liao, S. S., Hiipakka, R. A. (1995). Selective-Inhibition of Steroid 5 α-Reductase Isozymes by Tea Epicatechin-3-Gallate and Epigallocatechin-3-Gallate. Biochem Biophys Res Commun. 214(3). 833-838. … Continue reading 

What cell studies do show, however, is that green tea extract can dampen the downstream effects of DHT. In hair follicle cells, green tea extract can protect against DHT-induced death and lack of growth.^[26]Shin, S., Kim, K., Lee, M. J., et al. (2016). Epigallocatechin Gallate-Mediated Alteration of the MicroRNA Expression Profile in 5α-Dihydrotestosterone-Treated Human Dermal Papilla Cells. Ann … Continue reading 

The DHT-blocking mechanisms characterised for green tea appear to translate to in vivo DHT-blocking. Dietary intake of green tea, along with soy compounds, was found to reduce DHT levels in mice. However, intake of green tea alone was found to actually increase DHT.^[27]Zhou, J. R., Yu, L., Zhong, Y., Blackburn, G. L. (2003). Soy Phytochemicals and Tea Bioactive Components Synergistically Inhibit Androgen-Sensitive Human Prostate Tumors in Mice. J Nutr. 133(2). … Continue reading This suggests whole green tea, instead of green tea extract, may not effectively block DHT. 

For now, there is a lack of large, randomized controlled trials to indicate whether green tea extract, whether topical or oral, can effectively block DHT in humans. Thus, in a shampoo, its role is best considered mechanistically possible but not yet proven. 

Our evidence score – 6/100 (shampoo)

Example green tea extract shampoos:

• DrFormulas Best DHT Blocker Shampoo – $20.41
• Keeps Thickening Shampoo – $24
• Neofollics Hair Growth Stimulating Shampoo – $32.84

6. Sulforaphane Shampoo

Sulforaphane is a plant-derived compound known as a phytochemical. It is known for its antioxidant, anti-inflammatory, and even potential anti-cancer properties, and may have a novel mechanism for promoting hair growth as well. 

In the laboratory, sulforaphane has been shown to increase the concentration of an enzyme that can degrade DHT, known as 3α-hydroxysteroid dehydrogenase.^[28]Park, Y., Choi, K., Kim, H., Lee, J., Park, G., Kim, J., (2021). Sulforaphane, L-Menthol, and Dexpanthenol as a Novel Active Cosmetic Ingredient Composition for Relieving Hair Loss Symptoms. … Continue reading

But does this mean it can actually promote hair growth? In the same study, the hair growth potential of sulforaphane as a conditioner in those with androgenic alopecia was examined in an 18-week clinical trial.

The trial found that there was an 87% increase in visual hair growth at the crown and forehead line, and an increase in the number of hair follicles. While this was found to be statistically significant, it should be noted that this only translated to a difference of +2 hairs on average at 18 weeks compared to day one.

To make conclusions about the potential of sulforaphane against hair loss, we need more robust clinical trials. We also need more evidence of its use as a shampoo; the trial above used sulforaphane as a conditioner, where it would have had minimal contact with the scalp compared with a shampoo.

Figure 4: Five images per time point showing the scalp at baseline (0 week) and following use of a sulforaphane conditioner for 6, 12, and 18 weeks. Adapted from Figure 5.^[29]Park, Y., Choi, K., Kim, H., Lee, J., Park, G., Kim, J., (2021). Sulforaphane, L-Menthol, and Dexpanthenol as a Novel Active Cosmetic Ingredient Composition for Relieving Hair Loss Symptoms. … Continue reading. Image obtained in line with the Creative Commons License. 

If you want to learn more about sulforaphane for hair loss, read our article here.

Our evidence score – 4/100 (shampoo)

Currently, there are no sulforaphane shampoos on the market.

7. Melatonin Shampoo

Melatonin is not a traditional DHT blocker. It does not inhibit 5‑α‑reductase or bind with androgen receptors. Instead, melatonin appears to reduce the DNA changes that occur when androgen receptors are activated.^[30]Hao, L., Dong, Y., Zhang, J. J., et al. (2022). Melatonin decreases androgen-sensitive prostate cancer growth by suppressing SENP1 expression. Transl Androl Urol. 11(1). 91-103. Available at: … Continue reading

This has been studied in relation to prostate cancer, but it could also mean that when DHT binds androgen receptors, the receptors are not able to signal DNA changes that may result in hair loss. 

Melatonin has also been shown to reduce androgen levels in cells of the ovary.^[31]Yu, K., Wang, R. X., Li, M. H., et al. (2019). Melatonin Reduces Androgen Production and Upregulates Heme Oxygenase-1 Expression in Granulosa Cells from PCOS Patients with Hypoestrogenia and … Continue reading Although not hair follicle cells, this suggests melatonin could similarly reduce androgens (like DHT) at the scalp. 

Unfortunately, there isn’t any evidence to show that application of melatonin results in reduced blood DHT levels, but topical application of 0.1% melatonin has shown to decrease the rate of active hair loss for patients with early androgenic alopecia. However, not all results were statistically significant.^[32]Fischer, T.W., Burmeister, G., Schmidt, H.W. and Elsner, P. (2004). Melatonin increases anagen hair rate in women with androgenetic alopecia or diffuse alopecia. British Journal of Dermatology. … Continue reading 

A subsequent study analysing the results of five clinical studies using topical melatonin concluded that, overall, melatonin is an effective ingredient for androgenic alopecia. Leave-on, topical melatonin was found to not only be safe but also increase hair density, reduce hair loss, and increase hair strength.^[33]Fischer, T. W., Trüeb, R. M., Hänggi, G., Innocenti, M., Elsner, P. (2012). Topical Melatonin for Treatment of Androgenetic Alopecia. Int J Trichology. 4(4). 236-245. Available at: … Continue reading

Whether a rinse-off melatonin formula could produce similar results is not yet clear, but the topical evidence thus far indicates that melatonin could be a beneficial ingredient for androgenic alopecia.

Our evidence score – 4/100

Example melatonin shampoos:

• As I am Rosemary Shampoo – $9.99
• RevivSerums RevivHair Stimulating Shampoo – $29.00
• Kenogen Hair Growth Shampoo – $59.00 

8. Saw Palmetto Shampoo

Saw palmetto is a plant native to the United States. In the laboratory, extracts of saw palmetto have been found to inhibit the activity of 5‑α‑reductase.^[34]Blair, H. A. (2022). Hexanic Extract of Serenoa repens (Permixon®): A Review in Symptomatic Benign Prostatic Hyperplasia. Drugs Aging. 39(3). 235-243. Available at: … Continue reading,^[35]Buonocore, D., Verri, M., Cattaneo, L., Arnica, S., Ghitti, M., Dossena, M. (2018). Serenoa repens extracts: In vitro study of the 5α-reductase activity in a co-culture model for Benign Prostatic … Continue reading The effectiveness of saw palmetto has also been shown outside the lab. Oral administration of saw palmetto extracts at 320 mg per day has been shown to reduce DHT levels in male participants, confirming that saw palmetto can indeed inhibit 5‑α‑reductase when ingested.^[36]Di Silverio, F., Monti, S., Sciarra, A., et al. (1998). Effects of long-term treatment with Serenoa repens (Permixon®) on the concentrations and regional distribution of androgens and epidermal … Continue reading

In clinical trials, the topical application of saw palmetto for hair loss has received mixed results. Application of saw palmetto as a lotion has shown to marginally increase hair number compared to a placebo lotion after 50 weeks in those with androgenic alopecia.^[37]Morganti, P., Fabrizi, G., James, B., Bruno, C. (1998). Effect of gelatin-cystine and serenoa repens extract on free radicals level and hair growth. Journal of Applied Cosmetology. 16, 57-64. … Continue reading. It has also been observed that androgenic alopecia patients had improved hair strength and slightly thicker hair after application of a saw palmetto oil for 16 weeks.^[38]Sudeep, H.V., Rashmi, S., Jestin, T.V., Richards, A., Gouthamchandra, K., Shyamprasad, K. (2023). Oral and Topical Administration of a Standardized Saw Palmetto Oil Reduces Hair Fall and Improves the … Continue reading 

Based on the evidence, saw palmetto seems a promising natural ingredient for promoting hair growth. But it should be considered that both of the outlined trials appeared to count terminal hairs (i.e., long, thick hairs that contribute to hair fullness) as well as vellus hairs (i.e., fine “peach fuzz” hairs that don’t contribute to hair fullness), and use a leave-on formula, so the results are only tentative and do not justify the purchase of a rinse-off saw palmetto shampoo. 

However, the foundation is there for future clinical studies to build on these results and provide the proof-of-concept evidence needed to determine whether a saw palmetto shampoo can be effective against hair loss.

Our evidence score – 4/100 (shampoo)

Example saw palmetto shampoos:

• DrFormulas Best DHT Blocker Shampoo – $20.41
• Advanced Trichology DHT-Blocking Shampoo – $27.95
• Shapiro MD DHT Fighting Shampoo – $39.95

9. Pumpkin Seed Oil Shampoo

In the laboratory, pumpkin seed oil has been identified as a moderate inhibitor of 5-α-reductase and can interact with androgen receptors, preventing the conversion of testosterone to DHT and the binding of DHT. At 5 mg per mL, pumpkin seed oil could inhibit 5-α-reductase 70-95%.^[39]Heim, S., Seibt, S., Stier, H., Moré, M. I. (2018). Uromedic® Pumpkin Seed Derived Δ7-Sterols, Extract and Oil Inhibit 5α-Reductases and Bind to Androgen Receptor in Vitro. Pharmacol Pharm. 9(6). … Continue reading 

There are no studies demonstrating that pumpkin seed oil reduces DHT levels in humans. Administration of pumpkin seed oil extracts to rats has shown to reduce 5-α-reductase levels, showing that the outcomes of laboratory experiments in vitro are matched in vivo.^[40]Kang, X. C., Chen, T., Zhou, J. L., et al. (2021). Phytosterols in hull-less pumpkin seed oil, rich in ∆7-phytosterols, ameliorate benign prostatic hyperplasia by lowing 5α-reductase and … Continue reading

In a clinical trial of 60 women with androgenic alopecia, topical application of a pumpkin seed oil foam for three months increased the number of regrowing hairs compared to baseline, but not as much as 5% minoxidil. It should be noted that upright growing hairs aren’t the best endpoint for assessing outcomes, since these come and go with the natural hair cycle. Additionally, this study featured no placebo group, so whether these results were substantial against no treatment at all is unknown.^[41]Ibrahim, I. M., Hasan, M. S., Elsabaa, K. I., Elsaie, M. L. (2021). Pumpkin seed oil vs. minoxidil 5% topical foam for the treatment of female pattern hair loss: A randomized comparative trial. J … Continue reading

Nonetheless, the trial suggests topical pumpkin seed oil has the potential to support hair growth, but without further clinical studies, it is simply a marketing ingredient, not a science-backed one.

Our evidence score – 4/100 (shampoo)

Example pumpkin seed oil shampoos:

• BosleyMD Revive Nourishing Shampoo – $21.25
• Roman Revive Shampoo – $24
• Botanical Green Care Saw Palmetto & Cayenne Anti-Hair Loss Shampoo – $36.99

10. Rosemary Oil Shampoo

Rosemary oil is an essential oil and a common ingredient in products marketed towards hair loss. 

In the laboratory, rosemary oil extract has been found to inhibit the activity of 5-ɑ-reductase. Rosemary oil extract has also been shown to potentially prevent the interaction of DHT with androgen receptors, both effects resulting in improved hair growth in mice compared to control.^[42]Murata, K., Noguchi, K., Kondo, M., et al. (2013). Promotion of hair growth by Rosmarinus officinalis leaf extract. Phytother Res PTR. 27(2). 212-217. Available at: https://doi.org/10.1002/ptr.4712

Research is needed to test whether the same effect occurs within humans, although clinical trials with this essential oil do indicate that rosemary oil works similarly within the body.

Namely, a clinical trial with androgenic alopecia patients has shown that rosemary oil can increase hair count by a similar amount to 2% minoxidil following topical application for six months. However, while the results sound great, increases were not substantial in either group compared to baseline hair counts.^[44]Panahi, Y., Taghizadeh, M., Marzony, E. T., & Sahebkar, A. (2015). Rosemary oil vs minoxidil 2% for the treatment of androgenetic alopecia: a randomized comparative trial. Skinmed. 13(1). … Continue reading This would suggest:

• Rosemary oil only marginally improves hair count
• There may be quality issues with the data and conclusions, as minoxidil should significantly and progressively support hair growth over this time frame.

As it stands, there is some evidence to suggest that rosemary oil might have some action on DHT, but further clinical studies are needed to validate these results and indicate whether rosemary oil could be equally as effective when applied as a shampoo. 

Our evidence score – 4/100 (shampoo)

Example rosemary oil shampoos:

• Ulo Thickening Shampoo – $21.75
• Dandrene Exfoliating Anti-Dandruff Shampoo – $32
• Neofollics Scalp Therapy Exfoliating Shampoo – $32.84

Is a DHT-Blocking Shampoo Worth It?

Unlike supplements or leave-on topical products, shampoos have a short contact time with the scalp and are rinsed off quickly. Shampoos are also often used inconsistently. This does not give ample time or enough repeated exposure for ingredients to properly absorb into the scalp and affect hair growth. 

Some DHT-blocking ingredients show promise when used topically. However, there is limited evidence, laboratory or clinical, to show that they would have the same effect in a shampoo, except for ketoconazole. 

DHT-blocking shampoos contain a range of herbal extracts that may help hair look healthier and feel softer. If you find your DHT-blocking shampoo gives your hair a physical appearance boost, feel free to keep using it. However, the evidence for the use of DHT-blocking shampoos in hair loss regimens does not stack up with claims of hair regrowth when used alone. 

If you are interested in DHT-blocking, seek out FDA-approved oral DHT blockers such as finasteride, dutasteride, bicalutamide, flutamide, or spironolactone. If you want a chemical-free formula, find topical lotions, serums, or oils with DHT-blocking ingredients instead of shampoos. Both of these formulations offer longer contact time in and outside the body. 

However, DHT-blocking shampoos could be used alongside FDA-approved hair loss treatments or leave-on products with DHT-blocking ingredients if you choose, just do not rely on these shampoos alone to treat hair loss.

Final Remarks 

When considering a DHT-blocking shampoo, ingredient choice matters more than marketing. Ingredients like ketoconazole have the best evidence behind them to support their use in an anti-hair loss product.

But it’s not just the ingredients that matter, it’s the formulation as well. DHT blockers are more often incorporated into supplements and FDA-approved medications. This allows the ingredients to work from deep inside the body. Shampoos instead rely on repeated, short-term exposure to deliver the ingredients. 

Shampoo exposure like this may influence local DHT levels at the scalp, generally improve the scalp environment, and slow the progression of androgenic alopecia, but it will not act as a re-growth formula, and use of shampoo is unlikely to resolve androgenic alopecia when used alone. 

Finasteride is among the most effective drugs for androgenic alopecia. And while side effects are often overstated, it can lead to reduced libido or lowered sperm counts in some men. For this reason, many choose topical versus oral finasteride, hoping to limit the drug’s DHT-reducing effects to the scalp. But at certain doses, even topical finasteride can become systemic. So, to minimize side effects, which finasteride dosage, formula and application is best? 

In this article, we’ll review 

• About oral versus topical finasteride
• Why topical finasteride can still go systemic
• Why choosing the lowest percentage solution isn’t the only answer
• How to maximize finasteride gains, while minimizing side effects

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About Finasteride 

Finasteride, also known under the brand name Propecia or Proscar, is a prescription medication approved by the FDA for the treatment of androgenic alopecia (AGA). The anti-androgen works by reducing the production of Dihydrotestosterone (DHT), a hormone linked to pattern hair loss. In use since 1992, Finasteride is among the most powerful and well-studied drugs for hair loss.

Oral Finasteride

Oral finasteride stops AGA progression in 80-90% of men and, on average, leads to a 10% increase in hair count over two years.^[1]https://www.sciencedirect.com/science/article/pii/S0022202X15529357 For men wanting a “hands-off” approach to hair maintenance, oral finasteride can be an excellent option. With a once-daily pill, it’s expected that hair loss will stop at approximately 6 months, and thereafter, improve.

However, oral finasteride isn’t for everyone. While the risk of side effects are often overstated online, the drug appears to reduce libido in a certain percentage of men. Oral finasteride can also temporarily lower sperm counts, which might make conception more difficult during its first six months of use. In some men, the use of finasteride appears to increase anxiety and/or depression. While the true incidence and magnitude of these reports are hard to discern, it’s understandable that many are weary of taking this once daily pill.

Fortunately, recent improvements in finasteride’s delivery may mean we no longer need to throw the proverbial baby out with the bathwater.

Topical Finasteride

The biggest reason people seek out topical finasteride (instead of oral finasteride) is because they want to minimize systemic exposure to the drug, and in doing so, localize finasteride’s effects to the scalp.

While research is still in the early stages, evidence suggests that topical finasteride can produce similar levels of hair regrowth compared to oral finasteride, with a significantly reduced incidence of side effects.

Topical finasteride works identically to its oral counterpart: by inhibiting the type II 5-alpha reductase enzyme to reduce DHT. It is designed to target scalp DHT instead of systemic DHT levels.

However, limiting finasteride’s reach to scalp, not serum, DHT is harder than perhaps anticipated. To understand why, let’s take a closer look at scalp versus serum DHT.

Serum vs Scalp DHT 

There’s a lot of evidence that the hormone DHT is directly implicated in androgenic alopecia. In fact, research directly links DHT to all three of AGA’s defining characteristics:

1. Increased telogen:anagen ratio. DHT’s influence on DKK-1 expression increases hair shedding
2. Increased anagen cycling. DHT’s effects on signaling pathways limit the growth phase of hairs 
3. Hair follicle miniaturization. DHT’s effects on dermal papilla sizing thins hair with each cycle 

There are a wide variety of DHT reducers available, including prescription drugs, over-the-counter products, intradermal injections, and even herbal supplements. Finasteride reduces DHT in two ways. 

1. Oral finasteride reduces DHT everywhere in the body. Beyond just the scalp, it reduces DHT in the blood, brain, and prostate. 
2. Topical finasteride attempts to reduce DHT only where it is applied – in the scalp – with minimal effects on DHT levels elsewhere.

However, it’s far easier than most realize for topical finasteride to go systemic. And when it does, it potentially reduces DHT everywhere – leading to the very side effects it’s meant to prevent.

Topical Finasteride Can Still Go Systemic

Why? When it comes to lowering DHT (the goal of the drug), finasteride has a highly-sensitive, dose-dependent response curve. This means that while 0.01 mg of finasteride barely reduces any DHT at all, 0.1 mg reduces almost as much DHT as 5 mg, a much larger dose.

This implies that when applying topical finasteride, only a tiny fraction of it needs to go systemic in order to produce the same DHT-lowering effects as oral finasteride. If this happens, the purpose of using the topical formulation is completely defeated. 

Research suggests a 1% topical finasteride formulation, applied twice daily, is ‘non-inferior,’ meaning equivalent, to 1 mg oral finasteride tablets.^[2]https://www.ncbi.nlm.nih.gov/pubmed/19172031 And while that’s a positive in terms of hair growth, using this amount topically twice daily pretty much guarantees systemic absorption. In other words, if 1% topical is the equivalent of 1 mg oral, we can expect it to reduce serum DHT levels by 71%.

So what if we choose a formula with even lower percentages of the active drug? A study on 0.25% topical finasteride showed just a 35% reduction in serum DHT levels versus 55% for the oral medication, and yet similar outcomes for hair regrowth in both oral and topical groups.^[3]https://onlinelibrary.wiley.com/doi/10.1111/jdv.17738

So what if we go even lower? A study on 0.005% alcohol-based topical finasteride instructed participants to use the formulation twice daily, with 1 mL applied per session.^[4]https://dx.doi.org/10.3109%2F09546639709160517 This led to no appreciable changes in serum DHT levels… meaning that for this ultra-low topical formulation, there was little-to-no systemic absorption (and presumably, few-to-no side effects). The good news? This group still experienced great hair growth outcomes.

So Just Reach for the Lowest Percentage, Yes?

It’s tempting from the above to infer we’ve reached the end of our story. As long as we reach for the lowest percentage of topical finasteride, we can be free from worries about the drug’s systemic effects. But, reality is a bit more complicated than that.

Systemic absorption isn’t just about dilution percentages. Topical finasteride’s systemic absorption actually depends on (at least) for variables:

1. The drug’s formulation. Common carrier agents include alcohol and propylene glycol.
2. The amount applied per use. The amount of topical finasteride applied to the scalp greatly varies.
3. The application frequency. Applying the drug twice per day can more than double its effects on serum DHT. 
4. The days of application. Topical finasteride can take many days to “leak” into the blood before its final effects on serum DHT are realized.

For an example, see this figure from a 2014 study measuring how one versus two applications of 1 mL of 0.25% topical finasteride affected serum DHT levels.^[5]https://www.ncbi.nlm.nih.gov/pubmed/25074865 

Over a 24-hour period, what were the findings?

• One application (i.e., 1 mL of 0.25% topical finasteride) lowered blood DHT levels by ~20%
• Two applications (i.e., 2 mL total) lowered blood DHT levels by ~70%

As such, we need to factor in these variables if we plan on sticking with topical finasteride for the long-term. Otherwise, we risk lowering our DHT levels to the same degree as 1 mg of oral finasteride, which would defeat the purpose of using the topical in the first place.

Topical Finasteride and Serum DHT: What Do The Clinical Studies Say?

Let’s take a closer look at some of the studies mentioned above. In addition to the percentage of active drug in the formula, there are a few more variables to understand. How much of the topical was applied, and which carrier agents were used?

The table below shows how even a .25% formula, for example, can reduce DHT in the serum by 24-70% 

Based on this table, our total mg of daily finasteride exposure is probably the biggest factor in determining systemic leakage. And our total daily exposure (in mg) is a function of topical finasteride dilution (%) and the amount (mL) applied daily.

Knowing this, we can turn this table into a chart and sort it by mg of daily exposure. In doing so, we see a clear trend:

The good news? At both extremes of this chart – 0.091 mg and 2.275 mg daily – topical finasteride was shown to produce clinical results in improving hair parameters. Based on this, if we’re going for topical finasteride, we probably want to be prescribed topical finasteride solutions that net us daily exposure volumes of 0.228 mg and lower. After all, at 0.091 mg of topical finasteride daily, no systemic effects on DHT were observed.^[6]https://www.tandfonline.com/doi/abs/10.3109/09546639709160517

In other words, low dilutions (i.e., 1-2 mL of 0.005% to 0.02% of topical finasteride) confer significant benefits but at reduced risks of side effects due to lower systemic absorption – provided that guidelines for daily amounts (in mL) are also followed.

So What’s the Perfect Amount and Formula?

Our analyses from member-submitted lab tests and the clinical data suggest that 10-15% of topical finasteride will enter the bloodstream, at least when it’s formulated with alcohol and/or propylene glycol as carrier ingredients (as most compounding pharmacies do). So, if we apply 1-2 mL of 0.005% to 0.02% topical finasteride, this might equate to just 0.01-0.03 mg of systemic drug exposure.

For the overwhelming majority of people, that’s not enough systemic leakage to significantly lower DHT levels in the body. But it is enough to produce great hair loss outcomes. 

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Long-story short: stick to 1-2 mL of 0.005% to 0.02% topical finasteride solutions. This equates to roughly 0.1-0.2mg of daily finasteride exposure to the scalp. Any more than that, and there’s risk of significant systemic leakage, which defeats the purpose of using topical finasteride altogether.

How to Maximize Gains and Minimize Side Effects

Maximizing gains while minimizing the side effects of finasteride can be done, but it’s not a perfect science. We’ve outlined several tips below that we think might help. Due to individual variance, the most important step is to always start with testing.

1. Get Lab Tests for DHT

The goal with topical finasteride is to reduce the risk of side effects. To do this, we must minimize the amount of finasteride that leaks into the bloodstream. The best way to do this isn’t to rely on estimated metrics from clinical studies, but to collect personal data.

Get a serum DHT test before using the topical to establish a baseline. Then, DHT levels should be retested at one month to gauge just how much is going systemic. Testing is easier than most expect, and in our experience, the expenses are worth the peace of mind.

If future lab tests deviate from baseline, it’s an indication of just how much topical finasteride is going systemic. According to the clinical data, 30 days of application is more than enough time for finasteride to saturate at its maximum levels in the scalp and serum. 

As such, measuring DHT levels after one month of finasteride use offers a great reference point to see if topical finasteride is impacting serum DHT levels. If needed, changes can be made to the application or use frequency depending on any changes to your blood levels of DHT.

2. Understand That DHT Levels Fluctuate Diurnally

Keep in mind, some fluctuation in DHT levels is normal. DHT levels fluctuate throughout the day and across seasons. As such, 15-20% differences across tests are normal and expected. Anything beyond 20% suggests that topical finasteride might be having slight systemic effects.

Because of this fluctuation, however, it’s important to get blood draws done at the same time of day – preferably in the morning and while in a fasted state. Also, try not to make drastic changes to diet, lifestyle, or environment prior to testing. Heavy drinking, deviations from a typical daily diet, the introduction of creatine powders, and/or sleep deprivation can all influence DHT levels and muddy test results. In the 3-5 days prior to the second test, try to keep things as they were when you first went in for testing.

3. Avoid supplementing with Quercetin and/or Creatine

Maintaining systemic DHT levels, while maximizing the effects of finasteride, isn’t just about the drug. There are other activities that could potentially affect DHT levels. Supplementing with quercetin and/or creatine is one common mistake that could impact results.

Studies on mice suggest that quercetin can inhibit the DHT-reducing effects of finasteride.^[7]https://joe.bioscientifica.com/view/journals/joe/181/3/493.xmlWhile the translatability to humans has not yet been studied, the dosages used in these mouse models were comparable to what humans typically consume from quercetin supplements. As such, it may be best for those using finasteride to avoid this supplement.

When it comes to creatine, one study found that in training athletes, creatine supplementation increased serum DHT levels by over 70%.^[8]https://pubmed.ncbi.nlm.nih.gov/19741313/ While the study was small, we have to reconcile these findings with the reality that for the overwhelming majority of training athletes, creatine is unnecessary. Bodybuilders can still look great without using it, and so can the every-day gym goer. Competitive bodybuilders are, however, a different story.

4. Set Realistic Expectations and Track Progress

Finasteride is the best-studied intervention for androgenic alopecia. In order to appreciate its full effects, consider the following:

1. Know the timeline for results. Clinical studies show that finasteride improves pattern hair loss outcomes in 80-90% of men. Having said that, cosmetic degrees of hair regrowth don’t often occur until after 10-12 months of treatment. Moreover, the drug’s full effects typically take two years to manifest, with the biggest degrees of cosmetic regrowth occurring between year one and year two. As such, don’t expect any miracles in the first six months, it may take the full two years to see an effect. 
2. Track progress. It’s hard to know if something is improving without objective measurements. While not all of us have access to trichoscopic hair-counting equipment, most of us do have a smartphone, which can easily be used to take photos to track progress (particularly when the photosets are standardized). This can be done relatively effortlessly. 

Following the tips above allows for the best possible shot at measurable hair growth results, while minimizing the potential effects of systemic DHT reduction.

Summary

Oral finasteride works great for male pattern hair loss, but by significantly reducing serum DHT, it can cause unwanted side effects. 

Topical finasteride was developed as a solution, with a goal to reduce DHT in the scalp only. But when applied in high percentages or large amounts, it too, can go systemic and reduce serum DHT levels. 

To minimize the side effects of finasteride without missing out on the benefits, stick to 1-2 mL of 0.005% to 0.02% topical finasteride solutions. This equates to roughly 0.1-0.2mg of daily finasteride exposure to the scalp. 

The best way to ensure a reduced risk for side effects is to track serum DHT levels. Establish a baseline by taking one test before using finasteride, then test again one month later. 

Dihydrotestosterone (DHT) is a potent androgen hormone that can significantly impact hair loss. Its activity, however, isn’t just restricted to the scalp. What’s more, hair loss is a multifactorial condition, with a wide range of causes. As such, the solution to hair loss is much more complicated than simply eliminating DHT.

Many natural or pharmaceutical therapies seek to reduce, or rather, rebalance DHT levels. While lowering DHT can slow or even reverse hair loss, the hormone itself plays vital roles in sexual function, mood regulation, and overall well-being. Therefore, the goal should not be total suppression, but rather modulation that considers the balance between hair health and systemic androgen levels.

In this article, we will rank both natural and pharmaceutical DHT blockers from weakest to strongest, based on research, effectiveness, and risk of side effects.

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Understanding DHT: Why Blocking It Helps (and Hurts)

DHT is derived from testosterone through the enzyme 5-alpha-reductase. Once formed, DHT binds to androgen receptors and plays a major role in androgenic alopecia (AGA). In hair follicles genetically sensitive to DHT, such as those on the crown and frontal scalp, the hormone acts as a signal for miniaturization. Over time, the follicle shrinks, producing thinner, shorter hairs until it eventually becomes dormant.^[1]York, K., Meah, N., Bhoyrul, B., & Sinclair, R. (2020). A review of the treatment of male pattern hair loss. Expert Opinion on Pharmacotherapy. 21(5). 603-612. Available at: … Continue reading

By reducing DHT levels or blocking its receptor binding, therapies can interrupt this miniaturization cascade. The goal is to prevent DHT from triggering the cellular changes that cause follicles to shrink and enter a premature resting (telogen) phase. AGA is influenced not just by DHT levels but also by individual receptor sensitivity, local inflammation, and oxidative stress.

However, because of DHT’s wide-reaching activity, side effects of its reduction can include sexual dysfunction, decreased motivation, and mood changes, especially in individuals who are more hormonally sensitive. As such, careful consideration of different therapies and their potential impacts is essential if you choose to use a DHT-blocking treatment.^[3]Traish, A. M., Melcangi, R. C., Bortolato, M., Garcia-Segura, L. M., & Zitzmann, M. (2015). Adverse effects of 5α-reductase inhibitors: what do we know, don’t know, and need to know?. Reviews … Continue reading

Ranking the DHT Blockers: From Mild to Potent

We’ll rank DHT blockers based on their potency, as well as on the quality of evidence supporting their use for hair loss. You can learn more about our treatment metrics, including evidence quality, in our article.

Tier 1 – Mild / Natural DHT Blockers

Natural treatments, typically based on oils and herbs, are generally more gentle than pharmaceutical options. They tend to be less potent, but have far fewer side effects and are not typically subject to the same stringent regulation as pharmaceuticals.

EGCG (Evidence Quality – 6%)

Epigallocatechin gallate (EGCG), a catechin compound found in green tea, is another naturally derived compound that has attracted interest for its potential to influence hair follicle biology. As a potent antioxidant and anti-inflammatory molecule, EGCG helps protect follicular cells from oxidative stress and inflammation, both of which are exacerbated by androgen activity. 

 

EGCG appears to enhance cell-survival pathways such as Akt and Erk, supporting follicular cell proliferation while suppressing apoptotic signals that can trigger hair follicle regression.^[5]Kwon, O. S., Han, J. H., Yoo, H. G., Chung, J. H., Cho, K. H., Eun, H. C., & Kim, K. H. (2007). Human hair growth enhancement in vitro by green tea epigallocatechin-3-gallate (EGCG). … Continue reading

Laboratory studies also indicate that EGCG can partially inhibit 5AR, reducing the local generation of DHT.^[6]Hiipakka, R. A., Zhang, H. Z., Dai, W., Dai, Q., & Liao, S. (2002). Structure–activity relationships for inhibition of human 5α-reductases by polyphenols. Biochemical Pharmacology. 63(6). … Continue reading However, while this study showed that EGCG can inhibit 5AR in cell-free experiments, it did not have the same impact in cells. This suggests that it may not be able to enter cells and would have reduced impacts in humans.

This seems to be the case, and clinical evidence for EGCG in the treatment of hair loss remains limited. A small pilot study of topical EGCG found no visible changes in hair, although this research was conducted in people with no hair loss disorders.^[7]Kwon, O. S., Han, J. H., Yoo, H. G., Chung, J. H., Cho, K. H., Eun, H. C., & Kim, K. H. (2007). Human hair growth enhancement in vitro by green tea epigallocatechin-3-gallate (EGCG). … Continue reading Despite the lack of large-scale human trials, molecular findings do suggest EGCG contributes meaningfully to the cellular environment that supports hair growth and protection.

Catechins from green tea infusions are generally well tolerated. However, supplements should be used cautiously at high doses, particularly above 800 mg per day, as they have been linked to liver enzyme elevations in sensitive individuals.^[8]EFSA Panel on Food Additives and Nutrient Sources added to Food (ANS), Younes, M., Aggett, P., Aguilar, F., Crebelli, R., Dusemund, B., Filipič, M., Frutos, M. J., Galtier, P., Gott, D., … Continue reading

You can read more about the evidence for using EGCG for hair loss in our article here.

Pumpkin Seed Oil (Evidence Quality – 49%)

Pumpkin seed oil (PSO) is one of the most extensively studied non-pharmaceutical treatments for hair loss. In general, it is mild and well-tolerated. Its effects appear to arise from its profile of phytosterols and essential fatty acids, such as linoleic and oleic acid. These compounds have been shown to exhibit mild 5AR inhibitory activity in laboratory studies, potentially reducing local DHT formation in scalp tissues.^[9]Azizi, A., Mumin, N. H., & Shafqat, N. (2021). Phytochemicals with anti 5-alpha-reductase activity: a prospective for prostate cancer treatment. F1000Research. 10. 221. Available at: … Continue reading,^[10]Liang, T., & Liao, S. (1992). Inhibition of steroid 5α-reductase by specific aliphatic unsaturated fatty acids. Biochemical Journal. 285(2). 557-562. Available at: … Continue reading

Beyond hormonal modulation, pumpkin seed oil provides antioxidant and anti-inflammatory support, which can help protect hair follicles from oxidative damage and microinflammation – two key contributors to progressive miniaturization.^[11]Fahim, A. T., Abd-El Fattah, A. A., Agha, A. M., & Gad, M. Z. (1995). Effect of pumpkin-seed oil on the level of free radical scavengers induced during adjuvant-arthritis in rats. Pharmacological … Continue reading

A clinical trial carried out in Korea made waves in 2014 when it reported a 40% increase in hair count after 24 weeks. However, the formulation, Octa-Sabal Plus, included multiple additional herbal compounds, alongside pumpkin seed powder, not oil. This means we can’t attribute the growth reported to pumpkin seed oil.^[12]Cho, Y. H., Lee, S. Y., Jeong, D. W., Choi, E. J., Kim, Y. J., Lee, J. G., & Cha, H. S. (2014). Effect of pumpkin seed oil on hair growth in men with androgenetic alopecia: a randomized, … Continue reading 

You can read more about the controversial PSO study here.

Cold-pressed pumpkin seed oil is typically taken orally at doses ranging from 400 to 1000 mg daily, with results accumulating gradually over several months. The compound is generally well tolerated, with gastrointestinal discomfort being rare and mild.^[13]Hong, H., Kim, C. S., & Maeng, S. (2009). Effects of pumpkin seed oil and saw palmetto oil in Korean men with symptomatic benign prostatic hyperplasia. Nutrition Research and Practice. 3(4). … Continue reading Although PSO alone is unlikely to reverse established AGA, it may serve as a gentle adjunct for individuals seeking natural or preventive strategies to support long-term scalp and hair health.

Saw Palmetto (Evidence Quality – 54%)

Saw palmetto (Serenoa repens) is one of the most widely studied natural 5AR inhibitors and is sometimes called “nature’s finasteride.” It appears to reduce DHT by inhibiting Type II 5AR, reducing the binding of DHT to androgen receptor sites and increasing the conversion of DHT to a weaker metabolite called androstanediol.^[14]Suzuki, M., Ito, Y., Fujino, T., Abe, M., Umegaki, K., Onoue, S., Noguchi, H., & Yamada, S. (2009). Pharmacological effects of saw palmetto extract in the lower urinary tract. *Acta … Continue reading

Importantly, saw palmetto appears to reduce DHT selectively, with research showing decreases in DHT in the prostate but not in the blood. As such, it may cause fewer side effects than systemic DHT reducers.^[15]Fagelman, E., & Lowe, F. C. (2001). Saw palmetto berry as a treatment for BPH. Reviews in Urology. 3(3). 134-138. Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1476047/

Clinical studies have shown modest impacts of saw palmetto on hair loss. In one study, participants using oral extracts over several months showed reductions in hair shedding, increases in hair density, and subjective improvements in scalp coverage and hair quality.{ Importantly, however, this was an open-label study, where participants and researchers both knew what product they were receiving, so is not as strong a form of evidence as a randomzied controlled trial (RCT).^[16]Rossi, A., Mari, E., Scarno, M., Garelli, V., Maxia, C., Scali, E., Iorio, A., & Carlesimo, M. (2012). Comparative effectiveness of finasteride vs Serenoa repens in male androgenetic alopecia: a … Continue reading 

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In a recent RCT, a standardized, proprietary saw palmetto extract was given as either a 400mg oral capsule or 5 ml of topical formulation and compared to relevant controls. The study found a significant reduction in hair shedding in both oral and topical groups compared to their controls, alongside an increase in hair density of 5% and 7.5% respectively. However, this study also had significant drawbacks. For example, measurements of hair density were not well defined and may therefore include vellus hairs, which do not contribute to visible hair. Despite this, the study does provide some support for the use of saw palmetto in decreasing hair shedding and increasing hair thickness.^[17]Sudeep, H. V., Rashmi, S., Jestin, T. V., Richards, A., Gouthamchandra, K., & Shyamprasad, K. (2023). Oral and topical administration of a standardized saw palmetto oil reduces hair fall and … Continue reading

Evidence from benign prostatic hyperplasia suggests that an oral dose of 320 mg per day is optimal, with increases in dose above that resulting in no further improvements. For topical use, concentrations around 0.5 – 1% applied once or twice daily are common. Both routes are well tolerated, with infrequent reports of mild gastrointestinal discomfort or skin irritation. 

You can read about the differences between saw palmetto and finasteride in our article here.

Tier 2 – Over-the-Counter Pharmaceutical Options

Over-the-Counter Pharmaceutical Options bridge the gap between gentle natural therapies and prescription-strength DHT blockers, potentially offering clinically supported benefits with relatively low systemic risk.

Ketoconazole Shampoo (Evidence Quality – 54%)

Originally developed as an antifungal agent, ketoconazole helps normalize the scalp environment by reducing inflammation, fungal overgrowth, and excess sebum, all of which can worsen AGA. Beyond its antifungal activity, laboratory and clinical research suggest that ketoconazole exerts mild local antiandrogenic effects, likely through partial inhibition of 5AR and modulation of DHT activity within the scalp. 

Clinical evidence for men is stronger than for women. One 21-month study using 2% ketoconazole shampoo showed progressive improvement in hair shaft diameter and percentage of hairs in the growth (anagen) phase, reversing the slow decline seen in untreated AGA.^[18]Piérard-Franchimont, C., De Doncker, P., Cauwenbergh, G., & Piérard, G. E. (1998). Ketoconazole shampoo: effect of long-term use in androgenic alopecia. Dermatology. 196(4). 474-477. Available … Continue reading

Another study, which compared Ketoconazole with other shampoos, found that 1% ketoconazole reduced hair shedding by 17%, improved anagen hair by 4.9%, and lowered scalp sebum levels.^[19]Piérard-Franchimont, C., Goffin, V., Henry, F., Uhoda, I., Braham, C., & Piérard, G. E. (2002). Nudging hair shedding by antidandruff shampoos: A comparison of 1% ketoconazole, 1% piroctone … Continue reading Studies also show that ketoconazole performs well as an adjunct therapy, with synergistic effects when combined with finasteride.^[20]Perez, B. S. H. (2004). Ketoconazole as an adjunct to finasteride in the treatment of androgenetic alopecia in men. Medical Hypotheses. 62(1). 112-115. Available at: … Continue reading 

Evidence in women is limited, with only one published study investigating ketoconazole solution, rather than shampoo. They compared 2% ketoconazole to 2% minoxidil and reported meaningful regrowth in both groups, with ketoconazole producing improvements by the six-month mark and causing far fewer side effects.^[21]El-Garf, A., Mohie, M., & Salah, E. (2019). Trichogenic effect of topical ketoconazole versus minoxidil 2% in female pattern hair loss: a clinical and trichoscopic evaluation. Biomedical … Continue reading

Ketoconazole is generally well tolerated. Mild irritation, dryness, or temporary scalp tightness may occur, especially with 2% formulations or frequent use. Most regimens recommend applying it 2–3 times per week, leaving the shampoo on the scalp for 3–5 minutes before rinsing.

You can read our breakdown of the research into ketoconazole shampoos here.

You can also read about why 2% ketoconazole might be a better choice than 1% here.

Tier 3 – Prescription Pharmaceutical DHT Blockers

Prescription Pharmaceutical DHT Blockers represent the most potent and clinically validated options, offering stronger and more predictable suppression of DHT than natural therapies but with a greater need for careful monitoring of side effects.

Topical Finasteride (Evidence Quality – 69%)

Topical finasteride represents a new, more targeted approach to DHT inhibition, delivering the drug directly to the scalp while aiming to minimize systemic exposure. Like its oral counterpart, it blocks the Type II 5-alpha reductase enzyme. However, by focusing this activity locally within the hair follicle, topical formulations can achieve substantial reductions in scalp DHT while maintaining serum levels that are a fraction of those seen with oral dosing. This distinction is clinically important for individuals concerned about systemic side effects such as decreased libido or hormonal shifts.

Clinical research has consistently shown that topical finasteride can achieve similar improvements in hair density and regrowth as oral therapy. One 24-week study showed a 34.5% decrease in DHT, compared to 55.6% for oral finasteride. However, plasma concentrations were 100 times lower, indicating that systemic exposure is greatly reduced.^[22]Piraccini, B. M., Blume-Peytavi, U., Scarci, F., Jansat, J. M., Falqués, M., Otero, R., Tamarit, M. L., Galván, J., Tebbs, V., Massana, È., on behalf of the Topical Finasteride Study Group. … Continue reading

Topical finasteride is particularly appealing to men who respond well to oral therapy but wish to lower the risk of systemic adverse effects. When applied once daily at concentrations between 0.1% and 0.25%, it can stabilize shedding within four to six months, with visible improvements generally continuing over the course of a year.^[23]Mazzarella, G. F., Loconsole, G. F., Cammisa, G. A., Mastrolonardo, G. M., & Vena, G. A. (1997). Topical finasteride in the treatment of androgenic alopecia. Preliminary evaluations after a … Continue reading For optimal results, it can be combined with topical minoxidil to stimulate regrowth through complementary pathways.^[24]Wang, H., Chen, B., & Hong, X. (2020). The efficacy and safety of finasteride combined with topical minoxidil for androgenetic alopecia: A systematic review and meta-analysis. *Journal of … Continue reading  

Our members can find the ultimate guide to finasteride here.

Dutasteride (Evidence Quality – 77%)

Dutasteride is the most potent 5AR inhibitor currently available, targeting both Type I and Type II isoenzymes. This dual inhibition results in serum DHT reductions of up to 90 – 95%, creating a profoundly anti-androgenic environment within scalp follicles.^[25]Roehrborn, C. G., Marks, L. S., Fenter, T., Freedman, S., Tuttle, J., Gittleman, M., Morrill, B., & Wolford, E. T. (2004). Efficacy and safety of dutasteride in the four-year treatment of men … Continue reading Clinically, this translates into faster and often more pronounced regrowth compared to finasteride, particularly in individuals with advanced hair thinning.

Because dutasteride suppresses DHT more comprehensively, it may pose a slightly higher risk of hormonal side effects such as gynecomastia or reduced libido. However, head-to-head studies have suggested superior efficacy for dutasteride in both short-term and long-term endpoints. 

A meta-analysis, which combines results from multiple studies, indicated that dutasteride showed better efficacy in treating AGA.^[26]Zhou, Z., Song, S., Gao, Z., Wu, J., Ma, J., & Cui, Y. (2019). The efficacy and safety of dutasteride compared with finasteride in treating men with androgenetic alopecia: a systematic review and … Continue reading These results suggest that dutasteride is ~3 times more potent than finasteride in blocking Type II 5α-reductase and up to 100 times more potent against Type I. This dual inhibition reduces scalp DHT levels by over 50%, compared to approximately 41% with finasteride, leading to greater prevention of follicular miniaturization and enhanced regrowth response with similar levels of adverse effects.

Dutasteride has a relatively low evidence quality score compared to finasteride, though this is largely due to there being fewer studies. The studies that do investigate dutasteride have shown higher potency and effectiveness.

For detailed information on clinical trials, including dutasteride, check out our comprehensive summary.

Topical dutasteride formulations are now under active investigation. Concentrations ranging from 0.01% to 0.05% have produced significant gains in target-area hair counts, with studies suggesting that improvements associated with oral formulations can be achieved without drops in serum DHT.^[27]Panuganti, V. K., Madala, P. K., Grandhi, V. R., Alluri, C. V., Mohammad, J., KSSVV, S. R., & Dundigalla, M. R. (2025). A randomized, double-blind, placebo and active controlled Phase II study to … Continue reading

 

A 2018 randomized clinical study further demonstrated that topical dutasteride (0.02%) combined with microneedling significantly improved hair shaft thickness and patient satisfaction compared with microneedling alone, without notable systemic absorption or hormonal side effects. These findings suggest that localized delivery of dutasteride may enhance follicular response while minimizing systemic exposure and related adverse effects.^[29]Nada, E.A., El Sharkawy, R.E.E.D., Abd El-Maged, W. M., & Abo Elmagd, M. A. (2018). Topical dutasteride with microneedling in treatment of male androgenetic alopecia. Sohag Medical Journal. … Continue reading

Similarly, research published in 2024 looked into the impact of microneedling. However, in this study, topical dutasteride was combined with minoxidil. They found similar improvements in hair density and hair width in participants who had topical dutasteride and minoxidil treatment to those in patients who had oral dutasteride and topical minoxidil.^[30]Abu Obeid, M. N., Abdel Fattah, N. S., Elfangary, M. M., & Al Husseni, R. M. (2024). Comparison between Topical Minoxidil 5% Alone versus Combined with Dutasteride (Topical 0.02% through … Continue reading These results suggest that, in combination with other therapies (minoxidil or microneedling), topical dutasteride may be able to produce similar results to oral formulations but with a significantly lower chance of side effects.

A newly published Phase II trial has also drawn significant attention because it is the first study to test topical dutasteride alone, without microneedling. The results appear impressive: all topical doses improved hair parameters versus placebo, showed minimal impact on serum DHT (suggesting good scalp localization), and 1 ml daily of 0.05% topical dutasteride reportedly outperformed oral finasteride in key regrowth metrics.^[31]Panuganti, V. K., Madala, P. K., Grandhi, V. R., Alluri, C. V., Mohammad, J., Kssvv, S. R., & Dundigalla, M. R. (2025). A randomized, double-blind, placebo- and active-controlled phase II study … Continue reading

However, the study reports unusually high baseline hair counts, as well as inconsistencies in the placement and size of the 1 cm² target areas used for serial hair counts. These issues can dramatically skew results, creating the illusion of improvement even when none exists. Real-world data from users of low-dose topical dutasteride (0.01–0.02% applied daily or near-daily) also paint a more modest picture: good localization and serum DHT stability, but primarily maintenance rather than regrowth exceeding oral finasteride

For more information on the emerging potential of topical dutasteride formulations, read our article here.

Oral Finasteride (Evidence Quality – 99%)

As you can see from our evidence quality score, oral finasteride remains the most clinically validated pharmacological treatment for AGA. It acts as a selective inhibitor of the Type II 5AR enzyme, reducing systemic and scalp DHT levels by approximately 60–70%.^[32]Drake, L., Hordinsky, M., Fiedler, V., Swinehart, J., Unger, W. P., Cotterill, P. C., Thiboutot, D. M., Lowe, N., Jacobson, C., Whiting, D., Stieglitz, S., Kraus, S. J., Griffin, E. I., Weiss, D., … Continue reading This substantial suppression slows or halts follicular miniaturization, prolongs the growth (anagen) phase, and enables partial regrowth in many users. The standard 1 mg daily dose for AGA has been extensively studied and represents the optimal balance between efficacy and safety for most men.

Clinical trials have consistently confirmed the effectiveness of finasteride in both the short and long term. A 4-year, randomized study found that 1 mg of finasteride led to increased hair weight (46% vs placebo) and hair count (20% vs. placebo).^[33]Price, V. H., Menefee, E., Sanchez, M., & Kaufman, K. D. (2006). Changes in hair weight in men with androgenetic alopecia after treatment with finasteride (1 mg daily): three- and 4-year results. … Continue reading

You can find an in-depth overview of the clinical studies on finasteride here.

While highly effective, oral finasteride is not without potential drawbacks. A small percentage of users report side effects related to sexual function, including reduced libido, erectile difficulty, and diminished ejaculate volume. Most of these effects are mild and resolve upon discontinuation, although persistent symptoms have been reported in rare cases. Some users also report changes in mood or motivation, likely reflecting individual hormonal sensitivity. For those wishing to minimize systemic exposure, transitioning to topical finasteride or titrating to a lower dose (e.g., 0.25-0.5 mg daily) may be a suitable option.^[34]Gupta, A. K., Venkataraman, M., Talukder, M., & Bamimore, M. A. (2022). Finasteride for hair loss: a review. Journal of Dermatological Treatment. 33(4). 1938-1946. Available at: … Continue reading

There have also been reports of a condition that’s been named ‘post-finasteride syndrome’. While not widely accepted by the medical community, similar symptoms have been reported in a number of individuals who are taking finasteride. These symptoms can include sexual dysfunction, such as loss of libido and erectile dysfunction, neuropsychiatric symptoms like depression and anxiety, and physical changes like muscle atrophy and fatigue. Importantly, there have been cases where these symptoms have persisted after users have stopped taking the drug.

While the authors who published the original article on post-finasteride syndrome do highlight the lack of consistent evidence for persistent side effects found in clinical trials, they suggest that finasteride may act to worsen symptoms associated with sexual dysfunction and psychiatric conditions for some users who already have these issues.^[35]Pereira, A. F. J. R., & Coelho, T. O. A. (2020). Post-finasteride syndrome. Anais Brasileiros de Dermatologia. 95(3). 271-277. Available at: https://doi.org/10.1016/j.abd.2020.02.001

Overall, oral finasteride remains the gold standard for DHT suppression, providing robust and predictable results when used consistently. It’s also important to consider the potential side effects when choosing to take finasteride, and consult with your doctor if symptoms arise.

Honourable Mention – Pyrilutamide

Pyrilutamide (KX-826)

Pyrilutamide takes a different approach to androgen modulation. Rather than reducing DHT production, it acts as a topical androgen receptor antagonist, blocking DHT and testosterone from binding to their receptors in the follicle. By interfering with receptor activation, pyrilutamide aims to suppress the downstream gene expression that leads to follicular miniaturization.^[36]Koralewicz, M. M., & Szatkowska, O. A. (2024, July). Topical solutions for androgenetic alopecia: evaluating efficacy and safety. Forum Dermatologicum. 10(3). 61-70. Available at: … Continue reading

Clinical data show encouraging signals. Trials conducted in China and the United States suggest that topical formulations applied once or twice daily can produce measurable increases in hair counts over several months. Reported side effects are primarily mild local dermatitis, and systemic exposure appears very low. However, many of these results remain unpublished in peer-reviewed journals and have failed to demonstrate statistical superiority over placebo for some measurements.^[37]Kintor Pharmaceuticals. (2022). Developing Novel Drugs and Commercialization Platform. Available at: … Continue reading,^[38]Kintor Pharmaceutical Limited. (2023, March 28). Kintor Pharma Announces Completion of Subject Enrollment in Phase III Clinical Trial for KX-826 for Treatment of Male Androgenetic Alopecia in China. … Continue reading Because these reports have not been published in peer-reviewed journals, they can only currently be considered pre-releases, rather than academic papers. The absence of published, peer-reviewed, blinded, controlled data means that we can’t draw firm conclusions on pyrilutamide, even in the wake of the many press releases that Kintor has published.

To learn more about the research on Pyrilutamide and when to be cautious of press-release-style publications, read our in-depth article.  

For now, pyrilutamide should be viewed as an experimental therapy. Its mechanism is compelling and localized, offering a theoretical advantage over systemic antiandrogens. Still, robust, peer-reviewed clinical trials confirming efficacy and long-term safety are needed before it can be considered a mainstream treatment. Those interested in exploring it should do so only under medical supervision or within the context of formal clinical research.

Final Thoughts

DHT blockers span a broad spectrum, ranging from gentle, naturally derived modulators like pumpkin seed oil and EGCG to powerful prescription therapies such as finasteride and dutasteride. Natural options may improve scalp health and have a modest influence on hormonal activity, but their effects are typically gradual and limited. In contrast, pharmacological inhibitors act directly on the enzymatic pathways responsible for DHT synthesis, offering stronger and more predictable outcomes. Topical finasteride has emerged as a compelling middle ground, delivering scalp-level efficacy with minimal systemic impact, while dutasteride represents the upper limit of potency for those requiring more aggressive intervention.

Ultimately, the “best” DHT blocker depends on individual tolerance, goals, and the stage of hair loss. A well-balanced regimen typically combines a DHT inhibitor with a growth stimulant, such as minoxidil, alongside scalp care and lifestyle modifications. With consistent use and proper medical guidance, these approaches can collectively slow, halt, or even reverse the progression of AGA, helping individuals maintain fuller, healthier hair over time.

When someone notices a thinning crown, a widening part, or a receding hairline, it is natural to assume that the follicles in those areas are dying. But in androgenic alopecia (AGA), that is not usually what happens, at least not in the way most people mean it. 

AGA is primarily a condition of hair follicle miniaturization. The follicle often remains in the scalp, but it gradually shrinks and produces lower-quality hair fibers. A thick, long, pigmented terminal hair might become a shorter, finer, less pigmented vellus hair that contributes very little to visible coverage.

This, therefore, raises the question: if a follicle has not simply disappeared, could it recover and return to its former state as a terminal hair?

The short answer is sometimes. 

Treatments like finasteride and minoxidil can slow miniaturization and improve visible hair growth in many people. However, they must be used continuously to maintain their effects, and they do not reliably restore every follicle to the size or productivity it had before AGA began. Furthermore, while studies suggest that bald AGA scalps can retain some stem cell populations, this does not mean that all long-bald follicles are merely “asleep” and ready to be reactivated.

To understand why, we first need to look at how AGA affects the normal hair cycle.

What Happens to Hair Follicles in AGA?

A hair follicle is not a permanent, continuously growing structure. It repeatedly moves through a cycle of growth, regression, rest, and renewal. 

The three main phases are:^[1]Kloepper, J.E., Sugawara, K., Al-Nuaimi, Y., Gaspar, E., & Paus, R. (2010). Methods in hair research: How to objectively distinguish between anagen and catagen in human hair follicles. … Continue reading,^[2]Alonso, L., & Fuchs, E. (2006). The hair cycle. Journal of Cell Science. 119(Pt 3). 391-393. Available at: https://doi.org/10.1242/jcs.02793

• Anagen: The active growth phase. The follicle produces a hair shaft, and scalp hairs can remain in anagen for years.

• Catagen: A brief regression phase. Growth stops, the lower part of the follicle shrinks, and the hair-producing bulb moves upward.

• Telogen: The resting phase. The follicle remains relatively inactive before eventually returning to anagen. The old club hair may shed during this period or shortly before the next hair begins to grow.

In healthy scalp hair, anagen is unusually long. That is why terminal scalp hairs can grow to substantial lengths. But in AGA-prone areas of the scalp, the cycle gradually changes. 

Genetically susceptible hair follicles respond to androgen signaling, particularly dihydrotestosterone (DHT), by producing hairs that are progressively smaller with each cyle. The anagen phase shortens, meaning each hair has less time to grow. At the same time, the follicle that is produced is thinner and finer.^[4]Randall, V.A. (2008). Androgens and hair growth. Dermatologic Therapy. 21(5). 314-328. Available at: https://doi.org/10.1111/j.1529-8019.2008.00214.x,^[5]Sawaya, M.E., & Price, V.H. (1997). Different levels of 5-alpha-reductase type I and II, aromatase, and androgen receptor in hair follicles of women and men with androgenetic alopecia. Journal of … Continue reading 

This is called the terminal-to-vellus transition.

Terminal hairs are the thick, pigmented hairs that create most of the scalp’s visible coverage, whereas vellus hairs are much finer, shorter, and less pigmented. In AGA, a follicle may not abruptly become a true vellus follicle. Instead, it gradually moves along a spectrum, producing hairs that become increasingly vellus-like over repeated cycles. 

In practical terms, AGA does not usually mean that a hair follicle simply “falls out”. It means that the follicle becomes smaller and less capable of making a cosmetically useful hair.

Why AGA Does Not Look Uniform

One reason AGA can be difficult to assess in its early stages is that follicles do not miniaturize at the same speed. 

Two adjacent follicles can be at very different stages. One may still produce a thicker terminal hair, while the follicle beside it may produce a short, fine, miniaturized fiber. This produces a mixture of hair diameters within the same scalp area, a feature known as hair-diameter diversity, or anisotrichosis.

That mixture is one of the most useful signs of AGA under trichoscopy. Rather than a uniform reduction across all hairs, clinicians often observe increasing variation. Some hairs remain relatively thick, while others are much thinner and shorter. A 2024 cross-sectional study in men with AGA found that hair-diameter diversity increased with disease severity, while mean hair diameter declined and the proportion of thinner hairs rose.^[6]Kim, M.S., Kim, J., Lee, S.Y., et al. (2024). Quantitative measurement of hair diameter diversity as a diagnostic indicator of androgenetic alopecia in Korean males: A cross-sectional study. JAAD … Continue reading

This is why AGA often looks like reduced density rather than immediate baldness. The hairs may still be present, but an increasing proportion are too fine to provide meaningful coverage.

Are Miniaturized Follicles Dead or Dormant?

The short answer is that neither word is completely accurate.

Calling a miniaturized AGA follicle “dead” suggests that it has been physically destroyed, which is simply not the case.

AGA is classified as a non-scarring alopecia. Even when an area of scalp looks bald, miniaturized follicular structures may still remain. This differs from scarring alopecia, where inflammation can physically destroy follicles and replace them with fibrotic tissue. In those conditions, follicular openings can disappear, and the potential for spontaneous regrowth is much more limited.^[7]Vidal, C.I. (2015). Overview of alopecia: A dermatopathologist’s perspective. Missouri Medicine. 112(4). 308-312. Available at: https://pmc.ncbi.nlm.nih.gov/articles/PMC6170065/ 

But “dormant” is not quite right either.

A miniaturized AGA follicle may still cycle and produce a hair shaft. The issue is that the produced shaft may be too fine, short, or lightly pigmented to provide noticeable scalp coverage. In other words, it’s not necessarily inactive, but rather functioning at a reduced level.

It should be noted that AGA can still become difficult to reverse, especially in longstanding bald areas. But its biology is not identical to a scarring disorder. A miniaturized follicle and a physically destroyed follicle are not the same thing.

What Stem Cell Studies Actually Show

One influential study compared bald and haired scalps from men with AGA. Researchers found that bald scalp retained KRT15-positive cells associated with the hair follicle’s bulge region, a stem-cell niche located in the permanent portion of the hair follicle. However, they also found marked depletion of several additional activated progenitor-cell populations located near the bulge, including CD200-high/ITGA6-high and CD34-positive cells.^[8]Garza, L.A., Yang, C.C., Zhao, T., et al. (2011). Bald scalp in men with androgenetic alopecia retains hair follicle stem cells but lacks CD200-rich and CD34-positive hair follicle progenitor cells. … Continue reading

At first glance, that might sound like very good news. If stem cells are still there, perhaps the follicles can simply be switched back on.

But that conclusion goes beyond what the study showed.

A more cautious interpretation is that some of the hair follicle’s core machinery persists in the bald AGA scalp, while the processes required to activate those cells or convert them into the progenitor cells needed for robust hair production may be impaired.

Put differently, the issue may not be a total absence of follicular stem cells; it might be a failure of the signaling, activation, or stem-cell-to-progenitor conversion steps required to rebuild a normal terminal hair.

That is an important finding for regenerative hair loss research. It is not proof that every long-bald follicle can currently be restored with conventionally available treatments.

Can AGA Treatments Reverse Miniaturization?

The most accurate answer is: partially, in some follicles, in some people. 

That may sound less exciting than claims of “follicle revival” or “complete regrowth”, but it reflects what the clinical evidence actually supports. 

A positive response to treatment can include:

• A longer anagen phase, allowing hairs to grow for longer before entering regression.
• Increased hair-shaft diameter, making existing hairs more visible.
• A shift from producing very fine, vellus-like hairs toward producing thicker, more cosmetically meaningful hairs.
• Recruitment of follicles that were producing very little visible hair into a more productive growth cycle.
• Slower ongoing miniaturization, which can preserve density that would otherwise have been lost.

These changes can substantially improve scalp coverage. But they are not necessarily equivalent to full anatomical restoration of every affected follicle.

What Finasteride Studies Show

Finasteride reduces the conversion of testosterone to DHT by inhibiting type II 5-alpha-reductase. In men with AGA, this reduces DHT in serum and scalp tissue, thereby lowering one of the key androgenic signals that drives miniaturization in genetically susceptible follicles.^[10]Drake, L., Hordinsky, M., Fiedler, V., et al. (1999). The effects of finasteride on scalp skin and serum androgen levels in men with androgenetic alopecia. Journal of the American Academy of … Continue reading

Randomized trials have shown that finasteride can increase hair counts and improve photographic appearance compared with placebo in men with AGA.^[11]Kaufman, K.D., Olsen, E.A., Whiting, D., et al. (1998). Finasteride in the treatment of men with androgenetic alopecia. Journal of the American Academy of Dermatology. 39(4 Pt 1). 578-589. Available … Continue reading 

Long-term evidence is particularly useful here because AGA is progressive. In a five-year multinational study, men taking finasteride 1 mg daily showed durable improvements in hair count, investigator assessments, patient assessments, and clinical photographs, while the placebo group continued to lose hair over time.^[12]Shapiro, J., Kaufman, K.D., Olsen, E.A., Whiting, D., & Savin, R. (2003). Long-term (5-year) multinational experience with finasteride 1 mg in men with androgenetic alopecia. European Journal of … Continue reading

However, “finasteride works” should not be interpreted as “finasteride can restore your original hair density”.

Some men do see visible regrowth, while others maintain what they already have. Some improve in one area, like the crown, but not the frontal hairline. Some have a modest response despite a substantial reduction in DHT, while others do not experience meaningful cosmetic improvement.

This is because DHT reduction is only one part of the chain between drug exposure and visible hair growth. The final outcome depends on disease duration, degree of miniaturization, follicular biology, treatment adherence, age, genetics, and the amount of potentially recoverable hair remaining.

For many people, preventing further decline is not a treatment failure. In a progressive condition such as AGA, stabilizing hair loss can be a meaningful outcome.

What Does Minoxidil Do?

Minoxidil works through a different treatment pathway than finasteride. It does not meaningfully reduce DHT or remove the follicle’s underlying androgen sensitivity.

Instead, minoxidil appears to influence hair cycling and follicular productivity. Its exact mechanism is not fully understood, but research suggests that it can promote anagen activity, influence potassium channels and intracellular signaling, and affect growth-factor pathways within the follicular environment.^[13]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,^[14]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 

Clinically, minoxidil can increase total and non-vellus hair growth compared with a placebo. A systematic review and meta-analysis reported improvements in total and non-vellus hair counts with topical minoxidil.^[15]Fiedler, V.C., Alaitz, M., & Hayden, R.E. (2015). Topical minoxidil: Systematic review and meta-analysis of its efficacy in androgenetic alopecia. Journal of the American Academy of Dermatology. … Continue reading

In a 48-week trial in men with AGA, 5% topical minoxidil outperformed both 2% minoxidil and placebo for non-vellus hair count, investigator-rated scalp coverage, and patient-rated treatment benefit.^[16]Olsen, E.A., Dunlap, F.E., Funicella, T., et al. (2002). A randomized clinical trial of 5% topical minoxidil versus 2% topical minoxidil and placebo in the treatment of androgenetic alopecia in men. … Continue reading 

The important limitation is that minoxidil does not eliminate the underlying androgen sensitivity of AGA. That is why its benefits are generally treatment-dependent. If treatment is stopped, the hair that was being maintained or improved by minoxidil may gradually be lost.

Why Combination Therapy Can Help

Studies and reviews of combination minoxidil and finasteride treatment generally suggest better outcomes than monotherapy, at least for some patients.^[17]Gupta, A.K., Bamimore, M.A., & Foley, K.A. (2020). The efficacy and safety of finasteride combined with topical minoxidil for androgenetic alopecia: A systematic review and meta-analysis. Journal … Continue reading Using both makes biological sense. One treatment can slow the process driving miniaturization, while the other may improve the productivity of the remaining follicles. 

What About Microneedling, PRP, and Experimental Treatments?

Microneedling, platelet-rich plasma (PRP), low-level light therapy (LLLT), topical anti-androgens, and cell-based or regenerative approaches are frequently discussed in the treatment of AGA. 

Some of these interventions have encouraging signals.

For example, systematic reviews of PRP have found that PRP injections can improve hair density compared with control treatments in several small randomized trials. However, PRP preparation, platelet concentration, injection technique, treatment schedule, comparator treatment, and outcome measurement vary substantially between studies.^[18]Zhang, X., Ji, Y., Zhou, M., et al. (2023). Platelet-rich plasma for androgenetic alopecia: A systematic review and meta-analysis of randomized controlled trials. Journal of Cutaneous Medicine and … Continue reading

Microneedling combined with minoxidil has also shown better average hair-count outcomes than minoxidil alone in meta-analyses. But the evidence remains heterogeneous, with studies using different needle depths, devices, treatment intervals, and follow-up periods.^[19]Zhou, Y., Wang, J., Liu, Y., et al. (2025). Evaluating the efficacy and safety of combined microneedling with minoxidil versus minoxidil monotherapy for androgenetic alopecia: A systematic review and … Continue reading

The key issue is not whether these interventions can improve average hair-count measurements. Some certainly do. The question is whether those changes demonstrate anatomical reversal of miniaturization in longstanding follicles.

Right now, the answer is no.

Prolactin-Receptor Inhibitors

While the above treatments can be effective, they aren’t designed specifically to address the possibility that AGA involves defective communication between hair-follicle stem cells and the progenitor cells needed to build a robust terminal hair. 

That is one reason prolactin-receptor inhibitors have attracted attention.

The prolactin receptor is expressed in hair follicles, and experimental work suggests that prolactin signaling can influence hair-cycle regulation. New injectable antibodies, like Absci’s ABS-201, are being developed to block prolactin receptor signaling in people with AGA.

The appeal of this approach is straightforward. If miniaturized follicles retain some stem-cell populations but fail to generate enough active progenitor cells, a treatment that improves the follicle’s regenerative environment could, in theory, help more follicles return to productive growth. 

But “in theory” is the important phrase here.

HMI-115, which we have covered in more detail here, is one of the first PRLR-blocking treatments to reach early-stage clinical testing for AGA. In a company-reported open-label Phase 1b study, 12 male participants with AGA reportedly had a mean increase of 14 non-vellus hairs per cm2 after 24 weeks of treatment.^[20]Hope Medicine. (2024). Positive outcome from a Phase Ib study in Australia treating androgenetic alopecia with HMI-115. Company press release. Available at: … Continue reading This result is promising, but the study was small, lacked a placebo comparison, and has not yet provided the kind of peer-reviewed, full clinical dataset needed to determine how reliably HMI-115 improves hair density, caliber, or long-term outcomes.

ABS-201 is an anti-prolactin receptor antibody in the earlier stages of clinical development. Its ongoing Phase 1/2a HEADLINE trial is randomized, double-blind, and placebo-controlled, with planned measures including target-area hair count, hair width, and pigmentation.^[21]Absci. (2026). Absci announces positive interim Phase 1 data from the HEADLINE trial evaluating ABS-201 in androgenetic alopecia. Company press release. Available at: … Continue reading However, the company’s initial human update focused on safety and pharmacokinetics in the single-ascending-dose portion of the trial, rather than confirmed hair-growth efficacy. 

Absci has also reported ex vivo findings from human scalp tissue suggesting that PRLR blockade may prolong anagen and improve growth-associated follicular activity.^[22]Absci. (2025). Absci reports new human ex vivo data demonstrating that ABS-201 promotes hair follicle growth. Company press release. Available at: … Continue reading 

For now, prolactin-receptor inhibitors are best viewed as an intriguing test of a newer biological hypothesis: that improving the regenerative signaling environment of the follicle may complement conventional DHT-lowering and growth-promoting therapies. Whether this translates into clinically meaningful reversal of advanced miniaturization remains unknown.

Why Earlier Treatment Usually Produces Better Results

Early intervention tends to be more rewarding because, even if follicles are starting to produce finer, shorter hairs, they may still have greater regenerative capacity than follicles further along in the process.

There are two potential benefits to treating earlier:

• Preservation: Slowing miniaturization before thicker terminal hairs become very fine or disappear from view.

• Thickening: Improving the caliber, length, and visibility of hairs produced by follicles that remain viable but are already underperforming. 

This is why preventing further deterioration can be a successful outcome even without dramatic regrowth. 

Someone who began treatment while they still had a dense field of miniaturized hairs may see a substantial cosmetic improvement if enough of those hairs thicken. Someone with a longstanding slick-bald area may have fewer follicles capable of producing visible hair, even if some follicular structures remain in the scalp.

Does Fibrosis Create a Point of No Return?

Perifollicular inflammation and fibrosis have been observed in AGA, particularly around the upper follicle. Histological studies have identified inflammatory cell infiltrates and fibrotic changes in at least some of the affected scalp areas.^[23]Jaworsky, C., Kligman, A.M., Murphy, G.F., & Kennedy, J.W. (1992). Characterization of inflammatory infiltrates in male pattern alopecia: Implications for pathogenesis. British Journal of … Continue reading,^[24]Mahé, Y.F., Michelet, J.F., Billoni, N., et al. (2000). Androgenetic alopecia and microinflammation. International Journal of Dermatology. 39(8). 576-584. Available at: … Continue reading 

This has led to an understandable theory. Perhaps fibrosis gradually locks a follicle into a permanent non-responsive state. 

But the evidence is not strong enough to say that fibrosis is the sole cause of irreversible AGA.

AGA is a complex condition involving several factors, one of which may be fibrosis, but it should not be treated as the sole explanation for why recovery becomes harder. 

The Arrector Pili Muscle Hypothesis

Another proposed explanation involves the arrector pili muscle, the tiny smooth muscle attached to the hair follicle that causes goosebumps.

Research suggests that miniaturized hair follicles in AGA may lose their normal attachment to the arrector pili muscle. This is notable because miniaturized follicles in alopecia areata may preserve this attachment and can often regrow terminal hair when the autoimmune process resolves.^[25]Yazdabadi, A., Whiting, D., Rufaut, N., & Sinclair, R. (2012). Miniaturized hairs maintain contact with the arrector pili muscle in alopecia areata but not in androgenetic alopecia. International … Continue reading 

This has been proposed as one reason why AGA miniaturization may become harder to reverse than miniaturization in alopecia areata. However, this is best understood as a biological model rather than a clinically validated “point-of-no-return” test. No clinician can currently examine a scalp and use arrector pili attachment alone to calculate the chance that a particular follicle will regrow.

How Can You Estimate Whether a Hair Follicle Might Respond?

There is a non-invasive test that can prove whether a specific follicle is recoverable. 

But clinicians can look for clues to help estimate whether an area of the scalp still contains follicles capable of producing more visible hair. 

Visible Miniaturized Hairs

Fine, short hairs in an area of thinning are often more encouraging than completely smooth, long-bald skin. While this does not guarantee regrowth, it suggests that follicles in the area are still producing shafts, even if those shafts are currently too fine to provide useful density.

Hair-Shaft Diameter Diversity

A mixture of thick terminal hairs and fine miniaturized hairs is a hallmark of active AGA miniaturization. Trichoscopy can show this variation more clearly than the naked eye. It can also identify an increased proportion of vellus-like hairs, changes in follicular units, and regional density differences.^[26]Kuczara, A., Waskiel-Burnat, A., Rakowska, A., Olszewska, M., & Rudnicka, L. (2024). Trichoscopy of androgenetic alopecia: A systematic review. Journal of Clinical Medicine. 13(7). 1962. … Continue reading

Density Under Standardized Trichoscopy

A standardized trichoscopic examination or phototrichogram can help document:

• Hair density per square centimeter.
• Average shaft diameter.
• The proportion of terminal versus vellus-like hair.
• Changes in the same scalp area over time.

Duration and Speed of Progression

Duration matters, but it is not a precise predictor. 

An area that has been slick-bald for many years is generally less likely to respond than an area that has recently thinned and still contains visible miniaturized hairs. But there is no scientifically validated rule stating that follicles become irreversibly “dead” after a specific number of years. 

Speed also matters. Rapid recent thinning may warrant evaluation for additional contributors, such as telogen effluvium, inflammatory scalp disease, medication effects, nutritional deficiency, or endocrine conditions.

Duration and Speed of Progression

Duration matters, but it is not a precise predictor. 

An area that has been slick-bald for many years is generally less likely to respond than an area that has recently thinned and still contains visible miniaturized hairs. But there is no scientifically validated rule stating that follicles become irreversibly “dead” after a specific number of years. 

Speed also matters. Rapid recent thinning may warrant evaluation for additional contributors, such as telogen effluvium, inflammatory scalp disease, medication effects, nutritional deficiency, or endocrine conditions.

Response to an Adequate Treatment Trial

Ultimately, an individual’s response after a sufficiently long and consistent treatment trial is often more useful than a baseline prediction.

AGA treatments work slowly because hair cycling is slow. A short trial of a few weeks or a couple of months is generally not enough to judge whether miniaturized hairs are thickening or whether progression has stabilized. 

Photographs can help, but only if they are standardized.

For useful comparisons, take photographs with the same:

• Lighting
• Camera distance
• Camera angle
• Hair length
• Hairstyle or part placement
• Scalp dryness and hair product use
• Head position

Phone photographs alone cannot determine whether follicles are viable. They can show changes in coverage, but they cannot distinguish miniaturization from shedding, breakage, changes in hair length, or lighting changes.

A scalp biopsy is also not normally required solely to predict regrowth in typical AGA. Biopsy is generally reserved for uncertain cases, atypical presentations, or situations where scarring alopecia or another diagnosis needs to be excluded.

Is There a Proven Point of No Return?

No. 

There is currently no validated hair-diameter threshold, duration of baldness, Norwood stage, fibrosis score, or trichoscopic measurement that defines the exact point at which an AGA follicle becomes irreversibly non-responsive. 

Longstanding bald areas are less likely to produce substantial regrowth with existing medical treatments than areas containing numerous fine hairs. But less likely is not the same as impossible, and current evidence does not allow clinicians to calculate a precise individual probability from duration alone. 

This uncertainty can be frustrating. But it is better than false certainty in either direction. 

Final Thoughts

AGA miniaturization is best understood as a continuum rather than an on/off process. Affected follicles do not usually vanish all at once; instead, they gradually become smaller and produce hairs that are shorter, finer, less pigmented, and less able to cover the scalp. Because neighboring follicles can be at different stages of miniaturization, AGA often creates a mixture of thick terminal hairs and fine vellus-like hairs rather than uniform hair loss. This is also why “dead” and “dormant” are imperfect descriptions: a miniaturized follicle may still be present and may still produce a hair shaft, but it may no longer produce hair that contributes meaningfully to cosmetic density. 

Research suggesting that some follicular stem-cell populations persist in bald AGA scalp is biologically important, but it should not be interpreted as proof that long-bald follicles can currently be restored to their original state. The more realistic takeaway is that treatment can sometimes reverse part of miniaturization, particularly in follicles that are still producing fine, visible hairs. Finasteride, minoxidil, and combination approaches may help preserve existing hair, slow further diameter loss, and improve the thickness, length, or visibility of hair that remains responsive. This is why earlier treatment generally offers the greatest opportunity: the goal is not always dramatic regrowth or a return to original density, but preventing further deterioration while improving the follicles that are still capable of producing visible hair.

Oral minoxidil has become one of the most popular treatments for pattern hair loss, and for good reason. In clinical trials, it works just as well or even outperforms 5% topical minoxidil, with investigator assessments rating oral minoxidil as performing better than topical minoxidil. ^[1]Penha, M.A., Miot, H.A., Kasprzak, M., Müller Ramos, P. (2024). Oral Minoxidil vs Topical Minoxidil for Male Androgenetic Alopecia: A Randomized Clinical Trial. JAMA Dermatology. 160(6). 600-605. … Continue reading^[2]Ramos, P.M., 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: A randomized clinical trial. … Continue reading

Oral minoxidil is also affordable, convenient, and, with the increasing popularity of telemedicine, as accessible as ever.

But there’s a trade-off.

Oral and topical minoxidil work the same way. Minoxidil is enzymatically activated, converted into minoxidil sulfate (the active form of the drug), interacts with the cells in the hair follicle, and, in turn, enhances hair growth.

With the use of topical minoxidil, this activation process happens in the hair follicle itself. With oral minoxidil, some of this happens in the liver, in a metabolic process called first-pass metabolism.

The minoxidil and active minoxidil sulfate then travel through the blood to the scalp and into the hair follicles themselves, where they support hair growth. But because the blood delivers minoxidil sulfate throughout the whole body, it also results in significant exposure to different parts of the body, like the cardiovascular system.

As a result, oral minoxidil has an increased risk of cardiovascular side effects that we don’t typically see with topical minoxidil. These may include:

• Heart palpitations
• Tachycardia
• Fluid retention
• Dizziness
• Pericardial effusion
• and more

However, these side effects typically only occur once the active minoxidil sulfate reaches cardiovascular tissue via the bloodstream. If we can reduce the blood levels of active minoxidil sulfate, we can, in theory, reduce the risk of side effects with oral minoxidil while (hopefully) still maintaining the directionally better results.

This is the premise of sublingual minoxidil, a form of oral minoxidil that dissolves under the tongue.

This article explains the science behind sublingual minoxidil, why it works, and why, in all likelihood, it could be a better form of minoxidil.

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Is Oral Minoxidil Better Than Topical Minoxidil?

Topical minoxidil is one of two FDA-approved treatments for androgenic alopecia (AGA). It’s been studied since the 1980s. Regrowth tends to peak between months four and eight of treatment, and in people who keep using it, the gains hold through at least year five.

The catch is that it only works for about 40 to 60% of people who try it. Surveys of people who quit topical minoxidil find that most of them stopped because they didn’t see results.

The reason for this is twofold:

• Penetration. Only a small fraction of the minoxidil applied to the scalp makes it through the skin to the follicles.
• Activation. Minoxidil is a prodrug (i.e., it’s inactive until the body converts it). The conversion is done by an enzyme called sulfotransferase, which attaches a sulfate group to minoxidil and turns it into minoxidil sulfate. Minoxidil sulfate is the form of minoxidil that opens potassium channels in the follicle and stimulates growth. If the scalp doesn’t have enough sulfotransferase activity, minoxidil sits inactive in the skin and doesn’t produce an effect. And, as it turns out, a large share of people fall into this category: in one study of 120 patients, 40.8% had low sulfotransferase activity in their scalp.^[3]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 And the research suggests this likely makes a meaningful difference in the effectiveness of topical minoxidil: around 85% of patients with normal enzyme activity responded to topical minoxidil, compared to just 8.7% of those with low sulfotransferase activity.^[4]Goren, A., Shapiro, J., Roberts, J., Desai, N., Zarrab, Z., Pietrzak, A., Lotti, T. (2015). Clinical utility and validity of minoxidil response testing in androgenetic alopecia. Dermatologic Therapy. … Continue reading

Oral minoxidil, on the other hand, is metabolized differently. Instead, part of the oral minoxidil taken orally is activated by sulfotransferase in the liver. It then travels from the bloodstream to the scalp, where it delivers active minoxidil sulfate to hair follicles and supports growth. It also delivers inactive minoxidil, which is then activated by sulfotransferase enzymes in the scalp.

In other words, oral minoxidil overcomes both critical barriers to efficacy with topical minoxidil. It delivers more inactive minoxidil and supplies minoxidil sulfate to the follicle without having to rely on sulfotransferase enzymes in the scalp alone.

But the bloodstream doesn’t just deliver active minoxidil sulfate to the scalp, it also delivers it systemically, including to sensitive tissues like the cardiovascular system. Because minoxidil sulfate is a potent vasodilator (i.e., it relaxes the smooth muscle in blood vessel walls), it can have a significant effect on the cardiovascular system.

As a result, oral minoxidil carries a risk of cardiovascular side effects that we don’t typically see with topical minoxidil, where only around 1.4% of the applied dose reaches the bloodstream. These side effects are typically very rare, but can include:^[5]Jimenez-Cauhe, J., Lo Sicco, K.I., Shapiro, J., Hermosa-Gelbard, A., Burgos-Blasco, P., Melian-Olivera, A., Ortega-Quijano, D., Pindado-Ortega, C., Buendia-Castaño, D., Asz-Sigall, D., Vaño-Galvan, … Continue reading

• Heart palpitations and tachycardia (0.9 to 4% of patients)
• Fluid retention (1.3 to 10%)
• Dizziness or lightheadedness (1 to 1.7%)
• Pericardial effusion (extremely rare at doses used in hair loss)

But what if there was a way to deliver active minoxidil to the follicles without exposing the rest of the body to minoxidil sulfate? Could there be an opportunity for us to harness the benefits of oral minoxidil while minimizing the side effects?

Sublingual minoxidil might be the answer. Let’s unpack the research.

Oral vs. Sublingual Minoxidil: The Research

When taken sublingually, oral minoxidil bypasses first-pass hepatic metabolism. In other words, it skips metabolic processing in the liver, including by the sulfotransferase enzyme. So instead of minoxidil sulfate being delivered to follicles alongside the inactive minoxidil, sublingual minoxidil means only the inactive minoxidil is transported via the bloodstream to the scalp, not minoxidil sulfate.

With less active minoxidil sulfate in the bloodstream to interact with tissues other than the scalp, you would expect to see a lower rate of side effects.

And that’s exactly what researchers found.

Study #1

In a randomized, double-blind, placebo-controlled phase I trial, published in 2021, researchers tested the effects of three doses of sublingual minoxidil, 0.45 mg, 1.35 mg, and 4.05 mg, in 40 men and women with AGA. ^[6]Bokhari, L., Jones, L.A., Sinclair, R.D. (2022). Sublingual minoxidil for the treatment of male and female pattern hair loss: a randomized, double-blind, placebo-controlled, phase 1B clinical trial. … Continue reading

The sublingual minoxidil was considered effective. At 24 weeks, hair density improved in a dose-dependent way: roughly 45% of patients on 0.45 mg showed improvement in frontal density and 55% at the vertex, rising to nearly 67% in both areas with a 4.05 mg dose.

However, because there was no oral minoxidil group in this study, we don’t know how it compares to oral minoxidil for efficacy or side effects.

Study #2

In a hallmark study, researchers directly compared the efficacy and safety of oral minoxidil with sublingual minoxidil. ^[7]Sanabria, B., Miot, H.A., Sinclair, R., Chaves, C., Müller Ramos, P. (2025). Sublingual Minoxidil 5 mg versus Oral Minoxidil 5 mg for male androgenetic alopecia: A double-blind randomized clinical … Continue reading

110 men with AGA (Norwood-Hamilton 3V, 4V, and 5V) were enrolled. One group took 5 mg of sublingual minoxidil daily plus an oral placebo. The other took 5 mg of oral minoxidil daily plus a sublingual placebo. Total and non-vellus hair density were measured in the vertex by trichoscopy with hair-to-hair matching, and three dermatologists blind to treatment scored global photographs.

After 24 weeks:

• Total hair density rose by 24.5 hairs/cm² in the sublingual group and 21.8 hairs/cm² in the oral group.
• Terminal hair density rose by 7.8 hairs/cm² with sublingual and 7.4 hairs/cm² with oral.
• On global photographs of the crown, 42% of the sublingual group and 40% of the oral group were rated as improved.

While sublingual numbers were directionally a little higher, both sublingual and oral minoxidil were measured as having about the same impact on hair growth.

However, side effects are where the groups separated:

• Heart palpitations occurred in 4 of 43 men (9.3%) on oral minoxidil and 0 of 43 men (0%) on sublingual minoxidil.
• Hypertrichosis was the most common side effect on both routes and was nearly identical at most sites: beard growth in 47.9% vs. 48.8%, chest hair in 43.8% vs. 42.9%. The one exception was the upper back (43.8% sublingual vs. 18.6% oral), which the authors noted as an unusual result.
• Shedding, insomnia, headache, dizziness, and mild swelling were infrequent and similar across groups.

At the end of the study, the authors concluded that sublingual minoxidil and oral minoxidil were about on par in terms of efficacy. Both were well tolerated, with less frequent palpitations in the sublingual group. The authors attribute the absence of palpitations to minoxidil escaping hepatic metabolism.

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Study #3

The original publishers of the 2021 study revisited their original data, using hair-to-hair matching software to track the diameter of individual hairs from baseline to week 24.^[8]Sinclair, R., Sicinska, J., Bokhari, L., Kasprzak, M. (2025). Sublingual minoxidil increases fibre diameter in male androgenetic alopecia: a proxy for reversal of hair follicle miniaturization. … Continue reading

There were considerable differences across doses and placebo:

• In the placebo group, average hair fiber diameter fell by 2 µm over 24 weeks.
• At 0.45 mg, it also fell by 2 µm.
• At 1.35 mg, hair fiber diameter rose by 3 µm.
• At 4.05 mg, it rose by 6 µm, the largest gains in the thickest hairs.

Because hair follicle miniaturization and the resultant shrinking of hair diameter are significant drivers of pattern hair loss, thickening of hair diameter suggests sublingual minoxidil may address a significant underlying factor in hair loss.

Notably, this is the first human evidence that a minoxidil treatment thickens existing hairs, consistent with the vellus-to-terminal reconversion seen in a humanized mouse model.^[9]Gilhar, A., Keren, A., Paus, R. (2023). Vellus-to-terminal hair follicle reconversion occurs in male pattern balding and is promoted by minoxidil and platelet-rich plasma: in vivo evidence from a new … Continue reading

However, like the original study, we are limited in our ability to compare this directly to oral minoxidil.

Study #4

In a 2026 randomized, double-blind, placebo-controlled trial, researchers assessed the effect of sublingual minoxidil in transgender people recorded female at birth and taking full-dose testosterone.^[10]Tang, G.T., Leemaqz, S., Bhoyrul, B., Eisman, S., Kasprzak, M., Sicinska, J., Sinclair, R., Cheung, A.S. (2026). Treatment of androgenetic alopecia in transgender people receiving testosterone … Continue reading This group develops AGA at about 2.5 times the rate of cisgender women, and finasteride is generally a poor fit because it can interfere with masculinization.

Participants were randomized to sublingual minoxidil (titrated to 1.35 mg twice daily) or placebo for 24 weeks, then moved to 2.5 mg twice daily in an open-label extension through week 48. Blood pressure, heart rate, and testosterone were measured at every visit.

At 24 weeks, midfrontal total hair count rose by 15.7 hairs/cm² more on minoxidil than on placebo (p=0.03), and non-vellus hair count by 12.7 hairs/cm² more (p=0.04). At 24 weeks, sublingual minoxidil didn’t beat placebo for vertex hair growth but eventually outpaced placebo by week 48. Self-rated vertex improvement was 57% on minoxidil versus 30% on placebo. There was no difference between groups in postural hypotension, hypertrichosis, or any other side effect, and sublingual minoxidil didn’t impact blood pressure, heart rate, or testosterone levels.

Study #5

Andrés-Lencina and colleagues reviewed 87 patients (73 women, 14 men) treated with a compounded sublingual minoxidil spray at their clinic.^[11]Andrés-Lencina, J.J., Brisco, F., Ricart, J.M., Gómez-Zubiaur, A. (2025). Tolerance and Safety Profile of Sublingual Minoxidil in the Treatment of Androgenic Alopecia. Actas Dermo-Sifiliográficas. … Continue reading Median doses were 0.5 mg per day for women and 1 mg per day for men. Three months in, patients were surveyed by phone about side effects.

The authors compared their results against two large oral minoxidil series. Side effects were less frequent with sublingual minoxidil than in a 435-patient oral minoxidil study that used the same phone survey, and about as frequent as in a 1,404-patient oral minoxidil study that relied on medical records rather than patient surveys.^[12]Sanabria, B., de Nardo, V.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 Dermatology. … Continue reading^[13]Vañó-Galván, S., Pirmez, R., Hermosa-Gelbard, A., et al. (2021). Safety of low-dose oral minoxidil for hair loss: A multicenter study of 1404 patients. Journal of the American Academy of … Continue reading

Sublingual Minoxidil Studies: Where Do We Stand?

All in, while more research is needed, the existing research suggests sublingual minoxidil seems to perform on par with or directionally better than oral minoxidil. Even better, it seems to do so with a much lower risk of some side effects.

According to these studies, it seems the cardiovascular impact of minoxidil may be, in part, related to the spike of the active drug in the blood. If we can prevent a spike of active minoxidil sulfate in the blood, we can, in theory, reduce the risk of side effects with oral minoxidil while (hopefully) keeping the directionally better regrowth.

However, sublingual delivery doesn’t seem to reduce the risk of other side effects like hypertrichosis, insomnia, headache, dizziness, and fluid retention. However, all but hypertrichosis remained rare.

But What If I Have Low Sulfotransferase Levels In My Scalp?

If you have lower sulfotransferase levels in your scalp, you might be worried that sublingual minoxidil might not be as effective as oral minoxidil. After all, if the advantage of oral minoxidil is that it bypasses the need for minoxidil activation in the scalp, then we would expect that bypassing activation in the liver with sublingual minoxidil could theoretically lead to subpar results (compared to regular oral minoxidil).

Except this doesn’t seem to be true. In research comparing oral and sublingual minoxidil, they generally perform about the same despite the fact that sublingual minoxidil bypasses this essential step.

Why might this be the case? There are two reasons:

• Sublingual minoxidil bypasses sulfation in the liver, but it also bypasses glucuronidation. Glucuronidation is another metabolic process that occurs in the liver after taking oral minoxidil. Except instead of activating minoxidil, this process actually inhibits it. As a result, a portion oral minoxidil may be activated by the liver, but a portion is also be inhibited. In short, sublingual minoxidil might be more bioavailable even if it’s not converted to its active form before reaching the hair follicle. This might mean that sublingual minoxidil, by bypassing glucuronidation, supplies a larger amount of minoxidil to be converted to minoxidil sulfate in the follicle. In turn, more bioavailable amounts of minoxidil may make up for less minoxidil sulfate.
• The liver doesn’t contribute much at all to the efficacy of oral minoxidil. If oral minoxidil arrived at the follicle in its activated sulfate form (in sufficient amount), then the number of sulfotransferase enzymes present in your scalp shouldn’t affect response to oral minoxidil at all. But it, as it turns out, it does. In a 2020 study, researchers studying oral minoxidil found that low follicular sulfotransferase activity predicted weaker regrowth with oral minoxidil.^[14]Ramos, P.M., Goren, A., Sinclair, R., Miot, H.A. (2020). Oral minoxidil bio-activation by hair follicle outer root sheath cell sulfotransferase enzymes predicts clinical efficacy in female pattern … Continue reading In other words, even with oral minoxidil, sulfotransferase activity at the follicle is likely still a main reservoir of the active drug. As such, the reason oral minoxidil has less to do with bypassing scalp enzymes, and more to do with the amount of inactive minoxidil it delivers to the follicle. By delivering more minoxidil to the follicles, it overcomes the reduced absorption of topical minoxidil, producing a greater effect. It doesn’t mean the active minoxidil sulfate delivered to the scalp via the liver is inconsequential in oral minoxidil treatment, but rather that it’s not the most significant factor.

As a result, it doesn’t seem that there is a disadvantage to using sublingual minoxidil when it comes to expected growth potential.

Is There a Best Sublingual Minoxidil Dose?

Sublingual minoxidil has been tested at various doses in the research, as low as 0.45 mg and as high as 5 mg. While doses of 0.45 mg, 1.35 mg, 2.5 mg, 4.05 mg, and 5 mg have all shown favorable results, only 5 mg has data to support its non-inferiority to standard oral minoxidil. 1.35 mg and 2.5 mg were rated as more effective than placebo, but weren’t validated against standard oral minoxidil.

This doesn’t mean doses lower than 5 mg won’t be effective, but it is the most evidence-backed dose when it comes to sublingual minoxidil.

Is Sublingual Minoxidil Available Today?

Ulo just released their Sublingual Minoxidil Rx. It’s an orange-flavored, rapidly dissolving tablet that easily dissolves under the tongue. It’s a convenient, easy way to take oral minoxidil while harnessing the potential of sublingual delivery.

Sublingual Minoxidil From our partners at Ulo

Sublingual Minoxidil

A rapidly-dissolving sublingual tablet with minoxidil. Available in 1.25 mg and 2.5 mg doses. Prescribed 100% online. Choose a multi-month plan and get up to 30% plus a free gift bundle.

Free full-size gifts with 3-month+ plans Prescribed online, shipped to your door

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Sublingual deliveryDissolves under the tongue

*Only available in the U.S. Prescription requires an online medical consultation at no extra cost. Off-label products are not endorsed by the FDA. Free gifts included with select multi-month plans while supplies last. Ulo is a partner of Perfect Hair Health; we may earn a commission on purchases.

Bottom Line

Sublingual minoxidil made its way into research on the premise that its delivery route might have less of an impact on the cardiovascular system. And in a landmark head-to-head trial, researchers found exactly that. Heart palpitations occurred in 0% of men taking 5 mg of sublingual minoxidil, compared with 9% of men taking 5 mg of standard oral minoxidil. And importantly, it was just as effective: both groups grew the same amount of hair over six months.

Oral minoxidil’s cardiovascular effects are driven by a spike in the active form of minoxidil, minoxidil sulfate, in the blood. That surge in active minoxidil dips blood pressure and contributes to related side effects.

Sublingual minoxidil minimizes the spike in the active form of minoxidil by bypassing the first-pass metabolism responsible for its activation. Instead, minoxidil gets supplied directly to the scalp tissue, and at higher amounts than topical minoxidil.

This is also why sublingual minoxidil performs on par with oral minoxidil: by delivering higher amounts to the hair follicle, more minoxidil can be converted to the active form in the follicles. By providing a higher dose of minoxidil to follicles, both oral and sublingual minoxidil outperform topical minoxidil.

In general, research around sublingual minoxidil is still in its infancy. However, the early clinical data make it a reasonable option for anyone looking to explore other forms of minoxidil that are best suited to their needs and preferences when approaching hair loss.