Education. Evidence. Regrowth.
Prioritize knowledge. Make better choices.
Sort good studies from the bad.
Get bigger hair gains.
PhD's, resarchers, & consumer advocates.
Founder, researcher, & consumer advocate
Our team of PhD’s, researchers, & more
Discover how we conduct our research.
Have questions? Contact us.
Our library of before-after photos.
I have attached my before and afters of my progress since joining this group...
I’m convinced I’ve recovered to probably the hairline I had 3 years ago. Super stoked…
My friends actually told me, “Your hairline improved. Your hair looks thicker...
I also feel my hair has a different texture to it now…
Firstly thank you for your work in this field. I am immensely grateful that...
I just wanted to thank you for all your research, for introducing me to this method...
To be honest I am having fun with all this and I still don’t know how much...
I see a massive amount of regrowth that is all less than about 8 cm long...
150+ member experiences.
Scroll DownPopular treatments. But do they work?
Top-selling ingredients, quantified.
The truth about hair loss "best sellers".
Xyon Health
Strut Health
Happy Head
DS Laboratories
Advanced Trichology
Fully Vital
Xyon Health
DrFormulas
Revivogen MD
Standardized rubrics to evaluate all treatments.
Is this treatment well studied?
How much regrowth can you expect?
Is this treatment safe & sustainable?
Apps, tools, guides, freebies, & more.
100+ free articles.
Our team’s peer-reviewed studies.
Education. Evidence. Regrowth.
PhD's, resarchers, & consumer advocates.
Discover how we conduct our research.
Have questions? Contact us.
Our library of before-after photos.
Read the experiences of members
Finasteride and dutasteride are prescription medications that treat androgenic alopecia (AGA) by targeting the hormone pathway that drives follicle miniaturization. Because they share the same core mechanism and have similar effects on hair loss, understanding which treatment is the best choice for you is not straightforward.
In this article, we tackle the questions that come up most often when choosing between finasteride and dutasteride. We’ll break down how they differ biologically, what head-to-head studies really show about regrowth and side effects, and how oral versus topical use changes the equation, so you can make a more informed decision about which option makes sense for your hair loss and your goals.
Low-dose & full-strength finasteride 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.
*Only available in the U.S. Prescriptions not guaranteed. Restrictions apply. Off-label products are not endorsed by the FDA.
AGA is not a sudden shedding event but a slow remodeling of the hair follicle driven by androgen sensitivity. Across repeated hair cycles, susceptible follicles undergo progressive miniaturization: the growth phase (anagen) shortens with each cycle, while the rest phase (telogen) remains the same or lengthens.
Dihydrotestosterone (DHT) is the key androgen driving follicular miniaturization. An enzyme called 5α‑reductase (5AR) in the hair follicle converts testosterone to DHT. Because DHT is known to drive hair loss progression, many treatments for AGA target 5AR to reduce scalp DHT levels.[1]Asfour, L., Cranwell, W., & Sinclair, R. (2023). Male androgenetic alopecia. *Endotext [Internet].* Available at: https://www.ncbi.nlm.nih.gov/books/NBK278957/
Both finasteride and dutasteride can decrease levels of DHT in the body. They were originally created to treat a condition called benign prostate hyperplasia (BPH), but have been repurposed for AGA since their impact on hair growth was noticed. While finasteride is approved by the FDA for treating both BPH, dutasteride is approved only for BPH and is therefore used off-label for hair loss.
Finasteride is an inhibitor of Type II 5AR, which is highly expressed in hair follicles in androgen‑sensitive regions such as the scalp and prostate tissue. Type II is responsible for the conversion of testosterone to DHT inside miniaturizing scalp follicles, directly driving AGA‑related changes.[2]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
Dutasteride is a dual 5AR inhibitor, which means that it blocks Type I 5AR as well as Type II. Type I 5AR plays a more supportive role and is mainly found in sebaceous glands and skin, so it has a less direct impact on scalp follicular miniaturization.[3]Frye, S. V. (2006). Discovery and clinical development of dutasteride, a potent dual 5α-reductase inhibitor. *Current Topics in Medicinal Chemistry.* 6(5). 405–421. Available at: … Continue reading
Because of this dual action, dutasteride may decrease levels of DHT to a greater extent than finasteride. In fact, studies have shown that dutasteride may decrease DHT by 50% more than finasteride.

Figure 1. The structures of finasteride and dutasteride.[4]Wikimedia Commons. (n.d.). Azasteroid Pharmaceuticals [Image]. *Wikimedia Commons.* Available at: https://commons.wikimedia.org/wiki/File:Azasteroid_Pharmaceuticals.png (Accessed: November 2025) Image in the Public Domain.
Does that mean that dutasteride is the better option? Not necessarily. Lower DHT doesn’t necessarily translate into improved hair growth. What’s more, side effects associated with decreased DHT, particularly sexual dysfunction, can affect other aspects of health and well-being.
To understand the potential benefits and side effects of finasteride and dutasteride, we’ll dive into the science and studies that can help us make choices about treatment options.
It’s important to recognize that there are many different ways both finasteride and dutasteride can be taken. This includes the drug’s concentration, the frequency of administration, and the formulation used.
Oral finasteride and later oral dutasteride were designed to suppress DHT throughout the body, and they remain the most thoroughly studied options for AGA. Oral finasteride is most commonly prescribed at 1mg daily for AGA, while oral dutasteride is typically taken at 0.5mg daily. Some studies have tested a wider range of concentrations to investigate if there are any changes in benefit or risk.
Topical formulations were introduced later to change the risk profile without affecting the mechanism. Instead of lowering DHT systemically by default, topical finasteride was designed to concentrate drug activity in the scalp while limiting how much reaches the bloodstream.
Topical dutasteride represents the newest and least mature category, but evidence is promising. Because dutasteride is more potent than finasteride, even very low topical concentrations (around 0.01-0.05%) can meaningfully suppress scalp DHT. Importantly, both finasteride and dutasteride can and do enter systemic circulation when applied to the scalp, so safety concerns still need to be addressed.
Because there is a range of treatment options for both finasteride and dutasteride, there is also a web of comparisons we can make when trying to compare the two. First, we’ll compare oral formulations. These are best researched, and there are a number of head-to-head comparison studies we can use to assess their effectiveness.
Here is a summary of the clinical trials that compare oral finasteride and dutasteride treatment directly:
| Study Design and Population | Treatments | Impact on DHT | Hair Growth Comparison | |
| Study #1[5]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 | Randomized, placebo-controlled, double-blinded trial. 415 men with male pattern hair loss aged 21-45 years old; 24 weeks. | 5 mg finasteride; 0.05, 0.1, 0.5, or 2.5 mg dutasteride; placebo. | Serum DHT was significantly lower at 0.5 and 2.5 mg dutasteride than at 5 mg finasteride. 5mg finasteride decreased scalp DHT by 41%, while 0.5 and 2.5 mg dutasteride decreased it by 51% and 79% respectively. | The proportion of participants with at
least a 10% increase in hair counts was 41% for finasteride, and 48%, and 56% for 0.5 and 2.5 mg dutasteride, respectively. |
| Study #2[6]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 | Randomized, placebo-controlled, double-blinded trial. 917 men with AGA aged 20-50; 24 weeks. | 1 mg finasteride; 0.02, 0.1, or 0.5 mg dutasteride; placebo | Not assessed. | 0.5 mg dutasteride significantly improved hair growth compared to 1 mg finasteride. |
| Study #3[7]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 | Open-label, randomized study; no placebo control. 90 men with AGA aged 18-40; 24 weeks. | 1 mg finasteride; 0.5 mg dutasteride. | Not assessed. | Increase in total hair count was significantly higher in dutasteride compared to finasteride. |
| Study #4[8]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 | Retrospective chart review. 600 men over 18 with AGA. | 1 mg finasteride; 0.5 mg dutasteride. | Not assessed. | Dutasteride improved BASP basic M classification of AGA significantly better than finasteride. |
These RCTs directly comparing finasteride and dutasteride provide the best insight into their comparative efficacy. We’ll focus on 1 mg finasteride vs. 0.5 mg as these are the most commonly used doses. While these studies differ in design and duration, their findings are consistent across several clinically meaningful outcomes.
Key Takeaways from Trials
An important limitation to consider when interpreting these trials is the length of the studies. Most head-to-head RCTs run for 24 weeks, which may favor dutasteride if it is faster acting. Finasteride, by contrast, is known from longer studies to continue producing gains for 48 months, with hair counts typically plateauing only after around 2 years.[12]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
However, long-term data, though mostly retrospective rather than randomized, still suggest sustained superiority of dutasteride on global classification scales.[13]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
On paper, dutasteride often looks clearly superior to finasteride. But translating statistical superiority from randomized trials into real-world expectations requires more nuance. The practical difference between these drugs depends less on averages and more on what kind of hair loss someone has, how fast it’s progressing, and how much regrowth is biologically possible.
Blocking 5AR interferes with hormone activity and is known to cause some side effects. The most frequently discussed effects include:
As we’ve already noted, the dual action of dutasteride could mean that it poses an increased risk of side effects. To see whether the evidence backs this up, we’ll take a look at what randomized trials and retrospective studies tell us about the comparative risks of each treatment. Below is a summary of the head-to-head studies to date.
| Average incidence of side effects | Decreased libido | Ejaculation disorders | Erectile dysfunction | Breast enlargement and tenderness | |
| Study #1[15]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 | Finasteride 2.6% vs dutasteride 4.6% | Finasteride – 5 mg: 4%. Dutasteride – 0.1 mg: 3%; 0.5 mg: 1%; 2.5 mg: 13%. | Dutasteride – 0.1 mg: 4%; 0.5 mg: 1%; 2.5 mg: 13%. Finasteride – 5 mg: 1% | Dutasteride – 0.1 mg: 0%; 0.5 mg: 0%; 2.5 mg: 0%. Finasteride – 5 mg: 1% | Not assessed. |
| Study #2[16]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 | Finasteride 10.0% vs dutasteride 10.0% | Not assessed. | Not assessed. | Not assessed. | Not assessed. |
| Study #3[17]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 | Finasteride 13.4% vs dutasteride 11.5% | Finasteride – 1 mg: 6.7%. Dutasteride – 0.02 mg: 8.1%; 0.1 mg: 6.9%; 0.5 mg: 3.3%. | Finasteride – 1 mg: 3.9%. Dutasteride – 0.02 mg: 2.2%; 0.1 mg: 4.8%; 0.5 mg: 3.9%. | Finasteride – 1 mg: 5.6%. Dutasteride – 0.02 mg: 4.3%; 0.1 mg: 3.7%; 0.5 mg: 5.6%. | Finasteride – 1 mg: 0.6%. Dutasteride – 0.02 mg: 0.5%; 0.1 mg: 0.5%; 0.5 mg: 0.6%. |
| Study #4[18]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 | Finasteride 10.5% vs dutasteride 7.6% | Finasteride 0.7% vs dutasteride 1.2% | Not assessed | Finasteride 0% vs dutasteride 0.4% | Not assessed |
As we can see, across randomized and controlled studies comparing dutasteride and finasteride, the overall incidence of side effects is similar between the two drugs. When averaged across trials, total reported side effects occur at nearly identical rates (approximately 8-9% for both drugs).
In some studies, finasteride shows equal or higher rates of certain sexual side effects despite producing less DHT suppression. Importantly, these findings hold even when dutasteride reduces serum DHT by an additional 19-23% beyond finasteride and scalp DHT by significantly greater margins. The most closely scrutinized adverse effects, such as reduced libido, erectile dysfunction, and ejaculation disorders, do not follow a clear dose-response pattern with dutasteride.
Given that dutasteride suppresses systemic and scalp DHT substantially more than finasteride, the lack of a clear increase in side effects may seem counterintuitive.
DHT reduction alone does not appear to be a reliable predictor of side-effect risk. This suggests that once DHT is reduced beyond a certain threshold, further suppression may not meaningfully increase the likelihood of side effects, particularly if compensatory mechanisms come into play. For example, lowering of DHT below a certain level might activate hormonal mechanisms to redress the balance. Long-term studies further support this idea, showing that side-effect incidence with dutasteride tends to decrease over time rather than accumulate.
Dutasteride’s size and tissue accessibility might also play a role. It has a much higher molecular weight (around 528 daltons) than finasteride (372 daltons), which likely limits its ability to cross the blood–brain barrier. Finasteride, by contrast, is small enough to enter brain tissue more readily. Because androgen metabolism in the brain is implicated in libido and sexual function, a drug that primarily exerts its effects in peripheral tissues may suppress DHT more aggressively without proportionally increasing neurological side effects.
Reported rates of side effects with finasteride and dutasteride vary widely across studies largely because incidence is highly dependent on study design. The makeup of the participant groups can impact how likely they are to experience side effects. How side effects are defined and recorded can also influence estimates. Some studies rely on spontaneous self-reporting, while others use targeted questionnaires or direct investigator questioning. These different approaches produce different reporting rates.
Psychological and selection factors further complicate interpretation. Participants who expect problems are more likely to notice and report them, even in placebo groups (this is called the nocebo effect). This means the information that participants receive can impact side effects.
Most randomized controlled trials are short (e.g., 24 weeks), enroll relatively healthy participants, and use structured adverse-event reporting. This means they tend to capture early, transient side effects, while missing longer-term patterns such as spontaneous resolution or adaptation. In contrast, observational and retrospective studies follow broader populations over longer periods but rely on less standardized reporting, which can inflate or obscure true incidence.
As a result, short-term trials may overestimate persistent risk, while long-term datasets may underrepresent early intolerance.
Where trials discuss the resolution of side effects, one trial reported that around half of affected participants taking dutasteride reported spontaneous resolution of symptoms while continuing treatment.[19]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 By contrast, finasteride-associated side effects in these trials were less likely to resolve during ongoing treatment, even though many resolved after stopping the drug.
Oral Dutasteride Hair gains bigger than finasteride? Dutasteride makes this possible, 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.
*Only available in the U.S. Prescriptions not guaranteed. Restrictions apply. Off-label products are not endorsed by the FDA.
Post-Finasteride Syndrome (PFS) is a term used to describe persistent sexual, cognitive, or mood-related symptoms that continue for months after stopping finasteride. Its existence and prevalence remain highly debated among dermatologists, endocrinologists, and hair loss researchers.
While some clinicians argue that PFS represents a real, drug-induced condition affecting a very small subset of users, others contend that the available evidence is low quality, heavily confounded by psychological factors, media influence, and the high background rates of sexual dysfunction in adult men.[20]Traish, A. M. (2020). Post-finasteride syndrome: a surmountable challenge for clinicians. *Fertility and Sterility.* 113(1). 21–50. Available at: https://doi.org/10.1016/j.fertnstert.2019.11.030,[21]Trüeb, R. M., Régnier, A., Rezende, H. D., & Dias, M. F. R. G. (2019). Post-finasteride syndrome: an induced delusional disorder with the potential of a mass psychogenic illness?. *Skin … Continue reading
Critically, high-quality clinical trials of finasteride did not report persistent side effects after discontinuation, with symptoms resolving within three months in all affected participants.[22]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 Claims of PFS largely arise from case reports, small observational studies, and self-reported data, all of which suffer from major limitations such as lack of controls and small sample sizes.
One important exception is finasteride-induced gynecomastia (enlarged breast tissue in males), which is a well-documented side effect and can persist in a minority of cases even after stopping the drug, demonstrating that long-lasting tissue changes are possible, albeit rare.[23]Kaplan, S. A., Chung, D. E., Lee, R. K., Scofield, S., & Te, A. E. (2012). A 5-year retrospective analysis of 5α-reductase inhibitors in men with benign prostatic hyperplasia: finasteride has … Continue reading
If PFS is real, it is likely extremely rare, plausibly affecting fewer than 1 in 5,000 – 10,000 users. For users, the key takeaway is one of risk context: while persistent side effects cannot be ruled out entirely, their estimated risk appears very low when weighed against the well-established benefits of finasteride for AGA, especially when dosing strategies are used to minimize overall exposure.
After oral formulations, the next logical question is whether you can get the same DHT-blocking benefits where it matters most. That’s the core promise of topical finasteride and dutasteride formulations: to localize 5AR inhibition to the scalp and reduce the likelihood of systemic side effects.
The potential for using topical formulations opens up a host of new options for treating AGA. Like oral formulations, topicals can also come in a range of concentrations, but can also be delivered in a range of formulations and solutions, including:
Formulations can also be combined with physical methods, such as microneedling, or with other common pharmaceuticals, like minoxidil. This also means that the decisions we need to make when choosing the right hair loss treatment are more complicated. Again, we’ll focus on head-to-head trials that compare different topical and oral formulations, as well as what clinical studies can tell us about side effects.
Based on trials comparing topical dutasteride to other AGA treatments, the answer is a resounding yes. However, the challenge is that finasteride has a highly sensitive, logarithmic dose-response curve. In other words, you don’t need much finasteride in the bloodstream to create a big systemic DHT change. That’s why topical finasteride can still “leak” systemically, and why even small systemic absorption can defeat the original purpose of going topical.
To take a closer look, we’ll first see how topical formulations compare to oral.
Several trials directly comparing topical to oral finasteride show that topical treatment can improve target-area hair counts and other hair parameters similarly to oral dosing, while often producing less suppression of serum DHT and far lower measured systemic drug exposure.
In one Phase III trial, topical finasteride produced hair-count improvements comparable to oral finasteride. What’s more, the oral formulation reduced mean serum DHT by 55.6%, whereas topical finasteride reduced it by 34.5%, and sexual side effects were more associated with oral treatment.[24]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
Other randomized comparisons similarly report meaningful regrowth with topical finasteride, with most adverse events being local (irritation) and relatively few systemic complaints.[25]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
However, even at lower concentrations, topical finasteride can reduce serum DHT depending on how much you apply and how often you apply it. For example, one versus two daily applications of the same topical concentration can produce dramatically different serum DHT suppression, illustrating that frequency and volume can matter as much as concentration.[26]Caserini, M., Radicioni, M., Leuratti, C., Annoni, O., & Palmieri, R. (2014). A novel finasteride 0.25% topical solution for androgenetic alopecia: pharmacokinetics and effects on plasma androgen … Continue reading

Figure 2. Multiple daily doses of topical finasteride can reduce serum DHT more than a single dose. Adapted from Figure 3.[27]Caserini, M., Radicioni, M., Leuratti, C., Annoni, O., & Palmieri, R. (2014). A novel finasteride 0.25% topical solution for androgenetic alopecia: pharmacokinetics and effects on plasma androgen … Continue reading
There are a few key factors that impact absorption:
Topical dutasteride research is newer and still developing, but early findings are encouraging. The current literature suggests that topical dutasteride can meaningfully improve hair density and shaft caliber while producing minimal changes in serum DHT.
A randomized, placebo-controlled trial in 34 men found that microneedling plus 0.01% topical dutasteride produced significant improvements in hair thickness, density, and the vellus-to-terminal ratio, compared with microneedling plus saline.[28]Sánchez-Meza, E., Ocampo-Candiani, J., Gómez-Flores, M., Herz-Ruelas, M. E., Ocampo-Garza, J., Orizaga-y-Quiroga, T. L., Martínez-Moreno, A., & Ocampo-Garza, S. S. (2022). Microneedling plus … Continue reading
This is only a proof-of-concept study with a small sample size. However, it does demonstrate that topical dutasteride can drive clinically meaningful changes when follicular delivery is boostedby microneedling. But it also limits generalizability: microneedling itself is an active intervention, and it may not reflect what happens with topical dutasteride alone.
A newer Phase II trial tested 0.01%, 0.02%, and 0.05% topical dutasteride and reported dose-dependent improvements in total hair count and hair width versus placebo.[29]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
The authors also reported that 0.05% appeared to outperform oral finasteride in total hair count. That’s an attention-grabbing claim, but it should be interpreted cautiously. Unusually high baseline counts and possible inconsistencies in target-area placement, which could inflate apparent differences, raise concerns about the methodology used.

Figure 3. Oral finasteride (yellow line) reduces serum DHT levels more than topical Dutaseride (blue lines). Adapted from Figure 3.[30]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 Image used under Creative Commons License
A common objection is that dutasteride is too large to penetrate the skin well. At around 528.5 Daltons, it sits slightly above the widely cited 500 Dalton rule, which suggests that larger molecules struggle to cross the stratum corneum. In practice, dutasteride appears capable of penetrating the scalp, as it can suppress DHT and promote hair growth.
Topical regimens tend to perform best when they’re used alongside other treatments, rather than as a single agent. DHT drives miniaturization, but follicular stimulation, blood-flow signaling, and wound-healing pathways all influence whether a follicle can thicken and re-enter robust growth.
Microneedling consistently appears in the literature as an accelerator of topical outcomes. Controlled micro-injury activates wound-healing signals that can independently improve density and shaft diameter, while also enhancing follicular penetration and local drug exposure.
Combination with other treatments, primarily minoxidil, can also improve outcomes. The underlying logic is straightforward: minoxidil boosts growth, while dual 5AR blockade increases the probability that follicles remain protected from hormonal changes.
One study showed that adding microneedling to topical finasteride therapy alongside minoxidil can increase hair density and shaft diameter more than minoxidil alone.[31]Chang, Y., Zhang, W., Zhou, J., Lv, L., He, Q., Chen, Y., Wang, P., & Zhai, Q. (2025). Clinical efficacy of microneedle combined with 5% minoxidil solution and finasteride in the treatment of … Continue reading
Similarly, combining dutasteride with microneedling and minoxidil has also demonstrated promising results. In a small study, all patients used topical minoxidil 5%, while adding dutasteride, either systemically or locally, significantly improved hair density and shaft caliber compared with minoxidil alone. The strongest overall results were seen with topical dutasteride 0.02% delivered via monthly microneedling, which outperformed oral dutasteride plus minoxidil on objective measures while maintaining a more favorable safety profile.[32]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
Overall, the evidence suggests that topical regimens may be most effective when they combine anti-androgen suppression, follicular stimulation, and delivery-enhancing strategies.
Hair gains bigger than finasteride? Dutasteride makes this possible, 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.
*Only available in the U.S. Prescriptions not guaranteed. Restrictions apply. Off-label products are not endorsed by the FDA.
Choosing the right dose depends on both the medication and the clinical context. Finasteride, whether oral or topical, is generally the best starting point for most men beginning pharmacologic treatment for androgenetic alopecia. Its pharmacokinetics are more forgiving, dose adjustments are easier, and when side effects occur, they are often manageable with modest reductions in dose or changes in dosing frequency.
Dutasteride, in contrast, is better suited for men with aggressive, fast-progressing AGA or for those who have not responded well to finasteride. Its greater potency comes with less flexibility, largely due to its long half-life and sustained enzyme binding. As a result, dosing with dutasteride should be conservative and deliberate, with careful consideration of long-term exposure and tolerability.
The standard dose of oral finasteride for androgenetic alopecia is 1 mg once daily. This regimen has been used in the majority of randomized controlled trials and has consistently demonstrated improvements in key hair growth outcomes, including hair counts, hair shaft caliber, and investigator global photographic assessments.
A key pharmacologic feature of finasteride is its logarithmic dose–response curve. Most of the drug’s DHT-lowering effect occurs at relatively low doses, and by the time a daily dose of 1 mg is reached, inhibition of type II 5-alpha reductase is already close to maximal.
This explains why lower doses, such as 0.2–0.5 mg daily, can still meaningfully suppress both serum and scalp DHT, and why increasing the dose beyond 1 mg does not lead to proportionally greater hair regrowth. Instead, higher doses primarily increase systemic exposure and may raise the risk of side effects without offering additional cosmetic benefit.

Figure 4. The dose response of finasteride demonstrates that increasing the concentration of treatment doesn’t translate to increased DHT reduction.
From a practical standpoint, this dose–response relationship allows for flexibility in real-world use. Many individuals are able to maintain hair stabilization and regrowth with reduced dosing or alternate-day schedules, particularly after an initial period of stabilization.
When side effects do occur, they also tend to be dose-sensitive rather than all-or-nothing, meaning that lowering the dose or adjusting the dosing schedule is often sufficient to improve tolerability while preserving therapeutic benefit.
The standard oral dose of dutasteride for androgenetic alopecia is 0.5 mg once daily. This is the dose most consistently studied in clinical trials and the dose used in nearly all head-to-head comparisons with finasteride.
The reason dutasteride is prescribed at a lower milligram dose than finasteride comes down to its greater pharmacologic potency. Dutasteride’s pharmacokinetics are also different. The drug has a longer half-life (roughly 4–5 weeks), which means it accumulates in tissues over time.[33]Arif, T., Dorjay, K., Adil, M., & Sami, M. (2017). Dutasteride in androgenetic alopecia: an update. *Current Clinical Pharmacology.* 12(1). 31–35. Available at: … Continue reading
Because of this, missed doses tend to matter less for maintaining efficacy. However, the flip side is that if adverse effects occur, they may take weeks to months to fully resolve after discontinuation, as the drug slowly clears from the body.
These properties have important practical implications for dosing. Daily dosing is not always necessary to maintain clinical benefit, and some clinicians employ intermittent schedules, such as 0.5 mg taken two to three times per week, in an effort to balance efficacy with tolerability.
Topical finasteride dosing is often misunderstood because the percentage concentration listed on the label is not the most important variable. What ultimately determines both efficacy and systemic risk is total daily finasteride exposure, measured in milligrams per day.
This total exposure is shaped by several interacting factors: the concentration of finasteride in the solution, the volume applied per use, how often it is applied (once versus twice daily), and the vehicle or carrier used, such as alcohol or propylene glycol, which influences skin penetration.
The key principle underlying topical finasteride dosing is that finasteride is extremely potent systemically. Only a very small fraction of the drug needs to enter circulation to meaningfully suppress serum DHT. As a result, topical formulations can unintentionally behave like oral finasteride if dosing is too aggressive, even when the product is intended to act locally on the scalp.
An evidence-informed dosing range is 1-2 mL of a 0.005%-0.02% topical finasteride solution applied once daily. This corresponds to roughly 0.1-0.2 mg of finasteride applied to the scalp per day, with estimated systemic exposure in common carriers of approximately 0.01-0.03 mg per day.
Generally, high-concentration formulations (≥0.25-1%) should be avoided, especially when combined with large application volumes or twice-daily use. These regimens can suppress serum DHT to a degree similar to 1 mg of oral finasteride, effectively defeating the purpose of choosing a topical formulation in the first place.
Topical dutasteride dosing is less standardized than topical finasteride, largely because the evidence base is newer and consists of fewer clinical trials. That said, several consistent patterns are beginning to emerge from the available data.
Most studies have evaluated topical dutasteride in a concentration range of 0.01% to 0.05%, typically applied once daily. In many protocols, topical dutasteride has been paired with microneedling to enhance follicular delivery, although some studies suggest that meaningful efficacy can be achieved even without microneedling.[34]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
The practical takeaway is that low-concentration, low-volume topical dutasteride protocols appear to offer the best balance between efficacy and safety. Given the variability in formulations, vehicles, and individual skin permeability, optimal dosing is likely individualized, and careful titration remains essential as the clinical evidence continues to evolve.
Monitoring and risk management with finasteride or dutasteride are about using the minimum effective exposure while staying alert to tolerability over time. Ideally, treatment begins with a clear diagnosis of androgenetic alopecia, baseline photos, and, especially for topical or risk-averse users, optional baseline serum DHT testing to provide context for future changes.
Side effects, if they occur, should be addressed early with dose reduction, spacing doses, or switching delivery routes rather than abrupt discontinuation, since most are dose-sensitive and reversible. For topical users, repeat serum DHT testing after ~30 days can help confirm that systemic exposure remains low.
Ongoing monitoring should focus on objective progress via standardized photos every 3–6 months and general symptom awareness rather than day-to-day fluctuations.
Extra caution is warranted with dutasteride due to its long half-life and accumulation, making conservative dosing and deliberate adjustments especially important. When approached with planned checkpoints and proportional responses, both drugs can be used safely, predictably, and effectively over the long term.
Finasteride and dutasteride are among the most effective pharmacologic options for AGA, but they are not one-size-fits-all treatments. Choosing which drug to use depends on hair-loss pattern, rate of progression, prior treatment response, side-effect tolerance, and long-term goals.
Both drugs require consistent, long-term use to maintain results. Candidates should be comfortable with ongoing therapy and realistic timelines, as visible improvements often take 6-12 months, with maximal benefits closer to two years.
You’re starting treatment, or your AGA is early-to-moderate. Oral finasteride is the usual baseline because it’s effective for most men and has a long track record. It’s also more forgiving: if you need to adjust dose, frequency, or route due to side effects, finasteride is generally easier to fine-tune.
If you’re risk-averse or simply want the most studied on-label option for hair loss, finasteride is usually the logical starting point, especially if you can commit to consistent use and track progress with photos over months.
Your hair loss is aggressive, or you’re losing ground despite finasteride. Dutasteride’s broader 5AR inhibition often translates into greater average gains in hair counts and thickness in shorter head-to-head trials. Clinically, it’s most often considered when progression is rapid, miniaturization is extensive, or finasteride hasn’t provided adequate stabilization after a consistent trial.
Men without androgenetic alopecia – Finasteride and dutasteride are ineffective for conditions such as alopecia areata, telogen effluvium, traction alopecia, or scarring alopecias. Using them in these contexts adds risk without meaningful benefit.
Those highly risk-averse to hormonal manipulation – While most users tolerate these medications well, anyone uncomfortable with altering systemic hormone levels, even at low risk, may prefer non-hormonal options or topical-only approaches with careful dosing.
Men who experienced significant adverse effects previously – Dutasteride may be more appropriate for men with rapid progression, extensive miniaturization, or those who continue to lose ground despite consistent finasteride use. Its stronger and broader DHT suppression can provide an additional margin of control in these cases.
Men trying to conceive in the near term – Although evidence of fertility harm at hair-loss doses is limited, many clinicians advise avoiding systemic 5AR inhibitors when actively trying to conceive, particularly dutasteride due to its long half-life. This decision should be individualized and discussed with a clinician.
Those unable to maintain consistency – Oral therapies require daily (or structured intermittent) dosing, while topical therapies demand regular application and attention to volume and frequency. If adherence is unlikely, expected benefits drop substantially.
Finasteride and dutasteride, in their different formulations, are not competing “good vs bad” options. Instead, they are different tools for different stages and severities of androgenetic alopecia.
The real decision isn’t which drug suppresses more DHT on paper, but how much suppression you need to control your hair loss, and how much systemic exposure you’re comfortable carrying long term.
Finasteride has the longest safety record, strong long-term efficacy, and a forgiving dose–response curve that allows real-world flexibility. For early-to-moderate AGA, or for men prioritizing reversibility and adjustability, finasteride, either oral or carefully dosed topical, covers the majority of clinical needs.
When hair loss is aggressive, rapidly progressive, or insufficiently controlled on finasteride, dutasteride’s broader 5AR inhibition offers a higher ceiling of protection. Head-to-head trials consistently show greater average gains, and it does not show a clearly higher overall incidence of side effects in controlled studies despite stronger systemic and scalp DHT reduction.
Topical vs oral delivery, total daily exposure, application volume, and frequency often have a larger impact on outcomes and tolerability than the finasteride-vs-dutasteride label alone. Hair loss therapy is a long game. The optimal choice is not the strongest drug you can tolerate for a few months, but the strategy you can follow consistently for years with acceptable trade-offs.
References[+]
| ↑1 | Asfour, L., Cranwell, W., & Sinclair, R. (2023). Male androgenetic alopecia. *Endotext [Internet].* Available at: https://www.ncbi.nlm.nih.gov/books/NBK278957/ |
|---|---|
| ↑2 | 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.* 34(3). 617–623. Available at: https://doi.org/10.1677/jme.1.01725 |
| ↑3 | Frye, S. V. (2006). Discovery and clinical development of dutasteride, a potent dual 5α-reductase inhibitor. *Current Topics in Medicinal Chemistry.* 6(5). 405–421. Available at: https://doi.org/10.2174/156802606776743101 |
| ↑4 | Wikimedia Commons. (n.d.). Azasteroid Pharmaceuticals [Image]. *Wikimedia Commons.* Available at: https://commons.wikimedia.org/wiki/File:Azasteroid_Pharmaceuticals.png (Accessed: November 2025) |
| ↑5, ↑15, ↑19 | 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 inhibition in the treatment of male pattern hair loss: results of a randomized placebo-controlled study of dutasteride versus finasteride. *Journal of the American Academy of Dermatology.* 55(6). 1014–1023. Available at: https://doi.org/10.1016/j.jaad.2006.05.007 |
| ↑6, ↑10, ↑16 | 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 of the efficacy and safety of different doses of dutasteride versus placebo and finasteride in the treatment of male subjects with androgenetic alopecia. *Journal of the American Academy of Dermatology.* 70(3). 489–498. Available at: https://doi.org/10.1016/j.jaad.2013.10.049 |
| ↑7, ↑17 | 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 open-label, evaluator-blinded study. *Indian Journal of Dermatology, Venereology and Leprology.* 83. 47. Available at: https://doi.org/10.4103/0378-6323.188652 |
| ↑8, ↑11, ↑13, ↑18 | 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 androgenic alopecia in South Korea: a multicentre chart review study. *Annals of Dermatology.* 34(5). 349. Available at: https://doi.org/10.5021/ad.22.027 |
| ↑9 | 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 inhibition in the treatment of male pattern hair loss: results of a randomized placebo-controlled study of dutasteride versus finasteride. *Journal of the American Academy of Dermatology.* 55(6). 1014–1023. Available at: https://doi.org/10.1016/j.jaad.2006.05.007 |
| ↑12 | 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. *Journal of the American Academy of Dermatology.* 55(1). 71–74. Available at: https://doi.org/10.1016/j.jaad.2005.07.001 |
| ↑14 | Hirshburg, J. M., Kelsey, P. A., Therrien, C. A., Gavino, A. C., & Reichenberg, J. S. (2016). Adverse effects and safety of 5-alpha reductase inhibitors (finasteride, dutasteride): a systematic review. *The Journal of Clinical and Aesthetic Dermatology.* 9(7). 56–62. Available at: https://pmc.ncbi.nlm.nih.gov/articles/PMC5023004/ |
| ↑20 | Traish, A. M. (2020). Post-finasteride syndrome: a surmountable challenge for clinicians. *Fertility and Sterility.* 113(1). 21–50. Available at: https://doi.org/10.1016/j.fertnstert.2019.11.030 |
| ↑21 | Trüeb, R. M., Régnier, A., Rezende, H. D., & Dias, M. F. R. G. (2019). Post-finasteride syndrome: an induced delusional disorder with the potential of a mass psychogenic illness?. *Skin Appendage Disorders.* 5(5). 320–326. Available at: https://doi.org/10.1159/000497362 |
| ↑22 | 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.* 8(1). 20–23. Available at: https://doi.org/10.1046/j.1523-1747.2003.12167.x |
| ↑23 | Kaplan, S. A., Chung, D. E., Lee, R. K., Scofield, S., & Te, A. E. (2012). A 5-year retrospective analysis of 5α-reductase inhibitors in men with benign prostatic hyperplasia: finasteride has comparable urinary symptom efficacy and prostate volume reduction, but less sexual side effects and breast complications than dutasteride. *International Journal of Clinical Practice.* 66(11). 1052–1055. Available at: https://doi.org/10.1111/j.1742-1241.2012.03010.x |
| ↑24 | 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 |
| ↑25 | Hajheydari, Z., Akbari, J., Saeedi, M., & Shokoohi, L. (2009). Comparing the therapeutic effects of finasteride gel and tablet in treatment of the androgenetic alopecia. *Indian Journal of Dermatology, Venereology and Leprology.* 75. 47. Available at: https://doi.org/10.4103/0378-6323.45220 |
| ↑26 | Caserini, M., Radicioni, M., Leuratti, C., Annoni, O., & Palmieri, R. (2014). A novel finasteride 0.25% topical solution for androgenetic alopecia: pharmacokinetics and effects on plasma androgen levels in healthy male volunteers. *International Journal of Clinical Pharmacology and Therapeutics.* 52(10). 842–849. Available at: https://doi.org/10.5414/CP202119 |
| ↑27 | Caserini, M., Radicioni, M., Leuratti, C., Annoni, O., & Palmieri, R. (2014). A novel finasteride 0.25% topical solution for androgenetic alopecia: pharmacokinetics and effects on plasma androgen levels in healthy male volunteers. *International Journal of Clinical Pharmacology and Therapeutics.* 52(10). 842–849. Available at: https://doi.org/10.5414/CP202119 |
| ↑28 | Sánchez-Meza, E., Ocampo-Candiani, J., Gómez-Flores, M., Herz-Ruelas, M. E., Ocampo-Garza, J., Orizaga-y-Quiroga, T. L., Martínez-Moreno, A., & Ocampo-Garza, S. S. (2022). Microneedling plus topical dutasteride solution for androgenetic alopecia: a randomized placebo-controlled study. Journal of the European Academy of Dermatology & Venereology. 36(10). Available at: https://doi.org/10.1111/jdv.18285 |
| ↑29 | 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 evaluate the safety and efficacy of novel dutasteride topical solution (0.01%, 0.02%, and 0.05% w/v) in male subjects with androgenetic alopecia. Cureus. 17(8). e89309. Available at: https://doi.org/10.7759/cureus.89309 |
| ↑30 | 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 evaluate the safety and efficacy of novel dutasteride topical solution (0.01%, 0.02%, and 0.05% w/v) in male subjects with androgenetic alopecia. *Cureus.* 17(8). e89309. Available at: https://doi.org/10.7759/cureus.89309 |
| ↑31 | Chang, Y., Zhang, W., Zhou, J., Lv, L., He, Q., Chen, Y., Wang, P., & Zhai, Q. (2025). Clinical efficacy of microneedle combined with 5% minoxidil solution and finasteride in the treatment of androgenetic alopecia in males. *Archives of Dermatological Research.* 317(1). 428. Available at: https://doi.org/10.1007/s00403-025-03891-y |
| ↑32 | 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 microneedling or oral 0.5 mg) in treatment of androgenetic alopecia. *QJM: An International Journal of Medicine.* 117(Supplement_2). hcae175–207. Available at: https://doi.org/10.1093/qjmed/hcae175.207 |
| ↑33 | Arif, T., Dorjay, K., Adil, M., & Sami, M. (2017). Dutasteride in androgenetic alopecia: an update. *Current Clinical Pharmacology.* 12(1). 31–35. Available at: https://doi.org/10.2174/1574884712666170310111125 |
| ↑34 | 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 evaluate the safety and efficacy of novel dutasteride topical solution (0.01%, 0.02%, and 0.05% w/v) in male subjects with androgenetic alopecia. Cureus. 17(8). e89309. Available at: https://doi.org/10.7759/cureus.89309 |
Finasteride is one of the most effective and widely studied treatments for androgenic alopecia (AGA). It works by lowering dihydrotestosterone (DHT) levels at the scalp to slow or halt androgen-driven hair follicle miniaturization. While most men tolerate finasteride well and experience meaningful, long-term hair preservation, side effects can occur in a minority of users and are a legitimate concern for anyone considering or already using the medication.
Importantly, tolerance to finasteride varies from person to person. Factors such as baseline hormone levels, genetics, lifestyle, and overall health can influence how an individual responds. The goal of this article is to outline practical, evidence-informed strategies to help manage or reduce side effects, enabling thoughtful, safe decisions about finasteride use with appropriate medical guidance.
Low-dose & full-strength finasteride 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.
*Only available in the U.S. Prescriptions not guaranteed. Restrictions apply. Off-label products are not endorsed by the FDA.
Sexual side effects, such as decreased libido, erectile dysfunction, and ejaculation disorders, occur in a small minority of users. They are most commonly reported early in treatment and often improve or resolve on their own.[1]Hirshburg, J. M., Kelsey, P. A., Therrien, C. A., Gavino, A. C., & Reichenberg, J. S. (2016). Adverse effects and safety of 5-alpha reductase inhibitors (finasteride, dutasteride): a systematic … Continue reading
Breast tenderness and enlargement (gynecomastia) are sometimes reported. Gynecomastia in particular is well-documented and can persist in a minority of cases even after stopping the drug.[2]Kaplan, S. A., Chung, D. E., Lee, R. K., Scofield, S., & Te, A. E. (2012). A 5-year retrospective analysis of 5α-reductase inhibitors in men with benign prostatic hyperplasia: finasteride has … Continue reading
Some men report cognitive symptoms while taking finasteride, most commonly described as “brain fog” or reduced mental clarity, but these complaints have not been observed at meaningful rates in controlled clinical trials. If such effects occur, they are likely subtle and gradual, which may make them difficult to quantify or consistently attribute to the medication
There is a small number of cases where sexual, cognitive, or mood-related symptoms have persisted, leading to the development of the term post-finasteride syndrome (PFS).
PFS remains controversial: some clinicians consider it a genuine but extremely rare drug-related condition, while others argue that existing evidence is low quality and heavily confounded by psychological factors, reporting bias, and the high baseline prevalence of sexual dysfunction in men.[3]Traish, A. M. (2020). Post-finasteride syndrome: a surmountable challenge for clinicians. *Fertility and Sterility.* 113(1). 21–50. Available at: https://doi.org/10.1016/j.fertnstert.2019.11.030,[4]Trüeb, R. M., Régnier, A., Rezende, H. D., & Dias, M. F. R. G. (2019). Post-finasteride syndrome: an induced delusional disorder with the potential of a mass psychogenic illness?. *Skin … Continue reading
Low-dose & full-strength finasteride 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.
*Only available in the U.S. Prescriptions not guaranteed. Restrictions apply. Off-label products are not endorsed by the FDA.
It’s important to remember that the majority of men who use finasteride experience no noticeable side effects,
In the original large, randomized, placebo-controlled trial that led to FDA approval for AGA, sexual side effects were reported in about 4.2% of men taking finasteride versus 2.2% on placebo in the first year. This suggests a small absolute risk, and participants in the study who stopped taking finasteride due to side effects reported that they did not persist after the medication was discontinued.[5]Kaufman, K. D., Olsen, E. A., Whiting, D., Savin, R., DeVillez, R., Bergfeld, W., Price, V. H., et al. (1998). Finasteride in the treatment of men with androgenetic alopecia. *Journal of the American … Continue reading
In other trials, rates vary widely across studies depending on study design, definitions, and participant expectations.
Higher rates seen in some studies appear to be strongly influenced by the nocebo effect, where awareness of potential side effects increases reporting. More conservative analyses estimate that up to 10-15% of users may experience some form of sexual symptoms, most of which are mild, transient, and reversible.[6]Traish, A. M., Hassani, J., Guay, A. T., Zitzmann, M., & Hansen, M. L. (2011). Adverse side effects of 5α-reductase inhibitors therapy: persistent diminished libido and erectile dysfunction and … Continue reading
If you get severe side effects, stop and speak to your primary care physician.
Early evaluation helps rule out other medical, hormonal, or psychological contributors, establishes whether symptoms are plausibly related to finasteride, and prevents unnecessary continuation of treatment when modification or discontinuation is appropriate.
Prompt medical guidance also ensures that side effects are documented and managed correctly, rather than being compounded by anxiety, misinformation, or unsupervised dose changes. The strategies outlined below apply only to mild or moderate symptoms, should be considered only under clinician supervision, and are not appropriate for severe, rapidly worsening, or distressing effects, which warrant immediate medical review.
With that in mind, we can now look at ways to reduce the side effects of finasteride.
One of the most consistently observed patterns with finasteride and other 5α-Reductase (5AR) inhibitors is that many reported side effects improve or resolve with continued use, particularly when they are mild and occur early in treatment.
Clinical trials and follow-up data also suggest the side effects are most common in the first 12 months. This pattern supports the idea that early side effects often reflect a transient adjustment phase rather than a permanent intolerance.[7]Lowe, F. C., McConnell, J. D., Hudson, P. B., Romas, N. A., Boake, R., Lieber, M., Elhilali, M., et al. (2003). Long-term 6-year experience with finasteride in patients with benign prostatic … Continue reading,[8]Hudson, P. B., Boake, R., Trachtenberg, J., Romas, N. A., Rosenblatt, S., Narayan, P., Geller, J., et al. (1999). Efficacy of finasteride is maintained in patients with benign prostatic hyperplasia … Continue reading
Several biological mechanisms may explain this improvement. Androgen receptors and downstream hormone signaling can adapt to reduced DHT levels, central nervous system sensitivity to hormonal shifts may normalize, and early symptoms may be amplified by anxiety or expectancy effects that lessen with reassurance and time.
The standard dose of finasteride for AGA is 1 mg once daily, a regimen supported by large randomized controlled trials showing clear improvements in hair count, hair shaft thickness, and global photographic assessments.
However, a key pharmacologic feature of finasteride is its non-linear (logarithmic) dose–response curve, meaning that most of its DHT–lowering effect occurs at relatively low doses.

Figure 1. The dose response of finasteride demonstrates that increasing the concentration of treatment doesn’t translate to increased DHT reduction.
By the time a daily dose of 1 mg is reached, inhibition of 5AR is already near maximal. As a result, lower doses, such as 0.2–0.5 mg daily, can still meaningfully suppress serum and scalp DHT, often preserving much of finasteride’s hair-protective benefit. [9]Drake, L., Hordinsky, M., Fiedler, V., Swinehart, J., Unger, W. P., Cotterill, P. C., Thiboutot, D. M., et al. (1999). The effects of finasteride on scalp skin and serum androgen levels in men with … Continue reading
Increasing the dose beyond 1 mg does not produce proportionally greater hair regrowth, but instead primarily increases systemic exposure, which may raise the likelihood of side effects without additional cosmetic gain.
From a practical standpoint, this dose–response relationship allows for flexibility in real-world use. Because finasteride side effects tend to be dose-sensitive rather than all-or-nothing, reducing the daily dose is often an effective first adjustment for improving tolerability while maintaining therapeutic efficacy.
Finasteride’s pharmacology also allows for flexibility in dosing frequency. The drug binds tightly to 5AR, and suppression of DHT persists well beyond the drug’s short plasma half-life.[10]National Center for Biotechnology Information. (n.d.). Finasteride. *NCBI Bookshelf.* Available at: https://www.ncbi.nlm.nih.gov/books/NBK513329/ (Accessed: November 2025),[11]Steiner, J. F. (1996). Clinical pharmacokinetics and pharmacodynamics of finasteride. *Clinical Pharmacokinetics.* 30(1). 16–27. Available at: https://doi.org/10.2165/00003088-199630010-00002 In practical terms, this means that daily dosing is not strictly required to maintain meaningful inhibition of scalp DHT once steady-state suppression has been achieved.

Figure 2. Multiple doses of oral finasteride (square points) do not reduce serum DHT significantly more than a single dose over 36 hours. Adapted from Figure 3.[12]Caserini, M., Radicioni, M., Leuratti, C., Annoni, O., & Palmieri, R. (2014). A novel finasteride 0.25% topical solution for androgenetic alopecia: pharmacokinetics and effects on plasma androgen … Continue reading
Common clinician-guided intermittent regimens include 1 mg three times per week or 0.5 mg every other day, both of which can significantly reduce cumulative drug exposure while preserving much of finasteride’s therapeutic effect. Because DHT levels recover gradually rather than immediately, these schedules often maintain adequate androgen suppression for hair stabilization.
Intermittent dosing may be especially helpful for men who develop mild side effects on daily therapy, those who are particularly sensitive to hormonal changes, or individuals transitioning into a long-term maintenance phase after initial hair loss control.
If you want to understand more about finasteride dosing, you can read our in-depth article here.
Topical finasteride is designed to reduce DHT locally within the scalp while limiting systemic exposure, making it an attractive option for men who experience side effects with oral therapy. By delivering the drug directly to the scalp, topical formulations aim to suppress DHT activity in hair follicles without relying on sustained systemic circulation.
Randomized trials comparing topical and oral finasteride show that topical treatment can produce similar improvements in target-area hair counts and other hair growth parameters, while generally causing less suppression of serum DHT and lower measured systemic drug levels.[13]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
One trial demonstrated that topical finasteride reduced DHT in the blood by 34.5%, compared to 55.6% with oral finasteride. They also found that sexual side effects were more associated with oral treatment.[14]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
That said, finasteride’s highly sensitive, logarithmic dose–response curve means that even small amounts entering the bloodstream can suppress DHT. Total systemic exposure depends not only on concentration, but also on application volume, frequency, treated surface area, and formulation vehicle.
As such, topical treatments also require care when applying, and success with topical finasteride depends on consistent, measured application and adherence to the prescribed regimen.
When used thoughtfully, topical finasteride can preserve much of the hair benefit of oral therapy while reducing the risk of systemic side effects for many men.
Find out more about topical finasteride in our article.
As we’ve already seen, even low doses of finasteride can have a significant impact on hair growth. For men who are particularly sensitive to finasteride or who experience side effects even with standard topical formulations, ultra–low-dose topical finasteride may offer a further risk-reduction strategy.
These formulations typically use very low concentrations (e.g., 0.005%), aiming to provide localized scalp DHT suppression while minimizing systemic exposure as much as possible. Supporting this strategy, a small clinical study of 0.005% alcohol-based topical finasteride found appreciable changes in serum DHT levels, indicating little-to-no systemic absorption. Despite minimal systemic exposure, participants still experienced meaningful hair growth outcomes, suggesting that even ultra-low topical doses can be effective at the scalp level.[15]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
Ultra–low-dose topical finasteride has not been studied extensively in large randomized controlled trials. Observationally, many users report improved tolerability and stable hair outcomes, but responses are variable, and efficacy may be more modest than with higher doses.
Low-dose & full-strength finasteride 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.
*Only available in the U.S. Prescriptions not guaranteed. Restrictions apply. Off-label products are not endorsed by the FDA.
For men who develop erectile dysfunction while using finasteride, PDE5 inhibitors (such as sildenafil or tadalafil) can be an effective symptom-management option. These medications are well studied in urology, including in men treated with 5AR inhibitors for benign prostatic hyperplasia (BPH).[16]Casabé, A., Roehrborn, C. G., Da Pozzo, L. F., Zepeda, S., Henderson, R. J., Sorsaburu, S., Henneges, C., Wong, D. G., & Viktrup, L. (2014). Efficacy and safety of the coadministration of … Continue reading
In that setting, PDE5 inhibitors have consistently been shown to improve erectile performance and sexual confidence, even when the underlying hormonal environment is altered.
It’s important to be clear about what this strategy does (and doesn’t) do. PDE5 inhibitors do not reverse DHT suppression or directly address libido changes or ejaculatory volume in the same way they may improve erectile rigidity. However, for many men, symptom relief can meaningfully reduce distress and help prevent performance anxiety from amplifying the problem.
Because PDE5 inhibitors are prescription medications with cardiovascular considerations and potential drug interactions, they should be used only under clinician supervision, particularly in men with heart disease, low blood pressure, or those taking nitrates or certain alpha-blockers.[17]Lui, J. L., Shaw, N. M., Abbasi, B., Hakam, N., & Breyer, B. N. (2023). Adverse reactions of PDE5 inhibitors: an analysis of the World Health Organization pharmacovigilance database. *Andrology.* … Continue reading
Testosterone plays a vital role in sexual health and, like finasteride, is associated with a wide range of symptoms. Reduced libido, erectile changes, fatigue, or low mood overlap significantly with those of hypogonadism, thyroid dysfunction, or other hormonal imbalances.[18]National Center for Biotechnology Information. (n.d.). Dutasteride. *NCBI Bookshelf.* Available at: https://www.ncbi.nlm.nih.gov/books/NBK532933/ (Accessed: November 2025)
Improving total and free testosterone levels through lifestyle changes or medical treatment when indicated can therefore restore androgen balance and reduce the relative impact of DHT suppression in sensitive individuals.
In select cases, testosterone replacement therapy (TRT) may be considered, but only with careful specialist oversight. TRT can improve sexual function, energy, and quality of life, yet it may also accelerate AGA unless combined thoughtfully with hair-loss treatments.[19]Zhang, Y., Xu, J., Jing, J., Wu, X., & Lv, Z. (2018). Serum levels of androgen-associated hormones are correlated with curative effect in androgenic alopecia in young men. *Medical Science … Continue reading For these reasons, TRT should never be initiated solely to counter finasteride side effects without a clear medical diagnosis and a comprehensive discussion of risks, benefits, and long-term goals.
While lifestyle changes cannot reverse finasteride’s pharmacologic action on DHT, they can meaningfully improve erectile function, mood, energy levels, sleep quality, and overall androgen balance, all of which overlap with the most commonly reported finasteride-related complaints.
A wide body of evidence shows that diet, exercise, and weight management play a significant role in sexual function. Randomized trials demonstrate that intensive lifestyle programs can significantly improve erectile function, with a meaningful proportion of men regaining normal erectile performance over time.[20]Esposito, K., Giugliano, F., Di Palo, C., Giugliano, G., Marfella, R., D’Andrea, F., D’Armiento, M., & Giugliano, D. (2004). Effect of lifestyle changes on erectile dysfunction in obese men: … Continue reading,[21]Hehemann, M. C., & Kashanian, J. A. (2016). Can lifestyle modification affect men’s erectile function?. *Translational Andrology and Urology.* 5(2). 187. Available at: … Continue reading
Environmental and behavioral factors can also be reviewed. Excessive heat exposure (such as frequent sauna use), high alcohol intake, cannabis use, and certain medications (including antidepressants) can independently impair sexual function or mood and may confound the interpretation of finasteride-related symptoms.
Although no studies have looked specifically at lifestyle programs for finasteride side effects, strong evidence shows that improving fitness, diet, sleep, and stress can enhance the same areas (erectile function, mood, energy, and hormone balance) that many men find most affected.
Some men explore supplements marketed for testosterone support or sexual function, such as tongkat ali, in an effort to counter finasteride-related symptoms. Small studies suggest that tongkat ali may modestly increase testosterone or improve libido in certain populations, but the evidence is limited, inconsistent, and highly variable between individuals.[22]Leisegang, K., Finelli, R., Sikka, S. C., & Selvam, M. K. P. (2022). Eurycoma longifolia (jack) improves serum total testosterone in men: a systematic review and meta-analysis of clinical trials. … Continue reading
It’s critical to remember these supplements are experimental, not first-line solutions. Product quality, dosing, and purity can vary widely, and robust data on long-term safety or interactions with finasteride are lacking. While some individuals report subjective benefit, others notice no effect at all.
For these reasons, supplements should only be considered after established strategies have been explored and ideally discussed with a clinician, rather than relied upon as a primary way to manage side effects.
If side effects persist despite adjustments to dose, frequency, or formulation, it may be appropriate to change strategies altogether. Hair loss treatment is not all-or-nothing, and finasteride, while highly effective, is not the only option.
Many men choose to rely on non-hormonal treatments entirely. Options such as topical or oral minoxidil, microneedling, low-level laser therapy devices, platelet-rich plasma (PRP), or hair transplantation can provide meaningful benefits without altering androgen pathways.
You can read more about alternative treatments in our guides and in-depth articles on minoxidil, microneedling, low-level laser therapy devices, and platelet-rich plasma (PRP).
While these approaches may not match finasteride’s disease-modifying effect on DHT, they can still preserve or improve cosmetic density for many users.
If you’re using topical finasteride, you might consider switching to low-dose topical dutasteride. offer better scalp localization at very low application frequencies due to dutasteride’s stronger and longer-lasting binding to 5AR. When used carefully and infrequently, some patients tolerate topical dutasteride well while maintaining hair stabilization.
Finasteride side effects are often manageable with thoughtful adjustments to dose, dosing schedule, formulation, and supporting lifestyle factors. There is no single correct way to use finasteride. Personalization is key, and the right approach depends on individual biology, risk tolerance, and treatment goals.
Health should always come first. Any side effects warrant open discussion with a clinician, and treatment decisions should be made collaboratively rather than in isolation. With informed, flexible planning, many men are able to find a balance that protects both their hair and their overall well-being.
References[+]
| ↑1 | Hirshburg, J. M., Kelsey, P. A., Therrien, C. A., Gavino, A. C., & Reichenberg, J. S. (2016). Adverse effects and safety of 5-alpha reductase inhibitors (finasteride, dutasteride): a systematic review. *The Journal of Clinical and Aesthetic Dermatology.* 9(7). 56–62. Available at: https://pmc.ncbi.nlm.nih.gov/articles/PMC5023004/ |
|---|---|
| ↑2 | Kaplan, S. A., Chung, D. E., Lee, R. K., Scofield, S., & Te, A. E. (2012). A 5-year retrospective analysis of 5α-reductase inhibitors in men with benign prostatic hyperplasia: finasteride has comparable urinary symptom efficacy and prostate volume reduction, but less sexual side effects and breast complications than dutasteride. *International Journal of Clinical Practice.* 66(11). 1052–1055. Available at: https://doi.org/10.1111/j.1742-1241.2012.03010.x |
| ↑3 | Traish, A. M. (2020). Post-finasteride syndrome: a surmountable challenge for clinicians. *Fertility and Sterility.* 113(1). 21–50. Available at: https://doi.org/10.1016/j.fertnstert.2019.11.030 |
| ↑4 | Trüeb, R. M., Régnier, A., Rezende, H. D., & Dias, M. F. R. G. (2019). Post-finasteride syndrome: an induced delusional disorder with the potential of a mass psychogenic illness?. *Skin Appendage Disorders.* 5(5). 320–326. Available at: https://doi.org/10.1159/000497362 |
| ↑5 | Kaufman, K. D., Olsen, E. A., Whiting, D., Savin, R., DeVillez, R., Bergfeld, W., Price, V. H., et al. (1998). Finasteride in the treatment of men with androgenetic alopecia. *Journal of the American Academy of Dermatology.* 39(4). 578–589. Available at: https://doi.org/10.1016/S0190-9622(98)70007-6 |
| ↑6 | Traish, A. M., Hassani, J., Guay, A. T., Zitzmann, M., & Hansen, M. L. (2011). Adverse side effects of 5α-reductase inhibitors therapy: persistent diminished libido and erectile dysfunction and depression in a subset of patients. *The Journal of Sexual Medicine.* 8(3). 872–884. Available at: https://doi.org/10.1111/j.1743-6109.2010.02157.x |
| ↑7 | Lowe, F. C., McConnell, J. D., Hudson, P. B., Romas, N. A., Boake, R., Lieber, M., Elhilali, M., et al. (2003). Long-term 6-year experience with finasteride in patients with benign prostatic hyperplasia. *Urology.* 61(4). 791–796. Available at: https://doi.org/10.1016/S0090-4295(02)02548-7 |
| ↑8 | Hudson, P. B., Boake, R., Trachtenberg, J., Romas, N. A., Rosenblatt, S., Narayan, P., Geller, J., et al. (1999). Efficacy of finasteride is maintained in patients with benign prostatic hyperplasia treated for 5 years. *Urology.* 53(4). 690–695. Available at: https://doi.org/10.1016/S0090-4295(98)00666-9 |
| ↑9 | Drake, L., Hordinsky, M., Fiedler, V., Swinehart, J., Unger, W. P., Cotterill, P. C., Thiboutot, D. M., 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 Dermatology.* 41(4). 550–554. Available at: https://doi.org/10.1016/S0190-9622(99)80051-6 |
| ↑10 | National Center for Biotechnology Information. (n.d.). Finasteride. *NCBI Bookshelf.* Available at: https://www.ncbi.nlm.nih.gov/books/NBK513329/ (Accessed: November 2025) |
| ↑11 | Steiner, J. F. (1996). Clinical pharmacokinetics and pharmacodynamics of finasteride. *Clinical Pharmacokinetics.* 30(1). 16–27. Available at: https://doi.org/10.2165/00003088-199630010-00002 |
| ↑12 | Caserini, M., Radicioni, M., Leuratti, C., Annoni, O., & Palmieri, R. (2014). A novel finasteride 0.25% topical solution for androgenetic alopecia: pharmacokinetics and effects on plasma androgen levels in healthy male volunteers. *International Journal of Clinical Pharmacology and Therapeutics.* 52(10). 842–849. Available at: https://doi.org/10.5414/CP202119 |
| ↑13 | Hajheydari, Z., Akbari, J., Saeedi, M., & Shokoohi, L. (2009). Comparing the therapeutic effects of finasteride gel and tablet in treatment of the androgenetic alopecia. *Indian Journal of Dermatology, Venereology and Leprology.* 75. 47. Available at: https://doi.org/10.4103/0378-6323.45220 |
| ↑14 | 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 |
| ↑15 | 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 16-month therapy course. *Journal of Dermatological Treatment.* 8(3). 189–192. Available at: https://doi.org/10.3109/09546639709160517 |
| ↑16 | Casabé, A., Roehrborn, C. G., Da Pozzo, L. F., Zepeda, S., Henderson, R. J., Sorsaburu, S., Henneges, C., Wong, D. G., & Viktrup, L. (2014). Efficacy and safety of the coadministration of tadalafil once daily with finasteride for 6 months in men with lower urinary tract symptoms and prostatic enlargement secondary to benign prostatic hyperplasia. *The Journal of Urology.* 191(3). 727–733. Available at: https://doi.org/10.1016/j.juro.2013.09.059 |
| ↑17 | Lui, J. L., Shaw, N. M., Abbasi, B., Hakam, N., & Breyer, B. N. (2023). Adverse reactions of PDE5 inhibitors: an analysis of the World Health Organization pharmacovigilance database. *Andrology.* 11(7). 1408–1417. Available at: https://doi.org/10.1111/andr.13430 |
| ↑18 | National Center for Biotechnology Information. (n.d.). Dutasteride. *NCBI Bookshelf.* Available at: https://www.ncbi.nlm.nih.gov/books/NBK532933/ (Accessed: November 2025) |
| ↑19 | Zhang, Y., Xu, J., Jing, J., Wu, X., & Lv, Z. (2018). Serum levels of androgen-associated hormones are correlated with curative effect in androgenic alopecia in young men. *Medical Science Monitor.* 24. 7770. Available at: https://doi.org/10.12659/MSM.913116 |
| ↑20 | Esposito, K., Giugliano, F., Di Palo, C., Giugliano, G., Marfella, R., D’Andrea, F., D’Armiento, M., & Giugliano, D. (2004). Effect of lifestyle changes on erectile dysfunction in obese men: a randomized controlled trial. *JAMA.* 291(24). 2978–2984. Available at: https://doi.org/10.1001/jama.291.24.2978 |
| ↑21 | Hehemann, M. C., & Kashanian, J. A. (2016). Can lifestyle modification affect men’s erectile function?. *Translational Andrology and Urology.* 5(2). 187. Available at: https://doi.org/10.21037/tau.2016.02.05 |
| ↑22 | Leisegang, K., Finelli, R., Sikka, S. C., & Selvam, M. K. P. (2022). Eurycoma longifolia (jack) improves serum total testosterone in men: a systematic review and meta-analysis of clinical trials. *Medicina.* 58(8). 1047. Available at: https://doi.org/10.3390/medicina58081047 |
Dutasteride is one of the most powerful pharmacologic treatments for androgenic alopecia (AGA). Initially approved for benign prostatic hyperplasia, dutasteride is now commonly prescribed off-label for hair loss in men and, more recently, has gained attention in topical form to minimize systemic exposure. This has created an important clinical question: how do oral and topical dutasteride compare in terms of effectiveness, safety, and real-world practicality?
This article examines what the current scientific literature reveals about oral versus topical dutasteride, reviewing mechanisms of action, efficacy data, and safety profiles to help you make more informed treatment decisions.
Hair gains bigger than finasteride? Dutasteride makes this possible, 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.
*Only available in the U.S. Prescriptions not guaranteed. Restrictions apply. Off-label products are not endorsed by the FDA.
AGA is driven by increases in dihydrotestosterone (DHT). DHT binds to androgen receptors in hair follicles, triggering miniaturization that leads to thinner, shorter hairs. Dutasteride works by inhibiting an enzyme called 5α-reductase (5AR), which converts testosterone into DHT. Dutasteride is a dual 5AR inhibitor, meaning it blocks both type I and type II 5AR, leading to decreased DHT levels and ultimately halting the progression of AGA and restoring thicker hair.[1]Gerst, C., Dalko, M., Pichaud, P., Galey, J. B., Buan, B., & Bernard, B. A. (2002). Type-1 steroid 5α-reductase is functionally active in the hair follicle as evidenced by new selective … Continue reading,[2]Clark, R. V., Hermann, D. J., Cunningham, G. R., Wilson, T. H., Morrill, B. B., & Hobbs, S. (2004). Marked suppression of dihydrotestosterone in men with benign prostatic hyperplasia by … Continue reading

Figure 1. Structure of dutasteride, which is a dual 5AR inhibitor.[3]Wikimedia Commons. (n.d.). Dutasterid.svg [Image]. *Wikimedia Commons.* Available at: https://commons.wikimedia.org/wiki/File:Dutasterid.svg (Accessed: November 2025) Image used under Creative Commons License.
Oral Dutasteride Hair gains bigger than finasteride? Dutasteride makes this possible, 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.
*Only available in the U.S. Prescriptions not guaranteed. Restrictions apply. Off-label products are not endorsed by the FDA.
Oral dutasteride is absorbed through the gastrointestinal tract into systemic circulation, leading to significant and sustained reductions in DHT in the blood (serum). This includes reductions in scalp DHT, since less DHT is available systemically to diffuse into hair follicles.[4]Clark, R. V., Hermann, D. J., Cunningham, G. R., Wilson, T. H., Morrill, B. B., & Hobbs, S. (2004). Marked suppression of dihydrotestosterone in men with benign prostatic hyperplasia by … Continue reading,[5]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
The flip side is that any symptoms tied to systemic DHT suppression, such as sexual side-effects, are driven by this same mechanism. Given the long half-life and accumulation, systemic exposure persists even if doses are missed or therapy is stopped, and any adverse effects may take weeks to resolve.[6]Tsai, T.-F., Choi, G. S., Kim, B. J., Kim, M.-B., Ng, C. F., Kochhar, P., Jasper, S., Brotherton, B., Orban, B., & Lulic, Z. (2018). Prospective randomized study of sexual function in men taking … Continue reading
Topical dutasteride treatment might avoid some of these pitfalls: high exposure at the scalp and low exposure elsewhere can target delivery and avoid systemic issues. It is applied directly to the scalp in formulations such as:
These vehicles are designed to ensure that dutasteride can cross the stratum corneum (the outermost protective layer of the skin) and, ideally, remain localized within the scalp.
The effect of dutasteride on hair loss is well documented: multiple randomized placebo-controlled studies have been conducted over the last 25 years. Dutasteride was first developed as a treatment for benign prostatic hyperplasia and taken as a tablet. Early studies into dutasteride for hair loss therefore used oral formulations, with topical treatments developed later.
Here, we’ll take a look at the evidence supporting the use of oral dutasteride for hair loss. Many studies compare dutasteride with other treatments, most notably finasteride, or use the drug in combination with other therapies. We’ll focus on data showing the effect of dutasteride alone compared to placebo, but will also touch on comparisons with other popular treatments.
Below is a summary of the findings to date on the safety and efficacy of oral dutasteride:
| Study Design and Population | Treatments and Concentrations (Daily) | Hair Growth Outcomes | Systemic Effects | |
| Study #1[7]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 | Randomized, placebo-controlled, double-blinded trial. 415 men with male pattern hair loss aged 21-45 years old; 24 weeks. | 0.05, 0.1, 0.5, or 2.5 mg dutasteride; 5 mg finasteride. | Dose-dependent increase in total hair count vs placebo. Improved hair count vs finasteride. | Serum decrease in DHT level (92% at 0.5 mg). |
| Study #2[8]Stough, D. (2007). Dutasteride improves male pattern hair loss in a randomized study in identical twins. *Journal of Cosmetic Dermatology.* 6(1). 9–13. Available at: … Continue reading | Randomized, placebo-controlled, double-blinded trial. 17 pairs of identical twin males with
AGA; 12 months. |
0.5 mg dutasteride. | Significant increase in total hair counts in dutasteride-treated twins. | Not assessed. |
| Study #3[9]Eun, H. C., Kwon, O. S., Yeon, J. H., Shin, H. S., Kim, B. Y., Ro, B. I., Cho, H. K., et al. (2010). Efficacy, safety, and tolerability of dutasteride 0.5 mg once daily in male patients with male … Continue reading | Randomized, placebo-controlled, double-blinded trial. 153 men with male pattern hair loss aged 18-49; 6 months | 0.5 mg dutasteride. | Significant increase in total hair count. | Sexual dysfunction was reported in 4.1% of the treatment group and 2.7% of placebo (not statistically significant). |
| Study #4[10]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 | Randomized, placebo-controlled, double-blinded trial. 917 men with AGA aged 20-50; 24 weeks. | 0.02, 0.1, or 0.5 mg dutasteride; 1 mg finasteride | Increase in terminal hair count and width vs placebo. Significant increase in hair width vs dutasteride. | No significant changes in reported adverse events. |
| Study #5[11]Tsunemi, Y., Irisawa, R., Yoshiie, H., Brotherton, B., Ito, H., Tsuboi, R., Kawashima, M., Manyak, M., & ARI114264 Study Group. (2016). Long-term safety and efficacy of dutasteride in the … Continue reading | Open-label, prospective study, no control. 120 men with AGA aged 20-50; 52 weeks. | 0.5 mg dutasteride. | Increase in terminal hair count and hair width compared to baseline. | 12% of men experienced libido decrease and impotence, of which 50% and 57%, respectively, were not resolved by the end of the study. |
| Study #6[12]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 | Open-label, randomized study; no placebo control. 90 men with AGA aged 18-40; 24 weeks. | 0.5 mg dutasteride or 1 mg finasteride. | Increase in total hair count and width compared to baseline. Increase in total hair count was significantly higher in dutasteride than finasteride group. | Erectile dysfunction and loss of libido reported in 3 and 4 patients respectively. |
| Study #7[13]Tsai, T.-F., Choi, G. S., Kim, B. J., Kim, M.-B., Ng, C. F., Kochhar, P., Jasper, S., Brotherton, B., Orban, B., & Lulic, Z. (2018). Prospective randomized study of sexual function in men taking … Continue reading | Randomized, placebo-controlled, double-blinded trial. 117 men with AGA aged 23-50; 24 weeks. | 0.5 mg dutasteride. | Not assessed. | Incidence of sexual adverse events was approximately double in the dutasteride group (16% vs 8% in placebo). |
| Study #8[14]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 | Retrospective chart review. 600 men over 18 with AGA. | 0.5 mg dutasteride or 1 mg finasteride. | Greater improvements in BASP classifications of AGA compared to baseline were found in dutasteride vs finasteride. | Incidence of adverse events was higher in finasteride group (10.5%) than in dutasteride group (7.6%). |
While evidence for the efficacy of oral dutasteride is well established, research into topical dutasteride solutions started relatively recently. Below is an overview of the studies into the efficacy of topical dutasteride:
| Study Design and Population | Treatments and Concentrations (Daily) | Hair Growth Outcomes | Systemic Effects | |
| Study #1[15]Sánchez-Meza, E., Ocampo-Candiani, J., Gómez-Flores, M., Herz-Ruelas, M. E., Ocampo-Garza, J., Orizaga-y-Quiroga, T. L., Martínez-Moreno, A., & Ocampo-Garza, S. S. (2022). Microneedling plus … Continue reading | Randomized, placebo-controlled, double-blinded trial. 34 men with AGA aged 18-65; 20 weeks. | Microneedling with 0.01% dutasteride solution. Placebo was microneedling with saline solution. | Significant improvements in hair thickness, hair density, and vellous: terminal hair ratio. | Not assessed. |
| Study #2[16]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 | Randomized, placebo-controlled, double-blinded trial. 135 adult males aged 20-60 with AGA; 24 weeks. | 0.01%, 0.02%, or 0.05% topical dutasteride; 1mg oral dutasteride | Dose-dependent increase in total hair count and hair width. 0.05% solution showed significant improvement over finasteride in total hair count. | No change in serum DHT levels observed vs placebo. |
When comparing oral and topical dutasteride, the most important point to note is that there are currently no published clinical trials directly comparing the two formulations alone head-to-head for AGA. All comparisons must be made indirectly, using separate studies with different designs, populations, timelines, and formulations.
Despite this limitation, the evidence available for each formulation allows us to evaluate its strength and predictability. The current evidence quality for each formulation is as follows:
By our metrics, this means that both treatments have similar evidence quality overall. Longer-term data support oral dutasteride, while topical dutasteride remains less validated, largely due to fewer studies and limited long-term follow-up.
We’ll take a closer look at the strength of the evidence supporting both formulations.
Oral dutasteride can reduce serum DHT levels by up to 90% and scalp DHT levels by 51-79%.[17]Clark, R. V., Hermann, D. J., Cunningham, G. R., Wilson, T. H., Morrill, B. B., & Hobbs, S. (2004). Marked suppression of dihydrotestosterone in men with benign prostatic hyperplasia by … Continue reading,[18]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 Randomized controlled trials consistently demonstrate that dutasteride, particularly at the standard 0.5 mg daily dose, suppresses serum and scalp DHT and delivers some of the most robust regrowth outcomes documented for AGA.
A number of the studies outlined above include large sample sizes, often over 100 participants, with the largest including over 900.[19]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 Importantly, these cohorts should be large enough to detect changes in the incidence of adverse events, even if they are relatively rare. The replication of results in multiple trials using similar endpoints is a strong indicator of the efficacy of the drug.
Unfortunately, the longest of these RCTs only lasted 6 months, which may mean that lasting impacts on growth are overlooked. Similarly, side effects associated with long-term use over many years may be missed.
We can turn to longer studies using finasteride for some indication of how sustained benefits may be, given the similar mechanism of action of the two treatments. A 3-year trials using 1 mg daily doses of finasteride showed sustained improvement in hair growth over the course of the study, while placebo groups saw decreased hair counts.[20]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
A 10-year follow-up study concluded that improvements in hair growth, as determined by expert analysis of hair photographs, from finasteride do not worsen over time, and in 21% of cases, hair growth got even better after 5 years of treatment.[21]Rossi, A., Cantisani, C., Scarnò, M., Trucchia, A., Fortuna, M. C., & Calvieri, S. (2011). Finasteride, 1 mg daily administration on male androgenetic alopecia in different age groups: 10-year … Continue reading
While we can’t draw any firm conclusions about the long-term efficacy of dutasteride from studies using finasteride, these findings can indicate the impact of long-term inhibition of 5AR, which is also seen in dutasteride treatment.
Evidence for topical dutasteride is promising but remains less mature. Early clinical research indicates that topical formulations can meaningfully improve hair density, hair shaft diameter, and overall investigator-assessed regrowth, with efficacy in trials approaching that of oral therapy.
One small study with only 34 participants showed significant improvements in hair growth and thickness when combined with microneedling, compared to microneedling alone. Another study combined dutasteride formulations with minoxidil and also found that topical dutasteride delivered via microneedling produced hair density and thickness improvements similar to oral dutasteride, with fewer systemic side effects.[22]Sánchez-Meza, E., Ocampo-Candiani, J., Gómez-Flores, M., Herz-Ruelas, M. E., Ocampo-Garza, J., Orizaga-y-Quiroga, T. L., Martínez-Moreno, A., & Ocampo-Garza, S. S. (2022). Microneedling plus … Continue reading,[23]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
A recently published Phase II trial, the first to test topical dutasteride without microneedling, reported that all concentrations improved hair growth versus placebo, produced minimal changes in serum DHT, and that 1 ml daily of 0.05% appeared to outperform oral finasteride. However, concerns about unusually high baseline hair counts and inconsistencies in the placement and size of the 1 cm² target areas used for hair measurements raise questions about the reliability of these results.[24]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

Figure 2. Oral dutasteride (yellow line) reduces serum DHT levels more than topical Dutaseride (blue lines). Adapted from Figure 3.[25]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 Image used under Creative Commons License.
Real-world outcomes from low-dose topical dutasteride users (0.01–0.02% applied daily or near-daily) suggest more modest benefits, with good scalp localization and stable serum DHT noted as positives, rather than regrowth exceeding that with oral finasteride.
There have been some concerns raised about the ability of dutasteride to penetrate into the scalp. Dutasteride is a relatively large molecule, with one molecule weighing 528.5 Daltons (Da). There is a commonly cited rule, called the 500 Dalton Rule, that states that molecules should be under 500 Da in order to penetrate the skin. However, dutasteride has been demonstrated to be effective in topical formulations and can measurably lower DHT concentrations. What’s more, a small, unpublished study has also shown that the drug does penetrate into both the scalp and serum, even at low concentrations. As such, in this case, dutasteride does seem to penetrate the skin in the scalp, without the need for microneedling or injection.
Because dutasteride produces sustained suppression of DHT, safety considerations, particularly regarding hormonal and sexual side effects, are central to treatment selection. Most clinical trials record adverse events, while some studies are focused specifically on side-effects.[26]Tsai, T.-F., Choi, G. S., Kim, B. J., Kim, M.-B., Ng, C. F., Kochhar, P., Jasper, S., Brotherton, B., Orban, B., & Lulic, Z. (2018). Prospective randomized study of sexual function in men taking … Continue reading
Across randomized trials and long-term observational studies, the most consistently reported adverse effects of oral dutasteride involve sexual function, including:
Trials report overall total adverse event rates between 4 and 12%, with sexual adverse events such as decreased libido as high as 13%, although this was reported in higher doses (2.5mg daily).[27]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 At the standard 0.5mg daily dose, sexual side effects typically occur at a rate of between 1 and 5%. In the context of other popular treatments, comparisons with finasteride show no consistent increase in sexual side effects with dutasteride, despite dutasteride lowering serum DHT by an additional 20-30% beyond finasteride.[28]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
Most controlled studies show that the majority of sexual side effects resolve either during treatment or after discontinuation. However, due to dutasteride’s long half-life (4-5 weeks) and high tissue binding, systemic effects can persist. At standard 0.5mg daily dosing, serum DHT generally returns to 80% of baseline within 6 months of discontinuation.
Topical dutasteride is generally well tolerated, and reported adverse events are usually mild and localized, including:
These occur inconsistently and are formulation-dependent, influenced by solvent systems, penetration enhancers, and application volume.
The primary safety advantage of topical dutasteride is reduced systemic exposure. In trials, topical regimens in the 0.01–0.05% range produce minimal or no significant changes in serum DHT or testosterone.[29]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 When decreases in serum DHT are observed with topical use, they are generally smaller than those seen with oral dosing.[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
Dutasteride, whether oral or topical, is primarily used for AGA in men, though its use for hair loss remains off-label in the United States. Oral dutasteride is formally FDA-approved only for benign prostatic hyperplasia, while topical formulations exist solely through compounding pharmacies.
Oral dutasteride offers the simplest adherence burden: one capsule daily (or a modified intermittent schedule). This ease is a major factor behind its consistent outcomes. Topical dutasteride, while potentially safer from a systemic standpoint, requires regular scalp application and attention to dosing volume.
The effectiveness of topical formulations is heavily influenced by factors such as vehicle, scalp contact time, treated surface area, and individual skin permeability. These practical considerations can meaningfully shape both efficacy and systemic absorption.
Advanced vehicles such as nanoemulsions or nanoemulgels can increase scalp penetration by up to 1.5-fold compared to conventional solutions.[31]Ali, M. S., Alam, M. S., Alam, N., & Siddiqui, M. R. (2014). Preparation, characterization and stability study of dutasteride loaded nanoemulsion for treatment of benign prostatic hypertrophy. … Continue reading However, this may also increase systemic exposure. Application frequency can be adjusted to balance efficacy and hormonal safety. Because dutasteride binds to 5AR for prolonged periods, daily application is not always necessary.
Time on the scalp also matters. The longer a topical formulation remains in contact with the skin, the more dutasteride can penetrate the follicle. Most protocols recommend allowing at least four hours before washing the hair. Rinsing too soon can reduce efficacy, while prolonged contact increases both potency and the possibility of systemic absorption.
The size of the application area affects systemic exposure. Treating a small region, such as the crown, introduces less drug into circulation than applying the same concentration across the entire scalp. Patients with diffuse thinning often benefit from using lower volumes or concentrations to counterbalance the increased surface area.
As we can see, there is a wide range of factors to consider when making a treatment plan with topical dutasteride, which may make consistent application a challenge.
Off-label use of dutasteride in women is limited and generally reserved for postmenopausal women or women with documented hyperandrogenism or a strong family history of AGA. Due to the systemic androgenic impacts of the drug, it’s typically only used in cases where other therapies (minoxidil, spironolactone) are inadequate.
The key trade-off between oral and topical formulations is systemic potency versus localized targeting, balanced against differences in side-effect risk, convenience, and cost. Oral therapy is simpler and less variable; topical therapy requires consistent application but offers greater hormonal safety for risk-averse patients.
Combination therapy, most commonly topical dutasteride with minoxidil, can enhance outcomes through complementary mechanisms. Oral dutasteride may also be paired with topical agents in some cases.
Significant research gaps remain, including the absence of direct head-to-head oral-versus-topical trials, limited long-term safety data for topical dutasteride, and the lack of standardized dosing guidelines for topical formulations.
Dutasteride, whether oral or topical, represents one of the most powerful tools currently available for treating AGA. Oral dutasteride offers the most consistent and robust regrowth outcomes, supported by the strongest body of clinical evidence, but with predictable systemic hormonal suppression and long persistence after discontinuation.
Topical dutasteride, while still supported by a smaller and newer evidence base, offers a compelling alternative for patients seeking meaningful scalp-level efficacy with reduced systemic exposure. Its ultimate success depends heavily on formulation quality, dosing strategy, and adherence.
There is no universally “best” option: only the best option for specific circumstances. Treatment selection should be guided by hair-loss severity, prior treatment response, risk tolerance, reproductive plans, and long-term adherence capacity. As research continues to evolve, clinical guidance will become more precise. For now, optimal results come from choosing the formulation that best aligns with your goals and comfort with risk.
Oral Dutasteride Hair gains bigger than finasteride? Dutasteride makes this possible, 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.
*Only available in the U.S. Prescriptions not guaranteed. Restrictions apply. Off-label products are not endorsed by the FDA.
References[+]
| ↑1 | Gerst, C., Dalko, M., Pichaud, P., Galey, J. B., Buan, B., & Bernard, B. A. (2002). Type-1 steroid 5α-reductase is functionally active in the hair follicle as evidenced by new selective inhibitors of either type-1 or type-2 human steroid 5α-reductase. *Experimental Dermatology.* 11(1). 52–58. Available at: https://doi.org/10.1034/j.1600-0625.2002.110106.x |
|---|---|
| ↑2, ↑4, ↑17 | Clark, R. V., Hermann, D. J., Cunningham, G. R., Wilson, T. H., Morrill, B. B., & Hobbs, S. (2004). Marked suppression of dihydrotestosterone in men with benign prostatic hyperplasia by dutasteride, a dual 5α-reductase inhibitor. *The Journal of Clinical Endocrinology & Metabolism.* 89(5). 2179–2184. Available at: https://doi.org/10.1210/jc.2003-030330 |
| ↑3 | Wikimedia Commons. (n.d.). Dutasterid.svg [Image]. *Wikimedia Commons.* Available at: https://commons.wikimedia.org/wiki/File:Dutasterid.svg (Accessed: November 2025) |
| ↑5, ↑18 | 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 inhibition in the treatment of male pattern hair loss: results of a randomized placebo-controlled study of dutasteride versus finasteride. *Journal of the American Academy of Dermatology.* 55(6). 1014–1023. Available at: https://doi.org/10.1016/j.jaad.2006.05.007 |
| ↑6, ↑13, ↑26 | Tsai, T.-F., Choi, G. S., Kim, B. J., Kim, M.-B., Ng, C. F., Kochhar, P., Jasper, S., Brotherton, B., Orban, B., & Lulic, Z. (2018). Prospective randomized study of sexual function in men taking dutasteride for the treatment of androgenetic alopecia. *The Journal of Dermatology.* 45(7). 799–804. Available at: https://doi.org/10.1111/1346-8138.14329 |
| ↑7, ↑27 | 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 inhibition in the treatment of male pattern hair loss: results of a randomized placebo-controlled study of dutasteride versus finasteride. *Journal of the American Academy of Dermatology.* 55(6). 1014–1023. Available at: https://doi.org/10.1016/j.jaad.2006.05.007 |
| ↑8 | Stough, D. (2007). Dutasteride improves male pattern hair loss in a randomized study in identical twins. *Journal of Cosmetic Dermatology.* 6(1). 9–13. Available at: https://doi.org/10.1111/j.1473-2165.2007.00297.x |
| ↑9 | Eun, H. C., Kwon, O. S., Yeon, J. H., Shin, H. S., Kim, B. Y., Ro, B. I., Cho, H. K., et al. (2010). Efficacy, safety, and tolerability of dutasteride 0.5 mg once daily in male patients with male pattern hair loss: a randomized, double-blind, placebo-controlled, phase III study. *Journal of the American Academy of Dermatology.* 63(2). 252–258. Available at: https://doi.org/10.1016/j.jaad.2009.09.018 |
| ↑10, ↑19, ↑28 | 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 of the efficacy and safety of different doses of dutasteride versus placebo and finasteride in the treatment of male subjects with androgenetic alopecia. *Journal of the American Academy of Dermatology.* 70(3). 489–498. Available at: https://doi.org/10.1016/j.jaad.2013.10.049 |
| ↑11 | Tsunemi, Y., Irisawa, R., Yoshiie, H., Brotherton, B., Ito, H., Tsuboi, R., Kawashima, M., Manyak, M., & ARI114264 Study Group. (2016). Long-term safety and efficacy of dutasteride in the treatment of male patients with androgenetic alopecia. *The Journal of Dermatology.* 43(9). 1051–1058. Available at: https://doi.org/10.1111/1346-8138.13310 |
| ↑12 | 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 open-label, evaluator-blinded study. *Indian Journal of Dermatology, Venereology and Leprology.* 83. 47. Available at: https://doi.org/10.4103/0378-6323.188652 |
| ↑14 | 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 androgenic alopecia in South Korea: a multicentre chart review study. *Annals of Dermatology.* 34(5). 349. Available at: https://doi.org/10.5021/ad.22.027 |
| ↑15, ↑22 | Sánchez-Meza, E., Ocampo-Candiani, J., Gómez-Flores, M., Herz-Ruelas, M. E., Ocampo-Garza, J., Orizaga-y-Quiroga, T. L., Martínez-Moreno, A., & Ocampo-Garza, S. S. (2022). Microneedling plus topical dutasteride solution for androgenetic alopecia: a randomized placebo-controlled study. *Journal of the European Academy of Dermatology & Venereology.* 36(10).. Available at: https://doi.org/10.1111/jdv.18285 |
| ↑16, ↑25, ↑29 | 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 evaluate the safety and efficacy of novel dutasteride topical solution (0.01%, 0.02%, and 0.05% w/v) in male subjects with androgenetic alopecia. *Cureus.* 17(8). e89309. Available at: https://doi.org/10.7759/cureus.89309 |
| ↑20 | 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. *Journal of the American Academy of Dermatology.* 55(1). 71–74. Available at: https://doi.org/10.1016/j.jaad.2005.07.001 |
| ↑21 | Rossi, A., Cantisani, C., Scarnò, M., Trucchia, A., Fortuna, M. C., & Calvieri, S. (2011). Finasteride, 1 mg daily administration on male androgenetic alopecia in different age groups: 10-year follow-up. *Dermatologic Therapy.* 24(4). 455–461. Available at: https://doi.org/10.1111/j.1529-8019.2011.01441.x |
| ↑23, ↑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 microneedling or oral 0.5 mg) in treatment of androgenetic alopecia. *QJM: An International Journal of Medicine.* 117(Supplement_2). hcae175–207. Available at: https://doi.org/10.1093/qjmed/hcae175.207 |
| ↑24 | 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 evaluate the safety and efficacy of novel dutasteride topical solution (0.01%, 0.02%, and 0.05% w/v) in male subjects with androgenetic alopecia. *Cureus.* 17(8). e89309. Available at: https://doi.org/10.7759/cureus.89309 |
| ↑31 | Ali, M. S., Alam, M. S., Alam, N., & Siddiqui, M. R. (2014). Preparation, characterization and stability study of dutasteride loaded nanoemulsion for treatment of benign prostatic hypertrophy. *Iranian Journal of Pharmaceutical Research (IJPR).* 13(4). 1125. Available at: https://doi.org/10.3390/pharmaceutics14061152 |
Minoxidil is a medication that began as a treatment for hypertension (high blood pressure). However, after observing excess hair growth during the testing stages of the drug, minoxidil was repurposed as a treatment for hair loss. Topical minoxidil soon received FDA approval for the treatment of both male and female pattern hair loss, while oral minoxidil is also used as an off-label treatment for hair loss.[1]Suchonwanit, P., Thammarucha, S., & Leerunyakul, K. (2019). Minoxidil and its use in hair disorders: a review. Drug design, development and therapy. 2777-2786. Available at: … Continue reading
So, if minoxidil is a treatment for hair loss, why does it cause an increase in hair loss when you start using it? Yes, you did read that right – minoxidil can actually cause an increase in hair loss as part of what is often called the ‘dread shed.’ This phenomenon was demonstrated in a retrospective study of 435 patients with androgenic alopecia (AGA) who were prescribed low-dose oral minoxidil [≤5 mg per day] by the same clinic. Self-reported adverse events were recorded for each of the users and, of the 435 patients, 32% experienced increased hair shedding.[2]Sanabria, B., de Nardo Vanzela, T., Miot, H. A., & Ramos, P. M. (2021). Adverse effects of low-dose oral minoxidil for androgenetic alopecia in 435 patients. Journal of the American Academy of … Continue reading
This is evidently cause for concern – if you have just started minoxidil treatment to prevent hair loss, a sudden increase in hair loss is possibly the last thing you would hope and expect to experience. So what is it about minoxidil that causes this to happen, how long does it usually last, and is it actually a good thing? In this article, we will explore the hair cycle and minoxidil in detail to provide answers to each of these questions.
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.
*Only available in the U.S. Prescriptions not guaranteed. Restrictions apply. Off-label products are not endorsed by the FDA.
To understand why minoxidil can increase hair shedding, let’s first take a refresher on the hair cycle. Our hair is constantly going through a cycle of growing (anagen), regression and transition (catagen), resting (telogen), and shedding (exogen), which it repeats continuously.
Healthy hairs grow for anywhere between 2 and 8 years, and there is a correlation between the length and strength of a hair and the time spent in anagen. Catagen is the transition from anagen to telogen, a period of approximately 2 weeks during which the follicle regresses from the hair shaft and disconnects it from the blood supply, preventing any further growth. Telogen follows and lasts for 2-3 months, with a new hair shaft beginning to develop at the base of the follicle underneath the now resting hair shaft. Exogen then represents the transition from telogen to anagen, with the growing hair shaft pushing out the old hair shaft.[3]Natarelli, N., Gahoonia, N., & Sivamani, R. K. (2023). Integrative and mechanistic approach to the hair growth cycle and hair loss. Journal of clinical medicine. 12(3). 893. Available at: … Continue reading
In the healthy scalp, the percentage of hairs in each of the hair cycle stages is thought to remain fairly consistent. At any one time, evidence suggests that approximately 9% of the hairs on a healthy scalp are in the telogen phase (although there are some suggestions that this figure may actually be too high).[4]Natarelli, N., Gahoonia, N., & Sivamani, R. K. (2023). Integrative and mechanistic approach to the hair growth cycle and hair loss. Journal of clinical medicine. 12(3). 893. Available at: … Continue reading These hairs exist in a largely asynchronous fashion, with hair follicles progressing through the hair cycle according to their own unique pattern. Hair follicles undergo between 10 and 30 full cycles, and it is normal for up to 150 hairs to fall out per day without there being an underlying hair loss problem, as the hairs are constantly being replaced.[5]Bergfeld, W. (2009). Diffuse hair loss: its triggers and management. Cleve Clin J Med. 76(6). 361-370. Available at: https://doi.org/10.3949/ccjm.76a.08080 This keeps hair fall relatively consistent, preventing periods of significant hair shedding.
AGA, the hair loss condition for which topical minoxidil is an approved treatment, is caused by damage to the hair follicle that contributes to its miniaturization. This is when individual strands of hair become smaller and smaller over time, eventually becoming vellus hairs that are shorter, thinner, and more white, which makes them difficult to see. We have a previous article that explores AGA-induced hair loss in great detail, but let’s summarize the key characteristics below:
Although the exact mechanisms underlying AGA are yet to be fully understood, it is evident that AGA is a progressive and cumulative process that occurs due to harmful factors damaging the hair follicle and shortening the anagen phase.

Chemical Structure of Minoxidil. Adapted from:[6]Pubchem (no date). Minoxidil (Compound). Available at: https://pubchem.ncbi.nlm.nih.gov/compound/Minoxidil#section=2D-Structure (Accessed: June 2025
Minoxidil is also yet to be fully understood, but several mechanisms have been suggested that could explain how it reduces hair loss:
It is likely that minoxidil reduces hair loss through a combination of several mechanisms, including those noted above and perhaps others that are yet to be discovered.
So, we know the basics of the hair cycle, some of the mechanisms that contribute to pattern hair loss, and some of the mechanisms by which minoxidil may reduce hair loss. But what does all this have to do with the ‘dread shed ’? Fortunately, observing the effects of minoxidil is more straightforward than trying to understand how it works, and there is one key effect which is believed to contribute to the increase in shedding: shortening of the telogen phase.
As we previously discussed, a key characteristic of AGA is lengthening of the telogen phase, which causes an abnormal amount of scalp hair to be in a state of arrested growth at the same time. It is widely believed that minoxidil directly addresses this issue by both shortening the telogen phase and accelerating the telogen to anagen transition. In one study, application of topical minoxidil to rats caused a dramatic shortening of the telogen phase, falling from 20 days to just 1-2 days.[10]Mori, O., & Uno, H. (1990). The effect of topical minoxidil on hair follicular cycles of rats. The Journal of dermatology. 17(5). 276-281. Available at: … Continue reading In a separate study that was also conducted in rats, topical minoxidil caused a significant switch from the telogen to anagen phase as quickly as 10 days after beginning treatment (Figure 2).[11]Shatalebi, M. A., & Rafiei, Y. (2014). Preparation and evaluation of minoxidil foamable emu oil emulsion. Research in pharmaceutical sciences. 9(2). 123-133. Available at: … Continue reading

Figure 1: The percentage of rat hair follicles in the anagen and telogen phases following treatment with minoxidil. Control rats were not given any treatment, market formulation refers to standard topical minoxidil [5%], main formulation is minoxidil in a foamable emulsion, and blank formulation is the foamable emulsion without the minoxidil.[12]Shatalebi, M. A., & Rafiei, Y. (2014). Preparation and evaluation of minoxidil foamable emu oil emulsion. Research in pharmaceutical sciences. 9(2). 123-133. Available at: … Continue reading
We could only find one clinical study that has investigated the telogen-anagen shift in humans at an early stage after beginning minoxidil use. They conducted a 24-week trial in which men with AGA either applied topical minoxidil [5%] or topical cetirizine for the first 16 weeks, then stopped use for 8 weeks. Although the results were not statistically significant, they showed that minoxidil caused an increase in the percentage of anagen hair and a decrease in the percentage of telogen hair, supporting the idea that minoxidil rapidly induces shortening of the telogen phase.[13]Mostafa, D. H., Samadi, A., Niknam, S., Nasrollahi, S. A., Guishard, A., & Firooz, A. (2021). Efficacy of cetirizine 1% versus minoxidil 5% topical solution in the treatment of male alopecia: a … Continue reading
In accelerating the telogen to anagen transition, minoxidil also causes “hair follicle synchronization” or synchronization of the hair cycle. As we highlighted earlier, healthy scalps are somewhat ‘protected’ from significant hair shedding events due to the asynchronous nature of the hairs and their individual hair cycles. However, due to the increased density of telogen follicles in the AGA-affected scalp, minoxidil causes a greater-than-normal percentage of hairs to enter anagen at the same time. This syncing of the hair cycles then results in more hairs being pushed out at the same time.
So, to summarize the process that is believed to be the key factor behind the dread shed:
Until very recently, evidence of minoxidil-induced hair shedding was either anecdotal or provided by studies of minoxidil in which increased hair shedding was noted as an adverse event. However, a newly published study sought to investigate the shedding phase in detail.
In this 2025 study, 49 patients with AGA used topical minoxidil [2% or 5%] for 24 weeks. Total hair shedding was quantified daily by the participants, who self-assessed their hair fall after combing, after washing, and on the pillow after sleeping. This was then averaged every 4 weeks and compared to the level of hair shedding prior to starting treatment. They found that the participants who used 5% minoxidil exhibited increased hair shedding (relative to pre-treatment) for 4-8 weeks, while the participants who used 2% minoxidil exhibited increased shedding for 8-12 weeks (Figure 2).[14]Bi, L., Kan, H., Wang, J., Ding, Y., Huang, Y., Wang, C., Du, Y., Lu, C., Zhao, M., Sun, W. & Su, T. (2025). Whether the transient hair shedding phase exist after minoxidil treatment and does it … Continue reading

Figure 2: Relative hair loss in the 24 weeks after starting treatment with minoxidil. *p < 0.05, **p < 0.01, ***p < 0.001. (A) Hair loss across all patients. (B) Hair loss in patients using 2% topical minoxidil. (C) Hair loss in patients using 5% topical minoxidil.[15]Bi, L., Kan, H., Wang, J., Ding, Y., Huang, Y., Wang, C., Du, Y., Lu, C., Zhao, M., Sun, W. & Su, T. (2025). Whether the transient hair shedding phase exist after minoxidil treatment and does it … Continue reading
This study provides definitive evidence that minoxidil does cause an initial shedding phase. However, importantly, hair shedding eventually fell below baseline levels in both groups, indicating that the initial shedding phase is temporary and that minoxidil did begin to reduce hair loss.
The same authors investigating the minoxidil shedding phase also sought to determine whether the amount of shedding had any association with treatment efficacy. They compared peak relative hair shedding (within the first 12 weeks) to changes in AGA severity using the Basic and Specific classification (BASP), which is a universal hair loss classification system that is used to assess the distribution and severity of hair loss in men and women of all races. They also compared peak relative hair shedding to several trichoscopy measurements, including hair density, hair diameter, and terminal hair proportion.[16]Bi, L., Kan, H., Wang, J., Ding, Y., Huang, Y., Wang, C., Du, Y., Lu, C., Zhao, M., Sun, W. & Su, T. (2025). Whether the transient hair shedding phase exist after minoxidil treatment and does it … Continue reading
Interestingly, in the 5% minoxidil group, a significant association was found between the amount of initial hair shedding and hair density, hair diameter, and the proportion of terminal hairs. In other words, people who lost more hair in the ‘dread shed’ actually experienced greater outcomes from minoxidil treatment. Furthermore, participants who initially shed the most hair in both the 2% and 5% minoxidil groups demonstrated the greatest improvements in AGA severity by week 24.[17]Bi, L., Kan, H., Wang, J., Ding, Y., Huang, Y., Wang, C., Du, Y., Lu, C., Zhao, M., Sun, W. & Su, T. (2025). Whether the transient hair shedding phase exist after minoxidil treatment and does it … Continue reading
These results are very interesting – not only does the initial shedding phase indicate that the minoxidil is working, but more shedding may even predict better treatment outcomes! So, if you’ve just started treatment, don’t fear the shed!
Minoxidil is an FDA-approved treatment for AGA but, in some cases, it can cause increased hair shedding in the early stages of use. Known as the ‘dread shed,’ this phase is believed to be caused by minoxidil shortening the telogen phase of the hair cycle, causing old hairs to fall out. This shedding is even more pronounced due to the increased density of telogen hairs present in the scalps of people with AGA. However, this shedding is only temporary, typically lasting between 4 and 8 weeks. Moreover, people who experience more shedding in this initial phase may actually experience greater overall outcomes from their minoxidil treatment. So, if you have just started minoxidil and are noticing increased shedding, don’t panic – it is most likely a sign that the minoxidil is working.
References[+]
| ↑1 | Suchonwanit, P., Thammarucha, S., & Leerunyakul, K. (2019). Minoxidil and its use in hair disorders: a review. Drug design, development and therapy. 2777-2786. Available at: https://doi.org/10.2147/DDDT.S214907 |
|---|---|
| ↑2 | Sanabria, B., de Nardo Vanzela, T., Miot, H. A., & Ramos, P. M. (2021). Adverse effects of low-dose oral minoxidil for androgenetic alopecia in 435 patients. Journal of the American Academy of Dermatology. 84(4). 1175-1178. Available at: https://doi.org/10.1016/j.jaad.2020.11.035 |
| ↑3 | Natarelli, N., Gahoonia, N., & Sivamani, R. K. (2023). Integrative and mechanistic approach to the hair growth cycle and hair loss. Journal of clinical medicine. 12(3). 893. Available at: https://doi.org/10.3390/jcm12030893 |
| ↑4 | Natarelli, N., Gahoonia, N., & Sivamani, R. K. (2023). Integrative and mechanistic approach to the hair growth cycle and hair loss. Journal of clinical medicine. 12(3). 893. Available at: https://doi.org/10.3390/jcm12030893 |
| ↑5 | Bergfeld, W. (2009). Diffuse hair loss: its triggers and management. Cleve Clin J Med. 76(6). 361-370. Available at: https://doi.org/10.3949/ccjm.76a.08080 |
| ↑6 | Pubchem (no date). Minoxidil (Compound). Available at: https://pubchem.ncbi.nlm.nih.gov/compound/Minoxidil#section=2D-Structure (Accessed: June 2025 |
| ↑7 | 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 |
| ↑8 | Michelet, J. F., Commo, S., Billoni, N., Mahé, Y. F., & Bernard, B. A. (1997). Activation of cytoprotective prostaglandin synthase-1 by minoxidil as a possible explanation for its hair growth-stimulating effect. Journal of investigative dermatology. 108(2). 205-209. Available at: https://doi.org/10.1111/1523-1747.ep12334249 |
| ↑9 | Lachgar, Charveron, Gall, & Bonafe. (1998). Minoxidil upregulates the expression of vascular endothelial growth factor in human hair dermal papilla cells. British Journal of Dermatology. 138(3). 407-411. Available at: https://doi.org/10.1046/j.1365-2133.1998.02115.x |
| ↑10 | Mori, O., & Uno, H. (1990). The effect of topical minoxidil on hair follicular cycles of rats. The Journal of dermatology. 17(5). 276-281. Available at: https://doi.org/10.1111/j.1346-8138.1990.tb01641.x |
| ↑11, ↑12 | Shatalebi, M. A., & Rafiei, Y. (2014). Preparation and evaluation of minoxidil foamable emu oil emulsion. Research in pharmaceutical sciences. 9(2). 123-133. Available at: https://pmc.ncbi.nlm.nih.gov/articles/PMC4311290/ |
| ↑13 | Mostafa, D. H., Samadi, A., Niknam, S., Nasrollahi, S. A., Guishard, A., & Firooz, A. (2021). Efficacy of cetirizine 1% versus minoxidil 5% topical solution in the treatment of male alopecia: a randomized, single-blind controlled study. Journal of Pharmacy & Pharmaceutical Sciences. 24. 191-199. Available at: https://doi.org/10.18433/jpps31456 |
| ↑14, ↑16, ↑17 | Bi, L., Kan, H., Wang, J., Ding, Y., Huang, Y., Wang, C., Du, Y., Lu, C., Zhao, M., Sun, W. & Su, T. (2025). Whether the transient hair shedding phase exist after minoxidil treatment and does it predict treatment efficacy? A retrospective study in androgenetic alopecia patients. Journal of Dermatological Treatment. 36(1). 2480739. Available at: https://doi.org/10.1080/09546634.2025.2480739 |
| ↑15 | Bi, L., Kan, H., Wang, J., Ding, Y., Huang, Y., Wang, C., Du, Y., Lu, C., Zhao, M., Sun, W. & Su, T. (2025). Whether the transient hair shedding phase exist after minoxidil treatment and does it predict treatment efficacy? A retrospective study in androgenetic alopecia patients. Journal of Dermatological Treatment. 36(1). 2480739. Available at: https://doi.org/10.1080/09546634.2025.2480739 |
In recent years, there’s been an explosion of interest in caffeine shampoos / topicals and their potential to improve pattern hair loss (androgenic alopecia). The hope: that applying caffeine to our scalps might stimulate growth factors, improve blood flow, and maybe even reverse hair follicle miniaturization.
At first glance, caffeine use might look like a viable, natural intervention. But what does the research actually say?
In other words, does caffeine work? Is it a viable alternative to minoxidil? Is caffeine better if ingested, applied topically, or used as a shampoo? How much hair regrowth can we expect? And are there any longterm side effects?
This article dives in the science (and answers).
We’ll dispel a lot of common knowledge about caffeine’s efficacy for hair growth. We’ll also comb through the evidence, set realistic expectations, and reveal how to best use caffeine to maximize your chances of hair recovery.
Long-story short: caffeine isn’t a miracle cure. But it might not be completely useless, either.
The top natural ingredients for hair growth, all in one serum & supplement.
Take the next step in your hair growth journey with a world-class natural serum & supplement. Ingredients, doses, & concentrations built by science.
Topical caffeine is clinically shown to reduce hair shedding rates and improve anagen:telogen ratios in men with androgenic alopecia. Unfortunately, it’s still unclear just how effective caffeine-based topicals and shampoos are for improving pattern hair loss.
Caffeine shampoos/topicals fall under an intervention umbrella of “low risk, low reward”. In other words, caffeine’s risk of significant side effects is minimal, as is the amount of hair growth it may initiate.
Having said that, not all caffeine is created equally. While topical caffeine products have been shown to improve shedding rates and anagen:telogen ratios, oral caffeine might actually increase hair loss in those who have insulin resistance or are hypothyroid.
Of all clinical studies on topical caffeine for pattern hair loss, the best results seem to occur when topical caffeine is combined with ingredients like azelaic acid or drugs like minoxidil.
In any case, a 0.2% caffeine dilution for topical solutions and a 1% caffeine dilution for shampoo formulations seem to be the best studied (and most promising), so look for brands that meet these criteria.
If you’re going to use caffeine as a potential hair loss intervention, please understand that this stimulant is only clinically tested on androgenic alopecia, and that it’s likely not effective as a standalone treatment.
More information on the science behind caffeine – its mechanisms, as well as the optimal delivery methods, dilution, and more for hair recovery – can be found below.
Caffeine is a stimulant derived from plants – namely, coffee and tea. It’s the most popular stimulant on the planet.
As a stimulant, caffeine has a variety of effects on the human body – from better focus to improvements in endurance. But interestingly, the magnitude of these effect often vary per person, and as a result of differences in our genetic constitution, food consumption, and even past caffeine exposure.
In general, caffeine has been studied for its effects on:
And interestingly, vasodilation, cellular metabolism, cortisol, and thyroid hormones have all been studied as potential treatments to different hair loss disorders.
For instance, hair loss drugs like minoxidil improve hair growth by increasing vasodilation; thyroid drugs like levothyroxine help to improve hypothyroid-related hair loss by restoring thyroid functionality.
This begs the question: what sort of impact might caffeine have on our hair follicles?
Can caffeine – ingested orally or applied topically – mimic the mechanisms of hair loss interventions? And if so, are the effects of caffeine strong enough to actually improve hair loss outcomes?
These connective points are what prompted scientists to start studying caffeine as a potential hair loss intervention. And taking a deeper look, there is some mechanistic overlap in how this stimulant might improve hair loss outcomes.
Caffeine is one of the most popular stimulants. It’s well-studied in terms of its effects on vasodilation, cellular metabolism, and hormonal health. And interestingly, these research avenues have left scientists wondering if caffeine can also be reoriented as a hair loss solution.
It’s hard to say. On the one hand, caffeine does have some hair-promoting effects. On the other hand, caffeine also has some issues that may actually contribute to hair loss. All in all, the way it will effect you will boil down to (1) the dose and (2) the ingestion type (oral or topical), and (3) your genetic constitution.
Here are a few effects that caffeine has – both positive and negative – in regard to hair health.
Caffeine’s effects on blood flow vary depending on the mode of ingestion (i.e., topical versus oral) and the actual tissue being measured. Just see this chart demonstrating how oral caffeine impacts blood flow across body tissues.
(source)
Interestingly, both topical caffeine and oral caffeine seem to improve blood flow in microcapillary networks – the blood vessel networks that supply our peripheral tissues (i.e., skin) – and the same blood vessel networks that help support the growth of our hair follicles.
This is because in vascular smooth muscle cells, caffeine acts as a phosphodiesterase inhibitor. In other words, caffeine helps to block the enzyme phosphodiesterase.
This enzyme helps inactivate a molecule called cyclic adenosine monophosphate – a biological messenger molecule that regulates vasolidation (i.e., blood flow) in smooth muscle cells. In the absence of phosphodiesterase, more cyclic adenosine monophosphate accumulates, thus expanding vasodilation in smooth muscle tissues.
This is also why phosphodiesterase inhibitors are often prescribed for a variety of blood flow-related health conditions – i.e., erectile dysfunction, hypertension, and even vascular disease. They all help promote blood flow.
Caffeine happens to be one of these phosphodiesterase inhibitors. And while it’s a weak inhibitor, it still has an effect on these capillary networks.
But, there’s one caveat here. While it’s true that a defining characteristic of androgenic alopecia (AGA) is reduced blood flow, it’s still debated whether blood flow is a cause or consequence to hair follicle miniaturization. So, we don’t yet know if caffeine’s vasodilation effects will really have any impact to our hair.
Caffeine doesn’t just inhibit phosphodiesterase. It also inhibits adenosine receptors – a type of neural receptor that helps to regulate cellular metabolism and our own sense of “wakefulness”.
In the absence of caffeine, a molecule called adenosine normally binds to an adenosine receptor in our brain. When adenosine binds to an adenosine receptor, our brain’s neural activity begins to quiet. The end-result: we feel a bit sleepier.
Caffeine is an adenosine receptor antagonist. That means that when it’s ingested, caffeine blocks adenosine receptors so that adenosine cannot bind to them. This prevents the “quieting” of neural activity – and thus promotes longer periods of wakefulness.
Interestingly, there’s also evidence that caffeine’s inhibition of both phosphodiesterase and adenosine receptors may promote cellular metabolism. To put it more bluntly, caffeine ingestion might help to improve (1) energy utilization in the body, and (2) the mobilization of free fatty acids for energy usage.
This may have pro-hair effects, as many genes that are upregulating in balding scalp tissues tend to have an association with impaired cellular metabolism. But again, we just don’t know for sure.
Unfortunately, not all effects from caffeine are pro-hair. While improving cellular metabolism may help support the growth stage of our hair follicles, there are also consequences to the way in which caffeine improves cellular metabolism that may negatively impact our hair.
For instance, one study found that oral caffeine consumption decreased insulin sensitivity by 15% in healthy adults. That’s not good – especially for young men and women who are balding, as insulin resistance is almost always a commonly confounding factor in early-onset AGA.
Moreover, there’s also evidence that at high dosages, oral caffeine’s “liberation” of free fatty acids also promotes hyperglycemia and insulin resistance in peripheral tissues (i.e., our skin) – possibly as a result of increased stress hormones like cortisol. Which brings us to our second concern…
Evidence strongly implicates oral caffeine consumption and an increase in cortisol levels. Unfortunately, the hormone cortisol, when chronically elevated, can negatively impact hair-related bodily functions and in two major ways:
Another noteworthy mention is that coffee can also impair the absorption of thyroxine. So, if you are taking this medication for a thyroid disorder, it’s likely in your best interest to avoid consuming coffee around the same time. But, it’s unclear whether this effect is a result of the caffeine content or other compounds found in coffee.
Again, we don’t yet have any data correlating oral caffeine consumption to pattern hair loss. But these concerns are worth noting for anyone who’s balding and has had a history of hyperglycemia, insulin resistance, hypothyroidism, or adrenal dysregulation.
In contrast to high dose oral caffeine, it doesn’t seem like topical caffeine elicits the exact same anti-hair effects. Rather, topical caffeine (as a lotion or shampoo) might have some therapeutic benefit to our scalp hair.
For reference, in vitro studies in humans and in vivo studies in mice suggest that caffeine’s effects on (1) phosphodiesterase inhibition and (2) adenosine receptor binding probably will improve hair growth, and through a variety of means.
Specifically, topical caffeine might…
So, overall, it seems like mechanistic evidence supports at least the use of topical caffeine as a potential hair loss intervention. And this conclusion is why so many researchers have bothered studying caffeine lotions and shampoos for the improvement of AGA.
Caffeine is a (1) phosphodiesterase inhibitor and (2) an adenosine receptor antagonist. While its effects vary on a tissue-by-tissue basis, oral and topical caffeine seem to improve microcapillary networks in periphery tissues (where our hair follicles reside). Moreover, caffeine can help improve cellular metabolism by liberating free fatty acids for energy use. Improvements to both (1) vasodilation and (2) cellular metabolism should theoretically benefit our hair.
At the same time, oral caffeine seems to also increase insulin resistance in peripheral tissues. This is problematic – as reduced insulin sensitivity may interfere with the growth cycles of our hair follicles. Moreover, oral caffeine consumption can increase cortisol levels and decrease thyroid functionality – which may also negatively impact hair growth cycles.
Despite concerns of oral caffeine use for hair, evidence does support the use of topical caffeine for hair growth – at least from a mechanistic standpoint. In vitro research suggests that, in human hair follicles, topical caffeine helps to prolong anagen duration, increase IGF-1, inhibit cell death, and improve blood flow. While this doesn’t mean that these effects will translate in vivo, it does give credence to the idea that topical caffeine is worth testing as a hair loss intervention.
This all brings us to our next question: what does the clinical data say about topical caffeine and its use as a hair growth stimulant?
This is harder to answer than it may seem.
At face-value, the answer is yes. This is because there are a lot of studies showing that caffeine in a topical or shampoo (or caffeine in conjunction with minoxidil and/or azelaic acid) can improve hair loss outcomes.
For instance, this recent literature review on topical caffeine dives into over a dozen clinical studies, many of which report:
Reading these conclusions, it’s no wonder why caffeine topical sales have spiked in the last few years.
However, taking a closer look, these studies might not be as encouraging as their conclusions imply. Here’s why.
When it comes to research, not all peer-reviewed papers are created equally.
Some studies are published in predatory journals that circumvent the peer review process; others are published in low-ranking journals; others simply have major methodological concerns that draw the findings of those studies into question.
When it comes to the studies on caffeine and hair regrowth, it’s that last issue that’s most prevalent. That’s not to say that we should dismiss caffeine’s effects entirely. But, there are several concerns worth highlighting.
In the above literature review, most of the feature studies don’t measure hair count increases. Rather, they measure endpoints like patient self-satisfaction surveys, changes to anagen:telogen ratios, and a reduction in hair fall during “wash tests” or “tug tests”.
These measurements are difficult to standardize and are notoriously unreliable, meaning it can be hard to determine the true effectiveness of caffeine from any study designed this way.
In fact, it’s my belief that a lot of industry-funded research purposefully chooses these measurement endpoints because of their unreliability. For reference, these types of endpoints are why so many low-level laser therapy studies will report almost unbelievable hair improvement – i.e., “200% hair diameter increases” or “80% hair density improvements” in their clinical trials – while paradoxically, having no visual improvements to show subjects’ photographic assessments.
The bottom line: these measurement endpoints aren’t very strong, and some investigators who choose these endpoints may be doing so to deliberately skew caffeine’s perception of efficacy. But no matter what, the weaker the hair measurement endpoints, the less reliable the results.
Most of these studies measure topical caffeine alongside enhancer ingredients – like azelaic acid, minoxidil, or both – and not caffeine as a standalone treatment. This makes it hard to evaluate whether caffeine by itself is very effective.
In fact, there’s just one study that we could find that measured topical caffeine as a standalone treatment. Unfortunately, it measures topical caffeine versus minoxidil, not a placebo. That study’s takeaway? That topical caffeine is similarly effective to 5% minoxidil… at least when we compare weak measurement endpoints (see #1).
Of all the clinical research done on caffeine and hair growth, most of it is industry-funded.
At face-value, this isn’t necessarily a problem. After all, a significant portion of hair loss studies comes from industry-funded research teams. Where there’s financial incentive for a treatment, there will be attempts at peer-reviewed research to prove efficacy.
Having said that, this does become a problem when the studies are typically designed with poor measurement outcomes – such that the odds of achieving “favorable” results increases dramatically. Nearly all of the topical caffeine studies on AGA have this very problem. Compile that with the issue of almost never measuring caffeine alone, and you have even more problems (see #1 and #2).
One of the most frustrating aspects of hair loss products are that manufacturers will publish a study showing their product demonstrating benefit, but then sell you a product that’s different from the one studied.
This happens all the time with LLLT devices, and it seemingly also happens with caffeine products for hair loss.
Case in point: Alpecin’s study on a topical caffeine solution. The findings showed that this topical did improve hair loss outcomes. But ironically, Alpecin doesn’t sell this topical; it sells a caffeine shampoo. Topicals are leave-in for hours, whereas shampoos may only come into contact with the scalp for 60 seconds. It was this issue in addition to #1-#3 that got Alpecin banned in certain countries from saying their “shampoos” could reduce hair loss.
It was a combination of these issues that led researchers in the above literature review to conclude that while caffeine might help improve aspects of our hair, there isn’t yet enough evidence to support most claims being made by manufacturers.
Topical caffeine does have clinical research supporting its use for hair loss. However, in literature reviews of the dozen or so studies on topical caffeine, concerns of endpoint measurements, lacking study as a standalone treatment, conflicts of interest, and discrepancies in what’s studied versus sold to consumers raises red flags as to caffeine being a truly viable long-term solution.
Circling back to that literature review, there is accumulating evidence that caffeine can help reduce hair shedding from androgenic alopecia and even improve anagen:telogen ratios. It’s just that if we’re going to use it, we shouldn’t set our expectations at regrowth; we should set our expectations at a slowing of hair loss.
This leaves us with an interesting dilemma: if we want to leverage caffeine as a hair growth promoter, we need to do so in topical or shampoo form. And that means we need to know:
Sifting through the literature review, there are studies that answer these questions. But again, they’re all subject to significant bias.
Even still, we can use these studies to guide some caffeine best practices – at least for those who want to make the investment and try it out.
Oral caffeine likely doesn’t accumulate in the scalp at a high enough degree to elicit adverse or beneficial effects. However, it may have peripheral action through increased cortisol levels, and this may indirectly impede hair growth for those with insulin resistance and/or hypothyroidism.
Knowing this, the safest and most effective way to use caffeine for hair growth is through topical means, either through some sort of lotion or shampoo.
Considering one study found that caffeine solutions penetrate the hair follicle after 2 minutes and peak at 2 hours, a leave-on caffeine solution may be optimal over a shampoo formulation.
But to be clear: the answer likely depends on whatever other ingredients are also in the topical (i.e., azelaic acid, minoxidil, etc.). Here’s why.
So, from what we can garner from the limited studies available, a 0.2% solution for topical application seems to be somewhat effective. However, keep in mind that this is only for a leave-on treatment, not a shampoo.
We don’t really have much information on optimal shampoo dilution. A 1% dilution was the only concentration reported for caffeine shampoo alone, but this treatment wasn’t compared against a placebo and, so, results aren’t super applicable. Even still, 1% seems to be comparably effective to minoxidil.
A 1% caffeine, minoxidil 5%, and 1.5% azelaic acid topical was considered more effective than minoxidil alone, but we can’t extrapolate this 1% dilution to a caffeine-only shampoo.
0.2% for topical solutions and 1% for shampoo formulations is all we can really extract from the current body of evidence, but it should be noted that these recommendations aren’t necessarily reliable given the minimal evidence.
Like concentration, data on the frequency of use is also sparse. In the highest quality study, subjects used a 0.2% caffeine topical twice a day, every day. Another study instructed subjects to apply a caffeine lotion (unspecified concentration) once daily.
Other studies likely using shampoos most likely involved subjects using the treatment product however often they would normally shampoo their hair. So, it can be difficult to quantify just how often is optimal because use wasn’t standardized, as far as we can see.
With the knowledge we have, daily use of a topical seems to be optimal. Conversely, using a shampoo daily may be drying to the hair and the scalp, so it’s safe to say that using a caffeine-containing shampoo however often you would normally shampoo is probably best.
While no studies measure caffeine’s effectiveness for long enough to see if regrowth is sustained, we can assume – like nearly all topicals – that its hair-promoting effects will likely lessen over time.
The reasons why will be explained in a future article – one comparing the long-term outcomes of antiandrogenic versus non-antiandrogenic hair loss interventions. But the short answer is that we can liken any sort of topical formulation for hair loss – even minoxidil – as a bandaid that won’t necessarily fully address the underlying roots of the problem.
Topical caffeine may help to elongate the anagen phase of the hair cycle, improve anagen:telogen ratios, decrease hair shedding, and slow the progression of androgenic alopecia (AGA). But it’s by no means a miracle cure, and evidence so far suggests that this topical isn’t any better than 5% minoxidil.
The limited evidence we do have on topical caffeine is relatively biased, poorly designed, and has only been studied for androgenic alopecia. Until studies with better designs are published, it’s hard to say with certainty just how much of an effect topical caffeine will have on our hair.
Nevertheless, topical caffeine leave-on treatments have more quality evidence to support their use (as opposed to shampoos). 0.2% dilutions for topicals and 1% dilutions for shampoos seem to be the most promising. Moreover, the best way to utilize caffeine seems to be in conjunction with minoxidil and, possibly, azelaic acid.
Paradoxically, oral caffeine consumption may have an adverse effect on hair growth through increased cortisol release, increased hyperglycemia in periphery tissues, and potentially decreased thyroid functionality. For these reasons, anyone with a history of insulin resistance or hypothyroidism is probably better off avoiding oral caffeine altogether – particularly for hair health.
If you do decide to implement caffeine into your regrowth regimen, the first thing you’ll notice is how difficult it is to field the market. Almost all companies that have any merit in this space don’t quantify the caffeine dilution in their products. Considering most caffeine treatments are upwards of $35 USD, you may want to call around and see if their customer service representatives can give you more information.
Let us know if you have personal experience or testament in using (or excluding) caffeine. If you start using caffeine, report your progress here for others to see! Any questions or comments? Please reach out in the comments section.
In the last decade, thousands of dermatologists have started offering platelet-rich plasma (PRP) therapy as a treatment for hair loss. At first glance, PRP seems like an enticing therapy: a hands-free, drug-free approach to improve our hair thinning…
…but with a $1,000+ price tag, is the therapy worth it? Is PRP right for all hair loss sufferers? And if platelet-rich plasma therapy does work, how much hair can we expect to regrow?
This ultimate guide to platelet-rich plasma therapy uncovers the answers. Here we’ll reveal how platelet-rich plasma therapy works, how it compares to similar therapies, and what most dermatologists don’t tell you about their PRP “before-after” photos.
We’ll also reveal how hair regrowth from PRP depends largely on your form of hair loss, whether you combine PRP with other treatments, and the type of PRP your dermatologist provides (Acell, etc.).
If you’re considering PRP as a hair loss treatment, this guide will help you determine if the costs make sense for your situation and, if so, how to select the right provider.
The top natural ingredients for hair growth, all in one serum & supplement.
Take the next step in your hair growth journey with a world-class natural serum & supplement. Ingredients, doses, & concentrations built by science.
PRP is effective for androgenic alopecia and alopecia areata, but it’s expensive and requires ongoing injections to maintain results. It works best as an adjunct treatment alongside other hair loss therapies, and while it has helped both men and women, evidence suggests that it’s less effective for females overall. If you’re going to try PRP, don’t just go to any clinic; rather, vet your cosmetic surgeon by asking them a list of questions we’ve suggested (below).
Platelet-rich plasma therapy (PRP) is an injection-based therapy. It’s the injection of a modified version of our own blood into a tissue site – with the goal to accelerate healing, reduce scarring, and improve injury outcomes.
PRP has been used for dentistry, facial reconstruction surgery, orthopedics, sports injuries, acne scarring, and fat grafting. But in the last decade, it’s been given serious attention as a potential treatment for thinning hair.
PRP therapy is a multi-step process that involves drawing a sample of our blood, separating out its platelets, concentrating those platelets, and then re-injecting those platelets into a targeted location (like our scalp).
If you’re considering PRP, the procedure usually takes around an 30-90 minutes, and the process looks something like this:
Our blood volume contains roughly 55% plasma, 40-45% red blood cells, 6% platelets, and 1% white blood cells. Whenever our tissues incur a wound – for example, a paper cut – an inflammatory reaction begins, and our bodies will send blood to our injury site to initiate repair.
Interestingly, our platelets – which constitute just 6% of our blood volume – are responsible for a huge part of the entire repair process. Specifically, platelets do two things:
This begs the question: what if we could concentrate our platelets so that instead of sending only 6% of platelets to a wound tissue, we could send a much higher percentage? Would we see better injury outcomes? Would we see less scarring?
Well, this is exactly what platelet-rich plasma therapy does. In fact, recent advents in “centrifugation” – or the swirling, mixing, and separation of platelets from our blood – have enabled dermatologists to achieve blood platelet concentrations higher than 94%+. That’s a huge jump from the 6% typically carried within our normal blood volume.
And as of today, it seems like platelet concentrations do improve injury outcomes and scarring. Decades of studies show that, on average, if we concentrate high levels of plasma and send that plasma to an injury site, we can improve injuries, reduce scar tissue, and in doing so, maybe even regrow some hair.
There are several growth factors carried within plasma linked to hair growth, most notably:
And when injected into balding scalp tissues, the arrival of these growth factors can do a few things:
Yes. PRP’s mechanisms overlap with one of the ways by which massaging and microneedling improve hair loss: they both increase the number of growth factors in balding scalp regions. But, they do it in slightly different ways.
Massaging and microneedling first generate acute inflammation (i.e., micro-wounding), which then increases growth factors, which then helps to promote hair recovery. The order of operations is as follows:
Massaging / microneedling >> evokes micro-inflammation >> evokes platelets / growth factors >> decreases scarring proteins / increases angiogenesis >> reduces perifollicular fibrosis >> improves blood flow to miniaturizing hair follicles / increases follicle growth space >> increases hair growth
But there’s a key difference between PRP and these two therapies. With massaging and microneedling, you need to first evoke inflammation to increase growth factors to a wound site. With platelet-rich plasma, you essentially skip that first step, and instead, you simply inject platelets directly into the tissue of your choosing.
When it comes to balding scalp tissues, we can think of the mechanistic difference between these therapies as this:
Now, there is some wounding involved in PRP procedures. But that wounding / acute inflammation is a consequence to the injection of the platelets. In this way, PRP is sort of like a supercharged microneedling or massage session – only with many more platelets present.
This is a tricky question to answer.
If forced to give a one-word answer, then yes. Most studies on PRP show positive outcomes for hair loss. But if you’re going to invest thousands of dollars into the therapy, there are caveats of which you should be made aware.
The reality is that PRP’s effectiveness for regrowth depends on the study you reference and how you define the term, “effective”. Moreover, PRP efficacy varies greatly by:
We’ll cover all of this below. First, we’ll start with PRP’s issues. Then, we’ll dive into PRP’s benefits (and its effects on our hair).
Most PRP studies are conducted by dermatologists who offer PRP procedures at their clinics. That creates an incentive to achieve positive results – because those positive results might encourage patients to do the procedure at their specific clinic.
However, this problem isn’t necessarily game-ending. In fact, nearly all hair loss research contains some level of bias. For instance, despite our efforts to control for bias in our own study on the massages, technically you could argue that because this site conducted it, our results are at risk of bias, too.
In any case, there are plenty of well-controlled studies on platelet-rich plasma and hair loss. We’ve filtered for these. But if you go digging through the literature and find a PRP study with crazy results, just know that if it wasn’t included in our analysis, there’s probably a good reason why.
Nearly every PRP study has a different patient profile (i.e., ages and hair loss severities), methodology (i.e., injection methods, rounds, treatment regions), trial duration (i.e., three months versus two years), and hair assessment method.
For instance, here are just a few ways PRP studies have measured hair loss “improvements” (ranked from worst to best).
To be fair, this isn’t just a problem with PRP; it’s a problem with all of hair loss research. It’s why literature reviews have a hard time drawing conclusions about most treatments – because there are rarely apples-to-apples comparisons.
But again, we’ve sorted through all the PRP studies we could find to standardize the research (as best we can) and give you ballpark assessments of regrowth rates (i.e., increases to hair count in balding regions).
When you look into the research on minoxidil or finasteride, studies show that within 3-12 months of quitting either drug, your hair loss will return to what it was prior to the intervention. So, how long will results hold for platelet-rich plasma after quitting?
Well, it’s unclear how long results will last after you stop doing PRP treatments, but evidence suggests that a percentage of people will start seeing their hair return to baseline after a year.
Out of all PRP studies, the one with the longest follow-up period (two years) included 20 patients. Interestingly, four of them experienced a relapse in hair loss one-year post-PRP. In fact, their androgenic alopecia progressed beyond their pre-trial hair counts by the 16-month mark. This suggests that for about 20% of people, PRP’s effects start to wane 12-18 months after the treatment.
This wouldn’t be such an issue if the procedure were cheap, but it isn’t: several therapeutic rounds of PRP cost $1,000-$4,000+. So, if you’re going to give this procedure a try, make sure you’re financially comfortable with the investment.
Out of all the research on PRP, only two studies found that PRP was an ineffective treatment option. One study was on females with androgenic alopecia. The other study was on men with advanced androgenic alopecia (Norwood gradients 4+).
If you were to ask me why the first study failed to produce results, I would say that it was probably because (like most women with hair loss) the females in that study likely had other undiagnosed hair loss types (like telogen effluvium / hair loss related to a chronic condition).
And as far as the study on men with advanced androgenic alopecia (AGA) – we need to keep in mind that the investigation team only did two rounds of PRP injections. For what it’s worth, in all of the PRP studies which saw improvement, a minimum of three PRP injection rounds were performed. So, it’s likely that either this study didn’t do enough injections to see results, or that men with advanced AGA needed several more injections before PRP begins to repeat significant benefit.
In fact, the overwhelming majority of studies measure PRP alongside other hair loss treatments – like minoxidil, finasteride, or even a hair transplant. So, it’s important to delineate between the studies you reference when evaluating whether PRP is right for you (we’ve done this below).
This also brings up another problem: dermatologists showcasing their PRP results online often don’t tell you something important: that they’re showing you PRP results alongside drugs like minoxidil and finasteride.
This is incredibly disingenuous, and I suggest that if you’re shopping around for a PRP clinic, you call ahead and ask the doctor if the results they showcase on their website are from PRP alone. If they are, great. If they’re not, but they’re labeled to make it seem as such, then that means these dermatologists are intentionally misleading prospective patients, and they should lose your business (and their license to practice).
While we might’ve just painted a problematic picture for PRP, this isn’t the whole story. In fact, PRP is an incredibly effective treatment for hair loss under the right circumstances. This is all covered below.
PRP has shown great promise for the hair loss disorder alopecia areata. This is an autoimmune condition that leads to hair loss in patchy spots throughout the head. In some cases, it can advance to complete baldness (alopecia universalis).
In fact, studies show that PRP is very effective in treating at least 70% of alopecia areata cases. Here are some of the really promising photos (source):
When looking at PRP as a standalone treatment, most studies measuring hair counts suggest that the average patient will regrow 15 hairs per square centimeter (i.e., half the size of a penny). That’s about a 25-30% regrowth rate at 3-6 month follow-ups.
Quantitatively, that’s pretty impressive. For a benchmark, most studies on finasteride show just a 10% increase in hair count over two years.
Across studies, some of the less quantitative outcomes for PRP alone (at least at the 3-6 month mark) are:
Finally, a common trend mentioned among researchers is that PRP treatment seems to be more effective for patients with less severe forms of AGA. So, if you’re in the early stages of hair loss, PRP might be a great option for you.
In one study examining hair transplantation, two areas with 50 grafts each(not a lot to measure, especially for hair transplantation) were compared with or without PRP injections. The area with PRP had, on average, 46.75 units that survived compared to the non-PRP which had, on average, 41 units that survived.
While this isn’t that drastic of an increase – we have to keep in mind that transplant procedures are incredibly costly… and that means that every hair follicle unit counts.
So, if you’re considering a hair transplant, you’ve spent the finances to secure a skilled surgeon, and you still have some extra spending money you’d like to throw into improving your results – do it alongside PRP. Chances are your hair transplant survival rates will improve, as will your overall hair count.
In this study, 30 male participants received 6 PRP injections following microneedling sessions. At the six month follow-up, the average patient had a hair density increase of about 30%. This study also noted that the most significant improvement was seen in patients with less severe AGA.
In this study comparing the efficacy of PRP + minoxidil and PRP + finasteride, while both outcomes were deemed effective, the PRP + minoxidil treatment actually achieved significantly better results than the PRP + finasteride group. In fact, the PRP + minoxidil group showed five-fold better hair increases versus the PRP + finasteride group.
Now, you might read these results and think that makes no sense. Finasteride is clinically more effective than minoxidil. So, why would PRP + minoxidil outperform PRP + finasteride?
Well, the devil is in the details. For one, the sample size of each PRP subgroup was less than 15 people. So, it’s possible these differences might’ve been due to statistical noise which would’ve canceled itself out with subgroups of 150+ people.
And secondly, while a five-fold improvement might sound drastic, we’re actually dealing with the law of small numbers here. Yes, PRP + finasteride saw an additional hair count lift of 1% versus 5% for the PRP + minoxidil group. And yes, that is technically a five-fold improvement. But in all reality, that’s just a few percentage points better.
In this study comparing PRP + minoxidil + microneedling versus minoxidil alone, the earlier treatment proved to be much more effective than the latter, although exact numbers were not given in this study to show this. However, we can assume that PRP + minoxidil + microneedling is probably better than PRP + minoxidil, and that PRP + minoxidil is probably better than PRP alone.
PRP + Acell is a relatively new procedure that a lot of PRP practitioners are offering now. Acell is a protein matrix derived from pig bladder (you read that right) that creates a “scaffold” for new hairs. Acell essentially offers a platform by which all of our growth factors (and hair) can cling to. It also helps to stimulate stem cell activity.
[Note: since ACell is made from pig, people allergic to pig products should notify their physicians about their allergy prior to the treatment.]
There doesn’t seem to be any studies measuring the results of PRP + Acell compared to PRP alone, so it’s hard to objectively say whether it increases the effectiveness of PRP.
At least so far, there haven’t been any severe risks reported. However, some milder symptoms have been noted during and shortly after the procedure:
Androgenic alopecia treatments vary depending on your (1) finances, (2) willingness to invest time into a therapy, and (3) comfortability with FDA-approved drugs. Compared to some of the other AGA specific treatments, like standardized scalp massages and microneedling, PRP is a pricey option. At the same time, PRP is a lot less time consuming than microneedling or massaging because you may only go into a clinic for a handful of injection rounds before you start seeing results.
You are a great candidate for PRP if you…
You are not a great candidate for PRP if you…
When evaluating any hair loss therapy, it’s important to note that, sometimes, study results don’t match up to real-world results. On hair loss blogs and forums, there’s sometimes an inkling that this might be the case with PRP.
For starters, while there are positive patient stories with PRP, there are also many anecdotes of patients who tried PRP without success. This video is a perfect example. And if you dig deeper, you’ll probably find more negative than positive anecdotes.
This can be confusing – as most of the literature tends to describe PRP as seemingly beneficial. And even more troublesome, it’s also worth noting that I’ve spoken with dozens of readers who’ve tried PRP… and most of them have also reported negligible improvements.
This begs the question: is PRP that effective? And regardless of the answer, why might there be a discrepancy between studies’ results and patient reports?
For starters, it’s actually unclear if there are clinical versus real-world discrepancies for PRP. For instance, it’s possible that PRP treatments might just suffer from the “Yelp effect”. This is when someone with a negative experience is far more likely to leave a public review versus someone with a positive experience.
So, PRP might just be one of those treatments that have collected negative reviews over a period of years – much like finasteride and its reports of sexual side effects.
Secondly (and this is the more important point to make), clinical research does not always depict reality. For instance, while a 25-40% increase in hair count from PRP looks great on paper, it doesn’t always translate to cosmetic results.
This tends to be a problem with even the “best” FDA-approved treatments. Just take a look at these five men who did combination treatments of minoxidil, finasteride, laser combs, and even hair transplants – and their results after one year.
I’ll save you the suspense: their final “after” photos are darkened to obscure just how minimal their hair changes are. And, for the hundreds (to thousands) of dollars each of the men spent, their hair seems more-or-less cosmetically unchanged.
(Note: that video is just one of the reasons why, for most AGA sufferers, I recommend approaches like massaging / microneedling as a baseline for any regimen. Not only do these therapies enhance other hair loss treatments, but also without their inclusion, you’re statistically likely to see no cosmetic improvements from your other treatments).
Thirdly, we just learned that without follow-up sessions, PRP results will fade for 20% of patients starting 12-18 months after their last round of injections. So, if you’re reading a review of someone who got PRP once four years ago and never saw results (or is experiencing continued hair loss) – you’ll know that it’s probably because they didn’t do enough injection rounds and they didn’t keep up with the therapy.
In any case, it’s worth noting that of the readers with whom I’ve communicated, the ones who tried PRP + Acell all reported positive results. While there aren’t yet studies validating this combination therapy, it seems to be the most promising from an anecdotal standpoint (if that means anything to you).
If you’re going to invest $1,000+ into platelet-rich plasma, don’t give your money to the first PRP clinic you find.
Instead, find a few clinics near you that offer the procedure and make sure they have a proven track record. That means they should have a website with PRP before-after photos.
Make a list of these clinics. Then, call each clinic and ask if their online photos are of PRP alone or of PRP + finasteride / minoxidil.
If the photos are of PRP alone, great! If they’re of PRP + multi-therapies but advertised to represent only PRP… then hang up, cross them off your list, and consider reporting them the clinic to the Better Business Bureau.
Doing this should eliminate 60-70% of providers.
Next, call the remaining providers and ask about their PRP techniques. You’ll want to find a clinic that offers 1-4+ months between injection rounds. If someone offers you a package of 10 PRP sessions spaced out as one injection round per week, that goes against the literature’s recommendations (and our understanding of wound-healing timelines) – and you should probably find another provider.
Moreover, the actual PRP product that a clinic uses will vary by volume, number of injection rounds, color, platelet count, leukocyte count, and protein content. The best PRP providers will offer double-spin centrifugation preparation with an activator like thrombin or calcium chloride. While some evidence suggests that “platelet activators” are not necessary, they also don’t seem to hurt the procedure. In any case, it’ll be good to speak with your provider about all of this – so you can get a feel of whether they can actually answer these questions. If they can’t, then cross them off your list.
Lastly, ask your remaining clinics if they offer PRP + Acell. If they do (and the costs aren’t prohibitive), then this might be a better option versus PRP alone. If they don’t, it’s not the end of the world – and chances are you’ll still see benefit from the procedure.
Following this process should leave you a few great PRP clinic options. And, as long as you’re willing to commit to injections every 4-6 months, you should see a considerable lift in hair count… especially if you’re combining platelet-rich plasma with other therapies.
Platelet-rich plasma therapy is effective for both androgenic alopecia and alopecia areata, but the procedure is cost-prohibitive and requires repeated clinic visits to see sustained results. These factors are big turnoffs for most hair loss sufferers considering PRP as a treatment option.
PRP works best as an adjunct treatment alongside other hair loss therapies. So, don’t just try PRP as the only thing to help your hair. We recommend combining it with massaging and/or microneedling, and (if you’re comfortable), FDA-approved drugs (especially minoxidil) to maximize results. And, if you can, try to find a clinic that provides PRP + Acell.
While PRP can help both male and female hair loss sufferers, preliminary evidence suggests that it’s just not as effective for females. However, this might be because of the added complexities of female AGA – and the fact that women are so frequently misdiagnosed with AGA but instead actually have hair shedding disorders related to underlying chronic conditions.
Be careful about clinic selection for PRP. For instance, the photos you’ll see on most dermatology websites offering PRP are from patients doing PRP + finasteride / minoxidil (rather than PRP alone). The equivalent would be if I advertised a before-after photo of someone doing massaging + finasteride, but decided to position the photo as if the results were only from massaging. It’s just bad business. So, be aware of this. Call all clinics to confirm the regimens of their highlighted patients.
If you’re seeing improvements from PRP, chances are you’ve already navigated through this mess to find a good provider. So, steer the course and keep us posted with your progress!
Saw palmetto is often touted as nature’s finasteride. This herbal extract reduces levels of the hormone dihydrotestosterone (DHT). For this reason, it’s clinically demonstrated to improve hair growth in men with androgenic alopecia (AGA).
But is saw palmetto as effective as finasteride?
Not quite. In fact, a closer look into the research on saw palmetto reveals that taking this supplement also comes with risks.
That’s not to say that saw palmetto is ineffective. But if you’re going to opt for saw palmetto over finasteride, you’re going to want to weigh its benefits and risks. Specifically, you’re going to want to know how saw palmetto compares to finasteride in terms of its (1) ability to reduce DHT, (2) ability to regrow hair, and (3) reported side effects.
This Quick Win dives into the details (and answers). The bottom line: saw palmetto isn’t as powerful as finasteride, but it also comes with some upsides that may make it a better option, at leaast for certain hair loss sufferers.
Note: Quick Wins are short articles focused on answering one question about hair loss. Given their specificity, these articles are written in a more scientific tone. If you’re new to hair loss research, start with our long-form articles.
The top natural ingredients for hair growth, all in one serum & supplement.
Take the next step in your hair growth journey with a world-class natural serum & supplement. Ingredients, doses, & concentrations built by science.
Saw palmetto is a palm plant native to warm humid climates (Florida).
Thirty years ago, researchers discovered that certain polyphenol and lipid extracts of saw palmetto could reduce the activity of type II 5-alpha reductase – an enzyme our bodies use to make the hormone dihydrotestosterone (DHT).
DHT is the main hormone implicated in pattern hair loss, also called androgenic alopecia (AGA). And interestingly, the popular hair loss drug finasteride (Propecia®) reduces that same enzyme – type II 5-alpha reductase – to lower DHT levels and improve pattern hair loss outcomes in ~80% of men trying the drug.
Unfortunately, finasteride use is also associated with sexual side effects. This scares a lot of men away from trying the drug. It also leads many of them to wonder…
“If I use saw palmetto instead of finasteride, can I still regrow hair while also reducing my risk of side effects? After all, saw palmetto is natural, and natural often means safer.”
For starters, anything branded as “natural” isn’t always safer. Many natural supplements sold through Amazon and tested by third parties have been found to contain dangerous levels of heavy metals. Moreover, many popular natural extracts – i.e., green tea extract – have been associated with hepatic failure due to the metabolic demands these extracts can place on our livers. (For more information, see my master class).
In any case, if we’re to answer the question, “Is saw palmetto as effective as finasteride?”, we’ll need to evaluate saw palmetto versus finasteride in terms of its (1) expected hair regrowth, and (2) risk of side effects.
The rest of this Quick Win does just this.
“Hair regrowth” is a non-specific term, and most clinical studies on pattern hair loss define this term differently:
…the list goes on.
That’s why, whenever we’re diving in studies on hair loss, we standardize the term “hair regrowth” into two categories:
So, if we summarize the data on saw palmetto versus finasteride, how do these two interventions compare? (1) (2)
|
Saw Palmetto (320mg) |
Finasteride (1mg) |
|
| Response Rate | 60%; dependent on the dose and delivery (supplement or topical) | 80-90% |
| Regrowth Rate | 0-10%; potentially higher if used alongside other therapies | 10%, alongside thickening of miniaturizing hair |
The key takeaway: compared to finasteride, saw palmetto has a lower response rate and regrowth rate. And when we look at the individual studies that constitute these aggregated estimations, things look a little bleak.
To date, there’s only one clinical study directly comparing saw palmetto versus finasteride for the treatment of androgenic alopecia. The investigation team randomized 100 men with androgenic alopecia into two groups. They gave one group 320mg of saw palmetto and the other group 1mg of finasteride – every day, for two years. (3)
The results? After 24 months, 68% of finasteride users saw hair regrowth, while only 38% of men taking saw palmetto saw hair regrowth. Moreover, investigators noted that in the saw palmetto group, hair regrowth only occurred in the crown (i.e., vertex), and that the magnitude of regrowth was significantly less than finasteride.
In other words, saw palmetto achieves half the response rate of finasteride, and that if regrowth does occur, it’s not nearly as impressive as what finasteride achieves.
Having said that, it’s not all bad news. That same study also demonstrated that 45/50 men in the saw palmetto group saw a stop in hair loss over the two years that they took it. So, in this one study, saw palmetto showed a response rate of 90%.
This means it’s not a complete stretch to say that most men taking 320mg of saw palmetto daily should see an improvement in their pattern hair loss. It’s just that this improvement won’t be anywhere near on-par what is achievable with finasteride.
This likely has to do with the ways in which saw palmetto reduces DHT, and the amount of DHT that saw palmetto reduces.
Finasteride is a synthetic azosteroid. It reduces DHT by competing with (and binding to) a coenzyme that our bodies use to make type II 5-alpha reductase – the enzyme that converts free testosterone into DHT.
Conversely, saw palmetto competitively and non-competitively inhibiting type II 5-alpha reductase, reducing the binding of DHT to androgen receptors, and increasing the conversion of DHT to a weaker metabolite called androstanediol (4).
The long-story short is that these factors, along with differences in the half lives of both finasteride and saw palmetto, lead to differences in their abilities to lower DHT.
For reference, see this graph on the DHT-reducing capabilities of both saw palmetto and finasteride, as organized by different tissue sites.
The bottom line: saw palmetto is about half as effective as finasteride because it just doesn’t reduce as much DHT.
At this point, we’ve really only evaluated half of the question: is saw palmetto as effective as finasteride?
In terms of response rates and regrowth rates, the answer is no. But can saw palmetto make up for its lower efficacy by being a safer long-term supplement for hair loss sufferers?
Maybe.
Long-term clinical studies show that saw palmetto’s overall rate of side effects is just 2%. Moreover, if side effects do occur, they’re relegated more so to gastrointestinal distress than to sexual dysfunction. Even better, many studies on saw palmetto show no change in libido; some studies show improvement to sexual health (at least for men with enlarged prostates). (5) (6) (7)
The “Yelp effect” is a phenomenon where patrons of a business are far more likely to leave a review if their experience was negative rather than positive. Finasteride is a drug that suffers from the Yelp effect, meaning that its sexual side effects are often overstated and amplified online.
Having said that, side effects do occur. Moreover, the self-assessment questionnaires filled out by participants in large-scale clinical trials for finasteride were worded in such a way where under-reporting certain side effects were more likely than not (but that’s for another article).
In any case, finasteride use does come with a heightened risk of side effects. Depending on which study you cite, between 1% and 25% of finasteride users will report issues ranging from brain fog to depression to sexual dysfunction. (8) (9) Moreover, when side effects are reported, they seem to be of higher magnitude versus saw palmetto.
The bottom line:
It depends on your risk tolerance for side effects, and whether you plan on combining saw palmetto with other treatments, therapies, or procedures to make up for its lower response rates and regrowth rates.
There’s evidence that supplemental + topical saw palmetto, alongside other ingredients, might lead to better hair loss outcomes than just supplemental saw palmetto. Moreover, combining saw palmetto with massaging, microneedling, platelet-rich plasma therapy, or other interventions might help mitigate its lower efficacy.
Having said that, making these choices will depend entirely on someone’s needs, preferences, and unique hair loss situation.
Unlike finasteride, saw palmetto isn’t standardized. Serenoa repens growing conditions, extraction methods, and manufacturing practices can all impact the composition, bioavailability, and absorption of each saw palmetto supplement. In fact, these differences might explain the variances in response rates and regrowth rates seen across saw palmetto studies.
So, if you’re looking for a more comprehensive guide on how to use saw palmetto – including recommendations for dosages, extraction practices, and combinations therapies – see our saw palmetto ultimate guide here.
In order to evaluate whether saw palmetto is as effective as finasteride, we need to understand how the supplement compares in terms of (1) response rates, (2) regrowth rates, and (3) risk of side effects.
Saw palmetto isn’t as effective as finasteride in terms of its response rates or regrowth rates, but it also seems to cause fewer (and less severe) side effects. Because of this, making the choice to use saw palmetto over finasteride depends entirely on someone’s risk tolerance for side effects, as well as whether they plan on combining the supplement with other treatments, therapies, or procedures to make up for its less-impressive efficacy.
|
Saw Palmetto (320 mg) |
Finasteride (1 mg) |
|
| Response Rate | 60%; dependent on the dose and delivery (supplement or topical) | 80-90% |
| Regrowth Rate | 0-10%; potentially higher if used alongside other therapies | 10%, alongside thickening of miniaturizing hair |
| Side Effects | 2%; more relegated to gastrointestinal distress than sexual side effects | 1-25%; partly psychosomatic, but more severe than saw palmetto |
Otherwise, if you have any questions, please feel free to leave them in the comments section.

Latanoprost is a medication that was originally developed to treat glaucoma. Over the last two decades, research groups have also started testing it as a treatment for hair loss – including alopecia areata, androgenic alopecia, and telogen effluvium.
In this ultimate guide, we’ll explore the evidence on latanoprost, dive into the mechanisms and clinical data regarding hair growth, and identify who might be a good candidate for this experimental intervention. We’ll also specify which formulations, dilutions, and usage frequencies are reaping the best results in terms of both efficacy and safety.
Finally, we’ll uncover critical caveats with its use – including lesser-discussed (but significant) safety risks – and where to get latanoprost (should you choose to incorporate it into your regrowth regimen).
Low-dose & full-strength finasteride 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.
*Only available in the U.S. Prescriptions not guaranteed. Restrictions apply. Off-label products are not endorsed by the FDA.
Latanoprost is a drug developed to treat disorders of the eye – specifically, glaucoma. Originally formulated for delivery as eye drops, some users began reporting the elongation and/or regrowth of eyelash hairs.[1]https://jamanetwork.com/journals/jamaophthalmology/fullarticle/413134 Resultantly, researchers started investigating whether latanoprost – when formulated as a topical – might also enhance hair regrowth in other areas of the body, such as the scalp.
Latanoprost modulates levels of prostaglandin F2 – a substance our bodies produce that is derived from essential fatty acids (i.e., omega 6 fatty acids). More specifically, latanoprost stimulates the activity of the prostaglandin F2 alpha receptor. This allows for prostaglandin F2 levels to increase in cell sites, and when this occurs in eye tissues, it can reduce (or alleviate) ocular pressure and thereby improve cases of glaucoma.[2]https://www.ncbi.nlm.nih.gov/books/NBK540978/
There’s evidence that the eyelash hair regrowth reported by many latanoprost users isn’t just happenstance. For instance, as prostaglandin F2 activity increases…
Interestingly, many of the above mechanisms (i.e., improved vasodilation and prostaglandin modification) overlap with the suspected mechanisms of the FDA-approved hair loss drug, topical minoxidil. As such, it’s no surprise that in a case series on 300+ patients using eye drops of latanoprost to treat glaucoma, 77% saw hypertrichosis (i.e., additional hair growth) in the areas surrounding the eyes. [6]https://www.jaad.org/article/S0190-9622(01)70206-X/fulltext
With all of these cases, it’s also not out-of-the-question that latanoprost might also help regrow some scalp hair if reformulated as a topical.
In fact, this was corroborated by a 2002 study on primates (i.e., stump-tailed macaques) who happen to be one of the only other species to also suffer from pattern hair loss, or androgenic alopecia. Over an 8-month study, monkeys receiving a topical application of 0.5 ml x 0.005% to 0.05% latanoprost daily showed improvements to hair loss and cosmetic degrees of hair regrowth.

Fig. 1.Frontal bald scalp of a 10-year-old, female, macaque, showing sparce short vellus hairs in the bald scalp at pretreatment time (a). After 5 months of treatment with latanoprost 50 mg/ml, thickness and density of hair increased in upper central and lower lateral regions (b). After 3 months of latanoprost 500 ug/ml thickness and density of hair significantly increased in mid and lower lateral region.

Fig. 2.Sequential changes of average scores of categorical grades of hair growth in latanoprost and vehicle-treated monkeys.
The anecdotes on eyelash hair growth in glaucoma patients – and the preliminary evidence of hair regrowth on balding monkeys – certainly provides a strong enough signal to further investigate topical latanoprost as a hair loss treatment in humans.
So, over the last 20 years, what does the clinical evidence on latanoprost show?
While the data are limited (so far), clinical studies on latanoprost for hair loss have been conducted on both androgenic alopecia, telogen effluvium, and alopecia areata.
In its first-ever randomized, double-blinded, placebo-controlled clinical trial, researchers tested topical latanoprost on 16 men with early-stage androgenic alopecia.
Each participant received two drops of 0.1% latanoprost daily – one drop per receding temple region – equating to 0.1 mL of solution applied daily. In other words, each man applied 0.1 mg of latanoprost per day.[7]https://pubmed.ncbi.nlm.nih.gov/21875758/

Fig 1. Male subject with androgenetic alopecia (Norwood Hamilton scale grade III). Marked areas indicate minizone position for topical application of latanoprost and placebo solutions.
Over the course of 24 weeks, daily application of 0.1 mg of latanoprost…
The results were reflected statistically through phototrichogram data (i.e. the gold-standard for clinical research on hair loss disorders).

Fig 3. Number and percentage of anagen and telogen hairs/cm2 at baseline and 24 weeks. [8]https://pubmed.ncbi.nlm.nih.gov/21875758/
While the data seem encouraging, it’s important to point out three caveats. Across all latanoprost users:
In other words, latanoprost seemed to work well in half of participants, with the other half of participants showing hair loss stabilization or no response at all.
For what it’s worth, this is a common trait among hair loss drugs that target factors like histamine responses and/or prostaglandins – for instance, minoxidil and cetirizine. [9]https://perfecthairhealth.com/histamine-and-hair-loss-is-there-a-use-for-antihistamines/ For some, these drugs work wonders. For others, they see no effect. Why?
In our estimation, the dichotomies in responses are likely related to the following:
Therefore, this initial (albeit, small) clinical study on topical latanoprost suggests that it might have a place in treating some cases of hair loss, but not all.
In 2018, another research group investigated the use of topical latanoprost by itself (and combined with topical minoxidil) in the treatment of men and women with androgenic alopecia or telogen effluvium.[13]http://www.surgicalcosmetic.org.br/details/618/en-US/latanoprost-and-minoxidil–comparative-double-blind–placebo-controlled-study-for-the-treatment-of-hair-loss
First, the researchers split 123 participants into six groups, with each group testing one of the following:
Unfortunately, the investigators didn’t specify how much solution each participant applied once daily. Based on the photos of participants featured inside their study, many participants had moderate levels of hair loss and beyond, which would likely require at least 1-2 mL of solution to cover all balding regions. So, we can only make rough estimations as to how much daily exposure of these drugs each participant received.
Note: the absence of daily drug exposure volume is just one of the many flaws in this study. We’ll uncover more issues soon.
Over the course of 180-240 days, 25 of the 123 people withdrew from the study for reasons that the investigators state were “not related to the research” – though they don’t specify what those reasons were. Withdrawal rates were mostly equivalent across all six groups, which leaves us with 98 people and 16-18 participants per group for statistical comparisons.
Among those who remained, here are the key findings:
Here are some photos the investigators featured of participants using 5% minoxidil and 0.005% latanoprost – albeit from an extension period that ran up to 240 days:

Figure 1: Macro image of a female participant at the start and end periods (treatment with 5% minoxidil + 0.005% latanoprost)

Figure 2: Macro image of a male participant at the start and end periods (treatment with 5% minoxidil + 0.005% latanoprost)
And here is data regarding anagen hair counts (i.e., the number of “growing” hairs) across all groups and time periods (day 2, day 92, and day 182):

Graph 2: Number of anagen hairs by period and by treatment
First, let’s start off by interpreting a good signal from this study.
Topical formulations of latanoprost that are of higher volume and lower concentration might greatly minimize the risk of side effects.
If we recall from the 2011 study on topical latanoprost, two drops of 0.1% latanoprost totaling 0.1 mL of daily use led to skin irritation-related side effects in 50% of participants. But in this study on 0.005% to 0.01% latanoprost applied daily at 1-2 mL of volume, no adverse events were reported.
It might interest you to know that both of these studies likely exposed participants to the exact same total amount of latanoprost each day. It’s just that the 2011 study used a higher concentration (i.e., 0.1%) but with less volume of topical (i.e., 0.1 mL), whereas the 2018 study used a 10-20x lower concentration (i.e., 0.005% to 0.01%) but with 10-20x more volume (i.e., 1-2 mL).
Yet mathematically, both studies exposed their participants to ~0.1mg of latanoprost daily.
This is important, because it suggests that 0.1mg of latanoprost may become a lot more tolerable for hair loss patients when it is spread out over a larger area. So, if nothing else comes from this study, we’re at least encouraged by this signal.
So what else can we surmise?
1-2 mL daily of 0.005% latanoprost may improve hair counts for a portion of people with androgenic alopecia and/or telogen effluvium… particularly if combined with 5% minoxidil
According to the data presented by the research team, 0.005% latanoprost by itself was effective at improving hair parameters, as was 0.005% latanoprost + 5% minoxidil.
However, we need to keep in mind the response rates here: just 35% to 36% of participants in these groups saw visual regrowth. That’s not a lot, and it gives credence to the belief that while latanoprost might work for some people, it’s probably not appropriate for all hair loss sufferers.
Looking at all of the data from this study can be confusing. After all, we have 6 different groups statistically measured across one another, with varying methodologies applied for some groups (like extension time periods for those using 0.005% latanoprost + 5% minoxidil), and with poor clarity in writing regarding both results and discussion organizations.
Nonetheless, we’ve read online about some people presuming that this study gives us enough insights to include the following. So, before adopting similar opinions, please read our counterarguments below:
Fallacy #1: this study suggests that 0.01% latanoprost might be less effective than 0.005% latanoprost
It’s not abnormal to make this assumption given the data presented. After all, the groups using 0.005% latanoprost saw a 35% and 36% response rate, whereas the groups using 0.01% latanoprost saw a 6% and 0% response rate.
Moreover, it’s not unusual to see dose-dependent effects in medicine – where some drugs have a strong therapeutic benefit at lower concentrations but can have opposing or toxic effects at higher concentrations. We discuss these relationships in our guide on flutamide.
Nonetheless, there are significant methodological flaws in this study that do not allow us to jump to this conclusion. Here are a few:
As such, we need to be incredibly careful about drawing any efficacy or comparison conclusions from this study. It’s entirely possible that 0.005% and 0.01% latanoprost are equally effective… but that the groups receiving higher dilutions of latanoprost had poorer results because of participant sampling. Without better data, we just don’t know.
As an aside, when discussing this study across our own team, we were even apprehensive to mention the positive safety signal – as this 2018 study is so poorly designed that any conclusions whatsoever are potentially problematic and/or at-odds with the real-world experiences of latanoprost users.
Nonetheless, we have to work with the data currently available, and these two studies on topical latanoprost are all that we’ve got (so far) for androgenic alopecia.
So, what about other hair loss disorders, such as alopecia areata?
To date, there have been five publications (to which we could find) assessing topical latanoprost for alopecia areata. Here are their quick summaries and results:
A 2003 case report details the experience of an 11-year old female who experienced alopecia areata of the eyelashes after recovering from a viral illness. After multiple failed treatments, doctors eventually tested topical latanoprost – at an unknown dilution – which was applied daily for a period of six months. During that time, photographic assessments show a near full recovery of all lost eyelashes.[14]https://pubmed.ncbi.nlm.nih.gov/12724722/
A 2009 clinical study tested 0.005% latanoprost – at an unknown volume – on a total of 26 men and women with alopecia areata of the eyebrows and eyelashes. Participants applied latanoprost to just one side of the face, with the other side acting as an intra-patient “control”. After four months, researchers saw partial hair recovery in just one patient, and concluded that topical latanoprost was no more effective than applying nothing at all. Aside from a transient headache fro one patient, no adverse events were reported.[15]https://pubmed.ncbi.nlm.nih.gov/19620039/
Interestingly, these results were mirrored by prior clinical studies done on similar dilutions of topical latanoprost for eyelash-related alopecia areata from 2005 and 2008.[16]https://pubmed.ncbi.nlm.nih.gov/16310083/[17]http://www.iranjd.ir/article_98048_64fda5d6552e3e9d714cc2162d5686a4.pdf As such, it appears that the data (so far) suggest topical latanoprost does not improve this specific hair loss disorder for the overwhelming majority of people trying it.
Finally, a 2021 randomized clinical study tested daily applications of 0.005% latanoprost versus 0.05% betamethasone diproprionate (an autoimmune-related medication) for the treatment of scalp-related alopecia areata in 50 patients.[18]https://ijdvl.com/a-randomized-comparative-study-of-the-efficacy-of-topical-latanoprost-versus-topical-betamethasone-diproprionate-lotion-in-the-treatment-of-localized-alopecia-areata/
Unfortunately, the researchers did not specify the amount (in mL) of topical applied daily. As such, we cannot estimate daily exposure volumes.
Over a 16-week period, 24% of patients using 0.005% latanoprost saw improvements, whereas 56% of patients using 0.05% betamethasone diproprionate saw improvements. In fact, patients in the 0.05% betamethasone diproprionate group also tended to see a faster recovery and a more dramatic reduction of alopecia areata lesions.
Therefore, the researchers concluded that 0.05% betamethasone diproprionate was superior to 0.005% latanoprost in the treatment of scalp alopecia areata.
From what we can glean across all clinical studies on topical latanoprost for hair loss:
It’s easy to look at these studies and note that dilutions of 1-2 mL daily of 0.005% to 0.01% were well-tolerated for nearly all participants, with only a handful of minor, transient adverse events reported across all patient cohorts testing this formulation. As such, it’s easy to presume that topical latanoprost must be safe.
We have significant reservations with that conclusion.
After all, these topical latanoprost studies for hair growth ran – at most – 8 months. While no serious adverse events were reported during these short timeframes, there is a well-known phenomenon that occurs from long-term latanoprost use, and one that does not typically show up until after one full year of treatment: pigment changes.
In glaucoma patients, pigment changes of the iris begin to occur after one year of daily latanoprost use, and they worsen over time – affecting up to 10% of glaucoma patients.[19]https://www.ncbi.nlm.nih.gov/books/NBK540978/ Other studies suggest an incidence as high as 70%, depending on the eye color & duration of use.[20]https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1771317/
This is because regular latanoprost use increases melanin activity (i.e., the activity of cells that produce pigmentation in our skin, eyes, etc.). The effects, over time, can be quite dramatic. Just see the results from this patient, who was treated for glaucoma in their right eye with latanoprost (picture A) but not in their left eye (picture B). It’s as if we are looking at two different eyes. [21]https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1771317/
As such, a critical question remains: does latanoprost applied topically produce the same effects in the skin, hair, and (potentially) through the eyes via systemic absorption?
Unfortunately, we have no way of knowing… because the clinical studies have not yet been conducted. Moreover, none of the studies on topical latanoprost for hair loss ran even remotely long enough to measure if this effect would also apply to the scalp.
In cases of treatments producing serious, cosmetically-unwanted adverse events – like a darkening of scalp skin – we tend to err on the side of caution and say that without more data, most people should be seriously cautious about long-term use of topical latanoprost. Perhaps better data will demonstrate this is not a concern, but until we have that data, we don’t feel comfortable recommending topical latanoprost as a guinea pig experiment to members here… even despite its popularity online as an adjuvant hair loss treatment.
For more contraindications and side effects from latanoprost, please visit this resource.[22]https://www.ncbi.nlm.nih.gov/books/NBK540978/
You are likely a candidate for latanoprost if:
You are likely not a candidate for latanoprost if:
Latanoprost has some limited clinical data supporting its use for androgenic alopecia, but with response rates of 30-50%, it’s unlikely that this treatment is right for most hair loss sufferers. For these reasons, we recommend people use other prostaglandin analogues instead – such as minoxidil – and only resort to latanoprost if they’re using it as an add-on to their regimen and if they’re comfortable with the unknowns about its long-term safety profile.
For alopecia areata of the eyelashes, latanoprost is unlikely to help. For alopecia areata of the scalp, one small study found that topical latanoprost may help up to 25% of people. However, that same study also found that 0.05% betamethasone diproprionate was twice as effective at producing a response rate versus latanoprost, and that it also worked faster than latanoprost.
References[+]
| ↑1 | https://jamanetwork.com/journals/jamaophthalmology/fullarticle/413134 |
|---|---|
| ↑2, ↑19, ↑22 | https://www.ncbi.nlm.nih.gov/books/NBK540978/ |
| ↑3 | https://pubmed.ncbi.nlm.nih.gov/15854125/ |
| ↑4 | https://www.frontiersin.org/articles/10.3389/fphys.2020.594313/full |
| ↑5 | https://pubmed.ncbi.nlm.nih.gov/33854354/ |
| ↑6 | https://www.jaad.org/article/S0190-9622(01)70206-X/fulltext |
| ↑7, ↑8 | https://pubmed.ncbi.nlm.nih.gov/21875758/ |
| ↑9, ↑11 | https://perfecthairhealth.com/histamine-and-hair-loss-is-there-a-use-for-antihistamines/ |
| ↑10 | https://pubmed.ncbi.nlm.nih.gov/8496421/ |
| ↑12 | https://my.perfecthairhealth.com/courses/minoxidil/topical-minoxidil/ |
| ↑13 | http://www.surgicalcosmetic.org.br/details/618/en-US/latanoprost-and-minoxidil–comparative-double-blind–placebo-controlled-study-for-the-treatment-of-hair-loss |
| ↑14 | https://pubmed.ncbi.nlm.nih.gov/12724722/ |
| ↑15 | https://pubmed.ncbi.nlm.nih.gov/19620039/ |
| ↑16 | https://pubmed.ncbi.nlm.nih.gov/16310083/ |
| ↑17 | http://www.iranjd.ir/article_98048_64fda5d6552e3e9d714cc2162d5686a4.pdf |
| ↑18 | https://ijdvl.com/a-randomized-comparative-study-of-the-efficacy-of-topical-latanoprost-versus-topical-betamethasone-diproprionate-lotion-in-the-treatment-of-localized-alopecia-areata/ |
| ↑20, ↑21 | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1771317/ |
Finasteride is one of the most commonly-prescribed medications for treatment of male pattern hair loss—also known as androgenic alopecia (AGA). But it’s also used as an off-label treatment for female pattern hair loss. Evidence suggests this medication can help regrow hair in both sexes.
But what’s the best dose of finasteride for women with AGA? Unfortunately, it’s complicated. This article sets out to evaluate the data, uncover the answers, and provide recommendations based on the current landscape of clinical research.
Oral finasteride & 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.
*Only available in the U.S. Prescriptions not guaranteed. Restrictions apply. Off-label products are not endorsed by the FDA.
Finasteride is a drug developed to inhibit type II 5-alpha reductase. This is an enzyme in the body that converts free testosterone in dihydrotesterone (DHT).
Essentially, finasteride lowers DHT levels by reducing the amount of type II 5-alpha reductase circulating throughout our bodies. And by taking finasteride at 0.2 to 5.0 mg daily dosages, we can often reduce total DHT levels by 70%. [1]https://www.ncbi.nlm.nih.gov/books/NBK513329/
DHT is not just a metabolite of testosterone; it’s also the primary male hormone causally associated with androgenic alopecia.
We know this because studies have shown that men who cannot produce DHT are nearly fully-protected from going bald throughout a lifetime. Furthermore, clinical studies on DHT-lowering drugs – such as finasteride – show that if DHT levels are suppressed enough, 80-90% of men can arrest the progression of their pattern hair loss and even regrow 10-20% of their lost hair. [2]https://pubmed.ncbi.nlm.nih.gov/29407002/ [3]https://www.ncbi.nlm.nih.gov/books/NBK430924/
Similarly, studies on females with androgenic alopecia have shown that finasteride can also improve their hair loss outcomes. The evidence is less robust than for men, but finasteride is something many women should consider trying in order to improve their pattern hair loss.
In men, the FDA has approved the use of 1mg of finasteride for pattern hair loss. However, male and female hair loss cases are not always the same. Reducing DHT levels is often of therapeutic interest to fighting AGA – and for both sexes – but some clinical evidence suggests that females might need a different dose of finasteride versus males.
Finasteride has what is known as a dose-dependent, logarithmic response curve for DHT reduction. In other words: a little bit of finasteride reduces nearly as much DHT as a lot of finasteride. For an example, see this chart:
Clinical studies have demonstrated that 0.2 mg and 5.0 mg reduce nearly the same amount of finasteride: 69% versus 72%, respectively.
Because of this, a lot of people actually prefer to use lower dosages of finasteride than what is generally prescribed. This practice is also supported by clinical data. For instance, in men, 0.2mg of finasteride AGA at a statistically similar level as 1.0 mg of finasteride over the course of a year. [4]https://europepmc.org/article/med/15319158
But is the same true with females? Unfortunately, the data is less clear.
The FDA approves the use of 1 mg of finasteride for male pattern hair loss.[5]https://www.fda.gov/drugs/information-drug-class/5-alpha-reductase-inhibitor-information But the underlying causes of male and female pattern hair loss cases (androgens such as DHT) are not always the same. Furthermore, while reducing DHT levels is of therapeutic relevance in treating AGA in men and women, some clinical evidence suggests that females might need a different dose of finasteride versus males.
What does the available research tell us? Here are a few of the key studies on finasteride for women, and their main findings (summarized in the table below).
| Type of study | Number of patients | Patient condition | Finasteride dosage | Length of treatment | Assessment parameters | Outcomes | Reference |
| Double-blind, randomized control trial | 67 treated, 70 placebo | AGA, post-menopausal, normal serum testosterone | 1 mg, daily | 12 months | Hair counts, photographic assessment, self-assessment, scalp biopsies | Serum DHT reduction but no effect on hair loss outcomes compared to placebo | [6]https://pubmed.ncbi.nlm.nih.gov/10674382/[7]https://pubmed.ncbi.nlm.nih.gov/11050579/ |
| Randomized, unmasked trial | 12 finasteride, 12 flutamide, 12 cyproterone acetate with estradiol, 12 no treatment | 48 women, hyperandrogenic, age- and weight matched controls | 5 mg, daily | 12 months | Ludwig classification15 of female hair loss, self-assessment, and investigator assessment | No effect with finasteride | [8]https://pubmed.ncbi.nlm.nih.gov/11050579/ |
| Single-blind, placebo-controlled trial | 24 female patients included | AGA, age 23-38 years (mean 33) | 1 ml topical application (0.005%), twice daily to affected area | 16 months | Semi-quantitative investigator assessment, hair shedding quantification, self-assessment | Hair count and hair density improvements versus placebo (data not sex-stratified) | [9]https://www.tandfonline.com/doi/abs/10.3109/09546639709160517 |
| Small trial | 5 treated | Post-menopausal, normal androgen levels | 2.5 or 5 mg, daily | 18 months, review every 6 months | Self-assessment, investigator assessment, photographic assessment | Overall improvement | [10]https://pubmed.ncbi.nlm.nih.gov/15459533/ |
| Small trial | 10 treated | Post-menopausal | 1 mg, daily | 52-82 weeks | Self-assessment and photographic assessment | Overall improvement (9/10 patients) | [11]Ahn J, Cho SB, Kim MN, Ro BI. Finasteride treatment of female patterned hair loss in postmenopausal women. Korean J Dermatol. 2006;44:1094-1097. |
| Small trial | 6 treated | AGA, age 30-76 years (mean 46.5), normal androgen levels | 5 mg, daily | Weeks (not specified) | Retrospective questionnaire (self-assessment) | Overall improvement (5/6 patients) | [12]https://pubmed.ncbi.nlm.nih.gov/17454167/ |
| Small trial | 37 treated | Female pattern hair loss, pre-menopausal, age 19-50 years (mean, 33.7) | 2.5 mg, daily (+ oral contraceptive drospirenone and ethinyl estradiol) | 12 months | Self-assessment, photographic assessment, and hair-density scoring | Overall improvement by self-assessment (29/37), photographic improvement ((23/37), significant hair density improvement (12/37) | [13]https://pubmed.ncbi.nlm.nih.gov/16549704/ |
| Small trial | 41 treated | AGA, persistent adrenarche syndrome | 2.5 mg, daily (+ ethinyl estradiol) | 2 years | Not specified | Overall improvement | [14]https://pubmed.ncbi.nlm.nih.gov/19341939/ |
| Small trial | 4 treated | 36, 40, 60, and 66 years old, elevated testosterone and hyperandrogenism | 1.25 mg, daily | 6 months to 2.5 years | Photographic assessment and self-assessment | Stabilization of hair loss within 6-12 months, hair growth improvements in 6 months – 2.5 years | [15]https://pubmed.ncbi.nlm.nih.gov/12399766/ |
| Case study | 1 treated | 47-year-old, ‘male’ pattern hair loss, hysterectomy and ovariectomy, long-term hormone replacement | 2.5 mg, daily (+continued testosterone supplementation) | 10 months | Photographic assessment | Hair loss stabilization at 6 months, hair growth improvement at 10 months | [16]Hong JB, Chiu HC, Chan JY, Chen RJ, Lin SJ. A woman with iatrogenic androgenetic alopecia responding to finasteride. Br J Dermatol. 2007;156(4):754-755. doi:10.1111/j.1365-2133.2006.07719.x |
| Case study | 1 treated | 67-year-old, 18 month history of hair thinning, normal androgen levels | 5 mg, weekly | 12 months | Self-assessment and photographic assessment | Improvement, hair regrowth | [17]https://pubmed.ncbi.nlm.nih.gov/12366441/ |
| Case study | 1 treated | 51-year-old, 8 month history of hair thinning, normal androgen levels | 1 mg, daily | 12-13 months | Hair density measurements | Hair density increased versus baseline | [18]https://pubmed.ncbi.nlm.nih.gov/15844649/ |
There is conflicting data regarding the efficacy of finasteride for female pattern hair loss. Some studies report improvements while others do not.
There are some key variables to consider when weighing the available evidence:
Interpreting research data can be difficult and confusing. such as different studies using different dosages of finasteride and for varying lengths of time, measuring different hair loss outcomes, and using different numbers and ages of patients.
The specific type of hair loss is also a crucial variable.[19]https://pubmed.ncbi.nlm.nih.gov/30604525/ Often, studies reporting positive outcomes are based on patient self-reporting, which can be suspect and not meaningfully objective or quantitative in measuring true prevention or reversal of hair loss.
Given the dose-response relationship between finasteride and DHT levels, shouldn’t 1 mg be as effective as 5 mg? Why aren’t women getting consistent regrowth across doses within these ranges?
Other discrepancies are the time for which finasteride was given. In men, 1 mg of finasteride can be effective in 6-12 months, but it is possible that women require more long-term treatment regimens.[20]https://pubmed.ncbi.nlm.nih.gov/30604525/ Generally, success with finasteride in women has been reported in both the short- and long-term.[21]https://pubmed.ncbi.nlm.nih.gov/12399766/
Alternatively, the difference in observed efficacies between studies may be due to patient background and the type of hair loss. Hair loss in patients suffering from PCOS or adrenarche (i.e., high levels of adrenal gland activity) likely has a clear causal link to abnormal androgen signaling (and therefore suitable for finasteride), where hair loss in post-menopausal women may be more akin to age-related hair ‘thinning’, and not linked to testosterone or DHT, which may explain why some studies find no effect with finasteride.[22]https://pubmed.ncbi.nlm.nih.gov/10674382/[23]https://pubmed.ncbi.nlm.nih.gov/11050579/[24]https://pubmed.ncbi.nlm.nih.gov/12399766/
That said, finasteride is also reportedly effective in patients that are androgen-normal.20 Therefore, there needs to be more careful classification of the type of hair loss and the likely underlying mechanisms, as well as clear standardization of treatment outcome measurements.
Does finasteride work for women suffering from hair loss? If so, what is the ideal dosage?
Finasteride is most beneficial for women when their hair loss occurs alongside elevated androgen levels—much like hair loss in men.
It is likely that DHT is a major factor in a proportion of female hair loss cases. Finasteride is likely to be a beneficial part of a successful hair loss regimen in these cases. However, it is not clear that male and female pattern hair loss universally share the same underlying cause.
Finasteride may be less suitable in contexts of age-related hair thinning. Hair follicles are sensitive to all manner of different hormones and chemical signals, not just androgens such as testosterone and DHT.[25]https://pubmed.ncbi.nlm.nih.gov/32731328/
The best dose is one that maximizes the desired benefits (prevention and reversion of hair loss) while minimizing any undesirable side effects.
Finasteride can be effective at reducing DHT even in small doses. Because of this, experimentation with low levels of finasteride may lead to results with far less exposure to chemicals. Topical treatments may also be considered to further reduce systemic side effects.
Therefore, the best dose will be patient-subjective. Prior consideration of your history, goals regarding hair loss, and experimentation with dosages is needed before you will find the ideal routine for your hair health.
References[+]
| ↑1 | https://www.ncbi.nlm.nih.gov/books/NBK513329/ |
|---|---|
| ↑2 | https://pubmed.ncbi.nlm.nih.gov/29407002/ |
| ↑3 | https://www.ncbi.nlm.nih.gov/books/NBK430924/ |
| ↑4 | https://europepmc.org/article/med/15319158 |
| ↑5 | https://www.fda.gov/drugs/information-drug-class/5-alpha-reductase-inhibitor-information |
| ↑6, ↑22 | https://pubmed.ncbi.nlm.nih.gov/10674382/ |
| ↑7, ↑8, ↑23 | https://pubmed.ncbi.nlm.nih.gov/11050579/ |
| ↑9 | https://www.tandfonline.com/doi/abs/10.3109/09546639709160517 |
| ↑10 | https://pubmed.ncbi.nlm.nih.gov/15459533/ |
| ↑11 | Ahn J, Cho SB, Kim MN, Ro BI. Finasteride treatment of female patterned hair loss in postmenopausal women. Korean J Dermatol. 2006;44:1094-1097. |
| ↑12 | https://pubmed.ncbi.nlm.nih.gov/17454167/ |
| ↑13 | https://pubmed.ncbi.nlm.nih.gov/16549704/ |
| ↑14 | https://pubmed.ncbi.nlm.nih.gov/19341939/ |
| ↑15, ↑21, ↑24 | https://pubmed.ncbi.nlm.nih.gov/12399766/ |
| ↑16 | Hong JB, Chiu HC, Chan JY, Chen RJ, Lin SJ. A woman with iatrogenic androgenetic alopecia responding to finasteride. Br J Dermatol. 2007;156(4):754-755. doi:10.1111/j.1365-2133.2006.07719.x |
| ↑17 | https://pubmed.ncbi.nlm.nih.gov/12366441/ |
| ↑18 | https://pubmed.ncbi.nlm.nih.gov/15844649/ |
| ↑19, ↑20 | https://pubmed.ncbi.nlm.nih.gov/30604525/ |
| ↑25 | https://pubmed.ncbi.nlm.nih.gov/32731328/ |
Topical finasteride has emerged to meet demand for hair loss treatments that promise strong results with fewer systemic side effects than oral finasteride by concentrating action at the scalp while reducing overall drug exposure. Early studies suggest it can improve hair growth and lower scalp dihydrotestosterone (DHT) with less systemic absorption, but side effects are not eliminated, and long-term head-to-head data versus oral finasteride remain limited.
This article will cut through the “same results, fewer side effects” marketing narrative and set realistic expectations by focusing on what current clinical evidence and real-world user patterns actually support.
Finasteride is a 5-alpha reductase inhibitor, meaning that it blocks this enzyme from converting testosterone into DHT, the more potent androgen that drives miniaturization of sensitive scalp follicles in androgenic alopecia (AGA). The enzyme catalyzes this conversion in the scalp, skin, liver, and prostate. By inhibiting it, finasteride lowers both local (scalp/prostate) and circulating DHT.[1]Zito PM, Bistas KG, Patel P, et al. Finasteride. [Updated 2024 Feb 28]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Available from: … Continue reading

Finasteride structure
A standard 1 mg oral dose reduces DHT by roughly 60-70%, with some studies reporting around 70% suppression at steady state, and intraprostatic DHT falls by about 90%.[2]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,[3]Smith, A.B., Carson, C.C. (2009). Finasteride in the treatment of patients with benign prostatic hyperplasia: a review. Therapeutics and Clinical Risk Management. 5. 535-545. Available at: … Continue reading Because 5 alpha-reductase is expressed in multiple organs, this systemic inhibition affects DHT signaling throughout the body, not only in the scalp.
Sexual and mood-related side effects are not purely “in the mind”; they reflect altered androgen physiology in a subset of men whose tissues are more sensitive to a DHT drop, even though testosterone usually stays within the normal range or rises modestly. Reduced DHT can influence libido, erectile function, ejaculate volume, and, in some individuals, mood or energy, consistent with the hormone’s broader role beyond hair follicles.[4]Traish, A.M. (2017). Negative Impact of Testosterone Deficiency and 5ɑ-Reductase Inhibitors Therapy on Metabolic and Sexual Function in Men. Advances in experimental medicine and biology. 1043. … Continue reading
Topical finasteride aims to concentrate drug action in the scalp by delivering finasteride directly to hair follicles, potentially lowering local DHT while limiting how much drug reaches the bloodstream. However, percutaneous absorption still occurs, and pharmacokinetic studies do show measurable reductions in serum DHT with topical formulations, meaning systemic exposure is reduced compared to oral dosing, but not eliminated.[5]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
The evidence on topical finasteride’s side effect profile shows a nuanced picture – measurable systemic exposure, lower but not zero adverse event rates, and substantial variability between formulations and individuals.
The 2021 Piraccini trial, one of the largest randomized double-blind topical finasteride studies to date, tested a 0.25% finasteride spray applied once daily over 24 weeks in 458 men.[6]Piraccini, B.M., Blume-Peytavi, U., Scarci, F., Jansat, J.M., Falques, M., Otero, R., Tamarit, M.L., Galvan, J., Tebbs, V., Massana, E., Topical Finasteride Study Group. (2022). Efficacy and safety … Continue reading Plasma finasteride concentrations were over 100-fold lower than with oral finasteride. Serum DHT fell by 34.5% with topical use compared to 55.6% with a 1 mg oral tablet.
Caserini found that lower volumes (100-200 μL of 0.25% solution) reduced serum DHT by 24-26%, while higher volumes (300-400 μL) dropped it by 44-48%.[7]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 Even at the lowest tested doses, scalp DHT declined by roughly 47-52%, demonstrating effective local action with more limited systemic spillover.
Other studies report a range of serum DHT suppression with topical formulations, but all confirm that absorption is lower than oral administration, not absent. One hydroxyl-propyl chitosan formulation was designed specifically to retain finasteride in the reticular dermis near hair bulbs; repeated-dose rat experiments showed no detectable plasma finasteride and no accumulation in skin, although human data remain sparse.[8]Monti. D., Tampucci, S., Burgalassi, S., Chetoni, P., Lenzi, C., Pirone, A., Mailland, F. (2014). Topical formulations containing finasteride. Part I: in vitro permeation/penetration study and in … Continue reading
So to summarize, topical finasteride’s systemic exposure is markedly reduced compared to oral dosing, yet reductions in circulating DHT do still occur across most formulations (in human studies), meaning that some degree of systemic exposure is virtually unavoidable.
Clinical trials have monitored sexual dysfunction, dermatological reactions, and less common systemic complaints, though sample sizes and durations limit the ability to detect rare or delayed adverse events.
In the 2021 Piraccini study, 2.8% of topical finasteride users reported sexual adverse events (decreased libido, erectile dysfunction, and ejaculatory dysfunction) versus 4.8% on oral finasteride and 3.3% on placebo.
The similarity between the topical and placebo groups led some investigators to suggest that many reports may not be causally linked to the drug. However, a 2025 FDA pharmacovigilance analysis of adverse event reports (2019-2024) identified 32 cases involving topical finasteride formulations, most of which were compounded products, with complaints of erectile dysfunction, anxiety, brain fog, depression, fatigue, insomnia, decreased libido, and testicular pain.[9]US Food and Drug Administration. (2025). FDA alerts health care providers, compounders and consumers of potential risks associated with compounded topical finasteride products. FDA. Available at: … Continue reading What’s more, many of these symptoms reportedly persisted after discontinuation.
A separate analysis found that topical finasteride generated fewer signals for post-finasteride syndrome (PFS) – like events than oral finasteride, but erectile dysfunction remained the most consistently reported adverse event for both routes.[10]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

Figure 1: Association between finasteride use (topical vs. oral) and occurrence of adverse events (sexual and neuropsychiatric) between 2006and 2011 (inclusive) and across men.[11]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
Local reactions are the most common topical-specific side effects. A 2018 systematic review noted reports of erythema, contact dermatitis, and scalp irritation in several studies, though serious cutaneous adverse events were absent.[12]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
Rates of contact dermatitis ranged from 12-24% in some combination formulations (finasteride + minoxidil), though these were generally mild and did not lead to treatment discontinuation. The irritation effect likely derives from vehicle components (alcohol, propylene glycol) as well as the active drug.
Less frequently, trials have documented headaches, feeling about to faint, testicular pain, increased liver enzymes, and even bed-wetting in isolated cases. The 2025 FDA alert highlighted fatigue and insomnia among the systemic complaints associated with topical formulations, reinforcing that absorption can produce effects beyond the scalp.
Most published trials run 12-24 weeks with cohorts of 30-135 participants per arm, which may under-detect rare events (incidence <1%) or adverse effects that emerge only after prolonged exposure. Only a handful of studies have extended beyond six months, and none approach the multi-year observation periods needed to assess phenomena such as PFS.[13]Pereira, A.F.J.R., Coehlo, T, O. de 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 Recruitment through specialist dermatology centres may also select for patients more tolerant of medication, introducing survivorship bias.
Head-to-head data have shown that topical finasteride has a numerically lower, but not zero, incidence of systemic adverse events. In Piraccini’s trial, sexual side effects occurred in 2.8% of topical users versus 4.8% of oral users, representing an approximate halving of risk.
There are two important points often overlooked in clinical summaries, however:
Despite the reduced systemic exposure, some people still experience sexual, mood, and systemic adverse effects. Let’s take a look at the mechanisms why.
Human skin is not a uniform barrier. Stratum corneum thickness, lipid composition, hydration status, pH, and blood flow differ among individuals and even within scalp regions of a single person.
In vitro permeation studies using human cadaver scalp skin show that finasteride flux ranges of 1.1-20.1 μg/cm2/h, depending on vehicle choice, a roughly 18-fold variation. Live scalp skin likely exhibits even greater heterogeneity due to sebum content, follicle density, and individual differences in dermal blood flow, all of which influence how much drug reaches the bloodstream versus remaining confined to follicular tissue.[15]Farah, A.H., Brown, M.B., McAuley, W.J. (2020). Enhanced Follicular Delivery of Finasteride to Human Scalp Skin Using Heat and Chemical Penetration Enhancers. Pharmaceutical Research. 37(6). 112. … Continue reading
For topical finasteride to minimize systemic exposure, it needs to stay within the area of the hair follicle. Variability in penetration means some individuals absorb more systemically than others, despite using the same concentration and volume.
The formulation of a topical finasteride product isn’t just a minor detail; it’s one of the biggest determinants of how much of the medication actually enters the bloodstream. Not all vehicles behave the same way, and the differences can be dramatic. For example, in vitro research comparing common topical solvents on human scalp skin shows that propylene glycol (PG) and isopropyl alcohol (IPA) formulations allow far more drug to pass through the skin: roughly 62–81 µg/cm² over 24 hours. In contrast, dimethyl isosorbide (DMI), often marketed as a “low-penetration” carrier, delivered just 17.8 µg/cm² in the same timeframe.[16]Farah, A.H., Brown, M.B., McAuley, W.J. (2020). Enhanced Follicular Delivery of Finasteride to Human Scalp Skin Using Heat and Chemical Penetration Enhancers. Pharmaceutical Research. 37(6). 112. … Continue reading That’s a 4.5-fold reduction in systemic permeation, purely from changing the solvent.
More sophisticated delivery systems behave differently still. Liposomal and niosomal gels, for example, are designed to deposit the medication deeper into hair follicles while limiting diffusion into the bloodstream. And in controlled experiments, these vesicular carriers did exactly that: liquid-state liposomes delivered 2.1–2.3% of the applied dose into the skin, compared to only 0.76% from a standard hydroalcoholic solution.[17]Tabbakhian, M., Tavakoli, N., Jaafari, M.R., Daneshamouz, S. (2006). Enhancement of follicular delivery of finasteride by liposomes and niosomes: 1. In vitro permeation and in vivo deposition studies … Continue reading
In other words, depending on the vehicle, the same dose of finasteride can behave like a local scalp medication or something much closer to an oral drug.
At the opposite end of the spectrum are ethosomes, ethanol-rich vesicles that dramatically increase drug penetration. In one study, finasteride ethosomes produced 7.4-times higher transdermal flux than the same drug in an aqueous solution, reaching all the way into the dermis.[18]Rao, Y., Zheng, F., Zhang, X., Gao, J., Liang, W. (2008). In vitro Percutaneous Permeation and Skin Accumulation of Finasteride Using Vesicular Ethosomal Carriers. 9(3). 860-865. Available at: … Continue reading
This is the kind of penetration behavior that significantly raises the likelihood of systemic absorption.
The bottom line: two topical finasteride products with the same concentration can have completely different side-effect profiles, simply because the vehicles modulate how much drug gets through the skin. Hydroalcoholic sprays tend to penetrate more aggressively; liposomal or niosomal gels are usually more conservative; and individual biology, skin barrier integrity, inflammation, and sebaceous output add yet another layer of variability. This is why real-world responses to topical finasteride are so mixed, and why formulation needs to be taken as seriously as the dose itself.
Higher concentrations and larger volumes increase both local scalp DHT reduction and systemic spillover. As mentioned above, Caserini’s dose-response study found that applying 100-200 μL of 0.25% finasteride reduced serum DHT by 24-26%, whereas 300-400 μL volumes reduced it by 44-48%, approaching the efficacy of oral dosing at the higher end.[19]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
Users who apply larger volumes, cover a wider scalp area, or use higher-concentration formulations absorb more drug systemically, shifting the risk-benefit profile toward greater potential for side effects.
Finasteride has a terminal half-life of 5-6 hours in young men and 8 hours in older men.[20]Mysore, V. (2012). Finasteride and sexual side effects. Indian Dermatology Online Journal. 3(1). 62-65. Available at: https://doi.org/10.4103/2229-5178.93496 Although short, daily topical application leads to steady-state accumulation in plasma and skin tissues.
With topical dosing, measurable finasteride concentrations appear in plasma within hours and remain detectable for a full day; repeated daily application amplifies cumulative levels, particularly if absorption is higher than intended due to vehicle choice or individual skin permeability.[21]Tai, Z., Cui, Z., Shi, X., Li, H., Chai, R., Huang, Y., Fang, Y., Jia, D., Zhu, Q., Chen, Z. (2025). The Pharmacokinetics of Topical Finasteride 0.25% Spray in Chinese Adult Male Volunteers with … Continue reading
Even when two people experience the same level of DHT reduction, their bodies may not respond the same way. This is where individual biology plays a much bigger role than most clinical studies acknowledge. Variations in genes tied to 5α-reductase activity, androgen receptor sensitivity (including CAG repeat length), and enzymes involved in neurosteroid production, such as 3α-HSD, can all influence how strongly someone reacts to changes in DHT.[22]Cecchin, E., De Mattia, E., Toffoli, G., Mazzon, G., Cauci, S., Trombetta, C. (2014). A Pharmacogenetic Survey of Androgen Receptor (CAG)N and (GGN)N Polymorphisms in Patients Experiencing … Continue reading,[23]Rahimi-Ardabili, B., Pourandarjani, R., Habibollahi, P., Mualeki, A. (2006). Finasteride-induced depression: a prospective study. BMC Clinical Pharmacology. 6(7). Available at: … Continue reading
For one man, a 30% drop in circulating DHT might feel completely benign. For another, that exact same reduction might coincide with noticeable changes in libido, erectile quality, or overall sexual function.
Layered on top of genetics are factors like baseline hormone levels, underlying hypogonadism, and even a person’s psychophysiological sensitivity to small hormonal shifts. Together, these variables help explain why side effects remain so individualized and difficult to predict, and why two people using an identical topical finasteride formulation can walk away with very different experiences. This isn’t meant to alarm anyone, only to highlight that DHT suppression is not a one-size-fits-all phenomenon, and that understanding your own sensitivity is often just as important as choosing the right dose or vehicle.
Target the Lowest Effective Exposure
Adjust Volume and Frequency to Limit Systemic Load
Choose Vehicles Carefully
Implement Smart Application Strategies
Important: If you experience any side effects, we recommend first stopping and speaking to your primary care physician.
While topical finasteride carries a lower risk profile than its oral counterpart, some people may still need to exercise caution or avoid the drug entirely.
It should be mentioned that a history of side effects from oral finasteride does not mean that topical finasteride won’t work well for you; however, it does warrant a personalized, cautious approach. This approach might include starting with lower doses, extended monitoring, and communication with the prescribing physician about any potential symptoms.
For users unable to tolerate topical finasteride due to side effects or scalp irritation, several evidence-based alternatives exist.
Low Dose Oral Minoxidil
Oral minoxidil is a hair growth stimulant that bypasses the hormonal pathway entirely. Studies show high efficacy (e.g., 43% of men achieving excellent results with 5 mg), but it carries systemic risks such as hypertrichosis (excess body hair), fluid retention, and cardiovascular effects like tachycardia.[24]Vano-Galvan, S., Pirmez, R., Hermosa-Gelbard, A., Moreno-Arrones, O.M., Saceda-Corralo, D., Rodrigues-Barata, R., Jiminez-Cauhe, J., Koh, W.L., Poa, J.E., Jerjen, R., de Carvalho, L.T., John, J.M., … Continue reading
Alternative Topical Anti-Androgens
Fluridil is a topical anti-androgen designed to degrade in water (i.e., blood), minimizing systemic exposure. Clinical data are limited but suggest efficacy without affecting serum testosterone or sexual function.[25]Sovak, M., Seligson, A.L., Kucerova, R., Bienova, M., Hajduch, M., Bucek, M. (2002). Fluridil, a rationally designed topical agent for androgenetic alopecia: first clinical experience. Dermatologic … Continue reading
Clascoterone (17ɑ-proprionate) is an androgen receptor antagonist that competes with DHT at the follicle rather than reducing DHT production. It offers a different mechanism but is still under investigation for hair loss.[26]Devjani, S., Ezemma, O., Kelley, K.J., Stratton, S., Senna, M. (2023). Androgenetic Alopecia: Therapy Update. Drugs. 83(8). 701-715. Available at: PMID: 37166619
Pyrilutamide is a non-steroidal anti-androgen that binds to the androgen receptor with high affinity. Like fluridil, it is designed to metabolize into an inactive form upon entering systemic circulation, theoretically offering a safety advantage over finasteride.[27]Biospace. (2023). Kintor Pharma’s KX-826 and GT20029 for Treatment of Androgenetic Alopecia (AGA) and Acne Presented at AAD 2023. Biospace. Available at: … Continue reading
Non-Pharmaceutical Options
Microneedling creates micro-injuries in the scalp and stimulates growth factors (PDGF, VEGF) and activates Wnt/ꞵ-catening signaling, promoting hair regeneration even without concurrent drug use.[28]Dhurat, R., Sukesh, M.S., Ayhad, G., Dandale, A., Pal, A., Pund, P. (2013). A Randomized Evaluator Blinded Study of Effect of Microneedling in Androgenetic Alopecia: A Pilot Study. International … Continue reading
Low-level laser therapy (LLLT) devices use red light (650-655 nm) to stimulate mitochondrial activity in hair follicles, prolonging anagen and improving density with an excellent safety profile.[29]Egger, A., Resnik, S.R., Aickara, D., Maranda, E., Kaiser, M., Wikramanayake, T.C. (2020). Examining the Safety and Efficacy of Low-Level Laser Therapy for Male and Female Pattern Hair Loss: A … Continue reading
Some botanical supplements have some 5ɑ-reductase inhibitory properties. Saw palmetto and pumpkin seed oil have been shown to have mild 5ɑ-reductase inhibition.[30]Cho, Y.H., Lee, S.Y., Jeong, D.W., Choi, E.J., Kim, Y.J., Lee, J.G., Yi, H.Y., Cha, H.S. (2014). Effect of Pumpkin Seed Oil on Hair Growth in Men with Androgenetic Alopecia: A Randomized, … Continue reading,[31]Pilar, P., 2010. Potency of a novel saw palmetto ethanol extract, SPET-085, for inhibition of 5alpha-reductase II. Advances in Therapy. 27(8). 555-563. Available at: … Continue reading While less potent than finasteride (reducing DHT by ~30-40% vs. >60%), they may provide a viable “middle ground” for those seeking modest stabilization.
Topical finasteride offers a compelling middle path for those seeking the hair-growth benefits of 5-α-reductase inhibition with a lower likelihood of systemic side effects. But “lower” does not mean “none,” and responses vary widely depending on formulation, dose, skin permeability, and individual DHT sensitivity. The current research, while promising, remains short-term, and real-world patterns remind us that systemic exposure is still possible.
For many people, topical finasteride can be a safe, effective component of a broader hair-loss program. The key is approaching it strategically: start low, personalize dosing, choose the right vehicle, and monitor closely for changes. For others, especially those prone to hormonal side effects, alternatives ranging from anti-androgen topicals to non-pharmaceutical options may offer a better balance of efficacy and tolerability.
As with any AGA therapy, the best results come from matching the treatment to the individual, not the other way around.
References[+]
| ↑1 | Zito PM, Bistas KG, Patel P, et al. Finasteride. [Updated 2024 Feb 28]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK513329/ (Accessed: December 2025) |
|---|---|
| ↑2 | 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 with androgenetic alopecia. International Journal of Clinical Pharmacology and Therapeutics. 54(1). 19-27. Available at: https://doi.org/10.5414/CP202467 |
| ↑3 | Smith, A.B., Carson, C.C. (2009). Finasteride in the treatment of patients with benign prostatic hyperplasia: a review. Therapeutics and Clinical Risk Management. 5. 535-545. Available at: https://doi.org/10.2147/tcrm.s6195 |
| ↑4 | Traish, A.M. (2017). Negative Impact of Testosterone Deficiency and 5ɑ-Reductase Inhibitors Therapy on Metabolic and Sexual Function in Men. Advances in experimental medicine and biology. 1043. 473-526. Available at: https://doi.org/10.1007/978-3-319-70178-3_22 |
| ↑5 | 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 with androgenetic alopecia. International Journal of Clinical Pharmacology and Therapeutics. 54(1). 19-27. Available at: https://doi.org/10.5414/CP202467 |
| ↑6 | Piraccini, B.M., Blume-Peytavi, U., Scarci, F., Jansat, J.M., Falques, M., Otero, R., Tamarit, M.L., Galvan, J., Tebbs, V., Massana, E., Topical Finasteride Study Group. (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 |
| ↑7, ↑19 | 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 with androgenetic alopecia. International Journal of Clinical Pharmacology and Therapeutics. 54(1). 19-27. Available at: https://doi.org/10.5414/CP202467 |
| ↑8 | Monti. D., Tampucci, S., Burgalassi, S., Chetoni, P., Lenzi, C., Pirone, A., Mailland, F. (2014). Topical formulations containing finasteride. Part I: in vitro permeation/penetration study and in vivo pharmacokinetics in hairless rat. Journal of Pharmaceutical Sciences. 103(8). 2307-2314. Available at: https://doi.org/10.1002/jps.24028 |
| ↑9 | US Food and Drug Administration. (2025). FDA alerts health care providers, compounders and consumers of potential risks associated with compounded topical finasteride products. FDA. Available at: https://www.fda.gov/drugs/human-drug-compounding/fda-alerts-health-care-providers-compounders-and-consumers-potential-risks-associated-compounded (Accessed: December 2025) |
| ↑10 | 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 the United States Food and Drug Administration Adverse Event Reporting System. International Journal of Dermatology. Available at: https://doi.org/10.1111/ijd.17957 |
| ↑11 | 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 the United States Food and Drug Administration Adverse Event Reporting System. International Journal of Dermatology. Available at: https://doi.org/10.1111/ijd.17957 |
| ↑12 | 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 Dermatology. 17(4). 457-463. Available at: PMID: 29601622 |
| ↑13, ↑14 | Pereira, A.F.J.R., Coehlo, T, O. de 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 |
| ↑15, ↑16 | Farah, A.H., Brown, M.B., McAuley, W.J. (2020). Enhanced Follicular Delivery of Finasteride to Human Scalp Skin Using Heat and Chemical Penetration Enhancers. Pharmaceutical Research. 37(6). 112. Available at: https://doi.org/10.1007/s11095-020-02822-y |
| ↑17 | Tabbakhian, M., Tavakoli, N., Jaafari, M.R., Daneshamouz, S. (2006). Enhancement of follicular delivery of finasteride by liposomes and niosomes: 1. In vitro permeation and in vivo deposition studies using hamster flank and ear models. International Journal of Pharmaceutics. 1-2(323). 1-10. Available at: https://doi.org/10.1016/j.ijpharm.2006.05.041 |
| ↑18 | Rao, Y., Zheng, F., Zhang, X., Gao, J., Liang, W. (2008). In vitro Percutaneous Permeation and Skin Accumulation of Finasteride Using Vesicular Ethosomal Carriers. 9(3). 860-865. Available at: https://doi.org/10.1208/s12249-008-9124-y |
| ↑20 | Mysore, V. (2012). Finasteride and sexual side effects. Indian Dermatology Online Journal. 3(1). 62-65. Available at: https://doi.org/10.4103/2229-5178.93496 |
| ↑21 | Tai, Z., Cui, Z., Shi, X., Li, H., Chai, R., Huang, Y., Fang, Y., Jia, D., Zhu, Q., Chen, Z. (2025). The Pharmacokinetics of Topical Finasteride 0.25% Spray in Chinese Adult Male Volunteers with Androgenic Alopecia: A Phase I Study. Advances in Therapy. 42(3). 1494-1505. Available at: https://doi.org/10.1007/s12325-025-03106-w. |
| ↑22 | Cecchin, E., De Mattia, E., Toffoli, G., Mazzon, G., Cauci, S., Trombetta, C. (2014). A Pharmacogenetic Survey of Androgen Receptor (CAG)N and (GGN)N Polymorphisms in Patients Experiencing Long-Term Side Effects after Finasteride Discontinuation. The International Journal of Biological Markers. 29(4). 310-316. Available at: https://doi.org/10.5301/jbm.500095 |
| ↑23 | Rahimi-Ardabili, B., Pourandarjani, R., Habibollahi, P., Mualeki, A. (2006). Finasteride-induced depression: a prospective study. BMC Clinical Pharmacology. 6(7). Available at: https://doi.org/10.1186/1472-6904-6-7 |
| ↑24 | Vano-Galvan, S., Pirmez, R., Hermosa-Gelbard, A., Moreno-Arrones, O.M., Saceda-Corralo, D., Rodrigues-Barata, R., Jiminez-Cauhe, J., Koh, W.L., Poa, J.E., Jerjen, R., de Carvalho, L.T., John, J.M., Salas-Callo, C.I., Vincenzi, C., Yin, L., Lo-Sicco, K., Waskiel-Burnat, A., Starace, M., Zamorano, J.L., Jaen-Olasolo, P., Piraccini, B.M., Rudnicka, L., Shapiro, J., Tosti, A., Sinclair, R., Bhoyrul, B. (2021). Safety of low-dose oral minoxidil for hair loss: A multicenter study of 1404 patients. Journal of the American Academy of Dermatology. 84(6). 1644-1651. Available at: https://doi.org/10.1016/j.jaad.2021.02.054 |
| ↑25 | Sovak, M., Seligson, A.L., Kucerova, R., Bienova, M., Hajduch, M., Bucek, M. (2002). Fluridil, a rationally designed topical agent for androgenetic alopecia: first clinical experience. Dermatologic Surgery. 28(8). 678-685. Available at: https://doi.org/10.1046/j.1524-4725.2002.02017.x |
| ↑26 | Devjani, S., Ezemma, O., Kelley, K.J., Stratton, S., Senna, M. (2023). Androgenetic Alopecia: Therapy Update. Drugs. 83(8). 701-715. Available at: PMID: 37166619 |
| ↑27 | Biospace. (2023). Kintor Pharma’s KX-826 and GT20029 for Treatment of Androgenetic Alopecia (AGA) and Acne Presented at AAD 2023. Biospace. Available at: https://www.biospace.com/kintor-pharma-s-kx-826-and-gt20029-for-treatment-of-androgenetic-alopecia-aga-and-acne-presented-at-aad-2023 (Accessed: December 2025) |
| ↑28 | Dhurat, R., Sukesh, M.S., Ayhad, G., Dandale, A., Pal, A., Pund, P. (2013). A Randomized Evaluator Blinded Study of Effect of Microneedling in Androgenetic Alopecia: A Pilot Study. International Journal of Trichology. 5(1). 6-11. Available at: https://doi.org/10.4103/0974-7753.114700 |
| ↑29 | Egger, A., Resnik, S.R., Aickara, D., Maranda, E., Kaiser, M., Wikramanayake, T.C. (2020). Examining the Safety and Efficacy of Low-Level Laser Therapy for Male and Female Pattern Hair Loss: A Review of the Literature. Skin Appendage Disorders. 6(5). 259-267. Available at: https://doi.org/10.1159/000509001 |
| ↑30 | Cho, Y.H., Lee, S.Y., Jeong, D.W., Choi, E.J., Kim, Y.J., Lee, J.G., Yi, H.Y., Cha, H.S. (2014). Effect of Pumpkin Seed Oil on Hair Growth in Men with Androgenetic Alopecia: A Randomized, Double-Blind, Placebo-Controlled Trial. Evidence-Based Complementary and Alternative Medicine. 23. 549721. Available at: https://doi.org/10.1155/2014/549721 |
| ↑31 | Pilar, P., 2010. Potency of a novel saw palmetto ethanol extract, SPET-085, for inhibition of 5alpha-reductase II. Advances in Therapy. 27(8). 555-563. Available at: https://doi.org/10.1007/s12325-010-0041-6 |
After years of anticipation, we finally have the first-ever study testing topical dutasteride as a standalone treatment for androgenic alopecia (AGA). No microneedling, no formulations mixed with other ingredients, just topical dutasteride itself.
And the results?
Frankly, they are shocking.
According to the study, low-dose topical dutasteride outperformed oral finasteride for hair regrowth.
On the face of it, this is so surprising that it borders on unbelievable, especially given the 5+ years of real-world data we’ve collected from our members.
So, in this article, we’ll break down:
Hair gains bigger than finasteride? Dutasteride makes this possible, 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.
*Only available in the U.S. Prescriptions not guaranteed. Restrictions apply. Off-label products are not endorsed by the FDA.
Until now, only two small clinical studies have evaluated low-dose topical dutasteride. Both used it alongside microneedling and applied it just once every 1-4 weeks.
Nada et al. reported that adding low-dose topical dutasteride to a structured microneedling regimen improved hair density and shaft thickness more than microneedling alone, while only slightly reducing serum DHT, likely without meaningful systemic hormonal impact.[1]Nada, E.A., El-Dawla, R.E., El-Maged, W.M.A., Elmaged, M.A.A. (2018). Topical dutasteride with microneedling in treatment of male androgenetic alopecia. Sohag Medical Journal. 22(1). Available at: … Continue reading
30 men with AGA were randomized to either microneedling plus topical dutasteride 0.02% or microneedling alone for six months. Both groups received 13 microneedling sessions with a 1.5 mm Dermapen (12-needle cartridge) on a staggered schedule: weekly during the first 8 weeks, then gradually reduced to once every 2-4 weeks through month six. In the combination arm, up to 2 mL of 0.02% dutasteride
Sanchez-Meza et al. found that adding very low-dose topical dutasteride to microneedling produced greater clinical and trichoscopic improvement than microneedling with placebo, without reported sexual side effects and with much lower total dutasteride exposure than earlier work.[2]Sanchez-Meza, E., Ocampo-Candiani, J., Gomez-Flores, M., Herz-Ruelas, M.E., Ocampo-Garza, J., Orizaga-Y-Quiroga, T.L., Martinez-Moreno, A., Ocampo-Garza, S.S. (2022). Microneedling plus topical … Continue reading
34 men with AGA were randomized to microneedling plus 1 mL of 0.01% topical dutasteride (~0.1 mg) or microneedling plus 1 mL of saline as a placebo. Both groups received three treatment sessions spaced 4 weeks apart using a Dr. Pen Ultima A6 device set to a 2.5 mm needle depth, and outcomes were assessed over a 16-20 week period.
While both these studies showed mild hair regrowth, the effect is not from topical dutasteride alone, nor from daily use.
Furthermore, low-dose topical dutasteride showed almost no systemic dihydrotestosterone (DHT) suppression.
Across these studies, bloodwork suggested:
This makes sense. Dutasteride is a large, lipophilic molecule. At low concentrations, it tends to stay localized to the scalp unless dosing or penetration enhancers are significant.
Because early studies were promising, some of our members tried 0.01-0.02% topical dutasteride in the years that followed.
A dozen users also tracked blood DHT levels before and after treatment.
The results? Strong localization with minimal regrowth.
Instead, most people saw hair maintenance, not cosmetic improvement.
This aligns with the published studies: low-dose topical dutasteride appears to stabilize hair loss, with minimal systemic impact, but not drive substantial growth.
You can get more information about this and comparisons to topical finasteride here:
This new randomized, double-blind, placebo-controlled study appeared to be the gold standard of topical dutasteride research.[3]Panuganti, V.K., Mandala, P.K., Grandhi, V.R., Alluri, C.V., Mohammad, J., Rao, S., Dundigalla. (2025). A Randomized, Double-Blind, Placebo and Active Controlled Phase II Study to Evaluate the Safety … Continue reading
It was the first study to test topical dutasteride:
On paper, this looked like the definitive study that we have long needed.
135 men aged 20-60 with Norwood III vertex, IV, or V AGA were randomized across five treatment arms in a 2:2:2:2:1 ratio:
All participants were Asian men, average age of ~38 years. Baseline hair loss severity was balanced across groups.
Each 1 mL dose contained:
Importantly, the solution was nearly 30% dehydrated alcohol, a known penetration enhancer. This choice may have implications for systemic absorption and hair-count interpretation, though the authors claim systemic exposure remained minimal.
The researchers measured hair counts (total area hair counts) and hair widths (total area hair widths). Using a Dino-Lite microscope, researchers identified a 1.9 cm2 circular region at the vertex, clipped hairs to 0.5 – 1 mm, marked the center of the circle, and captured macrophotographs at baseline, week 12, and week 24.
The authors do not mention tattooing, ink permanence, or the use of a positioning device, which becomes critically important later.
Here’s where the shock factor begins.
At 24 weeks, the study reported:
The headline claim: “0.05% topical dutasteride significantly outperformed oral finasteride (p=0.0083)”
This is a remarkable result, and one that contradicts every known real-world case we’ve observed at similar dosing.
All active groups increased hair thickness, with results very close to oral finasteride:
Only the 0.05% topical and finasteride groups significantly beat placebo. The 0.05% topical did not significantly outperform finasteride in hair-width metrics.
At 24 weeks, the percentage of participants rated as having “moderate improvement” or better (GPA ≥ +2) was:
These numbers suggest a level of regrowth from 0.5 mg/week of topical dutasteride that we’ve simply never witnessed, not in our community, not in the medical literature, and not among clinicians who routinely prescribe topical dutasteride.
By week 24, 96.55% of 0.05% topical users were satisfied with the hair on top of their heads. This is far above the finasteride group (71.43%) and far above the placebo (33.33%).
Again, the magnitude of the difference warrants scrutiny.
This is where things do align with real-world experiences of low-dose topical users.
DHT Reductions
Testosterone Increases
The authors emphasize that topical dutasteride caused minimal systemic effects.
This is consistent with our members’ lab data – but inconsistent with the hair-growth magnitude reported.
According to the PK data:
The authors interpret this as “low systemic exposure”. But variability this large raises questions.
Across the entire study, no serious adverse events were reported, no withdrawals due to safety, minimal skin irritation, and all groups showed mild effects like “glazing” at similar rates.
This matches expectations for low-dose topicals.
For more than five years, we’ve tracked user outcomes from low-dose topical dutasteride at comparable or even higher weekly doses than used in this study.
Not once have we seen:
Even in dermatology clinics across the world, this simply isn’t observed. So, why would this study find such dramatically different results?
It comes down to two major methodological problems – both related to hair counts.
The average baseline hair density reported in the study was 305-330 hairs/cm2.
For context:
This would mean that severely balding scalps had triple the hair density of a normal, non-balding scalp, and that hair counts exceeded what is physiologically plausible.
Why might this happen?
Vellus hairs were counted.
The measurement area was bigger than stated.
Manual counting errors.
None of these possibilities inspires confidence in the baseline data.
This is the more serious problem, and the one most likely to invalidate the findings entirely.
When examining the study’s published before-and-after images, the measurement circles:

Figure 1: Representative hair growth images.[4]Panuganti, V.K., Mandala, P.K., Grandhi, V.R., Alluri, C.V., Mohammad, J., Rao, S., Dundigalla. (2025). A Randomized, Double-Blind, Placebo and Active Controlled Phase II Study to Evaluate the Safety … Continue reading
Take a close look at these images; the center point marks do not appear to be consistent (at least from these photos). This means that you really can’t compare the improvements over time, as the follow-up hair counts would have been conducted in slightly different areas of the scalp!
This is an enormous methodological flaw.
A shift of just 1-2 millimetres in circle placement can change hair counts by 50% or more, something we demonstrated in our 2021 publication.[5]Jnr, R.E., Ruiz, S. (2021). Conflicting Reports Regarding the Histopathological Features of Androgenic Alopecia: Are Biopsy Location, Hair Diameter Diversity, and Relative Hair Follicle … Continue reading

Fig 2: Circle A has 50% more hair than Circle B.[6]Jnr, R.E., Ruiz, S. (2021). Conflicting Reports Regarding the Histopathological Features of Androgenic Alopecia: Are Biopsy Location, Hair Diameter Diversity, and Relative Hair Follicle … Continue reading
Yet the improvements reported in this study were around 10-30%.
Meaning: These “improvements” could be fully explained by inconsistent circle placement, not actual regrowth.
This alone is enough to call the validity of the hair-count data into question.
This is one situation where we at PHH trust the real-world experiences of our members over a randomized, controlled clinical trial, because while the study appears rigorous on the surface, its hair-counting methods reveal inconsistencies significant enough to undermine its conclusions.
All available evidence still supports the following: low-dose topical dutasteride (0.01-0.05%) localizes well to the scalp, minimally suppresses serum DHT, effectively slows or stops hair loss, and rarely produces meaningful regrowth, whereas high-strength topical dutasteride (≥0.1%) is more likely to leak systemically, carry a greater risk of side effects, and generate visible regrowth approaching the results of oral finasteride.
References[+]
| ↑1 | Nada, E.A., El-Dawla, R.E., El-Maged, W.M.A., Elmaged, M.A.A. (2018). Topical dutasteride with microneedling in treatment of male androgenetic alopecia. Sohag Medical Journal. 22(1). Available at: https://smj.journals.ekb.eg/article_42083_24b61cbba4be9982db23c318414034c0.pdf (Accessed: December 2025) |
|---|---|
| ↑2 | Sanchez-Meza, E., Ocampo-Candiani, J., Gomez-Flores, M., Herz-Ruelas, M.E., Ocampo-Garza, J., Orizaga-Y-Quiroga, T.L., Martinez-Moreno, A., Ocampo-Garza, S.S. (2022). Microneedling plus topical dutasteride solution for androgenetic alopecia: a randomized placebo-controlled study. Journal of the European Academy of Dermatology and Venereology. 36(10). E806-e808. Available at: https://doi.org/10.1111/jdv.18285 |
| ↑3 | Panuganti, V.K., Mandala, P.K., Grandhi, V.R., Alluri, C.V., Mohammad, J., Rao, S., Dundigalla. (2025). A Randomized, Double-Blind, Placebo and Active Controlled Phase II Study to Evaluate the Safety and Efficacy of Novel Dutasteride Topical Solution (0.01%, 0.02%, and 0.05% w/v) in Male Subjects with Androgenetic Alopecia. Cureus. 17(8). E89309. Available at: https://doi:10.7759/cureus.89309 |
| ↑4 | Panuganti, V.K., Mandala, P.K., Grandhi, V.R., Alluri, C.V., Mohammad, J., Rao, S., Dundigalla. (2025). A Randomized, Double-Blind, Placebo and Active Controlled Phase II Study to Evaluate the Safety and Efficacy of Novel Dutasteride Topical Solution (0.01%, 0.02%, and 0.05% w/v) in Male Subjects with Androgenetic Alopecia. Cureus. 17(8). E89309. Available at: https://doi:10.7759/cureus.89309 |
| ↑5 | Jnr, R.E., Ruiz, S. (2021). Conflicting Reports Regarding the Histopathological Features of Androgenic Alopecia: Are Biopsy Location, Hair Diameter Diversity, and Relative Hair Follicle Miniaturization Partly to Blame? Clinical, Cosmetic and Investigative Dermatology. 14. 357-365. Available at: https://doi.org/10.2147/CCID.S306157 |
| ↑6 | Jnr, R.E., Ruiz, S. (2021). Conflicting Reports Regarding the Histopathological Features of Androgenic Alopecia: Are Biopsy Location, Hair Diameter Diversity, and Relative Hair Follicle Miniaturization Partly to Blame? Clinical, Cosmetic and Investigative Dermatology. 14. 357-365. Available at: https://doi.org/10.2147/CCID.S306157 |
Female hair loss remains a widely misunderstood and often under-treated condition, affecting nearly one-third of all women at some point in their lives and up to two-thirds after menopause. Unlike male pattern hair loss, research and treatment options for women have historically lagged, resulting in limited specialized solutions and significant emotional distress for those afflicted.
Minoxidil stands as the only FDA-approved medication for female pattern hair loss. Its efficacy is supported by robust data, particularly at the 2 and 5% concentrations for women. In this guide, we will showcase the six best minoxidil products for women, including the best overall, best value, and top specialized choices.
| Product | Strength | Format | Customization | Price | Best |
| Ulo Women’s Rx Minoxidil | 7% | Solution | High | $41.65 | Overall |
| Musely | 8% | Solution | High | $99 | Strength |
| Rogaine Women’s Foam | 5% | Foam | None | $49.97 | Sensitivity |
| Hers | 2%-5% | Solution/Foam | None | $30 | Value |
| Happy Head (Women’s Formula) | 6% | Solution | High | $79 | Alternative |
| Winona | 7% | Solution | None | $150 | Woman-centered care |
Before we get into our list, let’s first take a look at what female pattern hair loss is and how minoxidil works for women.
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.
*Only available in the U.S. Prescriptions not guaranteed. Restrictions apply. Off-label products are not endorsed by the FDA.
Female pattern hair loss (FPHL) is a chronic, non-scarring alopecia where genetically susceptible follicles on the central scalp progressively minaturize, leading to reduced hair density over time. Clinically, women usually show diffuse thinning over the crown and midline part with relative preservation of the frontal hairline rather than “bald patches”.[1]Bhat, Y.J., Saqib, N-U., Latif, I., Hassan, I. (2020). Female Pattern Hair Loss – An Update. Indian Dermatology Online Journal. 11(4). 493-501. Available at: … Continue reading
The Ludwig scale grades this pattern from I-III: mild central thinning (I), moderate widening of the part and density loss (II), and advanced, see-through vertex thinning (III). Trichoscopy and histology show increased hair shaft diameter variability and replacement of terminal hairs by finer, vellus-like hairs.[2]Kothari, C.R., Shivakumar, P. (2024). Trichoscopic Features in Female Pattern Hair Loss: 1-Year Hospital-Based Cross-Sectional Study. Clinical Dermatology Review. 8(2). 95-101. Available at: … Continue reading
FPHL arises from a mix of genetics, hormones, low-grade inflammation, oxidative stress, and microvascular and aging-related changes around the follicle. Unlike classic male pattern hair loss, many women have normal serum androgens, suggesting that local androgen sensitivity and non-androgen mechanisms both contribute.[3]Ramos, P.M., Miot, H.A. (2015). Female Pattern Hair Loss: a clinical and pathophysiological review. Anais Brasileiros de Dermatologia. 90(4). 529-543. Available at: … Continue reading
Minoxidil functions as a potassium channel opener that promotes vasodilation, increasing blood flow and improving microcirculation around hair follicles.[4]Hussein, R.S., Dayel, S.B., Abahussein, O., El-Sherbiny, A.A. (2024). Applications and efficacy of minoxidil in dermatology. Skin Health and Disease. 4(6). E472. Available at: … Continue reading
It is also a prodrug that must be converted by the sulfotransferase enzyme into its active form, minoxidil sulfate. This conversion helps extend the anagen (growth) phase while shortening the telogen (resting) phase, thereby shifting a greater number of follicles into active growth cycles.[5]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
Additional evidence indicates that minoxidil stimulates the expression of growth-promoting factors, such as vascular endothelial growth factor (VEGF), and activates the Wnt/β-catenin signaling pathway, both of which further support hair regrowth.[6]Gupta, A.K., Talukder, M., Shemer, A., Piraccini, B.M., Tosti, A. (2023). Low-Dose Oral Minoxidil for Alopecia: A Comprehensive Review. Skin Appendage Disorders. 9(6). 423-437. Available at: … Continue reading
While minoxidil does not directly address dihydrotestosterone (DHT), it can enhance the effectiveness of other therapies by targeting different biological pathways involved in hair loss. When used alongside anti-DHT treatments such as finasteride, which reduces the underlying hormonal driver of androgenic alopecia, minoxidil offers a complementary, non-hormonal mechanism of action. Clinical research demonstrates that the combined use of topical finasteride and minoxidil produces greater improvements in hair density in men compared to minoxidil alone.[7]Asad, N., Naseer, M., Ghafoor, R. (2024). Efficacy of Topical Finasteride 0.25% with Minoxidil 5% versus Topical Minoxidil 5% Alone in Treatment of Male Pattern Androgenic Alopecia. Journal of Drugs … Continue reading
In women, pattern hair loss is generally less strictly DHT-driven than in men, so microcirculation, oxidative stress, and local inflammatory pathways play a proportionately greater role.[8]Fabbrocini, G., Cantelli, M., Masara, A., Annunziata, M.C., Marasca, C., Cacciapuoti, S. (2018). Female pattern hair loss: A clinical, pathophysiologic, and therapeutic review. International Journal … Continue reading This helps explain why a vasodilatory, pro-anagen agent like minoxidil is often effective even when anti-androgens alone are insufficient.
Hormonal transitions like perimenopause/menopause, thyroid dysfunction, and polycystic ovary syndrome (PCOS) commonly unmask or accelerate FPHL by altering estrogen-androgen balance and cycling dynamics.[9]Aksenenko, M., Palkina, N., Komina, A., Ruksha, T. (2019). MiR-92a-1-5p and miR-328-3p Are Up-Regulated in Skin of Female Pattern Hair Loss Patients. Annals of Dermatology. 31(2). 256-259. Available … Continue reading
Over-the-counter (OTC) minoxidil for women typically comes at 2-5% concentrations, while prescription or compounded products may use 5-8% or higher strengths in customized products.
2% minoxidil is the classic, label-approved strength for women, with clear evidence of a benefit versus placebo.[10]van Zuuren, E.J., Fedorowicz, Z., Schoones, J. (2016). Interventions for female pattern hair loss. Cochrane Database of Systematic Reviews. 2016(5). CD007628. Available at: … Continue reading
Compounded “high-strength” minoxidil (5-8%+) is prescription only and relies in part on carrier agent formulation.[11]Sattur, S.S., Sattur, I.S. (2021). Pharmacological Management of Pattern Hair Loss. Indian Journal of Plastic Surgery. 54(4). 422-434. Available at: https://doi.org/10.1055/s-0041-1739254 Simply raising the percentage does not guarantee better results and may raise the risk of irritation, hypertrichosis, or systemic absorption of the drug.[12]Ghonemy, S., Alarawi, A., Bessar, H. (2021). Efficacy and safety of a new 10% topical minoxidil versus 5% topical minoxidil and placebo in the treatment of male androgenetic alopecia: a trichoscopic … Continue reading
So, with that in mind, let’s take a look at our top six minoxidil brands of 2025.
| Pros: | Cons: |
| ✓ Prescription-only 7% minoxidil, higher than standard OTC strengths | ✗Prescription products are only available in the USA |
| ✓ Optional evidence-based add-ons | |
| ✓ Quality-tested ingredients free of irritants | |
| ✓ Includes medical consultation and ongoing monitoring |
Ulo Women’s Rx Minoxidil+ is our go-to product for topical minoxidil treatment. It is designed for those who want more than “pink-labeled” 2-5% solutions and are comfortable with a prescription approach guided by specialists. The 7% concentrated and layered actives (including cetirizine 1%, tretinoin 0.01%, melatonin 0.01%, and caffeine 0.2%) target multiple facets of hair loss with a level of customization that goes beyond typical off-the-shelf products.
Bottom Line: Ulo offers the most precise, clinically guided minoxidil-based treatment for women in 2025, combining higher-strength therapy with thoughtful formulation and ongoing medical oversight.
| Pros: | Cons: |
| ✓ High-strength 8% prescription minoxidil. | ✗ Use of corticosteroids increases the risk of skin thinning. |
| ✓ Optional evidence-based add-ons like dutasteride and spironolactone for hormonal control. | ✗ Propylene glycol and ethyl alcohol base, which can sting or dry out sensitive scalps. |
| ✓ Additional scalp-supporting actives like tretinoin, ketoconazole, caffeine, and melatonin. | ✗ More expensive than simpler OTC or lower-strength prescription options. |
| ✓ Includes periodic medical follow-up. |
Musely’s 8% “Classic” Hair Topical is designed for women with advanced thinning or those who have plateaued on conventional strengths, combining high-dose minoxidil with potent anti-androgens and supportive ingredients in a single solution, including optional add-ons such as dutasteride 0.3%, spironolactone 0.075%, tretinoin 0.01%, ketoconazole 2%, hydrocortisone 1%, plus adjuncts like caffeine and melatonin.
It functions more as an intensive, prescription-only protocol than a starter product, and is best reserved for users willing to tolerate a stronger propylene glycol/ethyl alcohol vehicle, and possible skin thinning if using long-term due to the addition of corticosteroids.
Bottom line: For women with stubborn, progressive hair loss who have outgrown basic 5% formulas, Musely’s high-strength, multi-active topical offers one of the most powerful at-home options, provided they are comfortable with higher cost and higher irritation risk.
| Pros: | Cons: |
| ✓ Propylene-glycol-free foam vehicle, often better tolerated on sensitive or irritated scalps. | ✗No medical consultation or follow-up after buying |
| ✓ Widely available OTC | ✗ No customization. |
Rogaine Women’s Foam is a classic choice for those looking for a gentle-on-the-scalp option of minoxidil. The propylene-glycol-free foam base, robust clinical evidence, and once-daily 5% option make it a gentle yet effective starting point for treating female pattern thinning. It should be noted that if you wanted to try the lower dose option (2%), you need to buy the solution, which contains propylene glycol, and so may not be as beneficial for those with sensitive skin.
Bottom Line: Get the foam if you have a sensitive scalp or are a beginner, wanting a low-irritant minoxidil option.
| Pros: | Cons: |
| ✓ Budget-friendly option at around $30 for a 2-month supply. | ✗No advanced customization available. |
| ✓ Offers both 2% and 5% strengths at the same price. | |
| ✓ Available in solution and foam formats. |
Hers Minoxidil is designed for women who want a clinically supported minoxidil treatment without paying premium prices for branding or heavy telehealth layering. With standard 2 and 5% options in familiar vehicles, it delivers an approachable, budget-conscious package for those comfortable managing a simple daily routine themselves.
Bottom Line: For cost-conscious women who want an easy, no-frills entry into proven minoxidil therapy, Hers Minoxidil offers standard concentrations with good value.
| Pros: | Cons: |
| ✓ Prescription-strength 6% minoxidil, higher than standard OTC options but below ultra-high-dose protocols. | ✗ Uses a propylene glycol-containing vehicle, which can increase irritation, dryness, or stinging on sensitive scalps. |
| ✓ Customizable blends that include spironolactone, tretinoin, and hydrocortisone | ✗ Inclusion of topical corticosteroids carries a risk of skin thinning and barrier damage if used long-term. |
| ✓ Strong telehealth model with online prescribing and adjustments to treatments over time. | ✗ More expensive than generic 5% minoxidil and some standard telehealth offerings. |
| ✓ Good fit for women who need more than basic 2-5% formulas but do not want to jump straight to 8%+ multi-drug cocktails. |
Happy Head’s 6% formulas are aimed at women who want a personalized, prescription-only topical that goes beyond standard strengths while still staying below the most aggressive high-dose regimens. By combining minoxidil with spironolactone, retinoic acid, and short-term hydrocortisone in a single bottle, it offers a modular approach that can be tuned to individual tolerance and response rather than a one-size-fits-all solution. It should be noted that Happy Head uses corticosteroids in their topicals to offset the potential irritation from propylene glycol usage. However, this can cause skin thinning with long-term use.
Bottom line: For women who need a tailored, mid-high-strength minoxidil blend with added anti-androgens and supportive ingredients, but prefer not to escalate to ultra-high-dose, steroid-heavy cocktails, Happy Head provides a strong option.
| Pros: | Cons: |
| ✓ Women-focused clinic model that addresses broader menopausal health alongside hair loss. | ✗ Uses a propylene glycol-containing vehicle, which can increase irritation, dryness, or stinging on sensitive scalps. |
| ✓ Prescription-strength 7% minoxidil specifically targeted to menopausal and perimenopausal thinning. | ✗ No customization |
| ✓ Guided supportive care pathway, with structured programs, check-ins, and follow-up. | ✗ Premium pricing at around $150 for a 3-month supply. |
| ✓ Treatment plans that can integrate other menopause therapies where appropriate |
Winona’s 7% minoxidil is designed for women who want more than a stand-alone bottle and value a structured, woman-centered approach that fits into a broader menopause-care framework. The higher-strength prescription formula, combined with clear guidance, follow-up, and attention to hormonal context, makes it particularly suited to postmenopausal and perimenopausal hair loss rather than general early thinning. However, it should be noted that its carrier agent, propylene glycol, may be irritating for sensitive scalps.
Bottom line: For women seeking a guided, menopause-focused program built around prescription-strength minoxidil, Winona offers a structured, woman-centered care pathway, albeit at a higher price and with a more irritant-prone vehicle.
Setting realistic expectations is essential when beginning topical minoxidil for female pattern hair loss. Unlike quick cosmetic fixes, minoxidil works by gradually altering the hair growth cycle, and visible changes take time to develop.
| Timeframe | What to Expect | Clinical Evidence |
| Months 0-3 | An initial increase in shedding may occur as follicles shift out of the resting (telogen) phase and re-enter growth. This temporary “dread shed” phase typically improves within 4–8 weeks and is considered a normal response to treatment initiation. | [13]Nohria, A., Desai, D., Sikora, M., Mandal, S., Shapiro, J., Lo Sicco, K. (2024). Combating “dread shed”: The impact of overlapping topical and oral minoxidil on temporary hair shedding during … Continue reading |
| Months 3-6 | Early visible signs of improvement may appear, including reduced shedding and the emergence of fine, new hairs (vellus to terminal transformation), particularly along the part line and crown. | [14]Amit, K., Mansukh, G., Satyaprakash, M., Dhiraj, D., Hanmant, B. (2023). Real-World Effectiveness, Safety, and Tolerability of Cetosomal Minoxidil 5% Alone and a Fixed Drug Combination of Cetosomal … Continue reading |
| Months 6-12 | More noticeable cosmetic improvements are typically seen, including increased overall density, thickening of existing strands, and improved scalp coverage in areas of diffuse thinning. For many women, this is the point at which changes become easily visible in the mirror and in photos. | [15]Katz, H.I., Hien, N.T., Prawer, S.E., Goldman, S.J. (1987). Long-term efficacy of topical minoxidil in male pattern baldness. Journal of the American Academy of Dermatology. 16(3). 711-718. Available … Continue reading |
| Months 12+ | Hair density gains typically plateau. At this point, continued use is required to maintain results and prevent gradual regression back toward baseline. Stopping treatment may allow thinning to resume over time. | [16]Katz, H.I., Hien, N.T., Prawer, S.E., Goldman, S.J. (1987). Long-term efficacy of topical minoxidil in male pattern baldness. Journal of the American Academy of Dermatology. 16(3). 711-718. Available … Continue reading |
Topical minoxidil works by extending the anagen (growth) phase of the hair cycle and shortening the telogen (resting) phase, thereby increasing the amount of time that follicles spend actively producing hair. Maintaining this effect requires regular, consistent application. When doses are frequently missed, follicles spend less cumulative time in a growth-biased state, which reduces the likelihood of noticeable improvement.[17]Messenger, A.G., Rundegren, J. (2004). Minoxidil: mechanisms of action on hair growth. British Journal of Dermatology. 2(1). 186-194. Available at: … Continue reading
This principle is especially important in women, whose hair loss is often more diffuse and gradual, making subtle changes harder to notice in the early months. Because the human scalp hair cycle progresses slowly, with the anagen phase potentially lasting several years, many follicles need prolonged, uninterrupted exposure to minoxidil before visible gains in density and coverage can be achieved.[18]Hoover E, Alhajj M, Flores JL. Physiology, Hair. [Updated 2023 Jul 30]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Available from: … Continue reading
For this reason, most clinical guidance advises committing to at least six months of daily, consistent use before evaluating the effectiveness of treatment, with continued use required to sustain and build upon results.
You can find topical minoxidil in several different delivery vehicles, each with its own advantages in terms of scalp tolerability, ease of use, and fit for a woman’s lifestyle and hair type. In most cases, the “best” option is not defined by pure strength alone, but by how well the formula matches skin sensitivity, styling habits, and consistency of application.
Foam – Best for Sensitive Skin
Propylene glycol–free foam formulations were developed to reduce the risk of contact dermatitis, itching, and dryness that can occur with traditional liquid solutions. Clinical observations suggest that foam is generally better tolerated and faster-drying, making it a strong choice for women with sensitive scalps or those who wash and style their hair frequently.[19]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
Liquid – Best for Cost and Precision
Classic liquid solutions, usually formulated with alcohol and propylene glycol, remain widely available and affordable. While effective, they may cause itching, dryness, or flaking in some women. These solutions can work well for individuals without scalp sensitivity who prefer a more targeted, dropper-based application, especially along the part line.
Spray – Best for Quick, Even Coverage
Spray or mist-style applicators make it easier to cover larger areas of diffuse thinning, such as along the crown or upper scalp. However, they can be less precise, with some product landing on the hair shafts or surrounding skin rather than directly on the scalp.
Gel – Best for Targeted Areas
Gel or cream-gel formulations tend to stay in place, minimizing runoff and improving control. These are helpful for women treating specific areas of thinning, such as the temples, frontal hairline, or post-partum thinning zones.
Liposomal Delivery
Some prescription and premium products use liposomal or phospholipid-based carriers that are designed to improve follicular penetration while reducing irritation and systemic absorption. These advanced bases may be especially attractive for women who need stronger formulations but have experienced irritation with traditional vehicles.
Topical minoxidil is generally well tolerated by women, but like any active medication, it can produce local scalp irritation, a brief increase in shedding during the early treatment phase, and, in very rare cases, systemic side effects, particularly in individuals with underlying skin or cardiovascular conditions.
Common local reactions may include:
These symptoms are typically mild, tend to improve as the scalp adapts, and can often be reduced by switching to a foam-based formula, lowering concentration, or using a gentler vehicle.
Systemic and heart-related reactions are extremely uncommon with proper topical use. However, isolated case reports and safety data recommend seeking medical attention if symptoms such as chest tightness, heart palpitations, lightheadedness, dizziness, or unexplained swelling develop, as these could indicate increased systemic absorption or accidental ingestion. The risk of cardiovascular effects is significantly higher with oral minoxidil or improper dosing, where hypotension, tachycardia, and even heart failure have been reported.[20]Tripathee, S., Benyovszky, A., Devbhandari, R., Quiza, K., Boris, J. (2024). A Very Bad Hair Day: Minoxidil Ingestion Causing Shock and Heart Failure. Cureus. 16(8). E66039. Available at: … Continue reading
To minimize the risk of side effects, many clinicians recommend starting with once-daily application, gradually increasing only if tolerated. Women with reactive skin often benefit from foam formulations, lower-alcohol bases, or liposomal delivery systems, which can reduce irritation and improve comfort during long-term use.
Individuals with active inflammatory scalp conditions, such as psoriasis, eczema, or severe seborrheic dermatitis, are generally advised to first address the underlying condition before beginning minoxidil therapy. Applying treatment to an inflamed or compromised skin barrier can increase irritation, worsen symptoms, and lead to unpredictable absorption patterns.[21]Junge, A., Jic-Hoesli, S.R., Bossart, S., Simon, D., de Viragh, P., Hunger, R.E., Heidemeye, K., Seyed Jafari, S.M. (2025). Contact Dermatitis Caused by Topical Minoxidil: Allergy or Just Irritation. … Continue reading
Although topical minoxidil has lower systemic absorption than oral formulations, it is generally not recommended during pregnancy or while breastfeeding unless specifically advised by a healthcare provider. Women who are pregnant, trying to conceive, or nursing should consult a qualified medical professional to fully review potential risks and alternative treatment options.
A range of minoxidil-based options is available to support different needs among women experiencing hair thinning, from strength-focused prescriptions to gentle, sensitivity-friendly alternatives and highly customized compounded formulas. While each product relies on the same core ingredient, differences in concentration, delivery vehicle, add-on actives, and level of medical support can significantly influence both tolerability and long-term adherence.
Whichever option you choose, consistent use of minoxidil remains one of the most evidence-backed ways to slow progression and improve hair density in women with pattern hair loss. With today’s expanded access to prescription platforms, foam-based formulations, and individualized treatment models, it is now easier than ever to find an approach that aligns with your scalp sensitivity, stage of hair loss, and lifestyle needs.
References[+]
| ↑1 | Bhat, Y.J., Saqib, N-U., Latif, I., Hassan, I. (2020). Female Pattern Hair Loss – An Update. Indian Dermatology Online Journal. 11(4). 493-501. Available at: https://doi.org/10.4103/idoj.IDOJ_334_19 |
|---|---|
| ↑2 | Kothari, C.R., Shivakumar, P. (2024). Trichoscopic Features in Female Pattern Hair Loss: 1-Year Hospital-Based Cross-Sectional Study. Clinical Dermatology Review. 8(2). 95-101. Available at: https://doi.org/10.4103/cdr.cdr_123_21 |
| ↑3 | Ramos, P.M., Miot, H.A. (2015). Female Pattern Hair Loss: a clinical and pathophysiological review. Anais Brasileiros de Dermatologia. 90(4). 529-543. Available at: https://doi.org/10.1590/abd1806-4841.20153370 |
| ↑4 | Hussein, R.S., Dayel, S.B., Abahussein, O., El-Sherbiny, A.A. (2024). Applications and efficacy of minoxidil in dermatology. Skin Health and Disease. 4(6). E472. Available at: https://doi.org/10.1002/ski2.472 |
| ↑5 | 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 review. Advances in Dermatology and Allergology. 39(3). 472-478. Available at: https://doi.org/10.5114/ada.2020.99947 |
| ↑6 | Gupta, A.K., Talukder, M., Shemer, A., Piraccini, B.M., Tosti, A. (2023). Low-Dose Oral Minoxidil for Alopecia: A Comprehensive Review. Skin Appendage Disorders. 9(6). 423-437. Available at: https://doi.org/10.1159/0000531890 |
| ↑7 | Asad, N., Naseer, M., Ghafoor, R. (2024). Efficacy of Topical Finasteride 0.25% with Minoxidil 5% versus Topical Minoxidil 5% Alone in Treatment of Male Pattern Androgenic Alopecia. Journal of Drugs in Dermatology. 23(11). 1003-1008. Available at: https://doi.org/10.36849/JDD.7826 |
| ↑8 | Fabbrocini, G., Cantelli, M., Masara, A., Annunziata, M.C., Marasca, C., Cacciapuoti, S. (2018). Female pattern hair loss: A clinical, pathophysiologic, and therapeutic review. International Journal of Women’s Dermatology. 4(4). 203-211. Available at: https://doi.org/10.1016/j.ijwd.2018.05.001 |
| ↑9 | Aksenenko, M., Palkina, N., Komina, A., Ruksha, T. (2019). MiR-92a-1-5p and miR-328-3p Are Up-Regulated in Skin of Female Pattern Hair Loss Patients. Annals of Dermatology. 31(2). 256-259. Available at: https://doi.org/10.5021/ad.2019.31.2.256 |
| ↑10 | van Zuuren, E.J., Fedorowicz, Z., Schoones, J. (2016). Interventions for female pattern hair loss. Cochrane Database of Systematic Reviews. 2016(5). CD007628. Available at: https://doi.org/10.1002/14651858.CD007628.pub4 |
| ↑11 | Sattur, S.S., Sattur, I.S. (2021). Pharmacological Management of Pattern Hair Loss. Indian Journal of Plastic Surgery. 54(4). 422-434. Available at: https://doi.org/10.1055/s-0041-1739254 |
| ↑12 | Ghonemy, S., Alarawi, A., Bessar, H. (2021). Efficacy and safety of a new 10% topical minoxidil versus 5% topical minoxidil and placebo in the treatment of male androgenetic alopecia: a trichoscopic evaluation. Journal of Dermatological Treatment. 32(2). 236-241. Available at: https://doi.org/10.1080/09546634.2019.1654070 |
| ↑13 | Nohria, A., Desai, D., Sikora, M., Mandal, S., Shapiro, J., Lo Sicco, K. (2024). Combating “dread shed”: The impact of overlapping topical and oral minoxidil on temporary hair shedding during oral minoxidil initiation. JAAD International. 15. 220-224. Available at: https://doi.org/10.1016/j.jdin.2024.03.005 |
| ↑14 | Amit, K., Mansukh, G., Satyaprakash, M., Dhiraj, D., Hanmant, B. (2023). Real-World Effectiveness, Safety, and Tolerability of Cetosomal Minoxidil 5% Alone and a Fixed Drug Combination of Cetosomal Minoxidil 5% With Finasteride 0.1% in the Management of Androgenetic Alopecia (Inbilt Study). Cureus. 15(7). E41681. Available at: https://doi.org/10.7759/cureus.41681 |
| ↑15, ↑16 | Katz, H.I., Hien, N.T., Prawer, S.E., Goldman, S.J. (1987). Long-term efficacy of topical minoxidil in male pattern baldness. Journal of the American Academy of Dermatology. 16(3). 711-718. Available at: https://doi.org/10.1016/s0190-9622(87)70092-9 |
| ↑17 | Messenger, A.G., Rundegren, J. (2004). Minoxidil: mechanisms of action on hair growth. British Journal of Dermatology. 2(1). 186-194. Available at: https://doi.org/https://doi.org/10.1111/j.1365-2133.2004.05785.x |
| ↑18 | Hoover E, Alhajj M, Flores JL. Physiology, Hair. [Updated 2023 Jul 30]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK499948/ (Accessed: November 2025) |
| ↑19 | 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 |
| ↑20 | Tripathee, S., Benyovszky, A., Devbhandari, R., Quiza, K., Boris, J. (2024). A Very Bad Hair Day: Minoxidil Ingestion Causing Shock and Heart Failure. Cureus. 16(8). E66039. Available at: https://doi.org/10.7759/cureus.66039 |
| ↑21 | Junge, A., Jic-Hoesli, S.R., Bossart, S., Simon, D., de Viragh, P., Hunger, R.E., Heidemeye, K., Seyed Jafari, S.M. (2025). Contact Dermatitis Caused by Topical Minoxidil: Allergy or Just Irritation. Acta Dermato-Venereologica. 105. 42401. Available at: https://doi.org/10.2340/actadv.v105.42401 |