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Is hair loss treatment lifelong? It can be daunting to think that’s the case, as it seems quite a commitment. But while it’s true for most cases of androgenic alopecia, lifelong hair loss treatment may not be as scary as it seems. In this article, we will delve into the effects of stopping hair loss treatments and how a shift in perspective can improve how we feel about “lifelong” hair loss treatments. 

Is Hair Loss Treatment Lifelong?

The short answer is yes: hair loss treatments must be continued, or results gained will be lost. This is at least true for most cases of androgenic alopecia (more on this below). The longer answer is that:

• This isn’t true for all hair loss cases. There are plenty of situations where hair loss treatments are only temporary, as the hair regrowth sustains even after quitting. It depends on the type(s) of hair loss.
• “Lifelong” treatments aren’t as scary as they seem. The fact that some treatments might require a lifelong commitment should never be a reason not to try that same treatment, at least today.

Let’s first look at what we know about what happens when you quit a hair loss treatment.

What Happens if I Quit a Hair Loss Treatment?

Luckily, some studies explain what happens when you quit traditional hair loss treatments like minoxidil and finasteride. There is even a study looking at what happens if you stop microneedling.

What Happens if I Quit Minoxidil?

In 1999, a study explored the implications of discontinuing minoxidil after long-term use. The study yielded intriguing results, as the group that ceased minoxidil treatment observed a period of increased hair shedding and a temporary drop in hair counts, falling below their pre-treatment levels.

Four groups of 9 men with AGA were followed over two years, with each group receiving either 2% minoxidil, 5% minoxidil, a placebo, or no treatment. The 2% and 5% minoxidil groups displayed a notable increase in hair counts after three months, which reached a plateau but remained higher than those observed in the placebo and control groups.

Approximately two years into the study, at the 96-week mark, the individuals in the 2% and 5% minoxidil groups stopped their treatments. This discontinuation is evident in the data related to hair weights, which began to decline shortly afterward (see Figure 1). Three months later, around week 108, their hair loss had fallen well below the levels seen in the placebo group, even dipping below their initial hair counts. However, by week 120, three months later, the 2% and 5% minoxidil groups had rebounded and returned to a level comparable to their baseline hair counts before the study began.

It should be noted that any excess hair shedding experienced during this transition phase is usually not a permanent condition. With time, the hair adjusts to a new equilibrium without the presence of the drug, and excessive shedding should subside, returning to pre-treatment levels.

What Happens if I Quit Finasteride?

The informational insert for Propecia, a finasteride brand, indicates that hair loss typically resumes within 3 to 12 months after stopping the medication, and hair counts may revert to pre-treatment levels. This conclusion is grounded in the results from Phase II and III clinical trials, which were crucial for the FDA’s approval of finasteride for treating androgenic alopecia.

In these trials, a subset of participants received finasteride for an entire year. Subsequently, they were unknowingly switched to a group that received a placebo (a sugar pill) during the second year, corresponding to months 12-24 of the study. The researchers closely monitored and documented changes in hair counts for these participants from the start (month 0) throughout 24 months. They then compared these changes with those who continued using finasteride throughout the study and those who consistently received the placebo.^[2]Kaufman, K.D., Olsen, E.A., Whiting, D., Savin, R., DeVillez, R., Bergfeld, W., Price, V.H., van Neste, D., Roberts, J.L., Hordinsky, M., Shapiro, J., Binkowitz, B., Gormley, G.J. (1998). Finasteride … Continue reading

What the Findings Say

The study revealed that ceasing finasteride and switching to placebo resulted in hair counts falling back to their initial levels, or even slightly below, within 12 months after stopping the medication (Figure 2).

However, there are also interesting studies that can provide information about taking a break from finasteride.

Biological Effects of Finasteride After Quitting

Because finasteride has a terminal half-life of 5-7 hours, and it takes about 4-5 days for the drug to fully dissociate from tissues, its biological effects on hormone profiles can persist for approximately 30 days after discontinuation.

In practical terms, this means finasteride can continue to have a therapeutic impact in reducing scalp levels of dihydrotestosterone (DHT) even several weeks after discontinuing the medication (see Figure 3).

Exploring Alternative Finasteride Dosing Schedules

A study investigated whether a daily dose of 1 mg was necessary to maintain hair regrowth. Initially, a group of men was placed on a daily 1 mg finasteride regimen for a year. In the second year, the men were divided into two groups: one continued to take finasteride daily, while the other group adopted a 30-days-on, 30-days-off dosing schedule.^[5]Kim, K.H., Park, S.M., Lee, Y.J., Sim, W.Y., Lew, B.L. (2020). Similar efficacy of maintenance treatment of finasteride 1 mg every other month compared with finasteride 1 mg daily in Korean men with … Continue reading

The second group used finasteride for only half the time (i.e., 6 months as opposed to 12 months), yet both groups experienced similar improvements in hair parameters during the second year.

The underlying hypothesis for this result was that finasteride’s pharmacokinetics might allow for dosing schedules that alternate monthly. This approach could potentially accommodate those who wish to reduce their drug exposure or take breaks from the medication without significantly compromising their hair gains.

What If I Need To Stop Taking Finasteride For Any Other Reason?

When pausing finasteride use for an extended period exceeding 30 days, there is a higher risk of hair loss resuming due to the dissipation of the drug’s effects on scalp DHT levels. Both clinical withdrawal studies and anecdotal reports from finasteride users support this phenomenon.

Hair loss may not immediately return for many individuals but might become noticeable around the second or third month after quitting. To maintain the benefits of the drug on hair health, it is advisable to keep the withdrawal period beyond 30 days as short as possible.

If you want to learn more about the pharmacokinetics of finasteride and how you can maximize your treatment usage, you can follow these links:

• Finasteride: How Long Does It Stay In The Bloodstream?
• Finasteride: How Long Does It Stay Active in Scalp Tissue?
• What Happens If I Stop Using Finasteride?

What Happens if I Quit Microneedling?

Currently, there is only one clinical study evaluating the effects of microneedling cessation. This study compared the effects of using minoxidil only, microneedling only, and using both minoxidil and microneedling together.^[6]Bao, L., Zong, H., Fang, S., Zheng, L.i, Y. (2022). Randomized trial of electrodynamic microneedling combined with 5% minoxidil topical solution for treating androgenetic alopecia in Chinese males … Continue reading

The study involved 71 male participants with androgenetic alopecia (AGA), divided into three distinct treatment groups:

1. 5% minoxidil applied twice daily for 24 weeks (23 participants).
2. Microneedling sessions were conducted every 3 weeks, totaling 8 treatments (23 participants).
3. A combination of both treatments over 24 weeks (25 participants).

The researchers assessed changes in hair density and diameter at three-week intervals and conducted a six-month follow-up after the final treatment.

What the Findings Say

All groups exhibited significant increases in non-vellus hair density three weeks post-treatment. Notably, the combination group showed the most substantial increase in non-vellus hair density (56.45±7.82 roots per cm²), outperforming the ~28 increase in the minoxidil group and ~32 in the microneedling group.

These findings align with earlier research, particularly a paper by Dhurat et al., highlighting microneedling’s role in enhancing minoxidil’s effectiveness.

Six-Month Follow-Up Insights

Six months after the completion of the treatments, the study revealed intriguing long-term effects:

• In the minoxidil-only group, 90% of participants lost all newly acquired hair within six months post-treatment cessation, a finding consistent with previous minoxidil research.
• Conversely, in both the microneedling-only and the combination groups, 70% of participants retained some new hair, and 20% maintained all new hair growth (referenced in Figure 4).

Figure 4 illustrates the comparative hair regrowth across the three groups during the initial 24 weeks of treatment and the subsequent 24 weeks post-treatment.

These results suggest that microneedling, alone and in combination with minoxidil, offers more durable effects on hair maintenance, even after treatment discontinuation. The sustained impact in the combination group also indicates that microneedling may enhance minoxidil’s long-term effectiveness.

In summary, while managing hair loss often requires lifelong treatment, there are instances where benefits can continue even after the cessation of certain therapies. Studies have shown that minoxidil and finasteride necessitate ongoing use to maintain hair growth, as discontinuation can reverse benefits. However, treatments such as microneedling, alone or in combination with minoxidil, have demonstrated more enduring effects, offering sustained hair maintenance even after stopping the treatment.

How Can We Change Our Mindset About “Lifelong” Hair Loss Treatments?

Changing our mindset about lifelong hair loss treatment involves embracing it as a part of routine self-care, much like daily exercise or a balanced diet. It’s about viewing these treatments not as burdensome but as an empowering step toward self-confidence and well-being. Recognizing that consistency is key to success, we can integrate these treatments into our daily routines.

Let’s take a look at some ways that we can improve our mindset about long-term treatment.

1. Let hair care become part of a daily self-care routine.

Taking care of our hair is important to our overall health and well-being. We all have a daily skincare routine to maintain our skin’s health and appearance, and we can apply the same principles to our hair care routine.

Hair loss treatments should be viewed as a constructive practice that can help preserve and enhance our natural features. Whether we choose to use topical solutions, medications, or nutritional supplements, these treatments can help us maintain the health and vitality of our hair.

By adopting this mindset, we can reframe hair loss treatment as a positive and nurturing practice that empowers us to take control of our hair’s health, just like how we care for our skin, caring for our hair can be a normal and rewarding part of our daily wellness routine.

Another perspective:

2. Starting treatment today does not mean committing to that treatment forever.

Research shows that when someone quits treatment, their hair loss will resume. Within several months, their hair will return to its state before treatment. As you can see above, minoxidil users typically experience a loss of gains within 3-6 months, with an initial excess shedding period and then a return to baseline. For finasteride users, that timeframe is often 6-12 months (or longer), and quitting microneedling can take over 6 months to lose hair gains. 

Importantly, those same studies show people are never worse off after starting and then quitting hair loss treatments. 

This is critical because it means there is little risk when trying a hair loss treatment and later withdrawing it. By doing so, hair loss is not accelerated; it simply returns to baseline after quitting. In effect, the time spent on the treatment has slowed the progress of future hair loss.

It’s significantly easier to arrest the progression of hair loss than to regrow hair. That means that when fighting hair loss, time is of the essence. We speak about this in our treatment mistakes video series, which is available for members, particularly in the videos about balding speeds.

As such, trying a treatment today does not require a lifelong commitment to that treatment. Just by giving that treatment a shot, the rate of hair loss potentially slows down. If a decision is made later to quit or taper away from that treatment, the data strongly suggest that your efforts should never make things worse in the long-run.

Do Any Hair Loss Treatments Work Permanently, Even After Quitting Them?

For some cases of telogen effluvium and alopecia areata, yes. There may be conditional situations where this might be true for scarring alopecias.

For cases of androgenic alopecia, the clinical data suggests hair loss treatments need to be lifelong. Some studies have indicated that adding microneedling to minoxidil might enhance the staying power of minoxidil’s hair gains by several months,  even 6+ months after quitting both interventions.

We talk about these phenomena in this video. Remember that the data are preliminary, so don’t quit any treatments because of that study. 

So, why not take action now and begin a regrowth protocol to put yourself in the best possible future position? Any progress made will, at the very least, slow down the progression of hair loss over time, providing benefits even without a lifelong commitment to treatment.

When it comes to microneedling vs. platelet-rich plasma, which is better? Dermatologists often recommend platelet-rich plasma therapy (PRP) as a treatment for hair loss. This autologous therapy evokes the body’s natural healing response, as does microneedling. We look at what the research studies say about the effectiveness of these two treatments. Time and cost factors are also important considerations for most people.

What is Microneedling?

Microneedling, a minimally invasive cosmetic procedure, has emerged as a promising treatment for various forms of hair loss, including androgenic alopecia (AGA). This technique involves using specialized devices, like rollers of pens, equipped with fine needles to create controlled micro-injuries on the scalp.

These micro-injuries stimulate the body’s natural wound-healing processes, enhancing blood flow and promoting the release of growth factors essential for hair regeneration. This method not only improves hair density and thickness but also increases the efficacy of topical hair growth products by facilitating deeper penetration into the scalp.^[1]Dhurat, R., Sukesh, M.S., Avhad, G., Dandale, A., Pal, A., Pund, P. (2013). A Randomized Evaluator Blinded Study of Effect of Microneedling in Androgenetic Alopecia: A Pilot Study. International … Continue reading,^[2]English, R.S., Ruiz, S., DoAmaral, P. (2021). Microneedling and Its Use in Hair Loss Disorders: A Systematic Review. Dermatology and Therapy. 12. 41-60. Available at: … Continue reading

What is Platelet-Rich Plasma Therapy?

Platelet-rich plasma (PRP) therapy is increasingly recognized as an effective treatment for hair loss, particularly AGA. This procedure involves drawing a patient’s blood, processing it to concentrate platelets and growth factors, and injecting this enriched plasma into the scalp.

PRP therapy stimulates hair follicles, promotes new hair growth, and enhances hair density and thickness. The growth factors and proteins in PRP promote tissue repair and regeneration, making it a promising non-surgical option for hair loss. Clinical studies have also demonstrated the efficacy of PRP in improving hair count and thickness in individuals with hair loss.^[3]Gentile, P., Garcovich, S., Bielli, A., Scioli, M.G., Orlandi, A., Cervelli, V. (2015). The Effect of Platelet-Rich Plasma in Hair Regrowth: A Randomized Placebo-Controlled Trial. Stem Cells … Continue reading,^[4]Cervantes, J., Perper, M., Wong, L.L., Eber, A. E., Fricke, A.C.V., Wikramanayake, T.C., Jiminez, J.J. (2018). Effectiveness of Platelet-Rich Plasma for Androgenetic Alopecia: A Review of the … Continue reading

Microneedling vs. PRP: Which Is Better?

When hair loss patients visit dermatologists for advice, it’s not uncommon for those physicians to recommend autologous therapies. These hair loss therapies, such as platelet-rich plasma (PRP) therapy, PRP + Acell, adipose-derived stem cells, exosomes, and others, are derived from our tissues. These treatments must be conducted in a clinical setting and administered by a healthcare professional. While there is scientific evidence behind these therapies, it is also a significant cash cow for dermatologists, so it is no surprise that they recommend this treatment.

What these dermatologists won’t tell patients is that there is an alternative to PRP that:

1. Can be administered at home
2. Leverages the exact same mechanisms of action as PRP
3. Costs just a fraction of the price (usually 0.1% of the cost of a single PRP session)
4. Might be just as effective as PRP

That alternative is microneedling.

What Does the Clinical Evidence Say?

Two randomized, blinded, controlled clinical trials indicate that microneedling produces the same hair parameter improvements as PRP. Let’s take a closer look at these studies and determine if PRP has any benefits over microneedling.

Study 1 – Split Scalp Study Comparing Microneedling Alone to Microneedling with PRP

This one-year-long study included 30 male patients with varying degrees of androgenic alopecia. Each participant received treatments on different halves of their scalp – one half received microneedling only, and the other half of the scalp received microneedling and PRP together. The treatments were conducted over four months, with a follow-up evaluation three months after the final session. The effectiveness was measured using dermoscopic microphotographs and patient satisfaction scores.^[5]Aggarwal K, Gupta S, Jangra RS, Mahendra A, Yadav A, Sharma A. Dermoscopic Assessment of Microneedling Alone versus Microneedling with Platelet-Rich Plasma in Cases of Male Pattern Alopecia: A … Continue reading

The Results

• Hair Thickness and Density: Both treatments significantly improved hair thickness and density. The microneedling-only group nearly doubled the increase in hair thickness compared to the microneedling and PRP groups, though the difference between the groups was not statistically significant (Figure 1).
• Patient Satisfaction: Most patients reported moderate satisfaction with the treatment outcomes, noting reduced hair loss but not necessarily new hair growth.
• Long-Term Effects: A follow-up revealed that some patients experienced a recurrence of hair loss, indicating the need for ongoing or maintenance treatments.

The Conclusion

Both microneedling and PRP can effectively treat androgenic alopecia and improve hair parameters and patient satisfaction. However, adding PRP to microneedling did not show any significant additional benefits over microneedling alone.

Study 2 – PRP Compared to Saline Injection

Another study was conducted with 26 women with female pattern hair loss. The women were randomly assigned to receive either 10 mL of PRP or a normal saline placebo. The study’s primary endpoints were hair count and hair mass index (HMI), measured at baseline and after 26 weeks. Additionally, a patient survey was conducted to gauge personal perceptions of treatment effectiveness.^[7]Puig CJ, Reese R, Peters M. Double-Blind, Placebo-Controlled Pilot Study on the Use of Platelet-Rich Plasma in Women With Female Androgenetic Alopecia. Dermatol Surg. 2016 Nov;42(11):1243-1247. Doi: … Continue reading

The Results

• Hair Count and Mass: There was no statistically significant difference between the PRP and placebo groups regarding hair count and HMI after 26 weeks. This suggests that the needle insertion and the subsequent acute inflammation may be the reason for the improvement in hair growth, rather than the injection and the PRP (spoiler alert, you can get the same effect from just microneedling).
• Patient Survey: A small percentage (13.3%) of the treatment group reported substantial improvement in aspects like hair loss rate, hair thickness, and ease of hair management compared to the placebo group. However, these subjective improvements did not align with the objective measurements of hair count and HMI.

The Conclusion

This study, despite being well-designed, did not demonstrate a significant advantage of PRP over placebo in treating female androgenetic alopecia. The findings suggest that further research is needed to fully understand the role of PRP in hair loss treatment, including the possible contribution of the injection process beyond the growth factors in PRP.

So, it’s not looking great for PRP compared to microneedling. But are there any other redeeming qualities?

What About the Cost?

We know that PRP can improve hair loss outcomes, but it does not appear to be any more effective than microneedling. So does the cost make it more appealing?

No.

PRP is several times more expensive than microneedling. Let’s break it down a bit.

Microneedling Cost-Benefit

Let’s start with the costs:

• Initial investment: A microneedling device (roller or pen) can range from $10 – $200 for at-home devices.
• Replacement costs: Needles or cartridges, if applicable.
• Maintenance: Limited to cleaning and sterilizing the device.

Now, let’s see the benefits:

• Effectiveness: Proven to improve hair thickness and density in several studies.
• Convenience: This can be done at home.
• One-time cost: Mostly just the initial investment; very low ongoing costs.

Platelet-Rich Plasma Cost-Benefit

Costs:

• Per Session Cost: Each PRP session can range from $400 – $1300, depending on material quality and where you go.
• Annual cost: $1500 – $10,000 (assuming 3-4 sessions)
• Frequency: Initially, multiple sessions are needed, often 3-4 per year
• Maintenance: Every 6 – 12 months after the initial treatment to maintain hair regrowth.

Benefits:

• Effectiveness: Clinical studies show that it can stimulate hair growth and increase hair density (though microneedling can produce the same results).
• Professional Supervision: Performed by medical professionals, offering expertise and safety.

Based on the above information, it’s safe to say that you get more for your money with microneedling, given its effectiveness and significantly lower costs.

What About the Convenience / Ease of Use?

Several key differences become apparent when comparing the convenience and ease of use between microneedling and PRP.

Microneedling

Microneedling is notably convenient, especially with at-home devices. It allows individuals to perform the treatment at their own pace and in the comfort of their own homes, eliminating the need for frequent clinic visits. Furthermore, these devices are relatively straightforward to use. After an initial learning curve, users can quickly integrate the treatment into their routine. These sessions can also be relatively quick, often taking less than 10 minutes, and can be easily scheduled around personal routines and commitments.

If you want to learn more about integrating microneedling into your routine, look at our Ultimate Guide here.

Platelet-Rich Plasma

PRP therapy, on the other hand, is less convenient compared to microneedling due to the necessity of visiting a clinic or a healthcare provider for each session. This requires scheduling appointments, possibly taking time off work, and traveling to the clinic.

It is also not a self-administered treatment. It requires a skilled medical professional to draw the blood, process it to concentrate the platelets and inject it into the scalp. The process is more complex and clinical compared to miconeedling. Moreover, each PRP session, including preparation and treatment, takes longer than a typical microneedling session (treatment alone can take ~1 hour!), and the need to schedule and attend clinic appointments adds to the time commitment.

Overview Comparing Microneedling and PRP Therapy

Take a look at this overview table that we’ve created to get a quick comparison between the two treatments.

Criteria	Microneedling	PRP Therapy
Effectiveness	Similar improvements in hair count and thickness in comparative studies.
Cost per Session	Relatively low; cost primarily involves the purchasing of a microneedling device. This can range from less than $10 for a derma roller to ~$80+ for a derma pen. If you want an aesthetician to do it for you, it can cost $50 – $150 per session.	Higher. It involves the cost of blood draws, processing, and injections per session. The cost of just one injection can range anywhere from $400 – $1300, depending on the materials’ quality and where you go for treatment.
Total Cost for Treatment	There is a one-time cost for the device, which can be reused multiple times.	Treatments (3-4 rounds) could cost $1500 – $10,000.
Session Frequency	It can vary; typically, once a week to once every few weeks.	Every 4-6 weeks for the first 3-4 months, then maintenance treatments every 6- 12 months.
Ease-of-Use/Convenience	You can perform it at home but must learn the proper technique.	A healthcare professional must perform it in a clinical setting.
Recovery Time/Side Effects	Minimal; may include temporary redness or irritation.	Minimal; may include scalp tenderness, swelling, or mild pain at the injection sites.
Longevity of Results	Long-term consistent use is required for sustained results – however, some benefits may be retained even after the stoppage of treatment.	Periodic maintenance sessions are needed for sustained results.

In addition to saving time and money (which can amount to tens of thousands of dollars), it’s important to be cautious when following a dermatologist’s recommendation for PRP or any other autologous hair growth therapy. Instead, when weighing the options between microneedling and PRP, it may be wise to consider the benefits of microneedling.

How Does Microneedling Improve Hair Growth?

Microneedling is not just a superficial treatment; it has the ability to enhance hair growth by stimulating biological responses within the skin’s layers. This process involves the stimulation of the scalp at different depths, which activates a cascade of healing and rejuvenating mechanisms that are crucial for promoting healthier and thicker hair. Microneedling may contribute to hair regrowth by enhancing the effectiveness of topical treatments and stimulating the body’s natural healing processes. Let’s explore in more detail how microneedling can help with hair regrowth.

Enhances Drug Penetration

At shorter needle lengths (0.25 mm to 5 mm), microneedling can enhance the absorption and penetration of topical hair growth products such as minoxidil. By creating microchannels in the scalp, microneedling facilitates the delivery of these products to hair follicles, potentially maximizing their effectiveness. However, these needle lengths likely won’t evoke the growth factors necessary to encourage hair follicle proliferation.

Induces Growth Factor and Protein Secretion

At longer needle depths (1.5 mm to 2.5 mm), microneedling punctures the vascular networks in the dermis, which induces the release of growth factors and proteins. The body perceives these micro-injuries as wounds and activates an acute inflammatory response. Inflammation is a natural defense mechanism that recruits various cells and molecules to the injured site.

As part of this inflammatory wound-healing process, platelets in the blood release growth factors such as platelet-derived growth factor (PDGF), transforming growth factor-beta (TGF-β), and fibroblast growth factor (FGF). These growth factors are crucial in signaling nearby cells, including fibroblasts and keratinocytes. They stimulate these cells to migrate to the wounded area and begin tissue repair.

Fibroblasts in the scalp’s dermal layer (more on this below) respond to these growth factors by producing collagen and other proteins. Collagen is essential for the structural support of tissues, and it contributes to the overall health and strength of hair follicles.

Stimulates Bulge Stem Cells

Another aspect of the wound healing response is the activation of bulge stem cells. The bulge is a region located in the outer root sheath of the hair follicle, just below the sebaceous gland (Figure 2). It’s recognized as a niche for adult stem cells, essential for the regeneration and growth of hair follicles. These bulge stem cells can give rise to the various cell types that form the hair shaft and its surrounding structures. Activation of these cells is important for hair cycle progression and repair after injury.

(May) Promote Angiogenesis

Another suspected mechanism of microneedling is tissue remodeling, particularly in the form of angiogenesis: the formation of new blood vessel networks. The micro-injuries sustained during microneedling might stimulate increased blood circulation to the treated area, along with growth factors which, over a number of repeated sessions, might help grow new blood vessels in the microvascular networks supporting thinning hair follicles.. This increase in blood flow might deliver more essential nutrients and oxygen to hair follicles, which might improve their growth.

Note: microneedling-induced angiogenesis has been demonstrated in mouse models. However, it has not (yet) been demonstrated in human scalps – because the studies haven’t yet been conducted.^[5]https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5064188/ It’s suspected that repeated microneedling would also promote angiogenesis in human scalps. However, confirming this would require invasive and repeated biopsies from humans pre- and post-microneedling, which acts as a deterrent for human study. As more research is published, we’ll update this article.

(May) Reduce Scalp Fibrosis

Another suspected effect from microneedling is the potential reduction of scalp fibrosis or scarring, a common feature in individuals with AGA. Scalp fibrosis can hinder hair follicle function and might even drive aspects of hair follicle miniaturization. Microneedling has shown promise in breaking down scar tissue (for example, in acne patients). It’s not unreasonable to assume a similar histological effect might also occur in the scalp, and potentially promote a healthier scalp environment for hair growth. As is the case with angiogenesis, as research develops, we’ll update this article.

How is Microneedling Applied?

CB-03-01, also known as Breezula™ or clascoterone, is a topical medication generating interest as a potential therapy for androgenetic alopecia (AGA). It was developed by Cassiopea (now owned by Cosmo Pharmaceuticals) and is a synthetic androgen receptor antagonist. While it is primarily recognized for its potential in combating hair loss, particularly AGA, CB-03-01 has also exhibited efficacy in treating conditions like acne, hirsutism, polycystic ovary syndrome (PCOS), and seborrheic dermatitis. In this overview, we look at whether  CB-03-01  can impact hair follicles and its potential in treating hair loss, and we will also look at CB-03-01’s safety profile and mechanism of action, drawing from clinical trials and research findings.

Key Takeaways

• Drug. CB-03-01, also known as Breezula™ or clascoterone, is a topical synthetic androgen receptor antagonist developed by Cassiopea (now owned by Cosmo Pharmaceuticals). It competes with natural androgens like dihydrotestosterone (DHT) for binding to androgen receptors, making it a promising treatment for hair loss that may be caused by androgen signaling, particularly androgenetic alopecia.
• Clinical Data. Three Phase II trials for CB-03-01 have been conducted – two for male and one for female AGA – the results of one of these trials were not published. The published studies are summarized below:
  • Study 1: A study involving 293 women aged 18-55 with AGA. Of various treatments used, a 5% formulation of CB-03-01 was the only treatment that significantly improved, and only in women under 30.^[1]Cassiopea Spa, (2021). Cassiopea SpA Announces Topline Results of Phase II Proof of Concept Trial of Clascoterone Solution for the Treatment of Androgenetic Alopecia in Females. Bloomberg. Available … Continue reading 
  • Study 2: A study involving 400 men aged 18-55 with mild to moderate AGA.  A 7.5% concentration of CB-03-01 led to statistically significant improvements in hair length and width in the treated area. All treatment groups showed relative improvement compared to the control.^[2]Cassiopea Spa, (2021). Cassiopea Announces Very Positive Phase II Twelve Months Results for Breezula® (Clascoterone) in Treating Androgenetic Alopecia Bloomberg. Available at: … Continue reading 
  • Phase III trials of CB-03-01 are expected to be completed in January 2025.
• Safety. CB-03-01 has reportedly demonstrated minimal side effects, with common issues being mild skin reactions such as scaling, redness, and itching. However, there is too little published data to make a definitive statement regarding the safety of CB-03-01.
• Evidence Quality. CB-03-01 scored 36/100 for evidence quality by our metrics.
• Best Practices. This product is not currently available at a 5% concentration for treatment of AGA. However, when available, this may be most effective when used twice daily by women with AGA under 30, based on the available data.

What is CB-03-01?

CB-03-01, known by its brand name Breezula™ or clascoterone, is a topical synthetic androgen receptor antagonist owned by Cosmo Pharmaceuticals.^[3]Cosmo, (no date). Breezula. Cosmo Pharmaceuticals Available at: https://www.cosmopharma.com/pipeline/breezula (Accessed: 17 October 2023) An androgen receptor antagonist is a substance that can interfere with or block androgen hormones from working as they normally would.^[4]Kokal, M., Mirzakhani, K., Pungsrinont, T., Baniahmad, A. (2020). Mechanisms of Androgen Receptor Agonist- and Antagonist-Mediated Cellular Senescence in Prostate Cancer. Cancers (Basel). 12(7). … Continue reading CB-03-01 is a competitive antagonist, meaning it competes with natural androgen hormones in our bodies, such as dihydrotestosterone (DHT), for binding to the androgen receptor. CB-03-01 is primarily recognized for its potential in treating hair loss, particularly androgenetic alopecia. However, it has also been used to treat acne (under the brand name Winlevi), hirsutism (excess/unwanted facial hair in women), polycystic ovary syndrome (PCOS), and seborrheic dermatitis (Figure 1).

How Does CB-03-01 Work?

The mechanism of action of CB-03-01 (clascoterone) involves its interaction with androgen receptors in the skin, particularly in hair follicles and sebaceous glands. This compound is a selective androgen receptor antagonist with a specific affinity for androgen receptors.^[6]Cosmo, (no date). Breezula. Cosmo Pharmaceuticals Available at: https://www.cosmopharma.com/pipeline/breezula (Accessed: 17 October 2023) Androgens are a group of hormones that include testosterone and dihydrotestosterone (DHT), which play a role in the development and growth of hair, but which can also contribute to conditions like androgenetic alopecia (AGA, also known as male pattern hair loss) and acne when androgen hormone activity becomes abnormal or excessive.^[7]Handelsman, D.J. (2020). Androgen Physiology, Pharmacology, Use and Misuse. Endotext [Internet]. South Dartmouth (MA). Available at: https://www.ncbi.nlm.nih.gov/books/NBK279000/ (Accessed: 17 … Continue reading

Androgens like DHT normally activate androgen receptors to mediate their biological effects. CB-03-01 interferes with the ability of androgens to activate these receptors. In the context of hair loss, reducing androgen signaling can help slow down the miniaturization of hair follicles associated with androgenetic alopecia. By reducing the impact of androgens on hair follicles, CB-03-01 may help prevent hair follicle miniaturization and hair loss.

What is the Impact of CB-03-01 on Hair Follicle Biology?

There is one in vitro (or ‘test tube’) study that we could find that looks at how CB-03-01 could affect hair follicle biology. The study looked at dermal papilla cells (DPCs), which can be thought of as the hair follicle’s signaling center and which are negatively affected by testosterone in patients with AGA. DPCs from balding scalps grow slower than those of healthy scalps. They undergo a process called premature senescence, in which cells lose their ability to divide and grow.^[8]Bahta, A.W., Farjo, N., Farjo, B., Philpott, M. Premature senescence of balding dermal papilla cells in vitro is associated with p16(INK4a) expression. Journal of Investigative Dermatology. 218(5). … Continue reading 

Firstly, the researchers wanted to show that CB-03-01 could, in principle,  interfere with androgen receptor signaling. They used an experimental tool called androgen receptor reporter cells, which are commonly used to study the activity of androgen receptors. These cells were treated with 0.4 nM testosterone in the presence or absence of CB-03-01 or finasteride. The IC₅₀ value –  the drug concentration required to give half the maximal response  – was then calculated. CB-03-01 (called clascoterone here) had an IC₅₀ of  1.55×10^-6M, compared to 2.89×10^-6 M for finasteride. As a lower IC₅₀ value indicates that a drug is more effective, the results show that clascoterone is at least as potent as finasteride in inhibiting testosterone-induced androgen receptor activity; their IC₅₀ values are in the same order of magnitude (Figure 2).^[9]Rosetter, C., Rosette, N., Mazzetti, A., Moro, L., Gerloni, M. Cortexolone 17ɑ-Proprionate (Clascoterone) is an Androgen Receptor Antagonist in Dermal Papilla Cells in Vitro. Journal of Drugs in … Continue reading 

The researchers then treated reporter cells with 200 μM DHT with or without finasteride or CB-03-01 under three conditions (Figure 3).

1. Treated with DHT plus androgen receptor inhibitor (finasteride of CB-03-01) for 24 hours (to mimic once-daily application)
2. Treated with DHT plus androgen receptor inhibitor for 12 hours, then washed off and treated with DHT alone for a further 12 hours (to mimic once daily application and examine the metabolism of the drug)
3. Treated with DHT plus androgen receptor inhibitor for 12 hours, then washed off and treated with DHT plus androgen receptor inhibitor for a further 12 hours (to mimic twice-daily application)

In conditions 1 and 3, where CB-03-01 was continuously present, AR activity was significantly inhibited. This suggests that continuous exposure to the inhibitor effectively blocks androgen receptor activity. In condition 2, where CB-03-01 was removed after 12 hours, and the cells were exposed to DHT alone, the inhibitor’s effectiveness significantly decreased. The drug’s IC₅₀ was much higher in this case. This indicates a need for a continuous presence of the inhibitor for sustained antagonism of DHT-induced AR activity. The study also found finasteride was more effective when present for 24 hours than 12 hours (Figure 3), and CB-03-01 seemed to be as effective as finasteride at a similar concentration.

 

DPCs were treated with 200 μM DHT or vehicle control (0.1% DMSO) for 24 hours. The researchers found that exposure to high levels of DHT increased the expression of the androgen receptor in healthy dermal papilla cells. This mimicked the conditions found in the balding scalp, where DHT sensitivity contributes to hair loss. Additionally, the experiment revealed that exposure to high levels of DHT significantly increased the secretion of two cytokines: Interleukin-6 (IL-6) and basic fibroblast growth factor (bFGF) by DPCs (Figure 4A & B). 

The researchers then investigated whether clascoterone (CB-03-01) could antagonize the synthesis and secretion of these cytokines. They used enzalutamide as a positive control because it also acts as an androgen receptor antagonist, competing with DHT for binding to the androgen receptor. However, it would have been more useful to compare to finasteride, which is commonly used to treat AGA.

Clascoterone was found to be more effective at reducing the secretion of IL-6 compared to enzalutamide. The IC₅₀ (the concentration at which it inhibits 50% of IL-6 secretion) for clascoterone was much lower than that of enzalutamide, indicating that clascoterone more effectively reduced the secretion of this inflammatory cytokine (Figure 4B). However, neither of the drugs had any effect on bFGF (Figure 4C). 

The researchers finally performed cell viability assays to ensure the results were not due to cell death – this is important because cell viability changes could affect cytokine secretion. These assays showed that neither clascoterone nor enzalutamide significantly affected cell viability, indicating that the results were not an artifact caused by variations in cell death (Figure 4D).

 

So, we know that CB-03-01 can effectively compete with DHT for the androgen receptor, reducing the harmful effects of the hormone. However, these experiments were conducted in cells in a dish. Let’s move on to studies conducted on human patients.

Is CB-03-01 Clinically Effective at Treating Hair Loss?

CB-03-01 has undergone three Phase II trials, which have informed the dosage for an upcoming Phase III trial that is expected to be completed in 2025.  The first Phase II trial was a proof-of-concept study conducted in 2014 with 95 males with androgenetic alopecia. However, the Phase II trial results for male AGA were not publicly disclosed or published.^[13]Clinical Trials, (2017). A Phase 2 Study to Evaluate the Safety and Efficacy of CB-03-01 Solution, a Comparator Solution and Vehicle Solution in Males with Androgenetic Alopecia. Clinical Trials. … Continue reading

The second Phase II study was another proof-of-concept study for the use of CB-03-01 in the treatment of female pattern baldness. Once again, there have yet to be fully published results. However, Bloomberg did publish a press release summarizing the main findings.^[14]Cassiopea Spa, (2021). Cassiopea SpA Announces Topline Results of Phase II Proof of Concept Trial of Clascoterone Solution for the Treatment of Androgenetic Alopecia in Females. Bloomberg. Available … Continue reading. The trial enrolled 293 women aged 18 to 55, all experiencing androgenetic alopecia (AGA). The participants were divided into groups, with each group containing 70 individuals. The trial’s main objective was to evaluate the effects of different treatments over six months, comparing them to a control group that received a placebo (vehicle) and another group that used a 2% minoxidil solution.

All participants applied their assigned treatment twice daily. The treatment groups included two concentrations of CB-03-01, specifically 5% and 7.5%. The primary outcome measurements were changes in hair count and assessing hair growth over the six months of treatment.

Interestingly, only a subgroup of women under 30 using the 5% CB-03-01 solution showed statistically significant improvements in hair count, which was unexpected. Cassiopea mentioned that they were encouraged by the data and would further analyze it to identify further subgroups. However, since female-pattern hair loss typically occurs later in life for women (in their 50s or 60s), this treatment may not be appropriate for most patients. Therefore, further research is needed to determine its broader applicability.^[15]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 

Furthermore, although the press release mentioned that some participants were treated with 2% minoxidil, there was no information on how CB-03-01 performed compared to this. This highlights the issue of using press releases instead of peer-reviewed journal articles, as important data can be omitted.

The third phase II study recruited more than 400 male participants in Germany, aged 18-55, with mild to moderate AGA. All participants applied CB-03-01 at concentrations of 2.5%, 5%, 7.5% twice daily, or 7.5% once daily. The control group applied a  vehicle solution (once- or twice daily).^[16]Cassiopea Spa, (2021). Cassiopea Announces Very Positive Phase II Twelve Months Results for Breezula® (Clascoterone) in Treating Androgenetic Alopecia Bloomberg. Available at: … Continue reading Once again, the results were only available via a press release, so while some data was present we do not know if any has been omitted. It is reported that the results showed statistically significant improvements in target area hair counts and hair growth assessment scores across all active groups compared to the vehicle control. Notably, the highest change occurred in the 7.5% twice-daily group. This group also showed the highest statistically significant improvements in hair width in the treated area.

Two Phase III studies are awaiting recruitment, with expected completion dates in January 2025.^[17]Clinical Trials, (no date). CB-03-01. NIH. Available at: https://clinicaltrials.gov/search?cond=Hair%20Loss%2FBaldness&term=CB-03-01 (Accessed: 17 October 2023)

Is CB-03-01 Safe?

According to the Bloomberg press release, treatment-emergent adverse events (TEAEs) were mostly minimal, mild, or trace and unrelated to the study drug. However, very little detail is given. The most frequently observed local skin reactions across all treatment groups were minimal to mild scaling, redness, or minimal itching.^[18]Cassiopea Spa, (2021). Cassiopea SpA Announces Topline Results of Phase II Proof of Concept Trial of Clascoterone Solution for the Treatment of Androgenetic Alopecia in Females. Bloomberg. Available … Continue reading

In a Phase III trial of CB-03-01 for patients with facial acne, TEAEs were also generally mild in severity and similar to the control. The most common were pain, dryness, hypersensitivity at the site of application, redness, contact dermatitis, and headache.^[19]Hebert, A., Thiboutot, D., Gold, L.S., Cartwright, M., Gerlonim M., Fragasso, E., Mazzetti, A. (2020). Efficacy and Safety of Topical Clascoterone Cream, 1% for Treatment in Patients with Facial … Continue reading

CB-03-01 has yet to receive FDA approval for hair loss treatment, and certainly, more information on its safety and efficacy is required. The results from the upcoming Phase III studies should provide more information.

Can I Make CB-03-01 at Home?

We want to make it clear here – we do not endorse the use of homemade CB-03-01 (or any other treatment) as there may be issues with the purity of CB-03-01 and may lead to other unintended side effects. However, some people are buying powdered CB-03-01 and making a topical solution at home. CB-03-01 powder is widely available online for research and is easy to buy. As for a vehicle, some are using ethanol, propylene glycol (PG), and diethylene glycol monoethyl ether (DEGEE) at a 1:1:1 ratio, whereas others are using ethanol and PG alone.^[20]Reddit, (2020). Anyone know how to make your own CB0301 vehicle? Reddit. Available at: https://www.reddit.com/r/tressless/comments/l5y0di/anyone_know_how_to_make_your_own_cb0301_vehicle/ (Accessed: … Continue reading According to Selleckchem, it is soluble in both dimethylsulfoxide (DMSO) and ethanol.^[21]Selleckchem, (no date). Clascoterone. Selleckchem. Available at: https://www.selleckchem.com/datasheet/clascoterone-S689601-DataSheet.html (Accessed 17 October 2023)

Is CB-03-01 for Me?

While CB-03-01 is available under the brand name Winlevi for acne at a 1% concentration, it will not be available at the 5% dosage (which seemed effective in Phase II studies) until Phase III studies have been completed and FDA approval application has begun.

However, when it is available, you may want to try this treatment if:

• You are male or female 
• You are female and 30 or under
• You have AGA (this treatment targets androgen receptors, so it will not be beneficial for those with other types of hair loss)

 

Corticosteroids are a class of steroid hormones that have emerged as a treatment against, in particular, alopecia areata and scarring alopecia. These compounds, synthesized to mimic the activity of cortisol, a hormone produced by the adrenal glands, exhibit potent anti-inflammatory and immunosuppressive properties. This makes them effective in treating hair loss conditions where inflammation or an autoimmune response plays a critical role.

However, long-term corticosteroid use is not without potential drawbacks. When overused (or used for too long), topical corticosteroids are causally linked to hormonal changes, alterations to skin pigmentation, the creation of spider veins, and even skin thinning. Some adverse effects can be permanent – with the risk of irreversibility increasing alongside the dose and duration of use. Without usage breaks and/or careful dosing guidelines, long-term users of topical corticosteroids can inadvertently disfigure their skin.

In the last two years, we’ve observed a concerning trend in the hair loss industry: big-brand telehealth companies now add low-dose corticosteroids – i.e., 1% hydrocortisone and 0.01% fluocinolone – to their prescription hair growth topicals. They’re also recommending patients apply corticosteroids to their scalps up to twice daily, forever.
These corticosteroids undoubtedly help lower scalp inflammation and may offset skin irritation from ingredients like tretinoin (retinoic acid) – which is often paired with hair growth drugs, such as minoxidil, to enhance drug activation and penetration.

But is there any evidence that twice-daily use of topical corticosteroids – applied daily, forever, and with no pulse dosing or dosing breaks – is safe? Or are these telehealth companies exposing their patients to unknown risks, gambling with their health, and selling them into short-term hair gains without considering the long-term consequences?

This article will delve into the efficacy and long-term safety of corticosteroids – particularly as a therapy for hair loss disorders. We’ll explore corticosteroids and their therapeutic role in treating hair loss. We’ll also explore considerations for dosing and duration. This is particularly important for people who might be currently using topical corticosteroids on their scalps and who don’t understand the risks they might be exposing themselves to 5-10 years into the future.

What Role Do Corticosteroids Play in Treating Alopecia?

In the context of alopecia, corticosteroids reduce inflammation and suppress the immune system’s activity around hair follicles. This action can halt the progression of hair loss and, in many cases, stimulate hair regrowth. The application of corticosteroids in hair loss treatment can vary; they can be administered topically, injected directly into the scalp, or taken orally. 

Within the class of corticosteroids are:

Glucocorticoids: such as cortisol and cortisone, influence carbohydrate, fat, and protein metabolism.^[1]Macfarlane, D.P., Forbes, S., Walker, B.R. (2008). Glucocorticoids and fatty acid metabolism in humans: fuelling fat redistribution in the metabolic syndrome. Journal of Endocrinology. 197(2), … Continue reading They are anti-inflammatory, immunosuppressive, and vasoconstrictive (narrow blood vessels). Their anti-inflammatory effects occur through inhibiting inflammatory mediators and stimulating anti-inflammatory mediators. Their immunosuppressive effects occur through direct action on immune cells.^[2]Coutinho, A.E., Chapman, K.E. (2011). The anti-inflammatory and immunosuppressive effects of glucocorticoids, recent developments, and mechanistic insights. Molecular and Cellular Endocrinology. … Continue reading 

Mineralocorticoids: such as aldosterone, regulate electrolyte and water balance. They modulate ion transport in the renal tubules of the kidneys.^[3]Yang, J., Young, M.J. (2009). The mineralocorticoid receptor and its coregulators. Journal of Molecular Endocrinology. 43(2), 53-64. Available at: https://doi.org/10.1677/JME-09-0031

How is the Potency of a Corticosteroid Decided?

There are seven potency classifications for corticosteroids, which range from Class I – super potent corticosteroids to Class VII – least potent corticosteroids.^[4]Gabros, S., Nessel, T.A., Zito, P.M. (2023) Topical Corticosteroids. In: StatPearls [Internet]. Treasure Island (FL):  StatPearls Publishing. Available from: … Continue reading This is based on several factors, including its chemical structure, formulation, and the ability of the drug to cause vasoconstriction in the skin, which is often assessed through vasoconstrictor assays.^[5]Stoughton, R.B. (1992). The vasoconstrictor assay in bioequivalence testing: practical concerns and recent developments. International Journal of Dermatology. Available at: … Continue reading These assays measure the degree of skin blanching (induction of longer-than-normal skin paleness) induced by the corticosteroid. 

What are the Benefits of Corticosteroids in Treating Alopecia?

Corticosteroids are particularly beneficial in treating alopecia areata and scarring alopecias because they modulate inflammatory and immune response pathways. High potency, medium potency, and low potency have all shown some efficacy in treating alopecia, with the highest efficacy observed with high-potency corticosteroids under occlusion.^[6]Alsantali, A. (2011). Alopecia areata: a new treatment plan. Clinical Cosmetic and Investigational Dermatology. 4, 107-115. Available at: https://doi.org/10.2147/CCID.S22767 

However, it should be noted that their maximum usage durations depend on the potency of the corticosteroid. Super potent corticosteroids have a maximum duration of 3 weeks, high and medium potency have a maximum duration of 12 weeks, and low potency have no specified limit.^[7]Stacey, S.K., Mceleney, M. (2021). Topical Corticosteroids: Choice and Application. American Family Physician. 103(6). 337-343. Available at: … Continue reading Continuing to use corticosteroids after these time points may increase the risk of experiencing adverse effects.

What Risks Are Associated with Corticosteroid Use?

Topical corticosteroids can lead to both skin-related (cutaneous) and whole-body (systemic) side effects, with risk increasing with a larger area of application and higher potency of the drug.^[8]Stacey, S.K., Mceleney, M. (2021). Topical Corticosteroids: Choice and Application. American Family Physician. 103(6). 337-343. Available at: … Continue reading 

Some common skin-related effects can include:

• Skin thinning
• Stretch marks
• Spider veins
• Easy bruising and purpura
• Delayed wound healing 
• Hyper or hypopigmentation
• Acne and rosacea like eruptions
• Hypertrichosis (increased hair growth)
• Infections or aggravation of existing infections

Long-term use may lead to whole-body (systemic) effects. These can include:

• Hypothalamus-pituitary-adrenal activity suppression (characterized by weakened immunity, anxiety, midday fatigue, difficulty sleeping, depression, and aching joints, amongst others)
• Cushingoid appearance (moon face, acne, and thin, easily bruised skin, amongst others)
• Unwanted facial skin hair in women (hirsutism) 
• Impotence
• Menstrual irregularities
• Peptic ulcer disease
• Cataracts
• Increased intraocular pressure/glaucoma
• Myopathy
• Osteoporosis
• Vertebral compression fractures​

Some patients may also experience a rebound phenomenon – although this is rare in low-potency corticosteroids.

One case study shows a patient who experienced worsening rebound after being treated with first 0.5%, then 1% of hydrocortisone, and again after a 5-day course of clobetasol butyrate and then hydrocortisone.^[9]MEDSAFE, (2013). Steroid Rebound – A Topical Issue. MEDSAFE. Available at: https://www.medsafe.govt.nz/profs/PUArticles/June2013Steroid.htm (Accessed: 12 January 2023) It only resolved 3.5 months after stopping all steroid treatments.

However, a retrospective study of 300 patients found that patients who had received hydrocortisone 0.75% and precipitated sulfur 0.5% lotion for up to 15 years for common dermatological conditions of the face showed no evidence of rebound phenomenon, steroid acne, and perioral dermatitis.^[10]Harlan, S.L. (2008). Steroid acne and rebound phenomenon. Journal of Drugs in Dermatology. 7(6). 547-550. Available at: PMID:18561585

What are the Long-Term Effects and Safety Profiles of Low Potency Corticosteroids?

There is no specified limit on the duration of use of low-potency corticosteroids. But how safe are they really? Are there any long-term studies showing that these steroids are safe to use long-term?

We’ve collated the longest studies available for several low-potency corticosteroids to help us determine this.

Corticosteroid	Study: alopecia	Study: other indication	Safety profile (adverse effects?)	References
Alclometasone dipropionate 0.05%	N/A	Applied twice daily for 21 days in 31 patients with psoriasis. A comparative study with clobetasone butyrate cream 0.5%.	No reported adverse events.	[11]Aggerwal, A., Maddin, S. (1982). Alclometasone Dipropionate in Psoriasis: A Clinical Study. Journal of International Medical Research. 10, 414-418. Available at: … Continue reading
Desonide 0.05%	N/A	Twice daily application of either desonide 0.05% hydrogel or desonide 0.05% ointment in 46 patients with mild to moderate atopic dermatitis. The study length was 4 weeks.	No reported adverse events.	[12]Trookman, N.S., Rizer, R.L. (2011). Randomized Controlled Trial of Desonide Hydrogel 0.05% versus Desonide Ointment 0.05% in the Treatment of Mild-to-moderate Atopic Dermatitis. The Journal of … Continue reading
Fluocinolone acetonide 0.01%	N/A	Once daily application for 12 months alongside hydroquinone 4% and tretinoin 0.05% in 228 patients for treating facial melasma.	Six cases of telangiectasia (spider veins), 5 mild and 1 moderate.	[13]Torok, H.M., Jones, T., Rich, P., Smith, S., Tschen, E. (2005). Hydroquinone 4%, tretinoin 0.05%, fluocinolone acetonide 0.01%: a safe and efficacious 12-month treatment for melasma. Cutis. 75(1), … Continue reading
Hydrocortisone 1%	Applied twice daily to areas of hair loss for 2 cycles of 6 weeks on and 6 weeks off for a total of 24 weeks. 42 children with alopecia areata. Hydrocortisone 1% compared to clobetasol propionate 0.05%.	Twice daily application of either hydrocortisone 1% or desonide 0.05% for 5 weeks in 113 children with mild-to-moderate atopic dermatitis. 36 children continued the study through to 6 months.	Alopecia study: 2 patients in the hydrocortisone group experienced abnormal cortisol levels, which were resolved by the end of the study. One patient showed skin atrophy, which resolved by week 6.	[14]Lenane, P., Macarthur, C., Parkin, C.P., Krafchik, B., DeGroot, J., Khambalia, A., Pope, E. (2014). Clobetasol Propionate, 0.05%, vs. Hydrocortisone, 1% for Alopecia Areata in Children. A Randomized … Continue reading,[15]Jorizzo, J., Levy, M., Lucky, A., Shavin, J., Goldberg, G., Dunlap, F., Hinds, A., Strelka, L., Baker, M., Tuley, M., Czernielewski, J.M. (1995). Multicenter trial for long-term safety and efficacy … Continue reading,[16]Salava, A., Perala, M., Pelkonen, A.S., Remitz, A., Makela. (2022). Safety of tacrolimus 0.03% and 0.1% ointments in young children with atopic dermatitis: a 36-month follow-up study. Clinical and … Continue reading,[17]Sigurgeirsson, B., Boznanski, A., Todd, G., Vertruyen, A., Schuttelaar, M.L.A., Zhu, X., Schauer, U., Qaqundah, P., Poulin, Y., Kristjansson, S., von Berg, A., Nieto, A., Boguniewicz, M., Paller, … Continue reading
		Twice daily application of 1. Hydrocortisone 1% or, if needed, hydrocortisone-17-butyrate or 2. 0.03% tacrolimus ointment for a 3-7 day course until clearance was achieved in 152 young children (aged 1-3) with eczema. 3 year follow-up.	No side effects were observed for the hydrocortisone group.
		Application (not mentioned how often) of either pimecrolimus or 1% hydrocortisone in 2418 infants with atopic dermatitis. The treatment was used at the first signs/symptoms until clearance and initiated at the first signs/symptoms of atopic dermatitis. 5-year follow-up.	1% hydrocortisone was associated with an increased incidence of fever, cough, pharyngitis, viral rash, and lower respiratory tract infection.

A number of the corticosteroids did not have any studies conducted for alopecia areata. Furthermore, several studies did not report any side effects; however, the corticosteroids were only used for 21 – 28 days in these cases. The study using fluocinolone 0.01% was the longest and was used daily for one year, with few side effects, which is promising.^[18]Torok, H.M., Jones, T., Rich, P., Smith, S., Tschen, E. (2005). Hydroquinone 4%, tretinoin 0.05%, fluocinolone acetonide 0.01%: a safe and efficacious 12-month treatment for melasma. Cutis. 75(1), … Continue reading However, the researchers claimed that there were no signs of skin atrophy or thinning, but 6 patients did experience telangiectasia (otherwise known as spider veins) – which incidentally is a sign of skin thinning.^[19]Mount Sinai, (no date), Telangiectasia. Mount Sinai. Available at: … Continue reading

The only study that used a low-potency corticosteroid to treat alopecia areata was hydrocortisone 1%. In this study, participants applied hydrocortisone 1% or clobetasol propionate 0.05% twice daily to areas of hair loss for 2 cycles of 6 weeks on and 6 weeks off for 24 weeks. During this time, there were few adverse events reported. These were abnormal cortisol levels, which were resolved before the end of the study. Furthermore,  one patient who had extensive alopecia areata showed skin atrophy, which resolved by itself in 6 weeks.^[20]Lenane, P., Macarthur, C., Parkin, C.P., Krafchik, B., DeGroot, J., Khambalia, A., Pope, E. (2014). Clobetasol Propionate, 0.05%, vs. Hydrocortisone, 1% for Alopecia Areata in Children. A Randomized … Continue reading 

Furthermore, the only two studies that did include long-term follow-up either used very short pulses of the topical corticosteroid treatment or didn’t mention how often it was used at all.

It is clear from the above table that there is a distinct lack of long-term safety data for the use of corticosteroids in dermatological conditions and hair loss conditions. However, short-term or pulsed use (in the case of hydrocortisone) showed very few, if any, adverse effects.

What Role Do Telehealth Companies Play in The Sale and Use of Corticosteroid Treatments?

Telehealth companies provide a convenient alternative to accessing personalized medication and specialized knowledge that may not be readily available in general practice. Furthermore, you can do this from home, eliminating the need for travel and spending time in waiting rooms. You can buy compounded medications from these companies, including mixtures of finasteride, minoxidil, retinoids, and corticosteroids, amongst other treatments. 

However, it appears that some telehealth companies may not be providing enough information for the typical buyer to determine how often they should be using their products that contain corticosteroids.

Some of these companies are also burying the known safety concerns of low-potency corticosteroids deep within their website navigations, while also not clearly stating these concerns upfront to prospective consumers. This strategy might help to mitigate these companies from legal actions related to non-disclosures, while at the same time, not truly informing their customers of the very real (and uncertain) risks they may face 2, 3, or 5 years into the future while using their products.

Conclusion

Short-term or pulsed use of low-potency corticosteroids might be safe and effective for hair loss conditions such as alopecia areata. However, the long-term safety of these treatments is less clear, with a distinct lack of extensive, long-term studies. The risks of long-term corticosteroid use are well-documented, which underscores the importance of careful monitoring and following medical guidance when using these treatments. While telehealth companies offer convenience and access to a range of hair loss treatments, including those containing corticosteroids, there is a gap in providing comprehensive safety information and use guidelines that align with the currently available data. This lack of information raises concerns about the potential for overuse or misuse of these products.

Finasteride is an FDA-approved medication for androgenic hair loss in men. Clinical studies suggest that 1 mg daily of finasteride can improve hair loss in 80-90% of men with androgenic alopecia (AGA) – with 5- and 10-year studies demonstrating hair maintenance in a large portion of users who continue treatment. 

As such, many consider finasteride to be the gold-standard medical therapy for AGA. 

But what happens when someone stops using finasteride? How long are hair gains preserved? When does hair loss resume? And can someone quit finasteride, but keep their hair gains by replacing finasteride with other treatments and/or therapies? 

This article explores some of the studies attempting to answer these questions.^[1]https://pubmed.ncbi.nlm.nih.gov/9777765/^[2]https://pubmed.ncbi.nlm.nih.gov/11809594/^[3]https://www.oatext.com/Long-term-(10-year)-efficacy-of-finasteride-in-523-Japanese-men-with-androgenetic-alopecia.php

What Happens If I Stop Using Finasteride?

Package inserts for the drug Propecia® (brandname finasteride) suggest that within 3-12 months of quitting finasteride, hair loss resumes and hair counts return to where they were prior to starting the drug.

But what’s the basis for this statement? In other words, where’s the scientific support?

The evidence actually comes from the original Phase II and Phase III clinical trials that granted finasteride FDA-approval for the treatment of androgenic alopecia.^[4]https://pubmed.ncbi.nlm.nih.gov/9777765/

In a subset of finasteride users, participants were given the drug for a full year, then unknowingly switched into the placebo (i.e., sugar pill) group for the second year (i.e., months 12-24).

The investigators then charted these participants’ hair count changes from months 0-24, and compared those changes to those who continued using finasteride and those who were always receiving the placebo pill.

The results: unknowingly quitting finasteride led to a return to month 0 hair counts (actually, slightly below baseline) after 12 months of discontinuance. Just see the following chart. The group labeled Fin→Pbo is the group who took finasteride for year one, and a placebo pill for year two.

This chart provides the scientific backing for the claims made within the Propecia® package insert. It’s also the reason why manufacturers of finasteride state that the drug must be used for a lifetime in order to maintain any of the hair gained and/or preserved by the drug.

What If I Stop Taking Finasteride Temporarily?

Under some circumstances, it is possible to stop taking finasteride temporarily, and without losing much (or any) hair. This is because there is a delay between the time at which finasteride is discontinued and when hair loss resumes.

The reason for this delay is because of the way finasteride behaves in the body – i.e., the drug’s pharmacokinetics. More specifically, finasteride’s metabolism and timing of effects on the body depend on factors such as its:

• Terminal half-life
• Biological half-life
• Tissue dissociation timings

For a deep-dive into these topics, see these articles.

• Finasteride: How Long Does It Stay In The Bloodstream?
• Finasteride: How Long Does It Stay Active In Scalp Tissue?

Otherwise, here are the key takeaways:

1. Finasteride’s biological effects can last up to 30 days after quitting

Due to finasteride’s terminal half-life of 5-7 hours and tissue dissociation timing of 4-5 days, the drug can actually exert biological effects on hormone profiles even up to ~30 days after quitting.

That means that finasteride can continue to therapeutically lower scalp levels of dihydrotestosterone (DHT), even for weeks after quitting the medication.

Just see this chart, which shows that even after men quit using finasteride, it still took several weeks before their serum DHT levels returned to baseline.^[5]https://academic.oup.com/jcem/article/89/5/2179/2844345

(Note: these relationships assume that finasteride reachced full tissue distribution and a steady-state plasma level commensurate with 1-5 mg of daily use over a number of weeks. For those who only took finasteride a handful of times, the drug’s effects may only take a matter of days to reverse).

2. Users can take advantage of the pharmacokinetics of finasteride to reduce drug exposure and still preserve their hair gains

Finasteride is FDA-approved for androgenic alopecia at 1 mg daily doses. However, given the pharmacokinetics of the drug, some researchers have wondered if daily dosing is necessary.

One investigation group decided to explore this by putting a group of men on 1 mg of finasteride daily for a year. But for year two, they randomized the men into two groups: one group who would continue taking finasteride every day, and the other group who would start a 30 days-on, 30 days-off dosing approach.

The researchers found that both groups achieved comparable hair parameter improvements in year two – even despite the second group only technically using finasteride for half the time (i.e., a total of 6 months versus 12 months).^[6]https://jaad.org/retrieve/pii/S0190962220319289

The hypothesis: that finasteride’s pharmacokinetics allow for dosing schedules that alternate month-to-month. For those wanting to lower their drug exposure or simply “take breaks” from the medication – for any reason – this type of dosing might allow for this to happen without sacrificing much (or any) hair gains.

What If I Stop Finasteride For Longer Than One Month?

Say you’re troubleshooting side effects, or trying to conceive, and you decide to pause your use of finasteride for longer than one month.

Under these circumstances, there is a higher likelihood of hair loss resuming versus the 30-day withdrawal window. We see this reflected clinically in the withdrawal studies on finasteride, as well as anecdotally amongst members of our membership community.

This is because after 30 days of withdrawal, the effects of finasteride on scalp DHT levels have mostly worn off. This means that scalp DHT levels return to baseline, and under these circumstances, hair loss will eventually resume.

However, for many people, the resumption of hair loss doesn’t happen immediately. While there aren’t any studies of which we’re aware that track finasteride withdrawal versus hair count changes on a month-by-month basis, we have communicated with many finasteride users who’ve consistently reported, after quitting, that hair shedding and hair loss didn’t seem to pick back up again until months 2, 3, and beyond.

Even still, if you’re considering pausing finasteride use for any reason, try to keep the window of time beyond 30 days to a minimum. In doing so, you’ll put yourself in the best possible position for drug-related hair maintenance.

What If I Quit Finasteride And Replace It With Other Treatments?

We get this question all the time, and unfortunately, there’s no good clinical data to answer this question.

Scientifically speaking, finasteride’s mechanism of action is that it suppresses scalp DHT levels low enough to allow for hair cycle normalization and the partial reversal of hair follicle miniaturization. This typically occurs only at therapeutic levels of DHT reduction, which according to clinical studies for hair regrowth, seem to require lowering scalp DHT by 60-70%.

If someone quits finasteride and replaces the drug with other treatments, the preservation of any hair gains from finasteride will, for the most part, directly depend on the ability for those “replacement treatments” to suppress DHT levels to the same degree of finasteride.

For better or for worse, finasteride is one of the best tools we have to therapeutically and safely suppress scalp DHT levels enough to generate long-lasting hair growth – even despite its risk of side effects, which seem to affect 5-15% of users trying the drug.

Therefore, for anyone considering quitting finasteride, the most important question is to understand why. Then, we can create a roadmap or action plan based on that answer. For example:

• If quitting finasteride (as a male) to start to conceive: this can be done temporarily, and without a high risk of hair loss provided that you can conceive after month one of quitting but before month three of discontinuance.
• If quitting finasteride due to side effects: there’s a good chance that those side effects can be managed or eliminated with dose titration strategies, and/or the use of topical finasteride.
• If quitting finasteride because you want to try a natural approach to treating hair loss: we recommend first adding in a natural approach alongside finasteride use, rather than quitting finasteride abruptly.
• If quitting finasteride because you no longer want to use drugs to treat hair loss: we recommend watching this video to ensure your decision isn’t rooted in cognitive dissonance or misinformation.

If quitting finasteride for any other reason, please note that there are no studies exploring outcomes for men or women who withdraw from finasteride and replace the drug with other treatments.

Having said that, the totality of evidence strongly suggests that this is not necessarily a good gamble to make – as finasteride tends to suppress DHT levels in the scalp by a far larger margin (and for a far longer time period) than natural extracts such as saw palmetto. So, your expectation should be that hair loss, in all likelihood, will slowly resume.

Even still, we have seen success stories of people transitioning off finasteride and maintaining their hair gains. While this isn’t an approach we recommend unless absolutely necessary, here are the commonalities amongst people who’ve reported success with this:

1. They multi-target their hair loss. In other words, they replace finasteride use with an array of supplements, topicals, and stimulation-based interventions that target their hair loss from multiple angles: DHT reduction, growth stimulation, angiogenesis, and more.
2. They don’t immediately withdraw from finasteride. Instead, they add in all replacement interventions alongside finasteride use – and for at least 9-12 months. This allows for any potential synergies to occur between finasteride use and other therapies. Then, after achieving a new level of hair regrowth, they slowly wean away from finasteride via strategies such as topical finasteride and every-other-month oral dosing followed by titration – until after 3-5 months, they’re no longer using finasteride at all. Under the circumstances where users start noticing more hair fall, they hop back on finasteride until things stabilize. Under the circumstances whereby hair gains are maintained, they continue their drug withdrawal.

To reiterate, this is not something we actively recommend. But for those considering doing this, we recommend the above two strategies to minimize your downside risks.

Want Help With Your Hair Loss?

We offer one-on-one support to hair loss sufferers inside our membership community. This is where you can interact directly with hair loss researchers, access our library of product reviews, use our automated tools to build yourself a personalized regrowth plan, and protect yourself from the overwhelming negativity of most online hair loss forums.

If you’re interested in learning more, you can access our membership community right here.

Otherwise, we hope this article helps you make more informed decisions about your treatment choices.

In this article, we’ll explore the science behind topical finasteride, if incidental exposure to the drug comes with a risk of harming pregnant women and/or children, and strategies you can employ starting today to minimize inadvertently exposing your household to secondary finasteride exposure – all while still preserving your hair gains from the drug.

Topical Finasteride: Benefits & Drawbacks

Finasteride is the world’s most effective FDA-approved treatment for androgenic alopecia in men. Having said that, the drug is not safe for use in children or in pregnant woman – mainly because it inhibits an enzyme that is critical for proper fetal and adolescent development.

Oral formulations of finasteride are ingested by the user, and thereby eliminate almost all possibilities of incidental drug exposure to partners or other household members of the drug user. The only exception to this is a small amount of detectable finasteride in semen, which can be absorbed by a partner during periods of unprotected intercourse – and in amounts that are considered far below danger levels (even while pregnant).^[1]https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2018472/pdf/11785276.pdf

In recent years, interest has exploded in an alternative delivery vehicle for finasteride: topical finasteride. This is because preliminary studies suggest topical finasteride can confer similar hair improvements versus the oral formulations, but also better localize the effects of the drug mainly to the scalp – thus lowering the risk of finasteride’s side effects.

Having said that, the switch to topical formulations comes alongside new risks: incidental drug exposure to partners and other members of the household. But are these risks quantifiable, and if so, how can we reduce them?

How Might Incidental Exposure To Finasteride Occur?

After applying topical finasteride, there is often a period of time – up to 30 minutes – whereby that finasteride solution has yet to fully dry onto the scalp. During this period, it’s much easier for topical finasteride to find its way onto other household surfaces or people – particularly if contact is made with the scalp.

During this window of time (when topical finasteride isn’t yet fully dried), here a few ways inadvertent exposure to topical finasteride can occur:

1. Putting your head down on a pillowcase, thereby rubbing residual finasteride onto sheets that might be shared with your partner and/or children
2. Resting your head on couch pillows and/or furniture surfaces
3. Letting your partner and/or children play with your hair

In all of these scenarios, the amount of exposure to a partner or child will be relatively small. However, with repeated daily exposure throughout critical periods of development – such as a partner’s pregnancy or a child’s adolescence – each repeated contact comes alongside a cumulative increased risk of adverse events.

While the long-term effects of repeated, residual contact by spouses and/or children from topical finasteride have not been thoroughly investigated – and likely never will be (due to the difficulties of conducting such a study) – it goes without saying that it’s within our best interests not to expose our loved ones to unnecessary risks, particularly those that come with the potential for long-long adverse effects.

Topical Finasteride: How To Minimize Incidental Exposure To Loved Ones

Fortunately, when it comes to topical finasteride, there are great science-based management strategies that should allow you to keep using the medication while also minimizing – or even eliminating – your loved ones’ risks of incidental exposure. Here are a few that might take most of the risk off the table.

1. After applying topical finasteride, avoid physical contact for ~30 minutes

Depending on the carrier agents used for topical finasteride (alcohol, propylene glycol, etc.), most topicals should fully dry within a 30-minute window after application. At this point, most of the topical finasteride will remain trapped within the dried portion of the topical.

Once this window is reached, it’s far less likely that scalp contact with pillow cases, furniture, or even a partner’s hands will lead to appreciable leeching off the scalp. So, by making this very simple change, men and women can perhaps take most of the risk away regarding incidental finasteride exposure.

2. Wash pillow cases regularly, and try to dedicate a pillowcase just for the user of finasteride

Even after letting the topical dry, some topical finasteride (albeit significantly less) will leech onto the pillowcase or wherever else you might rest your head. While the amount will be substantially smaller than if you were to rest your hand on that pillowcase before the 30-minute time window for drying is completed, there’s still some topical finasteride that will end up in those sheets.

Under these circumstances, weekly washing of pillowcases is warranted. If that’s not of interest to you or your partner, you can instead dedicate one pillowcase to the person using topical finasteride that the other partner will not use.

If that’s not enough to create peace-of-mind, you can also consider wearing a loosely-fitting shower cap to bed. Some members of our membership community do this – particularly fathers with young boys who don’t want to leave any incidental exposure risks to chance.

3. Time your application windows for when you are out-of-the-house and/or unlikely to have skin contact with household members

Topical finasteride users can dramatically reduce the cumulative exposure risk to loved ones by timing their topical applications to periods where they are (mostly) outside of the home and/or unlikely to come into skin-to-skin contact with other household members. This can be done by either:

1. Applying topical finasteride at least 30 minutes before bed, then washing it out each morning
2. Applying topical finasteride prior to leaving for work, then washing it out after arriving home

If opting for either strategy, it’s critical to let topical finasteride site in the scalp skin for at least 6-12 hours. Otherwise, the diminishment in the drug’s contact time in the scalp may begin to hinder its efficacy. Here’s why.

How Long Should Topical Finasteride Stay on the Scalp Before Washing It Out?

When topicals are applied to the skin, there are multiple stages of absorption.

• Stage #1: the drug sits on the epidermis (the outermost layer of skin). Over several hours, some of the drug will absorb into the dermis, and some will evaporate.
• Stage #2: the drug absorbs percutaneously. This is when some of the drug moves from the epidermis into the dermis, where it can begin to affect hair follicles.
• Stage #3: the drug absorbs systemically. This is when some of the drug moves from the dermis into the bloodstream, where it can have systemic effects.

So, what’s the minimum amount of time topical finasteride must be left on the scalp to have an effect? First, one needs to know how much of the drug absorbs into the dermis over time.

To answer this, there is an in vitro study measuring percutaneous absorption of topical finasteride across various formulations: ethosomes, ethanol, liposomes, and aqueous (water). ^[2]https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2977015/

Here’s a chart showing the percent of topical finasteride that percutaneously absorbs (enters the dermis) over a 24-hour period:

According to these study results, if applying hydroethanolic finasteride to the scalp, then at the 10-hour mark, ~5 ug/cm² will have been absorbed percutaneously. By hours 22-24, that absorption rises to ~8 ug/cm². That means leaving the drug on the scalp for an additional 12-14 hours before washing it off only offers an additional 3 ug/cm² of percutaneous absorption.

So, say that to minimize a partner’s exposure to finasteride means only keeping it on the scalp for 10 hours before washing it off. This begs the question: is the 5 ug/cm² of absorbed finasteride enough to therapeutically lower scalp levels of dihydrotestosterone (DHT) and regrow hair?

Topical Finasteride: How Long Does It Need To Stay In The Scalp To Be Effective?

There aren’t any clinical studies attempting to answer this question. However, a look at surrogate data can help ballpark an answer.

First, a percentage of topical finasteride will absorb into the dermis, and a smaller percentage of topical finasteride absorbed into the dermis will later absorb into the bloodstream. This means after applying topical finasteride; people can use time-dependent DHT reductions in the bloodstream to “ballpark” how much DHT is likely also getting reduced in the scalp. This is, again, because there is more topical finasteride that percutaneously absorbs than systemically absorbs.

So, for lower dosages, the effects we see in the system can be used as signals for what’s happening, at a minimum, in the scalp skin.

In that regard, see this figure from a 2014 study measuring the effects of one versus two applications of 1 mL of 0.25% topical finasteride on serum DHT levels. ^[3]https://pubmed.ncbi.nlm.nih.gov/25074865

Six hours after applying 1 mL or 2 mL applications of 0.25% topical finasteride (2.275-4.550 mg of finasteride), serum DHT reductions flatline. This means that for the 2 mL application group (the black circle with a dotted line), there was enough systemic absorption by the 6-hour mark to effectively lower serum DHT levels as much as they would normally lower with 1 mg of oral finasteride.

Keep in mind that finasteride has an upper limit for its effects on serum DHT reduction. After hitting ~70% reduction in serum DHT, more finasteride doesn’t reduce serum DHT. The same is true with scalp DHT reductions.

So, the above study shows that with topical finasteride applications of 2.275 mg or higher in a hydroxypropyl chitosan delivery vehicle, systemic reductions in DHT equal that of 1 mg of oral finasteride. And with topical finasteride, since serum DHT reductions are sort of like “canaries in the coal mine” for scalp DHT reduction, we can take an educated guess that 6-12 hours after applying topical finasteride. There’s likely enough percutaneous absorption to therapeutically lower scalp DHT levels for hair regrowth. 

This is corroborated by a 1997 study suggesting that 2 mL daily of 0.005% topical finasteride (0.0912 mg of finasteride exposure) improved hair parameters for men with AGA and without affecting serum DHT levels – even after 16 months of treatment. ^[4]https://www.tandfonline.com/doi/abs/10.3109/09546639709160517

Taken together, all of the above evidence signals that, depending on the exposure level, 6-12 hours of exposure to topical finasteride should be enough to have a therapeutic effect on scalp DHT reductions (and hair growth).

Do these time windows apply to all topical finasteride formulations?

No. Obviously, the contact time required for topical finasteride to be effective depends on a number of factors:

1. The finasteride dilution (i.e., 0.01% vs. 0.1% topical finasteride)
2. The volume of topical applied (i.e., 1 mL vs. 2 mL)
3. The topical’s carrier ingredients (i.e., hydroxypropyl chitosan vs. ethanol vs. propylene glycol vs. liposomes)
4. The frequency of application (i.e., once-daily, twice-daily, every-other-day, etc.)

Nonetheless, a 6-12 hour contact window should allow for therapeutic efficacy of many big-brand topical finasteride formulations available to consumers currently. However, if you’d like to get specific about adjustments on an individual basis, we offer that level of support inside our membership community.

Final Thoughts

For the most part, occasional incidental exposure to topical finasteride should not cause problems for household members. With that said, there are certain groups at an elevated risk – particularly pregnant women and children – and in these groups, cumulative risk over a lifetime of incidental topical finasteride exposure has yet to be studied.

If this is a concern for you, men and women can minimize the risk of incidental drug exposure from topical finasteride by doing any (or all) of the following:

1. Avoiding all physical contact with the scalp for at least 30 minutes after topical finasteride application (so that it fully dries)
2. Dedicating a pillowcase to the topical finasteride user, and washing that pillowcase weekly
3. Wearing a loosely-fitting shower cap to bed
4. Timing topical finasteride applications to 6-12 hour windows where the user is out-of-the-house and/or unlikely to come into contact with household members

Using the evidence and strategies above, our hope is that topical finasteride users can minimize or even eliminate the risk of incidental exposure, all while preserving their hair gains.

Fluridil: Scientific Deep-Dive

Fluridil, otherwise known as topilutamide (or by the brand name Eucapil) is a topical medication that has been tested as a treatment for both androgenetic hair loss and hirsutism (excess facial hair growth in women). In 2021, the patent for fluridil expired, however, there have been no generic fluridil treatments that have come to the market. Fluridil has been approved for cosmetic use in Europe but does not have FDA or EMA approval as a treatment for androgenetic alopecia. You can however buy this product on shopping websites, such as Amazon, for around $83 (at the time of writing). But is fluridil worth your money?

In this article, we will look at how Fluridil works, what the clinical evidence for it is, and whether it is safe to use.

Key Takeaways

• • Drug. Fluridil is an anti-androgenic drug that is currently on the market for the treatment of androgenetic alopecia and hirsutism. It is known to reduce the gene expression of androgens. Due to its similar structure to other anti-androgens, it’s thought to also exert its effect by binding to androgen receptors. As it readily breaks down in aqueous solutions, some researchers believe that it is safer to use than other anti-androgens, and can be applied locally without the risk of side effects on the rest of the body.
  • Clinical Data. There are only two studies that have been completed for fluridil: one on men and one on women. 
    • The first study was 9 months long and completed on 43 men with diagnosed androgenetic alopecia (AGA) aged between 20-56, in which 2mls of 2% fluridil was topically applied once nightly. Researchers found that in the first 3 months, there was a significant increase in the number of growing hairs, and a significant decrease in the number of non-growing hair, with no effects on testosterone levels or perceived sexual libido and function. Furthermore, fluridil, or its by-products, was not found to be present in the serum. Researchers also found, however, that the positive effects on the number of growing hairs/non-growing hairs did not last past the 3-month mark, and were instead maintained. A small safety study completed alongside this determined that either 2% or 4% fluridil was ok to use without adverse effects.
    • The second study was 9 months long and only completed on 11 women, 2 of which had to drop out of the study due to adverse effects from the isopropanol that the fluridil was diluted in. The participants applied 2mls of 2% fluridil, once nightly. The researchers did not find any significant change in growing or non-growing hairs, however, they did measure an increase in hair thickness. Due to the small sample size, the lack of a placebo, and the fact that every participant had taken another anti-androgenic medication within 3 months of the beginning of the study, it’s not possible to conclude whether fluridil has any effect or not for women with AGA.

• Safety. Unlike oral anti-androgenic drugs, fluridil should only work at the point of application as it should break down once it comes into contact with the blood. Additionally, across the limited parameters of both the studies mentioned above, no serious adverse effects were reported, however as both of the studies were 9 months long, with small sample sizes, we have no real information about what the long-term effects of fluridil usage may be.
• Best Practices. Based on the limited clinical data, if you decide to use fluridil, you could apply 2ml of a 2% fluridil solution in isopropanol once, at night before bed on a dry scalp (it will degrade if your hair or scalp is wet). You might be a candidate for fluridil if you are male with AGA (as the data isn’t sufficient for females with AGA), are comfortable with using a product that has very limited efficacy or safety data, have potentially seen results using other anti-androgens (such as finasteride), and don’t mind limiting hair washing to once or twice a week. If you’re interested in trying fluridil, although it’s not approved by the FDA, you can buy it on shopping sites like Amazon, and it’s possible that you may see limited results, at least over the first 3 months of usage.

What is Fluridil?

As mentioned above, fluridil is a topical treatment that has been used in studies to determine its efficacy and safety in hair loss and excessive hair growth in women (hirsutism). 

Fluridil was synthesized alongside four other compounds in a study designed to discover a novel, topical anti-androgenic compound. ^[1]Seligson, A.L., Campion, B.K., Brown, J.W., Terry, R.C., Kucerova, R., Bienova, M., Hajduch, M., Sovak, M. (2003). Development of Fluridil, a Topical Suppressor of the Androgen Receptor in … Continue reading Androgens are linked to certain types of hair loss such as androgenetic alopecia.

The researchers were also searching for a compound that rapidly degraded (broken down) into non-harmful by-products in the blood so that it does not have effects at the systemic (whole-body) level (but rather limits its activity locally to the area of application). Out of the five total compounds synthesized, the researchers determined that fluridil best fit their criteria, which are described below:

1. Down-regulation of androgen receptors

The growth of prostate cancer is often androgen receptor-dependent.^[2]Fujita, K., Nonomura, N. (2019). Role of Androgen Receptor in Prostate Cancer: A Review. The World Journal of Men’s Health. 37(3), 288-295. Available at: https://doi.org/10.5534/wjmh.180040Therefore treating prostate cancer cells in a dish can be a useful way of seeing whether drugs have any anti-androgen receptor activity. In the human prostate cancer cell line LNCaP, fluridil reduced protein expression of androgen receptors by 40% at a concentration of 3μM, and by up to 95% at a 10μM concentration (Figure 1). Whilst this was not the most effective result, (BP-521 further reduced expression), it was the combination of this and results shown further down (Figure 2) that led the researchers to choose fluridil. Additionally, these compounds were compared to two other anti-androgen drugs (bicalutamide and hydroxyflutamide) and found that they did not decrease the expression of androgen receptors, indicating an additional mechanism of action of fluridil that other anti-androgen drugs may not have.

 

2. Degradation of the compound after incubation in human serum at 38°C

Fluridil was found to be the only compound that fully degraded in human serum by 48h of incubation (Figure 2). By contrast, BP-521, the compound that showed better down-regulation of androgen receptors barely showed any degradation, so did not match the criteria set by the researchers. 

Fluridil degrades into BP-34 which – as the researchers show in Figure 1 – doesn’t have a large effect on the expression of androgen receptors. It also degrades into a perfluorocarboxylic acid (PFCA) called trifluoroacetic acid (TFA) which mammals are thought to be insensitive to. ^[4]Solomon, K., Velders, G., Wilson, S., MAdronich, S., Longstreth, J., Aucamp, P., Bornman, J. (2016). Sources, Fates, Toxicity and Risks of Trifluoroacetic Acid and its Salts: Relevance to Substances … Continue reading

The researchers state that the by-products are non-toxic and that they should be processed rapidly by the kidneys because they are ionic. Ionic substances are attracted to water molecules and undergo dissociation, where they disperse throughout the water, and can therefore be excreted in the urine.^[5]Urine pH. (no date). University of Nottingham. Available at: https://www.nottingham.ac.uk/nmp/sonet/rlos/bioproc/kidneydrug/page_six.html (Accessed: 22 January 2022)

The researchers determined that based on their criteria, fluridil was the most promising in terms of its capacity to reduce androgen expression and due to its short half-life in aqueous solutions. This study however did not look at the efficacy of fluridil in the context of hair loss, and also did not provide data that established its safety in humans.

How does Fluridil work?

Androgenetic alopecia (AGA) is a form of hair loss with causes not yet fully understood, however, it is thought to be related to either excess androgens present, or an exaggerated response to androgens such as dihydrotestosterone (DHT). It affects both men and women and is characterized by progressive loss of hair over time in a particular pattern.^[7]Ho, C.H., Sood, T., Zito, PM. (2022). Androgenetic Alopecia. StatPearls [Internet]. Treasure Island (FL). Available at: https://www.ncbi.nlm.nih.gov/books/NBK430924/. (Accessed: 22 January 2023)

Fluridil belongs to a class of drugs known as non-steroidal anti-androgens (NSAAs). NSAAs are chemicals that stop androgens (like testosterone and DHT) from binding to their receptors. This means that androgens then can’t exert their effects, as they need to bind to these receptors to initiate the signaling events that can lead to hair follicle miniaturization, amongst other things. NSAAs may also be called androgen receptor antagonists, or androgen receptor blockers.  ^[8]Iverson, P., Melezinek, I., Schmidt, A. (2002). Nonsteroidal antiandrogens: a therapeutic option for patients with advanced prostate cancer who wish to retain sexual interest and function. BJUI … Continue reading ^[9]Ustuner, E.T. (2013). Cause of Androgenic Alopecia: Crux of the Matter. Plastic and Reconstructive Surgery. Global Open. 1(7), e64. Available at: https://doi.org/10.1097/GOX.0000000000000005

Receptors are specialized proteins in cells that allow specific chemicals to bind to them. In response to the correct chemical binding to the receptor, the receptor can exert downstream effects that have an impact on biology (a process known as signal transduction).^[10]Miller, E.J., Lappin, S.L. (2022). Physiology, Cellular Receptor. StatPearls [Internet]. Treasure Island (FL). Available at: https://www.ncbi.nlm.nih.gov/books/NBK554403/#_NBK554403_pubdet_ … Continue reading Other NSAAs include flutamide and bicalutamide. 

It’s important to note that there have been no studies to determine if this is really how fluridil works. Researchers have stated that this is because of fluridil’s instability in aqueous environments (meaning it is difficult to store, handle, and therefore study). Researchers hypothesize that because its structure is similar to other NSAAs, it has a similar mechanism of action, in addition to its ability to reduce the expression of androgen receptors. ^[11]Seligson, A.L., Campion, B.K., Brown, J.W., Terry, R.C., Kucerova, R., Bienova, M., Hajduch, M., Sovak, M. (2003). Development of Fluridil, a Topical Suppressor of the Androgen Receptor in … Continue reading

So, how fluridil actually works has not been fully determined, but is there any information on if and how fluridil affects hair follicles?

How can Fluridil have an impact on hair follicles?

Other than what has been hypothesized above (fluridil may be an androgen receptor inhibitor), it is not possible to know for sure exactly how fluridil might work on the hair follicle. As mentioned, there have been no studies in cells or isolated hair follicles in a dish  (which may be due to fluridil being unstable in aqueous environments). Cells and isolated hair follicles require physiological media solutions that contain all the nutrients needed to survive and grow, creating a barrier in experimentation with this drug/to experiment with this drug.

Furthermore, the only work completed on animals was in the initial paper in which the researchers completed skin irritant tests and absorption tests, where they found that fluridil was non-irritant at a concentration of 2% (the concentration at which they sell the product, although they don’t mention whether it’s weight/volume or volume/volume) and that there was no fluridil (or its by-products) detected in rabbit serum after a 1% solution was applied twice daily for 10 days. Samples were collected at 2, 5, 21, and 48 hours after treatment and then once every other day for the next 3 days. ^[12]Seligson, A.L., Campion, B.K., Brown, J.W., Terry, R.C., Kucerova, R., Bienova, M., Hajduch, M., Sovak, M. (2003). Development of Fluridil, a Topical Suppressor of the Androgen Receptor in … Continue reading

The most important thing however is whether, in humans, fluridil actually works and is safe to use. There have been two studies using fluridil in humans diagnosed with androgenetic alopecia. So let’s see if, regardless of knowing exactly how fluridil works, it is effective at treating hair loss.

Is Fluridil effective at treating hair loss?

There are currently only two studies that look at the efficacy and safety of fluridil in humans.

Study 1

The first study was a randomized, double-blind study to determine the efficacy and safety of a topical 2% fluridil solution on 43 men between 20-56 years of age with diagnosed AGA. ^[13]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. American … Continue reading Fluridil was dissolved in isopropanol to make the solution, because of its instability in water-based liquids. The participants were randomly assigned into two groups, 23 receiving the fluridil, and 20 receiving a placebo of just isopropanol. Participants were required to apply the fluridil or the placebo solution once nightly before bed, to avoid direct sun exposure and to only wash hair a maximum of twice a week using warm water.

After 3 months, the study then became open-label (all participants knew what they were receiving) and all participants began receiving the 2% fluridil solution with a further follow-up 6 months later (so the study was a total of 9 months long).

Data was collected through:

• Phototrichogram – an area of the hair is shaved (1.1cm2) and then photographed using a digital camera. Individual hairs/follicles are counted at baseline and at specific time points throughout.
• Calculating the ratio of growing (anagen) to non-growing (telogen) hairs.
• Global scalp imaging – photographs are taken of the entire scalp for subjective comparison.
• Blood collection – for measuring serum testosterone, measuring for the presence of serum fluridil and its by-products, and determining other relevant blood chemistry values.
• Self-perception questionnaire – for sexual function and libido

Results at 3 months

After 3 months, the number of growing to non-growing hairs was compared between the placebo and fluridil groups (Figure 3). The researchers found that the percentage of anagen hairs significantly increased from the baseline in the fluridil-treated group (75.68% at 0 months – 85.09% at 3 months) and the percentage of telogen hairs significantly decreased (25.41% at 0 months -14.61% at 3 months). The placebo group, however, also showed a significant decrease in the percentage of telogen hairs, however (29.51% at 0 months – 21.87 at 3 months) as well.

When comparing the fluridil-treated group to the placebo group after 3 months of treatment, the percentage of anagen hairs was higher in the fluridil (85.09% and 77.25% respectively). Furthermore, there were fewer telogen hairs in the fluridil-treated group than in the placebo group (14.61% and 21.87% respectively). 

At this point, the researchers decided that the effects of fluridil on hair growth were significant enough to change all participants to the treated group. It would however have been useful for the researchers to have stated what percentage of participants did see a positive effect.

Results at 9 months

To keep us all on track, by the end of the 9 months, the fluridil-treated group will have been using fluridil for 9 months, and the placebo group will have used the placebo for 3 months and then fluridil for 6 months. We’ll call the placebo group the ‘former placebo’ group now.

After counting growing and non-growing hairs, the researchers found that all groups now experienced significant increases in anagen hairs, and significant reductions in telogen hairs (Figure 4).

The researchers then compared the changes in growing and non-growing hairs after 3 months and 9 months for the fluridil-treated group and found that there were no significant differences, which indicates that there may be a limit to the effect that fluridil can have on hair growth, and that this limit might be achieved only within the first 3 months. Fluridil however did appear to maintain the number of growing/non-growing hairs after that. 

Let’s have a look at before-and-after images to see if this improvement shown in the data actually correlates to a visual improvement. Unfortunately, there is only one image shown (Figure 6), and we are left to wonder if this was the best case and if the reason that the others weren’t shown was that it was more difficult to see the improvements. Furthermore, there are no photos shown of anyone from the placebo group, so we cannot compare between groups. 

Other than measuring the number of growing/non-growing hairs, serum testosterone levels were also measured. Whilst variation between participants was observed, testosterone levels remained between the physiological range of 8-35 nm/L (Figure 7). Questionnaires also determined that participants did not experience any changes to libido or sexual performance either, however, it is not stated at what time points this data was collected. This is an indication that fluridil can only affect the hair follicle without leading to the systemic side effects that other anti-androgen drugs can cause. Additionally, the researchers did not detect fluridil or its by-product BP-34 in the serum of participants, further lending credence to this hypothesis.

A separate study within the same paper was completed with 20 male participants between the ages of 18-60. Patches containing 2,4, or 6% fluridil in either isopropanol or Vaseline Intensive Care Lotion were applied once a day for 21 days (excluding weekends) to determine if fluridil caused any irritancy to the skin. Isopropanol was also given alone as a control. 2% and 4% fluridil were found to be non-irritant and non-sensitizing. 6% fluridil however caused a slight degree of macular erythema (a rash with flat discolored areas of skin and small raised bumps).

So, to summarize, the data indicates that fluridil treatment leads to more growing hairs and fewer non-growing hairs. This effect however plateaus after 3 months, with no improvement or deterioration occurring after. Fluridil doesn’t appear to affect testosterone levels (which other anti-androgen medications can), and, holding up to the claim of hydrolyzation neither fluridil nor its by-product BP-34 were found to be present in the serum of participants throughout the study. There is only one comparison photo however, and while it does look like there is an improvement, it’s not possible to know if this was just the very best case or whether other participants also experienced a similar level of improvement. Of course, the long-term effects of fluridil (beyond 9-months) are unknown.

Study 2

The second study completed by the same research group was an open study. An open study is a study in which both participants and researchers are aware of what they are using. It sought to determine the efficacy and safety of a 2% fluridil solution in isopropanol on 11 female participants, aged 22-45, with diagnosed AGA. ^[19]Kucerova, R., Bienova, M., Novotny, R., Fiuraskova, M., Hajduch, M., Sovak, M. (2006). Current Therapies of Female Androgenetic Alopecia and Use of Fluridil, a Novel Topical Antiandrogen, Scripta … Continue reading

Participants were required to massage 2 ml of the fluridil solution into their scalps once a day, in the evening. 2 women discontinued the study due to itching and reddening that developed at the site after treatment. It was determined with an allergy study that this was due to the isopropanol causing irritation, rather than a reaction to the fluridil itself.

Participants were advised to only apply the solution to a dry scalp and to limit hair washes to a maximum of 2 times a week.

In this study, all 11 participants were treated with fluridil, so there was no placebo or a no-treatment group. A placebo group is useful in clinical trials as it provides a group to compare throughout the study. The participants are also aware that they are receiving the actual treatment without a placebo, which may influence the participant’s perception of the effect of the treatment. 

Several types of data were collected, including the following methods:

• Phototrichogram
• Global scalp imaging
• Hair Diameter measurement – an area of hair shaved and 3 weeks later ~50 new hairs collected and measured using a microscope.
• Changes in hair surface – five hairs from each patient were collected and prepared for scanning electron microscopy (SEM*).
• Evaluation by a physician (using a scoring system)

• Self-evaluation by participants (using a scoring system) to determine self-perception of hair growth and quality as well as effects on libido and sexual function.
• Blood tests – to measure serum testosterone, sex hormone binding globulin, other relevant blood chemistry, and serum fluridil or its by-products.

*(SEM is a special type of microscope that produces images of a sample by scanning the surface with electrons. These interact with the atoms that make up the sample, creating a much higher resolution image than might be obtained from a light-based camera). ^[20]Scanning Electron Microscopy. (no date). Nanoscience Instruments. Available at: https://www.nanoscience.com/techniques/scanning-electron-microscopy/ (Accessed: 22 January 2023)

Results

The authors of this study stated that they only included statistically significant data and what they considered to be “otherwise remarkable observations” in their results section.

The researchers found that fluridil treatment did not significantly increase the number of growing hairs or decrease the number of non-growing hairs over the whole study period (9 months), however, there was a significant improvement in hair diameter when it was measured at the 6 months and 9-month marks compared to the baseline. Whilst there are no images included in this paper, it is mentioned that the SEM images showed no changes in the overall morphology of the hair and that after evaluating global scalp images (photos taken from the top of the head) hair appeared to be thicker.

5 out of 11 participants reported that they perceived themselves to have reduced hair loss after 6 months of treatment. 1 out of 11 participants reported that they perceived their hair to have improved quality after 6 months, with another one reporting the same after 9 months. One person observed thickening of the hair (after 9 months), one reported new undergrowth (after 6 months) and one person reported accelerated hair growth (after 3 months). Undergrowth is the growth of short, fine hairs underneath longer hair.

So, not very convincing. We have measurements of hair diameter thickening but no data showing any increase in growing hairs or reduction in non-growing hairs. Moreover, the reported ‘positive’ data is almost entirely based on subjective patient self-reporting.

The safety data however does generally follow the same results as with the previous study on men, with no patients reporting adverse side effects. 

The blood chemistry data was within normal parameters throughout the study (measured at 3, 6, and 9 months) and there was no presence of fluridil or its by-products in the serum of any of the participants.

With regards to testosterone levels and sexual hormone binding globulin (SHBG), the researchers found no statistically significant differences between measurements taken at baseline and 9 months of treatment. There were however patients with higher than the physiological range of SHBG, which has been attributed to the fact that 8 out of 9 of the final patients were taking the combined oral contraceptive pill, which is known to increase SHBG. ^[22]Amiri, M., Tehrani, F.R., Nahidi, F., Kabir, A., Azizi, F. (2018). Comparing the Effects of Combined Oral Contraceptives Containing Progestins with Low Androgenic and Antiandrogenic Activities on the … Continue reading

So, why didn’t fluridil work in the same way for women as it did for men? Well, the researchers attribute this to the fact that the participants were taking cyproterone acetate (aka Diane 35) another anti-androgen, and (in some cases) contraceptive at least 3 months previous to the study. They determined that because they were taking Diane 35, it can be assumed that there was a sufficient anti-androgenic effect being exerted and so fluridil could not provide a further effect. 

But this is just one of several other problems with this study, such as:

• Small participant number
• No placebo
• Participants had been taking medication that may interfere with the efficacy of fluridil

Overall, we cannot conclude that fluridil has any real beneficial effect for women with AGA.

Is Fluridil safe?

Within the limited parameters of the published studies, fluridil doesn’t appear to have any treatment-related side effects. Furthermore, unlike taking oral anti-androgenic medications, fluridil should work only at the point of application and not have effects anywhere else in the body, due to its ability to degrade when it comes into contact with water.

However, fluridil has not been approved by the FDA or the European Medicines Agency as an anti-androgenic medication and is only approved for use in Europe as a cosmetic. The long-term effects of using fluridil are completely unknown.

Is Fluridil for me?

You may want to try fluridil if you:

• Are male with AGA.
• Want to either maintain the current status of hair loss or see short-term improvement and then a plateau.
• Are comfortable with using a product that has no FDA or EMA approval.
• Have no issues using a product that has very little recent (or otherwise) efficacy or safety data.
• Are ok with reducing hair washing to around once or twice a week.
• Have perhaps seen positive results with other anti-androgens (such as finasteride)

Whilst the previously mentioned points (easily degradable and topical application) may prove appealing, we cannot currently recommend using fluridil until more data becomes available. If you want to take the risk, however, it is possible that you may see some limited benefits.

 

Topical minoxidil is an FDA-approved treatment for male and female pattern hair loss, also known as androgenic alopecia (AGA).

Despite its popularity, not very many people continue using topical minoxidil for the long-run. In fact, one clinical study found that by the one-year mark, 95% of topical minoxidil users voluntarily quit applying the drug – with more than 2/3rds of them citing “low effect” as their rationale.^[1]https://pubmed.ncbi.nlm.nih.gov/17917938/

So, what sort of hair regrowth can we expect from minoxidil? Why do so many people quit using the topical? And what can we do to maximize minoxidil’s hair growth-promoting effects, and in doing so, set ourselves up for sustainable hair regrowth years into the future?

What Is Minoxidil?

Topical minoxidil is the only medication approved by the FDA for the treatment of androgenic alopecia (AGA) in both males and females. Since its use as an anti-hypertensive drug in 1979, researchers have long-noted a nearly universal “adverse event” in oral minoxidil users: unexpected new hair growth along the limbs, chest, face, and scalp.^[2]https://pubmed.ncbi.nlm.nih.gov/7030707/

This led to to the reformulation of minoxidil as a topical, and subsequent clinical trials to test its efficacy on treating AGA. In 1988 and 1992, 5% and 2% minoxidil became commercial available as an over-the-counter hair growth treatment for men and women, respectively.

How Does Minoxidil Work?

Researchers aren’t totally sure how minoxidil regrows hair.

Having said that, they suspect that minoxidil may work through at least one (or all) of the following mechanisms:

• Opening potassium ion channels – which increases blood, oxygen, and nutrient transport to balding regions (i.e., increased microcirculation)
• Modulation of prostaglandin analogues (i.e., decreased inflammation)
• Anti-androgenic activity in hair follicle sites (i.e., decreased dihydrotestosterone (DHT) – the hormone causally linked to baldness).

How Much Regrowth Should We Expect From Minoxidil?

For more information on these topics, see this article: Minoxidil: How Long Do Results Last (Even After Quitting)?

In this article, we’ll explore the history of minoxidil, how it became a hair loss drug, and the debate over its mechanisms of action for hair growth.

Despite decades of study, researchers still do not know how minoxidil promotes hair growth. But they do have some ideas, and these ideas have remained the subject of significant debate – even 70 years after the discovery of the drug.

What Is Minoxidil?

Minoxidil is a drug that was originally developed in the 1950’s by Upjohn Company, which later became a part of Pfizer. In early experiments, minoxidil consistently improved vasodilation in animals, which led to human trials as a potential treatment for hypertension (i.e., high blood pressure).

In 1979, the FDA approved the use of oral minoxidil as a treatment for hypertension. But during its clinical trials and post-marketing studies, “nearly all” oral minoxidil users reported excessive hair growth as a side effect – and even the development of new hair along the face, chest, back, and scalp.^[1]https://pubmed.ncbi.nlm.nih.gov/7030707/

This led to the reformulation of minoxidil as a topical, followed by clinical studies to evaluate topical minoxidil’s effectiveness in men and women facing androgenic alopecia (AGA) – one of the world’s most common hair loss disorders.

Throughout the 1980’s, a series of clinical studies consistently demonstrated that topical minoxidil was able to improve hair counts, increase hair thickness, and reduce hair shedding in male and female hair loss sufferers. And in 1988 and 1992, topical minoxidil at 5% and 2% formulations were approved by the FDA for male and female pattern hair loss, respectively.^[2]https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6691938/

How Does Minoxidil Work?

Despite decades of study, it’s still unclear exactly how minoxidil improves hair growth.

In animal studies, topical minoxidil has been shown to shorten the telogen (rest) phase of the hair cycle and stimulate the initiation of the anagen (active) stage of the hair cycle.^[3]https://pubmed.ncbi.nlm.nih.gov/14996087/ These effects also consistently translate to humans using minoxidil (oral and topical) to treat AGA. But despite knowing what minoxidil does to most hair follicles, researchers still aren’t exactly sure of the mechanisms governing the hair growth improvements.

With that said, investigation groups do have some ideas what might be going on. In particular, there are (at least) three suspected ways minoxidil might regrow hair: its activity as a vasodilator, as well as its anti-inflammatory and anti-androgenic effects.

We’ll explore arguments for and against each hypothesis – all to elucidate why there’s still debate.

Hypothesis #1: Vasodilation (i.e, Increased Blood Flow)

The hypothesis: minoxidil improves blood, oxygen, and nutrient transport to balding hair follicles – which stimulates more robust hair growth.

Argument For

Minoxidil opens potassium ion channels, which improves circulation in microvascular networks. These potassium channels are located in a variety of places – including the muscles of peripheral arteries and within and nearby the hair follicles themselves.^[4]https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6691938/^[5]https://faseb.onlinelibrary.wiley.com/doi/epdf/10.1096/fj.07-099424

The human scalp has a broad network of blood vessels, and is considered one of the most densely vascularized regions of the body. However, as AGA progresses, balding scalp regions undergo a loss of blood supply. For instance, clinical studies have shown 40% declines in transcutaneous oxygen levels in frontal balding regions versus non-balding controls.^[6]https://pubmed.ncbi.nlm.nih.gov/8628793/ Similarly, another study found that subcutaneous blood flow is 2.6x lower in balding versus non-balding scalps.^[7]https://www.jidonline.org/article/0022-202X(89)90189-9/pdf

Whether reduced blood supply is a cause or effect of the balding process is still debated – with research groups arguing both sides. However, current consensus is that if blood flow is causally linked to pattern hair loss, it is probably a secondary contributor to the balding process – rather than its root cause.

So, if minoxidil increases blood vessel diameters by opening potassium ion channels, more blood, oxygen, and nutrients might reach hair follicles and thereby lead to more robust hair growth.^[8]https://pubmed.ncbi.nlm.nih.gov/22409453/

Studies using Doppler devices (a measurement tool for blood flow) showed that minoxidil appears to do this. Specifically, minoxidil improve microvascular vasodilation in skin tissues supporting hair follicles, and that these improvements coincide with hair growth.^[9]https://pubmed.ncbi.nlm.nih.gov/10233226/

Other studies have found that minoxidil application grows new blood vessel openings surrounding the hair follicles themselves – a term known as fenestration.^[10]https://pubmed.ncbi.nlm.nih.gov/10233226/ Fenestration is a process supporting angiogenesis, or the growth and formation of new blood vessel networks.

Therefore, mechanistic, animal, and clinical data all suggest that minoxidil might work by improving blood flow to balding regions – and that this might be the main mechanism by which minoxidil regrows hair.

Argument Against

There are three main counterarguments to the idea that minoxidil might regrow hair by improving blood flow to balding regions:

1. Reduced blood flow is likely a consequence of androgenic alopecia, rather than a cause.

While minoxidil might increase blood flow, reductions to blood flow are not considered to be the fundamental driver of AGA. Instead, the evidence most strongly supports that the overwhelming majority of reductions to blood flow that occurs during the progression of AGA is a consequence of hair cycle-mediated hair follicle miniaturization, rather than a cause of hair loss.Because of the conflation of cause-and-effect, improving circulation to thinning regions cannot be the main way in which minoxidil regrows hair – much like an increase in ice cream sales is not the cause of more shark attacks, despite both being correlated. Instead, there must be some other unidentified variable at play (in the case of ice cream sales and shark attacks, it’s “nice weather”).Therefore, minoxidil must be working to regrow hair through some other mechanism outside of increased blood flow.

2. If minoxidil works primarily by increasing blood supply, why don’t other vasodilating medications also regrow hair?

If increasing blood circulation were truly a plausible treatment target for androgenic alopecia, why don’t other antihypertensive medications regrow hair? Why is it only minoxidil?This is further evidence that minoxidil probably doesn’t work primarily through increasing blood supply to miniaturized hairs. There must be some other mechanism at play.

3. Minoxidil has other suspected mechanisms beyond circulation enhancements.

These mechanisms include, but are not limited to, prostaglandin modulation and anti-androgenic effects – the latter of which is far closer to the suspected root cause of androgenic alopecia: dihydrotestosterone (DHT), a hormone that is causally associated with the balding process.

Altogether, these three arguments form the basis by which some people reject the idea that minoxidil works primarily through increasing blood supply. But – as is the case with many topics in hair loss research – the science isn’t completely settled, because there also counterpoints to each of the above counterarguments.

Rebuttals

While the case against minoxidil working through vasodilation might appear strong, there are also compelling rebuttals to each of the counterpoints raised.

1. “Reduced blood flow is likely a consequence of androgenic alopecia, rather than a cause.”

This can be true, and simultaneously, it can also be true that targeting secondary contributors to AGA – like reductions to blood supply – can still promote hair growth.This has even been demonstrated in the context of human hair loss, whereby targeting to reduce factors such as inflammation in the infundibulum (which is believed to be partly caused by microorganisms) and/or inflammation near the dermal papillae (which is believed to be driven by the hormone DHT) in AGA patients can still improve hair growth outcomes – even without necessarily resolving the root cause(s) of that inflammation.Moreover, despite minoxidil being an FDA-approved to treat AGA, its effects on hair growth are relatively mild – particularly in the long-run – whereby hair density improvements from minoxidil start trending downward after the first year of use. The steepness of minoxidil’s downward slope is not matched by other treatments like finasteride, which directly lower scalp DHT levels and, in doing so, lead to longer-term hair gains – probably because of the drug’s ability to address factors closer to the “root cause” of AGA.

Therefore, minoxidil’s mild and long-run diminishing effects on hair growth actually support the idea that the drug targets an accelerator or secondary contributor to the balding process – rather than something closer to its root cause. There is enough alignment in mechanistic, animal, and clinical data on minoxidil to suggest that this might be increased blood supply via fenestration of vascular networks nearby hair follicles.

2. “If minoxidil works primarily by increasing blood supply, why don’t other vasodilating medications also regrow hair?”

Other anti-hypertensive medications do improve hair growth in humans. So at the outset, this counterargument makes no sense.Studies have shown that medications like diazoxide and pinacidil also increase blood flow by opening the same potassium ion channels as minoxidil, and also promote hair growth in humans.^[11]https://faseb.onlinelibrary.wiley.com/doi/epdf/10.1096/fj.07-099424^[12]https://www.karger.com/Article/Pdf/248368^[13]https://journals.lww.com/cardiovascularpharm/abstract/1988/12002/clinical_pharmacology_of_pinacidil,_a_prototype.8.aspx^[14]https://www.sciencedirect.com/science/article/pii/S0022202X9290089M

This is important, because it suggests that the mechanism of vasodilation – i.e., opening potassium ion channels – likely matters for hair growth. Because in mechanistic and animal studies, vasodilation stimulated by opening potassium ion channels seems to also enhance the vasculature surrounding the hair follicles and the fenestration of microvascular networks, whereas other vasodilating medications working through other mechanisms might not achieve the same effect.

This is because other anti-hypertensive medications do not all target potassium ion channels. Therefore, other anti-hypertensive medications will not always have the same magnitude of effect on vasodilation as minoxidil, nor will they always influence vasodilation in areas relevant to hair growth – like the microvascular regions of the scalp skin.

For an example, just see our article on peppermint oil for hair growth – in which we reviewed research showing that menthol (which is widely labeled as a “vasodilator”) happens to cause vasodilation in the vascular endothelium but vasoconstriction in vascular smooth muscle tissues.

This degree of specificity matters, but the nuance tends to get left behind by people blindly assuming that all vasodilation medications must improve hair growth in order for vasodilation to be a worthy mechanism of action by which minoxidil might work.

That’s not a reasonable assumption. Depending on the medication, dosing schedule, delivery method, and regions of application – anti-hypertensive compounds can have a range of blood flow-related effects across organ sites, arteries, veins, and microvascular networks – some of which are paradoxical.

3. “Minoxidil has other suspected mechanisms beyond circulation enhancements.”

This is true. It is also true that these mechanisms might also contribute to minoxidil’s hair growth-promoting effects. However, these mechanisms of action remain speculative, and they are supported by low-quality studies (and conflicting research) regarding their plausibility.Therefore, the existence of this speculation does not disprove the possibility that minoxidil might still work through vascular fenestration of AGA-affected hair follicles. All mechanisms can simultaneously contribute to hair growth; there need not be a “one versus the other” mentality.

Hypothesis #2: Prostaglandin Modulation

The hypothesis: minoxidil modifies prostaglandin activity, and in doing so, reduces inflammation in balding regions.

Argument For

Prostaglandins are fatty acid derivatives that come from our ingestion of omega 6 fatty acids. These lipid derivatives can have hormone-like effects on the body, and are often involved in inflammatory processes. Specifically, prostaglandins tend to increase in response to tissue damage or infection – with different prostaglandins playing roles in both inflammation generation and inflammation resolution.

In 2012, a renowned research team from the University of Pennsylvania demonstrated that prostaglandin D2 (PGD2) and prostaglandin J2 (PGJ2) were elevated in balding regions, and that in mouse models, prostaglandin D2 inhibited hair lengthening.^[15]https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3319975/^[16]https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3982925/

Moreover, research from more than a decade prior had demonstrated that minoxidil appears to enhance the activity of prostaglandins associated with the growth phase of the hair cycle, and perhaps dampen prostaglandins associated with hair loss.^[17]https://pubmed.ncbi.nlm.nih.gov/9008235/

For these reasons, some researchers now believe that prostaglandin modifications are perhaps one of the ways in which minoxidil might regrow hair. In modifying prostaglandin activity, minoxidil might lower inflammation within certain hair follicle sites and, in doing so, improve hair growth outcomes.

Argument Against

When Garza et al.’s 2012 study on prostaglandin D2 was published, hair loss forums were enthralled with the possibility of developing and/or repurposing a new class of treatments for AGA: prostaglandin analogues. Excitingly, a drug developed to inhibit prostaglandin D2-mediated inflammation – setipiprant – was already undergoing clinical trials to treat asthma. As such, the drug developers repurposed the drug and began a clinical trial to see if it would also help fighting hair loss from AGA.

In 2021, the clinical trial evaluating setipiprant as a hair loss treatment was quietly published, and without a major press release. The results: the drug was well tolerated, but it did not work. Specifically, it produced no statistically significant effects on hair parameters versus the placebo group, whereas the study’s positive treatment-control group (who were taking oral finasteride) saw improvements to hair counts throughout the duration of the study.^[18]https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8526366/

Over the last two decades, other drugs with prostaglandin-modulating activities have also been tested to treat AGA – such as latanoprost and bimatoprost. While some clinical studies show a mild effect, these studies are poorly designed: they tend to have small sample sizes and poor methods (or no methods) of randomization for participants; they tend to include participants with other hair loss disorders in addition to AGA; and they tend to show relatively low response rates across participants, despite some endpoints achieving statistical significance.^[19]https://my.perfecthairhealth.com/courses/latanoprost/ This makes it difficult to ascertain any true effects on prostaglandin modulation for AGA – if any.

Finally, follow-up studies conducted by Garza et al. (and other research groups) have actually found conflicting results regarding the presence of prostaglandins throughout the progression of AGA – with some studies showing elevated pro-inflammatory and anti-inflammatory prostaglandin levels only during specific stages of the hair cycle or specific stages of AGA’s progression.^[20]https://pubmed.ncbi.nlm.nih.gov/33854354/

Altogether, these findings have significantly dampened excitement surrounding prostaglandin activity as an effective treatment target for AGA.

Rebuttals

Much like it is irresponsible to group together all anti-hypertensive medications as having the same effects on hair growth, we must also not make the same mistake by lumping together all prostaglandin analogues – setipiprant, latanoprost, bimatoprost, minoxidil, and more.

In other words, just because setipiprant failed its phase II clinical trials on AGA, and just because latanoprost appears to be inferior to minoxidil in terms of hair growth, this does not automatically mean that we can dismiss the possibility of prostaglandin modification as a potential treatment target for AGA, nor can we fully dismiss the idea that minoxidil does not work through prostaglandin modification.

Hypothesis #3: Androgen Receptor Antagonization

The hypothesis: minoxidil may reduce androgen activity in the scalp skin, and in doing so, regrow hair.

Argument For

An in vitro study published in 2014 suggested that minoxidil might make androgen receptor pathways less stable – thereby acting as a mild androgen receptor antagonist and/or anti-androgen (at least in cell culture studies).^[21]https://pubmed.ncbi.nlm.nih.gov/24742982/

Overwhelming evidence implicates the hormone DHT as causally associated with the balding process. Drugs like finasteride lower DHT levels in the scalp, and in doing so, consistently improve AGA outcomes across dozens of studies spanning tens of thousands of participants.

If the results of this in vitro study hold true in vivo, this would suggest that minoxidil might help lower hormones in the scalp that are causally associated with the balding process. In doing so, minoxidil might actually target hormonal causes of hair loss – even though the drug isn’t believed to change hormonal profiles in the (serum) blood or elicit significant anti-androgenic effects elsewhere throughout the body.^[22]https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6691938/

Argument Against

This 2014 in vitro study conflicts with other studies exploring whether minoxidil has anti-androgenic effects.

For instance, a 1987 study and a 2017 study both found that minoxidil doesn’t appear to affect androgens – with the latter study suggesting that minoxidil may even enhance androgenic activity in the scalp.^[23]https://pubmed.ncbi.nlm.nih.gov/3800423/^[24]https://pubmed.ncbi.nlm.nih.gov/30064598/

Therefore, it can just as easily be argued that minoxidil enhances androgenic activity in the scalp skin, rather than inhibits it.

Rebuttals

To our knowledge, there aren’t any strong rebuttals to these counterpoints. With such little evidence existing on this subject – and with the existing studies finding conflicting results – the jury is still out on whether minoxidil has any anti-androgenic effects at all.

Final Thoughts

The way in which minoxidil grows hair is still up for debate.

To date, there are (at least) three leading hypotheses, all of which have their problems:

1. Increased microcirculation to balding regions through vascular fenestration
2. Prostaglandin modulation – specifically related to PGE2
3. Anti-androgenic activity

What’s important to note is that there is not enough evidence to dismiss any of these suspected mechanisms. As such, all of them are still in the running, and all of them might contribute toward minoxidil hair growth-promoting effects.

With more research, we’ll hopefully have a final answer. And if we ever do, we’ll update this article with more information.

As we can see from the following chart, a doubling of the daily dose had a dramatic effect on serum DHT reductions.

Which Factors Influence How Often We Can Use Topical Finasteride?

If it isn’t already obvious, it’s impossible to answer the question, “Can I use topical finasteride less than once-daily?” without more context.

Each of the variables we’ve mentioned is critically important, because minor differences in any variable can dramatically change your total weekly finasteride exposure, and thereby the actual effectiveness of the drug.

This is particularly important for those who are trying to build a topical finasteride application schedule that prevents inadvertent exposure to family members, or for those who are opting for topical finasteride to lower their risk of side effects.

So, here’s a recap of the five critical factors influencing how much topical finasteride will actually penetrate into the scalp skin:

1. Topical Dilution (i.e., % finasteride). The higher the dilution, the less frequently you need to apply topical finasteride.
2. Carrier Vehicles (i.e., liposomes, alcohol, etc.). Liposomal vehicles are significantly less effective versus alcohol.
3. Application Dose (i.e., how many mL you apply each time). The higher the mL applied, the more drug exposure.
4. Application Frequency (i.e., how often you apply). The more frequent the application, the more drug exposure.
5. Scalp Contact Time (i.e., how many hours before washing out?). This is influenced by your % dilution and carrier vehicles.

Moreover, there’s a sixth factor that hasn’t yet gotten discussed: adjuvant treatments alongside topical finasteride.

If you’re combining topical finasteride with other ingredients or therapies that augment skin penetrability – i.e., retinoic acid, topical corticosteroids, or even microneedling – then you can expect more of the drug to penetrate the skin over the same time period.

That’s because these therapies wear down the stratum corneum (i.e. the outermost layer of skin), decrease the side of the epidermis, or create channels into the dermis for better drug penetration – all of which influence topical drug absorption.

What’s The Minimum Days Per Week I Can Apply Topical Finasteride?

To reiterate: the answer depends entirely on your topical dilution, carrier vehicles, application dose, how long you leave in that topical before washing it out, and your use of adjuvant therapies alongside topical finasteride.

Moreover, if someone isn’t experiencing side effects from finasteride, or if someone isn’t trying to limit other household members’ inadvertent exposure to the drug, then it doesn’t make much sense to adopt an alternate dosing schedule. It just introduces a level of complexity to your life that is, largely, unnecessary.

Nonetheless, if you are troubleshooting side effects, trying to limit a loved one’s inadvertent exposure to the drug, or simply traveling and wondering how long you can stop using topical finasteride before your hair starts falling out, you can lower your dosing frequency without necessarily hurting your hair gains.

The exact strategy will depend on why you’re doing this. For instance:

• If you’re troubleshooting side effects, you’ll likely want to lower your total weekly drug exposure. This is because total finasteride exposure is tied to side effect risks.
• If you don’t have any side effects, but you’re just trying to limit the amount of time you’re wearing topical finasteride around a partner, pregnant person, or family member – you may not want to lower your total weekly drug exposure. Instead, you may want to increase the dilution of your finasteride by a factor of 2x or more, but decrease the amount of time you wear in-the-house by washing it out more frequently, or only applying it on certain days of the week.
• If you don’t want to take topical finasteride with you on a vacation, chances are you can stop using it for 1-2 weeks (or more) without seeing much of a negative effect. After all, oral dosing studies showed that every-other-month daily doses were just as effective as every-month daily doses in the second year of use. Just make sure you reach scalp skin saturation points for finasteride before opting for this strategy – which you can likely achieve after ~30 days worth of applications.

Oral finasteride is a drug that helps lower levels of dihydrotestosterone (DHT) – the hormone causally associated with androgenic alopecia (AGA). Since 1997, the FDA has approved oral finasteride at 1 mg daily doses to treat AGA.^[1]https://www.ncbi.nlm.nih.gov/books/NBK513329/

Having said that, clinical studies also suggest that daily doses of finasteride as low as 0.2 mg can reduce nearly as much DHT as 1.0 mg daily, and lead to similar hair count improvements.^[2]europepmc.org/article/med/15319158

For these reasons, many finasteride users have wondered why physicians routinely prescribe 1 mg pills when they can potentially reap the same hair gains with 0.2 mg, or 1/5th the total drug exposure.

In this article, we’ll explore the science behind finasteride’s dosing, and if alternate dosing schedules make sense.

What’s the Ideal Oral Finasteride Dosage For Hair Growth?

In pharmaceutical settings, ideal doses are determined based on the perfect intersection whereby a drug maximizes benefit while minimizing side effects. For finasteride, that would be the dose that maximizes DHT reduction (and thereby hair regrowth) while minimizing the risk of adverse events.

To determine what this dose is, investigators must conduct a range of dosing studies on finasteride for the treatment of AGA – and then measure hair parameter outcomes against any perceived side effects.

Luckily for us, these studies have already been conducted.

Finasteride’s dose-dependent effects on serum DHT

Finasteride is a drug that lowers levels of the hormone DHT – which is causally linked to the balding process in men and women with androgenic alopecia.

A 1999 study sought to determine the effects of finasteride on DHT levels in the blood and scalp, depending on the dose someone took: 0.01 mg, 0.2 mg, 0.05 mg, 1.0 mg, or 5.0 mg.^[3]https://pubmed.ncbi.nlm.nih.gov/10495374/

The investigators found that finasteride had what’s known as a logarithmic, dose-dependent effect on DHT reduction. That’s just a fancy way of saying that a little finasteride had nearly the same effect on DHT as a lot of finasteride – and that with higher doses, the marginal reduction of DHT got smaller and smaller.

For instance, the above chart shows that while 0.01 mg daily of finasteride barely reduces any DHT, 0.2 mg daily reduces almost as much as DHT as 5 mg daily – even though 5 mg of finasteride 25x higher than the 0.2 mg dose.

Thus, the investigators concluded:

“In this study, doses of finasteride as low as 0.2 mg per day maximally decreased both scalp skin and serum DHT levels. These data support the rationale used to conduct clinical trials in men with male pattern hair loss at doses of finasteride between 0.2 and 5 mg.”

Interestingly, finasteride’s phase III clinical trials (which granted the drug FDA approval) tested a dose of 1 mg daily – and with impressive results on hair count parameters and a relatively low rate of reported side effects versus placebo.^[4]https://pubmed.ncbi.nlm.nih.gov/9777765/

But what about lower daily doses of finasteride? Might those also work to regrow hair – all while reducing drug exposure and perhaps side effects?

According to small clinical studies, yes – albeit with caveats.

Finasteride: dose-dependent effects on hair counts & side events

While the evidence is limited, there have been a handful of small clinical trials comparing different daily doses of finasteride on hair counts (and side effects) in men with androgenic alopecia.

One study tested daily doses of finasteride at 0.01 mg, 0.2 mg, 1.0 mg, and 5.0 mg versus placebo for 1-2 years. The researchers found that doses at or above 0.2 mg daily were effective at regrowing hair versus placebo, but that doses of 1.0 mg to 5.0 mg were directionally superior versus 0.2 mg doses.^[5]https://pubmed.ncbi.nlm.nih.gov/10495375/

Just see this chart for a breakdown of the numbers:

Moreover, here’s a chart visualizing the differences in hair counts across the full two years:

So, what about adverse events? That same study concluded:

“The incidence of these side effects with finasteride therapy was generally comparable to that observed with treatment with placebo, and there was no evidence of dose dependency or increased incidence with longer therapy out to 12 months. In addition, these side effects ceased in some patients while they continued to receive finasteride.”

In other words, the authors of the study found that while 1mg daily doses of finasteride produced directionally better – but not statistically significantly better – hair count improvements, these improvements did not come at the expense of a higher rate of side effects.

Thus, the investigators concluded that 1mg daily of finasteride was probably the best dose for treating androgenic alopecia.

Having said that, other studies haven’t shared the exact same conclusions.

For instance, a 2004 study on 414 Japanese men found that 1.0 mg daily doses of finasteride produced “numerically superior” results versus 0.2 mg daily, but that 1.0 mg daily doses also came with a numerically superior risk of side effects.^[6]https://www.researchgate.net/publication/8392775_Finasteride_in_the_treatment_of_Japanese_men_with_male_pattern_hair_loss

Similar to the other finasteride dosing study, none of the differences in hair count changes or side effect incidences were statistically significant. Nonetheless, the investigators felt the differences in results were still strong enough to note in the conclusions of their study.

Summary (so far)

Based on the totality of data currently available, this leads us to believe the following:

1. DHT reduction. Finasteride daily doses of 0.2 mg, 1.0 mg, and 5.0 mg all reduce nearly the same amount of DHT in the body.
2. Hair counts. Compared to 0.2 mg doses, 1.0 mg and 5.0 mg doses of finasteride result in directionally better hair counts over 1-2 years.
3. Side effects. Compared to 0.2 mg doses, 1.0 mg and 5.0 mg may also come with a directionally higher risk (or magnitude) of side effects.

So, if we choose to lean into these directional (but not statistically significant) results and believe that lower doses of finasteride come with a lower risk of side effects, the next question becomes: “How infrequently can I use finasteride and still see hair gains?”

Can I Use Finasteride Less Than Once Daily?

The answer depends on a number of factors, including finasteride’s:

• Terminal half-life (i.e., how long it takes for 50% of the drug to become inactivated)
• Tissue dissociation timing (i.e., how long it takes for finasteride to leave skin tissues)
• Biological half-life (i.e., how long it takes for finasteride’s effect on DHT to get cut in half)

We’ve covered these topics in great detail inside the following articles. For more information, please read:

• How Long Does Finasteride Stay In The Bloodstream?
• How Long Does Finasteride Stay In Scalp Tissues?

For now, here are the key takeaways from the literature:

1. Finasteride has a terminal half-life of 5-7 hours.
2. After multiple daily doses, finasteride reaches a tissue dissociation timing of 4-5 days.
3. Due to both of the above, finasteride’s effects on DHT suppression can remain for up to 14-30 days after quitting the drug.

On that note, one dosing study on finasteride found that after a year of daily use, every-other-month dosing of 1 mg daily of finasteride was just as effect as once-daily dosing – despite users in the first group using the drug for a total of 6 versus 12 months throughout the same year.^[7]https://jaad.org/retrieve/pii/S0190962220319289

Again, this is because finasteride’s effects don’t immediately dissipate upon cessation of the drug. They can last up to 14-30 days from the last dose – at least after reaching a certain saturation point in the body (which often requires a handful of days of use at 1 mg daily).

With all of this in mind, finasteride users who are interested in (1) achieving some hair gains, and (2) minimizing their drug exposure – all in hopes of lowering their risk of side effects – may be able to achieve this by reducing their dosing schedule of finasteride.

Alternate Dosing Schedules For Finasteride

To best conceptualize this, it’s easier to think of finasteride dosing in terms of weekly exposure levels, rather than daily. This is because finasteride’s effects on DHT can accumulate across doses, and because lower doses tend to have a similar impact on DHT as higher doses (up to a point).

For instance, those studies showing statistically equivalent efficacy of 0.2 mg versus 1.0 mg daily of finasteride represented dosing difference of 1.4 mg versus 7.0 mg weekly of finasteride.

So, how can we take into account finasteride’s biological half-life to build an alternate dosing schedule that might help support hair growth, albeit with a lower overall drug exposure?

We can likely do so by trying a finasteride dosing schedule of 0.5 mg, 3x weekly.

For most people, that would involve taking 0.5 mg of finasteride every Monday, Wednesday, and Friday. That’s ~1.5 mg weekly of exposure, which is roughly the same as 0.2 mg daily (or 1.4 mg weekly).

In that regard, you can achieve this by simply getting a standard prescription of finasteride for 1.0 mg daily. Companies like Hims, Keeps, and Roman (no affiliation!) often offer these bundled in 90-day supply.

Then, you can cancel that subscription product, buy a pill cutter, and just cut the pills in half.

You can take one-half pill every Monday, Wednesday, and Friday – which equates to 1.5 pills weekly.

If you received a 90-day supply of 1.0 mg daily of finasteride from any of these companies, this alternate dosing schedule should last you a total of 60 weeks – which is more than a year.

With this alternate dosing schedule, you also reduce your total costs of finasteride treatment to just a few dollars per month. So for those who are financially constrained, it’s potentially a wonderful option.

Whether or not these lower doses actually worsen hair count outcomes or lower side effect risks is still up for debate. Nonetheless, this reduced dosing schedule should – at a minimum – lower your overall drug exposure. For this reason, this alternate dosing schedule is also included as part of our guide on troubleshooting finasteride-related side effects.

We hope this article helps. If you’re looking for personal support on hair growth journey, you can receive personalized support and work with our team of researchers directly inside our membership community.